America’s Children 

and the Environment

Measures of Contaminants, Body Burdens, and Illnesses

Second Edition 

EPA 240-R-03-001

February 2003
I am pleased to present the U.S. Environmental Protection Agency’s second edition of

America’s Children and the Environment: Measures of Contaminants, Body Burdens, and

Illnesses. This report marks the progress we have made as a nation to reduce environmental risks faced by children.

The report contains good news for children including the continued decline in the

number of children with elevated blood levels, a reduction in children’s exposure to

secondhand smoke, and decreases in exposures to air pollution and contaminants in

drinking water.

Although we are encouraged by these findings, there is still much work to be done.

Asthma rates are increasing, too many children continue to have elevated blood lead

levels, the potential for mercury exposure in the womb is of growing concern, and there

is a disproportionate impact of childhood diseases on low-income and minority children. America’s Children and the Environment will help focus our efforts in addressing

these problems and others.

Protecting children’s health is an integral part of EPA’s mission, and the Agency has

taken great strides to improve the environment for children where they live, learn, and

play, including: 

■ Reducing emissions of diesel pollutants from trucks and buses, which will help

prevent hundreds of thousands of asthma attacks in children each year.

■ Adopting stringent restrictions on the use of the organophosphate pesticides

azinphos-methyl, chlorpyrifos, methyl parathion, and diazinon on food crops and

around the home.

■ Taking preventive action to reduce risks of exposure from environmental

contaminants, including our work with industry to ensure playground equipment is

no longer made with wood treated with arsenic-containing preservatives.

■ Establishing 12 Centers for Children’s Environmental Health and Disease

Prevention Research, in partnership with the Department of Health and Human

Services, to enhance scientific understanding of the relationships between

environmental contaminants and children’s health. 

■ Launching a comprehensive schools initiative to create healthier classrooms.

■ Implementing the Smoke-Free Home Pledge campaign, designed to protect

millions of children from the risks of secondhand tobacco smoke at home.

■ Working with other federal agencies to develop and implement the Interagency

Asthma and Lead Strategies to reduce the disproportionate impact of asthma on

minority and low-income children and to eliminate childhood lead poisoning by

the year 2010. 

■ Developing the Clear Skies Initiative, to reduce emissions of sulfur dioxide,

nitrogen oxides, and mercury from electric utilities by approximately 70 percent,

which will help reduce asthma attacks and respiratory infections. 

ii America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Foreword
As we move forward, EPA is committed to monitoring the success of our children’s

health efforts. The America’s Children and the Environment report, based on the best

data available at this time, is an important benchmark that EPA will use to guide our

future actions and measure progress. As our data and methods improve, we will work

to develop increasingly reliable children’s environmental health indicators that will help

us in reaching our children’s health goals. 

I want to thank the many individuals who contributed to this report for their hard work

and efforts. By monitoring trends, identifying successes, and pinpointing areas of concern,

we can continue to improve the health of our children and the health of all Americans.

Christine Todd Whitman 

Administrator

Foreword iii

Foreword

About This Report . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

Key Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

Summary List of Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

Part 1: Environmental Contaminants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

Outdoor Air Pollutants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

Indoor Air Pollutants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

Drinking Water Contaminants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

Pesticide Residues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

Land Contaminants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

Part 2: Body Burdens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49

Concentrations of Lead in Blood . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52

Concentrations of Mercury in Blood . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58

Concentrations of Cotinine in Blood . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62

Part 3: Childhood Illnesses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

Respiratory Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67

Childhood Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76

Neurodevelopmental Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86

Part 4: Emerging Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91

Mercury in Fish . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94

Attention-Deficit/Hyperactivity Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98

Part 5: Special Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101

Lead in California Schools . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103

Pesticides in Minnesota Schools . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111

Birth Defects in California . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116

Future Directions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119

Glossary of Terms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125

Appendix A: Data Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131

Appendix B: Data and Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147

Appendix C: Environmental Health Objectives in Healthy People 2010 . . 167

Appendix D: Environmental Health Objectives in EPA’s Strategic Plan . . . . 169

Table of Contents 1

Table of Contents
Tracey J. Woodruff

National Center for Environmental Economics

Office of Policy, Economics and Innovation

U.S. Environmental Protection Agency

San Francisco, CA 94105

Daniel A. Axelrad

National Center for Environmental Economics

Office of Policy, Economics and Innovation 

U.S. Environmental Protection Agency

Washington, DC 20460

Amy D. Kyle

School of Public Health

University of California Berkeley

Berkeley, CA 94720 

Onyemaechi Nweke

National Center for Environmental Economics

Office of Policy, Economics and Innovation

U.S. Environmental Protection Agency

Washington, DC 20460

Gregory G. Miller

National Center for Environmental Economics

Office of Policy, Economics and Innovation 

U.S. Environmental Protection Agency

Washington, DC 20460

2 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Authors
External Peer Reviewers*

Lara Akinbami, National Center for Health Statistics, Centers for Disease 

Control and Prevention, U.S. Department of Health and Human Services 

Joel Bender, American Chemistry Council 

Elinor Blake, California Department of Health Services

David Brown, Northeast States for Coordinated Air Use Management (NESCAUM)

Patricia Buffler, School of Public Health, University of California, Berkeley 

Suzan Carmichael, March of Dimes/California Birth Defects Monitoring Program,

California Department of Health Services

Gwen Collman, National Institute of Environmental Health Sciences, 

U.S. Department of Health and Human Services

Brenda Eskenazi, School of Public Health, University of California, Berkeley

Paul Garbe, National Center for Environmental Health, Centers for Disease 

Control and Prevention, U.S. Department of Health and Human Services

Fernando Guerra, San Antonio Metropolitan Health District 

Nadia Juzych, Michigan Public Health Institute

Linda Mazur, California Environmental Protection Agency

Maria Morandi, University of Texas, Houston

Swati Prakash, West Harlem Environmental Action, Inc.

Peggy Reynolds, California Department of Health Services 

Kristin Ryan, Division of Environmental Health, Alaska Department of

Environmental Conservation

Sam Sanchez, San Antonio Metropolitan Health District 

Ken Schoendorf, National Center for Health Statistics, Centers for Disease Control

and Prevention, U.S. Department of Health and Human Services

Kirk Smith, School of Public Health, University of California, Berkeley

Nancy H. Sutley, California Environmental Protection Agency

Daniel Swartz, Children’s Environmental Health Network

Diane Wagener, Office of Public Health and Science, U.S. Department of 

Health and Human Services

John Wargo, Yale School of Forestry and Environmental Studies

Cynthia Warrick, Howard University

Internal EPA Peer Reviewers

David Bennett, Office of Solid Waste and Emergency Response

John Bennett, Office of Water

Jeff Bigler, Office of Water

Ellen Brown, Office of Air and Radiation

Doreen Cantor, Office of Prevention, Pesticides, and Toxic Substances

Reviewers for 

America’s Children and

the Environment:

Measures of

Contaminants, Body

Burdens, and Illnesses

Reviewers 3

Reviewers

* Each listed reviewer participated in one or more of three peer review meetings: October 5, 2000 in

Washington, DC; March 28, 2001 in Berkeley, CA; November 15, 2001 in Washington, DC.
Wayne Garfinkel, Region 4

Rafael Gonzalez, Office of Solid Waste and Emergency Response

Dave Guinnup, Office of Air and Radiation

Lee Kyle, Office of Water

Karen Martin, Office of Air and Radiation

Ellie McCann, Office of Prevention, Pesticides, and Toxic Substances

David McKee, Office of Air and Radiation

Deborah Rice, Office of Research and Development

Ron Shafer, Office of Environmental Information

Roy Smith, Office of Air and Radiation

Carol Terris, Office of Prevention, Pesticides, and Toxic Substances

David Topping, Office of Prevention, Pesticides, and Toxic Substances

Glenn Williams, Office of Prevention, Pesticides, and Toxic Substances

Lynda Wynn, Office of Water

Federal Agency Contributors

Lara Akinbami, National Center for Health Statistics, Centers for Disease 

Control and Prevention, U.S. Department of Health and Human Services 

Rebecca Allen, EPA Office of Water

Thomas Bernert, National Center for Environmental Health, Centers for Disease

Control and Prevention, U.S. Department of Health and Human Services

Barry Gilbert, EPA Office of Air and Radiation

Brian Gregory, EPA Office of Air and Radiation

James Hemby, EPA Office of Air and Radiation

Lee Kyle, EPA Office of Water

David Mintz, EPA Office of Air and Radiation

Patricia Pastor, National Center for Health Statistics, Centers for Disease 

Control and Prevention, U.S. Department of Health and Human Services

Abraham Siegel, EPA Office of Water

Philip Villanueva, EPA Office of Prevention, Pesticides, and Toxic Substances

David Widawsky, EPA Office of Prevention, Pesticides, and Toxic Substances

Special thanks to Brad Hurley of ICF Consulting for his extensive work in document

preparation, formatting and editing the text and graphics, and logistical support in

preparing the report.

4 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Reviewers
About This Report 5

About This Report

merica’s Children and the Environment: Measures of Contaminants, Body Burdens, and

Illnesses is the U.S. Environmental Protection Agency’s second report on trends in

environmental factors related to the health and well-being of children in the United States.

America’s Children and the Environment brings together, in one place, quantitative information from a variety of sources to show trends in levels of environmental contaminants

in air, water, food, and soil; concentrations of contaminants measured in the bodies of

children and women; and childhood illnesses that may be influenced by exposure to

environmental contaminants.

EPA’s first report, America’s Children and the Environment: A First View of Available

Measures, published in December 2000, presented the results of EPA’s initial effort to

collect and analyze existing, readily available data on measures relevant to children’s

health and the environment. This second report improves on the first edition by adding

new measures for important contaminants, exposures, and childhood illnesses and by

including data for additional years. The report also includes more analysis of these

measures by race/ethnicity of children and family income.

What are the purposes of this report?

This report has three principal objectives. First, it presents concrete, quantifiable

measures for key factors relevant to the environment and children in the United States.

These measures offer a basis for understanding time trends for some factors and for

further investigation of others. Second, the report can inform discussions among policymakers and the public about how to improve federal data on children and the environment. Third, America’s Children and the Environment includes measures that can be used

by policymakers and the public to track and understand the potential impacts of environmental contaminants on children’s health and, ultimately, to identify and evaluate

ways to minimize environmental impacts on children. The authors and sponsors hope

this report will contribute to the effort to integrate the environmental health needs of

children into the nation’s policy agenda.

What’s new in this edition of the report? 

Most measures that were included in the first edition of America’s Children and the

Environment have been updated to include data for additional years. Several new measures have been added for this edition, and analyses by race/ethnicity and family income

are included where possible.

What’s new in the section on environmental contaminants?

● New measures of long-term exposures to outdoor air pollutants

● An improved measure of children’s proximity to hazardous waste sites

What’s new in the section on body burdens?

● A new measure that shows the full current distribution of blood lead levels in

children ages 1-5

● A new measure of mercury in the blood of women of child-bearing age

● A new measure of cotinine (a marker of exposure to environmental tobacco

smoke) in the blood of children

What’s new in the section on childhood illnesses?

● New measures of respiratory diseases 

● A new measure on mental retardation

A
A new section on emerging issues presents information about important aspects of

children’s environmental health for which data recently have become available. Topics

covered in this section include mercury in fish, an important source of mercury exposure

for people in the United States, and attention-deficit/hyperactivity disorder, which recent

research suggests may be associated in part with exposure to environmental contaminants.

Also new in this report is a special features section that presents important aspects of

children’s environmental health for which nationally representative data are not available. The special features are based on data from single states, and include:

● Lead in paint, water, and soils in California schools

● Pesticide use in schools in Minnesota

● Birth defects trends in California

How is the report structured?

The measures in the report focus on contaminants in the environment, contaminants in

the bodies of children and women, and illnesses for which there is reason to believe that

environmental exposures may play a role. Measures show trends over time whenever

possible.

The first part of the report presents measures reflecting trends in levels of environmental contaminants that are likely to affect children’s health. These measures show the percentages of children exposed to particular levels of contaminants in air, water, food, and

soil. Where data on actual environmental concentrations of contaminants are not available, the report presents surrogate measures.

The second part presents measures reflecting trends in concentrations of key contaminants

measured in the bodies of children and women. These data provide direct evidence of

exposures.

The third part presents measures that reflect trends in key childhood illnesses, the frequency or severity of which may be related to exposure to environmental contaminants.

The fourth part presents information about emerging issues for which data recently

have become available or that are new to this report.

The fifth part presents measures for important aspects of children’s environmental

health based on data from single states.

Ideally, it would be informative to include measures that reflect similar environmental

health concerns for children in all three of the report’s main topic areas—exposure to

contaminants in the environment (Part 1), concentrations of the same contaminants in

the bodies of children and women (Part 2), and illnesses for which these contaminants

have been found to play a role (Part 3). Although there are not sufficient data to fully

accomplish this goal, relationships among some of the measures in the three sections

are evident.

For example, Part 1 includes measures that reflect children’s exposures to outdoor air

pollutants over both the short and long term, while Part 3 includes measures for respiratory diseases, some of which are associated with air pollution. Similarly, for environmental tobacco smoke, a key pollutant of indoor air, Part 1 includes measures reflecting the

frequency of smoking in homes where children live; Part 2 includes a measure for concentrations of cotinine, a marker for exposure to environmental tobacco smoke, in the

blood of children; and Part 3 includes a measure on respiratory-related health effects that

6 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

About This Report
can in part be caused by exposure to environmental tobacco smoke. In another example,

Part 1 includes a measure on the percentage of children living in counties in which air

quality standards for lead were exceeded; Part 2 includes measures on concentrations of

lead in the blood of children; Part 3 includes a new measure for mental retardation in

children, which may be due in part to exposure to lead; and Part 5 has information

from California on lead in schools.

Appendix A provides tables showing the data on which the measures were based.

Appendix B describes the sources of the data used in this report and the methods for

calculating the measures. Appendix C has a list of health goals relevant to the topics in

this report, developed by Healthy People 2010, a collaborative effort coordinated by

the U.S. Department of Health and Human Services to establish national health objectives. Appendix D lists EPA’s Government Performance and Results Act goals that are

related to the measures in this report. These goals are set to achieve EPA’s overall objectives of clean air, clean and safe water, safe food, and the protection of America’s land.

The report includes a discussion of future directions, including ways in which the existing

measures could be improved and additional measures that may be included in future editions.

Why did EPA focus on measures for children?

Environmental contaminants can affect children quite differently than adults, both

because children may be more highly exposed to contaminants and because they may

be more vulnerable to the toxic effects of contaminants.

Children generally eat more food, drink more water, and breathe more air relative to

their size than adults do, and consequently may be exposed to relatively higher amounts

of contaminants. Children’s normal activities, such as putting their hands in their mouths

or playing on the ground, can result in exposures to contaminants that adults do not

face. In addition, environmental contaminants may affect children disproportionately

because their immune defenses are not fully developed and their growing organs are

more easily harmed.

How were the measures in this report selected?

Three principal criteria were used to select measures for the report: 1) importance to

the health of children, 2) availability of data for much or all of the United States, and

3) and sufficient quality of data to generate a reliable measure.

For environmental contaminants, five important media were identified: outdoor air, indoor

air, drinking water, food, and soil. For each of these media, data available from federal

environmental and health agencies were reviewed. The most informative sources that

provided national coverage (or close to it) and a reasonable assurance of reliability were

selected. If data about concentrations of key contaminants could be identified and were of

adequate quality, they were used. If not, the best available surrogate measure was selected.

The available data for concentrations of contaminants in the bodies of children and

women were reviewed, and the report presents selected contaminants for which several

years of data were available or for which health impacts had been well established. These

are lead, mercury, and cotinine (the latter of which reflects exposure to environmental

tobacco smoke)—pollutants long recognized as having important impacts on children’s

health. The report presents the best available information about the concentrations of

lead and cotinine in the blood of children, and about the concentrations of mercury in

the blood of women of child-bearing age.

About This Report 7

About This Report
For childhood illnesses associated with environmental contaminants, the report presents

measures of asthma and other respiratory conditions, childhood cancer, and neurodevelopmental disorders. The best available data to assess the frequency of these illnesses in children were selected, with measures structured to portray changes over time, where possible.

In cases where data are not available for a sufficient number of years, measures are

structured as snapshots; in future editions EPA expects to have data that can be used to

portray trends for those measures.

In the special features section, the report presents measures that reflect important aspects

of children’s environmental health for which data were not available at the national

level. These were chosen based on recommendations from peer reviewers and others. 

America’s Children and the Environment is intended to convey information about trends

in children’s environmental health in the United States. The key measures presented in

this report are based on the best available data to provide the most complete picture

possible at this time. There are certain data limitations and assumptions in some of the

measures, resulting in a degree of uncertainty for certain key measures and trends. As

data and methods improve, we aim to develop increasingly reliable indicators of children’s environmental health.

The America’s Children and the Environment report, and the key measures used in the

report, should not be construed as a definitive basis for planning specific policies or

projects. Other technical information also will be used to inform the activities of EPA

and other federal agencies concerning children’s environmental health. Emerging and

ongoing research will help shape these activities for years to come.

What are the sources for the data in this report?

Federal agencies provided the data for most of the measures. The data on environmental

contaminants generally are from data systems maintained by EPA and by state environmental agencies. Data on contaminants in blood and on respiratory diseases and

neurodevelopmental disorders are from the National Center for Health Statistics in the

Centers for Disease Control and Prevention. Cancer data are from the National Cancer

Institute. Population data from the Census Bureau were used to calculate the number

of children potentially exposed to environmental contaminants.

Data for the special features section are from the states of California and Minnesota. The

data on lead in schools are from a survey of schools in California. The data on pesticide

use in schools are from a survey of Minnesota schools. The data on birth defects are from

California’s birth defects monitoring program.

Detailed descriptions of the data sources are in Appendix B.

What groups of children are included in this report?

Most of the measures include all children in the United States under the age of 18,

representing approximately 72 million individuals based on the 2000 census. Exceptions

are noted in Appendix B.

In response to suggestions from peer reviewers, the report presents (where possible)

measures for groups of children of different races and ethnicities and for children living

in households with various levels of income. In some cases, these breakouts by race/ethnicity and family income are shown in the graphs, while in other cases they are included in the data tables found in Appendix A.

8 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

About This Report
The report uses five categories of race or ethnicity: White non-Hispanic, Black nonHispanic, Hispanic, American Indian/Alaska Native, and Asian or Pacific Islander. In

many cases, the data were insufficient to present results for the latter two categories.

The report uses three categories of family income: 1) below the poverty level (shown in

graphs and tables as < Poverty Level), 2) between the poverty level and twice the poverty

level (100-200% of Poverty Level), and 3) more than twice the poverty level (> 200%

of Poverty Level). “Poverty level” is defined by the federal government and is based on

income thresholds that vary by family size and composition. The category of incomes

between the poverty level and twice the poverty level represents households that have

relatively low incomes but are not below the officially defined poverty level. This category

frequently is used by the Centers for Disease Control and Prevention in its reporting of

health data and was recommended by peer reviewers for use in this report.

What years are included in this report?

The report includes data for each year from 1990 through 2000 whenever possible. In

many cases, data were available for only some of these years. In other cases, data available

before 1990 or after 2000 were included to provide an expanded depiction of trends.

Is this report available online?

This report is available at www.epa.gov/envirohealth/children. In addition, the Web site

includes links to other information on children’s environmental health, additional data

tables, information by state where such data are available, and references.

How does the information in America’s Children and the Environment

differ from what is proposed to be included in EPA’s forthcoming Report on

the Environment?

EPA is developing a report on the state of the environment in the United States, scheduled for publication in 2003. The Report on the Environment is intended to be a broadbased collection of national data depicting progress in addressing environmental problems and identifying remaining challenges. America’s Children and the Environment

focuses more specifically on data related to children and their related environmental

conditions. Both America’s Children and the Environment and the forthcoming Report on

the Environment rely on existing national data to describe current conditions and trends.

The forthcoming Report on the Environment will address a broader set of environmental

conditions and human health concerns. The Report on the Environment will be organized around five theme areas: 1) human health, 2) ecological health, 3) air, 4) water, and

5) land. America’s Children and the Environment is organized into three main sections: 

1) environmental contaminants, 2) body burdens, and 3) childhood health. A fourth

section of special features presents important measures for which data are available

from individual states but not for the nation.

What is the Office of Children’s Health Protection at EPA?

The Office of Children’s Health Protection (OCHP) supports and facilitates EPA’s efforts

to protect children from environmental threats. OCHP’s mission is to make the protection

of children’s health a fundamental goal of public health and environmental protection in

the United States. OCHP reviews EPA proposals for their impact on children and funds

work designed to improve the protection of children from environmental hazards.

About This Report 9

About This Report
What are the Office of Policy, Economics, and Innovation and the 

National Center for Environmental Economics at EPA?

The Office of Policy, Economics, and Innovation develops new approaches and provides

analysis to enable EPA to better address emerging environmental challenges. The office

addresses cross-cutting environmental management strategies, identifies emerging issues,

and serves as a catalyst for testing and institutionalizing integrative approaches to 

environmental protection. 

Within the Office of Policy, Economics, and Innovation, EPA’s National Center for

Environmental Economics (NCEE) provides economic and health analysis of important environmental issues for the regulatory and policy process. NCEE also conducts

research that will improve our current understanding of the impacts of environmental

contaminants on public health. NCEE’s staff includes specialists in air, water, solid

waste, cross-media economics, and children’s health risks. The center’s health scientists

emphasize new methods for assessing previously unidentified risks, assessing relationships

between exposures and disease, and developing tools to communicate this information

to the public.

10 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

About This Report
Key Findings 11

Key Findings

Outdoor Air Pollutants

■ In 1990, approximately 23 percent of children lived in counties in which the 

one-hour ozone standard was exceeded on at least one day per year. In 2001,

approximately 15 percent of children lived in such counties. This value fluctuated

during the intervening years, ranging from 13 to 28 percent. (Page 23)

■ In 1996-2001, significantly more children lived in counties that exceeded the eight-hour

ozone standard than in counties that exceeded the one-hour standard. In 2001, nearly

40 percent of children lived in counties that exceeded the eight-hour standard. (Page 23)

■ In 2000, approximately 27 percent of children lived in counties that exceeded the

PM-2.5 particulate matter standard. In 2001, approximately 25 percent of children

lived in such counties. (Page 23)

■ The percentage of days that were designated as having “unhealthy” air quality

(including days that were unhealthy for everyone as well as those that were

unhealthy for sensitive groups) decreased between 1990 and 1999, dropping 

from 3 percent in 1990 to less than 1 percent in 1999. The percentage of days

with “moderate” air quality remained around 20 percent between 1990 and 1999,

although an upward trend is suggested by the fact that the percentage of moderate

air quality days was higher in 1999 than for any other year in this analysis. (Page 25)

■ In 1990, on average, children were exposed to 31.9 micrograms per cubic meter 

of PM-10, which represents 64 percent of the standard for the year. By 1995, the

concentration had fallen to 54 percent of the standard, and it has remained at about

that level since. (Page 27)

■ In 2000, about 1 million children experienced an average PM-10 concentration

above the annual standard, down from about 2 million in 1990. (Page 28)

■ In 1996, all children lived in counties in which the combined estimated concentrations

of hazardous air pollutants exceeded the 1-in-100,000 cancer risk benchmark.

Approximately 95 percent of children lived in counties in which at least one hazardous

air pollutant exceeded the benchmark for health effects other than cancer. (Page 31)

Indoor Air Pollutants

■ The percentage of homes with children under 7 in which someone smokes on a

regular basis decreased from 29 percent in 1994 to 19 percent in 1999. (Page 33)

Drinking Water Contaminants

■ The percentage of children served by public water systems that reported exceeding a

Maximum Contaminant Level or violated a treatment standard decreased from 20

percent in 1993 to 8 percent in 1999. Every category of violation decreased between

1993 and 1999 except for nitrates and nitrites, which remained steady. (Page 37)

■ In 1993, approximately 22 percent of children lived in an area served by a public

water system that had at least one major monitoring and reporting violation. This

figure decreased to about 10 percent in 1999. The largest number of monitoring

and reporting violations occurred for the lead and copper standards. (Page 39)

Part 1: Environmental

Contaminants
Pesticide Residues

■ From 1994 to 2001, the percentage of food samples with detectable organophosphate

pesticide residues ranged between 19 percent and 29 percent. The highest detection

rates were observed during 1996 and 1997, while the lowest detection rate was

observed in 2001. (Page 41)

Land Contaminants

■ As of September 2000, about 0.8 percent of children lived within one mile of a

Superfund site listed on the National Priorities List (NPL) that had not yet been

cleaned up or controlled, down from about 1.3 percent in 1990. As of September

2000, about 1.3 percent of children lived within one mile of any Superfund site

listed on the Superfund NPL. (Page 43)

Concentrations of Lead in Blood

■ The median (50th percentile) concentration of lead in the blood of children 5 years

old and under dropped from 15 micrograms per deciliter (μg/dL) in 1976-1980 to

2.2 μg/dL in 1999-2000, a decline of 85 percent. (Page 55)

■ The concentration of lead in blood at the 90th percentile in children 5 years old and

under, representing the most highly exposed 10 percent of children in that age group,

dropped from 25 μg/dL in 1976-1980 to 4.8 μg/dL in 1999-2000. (Page 55)

■ Concentrations of lead in children’s blood differ by race/ethnicity and family income.

In 1999-2000, the median blood lead level in children ages 1-5 was 2.2 μg/dL. The

median blood lead level for children living in families with incomes below the poverty

level was 2.8 μg/dL and for children living in families above the poverty level it was

1.9 μg/dL. For all income levels, Black non-Hispanic children had a median blood

lead level of 2.8 μg/dL. White non-Hispanic children had a median blood lead level

of 2.1 μg/dL and Hispanic children had a median blood level of 2.0 μg/dL. (Page 57)

■ Approximately 300,000 children ages 1-5 (about 2 percent) had a blood lead level

of 10 μg/dL or greater in 1999-2000. (Page 59)

Concentrations of Mercury in Blood

■ EPA has determined that children born to women with blood concentrations above

5.8 parts per billion are at some increased risk of adverse health effects. About 8 percent

of women of child-bearing age had at least 5.8 parts per billion of mercury in their

blood in 1999-2000. (Page 61)

Concentrations of Cotinine in Blood

■ Cotinine is a marker of exposure to environmental tobacco smoke. In 1999-2000,

median (50th percentile) levels of cotinine measured in children were 56 percent lower

than they were in 1988-1991. Cotinine values at the 90th percentile, representing the

most highly exposed 10 percent of children, declined by 18 percent between 1988-

91 and 1999-2000. (Page 63)

12 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Key Findings

Part 2: Body Burdens
Respiratory Diseases

■ Between 1980 and 1995, the percentage of children with asthma doubled, rising

from 3.6 percent in 1980 to 7.5 percent in 1995. A decrease in the percentage of

children with asthma occurred between 1995 and 1996, but interpreting single-year

changes is difficult. (Page 71)

■ In 2001, 8.7 percent (6.3 million) of all children had asthma. (Page 71)

■ The percentage of children with asthma differs by race/ethnicity and family income.

In 1997-2000, more than 8 percent of Black non-Hispanic children living in families

with incomes below the poverty level had an asthma attack in the previous 12 months.

Approximately 6 percent of White non-Hispanic children and 5 percent of Hispanic

children living in families with incomes below the poverty level had an asthma attack

in the previous 12 months. (Page 73)

■ More than 6 percent of children living in families with incomes below the poverty

level had an asthma attack in the previous 12 months. About 5 percent of children

living in families with incomes at the poverty level and higher had an asthma attack

in the previous 12 months. (Page 73)

■ Emergency room visits for asthma and other respiratory causes were 369 per 10,000

children in 1992 and 379 per 10,000 children in 1999. (Page 75)

■ Hospital admissions for asthma and other respiratory causes were 55 per 10,000

children in 1980 and 66 per 10,000 children in 1999. (Page 77)

Childhood Cancer

■ The frequency of new childhood cancer cases has been fairly stable since 1990. The

age-adjusted annual incidence of cancer in children increased from 128 to 161 cases

per million children between 1975 and 1998. Cancer mortality decreased from 51

to 28 deaths per million children during the 1975-1998 period. (Page 79)

■ Leukemia was the most common cancer diagnosis for children from 1973-1998,

representing about 20 percent of the total childhood cancer cases. Incidence of

acute lymphoblastic leukemia was 24 cases per million in 1974-1978 and

approximately 28 cases per million in 1994-1998. Incidence of acute myeloid

leukemia was approximately 5 cases per million in 1974-98 and about the same 

in 1994-98. (Page 81)

Neurodevelopmental Disorders

■ In 1997-2000, about 6 children out of every 1,000 (0.6 percent) were reported to

have been diagnosed with mental retardation. (Page 87)

Key Findings 13

Part 3: Childhood

Illnesses

Key Findings
Mercury in Fish

■ Since 1995, most states have issued one or more advisories to warn people about

elevated concentrations of mercury in non-commercial fish. In some cases, advisories

tell people to avoid eating fish that they catch in particular areas or to avoid particular

species. In other cases, they tell people to limit the amount of fish that they consume.

Some advisories are directed at particularly susceptible groups, usually women of

child-bearing age and children. (Page 96)

Attention-Deficit/Hyperactivity Disorder

■ In 1997-2000, 6.7 percent of children ages 5-17 were reported to have been

diagnosed with attention-deficit/hyperactivity disorder (ADHD). (Page 99)

Lead in California Schools

■ Thirty-two percent of all public elementary schools surveyed in California had both

lead-based paint and some deterioration of paint. (Page 107)

■ Eighty-nine percent of all California schools studied had detectable levels of lead in

soils. Only 7 percent of the schools had lead levels in soil at or exceeding the EPA

hazard standard. (Page 109)

■ Approximately 15 percent of schools had lead levels in drinking water that exceeded

EPA’s drinking water standard on the first draw. Drinking water from approximately

6.5 percent of schools remained above the standard on the second draw. Second

draw samples are more representative of the lead concentrations that children are

exposed to during most of the day. (Page 111)

Pesticides in Minnesota Schools

■ Approximately 47 percent of responding school custodians in Minnesota reported

that they sprayed pesticides “as needed” in the classroom. Forty percent of the

responding custodians reported that their schools provided no notification of

pesticide use (such as notices in fumigated areas or pre- and postapplication letters to

students and teachers). (Page 115)

Birth Defects in California

■ Heart defects are the most common birth defect in California, with 1.8 cases per

1,000 live births in 1997-99. The rates of birth defects in California generally

remained constant during the 1990s. (Page 117)

14 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Key Findings

Part 5: Special Features

Part 4: Emerging Issues
Summary List of Measures 15

Summary List of Measures

Summary List of Measures Included in this Report

Name Description of Measure Year(s)

Environmental Contaminants

Outdoor Air Pollutants

Common Air Pollutants Percentage of children living in counties in which 1990-2001

air quality standards were exceeded

Percentage of children’s days with good, moderate, or 1990-1999

unhealthy air quality

Long-term trends in annual average concentrations of 1990-2000

criteria pollutants

Number of children living in counties with high annual 1990-2000

averages of PM-10

Hazardous Air Pollutants Percentage of children living in counties where estimated 1996

hazardous air pollutant concentrations were greater than 

health benchmarks

Indoor Air Pollutants

Environmental Tobacco Smoke Percentage of homes with children under 7 where 1994-1999

someone smokes regularly

Drinking Water Contaminants

Drinking Water Contaminants Percentage of children living in areas served by public 1993-1999

water systems that exceeded a drinking water standard 

or violated treatment requirements

Monitoring and Reporting Percentage of children living in areas with major violations 1993-1999

of drinking water monitoring and reporting requirements

Pesticide Residues Percentage of fruits, vegetables, and grains with 1994-2001

detectable residues of organophosphate pesticides

Land Contaminants Percentage of children residing within one mile of a 1990-2000

Superfund site

Body Burdens

Concentrations of Lead in Blood Concentration of lead in blood of children ages 1976-2000

5 and under

Median concentrations of lead in blood of children 1999-2000

ages 1-5, by race/ethnicity and family income

Distribution of concentrations of lead in blood 1999-2000

of children ages 1-5

Concentrations of Mercury in Blood Distribution of concentrations of mercury in blood 1999-2000

of women of child-bearing age

Concentrations of Cotinine in Blood Concentrations of cotinine in blood of children 1988-2000
Name Description of Measure Year(s)

Childhood Illnesses

Respiratory Diseases Percentage of children with asthma 1980-2001

Percentage of children having an asthma attack 1997-2000

in the previous 12 months, by race/ethnicity and 

family income

Children’s emergency room visits for asthma and 1992-1999

other respiratory causes

Children’s hospital admissions for asthma and other 1980-1999

respiratory causes

Childhood Cancer Cancer incidence and mortality for children under 20 1975-1998

Cancer incidence for children under 20 by type 1974-1998

Neurodevelopmental Disorders Children reported to have mental retardation, 1997-2000

by race/ethnicity and family income

Special Features

Lead in California Schools Percentage of California public elementary schools with 1994-1997

lead paint and some deterioration of paint

Percentage of California public elementary schools with 1994-1997

lead in soils

Percentage of California public elementary schools with 1994-1997

lead in drinking water

Pesticide Use in Minnesota Schools Frequency of application of pesticides in Minnesota 1999

K-12 schools

Birth Defects in California Number of birth defects in California per 1,000 live 1991-1999

births and fetal deaths

16 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Summary List of Measures
PART I

Environmental 

Contaminants
18 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Environmental Contaminants

racking environmental contaminants is an important step toward determining

whether environmental policies protect children. This section of the report presents information about environmental contaminants that can affect children and discusses how levels of these contaminants in the environment have changed over time.

Pollutants or contaminants that can affect the health of children can be found in air,

water, food, and soil. This section includes measures for contaminants in these media.

Most of the measures show the percentages of children who may be at risk from exposure to critical concentrations of pollutants.

This second edition of America’s Children and the Environment includes several new

measures that reflect pollutants in environmental media.

The report adds a new measure that describes trends in long-term concentrations of

pollutants in the air. This measure builds on the report’s first two measures for air pollution, which reflect daily exposures to air pollutants. Research suggests that exposure

to a few days of high concentrations of air pollutants or to many days of lower concentrations both can have adverse effects on health. The report also includes a new measure concerning pesticide residues in foods.

Describing the significance of pollutants in soils is a difficult problem because contamination often is localized and difficult to capture in a national report. To improve coverage

of contaminants in soil, this report replaces an earlier measure that showed the percentages

of children living in counties with a Superfund site with a new measure showing the

percentage of children who live within a mile of a Superfund site.

This report does not assess quantitative relationships between the measures for environmental contaminants and childhood illnesses. The report includes a qualitative discussion of the research that has looked at some of these relationships. 

The measures in this section do not account for many environmental contaminants that

are important for children but lack nationally representative data. Such contaminants

include those in dusts and soils in and near homes, and contaminants in soil from

sources other than Superfund sites. The measure on food contaminants addresses only

a few of the contaminants found in foods: selected pesticides used on certain items of

produce. The measure does not account for pathways, other than the diet, by which

children are exposed to pesticides. For example, pesticides may be transported into

homes from outdoors or from the workplace on skin, clothing, or shoes. Children then

may ingest pesticides when they put their hands in their mouths after touching contaminated surfaces or when they put objects in their mouths that have been contaminated

with pesticides.

The data used to develop the measures within this section vary in coverage and 

completeness, as summarized in the chart on the next page.

Environmental

Contaminants

T
Part 1: Environmental Contaminants 19

Environmental Contaminants

Coverage of Environmental Contaminant Measures

Description Geographic 

Topic of Measure Year(s) Coverage Notes

Outdoor Air Pollutants

Common Air E1: Percentage of children living 1990-2001 County-level Measure includes five common 

Pollutants in counties in which air quality data (criteria) air pollutants. Many counties 

standards were exceeded monitored only some common air 

pollutants and some counties did not 

monitor any.

E2: Percentage of children’s days 1990-1999 County-level Measure includes five common air 

with good, moderate, or unhealthy data pollutants.

air quality

E3: Long-term trends in annual 1999-2000 County-level Measure includes three common air 

average concentrations of criteria data pollutants.

pollutants

Hazardous Air E4: Percentage of children living in 1996 County-level Data for one year only; measure 

Pollutants counties where estimated hazardous data is based on estimates of ambient 

air pollutant concentrations were concentrations of 33 of the 

greater than health benchmarks 188 hazardous air pollutants 

in 1996 identified in the Clean Air Act.

Indoor Air Pollutants

Environmental E5: Percentage of homes with 1994-1999 National-level Measure is a surrogate for environTobacco Smoke children under 7 where someone data mental tobacco smoke in the home. 

smokes regularly Other indoor pollutants (e.g., 

combustion products, volatile organic 

compounds) would be relevant to 

include if data could be identified.

Drinking Water Contaminants

Drinking Water E6: Percentage of children living in 1993-1999 County-level Data on violations of standards are 

Contaminants areas served by public water systems data incomplete due to monitoring and 

that exceeded a drinking water reporting limitations. Measure is a 

standard or violated treatment surrogate for concentrations of 

requirements contaminants.

Monitoring and E7: Percentage of children living in 1993-1999 County-level Measure shows percentage of 

Reporting areas with major violations of data children living in areas where no

drinking water monitoring and information on drinking water 

reporting requirements contaminants is available; children 

may or may not be at risk.

Food Contaminants

Pesticide Residues E8: Percentage of fruits, vegetables, 1994-2001 National-level Surrogate for dietary exposure to 

and grains with detectable residues data residues of organophosphate pesticides. 

of organophosphate pesticides Other contaminants in food, such as 

other pesticides and industrial 

chemicals that are relevant to children, are not included.

