Translating Science to Policy - Columbia Center for Children`s

Transcription

Translating Science to Policy
Protecting Children’s Environmental Health
A Conference Held on March 30, 2009
Hosted by The Columbia Center for Children’s Environmental Health
in collaboration with WE ACT for Environmental Justice
COLUMBIA CENTER
FOR CHILDREN’S
ENVIRONMENTAL
HEALTH
MAILMAN SCHOOL OF PUBLIC HEALTH
Columbia University
Columbia Center for Children’s Environmental Health (CCCEH)
The Columbia Center for Children’s Environmental Health—part of the Mailman
School of Public Health at Columbia University—is a leading research organization
dedicated to understanding and preventing environmentally related disease in children. Founded in 1998, the Center conducts research in New York City, including a
study of mothers and children in Northern Manhattan and South Bronx, a World
Trade Center Study, as well as cohort studies in Krakow, Poland, and Chongqing,
China. Its mission is to improve the respiratory health and cognitive development of
children and to reduce their cancer risk by identifying environmental toxicants and
conditions related to poverty that increase their risk of disease. In NYC, the Center
collaborates with residents and partner organizations in Washington Heights, Harlem
and the South Bronx to share research findings with the local communities in ways
that are meaningful and usable in daily life. CCCEH is one of several National Centers
funded by the NIEHS and EPA and one of three Disease Investigation through
Specialized Clinically-Oriented Ventures In Environmental Research (DISCOVER)
Centers funded by the NIEHS. www.ccceh.org.
WE ACT for Environmental Justice
Founded in 1988, WE ACT for Environmental Justice (West Harlem Environmental
Action, Inc.) was New York’s first environmental justice organization created to build
community power to improve environmental health, policy and protection in communities of color. WE ACT is a nationally recognized organization in the field of community-based participatory research in partnership with the Mailman School of Public
Health at Columbia University. Based in Northern Manhattan, WE ACT advances its
mission through research, public education, advocacy, organizing, government
accountability, litigation, legislative affairs, and sustainable economic development.
WE ACT works for environmental and social justice on issues of land use, waterfront
development, brownfields redevelopment, transportation and air pollution, open
space and environmental health. In its first organizing campaign, WE ACT won a $1.1
million settlement of its lawsuit against the City regarding the North River sewage
treatment plant in late December 1993, as well as a monitoring role with the Natural
Resources Defense Council in the enforcement of the city-state consent agreement on
a five-year plan to fix the North River Plant. www.weact.org.
Mailman School of Public Health
The only accredited school of public health in New York City and among the first in
the nation, Columbia University Mailman School of Public Health pursues an agenda
of research, education, and service to address the critical and complex public health
issues affecting millions of people locally and globally. The Mailman School is the
recipient of some of the largest government and private grants in Columbia
University’s history. Its more than 1,000 graduate students pursue master’s and doctoral degrees, and the School’s 300 multi-disciplinary faculty members work in more
than 100 countries around the world, addressing such issues as infectious and chronic
diseases, health promotion and disease prevention, environmental health, maternal
and child health, health over the life course, health policy, and public health preparedness. www.mailman.columbia.edu.
A Conference Held on March 30, 2009
Hosted by The Columbia Center for Children’s Environmental Health
in collaboration with WE ACT for Environmental Justice
The conference was sponsored by:
The John Merck Fund, The New York Community Trust, Passport Foundation,
The National Institute of Environmental Health Sciences, and the US Environmental Protection Agency.
The Center’s work has been made possible by joint funding from:
The National Institute of Environmental Health Sciences
US Environmental Protection Agency
National Cancer Institute
Irving Institute for Clinical and Translational Research
Private Foundations, including:
The Atlantic Foundation, The Bauman Foundation, Beldon Fund, Blanchette Hooker Rockefeller Fund,
Educational Foundation of America, Energy Foundation, Gladys & Roland Harriman Foundation,
Johnson Family Foundation, The John Merck Fund, Alida R. Messinger Charitable Trust,
The John & Wendy Neu Family Foundation, The New York Community Trust, The New York Times Company Foundation,
Passport Foundation, Rockefeller Brothers Fund, Rockefeller Financial Services, Schmidt Family Foundation,
September 11 Children’s Fund, V. Kann Rasmussen Foundation.
And Individual Donors.
Translating Science to Policy: Protecting Children’s Environmental Health
Table of Contents
Conference Overview
Executive Summary ....................................................................................................................................................................................4
Children’s Environmental Health: A Decade of Research ..............................................................................................................6
Frederica Perera, DrPH
Professor and Director, Columbia Center for Children's Environmental Health and Disease Investigation
through Specialized Clinically-Oriented Ventures In Environmental Research (DISCOVER) Center,
Mailman School of Public Health, Columbia University
Partnership in Public Health Research: A Decade of Activism......................................................................................................7
Peggy Shepard
Executive Director, WE ACT for Environmental Justice
Conference Highlights: Keynote Speakers
Protecting Children’s Environmental Health .....................................................................................................................................8
Lisa P. Jackson, Administrator, US Environmental Protection Agency
The Promise: Children’s Environmental Health ...............................................................................................................................11
Linda S. Birnbaum, PhD, DABT, ATS
Director, National Institute of Environmental Health Sciences
Conference Highlights: Presentations*
Case Study 1: Air Pollution and Climate Change
Impact of Prenatal Exposure to Air Pollution from Traffic and Other
Fossil Fuel Combustion Sources on Children’s Health and Development ..........................................................................15
Professor and Director, Columbia Center for Children's Environmental Health and Disease
Investigation through Specialized Clinically-Oriented Ventures In Environmental
Research (DISCOVER) Center, Mailman School of Public Health, Columbia University
Fossil Fuels, Climate Change and Children’s Health: Impacts and Opportunities..........................................................17
Patrick Kinney, ScD
Associate Professor and Director, Program in Climate and Health,
Case Study 2: Pesticides and Integrated Pest Management
Prenatal Chlorpyrifos Exposure and Neurodevelopment:
How Exposure to a Common Pesticide Can Damage the Developing Brain.....................................................................19
Virginia Rauh, ScD
Professor and Deputy Director, Columbia Center for Children’s Environmental Health,
A Collaborative Effort to Evaluate the Impact of
Integrated Pest Management in New York City Public Housing ...........................................................................................21
Daniel Kass, MSPH
Assistant Commissioner, Environmental Surveillance and Policy,
New York City Department of Health and Mental Hygiene
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Table of Contents
Case Study 3: Endocrine Disruptors
The Health Effects of Endocrine Disruptors on the Growth and Development of Children ...................................... 24
Sandra Steingraber, PhD
Scholar in Residence, Division of Interdisciplinary and International Studies, Ithaca College
Translating Research Into Policy and Action
Translating Community-Based Research into Policy and Public Health Action.............................................................27
Peggy Shepard
Conference Highlights: Roundtable Discussions*
Panel 1: Addressing Urban Air Pollution and Climate Change
Brian Lehrer, MPH, Moderator
Host, WNYC and National Public Radio
Panel 1 Policy Recommendations ...................................................................................................................................................30
Rachel Miller MD, FAAAAI, Associate Professor of Medicine and Environmental Health Sciences
(in Pediatrics) at New York–Presbyterian Hospital/Columbia University Medical Center
John Balbus, MD, MPH, Chief Health Scientist, Program Director at Environmental Defense Fund
Michel Gelobter, PhD, Chief Executive Officer, Cooler, Inc.
Rohit Aggarwala, PhD, Director, Office of Long-Term Planning and Sustainability,
Mayor’s Office of Operations, City of New York
Cecil D. Corbin-Mark, MPhil, Deputy Director, WE ACT for Environmental Justice
Panel 2: Healthy Homes—Controlling Residential Pesticides and Consumer Products
Brian Lehrer, MPH, Moderator
Host, WNYC and National Public Radio
Panel 2 Policy Recommendations ...................................................................................................................................................35
Jay Feldman, MS, Executive Director, Beyond Pesticides
Philip Landrigan, MD, MSc, Director of the Children’s Environmental Health Center at
the Mount Sinai School of Medicine
Robin Whyatt, DrPH, Professor and Deputy Director of the Columbia Center for Children’s
Environmental Health, Mailman School of Public Health, Columbia University
Gina Solomon, MD, MPH, Senior Scientist, Natural Resources Defense Council (NRDC)
Erik Olson, Director of Chemical and Food Safety Programs, The Pew Charitable Trusts
Speakers and Panelists ............................................................................................................................................................................40
List of Key CCCEH Findings...................................................................................................................................................................43
Glossary of Terms ......................................................................................................................................................................................47
* Note: All case study and panel transcripts have been edited for length and clarity.
Additional materials, publications, and full videos of all the conference sessions are available online at
www.ccceh.org/conference09.
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Executive Summary
On March 30, 2009, the Columbia Center for
Children’s Environmental Health (CCCEH) hosted a
conference in collaboration with WE ACT for
Environmental Justice (WE ACT), the Center’s lead
community partner. The symposium focused on
three major environmental health concerns affecting children: air pollution, pesticides, and
endocrine disrupting chemicals in consumer products. The purpose of the conference was to share
the Center’s research findings and interventions
over the past ten years, and to discuss how such scientific findings can be translated into policies to
adequately protect children’s health.
During the past ten years, the Center has been
conducting cohort studies in New York City, Poland,
and China to identify the environmental and social
contributors to childhood disease and developmental disorders. Since 1998, CCCEH has followed a
cohort of over 700 Dominican and AfricanAmerican mothers and children in Northern
Manhattan and the South Bronx, and has partnered
with WE ACT and others to disseminate research
results to community residents and policymakers.
Community-academic partnerships such as this one
have demonstrated potential for improving environmental health. The conversion of New York City’s
bus fleet to clean diesel, the installation by the EPA
of permanent air monitors in Harlem and other
“hot spots,” and legislation to restrict the use of toxic
pesticides in New York City are among the initiatives
for which the partnership’s research and policy
work has been given substantial credit. While there
have been successes in reducing exposure to environmental pollutants over the past ten years, there
is still much to be done in developing policies that
adequately protect children’s environmental health.
Air Pollution & Climate Change
Fossil fuel combustion by motor vehicles, residential
boilers, and power plants release a host of toxic pollutants including polycyclic aromatic hydrocarbons
(PAH), fine particles, metals, sulfur and nitrogen
oxides, and volatile organic compounds, which
include precursors to ozone. CCCEH research has
shown that prenatal exposures to PAH are associated
with significantly reduced fetal growth, an increased
risk of developmental and behavioral problems,
reductions in IQ, asthma precursor symptoms, and
changes in gene expression associated with parental
reports of childhood asthma. Encouragingly, policy
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changes supported by these and other findings have
resulted in cleaner air in New York City.
Investigators at CCCEH have documented significant decreases in concentrations of airborne PAH
exposure between 1998 and 2006 in our cohort.
Fossil fuel burning can also adversely affect
children’s health through emissions of carbon dioxide (CO2), the major climate-altering gas. Climate
change is likely to impact children’s health in a variety of ways, including intensifying summer heat
and worsening air quality, prompting earlier and
more intense allergy seasons, and increasing risks
of mosquito-borne diseases like malaria and West
Nile virus. Higher temperatures accelerate the formation of ozone and exacerbate the toxicity of air
pollutants. Because of the close linkages between
CO2 and other combustion-related air pollutants,
policies aimed at mitigating global climate change
will also benefit local and regional air quality.
Similarly, policies to address air quality locally will
influence climate globally. An integrated policy
approach is clearly needed if we are to identify and
capitalize on win-win opportunities for climate and
health. This approach must pay special attention to
populations that are more vulnerable to the health
impacts of both climate change and air pollution
because of inadequate access to health care services, quality housing, financial resources, and social
support networks. There is a disproportionate burden of adverse effects from air pollution and climate change on disadvantaged communities in the
US and worldwide.
Residential Pesticides
The Center’s research has found links between prenatal exposure to common residential pesticides
and adverse health outcomes. In our NYC cohort,
high prenatal exposure to the organophosphate
pesticide chlorpyrifos was associated with significant deficits in birth weight and birth length, as
well as developmental delay, increased risk for
Attention-Deficit/Hyperactivity Disorder (ADHD)
and other behavioral problems. Taken together,
these findings indicate that residential use of chlorpyrifos at pre-ban levels resulted in detectable and
sometimes high levels of the chemical in umbilical
cord blood that were associated with neurobehavioral impairment.
This research has also shown that governmental regulations such as the 2000-2001 EPA restric-
Conference Overview
tions on residential use of chlorpyrifos and the pesticide diazinon succeeded in sharply lowering prenatal exposures, and have had positive impacts on
children’s health. Despite the residential ban on
chlorpyrifos, however, agricultural applications
continue in the US and abroad. Citing CCCEH data
at a September 2008 public hearing, the EPA’s
Scientific Advisory Panel unanimously concluded
that chlorpyrifos may act as a neurotoxicant in
human beings.
The Center’s research has also shown that
alternatives to the traditional use of residential pesticides are more effective and are less toxic.
CCCEH, the NYC Housing Authority, and the NYC
Department of Health and Mental Hygiene jointly
implemented and evaluated an integrated pest
management (IPM) approach in NYC. IPM is an
approach that primarily involves improving sanitary and structural conditions to deny pests food,
water, and movement, and includes the judicious
use of pesticides after an evaluation of need and the
hazard to human occupants. Investigators compared IPM to traditional practices with respect to
their impact on pests, allergens, pesticide use, and
resident satisfaction in several representative public
housing developments. Apartments receiving IPM
used fewer pesticides, had significantly lower
counts of cockroaches at three months, and had
greater success in sustaining these benefits after
three and six months. Residents of IPM apartments
also rated building services more positively. This
was just one example of using the results of scientific research to change public health practice.
Endocrine Disruptors
Endocrine disrupting chemicals interfere with the
production, release, transport, metabolism, binding
action or elimination of the natural hormones in the
body responsible for the maintenance of homeostasis and the regulation of developmental processes.
Recent studies indicate that when exposures occur
at specific times in utero and/or in early life, infant
and child development itself may be disrupted in
ways that can affect intelligence, reproductive development, the timing of puberty, fertility, and could
increase the risks of obesity and cancer. The Center’s
research on endocrine disrupting chemicals is
focusing on phthalates and bisphenol-A (BPA),
which are widely used in consumer products and in
food and beverage containers. Exposures are ubiquitous. For example, in the sample of women and
children in the CCCEH cohort evaluated thus far,
100% were exposed to phthalates in the air they
breathed and 100% had residues of phthalates and
BPA in their urine. High maternal phthalate exposure during pregnancy was associated with reduced
gestational age.
