AND THE ENVIRONMENT
Measures of Contaminants, Body Burdens, and Illnesses
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AND THE ENVIRONMENT
leasures of Contaminants, Body Burdens, and Illnesses
Second Edition
,.
Office of Children's
' "»n|th Protection
EPA 240-R-03-001
February 2003
NCEE0
NATIONAL CENTER FOR
ENVIRONMENTAL ECONOMICS
POLCY
ECONOM CS
INNOVAT ON
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Foreword
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 environ-
mental 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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
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Table of Contents
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 Ill
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
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Authors
Tracey J. Woodruff
National Center for Environmental Economics
Office of Policy, Economics and Innovation
U.S. Environmental Protection Agency
San Francisco, CA94105
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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Reviewers
External Peer Reviewers* Reviewers for
Lara Akinbami, National Center for Health Statistics, Centers for Disease America's Children and
Control and Prevention, U.S. Department of Health and Human Services the Environment:
Joel Bender, American Chemistry Council Measures of
Elinor Blake, California Department of Health Services Contaminants, Body
David Brown, Northeast States for Coordinated Air Use Management (NESCAUM) Burdens, and Illnesses
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 Juzyeh, 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
JJ J o J i
John Bennett, Office of Water
JeffBigler, Office of Water
Ellen Brown, Office of Air and Radiation
Doreen Cantor, Office of Prevention, Pesticides, and Toxic Substances
* 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.
Reviewers
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Reviewers
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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About This Report
Hmerica'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 informa-
tion 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 policy-
makers and the public about how to improve federal data on children and the environ-
ment. 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 envi-
ronmental 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 meas-
ures 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
About This Report
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About This Report
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 avail-
able. 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 percent-
ages 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 fre-
quency 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 areasexposure 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 respira-
tory 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 con-
centrations 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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 objec-
tives. 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 objec-
tives 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) 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
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About This Report
For childhood illnesses associated with environmental contaminants, the report presents
measures of asthma and other respiratory conditions, childhood cancer, and neurodevelop-
mental disorders. The best available data to assess the frequency of these illnesses in chil-
dren 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 chil-
dren'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 envi-
ronmental 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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About This Report
The report uses five categories of race or ethnicity: White non-Hispanic, Black non-
Hispanic, 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, sched-
uled for publication in 2003. The Report on the Environments intended to be a broad-
based collection of national data depicting progress in addressing environmental prob-
lems 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 &nA 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 w&. be organ-
ized 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
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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 impor-
tant 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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)
Parti: Environmental
Contaminants
Key Findings
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Key Findings
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)
Part 2: Body Burdens
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 (ug/dL) in 1976-1980 to
2.2 ug/dL in 1999-2000, a decline of 85 percent. (Page 53)
The concentration of lead in blood at the 90 percentile in children 5 years old and
under, representing the most highly exposed 10 percent of children in that age group,
dropped from 25 ug/dL in 1976-1980 to 4.8 ug/dL in 1999-2000. (Page 53)
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 ug/dL. The
median blood lead level for children living in families with incomes below the poverty
level was 2.8 ug/dL and for children living in families above the poverty level it was
1.9 ug/dL. For all income levels, Black non-Hispanic children had a median blood
lead level of 2.8 ug/dL. White non-Hispanic children had a median blood lead level
of 2.1 ug/dL and Hispanic children had a median blood level of 2.0 ug/dL. (Page 55)
Approximately 430,000 children ages 1-5 (about 2 percent) had a blood lead level
of 10 ug/dL or greater in 1999-2000. (Page 57)
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 59)
Concentrations of Cotinine in Blood
Cotinine is a marker of exposure to environmental tobacco smoke. In 1999-2000,
median (50 percentile) levels of cotinine measured in children were 56 percent lower
than they were in 1988-1991. Cotinine values at the 90 percentile, representing the
most highly exposed 10 percent of children, declined by 18 percent between 1988-
91 and 1999-2000. (Page 61)
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Key Findings
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 69)
In 2001, 8.7 percent (6.3 million) of all children had asthma. (Page 69)
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 71)
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 71)
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 73)
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 75)
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 77)
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 79)
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 85)
Part 3: Childhood
Illnesses
Key Findings
-------
Key Findings
Part 4: Emerging Issues 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 94)
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 96)
Part 5: Special Features 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 105)
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 107)
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 109)
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 113)
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 115)
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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
Hazardous Air Pollutants
Indoor Air Pollutants
Environmental Tobacco Smoke
Drinking Water Contaminants
Drinking Water Contaminants
Monitoring and Reporting
Pesticide Residues
Land Contaminants
Body Burdens
Concentrations of Lead in Blood
Concentrations of Mercury in Blood
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
Percentage of children living in counties where estimated 1996
hazardous air pollutant concentrations were greater than
health benchmarks
Percentage of homes with children under 7 where 1994-1999
someone smokes regularly
Percentage of children living in areas served by public 1993-1999
water systems that exceeded a drinking water standard
or violated treatment requirements
Percentage of children living in areas with major violations 1993-1999
of drinking water monitoring and reporting requirements
Percentage of fruits, vegetables, and grains with 1994-2001
detectable residues of organophosphate pesticides
Percentage of children residing within one mile of a 1990-2000
Superfund site
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
Distribution of concentrations of mercury in blood 1999-2000
of women of child-bearing age
1988-2000
Concentrations of Cotinine in Blood Concentrations of cotinine in blood of children
Summary List of Measures
-------
Summary List of Measures
Name
Description of Measure
Year(s)
Childhood Illnesses
Respiratory Diseases
Childhood Cancer
Neurodevelopmental Disorders
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
Cancer incidence and mortality for children under 20 1975-1998
Cancer incidence for children under 20 by type 1974-1998
Children reported to have mental retardation, 1997-2000
by race/ethnicity and family income
Special Features
Lead in California Schools
Pesticide Use in Minnesota Schools
Birth Defects in California
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
Frequency of application of pesticides in Minnesota 1999
K-12 schools
Number of birth defects in California per 1,000 live 1991 -1999
births and fetal deaths
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Environmental Contaminants
P|-»»/j KOFI rHfHt.PI I 1 racking environmental contaminants is an important step toward determining
^^| whether environmental policies protect children. This section of the report pres-
ents mf°rmati°n about environmental contaminants that can affect children and dis-
cusses 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 expo-
sure 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 pol-
lution, 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 concen-
trations both can have adverse effects on health. The report also includes a new meas-
ure concerning pesticide residues in foods.
Describing the significance of pollutants in soils is a difficult problem because contami-
nation 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 environ-
mental contaminants and childhood illnesses. The report includes a qualitative discus-
sion 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 contam-
inated 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Environmental Contaminants
Coverage of Environmental Contaminant Measures
Description
Topic of Measure Year(s)
Geographic
Coverage
Notes
Outdoor Air Pollutants
Common Air E1: Percentage of children living
Pollutants in counties in which air quality
standards were exceeded
E2: Percentage of children's days
with good, moderate, or unhealthy
air quality
E3: Long-term trends in annual
average concentrations of criteria
pollutants
Hazardous Air E4: Percentage of children living in
Pollutants counties where estimated hazardous
air pollutant concentrations were
greater than health benchmarks
in 1996
Indoor Air Pollutants
Environmental
Tobacco Smoke
E5: Percentage of homes with
children under 7 where someone
smokes regularly
1990-2001 County-level Measure includes five common
data (criteria) air pollutants. Many counties
monitored only some common air
pollutants and some counties did not
monitor any.
1990-1999 County-level Measure includes five common air
data pollutants.
1990-2000 County-level Measure includes three common air
data pollutants.
1996 County-level Data for one year only; measure
data is based on estimates of ambient
concentrations of 33 of the
188 hazardous air pollutants
identified in the Clean Air Act.
1994-1999 National-level Measure is a surrogate for environ-
data mental tobacco smoke in the home.
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
Contaminants areas served by public water systems
that exceeded a drinking water
standard or violated treatment
requirements
Monitoring and E7: Percentage of children living in 1993-1999
Reporting areas with major violations of
drinking water monitoring and
reporting requirements
Food Contaminants
Pesticide Residues E8: Percentage of fruits, vegetables, 1994-2001
and grains with detectable residues
of organophosphate pesticides
Land Contaminants
Hazardous E9: Percentage of children 1990-2000
Waste Sites residing within one mile of
a Superfund site
County-level Data on violations of standards are
data incomplete due to monitoring and
reporting limitations. Measure is a
surrogate for concentrations of
contaminants.
County-level Measure shows percentage of
data children living in areas where no
information on drinking water
contaminants is available; children
may or may not be at risk.
National-level Surrogate for dietary exposure to
data residues of organophosphate pesticides.
Other contaminants in food, such as
other pesticides and industrial
chemicals that are relevant to
children, are not included.
Site-specific Does not reflect exposures from sites
locations that may be hazardous but are not
included on the Superfund National
Priorities List. Proximity to a Superfund
site does not necessarily indicate that
children are exposed to contaminants.
Part 1: Environmental Contaminants
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Outdoor Air Pollutants
Common ("Criteria")
Air Pollutants
Air pollution contributes to a wide variety of adverse health effects. Six of the most
common air pollutantscarbon monoxide, lead, ground-level ozone, particulate matter,
nitrogen dioxide, and sulfur dioxideare 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 car-
bon 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 pollu-
tants 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 func-
tion, 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 res-
piratory effects serious enough to require emergency room visits and hospital admis-
sions.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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 mortal-
ity 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 stan-
dard 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 neu-
robehavioral 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 ele-
vated 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
Part 1: Environmental Contaminants
-------
Outdoor Air Pollutants
Exceedances of Short-
Term Air Quality
Standards
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 fre-
quently 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.