Land Contaminants

Hazardous E9: Percentage of children 1990-2000 Site-specific Does not reflect exposures from sites 

Waste Sites residing within one mile of locations that may be hazardous but are not 

a Superfund site included on the Superfund National 

Priorities List. Proximity to a Superfund 

site does not necessarily indicate that 

children are exposed to contaminants.
20 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Outdoor Air Pollutants

Air pollution contributes to a wide variety of adverse health effects. Six of the most

common air pollutants—carbon monoxide, lead, ground-level ozone, particulate matter,

nitrogen dioxide, and sulfur dioxide—are known as “criteria” pollutants because EPA

uses health-based criteria as the basis for setting permissible levels of these pollutants in

the atmosphere.

EPA periodically conducts comprehensive reviews of the scientific literature on health

effects associated with exposure to the criteria air pollutants. The resulting “criteria

documents” critically assess the scientific literature and serve as the basis for making

regulatory decisions about whether to retain or revise the National Ambient Air Quality

Standards (NAAQS) that specify the allowable concentrations of each of these pollutants

in the air. The standards are set at a level that protects public health with an adequate

margin of safety. However, the standards are not “risk free.” Even in areas that meet the

standards, there may be days when unusually sensitive individuals, including children,

experience health effects related to air pollution. This is especially the case for pollutants

such as ozone and particulate matter that do not have discernible thresholds below

which health effects are absent.

Some of the standards are designed to protect the public from adverse health effects

that can occur after being exposed for a short time, such as one hour or one day. Other

standards are designed to protect people from health effects that can occur after being

exposed for a much longer time, such as a year. For example, current standards for carbon monoxide are for short-term periods of one hour and eight hours. By contrast, the

current standard for nitrogen dioxide is for one year. The standards and the varying

time periods for which they apply are shown in Table 1 in Appendix B. Some pollutants have both short-term and long-term standards. 

Health effects that have been associated with each of these pollutants are summarized

below. This information is drawn from EPA’s criteria documents as well as more recent

studies.

Ground-level Ozone

Short-term (also known as “acute”) exposure to ground-level ozone can cause a variety

of respiratory health effects, including inflammation of the lung, reduced lung function, and respiratory symptoms such as cough, chest pain, and shortness of breath. It

also can decrease the capacity to perform exercise.1 Exposure to ambient concentrations

of ozone also has been associated with the exacerbation of asthma, bronchitis, and respiratory effects serious enough to require emergency room visits and hospital admissions.1 Some evidence suggests that high ozone concentrations may contribute to

increased mortality.1

Health effects associated with long-term (also known as “chronic”) exposure to ozone

are not as well established and documented as health effects associated with short-term

exposure, but long-term exposures also are of concern. In 1996, EPA’s criteria document for ozone concluded that there was insufficient evidence to determine whether

health effects resulted directly from long-term exposure, although the evidence suggested that long-term ozone exposure, along with other environmental factors, could be

responsible for health effects.1 Since 1996, a few studies suggest that long-term exposure

to ozone is associated with decreases in lung function in humans,2 increased prevalence

of asthma,3 increased development of asthma in children who exercise outdoors,4 and

exacerbation of existing asthma.5

Common (“Criteria”)

Air Pollutants
Part 1: Environmental Contaminants 21

Outdoor Air Pollutants

Particulate Matter

Particulate matter in the air (often called PM-10 or PM-2.5) has been found to cause

increased risk of mortality (death), hospital admissions and emergency room visits for

heart and lung diseases, respiratory effects, and decreases in lung function.6 Such health

effects have been associated with both short-term and long-term exposure to particulate

matter. Children and adults with asthma are considered to be among the groups most

sensitive to respiratory effects.6-10 Studies published since the release of EPA’s criteria

document for particulate matter have found further evidence of an association between

particulate matter and increased respiratory disease and symptoms in children with

asthma11 and increased hospitalizations or emergency room visits for persons with asthma.5, 12, 13 Studies also have confirmed that chronic exposure to particulate matter is

associated with mortality in adults14-16 and suggest that it may be associated with mortality in infants.17 Also, recent studies suggest that chronic exposure to particulate matter

may affect lung function and growth.18, 19 

Prior to 1997, the National Ambient Air Quality Standard for particulate matter was

based on particulate matter measuring 10 microns or less (PM-10). In 1997, the standard was revised to address the health risks from particulate matter measuring 2.5

microns or less (PM-2.5). 

Lead

Lead accumulates in bones, blood, and soft tissues of the body. Exposure to lead can

affect development of the central nervous system in young children, resulting in neurobehavioral effects such as lowered IQ.20

Sulfur Dioxide

Sulfur dioxide poses particular concerns for those with asthma, who are considered to be

especially susceptible to its effects.21 Short-term exposures of asthmatic individuals to elevated levels of sulfur dioxide while exercising at a moderate level may result in breathing

difficulties accompanied by symptoms such as wheezing, chest tightness, or shortness of

breath. Effects that have been associated with longer-term exposures to high concentrations

of sulfur dioxide, in conjunction with high levels of particulate matter include respiratory

illness, alterations in the lung’s defenses, and aggravation of existing cardiovascular diseases.

Carbon Monoxide

Exposure to carbon monoxide reduces the capacity of the blood to carry oxygen, thereby

decreasing the supply of oxygen to tissues and organs such as the heart. Short-term

exposure can cause effects such as reduced time to onset of angina pain, neurobehavioral

effects, and a reduction in exercise performance.22 Long-term exposure has not been

studied adequately in humans to draw conclusions regarding possible chronic effects,

though a recent study reported an association between long-term exposure to carbon

monoxide and other traffic-related pollutants and respiratory symptoms in children.23

Nitrogen Dioxide

Exposure to nitrogen dioxide has been associated with a variety of health effects.24

Effects include decreased lung function,23, 25, 26 increased respiratory symptoms or illness,7, 23, 27-29 and increased symptoms in children with asthma.11 Nitrogen dioxide also

is a major contributor to the formation of ground-level ozone.1
22 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Outdoor Air Pollutants

State agencies that monitor air quality report their findings to EPA. In turn, EPA

compares the measured values reported by states to the National Ambient Air Quality

Standards in order to determine whether pollutants exceed the established standards.

EPA uses the term “exceedance” to refer to a case in which a reported measurement of a

pollutant is higher than the standard. Appendix B includes a description of the methods

used to determine whether an exceedance has occurred. 

This measure uses EPA data on exceedances of short-term air quality standards in

counties in the United States. This data source simply indicates whether each standard

was exceeded at any time during a year. This measure shows the percentage of children

living in areas with any such exceedances, who thus may be exposed to poor daily air

quality at some point during a year. In addition, the measure includes exceedances of

the new ozone and particulate matter standards adopted in 1997. The ozone standard

is based on an eight-hour average ozone value. The new particulate matter standards are

for PM-2.5 and have both annual and 24-hour averaging periods. The annual PM-2.5

standard is intended to protect against both short-term and long-term health effects.

This measure does not differentiate between areas in which standards are exceeded frequently or by a large margin, and areas in which standards are exceeded only rarely or by

a small margin. The measure is based on exceedances of individual standards and does

not reflect any combined effect of multiple pollutants. Also, because the nature of health

effects varies significantly and the averaging times associated with different standards

vary widely, exceedances for different standards are not comparable. For example, the

ozone standard considers measured levels of ozone within a one-hour or eight-hour period

and health effects such as lung function decrements, respiratory symptoms, and hospital

admissions. In contrast, the averaging time for the lead standard is three months and is

based on health effects such as IQ decrements and hypertension. 

The graph shows the percentage of children who live in counties with exceedances for

any of four of the six criteria pollutants. Nitrogen dioxide is not included, as there is no

short-term standard for this compound. Sulfur dioxide also is not shown, since few

exceedances have been reported since 1993.

Exceedances of ShortTerm Air Quality

Standards

Healthy People 2010: Objective 8-01 of Healthy People 2010 aims to reduce 

the proportion of persons exposed to air that exceeds the levels of 

U.S. Environmental Protection Agency’s health-based standards for 

harmful air pollutants. See Appendix C for more information.
Part 1: Environmental Contaminants 23

Outdoor Air Pollutants

■ The highest number of exceedances is consistently reported

for ozone. In 1990, approximately 23 percent of children

lived in counties in which the one-hour ozone standard

was exceeded on at least one day per year. In 2001,

approximately 15 percent of children lived in such counties. Exceedances of the eight-hour ozone standard are

reported beginning in 1996. In 1996-2001, significantly

more children lived in counties that exceeded the eighthour ozone standard than in counties that exceeded the

one-hour standard.

■ In 2000, approximately 27 percent of children lived in

counties that exceeded the annual PM-2.5 standard. In

2001, approximately 25 percent of children lived in such

counties. (The standard is intended to protect against

both short-term and long-term health effects and thus

PM-2.5 is included in Measure E1.)

■ In 1990, approximately 10 percent of children lived in

counties in which the carbon monoxide standard was 

exceeded. In 2001, approximately 0.2 percent of

children lived in such counties.

■ From 1990 to 2001, the percentage of children living in

counties that exceeded the one-day standard for PM-10

fluctuated, but was as high as 10 percent in 1992 and

1995. The percentage remained around 2 to 3 percent

from 1996-2001.

■ Since 1992, on average, 2 percent of children lived in

counties that exceeded the three-month standard for lead.

In 2000, the three counties with reported lead exceedances

were Madison County, Illinois; Jefferson County,

Missouri; and Dallas County, Texas.

■ Few exceedances of the sulfur dioxide standard have

occurred since 1993. Consequently, it was not included

on the graph.

Measure E1

Percentage of children living in counties in which air quality standards were exceeded 

1990 1992 1994 1996 1998 2000 2001

0%

10%

20%

30%

40%

50%

Ozone

one-hour standard

Carbon

monoxide 

PM-10

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information 

Retrieval System

Lead

Ozone

 eight-hour standard

PM-2.5

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants (E1-E3) Respiratory (D1-D4)

Criteria Air Pollutants: lead (E1-E2) Lead in Blood (B1-B3) Neurodevelopmental (D7) Lead in Schools (S1-S3) Drinking Water: lead (E6-E7) 
24 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Outdoor Air Pollutants

EPA provides an Air Quality Index (AQI) that represents air quality for specific days

and is widely reported in newspapers and other media outlets in metropolitan areas.

The AQI is based on measurements of up to five of the six air quality criteria pollutants

(carbon monoxide, ground-level ozone, nitrogen dioxide, particulate matter, and sulfur

dioxide). Lead is not included in the AQI. The specific pollutants considered in the

AQI for each metropolitan area depend on which pollutants are monitored in that area.

Each pollutant concentration is given a value on a scale that is related to the air quality

standards for that pollutant. An AQI value of 100 for a criteria pollutant generally corresponds to the short-term National Ambient Air Quality Standard for that pollutant,

and is the level EPA has set to protect public health for a single day. Above this level,

pollutant-specific health advisories are issued. The daily AQI is based on the pollutant

with the highest index value on the scale that day. It does not add up values for more

than one pollutant. Therefore, it does not reflect the possible effects of simultaneous

exposure to high levels of multiple pollutants.

EPA has divided the AQI scale into categories. Air quality is considered “good” if the

AQI is between 0 and 50, posing little or no risk. Air quality is considered “moderate”

if the AQI is between 51 and 100. Some pollutants at this level may present a moderate health concern for a small number of individuals. Moreover, such a level may pose

health risks if maintained over many days. Air quality is considered “unhealthy for sensitive groups” if the AQI is between 101 and 150. Members of sensitive groups such as

children may experience health effects, but the general population is unlikely to be

affected. Air quality is considered “unhealthy” if the AQI is between 151 and 200. The

general population may begin to experience health effects, and members of sensitive

groups may experience more serious health effects.

Measure E2 on the following page is based on the reported AQI for counties of the

United States. (Not all counties have air quality monitoring stations.) This measure was

developed by reviewing the air quality designation for each day for each county and

weighting the daily designations by the number of children living in each county. The

overall measure reports the percentage of children’s days of exposure considered to be of

good, moderate, or unhealthy air quality.

The advantage of this approach, compared with that used in measure E1, is that it provides a sense of the intensity of pollution over the course of a year. This method provides data on the air quality category for each day, rather than simply reporting

whether a county ever exceeds any standard for any pollutant. However, the method

has some limitations. The AQI is based on the single pollutant with the highest value

for each day; it does not reflect any combined effect of multiple pollutants. It reflects

only short-term, daily pollution burdens. It does not include lead. The approach is

influenced by the frequency of measurements. Because the AQI is reported daily, pollutants that are measured daily—such as ozone—will appear to have more effect than

those that are measured less frequently, such as PM-10, which typically is measured

every six days. Also, the AQI is not well-suited for reporting concentrations of nitrogen

dioxide, because this pollutant does not have a short-term standard.

Daily Air Quality
Part 1: Environmental Contaminants 25

Outdoor Air Pollutants

■ The percentage of days that were designated as having

“unhealthy” air quality (including days that were unhealthy

for everyone as well as those that were unhealthy for

sensitive groups) decreased between 1990 and 1999,

dropping from 3 percent in 1990 to less than 1 percent in

1999. The percentage of days with “moderate” air quality

remained around 20 percent between 1990 and 1999,

although an upward trend is suggested by the fact that the

percentage of moderate air quality days was higher in 1999

than for any other year in this analysis. As the percentage

of either unhealthy or good air days decreases, the

percentage of moderate days would be expected to increase.

■ The coverage of monitoring for this measure, in terms

of area and percentage of days monitored, was largely

unchanged between 1990 and 1999. Approximately 30

percent of children’s days of exposure to air pollutants

were not monitored. This percentage includes days for

which no AQI was reported in counties where the AQI is

sometimes reported, as well as counties in which the AQI

is not reported at all. On days that were monitored, in

many cases only one or a few pollutants were monitored.

Measure E2

Percentage of children's days with good, moderate, or

unhealthy air quality

1990 1992 1994 1996 1998 1999

0%

10%

20%

30%

40%

50%

60%

Good

Moderate

No Monitoring Data

Unhealthy

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric

Information Retrieval System 

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants (E1-E3) Respiratory (D1-D4)
26 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Outdoor Air Pollutants

Most measures used to describe air pollution focus on days when pollutant levels are

high. This approach is appropriate because high pollution levels over short periods of

time, even less than a day, can contribute to many adverse health effects.1

Accumulated exposures to criteria air pollutants over longer periods of time also may

affect health. As it has for short-term exposures, EPA has set standards for longer time

periods for some pollutants. The concentrations of air pollutants in the long-term air

pollution standards established by EPA are not “risk-free.” Even in areas that meet the

standards, unusually sensitive individuals, including children, may experience health

effects related to air pollution. This is especially true for pollutants, such as particulate

matter, that do not have discernible thresholds below which health effects are absent.

Comparisons of pollutant concentrations with longer-term air quality standards can

help identify the pollutants that pose the greatest concerns. Such comparisons can provide a perspective on whether pollutants pose equal or different levels of concern with

regard to long-term exposure. 

Measure E3a presents trends in the long-term exposures of children to three of the six

criteria pollutants that have long-term standards: particulate matter, sulfur dioxide, and

nitrogen dioxide. This measure reflects annual averages of pollutants. It shows how the

average exposure of children compares with the applicable long-term National Ambient Air

Quality Standard, and how the long-term exposure has changed over the last several years.

The values shown in Measure E3a are all based on standards for individual pollutants,

and do not reflect any combined effect of multiple pollutants. For nitrogen dioxide and

sulfur dioxide, data are available only for 1996-1999. For PM-10, data are available for

1990-2000. EPA adopted a new standard for PM-2.5 (finer particles) in 1997, but several years of data on PM-2.5 were not available for this report. 

Measure E3b shows the number of children living in counties where long-term standards

for PM-10 have been exceeded. Exposure to particulate matter has increasingly been

recognized as a health concern. Health effects have been documented at concentrations

that are experienced in the United States today. 

In addition, as noted above, research suggests that there is no “safe” level of particulate

matter and that any exposure poses some risk.6 It is therefore valuable to track the

number of children who live in counties where particulate matter concentrations, while

not exceeding the standard, are relatively high. Measure E3b provides additional perspective on the concentrations of PM-10 to which children are exposed, by showing

the number of children who live in counties that exceed 80 percent of the long-term

standard. This is a somewhat arbitrary cutoff, as a different value (such as 90 percent or

75 percent) could have been chosen. However, the measure does provide an indication

of the percentage of children who are living in areas where measured concentrations are

fairly close to the standard and are of interest for tracking purposes. 

Long-Term Exposure to

Criteria Air Pollutants
Part 1: Environmental Contaminants 27

Outdoor Air Pollutants

■ In 1990, on average, children experienced a concentration

of 31.9 μg/m3 of PM-10, which represents 64 percent

of the standard for the year. By 1995, the concentration

had fallen to 54 percent of the standard, and it has

remained at about that level since. From 1990-2000,

between 55 and 66 percent of children lived in counties

with monitoring stations for PM-10.

■ In 1996, on average, children experienced a concentration

of 0.02 parts per million of nitrogen dioxide, which

represents 37 percent of the standard for the year. By

1999, this percentage had fallen to 34 percent of the

standard on average. During these years, between 45

and 47 percent of children lived in counties with

monitoring stations for nitrogen dioxide.

■ In 1996, on average, children living in counties with

monitoring stations experienced a concentration of

0.002 parts per million of sulfur dioxide, which represents

6.5 percent of the standard for the year. By 1999, this

percentage had fallen to 5.2 percent of the standard on

average. During these years, between 31 and 36 percent

of children lived in counties with monitoring stations 

for sulfur dioxide.

Measure E3a

Long-term trends in annual average concentrations of criteria pollutants 

1990 1992 1994 1996 1998 2000

0%

10%

20%

30%

40%

50%

60%

70%

Sulfur dioxide, percent 

of annual standard 

PM-10, percent

of annual standard 

Nitrogen dioxide, 

percent of annual standard

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information

Retrieval System

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants (E1-E3) Respiratory (D1-D4)
28 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Outdoor Air Pollutants

■ In 2000, about 1 million children experienced an

average PM-10 concentration above the annual

standard, down from about 2 million in 1990.

■ In 2000, about 2 million children experienced a relatively

high average concentration of PM-10 (greater than 80

percent of the annual standard), down from about 6

million children in 1990.

Measure E3b

Number of children living in counties with high annual averages of PM-10

1990 1992 1994 1996 1998 2000

Exceeding the 

long-term standard 

Exceeding 80 percent of the long-term standard

Number of children (millions)

1

2

3

4

5

6

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information 

Retrieval System

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants (E1-E3) Respiratory (D1-D4)
Part 1: Environmental Contaminants 29

Outdoor Air Pollutants

Hazardous air pollutants, also known as air toxics, have been associated with a number of

adverse human health effects, including cancers, asthma and other respiratory ailments,

and neurological problems such as learning disabilities and hyperactivity.30-38

The Clean Air Act identifies 188 substances as hazardous air pollutants. Examples include

benzene, trichloroethylene, mercury, chromium, and dioxin. EPA establishes standards

for hazardous air pollutant emissions for separate source categories. Hazardous pollutants

are emitted from sources that are grouped into three general categories: major sources,

area sources, and mobile sources. Major sources typically are large industrial facilities such

as chemical manufacturing plants, refineries, and waste incinerators. These sources may

release air toxics from equipment leaks, when materials are transferred from one location

to another, or during discharge through emission stacks or vents. Area sources typically are

smaller stationary facilities such as dry cleaners. Though emissions from individual area

sources often are relatively small, collectively their emissions can be of concern—particularly

where large numbers of sources are located in heavily populated areas. Mobile sources

include both on-road sources, such as cars, light trucks, large trucks and buses, and

non-road sources such as farm and construction equipment, lawn and garden equipment,

marine engines, aircraft, and locomotives.

Unlike the criteria air pollutants, hazardous air pollutants have no national air quality

standards that can be used to construct a health-based measure. Instead, the measure

shown here compares estimates of ambient concentrations for 33 hazardous air pollutants with health benchmark concentrations derived from scientific assessments conducted by EPA and other environmental agencies.32, 38-40

Hazardous Air

Pollutants
30 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Outdoor Air Pollutants

This analysis compares ambient concentrations of hazardous air pollutants with three

health benchmark concentrations. Two benchmarks reflect potential cancer risks, at levels of 1-in-100,000 risk and 1-in-10,000 risk. If a particular hazardous air pollutant is

present in ambient air at a 1-in-100,000 benchmark concentration, for example, one

additional case of cancer would be expected in a population of 100,000 people exposed

for a lifetime. The third benchmark concentration corresponds to the level at which

exposure to the hazardous air pollutant is judged to be of minimal risk; exposures above

this benchmark may be associated with adverse health effects other than cancer.

The three benchmarks generally reflect health risks to adults, rather than potential risks

to children or risks in adulthood stemming from childhood exposure. Benchmarks are

not available to reflect the latter concerns. Further, the benchmarks reflect risks of continuous exposure over the course of a lifetime. Potential risks from very high short-term

exposures, or from elevated exposures that may be experienced during childhood, are

not addressed by these benchmarks. Therefore, this analysis does not represent a prediction of actual cancer rates in children.

The estimates of ambient concentrations of 33 air toxics for the year 1996 were generated

as part of EPA’s National Air Toxics Assessment. A computer model provided estimates

for every county in the continental United States. The computer estimates generally are

consistent with the limited set of actual measurements of ambient air toxics concentrations available for 1996, though at many locations the model estimates are lower than

the measured concentrations.

Actual exposures may differ from ambient concentrations. Indoor concentrations of

hazardous air pollutants from outdoor sources may be slightly lower than ambient concentrations, though they can be significantly higher if any indoor sources are present.

Levels of some hazardous pollutants may be substantially higher inside cars and school

buses, and those higher levels would increase the risks.

This measure only considers exposures to air toxics that occur by inhalation. For many

air toxics, dietary exposures also are important. Air toxics that are persistent in the environment settle out of the atmosphere onto land and water, and then accumulate in fish

and other animals in the food web. For hazardous air pollutants that are persistent in the

environment, exposures through food consumption typically are greater than inhalation

exposures. Hazardous air pollutants for which these food chain exposures are important

include mercury, dioxins, and PCBs.41-43

Hazardous 

Air Pollutants and

Health Benchmarks

Healthy People 2010: Objective 8-04 of Healthy People 2010 focuses on reducing emissions of

hazardous air pollutants. See Appendix C for more information.
Part 1: Environmental Contaminants 31

Outdoor Air Pollutants

■ In 1996, all children lived in counties in which the

combined estimated concentrations of hazardous air

pollutant exceeded the 1-in-100,000 cancer risk

benchmark.

■ Eighteen percent of children lived in counties in which

hazardous air pollutants combined to exceed the 1-in10,000 cancer risk benchmark. The pollutants that

contributed most to this result were formaldehyde

(mostly from mobile sources) and chromium (mostly

from chromium electroplating). Formaldehyde is

considered by EPA to be a “probable human carcinogen”

and chromium is a “known human carcinogen.”

■ Approximately 95 percent of children lived in counties

in which at least one hazardous air pollutant exceeded

the benchmark for health effects other than cancer. In

almost all cases, this result was attributable to the

pollutant acrolein, which is a respiratory irritant. More

than 75 percent of acrolein emissions are from mobile

sources such as cars, trucks, buses, planes, and

construction equipment.

■ Exposures to diesel particulate matter are not included

in this measure, because of uncertainty regarding the

appropriate values to use as cancer benchmarks. Some

studies have found that cancer risks from diesel

particulate matter exceed those of the hazardous air

pollutants considered in this measure.44 Although EPA

does not endorse any particular cancer benchmark value

for diesel particulate matter, if the State of California’s

benchmark for diesel particulate matter were used in this

analysis, 98 percent of children would live in counties

where hazardous air pollutant estimates combined to

exceed the 1-in-10,000 cancer risk benchmark.

Percentage of children living in counties where estimated hazardous air pollutant

concentrations were greater than health benchmarks in 1996

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

Measure E4

SOURCE: U.S. Environmental Protection Agency, National Air Toxics Assessment

Cancer Benchmark:

1-in-100,000

Cancer Benchmark:

1-in-10,000

Benchmark for

Other Health Effects
32 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Indoor Air Pollutants

Children can be exposed to a number of air pollutants that come from sources inside

homes, schools, and other buildings. Indoor sources include combustion sources such

as gas stoves, fireplaces, and cigarettes; building materials such as treated wood and

paints, furnishings, carpet, and fabrics; and consumer products such as sprays, pesticides, window cleaners, and laundry soap. Indoor air pollutants also can come from

outside, as air pollution penetrates indoors. Information on the toxic effects of air pollutants from indoor sources indicates that they could pose health risks to children.45, 46

Children who are exposed to environmental tobacco smoke, also known as secondhand

smoke, are at increased risk for a number of adverse health effects, including lower respiratory tract infections, bronchitis, pneumonia, fluid in the middle ear, asthma symptoms, and sudden infant death syndrome (SIDS).47-52 Exposure to environmental tobacco smoke also may be a risk factor contributing to the development of new cases of

asthma.48, 53, 54 Young children appear to be more susceptible to the effects of environmental tobacco smoke than older children are.46, 48

Smoking in the home is an important source of exposure because young children spend

most of their time at home and indoors. The measure for environmental tobacco smoke

shows the percentage of homes with children under 7 in which someone smokes regularly. Most often the smoker in the home is a parent. 

This measure is a surrogate for the exposure of children to tobacco smoke. The data

come from a national survey and are available for 1994, 1996, and 1999. The measure

reflects the percentage of homes, rather than children, although it is expected that the

two would track closely.

Environmental 

Tobacco Smoke:

Smoking in the Home

Healthy People 2010: Objective 27-9 of Healthy People 2010 is to reduce the proportion of children

who are regularly exposed to tobacco smoke at home. See Appendix C for

more information.
Part 1: Environmental Contaminants 33

Indoor Air Pollutants

■ The percentage of homes with children under 7 in

which someone smokes on a regular basis decreased

from 29 percent in 1994 to 19 percent in 1999.

■ This measure shows the percentage of homes where a

regular smoker lives. However, some percentage of these

regular smokers may not actually smoke inside the

home. The percentage of children who are exposed to

secondhand smoke in the home thus may be smaller

than suggested by the graph above.

■ In 1999, an estimated 23.5 percent of adults were

current smokers, down from 25.0 percent in 1993.55

Percentage of homes with children under 7 where someone smokes regularly

0%

5%

10%

15%

20%

25%

30%

35%

Measure E5

1994 1996 1999

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Indoor Environments 

Division, Surveys on Radon Awareness and Environmental Tobacco Issues

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Environmental Tobacco Smoke (E5) Cotinine in Blood (B5) Respiratory (D1-D4)
34 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
The contaminants in drinking water are quite varied and may cause a range of diseases

in children, including acute diseases such as gastrointestinal illness, developmental

effects such as learning disorders, and cancer.56 Children are particularly sensitive to

microbial contaminants because their immune systems are less developed than those of

most adults.56 Children are sensitive to lead, which affects brain development,58-65 and

to nitrates and nitrites, which can cause methemoglobinemia (blue baby syndrome).66-68

Fertilizer, livestock manures, and human sewage are significant contributors of nitrates

and nitrites in groundwater sources used for drinking water.69-71

EPA sets drinking water standards for public water systems, referred to as Maximum

Contaminant Levels (MCLs).72 These standards are designed to protect people against

adverse health effects from contaminants in drinking water while taking into account

the technical feasibility of meeting the standard and balancing costs and benefits. EPA

has set MCLs for more than 80 microbial contaminants, chemicals, and radionuclides.

EPA also has developed regulations to protect drinking water sources and to require

treatment of drinking water. An important treatment-related regulation, the Surface

Water Treatment Rule, requires treatment of surface waters used for drinking water by

filtration to remove microbial contaminants.

Drinking water rules often are added or modified. For example, EPA established more

stringent filter performance requirements in 1998 to further strengthen protection

against microbial contaminants. In the same year, EPA also established new drinking

water standards for disinfection byproducts, exposure to which has been associated with

bladder cancer73 and possible reproductive effects.74 In 2000, EPA finalized standards

protecting against radionuclides in drinking water.75 In addition, EPA strengthened the

existing standard for arsenic in 2001. Changes in regulatory requirements may affect

the outcome of the measures presented in this report, as the resulting trends sometimes

may be related to changes in standards rather than changes in exposures.

Contaminants in

Children’s 

Drinking Water

Part 1: Environmental Contaminants 35

Drinking Water Contaminants
36 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Drinking Water Contaminants

One way to measure children’s risk of exposure to contaminated drinking water is to

identify public water systems that contain contaminants at levels greater than those

allowed by the drinking water standards. Ideally, concentrations for all chemical and

microbial contaminants in all drinking water systems would be available for analysis

to identify areas of risk for children. Currently this is not possible. The Safe Drinking

Water Information System (SDWIS) does not track concentrations of contaminants in

drinking water, but instead tracks the frequency with which standards are exceeded. 

Public water systems are required to monitor individual contaminants at specific time

intervals to assess whether they have achieved compliance with drinking water standards.

When a violation of a drinking water standard is detected, the public water system is

required to report the violation to state and federal governments. Information about

exceedances can be used as a surrogate for exposure to unacceptably high levels of

drinking water contaminants.

The reported violations received by the federal government are highly accurate, but violations may be under-reported in some cases because some public water systems fail to

fully monitor contaminants or report their monitoring results. Data identifying public

water systems that do not monitor or report their results are available. A review of the

federal SDWIS database published in October 2000 found that 68 percent of the microbial

contaminant violations, 19 percent of violations for other contaminants, and 11 percent

of treatment and filtration violations that should be included in the SDWIS database

are reported.76 As a result of these findings, many states have taken corrective steps to

improve their SDWIS data quality.

It also is important to consider information about water sources that are not included

in the SDWIS database. Because data are only available for public water systems, this

measure does not include children served by private water sources, such as wells or bottled water. Approximately 42 million people are served by private water systems that are

not required to monitor and report the quality of drinking water.77 Many people served

by private water supplies live in rural and agricultural areas, which may be at increased

risk for nitrate and nitrite contamination. Conversely, many children served by public

water systems may not drink the tap water or may use a water filtration device to further purify the water. Thus, the measure may overestimate the percentage of children

exposed to contaminated drinking water. 

A violation of “treatment and filtration” is defined as any failure in the treatment process,

or in operation and maintenance activities, or both, that may affect water quality.78 The

Surface Water Treatment Rule specifies the type of treatment and maintenance activities

that systems must use to prevent microbial contamination of drinking water.

Exceedances of

Drinking Water

Standards

Healthy People 2010: Objective 8-05 of Healthy People 2010 seeks to increase the number of

people served by community water systems that meet the regulations of the

Safe Drinking Water Act. See Appendix C for more information.
Part 1: Environmental Contaminants 37

Drinking Water Contaminants

■ The percentage of children served by public water systems

that reported exceeding a Maximum Contaminant Level

or violated a treatment standard decreased from 20 percent

in 1993 to 8 percent in 1999.

■ Every category of reported violation decreased between

1993 and 1999 except for nitrates and nitrites, which

remained steady. The largest decline was for violations

of the treatment and filtration standards.

■ From 1993-1999, approximately 0.2 percent of the

children served by public water systems were served by

systems that reported violations of the nitrate or nitrite

standard.

■ Between 1993 and 1999, fewer than 0.2 percent of all

children served by public water systems were served by

systems that had violations of the Total Trihalomethane

(TTHM) standard. Four recent epidemiological studies

have found significant associations between elevated

TTHM exposure and stillbirth or miscarriages, but

more study is necessary before any definitive conclusion

can be made.79-86

Measure E6

Percentage of children living in areas served by public water systems

that exceeded a drinking water standard or violated treatment requirements 

1993 1994 1995 1996 1997 1998 1999

0%

5%

10%

15%

20%

25%

Any health-based violations

Treatment and filtration

Microbial

contaminants

Chemical and radiation

Lead and copper

Nitrate/nitrite

SOURCE: U.S. Environmental Protection Agency, Office of Water, Safe Drinking Water Information System

(Percentages are estimated)

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants: lead (E1-E2) Lead in Blood (B1-B3) Neurodevelopmental (D7) Lead in Schools (S1-S3) Drinking Water: lead (E6-E7)
38 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Drinking Water Contaminants

Public water systems are required to monitor for contaminants and to report violations

of drinking water standards to EPA. However, some public water systems do not conduct all of the required monitoring. Not all systems report violations. Such water systems violate monitoring and reporting requirements.

Some monitoring and reporting violations, such as late reporting, are minor. However,

many water systems have major violations. For example, some water systems fail to collect any water samples during specified monitoring periods. Children who live in areas

that are not adequately monitoring for water contaminants or reporting violations may be

at risk, but the extent of any possible exposures in violations of drinking water standards

and their associated risks is unknown.

Monitoring and

Reporting
Part 1: Environmental Contaminants 39

Drinking Water Contaminants

■ In 1993, approximately 22 percent of children lived in

an area served by a public water system that had at least

one major monitoring and reporting violation. This

figure decreased to about 10 percent in 1999. 

■ The largest number of monitoring and reporting

violations occurred for the lead and copper standards.

Approximately 11 percent of children in 1993 were

served by public water systems with monitoring and

reporting violations for lead and copper, decreasing to

about 5 percent in 1995. The number has remained

relatively constant since then.

■ The percentage of children living in areas with a major

chemical and radiation monitoring violation declined

from approximately 8 percent in 1993 to about 3

percent in 1999.

Measure E7

Percentage of children living in areas with major violations 

of drinking water monitoring and reporting requirements

1993 1994 1995 1996 1997 1998 1999

0%

5%

10%

15%

20%

25%

Any major violation

Lead and copper

Chemical

and radiation 

Microbial contaminants

Treatment and filtration

SOURCE: U.S. Environmental Protection Agency, Office of Water, Safe Drinking Water Information System 

(Percentages are estimated)

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants: lead (E1-E2) Lead in Blood (B1-B3) Neurodevelopmental (D7) Lead in Schools (S1-S3) Drinking Water: lead (E6-E7)
40 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Pesticide Residues

Children may be exposed to pesticides and other contaminants in their food and through

day-to-day activities around the home. EPA regulates the amounts of pesticides in food,

termed “residues,” through standards called “food tolerances.” A tolerance is a legal limit

on the amount of pesticide residue in a particular food. 

Children’s exposures to pesticides may be higher than the exposures of most adults.

Pound for pound, children generally eat more than adults, and they may be exposed

more heavily to certain pesticides because they consume a diet different from that of

adults.87 Among the agricultural commodities that are consumed by children in large

amounts are apples, corn, oranges, rice, and wheat.

Organophosphate pesticides frequently are applied to many of the foods important in

children’s diets, and certain organophosphate pesticide residues can be detected in small

quantities. When exposure to organophosphate pesticides is sufficiently high, they

interfere with the proper functioning of the nervous system.88 There are approximately

40 organophosphates, and as a group they account for approximately half of the insecticide use in the United States. The majority of organophosphate use is on food

crops—including corn, fruits, vegetables, and nuts. In addition, organophosphate pesticides often have been used in and around the home. Examples of organophosphate pesticides include chlorpyrifos, azinphos methyl, methyl parathion, and phosmet.

The U.S. Department of Agriculture (USDA) collects annual data on pesticide residues in

food. Among the foods sampled by the USDA’s Pesticide Data Program in recent years

are several that are important parts of children’s diets, including apples, apple juice,

bananas, carrots, green beans, orange juice, peaches, pears, potatoes, and tomatoes. 

The chart on the following page displays the percentage of food samples with

detectable organophosphate pesticide residues reported by the Pesticide Data Program

from 1994 to 2001. The 34 organophosphates that were sampled in each of these years

are included; other organophosphates that have been added to the program in recent

years are excluded so that the chart represents a consistent set of pesticides for all years

shown. This measure is a surrogate for children’s exposure to pesticides in foods: If the

frequency of detectable levels of pesticides in foods decreases, it is likely that exposures

will decrease. However, this measure does not account for many additional factors that

affect the risk to children. For example, some organophosphates pose greater risks to

children than others do, and residues on some foods may pose greater risks than

residues on other foods due to differences in amounts consumed. In addition, year-toyear changes in the percentage of samples with detectable pesticide residues may be

affected by changes in the selection of foods that are sampled each year.

In accordance with the Food Quality Protection Act (FQPA) of 1996, EPA currently is

reassessing all food tolerances to assure that they comply with the FQPA’s “reasonable

certainty of no harm” standard, with a particular focus on protecting children’s health.

EPA has concluded that a substantial portion of the existing tolerances for organophosphate pesticides meet the stringent safety standards of the FQPA and that a significant

portion of the potential exposure to organophosphate pesticides is associated with only

a small number of uses of these compounds.

Pesticide Residues on 

Foods Frequently

Consumed by Children

Healthy People 2010: Objective 8-24 of Healthy People 2010 addresses exposure to common pesticides. See Appendix C for more information.
Part 1: Environmental Contaminants 41

Pesticide Residues

■ Between 1994 and 2001, the percentage of food samples

with detectable organophosphate pesticide residues

ranged between 19 percent and 29 percent. The highest

detection rates were observed during 1996 and 1997,

while the lowest detection rate was observed in 2001. 

■ Between 1993 and 2001, the amount of organophosphate

pesticides used on foods most frequently consumed by

children declined by 44 percent, from 25 million pounds

to 14 million pounds.89

■ In 1999-2000, EPA imposed new restrictions on the

use of the organophosphate pesticides azinphos methyl,

chlorpyrifos, and methyl parathion on certain food crops

and around the home, due largely to concerns about

potential exposures of children. 

Measure E8

Percentage of fruits, vegetables, and grains with detectable residues 

of organophosphate pesticides

1994 1995 1996 1997 1998 1999 2000 2001

0%

5%

10%

15%

20%

25%

30%

35%

SOURCE: U.S. Department of Agriculture, Pesticide Data Program

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Pesticide Residues (E8) Pesticide Use in Schools (S4)
42 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Land Contaminants

Abandoned and uncontrolled hazardous waste sites may pose risks to children who play

in or near them.90, 91 These sites also may cause pollution of drinking water, ambient

air, and foods. Superfund is the federal government’s program to clean up hazardous

sites. EPA’s principal mechanism for placing sites on Superfund’s National Priorities List

(NPL) is a scoring system that uses information from initial, limited investigations to

assess the relative potential of sites to pose a threat to human health or the environment.