Policy roundtables considered strategies for leveraging scientific findings into policies that better
protect environmental health. The first panel discussed options for reducing pollution from fossil
fuel burning in urban areas like New York City.
Panelists considered proposals that would target
emissions from vehicles, residential heating fuels,
and power plants. These included changes in infrastructure, such as renovating power plants with
updated technology, reforming transportation systems to be both environmentally and financially
sustainable, and replacing residential boilers to utilize energy more efficiently while emitting fewer
pollutants into the air. Other options included the
reduction of diesel emissions through stronger
idling regulations, retrofitting diesel fleets, and the
use of diesel particulate filters to reduce emissions
of black carbon.
Ensuring that the public is protected from
toxic chemicals such as pesticides, phthalates, and
BPA in the home and in common consumer products is also an urgent matter. Panelists in the second
roundtable underscored the ineffectiveness of the
current Toxic Substances Control Act. They agreed
that comprehensive legislative reform at the federal
level is needed to require manufacturers to show
that chemicals are safe before marketing, rather
than placing the burden on agencies and the public
to prove that each new chemical on the market
causes harm before it is regulated. Labeling of
chemicals like phthalates, BPA, and other endocrine
disruptors in consumer products is needed to
enable individuals to make informed decisions. A
consumer-based approach to this problem, however, is limited in effectiveness and cannot substitute
for regulation. When a chemical is removed from
the market, safe substitutes must be available.
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Children’s Environmental Health: A Decade of Research
Ten years ago, the
Columbia Center for
Children’s Environmental
Health (CCCEH) was
founded with the goal of
preventing environmentally related childhood disease
and developmental disorders. We focused on the
role of early-life exposure
to pollutants and adverse
social conditions, which
were suspected of being
among the earliest determinants of disease. Our ultimate goal was to document the effects of prenatal and childhood exposures and communicate our findings to help
reduce, and ultimately prevent, asthma, developmental disorders, and cancer in children.
Since 1998, we have been conducting international studies of pregnant women and their children in New York City, Poland, and China. We have
used an innovative research approach called
“molecular epidemiology,” which combines traditional epidemiological methods and environmental
monitoring with the measurement of biomarkers
(molecular changes that can be detected in blood or
urine) to estimate children’s exposure to pollutants
and their risk of disease. In New York City, for
example, we have been following a cohort of over
700 Dominican and African-American mothers and
children in New York City’s Washington Heights,
Harlem, and South Bronx neighborhoods, who are
disproportionately exposed to pollutant sources
such as diesel bus depots, major commercial roadways, and deteriorated public housing.
In 2000, we convened our first conference to
discuss the serious health threats to children in New
York City from environmental exposures, environmental justice, and the need for targeted research to
fill the gaps in knowledge. We outlined our innovative research approach, our very early findings, and
our plans for outreach and translation of results.
Since then, we have gathered compelling evidence of the multiple adverse health effects of earlylife exposures to common urban pollutants. Our
findings have identified links between specific health
hazards and their clinical consequences. The hazards
include prenatal exposure to air pollution from traffic and other combustion sources, second-hand
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tobacco smoke, residential pesticides, and pest allergens. The health outcomes include significantly
reduced fetal growth, increased risk of developmental and behavioral problems, respiratory symptoms
and asthma, and increased cancer risk. We have also
learned that exposure to multiple pollutants can lead
to more detrimental health outcomes in children
and that nutritional deficiencies, genetic predisposition, and poverty can exacerbate pollutant effects.
In March 2009, we held a second conference
in collaboration with WE ACT for Environmental
Justice, our lead community partner, to report on
our key findings, our intervention studies that
flowed from these findings, and to discuss ways to
translate this research into protective health policy.
We have made significant gains in scientific knowledge over the past decade, which will be described
in this report. Working in collaboration with WE
ACT and other members of our Community
Advisory Board, we have applied our findings to
interventions and health education materials for
parents, community members, health professionals, and policymakers.
Much more remains to be done, however. In
the coming years, we will address the longer-term
consequences of the pollutants we have been studying as well as the role of endocrine-disrupting chemicals, such as bisphenol-A (BPA) and phthalates, in
childhood disease. These chemicals are ubiquitous in
the environment and have been linked to obesity and
metabolic disorders, as well as to other health problems in children. We hope to better understand the
mechanisms involved in environmentally related disease, such as epigenetic modifications (changes in a
gene’s expression but not its fundamental DNA structure) and genotoxic mechanisms (DNA damage that
can cause mutations). This knowledge will be valuable in developing early warning indicators and
informing preventive policies.
We hope the conference proceedings
described in this report will stimulate discussion
and propel work forward for scientists, community
activists, and policymakers as they identify and
implement policies to protect environmental
health. We also hope that it will inspire new allies in
the effort to protect children’s health.
—Frederica Perera, DrPH
Professor and Director,
Columbia Center for Children's Environmental Health
Conference Overview
Partnership in Public Health Research: A Decade of Activism
Most advocates
approach their
mission in the spirit of, “We are not
here to fear the
future. We are here
to shape it.”
Over the past
20 years, I have
been proactively
engaged in the
grassroots national
environmental justice movement,
which has redefined environment to embrace all the
habitats where we live, work, play, and go to
school. Movement organizers, advocates, and academics have helped document that millions of
people in this nation do not have access to clean
air, clean water, a healthy home, a safe school, and
a sustainable community. We are engaged in studies that indicate that race, class, and income are
key determinants of health status, as are higher
environmental and occupational exposures. We
realize that longevity is increasing for many
Americans as mortality and morbidity increases for
residents in indigenous, and urban and rural communities of color and low income across this
nation and around the world.
We acknowledge that we live and work in a
context of race, class, and income as key determinants of health status, environmental protection,
and how land-use burdens and benefits are distributed. We understand that children, in their early
stages of development, are more vulnerable to environmental exposures, and that children of color are
disproportionately impacted by pollution and are
most disadvantaged. The dynamics of environmental injustice have led to excess exposure to environmental hazards, communities devoid of green benefits, and a lack of community-based participation
in democratic decision-making. It is these dynamics
that have seized my attention, commitment, and
energy for the last 20 years.
The important news is that there is a growing
awareness of community conditions that affect community health and sustainability. There is evidence
that community engagement and participation is
translating research to policy and practice. It is
reshaping the direction of many neighborhoods, creating opportunities where it seemed there were none.
We realize that the most powerful factors
shaping health and disparities are social and economic determinants such as poverty and discrimination. Community-wide environmental conditions influence health directly through toxins in air,
water, soil, and building materials. Health disparities are prominent in communities without access
to nutritious food, spaces for active living, effective
transportation systems, but with ready access to
unhealthy products like cigarettes, alcohol, and fast
foods. Combine these factors with lack of access to
quality medical care, and we describe the landscape
of disparities in communities like Northern
Manhattan and the South Bronx.
The results from the Center’s study here in
Northern Manhattan and the South Bronx are typical of exposures being experienced by other environmental justice communities in NYC and across
this country. Like other communities, Northern
Manhattan residents want and need to identify
environmental exposures that negatively impact
their health and quality of life.
WE ACT’s 10-year partnership with the
Columbia Center for Children’s Environmental
Health has answered community questions about
levels of indoor and outdoor toxins and allergens.
The collaboration has engaged residents, empowering them through trainings and evidence-based
environmental health campaigns to impact public
policy. The collaboration has enriched the science
and increased capacity at the community and academic levels. The Center’s research findings have
empowered residents and advocates to translate the
research into policy and practice. I believe and I
have observed that carefully designed CommunityBased Participatory Research (CBPR) that is committed to strong science, high level community involvement, engagement in policy steps and activities, and
the strategic use of study findings to help impact
policy is an important contributor to the broader
struggle for urban health and environmental justice.
—Peggy M. Shepard
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Lisa P. Jackson
Administrator, US Environmental Protection Agency
I’m pleased that I have an opportunity to address
you and meet with you so early in my tenure at EPA.
I hope it underscores for you the importance that I
assign to these issues, to children’s health. It’s also
very significant that we’re here in the middle of this
great city to talk about environmental protection.
When we talk about the environment or environmentalism, it typically brings to mind sweeping
landscapes and stunning vistas, pristine beaches,
mountains, but what usually doesn’t come to mind
for too many people still is an apartment building
or a city block, an urban playground, parking lots.
But that perception only tells part of the story. You
know very well that our cities and urban communities are home to some of the most significant
human health and environmental issues that we
face as a nation. That’s because environmental protection is about human protection, it’s about protecting our communities and our families, it’s about
safeguarding the places where Americans live and
work and play and learn. In that work, EPA and I as
the Administrator are committed to meeting people
where they are.
You do not have to label yourself as an environmentalist, and I don’t believe that all of you here
spend your days or nights thinking about wilderness preservation or sit up late at night, as too many
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of us do lately, talking and strategizing on climate
change. But we’ve all come to the conclusion that
children’s health is worth fighting for. Maybe you’re
a parent or a grandparent worried about loved
ones, or maybe you’ve noticed that the kids in your
neighborhood can’t go outside and play in the summer because it’s too dangerous to breathe the air.
Maybe the work of our friends in the environmental justice movement have moved you to action,
people like WE ACT have gotten through to you.
You understand that the children who get sick at
two and three times the average rate because their
air and water are dirty are often the same kids who
use emergency rooms as their primary healthcare
mechanism. And you know that that drives up
health costs for everyone, not to mention the strain
it puts on working mothers and fathers who have to
miss work to care for their children.
Whatever reasons bring you here to this
moment, we share the common ground of children’s health protection. And I say again that EPA is
committed to meeting you where you are and
working with you on the issues that we share. There
are simply too many important issues where we
can’t wait for a quorum of the American people to
decide that they are environmentalists before we
move forward with action. Children’s health is one
of those issues.
Ensuring that our children are not exposed to
toxins and pollution or other environmental
threats in their homes or in their schools or anywhere else is central to our work at EPA. Children’s
health was one of the top issues that I laid out in my
first day memo and sent to all employees in order to
establish priorities from day one. Children’s health
was reinforced by our first lady, Michelle Obama,
when she visited EPA last month and spoke to our
staff. She charged each employee there with a
responsibility, saying simply that the health and
safety of our children is our top priority.
Children’s health was also the driving force
behind one of our very first initiatives, the effort to
monitor dangerous particulate matter around
schools. When USA Today published this story, parents all across the nation read about dangerous air
in our schools; they read how children absorb toxic
pollutants in the same quantities as adults, meaning
they ingest a much higher dose because of their
lower body weights; they read about how children
are more vulnerable to asthma and other respiratory illnesses and susceptible to long-term complications that can affect them throughout their entire
lives. Then they sent their children to school wondering, as any parent would, if they were putting
them in harm’s way.
So in response to their concerns EPA has a
fundamental obligation to step in. We’ll work with
tribes, states, and local officials to determine which
schools are exposed to high levels of toxic air pollution. We have a strong focus on schools located near
large industries, big stacks, and in urban areas
where we know there’s a coming together of issues
that can affect children’s health. That will begin at
some schools in the coming weeks. Results will be
available to the public as quickly as we can provide
them so that the many concerned parents and
healthcare professionals, toxicologists, and risk
assessors can get critical information they deserve,
and so that we can all take action where it’s needed.
But that’s just the beginning. We have important
obligations to look ahead and be proactive about
preventing and where necessary mitigating the particular effects of climate change and those effects
on children’s health and welfare. We need to step
up our efforts to assess and manage chemical risk
especially those in looking how they are particularly
harmful to children. As this Center has shown, prenatal and early life exposures can have tragic lifelong effects, and we must be diligent in preventing
any possible dangers.
I’m also particularly concerned about eliminating disparities in environmental health and safety from minorities and low income populations.
You have all led the way on this, and I’m asking for
you to keep pushing. We need your help at EPA to
elevate this issue to the mainstream so that we can
create a sustainable and healthy environment for
children and adults in every single community in
our country.
These and many other issues—energy efficiency, public transportation, walkable neighborhoods, air quality, water quality, hazardous waste—
are all important to children’s health protection.
So I’m very proud today to announce some great
news in our children’s health work. Starting today
we have a new member on our team at EPA, Peter
Grevatt. Peter will serve as our senior advisor for
children’s environmental health. Peter brings to
the position a wealth of scientific, risk assessment,
environmental justice and children’s health experience. …
Now given Peter’s background in science, I
think I can speak for him, and I certainly know for
me the theme of this meeting, translating science
into policy, is praiseworthy indeed. It makes me
happy not just because I’m a scientist, but because
I’ve been working to communicate that science
must once again be the determining factor in EPA’s
decision making. If we return to science we will
make decisions on clean air and water that are
“… science must once again be the determining factor in EPA’s
decision making. If we return to science we will make decisions
on clean air and water that are based on human health. It will
lead us to places where we can identify and articulate very
clearly what it is we face and what it is we must do.”
based on human health. It will lead us to places
where we can identify and articulate very clearly
what it is we face and what it is we must do.
In just the past month we have begun the
arduous process of reexamining previous decisions
made at EPA largely because of questions about
whether science was trumped by politics. Whenever
that happens it may be a momentary victory for one
side or the other, but it dilutes our effectiveness at
EPA as an agency, it dilutes the American people’s
ability to look at EPA and see us as guardian of the
things they value, and it requires that we use our
time and resources to look back when we absolutely
need to be moving ahead.
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The second guiding principle for us at EPA is
the rule of law. The lawsuits that follow EPA are
probably inevitable, but there have been some
important times when lawsuits have crystallized
what we need to remember every day at EPA, and
that is that the laws are in place because Congress
“I’ve tried to send a clear, consistent message, and it’s a
message that I give you in hopes that you will join with me in
carrying it to everyone you work with. That message is that EPA
is back on the job.”
decided and the people determined that environmental action was needed. If we don’t uphold these
laws then we have let the system down, but more
importantly we are impacting and affecting people’s
health. When we don’t win a court case on particulate matter or ozone, it’s sad for the lawyers
involved but it’s tragic for human health.
Lastly, we must operate with unparalleled
transparency at EPA. Transparency will aid us in
making sure that science and the law come first,
and it will send a very clear signal to the American
people that we work for them. I want everyone to
know who I meet with and what I’m talking about,
and I want the American people to believe that EPA
is its advocate. It’s extraordinarily important that
people believe they can get inside the walls of the
EPA and that EPA is not governed by industry or any
one group or interest.
