A Decade of Children’s 

Environmental Health Research

Highlights from EPA’s 

Science to Achieve Results Program

Office of Research and Development

National Center for Environmental Research

SUMMARY REPORT

EPA/600/S-07/038 | December 2007 | http://www.epa.gov

EPA/600/S-07/038

A Decade of Children’s Environmental Health Research:

Highlights from EPA’s Science to Achieve Results Program

U.S. Environmental Protection Agency

Office of Research and Development (8101R)

http://www.epa.gov

December 2007
Disclaimer

The research described in this document has been funded wholly by the United States Environmental Protection 

Agency (EPA) under the Science to Achieve Results (STAR) grant program. The information provided does 

not necessarily reflect the views of the Agency, and no official endorsement should be inferred. Mention of 

trade names or commercial products does not constitute endorsement or recommendation by EPA for use. The 

information presented in this synthesis report is intended to provide the reader with insights about the progress 

and scientific achievements of STAR research grants. The report lists the grantees whose research is discussed, 

and it also indicates where more detailed peer-reviewed scientific data can be found. This report is not sufficiently 

detailed nor is it intended to be used directly for environmental assessments or decision making. Readers with 

these interests should instead consult the peer reviewed publications produced by the STAR grants and conduct 

necessary data quality evaluations as required for their assessments.

Acknowledgement

While this document was reviewed by both external and internal EPA reviewers chosen for their contributions to 

the field of children’s environmental health, it was also reviewed by some of the principal investigators whose 

research is discussed in the report. Dr. Cynthia F. Bearer of Case Western Reserve University under contract 

to ICF International provided additional review. Rebecca Brown of EPA’s National Center for Environmental 

Assessment; Michael Firestone, Ph.D. EPA’s Office of Children’s Health Protection; Hugh Tilson, Ph.D. EPA’s 

Office of Research and Development National Program Director for Human Health reviewed the report for EPA.

This report was prepared by ICF International of Fairfax, Virginia under EPA Contract No. 68-C-03-137, Work 

Assignments 03-5 and 04-3.
i

Contents

Glossary ................................................................................................................ ii

Executive Summary .................................................................................................. 1

Introduction............................................................................................................ 2

How This Report is Organized ..................................................................................... 3

Important Findings Across Life Stages .......................................................................... 8

Prenatal: Pollutant Exposure ...................................................................................... 8

Neonatal: Genetic Vulnerability ................................................................................. 10

Infant/Crawler: Early Immune Function ........................................................................ 12

Toddler: Behaviors that Affect Pollutant Exposure ............................................................ 14

Preschooler: Neurological Disorders ............................................................................ 16

School-Age: Asthma Intervention Programs ................................................................... 18

Children’s Health and The Environment: Emerging Trends, Current Work, And Future Directions.. 22

Interpreting Human Biomonitoring Information ............................................................... 23

Community-Based Risk Approaches: Exploring Interactions between Chemical

and Nonchemical Stressors ..................................................................................... 23

Epilogue........................................................................................................... 24

Links to Additional Information ................................................................................. 25

References ........................................................................................................... 26
ii

Allergic sensitization: Process by which a subject becomes increasingly allergic to a substance through 

repeated exposure to that substance. As the allergy develops, the response becomes worse with even short 

exposures to low concentrations eliciting severe reactions.

Arsenic: Heavy metal naturally occurring in the environment in various organic and inorganic forms. Typical 

sources of exposure to arsenic are from food, drinking water, and pesticides. 

Attention Deficit Hyperactivity Disorder (ADHD): A largely neurological developmental disorder characterized by 

a persistent pattern of inattention or hyperactivity-impulsivity, or both.

Autism: A developmental disability that results from a disorder of the human central nervous system. 

It is diagnosed using specific criteria for impairments to social interaction, communication, interests, 

imagination, and activities.

Autism Spectrum Disorder (ASD): A developmental and behavioral syndrome that results from certain 

combinations of characteristically autistic traits.

Biomarker: A biological substance (blood, DNA, saliva, breast milk, hair, etc.) used to indicate exposure, or 

early biological effect to an environmental chemical, or susceptibility to disease. 

Cell proliferation: Cell growth and multiplication.

CHAMACOS: The Center for the Health Assessment of Mothers and Children of Salinas, a project of the 

University of California at Berkeley Center for Children’s Environmental Health Research.

CHARGE: Childhood Autism Risks from Genetics and the Environment, a project of the University of California 

- Davis Center for the Study of Environmental Factors in the Etiology of Autism.

Chloropyrifos: Ubiquitous organophosphate pesticide widely used before an EPA ban on household use 

in 2001. 

Community-based participatory research (CBPR): A collaborative approach to research that equitably involves 

community and academic investigators in the research process and recognizes the unique strengths that 

each brings, particularly with the goal of achieving social change, to improve health outcomes and eliminate 

health disparities.

Detoxify: Removing harmful substances from the body through metabolic pathways.

Dichlorodiphenyl dichloroethene (DDE): A metabolite of DDT.

Dichlorodiphenyl trichloroethane (DDT): A synthetic crop pesticide widely used in the 1940s and 1950s and 

banned in the 1970s due to its harmful effects on wildlife and proclivity for bioaccumulation. 

Environmental neurotoxicants: Naturally occurring (e.g., mercury) or synthetic (e.g., pesticides) chemical 

agents that act specifically on nerve cells. 

Environmental tobacco smoke (ETS): Smoke generated from the burning end of a cigarette, pipe, or cigar and 

smoke that is exhaled by smokers. 

Exposure assessment: Evaluates the magnitude, frequency, and duration of human substance exposure. 

Genotype: Internally coded, inherited information used as a blueprint to build a living organism.

Inorganic arsenic: See arsenic.

Glossary
iii

Longitudinal birth-cohort studies: Typically long-term observational studies; often following mothers during 

pregnancy and/or babies from birth through several stages of the developmental. 

Manganese: Toxic metal similar to iron occurring naturally in the environment; exposure linked to cognitive 

and motor impairments.

Metabolites: Biological by-products of metabolism. Often used as a biomarker to confirm exposure to 

environmental factors. 

Microactivities: Individual, detailed behavioral characteristics comprising part of the exposure pathway.

Neurotoxic pesticides: Pesticides formulated to alter the normal functioning of the nervous system. See also, 

Environmental neurotoxicants.

Ovalbumin (OVA): A protein commonly used in research to stimulate an allergic reaction.

Ozone: An unstable form of oxygen found naturally in the stratosphere and troposphere. At ground level it is 

considered an air pollutant having harmful effects upon the respiratory system. 

Particulate-matter (PM): The summation of airborne molecules, both solid and liquid, that remain suspended 

in air. These molecules vary in toxicity due to their size (e.g., PM10, PM2.5) and /or composition.

Pathways: Refers to the numerous channels by which one can become exposed to environmental pollutants. 

Pervasive Developmental Disorder (PDD): A group of five disorders (Autistic Disorder, Rett’s Disorder, Childhood 

Disintegrative Disorder, Asperger’s Syndrome, and Pervasive Developmental Disorder Not Otherwise 

Specified) characterized by delays in development.

Pesticide drift: Term used to define the airborne release and distribution of pesticides/insecticides. 

Polybrominated diphenyl ethers (PBDEs): A bioaccumulating flame retardant substance found in many 

household products (e.g., electronics, furniture). 

Polychlorinated biphenyls (PCBs): An array of synthetic organic pollutants produced primarily for industrial 

processes in the 1950-60s and widely released into the environment. PCBs were banned in the US in 1977.

Polycyclic aromatic hydrocarbons (PAH): A carcinogenic organic molecule produced from the burning of 

organic substances such as coal, garbage, oil, and cigarettes. 

Respiratory syncytial virus (RSV): Virus causing respiratory tract infections, most commonly in infants 

and children. 

Spray Drift: See pesticide drift.

T-helper cell (Th1, Th2): A type of T cell that provides help to other cells in the immune response by 

recognizing foreign antigens and secreting substances called cytokines that activate T and B cells. 

Wheezing: Making a coarse whistling sound due to narrowed or obstructed air passages; symptomatic of 

asthma and/or reduced lung function.
EPA/National Institute of Environmental Health Sciences (NIEHS) 

Centers for Children’s Environmental Health and Disease Prevention Research Locations
1

Executive Summary

In 1997, Federal Executive Order 13045, Protection of Children from Environmental Health Risks and Safety Risks, 

mandated Federal agencies to place a high priority on identifying and assessing risks affecting children and to ensure 

their policies, standards, and programs address disproportionate risks to children. The Executive Order stimulated 

a wide array of research supported by the U.S. Environmental Protection Agency (EPA), particularly through the 

National Center of Environmental Research’s (NCER) extramural Science to Achieve Results (STAR) grant program. 

In 1998, the STAR grant program, which supports human health, ecology, economics and engineering sciences through 

grants, centers, and fellowships, initiated a diverse portfolio focused specifically on children’s environmental health 

research. The goal of this research is to better understand children’s genetic, life stage, and behavioral susceptibilities. 

The research also aims to better characterize child-specific harmful chemical exposures and to demonstrate cost effective, 

protective interventions, particularly at the household and community level. Since 1998, the STAR grant program has 

issued more than 10 research solicitations and awarded over 60 grants focusing on children’s environmental health, 

including: Centers for Children’s Environmental Health and Disease Prevention Research (21 Children’s Centers 

awards—11 currently active); Aggregate Exposure Assessment of Pesticide Exposure (3 grants); Biomarkers for 

Children’s Risks (8 grants); Children’s Vulnerability to Toxics (19 grants); Children’s Valuation (7 grants); and Early 

Indicators of Environmentally Related Disease (5 grants). To date, NCER has funded more than a hundred individual 

projects resulting in more than a thousand peer-reviewed articles in a wide array of scientific publications.

Since the passage of the Executive Order 10 years ago, this research has increased scientific knowledge of many 

aspects of children’s environmental health. For example, studies have shed light on how environmental exposures 

change across life stages from newborn to school-age children and some of the genetic factors that contribute to 

children’s vulnerability. Research has also provided insight on how to appropriately assess aggregate and cumulative 

exposures, suggested what biological markers in children’s urine or blood tell us about exposure or effects, and 

indicated what steps need to be taken in order to prevent harmful exposures, including which interventions are effective 

and sustainable. This is particularly the case for residential pesticide exposure, which was an articulated focus of the 

STAR grant program during the past 10 years. Some of the major research findings include the following:

•	 People metabolize pesticides differently based on their genotype; some faster, others slower. This finding is of

particular concern during pregnancy, as many babies do not develop the ability to metabolize some pesticides 

during the first two years of life, putting them at greater risks of health effects.

