Children's health

and the environment

GLOBAL PERSPECTIV
Edited by
J. Pronczuk-Garbino, MD

( . ) World Health
'\.~ Organization
~
 Children's health
and the environment
A global perspective
A RESOURCE MANUAL
FOR THE HEALTH SECTOR

J. Pronczuk-Garbino, MD
Editor-i n-Chief

tf;_'~~
~~ ~I' i!!~
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World Health
Organization
GENEVA
200 5

,
WHO Library Cataloguing-in-Publication Data

Children ' s health and the environment: a global perspective: a resource manual
for the health sector / J. Pronczuk-Garbino, editor-in-chief.

1.Child welfare 2.Environmental health 3.Environmental pollution

4.Manuals I.Pronczuk-Garbino, Jenny.

ISBN 9241562927 (NLM classsification: WA 320)

© World Health Organization 2005

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Contents
Acknowledgements vi
Preface vii

Section I. Introduction

Chapter 1. Children are not little adults

P. J. Landrigan and A. Garg 3
Chapter 2. Windows of susceptibility to environmental
exposures in children
S. G. Selevan, C. A. Kimmel and P. Mendola 17

Section II. How and when exposure occurs 27

Chapter 3. Where the child lives and plays
N. Chaudhuri and L. Fruchtengarten 29
Chapter 4. Where the child learns
J. Pronczuk
Chapter 5. Where the child works
M. Tennassee
Chapter 6. Where the child is under extreme stress
R. Bu-Hakah 54
Chapter 7. When the child uses alcohol and other drugs
M. Monteiro

Section III. Specific environmental threats: sources of exposure and

health effects 69
Chapter 8. Water quality
T. Boonyakarnkul, P. A. Kingston and K. M. Shea 71
Chapter 9. Sanitation and hygiene
J. Hueb 95
Chapter Air
10.
R. A. Etzel and K. Balakrishnan 107
Chapter 11. Foodborne hazards of particular concern for the young
D. B. Mahoney and G. C. Moy 133
Chapter 12. Poisonings and envenomings
I. Makalinao and A. D. Woolf 153
Chapter 13. Unintentional injuries in children
T. Guthrie, K. McGee and M. M. Thein 177
Chapter 14. Ionizing radiation
L. Kheifets and M. Repacholi 18 7
Chapter 15. Noise
C. F. Bearer 194
Chapter 16. Global environmental change and child health
A. J. McMichael, S. Bunyavanich and P. R. Epstein 202

iii
 Chapter 17. Emerging environmental threats: endocrine-disrupting
chemicals
T. Damstra 21 7

Section IV. The paediatric environmental history 225

Chapter 18. Paediatric environmental history-taking in developing

countries
J. Pronczuk 227
Chapter 19. The clinical environmental history: experience of
the USA
~J.&~ ~o

Section V. Taking action

Chapter 20. Taking action to protect children from environmental

hazards
S. Boese-O'Reilly and M. K. E. Shimkin 253

Section VI. Case studies 273

Chapter 21. Case studies 275

1. Thiomersal in children's vaccines-the
response of the United States
C. J. Clements 275
2. Silicosis among children in the agate industry
H. N. Saiyed 279
3. Protection against the sun in schools
S. Harper 28 3
4. Prevention of asbestos-related diseases-the
Finnish approach
A. Karjalainen 288
5. Informal markets of Tegucigalpa, Honduras:
adolescent participation in market clean-up
campaign
D. C. Kaminsky
6. Arsenic exposure and child health
M. Rahman 294
7. Household water treatment: a success story
J. T. Macy and R. E. Quick 299
8. Contaminated water distribution: an intervention
strategy to solve a public health problem
J. c. Semenza 30 3
9. A fiuorotic village
E. Dahi 306
10. Carbon monoxide poisoning in children in France
M. Mathieu-Nolf 30 9
11. Children deserve a smoke-free world
A. M. David, S. A. Tamplin and S. Pineda-Mercado 313

iv CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

 12. Improvement in respiratory symptoms in children
as a result of pollution control strategies in a
district of the city of Sao Paulo, Brazil
H. Ribeiro 316
13· Air pollution and pregnancy outcome
R. Sram 320
14· Asthma case study
G. W. K. Wong 323
15· Infant exposure to organochlorine contaminants
in breast milk
G. G. Moy 325
16. Escherichia coli 0157:H7 outbreak in Japanese
schoolchildren
H. Toyofuku and F. Kasuga 33 0
17· Health hazards of pesticide use: studies by Thai
schoolchildren
S. Wichanee, M. Tianponkrang, M. Jakiet and
H. Murphy 334
18. Psychosocial status and somatic outcomes
among the younger population of the Ukraine
affected by the Chernobyl nuclear plant accident
N. Korol 33 8
19· Hospitalization for asthma in children living near
an iron foundry in the United Kingdom
B. Olowokure, P. J. Saunders, R. C. Wilson and
R. L. Smith 342
20. An environmental education and research
learning programme: South Texas Environmental
Education and Research (STEER) 345

Index
347

CONTENTS v
Acknowledgements
The World Health Organization gratefully acknowledges the contributions of
many experts from around the world who framed the concept of this resource
manual, authored the various chapters, reviewed text, edited and designed the
publication, and provided invaluable advice during the long preparation
process.
The inspiration provided by the "green book" (Handbook of pediatric envi·
ronmental health) of the American Academy of Pediatrics (AAP) was pivotal for
this initiative, which was indeed strongly supported by AAP members, especially
by Dr Ruth Etzel, Dr Sophie Balk and Dr Kathy Shea. The advice provided by
WHO colleagues dealing with different aspects of human environmental health
was crucial in the initial conception of this manual, and is deeply appreciated.
We are very thankful to Dr Terri Damstra, who was always ready to provide new
ideas, inspiration and support. Ms Martha Shimkin worked with enthusiasm on
this manual, dealing with problems and always finding a solution. Thanks to
her encouragement and support, this project became a reality. We are especially
grateful to Dr Sonja Junge, who managed to recruit potential authors and follow
up until their manuscripts were produced and received in WHO and who sup-
ported this initiative up to its culmination. Ms Eva Rehfuess collected and col·
lated all the case studies in record time and her contribution is highly
appreciated. We are thankful to Ms Anne Marie Pfister for compiling the rough
first manuscripts; to Ms Caron Gibson who formatted texts and prepared
vignettes, and to Dr Cesar Chelala who reviewed the text. Ms Maya Kanetsuka
helped with enthusiasm during the final stages of preparation, and Dr Pat Butler
provided substantial editorial input, with great insight and personal dedication.
The support provided by the United States Environmental Protection Agency
(US EPA) to the preparation and publication of this manual is deeply appreci·
ated. Our thanks go to Ms Martha Berger, who envisioned the need for such
materials and for transferring knowledge and experience across the world.
We appreciate the efforts of all those who in one way or another contributed
to the production of the manual, and regret any omissions that may have
occurred. Our deep thanks go to all the authors, co-authors and reviewers from
different parts of the world who freely offered their precious time, work, experi.
ence and effort for the benefit of colleagues in the health sector, and overall for
the benefit of children everywhere.

Jenny Pronczuk de Garbino, MD

Editor-in-Chief

vi
Preface

Children face the excitement of a changing world, with many opportunities

and challenges; but they also encounter formidable barriers to their health,
development and well-being in the form of environmental threats. During recent
decades, new knowledge has emerged about the special vulnerability of children
to environmental risks in the places where they live, learn and grow. Children's
and adolescents' exposure to chemical, physical, and biological risks at home,
in school, in the playground, at work and elsewhere deserves our immediate
attention and needs to be recognized as an important threat to their develop-
ment and survival. Action to reduce the risks is required at global, regional and
national levels.
In 1999, a Task Force on Children's Environmental Health was set up by the
World Health Organization (WHO). Its activities culminated at the International
Conference on Children's Environmental Health: Hazards and Vulnerability, in
March 2002, with a pledge to promote action enunciated in the Bangkok State-
ment. WHO was urged to "incorporate children's environmental health into the
trainingfor health care providers and other professionals". At the World Summit on
Sustainable Development in September 2002, WHO called for a global move-
ment to create healthy environments for children. The proposal of a global
alliance was backed by many countries, as well as by representatives of non-
governmental organizations, the private sector, academia and international orga-
nizations. This worldwide call to action was the first of its kind, recognizing
children, both girls and boys, as the essence of sustainable development and
binding nations together in the search for healthy and safe lives for children.
As one of the action steps towards the protection of children's health and
environments, WHO has produced this resource manual for health care prac-
titioners. The manual, inspired by the American Academy of Pediatrics Hand-
book of pediatric environmental health (1999 and 2003), is intended as an
introductory resource tool for health care professionals around the world, and
especially in developing countries, who aim to increase their knowledge and
understanding of children and environmental health.
Health professionals in the "front line", dealing with children and adoles-
cents, and interacting with their families and communities, are well positioned
to recognize, investigate and help prevent environmentally related diseases.
They are in a strategic position to collect data, undertake research, stimulate
decision-makers to take action, and promote the education of family members
and the general public. This resource manual will enable health care providers
to playa proactive and preventive role and to assume their responsibilities,
expanding their horizons in the area of paediatrics, family and community
medicine.

vii
 While the design, content and compilation of the manual was coordinated
by WHO, the chapters have been contributed by experts in the field of paedi-
atric health and the environment. In most cases, the co-authors are from dif-
ferent parts of the world, sharing insights and expertise gained from their
professions, research activities and personal experiences. Each chapter was
reviewed by one or more experts in the field, as well as by WHO staff. Authors
verified their sources, made available at the end of each chapter, to provide
readers with additional sources of information. When possible, electronic
access has been encouraged, by provision of World Wide Web sites. WHO also
makes this publication available on its web site at www.who.intjceh.
With deepest appreciation of the many professionals who freely contributed
to this book in numerous ways, WHO is pleased to offer Children's health and
the environment as part of a concerted effort to increase the health, happiness,
and quality of life of our world's children.

viii CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

Introduction
 CHAPTER 1

Children are not little adults1

P. J. Landrigan
A. Garg
Center for Children's Health and the Environment,
Department of Community and Preventative Medicine,
Mount Sinai School of Medicine, New York, USA

Introduction
Children around the world today confront environmental hazards that were
neither known nor suspected a few decades ago. More than 80000 new syn·
thetic chemical compounds have been developed over the past 50 years. Chil·
dren are especially at risk of exposure to the 15000 of these chemicals produced
in quantities of 4500 kg or more per year, and to the more than 2800 chemicals
produced in quantities greater than 450000 kg per year. These high-production-
volume (HPV) chemicals are those most widely dispersed in air, water, food
crops, communities, waste sites and homes (1). Worldwide many thousands of
deaths occur as a result of poisoning, with the vast majority being among chil-
dren and adolescents after accidental exposure. Many hundreds of H PV chem-
icals have been tested for their potential human toxicity, but fewer than 20%
have been examined for their potential to cause developmental toxicity to
fetuses, infants, and children (1, 2).
Until about ten years ago, chemical exposure was principally a problem for
children in the developed countries. However, it is becoming a problem in devel-
oping countries as hazardous industries relocate there as a consequence of
globalization and in an effort to escape ever stricter labour and environmental
laws in the developed countries.
In addition to the hazards of new chemicals, children worldwide confront
traditional environmental hazards, including poor water quality and sanitation,
ambient and indoor air pollution, vector-borne diseases, unintentional injuries,
inadequate housing, and effects of climate variability and change.

Children's unique susceptibility

Children are highly vulnerable to environmental hazards for several reasons
(3, 4)· Children have disproportionately heavy exposures to environmental tox-
icants. In relation to body weight, children drink more water, eat more food, and
breathe more air than adults. Children in the first 6 months of life drink seven

'Reviewed by I. Makalinao, Department of Pharmacology and Toxicology, University of the

Philippines, College of Medicine, Manila, Philippines.

3
times as much water per kg of body weight and 1-5-year-old children eat 3-4
times more food per kg than the average adult. The air intake of a resting infant
is proportionally twice that of an adult. As a result, children will have substan-
tially heavier exposures than adults to any toxicants that are present in water,
food, or air. Two additional characteristics of children further magnify their expo-
sures: their hand-to-mouth behaviour, and the fact that they live and play close
to the ground.
Children's metabolic pathways, especially in the first months after birth, are
immature. Children's ability to metabolize, detoxify, and excrete many toxicants
is different from that of adults. In some cases, children may actually be better
able than adults to deal with some toxicants, e.g. paracetamol. Commonly,
however, they are less well able to deal with toxic chemicals and thus are more
vulnerable to them.
Children undergo rapid growth and development, and their developmental
processes are easily disrupted. The organ systems of infants and children
change very rapidly before birth, as well as in the first months and years of life.
These developing systems are very delicate and are not able to repair adequately
damage caused by environmental toxicants. Thus, if cells in an infant's
brain are destroyed by chemicals such as lead, mercury, or solvents, or if false
signals are sent to the developing reproductive organs by endocrine disruptors,
there is a high risk that the resulting dysfunction will be permanent and
irreversible.
Because children generally have more future years of life than adults, they
have more time to develop chronic diseases triggered by early exposures. Many
diseases that are caused by toxicants in the environment require decades to
develop. Many such diseases, including cancer and neurodegenerative diseases,
are now thought to arise through a series of stages that require years or even
decades from initiation to actual manifestation of disease. Carcinogenic and
toxic exposures sustained early in life, including prenatal exposures, appear
more likely to lead to disease than similar exposures encountered later.

Diseases in children possibly linked to environmental exposures

Children are exposed to a series of health risks from environmental hazards.
Environment-related illnesses are responsible for more than 4.7 million deaths
annually in children under the age of five (5). Both "basic" and traditional risks,
such as unsafe water, poor sanitation, indoor air pollution, poor food hygiene,
poor quality housing, inadequate waste disposal, vector-borne diseases and
hazards that cause accidents and injuries, as well as "modern" environmental
risks endanger children's health. Newly emerging environmental threats to the
health of children derive from high levels of natural or man-made toxic sub-
stances in the air, water, soil and food chain, global climate change and ozone
depletion, electromagnetic radiation and contamination by persistent organic
pollutants and chemicals that disrupt endocrine functions.

4 SECTION I: INTRODUCTION
 Environmental health
hazards Subclinical toxicity
The risks to children in their A critically important intellectual step in the
everyday environments are numer- development of understanding of children's
ous. But there are six groups of special susceptibility to chemical toxins has
environmental health hazards that been the recognition that environmental toxins
cause the bulk of environmentally can cause a range of adverse effects in children.
related deaths and disease among Some of these effects are clinically evident, but
children (12), as outlined below. others can be discerned only through special
testing and are not evident on the standard
Household water security examination-hence the term "subClinical toxi·
Contaminated water is the cause city". The underlying concept is that there is a
of many life-threatening diseases dose-dependent continuum of toxic effects, in
including diarrhoea, the second which clinically obvious effects have their sub-
biggest child-killer in the world. clinical counterparts (6, 1).
Diarrhoea is estimated to cause 1.3 The concept of subclinical toxicity has its origins
million child deaths per year-about in the pioneering studies of lead toxicity in
12% of total deaths of children clinicaHy asymptomatic children undertaken by
under five in developing countries. Herbert Needleman and colleagues (8). Needle-
Around the world, both biological man et at showed that children's exposure to
disease agents and chemical pollu- lead could cause decreased intelligence and
tants are compromising the quality altered behaviour, even in the absence of clini-
of drinking-water. Water contamina- cal symptoms of lead toxicity. The subclinical
tion can spread diseases such as toxicity of lead in children has subsequently
hepatitis B, dysentery, cholera and been confirmed in prospective epidemiological
typhoid fever. High levels of arsenic, studies (9). Similar subclinical neurotoxic ef-
lead or fluoride may lead to both fects have been documented in children exposed
acute and chronic diseases in in the womb to polychlorinated biphenyls
children. (PCBs) (10) and to methylmercury (11).

Hygiene and sanitation

Globally, 2.4 billion people, most of them living in periurban or rural areas
in developing countries, do not have access to any type of sanitation facilities.
Coverage estimates for 1990-2000 show that little progress was made during
this period in improving coverage. The lowest levels of service coverage are
found in Africa and Asia, where 48% and 31% of the rural populations, respec-
tively, do not have these services. Examples of sanitation-related diseases
include cholera, typhoid, schistosomiasis, and trachoma-a disease that causes
irreversible blindness, and currently affects about 6 million people, with another
500 million at risk of the disease.

1. CHILDREN ARE NOT LlTILE ADULTS

5
 Air pollution
Air pollution is a major environment-related health threat to children and a
risk factor for both acute and chronic respiratory disease as well as a range of
other diseases. Around 2 million children under five die every year from acute
respiratory infections (ARI) aggravated by environmental hazards. Indoor air
pollution is a major causal factor for ARI deaths in rural and urban areas of
developing countries. Outdoor air pollution, mainly from traffic and industrial
processes, remains a serious problem in cities throughout the world, particu-
larly in the ever-expanding megacities of developing countries. A major problem
is the continuing use of lead in petrol (13). It is estimated that a quarter of the
world's population is exposed to unhealthy concentrations of air pollutants such
as particulate matter, sulfur dioxide, and other chemicals.

Disease vectors
Numerous vector-borne diseases affect children's health. Their impact
varies in severity. Malaria is particularly widespread and dangerous, existing in
100 countries and accounting for more than 800000 deaths annually, mostly
in children under five. Schistosomiasis is a water-borne disease that mainly
affects children and adolescents, and is endemic in 74 developing countries.
Japanese encephalitis occurs only in south and south-east Asia, where it is
linked with irrigated rice production ecosystems. The annual number of clinical
cases is estimated at about 40000. Some 90% of cases are in children in
rural areas, and 1 in 5 of these children dies. Annual mortality due to dengue
is estimated at around 13000; more than 80% of these deaths occur in
children.

Chemical hazards
As a result of the increased production and use of chemicals, myriad chem-
ical hazards are nowadays present in children's homes, schools, playgrounds
and communities. Chemical pollutants are released into the environment by
uncontrolled industries or through leakage from toxic waste sites. In 2002 about
35 0000 people died as a result of poisoning, and 46000 were children and ado-
lescents exposed accidentally (www.who.intJevidenceJbod). Pesticides, clean-
ers, kerosene, solvents, pharmaceuticals and other products unsafely stored or
used at home are the most common causes of acute toxic exposure. Some result
in life-threatening poisoning. Chronic exposure to a number of persistent envi-
ronmental pollutants is linked to damage to the nervous and immune systems
and to effects on reproductive function and development, as exposure occurs
during periods of special susceptibility in the growing child or adolescent. Chil-
dren are quite vulnerable to the neurotoxic effects of lead in paint and air, which
may reduce their intelligence and cause learning disabilities and behavioural
problems, in particular reduced attentiveness. They are also vulnerable to the
developmental effects of mercury released into the environment or present as

6 SECTION I: INTRODUCTION
 a food contaminant. Another problem is asbestos, which is used extensively as
an insulator in the construction industry (14).

Injuries and accidents

In 2000 an estimated 685000 children under the age of 15 were killed by an
unintentional injury, accounting for approximately 20% of all such deaths
worldwide. Unintentional injuries are among the ten leading causes of death for
this age group. Worldwide, the leading causes of death from unintentional injury
among children are road traffic injuries and drowning, accounting for 21% and
19%, respectively. Unintentional injuries among children are a global problem,
but children and adolescents in certain regions of the world are disproportion-
ately affected. It is estimated that 98% of all unintentional injuries in children
occur in low- and middle-income countries, and 80% of all childhood deaths
from unintentional injuries occur in the African, South-East Asian and Western
Pacific regions.

Chronic effects of environmental hazards

Exposure to environmental hazards is known or suspected to be responsi-
ble for a series of acute and chronic diseases that, in the industrialized coun-
tries, have replaced infectious diseases as the principal causes of illness and
death in childhood.
Urbanization and pervasive poverty in developing countries aggravate both
"basic" and "modern" health risks. Developing countries therefore face a double
burden in paediatric environmental health.
The chronic diseases represent a "new paediatric morbidity", and include
the following.

Asthma
Asthma prevalence among children under 18 years of age has more than
doubled over the past decade in many industrialized and developed countries.
This increase is particularly evident in urban centres, where asthma has become
the leading cause of children's admissions to hospital and of school absen-
teeism (15, 16).
Ambient air pollutants, especially ground-level ozone and fine particulates
from automobile exhausts, appear to be important triggers of asthma. Asthma
incidence declines when levels of these pollutants drop (17). Indoor air pollu-
tion, including use of open fires for cooking and heating, insect dust, mites,
moulds and environmental tobacco smoke are additional triggers.
Sharp discrepancies in asthma by socioeconomic and racial or ethnic status
have been noted in certain countries. In New York City, hospital admission rates
for asthma are 21 times higher in the poorest communities than in the wealth-
iest ones (18). Globally, the International Study of Asthma and Allergies in Child-
hood (ISAAC) demonstrated a wide range in rates for symptoms of asthma. Up

1. CHILDREN ARE NOT LlTILE ADULTS

7
to 15-fold differences were found between countries, with a range of 2.1% to
4-4% in Albania, China, Greece, Indonesia, Romania and the Russian Federa-
tion, and 29.1% to 32.2% in Australia, New Zealand, Ireland and the United
Kingdom (19).

Childhood cancer
The reported incidence of cancer among children under 18 years of age in
the United States has increased substantially in the past 20 years (20). Indeed,
childhood cancer incidences around the world are on the rise. Industrialized
countries have succeeded in bringing the death rates from childhood cancer
down, thanks to improved treatment. Still, in the United States, the incidence
of acute lymphoblastic leukaemia (ALL), the most common childhood cancer,
increased by 27.4% from 1973 to 1990, from 2.8 cases per 100000 children to
3.5 per 100000. Since 1990, ALL incidence has declined in boys in the United
States, but continues to rise in girls. Between 1973 and 1994, incidence of
primary brain cancer (glioma) increased by 39.6%, with nearly equal increases
in boys and girls (21). In young white men, 20-39 years of age, although not in
black men, incidence of testicular cancer increased by 68%. The causes of these
increases are not known. In tropical Africa, Burkitt lymphoma is the most
common childhood malignancy. However, in Nigeria there was a marked
decrease in the relative frequency of Burkitt lymphoma from 37.1% in the period
1973 to 1990 to 19-4% between 1991 and 1999 which was seen partly as a con-
sequence of improved living conditions and greater control of malaria (22). The
risk of liver cancer is influenced by a number offactors; persistent infection with
the hepatitis B or C virus is strongly associated with this kind of malignancy.
Aflatoxins, one of the most potent mutagenic and carcinogenic mycotoxins, also
represent a major risk factor for hepatocellular carcinoma, especially in high-
incidence areas, i.e. south-east Asia and parts of Africa. Immunization against
hepatitis B or protection against hepatitis C and reduced aflatoxin exposure
would reduce the risk for liver cancer in these populations (23, 24)·

Lead poisoning
Countries that have succeeded in removing lead from petrol have accom-
plished a major public health goal that greatly benefits all citizens, especially
children. There have been significant studies of lead in blood before and after
elimination of lead from petrol in a number of industrialized countries. These
studies show conclusively a direct relationship between lead in petrol and lead
levels in children's blood. Still, even with the tremendous improvement in blood
lead levels in countries that have removed lead from petrol, there are other
sources of lead exposure. For example, in the USA, despite a 94% decline in
blood lead levels since 1976, an estimated 930000 preschool children in the
United States still have elevated blood lead levels (lOllgjdl or above) and suffer
from lead toxicity (25). These children are at risk of diminished intelligence,

8 SECTION I: INTRODUCTION
behavioural disorders, failure at school, delinquency, and diminished achieve-
ment (9). Rates of lead poisoning are highest in poor children from disadvan-
taged groups in urban centres. New immigrants to the United States are often
at high risk, because they tend to live in poor-quality housing, are not aware of
the dangers of lead-based paint, and may bring medications or cosmetics
containing lead from their home countries (25).
In the industrially developed countries, consumption of lead has decreased
sharply in the past two decades. This reduction reflects the phasing out of
leaded petrol and decreases in industrial use of lead (26). Major reductions in
human exposure and in population blood lead levels have resulted. By contrast,
in countries undergoing transition to industrialization, lead use in petrol as
well as in industry remains widespread, environmental contamination may be
intense, and blood lead levels in workers as well as in residents of communi-
ties near polluting industries have been reported to be dangerously elevated
(27-30). A study conducted in Romania examined lead levels in children from a
polluted municipality: only six children out of 42 had blood lead levels below
10Ilgjdl (27). A devastating experience in Trinidad and Tobago demonstrated
the impact of lead exposure on child health, in this case from battery recycling.
A six-year-old boy died from acute lead poisoning, with a blood lead level above
140llgjdl, and many children had to undergo chelating therapy and suffered
permanent damage from exposure to extremely high lead levels.

Developmental disorders
Developmental disorders, including autism, attention deficit disorder,
dyslexia and mental retardation affect 5-8% of the 4 million children born each
year in the United States (31). The causes are largely unknown, but exposure to
lead, mercury, PCBs, certain pesticides and other environmental neurotoxicants
are thought to contribute. An expert committee convened by the US National
Academy of Sciences concluded in July 2000 that 3% of all developmental dis-
orders in American children are the direct consequence of toxic environmental
exposures, and that another 25% are the result of interactions between envi-
ronmental factors and individual children's susceptibility (32).

Endocrine disruption
Endocrine disruptors are chemicals in the environment that have the capac-
ity to interfere with the body's hormonal Signalling system. The effects of these
chemicals have been well documented in experimental animals exposed in the
laboratory as well as in wildlife populations in contaminated ecosystems such
as the Great Lakes in North America.
While data on the human health effects of endocrine disruptors are still
scant, it would appear that the embryo, fetus and young child are at greatest
risk of adverse consequences following exposure to these chemicals, because
the human reproductive and endocrine systems undergo complex development

1. CHILDREN ARE NOT LlTILE ADULTS 9

in fetal life and thus are highly vulnerable to toxic influences. It is hypothesized,
but not proven, that endocrine·disrupting compounds may be responsible, at
least in part, for an increased incidence of testicular cancer, a reported doubling
in incidence of hypospadias (33) and the increasingly early onset of puberty in
young girls.

The international response to children's environmental health

The first major international development in children's environmental health
was the Declaration of the Environment Leaders of the Eight on Children's Envi-
ronmental Health, issued in Miami in 1997 by the group of highly industrialized
nations, the so-called G-8 (34). The Miami Declaration expressed the commit·
ment of these nations to children's environmental health and included specific
commitments to remove lead from petrol, to improve air quality, and to improve
the quality of drinking-water. The Declaration also called for improvements in
the scientific risk assessments that underpin environmental regulations to
explicitly incorporate children, and set forth international cooperation to do
further research on endocrine-disrupting chemicals. This Declaration has catal-
ysed developments in many international organizations and nongovernmental
organizations (NGOs).
In 2002, the World Health Organization (WHO) launched an initiative to
improve environmental protection of children, reflecting its major thrust at the
World Summit on Sustainable Development, which took place in Johannesburg,
South Africa. "Our top priority in health and development must be investing in
the future-in children and the young-a group that is particularly vulnerable
to environmental hazards," stated WHO's then Director-General, Dr Gro
Harlem Brundtland. She set forth the Healthy Environments for Children
Alliance which many international organizations, nations, NGOs and busi-
nesses have responded to and have begun to put into action.
A WHO working group on children's environmental health has been active
in bringing together participants from developed as well as developing coun-
tries since early 2000. The United Nations Environment Programme (UN EP),
the World Bank, and the United Nations Children's Fund (UNICEF) have joined
in partnership with WHO in these efforts.
The international community of NGOs is becoming active in children's envi·
ronmental health. An umbrella organization, the International Network of Chil-
dren's Environmental Health & Safety (INCHES), was formed to link grassroots
organizations in various countries. INCHES, in conjunction with a US NGO, the
Children's Environmental Health Network (CEH N) hosted a global conference
on children's environmental health in Washington in September 2001 to raise
international interest in children's environmental health. This was followed by
a WHO conference in Bangkok, Thailand, which considered environmental
threats to the health of children in South-East Asia and the Western Pacific (see
resulting statement below) (35). The Pan American Health Organization has

10 SECTION I: INTRODUCTION
developed a strategy to improve environmental health of children in the Amer-
icas and launched a regional workshop on children's environmental health in
200 3.

The Bangkok Statement

A pledge to promote the protection of Children's Environmental Health
We, the undersigned scientists, doctors and public health professionals, educators, envi-
ronmental health engineers, community workers and representatives from a number of inter-
national organizations, from governmental and non-governmental organizations in South
East Asian and Western Pacific countries, have come together with colleagues from differ-
ent parts of the world from 3 to 7 March 2002 in Bangkok, Thailand, to commit ourselves
to work jOintly towards the promotion and protection of children's health against environ-
mental threats.
Worldwide, it is estimated that more than one-Quarter of the global burden of disease (GBD)
can be attributed to environmental risk factors. Over 40% of the environmental disease
burden falls on children under 5 years of age, yet these constitute only 10% (jf the world
population. The environmental burden of pediatric disease in Asia and the Pacific countries
is not well recognized and needs to be Quantified and addressed.

We recognize
That a growing number of diseases in children have been linked to environmental exposures.
These range from the traditional waterborne, foodborne and vector-borne diseases and acute
respiratory infections to asthma, cancer, injuries, arsenicosis, fluorosis, certain birth defects
and developmental disabilities.
That environmental exposures are increasing in many countries in the region; that new
emerging risks are being identified; and that more and more children are being exposed to
unsafe environments where they are conceived and born, where they live, learn, play, work
and grow. Unique and permanent adverse health effects can occur when the embryo, fetus,
newborn, child and adolescent (collectively referred to as "children" from here onwards) are
exposed to environmental threats during early periods of special vulnerability.
That in developing countries the main environmental health problems affecting children are
exacerbated by poverty, illiteracy and malnutrition, and include: indoor and outdoor air pol-
lution, lack of access to safe water and sanitation, exposure to hazardous chemicals, acci-
dents and injuries. Furthermore, as countries industrialize, children become exposed to
toxicants commonly associated with the developed world, creating an additional environ-
mental burden of disease. This deserves special attention from the industrialized and devel-
oping countries alike.

1. CHILDREN ARE NOT LlTILE ADULTS 11

Box continued
That environmental hazards arise both from anthropogenic and natural sources (e.g. plant
toxins, fluoride, arsenic, radiations), which separately and in combination can cause serious
harm to children.
That restoring and protecting the integrity of the life-sustaining systems of the earth are inte-
gral to ensuring children's environmental health now and in the future. Therefore, address-
ing global changes such as human population growth, land and energy use patterns, habitat
destruction, biodiversity loss and climate change must be part of efforts to promote chil-
dren's environmental health.
That despite the rising concern of the scientific community and the education and social
sectors about environmental threats to children's health and development, progress has been
slow and serious challenges still remain.
That the health, environment and education sectors must take concerted action at all levels
(local, national, global), together with other sectors, in serious efforts to enable our coun-
tries to assess the nature and magnitude of the problem, identify the main environmental
risks to children's health and establish culturally appropriate monitoring, mitigation and pre-
vention strategies.

We affirm
That the principle" children are not little adull~' requires full recognition and a preventive
approach. Children are uniquely vulnerable to the effects of many chemical, biological and
physical agents. All children should be protected from injury, poisoning and hazards in the
different environments where they are born, live, learn, play, develop and grow to become
the adults of tomorrow and citizens in their own right.
That all children should have the right to safe, clean and supportive environments that ensure
their survival, growth, development, healthy life and well-being. The recognition of this right
is especially important as the world moves towards the adoption of sustainable development
practices.
That it is the responsibility of community workers, local and national authorities and policy-
makers, national and international organizations, and all professionals dealing with health,
environment and education issues to ensure that actions are initiated, developed and sus-
tained in all countries to promote the recognition, assessment and mitigation of physical,
chemical and biological hazards, and also of social hazards that threaten children's health
and quality of life.

We commit ourselves
To developing active and innovative national and international networks with colleagues, in
partnership with governmental, nongovernmental and international organizations for the
promotion and protection of children's environmental health, and urge WHO to support our
efforts in all areas, especially in the following four:

12 SECTION I: INTRODUCTION
 Box continued
1. Protection and Prevention-To strengthen existing programmes and initiate new
mechanisms to provide all children with access to clean water and air, adequate san-
itation, safe food and appropriate shelter:
• Reduce or eliminate environmental causes and triggers of respiratory diseases and
asthma, including exposure to indoor air pollution from the use of biomass fuels and
environmental tobacco smoke.
• Reduce or eliminate exposure to toxic metals such as lead, mercury and arsenic, to
fluoride, and to anthropogenic hazards such as toxic wastes, pesticides and persis-
tent organic pollutants.
• Reduce or eliminate exposure to known and suspected anthropogenic carcinogens,
neurotoxicants, developmental and reproductive toxicants, immunotoxicants and
naturally occurring toxins.
• Reduce the incidence of diarrhoeal disease through increased access to safe water
and sanitation and promotion of initiatives to improve food safety.
• Reduce the incidence of accidents, injuries and poisonings, as well as exposure to
noise, radiation, microbiological and other factors by improving all environments
where children spend time, in particular at home and at school.
• Commit to international efforts to avert or slow global environmental changes, and
also take action to lessen the vulnerability of populations to the impact of such
changes.

2. Health Care and Research-To promote the recognition, assessment and study of
environmental factors that have an impact on the health and development of children:
• Establish centres to address issues related to children's environmental health.
• Develop and implement cooperative multidisciplinary research studies in association
with centres of excellence, and promote the collection of harmonized data and their
dissemination.
• Incorporate children'S environmental health into the training for health care providers
and other professionals, and promote the use of the environmental history.
• Seek financial and institutional support for research, data coliection, education, inter-
vention and prevention programmes.
• Develop risk assessment methods that take account of children as a special risk group.

3. Empowerment and Education-To promote the education of children and parents about
the importance of their physical environment and their participation in decisions that
affect their lives, and to inform parents, teachers and caregivers and the community
in general on the need and means to provide a safe, healthy and supportive environ-
ment to all children:
• Provide environmental health education through healthy schools and adult education
initiatives.
• Incorporate lessons on health and the environment into all school curricula.

1. CHILDREN ARE NOT LlTILE ADULTS 13

Bl1xcontinued
• Empower children to identify potential risks and solutions.
• Impart environmental health expertise to educators, curriculum designers and school
ad ministrators.
• Greate and disseminate to families and communities culturally relevant information
about the special vulnerability of children to environmental threats and practical steps
to protect children.
• TeaclJfamilies ;ind the community to identify environmental threats to their children,
to .adopt practices that will reduce risks of exposure and to work with local authori-
ties and the private sector in developing prevention and intervention programmes.

4. Advocacy;...;...To advocate and take action onthe protection and. promotion of children's
environmental health at all levels,including political,administralive and community
levels:
• Use lessons learned to prevent environmental illness in children, for example by
promoting legislation for the removal of lead from all petrol, paints, water pipes and
ceramics, and for the provision of smoke-free environments in all public buildings.
• Sensitize decision,makers to the results of research studies and observations of com-
munityworkers arid primary health care providers that need to be accorded high
priority to safeguard clJildren's health .
• < Promote environmental he.alth policies that protect children.

• Raise the awareness of decision-makers and potential donors about known environ-
mental threats to children's health and work with them and other stakeholders to allo-
cate necessary resources to implement interventions.
• Work with the media to disseminate ·information on core children's environ-
mental health issues and locally relevant enVironmental health problems and potential
solutions.
For all 'flose concerned about the environmental health of children, the time to trans/ate
knowledge. ;nfo a6ti011 is now.
Bangkok, 7 MarcIJ 2002

References
1. us Environmental Protection Agency. Chemicals-in-commerce information system.
Chemical update system database, 199B. Washington, DC, July 1997.
2. National Academy of Sciences. Toxicity testing needs and priorities. Washington,
DC, National Academy Press, 1984.
3. US Environmental Protection Agency. Office of Pollution Prevention and Toxic
Substances. Chemical hazard data availability study: What do we really know about
the safety of high production volume chemicals? US EPA, Washington, DC, 1998.
4. National Academy of Sciences. Pesticides in the diets of infants and children.
Washington, DC, National Academy Press, 1993.

SECTION I: INTRODUCTION
 5· World Health Organization. Healthy environments for children. World Health
Organization, Geneva, 2002 (WHO/SDE/PHE/02.05).
6. Landrigan PJ, Suk WA, Amler RW. Chemical wastes, children's health and the Super-
fund Basic Research Program. Environmental Health Perspectives, 1999, 107:423-427.
7· Landrigan PJ. The toxicity of lead at low dose. British Journal of Industrial Medi-
cine, 1989, 46:593-596.
8. Needleman H L, Gunnoe C, Leviton A. Deficits in psychological and classroom
performance of children with elevated dentine lead levels. New England Journal
of Medicine, 1979, 3°0:689-695.
9· Bellinger D et al. Longitudinal analysis of prenatal and postnatal lead exposure
and early cognitive development. New England Journal of Medicine, 1987,
316 :1°37-1°43.
10. Jacobson JL, Jacobson SW, Humphrey HEB. Effects of in utero exposure to
polychlorinated biphenyls and related contaminants on cognitive functioning in
young children. Journal of Pediatrics, 1990, 116:38-45.
11. Grandjean Pet al. Cognitive deficit in 7-year-old children with prenatal exposure
to methylmercury. Neurotoxicology and Teratology, 1997, 19:417-428.
12. World Health Organization. Healthy environments for children. Initiating an alliance
for action. World Health Organization, Geneva, 2002 (WHO/SDE/PHE/02.06).
13· Landrigan PJ, Boffetta P, Apostoli P. The reproductive toxicity and carcino-
genicity of lead: a critical review. American Journal of Industrial Medicine, 2000,
38 :231- 243.
14· Nicholson WJ, Perkel G, Selikoff IJ. Occupational exposure to asbestos: popula-
tion at risk and projected mortalitY-198o-203°. American Journal of Industrial
Medicine, 1982, 3:259-311.
15· Mannino DM et al. Surveillance for asthma-United States, 1960-1996. Mor-
bidity and Mortality Weekly Report, 1998,47(55-1):1-28.
16. Centers for Disease Control and Prevention. Asthma mortality and hospitaliza-
tion among children and young adults-United States, 1980-1993. Morbidity and
Mortality Weekly Report, 1996, 45:350-353.
17· Friedman MS et al. Impact of changes in transportation and commuting behav-
iors during the 1996 summer Olympic Games in Atlanta on air quality and child-
hood asthma. Journal of the American Medical Association, 2001, 285:897-905.
18. Claudio Let al. Socioeconomic factors and asthma hospitalization rates in New
York City. Journal of Asthma, 1999, 36:343-350.
19· Children's health and environment: a review of evidence. Copenhagen, WHO
Regional Office for Europe, 2002 (Environmental Issue Report, No. 29).
20. Gurney JG et al. Trends in cancer incidence among children in the U.S. Cancer,
199 6 ,7 6 :53 2-4l.
21. Legler J M et al. Brain and other central nervous system cancers: recent trends
in incidence and mortality. Journal of the National Cancer Institute, 1999,
91:1382-139°.
22. Ojesina AI, Akang EEU, Ojemakinde KO. Decline in the frequency of Burkitt's
lymphoma relative to other childhood malignancies in Ibadan, Nigeria. Annals
of Tropical Paediatrics, 2002, 22:159-163.

1. CHILDREN ARE NOT LlTILE ADULTS 15

23. Henry SH, Bosch FX, Bowers Jc. Aflatoxin, hepatitis and worldwide liver cancer
risks. Advances in Experimental Medicine and Biology, 2002, 504:229-233.
24. Montesano R, Hainaut P, Wild CPo Hepatocellular carcinoma: from gene to
public health. Journal of the National Cancer Institute, 1997, 89:1844-1851.
25. Centers for Disease Control and Prevention. Lead poisoning-update. Morbidity
and Mortality Weekly Report, 1997,46:141-146.
26. Hernberg S. Lead poisoning in a historical perspective. AmericanJournal of Indus-
trial Medicine, 2000, 38:244-254.
27. Bindea V. Blood lead levels in children from Baia Mare, Romania. In: Proceedings
of the International Conference on Lead Exposure, Reproductive Toxicity and
Carcinogenicity, Gargagno, Italy, 7-9 June 1999, Lyon, International Agency for
Research on Cancer, 1999.
28. Bulat P et al. Occupational lead intoxication in lead smelter workers. In: Pro-
ceedings of the International Conference on Lead Exposure, Reproductive Toxicity and
Carcinogenicity, Gargagno, Italy, 7-9 June 1999, Lyon, International Agency for
Research on Cancer, 1999.
29. Chatterjee A et al. Pollution from a lead smelter in a residential area of Calcutta.
In: Proceedings of the International Conference on Lead Exposure, Reproductive
Toxicity and Carcinogenicity, Gargagno, Italy, 7-9 June 1999, Lyon, International
Agency for Research on Cancer, 1999.
30. Koplan J. Hazards of cottage and small industries in developing countries. Amer-
ican Journal of Industrial Medicine, 1996, 30:123-124.
31. Weiss B, Landrigan P. The developing brain and the environment: an introduc-
tion. Environmental Health Perspectives, 2000, 108 (SupPI.):373-374·
32. National Academy of Sciences. Scientific frontiers in developmental toxicology and
risk assessment. Washington, DC, National Academy Press, 2000.
33. Paulozzi LJ, Erickson JD, Jackson RJ. Hypospadias trends in two US surveillance
systems. Pediatrics, 1997, 100:831-834.
34. Declaration of the Environment Leaders of the Eight on Children's Environmental
Health. (http://www.library.utoronto.ca/g7 /environ ment/1997miami/children.
html).
35. International Conference on Environmental Threats to the Health of Children:
Hazards and Vulnerability. Bangkok, 3-7 March 2002 (http://www.who.int/
docstore/ peh / ceh / Bangkok/bangkokconf.htm).

SECTION I: INTRODUCTION
 CHAPTER 2

Windows of susceptibility to
environmental exposures in children
S. G. Selevan
National Center for Environmental Assessment/ORO
Environmental Protection Agency, Washington, ~C, USA

C. A. Kimmel
National Center for Environmental Assessment/ORO
Environmental Protection Agency, Washington, ~C, USA

P. Mendola
National Health and Environmental Effects Research
Laboratory/ORO
Environmental Protection Agency, Research Triangle Park,
NC, USA

Children have a unique susceptibility to chemical, biological and physical

environmental threats. Their tissues and organs grow rapidly, developing and
differentiating until maturity. The developmental and growth processes in the
fetus, infant, child, and adolescent can define periods of varying vulnerability to
environmental toxicants. Furthermore, the exposure patterns and behaviours
of children are very different from those of adults, and may result in greater
exposures.
A large number of anatomical, biochemical, and physiological changes occur
from early intrauterine life through adolescence. These maturational processes
may be altered by phYSical, biological, and chemical environmental factors at
various points in time. Furthermore, the changes with maturation may them-
selves substantially affect the absorption, distribution, metabolism, and elimi-
nation of chemicals present in the environment. The younger and less mature
the child, the more different its response may be from that of an adult. Addi-
tionally, recent evidence suggests that exposure of the embryo, fetus or young
child may affect the onset of diseases in adulthood, e.g. cardiovascular and neu-
rodegenerative diseases or cancer.
These susceptible developmental periods, called "windows of susceptibil-
ity", are times when a number of systems, including the endocrine, reproduc-
tive, immune, respiratory, and nervous systems, may be particularly sensitive
to certain chemicals and phYSical factors. Therefore, a new "child-centred"
approach to research, risk assessment and risk management is necessary to

17
identify, understand, control, and prevent childhood or adult diseases of
environmental origin.

Timing of exposure
Not only the level of exposure, but also its timing, may ultimately affect the
health outcomes observed in children. During the highly susceptible periods of
organ formation, timing of exposure is extremely important. For example, in the
case of prenatal exposures, the same type of exposure occurring at different
times is likely to produce a varied spectrum of malformations with the specific
outcomes observed dependent on the organ system(s) most vulnerable at the
time of exposure (Figure 2.1) (1).
In addition to highly sensitive windows for morphological abnormalities
(birth defects), there are also time windows important for the development of
physiological defects and morphological changes at the tissue, cellular and sub-
cellular levels (Figure 2.2) (2). An adaptation of the scheme in Figure 2.2 shows
the broader range of potential adverse outcomes from exposures during pre-
conceptional, prenatal, and postnatal development (Figure 2.3). Many of the
existing data are related to preconceptional and prenatal exposures (3). Data on
prenatal exposures are based mainly on studies of maternal exposure to
pharmaceuticals (e.g. diethylstilbestrol, thalidomide) and parental alcohol use,

Figure 2.1 Syndromes of malformation

A brief pulse of teratogenic treatment on the 10th day of gestatiol

would result in the following incidence of malformations:
35% brain defects
33% eye defects
24% heart defects
10% skeletal defects
6% urogenital defects
0% palate defects

Hypothetical representation of how the syndrome of malformations produced by a given agent

might be expected to change when treatment is given at different times. The percentage of
animals affected as well as the incidence ranking of the various types of malformations would be
different if treatment were given on day 12 or 14, for example. Reprinted from (1) with
permission of University of Chicago Press.

SECTION I: INTRODUCTION
Figure 2.2 Critical periods in human development

Schematic illustration of the sensitive or critical periods in human development. Dark grey
denotes highly sensitive periods; light grey indicates stages that are less sensitive to teratogens.
Reprinted from (2) with permission of WB. Saunders Co.

Figure 2.3 Reproductive outcomes and timing of maternal exposure

_ .T!~lacental cacinogenesi

_ •• ....!:.owered birth weight

Preterm delivey
III

_. _
Congenital malformations
.. _ .. --.
Spontaneous abortion
III
Subfertiliy
III
Menstrual disorders
III

.. _ .. _ .. - 1-1--+--+__II--+---I-----ill--+--+I____- - -
Preconception 0 2 3 4 5 6 7 8 9 Neonatal period
(fertilization) (birth)
Months of gestation

Timing of exposure

Solid lines indicate the most probable timing of exposure for a particular outcome; dotted lines
indicate less probable but still possible timing of exposure. Arrows suggest that a defined cut-off
point for exposure to a specific outcome is not known. Reprinted from (3) with permission of
Lippincott, Williams and Wilkins.

2. WINDOWS OF SUSCEPTIBILITY TO ENVIRONMENTAL EXPOSURES IN CHILDREN 19

smoking, and occupational exposures. Information on critical windows for expo-
sure during the postnatal period is scarce. Postnatal exposures have been exam-
ined in detail for only a few environmental agents, including lead, mercury, some
pesticides, and radiation.
Developmental exposures may result in health effects observed:

• prenatally and at birth, such as spontaneous abortion, stillbirth, low birth

weight, small size for gestational age, infant mortality, and malformation
(3-6);
• in childhood, such as asthma, cancer, neurological and behavioural
effects (7-10);
• at puberty, such as alterations in normal development and impaired
reproductive capacity (11, 12);
• in adults, such as cancer, heart disease, and degenerative neurological
and behavioural disorders (13-16).

In '999, a multidisciplinary group reviewed the data available on precon-

ceptional, prenatal, and postnatal developmental exposures and the subsequent
outcomes, looking in detail at the respiratory, immune, reproductive, nervous,
cardiovascular and endocrine systems, as well as general growth and cancer.
Clear limitations were found in the data available on developmental toxicity (5).'
Animal studies done for regulatory testing purposes are well controlled and
may include extended periods to simulate long-term human exposure. In
humans, the patterns of exposure are much more variable and must be care-
fully evaluated with systematic studies of environmental exposures and devel-
opmental effects. Early evidence of the effects of environmental exposures on
parents and children came from data on individuals with atypical exposures (e.g.
industrial or environmental accidents, poisoning). These studies of atypical
exposures provided information about associations between exposures and out-
comes but were not usually sufficient for extrapolation because of limitations
in the measurement of exposure and uncertainty as to whether exposure
occurred at a biologically plausible time. More recent studies have attempted
to better document exposures using environmental and biological sampling as
well as measuring the level and timing of exposure.
Exposure issues vary according to the time at which they occur: before con-
ception, prenatally, or postnatally. The preconceptional exposures of concern

'Developmental toxicity was defined as the occurrence of adverse effects on the developing
organism that may result from exposure prior to conception (either parent), during prena-
tal development, or postnatally to the time of sexual maturation. Adverse developmental
effects may be detected at any point in the lifespan of the organism. The major manifesta-
tions of developmental toxicity include death of the developing organism, structural abnor-
mality, altered growth, and functional deficiency.

20 SECTION I: INTRODUCTION
 may occur acutely prior to conception or result from an increased body burden
in either parent accumulated over a long period of exposure. Prenatally, expo-
sures often change throughout pregnancy, e.g. if a woman reduces her alcohol
consumption, quits smoking, or avoids using medicines. In addition to these
variations, the altered absorption, distribution, metabolism, and excretion of
chemicals during pregnancy result in changes in internal dosing (Table 2.1) (17).
For example, pregnant women have an increased cardiac output and pulmonary
function (they exchange about 72% more air over 8 hours at rest: 5000 litres in
pregnant women versus 2900 litres in nonpregnant women) (18). In practice,
studies of prenatal exposures in humans are difficult, as they are typically based
upon one or a few measurements of exposure, which are used to estimate expo-
sure for the entire pregnancy.
Difficulties also arise in studies of exposure in children, as these can vary
enormously over time. At different developmental stages, the biology, behav-
iour, settings, and activities of children can result in variable exposures which
may also be quite different from those of adults in the same environment
(Table 2.2). For example, the ratio of surface area to body mass in infants is
approximately 2.7 times that in adults; the respiratory minute ventilation rate is

Table 2.1 Physiological and toxicokinetic changes during pregnancya

PARAMETER PHYSIOLOGICAL CHANGE TOXICOKINETIC CHANGE
Absorption
Gastric emptying time Increased Absorption increased
Intestinal motility Decreased Absorption increased
Pulmonary function Increased Pulmonary exposure increased
Cardiac output Increased Absorption increased
Blood flow to skin Increased Absorption increased
Dermal hydration Increased Absorption +/-
Metabolism
Hepatic metabolism +/- Metabolism +/-
Extrahepatic metabolism +/- Metabolism +/-
Plasma proteins Decreased Metabolism +/-
Excretion
Renal blood flow Increased Increased renal elimination
Glomerular filtration rate Increased Increased renal elimination
Pulmonary function Increased Increased pulmonary elimination
Plasma proteins Decreased Elimination +/-
, Modified from Silvaggio & Mattison (17).

2. WINDOWS OF SUSCEPTIBILITY TO ENVIRONMENTAL EXPOSURES IN CHILDREN 21

N
N
Table 2.2 Differences between children and adults in certain parameters affecting environmental exposures

PARAMETER NEWBORN YOUNG CHILO OLDER CHILD ADULT REF.

Surface area: body mass (m2/kg) 0.067 0.047 0.033 0.025 (18)

Respiratory ventilation rates Infant Adult (18)

Respiratory volume (ml/kg per breath) 10 10
Alveolar surface area (m2) 3 75
Respiration rate (breaths/min) 40 15
Respiratory minute ventilation rate' 133 2
<1 year 1-10 years 11-19 years 20-64 years
Mean drinking-water intake (ml/kg per day) 43.5 35.5 18.2 19.9 (19)

Fruit consumption (g/kg per day (USA)) <1 year 3-5 years 12-19 years 40-69 years (21)

Citrus fruits 1.9 2.6 1.1 0.9

Other fruits (including apples) 12.9 5.8 1.1 1.3
Apples 5.0 3.0 0.4 0.4

Soil ingestion (mg/day)

Vl
500 (19)
rn
()
Pica child
-I 2.5 years 6 years Adult
(5
z Outdoors 50 20 20 b
..
Z Indoors 60 2 0.4
-I
Al
Differences in absorption of lead 42-53% 30-40% 18-24% 7-15% (19)
0
0
c
()
-I
, In mllkg of body weight per m' lung surface area per minute.
(5 b Gardening.
z
 more than 65 times greater (17), and consumption of drinking-water more than
twice that of adults on a body weight basis (19). Even over the relatively short
time span of childhood, exposure levels can vary widely.

Windows of susceptibility
Because of the variety of biological factors mentioned above, there is a
greater potential for adverse health effects in children than in adults. Children
are still developing in many ways and may be more vulnerable. They may be
less able to avoid exposure because of immature detoxification mechanisms.
Differences in metabolism, size, and behaviour may mean that they have higher
levels of exposure than adults in the same environment.
It is, therefore, crucial to identify and understand the importance of the
"windows of susceptibility" in children and the relationships between exposures
and developmental outcomes. This requires knowing the key periods of sus-
ceptibility for specific outcomes. Information on these critical windows has been
compiled in a number of reports (20). However, one of the main constraints in
identifying critical windows is the limited information on the exact timing and
sensitivity of various developmental stages. This underscores the importance
of collecting case-specific information and detailed exposure assessments in
children. For cancer, the situation is unique: tumours may be induced in a wide
variety of systems at many highly vulnerable developmental stages.
Several issues that are closely related to the windows of susceptibility in chil-
dren require further attention.

• The consequences of developmental exposures that are manifested in

adulthood and old age should be considered: the potential cascade of
events that might result in health effects in the adult is poorly understood.
For example, if intrauterine growth restriction (I UGR) is associated with
exposure to a particular agent, does it have the same later-life effects as
nutritionally induced IUGR?
• Limited data are available on gene-environment interactions, an area
identified as important for future research. Are those with certain genetic
traits more likely to develop cancer or other health conditions associated
with developmental exposures? Do these genetic traits impart greater
vulnerability during particular developmental stages?
• The peripubertalJadolescent period is under-represented in studies of
both exposure and outcomes in the current literature, despite the fact
that many organ systems-especially the endocrine system-undergo
significant development during this time.

More information is needed on windows of susceptibility in order to improve

the risk assessment of potential environmental health threats to children, ado-
lescents and adults. This requires increased interaction across different sci en-

2. WINDOWS OF SUSCEPTIBILITY TO ENVIRONMENTAL EXPOSURES IN CHILDREN 23

tific disciplines. For example, animal laboratory data can help clinicians and epi-
demiologists identify areas of potential concern in humans. Epidemiological
data can raise interest among laboratory researchers for developing mechanis-
tic data and exploring agent-target interactions. Clinicians may contribute case
reports that generate hypotheses for follow-up by other scientists. These inter-
actions could help develop more sensitive methods for both clinicians and
researchers for validation across species, and for enhancing the value of future
studies on children's environmental health.
In summary, increased knowledge and information about children's
windows of susceptibility to environmental agents will help to identify the par-
ticularly susceptible subgroups/ages and to plan for specific preventive actions.
Increased dialogue among scientists from various disciplines will help to fill in
the data gaps, improve measurement of exposures, and enhance the use of
information to address and prevent the adverse effects of environmental threats
on children's health.

References
1. Wilson JG. Embryological considerations in teratology. In: Wilson JG, Warkany
J, eds. Teratology: principles and techniques. Chicago, The University of Chicago
Press, 1965:256.
2. Moore KL, Persaud TVN. The de~eloping human: clinically oriented embryology.
Philadelphia, W.B. Saunders, 19]3:9 8 .
3. Selevan SG, Lemasters GK. The dose-response fallacy in human reproductive
studies of toxic exposures. Journal of Occupational Medicine, 19 8 7, 29:
45 1-454.
4. Herbst AL, Scully RE, Robboy SJ. Prenatal diethylstilbestrol exposure and
human genital tract abnormalities. National Cancer Institute Monographs, 1979,
51 :25-35·
5. Horta BL et al. Low birthweight, preterm births and intrauterine growth retar-
dation in relation to maternal smoking. Paediatric and Perinatal Epidemiology,
1997,11:140- 151.
6. Gonzalez-Cossio T et al. Decrease in birth weight in relation to maternal bone-
lead burden. Pediatrics, 1997, 100:85 6- 862 .
7. Hu FB et al. Prevalence of asthma and wheezing in public schoolchildren: asso-
ciation with maternal smoking during pregnancy. Annals of Allergy, Asthma and
Immunology, 1997, 79: 80- 84.
8. Drews CD et al. The relationship between idiopathic mental retardation and
maternal smoking during pregnancy. Pediatrics, 199 6 , 9T547-553·
9. van Duijn CM et al. Risk factors for childhood acute non-lymphocytic leukemia:
an association with maternal alcohol consumption during pregnancy? Cancer
Epidemiology, Biomarkers and Pre~ention, 1994, 3:457-4 60 .
10. Daniels JL, Olshan AF, Savitz DA. Pesticides and childhood cancers. En~iron­
mental Health Perspecti~es, 1997, 105:1068-1077.

SECTION I: INTRODUCTION
 11. Blanck HM et al. Age at menarche and tanner stage in girls exposed in utero
and postnatally to polybrominated biphenyl. Epidemiology, 2000, 11:641- 647.
12. Selevan SG et al. Blood lead concentration and delayed puberty in girls. New
England Journal of Medicine, 2003, 348:1527-1536.
13· Needleman H Let al. The long-term effects of exposure to low doses of lead in
childhood. An ll-year follow-up report. New England Journal of Medicine, 199 0 ,
322 :83-88.
14· Miller RW. Special susceptibility of the child to certain radiation-induced
cancers. Environmental Health Perspectives, 103 (Su ppl. 6) :41-44.
15· Wadsworth ME, Kuh DJ. Childhood influences on adult health: a review of recent
work from the British 1946 national birth cohort study, the MRC National Survey
of Health and Development. Paediatric and Perinatal Epidemiology, 1997,
11:2-20.
16. Osmond C et al. Early growth and death from cardiovascular disease in women.
British Medical Journal, 1993, 30T1519-1524.
17· Silvaggio T, Mattison DR. Comparative approach to toxicokinetics. In: Paul M,
ed. Occupational and environmental reproductive hazards: a guide for clinicians.
Baltimore, MD, Williams & Wilkins, 1993:25-36.
18. Snodgrass WR. Physiological and biochemical differences between children and
adults as determinants of toxic response to environmental pollutants. In:
Guzelian PS, Henry CJ, Olin SS, eds. Similarities and differences between children
and adults: implications for risk assessment. Wash ington, DC, ILS I Press, 199 2:
35-42 .
19· US Environ mental Protection Agency. Exposure factors handbook. Vol 1: General
factors. Washington, DC, 199T3-7 (EPA/600/P-95/002Fa).
20. Selevan SG, Kimmel CA, Mendola P, eds. Identifying critical windows of expo-
sure for children's health. Environmental Health Perspectives, 2000, 108(Suppi
3):449-597.
21. US Environmental Protection Agency. Exposure factors handbook. Vol. 2: Food
ingestion factors. Washington, DC, 199T9-13; 9-19 (EPA/600/P-95/002Fa).

2. WINDOWS OF SUSCEPTIBILITY TO ENVIRONMENTAL EXPOSURES IN CHILDREN 25

How and when exposure occurs
 CHAPTER 3

Where the child lives and plays

N. Chaudhuri
Environmental Health Professional, Paris, France

L. Fruchtengarten
Paediatrician and Medical Toxicologist,
Poison Control Centre of Sao Paulo, Brazil

Introduction
Children are more susceptible than adults to the action of environmental
toxicants. The environment where children live can cause or prevent illness, dis-
ability, and injury. A clean environment is essential for the good health and devel-
opment of children. There are numerous situations in the home and in schools
that may result in exposure to contaminants, such as presence of second-hand
smoke (environmental tobacco smoke), spraying of insecticides, and accumu-
lation of different materials in carpets.

The home environment

A healthy physical and psychosocial home environment is essential for the
normal development of children, especially during preschool years when they
spend much of their time at home. Poor quality housing and hazards found
inside the home can affect their health.
In developing countries, housing may be poorly constructed because of a
lack of high quality building materials and limited building skills. Housing may
be located on contaminated or disaster-prone sites; basic services, such as clean
water, sanitation, and waste storage and disposal may be limited; and there may
be chronic rodent and insect infestation and other vectors of disease. The use
of biomass stoves contributes to poor indoor air quality and overcrowded
housing may favour the transmission of disease and adversely affect the mental
health of children.
In the developed world, where basic services such as water, sanitation and
waste management are usually provided, unhealthy hOUSing is generally a result
of poor design, construction, or lighting, or of the use of unhealthy building
materials such as lead. Poor heating or ventilation systems may encourage the
development of mould and dust mites, triggering chronic diseases such as
asthma. Exposure to radon and electromagnetic fields may also occur.

29
Principles of healthy housing (1) Reduction of psychological and social stress:
Protection against communicable diseases: • adequate living space, privacy and
• safe water supply; comfort;
• sanitation; • personal and family security;
• disposal of solid wastes; • access to recreation and community
• drainage of surface water; amenities;
• personal and domestic hygiene; • protection against noise.
• safe food preparation; Access to supportive living environment:
• structural safeguards.
• security and emergency services;
Protection against injuries, poisonings and • health and social services;
chronic diseases: • access to cultural and other amenities.
• adequate structural features Protection of groups at special risk:
and furnishing;
• good air quality; • women and children;
• chemical safety; • displaced and mobile population;
• avoidance of use of • the aged, ill and disabled.
the home as workplace;

Psychosocial factors
Housing design can influence the ability of people to satisfy their needs in
terms of contact with others, privacy, play and development. Restricted oppor-
tunities for play and social isolation in high-rise apartments can produce psy-
chological distress in children.
Poor mental health, psychiatric disorders, psychological distress in children,
and worry have been found to be related to population density and overcrowd-
ing. However, the precise relationship between crowding and mental health
depends on many cultural and social factors, and both low and high population
densities can be detrimental to health.

Play spaces
Young children like to explore their environment, passing through an intense
hand-to-mouth discovery phase, which is necessary to their development; this
can place them at risk both inside and outside the home.
Because of their short stature and early crawling activities, they live much
closer to the floor than adults. Children are therefore at increased risk from
chemicals sprayed on gardens and fields, and during play in polluted industrial
sites. An eating disorder, mainly caused by a deficiency of iron, may lead chil-
dren to ingest soil and any associated toxicants.

SECTION II: HOW AND WHEN EXPOSURE OCCURS

 Playgrounds present a potential risk to children and should be made
safe and attractive. The majority of injuries are caused by falls. All play equip-
ment should be located on shock-absorbing surfaces, and climbing equipment
should have well defined foot and hand grips. All materials used in construc-
tion should be non-corroding and maintenance should be carried out regularly.
Sand pits should be free of dirt, clay, stones, sticks and other dangerous
materials.
Children should be encouraged to learn about water, its pleasures and its
dangers. Children can drown in very small amounts of water, and constant
supervision is needed. Pools should be covered when not in use. The chemical
treatment of swimming-pools can lead to excessive inhalation of chlorine and
nitric oxide by young children.

The indoor environment

Indoor air quality is influenced by outdoor air pollution, indoor sources of
pollution, the characteristics of the building and the habits of the residents.
High levels of indoor air pollution come from the use of open fires and ineffi-
cient stoves for cooking or heating, with combustion of biomass fuels, coal and
kerosene. Gas stoves or wood-burning units that have been poorly installed and
maintained, or that are inadequately ventilated, can increase indoor levels of
carbon monoxide, nitrogen dioxide and particles.
There is a risk of pollution by automobile fumes in homes with attached
garages. Tobacco smoke is a dangerous combustion product and a major
source offine particulate matter indoors. Pollution from traffic and industry may
also influence the quality of indoor air in urban areas.
Other pollutants not associated with fuel combustion may also be of
concern, including building materials such as asbestos, cement, and wood
preservatives. Volatile organic compounds may be released by various materi-
als including paints, glues, resins, stored petrol, polishing materials, perfumes,
spray propellants, building materials, personal care products and cleaning
agents. Formaldehyde, a component of some household products, can irritate
eyes, nose and airways. The most Significant sources of indoor allergens are
dust mites, and feathered and furry pets. Mattresses, upholstery and carpets
are primary reservoirs for such allergens.
Increased air exchange may dilute indoor airborne pollutants and prevent
moisture problems, but can be difficult to achieve in certain countries during
winter or with continuous use of air-conditioning in the summer.

Specific chemical contaminants

Lead
Lead is one of the most toxic chemical hazards found in houses. The main
source of lead in houses is deteriorating interior and exterior lead-based paint.
Lead from petrol or industrial sources may be brought into houses in contam-

3. WHERE THE CHILD LIVES AND PLAYS 31

inated dust and soil. Cottage industries that recycle lead batteries, particularly
if work is conducted indoors, can be an important source of household lead.
Other sources include ceramic pottery glazes, polyvinyl chloride and other plas-
tics, and cosmetics.
Children can be exposed to lead via two pathways-either by directly ingest-
ing paint chips or other lead-containing products (water from lead-based water-
pipes) or indirectly by ingesting lead-contaminated house dust or soil through
normal hand-to-mouth behaviour. Lead dust may also settle on food, creating
another route of exposure.

Asbestos
Another chemical contaminant of significance is asbestos, which is found
in ceiling and floor tiles, and as insulation. Exposure to asbestos may affect lung
function.

Volatile organic compounds

Volatile organic compounds (VOCs) significantly influence the quality of air
in homes. They are found widely in personal care and cleaning products, paints,
solvents, adhesives, furnishings, pesticides and building materials, and as a
byproduct of chlorinated drinking-water. Acute and chronic effects associated
with exposure to VOCs include irritation and sensitization of eyes, nose, lungs
and mucous membranes, narcotic effects and depression of the central nervous
system.

Particulate matter
Particulate matter is small solid or liquid particles suspended in the air.
In the developing world, the greatest source of particulates is the burning of
biomass fuels, such as wood, charcoal, crop residues and animal dung. In devel-
oped societies, sources include cleaning activities such as vacuuming and
dusting; heating, ventilation and air-conditioning systems; consumer products,
such as spray disinfectants, cleaners and repellents; unvented clothes dryers;
tobacco smoke; particles carried indoors from busy roads, incinerators and
industrial sources. Increased rates of respiratory infections in vulnerable groups,
such as children and those with pre-existing chronic respiratory disease, have
been associated with the presence of high concentrations of particles (3).

Nitrogen dioxide
Nitrogen dioxide is formed at high temperatures in gas appliances, such as
stoves, kerosene heaters and wood-burning stoves, as well as in cigarette
smoke. Health effects associated with nitrogen dioxide exposure include irrita-
tion of the mucous membranes of the lungs; provocation of asthmatic crises
either by direct pollutant effect or by inducing an allergic response in the
bronchi; increased incidence of respiratory infections, sore throats, and colds.

SECTION II: HOW AND WHEN EXPOSURE OCCURS

 Carbon monoxide
Carbon monoxide is a colourless, odourless gas, produced by the incom-
plete combustion of carbon-containing fuels, including coal, natural gas,
biomass, and oil. Cigarette smoke can also produce high levels of carbon
monoxide. Poorly functioning heating devices (stoves and furnaces), poor ven-
tilation and poor elimination of combustion by-products are the usual sources
of carbon monoxide indoors. Carbon monoxide is extremely toxic and exposure
can be fatal. In the United Kingdom, for example, more children die from carbon
monoxide poisoning than from any other poisoning (4). Acute effects include
headache, fatigue and impaired exercise tolerance. Higher concentrations
produce a wide range of symptoms that resemble those of gastroenteritis,
influenza, cerebrovascular disease and drunkenness. Chronic exposure can
produce headache, fatigue, confusion, dizziness, chest pain, visual distur-
bances, nausea, diarrhoea, and abdominal pain.

Pesticides
Residual insecticides have played an important role in vector control activi-
ties. Concerns exist, however, over the prolonged use of pesticides, including
the development of resistance in
pest species, and exposure of chil-
dren to residues. Pesticides may Radiation
also be found in breast milk. Radiation is carcinogenic to humans, and chil-
Commonly used insecticides dren and fetuses are especially sensitive to its
include pyrethroids, chlorpyrifos, effects. This is probably due to the higher rate
diazinon, propoxur, dichlorvos, of cell division during growth and development.
malathion and piperonyl butoxide. While some exposure comes from natural
Children are at increased risk of radiation, most people are also exposed to
exposure to pesticides used in resi-
man-made radiation. The biggest source of this
dential areas because of higher con-
is medical radiation, from diagnostic X-rays and
imaging techniques, cancer treatments, etc.,
centrations near the floor and the
though these procedures do provide benefits to
persistence of some insecticides on
patients. Children may be exposed to radiation
carpets, furniture and soft toys.
in their homes and communities, from television
Activities of young children, such as
sets, nuclear weapons tests, waste generated
crawling, playing on the floor,
from the production of nuclear power, and radon
playing outdoors and hand-to-
from soil and stone. High levels. of radiation
mouth behaviour, contribute to exposure have been linked to cancer: childhood
higher exposure. Ingestion and exposure, in particular, increases the risk .of
inhalation of, and contact with, leukaemia, and breast and thyroid cancer. Health
house dust can be primary routes of risks are higher for .children than fora:dults.
exposure for small children. Acci- Whenever possible,medieaIX-rayexaminations
dental exposures may also occur of children should be avoided; in,any case, tqe
when pesticides spill, leak or are radiation dMes snould be kept toa minimum.
improperly used, because label

3· WHERE THE CHILD LIVES AND PLAYS

33
instructions are not followed or pesticides are placed in unmarked containers
or in unsafe places.
In some countries, the pesticide chlorpyrifos is frequently used indoors,
where it can accumulate on soft toys, furniture and carpets and later volatilize
in the air. Under these conditions children may be exposed to high levels. Pes-
ticides used to treat head lice, such as lindane, are considered as possibly car-
cinogenic (5). Few studies have examined the potential health effects of chronic
exposure to insecticides used to control Chagas disease or malaria.
Health effects associated with pesticide use may include endocrine disrup-
tion, behavioural abnormalities, cancers and damage to the immune system.
Integrated pest management (IPM) techniques, which use the least possible
amount of pesticide, are recommended to avoid unnecessary exposure.

Second-hand tobacco smoke

Tobacco smoke is a mixture of gases and particles. Second-hand tobacco
smoke includes sidestream smoke, the smoke emitted from a burning cigarette,
cigar, or pipe, and mainstream smoke from the smoker. Health effects in infants
have been correlated with close contact with smoking mothers (6). Acute health
effects include eye, nose and throat irritation. Other effects include cancer, lower
respiratory tract infections, respiratory symptoms (cough, phlegm and wheez-
ing), childhood asthma, retarded lung growth and development, and middle ear
disease. Some evidence exists that second-hand smoke is related to sudden
infant death syndrome.

Specific biological contaminants

Dampness and mould
Dampness in a dwelling can promote the growth of several agents, such as
viruses, bacteria, dust mites and mould. Damp conditions are related to pre-
vailing climatic conditions, poor housing design and construction, and poor
ventilation.
Condensation, in combination with organic materials found on walls (such
as wallpaper paste), ceilings and floors, provides a good medium for mould
growth. Kitchens and bathrooms are particularly prone to mould growth
because of the moist conditions. The health effects of moulds include respira-
tory allergies, such as asthma, rhinitis, bronchitis, alveolitis, fever, chills, hoarse-
ness, fatigue, coughing, and wheezing.

Dust mites
Dust mites are microscopic organisms, which tend to breed at a constant
temperature of around 25°C and a relative humidity of between 70% and 80%.
They do not survive in cool and dry conditions. Furnishing, flooring materials,
heating systems and type of house also influence the concentration of mites,
which are mostly found on soft furnishings, such as sofas, fabrics, carpets,

34 SECTION II: HOW AND WHEN EXPOSURE OCCURS

sheets, duvets, pillows and mattresses. Health effects associated with dust mite
exposure include allergic reactions, bronchial asthma, allergic rhinitis and atopic
dermatitis.

Pets and livestock

In many developing countries, people share their home with domestic
animals, including sheep, pigs, cattle and poultry. Animal diseases may be trans-
mitted to children through contact or via soil and dust. These diseases include
anthrax, tetanus, brucellosis, tuberculosis, listeriosis, salmonellosis, rabies,
psittacosis, larva migrans, histoplasmosis and mycotic dermatophytosis.
In industrialized countries, approximately 50% of households have some
type of animal living in the home. Dogs, cats and other companion animals
have been shown to produce health benefits. However, up to 60% of asthmatic
patients show an IgE mediated hypersensitivity to cat or dog allergen. Many
allergic individuals are not willing to give up a family pet for psychological
reasons. In this case, pets should be kept out ofthe bedroom, and should prefer-
ably stay outdoors or in a well ventilated area. Soft furnishings, such as carpets
or sofas, should be removed or cleaned regularly.

Water and sanitation

The availability of water of good quality is essential for children's health.
Unsanitary conditions and practices in households, such as unsafe waste dis-
posal and unhygienic behaviour in child care and food preparation, account for
a large number of diseases that are transmitted via water, food and contact
between individuals. Diseases such as diarrhoea, intestinal parasitic infection
and resulting malnutrition, anaemia and retarded growth, blindness from tra-
choma, and arsenic poisoning have all been attributed to an unsafe water supply
and inadequate sanitation.
Chemical contaminants may be introduced into drinking-water by various
means. Naturally occurring chemicals, such as arsenic and radon, may dissolve
in groundwater. Industrial and human wastewater may be discharged into
surface water or groundwater. Pesticides and fertilizers applied to land and
crops may wash into water sources. Lead may leach from pipes during water
distribution. As far as possible, water sources should be protected to prevent
chemical or microbiological contamination. Water treatment plants should be
designed and operated to take all these factors into consideration to avoid
health hazards.
Health benefits accrue from the provision of sufficient quantities of water
through good quality community facilities, and even more so from household con-
nections. As regards sanitation, health benefits are achieved through facilities
ranging from hygienic on-site sanitation to flushing toilets to sewerage systems
with effective wastewater treatment. The full health benefits of water supply and
sanitation facilities can only be achieved in combination with hygiene education.

3. WHERE THE CHILD LIVES AND PLAYS 35

 Crowding and density
Accidents There are several hypotheses
EnVironmental hazards associated with home about the health effects of crowding
accidents may be related to bad design, poor and population density. Crowding is
quality of housing materials, poor maintenance, a perceived condition (lack of
or use of defective and improperly installed equip- privacy, social demands) whereas
ment and appliances. Injuries, falls, burns and density refers to the amount of space
poisonings may resultfrom inadequate storage of available. High population density
poisonous substances and dangerous items such may increase the risk of early and
as medicines and cleaning products; poorly repeated disease transmission in
placed or maintained heat sources such as open children. In addition, it increases the
fires, and wood, oil, gas or kerosene burners; risk of repeated exposure to toxins.
inadequate floor coverings and surfaces; poorly Intensive exposure at home (sec-
designed stairways and storage areas; and
ondary cases) increases the severity
improperly designed or installed windows.
of infection and the case-fatality
ratio for infectious diseases, such as
measles, chickenpox, pertussis and
poliomyelitis. However, high population density may have some positive effects,
e.g. children may get mild forms of viral infections which stimulate the immune
system and protect against more severe infection.

Outdoor air
Outdoor air pollution can influence the quality of air found in the house-
hold. The effect is dependent on various factors, including the concentration
of outdoor pollutants, the rate of infiltration, the reactivity of the contaminant,
the efficiency of any mechanical filtration system and, for solids, particle size
and shape. Some pollutants that have been identified as particularly hazardous
include total suspended particulates (>l0/-lg) and fine particulates «l0/-lg)
from diesel exhaust, sulfur dioxide, sulfuric acid, polycyclic aromatic hydrocar-
bons, nitrous oxides, ozone, carbon monoxide and heavy metals such as lead.

Vector-borne diseases
Several vector-borne diseases, such as malaria, Chagas disease and dengue
fever are related to housing construction and design. Malaria risk has been shown
to be greater for people living in poorly constructed houses (e.g. with incomplete
thatched roofs) than for those living in houses with complete brick and plaster
walls and tiled roofs. Malaria risk also increases if housing is located near a body
of water where mosquitoes can breed. Similar results have been found for dengue
fever, where people living in houses that are fully screened are at lowest risk.
Chagas disease, which is caused by a protozoan parasite, Trypanosoma cruzi,
is transmitted to humans by triatomine bugs. Triatomine bugs proliferate in
houses made of earth, wood, and roughly plastered wattle daub, in thatch and
palm roofs on a timber structure, and in walls of split and flattened bamboo.

SECTION II: HOW AND WHEN EXPOSURE OCCURS

Replacement of uneven, cracked, earth floors by cement or ceramic tiles has
reduced infestation rates of Triatoma dimidiata. Replacement of palm-thatched
roofs by corrugated tin sheets or ceramic tiles also decreases the number of
infestations.
Cockroaches can be vectors of disease, such as dysentery, salmonellosis,
hepatitis A, poliomyelitis, and legionnaire disease (7); cockroach antigens are also
important provokers of asthma. Housing conditions and housekeeping practices
influence the severity of cockroach infestations, which are fostered by the presence
of food through improper storage or disposal, water from leaky pipes and taps,
and points of entry such as cracks, crevices and holes in plasterwork and flooring.

Four key vector-borne diseases

A considerable proportion of the disease burden for four key vector-borne diseases-
malaria, schistosomiasis, Japanese encephalitis and dengue/dengue haemorrhagic fever-
falls on children under 5 years of age. Because of the vastness of this topic, readers are
referred to WHO manuals and guidelines on such diseases (see www.who.intltdr and
www.who.intlceh/risks). The particular concerns for children in relation to vector-borne
diseases are summarized here.
In sub-Saharan Africa and in many countries in Asia and Latin America, children under 5
years suffer high mortality and morbidity due to malaria. In older children malaria remains
an important cause of mortality and morbidity and significantly contributes to low educa-
tional achievement. Schistosomiasis is a waterborne disease that affects children and ado-
lescents mainly because of lack of hygiene and specific behaviour, such as playing and
swimming in contaminated water. High infection rates and individual worm loads produce a
debilitating infection which may cause severe damage to liver and kidneys over many years,
and can result in premature death. The occurrence of Japanese encephalitis is restricted
to south and south-east Asia, where it is associated with irrigated rice production ecosys-
tems. The annual number of clinical cases is estimated at between 30000 and 50000, some
90% of which are in children in rural areas. Dengue affects mainly urban populations (the
Aedes species that transmit dengue are adapted to the man-made environment), and the
infection can develop into dengue haemorrhagic fever or dengue shock syndrome with high
levels of mortality. Annually, mortality due to dengue fever is estimated at around 13000;
more than 80% of these deaths occur in children.
Several methods are available for controlling these diseases. A combination of four inter-
ventions in different settings is proposed for the mosquito-borne diseases: the use of
insecticide-impregnated mosquito nets; the screening of windows, doors and eaves of
houses; the application of zooprophylaxis in places where mosquitoes are distinctly zoophilic;
and the use of insect repellents. For the control of schistosomiasis, a combination of case
detection and drug treatment is most cost-effective in the short term, but as prevalence drops
it becomes increasingly expensive. Environmental management and community health edu-
cation are then needed to make the achievement of drug treatment sustainable.

3. WHERE THE CHILD LIVES AND PLAYS 37

 Specific physical factors
Electric and magnetic fields
Extremely low frequency (ELF) electric and magnetic fields are produced by
the movement of charged particles, such as the transmission of electricity
through power lines. Electric fields arise from electric charges. Common mat·
erials such as wood and metal can shield against them. The motion of electric
fields gives rise to magnetic fields, which are not easily shielded and are there-
fore of most concern for health.
Electric and magnetic field strength in homes depends on many factors,
including the distance from local power lines, the number and type of electri-
cal appliances used in the home, and the configuration and position of house-
hold electrical wiring. Both fields decrease rapidly with distance.
The International Agency for Research on Cancer (IARC) has concluded that
ELF magnetic fields above 0-4 microtesla are possibly carcinogenic to humans
(8), based on consistent statistical associations of high-level magnetic fields in
residential areas with increased risk of childhood leukaemia.

Noise
Noise pollution is an often overlooked environmental risk that can be detrimental to human
health. As with many other environmental health concerns, children are more vulnerable than
adults to noise pollution. This is because of behavioural factors, such as a child's inability
to move away from a noisy situation, or a teenager's tendency to listen to loud music.
Children and teenagers can have problems with learning, language development, and con-
centration, as well as hearing damage and tinnitus, from overexposure to noise. Exposure
to excessive noise in the womb can cause babies to be born with high-frequency hearing
loss. Exposure to noise above 70 decibels (dB) can cause physiological changes, such as
an increase in heart rate and blood pressure. It is likely that children are routinely exposed
to levels of noise even higher than this (2).
Noise pollution is not always as obvious as air or water pollution, but it is important to protect
children from its harmful effects. Parents should discourage children from playing with loud
toys and listening to loud music. Hearing protection should be used in cases where noise
cannot be avoided, such as in work situations.

Radon
Radon is an inert radioactive gas that arises from the decay of radium 226
contained in various minerals found in soil and rock. The main source of radon
gas is soil, so that highest concentrations are found in basements. Some evi·
dence exists to suggest that 5-15% of lung cancer deaths may be associated
with residential radon exposure.

SECTION Ii: HOW AND WHEN EXPOSURE OCCURS

 References
1. Health principles of housing. Geneva, World Health Organization, 198 9.
2. Roche AF et al. Longitudinal study of hearing in children: baseline data con-
cerning auditory thresholds, noise exposure, and biologic factors. journal of the
Acoustic Society of America, 1978, 64:1593-1616.
3· Goren A et al. Respiratory problems associated with exposure to airborne parti-
cles in the community. Archives of Environmental Health, 1999, 54: 16 5-171.
4· Flanagan RJ, Rooney C. Recording acute poisoning deaths. Forensic Science Inter-
national, 2002, 128:3-19.
5· Overall evaluations of carcinogenicity to humans. Lyon, International Agency for
Research on Cancer (www.iarc.fr).
6. Prietsch SO et al. [Acute disease of the lower airways in children under five years
of age: role of domestic environment and maternal cigarette smoking.JJournal
of Pediatrics (Rio de janeiro) , 2002, 78:415-422 [in Portuguese].
7· Baumholtz MA et al. The medical importance of cockroaches. International
journal of Dermatology, 1997, 36:90-96.
8. Non-ionizing radiation, Part 1: static and extremely low-frequency (ELF) electric
and magnetic fields. Lyon, International Agency for Research on Cancer, 2002
(IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 80).

3· WHERE THE CHILD LIVES AND PLAYS

39
CHAPTER 4

Where the child learns

J. Pronczuk
Department for the Protection of the Human Environment,
World Health Organization, Geneva, Switzerland

A healthy school environment is crucial for protecting children's health

and promoting effective learning. Throughout the world, most children
attend primary school, spending up to eight hours a day for nine months
a year within classrooms and laboratories or in playgrounds and the sur-
rounding school areas. Myriad physical, chemical and biological threats
to children's health and development may be present inside or near the
school (1).
A contaminated school environment can cause or exacerbate health prob-
lems such as infectious diseases or asthma, which can reduce school atten-
dance and adversely affect learning ability. Pollutants in the school environment
may also be associated with chronic health effects, such as cancer or neuro-
logical diseases, that may appear much later in life.
Environmental threats vary considerably among schools in urban and rural
areas, within communities, countries and regions. The health and pollution
problems are generally related to levels of prosperity, and some may exist only
in certain climates or geographical areas, but many problems are global.
Contaminated water or food can result in diarrhoeal disease, which is more
common in poor countries, but may also affect schoolchildren in industrialized
countries. Air pollution around a school may result from industries or heavy
traffic, and this happens both in developed and developing countries. Exposure
to lead in paint is a risk in the old urban schools of some industrialized
countries. Exposure of schoolchildren to pesticides may occur following their
application to combat vectors of disease or may result from drift after field
application in agricu Itu ral areas (2).
Infectious diseases carried by water and physical risks associated with poor
construction and maintenance are examples of risks children face in schools
throughout the world.

What is the physical school environment?

The physical school environment includes the school building and all its con-
tents (physical structure, furniture, chemicals and biological agents in use or
storage), the site on which the school is located, and the surrounding environ-
ment (air, water, materials that children use or touch, nearby land uses and
roadways) (3).
 What are the main threats in the school environment?
Potential environmental threats present in the school and surroundings
include indoor and outdoor air pollution, contaminated drinking- and recrea-
tional water, lack of sanitation, contaminated food, vector-borne diseases,
unsafe buildings, and ultraviolet radiation. Other conditions that can adversely
affect children are extreme temperatures (very cold or hot buildings), lack of
light and ventilation, and overcrowding.
Lack of adequate sanitation facilities not only represents a health threat to
children but also leads to absenteeism, especially among girls (who in some
countries leave school once they reach adolescence, because of the lack of
adequate toilets).
In urban areas, children are exposed to outdoor air pollution from industry
and traffic exhaust on their way to school, and these pollutants may enter the
classrooms. Many children spend much of their school day indoors. The air they
breathe inside their school may be more polluted than outdoor air. For example,
in many rural schools, biomass fuels are used for heating and for the prepara-
tion of school meals, potentially exposing children to high levels of indoor air
pollution. Carbon monoxide, resulting from inadequate combustion in heating
devices, poses a very severe risk to the health and life of children. Indoor air
pollution results also from deficient heating systems, as well as mould, cock-
roach and rat detritus, and lack of ventilation. Poor indoor air quality may
increase the incidence of asthma, allergies, and infectious and respiratory dis-
eases, and also affect the performance of intellectual tasks involving concen-
tration, calculation, and memory (1).
In some parts of the world, rural areas are polluted by the smoke from
burning forests ("haze"). Drinking- and recreational water in schools may be
contaminated with metals (e.g. lead and arsenic), fluorides, organic solvents,
viruses and bacteria. Vector-borne diseases, such as malaria, yellow fever, and
dengue fever, may also affect children at school. Unsafe building structures
increase the risk offalls, trauma and lesions. This may be the case especially in
schools that are installed in old houses, which are totally unfit for educational
purposes. Old buildings may have lead in paint, asbestos insulation, and mould
in the walls.
New schools may be constructed on undesirable land, on sites that pose
health hazards. A famous example in the USA is the Love Canal dumpsite
in Niagara Falls, New York, where schools constructed on a former indus-
trial landfill were closed after testing showed excessive levels of contamina-
tion (4).
Exposure to ultraviolet radiation occurs when children play and do sports in
non-shaded areas around the school.
Children's behaviour may increase the risks of exposure (e.g. exploring dan-
gerous areas, touching objects and placing fingers in the mouth, not washing
the hands, rubbing the eyes). Adolescents often tend to act on impulse and take

4. WHERE THE CHILD LEARNS 41

risks (e.g. climbing and jumping or experimenting with drugs) and may lack the
experience to judge the risks associated with their behaviour.

What health effects can result from an adverse school

environment?
Acute respiratory infections (ARI). They are the most common disease in
children throughout the world, and pneumonia is the biggest cause of child-
hood mortality. ARI are linked to indoor and outdoor air pollution and other
environmental factors (5).
Asthma. Asthma and chronic respiratory illnesses such as bronchitis are
growing problems, especially in industrialized countries. Both indoor and
outdoor air pollution may increase the severity of the disease. Wood smoke,
moulds, and many volatile chemicals found in indoor environments can affect
the respiratory function in schoolchildren. School absenteeism associated with
these respiratory diseases can adversely affect both intellectual and emotional
development (6).
Diarrhoeal diseases. The second most common global illness affecting
young children and a major cause of death in low-income countries, diarrhoeal
diseases are closely associated with poor sanitation, poor hygiene, and lack of
access to clean water and food. Although diarrhoeal diseases are most deadly
in the developing world, they are also a significant health threat in developed
countries (7).
Vector-borne diseases. Mosquitoes, ticks, rodents, and flies may be present
in the school and are significant disease vectors. Mosquitoes can transmit
malaria, dengue fever, yellow fever, filariasis, and Japanese encephalitis. Ticks
can transmit Lyme disease, tick-borne encephalitis, and different fevers.
Rodents are capable of spreading plague (transmitted from rats to humans by
fleas). leptospirosis, and various viral and rickettsial diseases. In sub-Saharan
Africa, tsetse flies can cause trypanosomiasis (8).
Foodborne disease. In developing countries, a polluted environment, lack of
safe water supply and poor sanitation increase the likelihood offood becoming
contaminated. However, in all countries outbreaks of food borne illness may
result from improper food handling, such as use of contaminated equipment,
contamination by infected persons, use of contaminated raw ingredients, cross-
contamination, and addition oftoxic chemicals or use offood containing natural
toxins (9).
Accidents and injuries. In high-income countries road traffic accidents are
the most common cause of death among school-age children (5 out of every
100000 deaths) and in low- and middle-income countries they are the third
leading cause of death along with drowning (nearly 15 out of every 100000
deaths). Children attending schools located near busy roads or water bodies are
at increased risk of these types of accidents. Falls and other accidents within

SECTION II: HOW AND WHEN EXPOSURE OCCURS

42
 the school grounds can occur as a result of poor construction and poor main-
tenance (10).
Poisoning. Children can be poisoned at school as a result of the improper
storage or application of pesticides, or from exposure to lead in paint chips and
air, or chemicals in cleaning products. The effects oflong-term exposure to lead,
pesticides and other pollutants on children's health and development are likely
to outweigh the effects of acute poisonings (10).
Cancer. Some environmental childhood exposures, such as to ioniz-
ing and ultraviolet radiation, environmental tobacco smoke, some pesticides,
solvents, radon and arsenic, may contribute to the cancers that develop in
adulthood (2).
Developmental disabilities. Environmental factors are suspected to playa
role in the "epidemic" of learning and behavioural disabilities observed in some
parts of the world. Developmental disabilities are believed to be a significant
and frequently undetected health problem in developing countries, where mal-
nutrition and parasitosis (especially helminth infections) may contribute to
these illnesses (11). For example, in India, undernourished rural children 10-12
years of age had learning deficiencies when compared with normally nourished
children. Schools could play an important role in ensuring that students have
nutritious food to eat every day.
Exposure to toxic substances such as lead and mercury may induce devel-
opmental disorders. Children may suffer permanent brain damage from expo-
sure to lead, causing learning disabilities, hearing loss, reduced attention span,
and behavioural abnormalities.