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In closing, let me say that right now we have
extraordinary opportunities to protect public
health and the environment, probably greater than
any other time in the history of the EPA. We’ve
moved beyond the false choice between having a
green economy and having a green environment,
and we have risen above many of the past divides
that have often slowed down environmental protection and set us back for years. Today in Congress
and throughout the country there is tremendous
bipartisan support for green jobs, smart growth,
clean energy, a long list of ideas and innovations
that will grow our economy and improve our planet. And we have the support of extraordinary people like you.
So when I speak to reporters and industry
leaders, community members, stakeholders, I’ve
tried to send a clear, consistent message and it’s a
message that I give you in hopes that you will join
with me in carrying it to everyone you work with.
That message is that EPA is back on the job. I’m
asking you to keep doing exactly what you’re
doing, continue to gather the best science, then
use that information to organize and engage people in your communities, talk to parents about
why this matters, show someone that whether
they count themselves as an environmentalist or
not, clear air and clean water affects them and the
people around them every day. Please educate
young people so that they can carry the torch for
the next generation.
The Promise: Children’s Environmental Health
Linda S. Birnbaum, PhD, DABT, ATS
Director, National Institute of Environmental Health Sciences
National Toxicology Program
Environmental health sciences provide critical
investments into children’s health. We’re interested
in prevention here, and that’s really the power of
environmental health. When I look at the mission
of my Institute, it is to protect the American public
from diseases and health conditions associated
with the environment. We need to remove the
toxic agents from human exposure before disease
happens.
When we’re talking about environmental
health sciences and children’s health, we’re really
talking about the issues of early prevention. And
what does early prevention get us? It gets us years,
decades, a lifetime of improved health. It can lead
to reductions in early mortality and morbidity. It
can decrease the instances of fetal or childhood
exposures causing diseases in adulthood. You’ve
already heard somewhat about that this morning,
and I’m going to come back to the latent effects of
early life exposures. It can improve the quality of
life. And, from an economic point of view, and we
are always being asked to balance economic benefits with risks, it can decrease the expenditures on
healthcare while improving individual productivity
in the schools and the workplaces throughout life.
I want to talk about a children’s success story,
and that’s the story of lead. Lead as an additive was
removed from gasoline in the mid-70s as well as
from paint, and it started a downward trend.
Actually, it was amazing. From 1976 to 1988 there
was a dramatic decline in the amount of lead measured in children’s blood in the American population. I can tell you from a regulatory perspective no
one expected that taking lead out of gasoline would
bring about the very rapid decrease that ensued. As
a follow-up, CDC reported that the percent of children with elevated blood lead dropped from 9% in
1988 to 1.4% in 2004.
When the regulatory limit of ten parts per
deciliter was set, the idea was that it was protective
against the adverse effects of lead on child’s IQ. But
what we’re now understanding is that there appears
to be no safe level of lead. Even at lower levels, we
can still see relationships. It became harder to see the
IQ effects (although you can see them on a popula-
tion basis), but we can see the behavioral effects associated with lead. I think this is a very important message to get out there—that we need to continue to be
vigilant and to continue to reduce these exposures.
We’re all here really celebrating the success of
the Centers for Children’s Environmental Health
“We need to remove the toxic agents from human exposure
before disease happens.”
and Disease Prevention program, and specifically
the marvelous program that exists here at
Columbia. This is a federal partnership, and it’s the
kind of thing the government can and should do
more of. In this case, it’s a partnership between
NIEHS and the US EPA. The overall goal of this partnership was to establish a national network fostering communication, innovation, and research
excellence in children’s environmental health in
order to reduce the burden of morbidity among
children as a result of exposure to harmful environmental agents.
We have 13 centers, 12 of which are co-funded
by NIEHS and EPA. These centers are addressing a
variety of environmentally-related issues, and the
focus is to stimulate new and existing research on the
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role of environment in the etiology of disease and
dysfunction. All too often we’re looking for diseases,
and what we really need to be looking at is putting
more children in an at-risk category, whether it’s at
risk for their behavior, at risk for their intellectual
success, at risk for their future. We need to develop
novel effective interventions and prevention strategies, and we heard about some of those this morning. Again, it’s much better to prevent the problem
than to try to treat or cure it once it has occurred.
“We need to promote the translation of basic research findings
into applied intervention and prevention methods. We need to
enhance the awareness of the public and medical professionals
of detection, treatment, and prevention—and I keep stressing
prevention. I think the public partnerships that these children’s
centers have are really an example for how the biomedical
research establishment needs to be moving in the 21st Century.”
We need to promote the translation of basic
research findings into applied intervention and
prevention methods. We need to enhance the
awareness of the public and medical professionals
of detection, treatment, and prevention—and I keep
stressing prevention. I think the public partnerships that these children’s centers have are really an
example for how the biomedical research establishment needs to be moving in the 21st Century.
I’m going to briefly give a couple of examples
of some of the different kinds of focuses that we
have in these environmental centers. You’ve already
heard somewhat about environmental health and
asthma, which is still a work in progress. We know
that the increase in asthma is really of epidemic
proportions. Right now in the US we have at least 22
million people with physician-diagnosed asthma,
and 6 million of those people are children.
Researchers funded by NIEHS within our Institute
and our intramural program have identified dust
mites and roach allergens, cockroaches, as common
triggers in initiating asthma and asthmatic
episodes. These environmental agents not only can
cause the disease, they exacerbate and promote it.
Here you have two opportunities for prevention.
The first is to stop the disease from ever happening,
which is the best. The second is to stop it from
being reintroduced or progressing.
Many of the centers, like this one, are exploring the roles of outdoor pollution as well as indoor
pollution, and the role of maternal smoking. We’re
also understanding that there are genetic suscepti-
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bilities. What we’re looking at in many cases are
interactions between the epigenome and environmental exposure in the induction of these diseases. I
know that here at Columbia you’re looking at pollutants from vehicle exhaust, indoor residential heating and power generation, and finding that many of
these pollutants may actually alter the structure of
DNA and chromosomes in the womb.
The increased susceptibility of the developing
organism is well known. In utero, infantile, and
pubertal stages are all times of rapid growth and
extensive differentiation. It’s at these times that you
have opportunities for initiation of lesions and promotions of altered cells. We all know that development is a highly integrated process. The idea of latent
effects of early exposure comes from some key epidemiological work done in the United Kingdom,
which is known as the “Barker Hypothesis.” This is
the growing body of research that suggests that many
chronic adult diseases and disorders, including asthma, diabetes, obesity, even heart disease for example, can be traced back to exposures that occur in
utero or during early childhood.
I just want to briefly mention some of the
work that NIEHS is doing related to early exposures. NIEHS is partnering with the National
Cancer Institute in funding four breast cancer and
the environment research centers that are investigating the impact of prenatal and childhood exposures on mammary gland development, and on the
potential of exposures to alter risk of breast cancer
in adulthood.
In addition to asthma and cancer, another key
issue is neurodevelopment and neurological diseases. We support basic research to determine the
mechanisms and pathways by which toxicants can
disrupt the developing brain. A point that I should
make is that brain development does not stop at
birth. It does not stop at two years of age. In fact,
there’s growing evidence that, in humans, the brain
continues to develop until about 25 years of age (so
when you’re dealing with your teenagers and you
know that they’re not full adults, it’s true.)
Neurotoxicants being studied by NIEHS-sponsored
research includes a variety of metals, such as lead,
mercury and manganese, pesticides, tobacco
smoke, and a whole bunch of persistent organic
pollutants such as PCBs. In the past we have studied
the dioxins, and it’s a success of the regulatory
agency that dioxin levels have gone way down. But
now there’s a lot of focus on polybrominated
diphenyl ethers (PBDEs) and other brominated
flame retardants, which we’re finding in exponentially increasing levels in our environment and in
our people. They’ve been put there to provide fire
safety. I’m not terribly concerned about going up in
smoke, but I am concerned about what’s happening
to our population by exposure to these compounds.
In addition to looking at early life exposure
and development neurotoxicity, we’re also looking
at the associations with neurodegenerative syndromes. Autism is clearly a neurodevelopmental
condition. I should mention we shouldn’t just be
talking about “autism,” just like we don’t just talk
about “cancer.” We’re talking about a spectrum of
disorders, and they may have different and multiple
causes when you talk about autism spectrum. We’re
dealing with Attention-Deficit/Hyperactivity
Disorder (ADHD). Again, this is not one condition—
there are multiple conditions and multiple causes.
We are also looking at adult onset diseases, such as
Parkinson’s disease and Alzheimer’s. Again, these
may be rooted in early environmental exposures.
Many of our NIEHS centers focus on neurodevelopmental outcomes.
I want to come back to autism now because we
know that there is an epidemic of autism in the population, and it cannot all be explained by changes in
classification of the disorder or better diagnosis. One
of our children’s centers that really focuses on that is
at the University of California at Davis, which is conducting the first large-scale epidemiologic study of
children with autism, looking at a wide range of environmental exposures and effects on early development of over 1,000 California children. At the same
time, we have NIEHS-sponsored investigators looking
at new and improved animal and cellular models for
autism and ADHD. This will help us determine how
neurotoxic substances may impact both brain development and behavior. Interestingly, we have tended
to think about the immune system and allergies, or
responses to certain other stressors. The immune system plays a key role in brain development as well, and
there appear to be interactions. If you have one autistic child or if there’s autism in a family there is clearly
some kind of both genetic and environmental susceptibility factors going on here. One of the most exciting
things we’re doing is enrolling mothers of autistic
children who are pregnant with a subsequent child to
look at prenatal, neonatal, and early postnatal exposures to see if we can pick up an association in this
more susceptible population.
The other thing I want to mention is that in
2006 Congress passed the Interagency Autism Act,
which provides for a national strategy on dealing
with autism and autism-based research. I serve on
the coordinating committee for that, along with the
heads of National Institutes of Child Health and
Developmental and Neurological Disorders, and
Mental Health, for example. This is also a coordinating committee that not only involves the leaders
of the research community, but involves citizens’
action groups and advocacy groups so we can work
together to move faster in dealing with these serious environmental diseases.
Endocrine disruptors are exogenous agents
that interfere with the production, release, transport, metabolism, binding action or elimination of
the natural hormones in the body responsible for
the maintenance of homeostasis and the regulation
of developmental processes.
One point I want to make is that what is normal for me may not be normal for you. We all have
our own balance of different hormones in our different systems. What is normal has a distribution. I
used to talk about in the dioxin field where we knew
that exposure to dioxin could reduce circulating
testosterone levels by 10%—for a male who is in the
average of that, or the mean of that distribution, a
10% reduction means nothing. But for a male who’s
at the low end, a 10% reduction can make him infertile. When we’re talking about exogenous chemicals
that are endocrine disruptors, they’re not adding
onto a control of 0. They’re adding onto a background that already exists. Depending on where
that background is, it may cause a problem for some
people and not for other people.
“As we move into the 21st Century, we’re beginning to realize
that the developmental period is a critical time for disruption,
not only by endocrine disrupting agents but by other toxicants.”
Environmental exposures to endocrine disruptors are suspected of being associated with the
earlier and earlier puberty we’re finding in young
girls, with increasing incidences of genital malformation that are being detected in the population,
and with the dramatic increase in testicular cancer
in males. This is not only in our country, it is pretty
much worldwide. NIEHS has supported a number
of studies, both experimental and epidemiological
studies, looking at endocrine disruptor activities.
For example, BPA, which you heard mentioned this morning, is often called a weak environmental estrogen. But weak is context-dependent. It
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may be weak in terms of its ability to work on
nuclear estrogen receptors, but it is equipotent
when it comes to the newly-discovered membrane
estrogen receptors. And BPA is only one of a plethora of environmental endocrine disruptors, or in this
case environmental estrogens, which act in an additive fashion. So when we look at one compound at a
“The lives of our children are our most cherished and prized
responsibilities. Our children’s health reflects how we are doing
both as a nation and the world.”
time we may miss the boat. Nevertheless, BPA in
experimental studies clearly causes changes in the
mammary gland and in the development that were
time and dose dependent. …
As we move into the 21st Century, we’re beginning to realize that the developmental period is a
critical time for disruption, not only by endocrine
disrupting agents but by other toxicants. We’re
beginning to emphasize the use of perinatal dosing
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regimes in our toxicology and carcinogenicity studies. We’re also focusing on the important understanding that it’s not so much what you get on a daily
basis but it’s what’s really in your bodies that’s really
important. For some chemicals, which are persistent
and biocumulative, you are what you’ve been
exposed to for the last month, year, multiple years.
For other things, it could be very much what you’re
getting on a daily basis. But if we want to compare
our animal data to our human data we have to look
at the internal dose. That has been kind of a late
understanding in the field. …
So when we talk about children’s health, in
some ways our children’s health is a report card on
what the future adult health of the American population will look at. Kids, along with the ill and the
elderly, are the most vulnerable parts of our population. The lives of our children are our most cherished and prized responsibilities. Our children’s
health reflects how we are doing both as a nation
and the world. May our report cards give us
increasingly A’s in this area.
Conference Highlights: Presentations
Case Study 1: Air Pollution and Climate Change
This case study focused on the effects of fossil-fuel related air pollution on children’s health, and the linkages between fossil fuel
combustion, climate change, and human health. Dr. Frederica Perera discussed the Center’s findings about the health effects of
prenatal and early-life exposure to air pollution from traffic in New York City, which include low birth weight, respiratory
effects, neurodevelopmental disorders, and potentially increased cancer risk. Dr. Patrick Kinney then reviewed the effects of
global climate attributable to carbon dioxide (CO2, one of the main greenhouse gases) on children’s health. The predicted
effects in children of global warming caused by CO2 from fossil fuel combustion include heat stroke, increased risk of infectious
disease, allergies and asthma, and malnutrition from food shortages. These two pathways of health effects are closely related,
and interact with each other (see Figure 1). Reducing fossil fuel pollution in New York City and across the country will therefore
have multiple, complementary benefits..