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Outdoor Air Pollutants
Measure El
Percentage of children living in counties in which air quality standards were exceeded
Ozone
eight-hour standard
Carbon
monoxide
2000 2001
SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information
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 coun-
ties. Exceedances of the eight-hour ozone standard are
reported beginning in 1996. 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 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 El.)
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 2001, 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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Criteria Air Pollutants (E1-E3)
Respiratory (D1-D4)
Criteria Air Pollutants: lead (E1-E2)
Drinking Water: lead (E6-E7)
Lead in Blood (B1-B3) Neurodevelopmental (D7)
Special Features
Lead in Schools (S1 -S3)
Part 1: Environmental Contaminants
-------
Outdoor Air Pollutants
Daily Air Quality 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, paniculate 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 cor-
responds 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 moder-
ate 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 sen-
sitive 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 pro-
vides a sense of the intensity of pollution over the course of a year. This method pro-
vides 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, pollu-
tants that are measured dailysuch as ozonewill 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Outdoor Air Pollutants
Measure E2
Percentage of children's days with good, moderate, or
unhealthy air quality
No Monitoring Data
Moderate
Unhealthy
1998 1999
SOURCE
iency, Office of Air £
Aerometric
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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants (E1-E3)
Respiratory (D1-D4)
Part 1: Environmental Contaminants
-------
Outdoor Air Pollutants
Long-Term Exposure to Most measures used to describe air pollution focus on days when pollutant levels are
Criteria Air Pollutants 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 pro-
vide 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 sev-
eral 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 per-
spective 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Outdoor Air Pollutants
PM-10, percent
of annual standard
Nitrogen dioxide,
percent of annual standard
Sulfur dioxide, percent
of annual standard
In 1990, on average, children experienced a concentration
of 31.9 ug/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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants (E1-E3)
Respiratory (D1-D4)
Part 1: Environmental Contaminants
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Outdoor Air Pollutants
Exceeding 80 percent of the long-term standard
Exceeding the
long-term standard
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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants (E1-E3)
Respiratory (D1-D4)
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Outdoor Air Pollutants
Hazardous air pollutants, also known as air toxics, have been associated with a number of Hazardous Air
adverse human health effects, including cancers, asthma and other respiratory ailments, Pol III tail tS
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 concernparticularly
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 pollu-
tants with health benchmark concentrations derived from scientific assessments con-
ducted by EPA and other environmental agencies.32'38'40
Part 1: Environmental Contaminants
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Outdoor Air Pollutants
Hazardous
Air Pollutants and
Health Benchmarks
This analysis compares ambient concentrations of hazardous air pollutants with three
health benchmark concentrations. Two benchmarks reflect potential cancer risks, at lev-
els of l-in-100,000 risk and l-in-10,000 risk. If a particular hazardous air pollutant is
present in ambient air at a l-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 con-
tinuous 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 predic-
tion 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 concentra-
tions 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 con-
centrations, 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 envi-
ronment 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
Healthy People 2010:
Objective 8-04 of Healthy People 2010 focuses on reducing emissions of
hazardous air pollutants. See Appendix C for more information.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Outdoor Air Pollutants
Measure E4
Percentage of children living in counties where estimated hazardous air pollutant
concentrations were greater than health benchmarks in 1996
Cancer Benchmark:
1-in-100,000
Cancer Benchmark:
1-in-10,000
Benchmark for
ther Health Effects
SOURCE: U.S. Environmental Protection Agency, National Air Toxics Assessment
In 1996, all children lived in counties in which the
combined estimated concentrations of hazardous air
pollutant exceeded the l-in-100,000 cancer risk
benchmark.
Eighteen percent of children lived in counties in which
hazardous air pollutants combined to exceed the 1-in-
10,000 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 l-in-10,000 cancer risk benchmark.
Part 1: Environmental Contaminants
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Indoor Air Pollutants
Environmental
Tobacco Smoke:
Smoking in the Home
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, pesti-
cides, 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 pol-
lutants 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 respi-
ratory 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 regu-
larly. 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.
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Indoor Air Pollutants
Measure E5
Percentage of homes with children under 7 where someone smokes regularly
SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Indoor Environments
Division, Surveys on Radon Awareness and Environmental Tobacco Issues
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
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Environmental Tobacco Smoke (E5) Cotinine in Blood (B5)
Respiratory (D1-D4)
Part 1: Environmental Contaminants
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America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Drinking Water Contaminants
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
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Drinking Water Contaminants
Exceedances of
Drinking Water
Standards
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 vio-
lations 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 bot-
tled 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 fur-
ther 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.
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Drinking Water Contaminants
Any health-based violations
Chemical and radiation
Lead and copper
Nitrate/nitrite
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.7?-86
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants: lead (E1-E2)
Drinking Water lead (E6-E7)
Lead in Blood (B1-B3) Neurodevelopmental (D7)
Lead in Schools (S1 -S3)
Part 1: Environmental Contaminants
-------
Drinking Water Contaminants
Monitoring and Public water systems are required to monitor for contaminants and to report violations
Reporting of drinking water standards to EPA. However, some public water systems do not con-
duct all of the required monitoring. Not all systems report violations. Such water sys-
tems 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 col-
lect 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Drinking Water Contaminants
Measure E7
Percentage of children living in areas with major violations
of drinking water monitoring and reporting requirements
Any major violation
Lead and copper
SOURCE: U.S. Environmental Protection Agency, Office of Water, Safe Drinking Water Information System
(Percentages are estimated)
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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants: lead (E1-E2)
Drinking Water lead (E6-E7)
Lead in Blood (B1-B3) Neurodevelopmental (D7)
Lead in Schools (S1 -S3)
Part 1: Environmental Contaminants
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Pesticide Residues
Pesticide Residues on
Foods Frequently
Consumed by Children
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 insec-
ticide use in the United States. The majority of organophosphate use is on food
cropsincluding corn, fruits, vegetables, and nuts. In addition, organophosphate pesti-
cides often have been used in and around the home. Examples of organophosphate pes-
ticides 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-to-
year 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 organophos-
phate 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.
Healthy People 2010:
Objective 8-24 of Healthy People 2010 addresses exposure to common pes-
ticides. See Appendix C for more information.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Pesticide Residues (E8)
Pesticide Use in Schools (S4)
Part 1: Environmental Contaminants
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Land Contaminants
Hazardous Waste Sites 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 subtrac-
tion 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 indi-
cates 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 neces-
sary 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 contam-
inants 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.
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Land Contaminants
All Superfund sites not yet cleaned up or controlled
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.
Part 1: Environmental Contaminants
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16. D. E. Abbey, N. Nishino, W. F. McDonnell, R. J. Burchette, S. F. Knutsen, W. Lawrence Beeson and J. X. Yang.
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17. T. J. Woodruff, J. Grillo and K. C. Schoendorf. 1997. The relationship between selected causes of postneonatal infant
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America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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28. M. Studnicka, E. Hackl, J. Pischinger, C. Fangmeyer, N. Haschke, J. Kiihr, R. Urbanek, M. Neumann and T. Frischer.
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29. S. Walters, M. Phupinyokul and J. Ayres. 1995. Hospital admission rates for asthma and respiratory disease in the
West Midlands: their relationship to air pollution levels. Thorax 50 (9):948-54.
30. 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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31. T J. Woodruff, J. C. Caldwell, Y J. Cogliano and D. A. Axelrad. 2000. Estimating cancer risk from outdoor
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33. G. D. Leikauf, S. Kline, R. E. Albert, C. S. Baxter, D. I. Bernstein and C. R. Buncher. 1995. Evaluation of a possible
association of urban air toxics and asthma. Environmental Health Perspectives 103 (Suppl. 6):253-71.
34. P. Grandjean, E. Budtz-Jorgensen, R. E White, P. J. Jorgensen, P. Weihe, F. Debes and N. Keiding. 1999.
Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. American
Journal of Epidemiology 150 (3):301-5.
Part 1: Environmental Contaminants
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35. J. L. Jacobson and S. W. Jacobson. 1997. Teratogen update: polychlorinated biphenyls. Teratology 55:338-347.
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low doses of lead in childhood, an 11-year follow-up report. New England Journal of Medicine 322 (2):83-8.
37. M. Marlowe, A. Cossairt, C. Moon, J. Errera, A. MacNeel, R. Peak, J. Ray and C. Schroeder. 1985. Main and interaction
effects of metallic toxins on classroom behavior. Journal of Abnormal Child Psychology 13 (2): 18 5-98.
38. J. C. Caldwell, T. J. Woodruff, R. Morello-Frosch and D. A. Axelrad. 1998. Application of health information to haz-
ardous 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
Protection Agency, Office of Environmental Health Hazard Assessment, 1999.
http://www.oehha.ca.gov/air/cancer_guide/hsca2.html.
40. California Environmental Protection Agency. All Chronic Reference Exposure Levels Adopted by OEHHA as of May 2000.
California Environmental Protection Agency, Office of Environmental Health Hazard Assessment, 2000.
http://www.oehha.ca.gov/air/chroni c_rels/AllChrels.html.
41. National Research Council. 2000. Toxicological Effects of Methylmercury. Washington, DC: National Academy Press.
http://books.nap.edu/catalog/9899.html?onpi_newsdoc071100.
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/96lO.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/600/6-90/006E 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 (l):36-4l.
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. E Hovell, E. O. Meltzer and S. B. Meltzer. 2000. Involuntary smoking and asthma.
Current Opinions in Pulmonary Medicine 6:31-6.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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54. A. Lindfors, M. Y 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 adultsUnited States, 1999.