•	 Children living close to major roadways in Southern California have a higher risk of asthma.

•	 EPA’s ban on two household pesticides (diazinon and chlorpyrifos) resulted in a rapid decrease in exposures in

New York City. Children born after the ban were also healthier.

•	 Integrated Pest Management (IPM) can be effectively implemented in urban areas to reduce both pesticide and

allergen triggers.

•	 Community partners play a critical role in informing, implementing, and translating children’s environmental

health research.

While much has been discovered in the last 10 years, there is still much to learn about children’s environmental 

health. Building on the many lessons learned in characterizing pesticide exposures during early development and in 

investigating the multiple impacts of indoor and outdoor air pollution on childhood asthma, NCER is now broadening 

its focus. Recently, the STAR grant program has increased its support for research on less characterized, though 

increasingly common, chemicals (for example, plasticizers and flame retardants) and chronic childhood ailments 

(for example, autism and other developmental disabilities). The STAR grant program will continue to work closely 

with Federal, state, and community partners to disseminate these and many other findings in order to create healthier 

environments and nurture healthier children. The STAR grant program also anticipates continuing, even broadening, 

Federal partnerships for future research efforts that build upon the progress that has already been made. For more 

information about NCER and the STAR grant program, please visit http://www.epa.gov/ncer. For more information 

on the Children’s Centers, please visit http://www.epa.gov/ncer/childrenscenters.
2

Introduction

Scientists are finding increasing evidence that 

exposure to some environmental factors jeopardizes 

children’s health and may relate to large increases 

in the number of children diagnosed with asthma, 

Attention Deficit/Hyperactivity Disorder (ADHD), 

autism, and developmental impairment. Evidence 

is also strong that environmental health risks 

disproportionately affect children. Their nervous, 

immune, digestive, and other bodily systems are still 

developing while they receive disproportionately 

greater exposure to pollutants. They eat more food, 

drink more fluids, and breathe more air in relation to 

their body weight than adults do. 

To address the increasingly evident disproportionate 

environmental health risks for children, President 

Bill Clinton signed Federal Executive Order 

13045, Protection of Children from Environmental 

Health Risks and Safety Risks, on April 21, 1997 

(62 FR 19883). This Order mandated Federal 

agencies to place a high priority on identifying and 

assessing risks affecting children and to ensure their 

policies, programs, activities, and standards address 

disproportionate risks to children.

In response, EPA’s NCER started a research program 

focusing on children’s environmental health issues 

through its STAR grant program. In the 10 years 

since the Executive Order was signed, NCER has 

developed a research portfolio of more than a 

hundred individual projects the results of which have 

appeared in more than a thousand peer-reviewed 

publications. Policymakers at state and local levels 

have used STAR grant research results to frame 

legislation and regulations. These results also 

have contributed to various approaches used to 

assess risk, and they have provided guidance to 

the public in creating safer, healthier environments 

(CHPAC-BOSC Workgroup 2007). 

In addition, NCER and NIEHS have established the 

Centers for Children’s Environmental Health and 

Disease Prevention Research (“Children’s Centers”). 

This multidisciplinary research effort applies 

community-based, participatory research (CBPR) 

and innovative techniques in the investigation of 

environmental stressors on widespread childhood 

disorders such as asthma, autism, and learning 

disabilities. This research is also seeking effective 

strategies to reduce children’s exposure to these 

environmental stressors. 

The first eight Children’s Centers, established in 1998, 

set out to study the effects of environmental factors 

such as pesticides and air pollution on childhood 

asthma and children’s growth and development. In 

2001, four more Children’s Centers opened to study 

the basis of neurodevelopmental and behavioral 

disorders such as autism. Additional Children’s 

Centers began investigations in 2004 and 2007 

on how exposure to mixtures of chemicals affects 

children’s health and which environmental pollutants 

cause disparities in birth outcomes. Since 1998, EPA 

has awarded 21 Children’s Center grants that have 

fostered a collaborative network of pediatricians, basic 

scientists, epidemiologists, and community advocates 

across the United States, seeking to improve the health 

and environments of children. 

This report highlights some important research 

findings from the STAR research grants, including 

the Children’s Centers during the past 10 years. It also 

describes how this scientific research is developing 

ways to improve the health of our nation’s children. 
3

How This Report is Organized

To assist implementation of the 1997 Executive Order, 

the EPA Risk Assessment Forum drafted a document, 

Guidance on Selecting Age Groups for Monitoring 

and Assessing Childhood Exposures to Environmental 

Contaminants (Age Grouping Guidance) (EPA 2005) 

to complement existing EPA guidance and experience 

aimed at improving the accuracy and consistency of 

children’s exposure assessments. The Age Grouping 

Guidance describes logical children’s age groupings 

for more uniform monitoring studies and exposure 

assessments. The document divides age groups 

according to specific developmental stages (table 1).

Table 1. Recommended Childhood Age Groups for 

Agency Exposure Assessments (EPA 2005)

Age Groups 1 Year Age Groups 1 Year

Birth to < 1 month 1 to < 2 years

1 to < 3 months 2 to < 3 years

3 to < 6 months 3 to < 6 years

6 to < 12 months 6 to < 11 years

11 to < 16 years

16 to < 21 years

This summary report uses age groups similar to those 

used in the Age Grouping Guidance to illustrate 

children’s vulnerabilities at different developmental 

stages and the disproportionate effects of some 

environmental exposures for children of certain age 

groups (table 2). This report combines several age 

groups based on similarities of their exposure characteristics. Additionally, it highlights information from 

the prenatal lifestage, which is not listed in EPA’s Age 

Grouping Guidance, yet it does not include the 

adolescent life stage (11 to <21 years) because NCER 

has yet to fund studies of this age group. Investigators 

in the Children’s Centers are following children from 

birth throughout the various stages of development in 

several long-term, longitudinal birth-cohort studies.

“At EPA, we are committed to protecting 

human health and the environment 

for all our residents, including our 

most vulnerable citizens. By promoting 

children’s health research, we are 

working to provide a healthier start for 

every child born in America.”

— Stephen L. Johnson, EPA 

Administrator

Highlights of NCER-supported findings in basic 

science, exposure assessment, epidemiology, and 

intervention for each of the life stages are featured at 

the end of this section (table 3). The chapters that 

follow report six case studies illustrating that 

childhood is a significantly vulnerable period for 

exposure to environmental factors and that health 

outcomes can vary with a child’s age at exposure. 

Although the research studies often span multiple life 

stages, each case study focuses on susceptibility, 

health outcomes, or interventions at one of the six life 

stages. Case studies discuss research findings and their 

implications for public policy in the following 

key issues: 

•	 Fetal vulnerability, growth, and development

related to prenatal pollutant exposure

•	 Genetic differences in newborns that may

contribute to susceptibility

•	 Immune development, allergic sensitization, and

allergic and chemical response during the infant 

and crawler life stage

•	 The effect a toddler’s behavior has on exposure

to pollutants

•	 Autism, autism spectrum disorder (ASD), and

ADHD as health outcomes of pollutant exposure

•	 The effectiveness of various asthma intervention

programs

References to published results in the scientific literature 

are provided throughout the report and in the References 

section. In instances where research results have not 

yet been published, EPA grant numbers (e.g., R831710) 

have been provided. Full information on these grants 

may be found by visiting http://www.epa.gov/ncer and 

performing a search on the relevant grant number.
4

Table 2. Definition of Life Stages and Examples of Exposure Characteristics (EPA 2005)

Life Stage Age 

Group

Characteristics 

Relevant to 

Oral and Dermal Exposure

Characteristics 

Relevant to 

Inhalation 

Exposure

Anatomy and Physiology Characteristics

Prenatala

Before 

Birth

Neonatal

Birth to < 

3 months

•	Breast and

bottle feeding

•	Hand-tomouth activity

•	Time spent

sleeping 

•	Time spent

sedentary

•	Rapid growth and weight gain

•	Increased proportion of body fat

•	Increased skin permeability

•	Deficiencies in liver enzyme activity (affecting ability to breakdown chemicals)

•	Immature immune system functions

•	High oxygen requirements (increased

inhalation rates)

•	More alkaline stomach fluids (affecting

function and digestion)

•	Increased extracellular fluid

•	Less kidney function than predicted by

surface area

Infant/Crawler

3 to < 6 

months

•	Introduction

of solid food

•	Increased

contact with 

surfaces

•	Increased

object and 

hand-tomouth activity

•	Breathing

zone close to 

the floor

•	Rapid growth and weight gain

•	Increased proportion of body fat

•	Deficiencies in liver enzyme activity

•	Immature immune system functions

•	Increased extracellular fluid

•	Kidney function less than predicted by

surface area

6 to < 12 

months

•	Expanded

food 

consumption

•	Increased

floor mobility (surface 

contact)

•	Increased

likelihood to 

put nonfood 

items in 

mouth

•	Development

of personal 

dust clouds

•	Rapid growth and weight gain

•	Increased body fat begins to level off

•	Deficiencies in liver enzyme activity (affecting ability to breakdown chemicals)

•	Immature immune system functions

•	Rapid decrease in extracellular fluid

•	Kidney function more predictable by

surface area
5

Life Stage Age 

Group

Characteristics 

Relevant to 

Oral and Dermal Exposure

Characteristics 

Relevant to 

Inhalation 

Exposure

Anatomy and Physiology Characteristics

Toddler

12 to 

< 24 

months

•	Consumption

of full range 

of foods

•	Participation

in increased 

play activity

•	Demonstration

of curiosity 

accompanied 

with poor 

judgment

•	Cessation of

breast and 

bottle feeding

•	Walking

upright, 

running, and 

climbing

•	Occupy wider

variety of 

breathing 

zones

•	Engage in

more vigorous 

activities

1 to < 3 yearsb

: 

•	Some liver enzyme activities peak, then

fall back to adult range

•	Most immune system functions mature

•	Extracellular fluid more consistently

related to body size

Preschooler

2 to < 6 

years

•	Onset of

wearing 

adult-style 

clothing 

•	Decreased

hand-tomouth 

activities 

•	Increased

time outdoors

3 to < 8/9 yearsb

: 

•	Relatively stable weight gain and

skeletal growth (as opposed to a period 

marked by growth spurts)

School-Age

6 to < 11 

years

•	Decreased

oral contact 

with hands 

and objects

•	Decreased

dermal 

contact with 

surfaces

•	Time spent

in school 

environments

•	Participation

in sports 

activities 

8/9 to < 16/18 yearsb

: 

•	Rapid skeletal growth

•	Rapid reproductive and endocrine

system changes, including puberty

a

 This life stage was not addressed in EPA’s Age Grouping Guidance.

b

 The age categorization of anatomy and physiology characteristics differs slightly from the age categorization for 

behavioral development. 
6

Table 3. Summary of Relevant Research Findings Across Life Stages 

Prenatal Neonatal: Birth to <3 months Infant/Crawler

•	Babies exposed before birth to

higher levels of organophosphate (OP) insecticides have a

shorter gestation period, smaller

birth weight, shorter length, and

decreased head circumference,

and show delay in neurodevelopment up to age 3 (R827039C004,

R831710C001). For example,

babies exposed prenatally to chlorpyrifos and diazinon weighed

less at birth by an average of 6.6

ounces, which is equivalent to that

seen in babies born to women

who smoked during pregnancy

(R827027C003).