What is a healthy physical school environment?

WHO defines a health promoting school as "one that constantly strength-
ens its capacity as a healthy setting for living, learning and working". A health-
ful school environment protects students and staff against immediate injury or
disease, promotes prevention activities, and teaches about risk factors that
might lead to disease or disability.
Access to safe water and sanitation and shelter from the elements are the
basic necessities for a healthy physical learning environment. Equally important
is protection from biological, physical, and chemical risks that can threaten chil-
dren's health (see box below).

Why do children need a safe school environment?

Children require safe schools, with clean water to drink, adequate sani-
tation facilities for boys and girls, clean air to breathe, safe and nutri-

4· WHERE THE CHILD LEARNS

43
 tious food, and a clean and quiet
Components of a healthy school place to learn and play. This allows
them to grow and develop nor-
environment
Provision of basic necessities mally, and enhances their learning
Shelter capacity.
Warmth Fu rthermore, schools represent
Water an example for the community. As
Food people become aware of how envi-
Light ronmental risks are dealt with at
Ventilation school they will recognize ways to
Sanitary facilities make other environments (home,
Emergency medical care playground, workplace) safer. In
addition, students who learn about
Protection from biological threats the link between the environment
Moulds and health will be able to recognize
Waterborne pathogens and remedy health threats in their
Foodborne pathogens own homes when they become
Vector-borne diseases adults.
Venomous animals It is therefore important to
Rodents provide the information that will
Hazardous insects help people understand the rela-
tionship between the environment
Protection from physical threats
and health, identify key hazards in
Traffic and transport
the places where children live, play,
Violence and crime
learn and work, in particular in the
Accidents
school environment, and recognize
Radiation
children's special vulnerability and
Protection from chemical threats exposure to environmental health
Air pollution threats. The health care provider
Water pollution should be able to detect and prevent
Pesticides those childhood diseases and
Hazardous waste effects that may be linked to the
Hazardous materials and finishes environment where the child learns.
Cleaning agents

SECTION II: HOW AND WHEN EXPOSURE OCCURS

44
 References
1. The physical school environment. An essential component of a health-promoting
school. Geneva, World Health Organization, 2003.
2. Sanborn M et al. Pesticides literature review. Toronto, Ontario College of Family
Physicians, 2004 (www.ocfp.on.ca).
3· School health and youth health promotion. Geneva, World Health Organization
(www.who.int/hpr/gshi/index.htm ).
4· Brown P, Clapp R. Looking back on Love Canal. Public Health Reports, 2002,
11]:95-98.
5· Health and environment in sustainable development. Five years after the Earth
Summit. Geneva, World Health Organization, 1997.
6. Aubier M. Air pollution and allergic asthma. Revue des Maladies Respiratoires,
2000,1J:l59-165·
7· Martines J et al. Diarrhoeal diseases. In: Jamison DT et aI., eds. Disease control
priorities in developing countries. Oxford, Oxford Medical Publications, 1993.
8. Vectors of diseases, hazards and risks for travelers. Part 1. Weekly Epidemiologi-
cal Record, 2001, 76:189-196.
9· International Life Sciences Institute. Global approach to prevent, detect, and
treat food-borne disease. ILSI News, 1997, 159.
10. Healthy environments for children: initiating an alliance for action. Geneva, World
Health Organization, 2002.
11. Oberhelman RA et al. Correlations between intestinal parasitosis, physical
growth, and psychomotor development among infants and children from rural
Nicaragua. AmericanJournal of Tropical Medicine and Hygiene, 1998, 58:470 -475.

4. WHERE THE CHILD LEARNS

45
CHAPTER 5

Where the child works 1

M. Tennassee
Division of Health and Environment, Pan American Health
Organization, Washington, DC, USA

Introduction
Every day, around the world, millions of children go to work instead of
school. The main reason for this is poverty, especially in developing countries.
But poverty is not the only reason for the existence of child labour; other factors
playa role, including inefficiency in educational systems and in enforcement of
relevant legislation, and lack of public awareness (1).
Children are different from adults in anatomy, physiology and psychology.
They are more vulnerable to hazards, such as long hours at work, exposure
to chemicals and physical risk factors, and psychological conditions. Many
children work in dangerous occupations and industries, and are exposed to
extremely dangerous situations and exploitative and abusive conditions. Dan-
gerous occupations are included in Convention No. 182 of the International
Labour Organization (ILO) on the worst forms of child labour. Governments,
employers, workers' organizations, universities, nongovernmental organiza-
tions (NGOs), occupational health profeSSionals and other interested parties
need to work together to establish programmes to eliminate these dangerous
forms of child labour and to protect children at work.

Characteristics and trends in child labour

In 2002, ILO estimated the number of working children aged between 5 and
14 years to be about 211 million worldwide. Of these, 127.3 million are in the
Asia-Pacific region, 48 million in sub-Saharan Africa, 17-4 million in Latin
America and the Caribbean, and 13-4 million in the Eastern Mediterranean and
North Africa (2). Developed and transition economies have the lowest numbers
of child labourers, with 2.5 million and 2-4 million, respectively.
According to the World Bank (1), in general, child labour participation rates
in the workforce are much higher in rural than in urban areas, and three-
quarters of working children work in a family enterprise. In rural areas, 90 %
of working children are engaged in agricultural or similar activities, while their
urban counterparts are found mainly in trade and services, with fewer in man-
ufacturing and construction. The same report of the World Bank found relatively

'Reviewed by Dr Gerry Eijkemans, Occupational and Environmental Health, WHO, Geneva,

Switzerland.
 few child workers in export industries (such as textile, clothing, carpets, and
footwear) compared with the numbers involved in activities geared to domes-
tic consumption.
In the United States, more than 5 million adolescents under 18 years are
legally employed, and a further 1-2 million are believed to be employed in vio-
lation of wage, hours, or safety regulations (3). According to household surveys
(4), there are 11.6 million children between 10 and 14 years old working in Latin
America and the Caribbean. If children under 10 years working in domestic
service are included, the total child workers in Latin America and the Caribbean
reach almost 18 million. The ILO estimates that one in five children in Latin
America is economically active (Table 5.1).

Table 5.1 Economically active child population in Latin America

COUNTRY TOTAL POPULATION ECONOMICALLY ACTIVE
AGEO 10-14 YEARS POPULATION 10-14 YEARS
NO. %
Argentina 3197582 214238 6.70
Bolivia 386222 54549 14.10
Brazil 16664591 1935269 11.61
Chile* 755227 14914 2.00
Colombia* 2327823 367796 15.80
Costa Rica* 203893 26009 12.80
Ecuador 1391433 420663 30.20
EI Salvador 661176 85516 12.90
Guatemala 1325725 316061 23.80
Haiti 847706 158182 18.66
Honduras 778714 88264 11.30
Mexico 10934134 1233353 11.30
Nicaragua 575137 42310 7.35
Panama 278631 12603 4.50
Paraguay 602417 49097 8.15
Peru* * 4928899 801033 16.20
Dominican Republic 871144 42302 4.80
Uruguay 253846 5278 2.08
Venezuela 3205592 80781 2.52
TOTAL 50189892 5948720 11.85
'Figures refer to population aged 12 to 14 years.
'*Figures refer to population aged 6 to 14 years.
Source: ref. 5.

5. WHERE THE CHILD WORKS

47
 Working conditions
There are some conditions that increase the risk to child workers. As noted
in an earlier chapter, children are not "little adults". Most biological systems in
the human body do not mature until about the age of 18. Many differences in
anatomy, physiology, and psychology distinguish children from adults. These
differences may translate into unique risk factors for occupational injuries and
illnesses (6), stemming from the nature of the work or from poor working con-
ditions. Because they are physically immature, children are more vulnerable to
the effects of arduous work and exposure to dangerous chemical substances.
Children are not physically suited to long hours of strenuous and monotonous
work and they suffer the effects of fatigue more than adults. Such labour can
have an effect on their intellectual development and physical health. Although
most working children combine work and school, often child labourers lack edu-
cational opportunities (2, 7).
What is particularly important is not so much the fact that the child works,
but the conditions in which he or she works. There is a huge difference between
a child who does 2 hours of light work a day, after going to school, and one who
works long hours in hazardous conditions. It is fundamental to make this dis-
tinction in order to prioritize action at national and local level.

Risk factors related to the physical environment

Most information about the health outcomes of child workers relates to
injuries, but illness may also result when children and adolescents are exposed
to hazardous materials, processes or tasks, or working conditions. Child
workers may be exposed to pesticides during farm work, benzene during work
at petrol stations, lead during vehicle repair, asbestos and silica during con-
struction and maintenance work, and loud noise during manufacturing, con-
struction, and farm work, to name a few. Exposures to hazardous materials and
working conditions may result in immediate illness or illness that is not detected
for months or years after exposure. In both cases, the association with work
exposure mayor may not be recognized (Table 5.2) (6).
According to ILO (9), a large number of working children are affected by
various phYSical, chemical and biological hazards; more than two-thirds (69%)
of them are found in the same countries. Many children suffer injuries or illness,
including punctures, burns and skin diseases, eye and hearing impairment, res-
piratory and gastrointestinal illnesses, fever, and headache from excessive heat.
The surveys carried out so far have assisted in identifying the specific industries
and occupations that are harmful to children. According to ILO (4), hazardous
workplaces for children include brick mould factories, mines, quarries, market-
places, rocketry manufacturing sites, domestic service, and agriculture.
Although more than two-thirds (70-4%) of all working children are in the agri-
cultural sector, where a large proportion of injuries occur, injuries also occur in
the construction, mining and transport sectors (10).

SECTION II: HOW AND WHEN EXPOSURE OCCURS

 Table 5.2 Some examples of hazardous agents to which working children may
be exposed
HAZARDOUS AGENT SOURCES OF EXPOSURE HEALTH EFFECTS
Biological agents
Contact with bacteria or Abattoirs, agricultural Anth rax, asth ma,
viruses, through contact animals, bone and meat brucellosis, catarrh,
with domestic and wild processing, butcher's shops, dermatitis, herpes, Q fever,
animals ivory and horn processing, leptospirosis, rabies, rat bite
poultry, stock, tanneries fever, ringworm,
salmonellosis,
toxoplasmosis, tuberculosis
Cotton, flax, linen Mixing and carding rooms, Byssinosis
rope-making, textiles,
twine-making, bali-pressing
plants, cotton ginneries

Physical agents
Compressed air Deep-sea diving Decompression sickness
Noise Textile engineering works, Hearing impairments
boilers, explosives,
compressors

Chemical agents
(including metals)
Organophosphorus Use of pesticides in Severe poisoning,
compounds agriculture neurological impairment,
death
Chromium and its Production or use of Asthmatic bronchitis,
compounds chromium salts, chromium impaired lung function,
plating, leather tanning, lung cancer, ulcerations and
metallurgy, refractory perforation of nasal septum
bricks
Coal dust (associated with Coal mines Anthracosilicosis (pulmonary
silica) coal tar derivatives fibrosis), lung cancer
Asbestos dust Brake linings, cement filter Asbestosis (pulmonary
for plastics, fire smothering fibrosis), lung cancer
blankets, mining of
asbestos, safety garments,
thermal and electrical
insulation

Source: Modified from ref. 8.

Factors related to work organization (amount of safety training and super-

vision) may increase the risk of injuries and illnesses among children and
adolescents. In a telephone survey, cited by the US National Institute for
Occupational Safety and Health (NIOSH) (6),54% of workers aged 14 to 16
years with work injuries reported receiving no training in methods to prevent

5· WHERE THE CHILD WORKS

49
their injuries. According to NIOSH, in the United States, every year at least 70
children under 18 years die at work, and more than 77000 are injured severely
enough to seek care in emergency departments (6).
The usual routes of exposure of children at work are:

• dermal-especially to chemicals such as pesticides (in lawn care and

agriculture), nicotine (while harvesting tobacco) and solvents (in vehicle
bodywork repair);
• inhalation-from metal fumes (such as lead), ammonia, isocyanates and
shellac;
• ingestion-of dangerous agents such as lead and other heavy metals
(10).

Child labour is more common in rural areas and concentrated in the infor-
mal sector of the economy. In some countries, a significant percentage of
working children are under the age of 10. Children not only work long hours
and may be exposed to physical, psychological, and social hazards that prevent
their normal development; they may also suffer intolerable exploitation such as
slavery, servitude, forced labour, and sexual abuse.
In urban areas, children can be found working in trade, domestic service,
construction and manufacturing sectors, as well as begging and performing dif-
ferent tasks on the street.
In manufacturing, they may suffer serious cuts, fractures, burns, skin dis-
eases, and respiratory illnesses. Table 5.3 shows some potential job-related
exposures of child workers.

Psychosocial risk factors

"Child labour damages children's physical and mental health ... Working
children are more vulnerable than adult workers not only for physiological
reasons, but also because of a combination of psychological and social reasons.
Some children at work are under psychological stress. The motivation for them
to start working and to retain the job is to contribute to the financial support of
the family, which is a heavy responsibility at an early age .... [they] may prefer
to face a challenge rather than be considered weak by the other playmates and
therefore may attempt the riskiest tasks" (8).
The psychosocial risk factors are extremely important in children who work
under the unconditional worst forms of child labour, such as defined in ILO con-
vention C182 (1999). In slavery and forced labour systems, the most common
of which is debt bondage, children work to payoff a debt or other obligations
incurred by the family. There are also less "formal" types of child slavery and
forced labour, in which rural children are lured to the city with false promises
of work, only to be forced into domestic service or sweatshops. Children are

SECTION II: HOW AND WHEN EXPOSURE OCCURS

50
 Table 5.3 Potential job-related exposures of child workers

Bloodborne pathogens-in nursing homes and hospitals

Cleaning agents-in restaurants, nursing homes, schools
Pesticides-in lawn care, farm work, and when buildings are sprayed
Isocyanates-during vehicle bodywork repair or roofing with newer forms of roofing materials
Benzene-when pumping petrol
Lead-from radiators in vehicle repair and home renovation
Asbestos-in vehicle brake repair, renovation/demolition of old buildings
Solvents-in T-shirt screening
Second-hand smoke-in restaurants and bars
Heat-in washing dishes, in working outdoors in hot weather
Cold-in outdoor jobs in cold weather
Wood dusts-in furniture making
Fumes and eye damage-in welding
Chemicals and dyes-in cosmetic manufacture
Biological/infectious hazards-in farming, work with animals
Noise-induced hearing loss-in farms and factories
Nicotine-in harvesting of tobacco

Source: adapted from ref. 11.

also being used in drug trafficking in many cities of Latin America, and are them-
selves victims of drug trafficking organized by criminal networks.
As they grow, children experience profound psychological changes as well
as physical and physiological ones. The psychological transition is often less
visible than the physical one, requires more time to complete, and typically lags
behind physical maturation. Thus psychological immaturity may be obscured
by a relatively mature physical appearance in an adolescent. As a result, a child
worker may be aSSigned to a task for which he or she is emotionally or cogni-
tively unprepared. In addition, young workers often do not have adequate experi-
ence to judge their ability to complete an assignment safely. There is no easy
way of characterizing the complex psychological development that takes place
during adolescence and the potential consequences for working adolescents. A
general lack of work experience, coupled with normal adolescent psychological
development, places adolescents at high risk of injury at work.
It is important to mention the situation of live-in child domestic workers,
i.e. children who work full-time in other people's households, doing domestic
chores, caring for children, running errands, etc., in exchange for room, board,
care, and some remuneration (12). The number of children in this position is
literally uncountable at present because of the "hidden" nature of the work,

5· WHERE THE CHILD WORKS

51
which lies largely beyond the scope of conventional labour market mechanisms.
However, improved statistical survey methods being pioneered by the I LO indio
cate that the practice, especially in the case of girls, is extensive. In Brazil, for
example, 22% of working children are employed in domestic service. The major·
ity of child domestic workers are between 12 and 17 years old, but some surveys
have identified children as young as 5 or 6 years. Their hours of work are usually
long-1 5 or 16 hours a day is not uncommon. There is also alarming evidence
of physical, mental and sexual abuse (12).
Child domestic workers usually come from poor families and the majority
will probably remain poor throughout their lives. Work as a child domestic
worker perpetuates poverty, as it usually does not allow for an education. In
addition, it is rare for the child to receive payment directly, if at all; wages may
be paid directly to the parents, if contact is maintained, but often the employer
provides food, shelter and clothing instead of payment. Regardless of the type
of employment, the assigned duties often go beyond the children's ability.
Children may often work 15 or more hours a day, seven days a week. In
studies that have examined their physical wellbeing, children complain of
fatigue, headaches and other health problems. Accidents are a risk, in particu-
lar when the child is exhausted. There are hazards associated with cooking,
boiling water, chopping vegetables, using cleaning fluids and carrying heavy
items. Burns are relatively common among child domestic workers. The Inno-
centi Digest on Child Domestic Work, issued in May 1999, states that the pos-
sibility of sexual abuse or exploitation presents risks of sexually transmitted
diseases and early pregnancy in these girls. Usually pregnancy leads to dismissal
and in some countries rejection by the girl's own family. In addition, the isola-
tion and ill-treatment that child domestic workers endure may lead to low self-
esteem. Health care providers should be alert to any signs, symptoms, or
indications that may suggest that there is child labour. In this case, they should
explain and discuss the problem with parents and care-givers and involve the
relevant social actors who could take appropriate action.

References
1. Fallon PRo Child labour: issues and directions for the World Bank. Washington, DC,
World Bank, 1998.
2. Every child counts: new global estimates on child labour. Geneva, International
Labour Office, 2002 (www.ilo.org).
3- American Academy of Pediatrics, Committee on Environmental Health. The
hazards of child labour. Pediatrics, 1995, 9s:3 11 -3 13·
4. Action against child labour 1999-2001. Progress and future priorities. Geneva, Inter-
national Programme on the Elimination of Child Labour, International Labour
Office, 2001.
5. International Programme on the Elimination of Child Labour. Working Document,
San Jose, International Labour Office, 2002 (Brochure).

SECTION II: HOW AND WHEN EXPOSURE OCCURS

 6. National Institute for Occupational Safety and Health. Child labour research
needs. Recommendations from the NIOSH Child Labour Working Team. Washing-
ton, DC, US Department of Health and Human Services. Public Health Service.
Centers for Disease Control and Prevention, 1997.
7· Action against child labour: lessons and strategic priorities for the future. A synthesis
report. Geneva, International Labour Office, 1997.
8. Forastieri V. Children at work. Health and safety risks. 2nd ed. Geneva, Interna-
tional Labour Office, 2002, 169 pages.
9· International Programme on the Elimination of Child Labour. Action against child
labour. Achievements, lessons learned and indicators for the future (199 8- 1999).
Geneva, International Labour Office, 1999.
10. Fassa AG. Health benefits ofeliminating child labour. Geneva, International Labour
Organization, 2003.
11. Workplaces. In: Handbook of pediatric environmental health. Elk Grove Village, IL,
American Academy of Pediatrics, 1999:295-3 0 4.
12. Child domestic work. Innocenti Digest. New York, United Nations Children's Fund,

1999·

5· WHERE THE CHILD WORKS

53
CHAPTER 6

Where the child is under extreme stress1

R. Bu-Hakah
Department of Emergency and Humanitarian Action, World
Health Organization, Geneva, Switzerland

How and when does exposure happen?

Too many children throughout the world are confronted with extreme stress
from a variety of sources, including war and conflict, environmental disasters,
physical and emotional abuse, loss of parents and being forced to abandon their
homes. In such situations, survival becomes the child's instinctive and primary
concern.

Mechanisms of exposure
Under extreme circumstances, such as floods, droughts, environmental and
technological disasters, and wars and conflict situations, and the consequent
displacement and refugee movement, the whole spectrum of threats to chil-
dren's health changes. Extreme situations can be described in terms of four
characteristics:

• speed of onset (sudden or gradual);

• duration;
• type (natural, technological, conflict);
• impact.

Children's exposure to these threats can be (1) sudden or slow, (2) acute or
chronic, (3) direct or indirect, (4) purposeful or unintentional. Exposure may
occur in the familiar environment, with minimal change in its physical charac-
teristics. Alternatively, exposure can take place in a completely new environ-
ment, as in the case of refugee children. Table 6.1 summarizes the various
situations, their characteristics, effects and consequences.
Despite the characterizations mentioned above, there is tremendous com-
plexity surrounding each extreme situation. For example, an earthquake can
occur in a known physical environment but it causes the destruction of
familiar landmarks, such as homes, schools and churches. An unfamiliar and

'Reviewed by C. Corvalan, Department for the Protection of the Human Environment, World
Health Organization, Geneva, Switzerland; A_ Loretti, Department of Emergency and
Humanitarian Action, World Health Organization, Geneva, Switzerland; D. Rasmussen,
Department of Emergency and Humanitarian Action, World Health Organization, Geneva,
Switzerland.

54
 >" Table 6.1 Summary of various types of traumatic situations, their characteristics, initial effects and consequences
:E
I
en SITUATION
;0 ONSET INCREASED NEW RISKS CHANGE IN BREAKDOWN OF
en VIOLENCE INCREASED
-I
EXPOSURE TO SURROUNDINGS SOCIETY/COMMUNITY POVERTY
I ENVIRONMENTAL STRUCTURE
en
()
THREATS
I
r= Drought slow +
0 + +
Vi Flood sudden ++ ++ + or ++
c +
z Earthquake sudden +++
0
++ +++ +
en Volcano sudden +++
;0
en
++ +++ +
X War sudden + +++
-I +++ ++ +++ +
;0
en chronic + ++ +++
s::: +++ +++ +
en Refugee/displacement chronic +
til
++ +++ +++ +++ +
-I Technological slow ++
;0
en ++ +++ +
til
til
sudden +++ +++ ++ +
+, slight; ++, moderate; +++, significant; -, no change.

V1
V1
unsettled environment surrounds the child when he or she is on the move, dis-
placed or seeking refuge in another province or in another country as a result
of a natural disaster or conflict. Alternatively, in conflicts and ongoing wars, the
physical environment may be only mildly damaged but the normal life activities,
and even the societal structure, change.
Under these extreme circumstances, the risk of exposure to environmental
threats is typically increased. There may be greater potential for water- and food-
borne diseases, poisoning, air pollution, electrocution, traffic accidents and
other injuries. Other risks may be rare, unforeseen or unconventional, includ-
ing injury by landmines and unexploded ordnance, exposure to nuclear radia-
tion or depleted uranium, or spewing of hot ashes and burning lava from a
volcanic eruption. Sadly, in some countries these formerly unanticipated threats
are becoming commonplace. In Angola, for example, which is plagued with an
extraordinary number of landmines, the probability of stumbling on a land mine
is higher than that for any other trauma (1,2).

Health consequences
The consequences of extreme stress can be severe in both physical and psy-
chological terms. Lack of adequate nutrition, unavailability of water, spread of
communicable disease, exposure to toxic chemicals, loss of housing and
increased violence are just some of the physical threats that confront children
in such situations. Children living in war zones or areas of conflict are subject
to violence, which they either witness or experience directly. Environmental
threats may provoke respiratory illnesses, enteric infections, and vector-borne
diseases. Many children die in infancy, and maternal mortality and incidence of
miscarriage and stillbirth often rise significantly. During flight from an acute
threat, such as war or natural disaster, children often become separated from
their families and their communities and ethnic groups. Many are orphaned.
In some countries, large numbers of children have been kidnapped to serve
as "military slaves" or recruited as child soldiers in prolonged situations of
conflict.
Emotional trauma, depression, grief and fear are some of the psychological
effects manifested in children under extreme stress. In a war situation, children
may become accustomed to violence, losing the ability to empathize, and may
become aggressive. In one study, emotional and stress disorders were observed
in children in situations of extreme stress, in the form of sleep disorders and
nightmares. Children become fearful, their personalities may change, they
become withdrawn, and are unable to play (3)·

What to do for a child who is extremely stressed

The United Nations Children's Fund (UNICEF) publication, Factsfor life (4),
serves as an excellent resource on assisting children who are especially stressed.
This publication offers key messages on addressing the challenges that children

SECTION II: HOW AND WHEN EXPOSURE OCCURS

 confront in such situations. Provid-
ing access to basic nutrition, water Key messages on action in emergency
and sanitation are the first chal- situations
lenges. Consideration of psycho- What every family and community has a right to
logical stability, stress management know about disasters and emergencies
and emotional health is important
for children, both during and after 1. In disaster or emergency situations, children
should receive essential health care, includ-
the crisis. Other important steps for
ing measles vaccination, adequate food and
alleviating stressful situations are
micronutrient supplements.
summarized in the box opposite.
2. Breastfeeding is particularly important in
emergency situations.
Remedial action, prevention
3. It is always preferable for children to be cared
and education
for by their parents or other familiar adults,
Disasters can kill large numbers especially during conflict situations, because
of people at one time. The number it makes children feel more secure.
will depend on the vulnerability or 4. Violence in the home, war and other disas-
susceptibility of a community to ters can frighten and anger children. When
hazards and its resilience. Emer- such events occur, children need special
gency preparedness at the individ- attention, extra affection and the opportunity
ual, community and national level to express their feelings and to describe their
can alleviate the physical and emo- experiences in ways that are appropriate for
tional effects on all citizens. Chil- their age.
dren largely depend on families, 5. Landmines and unexploded ammunition are
communities and other sources of extremely dangerous. They should never be
aid to prepare for disasters. Infor- touched or stepped over. Establish safe play
mation resources are available that areas for children and warn them not to play
provide guidelines and recommen- with unknown objects.
dations for emergency prepared- Source: ref. 4.
ness for different types of situations
(5)· These are summarized in
Table 6.2.

6. WHERE THE CHILD IS UNDER EXTREME STRESS

57
 Table 6.2 Summary of emergency preparedness and mitigation

NATIONAL LEVEL COMMUNITY LEVEL FAMILY LEVEL HEALTH PROFESSIONAL

OISASTER
V1
00
National disaster plan Community disaster committee Family disaster plan: Participation or identifying community
Natural disasters
knowing what disasters are disaster committee
Earthquake Disaster committee Participation of sector/
Floods societies representatives from most likely to happen, Training in disasters and emergencies
National drills
Drought health, water, engineering, learning about community Participating in drills
Landslide Organization of training and police, fire fighters, civil warning signals,
re-certification for health, Maintain updated knowledge and
Volcanic eruption defence, education, local knowing location of
search and rescue teams, information about hazards
Bush fires media, clerics and social emergency shelters,
Cyclones police, army workers Ensuring that health facility/workplace
knowing where family has a disaster plan and reducing its
Early warning system Community disaster plan, members are likely to be and vulnerability to disasters
Communication networks and education campaign targeting ensure numbers/contacts,
alternatives schools, health facilities and Participating in public education and
explaining danger of fire, information campaigns, distributing
Laws industrial plants
severe weather, floods, and information material
Hazard mapping Hazard identification at the earthquakes to children,
Vl
en level of community Educating families and children about
...,
n Insurance having a place to meet outside disaster risks and protection
6 Drills and simulation house in case of a disaster,
z Disaster funds Identification of possible Preparing with social workers for
stocks for at least 3 days, support in case of a disaster
Public information campaigns shelter facilities
I supplies, change of clothes,
o (media, schools, health Emergency stocks Ensuring stocks of essential drugs and
:E facility) for public education, blankets,
supplies
}>
warning and for support Early warning system based on sanitation supplies,
z Disease surveillance networks and
o during response communication facilities and first-aid kit and prescriptions,
:E networks alternatives
I
en Emergency stocks (food, water learning how to turn off water,
Z purification, drugs and medical Evacuation routes, electric fuse box and gas,
en responsibilities and plans
X
'0
supplies) keeping radio and batteries,
oVl Health facilities assessments First aid courses and volunteer taking first-aid course.
c training and identification
and reduction of vulnerability
'"en Coordination with other
o
n Evacuation plans and
n responsibilities neighbouring communities
c
'"
Vl
Development of provincial/
district and sector-specific
disaster plans
 Epidemics In addition to above and In addition to the above Health education on basic Training and keeping updated
0 especially for the Ministry of (disaster committee): hygiene and disease
:E Health: knowledge
I Updated lists of health transmission, protective
en
Procedures for obtaining funds Simulations and drills
;u
en providers, laboratories, measures, signs of some
--I and other resources such as pharmacists and facilities epidemic diseases Delivering health education
I messages
en transportation, drugs, vaccines, Training on home-based care
n Identification of alternatives
I
health workers Participating in community activities
for health facilities and Immunization and regular with health focus
c-
O Intersectoral collaboration isolation wards visits to health facilities
Vl
Coordination with private Distributing information booklets
C Public health community List of emergency contacts
Z sector and with NGOs, and brochures about epidemic
0
disaster plan (doctor, nurse, health worker) diseases
en implementation of key
;u Public education and
en environmental measures Documenting cases and reporting
X information campaign (media
--I
;u Surveillance systems activated cases of epidemic prone diseases
en and special events) and
;;: and level of alert heightened community health education Ensuring and advocating
en
Vl
Training of health care staff, programmes environmental protection measures
--I
;u
en and a core of epidemiologists such as sanitization of food
First aid/volunteers training
Vl
Vl preparation areas, spraying, solid
Ensuring communication Dissemination of simplified waste disposal, disinfecting and
systems at health facility and protocols and flowcharts to protecting water sources
timely reporting teachers, social workers
Establishing network of Early warning and reporting
laboratories and procedures for procedures
collection and testing samples
Health education in school
Case management protocols curricula/youth clubs
Public health mapping Ensuring regular and adequate
implementation of
environmental measures for
controlling infections such as
spraying, sanitization of food
V1
preparation areas, solid waste
\0 disposal, disinfecting and
protecting water sources
 Table 6.2 continued
0'1
o COMMUNITY LEVEL FAMILY LEVEL HEALTH PROFESSIONAL
DISASTER NATIONAL LEVEL
Ensure access to information Training in first aid/trauma care
Armed conllicts In addition to the above: In addition to the above:
Evacuation routes Participate in community activities
Focus on advocacy for peace Develop community
and negotiation for contingency plan Access to shelter Training in counselling and
preventing conflict Train community health psychological support
Information to children and
Preparing in case negotiations workers on counselling and logical explanation provided Network with other health
fail psychological support professionals
First-aid kit and essential
Coordinating mechanisms of Strengthen community supplies stock Advocate for peace
health-related interventions participation and consultation Contacts lists, addresses of Ensure that health facilities have
mechanisms relatives disaster plan and stocks in place
Vulnerability assessment
Identify possible reception Identify vulnerable areas in health
Information collection, Maps
Vl sites in case of displaced facilities
rn analysis and management
C1 population
systems
(5 Conduct vulnerability
z Develop contingency plans,
assessments
security issues
I Prepare stocks of emergency
~ Training on war surgery
supplies, identify supply
» Identification of safe facilities routes
z
o Blood transfusion campaigns
:E Evacuation routes and
I
rn Special arrangements and procedures
Z agreements for wounded/
rn Security issues
X deaths
"o
Vl Mass casualty management
C

""orn Identification of intensive

()
care facilities and
()
C development of referral
""
Vl protocols
 '"
l2'
I
en
Al
en Technological In addition to the above: In addition to the above: In addition to the above:
--I In addition to the above:
I accidents Implement local awareness
en Coordinate with local Be familiar with hazards Participate in emergency planning
n and preparedness plans for industry emergency plans
I around them, alarm signals,
r- emergencies at local level Training on identification and
0 Raise public awareness and evacuation plans
management of toxic spillages
Vl Engaging industries and mobilize support for Ensuring that doors and
C communities emergency plan Procedures and protocols
Z windows are equipped with
0 disseminated
en Enforce implementation of Improve fire fighting tight fastenings
Al
labelling, sites planning, Identification of possible
en capacities at plants and in
X
--I storage facilities monitoring surrounding areas decontamination areas
Al
en and regulation Drills and simulation exercise
s::
en
Evaluate risk and hazards of
Vl Requirements of insurance storage sites and map them, Stock of protective equipment and
--I
Al
en
for industries handling review plans regularly supplies
Vl hazardous chemicals
Vl
Regular inspection of
chemical plants and storage
facilities
Land use planning and zoning
Maintain monitoring and
database about transportation
hazards
Conduct drills, evacuation
exercises
Monitor pollution level and
report incidents

S'
 Table 6.2 continued
0'1
HEALTH PROFESSIONAL
'" DISASTER NATIONAL LEVEL COMMUNITY LEVEL FAMILY LEVEL

In addition to the above: In addition to the above: In addition to the above: In addition to the above:
Terrorist attacks
Family kit Preparing and training health care
Mass casualty plans Maintaining databases of
specialists, laboratories and Water (for at least 3 days) staff to deal with stress and anxiety
Ensure surveillance systems are and to provide counselling and advice
essential supplies providers Food: canned meats, fruits,
able to detect unusual pattern of
Participation of health providers vegetables, sugar, high-energy Training/refresher course in trauma
diseases or injuries
in preparedness activities food, food for infants care, triage
Coordination and intersectoral
Report suspicious incidents and First aid supplies: bandages, Training and awareness of signs and
collaboration
coordinate with national levels gauze, scissors, tape, safety pins, symptoms of diseases, exposure to
Evaluation of health facilities chemical agents, decontamination,
soap, antiseptic, thermometer,
preparedness Mobilization plans for personal protective equipment,
volunteers and community pain reliever
Disaster plans, practice drills support and therapy
Vl members Clothing and bedding
rn Stockpile appropriate drugs, Tools and supplies (paper cups, Simulation exercises, drills
C1 Emergency plans to ensure
(5 antidotes and vaccines plates, battery-operated radio, Stocks of antidotes, drugs and
alternatives to main utilities
z Prepare educational materials such as electricity and water batteries, flashlight, can opener protective equipment maintained
I
that will inform and reassure the sources or knife, fire extinguisher, Documenting and reporting
o public during and after compass, paper, pencil, whistle,
:E Mass communication systems Health facilities plans
» biological or chemical attack map, toilet paper, chlorine
z Mechanisms for informing
o Disseminate public health Special items for specific needs
health providers on possible
:E guidelines to local level of infants, the elderly and family
I threats
rn
Z Collection, analysis and documents
Expertise of epidemiologists
rn
X
information sharing
"0 enhanced and resources
oVl available
C
;<:J
rn Drills and exercises
o
n Prepare adaptation of
n
c educational material to be
;<:J
Vl distributed in case of an attack
 References
1. Chaloner EJ. The incidence of landmine injuries in Kuito, Angola. Journal of the
Royal College of Surgeons of Edinburgh, 1996,41:398-400.
2. Landmine-related injuries, 1993-1996. Morbidity and Mortality Weekly Report,
1997,46 7 24.
3· McDermott 8M, Palmer LJ. Post disaster emotional distress, depression and
event-related variables: findings across child and adolescent developmental
stages. Australian and New Zealand Journal of Psychiatry, 2002, 36 :754.
4· Facts for life, 3rd ed. New York, United Nations Children's Fund, 2002.
5· Health action in crises: reducing the impact of crises on people's health. Geneva,
World Health Organization, 2003.

6. WHERE THE CHILD IS UNDER EXTREME STRESS

CHAPTER 7

When the child uses alcohol and

other drugs1
M. Monteiro
Department of Mental Health and Substance Dependence,
World Health Organization, Geneva, Switzerland

Introduction
There has been a considerable increase worldwide in the production and
consumption of psychoactive drugs, including new drugs such as ecstasy,
amfetamines, and other synthetic substances. Five of the ten leading causes
of disability worldwide are mental disorders, including alcohol dependence (1).
In 2000, alcohol, tobacco and illicit drug use ranked among the top twenty
risks to health worldwide, with tobacco and alcohol among the top five (2).
Psychoactive drugs are substances that, when taken into a living organism,
may modify its perception, mood, cognition or behaviour. They include alcohol,
tobacco, volatile solvents, illicit drugs and psychotropic medications (prescribed
or taken illicitly or not as prescribed). There has been an increase in the avail-
ability and use of alcohol, tobacco and other drugs among children and young
people, marked by a change in the social context in which drugs are taken and
in patterns of drug use.

Routes of exposure: how do children gain access to alcohol

and drugs?
Globalized marketing and trade in many consumer goods, improvements in
transportation networks, increases in disposable incomes, and rapid social
changes are some of the factors related to the increase in the availability of
alcohol and other drugs worldwide. Populations have been brought into contact
with each other's customs and behaviour through tourism, migration, and inter-
nal displacements, particularly from rural to urban areas, bringing new cultural
norms and attitudes towards alcohol and other drug use. Rapid urbanization
leads to overcrowding, adverse living conditions, poor sanitation, and lack of
access to recreational activities, placing an increased burden on the lives of chil-
dren and their parents. Changes in work opportunities, and social isolation and
disintegration are also related to an increase in the consumption of alcohol,
tobacco and other drugs.

'Reviewed by V. Poznyak, Department of Mental Health and Substance Dependence, World

Health Organization, Geneva, Switzerland.
 In some parts of the world, the majority of the population remains in poverty,
and destitution has increased. In some places particularly affected by famine
and warfare, government functions have essentially ceased and illicit drug pro-
duction has flourished. In others, the economic power of the illicit drug market
has become a threat to the stability of the government and its ability to
function (3).

Substance use and health in children and adolescents

Alcohol and other substance use is related to key determinants of popula-
tion health, such as poor education, low income and social status, lack of social
support networks, unemployment and adverse working conditions, unhealthy
physical environments, and lack of or inadequate access to health services (4).
It is also an independent determinant of population health linked to overall mor-
tality and hospitalizations. Risky patterns of alcohol consumption are more
prevalent among young males, and unemployed or poorly educated individ-
uals; consumption is increasing in developing societies where drinking is not
part of the tradition and culture, and where alcohol is very cheap (5). Poor
health and living conditions can also lead to alcohol and other substance use
problems, and drug use can serve as a paradigm for understanding and
analysing inequalities and inequities in health (4, 6).
Alcohol and other drug use needs to be seen as multidimensional and
complex behaviour, which cannot simply be said to be the result of a "free
choice". It often occurs in the context of difficult social, environmental and
economic conditions, in which the freedom to choose whether or not to take a
substance is seriously compromised by several individual and environmental
factors. Alcohol and other drug use may serve as coping strategies in dealing
with difficult life circumstances, including physical, emotional and sexual abuse
at home (7).
The role of psychoactive substances in the lives of children and adolescents
is related to the environmental conditions in which they live. They can
serve to solve temporary problems including hunger, boredom, fear, feelings
of shame, depression, hopelessness, lack of medicine and medical care,
difficulty falling asleep because of noise or overcrowding, cold or heat,
tiredness, risk of attack and abuse, lack of recreational facilities or
after-school activities, social isolation, lack of proper parenting, loneliness and
physical pain.
Under difficult economic and social conditions young people may resort to
d rug dealing in order to make enough money to provide basic needs and a better
quality of life for themselves and their families. Trafficking of small amounts of
illicit drugs provides an appealing opportunity for young people, who are often
na"ive about the legal consequences of their acts, may feel protected by gangs
or see no other opportunity to obtain goods and services advertised Widely in
the media.

7. WHEN THE CHILD USES ALCOHOL AND OTHER DRUGS

 Alcohol and other substance use problems are growing faster in societies
undergoing rapid social change and as a result of the globalization of markets
and increases in the availability of these substances (both legal and illegal), par-
ticularly in countries without strong policies to counteract these problems. For
example, alcohol consumption is increasing rapidly in eastern Europe and Asia
(8). Intravenous drug use is the major factor in the spread of human immuno-
deficiency virus in eastern Europe and Asia (9), where new trafficking routes
have been established, and rapid socioeconomic changes are taking place (10).
The age at which people start to use drugs and tobacco is decreasing.
Patterns of drug use depend on the living conditions of children and young
people. For example, studies have found that between 25% and 90% of street
children use psychoactive substances of some kind. Other marginalized and
vulnerable groups, such as gypsies, indigenous populations, sex workers,
homeless people and prisoners, also have relatively high rates of use and
related problems. These behaviours often begin in early adolescence and can
interfere with development, affect school performance, and be linked with other
behavioural problems that can have an impact later in life (11, 12).
Schoolchildren also use alcohol, tobacco and other drugs. Marketing and
promotion of alcohol and tobacco create a permissive environment that
glamorizes the use of these substances, and links their use with particular
lifestyles which are often very appealing to young people but are unaffordable
or unrealistic. Experimentation with other drugs, often illicit, is related not only
to access and street price, but also to youth culture.
Profiles of problems can vary dramatically from region to region, even for
the same drug. Health consequences are strongly related to the characteristics
of the d rug itself, the mode of ad mi n istration and the pattern of use. Social con-
sequences of drug use are determined not only by the behaviour of the user but
also by the reaction of those in the social environment. These include the levels
of tolerance towards alcohol and other drug use, existing laws and their enforce-
ment, and cultural norms regarding drug use and consequences.

Remedial action, prevention and education

The environment can also offer a range of protective factors that decrease
the chances of a child or young person using alcohol and other drugs. These
include limited availability of drugs and alcohol, restricted access, opportuni-
ties for education and leisure activities, support for parents and youth groups,
a culture that is not permissive towards alcohol and other drug use, an envi-
ronment that promotes dialogue and offers opportunities for young people to
express their views, and opportunities for confidential counselling and infor-
mation on substance use and related topics. Positive and strong attachments
or close relationships with other people, either parents, relatives or friends, can
have a positive influence on the behaviour of young people. Negative attach-
ments are connections to people or institutions associated with substance use,

66 SECTION II: HOW AND WHEN EXPOSURE OCCURS

 abuse or exploitation, such as drug syndicates or peers who use drugs: such
attachments make substance use more likely. Finally, young people need to
develop physical, psychological, social, moral and vocational competencies as
a part oftheir healthy development, in order to be less likely to harm themselves
with psychoactive drugs.
I n conclusion, the environment in which children and adolescents live can
have both risk and protective factors that strongly influence the decision to
experiment with a psychoactive substance or to continue to use it, as well as
the health and social consequences. Rather than just trying to convince indi-
vidual users to avoid any contact with drugs, environmental responses need to
be promoted to strengthen protective factors and weaken the risk factors that
contribute to substance use among young people.

References
1. The World Health Report 1999: making a difference. Geneva, World Health Orga-
nization, 1999.
2. The World Health Report 2002: reducing risks, promoting healthy life. Geneva, World
Health Organization, 2002.
3· WHO Expert Committee on Drug Dependence: twenty-eighth report. Geneva, World
Health Organization, 1993 (WHO Technical Report Series, No. 83 6).
4· Single E. Substance abuse and population health. Paper presented at the
Workshop on Addiction and Population Health, Edmonton, June 1999
(http://www.ccsa.ca/ADH/single.htm) .
5· Room R et al. Alcohol in a changing world: drinking patterns and problems in
de~eloping societies. Helsinki, Finnish Foundation of Alcohol Studies, 2002.
6. Leon DA, Walt G, Gilson L. International perspectives on health inequalities and
policy. British Medical Journal, 2001, 322:591-594.
7· Radford J, King A, Warren W. Street youth and AIDS. Kingston, Health and Welfare
Canada, 1989.
8. Global status report alcohol. Geneva, World Health Organization, 1999.
9· AIDS epidemic update: December 2000. Geneva, Joint United Nations Programme
on AIDS, World Health Organization, 2000 (UNAIDS/oO.44E; WHO/CDS/CSR/
EDC/2000·9) .
10. Global illicit drug trends, 2000. Vienna, United Nations International Drug Control
Programme, 2000 (ODCCP Studies on Drugs and Crime).
". Brown SA et al. Conduct disorder among adolescent alcohol and drug misusers.
Journal of Studies on Alcohol, 1996, 5]:314-324.
12. Linskey M, Hall W. The effects of adolescent cannabis use on educational attain-
ment: a review. Addiction, 2000, 95:1621-163°.

7· WHEN THE CHILD USES ALCOHOL AND OTHER DRUGS

 Specific environmental threats:
sources of exposure and health effects
 CHAPTER 8

Water quality1
1. Boonyakarnkul
Sanitation and Health Impact Assessment Division,
Department of Health, Ministry of Public Health, Bangkok,
Thailand

P. A. Kingston
Queensland Environmental Protection Agency, Brisbane,
Australia

K. M. Shea
Division of Occupational and Environmental Medicine,
Department of Community and Family Medicine, Duke
University Medical Center, Raleigh, USA

Overview
Viewed from space the earth appears to be mostly water; but only 2.5% of
that water is fresh, and most of that lies frozen and inaccessible. As a result,
less than 1% of fresh water is accessible in lakes, river channels and under-
ground. Geography, environment, and pollution from human activities reduce
this by a further two-thirds, and what remains is unequally distributed around
the world (1).
It is estimated that between 1990 and 2000, the global population increased
from 5.25 billion to over 6 billion, an increase of over 15%. Within that total,
there was a 25% increase in the urban population, and an 8% increase in the
rural sector. This population increase meant that an additional 800 million
people required access to safe water supplies, just to maintain coverage at a
constant level. During this period an additional goo million people gained
access to an improved source of water, resulting in an increase in coverage from
77% to 82%. Despite these gains, there are still more than 1.1 billion people, or
1/6 of the world's population, without access to adequate sources of drinking-
water (2).
The decade also saw a marked shift in the urban-rural population ratio; by
2000, the proportion of urban dwellers had risen from 43.5% to 47%, and the
growth showed no signs of slowing. The rate of urbanization is greater in the
developing world, particularly in Africa and Asia, and this, together with lower

'Reviewed by J. Bartram and J. Hueb, Department for the Protection of the Human Envi-
ronment, Water, Sanitation and Health, World Health Organization, Geneva, Switzerland.
 levels of safe water supply, make these locations particularly vulnerable to the
risk of water-related diseases_ By 2000,81% of Asians and only 64% of Africans
had access to safe sources of drinking-water, despite worldwide efforts.
Even with the modest increases in water supply coverage, there is evidence
that, because of the rural to urban shift, urban water supply coverage has
decreased, and the total number of people who lack access to water supply has
remained constant. With urban populations in the developing world expected
to double over the next 25 years, the water supply sector faces enormous chal-
lenges. In rural areas, considerable work and investment will be needed to
narrow the existing gap in coverage.
It should be noted that access to safe water, provision of sufficient supplies
of water, and access to sanitation are three factors that together can contribute
to the health and safety of the
world's population. A lack of ad-
equate water supplies of good qual-
Household water treatment: ity, together with poor sanitation,
a success story exacts a high health toll, particularly
Diarrhoeal diseases are a leading cause of illness
in rural areas, hindering both social
and death among children under 5 years old in
and economic development. This
developing countries; they are associated with
makes the promotion of hygienic
approximately 1.6 million deaths in these
children every year. Provision and use of micro- behaviour a high priority.
biologically safe drinking-water are key to Diarrhoea is the major public
decreasing diarrhoeal disease in children. Dis- health problem caused by unsafe
cover how the Safe Water System, led by the water and lack of sanitation. To give
Pan American Health Organization and World an indication of the scale of health
Health Organization, with support from the problems caused by lack of safe
United States Centers for Disease Control and water, there are approximately 4
Prevention, has improved household manage- billion cases of diarrhoea each year,
ment of clean and disinfected drinking-water in causing 1.8 million deaths. These
poor areas of South and Central America (Case deaths occur mostly among children
study 7, page 299). under the age of five and represent
15% of all deaths in this age group
in developing countries. Waterborne
intestinal worms infect nearly 10% of the population of the developing world,
leading to malnutrition, anaemia, and retarded growth. Some 6 million people
are blind from trachoma, while research suggests that provision of safe water
could reduce infections by 25%. Some 200 million people are infected with
schistosomiasis, while the provision of safe water and sanitation could reduce
infections by as much as 77% (2). Contamination of drinking-water by chemi-
cals, particularly arsenic and fluoride, has been increasingly recognized as a
major health problem in some parts of the world (3)·
Interventions in water supply and sanitation and the promotion of hygienic
practices have been shown to lower dramatically the incidence of waterborne

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

diseases, particularly in infants and children, who-because of their physiolo-
gical immaturity-are at higher risk (4). These health risks vary by climate, ge-
ography, economic development, education, and by urban/rural status, and are
particularly acute among the rural poor of developing countries.

Major contaminants of water

The primary public health concern regarding water contamination is micro-
biological contamination of drinking-water. Water-related infections can be
classified in four categories: waterborne diseases (directly acquired from
drinking-water), water-washed (indirectly acquired) diseases, water-based dis-
eases, and diseases transmitted by water-related insect vectors (see Table 8.1).
Water contains many trace elements and minerals which, depending on
their concentration, may be inert, beneficial, or toxic. Some minerals can be
beneficial at low concentrations but toxic at higher levels. These minerals may
occur naturally, arising from the surrounding geological features, particularly
in groundwater. Chemicals may also
be introduced into water from
human activities, particularly into Table 8.1 Examples of water-related
surface waters. Contamination may infections
be from agricultural chemicals, such
Waterborne diseases
as pesticides and fertilizers, human
• Cholera
activity, such as waste disposal, • Poliomyelitis
urban run-off from human settle- • Diarrhoeal diseases
ments, industrial chemicals, or the • Roundworm
• Enteric fevers: typhoid
process of water treatment itself.
• Whipworm
Many of these substances are • Hepatitis A
not harmful to humans, or are
Water-washed diseases
present in concentrations so low as
• Scabies
to cause no health effects. However, • Typhus
some are known to cause serious • Trachoma
health effects at low concentrations, • Louse infestation
• Leishmaniasis
and treatment is needed to remove
or reduce their concentration in Water-based diseases
drinking-water. • Schistosomiasis
• Dracunculiasis (guinea-worm disease)
Guideline values for a number of
contaminants of drinking-water are Diseases transmitted by water-related insect
given in Appendix 8.1. vectors
• Malaria
• Onchocerciasis
Mechanisms of exposure • African trypanosomiasis
Contamination of water can be • Yellow fever
conveniently divided into two cat- • Dengue
egories-biological and chemical. • Filariasis

Exposure to biologically contami- Source: ref. 5.

8. WATER QUALITY
73
nated materials often results in acute health effects, such as outbreaks of gas-
troenteritis and diarrhoea, allowing the source of contamination to be quickly
traced. Exposure of the skin during bathing and recreational water use can also
be important, particularly with infectious diseases such as schistosomiasis and
amoebic meningoencephalitis.
While there are many clear instances of directly acquired (waterborne)
disease, such as outbreaks of cholera and typhoid, a large number of less dra-
matic diseases, resulting from infections or from chronic exposure to toxic
chemicals, can reduce work capacity and quality of life. Major outbreaks, which
occur in both developed and developing countries, are usually transmitted by
the faecal-oral route and may not be effectively detected. Diseases that are
either very common or localized are even more difficult to address, as often only
the sufferer and local health care workers are aware of their extent. Disease may
also result from the consumption of foods that have been grown on land irri-
gated with contaminated water, or from fish or fish products gathered from
contaminated water sources.
Indirectly acquired (water-washed) disease occurs when the quantity of safe
water is insufficient, resulting in low levels of personal and domestic hygiene, and
allowing the spread of diseases, such as scabies, trachoma, and louse infestation.
Adequate quantities of safe water are required for consumption and to
promote hygienic behaviour. The quantity of water used often depends on the
ease of access: greater quantities of water will be used if it is readily available,
while if it is in short supply, people will use less or will turn to unsafe water
sources.
Water quality and sanitation are directly linked, and it is of the greatest
importance to protect water supplies from contamination by human faeces.
Nevertheless, improvements in sanitation alone are less effective than an
improved water supply in preventing disease. Children are the main victims of
diarrhoea and other faecal-oral disease, and are also the most likely source
of infection, so both the safe disposal of their faeces and hygiene education are
of critical importance.
Chemical contamination, though less easy to determine, is often self-
limiting, as high levels of contamination usually result in water becoming
undrinkable because of its taste, smell, or colour. However, some chemical
contaminants produce long-term health effects at concentrations undetectable
by the consumer; these include inorganic chemicals such as arsenic, fluoride,
lead, nitrates, and selenium.
The major pollutants found in drinking-water are listed in Table 8.2.

Microbial contamination
Occurrence
Microbial contamination usually results from the contamination of water
with human or animal faeces. If drinking-water is contaminated with faeces,

74 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

?"
~ Table 8.2 Selected water pollutants, their common sources and major adverse health outcomes
~
rn
Al
,() CONTAMINANT COMMON SOURCES MAJOR ADVERSE HEALTH OUTCOMES
C
>
r Inorganic chemicals WHO
~ guideline value
(mgllitre)
Arsenic 0.01 Natural erosion, pesticide run-off, coal burning, Skin damage, circulatory damage, increased risk of cancer
smelting, glass and electronic production waste
Fluoride 1.5 Natural erosion, discharge from fertilizer and Bone disease, mottled teeth
aluminium factories
Lead 0.01 Natural erosion, plumbing, solder, lead-glazed Impaired growth and development, behavioural problems, kidney
ceramics, old paint, deposits from leaded petrol damage
Mercury (inorganic) 0.001 Natural erosion, discharge from refineries and Kidney damage
factories, run-off from landfills and croplands
Nitrite/n it rate 3/50 Run-off from fertilized land, septic tanks, sewers, Methaemoglobinaemia in young infants
erosion from natural deposits
Selenium 0.01 Natural erosion, occupational exposure Nail deformities, gastrointestinal problems, dermatitis, dizziness

Organic chemicals
Disinfection by-products Drinking-water disinfection Increased risk of cancer
Dioxins Combustion by-products, discharge from chemical Reproductive problems, increased risk of cancer
plants
Methylmercury Contaminated fish Impaired neurological development
Pesticides Urban and rural run-off Multiple, including endocrine and neurological damage
Polychlorinated biphenyls Transformers, industry, run-off from landfills Impaired neurological development, increased risk of cancer, skin
changes
"-I
VI
"-J
Table 8.2 continued
0\
CONTAMINANT COMMON SOURCES MAJOR ADVERSE HEALTH OUTCOMES
Radionuclides
Radium Natural erosion Increased risk of cancer

Bacteria
Campylobacter Human and animal faeces Gastroenteritis, Guillain-Barre syndrome
Escherichia coli Human and animal faeces Gastroenteritis
Escherichia coli 0157: H7 Human and animal faeces Bloody diarrhoea, haemolytic uraemic syndrome
Salmonellae Human and animal faeces Enteric fever, gastroenteritis
Shigellae Human faeces Dysentery
Vibrio cholerae Human and animal faeces Dysentery
Vl
rn
n
--I
Viruses
is Enterovirus Human faeces Gastroenteritis
z
Poliovirus Human faeces Poliomyelitis
..
Vl
-a Hepatitis A virus Human faeces Hepatitis A
rn
Q Rotavirus Human faeces Gastroenteritis
-n
n
rn Parasites
z
:s:; Cryptosporidium Human and animal faeces Gastroenteritis
;;0
0 Entamoeba Human faeces Gastroenteritis
z
s:rn Giardia Human and animal faeces Gastroenteritis, anaemia
z
);! Schistosoma Human faeces/infected snails Schistosomiasis
r
--I
I Natural toxins
;;0
rn Microcystins Cyanobacteria in nutrient-rich surface waters Gastrointestinal, neurological effects
~
Vl
Source: compiled from data in ref. 6.
pathogens are likely to be widely and rapidly dispersed. If the contamination is
recent, and if the faeces are from carriers of communicable enteric diseases,
the microorganisms (bacteria, viruses, or protozoa) that cause these diseases
may be present in the water. The diseases range from mild gastroenteritis to
severe and sometimes fatal diarrhoea, dysentery, hepatitis, cholera, or typhoid.
Helminths and amoebae may also be transmitted in water and are common in
poor quality water supplies. There are also some organisms of environmental
origin that may cause disease in humans in certain circumstances, e.g.
Legionella may be transmitted through aerosols. Some toxins occur naturally,
particularly in nutrient-rich surface waters where there is high algal growth.

Health considerations
Adverse health effects arise primarily from the ingestion of pathogenic bac-
teria. People with low immunity, including infants, young children, the sick and
the elderly are particularly vulnerable to microbial contamination even from ordi-
narily mild pathogens. Outbreaks of waterborne disease can lead to infection
across a wide community.

Chemical contamination
Arsenic
Occurrence
Arsenic is a naturally occurring element, which can be introduced into water
through the dissolution of minerals, from industrial effluent (drainage from
goldmines) and from atmospheric deposition (burning of fossil fuels and
wastes). These sources make Significant contributions to arsenic concentrations
in drinking-water and may be harmful to health (7). The body rapidly excretes
organic forms of arsenic, and it is the inorganic trivalent form that is of most
concern.
While concentrations in natural water are generally less than 0.005 mgjlitre,
some countries have reported very high concentrations particularly in ground-
water supplies. In Bangladesh, for example, over 25000 wells are contaminated
with arsenic at levels above 0.05 mgjlitre. Food is also a significant source
of arsenic, but usually in highly
complex forms that are biologi-
cally unavailable and essentially Arsenic exposure and child health
non-toxic. In an effort to reduce the occurrence of diar-
rhoeal disease in Bangladesh, tube wells were
Health considerations installed in the 1970s and 1980s. Unfortunately,
Although studies indicate that many of these wells were contaminated with
arsenic may be essential for some arsenic and resulted in serious health effects.
animal species, there is no indica- Read about the case, actions taken and lessons
tion that it is essential for humans. learned in Case study 6, page 294.
Arsenic compounds are readily

8. WATER QUALITY 77
 absorbed by the gastrointestinal tract, and then bind to haemoglobin and are
deposited in the liver, kidneys, lungs, spleen, and skin. Inorganic arsenic does
not appear to cross the blood-brain barrier, but can cross the placenta (8).
Approximately 45-85% of ingested arsenic is excreted in the urine within 1-3
days. The major health effects are caused by low-level chronic exposure from
the consumption of arsenic-contaminated water. A number of studies in
Bangladesh and West Bengal have documented the effects of consuming water
containing elevated concentrations of arsenic (>0.3 mgjlitre). Consumption
over periods of 5 to 25 years was reported to produce skin lesions, skin
cancer, vascular disease, effects on the nervous system, and possibly cancer
of other organs (9). The only available treatment for chronic arsenic poisoning
is to remove the patient from the source of exposure and provide supportive
care.

Fluoride
Occurrence
Fluoride occurs naturally in soil and water, and is a by-product of industrial
activities such as the aluminium and fertilizer industries. It is also added
to drinking-water to help prevent
dental caries. Concentrations in
surface water are usually relatively
A, Huorotic village
low «0.5 mgjlitre) while deeper
'An estimated 100 million people suffer health
groundwater wells in areas high in
e~el::tsjromoverexposure tofluoride. A Wide
·sttip.from N.orthto South Africa, and including fluoride minerals may have concen-
trations as high as lOmgjlitre.
the@~~t~nArab RepI.lblic! Jordan, Egypt, Sudan,
~t~ii(1)pia; K~nya,theUnitedRepublicof Tanzania
.. and.routh Africa; is known to have high con- Health considerations
centrafi(}n!){.lUluoride in groundwater asairesult Fluoride may be an essential
of the natural.weathering of yolcanic andsedi~ trace element for humans, but this
mentaryrocKs:ln one village of 2000 people, has yet to be established. It is widely
95%0{. childr~n are affected by dental fluorosis. dispersed in the environment, and
Other effects, such as skeletalfluorosls and crip" all living organisms tolerate modest
piing fluorosis, are. also present in this village, amounts. Fluoride is absorbed
as in other parts oUMs?-caIiM "Atrican· fitJo- quickly following ingestion, but is
ride; belt" . Head abo~t: the effects. suffered by not metabolized, and diffuses
children and learn how reduGingexposureto throughout the body. About 40% is
fIUorigeic<urhi'Hp (Case study 9, page a06}. excreted in urine within 9 hours, and
50% over 24 hours.
Fluoride has an affinity for min-
eralizing tissues of the body-in young people the bones and teeth, and in older
people the bones. As the excretion rate is greater in adults, mineralization is
proportionally less than in children. The most readily identifiable health effects
of consuming water with elevated levels of fluoride are a mottling of the teeth,

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

known as fluorosis, and sclerosis of the bones. Children are particularly affected
by fluorosis, because teeth take up fluoride during their formation (10).
Fluoride has been shown to be effective in preventing dental caries, from
the observed association of low dental caries with naturally occurring fluoride
in drinking-water (at about 1 mgjlitre). As a result, many health authorities
around the world, including the World Health Organization, recommend fluo-
ridation of public water supplies as an important public health measure.
However, at concentrations above 1.5 mgjlitre fluoride may affect tooth miner-
alization in children leading to a mottling of the teeth, which can in some
cases be unsightly. Where exposure to high fluoride concentrations in drinking-
water has occurred over prolonged periods (several years), skeletal fluorosis
may appear. If the exposure is removed, some of the effects may be reversible,
and the fluoride levels in bone gradually decline. The regular consumption of
water with fluoride concentrations above 4 mgjlitre, however, can cause
progressively increasing skeletal fluorosis. This is the maximum acceptable
level in drinking-water. People with kidney impairment may retain fluoride to a
greater degree, thus lowering their margin of safety for fluoride intake (11).
Patients with evidence of exposure to fluoride should avoid the contaminating
source.

Lead
Occurrence
Lead may be found in drinking-water at high levels. This is most commonly
a result of human activities, particularly where lead piping is still being used, or
water supply fittings use leaded solders. Concentrations are affected by factors
such as water acidity, water hardness, and contact time with water. Urban run-
off, particularly where leaded fuels are common, is a source of lead contami-
nation, particularly of surface waters (11).

Health considerations
Lead is a neurodevelopmental toxicant. It interferes with haem synthesis,
and can damage the peripheral nervous system, the kidneys, and the repro-
ductive system. It can be absorbed by the body through inhalation, ingestion,
or placental transfer. In adults, approximately 10% of ingested lead is absorbed,
but in children this figure can be 4-5 times higher. After absorption, the lead is
distributed in soft tissues such as the kidneys, liver, and bone marrow, where it
has a biological half-life in adults of less than 40 days. In skeletal bone lead may
persist for 20 to 30 years. Lead is a cumulative poison, and can severely affect
the central nervous system. Infants and fetuses are the most susceptible. Pla-
cental transfer of lead occurs in humans as early as the 12th week of gestation
and continues throughout development.
Many epidemiological studies have been carried out on the effects of lead
exposure on the intellectual development of children. Although there are some

8. WATER QUALITY 79
 conflicting results, on balance the studies demonstrate that exposure to lead
adversely affects intelligence.
Other adverse effects associated with exposure to high amounts of lead
include kidney damage, and interference with the production of red blood cells
and the metabolism of calcium needed for bone formation (11).

Nitrates and nitrites

Occurrence
Nitrates and nitrites occur primarily as a result of run-off from the agricul-
tural use offertilizers and bacterial action on animal wastes. The intensification
oHarming practices and sewage effluent disposal to streams have led to increas-
ing amounts of nitrate in some waters, particularly groundwater. Nitrite is
formed by the reduction of nitrate in poorly oxygenated waters and is relatively
unstable. It is rapidly oxidized to nitrate and is rarely present in well oxygenated
or chlorinated supplies. Other processes reduce it to other compounds such as
ammonia. While food is the major source of nitrate intake for adults, bottle-fed
infants may be exposed to nitrates if contaminated water is used for mixing
formula.

Health considerations
The toxicity of nitrate in humans is thought to be solely due to its reduction
to nitrite. The major biological effect of nitrite in humans is its involvement in
the oxidation of normal haemoglobin to methaemoglobin, which is unable to
transport oxygen to the tissues, a condition known as methaemoglobinaemia
or more commonly, "blue baby syndrome". Young infants and pregnant women
are most susceptible to methaemoglobin formation. Laboratory experiments
with animals suggest that neither nitrite nor nitrate acts directly as a carcino-
gen, but there is concern that nitrite may react with foods rich in secondary
amines to form N-nitroso compounds in the stomach, many of which are known
to be carcinogenic in animals. Some
epidemiological evidence suggests
Contaminated water distribution a relationship between nitrate and
In an area of Uzbekistan, a study was undertaken gastric cancer in humans, but this
to determine the causes of increased diarrhoeal has yet to be confirmed (11).
disease during certain seasons. It was found
that agricultural irrigation reduced water supply Selenium
during certain months, and as a result an over- Occurrence
haul of the water supply and quality manage- Selenium, although widespread
ment were carried out. Case study 8 (page 303) in the environment, is generally
illustrates the usefulness of field epidemiology found in very low concentrations.
as an analytical tool to address a problem and There are some regions where
guide policy and decision-making. elevated levels have resulted in
health effects, and groundwater

80 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

concentrations as high as 6 mgjlitre have been reported in the United States,
for example.

Health considerations
Selenium is an essential element for many species, including humans.
Selenium deficiency in humans is not well established but may include a chronic
disorder of the heart muscle and cancer. The gastrointestinal tract effectively
absorbs most water-soluble selenium compounds, which are then distributed
to most organs, with the highest concentrations found in the kidneys, liver, and
spleen. The toxicity of selenium varies considerably depending on the com-
pound, with selenite and selenate being more toxic than the sulfide. There have
been a number of reports of ill-effects attributed to short-term and long-term
exposure to selenium, most of which have been linked to occupational expo-
sure or accidental poisoning. Acute or chronic nutritional toxicity is compara-
tively rare. Intakes above about 1 mgjday over prolonged periods may produce
nail deformities characteristic of selenosis. Other features of excess selenium
intake include non-specific symptoms, such as gastrointestinal disturbances,
dermatitis, dizziness, lassitude, and a garlic odour on the breath (11).

Mercury
Occurrence
Mercury occurs naturally in drinking-water at extremely low levels, but con-
tamination can result from industrial emissions or spills. Inorganic mercury
compounds are generally insoluble in water and the major concern is the
organic methylmercury, formed from inorganic mercury by bacteriological
action. Methylmercury is known to accumulate in fish and fish products, and
the consumption of these foods may cause human illness (12).

Health considerations
A developmental neurotoxicant, when exposure occurs in utero methylmer-
cury interferes with neuronal migration, organization of brain nuclei and layer-
ing of the cortex. These experimental findings are consistent with the severe
cerebral palsy, seizure disorders, blindness, deafness and mental retardation
that have been documented in children whose mothers ate heavily contami-
nated fish during pregnancy (13). More subtle neurodevelopmental deficits have
been observed in some children who received much lower exposures in utero
(14). Methylmercury can also damage the brain after birth. Long-term exposures
outside the developmentally vulnerable periods also cause central nervous
system damage. Progressive signs include paraesthesia, ataxia, tremor, and
muscle spasticity, leading to coma and death.
Studies of workers occupationally exposed to mercury have reported health
effects including tremors, mental disturbances, and gingivitis. Methylmercury
compounds are almost completely absorbed by the gastrointestinal tract and

8. WATER QUALITY 81
can cross biological membranes, especially in the brain, spinal cord, and periph-
eral nerves. The main effects of methylmercury poisoning are severe, irre-
versible, neurological disorders and mental disability. In Minamata Bay, Japan,
two major epidemics of methylmercury poisoning were caused by the release
of methylmercury and other mercury compounds from industrial processes.
These compounds accumulated in fish, which were subsequently eaten by
humans. Other countries have reported cases of poisoning caused by mercury
contamination of bread and cereals (11).
Less than 15% of inorganic mercury in drinking-water is absorbed by the gas-
trointestinal tract. Inorganic mercury compounds have a long biological half-life,
accumulating in the kidneys where the toxic effects may lead to kidney failure.

Pesticides
Occurrence
Pesticides are of increasing concern due to their widespread and often indis-
criminate use. In both urban and rural settings, pesticides may reach water sup-
plies from agricultural run-off. While not specifically removed by conventional
water treatment processes, natural filtration and biodegradation prior to and
during treatment means that these substances are rarely detected in treated
water. However, elevated levels are often found in rural areas where intensive
agricultural practices can result in direct contamination of the water source.

Health considerations
Public health concerns regarding pesticides arise from their potential to
cause poisoning and to accumulate in the body. These chemicals can be
absorbed by the oral, inhalation, and dermal routes; health effects depend on
the specific type of pesticide. For instance, organophosphorus compounds
produce an anticholinergic syndrome (salivation, vomiting, diarrhoea, etc.),
while organochlorine compounds induce neurological signs and symptoms.

Disinfection by-products
Occurrence
Disinfection by-products (DBPs) occur when treatment chemicals such as
chlorine are added to water to control microbial contamination, where they
combine with organic materials (15).

Health considerations
A variety of halogenated DBPs found in treated drinking-water have been
linked to cancer in laboratory animals at high doses (15, 16). There are few data
on the effects of low doses on humans, particularly infants and children. While
there is some concern that these chemicals may pose a health risk, the poten-
tial risks arising from not treating drinking-water are considerably greater, and
the disinfection of water should never be compromised as a result (11, 17).

82 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Radionuclides
Occurrence
Radionuclides occur naturally in the environment from deposits of radioactive
minerals, and from the disposal and storage of radioactive materials. Concen-
trations in surface waters are likely to be extremely low, and groundwater con-
centrations vary according to the type of aquifer minerals and dissolved anions.

Health considerations
Radioactive materials cause changes in the DNA of cells, with an increased
risk of cancer being the most serious outcome. The most common exposure
route is via the respiratory system by inhalation of aerosolized droplets (11). The
US Environmental Protection Agency estimates that 168 cancer deaths per year
in the USA are related to radon in water, of which 89% are lung cancers, and
11% stomach cancers (18).

Diagnosis
Diagnosis of illnesses suspected to be caused by contaminated water sup-
plies requires a thorough knowledge of the history of exposure, a complete phys-
ical examination of the patient and, where possible, confirmatory laboratory
tests. Standard stool cultures, tests for ova and parasites, and measurement of
antibody titres may be feasible for patients who present at hospitals or health
care centres. Laboratory tests are more likely to be useful for microbial expo-
sures and acute effects from chemical exposures than for chronic low-dose
chemical exposures. Testing for low concentrations of chemicals requires
sophisticated analytical techniques unlikely to be found outside research set-
tings. Measuring methaemoglobin in the blood will confirm acute nitrate poi-
soning. Testing blood lead levels can indicate lead exposure. Urinary arsenic
levels are of limited value as arsenic is rapidly excreted from the body. None of
these tests however, will identify the source of exposure, which is important for
case management and prevention of further exposure. If elevated levels of
chemical contaminants are known to exist then exposure can be inferred, and
confirmed by detailed patient and environmental histories and by chemical and
microbiological analyses.

Treatment guidelines
Diarrhoeal illness is treated by controlling the infection and by aggressive
fluid management. Antimicrobial drugs are used only in cases of severe cholera
and bloody diarrhoea (dysentery). In young children, the most common cause
of death is from dehydration. Correct management may prevent up to 90% of
deaths (19). Dehydration can usually be treated using oral rehydration fluids.
Intravenous rehydration may be needed in cases of severe dehydration, or where
the patient cannot drink or absorb water. The rehydration treatment of diar-
rhoeal disease is summarized in the box below.

8. WATER QUALITY
Guidelines for treating children and adults with some dehydration
Approximate amount of ORS' solution to give in the first 4 hours

Age b Less than 4-11 12-23 2-4 years 5-14 years 15 years or
4 months months months older
Weight Less than 5 kg 5-7.9 kg 8-1 0.9 kg 11-15.9kg 16-29.9kg 30kg or
more
In ml 200-400 400-600 600-800 800-1200 1200-2200 2200-4000
In local
measure
, Oral rehydration salts.
b Use the patient's age only when you do not know the weight. The approximate amount of ORS required (in ml)
can also be calculated by multiplying the patient's weight in kg by 75.

• If the patient wants more ORS than shown, give more.

• Encourage the mother to continue breastfeeding her child.
• For infants under 6 months who are not breastfed, if using the old so-called standard
WHO ORS solution containing 90 mmol/L of sodium, also give 100-200 ml clean water
during this period. However, if using the new reduced (low) osmolarity ORS solution con-
taining 75 mmol/L of sodium, this is not necessary.
NOTE: During the initial stages of therapy, while still dehydrated, adults can consume up to
750 ml per hour, if necessary, and children up to 20 ml per kg body weight per hour.

Sources of infection should be identified and made safe. If the infected

person is potentially contagious, isolation, strict hand-washing by staff, and
the safe disposal of faeces are the recommended control measures. For non-
infectious diseases resulting from contaminated water supplies, treatment
involves removing the patient from the source of exposure and providing sup-
portive care. In some cases the use of a specific pharmaceutical or antidote may
be indicated (e.g. succi mer for lead, atropine for organophosphorus pesticides,
methylene blue for reversal of methaemoglobinaemia).

Registration, recording and reporting of data

It is critical that information is registered and recorded after diagnosis. Some
diseases are notifiable by law.
A systematic approach to recording this information is vital in building up
a knowledge base. It provides a basis for effective communication both within
the health care system and with the community, and ensures that the relevant
authorities receive the information they need to make informed decisions and
respond appropriately to the sources of contamination and disease. The har-

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 monized recording of clinical case data will show trends over time and seasonal
occu rrence.

Prevention, remedial action, and education

Prevention of contamination is an essential feature of effective water quality
management. A comprehensive assessment of the water supply system enables
effective risk management strategies to be identified from the source to the con-
sumer. When a situation that can give rise to water contamination is recognized,
preventive strategies can be identified to minimize the exposure (1J).
Surface and groundwater sources should be protected from contamination.
Possible sources of contamination include animal and human waste, agricul-
ture, industry, mining and quarrying run-off, and the disposal of hazardous
wastes. These and other polluting activities should be identified and controlled,
or where feasible, excluded from the water catchment area.
Groundwater in deep or confined aquifers is usually protected from local
sources of contamination and microbiological quality is generally high.
However, groundwater supplies may contain high concentrations of naturally
occurring elements with health or aesthetic effects.
Groundwater with a high salinity may be unpalatable, while high levels of
nitrates, arsenic, boron, fluoride and radionuclides may make water unfit for
use. Groundwater may also be polluted by some practices, such as drilling of
wells.
Even in areas without safe drinking-water systems, home treatment is pos-
sible. Filtration can remove some microbial contamination and parasites, as can
disinfection and boiling. While it is possible to remove some chemical conta-
minants, methods tend to be expensive and the costs must be weighed against
the risks involved in drinking water with potentially high levels of chemical con-
taminants. Water treatment carried out in the home requires scrupulous and
continuous maintenance to ensure a safe and effective supply (7, 77).
Education is Vitally important to ensure that consumers of water understand
the routes by which contaminants may enter the system. Health promotion
activities are needed to show the importance of correct hygiene regarding both
sanitation and water supply, particularly for those most at risk. Communities
should be involved to ensure that everyone understands the importance of clean
water to health, and that the protection of safe water sources is essential in
reducing health risks.

8. WATER QUALITY
APPENDIX 8.1
1
Guideline values for drinking-water contaminants

Inorganic constituents
GUIDELINE VALUE REMARKS
(mg/lilre)

Antimony 0.005 (P)'

4
Arsenic 0.01b (P) For excess skin cancer risk of 6 x 10-

Barium 0.7
Beryllium NAD C
Boron 0.5 (P)
Cadmium 0.003
Chromium 0.05 (P)
Copper 2 (P) Based on acute gastrointestinal effects
Cyanide 0.07
1.5 Climatic conditions, volume of water consumed, and
Fluoride
intake from other sources should be considered when
setting national standards
0.01 It is recognized that not all water will meet the
Lead
guideline value immediately; meanwhile, all other
recommended measures to reduce the total exposure
to lead should be implemented
Manganese 0.5 (P) ATO d
Mercury (total) 0.001
Molybdenum 0.07
Nickel 0.02 (P)
Nitrate (as NOd 50 (acute)
Nitrite (as NOd 3 (acute)
0.2 (p}(chronic)
Selenium 0.01
Uranium 0.002 (P)

, Based on ref. 17·

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

86
 Organic constituents

GUIDELINE VALUE REMARKS

(Ilo/litre)
Chlorinated alkanes
Carbon tetrachloride 2
Dichloromethane 20
1,1-dichloroethane NAD
1,2-dichloroethane 30 b For excess risk of 10-5
1,1,1-trichloroethane 2000 (P)
Chlorinated ethenes
Vinyl chloride 5b For excess risk of 10-5
1,1-dichloroethene 30
1,2-dichloroethene 50
Trichloroethene 70 (P)
Tetrachloroethene 40
Aromatic hydrocarbons
Benzene lO b For excess risk of 10-5
Toluene 700 ATO
Xylenes 500 ATO
Ethylbenzene 300 ATO
Styrene 20 ATO
Benzo [a] pyrene 0.7 b For excess risk of 10-5
Chlorinated benzenes
Monochlorobenzene 300 ATO
1,2-dichlorobenzene 1000 ATO
1,3-dichlorobenzene NAD
1,4-dichlorobenzene 300 ATO
Trichlorobenzenes (total) 20 ATO
Miscellaneous
Di(2-ethylhexyl)adipate 80
Di(2-ethylhexyl)phthalate 8
Acrylamide 0.5 b For excess risk of 10-5
Epichlorohydrin 0.4 (P)
Hexachlorobutadiene 0.6
Edetic acid (EDTA) 600 Applies to the free acid
Nitrilotriacetic acid 200
Dialkyltins NAD
Tributyltin oxide 2
Microcystin-LR 1 (P) Applies to total microcystin-LR
(free plus cell-bound)

8. WATER QUALITY
Pesticides
GUIDELINE VALUE REMARKS
(J.1u/litre)
20 b For excess risk of 10-5
Alachlor
Aldicarb 10
Aldrin/dieldrin 0.03
Atrazine 2
Bentazone 300
Carbofuran 7
Chlordane 0.2
Chlorotoluron 30
Cyanazine 0.6
OOT 2
1b For excess risk of 10-5
1,2-dibromo-3-chloropropane
OA-15 b (P) For excess risk of 10-5
1,2-dibromoethane
2,4-dichlorophenoxyacetic acid (2,4-0) 30
1,2-dichloropropane (1,2-0CP) 40 (P)
1,3-dichloropropane NAO
20 b For excess risk of 10-5
1,3-dichloropropene
Oiquat 10 (P)
Heptachlor and heptachlor epoxide 0.03
1b For excess risk of 10-5
Hexachlorobenzene
Isoproturon 9
Lindane 2
(4-chloro-2-methylphenoxy)acetic acid (MCPA) 2
Methoxychlor 20
Metolachlor 10
Molinate 6
Pendimethalin 20
gb (P) For excess risk of 10-5
Pentachlorophenol
Permethrin 20
Propanil 20
Pyridate 100
Simazine 2
Terbuthylazine (TBA) 7
Trifluralin 20

Chlorophenoxy herbicides other than 2,4-0 and MCPA

2,4-0B gO
Oichlorprop 100
Fenoprop 9
4-( 4-chloro-2-methylphenoxy)butanoic acid NAO
(MCPB)
Mecoprop 10
2,4,5-T 9

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

88
 Disinfectants and disinfectant by-products
DISINFECTANTS GUIDELINE VALUE REMARKS
(mg/litre)
Monochloramine 3
Di- and trichloramine NAD
Chlorine 5 ATO. For effective disinfection there should be
a residual concentration of free chlorine of
0.5 mgilitre after at least 30 minutes contact
time at pH < 8.0
Chlorine dioxide A guideline value has not been established
because of the rapid breakdown of chlorine
dioxide and because the chlorite guideline value
is adequately protective for potential toxicity
from chlorine dioxide
Iodine NAD
DISINFECTANT BY- GUIDELINE VALUE REMARKS
PRODUCTS (j.Lg/litre)
Bromate 10b (P) For 7 x 10-5 excess risk
Chlorate NAD
Chlorite 700 (P)

Chlorophenols
2-chlorophenol NAD
2,4-dichlorophenol NAD
2,4,6-trichlorophenol 200 b For excess risk of 10-5, ATO
Formaldehyde 900
3-chloro-4-dichloromethyl- NAD
5-hYdroxY-2(5H)-furanone (MX)
Trihalomethanes The sum of the ratio of the concentration of
each to its respective guideline value should not
exceed 1
Bromoform 100
Dibromochloromethane 100
Bromodichloromethane 60 b For excess risk of 10-5
Chloroform 200

Chlorinated acetic acids

Monochloroacetic acid NAD
Dichloroacetic acid 50 (P)
Trichloroacetic acid 100 (P)
Chloral hydrate 10 (P)
(trich loroacetaldehyde)
Chloroacetone NAD

8. WATER QUALITY
89
DISINFECTANTS GUIDELINE VALUE REMARKS
(flg/litre)
Halogenated acetonitriles
Dichloroacetonitrile 20 (P)
Dibromoacetonitrile 70 (P)
Bromochloroacetonitrile NAD
Trich loroaceton itri Ie NAD
Cyanogen chloride 70
(as CN)
Chloropicrin NAD

, (P)-Provisional guideline value. This term is used for constituents for which there is some evidence of a
potential hazard but where the available information on health effects is limited; or where an uncertainty
factor greater than 1000 has been used in the derivation of the tolerable daily intake (TOI). Provisional
guideline values are also recommended: (1) for substances for which the calculated guideline value would be
below the practical quantification level, or below the level that can be achieved through practical treatment
methods; or (2) where disinfection is likely to result in the guideline value being exceeded.
b For substances that are considered to be carcinogenic, the guideline value is the concentration in drinking-
water associated with an excess lifetime cancer risk of 10-5 (one additional cancer per 100000 of the
population ingesting drinking-water containing the substance at the guideline value for 70 years).
Concentrations associated with estimated excess lifetime cancer risks of 10-4 and 10-6 can be calculated by
multiplying and dividing, respectively, the guideline value by 10.
In cases in which the concentration associated with an excess lifetime cancer risk of 10-5 is not feasible as
a result of inadequate analytical or treatment technology, a provisional guideline value is recommended at a
practicable level and the estimated associated excess lifetime cancer risk presented.
It should be emphasized that the guideline values for carcinogenic substances have been computed from
hypothetical mathematical models that cannot be verified experimentally and that the values should be
interpreted differently from TO I-based values because of the lack of precision of the models. At best, these
values must be regarded as rough estimates of cancer risk. However, the models used are conservative and
probably err on the side of caution. Moderate short-term exposure to levels exceeding the guideline value for
carcinogens does not significantly affect the risk.
o NAO-No adequate data to permit recommendation of a health-based guideline value.
d ATO-Concentrations of the substance at or below the health-based guideline value may affect the

appearance, taste, or odour of the water.

Chemicals not of health significance at concentrations normally found

in drinking-water

CHEMICAL REMARKS
Asbestos U
Fluoranthene U
Glyphosate U
Silver U
Tin U

U-It is unnecessary to recommend a health-based guideline value for these compounds because they are not
hazardous to human health at concentrations normally found in drinking-water.

90 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Bacteriological quality of drinking-water'

ORGANISMS GUIDELINE VALUE

All water intended lor drinking
E. coli or thermotolerant coliform bacteriab,c Must not be detectable in any 100-ml sample
Treated water entering the distribution system
E. coli or thermotolerant coliform bacteria b Must not be detectable in any 1OO-ml sample
Total coliform bacteria Must not be detectable in any 100-ml sample
Treated water in the distribution system
E. coli or thermotolerant coliform bacteria b Must not be detectable in any 100-ml sample
Total coliform bacteria Must not be detectable in any 100-ml sample.
In the case of large supplies, where
sufficient samples are examined, must not
be present in 95% of samples taken
throughout any 12-month period

, Immediate investigative action must be taken if either E. coli or total coliform bacteria are detected. The
minimal action in the case of total coliform bacteria is repeat sampling; if these bacteria are detected in the
repeat sample, the cause must be determined by immediate further investigation.
b Although E. coli is the more precise indicator of faecal pollution, the count of thermotolerant coliform

bacteria is an acceptable alternative. If necessary, proper confirmatory tests must be carried out. Total
coliform bacteria are not acceptable indicators of the sanitary quality of rural water supplies, particularly in
tropical areas where many bacteria of no sanitary significance occur in almost all untreated supplies.
c It is recognized that in the great majority of rural water supplies in developing countries faecal contamination
is widespread. Under these conditions, the national surveillance agency should set medium-term targets for
the progressive improvement of water supplies, as recommended in the Guidelines for drinking-water quality,
released by WHO (www.who.int/water_sanitation_health/dwq)

Radioactive constituents of drinking water

SCREENING VALUE (Bq/litre)

Gross alpha activity 0.1
Gross beta activity

8, WATER QUALITY
91
Substances and parameters in drinking-water that may give rise to complaints
from consumers
LEVELS LIKELY TO GIVE RISE REASONS FOR CONSUMER
TO CONSUMER COMPLAINTS a COMPLAINTS

Physical parameters
Colour Appearance
Taste and odour Should be acceptable
Temperature Should be acceptable
Turbidity 5 NTU' Appearance; for effective terminal
disinfection, median turbidity =
1 NTU, single sample = 5 NTU

Inorganic constituents
Aluminium 0.2 mg/litre Depositions, discoloration
Ammonia 1.5 mg/litre Odour and taste
Chloride 250 mg/litre Taste, corrosion
Copper 1 mg/litre Staining of laundry and sanitary
ware (health-based provisional
guideline value 2 mg/litre)
Hardness High hardness: scale deposition,
scum formation
Low hardness: possible
corrosion
Hydrogen sulfide 0.05 mg/litre Odour and taste
Iron 0.3 mg/litre Staining of laundry and sanitary
ware
Manganese 0.1 mg/litre Staining of laundry and sanitary
ware (health-based guideline value
0.5 mg/litre)
Dissolved oxygen Indirect effects
pH Low pH: corrosion
High pH: taste, soapy feel
Preferably <8.0 for effective
disinfection with chlorine
Sodium 200 mg/litre Taste
Sulfate 250 mg/litre Taste, corrosion
Total dissolved solids 1000 mg/litre Taste
Zinc 3 mg/litre Appearance, taste

Organic constituents
Toluene 24-170 ~g/litre Odour, taste (health-based guideline
value 700 ~g/l)
Xylene 20-1800 ~g/litre Odour, taste (health-based guideline
value 500 ~g/l)
Ethylbenzene 2-200 ~g/litre Odour, taste (health-based guideline
value 300 ~g/l)

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 LEVELS LIKELY TO GIVE RISE REASONS FOR CONSUMER
TO CONSUMER COMPLAINTS' COMPLAINTS
Styrene 4-2600 /-lg/l itre Odour, taste (health-based guideline
value 20/-lg/l)
Monochlorobenzene 10-120/-lg/litre Odour, taste (health-based guideline
value 300/-lg/l)
1,2-dichlorobenzene 1-10/-lg/litre Odour, taste (health-based guideline
value 1000 /-lg/l)
1,4-dichlorobenzene 0.3-30 /-lg/litre Odour, taste (health-based guideline
value 300/-lg/l)
Trichlorobenzenes (total) 5-50/-lg/litre Odour, taste (health-based guideline
value 20/-lg/l)
Synthetic detergents Foaming, taste, odour

Disinfectants and disinfectant by-products

Chlorine 600-1000 /-lg/litre Taste and odour (health-based
guideline value 5/-lg/l)
Chlorophenols
2-chlorophenol 0.1-10/-lg/litre Taste, odour
2,4-dichlorophenol 0.3-40 /-lg/litre Taste, odour
2,4,6-trichlorophenol 2-300/-lg/litre Taste, odour (health-based guideline
value 200/-lg/l)

a The levels indicated are not precise numbers. Problems may occur at lower or higher values according to
local circumstances. A range of taste and odour threshold concentrations is given for organic constituents.
b TCU, true colour unit.
C NTU, nephelometric turbidity unit.

References
1. Water for health-taking charge. Geneva, World Health Organization, 2001.
2. WHO/UNICEF Joint Monitoring Programme for Water Supply and Sanitation.
Global water supply and sanitation assessment 2000 report. Geneva, World
Health Organization, United Nations Children's Fund, 2000 (http://www.
who. int/water_san itation_health/G lobassess ment/G lobah. htm#Top).
3. Smith AH, Lingas EO, Rahman M. Contamination of drinking-water by arsenic
in Bangladesh: a public health emergency. Bulletin of the World Health
Organization, 2000, 78:1093-1103 (http://www.who.int/bulletin/pdf/2000/
issue9/bu0751.pdf) .
4. Special considerations based on age and developmental stage. In: Etzel RA, Balk
SJ. Handbook of pediatric environmental health. Elk Grove Village, American
Academy of Pediatrics, 1999:9-19.
5. Satterthwaite D et al. The environment for children. New York, United Nations
Children's Fund & Earthscan, 1996.
6. Environmental Protection Agency. Drinking water contaminant candidate list. 1998
(www.epa.gov/safewater/ccl/cclfs.html) .
7. United Nations Synthesis Report on Arsenic in Drinking Water (http://www.who.int/
water_san itation_health / dwq/ arsen ic3/ en/ pri nt.htm I).