Sites with scores indicating a high risk potential are proposed for addition to the NPL.

EPA then accepts public comments on sites, responds to comments, and finalizes the

listing for those sites that continue to meet the requirements for addition to the list.

Sites on the NPL are studied in detail and cleaned up to the extent necessary to protect

human health and the environment. Cleanup has been completed at more than 250 of

approximately 1,500 sites to date, and EPA has removed those sites from the NPL.

From 1990-2000, 294 sites were added to the NPL. Because the addition and subtraction of sites on the NPL is a continuous process, the number of sites on the NPL

stayed relatively constant during this period. The removal of sites from the NPL indicates a decreased risk of exposure to hazardous contaminants. Conversely, the addition

of sites to the NPL in recent years does not necessarily reflect an increase in hazards to

children. Most of the newly listed sites have been contaminated for many years, many

have had exposure restrictions (e.g., fences, or partial cleanups), and their addition to

the NPL in the 1990s means only that EPA has recognized the contamination and that

the administrative processes required for listing have been completed.

Sites at which substantial cleanup work has been completed may be designated as having

reached “Construction Completion.” This means that any physical construction necessary to reduce potential exposures has been completed, and other controls are in place

to prevent exposure while final cleanup levels are being achieved. Sites with controlled

pollution sources represent a level of site remediation at which potential exposures have

been significantly reduced, although additional cleanup work remains.

Residence within a mile of a Superfund site is a surrogate measure for exposure to contaminants found at these sites. This measure covers the entire nation and includes data for

multiple years. However, residence near a hazardous waste site does not directly represent

risks of adverse health effects; the hazards posed to children may vary significantly across

the different Superfund sites. In particular, sites that have been controlled (those that

have reached Construction Completion) are less likely to pose a hazard than those that

are uncontrolled. Some children living near an uncontrolled Superfund site may have

relatively low exposure to contaminants originating from that site, while others may

have high exposure. This surrogate measure does not imply any specific relationship

between childhood illness and a child’s proximity to a Superfund site. 

This measure may underestimate the number of children living near hazardous waste

sites, since many hazardous sites are not included on the Superfund NPL. For example,

the NPL does not include contaminated sites managed by states or addressed as part of

the Resource Conservation and Recovery Act corrective action program. Also, this

measure most likely underestimates the number of children residing within one mile of

a Superfund site, as each site is represented by a single point even though many sites

are spread over large areas.

Hazardous Waste Sites

Healthy People 2010: Objective 8-12 of Healthy People 2010 addresses the mitigation of hazardous waste sites on the National Priority List. See Appendix C for more

information.
Part 1: Environmental Contaminants 43

Land Contaminants

■ As of September 2000, about 0.8 percent of children

lived within one mile of a Superfund site listed on the

National Priorities List (NPL) that had not yet been

cleaned up or controlled, down from about 1.3 percent

in 1990. As of September 2000, about 1.3 percent of

children lived within one mile of any Superfund site

listed on the Superfund NPL.

■ More than 750 out of the approximately 1,500 sites 

on Superfund’s NPL have reached Construction

Completion, indicating that potential for exposure has

been significantly reduced and controlled. For these

sites, any physical construction necessary to reduce

potential exposures has been completed, and other

controls are in place to prevent exposure while final

cleanup levels are being achieved. Final cleanup has

been completed at more than 250 of these sites and

they have been removed from the NPL. 

■ As of 2000, approximately 500,000 children lived

within one mile of a Superfund site that had been

cleaned up or controlled since 1990. 

Measure E9

Percentage of children residing within one mile of a Superfund site

1990 1992 1994 1996 1998 2000

0%

1%

2%

3%

4%

5%

All Superfund sites

All Superfund sites not yet cleaned up or controlled

SOURCE: U.S. Environmental Protection Agency, Superfund NPL Assessment Program (SNAP) Database
44 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

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Part 1: Environmental Contaminants 45

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46 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

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36. H. L. Needleman, A. Schell, D. C. Bellinger, A. Leviton and E. N. Allred. 1990. The long term effects of exposure to

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38. J. C. Caldwell, T. J. Woodruff, R. Morello-Frosch and D. A. Axelrad. 1998. Application of health information to hazardous air pollutants modeled in EPA’s cumulative exposure project. Toxicology and Industrial Health 14 (3):429-454.

39. California Environmental Protection Agency. Hot Spots Unit Risk and Cancer Potency Values. California Environmental

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41. National Research Council. 2000. Toxicological Effects of Methylmercury. Washington, DC: National Academy Press.

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42. U.S. Environmental Protection Agency. 1996. Mercury Study Report to Congress, Volumes I to VII. Washington, DC:

Office of Air Quality Planning and Standards. http://www.epa.gov/oar/mercury.html.

43. U.S. Environmental Protection Agency. 2000. Deposition of Air Pollutants to the Great Waters: Third Report to Congress.

Washington, DC. http://www.epa.gov/oar/oaqps/gr8water/.

44. South Coast Air Quality Management District. 1999. Multiple Air Toxics Exposure Study II.

http://www.aqmd.gov/matesiidf/matestoc.htm.

45. U. Diez, T. Kroessner, M. Rehwagen, M. Richter, H. Wetzig, R. Schulz, M. Borter, G. Metzner, P. Krumbiegel and

O. Herbarth. 2000. Effects of indoor painting and smoking on airway symptoms in atopy risk children in the

first year of life: results of the Leipzig Allergy High-Risk Children Study. International Journal of Hygiene and

Environmental Health 203:23-28.

46. National Academy of Sciences. 2000. Clearing the Air: Asthma and Indoor Air Exposures. Washington, DC: 

National Academy Press. http://books.nap.edu/catalog/9610.html.

47. E. Dybing and T. Sanner. 1999. Passive smoking, sudden infant death syndrome (SIDS) and childhood infections.

Human and Experimental Toxicology 18:202-205.

48. U.S. Environmental Protection Agency. 1992. Respiratory Health Effects of Passive Smoking: Lung Cancer and Other

Disorders. Washington, DC. EPA/600/6-90/006F. http://cfpub.epa.gov/ncea/cfm/ets/etsindex.cfm.

49. M. S. Benninger. 1999. The impact of cigarette smoking and environmental tobacco smoke on nasal and sinus disease:

a review of the literature. American Journal of Rhinology 13:435-438.

50. B. P. Lanphear, C. A. Aligne, P. Auinger, M. Weitzman and R. S. Byrd. 2001. Residential exposures associated with

asthma in U.S. children. Pediatrics 107 (3):505-11.

51. D. M. Mannino, J. E. Moorman, B. Kingsley, D. Rose and J. Repace. 2001. Health effects related to environmental

tobacco smoke exposure in children in the United States: data from the Third National Health and Nutrition

Examination Survey. Archives of Pediatrics and Adolescent Medicine 155 (1):36-41.

52. P. J. Gergen, J. A. Fowler, K. R. Maurer, W. W. Davis and M. D. Overpeck. 1998. The burden of environmental tobacco

smoke exposure on the respiratory health of children 2 months through 5 years of age in the United States: Third

National Health and Nutrition Examination Survey, 1988 to 1994. Pediatrics 101 (2):E8.

53. D. R. Wahlgren, M. F. Hovell, E. O. Meltzer and S. B. Meltzer. 2000. Involuntary smoking and asthma. 

Current Opinions in Pulmonary Medicine 6:31-6.
Part 1: Environmental Contaminants 47

References

54. A. Lindfors, M. V. Hage-Hamsten, H. Rietz, M. Wickman and S. L. Nordvall. 1999. Influence of interaction of 

environmental risk factors and sensitization in young asthmatic children. Journal of Allergy and Clinical

Immunology 104:755-62.

55. Centers for Disease Control and Prevention. 2001. Cigarette smoking among adults—United States, 1999. 

Morbidity and Mortality Weekly Report 50 (40):869-73.

56. U.S. Environmental Protection Agency. Drinking Water Contaminants. EPA Office of Water, 2001.

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57. A. M. Garcia, S. A. Fadel, S. Cao and M. Sarzotti. 2001. T cell immunity in neonates. Immunologic Research

22 (2-3):177-90.

58. D. Bellinger, A. Leviton, C. Waternaux, H. Needleman and M. Rabinowitz. 1987. Longitudinal analyses of prenatal

and postnatal lead exposure and early cognitive development. New England Journal of Medicine 316 (17):1037-43.

59. R. W. Tuthill. 1996. Hair lead levels related to children’s classroom attention-deficit behavior. Archives of

Environmental Health 51 (3):214-20.

60. H. L. Needleman, J. A. Riess, M. J. Tobin, G. E. Biesecker and J. B. Greenhouse. 1996. Bone lead levels and delinquent

behavior. Journal of the American Medical Association 275 (5):363-9.

61. H. L. Needleman, A. Schell, D. Bellinger, A. Leviton and E. N. Allred. 1990. The long-term effects of exposure to

low doses of lead in childhood. An 11-year follow-up report. New England Journal of Medicine 322 (2):83-8.

62. H. L. Needleman. 1990. What can the study of lead teach us about other toxicants? Environmental Health Perspectives

86:183-9.

63. B. Minder, E. A. Das-Smaal, E. F. Brand and J. F. Orlebeke. 1994. Exposure to lead and specific attentional problems

in schoolchildren. Journal of Learning Disabilities 27 (6):393-9.

64. A. L. Mendelsohn, B. P. Dreyer, A. H. Fierman, C. M. Rosen, L. A. Legano, H. A. Kruger, S. W. Lim and 

C. D. Courtlandt. 1998. Low-level lead exposure and behavior in early childhood. Pediatrics 101 (3):E10.

65. J. Calderon, M. E. Navarro, M. E. Jimenez-Capdeville, M. A. Santos-Diaz, A. Golden, I. Rodriguez-Leyva, 

V. Borja-Aburto and F. Diaz-Barriga. 2001. Exposure to arsenic and lead and neuropsychological development 

in Mexican children. Environmental Research 85 (2):69-76.

66. L. Knobeloch, B. Salna, A. Hogan, J. Postle and H. Anderson. 2000. Blue babies and nitrate-contaminated well water.

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67. S. K. Gupta, R. C. Gupta, A. K. Seth, A. B. Gupta, J. K. Bassin and A. Gupta. 2000. Methaemoglobinaemia in areas

with high nitrate concentration in drinking water. National Medical Journal of India 13 (2):58-61.

68. T. Saito, S. Takeichi, M. Osawa, N. Yukawa and X. L. Huang. 2000. A case of fatal methemoglobinemia of unknown

origin but presumably due to ingestion of nitrate. International Journal of Legal Medicine 113 (3):164-7.

69. M. Nugent, Kamrin, M.A., Wolfson, L., D’Itri, F.M. Nitrate - A Drinking Water Concern, 1993.

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70. U.S. Environmental Protection Agency. National Primary Drinking Water Regulations: Consumer Factsheet on

NITRATES/NITRITES. EPA Office of Water, 2001. http://www.epa.gov/safewater/dwh/c-ioc/nitrates.html.

71. U.S. Environmental Protection Agency. Ground Water and Drinking Water: Appendix D glossary. EPA Office of

Water, 2001. http://www.epa.gov/safewater/wot/appd.html.

72. U.S. Environmental Protection Agency. Current Drinking Water Standards. EPA Office of Water, 2001.

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73. G. A. Boorman. 1999. Drinking water disinfection byproducts: review and approach to toxicity evaluation.

Environmental Health Perspectives 107 (Suppl. 1):207-17.
48 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

References

74. M. J. Nieuwenhuijsen, M. B. Toledano, N. E. Eaton, J. Fawell and P. Elliott. 2000. Chlorination disinfection byproducts

in water and their association with adverse reproductive outcomes: A review. Occupational and Environmental

Medicine 57 (2):73-85.

75. National Primary Drinking Water Regulations and National Primary Drinking Water Regulations Implementation.

40 CFR Parts 141 and 142. http://www.access.gpo.gov/nara/cfr/waisidx_01/40cfrv19_01.html.

76. U.S. Environmental Protection Agency. 2000. Data Reliability Analysis of the EPA Safe Drinking Water Information

System/Federal Version (SDWIS/FED). Washington, DC: EPA Office of Water. EPA 816-R-00-0200. 

77. U.S. Geological Survey. 1998. Estimated Use of Water in the United States in 1995. Denver, CO. USGS Circular 1200.

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78. U.S. Environmental Protection Agency. Fact Sheet: Surface Water Treatment Rule. EPA Office of Water, 2001.

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79. F. Bove, Y. Shim and P. Zeitz. 2002. Drinking water contaminants and adverse pregnancy outcomes: a review.

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80. L. Dodds, W. King, C. Woolcott and J. Pole. 1999. Trihalomethanes in public water supplies and adverse birth outcomes.

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81. L. Dodds and W. D. King. 2001. Relation between trihalomethane compounds and birth defects. Occupational and

Environmental Medicine 58 (7):443-6.

82. W. D. King, L. Dodds and A. C. Allen. 2000. Relation between stillbirth and specific chlorination by-products in

public water supplies. Environmental Health Perspectives 108 (9):883-6.

83. D. A. Savitz, K. W. Andrews and L. M. Pastore. 1995. Drinking water and pregnancy outcome in central North Carolina:

source, amount, and trihalomethane levels. Environmental Health Perspectives 103 (6):592-6.

84. S. H. Swan, K. Waller, B. Hopkins, G. Windham, L. Fenster, C. Schaefer and R. R. Neutra. 1998. A prospective

study of spontaneous abortion: relation to amount and source of drinking water consumed in early pregnancy.

Epidemiology 9 (2):126-33.

85. K. Waller, S. H. Swan, G. DeLorenze and B. Hopkins. 1998. Trihalomethanes in drinking water and spontaneous

abortion. Epidemiology 9 (2):134-40.

86. K. Waller, S. H. Swan, G. C. Windham and L. Fenster. 2001. Influence of exposure assessment methods on risk estimates

in an epidemiologic study of total trihalomethane exposure and spontaneous abortion. Journal of Exposure Analysis

and Environmental Epidemiology 11 (6):522-31.

87. National Research Council. 1993. Pesticides in the Diets of Infants and Children. Washington, DC: National Academy

Press. http://www.nap.edu/catalog/2126.html?se_side.

88. B. Eskenazi, A. Bradman and R. Castorina. 1999. Exposures of children to organophosphate pesticides and their

potential adverse health effects. Environmental Health Perspectives 107 (Suppl. 3):409-19.

89. Doane Marketing Research. AgroTrack Row and Specialty Crop Studies, 1993-2001. 

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90. E. J. Stanek, 3rd and E. J. Calabrese. 2000. Daily soil ingestion estimates for children at a Superfund site. 

Risk Analysis 20 (5):627-35.

91. P. J. Landrigan, W. A. Suk and R. W. Amler. 1999. Chemical wastes, children’s health, and the Superfund Basic

Research Program. Environmental Health Perspectives 107 (6):423-7.
PART 2

Body Burdens:

Contaminants in the

Bodies of Women and

Children
50 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
easurements of the levels of pollutants in children’s bodies provide direct information about exposures to environmental contaminants. Also, measurements in

women who may become pregnant, currently are pregnant, or currently are breastfeeding provide information about exposures that potentially can affect conception, the

fetus, and/or the developing child. These “body burden” measurements most often are

taken from blood samples, but also can come from urine or hair.

This edition of America’s Children and the Environment includes new body burden

measurements for mercury and cotinine. The first new measure shows concentrations

of mercury in the blood of women of child-bearing age, defined as between the ages of

16 and 49. This measure is important because studies have shown that prenatal exposure to mercury can cause adverse neurological and developmental effects in children.

The second new measure shows levels of cotinine in the blood of children. Cotinine is

a breakdown product of nicotine. Children who have been exposed to environmental

tobacco smoke (ETS) have cotinine in their blood. Exposure to ETS increases the risk

of a number of adverse health effects, including lower respiratory tract infections, bronchitis, pneumonia, ear infections, asthma symptoms, and sudden infant death syndrome (SIDS).

This report also includes updated data on lead in the blood of children. This measure is

directly related to adverse neurological and developmental effects in children. The data

on concentrations of lead in blood (called “blood lead”) depict a trend over 25 years.

One limitation of body burden measures is that they reveal few clues to the source(s) of

exposure. For example, lead in children’s blood may come from exposure to airborne

sources, contaminated water or food, or contaminated soil or dust. 

The measures in this section do not account for many environmental contaminants that

are important to children but for which data are not available on a national scale, or for

which information is lacking to evaluate health significance. For example, data are now

available for a number of other environmental contaminants—such as pesticides and

heavy metals—in children’s blood and urine. However, no information is available to

show how these concentrations relate to health risks. Also, it is not currently possible

to show trends for these contaminants because data are available for only one year.

Body Burdens

Part 2: Body Burdens 51

Body Burdens: Contaminants in the Bodies of Women and Children

M
52 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Concentrations of Lead in Blood

Lead is a major environmental health hazard for young children. Childhood exposure

to lead contributes to learning problems such as reduced intelligence and cognitive

development.1-3 Studies also have found that childhood exposure to lead contributes to

attention-deficit/hyperactivity disorder4 and hyperactivity and distractibility;5-7 increases

the likelihood of dropping out of high school, having a reading disability, lower vocabulary, and lower class standing in high school;8 and increases the risk for antisocial and

delinquent behavior.9 A blood lead level of 10 micrograms per deciliter (μg/dL) or greater

is considered elevated,10, 11 but there is no demonstrated safe concentration of lead in

blood.12 Adverse health effects can occur at lower concentrations.2, 13, 14

In the past, ambient concentrations of lead from leaded gasoline were a major contributor

to blood lead levels in children.14 Today, elevated blood lead levels are due mostly to

ingestion of contaminated dust, paint and soil.10 Soil and dust that are contaminated with

lead are important sources of exposure because children play outside, and very small

children frequently put their hands in their mouths.15, 17 Deterioration of lead-based

paint can generate contaminated dust and soil, and past emissions of lead in gasoline

that subsequently were deposited in the soil also contribute to lead-contaminated soil and

house dust.15-17 As of 1998-2000, lead-based paint was present in 40 percent of U.S.

homes.18 16 percent of homes had dust lead hazards, and 7 percent of homes had soil lead

hazards.18 Some small fraction of children also are exposed through direct ingestion of

lead-containing paint chips.19

Although the concentration of lead in blood is an important indicator of risk, it reflects

only current exposures. Lead also accumulates in bone. Recent research suggests that

concentrations of lead in bone may be more related to adverse health outcomes in children than are concentrations in blood.20 This finding suggests that concentrations in

bone may better reflect the net burden of exposure. However, methods for measuring

lead in bone are more time-consuming and expensive than those for measuring lead in

blood, and nationally representative data are not available.

Lead in the Blood of

Children

Healthy People 2010: Objective 8-11 of Healthy People 2010 aims to totally eliminate elevated

blood lead levels in children. See Appendix C for more information.
53 Part 2: Body Burdens

Concentrations of Lead in Blood

■ The median concentration of lead in the blood of children 5 years old and under dropped from 15 micrograms

per deciliter (μg/dL) in 1976-1980 to 2.2 μg/dL in

1999-2000, a decline of 85 percent.

■ The concentration of lead in blood at the 90th percentile

in children 5 years old and under dropped from 25 μg/dL

in 1976-1980 to 4.8 μg/dL in 1999-2000.

■ In 1978, about 4.7 million children ages 1-5 had blood

lead levels at or greater than 10 μg/dL, which is considered elevated. By 1999-2000, this number had declined

to about 300,000.

■ The decline in blood lead levels is due largely to the

phasing out of lead in gasoline between 1973 and 199521

and to the reduction in the number of homes with leadbased paint from 64 million in 1990 to 38 million in

2000.18 Some decline also was a result of EPA regulations reducing lead levels in drinking water, as well as

legislation banning lead from paint and restricting the

content of lead in solder, faucets, pipes, and plumbing.

Lead also has been eliminated or reduced in food and

beverage containers and ceramic ware, and in products

such as toys, mini-blinds, and playground equipment.

Measure B1

Concentration of lead in blood of children ages 5 and under

Micrograms of Lead per Deciliter of Blood (

μg/dL)

0

5

10*

15

20

25

30

90th percentile

(10 percent of children have

this blood lead level or greater)

Median value

(50 percent of children 

have this blood lead 

level or greater)

1976-1980 1988-1991 1992-1994 1999-2000

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, 

National Health and Nutrition Examination Survey

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants: lead (E1-E2) Lead in Blood (B1-B3) Neurodevelopmental (D7) Lead in Schools (S1-S3) Drinking Water: lead (E6-E7) 

* 10 μg/dL of blood lead has been identified by CDC as elevated, which indicates need for intervention.22 There is no demonstrated safe

concentration of lead in blood.12 Adverse health effects can occur at lower concentrations.2,13,14
54 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Concentrations of Lead in Blood

Concentrations of lead in children’s blood differ by race/ethnicity and family income.

This measure presents blood lead levels by race/ethnicity and family income for children

ages 1-5, a period when lead is particularly harmful to the developing brain and nervous

system.22 Measures of blood lead by race/ethnicity and income can help identify the

groups that are at greatest risk.

Blood lead levels are highest for younger children, because their exposure per pound of

body weight is greater due to their smaller size. In addition, young children play in certain ways that can increase their exposure to lead. For example, they play and crawl on

the ground and frequently put their hands in their mouths. Blood lead levels tend to

reflect more recent exposures.

Blood Lead by

Race/Ethnicity and

Family Income
55 Part 2: Body Burdens

Concentrations of Lead in Blood

■ In 1999-2000 the median blood lead level in children

ages 1-5 was 2.2 μg/dL. The median blood lead level

for children living in families with incomes below the

poverty level was 2.8 μg/dL and for children living in

families above the poverty level it was 1.9 μg/dL.

■ In 1999-2000, White non-Hispanic children ages 

1-5 had a median blood lead level of about 2 μg/dL,

unchanged from the level in 1992-1994. 

■ In 1992-1994, Black non-Hispanic children ages 1-5 had

a median blood lead level of 3.9 μg/dL and in 1999-

2000 they had a median blood lead level of 2.8 μg/dL. 

■ In 1992-1994, Hispanic children ages 1-5 had a median

blood lead level of 2.6 μg/dL and in 1999-2000 they

had a median blood lead level of 2.0 μg/dL.

Median concentrations of lead in blood of children ages 1-5, by race/ethnicity 

and family income, 1999-2000 

012345

Measure B2

All Incomes

All Incomes

All Incomes

< Poverty Level

< Poverty Level

< Poverty Level

100-200% of Poverty Level

100-200% Poverty Level

100-200% of Poverty Level

>200% of Poverty Level

> 200% of Poverty Level

> 200% of Poverty Level

All Incomes

< Poverty Level

100-200% of Poverty Level

> 200% of Poverty Level

Black

nonHispanic

Hispanic

All

Races/

Ethnicities

White

nonHispanic

Median concentrations of lead in blood (μg/dL)

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, 

National Health and Nutrition Examination Survey

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants: lead (E1-E2) Lead in Blood (B1-B3) Neurodevelopmental (D7) Lead in Schools (S1-S3) Drinking Water: lead (E6-E7) 
56 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Concentrations of Lead in Blood

A blood lead level of 10 micrograms per deciliter (μg/dL) or greater is considered elevated, but there is no demonstrated safe concentration of lead in blood. Adverse health

effects can occur at lower concentrations. A growing body of research has shown that

there are measurable adverse neurological effects in children at blood lead concentrations as low as 1 μg/dL.2, 13, 23 EPA believes that effects may occur at blood lead levels so

low that there is essentially no “safe” level of lead.12 This measure shows the distribution of blood lead levels among children ages 1-5 for the years 1999-2000, the most

current years for which data are available.

Distribution of 

Concentrations of 

Lead in Blood in

Children Ages 1-5
57 Part 2: Body Burdens

Concentrations of Lead in Blood

■ In 1999-2000, the concentration of lead in blood at

the 90th percentile in children ages 1-5 was 4.8 μg/dL,

meaning that 10 percent of children had blood lead

levels above this concentration and 90 percent had

blood lead levels below it.

■ In 1999-2000, the median blood lead level of children

ages 1-5 was 2.2 μg/dL, meaning that 50 percent of

children had blood lead levels above this concentration

and 50 percent had blood lead levels below it.

■ Approximately 300,000 children ages 1-5 (about 2 percent) had a blood lead level of 10 μg/dL or greater in

1999-2000.

Measure B3

Distribution of concentrations of lead in blood of children ages 1-5, 1999-2000

Percentage of children

0%

5%

10%

15%

20%

25%

30%

35%

0 2 3 4 5 6 7 > 7 1

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, 

National Health and Nutrition Examination Survey

Concentration of lead in blood (μg/dL)

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants: lead (E1-E2) Lead in Blood (B1-B3) Neurodevelopmental (D7) Lead in Schools (S1-S3) Drinking Water: lead (E6-E7) 
58 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Concentrations of Mercury in Blood

Prenatal exposure to methylmercury can cause adverse developmental and cognitive

effects in children, even at low doses that do not result in effects in the mother.24-26

Infants and children are particularly sensitive to the effects of neurotoxic agents such as

methylmercury.27 Children who are exposed to low concentrations of methylmercury

prenatally are at increased risk of poor performance on neurobehavioral tests, such as those

measuring attention, fine motor function, language skills, visual-spatial abilities (like

drawing), and verbal memory.26, 28 There is some evidence that exposure to methylmercury

also can affect the cardiovascular,29 immune,30, 31 and reproductive systems.32

The measure presented here shows blood mercury concentrations in women of childbearing age (16-49 years). Monitoring the concentrations of mercury in the blood of

women of child-bearing age can help identify the proportion of children who may be

at risk. Based on recent studies of children born to women who consumed fish that

contained mercury, EPA has determined that children born to women with blood

mercury concentrations above 5.8 parts per billion are at some increased risk of adverse

health effects.33 EPA’s reference dose (RfD) for methylmercury is 0.1 micrograms per

kilogram body weight per day. This dose is approximately equal to a concentration of

5.8 parts per billion mercury in blood. Although the prenatal period is the most sensitive

period of exposure, exposure to mercury during childhood also could pose a potential

health risk.32

People are exposed to methylmercury mainly through eating fish contaminated with

methylmercury. Mercury that ends up in fish may originate as emissions to the air.

Mercury released into the atmosphere can travel long distances on global air currents

and be deposited in areas far from its original source.35, 36 The largest human-generated

source of mercury emissions in the United States is the burning of coal. Other sources

include the combustion of waste and industrial processes that use mercury.36

Mercury usually is released in an elemental form and later converted into methylmercury

by bacteria. Methylmercury is more toxic to humans than other forms of mercury, in

part because it is more easily absorbed in the body.36 Methylmercury accumulates through

the food chain: fish that live a long time and that eat other fish can accumulate high

levels of methylmercury.

People also can be exposed to inorganic mercury at work, through ritualistic uses of

mercury, and from dental restorations with mercury-silver amalgams.36 Inorganic mercury is less readily absorbed than methylmercury and is not known to cause the types

of health effects discussed in this section.

Prenatal Exposure to

Methylmercury

Healthy People 2010: Objective 8-10 of Healthy People 2010 addresses the reduction of

contaminants (such as mercury) in fish. See Appendix C for more

information.
59 Part 2: Body Burdens

Concentrations of Mercury in Blood

■ EPA has determined that children born to women with

blood concentrations of mercury above 5.8 parts per 

billion are at some increased risk of adverse health effects.33

About 8 percent of women of child-bearing age had at

least 5.8 parts per billion of mercury in their blood in

1999-2000.

■ Current research indicates that there is no safe level of

methylmercury in the blood within the range of exposures

measured in the human studies of the health effects of

mercury, which were as low as 1 part per billion.33 About

50 percent of the women of child-bearing age in the

United States have at least 1 part per billion of mercury

in their blood. 

■ The graph shows reported concentrations of mercury

in blood from the National Health and Nutrition

Examination Survey. These figures are for total mercury,

which includes methylmercury and other forms of

mercury. However, most of the mercury in the blood 

of participants in the survey was methylmercury, so 

the measured concentrations are a good indication of

methylmercury concentrations.37

■ The National Academy of Sciences (NAS) and EPA have

determined that 58 parts per billion of mercury in the

blood of pregnant women corresponds to approximately

a doubling in the risk of poor performance on a specific

neurodevelopmental test.32-34 The NAS and EPA also

have concluded that 32 parts per billion of mercury in the

blood of pregnant women corresponds to approximately

a doubling in the risk of abnormal performance on a

range of neurodevelopmental tests.32-34 Data from the

National Health and Nutrition Examination Survey

showed no measured blood mercury concentrations

greater than or equal to 58 parts per billion in women

of child-bearing age. A small percentage of women (less

than 1 percent) have blood mercury concentrations

greater than 30 parts per billion.

Measure B4

0%

10%

20%

30%

40%

50%

60%

EPA's Reference Dose

0 2 3 4 5 6 7 > 7 1

Distribution of concentrations of mercury in blood of women of 

child-bearing age, 1999-2000

Percentage of women of child-bearing age

Concentration of mercury in blood (parts per billion)

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, 

National Health and Nutrition Examination Survey

Note: EPA's reference dose (RfD) for methylmercury is 0.1 micrograms per kilogram body weight per day. 

 This is approximately equal to a concentration of 5.8 parts per billion mercury in blood. 

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Mercury in Blood (B4) Neurodevelopmental (D7)
60 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Concentrations of Cotinine in Blood

Exposure to environmental tobacco smoke (ETS) is an important health risk for children. Children who are exposed to environmental tobacco smoke are at increased risk

for a number of adverse health outcomes, including lower respiratory tract infections,

bronchitis, pneumonia, fluid in the middle ear, and sudden infant death syndrome

(SIDS).38-40 ETS also can play a role in the development and exacerbation of asthma,

particularly for children under 6 years old.41-46 Young children appear to be more susceptible to the effects of environmental tobacco smoke than are older children.40, 44

Cotinine is a breakdown product of nicotine in blood. Measurements of cotinine in

blood serum are a marker for exposure to environmental tobacco smoke in the previous

1 to 2 days.47 Children can be exposed to ETS in their homes or in places where people

are allowed to smoke, such as some restaurants. This measure presents cotinine levels

for non-tobacco-users only. Children who smoke were excluded from these statistics.

Cotinine in the 

Blood of Children

Healthy People 2010: Objective 27-9 of Healthy People 2010 is to reduce the proportion of 

children who are regularly exposed to tobacco smoke at home. See

Appendix C for more information.
61 Part 2: Body Burdens

Concentrations of Cotinine in Blood

■ In 1999-2000, median (50th percentile) levels of cotinine measured in children were 56 percent lower than

they were in 1988-1991.

■ Cotinine values at the 90th percentile, representing the

most highly exposed 10 percent of children, showed a

smaller relative decline (18 percent) from 1988-1991 to

1999-2000.

■ Eighty-five percent of children had detectable levels of

cotinine in 1988-1991;41 between 50 and 75 percent of

children had detectable levels of cotinine in 1999-2000

(data not shown).

■ The reduction in children’s cotinine levels is in part

attributable to a decline in the percentage of adults who

smoke. In 1999, an estimated 23.5 percent of adults were

current smokers, down from 25.0 percent in 1993.48

■ In 1988-91, median concentrations of cotinine in blood

were about 0.6 nanograms per milliliter (ng/mL) for

Black non-Hispanic children and about 0.2 ng/mL for

White non-Hispanic children and Hispanic children.

Measure B5

Concentrations of cotinine in blood of children

Serum cotinine concentrations (ng/mL)

0.0

0.5

1.0

1.5

2.0

2.5

3.0

90th percentile

(10 percent of children have this

serum cotinine level or greater) 

50th percentile

(50 percent of children have this 

serum cotinine level or greater)

1988-1991

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, 

National Health and Nutrition Examination Survey

1999-2000

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Environmental Tobacco Smoke (E5) Cotinine in Blood (B5) Respiratory (D1-D4)
62 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

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early cognitive development. New England Journal of Medicine 316 (17):1037-43.

2. A. J. McMichael, P. A. Baghurst, N. R. Wigg, G. V. Vimpani, E. F. Robertson and R. J. Roberts. 1988. Port Pirie

Cohort Study: environmental exposure to lead and children’s abilities at the age of four years. New England

Journal of Medicine 319 (8):468-75.

3. B. P. Lanphear, K. Dietrich, P. Auinger and C. Cox. 2000. Cognitive deficits associated with blood lead concentrations

<10 micrograms/dL in U.S. children and adolescents. Public Health Reports 115 (6):521-9.

4. R. W. Tuthill. 1996. Hair lead levels related to children’s classroom attention-deficit behavior. Archives of 

Environmental Health 51 (3):214-20.

5. J. Calderon, M. E. Navarro, M. E. Jimenez-Capdeville, M. A. Santos-Diaz, A. Golden, I. Rodriguez-Leyva, V. Borja-Aburto

and F. Diaz-Barriga. 2001. Exposure to arsenic and lead and neuropsychological development in Mexican children.

Environmental Research 85 (2):69-76.

6. A. L. Mendelsohn, B. P. Dreyer, A. H. Fierman, C. M. Rosen, L. A. Legano, H. A. Kruger, S. W. Lim and 

C. D. Courtlandt. 1998. Low-level lead exposure and behavior in early childhood. Pediatrics 101 (3):E10.

7. B. Minder, E. A. Das-Smaal, E. F. Brand and J. F. Orlebeke. 1994. Exposure to lead and specific attentional problems

in schoolchildren. Journal of Learning Disabilities 27 (6):393-9.

8. H. L. Needleman, A. Schell, D. C. Bellinger, A. Leviton and E. N. Allred. 1990. The long term effects of exposure to

low doses of lead in childhood, an 11-year follow-up report. New England Journal of Medicine 322 (2):83-8.

9. H. L. Needleman, J. A. Riess, M. J. Tobin, G. E. Biesecker and J. B. Greenhouse. 1996. Bone lead levels and delinquent

behavior. Journal of the American Medical Association 275 (5):363-9.

10. Centers for Disease Control and Prevention. 1997. Screening Young Children for Lead Poisoning: Guidance for State

and Local Public Health Officials. Atlanta, GA. http://www.cdc.gov/nceh/lead/guide/guide97.htm.

11. Centers for Disease Control and Prevention. 2002. Managing Elevated Blood Lead Levels Among Young Children:

Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Atlanta, GA.

http://www.cdc.gov/nceh/lead/CaseManagement/caseManage_main.htm.

12. U.S. Environmental Protection Agency. 1997. Integrated Risk Information System (IRIS) Risk Information for 

Lead and Compounds (Inorganic). Washington, DC: National Center for Environmental Assessment.

http://www.epa.gov/iris/subst/0277.htm#reforal.

13. B. P. Lanphear, K. Dietrich, P. Auinger and C. Cox. 2000. Cognitive deficits associated with blood lead concentrations

<10 microg/dL in U.S. children and adolescents. Public Health Reports 115 (6):521-9.

14. E. K. Silbergeld. 1997. Preventing lead poisoning in children. Annual Review of Public Health 18:187-210.

15. H. Mielke and P. Reagan. 1998. Soil is an important pathway of human lead exposure. Environmental Health

Perspectives 106 (Suppl. 1):217-229.

16. H. W. Mielke. 1999. Lead in the inner cities. American Scientist 87:62-73.

17. President’s Task Force on Environmental Health Risks and Safety Risks to Children. 2000. 

Eliminating Childhood Lead Poisoning: A Federal Strategy Targeting Lead Paint Hazards.

http://www.hud.gov/offices/lead/reports/fedstrategy2000.pdf.

18. D. E. Jacobs, R. P. Clickner, J. Y. Zhou, S. M. Viet, D. A. Marker, J. W. Rogers, D. C. Zeldin, P. Broene and W.

Friedman. 2002. The prevalence of lead-based paint hazards in U.S. housing. Environmental Health Perspectives

110 (10):A599-606.
63 Part 2: Body Burdens

References

19. M. D. McElvaine, E. G. DeUngria, T. D. Matte, C. G. Copley and S. Binder. 1992. Prevalence of radiographic 

evidence of paint chip ingestion among children with moderate to severe lead poisoning, St Louis, Missouri, 

1989 through 1990. Pediatrics 89 (4 Pt 2):740-2.

20. H. Hu. 1998. Bone lead as a new biologic marker of lead dose: recent findings and implications for public health.

Environmental Health Perspectives 106 (Suppl. 4):961-7.

21. U.S. Environmental Protection Agency. 2000. National Air Quality and Emissions Trends Report, 1998. 

Research Triangle Park, North Carolina: EPA Office of Air Quality Planning and Standards. 454/R-00-003.

http://www.epa.gov/oar/aqtrnd98/toc.html.

22. Centers for Disease Control and Prevention. 1991. Preventing Lead Poisoning in Young Children. Atlanta, GA.

http://www.cdc.gov/nceh/lead/publications/pub_Reas.htm.

23. J. Schwartz. 1994. Low-level lead exposure and children’s IQ: a meta-analysis and search for a threshold.

Environmental Research 65 (1):42-55.

24. P. Grandjean, R. F. White, A. Nielsen, D. Cleary and E. C. de Oliveira Santos. 1999. Methylmercury neurotoxicity in

Amazonian children downstream from gold mining. Environmental Health Perspectives 107 (7):587-91.

25. P. Grandjean, P. Weihe, R. F. White and F. Debes. 1998. Cognitive performance of children prenatally exposed to

“safe” levels of methylmercury. Environmental Research 77 (2):165-72.

26. P. Grandjean, P. Weihe, R. F. White, F. Debes, S. Araki, K. Yokoyama, K. Murata, N. Sorensen, R. Dahl and 

P. J. Jorgensen. 1997. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury.

Neurotoxicology and Teratology 19 (6):417-28.