Impact of Prenatal Exposure to Air Pollution from Traffic and Other
Fossil Fuel Combustion Sources on Children’s Health and Development
Professor and Director, Columbia Center for
Children’s Environmental Health, Mailman School
of Public Health, Columbia University
Air pollution from the burning of fossil fuels
adversely affects children’s health in many ways. In
New York City (NYC), major sources are local-transportation vehicles, including buses, trucks, and
automobiles. Diesel fuel is a particularly important
source of pollutants. Nationwide, coal burning is
widely used in power generation and industry, and
is a major contributor to air pollution. These pollutants can be locally generated as well as transported
to NYC from areas upwind. The complex mix of
pollutants in urban ambient air includes polycyclic
aromatic hydrocarbons (PAH), fine particles, sulfur
and nitrogen oxides, mercury, and other metals
from fossil fuel burning.
We know from many lines of research that the
developing fetus, infant, and young child are especially susceptible to effects of toxic pollutants, and
also to psychosocial and other physical stressors such
as heat. Compared to older children and adults, the
very young have less efficient systems to detoxify
chemicals or repair damage; and their rapid growth
and higher rates of cell proliferation put them at
greater risk. Over the span of their lives there is more
time for cancer and other serious chronic diseases,
such as cardiovascular and neurodegenerative diseases, to develop. We are now aware that harmful
early-life exposures can affect health over the life
course, not only in childhood, but also in adolescence and in middle and older age. We are also
beginning to understand that early exposures can
result in heritable effects across generations.
There is an urgent need to prevent environmentally-related disease, in NYC and elsewhere.
Figure 1
High rates of low birth weight, developmental
delay, and asthma in children were obvious to us
ten years ago. They are even more obvious now. In
CCCEH’s Mothers & Newborns study in Northern
Manhattan and the South Bronx, we have found a
30% incidence of asthma and a high incidence of
developmental problems. African-American populations have much higher rate of low birth weight
and preterm delivery than other populations. In the
US, rates of developmental disorders, asthma, and
certain childhood cancers have been increasing in
recent decades. Common environmental exposures
are known or suspected of contributing to this
increase, along with adverse social conditions,
genetic susceptibility, and nutritional deficits.
Studies & Design
The Center has been carrying out longitudinal studies
of mothers and children in NYC, Poland, and China,
as well as a study of health effects in the aftermath of
the World Trade Center disaster. All these cohort
studies are complementary because they are investigating common pollutants using the same molecular
methods. These methods involve the analysis of bio-
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logic samples like umbilical cord blood, urine or placental tissue for biologic markers indicating the level
of pollutant exposure, the preclinical damage resulting from the exposure, or genetic or nutritional susceptibility to the exposure. The biomarkers are
embedded in population studies—an approach
known as molecular epidemiology. Our study populations include young, healthy, non-smoking women
recruited during pregnancy. A total of 2,000 mothers
and 2,000 children have been enrolled in these studies. Our largest study is in NYC, where over 700
African-American and Dominican mother-child pairs
living in Harlem, Washington Heights, and the South
Bronx have been enrolled.
We use a molecular epidemiologic approach in all
our studies to better document the early warning signs
of disease risk or susceptibility. Two examples of biomarkers include epigenetic changes and chemical-DNA
adducts, which can be measured in blood. When epigenetic changes occur, the structure of DNA is not
changed, but the expression of the gene is altered. Since
gene expression is tightly choreographed during early
development, unprogrammed epigenetic changes can
result in developmental and health problems. DNAadducts are formed by the direct interaction of a chemical (such as PAH) with DNA. Adducts are considered a
marker of potentially increased cancer risk because they
can lead to mutation and even to cancer.
In the NYC study, as in the other cohorts, we have
taken repeat measures of exposure, biomarkers, and
outcomes from pregnancy into childhood. Exposure
assessment is done through personal and residential
air monitoring. We obtain extensive questionnaire
data, as well as geographic information about neighborhood-level characteristics (see Figure 2). In our
analyses, we control for factors that could confound
associations between the pollutants of concern and
health effects, such as socioeconomic status and age.
Figure 2
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CCCEH Research Results
We have found that exposure to pollution in the air is
widespread in our NYC cohort—100% of pregnant
mothers were exposed to PAH in air; 40% were also
exposed to environmental tobacco smoke (ETS); and
40% of mothers reported experiencing material
hardship during pregnancy. This is clearly a population in which both physical toxicants and psychosocial stressors are prevalent.
DNA adducts were detected in 40% of the
maternal and newborn cord bloods. We also compared the levels of PAH-DNA adducts in maternal and
cord blood within and across our NYC, World Trade
Center, Polish, and Chinese study populations.
Despite the natural protection that the placenta provides in reducing fetal exposure, levels of DNA damage in mothers and children were similar within
each population. This finding indicates that the fetus
may be significantly more susceptible to DNA damage from air pollution than adults.
Prenatal exposure to PAH measured by personal
backpack air monitors or by PAH-DNA adducts in
cord blood was associated with reduced birth weight
and head circumference among African-Americans
and, across the entire population, with developmental delays at age 3, attentional and behavioral problems, and reduced IQ scores at age five. Prenatal PAH
exposure in conjunction with postnatal exposure to
secondhand smoke was associated with increased respiratory symptoms. We have also found that an epigenetic alteration in cord blood that was associated with
prenatal PAH exposure was a predictor of subsequent
childhood asthma. This was the first such report.
Finally, we have found that prenatal PAH exposure
was linked to significantly higher frequency of stable
chromosomal alterations in newborns.
Conclusions
Our scientific findings have serious implications for
children’s health, but there is also good news in that
data such as ours can spur action that yields immediate benefits. In NYC, for example, we have seen
that personal prenatal exposure to PAH in our
cohort declined significantly in recent years as a
result of NYC’s efforts to clean up its fleet of buses,
restrict idling, and reduce congestion. As shown in
Figure 1, children’s health doubly benefits from
curbing of fossil fuel combustion emissions. In conclusion, our findings underscore the critical need to
identify risks from early-life environmental exposures as a key to prevention of childhood disease
and developmental impairment.
Case Study 1 : Air Pollution and Climate Change
Fossil Fuels, Climate Change and Children’s Health: Impacts and Opportunities
Patrick Kinney, ScD
Associate Professor and Director, Program in Climate and Health, Mailman School of Public Health,
Columbia University
Health Impacts of Climate Change
There are several ways that climate change can filter
through various environmental and ecological systems to affect human health (see Figure 4). Health
effects related to climate change that we expect to
see in children in New York City and elsewhere
include heat-wave-related illnesses. We also expect
impacts on air quality. At higher temperatures, airquality problems that we’re already dealing with,
such as summer smog, generally become more
severe. But there’s a range of more complex potential consequences that we’re only beginning to
understand, including
changes in the prevalence of vector-borne
diseases. West Nile
Virus is an example of
a vector-borne disease
that emerged in the
last seven or eight
years, and is now all
over the United States.
We are only beginning
to understand the ways
in which meteorological changes related to
precipitation and temperature will affect the
spread of disease. To
date, we do not have
enough scientific research underpinning this to
understand all these connections. An important goal
for the future is to fill the gaps.
There is a range of health-based air-quality standards that the US Environmental Protection Agency
administers, such as carbon monoxide, nitrogen
dioxide, lead, and sulfur dioxide. Since the EPA started working on pollution control in the early 1970s
they have succeeded in reducing concentrations of
these four pollutants in the United States. Regulation
of ozone and fine particles, on the other hand, is a
more challenging task. There has been less success in
reducing ozone concentrations and fine particle concentrations (also called PM2.5), which are the smallest
pollution particles and can penetrate most deeply
into our lungs. But these are only a handful of pollutants; the mix of pollutants in the environment, especially in New York City, is much more complex. There
are many other pollutants, including chemicals such
as polycyclic aromatic hydrocarbons (PAH), that have
been shown by the Center’s research to play specific
roles in a variety of adverse health impacts.
We can also tease apart the composition of
fine particles and find that they are composed of a
variety of chemicals drawn from many different
sources, including organic compounds, elemental
compounds, mercury, and nickel, among other
substances. To really understand the health impli-
Intergovernmental Panel on Climate Change
In New York City and in most urban areas in the US,
we burn fossil fuels for essentially three purposes:
transportation, electric power generation, and space
heating for residential and commercial buildings.
Nationally, fossil fuel combustion in the City and
upwind of the City is producing large amounts of
carbon dioxide (CO2), which contributes to global
climate change (see Figure 3). All of this combustion
and production of CO2 in the United States contributes significantly to global climate change.
Historically, the US has emitted more CO2 than any
other nation—we have approximately 6% of the
world’s population and on average produce about
25% of annual CO2 emissions, so we’re doing more
than our share to contribute to global warming.
Figure 3
Figure 4
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cations, and also the climatological relationships,
we need to fully examine the constituent elements
of the particles.
Climate impacts and human health impacts
from air pollution are two sides of the same coin.
When we burn fossil fuels we know that the toxic
emissions have immediate impacts on children’s
health. At the same time, we also emit carbon dioxide
that is diffusing globally and contributing in important
ways to climate change, which has a variety of adverse
health impacts. Climate change itself can influence air
pollution, resulting in direct health effects
Projected Effects of Climate Change
I also want to mention the New York Climate and
Health Project, a project started at Columbia that was
designed to examine whether climate change could
have adverse effects on human health, particularly in
the New York region. First, we developed a modeling
system that took global climate change models and
linked them with regional climate and air quality
models. We do not know exactly how global and
domestic policy will evolve for the next 50 to 100
years, so we looked at a range of potential scenarios
for greenhouse gas growth. We looked at several different time slices: the 2020s, 2050s, and 2080s.
Figure 5 includes a map of counties across the
eastern United States and shows how the number of
summer ozone exceedence events might change in
the 2020s compared to the 1990s. An exceedance day
occurs when the eight-hour maximum ozone concentration measured on that day is higher than the
health-base standard that the EPA sets. The orange
and red counties are areas where our modeling projects that exceedence days for ozone standards could
increase from 25 to 80 additional days. This is just an
Figure 5
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example of the kind of work one can do to link the
latest models with our understanding of the health
standards and health effects of air pollution.
Call to Action
There are some important take-home messages.
First, we need to take action to reduce emissions
from fossil fuels because it is a win-win opportunity. We can have immediate improvements in children’s health via reductions in local and regional
concentrations of particulate matter, ozone, and a
variety of other toxic pollutants from the fossil fuel
combustion. Meanwhile, we have the great benefit
of reducing our contribution to global climate
change by reducing CO2 emissions. Because climate
change and immediate human health impacts are
so intricately linked through the combustion of fossil fuels we really ought to be thinking about them
together; we should be analyzing them and controlling them in a systematic, integrated way.
As we do that, we need to consider the environmental-justice aspects of the question. Both the
costs and benefits of our improved air quality
should be distributed equitably, nationally and
internationally. There’s a huge global equity issue in
the case of climate change. As I mentioned before,
the US has been disproportionately responsible for
the problem, but the effects are likely to be especially striking in some developing countries. Even
within the United States, the equity issue is very
important. The communities where toxic air pollutants are affecting children the most tend to be
underprivileged neighborhoods that face all sorts of
other environmental health risks, too. As we begin
to address the problem of climate change along
with toxic air pollutants, we need to make sure that
we put a special emphasis on improving the situation in places that are already most burdened.
We also need to move aggressively to rein in
greenhouse gas emissions. Some of the more aggressive proposals in Washington are aiming for an 80%
reduction in greenhouse gas emissions by 2050. If
met, that goal will stabilize the climate, but it will
also impart tremendous health benefits. We should
swiftly implement near-term emission reduction
strategies, ones that we can identify as having the
greatest immediate health benefit for children, particularly in communities that bear the greatest pollution-related health burdens. In other words, let’s
look at the various mitigation options that can
achieve reductions in greenhouse gases, and start
with the ones that are going to have the most immediate benefits for children’s health in the near term.
This case study focused on the Center’s findings about the effects of chlorpyrifos on children’s neurodevelopment, and a
related intervention to reduce exposure to residential pesticides in New York City public housing. Dr. Virginia Rauh discussed how prenatal exposure to chlorpyrifos negatively affects children’s growth and neurobehavioral development.
Daniel Kass, Assistant Commissioner of Environmental Surveillance and Policy for the New York City Department of
Health and Mental Hygiene, then discussed a successful intervention program that used Integrated Pest Management, a
lower-toxicity pest-control method, in place of traditional pesticide spraying in public housing. City health officials collaborated with the New York City Housing Authority and CCCEH on the program. This case study demonstrates how sound
scientific findings about the effects of toxic exposures can be used to reduce harmful environmental exposures in practice.
Prenatal Chlorpyrifos Exposure and Neurodevelopment: How Exposure to
a Common Pesticide Can Damage the Developing Brain
Virginia Rauh, ScD
Professor and Deputy Director, Columbia Center for Children’s Environmental Health,
Chlorpyrifos is a broadband organophosphate
insecticide, typically used as an insecticide for agricultural purposes, but has also been employed to
control pests in residential and commercial settings. It is also registered for use on farms. This is
the same substance that was initially introduced as
a nerve gas in warfare, so it would seem reasonable
to expect that it might be harmful to human beings.
Exposure data have shown that use of this particular substance has been relatively widespread in
New York City. Figure 6 shows some of the indicators
of social and economic status in our cohort. When
we started our New York City cohort study at the end
of the 1990s, chlorpyrifos exposure was found in virtually 99% of personal and indoor air samples from
the enrolled mothers, and 70% of blood samples collected from mothers and newborns at delivery.
Diazinon, which belongs to the same class of
organophosphate pesticides and has been used for
similar purposes, was also frequently detected in this
population. It’s interesting that the exposure in this
urban setting was higher than New York State agricultural exposures, and perhaps this says something
about the prevalence of cockroaches in New York
City apartments. Maternal and newborn blood levels
were highly correlated in our sample, suggesting that
these insecticides readily crossed the placenta.
So why bother to study the adverse effects of
such chemicals? There are approximately 5,000 new
chemicals introduced in the United States each year,
and EPA estimates that perhaps a quarter of these
chemicals may be neurotoxic. These are not chemicals regulated by the Food and Drug Administration
Figure 6
(FDA), but they can be found in commonly used
household products. The developing human organism is extremely vulnerable, so children are going to
be more susceptible to the possible neurotoxic
effects of these chemicals. Epidemiologic and testing
data are key to the task of setting safety standards.
There are several possible biological pathways
by which organophosphate exposures might harm
the developing organism. The primary pathway
from a biological perspective is thought to be
cholinesterase inhibition. Recent work from animal
studies, however, suggests that some neurodevelopmental toxicity may be unrelated to this mechanism
and may occur at slightly lower levels of exposure.