8. WATER QUALITY 93
8. Kreiss K. Arsenic toxicity. Atlanta, GA, US Department of Health and Human
Services, Agency of Toxic Substances and Disease Registry, 1990 (Case Studies
in Environmental Medicine, NO·5)·
9. International Programme on Chemical Safety. Arsenic. Geneva, World Health
Organization, 1981 (Environmental Health Criteria No. 18).
10.Marcus R. Agents affecting calcification and bone turnover. In: Hardman JG,
Limbird LE. Goodman 11( Gillman's the pharmacological basis of therapeutics, 9 th
ed. New York, McGraw-Hili, 199 6 :153 8- 1539.
". National Health and Medical Research Council. Australian drinking water guide-
lines and framework for management of drinking water quality (http:f jwww.
health .gov.au j n h m rcj pu bl ications jsynopsesj eh1 9 s yn.htm).
12. Wheeler M. Measuring mercury. Environmental Health Perspectives, 199 6 ,
104:826-831 (http://ehpnet1.niehs.nih.govjdocsj1 996j1 04- 8 jfocus.html).
13. Goyer RA. Toxic effects of metals. In: Klaassen CD. Casarett 11( Doull's toxicology:
the basic science of poisons, 5th ed. New York, McGraw-Hili, 199 6 :6 9 1-73 6 .
14. Grandjean Pet al. Cognitive deficit in 7-year-old children with prenatal exposures
to methylmercury. Neurotoxicology and Teratology, 1997, 6:417-4 28 .
15. International Programme on Chemical Safety. Disinfectants and disinfectant by-
products. Geneva, World Health Organization, 1999 (WHO Environmental
Health Criteria No. 216) (www.inchem.orgjdocumentsjehcjehcjehc216.htm).
16. Booker SM. TNP taps disinfection by-products for study. Environmental Health
Perspectives, 2000, 108:A64-A66.
17. Guidelines for drinking-water quality, 3rd ed. Geneva, World Health Organization,
2004 (www.who.intjdocstorejwater_sanitation_healthjGDWQ jU pdati ngj
draftguideljdraftchap1 .htm).
18. US Environmental Protection Agency. Proposed radon in drinking water rule.
EPA 815-F-99-009, 2000 (http://www.epa.gov/safewater/radon/proposal.html).
19. The treatment of diarrhoea. A manual for physicians and other senior health workers.
Geneva, World Health Organization, 2003 (WHOjFCHjCAHj03-7).

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

94
CHAPTER 9

Sanitation and hygiene

J. Hueb
Water, Sanitation and Health, Department for the
Protection of the Human Environment, World Health
Organization, Geneva, Switzerland

Introduction
Global sanitation needs are enormous. An estimated 42% of the world's
population has no access to sanitation facilities. In sub-Saharan Africa and
South Asia, the situation is critical, with 64% and 63% of the respective popu-
lations without adequate sanitation facilities. Of the 2.6 billion people without
access to sanitation services, 75% live in Asia (Figure 9.1) (1).
Although major improvements have been made over the past decade
(Figure 9.2), the world population not served with adequate sanitation has
hardly decreased (see Appendix 9.1), primarily because of rapid population
growth among the poorest sectors of society, particularly in isolated rural com-
munities and periurban slums. Sanitation has been given a low priority com-
pared with other development issues. One assessment found that only 20% of
the total investment in water supply and sanitation infrastructure over the 1990S
was dedicated to sanitation (1, 2).
In developed countries, nearly all human excreta are collected safely in
sewerage systems or septic tanks; however, not all wastewater is treated before
being discharged to the environment. In developing countries, the percentage
of treated wastewater is discouragingly low: 14% in Latin America and the
Caribbean; 34% in Asia; and practically no treatment at all in Africa (1).
Lack of access to sanitation services aggravates and in turn is aggravated
by poverty, inequity and poor health. Without access to these basic services,
people, especially children, miss out on opportunities to improve their own lives
with dignity and good health. As long as the human right of access to adequate
sanitation and safe water supply is denied to the poor, the health status of mil-
lions of children around the world will not improve in a sustainable manner.

Health aspects of sanitation

Lack of sanitation is a critical determinant in the contamination of drinking-
water by microbes. Faecal pollution of drinking-water can lead to a number of
diseases, including cholera, typhoid fever, paratyphoid fever, salmonellosis,
shigellosis, giardiasis, hepatitis and poliomyelitis. Of particular concern is
the evidence that the burden of disease associated with the lack of sanitation
services falls disproportionately upon children. In 2000, for example,

95
Figure 9.1 Global population without access to improved sanitation (unserved population in
2002: 2.6 billions)

Oceania Developed countries

0% 1%
Latin America & the Caribbean European countries in CIS
5% 1%
Asian countries in CIS
1%
Sub-Saharan Africa

Eastern Asia
Northern Africa 29%
1%

Western Asia
1%

South-eastern Asia
8%

Source: ref. 1.
CIS, Commonwealth of Independent States (countries of the former Union of Soviet Socialist Republics).

Figure 9.2 Global access to improved sanitation, 1990, 2002

100
1111990 .2002
90
'0
'"2: 80
'"c 70
<J)

0
~ 60
=>
c.
0
c. 50
'0
40
'"
Cl
.;g
c 30
'"e
'" 20
0-

10
0

a Source: ref. 1.
CIS, Commonwealth of Independent States (countries of the former Union of Soviet Socialist Republics).

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

96
Table 9.1 Main diseases related to poor sanitation

DISEASE ANNUAL NO. ANNUAL NO. CAUSAL RELATIONSHIP TO POOR

OF CASES OF DEATHS SANITATION
(THOUSANDS) (THOUSANDS)
Diarrhoeal diseases 4000000 1800 Unsafe excreta disposal; poor
personal and domestic hygiene;
unsafe drinking-water
Ascariasis and other 1500000 100 Unsafe excreta disposal; poor
diseases caused by personal and domestic hygiene
intestinal helminths
Schistosomiasis 200000 200 Unsafe excreta disposal; poor
personal and domestic hygiene
Trachoma 150000 Poor personal and domestic hygiene
Poliomyelitis 114 Unsafe excreta disposal
Bancroftian filariasis 72800 Unsafe disposal of excreta; poor
domestic hygiene; wastewater
disposal and drainage

approximately 60% of the 2.1 million deaths from diarrhoeal diseases were
among children under five years of age (2). The data clearly show that children
cannot be healthy without access to adequate sanitation and a safe water supply.
Providing access to sanitation and hygiene interrupts the disease transmission
cycle and reduces the incidence of infectious diseases.
Water-borne diseases (see Chapter 8) are transmitted by contaminated
drinking-water. Contaminated water is a direct result of a lack of adequate
sanitation facilities, poor wastewater treatment, and unhygienic behaviour.
Water-washed diseases, which produce skin and eye infections, are caused
by a lack of soap and insufficient water for washing hands and clothes and for
personal hygiene. Again, children are particularly vulnerable to these diseases.
The main water-washed diseases are scabies, trachoma, leishmaniasis, typhus,
and louse infestation. Trachoma, for example, is an infectious disease that can
lead to blindness (3). Children are often a reservoir for the bacteria that cause
trachoma.
Water-based diseases are transmitted to aquatic hosts, such as freshwater
crustaceans, which may then be ingested by people. The main water-based
diseases are schistosomiasis and dracunculiasis (guinea-worm disease).
Water-related vector-borne diseases are caused by bacteria, viruses and
parasites (protozoa and helminths) that are transmitted by water-related agents
(vectors or intermediate hosts). Often, the vector is an insect that transmits
infectious agents from one infected person to another, or from infected animals
to people (4). The main water-related vector-borne diseases are malaria, African
trypanosomiasis, dengue, onchocerciasis, yellow fever and filariasis.
Inadequate water supply, sanitation and hygiene are estimated to be respon-
sible for 4.0% of all deaths and 5.7% of the total disease burden in disability-

9. SANITATION AND HYGIENE 97

adjusted life years (DALYs).' Most of this burden could be prevented with inter-
ventions to improve sanitation. Other diseases related to water supply, sanita-
tion and hygiene remain to be evaluated (5). Also, the burden of hygiene-related
diseases needs to be analysed separately for water-, sanitation- and hygiene-
related risk factors. Estimates of morbidity and mortality related to poor sani-
tation are shown in Table 9.1 for selected main diseases.

Barriers to progress in sanitation

The barriers to improving sanitation are complex and interrelated. The main
problems are listed below (6):

• A lack of political will: governments have little interest in dealing with

sanitation issues.
• Low prestige and recognition: promoting low-cost sanitation and hygiene
education has never been popular with politicians and technical staff
because such projects carry little prestige.
• Poor policy on sanitation at global and country level.
• Poor institutional framework: responsibilities for sanitation are frag-
mented and poorly coordinated among country agencies.
• Inadequate and poorly used resources: scarce financial resources are fre-
quently used inefficiently, such as for improving existing services.
• Inappropriate approaches: frequently, the approach used to provide
sanitation services is not in line with local culture, technical limitations
or affordability criteria.
• Failure to recognize the disadvantages of conventional excreta manage-
ment systems. Although water-borne sanitation systems have been used
successfully in many parts of the world, often the wastewater is not
treated before being discharged to rivers, lakes or the ocean. In many
situations, on-site alternatives are more appropriate in terms of both
cost and their low impact on the environment.
• Neglect of user preferences: sanitation programmes should consider user
preferences for affordability, cultural aspects, etc.
• Ineffective promotion and low public awareness: often both the potential
users of sanitation services and those responsible for policy and decision-
making are not aware or convinced of the importance of good sanitation
for health.
• The low importance given to women and children: women are potential
agents of change in hygiene education, and children are the most
vulnerable to poor sanitation.

'DALY = the sum of years of potential life lost due to premature mortality and years of pro-
ductive life lost due to disability.

98 SECTION Iii: SPECIFIC ENVIRONMENTAL THREATS

 Lessons learned
• Sanitation development should not be based on a supply-driven
approach, which frequently runs into problems (7). With such an
approach, for the same type of service, the investment per capita is nor-
mally higher, since the population does not participate. Users may not
be willing to pay for the recurrent costs of facilities that were selected
without their participation. This also leads to insufficient cost-recovery,
making it impossible to operate and maintain the facilities effectively.
Also, such investments are generally focused on improving services for
those already served, and the unserved or underserved poor are not con-
sidered a priority. Supply-driven approaches may also not consider the
environmental impact of a programme, such as when flushing toilets are
connected to a sewerage system with no wastewater treatment.
• An adequate institutional framework is a major factor facilitating sector
development. Centrally managed sanitation services, especially in urban
areas, tend to be hampered by ineffective financial performance and a
rigid bureaucracy, and to have little budget autonomy. Decentralization
of services appears to be an effective alternative. However, in moving
from a centralized to an effective decentralized management system, the
central agencies have a vital role to play in organizing the decentralized
agencies, mobilizing resources for investment and recurrent costs, and
providing strong technical and financial support, during at least the
transition process. As the decentralization process progresses, the
central agencies should act as facilitators of services, rather than as
providers.
• The operation and maintenance of sanitation systems have been tradi-
tionally neglected. This is true both of large sewerage systems and of
small-scale family-owned sanitation facilities. Many small systems fall
into disrepair as early as a few weeks after their installation. A number of
large wastewater treatment plants that use sophisticated instrumentation
and equipment are operated manually because of a lack of knowledge
about the system, a lack of spare parts, or simply a lack of interest in
making the most of the facility. Operation and maintenance should there-
fore not be viewed as purely technical issues, since they have connections
with many institutional and management issues.
• Hygiene behaviour has often been the missing link between sanitation,
water supply and health. While past efforts have built new water supply
and sanitation systems, little has been done to maximize the health
benefits from these efforts by changing the behaviour of people. Neglected
school sanitation is a typical indicator that hygiene education is not
a priority in schools, especially in poor urban agglomerations and in
rural areas. According to a 1995 pilot survey conducted in 14 develop-
ing countries, the average number of children per toilet in urban

9. SANITATION AND HYGIENE 99

 schools was often more than 50. None of the 14 countries had increased
the number of school toilets by more than 8% since 1990, suggesting
that they were barely managing to keep up with the rise in student
populations (8).

Future perspectives
Even though sanitation coverage increased from 45% to 58% globally during
the 1990s, it is still far below the water supply coverage (82% in 2000). The
Asian region, which had a sanitation coverage of only 27% in 1990, made
great progress and coverage increased to 47% by 2000. Coverage in Africa,
by contrast, was essentially unchanged (59% in 1990; 60% in 2000). If these
trends continue, Asia is more likely than Africa to achieve the target set at the
World Summit on Sustainable Development in Johannesburg, South Africa, in
August 2002 of halving the proportion of people unserved by 2015. Coverage
in Latin America and the Caribbean increased from 72% in 1990 to 78 % in
2000.
Currently, 2-4 billion people globally do not have access to any type of san-
itation facility and are thus heavily exposed to health risks. To achieve the target
set in Johannesburg, an additional 1870 million people will need to be provided
with sanitation facilities between 2000 and 2015 (taking 1990 as the baseline
year). Even if the target is achieved, more than 2 billion people (28% of the 201 5
population) will remain unserved.
The task will involve the mobilization of significant financial and human
resources, and will require (6):

• a change in political attitude;

• the formulation and implementation of policies at all levels;
• a better organization of the sanitation subsector at country level;
• the use of affordable approaches and technologies that can be operated
and maintained by households, communities or agencies in charge;
• that user preferences be considered;
• that people, especially women and children, become a central concern.

Three principles are fundamental for introducing sanitation systems that are
sustainable socially, economically and ecologically (1):

• Equity. All segments of society should have access to safe, appropriate

sanitation systems, adapted to their needs and means.
• Health promotion and protection from disease. Sanitation systems should
prevent users and others from contracting excreta-related diseases, and
should interrupt the cycle of disease transmission.
• Protection of the environment. Sanitation systems should neither pollute
ecosystems nor deplete scarce resources.

100 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 The construction and maintenance of sanitation facilities in rural or poor
periurban areas are often carried out by the users themselves. In urbanized
areas, public or private organizations generally manage the sewerage system
and raise service charges. Increasingly, people in rural and many periurban areas
are adopting on-site sanitation (e.g. pit latrines). A marketing approach is
needed, with a focus on developing and distributing products that match con-
sumer needs in both quality and price. In turn, this requires understanding the
reasons why people want sanitation (1).
Hygiene education, especially in primary schools, should be a fundamental
component of sanitation and water-supply programmes. Much of the health
benefit of water supply and sanitation is realized through changes in behaviour
and improved hygiene. To obtain the full health benefits of sanitation pro-
grammes, key issues will need to be addressed, including: how to change habits
and long-held beliefs about hygiene; how to discuss sanitation issues in
societies where the topic is unmentionable; and how to achieve the necessary
commitment of effort and time. Involving children in the process would offer
hope for sustainability, because as the children grow, they will continue to imple-
ment better sanitation practices and influence their own children and commu-
nity to do the same (6).

9· SANITATION AND HYGIENE

101
~

0
N

APPENDIX 9.1

Regional and global use of improved drinking water and sanitation in 1990 and 2002
1990 POPULATION (THOUSANDS) 2002 POPULATION (THOUSANDS)
% TOTAL POPULATION POPULATION %
TOTAL POPULATION POPULATION SERVED
UNSERVEO SERVED POPULATION SERVED UNSERVED
POPULATION SERVED
107765 95 2980995 2820494 160501 95
Worldwide Urban water 2273241 2165476
63 3243990 2328654 915336 72
Rural water 2990351 1893020 1097331
1205096 77 6224985 5149148 1075837 83
Total water 5263592 4058496
79 2980995 2413465 567530 81
Urban sanitation 2273241 1804813 468428
25 3243990 1192692 2051298 37
Vl
rn Rural sanitation 2990351 752651 2237700
n 2706128 49 6224985 3606157 2618828 58
--I Total sanitation 5263592 2557464
0 0 100 744438 744438 0 100
z Developed Urban water 672945 672945
2612 99 248708 233786 14922 94
.. countries Rural water 261158 258546
Vl 2612 100 993146 978224 14922 98
'1:l Total water 934103 931491
rn
0 100 744438 744438 0 100
Q Urban sanitation 672945 672945
-n 99 248708 228811 19897 92
n Rural sanitation 261158 258546 2612
2612 100 993146 973249 19897 98
rn Total sanitation 934103 931491
z
:::; 4968 97 179798 177 029 2769 98
;0
Countries Urban water 184339 179371
0 16838 83 101172 82775 18397 82
z in CIS Rural water 97360 80522
s:: 92 280970 259804 21166 92
rn Total water 281699 259892 21807
z 93 179798 166276 13522 92
Urban sanitation 184339 171598 12741
~ 68 101172 66310 34862 66
c- Rural sanitation 97360 66184 31176
--I 84 280970 232586 48384 83
I Total sanitation 281699 237781 43918
;0
rn
~
Vl
 Developing Urban water 1415957 1313161 102796
'P 93 2056759 1899027 157732 92
V1 countries Rural water 2631833 1553952 1077881
» 59 2894110 2012094 882016 70
z Total water 4047790 2 867113 1180677 71 4950869 3911121 1 039748 79
~ Urban sanitation 1415957 960270 455687 68 2056759
'-i 1 502751 554008 73
(5 Rural sanitation 2631833 427921 2203912 16 2894110
z 897571 1996539 31
Total sanitation 4047790 1388191 2659599
» 34 4950869 2400322 2550547 48
z
0 European Urban water 152300 149254 3046
I
98 147422 145948 1474 99
-< countries in Rural water 62513 54386 8127 87
C) 59772 53795 5977 90
CIS Total water 214813 203640 11173
en 95 207194 199743 7451 97
z Urban sanitation 152300 144685 7615 95
en 147422 140051 7371 95
Rural sanitation 62513 48760 13753 78 59772 46024 13748 77
Total sanitation 214813 193445 21368 90 207194 186075 21119 90
Asian Urban water 32039 30117 1922 94 32376 31081 1295 96
countries in Rural water 34847 26135 8712 75 41400 28980 12420 70
CIS Total water 66886 56252 10634 84 73776 60061 13715 82
Urban sanitation 32039 26913 5126 84 32376 26225 6151 81
Rural sanitation 34847 17424 17424 50 41400 20286 21114 49
Total sanitation 66886 44336 22550 66 73776 46511 27265 63
Northern Urban water 57349 54482 2867 95 76101 73057 3044 96
Africa Rural water 60719 49790 10929 82 71217 59822 11395 84
Total water 118068 104271 13797 88 147318 132879 14439 90
Urban sanitation 57349 48173 9176 84 76101 67730 8371 89
Rural sanitation 60719 28538 32181 47 71217 40594 30623 57
Total sanitation 118068 76711 41357 65 147318 108324 38994 73
Sub- Urban water 141445 115985 25460 82 241439 197980 43459 82
Saharan Rural water 362929 130654 232275 36 443334 199500 243834 45
Africa Total water 504374 246639 257735 49 684773 397480 287293 58
Urban sanitation 141445
-
0
w
Rural sanitation
Total sanitation
362929
504374
76380
87103
163483
65065
275826
340891
54
24
32
241439
443334
684773
132791
115267
248058
108648
328067
436715
55
26
36
2

1990 POPULATION (THOUSANDS) 2002 POPULATION (THOUSANDS)

POPULATION % TOTAL POPULATION POPULATION %
TOTAL POPULATION UNSERVED SERVED
POPULATION SERVED UNSERVED SERVED POPULATION SERVED

21972 93 409168 388710 20458 95

Latin Urban water 313879 291907
53612 58 126458 87256 39202 69
America & Rural water 127647 74035
75583 83 535626 475966 59660 89
the Total water 441526 365943
56498 82 409168 343701 65467 84
Caribbean Urban sanitation 313879 257381
82971 35 126458 55642 70816 44
Rural sanitation 127647 44676
139469 69 535626 399343 136283 75
Total sanitation 441526 302057
Vl
en 3672 99 548285 509905 38380 93
Eastern Urban water 367169 363497
Cl Rural water 859254 515552 343702 60 826553 562056 264497 68
(5 Asia 302877 78
z 1226423 879050 347373 72 1374838 1071961
Total water 69
234988 132181 64 548285 378317 169968
.. Urban sanitation 367169
799106 7 826553 247966 578587 30
Vl
-0 Rural sanitation 859254 60148
en
931287 24 1374838 626283 748555 45
() Total sanitation 1226423 295136
:':! 26246 94
()
311514 280363 31151 90 437431 411185
South Asia Urban water 80
en
310707 64 1042856 834285 208571
z Rural water 863076 552369
:'0 341859 71 1480287 1245470 234817 84
;u Total water 1174590 832731
0 143296 54 437431 288704 148727 66
z Urban sanitation 311514 168218
802661 7 1042856 250285 792571 24
$
en Rural sanitation 863076 60415
z 945957 20 1480287 538989 941298 37
Total sanitation 1174590 228633
}:!
r
--j
I
;u
en
~
Vl
 'P
V1
»
Z
~
'-i
(5
Z
» South- Urban water 138937 126433 12504 91
z 221161 201257 19904 91
0 eastern Asia Rural water 300989 195643 105346 65 314451 220116 94335 70
I Total water
-< 439926 322076 117850 73 535612 421372 114240
Cl 79
Urban sanitation 138937 93088 45849 67 221161 174717
rn 46444 79
z Rural sanitation 300989 117386 183603 39 314451 154081
rn 160370 49
Total sanitation 439926 210474 229453 48 535612 328798 206814 61
Western Urban water 84161 79111 5050 94 121130 115074 6057 95
Asia Rural water 52283 33984 18299 65 62831 46495 16336 74
Total water 136444 113095 23349 83 183961 161568 22393 88
Urban sanitation 84161 80795 3366 96 121130 115074 6056 95
Rural sanitation 52283 27187 25096 52 62831 30787 32044 49
Total sanitation 136444 107982 28462 79 183961 145861 38100 79
Oceania Urban water 1503 1383 120 92 2044 1860 184 91
Rural water 4936 1925 3011 39 6410 2564 3846 40
Total water 6439 3308 3131 51 8454 4424 4030 52
Urban sanitation 1503 1247 256 83 2044 1717 327 84
Rural sanitation 4936 2468 2468 50 6410 2949 3461 46
Total sanitation 6439 3715 2724 58 8454 4666 3788 55
Source: rei. 1.
CIS, Commonwealth 01 Independent States (countries 01 the lormer Union 01 Soviet Socialist Republics).

-
o
'"
 References
1. WHO/UNICEF Meeting the MOG drinking Water and Sanitation target. Geneva,
World Health Organization, United Nations Children's Fund, 200 4.
2. The World Health Report 2000. Health systems: improving peiformance. Geneva,
World Health Organization, 2000.
3. Children in the new millennium-environmental impact on health. Geneva, World
Health Organization, 2002.
4. Cairncross S, Feachem RG. Environmental health engineering in the tropics: an
introductory text. Chichester, John Wiley and Sons, Ltd, 1983.
5. Pruess A et al. Estimating the burden of disease from water, sanitation and
hygiene at a global level. Environmental Health Perspectives, 2002, 110:537-542 .
6. Sanitation promotion. Geneva, World Health Organization, 199 8 .
7. Wright A. Toward a strategic sanitation approach: improving the sustainability of
urban sanitation in developing countries. Washington, DC, UNDP/World Bank
Water and Sanitation Programme, 1997·
8. The progress of nations. New York, United Nations Children's Fund, 1997·

106 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 CHAPTER 10

R. A. Etzel
Department of Environmental and Occupational Health,
School of Public Health and Health Services, George
Washington University, Washington, DC, USA

K. Balakrishnan
College of Allied Health Sciences, Sri Ramachandra
Medical College and Research Institute, Porur, India

INDOOR AIR
Overview
Indoor air pollutants are now recognized to pose potential health risks to
exposed children throughout the world (1,2). Indoor air pollutants have various
sources and hazard profiles. Some key indoor air pollutants and their sources
are listed in Table 10.1.
Indoor air quality problems are strikingly different between developed and
developing nations. The most Significant factor affecting indoor air quality in
rural areas of developing countries is emissions from combustion of biomass
fuels (wood, dung and crop residues) and coal used for cooking and heating.
Use of open fires for cooking and heating in poorly ventilated homes exposes
an estimated 2-4 billion people to concentrations of particulate matter and
gases up to 60 times higher than ambient concentrations (3, 4).
Women who cook with these fuels and children, who often stay close to their
mothers, are usually the most exposed groups (5-8). Although solid fuels make
up only 10-15% of total fuel use, indoor exposures are likely to exceed outdoor
exposures globally since nearly half the world's population cooks and heats their
homes with biomass fuels.
Indoor air quality has also become a health concern in developed countries
in recent years as rising energy costs have led to building designs that reduce
air exchange. In addition, new synthetic materials are now widely used in home
furnishings. As a result, there are a range of airborne pollutants in indoor
environments, including particulate matter, gases, vapours, biological materi-
als, and fibres (9, 10). In homes, common sources of air pollutants include
tobacco smoke, gas and wood stoves, and furnishings and construction
materials that release organic gases and vapours. Allergens and biological

'Reviewed by D. Schwela, Physical and Chemical Exposure Unit, Institute for Health and
Consumer Protection, Joint Research Centre, Ispra, Italy.

10 7
Table 10.1 Principal pollutants and sources of indoor air pollution, grouped
by origin

PRINCIPAL POLLUTANTS SOURCES

Predominantly outdoor
sources
Sulfur dioxide, suspended particulate Fuel combustion, smelters
matter, respirable suspended particles
Ozone Photochemical reactions
Pollens Trees, grass, weeds, plants
Lead, manganese Automobiles
Lead, cadmium Industrial emissions
Volatile organic Petrochemical solvents, vaporization of unburned
compounds, polycyclic aromatic fuels
hydrocarbons

Indoor and outdoor sources

Oxides of nitrogen, carbon monoxide Fuel burning
Carbon dioxide Fuel burning, metabolic activity
Suspended particulate matter, respirable Environmental tobacco smoke, resuspension of dust,
suspended particles condensation of vapours and combustion products
Water vapour Biological activity, combustion, evaporation
Volatile organic compounds Volatilization, fuel burning, paint, metabolic activity,
pesticides, insecticides, fungicides
Spores Fungi, moulds

Predominantly indoor sources

Radon Soil, building construction materials, water
Formaldehyde Insulation, furnishing, environmental tobacco smoke
Asbestos Fire-retardant, insulation
Ammonia Cleaning products, metabolic activity
Polycyclic aromatic hydrocarbons, Environmental tobacco smoke
arsenic, nicotine, acrolein
Volatile organic compounds Adhesives, solvents, cooking, cosmetics
Mercury Fungicides, paints, spills or breakage of mercury-
containing products, Santeria (traditional medicine in
some Latin American countries)
Aerosols Consumer products, house dust
Allergens House dust, animal dander

Source: ref. 3.

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

108
materials include animal dander, faecal material from house dust mites and
other insects, fungal spores, and bacteria.

Main indoor air pollutants

Solid fuel smoke
Air pollutants emitted from combustion of biomass fuels, such as wood,
woodchips, agricultural produce and cow dung, are the result of incomplete
combustion and are practically the same for any type of biomass. However,
the amount and characteristics of the pollutants produced depend on several
factors including composition of the fuel, combustion conditions (temperature
and air flow), mode of burning, and even shape of the fireplace (11). Hundreds
of different chemical substances are emitted during the burning of biomass
fuels, in the form of liquids (suspended droplets), solids (suspended particles),
and gases such as nitrogen dioxide (N0 2 ) and sulfur dioxide (50 2 ) (12). The
aerosol mixture of very fine solid and liquid particles, or "smoke", contains
particles in the inhalable range, i.e. less than 10Ilm in diameter.
The aerosol produced from burning solid fuel is made up of organic and inor-
ganic matter. In addition to particulates, it contains many toxic and carcinogenic
compounds, including polycyclic aromatic hydrocarbons (PAHs), benzene, and
formaldehyde. The inorganic matter is mostly ash and is produced in very small
amounts during regular combustion in stoves. Smoke from burning coal has all
of the above in addition to high levels of sulfur and toxic elements such as heavy
metals and fluorine, depending on the geographical location.
Combustion pollutants are also emitted from gas ranges, particularly when
they function incorrectly or are used as space heaters. Combustion of natural
gas results in the emission of nitrogen dioxide (N0 2 ) and carbon monoxide
(CO). Levels of N0 2 in the home generally increase during the winter, when ven-
tilation is reduced to conserve energy. During the winter, average indoor con-
centrations of N0 2 in homes with gas cooking stoves may be twice as high as
outdoor levels. Some of the highest indoor N0 2 levels have been measured in
homes where ovens were used as space heaters (12).

Routes of exposure
Exposure to the products of solid fuel combustion is essentially an everyday
occurrence in homes that use these fuels. Recent large-scale assessments of
household level concentrations and exposures have shown that concentrations
of respirable particulate matter (used as an indicator pollutant for overall levels
of biomass smoke) in kitchens and living areas during the cooking period can
be several thousand Ilg per ml, while 24-hour average concentrations are around
several hundred Ilg per ml. Households that have indoor kitchens that are not
partitioned from the living area have the highest concentrations (13, 14). Young
children who spend a considerable time with their mother indoors are at high
risk of high exposure.

10. AIR 109

 In homes where coal is burned, concentrations of particulate matter, sulfur
dioxide and fluorine have been found to reach 10-100 times the standards set
for outdoor air. In cold regions, the use of coal for heating further compounds
the situation as these stoves are often kept burning all day long. Release of
certain pollutants, such as lead, arsenic and fluorine, where food grains are
stored creates the potential for secondary routes of exposure through con-
taminated food (15).

Health effects in children

While exposure to solid fuel smoke has been associated with several health
effects in women who cook with these fuels, including chronic bronchitis in
biomass users and lung cancer in coal users, there is strong evidence that high
levels of indoor smoke are an important risk factor for acute lower respiratory
illnesses in children (16, 17). Acute lower respiratory illnesses in children are a
leading contributor to infant mortality. In certain situations, e.g. where coal con-
tains high amounts of arsenic or fluorine, the potential for secondary toxicity
exists. Arsenic-induced skin lesions and skeletal fluorosis have been docu-
mented in children in communities using so-called "dirty coal".
Exposure to high levels of N0 2 and 50 2 may result in acute mucocutaneous
irritation and respiratory effects. The relatively low water solubility of N0 2 results
in minimal irritation of the mucous membranes of the upper airway; the prin-
cipal site of toxicity is the lower respiratory tract (18). In contrast, the high water
solubility of 50 2 makes it extremely irritating to the eyes and upper respiratory
tract. Whether exposure to the relatively low levels of these gases in houses is
associated with any health effects remains to be determined. Exposure to in hal-
able particles in wood smoke may result in irritation and inflammation of the
upper and lower respiratory tract, resulting in rhinitis, cough, wheezing, and
worsening of asthma (19).

Diagnosis
The specific etiology of a respiratory illness may be difficult to establish
because most respiratory signs and symptoms are nonspecific and may
occur only in association with significant exposure. The effects of low exposures
may be mild. Multiple pollutants may be involved in a given situation. Estab-
lishing an environmental cause for a respiratory illness is further complicated
by the similarity of effects to those of allergies and respiratory infections. Diag-
nosis of an environmentally related disease requires a high index of suspicion
and a thorough environmental history. While health workers cannot always
assess the causal association between indoor air and health effects, they
should consider a possible environmental cause when a child's illness does not
follow usual patterns. Exposure reduction should be recommended whenever
possible.

110 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Registering the data
Health or environmental databases for registering data on childhood acute
respiratory infections and household fuel use are unlikely to be available in
developing country settings where such exposures predominate. In this case,
an entry may be made on the patient's health chart to indicate the main type of
fuel such as natural gas or renewables (e.g. solar heat or biomass fuel used in
the home for cooking or heating).

Remedial action, prevention, and education

Recognition that indoor air pollution from solid fuel use is a potential source
of significant health risks to children is relatively new. Existing community health
and education programmes may not therefore be specifically focused on raising
awareness of the threats from indoor air pollution. While interventions to reduce
exposure to solid fuel smoke are difficult to implement and often involve sub-
stantial cost (such as switching to clean fuels or installing better ventilation
systems), health workers can recommend simple behavioural interventions,
such as keeping children away from the stove during cooking, using lids on pots
during cooking, using dry wood, and cooking outdoors, whenever possible. This
may be difficult in some areas, yet the need to reduce exposure of children
remains. This information could be disseminated through community health or
social workers.

Second-hand tobacco smoke

Environmental tobacco smoke (ET5) or second-hand smoke is exhaled
smoke or smoke released from the smouldering end of cigarettes, cigars, and
pipes. Environmental tobacco
smoke is composed of more than
3800 chemical compounds. Children deserve a smoke-free world
Smoking tobacco is dangerous,both for users
Routes of exposure and for those nearby. Growing evidence points
Around 700 million, or almost to second-hand smoke as an important factor in
half, of the world's children breathe health problems such as sudden infant death
air polluted by tobacco smoke, par- syndrome, asthma, and pulmonary and middle
ticularly at home (20). Because. ear infections. The tobacco industry has suc-
many young children spend a large cessfully lobbied worldwide to open doors for
proportion of their time indoors, tobacco crops, cigarette manufacture, and sales.
they may have significant exposure However, some countries are learning to fight
to second-hand smoke. This expo- back. Read how the Philippines established a
sure may occur in a variety of envi- Clean Air Act in 1999, which i:ncluded the right
ronments, such as in homes, child for children to learn in a smoke-free setting
care settings, and motor vehicles (Case study 11, page 313).
(21) .

10. AIR 111

 Mechanism of action and clinical effects in children
Infants whose mothers smoke are 38% more likely to be hospitalized for
pneumonia than those whose mothers do not smoke. The number of hospital-
izations increases with the number of cigarettes the mother smokes each day
(22, 23). Infants with two smoking parents are more than twice as likely to have
had pneumonia than infants whose parents do not smoke (24, 25).
Children whose parents smoke are about 60% more likely to develop middle
ear effusion, as measured by tympanometry; overall, between 8% and 15% of
middle ear effusions are attributable to passive smoking (26). In one study, at
least one-third of cases of middle ear effusion among children were attributable
to passive smoking (27).
Children whose mothers smoke may be more likely to develop asthma.
Children with asthma whose parents smoke may have more frequent exacerba-
tion and more severe symptoms (28-30). Conversely, if asthmatic children's
exposure to cigarette smoke is reduced, their asthmatic symptoms will be less
severe (]1).
There is substantial evidence linking exposure to ETS to sudden infant death
syndrome (J2). This association appears to be independent of birth weight and
gestational age (33). Most reviewers consider the association to be causal (]4).

Registering the data

It may be difficult to determine the extent of a child's exposure to ETS.
At each clinic visit, the child's parents should be asked about their smoking
behaviour. Every child's medical chart should include in a prominent place
information about smoking and passive smoking.

Remedial action, prevention, and education

Discussions related to ETS exposure and parental smoking are appropriate
in the context of paediatric visits. Most parents do not want to damage the
health of their children. Messages about risks to children from ETS may become
an important factor in their decision to quit smoking. When a child has a
medical condition exacerbated by ETS exposure (e.g. asthma or recurrent otitis
media), parent education is an important element of the child's medical care.
The health worker should advise the parents to reduce their child's exposure to
ETS and to attempt to quit smoking. Smoking cessation counselling by physi-
cians has been found to almost double smoking cessation rates. In the United
States, approximately 10% of smokers who received smoking cessation coun-
selling from a physician stopped smoking (35). Although this may not seem sig-
nificant within the context of an individual practice, it reflects a tremendous
public health impact at the population level. Over time, advice from physicians
may also influence other family members to stop smoking.
Smoking cessation by parents is the most effective means of reducing their
children's exposure to ETS. Even if the parents and other family members do

112 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

not quit, efforts to reduce their chil-
dren's exposure to ETS may reduce Carbon monoxide pOisoning in children
their risk of disease and may also in France
motivate those who smoke to quit. An unusually high incidence of carbon monox-
ide pOisoning was noted in the north of France
Carbon monoxide in the 1980s, associated with the use of
Carbon monoxide (CO) is a kerosene lamps. Public health authorities
colourless, odourless, tasteless responded by implementing monitoring, report-
toxic gas that is produced by the ing of cases and strict regulations requiring
incomplete combustion of carbon- the lamps to have carbon monoxide detection
based fuels. devices. These measures resulted in a noticeable
decrease in poisonings the following year. Learn
Routes of exposure how ongoing surveillance is necessary to
Un intentional exposu re to CO protect public health and why carbon monoxide
can be largely attributed to smoke
is particularly hazardous to children in Case
study 10, page 309.
from fires, automobile exhaust,
faulty or improperly vented com-
bustion appliances, and tobacco
smoke. Confined, poorly ventilated spaces such as garages, caravans, tents, and
boats are particularly liable to have elevated levels of CO. Common sources of
CO exposure are wood and coal fires, gas furnaces and heaters, gas ranges and
ovens, gas clothes dryers, other fuel-powered equipment and appliances, fire-
places, and charcoal grills. Exposure to CO may occur in and around automo-
biles when there is inadequate combustion resulting from substandard vehicle
maintenance and poor ventilation.

Mechanism of action and clinical effects in children

Intoxication from exposure to CO and the resultant tissue hypoxia affect mul-
tiple organ systems. Systems with high metabolic rates and high oxygen demand
are preferentially affected. Carbon monoxide is inhaled, diffuses across the
alveolar-capillary membrane, and is measurable in the bloodstream as carboxy-
haemoglobin. CO has approximately 240 times greater affinity for haemoglobin
than oxygen, and decreases the oxygen-carrying capacity of the blood. Carbon
monoxide in the bloodstream also causes a leftward shift of the oxyhaemoglo-
bin dissociation curve, causing decreased delivery of oxygen to the tissues.
The clinical presentation of CO intoxication is highly variable and the sever-
ity of the symptoms may not correlate to carboxyhaemoglobin levels in the
blood. Low levels of carboxyhaemoglobin may be present in cases of severe
poisoning. Symptoms of CO intoxication include: headache, dizziness, fatigue,
weakness, drowsiness, nausea, vomiting, loss of consciousness, skin pallor, dys-
pnoea on exertion, palpitations, confusion, irritability, and irrational behaviour.
The prevalence of unintentional nonfatal CO poisonings is difficult to estimate
because early symptoms of intoxication are often nonspecific (3 6, 37).

10. AIR 113

 Infants and children are particularly susceptible to CO toxicity because of
their higher metabolic rates (38). The fetus is especially vulnerable to maternal
CO intoxication. The risk of complications increases with the severity of the
maternal poisoning, as the amount of oxygen available to the fetus decreases.

Diagnosis
A thorough history and physical examination, as well as a high index of clin-
ical suspicion, are necessary to diagnose CO poisoning. Health workers should
consider the possibility of CO exposure when people living in the same house-
hold present with similar nonspecific symptoms. Initial laboratory findings may
be misleading.
The measurement of carboxyhaemoglobin levels in the blood enables the
degree of exposure to be assessed. An elevated level may confirm the diagno-
sis of CO intoxication: low or moderately increased levels must be interpreted
with caution. Baseline levels of carboxyhaemoglobin are typically 0.3-0.7% in
nonsmokers, while those in smokers typically range from 3% to 8%, although
higher values have been reported.

Treatment guidelines
Patients who have been exposed to CO should be removed from the source
immediately. Therapy consists of the administration of 100% oxygen through a
tight-fitting non-rebreather mask at a flow rate of 10 litres/min.

Registering the data

Carbon monoxide exposure and poisoning should be reported to the local
health department.

Remedial action, prevention, and education

Primary prevention of CO poisoning involves prevention of exposure to
known sources (39).
Smoke detectors and carbon monoxide detectors, when used properly, may
provide an early warning and prevent unintentional CO-related deaths. Carbon
monoxide detectors measure the amount of CO that has accumulated in the
air, and sound an alarm when the CO in the air corresponds to a 10% carboxy-
haemoglobin level in the blood.
Several countries, including Canada and Japan, have set gUidelines for CO
in indoor air. Health Canada recommends that the acceptable short-term expo-
sure range for carbon monoxide in indoor air is less than or equal to 11 parts
per million (ppm) (eight-hour average concentration), or less than or equal to
25 ppm (one-hour average concentration) (40).
The American Society of Heating, Refrigerating and Air Conditioning Engi-
neers recommends an exposure limit of no more than 9 ppm in a living space,
while Japan has an indoor standard that limits exposure to 10 ppm for any dura-

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

tion (40). However, these guidelines may not provide sufficient protection for
infants and children.

Volatile organic compounds

Indoor concentrations of volatile organic compounds (VOCs) are greater
than outdoor concentrations. Many household furnishings and products
contain VOCs as residues or carriers (9, 41). These include chemicals such as
aliphatic and aromatic hydrocarbons (including chlorinated hydrocarbons),
alcohols, and ketones, in products such as finishes, rug and oven cleaners,
paints and lacquers, and paint strippers. Formaldehyde is found primarily in
building materials and home furnishings (9-10,43). Since product labels do not
always specify the presence of organic compounds, the specific chemicals to
which a product user may be exposed can be difficult to discern. At room tem-
perature, VOCs are released as gases or vapours from furnishings or consumer
products. In the United States, consumer surveys conducted by the Environ-
mental Protection Agency (EPA) and measurements ofVOCs in residential and
nonresidential buildings showed that exposure to VOCs is widespread and
highly variable. In general, VOCs are likely to be higher in recently constructed
or renovated buildings than in older buildings. Once building-related emissions
decrease, consumer products are the predominant source of exposure.
Formaldehyde is one of the most common indoor air contaminants.
It is used in hundreds of products, such as urea-formaldehyde and phenol-
formaldehyde resin, which are used to bond laminated wood products and to
bind wood chips in particle board; as a carrier solvent in dyeing textiles and
paper products; and as a stiffener, wrinkle resistor, and water repellant in floor
coverings (e.g. rugs and linoleum) (9, 10). Toxicology reports indicate that
exposure to VOCs may result in dermal, mucocutaneous, and nonspecific
effects. Epidemiological studies delineating the acute and chronic health effects
of residential exposure to low levels ofVOCs are limited, reflecting the difficulty
of characterizing exposures and identifying effects of components of complex
mixtures.
Depending on the dominant compounds and route and level of exposure,
signs and symptoms may include upper respiratory tract and eye irritation,
rhinitis, nasal congestion, rash, pruritus, headache, nausea, and vomiting.
These effects are drawn from limited studies of occupationally exposed adults.
It is unlikely that exposures of the same magnitude would be found in a typical
home environment.
Volatile organic compounds have only recently attracted study, and it is still
largely unknown which VOCs are associated with specific health effects. Data
on children are extremely limited.
The effects of exposure to formaldehyde have received more attention. Expo-
sure to airborne formaldehyde can result in conjunctival and upper respiratory
tract irritation (i.e. burning or tingling sensations in eyes, nose, and throat);

10. AIR 115

these symptoms are temporary and resolve when exposure stops. Formalde-
hyde may exacerbate asthma in some infants and children.
Several questions may help to identify exposure to VOCs. These include:
Does the family live in a new home with large amounts of pressed wood prod-
ucts? Is there new pressed wood furniture? Have household members recently
worked on craft or graphic materials? Are chemical cleaners used extensively?
Has the home recently been renovated? Has anyone recently used paints,
solvents, or sprays in the home?
Prevention strategies include increasing ventilation and avoiding storage of
opened containers of paint and similar materials within the home. If formalde-
hyde is thought to be the cause of the problem, the source should be identified
and, if possible, removed. Measuring levels of formaldehyde in the air is usually
not necessary. If it is not possible to remove the source, exposure can be
reduced by coating cabinets, panelling, and other furnishings with polyurethane
or other nontoxic sealants, and by increasing the amount of ventilation in the
home. Formaldehyde concentrations decrease rapidly over the first year after a
product is manufactured.

Moulds
Moulds are ubiquitous in the outdoor environment, and can enter the home
through doorways, windows, heating and ventilation systems, and air condi-
tioning systems. Moulds also develop in damp indoor environments, and pro-
liferate where there is excessive moisture, such as from leaks in roofs, walls,
plant pots, or pet urine. The most common indoor moulds are Cladosporium,
Penicillium, Aspergillus, and Alternaria (44).
Moulds have been associated with both allergic reactions and toxic effects.
Some children who are exposed to moulds have allergic effects manifesting as
persistent upper respiratory tract symptoms, such as rhinitis, sneezing, and eye
irritation, and lower respiratory tract symptoms such as coughing and wheez-
ing (45-47).
Toxic effects may be produced by inhalation of mycotoxins, lipid-soluble
toxins that are readily absorbed by the airways (48). Species of mycotoxin-
producing moulds include Fusarium, Trichoderma, and Stachybotrys (49).
Stachybotrys has been associated with acute pulmonary haemorrhage in young
infants in Ohio (48, 50), Missouri (51), and Delaware (52), and with pulmonary
haemosiderosis in a 7-year old child in Texas (53).
Several questions may help to identify exposure to moulds. They include:
Has the home been flooded? Is there any water-damaged wood or cardboard in
the house? Has there been a roof or plumbing leak? Have occupants seen any
mould or noticed a musty smell?
Although no indoor guidelines for fungi have been set, experts have sug-
gested that even '50 colony-forming units (CFU) per ml is considered to be high
if there are dominant species of mould along with a few other species (54, 55).

116 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

The "tolerable" levels for airborne fungi are around 200CFUjm J (56). This is
exclusive of the toxigenic fungi, which are considered unacceptable in indoor air
(57)·
Prevention includes cleaning up water and removing all water-damaged
items (including carpets) within 24 hours of a flood or leak. If this is done, toxic
mould will not have the opportunity to grow. If some mould is already present,
the affected area needs to be washed with soap and water, and then with a solu-
tion of 1 part bleach to 9 parts water. Protective gloves should be worn during
these operations.

Treatment guidelines
Clinical symptoms due to exposure to indoor moulds are usually short-lived,
and cease with elimination of exposure. Treatment of most mould-related ill-
nesses includes relief of symptoms and elimination of the water source. Chil-
dren with lower respiratory symptoms may need to be evaluated for possible
allergies and asthma.

Registering the data

Data on health problems due to biological agents are rarely reported to the
local health department, primarily because it is very difficult to pinpoint the
specific cause.

Mercury vapour
Mercury vapour is a potentially dangerous indoor air pollutant.

Routes of exposure
Elemental mercury is used in sphygmomanometers, thermometers, and
thermostat switches. Elemental mercury is also used in some folk rituals, such
as Santeria, which is practised in some parts of the Caribbean. Because of its
attractive appearance, schoolchildren may bring home mercury from science
classes.

Mechanism of action and clinical effects in children

Elemental mercury is liquid at room temperature and readily volatilizes to a
colourless and odourless vapour. When inhaled, elemental mercury vapour easily
passes through the pulmonary alveolar membranes and enters the blood, where
it is distributed primarily into red blood cells and the central nervous system.
Inhalation of the vapours from heated mercury can be very dangerous. At high
concentrations, mercury vapour produces an acute necrotizing bronchitis and
pneumonitis, which can lead to death due to respiratory failure. Fatalities have
resulted from heating elemental mercury in inadequately ventilated areas.
Long-term exposure to mercury vapour primarily affects the central nervous
system. Early nonspecific signs include insomnia, forgetfulness, loss of appetite,

10. AIR
and mild tremor, and may be misdiagnosed as psychiatric illness. Continued
exposure leads to progressive tremor and erethism, a syndrome characterized
by red palms, emotional lability, and memory impairment. Salivation and exces-
sive sweating are accompanying autonomic signs. The child's developing brain
may be especially vulnerable to mercury vapour toxicity.
Mercury also accumulates in the kidneys. Renal toxicity includes proteinuria
and nephrotic syndrome, alone or in addition to other signs of mercury expo-
sure. Isolated renal effects may be immunological in origin.
Acrodynia (painful extremities) is a hypersensitivity response to mercury
that has been reported in children exposed to mercury from interior latex paint
containing phenyl mercury as a preservative (58, 59). Since the carbon-mercury
chemical bond of phenylmercury is relatively unstable, elemental mercury can
be released from painted walls.

DiagnosiS
Mercury should be measured in a 24-hour urine collection, using a special
mercury-free container from an environmental laboratory. In sensitive in-
dividuals, effects may already be seen at urine mercury values of around 100
micrograms per litre (3).

Treatment guidelines
The most important step is to identify the source of the child's exposure and
remove it.

Registering the data

Children with documented mercury poisoning should be reported to the
health authorities.

Remedial action, prevention, and education

Although there are no standards for indoor air, the Agency for Toxic Sub-
stances and Disease Registry suggests that residential air mercury levels should
be not higher than 0.5 micrograms per cubic metre (37)·

OUTDOOR AIR
Overview
Outdoor air pollutants typically exist as part of a complex mixture of
multiple pollutants. In many countries, however, only a few air pollutants are
regularly monitored to assess air quality. WHO has developed and published
guidelines for air quality (3) covering about 50 compounds with noncarcino-
genic health endpoints and 30 compounds with carcinogenic health endpoints,
including respirable particulate matter, sulfur compounds, carbon monoxide,
lead, nitrogen oxides, and ozone.

118 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Key pollutants
Particulate matter
Particulate matter is a generic term for a variety of materials with many dif-
ferent characteristics. Both solid particles and liquid droplets are included, and
the particle or droplet size can range from slightly above the molecular level
(invisible to the naked eye) to dust
particles several hundred microns in
diameter. Solid particulate matter is
generated by the incomplete com- Respiratory illness among children in
bustion of organic matter, or can Sao Paulo, Brazil
come from the mechanical break- The city of Sao Paulo, Brazil, is one of the largest
down of solid matter (such as rocks in the world, with over 40000 industries and
and sOil). Fine and ultra-fine par- nearly 6 million registered vehicles. In the 1970s
and 1980s, industries sprang up, many of which
ticulate matter is emitted by diesel
were indiscriminately situated in residential
engines and power plants, and can
areas. By 1980, respiratory diseases were the
be found in the smoke of forest
second largest cause of death in the city. A
fires.
series of public pOlicies, including the establish-
Particle size is the major factor
ment of clean air regulations, and programmes
determining where in the respiratory to promote control of air pollution and industrial
system the particles will be depo- zoning, have since led to reduced health risks in
sited. Particles larger than 10 11 m the city (Case study 12, page 316).
in diameter are filtered out as air
passes through the nose, while
smaller particles reach the lower
airways. Children, however, fre-
quently breathe through their
mouths, thus bypassing the nasal
filtration mechanism. Particles
Air pollution and pregnancy outcome
There is widespread concern over the health
smaller than 2.511m are able to pen-
effects of ambient air pollution. Support is
etrate deeply into the lungs. The par-
growing for the idea that several adverse preg-
ticles that reach the alveoli (the
nancy outcomes may be the result of maternal
terminal air pockets of the lungs)
or paternal exposure to airborne pollution. A
stay there permanently. Thus an
consistent relationship between maternal expo-
adolescent who has lived in a pol- sure to fine particles in early gestation and
luted city for many years has intrauterine growth retardation was recently
"blacker" lungs than one who has observed in a highly polluted district of North-
lived in a polluted city for a shorter ern Bohemia in the Czech Republic. One pOSSi-
time. Particulate matter with a ble explanation for this finding is that some
diameter smaller than 10 11m is associated copollutants, such as polycyclic aro-
called PM lO • The fine particles are matic hydrocarbons, may interfere with fetal
often the most toxic. development. Read about this, in Case study 13,
Diesel automobile exhaust gen- page 320).
erates particles smaller than 111m;

10. AIR
119
 these remain suspended in the atmosphere for long periods of time and are
more likely to be inhaled.

Sulfur compounds
Sulfur-containing compounds include sulfur dioxide (50 2 ) , sulfuric acid
aerosol (H 2 S0 4), sulfate particles, and hydrogen sulfide (H 2 S). The primary
source of sulfur dioxide is from burning coal; thus, major emitters of sulfur
dioxide include coal-fired power plants, smelters, and pulp and paper mills.
Sulfuric acid aerosol is formed in the atmosphere from the oxidation of sulfur
dioxide in the presence of moisture.
Facilities that either manufacture
or use acids can also emit sulfuric
Childhood asthma in China, Hong Kong, acid aerosol. Hydrogen sulfide is
Special Administrative Region emitted from a variety of indus·
Childhood asthma is common in Hong Kong, trial processes, including oil refining,
SAR. High levels of ambient air pollution are now wood pulp production and waste-
thought to be an important factor contributing water treatment, as well as from the
to asthma morbidity. The main sources of operation of geothermal plants and
outdoor pollution in Hong Kong include auto- landfills. Hydrogen sulfide, which
mobile exhaust and burning of fossil fuels by has an odour similar to that of
various factories. The incidence of asthma in rotten eggs, is easily detected at
children was reduced after fuel regulations were
levels that are far below those asso-
established in 1990 (Case study 14, page 323).
ciated with physiological effects.

Carbon monoxide
Large amounts of carbon monoxide enter the outdoor air primarily through
the incomplete combustion of motor vehicle fuels.

Lead
The use of leaded petrol in motor vehicles is an important source of lead
exposure for children. In the absence of stringent controls on automobile emis·
sions and volume of traffic, the use of leaded petrol in some major cities of the
developing world creates the potential for serious risks to children (3)· Paint and
soil are generally the most common sources of lead exposure for children in
countries that have eliminated lead from petrol, but industrial operations, such
as battery recycling or lead smelters, can also generate potentially harmful lead
emissions.

Nitrogen oxides
Motor vehicle emissions contribute to outdoor levels of nitrogen oxides.
However, the levels of nitrogen oxides outdoors are generally lower than those
found indoors.

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

120
 Ozone
Ozone (OJ) is a pervasive outdoor air pollutant (59). Outdoor ozone and
other photochemical oxidants are secondary pollutants formed in the atmos-
phere from a chemical reaction between volatile organic compounds and nitro-
gen oxides in the presence of sunlight. The primary sources of these precursor
compounds include motor vehicle exhaust fumes, chemical factories and
refineries. Ozone is the principal component of urban summer smog. Levels of
ozone are generally highest on hot summer days, reaching a maximum in the
late afternoon. It is common for outdoor air pollutants to occur together; for
example, when ozone levels are high, levels of fine particles and acid aerosols
may also be high.

Routes of exposure
The main pathway of exposure to air pollution is through inhalation. Sub-
stances (such as mercu ry) released into the atmosphere can, however, enter the
hydrological cycle as a result of atmospheric dispersion and precipitation.
Similarly, deposition of suspended particulate matter occurs. Thus, material that
was originally released into the atmosphere can be ingested as a result of the
subsequent contamination of water, soil, or vegetation.

Mechanism of action and clinical effects in children

Children are especially vulnerable to outdoor air pollution for several
reasons. First, the lungs are growing rapidly during the first year of life and the
number of air sacs increases until the fourth year of life. Exposure to pollutants
during infancy and childhood can decrease the rate of lung development (61).
Second, because children tend to spend more time outside than adults, and are
often physically active, they have a greater likelihood of exposure to pollutants.
Because of their higher metabolic rate, children breathe more rapidly and inhale
more pollutants per kg of body weight than adults (37). In addition, because
airway passages in children are narrower than those in adults, irritation caused
by air pollution can result in proportionally greater airway obstruction. Unlike
adults, children may not cease vigorous outdoor activities when bronchospasm
occurs.
Infants and children have an increased susceptibility to CO toxicity because
of their higher metabolic rate (62-64). Carbon monoxide in the bloodstream
causes a leftward shift of the oxyhaemoglobin dissociation curve, resulting in
reduced oxygen delivery to the tissues. Tissue hypoxia from exposure to carbon
monoxide preferentially affects organ systems with a high metabolic rate and
high oxygen demand.
In children, acute health effects associated with outdoor air pollution include
respiratory symptoms, such as wheezing and cough, serious lower respiratory
tract infections, and exacerbation of asthma (65, 66). Increases in the number

10. AIR 121

of admissions to hospital emergency departments have been observed when air
pollution levels are elevated, which commonly occurs in major urban areas (67,
6B). Historically, episodes of very heavy air pollution (such as the London smog
Of1952) have been linked with increased death rates among adults and children
(69-71). Most ofthe short-term respiratory effects of outdoor air pollution, such
as cough or shortness of breath, are thought to be reversible.
Because children with asthma have increased airway reactivity, the effects
of air pollution on the respiratory system can be more serious for them (72).
Some evidence suggests that exposure to ozone can increase bronchial reac-
tivity to inhaled allergens (7], 74). New diagnoses of asthma are associated with
strenuous exercise by children in communities with high concentrations of
ozone (75).
The effects of repeated or long-term exposures to outdoor air pollution on
the developing lungs of children are not well understood, primarily because of
the methodological difficulties of long-term studies. Long-term exposure to
ozone is linked to chronic respiratory symptoms and small deficits in pulmonary
function tests. A study of 17-21-year-old college students in California demon-
strated that lifetime exposure to ambient ozone was negatively associated with
lung function measures reflecting small-airway physiology (forced expiratory
flow rate between 25% and 75% of forced vital capacity (FEF 25-75%) and forced
expiratory flow rate at 75% of forced vital capacity (FEF7s%)) (76). These pul-
monary function measures are considered early indicators of pathological
changes that could progress to chronic obstructive lung disease. A similar study
of Connecticut college students detected an association between living for four
or more years in areas of the United States with high levels of ozone, dimin-
ished forced expiratory volume in 1 second (FEV,), and diminished FEF 25-75%(77).
The study also demonstrated that chronic phlegm, wheezing, and a higher com-
posite respiratory symptom index were more common in students who had lived
for a long period in areas with high ozone concentrations (7B).
Chronic exposure to ozone pollution has been associated with de novo devel-
opment of chronic lung disease, mild pulmonary fibrosis, and modest increases
in small airway obstruction (79, Bo). Some evidence has linked ozone to chronic
lung scarring, especially at the broncho-alveolar junction (66, B1).
Long-term intermittent exposure to acid aerosols is associated with a higher
probability of reported bronchitis among 8-12-year-old children. Asthma, per-
sistent wheeze, chronic cough and chronic phlegm were not associated with
higher levels of acid aerosols. Long-term exposure to acid aerosols was associ-
ated with statistically significant decrements in forced vital capacity (FVC) and
FEV, (B2-B4).
Several studies have noted an association between particulate air pollution
and mortality among persons of all ages (B5), as well as low birth weight,
intrauterine growth retardation and postneonatal infant death. Table 10.2 shows
results of a recent meta-analysis of the health effects of particulates (B6).

122 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Table 10.2 Increase in health-related parameters associated with a 10f,lg/nt
increase in PMIO
PARAMETER INCREASE
Total mortality rate 1%
Cardiovascular mortality rate 1.4%
Respiratory mortality rate 3.4%
Respiratory-related hospitalizations 0.8%
Asthma-related hospitalizations 1.9%
Asthma-related emergency department visits 3.4%
Asthma exacerbations 3%
Source: ref. 86.

Diagnosis
A specific etiology for respiratory illness may be difficult to establish because
most signs and symptoms are nonspecific and may occur only in association
with significant exposure. The effects of low·level exposure may be mild.
Furthermore, multiple outdoor air pollutants may be involved. Establishing the
environmental cause of a given respiratory illness is further complicated by the
similarity of effects to those associated with allergies and respiratory infections.
Diagnosis of an environmentally related disease requires a high index of suspi-
cion and a thorough environmental history. While health workers cannot always
assess the causal association between outdoor air and health effects, they
should consider a possible environmental cause when a child's illness does not
follow usual patterns. Ways to reduce exposure should be recommended.

Treatment guidelines
The treatment of symptoms and the use of medication should be based on
the usual clinical indications. A therapeutic regimen should not be changed in
response to periods of poor air quality unless there is a clear indication of a
change in a patient's respiratory symptoms. However, it might be advisable to
recommend restriction of strenuous physical activity during periods of poor air
quality.

Registering the data

There are no standard ways of reporting illnesses and deaths thought to be
due to outdoor air pollution to the local health department. In some areas
affected by severe temperature inversions, public health officials review and
record emergency department records during temperature inversions to see if
morbidity and mortality from respiratory and other causes increase. It has to be
kept in mind that a causal link between a given disease episode and exposure
to air pollutants may not be established.

10. AIR 123

 Remedial action, prevention, and education
In many countries, national environment or health ministries have the
authority to set standards for air pollutants to protect the health of people. In
some cases, such as in the USA, these standards take into account people with
specific sensitivities, including children and those with asthma in the standard-
setting process. The WHO ambient air quality guidelines for selected pollutants
are shown in Table 10-3. As another example, the US ambient air quality stan-
dards are given in Table lOA.

Table 10.3 Guideline values for individual substances based on effects other than
cancer or odour/annoyance

SUBSTANCE TIME-WEIGHTED AVERAGE AVERAGING TIME

Cadmium 5 ng/m 3 annual

Carbon disulfide 1OOllg/m3 24 hours
Carbon monoxide 100mg/m 3 15 minutes
60mg/m 3 30 minutes
30mg/m 3 1 hour
10mg/m 3 8 hours
1,2-Dichloroethane 0.7mg/m 3 24 hours
Dichloromethane 3mg/m 3 24 hours
0.45mg/m 3 1 week
Fluoride
Formaldehyde 0.1 mg/m 3 30 minutes
Hydrogen sulfide 15Ollg/m3 24 hours
Lead 0.51lg /m3 annual
Manganese 0.151lg /m3 annual
Mercury 11lg /m3 annual
Nitrogen dioxide 2OOllg/m3 1 hour
4Ollg/m3 annual
Ozone 12Ollg/m3 8 hours
Particulate matter Dose-response
Platinum
PCBs
PCDDs/PCDFs
Styrene 0.26mg/m 3 1 week
Sulfur dioxide 5OOllg/m3 10 minutes
1251lg/m3 24 hours
5Ollg/m3 annual
Tetrachloroethylene 0.25 mg/m 3 annual
Toluene 0.26mg/m 3 1 week
Vanadium 11lg /m3 24 hours

Source: ref. 3.

124 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Table 10.4 US national ambient air quality standards (NAAQS) 1997
POLLUTANT AMBIENT AIR LIMIT AVERAGING TIME
Ozone 0.08ppm 8h
PM 10 50/lg/m 3 Annual arithmetic mean
150/lg/m 3 24h
PM 25 15/lg/m 3 Annual arithmetic mean
65/lg/m 3 24h
Sulfur dioxide 0.03ppm Annual arithmetic mean
0.14ppm 24h
Nitrogen dioxide 0.053ppm Annual arithmetic mean
Carbon monoxide 9ppm 8h
35ppm 1h
Lead 1.5/lg/m 3 24h

Many countries have adopted WHO's guidelines as national standards. In

countries that enforce air quality standards, the ambient concentrations of the
pollutants listed in Table lOA have decreased overall over the past decade,
although fine and ultra-fine particulate matter has increased, and ozone has not
decreased significantly. Large numbers of people are still exposed to potentially
unhealthy levels of all these pollutants. Table 10.5 shows an example of
standard index values with corresponding pollutant concentrations and health
effects.
Prevention efforts have largely focused on the short-term effects of air pollu-
tion. Short-term exposure to ozone aggravates childhood asthma, leading to
increased emergency visits to health facilities for acute asthma attacks. Recent
research has explored whether dietary antioxidant supplementation (4 001 U of
vitamin E and 500mg of vitamin C) affects ozone-induced bronchial hyper-
responsiveness in persons with asthma. In several, but not all, studies of adults,
dietary supplementation was associated with higher lung function values during
periods of ozone pollution (87, 88). It is not yet known whether dietary antioxidant
supplementation is helpful in reducing symptoms among children with asthma
exposed to ozone. Future research efforts should therefore include children.
In his 1962 report on motor vehicles, air pollution, and health (89), the
United States Surgeon General stated:

"As in other problems affecting the public health, it is important that, as

needed research proceeds on the problem of pollution emissions from
motor vehicles, all practicable steps be taken to minimize such pollution
rather than waiting until the results of all the needed research are available."

This remains as true today as it was over 40 years ago.

10. AIR
12 5
 Table 10.5 Pollution standard index values with corresponding pollutant concentrations and health effects
-'"
0'1 INDEX AIR POLLUTANT LEVELS HEALTH
EFFECT
GENERAL HEALTH EFFECTS CAUTIONARY STATEMENTS
VALUE QUALITY
LEVEL PM S02 CO 03 N0 2 DESCRIPTOR
(24-h} (24-h} (S-h) (1-h) (1-h)
J.1g/m J.1g/m ppm ppm ppm
50 0.6 2.0 Premature death of ill and All persons should remain indoors, keeping
500 Significant 600 2620
elderly. Healthy people will windows and doors closed. All persons
harm
experience adverse should minimize physical exertion.
symptoms that affect their
normal activity.
40 0.5 1.6 Hazardous Premature onset of certain The elderly and persons with existing disease
400 Emergency 500 2100
diseases in addition to should stay indoors and avoid physical
significant aggravation of exertion. General population should avoid
symptoms and decreased outdoor activity.
V>
rn exercise tolerance in healthy
n
--I persons.
is The elderly and persons with existing heart or
z 300 Warning 420 1600 30 0.4 1.2 Significant aggravation of
.. Very symptoms and decreased lung disease should stay indoors and reduce
V>
unhealthy exercise tolerance in persons physical activity.
"rnQ with heart or lung disease,
on
nrn with widespread symptoms
in the healthy population.
z
< 0.2 0.6 Mild aggravation of Persons with existing heart or respiratory
;;; 200 Alert 350 800 15
0 Unhealthy symptoms in susceptible ailments should reduce physical exertion and
z outdoor activity.
s:
rn
persons, with irritation
z symptoms in the healthy
):! population.
r
--I
:r:
;0 100 NAAQS 1 150 365 9 0.12
rn Moderate
~
V>

NMQS: National Ambient Air Quality Standards.

 References
1. Bruce N, Perez-Padilla R, Albalak R. Indoor air pollution in developing countries:
a major environmental and public health challenge. Bulletin of the World Health
Organization, 2000, 78:1078-1092.
2. Smith KR, Mehta s. The burden of disease from indoor air pollution in devel-
oping countries. Comparison of estimates. Paper presented at the USAlDj
WHO Global Technical Consultation on the Health Impacts of Indoor Air Pollution
and Household Energy in Developing Countries, 3-4 May 2000, Washington,
DC.
3. Air quality guidelines for Europe, 2nd ed. Copenhagen, WHO Regional Office for
Europe, 2000 (European Series, No. 91).
4. Gordon B, Mackay R, Rehfuss E. Inheriting the world: the atlas of children's health
and the environment. Geneva, World Health Organization, 2004.
5. Parikh J, Pandey V. Biofuels, pollution and health linkages. Economic and Politi-
cal Weekly, 2000, 35:4125-4137.
6. Saksena S et al. Patterns of daily exposure to TSP and CO in the Garhwal
Himalaya. Atmosphere and Environment, 1992, 26A :2125-2134.
7. Albalak R et al. Assessment of PM lO concentrations from domestic biomass fuel
combustion in rural Bolivian highland villages. Environmental Science and Tech-
nology, 1999, 33:2505-2509.
8. Balakrishnan K et al. Daily average exposures to respirable particulate matter
from combustion of biomass fuels in rural households of Southern India. Envi-
ronmental Health Perspectives, 2002, 110:1069-1075.
9. Spengler JD. Sources and concentrations of indoor air pollution. In: Samet JM,
Spengler J D, eds. Indoor air pollution. A health perspective. Baltimore, M D, Johns
Hopkins University Press; 1991.
10. US Environmental Protection Agency. Indoor air pollution: an introduction for
health professionals. Washington, DC, US Government Printing Office, 1994 (EPA
523-217/81322) .
11. Smith KR. Biomass fuels, air pollution and health. A global review. New York,
Plenum Press, 1987.
12. Lambert WE, Samet JM. Indoor air pollution. In: Harber P, Schenker M B, Balmes
JR, eds. Occupational and environmental respiratory disease. St Louis, MO, Mosby,
199 6 :784-807.
13. Parikh J et al. Exposure from cooking with biofuels: pollution monitoring and
analysis for rural Tamil Nadu, India. Energy, 2000, 26:949-962.
14. Balakrishnan K et al. Exposure assessment for respirable particulates associated
with household fuel use in rural districts of Andhra Pradesh, India. Journal
of Exposure Analysis and Environmental Epidemiology, 2004, 14(suppl 1):
S14-S2 5·
15. Smith KR, Liu Y. Indoor air pollution in developing countries. In: Samet JM, ed.
Epidemiology of lung cancer. New York, Marcel Dekker, 1994.
16. Smith KR et al. Indoor air pollution in developing countries and ALRI in children.
Thorax, 2000, 55:518-532.

10. AIR 127

17. Ezzati M, Kammen DM. Quantifying the effects of exposure to indoor air pollu-
tion from biomass combustion on acute respiratory infections in developing
countries. Environmental Health Perspectives, 2001, 1°9:481-489.
18. Samet JM et al. Nitrogen dioxide and respiratory illnesses in infants. American
Review of Respiratory Disease, 1993, 148:1258-1265.
19. Robin LF et al. Wood-burning stoves and lower respiratory illnesses in Navajo
children. Pediatric Infectious Disease Journal, 1996, 15:859-865.
20. International consultation on environmental tobacco smoke (ETS) and child health.
Geneva, World Health Organization, 1999 (WHO/NCD/TFI/99.1O).
21. American Academy of Pediatrics, Committee on Environmental Health.
Environmental tobacco smoke: a hazard to children. Pediatrics, 1997, 99:639-
64 2 .
22. Colley JR, Holland WW, Corkhill RT. Influence of passive smoking and parental
phlegm on pneumonia and bronchitis in early childhood. Lancet, 1974,
2:1031- 1034.
23. Fergusson DM, Horwood LJ, Shannon FT. Parental smoking and respiratory
illness in infancy. Archives of Diseases in Children, 1980, 55:358-361.
24. Harlap S, Davies AM. Infant admissions to the hospital and maternal smoking.
Lancet, 1974, 1:529-532.
25. Rantakallio P. Relationship of maternal smoking to morbidity and mortal-
ity of the child up to the age of five. Acta Paediatrica Scandinavica, 1978, 67:
621-631.
26. Etzel RA et al. Passive smoking and middle ear effusion among children in day
care. Pediatrics, 1992, 9°:228-232.
27. Ey J Let al. Passive smoke exposure and otitis media in the first year of life. Pedi-
atrics, 1995, 95:67°-677.
28. Chilmonczyk BA et al. Association between exposure to environmental tobacco
smoke and exacerbations of asthma in children. New England Journal of Medi-
cine, 1993, 328:1665-1669.
29. Martinez FD, Cline M, Burrows B. Increased incidence of asthma in children of
smoking mothers. Pediatrics, 1992, 89:21-26.
30. Weitzman M et al. Maternal smoking and childhood asthma. Pediatrics, 1990,
85:5 0 5-5 11 .
31. Murray AB, Morrison BJ. The decrease in severity of asthma in children of
parents who smoke since the parents have been exposing them to less cigarette
smoke. Journal of Allergy and Clinical Immunology, 1993, 91:102-110.
32. Anderson HR, Cook DG. Health effects of passive smoking. 2. Passive smoking
and sudden infant death syndrome: review of the epidemiologic evidence.
Thorax, 1997, 53:1003-1009.
33. Taylor JA, Sanderson M. A reexamination of the risk factors for the sudden infant
death syndrome. Journal of Pediatrics, 1995, 126:887-891.
34. Tamburlini G, von Ehrenstein 0, Bertollini R, eds. Children's health and environ-
ment: a review of evidence. Luxembourg, Office for Official Publications of the
European Communities (on behalf of the European Environmental Agency and
WHO Regional Office for Europe). 2002.

128 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 35· Fiore MC et al. Smoking cessation: information for specialists. Clinical practice
guideline. Quick reference guide for smoking cessation specialists, No. 18. Rockville,
MD, Centers for Disease Control and Prevention, 1996 (Publication AHCPR
96-06 94).
36 . Baker MD, Henretig FM, Ludwig S. Carboxyhemoglobin levels in children
with nonspecific flu-like symptoms. Journal of Pediatrics, 1988, 113:501-
50 4.
37· Heckerling PS et al. Occult carbon monoxide poisoning in patients with neuro-
logic illness. Clinical Toxicology, 1990, 28:29-44.
38 . Etzel RA, ed. Pediatric environmental health, 2nd ed. Elk Grove Village, IL, Amer-
ican Academy of Pediatrics 2003.
39· Samet J. Environmental controls and lung disease. Report of the ATS Workshop
on Environmental Controls and Lung Disease. American Review of Respiratory
Disease, 1990, 142:915-939.
4 0 . Health Canada. Exposure guidelines for residential indoor air quality: a report to the
federal-provincial advisory committee on environmental health. Ottawa, Health
Canada, 1989 (Publication #H46-2/90-156E).
41. American SOciety of Heating, Refrigerating, and Air Conditioning Engineers
(ASH RAE). Ventilation for acceptable indoor air quality. Atlanta, GA, ASHRAE,
19 8 9 (ASHRAE Standard 62-1989).
4 2 . Wallace LA. Volatile organic compounds. In: Samet JM, Spengler JD, eds. Indoor
air pollution: a health perspective. Baltimore, MD, Johns Hopkins University Press,
1991 :252- 272.
43· Molhave L. Indoor air pollution due to organic gases and vapours of solvents in
building materials. Environment International, 1982, 8:117-12 7.
44· American Academy of Pediatrics, Committee on Environmental Health. Toxic
effects of indoor molds. Pediatrics, 1998, 101 :712-7 14.
45· Dales RE et al. Respiratory health effects of home dampness and molds
among Canadian children. American Journal of Epidemiology, 1991, 134:196-
20 3.
4 6 . Jaakkola JjK, Jaakkola N, Ruotsalainen R. Home dampness and molds as
determinants of respiratory symptoms and asthma in pre-school children.
Journal of Exposure Analysis and Environmental Epidemiology, 1993, 3=1 2 9-
142 .
47· Verhoeff AP et al. Damp housing and childhood respiratory symptoms: The role
of sensitization to dust mites and molds. AmericanJournal of Epidemiology, 1995,
141:103-110.
4 8 . Dearborn DG et al. Overview of investigations into pulmonary hemorrhage
among infants in Cleveland, Ohio. Environmental Health Perspectives, 1999, 107
(SUPp I 3):495-499.
49· Croft WA, Jarvis BB, Yatawara CS. Airborne outbreak of trichothecene toxicosis.
Atmospheric Environment, 1986, 20:549-55 2.
50. Etzel RA et al. Acute pulmonary hemorrhage in infants associated with exposure
to Stachybotrys atra and other fungi. Archives of Pediatrics and Adolescent Medi-
cine, 1998, 152:757-762.

10. AIR
12 9
51. Flappan SM et al. Infant pulmonary hemorrhage in a suburban home with water
damage and mold (Stachybotrys atra). Environmental Health Perspectives, 1999,
107:9 2 7-93 0 .
52. Weiss A, Chidekel AS. Acute pulmonary hemorrhage in a Delaware infant
after exposure to Stachybotrys atra. Delaware Medical Journal, 2002, 74:3 6 3-
368 .
53. Elidemir 0 et al. Isolation of Stachybotrys from the lung of a child with pulmonary
hemosiderosis. Pediatrics, 1999, 104:964-966.
54. Flannigan B, McCabe EM, McGarry F. Allergic and toxigenic microorganisms in
houses. Society for Applied Bacteriology, Symposium Series, 199 1, 20:61S.
55. Gravesen S, Frisvad )C, Samson RA. Microfungi. Copenhagen, Munksgaard,
1994:473·
56. Wilson CEo Sudden infant death syndrome and Canadian Aboriginals: bacteria
and infections. FEMS Immunology and Medical Microbiology, 1999, 25:221-226.
57. Miller )D et al. Fungi and fungal products in some Canadian houses. Interna-
tional Biodeterioration, 1988, 24:103-120.
58. Agocs MM et al. Mercury exposure from interior latex paint. New EnglandJournal
of Medicine, 1990, 32 P 0 96-1101.
59. Hirschmann SZ, Feingold M, Boylen G. Mercury in house paint as a cause of
acrodynia: effect of therapy with N-acetyl-D,L-penicillamine. New EnglandJournal
of Medicine, 1963, 269:889-893.
60. US Environmental Protection Agency. 1997 National air quality: status and trends.
Office of Air and Radiation, 1998 (http://www.epa.gov/oar/aq trnd 97 /brochure/
n02html).
61. Dietert RR et al. Workshop to identify critical windows of exposure for children's
health: immune and respiratory systems work group summary. Environmental
Health Perspectives, 2000, 108(Suppi 3):48 3-49 0 .
62. Koren G et al. A multicenter prospective study of fetal outcome following acci-
dental carbon monoxide poisoning in pregnancy. Reproductive Toxicology, 199 1,
5:397-40 3.
63. Longo LD. The biological effects of carbon monoxide on the pregnant woman,
fetus, and newborn infant. American Journal of Obstetrics and Gynecology, 1977,
129:69-103.
64. Vreman H), Mahoney Jj, Stevenson DK. Carbon monoxide and carboxyhemo-
globin. Advances in Pediatrics, 1995, 4 2 :3 0 3-3 2 5.
65. Bates DV. The effects of air pollution on children. Environmental Health Perspec-
tives, 1995, 103(SUPPI. 6):49-53·
66. Committee of the Environmental and Occupational Health Assembly of the
American Thoracic Society. Health effects of outdoor air pollution. American
Journal of Respiratory and Critical Care Medicine, 1996, 153:3-5 0 .
67. World Health Organization and United Nations Environment Programme. Urban
air pollution in megacities of the world. Cambridge, MA, Blackwell, 199 2 .
68. Schwela D. Air pollution and health in urban areas. Reviews on Environmental
Health, 2000, 15:13-42.

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

69. Dockery DW, Pope CA. Acute respiratory effects of particulate air pollution.
Annual Review of Public Health, 1994, 15:107-132.
70. Smithard HER. The 1952 fog in a metropolitan borough. Monthly Bulletin of the
Ministry of Health, February 1954:26-35.
71. Etzel RA, French JG. Air pollution. In: Noji EK, ed. The public health consequences
of disasters. New York, Oxford University Press, 1997:336-353.
72. American Academy of Pediatrics, Committee on Environmental Health. Ambient
air pollution: respiratory hazards to children. Pediatrics, 1993, 91:1210-1213.
73. Hanania NA et al. Effect of exposure to low levels of ozone on the responses to
inhaled allergen in allergic asthmatic patients. Chest, 1998, 114:752-756.
74. Molfino NA et al. Effects of low concentrations of ozone on inhaled allergen
responses in asthmatic subjects. Lancet, 1991, 338:199-2°3.
75. McConnell R et al. Asthma in exercising children exposed to ozone: a cohort
study. Lancet, 2002, 359:386-391.
76. Kunzli N et al. Association between lifetime ambient ozone exposure and pul-
monary function in college freshmen-results of a pilot study. Environmental
Research, 1997, 72:8-23.
77. Galizia A, Kinney PL. Long-term residence in areas of high ozone: associations
with respiratory health in a nationwide sample of nonsmoking young adults.
Environmental Health Perspectives, 1999, 107:675-679.
78. Gilliland FD et al. The effects of ambient air pollution on school absenteeism
due to respiratory illnesses. Epidemiology, 2001, 12:43-54.
79. Abbey DE et al. Long-term ambient concentrations of particulates and oxidants
and development of chronic disease in a cohort of non-smoking California res-
idents. Inhalation Toxicology, 1995, 7:19-34.
80. Abbey DE et al. Long-term ambient concentrations of total suspended particu-
lates, ozone, and sulfur dioxide and respiratory symptoms in a non-smoking
population. Archives of Environmental Health, 1993, 48:33-46.
81. Berglund D, Abbey D. Long-term effects of air pollution. Western Journal of
Medicine, 1996, 165:14°.
82. Spengler J D et al. Health effects of acid aerosols on North American children:
air pollution exposures. Environmental Health Perspectives, 1996, 104:492-
499·
83. Dockery DW et al. Health effects of acid aerosols on North American children:
respiratory symptoms. Environmental Health Perspectives, 1996, 104:500-505.
84. Raizenne M et al. Health effects of acid aerosols on North American children:
pulmonary function. Environmental Health Perspectives, 1996, 104:5°6-514.
85. Dockery DW et al. An association between air pollution and mortality in six US
cities. New England Journal of Medicine, 1993, 329:1753-1759.
86. Dickey J et al. Part VII. Air pollution: overview of sources and health effects.
Disease of the Month, 2000, 46:566-589.
87. Romieu I et al. Antioxidant supplementation and respiratory functions among
workers exposed to high levels of ozone. AmericanJournal of Respiratory and Crit-
ical Care Medicine, 1998, 158:226-232.

10. AIR
88. Trenga C, Koenig JQ, Williams pv. Dietary antioxidants and ozone-induced
bronchial hyperresponsiveness in adults with asthma. Archives of Environmental
Health, 2001, 56:242.
89. United States Division of Air Pollution. Motor vehicles, air pollution and health: a
report of the Surgeon General to the U. S. Congress. Washington, DC, US Public
Health Service, Division of Air Pollution, 1962.

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CHAPTER 11

Foodborne hazards of particular concern

for the young
D. B. Mahoney
International Food Safety Consultant, Canberra, Australia

G. C. Moy
Food Safety Department, World Health Organization,
Geneva, Switzerland

Introduction
While the nutritional adequacy of the diets of infants and children is a major
concern for much of the world, there is also concern in many countries about
the safety of the foods they consume. Indeed, the International Conference on
Nutrition declared that " ... access to nutritionally adequate and safe food is a
right of each individual (1). Notwithstanding the advances in the knowledge and
tools to ensure food safety, food borne diseases are widespread and have con·
siderable impact on communities in both developing and developed countries.
For many food borne hazards, the susceptibility of the host is all·important.
Generally the young, pregnant women, persons over 60 years, and those who
are ill or immunocompromised are the most vulnerable to food borne illness.
This chapter discusses the food borne risks for three subgroups, namely: (1)
the developing fetus; (2) breastfed and bottle-fed infants; and (3) children and
infants receiving complementary food. In general, food borne illness can be
reduced by preventing contamination, through improved production, process-
ing and handling, and by educating people to avoid high-risk foods and to
prevent contamination during food preparation. Success in educating con-
sumers requires an understanding of who is most at risk, and techniques that
motivate consumers to change their behaviour and follow food safety recom-
mendations. This chapter presents specific measures that can be taken by those
responsible for infants and children to help reduce their risk of foodborne
disease.

Foodborne hazards
The agents responsible for food borne disease include bacteria, viruses and
parasites, as well as a range of chemicals, including biotoxins and heavy metals.
The adverse health effects of food borne illness range from mild gastroenteritis
(including diarrhoea and vomiting) to life-threatening neurological, renal or
hepatic syndromes, congenital anomalies and cancer. The risks posed by the

133
 presence of microorganisms and chemicals in the food supply are of concern
worldwide. However, consumers' judgement of hazards and perception offood
safety risks are often at variance with those of the scientific community. Con-
sumers' perceptions in particular are shaped by a number offactors, including
personal experience, access to information about food safety, trust in sources
of information, and baseline food safety risk levels. Hence, while the public
may be concerned about food additives and new technologies, they may fail to
recognize the major risks resulting from food contaminated by pathogenic
microorganisms.
In terms of acute illness, food·
borne disease caused by pathogenic
microorganisms or their toxins is
Infant. exposure to organochlo.rine
more significant for children than
contaminants in bres.st milk
Tile ·benefits of breastreed.ing infantsfwfiTl birth is generally acknowledged, even
for at least. six months are beyond question .. At among health care professionals.
the. same· time,. certainchemic.als, in particular Even mild bouts of gastroenteritis
organochlorines, .can enter thefo.odchainand pose serious threats to children, as
be stored in fatty tissue. In breastfeeding they can lead to dehydration and
women, these chemicals can then contaminate even death if not treated properly.
the breast milk, and can have adverse health This is especially significant in chil-
effects in the child. Whilebreastfeeding is dren who are malnourished.
optimal and should be. prQmotedi steps can be The duration of food borne
taken to reduce exposure to harmful chemicals. disease may vary from a few days in
Case study 15,.page 325 describes wllat gov- the majority of infections, to weeks
ernments, profeSs!onals.and Individuals·can do or months with agents such as
to avoid exposure of mothers and children to hepatitis A virus or Brucella. In the
hamiful chemicals and tQ respond to health case of toxoplasmosis, infants may
concerns: experience irreversible developmen-
tal and neurological deficits.
Noninfectious foodborne illness
arises from exposure to raw and processed food contaminated by toxic chemi-
cals. Such toxic chemicals include residues of pesticides and veterinary drugs,
industrial pollutants, heavy metals, biotoxins, and certain substances used
improperly in food processing. While illness may be acute, the effects of par-
ticular concern are generally chronic and irreversible, such as developmental
deficiencies and cancer.

Magnitude of the food safety problem

Unfortunately, data on the incidence and severity offoodborne illness in the
general population are limited in most countries. Where such data are collected
through surveillance programmes, most cases of food borne illness are not
reported, either because medical treatment is not sought or, when treatment is
sought, specimens are not taken to allow diagnostic tests to identify the food·

134 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

borne pathogen. Also, certain pathogens transmitted via food may also be
spread through water or by person-to-person contact, and this may obscure the
role offood as a vehicle for transmission. In addition, some food borne illness
is caused by hitherto unknown pathogens, and thus cannot be diagnosed. Many
pathogens, such as Campylobacter jejuni, Escherichia coli O'57:H7 and Cyclospora
cayetanensis, were not recognized as causes of food borne illness twenty years
ago.
Foodborne illnesses that are nationally reportable in certain developed
countries include typhoid fever, cholera, hepatitis A, E. coli O'5TH7 infection,
haemolytic uraemic syndrome, salmonellosis, and shigellosis. Reporting
requirements are stipulated by local and national regulations. In developing
countries (excluding China), food borne pathogenic microorganisms are esti-
mated to cause up to 70% of the roughly 1.5 billion annual episodes of diar-
rhoea, and a related 3 million deaths in children under the age of five (2). In the
United States it is estimated that 76 million illnesses, 325000 hospitalizations
and 5000 deaths result each year from food borne illnesses (3). While the figure
for morbidity suggests that one in three persons becomes ill each year, food-
borne disease is expected to be more prevalent among the young.

Risk analysis
An important tool for the control and prevention offoodborne illness is accu-
rate and reliable data on the risks. Such information is essential for food safety
managers to develop countermeasures.
Risk analysis has three components: risk assessment, risk management, and
risk communication. Risk assessment involves a sCientifically based process
designed to identify hazards and their adverse health effects, estimate likely risk
and provide an indication of the uncertainties. The risk assessment should
inform the selection of risk management options, such as establishing food
standards, defining food processing and handling guidelines, and developing
food safety messages to protect consumers. While there are good data on
chemical risks to consumers, microbiological risk assessment is a developing
science.

Specific hazards of particular concern

Foodborne protozoa
Toxoplasma gondii
Toxoplasmosis is a widespread parasitic disease that usually causes no
symptoms in healthy human hosts. In pregnant women the organism T. gondii
may infect the fetal brain, eyes and other tissues, even if the woman is asymp-
tomatic. The infection can trigger miscarriage, stillbirth and preterm birth, or
lead to mental retardation and blindness in the infant. The fetus is presumed
to be at risk only if the mother has a primary, active infection during the
pregnancy.

11. FOODBORNE HAZARDS OF PARTICULAR CONCERN FOR THE YOUNG 135

 The birth prevalence of congenital toxoplasmosis throughout the world
ranges from less than 1 to 10 per 10000 live births (4-6). The age of the fetus
may be a factor in maternal transmission, with the risk of fetal infection low
during the first 8 weeks of pregnancy, and infection resulting mainly in sponta-
neous termination of the pregnancy. In one study, up to 90% of infected infants
did not exhibit overt clinical signs of disease at birth (7). Of those with symp-
toms, many had severe neurological and development problems. In another
study, visual impairment was observed in all children with congenital toxoplas-
mosis, while 74% had severe visual impairment (8). Of those with subclinical
congenital infection at birth, up to 85% may develop chronic recurring eye
disease and learning difficulties. The long-term impact carries high economic
and societal costs.
Toxoplasmosis can be contracted by eating raw or undercooked meat or
from exposure to the faeces of infected cats. Cats are an important host, with
the parasite infecting the cells lining the cats' intestines. Farm animals may
become infected when they ingest food or water contaminated by faeces from
infected cats.

Giardia lamblia
c. lamblia is spread through the faecal-oral route, either directly by person-
to-person contact or through contaminated food or water. The parasite infects
the small intestine and may cause diarrhoea, abdominal cramps and bloating,
and result in malabsorption and weight loss.
Children are infected more frequently than adults, and the parasite is com-
monly found in day-care centres. The Centers for Disease Control and Preven-
tion in the USA reports that giardiasis has been identified in 10-15% of children
who have not been toilet-trained attending these centres. Approximately
20-25% of day-care staff and family contacts of infected children also become
infected.

Foodborne bacteria
Listeria monocytogenes
L. monocytogenes may cause a mild form of gastrointestinal illness in healthy
adults. While such infections are uncommon and cause few or no symptoms in
healthy people, they may be very serious for pregnant women. Women infected
with L. monocytogenes during pregnancy may transmit the infection to the fetus,
possibly leading to spontaneous abortion, fetal death, or subsequent visual,
mental, or other health problems in the infant. Outbreak data show that the
incubation period ranges from 2 to 6 weeks for the invasive disease. Listeriosis
results in an estimated 2500 serious illnesses and 500 deaths in the United
States each year (9).
Pregnant women are about 20 times more likely than other adults to get sick
from L. monocytogenes. The organism is typically found in raw meat, deli-

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

catessen products, including processed ready-to-eat meat products, soft
cheeses, unpasteurized dairy products and chilled smoked seafood.

Salmonella species
Salmonellosis results from consuming food contaminated by Salmonella
spp. Infected persons develop diarrhoea, fever, and abdominal cramps between
12 and 72 hours after eating the contaminated food. The illness usually lasts
4-7 days, and most people recover without treatment. In vulnerable groups,
such as the young, Salmonella infection may spread beyond the intestine to the
bloodstream and cause a more severe systemic disease.
Salmonellae are found in the intestinal tracts of animals and humans, and
some individuals are chronic carriers of the organism. Humans usually become
infected by eating food contaminated with animal faeces, especially raw and
undercooked foods of animal origin, such as beef, poultry, milk, and eggs. Food
may also become contaminated through cross-contamination and poor hygiene
of food handlers.