27. P. M. Rodier. 1995. Developing brain as a target of toxicity. Environmental Health Perspectives 103 Suppl 6:73-6.

28. T. Kjellstrom, P. Kennedy, S. Wallis and C. Mantell. 1986. Physical and mental development of children with prenatal

exposure to mercury from fish. Stage 1: Preliminary tests at age 4. Sweden: Swedish National Environmental

Protection Board. 

29. N. Sørensen, K. Murata, E. Budtz-Jørgensen, P. Weihe and P. Grandjean. 1999. Prenatal methylmercury exposure as a

cardiovascular risk factor at seven years of age. Epidemiology 10 (4):370-5.

30. L. I. Sweet and J. T. Zelikoff. 2001. Toxicology and immunotoxicology of mercury: a comparative review in fish and

humans. Journal of Toxicology and Environmental Health. Part B, Critical Reviews 4 (2):161-205.

31. N. Brenden, H. Rabbani and M. Abedi-Valugerdi. 2001. Analysis of mercury-induced immune activation in

nonobese diabetic (NOD) mice. Clinical and Experimental Immunology 125 (2):202-10.

32. National Academy of Sciences. 2000. Toxicological Effects of Methylmercury. Washington, DC: National Academy

Press. http://books.nap.edu/catalog/9899.html?onpi_newsdoc071100.

33. U.S. Environmental Protection Agency. 2001. Integrated Risk Information System (IRIS) Risk Information for

Methylmercury (MeHg). Washington, DC: National Center for Environmental Assessment.

http://www.epa.gov/iris/subst/0073.htm.

34. U.S. Environmental Protection Agency. 2001. Water Quality Criterion for the Protection of Human Health:

Methylmercury. Washington, DC. http://www.epa.gov/waterscience/criteria/methylmercury/merctitl.pdf

35. W. F. Fitzgerald, D. R. Engstrom, R. P. Mason and E. A. Nater. 1998. The case for atmospheric mercury contamination

in remote areas. Environmental Science and Technology 32 (1):1-7.

36. U.S. Environmental Protection Agency. 1996. Mercury Study Report to Congress Volumes I to VII. Washington, DC:

Office of Air Quality Planning and Standards. EPA-452-R-96-001b. http://www.epa.gov/oar/mercury.html.
64 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

References

37. Centers for Disease Control and Prevention. 2001. National Report on Human Exposure to Environmental Chemicals.

Atlanta, GA: Department of Health and Human Services. 01-0379. http://www.cdc.gov/nceh/dls/report.

38. M. S. Benninger. 1999. The impact of cigarette smoking and environmental tobacco smoke on nasal and sinus disease:

a review of the literature. American Journal of Rhinology 13 (6):435-8.

39. E. Dybing and T. Sanner. 1999. Passive smoking, sudden infant death syndrome (SIDS) and childhood infections.

Human and Experimental Toxicology 18 (4):202-5.

40. U.S. Environmental Protection Agency. 1992. Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders.

Washington, DC: EPA Office of Research and Development. http://cfpub.epa.gov/ncea/cfm/ets/etsindex.cfm.

41. D. M. Mannino, J. E. Moorman, B. Kingsley, D. Rose and J. Repace. 2001. Health effects related to environmental

tobacco smoke exposure in children in the United States: data from the Third National Health and Nutrition

Examination Survey. Archives of Pediatrics and Adolescent Medicine 155 (1):36-41.

42. B. P. Lanphear, C. A. Aligne, P. Auinger, M. Weitzman and R. S. Byrd. 2001. Residential exposures associated with

asthma in U.S. children. Pediatrics 107 (3):505-11.

43. P. J. Gergen, J. A. Fowler, K. R. Maurer, W. W. Davis and M. D. Overpeck. 1998. The burden of environmental tobacco

smoke exposure on the respiratory health of children 2 months through 5 years of age in the United States: Third

National Health and Nutrition Examination Survey, 1988 to 1994. Pediatrics 101 (2):E8.

44. National Academy of Sciences. 2000. Clearing the Air: Asthma and Indoor Air Exposures. Washington, DC: 

National Academy Press. http://books.nap.edu/catalog/9610.html.

45. A. Lindfors, M. V. Hage-Hamsten, H. Rietz, M. Wickman and S. L. Nordvall. 1999. Influence of interaction of 

environmental risk factors and sensitization in young asthmatic children. Journal of Allergy and Clinical

Immunology 104:755-62.

46. D. R. Wahlgren, M. F. Hovell, E. O. Meltzer and S. B. Meltzer. 2000. Involuntary smoking and asthma. 

Current Opinions in Pulmonary Medicine 6:31-6.

47. J. L. Pirkle, K. M. Flegal, J. T. Bernert, D. J. Brody, R. A. Etzel and K. R. Maurer. 1996. Exposure of the U.S. 

population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey, 

1988 to 1991. Journal of the American Medical Association 275 (16):1233-40.

48. Centers for Disease Control and Prevention. 2001. Cigarette smoking among adults—United States, 1999. 

Morbidity and Mortality Weekly Report 50 (40):869-73.
PART 3

Childhood Illnesses
ata on trends in childhood diseases and disorders provide important information

on successes and shortcomings in efforts to protect children’s health. Many

important diseases and other health disorders affect children. The causes of many of

these conditions are not well established. In some cases environmental contaminants

are known to play a role. In other cases clues suggest that environmental factors are

important, but definitive proof is lacking. 

This section of the report focuses on important childhood diseases and disorders for which

evidence or clues indicate or suggest some influence by environmental contaminants,

and for which nationally representative data are available. These diseases and disorders

are asthma, acute bronchitis and acute upper respiratory infections, cancer, and—new

for this edition—neurodevelopmental disorders. Other diseases and disorders that may

be influenced partially by environmental contaminants include other respiratory diseases,

waterborne diseases, methemoglobinemia, and birth defects.

It is very difficult to develop conclusive evidence that environmental contaminants

cause or contribute to the incidence of childhood health effects, particularly those

effects occurring in a relatively small proportion of children or effects with multiple

causes. In cases where exposure to an environmental contaminant results in a relatively

modest increase in the incidence of a disease or disorder, many children would need to

be included in a study in order to detect a true relationship. In addition, there may be

factors that are related to both the exposure and the health effect (like socioeconomic

status) that can make it difficult to detect a relationship between exposure to environmental contaminants and disease. There may, however, be suggestive (rather than

conclusive) evidence from studies in humans and/or laboratory animals to suggest that

exposures to environmental contaminants contribute to the incidence of a childhood

health effect.

Tracking childhood diseases and disorders is an important element of research on

potential links between health effects and exposure to environmental contaminants.

Tracking establishes a basis for comparison so that increases or decreases in the incidence of a disease or disorder can be detected, often yielding important clues to its

causes. Tracking helps researchers determine whether past and current actions have

been effective in reducing the incidence of a disease or disorder. It also helps to identify

opportunities for further action.

It can be difficult to assess the contribution of environmental exposures to childhood

illnesses. Even though environmental exposures can contribute to some childhood 

illnesses, other factors may be more important, such as family history, nutrition, and

socioeconomic factors. In addition, there can be interactions between environmental and

genetic factors. This report does not address illnesses that may result from childhood

exposures to environmental contaminants but do not manifest themselves until adulthood.

Childhood

Illnesses

66 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Childhood Illnesses

D
Respiratory diseases can greatly impair a child’s ability to function, and are an important

cause of missed school days and limitations to activities. Important respiratory diseases

in children include asthma, bronchitis, and upper respiratory infections. 

In 1994-96, 24 percent of children with asthma had to limit their activities due to their

asthma, and the disease caused children to miss 14 million days of school.1 Studies have

shown that outdoor and indoor air pollution cause some respiratory symptoms and

increase the frequency or severity of asthma attacks.2-15

Two types of measures of respiratory diseases are presented here. The first set of measures

(D1 and D2) focuses on the percentage of children who have asthma. The second set

(D3 and D4) reports on cases of respiratory illness severe enough to require a visit to

the emergency room or admission to the hospital.

Respiratory Diseases

in Children 

Part 3: Childhood Illnesses 67

Respiratory Diseases
Asthma is a disease of the lungs that can cause wheezing, difficulty in breathing, and

chest pain. It is the most common chronic disease among children and is costly in both

human and monetary terms.15

Asthma varies greatly in severity. Some children who have been diagnosed with asthma

may not experience any serious respiratory effects. Other children may have mild symptoms or may respond well to management of their asthma, typically through use of

medication. Some children with asthma may suffer serious attacks that greatly limit their

activities, result in visits to emergency rooms or hospitals, or, in rare cases, cause death.

Asthma among children is increasing in the United States. Researchers do not understand

completely why children develop asthma. The tendency to develop asthma can be inherited, but genetic factors alone are unlikely to explain the significant increases that have

occurred in the last 20 years.15

Research on environmental factors that exacerbate or may contribute to causing asthma

has focused on environmental agents found outdoors and indoors. The Institute of

Medicine concluded that exposure to dust mites causes asthma in susceptible children.15

Cockroaches and tobacco smoke are likely to cause asthma in young children.15 Other

studies have evaluated the role of indoor air pollutants such as nitrogen dioxide, pesticides, plasticizers, and volatile organic pollutants. Some of these pollutants may play a

role in asthma.15 One recent study suggests that chronic exposure to ozone may be

associated with the development of asthma in children who exercise outside,16 and two

other studies suggest that chronic exposure to particulate matter may affect lung function and growth.17, 18

Environmental factors may increase the severity or frequency of asthma attacks in children

who have the disease. Children with asthma are particularly sensitive to outdoor air

pollutants, including ozone, particulate matter, and sulfur dioxide.2-14, 19 These pollutants

can exacerbate asthma, leading to difficulty in breathing, an increased use of medication,

visits to doctors’ offices, trips to emergency rooms, and admissions to the hospital. In

addition, one study reported a relationship between exposure to hazardous air pollutants

and increases in chronic respiratory symptoms that are characteristic of asthma.20

Data from the National Health Interview Survey were used to estimate the prevalence of

childhood asthma. For 1980 to 1996, the percentage of children reported to have asthma

in the preceding 12 months is shown. In 1997, the survey’s method for measuring

childhood asthma changed. For 1997 to 2001, the measure shows the percentage of

children who had ever been told by a doctor or health professional that they have asthma,

as well as the percentage of children who were ever diagnosed with asthma and who

had an asthma attack in the preceding 12 months. Some children may have asthma

when they are young and outgrow it as they get older, or their asthma may be wellcontrolled through medication and by avoiding triggers of asthma attacks. In such cases,

children may have asthma but may not have experienced any attacks in a long time. 

Asthma 

68 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Respiratory Diseases
Part 3: Childhood Illnesses 69

Respiratory Diseases

■ Between 1980 and 1995, the percentage of children

with asthma doubled, from 3.6 percent in 1980 to 7.5

percent in 1995. A decrease in the percentage of children with asthma occurred between 1995 and 1996,

but it is difficult to interpret single-year changes.

■ It is difficult to obtain an accurate measurement of how

many children have asthma, because asthma is a complex

disease that can be difficult to differentiate from other

wheezing disorders, especially in children under the age

of 6 years. Prior to 1997, the percentage of children with

asthma was measured by asking parents if a child in their

family had asthma during the previous 12 months. In

1997-2001, a parent was asked if his or her child had ever

been diagnosed with asthma by a health professional. If 

the parent answered yes, then he or she was asked if 

the child had an asthma attack or episode in the last 

12 months. The percentage of children with an asthma

attack in the last 12 months measures the population

with incomplete control of asthma. For 1997-2001,

available data do not distinguish between those children

who may no longer have active asthma and those whose

asthma is well controlled.

■ Starting in 2001, the National Health Interview Survey

included a question that allows the estimation of the

percentage of children who currently have asthma. The

results indicate that 8.7 percent (6.3 million) of children had asthma in 2001.

Measure D1

Percentage of children with asthma

1980 1982 1984 1986 1988 1990 1992 1994 1996

0%

2%

4%

6%

8%

10%

12%

14%

Children with asthma

in the past 12 months 

Note: The survey questions for asthma changed in 1997; data before 1997 cannot be directly compared to data in 1997 and later.

Children ever 

diagnosed 

with asthma 

Children ever 

diagnosed with 

asthma and having 

an asthma attack in 

the past 12 months 

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics,

National Health Interview Survey

1998 2001

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants (E1-E3) Respiratory (D1-D4)

Environmental Tobacco Smoke (E5) Cotinine in Blood (B5) Respiratory (D1-D4)
Children of lower-income families and children of color are more likely to have had an

asthma attack in the previous 12 months. These children may face barriers to medical

care, or they may have less access to routine medical care and instructions for asthma

management than other children do. These factors can increase the severity and impact

of the illness.21-24 Data for 1997-2000 show that the percentage of children with asthma

having an asthma attack in the last 12 months differs by racial and ethnic groups and

by family income. 

The Institute of Medicine concluded that exposure to dust mites causes asthma in susceptible children.15 Cockroaches and tobacco smoke are likely to cause asthma in young

children.15 Research suggests that lower income children are more likely to live in

homes with higher exposure to cockroach allergens.25, 26 The first nationally representative survey of allergens in U.S. housing reported higher levels of dust mite allergen in

bedding from lower income families.27 Although some studies found higher dust mite

allergen levels in the homes of higher income families, those studies were conducted in

smaller geographic areas.25, 26

Percentage of Children

Having an Asthma

Attack in the Previous

12 Months, by

Race/Ethnicity and

Family Income

70 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Respiratory Diseases
Part 3: Childhood Illnesses 71

Respiratory Diseases

■ In 1997-2000, 5.5 percent of all children had an

asthma attack in the previous 12 months.

■ More than 8 percent of Black non-Hispanic children

living in families with incomes below the poverty level

had an asthma attack in the previous 12 months.

■ Approximately 6 percent of White non-Hispanic

children and 5 percent of Hispanic children living in

families with incomes below the poverty level had an

asthma attack in the previous 12 months.

■ More than 6 percent of children living in families with

incomes below the poverty level had an asthma attack

in the previous 12 months. About 5 percent of children

living in families with incomes at the poverty level and

higher had an asthma attack in the previous 12 months.

Percentage of children having an asthma attack in the previous 12 months,

by race/ethnicity and family income, 1997-2000 

0% 2% 4% 6% 8% 10%

Measure D2

> 200% of Poverty Level

100-200% of Poverty Level

< Poverty Level

> 200% of Poverty Level

100-200% of Poverty Level

< Poverty Level

> 200% of Poverty Level

100-200% of Poverty Level

< Poverty Level

100-200% of Poverty Level

> 200% of Poverty Level

< Poverty Level

All Incomes

All Incomes

All Incomes

All Incomes

Hispanic

All

Races/

Ethnicities

White

nonHispanic

Black

nonHispanic

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics,

National Health Interview Survey

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants (E1-E3) Respiratory (D1-D4)

Environmental Tobacco Smoke (E5) Cotinine in Blood (B5) Respiratory (D1-D4)
Children who visit emergency rooms or are hospitalized for respiratory diseases—such

as asthma, upper respiratory infections, and acute bronchitis—represent the most severe

cases of respiratory effects.

Only a fraction of children with respiratory diseases are admitted to the hospital.

Hospital admissions and emergency room visits for respiratory diseases can be related to

a number of factors besides air pollution, such as lack of access to primary health care

and instructions for asthma management. Changes in hospital admissions and emergency

room visits over time may reflect changes in medical practices, asthma therapy, and access

to and use of care.28, 29

There is extensive scientific evidence that exposure to air pollution from outdoor and

indoor sources can exacerbate existing respiratory conditions.12-14 For children with

these conditions, exposure to air pollution can lead to difficulty in breathing, increased

use of medication, visits to the doctor’s office, trips to the emergency room, and in

some cases admission to the hospital.30-33 For example, outdoor air pollution can cause

asthma attacks in children, which can lead to emergency room visits.8, 9, 34, 35 A recent

study found that increased ozone concentrations in the summer were related to increased

respiratory-related hospital and emergency room visits for children under the age of

two.19 Studies conducted in the northeastern United States indicate that air pollution

during the summer was associated with approximately 6-24 percent of all hospital

admissions for asthma.36

Recent analyses also have suggested that exacerbation of asthma from exposure to air

pollution can be more severe among lower-income people than in other populations.37, 38

Emergency Room Visits

and Hospitalizations 

for Respiratory Diseases

72 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Respiratory Diseases
Part 3: Childhood Illnesses 73

Respiratory Diseases

■ Emergency room visits for asthma and other respiratory

causes were 369 per 10,000 children in 1992 and 379

per 10,000 children in 1999. 

■ Trends in individual causes of emergency room visits

remained fairly stable between 1992 and 1999. In 1999,

hospitals reported 239 emergency room visits per 10,000

children for acute upper respiratory infections, 104 visits

per 10,000 children for asthma, and 35 visits per

10,000 children for acute bronchitis.

■ Data on children’s emergency room visits for asthma

and other respiratory causes by race and ethnicity are

shown in the data tables in Appendix A.

Measure D3

Children's emergency room visits for asthma and other respiratory causes 

1992 1993 1994 1995 1996 1997 1998 1999

Visits per 100,000 children

0

100

200

300

400

500

600

700

All asthma and

other respiratory causes

Acute upper respiratory

infections

Asthma

Acute bronchitis

Measure D3

Children's emergency room visits for asthma and other respiratory causes 

1992 1993 1994 1995 1996 1997 1998 1999

Visits per 10,000 children

0

100

200

300

400

500

All asthma and other 

respiratory causes

Acute upper 

respiratory infections

Asthma

Acute bronchitis

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics,

National Hospital Ambulatory Medical Care Survey

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants (E1-E3) Respiratory (D1-D4)

Environmental Tobacco Smoke (E5) Cotinine in Blood (B5) Respiratory (D1-D4)
74 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
Part 3: Childhood Illnesses 75

Respiratory Diseases

■ Hospital admissions for asthma and other respiratory

causes were 55 per 10,000 children in 1980 and 66 per

10,000 children in 1999. 

■ Hospital admissions for asthma alone increased from 21

per 10,000 children in 1980 to 29 per 10,000 children in

1999. Hospital admissions for acute bronchitis increased

from 16 per 10,000 children in 1980 to 29 per 10,000

children in 1999. Hospital admissions decreased for

acute upper respiratory infections from 18 per 10,000

children in 1980 to 8 per 10,000 children in 1999.

■ Asthma hospitalizations accounted for about 7 percent

of all hospitalizations for children aged 0-14 in 1999,

and asthma was the fourth leading cause of non-injuryrelated hospital admissions in that year.39

■ Acute bronchitis accounted for about 8 percent of all

hospitalizations for children aged 0-14 in 1999. Acute

bronchitis was the third leading cause of non-injury

related hospital admissions in that year.39

■ Children aged 0-14 represented 40 percent of asthma

hospitalizations for all ages (children and adults) during

1999.39

■ Children’s access to primary and preventive care also

plays a role in the number of hospitalizations.

■ Data on children’s hospital admissions for asthma and

other respiratory causes by race and ethnicity are shown

in the data tables in Appendix A.

Measure D4

Children's hospital admissions for asthma and other respiratory causes 

1980 1985 1990 1995

Admissions per 10,000 children

0

10

20

30

40

50

60

70

80

1999

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, 

National Hospital Discharge Survey

All asthma and other respiratory causes

Asthma

Acute bronchitis

Acute upper respiratory infections

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants (E1-E3) Respiratory (D1-D4)

Environmental Tobacco Smoke (E5) Cotinine in Blood (B5) Respiratory (D1-D4)
Cancer in childhood is quite rare compared with cancer in adults, but it still causes

more deaths than any factor, other than injuries and accidents, among children 1-19

years of age.40

Childhood cancer is not a single disease, but includes a variety of malignancies. The

forms of cancer that are most common vary according to age.

The annual incidence of childhood cancer increased from 1975 until about 1990. The

frequency of the disease appears to have become fairly stable overall since 1990.

Mortality has declined substantially during the last 25 years, due largely to improvements in treatment. 

The causes of cancer in children are poorly understood, though in general it is thought

that different forms of cancer have different causes. Established risk factors for the

development of childhood cancer include family history, specific genetic syndromes,

radiation, and certain pharmaceutical agents used in chemotherapy.40 Evidence from

epidemiological studies suggests that environmental contaminants such as pesticides

and certain chemicals, in addition to radiation, may contribute to an increased frequency of some childhood cancers.40, 41 Some studies have found that children born to parents who work with or use such chemicals are more likely to have cancer in childhood.40, 42 It may be that the chemicals cause mutations in parents’ germ cells that

increase the risk of their children developing certain cancers, or perhaps the parental

exposure is passed on to the child while in utero, affecting the child directly. Children’s

direct exposures to such chemicals also may contribute to cancer.

Cancer Incidence and

Mortality

76 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Childhood Cancer
Part 3: Childhood Illnesses 77

Childhood Cancer

■ The frequency of new cancer cases has been fairly stable

since 1990. The age-adjusted annual incidence of cancer

in children increased from 128 to 161 cases per million

children between 1975 and 1998. Cancer mortality

decreased from 51 to 28 deaths per million children

during the 1975-1998 period.

■ Rates of cancer incidence vary by age. Rates are highest

among infants, decline until age 9, and then rise again

with increasing age. Between 1986 and 1995, children

under 5 and those aged 15-19 experienced the highest

incidence rates of cancer at approximately 180 cases per

million. Children aged 5-9 and 10-14 had lower incidence

rates at approximately 100 and 110 cases per million

respectively.

■ Between 1994 and 1998, incidence rates of cancer were

highest among White non-Hispanics at 172 per million

for boys and 156 per million for girls. Hispanics were

next highest at 150 per million for boys and 141 per

million for girls. Asians and Pacific Islanders had an

incidence rate of 150 per million for boys and 132 per

million for girls. Black non-Hispanic children had a rate

of 133 per million for boys and 117 per million for

girls. American Indians and Alaska Natives had the

lowest rate at 82 per million for boys and 62 per

million for girls. Data on childhood cancer incidence

and mortality by race and ethnicity are shown in the

data tables in Appendix A.

Measure D5

Cancer incidence and mortality for children under 20

1975 1980 1985 1990 1995

Cases per million children

0

50

100

150

200

Incidence

Mortality

1998

SOURCE: Incidence data from National Cancer Institute, Surveillance, Epidemiology, and End Results Program; 

mortality data from Centers for Disease Control and Prevention, National Center for Health Statistics, 

National Vital Statistics System
Trends in the total incidence of childhood cancer are useful indicators for assessing the

overall burden of cancer among children. However, broad trends mask changes in the

frequency of individual cancers. Individual cancers often have patterns that diverge from

the overall trend. Moreover, environmental factors may be more likely to contribute to

some childhood cancers than to others.

Ionizing radiation, such as from x-rays, is a known cause of leukemia and brain tumors.43, 44

There is suggestive—but not conclusive—evidence that parental exposures to certain

chemicals may be a cause of leukemia, brain cancer, non-Hodgkin’s lymphoma, and

Wilms’ tumor in children.40, 42, 45

A number of studies have evaluated the relationship between pesticide exposure and

certain types of childhood cancer. Although the evidence is suggestive of a link, it is not

conclusive.40 Most studies of the relationship between pesticide exposure and leukemia

and brain cancer show increased risks for children whose parents used pesticides at home

or work, as well as for children who may be exposed to pesticides in the home.46-49

Evidence is limited but suggestive that non-Hodgkin’s lymphoma in children may be

linked to parental pesticide exposure and exposure to pesticides in the home.47 There

is some evidence linking pesticide use to Wilms’ tumor and Ewing’s sarcoma.47

There is also suggestive, though not conclusive, evidence that maternal and paternal

exposure to solvents may increase the risk of childhood cancers. A recent review found

that there is strong evidence for an association between paternal exposure to solvents—

including benzene, carbon tetrachloride, and trichloroethylene—and childhood leukemias.42

A number of studies also find a link between childhood cancer and paternal employment in

occupations related to motor vehicles or involving exposure to exhaust gas.42 In addition,

a recent study found an association between living close to areas with heavy traffic and

childhood leukemia.50 The authors of these studies suggest that the link in these cases

may be benzene, which is associated with leukemia in adults.42, 50

Types of Childhood

Cancer

78 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Childhood Cancer
Part 3: Childhood Illnesses 79

Childhood Cancer

■ Leukemia was the most common cancer diagnosis for

children from 1973-1998, representing about 20

percent of total cancer cases. Incidence of acute

lymphoblastic leukemia was 24 cases per million in

1974-1978 and approximately 28 cases per million in

1994-1998. Rates of acute myeloid leukemia were

approximately 5 cases per million in 1974-98 and about

the same in 1994-98.

■ Central nervous system tumors represented about 17

percent of childhood cancers. The incidence of central

nervous system tumors was approximately 23 cases per

million in 1974-1978 and 27 per million in 1994-1998.

■ Lymphomas, which include Hodgkin’s disease and nonHodgkin’s lymphoma, represent approximately 15 percent

of childhood cancers. Incidence of Hodgkin’s disease was

roughly 14 cases per million in 1974-1978 and 13 per

million in 1994-1998. There were approximately 9 cases

of non-Hodgkin’s lymphomas per million children in

1974-1978 and 11 per million in 1994-1998.

Cancer incidence for children under 20 by type

Cases per million children

0

5

10

15

20

25

30

35

Measure D6a

Acute

lymphoblastic

Acute

myeloid

Central

nervous

system tumors

Hodgkin's

lymphoma

Leukemias

Non-Hodgkin's

lymphoma Thyroidcarcinoma

Malignant

melanoma

Lymphomas Carcinomas and other

epithelial neoplasms 

1974-1978 1979-1983 1984-1988 1989-1993 1994-1998 

SOURCE: National Cancer Institute, Surveilliance, Epidemiology, and End Results Program
Cancer incidence for children under 20 by type

Cases per million children

0

5

10

15

20

25

30

35

Measure D6b

Germ cell

tumors

Soft tissue

sarcomas

Osteosarcoma Ewing's sarcoma Neuroblastoma

Wilms'

tumor 

HepatoMalignant Bone Tumors blastoma

1974-1978 1979-1983 1984-1988 1989-1993 1994-1998 

SOURCE: National Cancer Institute, Surveilliance, Epidemiology, and End Results Program

80 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Childhood Cancer

■ Different types of cancer affect children at different ages.

Neuroblastomas and Wilms’ tumor (tumors of the kidney)

are usually found only in very young children. Nervous

system cancers and leukemias are most common through

age 14 (leukemias being highest among 0-4 year olds);

lymphomas, carcinomas, and germ cell and other gonadal

tumors are more common in those 15-19 years old.40
Part 3: Childhood Illnesses 81
Researchers estimate that between 3 and 8 percent of the babies born in the United States

each year will be affected by neurodevelopmental disorders such as attention-deficit/

hyperactivity disorder or mental retardation.51 Neurodevelopmental disorders are disabilities in the functioning of the brain that affect a child’s behavior, memory, or ability

to learn. These effects may result from exposure of the fetus or young child to certain

environmental contaminants, though current data do not indicate the extent to which

environmental contaminants contribute to overall rates of neurodevelopmental disorders

in children. A child’s brain and nervous system are vulnerable to adverse impacts from

pollutants because they go through a long developmental process beginning shortly

after conception and continuing through adolescence.52, 53

Studies have found that several widespread environmental contaminants can damage

children’s developing brain and nervous system. Childhood exposure to lead contributes

to learning problems such as reduced intelligence and cognitive development.54-56 Studies

also have found that childhood exposure to lead contributes to attention-deficit/

hyperactivity disorder57 and hyperactivity and distractibility;58-60 increases the likelihood

of dropping out of high school, having a reading disability, lower vocabulary, and lower

class standing in high school;61 and increases the risk for antisocial and delinquent

behavior.62

Methylmercury also has negative impacts on children’s neurological development. Studies

of children whose mothers had high intakes of mercury-contaminated seafood prior to

conception found adverse impacts on intelligence63, 64 and decreased functioning in the

areas of language, attention, and memory.65 Particularly high levels of exposure to mercury in the womb have been found to cause mental retardation.66, 67

Several studies of children exposed to elevated levels of polychlorinated biphenyls (PCBs)

have linked these contaminants to neurodevelopmental effects, including lowered intelligence and behavioral deficits such as inattention and excessive reaction to stimulation.

Most of these studies find that the effects are associated with exposure in the womb

resulting from the mother having eaten food contaminated with PCBs.68-73 Adverse

effects on intelligence and behavior also have been found in children of women who

were highly exposed to mixtures of PCBs, chlorinated dibenzofurans, and other pollutants prior to conception.74-76

Human studies also suggest that exposures to other metals such as cadmium and arsenic

may have adverse effects on neurological development.58, 77-79 Other types of pollutants

also have been associated in animal studies with neurodevelopmental effects. Numerous

toxicological studies link both prenatal and postnatal exposure to organophosphate pesticides to neurodevelopmental effects.80 A recent study of brominated flame retardants

found that two of these compounds caused adverse effects on behavior, learning, and

memory in animals.81

Neurodevelopmental

Disorders in Children

82 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Neurodevelopmental Disorders

Healthy People 2010: Objective 16-14 of Healthy People 2010 calls for a reduction in the occurrence of developmental disabilities. See Appendix C for more information.
Mental retardation is a neurodevelopmental disorder that, in some cases, is related to

exposures to environmental contaminants such as lead. A measure of mental retardation

in children is presented here. A second neurodevelopmental disorder, attention-deficit/

hyperactivity disorder, is discussed in the Emerging Issues section of this report. Although

the studies described above have related lead, PCBs, mercury, and perhaps other contaminants

to adverse neurodevelopmental effects in humans, it is not currently possible to determine

the extent to which environmental contaminants contribute to developmental disorders.

Part 3: Childhood Illnesses 83

Neurodevelopmental Disorders

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants: lead (E1-E2) Lead in Blood (B1-B3)

Drinking Water: lead (E6-E7) Mercury in Blood (B4) Neurodevelopmental (D7) Lead in Schools (S1-S3)
The most commonly used definitions of mental retardation emphasize subaverage intellectual functioning before the age of 18, usually defined as an intelligence quotient

(IQ) less than 70 and impairments in life skills such as communication, self-care, home

living, and social or interpersonal skills. Different severity categories, ranging from mild

retardation to severe retardation, are defined on the basis of IQ scores.82

Researchers have identified many causes of mental retardation, including genetic disorders, traumatic accidents, and prenatal events such as maternal infection or exposure to

alcohol.82, 83 Exposure to lead and exposure to particularly high levels of mercury also

have been shown to cause mental retardation.66-67, 84 Furthermore, lead, mercury, and

PCBs all have been found to have adverse effects on intelligence and cognitive functioning

in children. Exposure to these environmental contaminants therefore has the potential

to increase the proportion of the population with IQ less than 70, thus increasing the

incidence of mental retardation in an exposed population.85

The causes of mental retardation are unknown in 30 to 50 percent of all cases.83 The

causes are more frequently identified for cases of severe retardation (IQ less than 50).

The cause of mild retardation (IQ between 50 and 70) is unknown in more than 75

percent of cases.86, 87

This measure on the prevalence of mental retardation among U.S. children presents

data obtained from the National Health Interview Survey (NHIS). Although the NHIS

provides the best national-level data available, NHIS data likely underestimate the

prevalence of mental retardation. Reasons for this understatement may include late identification of affected children and the exclusion of institutionalized children from the NHIS

survey population. Further, the NHIS relies on parents reporting that their child has

been diagnosed with mental retardation, and accuracy of parental responses could be

affected by cultural and other factors. 

Mental Retardation

84 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Neurodevelopmental Disorders
Part 3: Childhood Illnesses 85

Neurodevelopmental Disorders

■ In 1997-2000, about 6 children out of every 1,000 were

reported to have been diagnosed with mental retardation.

■ Reported rates of mental retardation were 10 per 1,000

Black non-Hispanic children, 6 per 1,000 White nonHispanic children, and 5 per 1,000 Hispanic children.

■ 12 children out of every 1,000 living in families with

incomes below the poverty level were reported to have

mental retardation. Reported rates of mental retardation

were lowest for children living in families with higher

incomes. 

Children reported to have mental retardation, by race/ethnicity

and family income, 1997-2000 

0

2

4

6

8

10

12

14

Measure D7

All White

nonHispanic

Black

nonHispanic

Hispanic < Poverty

Level 

100-200% 

of Poverty

Level 

> 200%

of Poverty

Level 

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics,

National Health Interview Survey

Cases per 1,000 children
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19. R. T. Burnett, M. Smith-Doiron, D. Stieb, M. E. Raizenne, J. R. Brook, R. E. Dales, J. A. Leech, S. Cakmak and 

D. Krewski. 2001. Association between ozone and hospitalization for acute respiratory diseases in children less

than 2 years of age. American Journal of Epidemiology 153 (5):444-52.

20. J. H. Ware, J. D. Spengler, L. M. Neas, J. M. Samet, G. R. Wagner, D. Coultas, H. Ozkaynak and M. Schwab. 1993.

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22. H. J. Farber, C. Johnson and R. C. Beckerman. 1998. Young inner-city children visiting the emergency room (ER)

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24. M. R. Price, J. M. Norris, B. Bucher Bartleson, L. A. Gavin and M. D. Klinnert. 1999. An investigation of the medical

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26. B. P. Leaderer, K. Belanger, E. Triche, T. Holford, D. R. Gold, Y. Kim, T. Jankun, P. Ren, J. E. M. Jr., T. A. PlattsMills, M. D. Chapman and M. B. Bracken. 2002. Dust mite, cockroach, cat, and dog allergen concentrations in

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32. R. C. Gwynn, R. T. Burnett and G. D. Thurston. 2000. A time-series analysis of acidic particulate matter and daily

mortality and morbidity in the Buffalo, New York, region. Environmental Health Perspectives 108 (2):125-33.

33. G. Thurston, I. Kazuhiko, C. Hayes, D. Bates and M. Lippmann. 1994. Respiratory Hospital Admissions and

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37. R. C. Gwynn and G. D. Thurston. 2001. The burden of air pollution: impacts among racial minorities.

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38. E. Nauenberg and K. Basu. 1999. Effect of insurance coverage on the relationship between asthma hospitalizations

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41. S. H. Zahm and S. S. Devesa. 1995. Childhood cancer: overview of incidence trends and environmental carcinogens.

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42. J. S. Colt and A. Blair. 1998. Parental occupational exposures and risk of childhood cancer. Environmental Health

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43. J. Boice, J.D. and R. W. Miller. 1999. Childhood and adult cancer after intrauterine exposure to ionizing radiation.

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44. R. Doll and R. Wakeford. 1997. Risk of childhood cancer from fetal irradiation. British Journal of Radiology 70:130-139.

45. S. H. Zahm. 1999. Childhood leukemia and pesticides. Epidemiology 10:473-475.

46. J. D. Buckley, L. L. Robison, R. Swotinsky, D. H. Garabrant, M. LeBeau, P. Manchester, M. E. Nesbit, L. Odom, 

J. M. Peters and W. G. Woods. 1989. Occupational exposures of parents of children with acute nonlymphocytic

leukemia: a report from the Children’s Cancer Study Group. Cancer Research 49 (4030-4037).

47. S. H. Zahm and M. H. Ward. 1998. Pesticides and childhood cancer. Environmental Health Perspectives

106 (Suppl. 3):893-908.

48. M. Feychting, N. Plato, G. Nise and A. Ahlbom. 2001. Paternal occupational exposures and childhood cancer.

Environmental Health Perspectives 109 (2):193-6.

49. X. Ma, P. A. Buffler, R. B. Gunier, G. Dahl, M. T. Smith, K. Reinier and P. Reynolds. 2002. Critical windows of

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50. R. L. Pearson, H. Wachtel and K. L. Ebi. 2000. Distance-weighted traffic density in proximity to a home is a risk factor

for leukemia and other childhood cancers. Journal of the Air and Waste Management Association 50 (2):175-80.

51. B. Weiss and P. J. Landrigan. 2000. The developing brain and the environment: an introduction. Environmental Health

Perspectives 108 Suppl. 3:373-4.

52. D. Rice and S. Barone, Jr. 2000. Critical periods of vulnerability for the developing nervous system: evidence from

humans and animal models. Environmental Health Perspectives 108 Suppl. 3:511-33.

53. P. M. Rodier. 1995. Developing brain as a target of toxicity. Environmental Health Perspectives 103 Suppl. 6:73-6.

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55. A. J. McMichael, P. A. Baghurst, N. R. Wigg, G. V. Vimpani, E. F. Robertson and R. J. Roberts. 1988. Port Pirie

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56. B. P. Lanphear, K. Dietrich, P. Auinger and C. Cox. 2000. Cognitive deficits associated with blood lead concentrations

<10 micrograms/dL in U.S. children and adolescents. Public Health Reports 115 (6):521-9.

57. R. W. Tuthill. 1996. Hair lead levels related to children’s classroom attention-deficit behavior. Archives of

Environmental Health 51 (3):214-20.

58. J. Calderon, M. E. Navarro, M. E. Jimenez-Capdeville, M. A. Santos-Diaz, A. Golden, I. Rodriguez-Leyva, V. Borja-Aburto

and F. Diaz-Barriga. 2001. Exposure to arsenic and lead and neuropsychological development in Mexican children.

Environmental Research 85 (2):69-76.

59. A. L. Mendelsohn, B. P. Dreyer, A. H. Fierman, C. M. Rosen, L. A. Legano, H. A. Kruger, S. W. Lim and 

C. D. Courtlandt. 1998. Low-level lead exposure and behavior in early childhood. Pediatrics 101 (3):E10.

60. B. Minder, E. A. Das-Smaal, E. F. Brand and J. F. Orlebeke. 1994. Exposure to lead and specific attentional problems

in schoolchildren. Journal of Learning Disabilities 27 (6):393-9.

61. H. L. Needleman, A. Schell, D. C. Bellinger, A. Leviton and E. N. Allred. 1990. The long term effects of exposure to

low doses of lead in childhood, an 11-year follow-up report. New England Journal of Medicine 322 (2):83-8.