This is a very important point because EPA uses
cholinesterase inhibition as the biomarker to establish safety standards. Unfortunately, the burden has
19
rested on academic communities and centers like
our own to determine whether there are dangers to
the developing brain via other pathways, and to
examine the relevant levels of exposure and effects
from these pathways.
Health Effects
There have been a number of findings to date suggesting adverse effects of chlorpyrifos exposure on
the developing child. In 2004, Dr. Robin Whyatt and
Center investigators showed that early exposure during the prenatal period to chlorpyrifos resulted in a
150-gram reduction in birth weight in the infants of
women who were highly exposed. The 200-gram
reduction in birth weight associated with active
maternal smoking in pregnancy is considered a
developmentally meaningful reduction in birth
weight, and the chlorpyrifos effect is comparable.
Importantly, the affected children appeared to be
growth restricted. This means that, rather than being
born early, these children may have completed gestation but did not grow normally. In fact, the infants in
our cohort whose mothers were highly exposed to
chlorpyrifos in utero were twice as likely to be born
below the tenth percentile in size for gestational age.
In 2001, EPA phased out and banned the sale
of chlorpyrifos for all residential and indoor use.
However, many agricultural uses are still permitted.
The residents of farming communities, and the
agricultural workers themselves, continue to be
exposed. Exposure also occurs through residues on
food. Replacement pesticides are now being used,
in particular pyrethroids and carbamates, for pest
control in homes and apartments. The long-term
Figure 7
20
effects of chlorpyrifos on children and adolescents
are still unknown.
Following EPA’s regulatory action, we found
that chlorpyrifos levels in air and blood samples
began to drop immediately. It was amazing to see
the average exposure levels drop among pregnant
women in this New York City cohort. We had direct
evidence that the levels of chlorpyrifos were
reduced in the air that was breathed as well as in
umbilical cord blood samples. Both measures
dropped precipitously over the period immediately
following the ban.
To touch upon a few of the highlights from the
Center’s pesticide research, we examined children’s
developmental progress over the first three years of
life. The Bayley Scales of Infant Development are a
broadband test of child development, and showed
significant deficits associated with high exposure.
By 36 months, children with high pesticide exposure were starting to fall off developmentally by 3 to
5 points, on average, as compared to those with low
exposure. The size of this deficit is educationally
meaningful in the early preschool years, and in fact
can push whole groups of children into the developmentally delayed category. We saw the same kind
of findings in motor and mental development.
Another worrisome finding concerned possible effects in the neurobehavioral domains. We
found evidence that a higher proportion of exposed
children were showing attention deficit problems,
as compared to those with lower exposure. These
problems included hyperactivity and impulsivity.
The nature of these attentional problems is not yet
clear, and we are continuing to follow the children
to ages when the clinical assessment of behavior
problems is more reliable. We also found evidence
that some children had developmental problems
related to socialization and self-regulation.
We have continued to follow the children over
the course of the last few years. The bulk of children
are now reaching the 5-year age range and some have
reached 9-10 years of age. Figure 7 shows the developmental trajectory. At 7 years of age we’re already finding some deficits in the areas of working memory. This
might be expected if the primary mechanism is affecting attention and self-regulation, with possible effects
on full-scale IQ measures. These types of deficits could
affect learning and school performance. We are now
working to better understand these functional and
behavioral results with new studies, including through
the use of MRI (magnetic resonance imaging) to identify possible anatomical changes in the brain that may
accompany these functional disturbances.
A Collaborative Effort to Evaluate the Impact of Integrated Pest Management
in New York City Public Housing
Daniel Kass, MSPH
Assistant Commissioner, Environmental Surveillance and Policy, New York City Department
of Health and Mental Hygiene
When we first launched this joint integrated pest
management program I am about to describe,1 we
suspected that cockroaches would be a common
problem. We now know from our own Department
of Health survey that this is true. But contrary to
urban myth, not every New Yorker is subject to the
pests. Based on our survey work, 30% of New York
City residents have cockroaches in their household
(see Figure 8). The disparities by income and race
are enormous. The same patterns of disparity are
also apparent when looking at mice. Slightly fewer
households—about 25%—report mice in their buildings. In these housing-related conditions, income
and race and ethnicity are predictive of disproportionate burden.
The same disparate patterns apply to the methods by which households try to control pests. About
one in five families in New York use aerosol products like sprays or bombs and foggers, but their use
is especially common among low-income, nonWhite populations in New York City. This is partly
due to the fact that these families receive less professional pest control, and because they have more
pests. In addition to legal, commercial pesticides
being used, people sometimes use illegal pesticides
to control pests.
City’s rental apartments and a substantial portion of
the population. If we could influence better pest
control in this type of institution, we felt that we
could pave the way for expansion across both governmental agencies and into the private sector.
Our study addressed three critical questions:
1) whether an integrated pest management (IPM)
approach was superior to traditional, pesticidebased approaches at reducing pest populations,
particularly cockroaches and mice; 2) whether IPM
was more effective at reducing residents’ own use of
hazardous pesticides; and 3) whether IPM was effective at reducing exposure to key cockroach and
mouse allergens.
This program was conducted in two neighborhoods within New York City: East Harlem, in
Manhattan; and Bushwick, in Brooklyn. Both neighborhoods have high rates of asthma, relative to
both the city’s and the nation’s average. The essential design of the study involved comparing an
intervention group of buildings to a control group
of buildings. Our intervention occurred in 13 buildings in 280 apartments.
We performed the IPM intervention in the
experimental buildings, while allowing traditional
pest control to continue in the control buildings.
Study Design
With funding from EPA and the City Council, we
established a valuable collaboration among the New
York City Housing Authority (NYCHA)’s Technical
Services Department, the Health Department, and
the Columbia Center for Children’s Environmental
Health. New York City has the largest housing
authority in North America. It is home to at least
400,000 residents, has 180,000 apartments in 340
developments, and includes 2,600 buildings. The
housing authority represents 8.3% of all of New York
1. Kass D, McKelvey W, Carlton E, Hernandez M, Chew G, Nagle S,
Garfinkel R, Clarke B, Tiven J, Espino C, Evans D. Effectiveness of
an integrated pest management intervention controlling cockroaches, mice, and allergens in New York City public housing.
Environmental Health Perspectives, 117(8): 1219-1225, 2009.
Figure 8
21
Traditional pest control as generally practiced by the
Housing Authority and private landlords often
involves a combination of professional pesticide use
and residents’ own use of chemicals. Sometimes,
traditional pest control means no pest control services at all. A combination of interviews, objective
measures of pests by trapping, residents’ self-reported sightings of pests, and tracking the frequency of
improvement or deterioration of conditions allowed
us to assess the status of residences in terms of pest
control at three points in time: baseline, three
months, and six months.
Unemployed residents within public housing
were hired to form an integrated pest management
team. We trained them and arranged for them to be
licensed by the State to be pesticide applicators. The
intervention involved very simple but labor-intensive approaches for deep cleaning, including HEPAvacuuming wall cavities (HEPA vacuums contain a
special filter that is able to trap very fine dust particles.) The goal was to reduce both pests and allergen
build-up by caulking and sealing cracks and
crevices; patching holes in walls with careful use of
gel baits, containers, and boric acid in wall cavities;
and providing safer cleaning supplies to residents
themselves. Due to our limited resources, we did
not provide extensive residential education.
Results
Baseline results showed that cockroach levels measured by the number trapped weekly were higher in
the IPM group than in the control group. At three
and six months after the intervention began, there
was a significant decline in the median weekly
trapped cockroaches in kitchens in the intervention
Figure 9
22
group, whereas we saw a pattern of growth and
then modest reduction in control apartments—
essentially little change at all (see Figure 9).
Success in our intervention was defined as
either substantially reducing within an apartment
the number of cockroaches, or staying cockroach
free over time. The IPM intervention apartments
were three times more likely to show successful
reductions in pests than control apartments. The
study also asked about residents’ own sightings of
cockroaches, to assess how people felt about the
intervention’s impact. In the IPM apartments, there
was a sharp and sustained decline of sightings at 3
and 6 months. In the control apartments, there was
no change at 3 months, and some decline at 6
months. Changes in the levels of allergens were also
evaluated in the apartments. Though the program
confined its interventions to kitchens and bathrooms, we found meaningful reductions in cockroach allergens in bedrooms. Bedrooms in IPM
apartments at 3 months had just 60% the levels of
control apartments, and 40% their levels at 6
months.
We also tracked individual’s self-reported use
of legal and illegal pesticide products. Figure 10
shows a decline in use of these products among
people who received IPM services, and very little
change in the use of such products by people in
control apartments. If people continued to have
cockroaches at the end of the intervention, they
were more likely to continue to use these products.
If we can reduce pests, we ultimately reduce the use
of hazardous products.
There are some important limitations to this
study. It employed a quasi-experimental design,
which limits the generalizability of the findings. We
did not randomize the selection of buildings, but
we tried to match them within a development.
NYCHA was more likely to visit control apartments to spray or offer to spray pesticides.
Normally, a significant proportion of residents
refuse or do not make their homes available for
these scheduled visits. Given the nature of this
study, however, it is likely the NYCHA reached a
greater proportion of control apartments than
would otherwise be expected.
Because residents within a development share a
resident association, we believe that the information
about this program was spread from experimental to
control groups, perhaps lessening the estimation of
the intervention’s impact, since the control group
may have benefited from IPM techniques too.
There were also a few important implications
of this study. This program employed a very simple
intervention, with low costs and minimal participant engagement. This intervention can be more
easily replicated and scaled than other programs
evaluated in the literature. A single visit averaging 8
to 12 person-hours can have significant impact on
pest populations, on residents’ use of pesticides,
and on the allergen levels in apartments. Although
we didn’t measure the impact of actual pesticide
exposure, I think that the studies that have happened here at CCCEH and elsewhere really do close
the loop. When both pest populations and pesticide
use decline, detrimental exposure declines too. We
hope that this kind of work ultimately leads to a
reduction in both the risk of acute poisoning events
and chronic effects from pesticide exposures.
As a result of this effort, NYCHA now has new
protocols in place. It has trained all its exterminators on IPM and routinely uses gels and containerized baits rather than spray pesticides. NYCHA
reserves the use of pyrethroids for severe circumstances and for basement spaces away from areas of
common exposure. Where possible, NYCHA has
begun to renovate its kitchens with IPM in mind;
cabinets can be ordered precaulked and their contracts for installation involve closing wall cavities,
applying boric acid before they do so, and sealing
cabinets neatly against the wall.
There have been important policy changes as a
result of our collaborative work. In December 2008,
the New York City Board of Health amended our
health code. The revised Article 151, which pertains
to pest infestations, clarifies pest control as a preventive practice and not just a responsive practice.
Where the Department of Health orders abatement,
Article 151 now prohibits pesticide pest prevention
and control without also addressing underlying
conditions that contribute to infestations. And the
Department of Health is now authorized to mandate a pest management plan where needed. We
hope that this raises the expectation of what constitutes good pest control service throughout the private sector.
There are still many things we need to do.
We’re preempted by New York State from regulating
pesticides, and we are in an unfortunate situation
in New York City. Despite significant improvements
at both the State and EPA around recognizing the
health impacts of pesticide use, there is a lack of
Figure 10
understanding about the way pesticides need to be
regulated in an urban environment. Pest control
cannot substitute for preventive maintenance.
Multi-unit dwellings require a different kind of regulatory practice, and the pest control decisions of
individuals do not just influence what happens in
that apartment but affect residents of neighboring
apartments, too. In addition, the continued availability of legal but ultimately ineffective and unsafe
pesticides is not beneficial.
I want to credit the folks at the Housing Authority—Brian
Clark, Julius Tiven, Louis Ponce, and Jamal Rashid in particular—for taking a chance on these innovations. Thanks
also to Marta Hernandez and Wendy McKelvey at the
Health Department, and Dave Evans and Ginger Chew at
Columbia University.
23
This case study focused on the health effects of early-life exposure to phthalates and bisphenol-A, two synthetic chemicals
commonly found in plastics and consumer products that interfere with the body’s endocrine system. These chemicals can
mimic or block naturally occurring hormones in the body, and thus are capable of disrupting early development. An abbreviated version of Dr. Steingraber’s remarks appear here. The full transcript is available online at www.ccceh.org/conference09.
The Health Effects of Endocrine Disruptors on the Growth
and Development of Children
Sandra Steingraber, PhD
Scholar in Residence, Division of Interdisciplinary and International Studies, Ithaca College
…. Translating the empirical evidence of a serious
systematic problem into a rational public policy has
one set of challenges when the public is aware and
familiar with the problem. It has another set of challenges when the public is largely unaware that the
problem exists, or at least is not conversant with the
scope of the problem. Nowhere in pediatric environmental health is that more true than endocrine disruption. I say this with a particular sadness, because
as an ecologist and a public scientist I’ve been
researching and writing about endocrine disruption
for 15 years, as have my esteemed colleagues.
In spite of the media attention that this work
has received and in spite of the Congressional briefings and the testimonies and town hall meetings and
grand rounds that we’ve all done, most people still
consider their hormones as a private, innate, intimate, interior part of themselves, and not a signaling mechanism, a tuning fork, that responds to messages streaming in from the environment that we
24
inhabit. Nor is it common knowledge that common
chemical contaminants at vanishingly small concentrations can interfere with natural signals controlling human development in pregnancy, infancy,
childhood, and adolescence. Chemicals used in
farming have demonstrable links to early pregnancy
loss. For example, the pesticide methoxychlor is
known to interfere with para-hormonal signals that
guide embryonic implantation in the uterus.
Let me be specific. When a woman who wants
to get pregnant and is having a tough time of it goes
to the pharmacy to purchase a home ovulation predictor kit in an attempt to increase the efficacy of
her efforts, does she, as she reaches for the box on
the shelf, think about weed control in cornfields?
She should. The weed killer Atrazine, the number
two pesticide used in the US, which is banned for
use in Europe because it is an endocrine disrupter,
is used for this purpose. It’s known to interfere with
a hormone from the pituitary to the ovary that governs ovulation. When this woman finds out that she
has endometriosis and decides to undergo laparoscopic surgery, does she ask herself as she slips
under the anesthesia, “Hmm, I wonder about the
possible connection between my painful periods
and our nation’s waste disposal practices.” She
should. Municipal waste incineration is a leading
source of dioxin, which is a chlorinated hydrocarbon that has been linked in primates to
endometriosis. If she does succeed in achieving
pregnancy only to suffer the acute and particular
grief of miscarriage, does she call her mother to talk
about agriculture? She might.