Morbidity and Mortality Weekly Report50 (40):869-73.
56. U.S. Environmental Protection Agency. Drinking Water Contaminants. EPA Office of Water, 2001.
http://www.epa.gov/safewater/hfacts.html#Inorganic.
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. E 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,
Y 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.
Environmental Health Perspectives 108 (7):675-8.
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): 5 8-61.
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'ltri, EM. Nitrate - A Drinking Water Concern, 1993.
http://www.gem.msu.edu/pubs/msue/wq 19p 1 .html.
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.
http://www.epa.gov/safewater/mcl.html.
73. G. A. Boorman. 1999. Drinking water disinfection byproducts: review and approach to toxicity evaluation.
Environmental Health Perspectives 107 (Suppl. 1):207-17.
Part 1: Environmental Contaminants
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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_01/40cfrvl9_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 ofWater in the United States in 1995. Denver, CO. USGS Circular 1200.
http://water.usgs.gov/watuse/pdfl995/html/.
78. U.S. Environmental Protection Agency. Fact Sheet: Surface Water Treatment Rule. EPA Office of Water, 2001.
http://www.epa.gov/ogwdwOOO/smallsys/ndwac/surface.html.
79. F. Bove, Y. Shim and P. Zeitz. 2002. Drinking water contaminants and adverse pregnancy outcomes: a review.
Environmental Health Perspectives 110 (Suppl. l):6l-74.
80. L. Dodds, W King, C. Woolcott and J. Pole. 1999. Trihalomethanes in public water supplies and adverse birth outcomes.
Epidemiology 10 (3):233-7.
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Body Burdens: Contaminants in the Bodies of Women and Children
I easurements of the levels of pollutants in children's bodies provide direct infor-
I mation 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 expo-
sure 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, bron-
chitis, pneumonia, ear infections, asthma symptoms, and sudden infant death syn-
drome (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 contaminantssuch as pesticides and
heavy metalsin 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
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Concentrations of Lead in Blood
Lead in the Blood of
Children
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 vocab-
ulary, 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 (ug/dL) or greater
is considered elevated,10' n 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 chil-
dren 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.
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Concentrations of Lead in Blood
90th percentile
(10 percent of children have
this blood lead level or greater)
(50 percent of children
have this blood lead
level or greater)
The median concentration of lead in the blood of chil-
dren 5 years old and under dropped from 15 micrograms
per deciliter (ug/dL) in 1976-1980 to 2.2 ug/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 ug/dL
in 1976-1980 to 4.8 ug/dL in 1999-2000.
In 1978, about 4.7 million children ages 1-5 had blood
lead levels at or greater than 10 ug/dL, which is consid-
ered elevated. By 1999-2000, this number had declined
to about 430,000.
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 lead-
based paint from 64 million in 1990 to 38 million in
2000.18 Some decline also was a result of EPA regula-
tions 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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants: lead (E1-E2)
Drinking Water: lead (E6-E7)
Lead in Blood (BT-B3)
Neurodevelopmental (D7)
Lead in Schools (S1 -S3)
* 10 |ig/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
Part 2: Body Burdens
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Concentrations of Lead in Blood
Blood Lead by Concentrations of lead in children's blood differ by race/ethnicity and family income.
Race/Ethnicity and This measure presents blood lead levels by race/ethnicity and family income for children
Familv Income a&es ^' a Peri°d wnen lea
-------
Concentrations of Lead in Blood
In 1999-2000 the median blood lead level in children
ages 1-5 was 2.2 ug/dL. The median blood lead level
for children living in families with incomes below the
poverty level was 2.8 ug/dL and for children living in
families above the poverty level it was 1.9 ug/dL.
In 1999-2000, White non-Hispanic children ages
1-5 had a median blood lead level of about 2 ug/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 ug/dL and in 1999-
2000 they had a median blood lead level of 2.8 ug/dL.
In 1992-1994, Hispanic children ages 1-5 had a median
blood lead level of 2.6 ug/dL and in 1999-2000 they
had a median blood lead level of 2.0 ug/dL.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants: lead (E1-E2)
Drinking Water: lead (E6-E7)
Lead in Blood (BT-B3)
Neurodevelopmental (D7)
Lead in Schools (S1 -S3)
Part 2: Body Burdens
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Concentrations of Lead in Blood
Distribution Of A blood lead level of 10 micrograms per deciliter (ug/dL) or greater is considered elevated,
Concentrations Of kut tnere is no demonstrated safe concentration of lead in blood. Adverse health effects
Lead in Blood in can occur at l°wer concentrations. A growing body of research has shown that there are
Ph'IH A 11 measurable adverse neurological effects in children at blood lead concentrations as low as
" 1 ug/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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Concentrations of Lead in Blood
In 1999-2000, the concentration of lead in blood at
the 90 percentile in children ages 1-5 was 4.8 ug/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 ug/dL, meaning that 50 percent of
children had blood lead levels above this concentration
and 50 percent had blood lead levels below it.
Approximately 430,000 children ages 1-5 (about 2 per-
cent) had a blood lead level of 10 ug/dL or greater in
1999-2000.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants: lead (E1-E2)
Drinking Water: lead (E6-E7)
Lead in Blood (BT-B3)
Neurodevelopmental (D7)
Lead in Schools (S1 -S3)
Part 2: Body Burdens
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Concentrations of Mercury in Blood
Prenatal Exposure to
Methyl mercury
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 child-
bearing 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 (PvfD) 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 mer-
cury is less readily absorbed than methylmercury and is not known to cause the types
of health effects discussed in this section.
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Concentrations of Mercury in Blood
Measure B4
Distribution of concentrations of mercury in blood of women of
child-bearing age, 1999-2000
7 > 7
body weight pe
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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Mercury in Blood (B4) Neurodevelopmental (D7)
Special Features
Part 2: Body Burdens
-------
Concentrations of Cotinine in Blood
Cotinine in the
Blood of Children
Exposure to environmental tobacco smoke (ETS) is an important health risk for chil-
dren. 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 sus-
ceptible 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.
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Concentrations of Cotinine in Blood
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)
In 1999-2000, median (50th percentile) levels of coti-
nine 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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Environmental Tobacco Smoke (E5) Cotinine in Blood (B5)
Respiratory (D1-D4)
Part 2: Body Burdens
-------
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. Y Vimpani, E. E 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. l):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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
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):96l-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 (l):42-55.
24. P. Grandjean, R. E 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): 5 87-91.
25. P. Grandjean, P. Weihe, R. E White and E 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. E White, E Debes, S. Araki, K. Yokoyama, K. Murata, N. Sorensen, R. Dahl and
P. ]. Jorgensen. 1997. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury.
Neurotoxicology and Teratology 19 (6):4l7-28.
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. Sorensen, K. Murata, E. Budtz-J0rgensen, 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 ofToxicology and Environmental Health. Part B, Critical Reviews 4 (2):l6l-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 E 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 (l):l-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.
Part 2: Body Burdens
-------
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 (l):36-4l.
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/96lO.html.
45. A. Lindfors, M. Y 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.
o/
46. D. R. Wahlgren, M. E 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 27'5 (16):1233-40.
48. Centers for Disease Control and Prevention. 2001. Cigarette smoking among adultsUnited States, 1999.
Morbidity and Mortality Weekly Report50 (40):869-73.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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-------
Childhood Illnesses
Childhood
Illnesses
ata on trends in childhood diseases and disorders provide important information
I 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, andnew
for this editionneurodevelopmental 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 environ-
mental 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 inci-
dence 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Respiratory Diseases
Respiratory diseases can greatly impair a child's ability to function, and are an important Respiratory Diseases
cause of missed school days and limitations to activities. Important respiratory diseases jn Children
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.
Part 3: Childhood Illnesses
-------
Respiratory Diseases
Asthma 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 symp-
toms 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 inher-
ited, 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, pesti-
cides, 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 func-
tion 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 well-
controlled 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Respiratory Diseases
Percentage of children with asthma
Measure Dl
Children ever
diagnosed
with asthma
Children with asthma
in the past 12 months
Children ever
diagnosed with
asthma and having
an asthma attack in
the past 12 months
1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2001
SOURCE:
Note: The survey
for asthma chanp
)re 1997 cannot be directly compared tc
' and later.
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 chil-
dren 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 1997-2000,
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 chil-
dren had asthma in 2001.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Criteria Air Pollutants (E1-E3)
Respiratory (D1-D4)
Environmental Tobacco Smoke (E5) Cotinine in Blood (B5)
Respiratory (D1-D4)
Special Features
Part 3: Childhood Illnesses
-------
Respiratory Diseases
Percentage of Children
Having an Asthma
Attack in the Previous
12 Months, by
Race/Ethnicity and
Family Income
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 sus-
ceptible 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 representa-
tive 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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Respiratory Diseases
Measure D2
Percentage of children having an asthma attack in the previous 12 months,
by race/ethnicity and family income, 1997-2000
Hispanic
!00-200%ofPove
0% of Poverty Level
200% of Poverty Level
00-200% of Pove|ty Level
Poverty Level
Races/
Ethnicities
> 200% of Poverty Level
100-200% of Povet ry Level
Poverty Level
All Incomes
SOURCE: Centers for Disease Control and P
National Health Interview Survey
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.
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)
Part 3: Childhood Illnesses
-------
Respiratory Diseases
Emergency Room Visits
and Hospitalizations
for Respiratory Diseases
Children who visit emergency rooms or are hospitalized for respiratory diseasessuch
as asthma, upper respiratory infections, and acute bronchitisrepresent 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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Respiratory Diseases
Measure D3
Children's emergency room visits for asthma and other respiratory causes
All asthma and other
respiratory causes
Acute upper
respiratory infections
Acute bronchitis
SOURCE:
s for Disease
and Prevention, Nations
ry Medical Care Survey
ealth Statistics,
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.