Escherichia coli 0157:H7

E. coli 015TH7 is an emerging cause offoodborne illness, and has rapidly
become a major cause of bloody diarrhoea and acute renal failure. The infec-
tion can be fatal, especially in chil-
dren. The largest outbreak recorded
so far was in Japan in 1996 (see Escherichia coli 0157:H7 outbreak in
Box). Japanese schoolchildren
In some people, particularly chil- School lunch programmes in Japan were to
dren under 5 years of age and the blame for several outbreaks of Escherichia coli
elderly, the infection can lead to the 0157:H7 infection in 1996. Several problems
development of haemolytic uraemic were found in growth, distribution and manage-
syndrome. Between 2% and 7% of ment of food that could have been the cause of
infections in the United States led nearly 10000 children becoming ill and five
to this complication. Haemolytic dying in more than eight outbreaks over a six-
uraemic syndrome is the principal month period. Changes to the school lunch pro-
cause of acute kidney failure in chil- gramme management led to improved food
dren, and most cases are caused by safety and reduced the incidence of foodborne
E. coli 015TH7. illness (Case study 16, page 330).
E. coli 0157:H7 infection has
been associated with eating under-
cooked, contaminated minced beef. Because the organism lives in the intestines
of healthy cattle, preventive measures on cattle farms and during meat pro-
cessing are being investigated. Infection has also occurred after consumption
of unpasteurized milk, unpasteurized apple cider, sprouts, lettuce, and salami.
Person-to-person transmission is important in families and child care centres,
especially among toddlers who are not toilet-trained.

11. FOODBORNE HAZARDS OF PARTICULAR CONCERN FOR THE YOUNG 137

 Clostridium botulinum
Botulism is a rare, acute, descending flaccid paralysis caused by the neuro-
toxin produced by C. botulinum_ Intoxication results from ingestion oHood con-
taminated with the preformed toxin. Typical food vehicles include low-acid
canned foods that have been improperly heat-processed, such as asparagus,
green beans, and corn; more unusual sources have included chilli peppers,
chopped garlic, tomatoes stored in oil, and smoked vacuum-packed fish.
Infant botulism is a recognized variant first described in 1976. The illness in
infants is caused by ingestion of C. botulinum spores, which subsequently ger-
minate, multiply, and release toxin in the infant's large intestine. A unique epi-
demiological feature of infant botulism is that all cases occur in children less
than one year of age, with 95% of cases occurring in the first 6 months of life.
Honey is a reservoir for C. botulinum and epidemiological studies have impli-
cated honey consumption as a risk factor.
The clinical features include constipation, poor feeding, weakness, hypoto-
nia, dysphasia and, in severe cases, flaccid paralysis and respiratory failure. All
forms of botulism can be fatal and are considered medical emergencies.

Other pathogenic bacteria

A range of other bacteria are responsible for outbreaks of food borne disease.
Organisms such as Campylobacter jejuni, Staphylococcus aureus, Bacillus cereus,
Clostridium perfringens, Shigella spp. and Vibrio spp., especially Vibrio cholerae,
are commonly implicated in outbreaks associated with specific foods.

Foodborne viruses
Rotaviruses, hepatitis A, and noroviruses
Hepatitis A and gastroenteritis viruses, such as rotaviruses, noroviruses,
astroviruses, and other caliciviruses are more often transmitted via food than
other viruses. Viruses are considered the most common cause of infectious gas-
troenteritis (10), but except for rotaviruses, they are rarely identified. All food-
borne viruses are shed in faeces and infect by being ingested.
The main symptoms of viral gastroenteritis are watery diarrhoea and vom-
iting. Patients may also have headache, fever and abdominal cramps. Symp-
toms occur 1 or 2 days after infection and last for 1-10 days. People with viral
gastroenteritis almost always recover without long-term problems. However
gastroenteritis can be serious for infants and young children, who are at risk of
dehydration from loss of fluids through vomiting or diarrhoea.
Food may be contaminated by food handlers who have viral gastroenteritis,
especially if their personal hygiene is poor. Raw and undercooked shellfish
grown in polluted waters are also an important vehicle for viral gastroenteritis.
Rotavirus infection is the most common cause of severe viral diarrhoea in
infants and young children under 5 years old, resulting in the hospitalization of
approximately 55000 children each year in the United States. The incubation

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

period for rotavirus disease is approximately 2 days, followed by vomiting and
watery diarrhoea for 3-8 days. The primary mode of transmission is faecal-oral.
The virus is stable in the environment, and transmission occurs through inges-
tion of contaminated water or food and contact with contaminated surfaces.

HIV and other viral infections

Breast milk may be a source of viral infection in nursing infants whose
mothers have acquired HIV or cytomegalovirus (11) infections. Mother-to-child
transmission of H IV can occur in utero, at delivery, or after birth through breast-
feeding. Data from various studies estimate transmission rates, without anti-
retroviral intervention, of 15-30% in the absence of breastfeeding, 25-35% if
there is breastfeeding up to 6 months, and 30-45% if breastfeeding is contin-
ued for 18-24 months (12).
Policies and strategies are evolving as more evidence becomes available
from research, but more needs to be known about the factors that influence
transmission rates and the risks associated with alternative feeding strategies.
For women who know they are HIV-positive and where infant mortality is high,
exclusive breastfeeding may still result in fewer infant deaths than feeding
breast-milk substitutes. A WHO Technical Consultation (13) recommended the
following approaches to prevention of mother-to-child transmission:

• When replacement feeding is acceptable, feasible, affordable, sustainable

and safe, avoidance of all breastfeeding by H IV-infected mothers is rec-
ommended. Otherwise, exclusive breastfeeding is recommended during
the first months of life.
• To minimize HIV transmission risk, breastfeeding should be discontin-
ued as soon as feasible, taking into account local circumstances, the indi-
vidual woman's situation and the risks of replacement feeding (including
infections other than HIV and malnutrition).
• When H IV-infected mothers choose not to breastfeed from birth or stop
breastfeeding later, they should be provided with specific guidance and
support for at least the first 2 years of the child's life to ensure adequate
replacement feeding. Programmes should strive to improve conditions
to make replacement feeding safer for HIV-infected mothers and
families.

Countries should have in place a comprehensive national infant and young

child feeding policy which includes information on HIV and infant feeding. Such
a policy should lead to guidelines for health workers on how to protect, promote
and support breastfeeding in the general population, while giving adequate
support to H IV-positive women to enable them to select the best feeding option
for themselves and their babies. The policy and gUidelines should be based on
the local situation, including an assessment of feeding options.

11. FOODBORNE HAZARDS OF PARTICULAR CONCERN FOR THE YOUNG 139

 Chemical contaminants
Infants and children have a special vulnerability to acute, subacute and
chronic effects of chemicals present in their food. There is an urgent need for
recognition, evaluation and action to address potential contaminant problems.
This is especially important in developing countries, where the likelihood oftoxic
exposures is magnified by the unsafe use of chemicals, increased pollution, and
sometimes a lack of awareness of environmental hazards.
The distinctive diet and physiological immaturity of infants and children
make them particularly susceptible to the toxic effects of certain chemicals.
Another important factor is their greater exposure. Compared with adults, chil-
dren consume more food and water and breathe more air per kg of body weight.
The skin surface area of an infant per unit of body weight is double that of adults.
The normal respiratory volume of a resting infant in relation to body weight is
twice that of a resting adult. Food consumption by infants per unit of body
weight is approximately twice that of adults. In addition, a child's diet is usually
less varied than an adult's, with children consuming larger proportions of milk,
fruit and fruit juices.

Pesticides
Pesticides perform an important role in maximizing agricultural production
and protecting the food supply. But because of their inherent toxicity and wide-
spread use, pesticides also pose a threat to public health, particularly to infants
and children.
Epidemiological studies and laboratory studies in animals contribute to a
growing body of evidence linking pesticide exposure to adverse health effects
including cancer, birth defects, reproductive harm, neurological and develop-
mental toxicity, immunotoxicity and disruption of the endocrine system. A major
concern for the young is that, during the first six years of life, the child's central
nervous system is still developing and is likely to be vulnerable to neurotoxic
pesticides.
Most major classes of pesticides, including the organochlorines, organo-
phosphorus compounds, carbamates, chlorophenoxy herbicides, and pyre-
throids, have been shown to adversely affect the developing nervous system of
laboratory animals, altering neurological function and causing subtle neuro-
behavioural impairments. Many of these pesticides share a common mecha-
nism of toxicity, but their cumulative impact on children's health has not yet
been fully assessed.

Persistent organic pollutants

Persistent organic pollutants (POPs) are a group of toxic chemical sub-
stances that persist in the environment, bioaccumulate along the food-chain,
and are a risk to human health. Twelve substances were initially classified as

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 POPs under the Stockholm Convention (14): aldrin, chlordane, dichlorodiphenyl-
trichloroethane (DDT), dieldrin, endrin, heptachlor, mirex, toxaphene, poly-
chlorinated biphenyls (PCBs), hexachlorobenzene, dioxins and dibenzofurans.
Most of these, with the exception of DDT used for malaria control, have been,
or are in the process of being, phased out.
POPs resist biodegradation and are insoluble in water, but are readily stored
in fatty tissue where concentrations can reach 70000 times the background
level. Long-lived species of fish, birds and mammals, including humans, have
the greatest concentrations. These pollutants may accumulate in fatty tissues
in the human body for many years, and may be passed to infants in breast milk.
The potential health effects of POPs include cancer, allergies, hypersensi-
tivity and disorders of the nervous and immune systems. Of particular concern
are dioxins (including dibenzofurans and dioxin-like PCBs) which may function
as endocrine disrupters. Low-level exposure to such substances is particularly
critical for the fetus and infants, because of their very low levels of circulating
hormones. Dioxins can pass through the placenta directly to the fetus, and may
cause developmental problems. Breastfeeding infants can receive up to '4% of
their lifetime exposure to dioxins through breast milk. Because reproductive and
developmental processes are extremely sensitive to endocrine-disruptive com-
pounds, there is an urgent need for better risk characterization and improved
evaluation procedures (15). In any case, it may be prudent to reduce the use and
emissions of these substances and to establish limits for their presence in food
and animal feed. An assessment of the current knowledge on endocrine dis-
rupters has been prepared by WHO through the International Programme on
Chemical Safety (16).

Mercury
Mercury occurs naturally in soils and rocks but is also used in a number of
industrial applications. Organic mercury, principally in the form of methylmer-
cury, is the most hazardous form.
Food is the main source of exposure to methylmercury and, for the fetus,
the main source of exposure is the maternal diet. The highest levels of mercury
in food are typically found in fish, particularly the long-lived, large, predatory fish
at the top of the food chain, e.g. shark, swordfish, and tuna.
For the vast majority of consumers, the level of mercury in fish does not
pose any significant health risk. However, the fetus and young children are more
vulnerable to the harmful effects of mercury than adults. Mercury is toxic to the
developing fetal brain, and exposure in the womb may lead to neurobehavioural
effects such as deficits in motor skills, attention, language, visual-spatial skills
and memory. The Codex Alimentarius Commission has established guideline
levels for total mercury in predatory and non-predatory fish. In some countries,
pregnant women are advised to limit their consumption of certain fish.

11. FOODBORNE HAZARDS OF PARTICULAR CONCERN FOR THE YOUNG

..........----------------
 lead
Lead occurs naturally in the environment and has many industrial uses.
Small amounts of lead can be harmful, especially to the fetus, infant and young
child. During pregnancy, especially in the last trimester, lead can cross the pla-
centa. Cognitive and growth defects may occur in infants whose mothers are
exposed to lead during pregnancy. Lead exposure is also serious for young chil-
dren because they absorb it more easily than adults and are more susceptible
to its harmful effects. Even low-level exposure may reduce intelligence, result in
learning disabilities and behavioural abnormalities, and cause kidney damage.
Airborne lead from automobile exhaust may contaminate crops or soil; lead
may also be introduced into water by certain household water systems. Lead
can enter food, especially acidic food such as fruit juice, from lead-based glazes
and lead-soldered cans. Infants may also ingest lead in breast milk.
There is no threshold level believed to be safe for infants and young chil-
dren. However, the Joint FAO/WHO Expert Committee on Food Additives
(JECFA) has established a provisional tolerable weekly intake (PTWI) for lead of
0.025 mg/kg of body weight (17).

Nitrate and nitrite

The major acute toxic effect of nitrate and nitrite poisoning is development
of methaemoglobinaemia, a condition in which more than 10% of the haemo-
globin is transformed into methaemoglobin, thereby reducing the oxygen-
carrying capacity of the blood. When transformation exceeds 70%, the condi-
tion can be fatal.
Neonates are at special risk because of a transient deficiency in met-
haemoglobin reductase and the greater susceptibility of haemoglobin F (fetal
haemoglobin) to oxidation. Near-adult levels of methaemoglobin reductase
and haemoglobin A are reached by 4 months of age.
Most clinical cases of neonatal methaemoglobinaemia occur from drinking
water or water-based formulations with high nitrate or nitrite content, i.e. nitrate
levels in drinking-water of more than 100 mg per litre. Cases of methaemoglo-
binaemia have also been reported in infants fed with vegetable preparations in
which nitrate has been converted to nitrite through bacterial action.

Mycotoxins
The growth of moulds on agricultural commodities may result in the pro-
duction of mycotoxins. For example, aflatoxins are produced by Aspergillus jlavus
growing on corn, peanuts and other nuts. These toxins are human carcinogens
and considered one of the most dangerous contaminants of food and animal
feed. Patulin is a mycotoxin produced by certain species of Penicillium,
Aspergillus, and Byssochylamys moulds, and has been found in high levels in
apple juice made from damaged and bruised apples. On the basis of adverse
effects observed in animal studies, the Codex Alimentarius Commission has

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

proposed a limit for patulin of 5o)..lgjkg in apple juice and apple juice ingredi-
ents in other beverages. In deriving this limit, apple juice consumption by chil-
dren was considered because they consume higher amounts relative to their
body weight than other age groups. Avoiding consumption of bruised apples
can also reduce exposure to patulin.
Ethyl alcohol can also be considered a mycotoxin, because it is produced by
microorganisms and is toxic to humans. In particular, intake of ethyl alcohol by
pregnant women can seriously injure the fetus. Ethyl alcohol is present in many
fermented beverages, such as beer and wines, and is used as an ingredient in
various foods.

Food additives and dietary supplements

Public health concerns about the use of food additives, such as preserva-
tives, artificial colouring agents, flavour enhancers, sweeteners, and antimicro-
bials, are generally unfounded. Most developed countries have registration and
approval processes which are designed to ensure that only substances that have
met exacting safety assessments are used. JECFA provides reference intakes for
a range of direct and indirect food additives. An acceptable daily intake (ADI)
may be established for a chemical and its toxicologica"y significant degradation
and metabolic products if data demonstrate that exposure to the chemical under
its proposed conditions of use would pose no appreciable risk to the consumer
over a lifetime. JECFA has, however, stated that ADls should not be considered
applicable to neonates and infants up to the age of 12 weeks (18). In addition,
there is some evidence to suggest that certain food additives may produce spe-
cific effects in children, such as attention and hyperactivity disorders.
The consumption of supplementary vitamins and minerals is indicated in
certain situations, but excessive use may pose health problems. Commercial
fortified products include vitamin D fortified milk, iodized salt, and iron-
supplemented cereals. In addition, there is widespread promotion of the use by
pregnant women of folic acid supplements to prevent spina bifida, vitamin K to
prevent haemorrhagic disease of the newborn, and vitamin A to reduce the risk
of xerophthalmia in infants. However, there are also dangers associated with
excessive intake of vitamins and minerals. For example, excess vitamin A can
result in bone disease and increased intracranial pressure, while excess vitamin
D can cause kidney disease. Such excesses are unlikely to be a result of dietary
intake, but rather of excessive use of supplements. Consequently, it is best to
seek a physician's advice before taking such supplements.

Protecting the young

The appropriate advice on how to minimize or avoid food safety risks
depends on the type of hazard, the nature of the food, the age of the consumer,
environmental conditions and other factors. Here, we consider three groups,
namely: (a) the developing fetus, (b) breastfed and bottle-fed infants, and (c)

11. FOODBORNE HAZARDS OF PARTICULAR CONCERN FOR THE YOUNG 143

infants receiving complementary foods, and children. The principal foodborne
hazards and risk reduction strategies for each of these three groups are
described.

The developing fetus

The developing fetus is at risk from infectious agents and toxic chemicals
that may cross the placenta. Obviously, the exposure of the fetus is a result of
exposure of the woman during pregnancy and, in some cases, before pregnancy.
Because of the potential adverse health outcome for the developing fetus,
women should be informed about these foodborne hazards. Table 11.1 lists the
hazards, adverse health effects and possible risk reduction strategies.

Breastfed and bottle-fed infants

Breast milk is the most nutritious and safest food for the newborn infant.
Exclusive breastfeeding minimizes exposure of the infant to food borne and
waterborne pathogenic microorganisms, and confers protection to the infant
through the anti-infective properties of breast milk. However breastfed infants
can be at risk from a range of chemicals that may be present in breast milk.
These may come from the maternal diet during nursing, but may also
come from the release of substances that had accumulated in the mother's
adipose tissue. Certain infectious agents may also be transmitted through
breast milk.
Bottle-fed infants may be exposed to a range of food- and waterborne
pathogens. Bacterial contamination of bottles is an important source of diar-
rhoea in infants. This is particularly a problem in developing countries and in
other situations where environmental sanitation is poor. Breast-milk substi-
tutes, such as powdered infant formula, may contain viable pathogenic micro-
organisms. Infections in infants fed with contaminated formula products
containing Salmonella spp. and other bacteria from the family Enterobacteri-
aceae have been reported. In some countries, teats contaminated with N-
nitrosamines can still be found. Table 11.2 lists the hazards, adverse health
effects and possible risk reduction strategies.

Infants receiving complementary food, and children

When infants reach the age of about 6 months, they should normally be
given complementary foods to meet their evolving nutrient requirements. With
the introduction of such foods, infants may be exposed to a range of contami-
nants. These include pathogenic microorganisms and their toxins, and various
chemical contaminants of foodstuffs, e.g. lead, mercury and pesticides. Diar-
rhoea is a leading cause of death in children under the age offive. In develop-
ing countries, diarrhoeal disease may be responsible for over 40% of all deaths
in children (24). Contaminated complementary foods account for a substantial
proportion of diarrhoeal illness among infants and young children (25). Such

144 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

o"
o
o
OJ Table 11.1 Foodborne hazards for the developing fetlls
o
'"
Z
Tn DISEASE/AGENT HAZARD RISK REDUCTION MEASURES
I
i(j Toxoplasmosis Women infected during pregnancy may transmit the • Avoid raw and undercooked meat.
}>-
(Toxoplasma gondii) infection to the fetus, possibly leading to stillbirth or • There is currently insufficient evidence to confirm that treating
'"
o
Vl birth defects, e.g. hearing or visual impairments, mothers who seroconvert during pregnancy can prevent fetal
o mental retardation. infection and improve infant outcomes (19).
:g"
listeriosis Women infected during pregnancy may transmit the Listeria is destroyed by cooking, but will grow at refrigeration temperatures.
n'"
--j

c (Listeria monocytogenes) infection to the fetus, possibly leading to spontaneous • Do not eat refrigerated pates, meat spreads, or cold meats.
);: abortion or infants born with visual, mental, or other • Do not drink unpasteurized milk or eat foods that contain unpasteurized milk.
'"
n problems. • Do not eat soft cheese or blue-vein cheese.
o The increased use of refrigeration to prolong the • Do not eat prepared or stored salads.
z
n • Do not eat refrigerated smoked seafood such as salmon, trout, tuna, or
Tn shelf-life of food has contributed to the emergence
'"
Z of L. monocytogenes as a food hazard. mackerel.
• Do not eat raw fish such as sashimi, sushi, ceviche, roe, mussels or oysters.
"o
• Do not eat refrigerated foods that are past their expiry dates.
'"
--j
I
Tn Heavy metals (lead, Heavy metals may cross the placenta resulting in Methylmercury:
oc-< mercury) exposure of the developing fetus. • Avoid consuming large amounts of fish that bioaccumulate methylmercury,
z These substances can be neurotoxic, result in such as large predatory fish.
Cl
reduced intelligence, and lead to behavioural Lead:
problems. • Avoid ceramic dishes and canned food with lead-soldered seams.
• Wash vegetables and fruit thoroughly.
• Avoid food produced or prepared near busy roads.

~
V1
~

~
0\

Table 11.1 continued

RISK REDUCTION MEASURES
DISEASE/AGENT HAZARD
Pregnant women should avoid foods that may contain high levels of POPs.
POPs may cross the placenta resulting in exposure
Persistent organic
pollutants
including dioxins and of the developing fetus. NOTE: It is important to reduce the use and emissions of POPs and to establish
polychlorinated biphenyls POPs may cause behavioural problems, hormone limits for food and animal feed.
disturbances, and cancer.
Vl
Fetal alcohol syndrome and other alcohol-related conditions can be prevented by
en Drinking of alcohol during pregnancy can cause birth avoiding alcohol use and food containing alcohol during pregnancy.
C1 Ethyl alcohol
defects and developmental disabilities. Children
o
z exposed to alcohol in the womb can suffer an array
of disorders, from subtle changes in intelligence to
Vl
""C
profound mental retardation. They may also suffer
en growth retardation and be born with birth defects.
Q
"T1
nm One of the most severe outcomes is letal alcohol
Z
syndrome (FAS), which includes three abnormalities
::; -disorder of the brain, growth retardation, and
Al
oZ facial malformation.
s:en
Z
:;!
r--
--I
I
Al
en
~
Vl
 Table 11.2 Faadbarne hazards far breastfed and battle-fed infants

DISEASE/AGENT HAZARD RISK REDUCTION MEASURES

:""'
."
0 Pathogenic Exposure to pathogenic organisms such as Salmonella spp., • Breast milk is the safest food for infants.
0 microorganisms E. coli 0157: H7, Campylobaeter jejuni, Staphylococcus aureus, • Select good quality infant formula (20).
0
OJ
0 Bacillus cereus, Clostridium perfringens, Shigella spp., Vibrio • Use safe or boiled water when preparing formula.
;0
z spp., Giardia lamblia, and foodborne viruses, resulting in • Do not store prepared formula.
m
gastroenteritis and associated illnesses. • Wash and boil bottles and teats after every feeding. If possible, use a cup
I
;p
N Such agents have high rates of morbidity and mortality, with instead.
;p • Wash hands after changing the baby, using the toilet, handling raw food or
;0 mortality directly due to dehydration and indirectly due to
0 touching animals.
Vl reduced resistance to disease.
0
."
• Follow safe food handling practices (see Table 11.3).
";p
;0 POPs Exposure of the infant can lead to behavioural problems, • Avoid excessive weight loss during breastfeeding.
-i
n including hormone disturbances, and cancer.
c dioxins and NOTE: It is important to reduce the use and emissions of POPs and to establish
):: Human breast milk may contain lipophilic POPs.
;0 PCBs limits for food and animal feed.
n
0
z Heavy metals Exposure of the infant to substances such as methylmercury Methylmercury:
n
m
;0
(lead, mercury) and lead. • Lactating mothers should avoid consuming large amounts of fish that
z bioaccumulate methylmercury, such as large predatory fish.
." Heavy metals can be neurotoxic, result in reduced intelligence,
0 and lead to behavioural problems. lead:
;0
-i • Lactating mothers should avoid ceramic dishes and canned food with
I
m lead-soldered seams.
-< • Wash vegetables and fruit thoroughly.
0
c • Avoid food produced or prepared near busy roads.
zC)
Infant botulism Ingested Clostridium botulinum spores may germinate, grow Children less than 12 months old should not be fed honey.
and produce toxin. Spores have been found in honey.

HIV Breast milk may be a vehicle for transmission of HIV. HIV-positive mothers should seek advice (21-23).

Methaemo- Ingestion of nitrate and nitrite by infants results in the Ensure well-water and water used to prepare breast-milk substitutes is low in
.j>.
'-J
globinaemia formation of methaemoglobin which reduces the oxygen- nitrate .
carrying capacity of blood.

POPs, Persistent organic pollutants: PCBs, polychlorinated biphenyls; HIV, human immunodeficiency virus.
foods may also expose infants to toxic chemical substances. Table 11-3 lists the
hazards, adverse health effects and possible risk reduction strategies.

Conclusions
Protecting the health of fetuses, infants, and young children requires vig-
ilance over the types of food consumed by pregnant mothers, special precau-
tions for bottle-fed infants, care in selection and preparation of complementary
foods, and supervision of food consumed by young children.
Pregnant women should avoid consumption of high-risk foods. Bottle-fed
infants should be provided with good quality breast-milk substitutes that have
been prepared and stored in a hygienic manner. Good hygienic practices are
essential in the preparation of complementary foods, and infants and children
should not be exposed to high-risk foods and ingredients.
Good hygienic practices should be employed in all food handling and prepa-
ration activities. Refrigeration is necessary for most foods, as food should not
be kept for more than two hours at room temperature. This is especially impor-
tant for meats, seafood, and dairy products. The food handler's hands, equip-
ment and preparation surfaces must be clean. All fruits and vegetables should
be thoroughly washed and the outer leaves of leafy vegetables should be
removed, especially if they are to be eaten raw. Cross-contamination must be
avoided, with ready-to-eat foods kept separate from raw foods. Finally, thorough
cooking, especially of meats, poultry, eggs and fish, is indispensable to avoid
food borne illness. Meats should have an internal temperature of at least 70°e.
This is especially important for minced meat products. Leftover foods and ready-
to-eat foods should be heated until they are steaming before being consumed.
As a simple guide for consumers, WHO's Five keys to safer food (27) should be
promoted.
It is important that food safety strategies focus upon improving knowledge
and effectively communicating with consumers, including mothers, about the
risks associated with specific foods and eating habits. Education to prevent
food borne illnesses should target pregnant and nursing mothers, as well as
doctors, public health nurses and nutritionists in health clinics. Children them-
selves might also be considered targets for food safety messages (28).

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 -n
o
o Table 11.3 Foodborne hazards for infants receiving complementary food, and children
o
(Xl
o DISEASE/AGENT
AJ
Z
HAZARD
rn RISK REDUCTlDN MEASURES (26)
I Pathogenic Exposure to pathogenic organisms such as Salmonella spp.,
»
N microorganisms • Cook all food thoroughly.
» E. coli 0157:H7, Campylobacter jejuni, Staphylococcus aureus,
AJ • Avoid storing cooked food.
o Bacillus cereus, Clostridium perfringens, Shigella spp., Vibrio
Vl
spp., Giardia lamblia, and foodborne viruses, resulting in • Avoid contact between raw foodstuffs and cooked foods.
o-n • Wash fruits and vegetables.
gastroenteritis and associated illnesses.
;g • Use safe water.
AJ
-1
Such agents have high rates of morbidity and mortality, with • Wash hands repeatedly.
n
C
mortality directly due to dehydration and indirectly due to • Protect food from insects, rodents and other animals.
'}:;: reduced resistance to disease. • Store non-perishable foodstuffs in a safe place.
AJ
n • Keep all food preparation premises meticulously clean.
o • Purchase food from reliable sources.
z
n • Practise good personal hygiene during food handling and preparation
rn
AJ
Z
activities.
-n
o • Do not eat or drink foods containing raw eggs, or raw unpasteurized milk
AJ and fruit juice.
-1
I
rn
• Avoid keeping food at room temperature for more than 2 hours.
• Ensure that persons with diarrhoea, especially children, wash their hands
d
C
after using the toilet.
Z
[)
Haemolytic Ingestion of E. coli 0157:H7 in food may lead to infection and
uraemic in severe cases to the development of haemolytic uraemic • Avoid eating salami, raw milk, and hard-to-clean vegetables, like sprouts
syndrome and lettuce .
syndrome in infants and young children.
• Cook all meat thoroughly.
• Practise good personal hygiene during food handling and preparation
activities.
• Drink only pasteurized fruit juice.
~
~
 -
V 'I
o

Table 11.3 continued

RISK REDUCTION MEASURES (26)
DISEASE/AGENT HAZARD
Select food likely to be low in these substances.
Exposure of infants and young children can lead to behavioural
POPs
including dioxins problems, hormone disturbances, and cancer.
and PCBs
Wash fruits and leafy vegetables, and peel other vegetables to avoid ingesting
Organophos- Neurotoxicity, with young children at risk because of high
consumption on body weight basis of certain foods. pesticides.
phorus pesticides
Exposure of infants and young children to substances such as Methylmercury:
Heavy metals • Avoid consuming large amounts of fish that bioaccumulate methylmercury,
(lead, mercury) methylmercury and lead. These substances can be neurotoxic,
such as large predatory fish.
V1
rn result in reduced intelligence, and lead to behavioural
Lead:
C4 problems. • Avoid ceramic dishes and canned food with lead-soldered seams.
6
z • Wash vegetables and fruit thoroughly.
• Avoid food produced or prepared near busy roads.
V1

"rnQ • Avoid eating bruised apples.

-n Patulin Mycotoxin found in apple juice. Codex limit of 50 ~g/kg of
• Avoid apple juice made from damaged or mouldy apples.
n apple juice is proposed.
rn
Z
:::; • Ensure well-water and water used in food contains low levels of nitrate.
;;0 Methylhaemo- Ingestion of nitrate and nitrite by infants results in the
o globinaemia formation of methaemoglobin which reduces the oxygen-
z
;;: carrying capacity of blood.
rn
Z
);! POPs. Persistent organic pollutants; PCBs, polychlorinated biphenyls.
r
-1
I
;;0
rn
~
V1
 References
1. World Declaration on Nutrition. A plan of action for nutrition adopted on 11 Decem-
ber 1992 by the International Conference on Nutrition. Rome, Geneva, Food and
Agriculture Organization of the United Nations and World Health Organization,
199 2 .
2. Kaferstein FK. Food safety: a commonly underestimated public health issue.
World Health Statistics Quarterly, 1997, 50 :3-4.
3· Mead Pet al. Food-related illness and death in the United States. Emerging Infec-
tious Diseases, 1999, 5:607-625.
4· Gilbert RE. Epidemiology of infection in pregnant women. In: Petersen E,
Amboise-Thomas P, eds. Congenital toxoplasmosis: scientific background, clinical
management and control. Paris, Springer-Verlag, 2000.
5· Evengard B et al. Low incidence of toxoplasma infection during pregnancy and
in newborns in Sweden. Epidemiology and Infection, 2001, 127:121-127.
6. Neto EC et al. High prevalence of congenital toxoplasmosis in Brazil estimated
in a 3 year prospective neonatal screening study. International Journal of
Epidemiology, 2000, 29:941-947.
7· Wallon M et al. Toxoplasma infections in early pregnancy: consequences and
management. Journal of Gynecology and Obstetrics and Biology of Reproduction,
2002,3 1:478-484.
8. Lipka B et al. Visual and auditory impairment in children with congenital
cytomegalovirus and Toxoplasma gondii infection. przegl Lek, 2002, 59(SuPPI.
1)70 -7 2.
9· Multistate outbreak of listeriosis-United States, 2000. Morbidity and Mortality
Weekly Report, 2000,49:1129-11 30 .
10. Wilhelmi I, Roman E, Sanchez-Fauquier A. Viruses causing gastroenteritis. Clin-
ical Microbiology and Infection, 2003, 9: 247-262.
11. Hamprecht K et al. Epidemiology of transmission of cytomegalovirus from
mother to preterm infant by breastfeeding. Lancet, 2001, 357:5 13-5 18 .
12. De Cock KM et al. Prevention of mother-to-child HIV transmission in resource-
poor countries-translating research into policy and practice. Journal of the
American Medical Association, 2000, 28 3: 11 75-11 82.
13· New data on the prevention of mother-to-child transmission of HIV and their
policy implications. WHO Technical Consultation on Behalf of the UNFPAj
UNICEFjWHOj UNAIDS Inter-Agency Task Team on Mother-to-Child
Transmission of HIY. Geneva, World Health Organization, 2001 (WHOjRHRj
01.28).
14· Stockholm Convention on Persistent Organic Pollutants. Nairobi, United Nations
Environment Programme, 2001 (www.pops.int).
15· Cooper RL, Kavlock RJ. Endocrine disrupters and reproductive development: a
weight-of-evidence overview. Journal of Endocrinology, 1999, 15 2 :159-166.
16. IPCS global assessment of the state-of the-science on endocrine disrupters. Geneva,
World Health Organization, 2002 (http://www.who.int/pcs/emerg_site/edc/
global_edcTOC.htm).

11. FOODBORNE HAZARDS OF PARTICULAR CONCERN FOR THE YOUNG

17. Safety evaluation of certain food additives and contaminants. Geneva, World Health
Organization, 2000 (WHO Food Additives Series No. 44)·
18. IPCS. Principles for evaluating health risks from chemicals during infancy and early
childhood: the need for a special approach. Geneva, World Health Organization,
19 86 (Environmental Health Criteria, No. 59)·
19. Peyron F et al. Treatments for toxoplasmosis in pregnancy (Cochrane review).
Oxford, Update Software, 2001 (The Cochrane Library, Issue 4)·
20. FAO/WHO. Codex Alimentarius. Codex Standard for Infant Formula. Rome,
FAO/WHO Codex Alimentarius Commission, 1997 (CX-STAN 07 2).
21. HIV and infant feeding. Guidelines for decision-makers. Geneva, World Health

Organization, 1998 (WHO/FRH/NUT/CHD/9 8 .1).

22. H IV and infant feeding. A guide for health care managers and supervisors. Geneva,
World Health Organization, 1998 (WHO/FRH/NUT/CHD/9 8 .2).
23. H IV and infant feeding. A review ofH IV transmission through breastfeeding. Geneva,
World Health Organization, 1998 (WHO/FRH/NUT/CHD/9 8 .3)·
24. Fikree F et al. Time to focus child survival programs on the newborn: assess-
ment of levels and causes of infant mortality in rural Pakistan. Bulletin of the
World Health Organization, 2002, 80:271- 277.
25. Motarjemi Y et al. Contaminated weaning food: a major risk factor for diarrhoea
and associated malnutrition. Bulletin of the World Health Organization, 1993,
71:79-9 2 .
26. Basic principles for the preparation of safe food for infants and young children.
Geneva, World Health Organization, 1996 (WHO/FNU/FOS/9 6 .6).
27. Five keys to safer food. Geneva, World Health Organization, 2001 (http://www.
who.i nt/fsf/Docu ments /5keys-1 D-eng. pdf).
28. Williams T et al. Food, environment and health: a guide for primary school teach-
ers. Geneva, World Health Organization, 199 0 .

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 CHAPTER 12

Poisonings and envenomings 1

I. Makalinao
Department of Pharmacology and Toxicology, University of
the Philippines, College of Medicine, Manila, Philippines

A. Woolf
Harvard Medical School and American Association of
Poison Control Centers, Boston, USA

POISONING
Overview
Poisonings extract an enormous toll worldwide, not only in terms of human
suffering and death, but also in terms of social and economic losses associated
with premature death, reduced human functioning, lost potential and produc-
tivity, and the costs of treatment. Exposures can be categorized according to the
circumstances: (i) acute, one-time events; (ii) subacute or time-limited expo-
sures; and (iii) chronic poisoning. While the chronic effects of toxicants such
as tobacco, nicotine, chemical inhalants, alcohol, and illegal drugs are major
public health concerns and often have their roots in childhood and early ado-
lescence, they are outside the scope of this chapter. Likewise suicide by poi-
soning, often with pharmaceuticals, is a serious phenomenon, and is especially
common among adolescent women in developed countries. However, such
exposure will not be addressed here.

Incidence and Significance

Poisonings and toxic exposures are among the most prevalent public health
problems affecting children in the world today. In 1990, there were 139 million
cases of poisoning, with about 242000 deaths (1). In 2001, it was estimated
that over 50000 deaths in children under 14 years were due to unintentional
poisoning (2). In Finland, more than 37000 calls are made to the national
poison centre annually, and 60% of the poisonings involve children under the
age of 6 (3)· In Viet Nam, over 9000 hospitalizations for poisoning were
recorded annually, with a mortality of B% (4). Agricultural poisonings from
organophosphorus compounds and paraquat are particularly problematic,
along with a new rodenticide, trifluoracetamide.ln the United States, 64 poison
centres reported more than 2.2 million poisonings in 2001, of which 9 2 . 2 %

'Reviewed by J. Pronczuk, Department for the Protection of the Human Environment, World
Health Organization, Geneva, Switzerland.

153
 occurred in a residence and 51.6% involved children younger than 6 years (5)·
There were 1074 fatalities reported by these same centres. In Sri Lanka, the
death rate from poisoning was found to be 43 per 1000 total deaths (6).
Poisonings are expensive, accounting for 1-5% of hospitalizations of chil-
dren in the USA (7). Miller estimated the lifetime losses related to poisonings
in the USA in 1992 alone at about US$ 50 billion, with US$ 3 billion in direct
medical spending (8).

Severity and vulnerable populations

Poisonings can be graded clinically on the basis of the duration (e.g.
minutes, hours, days, or years) and the dose, as well as the relative sensitivity
of the host to the toxicant's harmful effects. The potency of the toxic agent, in
terms of its inherent ability to cause cellular injury and the nature of its toxic-
ity, is also a determinant of the clinical importance of an exposure. The grada-
tion of exposure along these four axes has important clinical implications in
terms of the severity of the injury and the extent of likely disability.
Developmentally, children are most vulnerable to poisoning when they start
to walk and climb. At the same time, they exhibit pincer grasp and other intri-
cate finger and hand movements, and start to explore objects orally without the
cognitive ability to recognize which items are edible. As has been discussed
earlier, infants and young children also differ from older children, adolescents,
and adults in how they are exposed to toxicants and how they absorb, distrib-
ute, detoxify, and eliminate xenobiotics. Their diets are different, and so they
may be exposed to excessive amounts of certain toxicants in contaminated
foods. Their respiratory rate is faster
than that of adults, so that they are
exposed to higher quantities of
Pesticide exposure
inhaled toxicants.
Rural children in developing countries come into
There are also special paediatric
close contact with pesticides, playing in the
populations who are particularly vul-
family fields. Children help in the fields, live in
nerable to poisoning. The unborn
houses where pesticides are stored, and may be
more exposed to pesticides in inappropriate fetus is sensitive to any toxicants
containers, leading to accidental poisoning. that pass through the placenta, and
Thailand, a major user of pesticides, embarked to the direct teratogenic effects of
on an education programme in selected school radiation. Infants who are breast-
districts to improve awareness of the hazards of feeding may inadvertently receive
pesticides, their health effects and the symp- doses of harmful chemicals, such as
toms of poisonings (Case study 17, page 334). dioxin and some mycotoxins,
through breast milk.

Routes of exposure
Children can encounter toxic exposures in many different places. However,
over 9 0 % of early childhood poisonings reported to poison centres occur in the

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

154
child's home or in that of a grandparent or other carer. The home environment
often contains an assortment of medicines, cooking and heating fuels, auto-
mobile supplies, cleaning agents, paints, solvents, and chemicals useful in
everyday life. Often these are accessible to infants and young children, who may
poison themselves by swallowing a substance or spilling a caustic chemical on
their skin or in their eyes.
Many children in developing countries work full-time to help support their
families, and they may be exposed to chemical solvents, pesticides, heavy
metals, and other agents in the workplace (9). For example, children working in
the gold mining industry in Brazil or the Philippines risk significant mercury-
related neurotoxicity, as this metal is used in the gold extraction process.
Unsanitary drinking-water contaminated with infectious agents or natural or
man-made toxicants affects millions of children (see Chapter 8). The contami-
nation of wells used for drinking-water with arsenic in areas of West Bengal and
Bangladesh is a poisoning epidemic on an unprecedented scale, affecting an
estimated 20 million people in Bangladesh (10).

Disasters
Environmental disasters can cause poisoning epidemics, such as the explo-
sion in Bhopal, India, in 1984, which led to diisocyanide gas poisoning, or the
radiation exposure in Ukraine related to the 1986 Chernobyl nuclear reactor
disaster.

Epidemics
Epidemics from contaminated foodstuffs represent an important risk.
During May and June 1981, an outbreak of pulmonary and gastrointestinal
illness in Spain, affecting over 19828 people and causing 315 deaths, was traced
to an illegally marketed, rapeseed-based cooking oil (11). Gupta & Singh
reported periodic outbreaks of "epidemic dropsy" in New Delhi, India, from
ingestion of mustard oil contaminated by Argemone mexicana ("prickly poppy")
oil (12). Over 1726 people, including a disproportionately high number of chil-
dren, were stricken in 1998 with erythema, rashes, fever, vomiting, diarrhoea,
bilateral lower limb oedema and calf tenderness, hypotension, and occasional
heart failure and ocular involvement.
Poisoning epidemics have also been caused by locally formulated, unregu-
lated and impure medications. In 1995-1996, at least 109 Haitian children suf-
fered acute renal failure, and 85 died, from the use of locally formulated and
unregulated paracetamol adulterated with diethylene glycol (13).

Health effects
Drugs and chemicals may induce injury at the organ and cellular levels,
through idiosyncratic adverse reactions, an extension of their dose-response
pharmacology, direct or indirect toxic interactions at the cellular level with cor-

12. POISONINGS AND ENVENOMINGS 155

responding physiological perturbations, or additive or synergistic actions with
other toxic agents. Toxicants cause cellular injury through a variety of mecha-
nisms. They may interfere with energy production (e.g. cyanide, salicylates,
iron) or neurotransmission (e.g. botulin, tetrodotoxin), block receptors (e.g.
organophosphorus and carbamate pesticides) or subcellular channel function
(e.g. calcium channel blockers). They may interfere with essential membrane-
associated electrolyte pumps (e.g. digitalis), create protein adducts or other rad-
icals that injure cell membranes (e.g. paracetamol), promote oncological
transformation (e.g. benzene), or deplete cofactors essential to normal physi-
ology (e.g. isoniazid).
Toxicants tend to affect the gastrointestinal tract first, inducing nausea and
vomiting, often accompanied by intense abdominal pain. Some ingested
poisons (e.g. iron, castor bean, food borne toxicants) can produce haemorrhagic
diarrhoea. Severe poisonings affect the vital signs early. Cardiovascular changes
may include tachycardia and hypertension (e.g. amfetamines, cocaine), or
bradycardia and hypotension (e.g. beta blockers, calcium channel blockers).
Metabolic poisons, such as salicylates, iron, and cyanide, may initially increase
the respiratory rate and then produce respiratory arrest. Others, such as opiates,
barbiturates, gamma-hydroxybutyrate (G H B), and muscle relaxants, induce
coma and depress respiration early in the course of the poisoning. Seizures are
common soon after an overdose of neurotoxicants such as isoniazid, strych-
nine, camphor and bupropion. Some agents, notably paracetamol and Amanita
mushrooms, may take hours before producing signs of life-threatening toxicity.
Many environmental toxicants have multisystem effects. For example,
organophosphorus pesticides affect the gastrointestinal, neurological, cardio-
vascular, and pulmonary systems through cholinergic stimulation, producing
characteristic increased sweating, vomiting and diarrhoea, seizures, bradycar-
dia, lacrimation, salivation, bronchorrhoea and respiratory distress, and incon-
tinence. Such constellations of symptoms and signs reflect the physiological
perturbations typically produced by a particular class of toxic agents.

Management
Early medical care for the poisoned child can prevent complications, some
of which may be life-threatening. The four basic tenets in the treatment of the
poisoned child are described below.

• Supportive care. This includes resuscitation, administration of oxygen,

intravenous fluids, anticonvulsants, antiemetics, vasoactive drugs, and
other critical care measures .
• Decontamination. This involves removing the toxicant before it can be
absorbed or cause an injury. Thus, poison on the skin or in the eye should
be washed off. Victims of an inhalation poisoning should be removed
from the contaminated environment and given oxygen. Gastrointestinal

SECTION Iii: SPECIFIC ENVIRONMENTAL THREATS

 procedures (such as evacuating the stomach by lavage with an orogas-
tric tube or giving activated charcoal orally) may be important for the
patient who has swallowed poison if they can be performed early.
• Enhanced elimination. This includes advanced extracorporeal techniques,
such as haemodialysis or haemoperfusion, for selected poisonings. Alka-
linization of urine, in order to "trap" the ionized species of certain drugs
with an acidic pK (e.g. salicylates, methotrexate or phenobarbital), can
also enhance elimination. Repeated doses of oral charcoal every 2-4
hours can help eliminate certain drugs by enhancing their dialysis out of
the splanchnic blood back into the lumen of the gastrointestinal tract, or
by interfering with their enterohepatic circulation.
• Antidote administration. For a few toxicants, specific antidotes can block
their injurious effects or reverse physiological disturbances.

Antidotes
Antidotes work by a variety of mechanisms:

• adsorbing the toxicant before it can be absorbed into the body (e.g. acti-
vated charcoal);
• blocking the metabolism of a nontoxic compound to a more toxic
metabolite (e.g. use of ethanol or 4-methylpyrazole to block methanol or
ethylene glycol metabolism);
• chelating the toxicant out of the bloodstream (e.g. sodium calcium
edetate, dimercaptosuccinic acid for lead poisoning; deferoxamine for
iron poisoning);
• correcting the physiological perturbations induced by a poison (e.g.
atropine to treat the cholinergic effects of organophosphorus pesticide
poisoning);
• supplying a cofactor needed to correct physiological functioning or detox-
ify a drug or chemical (e.g. acetylcysteine for paracetamol poisoning; pyri-
doxine for isoniazid poisoning);
• reversing the toxic effects at the receptor site in affected organ systems
(e.g. flumazenil for benzodiazepine poisoning; naloxone for opiate poi-
soning; pralidoxime for organophosphorus poisoning);
• treating the toxic effects directly (e.g. diphenhydramine for the syndrome
of dystonia associated with acute neuroleptic poisoning).

Data sources
Public health authorities need to understand local and regional variations in
the causes of poisonings and toxic exposures in order to formulate regulations
and other measures that meet local and regional priorities (14). Information
about morbidity and mortality from toxic exposures, including the numbers of
hospitalizations and deaths due to poisonings, emergency department and out-

12. POISONINGS AND ENVENOMINGS 157

patient visits, and telephone calls to poison centres, might be found in reg-
istries_ Information about toxicants and their effects is available on several
web sites (e.g. www.inchem.org).

Poisoning prevention
Both active and passive prevention measures can limit injuries from toxic
exposures among children. One-time childhood poisonings can be reduced
through the use of child-resistant packaging for both drugs and chemicals, and
by preferring nontoxic chemicals for household use. Discouraging the use of
more toxic drugs, such as propoxyphene, harmful commercial products, such
as thallium-containing rodenticides, and dangerous agricultural products, such
as paraquat, will also reduce the incidence of childhood poisoning.
Poison control centres are a key resource for preventing poisoning in many
parts of the world. In some countries, advice from poison centres is accessible
only to health care professionals; in others, the poison centre is accessible to
the general public, and provides advice on both medically serious and trivial
toxic exposures. Poison centres offer professional medical advice and triage
designed to treat and limit the injurious effects of poisoning. They can also serve
as a lead agency in public education outreach campaigns directed either to the
entire population or to vulnerable groups.
Active poisoning prevention measures include education of the public in
order to change their lifestyles and behaviour. The home should be made a safe
environment for children, ideally with a "safe area", as well as constant vigilance
and close supervision by carers. The "four Rs" of poisoning prevention are
important for parents of young children:

• Recognize what chemicals, cleaners, plants, drugs, and other products

represent a poisoning hazard and are present in the household.
• Remove poisonous products from the reach of children by throwing them
away or locking them in high cabinets.
• Be ready should a poisoning event occur. This may include having the
telephone number of the local poison centre on hand and knowing first
aid for different types of toxic exposure.
• Respond appropriately to a poisoning event. This includes the basic tenets
of first aid: washing the skin in the case of a dermal exposure, flushing
the eyes under a stream of running water in the case of an ocular expo-
sure, or getting the patient safely to fresh air in the case of a toxic inhala-
tion. Where local poison centres exist, calling for information and help
can be a crucial aspect of first aid.

Public health programmes

Poisoning prevention also entails disaster preparedness at local, regional,
and national levels. Releases of hazardous chemicals from factories or during

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

transport or fires can lead to a disaster. Public health agencies must develop
comprehensive plans that address the multiple possible environmental toxic
exposures at a programme level. Recently Carlson & Tamburlini outlined a
rationale and guiding principles for the development of national policies on chil-
dren's environmental health, which included various types of poisoning (e.g.
lead, tobacco, pesticides) as priority health outcome and exposure indicators
(14)·

Regulatory measures
Many countries have yet to enact regulatory measures to safeguard children
from toxic exposures and poisonings. Recently the Bangkok Statement (see
Chapter 1) endorsed recommendations for poisoning prevention to include a
ban on leaded petrol and increased use of child-resistant packaging. The ban
on leaded petrol should be extended to all countries. The requirement that drugs
be packaged in child-resistant containers and that kerosene and other fuels be
kept in childproof bottles (with special taps) are measures with proven effec-
tiveness in preventing poisoning. Restrictions on child labour, regulating the
age of eligibility, types of occupations, and hours per week will also help protect
children from workplace-associated toxicants.

Specific toxicants
Paracetamo/
Paracetamol is a popular, nonprescription medication taken for the relief of
pain or treatment of fever. The toxic one-time dose is 150 mg/kg of body weight
in children or 7.5 g in adolescents. High-risk groups vulnerable to the hepato-
toxic effects of paracetamol include alcohol-dependent people, suicidal adoles-
cents, and pregnant women and their unborn children.
When taken in overdose, the normal hepatic conjugation pathways for
the detoxification of paracetamol become saturated. Excess paracetamol is
processed via P450 oxidative degradation to a reactive intermediate compound,
N-acetylbenzoquinonimine (NAMBQI). In paracetamol poisoning, the cofactor
glutathione required to detoxify NAMBQI is quickly exhausted. Without enough
glutathione to detoxify it, NAM BQI destroys hepatocytes.
Patients may not show symptoms of toxicity for the first 12 hours or so, then
complain of nausea, vomiting, and abdominal pain. Hepatitis supervenes within
24-36 hours post-ingestion and peaks at 72-96 hours, progressing to fulminant
hepatic necrosis in severe poisoning. Complications include hepatorenal failure,
acidosis, encephalopathy with cerebral oedema, severe coagulopathy, and
death.
Clinical severity can be gauged using the Rumack-Mathews nomogram, in
which the plasma paracetamol level is plotted against time post-ingestion to
predict hepatitis. For example, a plasma paracetamol concentration of 150
/lg/ml or more at 4 hours post-ingestion suggests a possible risk of hepatitis,

12. POISONINGS AND ENVENOMINGS 159

whereas a level of 200~g/ml or more at 4 hours warns of probable hepatitis.
Other relevant blood tests include liver and renal function tests and, in severe
cases, measures of coagulation. The patient's neurological status should be
carefully assessed periodically over the course of the hospitalization.
Treatment of paracetamol poisoning is directed towards preventing the
drug's absorption using oral activated charcoal. The antidote is acetylcysteine,
which supplies more than enough glutathione and sulfur to detoxify
paracetamol.

Carbon monoxide
Carbon monoxide is a colourless, odourless gas emitted as a product of
combustion. Sources include furnaces, hot water heaters, propane or gasoline
space heaters, barbecues, fireplaces, wood stoves, and gas dryers. In many
countries, especially in rural areas, the use of charcoal in domestic heating
devices is common, exposing inhabitants to carbon monoxide poisoning.
House fires produce high concentrations of carbon monoxide and other toxic
gases. Methylene chloride, found in chemical paint strippers, absorbed by
inhalation or dermal absorption, is metabolized endogenously to carbon
monoxide. The pregnant woman and her unborn child are particularly suscep-
tible to the toxic effects of carbon monoxide exposure.
Carbon monoxide interferes with cytochrome oxidase function and disrupts
cellular respiration. The gas also binds to haemoglobin and myoglobin; normal
oxygen unloading cannot occur, causing hypoxic injury at the cellular level. The
half-life of carbon monoxide in the blood is 4-6 hours in room air, 90 minutes
in 100% oxygen, and 20 minutes in hyperbaric oxygen.
Symptoms of carbon monoxide poisoning are similar to, and may be con-
fused with, those of influenza. Patients with mild poisoning may have poor
appetite, confusion, lethargy, muscular aches, nausea, vomiting and headache.
In patients with severe poisoning there may be confusion, seizures and coma.
Delayed symptoms (2-3 weeks after exposure) include confusion, poor memory,
behavioural changes, irritability, poor concentration, focal neurological findings,
weakness, and myoclonus.
Carboxyhaemoglobin levels in blood are often above 15-20% in the poisoned
patient. Levels above 60% are usually lethal. However, a history of the dose and
duration of exposure ("carbon monoxide soaking") is more often prognostic of
outcome than the blood carboxyhaemoglobin level. Psychometric testing of
patients with carbon monoxide poisoning reveals deficits in speech, orientation,
and memory, many of which persist as sequelae.
Patients suffering from carbon monoxide poisoning should be moved to
fresh air as soon as possible, and receive 100% oxygen. Hyperbaric oxygen
therapy has also been found to be effective.

160 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Caustic agents
Caustic household products include drain-clearing agents, toilet bowl and
oven cleaners, and chrome and metal cleaners. Cement cleaners and rust
removers may contain hydrofluoric acid, an extremely potent acid that can also
cause systemic hypocalcaemia, even after dermal exposure.
The alkaline corrosives stick to oesophageal tissues producing transmural
liquefaction necrosis, a saponification of available tissue fats and proteins.
ingestion of acid produces a more superficial chemical burn, with eschar for-
mation and a coagulative necrotic lesion, that can extend through the oesoph-
agus and into the stomach.
Patients may be remarkably symptom-free, even after a significant exposure
to alkali. initial symptoms of caustic poisoning include crying, hypersalivation,
drooling, and swollen red lips and gums. Young children may refuse to feed;
older children may complain of throat pain and significant dysphagia. Reddish
or pale areas of burning may be visible around the mouth or on the lips, tongue,
oropharyngeal surfaces or palate. Splash burns may be evident elsewhere on
the skin or in the eyes. Respiratory symptoms, including wheezing and hypoxia,
indicate aspiration of the product.
Determination of the pH of the affected tissues or the suspect product can
confirm a caustic exposure. A chest radiograph in the patient with respiratory
symptoms may show free air in tissues or a pneumomediastinum or pneu-
mothorax. Arterial blood gas analysiS often reveals a respiratory acidosis and
hypoxaemia if the patient has aspirated caustic material into the lungs, or a
metabolic acidosis after significant acid absorption.
Patients suffering from caustic poisoning should be given nothing by mouth;
vomiting should be avoided and ipecacuanha should not be given. "Neutral-
ization" (e.g. giving vinegar to counteract an alkali) exacerbates injury and is
normally contraindicated. To treat patients who have swallowed a large amount
of strong mineral acid, carefully instil saline into the patient's stomach using a
nasogastric tube. Endoscopy of the upper gastrointestinal tract should be per-
formed 6-24 hours after ingestion. For severely burned patients, steroids can
be given to limit in-migration of inflammatory cells and reduce the risk of later
stricture formation. Some patients may require a period of total parenteral nutri-
tion, or feeding through a gastrostomy until the oesophagus heals. Parenteral
anti reflux drugs are adjunctive therapy. Antibiotics may be necessary to treat
subsequent bacterial oesophagitis or gastritis. Surgical revision or colonic inter-
position may be necessary later.

Cyanide
Cyanide is found in jewellery polish, plants (cassava, apricot pits). medica-
tions such as sodium nitroprusside, smoke from some house fires, and nitriles
used in industry. it is used as an intermediate in the manufacture of paper, tex-
tiles, and plastics, in electroplating, and in extracting gold from ore.

12. POISONINGS AND ENVENOMINGS

 The cyanide (CN) molecule is a potent direct vasodilator, and disrupts mito-
chondrial cytochrome oxidase, interfering with cellular oxidative metabolism.
CN is metabolized by the enzyme rhodanase in the liver to the less toxic metabo-
lite, thiocyanate (SCN), which is freely excreted in the urine.
Sometimes a person who has swallowed cyanide has a premonitory "feeling
of dread", with an odour of bitter almonds. Nausea, vomiting, confusion,
lethargy, and tachycardia are early manifestations of poisoning. These qUickly
progress to coma and shock; seizures and metabolic acidosis may intervene at
any time. Death is from respiratory failure and cardiac arrest.
Levels of CN in serum and red blood cells are elevated in the poisoned
patient. Arterial blood gases show a profound metabolic acidosis, or a mixed
acidosis in patients who are in respiratory failure. The whole blood lactate level
is elevated.
Management of the poisoned patient includes supportive measures, such
as administration of oxygen and dextrose-containing intravenous fluids. Anti-
convulsants may also be necessary.
In many countries, hydroxocobalamin or other cobalt-containing antidotes
are available. An alternative treatment involves three phases: (i) inhalation of
amyl nitrite pearls induces a 3-5% methaemoglobinaemia, which with free blood
CN forms cyanomethaemoglobinaemia; (ii) intravenous administration of
sodium nitrite induces 25-30% methaemoglobinaemia, which can capture
larger amounts of free CN; (iii) intravenous administration of sodium thiosul-
fate, which reacts with cyanomethaemoglobin to form thiocyanate ion, which is
less toxic and is excreted by the kidneys.

Ethylene glycol
Ethylene glycol is present in automobile antifreeze and refrigerants,
and is used as a common commercial solvent and in photographic develop-
ing. It is sweet-tasting and can be attractive to young children. Diethylene
glycol, a similar substance, has sometimes been used as a solvent in the
preparation of counterfeit medicines, causing the death of a large number of
children.
The parent compound is metabolized by hepatic alcohol dehydrogenase to
the more toxic glycoaldehyde, glycolic acid, glyoxalic acid, and oxalate deriva-
tives. All of these are capable of causing direct injury to cell membranes.
Oxalates combine with available calcium to produce symptomatic hypocal-
caemia. Calcium oxalate crystals precipitate in the neurons or in renal tubules,
exacerbating cellular injury.
Patients who swallow ethylene glycol may initially appear inebriated, with
ataxia and confusion. Coma and seizures also occur. A severe metabolic acido-
sis evolves over hours and may be accompanied by congestive heart failure,
hypotension, hypocalcaemic tetany and subsequently acute oliguric renal
failure.

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Ethylene glycol blood concentrations are rarely available; however blood
osmolality shows a gap between measured and calculated values. A urinalysis
shows an active urinary sediment and calcium oxalate crystals. Hypocalcaemia
and abnormal renal function tests are also often present.
Management includes supportive care and intravenous fluids. An enzyme-
blocking antidote such as ethanol or 4-methylpyrazole is indicated for ethylene
glycol blood levels of 20 mg/dl or above. Haemodialysis is reserved for patients
with confirmed exposure, who manifest worsening acidaemia or blood ethylene
glycol concentrations above 50 mg/di.

Herbal medicines and dietary supplements

Herbal preparations contain numerous different chemicals and substances.
Dietary supplements frequently contain vitamins, amino acids, ephedrine, caf-
feine, or hormones. Contaminants and adulterants may be present if quality
control is poor. Chinese patent medicines and Ayurvedic remedies may be con-
taminated by heavy metals, such as arsenic or lead, or contain pharmaceuticals
(e.g. corticosteroids). Some remedies, especially Asian patent medicines, may
contain aconite, a cardiotoxin capable of producing severe bradyarrhythmias, or
drugs such as phenylbutazone, a nonsteroidal anti-inflammatory agent capable
of causing aplastic anaemia. Homeopathic medicines are usually highly diluted
and thus pose little medical risk.
Different herbs may have toxicity for specific organ systems. For example
"chaparral", "germander" andjin bu huan, are all hepatotoxic. Pyrrolizidine alka-
loid-containing teas (e.g. comfrey, symphytum, heliotrope) are capable of
causing hepatic venous occlusion (Budd-Chiari syndrome).
Signs of poisoning vary according to the herb or dietary supplement
ingested. Agents containing ephedrine or caffeine may cause nausea and diar-
rhoea, tremulousness, anxiety, tachycardia and hypertension.
The identification of ingredients is key to the successful management of
toxic reactions to herbal products and dietary supplements. Consulting a poison
control centre or Internet site can be helpful. Treatment of inadvertent poison-
ing might include activated charcoal and supportive measures, depending on
the nature of the toxicants.

Hydrocarbons
Many household products used as fuels, cleaners, and solvents contain
hydrocarbons such as kerosene, gasoline, turpentine, or mineral spirits. Hydro-
carbons that have low viscosity and high volatility are most easily aspirated into
the lungs. Hydrocarbons are usually absorbed in large amounts by inhalation,
because of high vapour pressures, or via dermal absorption, because of their
lipid solubility and solvent properties.
Hydrocarbon-containing products can cause life-threatening chemical pneu-
monitis if inhaled, either accidentally or deliberately. They are often toxic to the

12. POISONINGS AND ENVENOMINGS

nervous system, causing inebriation, slurred speech, ataxia, and coma. Young
solvent abusers who inhale hydrocarbons may suffer "solvent encephalopathy",
a chronic syndrome of behavioural changes (garrulousness, aggression),
seizures, poor memory, slowed cognition, motor changes, and dementia.
"Sudden sniffing death" may occur as a result of lethal arrhythmia caused by a
rise in blood catecholamines after the acute inhalation of highly concentrated
hydrocarbon-containing solvents (e.g. toluene).
Pulmonary symptoms and signs of hydrocarbon poisoning include tachyp-
noea, cough, wheezing, and cyanosis. Children who vomit after ingesting a
hydrocarbon-containing product have an increased risk of aspiration. Life-
threatening complications, including chemical pneumonia, hypoxaemia, adult-
type respiratory distress syndrome, and respiratory failure can develop in severe
poisoning.
Specific hydrocarbons may also have intrinsic, extrapulmonary toxicity.
Benzene exposures are linked to the development of aplastic anaemia and later
leukaemia. Toluene can cause tubular necrosis and renal failure. Carbon tetra-
chloride poisoning causes an irreversible hepatic necrosis. Methylene chloride
(paint stripper) is converted in the liver to carbon monoxide and may produce
the typical symptomatology of carbon monoxide poisoning.
Blood assays for hydrocarbons are not usually available. A chest radiograph
should be obtained at presentation, if the child has respiratory symptoms, or
between 4 and 6 hours post-ingestion if the child is not initially symptomatic.
The blood count often demonstrates leukocytosis, even without bacterial infec-
tion. Monitoring of blood gases and neurological and pulmonary function is
important for severely poisoned children. Monitoring of blood counts (e.g. in
benzene poisoning), renal function (e.g. in toluene poisoning), carboxyhaemo-
globin (in methylene chloride poisoning), or liver function (e.g. in carbon tetra-
chloride poisoning) may be necessary in selected cases.
The treatment of children with hydrocarbon poisoning includes oxygen
administration and, if necessary, mechanical ventilation. Steroids and bron-
chodilators are not effective, unless the patient has significant bronchospasm.
Bacterial secondary infection is a common complication 48-72 hours after the
onset of symptoms and may require the use of antibiotics.

Iron
Multivitamins and iron supplements intended for pregnant women and
adults are highly toxic to children (and attractive, as they may be colourful and
sweet). The toxic dose of free iron is 40 mgjkg of body weight (155 mg of ferrous
fumarate = 65 mg of free iron; 30 mg of ferrous sulfate = 6 mg of free iron). Chil-
dren's multivitamins with iron do not contain, in general, enough iron to pose
a risk of toxicity.
Free iron acts as an oxidizing agent and a mitochondrial poison, interfering
with electron transport because of its reduction-oxidation potential. The cell

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

reverts to anaerobic metabolism, generating organic acids. I ron also causes
injury and corrosion to the gastrointestinal mucosal lining. Free iron destroys
hepatic cells, with unloading of glucose and the release of histamine, bradykinin,
and other vasoactive substances, which contribute to vascular injury and the
development of shock.
Early signs of severe iron poisoning include nausea, vomiting, diarrhoea,
and haemorrhagic gastritis. Hypotension, shock, confusion, lethargy, and coma
may develop early in the course of severe poisoning. Metabolic acidosis is
evident, along with an initial hyperglycaemia, giving way to hypoglycaemia later.
Severe hepatitis evolves within 24-48 hours of ingestion. Complications of
severe iron poisoning include hepatorenal syndrome, coagulopathy, bleeding,
and encephalopathy. Septicaemia with unusual organisms, such as Yersinia ente-
rocolitica or Listeria monocytogenes, sometimes develops on the third or fourth
day after poisoning. Late sequelae in survivors include cirrhosis or gastric
strictures.
Measurement of blood iron concentrations can help gauge the clinical sever-
ity of poisoning, and is best done 4 hours after ingestion. Levels greater than
500/lgjdl are associated with toxicity; those greater than 1000/lgjdl are life-
threatening. Unabsorbed iron pills may be radio-opaque in abdominal radio-
graphs. Serial blood counts, glucose, liver function, and coagulation tests are
all helpful in monitoring a patient's condition.
Activated charcoal should not be given as it does not adsorb heavy metals.
Ipecacuanha given orally with water produces vomiting within 20 minutes. Large
numbers of iron pills in the gut can also be evacuated with whole bowel irriga-
tion using polyethylene glycol. Coagulation defects in life-threatening cases may
require supportive measures, such as vitamin K or fresh frozen plasma. Defer-
oxamine is an antidote for iron poisoning. When given intravenously it chelates
free iron in blood to produce a soluble non-toxic product, ferrioxamine, which
is excreted in the urine, giving it a pinkish hue (vin rose urine).

Lead
Lead is highly toxic to children. Both acute and chronic poisoning result from
exposure to different sources of lead.
Children are vulnerable to lead in painted and plastered surfaces in homes
and other buildings. Lead in dust or outdoor soil may be ingested by young chil-
dren through their hand-to-mouth activities. Lead in petrol is released in auto-
mobile exhaust and may be inhaled. Lead can also contaminate water supplies,
canned foods, traditional medicines, cosmetics and other household products.
Lead interferes with haem synthesis and other enzyme-mediated systems,
and with the normal neuronal arborealization and synaptogenesis during the
development of the central nervous system. It also affects bone metabolism and
causes renal injury and hypertension. The absorption of lead is increased in chil-
dren with iron and calcium deficiency.

12. POISONINGS AND ENVENOMINGS

 Lead poisoning is usually defined as a blood lead level of 10 I-lgjd I or higher.
However, there is growing concern about neurodevelopmental effects resulting
from exposures where the blood lead levels are below lOl-lgjdl. Early signs of
poisoning include a microcytic anaemia, with basophilic stippling and elevated
red blood cell porphyrin levels. Neurobehavioural problems caused by
plumbism in children include poor appetite and irritability, with hyperactivity
and an inability to focus.
Neurodevelopmental delays and learning problems are common in lead-
poisoned children, especially in relation to speech acquisition, visual-motor
integration, and higher-order cognitive functions. In severe lead poisoning,
encephalopathy may occur as well as complications, such as peripheral neu-
ropathies, cerebral oedema, and deafness. Blood lead levels of 70 I-lgjdl and
above are associated with life-threatening sequelae related to cerebral oedema
and lead encephalopathy.
An abdominal radiograph may be positive if the child has recently eaten
plaster or paint chips containing lead; bone films may demonstrate metaphy-
seal "lead" lines in chronic poisoning. Children tend to suffer abdominal colicky
pain.
A singularly important aspect in the prevention of childhood lead poisoning
is the abandonment of lead-containing petrol by countries around the world.
Another important measure is the reduction of the lead hazard in the home,
day-care centre, and other environments where children spend appreciable
amounts oftime. Children's hand-to-mouth behaviour should be monitored and
pica should be discouraged. Measures such as frequent hand-washing, damp
mopping of floors, and dusting can cut down on lead-containing interior dust.
Water, old lacquer or paint on cribs and furniture, imported ceramics, pots and
pans, herbal remedies, and cosmetics can be unexpected sources of lead. A diet
containing high levels of iron and calcium can reduce absorption of lead by
children.
Children who have been poisoned by lead can be treated with chelating med-
ications including meso-2,3-dimercaptosuccinic acid, sodium calcium edetate,
and dimercaprol (15).

Methanol
Methanol, present in some paint thinners and de-icing compounds, is still
found in some household products. As little as 1 tablespoon of methanol can
cause life-threatening symptoms in a young child.
Methanol is metabolized by hepatic alcohol dehydrogenase to formaldehyde
and formate. These compounds injure cells in the brain and the eyes. Clinical
findings of poisoning include severe metabolic acidosis with a high anion gap.
Patients may complain of spots before their eyes, "snow" vision, blurring, and
a narrowed visual field. Central nervous system effects include inebriation, con-
fusion, ataxia, slurred speech, coma, seizures, and amblyopia.

166 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Laboratory findings include a high anion metabolic acidosis. In methanol
poisoning there is an osmolar gap between the measured and the calculated
serum osmolality. Blood methanol levels over 20 mgjdl confirm the diagnosis.
Measurement of blood methanol can be used to gauge the patient's prognosis.
Alcohol dehydrogenase blockers, including ethanol or 4-methylpyrazole, are
effective antidotes for methanol poisoning. Haemodialysis is necessary for
patients with blood methanol levels of 50 mgjdl or higher and for those with
confirmed exposure history and severe acidaemia.

Mushrooms
Only a few species of fungi are poisonous. Small children may eat mush-
rooms while playing and exploring, and occasionally severe poisoning may
occur. The most common circumstance leading to serious toxicity is the inges-
tion of misidentified fungi as food. In the majority of cases, the ingestion of
non-edible mushrooms produces mild gastrointestinal effects. However, some
species are highly toxic. Amanita phalloides is one of the most toxic species: its
amatoxins produce liver, kidney, pancreatic and gastrointestinal effects, and poi-
soning may be lethal.
Amanita muscaria-the typical red and white, colourful and attractive mush-
room-produces very mild and self-limiting gastrointestinal and hallucinogenic
effects. Mushrooms of the genus Cortinarius are nephrotoxic and may cause
renal failure. In case of suspected or known mushroom ingestion, health per-
sonnel should keep the patient under clinical observation and contact an orga-
nization that can assist in the identification of the mushroom (e.g. botanical
garden, university, or poisons centre). Specific treatment is required in case of
poisonous mushroom ingestion and a poisons centre should be consulted.

Plants
Poisoning by plants is very common in children, but the large majority of
such exposures are medically trivial. With few exceptions, once the plant has
been identified, parents whose child has swallowed a few leaves or berries can
be given simple reassurance.
Many plant compounds, such as terpenes, alkaloids, phytotoxicants,
saponins, and cardiac glycosides, have pharmacological properties and may be
toxic .

• Solanines (Jerusalem cherry (Solanum pseudocapsicum); nightshade

family) cause gastrointestinal complaints, shock, and convulsions .
• Abrin: The rosary pea (Abrus precatorius) contains a phytotoxin, abrin,
which causes vomiting, tremors, delirium, shock and uraemia. Even 1 or
2 ingested castor beans (Ricinus communis) can result in a life-threaten-

ing episode of nausea, vomiting, diarrhoea, haemolysis, renal failure, and

dehydration in a child.

12. POISONINGS AND ENVENOMINGS

 • Oxalate: Oxalate-containing plants (Jack-in-the-pulpit, philodendron, dief-
fenbachia) cause mouth and throat pain, swelling, and dysphagia.
• Aconitine: Grayanotoxicants (andromeda, azalea) and aconitine (monks-
hood (Aconitum napel/us)) cause bradyarrhythmias.
• Glycosides: The foxglove (Digitalis purpurea). oleander (Nerium oleander)
and yellow oleander (Thevetia peruviana) contain cardiac glycosides that
cause dysrhythmias, hypotension, hyperkalaemia, and coma.
• Scopolamine: Datura stramonium (Jimsonweed) causes an anticholinergic
syndrome with hallucinations.
• Holly berries (I/ex spp.) produce severe vomiting and diarrhoea. Poke-
weed (Phytolacca americana) can produce gastrointestinal cramps, visual
disturbances, diarrhoea, weakness, and subsequent death.
• Water hemlock (Cicuta maculata) is known to contain a neurotoxin
capable of producing lethal seizures, while poison hemlock (Conium mac-
ulatum) is an autonomic nervous system depressant, causing coma and
respiratory arrest.

Decontamination of the patient may be necessary if a poisoning involves a

highly toxic plant. Ipecacuanha may be useful where the plants, berries or mush-
rooms are known to be highly toxic and vomiting can be induced within 20-30
minutes of ingestion. Activated charcoal can also be a useful adsorbant of tox-
icants in plants, if administered orally in a timely fashion.
Prevention of plant poisoning requires vigilance by parents of young chil-
dren. Parents should survey their land, removing any toxic mushrooms or toxic
plants such as poison ivy or deadly nightshade. Indoor plants should be kept
well out of reach and should be nontoxic. Parents of young children should
check with their poison control centre for identification of suspect plants or for
advice about which ornamental plants are safe.

Salicy/ales
Salicylate poisoning may occur in young children who ingest the pharma-
ceutical, especially when it resembles a sweet. However, the incidence of expo-
sure seems to have decreased. Children can also be poisoned by ingesting
ointments and liniments that contain methylsalicylate.
At the cellular level, salicylates uncouple oxidative phosphorylation. The cell
converts to anaerobic metabolism, utilizing fat and other substrates and pro-
ducing free fatty acids and lactate. This results in a high anion gap metabolic
acidosis. Salicylates are also irritants, and can be potentially corrosive to gas-
trointestinal mucosa. Antiplatelet actions of salicylates are such that the patient
can develop a bleeding diathesis. Salicylates also stimulate the central respira-
tory centre in the hypothalamus, which accounts for a primary respiratory alka-
losis often seen early in poisoning. Salicylate poisoning also causes imbalances
of both fluids and electrolytes. Electrolytes cross membranes to buffer acid-base

168 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 abnormalities, resulting in total body deficits of potassium, calcium, and mag-
nesium. Intracellular ionic shifts and fluid losses can cause severe dehydration.
Occasionally a syndrome of inappropriate release of antidiuretic hormone is
seen in salicylate poisoning, causing fluid to move into the interstitial spaces
and metabolic derangements.
Classic findings in acute salicylism include hyperventilation, diaphoresis, tin-
nitus and acid-base disturbances. Other symptoms and signs of poisoning are
nausea, vomiting, abdominal pain, fever, haemorrhagic gastritis, respiratory
alkalosis, deep, rapid (Kussmaul-type) respirations, metabolic acidosis, hepati-
tis, confusion, lethargy, coma and seizures.
Blood analysis may reveal hypernatraemia, hypochloraemia, hypokalaemia
and hypocalcaemia. Arterial blood gases often reveal an acidosis with a base
deficit. Hyperglycaemia is evident early, hypoglycaemia later. Elevated ammonia
levels, abnormal liver function tests and laboratory evidence of coagulopathy
are seen in life-threatening salicylism. Blood salicylate levels can suggest the
severity of toxicity: 30 to 60 mgjdl indicates mild to moderate toxicity; 60 to
100 mgjdl reflects severe poisoning; and levels above 100 mgjdl are life-
threatening.
Repeated doses of activated charcoal every 3-4 hours may help prevent the
absorption of salicylate and enhance its elimination. The alkalinization of urine
to a pH oh·S-8.0 enhances elimination because of the low pK of the drug. The
ionized form predominates, is "trapped" in renal tubules, and then excreted in
urine. Haemodialysis should be considered forthe salicylate-poisoned child who
develops any of the following:

• noncardiogenic pulmonary oedema;

• cerebral oedema;
• worsening coma despite decontamination;
• severe metabolic derangements;
• acute renal failure;
• seizures;
• a salicylate blood concentration of 80-100 mgjdl after a one-time over-
dose;
• a salicylate blood level above 60mgjdl in a patient who is taking aspirin
regularly.

ENVENOMING
Venomous animals deliver a poison from a highly developed secretory gland
through a bite or sting. The venom is important for their survival, as they use
it for defence, overcoming prey, and digesting food. Venomous animals can be
found in all types of habitat. They may be found close to where children live,
learn and play, particularly-but not exclusively-in rural areas. Although

12. POISONINGS AND ENVENOMINGS 169

venomous species exist in all parts of the world, children living in tropical
countries may have a greater chance of being exposed to venomous bites and
stings.
Children may be exposed to a number of venomous creatures. While at
home or in areas where they play, they may be bitten by snakes, spiders, cen-
tipedes, or millipedes, or stung by scorpions, bees or wasps. At the beach, chil-
dren may be exposed to envenomation from cone shells, stinging fish, stonefish,
jellyfish, sea stars and sea urchins. The American Association of Poison Control
Centers (AAPCC) in 2002 (16) reported that 1305 of the 15687 scorpion stings
in the USA were in children less than 6 years old. Other exposures in this age
group were to centipedes and millipedes (315 out 2051), bees, wasps and
hornets (2494 out of 12632), coelenterates (116 out of1329) and fish (33 out of
1389) (16).
Treatment and details of specific types of envenomation will not be dis-
cussed here. In case of a bite or sting, the appropriate health care facility should
be consulted (e.g. a poisons control centre); in some countries, an experienced
toxicologist may be contacted for advice. Life-threatening envenomation in chil-
dren may warrant admission to an intensive care unit and the administration
of specific antivenin.
Diagnosis of envenomation may pose a unique challenge to the health care
provider, especially when there were no witnesses to the exposure and the child
is not old enough to give an accurate account of it. Patients may present with
nonspecific symptoms. For instance, incessant crying in children may be one of
the initial signs of a scorpion sting, even before the actual lesion becomes man-
ifest. It is important to consider the possibility of envenoming in cases of unex-
plained collapse, convulsions, bleeding or coagulopathy, paralysis, myolysis,
renal failure, local tissue injury, pain, increased salivation, lacrimation and
sweating.
The unique vulnerability of children may increase the potential for any given
exposure to be life-threatening. Some case reports suggest that the smaller
volume of children may predispose them to a higher morbidity than the adults
(4, 5, 8, 11). However, the existing grading scores for severity of snakebite are
mostly based on adult data. Various gUidelines based on adults have correlated
severity with amount of oedema, which may not be accurate in children.
Children and adolescents can benefit from education on how to prevent
snakebites. Preventive measures such as wearing protective clothing and not
reaching blindly into areas where snakes hide, may reduce the incidence of
snakebite.

Snakebites
While adults are generally wary of snakes, children may not understand the
potential danger and may even attempt to pick them up. The major venomous
snakes are as follows:

17 0 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 • Elapidae-cobras, kraits, mambas and coral snakes;
• Hydrophyidae-true sea snakes;
• Laticaudidae-sea kraits;
• Viperidae-pit vipers;
• Crotalidae-rattlesnakes, water moccasins, copperheads, American and
Asian bushmasters;
• Colubridae-boomslang and birdsnake of Africa and red necked keel back
of Asia.

Snake venoms are complex mixtures of proteins with enzymatic actions.

They may produce local or systemic effects. Clinical effects may range from local
tissue swelling to significant neurotoxicity. Pit viper bites may produce signifi-
cant disseminated coagulopathy and bleeding.

Spider bites
There are over 30000 species of spiders in the world (17), but only a few
produce venoms that cause significant injury or death in humans. However,
most fatalities are among children, the elderly or individuals with a pre-existing
medical condition. The spiders most commonly associated with significant
envenomation are the black widow (Latrodectus) and the brown recluse
(Loxosceles) .
The black widow spider is found in Africa, Asia, Australia, Europe and USA.
Only the female, recognized by its shiny black colour and characteristic red,
yellow or orange hourglass marking on the underside of the large globular
abdomen, is capable of human envenomation. Diagnosis can be challenging,
especially in very young children who are not able to explain that they have been
bitten. The symptoms may be misdiagnosed as acute appendicitis if the child
presents with severe abdominal pain associated with abdominal rigidity, espe-
cially if the characteristic lesion or "halo" remains unnoticed.
Brown recluse spiders are usually found in uncleaned, dusty areas in the
home. The bite is often not painful at the outset and may remain unnoticed for
up to 24 hours, after which a painful purple papule develops. Tissue necrosis
may develop up to one week later. The venom contains cytotoxic enzymes.
Haemolytic anaemia may follow a Loxosceles bite in children.

Scorpion
Scorpions have an elongated segmented body, similar to the shrimp, with a
long mobile tail. The venom is contained in a vesicle found in the telson, which
is the last segment of the tail. Morbidity and mortality from scorpion stings is
higher in children than adults (18). Children may have more severe signs and
symptoms because severity is dependent on body weight. Diagnosis in young
children with unexplained crying and agitation may be difficult because of the
absence of local signs. Different species of scorpions produce different clinical

12. POISONINGS AND ENVENOMINGS 17 1

syndromes. The yellow scorpion (Leiurus quinquestriatus) found in north Africa,
Jordan, Lebanon, Saudi Arabia, Syrian Arab Republic, and Turkey may produce
a hyperadrenergic state with high levels of catecholamines, cholinergic signs,
cardiovascular collapse and eventually death. The South African Tityus scorpi-
ons may produce hypertension, cholinergic signs, convulsions and death. The
only American genus of clinical significance is Centruroides (18).

Millipedes and centipedes

Children may pick up millipedes out of curiosity. While millipedes do not
bite, when handled they discharge toxic substances that may irritate the skin or,
in severe cases, produce local tissue changes and even necrosis. Some can
cause conjunctival irritation by spraying a highly irritating and repugnant secre-
tion. Children who pick up centipedes may receive a painful bite, that produces
localized swelling and erythema, which may later progress to lymphangitis or
lymphoedema; symptoms generally subside in 48 hours (18).

Hymenoptera
Bees, wasps, hornets and ants belong to the order Hymenoptera, charac-
terized by a stinging apparatus situated at the end of the abdomen, in the
females. Bees have a barbed stinger with lances that attaches to the skin and
continues to inject venom even if the insect dies. Wasps and hornets have
unbarbed stingers, and can inflict multiple stings. The stings cause local pain,
redness and swelling, and rarely cause severe toxicity. However, multiple stings
or stings near the mouth or neck may be life-threatening. In some children, a
single sting may produce a potentially fatal anaphylactic reaction within 30
minutes. These children present with rash, itching, angio-oedema, nausea, vom-
iting, hypotension, bronchospasm and eventually collapse. A child may go into
anaphylactic shock as a result of sensitization from a previous exposure.
Deaths from bee stings in the United States are more common than from
all other venomous creatures. Treatment of local effects may require the use of
antihistamines, corticosteroids, and cooling lotions. The bee sting should be
removed immediately, by scraping or pinching. Anaphylactic reactions require
the use of epinephrine and immediate supportive care.

Aquatic animals
There are some 100 known toxic species of coelenterates and aquatic inver-
tebrates. The venom is often found in stinging cells called nematocysts. Most
of the toxins contain a complex mixture of polypeptides and proteins, includ-
ing catecholamines, histamines, hyaluronidases, kin ins, fibrinolysins, and
cardiotoxins.
Jellyfish stings may cause death in humans. The "true" jellyfish, the Scypho-
zoans, are found throughout the world, and have tentacles arranged radially
round the bell and even inside the bell. The Cubozoans-the "box" jellyfish, par-

172 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

ticularly the Chirodropids-have caused many deaths in humans in tropical and
subtropical waters. The tentacles arise from the corners of the box or cube.
When the jellyfish touch the skin, the thread tube that is tightly coiled in each
nematocyst is locked in position by a set of spines. The thread tube fires at
tremendous speed through the skin in just a few thousandths of a second.
The Irukandji jellyfish, found in northern Australia, mostly lives in deep
waters but can be washed onto beaches during the summer months. The bell
is transparent making it almost impossible to be seen in water. On initial contact
the tentacles may be just 5-7cm long, but these can increase to 60-70cm when
the Irukandji has its prey. The initial envenomation may not be noticed, since
there is hardly any mark from the jellyfish bell. The skin may then develop a
"goose pimple effect", which lasts for approximately 30 minutes, and redness,
which may last for several days. This latent period, called the Irukandji syn-
drome, ranges from 5 to 50 minutes and is followed by severe and distressing
systemic symptoms, namely pain, catecholamine excess and global cardiotoxi-
city leading to pulmonary oedema. Low back pain is characteristic, with the
victim experiencing a dull aching at the sacral area and difficulty walking. Muscle
cramps are often described as unbearable and coming on in "waves". Victims
are usually restless, moving continuously in an effort to get comfortable. They
usually have a sense of impending doom. In severe envenomation, sweating is
highly profuse and generalized and piloerection is observed.
In 1996, the last recorded death from box jellyfish (Chironexjleckeri) enven-
omation in Australia was in a 3-year-old girl from the remote Northern Territory
aboriginal community. According to Currie, the last ten deaths from jellyfish
stings in the Northern Territory have all been in children, which shows the
greater risk for a smaller body exposed to the millions of stinging cells on jel-
lyfish tentacles. Because the efficacy and safety of the antivenom are uncertain,
prevention is of paramount importance. Children should therefore not enter the
sea when there may be jellyfish present (19).
Physalia are not real jellyfish, but a hydroid of the order siphonophora. They
appear on beaches during the summer months, and have a sting similarto that
of jellyfish. Physalia have a gas-filled sac that floats in water. Common examples
include the bluebottle, Portuguese man-of-war and Pacific man-of-war. Pain
accompanies the initial envenomation.

12. POISONINGS AND ENVENOMINGS 173

Scorpion bite
A 28-month-old girl with witnessed scorpion sting to the right big toe. She cried continu-
ously for 30 minutes. The child was tachycardic with a heart rate of 176 bpm and a respira-
tory rate of 36/min, and had increased salivation, agitation and wheezing. At the hospital the
child presented opsoclonus or roving eye movements. The scorpion was identified as a C.
sculpturatus. The child's clinical status improved rapidly, and she was discharged from the
emergency room after 2 hours. Five weeks later she was stung again by a small scorpion,
on her foot. She presented with excessive salivation and secretion from mouth and nose,
wheezing, supraventricular tachycardia and gross motor agitation. One hour after enveno-
mation, the child was noted to have a body temperature of 38.2°C, heart rate of 150 bpm,
respiratory rate of 40/min with gross motor agitation and opsoclonus and copious oral secre-
tions. One vial of the intravenous Centruroides antivenom was given. Symptoms resolved
after one hour at the emergency department and the patient was discharged after 4 hours
with specific instructions to watch out for signs of serum sickness. Follow-up was conducted
by telephone.
NOTE: ATROPINE IS NOT ROUTINELY RECOMMENDED IN TREATING SYSTEMIC TOXICITY FROM THE DANGEROUS
SCORPIONS OF ASIA, THE MIDDLE EAST AND SOUTH AFRICA. Atropine may potentiate the sympathetic effects of the
venom itself leading to an "autonomic storm" with transient cholinergic effects and a sustained hyperadrenergic state.

Spider bite
The father of a previously well child found his 8-month-old boy extremely lethargic, listless
and covered with vomitus. He noticed that the child had two puncture marks over the dorsal
web space of the right third and fourth fingers. A large spider was found on the bed. The
child presented with cholinergic signs, increased sweating, salivation, tongue fasciculation,
piloerection and progression of lethargy. During transportation to the hospital the child was
given two vials of Funnel Web Spider antivenom (recommended by the on-call toxinologist
at the Australian Venom Research Laboratory) and an immediate reversal of symptoms was
noted. The spider was identified by the Natural History Museum of Queensland as a male
Hadronyche infensa.

Agelenopsis aperta envenomation

Previously thought as harmless, this spider has now been shown to be dangerous. A nine-
year-old boy was initially unaware that the spider had bitten him, until a red mark was ooted
on his neck. He suffered from neck rigidity and pharyngeal swelling with fronto-occipital
headache after 10 minutes. Later there was nausea and disorientation. A red papule on the
bite site was noted. He developed myalgia and arthralgia, general malaise, headache, and
unsteadiness with heaviness in the legs. Because of the rarity of positive identification, all
spiders caught in the act of biting should be properly identified by qualified arachneiologists.
The spider in this case was caught by one of the boy's classmates while still on the neck of
the victim, allowing for the recognition of this species and its potential for toxicity.

'74 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Acknowledgement
Dr Woolf's work is supported in part by funds from the Comprehensive Envi-
ronmental Response, Compensation, and Liability Act (CERCLA) trust fund,
through a cooperative agreement with the Agency for Toxic Substances and
Disease Registry, Public Health Service, US Department of Health and Human
Services. The authors assume sole responsibility for the contents of this chapter;
the views expressed are not necessarily those of the Agency for Toxic Substances
and Disease Registry.

References
1. Murray CJL, Lopez AD. Global health statistics. A compendium ofincidence, preva-
lence, and mortality estimates for over 200 conditions. Boston, MA, Harvard School
of Public Health, 1996.
2. Mental health. New understanding, new hope. The World Health Report 2001.
Geneva, World Health Organization, 2001.
3· Hoppu K. Forty years of poison information service in Finland-what has changed
and what has not. Journal of Toxicology and Clinical Toxicology, 2001,39: 276.
4· Du NT, Due B, Due P. Epidemiology of acute poisonings in Viet Nam.Journal of
Toxicology and Clinical Toxicology, 2001, 39:5 27-5 28 .
5· Litovitz TL, Klein-Schwartz W, Rodgers G et al. 2001 annual report of the Amer-
ican Association of Poison Control Centers Toxic Exposure Surveillance System.
American Journal of Emergency Medicine, 2002:39 1-45 2 .
6. Senanayake N, Peiris H. Mortality due to poisonings in a developing agricultural
country: trends over 20 years. Human and Experimental Toxicology, 1995,
14:808-811 .
7· Woolf A, Wieler J, Greenes D. Costs of poison-related hospitalizations at an
urban teaching hospital for children. Archives of Pediatric and Adolescent Medi-
cine, 1997, 151:719-723.
8. Miller TR, Lestina DC. Costs of poisoning in the United States and savings from
poison control centers: a benefit-cost analysis. Annals of Emergency Medicine,
1997, 29:239-245.
9· Woolf AD. Health hazards for children at work. Journal of Toxicology and Clinical
Toxicology, 2002, 40:477-482.
10. The Bangladesh arsenic mitigation water supply project; addressing a massive public
health crisis. Washington, DC, World Bank, 1999 (http://wblm018.woridbank.org/
sar/sa.nsf).
11. Kilbourne EM et al. Clinical epidemiology of toxic-oil syndrome. New England
Journal of Medicine, 1983, 309:1408-1414.
12. Gupta SK, Singh U. Epidemic dropsy: treatment, prevention and future planning.
In: Gupta SK, ed. Poisoning, poison control, and environmental toxicology. New
Delhi, Utkarsh Prints, 2000.
13· O'Brien KL et al. for the Acute Renal Failure Investigation Team. Epidemic of
pediatric deaths from acute renal failure caused by diethylene glycol poisoning.
Journal of the American Medical Association, 199 8 ,279: 11 75- 11 80.