If this woman carries her pregnancy into the
third trimester only to give birth prematurely and
spends the first days of her new life as a mother praying in the neonatal intensive care unit over an incu-
bator, does she start to wonder about nail polish?
Does she ask herself whether the date of her child’s
birthday might have anything to do with our nation’s
failure to regulate endocrine disruptors in cosmetics
and personal care products? She might. Phthalates
are the latest chemical to join DDT and PCBs and the
club of chemicals with the power to shorten human
gestation. In the case of PCBs we even understand
the mechanism. PCBs can alter the way calcium flows
through uterine muscle tissue, through the calcium
channels, overriding the balance of estrogen and
progesterone that prevent taut muscle tissue from
contracting in late pregnancy. Calcium is needed for
muscular contractions. Pre-term birth is the leading
cause of disability in the United States.
If her child is a son and he’s diagnosed with a
genital malformation, un-descended testicles or
hypospadias, does the mother start to wonder
about building material specs? She could, because
phthalates are also a compound in vinyl, which is a
building material, and is known to shorten urogenital distance and be a male reproductive toxicant.
If her child is a daughter who grows up into a
fourth grader and one night is taking a bath and
looks up at her mother and says, “Mama, there’s
something hard that hurts inside my chest.” And
the mother discovers that the lump in her ten-yearold chest is a breast bud, and says, “Well, honey,
you’re just growing your breasts,” and the daughter
cries and says, “But I’m not ready for that,” does the
mother think about the world’s plastics manufacturing? She might. Bisphenol-A is a plasticizer used
to prevent polycarbonate from cracking. It’s found
in the urine of most schoolgirls at levels capable of
accelerating sexual maturation in female juvenile
rats, and early puberty is an outcome of bisphenolA exposure in mammal studies.
I am the author of a monograph on the environmental contributions to early puberty in girls
(“The Falling Age of Puberty in US Girls.”1) I spent
two years studying the neuroendocrinology of
pubertal onset, and I tried as a parent to do everything right. In spite of my work and the work of Our
Stolen Future and WE ACT and many in this room,
there is still low public awareness about the exquisite communion between our neuroendocrine system and the ecological world. There’s a huge cultural blindness because, in this culture, we see health
as an individual thing—as if we were all captains of
our own health boats—and if we do see larger forces
at work, we attribute them to genetics or to lifestyle.
The idea that the environment might be another leg
of that triangle of genetics, lifestyle, and environment is not evident to most people still.
Our public policy around endocrine disruptors
can’t wait for a public education campaign to bring
the whole populace up to speed on this and create
the cultural sea change that would be necessary to
“Our public policy around endocrine disruptors can’t wait for a
public education campaign to bring the whole populace up to
speed on this and create the cultural sea change that would be
necessary to recognize the communion between our bodies and
the environment. Policy needs to precede and serve as that
educator.”
recognize the communion between our bodies and
the environment. Policy needs to precede and serve
as that educator. In this, I think the example of secondhand smoke is a good one for us. When New York
State banned public smoking a few years ago, it
served to de-normalize tobacco smoke.
In some cases—and this is probably the most
controversial thing I say—I believe that public education in the absence of decent public policy actually
works at cross-purposes. For the past eight years,
we’ve had no real chance to make meaningful
national environmental health policy, nor even
invest in basic science. The Bush administration
worked to defund the National Children’s Study, for
example. (Happily, it failed.) Into the breach stepped
advocacy groups that tried to educate the public
about endocrine disruption. They directed their
efforts at parents, whom they addressed as shoppers
and consumers—not as citizens. Hence, toxicity
began to be seen as a choice. Nonprofit advocacy
groups provided us with websites on lead and cadmium in children’s toys. We were offered websites
on safe cosmetics. We were told how to avoid
formaldehyde in plywood and why to avoid vinyl
shower curtains. We were urged not to microwave in
plastic. Vigilant parenting replaced meaningful
chemical policy reform. That task required that
every parent become a chemical engineer and a risk
assessor. We became our own regulatory agencies.
And there was a backlash against this. Most
recently Peggy Orenstein, an otherwise very thoughtful journalist who writes for The New York Times
Sunday magazine, wrote an article called “Toxic
Paradox.” In it, she describes her reaction to being
1. Available on the Breast Cancer Fund website:
http://www.breastcancerfund.org/site/c.kwKXLdPaE/b.3266509/k.27C1/Falling_Age_of_Puberty_Main_Page.htm
25
presented with evidence of dangerous air pollution
near her child’s school. Already worn out from trying
to keep harmful pesticides and harmful toys away
from her child, her response is to kill the messenger.
Sociologist Rebecca Altman wrote a counterpoint to that essay in Environmental Health News. She
points out the plight of parents who have gone
green at home only to recognize the modest effects
of their actions for kids overall means that we have
to feverishly scan the internet for green products to
avoid headline-grabbing chemicals, only to learn
that research implicates another chemical and
another product, so that our efforts become only
partial solutions until they’re finally part of the
problem, too, because we don’t want to hear anything more about air pollution because we’ve had
it. We’ve already used up all our anxiety about this,
trying to find the right lunchbox.
I’m going to close now by talking about some
new science. And here I’m going to speak from the
perspective of a mother of two school-aged children, one a son and one a daughter. I’ll start with
phthalates, which are a male reproductive toxicant
and therefore a pediatric heath threat to my son,
Elijah, who is seven.
Phthalates provide car interiors with their
unmistakable new-car smell. You’ve all smelled
phthalates. They are an ester of 1,2-benzenedicarboxylic acid. They’re used to soften plastic, namely
a form of plastic called vinyl, which is 50% chlorine
by weight. There are many kinds of phthalates.
Those with high molecular weights are used in
vinyl. Those with lower molecular weights are an
oily substance used in perfumes and hair spray and
personal care products.
Phthalates have as their target of endocrine
disruption the testicle. They are linked to lower
sperm concentration and motility.2 Earl Gray’s lab
at EPA has looked closely at phthalates and explicated the vulnerability of the fetal male genital tract to
endocrine disruption by phthalates. Gray and his
team looked at a birth defect called hypospadias, in
which the urethra does not roll up and have its
opening at the tip of penis but rather along the
shaft somewhere.3 There’s a name called phthalate
syndrome for this combination of different kinds of
male reproductive disorders. It’s one subset of
what’s called testicular dysgenesis syndrome, which
is a frightening phrase for a mother to say.
One billion pounds of phthalates are manufactured each year. Researchers here at the
Columbia Center for Children’s Environmental
Health, as part of their Mothers and Newborns
Study in Harlem and the Bronx, persuaded very
pregnant women in the last trimester to wear a
backpack containing a personal air monitor. The
monitors measured actual levels of phthalates in
the air that women breathed during pregnancy. The
researchers found that almost 100% of these women
had phthalates in their personal air samples. Most
troubling: one form of phthalate, DEHP, was associated with shorter gestation.
Perfume use is linked to higher level of urinary metabolites of phthalates in women of reproductive age. We need to know how much phthalates
come to us from inhalation and by ingestion in
food. What we do know is that 95% of us have
phthalates in our urine.
Bisphenol-A is a plasticizer used to soften
polycarbonate. It’s used in food and beverage containers. The CDC estimates that bisphenol-A is
found in 92.6% of Americans’ urine. It’s higher in
children and teenagers than in adults. A pilot study
by Mary Wolff found bisphenol-A routinely in the
urine of six- to eight-year-old girls.4 Bisphenol-A
was first synthesized in 1891 as a pharmaceutical
estrogen, but DES, Diethylstilbestrol, was found to
be more potent so bisphenol-A was abandoned for
that purpose. It has been linked to diabetes and
obesity, and early puberty, which in turn is linked
to increased risk of breast cancer. Early puberty is
also linked to increased risk of violent victimization
during adolescence, increased risk for depression
and substance abuse, and early sexual initiation.
Bisphenol-A triggers early onset of sexual maturation in female rodents and stimulates breast development. The stimulation of breast development is
the target of bisphenol-A. In animals studies
bisphenol-A exposure in infancy makes breast tissue more sensitive to estrogens at puberty. …
2.Hauser R et al. “Altered semen quality in relation to urinary concentrations of phthalate monoester and oxidative metabolites.”
Epidemiology. 2006 Nov 17(6):682-91.
3. Wilson VS et al. “Phthalate ester-induced gubernacular lesions are associated with reduced insl3 gene expression in the fetal rat
testis.” Toxicol Lett. 2004 Feb 2:146(3):207-15.
4. Wolff MS et al. Pilot study of urinary biomarkers of phytoestrogens, phthalates, and phenols in girls. Environmental Health
Perspectives. 2007 Jan 115(1):116-21.
26
Translating Community-Based Research into Policy and Public Health Action
Peggy Shepard
Studies tell us that race, class, and income are key
determinants of health status, as well as higher
environmental and occupational exposure. Yet,
despite the fact that longevity is increasing for
many Americans, mortality and morbidity has
increased for others. One concern in addressing
expanding health disparities is that the emphasis is
not on primary prevention.
The good news is that there is a growing
awareness of community conditions for health. We
realized that the most powerful factors shaping
health and disparities are social and economic
determinants. First, we have root factors of poverty
and discrimination that play out at the community
level. Then there are community-wide environmental conditions that influence health directly
through toxins in air, water, soil, and building
materials. Indirectly, those affected by health disparities tend to live in environments without access
to nutritious food, spaces for active living, effective
transportation systems, but they have ready access
to unhealthy products like cigarettes, alcohol, and
fast foods. Combine these factors with lack of access
to quality medical services and we have a good picture of the landscape of health disparities for communities like Northern Manhattan and the South
Bronx. The results from the Center’s study here are
typical of exposures being experienced by other
environmental justice communities around New
York City and around the nation.
As a long time environmental justice advocate,
I know that race and socioeconomic status are
important risk factors locally and globally for predicting the location of noxious facilities, the levels
of exposure, health disparities, and the effects of
climate change. The dynamics of environmental
injustice have led to excess exposure to environmental hazards, community devoid of green benefits, and lack of participation in democratic decision-making that affects the lives of residents. It’s
these dynamics that have seized my attention, my
commitment and energy over the last 20 years.
When I first began organizing around these
issues in 1985, I recognized that the lack of scientific
literacy, information, and context was and continues to be a factor that contributes to the inaction of
policymakers and to the systemic exclusion of lowincome communities of color from decision making. As a result, WE ACT was founded in 1988 to
institutionalize advocacy and organizing in
Northern Manhattan, to build community power, to
improve environmental health, policy and protection in communities of color. We believe that we’re
having impact on the field through new models of
community-based environmental action, combining community organizing with policy initiatives at
the local, state and federal levels. We have helped
advance the perception and reality that it can be
beneficial to work with affected communities
whether the goal is to document environmental
exposures, intervene in housing hazards, or develop a waterfront park for active living the way we
now have at 125th Street and the Hudson.
To address some of these concerns, the environmental justice movement has raised its voice
with disempowered communities and we’ve taken
action to develop the community capacity to
become effective stewards of healthy homes and
healthy schools. We organized residents to engage
directly in the design and implementation of solutions that make sense, solutions that lead to sustainable homes and healthy schools, and schools
that we will not allow to be built on brownfield sites
with no environmental review, the situation we
now have with the City refusing to allow environmental review on leased sites.
27
So we have a moral obligation to help stop the
bad stuff, as reported in a recent New York Times article on green groups and diversity. But guess what?
When we stop the bad stuff and impact the political
will, we will bring the good stuff, too. And that paradigm has sparked the new green economy,
renewed investment in our built environment, and
catalyzed exciting new collaborations that are making a difference. By taking action, families and
advocates who supported a lead poisoning bill in
2004 helped improve the potential for many of our
“I believe we need a clear dialogue between researchers and
practitioners aimed at highlighting the role of community
conditions in shaping health disparities.”
children. Over 90% of new lead poisoning cases are
children of color living in the ten worst neighborhoods for lead poisoning risk. By taking action, WE
ACT stopped the City from reopening and tripling
the size of Manhattan’s only 24-hour marine transfer station (MTS) that would have drawn 300 diesel
trucks per day to West Harlem. “We have the lion’s
share, not the fair share,” we said, and the Mayor
heard that and he changed course in developing the
City’s solid waste plant. As a result, the City has
agreed to work with WE ACT and Community Board
9 to organize residents in a planning charette for
the community reuse of the 27,000 square foot MTS
facility in the Hudson River. That marine transfer
station will now be transferred to the Parks
Department by Department of Sanitation, and that
facility, adjacent to the new West Harlem waterfront
park, will be renovated to community use. Looking
back, if it were not for the hundreds of residents
who mobilized around the operations of the North
River Sewage Treatment Plant back in the ‘80s and
‘90s, the City would not have committed $55 million to fix the plant, to stop the odors and emissions
that were making people sick, and WE ACT might
not be here as a partner with the Children’s Center.
It was that campaign to stop odors and emissions from North River that were making kids and
families sick that led to the community demanding
health studies to understand their exposure to pollutants. It has been the air quality data on exposure and
outcomes that has led to the MTA using cleaner fuels,
hybrid technology, and diesel retrofits on all its buses.
The MTA has the largest fleet in the nation, and houses one-third of that fleet in northern Manhattan
neighborhoods. WE ACT’s 18-year campaign, “Clean
Fuel, Clean Air, Good Health,” has made a difference
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in New York City’s public health, and the data from
two Columbia centers and the help of allies like
Environmental Defense Fund and the Natural
Resources Defense Council have helped us create real
change here in this community.
Ten years ago WE ACT began a partnership with
the Children’s Center. Earlier we had begun working
with researchers like Pat Kinney and Mary Northridge
and the NIEHS Center for Health in Northern
Manhattan to engage residents in documenting exposure of students in the West Harlem community to
diesel. That collaboration yielded important data for
the community as well as four peer-reviewed published articles on air quality and the value of academic
community partnerships. It has been a rewarding
experience to educate youth as field technicians to
engage in community-based participatory research
and to co-author articles in our work.