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)
Part 3: Childhood Illnesses
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America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Respiratory Diseases
All asthma and other respiratory causes
Acute upper respiratory infections
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-injury-
related 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.
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)
Part 3: Childhood Illnesses
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Childhood Cancer
Cancer Incidence and
Mortality
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 improve-
ments 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Childhood Cancer
Measure D5
Cancer incidence and mortality for children under 20
Incidence
SOURCE:
nal Cancer Institute, Surveillance, Epidemiology, and End Results Program;
s for Disease Control and Prevention, National Center for Health Statistics,
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.
Part 3: Childhood Illnesses
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Childhood Cancer
Types of Childhood
Cancer
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 suggestivebut not conclusiveevidence 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 trichloroethyleneand 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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 non-
Hodgkin'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.
Part 3: Childhood Illnesses
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Childhood Cancer
Measure D6b
Cancer incidence for children under 20 by type
Sort tissue
Malignant Bone Tumors
Neuro-
blastoma
blastoma
SOURCE: National CE
ts Program
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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Part 3: Childhood Illnesses
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Neurodevelopmental Disorders
Neurodevelopmental
Disorders in Children
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 dis-
abilities 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 mer-
cury in the womb have been found to cause mental retardation.66'67
Several studies of children exposed to elevated levels of poly chlorinated biphenyls (PCBs)
have linked these contaminants to neurodevelopmental effects, including lowered intel-
ligence 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 pollu-
tants 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
lexicological studies link both prenatal and postnatal exposure to organophosphate pes-
ticides 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
Healthy People 2010:
Objective 16-14 of Healthy People 2010 calls for a reduction in the occur-
rence of developmental disabilities. See Appendix C for more information.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Neurodevelopmental Disorders
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.
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)
Part 3: Childhood Illnesses
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Neurodevelopmental Disorders
Mental Retardation The most commonly used definitions of mental retardation emphasize subaverage intel-
lectual 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 disor-
ders, 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 (IQless 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 identi-
fication 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 non-
Hispanic 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.
Part 3: Childhood Illnesses
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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
behavior. Journal of the American Medical Association 275 (5):363-9.
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
Environmental Protection Board. 3642.
64. K. S. Crump, T. Kjellstrom, A. M. Shipp, A. Silvers and A. Stewart. 1998. Influence of prenatal mercury exposure upon
scholastic and psychological test performance: benchmark analysis of a New Zealand cohort. Risk Analysis 18 (6):701-13.
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):4l7-28.
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 (l-3):59-62.
67. F. Bakir, H. Rustam, S. Tikriti, S. F. Al-Damluji and H. Shihristani. 1980. Clinical and epidemiological aspects of
methylmercury poisoning. Postgraduate Medical Journal 56 (651):1-10.
68. T. Darvill, E. Lonky, J. Reihman, P. Stewart and J. Pagano. 2000. Prenatal exposure to PCBs and infant performance
on the Fagan test of infant intelligence. Neurotoxicology 21 (6):1029-38.
69. J. L. Jacobson and S. W. Jacobson. 1996. Intellectual impairment in children exposed to polychlorinated biphenyls in
utero. New England Journal of'Medicine 335 (ll):783-9.
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
environmental exposure to polychlorinated biphenyls and dioxins on cognitive abilities in Dutch children at
42 months of age. Journal of Pediatrics 134 (l):33-4l.
72. 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 (l):21-9.
Part 3: Childhood Illnesses
-------
References
73. J. Walkowiak, J. A. Wiener, A. Fastabend, B. Heinzow, U. Kramer, E. Schmidt, H. J. Steingruber, S. Wundram and
G. Winneke. 2001. Environmental exposure to polychlorinated biphenyls and quality of the home environment:
effects on psychodevelopment in early childhood. Lancet358 (9293): 1602-7.
74. W. J. Rogan, B. C. Gladen, K. L. Hung, S. L. Koong, L. Y. Shih, J. S. Taylor, Y. C. Wu, D. Yang, N. B. Ragan and
C. C. Hsu. 1988. Congenital poisoning by polychlorinated biphenyls and their contaminants in Taiwan.
Science 2^1 (4863):334-6.
75. Y C. Chen, Y. L. Guo, C. C. Hsu and W. J. Rogan. 1992. Cognitive development of Yu-Cheng ("oil disease") children
prenatally exposed to heat-degraded PCBs. Journal of the American Medical Association 268 (22):3213-8.
76. Y. C. Chen, M. L. Yu, W. J. Rogan, B. C. Gladen and C. C. Hsu. 1994. A 6-year follow-up of behavior and activity
disorders in the Taiwan Yu-cheng children. American Journal of Public Health 84 (3) :415-21.
77. M. Marlowe, A. Cossairt, C. Moon, J. Errera, A. MacNeel, R Peak, J. Ray and C. Schroeder. 1985. Main and interaction
effects of metallic toxins on classroom behavior. Journal of Abnormal Child Psychology 13 (2):185-98.
78. S. M. Stewart-Pinkham. 1989. The effect of ambient cadmium air pollution on the hair mineral content of children.
Science of the Total Environment 78:289-96.
79. R. W. Thatcher, M. L. Lester, R. McAlaster and R. Horst. 1982. Effects of low levels of cadmium and lead on
cognitive functioning in children. Archives of Environmental Health 37 (3): 159-66.
80. 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.
81. P. Eriksson, E. Jakobsson and A. Fredriksson. 2001. Brominated flame retardants: a novel class of developmental neu-
rotoxicants in our environment? Environmental Health Perspectives 109 (9):903-908.
82. S. R. Schroeder. 2000. Mental retardation and developmental disabilities influenced by environmental neurotoxic
insults. Environmental Health Perspectives 108 (Suppl. 3):395-9.
83. D. K. Daily, H. H. Ardinger and G. E. Holmes. 2000. Identification and evaluation of mental retardation.
American Family Physician 61 (4): 1059-67, 1070.
84. O. David, S. Hoffman, B. McGann, J. Sverd and J. Clark. 1976. Low lead levels and mental retardation.
Lancet 2 (8000): 1376-9.
85. B. Weiss. 2000. Vulnerability of children and the developing brain to neurotoxic hazards. Environmental
Health Perspectives 108 (Suppl. 3):375-81.
86. C. Murphy, C. Boyle, D. Schendel, P. Decoufle and M. Yeargin-Allsopp. 1998. Epidemiology of mental retardation
in children. Mental Retardation and Developmental Disabilities Research Reviews^ (1):6-13.
87. J. Flint and A. O. Wilkie. 1996. The genetics of mental retardation. British Medical Bulletin 52 (3):453-64.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Emerging Issues
I he links between environmental contaminants and childhood diseases and disorders
| are receiving increasing attention and research. We can expect that our understanding
Emerging
of how children's health may be influenced by environmental factors will continue to I S S U 6 S
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
-------
Emerging Issues
Mercury in Fish Some pollutants build up in the bodies offish and other animals, reaching high con-
centrations 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 con-
vert 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 mercu-
ry from fish that people catch for their own use. Fish advisory information is not a sur-
rogate 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 advi-
sory 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-contami-
nated 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Emerging Issues
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 statesConnecticut, Indiana, Kentucky, Maine, Maryland,
Massachusetts, Michigan, Minnesota, Missouri, New Hampshire, New Jersey,
North Carolina, North Dakota, Ohio, Pennsylvania, Vermont and Wisconsinup
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.
Related Measures: Environmental Contaminants Body Burdens Childhood Illnesses Special Features
Mercury in Blood (B4) Neurodevelopmental (D7)
Part 4: Emerging Issues
-------
Emerging Issues
Attention-
Deficit/Hyperactivity
Disorder
Attention-deficit/hyperactivity disorder (ADHD) is a disruptive behavior disorder charac-
terized by ongoing inattention and/or hyperactivity-impulsivity occurring in several set-
tings 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 aca-
demic 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 con-
taminants 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 impul-
sivity, 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 1997-2000.
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 psychi-
atric 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Emerging Issues
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 ADHDthe highest of any group.
Two to three times more boys than girls are diagnosed with ADHD.35
Part 4: Emerging Issues
-------
References
1. J. R. D. Guimaraes, J. Ikingura and H. Akagi. 2000. Methyl mercury production and distribution in river water-sediment
systems investigated through radiochemical techniques. Water, Air, and Soil Pollution 124 (1-2):113-124.
2. C. Y. Chen, R. S. Stemberger, B. Klaue, J. D. Blum, P. C. Pickhardt and C. L. Folt. 2000. Accumulation of heavy met-
als in food web components across a gradient of lakes. Limnology and Oceanography 45 (7): 1525-1536.
3. R. P. Mason, J. R. Reinfelder and F. M. M. Morel. 1995. Bioaccumulation of mercury and methylmercury. Water, Air,
and Soil Pollution 80:915-921.
4. R. Dietz, F. Riget, M. Cleemann, A. Aarkrog, P. Johansen and J. C. Hansen. 2000. Comparison of contaminants from
different trophic levels and ecosystems. Science of the Total Environment 245 (1-3):221-231.
5. C. C. Gilmour and G. S. Riedel. 2000. A survey of size-specific mercury concentrations in game fish from Maryland
fresh and estuarine waters. Archives of Environmental Contamination and Toxicology 39 (l):53-59.
6. R. M. Neumann and S. M. Ward. 1999. Bioaccumulation and biomagnification of mercury in two warmwater fish
communities. Journal of Freshwater Ecology 14 (4):487-498.