•	Approximately 40 percent of

babies exposed before their birth

to a mixture of polycyclic aromatic hydrocarbons (PAHs) primarily from traffic sources and environmental tobacco smoke (ETS)

have genetic damage that can be

linked with increased cancer risk

(R827027C003).

•	Increases in maternal levels of

dichlorodiphenyl trichloroethane

(DDT), a pesticide, during pregnancy decrease scores on the

Mental Development Index at 2

years of age. Each 10-fold increase

in DDT level is associated with a 2-

to 3-point decrease in mental development (R831710C001).

•	Prenatal exposure to lead or

tobacco smoke has been implicated

as a precursor of Attention Deficit/

Hyperactivity Disorder (ADHD) in

children, possibly accounting for

as many as one in three cases of

ADHD in children (R829389).

•	Maternal levels of ortho-substituted

polychlorinated biphenyls (PCBs),

one form of the class of compounds

that compose PCBs, are associated

with reduced weight gain up to 17

years of age in girls but not boys,

suggesting that prenatal exposure

to PCBs may affect female growth

(R831711).

•	Human respiratory syncytial virus

(RSV) infection in the first year of

life increases the risk of asthmatic

symptoms later in life. RSV affects

the receptors in the airway that

interact with environmental agents,

which may explain why children

with RSV-induced asthma are especially sensitive to their environment

(R826711003).

•	Very low expression of the paraoxonase1 (PON1) enzyme, an enzyme

that facilitates the breakdown of

pesticides into a less toxic form,

is a major predictor of young children’s susceptibility to the toxic

effects of some OP insecticides

(R831709). For example, decreases

in the PON1 gene cause some newborns to be 26 to 50 times more

susceptible to adverse health outcomes from exposure to certain

OP pesticides than other newborns

(R831710C003).

•	Rat pups exposed to PCBs at the

same level as babies breast-fed by

mothers who live in high-PCB environments have developmental and

auditory abnormalities, specifically,

the ability for the brain to interpret

auditory cues (R829388C005).

•	Children in farmworker families

may be particularly vulnerable to

pesticides because they often are

exposed to these chemicals from

multiple pathways such as pesticide

drift from agricultural fields, takehome exposure from their parents,

and breast milk from mothers who

work or have worked in the fields

(Bradman et al. 2007; R831710).

•	Children living within 75 meters of

a major roadway have an increased

risk of developing asthma. This

effect was stronger in girls and in

children without a family history of

asthma (R831861).

•	Early life exposures to traffic-related

pollutants in urban environments

appear to affect the immune system

by increasing allergic responses,

which can lead to respiratory symptoms in children as young as 2

years of age (Al-alem et al. 2006;

R827027).

•	Developmental exposure to noncoplanar PCBs, one of the many

forms of compounds that compose

the class of PCBs, increases the

chance of a seizure. PCB exposure

for autistic children is particularly

dangerous because these children

have a particularly high rate (about

30 percent) of seizure disorders

(R829388).

•	Placental tissues with higher

concentrations of dichlorodiphenyl

dichloroethene (DDE), a pesticide

breakdown product, showed a

correlation with increased levels of

type 2 T-helper cells (Th2) cytokines

(R830825). Elevated levels of these

cells in very young children are a

possible indicator for the development of asthma and other immune

system disorders.
7

Toddler: 1 to <2 years Preschooler: 2 to <6 years School-Age: 6 to <11 years

•	About 30 percent of children with

Autistic Spectrum Disorder (ASD)

exhibit loss of neurological and

behavioral function during their first

few years of life (12 to 30 months

of age). This loss coincides with

the onset of children’s physical

capacity to explore their environment, and, combined with repetitive behavior typical of ASD, it

increases their exposure to environmental neurotoxicants. Autistic children also appear to have a different

genetic or biochemical susceptibility

(R829391).

•	Toddlers in farmworker communities accumulate more pesticides

on their clothing (socks and union

suits) compared with younger,

crawling children. In addition, toddlers show higher urinary metabolite

levels than infants (R826709C003).

•	Pesticide levels on children’s

hands are associated with pesticide metabolite levels in their urine,

which means that their frequent

hand-to-mouth behavior may cause

them to ingest chemicals that they

come in contact with (R827440).

•	Exposure to lead during early childhood increases the risk of illegal

behavior as an adult. There is a

relationship between neuropsychological functioning in adolescence

and police contacts in early adulthood, indicating a link between

early lead exposure and adult antisocial activities (R829389C004).

•	Children with iron deficiency

retain more lead in their bodies.

Childhood iron deficiency modifies

behavior such as increasing pica

(the desire to eat substances not

normally eaten) and hand-to-mouth

activity. These modified behaviors

can increase children’s exposure

to environmental lead. Correlation

between iron deficiency and blood

lead levels is strongest among children aged 1 to 2 years (Bradman et

al. 2001; R826709C003).

•	Mouse allergen exposure and

asthma-related outcomes have

a strong and consistent relationship. Children with high exposure to mouse allergens have more

asthma-related unscheduled doctor

visits, emergency department visits,

and hospitalization than unexposed

children (R832139C001).

•	Elevated indoor particulate matter

(PM) levels are associated with

increased respiratory symptoms in preschool-aged children

(R832139C001).

•	Children with organic diets show

lower median OP metabolite levels

in their urine than children with

conventional diets (Curl et al. 2003;

R825171).

•	Boys who spend the greatest

amount of time playing outdoors

have the highest pesticide exposure levels of any childhood group.

Similarly, children who play extensively in laundry rooms and entryways exhibit higher rates of pesticide metabolites in urine than those

who do not play, or play less, in

these areas. Additionally, frequent

hand washing does little to reduce

children’s pesticide exposures in

households where chemical contamination is readily accessible

(R827443).

•	Floor dust appears to be the major

source of exposure to OPs for young

children (accounting for 68.8 percent), followed by solid food (18.8

percent) and beverages (10.4 percent). Air and water contribute less

than 2 percent to the total aggregate exposure (R825169).

•	Autistic children showed higher

levels of leptin (a hormone that

affects the regulation of body

weight, metabolism, and reproductive function, and influences

the immune system) in their blood

when compared to typically developing children (Ashwood et al.

2007; R829388C002).

•	An increased risk of respiratoryrelated school absences occurs in

asthmatic and nonasthmatic children exposed to ETS (Gilliland et al.

2003; R831861).

•	Placing air cleaners containing high-efficiency particulate air

(HEPA) filters in inner-city asthmatic

children’s bedrooms can achieve

a substantial, sustained improvement in indoor PM levels, one major

cause of respiratory problems in

children (Eggleston et al. 2005;

R832139C002).

•	Rural lifestyles may not protect children against developing asthma.

Prevalence of asthma in rural areas

is comparable to prevalence in large

Midwestern cities (R826711C001).

•	High levels of PM and ozone are

associated with worsening pulmonary function and increased asthmatic symptoms among children from Detroit, Michigan, who

have moderate to severe asthma

(R826710C002).

•	Disadvantaged asthmatic children in urban areas appear to be

at increased risk for higher residential allergen levels, elevated air-pollution exposure, and higher levels

of asthma triggers in the home

(Breysse et al. 2005; R832139).

•	Children exposed to manganese and arsenic in the environment score lower on general intelligence tests and tests for memory

(Wright et al. 2006; R831725).

References to published results in the scientific literature are provided throughout the report and in the References section. In 

instances where research results have not yet been published, EPA grant numbers (e.g., R831710) are provided. Full information on these grants may be found by visiting http://www.epa.gov/ncer and performing a search on the relevant grant number.
8

Important Findings Across Life Stages

The six case studies in this section of the report 

highlight NCER-supported findings for each of the six 

life stages (table 2).

Prenatal: Pollutant Exposure

Every day, people are exposed to many different 

environmental pollutants ranging from pesticides used 

to control cockroaches in the home to particulate 

matter (PM) generated from combustion engines in

vehicles. Pesticides in particular are a major problem. 

Large quantities are applied in urban communities to 

control vermin, especially in some low-income areas. 

For example, the amount of one common insecticide, 

chlorpyrifos, applied in one urban borough of 

Manhattan in 1997 exceeded the total amount of all

pesticides applied in any other single county in all of 

New York, including in upstate agricultural regions 

(Landrigan et al. 1999). Exposure to pesticides is of 

special concern for certain sensitive groups such as 

pregnant women, infants, and children.

Prenatal and early postnatal periods are critical 

life stages, and they require careful assessment for 

pesticide exposure. In early life, the nervous system is 

still developing, and it is more susceptible to effects 

from exposure to neurotoxic pesticides. STAR research 

results have significantly increased knowledge 

of prenatal pollutant exposure. For example, one 

significant finding is that exposure to certain 

pesticides can have adverse effects on birth size and 

neurodevelopment (Bradman and Whyatt 2005). 

What contributes to fetal vulnerability?

Many physiological characteristics of a growing fetus

make it more likely to suffer a health effect from 

exposure to environmental pollutants. Some metabolic 

activities such as clearance by the kidneys and enzyme 

activity in the liver are immature, and these activities 

often are easily disrupted during development because 

they are highly variable throughout gestation and 

following birth (Landrigan et al. 1999, Corrion et al. 

2005). Greater absorption or retention rates of toxic 

substances, a reduced ability to detoxify chemicals 

and repair damage to DNA, and a higher rate of 

cell proliferation are other factors that contribute to 

a fetus’s susceptibility to health risks (Perera et al. 

2005). STAR research results have demonstrated some 

of the effects of fetal vulnerability. For example, in 

one study of a group of minority women and their 

infants, scientists measured women’s exposure to 

Pounds by county

1,300,000–2,587,057 lbs.

500,000–1,300,000 lbs.

120,000–500,000 lbs.

2,155–120,000 lbs.