Now, fortunately, the ten years of work with
the Children’s Center has yielded answers about
environmental exposures that community residents have wanted to know. This data has addressed
our concerns. These research findings have
empowered residents and advocates, and the partnership was chosen as one of ten Kellogg
Foundation case studies that was authored by
Meredith Minkler and published in the New York
Academy of Medicine’s “Journal of Urban Health.” It
found that carefully designed community-based
participatory research that is committed to strong
science, high level community involvement,
engagement in policy steps and activities, and the
strategic use of study findings to help impact policy
can be an important part of the broader struggle for
urban health and environmental justice. The paper
cited accomplishments like the partnership’s role in
the conversion of New York City’s bus fleet to clean
diesel, and the installation by the EPA of permanent
air monitors in Harlem and other hotspots.
With Columbia researchers, we have developed a daylong training for 60 community health
educators, and over 300 community residents have
graduated from a six-week environmental health
and justice leadership training program. We’ll continue working with our graduates in a new stakeholder collaborative supported by EPA’s CARE program that will identify, prioritize and reduce risks
in northern Manhattan communities.
During these years, WE ACT has also been
principal investigator on several NIEHS grants that
have allowed us to develop relationships with academics and to build our capacity to engage in community-based research, and advise the Center on
communication with participants and on other ethical issues. We have been able to hire staff with
advanced degrees in environmental health and science, and provide technical assistance with our
local, regional and national environmental justice
community. And we have leveraged additional
funding for our partnerships from foundations that
understand the importance of building healthy
communities with residents.
By making environmental data and research
accessible and relevant to community residents
through City-wide campaigns, such as Our Housing
is Our Health, that translate relevant findings into
practice and policy, the partnership helps ensure
that City policies related to environmental health
and indoor air quality are informed by the latest
and most relevant research. Through the campaign,
member groups around the City are linking their
organizing and advocacy work with legal strategies
across traditionally very separate fields, such as civil
rights, land use, housing, environmental and public
policy, to change policy in housing violations that
contribute to poor indoor air quality and an epidemic of respiratory disease. One campaign
achievement was getting the City’s health and housing agencies together in the same room so that they
could develop consistent guidelines for mold remediation. We developed a report on mold in housing,
“The Silent Epidemic,” with the Public Advocate’s
office, and we held state government accountable
to implementing a state mold task force that had
been legislated but never created.
Center findings have been employed in securing support from council members for passage of
Local Law 36 on pesticide notification and Local
Law 37 on Pesticide Use Reduction Act. We have
helped achieve legislative aims, such as the Diesel
Emission Reduction Act of 2006, and we’re working
to strengthen the state’s anti-idling regulations for
school buses and to hasten the use of the best alternative technology for school bus conversions, the
dirtiest vehicles on the road.
Most recently the Just Green statewide coalition that WE ACT helped to develop and convene
has facilitated a legislative initiative in the State
Senate on bisphenol-A, and we are working with
our local State Senator, Bill Perkins, who will introduce a bill on comprehensive chemical policy
reform. So these are some changes we can believe
in and get behind. “Where we live, work, play, go to
school”—you hear that a lot now. That’s the way the
environmental justice movement redefined the
environment 18 years ago. Our vision and agenda
for the coming decade places communities at the
center of dialogue, planning, action and change.
What are some of the lessons I would like to
share with you? I’ve learned that community-based
participatory research partnerships are critical to
understanding place-based exposure of families,
getting the expertise of affected residents, and for
studying cumulative risk and synergistic effects of
pollution. We need to ensure translation of research
findings to participants, and to community residents. We need to make sure that our communities
understand government regulations and mobilize
for policy reform. We need to expand the capacity
and training of low-income communities of color to
improve children’s health, and we need to develop
new partners across interdisciplinary sectors. And
we must ask ourselves how do we lay the groundwork for a movement to reduce health disparities? I
believe we need a clear dialogue between
researchers and practitioners aimed at highlighting
the role of community conditions in shaping health
disparities. We need to make houses and apartments healthy homes by examining the built environment where poverty, environmental conditions,
and poor design combine to cause or exacerbate
disease. We need to build health considerations into
land use, zoning, permitting, community design,
and other urban planning decisions that shape the
long-term nature of our built environment. And we
need to study the concept of health impact assessments being tried out in San Francisco, where the
community identifies its idea of the physical and
social characteristics of healthy neighborhoods and
then the city develops a process to incorporate
those elements as goals of the rezoning process.
We need to focus on the long view and ask
ourselves: Are we living longer, healthier lives, are
we building strong human communities, are we
handing down to our children a world that is deteriorating or a place whose natural heritage is being
revitalized? Those are key questions that represent
great challenges but also great opportunities. It has
been my pleasure and excitement to be here today
to really look at the breadth and scope of what we
have learned over the last ten years and to summarize that for you and to talk to you about how we
have been able to translate this wonderful research
into policy.
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This panel discussed viable options for reducing the effects of air pollution and climate change in urban areas like New York
City. Panelists discussed policy proposals that would target sources of air pollution that contribute to climate change and
more immediate adverse health outcomes (discussed in the cases studies), such as reducing vehicle emissions and idling.
Others suggested changes in infrastructure, such as repowering power plants with cleaner fuel alternatives and replacing
boilers in homes to utilize energy more efficiently and emit fewer pollutants in the air. Several panelists noted the disproportionate burden of adverse effects from air pollution and climate change on disadvantaged communities. In light of the big
challenge presented by urban air pollution and climate change, the panelists emphasized the need to work together to advocate for effective policy changes at the city, state, and federal levels.
Brian Lehrer, MPH, Host,
The Brian Lehrer Show,
WNYC Radio, am820, 93.9fm
It is my honor to be at this conference. This is truly a new day
in the United States for opportunities to make environmental
policy. The Obama administration knows that they have a
window of opportunity right
now. It would seem logical to
me that they try to use the
political capital that they have,
and the honeymoon period
that a new administration has, to do as much as
they can. This is the perfect time to be having this
conference to talk about the intersection of science
and policy. I’m delighted to moderate two great
panels today.
Rachel Miller MD, FAAAAI, Associate Professor
of Medicine and Environmental Health Sciences
(in Pediatrics) at New York–Presbyterian Hospital/
Columbia University Medical Center
As a lung physician I think that it’s important to
keep in mind the statistics about asthma.
Approximately nine million children have a lifetime
asthma diagnosis. We are aware that there is unfortunately a substantial disparity in susceptibility
according to socioeconomic groups, which is closely
related to ethnicity. Also keep in mind that there
were approximately 3,780 deaths from asthma in
the US in one year, which calculates to about ten
people a day who die from asthma annually.
On the brighter side, due to advances in treatment, between 1990 and 2000 asthma hospitalizations
in New York City have actually decreased by 17%, which
exceeds the 13% reduction that had been seen nationwide during this same time interval. And very fortunately, there actually has been a 35% decrease in pediatric admissions for asthma between 1997 and 2000.
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Living in areas with high volumes of traffic has
been associated with respiratory problems and
asthma in children. In particular, exposure to diesel
emissions is a big focus of our medical research.
This includes reports that higher levels of fine
ambient particulate matter, which includes diesel
exhaust emissions, has been associated with
decreased lung function among children living in
cities, including New York. Higher diesel exposure
has been associated with a greater likelihood of
developing allergies. In addition to diesel and particulate matter, other air pollutants have been associated with respiratory problems. These include
exposure to polycyclic aromatic hydrocarbons
(PAH), nitrogen dioxide, and ozone and sulfur dioxide. PAH have been associated with higher rates of
cough, wheeze, and possible asthma and ear infections in infant children. Prenatal exposure to nitrogen dioxide has been associated with impaired lung
function. Ozone and sulfur dioxide have been associated with emergency room visits for asthma.
There are many mechanisms as to why air pollution may be a problem for breathing and for the
lung. We know from a number of studies that air
pollution exposure, meaning air pollution exposure
prenatally in the womb and also shortly thereafter
when the lungs are continuing to develop, can actually affect lung development. There have been a
number of immune changes that have been associated with air pollution exposure, including effects
on our overall inflammatory response, the differentiation of some of our immune cells, and the production of some of our mediators, such as cytokine,
as well as processes related to oxidative stress. I’d
also like to mention that diesel exposure has been
associated with changes in airway remodeling,
which refers to what we think are permanent
changes in the cell structure of our lungs that diesel
pollution may induce.
There is some good news that I’d like to highlight, in which we’re able to document improve-
ments. One large study in
Switzerland documented
significant declines in ambient exposure to particulate
matter over an 11-year period between 1991 and 2002.
This was associated with
improvements in lung function. Furthermore, CCCEH
has documented reductions
in the ambient levels of PAH
from 1998 to 2006 in our
NYC cohort. In addition to
our research, we translate
our findings through
newsletters, through medical associations, and
Panelists R. Miller, J. Balbus, R. Aggarwala, M. Gelobter, and C. Corbin-Mark
through review articles so we
Diesel Emissions Reduction Act—which authorized
can get this information out to doctors and families
$500 million for putting diesel filters on existing
and parents and legislators. There’s clearly much
diesel engines. It was one of those semi-funded
more that we need to do, however.
mandates. A lot of that money wasn’t actually approJohn Balbus, MD, MPH, Chief Health Scientist,
priated, but $300 million has been appropriated in
Program Director, Environmental Defense Fund
the Stimulus Bill, and EPA has just announced grants
My comments will address the policy interventions
for localities, cities, and states to apply for diesel
that can be taken to get at this complex intersection
reductions. So that’s a way to get at all of these existof urban life, climate change, and children’s harming diesel engines that aren’t going away anytime
ful exposures to air pollution. New Yorkers as a
soon that are in the meantime spewing out a lot of
group have the smallest carbon footprint per perharmful pollution and black carbon.
son in America, yet they still breathe some of the
We’ve been hearing a lot about black carbon
most polluted air east of California. A lot of that
from a health perspective, especially its respiratory
pollution wafts in from the west from coal-fired
impacts. There are also some alarming neurodevelpower plants and industrial facilities, but a lot of a
opmental impacts that seem to be associated with
child’s exposure in the City comes from very local
black carbon, and good studies are being done out of
sources, such as school buses, trucks on the street,
the Harvard School of Public Health looking at trafhighways nearby, and building chimneys. How do
fic-associated black carbon exposures and decreased
we get at that nexus of greenhouse gas reduction
neurodevelopment. There’s also a lot of new science
and protecting children’s health from these harmful
and concern about black carbon as a greenhouse gas.
air pollutants? It’s not necessarily the easiest thing.
People are saying that black carbon is the secondObviously there’s some relatively low-hanging fruit
strongest contributor to global warming after carbon
that we have in terms of fuel efficiency and building
dioxide. It’s much shorter-lived, so it doesn’t have the
efficiency. I’m not going to talk a lot about them,
same implications long-term, but in the near term it
but reducing carbon dioxide really requires shifting
seems to have a very significant impact, and it may be
our complete transportation-energy infrastructure
a very important bridge between a carbon-based and
away from fossil fuels. That’s a big policy question.
a non-carbon-based energy system.
There’s a lot that needs to be done.
Although New Yorkers have a very small carWhat I want to do in three to five minutes is to
bon footprint in terms of CO2 per capita, we can
keep it really simple, and I’m going to boil it down to
definitely shrink the black carbon footprint. In
three letters: DPF. It stands for a diesel particulate
doing so, we not only score a big win for children’s
filter. If you place a DPF on the tailpipe of a diesel
environmental health, especially in areas that are
engine, it takes out about 90% of the diesel particuhardest hit by asthma and exposure to diesel pollulate, most of which is made out of black carbon.
tion, but we also can do a short-term, much-needThere is a bill that was passed several years ago—the
ed fix on global warming.
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There are other things that need to be done.
One of the other obvious low-hanging fruits in a city
like New York is doing away with engine idling, and
the City is taking this up, having just signed into law a
much tougher one-minute idling law. Enforcing this
law saves fuel, saves money, and saves children’s
lungs. We’re also working with New York City to try to
clean up the dirty fuels that are used in buildings. We
“We need to keep children at the center of our concerns and at
the center of our plans about climate change and air pollution.
Not only are they especially vulnerable to the harmful effects of
tailpipe and smokestack pollution, but they and their children
are going to have to live on the planet that we leave to them.”
worked for a long time to get the gasoline cleaner and
to get the sulfur content of diesel cleaner, but buildings in New York are burning some of the dirtiest
fuels. Shifting from the number 4 and 6 heating oils,
which have high pollutant content, to cleaner types of
fuels are policies that really are low-hanging fruit.
They can be done very quickly at the local level in a
city like New York, or in any city around the country.
Bigger issues require addressing our transportation system, addressing transportation efficiency, and moving toward non-motorized forms of
transportation whenever possible. These are very
important for children’s health and for reduction of
greenhouse gases.
It is a lot to do, but there are so many win-win
situations out there that are good for the economy,
good for children’s health, and good for long-term
sustainability. We really have to seize this opportunity, seize the funding mechanisms that have just been
put into place, and start acting on them. We really
need to keep children at the center of our concerns
and at the center of our plans about climate change
and air pollution. Not only are they especially vulnerable to the harmful effects of tailpipe and
smokestack pollution, but they and their children
are going to have to live on the planet that we leave
to them, so we’ve got to make that the atmosphere is
as clean as it can be both in terms of greenhouse
gases and in terms of toxic air pollutants.
Michel Gelobter, PhD, CEO, Cooler, Inc.
I have five points to discuss how we can achieve some
of these changes. First of all, I’d like to say that it’s our
time to fix this problem. We’re at an unprecedented
moment of debt accumulation, as we’re all aware,
unfortunately. The bailout is likely to leave each and
every American with a $75,000 debt. It’s better than
Iceland, where they have a million dollar per capita
32
debt, but it’s huge. At the level of climate, we each emit
12 times more than we should. In this country, we
should be able to have a sustainable, stable atmosphere
and climate. We’re at a moment when it has become
clear that we’ve been managing our resources completely unsustainably, borrowing from the future, and
continuing to do so to dig ourselves out of the economic and environmental holes we’ve dug ourselves into.
I’m sure people at this conference are aware that fossil
fuels are like cigarettes or tobacco for the planet as a
whole. They take money out of our communities, they
pollute our environment, they lead to all the impacts
and effects on children’s health, and they waste our
lives and our resources. The first point is that this is the
time to act on the kinds of things we’re talking about at
this conference, and we have a grave responsibility
that’s tied to the crisis in our country today.
The second is that there is a tremendous
opportunity in working on climate change because
it’s one of the few issues where there’s almost a
complete confluence between justice and efficiency.