7. P. Grandjean, P. Weihe, P. J. Jorgensen, T. Clarkson, E. Cernichiari and T. Videro. 1992. Impact of maternal seafood
diet on fetal exposure to mercury, selenium, and lead. Archives of Environmental Health 47 (3): 185-195.
8. G. J. Myers and P. W. Davidson. 2000. Does methylmercury have a role in causing developmental disabilities in chil-
dren? Environmental Health Perspectives 108 (Suppl. 3):413-20.
9. H. Galal-Gorchev. 1993. Dietary intake, levels in food and estimated intake of lead, cadmium, and mercury. Food
Additives and Contaminants 10 (1): 115-28.
10. 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.
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): 5 87-91.
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 contamina-
tion in remote areas. Environmental Science and Technology 32 (l):l-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).
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
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 recep-
tor 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 E 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 (ll):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 envi-
ronmental exposure to polychlorinated biphenyls and dioxins on cognitive abilities in Dutch children at 42
months of age. Journal of Pediatrics 134 (l):33-4l.
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 (l):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/sr 10_206.pdf.
Part 4: Emerging Issues
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Special Features
C r\f^f\rt I ^^3 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 child-
hood conditions for which there is some suspected environmental influence, using data
from California.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Lead in California Schools
Elevated levels of lead in blood remain an important childhood environmental health
hazard in the United States. Childhood exposure to lead contributes to learning prob-
lems 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 SI-S3 present data from this hazard assessment.
Lead in California's
Public Elementary
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.
Part 5: Special Features
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Lead in California Schools
Deteriorated
Lead-containing
Paint in California's
Public Elementary
Schools
The presence of lead-containing paint in environments where children reside or spend
timeincluding homes, schools, and childcare facilitiesdoes 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 ten-
dency 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.
* 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-surface-
area 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 lead-
contaminated 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Lead in California Schools
Measure SI
Percentage of California public elementary schools with lead paint
and some deterioration of paint, 1994-1997
Any Detectable Lead
> 600 ppm
> 5,000 ppm
Schools Built
Before 1940
Schools Built
1940-1959
Schools Built
1960-1979
Schools Built
1980-1995
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, 1 998
Thirty-seven percent of all public elementary schools sur-
veyed 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.)
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants: lead (E1-E2)
Drinking Water: lead (E6-E7)
Lead in Blood (B1-B3) Neurodevelopmental (D7)
Lead in Schools (ST-S3)
Part 5: Special Features
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Lead in California Schools
Soil Lead-contaminated soil poses an exposure risk to children. EPA's hazard standard for
Neai" California's Public ^ea<^ m so^ ^s ^00 parts per million by weight in play areas, and 1,200 parts per million
Elementary Schools ^n '3are so^ ^n ^ remamder 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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Lead in California Schools
Measure S2
Percentage of California public elementary schools with lead in soils, 1994-1997
Schools with detectable
lead in soils
Schools with > 400 ppm
lead in soils
Schools Built
Before 1940
Schools Built
1940-1979
SOURCE: California Department of Health Services, Childhood Lead Poisor
Lead Hazards in California's Public Elementary Schools and Child C
Schools Bu
1980-199
~-acilities. April, 1998
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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants: lead (E1-E2)
Drinking Water: lead (E6-E7)
Lead in Blood (B1-B3) Neurodevelopmental (D7)
Lead in Schools (ST-S3)
Part 5: Special Features
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Lead in California Schools
Drinking water may be contaminated with lead through contact with lead pipes found
Drinking Water in m older buildings, brass faucets, and copper pipes with lead solder. The use of pipes,
California's Public 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
Elementary Schools , . . 1C £.. , , ,. . T , ,
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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Lead in California Schools
Percentage of California public elementary schools
with lead in drinking water, 1994-1997
Schools with detectable
lead in drinking water
Schools with > 15 ppb lead
in drinking water
Measure S3
Schools with > 15 ppb lead in
drinking water at 1st draw
Schools with > 15 ppb lead in
drinking water at 2nd draw
Schools Built
Before 1940
SOURCE: Califor
Schools Built
1940-1979
Hazards in California's Put
Schools Built
1980-1995
ry Schools and
'.are Facilities. April, 1998
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.
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Criteria Air Pollutants: lead (E1-E2)
Drinking Water: lead (E6-E7)
Lead in Blood (B1-B3) Neurodevelopmental (D7)
Lead in Schools (ST-S3)
Part 5: Special Features
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America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Pesticides in Minnesota Schools
Children may be exposed to pesticides in their diets and through contact with pesticides Pesticide Use in Schools
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 statesArizona, California, Connecticut,
Massachusetts, New Hampshire, and New Mexicorequire 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 conven-
tional approaches to pest control.32 Currently, approximately 10 states require the adop-
tion 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 poten-
tially hazardous to children weeks and months after application.34'37
Healthy People 2010: Objective 8-24 of Healthy People 2010 aims to reduce
exposure to pesticides. See Appendix C for more information.
Part 5: Special Features
-------
Pesticides in Minnesota Schools
Pesticide Use in Legislation recommending the use of Integrated Pest Management (IPM) in schools
Minnesota's Public and was introduced in Minnesota in 1999 and again in 2000. In response to increased
Private Schools 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 second-
ary (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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Pesticides in Minnesota Schools
Measure S4
Frequency of application of pesticides in Minnesota K-12 schools, 1999
Cafeteria and kitchen/food storage area
Locker rooms and gymnasium
Classrooms
- 20%
Sprayed
As Needed
Once
per Month
1-4 Times
SOURCE: C.J. Olson Market Research Inc. for Minnc
Regarding Pest Management in Minnesota
No Answer /
Other / Dont Know
Quantitative Research
K-12 Schools. 1999
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 post-
application letters to students and teachers).
Related Measures: Environmental Contaminants Body Burdens
Childhood Illnesses
Special Features
Pesticide Residues (E8)
Pesticide Use in Schools (54)
Part 5: Special Features
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Birth Defects in California
Birth Defects 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 insuf-
ficient 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 environ-
mental 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 Pvico had some type of existing birth defects moni-
toring 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Birth Defects in California
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.
Part 5: Special Features
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34. S. Gurunathan, M. Robson, N. Freeman, B. Buckley, A. Roy, R. Meyer, J. Bukowski and P. J. Lioy. 1998.
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Part 5: Special Features
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54. L. S. Engel, E. S. O'Meara and S. M. Schwartz. 2000. Maternal occupation in agriculture and risk of limb defects in
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America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Future Directions
Future Directions for
America's Children and
the Environment
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 environ-
mental contaminants. In addition, the data would permit characterization of subgroups of
each disease for which environmental contributions to the conditions are most relevant.
Part 1: Environmental
Contaminants
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 com-
parable. 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 avail-
ability of health benchmarks that are specifically based on effects from exposures during
childhood.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Future Directions
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 information presented on states
with fish consumption advisories for mercury. 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 improve-
ment 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 cost-
benefit 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
-------
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 includ-
ing 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 improve-
ment 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 poten-
tial 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 Part 2: Body Burdens
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 child-
bearing 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 contami-
nants in breast milk, which is an important source of exposure for infants.
Future Directions
-------
Future Directions
Part 3: Childhood
Illnesses
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 contami-
nants play in the prevalence of some childhood diseases.
Additional data collected by states or collected at the state level for some of the child-
hood 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 neu-
rodevelopmental 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.
Part 5: Special Features
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 hyperac-
tivity, inattention, and impulsivity. Also referred to as ADD
(attention deficit disorder).
Benzene:
A colorless, volatile, flammable, toxic liquid aromatic hydro-
carbon (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 bat-
teries, 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 environ-
ment 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 harm-
ful 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
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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 mate-
rials 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 con-
trol 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 prod-
ucts (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 concen-
trations 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
-------
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 drink-
ing water as delineated by the National Primary Drinking
Water Regulations. These levels are based on consideration
of health risks, technical feasibility of treatment, and cost-
benefit 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 agentssuch as
nitritesconvert a larger proportion of hemoglobin into
methemoglobin.
Methylmercury:
An organic form of mercury, created from metallic or ele-
mental 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 (|jg):
One-millionth of a gram.
Mg/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, paniculate 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 investi-
gates 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Glossary of Terms
Nitrogen Dioxide (NO2):
A chemical that results from nitric oxide combining with
oxygen in the atmosphere; a major component of photo-
chemical 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 signifi-
cant 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:
Pvadioactive 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 esti-
mate, with uncertainty spanning perhaps an order of mag-
nitude, 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 com-
monly used solvents, such as TCE, are important environ-
mental 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" pol-
lutants for which EPA has set national ambient air quality
standards.
Glossary of Terms
-------
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 feed-
stocks, 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Appendix A: Data Tables
Part 1: Environmental Contaminants
Table El
Percentage of children living in counties in which air quality standards were exceeded
1990-1995
Ozone one-hour standard
PM-10
Carbon monoxide
Lead
Sulfur dioxide
Nitrogen dioxide
Any standard*
1996-2001
^^^^^^^m
Ozone one-hour standard
Ozone eight-hour standard
PM-10
PM-2.5
Carbon monoxide
Lead
Sulfur dioxide
Nitrogen dioxide
Any standard*
22.7%
8.0%
9.4%
2.2%
0.5%
3.7%
28.0%
1996
16.5%
39.1%
1.5%
5.6%
1.6%
0.1%
0.0%
19.8%
1991
25.2%
6.3%
8.4%
6.0%
2.1%
3.7%
31 .8%
1997
18.6%
38.9%
2.4%
3.7%
1.4%
0.1%
0.0%
21 .9%
1992
16.9%
9.6%
6.1%
1.8%
0.1%
0.0%
20.9%
1998
20.8%
48.5%
2.0%
4.3%
1.6%
0.1%
0.0%
23.7%
* Does not include ozone eight-hour or PM-2.5 standards.
SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric
1993
21.1%
2.6%
5.0%
2.1%
0.5%
0.0%
24.2%
1999
21 .7%
46.9%
2.1%
3.7%
0.2%
0.1%
0.0%
24.0%
Information
1994
19.3%
2.3%
6.4%
1.7%
0.1%
0.0%
23.5%
2000
13.3%
27.9%
2.4%
27.2%
3.8%
0.5%
0.1%
0.0%
15.5%
Retrieval System
1995
27.8%
10.0%
4.9%
1.8%
0.1%
0.0%
30.8%
2001
15.0%
39.8%
3.2%
25.4%
0.2%
1.0%
0.0%
0.0%
18.5%
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
Percentage of children living in counties in which air quality standards were exceeded,
by family income, 1999
Carbon monoxide
Sulfur dioxide
Nitrogen dioxide
Ozone
Lead
PM-IO
All Incomes
3.7%
0.1%
0.0%
21.7%
0.2%
2.1%
< Poverty Level
4.5%
0.1%
0.0%
20.9%
0.1%
2.1%
100-200% of
Poverty Level
4.3%
0.1%
> 200% of
Poverty Level
3.2%
0.1%
19.4%
0.2%
2.2%
22.7%
0.2%
2.0%
SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information Retrieval System
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Appendix A: Data Tables
Table E2
Percentage of children's days with good, moderate, or unhealthy air quality
1990-1995
Pollution Level
Good
Moderate
Unhealthy
No Monitoring Data
1990
43.6%
20.6%
3.0%
32.8%
1991
44.2%
21.0%
3.0%
31.8%
1992
47.7%
18.4%
2.7%
31.2%
1993
46.9%
19.2%
2.3%
31.6%
1996-1999
Pollution Level
Good
Moderate
Unhealthy
No Monitoring Data
1996
48.9%
19.1%
1.7%
30.3%
1997
48.8%
19.0%
1.3%
30.9%
47.1%
20.7%
1.3%
30.9%
1999
46.6%
21.9%
0.9%
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
Pollution Level
Good
Moderate
Unhealthy
No Monitoring Data
White non-
Hispanic
44.4%
18.7%
0.6%
36.4%
Black non-
Hispanic
33.4%
14.6%
51.d
Hispanic
51 .0%
22.6%
0.9%
25.6%
American Indian/
Alaska Native
60.0%
27.4%
1.3%
11.3%
Asian or
Pacific Islander
48.9%
33.2%
1.9%
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
Pollution Level
Good
Moderate
Unhealthy
No Monitoring Data
All Incomes*
46.9%
22.0%
0.9%
30.2%
< Poverty Level
44.9%
22.3%
0.9%
31.9%
100 -200% of
Poverty Level
42.5%
21.4%
0.9%
35.2%
> 200% of
Poverty Level
49.0%
22.1%
0.8%
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
Appendix A
-------
Appendix A: Data Tables
Table E3a
Long-term trends in annual average concentrations of criteria pollutants
1990-1993
PM-10, percent of annual standard
1994-1997
PM-10, percent of annual standard
Nitrogen dioxide, percent of annual standard
Sulfur dioxide, percent of annual standard
56.;
1992
56.8%
1996
52.4%
37.3%
6.5%
1993
55.8%
1997
52.6%
34.9%
5.6%
1998-2000
PM-10, percent of annual standard
Nitrogen dioxide, percent of annual standard
Sulfur dioxide, percent of annual standard
53.9%
33.9%
5.2%
2000
53.3%
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
Exceeding 80% of the
long-term standard
Exceeding the long-term standard
1990
5,978,059
1,844,770
1991
6,347,396
3,424,292
1993
1994
4,671,899 4,350,278 1,432,268
169,004 536,520 435,493
1995
3,019,285
131,590
1996-2000
Exceeding 80% of the
long-term standard
Exceeding the long-term standard
1996
2,464,947
60,243
2,074,549
788,945
165,431
0
1999
2,029,422
1,017,791
2000
1,830,579
874,734
SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Aerometric Information Retrieval System
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
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
Cancer, one in 10,000
Other health effects
100%
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
Health Benchmark
Cancer, one in 100,000
Cancer, one in 10,000
Other health effects
All Incomes
100%
18%
< Poverty Level
100%
22%
100-200% of
Poverty Level
100%
17%
> 200% of
Poverty Level
100%
17%
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
SOURCE: U.S. Environmental Protection Agency, National Air Toxics Assessment
Table E5
Percentage of homes with children under 7 where someone smokes regularly
SOURCE: U.S. Environmental Protection Agency, Office of Air and Radiation, Indoor Environments Division, Surveys on Radon Awareness and
Environmental Tobacco Issues
Appendix A
-------
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
Lead and copper*
Microbial contaminants
Chemical and radiation
Nitrate/nitrite
Treatment and filtration
Any health-based violations
1998-1999
Type of standard violated
Lead and copper*
Microbial contaminants
Chemical and radiation
Nitrate/nitrite
Treatment and filtration
Any health-based violations
1993
2.2%
4.7%
0.23%
10.7%
20.2%
1998
1.6%
2.8%
1.2%
0.17%
3.4%
1994
0.9%
7.5%
4.7%
0.12%
8.1%
15.5%
1995
1.4%
4.1%
2.2%
0.25%
4.5%
12.0%
1997
1.7%
3.6%
2.4%
0.37%
3.6%
10.7%
2.5%
1.0%
0.21%
3.0%
* Lead and copper represents the lead and copper rule, which Is a set of standards and Implementation measure;
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
Lead and copper
Microbial contaminants
Chemical and radiation
Treatment and filtration
Any major violation
1998-1999
Type of standard violated
Lead and copper
Microbial contaminants
Chemical and radiation
Treatment and filtration
Any major violation
1993
11.3%
2.2%
8.1%
1.6%
21.6%
1998
5.5%
1.9%
3.8%
0.5%
10.6%
6.7%
2.6%
5.8%
0.6%
14.2%
1999
5.4'
1.4'
2.8'
1.0'
9.9'
5.3%
2.1%
5.5%
0.4%
11.7%
1997
5.8%
2.0%
3.5%
0.3%
10.9%
SOURCE: U.S. Environmental Protection Agency, Office of Water, Safe Drinking Water Information System
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Appendix A: Data Tables
Table E8
Percentage of fruits, vegetables, and grains with detectable residues of organophosphate pesticides
1994
20.8%
1995
24.4%
1996
29.4%
1997
28.8'
22.
1999
24.4%
SOURCE: U.S. Department of Agriculture, Pesticide Data Program
2000
23.2%
2001
19.1%
All Superfund sites
All Superfund sites not yet
cleaned up or controlled
1.2%
1.2%
1.3%
1.1%
1.3%
1.2% 1.1% 1.1% 1.0%
SOURCE: U.S. Environmental Protection Agency, Superfund NPL Assessment Program (SNAP) Database
1.3%
2000
1.3%
0.8%
Table E9
Percentage of children residing within one mile of a Superfund site
Part 2: Body Burdens
Table Bl
Concentrations of lead in blood of children ages 5 and under
50th percentile
90th percentile
Blood lead concentrations Qjg/dL)
76-1980 1988-1991 1992-1994 1999-2000
15.0 3.5 2.6 2.2
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
All Races/Ethnicities
White non-Hispanic
Black non-Hispanic
Hispanic
All Incomes
2.2
2.1
2.8
2.0
< Poverty Level
2.8
2.8
3.6
2.4
Blood lead concentrations
100-200% of
Poverty Level
1.9
1.7
2.6
1.7
SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health and Nutrition Examination Survey
Appendix A
-------
Appendix A: Data Tables
Table B3
Distribution of concentrations of lead in blood of children ages 1-5,1999-2000
Blood lead concentrations Qjg/dL)
4-5 5-6
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)
3-4 4-5 5-6
4% 4% 2%
10-11
11-12 12-13
13-14
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
90th percentile
50th percentile
Serum cotinine concentrations (ng/mL)
1988-1991 1999-2000
2.16 1.78
0.25 0.11
SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health and Nutrition Examination Survey
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
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
All races/ethnicities
White non-Hispanic
Black non-Hispanic
Hispanic
All Incomes
0.25
0.23
0.59
0.19
Serum cotinine concentrations (ng/mL)
100-200% of > 200% of
< Poverty Level
0.66
1.15
0.80
0.21
Poverty Level
0.34
0.38
0.77
0.17
Poverty Level
0.16
0.16
0.24
0.12
Unknown
Income
0.30
0.37
0.47
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 Dl
Percentage of children with asthma
1980-1985
Percentage of children with
asthma in the past 12 months
1980
3.6%
1981
3.7%
1982
4.1%
1983
4.5%
1984
4.3%
1985
4.8%
1986-1991
^^m
Percentage of children with
asthma in the past 12 months
1986
5.1%
1987
5.3%
1988
5.0%
1990
5.8%
1991
6.4%
1992-1996
Percentage of children with
asthma in the past 12 months
1992
6.3%
1993
7.2'
1995
7.5%
1996
6.2%
1997-2001*
Children ever diagnosed with
asthma and having an asthma
attack in the past 12 months
Children ever diagnosed with asthma
1997
5.4%
1998
1999
5.3%
10.8%
2000
2001
5.7%
12.6%
* Note: The survey questions for asthma changed in 1997; data before 1997 cannot be directly compared to data in 1997 and late
SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health Interview Survey
Appendix A
-------
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
All races/ethnicities
White non-Hispanic
Black non-Hispanic
Hispanic
All Incomes
5.4%
5.2%
7.2%
4.6%
< Poverty Level
6.4%
6.1%
8.5%
5.0%
100 -200% of
Poverty Level
5.5%
5.5%
7.2%
3.9%
> 200% of
Poverty Level
5.3%
5.1%
6.3%
5.2%
Unknown
Income
4.9%
4.7%
6.5%
4.3%
SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health Interview Survey
1992 1993
All asthma and other respiratory causes 369.1 406.6
Acute upper respiratory infections 221.9 248.7
Asthma 97.6 107.1
Acute bronchitis 49.6 50.8
Table D3
Children's emergency room visits for asthma and other respiratory causes
1992-1997
Rate per 10,000 children
1994 1995 1996 1997
392.4 357.2 356.4 374.6
246.8 227.4 206.4 214.0
105.1 92.6 114.4 112.1
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
Children's emergency room visits for asthma and other respiratory causes,
by race/ethnicity, 1997-1999
White non-Hispanic
Black non-Hispanic
Hispanic
Rate per 10,000 children
1997 1998 1999 1997-1999
298.4 311.9 317.7 309.3
826.5 811.7 663.9 767.3
384.6
* Annual estimates for Hispanic ethnicity are unreliable for asthma.