Total pounds of pesticide products 

applied by commercial applicators 

and sold to farmers in 1997 

in New York State, by county

Source: Adapted from Landrigan et al. 1999
9

several pollutants including airborne polyaromatic 

hydrocarbons (PAHs) (which were monitored during 

pregnancy) and chlorpyrifos (which was measured 

from the mother and infant at birth). The results 

show that exposure to PAHs and pesticides during 

pregnancy impairs fetal growth and development 

(Perera et al. 2003). The study results also show that 

the developing fetus may be 10 times more susceptible 

to DNA damage from before-birth exposure to PAHs 

than the mother is (Perera et al. 2004, 2005). 

Another study has shown the effect on an infant’s 

growth from exposure before birth to certain 

pesticides. This study enrolled pregnant women at 

prenatal clinics in January 1998 and followed them 

until January 2004, capturing data from a critical 

period when EPA began to phase out residential use 

of chlopyrifos in 2001. This study included women 

exposed to higher levels of pesticides during the 

phase-out period as well as women exposed after 

the phase-out period. Infants exposed prenatally to 

pesticides before the EPA phase-out of chlorpyrifos 

showed significantly reduced birth weight and shorter 

length (Whyatt et al 2004, 2005). Other studies 

showed that infants were born with low activity levels 

of an enzyme, paraoxonase 1 (PON1), which affects 

the metabolism and detoxification of pesticides 

(Furlong et al. 2006). Infants with prenatal pesticide 

exposure and low PON1 enzyme levels had smaller 

head circumferences (Berkowitz et al. 2004, Wolff et 

al. 2007).

These results cause concern because outcomes such as 

a smaller head circumference correlate with reduced 

intelligence quotient levels and decreased cognitive 

function in later years. Study results indicate early-life 

exposures are more likely to lead to adverse health 

outcomes than similar exposures encountered later 

in life. Even more troubling are results that show the 

deficits sustained in early life may persist throughout 

life (Landrigan et al. 1999). For example, one study 

showed that prenatal PAH exposure led to cognitive 

development issues later in life, including higher risk 

for performance deficits in language, reading, and 

math in early school years (Perera et al. 2006).

How do we measure exposures relevant to fetal 

growth and development?

Measuring exposure to environmental pollutants is

difficult for a number of reasons. Exposure can vary 

widely across age groups depending on factors such 

as the amount and type of chemical used and daily 

patterns of life. Exposure can be of different durations 

and magnitudes such as short-term, high-level 

pesticide applications versus long-term, low-level 

pesticide applications. Some pollutants do not persist 

in the body for a long time, making them hard to 

measure without frequent sampling (Bradman and 

Whyatt 2005, Fenske et al. 2005). Because prenatal 

development is so critical, it is particularly important 

to assess maternal exposure to environmental 

chemicals during pregnancy to make subsequent 

associations with infant health (Fenske et al. 2005).

In general, maternal and infant exposures typically 

are measured using one or more of the currently 

available techniques; scientists take the advantages 

and limitations of each method into account 

when designing a research study. The techniques 

currently used include (Bradman and Whyatt 2005, 

Fenske et al. 2005): 

•	 Biological monitoring—Uses biomarkers 

(biological substances (blood, DNA, saliva, 

breast milk, urine, hair, etc.) to indicate exposure, 

or early biological effect to an environmental 

chemical, or susceptibility to disease) to provide a 

direct measure of the concentration of a pollutant 

in the body at a given time. 

•	 Environmental monitoring—Uses environmental 

samples such as air, dust, diet, and drinking 

water to characterize residential contamination 

and provide a measure of potential exposure 

to the pollutant.
10

•	 Survey questionnaire—Uses participant 

surveys to collect general information on a 

person’s habits and use of chemicals (typically 

conducted as a supplement to biological and 

environmental monitoring).

•	 Ecological methods—Uses geographic 

information systems and other techniques to 

help map the relative locations of populations 

potentially exposed to pollutant sources.

While biological monitoring appears to be one of 

the best ways to assess exposure, all biomarkers 

have limitations, and certain methods may not truly 

represent the full extent of exposure. For example, 

pollutants measured in blood represent only a 

snapshot of exposure because the body constantly 

metabolizes, redistributes, and eliminates chemicals 

(Ostrea et al. 2002). Additionally, drawing blood is 

invasive, especially when children are involved. Some 

scientists (Corrion et al. 2005) are looking for more 

innovative techniques that address this problem, such 

as sampling maternal and umbilical cord whole blood 

rather than blood serum (because pesticides are more 

likely to concentrate in red blood cells). One reason 

blood sampling is attractive for biological monitoring 

is because, unlike urine, blood is highly regulated, 

and factors such as water intake are less likely to 

alter concentrations.

Other studies indicate that meconium, the first set of 

stools of a newborn, is a useful biomarker of prenatal 

exposure to pollutants such as pesticides. Meconium is

a direct measure of exposure before birth (Ostrea et al. 

2006, Whyatt and Barr 2001, Bearer et al. 2005), and 

the main advantage over other biological measures is 

that it has a wide window of exposure time. Meconium

starts forming at the beginning of the second trimester 

and is not excreted until after birth. Although 

it provides a cumulative prenatal measurement, 

meconium is more difficult to analyze when compared 

with blood or urine (Ostrea et al. 2006). 

Neonatal: Genetic Vulnerability

Like the developing fetus, neonates (birth to <3 

months) are more susceptible to health effects from 

pollutant exposure than adults because they are still 

developing. Additionally, genetic differences can 

increase their vulnerability to pollutants such as 

pesticides, secondhand smoke, and air toxics. Genetic 

differences may occur either as a difference in a gene 

itself or in how the information from a gene is 

processed. Genetic differences can significantly affect 

metabolism and cause increased susceptibility for 

children at all life stages, but the neonatal period is 

unique in that newborns display some genetic 

characteristics that are different from those observed 

for adults or even older children. 

An important example of a genetic difference in 

neonates involves an enzyme that plays a key role in 

protecting humans against toxic effects of pesticides. 

Enzymes are proteins that help to accelerate chemical 

reactions in the body, and in this case, the enzyme 

PON1 facilitates the breakdown of pesticides into a 

less toxic form. For several decades, scientists have 

shown that high levels of PON1 are protective against 

nervous system effects associated with exposure 

to pesticides during development. More recently,

researchers have demonstrated that having low levels 

of PON1 results in greater sensitivity to these harmful 

effects. By knocking out the PON1 gene in neonatal 

mice—an animal model often used as a substitute 

for humans—researchers demonstrated an increase 

in sensitivity to certain insecticide exposures when 

compared with mice that still had the PON1 gene 

(Furlong et al. 2005). 

In several Children’s Center projects, researchers have 

shown that the enzyme PON1 is typically not fully 

functional until after birth. Even after birth, newborns 

and infants have very low levels of this enzyme. The 

results of a review of active PON1 levels in humans 

show that the enzyme levels increase from birth 

through infancy (Costa et al. 2003). PON1 levels reach 

a plateau at different ages in individuals anywhere 

from 15 to 25 months, depending on factors such as 

the individual’s genetic background. Before the levels 

plateau, an infant is much more vulnerable to health 

effects resulting from exposure to pesticides.
11

“People have this remarkable difference 

in enzymes that defend their health 

from pesticide exposure. In developing 

regulatory standards for safe levels of 

exposure, we need to protect the most 

sensitive in a population, particularly 

because children and unborn fetuses 

are involved.”

— Dr. Nina Holland, 

UC Berkeley

Researchers observed variability not only in reaching 

the plateau, but also in the range of PON1 levels 

among newborns when compared with their mothers. 

Levels of this critical enzyme varied by 26-fold in 

newborns compared with only 14-fold among mothers 

(Furlong et al. 2006). Even considering the variability 

among individuals, average PON1 levels in children 

were four times lower than the PON1 levels in the 

mothers, demonstrating that infants clearly are a more 

vulnerable population in their ability to detoxify 

certain commonly used insecticides (Chen et al. 2003, 

Furlong et al. 2006). Researchers confirmed the 

observation that PON1 levels are lower in children, 

and that the differences between adults and children 

vary by ethnicity: The average PON1 level in adults 

compared with newborns was 2.6 times higher for 

African Americans, 3.6 times greater in the Caribbean 

Hispanic population, and 4.6 times greater for 

Caucasians (Chen et al. 2003). 

In addition to studies that focus on pesticides, some 

STAR research studies focus on early exposure to 

environmental tobacco smoke (ETS), air toxics, and 

other pollutants encountered in the neonatal period. 

For example, scientists investigated long-term genetic 

effects of prenatal exposure to ETS through maternal 

smoking and early life exposures (Gilliland et al. 2001, 

2002a, 2002b). The researchers found a candidate 

gene that reduces the effects of the exposure to ETS by 

detoxifying some of the harmful chemicals associated 

with smoking. Because tobacco-related toxins are 

more harmful to a developing fetus or infant than 

to the mother, the presence of this candidate gene, 

glutathione S transferase M1 (GSTM1), may be

especially important during the early life stages. More

specifically, the adverse effects of prenatal exposure 

to maternal smoking (e.g., asthma, wheezing) were 

predominantly observed in children with a variation of 

GSTM1, the null genotype, which lacks the enzyme

that helps to detoxify the pollutants associated with 

ETS (Gilliland et al. 2002a). Damage during fetal 

development in particular can permanently alter the 

structure or function of the lungs, and thus can lead 

to postnatal vulnerabilities (Gilliland et al. 2003). In 

addition, large deficits in lung function are found in 

school-aged children with both early-onset asthma and 

before-birth exposure to maternal smoking regardless 

of whether the child had ETS exposure later in life 

(Gilliland et al. 2001, Gilliland et al. 2003, Li et al. 

2005). These results further emphasize the importance 

of early exposure and confirm that exposure before 

birth to maternal smoking is a critical risk factor for 

childhood asthma.

Strikingly, environmental exposures also may change 

genetic susceptibility. Results from STAR research 

show a new association between smoking during 

pregnancy and a child’s risk of asthma that extends 

beyond one generation (Li et al. 2005). These 

groundbreaking results show an increased risk of 

asthma across multiple generations, meaning that 

if a woman smokes during pregnancy, her child’s 

risk of developing asthma increases, and even if that 

child doesn’t become a smoker in adulthood, the 

next generation (grandchildren) will still have an 

increased risk. Potentially, this could occur through 

epigenetic mechanisms (interactions between genes 

and the environment that produce differences between 

cells during development before birth, but that do 

not involve changes to the underlying DNA). The 

researchers suggest that tobacco products may affect 

both immune function and pollutant detoxification 

mechanisms in the offspring by altering DNA patterns 

in the fetal cells (Li et al. 2005). This alteration would 

result in an increased genetic susceptibility to asthma 

affecting one generation to the next.