62. H. L. Needleman, J. A. Riess, M. J. Tobin, G. E. Biesecker and J. B. Greenhouse. 1996. Bone lead levels and delinquent

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63. T. Kjellstrom, P. Kennedy, P. Wallis and C. Mantell. 1989. Physical and mental development of children with prenatal

exposure to mercury from fish. Stage 2: Interviews and psychological tests at age 6. Solna, Sweden: National Swedish

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64. K. S. Crump, T. Kjellstrom, A. M. Shipp, A. Silvers and A. Stewart. 1998. Influence of prenatal mercury exposure upon

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65. P. Grandjean, P. Weihe, R. F. White, F. Debes, S. Araki, K. Yokoyama, K. Murata, N. Sorensen, R. Dahl and 

P. J. Jorgensen. 1997. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury.

Neurotoxicology and Teratology 19 (6):417-28.

66. M. Harada, H. Akagi, T. Tsuda, T. Kizaki and H. Ohno. 1999. Methylmercury level in umbilical cords from patients

with congenital Minamata disease. Science of the Total Environment 234 (1-3):59-62.

67. F. Bakir, H. Rustam, S. Tikriti, S. F. Al-Damluji and H. Shihristani. 1980. Clinical and epidemiological aspects of

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68. T. Darvill, E. Lonky, J. Reihman, P. Stewart and J. Pagano. 2000. Prenatal exposure to PCBs and infant performance

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69. J. L. Jacobson and S. W. Jacobson. 1996. Intellectual impairment in children exposed to polychlorinated biphenyls in

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70. J. L. Jacobson and S. W. Jacobson. 1997. Teratogen Update: Polychlorinated Biphenyls. Teratology 55:338-347.

71. S. Patandin, C. I. Lanting, P. G. Mulder, E. R. Boersma, P. J. Sauer and N. Weisglas-Kuperus. 1999. Effects of 

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G. Winneke. 2001. Environmental exposure to polychlorinated biphenyls and quality of the home environment:

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80. B. Eskenazi, A. Bradman and R. Castorina. 1999. Exposures of children to organophosphate pesticides and their

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PART 4

Emerging Issues
92 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
93

Emerging Issues

he links between environmental contaminants and childhood diseases and disorders

are receiving increasing attention and research. We can expect that our understanding

of how children’s health may be influenced by environmental factors will continue to

improve with more research and better data about both environmental contaminants

and health outcomes.

This section presents information about important aspects of children’s environmental

health for which data recently have become available. Additional research in these areas

will be useful to better determine how particular exposures to environmental contaminants might contribute to these particular health areas. It is important to identify emerging issues and new data sources in order to continue to expand our understanding of children’s environmental health.

This section includes two emerging issues: mercury concentrations in fish, and attention-deficit/hyperactivity disorder (ADHD).

Part 4: Emerging Issues

T Emerging 

Issues
Some pollutants build up in the bodies of fish and other animals, reaching high concentrations at upper levels of the food chain. For mercury, this “bioaccumulation”

process occurs primarily in aquatic systems such as lakes or oceans. Mercury that is

deposited from air currents or released to water bodies tends to become attached to

particles and deposited into sediments. There, under certain conditions, bacteria convert metallic or elemental forms of mercury into methylmercury.1 Methylmercury can

be absorbed in particles or from the water by small creatures such as shrimp or other

invertebrates, which then are consumed by predators including fish.2 As each organism

builds up methylmercury in its own tissues, and as smaller fish are eaten by larger fish,

concentrations of methylmercury can accumulate, particularly in those of large fish that

live a relatively long time.3-6 Examples of other chemicals that bioaccumulate include

dioxins, PCBs, and chlorinated pesticides such as DDT or chlordane. Some of these

chemicals also may pose risks to children.

Fish are the most common source of exposure to methylmercury for most people in the

United States7, 8 and in many countries around the world.9 As noted in Part 2 of this

report, about 8 percent of women of child-bearing age have blood mercury concentrations greater than 5.8 parts per billion (equivalent to EPA’s reference dose) based on

data from the Centers for Disease Control and Prevention. EPA has determined that

children born to such women may be at some increased risk of potential adverse health

effects.10 Chemicals accumulated by women may pass through the umbilical cord, contributing to prenatal exposure in children. Prenatal exposure to such levels of

methylmercury may cause developmental and cognitive effects in children, even at doses

that do not result in effects in women who are or may become pregnant.11-13

Some proportion of mercury that ends up in fish originates as emissions to the air.

Mercury released into the atmosphere can travel long distances on global air currents

and be deposited in areas far from its original source.14, 15 The largest human-generated

source of mercury emissions in the United States is the burning of coal, which is

roughly one percent of mercury in the global pool. Other sources include the combustion of waste and industrial processes that use mercury.14

Information regarding warnings to the public about elevated concentrations of

methylmercury in fish provides some indication of the likelihood of exposure to mercury from fish that people catch for their own use. Fish advisory information is not a surrogate for exposure to the general population, because most people eat only commercial

fish that they purchase in stores or restaurants. However, there are subpopulations who

do consume fish they have caught from waters covered by fish advisories, and fish advisory information is an indirect surrogate for exposure to these populations.

The scope of the warnings issued by states varies considerably. States typically advise

people to reduce their consumption of contaminated fish by switching to less-contaminated species or to smaller fish that have not accumulated as much mercury. For

methylmercury, which accumulates in muscle tissue, changes in cooking practices such

as trimming fat or cooking over a grill do not reduce exposure. States often provide

guidance about the maximum number of meals of fish that can be safely consumed.

Some warnings apply to entire states, others are issued for individual lakes or streams.

States also issue warnings for other contaminants besides mercury.

Mercury in Fish

94 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Emerging Issues
95

A review of fish advisories for mercury indicates the following:

■ Most states issue advisories to warn people about elevated concentrations of

mercury in non-commercial fish. In 2001, 44 states had advisories in effect for

mercury in non-commercial fish. In some cases, advisories tell people to avoid

eating fish from a particular area or a particular species. In other cases, they tell

people to limit the amount of fish that they consume in general from a specified

body of water. Some advisories are directed at protecting particularly susceptible

groups, usually women of child-bearing age and children.

■ Statewide advisories have shown the greatest increase. In 2001, statewide advisories

were in effect for 17 states—Connecticut, Indiana, Kentucky, Maine, Maryland,

Massachusetts, Michigan, Minnesota, Missouri, New Hampshire, New Jersey,

North Carolina, North Dakota, Ohio, Pennsylvania, Vermont and Wisconsin—up

from five states in 1995. Another nine states have statewide advisories for mercury

in their coastal waters. Increased public health concerns have led to increased

monitoring and this may explain, in part, the observed increase in statewide

advisories.

■ State programs for monitoring contaminants in fish and issuing advisories vary

greatly. The absence of a state advisory does not necessarily indicate that there is no

risk of exposure to unsafe levels of mercury in recreationally caught fish. Likewise,

the presence of a state advisory does not indicate that there is a risk of exposure to

unsafe levels of mercury in recreationally caught fish, unless people consume these

fish at levels greater than those recommended by the fish advisory.

■ Although some states monitor fish in a large number of water bodies, other states

monitor few or none. The relationship between monitoring, setting of fishing

advisories, and frequency of fishing has not been evaluated by EPA. Also, the

concentration of mercury that triggers an advisory varies from state to state. As a

result, the number of advisories does not directly represent the severity of

contaminants in recreationally caught fish. It also reflects the extent of monitoring

and the way that states assess risk.

EPA will work with other agencies to evaluate the feasibility of developing a measure

more closely related to exposures that reflect mercury concentrations in fish intended

for human consumption, for inclusion in future reports.

Part 4: Emerging Issues

Emerging Issues

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Mercury in Blood (B4) Neurodevelopmental (D7)
Attention-deficit/hyperactivity disorder (ADHD) is a disruptive behavior disorder characterized by ongoing inattention and/or hyperactivity-impulsivity occurring in several settings and more frequently and severely than is typical for individuals in the same stage of

development.17 ADHD can make family and peer relationships difficult, diminish academic performance, and reduce vocational development. 

A diagnosis of ADHD considers whether a child is hyperactive, inattentive, or impulsive, at

levels that are higher than expected for a child’s developmental stage, and whether the

behaviors occur on a continual basis in different settings (for example, both at school

and at home) and whether the behaviors interfere with the child’s ability to function

in those settings.17, 18

As the medical profession has developed a greater understanding of ADHD through

the years, the name of this condition has changed. The American Psychiatric Association

adopted the name “attention deficit disorder” in the early 1980s and revised it to

“attention-deficit/hyperactivity disorder” in 1987.19

Research on this disorder is ongoing and extensive, and new findings are frequently

reported, but the causes of ADHD are unknown. Research indicates that there are

genetic influences on the incidence of ADHD.18, 20-22 The role of environmental contaminants in contributing to ADHD is unknown, as few studies have looked explicitly at

the relationship between ADHD and exposures to environmental contaminants.

However, many of the behaviors that are observed in children with ADHD also have

been associated with elevated exposures to certain environmental contaminants. Several

studies have found relationships between attention problems, hyperactivity, and impulsivity, which are the common behaviors of ADHD, and exposures to lead23-28 and

PCBs.29-32 Animal studies provide supporting evidence that exposures to PCBs and lead

may contribute to ADHD.28, 33

Data on the prevalence of ADHD among U.S. children are available from the National

Health Interview Survey (NHIS), conducted by the National Center for Health

Statistics of the Centers for Disease Control and Prevention, for the years 1997-2001.

Although the NHIS provides the best data available, it is difficult to develop estimates

of the prevalence of ADHD for a variety of reasons. Diagnosis of ADHD relies on

recognition of various types of behaviors in different combinations, and therefore

requires a certain amount of judgment on the part of a doctor, similar to other psychiatric disorders. Many other problems, including anxiety disorders, depression, and

learning disabilities, can be expressed with signs and symptoms that resemble those of

ADHD. As many as half of those with ADHD also have other mental disorders, which

can make it harder to diagnose and treat ADHD.34

A diagnosis of ADHD depends not only on the presence of particular symptoms and

behaviors in a child, but on concerns being raised by a parent or teacher about the

child’s behavior and on the child’s access to a doctor to make the diagnosis. Further, the

NHIS relies on parents reporting that their child has been diagnosed with ADHD. 

It is unclear whether the percentage of children with ADHD has increased in recent

years. Although recently more children have been diagnosed with and treated for ADHD,

this increase may not reflect an increase in incidence, but rather greater awareness of the

condition due to media attention, development of effective treatments, or other factors.

Continued tracking of ADHD in the coming years should be useful for evaluating

trends in diagnosis of ADHD.

AttentionDeficit/Hyperactivity

Disorder

96 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Emerging Issues
97

It is most informative to focus on ADHD statistics for children 5-17 years old, because it

is difficult to diagnose ADHD in younger children. Data from the NHIS indicate that:

■ In 1997-2000, 6.7 percent of children ages 5-17 were reported to have been

diagnosed with attention-deficit/hyperactivity disorder (ADHD). 

■ Eight percent of White non-Hispanic children, 5 percent of Black non-Hispanic

children, and nearly 4 percent of Hispanic children were reported to have ADHD.

■ Almost 14 percent of White non-Hispanic children living in families with incomes

below poverty level were reported to have ADHD—the highest of any group.

■ Two to three times more boys than girls are diagnosed with ADHD.35

Part 4: Emerging Issues

Emerging Issues
98 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

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11. P. Grandjean, R. F. White, A. Nielsen, D. Cleary and E. C. de Oliveira Santos. 1999. Methylmercury neurotoxicity in

Amazonian children downstream from gold mining. Environmental Health Perspectives 107 (7):587-91.

12. P. Grandjean, P. Weihe, R. F. White and F. Debes. 1998. Cognitive performance of children prenatally exposed to

“safe” levels of methylmercury. Environmental Research 77 (2):165-72.

13. P. Grandjean, P. Weihe, R. F. White, F. Debes, S. Araki, K. Yokoyama, K. Murata, N. Sorensen, R. Dahl and P. J.

Jorgensen. 1997. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury.

Neurotoxicology and Teratology 19 (6):417-28.

14. U.S. Environmental Protection Agency. 1996. Mercury Study Report to Congress, Volumes I to VII. Washington, DC:

Office of Air Quality Planning and Standards. http://www.epa.gov/oar/mercury.html.

15. W. F. Fitzgerald, D. R. Engstrom, R. P. Mason and E. A. Nater. 1998. The case for atmospheric mercury contamination in remote areas. Environmental Science and Technology 32 (1):1-7.

16. U.S. Environmental Protection Agency. 2001. EPA National Advice on Mercury in Freshwater Fish for Women Who Are

or May Become Pregnant, Nursing Mothers, and Young Children. EPA Office of Water.

http://www.epa.gov/ost/fishadvice/advice.html.

17. American Psychiatric Association. 2000. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Text

Revision. Washington D.C.: American Psychiatric Association.

18. National Institute of Mental Health. 1994. Attention Deficit Hyperactivity Disorder. 96-3572.

http://www.nimh.nih.gov/publicat/adhd.cfm.

19. National Institute of Mental Health. 2000. Attention Deficit Hyperactivity Disorder (ADHD) – Questions and Answers.

http://www.nimh.nih.gov/publicat/adhdqa.cfm (cited October 15, 2001).
Part 4: Emerging Issues 99

References

20. A. Thapar, J. Holmes, K. Poulton and R. Harrington. 1999. Genetic basis of attention deficit and hyperactivity.

British Journal of Psychiatry 174:105-11.

21. Y.C. Ding, H.C. Chi, D.L. Grady, A. Morishima, J.R. Kidd, K.K. Kidd, P. Flodman, M.A. Spence, S. Schuck, J.M.

Swanson, Y.P. Zhang and R.K. Moyzis. 2002. Evidence of positive selection acting at the human dopamine receptor D4 gene locus. Proceedings of the National Academy of Sciences 99(1):309-14.

22. A. Kirley, Z. Hawi, G. Daly, M. McCarron, C. Mullins, N. Millar, I. Waldman, M. Fitzgerald and M. Gill. 2002.

Dopaminergic system genes in ADHD: toward a biological hypothesis. Neuropsychopharmacology 27(4):607-19.

23. J. Calderon, M. E. Navarro, M. E. Jimenez-Capdeville, M. A. Santos-Diaz, A. Golden, I. Rodriguez-Leyva, V. Borja-Aburto

and F. Diaz-Barriga. 2001. Exposure to arsenic and lead and neuropsychological development in Mexican children.

Environmental Research 85 (2):69-76.

24. A. L. Mendelsohn, B. P. Dreyer, A. H. Fierman, C. M. Rosen, L. A. Legano, H. A. Kruger, S. W. Lim and 

C. D. Courtlandt. 1998. Low-level lead exposure and behavior in early childhood. Pediatrics 101 (3):E10.

25. B. Minder, E. A. Das-Smaal, E. F. Brand and J. F. Orlebeke. 1994. Exposure to lead and specific attentional problems

in schoolchildren. Journal of Learning Disabilities 27 (6):393-9.

26. H. L. Needleman, A. Schell, D. C. Bellinger, A. Leviton and E. N. Allred. 1990. The long term effects of exposure to

low doses of lead in childhood, an 11-year follow-up report. New England Journal of Medicine 322 (2):83-8.

27. H. L. Needleman, J. A. Riess, M. J. Tobin, G. E. Biesecker and J. B. Greenhouse. 1996. Bone lead levels and delinquent

behavior. Journal of the American Medical Association 275 (5):363-9.

28. D. C. Rice. 1996. Behavioral effects of lead: commonalities between experimental and epidemiologic data.

Environmental Health Perspectives 104 (Suppl. 2):337-51.

29. J. L. Jacobson and S. W. Jacobson. 1996. Intellectual impairment in children exposed to polychlorinated biphenyls in

utero. New England Journal of Medicine 335 (11):783-9.

30. J. L. Jacobson and S. W. Jacobson. 1997. Teratogen Update: Polychlorinated Biphenyls. Teratology 55:338-347.

31. S. Patandin, C. I. Lanting, P. G. Mulder, E. R. Boersma, P. J. Sauer and N. Weisglas-Kuperus. 1999. Effects of environmental exposure to polychlorinated biphenyls and dioxins on cognitive abilities in Dutch children at 42

months of age. Journal of Pediatrics 134 (1):33-41.

32. P. Stewart, J. Reihman, E. Lonky, T. Darvill and J. Pagano. 2000. Prenatal PCB exposure and neonatal behavioral

assessment scale (NBAS) performance. Neurotoxicology and Teratology 22 (1):21-9.

33. D. C. Rice. 2000. Parallels between Attention Deficit Hyperactivity Disorder and behavioral deficits produced by

neurotoxic exposure in monkeys. Environmental Health Perspectives 108 (Suppl. 3):405-408.

34. National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention. 2002.

What is Attention-Deficit-Hyperactivity Disorder? http://www.cdc.gov/ncbddd/adhd/what.htm (Cited February 19,

2003).

35. P. N. Pastor and C.A. Reuben. 2002. Attention-deficit disorder and learning disability: United States, 1997-98.

National Center for Health Statistics. Vital Health Statistics 10 (206).

http://www.cdc.gov/nchs/data/series/sr_10/sr10_206.pdf.

PART 5

Special Features
his Special Features section presents measures of environments and health disorders for which data are available only for individual states, not for the nation as a

whole.

The measures in this section address potential exposures to lead and pesticides at schools,

an environment where children spend a significant portion of their time. The data on

lead in schools are from California; the data on pesticides in schools are from Minnesota.

The final measure in this section presents trends in birth defects, a collection of childhood conditions for which there is some suspected environmental influence, using data

from California.

Special

Features

102 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Special Features

T
Elevated levels of lead in blood remain an important childhood environmental health

hazard in the United States. Childhood exposure to lead contributes to learning problems such as reduced intelligence and cognitive development.1-3 Studies also have found

that childhood exposure to lead contributes to attention-deficit/hyperactivity disorder4

and hyperactivity and distractibility;5-7 increases the likelihood of dropping out of high

school, having a reading disability, lower vocabulary, and lower class standing in high

school;8 and increases the risk for antisocial and delinquent behavior.9 There is no

demonstrated safe concentration of lead in blood, and adverse health effects can occur

at very low blood lead levels.2, 3, 10

Ingestion of dust and soil contaminated mainly by deteriorated lead-based paint and by

past emissions of leaded gasoline deposited in the soil are the main sources of lead

exposure.11-13 Direct ingestion of paint chips can be important in some cases.14 Other

sources of lead exposure in the United States include drinking water, soil and dust,

canned food and drink, lead-glazed ceramics, and industrial plant emissions.11, 15

In 1992, the California Legislature approved the Lead-Safe Schools Protection Act.

Following approval of this legislation, the California Department of Health Services

conducted a study to determine the prevalence of lead and lead hazards in the state’s

public elementary schools, including elementary school buildings that house day care

centers and preschools. Measures S1-S3 present data from this hazard assessment.

Lead in California's

Public Elementary

Schools

Part 5: Special Features 103

Lead in California Schools

Healthy People 2010: Objective 8-11 of Healthy People 2010 aims to eliminate elevated blood

lead levels in U.S. children. See Appendix C for more information.
The presence of lead-containing paint in environments where children reside or spend

time—including homes, schools, and childcare facilities—does not always result in

exposure. However, it creates a potential for exposure, particularly if the paint is 

deteriorated and accessible to children. 

Deteriorated paint is more prevalent in old and poorly maintained buildings. According

to the National Center for Education Statistics, 75 percent of all public elementary schools

nationwide were built before 1970, and about 14 percent of these schools have never

been renovated.16 Sixteen percent of these pre-1970 schools were renovated before 1980,

the period preceding and immediately after the Consumer Product Safety Commission’s

1978 rule limiting the amount of lead allowed in paint to 600 parts per million.16

Therefore, about one-third of the nation’s oldest schools (those built before 1970) were

never renovated or were renovated before limits were placed on the amount of lead in

paint. Recent housing survey estimates from the U.S. Department of Housing and

Urban Development (HUD) suggest that 25 percent of housing units with one or

more children under the age of 6 have significant lead-based paint hazards.* 17, 18

Children under the age of six are particularly vulnerable to lead exposure and its adverse

effects because of age-related risk factors such as hand-to-mouth behavior, pica (a tendency to mouth or attempt to consume non-food objects),19 small body mass, and a

developing brain and nervous system. Currently, 60 percent of children aged three to

five are enrolled in day care or similar programs and more than 7.8 million children are

enrolled in pre-kindergarten to first grade.20 Lead hazards within the school environment

may be an important contributor to exposure.

In its study of the prevalence of lead and lead hazards in California public elementary

schools, the California Department of Health Services collected a maximum of four

interior and seven exterior paint chip samples from each of the 200 schools studied.

Where possible, paint chip samples were obtained from areas where the paint was 

visibly deteriorated.

Deteriorated 

Lead-containing 

Paint in California’s

Public Elementary

Schools

104 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Lead in California Schools

* The Department of Housing and Urban Development defines a “significant lead-based paint hazard”

as: a) deteriorated lead-based paint (paint containing 0.5 percent by weight or 1 milligram per square

centimeter of lead) of more than 20 square feet (exterior) or two square feet (interior) on large-surfacearea components, or damage to more than 10 percent of the total surface area of interior small surface

area components; or b) lead-contaminated dust on floors with 40 micrograms or greater of lead per

square foot, dust on window sills with 250 micrograms or greater of lead per square foot; or c) bare leadcontaminated soil of more than 9 square feet with a soil lead concentration of 1,200 parts per million

or greater, or 400 parts per million for bare soil in an area frequented by a child under the age of six.
Part 5: Special Features 105

Lead in California Schools

■ Thirty-seven percent of all public elementary schools surveyed in California had both lead-containing paint and

some deterioration of paint. Thirty-two percent of these

schools had lead-based paint and some deterioration. The

term “lead-containing paint” refers to paint containing

any detectable level of lead. “Lead-based” paint refers to

paint containing at least 5,000 parts per million of lead. 

■ Generally, the proportion of schools with lead-containing

paint and some deterioration of paint decreased as the

age of the schools decreased. Most (72 percent) of the

California schools built before 1940 had lead-containing

paint and some deterioration, compared with only 3

percent of the schools built between 1980 and 1995. A

similar trend was observed for paint deterioration and

lead in paint at or exceeding the Consumer Product Safety

Commission and EPA/HUD standards (600 parts per

million and 5,000 parts per million respectively).

■ Ninety percent of all schools surveyed had lead-containing

paint. All pre-1980 schools and 45 percent of schools

built between 1980 and 1995 had lead-containing

paint. (Data not shown.)

Percentage of California public elementary schools with lead paint 

and some deterioration of paint, 1994-1997

0%

20%

40%

60%

80%

Measure S1

Schools Built

Before 1940

Schools Built

1940-1959

Schools Built

1960-1979

Schools Built

1980-1995

Any Detectable Lead > 600 ppm > 5,000 ppm

All Schools

SOURCE: California Department of Health Services, Childhood Lead Poisoning Prevention Branch. 

Lead Hazards in California's Public Elementary Schools and Child Care Facilities. April, 1998

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants: lead (E1-E2) Lead in Blood (B1-B3) Neurodevelopmental (D7) Lead in Schools (S1-S3) Drinking Water: lead (E6-E7) 
Lead-contaminated soil poses an exposure risk to children. EPA’s hazard standard for

lead in soil is 400 parts per million by weight in play areas, and 1,200 parts per million

in bare soil in the remainder of the yard. EPA recommends measures to reduce exposure

when lead in soil is at or above these hazard standards.21 Exposure to soil lead levels

lower than the hazard standards also may pose some risk. Current research shows there

is no safe level of lead in blood.2, 3, 10

Deteriorated exterior lead-based paint and fallout from air-borne emissions may lead to

contamination of soil in schoolyard areas. Some of the widespread lead in U.S. soils,

especially around busy roadways, is attributable to automobile emissions before leaded

gasoline was phased out.22, 23

Lead-contaminated Soil

Near California’s Public

Elementary Schools

106 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Lead in California Schools
Part 5: Special Features 107

Lead in California Schools

■ Eighty-nine percent of all California schools in the study

(public elementary schools) had detectable levels of lead

in soils. Only 7 percent of the schools had lead levels in

soil at or exceeding the EPA hazard standard.

■ All buildings built before 1940 had detectable levels of

lead in soils, and 30 percent exceeded the EPA hazard

standard.

■ None of the schools built after 1980 had levels of lead

in soils at or exceeding the EPA hazard standard. 

■ The typical lowest concentration of lead that the method

could measure for the soil sample analysis was 20 parts

per million, with a range of 3.7 parts per million to 151

parts per million.

Percentage of California public elementary schools with lead in soils, 1994-1997 

0%

20%

40%

60%

80%

100%

Measure S2

All Schools Schools Built

Before 1940

Schools Built

1940-1979

Schools Built

1980-1995

Schools with detectable

lead in soils 

Schools with 400 ppm

lead in soils 

SOURCE: California Department of Health Services, Childhood Lead Poisoning Prevention Branch. 

Lead Hazards in California's Public Elementary Schools and Child Care Facilities. April, 1998

>

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants: lead (E1-E2) Lead in Blood (B1-B3) Neurodevelopmental (D7) Lead in Schools (S1-S3) Drinking Water: lead (E6-E7) 
Drinking water may be contaminated with lead through contact with lead pipes found

in older buildings, brass faucets, and copper pipes with lead solder. The use of pipes,

plumbing fittings, fixtures, or flux that are not “lead-free” in the installation and repair

of non-residential facilities was prohibited in June, 1986.24 EPA’s action level for lead in

drinking water is 15 parts per billion, and the Maximum Contaminant Level Goal

(MCLG) is zero.25 The MCLG is the concentration in drinking water at which no known

or anticipated adverse effect on the health of persons would occur and which allows an

adequate margin of safety.

On average, lead in drinking water accounts for an estimated 10-20 percent of total lead

exposure in young children.26 “First draw” water from pipes that have not been flushed

tends to have higher lead content but are not representative of typical concentrations.26 

Lead-contaminated

Drinking Water in

California’s Public

Elementary Schools

108 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Lead in California Schools
109

■ Detectable amounts of lead were reported in drinking

water at 53 percent of all schools in the California study.

First draw samples from 15.5 percent of participating

schools (31 out of 200 schools) exceeded the EPA hazard

standard of 15 parts per billion. Drinking water from

approximately 6.5 percent of participating schools

remained above the standard on the second draw.

Second-draw samples are more representative of the lead

concentrations that children are exposed to during most

of the day. Data for first- and second-draw samples are

available only for all schools combined, and not for

schools grouped by year of construction.

■ The percentage of schools with lead contamination

exceeding the EPA standard decreased as the age of the

schools decreased. 

■ The lowest concentration of lead measurable in the

water analysis was 5 parts per billion.

Percentage of California public elementary schools 

with lead in drinking water, 1994-1997 

0%

20%

40%

60%

80%

Measure S3

Schools Built All Schools

Before 1940

Schools Built

1940-1979

Schools Built

1980-1995

Schools with detectable

lead in drinking water 

Schools with 15 ppb lead 

in drinking water 

Schools with 15 ppb lead in

drinking water at 1st draw

Schools with 15 ppb lead in 

drinking water at 2nd draw

SOURCE: California Department of Health Services, Childhood Lead Poisoning Prevention Branch.

Lead Hazards in California's Public Elementary Schools and Child Care Facilities. April, 1998

>

>

>

Part 5: Special Features

Lead in California Schools

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Criteria Air Pollutants: lead (E1-E2) Lead in Blood (B1-B3) Neurodevelopmental (D7) Lead in Schools (S1-S3) Drinking Water: lead (E6-E7) 
110 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
Children may be exposed to pesticides in their diets and through contact with pesticides

used in homes, schools, and day care centers. Children are particularly vulnerable to the

effects of pesticides because of their unique susceptibilities and relatively high exposures

compared with adults.27-30 Because children spend a significant portion of time at school,

this setting may be an important contributor to overall exposure. 

There is no federal statute requiring the collection of data on pesticide use in schools;

thus there is no nationwide information on the amount of pesticides used in the nation’s

110,000 schools.31

Few states require reporting of pesticide use. For those states that do, the information

collected generally is not adequate to assess exposure. Some states have regulated and/or

assessed the use of pesticides in schools. In 1995, Louisiana passed a law requiring its

school districts to report the amount of pesticides used annually. In New York, commercial applicators are required by a 1996 law to report the amount of a specific pesticide used and the location where it was applied. Six states—Arizona, California,

Connecticut, Massachusetts, New Hampshire, and New Mexico—require commercial

applicators to report the amount of specific pesticides used, but not the locations where

the pesticides are applied.31

In recent years, EPA has recommended that schools undertake Integrated Pest

Management (IPM) to reduce pesticide use. An IPM program for schools may include

redesigning and repairing structures, improving sanitation, employing pest-resistant

varieties of plants, establishing watering and mowing practices that minimize the need

for pesticides, and applying pesticides judiciously. IPM programs frequently are more

economical and less hazardous to people, the environment, and property than conventional approaches to pest control.32 Currently, approximately 10 states require the adoption of IPM in schools.33

In 1999 the state of Minnesota conducted a survey on pesticide use in schools. The

results presented here focus on indoor uses of pesticides, because pesticide residues can

be persistent indoors,34-36 and because children spend most of their time indoors when

they are at school. Some pesticides have been detected at indoor concentrations potentially hazardous to children weeks and months after application.34, 37

Pesticide Use in Schools

Part 5: Special Features 111

Pesticides in Minnesota Schools

Healthy People 2010: Objective 8-24 of Healthy People 2010 aims to reduce 

exposure to pesticides. See Appendix C for more information.
Legislation recommending the use of Integrated Pest Management (IPM) in schools

was introduced in Minnesota in 1999 and again in 2000. In response to increased

awareness and concern about the issue of pesticides in schools, the state conducted a

survey in 1999 on current pest management practices in kindergarten through secondary (K-12) schools.

This measure presents data from the survey on the frequency of pesticide use and some

information about how these pesticides were used. The measure is only a surrogate for

exposure. The frequency with which pesticides are used is an indicator of potential

exposure because the risk of exposure increases with the frequency of pesticide use. This

measure does not provide information about the toxicity of pesticides used or details

about how they were applied and thus cannot provide a complete representation of the

risk of adverse effects following exposure.

Pesticide Use in

Minnesota’s Public and

Private Schools

112 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Pesticides in Minnesota Schools
113

■ Approximately 47 percent of responding school custodians

reported that they sprayed pesticides “as needed” in the

classroom. A little over a third (34 percent) reported the

same frequency of pesticide use in locker rooms and

gymnasiums, cafeterias, kitchens, and food storage areas.

■ Most (64 percent) responding custodians reported that

their schools engaged the services of contractors to apply

pesticides routinely, and that most of these contractors

(90 percent) had applicator certification and licenses.

However, the survey reported that facility directors,

custodial and maintenance staff, and teachers also were

engaged in routine pesticide application in schools.

■ The indoor pesticides reported as the most commonly used

were Saga WP, Demand CS, Tempo WP (all pyrethroids),

and Borid. However, a variety of pesticides including the

organophosphates Dursban (chlorpyrifos) and Diazinon

were used indoors in some schools. An agreement between

EPA and registrants of Dursban cancelled the pesticide’s

use in schools, parks, and other settings where children

may be exposed. This phase-out resulted in the

termination of retail sales by December, 2001.38

■ Forty percent of the responding custodians reported

that their schools provided no notification of pesticide

use (such as notices in fumigated areas or pre- and postapplication letters to students and teachers).

Frequency of application of pesticides in Minnesota K-12 schools, 1999 

Percentage of schools

0%

10%

20%

30%

40%

50%

Cafeteria and kitchen/food storage area 

Locker rooms and gymnasium 

Classrooms 

Measure S4

Sprayed Not Sprayed

As Needed 

Once

per Month

1-4 Times

per Year

No Answer /

Other / Don't Know

SOURCE: C.J. Olson Market Research Inc. for Minnesota Department of Agriculture. Quantitative Research 

Regarding Pest Management in Minnesota K-12 Schools. 1999

Pesticides in Minnesota Schools

Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features

Pesticide Residues (E8) Pesticide Use in Schools (S4)

Part 5: Special Features
Birth defects are the leading cause of infant death in the first year of life, accounting for

about 20 percent of infant deaths in 1999.39 The term “birth defects” covers a range of

structural defects of the limbs or mouth, defects that affect development of the spinal

cord, and defects of internal organs, such as the heart. Infants who do not die from birth

defects often have lifelong disabilities, such as mental retardation, heart problems, or

difficulty in performing everyday activities such as walking.

Some birth defects are inherited. Other risk factors for birth defects include prenatal

exposure of the fetus to certain pharmaceuticals, such as Accutane; alcohol; and insufficient folate in a woman’s diet. The causes of a significant portion of birth defects are

unknown, but research suggests that defects could be influenced by environmental

factors.40 Several environmental contaminants cause birth defects when pregnant

women are exposed to high concentrations. Mercury poisoning in Minamata, Japan,

resulted in birth defects such as deafness and blindness.41 Prenatal exposures to high

concentrations of polychlorinated biphenyls (PCBs) have resulted in stained and acned

skin and deformed nails in children.42 However, the relationship between exposure to

lower concentrations of environmental contaminants and birth defects is less clear.

A number of epidemiological studies have evaluated the relationship between environmental and occupational exposures and birth defects. A recent scientific review that

evaluated multiple studies of women’s occupational exposure to organic solvents found

an increased risk for birth defects such as heart defects and oral cleft defects.43 Studies

of fathers have found that certain occupations are associated with birth defects in their

children.44-46 Studies evaluating the role of pesticides in birth defects have found an

association between maternal and paternal exposure to pesticides and increased risk of

offspring having or dying from birth defects.44-54

There currently is no national monitoring system for birth defects. However, most states

have some type of birth defects monitoring program. At the end of 2000, 45 of the

states, the District of Columbia, and Puerto Rico had some type of existing birth defects

monitoring program.55 The type of tracking varies widely among the states. A small portion of these states have the most complete type of tracking system, which includes

actively researching medical records for birth defects and following children through the

first year of life. The remaining states have some type of monitoring program, but do not

have all the aspects of a complete surveillance system. California has monitored birth

defects since 1983 and has a monitoring program that is considered most complete.

Data from California for several major defects are presented here.

Birth Defects

114 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Birth Defects in California
115

■ Heart defects are the most common birth defect in

California, with 1.8 cases per 1,000 live births and fetal

deaths in 1997-99.

■ The rates of birth defects in California generally

remained constant during the 1990s. 

■ Other important defects not shown here are neural tube

defects and defects of the reproductive system, such as

hypospadias. During the 1990s, there were six cases of

neural tube defects per 10,000 (0.6 per 1,000) live

births and fetal deaths. There were insufficient data to

determine a trend over the 1990s. Data on hypospadias

are not available from the state of California.

Number of birth defects in California per 1,000 live births and fetal deaths

0.0

0.5

1.0

1.5

2.0

2.5

Measure S5

Heart Defects Oral Cleft Defects Down Syndrome Intestinal Defects Limb Defects

1991 – 1993 1994 – 1996 1997 – 1999 

SOURCE: California Birth Defects Monitoring Program

Part 5: Special Features

Birth Defects in California
116 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

References

1. D. Bellinger, A. Leviton and C. Waternaux. 1987. Longitudinal analyses of prenatal and postnatal lead exposure and

early cognitive development. New England Journal of Medicine 316 (17):1037-43.

2. A. J. McMichael, P. A. Baghurst, N. R. Wigg, G. V. Vimpani, E. F. Robertson and R. J. Roberts. 1988. Port Pirie

Cohort Study: environmental exposure to lead and children’s abilities at the age of four years. New England

Journal of Medicine 319 (8):468-75.

3. B. P. Lanphear, K. Dietrich, P. Auinger and C. Cox. 2000. Cognitive deficits associated with blood lead concentrations

<10 micrograms/dL in U.S. children and adolescents. Public Health Reports 115 (6):521-9.

4. R. W. Tuthill. 1996. Hair lead levels related to children’s classroom attention-deficit behavior. Archives of Environmental

Health 51 (3):214-20.

5. J. Calderon, M. E. Navarro, M. E. Jimenez-Capdeville, M. A. Santos-Diaz, A. Golden, I. Rodriguez-Leyva, V. Borja-Aburto

and F. Diaz-Barriga. 2001. Exposure to arsenic and lead and neuropsychological development in Mexican children.

Environmental Research 85 (2):69-76.

6. A. L. Mendelsohn, B. P. Dreyer, A. H. Fierman, C. M. Rosen, L. A. Legano, H. A. Kruger, S. W. Lim and 

C. D. Courtlandt. 1998. Low-level lead exposure and behavior in early childhood. Pediatrics 101 (3):E10.

7. B. Minder, E. A. Das-Smaal, E. F. Brand and J. F. Orlebeke. 1994. Exposure to lead and specific attentional problems

in schoolchildren. Journal of Learning Disabilities 27 (6):393-9.

8. H. L. Needleman, A. Schell, D. C. Bellinger, A. Leviton and E. N. Allred. 1990. The long term effects of exposure to

low doses of lead in childhood, an 11-year follow-up report. New England Journal of Medicine 322 (2):83-8.

9. H. L. Needleman, J. A. Riess, M. J. Tobin, G. E. Biesecker and J. B. Greenhouse. 1996. Bone lead levels and delinquent

behavior. Journal of the American Medical Association 275 (5):363-9.

10. E. K. Silbergeld. 1997. Preventing lead poisoning in children. Annual Review of Public Health 18:187-210.

11. J. L. Pirkle, R. B. Kaufmann, D. J. Brody, T. Hickman, E. W. Gunter and D. C. Paschal. 1998. Exposure of the 

U.S. population to lead, 1991-1994. Environmental Health Perspectives 106 (11):745-50.