12. POISONINGS AND ENVENOMINGS

175
'4. Carlson J, Tamburlini G. Policy development. In: Tamburlini G, van Ehrenstein
0, Bertollini R, eds. Children's health and environment: a review of evidence,
Copenhagen, WHO Regional Office for Europe and European Environment
Agency, 2002.
, 5. Bates N et al. eds. Paediatric toxicology: handbook of poisoning in children. London
and Basingstoke, Macmillan Reference, , 997·
,6. American Association of Poison Control Centers. 2002 Annual report of the
American Association of Poison Control Centers Toxic Exposure Surveillance System.
American Journal of Emergency Medicine, 2' :353·
'7. Diaz JH. The global epidemiology, syndromic classification, management and
prevention of spider bites. American Journal of Tropical Medicine and Hygiene,
2004, 7' :239-250 .
,8. Casarett and Doull's Toxicology: The basic science of poisons, 5th ed. New York,
McGraw-Hili, '996.
'9. Currie B et al. Jellyfish envenomation in the Northern Territory of Australia.
Toxicon, , 992, 30:501.

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 CHAPTER 13

Unintentional injuries in children

1. Guthrie
Children's Institute, University of Cape Town, South Africa

K. McGee
Department of Injuries and Violence Prevention, World
Health Organization, Geneva, Switzerland

M. M. Thein
Home Safety Committee, National Council of Singapore,
Singapore

Overview
Childhood injuries are a major public health problem worldwide. In 2000,
an estimated 973000 children under the age of 15 were killed by an injury (1).
Approximately 20% of all injuries worldwide occur in children under 15, and
injuries were among the 10 leading causes of death for this age group. Injuries
accounted for nearly 10% of the total burden of disease in children. Of the
injury deaths among children, 84% were due to unintentional injuries, with
almost 32% of these caused by drowning and almost 25% by road traffic injuries
(Figure 13.1).
Until recently, injuries were frequently referred to as accidents. However,
there is growing consensus that using the term accident implies a degree of
inevitability. This traditional view of injuries as accidents suggests that they are
random events, an unavoidable part of the world in which children live. During
the past few decades, public health professionals have recognized that injuries
are preventable. Injuries have been taken out of the realm of chance and placed
squarely in the realm of science, where they can be studied and approaches to
their prevention can be planned.
An injury is "a bodily lesion at the organic level, resulting from acute expo.
sure to energy (mechanical, thermal, electrical, chemical or radiant) in amounts
that exceed the threshold of physiological tolerance. In some cases (e.g. drown.
ing, strangulation, freezing), the injury results from an insufficiency of a vital
element" (2). Injuries are typically divided into two categories: unintentional
injuries, which comprise road traffic injuries (RTls), drowning, burns, poison.
ing, and falls; and intentional injuries, which arise from deliberate acts of
violence against oneself or others.
In this chapter we will discuss the epidemiology and risk factors of unin.
tentional injuries among children aged 0 to 14 years, particularly those linked

177
Figure 13.1 Distribution of unintentional injuries by cause among children under 15 years in
2000

24.7% Road traffic injuries (RTI)

7.4% Poisonings

4.0% Falls

to the children's environment. We also discuss measures that can be taken to

prevent injuries among children.

Magnitude of the problem

Unintentional injuries among children are a global problem; however,
children and adolescents in certain regions ofthe world are disproportionately
affected. It is estimated that 98% of all unintentional injuries in children occur
in low- and middle-income countries. Children in the African, South-East Asian
and Western Pacific regions account for 80% of all childhood unintentional
injuries (Figure 13.2) (1).
Among high-income countries, injury continues to be a leading cause of
death among children. For example, in the United States of America in 2000,
unintentional injury was the leading cause of death among children aged 1-14
years (3). In Finland, between 1971 and 1996, injuries were the leading cause of
death in children aged 1-14 years (4). In Australia, injuries are the leading cause
of death in children aged 1-14 years, accounting for nearly half of all deaths in
this age group (5). Unintentional injuries make up 90% of all child injury deaths
in Australia. A recent study by UNICEF revealed that every year injuries kill more
than 20000 children aged 1-14 years in the countries of the Organisation for
Economic Co-operation and Development (OECD) (6).

Figure 13.2 Distribution of unintentional injuries among children 0-15 years, by sex and
region, in 2000
20
OJ
0\ 15
~
~ 10 Females
~
~ 5
o
Africa Americas Eastern
Mediterranean
••
Europe South-East
Asia
Western
Pacific
Region

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 In Bangladesh, a community-based study found that drowning accounted
for between 10% and 15% of all child deaths over the 12 years of the study (7).
In rural areas of the Islamic Republic of Iran, unintentional injuries are
responsible for 41% of all deaths of children aged between 1 and 14 years (8).
A community-based study in Jordan found that 60% of sample families lived in
conditions that exposed their small children to a range of significant dangers,
including exposed kerosene heaters (9). Many of the Central and Eastern
European countries have significantly higher child injury mortality rates than
Western European countries; for example, Latvia has a rate of 38-4 per 100000
population versus 5.2 per 100000 in Sweden (6). Deaths from injury account
for almost the entire east-west gap in overall child mortality in Europe (10). In
Croatia, injuries are responsible for 36% of all deaths in childhood and 52.5%
of total mortality in the 5-14 year age group (11).
While mortality is an important indicator, it is important to realize that for
each injury death, there are several thousand injury survivors who are left with
permanent disabilities. Data on nonfatal childhood unintentional injuries and
associated disability among children are relatively scarce. Nonetheless, a study
in the Netherlands during 1991-1995 found that for every death among children
under 14 caused by a home or leisure injury, there were 160 hospital admissions
and 2000 visits to accident and emergency departments (12). If this proportion
is extrapolated to child injury deaths in the OECD countries, there would
be approximately 50 million accident and emergency department visits and
4 million hospital admissions each year (6). To measure nonfatal outcomes,
WHO uses the disability-adjusted life year (DALY).' It is estimated that, in 2000,
32% of the DALYs lost to injury globally were among children aged 0-14 years.
A recent review of children's injuries in low-income countries revealed a
good deal of consistency between WHO data and other sources with regard to
common causes of childhood unintentional injuries (13). These causes are
reviewed below.

Road traffic injuries

RTls among children include injuries to pedestrians, cyclists, and motor
vehicle occupants. WHO estimates that, in 2000, over 190000 children died as
a result of road traffic injuries. RTls account for 48% of child injury deaths in
the EU as a whole (14) and 41% in the OECD countries (6). RTls cause the most
serious injuries, including head and abdominal injuries, and in some places,
particularly urban areas, RTls are the most common cause of injuries that
require emergency care (13). For example, in Thailand, RTls were found to be
the most common cause of injury in children over one year of age (15). The

'Disability Adjusted Life Years: the sum of years of potential life lost due to premature mor·
tality and the years of productive life lost due to disability.

13. UNINTENTIONAL INJURIES IN CHILDREN 179

majority of children who die as a result of RTls are not car occupants but
pedestrians and cyclists. In South Africa, over 40% of children under 19 years
who suffered an RTI were pedestrians (16). In Ethiopia, 84% of all persons who
die in traffic crashes are pedestrians (17).

Drowning
In 2000, an estimated 229000 children died from drowning. Half of the
global mortality due to drowning occurs among children aged 0-14 years (18),
with children under 5 years having the highest drowning mortality rates. There
is a large disparity among children worldwide with regard to drowning; more
than 90% of drowning deaths occur in low- and middle-income countries,
while drowning rates in high-income countries are declining. In Uganda, a
population-based community survey in a rural district found that drowning was
the leading cause of injury death (19). A review of deaths among children aged
1-12 years in a rural district in India found that drowning was the single largest
cause of death for this age group during the 7-year study period (20). In Mexico,
from 1985 to 1990, 3408 children aged 1-4 years died as a result of drowning,
making it the leading cause of death for this age group (21).

Other causes of childhood unintentional injuries

There is some evidence that falls are a common cause of childhood injury.
A community survey in Brazil showed that over 46% of injuries among children
aged 1-10 years were caused by falls (22). A study in the United Kingdom found
that 42% of visits to emergency departments by children under 14 years were
for treatment of cuts or lacerations resulting from a fall (23). In addition, a review
of public hospital admissions in New Zealand over a 10-year period showed that
falls were the leading cause of morbidity among children aged under 14 years
(24). WHO estimates that over 32000 children died from a fall in 2000.
Burns are also an important public health issue, particularly in terms of mor-
bidity and long-term disability, and especially in the developing world; WHO
estimates that more than 95% of fire-related burns occur in low- and middle-
income countries. Burns and scalds are the third leading cause of death for chil-
dren in the EU (14). A study in Kuwait found that during the 16-year study period,
the majority of burn patients were children aged 0-5 years (25). An epidemio-
logical study of childhood injury in the United Arab Emirates found that in the
group under 5 years of age, the most common cause of trauma was burns and
scalds (64%) (26). A four-year study in Afghanistan found that 63% of patients
admitted to a Red Cross hospital for burns were children (27).
Acute unintentional poisoning also causes numerous deaths and health care
visits each year. In 2000, almost 70000 children died from unintentional poi-
soning. The youngest children seem to be at the greatest risk. For example, a
study in Zimbabwe found that over 45% of poisoning cases occurred in chil-

180 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

dren below the age of 5 years (28). In Saudi Arabia, 63% of the poisoning cases
seen over the seven-year study period were in children aged 1-3 years (29). In
the United States of America, children under 5 years have the highest rate of
poisoning-related emergency department visits (30).

Routes of exposure and risk factors

A number of factors playa role in children's vulnerability to injury. Some of
these are personal factors that are not modifiable; others are related to the chil-
dren's environment and in many cases are modifiable. One personal risk factor
is age; many studies show that for specific types of injuries, such as poisoning
and burns, very young children are at highest risk. Sex is also a risk factor for
injury among children. Boys account for most injuries in almost all studies
where figures are disaggregated by sex (13). For example, boys aged 5-14 years
in low- and middle-income countries are more than twice as likely to drown,
more than twice as likely to be injured in falls, and about 80% more likely to be
killed or injured in road traffic crashes than girls (31). Although sex and age are
not susceptible to modification, awareness of the increased likelihood of spe-
cific injuries being associated with certain age and sex groups allows preven-
tion programmes to be targeted to these high-risk groups.
Other risk factors associated with childhood unintentional injury include
socioeconomic status and environmental factors, many of which are closely
linked. There is evidence that children living in poverty are disproportionately
affected by injuries. Economic poverty can influence injury patterns in numer-
ous ways. For example, poor children frequently live in areas with high traffic
density, are more likely to travel on foot or by bicycle than by car, and typically
have inadequate play areas. Children from affluent families are more likely to
sustain nonfatal injuries as passengers inside a vehicle, while poor children
more frequently sustain fatal injuries as pedestrians (32). In many low- and
middle-income countries, substandard housing contributes to the risk of injury.
Approximately 600 million city residents in Africa, Asia and Latin America live
in "life- and health-threatening homes" (33). In addition, affluent families are
able to install a range of safety devices, such as smoke detectors, safety gates,
and window guards, that make the home environment safer for children.
There is some evidence of rural-urban differences in injury rates, though
most of this evidence is from high-income countries. In industrialized coun-
tries, such as Canada, New Zealand, and the USA, rural residents have higher
rates of fatal unintentional injuries than urban residents (J2). This may be
particularly relevant for certain types of injuries. For example, the circumstances
in which drowning occurs can differ between rural and urban settings:
drowning in streams, wells, dams, cisterns or while fishing is more common in
rural areas of low- and middle-income countries (34). While drowning in open
bodies of water, falls from trees, burns from open fires and high-speed car

13. UNINTENTIONAL INJURIES IN CHILDREN

crashes are important causes of death for rural residents, injuries as a pedes-
trian, a cyclist or as a passenger on public transport are more common for urban
residents.

Remedial action, prevention and education

Overall, there are three general approaches to injury prevention: (1) educa-
tion to promote behaviour change (so that individuals avoid risk and policy- and
decision-makers generate informed decisions); (2) environmental modification
to create safer surroundings; and (3) legal requirements and prohibitions to
reduce risk (35). These are commonly known as the "three Es" of injury pre-
vention: education, engineering, and enforcement.
Reducing deaths and disabilities from childhood unintentional injury is chal-
lenging but there are numerous examples of successful interventions. Lessons
can be learned from high-income countries where the incidence and severity of
childhood injuries have decreased in recent decades. Caution should be exer-
cised, however, in transferring these interventions to low- and middle-income
countries. For example, use of child safety seats in cars would be of compara-
tively limited value in settings where the vast majority of road traffic injury
victims are pedestrians. It is important to identify the factors that contribute to
the risk of injury among certain populations. For instance, childhood burns may
be more commonly due to hot bath scalds, as in Japan (36), or to dropping a
hot liquid while unsupervised, as in the Netherlands (37). Or the most common
agent in unintentional poisoning among children may be kerosene, paraffin, or
petroleum, as in many developing countries, or medicaments and household
chemicals, as in many developed countries.

Modifications and improvements for avoiding specific types

of injury
Road traffic injuries
There are numerous measures that can be taken to prevent RTls among
children. These include:

• reduced speed limits-in the United Kingdom, the introduction of 20

miles per hour (32 kmjhour) speed limits resulted in a 70% decrease in
child pedestrian collisions (14);
• traffic slowing measures such as speed bumps;
• safer vehicle car fronts-a large proportion of deaths and serious injuries
among pedestrians and cyclists could be prevented this way (38);
• sidewalks and roadway barriers, such as chains and fences, designed to
physically separate pedestrians from vehicles (39);
• mandatory use of safety belts and child safety seats. Where this is not fea-
sible because of a large number of vehicles without functional safety belts,
governments should ban importation of vehicles without such belts;

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 • use of helmets by riders on non-motorized and motorized cycles.
Numerous studies have shown that helmets are effective in reducing
head injuries in many settings.

Poisoning
Measures to prevent poisoning among children include:

• use of childproof caps for pesticide, medicine and fuel containers;

• establishment of poison control centres;
• community-based prevention education programmes to change storage
habits in the home and improve knowledge of first aid.

Drowning
Measures to prevent drowning among children include:

• fencing and barriers around open bodies of water, and covers on

wells;
• education about risks of drowning and need for closer supervision;
• training in resuscitation.

Burns
Measures to prevent burns among children include:

• raising or enclosing cooking areas;

• introduction of an electricity supply to reduce dependence on candles and
kerosene;
• safe stove design;
• improved house construction;
• installation of smoke detectors and sprinkler systems;
• education about first aid for burns;
• regulation of water temperature;
• use of flame-retardant fabrics.

Falls
Measures to prevent falls by children include:

• installation of fences, roof rails, stair rails, stair gates, window bars, well
covers, and window guards;
• improved recreational space for children with safe equipment and
surroundings.

In addition, there are some other simple, cost-effective prevention strategies

to consider:

13· UNINTENTIONAL INJURIES IN CHILDREN

 • development of national policies on injury prevention to advocate greater
resources;
• systematic surveillance for injuries;
• education for community members in first aid;
• coordinated emergency services;
• improved enforcement of existing laws.

References
1. Global burden of disease 2000 database, Version 1. Geneva, World Health
Organization,2001.
2. Baker SP, O'Neill B, Karpf RS. The injury fact book. Lexington, MA, Lexington
Books, 1984.
3- National Center for Injury Prevention and Control, Centers for Disease Control
and Prevention. WISQARS leading causes of death reports, 1999-2000
(http://webapp.cdc.gov/sasweb/ncipc/leadcaus10.html).
4. Parkkari J et al. Childhood deaths and injuries in Finland in 1971-1995. Interna-
tional Journal of Epidemiology, 2000, 29:516-523-
5. Kidsafe, The Child Accident Prevention Foundation of Australia. 10 key facts about
child injury in Australia (http://www.kidsafe.com.au/tenfacts.pdf).
6. UNICEF. A league table of child deaths by injury in rich nations. Florence, UNICEF
Innocenti Research Centre, 2001 (Innocenti Report Card NO.2).
7. Ahmed MK, Rahman M, van Ginneken J. Epidemiology of child deaths due to
drowning in Matlab, Bangladesh. International Journal of Epidemiology, 1999,
28:3 06-31l.
8. Soori H, Naghavi M. Childhood deaths from unintentional injuries in rural areas
of Iran. Injury Prevention, 1998,4:222-224.
9. Janson Set al. Accident risks for suburban pre-school Jordanian children.Journal
of Tropical Pediatrics, 1994, 40:88-93.
10. Sethi D et al. High childhood mortality from injuries in transition countries:
action is needed. Eurohealth, 2000, 6:47-50.
11. McKee M, Oreskovic S. Childhood injury: call for action. Croatian MedicalJournal,
2002, 43=375-378.
12. Deaths and injuries due to accidents and violence in the Netherlands 1998-1999.
Amsterdam, Consumer Safety Institute, 2000.
13. Bartlett SN. The problem of children's injuries in low-income countries: a review.
Health Policy and Planning, 2002, 1Tl-13.
14. Priorities for child safety in the European Union: agenda for action. Amsterdam,
European Child Safety Alliance, 2001.
15. Ruangkanchanasetr S et al. Epidemiology and risk factors of injury in Thai chil-
dren. Southeast Asian Journal of Tropical Medicine and Public Health, 1991,
22: 127-132.
16. Child Accident Prevention Foundation of Southern Africa (Childsafe).
(www.altonsa.co.zajchildsafe).
17. Taft C et al. Childhood unintentional injury worldwide: meeting the challenge. Wash-
ington, DC, Safe Kids Worldwide, 2002.

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 18. Peden M, McGee K, Sharma G. The injury chartbook: a graphical overview of the
global burden of injuries. Geneva, World Health Organization, 2002.
19· Kobusingye 0, Guwatudde D, Lett R. Injury patterns in rural and urban Uganda.
Injury Prevention, 2001, 7:4 6-5 0 .
20. Bose A, George K, Joseph A. Drowning in childhood: a population based study.
Indian Pediatrics, 2000, 37=80-83.
21. Celis A. Home drowning among preschool age Mexican children. Injury Preven-
tion, 1997, 3:252-256.
22. del Ciampo LA et al. Incidence of childhood accidents determined in a study
based on home surveys. Annals of Tropical Paediatrics, 2001, 21:239-243.
23· Laing GL, Logan S. Patterns of unintentional injury in childhood and their rela-
tion to socio-economic factors. Public Health, 1999, 113: 2 91- 2 94.
24· Kypri K et al. Child injury morbidity in New Zealand, 1987-1996. journal of
Paediatrics and Child Health, 2001, 37: 22 7-234.
25· Bang RL. Burn mortality during 1982 to 1997 in Kuwait. European journal of
Epidemiology, 2000, 16:731-739.
26. Bener A, AI-Salman KM, Pugh RNH. Injury mortality and morbidity among
children in the United Arab Emirates. European journal of Epidemiology, 1998,
14: 175- 178.
27· Calder F. Four years of burn injuries in a Red Cross hospital in Afghanistan.
Burns, 2002, 28:563-5 68 .
28. Tagwireyi D, Ball DE, Nhachi CFB. Poisoning in Zimbabwe: a survey of eight
major referral hospitals. journal of Applied Toxicology, 2002, 22:99- 10 5.
29· Izuora GI, Adeoye A. A seven-year review of accidental poisoning in children at
a military hospital in Hafr AI Batin, Saudi Arabia. Annals of Saudi Medicine, 2001,
21:13-15.
30. McCraig LF, Burt CWO Poisoning-related visits to emergency departments in
the United States, 1993-1996. journal of Toxicology-Clinical Toxicology, 1999,
7:81 7-826.
31. Krug EG, Sharma GK, Lozano R. The global burden of injuries. Americanjournal
of Public Health, 2000, 90:523-526.
32 . Barss P et al. Injury prevention: an international perspective. Epidemiology, surveil-
lance and policy. New York, Oxford University Press, 1998.
33· Global Urban Observatory and Statistics Unit, UN Human Settlements Pro-
gramme. Human settlements conditions and trends (http://www.unhabitat.org/
habrdd ji ntrod uction jhtml).
34· Sethi D, Zwi A. Challenges of drowning prevention in low- and middle-income
countries. Injury prevention, 199 8 ,4: 162.
35· Christoffel T, Gallagher SS. Injury prevention and public health: practical
knowledge, skills, and strategies. Gaithersburg, MD, Aspen Publishers, Inc.,
1999·
36. Fukunishi K et al. Epidemiology of childhood burns in the Critical Care Medical
Center of Kinki University Hospital in Osaka, Japan. Burns, 2000, 26:4 6 5-
4 6 9.

13· UNINTENTIONAL INJURIES IN CHILDREN

37. den Hertog PC, Blankendaal FACM, ten Hag SM. Burn injuries in the Nether-
lands. Accident Analysis and Prevention, 2000, 32 :355-3 64.
38. Priorities for EU motor vehicle safety design. Brussels, European Transport Safety
Council, 200l.
39. Forjuoh SN, Li G. A review of successful transport and home injury interventions
to guide developing countries. Social Science and Medicine, 199 6 , 43:1551-1560.

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

186
CHAPTER 14

Ionizing radiation
L. Kheifets
M. Repacholi
Department for the Protection of the Human Environment,
Radiation and Environmental Health, World Health
Organization, Geneva, Switzerland

Introduction
Ionizing radiation is a known carcinogen to which children are particularly
vulnerable. Relevant exposures include pre- and postnatal irradiation for
medical reasons, radon in the home, and accidental radiation releases. In some
cases, children may receive higher doses than adults because of higher intake
and accumulation. Furthermore, sensitivity to radiation is highest early in life
(1). Although the mechanism of greater susceptibility is not well understood, it
is likely to be linked to greater cell division in growing and developing tissues.
In addition, a longer expected lifetime, with a resultant increased chance of
repeated exposure and accumulated damage, also leads to higher cancer risk
for children. Fetuses might be particularly sensitive to ionizing radiation, since
their tissue cells are not only undergoing high rates of division, but are also dif-
ferentiating into mature functional cells.

Sources and exposures

All life on earth has evolved with continuous exposure to natural radiation,
which was far higher in prehistoric times. Natural radiation is the major source
of human radiation exposure and comes from external sources and from
radionuclides accumulated within the body. External sources include cosmic
radiation from remote parts of the universe and the sun, and terrestrial radia-
tion from the ground and from building materials. Radionuclides are introduced
into the body through food, water and air. In general, the highest exposure is to
radon, a radioactive gas produced from the decay of uranium and radium in the
earth's crust. The fact that radon is a gas means that it can diffuse into water
or through soil into homes and bUildings.
In addition to natural radiation, most individuals are exposed to man-made
radiation. The largest source of man-made radiation is medical irradiation,
which includes diagnostic X-rays and other imaging techniques. Radiation is
also used therapeutically to treat cancer and, historically, enlarged tonsils,
adenoids or thymus, as well as some viral and fungus infections (notably tinea
capitis or infection of the scalp). Medical radiation, when used judiciously, offers
enormous direct benefits to patients. Other sources of radiation include con-
sumer products (e.g. televisions, fertilizers), nuclear weapons tests, the pro-
duction of nuclear power, and the disposal of nuclear and other radioactive
waste.
In terms of human exposure, the dose and risk depend on many factors.
Exposure can be external or internal, for example through intake of radionu-
c1ides from air or food. The intensity of cosmic radiation depends on the alti-
tude. The dose in the mountains is more than twice that at sea level. Still higher
doses are found at altitudes used by aircraft, particularly for intercontinental
flights. The level of terrestrial radiation depends on the composition of the soil
and the use of certain building materials (e.g. granite). Unusually high expo-
sures from terrestrial radiation have been reported in some areas of Brazil,
India, the Islamic Republic of Iran and Kenya.
Concentrations of radon in soil exhibit a large geographical variability. In
addition, the concentration of radon in buildings will depend on the amount
of ventilation, with high concentrations in poorly ventilated areas, such as the
basement, especially in winter, when windows are kept closed. Children may
also receive relatively high doses in households that use groundwater wells with
high concentrations of radon in the water.
The level of exposure to medical radiation, especially for diagnostic pur-
poses, depends on accepted practice and varies from country to country. Pro-
cedures are checked periodically to ensure that the optimum dose is used. In
addition to the frequency of use of various procedures, the doses received will
depend on the equipment used. It should be noted, however, that use of medical
procedures involving radiation in children is relatively rare. On the other hand,
children might have a higher uptake and accumulation of radioactive isotopes
(e.g. iodine '3' in the thyroid).

Types of radiation and biological effects

Ionizing radiation produces charged particles (ions) in the materials or
tissues in which it is absorbed. When this happens in molecules of biological
importance, it may lead to recognizable damage. There are various types of
ionizing radiation: alpha, beta and gamma radiation, X-rays and neutrons. Their
effects vary, but all can be damaging. Cellular damage from ionizing radiation
depends on the type of radiation, the deposition rate, and the distribution
through the tissue. Biological effects also depend on the radiosensitivity of the
tissue exposed.
Two kinds of effects of radiation on tissues are observed. Deterministic effects
occur when a large number of cells have been damaged, stem cells have lost
their capacity to divide, or tissue structure or function is affected. These effects
occur at doses above a threshold, with the probability of occurrence and the
severity of effects increasing sharply above this threshold. To the extent that the
organism is able to compensate for the loss of cells, the harm may be tempo-

,88 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

rary. Examples of deterministic effects are nausea, diarrhoea, skin damage and
cataracts.
Stochastic effects occur when cells are not killed, but are modified. Some of
the changes may persist in daughter cells. Examples of stochastic effects are
cancer and hereditary diseases in children or subsequent descendants of indi-
viduals who have been exposed to radiation, especially if the genital organs were
exposed. Ionizing radiation is a complete carcinogen since it can act to initiate,
promote and progress cellular changes that lead to cancer. The dose of radia-
tion received by an individual affects the probability of cancer, but not its aggres-
siveness. Radiation-induced cancer is indistinguishable from cancer from other
causes. The probabilistic nature of this risk means that children have more time
to accumulate exposures and damage, and more time after exposure to develop
the disease.

Health effects
With increasing dose, the severity of acute effects increases from transient
pathological changes to immediate death (Table 14.1).
Much of the available evidence about the effects of ionizing radiation on
human populations stems from the experiences of the survivors of the atomic
bombs exploded over Hiroshima and Nagasaki in 1945 (the Life Span Study or
LSS (3)), from follow-up of patients exposed to radiation for diagnostic or
therapeutic reasons, and from the radiation accident that occurred in 1986
at the Chernobyl nuclear power plant in the Ukraine.
LSS includes a cohort of85000 survivors who received total body exposure
and for whom individual estimates of radiation exposure have been calculated.
This population, of all ages and both sexes, has been carefully followed up for

Table 14.1 Effects of whole body exposure to ionizing radiation

WHOLE BOOY OOSE (Gy) SYMPTOMS SURVIVAL TIME

20 Damage to the central Death within a few hours to a few days
nervous system
8-20 Damage to the gut Death after about two weeks
3.5 Bone marrow damage 50% of patients will survive; the rest
will die in 1-2 months
0.5-3 Bone marrow damage All survive; stochastic effects, some
causing transient resulting in death, may occur later in life
reduction in the number
of blood cells
Under 0.5 Stochastic effects may All survive; stochastic effects, some
occur later in life resulting in death, may occur later in life

Source: ref. 2.

14. IONIZING RADIATION 189

many years since 1950. Available data include results of numerous clinical tests,
as well as a comprehensive monitoring of both cancer development and mor-
tality. Large numbers, relatively good dose information encompassing a wide
range of exposure and a broad demographic composition make this study the
most important source of information on radiation risk. Of particular relevance
here are two groups: children who were under 10 years of age at the time of the
explosions (approximately 5% ofthe cohort) and 1630 people who were exposed
to the bombing in utero.
Numerous studies of radiotherapy and diagnostic irradiation have been con-
ducted. The most relevant findings from these studies for particular cancers are
presented below. Overall the studies were limited in terms of their size, the sex
and age distribution of the study populations, and the organs irradiated. Nev-
ertheless, they provide important information complementary to the LSS study
because they cover many different countries, represent a broad range of doses
(high for radiation therapy and low for diagnostic procedures), and encompass
various types of ionizing radiation. They are particularly valuable in providing
additional information of risks for particular cancers and for particular ages.
As a result of the explosion at the Chernobyl nuclear power plant, large areas
of Belarus, the Russian Federation and Ukraine were contaminated. As a result
millions of people were exposed to low levels of radiation over an extended time
period. Several studies of residents of the contaminated area, their offspring
and clean-up workers are currently under way. Most of the information is limited
by lack of reliable individual doses and difficulties in conducting studies because
of population resettlement, changes in food supply, and restrictions on the
activities of individuals and families. The break-up of the Soviet Union exacer-
bated these difficulties, through differences in registration criteria, follow-up
mechanisms, dose-reconstruction methods and compensation laws. WHO
established the International Programme on the Health Effects of the Chernobyl
Accident (IPHECA) to support national programmes, monitor health conse-
quences and indicate future work needed to ensure that maximum information
is gained from this disaster (4).

Cancer
Epidemiological studies have shown that exposure to high levels of ionizing
radiation leads to an increased risk of cancer. Exposure in childhood, in partic-
ular, increases risk of leukaemia, and breast and thyroid cancer. Age dependence
for these cancers, which are among the diseases most readily induced by
radiation, is complex, and generally tracks changes in background rates, i.e.
increase in the risk due to radiation is proportional to the overall increase in
cancer risk due to ageing.
The radiation exposure from a single diagnostic procedure is usually small.
However, many people undergo radiological examinations, some of them rather
frequently, making these procedures the highest man-made source of radiation

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

exposure. Because of the increased lifetime risk per unit dose for children, the
potentially higher doses, and the increasing frequency of paediatric computer-
ized tomography (CT) examinations, diagnostic procedures that use radiation
can lead to a small, but non-negligible, increase in risk of cancer (5). While these
procedures are undisputedly beneficial, the magnitude of exposure of children
can often be reduced without significant loss of information.

Leukaemia
Studies of survivors of atomic bomb explosions showed an increased risk
in both incidence of leukaemia and associated mortality. Furthermore, the risk
of leukaemia from radiation is higher than for other risk factors and occurs
earlier than for solid cancers. Leukaemia risk is best described by non-linear fit;
risk is higher for exposures that occur in childhood, but tends to begin to
decrease 10-15 years after exposure (6). Most of the studies of radiotherapy and
diagnostic irradiation confirm an increase in leukaemia risk at high doses.
The observed association between childhood leukaemia and in utero expo-
sure to diagnostic X-rays has been interpreted as providing further support for
the etiological role of ionizing radiation, despite methodological limitations of
some of the studies.

Breast cancer
Breast cancer risk was associated with radiation exposure in the LSS cohort
and among several medically exposed groups. The risk increases with dose lin-
early and is particularly high for those exposed at young ages. The risk of breast
cancer was increased in women who were under 10 years of age at the time of
the atomic bomb explosion-a time when girls have little or no breast tissue.
Women who developed early-onset breast cancer might have been genetically
susceptible to radiation (7). On the basis of these findings, it is recommended
that breasts should be shielded when possible during diagnostic or therapeutic
radiation (8).

Thyroid cancer
Thyroid gland tissue is highly susceptible to radiation during childhood. In
the LSS cohort a significant association was found between radiation dose and
risk of thyroid cancer for those exposed before 19 years of age. Irradiation in
childhood for benign conditions, as well as therapeutic exposure, can increase
the risk of thyroid cancer. Risk is highest for children and decreases with
increased age at exposure. The excess risk can be observed for many years after
exposure and is highest 15-30 years after exposure (6). The most dramatic
finding after the Chernobyl incident was a large increase in thyroid cancers in
children. Some 2000 children have now been diagnosed with thyroid cancer,
and in some locations where contamination was highest, as in the Gomel
region, the incidence of this cancer increased over 100-fold.

14. IONIZING RADIATION

 Brain cancer
Ionizing radiation is related to brain tumours, although the relationship is
weaker than for the cancers described above. Most brain tumours associated
with ionizing radiation are benign, but an increase in malignant brain tumours
has been observed in patients who received radiotherapy. The evidence is
strongest for those exposed before age 20 years (9)·

Mental retardation
Fetal exposure to radiation has been associated with severe mental retar-
dation in the LSS study. A dose-dependent relationship with reduced head cir-
cumference was reported (10). The risk depended on gestational age, and was
most severe at 8-15 weeks.
As a result, it is recommended that, because of the potentially high expo-
sure of the head of an infant during (T scans (around 100mGy), frequent
radiological examinations over short periods should be avoided, particularly
when other imaging techniques are available.

Indoor radon
The evidence of carcinogenicity of radon comes largely from studies of
lung cancer in uranium miners. The risk of lung cancer from radon is
much higher for smokers. Ecological and analytical studies carried out in several
countries have not provided any evidence of an association between indoor
radon and childhood cancer risk (11). Although indoor radon exposure has
been postulated to cause leukaemia, recent evidence does not support such an
association (12).

References
1. Ionizing radiation, Part 1: X- and gamma-radiation, and neutrons. Lyon, Interna-
tional Agency for Research on Cancer, 2000 (IARC Monographs on the Evalua-
tion of the Carcinogenic Risk to Humans, Volume 75)·
2. Diagnosis and treatment of radiation injuries. Vienna, I nternational Atomic Energy
Agency, 1998 (Safety Reports Series No.2).
3. Radiation Effects Research Foundation. Life Span Study reports. (www.rerf.or.jp/
eigo /titles/lsstitle.htm).
4. WHO. Children affected by the Chernobyl accident. Geneva, World Health Orga-
nization (www.who.int/ionizing_radiation/research/children/en /i ndex.html).
5. Brenner DJ et al. Estimated risks of radiation-induced fatal cancer from pediatric
CT. American Journal of Roentgenology, 2001, 176: 28 9- 29 6 .
6. United Nations Scientific Committee on the Effects of Atomic Radiation. Report
to the General Assembly, United Nations, New York, Volume II: Effects. New York,
United Nations, 2000.
7. Land CEo Early-onset breast cancer in A-bomb survivors. Lancet, 1993, 342:
237·

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 8. American Academy of Pediatrics. Risk of ionizing radiation exposure to children:
a subject review. Pediatrics, 1998, 101 :717-719.
9· Tilyou SM. NRC issues interim rule on medical use of radionuciides.Journal of
Nuclear Medicine, 1990, 31:20A-21A.
10. Lee S, Otake M, Schull WJ. Changes in the pattern of growth in stature related
to prenatal exposure to ionizing radiation. International Radiation Biology, 1999,
75: 1449-145 8 .
11. Little J. Epidemiology of childhood cancer. Lyon, International Agency for Research
on Cancer, 1999 (IARC Scientific Publications No. 149).
12. Kiriou JC et al. A comparison of doses and techniques between specialist and
non-specialist centers in the diagnostic X-ray imaging of children. BritishJournal
of Radiology, 1996, 69:437-450.

'4. IONIZING RADIATION 193

CHAPTER 15

Noise 1
c. F. Bearer
Departments of Pediatrics and Neurosciences, Case
Western Reserve University; Division of Neonatology,
Mary Anne Sears Swetland Environmental Health Center,
Rainbow Babies and Children's Hospital, Cleveland, OH,
USA

What is noise?
Noise is undesirable sound. Sound is vibration in a medium, usually air. It
has frequency (pitch), intensity (loudness), periodicity, and duration.
The frequency of sound is measured in cycles per second or hertz (Hz):
1 Hz = 1 cycle per second. People can hear frequencies ranging from 20 to
20000 Hz, but are most sensitive to sounds in the range of 500 to 3000 Hz,
the band that includes human speech.
The loudness of sound is measured in terms of pascals (Pa) or decibels
(dB). One Pa is 1 x lO-s standard atmospheres of pressure. The sound limits of
human hearing are 0.00002 Pa (the weakest sound that a keen human adult ear
can detect under quiet conditions) to 200 Pa (the pressure that causes pain in
the adult ear). The decibel expresses the energy of a sound in comparison with
a reference sound, usually 0.00002 Pa. The dB SPL (sound pressure level) of
one sound (p1) is therefore: 20 logw(p1 Jp2) where p2 is 0.00002 Pa. Noise in a
quiet room may be 40dB, while a pneumatic drill may produce 130dB. Human
speech is approximately 50dB SPL. The perceived loudness of sound varies with
the frequency. For example, to match the perceived loudness of a 1000 Hz
40dB SPL tone requires over 80dB SPL at 50Hz and over 60dB SPL at
10000 Hz. The 40dB SPL equivalency curve is used to determine the sound
intensity, referred to as the decibel weighted by the A scale, or dBA.
Periodicity refers to either continuous sound or impulse sound.

Routes of exposure
Sound waves enter the ear through the external auditory canal and vibrate
the ear drum. This vibration travels through the three ossicles of the middle ear
(the malleus, incus and stapes), to the oval window, causing the fluid of the
inner ear, the cochlea, to vibrate. Within the cochlea, the basilar membrane
covers the organ of Corti which is composed of the hair cells. Each hair cell

'Based on the Handbook of Pediatric Environmental Health of the American Academy of

Pediatrics.

194
responds to a specific frequency and converts this signal to a nerve impulse.
The impulses travel up the auditory nerve to be interpreted as sound by the
brain. Loss of hearing originating in the external auditory canal, ear drum, ossi-
cles or middle ear is called conductive hearing loss and is usually treatable. Loss
of hearing originating in the cochlea or auditory nerve is called sensorineural
hearing loss and is usually permanent.
Sound vibration may also be transmitted to the body directly through the
skin as vibration, but this will not be discussed here.

Systems affected
Noise-induced hearing loss
Although noise pollution receives little public attention, there is evidence
that current environmental levels of noise are damaging our hearing. A study
on deafness among college students conducted in 1990 could find no students
unexposed to loud music to serve as controls (1). Among the controls who had
low exposure, noticeable hearing loss was found. Statistics from the University
of Washington Occupational Medicine Clinic in Seattle show that nearly 10%
of the 1424 persons evaluated between 1982 and 1987 showed noise-induced
hearing loss (N IH L). Approximately 50% of these people had been exposed to
hazardous noise at work. Susceptibility to NIHL is highly variable; while some
individuals are able to tolerate high noise levels for prolonged periods of time,
others in the same conditions will rapidly lose hearing. NIHL results from
trauma to the hair cells of the cochlea. Prolonged exposure to sounds louder
than 85 dBA is potentially injurious. Continuous exposure to hazardous levels
of noise tends to have its maximum effect in the high-frequency regions of the
cochlea. NIHL is usually most severe around 4000Hz with downward exten-
sion toward speech frequencies with prolonged exposure. This pattern of loss
of frequency perception is true regardless of the pitch of the noise exposure.
Impulse noise is more harmful than continuous noise since it bypasses the
body's natural protective reaction, the dampening of the ossicles mediated by
the facial nerve.
Exposure to loud noise may result in a temporary decrease in sensitivity of
hearing and tinnitus. This condition, called temporary threshold shift (TTS).
lasts for several hours depending on the degree of exposure.

Physiological effects
Noise causes a stress response. The hypothalamic-pituitary-adrenal axis is
sensitive to noise intensities as low as 65dBA, resulting in a 53% increase in plasma
17-0H-corticosteroid levels. Increased excretion of adrenaline and noradrenaline
has been demonstrated in humans exposed to noise at 90dBA for 30 minutes.
Noise contributes to sleep deprivation. Noise at 40-45 dBA results in a
10-20% increase in awakening or EEG arousal changes. Noise at 50dBA results
in a 25% probability of arousal features on EEG.

15. NOISE 195

 Noise has undesirable cardiovascular effects. Exposure to noise greater than
70dBA increases vasoconstriction, heart rate and blood pressure. A case of
persistent ventricular fibrillation upon arousal from sleep by noise has been
reported (2).

Psychological effects
Exposure to moderate levels of noise can cause psychological stress. Annoy·
ance, inability to concentrate and symptoms such as headaches, tiredness and
irritability are common psychological reactions to noise. The degree of annoy-
ance is related to the nature of the sound. Intense noise can cause personality
changes and a reduced capacity to cope. Sudden and unexpected noise can
cause a startle reaction which may provoke physiological stress responses.
Work performance may be affected. At low levels, noise can improve per-
formance of simple tasks. However, noise may impair complex intellectual func-
tions and performance of complex tasks.

Paediatric exposures
Little work has been done to estimate children's exposure to noise. Avail-
able data suggest that children are routinely exposed to more noise than the
24-hour equivalent noise exposures (Leq24) of 70dbA recommended as an
upper limit by the United States Environmental Protection Agency (EPA) in 1974
(3,4). A longitudinal study of hearing in suburban and rural Ohio children aged
6-18 years found that Leq24s varied from 77 to 84db, and were higher for boys
than girls (5).

Developmental sensitivity
There is little evidence to suggest that the organs of hearing are more sen-
sitive to NIHL in children than adults. Children are at increased risk of expo-
sure to noise for behavioural reasons: infants cannot remove themselves from
noise, and cannot communicate if they cannot hear adult speech. Older chil-
dren may play with firecrackers or cap pistols, while teenagers may listen to loud
rock music.

Clinical effects
There is evidence to suggest that: (1) exposure to excessive noise in utero
may result in high·frequency hearing loss in the newborn, and may be associ·
ated with prematurity and intrauterine growth retardation; (2) exposure to noise
in the NICU may result in cochlear damage, and (3) incorporation of individu-
alized environmental care (including reduction of noise) in the management of
premature infants decreases the time they spend on the ventilator, and appears
to allow more normal maturity of the central nervous system as measured by
quantitative EEG (6, 7). Very few studies have been done on the clinical effects
of noise on children.

SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 NIHL
A longitudinal study of hearing was conducted in suburban and rural Ohio
children aged 6-18 years. While there was no clear relationship between noise
exposure and hearing loss, the hearing loss that was evident was greater at
higher frequencies than lower ones, and sex differences in hearing acuity
became greater with age; both observations are consistent with a developing
noise-induced hearing loss (5). Auditory screening of 3322 children attending
schools within 2 miles of Logan Airport in Boston, Massachusetts (USA), was
conducted, and follow-up examinations performed to permit classification of
the type of hearing loss (8). Children living directly under the flight paths or
immediately adjacent to runways did not have a higher incidence of bilateral
sensorineural or mixed hearing loss than the sample average. Hearing acuity
among children without diagnosis of hearing loss was unrelated to distance
from the flight path or duration of residence.

Physiological effects
A stress response consisting of acute terror and panic has been described
in children exposed to sonic booms in Labrador, Canada (9), and in Germany.
Biochemical evidence of the stress response was found in elevated urinary cor-
tisollevels. Hypertension accompanied a 30-minute exposure to 100dBA in 60
children aged 11-16 years.

School performance
In a comparison of schoolchildren aged 8-10 years living in lower or upper
floors of a 32-floor apartment building, reading achievement and auditory dis-
crimination were poorer among those living in lower-floor apartments where
noise levels from adjacent highways were higher (10). The range of noise levels
was not large: the interior apartment noise levels varied from 55 to 66 dBA.
Reading performance is negatively affected by noise either in the classroom or
in the home. Bronzaft & McCarthy (11) showed that children aged 6, 8, and 10
in classrooms on the side of the school building adjacent to elevated trains had
poorer reading performance than children from the quieter side of the same
building. Classroom noise varied from 59dBA when trains were not passing, to
89 dbA when they were. Aircraft noise was inversely related to the percentage of
children whose reading ability was below average in a study of children in New
York City (12). In a study of children in 15 schools in California, reading level was
inversely related to freeway noise (13).

Effects on parenting
There is a growing body of evidence that noise and crowding adversely affect
the interactions of carers with infants and toddlers (14-16). Parents in noisy
environments were less likely to be highly involved in their child's activities, and
less likely to be verbally responsive to their child.

15. NOISE 197

 Diagnosis
The typical finding in noise-induced hearing loss is a dip in hearing thresh-
old around 4000 Hz on an audiogram. Health care providers who lack the
capacity to perform pure tone audiograms should refer their patients for
evaluation. Audiological evaluation, including pure tone audiometry, should be
performed for noise-induced hearing loss on any child with a history of:

• in utero exposure to excessive noise because of maternal occupation or

recreational activities;
• playing with cap pistols or other loud "impulse" toys;
• an occupation with excessive noise exposure;
• poor school performance;
• short attention span;
• complaints of ringing in the ears, a feeling of fullness in the ears, muf-
fling of hearing, or difficulty in understanding speech.

Adolescents should be screened yearly because of their propensity to listen

to loud music.
The American Academy of Pediatrics (AAP) currently recommends objective
hearing screening for high-risk newborns (17, 18) and at 4,5,12 and 18 years of
age (19).

Treatment of clinical symptoms

There is no treatment for permanent noise-induced hearing loss.

Prevention of exposure
Questions about noise exposure should be part of routine health visits.
Parents should be encouraged to reduce the noise exposure of their children
by:

1. avoiding loud noises, especially loud impulse noise, whenever possible;

2. avoiding loud toys, especially cap pistols and firecrackers;
3. turning off televisions, computers, and radios when not in use;
4. reducing the volume of televisions, computers, and radios; a good rule of
thumb is that volume levels should be such that one does not need to raise
one's voice during normal conversation;
5. creating a "stimulus haven", the quietest room in the house for play and
interactions with infants and toddlers.

When reducing noise is impossible, hearing protectors should be worn.

There are two types, ear plugs and ear muffs. Ear plugs should fit properly; they
should require a slight tug to remove them. Ear muffs are the most effective
type of ear protector available. They have cups lined with sound-absorbing mat-

198 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 erial that are held against the skull with a spring band or oil-filled ring that pro-
vides a tight seal.
Unfortunately, environmental noise is often not under the control of the
hearer, which makes noise reduction and hearing protection difficult. Govern-
ment regulations are needed to protect parents and children. The standard for
the workplace is no more than 8 hours of exposure to 90 dBA, 4 hours to
9SdBA, 2 hours to 100dBA, with no exposure allowed to continuous noise
above llSdBA or impulse noise above 140dBA. In other settings, environmental
noise is expressed as a day-night average sound level (DN L). For the protection
of public health, the US Environmental Protection Agency proposed a DN L of
SSdB during waking hours and 4SdB during sleeping hours in neighbourhoods,
and 4SdB during the day and 3SdB at night in hospitals.
Table 15.1 lists some common environmental noises and their potential
effects.

Table 15.1 Decibel ranges and effects of common sounds

EXAMPLE SOUND PRESSURE EFFECT OF EXPOSURE
(dBA)
Breathing 0-10 Threshold of hearing
Whisper, rustling leaves 20 Very quiet
Quiet rural area at night 30
Library, soft background music 40
Quiet suburb (daytime), 50 Quiet
conversation in living room
Conversation in restaurant, average 60 Intrusive
office, background music, chirping
bird
Freeway traffic at 15 m, vacuum cleaner, 70 Annoying
noisy office or party, television
Garbage disposal, washing machine, 80 POSSible hearing damage
average factory, freight train at 15 m,
dishwasher, arcade games
Busy urban street, diesel truck, food 90 Hearing damage (8 hr
blender exposure), speech interference
Jet take-off (305 m away), subway, 100
outboard motor, power lawn mower,
motorcycle at 8 m, farm tractor, printing
plant, jackhammer, garbage truck
Steel mill, riveting, automobile horn at 110
1 m, boom box stereo held close to ear
Thunderclap, textile loom, live rock 120 Human pain threshold
music, jet take-off (161 m away), siren,
chain saw, boom stereo in cars

15· NOISE
199
Table 15.1 continued

EXAMPLE SOUND PRESSURE EFFECT OF EXPOSURE

(dBA)

Armoured personnel carrier, jet take-off 130

(100 m away), earphones at loud level
Aircraft carrier deck 140
Jet take-off (25 m away), 150 Eardrum rupture
toy cap pistol, firecracker

References
1. West PD, Evans EF. Early detection of hearing damage in young listeners result-
ing from exposure to amplified music. British Journal of Audiology, 1990,
24: 89-10 3.
2. Kam PC, Kam AC, Thompson JF. Noise pollution in the anaesthetic and inten-
sive care environment. Anaesthesia, 1994, 49:982-986.
3. Dejoy DM. Environmental noise and children: review of recent findings.Journal
of Auditory Research, 1983, 23:181-194.
4. Von Gierke H. Noise: how much is too much? Noise Control EngineeringJournal,
1975, 5: 2 9-34.
5. Roche AF, Chumlea WC, Siervogel RM. Longitudinal study of human hearing: its
relationship to noise and other factors. III. Results from the first five years.
Aerospace Medical Research Laboratory, 1982 (Report no. AFAMRL-TR-82-68).
6. Als H et al. Individualized behavioral and environmental care for the very
low birth weight preterm infant at high risk for bronchopulmonary dysplasia:
neonatal intensive care unit and developmental outcome. Pediatrics, 1986,
78:1123-1132.
7. Buehler DM et al. Effectiveness of individualized developmental care for low-risk
preterm infants: behavioral and electrophysiologic evidence. Pediatrics, 1995,
9 6 :9 23-93 2 .
8. Andrus WS, Kerrigan ME, Bird KT. Hearing in para-airport children. American
Space and Environmental Medicine, 1975, 46:740-742.
9. Rosenberg J. Jets over Labrador and Quebec: noise effects on human health.
Canadian Medical Association Journal, 1991, 144:869-875.
10. Cohen S, Glass DC, Singer JE. Apartment noise, auditory discrimination, and
reading ability in children. Journal of Experimental Social Psychology, 1973,
9:40 7-4 22 .
11. Bronzaft AI, McCarthy DP. The effect of elevated train noise on reading ability.
Environment and Behaviour, 1975, 7=517-528.
12. Green KB, Pasternack BS, Shore RE. Effects of aircraft noise on reading ability
of school-age children. Archives of Environmental Health, 1982, 37=24-31.
13. Lukas JS, Dupree RB, Swing Jw. Effects of noise on academic achievement and
classroom behavior. Office of Noise Control California Department of Health Ser-
vices, 1981 (Report no. FHWA/CA./DOHS-81/0l).

200 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 14· Wachs TO, Chan A. Specificity of environmental action as seen in physical and
social environment correlates of three aspects of twelve month infants' com-
munication performance. Child Development, 1986, 57= 14 64-1475.
15· Wachs TO, Camli O. Do ecological or individual characteristics mediate the influ-
ence of the physical environment upon maternal behavior. Journal of Environ-
mental Psychology, 1991, 11 :249-26 4.
16. Wachs TO. Nature of relations between the physical and social microenviron-
ment of the two-year-old child. Early Development and Parenting, 1993, 2:81-87.
17· American Academy of Pediatrics, Joint Committee on Infant Hearing. Joint Com-
mittee on Infant Hearing 1990 Position Statement. AAP News, 1991, 7.
18. American Academy of Pediatrics, Committee on Environmental Health. Noise:
a hazard to the fetus and newborn. Pediatrics, 1997, 100:724-7 2 7.
19· American Academy of Pediatrics, Committee on Psychosocial Aspects of Child
and Family Health. Guidelines for health supervision, 2nd ed. American Academy
of Pediatrics, 1988.

15· NOISE
201
CHAPTER 16

Global environmental
change and child health 1,2
A. J. McMichael
National Centre for Epidemiology and Population Health,
The Australian National University, Canberra, Australia

s. Bunyavanich
Department of Medicine, Massachusetts General Hospital,
Harvard Medical School, Boston, MA, USA

P. R. Epstein
Center for Health and the Global Environment, Harvard
Medical School, Boston, MA, USA

Introduction
The distinctive aspect of global environmental change is its scale. For the
first time, humankind is exerting sufficient pressure on the earth's biophysical
systems to cause changes in some environmental processes and conditions at
the global level. Several such environmental changes have now been confirmed,
in particular stratospheric ozone depletion and climate change. There is also a
human-induced global change in the elemental cycles of nitrogen, sulfur and
potassium. Various other environmental changes are now occurring worldwide,
in rather more mosaic fashion. These include depletion of fresh water, degra-
dation of agroecosystems, depletion of fisheries, and the dissemination of per-
sistent organic pollutants (POPs).
These large-scale environmental changes do not necessarily pose qualita-
tively new risks to health. Rather, they amplify and extend the health risks posed
by many existing environmental hazards. These include extreme weather events,
thermal stress, food and water shortages, toxic POPs, and increased ultraviolet
radiation at middle to high latitudes. More important risks to health will prob-
ably come from the disruption of ecological processes or systems. For example,
changes in land use, climatic conditions and surface water distribution will influ-
ence the geographical range and density of disease vectors, such as mosqui-
toes, ticks and water-snails. Likewise, many of these environmental changes will

'Reviewed by D. Schwela, Physical and Chemical Exposure Unit, Institute for Health and Con-
sumer Protection, Joint Research Centre, Ispra, Italy.
'Some of the material in this chapter is adapted from Bunyavanich S, Landrigan CP, McMichael
AJ, Epstein PRo The impact of climate change on child health. Ambulatory Pediatrics, 20 0 3,
3:47-55·

202
affect crop production, fruit and vegetable production, and animal husbandry,
with particular consequences for child nutrition and development.
A well-known example of these environmental changes is global climate
change. This phenomenon results from the recent rapid increase in human-
induced greenhouse gas emissions, altering the properties of the lower atmos-
phere, and thereby causing a change in world climate. This has widespread
consequences for human health, and poses some particular risks to children's
health.
There are three pathways by which global climate change may affect child
health (1). These are via:

1. The immediate environmental consequences of the processes that cause

climate change, such as burning offossil fuels and forests. The toxic air pol-
lutants produced can cause or exacerbate cough, asthma and some child-
hood respiratory infections, particularly within the urban environment.
2. The direct impact of altered climatic conditions. Heat waves may increase
the incidence of heat stroke in children; a greater intensity and frequency of
natural catastrophes related to weather will increase drowning, dehydration,
gastrointestinal illness, and psychological trauma (e.g. from disruption of
family and community social networks).
3. The indirect impacts caused by ecological disturbances. Malnutrition and
childhood stunting will occur in food-insecure populations as a consequence
of climatic effects on food production. Increased production of pollen and
fungal spores may exacerbate allergies and asthma. Higher temperatures
and increased flooding will tend to expand the geographic range of malaria,
dengue, various types of encephalitis, and tick-borne diseases, leading to
greater morbidity and, especially among children, mortality. Even more
complex ecological disturbances underlie the increased risk of diseases such
as hantavirus pulmonary syndrome, where, for example, drought followed
by heavy rains disturb the balance between rodents and their predators, and
increase human exposure to viruses excreted by rodents.

To date, there has been little empirical research specifically into the health
impacts on children of global environmental changes (1). This may reflect the
large spatial scale and rapid pace of environmental change, which mean that,
as yet, there are few local, clear-cut, acute health impacts. Further, the mathe-
matical modelling of the future health impact of climate change (and other
global environmental changes) has, to date, not specifically addressed child
health. Most such modelling has either encompassed the full age range or has
been confined to adult health outcomes (e.g. heart attacks and strokes during
heat waves). Further, there are well recognized limitations in the mathematical
and statistical models that have been developed for this type of research, which
is still in its early stages. The difficulties in modelling future processes include

16. GLOBAL ENVIRONMENTAL CHANGE AND CHILD HEALTH

handling the various scientific uncertainties and the unavoidable demographic,
economic, and technological contextual uncertainties about future human soci-
eties and behaviour.
In this chapter we focus on the impact of global climate change on child
health, as an illustration of how global environmental changes in general can,
or may in the future, affect children's health.

Global climate change and children's health

Human communities are accustomed to climatic conditions that vary on
daily, seasonal and interannual time scales. The recent and growing concern
over global climate change is caused by the accumulating evidence that the
average climatic conditions, measured over extended time periods (conven-
tionally 30 years or longer), are changing as a result of human activities that
produce various greenhouse gases, especially carbon dioxide and methane.
Temperature records since the 1860s (see Figure 16.1) show that global
warming has occurred, including a 0.6 °C increase in surface temperature during
the twentieth century (2). The Intergovernmental Panel on Climate Change
(I PCC) has concluded that most of the climate change observed since 195 0 is
due to human alteration of the lower atmosphere (troposphere), and that future
climate change will have far-reaching effects on the environment and health.
The IPCC predicts a rise in average world surface temperature of lA-5.8 °C by
2100 (2). The range of uncertainty in this prediction reflects both the scientific
uncertainties and the societal and developmental uncertainties mentioned
above.

Figure 16.1 Observed global average land and sea surface temperatures from 1860 to 2000

0.6

Q.
"i6' 0.4
E
0
c
ro
OJ 0.2
Z
ro
o~average
Q; 0.0
0- 1961-90
E
~
c -0.2
ro
OJ

i
ro
.D -0.4
0 Global
\3 _ _ Global (30y filter)
-0.6
1860 1880 1900 1920 1940 1960 1980 2000
Year

Source: Climatic Research Unit, Norwich, England.

204 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Such a rise in average world temperature would be faster than any since
the inception of agriculture around 10000 years ago. Predictions for precipita-
tion and wind speed are less consistent, but also suggest significant changes.
We should note also that climatologists are increasingly concerned that dis-
ruption of the climate system may exceed critical thresholds, causing abrupt
rather than gradual climate change and an associated rapid shift in health
effects (j, 4).
Over the past two decades, an increasing rate of changes in natural physi-
cal and biological processes, attributable to warmer temperatures, has been
reported. For example, sea ice and glaciers have been diminishing in volume,
bird nesting has begun earlier, and animal and insect migration patterns have
changed. To date, however, there is relatively little empirical evidence of the
impact of recent climatic trends on human health, and very little such evidence
refers specifically to children.
Children may be an especially susceptible group, because of both their devel-
oping physiology and their anticipated lifelong exposure to altered climatic and
environmental conditions. Worldwide, two-thirds of all preventable disease and
premature death due to environmental concerns occurs in children (5). Global
climate change will almost certainly increase the influence of environmental
conditions and processes on health, especially in children.
The economic activities that cause increased emission of greenhouse gases,
particularly fossil fuel combustion and the burning of forests and other vegeta-
tion, may also produce immediate local environmental hazards to health. The
most obvious example is that of urban air pollution, comprising a mix of power-
plant emissions, industrial smoke and gases, and traffic exhaust gases. The
impact on child health of this mix of ambient air pollutants-including fine par-
ticulates, lead compounds, carbon monoxide, nitrogen oxides, sulfur oxides,
and ozone-is described elsewhere in this volume. The following review focuses
on the other two large-scale causal pathways, direct and indirect, that connect
climate change to risks to health.

Direct health effects from altered climatic conditions

Thermal extremes: heat stroke
It is predicted that small changes in mean climate conditions will trigger rel-
atively large changes in the frequency and severity of heat waves (2). Heat waves
are therefore expected to increase in number and intensity in the future.
By extrapolation from many prior studies, any future increase in the fre-
quency and severity of heat waves will increase the risks of death and serious
illness. The very old, the very young and the sick are particularly vulnerable to
thermal stress (4). Children are less able than adults to modify their local
(usually domestic) climate, especially if a heat wave is sudden and severe. In
children, heat stroke is the most serious outcome of central or peripheral
impairment of body temperature regulation, and may result in death.

16. GLOBAL ENVIRONMENTAL CHANGE AND CHILD HEALTH 20 5

 Weather disasters: drowning, dehydration, diarrhoeal disease, and
psychological trauma
The hydrological cycle accelerates with global warming (6-10). As heat
energy accumulates in the deep ocean, more water evaporates (2), causing
increased intensity and frequency of precipitation. Evaporation from soil may
also be increased, causing drought. Models indicate that there will be more
heavy deluges, with flooding (11-13), and more frequent and longer droughts
(14) .
Extreme weather events such as heavy precipitation, severe storms, floods,
droughts, and cyclones may have increased in frequency, duration, and inten-
sity in some regions over the past century. An increase in the frequency of large
floods over the twentieth century has recently been demonstrated (11), and
several-fold increases in the frequency of what are cu rrently considered extreme
wet seasons are predicted for various regions, using a range of climate models
(15). Recent climate catastrophes, such as Hurricane Mitch in Honduras, have
had major adverse health impact. Over the past decade, floods in Bangladesh,
China, various parts of Europe, Mozambique and Venezuela have taken a con-
siderable toll on human life and well-being.
Severe weather events have many effects on child health. Studies of earth-
quakes indicate that women and young children are more vulnerable to the
acute impacts of natural disasters (16) and famines (17). Floods cause child
injuries and death by drowning, and also compromise clean water supplies,
fostering epidemics of diarrhoea. In Peru, hospital admissions for paediatric
diarrhoea were 50% above the seasonal norm after precipitation and flooding
related to the EI Nino-Southern Oscillation (EN SO). Following Hurricane Mitch,
30000 cases of cholera occurred in Central America (18). A review of 548
reported gastrointestinal infection outbreaks between 1948 and 1994 in the
United States revealed that 68% of cases were preceded by precipitation events
above the 80th percentile (19).
Weather disasters devastate homes, spawning refugee communities that are
likely to have poor public health. Basic life support systems, including water,
forests and other natural resources, may also be undermined by climate change.
Food production and availability are impaired by droughts and floods. Children
are especially vulnerable to the emotional trauma caused by sudden changes in
living routines and social networks, and the social disruption, economic damage
and population displacement caused by weather disasters can impair their psy-
chological and social development.

Diarrhoeal disease
Diarrhoeal disease is one of the most important causes of ill-health in the
world. It is highly sensitive to climatic conditions and shows strong seasonal
variations in many locations (20). The usually positive correlation of diarrhoeal
disease with temperature reflects the fact that most cases in tropical develop-

206 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

ing countries are caused by bacteria, entamoebae and protozoa (21), all ofwhich
are favoured by high temperatures.
Deaths from gastrointestinal infectious disease are especially high in chil-
dren. An estimated 3-4 million children die each year from diarrhoeal diseases,
predominantly in poorer countries (22). Children consume more water per kg
of body mass than adults, giving them an increased relative exposure to water-
borne pathogens. Further, with their less well developed immune systems, chil-
dren are less able to counteract microbes (23) or to compensate for a given level
of dehydration.
Several recent studies have used time-series analysis to correlate measure-
ments of temperature and relative humidity with the incidence of diarrhoeal
disease in children. A 6-year study in Lima, Peru, showed, on average, an 8%
increase in daily hospital admissions for each degree increase in temperature
(24). This analysis controlled for seasonal variations and long-term trends, thus
imparting high confidence to the observed relationship of diarrhoeal disease
with temperature. A similar time-series analysis in Fiji assessed the relationship
of monthly reported incidence of diarrhoea to variations in temperature and
rainfall, allowing for the effects of seasonal variation and long-term trends (25).
The reported incidence increased by approximately 3% for each degree increase
in temperature, by 2% per unit increase in rainfall above 5 x 10-5 kgjm2 per
minute (average rainfall conditions), and by 8% per unit decrease in rainfall
below this level.
These studies indicate that future changes in mean climatic conditions and
in the occurrence of extreme weather events are likely to Significantly affect the
incidence of diarrhoeal disease in children. As well as meteorological influences
on microbial exposures, child diarrhoeal disease may also increase because
drinking-water becomes contaminated by toxins from warming-induced algal
blooms.

Indirect health effects resulting from ecological alterations

Food availability: malnutrition, growth retardation, and
developmental delay
Childhood malnutrition was estimated to account for 15.9% of the total
burden of premature death and disabling disease in 1990 (26). A multiplicity of
biological, social, political, and economic factors affect the incidence of mal-
nutrition, but one of the fundamental determinants is the availability of staple
foods, predominantly cereal grains.
Climate change has many effects on food availability (27). Because there is
more carbon dioxide in the atmosphere, plants take up more CO 2 and less nitro-
gen (28). Plant protein content is thus reduced, with less nitrogen available as
building-blocks. Although elevated atmospheric carbon dioxide may increase
plant biomass, the nutritional content of the biomass may be impaired. Further,
the increased carbon-to-nitrogen ratio, by reducing the synthesis of alkaloids

16. GLOBAL ENVIRONMENTAL CHANGE AND CHILD HEALTH 20 7

and other nitrogen-based plant defences, may increase the eating of plants by
insects, rodents and other pests (29). Increased evaporation may reduce soil
moisture, while flooding may cause some arable land to become saline. Climate
change can also reduce parasite resistance in livestock (30).
Figure 16.2 shows the estimated impact on cereal grain production in sub-
Saharan Africa of standard scenarios of climate change, over three time periods
in the coming century, as modelled by scientists at the Hadley Research Centre,
United Kingdom Meteorology Office (31). Cereal grains account for around two-
thirds of total food energy for human populations, and therefore represent an
important index of future food supplies. This study, which incorporated esti-
mates of future trends in population growth, economic development, govern-
mental policies on pricing, world food trading and agricultural technological
developments, found that global climate change would result in a 5-10% drop
in total yield. Importantly, this deficit would occur very unevenly around the
world, with most of the shortfall occurring in low-latitude countries where
food insecurity is often already present, especially in South Asia, the Eastern
Mediterranean, North Africa, parts of sub-Saharan Africa, parts of Central
America and the northern part of South America.
The above-mentioned modelling studies, collectively, forecast that an addi-
tiona l 4 0 to 300 million people will become hungry by 2060 as a result of climate
change (27-32). The IPCC has concluded with "medium confidence" that "mod-
elling studies have indicated that climate change would increase the number of
hungry and malnourished people in the world later in the twenty-first century
by 80 to 90 million" (4). Most of this hungry population would be children, who
require three to four times more food than adults in proportion to their body
size (33). Food shortage in critical areas will therefore contribute to child mal-
nutrition and, hence, to retarded growth and development. Undernourishment

Figure 16.2 Estimated impact of standard scenario of global climate change on production of
cereal grains in sub-Saharan Africa, in the 2020s, 2050s and 2080s

Reference scenaro Climate change scenari

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SECTION III: SPECIFIC ENVIRONMENTAL THREATS

208
is a well-studied fundamental cause of impaired physical and intellectual devel-
opment in children, low productivity in adults, and susceptibility to infectious
disease (34, 35)·

Increased aeroallergens: allergies

Human allergic response to airborne plant pollens is a widespread envi-
ronmental contributor to hay fever, allergenic rhinitis and allergenic asthma
(36-39). Sensitization to allergens in early childhood can cause an allergic
(including asthmatic) disposition (40).
Ambient pollen levels may rise in response to higher atmospheric carbon
dioxide concentrations and higher temperatures (41, 42). Pollen counts have
been rising, and this may be partly a result of increased carbon dioxide, warmer
winters, the earlier arrival of spring, or excess of nitrogen (43). Thus, climate
change may already be contributing to the increased incidence of hay fever and
asthma that has occurred in many parts of the world in recent decades.

Malaria, dengue fever, and other vector-borne diseases

The reproduction and survival of blood-feeding vector organisms, such as
mosquitoes and ticks, are greatly affected by climate and other ecological
factors. Higher temperatures, changes in precipitation, and altered climate
variability may therefore change the distribution of vector-borne diseases, both
spatially and seasonally (44-48). Immunologically naive populations may thus
face unfamiliar pathogens. In some locations, climate change may actually lead
to decreased vector-borne disease transmission because of reduced rainfall or
excessively high temperatures.
In general, without strong public health defences, the anticipated increases
in range and seasonality of pathogens and their vector organisms will cause a
greater incidence of various infectious diseases. Children are particularly sus-
ceptible to malaria, dengue fever and various forms of encephalitis.

Malaria
Malaria is the world's most serious vector-borne disease. Around 40% of
the world's population currently lives in malaria-endemic areas. Various math-
ematical modelling studies have estimated that increased temperatures will
expand the geographical range of conditions conducive to malaria transmission,
both to higher altitudes and higher latitudes (49-51). Further, elevated temper-
atures, in combination with conducive patterns of rainfall and surface water,
will extend the transmission season in some locations. Some data suggest
that global warming may have already exacerbated malaria incidence, especially
in areas where transmission is limited by low temperatures or high altitude
(52).
Ch ildren experience disproportionately high levels of both morbidity and
mortality from malaria. Young children have little specific immunity to malarial

16. GLOBAL ENVIRONMENTAL CHANGE AND CHILD HEALTH 20 9

species and may therefore suffer yearly attacks of debilitating and potentially
fatal disease. Children are also more susceptible to cerebral malaria and to the
hypoglycaemia that is secondary to malaria, both of which can lead to neuro-
logical damage and, often, death (53).
While excessive heat kills mosquitoes, warmer average temperatures within
their survival range increase their reproduction, biting activity, and the rate at
which pathogens mature within them, including the malaria parasite, Plasmod-
ium. Furthermore, warm nights and warm winters in particular favour insect
maturation and survival. This is the specific warming pattern that climate
change induces, and mosquitoes will therefore probably mature faster and live
longer with climate change.

Dengue fever
Dengue fever is the world's most common mosquito-borne viral disease.
The disease is currently endemic in much of tropical Asia, the South Pacific
islands, tropical Africa, the Caribbean, and Central and South America. Dengue
is characterized by fever, myalgia or arthralgia, rash, leukopenia, and lym-
phadenopathy. Children are more likely to experience overt, serious, disease.
Dengue haemorrhagic fever is a severe, often fatal, febrile disease caused by
serial infection with several strains of the dengue virus (54). Dengue outbreaks
in urban areas infested with Aedes aegypti can be explosive, involving up to three-
quarters of the population.
Aedes aegypti, a daytime biting mosquito, is the principal vector and is highly
urbanized. It breeds in water stored for drinking or bathing and in collected
rainwater. I ncreased flooding and precipitation as a result of climate change
will therefore increase the presence of stagnant water breeding sites, thereby
fostering dengue virus propagation. Modelling studies indicate that global
warming will increase the geographical range of dengue (55).

Encephalitis and other vector-borne diseases

Greater climate variability will increase the incidence and geographical dis-
tribution of other vector-borne diseases, including mosquito-borne encephali-
tis, tick-borne encephalitis, and Lyme disease. Children are especially vulnerable
to mosquito and tick bites, because they tend to play outside and are closer to
the ground where ticks and mosquitoes can be found. The reported incidence
of Lyme disease in the USA is highest among children aged 5-10 years, almost
twice that among older children and adults (56).
Warm winters encourage the overwintering of ticks. Global climate change
will therefore foster the geographical spread of tick-borne diseases. A recent
study in Sweden showed that a decade of milder winters and earlier springs in
the 1980s was related to a significant increase in the range and incidence of
tick-borne encephalitis (57).

210 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Ultraviolet exposure: sunburn, skin cancer, and immunosuppression
Global climate change does not include depletion of stratospheric ozone per
se. However, certain gases (such as the chlorofluorocarbons) contribute to both
phenomena, which interact with one another.
Stratospheric ozone provides protection to life on earth by filtering out much
of the incoming solar ultraviolet (UV) radiation. In mammals and other animals,
this radiation can cause oxidative damage (and hence cancer) and suppression
of the immune system. Industrial activity and biomass burning have resulted
in the emission of particular gases, especially halogenated fluorocarbons, that
undergo photolytic release of high-energy "free radicals", which destroy strato-
spheric ozone. Consequently, ozone depletion has been observed since the early
1970s, and has caused a 5-10% seasonal (late winter and early spring) increase
in UV radiation exposure at middle to high latitudes.
Since ozone depletion is causing greater ground-level UV radiation expo-
sure, it can be presumed to be contributing to sunburn in children at middle to
high latitudes. Children's skin and eyes burn more easily than those of adults.
Childhood sunburn significantly increases the risk of malignant melanoma later
in life (58-60).
UV radiation also suppresses immune system activity, both local and sys-
temic, in animals and humans (61). Although further research is needed on this
relationship, there is a theoretical possibility that such immune suppression
may pose a health risk to children by increasing their susceptibility to infectious
agents.

Other global environmental changes

The impact on human health has been most completely assessed for global
climate change and stratospheric ozone depletion. Meanwhile, many other
large-scale environmental changes will also have consequences for child health
around the world.
In 2001, a network of international agencies and environmental conventions
initiated the Millennium Ecosystem Assessment Project, to assess the causes
and extent of ecosystem changes in the world, the projected future scenarios of
such changes, and how these are affecting and will affect the well-being and
health of human populations. This is a scientifically challenging task, since the
scope of ecosystem disruption and biodiversity losses is broad and multi-
faceted. The causal connections with human health outcomes will generally be
harder to discern and quantify than has been the case for climate change and
ozone depletion.
It is clear, however, that such things as the loss of wetlands and the degra-
dation of arable land will reduce the natural cleansing of freshwater supplies
and the productivity of agro-ecosystems, respectively. The latter will also be
affected by such things as the loss of plant pollinators, the shortage of fresh-

16. GLOBAL ENVIRONMENTAL CHANGE AND CHILD HEALTH 211

water supplies, and the encroachment of invasive introduced species. The
spread of megacities in many developing countries also jeopardizes the reten-
tion of good arable land, since cities, historically, have usually been built on
good land near rivers and coastlines.
We still have much to learn about the myriad ways in which global environ-
mental changes will affect the health of human populations. In the meantime,
we should remember that we are now depleting and disrupting the earth's life-
support systems. In the medium to long term, this will inevitably reduce the
carrying capacity of the biosphere for healthy human life.

Prevention options
Primary prevention is always preferred in public health. This applies partic-
ularly in this setting, where environmental change processes may acquire
momentum and may induce irreversible changes in important components of
the biosphere's life-support systems.
In relation to climate change, the prime requirement is for governments and
populations everywhere to modify technological choices and economic prac-
tices, so as to greatly reduce the global emission of greenhouse gases. The IPCC
and other expert commentators estimate that we need to eliminate around two-
thirds of current emissions in order to stabilize the lower atmosphere and its
climate at acceptable (apparently not dangerous) levels. This will not prove
easy-as is already evident from the inability of most countries to achieve their
Kyoto Protocol targets, agreed in '997. This protocol was developed within the
UN Framework Convention on Climate Change, originally formulated at the UN
Conference on Environment and Development, Rio de Janeiro, Brazil, in '992
(62).
Given that the process of climate change is already under way-as are other
global environmental changes-and that the world is committed to the contin-
uation of such change over at least several decades, societies must now also
seek adaptations that will lessen its adverse health impacts. Many of the
climate-amplified risks to children's health would be lessened by strengthening
public health infrastructure and environmental management-including sani-
tation, fresh water provision, immunization programmes, mosquito control,
improved housing quality, and better and more secure nutrition.
There is also a need for increased education of primary and secondary
schoolchildren about the need for communities to think and act in ecologically
sustainable ways, and about the ways of lessening personal and family expo-
sure to environmental hazards consequent upon global environmental changes.
Finally, there are some risk-reducing responses that are specific to the hazards
of environmental change-such as strengthening coastal defences against
rising seas, managing local and regional fisheries sustainably in order to main-
tain nutritional (especially protein) supplies, and altering clothing and recrea-
tional behaviour to reduce exposure of children to ultraviolet radiation.

212 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Conclusion
The impacts of global environmental change on child health span a wide
spectrum, covering respiratory health, temperature regulation, trauma, nutri-
tion, development, allergy, infectious disease, mental health, skin cancer, and
immunological changes. Nevertheless, there remains a serious lack of empiri-
cal data on how climate change specifically affects child health. Much of this
knowledge gap reflects the fact that global climate change is a recent and inher-
ently slow process. Furthermore, scientific and popular consensuses have only
recently converged in recognizing that climate change and the other global envi-
ronmental changes require both research and policy attention.
We need more research on how changes in temperature, precipitation and
extreme weather events, and their resultant ecological changes, affect children's
health. Because many aspects of the physiology and metabolism of children
differ markedly from those of adults, several of the health impacts in children,
of climate change and other global environmental changes are likely to be
distinctive.
To protect children fully from these health consequences will require a sub-
stantial change in our pattern of economic activities and in our technology
choices. By understanding better the range and extent of risks posed by
climate change, stratospheric ozone depletion and other global environmental
changes, we will strengthen the contribution of the health sciences to the
ongoing public debate over the future, sustainable, management of the
biosphere.

References
1. Bunyavanich S et al. The impact of climate change on child health. Ambulatory
Pediatrics, 2003, 3:47-55.
2. Intergovernmental Panel on Climate Change. Third Assessment Report of Working
Group 1: The Science of Climate Change. Cambridge, Cambridge University Press,
2001.
3. Broecker WS. Thermohaline circulation, the Achilles heel of our climate system:
Will man-made CO 2 upset the current balance? Science, 1997, 278:1582-1588.
4. Intergovernmental Panel on Climate Change. Climate change 2000. Impacts,
adaptation, and vulnerability. Third Assessment Report, Volume 11. Cambridge,
Cambridge University Press, 2001.
5. McMichael Aj, Kjellstrom T, Smith K. Environment and health. In: Merson M,
Black R, Mills A, eds. International public health. Gaithersburg, MD, Aspen Press,
2000:379-430 .
6. Cubasch UG et al. Projections offuture climate change. In: Houghton jT et aI.,
eds. Climate Change 2001: The scientific basis. Contribution of Working Group I to
the Third Assessment Report of the Intergovernmental Panel on Climate Change.
Cambridge, Cambridge University Press, 2001.
7. Church j. How fast are sea levels riSing? Science, 2001, 294:802-803.

16. GLOBAL ENVIRONMENTAL CHANGE AND CHILD HEALTH 21 3

8. Kattenberg A et al. Climate models projections of future climate. In: Houghton
J et al. eds., Climate change 1995. Cambridge, Cambridge University Press,
199 6 :28 5-357.
9. Karl T, Knight R, Plummer N. Trends in high-frequency climate variability in the
twentieth century. Nature, 1995, 377:217-220.
10. Whetton Pet al. Implications of climate change due to the enhanced greenhouse
effect on floods and droughts in Australia. Climate Change, 1993,25.
11. Milly P et al. Increasing risk of great floods in a changing climate. Nature, 2002,
4 15:514-5 17.
12. White KS et al. Technical summary. Climate change 2001: Impacts, adaptation,
and vulnerability. In: McCarthy J et al. eds., Climate change 2001: impacts, adap-
tation, and vulnerability. Cambridge, Cambridge University Press, 2001.
13. Easterling D. Climate extremes: observations, modeling, and impacts. Science,
2000, 289:2068-2074.
14. Epstein P. Climate change and emerging infectious diseases. Microbes and Infec-
tion, 2001, 3747-754.
15. Palmer TN, Raisanen J. Quantifying the risk of extreme seasonal precipitation
events in a changing climate. Nature, 2002, 415:512-514.
16. Beinin C. An examination of health data following two major earthquakes in
Russia. Disasters, 1981, 5:142-146.
17. Rivers JPw. Women and children last; an essay on sex discrimination in disas-
ters. Disasters, 1982, 6:256-267.
18. Epstein P. Climate and health. Science, 1999, 285:347-348.
19. Curriero F et al. The association between extreme precipitation and waterborne
disease outbreaks in the United States, 1948-1994. American Journal of Public
Health, 2001, 91:1194-1199.
20. Drasar BS, Tomkins AM, Feachem RG. Seasonal aspects of diarrhoeal disease. Sea-
sonal dimensions to rural poverty. Brighton, University of Sussex, 1978.
21. Black RE, Lanata CF. Epidemiology of diarrhoeal disease in developing countries.
In: Blaser MJ et al. eds. Infections of the gastrointestinal tract. New York, Raven
Press, 1995:13-36.
22. Health and environment in sustainable development : 5 years after the Earth
Summit. Geneva, World Health Organization, 2002 (http://www.who.int/
archivesjinf-pr-l 997 jenjpr97-47 .html).
23. Children and drinking water standards. Washington, DC, United States Environ-
mental Protection Agency Office of Water, 1999 (81 5K-99-001).
24. Checkley W et al. Effect of EI Nino and ambient temperature on hospital ad-
missions for diarrhoeal diseases in Peruvian children. Lancet, 2000, 355:442-
45 0 .
25. Singh RB et al. The influence of climate variation and change on diarrhoeal
disease in the Pacific Islands. Environmental health perspectives, 2001,
10 9: 155-159.
26. Murray C)L, Lopez AD. The global burden of disease. Cambridge, MA, Harvard
School of Public Health (on behalf of the World Health Organization and the
World Bank), 1996.

214 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 27· McMichael AL. Impact of climatic and other environmental changes on food
production and population health in the coming decades. Proceedings of the
Nutrition Society, 2001, 60:195-201.
28. Campbell B et al. Impacts of atmospheric composition and climate change on
temperate and tropical pastoral agriculture. In: Bouma W, Pearman G, Manning
M, eds. Greenhouse. Coping with climate change. Melbourne, CSIRO, 1996:171-189.
29· Coley P. Possible effects of climate change on plant/herbivore interactions in
moist tropical forests. Climatic Change, 1998, 39:455-472 .
30 . Coop R, Holmes P. Nutrition and parasite interaction. International Journal of
Parasitology, 1996, 26:951-962.
31. Parry M et al. Climate change and world food security: a new assessment. Global
Environment Change-Human and Policy Dimensions, 1999, 9: S51- 67.
2
3 . Parry M, Rosenzweig C. Food supply and risk of hunger. Lancet, 1993,
342:1345-1347.
33· How EPA protects children's health. Washington, DC, Environmental Protection
Agency, 2002 (http://www.epa.gov/epahome/chm_factsheet.html).
34· Chandra R. Nutrition, immunity, and infection: present knowledge and future
directions. Lancet, 1983, 1:688-6 91.
35· McMichael A, Haines A. Global climate change: the potential effects on health.
British Medical Journal, 1997, 315:805-809.
36 . Something in the air: airborne allergens. Bethesda, MD, National Institutes of
Health, 1993.
37· D'Amato G, Liccardi G, D'Amato M. Environmental risk factors (outdoor air pol-
lution and climatic changes) and increased trend of respiratory allergy. Journal
of Investigational Allergology and Clinical Immunology, 2000, 10: 123-128.
38. Arrighi H. US asthma mortality: 1941-1989. Annals of Allergy, Asthma, and
Immunology, 1995,74:321 -3 2 6.
39· Wuthrich B. In Switzerland, pollinosis has really increased in the last decade.
Allergy and Clinical Immunology News, 1991, 3:41-44.
0
4 . Wahn U et al. Indoor allergen exposure is a risk factor for sensitization during
the first three years of life. Journal of Allergy and Clinical Immunology, 1997,
997 63-7 6 9.
41. Ziska L, Caulfield F. The potential influence of rising atmospheric carbon dioxide
on public health: pollen production of common ragweed as a test case. World
Resources Review, 2000, 12:449-457.
4 2 . Reekie J, Hinkleton P, Reekie E. Effects of elevated CO 2 on time of flowering in
four short-day and four long-day species. Canadian Journal of Botany, 1994,
72 :533-53 8.
43· Wayne Pet al. Production of allergenic pollen by ragweed (Ambrosia artemisiifo-
lia L.) is increased in CO 2 -enriched atmospheres. Annals of Allergy, Asthma and
Immunology, 2002, 8:279-282.
44· Patz J, Reisen W. Immunology, climate change and vector-borne diseases. Trends
in Immunology, 2001, 22:17 1- 172 .
45· Epstein P. Emerging diseases and ecosystem instability: new threats to public
health. AmericanJournal of Public Health, 1995,85: 168-172.

16. GLOBAL ENVIRONMENTAL CHANGE AND CHILD HEALTH

21 5
4 6 . Sutherst R. The vulnerability of animal and human health to parasites under
global change. International Journal of Parasitology, 2001, 31:933-948 .
47. Rogers D, Randolph S. The global spread of malaria in a future, warmer world.
Science, 2000, 289:1763-1765.
4 8 . Patz ) et al. Effects of environmental change on emerging parasitic diseases.
International Journal of Parasitology, 2000, 30 :1395-14 0 5.
49. Sutherst R. Arthropods as disease vectors in a changing environment. Environ-
mental Change and Human Health, 1993: 124-145.
50. Reiter P. Climate change and mosquito-borne disease. Environmental Health Per-
spectives, 2001, 109:141-161.
51. Martens P. How will climate change affect human health? American Scientist,
1999, 87:534-541·
52. Epstein P et al. Biological and physical signs of climate change: focus on
mosquito-borne infectious diseases. Bulletin of the American Meteorological
Society, 1998, 79:40 9-4 17.
53. Krause P. Malaria (Plasmodium). In: Behrman RE et al. eds. Nelson textbook of
pediatrics. WB Saunders and Co., Philadelphia, 2000.
54. Halstead B. Dengue fever/dengue hemorrhagic fever. In: Behrman RE et al. eds.
Nelson textbook of pediatrics. WB Saunders and Co., Philadelphia, 2000.
55. Hales S et al. Potential effect of population and climate changes on global dis-
tribution of dengue fever: an empirical model. Lancet, 2002, 360:830-834.
56. Shapiro E. Lyme disease (Borrelia burgdotfen). In: Behrman RE et al. eds. Nelson
textbook of pediatrics. WB Saunders and Co., Philadelphia, 2000.
57. Lindgren E, Gustafson R. Tick-borne encephalitis in Sweden and climate change.
Lancet, 2001, 358:16-18.
58. Ozone depletion glossary. Washington, DC, Environmental Protection Agency,
2002 (http://www.epa.gov/dots/ozone/defns.htmigods).
59. Fitzpatrick T. The skin cancer cascade: from ozone depletion to melanoma-
some definitions and some new interpretation. Journal of Dermatology, 199 6 ,
23:816-820.
60. Skin cancer fact sheet. Atlanta, GA, American Cancer Society, 199 6 .
61. Melanoma risk factors fact sheet. Schaumberg, IL, American Academy of Derma-
tology, 1997·
62. United Nations Framework Convention on Climate Change. New York, United
Nations (www.unfccc.int).

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216
CHAPTER 17

Emerging environmental threats:

endocrine-disrupting chemicals
T. Damstra
Department for the Protection of the Human Environment,
International Programme on Chemical Safety, World Health
Organization, Geneva, Switzerland

Introduction
The knowledge that environmental exposures to chemicals can significantly
affect children's health is not new. However, recently there has been growing
concern that children may be adversely affected by exposure to a group of chem-
icals that have the potential to alter the normal functioning of the endocrine
system in wildlife and humans. Concerns regarding exposure to these
endocrine-disrupting chemicals (EDCs) are primarily related to: (1) adverse
effects observed in certain wildlife, fish, and ecosystems; (2) the increased inci-
dence of certain endocrine-related human diseases; and (3) endocrine disrup-
tion observed in laboratory experimental animals exposed to certain
environmental chemicals.
Potential adverse health outcomes are mainly neurodevelopmental and neu-
robehavioural abnormalities, reproductive disorders, immune impairment, and
certain hormone-related cancers (1). Children may be particularly susceptible to
exposure to EDCs during critical periods of development. Both the nature and
severity of health outcomes may depend on the developmental stage at which
exposure occurs.
Although most of the concerns regarding EDCs have focused on persistent
organic pollutants (POPs), a variety of chemical classes including natural and
synthetic hormones, plant constituents, pesticides, compounds used in the plas-
tics industry and in consumer products, and other industrial by-products and
pollutants are potential EDCs. They are often pervasive and widely dispersed in
the environment. Some are persistent, can be transported long distances, and
have been found in virtually all regions of the world. Others are rapidly degraded
in the environment or human body, or may be present for only short periods of
time. This enormous diversity means that it is not possible to define a "typical"
EDC, and each chemical or mixture must be carefully evaluated.

Mechanisms of action
Research has shown that disruption of the endocrine system can occur
through various mechanisms. Some chemicals may mimic a natural hormone,

21 7
whereas others may block the effects of hormones. Some may interfere
with hormone synthesis, transport, or metabolism (2). Exposure to EDCs
during critical developmental stages, when programming of the endocrine
system is occurring, may result in changes in growth, development, rep-
roduction, and behaviour, whereas exposure at other time periods might not
result in any significant effects. Cross-talk between various components of the
endocrine-system may also have different consequences at various life stages
and effects may occur in systems other than the system predicted to be affected
(3)·

Potential health effects

A variety of field investigations and laboratory studies have shown that
exposure to certain EDCs has contributed to adverse effects in some wildlife
populations, including mammals, birds, reptiles, and molluscs (4). Effects range
from subtle changes to permanent alterations. For example, reproductive and
immune dysfunction has been reported in various species of mammals, partic-
ularly aquatic species at the top of the food chain. Exposure to polychlorinated
biphenyls (PCBs) and dichlorodiphenyltrichloroethylene (DDE) has been shown
to adversely impact the reproductive function of Baltic seals (5). Studies on fish
have shown that exposure to certain constituents present in pulp and paper mill
effluents and sewage treatment effluents may function as EDCs and contribute
to alterations in reproductive development (6). Another example is masculin-
ization in female gastropods due to exposure to tributyltin (used in antifouling
paints), which has resulted in a global population decline in a number of gas-
tropod species (7). These are but a few examples of the breadth of responses
observed in a wide variety of wildlife species. For humans, evidence of causal
associations between low-level exposure to EDCs and adverse health outcomes
is less clear-cut.