PON1 Enzyme Activity

Average PON1 activity for all genotypes and race/ethnicities 

for mothers and neonates.

Source: Chen et al. 2003 (Tables 2 and 3); median of all values plotted; error bars 

represent the range in the means for the various genotypes.

0

40

80

120

160

Maternal Neonate
12

Infant/Crawler: Early Immune Function

Allergic sensitization and responses to allergies and 

chemicals have become the focus of much STAR grant 

research, especially for infants/crawlers (3 to <12 

months old) whose immune systems are still in the 

early stages of development. One reason for this focus 

is because asthma is the most common chronic disease 

among children. Asthma is an immune system disorder 

manifested when the airways in the lungs strongly 

react to various factors, such as stress, allergens, 

temperature, exercise, and air pollutants in the air that 

generally pose no risk to individuals with healthy 

immune systems. In individuals susceptible to asthma, 

reaction to these factors can cause the airways to 

become irritated and inflamed, and may evoke 

symptoms such as wheezing, coughing, chest 

tightness, and difficulty breathing. Although a large 

body of evidence has linked life style and 

environmental exposures to asthma, the timing of such 

environmental exposures during early development 

also may be critical to how children become 

susceptible to allergens that previously had no effect 

(that is, allergic sensitization), as well as the later 

development of asthma. 

One way scientists are exploring the relationship 

between asthma and age is to measure biomarkers that 

indicate this immune system disorder. Researchers 

compared levels of type 1 and type 2 T-helper cells 

(Th1 and Th2) in infants to observe relationships 

caused by exposure to pesticides, natural toxins, 

and allergens and compared the data to the resulting 

incidence of asthma (Duramad et al. 2006). The 

selected infants were subjects of the Center for 

Health Assessment of Mothers and Children of

Salinas (CHAMACOS) birth-cohort study. The study

comprises infants of farm workers in rural areas. 

Infants in this study population may have experienced 

greater exposure to pesticides because of their 

proximity to fields and contact with pesticide residues 

brought home by their parents. Researchers took 

blood samples from the infants at 12 and 24 months 

to measure the amount of Th1 and Th2 cells. The 

results indicated that infants who live with agricultural 

workers and whose mothers work in the field had 

higher levels of Th2 cells than infants who did not 

meet these criteria. These are important findings 

because 2-year-old children diagnosed with asthma 

and wheezing exhibit a significant increase in Th2 

levels, which means that elevated levels of these cells 

in very young children can perhaps indicate the onset 

of respiratory or other immune system disorders. 

Using Biomarkers to Discover 

Asthma in Children

Biomonitoring is the measurement of a 

substance—or its breakdown product, 

known as a metabolite—in biological 

samples such as blood or urine. 

Researchers measure biomarkers and 

then use the data to assess the presence 

of a pollutant such as a pesticide or a 

condition such as asthma. Because the 

balance between Th1 and Th2 cells is 

important in the development of asthma, 

scientists have examined the levels 

of these cells in blood as a possible 

indicator of asthma in children. These 

cells are part of the immune system 

and belong to a group of cells essential 

to controlling viruses and bacteria. Th1 

cells tend to provide general protective 

immunity; Th2 cells may play an 

important role in the functional changes 

of allergic diseases, including asthma. 

Animal studies also have concentrated on the 

importance of age and early immune system 

development, allergic sensitization, and allergic and 

chemical response. One such study focused on the 
13

relationship between age and the onset of allergies in 

mice (Rumold et al. 2001). Investigators for this study 

examined the effect of age on the response to 

environmental ETS and its possible role in 

sensitization to normally harmless substances. 

Studying how ETS affects infants and crawlers is very 

important because secondhand smoke exposure causes 

numerous problems in children, such as slower lung 

growth, acute respiratory infections, ear problems, and 

more frequent and severe asthma attacks. In the study, 

young mice aged 2 to 3 weeks and adult mice aged 6 

to 8 weeks received exposure to (1) ETS, (2) a protein 

called ovalbumin (OVA) that stimulates an immune 

response but that is typically harmless, or (3) both ETS 

and OVA. Investigators measured the animal’s ability 

to respond and defend itself based on levels of two 

immunoglobulins (Ig), IgE and IgG1. IgE is an 

antibody class that plays a role in allergic responses; it 

binds to allergens and triggers the release of 

histamines (important substances involved in many 

allergic reactions). IgG1 is a subclass of IgG, which 

provides the majority of antibody-based immunity 

against invading pathogens. Researchers detected the 

antibodies in both adult and young mice exposed to 

both ETS and OVA. Because exposure to ETS and 

OVA together created an allergic response, but not 

OVA or ETS exposure alone, results suggest that ETS 

can create allergic sensitization to otherwise harmless 

substances. Furthermore, the young mice had 

significantly higher antibody levels, which may explain 

why exposure to secondhand smoke is a major risk 

factor for the development of allergies in 

young children.

http://ehs.sph.berkeley.edu/chamacos

What is an antibody?

An antibody is a protein whose 

primary responsibility is defending the 

body as part of the immune system. 

In response to bacteria or viruses, 

mature B cells or plasma cells, make 

antibodies. In mammals, there are 

five classes of antibodies. Each class 

is named with an “Ig” prefix, which 

stands for immunoglobulin – another 

name for an antibody. These antibody 

classes – IgA, IgD, IgE, IgG and 

IgM – differ in their biologic properties, 

their function, where they are found in 

the body, and their ability to interact 

with various substances that stimulate 

antibody production.
14

Toddler: Behaviors that Affect 

Pollutant Exposure

Children are often exposed to contaminants at levels 

that are equal to, or greater than, adult levels of 

exposure (Black et al. 2005; Harnley et al. 2005). 

Relative to their body weight, children typically eat 

more food, drink more water, and breathe in more air 

than adults, and because they are less able than adults 

to rid their bodies of contaminants or reduce the 

toxicity of pollutants, the effects in children associated 

with these exposures can be greater (Eskenazi et al. 

1999; Bearer 2000). Children also may have a greater 

level of exposure to contaminants because they tend to 

put items in their mouth, they are closer to potentially 

contaminated floors and surfaces, and they spend more 

time inside the home. 

By spending a significant portion of their time 

inside, children are exposed to a complex mix of 

contaminants including pesticides that come from 

numerous sources such as outdoor air, tracked-in 

particles, and various indoor sources that can vary in 

nature by geographic region (Lioy 2006; Akland et 

al. 2000). For example, researchers have measured 

pesticide contamination levels in the homes of families 

living close to agricultural activities (Freeman et al. 

2004; Shalat et al. 2003; Eskenazi et al. 1999). In one 

agricultural community, children had 3.5 to 13 times 

higher urinary pesticide metabolites than children 

in the National Health and Nutrition Examination 

Survey (NHANES) database, a database containing 

information on the health and nutritional status of 

adults and children in the United States (Shalat et al. 

2003). This exposure to pesticides from agricultural 

application is a concern for children living in homes 

adjacent to or in close proximity of agricultural fields 

and orchards (Ramaprasad et al. 2004). 

In addition to the amount of time spent indoors, 

children’s other activities also greatly influence their 

potential exposure to environmental contaminants 

(Black et al. 2005). The frequency, duration, and 

nature of a child’s interaction with contaminated media 

determine the degree of a child’s exposure. Young 

children, through a number of normal activities and 

behaviors, have the potential to sustain substantial 

exposure to contaminants such as pesticides. For 

example, studies demonstrate that toddlers (children 

ages 12 months to <2 years) have higher levels of 

pesticides on their clothing, as well as higher 

concentrations of urinary metabolites, when compared 

with younger infants (Bradman et al. 2007). Toddlers 

are extremely susceptible to pesticide exposure in the 

indoor environment because of their characteristic 

behaviors. At the toddler stage, children consume a 

full range of foods because breast- and bottle-feeding 

cease. They participate in increased play activities, are 

extremely curious, and exercise poor judgment. 

Toddlers walk upright, run, climb, occupy a wider 

variety of breathing zones, and engage in more 

vigorous activities than younger infants do 

(EPA 2005).

“Pesticide exposure isn’t a great idea for 

adults, but it poses a particular concern 

in regards to children. These smallest 

humans, who spend a lot of time close 

to the floor and with their hands in their 

mouths, can encounter much higher 

doses relative to their body weights.”

— Phillips 2005
15

Furthermore, toddlers have several microactivities 

that help determine their level of exposure. Toddlers 

frequently insert objects or hands into their mouths; 

demonstrate poor food handling skills; and use objects 

such as toys, bottles, pacifiers, and blankets in the 

home that may affect exposure (Black et al. 2005; 

Freeman et al. 2001a; Akland et al. 2000). The activity 

of eating and food contamination is a specific concern 

(and this finding extends to children 3 years of age 

as well as toddlers). In fact, research results suggest 

that poor food handling skills can increase a child’s 

potential for exposure from hand-to-food, food-tosurface, and hand-to-surface contacts to pesticides 

(Akland et al. 2000). Children spend a significant 

portion of their waking hours engaged in eating and 

other activities during which their hands are exposed 

to contaminated surfaces. For example, Freeman et al. 

(2001b) reported that 63 percent of toddlers ate food 

that had been on the floor. 

While researchers have evaluated some microactivities, 

much remains unknown. Identifying the link between 

a child’s behavior and the resulting amount of a 

contaminant that enters a child’s body is an extremely 

important step in determining the significance of 

an exposure (Black et al. 2005). A number of novel 

methods have helped determine the link between 

behavior and dose. One new approach developed 

at the University of Washington Center for Child 

Environmental Health Risks Research involves the 

use of global positioning system technology for 

characterizing children’s activity patterns (EPA 2007a). 

Another novel method involves the use of laser-based, 

real-time measurement of pesticide spray drift, a 

frequent occurrence in agricultural communities. 

Path traveled by one child (6-hour sampling time) on a 

weekday during school hours.

Why the potential for food 

contamination while eating is a 

specific concern for children:

• Approximately 20 to 80 percent of a 

child’s dietary exposure results from 

handling his or her food. 

• A child’s hands contact contaminated 

surfaces up to 32 times during eating. 

• A child’s contaminated hands then contact 

his or her food 10 to 39 times before it 

enters his or her mouth during eating. 

Source: Akland et al. 2000. 