12. B. P. Lanphear, T. D. Matte, J. Rogers, R. P. Clickner, B. Dietz, R. L. Bornschein, P. Succop, K. R. Mahaffey, S. Dixon,

W. Galke, M. Rabinowitz, M. Farfel, C. Rohde, J. Schwartz, P. Ashley and D. E. Jacobs. 1998. The contribution

of lead-contaminated house dust and residential soil to children’s blood lead levels. A pooled analysis of 12 epidemiologic studies. Environmental Research 79 (1):51-68.

13. M. Weitzman, A. Aschengrau, D. Bellinger, R. Jones, J. S. Hamlin and A. Beiser. 1993. Lead-contaminated soil 

abatement and urban children’s blood lead levels. Journal of the American Medical Association 269 (13):1647-54.

14. M. D. McElvaine, E. G. DeUngria, T. D. Matte, C. G. Copley and S. Binder. 1992. Prevalence of radiographic evidence

of paint chip ingestion among children with moderate to severe lead poisoning, St Louis, Missouri, 1989 through

1990. Pediatrics 89 (4 Pt 2):740-2.

15. United States Environmental Protection Agency. 2001. Lead Phase-out [Web site], 2001.

http://www.epa.gov/oia/tips/lead2.htm.

16. C. Rowand. 1999. How Old Are America’s Public Schools? Washington, DC: Department of Education. 

National Center for Education Statistics (NCES). NCES 1999-048. 

http://nces.ed.gov/pubs99/quarterlyapr/4-elementary/4-esq11-h.html.

17. D. E. Jacobs, R. P. Clickner, J. Y. Zhou, S. M. Viet, D. A. Marker, J. W. Rogers, D. C. Zeldin, P. Broene and 

W. Friedman. 2002. The prevalence of lead-based paint hazards in U.S. housing. Environmental Health

Perspectives 110 (10):A599-606.
Part 5: Special Features 117

References

18. U.S. Department of Housing and Urban Development. 2001. National Survey of Lead and Allergens in Housing. Final

Report. Volume 1: Analysis of Lead Hazards. Washington, DC. http://www.hud.gov/lea/HUD_NSLAH_Vol1.pdf.

19. United States Environmental Protection Agency. 1998. Risk Analysis to Support Standards for Lead in Paint, Dust and

Soil. Washington, DC. EPA 747-R-97-006. http://www.epa.gov/lead/403risk.htm.

20. J. Wirt, S. Choy, D. Gerald, S. Provasnik, P. Rooney, S. Watanabe, R. Tobin and M. Glander. 2001. The Condition of

Education 2001. Washington, DC: U.S. Department of Education. National Center for Education Statistics.

NCES 2001-072. http://nces.ed.gov/pubsearch/pubsinfo.asp?pubid=2001072.

21. Lead-Based Paint Poisoning Prevention in Certain Residential Structures. 40 CFR§745.65( c).

http://www.access.gpo.gov/nara/cfr/waisidx_01/40cfr745_01.html.

22. H. W. Mielke. 1999. Lead in the inner cities. American Scientist 87:62-73.

23. H. Mielke and P. Reagan. 1998. Soil is an important pathway of human lead exposure. Environmental Health

Perspectives 106 (Suppl. 1):217-229.

24. Prohibition on Use of Lead Pipes, Solder, and Flux. 42 U.S.C. 300g-6. http://www4.law.cornell.edu/uscode/42/300g-1.html.

25. National Primary Drinking Water Regulations. 40CFR1.141:

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26. United States Environmental Protection Agency. 1993. Lead in Your Drinking Water: Actions You can Take to Reduce

Lead in Drinking Water. Washington, DC. EPA 810-F-93-001. http://www.epa.gov/safewater/Pubs/lead1.html.

27. S. H. Zahm and S. S. Devesa. 1995. Childhood cancer: overview of incidence trends and environmental carcinogens.

Environmental Health Perspectives 103 (Suppl. 6):177-184.

28. L. R. Goldman. 1995. Children—unique and vulnerable: environmental risks facing children and recommendations

for response. Environmental Health Perspectives 103 (Suppl. 6):13-18.

29. B. Eskenazi, A. Bradman and R. Castorina. 1999. Exposures of children to organophosphate pesticides and their

potential adverse health effects. Environmental Health Perspectives 107 (Suppl. 3):409-19.

30. National Research Council. Committee on Pesticides in the Diets of Infants and Children. 1993. 

Pesticides in the Diets of Infants and Children. Washington, DC: National Academy Press. 0309048753.

http://www.nap.edu/catalog/2126.html?se_side.

31. U.S. General Accounting Office (GAO). 1999. Pesticides: Use, Effects, and Alternatives to Pesticides in Schools.

Washington, DC: GAO. GAO/RCED-00-17. http://www.gao.gov/new.items/rc00017.pdf.

32. U.S. Environmental Protection Agency. 1993. Pest Control in the School Environment: Adopting Integrated Pest

Management. Washington, DC: United States Environmental Protection Agency. EPA-735-F-93-012.

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33. K. Owens and J. Feldman. 2002. The Schooling of State Pesticide Laws Regarding Schools, 2002 Update. 

Pesticides and You 22 (1):14-17.

34. S. Gurunathan, M. Robson, N. Freeman, B. Buckley, A. Roy, R. Meyer, J. Bukowski and P. J. Lioy. 1998.

Accumulation of chlorpyrifos on residential surfaces and toys accessible to children. Environmental Health

Perspectives 106 (1):9-16.

35. J. C. Wallace, L. P. Brzuzy, S. L. Simonich, S. M. Visscher and R. A. Hites. 1996. Case study of organochlorine 

pesticides in the indoor air of a home. Environmental Science and Technology 30:2715-2718.

36. R. W. Whitemore, F. W. Immerman, D. E. Camann, A. E. Bond, R. G. Lewis and J. L. Schaum. 1994. 

Non-occupational exposures to pesticides for residents of two U.S. cities. Archives of Environmental 

Contamination and Toxicology 26 (1):47-59.
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37. R. G. Lewis, C. R. Fortune, F. T. Blanchard and D. E. Camann. 2001. Movement and deposition of two 

organophosphorus pesticides within a residence after interior and exterior applications. Journal of the 

Air and Waste Management Association 51 (3):339-51.

38. U.S. Environmental Protection Agency. 2000. Chlorpyrifos Revised Risk Assessment and Agreement with Registrants.

Washington, DC: United States Environmental Protection Agency. 7506C.

http://www.epa.gov/pesticides/op/chlorpyrifos/agreement.pdf.

39. National Center for Health Statistics. 2001. Health, United States, 2001 With Urban and Rural Health Chartbook.

Hyattsville, Maryland. http://www.cdc.gov/nchs/data/hus/hus01.pdf.

40. K. Nelson and L. B. Holmes. 1989. Malformations due to presumed spontaneous mutations in newborn infants. 

New England Journal of Medicine 320 (1):19-23.

41. M. Harada, H. Akagi, T. Tsuda, T. Kizaki and H. Ohno. 1999. Methylmercury level in umbilical cords from patients

with congenital Minamata disease. Science of the Total Environment 234 (1-3):59-62.

42. W. J. Rogan. 1982. PCBs and cola-colored babies: Japan, 1968, and Taiwan, 1979. Teratology 26 (3):259-61.

43. K. I. McMartin, M. Chu, E. Kopecky, T. R. Einarson and G. Koren. 1998. Pregnancy outcome following maternal

organic solvent exposure: a meta-analysis of epidemiologic studies. American Journal of Industrial Medicine 34

(3):288-92.

44. A. Irgens, K. Kruger, A. H. Skorve and L. M. Irgens. 2000. Birth defects and paternal occupational exposure.

Hypotheses tested in a record linkage based dataset. Acta Obstetricia et Gynecologica Scandinavica 79 (6):465-70.

45. H. Dimich-Ward, C. Hertzman, K. Teschke, R. Hershler, S. A. Marion, A. Ostry and S. Kelly. 1996. Reproductive

effects of paternal exposure to chlorophenate wood preservatives in the sawmill industry. Scandinavian Journal of

Work Environment and Health 22 (4):267-73.

46. B. M. Blatter and N. Roeleveld. 1996. Spina bifida and parental occupation in a Swedish register-based study.

Scandinavian Journal of Work Environment and Health 22 (6):433-7.

47. B. M. Blatter, R. Hermens, M. Bakker, N. Roeleveld, A. L. Verbeek and G. A. Zielhuis. 1997. Paternal occupational

exposure around conception and spina bifida in offspring. American Journal of Industrial Medicine 32 (3):283-91.

48. E. M. Bell, I. Hertz-Picciotto and J. J. Beaumont. 2001. A case-control study of pesticides and fetal death due to 

congenital anomalies. Epidemiology 12 (2):148-56.

49. E. M. Bell, I. Hertz-Picciotto and J. J. Beaumont. 2001. Pesticides and fetal death due to congenital anomalies: 

implications of an erratum. Epidemiology 12 (5):595-6.

50. G. M. Shaw, C. R. Wasserman, C. D. O’Malley, V. Nelson and R. J. Jackson. 1999. Maternal pesticide exposure from

multiple sources and selected congenital anomalies. Epidemiology 10 (1):60-6.

51. C. A. Loffredo, E. K. Silbergeld, C. Ferencz and J. Zhang. 2001. Association of transposition of the great arteries in

infants with maternal exposures to herbicides and rodenticides. American Journal of Epidemiology 153 (6):529-36.

52. A. M. Garcia, F. G. Benavides, T. Fletcher and E. Orts. 1998. Paternal exposure to pesticides and congenital 

malformations. Scandinavian Journal of Work Environment and Health 24 (6):473-80.

53. A. M. Garcia, T. Fletcher, F. G. Benavides and E. Orts. 1999. Parental agricultural work and selected congenital 

malformations. American Journal of Epidemiology 149 (1):64-74.

54. L. S. Engel, E. S. O’Meara and S. M. Schwartz. 2000. Maternal occupation in agriculture and risk of limb defects in

Washington State, 1980-1993. Scandinavian Journal of Work Environment and Health 26 (3):193-8.

55. F. J. Meaney. 2001. Introduction: Birth defects surveillance in the United States. Teratology 64:S1-S2.
Future Directions
Part 1: Environmental

Contaminants

his section discusses improvements that could be made to the measures in the report,

improvements to the data sources used for the measures, and new measures that

may be included in future reports.

Characteristics of Ideal Measures

Ideally, data sources for measures in all three parts of the report would provide information

collected in a consistent manner for all of the nation’s children. Data also would be

available for 10 years or more to provide information about changes over time, and to

show whether the changes were statistically significant. Information would be available

on differences among geographic areas, by race/ethnicity, and by economic status.

For environmental contaminants, ideal measures would be nationally representative

measurements of concentrations of environmental contaminants in air, water, food,

and soil that can affect children’s health. The measures would reflect the potential for

children to be exposed to these pollutants. 

For concentrations of contaminants measured in children and women of child-bearing

age, ideal measures would reflect concentrations of the key pollutants in their bodies

that pose a risk of adverse health effects. 

For childhood illnesses, ideal measures would identify the percentage of children in whom

important health conditions may have been caused by or exacerbated in part by environmental contaminants. In addition, the data would permit characterization of subgroups of

each disease for which environmental contributions to the conditions are most relevant.

Common Air Pollutants

The measures for criteria air pollutants are based on three kinds of data: exceedances of

national standards, reports of daily air quality generated through the Air Quality Index,

and measured concentrations of air pollutants in all counties.

An important future direction would be to estimate health risks associated with ambient

concentrations of criteria air pollutants. Such measures would link air quality data with

health outcomes. This measure would be risk-based and would incorporate current

knowledge about the link between air pollution and health outcomes.

Hazardous Air Pollutants

The measure in this report for hazardous air pollutants (air toxics) is based on data from

the year 1996 only. The previous edition of the report showed data based on EPA’s

1990 modeling of ambient concentration of hazardous air pollutants, but the 1990

results are not included in the current measure because of differences in the way the

modeled results are reported for 1990 and 1996. Hazardous air pollutant data will be

developed for every three years starting with 1996, and years after 1996 will be comparable. Future reports will incorporate trends in hazardous air pollutants and their

possible relationships to children’s health. 

The measure in this report uses health benchmarks that are based on lifetime exposures,

and the data and methods used to establish the benchmarks are based on responses in

mature organisms (animals and humans). For future reports EPA will explore the availability of health benchmarks that are specifically based on effects from exposures during

childhood.

Future Directions for

America's Children and

the Environment

120 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Future Directions

T
Data from air toxics monitoring programs also could be considered for inclusion in future

editions of this report. Currently, national data on air toxics monitoring are limited,

and much of the monitoring and data collection are performed at the state level. 

The hazardous air pollutant measures in this report also are limited in that they represent

the presence of these pollutants in ambient air only. For certain hazardous air pollutants

that are persistent in the environment, greater exposures occur in food. These pollutants

settle out of the air onto land and into bodies of water, and are taken up in the food

chain. This pathway of exposure is addressed in part by the current measure on mercury

in fish. Related measures for other contaminants will be considered for future reports

(see the section on food contaminants below).

Indoor Air Pollutants

Indoor exposure to secondhand smoke is represented by a surrogate measure reflecting

the percentage of homes of children where people smoke. The most important improvement would be to add data about sources of other indoor air pollutants, such as consumer

products, gas stoves, and furnishings, for both homes and schools. To date no nationally

representative data on air contaminants in homes, schools, and other indoor environments

in which children may spend large amounts of time have been identified, but efforts to

explore possible measures will continue.

Drinking Water Contaminants

The measures for contaminants in drinking water reflect violations of national standards.

These measures do not distinguish among the impacts of various concentrations of

contaminants. The data on drinking water contaminants are less complete than those

used for the air measures because there is less monitoring and reporting of water 

contaminants. In addition, the drinking water contaminant measures in this report rely

on the Maximum Contaminant Level (MCL) standards. The MCL standards are based

partly on health considerations but also take into account technical feasibility and costbenefit considerations.

Each MCL also has a corresponding Maximum Contaminant Level Goal (MCLG),

which is based only on health considerations. The MCLGs could be considered for

measures in future reports.

Actual measured contaminant concentrations would provide the most relevant measures

of potential risks to children. The most complete data on contaminants in drinking

water are collected at the state level; information from the states would have to be

compiled nationally to improve the measures for drinking water. 

Another limitation of the data on drinking water is that many water systems do not

adequately monitor for contaminants, so no information about potential risks to children

in those areas is available. Future reports will consider data on such water systems

collected at the state level.

Surface Water Contaminants

In the future, EPA would like to characterize the risks posed to children when they

swim in waters contaminated with bacteria. Children are at greater risk of illness while

swimming than adults are because of their longer exposure times and more frequent

accidental ingestion of water. Data for monitoring recreational waters currently are

being collected and will be considered for future reports.

Future Directions 121

Future Directions
Food Contaminants

Dietary exposures to pesticides are represented in this report by a measure of

organophosphate pesticide residues on foods. This measure does not represent 

actual exposures or risks to children from pesticides. 

As required by the Food Quality Protection Act, EPA currently is conducting a 

cumulative risk assessment for the organophosphate pesticides. For the first time ever,

this scientific assessment evaluates the potential risks to children from the combined

estimates of all contributing organophosphate residues in food and drinking water

consumption, and from activities around the home. EPA already has imposed various

restrictions on many individual uses of organophosphates, particularly those that may

pose greater risk to children from dietary and residential sources. These restrictions, and

others that may be imposed as a result of the cumulative assessment, are expected to

lower children’s potential exposure to these pesticides and thereby reduce potential

health risks. EPA will evaluate the outputs from the cumulative risk assessments to

determine how they may be used in developing measures that better reflect increases 

or decreases in pesticide exposure or risk. In addition, the Agency expects to add

measures of pesticide exposures to the body burdens section of the report.

EPA also will examine the available data on the presence of other types of contaminants in

foods. As noted above, some hazardous air pollutants find their way into the food chain

after being deposited from the atmosphere, and their presence in food can pose more of

a risk to women of child-bearing age than their presence in the air. This report includes

information on states with fish consumption advisories for mercury. If feasible, future

reports will better characterize the risks posed by the consumption of fish contaminated

with mercury, PCBs, and other toxicants that affect neurological development, by including measures more closely related to exposures.

Finally, some children may be exposed to particularly elevated levels of contaminants in

food, including children in homes where much of the diet comes from subsistence fishing.

EPA will explore the availability of suitable data regarding such differential exposures

for future reports.

Land Contaminants

For contaminants in soil, this report includes a measure of the percentage of children

living within a mile of a Superfund site. This measure has the advantage of assessing

only children who live near a site, but living near a site does not necessarily mean that

they are exposed to contaminants. Also, there are other types of sites and land that may

be contaminated but are not classified as Superfund sites. The most important improvement to this measure would be to include data on contaminants in soil, but nationally

representative data are not currently available. A measure of children living in proximity

to “Brownfield” sites also will be considered for future reports. State databases with

information about contaminated sites also may be useful.

122 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Future Directions
Other Contaminated Media

Key additional data needs for environmental contaminants focus on exposure pathways

and environments that are particularly important for children. A number of contaminants

may gather on household surfaces, including those found in indoor air, contaminants

in soil that are tracked into the home, and those from the workplace that inadvertently

are brought into the home on the parents’ clothes or body. Young children may frequently be exposed to environmental contaminants that gather on floors and other surfaces

in the home through hand-to-mouth and object-to-mouth contact. Data available for

these exposure scenarios are limited.

Deteriorated lead-based paint, and the contaminated dust and soil it generates, is an

important contributor to childhood lead exposures, particularly in the home. The U.S.

Department of Housing and Urban Development (HUD) and the National Institute of

Environmental Health Sciences recently conducted a survey of lead hazards in the

home, with data collected from 1998-2000; HUD will repeat this survey in 2004.

Measures drawn from the data gathered in these surveys will be considered for future

editions of America’s Children and the Environment.

Focusing on Children’s Environments

This report includes measures related to potential exposures to children at school.

Future work will consider other measures reflecting settings where children spend time.

Additional measures related to where children live, go to school, and spend significant

time (such as playgrounds) will be considered, as will measures on children’s proximity

to sources of exposures that may affect their health, such as highways, areas of high

traffic, or hazardous waste sites.

Child care centers are a particularly important environment where many young children

spend a substantial portion of their time. The U.S. Department of Housing and Urban

Development, the Consumer Product Safety Commission, and EPA are conducting a

survey of environmental hazards in child care centers. Data from this survey will be

considered for future editions of this report, and the availability of other data on potential exposures to environmental contaminants in child care centers will be examined.

This report includes body burden data for lead and cotinine concentrations in the blood

of children, and mercury concentrations in the blood of women of child-bearing age.

These measures were chosen because it was possible to identify the health significance

of the measured concentrations or multiple years of data were available. Future work will

include more contaminants as multiple years of data become available. The development

of methods for evaluating health implications of the available body burden data will be

considered.

In future reports, EPA will present available body burden data (for women of childbearing age) on contaminants for which prenatal exposure has been associated with

childhood health effects, as with mercury. Cotinine will be considered as a possibility

for this type of measure. In addition, future work will consider data related to contaminants in breast milk, which is an important source of exposure for infants.

Part 2: Body Burdens

Future Directions 123

Future Directions
The current report includes measures for respiratory-related diseases, with an emphasis on

asthma; measures for childhood cancer; and measures for neurodevelopmental disorders

in children. All of these are complex conditions with multiple causes, and at present

available data do not allow scientists to determine the role that environmental contaminants play in the prevalence of some childhood diseases.

Additional data collected by states or collected at the state level for some of the childhood illnesses will be assessed for future reports. In particular, future work will assess

available data on childhood cancers by state. 

In future work other datasets will be considered to supplement the estimates for neurodevelopmental disorders, which are based on parents’ responses to the National Health

Interview Survey. Potential data sources include registries of clinically diagnosed cases,

which are available in select areas, and the percentage of children taking medications to

treat certain neurodevelopmental disorders such as ADHD.

Additional measures reflecting emergency room visits for respiratory effects and 

hospitalizations for respiratory effects are included in this edition of the report. Minor

respiratory symptoms, such as increasing cough and declines in lung function, are

influenced by environmental factors but are not included in this report. Future work

will focus on identifying appropriate data sources for such measures. 

No nationally representative data are available for a number of other childhood diseases

that may be in part caused by exposure to environmental contaminants such as birth

defects and waterborne diseases. This report’s Special Features section includes data on

birth defects in California. Future reports will consider data from other states. 

Environmental factors also may affect human reproduction, contributing to effects such

as earlier age at puberty. These effects are important to monitor, and if suitable data

become available they will be included in future reports. However, appropriate data

sources for these and other important childhood diseases and disorders may not exist.

This report includes measures based on data from selected states on potential exposures 

to lead and pesticides in schools, and on birth defects. Future reports will include

additional topics in this section that are important to children’s health, but for which

nationally representative data are not currently available. EPA will consider topics

describing the contributions of different pathways of exposures to children, such as

information on the multiple ways in which children may be exposed to pesticides.

In the future, EPA will evaluate new information on the sources of the contaminants in

the environment now included in Part 1. This information would complete the path

from source to contaminants to body burdens to health effects, and would help identify

priorities for future policies.

Part 5: Special Features

124 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Future Directions

Part 3: Childhood

Illnesses
Glossary of Terms
Air Toxics:

Synonym for “hazardous air pollutants.” (See below).

Ambient Air:

Outdoor air, any unconfined portion of the atmosphere,

open air.

Asthma:

A chronic inflammatory disorder of the lungs. Symptoms

include wheezing, breathlessness, chest tightening, and

cough.

Attention-Deficit/Hyperactivity Disorder (ADHD):

A disorder in which the prominent symptoms are hyperactivity, inattention, and impulsivity. Also referred to as ADD

(attention deficit disorder).

Benzene:

A colorless, volatile, flammable, toxic liquid aromatic hydrocarbon (C6H6) used in organic synthesis, as a solvent, and

as a component of motor fuel. Benzene is a known human

carcinogen and an important hazardous air pollutant.

Cadmium:

A heavy metal used primarily for metal plating and coating

operations, in applications such as transportation equipment,

machinery and baking enamels, photography, and television

phosphors. It also is used in nickel-cadmium and solar batteries, and in pigments. It also is found in cigarette smoke

and is an important hazardous air pollutant.

Carcinoma:

A form of cancer that begins in the tissues lining or 

covering an organ.

Carbon Monoxide (CO):

A colorless, odorless, poisonous gas produced by incomplete

combustion of fossil fuels; one of the six “criteria” pollutants

for which EPA has set National Ambient Air Quality

Standards under the Clean Air Act.

Carbon Tetrachloride:

A manufactured compound, most often found as a colorless

gas. Because of its harmful effect on the ozone layer, the

production and use of carbon tetrachloride in industrialized

nations was banned in 1996 under the Montreal Protocol

on Substances that Deplete the Ozone Layer. It is highly

persistent and remains at levels of concern in the environment in the United States; it is an important hazardous air

pollutant. 

Cardiopulmonary Mortality:

Death due to malfunction of the heart and lungs; also refers

to the death rate from these causes.

Cardiovascular Effects:

Health effects related to the heart and circulatory system.

Chlorinated Dibenzofurans (CDFs):

A family of 135 individual compounds with varying harmful health and environmental effects. CDFs typically are

released to the environment through the incineration of

municipal and industrial waste, accidental combustion of

polychlorinated biphenyls (PCBs), and the manufacture of

certain metals and paper products.

Chromium:

A heavy metal that is an important hazardous air pollutant.

(See “heavy metals.”) It is used for making steel, dyes and

pigments, chrome plating, leather tanning, and wood

preservation

Contaminant:

Any physical, chemical, biological, or radiological substance

or matter in air, water, or soil that can have adverse health

effects.

Cotinine:

A major metabolite of nicotine found in blood and urine.

Currently regarded as the best biomarker for exposure of

both active smokers and of nonsmokers to environmental

tobacco smoke.

Criteria Pollutant:

One of the six pollutants for which EPA is required to set

National Ambient Air Quality Standards to protect human

health and welfare. Criteria pollutants include ozone

(ground-level), carbon monoxide, particulate matter, sulfur

dioxide, lead, and nitrogen oxides. They are called “criteria”

pollutants because the Clean Air Act required EPA to

describe the criteria for setting or revising standards.

Deciliter:

One-tenth of a liter (0.1 liter).

Diesel:

A petroleum-based fuel. Diesel exhaust is an important

source of particulates and other pollutants that adversely

affect human health.

126 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Glossary of Terms
Dioxins:

A group of harmful chemical compounds that are released

into the air from combustion processes such as commercial

or municipal waste incineration and from burning fuels

such as wood, coal, or oil.

Disinfection Byproducts:

Organic and inorganic compounds that often result from the

reaction between a disinfectant and naturally occurring materials in water; chloroform is a commonly found example.

Down Syndrome:

A genetic condition usually caused by having an extra copy

of the 21st chromosome. Also called trisomy 21.

Environmental Tobacco Smoke:

Mixture of smoke exhaled by a smoker and the smoke from

the burning end of the smoker’s cigarette, pipe, or cigar.

Also known as secondhand smoke. Environmental tobacco

smoke is an important indoor air pollutant.

Epidemiological Studies:

Studies that research the incidence, distribution, and control of disease in a population.

Ewing’s Sarcoma:

A type of bone cancer that usually forms in the middle

(shaft) of large bones

Exacerbation of Asthma:

Increase in the frequency or severity of asthma attacks or

symptoms in individuals who have asthma.

Exposure:

Human contact with environmental contaminants in media

including air, water, soil, and food.

Formaldehyde:

A colorless, pungent-smelling gas; an important hazardous

air pollutant. High concentrations may trigger attacks in

people with asthma. Sources include environmental tobacco

smoke and other combustion sources; pressed wood products (such as particle board); and certain textiles, foams,

and glues.

Gastrointestinal:

Relating to, affecting, or including the stomach and/or

intestine.

Germ Cell Tumor:

A type of tumor found in the ovaries or testicles.

Gonadal Tumor:

Tumor specific to the gonads.

Ground level ozone:

Ground-level ozone (smog) is formed by a chemical reaction

between volatile organic pollutants (VOCs) and oxides of

nitrogen (NOx) in the presence of sunlight. Ozone concentrations can reach unhealthy levels when the weather is hot

and sunny with little or no wind. Ozone at the ground level

causes adverse effects on lung function and other adverse

respiratory effects. It is one of the six “criteria” pollutants

for which EPA has adopted National Ambient Air Quality

Standards.

Hazardous Air Pollutants:

Air pollutants identified in the Clean Air Act Amendments

of 1990 as reasonably expected to cause or contribute to

irreversible illness or death. Such pollutants include

asbestos, beryllium, mercury, benzene, coke oven emissions,

radionuclides, and vinyl chloride. A total of 188 hazardous

air pollutants are listed in section 112(b) of the Clean Air

Act, as amended in 1990. There are no ambient air quality

standards for these pollutants.

Heavy Metals:

Metallic elements with high atomic weights, e.g., mercury,

chromium, cadmium, arsenic, and lead; can damage living

things at low concentrations.

Hodgkin’s Lymphoma:

A cancer of the lymphatic system that is characterized by

enlargement of lymph nodes, the spleen, or other lymphatic

tissue.

Hypospadias:

A birth defect found in boys in which the urinary tract

opening is not located properly at the tip of the penis.

Immunodeficiency:

A disorder in which the immune system is reduced or

absent.

Ionizing Radiation:

Radiation that can strip electrons from atoms, i.e., alpha,

beta, and gamma radiation. High doses can causes massive

tissue damage; lower doses can lead to cancer and harmful

genetic mutations.

Glossary of Terms 127

Glossary of Terms
Leukemia:

A cancer in which the body produces a large number of

abnormal blood cells. 

Lymphocytic Leukemia:

The most common form of childhood leukemia, also

known as lymphoblastic leukemia. In this disease, the bone

marrow produces large quantities of immature lymphocytes

(white blood cells). 

Lymphoma:

Lymphomas are tumors in the lymph system, which is

responsible for fighting diseases in the body and is part of

the immune system.

Maximum Contaminant Level (MCL):

The highest level of a contaminant that is allowed in drinking water as delineated by the National Primary Drinking

Water Regulations. These levels are based on consideration

of health risks, technical feasibility of treatment, and costbenefit analysis.

Media:

Specific environments such as air, water, food, and soil.

Mercury:

A heavy metal that is highly toxic if breathed or swallowed.

The organic form of mercury, methylmercury, bioaccumulates

in ecosystems and can cause adverse effects on children

exposed before birth or adults at higher concentrations. The

largest human-generated source of mercury emissions in the

United States is the burning of coal. Other sources include

the combustion of waste and industrial processes that use

mercury.

Methemoglobinemia:

A condition that reduces the ability of the blood to transport

oxygen throughout the body for essential metabolism; it is

due to the replacement of hemoglobin with methemoglobin

in the blood. A small amount of methemoglobin is present

in the blood normally, but injury or toxic agents—such as

nitrites—convert a larger proportion of hemoglobin into

methemoglobin.

Methylmercury:

An organic form of mercury, created from metallic or elemental mercury by bacteria in sediments. Methylmercury is

easily absorbed into the living tissue of aquatic organisms

and is not easily eliminated. Therefore, it accumulates in

organisms at the top of food chains such as tuna or humans.

It can cause adverse effects in children exposed before or

after birth.

Microgram (μg):

One-millionth of a gram.

μg/dL:

Microgram per deciliter.

Microorganisms:

Tiny living organisms that can be seen only with the aid of

a microscope. Some microorganisms can cause acute health

problems when consumed in drinking water. Also known as

microbes.

Monitoring and Reporting Violation:

Violation of monitoring and reporting requirements that

specify how and when water must be tested for the presence

of contaminants as defined by the Safe Drinking Water Act.

Mortality:

The number of deaths in a population, or death rate.

Myeloid Leukemia:

One form of cancer of the blood-forming tissue, primarily

the bone marrow and lymph nodes.

National Ambient Air Quality Standards (NAAQS):

Standards established by EPA for maximum allowable 

concentrations of six “criteria” pollutants in outdoor air.

The six pollutants are carbon monoxide, lead, ground-level

ozone, nitrogen dioxide, particulate matter, and sulfur

dioxide. The standards are set at a level that protects public

health with an adequate margin of safety.

National Priorities List:

List of sites under EPA’s Superfund program, which investigates and cleans up hazardous sites nationwide. Sites on the

National Priorities List have undergone preliminary assessment

and site inspection and have been determined to require

remediation due to potential threats to persons living or

working near the site.

Neuroblastomas:

Cancer that arises in immature nerve cells and affects mostly

infants and children.

Nitrates and Nitrites:

Nitrogen-oxygen chemical units that combine with various

organic and inorganic compounds. Once taken into the body,

nitrates are converted into nitrites. The greatest use of nitrates

is as a fertilizer. Other sources include animal manure and

human sewage.

128 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Glossary of Terms
Nitrogen Dioxide (NO2):

A chemical that results from nitric oxide combining with

oxygen in the atmosphere; a major component of photochemical smog. One of the six “criteria” pollutants for

which EPA has set national ambient air quality standards.

Nitrogen Oxides:

A family of highly reactive gases (including nitrogen dioxide,

above) that form when fuel is burned at high temperatures.

Emitted principally from motor vehicle exhaust and stationary

sources such as electric power plants and industrial boilers.

Non-Hodgkin’s Lymphoma:

A group of cancers of the lymphoid system.

Oral Cleft Defects:

An abnormal opening in a structure around the mouth and

face. Clefts may occur in the lip, the roof of the mouth

(hard palate), or the tissue in the back of the mouth (soft

palate).

Organophosphate Pesticides:

A group of approximately 40 closely related pesticides that

affect functioning of the nervous system. Examples include

chlorpyrifos, phosmet, and methyl parathion.

Ozone:

A gas that results from complex chemical reactions between

nitrogen dioxide and volatile organic compounds; the major

component of smog. Ozone at the ground level is one of

the six “criteria” pollutants for which EPA has established

national ambient air quality standards.

Particulate Matter:

Particles in the air, such as dust, dirt, soot, smoke, and

droplets. Small particles (PM-10 or PM-2.5) have significant effects on human health. Particulate matter is one of

the six “criteria” pollutants for which EPA has established

national ambient air quality standards.

Plasticizers:

Small, often volatile molecules that are added to hard, stiff

plastics to make them softer and more flexible.

Polychlorinated Biphenyls (PCBs):

A group of toxic, persistent chemicals used in electrical

transformers and capacitors for insulating purposes, and in

gas pipeline systems as a lubricant. The sale and new use of

PCBs were banned by law in 1979 although large reservoirs

of PCBs remain in the environment.

Poverty Level:

An income level below which an individual or family is

considered poor. The U.S. Census Bureau defines poverty

level based on a set of money income thresholds that vary

by family size and composition. If a family’s total income is

less than that family’s threshold, then that family, and every

individual in it, is considered poor. The Census Bureau

updates its poverty thresholds annually. In 2000, a family

of two adults and two children with total income below

$17,463 was considered below the poverty level. Tables

showing the Census Bureau’s poverty thresholds are available

at http://www.census.gov/hhes/poverty/threshld.html.

Prenatal:

Occurring, existing, or performed before birth.

Radionuclides:

Radioactive isotopes or unstable forms of elements.

Retinoblastomas:

Tumors of the eye.

Respiratory Effects:

Effects on the process of breathing or on the lungs.

Respiratory Mortality:

Death or the death rate due to respiratory illness.

Reference Dose (RfD):

Oral reference dose. EPA defines a reference dose as an estimate, with uncertainty spanning perhaps an order of magnitude, of a daily oral exposure to the human population

(including sensitive subgroups) that is likely to be without

an appreciable risk of deleterious effects during a lifetime.

Solvents:

Substances used to dissolve another substance. Some commonly used solvents, such as TCE, are important environmental contaminants.

Sudden Infant Death Syndrome (SIDS):

The sudden and unexpected death of an apparently healthy

infant, without an apparent cause.

Sulfur Dioxide (SO2):

A pungent, colorless, gaseous pollutant formed primarily by

the combustion of fossil fuels. One of the six “criteria” pollutants for which EPA has set national ambient air quality

standards.

Glossary of Terms 129

Glossary of Terms
Superfund:

An EPA program to remediate sites contaminated by release

of hazardous substances. Activities include establishing a

National Priorities List, investigating sites for inclusion on

the list, determining their priority, and conducting and/or

supervising cleanup and other remedial actions. Superfund is

operated under the legislative authority of the Comprehensive

Environmental Response, Compensation and Liability Act

of 1980 (CERCLA). Some remedial actions are funded

directly by Superfund, through a tax on chemical feedstocks, but the majority are paid for by parties that are

liable for the release of the hazardous substances.

Trichloroethylene (TCE):

A stable, low boiling-point colorless liquid, toxic if inhaled.

Used as a solvent or metal decreasing agent, and in other

industrial applications.

Volatile Organic Pollutants:

Carbon-containing compounds that easily go from a solid

to a gaseous form at normal temperatures. Sources include

household products such as paints, paint strippers, and

other solvents; wood preservatives; aerosol sprays; cleansers

and disinfectants; moth repellents and air fresheners; stored

fuels and automotive products; hobby supplies; dry-cleaned

clothing.

Wilms’ Tumor:

A kidney cancer that occurs in children usually younger

than 5 years.

130 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Glossary of Terms
APPENDIX A

Data Tables
132 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix A: Data Tables

Part 1: Environmental Contaminants

Table E1

Percentage of children living in counties in which air quality standards were exceeded

1990-1995

1990 1991 1992 1993 1994 1995

Ozone one-hour standard 22.7% 25.2% 16.9% 21.1% 19.3% 27.8%

PM-10 8.0% 6.3% 9.6% 2.6% 2.3% 10.0%

Carbon monoxide 9.4% 8.4% 6.1% 5.0% 6.4% 4.9%

Lead 2.2% 6.0% 1.8% 2.1% 1.7% 1.8%

Sulfur dioxide 0.5% 2.1% 0.1% 0.5% 0.1% 0.1%

Nitrogen dioxide 3.7% 3.7% 0.0% 0.0% 0.0% 0.0%

Any standard* 28.0% 31.8% 20.9% 24.2% 23.5% 30.8%

1996-2001

1996 1997 1998 1999 2000 2001

Ozone one-hour standard 16.5% 18.6% 20.8% 21.7% 13.3% 15.0%

Ozone eight-hour standard 39.1% 38.9% 48.5% 46.9% 27.9% 39.8%

PM-10 1.5% 2.4% 2.0% 2.1% 2.4% 3.2%

PM-2.5 27.2% 25.4%

Carbon monoxide 5.6% 3.7% 4.3% 3.7% 3.8% 0.2%

Lead 1.6% 1.4% 1.6% 0.2% 0.5% 1.0%

Sulfur dioxide 0.1% 0.1% 0.1% 0.1% 0.1% 0.0%

Nitrogen dioxide 0.0% 0.0% 0.0% 0.0% 0.0% 0.0%

Any standard* 19.8% 21.9% 23.7% 24.0% 15.5% 18.5%

* Does not include ozone eight-hour or PM-2.5 standards.