Reproductive effects
Much of the concern about human health effects resulting from EDC expo-
sure has focused on adverse effects on reproductive development and function,
including decreased semen quality (i.e., reduced numbers, motility, and altered
morphology of sperm); male reproductive tract abnormalities (e.g. hypo-
spadias and cryptorchidism); altered sex ratio; endometriosis; precocious
puberty; and early menarche. A number of studies have reported a decline in
sperm counts in several countries (8-10). The available data suggest important
variations in sperm count between different countries, various regions within
the same country or between various districts of the same city; however, these
data must be interpreted with caution. All the studies published to date have
been retrospective and report data from men recruited for other purposes. There
are a number of confounding factors (e.g. age, seasonal variations, methods of
collecting sperm) that can influence sperm count making it difficult to compare

218 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

data between locations or from one time to another. These preliminary obser-
vations require further study.
Concerns have also been raised about the effects of EDCs on female repro-
ductive tissues and pregnancy outcomes. Exposure to certain EDCs (e.g.
2,3,7,8-tetrachlorodibenzyl-p-dioxin (TCDD) and PCBs) has been reported to be
associated with endometriosis, but the studies remain equivocal (11). Concerns
that EDCs may cause spontaneous abortion and affect fecundity and fertility
have also been raised but studies are inconsistent and suggest only a weak asso-
ciation at relatively high exposure levels (12). There have also been isolated
reports of precocious puberty resulting from foods possibly contaminated with
estrogenic compounds (13). but the mechanisms of action are unclear, and
other factors (e.g. nutrition) must also be considered.

Cancer
Increases in the incidence of certain hormone-related cancers in many parts
of the world are often cited as evidence that exposure to EDCs has had adverse
health effects. Of particular concern are increases in breast cancer and testicu-
lar cancer. Numerous epidemiological studies, as well as laboratory studies,
have been conducted to determine whether exposure to organochlorine chem-
icals contributes to an increased risk of breast cancer (14-16). Overall, the
current scientific evidence (including meta-analyses of human studies) does not
support a direct association between exposure to environmental EDCs and
increased risk of breast cancer (17); however, all the studies published to date
have measured EDC exposure levels in adult women. The claim that the time
of life when exposure takes place (e.g. prenatal, neonatal, childhood, adoles-
cence) may be the most critical factor is supported by human data on radiation
and smoking, and by basic research in animal models (18, 19). Adult women,
currently at risk for breast cancer, may have been exposed to exogenous EDCs
in utero or during infancy, childhood, or adolescence in the mid-twentieth
century when contaminant levels of organochlorines were higher. Research is
urgently needed to address the role of timing of exposure to environmental
chemicals, as well as the contributions of diet, lifestyle, and genetic profile to
the overall risk of breast cancer.
While there are marked differences in incidence of testicular cancer among
countries, there have been reports that testicular cancer incidence has increased
since the 1960s in certain countries (20,21); however, there have been no epi-
demiological studies to examine a direct linkage between exposure to estrogenic
or anti-androgenic compounds and testicular cancer (22). Unfortunately, animal
models for germ cell (testicular) tumours in men do not currently exist.
Although the data are limited, some evidence suggests that the incidence of
cryptorchidism and hypospadias may show geographical differences similar to
those of testicular cancer, and research on the etiology of this syndrome is
needed.

17. EMERGING ENVIRONMENTAL THREATS: ENDOCRINE-DISRUPTING CHEMICALS 219

 Neurological and immunological effects
The neuroendocrine and immune systems play an integrative role in orches-
trating critical physiological functions, which may be disrupted through a variety
of mechanisms, including endocrine-disrupting mechanisms. Certain EDCs
have been shown to cause neurotoxic and immunotoxic effects (23, 24). Of par-
ticular concern are the potential effects of exposure to these contaminants on
the developing nervous and immune systems, since exposure during these
critical periods may result in irreversible changes, which may not be apparent
until later in life.
Numerous studies have investigated the effects of prenatal and early post-
natal exposure to PCBs in newborn and young children (25). Studies in humans
who consumed high amounts of contaminated fish from the Great Lakes (26,
27) or accidentally contaminated rice oil (28, 29) have shown that PCBs con-
tribute to neurobehavioural changes in newborn children and that some of these
changes persist through childhood. Changes included motor immaturity,
abnormal reflexes, and low psychomotor scores. Subtle neurobehavioural alter-
ations have also been observed in children born to mothers exposed to lower
PCB levels (30). PCBs are known to interfere with thyroid hormones, which are
critical for normal brain development (31).
The immune system may also be perturbed as a result of exposure to envi-
ronmental contaminants, although for most chemicals the mechanism of action
is unclear (32). Immunological changes have been observed in human popula-
tions exposed to mixtures of PCBs, dibenzodioxins, and dibenzofurans (33).
Findings included increased susceptibility to respiratory tract infections in
adults and their children (34). and increased prevalence of ear infections in
infants (35). Infants exposed in utero or via breastfeeding appear to be particu-
larly vulnerable. Animal data support the immunotoxicity of PCBs and diben-
zodioxins (36). There is evidence of perturbed immune function at high
exposure levels, but data at lower levels are sparse, and further research is
needed.

Sources and timing of exposure

As has already been mentioned, the timing of exposure is critical to under-
standing the potential long-term health effects of EDC exposure in children
(prenatal and postnatal). Lack of adequate exposure data is often the weakest
link in attempts to determine whether exposure to EDCs poses an emerging
environmental threat. Data on the magnitude and trends of EDC exposure in
children, particularly in developing countries, are almost completely lacking.
Potential sources of exposure in children include: transplacental migration, con-
taminated breast milk or food, contaminated air and groundwater, and conta-
minants in toys and other consumer products. Global coordinated efforts are
needed to collect data on exposure.

220 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 Research needs
Data have clearly shown that POPs and EDCs are toxic at relatively high con-
centrations. The question remains whether adverse effects occur from low-level
chronic exposures. Information on timing of exposures is critical for under-
standing potential effects in children, and studies are urgently needed to address
the long-term effects of exposure during critical development stages. Significant
data gaps remain that often limit our abilityto estimate the risks of environmental
exposures to POPs and EDCs. Internationally and nationally, decision-making on
the possible deleterious effects of chemical exposure is increasingly governed by
the precautionary principle when scientific knowledge is uncertain. The influence
of endocrine disruptors on adverse health outcomes has yet to be definitely estab-
lished. However, it is clear that the risk from endocrine disruptors is important
at certain stages (preconception, prenatal and postnatal), and further research
is required to identify the windows of exposure that are critical for children's
health in terms of the irreversibility of the effects.

References
1. Global assessment of the state-of the-science of endocrine disrupting chemicals.
Geneva, World Health Organization, 2002.
2. McLachlan JA, Korach KS. Symposium on estrogens in the environment III. Envi-
ronmental Health Perspectives, 1995, 103:173.
3. Olea N et al. Inadvertent exposure to xenoestrogens in children. Toxicology and
Industrial Health, 1999, 15:151-158.
4. Ankley GT, Giesy JP. Endocrine disruptors in wildlife: a weight of evidence per-
spective. In: Kendall R et al. eds. Principles and processes for assessing endocrine
disruption in wildlife. Pensacola, FL, SETAC Press, 1998:349-368.
5. Reijnders PJH. Reproductive and developmental effects of endocrine disrupting
chemicals on marine mammals. In: O'Shea TJ et al. eds. Marine mammals and
persistent ocean contaminants: proceedings of the Marine Mammal Commission
Workshop, Keystone, Colorado, 12-15 October 1998. Bethesda, MD, Marine
Mammal Commission, 1999:139-143.
6. Van Der Kraak G et al. A comparison of bleached kraft mill effluent, 17-b-
estradiol, and b-sitosterol effects on reproductive function in fish. In: Kendall RJ
et al. eds. Principles and processes for evaluating endocrine disruption in wildlife.
Pensacola, FL, SETAC Press, 1998:249-265 (SETAC Technical Publication).
7. Matthiessen P, Gibbs PE. Critical appraisal of evidence for tributyltin-mediated
endocrine disruption in molluscs. Environmental Toxicology and Chemistry, 1998,
1T37-43·
8. Sharpe RM, Skakkebaek NE. Are estrogens involved in falling sperm counts and
disorders of the male reproductive tract? Lancet, 1993, 341 :1392-1395.
9. Larsen SB et al. Semen quality and sex hormones among organic and traditional
Danish farmers. ASCLEPIOS Study Group. Occupational Environmental Medicine,
1999,5 6 :139-144.

17. EMERGING ENVIRONMENTAL THREATS: ENDOCRINE·DISRUPTING CHEMICALS 221

10. Carlsen E et al. Evidence for decreasing quality of semen during past 50 years.
British Medical Journal, 1992, 3°5:6°9-613.
11. Lebel G et al. Organochlorine exposure and the risk of endometriosis. Fertility
and Sterility, 1998, 69:221-228.
12. Joffe M. Time trends in biological fertility in Britain. Lancet, 2000, 355:1961-1965.
1} Colon I et al. Identification of phthalate esters in the serum of young Puerto
Rican girls with premature breast development. Environmental Health Perspec-
tives, 2000, 108:895-900.
14. Hoyer AP et al. Repeated measurements of organochlorine exposure and breast
cancer risk (Denmark). Cancer Causes and Control, 2000, 11:177-184.
15. van't Veer P et al. DDT (dicophane) and postmenopausal breast cancer in
Europe; case control study. British MedicalJournal, 1997, 315:81-85.
16. Dorgan JF et al. Serum organochlorine pesticides and PCBs and breast cancer
risk: results from a prospective analysis (USA). Cancer Causes Control, 1999,
10:1-11.
17. Laden F et al. 1,1-Dichloro-2,2,-bis(p-chlorophenyl)ethylene and polychlorinated
biphenyls and breast cancer: combined analysis of five US studies. Journal of the
National Cancer Institute, 2001, 93768-775.
18. Tokunaga M, Land CE, Yamamoto T. Incidence of female breast cancer among
atomic bomb survivors, Hiroshima and Nagasaki. Radiation Research, 1987,
112:243-272.
19. Palmer JR, Rosenberg L. Cigarette smoking and the risk of breast cancer. Epi-
demiology Review, 1993, 15:145-156.
20. Adami H et al. Testicular cancer in nine Northern European countries. Interna-
tional Journal of Cancer, 1994, 59:33-38.
21. Bergstrom Ret al. Increase in testicular cancer incidence in six European coun-
tries: a birth cohort phenomenon. Journal of the National Cancer Institute, 1996,
88:7 27-733.
22. An updating of IARC Monographs, Vols 1-42. Lyon, International Agency for
Research on Cancer, 1987 (IARC Monographs on the evaluation of the carcino-
genic risk of chemicals in humans, Supplement 192).
23. International Programme on Chemical Safety. Principles and methods for assess-
ing direct immunotoxicity associated with exposure to chemicals. Geneva, World
Health Organization, 1996 (Environmental Health Criteria No. 180).
24. International Programme on Chemical Safety. Neurotoxicity risk assessment for
human health: principles and approaches. Geneva, World Health Organization,
2001 (Environmental Health Criteria No. 223).
25. Schantz SL. Developmental neurotoxicity of PCBs: what do we know and where
do we go from here? Neurotoxicology and Teratology, 1996, 18:217-227.
26. Stewart P, Darvill T, Lonky E. Assessment of prenatal exposure to PCBs from
maternal consumption of Great Lakes fish: an analysis of PCB pattern and con-
centration. Environmental Research, 1999, 80:S87-S96.
27. Lonky E, Reihman J, Darvill T. Neonatal behavioral assessment scale perfor-
mance in humans influenced by maternal consumption of environmentally con-
taminated Lake Ontario fish. Journal of Great Lakes Research, 1996, 22:198-212.

222 SECTION III: SPECIFIC ENVIRONMENTAL THREATS

 28. Hsu CC, Yu MLM, Chen YCJ. The Yu-Cheng rice oil poisoning incident. In:
Schechter A, ed. Dioxins and health. New York, Plenum Press, 1994:661-684.
29· Rogan WJ, Gladen Be. PCBs, DDE, and child development at 18 and 24 months.
Annual Reviews in Epidemiology, 1991, 1:40 7-4 13.
30. Winneke G et al. Developmental neurotoxicity of polychlorinated biphenyls
(PCBs): cognitive and psychomotor functions in 7-month old children. Toxicol-
ogy Uters, 1998, 102/103:423-428.
31. Porterfield SP, Hendry LB. Impact of PCBs on thyroid hormone directed brain
development. Toxicological Industrial Health, 1998, 14: 103-120 .
32 . Van Loveren H et al. Report of the Bilthoven symposium: Advancement of epi-
demiological studies in assessing the human health effects of immunotoxic
agents in the environment and workplace. Biomarkers, 1999,4: 135-157.
33· Weisglas-Kuperus N et al. Immunologic effects of background prenatal and post-
natal exposure to dioxins and polychlorinated biphenyls in Dutch infants. Pedi-
atric research, 1995, 38:404-410.
34· Yu ML, Hsin JW, Hsu ce. The immunological evaluation of the Yucheng
children. Chemosphere, 1998,37:1855-1865.
35· Muckle G et al. Prenatal exposure of the northern Quebec Inuit infants to
environmental contaminants. Environmental Health Perspectives, 2001,
109:1291-1299.
3 6 . Vos JG, De Heer C, Van Loveren H. Immunotoxic effects of TCDD and toxic
equivalency factors. Teratogenesis, Carcinogenesis and Mutagenesis, 1997/9 8 ,
1T 2 75- 28 4·

17· EMERGING ENVIRONMENTAL THREATS: ENDOCRINE·DISRUPTING CHEMICALS 223

The paediatric environmental history
CHAPTER 18

Paediatric environmental history-taking

in developing countries1
J. Pronczuk
Protection of the Human Environment, World Health
Organization, Geneva, Switzerland

Introduction
Over the past decade, evidence about the association between the environ-
ment and children's health has increased, as has knowledge about children's
particular susceptibility to environmental exposures. The fetus, the child and
the adolescent may be exposed to physical, chemical and biological risks during
crucial periods of growth and development. These exposures may not only
cause disease in childhood but also have an impact on health during adulthood.
Health professionals are in a key position to identify children at risk, advise
parents on ways to reduce the risk, and recommend actions to policy-makers.
They should be able to recognize and assess the environmental health threats
present in the places where children and adolescents live, learn, play, and work.
They should also know that the threats are greater in low-income populations
and marginalized communities, in degraded environments and when children
and adolescents are living under extreme stress (e.g. during civil unrest, or in
refugee camps).
Front-line health care providers dealing with children's health issues have
specific roles and responsibilities: they should be able to take a detailed history
of environmental exposure that will allow any resulting diseases to be detected
and treated. Health care providers should be able to identify potential exposure
to chemical, physical and biological agents, and should know how these could
cause or trigger respiratory, gastrointestinal or neurological diseases. They
should also be aware of potential reproductive, endocrine and neurobehavioural
toxicity, understand the mechanisms of environmental disease and know the
biomedical techniques available for the study and monitoring of environmental
exposures. This knowledge will enable more effective primary care of the child
and his or her family, improve the quality of medical surveillance, and contribute
to the prevention of environmentally related diseases.

'Reviewed by R. A. Etzel, Department of Environmental and Occupational Health, School of

Public Health and Health Services, George Washington University, Washington, DC, USA.
Additional input provided by: C. Alonzo (Uruguay), N. Chauduri (Canada), L. Corra
(Argentina), I. Makalinao (Philippines), and K. Shea (USA).

227
 In spite of the growing concern about health and the environment, and the
demands of communities for advice on environmental matters from health care
professionals, environmental health is seldom taught in medical and nursing
schools. Health professionals in many countries, especially developing coun-
tries, lack training in and knowledge of the clinical recognition, management
and prevention of diseases linked to the environment. Few clinicians are able
to elicit information about the home, the school or the playground as part of
the demographic and social history.
The need to incorporate training on health and the environment into medical
and nursing curricula is obvious. However, it is likely to be a lengthy process,
and immediately applicable solutions are required. Taking an environmental
history is one way in which health professionals can learn and apply basic envi-
ronmental health concepts immediately.
The paediatric environmental history (PEH) is a tool for identifying and
assessing children's exposure to environmental health threats and for respond-
ing with effective therapeutic and preventive measures. It is also a key
mechanism for collecting case data in a harmonized manner and bUilding
the evidence required for interventions to eliminate or reduce environmental
health threats and improve the quality of life of children within their families
and communities. Furthermore, it provides an opportunity for close interaction
between the health professional and parents, and also among clinicians,
environmental scientists, researchers, educators, policy-makers, and members
of the community.

What is the PEH?

The PEH is a series of basic concise questions that enables health profes-
sionals to identify children's risks of exposure to environmental threats and their
special vulnerabilities.
Some questions cover general issues and are applicable throughout the
world. Others are more specific and should be tailored to the local situation and
needs and to the age group that is being addressed. The questions should be
adapted to the epidemiological trends observed in the population group and
the sociocultural, economic and geographic characteristics of the area where
the child lives. In developing countries, the PEH requires careful consideration
of the specific risk factors that are found in run-down and poor environments
and also the special vulnerability factors that children may have, for example,
malnutrition.

Key areas
1. What are the potential environmental hazards?
• Identify the different hazards that may be present in the environments
where children spend most of their time: physical, chemical and biologi-
cal hazards (including their sources).

228 SECTION IV: THE PAEDIATRIC ENVIRONMENTAL HISTORY

2. How are children exposed?
• In the places where children spend most of their time: home and sur-
roundings, school, playground and recreational areas, streets, fields, work
and other places, in urban and rural settings. Include nearby hazardous
and waste sites.
• Through media that originate or carry the agents: water, air, food, soil and
objects.
• As a consequence of activities such as: eating, drinking, playing, explor-
ing, learning, working, and others.
• Through specific behaviours according to age group or circumstances
(e.g. crawling, tasting and "hand-to-mouth" behaviour in a toddler;
hobbies and drug-taking in adolescents).
]. What are the main effects observed?
• Requires consideration of special vulnerabilities ("windows of
susceptibility") .
• During different periods of development: in utero, postnatal period,
toddler, infant, school-age and adolescence.
• Encompasses clinical and subclinical effects on organs, systems or func-
tions, and on the development of the child or adolescent.

Developing and using the PEH questions

The questions should be prepared locally, taking into consideration the three
key areas mentioned above. They should address the main environmental
threats present in the places where children spend most of their time, the tox-
icants and pathologies most commonly encountered, and unhealthy behaviours
and conditions observed.
The harmonization of these questionnaires in the health sector offers a
number of advantages. First, the comparability of the data collected offers the
potential for cooperative research studies and publication of observations. Sec-
ondly, there are increased facilities for generating reports (e.g. annual reports
on the status of children's environmental health, use of indicators of children's
environmental health). Thirdly, increased communications, sharing of experi-
ences and awareness about local environmental problems may facilitate action,
e.g. to find common solutions.
The harmonization of the PEH requires a common terminology and case
definitions. Electronic data entry offers the possibility of creating a database that
could provide valuable information for interventions and for the follow-up of
environmental health problems in the area.
The preparation of the harmonized questionnaire requires consultation
among health professionals and agreement on the basic set of questions. It also
requires close collaboration with other sectors, such as environment, education
and labour, and with the community and decision-makers (in order to ensure
completeness and facilitate communications). A list of the potential issues to

18. PAEDIATRIC ENVIRONMENTAL HISTORY·TAKING IN DEVELOPING COUNTRIES 229

address in the PEH questions for developing areas is provided in Appendix 18.1.
This list may be used as a basis for evaluating the main environmental health
risks to children in the area and for preparing a locally adapted PEH.

Who takes the PEH, when and how?

Health care professionals dealing with infants, children and adolescents
can take the PEH. They may be the paediatricians, family doctors, primary
health care workers or nurses dealing with children and adolescents, or the res-
idents and medical and nursing students and midwives who care for pregnant
women.
The decision on who takes charge will depend on the characteristics of
the health system and the availability of health personnel. In some instances,
part of the environmental history-taking may be done by a social worker or envi-
ronmental officer who can visit the home, school, playground or other places
where children spend their time. Environmentally trained staff in health care
facilities would offer tremendous advantages, as they would be in a position to
identify and assess the potential threats in the child's environment, inform
the health care providers and authorities, and educate parents, teachers and
communities.
A PEH may be taken when children, whether symptomatic or asymptomatic,
are seen at a medical facility or during a home visit. It is crucial to take a PEH
when children with acute or chronic disease come to emergency rooms, out-
patient clinics, primary health care centres or private medical offices. It is also
a highly significant preventive tool when used during routine health surveillance
visits.
In some special cases, the PEH may be a key tool for addressing public
health problems, such as clusters of paediatric disease, uncommon cases or
symptoms, epidemics of unknown origin, or changes in epidemiological trends
in a given area.

How much time should be devoted to the PEH?

A basic set of questions should be part of the normal medical history-taking,
but in special cases, when an environmental cause or trigger of disease is sus-
pected, more time and patience will be required.
Taking a PEH requires the clear formulation of specific questions to parents,
children (depending on age) and carers. If possible, a home audit should be
made by parents and carers and a simple questionnaire completed on the char-
acteristics of the places where children spend most of their time, their activities
and their behaviour.

Barriers to the PEH

The main obstacles to the use of the PEH include: (a) lack of awareness of
health professionals and decision-makers about the importance of environ-

SECTION IV: THE PAEDIATRIC ENVIRONMENTAL HISTORY

 mental factors, (b) lack of training
and information on environmental
South Texas Environmental Education
health issues, (c) limited time avail-
and Research Center (STEER)
able for the paediatric consultation, A good example of home audits is found in the
(d) overstretched health facilities South Texas Environmental Education and
and lack of personnel, and (e) lack Research Center (STEER) training programme
of motivation. These barriers may used by medical and nursing students at the
be overcome by incorporating envi- University of Texas Health Science Center in San
ronmental health into the curricula Antonio. The STEER programme sends students
of medical and nursing schools, out on "environmental health house calls", tar-
increasing awareness of health geting houses that have children with. asthma.
authorities, disseminating informa- Families in the area with children who have
tion and strengthening health facili- asthma volunteer to open their homes to the stu-
ties. Also, health workers in training dents. Under professional supervision, the stu-
could carry out home visits. Many dents visit the family home three times,
developing countries require newly observing its characteristics, identifying poten-
graduated medical students to work tial "triggers" and learning about the relationship
for some years in a rural setting between illness and the environment of their
before practising in urban areas, patient. This innovative programme is described
and could use these graduates to in Case Study 20, page 345.
promote the use of environmental
home audits in rural areas.

18. PAEDIATRIC ENVIRONMENTAL HISTORY-TAKING IN DEVELOPING COUNTRIES 23

1
APPENDIX 18.1

Taking a paediatric environmental

history in developing areas
Main issues for consideration in developing a local harmonized
questionnaire
Places
1. Where does the child live?
Home
Is it a separate dwelling, a multiunit dwelling, a temporary structure or some-
thing else?
What is the family structure, how many members are there?
Socioeconomic status of the household?
What is the building made of? (Wood, brick, mud, cardboard, ... ?)
What is the age of the building?
Is there mould on the walls?
How well ventilated and lit is it?
Are there any odours?
Has there been any recent painting or refurbishing?
Do family members smoke at home? What do they smoke? How
much?
Are pesticides used indoors? How?
Are there cockroaches? Mites? Rats?
Are there pets (dogs, cats, birds) or other animals?
How often is the place cleaned?
Which chemicals are used for cleaning?
Where and how is the cooking done?
How is the home heated?
Type of stove, exhaust and fuels used (see section 12 below)
Type of water supply (see section 11 below)
Access to sanitation (see section 5 below)
Does the child have a place of his/her own?
Is it shared? With whom?
Is the home a workplace too?

Location
Is the home in an urban, periurban or rural area?
Is it in a shanty town?
Is it next to a sea, lake or water extension?
Is it near a waste site? industrial site? mining area? transformers? high-
tension electric line?
Is it in an area of high-density traffic?

SECTION IV: THE PAEDIATRIC ENVIRONMENTAL HISTORY

 If in a rural area, are pesticides used locally? How and when?
Where are agrochemicals stored?
Are there any particular poisonous animals?

Street
If the child lives on the street-where does he/she sleep?
Who else lives in the group?
What are the characteristics of the living place?

2. Where the child plays

Outdoors
Where is the outdoor playground?
Is there protection from excessive sun radiation? Are there trees?
Is it a high-risk area? (e.g. near a creek, pond, ravine ... )
Is it near an industrial area? Mining area? High-traffic area? Agricultural area
where pesticides are being applied?

Indoors
The indoor playground-same questions as for Home-see section 1 above)
Hobbies (see section 15)

3· Where the child learns

Same questions as for Home (section 1) applied to:
- child care centres;
- school;
- community house;
- workshop.

4· Where the child works

Characteristics of the place/activity:
- cottage industry;
- factory;
- rural area, plantation, farm;
- street (street vendors);
- waste sites (scavengers);
- manufacturing processes;
- mining;
- textiles;
- chemicals used.

5· Sanitation and hygiene (in all places covered by sections 1-4)

Sanitation facilities
Latrines

18. PAEDIATRIC ENVIRONMENTAL HISTORY-TAKING IN DEVELOPING COUNTRIES 233

 Wastewater irrigation
How is hygiene maintained?
Type of water treatment plant

Risks (chemical, physical, biological)

6. Exposure to chemicals
Pesticides?
Lead, mercury, arsenic, fluoride?
Solvents?
Gases and fumes?
Persistent organic pollutants?
Others (see section 24 below).

7. Exposure to radiation
Is the child overexposed to ultraviolet radiation? Are there any effects on the
skin? On the eyes? Phototoxicity? Photoallergy?
Is the child exposed to ionizing radiation: X-rays, gamma rays, radon?
Did the child receive X-rays while in the womb?
What are the possible sources of exposure (including diagnostic proce-
dures) ?
Is the child exposed to electromagnetic fields?

8. Noise exposure
Is the child exposed to undesirable sounds? During the day or night? At
school? Home? Work? Recreational area?
Have the sounds affected the child's health and well being?
Possible sources of noise:
- traffic;
- work, industry;
- music;
- airport.

9. Exposure to adverse and extreme environmental conditions

Is the child stressed by extreme conditions?
_ extreme/adverse climatic conditions (e.g. mountains, hot or cold
weather, storms, weather disaster);
- drought;
- floods;
- environmental degradation;
- technological disasters;
- war;
_ social conflict and postconflict circumstances;

SECTION IV: THE PAEDIATRIC ENVIRONMENTAL HISTORY

234
 refugee camp;
imprisonment.

10. Exposure to vector-borne diseases

Is the child exposed to parasitic or infectious diseases?
- malaria;
- filariasis;
- onchocerciasis;
- schistosomiasis;
- trypanosomiasis;
- leishmaniasis;
- dracunculiasis;
- hookworm;
- Toxocara canis;
- trachoma;
ringworm;
arboviral diseases (dengue, yellow fever, encephalitis, other).

Media
11. Water
Is there access to a safe water supply?
What are the water pipes made of?
Is there a home treatment system?
How are the water sources protected?
Is drinking-water stored in the house? How?
Are there potential sources of contamination? (chemicals, germs, parasites,
radionuclides)
Specific problems: nitrites and nitrates, arsenic, fluorides, lead.
Are there risks posed by recreational waters?
Is the recreational water near an industrial site? A petrochemical plant?
Is there pesticide pollution?
Water quality of ponds, dams and pools
Exposure to algal blooms.

12. Air quality

Sources of indoor air pollution:
- combustion products (carbon monoxide, nitrogen dioxide, sulfur
dioxide);
household materials (volatile organic compounds, hydrocarbons,
alcohols, ketones);
moulds (indoor);
allergens (cockroaches, dust mites);

18. PAEDIATRIC ENVIRONMENTAL HISTORY·TAKING IN DEVELOPING COUNTRIES 235

 pets and other animals;
environmental tobacco smoke;
asbestos, polyurethane, flame-retardants;
- ventilation and air-conditioning.
Sources of outdoor air pollution:
coal use, power generation, motor vehicles;
haze (e.g. from forest fires);
burning in the open;
incinerators;
- waste sites;
- use of pesticides.
Types of pollutants: sulfur compounds, ozone, particulate matter, carbon
monoxide, nitrogen dioxide, volatile organic compounds, lead, etc.

'3. Food and diet

Is the child exposed to chemical food contaminants?
- pesticides and persistent organic pollutants;
_ food additives and preservatives (colouring, flavouring and other
agents added intentionally);
- breast milk contaminants;
_ toxins (mycotoxins, pyrrolizidine alkaloids, aquatic microorganisms,
toxins in fish and seafood);
pathogens (viruses, bacteria, toxins, parasites);
- hormones;
- pesticides.
Are dietary supplements used, such as vitamins and minerals?
Is food genetically engineered?

'4. Clothing and objects

Quality and materials of:
- plastic toys;
- wooden painted toys;
furry toys;
pacifiers;
clothing (textiles, colour, flame retardants);
diapers;
school and art materials (paint, crayons).

Activities
'5. Hobbies
Painting-paint and solvents used?
Model-building-glue and solvents used?
Pottery-pigments, paints used?

SECTION IV: THE PAEDIATRIC ENVIRONMENTAL HISTORY

 Gardening-pesticides used?
Woodwork-chemicals used?

16. Activities
Eating habits (type of diet, food quality).
Drinking habits (alcohol use and abuse, soft drinks)
Playing habits
Learning habits
Working habits
Scavenging (time spent near garbage)
Exploring
Testing (trying drugs, eating unknown berries, pica)

17. Sports
Type of sport
Sports area (see section 2)
Injuries (see section 23)
Toxic exposures (see section 24)
Use of energizing drugs, application of poultices?

Behaviour
18. Personal hygiene and habits
How often does the child bathe? How? Where? With what (type of
soap/cleansing product)?
How often are the hands and face washed?
Are the clothes washed regularly?
What type of diapers are used?
Does the child have lice? How is the infestation treated?
Does the child play on the floor? Carpet?
How and how often is the child's bedroom and play area cleaned?
Which chemicals are used to clean the home?
Does the child have pica? Does the child have hand-to-mouth activities?

19. Cultural history

Use of alternative medicines or cosmetics
Cultural practices
Religious practices
Traditions involving the use of chemical substances.

20. Transport
What transport does the child use?
individual or collective;
- bicycle;

18. PAEDIATRIC ENVIRONMENTAL HISTORY·TAKING IN DEVELOPING COUNTRIES 237

 - motorcycle;
- horse;
- other.
Characteristics of bus (street or school)? Bus stop? Characteristics of car,
truck?

Vulnerability (during different periods of development)

21. Special vulnerability
Age: "windows of vulnerability"-in utero, postnatal period, toddler, infant,
school-age, adolescence.
Previous diseases (respiratory, gastrointestinal, neurological, renal, hepatic,
other).

Clinical effects
22. Specific health problems that may have an environmental cause or trigger
Asthma
Bronchitis, bronchiolitis
Pneumonia
Allergies
Immune disorders
Diarrhoea
Polyneuropathy
Attention deficit disorders
Learning disorders
Altered behaviour
Skin effects: neurodermatitis, eczema
Urinary infection
Early puberty
Cancer (brain, leukaemia, other)
Multiple chemical sensitivity syndrome
Sudden infant death syndrome
Poisoning (lead, mercury, pesticides, carbon monoxide) (see section 23)
Drug abuse, overdose
Silicosis
Arsenicosis
Fluorosis
Home accidents: lesions, sequelae
Malformations
Sterility in adolescents and young adults
Repeated abortions in adolescents and young adults

SECTION IV: THE PAEDIATRIC ENVIRONMENTAL HISTORY

 23. Accidents and injuries
Has the child suffered from the following?
- Traffic-related injuries and diseases
Home accidents
Risk of drowning and water-related accidents
Exposure to fire and fumes; burns
Exposure to electricity
- Sports-related injuries
- Exposure to violence (in the home)
- Animal bite (cat, dog, other).

24. Poisonings
Has the child been poisoned? When?
Was the poisoning accidental, intentional or occupational?
Was the exposure acute or low-level and chronic?
Where did it occur? (home, school, street, workplace, ... )
What was the cause?
- pesticide (organophosphorus, organochlorine, rodenticide, herbi-
cide, fungicide);
metal (lead, arsenic, mercury, cadmium, iron);
- household product (solvent, kerosene, detergent);
- pharmaceutical (analgesic, cough syrup, psychoactive drug, adulter-
ated medicine);
- drug abuse;
- alcohol;
- traditional medicine (herbal and other preparations).

25. Envenoming
Has the child been stung or bitten? When? Where?
snake
scorpion
spider
bee or wasp.

18. PAEDIATRIC ENVIRONMENTAL HISTORY-TAKING IN DEVELOPING COUNTRIES 239

CHAPTER 19

The clinical environmental history:

experience in the USA1
S. J. Balk
Children's Hospital, Montefiore, New York, USA

A child's surroundings-the physical environment-may have an impact on

his or her health. Numerous chemical toxicants have been shown to affect chil-
dren's health and development. Paediatricians and other clinicians who give
medical care to infants, children and adolescents should enquire about the
child's surroundings in order to uncover potential chemical and physical
hazards, and to provide guidance about avoiding or reducing them. Questions
about the child's environment should be an integral part of the routine health
history, along with questions about nutrition, sleep, development, and injury
prevention.
Paediatricians can include environmental health questions during routine
health care visits (check-ups). In addition, when a child presents with symp-
toms of illness, clinicians should consider environmental etiologies as part of
the differential diagnosis (1).

Integrating environmental health questions into the routine

health visit
A few basic questions about the child's surroundings (the dwelling, child
care setting or school setting) are integral to a complete health history. These
are outlined below.

1: Where does the child live or spend time?

Children may spend time in their own home or the home of a child care
provider or babysitter, and at school. Playtime may be spent in a playground.
Infants and young children often spend 80-90% of their time indoors, either in
their own home or in a child care (day-care) setting.
Important aspects of the indoor setting are described below.

Type of dwelling
Children generally live with their family in an individual home, apartment,
or mobile home. In private homes, children may be exposed to lead or asbestos.

'Based on the Handbook of Pediatric Environmental Health of the American Academy of

Pediatrics.
They may encounter radon in basements or the ground floor. Children living in
mobile homes may be exposed to formaldehyde, a respiratory and dermal irri-
tant commonly found in particle board and pressed wood materials used in
these dwellings.

Age and condition of the dwelling

Homes and apartment buildings, especially those built many years ago, may
contain lead paint. As paint ages, it may peel, flake or "chalk", particularly from
poorly maintained surfaces and those that are subject to friction, such as
windows. Young children may be exposed to deteriorated lead paint through
normal hand-to-mouth activity. Homes that have been damaged by floods or
leaks may have problems with growth of mould. Homes built to conserve energy
("tight" homes) may have poor ventilation, exposing occupants to high levels
of indoor air pollutants.

Ongoing or planned renovation

Often parents renovate a room in preparation for the birth of a baby, or
shortly after the baby's birth, possibly exposing the pregnant woman, or the
infant, to lead or asbestos.

Sources and uses of heat

Parents may heat the home, fully or in part, using wood burned in a wood
stove or fireplace. Respiratory irritants such as nitrogen dioxide (N0 2 ), particu-
lates and polycyclic aromatic hydrocarbons are found in wood smoke. Children
exposed to smoke may experience the onset or worsening of respiratory symp-
toms especially when there is poor ventilation or the stove or fireplace is poorly
maintained.
Natural gas cooking stoves are used in over half of homes in the USA.
Parents whose homes are inadequately heated may use the stove for supple-
mental heat in the winter, exposing children to nitrogen dioxide released during
the combustion of natural gas.
Carbon monoxide (CO) may be released from improperly functioning stoves,
fireplaces and furnaces, with potentially fatal results.

Pesticides
Pesticides may be used to control indoor infestations of insects such as ants
and cockroaches. Outdoors, pesticides may be used to control insects, herbi-
cides to control weeds and unwanted plants, and fungicides to control moulds.
Children are exposed through inhalation, ingestion and dermal absorption of
these chemicals as they crawl or play on treated surfaces. Health workers should
determine whether parents use pesticides and similar products, make them
aware of potential dangers, and encourage them to use safer methods of pest
and weed control.

19. THE CLINICAL ENVIRONMENTAL HISTORY: EXPERIENCE IN THE USA

 Outdoor environment-proximity to hazards in the community
Health workers should be aware of outdoor hazards in their community.
Lakes and streams used for fishing may be contaminated with chemicals;
children may play near contaminated dump sites and waste sites or be
exposed to pesticides in fields. Renovations may result in the release of toxic
contaminants.

Cultural uses of toxic materials

Health workers should take into account patients' cultural backgrounds. For
example, some children from Central America may be exposed to elemental
mercury, which is sprinkled in the home during a religious ritual performed by
practitioners of Santeria.

School exposures
Pollutants may be present in school buildings, especially those that are old
and deteriorating. Pollutants may be released during school renovations. In
addition, children may be exposed to toxic materials during certain school activ-
ities, such as arts and crafts.

Populations particularly at risk

In the USA, certain communities may be disproportionately at risk for envi-
ronmental exposures. These are likely to be members of ethnic minority groups
and low-income populations. Because children are also disproportionately
affected by environmental exposures (see Chapter 2), children from poor and
minority groups may be the most affected by environmental toxicants. For
example, in 1991-94, lO% of children under 6 years from low-income families
had elevated blood lead levels (greater than lOflgjdl), compared with 1% of chil-
dren from high-income families; more than 11% of African-American children
had elevated lead levels compared with 4% of Hispanic children and 2·3% of
white non-Hispanic children (2).
Some ethnic minorities may be more exposed to certain contaminants in
food because of dietary habits. For example, Native Americans and subsistence
fishers are likely to be more exposed to contaminants in fish, such as mercury
and polychlorinated biphenyls. Children of agricultural workers may be more
exposed to pesticides, either directly in fields or brought home on parents' cloth-
ing and shoes.

2: Is the child exposed to environmental tobacco smoke through parental

smoking? Is the child or teenager a smoker?
In the USA, over 40% of children aged between 2 months and 11 years live
with a parent who smokes (3). Environmental tobacco smoke (ETS, or "second-
hand smoke") comprises the smoke exhaled by the smoker ("mainstream
smoke") and the smoke from the smouldering end of a cigarette, pipe or cigar

SECTION IV: THE PAEDIATRIC ENVIRONMENTAL HISTORY

("sidestream smoke"). ETS is composed of more than 3800 chemical com-
pounds. It contains fine particulates (less than 2.Sllm in diameter, a size that
reaches the lower airways) in concentrations that may be 2-3 times that of the
outside air. ETS primarily affects the respiratory tract of children. Children
exposed to ETS have higher rates of lower respiratory infections, more persis-
tent middle-ear effusions, and more frequent and more severe asthma exacer-
bations. Infants exposed to ETS have a higher incidence of sudden infant death
syndrome ("cot death"). Children whose parents smoke are more likely to
become smokers themselves.
Paediatricians, or other physicians who care for children, can play an impor-
tant role in counselling parents who smoke. They may be the only medical staff
that parents visit regularly. Thus they have opportunities to help eliminate or
decrease children's exposure to ETS by helping parents to quit smoking. The
first step is to ask about smoking habits; these questions should become an
integral part of the routine paediatric health history.
In 2000, the US Public Health Service published its clinical practice
guideline, Treating tobacco use and dependence, which describes how even
brief counselling (3 minutes or less) can be effective in increasing quit rates
(4). A "s As" approach ("ask, assess, advise, assist, arrange follow-up") is
suggested:

• Paediatricians should ask parents about smoking habits.

• If parents smoke, paediatricians should assess willingness to quit smoking
and should advise parents who smoke to quit.
• If the parents are willing, paediatricians should assist them by providing
counselling and information about medications, such as nicotine replace-
ment therapies (N RT).
• They should arrange follow-up for this issue on future visits; the issue
should be addressed at every visit.

Pharmacotherapies, including N RT (such as nicotine patches and gum) and

oral amfebutamone, have been shown to increase quit rates. Paediatricians
should become familiar with these approaches in order to discuss them with
parents.
All smokers should be encouraged to quit. It is important to ask
about reasons for tobacco use (such as for energy, tactile sensation, because
smoking is pleasurable, to relax, to relieve cravings, or because it is a habit)
in order to suggest specific coping strategies. The paediatrician can then
ask questions directed towards determining whether the smoker is ready to
quit. These questions involve the "stages of change". In the pre-contemplative
phase, the smoker talks about quitting in an abstract way, without having
any plans to do so. In the contemplative phase, the smoker begins to seriously
consider quitting within the next six months, but has no plans to quit, and

19. THE CLINICAL ENVIRONMENTAL HISTORY: EXPERIENCE IN THE USA 243

has not had one tobacco-free day within the past year. In the preparative phase,
the smoker plans to quit in the next 6 months, and has had a 24-hour quit
attempt in the past year. Strategies appropriate to each phase have been
summarized (4).
Some 90% of smokers begin to smoke as teenagers. The average smoker
begins to smoke at age 12; 3000 children and adolescents in the USA begin
smoking each day. Obtaining accurate smoking histories from children and
teenagers is often more challenging than obtaining similar histories from adults.
They may be reluctant to discuss smoking with paediatricians. Their concerns
about maintaining confidentiality must be addressed. With children and young
teenagers, a direct approach to questioning may be awkward; clinicians may
first have to ask about other lifestyle matters, such as hobbies, sports activities
and friends, before asking about smoking. It may help to ask first about the peer
group-HDo any of your friends smoke?"-before asking directly if the patient
smokes. For patients who are not yet smokers but have a favourable attitude
towards smoking, clinicians can point out the influence of tobacco advertise-
ments on young people, using magazines with cigarette advertisements as
teaching aids. High school students usually have the capacity to understand the
short-term and long-term health consequences of smoking. Short-term conse-
quences include cough and sputum production; shortness of breath; reduced
athletic performance; recurrent upper respiratory infections; stained teeth and
fingers; bad breath; risk of fires; and exposing others, including younger sib-
lings, to ETS. The cost of cigarettes may also serve as a deterrent to the teenage
smoker (5).
Strategies adopted at the consultation can aid in history-taking and smoking
cessation efforts. Such interventions include the following:

(1) Systematic assessment of patient's or parent's smoking: smoking status can be

added as an item on the office intake form filled out by the parent or teenage
patient. Office systems, such as tobacco-use status stickers or adding
tobacco use as a vital sign, are helpful in reminding clinicians to gather this
information.
(2) Involving staff members in smoking cessation history-taking and education:
because cessation rates increase with the number of contacts a patient has
with staff, the goal is to have all professionals, including receptionists, ask
about smoking as part of the visit. Nurses and health educators can be a
vital part of this effort.
(3) Providing patient education materials: materials are available free or at low
cost from local affiliates of the American Cancer Society, American Heart
Association, American Lung Association, and the National Cancer Institute's
Cancer Information Service. Many agencies also provide self-help materials.
(4) Utilizing local resources: paediatricians can compile a list of local agencies or
programmes to be given to motivated patients.

244 SECTION IV: THE PAEDIATRIC ENVIRONMENTAL HISTORY

(5) Office policy: the office should have signs indicating that the office has a no-
smoking policy. Staff should not smoke in or near the office. There should
be no literature with pro-smoking messages in the waiting room.

3: Is tap water or well-water used?

Whether the supply of water is safe is generally well known locally. Most
industrialized countries provide universal access to safe drinking-water. Many
developing countries, however, do not have the necessary infrastructure and
have not overcome the barriers to providing adequate supplies of safe water to
their citizens. Often, water is safe in the cities but not in rural or peri urban sites.
In addition, even where water is considered safe, contamination, for example
with lead and nitrates, is still a potential hazard. Paediatricians should enquire
about the source of water. Tap water used to reconstitute infant formula, or given
directly to the infant, may be contaminated with bacteria or chemicals, such as
lead from pipes. To avoid possible contamination, parents can consider boiling
water or testing it for specific contaminants. Alternatively, in the morning or
whenever the water has been standing for hours in the pipes, parents may run
the water for two minutes, or until cold, before giving it to an infant.
Well-water or water in rural sites, in particular, may be contaminated with
high levels of nitrates, which may result in methaemoglobinaemia in young
infants. Parents who use well-water should be advised to have the water tested
for nitrates before using it to reconstitute infant formula.
Boiling water for one minute is sufficient to kill microorganisms. Over-
boiling of water should be discouraged as this will concentrate contaminants
such as lead and nitrates.

4: Is the child protected from excessive sun exposure?

The incidence of all skin cancers, including squamous cell carcinoma, basal
cell carcinoma, and cutaneous malignant melanoma, has risen dramatically in
the USA in recent years. The incidence is highest in persons with light skin and
light eyes, those who burn easily rather than tan, and those living closer to the
equator where the sun's rays are strongest. The ultraviolet (UV) spectrum of
sunlight is implicated in the development of skin cancer. Squamous cell and
basal cell carcinomas appear to be related to chronic cumulative sun exposure.
Malignant melanoma is related to the occurrence of blistering sunburn in child-
hood. As 80% of lifetime sun exposure occurs during the first 18 years of life,
paediatricians should enquire about sun exposure in order to advise about pre-
ventive measures.

Prevention advice
(1) Avoid exposure. Young infants should be kept out of direct sunlight when-
ever possible because of the possibility of heat stroke. Infants and children
should be dressed in clothing that is cool and comfortable, such as light-

19. THE CLINICAL ENVIRONMENTAL HISTORY: EXPERIENCE IN THE USA 245

 weight cotton shirts and trousers, which offer some protection. Lycra shirts,
which let in little light, are gaining popularity in Australia, which has the
world's highest incidence of melanoma. A hat with a brim, facing forwards,
offers some protection for the face and eyes. For older children and ado-
lescents, activities should be timed to avoid peak sun exposure hours
(lOhoo to 16hoo).
(2) Consulting the Ultraviolet Index. The Ultraviolet (UV) Index was developed
in 1994 by the US National Weather Service in consultation with the US Envi-
ronmental Protection Agency and the Centers for Disease Control and Pre-
vention. The UV Index predicts the intensity of UV light for the following day.
The UV Index may be found in the weather section of newspapers, and is
sometimes discussed during weather reports on the radio and television.
(3) Use sunscreen. Sunscreens prevent or diminish sunburn. There is contro-
versy about the ability of sunscreens to prevent melanoma; some studies
suggest that sunscreen use, by allowing increased time in the sun, increases
the risk of melanoma. Nevertheless, using sunscreen with frequent reappli·
cations is still recommended as part of a programme of sun avoidance for
children and adults.
(4) Protect eyes. A hat with a brim can reduce exposure to UV by 50%. Sun-
glasses should be worn when the sun is strong enough to cause sunburn.
Parents should choose sunglasses that block out 99% of UV rays.

5: Are there any hazards relating to occupation of adolescent or parent?

Parental occupations
Chemicals and dusts in the workplace may be brought into the home on
parents' skin, clothes, shoes and belongings if the parent does not shower and
change clothes at work. These substances may also contaminate cars. Pesti·
cides may be brought home by agricultural workers. Lead poisoning has been
described in children whose parents worked in the lead industry (6); elevated
mercury levels were found in children whose parents were employed in a
mercury thermometer plant (7); asbestos-related lung diseases, including fatal
malignant mesothelioma, have been reported in family members of asbestos
workers (8). Paediatricians should ask about mothers' and fathers' occupations
(9). They should encourage parents employed in dangerous occupations to
shower before leaving the work site and to leave potentially contaminated items
there. In addition, children should not be allowed to play in areas where parents
work with toxic substances, such as artists' paints that may contain lead or other
harmful substances.

Employment among adolescents

Teenagers may be employed, allowing them to accumulate skills, earn
money, and assume responsibility. More than 80% of high school students
in the USA are employed as part of their normal schedule. These teenagers

SECTION IV: THE PAEDIATRIC ENVIRONMENTAL HISTORY

may be exposed to hazardous work conditions, including chemical exposures
(10).
Many countries have established laws that regulate employment of children.
These laws often set standards for minimum ages for employment, maximum
daily and weekly work hours permissible, prohibition of certain types of work,
prohibition of night work, and registration of minors for employment. Often,
children must visit a physician to obtain a certificate of physical fitness before
becoming employed. This provides the paediatrician with the opportunity to
inquire about the nature of employment, whether paid or voluntary. In the infor-
mal sector, children work without such support and infrastructure. Questions
about employment should also be part of the complete adolescent health
history.
Children and teenagers should be asked about where they work, how many
hours, and whether they are exposed to any chemicals, dusts or metals. Those
with chronic illnesses may be susceptible to hazards in certain job situations
(such as a previously well-controlled patient with asthma working as a server in
a restaurant, whose condition is exacerbated after exposure to cigarette smoke
in the restaurant).
Paediatricians should talk to parents about the potential risks and benefits
of their child's employment. Parents may be unaware of the nature of the child's
job, especially possible hazards.

How to understand children's medical history, the surroundings,

and the link between observed effects and potential
environmental causes
Because illnesses or symptoms may result from environmental exposures,
health care workers should consider environmental etiologies in their differen-
tial diagnoses (Goldman, Shannon & Wolff, Personal Communication, 1999).
Asthma, upper respiratory symptoms and middle-ear effusion can result
from exposure to environmental tobacco smoke. Asthma and allergies can
result from exposure to certain indoor air pollutants. Recurrent abdominal pain,
constipation, irritability, seizures and unexplained coma can result from lead
poisoning. Headaches may be the result of acute or chronic exposure to carbon
monoxide from improperly vented heating sources, formaldehyde, or chemicals.
Idiopathic pulmonary haemorrhage in young infants has been linked to expo-
sure to certain toxigenic moulds.
When faced with an illness or symptom that may have an environmental
etiology, the health worker should give careful consideration to all aspects of
the child's physical surroundings, incorporating the areas detailed in question
1 above. The environmental etiology of illness is not always obvious. For
example, an 8-month-old girl with persistent hypertonicity was initially thought
to have cerebral palsy. Her paediatrician, not satisfied with the diagnosis, dis-
covered that her symptoms were related to chronic poisoning with diazinon, an

19. THE CLINICAL ENVIRONMENTAL HISTORY: EXPERIENCE IN THE USA 247

organophosphorus insecticide that had been sprayed inside the home. Symp-
toms resolved when the family moved out of the home (11). In another instance,
acrodynia (painful extremities, a syndrome in children associated with mercury
exposure) was found to be associated with exposure to latex paint to which
mercury had been added as a fungicide (12).
Symptoms may be nonspecific or common to other medical problems. A
history of environmental exposure may be missed unless the clinician seeks a
specific history (13). It is particularly important to obtain this history if the con-
dition is not typical or is unresponsive to usual treatment. Questions should
cover:

• Location: whether symptoms are worse or better in a particular location

such as home, school or child care setting.
• Time: whether symptoms are worse or better at certain times, such as at
weekends (when the child is at home), or during the week (when the child
may be out of the home in a child care setting, school or work).
• Particular activities: symptoms may be worse when the child engages in
a hobby or other activities that result in certain exposures.
• Common symptoms: whether other children or adults are experiencing
similar symptoms, suggesting a common exposure.

References
1. Etzel RA, Balk SJ, eds. The handbook of pediatric environmental health. Elk Grove
Village, IL, American Academy of Pediatrics, 1999.
2. Centers for Disease Control and Prevention. Update: blood lead levels-United
States; 1991-1994. Morbidity and Mortality Weekly Report, 1997, 46:141-
146.
3. Centers for Disease Control and Prevention. Strategies for reducing exposure to
environmental tobacco smoke, increasing tobacco use cessation, and reducing
initiation in communities and health care systems. Morbidity and Mortality
Weekly Report, 2000, 49(RR12):1.
4. Treating tobacco use and dependence. A clinical practice guideline.Journal of the
American Medical Association, 2000, 283:3244-3254.
5. Heymann RB. Tobacco: prevention and cessation strategies. Adolescent Health
Update, 1997, 9:1-8.
6. Watson WN, Witherell LE, Giguerre Gc. Increased lead absorption in children of
workers in a lead storage battery plant. Journal of Occupational Medicine, 1978,
20:]59-76l.
7. Hudson P) et al. Elemental mercury exposure among children of thermometer
plant workers. Pediatrics, 1987, 79:935-938.
8. Kilburn KH et al. Asbestos disease in family contacts of shipyard workers. Amer-
ican Journal of Public Health, 1985,75:615-617.
9. Chisolm )). Fouling one's own nest. Pediatrics, 1978, 62:614-617.

SECTION IV: THE PAEDIATRIC ENVIRONMENTAL HISTORY

 10. Pollack S et al. Pesticide exposure and working conditions among migrant farm-
worker children in western New York State. 1990 American Public Health Associ-
ation Annual Meeting Abstracts: 317.
11. Wagner SL, Orwick DL. Chronic organophosphate exposure associated with tran-
sient hypertonia in an infant. Pediatrics, 1994, 94:94-97.
12. Centers for Disease Control and Prevention. Mercury exposure from interior latex
paint. Morbidity and Mortality Weekly Report, 1990, 39: 12 5.
13· Agency for Toxic Substances and Disease Registry. Case studies in environmental
medicine: taking an exposure history. Atlanta, GA, US Department of Health and
Human Services, 199 2 .

19· THE CLINICAL ENVIRONMENTAL HISTORY: EXPERIENCE IN THE USA

249
Taking action
CHAPTER 20

Taking action to protect children from

environmental hazards1
s. Boese-O'Reilly
Children's Environmental Health Professional, Munich,
Germany

M. K. E. Shimkin
MShimkin Consulting, Alexandria, USA

In protecting children's environmental health, every level has a role to play,

from members of the family and community to local, regional, national and
international bodies. Everyone has a part in offering children the best chances
in life, and in making a difference in how they live, grow, play, learn, develop
and eventually work and become productive members of society. While note-
worthy accomplishments at all levels reach a variety of people, much remains
to be done to sustain progress and intenSify change. Certain countries have
leapt into action while others hardly know of the concern. Global movements
will narrow gaps between countries in the level of effort and involve progres-
sively more regions of the world, enhancing opportunities for children in all
countries to have healthy and productive lives.

Families, carers and teachers

Parents, child care providers and teachers can make a tremendous differ-
ence in the health of children through actions at home, in the child care setting
and at school. These adults can provide role models for healthy behaviour and
teach and guide children to create healthy environments. Efforts to motivate
teachers in Chinese schools to refrain from smoking, for example, have
improved the quality of indoor air in the schools and may influence children not
to smoke. "Tools for Schools" is a programme in the USA that teaches children,
teachers and administrative staff to conduct indoor air audits in schools and
take action to remedy sources of pollution. In Australia, many schools are
joining the SunSmart Schools Program, which involves the whole school com-
munity in protecting children from overexposure to the sun. Parents, child care
providers and teachers can find success acting alone or with others to improve

'Reviewed by M. Berger, Office of Children's Health Protection, Environmental Protection

Agency (EPA), Washington, DC, USA; I. Corra, Asociaci6n Argentina de Medicos por el
Medio Ambiente (AAMMA), Buenos Aires, Argentina; J. Pronczuk, Department for the Pro-
tection of the Human Environment, World Health Organization, Geneva, Switzerland.

253
 children's environmental health. Individual and local level effort will make a dif-
ference for children and may have greater impact than anticipated.

Ideas for action at the local level

The United States Environmental Protection Agency has developed "Tips to
protect children from environmental risks" (1), which have been disseminated
through doctor's offices, schools and on the Internet. These are practical, action-
oriented steps that parents and carers can take to protect children. Any
individual or group could develop similar tips and share them as part of a
community education effort, focusing on local issues of greatest concern for
children's well-being. WHO has put together messages for creating healthy envi-
ronments for children as shown in Fig. 20.1 (2).

Tips to protect children from environmental risks a

Help children breathe easier
• Don't smoke and don't let others smoke in your home or car.
• Keep your home as clean as possible. Dust, mould, certain household pests, second-
hand smoke, and pet dander can trigger asthma attacks and allergies.
• Limit outdoor activity on "ozone alert" days when air pollution is especially harmful.
• Walk, use bicycles, join or form carpools, and take public transportation.
• Limit motor vehicle idling.
• Avoid open burning.

Protect children from lead poisoning

• Get kids tested for lead by their doctor or health care provider.
• Test your home for lead paint hazards if it was built before 1978.
• Wash children's hands before they eat; wash bottles, pacifiers, and toys often.
• Wash floors and window sills to protect kids from dust and peeling paint contami-
nated with lead-especially in older homes.
• Run the cold water for at least 30 seconds to flush lead from pipes.

Keep pesticides and other toxic chemicals away from children

• Store food and trash in closed containers to keep pests from coming into your home.
• Use baits and traps when you can; place baits and traps where kids can't get them.
• Read product labels and follow directions.
• Store pesticides and toxic chemicals where kids can't reach them-never put them
in other containers that kids can mistake for food or drink.
• Keep children, toys, and pets away when pesticides are applied; don't let them play
in fields, orchards, and gardens after pesticides have been used for at least the time
recommended on the pesticide label.
• Wash fruits and vegetables under running water before eating-peel them before
eating, when possible.

254 SECTION V: TAKING ACTION

 Box continued
Protect children from carbon monoxide (CO) poisoning
• Have fuel-burning appliances, furnace fluids, and chimneys checked once a year.
• Never use gas ovens or burners for heat; never use barbecues or grills indoors or in
the garage.
• Never sleep in rooms with un-vented gas or kerosene space heaters.
• Don't run cars or lawnmowers in the garage.
• Install a CO alarm that meets UL, lAS, or Canadian standards in sleeping areas.

Protect children from contaminated fish and polllJted water

• Be alert for local fish adVisories and beach closings. Contact your local health
department.
• Take used motor oil to a recycling centre; properly dispose of toxic household
chemicals.
• Learn what's in your drinking-water-call your local public water supplier for annual
drinking water quality reports; for private drinking-water wells, have them tested annu-
ally by a certified laboratory. Call 1-800-426-4791 or contact www.epa.gov/safewater
for help.

SafeglJard children from high levels of radon

• Test your home for radon with a home test kit.
• Fix your home if your radon level is 4 pCi/L or higher. For help, call your state radon
office or 1-aOO-SOS-RADON.

Protect children from too mlJch SlJn

• Wear hats, sunglasses, and protective clothing.
• Use sunscreen with SPF 15+ on kids over six months; keep infants out of direct
sunlight.
• Limit time in the midday sun-the sun is most intense between 10 and 4.

Keep children and merclJry apart

• Eat a balanced diet but avoid fish with high levels of mercury.
• Replace mercury thermometers with digital thermometers.
• Don't let kids handle or play with mercury.
• Never heat or burn mercury.
• Contact your state or local health or environment department if mercury is spilled-
never vacuum a spill.
aOeveloped by the US Environmental Protection Agency.

20. TAKING ACTION TO PROTECT CHILDREN FROM ENVIRONMENTAL HAZARDS 255

Figure 20.1 Messages for creating healthy environments for children (WHO)

WORLD HEALTH DA:V.7APRIL 2003

H!e.~J~~;y
!Enyironm·.· .·•. e~ts .; <;:,;"<""

for·······C!h~ftd!ren·

SECTION V: TAKING ACTION

 Figure 20. 1 Continued

20. TAKING ACTION TO PROTECT CHILDREN FROM ENVIRONMENTAL HAZARDS 257

Figure 20.1 Continued
•. "'~U·"":'" t"1""'~"''''' ~"''' ............. .
"bugs",Oisprea<l-"
".'~~niand~leVe!,of
" ,..... distf'l<'<i>\idren""!'l
J¢arrung,
• High level> of ak pollution i"
pnd around schpol'i cause
respiratory probJefl1S' ~t~·ldrert.

SECTION V: TAKING ACTION

 Communities and local governments
Enforcement of environmental regulations, housing initiatives, school and
hospital administration, disease surveillance and reporting, and other public
services usually fall within the juris-
diction of local governments, offer-
ing many opportunities to make
communities "child friendly" in the Community meetings lead to reduction
in childhood asthma
environmental health context. Local
Particulate matter and harmful fumes are by-
governments often serve as first-line
products of the combustion process used in
response to environmental inci-
foundries that melt scrap iron. Residents of
dents and are the key communica-
Sandwell, an urban area in the United Kingdom,
tors with the general public. Not
became concerned about the respiratory health
only are they responsible for com- of their children, who attended schools close to
municating about risk and public such a foundry, and organized a public meeting
safety, they also are the inter- to discuss the issue. The resulting measures
mediaries between national policy- taken by the foundry management led to a sig-
makers and citizens. They can take nificant reduction in asthma-related hospital
proactive and preventive steps admissions of schoolchildren in the area (Case
by promoting community events, Study 19, page 342).
sponsoring poison control centres,
and creating innovative ways to
educate and protect the public,
especially children. The G8 Declaration 1997
The United States EnVironmental Protection
National governments Agency ushered children's environmental health
The words of a head of state can into the international arena, through its insis-
generate attention, political will tence on the importance of children's environ-
and funding. National governments mental health for discussion by environment
can gear environmental protection leaders of the group of eight highly industrial-
systems and structures to improve ized countries (G-8) in 1997. With the unani-
children's environmental health, mous adoption of the Declaration of the
supporting decentralized initiatives Environment Leaders of the Eight on Children's
and working to formulate regula- Environmental Health, the world took notice that
children, both in developing and industrialized
tions and comply with national
countries, could be at more risk from envir-
mandates. National governments
onmental threats than had previously been
are the ultimate champions for chil-
assumed. Not only did the Declaration help
dren's environmental health, and
focus the G-8 national governments on improv-
should monitor it through data
ing poliCies and efforts within their own borders,
collection and analysis. They it also inspired other international bodies to call
should support communication and for actions to protect children's environmental
national public awareness efforts, health, heightening the awareness of other
pilot actions, specific projects and country leaders.
more. In addition, national govern-

20. TAKING ACTION TO PROTECT CHILDREN FROM ENVIRONMENTAL HAZARDS 259

ments should contribute to international efforts that spread the message
beyond their borders, promote collaboration and strengthen the agenda at
home.

International and global efforts

Over recent years, the international agenda has given considerable attention
to children's environmental health, setting a framework for action by individ-
uals and entities worldwide. Recent examples of progress on the international
front include the following:

• At the World Summit on Sustainable Development in Johannesburg,

South Africa, September 2002, the World Health Organization called for
a global movement to improve children's environmental health, moti-
vating countries, United Nations agencies and non-governmental orga-
nizations to create a "mass movement for children's environmental
health". The organization has since taken steps to form a global Healthy
Environments for Children Alliance to support countries as they strive to
improve children's environmental health through national and local
efforts (2). WHO programmes and regional offices have begun facilitat-
ing regional and national efforts to improve children's environmental
health (5).
• The Commission for Environmental Cooperation of North America
adopted an agenda for action on children's health and environment in
June 2002 (4).
• In May 2002, the United Nations convened a General Assembly Special
Session on children, which hosted side events on children's environ-
mental health and resulted in a document that stressed the environment
as an integral element of child health and welfare (5).
• Countries of South-East Asia and the Western Pacific were addressed
by the International Conference on Children's Environmental Health:
Hazards and Vulnerability, which took place in Bangkok, Thailand, in
March 2002, resulting in the Bangkok Statement: a pledge to promote
the protection of children's environmental health (see Chapter 1). The
Statement urged the World Health Organization to support efforts in the
region to improve children's environmental health.
• The United Nations Millennium Development Goals published in Sep-
tember 2001 called for a two-thirds decrease in the under-five mortality
rate by 2015, which will require action to reduce illness and death from
diarrhoeal disease and acute respiratory infections, two leading environ-
ment-related causes of death worldwide.
• The Budapest Conference held in 2004 focused on "the future of our chil-
dren" and adopted, through its Declaration, a children's environmental
and health action plan for Europe (CEHAPE).

260 SECTION v: TAKING ACTION

 Ready ... set ... go!
From very small, local, community-based steps to dramatic international
accords, children's environmental health continues to gain momentum, expand
its audience and increase in significance. There is growing recognition that envi-
ronmental health is both a right of children and the basis for sustainable devel-
opment. Simple actions can improve the lives of children and give them the
best possible opportunities.
With the goals of increasing public awareness, defining the roles and respon-
sibilities of health professionals, and achieving government buy-in and policy
change, four action areas have been defined: communication, education, advo-
cacy and research. Efforts to inform people about children's environmental
health have tremendous potential. As people become more informed, health
professionals will need more knowledge to answer their questions. As health
professional training changes to incorporate the recognition and management
of environmental exposures and the particular vulnerabilities of children, health
workers will add to the awareness and information sources of parents and of
children themselves. As the competence of health professionals increases, they
will begin to identify gaps in knowledge and research needs, make recommen-
dations to policy-makers, and advocate for change to protect health and prevent
disease. As people become more informed and health professionals more vocal,
government officials will set policies that protect children from environmental
harm. As governments champion country efforts, national movements will
start that will serve to raise public awareness and improve professional educa-
tion. Action targeted to any of these areas will result in positive effects all
around.

Communication and public awareness

Communication and public awareness efforts involve a broadly based
approach to inform people of all ages and functions, from children to heads of
state, leading to an increased understanding of the importance of protecting
children from environmental harm. Internet resources are powerful mecha-
nisms to facilitate information exchange, allowing participation of individuals,
communities and national groups in global efforts. Both formal and informal
actions to raise public awareness have proven successful.

Education
Actions in the area of education aim to increase the competence of health
professionals, especially those dealing with children. They need to learn how to
recognize and manage the health effects of environmental exposures, and to
break the cycle of exposure, illness, treatment and re-exposure. Physicians,
nurses, midwives and other health professionals are in the front line of chil-
dren's environmental health, and can use their clinical experience, scientific
expertise and research efforts to work closely with children of all ages, their

20. TAKING ACTION TO PROTECT CHILDREN FROM ENVIRONMENTAL HAZARDS 261

 parents, families and carers. Increasing competence of health professionals in
children's environmental health can have significant influence, leading to
greater public understanding and awareness, improved diagnosis and treatment
of environmentally related diseases, and extended advocacy efforts to promote
policies that protect environmental health. The general outline of courses
offered by WHO is presented in the box below.

Children's environmental health for health care provider

Contents of a training course
1. New knowledge on the vulnerability of children to environmental hazards
a Why are children more vulnerable than adults?
b The developing child and the effects of neurotoxicants (lead, mercury, manganese,
PCBs)
c Lung development and the effects of environmental pollutants
d Vulnerability to pesticides: new data and growing concern
e Genes as a target for environmental toxicants, malnutrition, micronutrients and toxic
effects (including methylmercury, arsenic)
The effects of UV radiation on eyes, skin and the immune system
g Other examples.

2. How, when and where does exposure occur? Environmental threats in specific set-
tings and circumstances, in utero and during childhood and adolescence: "children
growing in an adult-size world"
a The poor home: particular risks (shanty towns); living near waste sites; polluted urban
areas; rural areas; street children; parental exposure
b Where the child plays: playgrounds (outdoors, indoors); recreational areas; hobbies
c Where the child learns: child care centres; schools
d Where the child works: cottage industry; factory; rural areas; street vendors; domes-
tic workers; scavengers
e Where the child is especially stressed: extreme and adverse climatic conditions (e.g.
mountains, hot and cold weather); environmental and technological disasters (floods
and droughts); war; conflict and postconflict circumstances; refugee camps
Exposure of parents: transgenerational effects.

3. Understanding the main environmental threats and seUing the priorities for action
a Access to safe drinking-water and sanitation
b Indoor air pollution: open fireplaces indoors, environmental tobacco smoke (parents);
solvents; moulds; pet dander; other
c Ambient air pollution and the health of children from rural and urban areas: sulfur
dioxide (S02); nitrogen oxides (NO,); diesel fumes; fine particulate matter; lead;
benzene; open burning (waste and other); other
d Asthma and other respiratory diseases in children: role of the environment

SECTION V: TAKING ACTION

 Box continued
e Traffic-related paediatric pathology. Giving priority to children in township develop-
ment planning: "child-size traffic". Rural traffic accidents
Non-intentional, intentional and environmental toxic exposures
g Exposure to pesticides: acute and chronic effects
h Endocrine disrupters
Drugs of abuse
j The working child
k Lifestyle changes influencing housing, transport and children's social surroundings

4. Assessing the global burden of environmental threats to the health of children

a The concept of global environmental burden of disease (GEBD) in children
b Harmonized procedures, tools and methodologies; guidance for assessing the GEBD
in children; indicators of children's environmental health
c Information available in developing and industrialized countries/regions; national
profiles
d Priorities identified (inc!. main controversial issues)

5. Controversial issues, dilemmas and knowledge gaps in the area of children's envi-
ronmental health (CEH)
a The risks of living near hazardous waste sites, landfills and open burnings
b Asthma: the contribution of indoor and outdoor environments
c The potential effects of climate change (emerging infectious diseases and climate
refugees)
d Noise, hearing loss and other health effects in children
e What is known about endocrine disrupters and CEH?
f Cancer and environmental factors: how much do we know?
g Birth defects, reproductive disorders and environmental factors
h Is there a "safe" blood lead and mercury level in children?
The potential effects of exposure to low chronic radiation levels and electromagnetic
fields
j Problems posed by cyanobacteria in water and other contaminants
k Parental exposure

6. Ensuring the appropriate risk assessment in developing children

a Setting environmental guidelines and standards.
b Considering variability in exposure and response
c Critical windows of exposure
d Special consideration of developmental effects
e Cumulative toxicity/mixtures, multiple exposures
f Recommendations for improved methodologies for exposure assessment and deter-
mining health effects

20. TAKING ACTION TO PROTECT CHILDREN FROM ENVIRONMENTAL HAZARDS 26 3

Box continued
7. Incorporating CEH issues in the work of child health professionals
a Recognizing the links between paediatric morbidity and environmental threats in the
micro- and macroenvironments of children
b Clinical observations: harmonized case data collection and analysis
c Taking the paediatric environmental history: from symptoms to etiology to prevention
d Detecting emerging diseases and signals of environmental illness in the community
e Reporting and publishing observations
f Undertaking research studies
g Evidence-based interventions: illustrative cases
h Communicating with parents, teachers, the community, media, local authorities and
decision-makers

Advocacy and public policy

These activities aim to improve the state of the environment and target poli-
cies towards children's health, so that local, regional and national governments
act to improve both the environment and the health of children and those
around them. In many countries, governments lead the effort. In other coun-
tries, policy-makers react to public and professional demands. All levels of
society can advocate for children's environmental health and influence policy
agendas. A global effort to develop children's environmental health indicators
is under way, coordinated by the World Health Organization and the United
Nations Children's Fund (UNICEF). Indicators of children's environmental
health offer a tool to policy-makers for determining priorities and measuring
progress towards set goals. Governments have the opportunity to join the global
initiative on children's environmental health indicators by contacting WHO or
UNICEF.

Research
Promotion of collaborative research in children's environmental health in
developing and developed countries is essential if problems are to be addressed
in their national and global contexts. The results of appropriate studies can be
used in strategies for prevention, intervention, and remedial action, and as a
foundation for evidence-based public health policies in countries. Collaborative
activities would also result in technology transfer and capacity building, and in
the development of a network of trained scientific collaborators throughout the
developing world.

SECTION v: TAKING ACTION

 National profiles and indicators
WHO has developed indicators of children's health and the environment
and other tools to assist countries in assessing the status of children's health
and determining the readiness of governments to effect change. A format for
doing rapid assessments that may help countries to prepare their national
strategies is shown in the box below.

Outline for preparing national profiles on the status of children's

environmental health
NOTE: please use the boxed headings as subheadings in the country/local profile you
develop. Use the questions proposed as a guide for obtaining and collating information and
developing an overall assessment of each area. These questions are intended to provide
some orientation on the type of information that is relevant for assessing the status of chil-
dren's health and the environment. Develop up to three paragraphs for each of the under-
lined headings, expanding even beyond the questions provided, as deemed necessary. Please
take into account for each question the potential gender, rural/urban, cultural and ethnicity
issues. Tables necessary to make a pOint can be annexed. The profiles should cover both
existing situations, observations and ongoing activities as well as potential opportunities for
actions that could be implemented at the country level. Profiles should be dated: once the
initial profile is done, successive ones may be prepared on an annual basis to assess
progress made and/or changes observed concerning the status of children's health and the
environment in the country.

INTRODUCTION
Overview of children's environmental health in the country
Provide a general synopsis of the country's views and position on children's environmental
health, for example, the awareness level of government officials (especially in the health and
environment sectors) and the acceptance of this as a distinct issue.

Key environmental issues

WHO lists the following key environmental risks for child ren: unsafe water, air pollution
(indoor/outdoor), poor food hygiene, poor sanitation and inadequate waste disposal, vector-
borne diseases and exposure to chemicals (agrochemicals, industrial chemicals, persistent
toxic substances, natural toxins and other). In addition, children's health is endangered by
other environmental risk factors, such as: poor housing, environmental degradation and the
the so-called "emerging" threats (e.g. global climate change, ozone depletion, radiation,
exposure to endocrine-disrupting compounds, and others). Prioritize these for your country
according to the impact they have on children's health, development and well-being. Add
areas of focus if necessary. Propose a prioritized list of environmental concerns for chil-
dren's health in your country.

20. TAKING ACTION TO PROTECT CHILDREN FROM ENVIRONMENTAL HAZARDS 265

Key causes of infant and under-tive mortality/morbidity
This information is normally readily available from WHO websites or in the WHO represen-
tations in the country. List the top five causes of illness and death for children under one,
for children five and under, for children up to 14 and for children as a whole. As the age
groups of children vary somewhat from country to country, please define the age group that
you are reporting (e.g. some use 18 and under, some 20 and under).

Burden of disease related to environment in children

WHO has some information available on its website (www.who.intlphe/health-topics, search
for "environmental burden of disease") and at the WHO representation. WHO reports that
environmental threats may cause up to one-third of the global burden of disease. What does
the country report? Are there any significant differences between boys and girls or between
rural and urban children? Has this issue been addressed at the country level or does it remain
to be done?

ECONOMIC STATUS AND ETHNIC GROUPS

Economic spread between poorest and wealthiest
What is the percentage share of income or consumption for the wealthiest 10% of the pop-
ulation? What is the percentage share of income or consumption for the poorest 10% of the
population?

Information on high risks/Vulnerable groups and demographic profile of countries

Provide the approximate numbers or percentages of each ethnic population group in your
country and the geographic areas they occupy. To what extent are environment and health
statistics or any other statistics routinely desegregated by socioeconomic status or ethni-
city? Do national environmental or other sectoral policies make specific reference to ethnic
groups or to groups that are geographically isolated? Is there any evidence of the impact of
ethnicity or socioeconomic status on the burden of disease related to environmental threats?
Are there any activities on ethnic minorities (and their children) undertaken by international
institutions or nongovernmental organizations to which an environment and health com-
ponent might be added?

NATIONAL GOVERNMENT ROLE

National pOlicies
Are there specific national pOlicies or stated priorities that support the protection of chil-
dren's environmental health? Are there specific national policies or stated priorities that seem
to run counter to the objectives of increasing protection of children from environmental
threats (e.g. lax pesticide or toxic chemical regulations, persistence of lead in gasoline
despite the proven health benefits of removing it)?

Health sector
How does the health sector address environmental health in general and children's environ-
mental health specifically? Is there legislation to protect public health from environmental

266 SECTION V: TAKING ACTION

 hazards and is this legislation well-implemented? Is there any action to protect vulnerable
sub-populations or children in particular? Are the medical, nursing and health-care profes-
sional communities informed and/or trained on environmental threats to human and-more
specifically-on children's health? Are there health facilities that promote environmental
health or children's environmental health? Describe the differences in approaches to envi-
ronmental health in rural and urban settings. In the specific area of chemicals, is there a
Poisons Centre in your country or a toxicology or other unit that deals with toxic exposures
in children? Where are pOisoned children seen and treated? Are chronic, low-level exposures
to chemicals in children being considered? Has any action been taken concerning the poten-
tial effects of persistent toxic substances (and POPs)?

Environment sector
Discuss the country's environmental legislation and its level of enforcement. Is human health
considered by the environmental legislation and/or is protecting human health part of the
mandate of the environment ministry? Are there any specific considerations concerning chil-
dren? Are specific media, such as water, air, soil, food, or chemical safety covered by envi-
ronmental legislation? If so, list which media are covered and list any gaps. Does the
environment ministry coordinate well with other ministries, such as health or education and,
if so, which ones? Has the country signed the international conventions/treaties dealing with
toxic chemicals/pollutants (e.g. The Stockholm Convention on Persistent Organic Pollution,
The Basel Convention on the Control of Transboundary Movements of Hazardous Wastes
and their Disposal, and The Rotterdam Convention for Prior Informed Consent)? Have the
actions taken in the context of these conventions/treaties considered the potential impact on
children's environmental health?

Education
What is the level of literacy in the country? How many children go to school, and up to what
levels? Is attendance in the schools required up to a certain age? Are there differences in
male/female school attendance? For elementary school and for high school, what are the
opportunities for health and environmental education? Is there an environmental or a health
curriculum taught in these grade levels? If so, are these taught in both rural and urban
schools? Would environmental health education through elementary schools be possible
and/or acceptable in the school systems?

Other pertinent ministry/sector

If applicable, list other pertinent ministries or governmental agencies that deal with children's
health and the environment (e.g. in certain countries some of the environmental issues may
be regulated through the ministries of agriculture, industry, youth, social well-being or
others). In many countries there are ministries of culture, science, education, welfare, and
family and youth that may playa role in the protection of children's environmental health.
What are the ministries or agencies at the national government level which would playa role
in implementing a national action plan on children's environmental health? List and describe
the role they play.

20. TAKING ACTION TO PROTECT CHILDREN FROM ENVIRONMENTAL HAZARDS 267

 SOCIETY ROLE
Communities
Do the governmental units at the community level (e.g. county seats, communal or city gov-
ernments) playa role in the protection of environmental human health-and more specifi-
cally-children's environmental health? If not, what role could they play, or might they take,
at a local level to better protect children from environmental threats? Do they have the ability
to pass local legislation? Are they charged with enforcing national legislation? Could they be
encouraged to carry out public information campaigns on children's environmental health?

Nongovernmental organizations (NGOs)

Do NGOs playa strong role in building stakeholder input and public participation? What are
the key NGOs (both national and international) involved in activities aiming at the protection
of children's environmental health, organizing national campaigns on children's environ-
mental health or promoting children's chemical safety? If none has been doing this, which
one could eventually be interested in this area? What roles might they play?

Professional associations
Do professional associations playa strong role in building stakeholder input and public par-
ticipation? What are the key professional associations (both national and international) that
would become involved in children's environmental health? (e.g. paediatric, medical, toxi-
cological, family doctors, occupational medicine, nursing, primary health care, and any other
societies). What roles might they play?

Academia
What academic institutions (e.g. academies, post-graduate schools) could promote chil-
dren's environmental health through research, advocacy, publications, medical education (of
medical and postgraduate students and continuing medical education), development/use of
children's environmental history taking, and development/use of indicators? What role would
each play?

Private sector
Are there any private companies that would likely be interested in promoting the safety and
health of children in the country? For example, pharmaceutical, hygiene and cosmetic prod-
ucts companies, agricultural chemical companies, water companies, food and beverage pro-
ducers? What roles could the private sector take-considering after all ethical aspects
involved-in the different areas (e.g. financing activities, public advertisements, educational
campaigns, or advocating in favour of national legislation)?

SCIENCE
State of the sCience in the country (in relation to children's environmental health)
Has anyone in the country conducted research and published results on topics related to
environmental health or children's environmental health (e.g. on the risk factors mentioned

268 SECTION Y: TAKING ACTION

 above, on children's settings, on specific topics such as chemical safety and poisonings)?
Name the country's science ministry or unit in the government that conducts research and
publishes findings. Is environment or health legislation based on scientific findings?

Capabilities to conduct research

What institutions promote science and research in the country? Does the national govern-
ment invest in research and development? What type of scientific publications are released
in the country? Is financing available to support research at universities, hospitals, labora-
tories or other facilities? Which institutions would most likely be interested in research on
children's environmental health?

Research needs
List the top priority research needs around the topic of children's environmental health in
the country. Is research on these topics under way? Are there barriers to conduct this
research and, if so, what would help overcome the barriers? What are the needs? What are
the top three ways in which an international organization or other countries or organizations
could support research?

DATA AND REPORTING

Information systems and centres
Does the country have a centralized information gathering function on children's health data
(e.g. health surveillance system, clinical case recording)? Does the country have national
or private information centres, for example on health, demographics or environment? Does
the country require reporting of certain paediatric diseases to support public health surveil-
lance and disease prevention and, if so, how is that information gathered and where? Are
there poison control centres in the country and, if so, do they record incoming and outgo-
ing information in a harmonized manner? Does the country report indicators on environ-
ment or health? Does the country put out regular reports on disease, public health or
environmental conditions? If so, how are they accessed by the public?

Data quality
The WHO national offices are most likely involved in data gathering on health, and local
UNICEF and UNDP offices probably work on information collection systems, as well. Do
these offices judge data quality as good enough to be useful and representative? Are there
other entities that collect data on health, environment or status of children in the country?
Can the national work on Millennium Development Goals help to clarify and address barri-
ers to data quality in the country?

COMMUNICATION
Avenues of communication
What are the most effective means for disseminating information in the country (e.g. tele-
vision, radio, newspaper, and role-playing)? Are these the same for both rural and urban

20. TAKING ACTION TO PROTECT CHILDREN FROM ENVIRONMENTAL HAZARDS 269

settings? If not, list by rural and urban. What are the most effective means for communica-
tions through schools, adult literacy programmes, country or local governments? Are there
other innovative means of communication, for example through local libraries, street thea-
tres, radiofTV educational "soap operas", fairs or other local events?

Success stories in communication

Do you know of any local success stories in widespread communication on important topics
related to health and the environment? (e.g. use of radio-based literacy programmes tar-
geting children in rural areas may increase adult and child literacy and lead to a decrease in
child agricultural workers and improve matriculation in rural schools). Could these successes
be repeated, this time carrying a message for children's environmental health?

CONCLUSION
Summary of the country status of children's environmental health and opportunities
for action
Given your findings, in a page or less, summarize your assessment of the country's poten-
tial, capacity and interest to take action to improve the environmental health of its children.
What specific actions in this area are recommended? What are the areas/issues for natural
success? What are the areas/issues where urgent actions are required? What are the key
barriers or areas that need to be addressed to achieve success? Who (individuals and orga-
nizations) are the key players?
Annexes. Please provide any samples of useful or illustrative materials, such as educational,
awareness building, information gathering, data collection forms, educational programmes,
photographs, maps, charts, other.

A special invitation for nongovernmental organizations

Nongovernmental organizations (NGOs) have excellent opportunities to
promote awareness of environmental hazards to children. They can use radio,
television, newspaper advertisements, street theatre, health fairs, and other
innovative ways to improve public awareness, increase training for health care
professionals, enhance access to information and advocate better policies. The
information era affords enormous potential to broadcast messages, reaching
urban and rural areas alike. Religious leaders can also have a strong impact,
reaching receptive audiences who want to take actions that benefit children.
Many NGOs actively promote activities that support the environment, from
nature conservation to sustainable development, but there are relatively few in
the field of environmental health or environmental medicine, particularly dealing
with the special vulnerability of children. Two organizations that have reacted
to the realization that children are particularly susceptible to environmental risks

27 0 SECTION Y: TAKING ACTION

 are the International Society of Doctors for the Environment (ISDE;
www.isde.org) and the International Network for Children's Health and Envi-
ronmental Safety (INCHES; www.inchesnetwork.net). Some countries have
national networks for children's environmental health, such as the United States
Children's Environmental Health Network (CEHN; www.cehn.org), the
Canadian Institute for Child Health (CICH; www.cich.ca) and the German
Network for Children's Health and Environment (www.kinder-agenda.de). The
web sites of these national networks are rich in information resources and links.

Conclusion
Pollution and other environmental threats do not recognize borders. Action
is required at all levels: even local, community-based activities may end up
having great influence around the world. The history of children's environmen-
tal health demonstrates how local actions may have a global impact: a non-
governmental organization with a clear mission convinces a minister of
environment, who motivates an international declaration, boosting children's
environmental health into the mainstream international agenda. Not only do
actions at the different levels affect those in the immediate area, they also create
energy for public good with worldwide benefits. Everyone at every level can do
something to improve children's environmental health and advance sustainable
development while contributing to the health, increased productivity and well-
being of children around the globe.

References
1. Tips to protect children from environmental risks. US Environmental Protection
Agency, 2004 (http:j jyosemite.epa.gov jochpjochpweb.nsfjcontentjtips).
2. Healthy environments for children alliance. Geneva, World Health Organization,
2003 (http://www.who.int/heca/enf).
3· Children's environmental health. Geneva, World Health Organization, 2004
(http://www.who.int/ceh/en).
4· Commission for Environmental Cooperation of North America. Cooperative
agenda for children's health and the environment in North America. Montreal, 2002
(http:j jwww.cec.orgjfilesjpdfjPOLLUTANTSjChildren_coop_agenda-en.pdf).
5· A worldfit for children. New York, United Nations, 2002 (http://www.unicef.org/
specialsess ion jwffcji ndex.html).

20. TAKING ACTION TO PROTECT CHILDREN FROM ENVIRONMENTAL HAZARDS 27 1

Case stud ies
CHAPTER 21

Case studies
1. THIOMERSAl IN CHilDREN'S VACCINES-
THE RESPONSE OF THE UNITED STATES

C. J. Clements
Expanded Programme on Immunization, Department of
Vaccines and Biologicals, World Health Organization,
Geneva, Switzerland

Thiomersal is an organic mercurial compound that has been used for over
60 years as an antimicrobial agent in vaccines and other pharmaceutical
products to prevent unwanted bacterial and fungal growth in the opened vaccine
vial. When vials contain multiple doses of vaccine, the rubber stopper has to be
punctured several times to withdraw doses; the liquid vaccine is thus exposed
to the possibility of contamination. To avoid this, thiomersal is used in multidose
presentations of vaccines such as diphtheria-tetanus-whole cell pertussis (DTP)
and tetanus toxoid (TI), as well as certain formulations of diphtheria·tetanus·
acellular pertussis (DTaP), hepatitis Band Haemophilus injluenzae type b (Hib)
vaccines, but not in live bacterial or viral vaccines. Vaccine preservatives, includ·
ing thiomersal, have probably prevented illness and death in countless infants
over the years by reducing the risk of contamination of opened multidose vials.
In certain vaccines, thiomersal is also used during the manufacturing processes.
Although the mercury-containing preservative is known to cause local skin
reactions when applied topically, it has been considered safe and highly effec·
tive when used in vaccines. However, in mid-1999, the chemical came under
public and professional scrutiny because of its presence in certain vaccines that
are included in childhood immunization schedules (1).
Questions regarding the safety of thiomersal in vaccines have arisen pri-
marily because of recent studies suggesting adverse effects in children from in
utero exposure to methylmercury (a similar organic mercury compound) at
levels previously considered safe (2, 3) and the reduction by the US EPA of the
recommended limits on methylmercury exposure (4).' Data on human health

'WHO, the us Environmental Protection Agency (EPA), the US Agency for Toxic Substances
and Disease Registry (ATSDR), and the US Food and DrugAdministration (FDA) have developed
recommendations for safe exposure to methylmercury in the diet. These range from 0.7 ~g/kgof
body weight per week (EPA) to 3.3 ~g/kg of body weight per week (WHO) and include a safety
margin. Applyingthese guidelines to a female infant in the lowest 5th percentile ofweight between
birth and 14 weeks, the period during which most infant vaccines are given, results in limits of
safe total methylmercury exposure of between 34~g (EPA) and 159~g (WHO). Application of
these guidelines to thiomersal, which is metabolized to ethyl mercury, assumes that the toxicity
of ethyl mercury is the same as that of methylmercury (still an unresolved question).

275
Table 21.1 Mercury exposure from thiomersal in typical immunization schedules

VACCINES' HEPATITIS B (HB) VACCINE MERCURY DOSE (~g)

AGE OF
INFANT SCHEME A SCHEME B SCHEME A SCHEME B

BeG, OPV 0 HB 1 12.5

Birth
HB 2 HB 1 62.5 62.5
6 weeks DTP 1, OPV 1, Hib 1
HB 2 50 62.5
10 weeks DTP 2, OPV 2, Hib 2
HB 3 HB 3 62.5 62.5
14 weeks DTP 3, OPV 3, Hib 3
9 months Measles, yellow fever
187.5 187.5
Total potential exposure of infants
TT1-as soon as possible in pregnancy or as early as 25
Women of
childbearing possible in the childbearing years
age, and TT2-at least 4 weeks after TT1 25
especially 25
TT3-at least 6 months after TT2
pregnant 50
women TT 4 and TT5-at least one year after the previous TT dose

125*
Total potential exposure of women through TT

'DPV = oral poliovirus vaccine; DTP, diphtheria, tetanus, pertussis; BCG, bacille Calmet\e-Guerin; Hib1,
Haemophilus influenzae type b; HB, hepatitis B; n, tetanus toxoid.

effects of low level exposure to ethylmercury, the metabolite of thiomersal are

lacking. Nonetheless, the tolerance of the public for risk without obvious benefit
to the individual has diminished (5). The combination of these factors has led
to an altered perception of mercury-containing products. As a result, the gradual
removal of the preservative from vaccines is being supported by the US Public
Health Service (USPHS), WHO, and industry (6, 7)· At present, however, sci-
entific investigation has not found conclusive evidence of harm from thiomer-
sal in vaccines. In June 2003 experts convened by the Food and Agriculture
Organization of the United Nations (FAO) and WHO reviewed additional infor-
mation on methylmercury and recommended a reduced provisional tolerable
weekly intake (PTWI) of 1.6 ~g per kg of body weight, in order to protect the
developing fetus (this new recommendation replaces the prior one of a dietary
lim it of 3-3 ~g per kg of body weight per week).