This tracking technique will help in estimating 

community residents’ and bystanders’ exposure to 

pesticide drift (EPA 2007a; Tsai et al. 2005). A third 

new approach uses videotaping to capture behaviors 

and detail needed to quantify exposures. (See text box 

on page 16.)

As concerns regarding environmental contaminants 

and their effects on children’s health continue to 

increase, the need continues for more knowledge about 

how children’s activities influence their exposure. 

This knowledge will help in the development of 

improved risk assessment models, which subsequently 

will promote our understanding of the risks 

environmental contaminants pose to children’s health. 

In turn, policymakers will have more information 

when designing strategies to reduce exposure to 

contaminants and developing methods to protect 

children’s health. If communicated effectively, this 

increased knowledge will help members of the public 

protect themselves and their children from pollutant 

exposures.
16

Preschooler: Neurological Disorders

The number of preschoolers diagnosed with 

neurodevelopmental disorders such as autism, ASD, 

Pervasive Developmental Disorder (PDD), and ADHD 

has been increasing recently. In California alone, a 

210-percent increase in the number of diagnosed cases 

of profound autism in children has been recorded in 

the past 10 years. Centers for Disease Control and 

Prevention (CDC) data released in 2007 show a high 

number of cases of ASD in several particular areas in 

the United States—approximately 1 in 150 children in 

those areas are diagnosed with an ASD by the time they 

are 8 years old. 

This sudden rise in the number of children exhibiting 

neurodevelopmental disorders is worrisome because 

scientists have little understanding of the causes and 

contributing environmental factors. The preschooler 

group, 2 to <6 years of age, is of particular 

significance because the symptoms associated 

with ASD generally begin before 3 years of age. 

Consequently, the scientific community is examining 

numerous factors such as environmental influences to 

find an explanation for the increasing trend in this age 

group (CDC 2007).

One environmental influence under study by 

researchers is early exposure to pesticides, an 

area that may reveal important information about 

neurodevelopmental disorders in children. For 

example, researchers are exploring the relationship 

between chlorpyrifos (a pesticide used in homes to 

kill cockroaches until 2001 when it was banned from 

residential sales) and neurodevelopmental disorders 

in preschool children through 3 years of age (Rauh et 

al. 2006). The investigators are finding that children 

who were exposed to high levels of chlorpyrifos before 

birth have greater developmental delays in motor 

and mental skills when compared with children who 

received low exposures. Researchers assess motor 

skills by examining endpoints like crawling, walking, 

reaching, and grasping; and cognitive development by 

studying how a child perceives, thinks, and gains an 

understanding of the world. By 3 years of age, children 

with high exposure to pesticides before birth were 11 

times more likely to have attention problems, 6.5 times 

more likely to have ADHD diagnosis, and 5 times more 

Videotaping: A Tool Capable of 

Capturing Children’s Microactivities 

(Freeman et al. 2001a) 

Children’s microactivities are not well 

documented, and understanding how 

exposures occur requires recording 

how children behave during specific 

activities. Detailed information about 

microactivities is difficult to obtain 

from questionnaires because many 

microactivities are behaviors that 

caretakers barely notice and cannot 

recall. A potential solution is to get 

information on microactivities from 

direct or videotaped observations.

For example, during the Minnesota 

Children’s Pesticide Exposure Study 

(MNCPES)—a population-based study 

in the National Human Exposure 

Assessment Survey—researchers 

videotaped 19 of the 102 children for 

four consecutive hours of normal daily 

activities. The purpose of the MNCPES 

was to characterize children’s exposure 

to residential pesticides and evaluate 

the contribution of children’s activities to 

their exposures.

Observational data from MNCPES 

expanded the existing microactivity 

database of observational studies, 

including the knowledge that most of 

children’s frequent contacts with the 

environment are short (typically less 

than 5 seconds in duration). Although 

the MNCPES observed children 

older than 3 years, the videotaping 

method is applicable for children of all 

ages. Improved understanding of the 

variability of microactivities will help 

protect the most vulnerable children.
17

likely to have PDD diagnosis than children with low 

exposure. These results show that not only is there an 

association between prenatal exposures to high levels 

of pesticides and neurodevelopmental delays, but also 

that symptoms of these delays begin to present 

strongly during preschool years.

Types of Neurodevelopmental 

Disorders

Autism—A developmental disability that 

results from a disorder of the human 

central nervous system. It is diagnosed 

using specific criteria for impairments 

to social interaction, communication, 

interests, imagination, and activities.

Autism Spectrum Disorder— 

A developmental and behavioral 

syndrome that results from certain 

combinations of characteristically 

autistic traits. 

Pervasive Developmental 

Disorder—A group of five disorders 

(Autistic Disorder, Rett’s Disorder, 

Childhood Disintegrative Disorder, 

Asperger’s Syndrome, and Pervasive 

Developmental Disorder Not Otherwise 

Specified) characterized by delays 

in development. 

Attention Deficit Hyperactivity 

Disorder—A largely neurological 

developmental disorder characterized 

by a persistent pattern of inattention or 

hyperactivity-impulsivity, or both.

http://beincharge.ucdavis.edu/ 

To better understand autism and its underlying causes, 

investigators at UC Davis are conducting a large-scale 

study called CHARGE (Childhood Autism Risks from 

Genetics and the Environment), examining potential 

genetic and environmental causes and triggers of 

autism (Hertz-Picciotto et al. 2006). The CHARGE 

investigators are particularly interested in studying the 

role the immune system plays in autism. The study 

enrolled children 2 to 5 years of age in Northern 

California diagnosed with autism. One of the key 

findings of this study showed higher levels of the 

hormone leptin in their blood (Ashwood et al. 2007). 

Leptin, a hormone known for its important effects on 

regulating body weight, metabolism, and reproductive 

function, also influences the immune system. When 

the body has too little of this hormone, the immune 

system is less responsive. Researchers identified 

children in the study who were diagnosed with early 

onset autism and regressive autism. Early onset autism 

refers to children with early delays in the development 

of language or social skills, or both; regressive autism 

refers to children who develop some language or social 

skills, or both, but who, between the ages of 18 to 24 

months, lose those skills. Children diagnosed with 

early onset autism had significantly higher blood levels 

of leptin as compared with children diagnosed with 

regressive autism. This finding is important because 

leptin may be the first biomarker to distinguish 

children with early onset autism from children with 

regressive autism. Because of its role in the immune 

system, leptin also may be an important biomarker of 

susceptibility to environmental triggers such as 

pollutants and pesticides.

Because the early interplay between toxic exposures, 

immune function, and neurological development appear 

to be strongly linked, the CHARGE investigators are 

evaluating blood samples from autistic children for 

other biomarkers of the immune system. Investigators 

found that children with autism have significantly 

lower levels of certain antibodies, show a significantly 

decreased response to some vaccinations for prevention 

of bacterial diseases, and have significantly increased 

levels of certain proteins that help amplify inflammatory 

reactions (EPA Grant Number R829388C002). The 

blood samples also show that autistic children have 

higher levels of natural killer cells and CD8 cells, 

which play similar roles in the immune system (EPA 

Grant Number R829388C003). Both cell types attack 

and destroy many foreign cells—natural killer cells kill 

right away; CD8 cells are more specific and follow a 

process before attacking and killing the foreign cell. 

The observed different levels of antibodies and cells in 

the immune systems of autistic children are significant 

because they indicate that autism may be linked to 

environmental triggers affecting the immune system.
18

Environmental Exposures

Assessed in the CHARGE Study

Biospecimens:

 Blood

 Hair (past exposures) 

 Baby lock (first year of life)

 Mother’s hair (if long enough, prenatal)

 Urine

 Buccal cells

Interviews:

 Diet

 Residential information

 Lifestyle

 Consumer products

 Medical history

Linkage to exposure databases

 Air pollution, water contamination,

 pesticide use, hazardous waste sites

Medical records

Pesticides

Metals

Organic pollutants

(PCBs, PBDEs, phthalates) 

Viruses, bacteria 

& other infections

Medical procedures 

& pharmaceuticals

School-Age: Asthma 

Intervention Programs

Asthma is the most common chronic disease of 

childhood in the developed world. In the United States, 

pediatric asthma affects approximately five million 

children under the age of 18 (Keeler et al. 2002). 

Furthermore, the prevalence rate of pediatric asthma 

(under 18 years of age) in the United States increased by 

61 percent from 1982 to 1994 (Keeler et al. 2002), and 

the mortality rate from pediatric asthma increased by 78 

percent from 1980 to 1993 (Keeler et al. 2002; Clark et 

al. 1999). Children in urban areas, especially poor and 

minority children, represent a sensitive subpopulation 

because they spend a significant portion of their time 

indoors where irritating and allergenic substances are 

prevalent. This indoor exposure to allergens may 

increase a child’s susceptibility to allergic sensitization, 

respiratory symptoms, and ultimately the development 

of asthma (Limb et al. 2005; Perera et al. 2002). While 

the consequences for the current U.S. population 

afflicted with pediatric asthma are unknown, large 

deficits in lung function persist into adulthood. The 

extent of the deficits associated with asthma is greater 

than it is with smoking (Berhane et al. 2000).

Children and Asthma Video

“Each year, asthma kills more than 600 

American children, and since 1980 the 

incidence of the disease has doubled 

and now affects over 5 million children 

in the U.S. Low-income children living 

in urban areas are at highest risk, but 

the disease cuts across socioeconomic 

and geographic boundaries.”

View the video: 

http://www.epa.gov/ncer/childrenscenters/

multimedia.html#child_asthma 

Research results indicate that in addition to genetic 

disposition, demographic variables, and psychosocial 

stressors, indoor environmental exposures may 

contribute significantly to the worldwide increase 

of asthma (Eggleston et al. 2005; Keeler et al. 

2002; Rauh et al. 2002). In fact, 80 to 90 percent of 

asthmatic children become sensitized to airborne 

environmental allergens beginning at school age (6 

years of age and less than 11 years of age) (Zeldin et 

al. 2006). Some of the strongest associations between 

asthma and indoor allergen exposure have been found 

with dust mites, rodents, pets, and cockroaches (Zeldin 

et al. 2006; Kinney et al. 2002; Rauh et al. 2002). 

Exposure to ETS during childhood also appears to play 

an important role in asthma causation and aggravation 

(Zeldin et al. 2006).
19

While investigators have identified environmental 

allergens as a potential cause for childhood asthma, 

the actual concentration of allergens that a child 

is exposed to remains uncertain (Zeldin et al. 