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information Retrieval System

Addendum 1 to Table E1

Percentage of children living in counties in which air quality standards were exceeded, 

by race/ethnicity, 1999

All Races/ White non- Black non- American Indian/ Asian or

Ethnicities Hispanic Hispanic Hispanic Alaska Native Pacific Islander

15.5% 10.6% 16.2% 31.4% 7.6% 24.5%

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information Retrieval System

Addendum 2 to Table E1

Percentage of children living in counties in which air quality standards were exceeded, 

by family income, 1999

100-200% of > 200% of

All Incomes < Poverty Level Poverty Level Poverty Level

Carbon monoxide 3.7% 4.5% 4.3% 3.2%

Sulfur dioxide 0.1% 0.1% 0.1% 0.1%

Nitrogen dioxide 0.0% 0.0% 0.0% 0.0%

Ozone 21.7% 20.9% 19.4% 22.7%

Lead 0.2% 0.1% 0.2% 0.2%

PM-10 2.1% 2.1% 2.2% 2.0%

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information Retrieval System
Appendix A 133

Appendix A: Data Tables

Table E2

Percentage of children’s days with good, moderate, or unhealthy air quality

1990-1995

Pollution Level 1990 1991 1992 1993 1994 1995

Good 43.6% 44.2% 47.7% 46.9% 45.7% 47.2%

Moderate 20.6% 21.0% 18.4% 19.2% 20.5% 19.7%

Unhealthy 3.0% 3.0% 2.7% 2.3% 2.3% 2.2%

No Monitoring Data 32.8% 31.8% 31.2% 31.6% 31.5% 30.8%

1996-1999

Pollution Level 1996 1997 1998 1999

Good 48.9% 48.8% 47.1% 46.6%

Moderate 19.1% 19.0% 20.7% 21.9%

Unhealthy 1.7% 1.3% 1.3% 0.9%

No Monitoring Data 30.3% 30.9% 30.9% 30.7%

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information Retrieval System

Addendum 1 to Table E2

Percentage of children’s days with good, moderate, or unhealthy air quality, by race/ethnicity, 1999

White non- Black non- American Indian/ Asian or

Pollution Level Hispanic Hispanic Hispanic Alaska Native Pacific Islander

Good 44.4% 33.4% 51.0% 60.0% 48.9%

Moderate 18.7% 14.6% 22.6% 27.4% 33.2%

Unhealthy 0.6% 0.4% 0.9% 1.3% 1.9%

No Monitoring Data 36.4% 51.6% 25.6% 11.3% 16.0%

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information Retrieval System

Addendum 2 to Table E2

Percentage of children’s days with good, moderate, or unhealthy air quality, 

by family income, 1999

100-200% of > 200% of

Pollution Level All Incomes* < Poverty Level Poverty Level Poverty Level

Good 46.9% 44.9% 42.5% 49.0%

Moderate 22.0% 22.3% 21.4% 22.1%

Unhealthy 0.9% 0.9% 0.9% 0.8%

No Monitoring Data 30.2% 31.9% 35.2% 28.0%

* Values for All Incomes in this table differ from 1999 values in Table E2 due to rounding.

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information Retrieval System
134 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix A: Data Tables

Table E3a

Long-term trends in annual average concentrations of criteria pollutants

1990-1993

1990 1991 1992 1993

PM-10, percent of annual standard 63.7% 63.8% 56.8% 55.8%

1994-1997

1994 1995 1996 1997

PM-10, percent of annual standard 56.3% 54.0% 52.4% 52.6%

Nitrogen dioxide, percent of annual standard 37.3% 34.9%

Sulfur dioxide, percent of annual standard 6.5% 5.6%

1998-2000

1998 1999 2000

PM-10, percent of annual standard 51.2% 53.9% 53.3%

Nitrogen dioxide, percent of annual standard 35.3% 33.9%

Sulfur dioxide, percent of annual standard 5.4% 5.2%

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information Retrieval System

Table E3b

Number of children living in counties with high annual averages of PM-10

1990-1995

1990 1991 1992 1993 1994 1995

Exceeding 80% of the 

long-term standard 5,978,059 6,347,396 4,671,899 4,350,278 1,432,268 3,019,285

Exceeding the long-term standard 1,844,770 3,424,292 169,004 536,520 435,493 131,590

1996-2000

1996 1997 1998 1999 2000

Exceeding 80% of the 

long-term standard 2,464,947 2,074,549 165,431 2,029,422 1,830,579

Exceeding the long-term standard 60,243 788,945 0 1,017,791 874,734

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information Retrieval System
Appendix A 135

Appendix A: Data Tables

Table E4

Percentage of children living in counties where estimated hazardous air pollutant concentrations

were greater than health benchmarks in 1996

Health Benchmark

Cancer, one in 100,000 100%

Cancer, one in 10,000 18%

Other health effects 95%

SOURCE: U.S. Environmental Protection Agency, National Air Toxics Assessment

Addendum 1 to Table E4

Percentage of children living in counties where hazardous air pollutant concentrations were greater

than health benchmarks in 1996, by family income

100-200% of > 200% of

Health Benchmark All Incomes < Poverty Level Poverty Level Poverty Level

Cancer, one in 100,000 100% 100% 100% 100%

Cancer, one in 10,000 18% 22% 17% 17%

Other health effects 95% 94% 93% 96%

SOURCE: U.S. Environmental Protection Agency, National Air Toxics Assessment

Addendum 2 to Table E4

Percentage of children living in counties where hazardous air pollutant concentrations were greater

than health benchmarks in 1996, by race/ethnicity

All Races/ White non- Black non- American Indian/ Asian or

Health Benchmark Ethnicities Hispanic Hispanic Alaska Native Pacific Islander Hispanic

Cancer, one in 100,000 100% 100% 100% 100% 100% 100%

Cancer, one in 10,000 18% 12% 28% 8% 34% 31%

Other health effects 95% 94% 99% 87% 99% 95%

SOURCE: U.S. Environmental Protection Agency, National Air Toxics Assessment

Table E5

Percentage of homes with children under 7 where someone smokes regularly

1994 1996 1999

28.7% 27.6% 19.0%

SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Indoor Environments Division, Surveys on Radon Awareness and

Environmental Tobacco Issues
136 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix A: Data Tables

Table E6

Percentage of children living in areas served by public water systems that exceeded a drinking

water standard or violated treatment requirements

1993-1997

Type of standard violated 1993 1994 1995 1996 1997

Lead and copper* 2.2% 0.9% 1.4% 1.6% 1.7%

Microbial contaminants 8.3% 7.5% 4.1% 4.3% 3.6%

Chemical and radiation 4.7% 4.7% 2.2% 1.8% 2.4%

Nitrate/nitrite 0.23% 0.12% 0.25% 0.20% 0.37%

Treatment and filtration 10.7% 8.1% 4.5% 3.7% 3.6%

Any health-based violations 20.2% 15.5% 12.0% 10.7% 10.7%

1998-1999

Type of standard violated 1998 1999

Lead and copper* 1.6% 1.5%

Microbial contaminants 2.8% 2.5%

Chemical and radiation 1.2% 1.0%

Nitrate/nitrite 0.17% 0.21%

Treatment and filtration 3.4% 3.0%

Any health-based violations 8.6% 8.0%

* Lead and copper represents the lead and copper rule, which is a set of standards and implementation measures.

SOURCE: U.S. Environmental Protection Agency, Office of Water, Safe Drinking Water Information System

Table E7

Percentage of children living in areas with major violations of drinking water monitoring and

reporting requirements

1993-1997

Type of standard violated 1993 1994 1995 1996 1997

Lead and copper 11.3% 6.7% 5.3% 5.2% 5.8%

Microbial contaminants 2.2% 2.6% 2.1% 1.6% 2.0%

Chemical and radiation 8.1% 5.8% 5.5% 4.8% 3.5%

Treatment and filtration 1.6% 0.6% 0.4% 0.5% 0.3%

Any major violation 21.6% 14.2% 11.7% 10.9% 10.9%

1998-1999

Type of standard violated 1998 1999

Lead and copper 5.5% 5.4%

Microbial contaminants 1.9% 1.4%

Chemical and radiation 3.8% 2.8%

Treatment and filtration 0.5% 1.0%

Any major violation 10.6% 9.9%

SOURCE: U.S. Environmental Protection Agency, Office of Water, Safe Drinking Water Information System
Appendix A 137

Appendix A: Data Tables

Table E8

Percentage of fruits, vegetables, and grains with detectable residues of organophosphate pesticides

1994 1995 1996 1997 1998 1999 2000 2001

20.8% 24.4% 29.4% 28.8% 22.1% 24.4% 23.2% 19.1%

SOURCE: U.S. Department of Agriculture, Pesticide Data Program

Table E9

Percentage of children residing within one mile of a Superfund site

1990 1992 1994 1996 1998 2000

All Superfund sites 1.2% 1.2% 1.3% 1.3% 1.3% 1.3%

All Superfund sites not yet

cleaned up or controlled 1.2% 1.1% 1.1% 1.0% 1.0% 0.8%

SOURCE: U.S. Environmental Protection Agency, Superfund NPL Assessment Program (SNAP) Database

Part 2: Body Burdens

Table B1

Concentrations of lead in blood of children ages 5 and under

Blood lead concentrations (μg/dL)

1976-1980 1988-1991 1992-1994 1999-2000

50th percentile 15.0 3.5 2.6 2.2

90th percentile 25.0 9.4 7.1 4.8

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health and Nutrition Examination Survey

Table B2 

Median concentrations of lead in blood of children ages 1-5, by race/ethnicity and family income,

1999-2000

Blood lead concentrations (μg/dL)

100-200% of > 200% of Unknown

All Incomes < Poverty Level Poverty Level Poverty Level Income

All Races/Ethnicities 2.2 2.8 1.9 1.9 2.9

White non-Hispanic 2.1 2.8 1.7 2.0 3.2

Black non-Hispanic 2.8 3.6 2.6 2.2 2.7

Hispanic 2.0 2.4 1.7 1.6 2.3

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health and Nutrition Examination Survey
138 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix A: Data Tables

Table B3

Distribution of concentrations of lead in blood of children ages 1-5, 1999-2000

Blood lead concentrations (μg/dL)

< 1 1-2 2-3 3-4 4-5 5-6 6-7 > 7

10% 36% 24% 14% 6% 3% 2% 5%

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health and Nutrition Examination Survey

Table B4

Distribution of concentrations of mercury in blood of women of child-bearing age, 1999-2000

Blood mercury concentrations (parts per billion)

< 1 1-2 2-3 3-4 4-5 5-6 6-7

51% 23% 8% 4% 4% 2% 2%

7-8 8-9 9-10 10-11 11-12 12-13 13-14 > 14

1% 1% 0% 1% 1% 1% 0% 1%

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health and Nutrition Examination Survey

Table B5

Concentrations of cotinine in blood of children

Serum cotinine concentrations (ng/mL)

1988-1991 1999-2000

90th percentile 2.16 1.78

50th percentile 0.25 0.11

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health and Nutrition Examination Survey
Appendix A 139

Appendix A: Data Tables

Addendum to Table B5

Median concentrations of cotinine in blood of children ages 4-17, by race/ethnicity and 

family income, 1988-1991

Serum cotinine concentrations (ng/mL)

100-200% of > 200% of Unknown

All Incomes < Poverty Level Poverty Level Poverty Level Income

All races/ethnicities 0.25 0.66 0.34 0.16 0.30

White non-Hispanic 0.23 1.15 0.38 0.16 0.37

Black non-Hispanic 0.59 0.80 0.77 0.24 0.47

Hispanic 0.19 0.21 0.17 0.12 0.19

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health and Nutrition Examination Survey

Part 3: Childhood Illnesses

Table D1

Percentage of children with asthma

1980-1985

1980 1981 1982 1983 1984 1985

Percentage of children with

asthma in the past 12 months 3.6% 3.7% 4.1% 4.5% 4.3% 4.8%

1986-1991

1986 1987 1988 1989 1990 1991

Percentage of children with 

asthma in the past 12 months 5.1% 5.3% 5.0% 6.1% 5.8% 6.4%

1992-1996

1992 1993 1994 1995 1996

Percentage of children with 

asthma in the past 12 months 6.3% 7.2% 6.9% 7.5% 6.2%

1997-2001*

1997 1998 1999 2000 2001

Children ever diagnosed with 

asthma and having an asthma 

attack in the past 12 months 5.4% 5.3% 5.3% 5.5% 5.7%

Children ever diagnosed with asthma 11.4% 12.1% 10.8% 12.3% 12.6%

* Note: The survey questions for asthma changed in 1997; data before 1997 cannot be directly compared to data in 1997 and later.

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health Interview Survey
140 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix A: Data Tables

Table D2

Percentage of children having an asthma attack in the previous 12 months, by race/ethnicity and

family income, 1997-2000

100-200% of > 200% of Unknown

All Incomes < Poverty Level Poverty Level Poverty Level Income

All races/ethnicities 5.4% 6.4% 5.5% 5.3% 4.9%

White non-Hispanic 5.2% 6.1% 5.5% 5.1% 4.7%

Black non-Hispanic 7.2% 8.5% 7.2% 6.3% 6.5%

Hispanic 4.6% 5.0% 3.9% 5.2% 4.3%

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health Interview Survey

Table D3

Children’s emergency room visits for asthma and other respiratory causes

1992-1997

Rate per 10,000 children

1992 1993 1994 1995 1996 1997

All asthma and other respiratory causes 369.1 406.6 392.4 357.2 356.4 374.6

Acute upper respiratory infections 221.9 248.7 246.8 227.4 206.4 214.0

Asthma 97.6 107.1 105.1 92.6 114.4 112.1

Acute bronchitis 49.6 50.8 40.5 37.1 35.6 48.5

1998-1999

1998 1999

All asthma and other respiratory causes 389.2 378.7

Acute upper respiratory infections 218.9 239.0

Asthma 124.4 104.5

Acute bronchitis 45.9 35.1

Note: Respiratory infections are ICD-9 codes 464 and 465, acute bronchitis is ICD-9 code 466, and asthma is ICD-9 code 493.

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Hospital Ambulatory Medical Care Survey

Addendum to Table D3

Children’s emergency room visits for asthma and other respiratory causes, 

by race/ethnicity, 1997-1999

Rate per 10,000 children

1997 1998 1999 1997-1999

White non-Hispanic 298.4 311.9 317.7 309.3

Black non-Hispanic 826.5 811.7 663.9 767.3

Hispanic *** 384.6

* Annual estimates for Hispanic ethnicity are unreliable for asthma.

SOURCE: Centers for Disease Control and Prevention, National Hospital Ambulatory Medical Care Survey
Appendix A 141

Appendix A: Data Tables

Table D4

Children’s hospital admissions for asthma and other respiratory causes

1980-1985

Rate per 10,000 children

1980 1981 1982 1983 1984 1985

All asthma and other respiratory causes 54.7 56.1 55.3 61.4 50.4 56.6

Acute upper respiratory infections 17.6 17.7 12.7 19.4 11.4 14.1

Acute bronchitis 16.2 16.3 16.9 18.3 13.5 17.1

Asthma 21.0 22.2 25.7 23.6 25.5 25.4

1986-1991

1986 1987 1988 1989 1990 1991

All asthma and other respiratory causes 49.9 52.3 52.5 58.8 54.5 62.8

Acute upper respiratory infections 10.0 12.8 9.5 11.8 8.3 11.4

Acute bronchitis 12.6 13.5 14.6 19.1 17.8 20.7

Asthma 27.3 25.9 28.5 27.9 28.4 30.7

1992-1997

1992 1993 1994 1995 1996 1997

All asthma and other respiratory causes 61.1 56.3 54.2 66.1 57.5 68.0

Acute upper respiratory infections 7.2 9.0 7.1 8.2 5.9 7.7

Acute bronchitis 22.9 21.7 20.0 24.7 21.3 27.3

Asthma 31.0 25.6 27.1 33.1 30.3 33.0

1998-1999

1998 1999

All asthma and other respiratory causes 50.3 66.4

Acute upper respiratory infections 5.9 8.4

Acute bronchitis 19.5 29.2

Asthma 24.9 28.8

Note: Respiratory infections are ICD-9 codes 464 and 465, acute bronchitis is ICD-9 code 466, and asthma is ICD-9 code 493.

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Hospital Discharge Survey

Addendum to Table D4

Children’s hospital admissions for asthma and other respiratory causes, 

by race/ethnicity, 1997-1999*

Rate per 10,000 children

1997 1998 1999 1997-1999

White 45.6 34.3 45.5 41.8

Black 107.7 78.6 99.2 95.2

* Estimates for ethnicity not available. Race categories include children of Hispanic ethnicity.

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Hospital Discharge Survey
142 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix A: Data Tables

Table D5

Cancer incidence and mortality for children under 20

1975-1980

Rate per million children

1975 1976 1977 1978 1979 1980

Incidence 128 141 141 144 145 142

Mortality 51 51 50 45 46 46

1981-1986

1981 1982 1983 1984 1985 1986

Incidence 138 144 144 154 157 157

Mortality 44 45 43 39 38 38

1987-1992

1987 1988 1989 1990 1991 1992

Incidence 152 151 166 155 162 160

Mortality 36 35 35 34 34 33

1993-1998

1993 1994 1995 1996 1997 1998

Incidence 161 156 158 162 156 161

Mortality 33 32 30 29 29 28

SOURCE: Incidence data from National Cancer Institute, Surveillance, Epidemiology, and End Results Program; mortality data from Centers for Disease

Control and Prevention, National Center for Health Statistics, National Vital Statistics System

Addendum 1 to Table D5

Cancer incidence for children under 20 by race/ethnicity and gender, 1994-1998

Rate per million children

Male Female

All races/ethnicities 167 150

White non-Hispanic 172 156

Black non-Hispanic 133 117

Hispanic 150 141

American Indian/Alaska Native 82 62

Asian or Pacific Islander 150 132

SOURCE: National Cancer Institute, Division of Cancer Control and Population Sciences. Surveillance, Epidemiology, and End Results Program 1994-1998

Addendum 2 to Table D5

Age-adjusted cancer mortality rates for children under 20 by race/ethnicity and gender, 1994-1998

Rate per million children

Male Female

All races/ethnicities 33 26

White non-Hispanic 34 26

Black non-Hispanic 33 29

Hispanic 35 27

American Indian/Alaska Native 25 19

Asian or Pacific Islander 30 24

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Vital Statistics System
Appendix A 143

Appendix A: Data Tables

Table D6

Cancer incidence for children under 20 by type

Rate per million children

1974-78 1979-83 1984-88 1989-93 1994-98

Acute lymphoblastic leukemia 23.7 24.9 27.6 28.2 28.3

Acute myeloid leukemia 5.2 4.9 3.8 5.1 4.8

Central nervous system tumors 23.2 22.2 27.9 30.1 27.3

Hodgkin’s lymphoma 13.9 14.2 14.1 14.1 12.8

Non-Hodgkin’s lymphoma 9.1 9.5 10.4 10.2 11.2

Thyroid carcinoma 4.8 4.8 5.1 5.1 5.4

Malignant melanoma 3.9 4.3 5.4 6.5 6.2

Germ cell tumors 8.3 9.9 9.7 11.7 11.7

Soft tissue sarcomas 10.0 10.7 10.9 11.4 11.6

Osteosarcoma 3.8 4.8 5.0 5.0 5.5

Ewing’s sarcoma 2.4 3.5 3.4 3.0 3.1

Neuroblastoma 7.3 7.2 7.9 7.7 8.0

Wilms’ tumor 5.4 6.5 5.6 6.3 6.5

Hepatoblastoma 0.7 0.7 1.1 1.2 1.4

SOURCE: National Cancer Institute, Division of Cancer Control and Population Sciences. Surveillance, Epidemiology, and End Results Program 1994-1998

Addendum to Table D6

Cancer incidence for children under 20 by age and type, 1994-1998

Rate per million children

Ages 0-4 Ages 5-9 Ages 10-14 Ages 15-19

Lymphocytic leukemia 61.0 30.6 18.4 14.9

Acute non-lymphocytic leukemia 9.7 4.3 6.5 7.8

Hodgkin’s lymphoma 0.9 3.7 11.8 32.0

Non-Hodgkin’s lymphoma 3.6 5.9 7.7 13.2

CNS and miscellaneous intracranial 

and intraspinal neoplasms 34.5 29.7 25.0 19.2

Neuroblastoma and 

ganglioneuroblastoma 25.7 3.2 0.8 0.4

Wilms’ tumor 18.8 4.8 0.8 0.3

Hepatic tumors 4.6 0.6 0.5 1.2

Osteosarcoma 0.2 2.6 7.9 8.9

Ewing’s sarcoma 0.6 2.2 4.2 4.7

Soft tissue sarcomas 11.1 7.9 10.5 15.0

Germ cell, trophoblastic,

other gonadal neoplasms 7.2 2.1 7.2 28.1

Epithelial and unspecified 3.1 3.3 11.6 40.5

SOURCE: National Cancer Institute, Division of Cancer Control and Population Sciences. Surveillance, Epidemiology, and End Results Program 1994-1998
144 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix A: Data Tables

Table D7

Children reported to have mental retardation, by race/ethnicity and family income, 1997-2000

Cases per 1,000 children

All 6

White non-Hispanic 6

Black non-Hispanic 10

Hispanic 5

< Poverty Level 12

100-200% of Poverty Level 10

> 200% of Poverty Level 4

Unknown Income 6

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health Interview Survey

Part 4: Emerging Issues

Table EI1

Number of states with advisories for methylmercury in non-commercial fish

1995 2000

Freshwater advisories 32 37

Coastal and estuarine advisories 7 13

Statewide advisories 5 12

SOURCE: U.S. Environmental Protection Agency, Office of Water. National Listing of Fish and Wildlife Consumption Advisories

Table EI2

Percentage of children ages 5-17 reported to have attention-deficit/hyperactivity disorder, 

by race/ethnicity and family income, 1997-2000

100-200% of > 200% of Unknown

All Incomes < Poverty Level Poverty Level Poverty Level Income

All races/ethnicities 6.7% 7.7% 7.5% 6.9% 4.8%

White non-Hispanic 8.0% 13.6% 9.3% 7.5% 6.1%

Black non-Hispanic 5.1% 5.6% 6.5% 4.9% 3.4%

Hispanic 3.8% 3.5% 3.9% 5.1% 2.3%

American Indian/Alaska Native 6.9%

SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health Interview Survey
Appendix A 145

Appendix A: Data Tables

Part 5: Special Features

Table S1

Percentage of California public elementary schools with lead paint and some 

deterioration of paint, 1994-1997

Schools Built Schools Built Schools Built Schools Built

Before 1940 1940-1959 1960-1979 1980-1995 All Schools

Any detectable lead 72.2% 46.3% 20.5% 3.1% 37.4%

≥ 600 ppm 72.2% 46.3% 18.2% 3.1% 36.9%

≥ 5,000 ppm 63.9% 41.8% 13.6% 0% 31.8%

SOURCE: California Department of Health Services, Childhood Lead Poisoning Prevention Branch. Lead Hazards in California’s Public Elementary Schools

and Child Care Facilities, April 1998

Table S2

Percentage of California public elementary schools with lead in soils, 1994-1997

Schools Built Schools Built Schools Built

Before 1940 1940-1979 1980-1995 All Schools

Schools with detectable lead in soil 100.0% 94.4% 60.5% 89.0%

Schools with soil lead > 400 ppm 29.7% 2.4% 0.0% 7.0%

SOURCE: Childhood Lead Poisoning Prevention Branch, California Department of Health Services. Lead Hazards in California’s Public Elementary Schools

and Child Care Facilities, April 1998

Table S3

Percentage of California public elementary schools with lead in drinking water, 1994-1997

Schools Built Schools Built Schools Built

Before 1940 1940-1979 1980-1995 All Schools

Schools with detectable 

lead in drinking water 68.6% 52.4% 42.1% 53.3%

Schools with > 15 ppb 

lead in drinking water 31.4% 16.1% 13.2% 18.3%

Schools with > 15 ppb 

lead in drinking water at first draw* 15.5%

Schools with > 15 ppb lead in 

drinking water at second draw* 6.5%

* Data for first- and second-draw samples are available for all schools only.
Table S4

Frequency of application of pesticides in Minnesota K-12 schools, 1999

Percentage of schools

Cafeteria and kitchen Locker Rooms

food storage areas and gymnasium Classrooms

Sprayed as needed 34.0% 33.5% 46.7%

Sprayed once a month 16.4% 3.7% 2.7%

Sprayed 1 - 4 times per year 24.0% 15.3% 12.5%

Not sprayed 16.9% 28.8% 25.6%

No answer / other / don’t know 8.7% 18.7% 12.5%

SOURCE: C.J. Olson Market Research Inc. for Minnesota Department of Agriculture. Quantitative Research Regarding Pest Management in 

Minnesota K-12 Schools. 1999

Table S5

Number of birth defects in California per 1,000 live births and fetal deaths

1991-1993 1994-1996 1997-1999

Heart defects 1.80 1.98 1.79

Oral cleft defects 1.60 1.67 1.50

Down Syndrome 1.34 1.28 1.28

Intestinal defects 0.73 0.73 0.56

Limb defects 0.46 0.46 0.38

SOURCE: California Birth Defects Monitoring Program

146 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix A: Data Tables
APPENDIX B

Data and Methods
Air Quality Exceedances (Measure E1)

EPA’s Office of Air Quality Planning and Standards has set health-based National

Ambient Air Quality Standards (NAAQS) for six common pollutants, often referred to

as criteria pollutants. These standards are shown in Table 1 below.

Air Quality Exceedances

State and local environmental agencies conduct air monitoring programs to measure

concentrations of these pollutants. The individual measurements are submitted to EPA

for inclusion in a national database called the Aerometric Information Retrieval System.

EPA, as part of its data management system, identifies instances in which levels of air

pollutants measured in the air are greater than the air quality standards. Each of these

events is called an “exceedance.” An exceedance occurs when a measured concentration

exceeds a target value that is actually higher than the air quality standard. Concentrations

measured in the air must be averaged over a time period set in accordance with the

standard for that pollutant. The target values used to identify exceedances are shown in

Table 1 below.

Agency Contact:

David Mintz (mintz.david@epa.gov)

U.S. EPA, Office of Air Quality Planning and Standards (OAQPS)

(919) 541-5224

Common Air Pollutants

(Measures E1-E3)

148 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix B: Data and Methods

Table 1: National Ambient Air Quality Standards (NAAQS) and the Values Used to Define

Exceedances by EPA

Target value to 

Pollutant Duration of Standard Standard define exceedance

Carbon monoxide Eight-hour average 9 ppm 9.5 ppm

One-hour average 35 ppm Not applicable

Nitrogen dioxide One year average 0.053 ppm 0.0535 ppm

Ozone One-hour averagea 0.12 ppm 0.125 ppm

Eight-hour average 0.08 0.085 ppm

Lead Three-month average 1.5 μg/m3 1.55 μg/m3

Particulate matter under 10 microns One-day (24 hour) average 150 μg/m3 155 μg/m3

One year average 50 μg/m3 Not applicable

Particulate matter under 2.5 microns One-day (24 hour) average 65 μg/m3 Not applicable

One year average 15 μg/m3 Not applicable

Sulfur dioxide One-day (24 hour) average 0.14 ppm 0.145 ppm

One year average 0.03 ppm Not applicable

a The ozone 1-hour standard applies only to areas that were designated non-attainment when the ozone 8-hour standard was adopted in July 1997.
Methods for Air Quality Exceedances (Measure E1)

Measure E1 uses exceedances reported by EPA based on its Aerometric Information

Retrieval System. EPA reported counties that exceeded the various standards on at

least one day per year. The measure reports the percentage of children living in

these counties, obtained by dividing the number of children in counties exceeding

the standards on at least one day per year by the total number of children in the

United States. Counties were identified that exceeded the following standards at

any time during the year:

■ Carbon monoxide: one-hour standard

■ Ozone: one-hour standard and eight-hour standard

■ PM-10: one-day standard

■ PM-2.5: annual standard 

■ Sulfur dioxide: annual standard

■ Nitrogen dioxide: annual standard

■ Lead: three month standard

Air Quality Index (Measure E2)

Measure E2 is based on the Air Quality Index (AQI) developed by EPA to report daily

air quality. The AQI converts measured pollutant concentrations to a number on a scale

from 0 to 500. In general, scores of 100 indicate that a daily standard has been reached.

Agency Contact:

AIRS Hotline

U.S. EPA, Office of Air Quality Planning and Standards (OAQPS)

(800) 334-2405

Long-Term Exposure to Criteria Pollutants (Measure E3)

Measure E3a uses concentrations of air pollutants measured at monitoring stations

across the United States and reported in EPA’s AIRS system. Measured concentrations

at each monitoring station were averaged by month and then by county. Annual values,

weighted by population, then were calculated. These annual averages of the measured

concentrations were compared with the applicable air quality standards to generate the

measure shown on the graph.

The measure shown for PM-10 is the average annual concentration experienced by

children in the United States, expressed as a percentage of the annual standard of 50

micrograms per cubic meter (μg/m3). The measure shown for nitrogen dioxide is the

average annual concentration experienced by children, expressed as a percentage of the

annual standard of 0.053 parts per million. The measure for sulfur dioxide is the average annual concentration experienced by children, expressed as a percentage of the

annual standard of 0.03 parts per million. 

Measure E3b uses the same data source for measured concentrations. This measure

reports the number of children living in counties with concentrations of PM-10 that

exceed the specific levels. The data for measured concentrations, averaged as in the

previous measure, were used to identify counties within the stated criteria. Census data

were used to calculate the number of children in these counties.

Appendix B 149

Appendix B: Data and Methods
The measure on hazardous air pollutants was developed using information from EPA’s

National Air Toxics Assessment (NATA) for 1996. As part of NATA, EPA estimated

ambient concentrations of hazardous air pollutants for every county in the continental

United States. EPA used a computer dispersion model, the Assessment System for

Population Exposure Nationwide (ASPEN), to estimate these concentrations. As a key

input to the model, EPA compiled a 1996 national emissions inventory of air toxics

emissions from outdoor sources. The types of emissions sources in the inventory

include major stationary sources (e.g., large waste incinerators and factories), area and

other sources (e.g., dry cleaners, small manufacturers, wildfires), and both on-road and

non-road mobile sources (e.g., cars, trucks, boats). 

Although computer modeling of hazardous air pollutant concentrations necessarily requires

simplifying assumptions and introduces significant uncertainties, no other method is

available for assessing air toxics concentrations nationally. Direct measurements of

ambient air toxics concentrations are available for only a subset of air toxics in relatively

few locations. In order to understand the limitations of the modeled ambient concentration estimates, EPA compared these estimates to available monitoring data from 1996

for seven pollutants as a “reality check.” The comparisons generally show that the model

estimates are lower than the monitored concentrations for these pollutants.

EPA used 1996 data because emissions inventories from that year are the most complete

and up-to-date available. The 33 air pollutants analyzed in NATA were identified as

priority pollutants in EPA’s Integrated Urban Air Toxics Strategy. This set includes 32

air toxics that are a subset of EPA’s list of 188 toxic air pollutants plus diesel particulate

matter, which is used as a surrogate measure of diesel exhaust. EPA has determined that

diesel exhaust is likely to be carcinogenic to humans by inhalation at environmental

levels of exposure and has listed it as a mobile source air toxic.

More information on NATA is available at http://www.epa.gov/ttn/atw/nata/

Agency Contact:

Roy Smith (smith.roy@epa.gov)

U.S. EPA, Office of Air Quality Planning and Standards

(919) 541-5362

Methods for Hazardous Air Pollutants (Measure E4)

Data

Ambient concentrations: Average concentrations of 33 hazardous air pollutants

(HAPs) in ambient (outdoor) air for each county in the continental United States

were obtained from EPA’s National Air Toxics Assessment (NATA). These values are

computer-generated estimates of the annual ambient concentrations of the HAPs

for 1996. The modeled concentrations, along with more information, are available

at http://www.epa.gov/ttn/atw/nata/

Dose-response information: EPA’s risk assessments for potentially carcinogenic HAPs

typically provide a unit risk estimate (URE), which is an estimate of the excess cancer

risk resulting from a lifetime of continuous exposure to a pollutant at a concentration

of one microgram per cubic meter (1 μg/m3) in air. UREs are estimated by extrapolation of data from laboratory animal studies, or in some cases, human studies (typically of workers who are exposed on the job). Many of the UREs are considered

“upper bound,” meaning they are an upper estimate of risks from a given exposure

level. For several of the more important hazardous air pollutants, including chromium

Hazardous Air

Pollutants (Measure E4)

150 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix B: Data and Methods
and benzene, the cancer risk estimates are based on the statistical best fit to human

data, and therefore are less conservative than estimates based on statistical upper

confidence limits developed from animal data.

The assessments also provide a reference concentration (RfC) for effects other than

cancer, which is an estimate of the concentration in air that is likely to be without

appreciable risks of deleterious effects during a lifetime. UREs and RfCs for pollutants

assessed in NATA were compiled and discussed in Health Effects Information Used

in Cancer and Noncancer Risk Characterization for the NATA 1996 National-Scale

Assessment, available at: http://www.epa.gov/ttn/atw/nata/natsa4.html (click on “Health

Effects Criteria”). The values from that document were used for this analysis. 

Population data: U.S. Census estimates of the number of children, ages 0-17, in

each county in the continental United States were obtained for 1996. 

Analysis: Cancer Risk Benchmarks

The lifetime cancer risks posed by HAPs in each county were calculated by multiplying the ambient concentration of each HAP by the inhalation unit risk estimate

(URE) of that HAP. The risk estimates for all modeled HAPs with cancer unit risk

estimates then were summed together to provide a combined cancer risk estimate.

The counties for which this value exceeded 1-in-100,000 and 1-in-10,000 were

identified, producing two lists of counties. For each list of counties, the number of

children ages 0-17 in the identified counties was summed together. The resulting

value then was divided by the number of children ages 0-17 in all counties in the

continental United States, yielding the percentage of children living in counties

where the concentrations of carcinogenic hazardous air pollutants exceeded the

two benchmark cancer risk levels.

Analysis: Benchmark for Other Health Effects

A hazard quotient (HQ) was calculated for each HAP with a reference concentration

(RfC). The HQ is equal to the modeled ambient concentration divided by the RfC.

An HQ greater than one indicates that the concentration of a HAP is greater than

that HAP’s reference concentration. Counties in which the HQ for any HAP

exceeded one were identified. The number of children ages 0-17 in the identified

counties was summed together. The resulting value was then divided by the number

of children ages 0-17 in all counties in the continental United States to yield the

percentage of children living in counties where the concentration of one or more

hazardous air pollutants exceeded the health benchmark for effects other than cancer.

Surveys on Radon Awareness and Environmental Tobacco Smoke Issues 

In 1994 and 1996, EPA’s Indoor Environments Division commissioned a commercial

contractor, Survey Communications, Inc., to conduct surveys on radon awareness and

environmental tobacco smoke issues. Approximately 31,000 households in the 50 states

were contacted in 1994 and 1996. All interviews were conducted by telephone using a

random digit dialing sampling methodology. Both the 1994 and the 1996 surveys

asked whether the household included any children under the age of 7. In addition,

they asked the following:

■ Does anyone in your household smoke cigarettes, cigars, or a pipe?

■ Do you allow anyone to smoke in your home on a regular basis?

In the 1994 survey, 6,411 households had children under the age of 7. In the 1996 survey,

6,851 households had children under the age of 7. The percentages of homes with children

Indoor Air Pollutants

(Measure E5)

Appendix B 151

Appendix B: Data and Methods
under the age of 7 in which someone smokes, or in which someone smokes regularly,

were obtained by crossing the question on children with the appropriate question on

smoking in the household.

In 1999, EPA commissioned the Center for Survey Research and Analysis at the

University of Connecticut to conduct a similar but much smaller survey. The results of

this survey were based on 1,005 telephone interviews with respondents located in the

contiguous 48 states, using a random digit dialing sampling methodology. The survey

questions regarding smoking in the home were similar to the questions in the 1994 and

1996 surveys. In the 1999 survey there were 225 households with children under the

age of 7. Although the 1999 survey was substantially smaller than the 1994 and 1996

surveys, all three surveys were designed to produce nationally representative samples.

Agency Contact:

Philip Jalbert (jalbert.philip@epa.gov)

U.S. EPA, Office of Air and Radiation

(202) 564-9431

Safe Drinking Water Information System (SDWIS) 

The Safe Drinking Water Information System (SDWIS) is the national regulatory compliance database for EPA’s drinking water program. SDWIS includes information on the

nation’s 170,000 public water systems and data submitted by states and EPA regions in

conformance with reporting requirements established by statute, regulation, and guidance.

EPA sets national standards for drinking water. These requirements take three forms:

maximum contaminant levels (MCLs, the maximum allowable level of a specific contaminant in drinking water), treatment techniques (specific methods that facilities must

follow to remove certain contaminants), and monitoring and reporting requirements

(schedules that utilities must follow to report testing results). States report any violations of these three types of standards to EPA.

Water systems must monitor for contaminant levels on fixed schedules and report to EPA

when a maximum contaminant level has been exceeded. States also must report when

systems fail to meet specified treatment techniques. More information about the maximum contaminant levels can be found at http://www.epa.gov/OGWDW/mcl.html.

EPA sets minimum monitoring schedules that drinking water systems must follow. These

minimum reporting schedules (systems may monitor more frequently) vary by the size of

the water system as well as by contaminant. Some contaminants are monitored daily, others

need to be checked far less frequently (the longest monitoring cycle is every nine years). For

example, at a minimum, drinking water systems will monitor continuously for turbidity,

monthly for bacteria, and once every four years for radionuclides.

A monitoring and reporting violation occurs when the system did not perform the

required testing, take adequate samples, or report a violation as required. Only major

monitoring and reporting violations are used in this report.

SDWIS includes data on the total population served by each public water system and the

state in which the public water system is located. However, SDWIS does not include the

number of children served. The numbers of children served by the public water systems

were estimated by determining the ratio of children in the state in which the public water

system is located and multiplying the ratio by the number of people served by that public

water system.

Drinking Water

Contaminants

(Measures E6-E7)

152 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix B: Data and Methods
For more information see the EPA’s SDWIS Web site at

http://www.epa.gov/safewater/sdwisfed/sdwis.htm.

Agency Contact:

Abraham Siegel (siegel.abraham@epa.gov)

U.S. EPA, Office of Ground Water and Drinking Water

(202) 564-4637

Methods for Drinking Water Contaminants (Measure E6 and E7)

Safe Drinking Water Information System (SDWIS) Data

The SDWIS database was used to examine national compliance with the Safe

Drinking Water Act. Three data files were prepared using data from SDWIS:

■ Public Water Systems (PWSs): Describes the public water systems in

the United States. Includes data fields with unique PWS Identification

numbers and an estimate of the total population served by each PWS.

■ SDWIS Maximum Contaminant Level (MCL) Violations: Describes PWS MCL

violations. Includes specific violation codes and contaminant group data.

■ SDWIS Monitoring and Reporting (MR) Violations: Describes PWS

monitoring and reporting violations. 