Management and intervention

The addition of new vaccines to the recommended childhood immunization
schedule during the past decade has increased the potential exposure of infants
to mercury from vaccines. In July 1999, an FDA review found that some infants
might receive more mercury from vaccines than was considered safe according
to certain national guidelines (8). The USPHS and American Academy of
Pediatrics (AAP) issued a joint statement concerning thiomersal in vaccines (6)

SECTION VI: CASE STUDIES

and the AAP released an interim report to clinicians (9) recommending that
thiomersal be removed from vaccines as soon as possible, while encouraging
maintenance of efforts to ensure high vaccination levels. These events prompted
international debate about preservatives and their safety as well as controversy
over immunization recommendations for thiomersal-containing vaccines. One
recommendation in the joint statement and interim report to clinicians was
deferral of hepatitis B vaccination until 2-6 months of age for infants born to
mothers at low risk of hepatitis B disease. An editorial in the Journal of the
American Medical Association soon followed suggesting that the authorities should
express a preference for thiomersal-free DTaP and Hib vaccines for infants (10).
The USPHS and various US vaccine advisory bodies, including the AAP,
Advisory Committee on Immunization Practices (ACIP), and the American
Academy of Family Physicians, continue to recommend the policy of moving
rapidly to vaccines that are free of thiomersal as a preservative (2, 11), citing the
desirability to minimize human exposure to mercury from all sources (1). With
the approval in the United States of a single antigen thiomersal-free hepatitis B
vaccine in August '999, the ACI P recommended that the birth dose of hepati-
tis B vaccine be resumed for all infants (12). The FDA approved an additional
preservative-free hepatitis B vaccine in March 2000 and a preservative-free DTaP
vaccine in March 2001. In the USA, additional proposals to remove thiomersal
as a preservative from other vaccines have been announced by manufac-
turers, and new vaccines under development are not being formulated with
thiomersal.

Wider implications
In the USA, recent progress in reducing exposure to thiomersal in vaccines
has relied mainly on reformulation of thiomersal-containing products into
single-dose vials that do not require a preservative. This is not feasible in many
developing countries for a number of reasons. For many vaccines there is no
obvious alternative preservative, thus leaving many local producers with the
option of either producing the vaccines in multidose containers without a
preservative (greatly increasing risk of contamination) or in single-dose prepa-
rations (too expensive in terms of manufacture, storage and delivery). The cost
of switching to single doses is high; the cold chain does not currently have the
capacity to cope with the increased volume, and local vaccine producers could
not easily adjust to increased demands on the manufacturing process caused
by conversion to single-dose containers.
The theoretical risk from exposure to thiomersal has to be balanced against
the known high risk of having no preservative in vaccines. Therefore, WHO (13),
UNICEF, the European Agency for Evaluation of Medicinal Products (EMEA),
and other key agencies continue to recommend the use of vaccines containing
this preservative because of the proven benefit of vaccines in preventing death
and disease and the lack of data indicating harm. Additional studies are planned

21. CASE STUDIES 277

or under way to address the gaps in knowledge on the potential health effects
of thiomersal in vaccines.

Acknowledgements
This article draws on material published in Drug Safety and is used with per-
mission (Clements CJ et al. Thiomersal in vaccines - is removal necessary?
Drug Safety, 2001, 24:567-574).

References
1. US Pharmacopeia 24. Rockville, MD, US Pharmacopeial Convention, 1999:1644.
2. Centers for Disease Control and Prevention. Recommendations regarding the
use of vaccines that contain thimerosal as a preservative. Morbidity and Mortal-
ity Weekly Report, 1999, 48:996-998.
3. Grandjean Pet al. Cognitive deficit in 7 year old children with prenatal exposure
to methylmercury. Neurotoxicology and Teratology, 1997, 6:417-428.
4. Environmental Protection Agency. Integrated risk information system. Cincinnati,
OH, EPA Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, 1994 (http://www.epa.govjiriswebp/iris/index.
html).
5. Covello VT, Sandman PM, Siovic P. Guidelines for communicating information
about chemical risks prospectively and responsively. In: Mayo DG, Hollander D,
eds. Acceptable evidence: science and values in risk management. New York, Oxford
University Press 1991:66-90.
6. Centers for Disease Control and Prevention. Notice to readers: Thimerosal in
vaccines - A joint statement of the American Academy of Pediatrics and the
Public Health Service. Morbidity and Mortality Weekly Report, 1999, 48:563-565.
7. World Health Organisation. Thiomersal as a vaccine preservative. Weekly Epi-
demiological Record, 2000, 75:12-16.
8. Ball LK, Ball R, Pratt RD. An assessment ofthimerosal use in childhood vaccines.
Pediatrics, 2001, 107:1147-1154.
9. American Academy of Pediatrics. Committee on Infectious Diseases and Com-
mittee on Environmental Health. Thimerosal in vaccines - an interim report to
clinicians. Pediatrics, 1999, 104:570-574.
10. Halsey NA. Limiting infant exposure to thimerosal in vaccines and other sources
of mercury. Journal of the American Medical Association, 1999, 282:1763-1766.
11. Centers for Disease Control and Prevention. Summary of the joint statement on
thimerosal in vaccines. Morbidity and Mortality Weekly Report, 2000,49:780-782.
12. Centers for Disease Control and Prevention. Availability of hepatitis B vaccine
that does not contain thimerosal as a preservative. Morbidity and Mortality
Weekly Report, 1999, 48780-782.
13. Children's vaccines - safety first. Geneva, World Health Organization (Note to the
press No. 18, 9 July 1999).

SECTION VI: CASE STUDIES

 2. SILICOSIS AMONG CHilDREN IN THE AGATE INDUSTRY

H. N. Saiyed
National Institute of Occupational Health, Indian Council of
Medical Research, Ahmedabad, India

Agate is a hard, semiprecious stone, a variety of chalcedony, with striped

or clouded colouring and contain-
ing a large quantity of free silica
(>60%). It is used to make cheap
jewellery and various articles of
decoration (Figure 21.1). Process-
ing of agate stone comprises
several steps, including chipping,
baking, grinding, polishing, and
drilling. Dust is generated mainly
during the grinding process. A
small quantity of dust is also gen-
erated during chipping. The agate
industry is located in Khambhat
(also known as Cam bay) town and
surrounding villages of Gujarat
State and Jaipur city of Rajasthan
State in Western India, and
employs about 50000 people.
Grinding of the stones is carried
out indoors or under open shade,
on an electric emery. The machin-
ery is primitive and the health and
safety ofthe workers is usually dis- Figure 21.1 Jewellery and decorative articles made
regarded. Dust generated during from agate
grinding pervades the work envi-
ronmentaswell asthecommunity.
Children may be exposed in the
community, when they accom-
pany their mothers to work (Figu re
21.2), or when they themselves are
employed in the industry.

Silicosis and
silicotuberculosis
Silicosis is the most
common and ancient of all occu- Figure 21.2 Grinding of agate stone under open shade

21. CASE STUDIES 279

pational diseases of the lu ngs and, even today, it is among the most serious occu-
pational diseases. It is an irreversible fibrosis of the lungs caused by repeated
inhalation over a long period of time of fine particles containing free silica.
Repeated exposure to silica dust results in fibrosis of the lungs. The disease is
characterized by insidious onset of shortness of breath followed by cough, with or
without expectoration. Exposure to silica dust also impairs the defence mecha-
nism of the lungs against infection, in particular tuberculosis. A high incidence of
tubercu losis is com mon among the working population exposed to silica.

Diagnosis of silicosis
The diagnosis of silicosis is based on the occupational history combined
with typical radiological features consisting of fine bilaterally symmetrical
nodular shadows on chest X-ray. To promote reproducibility and uniformity in
reporting, the International Labour Organization (ILO) has devised the Inter-
national Classification of Pneumoconiosis Radiographs for coding of radiolo-
gical abnormalities (1). The abnormal shadows due to pneumoconiosis are
coded as p, q, or r, depending on size and shape, and as 0, 1, 2, or 3 according
to their density or profusion. Category 0 means no pneumoconiosis and 1, 2,
and 3 correspond to increasing numbers of opacities per unit area, and usually
reflect the severity of pneumoconiosis. These four categories are further sub-
divided into twelve subcategories 0/-, 0/0, 0/1, 1/0, 1/1, 1/2, 2/1 ... 3/3 and
3/+. The categorization is made by comparing the chest radiograph of the
patient with the standard radiographs supplied by ILO.
Silicosis is not confined to the developing countries, although the situation
there is alarming. For example, according to the American Lung Association (2),
about 1.6 million workers in the USA are at risk of silicosis, and 60000 are
expected to suffer from it.

Prevalence of silicosis and tuberculosis in children

Normally, silicosis does not occur in the general population in the absence
of occupational exposure. However, a high prevalence of non-occupational
pneumoconiosis due to exposure to free silica has been reported from a resi-
dential area in India, close to the agate industry (3). To find out the prevalence
of silicosis and silicotuberculosis in agate grinders and the surrounding com-
munity, the National Institute of Occupational Health (N IOH), Ahmedabad,
recently carried out an environmental and epidemiological study in 2050
subjects who were exposed to silica dust, either occupationally or non-
occupationally (unpublished report). The study population included 230
children, of whom 58 (25.2%) had worked for a period as agate grinders. The
radiological findings of these 230 children are shown in Table 21.2.
A total of 28 children (12.1%) showed radiological evidence of silicosis of cat-
egory 1/0 or 1/2. There were 27 (11.7%) cases of silicosis category 1/0 and one girl
aged 17 years who was working as a grinder showed category 1/2 silicosis on X-ray.

280 SECTION VI: CASE STUDIES

Table 21.2 Distribution of cases of silicosis and tuberculosis in children exposed
to silica dust

AGE GROUP CATEGORY OF SILICOSIS TUBERCULOSIS

(YEARS) 0/0 0/1 1/0 1/2
<10 7/10 (70%) 3/10 (30%) 2/10 (20.0%)
11-15 121/148 (81.8%) 7/148 (4.7%) 20/148 (13.5%) 10/148 (6.8%)
16-18 61/72 (84.7%) 6/148 (8.3%) 4172 (5.6%) 3172 (4.2%)

Total 189/230 13/230 27/230 1/230 15/230 (6.5%)

(82.2%) (5.7%) (11.7%) (0.4%)

The overall prevalence of tuberculosis as diagnosed from X-ray was 6.5%.

This is much higher than the prevalence reported in other studies. For example
a recent tuberculin survey in northern India in 4200 children below 14 years
showed an overall infection prevalence of 2-4% (4). Similarly a radiological study
of a population in the North Arcot district of South India showed a tuberculo-
sis prevalence of 1.7% in subjects above 14 years (5). The high prevalence of
tuberculosis among the children could be attributed to occupational and non-
occupational exposure to silica dust from the agate industry. Moreover, in a pre-
vious study, a prevalence of tuberculosis of about 42% in adult men and women
working as grinders in the agate industry was reported (6). This adult popula-
tion, particularly working mothers, may act as a source of infection to children.

Prevention and control of silicosis and silicotuberculosis

In 1997, the Ministry of Health and Family Welfare of India initiated the
National Silicosis Elimination Programme, a long-term scheme, for which
NIOH, Ahmedabad, is the nodal agency. The programme consists of: (1) iden-
tification of high-risk small and cottage industries, through environmental and
epidemiological surveys, including surveys of the surrounding community; (2)
development of simple devices for dust control in the community and work envi-
ronment; (3) treatment of workers who suffer from dust-induced diseases; (4)
strengthening of regulatory mechanisms through technical support for dust
monitoring; and (5) awareness programmes for workers, employers, medical
officers and factory inspectors.
The agate industry is part of this programme. As mentioned earlier, an envi-
ronmental epidemiological study has already been completed. The cases of sil-
icosis and tuberculosis detected during the survey were referred to the local
health authorities for appropriate management. The government health depart-
ment has opened a special clinic for agate workers at Khambhat for diagnosis
and management of silicosis and silicotuberculosis. A 300 mA X-ray machine
and supplies of medicine have been provided to the centre for surveillance of
silicosis and tuberculosis.

21. CASE STUDIES

 The major challenge was to develop an appropriate dust control device accept-
able to the workers and the owners. Several models of a local exhaust system were
tried. Our initial attempt was to incorporate an exhaust system into the grinding
machine. These models were not accepted by the workers because they required
changes in their working posture. Finally we have developed a model of an exhaust
system that fits over the cutting machine. This model does not require the workers
to change posture and has met with a positive response. The efficacy of the local
exhaust in reducing dust levels is about 90-95% as shown by an industrial hygiene
survey. Model exhaust systems have been installed in six units and have been
working satisfactorily over a period of one year.
For the long term, the State Government plans to relocate the industry
outside the town by providing land and other infrastructure. It is proposed to
form a cooperative society for the workers and the owners to take care of the
environmental and occupational health problems. I n addition, education pro-
grammes for the workers and the community are organized to ensure success-
ful implementation of the silicosis elimination programmes.

Conclusions
An environmental epidemiological study of the agate industry demonstrated
the poor working conditions in this cottage industry, and the serious health
problems not only among the workers but also in the surrounding community.
Children are very vulnerable to silicosis and tuberculosis through direct and
indirect exposure, particularly through their mothers. Identification of industries
with high occupational and environmental exposure to silica is important. Com-
mitment from all parts of society - factory owners, workers, factory inspectors,
medical officers, people living in the surrounding area and government author-
ities - is essential. A silicosis elimination programme should be incorporated
in the national tuberculosis elimination programme in developing countries
where tuberculosis is still a major health problem.

References
1. International Labour Organization. Guidelines for the use of ILO International
Classification of Radiographs of Pneumoconioses. Geneva, ILO, 1980 (Occupational
Safety and Health Series, No. 22).
2. American Lung Association (www.lungusa.org).
3. Saiyed HN et al. Non-occupational pneumoconiosis at high altitude villages in
central Ladakh. British Journal of Industrial Medicine, 199 1, 48:825-829.
4. Pattanaik D et al. Prevalence of tuberculosis infection in children below fourteen
years in rural Haryana. Indian Pediatrics, 2002, 39:]0-74·
5. Datta M et al. Tuberculosis in North Arcot district ofTamilnadu. A sample survey.
The Indian Journal of Tuberculosis, 2000, JuIY:47.
6. Sadhu SG et al. A follow up study of health status of small scale agate industry
workers. Indian Journal of Industrial Medicine, 1995, 41 :101-10 5.

282 SECTION VI: CASE STUDIES

 3. PROTECTION AGAINST THE SUN IN SCHOOLS

s. Harper
School of Nutrition and Public Health, Deakin University,
Victoria, Australia

The problem
Australia has the highest incidence of skin cancer in the world - one out
of two Australians will develop some form of skin cancer during their lifetime.
There are three forms of skin cancer - basal and squamous cell carcinomas
(or common skin cancers) and melanoma. The annual incidence of common
skin cancers, which comprise about 78% of new cancer cases in Australia each
year, is 1000 per 100000 people (1). Melanoma incidence is 30 per 100000
people per year (1), and most of the 1200 skin-cancer-related deaths occurring
annually result from melanoma. Excluding common skin cancers, melanoma is
the third most common cancer in women and the fifth most common in men -
it is also the most common cancer in people aged 15-44 years (2). Skin cancer
is Australia's most costly cancer - direct costs of treatment have been esti-
mated at US$ 5.70 per person per year (3). Yet it is almost totally preventable
through sensible behaviour to protect against the sun.
Exposure to ultraviolet (UV) radiation from the sun, particularly during child-
hood and adolescence, is the most significant risk factor for development of
skin cancer in later life (2,4). It has been estimated that up to 80% of total life-
time exposure occurs during childhood (4). Both short, sharp shocks of sunburn
and cumulative exposure over a number of years increase skin cancer risk.
Although melanoma can develop during late adolescence, skin cancer is not
usually seen in people under 40 years of age.
Australia receives high levels of UV radiation as a result of its proximity to
the equator. The incidence of common skin cancers is related to latitude, and
is highest in northern Australia (5). Fair-skinned people, who make up the major-
ity of the population, are most at risk. Australians enjoy an outdoor lifestyle,
and since the early 1900S there has been a belief that suntanned skin looks
attractive and healthy.

Management and intervention

Because children are at school five days a week during the period when UV
levels are at their peak, schools can directly influence the UV radiation exposure
of their students. In addition, schools are ideally placed to educate students and
the wider community through curriculum programmes and role models. Devel-
opment of good habits during childhood can contribute to sensible behaviour
in the sun later in life.
The SunSmart Campaign of the Anti-Cancer Council of Victoria has four sub-
programmes - schools, media and public education, community support and

21. CASE STUDIES

 sponsorships (6). The campaign has a strong empirical base - ongoing
research and evaluation determine its direction and content. This multifaceted
approach, which ensures that the messages promoted through schools are re-
inforced at the broader community level, has been a major factor in the success
of the programme. The Schools Program also has the endorsement of the
Department of Education and other key educational and health bodies.
The SunSmart Schools Program emphasizes a whole school approach to
protection against the sun (see Box). The key element is policy development,
which as far as possible involves the whole school community - this increases
the likelihood of broad support for and long-term sustainability of the chosen
strategies. With the possible exception of shade development, most strategies
can be implemented quite easily and at low cost to the school and to parents.
Schools implementing an approved policy can apply for accreditation as a
SunSmart School. Successful schools receive a large (6ocm x 90cm) metal
SunSmart School sign, which both recognizes and promotes the school com-
munity's commitment to sun protection. A small joining fee partially covers the
cost of producing and distributing the sign, and every school that applies,
whether successful or not, receives a free copy of a teacher resource book, which
can be used as the basis for development of curriculum programmes in sun
protection.
Changes in staff and priorities can influence the level of support for the pro-
gramme. However, growing awareness of what the SunSmart School sign rep-
resents has raised parental expectations and encouraged schools to maintain
their commitment to protection.

A SunSmart school day

Liam, aged 8 years, is a Grade 3 student at a SunSmart School. A typical school day might
be as follows.
Before Liam leaves home, he applies SPF 30+ sunscreen and checks his school bag to ensure
that he has packed his broad-brimmed school hat, sunscreen and swimming gear. After being
dropped off, he walks into the school grounds past the SunSmart School sign on the front
fence.
Liam's first class is physical education, in which students practise for the next day's swim-
ming sports. The school conducts outdoor classes early in the morning whenever possible
to avoid the period when the UV level is at its highest. Students who did not apply sunscreen
before coming to school are given some from the school supply. The students and their
teacher wear hats on the way to the swimming-pool, and at all times while out of the water.
Some students wear special protective "sun suits", and those who do not are required to
put on a T-shirt when not in the water. At the end of the session, students are reminded to
reapply their sunscreen.

SECTION VI: CASE STUDIES

 Box continued
During the morning break, Liam helps to water the new trees the students planted recently
to provide more shade and improve the school environment. Students raised the funds to
purchase the trees and selected them themselves as part of the school's heatthand envi-
ronmental studies programme.
Later, Uam's class discuss the results of their homework assignment, in which they were
required to watch the television news or look in the newspaper and record maximum tem-
peratures and UV levels and the times of day at which they occurred. The class then dis-
cusses what this means in terms of the times of day it is safest to be outside, and what
precautions they should take. Students are asked to produce a poster showing what they
have learnt-these will be displayed in the local pharmacy as part of a promotion for sun
protective merchandise.
Shortly before the lunch break, Liam's teacher reminds the class to reapply their sunscreen
and demonstrates how to do it properly. Students eat their lunches in their classrooms before
going outside. Teachers wear broad-brimmed hats while on playground duty, and students
without approved hats are required to stay in a special shaded area. Five students who are
considered to have been particularly SunS mart receive tokens that they later give to their
teachers. These tokens contribute to class paints and at the end of the term the most
SunSmart class is rewarded with a special treat, such as an excursion.
Following afternoon classes, there is a brief assembly, where students are reminded about
the arrangements for the twilight swimming carnival the next day. There will be no school
in the morning and the event is to begin at 3 pm. A prize will be awarded to the most
SunSmart team and students are reminded to bring their hats, sunscreen and clothing to
cover up between events. A newsletter, explaining the arrangements to parents, inviting them
to attend and encouraging them to wear protective clothing is distributed before students
are dismissed for the day.

Evaluation and follow-up

Over 70% of Victorian primary schools have become SunSmart Schools since
the programme began in '994. The following comments from three school prin-
cipals reflect some of the outcomes achieved in participating schools and the
advantages of the whole-school approach.

"It's wondeiful to see the 'growth' in children's/parent's awareness since we first

became a SunSmart school. "
"We continue to see it as an important part of our school culture and
curriculum. "
"Children respond positively and have incorporated good habits in personal
sun/skin care."

21. CASE STUDIES

 Baseline data regarding protection practices in a sample of Victorian schools
were collected in 1998, with a follow-up study scheduled for 2001 and subse-
quently every three years. Unpublished data indicate significant improvements
in policy and practices since the introduction of the programme.
It is too early to evaluate the programme's impact on skin cancer rates,
which in any case cannot really be assessed independently of the broader cam-
paign. However, there is evidence of changes in frequency of sunburn and in
attitudes and behaviour relating to wearing a hat and using sunscreen (7).
Recent trends in skin cancer rates also suggest that education campaigns may
be beginning to have an effect (8).
However, the Schools Program does face some challenges. Because skin
cancer does not usually develop until later in life, it can be difficult to convince
people that protection is important. This applies especially to adolescents, for
whom the desire for a suntan is often driven by a more immediate need for peer
acceptance. Furthermore, protective clothing is generally perceived by young
people as unfashionable. Also, the majority of skin cancers are not life-
threatening, and in a society with relatively good access to medical services,
there can be a tendency to believe that because suspicious spots are easily
removed, skin cancer is not a serious problem. This is exacerbated by the fact
that political priorities focus on funding treatment as opposed to prevention.

Application to other health problems and settings

Protection against the sun is a relatively easy issue (compared, for example,
with issues such as tobacco, drugs, HIVjAIDS) for schools to begin with when
attempting to implement a whole school approach to health, as exemplified by
the Health Promoting Schools Framework (9). It is important however, that
schools focus on strategies that are realistic and achievable in the context
of their own school community; endorsement by key educational bodies is
particularly important.
Recognition of good practice is essential, but while accreditation has been
a successful element of the SunSmart Schools Program, it may not always be
appropriate. For example, it is generally less relevant for Australian secondary
schools, where differences from the primary school setting and adolescent atti-
tudes towards sun protection necessitate a different approach.
A national programme based on the Victorian model was implemented in
Australia in 1998 (10), and the principles of the SunSmart Schools Program can
be readily applied in other institutional settings such as child care centres and
pre-schools. Elements of the SunSmart Schools Program are now also being
adopted in other countries with high skin cancer rates, such as the United
States.

286 SECTION VI: CASE STUDIES

 References
1. Australian Institute of Health and Welfare (AIHW) and Australasian Association
of Cancer Registries (AACR). Cancer in Australia 1995: Incidence and mortality data
for 1995 and selected data for 1996. Canberra, Australian Institute of Health and
Welfare, 1996 (Cancer Series No. 10).
2. Khlat M et al. Mortality from melanoma in migrants to Australia: variation by
age at arrival and duration of stay. American Journal of Epidemiology, 199 2 ,
135: 1103-111 3.
3· Carter R, Marks R, Hill D. Could a national skin cancer primary prevention cam-
paign in Australia be worthwhile? An economic perspective. Health Promotion
International, 1999, 1473-82.
4· Marks Ret al. The role of childhood exposure to sunlight in the development of
solar keratoses and non-melanocytic skin cancer. Medical Journal of Australia,
1990, 152:62-66.
5· Giles GG, Marks R, Foley P. Incidence of non-melanocytic skin cancer treated in
Australia. British Medical Journal, 1988, 29 6 :13-18.
6. Sinclair C et al. From Slip! Slop! Slap! to SunSmart: a profile of a health educa-
tion campaign. Cancer Forum, 1994, 18: 183-187.
7· Hill D et al. Changes in sun-related attitudes and behaviour and reduced sunburn
prevalence. European Journal of Cancer Prevention, 1993, 2:447-45 6 .
8. Staples M, Marks R, Giles G. Trends in the incidence of non-melanocytic skin
cancer (NMSC) treated in Australia 1985-1995: are primary prevention programs
starting to have an effect? International Journal of Cancer, 199 8 , 78 :144-14 8.
9· WHO Global School Health Initiative. Health promoting schools. Geneva, World
Health Organization, 1998.
10. Dobbinson S et al. A national approach to skin cancer prevention: the National
SunSmart Schools Program. MedicalJournal of Australia, 1998, 16 9:5 13-5 14.

21. CASE STUDIES

 4. PREVENTION OF ASBESTOS-RELATED DlSEASES-
THE FINNISH APPROACH

A. Karjaiainen
Finnish Institute of Occupational Health, Helsinki, Finland

Asbestos has been widely used in modern societies. In Finland, some 250
applications and products containing asbestos have been identified in the con-
struction industry. The main asbestos-containing products are construction
sheets and thermal, fire and acoustic insulation materials (sprayed asbestos or
asbestos laggings). Further uses include asbestos blankets, ropes and yarns,
flooring materials, bitumen felts, adhesives, putties, plasters, ceramic tiles,
paints, and friction materials (e.g. car brakes). In Finland, the use of asbestos-
containing construction materials continued into the 1980s but was especially
common from the 1950S to the 1970s. Owing to its physicochemical structure,
asbestos is an extremely stable substance. All stages in the use and handling of
asbestos products may release asbestos fibres that pose a risk to the workers and
the entire population through the general environment and consumer products.
Asbestos is known to cause mesothelioma, lung cancer, lung fibrosis
(asbestosis), pleural plaques, pleural effusions and fibrotic lesions of the
visceral pleura. In addition, asbestos is suspected to increase the risk for
malignant diseases of the larynx and some gastrOintestinal organs. Prevention
of asbestos-related diseases relies on elimination of exposure to asbestos-
containing dust. The heaviest exposures occur in occupational settings, and pre-
ventive strategies therefore focus on the protection of the working population.
In Finland, 120-130 cases of asbestos-related cancer, 120 cases of asbestosis,
and 350 cases of asbestos-related pleural disease were reported as occupational
diseases each year during the late 1990s. For Western Europe, the number of
male deaths from mesothelioma alone is expected to almost double from 5000
in 1998 to about 9000 in 2018 (1).
While the risk of disease is highest among those with heavy exposure, a safe
level of exposure does not exist. Even low environmental exposures in domes-
tic or public buildings, in outdoor environments, or from consumer products
containing friable asbestos pose a potential risk. Asbestos-related diseases have
a latency time of 20-40 years from the onset of exposure to the occurrence of
disease. This makes children, whose remaining life expectancy is long, an espe-
cially vulnerable group for asbestos hazards. Children also breathe more air per
kilogram of body weight per day. Little is known about the possible long-term
consequences of low-level asbestos exposure during childhood. However, cases
of mesothelioma have been reported among the grown children of asbestos
workers (2). In some areas, uncontrolled environmental exposures starting
during childhood contribute Significantly to the total burden of asbestos-related
disease (3, 4)·

288 SECTION VI: CASE STUDIES

 In Finland, legislative measures to gradually restrict exposure to asbestos
started in the mid-1970s. However, in the mid-1980s society became increas-
ingly concerned about the sufficiency and scale of the measures planned and
implemented. In response, the Ministry of Social and Health Affairs requested
the Institute of Occupational Health to prepare a proposal on how to tackle the
problem. Consequently, a nationwide Asbestos Programme was carried out in
1987-92 in close cooperation between government authorities, labour market
organizations, occupational health and labour protection personnel, other inter-
est groups and the mass media, with the common goal of preventing all expo-
sure to asbestos, both occupational and non-occupational (5). The legislative
and administrative actions of the programme were set out by the national
Asbestos Committee in its final report (6). The committee report lists 27
measures falling under the responsibility of six ministries. The two main sets
of measures proposed were a total ban on all new use of asbestos and
asbestos-containing products, and improved control and stricter regulations
concerning removal of existing asbestos. These measures gained widespread
support and were rapidly incorporated into the Finnish legislation.
The Committee also proposed more stringent measures to ensure a safe
living environment for children and the general population. The Committee esti-
mated that two-thirds of all the asbestos used in Finland was still in place in
bUildings in the late 1980s, and that one-third of all buildings still had some
asbestos-containing materials. This proportion was estimated to be higher for
public buildings than for domestic dwellings. Consequently, the following was
agreed on:

In 1989, the National Board of Health issued recommendations on asbestos

abatement in schools, kindergartens, hospitals and other public buildings. These
recommendations underlined that before any removal work, the buildings
should be inspected for possible release of asbestos fibres. In case of such a pos-
sibility, the abatement work should be peiformed during school or kindergarten
holidays. The recommendations also addressed the isolation ofthe work site from
remaining facilities, appropriate ventilation during the abatement work, clean-
ing, and measurements necessary to assess the effectiveness of cleaning. These
principles were integrated into the regulations concerning asbestos abatement
work.
In 1990, the guidebook on the maintenance of houses published by the
National Board of Health determined less than 0.01 fibres/cm 3 as a standard for
airborne asbestos in dwellings. This limit value is 30 times lower than the current
standard for occupational exposure. During normal activities, the observed con-
centrations in domestic dwellings, schools and other public buildings were clearly
below the limit. In situations, where asbestos materials were processed or
demolished, the limit value was commonly exceeded even in adjacent parts of
the building.

21. CASE STUDIES

 A total ban on the use of asbestos has been in force in Finland since 1994
and only licensed companies using special techniques and trained personnel
are allowed to remove asbestos. The remaining challenge for the prevention
of asbestos-related diseases is to ensure that the special asbestos abatement
techniques are always applied. The State Asbestos Committee recommended
that all buildings that are likely to contain asbestos, as a result of their age and
type, should be systematically inspected and any asbestos-containing materials
marked. If these are intact, closed and do not release asbestos fibres, they can
be left in place and should be properly removed when the building is next
renovated. If the asbestos-containing materials are friable and release asbestos
fibres, they should be immediately removed or securely covered. The State
Council Resolution on Asbestos Work (1380/94) further emphasizes that the
constructor is obliged to ensure that materials to be demolished do not contain
asbestos. If this is not ensured, the demolition work has to be carried out
according to regulations concerning asbestos abatement work.
In addition to a solid legislative background, the prevention of asbestos
hazards relies on a widespread public awareness. The national asbestos pro-
gramme initiated an intensive information campaign to guarantee that poten-
tial asbestos hazards are always identified and appropriate measures taken to
eliminate them (5). On several occasions, alert environmental protection per-
sonnel, school and kindergarten personnel, or parents have identified poten-
tially dangerous situations in schools or kindergartens with friable or broken
asbestos materials, or even outdoor environments located close to asbestos-
producing or manufacturing facilities.

References
1. Peto ) et al. The European mesothelioma epidemic. British Journal of Cancer,
1999, 79:666-672.
2. Anderson HA. Family contact exposure. In: Proceedings of the World Symposium
on Asbestos, Montreal, 25-27 May 1982. Montreal, Canadian Asbestos Informa-
tion Centre, 1982: 349-362.
3. Dumortier P et al. The role of environmental and occupational exposures in
Turkish immigrants with fibre-related disease. European Respiratory Journal, 2001,
17:9 22-9 27.
4. Luce D et al. Environmental exposure to treolite and respiratory cancer in New
Caledonia: a case-control study. American Journal of Epidemiology, 2000,
15 1:259-265.
5. Huuskonen MS et al. Finnish Institute of Occupational Health Asbestos
Program 1987-92. American Journal of Industrial Medicine, 1995, 28:123-142.
6. Asbestos Committee. [Final report 66/1989.] Helsinki, Ministry of Labour, 1990
(in Finnish, English summary).

29 0 SECTION VI: CASE STUDIES

 5. INFORMAL MARKETS OF TEGUCIGALPA, HONDURAS:
ADOLESCENT PARTICIPATION IN MARKET CLEAN-UP
CAMPAIGN

D. C. Kaminsky
Fundaci6n Desarol/o, Amistad y Respuestas (FUNDAR),
Tegucigalpa, Honduras

Description of the problem

Project Alternatives, a nongovernmental organization, introduced an inte-
grated approach to the provision of primary health care and education services
for a population of working street children and adolescents and their families
in the informal market sector of the capital city of Honduras, Tegucigalpa.
Most of the children assist their family (usually a working single mother) in
selling goods at a small stall or while walking through the markets and the
surrounding streets. The goods vary from vegetables and fruits to candies,
women's stockings, etc. Thousands of children and adolescents are found in
the six markets. Multiple interventions included health education, primary
health care, recreation activities, youth clubs and a "school for parents". The
integrated approach was taken in order to address the multiple risks and inter-
actions that determine the health and well-being of the children and young
people. Also, there was a desire to provide a menu of activities whereby the
beneficiaries could select those most interesting and important to them at
different points in time.
Youth clubs were established in each market. Usually the clubs were com-
posed of 25-50 adolescents and met once a week. This organization scheme
provided the opportunity for the young people to have a voice in planning and
conducting the various activities of the project, allowed a space and time for
recreational activities for those who usually did not have this opportunity, and
provided an organizational scheme for health education sessions, other train-
ing sessions and special activities.
In the informal markets, regular waste disposal was almost non-existent.
Waste was thrown on the ground near the vending stalls and left to rot, attract
flies, and occaSionally be carried away to an open municipal dump nearby.
Municipal control standards defining hygienic practices applied but were not
enforced. The exposed population group was the adult vendors, their working
children and their customers. Cholera and other diarrhoea problems are
endemic in the country, thus the sanitary conditions of these markets provide
the perfect setting for the development of an epidemic. Fortunately, there has
not been an epidemic in these markets in recent years.
Project Alternatives introduced a waste management programme into its
ongoing interventions as a special activity. Funds to support this special
activity were taken from the general fund of the organization. The programme

21. CASE STUDIES

operated in six different market areas in various parts of the capital city. Some
training activities were conducted in the open drop-in centre of the organiza-
tion, which is five minutes walking distance from three of the six markets.

Management and intervention

The mothers of the working children, through the education activities of the
School for Parents, were made aware of the potentially grave health conse-
quences of the prevalent sanitary conditions of their workplace. Promotion of
participation of children and adolescents was a cornerstone of the programme.
Thus the conditions were right for the adolescents to take an active role in a
market clean-up programme. At the same time as the mothers were talking with
their children about the lack of proper waste disposal in the marketplace, the
youth clubs from the six different market areas were forming a Youth Advisory
Council with representation from all markets. The market waste disposal cam-
paign was taken on by the Youth Advisory Council as the first joint project con-
ducted under a common planning scheme for all markets. Besides the School
for Parents, the Youth Advisory Council also coordinated mass clean-up cam-
paigns of the Mayor's Office and the Fire Department when the markets would
be closed for one day periodically and the firemen would wash down the streets
with their fire hoses. The local Market Vendors' Associations also participated
in the planning of all activities.
A formal plan of action was prepared by the Youth Advisory Council.
Activities included health education sessions for the adult market vendors,
and for the first time the placing of waste barrels in the markets. The barrels
were painted with a message and the name of Project Alternatives. Carts were
provided for carrying away the waste to the common disposal area, from
where the municipal garbage disposal trucks transported it to a landfill outside
the city. Health education posters were created by the young people and hung
in various stalls and passageways of the markets. The young people also
went through the markets collecting the waste, to serve as an example of
the conduct they were promoting. The administrators of the market encouraged
the vendors to use the newly placed barrels. The vendors reacted favourably
and were receptive to these new ideas. The youth clubs of each individual market
were responsible for the activities in their area and Council members monitored
the activities. Approximately 100 young people were involved in the campaign.
All the work was facilitated, planned and introduced under the gUidance of
the street education staff of Project Alternatives. The timetable for the inter-
vention was as follows: one month before the mass campaign, health educa-
tion activities were carried out in the markets both with groups and at the
individual stalls; during this same time the barrel posters were purchased and
painted; close to the campaign, coordination was established with the Mayor's
office and the firemen. The campaign was carried out on a different day in each
of the markets.

SECTION VI: CASE STUDIES

 Follow-up and reference to other settings
The barrels were painted two more times at 6-week intervals in order to keep
them looking new and attractive. During the 6 months following the mass
campaign, young people made weekly visits to the stalls and conducted related
health education activities, with the objective of reinforcing the use of the barrels
for waste management in the markets and of promoting recognition of health
risks related to an inadequate waste disposal system.
The factors that contributed to the success of this intervention included the
role played by the mothers, who brought the situation and the need for a control
programme to the attention of the young people. They allowed the young people
to leave their selling activities in order to participate in the campaign, and they
attended the group and individual health education orientation sessions. The
coordination with official sectors of the city and the markets, and the Youth
Advisory Council, were also important. Project Alternatives enjoyed an excellent
reputation and working relationship with the municipal authorities and the
market administrators through its permanent presence and activities in the
markets, so that it was not difficult to obtain the cooperation and assistance
of these entities.

21. CASE STUDIES

293
 6. ARSENIC EXPOSURE AND CHILD HEALTH

M. Rahman
Public Health Sciences Division, ICDDR, B Centre for
Health and Population Research, Dhaka, Bangladesh

Introduction
Historically, surface waters in Bangladesh have been contaminated with bac-
teria, causing a significant burden of acute gastrointestinal diseases. In the
1970S and 1980s, tube-wells were installed throughout the country to provide
an alternative safe water source, resulting in a decrease in the incidence of diar-
rhoeal diseases. However, a major proportion of the tube-wells contain levels
of arsenic that far exceed WHO's guideline limit of 1ollg/l, and even the less
stringent standard of 50 Ilg/1 set by the Government of Bangladesh. Since 1993,
the occurrence of arsenicosis, a term used to describe the symptoms associ-
ated with chronic ingestion of arsenic, has been marked and widespread. Today,
an estimated 97% of the rural population use tube-well water for drinking,
cooking, and irrigation, and a recent report from the World Bank estimates that
20 million inhabitants of Bangladesh rely on arsenic-contaminated drinking-
water. Young children are now also showing signs of chronic arsenic poisoning.

Review of the impact of arsenic on child health

Health effects of arsenic exposure
Arsenic is an enzyme poison that affects almost all organ systems.
Characteristic skin lesions and skin cancer represent the most important

Table 21.3 Characteristics of Bangladesh and the extent of arsenic contamination

of tube-well water

CHARACTERISTICS
Total area (km2) 148393
Total number of districts 64
Total population (million) 120
Total children <14 years (million) 44.4
Number of districts with arsenic in tube-well water> 50llg/1 42
Area of arsenic-affected districts (km2) 92106
Population in affected districts (million) 79.9
Number of districts with identified patients with arsenic-induced skin lesions 25
Children in affected districts <14 years (million) 29.5
Children in affected districts <4 years (million) 7.4
Children in affected districts <9 years (million) 16.7

Source: refs 1 and 2.

294 SECTION VI: CASE STUDIES

health effect of chronic ingestion of inorganic arsenic. A cross-sectional survey
of four rural villages revealed a 29% prevalence of arsenic-related skin lesions
among Bangladeshis over 30 years of age. Furthermore, Milton et al. (3)
reported an association between chronic arsenic ingestion and "chronic bron-
chitis" among 94 individuals with arsenic-associated skin lesions in three
Bangladeshi villages. The mean concentration of arsenic in drinking-water was
614/-lgjl.

Effects on reproduction
There is some evidence that arsenic exposure is associated with adverse
reproductive and developmental outcomes. Women working in highly exposed
jobs in a Swedish copper smelter had higher rates of abortion (28% versus
14%), and gave birth to babies of lower birth weight than nearby residents (3.087
versus 3.394 kg). In addition, smelter employees who worked during pregnancy
had higher rates of congenital malformations than employees who did not work
during pregnancy. In Hungary, exposure to drinking water containing more than
100/-lgjl of arsenic was associated with increased rates of spontaneous abor-
tion and stillbirths. In Chile, rates offetal, neonatal, and postnatal infant mor-
tality were all elevated with high arsenic exposure.

Effects of arsenic in children

Limited information exists on possible health effects among exposed chil-
dren. A study on child growth and intellectual ability in Thailand revealed that
chronic arsenic exposure as assessed by arsenic concentrations in hair was
related to a decrease in intelligence quotient. The possible impact of arsenic on
children has not received sufficient attention to date, but the collective evidence
from human and laboratory studies suggests a large potential for adverse effects
on child health and development.

Safe water options

Both governmental and nongovernmental organizations have recognized an
urgent need to provide safe drinking-water to arsenic-affected areas of
Bangladesh. Four potential sources of arsenic-free drinking-water have
been identified, namely: (1) treated surface water, (2) rainwater, (3) treated
groundwater, and (4) deep aquifers. Once a safe water source has been made
available, continuous monitoring of its operation and maintenance is necessary
over several months, to ensure that people do not return to using tube-well
water.

Treated surface water

Filtering pond surface waters through a large tank filled with sand and
gravel - the community-based pond sand filter - can remove bacteria and
provide safe water for drinking and cooking.

21. CASE STUDIES 295

 Rainwater harvesting
Rainwater harvesting is already being introduced in arsenic-affected areas
and can supply enough water for drinking and cooking throughout the dry
season. The harvesting system uses a tin rooftop or plastic sheet to collect rain-
water, which is then transferred into large cement tanks, where it can be stored
indefinitely without bacterial contamination.

Deep aquifers
The deep aquifer of the underground water table is arsenic-free in most areas
of Bangladesh, and may provide a good alternative water source to replace the
arsenic-contaminated shallow aquifer.
In many regions of Bangladesh, especially in the southern part of the
country, the alternative water sources currently in place, i.e. treated surface
water, arsenic removal technologies and rainwater harvesting, are not viable
throughout the year or are beyond the reach of the poor communities. The Gov-
ernment of Bangladesh, with financial support from the World Bank and the
Danish and Swiss Development Agencies, has recently initiated the Bangladesh
Arsenic Mitigation Water Supply Project (BAMSWP) to provide one deep tube-
well for each group of 50 families.

Treatment of groundwater
Treatment of groundwater is also a potential option in rural Bangladesh. The
following arsenic removal techniques are available:

Three Koishi filter

This filter is normally used to remove arsenic at the household level. It is
simple to construct out of materials that rural people are familiar with, and is
based on a technology that is endogenous in Bangladesh. However, the flow-
rate of water through the system is low and the amount of water produced is
small. Despite these limitations, it is cost-effective, convenient and frequently
used in rural communities.

Alcan/Buet-activated alumina
This method of arsenic removal is commonly employed at the community
level. Technically, the system is very effective, at least in the short term and,
because it is easy to use, is well accepted. Filtration rates are good in terms of
serving the demand of the community. Although the initial cost is very high, the
method is cost-effective in long-term use and in rural communities.

Steven/Tetrahedrons method
The Steven/Tetrahedrons method is also used at the community level to
remove arsenic but is less effective than the Alcan/Buet-activated alumina
method.

SECTION VI: CASE STUDIES

29 6
 Communication and awareness raising
Bangladesh is divided into six divisions, 64 districts, 464 upazillas and
several thousand unions. Supportive health campaigns and awareness
raising at the upazilla and union level form an essential part of any approach
to mitigate arsenic-related health problems. A baseline survey needs to be con-
ducted throughout the affected upazillas to assess knowledge, attitudes and
practices regarding arsenic contamination of tube-wells, patterns of water use
in the community, the prevalence of arsenicosis, and the availability of local
resources. Various governmental and nongovernmental stakeholders should be
involved in raising awareness with a special focus on improving children's
health.

Sensitization meetings
Sensitization meetings at the upazilla and union levels should be held to
raise awareness and generate commitment among key stakeholders, and to
mobilize the rural community, especially women and children.

Courtyard meetings
In Bangladesh, water for domestic purposes is mostly collected and handled
by women. Courtyard meetings could serve to disseminate important informa-
tion on the health hazards of arsenic and the importance of safe drinking-water,
and could ultimately inspire women to implement arsenic-free safe water
options at their own cost.

Tea stall sessions

Men usually attend the local weekly bazaar to buy necessary goods and to
exchange information in tea stalls. These tea stalls provide an opportunity to
disseminate health messages to men, who dominate the decision-making
process at the household level.

School health programmes

Children can successfully convey messages to their families and ultimately
bring about changes in the family environment. Young adolescents should be
provided with information on arsenic, safe drinking-water and sanitation
through a variety of teaching methods and classroom activities. A rally could be
organized by students, teachers and community leaders to raise awareness in
the community.

Training of traditional medical practitioners

In Bangladesh, there is one physician per 4866 population (4). which is
grossly inadequate. As a result, a large number of people seek medical services
from rural traditional medical practitioners, who form an essential part of
Bangladesh's health care system, espeCially in the rural community. These

21. CASE STUDIES 297

traditional healers can playa crucial role in disseminating information about
arsenic.

Conclusions
An increase in adverse health effects and more widespread knowledge
about the gravity of the situation has led to panic in many affected commu-
nities. Children suffering from arsenicosis are often isolated by their school mates,
illustrating that arsenicosis is not only a major health hazard but also a large
psychosocial burden. Arsenic-related problems must be addressed through an
integrated, comprehensive approach to mitigate the sufferings of the affected
population.

References
1. Chowdhury UK et al. Groundwater arsenic contamination in Bangladesh and
West Bengal, India. Environmental Health Perspectives, 2000, 108:393-337·
2. Health and demographic surveillance system. Matlab, ICOOR, B, 2001
(http:f j202.136.7.26jorgjorgunits.jsp?idOetails+58&search I0=5 8).
3. Milton AH, Rahman M. Respiratory effects and arsenic contaminated well water
in Bangladesh. International Journal of Environmental Health Research, 2002,
12:175-179.
4. Bangladesh Bureau of Statistics. Statistical pocketbook. 2000 (www.sdnpbd.orgj
sd ijstatisticapocketbookji ndex.htm).

SECTION VI: CASE STUDIES

 7. HOUSEHOLD WATER TREATMENT: A SUCCESS STORY

J. 1. Macy
R. E. Quick
Safe Water System, Centers for Disease Control and
Prevention, Atlanta, GA, USA

Description of the problem

Diarrhoeal diseases, which are frequently transmitted by contaminated
water, are a leading cause of illness and death among children under 5 years
old in developing countries. Human or animal faeces often contaminate unpro-
tected sources of surface water (such as rivers, lakes, or springs) and ground-
water (such as shallow wells). Piped water can become contaminated through
cracks or unofficial connections in water lines. Also, if piped water is not
adequately treated, the water delivered to the tap may be contaminated. Water
can become contaminated during transport if carried in dirty containers or
touched by dirty hands. Stored water can become contaminated if it is stored
in a dirty or uncovered container, removed with a dirty cup, or touched by soiled
hands.
Worldwide, over 1.1 billion people lack access to protected water supplies.
Rural villages in Nyanza Province in western Kenya provide a good example of
a population without access to safe water. The communities rely on unprotected
surface water sources. In 1999, a survey conducted by CARE, an international
nongovernmental organization, revealed that 66% of the population in this
impoverished region lacked access to improved water supplies, and 47% of chil-
dren younger than 5 years had experienced diarrhoea in the preceding 2 weeks.
The populations of most of the surveyed villages did not have access to health
care. When a child is sick with diarrhoea, the mother treats the child at home,
usually with traditional remedies, and is unable to earn money for the family.

Management and intervention

In response to the problem of lack of access to safe water, the United States
Centers for Disease Control and Prevention (CDC) and the Pan American Health
Organization/World Health Organization (PAHO/WHO) developed the Safe
Water System, a household-based water quality intervention (www.cdc.gov/safe-
water). The intervention has three main components: (1) point-of-use treatment
with locally produced sodium hypochlorite solution; (2) safe storage through
the use of containers with a narrow mouth, tight-fitting lid, and a spigot for
removing water; and (3) behaviour change techniques, such as social market-
ing, community mobilization, motivational interviewing, and hygiene education.
In projects in Africa, South America, and Central Asia, families who used the
Safe Water System had 44-85% fewer episodes of diarrhoea than families who
did not.

21. CASE STUDIES 299

 The CARE-CDC Health Initiative, which was created through a grant from
the Woodruff Foundation to foster increased collaboration between the two
organizations, awarded a grant to CARE Kenya in October 1999 to implement
the Safe Water System in Nyanza Province. A total of 72 communities with a
population of 45000 people were selected for the project on the basis of having
very limited or no access to protected water supplies. The different sectors and
organizations involved in planning and implementing the intervention included
CARE, CDC, a private company that produces sodium hypochlorite solution,
and management committees at the local level that used participatory hygiene
and sanitation transformation (PHAST) methods. Formative research con-
ducted by CARE revealed that 91% of households stored drinking-water in open-
mouthed clay pots and that these pots were preferred over plastic jerry cans.
Laboratory and village-based studies determined that contaminated surface
water treated with an adequate dose of sodium hypochlorite retained free
chlorine residuals greater than 0.2 mgjl for 24 hours and had no detectable
bacterial contamination.
Responding to the preference for storing water in clay pots, the project
worked with the Oriang Women Pottery Group to produce improved pots with
narrow mouths, fitted lids, and spigots. Point-of-use water treatment was pro-
moted through the use of 1% sodium hypochlorite solution that was manufac-
tured in Kenya and packaged in a bottle with an 8-ml cap that served as a dosing
device.
The behaviour change techniques used in this project included community
mobilization and social marketing. The disinfectant solution was sold under the
brand name Klorin at a price affordable to the target population. Promotional
activities included puppet shows, skits, dancers dressed in Klorin bottle cos-
tumes, a truck with a loudspeaker system, soccer tournaments, public demon-
strations of the product, and Klorin quizzes with prizes. Village health
promoters received T-shirts, water vessels, or Klorin bottles as incentives for
meeting sales targets. To encourage improved water storage, the modified clay
pots were subsidized and packaged with a free bottle of Klorin during the pro-
motional period.
The project encountered difficulties. Daily power blackouts of up to 18 hours
hindered product procurement and delayed implementation by 3 months. In
addition, poor road conditions and large distances between communities made
product distribution difficult. Despite these challenges, the project was ulti-
mately successfully implemented.

Evaluation, follow-up and relevance to other settings

Six months after introducing the Safe Water System, product adoption was
monitored in a random sample of 20% of households in 12 project villages.
Water stored in 58 (33.5%) of173 households had detectable free chlorine levels,

300 SECTION VI: CASE STUDIES

indicating use of Klorin, and 32 (18.5%) of 173 households were using the
modified clay pots.
To evaluate the health impact of the intervention, active diarrhoea surveil-
lance, which consisted of weekly home visits by field workers trained by CARE
to ask about diarrhoea episodes in children less than 5 years old in the preced-
ing 7 days, was conducted for 8 weeks in 12 intervention and six comparison
communities. Klorin use was also measured weekly by testing stored water for
free chlorine. The surveillance data were analysed to determine adherence to
Klorin use and the effect of various factors on diarrhoea rates. During the 8
weeks, 37-60% of households in intervention communities had free chlorine
levels over 0.2 mgjl in their water. Overall, there was a 74% lower risk of diar-
rhoea in intervention communities than in comparison communities. House-
holds using Klorin had a 58% lower diarrhoea risk than households not using
Klorin, and households with latrines had a 45% lower diarrhoea risk than house-
holds without latrines.
Several factors contributed to the success of this intervention. First, CARE
conducted thorough formative research to identifY the local knowledge, atti-
tudes, and practices related to water and diarrhoeal disease. Second, CARE
obtained support early in the project from Kenyan government officials, com-
munity management committees, and leaders of women's groups. Third, CARE
used a participatory approach to mobilize the community, which motivated and
empowered the population. Fourth, the local community identified poor water
quality and diarrhoea as their highest priority problems, so they were motivated
to adopt the Safe Water System. Fifth, because the Safe Water System is a simple
and inexpensive intervention, it was adopted by a large percentage of the target
population. Sixth, social marketing activities conducted by CARE helped make
the disinfectant solution and improved clay pots accessible.
To build on the momentum of these successes, the project is looking for
opportunities to expand. In particular, CARE will engage the private sector by
recruiting commercial establishments to sell Klorin at the current low price. To
address the issue of economic sustainability, a Kenyan economist is conduct-
ing a cost-effectiveness study of the Safe Water System in this setting. In addi-
tion, further research on behaviour change strategies will be done to determine
the approach that is most effective in motivating sustained use of the Safe Water
System. The Safe Water System is relevant in any developing country setting
where water quality is a problem. Successful projects in countries other than
Kenya have demonstrated the intervention's practicality and usefulness. In
Zambia, a pilot social marketing trial in a periurban slum rapidly expanded in
response to a cholera epidemic and is now national in scope. The number of
bottles of disinfectant sold has grown every year, and sales exceeded 1 million
bottles in 2001. In Madagascar, CARE, Population Services International, and
CDC launched a Safe Water System project in 30 poor neighbourhoods in urban

21. CASE STUDIES 301

Antananarivo during a cholera epidemic, which immediately led to expansion
beyond the project site. A series of three cyclones over a g-week period accel-
erated demand to the point where the project grew to national scale in less than
a year. These experiences demonstrate that there is a need, desire, and market
for point-of-use water quality interventions in diverse communities throughout
the developing world.

SECTION VI: CASE STUDIES

302
 8. CONTAMINATED WATER DISTRIBUTION: AN INTERVENTION
STRATEGY TO SOLVE A PUBLIC HEALTH PROBLEM

J. C. Semenza
School of Community Health, Portland State University,
Portland, OR, USA

Description of the problem

Extensive irrigation of cotton fields has depleted water resources along the
Amudaria River leading to increased salinity and decreased fish population in
the Aral Sea. Uzbekistan has been disproportionately affected by the Aral Sea
crisis: along with declining socioeconomic status, the overall health of the pop-
ulation has deteriorated as a consequence of this environmental degradation.
To examine the health impact of this environmental crisis, we collected
passive surveillance data from the Sanitary Epidemiologic Services (SES) in
Nukus, a city of2ooooo residents, located 250 km south of the Aral Sea. While
rates of cancer and other chronic diseases were stable over the past decade
(with the exception of anaemia in women), we noted a marked seasonal pattern
in the occurrence of diarrhoea and dysentery each year. There was a tenfold
increase in diarrhoeal diseases duringthe summer months, with up to 180 cases
a month. The problem disproportionately affected children under five years of
age. Furthermore, the actual number of enteric cases was probably much higher,
because the SES data only reflect cases that were treated in hospital.
Exposure to gastrointestinal pathogens can arise from several sources, such
as surface water, household water containers, foods and drinks, poor personal
hygiene and sanitation, or municipal water supplies. In order to improve the
situation and take public health action to create a healthy environment for
children, the most significant route of transmission had to be identified.

Management and intervention

We examined food-handling practices, personal hygiene and sanitation in
the city of Nukus, but were not able to identify a significant overriding problem.
In fact, personal hygiene practices, such as hand-washing before eating,
appeared to be better than in the United States. We also evaluated the chlori-
nation procedures at the water treatment plants in Nukus and concluded that,
theoretically, the two-step chlorination procedure was adequate.
The pathway for diarrhoeal infections can be determined by establishing a
reference population. One possible source of exposure, such as the water
supply, is eliminated in this reference population and the impact on diarrhoeal
rates is monitored. By creating such a reference population, which differs in only
one respect (i.e. the water supply), conclusions can be drawn regarding the
mechanism of disease transmission. If the intervention does not have an impact
on diarrhoeal disease rates, the water supply is not contaminated; conversely,

21. CASE STUDIES

if the rates are reduced considerably the water supply is the likely source of the
contamination.
We conducted a randomized intervention study involving a total of 240
households, each with at least one child under five years of age, 120 with and
120 without access to municipal piped water (1). The intervention consisted of
providing a narrow-necked water container with a spout that prevented recont-
amination once the water had been disinfected with chlorine. Of the 120 house-
holds without access to piped water, 62 households received the intervention
and were monitored for diarrhoea for 9/2 weeks during the summer months
(when the highest rates were observed), along with two control populations:
households with and without access to piped water.
A group of local interviewers visited the households in the study twice a week
and asked an adult family member about diarrhoea or dysentery among the
family members. Intervention and no-intervention households were surveyed in
an identical manner.
The intervention was conducted as a collaborative effort between scientists
from the Centers for Disease Control and Prevention (CDC), SES, US Agency
for International Development (USAI D), and local physicians and municipal
officials.

Evaluation and effectiveness of intervention

In the intervention households we found a dramatic reduction in childhood
diarrhoeal rates. Children with access to disinfected water through their water
container were three times less likely to suffer from diarrhoea or dysentery than
the control group (42.2 episodes per 1000 children per month versus 127.7
episodes). Despite the fact that children in this intervention group did not have
piped water at home and thus were of considerably lower socioeconomic status,
they were half as likely to have diarrhoea as children in households with access
to piped water (84-4 episodes per 1000 children per month). These data indi-
cate that the deteriorating water distribution system in the city was contami-
nated, since children who drank tap water were more likely to get sick than
children in the intervention group. We also found that 30% of the households
with piped water lacked detectable levels of chlorine residues in their tap water,
increasing the risk for diarrhoea, in spite of the two-stage chlorination pro-
cedure. In at least 42% of the households, water pressure had been intermit-
tent in the two days prior to the interview.
On the basis of these epidemiological data we were able to implicate the
water distribution system as the main source of disease transmission: lack of
water availability (due to the Aral Sea crisis) and low water pressure allow
contaminated water to be drawn into the drinking water lines where it depletes
chlorine residues. This cross-contamination explains why subjects who drink
tap water with inadequate residual chlorine are more likely to develop diarrhoea.

SECTION VI: CASE STUDIES

It also explains why subjects who have access to household water treatment
suffer from fewer diarrhoeal episodes than those who drink tap water.

Conclusions
On the basis of these findings, with the support of USAI D, city engineers
increased water availability, allowing water pressure to be maintained in the dis-
tribution system. Leaks and water losses were minimized and chlorination was
closely monitored by municipal officials. These relatively inexpensive modifica-
tions are expected to reduce diarrhoeal rates in Nukus and to have a positive
impact on children's health, in contrast to other costly measures such as reverse
osmosis technology. Installing reverse osmosis technology to purify drinking-
water would have minimal impact on water quality since cross-contamination
would introduce gastrointestinal pathogens into the drinking-water.
Since the neighbourhoods without access to piped water were permanent
and long-standing rather than temporary, this intervention demonstrated the
feasibility of providing disinfected water to a disenfranchised population. The
intervention was well accepted by participants who realized the positive impact
it had on their health. Bleach, as a source of chlorine, and water containers are
readily available on local markets. However, the water containers used for this
study suffered from leaks and punctures suggesting the need for a more durable
type of container. Furthermore, the price of locally available water containers
was more than the study participants were willing to pay. Therefore, access to
these water containers remains a hurdle for widespread implementation of
household water treatment (see also Case Study 7).
This simple community intervention provides evidence for a cost-effective
public health solution that can be adapted in other settings where deteriorating
water treatment facilities and distribution systems pose a threat to children's
health. Furthermore, this case study in Uzbekistan illustrates how field epi-
demiology can be used as an analytical tool to address a children's environ-
mental health problem and to guide public health policy decisions.

Reference
1. Semenza JC et al. Water distribution system and diarrhoeal disease transmis-
sion: A case study in Uzbekistan. American Journal of Tropical Medicine and
Hygiene, 1998, 59:941-946.

21. CASE STUDIES

 9. A FLUOROTIC VILLAGE

E. Dah;
Environmental Development Co-operation Group, Soborg,
Denmark

The village
Ngungongare is a village of 2000 inhabitants in northern United Republic
of Tanzania. It lies at the foot of Mount Meru, within the Rift Valley, which con-
stitutes a large part of the African "fluoride belt", stretching from the Syrian
Arab Republic and Jordan through Egypt, Sudan, Ethiopia, Kenya, and the
United Republic of Tanzania down to South Africa. Natural weathering of the
volcanic and sedimentary rocks releases the fluoride ion from its complex
compounds into the natural waters.

Fluorosis
In Ngungongare, about 80% of adults and 95% of children are affected by
dental fluorosis. The adults who are not affected usually grew up in a low-fluo-
ride area. Healthy children are usually newcomers or still have milk teeth.
Nine-year-old Rebecca is a typical fluorotic child of Ngungongare, where she
was born and has lived throughout her life. Her severe dental fluorosis is illus-
trated in Figure 2l.3. Her parents, however, are "immigrants", with healthy,
regular, white teeth. Rebecca tries to avoid smiling and, when she does, she
covers her teeth in shame. All her teeth are affected, and some show deep black
erosions. Rebecca says that her teeth cause her pain when she has cold or hot
drinks or eats hard food.
Rebecca's arms and legs seem to be quite normal, with slight swelling
at the joints. So far she does not feel huma, as the early signs of fluorosis
associated with rheumatic fever and pain in the joints are called in Swahili.
Rebecca and her parents do not know that it is only a question of time before
she suffers from non-skeletal fluorosis and that in the long term she may suffer
disability. She is still too young to
understand that this irreversible
disability may be detrimental for
her future social life and working
opportunities.
But Rebecca is more fortunate
than others. Some children of her
age already have deformities in
their extremities, as shown in Figure
21.4. For example, Richard's elbows,

Figure 21.3 Dental fluorosis knees and ankles are enlarged and

SECTION VI: CASE STUDIES

 rigid. He suffers from the first stage
of skeletal fluorosis but is still
capable of moving around and
herding cattle. Up to 10% of the chil-
dren of primary school age suffer
from skeletal fluorosis; these chil-
dren are at very high risk of crippling
fluorosis later in life. Skeletal defor-
mities, rigidity and pain in the joints,
in addition to huma and teeth dis-
coloration and decay, are common
among the elderly in the village. Figure 21.4 Skeletal fluorosis

The water
When Rebecca is asked if she
knows the reason for her teeth dis-
coloration and deterioration, she
answers "ni maji"; it is the water. In
a fluorotic village like Ngungongare,
not only the water, but also air, soil
and crops contain fluoride at con-
centrations well above normal. Fur-
thermore, the local people tend to
use magadi, a carbonate/bicarbon-
ate salt that contains high concen-
trations of fluoride, as a food
additive. In some countries, indus-
trial and air pollution, especially due
to the burning of coal, may also
cause fluorosis. However, for a
typical fluorotic village like Ngun-
gongare, research has shown that
exposure through drinking-water
and water used in cooking is far Figure 21.5 A domestic defluoridation filter
more significant than all other expo-
su res taken together.
For decades, the villagers have been using the water from surrounding
springs whose fluoride concentrations vary between 2 and 8 mg/1. In recent
years, some families have started to collect rainwater for drinking during the
few months of the year when this is possible. A piped water scheme has been
made available to meet the increasing demand for water. However, this does
not solve the fluorosis problem but, on the contrary, worsens it, in part because

21. CASE STUDIES

 the piped water contains higher fluoride concentrations (of 12-21 mgjl), and in
part because the villagers now obtain less water from the springs and rain, as
the tap stands are easily accessible.

Similarity to arsenic
Fluoride shares some of its unfortunate properties with arsenic. In both
cases the water is usually without colour, turbidity, smell or taste, yet it contains
the agent at highly toxic levels. In both cases, equipment, chemicals and skilled
personnel are needed to measure the agent in the water. In both cases, the effect
on health does not appear immediately but with delay, and is irreversible. The
appropriate technology to remove both toxic agents from the water is available,
but experience with implementation is limited. And in both cases, the health
problems prevail mainly in developing countries with severe socioeconomic
constraints.

Mitigation
It has been estimated that more than 100 million people in the world suffer
from one or more types offluorosis. As in Ngungongare, the fluorosis problem
is increasing, mainly as a result of general improvements in life expectancy and
the increased use of groundwater. Providing piped supplies of safe water to fluo-
rotic areas is often not possible. In these cases, the only solution to the
problem is to install community or domestic defluoridation units for treatment
of the water to be used for drinking and food preparation.
Any reduction in fluoride exposure would be beneficial, but to ensure healthy
teeth for newborn children, the concentration of fluoride must be brought
down to about 0.5 mgjl, i.e. far below what has
been considered the "maximum allowable" and
"optimum recommended" levels. Defluoridators
are simple, workable and affordable and can be
made using local materials and manpower. Figure
21.5 shows such a domestic defluoridator. It can
be based on bone char, activated alumina or any
other fluoride sorption medium. But such units
can only be sustained if the family is disciplined
and motivated and if capacity-building, logistic
support and professional services are provided.
An alternative solution is shown in Figure 21.6, a
community unit ensuring that the water is taken
only for drinking and cooking.
Mitigation of fluorosis will be a great chal-
Figure 21.6 A community lenge for nongovernmental organizations and
def/uoridation plant donors in the decades to come.

SECTION VI: CASE STUDIES

 10. CARBON MONOXIDE POISONING IN CHILDREN IN FRANCE

M. Mathieu-Nolf
Poison Control Centre, Lille, France

Description of the problem

Carbon monoxide (CO) is a tasteless, odourless, and non-irritating gas pro-
duced by the incomplete combustion of organic materials. The most common
sources of CO include improperly maintained and poorly ventilated home or
water heating systems (unvented or defective gasjcoaljwoodjfuel stoves and
fireplaces, kerosene space heaters, water heaters), cooking devices (gas
burners, barbecues), car exhausts, and cigarette smoke. Most of these sources
are found indoors, where young children spend most of their time.
CO poisoning is a leading cause of accidental and fatal poisonings in many
countries. In France, between 5000 and 8000 poisonings occur every year
(10-15 cases per 100000 inhabitants) with about 25% affecting children under
15 years of age. Up to 400 people die from CO poisoning every year, of whom
16-4% are children.
When inhaled, CO is readily absorbed from the lungs into the bloodstream
and prevents oxygen uptake by binding to haeminic proteins. In addition to
hypoxaemic hypoxia, CO poisoning induces histotoxic hypoxia. Carboxyhaemo-
globin dissociation begins as soon as the patient is removed from the CO envi-
ronment. Beyond the high risk of immediate death during intoxication,
moderate to severe poisonings can lead to long-term effects including memory
impairment, personality alterations, signs of parietal dysfunction and, more
rarely, motor symptoms (hemiplegia, akinesia). In children, temporary cortical
blindness and involuntary movements have also been reported. To date, there
is little information about the risk of delayed neurological sequelae in infants
with CO poisoning. Generally, the long-term consequences of CO poisoning in
children are likely to be underestimated.
The frequency of CO intoxication varies between different regions depend-
ing on local heating or cooking habits, the socioeconomic situation, and
weather conditions. For example, the morbidity incidence rate varies between
17.5 per 100000 inhabitants in the Paris area and 24 per 100000 inhabitants
in the northern region. The high incidence in the north is a likely consequence
of the coal mining industry, which was active until 1980, the high rate of un em-
ployment and frequent fog.
As almost 30% of CO poisoning cases are misdiagnosed at first, the risk of
inadequate treatment is high. Despite efforts to improve prevention, medical
education and public information, intoxication remains frequent and severe,
and is too often overlooked. Early recognition and correct treatment and follow-
up of CO poisoning in children are crucial for the prevention of recurrence and
long-term health effects.

21. CASE STUDIES

 Management and intervention
Considering the high incidence of CO poisoning in the north of France, a
systemic approach was adopted to act on the multiple factors responsible for
CO poisoning.

Decreasing risk of CD exposure

A continuous surveillance system was set up by the regional poison centre
(PC) in 1986. This toxicovigilance programme follows up every case of CO poi-
soning that results in hospitalization. Data are collected from a network involv-
ing the Critical Care Unit and Hyperbaric Centre of Lille University Hospital,
every emergency department, paediatric unit and critical care unit of the regional
and general hospitals, medical rescue services, fire-fighters and environmental
health engineers at regional and departmental public health services. CO poi-
sonings are classified as certain, probable, suspected, not related, or unknown.
For every case, a systematic follow-up is carried out by medical staff of the
poisons centre by telephone or visits at 1, 3, 6 and 12 months after the poison-
ing occurred. To obtain information on deaths outside hospitals from CO poi-
soning (82% of victims are found dead at home or die before reaching hospital)
the poisons centre set up a complementary surveillance programme to record
all deaths, using other sources of information, such as forensic departments.
The two surveillance systems are used to monitor the frequency, severity and
mortality from CO poisoning, and to identify high-risk circumstances or popu-
lations. When the surveillance system detects a sudden increase in the inci-
dence of CO poisoning an alert is sent to health, environment and consumer
authorities, and to the general public via the media. For example, a rapid
increase in the incidence of CO poisoning in the north of France was detected
in 1989 related to the introduction of kerosene space heaters. National health
authorities and the consumer council were alerted, and as a result manufac-
turers were obliged to equip heaters with CO detectors and other safety devices.
During the following four years, only one case of CO poisoning was recorded.
However, after a change in regulations, six new cases were recorded in 1994
and the incidence of CO poisonings has been increasing ever since. New tech-
nical preventive measures are currently under investigation.

Increasing awareness and skills of health professionals

Training and continuous education programmes for medical students,
physicians and paramedics were developed aimed at preventing complications
and sequelae. The programme emphasizes the risk of misdiagnosis and inad-
equate treatment. Health professionals are encouraged to pay particular atten-
tion to high-risk populations such as pregnant women and children.
Data on CO poisoning in 140 children and 774 adults, collected at the Lille
University Hospital, illustrated the risk of misdiagnosis in infants. While
headache, nausea, and coma were less frequent in children than adults, uncon-

310 SECTION VI: CASE STUDIES

sciousness, convulsions, and lethargy were more frequent. Neurological exam-
inations found fewer abnormal plantar responses and more flaccidity in chil-
dren than in adults. Many of the early manifestations of CO poisoning are
difficult or impossible to observe in infants. Especially in neonates and toddlers,
CO poisoning is frequently interpreted as gastroenteritis.
The training courses were reformulated and improved to take into account
the particular difficulties of correct diagnosis and treatment in children.

Decreasing the recurrence rate

CO intoxication frequently recurs if no preventive measures are taken. The
Hyperbaric Centre and Emergency Department of Lille University Hospital and
public health engineers developed a programme to decrease the rate of recur-
rence. Information on the reasons for CO poisoning and preventive measures
is given to patients by medical staff just before the patient is discharged from
hospital, when he or she is most likely to be receptive to the health message.
Furthermore, the physician proposes that a public health engineer should visit
the patient's home to identify sources of CO and other factors relevant to CO
poisoning. Since the implementation of this programme in 1986, the surveil-
lance system has recorded a progressive decrease in the recurrence rate from
4.5% in 1993 to 1.5% in 2000. While this trend is encouraging, efforts must be
maintained.

Evaluation, follow-up and relevance to other settings

The implementation of a surveillance system prior to preventive action has
been the key factor for success. The system monitors data on CO poisonings
with a short-response time to provide up-to-date information to consumer asso-
ciations and other bodies. As it allows vulnerable subpopulations and risk
behaviours to be identified, prevention messages can be focused on these
groups and have greater impact.
A large multidisciplinary and highly motivated group consisting of physi-
cians and other health professionals, firemen, social workers, manufacturers,
heating professionals, and consumers was essential to raise awareness and
improve skills in relation to CO poisoning among health professionals and the
general public. Use of intermediary persons to convey the message was found
to be very effective.
Despite a multifaceted prevention programme the number of CO poison-
ings remains high. However, improved information dissemination, regulatory
measures and the implementation of specific social aids could further reduce
the incidence.

Conclusion
The approach to CO poisoning described can be taken as a model for an
efficient toxicovigilance system to monitor other environmental poisons and

21. CASE STUDIES 311

pollutants, such as lead. The evolution in data collection from simple data
recording via telephone calls to the active collection of representative and mean-
ingful data is essential for preventive action, and points to a much wider role
and responsibility for poison centres.

SECTION VI: CASE STUDIES

312
 11. CHILDREN DESERVE A SMOKE-FREE WORLD

A. M. David
S. A. Tamplin
Tobacco Free Initiative,
WHO Regional Office for the Western Pacific, Manila,
Philippines

S. Pineda-Mercado
Philippines Department of Health, Department of Health
Promotion and Health Education, University of the
Philippines, Manila, Philippines

Tobacco use contributes significantly to premature mortality and the burden

of chronic disease and disability in the Western Pacific Region. While the health
impact of the tobacco epidemic on smokers is well documented, the effect on
children exposed to second-hand smoke is less frequently recognized. Never-
theless, a growing body of evidence points to second-hand smoke as an impor-
tant risk factor for sudden infant death syndrome, asthma, and pulmonary and
middle ear infections in children (1).
The Philippines has 76 million inhabitants; about 40% are under the age of
15. One in three adults smokes, and an estimated 60% of households have at
least one smoker (1). Therefore, the number of children potentially at risk from
exposure to second-hand smoke in the home is considerable. In addition, before
1999, no national legislation existed to ensure smoke-free public places.
The influential lobby of the tobacco industry and the tobacco farmers' asso-
ciation from the northern provinces presented a barrier to policy changes
regarding tobacco control and provisions for smoke-free public places. A strong
and unequivocal message was needed to demonstrate that support for tobacco
control would be in the interest of the majority of the population, particularly
vulnerable groups such as children.
Working in partnership with the Philippine Department of Health, UNICEF
and a private advertising company, WHO developed a communications and
advocacy strategy with the aim of empowering nonsmokers to speak up and
defend their right to clean, smoke-free air. The precampaign survey indicated
that, while most tobacco control advertising focused on health risks to the
smoker, nonsmokers believed that they were also at risk. In addition, the non-
smoking survey respondents reported feeling annoyed and resentful when
exposed to tobacco smoke, but were reluctant to speak up, even in areas des-
ignated as nonsmoking.
WHO created three television advertisements, set in the family environment,
the workplace and a coffee bar, carrying the message: "It's OK to say you mind."
These focused on the dilemma nonsmokers face when persons near them light

21. CASE STUDIES

up, and their hesitation to address the issue. In all three advertisements, the
individuals who find the courage to speak up for themselves are surprised to
find that smokers, even teenagers, are responsive and willing to stop smoking
when asked.
One of the advertisements attempted to relate the nonsmoker's right to
clean air with the high value Filipinos give to their children's welfare. Filipinos
treasure their offspring, and this is even reflected in national policy. The Decla'
ration of Policy of the Child and Youth Welfare Code states: "The child is one of
the most important assets of the nation. Every effort should be exerted to promote
its welfare and enhance its opportunities for a useful and happy life." Filipino
parents are willing to sacrifice much for their children's sake. Thus, when made
aware that they are unintentionally exposing their children to a health hazard,
many parents will give up their hazardous behaviour. The advertisement illus-
trates this by depicting a family with three young children and a father who
smokes at the dinner table. After hearing one of the children coughing in the
background, the eldest son gently speaks up and asks his father not to smoke.
The father is momentarily taken aback, but realizing that his smoking is
adversely affecting his children, he apologizes and puts out his cigarette.
All three advertisements were run on national television from October 1999
to January 2000 using commercial and public television stations. A postcam-
paign survey to assess the impact of the communications campaign was carried
out in February 2000. This survey showed that the advertisement featuring the
smoking father and his children was the best remembered among both smokers
and nonsmokers (Table 21-4), and that the visual elements and message were
the most recognized (2). Graduate students at the College of Mass Communi-
cations of the University of the Philippines evaluated locally produced tobacco
control-related TV advertisements from 1992 to 2000, based on visual attrac-
tiveness, audience recall, cultural relevance and overall impact. This particular
advertisement was considered to be one of the most effective in conveying the
powerful health message to refrain from tobacco use.
While a child's right to a safe and healthy environment is not yet anchored
within the Convention on the Rights of the Child, the Philippines' Child and
Youth Welfare Code states clearly that "every child has the right to live in a

Table 21_4 Audience recall of television advertisements

TELEVISION ADVERTISEMENT AUDIENCE RECALL (%)

SMOKERS (n = 81) NONSMOKERS (n = 75)
1: Family at dinner 31% 23%
2: Peer group 1% 11%
3: Workplace 9% 12%

SECTION VI: CASE STUDIES

community and a society that can offer him an environment free from pernicious
influences and conducive to the promotion of his health and the cultivation of his
desirable traits and attributes." Partly as a result of the media exposure gener·
ated by the television campaign, both the public and the private sector started
to show interest in tobacco control as a means to protect the rights of children
to a clean and healthy environment. For example, the Philippine Paediatric
Society and the National Asthma Movement started to include sessions on
tobacco as an environmental hazard to children in their various conferences and
national congresses. The National Institutes of Health and the Department of
Health held a research forum for the media and academia on the effects of
involuntary exposure to tobacco smoke among infants and children. The Depart·
ment of Health chose the theme of protecting children from tobacco smoke in
its tobacco control campaign. On World No Tobacco Day 2000, they organized
a Youth Congress where young people from each of the political districts held
a symbolic session at the National Congress to pass tobacco control legislation.
These young people gave impassioned speeches on why it is critical for the gov·
ernment to speak up on behalf of all Filipino children and take action to pre·
serve their right to a clean, tobacco-free environment.
The Philippine Clean Air Act, ratified in '999, has been in the process of
implementation since 2000. It includes a provision for smoke-free enclosed
public places and public transport. While enforcement needs to be improved,
it represents significant progress towards ensuring a healthy indoor environ-
ment for children. A new alliance of government and nongovernmental organi-
zations is continuing political advocacy for tobacco control using the issue of
safeguarding children's health as a major theme.
Emphasizing the hazardous effect of exposure to second-hand smoke on
children's health can also serve as a means to broaden the audience for tobacco
control advocacy. By demonstrating the consequences of indirect exposure to
tobacco smoke, nonsmokers - who form the majority of the population but
are often left out of typical tobacco control messages - can be engaged in
tobacco control. Policy leaders and legislators may not always be receptive to
the health arguments for controlling tobacco use. However, these key political
leaders are sensitive to issues that involve infringement of the rights of vulner-
able groups, particularly children. Framing tobacco control as a means of pro-
tecting children's rights to clean air and a healthy environment can be a potent
tool towards mobiliZing support for tobacco-free environments.

References
1. International Consultation on Environmental Tobacco Smoke (ETS) and Child
Health, 11-14 January 1999. Geneva, World Health Organization, 1999 (back-
ground papers).
2. Taylor Nelson Sofres Philippines. Campaign effectiveness survey, 2000. Manila,
2000.

21. CASE STUDIES

 12. IMPROVEMENT IN RESPIRATORY SYMPTOMS IN CHilDREN
AS A RESULT OF POllUTION CONTROL STRATEGIES
IN A DISTRICT OF THE CITY OF SAO PAULO, BRAZil

H. Ribeiro
School of Public Health, University of Sao Paulo, Brazil

Sao Paulo, Brazil, an urban sprawl of 1051 square kilometres and 16.7 million
inhabitants, is one of the biggest cities in the world. Over 40000 potentially
polluting industries and 5.7 million vehicles are currently registered.
During the 1970s, emissions from factories had an important influence on
health problems as industrial activities of a diverse nature dominated the
economy of the region until the 1980s. The installation of industrial plants close
to residential areas was common and, in several cases, this resulted in severe
health risks. Respiratory diseases were the second largest cause of death in Sao
Paulo in 1980. The process of industrialization and land occupation, together
with meteorological conditions unfavourable to the dispersion of pollutants (fre-
quent low altitude thermal inversions during winter in a topography formed by
a floodplain surrounded by mountains in the north and north-east, receiving
predominant winds from the ocean in the south-east) resu Ited in the deterio-
ration of air quality.
The average concentration of sulfur dioxide and particulate matter in air in
the metropolitan area for 1973-1984 was mapped by this author. A survey was
conducted at seven schools of the government school system in three neigh-
bourhoods of Sao Paulo, to assess the influence of air pollution on respiratory
symptoms of children between 11 and 13 years of age. The three neighbourhoods
had a similar family income but distinct pollution levels reflecting different types
of land use. The first district, which was used as a control area, was a water-
shed protection area surrounded by parks; the second was a blue collar worker's
district with more modern industrial plants and medium pollution level, close
to the air quality standard limits of the national Environment Bureau (CETESB)
(1); the third showed very high levels of pollution throughout the year. The age
group was chosen because children are more sensitive to air pollution, do not
smoke and are not affected by occupational pollution. Children may receive a
higher dose of outdoor pollutants than adults because they have a higher
minute ventilation per unit body mass, are generally more physically active, and
spend more time outdoors than adults (2). The research tool employed was a
questionnaire developed by Ferris and a team from the Pulmonary Disease Divi-
sion of the US National Heart, Lung and Blood Institute in the Epidemiology
Standardization Project (3). Between 100 and 150 questionnaires were com-
pleted in each of the three neighbourhoods.
The area where pollution levels were highest was Tatuape, an old industrial
district with mixed land use: workers' houses located among large factories,

SECTION VI: CASE STUDIES

some built before 1920 and others in the 1940S and 1950S, with little or no pol-
lution control. A dense population and a significant number of children were
exposed to pollution levels that largely surpassed the national primary standards
for annual average concentrations limit of 8ollg/m3. In Tatuape, the average
annual concentration of sulfur dioxide was 124Ilg/m3, and of particulate matter
1271lg/m3 during the period 1973-1986 (Fig. 21.7). A strong correlation was
found between levels of sulfur dioxide and particulate matter and respiratory
symptoms in children.

Management and intervention

Air quality management in Sao Paulo started in 1976, when air quality stan-
dards and emission standards were set for stationary sources. Initially, stan-
dards were set for four major pollutants - particulate matter, carbon monoxide,
sulfur dioxide and photochemical oxidants - with levels similar to the primary
standards of the US Environmental Protection Agency (USEPA). In 1990, these
were revised and the new air quality standards incorporated primary standards
for the protection of public health, and secondary standards for the protection
of the environment and for human well-being in relation to suspended parti-
cles, inhalable particles (PM lO), smoke, sulfur dioxide, carbon monoxide, nitro-
gen dioxide and ozone.
In addition to the standards, regulatory mechanisms, improved technology,
and the transfer of many heavy industries to other parts of the state and of the
country have reduced industrial sources of air pollution to the point where vehi-
cles are the main sources of air pollution in the city. At first, control programmes
were initiated by the State Government, in part as a response to growing inter-
national pressure following the UN Conference in Stockholm in 1972, and were
financed by State Government, private and public industries, and the World
Bank. In 1980, a law was passed to regulate industrial zoning for the areas where
pollution problems were acute. These policies and increased media coverage
contributed to increased awareness among the general public in the 1980s and
1990s. This was also greatly influenced by the preparations for the UN Confer-
ence on Environment and Development which took place in Rio de Janeiro in
1992. Nongovernmental organizations, universities and research institutes
played an important role in awareness raising and in training professionals and
local authorities to face the problem.
Sulfur dioxide concentrations fell as a result of the industrial pollution con-
trols adopted in 1982, lower limits for sulfur levels in fuel oil, and the substitu-
tion of fuel oil by natural gas. In Tatuape, sulfur dioxide levels dropped from
1241lg/m3 in 1973-1983 to 401lg/m3 in 1990-1998 (Fig. 21.7) (4,5). The con-
centration of particulate matter also decreased significantly in the district, as
many industries moved to other areas, making room for residential land use.
Levels of particulate matter dropped from 1271lg/m3 in 1973-1983 to 651lg/m3
in 1991-1992. From 1992, smoke levels were also monitored. Between 1992 and

21. CASE STUDIES

Figure 21.7 Annual mean levels of sulfur dioxide in Tatuape
160
140
120
ME 100
"-
en 80
E
60
40
Seconda~standard
20
0
1973 1975 1977 1979 1981 1983 1985 1987 1989 1991 1993 1995 1997
Year

Source of data: ref. 4.

Figure 21.8 Annual mean smoke levels in Tatuape

120

1
E
':~~_';;"L;.
40
Primary standard
\
Secondary standard
20

o
19841985 1986 1987 19881989 1990 1991 19921993 199419951996 1997 1998
Year

Source of data: ref. 5.

1997, smoke concentrations were on average 61 flgjm 3, close to the primary air
quality standard limit of 60 flgjm 3 and above the secondary air quality standard
limit of 40flgjm3 (Fig. 21.8).

Effect of pollution control on children's health

The first survey, conducted in 1986, indicated that symptoms of respiratory
disease tended to increase with higher pollution levels. In Tatuape, there was a
higher prevalence rate of 26 of the 35 symptoms studied (72.2%) than in areas
with lower pollution levels.
Twelve years later, in 1998, a second survey was undertaken (3) to evaluate
the impact of pollution management programmes on pollution levels and res-
piratory symptoms among children. In 1998, Tatuape had a higher prevalence
of only 12 of the 35 symptoms (34%) studied when compared with the other

SECTION VI: CASE STUDIES

 two areas. The prevalence of symptoms in the other two neighbourhoods
increased between 1986 and 1998; pollution control programmes were less
effective there and largely neutralized by the higher number of cars in the streets.
In Tatuape, the prevalence of 19 indicators decreased: cough with cold (by
6·3%); phlegm with cold (12-3%); phlegm on most days (6.2%); congested chest
more than one week per year (6.7%); wheezing with cold (3.2%); chest illness
which caused lack of activity for more than three days a year (0.7%); chest illness
with more phlegm (3%); measles (1204%); sinus trouble (1.5%); pneumonia
(1.8%); whooping cough (2.3%); frequent ear infection (age group 0-2 years:
5. 2%; age group 2-5 years: 1.3%; above 5 years: 2.9%); surgical removal of
tonsils or adenoid (9·3%); asthma diagnosed by doctor (1.4%); having to take
medicine for asthma (0.3%); heart problem (2.9%).

Conclusions
Public policies and programmes to control air pollution and for industrial
zoning have proved to be important tools in reducing health risks. Levels of
most air pollutants, with the exception of ozone, decreased and are below or
close to the acceptable limits. Respiratory diseases fell from second to fourth
leading cause of death in Sao Paulo. Nevertheless the effectiveness of the pro-
grammes is unequally distributed in the urban area. It is important that, in addi-
tion to emission control programmes and industrial zoning, an environmental
plan, which incorporates health, traffic, public transportation and housing
sectors, is elaborated and put in practice with community support.

References
1. Companhia de Tecnologia de Saneamento Ambiental (www.cetesb.sp.gov.br).
2. Committee of the Environmental and Occupational Health Assembly of the
American Thoracic Society. Health effects of outdoor air pollution. American
Journal of Respiratory and Critical Care Medicine, 1996, 15B-5 0 .
3· Ferris BG. Epidemiology standardization project. American Review of Respiratory
Disease, 1978, 118:1-120.
4· Ribeiro H. Air pollution and respiratory disease in Sao Paulo (1986-1998). Ninth
International Symposium in Medical Geography. University of Montreal, Canada,
2000.

5· Companhia de Tecnologia de Saneamento Ambiental (CETESB). Relat6rios de

qualidade do ar no estado de Sao Paulo. Sao Paulo, CETESB 1980 to 2000.

21. CASE STUDIES

 13. AIR POLLUTION AND PREGNANCY OUTCOME

R. Sram
Laboratory of Genetic Ecotoxicology, Institute of
Experimental Medicine, Academy of Sciences of the Czech
Republic, Prague, Czech Republic

There is widespread concern over the health effects of ambient air pollution.
Support is growing for the idea that several adverse pregnancy outcomes may
be the result of maternal or paternal exposure to airborne pollution. A consis-
tent relationship between maternal exposure to fine particles in early gestation
and intrauterine growth retardation (IUGR) was recently observed in a highly
polluted district of Northern Bohemia in the Czech Republic. One possible
explanation for this finding is that, not the particles themselves, but some asso-
ciated co-pollutants, such as polycyclic aromatic hydrocarbons (PAH), may
interfere with fetal development.
The Teplice district is one of four mining districts in Northern
Bohemia, where power plants produce approximately 50% of the
electricity for the Czech Republic. These power plants burn brown coal
that is rich in sulfur and, together with glass production, chemical manufac-
turing and the petrochemical industry represent a major contributor to air
pollution. In 1988, Northern Bohemia produced 47% of the sulfur
dioxide emissions and 39% of the nitrogen oxide emissions in the Czech
Republic.
This pollution significantly affects the health of the approximately 500000
inhabitants of the region, leading to decreased life expectancy, increased inci-
dence of cancer, cardiovascular diseases, and immune deficiencies in children,
and a number of reproductive and behavioural abnormalities. In November
'990, the Czech Government initiated the Teplice Programme to provide sci-
entifically valid information on environmental health problems in the Northern
Bohemian mining districts.

Management and intervention

A population-based study of pregnancy outcomes evaluated the impact of
air pollution and lifestyle on the outcome of all pregnancies delivered in hospi-
tal, using biomarkers as a measure of exposure. The study group included all
7800 single births in the Teplice and Prachatice (control, without pollution) dis-
tricts between 1994 and '998. Only full-term births of mothers of European
origin were included.
Low birth weight (LBW; defined as below 2500g), premature birth (less than
37 weeks) and intrauterine growth retardation (IUGR) were chosen as the main
reproductive outcomes. IUGR is an important predictor of neonatal morbidity
and mortality as well as of diseases later in life, such as non-insulin-dependent

320 SECTION VI: CASE STUDIES

diabetes, hypertension and coronary heart disease. Two basic approaches were
combined:

• In a prospective cohort study, the simultaneous effects of air pollution

and several other factors on pregnancy outcomes were analysed, and crit-
ical windows of exposure considered for different outcomes .
• In a nested case-control study a sample of cases with diverse adverse
outcomes and systematically selected controls were studied.