2006). “Exposure dose” is dependent on both the 

Table 4. Allergen Characteristics and Possible Exposure-Reduction Methods

Allergen Characteristics Exposure-Reduction Methods

Dust Mite

•		Carried	on	relatively	large	particles	(10	to	30	

micrometers) that do not remain airborne for long

•	Infestation	on	fabrics,	especially	bedding	

•		Fitting	allergen-proof	encasings	to	the	mattress	and	

pillow

• 	Vacuuming,	cleaning,	and	washing	all	bedding	

regularly 

•	Relocating	the	bedroom

•	Applying	pesticides	designed	to	kill	mites

•	Dehumidifying

•	Removing	wall-to-wall	carpeting	

Pet

•		Carried	on	small	particles	that	remain	airborne	and	

are extremely adherent to surfaces and clothing

•	Using	air	filters

•	Removing	pet

•	Removing	carpets,	furniture,	and	other	reservoirs

•	Purchasing	new	bedding

concentration inhaled and the duration of exposure 

(Eggleston 2005). The most effective method of 

reducing exposure dose is to remove the source of the 

contaminant (Eggleston 2005). To achieve adequate 

source removal, it is necessary to conduct further 

research to better understand and address the sources 

of indoor and outdoor pollutants (Keeler et al. 2002). 

Research in this area is making progress. For example, 

studies have demonstrated that more than threequarters of U.S. homes have detectable concentrations 

of mouse allergen. Although mouse allergen is 

almost ubiquitous in inner-city homes and occurs in 

approximately 75 percent of middle-class suburban 

homes, analyses of settled dust concentrations of 

mouse allergen indicate that indoor levels are 10-fold 

higher in inner-city homes than suburban homes 

(Matsui et al. 2005). Studies have suggested that the

distribution of cockroach allergen is dependent on the 

built environment and that cockroach allergen persists 

for months after successful pest control (Eggleston 

2005; Eggleston 2003). While it is impossible to make 

indoor environments allergen free, proven effective 

intervention methods for reducing most indoor 

allergens have been developed based on this increasing 

knowledge base (table 4). It is important to recognize 

that each intervention method requires a somewhat 

different approach.
20

Allergen Characteristics Exposure-Reduction Methods

Rodent 

•		Carried	on	particles	that	are	small	and	remain	

airborne

•		Widely	distributed	and	commonly	found	in	homes	

that are not infested with mice

•		Applying	Integrated	Pest	Management	(IPM)	to	

reduce exposures by combining nonchemical

approaches, education, and information on the 

life cycles of pests and their interactions with the 

environment

•		Removing	basic	rodent	survival	elements	such	as	air,	

moisture, food, and shelter by sealing cracks and 

crevices

•	Carefully	placing	least-toxic	baits	and	gels

•	Maintaining	properties

•	Sanitizing	properties	to	remove	the	allergen

•	Educating	residents

•		Specially	training	professionals	to	conduct	

interventions

Cockroach 

•		Resembles	mite	allergens	with	up	to	80	percent	of	

aeroallergens carried on larger particles (>10 micrometers) that are detectable mainly after vigorous 

activity and settle rapidly

•		Highly	mobile;	therefore,	spreads	widely	throughout	

the home, especially in bedding and kitchens

•		Concentrates	behind	appliances	and	in	cracks	and	

crevices

•	Using	IPM	

•	Cleaning	to	remove	food	sources,	grease,	food	debris

•		Storing	food	in	plastic	containers	kept	in	a	

refrigerator

Environmental Tobacco Smoke 

•		Widespread	exposure—approximately	15	million	

children in the United States are exposed to 

environmental tobacco smoke (ETS) 

•		Restricts	lung	growth	and	development,	which	

results in reduced pulmonary function

•		Removing	sources	of	cigarette	smoke	from	the	

indoor environment

Sources: Apter and Eggleston 2005; Brenner et al. 2003; Clark 1999; Eggleston 2005; Gilliland et al. 2000; Matsui et al. 

2005; Phipatanakul et al. 2004

While these personal-level interventions are helpful, 

researchers recognize that to successfully combat 

the rising pediatric asthma prevalence rate, more 

community-based participatory approaches to 

interventions are needed. Urban environments are 

complex; they consist of a network of factors that 

potentially contribute to environmental allergens. 

Urban areas often contain multifamily residences, 

a high density of grocery stores and restaurants, 

substandard housing maintenance, and an inadequate 

sanitation infrastructure. All of these factors 

potentially could increase the prevalence and 

concentrations of environmental allergens; therefore, 

it is important to target asthma interventions at the 

community level (Chew et al. 2003). Researchers 

are beginning to recognize the value of including the 

intended beneficiaries in the planning, implementation, 

and evaluation of research (Parker et al. 2003; Clark et 

al. 1999). Involving community partners in collecting, 

analyzing, interpreting, and disseminating the research 

results, as well as developing, implementing, and 

evaluating household-, community-, and policy-level 

strategies aimed at reducing exposures and improving 

children’s health, will help make interventions 

successful (Keeler et al. 2002; Clark et al. 1999).

Several CBPR projects (some completed, some in 

progress) have actively involved community members 

in the research. The following projects investigated 

multiple exposures and susceptibility factors that may 

disproportionately affect children and the interactions 

between community members: 
21

•	 Community Action Against Asthma (CAAA): 

The overall goal of this CBPR project is to better 

understand environmental triggers and psychosocial 

factors such as family tensions, physical activity, 

anxiety and stress, and friends and peer pressure 

on children with asthma. Understanding this 

cause-and-effect relationship will help reduce 

various asthma triggers through household- and 

neighborhood-level interventions. Specifically, the 

CAAA study conducts research on the effects of 

environmental exposures on the residents of Detroit, 

Michigan, through a CBPR process. Participants

and researchers are involved in all aspects of the 

design and conduct of research, and all parties 

involved receive the study results. The study uses the 

research to design, in collaboration with all partners, 

interventions to reduce identified environmental 

exposures (Keeler et al. 2002).

•	 Inner-City Asthma Study: The overall goal of 

this project was to design intervention strategies to 

reduce allergen and particulate exposures. Results 

show that airborne particulates and allergens 

affect asthma synergistically. The intervention 

involved the following approaches: home-based 

education, cockroach and rodent extermination, 

mattress and pillow encasings, and cleaning with 

high-efficiency particulate air (HEPA) filters. The 

research results indicate that an intervention that 

combines strategies to reduce indoor pollutants 

and allergens simultaneously with education of 

residents in inner-city homes substantially reduces 

exposure levels of particulate matter and allergens. 

The research results also indicate modest reductions 

of symptoms in asthmatic children who live in 

homes treated with this combination intervention 

(Eggleston et al. 2005).

•	 National Cooperative Inner-City Asthma Study: 

This study consisted of a family-focused asthma 

intervention for low-income, inner-city children 

with moderate to severe asthma and their family 

members. The research focused on both problem 

solving and asthma education so that participants 

would have an improved understanding of the 

disease and gain the skills to avoid asthma 

triggers. The study demonstrated how common 

environmental allergens are in inner-city homes 

and how strongly sensitization and asthma 

morbidity relate to exposure. The current preferred 

approach is using IPM combined with pesticide

application, accompanied with family education and 

maintenance of the built environment (Chew et al. 

2003; Eggleston 2003; Rauh et al. 2002).

•	 Integrated Pest Management Study in East 

Harlem, New York City: This study was a twopronged prevention and intervention program to 

test whether IPM techniques in combination with

education targeted at the household level could 

reduce cockroach allergens and decrease reliance 

on chemical pesticides in the urban home. Although 

the study demonstrated that IPM techniques are

effective and relatively economical, success depends 

on direct involvement of the community residents 

in the development and implementation phases and 

education and guidance from pest control experts. 

Building managers, superintendents, and others 

who provide services to urban residences also must 

support the IPM efforts (Brenner et al. 2003).

Columbia University Center for Children’s 

Environmental Health has been honored 

with an Excellence Award from the EPA 

Office of Children’s Health Protection 

for its Integrated Pest Management 

interventions. This program trains and 

educates tenants to use IPM practices, 

which include reducing the levels of toxic 

pesticide use inside their homes and 

sealing cracks and crevices, as well as 

reducing asthma-triggering pet allergens.

Although researchers have made progress in 

establishing the causes of the rising rate of pediatric 

asthma, the need continues for a better definition of 

susceptible populations and a better understanding 

of the effect of allergens on susceptible individuals. 

Protecting children’s health will require identifying 

preventable risks and rapidly translating this 

knowledge into protective policies and interventions 

(Perera et al. 2002). Continued CBPR will give 

researchers and policymakers a better understanding 

of the interactions between multiple exposures and 

susceptibility factors that disproportionately affect 

certain populations (Perera et al. 2002), and CBPR 

can help make policymakers aware of susceptible 

populations when they formulate new standards and 

policies (Lewis et al. 2005; Clark et al. 1999). For 

example, researchers using CBPR could address the 

fact that asthma is especially prevalent in urban and 

minority populations (Keeler et al. 2002; Kinney 

et al. 2002; Clark et al. 1999). Researchers and 

policymakers using CBPR could develop effective and 

sustainable strategies for communities with susceptible 

populations such as disproportionately high levels of 

exposure to ETS and allergens and people who lack 

access to medical care, financial resources, and social 

support to effectively manage the disease long-term 

(Clark et al. 1999). 
22

Children’s Health and The Environment: 

Emerging Trends, Current Work, And Future Directions

Over the past fifty years, the trends in health threats 

to the Nation’s children have changed significantly. 

By creating safer drinking water and healthier 

environments, we have made tremendous progress 

in reducing childhood infectious diseases and infant 

mortality. Science-based policies have brought public 

health successes in certain areas of environmental 

health. For example, lead exposure prevention 

programs have reduced the average blood lead levels 

of children in the United States. Additionally, advances 

in asthma research have enabled pediatricians to 

detect the warning signs of respiratory distress 

earlier and to intervene through environmental and 

clinical management. Today, scientists now face 

increasingly complex questions and must deal with 

chronic health challenges affecting children, including 

impairments in growth and development, increased 

rates of preterm birth and low birth weight (LBW) 

babies, childhood obesity, Type 2 diabetes, and poorly 

understood developmental disabilities such as autism. 

Identifying the potential role of the environment in the 

development or progression of these diseases is further 

complicated by the emergence of many new chemicals 

in both domestic and international markets that are 

increasingly ubiquitous at low levels.