SOURCE: Centers for Disease Control and Prevention, National Hospital Ambulatory Medical Care Survey
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Appendix A: Data Tables
Table D4
Children's hospital admissions for asthma and other respiratory causes
1980-1985
1980
All asthma and other respiratory causes 54.7
Acute upper respiratory infections 17.6
Acute bronchitis 16.2
Asthma 21.0
Rate per 10,000 children
1981
56.1
17.7
16.3
22.2
1982
55.3
12.7
16.9
25.7
1983
61.4
19.4
18.3
23.6
1984
50.4
11.4
13.5
25.5
1985
56.6
14.1
17.1
25.4
1986-1991
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
All asthma and other respiratory causes 61.1
Acute upper respiratory infections 7.2
Acute bronchitis 22.9
Asthma 31.0
1997
68.0
7.7
27.3
33.0
1998-1999
1998
All asthma and other respiratory causes 50.3
Acute upper respiratory infections 5.9
Acute bronchitis 19.5
Asthma 24.9
1999
66.4
8.4
29.2
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*
White
Black
Rate per 10,000 children
1997 1998 1999 1997-1999
45.6 34.3 45.5 41.8
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
Appendix A
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Appendix A: Data Tables
Table D5
Cancer incidence and mortality for children under 20
1975-1980
Rate per million children
Incidence
Mortality
1981-1986
^^m
Incidence
Mortality
1987-1992
^^H
Incidence
Mortality
1993-1998
^^m
Incidence
Mortality
1975
128
51
1981
138
44
1987
152
36
1993
161
33
1976
141
51
1982
144
45
1988
151
35
1994
156
32
1977
141
50
1983
144
43
1989
166
35
1995
158
30
1978
144
45
1984
154
39
1990
155
34
1996
162
29
1979
145
46
1985
157
38
1991
162
34
1997
156
29
1980
142
46
1986
157
38
1992
160
33
1998
161
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
All races/ethnicities
White non-Hispanic
Black non-Hispanic
Hispanic
American Indian/Alaska Native
Asian or Pacific Islander
Rate per million children
Male Female
150
156
167
172
133
150
82
150
117
I4l
62
132
SOURCE: National Cancer Institute, Division of Cancer Control and Population Sciences. Surveillance, Epidemiology, and End Results Program 1994-1998
Age-adjusted cancer mortality rates for children under 20 by race/ethnicity and gender, 1994-1998
All races/ethnicities
White non-Hispanic
Black non-Hispanic
Hispanic
American Indian/Alaska Native
Asian or Pacific Islander
Rate per million children
Male Female
26
26
29
33
34
33
35
25
30
27
19
24
SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Vital Statistics System
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Appendix A: Data Tables
Table D6
Cancer incidence for children under 20 by type
1974-78
Acute lymphoblastic leukemia
Acute myeloid leukemia
Central nervous system tumors
Hodgkin's lymphoma
Non-Hodgkin's lymphoma
Thyroid carcinoma
Malignant melanoma
Germ cell tumors
Soft tissue sarcomas
Osteosarcoma
Ewing's sarcoma
Neuroblastoma
Wilms' tumor
Hepatoblastoma
23.7
5.2
23.2
13.9
9.1
4.8
3.9
8.3
10.0
3.8
2.4
7.3
5.4
0.7
1979-83
24.9
4.9
22.2
14.2
9.5
4.8
4.3
9.9
10.7
4.8
3.5
7.2
6.5
0.7
Rate per million children
1984-88
27.6
3.8
27.9
14.1
10.4
5.1
5.4
9.7
10.9
5.0
3.4
7.9
5.6
1989-93
28.2
5.1
30.1
14.1
10.2
5.1
6.5
11.7
11.4
5.0
3.0
7.7
6.3
1.2
1994-98
28.3
4.8
27.3
12.8
11.2
5.4
6.2
11.7
11.6
5.5
3.1
8.0
6.5
1.4
SOURCE: National Cancer Institute, Division of Cancer Control and Population Sciences. Surveillance, Epidemiology, and End Results Program 1994-1998
Cancer incidence for children under 20 by age and type, 1994-1998
Ages 0-4
Lymphocytic leukemia 61.0
Acute non-lymphocytic leukemia 9.7
Hodgkin's lymphoma 0.9
Non-Hodgkin's lymphoma 3.6
CMS and miscellaneous intracranial
and intraspinal neoplasms 34.5
Neuroblastoma and
ganglioneuroblastoma 25.7
Wilms' tumor 18.8
Hepatic tumors 4.6
Osteosarcoma 0.2
Ewing's sarcoma 0.6
Soft tissue sarcomas 11.1
Germ cell, trophoblastic,
other gonadal neoplasms 7.2
Epithelial and unspecified 3.1
Rate per million children
Ages 5-9 Ages 10-14
Ages
30.6
4.3
3.7
5.9
29.7
3.2
4.8
0.6
2.6
2.2
7.9
2.1
3.3
18.4
6.5
11.8
7.7
25.0
0.8
0.8
0.5
7.9
4.2
10.5
7.2
11.6
15-19
14.9
7.8
32.0
13.2
19.2
0.4
0.3
1.2
8.9
4.7
15.0
28.1
40.5
SOURCE: National Cancer Institute, Division of Cancer Control and Population Sciences. Surveillance, Epidemiology, and End Results Program 1994-1998
Appendix A
-------
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
White non-Hispanic
Black non-Hispanic
Hispanic
^^
< Poverty Level
100-200% of Poverty Level
> 200% of Poverty Level
Unknown Income
6
10
5
12
10
4
6
SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health Interview Survey
Part 4: Emerging Issues
Freshwater advisories
Coastal and estuarine advisories
Statewide advisories
1995
32
7
5
2000
37
13
12
Table Ell
Number of states with advisories for methylmercury in non-commercial fish
SOURCE: U.S. Environmental Protection Agency, Office of Water. National Listing of Fish and Wildlife Consumption Advisorie.
Table EI2
Percentage of children ages 5-17 reported to have attention-deficit/hyperactivity disorder,
by race/ethnicity and family income, 1997-2000
All races/ethnicities
White non-Hispanic
Black non-Hispanic
Hispanic
American Indian/Alaska Native
100-200% of > 200% of Unknown
All Incomes < Poverty Level Poverty Level Poverty Level Income
6.7% 7.7% 7.5% 6.9% 4.8%
8.0% 13.6% 9.3% 7.5% 6.1%
5.1% 5.6% 6.5% 4.9% 3.4%
3.8% 3.5% 3.9% 5.1% 2.3%
6.9%
SOURCE: Centers for Disease Control and Prevention, National Center for Health Statistics, National Health Interview Survey
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
-------
Appendix A: Data Tables
Part 5: Special Features
Table SI
Percentage of California public elementary schools with lead paint and some
deterioration of paint, 1994-1997
Any detectable lead
> 600 ppm
> 5,000 ppm
Schools Built
Before 1940
72.2%
72.2%
63.9%
Schools Built
1940-1959
46.3%
46.3%
41.8%
Schools Built
1960-1979
20.5%
18.2%
13.6%
Schools Built
1980-1995
3.1%
3.1%
All Schools
37.4%
36.9%
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
Percentage of California public elementary schools with lead in soils, 1994-1997
Schools with detectable lead in soil
Schools with soil lead > 400 ppm
Schools Built
Before 1940
100.0%
29.7%
Schools Built
1940-1979
94.4%
2.4%
Schools Built
1980-1995
60.5%
All Schools
39.C
7.C
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
Percentage of California public elementary schools with lead in drinking water, 1994-1997
Schools with detectable
lead in drinking water
Schools with > 15 ppb
lead in drinking water 31.4%
Schools with > 15 ppb
lead in drinking water at first draw*
Schools with > 15 ppb lead in
drinking water at second draw*
* Data for first- and second-draw samples are available for all schools only.