To evaluate the exposure, response and state of the mother and her child,
selected biomarkers were determined in venous blood, cord blood and placenta.
Different metabolic genotypes were also determined to estimate the magnitude
of the variation in genetic susceptibility to exposure to air pollution.
A considerably higher prevalence of all adverse outcomes was found in the
highly polluted district of Teplice than in Prachatice; this difference remained
significant even after adjustment for ethnic and social composition and smoking
habits. A significant and dose-dependent relationship between risk of fetal
growth retardation and levels of fine particles (PM lO , PM 2S ) was observed in
Teplice region. IUGR risk increased 1.19 times with every 101lg/m 3 increase in
PM lO exposure during the first month of gestation. No similar association was
observed in Prachatice. On the other hand, a strong dose-related association
between lUG R risk and concentration of carcinogenic polycyclic aromatic hydro-
carbons was found in both Teplice and Prachatice. IUGR risk increased 1.22
times with every 10 ng/m3 increase of PAH in early pregnancy. These findings
suggest that the first gestational month is a critical period for the effects of air
pollution on fetal growth. This is in agreement with the current hypothesis that
lUG R is triggered by an abnormal reaction between the trophoblast and uterine
tissues during the first week of pregnancy. Also, IUGR is one of the
most common consequences of mutagenic exposure around the time of
implantation.
PAHs are mostly adsorbed on the surface of fine particles. The above results
suggest that PAHs rather than the particles themselves primarily influence fetal
growth. PAHs are known to inhibit epidermal growth factor receptors and to
alter early trophoblast proliferation. In this way fetoplacental exchange of oxygen
and nutrients may be reduced and fetal growth could be impaired. The main
source of PM lO and PAHs is local heating, especially using coal. Air pollution
increasing IUGR is probably present in all large towns in the Czech Republic
during the winter season.
The impact of exposure to environmental tobacco smoke (ETS) was
analysed in the same cohort of mothers; it was shown that passive smoking
reduced the birth weight of infants delivered by nonsmoking mothers and also
increased the risk of delivery oflow-birth-weight infants by nonsmoking mothers
1.5 times. On the basis of the study, it was estimated that every year approxi-

21. CASE STUDIES 321

mately 47 0 babies are born with low birth weight caused by the exposure of non-
smoking mothers to ETS. ETS exposure also contributed to birth weight reduc-
tion in babies of smoking mothers.

Conclusions and relevance to other settings

Spurred by the results of the Teplice Programme, the Czech Government
invested US$ 200 million in Northern Bohemia to replace coal heating by gas,
using modern technology. As a result, atmospheric concentrations of sulfur
dioxide and suspended particulate matter in the year 2000 had fallen to approx-
imately 15% of the levels in 1990. This substantial decrease in air pollution is a
major success story of the recent introduction of an environmental policy in the
Czech Republic.
The Teplice Programme showed for the first time that air pollution may
adversely affect human reproductive outcomes, including fetal growth. The
induced changes appear to include not only observable birth defects but also
subtle functional changes affecting their carriers throughout their lives. From
their conception, children's complex development is vulnerable to environ-
mental hazards as well as being affected by their mothers' lifestyle such as cig-
arette smoking or poor diet.
The adverse impact of air pollution on reproductive health is a topic of
increasing public health concern. The information presented in this case study
should provide new inputs for prenatal care worldwide. This new understand-
ing about children's vulnerability to air pollution should be disseminated to
medical professionals and should be included in postgraduate medical educa-
tion for gynaecologists and paediatricians. We are slowly reaching an under-
standing of how important the first month of pregnancy is for the future health
of the child.

SECTION VI: CASE STUDIES

322
 14. ASTHMA CASE STUDY

G. W. K. Wong
Department of Paediatrics, Chinese University of Hong
Kong, China, Hong Kong Special Administrative Region

Asthma is one of the most common chronic disorders affecting children in

the developed and developing world (1). The prevalence of asthma in children
varies widely from less than 5% to more than 30% in different countries. Envi-
ronmental pollution is one of the important factors contributing to asthma.
Environmental pollution, in general, is a more significant problem in the devel-
oping world. Most of the outdoor pollutants, including ozone (OJ, sulfur
dioxide (50 2 ), and nitrogen dioxide (N0 2 ) , are related to combustion of fossil
fuels.
In Hong Kong SAR, childhood asthma is a common disorder (2). The main
sources of outdoor pollution include automobile exhaust and burning of fossil
fuels by various factories. Exposure to 502 has been linked to the development
of airway inflammation and bronchial hyperresponsiveness (BHR). The level of
atmospheric 50 2 is highly dependent on the sulfur content of the fuel used in
the community. An increasing level of atmospheric 50 2 is associated with an
increasing rate of hospitalization of Hong Kong children for asthma (3). There
have been several studies investigating the effect of 50 2 on children's lung
health in different districts in Hong Kong SAR. Kwai Tsing district has more than
8000 industrial outlets and air pollution is known to be a big problem. The
Southern district is primarily residential and the level of pollution is low.
Table 21.5 shows the dramatic differences between the air quality in these
two areas in 1989. Pollutants, including SO" N0 2 and respirable suspended par-
ticulates (RSP), were significantly higher in the Kwai Tsing district (4). Children
from primary schools from the two districts were invited to participate in a ques-

Table 21.5 Air quality, respiratory symptoms and bronchial hyper-responsiveness

in two districts in Hong Kong SAR

SOUTHERN KWAI TSING

3
Air quality (J.!g/m )

S02 9 117
N0 2 21 40
RSP 30 54
Respiratory symptoms n= 1486 n = 2027
Wheezing 4% 100%
Doctor-diagnosed asthma 3% 6%

RSP, Respirable suspended particles.

21. CASE STUDIES

Table 21.6 Results of histamine challenge in children

PERCENTAGE SHOWING BHR

1990 1991 1992
Southern district 22.6 15.8 10.9
Kwai Tsing 27.4 24.2 12.2

BHR. Bronchial hyperresponsiveness.

tionnaire survey and bronchial challenge test. Symptoms of wheezing and

BHR were significantly more common in the Kwai Tsing district.
In July 1990, new government fuel regulations were implemented and the
sulfur content of fuel was restricted to a maximum of 0.5%. This resulted in a
rapid reduction in atmospheric 50 2 level by more than 80%. A follow-up study
of the cohort was performed yearly for two years after the implementation of
the new regulation. For children from the polluted Kwai Tsing district, the per-
centage with BHR decreased significantly from 27.4% to 12.2% (Table 21.6) (4).
Such reduction in atmospheric 50 2 should also reduce morbidity in asthmatic
children, such as asthma attacks and hospitalization (3).
These sequential analyses of children for BHR demonstrated the effect of
successful environmental control on the level of outdoor air pollution. The
health benefits were objectively documented by the significant reduction of BH R
in schoolchildren.

References
1. The International Study of Asthma and Allergies Steering Committee. Worldwide
variation in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis,
and atopic eczema: ISAAC. Lancet, 1998,351:1225-1232.
2. Wong GWK et al. Prevalence of respiratory and atopic disorders in Chinese chil-
dren. Clinical and Experimental Allergy, 2001, 31:1225-1231.
3. Wong GWK et al. Temporal relationship between air pollution and hospital
admissions for asthmatic children in Hong Kong. Clinical and Experimental
Allergy, 2001, 31:565-569.
4. Tam AYC et al. Bronchial responsiveness in children exposed to atmospheric pol-
lution in Hong Kong. Chest, 1994, 106:1056-1060.

SECTION VI: CASE STUDIES

 15. INFANT EXPOSURE TO ORGANOCHLORINE CONTAMINANTS
IN BREAST MILK

G. c. Moy
Food Safety Department, World Health Organization,
Geneva, Switzerland

Description of the problem

Although its benefits are beyond question, breastfeeding should not be seen
as necessarily free of risk (1). Many contaminants are found at elevated levels
in breast milk and most of these arise from the mother's consumption of con-
taminated foods. Few of the chemicals employed in agriculture and industry
have been thoroughly investigated for their potential toxicity to animals and
humans. Information is particularly scant about their long-term effects on
infants and children. In general, the risk assessment and emergency planning
that underpin the regulation of environmental contaminants and other chemi-
cals in food have not considered the potential contamination in human milk
and its public health dimension.

Risk assessment of exposure to organochlorine contaminants

Physiological factors may cause toxic effects in infants exposed to contam-
inants in their food (breast milk or formula) to be more serious than those in
similarly exposed adults. As infants generally depend on only one source of
food, the levels of contaminants in that food are of greater concern than when
a variety of foods is consumed in the diet (2).
Organochlorine compounds gained prominence about 50 years ago, partic-
ularly as pesticides. Their use was subsequently curtailed as their negative
effects on non-target species became known. Initially believed to have low mam-
malian toxicity, organochlorine compounds are now known to have a range of
toxic effects, including immunotoxicity, carcinogenicity, neurotoxicity, reproduc-
tive disorders and interference with infant and child development. Because of
their stability and fat solubility, many of these compounds accumulate in the
environment, especially in long-lived species at the top of the food chain, such
as polar bears and humans. Breast milk contaminants arising from food may
include food additives, residues of pesticides, residues of veterinary drugs used
in food-producing animals, and environmental pollutants.
Twelve organochlorine compounds - dioxins and related dibenzofurans,
dieldrin, endrin, heptachlor, hexachlorobenzene (HCB), hexachlorocyclohexane,
mirex, polychlorinated biphenyls, toxaphene, and DDT (dichlorodiphenyl-
trichloroethane isomers and degradation products) - were the initial focus of
the 2001 Stockholm Convention on Persistent Organic Pollutants (POPs). The
Convention is intended to protect human health and the environment by
phasing out the production and use of these compounds. All these POPs have

21. CASE STUDIES

been found in breast milk to different degrees. Two of them, DDT and HCB, will
be discussed here for illustrative purposes. More detailed assessments of POPs
in breast milk are available elsewhere (3,4)·
One of the best known POPs, DDT was widely used in agriculture and public
health in many countries. Because its use was discontinued some time ago in
the majority of developed countries, mean DDT intake in breast milk is well
below the tolerable daily intake (TDI).' In contrast, many developing countries
and some European countries, report DDT levels in breast milk above the
current TDI. However, mean concentrations in the population have declined in
much of the world as a result of the restrictions on the use of DDT. No con-
firmed adverse health effects have been reported in infants exposed to DDT
while suckling, even in communities where the reference level was frequently
exceeded (4).
Only a few countries have reported levels of HCB in human milk to
GEMS/Food. 2 There are wide deviations in the observed HCB levels, some of
which exceed the TDI many times. There is, moreover, no clear pattern between
industrialized and developing countries. HCB contamination of breast milk
cannot necessarily be expected to decrease as long as inadequately controlled
synthetic processes result in continued production and dispersion of HCB as a
product of the chemical industry and waste disposal operations.

Considerations for risk management

Human breast milk is the natural and best food for infants, has the optimal
composition to meet their nutritional needs in early life, and provides immuno-
logical, psychological and economic advantages (5-9). As a general rule, WHO
recommends that all infants should be fed exclusively on breast milk from birth
up to 6 months of age (10).
The health benefits of breastfeeding are especially great where the family sit-
uation is suboptimal, which frequently occurs in developing countries or in dis-
advantaged subgroups in developed countries (11). Hence, any advice to reduce
breastfeeding on grounds of contaminant-mediated harm to the child is only
appropriate if the risk to the child's health is sufficiently great to outweigh the
benefits of breastfeeding.
In a number of countries, groups of mothers with known or suspected high
levels of a contaminant in their breast milk, caused by either acute intoxication
or low levels of sustained exposure, have been advised by health professionals

'Standard reference intakes such as the acceptable daily intake (ADI), the provisional tolerable
weekly intake (PTWI), and the tolerable daily intake (TDI) are jointly established by WHO
and the Food and Agriculture Organization of the United Nations (FAO).
'GEMS/Food is an international data collection and assessment activity undertaken by WHO
to examine the health Significance of levels and trends of chemicals in food and the diet,
including breast milk.

SECTION VI: CASE STUDIES

and public health authorities to reduce exposure to their nursing infants. For
example, lactating women involved in mass intoxications and occupationally
exposed pregnant women have been advised not to breastfeed at all, or to do
so for a limited time.
Some governments have advised women who are pregnant, lactating, or
plan to become pregnant in the near future not to eat fish of several species
harvested in particularly polluted areas. This recommendation was based on
concerns not only about organochlorine compounds, but also mercury. Sweden
also recommended that breastfeeding women should not lose large amounts
of weight abruptly, in order to avoid release of contaminants stored in fat (12).
A similar recommendation against weight loss had been issued by a consulta-
tion convened by the WHO Regional Office for Europe (13).
In 1993, the US National Academy of Sciences/National Research Council
called for improvements in the animal testing protocols used in regulatory deci-
sions about suitability for use, including information about effects of lactation
exposures (14). Subsequently, the Food Quality Protection Act of 1996 was
enacted which requires that testing protocols for chronic toxicity and carcino-
genicity be modified to include in utero exposure during the last trimester, lac-
tation exposure, and post-weaning dietary exposure. Where these data are not
available, the law stipulates that an additional safety factor of up to lo-fold be
applied. Similar requirements to improve testing protocols to protect unborn
and nursing infants are being considered by other countries and international
organizations.

Perspective and concluding remarks

Few countries systematically assess levels of organochlorine components in
human breast milk. In the light of suspected high levels of many contaminants
in breast milk, the following considerations are offered to assist responsible
authorities and relevant health and environmental professionals in responding
to health concerns:

• Basic monitoring and assessment programmes for breast milk need to

be established in all countries for at least the contaminants of priority
concern. However, at present the routine screening of individual breast-
milk samples to estimate the potential health risk to individual infants
does not appear to be cost-effective.
• Responsible authorities should examine their food monitoring and
control programmes to assess whether greater attention should be paid
to foods known to be potentially high in breast milk contaminants, and
whether tolerable residue levels in these foods should be changed to
protect women of childbearing age.
• National response plans for large-scale intoxications, either through
occupational exposure or highly contaminated foods, need to be

21. CASE STUDIES

 established or strengthened. Epidemiological studies linked to the
monitoring of food and breast milk are urgently needed to assess the
possible long-term health hazards from the intake of contaminated
breast milk .
• If warranted, dietary recommendations may be formulated for lactating
mothers and women intending to become pregnant based on levels of
contaminants in national diets. These recommendations may include
limiting consumption of heavily contaminated foods, such as certain
fish and avoiding extreme weight loss during pregnancy and while
breastfeeding .
• Primary preventive measures to control and reduce the introduction of
organochlorine chemicals into the environment are the most effective
way to minimize exposure.

References
1. International Programme on Chemical Safety. Principles for evaluating health risks
from chemicals during infancy and early childhood: the need for a special approach.
Geneva, World Health Organization, 1986 (Environmental Health Criteria No.
59)·
2. FAO/WHO. Food consumption and exposure assessment of chemicals. Report
of a Joint FAO/WHO Consultation, Geneva, 10-14 February 1997· Geneva, World
Health Organization 1997 (unpublished document WHO/FSF /FOS/97·5)·
3. Levels of PCBs, PCDDs and PCDFs in human milk. Report of a second round of
WHO-coordinated exposure study. Copenhagen, WHO European Centre for Envi-
ronment and Health, 1996 (Environmental Health in Europe NO·3)·
4. GEMS/Food international dietary survey: Infant exposure to certain organochlorine
contaminants from breast milk - a risk assessment. Geneva, World Health Orga-
nization 1998 (unpublished document WHO/FSF/FOS/9 8 A)·
5. Kovar M et aL Review of the epidemiologic evidence for an association between
infant feeding and infant health. In: Foege W, ed. Report of the Task Force on the
Assessment of the Scientific Evidence Relating to Infant-Feeding Practices and Infant
Health. Pediatrics, 1984, 74(SUppL): 61 5- 638.
6. Jason J, Nieburg P, Marks J. Mortality and infectious disease associated with
infant-feeding practices in developing countries. In: Foege W, ed. Report of the
Task Force on the Assessment of the Scientific Evidence Relating to Infant-Feeding
Practices and Infant Health. Pediatrics, 1984, 74(SUppL):702 -7 27·
7. Lawrence R. Breastfeeding, a guide for the medical profession. St Louis, MO, CV
Mosby Co., 1989.
8. Rogan W. Should the presence of carcinogens in breast milk discourage breast
feeding? Regulatory Toxicology and Pharmacology, 1991, 13:228-240.
9. Habicht J, Da Vanzo J, Butz W. Does breastfeeding really save lives, or are appar-
ent benefits due to biases? American Journal of Epidemiology, 123:279-290.
10. Global Strategy for Infant and Young Child Feeding. Geneva, World Health Orga-
nization,2001 (document A54/INF.DOC./4)·

SECTION VI: CASE STUDIES

 11. Macintyre UE, Walker ARP. Lactation - how important is it? Journal of the Royal
Society for Health, 1994, 114:20-28.
12. Siorach S. Kvicksilver och andra frammande amnen i fisk - atgarder for aU
begransa halsoriskerna. [Measures to reduce health risks from mercury and
other chemical contaminants in fish.] Var Foda, 1992,44:163-170 (in Swedish
with English summary).
13· PCBs, PCDDs and PCDFs in breast milk: assessment of health risks. Copenhagen,
WHO Regional Office for Europe, 1988 (Environmental Health Series No. 29).
14· National Academy of Sciences, National Research Council. Pesticides in the Diets
of Infants and Children. Washington, DC, National Academy Press, 1993.

21. CASE STUDIES

 16. ESCHERICHIA COLI 0157:H7 OUTBREAK IN JAPANESE
SCHOOLCHILDREN

H. Toyofuku
Food Safety Department, World Health Organization,
Geneva, Switzerland

F. Kasuga
Department of Biomedical Food Research, National
Institute of Infectious Diseases, Shinjuku-ku, Japan

Escherichia coli 0157:H7 infection can cause severe bloody diarrhoea and
abdominal cramps. Usually, little or no fever is present, and the illness resolves
within 5-10 days. However, in 2-7% of cases, particularly in children under 5
years of age and the elderly, the infection can lead to a complication called
haemolytic uraemic syndrome, in which red blood cells are destroyed and the
kidneys fail, sometimes causing death.

Description of foodborne outbreaks within the school system

In 1996, there were a large number of outbreaks of food borne disease in
Japanese schools (Table 21.7). Infections due to E. coli 0157:H7 were of partic-
ular significance as these caused 8 of the 18 outbreaks (Table 21.8), and were
responsible for five children dying. Comprehensive investigation results are
available for two outbreaks. These cases illustrate the need for good hygiene
practices during the preparation and distribution of school lunches. The iden-
tification of the source of contaminated food was important for the design of
measures to prevent future incidents of a similar nature.
In July 1996, Sakai City experienced the largest outbreak of E. coli 015TH7
infection ever reported, causing three child deaths. Among the 47643 school-
children in three Sakai school districts, 8355 displayed symptoms, and 398 had

Table 21.7 Foodborne outbreaks in Japan and within the school system

YEAR TOTAL SCHOOL LUNCH SYSTEM

NO. OF NO. OF NO. OF NO. OF NO. OF NO. OF
OUTBREAKS CASES DEATHS OUTBREAKS CASES DEATHS
1996 1217 46327 15 18 11651 5
1997 1960 39989 8 8 2325 0
1998 3010 46179 9 8 3901 0
1999 2697 35214 7 8 1503 0
2000 2198 42568 4 5 547 0

Source: Based on Food Poisoning Statistics 1996-2000, Ministry of Health, Labour and Welfare, Japan.

33 0 SECTION VI: CASE STUDIES

Table 21.8 E. coli 0157: H7 outbreaks in Japanese schools in 1996

AREA OF OUTBREAK MONTH CASES

(DEATHS)
Oku-town, Okayama Prefecture May 468 (2) Primary school
Tojo-cho, Hiroshima Prefecture May 185 Primary school
Gifu City, Gifu Prefecture June 395 Primary school
Sakai-town, Gunma Prefecture June 138 Primary school
Niimi City, Okayama Prefecture June 360 Primary school
Sakai City, Osaka Prefecture July 7966 (3) Pri mary school
Morioka City, Iwate Prefecture September 121 Primary school
Obihiro City, Hokkaido Prefecture October 158 Kindergarten

Source: Ministry of Heath and Welfare of Japan, 8 May 1998.

to be hospitalized (1). White radish sprouts from a single farm were the only
uncooked food implicated in all meals.
At the end of September, Morioka City also experienced an outbreak of E.
coli 015TH7 infection, involving more than 121 cases. Salad and seafood sauce
prepared in the school kitchen were identified as the vehicles for transmission
(2).

Management and intervention

The school lunch programme in Japan has been in operation since 1954. It
represents a unique system in which the same menu may be prepared from the
same raw materials for all schools in a given district. Individual school kitchens
or the district's school lunch centre is responsible for the final preparation and
distribution of the meals (3). This system increases the risk that many children
may be infected simultaneously.
In the case of Sakai, the most likely source of contamination was identified
to be the seed of white radish sprout. E. coli 015TH7 grow rapidly in radish
seeds at the time of germination (4). Viable E. coli 015TH7 organisms have
been demonstrated in the inner tissues of radish sprouts grown from experi-
mentally contaminated seed.
During the investigation it became apparent that neither the distribution
centre, nor the trucks used for delivery to the schools, nor the school kitchens
had freeZing or refrigeration equipment. Furthermore, there was no testing of
random food samples for bacteria after food was delivered to distribution
centres or school kitchens.
In the case of Morioka, baskets containing cooked food were left on the
kitchen floor for up to two hours. As workers entered the kitchen without chang-
ing or disinfecting their shoes, the food may have become contaminated
through splashes from the wet kitchen floor. The same sink was used for cooling
the cooked food and thawing and washing the raw materials without any clean-

21. CASE STUDIES 33 1

ing between the two operations. Furthermore, some ingredients of the salad
were cooked for too short a time and at insufficient temperatures, and after
cooking were left at ambient temperature (2).
School lunch is considered an essential part of education, and is therefore
under the jurisdiction of the Ministry of Education, Culture and Science, rather
than the Ministry of Health, Labour and Welfare. In April 1997, the Ministry of
Education, Culture and Science published the Standard of good hygienic practice
in school kitchens, which enforces the improvement of kitchen facilities, thor-
ough cooking, and prevention of cross-contamination through the separation
of raw and cooked materials (5). This standard was prepared in accordance with
directives issued by the Ministry of Health and Welfare, including a hygiene
control manual for large-scale catering facilities (including school kitchens and
school lunch preparation and distribution centres), and a manual on foodborne
outbreak investigation for inspectors.
The Ministry of Education, Culture and Science also started on-site inspec-
tions in selected school kitchens that had been affected by the outbreaks, to
evaluate compliance with the standards. The results showed that, despite some
improvements, further efforts were needed to educate kitchen workers on how
to prevent growth of pathogens. Cooking time and temperature must be appro-
priately controlled. Cross-contamination and excessive storage time at room
temperature should be avoided. High-risk foods, such as raw radish sprouts,
should not be included in the school lunch menus until effective control
methods can be implemented (3).
Since 1998, as a result of the many efforts to reduce the risk offoodborne
infections, the number of cases has decreased (Table 21.7). Advocacy to
promote essential food safety practices could improve the health situation in
many countries. The five keys to safe food promoted by WHO are applicable
throughout the world:

1. Keep clean.
2. Separate raw and cooked food.
3. Cook thoroughly.
4. Keep food at safe temperature (below SoC or above 60°C).
S. Use safe water and raw materials.

References
1. Michino H et al. Massive outbreak of Escherichia coli 015TH7 in school children
in Sakai City, associated with consumption of white radish sprouts. American
Journal of Epidemiology, 1999, 150:]87-796.
2. Shinagawa K et al. [Outbreak of Escherichia coli 015TH7 in school children in
Morioka City, the responses and challenges.] Bulletin of the National Institute of
Public Health, 1997,46:104-112 (in Japanese).

332 SECTION VI: CASE STUDIES

 3· Michino H, Otsuki K. Risk factor in causing outbreaks oHood-borne illness orig-
inating in school lunch facilities in Japan. Journal of Veterinary and Medical
Science, 2000, 62:SS7-S60.
4· Hara-Kudo Y et al. Potential hazard of radish product as a vehicle of Escherichia
coli 01STH7.Journal of Food Protection, 1997, 60:112S-112 7.
S· Report on the improvement of hygiene practice in school lunch system. Tokyo,
Ministry of Education, 1998 (in Japanese).

21. CASE STUDIES

333
 17. HEALTH HAZARDS OF PESTICIDE USE: STUDIES BY THAI
SCHOOLCHILDREN

s. Wichanee
Khao Praya Sangkharam School, Kan Sak District,
Thailand

M. Tianponkrang
Thai Education Board, Bangkok, Thailand

M. Jakiet
Thai Education Board, Bangkok, Thailand

H. Murphy
FAD Programme for Community IPM, Rome, Italy

The problem
Rural children in developing countries come into closer contact with
pesticides than their urban counterparts because in many cases their families
use pesticides in small-scale farming. Their playgrounds are the family field,
and toys are made from anything lying around, including colourful pesticide
containers. Children also frequently participate in agricultural practices, helping
weed or harvest freshly sprayed fields. As the households of private land-
owners are usually small, pesticides are frequently stored in living areas. Finally,
pesticides decanted into smaller containers (e.g. beverage bottles) or recycled
containers (for food or water storage) can lead to accidental poisonings
(1). Children are more susceptible than adults to the toxic effects of pesticides
because of their low body weight and rapid metabolism (2). As children's
ability to detoxify and excrete pesticides is not yet fully developed, they are
more vulnerable to long-term, adverse developmental effects (3). A total of
'7' cases of pesticide poisoning among children between 0 and '4
years
of age were reported to the newly expanded and centralized Thai Poison
Control Centre in Bangkok in 2000 (4). Another 495 were reported in
young adults ('5-24 years of age). As nationwide coverage continues to be
strengthened and standardized, these figures will no doubt increase in the
future.
Thailand is the biggest consumer of pesticides in South Asia, spending over
US$ 247 million on pesticides each year (5). Some 77% of its agriculture sector
is made up of private landholders (6); 73% of imported pesticides are highly
toxic to human health as categorized by the World Health Organization (5).
These include class la (extremely hazardous) products, such as methyl
parathion, mevinphos, and alachlor, and class Ib (highly hazardous) products,
such as monocrotophos and methamidophos (7).

334 SECTION VI: CASE STUDIES

 The Thai Education Foundation, with support from the community Inte-
grated Pest Management (IPM) programme of the Food and Agriculture Orga-
nization of the United Nations has been testing an innovative strategy to raise
awareness of these hazards among the rural population. Schools aim to iden-
tify the toxic pesticides available in the farming communities, and the hazardous
ways of applying, storing and discarding them. The children also assess the
acute health effects suffered by their parents by conducting a health history and
examination before and after spraying. The goal is to raise awareness among
children and their parents about the hazards of pesticides and to eliminate expo-
sure and the resulting adverse health effects.

Management and intervention

The pilot test was conducted at the Khao Praya Sangkharam School in Kan
Sak District, Utai Thani Province where a programme of integrated pest man-
agement was part of the science programme. Students learned about ecology
and nonchemical pest control methods through experiments on crops growing
within the school grounds. A health component was added to the programme,
in which 27 eighth grade students gained a better understanding of the poten-
tial health effects of pesticides by conducting surveys among their farming
parents.
Five topics were covered:

• classifying common pesticides by chemical family and WHO health

hazard level;
• calculating the amounts sprayed per season;
• hazards of handling pesticides and routes of exposure;
• household storage and disposal hazards; and
• the signs and symptoms of pesticide poisoning.

One topic per day was presented in the classroom through games and prac-
tical exercises. Each afternoon and evening the students, as homework, gath-
ered information on the topic from their parents and household. This included
estimating the seasonal amounts of pesticide their parents used, observing
spraying, taking a simple health history and examination, and recording the data
on a body map, surveying their own household, and making a list of the
pesticides used. The following morning, the data for each topic were analysed
in the classroom, first in small groups then for the entire class. The findings
were presented on posters and discussed with the parents in a community
meeting.

Evaluation and follow-up

To evaluate the impact of their efforts, the 27 students repeated the
survey 4 months later, at the end of the semester. In addition, the students

21. CASE STUDIES 335

 themselves were tested and observed in discussion about what they had
learned. In terms of the impact on parents, the students detected changes in
household storage and disposal and spraying practices, and a reduction in
adverse health effects.

Results. of the second survey

Household pesticide storage and disposal practices improved. Initially, stu-
dents identified that pesticides were stored in areas where children played
(under their houses on stilts, in the garden, hanging from trees). After four
months, the proportion of houses defined as "child unsafe" had decreased
fromB4% to 45%. Pesticide storage and disposal that were potentially cont-
aminating food, water and livestock improved by 31%, 22%, and 20% respec-
".
~
.... tively. Homes recycling pesticide containers diminished from 16% to 5%.

)·.. · ~·.••....·.·. .··7

....
... ;: Students reported that their parents took greater care to protect themselves
during spraying. All wore rubber gloves and boots and none smoked during
.~

the spray operation.

Of the 18 signs and symptoms of health effects initially reported by parents,

if
an but two decreased in frequency. For instance during the first survey, 23%
reported an episode of vomiting and 28% uncoordinated gait associated with
a spray operation. The corresponding figures in the second reporting period
were 0 and 6%.

In a written examination, all students were able to identify the most haz-
ardous pesticide classification, 63% one sample product, and 81% the correct
common and brand names. They were able to calculate correctly the amounts
of pesticide used by their parents, and could correctly identify hazardous spray-
ing, storage and disposal practices. The students' understanding was also
clearly demonstrated by what they had to say at the end of the studies:

• "Chemical pesticides should be kept up high out of the reach of children.

Recycling the containers should be prohibited and the empty containers
must be buried, and must not be used as toys by the children."
• "There is a risk that kids may touch a chemical container before they eat
or drink. This potential risk will only be reduced if pesticides are correctly
stored."
• "If we do not stop using chemical substances in our Village, the envi-
ronment and especially our health will be affected."
• "I would like to make my parents and relatives realize how poisonous
chemical substances are. Also, we would like the farmers in our village

SECTION VI: CASE STUDIES

 to decrease or even stop using chemicals. The introduction of biological
agents should be encouraged."
• "In Uthaithani and some other provinces, chemicals are still applied on
a large scale, and some banned substances are still available. I will try to
convince my parents and neighbours to avoid using chemicals in our
village. I will also ask for help from the health agents to increase under-
standing about the chemicals."

One student and her teacher presented the class's findings to the governor.
He was so impressed that he requested all the schools in the province to
conduct similar studies. To date, 31 other schoolteachers have been trained in
this methodology. Of the 11 schools that are planning studies, six have com-
pleted pilot tests, and another two have surveyed their entire community. The
Thai Ministry of Education has also visited demonstration areas and will be
adding an environmental education component to the curriculum, which will
include these pesticide-related health studies.

Application to other health problems and settings

This is an example of nonformal discovery learning, which is highly relevant
for children. This powerful educational method stimulates observation and
communication skills, involves mathematics and art, and promotes critical
thinking. Furthermore, students act as agents for change in the community as
well as child-to-child and child-to-parent educators. Although the data are not
validated by outside specialists, they illustrate the hazards of pesticide use in a
rural farming community.
This methodology can be applied to a range of other public health issues
that require change in behaviour based on community data. For instance, sur-
veillance of diarrhoea incidence, with promotion ofhand-washing or food safety,
monitoring of indoor air, and immunization coverage or campaigns are activi-
ties in which schoolchildren could be involved.

References
1. Murphy HH, Sanusi A. Pilot studies on the use and health effects of paraquat:
Pasaman, Sumatra 8arat. Jakarta, FAOjIPM, 1998.
2. United States Environmental Protection Agency. Protecting children from pesti-
cides. 2002 (www.epa.govjpesticidesjfactsheetsjkidpesticide.htm ).
3. Landrigan PJ et al. Pesticides and inner-city children: exposures, risks, and pre-
vention. Environmental Health Perspectives, 1999, 107(Suppi 3):431-437.
4. National Poison Control Center, Ministry of Health, Bangkok, Thailand.
5. The pesticide industry. Toxic Trail (http://www.toxictrail.org).
6. Ministry of Agriculture. Bangkok, Thailand (www.alro.go.th).
7. International Programme of Chemical Safety. The WHO recommended classifica-
tion of pesticides by hazard and guidelines to classification 1998-1999. Geneva,
World Health Organization, 1998 (WHOjPCSj98.21).

21. CASE STUDIES 337

 18. PSYCHOSOCIAL STATUS AND SOMATIC OUTCOMES
AMONG THE YOUNGER POPULATION OF THE UKRAINE
AFFECTED BY THE CHERNOBYL NUCLEAR PLANT ACCIDENT 1

N. Korol
Research Laboratory for Population Health of Radiation
Exposed Children, Academy of Medical Science of Ukraine,
Kiev, Ukraine

On 26 April 1986 the largest disaster in the history of the nuclear industry
took place at unit IV of Chernobyl's nuclear power plant. The radioactive fall-
out led to the contamination of 2218 Ukrainian cities, towns and villages in an
area of 50500 km\ with a population of 17.5 million, including 2.5 million chil-
dren under 7 years. The collective thyroid exposure dose for the Ukrainian pop-
ulation was estimated as 1300000 person-Gy (1). The magnitude of the
collective effective exposure dose of the Ukrainian population is estimated at
50000 person-Sv over 10 years, excluding thyroid exposure.
Numerous epidemiological studies on children living in the contaminated
areas confirmed that a dramatically increased thyroid cancer incidence was
associated with exposure to radioactive iodine. From 1986 to 2000, 1900 cases
of thyroid cancer were registered among people who were under 18 years of age
at the time of the accident (2). While the incidence of thyroid cancer was 0.1
per 100000 in 1986, by 1990 it had increased to 1.5 per 100000. A maximum
incidence of5.2 per 100000 was observed in 1996 (1,2).
Even though the accident occurred more than 15 years ago, it stili affects
many Ukrainians in all aspects of their life. Beside the direct health effects, such
as childhood thyroid cancer, caused by exposure to ionizing radiation, psycho-
logical and social effects play an increasingly important role. As a consequence
of evacuation, discrimination, confusion about safe dose limits, departure of
people with high socioeconomic status, changes in lifestyles, and insecurity
about the level of contamination offood, Chernobyl produced chronic stress in
children and adolescents. The 3000 children who were evacuated from the
immediate surroundings of Chernobyl in April 1986 received the highest doses
of ionizing radiation and therefore form the highest risk group. Many of these
children and adolescents personally remember the chaotic and poorly organized
evacuation and grew up under psychological pressure in an environmentally
aggressive society.
In Ukraine, investigations of health effects of the Chernobyl accident among
young people are conducted by the Research Laboratory for Population Health

'Reviewed by Dr Zhanat Carr, Radiation and Environmental Health, WHO, Geneva,

Switzerland.

SECTION VI: CASE STUDIES

which was set up in October 1986 at the Research Centre for Radiation Medi-
cine (RCRM). Since then, the Laboratory has been collecting epidemiological
data on health status of the affected children. A total of 3000 evacuated chil-
dren and adolescents have been regularly examined at the RCRM since 1986.
The clinical surveillance programme includes: physical examination, biochemi-
cal and haematological analysis, and ultrasound imaging of the thyroid gland
and abdomen. For the psychological examination, a general health question-
naire (GHQ-12) was used.
A serious deterioration in the health status of the evacuated children
has been observed. The number of children officially classified as healthy
gradually decreased from 31% in 1987 to 4% in 2000. This index among
the same age group in Kiev showed a similar trend but without any statistically
significant difference (32% in 1987 and 26% in 2000). There are no data
on pre-Chernobyl levels. The proportion of children officially classified as
disabled is four times higher among those evacuated from Chernobyl
than among other Ukrainian children. Furthermore, there appears to be an ele-
vated prevalence of peptic disease, cardiovascular disorders, and nervous and
immune system disorders. Psychological stress seems to be a major risk factor
for these conditions.
Psychological and social examinations showed that these children have
been under constant psychological stress since the Chernobyl accident. During
the first few years, many children had fatalistic ideas, expecting to develop
cancer themselves or that it would develop in members of their family. After
1997, the Government stopped providing social support for Chernobyl victims,
such as extra housing, school and job opportunities. As a result, the psycho-
logical and social problems changed: anxiety is still very common, but its man-
ifestation has changed. In 1987, Chernobyl children's role was emphasized as
a role of victims, expecting social privileges. In contrast, by 1999, they attempted
to downplay the fact that they belonged to the affected population, because
they feared discrimination in education, work and marriage as "Chernobyl
victims".
It appears that psychosomatic effects triggered by the Chernobyl disaster
have a more significant impact on the population than radiation-induced cancer.
While cancer has a dramatic impact on individuals, it only affects a small
number of people, and there is little opportunity for population risk manage-
ment. In contrast, public health interventions aimed at modifying psycho-
somatic effects can have a significant positive impact on the health and health
perception of the whole population. Based on the outcomes of our study, the
following directions have been proposed:

1. Treatment:
treat chronic stress related to self-identification as a victim, as any other
stress

21. CASE STUDIES 339

2. Information:
educate local communities and explain the nature of radiation effects and
separate psychosomatic outcomes; explain any restrictions on physical or
intellectual activity, and recommend appropriate nutritional diets.
3- Training:
give basic training in mental health promotion, including the need for per·
sonal warmth, active listening, calm communication, and empathetic
response.
4. Counselling theory and practice:
group work, case management, group counselling, counselling children and
families, and relationship consultation.

A further issue of increasing importance is the reproductive health of the

younger population, especially teenagers. This mentally immature but physically
developed group is at high risk because of their specific psychological profile.
For example, many take the attitude: "We have all been exposed. We will die
soon. Let us enjoy ourselves!" This leads to reckless behaviour, such as alcohol
and drug consumption, smoking, and unsafe sex. Furthermore, it has been sug·
gested that exposure to ionizing radiation may lead to alterations in immune
response that may change personal resistance to virus infections, e.g. human
papilloma virus (HPV), genital herpes and human immunodeficiency virus
(H IV). The prevalence of sexually transmitted diseases (STOs) among Cher·
nobyl victims is much higher than the average for Ukraine. Many married
couples choose to have an abortion because of fear of congenital malforma·
tions or other inherited disease allegedly resulting from exposure to ionizing
radiation. It is very important to develop educational reproductive health pro·
grammes for adolescents affected by the Chernobyl disaster, as well as for young
married couples, pregnant women and parents concerned about the effects on
their children of their exposure to ionizing radiation. These should include the
following elements:

1. Identification of behaviours that put adolescents at risk of reproductive

health problems, using questionnaires, psychological tests and voluntary
anonymous screening for STOs; work with the parents of at·risk adolescents.
2. Educational literature and a website to inform adolescents about reproduc·
tive health, safe sex, and risks.
3. Training seminars for public health specialists and support groups, 24·hour
hot·lines and counselling for adolescents including those adolescents with
an STO or drug dependence.
4. Scientific and popular literature explaining biological effects of exposure to
ionizing radiation; genetic counselling for young married couples.
5. Support centres for pregnant women and young parents, and information
about prenatal and postnatal hygiene and child care.

340 SECTION VI: CASE STUDIES

 6. Scientific and popular literature about psychological therapy, social orienta-
tion, life planning skills and legal counselling.

The experience of Chernobyl illustrates that neither the former USSR nor the
international community were prepared to manage a nuclear disaster. It took
13 years for formal agreements to be reached between the governments of the
affected areas and donor countries. While much attention has been given to the
increase in thyroid cancer among children and adolescents, to date no interna-
tional study has been conducted to investigate all long-term health effects in
the aftermath of Chernobyl. From a public health point of view, psychological
and reproductive health problems are likely to playa much bigger role than the
observed increase in thyroid cancer rates, and there is an urgent need for effec-
tive health promotion programmes.

References
1. United Nations Scientific Commission on Effects of Atomic Radiation. Exposures
and effects of the Chernobyl Accident. In: Sources and effects of ionizing radiation.
UNSCEAR 2000 report to the General Assembly. New York United Nations, 2000,
Annex ).
2. Tronko N et al. Thyroid cancer in children and adolescents of Ukraine having
been exposed as a result of the Chernobyl accident (1s-year expertise of investi-
gations). International Journal of Radiation Medicine, 2002, 4:222-232.

21. CASE STUDIES

341
 19. HOSPITALIZATION FOR ASTHMA IN CHILDREN LIVING NEAR
AN IRON FOUNDRY IN THE UNITED KINGDOM

B. Olowokure
Department of Public Health, Sandwell Health Authority,
West Bromwich, England

P. J. Saunders
Department of Public Health and Epidemiology, University
of Birmingham, England

R. C. Wilson
Department of Public Health and Epidemiology, University
of Birmingham, England

R. L. Smith
West Midlands Cancer Intelligence Unit, University of
Birmingham, England

Setting and background

Sandwell is an urban area in the heart of the West Midlands, England. Over
a number of years the local department of public health has received complaints
from a local community regarding emissions from a nearby foundry. The foundry
is one of 30 in Sandwell and was established in 1936. It is surrounded by resi-
dential property with a number of schools within a few hundred yards. The
foundry melts scrap iron and, although the principal by-product of the com-
bustion process is ferrous fume and particulate matter, a complex mix of air
pollutants that are incompletely characterized is produced.
Nearby residents have repeatedly complained of noise, unpleasant odours,
visible smoke and a fine dust that covers windows and parked vehicles.
However, the community was particularly concerned about the possible adverse
effects of the emissions on the respiratory health of their children. Following
a public meeting where residents voiced their concern to representatives
of the foundry, the local council, and the local department of public health,
it was agreed that the local department of public health would examine the
communities' health concerns. Two studies were undertaken: the first examined
hospital admissions for asthma from 1994 to 1996; the second was a ques-
tionnaire survey in 1995 of parents of 6-7-year-old children in three schools
close to the foundry. Both showed that there were no significant differences
between the "exposed" population and the rest of Sandwell with regard to res-
piratory health.

SECTION VI: CASE STUDIES

34 2
 The intervention
In 1997 foundry management installed dry-bag filters on all emission points.
Dry-bag filtration is a process that is primarily used to remove particulate matter
and is considered best practice. A further study was therefore undertaken, using
a geographical and epidemiological approach, to assess whether the children's
respiratory health changed following the introduction of the intervention.

Evaluating effectiveness of the intervention

To define the study area and population a geographical information system
was used to construct a series of three concentric 7so-m bands centred on the
foundry (Figure 21.9). A line was drawn through the foundry, from north to
south, dividing the study area into two areas of probable exposure to air pollu-
tion, based on the prevailing wind direction. These were then designated as
high-risk (downwind) and low-risk (upwind) areas. The impact of the interven-
tion was then assessed by examining hospital admission rates for asthma in
children under 15 years in the 2 years before the intervention, and in the 2 years
after the filters had been operating for 1 year.
Figure 21.10 shows that, prior to the introduction of the intervention, hos-
pital admission rates for asthma in the high-risk area (11.5/1000) were signifi-
cantly higher than in the low-risk area (6-4/1000). After introduction of the
filters, there was a threefold reduction in admission rates for children in the
high-risk area (3.9/1000). There was also a fall in the low-risk area to 3. 1/ 1000 ,

Figure 21.9 Study area showing area of study

21. CASE STUDIES

343
 12
0 • Low exposure
0
0 10
High exposure
'"
~
r: 8
c:
0
.~ 6
'E
-a
<1l
4
]
'0.
I
'"0 2

0
1995/1997 1998/2000
Figure 21.10 Hospital admission rates for asthma in children under 15 years before and after
the intervention

and the difference between the areas was no longer statistically significant. In
the high-risk area, the fall in admission rates was mainly due to a large and sig-
nificant fall in admission rates for children under 5 years of age, with smaller
reductions in those aged 5-9 years and 10-14 years. A similar but less dramatic
fall was seen in those under 5 years in the low-risk area. Overall, statistically sig-
nificant trends were not identified in relation to increasing distance from the
foundry.

Conclusions
• The intervention had a positive impact on children's respiratory health in
the exposed population.
• The methodology used in the study is relatively simple and provides a
useful approach to examining environmental health problems, although
there are limitations associated with this type of study.
• Responding to reported adverse health events perceived to be associated
with a source of environmental pollution is a difficult but important part
of the public health function.
• Communities should not suffer in silence but be advocates for the health
of their children.

SECTION VI: CASE STUDIES

344
 20. AN ENVIRONMENTAL EDUCATION AND RESEARCH LEARNING
PROGRAMME: SOUTH TEXAS ENVIRONMENTAL EDUCATION
AND RESEARCH (STEER)

The South Texas Environmental Education and Research (STEER) Center, a

part of the University of Texas Health Science Center at San Antonio, Texas, USA,
implements courses on environmental public health matters addressing
medical students and residents and nursing and public health students. The
team instructors are from the Health Science Center and the University of Texas-
Houston School of Public Health, and include local educators, health profes-
sionals, engineers, sanitarians and community leaders. These professionals
provide a hands-on approach to learning, so that trainees join in health fairs,
meet local residents, and see living conditions on both sides of the Mexican-
American border.
Part of a STEER student's training involves making an "environmental house
call", which is described in the box below.

EnVironmental house calls

Families with children who have asthma volunteer to let the students into their homes. Under
professional supervision, the students visit the family home three times. They learn about
the relationship between illness and the environment.
"Before coming here, I would have never thought to do home visits to identity allergens in
the environments of children with asthma," said Liz Lowenthal, a fourth-year student at
Baylor College of Medicine. "Now I want to find a way to make such visits routine for my
patients who have multiple hospitalizations for asthma exacerbations."
On the initial visit, students look for air contaminants that might contribute to asthma: mould,
tobacco smoke, dust from unpaved roads, car and truck exhaust, combustion byproducts
and allergens. On the second visit, students conduct selected testing for carbon dioxide,
carbon monoxide, allergens, mould and airborne particulate matter.
On their third and final visit, the students and the host family members discuss exposures
that concern them, ask questions, and consider ways to reduce irritants at home. The house
calls are supported by the US Environmental Protection Agency and the National Environ-
mental Education and Training Foundation. The goal is to develop a protocol for educational
house calls that medical and nursing schools can use to teach their students.

21. CASE STUDIES 345

 Index

Abrin poisoning 167 unintentional injuries 7, 178, 181

Academia 268 vector-borne diseases 37, 42, 210
Acceptable daily intake (ADI) 143 venomous animals 171, 172
Accidents 7 water quality 71-72
history-taking 239 African fluoride belt 78, 306
home 36,181 Agate industry 279-282
school children 42-43 Age, unintentional injuries and 181
terminology 177 Agelenopsis aperta envenomation 174
see also Unintentional injuries Agency for Toxic Substances and
Acid ingestion/burns 161 Disease Registry (ATSDR) 275
Aconite 163 Air intake 3-4,22, 121
Aconitine 168 Air pollution 6, 107-132
Acrodynia 118, 248 asthma and 7, 120, 121-122, 123,
Action, taking see Environmental health 323-3 24, 342-344
protection health effects 119,121-123
Activities, history-taking 236-237 history-taking 235-236
Acute lymphoblastic leukaemia (ALL) 8 indoor see Indoor air pollution
Acute respiratory infections (ARI) 6, management and intervention
110, 121-122 317-3 18
Adolescents 23 near iron foundry 342-344
affected by Chernobyl disaster 340 outdoor 36,41,118-125
market clean-up campaign 291-293 pregnancy outcome and 119,
occupational history 246-247 320-3 22
smoking 244 quality standards 124-125, 126, 317
sun protection 286 in Sao Paulo, Brazil 119,316-319
Advertising campaign, tobacco control standard index values 126
313-3 15 see also specific pollutants
Advisory Committee on Immunization Aircraft noise 197
Practice (ACI P) 277 Albania 8
Advocacy 264 Alcan/Buet-activated alumina 296
Aedes aegypti mosquitoes 210 Alcohol use 64-67, 143
Aerosols 108 health effects 65-66
Afghanistan 180 in pregnancy 146
Aflatoxin 8, 142 remedial action, prevention and
Africa education 66-67
child labour 46 routes of exposure 64-65
childhood cancer 8 Alkali ingestion/burns 161
food insecurity 208 Alkalinization of urine 157, 169
impact of climate change 208, 210 Allergens
sanitation and hygiene 5, 95, 100, airborne (aeroallergens) 209
103 indoor 31,35, 108

347
Allergies 247 vector-borne diseases 37, 210
climate change and 209 venomous animals 171
moulds 116 water quality 71-72
Amanita poisoning 167 Asthma 7-8,42,247
American Academy of Pediatrics (AAP) air pollution and 7, 120, 121-122,
276-277 12 3, 323-3 24, 342-344
Americas antioxidant supplementation and 125
impact of climate change 206, 208, community measures to prevent 259
210 environmental house calls 345
unintentional injuries 178 in Hong Kong 120,323-324
water quality 72 household pets and 35
Ammonia 108 near iron foundry 342-344
Anaphylactic reactions, hymenoptera solid fuel smoke exposure and 110
stings 172 tobacco smoke exposure and 112
Angola 56 Atomic bomb survivors 189-190,191
Animals Attention deficit disorder 9
aquatic 172-173 Audiometry 198
domestic 35 Australia
effects of endocrine disrupters 218 asthma 8
as parasite hosts 136 sun protection 246, 253, 283-287
venomous 169-174 unintentional injuries 178
Ant stings 172 venomous animals 171,173,174
Antidotes, poison 157 Autism 9
Antioxidant supplementation 125 Ayurvedic remedies 163
Apple juice 142-143, 150
Aquatic animals, venomous 172-173 Bacteria
Aquifers, deep 85, 296 in breast-milk substitutes 144
Aral Sea 303 food borne 136-138
Armed conflicts see Wars and conflicts in water 76
Arsenic Bacteriological quality, drinking-water
in air 108, 110 guidelines 91
health risks 77-78,294-295 Bangkok Statement (2002) 11-14, 159,
in water 75, 77-78, 86, 294-2 98 260
Arsenicosis 294, 298 Bangladesh
Asbestos 7, 108, 288 arsenic exposure 77,78, 155,
Asbestos-related diseases, prevention 294- 29 8
288-290 floods 206
Ascariasis 97 unintentional injuries 179
Asia Bangladesh Arsenic Mitigation Water
child labour 46 Supply Project (BAMSWP) 296
food insecurity 208 Bee stings 172
sanitation and hygiene 5, 95, 100, Behaviour, history-taking 237-238
103, 104-10 5 Belarus 190
substance use 66 Benzene 109, 164
unintentional injuries 181 Bhopal chemical disaster (1984) 155

CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

 Biological hazards Burns 180, 182
child workers 49 prevention 183
home environment 34-35 working children 52
water 73-74
Bites, venomous 169-174 Cadmium 108
Black widow spider bites 171 Canada
Blue baby syndrome 80 indoor air quality 114
Boiling, water 245 noise exposure 197
Bottle-fed infants 144, 147 unintentional injuries 181
Botulism 138 Canadian Institute for Child Health
infant 138, 147 (CICH) 271
Box jellyfish stings 172-173 Cancer 8,43
Brain cancer, primary 8, 192 asbestos-related 288
Brain damage endocrine-disrupting chemicals and
lead exposure 8-9, 43, 79-80 21 9
mercury poisoning 81-82, 118 magnetic fields and 38
Brazil radiation-induced 33,189,19°-192,
child labour 52 33 8 , 339
radiation exposure 188 see also specific types of cancer
respiratory diseases 119, 316-319 Carbon dioxide 108, 207
toxic exposures 155 Carbon monoxide (CO) 33, 108,
unintentional injuries 180 113-11 5,3 0 9
Breast cancer 191,219 detectors 114
Breast milk 144 environmental history 241
organochlorine compounds 134, exposure limits 114-115
325-3 2 9 outdoor air 120
persistent organic pollutants 141, poisoning 113-114,121,160,309-312
220, 325-326 prevention of exposure 255,310-312
Breastfeeding 57, 326-327 sources 41,113,160,309
hazards 144, 147, 154 Carbon tetrachloride poisoning 164
virus transmission 139 Cardiovascular effects
Bronchial hyperresponsiveness (BH R) noise 196
323, 324 poisons 156
Bronchitis 122 CARE 299-302
Brown recluse spider bites 171 Carers, environmental health protection
Brucella 134 253- 254
Budapest Conference (2004) 260 Caribbean
Building materials 31 child labour 46, 47
Buildings mercury exposure 117
asbestos in 288, 289-290 sanitation and hygiene 95, 100, 104
school 41 Caustic agent ingestion/burns 161
see also Housing Centers for Disease Control and
Burden of disease, environmental Prevention (CDC) 246, 299, 300,
266 301 -3 02 , 30 4
Burkitt lymphoma 8 Centipedes, venomous 172

INDEX
349
Cereal grain production 208 Chlorination
Chagas disease 36-37 by-products in water 82, 89
Charcoal, activated 157,165,168,169 household water supply 300-302,
Chemicals 3 30 4, 30 5
detoxification 4 inadequate 304-305
drinking-water guideline values Chlorpyrifos 34
86-90 Cholera 301-302
endocrine-disrupting see Endocrine- Chronic effects of environmental
disrupting chemicals hazards 7-10
food additives 143 Clean Air Act, Philippine 315
foodborne 134, 140- 143 Climate change, global (global
health hazards 6-7 warming) 202, 204-211
high-production volume (H PV) 3 direct health effects 205-207
history-taking 234, 246 indirect health effects 207-211
household contaminants 31-34 pathways of impact on health 203
occupational exposures 48, 49 prevention options 212
protection from exposure 158-159, Clostridium botulinum 138, 147
254 Clothing 236
subclinical toxicity 5 CO see Carbon monoxide
waterborne 35, 73. 74, 75, 77-8 3, 155 Coal burning 109, 110
see also Persistent organic pollutants; Cockroaches 37
Poisoning; specific chemicals Coelenterate stings 172-173
Chernobyl nuclear reactor disaster Commission for Environmental
(1986) 155, 18 9,19 0 ,19 1, Cooperation of North America
33 8-341 260
Child mortality 266 Communication
"Children are not little adults" principle arsenic-related health problems
3-4,12 297-2 98
Children's environmental and health in environmental health protection
action plan for Europe (CEHAPE) 261, 26 9-270
260 Communities
Children's environmental health environmental protection role 259
(CEH) national profiles 268
education 262-264 water treatment 295
national profiles and indicators Complementary foods 144-147,
26 5-270 149-150
Children's Environmental Health Computed tomography (CT scan) 191,
Network (CEHN) 10-11,271 19 2
Children's environmental history see Conflicts, armed see Wars and conflicts
Paediatric environmental Congenital malformations 18
history Cooking 148
Chile 295 Cooking oils, toxic 155
China 8, 206, 253 Cooking stoves/fires 31,107,109,241
Chinese patent medicines 163 see also Fuel combustion emissions
Chironex jleckeri stings 173 Cortinarius poisoning 167

CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

35 0
 Courtyard meetings, in Bangladesh Density, high population 30, 36
297 Dental caries 79
Crisis situations see Extreme stress Dental fluorosis 306
Critical periods in development 19, Developed countries, sanitation and
23-24 hygiene 102
Croatia 179 Developing countries
Crowding 30, 36 environmental history-taking
Cryptorchidism 219 227-239
Cultural history-taking 237, 242 food borne illnesses 135
Cyanide (CN) poisoning 161-162 sanitation and hygiene 5, 103
Cycle helmets 183 Developmental delay
Cyclones 58, 205 climate change and 207-209
Czech Republic, air pollution and lead poisoning 43, 79-80, 166
pregnancy outcome 119, Developmental disorders 9, 43
320-3 22 Developmental processes
critical or sensitive periods 19
Dampness 34 psychological 51
Data 269 susceptibility to disruption 4,
DDE 17-18
(dichlorodiphenyltrichloroethylene) timing of exposure 18-24
218 windows of susceptibility 17-18
DDT (dichlorodiphenyltrichloroethane) Developmental toxicity 20
141,3 25-326 Diarrhoeal diseases 5, 42
Deafness see Hearing loss climate change and 205-206
Deaths 4 foodborne 135, 138- 139, 144-147
cancer 8 Kenya case study 299-302
diarrhoeal disease 5, 72 treatment guidelines 83-84
foodborne illnesses 135 Uzbekistan case study 303-305
poisoning/toxic exposures 153, 154 water/sanitation-related 72, 97
poor sanitation-related 97-98 weather disasters and 205
unintentional injuries 7, 177, 178-179 Diazinon 247-248
vector-borne diseases 6 Dibenzofurans 141,220, 325-326
Debt bondage 50 Dichlorodiphenyltrichloroethane (DDT)
Decibels (dB) 194 141,3 25-326
Declaration of the Environment Dichlorodiphenyltrichloroethylene
Leaders of the Eight on Children's (DDE) 218
Environmental Health (Miami Dieldrin, in breast milk 325-326
1997) (G-8) 10, 259 Diesel automobile exhaust 119-120
Deferoxamine 165 Diet
Defluoridation, water 307, 308 breastfeeding mothers 327,
Dehydration 328
treatment guidelines 83-84 history-taking 236, 242
weather disasters and 205 see also Food
Dengue (and dengue fever) 6, 36, 37 Dietary supplements 143, 163
climate change and 209, 210 Diethylene glycol 162

INDEX
35 1
Dioxins Eastern Mediterranean
in breast milk 141,325-326 child labour 46
endocrine-disrupting effects 219, food insecurity 208
220 unintentional injuries 178
food borne 141,146,147,150 Ecological disturbances, global climate
waterborne 75 change 203, 207-211
Di phtheria-tetan us-acell ular pertussis Economic status 266
(DTaP) vaccine 275, 277 Ecosystem changes 211-212
Diphtheria-tetanus-whole cell pertussis Education
(DTP) vaccine 275, 27 6 in environmental health protection
Disability, unintentional injuries 179 261-264
Disability-adjusted life years (DALYs) national profiles 267
9 8 , 179 EI Nino-Southern Oscillation (ENSO)
Disasters 20 5
natural see Natural disasters Electric fields 38
poisoning 155 Emergency situations see Extreme
Diseases, environment-related 4 stress
Disinfectants, in water 89 Employment
Disinfection by-products (DBPs) 75, adolescents 246-247
82, 89-90 see also Working children
Displaced/refugee children 54-56 Encephalitis, vector-borne 2lO
Domestic workers, live-in 51-52 Endocrine-disrupting chemicals (EDCs)
Drinking-water, contaminants see under 9-10, 141, 21 7-22 3
Water mechanisms of action 217-218
Dropsy, epidemic 155 potential health effects 218-220
Droughts 54, 55, 58, 20 5 research needs 221
Drowning 7,31,180 sources and timing of exposure 220
prevention 183 Endometriosis 219
risk factors 181 Endrin, in breast milk 325-326
in schools 42 Envenoming 169-174
weather disasters and 205 history-taking 239
Drug trafficking 51, 65 Environment
Drug use 64-67 home 29-39
health effects 65-66 play 30-31
remedial action, prevention and school 40-45
education 66-67 working 46-53
routes of exposure 64-65 Environment sector, national profiles
Dust mites 34-35 267
Dyslexia 9 Environmental change, global see
Global environmental change
Ear Environmental exposures see
effusions, middle 112, 247 Exposures, environmental
hearing function 194-195 Environmental health hazards 3, 5-10
protectors 198-199 chronic effects 7-10
Earthquakes 54-56, 58 diseases linked to 4

CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

35 2
 history taki ng 228 Ethnic minority groups
international response 10-14 environmental exposure risk and
unique susceptibility 3-4 242
windows of susceptibility 17-25 national profiles 266
Environmental health protection Ethyl alcohol (ethanol) 143, 146
253-2 71 consumption see Alcohol use
action areas 260-264 as poison antidote 163,167
families, carers and teachers Ethylene glycol poisoning 162-163
253-2 54 Ethylmercury 276
international and global efforts Europe
10-14,260 children's environmental and health
at local level 254-259 action plan (CEHAPE) 260
national governments 259-260 substance use 66
national profiles and indicators unintentional injuries 178, 179, 180
26 5-26 9 venomous animals 171
nongovernmental organizations Excreta see Faeces
26 9-2 70 Exposures, environmental
Environmental history children vs adults 3-4, 21-23
clinical 240-249 difficulties in studying 20-22
paediatric see Paediatric history taking 229
environmental history timing 18-24
Environmental house calls 345 windows of susceptibility 17-18,
Environmental Protection Agency (EPA) 23-24
(US) Extreme stress 54-63
G8 Declaration 1997 and 259 causes 54
methylmercury exposure limits 275 health consequences 56
noise exposure limits 196, 199 history-taking 234-235
tips to protect children 254-255 mechanisms of exposure 54-56
Ultraviolet Index 246 methods of alleviation 56-57,
volatile organic compounds 115 58-62
Environmental tobacco smoke (ETS) Eye
34, 111-113 irritation 110, 115-116
advertising campaign 313-315 protection 246
health effects 112
history taking 112, 242-243 Facts for life (UNICEF 2002) 56-57
pregnancy outcome and 321-322 Faeces (excreta)
remedial action, prevention and contamination of water 74-77
education 112-113,243-244, 253 management systems 95, 98
EPA see Environmental Protection see also Sanitation
Agency Falls 42-43, 180
Epidemic dropsy 155 prevention 183
Epidemics 59 risk factors 181
Erethism 118 Family, environmental health protection
Escherichia coli 0157: H7 137, 149, 253-254
33 0 -333 Fetal alcohol syndrome 14 6

INDEX
353
Fetus Food and Drug Administration (FDA)
food borne hazards 144, 145-14 6 (US) 275, 27 6 , 277
radiation sensitivity 187,192 Food Quality Protection Act 1996
vulnerability to toxicants 154 (USA) 327
see also Prenatal exposures Foodborne hazards 133-152
Fiji 207 breast- and bottle-fed infants 144,
Filariasis, Bancroftian 97 147,3 25
Finland children/infants receiving
asbestos-related disease prevention complementary foods 144-148,
288-290 149-150
poisonings 153 developing fetus 144, 145-14 6
unintentional injuries 178 history-taking 236
Fires magnitude of problem 134-135
burn injuries 18o risk analysis 135
bush 58 in schools 42, 330-332
cooking see Cooking stoves/fires see also specific hazards
see also Fuel combustion emissions Formaldehyde 31,108,109,115-116
First aid, poisonings 158 France, carbon monoxide poisoning
Fish 113,3 0 9-3 12
in diet of breastfeeding mothers 32 7, Fruit consumption 22
Fuel combustion emissions (including
328
endocrine-disrupting chemicals 218, smoke) 109-111,205
220 asthma and 110, 323, 324
mercury contamination 141 components 32-33, 109
protection from contaminated 255 health effects 11 0, 203
Floods 54, 55, 58, 20 5 history-taking 241
Fluoride 78-79 indoor air 31, 107, 109-111
health aspects 78-79 pregnancy outcome and 320-322
in water 75, 78, 86, 30 7-3 08 routes of exposure 109
Fluorine 110 in Sao Paulo, Brazil 317-318
Fluorosis 78, 79, 110 in schools 41
case study 306-308 Fungi
crippling 307 airborne 116-117
dental 306 poisonous 167
mitigation 308 see also Moulds; Mycotoxins
non-skeletal (huma) 306, 307 Furnishings, home 115
skeletal 307
Food Gas cooking 109
availability, climate change and Gasoline, leaded see Petrol, leaded
207-20 9 Gastroenteritis 134
complementary 144-147, 149-150 viral 138-139
intake 3-4, 140 see also Diarrhoeal diseases
safety 148, 332 GEMS/Food 326
see also Diet Gene-environment interactions
Food additives 143 23

CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

354
German Network for Children's Health Hearing loss 195
and Environment 271 noise-induced see Noise-induced
Germany 197 hearing loss
Giardia lamblia 136 Heat stroke 205
Glioma 8 Heat waves 203, 205
Global efforts, environmental Heating devices
protection 260 carbon monoxide emission 113,160,
Global environmental change 202-216 310
effects on children's health 204-212 history-taking 241
pathways of health effects 203 indoor air pollution 31, 107, 109
prevention options 212 see also Fuel combustion emissions
Global warming see Climate change, Helmets, cycle 183
global Helminths (worms) 72, 97
Glycoside-containing plants 168 Hemlock poisoning 168
Gold mining industry 155 Hepatitis A 134, 138-139
Governments Hepatitis B
assessing role 266-267 cancer risk 8
environmental protection 259-260 vaccine 275, 276, 277
Greece 8 Hepatitis C 8
Greenhouse gases 203, 212 Heptachlor, in breast milk 325-326
Groundwater safety 85 Herbal medicines 163
Growth retardation 207-209 Hexachlorobenzene (HCB), in breast
milk 325-326
Haemolytic uraemic syndrome 137, Hexachlorocyclohexane, in breast milk
149,33 0 325-3 26
Haemophilus injluenzae type b (Hib) History, paediatric environmental see
vaccine 275, 276, 277 Paediatric environmental history
Haiti 155 Hobbies 236-237
Hantavirus pulmonary syndrome 203 Holly berries 168
Headaches 247 Home 29-39
Health problems, history-taking 238 air pollution see Indoor air pollution
Health professionals 261 audits 230, 231
carbon monoxide poisoning and biological contaminants 34-35
310-3 11 chemical contaminants 31-34
education and training 261-264, crowding and density 36
345 environmental history 232-233,
Health protection, environmental see 240- 241
Environmental health protection indoor environment 31
Health sector, national profiles physical hazards 38
266-267 toxic exposures 6, 36, 155
Healthy Environments for Children unintentional injuries 36, 181
Alliance 10, 260 water and sanitation 35
Hearing 194-195 water containers 300, 304, 305
screening 198 water treatment 72, 85, 299-302,
temporary threshold shift (TIS) 195 30 4-3 0 5

INDEX
355
Homeopathic medicines 163 toxic exposures 155
Honduras unintentional injuries 180
informal markets 291-293 Indonesia 8
weather disasters 206 Indoor air pollution 31,107-118
Hong Kong, asthma 120, 323-324 main pollutants and sources 108,
Hornet stings 172 10 9-118
House calls, environmental 345 prevention 253
House dust mites 34-35 in schools 41
Housing Indoor environment 31
environmental history 240-241 history-taking 240-241
healthy, principles 30 Infant feeding
psychosocial factors 30 hazards 144, 147
unhealthy 29 HIV-positive women 139
unintentional injury risk 181 see also Breastfeeding
Human immunodeficiency virus (HIV) Infant mortality 266
drug use and 66 Infections
mother-to-child transmission 139, food borne 134
147 water-related 73, 77, 95-97
Hungary 295 see also Vector-borne diseases;
Hurricane Mitch 205 specific infections
Hydrocarbon-containing products Information systems and centres
16 3-164 26 9
Hydrofluoric acid 161 Injuries
Hydrogen sulfide 120 definition 177
Hygiene 5, 95-106 intentional 177
barriers to improving 98 unintentional see Unintentional
education 101 injuries
food handling/preparation 148 Innocenti Digest on Child Domestic
future perspectives 100-101 Work (1999) 52
health aspects 72-]3, 74, 95-9 8 Insecticides 33-34,248
history-taking 233-234, 237 I ntegrated pest management (I PM) 34,
informal markets in Honduras 335
29 1- 2 93 I ntellectual development
recommendations for improving effects of lead 8-9, 43, 79-80
99-100 see also Mental retardation
see also Sanitation; Water Intergovernmental Panel on Climate
Hymenoptera stings 172 Change (IPCC) 204,208,212
Hypospadias 10,219 International Agency for Research on
Cancer (IARC) 38
Immunological effects International initiatives 10-14,
endocrine-disrupting chemicals 220 260
ultraviolet radiation 211 International Labour Organization
India (ILO)
radiation exposure 188 on child labour 46, 48, 52
silicosis and agate industry 279-282 diagnosis of silicosis 280

CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

 International Network of Children's forced 50
Environmental Health & Safety Land, school buildings 41
(INCHES) 10-11,271 Landmines 56, 57
International Programme on the Health Landslides 58
Effects of the Chernobyl Accident Latin America
(I PH ECA) 190 child labour 46, 47, 51
I nternational Society of Doctors for the sanitation and hygiene 95, 100, 104
Environment (ISDE) 271 unintentional injuries 181
International Study of Asthma and Latvia 179
Allergies in Childhood (ISAAC) 7 Lead 79-80
Intestinal worms 72, 97 absorption 22
Intoxication see Poisoning airborne 108, 120
I ntrauterine growth restriction (I UG R) environmental history 241, 242
23 in food 142, 145, 147, 150
air pollution and 119, 320-321 household exposure 31-32
Intravenous drug use 66 in petrol 6, 8, 9, 120, 159
Ipecacuanha 165, 168 poisoning 6, 8-9, 43, 79-80,
Iran, Islamic Republic of 179, 188 165-166, 247
Ireland 8 protection from exposure 166, 254
Iron foundry, asthma near 342-344 subclinical toxicity 5
Iron poisoning 164-165 in water 75, 79, 86
Irukandji jellyfish stings 173 Learning deficiencies see Mental
retardation
japan Lebanon 172
atomic bomb survivors 189 Leukaemia
Escherichia coli 0157: H7 outbreak acute lymphoblastic (ALL) 8
137,330-333 electric and magnetic fields and 38
indoor air quality 114-115 radiation-related risk 191, 192
methylmercury poisoning 82 Life Span Study (LSS) 189--:190,191
unintentional injuries 182 Lindane 34
japanese encephalitis 6, 37 Listeria monocytogenes (listeriosis)
jellyfish stings 172-173 13 6- 137, 145
joint FAO/WHO Expert Committee on Liver cancer 8
Food Additives (JECFA) 142, 143 Livestock 35
jordan 172 Local governments, environmental
protection 259
Kenya Local level, environmental protection
household water treatment 299-302 254-259
radiation exposure 188 Lung cancer 192
Klorin 300-301 Lung function tests 122
Kuwait 180 Lyme disease 210
Kyoto Protocol (1997) 212
Madagascar 301-302
Labour Magnetic fields, extremely low
child see Working children frequency (ELF) 38

INDEX
357
Malaria 6, 36, 37 Microorganisms
climate change and 209-210 in breast-milk substitutes 144, 147
control methods 37 food borne 135, 149
Malformations, congenital 18 waterborne 74-77
Malnutrition 207-209 see also Bacteria; Viruses
Manganese 108 Millennium Development Goals 260
Markets, informal, clean-up campaign Millennium Ecosystem Assessment
29 1- 2 93 Project 211
Medications Millipedes, venomous 172
child-proof containers 158,159 Minamata Bay, Japan 82
poisoning prevention 158 Mirex, in breast milk 325-326
toxic contaminants/adulterants 155, Mosquito-borne diseases 36, 37,42
16 3 climate change and 209-210
Melanoma, malignant 211, 245, 246, Motor vehicle emissions 31,119-120,
28 3 121, 125
Mental health problems see Moulds 34
Psychological problems airborne 116-117
Mental retardation (learning deficiency) food 142-143
9 Mozambique 206
radiation-induced 192 Mucous membrane irritation, solid fuel
role of schools 43 smoke 110
Mercury 81-82, 248 Mushroom poisoning 167
in food 141,145,147,150 Mustard oil, contaminated 155
prevention of exposure 255 Mycotoxins
toxicity 6-7, 81-82, 117-118 airborne 116
in vaccines 275-278 food borne 142-143
vapour 108, 117-118
in water 75,81,86 National governments
Mesothelioma 288 assessing role 266-267
Metabolism 4 environmental protection 259-260
Metals, heavy National Institute for Occupational
foodborne 145, 147, 150 Safety and Health (NIOSH) (US)
see also Lead; Mercury 49-5 0
Methaemoglobinaemia 80, 142, 147, National Institute of Occupational
15 0 Health (NIOH) (India) 280,281
Methanol poisoning 166-167 National profiles and indicators
Methylene chloride poisoning 160, 26 5-270
164 Natural disasters 54-56
Methylmercury 75, 81-82, 147, 150 global climate change and 203, 206
exposure guidelines 275 preparedness and mitigation 57, 58
sources of exposure 81,141 Neonates
thiomersal in vaccines and 275-276 nitrate/nitrite poisoning 142
4-Methylpyrazole 163, 16 7 noise exposure 196
Mexico 180 Netherlands, unintentional injuries
Miami (G8) Declaration (1997) 10,259 179,182

CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

Neurobehavioural effects, endocrine- Oral rehydration solutions (ORS) 84
disrupting chemicals 220 Organochlorine compounds 134, 140
Neurodevelopmental delay see in breast milk 134, 325-329
Developmental delay endocrine disrupting effects 219
Neurological disorders see also Persistent organic pollutants
congenital toxoplasmosis 136 Organophosphorus compounds 150,
mercury poisoning 81-82, 117-118 153
in poisonings 156 health effects 82, 140, 156
New Zealand history-taking 248
asthma 8 Otitis media 112
unintentional injuries 180, 181 Outdoor environment, history-taking
Nicotine 108 242
Nicotine replacement therapy (N RT) Oxalate-containing plants 168
243 Ozone
Nigeria 8 air pollution 108, 121, 122, 125
Nitrites / nitrates depletion of stratospheric 202,
adverse health effects 80 211
in food 142, 147, 150
in water 75, 80, 86 Paediatric environmental history
Nitrogen dioxide (NO,) 32, 109, 110 (PEH)
Nitrogen oxides 108, 120 barriers to taking 230-231
Noise 38, 194-201 developing countries 227-239
effects on children 196-197 development and use 229-230
effects on parenting 197 interpretation 247-248
history-taking 234 key areas covered 228-229
prevention of exposure 198-199 main questions to ask 232-239
routes of exposure 194-195 personnel involved 230
systems affected 195-196 scope 228
Noise-induced hearing loss (NIHL) 38, time and place 230
195 US experience 240-249
in children 196,197 Pan American Health Organization
diagnosis 198 (PAHO) 10-11,72,299
specific sounds 199-200 Paracetamol
treatment 198 poisoning 159-160
Nongovernmental organizations unregulated adulterated 155
(NGOs) 10-11 Paraquat 153, 158
market clean-up campaign in Parasites
Honduras 291-293 foodborne 135-136
national profiles 268 waterborne 76
opportunities for 270-271 Parents
Norwalk-like viruses 138-139 effects of noise 197
environmental health protection
Occupational history 253-254
adolescents 246-247 occupational history 246
parents 246 smoking 111-113, 242-243, 314

INDEX
359
Participatory hygiene and sanitation home environment 38
transformation (PHAST) methods school environment 41-42
300 Plants, poisonous 167-168
Particulate matter, airborne Play spaces 30-31
asthma and 343-344 environmental history 233, 240-241
health effects 122, 123 Playgrounds 31
indoor air 32, 108 Pneumoconiosis 280
outdoor air 36, "9-120, 316, Pneumonia, maternal smoking and
317-3 18 112
pregnancy outcome and 320,321, Poison control centres 158
322 Poisoning (intoxication) 6-7, 153-169,
solid fuel smoke 109 180-181
Pascals (Pa) 194 breastfeeding advice 326-328
Patulin 142-143, 150 data sources 157-158
Pedestrians 18o, 182 disasters 155
Persistent organic pollutants (POPs) epidemics 155
in breast milk 141,220,325-326 health effects 155-156
as endocrine disrupters 141,217 history-taking 239, 242
food borne 14°-141,146,147,15° home 36, 155
research needs 221 incidence and significance 153-154
see also Endocrine-disrupting management 156-157
chemicals; Organochlorine pesticides 334, 336
compounds prevention 158-159, 183
Peru 206, 207 routes of exposure 154-155
Pesticides 33-34, 82 school children 43
acute poisonings 334, 336 severity and vulnerability 154
in breast milk 325-326 see also Envenoming; specific poisons
environmental history 241 Pokeweed poisoning 168
in food 140, 150 Policy, public 264
health concerns 82, 140 Poliomyelitis 97
protection from exposure 254 Pollens 108, 209
routes of exposure 155 Polychlorinated biphenyls (PCBs)
Thai education programme 154, in breast milk 325-326
334-337 endocrine-disrupting effects 218,
in water 75, 82, 88 21 9,220
Petrol, leaded 6, 8, 9, 120, 159, 166 in food 141,146,147
Pets 35 in water 75
Phenylbutazone 163 Polycyclic aromatic hydrocarbons
Philippines (PAHs) 108, 109
tobacco control campaign "1, pregnancy outcome and 320,
313-3 15 321
toxic exposures 155 POPs see Persistent organic pollutants
Physalia stings 173 Population density, high 30, 36
Physical hazards Population Services International
child workers 48-50 , 51 301 -3 02

CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

 Postnatal exposures Psychosocial risk factors
difficulties in studying 21-23 home environment 30
windows of susceptibility 20 working children 50-52
Poverty Puberty 23
environmental exposure risk and early onset 10, 219
242 susceptibility to environmental
extreme situations 55 hazards 20
illicit drug production and 65 see also Adolescents
unintentional injuries and 181 Public awareness
working children 46, 52 arsenic-related health problems
Preconceptual exposures 18,19, 297-2 98
20-21 environmental health protection 261
Pregnancy Public policy 264
child domestic workers 52 Pulmonary haemorrhage, idiopathic
food borne hazards 135-137, 144, 247
145-14 6
outcome, and air pollution 119, Radiation, ionizing 33, 187-193
320-3 22 health effects 189-192
physiological and toxicokinetic history-taking 234
changes 21 sources and exposures 187-188
see also Prenatal exposures types and biological effects
Premature infants, noise exposure 188-189
19 6 see also Chernobyl nuclear reactor
Prenatal exposures disaster
difficulties in studying 21 Radionuclides, in water 76, 83, 91
endocrine-disrupting chemicals Radon 38, 83, 187
220 carcinogenicity 192
excessive noise 196 prevention of exposure 255
timing 18-20 sources and exposures 108, 188
see also Fetus Rainwater harvesting 296
Private sector 268 Reading performance, noise exposure
Professional associations 268 and 197
Project Alternatives 291-293 Refrigeration 148
Protozoa, foodborne 135-136 Refugee children 54-56
Psychological problems Rehydration treatment 83-84
after Chernobyl disaster 338-341 Reporting 269
after weather disasters 205 Reproductive health effects
extremely stressed ch i Id ren arsenic 295
56 Chernobyl disaster 340
housing and 30 endocrine-disrupting chemicals
working children 50 218-21 9
Psychological stress 30 see also Pregnancy
after Chernobyl disaster 338-341 Research 264, 269
noise-induced 196 Research Centre for Radiation Medicine
working children 50 (RCRM), Ukraine 339

INDEX
Respiratory illnesses (and symptoms) Sanitation 5, 35, 74, 95-106
247 barriers to improving 98
air pollution-related 11 0, 119, future perspectives 100-101
121-122, 123 global access 95, 96, 102-10 5
environmental history 241 health aspects 72-73, 95-98
mould allergies 116 history-taking 233-234
in poisonings 156 informal markets in Honduras
prevention 254 29 1- 2 93
in Sao Paulo, Brazil 119,316-319 recommendations for improving
see also Asthma 99-100
Respiratory infections, acute (ARI) 6, school 41,99-100
110, 121-122 see also Hygiene; Water
Respiratory tract Santeria 117
deposition of inhaled particles Sao Paulo, Brazil, respiratory illnesses
119-120 119,3 16-3 19
irritation 110,115-116 Saudi Arabia 172, 181
Respiratory ventilation rates 3-4, 22 Scalds 180
Risk-taking behaviour 42 Schistosomiasis 6, 37, 72, 97
Road traffic injuries (RTls) 7, 179-180 School (s)
prevention 182-183 arsenic awareness raising 297
risk factors 181 asbestos exposure 289, 290
schoolchildren 42 child health protection 253-254
Rodents 42 food borne disease outbreaks
Romania 8,9 330-33 2
Rotaviruses 138-139 history-taking 233, 242
Rural areas hygiene education 101
child labour 46, 50 performance, noise exposure and
indoor air pollution 107 197
pesticide exposure 82, 154 pesticide education 335-337
school environment 41 sanitation 41,99-100
unintentional injuries 179, 180, sun protection 283-287
181-182 School environment 40-45
vector-borne diseases 6 health effects of adverse 42-43
water supply/sanitation 5, 71-7 2 , healthy 43, 44
101, 102-105 main threats 41-42
Russian Federation 8, 190 need for safe 44
physical, components 40
Safe Water System 299-302 Science, national profile 268-269
Safety seats, child 182 Scopolamine-containing plants 168
Salicylate poisoning 168-169 Scorpion stings/bites 170, 17 1- 172 ,
Salmonella species (salmonellosis) 174
137 Selenium 80-81
Sand pits 31 health aspects 81
Sanitary Epidemiologic Services (SES) in water 75, 80-81, 86
30 3,3 0 4 Selenosis 81

CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

Sensitive periods in development 19, Solvent encephalopathy 164
23-24 Sound 194
Sensitization meetings, in Bangladesh day-night average level (DNL) 199
297 decibel ranges and effects 199-200
Sewerage systems 95, 98, 99 see also Noise
Sex differences, unintentional injuries South Africa, road traffic injuries 180
181 South-East Asia
Sexual abuse 52 Bangkok statement (2002) 10-14,
Sexually transmitted diseases (STDs) 260
340 childhood cancer 8
Silicosis/silicotuberculosis 279-282 unintentional injuries 7, 178
diagnosis 280 vector-borne diseases 6, 37
prevalence in children 280-281 South Texas Environmental Education
prevention and control 281-282 and Research Center (STEER) 231,
Skeletal fluorosis 307 345
Skin cancer Spain, toxic cooking oil (1981) 155
arsenic-related 294-295 Sperm counts 218-219
sunlight exposure and 211, 245, 283, Spider bites 171, 174
286 Spores, fungal 108
Skin lesions, arsenic-related 294-295 Sports 237
Slavery, child 50 Sri Lanka 154
Sleep deprivation, noise-induced 195 Steven/Tetrahedrons method, arsenic
Smog, urban summer 121 removal 296
Smoke see Fuel combustion emissions; Stings, venomous 169-174
Tobacco smoke Stockholm Convention on Persistent
Smoke detectors 114 Organic Pollutants (2001) 141,
Smoking, tobacco 325-3 26
cessation advice 112-113, 243-244 Street children
control, Philippines lll, 313-315 history taking 233
education materials 244 substance use 66
history-taking 242-245 Stress
parents 111-113, 242- 243, 314 extreme see Extreme stress
passive see Environmental tobacco psychological see Psychological
smoke stress
prevention 112-113,253 response, to noise 195, 197
Snakebites 170-171 Subclinical toxicity 5
Society role, national profile 268 Substance use 64-67
Socioeconomic status Sudden infant death syndrome 112
national profiles 266 Sudden sniffing death 164
unintentional injuries and 181 Suicide 153
see also Poverty Sulfur compounds, airborne 120
Sodium hypochlorite 300 Sulfur dioxide (S02)
Soil ingestion 22, 30 asthma and 323-324
Solanine poisoning 167 indoor air 108, 109, 110
Solvent abuse 163-164 outdoor air 120,316,317-318,322

INDEX
Sulfuric acid aerosol 120 pesticide education programme 154,
Sunburn 211 334-337
Sunglasses 246 road traffic injuries 179
Sunlight exposure 245-246 Thermal extremes 205
protection from 245-246, 255, Thiomersal, in vaccines 275-278
28 3-28 7 Three Kolshi filter 296
see also Ultraviolet (UV) radiation Thyroid cancer 191, 338
exposure Ticks 42, 210
Sunscreens 246 Tobacco control, in Philippines 111,
SunSmart Schools Program 253, 313-3 15
283-286 Tobacco smoke 31,32,33
Surface area: body mass ratio 22 second-hand see Environmental
Sweden tobacco smoke
arsenic exposure 295 Tobacco smoking see Smoking,
breastfeeding advice 327 tobacco
tick-borne encephalitis 210 Toluene poisoning 164
unintentional injuries 179 Toxaphene, in breast milk 325-326
Swimming pools 31,284 Toxic exposure see Poisoning
Symptoms, clinical 247-248 Toxins
Syrian Arab Republic 172 microbial 76
see also Mycotoxins
Tanzania, United Republic of, fluorosis Toxoplasmosis (Toxoplasma gondii) 134,
306 -3 08 135-136 , 145
Tap water Trachoma 5, 72, 97
contaminated 304-305 Traditional medical practitioners, in
history-taking 245 Bangladesh 297-298
Tea stall sessions, in Bangladesh 297 Training, health professionals 261-264,
Teachers 310-3 11 , 345
environmental health protection Transport, history-taking 237
253- 2 54 Traumatic injuries see Injuries
see also School(s) Traumatic situations see Extreme stress
Teas, herbal 163 Triatomine bugs 36-37
Technological disasters 54, 55, 61 Tributyltin 218
Teenagers see Adolescents Trifluoracetamide 153
Tegucigalpa, Honduras, informal Trinidad and Tobago 9
markets 291-293 Trypanosoma cruzi 36-37
Television advertising, tobacco control Tsetse flies 42
313-3 15 Tuberculosis, silica dust exposure and
Terrorist attacks 62 279-282
Testicular cancer 8, 10, 219 Turkey 172
Tetanus toxoid (TT) vaccine 275, 276
2,3,7,8-Tetrachlorodibenzyl-p-dioxin Uganda 180
(TCDD) 219 Ukraine, Chernobyl disaster (1986) 155,
Thailand 189, 19 0 , 33 8-34 1
arsenic exposure 295 Ultraviolet (UV) Index 246

CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

Ultraviolet (UV) radiation exposure food borne illnesses 135, 136, 138
climate change and 211 lead poisoning 8-9
history-taking 234, 245 noise exposure 196, 197
protection measures 245-246, 255, noise protection guidelines 199
28 3-28 7 organochlorines in breast milk 327
at school 41 poisonings 153-154
UNICEF see United Nations Children's school environment 41
Fund severe weather events 206
Unintentional injuries 7, 177-186 smoking cessation 112
causes 178, 179-181 thiomersal in vaccines 275-278
child workers 48-50, 52 unintentional injuries 178, 181
history-taking 239 vector-borne diseases 210
home 36, 181 venomous animals 170,171,172
magnitude of problem 178-179 water-borne disease 83
remedial action, prevention and Urban areas
education 182-184 air pollution 6,121,122
routes of exposure and risk factors alcohol and drug use 64
181-182 asthma prevalence 7
school children 42-43 child labour 46, 50
terminology 177 lead poisoning 9
see also Drowning; Road traffic school environment 40,41
injuries unintentional injuries 179, 181-182
United Arab Emirates 180 water supply/sanitation 71-72, 99,
United Kingdom 101,102-105
asthma 8, 342-344 US Agency for International
carbon monoxide poisoning 33 Development (USAID) 304, 305
environmental health protection 259 US Public Health Service (US PHS)
unintentional injuries 180, 182 276-277
United Nations 260 Uzbekistan, contaminated water
United Nations Children's Fund distribution 80, 303-305
(UNICEF) 10, 56-57, 264, 313
United Nations Environment Vaccines, thiomersal in 275-278
Programme (UNEP) 10 Vector-borne diseases 6, 36-37
United States (USA) climate change and 203, 209-210
air pollution 114, 115, 116, 122, 125 history-taking 235
air quality standards 124, 125 housing quality and 36-37
asthma 7 in schools 42
child labour 47, 49-50 water-related 73, 97
childhood cancer 8 Vectors, disease 6
clinical environmental history Venezuela 206
24 0- 249 Venomous animals 169-174
developmental disorders 9 Ventilation, home 116
environmental education and Viet Nam 153
research 231, 345 Violence, extreme situations 55, 56,
environmental health protection 253 57

INDEX
Viruses registration, recording and reporting
food borne 138-139 of data 84-85
waterborne 76 treatment guidelines 83-84
Visual impairment, congenital Water-related infections n 77, 95-97
toxoplasmosis 136 Water-related vector-borne diseases 73,
Vitamin A 143 97
Vitamin C 125 Water supply
Vitamin D 143 access to safe 71-72, 102-105
Vitamin E 125 arsenic-free, in Bangladesh 295-296
Vitamin supplements 143 contaminated, in Uzbekistan 80,
Volatile organic compounds (VOCs) 30 3-3 0 5
32,108,115-116 household 5, 35
Volcanic eruptions 55, 56, 58 protection 85, 255
Vulnerability, history-taking 238 quantity 74
school 41
Wars and conflicts 54, 55, 56, 60 Water treatment
Wasp stings 172 arsenic removal techniques 296
Waste disposal, informal markets in community 295
Honduras 291-293 defluoridation 307, 308
Wastewater management 95, 98, household 72, 85, 299-302, 304-305
99 Water-washed (infectious) diseases 73,
Water 71-94 74,97
arsenic contamination 75, 77-78, 86, Waterborne (infectious) diseases 73,
294- 29 8 97
boiling 245 Weather disasters 205
chemical contaminants 35, 73, 74, Weight loss, breastfeeding mothers
75, 77-8 3, 155 32 7
fluoride content 75, 78, 86, 307-308 Well-water, history-taking 245
guideline values for contaminants Western Pacific
86-93 Bangkok statement (2002) 10-14,
history-taking 235, 245 260
intake of children 3-4, 22 child labour 46
major contaminants 73, 75-76 unintentional injuries 7, 178
microbial contamination 74-77 WHO see World Health Organization
play, hazards 31 Windows of susceptibility 17-18, 23-24
storage containers 300, 304, 305 Woodruff Foundation 300
vapour 108 Working children 46-53
see also Drowning; Sanitation characteristics and trends 46-47
Water-based (infectious) diseases 73, conditions 48
97 history-taking 233, 246-247
Water-related illnesses 35, 72, 73 informal markets in Honduras
diagnosis 83 29 1- 293
mechanisms of exposure 73-74 physical risks 48-50
prevention, remedial action and psychosocial risks 50-52
education 85 toxic exposures 155

CHILDREN'S HEALTH AND THE ENVIRONMENT A GLOBAL PERSPECTIVE

World Bank 10, 46-47 national profiles and indicators
World Health Organization (WHO) 26 5-270
air quality guidelines 124 Safe Water System 299-302
drinking-water quality guidelines tobacco control advertising 313-314
86-93 World Summit on Sustainable
environmental protection initiatives Development, Johannesburg
10-11, 260, 264 (2002) 10, 260
messages for healthy environments
25 6- 258 Zambia 301
methylmercury exposure limits 275 Zimbabwe 180-181

INDEX