As discussed in this report, STAR research is starting 

to address these more complex questions. For example, 

EPA-funded researchers are providing cutting edge 

epidemiology and basic science insights to answer 

questions about:

•	 LBW and Preterm Birth: LBW babies and 

babies born before term (preterm birth) are at 

increased risk for various health problems (Stevens 

et al. 2002). Despite overall improvements in 

prenatal care in the United States, rates of LBW 

and preterm births continue to rise ( Hamilton, 

et al 2006). STAR researchers have published 

scientific findings on the association between certain 

environmental exposures (e.g. organophosphate 

pesticides and air pollution) in the womb and 

increased risk of preterm birth and low birth weight 

babies. Furthermore, in 2007, EPA launched a new 

Children’s Center at Duke University that seeks to 

understand the disparities in adverse birth outcomes, 

particularly in the American South as they relate 

to environmental exposures, complex genetic 

interactions, and community-level influences. 

•	 Childhood Obesity: Rates of childhood obesity 

in America are increasing; an estimated 17 percent 

of children and adolescents aged 12-19 years are 

overweight ( CDC 2007). Obesity is a complex issue 

related to lifestyle, environment, and genes. Recent 

data have shown that there are plausible biological 

mechanisms through which chemical exposures 

can disrupt hormonal processes. STAR research is 

investigating the links between early life exposures 

to endocrine disrupting chemicals and childhood 

obesity, early pubescent development, and Type 2 

diabetes.

•	 Autism Spectrum Disorder: Once reported to 

have an incidence rate in the single digits per 1000, 

ASD today affects one out of every 150 children 

( Rice 2007). Researchers are at the starting point 

in understanding how genetics, environmental 

exposures, maternal infections, and other factors 

can impact child neurodevelopment. For example, 

the summer of 2007 marked the initiation of the 

EPA/NIEHS supported Markers of Autism Risks in 

Babies—Learning the Early Signs (MARBLES)

study. The lead investigators of MARBLES will

monitor the environmental and genetic influences 

on pregnancies at higher risk of autistic outcomes 

( http://marbles.ucdavis.edu/).

“In the South, there is a unique social, 

economic, and demographic context 

in which environmental exposures play 

out. Poor birth outcomes aren’t just an 

immediate problem -- the effects can be 

very long lasting. Survivors of poor birth 

outcomes are at increased risk for serious 

illnesses later in life.”

— Dr. Marie Lynn Miranda, Duke 

University Children’s Center Director

As the science from the past ten years is reviewed, it 

is clear that EPA-funded research has led to important 

advances in understanding how environmental factors 

affect children’s health. This robust body of work 

has also informed policies that protect public health. 

As EPA looks to the future, however, it is equally 

clear that important work remains to be done. EPA, 
23

along with several other Federal Agencies, will begin 

working together to answer some of these more 

complex questions through a landmark study – the 

National Children’s Study – that will examine the 

effects of environmental influences on the health and 

development of more than 100,000 children across the 

United States, following them from before birth until 

age 21. This study defines the term “environment” 

broadly by considering natural and man-made 

environmental factors, biological and chemical factors, 

physical surroundings, social factors, behavioral 

influences and outcomes, genetics, cultural influences, 

and geographic locations. The NCS will be one of the 

richest information resources available for answering 

questions related to children’s health and development 

and will form the basis of child health guidance, 

interventions, and policy for generations to come. 

http://www.nationalchildrensstudy.gov

While EPA-funded research will provide some of 

the foundation for this major landmark study by 

advancing the science and creating the tools needed 

for conducting longitudinal epidemiology studies, 

NCER’s STAR program will also continue to work 

in major emerging areas of scientific inquiry such as 

advanced methods for interpreting biomonitoring data 

and community-based risk assessment.

Interpreting Human Biomonitoring 

Information

Human biomonitoring data is collected as a way of 

assessing exposure, susceptibility, and effects by 

researchers involved in many types of environmental 

health studies, including long term studies of the 

association between human exposure to environmental 

chemicals and resulting health effects. Advances in 

measurement technology have made biomonitoring 

more popular as a way to track health and monitor 

trends in exposure or disease. There are efforts at 

the Federal and State levels to collect information 

on human exposure to environmental chemicals and 

also to use biomonitoring data to assess the public 

health impacts of policy decisions. There are still 

data gaps, however, in our understanding of what 

certain biomarkers actually mean in terms of exposure 

and dose. STAR research is starting to fill some of 

these knowledge gaps through a program designed 

to develop methods and models to interpret and 

understand biomonitoring data. Using sophisticated, 

state-of-the-science modeling techniques, STAR 

researchers are making headway into this important 

area of science. These results will be informative 

for scientists and policy makers who rely on 

biomonitoring data – including those researchers 

working in children’s environmental health. A better 

understanding of biomarker data will help us more 

accurately assess a child’s exposure and risk and 

can eventually contribute to broader knowledge of 

children’s environmental health. This program will 

help answer questions like what exposure must have 

occurred to create the measured biomonitoring level 

and, based on the measured biomonitoring level, how 

much of this chemical reached a point in the body 

where it could potentially do harm.

Community-Based Risk Approaches: 

Exploring Interactions between Chemical 

and Nonchemical Stressors 

An important emerging area of environmental 

health science is investigating how chemical and 

nonchemical stressors – in combination – can impact 

health outcomes. NCER is leading an effort to explore 

the opportunities and challenges of this question in 

greater detail by initiating a program on conducting 

risk assessments that take into account both chemical 

and nonchemical stressors in a community and 

the potential health impact of those stressors when 

combined. It is likely that STAR research will fill an 

important role in this emerging area. It is anticipated 

that specific research needs will be identified in 

the areas of: (1) methods to measure chemical and 

nonchemical stressors, susceptibility factors, and 

health outcomes at the community level; (2) the 

physiological impacts on nonchemical stressors 

and the impact on health outcomes associated with 

environmental chemical exposures; and (3) statistical 

methods for assessing community and cumulative risk.

The ability to conduct community-level risk 

assessments that account for the many chemical and 

nonchemical stressors faced by the population relies 

on the use of well-developed tools and methods to 

accurately understand exposures to all stressors, the 

interactions between stressors, the biological impacts 
24

of those stressors, and the best way to combine and 

analyze the information in a way that is useful for risk 

assessors and managers. This type of assessment will 

move the science of risk assessment and environmental 

health forward.

Epilogue

Ten years ago, scientists were just beginning to 

answer pressing health and policy questions such 

as: How do children’s behaviors impact exposure to 

environmental toxins? How do children’s behaviors 

and exposures change over time? Can we identify 

biological susceptibilities that increase risk of health 

effects in children? Do exposures in the womb 

lead to health effects in children, and if so, to what 

extent? Are there effective ways to reduce children’s 

exposures to environmental chemicals? Can these 

effective interventions actually improve children’s 

health outcomes?

During the past ten years, with the emergence of 

biological monitoring, advanced exposure methods, 

and the rapidly proliferating science of human DNA 

analysis, STAR-supported researchers and community 

partners began answering these questions. Moreover,

many scientists participated directly or indirectly 

in creating more protective policies based on sound 

science for children at the state and local levels. 

Yet many of our most daunting challenges in 

children’s health protection may lie ahead. In the 

future, increasingly complex questions are likely to 

arise as the trends in low dose chronic exposures to 

multiple new chemicals continue across life stages. 

Additionally, global warming, nanotechnology, and 

urbanization each present potential risks for children’s 

health. Yet they also present an opportunity to design 

safer, more sustainable environments. 

NCER’s STAR program will continue to build upon 

the successes of the past ten years by supporting the 

scientific leaders of tomorrow. Together with our 

federal, academic, and community partners, EPA 

will step boldly toward answering the questions that 

will help create a cleaner environment and healthier 

communities for the Nation’s children.
25

Links to Additional Information

For more information on the Children’s Centers 

and NCER’s STAR grant program, see the links 

below. Other important sources for children’s health 

information are also provided.

EPA. Children’s Centers. Available online at http://

www.epa.gov/ncer/childrenscenters/ or http://

www.niehs.nih.gov/research/supported/centers/

prevention/.

The Children’s Centers are funded jointly

by EPA’s STAR grants, NIEHS, and CDC to

conduct laboratory, clinical, and behavior

studies on the environmental factors influencing

children’s health.

EPA. NCER. Available online at 

http://www.epa.gov/ncer/.

NCER supports scientific research across the

country on a wide variety of environmental issues.

Researchers use these results to develop and

support national environmental policies and

goals. The NCER STAR grant program partially

funds the Children’s Centers and provides other

grants to focus on children’s health.

CDC. Pediatric Environmental Health Specialty 

Units (PEHSUs). Available online at http://www.

atsdr.cdc.gov/HEC/natorg/pehsu.html. 

Funded by the Agency for Toxic Substances and

Disease Registry (ATSDR) and EPA, PEHSUs

consist of representatives from pediatric and

environmental clinics who provide education and

consultation to health professionals in the field

of children’s environmental health. Currently,

13 PEHSUs are in operation across the United

States, Canada, and Mexico.

Children’s Environmental Health Network (CEHN). 

Available online at http://www.cehn.org/.

CEHN is a nonprofit organization that, among

other endeavors, promotes research in the

field of children’s health. CEHN stimulates

research in five priority research areas: asthma

and respiratory diseases, childhood cancer,

neurodevelopmental effects, endocrine and

sexual disorders, and cross-cutting issues.

EPA. Office of Children’s Health Protection 

(OCHP). Available online at http://yosemite.epa.

gov/ochp/ochpweb.nsf/content/homepage.htm. 

OCHP works with other EPA Offices and other

Federal Agencies to promote scientific research

in children’s environmental health, including the

Toxicity and Exposure Assessment for Children’s

Health (TEACH) program and the National

Children’s Study.

EPA. TEACH. Available online at http://www.epa.

gov/teach/. 

The TEACH Web site and database include

information on scientific research and Federal

regulations relating to children’s environmental

health. Currently, TEACH provides nonbiased

information from numerous sources on 18

chemicals of concern.

EPA. Voluntary Children’s Chemical Evaluation 

Program (VCCEP). Available online at

http://www.epa.gov/oppt/vccep/. 

VCCEP was developed in response to the

Chemical Right-to-Know Initiative, and compiles

information from companies that manufacture

and import products that contain one or more of

the 23 chemicals identified as risks to children.

National Institutes of Health (NIH). National 

Children’s Study. Available online at 

http://www.nationalchildrensstudy.gov/.

Beginning this year, the National Children’s Study

will track the physical and mental health of more

than 100,000 children from before birth until age

21 in an effort to determine the environmental

factors that affect children’s health.

World Health Organization (WHO). Child and 

Adolescent Health and Development (CAH). 

Available online at 

http://www.who.int/child-adolescent-health/. 

CAH gathers data on children from birth

through 19 years of age, focusing on the burden

of disease and the effectiveness of public

health interventions
26

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