Schools Built
1940-1979
52.4%
16.1%
Schools Built
1980-1995
42.1%
13.2%
All Schools
53.3%
18.3%
15.5%
6.5%
Appendix A
-------
Appendix A: Data Tables
Sprayed as needed
Sprayed once a month
Sprayed 1 - 4 times per year
Not sprayed
No answer / other / don't know
Cafeteria and kitchen
food storage areas
34.0%
16.4%
24.0%
16.9%
Percentage of schools
Locker Rooms
and gymnasium
33.5%
3.7%
15.3%
18.7%
Table S4
Frequency of application of pesticides in Minnesota K-12 schools, 1999
SOURCE: CJ. 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
Heart defects
Oral cleft defects
Down Syndrome
Intestinal defects
Limb defects
1991-1993
1.80
1.60
1.34
0.73
0.46
1994-1996
1.98
1.67
1.28
0.73
0.46
1997-1999
1.79
1.50
1.28
0.56
0.38
SOURCE: California Birth Defects Monitoring Prog
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Appendix B: Data and Methods
Common Air Pollutants Air Quality Exceedances (Measure E1)
(Measures E1-E3) 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
Table 1: National Ambient Air Quality Standards (NAAQS) and the Values Used to Define
Exceedances by EPA
Pollutant
Carbon monoxide
Nitrogen dioxide
Ozone
Lead
Particulate matter under 10 microns
Particulate matter under 2.5 microns
Sulfur dioxide
Duration of Standard
Eight- hour average
One-hour average
One year average
One-hour averagea
Eight- hour average
Three-month average
One-day (24 hour) average
One year average
One-day (24 hour) average
One year average
One-day (24 hour) average
One year average
Standard
9 ppm
35 ppm
0.053 ppm
0.12 ppm
0.08
1 .5 pg/m3
150 Mg/m3
50 Mg/m3
65 Mg/m3
15 Mg/m3
0.14 ppm
0.03 ppm
1 Ul fc^l » Ul \M\^ l\J
define exceedance
9.5 ppm
Not applicable
0.0535 ppm
0.125 ppm
0.085 ppm
1.55 Mg/m3
155 Mg/m3
Not applicable
Not applicable
Not applicable
0.145 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Appendix B: Data and Methods
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: eight-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 (ug/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 aver-
age 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 I
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Appendix B: Data and Methods
Hazardous Air
Pollutants (Measure E4)
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 concen-
tration 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 jL/g/m3) in air. UREs are estimated by extrapo-
lation of data from laboratory animal studies, or in some cases, human studies (typi-
cally 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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 NATAwere 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 0-1 7, 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 multi-
plying 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 0-1 7 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 0-1 7 in the identified
counties was summed together. The resulting value was then divided by the number
of children ages 0-1 7 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 I
-------
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 Pvadiation
(202) 564-9431
Drinking Water
Contaminants
(Measures E6-E7)
Safe Drinking Water Information System (SDWIS)
The Safe Drinking Water Information System (SDWIS) is the national regulatory com-
pliance 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 con-
taminant 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 viola-
tions 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 maxi-
mum 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 I
-------
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: 1 038, 1040, 1 041
Inorganic chemicals: 1005, 1 01 0, 1015, 1020, 1 024, 1025, 1035, 1 045, 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 peo-
ple 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Appendix B: Data and Methods
Pesticide Data Program
The U.S. Department of Agriculture (US DA) 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 rec-
ommendation that pesticide residue monitoring programs target foods that are highly
consumed by children, and that the analytical testing methods used in these monitor-
ing efforts should be standardized, validated, and subject to strict quality control and
quality assurance programs. Since 1994 PDP has modified its commodity testing pro-
file 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 but-
ter, 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 con-
taining 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 list-
ing of sites; e.g., Hazard Pranking 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)
Land Contaminants
(Measure E9)
Appendix I
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Appendix B: Data and Methods
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 addi-
tion to the NPL, and date deleted from the NPL (where applicable). The latitude-
longitude 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 CIS 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-longi-
tude 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 charac-
teristics, 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 ug/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 (cljl@cdc.gov)
National Center for Health Statistics
(301) 458-4292
Concentrations of
Lead in Blood
(Measures B1-B3)
Appendix I
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Appendix B: Data and Methods
Concentrations of National Health and Nutrition Examination Survey
Mercury in the Blood Of 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."
Women of Child-bearing
Age (Measure B4)
Concentrations of
Cotinine in Blood
(Measure B5)
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).
Respiratory Diseases
(Measures D1-D4)
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 characteris-
tics, 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 popula-
tion. 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.E Moore, VL. 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.E Moore, C.L. Moriarity, and V.L. Parsons. 2000. Design and esti-
mation 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.
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Appendix B: Data and Methods
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 rep-
resented 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 esti-
mate asthma prevalence were changed. For asthma up to 1996, Measure Dl uses the
parent's response to the following question "Did have asthma in the
past 12 months?" For asthma in 1997-2000, Measures Dl and D2 use parents'
response to the following two questions: "Has a doctor or other health professional
EVER told you that had asthma?" and if yes, "During the past 12
months, has had an episode of asthma or an asthma attack?"
In 2001, the NHIS added the following new question: "Does 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 (Iem3@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 hos-
pital staff in data collection procedures. Hospital staff are instructed to complete
patient record forms for a systematic random sample of patient visits during a random-
ly assigned four-week reporting period. Data are obtained on demographic characteris-
tics of patients; expected source(s) of payment; patients' complaints; physicians' diag-
noses; 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/ahcdl.htm
Appendix I
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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 short-
stay hospitals in the United States. The NHDS collects data from a sample of approxi-
mately 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
Childhood Cancer
(Measures D5-D6)
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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Appendix B: Data and Methods
National Health Interview Survey Neurodevelopmental
Data on the prevalence of attention-deficit/hyperactivity disorder and mental retardation Disorders
are from the National Health Interview Survey (NHIS). See above for description of (Measure D7)
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 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 had attention deficit disorder?"
National Listing of Fish and Wildlife Advisories Advisories for
EPA's Office of Water maintains a database that includes all advisories issued by states, Methylmercury in
territories, and tribes to warn people to reduce or eliminate consumption offish due Non-Commercial FlSn
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://map Lepa.gov/
Agency Contact:
Jeff Bigler (bigler.jeff@epa.gov)
U.S. EPA, Office of Water
(202) 566-0389
Appendix I
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Appendix B: Data and Methods
Lead in California
Public Elementary
Schools and
Childcare Facilities
(Measures S1-S3)
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 collec-
tion of data was completed in 1997.
The Department of Health Services randomly selected 200 of the 5,041 public elemen-
tary 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 geo-
graphically representative sample. Schools with both public and private pre-kinder-
garten and childcare programs located on their premises were included in the sample.
Trained field staff collected the samples and an accredited commercial laboratory con-
ducted 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 build-
ing 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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Appendix B: Data and Methods
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 prac-
tices in K-12 schools, funded by EPA. The purpose of the survey was to obtain statisti-
cally 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, CJ. Olson Market Research, Inc. A pre-
test 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' question-
naires 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
Pesticide Use in
Minnesota's K-12
Schools (Measure S4)
California Birth Defects Monitoring Program
The California Birth Defects Monitoring Program registry is a population-based reg-
istry 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 pop-
ulation 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 thor-
ough 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.
Birth Defects
(Measure S5)
Appendix I
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Appendix B: Data and Methods
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 med-
ical 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/
Child Population Data 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 popu-
lation data were estimated by the Census Bureau using information on births, deaths,
domestic migration, and international migration. Individual age populations were com-
piled for children ages 0 to 17 at the county level for each year 1990 to 1999. A com-
plete 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 multi-
ple 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
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Appendix B: Data and Methods
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-overlap-
ping 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 correc-
tion factor, consisting of the ratio of Black non-Hispanics to total Blacks, was calcu-
lated 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 non-
Hispanic, 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 them-
selves with a single race if that category were the only option. Major bi-racial cate-
gories identified by the authors were: White/Black, White/AIAN, White/API, and
Black/AIAN. In this analysis, equations were derived for apportioning these four bi-
racial 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 multi-
ple 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).
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.
Appendix I
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Appendix B: Data and Methods
Methods for Obtaining Counts of Children under Age 18 by
Race/Ethnicity
The Census Bureau provides county-specific population estimates by race and eth-
nicity 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 15-1 7). Census Bureau files on population by county provide esti-
mates of people for each age (i.e., 15 year olds, 1 6 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 15-1 7. This scaling factor was multiplied by the estimat-
ed 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 (house-
holds 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 pover-
ty range from the 1990 population data to estimate the number of children, by
county, in the three income categories.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Appendix C: Environmental Health Objectives in Healthy People 2010
ealthy People 2010, coordinated by the U.S. Department of Health and Human
I 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 chil-
dren'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 pol-
lutants.
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 expo-
sure 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.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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Appendix D: Environmental Health Objectives in EPA's Strategic Plan
Relevant Environmental
Health Objectives in
EPA's 2000-2005
Strategic Plan
EPA's mission is to protect human health and to safeguard the natural environmentair,
water, and landupon 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 recre-
ation 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 stan-
dard of "reasonable certainty of no harm" will be eliminated.
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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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 migra-
tion to lower-risk pesticides and pesticide management practices, improving educa-
tion of the public and at-risk workers, and forming "pesticide environmental part-
nerships" 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 com-
prises 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, stor-
age, 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 envi-
ronmental information.
Through 2006, EPA will continue to improve the reliability, capability, and security
of EPA's information infrastructure.
Appendix D
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United States
Environmental Protection
Agency
United States
Environmental Protection Agency
1809/1107A
Washington, DC 20460
Office of Policy, Economics and Innovation
National Center for Environmental Economics (1809)
Office of Children's Health Protection (1107A)
EPA240-R-03-001
February 2003
Recycled/Recyclable
Printed with Vegetable Oil Based Inks on Recycled Paper
(Minimum 50% Postconsumer) Process Chlorine Free
America's Children and the Environment: Measures of Contaminants, Body Burdens, and Illnesses
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