Population Data

Census data on county-level population by age for every county in the United

States was obtained from the U.S. Census Bureau. The census population under the

age of 18 was summed by county for each state. Subsequently, the proportion of

individuals under the age of 18 to the total population in each state was calculated.

A census data file was generated containing the proportion of children under the

age of 18 living in a given state for each year between 1990 and 2000.

Analysis for Measure E6: Percentage of children living in areas served by public

water systems that exceeded a drinking water standard or violated treatment

requirements

Data files for Public Water Systems (PWSs), MCL violations and the proportion of

children residing within each state were linked by PWS identification number, year,

and state. The contaminant and violations codes in the SDWIS MCL Violations file

described the type of drinking water standard that was violated. Querying these

codes (listed below) generated the data in Measure E6.

■ All health-based: All SDWIS MCL violations

■ Lead and copper: Violation codes 57-63

■ Microbial Contaminants: Violation codes 21 and 22

■ Chemical and radiation: All applicable contaminant codes*

■ Treatment and filtration: Violation codes 41 and 42

■ Nitrate and nitrite: Contaminant codes 1038, 1040, and 1041

—————————————

* The applicable contaminant and violations codes for chemical and radiation are as follows:

Total trihalomethanes: 2950 continued on following page

Appendix B 153

Appendix B: Data and Methods
Volatile organic chemicals: 2326, 2378, 2380, 2955, 2964, 2968, 2969, 2976, 2977,

2979, 2980, 2981, 2982, 2983, 2984, 2985, 2987, 2989, 2990, 2991, 2992, 2996

Synthetic organic contaminants: 2005, 2010, 2015, 2020, 2031, 2032, 2033, 2034, 2035,

2036, 2037, 2039, 2040, 2041, 2042, 2046, 2050, 2051, 2063, 2065, 2067, 2105, 2110,

2274, 2306, 2383, 2931, 2946, 2959

Nitrate/nitrite: 1038, 1040, 1041

Inorganic chemicals: 1005, 1010, 1015, 1020, 1024, 1025, 1035, 1045, 1074, 1075,

1085, 1094

Radiological contaminants: 4000, 4010, 4101

Analysis for Measure E7: Percentage of children living in areas with major

violations of drinking water monitoring and reporting requirements

Data files for public water systems, monitoring and reporting violations, and the

proportion of children residing within each state were linked by PWS identification

number, year, and state. Querying the violation codes listed below generated the

various trend lines of Measure E7:

■ Any major violation: Only major violations selected.

■ Lead and copper: Violation codes 51-56

■ Microbial contaminants: Violation codes 23 and 25

■ Chemical and radiation : Violation code 03

■ Treatment and filtration: Violation codes 31 and 36

The initial query resulted in a single table containing merged data on MR violation,

PWSs, and census information. Because a PWS can have multiple violations of the

same MR rule in the same year, duplicates had to be removed in a second query.

The second query selected PWSs only once per year if they reported multiple MR

violations in the same contaminant category for that year. The total number of people served by a PWS violating the selected MR violation in a given state was then

summed and multiplied by the appropriate proportion of children under the age of

18 living in that state during a given year between 1990 and 2000. The estimate of

children age 18 and under served by a PWS violating a MR rule was then summed

for all 50 states. The percentage of all children was calculated and presented in

Measure E7. The estimate assumes an even geographic distribution by county of

individuals under the age of 18 in each state.

154 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix B: Data and Methods
Pesticide Data Program 

The U.S. Department of Agriculture (USDA) has been conducting the Pesticide Data

Program (PDP) since 1991 and has published its findings for calendar years 1991

through 2000. PDP continues to focus on the National Academy of Sciences’ 1993 recommendation that pesticide residue monitoring programs target foods that are highly

consumed by children, and that the analytical testing methods used in these monitoring efforts should be standardized, validated, and subject to strict quality control and

quality assurance programs. Since 1994 PDP has modified its commodity testing profile to include not only fresh fruits and vegetables, but also canned and frozen fruits

and vegetables, fruit juices, whole milk, wheat, soybeans, oats, corn syrup, peanut butter, and poultry. In 2001, PDP collected and analyzed more than 12,000 food samples.

More information is available at http://www.ams.usda.gov/science/pdp.

Each sample of food tested in the PDP is analyzed to determine whether the residues of

a variety of different pesticides are present. The number of organophosphate pesticides

and metabolites analyzed by PDP has increased from 34 in 1994 to 77 in 2001, and

measurement techniques have become more sensitive during that time. In order to

maintain comparability across the years 1994 to 2001, the organophosphate detection

rates reported in this measure include only detections of the original 34 pesticides

included in the PDP at or above the original limits of detection available in 1994. 

Agency Contact:

Martha Lamont (Martha.Lamont@usda.gov)

USDA, Agricultural Marketing Service

Tel: (703) 330-2300

Superfund NPL Assessment Program Database 

The Superfund NPL Assessment Program (SNAP) is a relational database system containing data for proposed, final, and deleted National Priorities List (NPL) sites. The

majority of the information contained in SNAP is the data that support the NPL listing of sites; e.g., Hazard Ranking System (HRS) scoring factors, site narratives, site

characteristics, contaminants, locational information, proposed and final Federal Register

dates and citations, etc. For the most part, the data contained in SNAP are a snapshot

at the time of NPL proposal and listing, although SNAP also contains a minimal amount

of data (date and status) on Construction Completions, partial deletions, and deletions.

This information allows SNAP to give an accurate overall picture of the status of the NPL

on a real-time basis. All of the data contained in SNAP are publicly available information.

Agency Contact:

Terry Jeng (jeng.terry@epa.gov)

U.S. EPA, Office of Solid Waste and Emergency Response

(703) 603-8852

Pesticide Residues 

(Measure E8)

Appendix B 155

Appendix B: Data and Methods

Land Contaminants

(Measure E9)
Methods for Land Contaminants (Measure E9)

Superfund Data

Data describing the physical location of sites listed on the Superfund National Priorities

List (NPL) were acquired from EPA’s Superfund NPL Assessment Program (SNAP)

Database (http://www.epa.gov/superfund/sites/query/advquery.htm). Data fields for each

site included parameters such as address, latitude, longitude, date of proposed addition to the NPL, and date deleted from the NPL (where applicable). The latitudelongitude values associated with each NPL site represented an estimate of the geographic

center of the site. For a given year, all sites on the NPL or proposed for addition to the

NPL on or before September 30th were selected. Sites deleted from the NPL prior to

or on September 30th of the same year were then removed. Sites were selected for

the period between 1990 and 2000 and the results were exported for use in

ArcView GIS version 3.2. 

Census Data

U.S. Census data from 1990 and 2000 at the census block level were compiled and

processed to obtain fields of information not readily available from the U.S. Census

Bureau. The variables in this data set include total population, population under 18,

and the latitude and longitude of each census block centroid. The census block

centroid latitude-longitude data corresponded to a point at the geographic center of

each U.S. census block.

GIS Analysis

Biannual Superfund data as well as the 1990 and 2000 U.S. Census block-level

demographic data were imported into ArcView GIS version 3.2. The latitude-longitude points for each Superfund site and census block centroid were plotted using

the GIS software. For years prior to 2000, 1990 census block centroids falling within

a one mile radius of a Superfund site were selected, on a year-by-year basis

between 1990 and 1998. The total number of children associated with the selected

census block centroids was then calculated and presented as a percentage of the

total number of people under the age of 18 living in the United States. For 2000,

U.S. Census block-level population data were used when selecting centroids within

a one-mile radius of sites on the NPL in 2000. The total number of children living

within one mile of a site on the NPL was summed and presented as a percentage of

the total number of children under the age of 18 living in the United States.

156 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix B: Data and Methods
National Health and Nutrition Examination Survey 

Data on children’s blood lead levels were obtained from the National Health and

Nutrition Examination Surveys (NHANES) II and III, and NHANES 1999-2000,

conducted by the National Center for Health Statistics. The survey is designed to assess

the health and nutritional status of the non-institutionalized civilian population with direct

physical examinations and interviews, using a complex multi-stage, stratified, clustered

sampling design. Interviewers obtain information on personal and demographic characteristics, including age, household income, and race and ethnicity by self-reporting or

as reported by an informant. The first survey, NHANES I, was conducted during the

periods 1971-1974 and 1974-1975; NHANES II covered the period 1976-1980; and

NHANES III covered the period 1988-1994. Only NHANES II and III, however,

contain data on blood lead levels. NHANES II provided blood lead data for children

ages 6 months to 5 years; NHANES III provided data on children ages 1-5 years.

Descriptions of the survey design, the methods used in estimation, and the general

qualifications of the data are presented in the following:

■ Plan and Operation of the Second National Health and Nutrition Examination

Survey, 1976-80: Programs and Collection Procedures, Series 1, No. 15. Vital and

Health Statistics, Hyattsville, MD: National Center for Health Statistics.

■ Plan and Operation of the Third National Health and Nutrition Examination

Survey, 1988-94: Series 1: Programs and Collection Procedures, No. 32. Vital and

Health Statistics, Hyattsville, MD: National Center for Health Statistics.

Starting in 1999, NHANES changed to a continuous survey visiting 15 U.S. locations

per year and surveying and reporting for approximately 5,000 people annually. Body

burden data from NHANES 1999-2000 are presented in:

■ Second National Report on Human Exposure to Environmental Chemicals.

Atlanta, GA: Centers for Disease Control and Prevention, National Center for

Environmental Health, January 2003.

The percentage of children with blood lead levels greater than 10 μg/dL is influenced

by the proportion of nonresponses within each category. Families with incomes below

the poverty level had a lower response rate than families with incomes at or above the

poverty level. The percentages are thus the best estimates available, but may be biased

by the variation of nonresponses by family income.

NHANES Web site: www.cdc.gov/nchs/nhanes.htm

Second National Report on Human Exposure to Environmental Chemicals:

www.cdc.gov/exposurereport/

Agency Contact:

Clifford Johnson (clj1@cdc.gov)

National Center for Health Statistics

(301) 458-4292

Concentrations of

Lead in Blood

(Measures B1-B3)

Appendix B 157

Appendix B: Data and Methods
National Health and Nutrition Examination Survey 

Data on mercury levels were obtained from the National Health and Nutrition

Examination Survey (NHANES) 1999-2000, conducted by the National Center for

Health Statistics. See above for description of NHANES under “Concentrations of

Lead in Blood.”

National Health and Nutrition Examination Survey 

Data on children’s cotinine levels were obtained from the National Health and

Nutrition Examination Survey (NHANES) III and NHANES 1999-2000, conducted

by the National Center for Health Statistics. See above for description of NHANES

under “Concentrations of Lead in Blood.”

Only cotinine levels for nonsmoking children were used. Children were classified as

smokers if they had a serum cotinine level greater than 10 nanograms per milliliter

(ng/mL).

National Health Interview Survey

Data on the prevalence of asthma and other respiratory diseases are from the National

Health Interview Survey (NHIS), a continuing nationwide sample survey of the civilian

noninstitutionalized population in which data are collected by personal household

interviews. Interviewers obtain information on personal and demographic characteristics, including race and ethnicity, by self reporting or as reported by an informant for

children under 18 years of age. Investigators also collect data about illnesses, injuries,

impairments, chronic conditions, activity limitation caused by chronic conditions, use

of health services, and other health topics. For most health topics, the survey collects

data over an entire year.

The NHIS sample includes an over-sample of Black and Hispanic persons and is

designed to allow the development of national estimates of health conditions, use of

health services, and health problems of the U.S. civilian non-institutionalized population. Over the years, the response rate for the ongoing part of the survey has run

between 94 and 98 percent. In 2000, interviewers collected information on 32,374

persons 18 years or older, and 13,376 children ages 0-17 years old.

Descriptions of the survey design, the methods used in estimation, and the general

qualifications of the data are presented in the following: 

■ Massey, J.T., T.F. Moore, V.L. Parsons, and W. Tadros. 1989. Design and estimation

for the National Health Interview Survey, 1985-1994. Vital and Health Statistics 2

(110). Hyattsville, MD: National Center for Health Statistics.

■ Botman S.L., T.F. Moore, C.L. Moriarity, and V.L. Parsons. 2000. Design and estimation for the National Health Interview Survey, 1995-2004. Vital Health

Statistics 2 (130). Hyattsville, MD: National Center for Health Statistics.

■ Bloom B, and L. Tonthat. 2002. Summary Health Statistics for U.S. Children:

National Health Interview Survey, 1997. Vital Health Statistics 10 (203).

Hyattsville, MD: National Center for Health Statistics. 

Concentrations of

Mercury in the Blood of

Women of Child-bearing

Age (Measure B4)

Concentrations of

Cotinine in Blood

(Measure B5)

158 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix B: Data and Methods

Respiratory Diseases

(Measures D1-D4)
Where possible, the report presents breakouts of the NHIS data for three family

income levels: below poverty level; between poverty level and twice the poverty level

(shown in graphs and tables as 100-200% of Poverty Level); and greater than twice the

poverty level (>200% of Poverty Level). For approximately 15 percent of children represented in the NHIS, family income information needed for this classification was not

available. These children are not included in the graphs showing statistics by income

level. Statistics for these children are included in the data tables in Appendix A, under

“unknown income.”

In 1997, the NHIS underwent a major redesign in which the questions used to estimate asthma prevalence were changed. For asthma up to 1996, Measure D1 uses the

parent’s response to the following question “Did <child’s name> have asthma in the

past 12 months?” For asthma in 1997-2000, Measures D1 and D2 use parents’

response to the following two questions: “Has a doctor or other health professional

EVER told you that <child’s name> had asthma?” and if yes, “During the past 12

months, has <child’s name> had an episode of asthma or an asthma attack?”

In 2001, the NHIS added the following new question: “Does <child’s name> still have

asthma?” This question was used to estimate the percentage of children who currently

have asthma.

NHIS Web site: http://www.cdc.gov/nchs/nhis.htm

Agency Contact:

Laura Montgomery (lem3@cdc.gov)

National Center for Health Statistics

(301) 436-3650

National Hospital Ambulatory Medical Care Survey

Data on asthma emergency room visits were obtained from the National Hospital

Ambulatory Medical Care Survey (NHAMCS). The NHAMCS is designed to collect

data on ambulatory care services in hospital emergency and outpatient departments.

Findings are based on a national sample of visits to the emergency departments and

outpatient departments of noninstitutional general and short-stay hospitals, exclusive of

federal, military, and Veterans Administration hospitals, located in the 50 states and the

District of Columbia. Annual data collection began in 1992.

Specially trained interviewers visit the hospitals prior to their participation in the survey

to explain survey procedures, verify eligibility, develop a sampling plan, and train hospital staff in data collection procedures. Hospital staff are instructed to complete

patient record forms for a systematic random sample of patient visits during a randomly assigned four-week reporting period. Data are obtained on demographic characteristics of patients; expected source(s) of payment; patients’ complaints; physicians’ diagnoses; diagnostic and screening services; procedures; medication therapy; disposition;

types of health care professionals seen; causes of injury where applicable; and certain

characteristics of the hospital, such as the type of ownership.

Respiratory infections are ICD-9 codes 464 and 465, acute bronchitis is ICD-9 code

466, and asthma is ICD-9 code 493.

NHAMCS Web site: http://www.cdc.gov/nchs/about/major/ahcd/ahcd1.htm

Appendix B 159

Appendix B: Data and Methods
Agency contact:

Hospital Care Statistics Branch

National Center for Health Statistics

(301) 458-4600

National Hospital Discharge Survey

Data on asthma hospitalizations were obtained from the National Hospital Discharge

Survey (NHDS). The NHDS is a national probability survey designed to meet the

need for information on characteristics of inpatients discharged from non-federal shortstay hospitals in the United States. The NHDS collects data from a sample of approximately 270,000 inpatient records acquired from a national sample of approximately

500 hospitals. Only hospitals with an average length of stay of fewer than 30 days for

all patients, general hospitals, or children’s general hospitals are included in the survey.

Federal, military, and Department of Veterans Affairs hospitals, as well as hospital units

of institutions (such as prison hospitals), and hospitals with fewer than six beds staffed

for patient use, are excluded. Data from the NHDS are available annually.

Respiratory infections are ICD-9 codes 464 and 465, acute bronchitis is ICD-9 code

466, and asthma is ICD-9 code 493.

NHDS Web site: http://www.cdc.gov/nchs/about/major/hdasd/nhdsdes.htm

Agency Contact:

Hospital Care Statistics Branch

National Center for Health Statistics

(301) 458-4321

Surveillance, Epidemiology, and End Results Program 

The population-based data used for incidence of cancer are from the Surveillance,

Epidemiology, and End Results (SEER) Program of the National Cancer Institute

(NCI). Information from five states (Connecticut, Hawaii, Iowa, New Mexico, and

Utah) and five metropolitan areas (Atlanta, Georgia; Detroit, Michigan; Los Angeles,

California; San Francisco-Oakland, California; and Seattle-Puget Sound, Washington)

accounting for approximately 14 percent of the United States’ population are included.

The participating regions were selected primarily for their ability to operate and maintain

a population-based cancer reporting system and for their epidemiologically significant

population subgroups. With respect to selected demographic and epidemiologic factors,

they are, when combined, a reasonably representative subset of the U.S. population.

The mortality data for all cancer deaths among children in the United States are from

data based on underlying cause of death from the National Vital Statistics System,

administered by the National Center for Health Statistics. Mortality data are obtained

by NCI and provided for all causes of cancer.

All rates are age-adjusted to the 1970 U.S. standard population.

SEER Web site: http://seer.cancer.gov

Agency Contact:

Surveillance, Epidemiology, and End Results Program

National Cancer Institute

(301) 496-8510

Childhood Cancer

(Measures D5-D6)

160 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix B: Data and Methods
National Health Interview Survey 

Data on the prevalence of attention-deficit/hyperactivity disorder and mental retardation

are from the National Health Interview Survey (NHIS). See above for description of

the NHIS under “Respiratory Measures.” For mental retardation, the measure uses

parents’ responses to this question: “Has a doctor or health professional ever told you

that <child’s name> had mental retardation?” For attention-deficit/hyperactivity disorder,

the measure uses parents’ responses to this question: “Has a doctor or health professional

ever told you that <child’s name> had attention deficit disorder?” 

National Listing of Fish and Wildlife Advisories

EPA’s Office of Water maintains a database that includes all advisories issued by states,

territories, and tribes to warn people to reduce or eliminate consumption of fish due

to chemical contamination. Most of the advisories are for non-commercial fish that

people catch for their own use, but some advisories issued by states for commercial fish

also are included. Some of the advisories apply to entire states; others apply only to

specified water bodies such as lakes or rivers. This database can be searched by state,

by type of fish, or by contaminant. The database was used for Measure E9, which

reports the number of women of child-bearing age living in states that have issued

advisories for mercury in non-commercial fish. The database includes advisories 

issued through the year 2000. A fact sheet describing the database is available at

http://www.epa.gov/ost/fish/advisories/factsheet.pdf.

The Office of Water also has produced extensive guidance to assist states and tribes in

developing and issuing advisories. These guidance documents are available at

http://www.epa.gov/ostwater/fish/guidance.html.

The National Listing of Fish and Wildlife Advisories database is available at:

http://map1.epa.gov/

Agency Contact:

Jeff Bigler (bigler.jeff@epa.gov)

U.S. EPA, Office of Water 

(202) 566-0389

Appendix B 161

Appendix B: Data and Methods

Neurodevelopmental

Disorders 

(Measure D7)

Advisories for

Methylmercury in

Non-Commercial Fish 
California Department of Health Services Study on 

Lead Contamination in California Schools

After the California state legislature passed the Lead-Safe Schools Protection Act in

1992, the Childhood Lead Poisoning Prevention Branch of the California Department

of Health Services commissioned a study to determine the extent of lead contamination

in paint, soil and water in California schools. The study began in 1994 and the collection of data was completed in 1997.

The Department of Health Services randomly selected 200 of the 5,041 public elementary schools in California to participate in the study. The participating schools were

selected to reflect the statewide distribution of school buildings by age (the age of the

building is a predictor of the presence of lead). The selection process also yielded a geographically representative sample. Schools with both public and private pre-kindergarten and childcare programs located on their premises were included in the sample.

Trained field staff collected the samples and an accredited commercial laboratory conducted the analysis. Samples in all media were analyzed using Flame Atomic Absorption

Spectroscopy. Paint and soil samples were taken from the oldest building in the school

and the youngest children’s classroom. In 76.5 percent of the schools, the oldest building also housed the youngest children’s classroom. Water samples also were taken from

the oldest building except in cases in which there was no water outlet in the building.

Paint chip samples were taken from walls, doors, or windows. Wherever possible, they

were obtained from areas where the paint was visibly deteriorated. Soil samples were

collected from within five feet of painted walls or windows, from play areas, and from a

location on the school grounds that was as far away from any building as possible. Water

samples were taken from outlets located both inside and outside the school buildings.

More information on study design, methods, and results is available at

http://www.dhs.ca.gov/childlead/schools/sitemap.htm

Agency Contact:

Jill Garellick (jgarelli@dhs.ca.gov)

Lead-Safe Schools Project

California Lead Poisoning Prevention Branch

California Department of Health Services

(510) 622-4959

Ginger Reames (greames@dhs.ca.gov)

Lead-Safe Schools Project

California Lead Poisoning Prevention Branch

California Department of Health Services

(510) 622-4966

162 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix B: Data and Methods

Lead in California

Public Elementary

Schools and 

Childcare Facilities

(Measures S1-S3) 
Minnesota Survey on Pesticide Use in K-12 Schools

In 1998, the Minnesota Department of Agriculture and the University of Minnesota

jointly established an Integrated Pest Management (IPM) workgroup in response to

growing concerns about pesticide use in K-12 schools in the state. The workgroup

included representatives from both founding organizations; the Minnesota Office of

Environmental Assistance; the Minnesota Department of Children, Families and

Learning; the Minnesota Department of Health; and the St. Paul Public Schools.

In 1999, the workgroup commissioned a statewide survey of pest management practices in K-12 schools, funded by EPA. The purpose of the survey was to obtain statistically reliable statewide data that would provide general information about current pest

management practices in K-12 schools. 

The survey questionnaires were designed by the workgroup and the survey was formatted

and conducted by an independent contractor, C.J. Olson Market Research, Inc. A pretest was mailed out to 25 superintendents and 25 head custodians (those who received

the pre-tests were not contacted again). The final survey questionnaires were mailed to

330 superintendents out of the 355 districts in the state, and to a random sample of

1,160 public and private K-12 schools out of 2,197 school buildings in the state. The

questionnaires mailed to the schools were addressed to principals, who were instructed

to ask head custodians to complete the questionnaires. 

Response to the questionnaires was voluntary. The overall response rate for the entire

survey was 36 percent. One hundred and sixty eight (168) superintendents’ questionnaires and 375 head custodians’ questionnaires were processed. The responses from the

head custodians were used for this report. 

More information about the survey is available at

http://www.mda.state.mn.us/IPM/PestMgmtinSchools.html

Agency Contact:

Jeanne Ciborowski (jeanne.ciborowski@state.mn.us)

Minnesota Department of Agriculture

(651) 297-3217

California Birth Defects Monitoring Program

The California Birth Defects Monitoring Program registry is a population-based registry for babies born in the following counties in California: Fresno, Kern, Kings, Los

Angeles, Madera, Merced, San Francisco, San Joaquin, Santa Clara, Stanislaus, and

Tulare. These counties represent about 45 percent of the state population. Experience

in monitoring California rates and trends since 1983 shows that the rates from the

eight Central Valley counties are reflective of those throughout California: both urban

and rural areas are included, all major racial/ethnic groups are present in the birth population in similar proportions to what is seen in California as a whole, and the high

quality of diagnostic practices in the primary hospitals and referral centers yield thorough and accurate case identification in medical records. This sampling of California’s

birth population is the same as that used by the Centers for Disease Control and

Prevention for the National Birth Defects Prevention Study.

Appendix B 163

Appendix B: Data and Methods

Pesticide Use in

Minnesota’s K-12

Schools (Measure S4)

Birth Defects 

(Measure S5)
Babies born with birth defects serious enough to require medical treatment or to cause

disability are included in the registry. These birth defects are listed in codes 740-759 of

the International Classification of Diseases (ICD) and include structural birth defects

such as missing limbs and malformed organs, chromosome abnormalities such as Down

syndrome, and birth defects patterns such as fetal alcohol syndrome. The cases are

ascertained actively through data gathering from medical facilities and review of medical records. Birth defects diagnoses made prenatally, after birth, and up to one year of

age are included in the registry.

Agency Contact:

Gretta Petersen (gpe@cbdmp.org)

California Birth Defects Monitoring Program

(888) 898-2229

http://www.cbdmp.org/

U.S. Census County-Level Data 

County population estimates were obtained from the U.S. Census Bureau. For 1990,

data from the decennial census were used directly. For subsequent years, county population data were estimated by the Census Bureau using information on births, deaths,

domestic migration, and international migration. Individual age populations were compiled for children ages 0 to 17 at the county level for each year 1990 to 1999. A complete description of the population estimation methodology can be found on the Census

Bureau’s Methodology for Estimates of State and County Total Population Web page at

http://www.census.gov/population/methods/stco99.txt and on the Census Bureau’s

Methodology for Estimating County Population by Age and Race Web site at

http://www.census.gov/population/estimates/county/casrh_doc.txt.

The U.S. Census Bureau population estimates for 1990 to 1999 classify the population

among six race/ethnic categories, which herein are referred to as the unadjusted race

categories. These categories are White non-Hispanic, White Hispanic, total Black

(Hispanic and non-Hispanic), total American Indian (Hispanic and non-Hispanic),

and total Asian and Pacific Islander (all races with Hispanic origin indicated). U.S.

Census data were adjusted to reflect five separate race/ethnic categories that were used

in this report: White non-Hispanic, Black non-Hispanic, American Indian and Alaska

Native non-Hispanic, Asian and Pacific Islander non-Hispanic, and Hispanic. 

For the 2000 census, individuals were allowed to report two or more race groups when

responding to the census. As with the 1990 census, individuals may indicate whether

they are of Hispanic origin in addition to indicating their race. Persons reporting multiple races in the 2000 data were assigned to one of the five race/ethnicity categories used

in this report (Black non-Hispanic, White non-Hispanic, American Indian and Alaska

Native Non-Hispanic, Asian and Pacific Islander non-Hispanic, and Hispanic) using

the method described below.

Census data also were used to derive children’s population counts for three income

categories: 1) households with income below poverty level; 2) households with

income greater than or equal to poverty level but less than twice the poverty level; and

3) households with income equal to or greater than 200 percent of poverty level. The

Census Bureau defines poverty level based on a set of money income thresholds that

vary by family size and composition. If a family’s total income is less than that family’s

threshold, then that family, and every individual in it, is considered poor. The Census

164 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix B: Data and Methods

Child Population Data
Bureau updates its poverty thresholds annually. In 2000, a family of two adults and two

children with total income below $17,463 was considered below the poverty level.

Tables showing the Census Bureau’s poverty thresholds are available at 

http://www.census.gov/hhes/poverty/threshld.html.

Agency Contact:

U.S. Census Bureau

Population Estimates Branch

(301) 457-2385

http://www.census.gov/population/www/estimates/countypop.html

Methods for Race Adjustment for 1990-1999 County Census Data

The overlapping race and ethnicity categories were adjusted into the non-overlapping categories of White non-Hispanic, Black non-Hispanic, American Indian and

Alaska Native (AIAN) non-Hispanic, Asian and Pacific Islander (API) non-Hispanic,

and Hispanic, for children under the age of 18. Census data provide 1990-1999

population estimates by “Race by Hispanic origin” (e.g., percentage of Black

Hispanic and Black non-Hispanic) but do not provide these data by sex or age,

except for White Hispanics and White non-Hispanics. An Hispanic ethnicity correction factor, consisting of the ratio of Black non-Hispanics to total Blacks, was calculated for all Blacks. This ratio was multiplied by the total number of Black children

to estimate the number of Black non-Hispanic children. A similar procedure was

followed for AIAN and API children. The analysis assumed that the ratio of Hispanic

to non-Hispanic children in each race category was the same as the corresponding

ratio for the total population. The Hispanic ethnicity correction factors for Black,

AIAN, and API were applied to the population of children on a county-by-county

basis. This method created five mutually exclusive race/ethnicity categories: Black

non-Hispanic, White non-Hispanic, AIAN non-Hispanic, API non-Hispanic, and

Hispanic, for children 17 and under.

Methods for Race Adjustment for 2000 County Census Data

Starting in 2000, persons can report multiple races to describe their race on the

census form. This analysis uses the bridging methodology by Parker and Makuc1 for

assigning non-Hispanic persons who report multiple race categories to four mutually

exclusive race categories: White non-Hispanic, Black non-Hispanic, AIAN nonHispanic, and API non-Hispanic. The Parker and Makuc methodology is based on

race information collected from the 1993-1995 National Health Interview Survey.

In this survey, respondents who reported multi-racial categories also were asked to

report a single race with which they would identify themselves. Parker and Makuc

calculated proportions of multi-racial respondents who would have identified themselves with a single race if that category were the only option. Major bi-racial categories identified by the authors were: White/Black, White/AIAN, White/API, and

Black/AIAN. In this analysis, equations were derived for apportioning these four biracial categories into single-race categories using the proportions reported by Parker

and Makuc. Race combinations other than the major bi-racial groups identified by

Parker and Makuc were grouped under the category of “multiple race.” The multiple race category was further split into the four single-race categories using the

national distribution of the four single-race categories in the United States (e.g.,

71.3 percent of “multiple race” respondents were considered White). 

Appendix B 165

Appendix B: Data and Methods

1 Parker, J.D. and Makuc, D.M. 2002. Methodological implications of allocating multiple

race data to single race categories. Health Services Research 37 (1): 203-15.
Methods for Obtaining Counts of Children under Age 18 by

Race/Ethnicity

The Census Bureau provides county-specific population estimates by race and ethnicity for each year from 1990-1999 for several age groups, including ages 15-19.

For the measures in this report, which are focused on children under age 18, it was

therefore necessary to estimate the portion of the population age 15-19 that is under

age 18 (i.e., ages 15-17). Census Bureau files on population by county provide estimates of people for each age (i.e., 15 year olds, 16 year olds, etc.) for each year.

A scaling factor was calculated for each county, for each year, as the proportion of

15-19 year olds who are ages 15-17. This scaling factor was multiplied by the estimated population ages 15-19 for each race/ethnicity to estimate the number of children

ages 15-17, by race/ethnicity, for each county for 1990- 1999. This calculation

assumes that the proportion of 15-19 year olds that is 15-17 years old is constant

across the race/ethnicity categories in each county.

Methods for Calculating Population by Ratio of Income to Poverty Level

Population counts by the three categories of income to poverty level ratio (households with income below poverty level, households with income greater than or

equal to poverty level but less than twice the poverty level, and households with

income equal to or greater than 200 percent of poverty level) are available for the

1990 census but are not estimated by the Census Bureau for the intercensal years

1991 to 1999. For the intercensal years, the Census Bureau’s county-level children’s

population estimates were multiplied by the percentage of children in a given poverty range from the 1990 population data to estimate the number of children, by

county, in the three income categories. 

166 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix B: Data and Methods
APPENDIX C

Environmental

Health Objectives in 

Healthy People 2010
ealthy People 2010, coordinated by the U.S. Department of Health and Human

Services, Office of Disease Prevention and Health Promotion, establishes national

health objectives for the first decade of the new millennium. Launched in January 2000,

Healthy People 2010 seeks to increase the quality and number of years of healthy life and

to eliminate health disparities among Americans.

Healthy People 2010 includes a number of goals and objectives that relate to the children’s environmental health risks considered in America’s Children and the Environment.

Objective 8-1 is to reduce the proportion of persons exposed to air that does not meet

the U.S. Environmental Protection Agency’s health-based standards for harmful air pollutants.

Objective 8-4 is to reduce air toxic emissions to decrease the risk of adverse health

effects caused by airborne toxics.

Objective 8-5 is to increase the proportion of persons served by community water 

systems who receive a supply of drinking water that meets the regulations of the Safe

Drinking Water Act.

Objective 8-10, currently under development, is to reduce the potential human exposure to persistent chemicals by decreasing fish contaminant levels.

Objective 8-11 is to eliminate elevated blood lead levels in children.

Objective 8-12 is to minimize the risks to human health and the environment posed by

hazardous sites. 

Objective 8-24 is to reduce exposure to pesticides as measured by urine concentrations

of metabolites.

Objective 16-14 is to reduce the occurrence of developmental disabilities.

Objective 24-2a is to reduce hospitalizations for asthma for children under 5.

Objective 27-9 is to reduce the proportion of children who are regularly exposed to

tobacco smoke at home.

Healthy People 2010 is available at www.health.gov/healthypeople or by calling 

1(800) 367-4725.

168 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

Appendix C: Environmental Health Objectives in Healthy People 2010

H
APPENDIX D

Environmental Health

Objectives in EPA's

Strategic Plan
170 America’s Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses

EPA’s mission is to protect human health and to safeguard the natural environment—air,

water, and land—upon which life depends. The agency’s 2000-2005 Strategic Plan lays

out long-term goals and shorter-term objectives for fulfilling that mission. 

The plan’s 10 long-term goals establish EPA’s major priorities for the five-year period.

These include 1) clean air; 2) clean and safe water; 3) safe food; 4) preventing pollution

and reducing risk in communities, homes, workplaces, and ecosystems; 5) better waste

management, restoration of contaminated waste sites, and emergency response; 6) reduction

of global and cross-border environmental risks; 7) quality environmental information;

8) sound science, improved understanding of environmental risk, and greater innovation

to address environmental problems; 9) a credible deterrent to pollution and greater

compliance with the law; and 10) effective management.

A number of objectives in the plan relate to the risks to children’s environmental

health considered in America’s Children and the Environment. Those selected objectives

are presented here.

The full text of EPA’s 2000-2005 Strategic Plan is available at

http://www.epa.gov/ocfo/plan/2000strategicplan.pdf.

Goal 1: Clean Air

Objectives:

■ Reduce the risk to human health and the environment by protecting and improving

air quality so that air throughout the country meets national clean air standards by

2005 for carbon monoxide, sulfur dioxide, nitrogen dioxide, and lead; by 2012 for

ozone; and by 2018 for particulate matter.

■ By 2020, eliminate unacceptable risks of cancer and other significant health problems

from air toxic emissions for at least 95 percent of the population, with particular

attention to children and other sensitive subpopulations, and substantially reduce

or eliminate adverse effects on our natural environment.

Goal 2: Clean and Safe Water

Objectives:

■ By 2005, protect human health so that 95 percent of the population served by

community water systems will receive water that meets health-based drinking water

standards, consumption of contaminated fish and shellfish will be reduced, and

exposure to microbial and other forms of contamination in waters used for recreation will be reduced.

■ By 2005, reduce pollutant loadings from key point and nonpoint sources by at least

11 percent from 1992 levels. Air deposition of key pollutants will be reduced to

1990 levels.

Goal 3: Safe Food

Objectives:

■ By 2006, reduce public health risk from pesticide residues in food from pre-Food

Quality Protection Act levels (pre-1996).

■ By 2008, use on food of current pesticides that do not meet the new statutory standard of “reasonable certainty of no harm” will be eliminated.

Relevant Environmental

Health Objectives in

EPA’s 2000-2005

Strategic Plan

Appendix D: Environmental Health Objectives in EPA’s Strategic Plan
Goal 4: Preventing Pollution and Reducing Risk in Communities, Homes,

Workplaces, and Ecosystems

Objectives:

■ By 2005, public and ecosystem risk from pesticides will be reduced through migration to lower-risk pesticides and pesticide management practices, improving education of the public and at-risk workers, and forming “pesticide environmental partnerships” with pesticide user groups.

■ By 2007, significantly reduce the incidence of childhood lead poisoning and reduce

risks associated with polychlorinated biphenyls (PCBs), mercury, dioxin, and other

toxic chemicals of national concern.

■ By 2005, 16 million more Americans than in 1994 will live or work in homes,

schools, or office buildings, with healthier indoor air.

■ By 2005, facilitate the prevention, reduction, and recycling of toxic chemicals and

municipal solid wastes, including PBTs. In particular, reduce by 20 percent the

actual (from 1992 levels) and by 30 percent the production-adjusted (from 1998

levels) quantity of Toxic Release Inventory-reported toxic pollutants that are

released, disposed of, treated, or combusted for energy recovery, half through source

reduction.

Goal 5: Better Waste Management, Restoration of Contaminated Waste

Sites, and Emergency Response

Objectives:

■ By 2005, EPA and its federal, state, tribal, and local partners will reduce or control

the risk to human health and the environment at more than 374,000 contaminated

Superfund, RCRA, underground storage tank (UST), and brownfield sites and have

the planning and preparedness capabilities to respond successfully to all known

emergencies to reduce the risk to human health and the environment. (Total comprises 1,105 NPL sites, 1714 RCRA facilities, 370,000 UST cleanups initiated or

completed, and 1,500 brownfield properties.)

■ By 2005, EPA and its federal, state, tribal, and local partners will ensure that more

than 277,000 facilities are managed according to the practices that prevent releases

to the environment. (Total comprises 6,500 RCRA hazardous waste treatment, storage, and disposal facilities, and municipal solid waste landfills; 264,000 USTs, and

7,100 oil facilities.)

Goal 7: Quality Environmental Information

Objectives:

■ Through 2006, EPA will continue to increase the availability of quality health and

environmental information through educational services, partnerships, and other

methods designed to meet EPA’s major data needs, make data sets more compatible,

make reporting and exchange methods more efficient, and foster informed decision

making.

■ By 2006, EPA will provide access to new analytical or interpretive tools beyond

2000 levels so that the public can more easily and accurately use and interpret environmental information.

■ Through 2006, EPA will continue to improve the reliability, capability, and security

of EPA’s information infrastructure.

Appendix D 171

Appendix D: Environmental Health Objectives in EPA’s Strategic Plan