Climate change is a problem of justice, inter- and
intragenerationally. Some people have used more of
the atmosphere than they had a right to, than was
sustainable, and are precluding the use of that
atmosphere and those resources for others, have
precluded it, and will continue to do unless we take
action. So it’s clearly a justice problem.
But the second point is if you solve it by sort of
handing a lot of capital to the polluters—for example, giving permits to polluters in a cap and trade
system—I call it paying the pusher for the cure.
That’s not an efficient solution. It’s one that wastes
capital and it’s one in which there will be tremendous credit default swaps, which will not work. The
right way to do it is to make us all owners of the
solution, make us all owners of the capital we have
to invest to move away from fossil fuels, and make
us all owners of the right to emit by charging polluters, making them pay, and making sure that the
resources we get from those charges go back to our
communities in ways that help us transition to a
clean energy future.
The fourth point is not to let them make us
own the problem. A lot of us in this field believe it’s
going to be so difficult. That’s true—it will be hard
for those of us who are activists. But the world we
want and the world we’re headed toward will be
much better. Let’s take, for example, the war in
Iraq, which was about oil. It’s estimated that that
war will have cost $3.5 trillion. What’s $3.5 trillion?
$3.5 trillion equates to a $100,000 piece of land with
a $250,000 home on it, $60,000 worth of furniture,
and a $40,000 car in the garage for each and every
person in the State of New York. Having spent that,
there would still be enough money left to build 250
libraries at a cost of $10 million, and 500 schools at
a cost of $20 million apiece. The rest of the money
could be placed in an interest-bearing account to
fund 10,000 teachers, 10,000 librarians, and 10,000
nurses at an annual salary of $65,000 apiece, and
still we’d have enough money left to pay each and
every resident in the State of New York $8,500 a
year, not just this year, but forever. That’s $3.5 trillion. So the next time someone tells you that where
we’re headed is hard, you tell them about how hard
what we’re doing today is.
And finally, the last point is to hold hands. The
solution really is a battle between a 90-minute commute in a car to a tract home, and walking. Those of
you who live in New York get to do this every day,
walking to school with your kids, five fingers in
your fingers, or linking arms with your partner as
you walk to and from work. It’s about community,
and it’s about the five fingers on your hands.
Rohit Aggarwala, PhD, Director, Office of Long-Term
Planning and Sustainability, Mayor’s Office of
Operations, City of New York
I have two broader issues I’d like to discuss. One is to
build on something John said about the low-hanging
fruit. I think one of the things we all have to bear in
mind is that the low-hanging fruit is still pretty high
up, and it requires a certain amount of work to get.
And as Michel said, the real challenge here is going
after the areas where solutions can clean the air, can
promote justice, can protect the planet, and can also
pay for themselves and save us money.
The remarkable thing is how many of those
opportunities we as a society, as a nation, as a City,
leave on the table because organizing ourselves to
get there, even when the economics makes sense,
can be very difficult. Here are a couple of examples.
One is in power plants. We are committed to exploring and bringing large amounts of renewable energy
to the City, but we do know that’s some time away.
There are shorter-term opportunities that involve
fossil fuels, but involve far less fossil fuels than we
currently have. And yet we face, both within the City
and due to the regulatory structure that the State
imposes, tremendous obstacles to things such as the
repowering of power plants where you can replace a
natural gas turbine that’s 30 years old, install a new
one, get more power out of it, have half as much
carbon emissions, half as much natural gas consumption, and 90% less criteria pollutants emitted
from that power plant. The economics makes sense
if you look at it in one way, but when you take into
account the way electricity prices are set, you’ve got
to get a number of people aligned in order to make
those opportunities a reality for the City.
And yet opportunities can be very powerful.
We did our carbon inventory for New York City and
looked at the years from 2005 to 2007. The singlelargest improvement in our carbon footprint was
the opening of the new power plant in Astoria. It’s
surprising to think that a big 500-megawatt fossil
fuel power plant contributed a 5% reduction in New
York City’s entire carbon footprint. But it’s true
because it pushed obsolete, less-efficient power supplies out of our supply stack.
We also know that there are huge opportunities to make our buildings more efficient. By changing light bulbs, insulating pipes, fine tuning boilers,
and doing things that may not require much in the
way of capital investment, individuals could get a 5%
reduction in energy consumption, 5% less pollution
in the air, and reduce the amount of electricity we
consume. Overall, these simple changes can lead to
a reduction in fossil fuels. Yet we still have tremendous barriers in the way leases are structured, in the
way our incentives are organized, in the way our tax
code is organized, and in the way we do not require
these things citywide to achieving them.
I think one of the things I have learned in the
past two or three years now is that we have to think
about this differently. I think some of the opportunities that we’ve been exploring, with the
Environmental Defense Fund and with WE ACT and
with others, show that we are now more comfortable with the idea of pushing people to places they
ought to go. I also think as a City, we are focused
most on those places that save us money, clean the
air, and reduce carbon to start.
Cecil D. Corbin-Mark, MPhil, Deputy Director,
WE ACT for Environmental Justice
Just for basics, how are air pollution and climate
change linked, and how does that connect to our
public health? In terms of climate change, the sun
heats the Earth, and two-thirds of that heat gets
absorbed in the Earth and the remainder returns to
the atmosphere. The greenhouse gas effect is a
result of our production systems, transportation
systems, and our energy systems. These systems are
putting gases into the air that essentially trap more
of that heat than the planet was designed to contain. Some of those gases are produced by things
like diesel buses that burn diesel fuel and put car-
33
bon into the air, or power plants that may be in
your neighborhoods that also put fossil fuels into
the air. In terms of climate, we’re seeing some
impacts like heat waves and impacts that are causing more respiratory illnesses.
For more than a decade now, we’ve been in a
partnership with the CCCEH and other research
“Even in rich countries like the United States it’s the poorest and
the most vulnerable communities that will ultimately feel the
harshest effects of climate change, or are feeling them already.
In Northern Manhattan, we are looking for policies that will
recognize that we already have particular health burdens, and
that we need to be able to put those health burdens into the
climate change policy framework.”
centers at Columbia. CCCEH research findings have
shown that the abundance of diesel pollution in
Northern Manhattan and the South Bronx is directly
linked to decreasing circumference of heads of the
babies in our communities, lower birth weight, and
early onset of asthma and other types of respiratory
illnesses. This is not a surprise to many of the residents that we organized with. We know that our
communities are more polluted and are more
adversely impacted with health outcomes, including
asthma and low birth weight. We also know that
these health outcomes contribute to other types of
social problems, including poor performance in
schools.
WE ACT has taken up the challenge of figuring
out how to take those scientific research findings that
we’ve done in partnership with residents in the community and with our research team, and translate
them into policies that create changes that bring
about a cleaner environment and reduce some of the
negative impacts of climate change. We’ve taken some
of those findings and created policy vehicles like the
Environmental Justice Leadership Forum, which is
composed of 30-plus organizations across the United
States, and across 16 states and the District of
Columbia. Through that forum, we are trying to
impact the national debate on climate policy.
What are we looking for in terms of the outcomes of that policy debate? We’re looking to have
policies that place public health at the center of the
climate change debate. Why? Because we know that
even in rich countries like the United States it’s the
poorest and the most vulnerable communities that
will ultimately feel the harshest effects of climate
34
change, or are feeling them already. In Northern
Manhattan, we are looking for policies that will recognize that we already have particular health burdens, and that we need to be able to put those health
burdens into the climate change policy framework.
At the state level, we’re also looking at the
Regional Greenhouse Gas Initiative, which is a compact made up of the 11 northeastern states. It creates
a system where they’re trading pollutants. They have
had two auctions already. We’re looking at the revenue that is being generated in that process, which
could help address some of the public health issues
in communities that we know are on the forefront
line of climate change. We’re also looking at creating
resources that will help convert boilers in our community, because we know that the boilers in our
buildings burn some of the dirtiest fuel. And lastly,
on the city level, we have been working with PlaNYC
2030 to look at how we can generate a public health
discussion about climate change. We are placing
some of our communities at the forefront of the initiatives that the Mayor’s office has developed, along
with the advisory body on PlaNYC 2030.
I’d like to raise the issue of climate policy and
public health. In the focus on climate change, we’ve
actually lost sight of the fact that we have significant
laws in place to help deal with criteria pollutants.
Those are pollutants like PM2.5 that come from the
combustion of things like diesel. One of the things that
has happened is we’ve lost sight of regulating those
particular pollutants. We believe that before we get
thrust into a climate change policy that is only focused
on carbon, we need to recognize that there are co-pollutants in our communities that make us equally as ill.
These are the things that need to be linked in the long
run for us.
I think Michel was right when he said we have a
historical opportunity to deal with this challenge
before us. Dr. Martin Luther King talked about the
urgency of now. The other thing that he said shortly
after that was not to allow ourselves to be tranquilized
by the pill of gradualism. I believe that if we don’t seek
bold solutions with regards to this, if we don’t take the
policy findings that are coming out of the Center and
the community-based research approach that we do
and really translate them into bold issues that put
public health at the center of climate change, reduce
urban air pollution, and recognize that some communities are more vulnerable than others, we will be
doomed to the pill of gradualism.
Panel 2: Healthy Homes—Regulating Residential Pesticides and Consumer Products
This roundtable considered how best to ensure that the public is protected from toxic chemicals like phthalates and BPA in
the home and in common consumer products. A common refrain was the ineffectiveness of the current Toxic Substances
Control Act, and the need for comprehensive legislative reform at the federal level. According to the US Government
Accountability Office (GAO), fewer than 200 chemicals out of the 82,000 on the market have been required to be tested
under the current law, and EPA has assessed fewer than 2% of the chemicals that are in its inventory.
There was strong support for the proposed Kid-Safe Chemicals Act, introduced in the previous Congress, because it
includes a range of systematic reforms instead of relying on a chemical-by-chemical approach to regulation. Panelists
underscored the need to reverse the burden of proof so that the chemical industry is responsible for establishing the safety
of their chemicals, rather than requiring the public sector to prove that each new chemical causes harm before it is regulated. Panelists suggested requiring labeling of chemicals like phthalates and other endocrine disruptors in consumer products
so individuals can make informed decisions in the absence of other restrictions. Regardless of the policy solutions implemented, there is an ongoing need to promote safe substitutes when a chemical is removed from the market. They also noted
that, with a new presidential administration, environmental health policy is now at a critical crossroads.
Jay Feldman, MS, Executive Director,
Beyond Pesticides
My thesis today is that, as a result of what we’ve
heard here today and what the scientific literature
supports, we need to shatter the conventional wisdom that drives pesticide policy—that toxic pesticides are necessary to our quality of life, food production, public health and environmental management. We’re sort of in between the age of risk
assessment and the precautionary principle. We
need to move with some urgency to the transformation of public policy toward precaution. Today
we’re looking at pesticide policies that are driven by
risk assessments, despite the fact that there are
known uncertainties associated with risk assessments. We don’t know much about mixtures, we
don’t know much about inert ingredients or
endocrine disruptors, as you heard. We don’t know
much about the inverse dose response curve. We
assume that dose makes the poison. We do very little under risk assessment to look at the disproportionate effects on people of color and those with
elevated risk factors. We’re not looking at low dose
or sub-lethal effects.
Policymakers continue to advance changes in
risk assessment. Improving a bad situation, however,
does not achieve the environmental public health
goals that we hear about from people who are living
in communities at risk. Consider the disproportionate risk of kids in New York City. African-American
inner city children suffer elevated asthmatic conditions caused or triggered by pesticide products that
meet the current health-based risk assessment standards. African-Americans are four to six times more
likely than whites to die from asthma. Therefore any
time our policies allow regulators to permit uses of
Panelists E. Olson, G. Solomon, R. Whyatt, P. Landrigan, and J. Feldman
pesticides with known asthma or respiratory effects,
our policies essentially impact the African-American
community disproportionately.
Noted English epidemiologist Austin Bradford
Hill actually got us to start thinking about the precautionary principle back in the ’60s when he said,
“All scientific work is incomplete. Whether it is observational or experimental, all scientific work is liable
to be upset or modified by advancing knowledge.
That does not confer upon us a freedom to ignore
the knowledge we already have or to postpone the
action that appears to be demanded at a given time.”
This same conclusion was reached in the recent book
written by Philip Shabecoff, former New York Times
reporter, and Alice Shabecoff, Poison Profits—The Toxic
Assault on Our Children, in which the authors refer to
the industry and its co-conspirator EPA—that’s the
authors’ characterization—that their actions amount
to crimes against children. Too often we let our sense
of what is possible politically cloud our sense of what
is scientifically appropriate or really necessary.
35
Now we’ll hear a lot on this panel perhaps, and
have heard somewhat throughout this conference,
about health-based standards, but the underlying
risk assessments that those standards are based on
still drive the use of unnecessary toxic substances.
And this is where I transition to alternative practices. We heard earlier from the city health officials
and others who talked about IPM, integrated pest
management. As a policy we have to look into how
it is put into action. But these ideas embrace caution—that in the face of inadequate knowledge we
need to prevent use and advance precaution.
“Risk assessment without safer substitutes is bad policy
in the 21st century.”
EPA has something they call the Pesticide
Stewardship Program. It’s a grant program that
works with the users of pesticides. In that program,
the agency is advancing this concept of risk mitigation, or reducing risk. In contrast, policies like the
one in New York City, or San Francisco’s precautionary risk policy, or the pesticide-free parks policy in
Wichita, Kansas, or the Washington, DC policy that
stopped the spraying for West Nile Virus because of
elevated asthma rates in the city—all of these policies
are essentially embracing the notion of precaution.
So what policies should we be looking at in
terms of models? The model that I look to is the
Organic Foods Production Act, which is a law I
helped write. It’s aimed at avoiding the vulnerabilities that lead to pest problems, proper fertilization,
inter-cropping, rotations, establishing acceptable
materials, biological controls, pheromones, traps,
and ensuring certification, enforcement and democratic decision making. This can be applied to home
use products as well in the context of IPM, defining
practices and acceptable least-toxic chemicals to be
used only as a last resort.
How do I know this can be done? Because I’m
working with people in the private sector that are
actually doing it. In public housing projects in
Gary, Indiana, and Portsmouth, Virginia, they have
done the same thing that we’re told is being done
in New York, which is to reduce pesticide use and
create a higher percentage of pest-free units—
going from 6% in Portsmouth, Virginia, to 80%
after the adoption of an integrated pest—management program.
Here’s my bottom line: we’re seeing around
the country and in Europe the adoption of policies
that link the availability of safer alternatives to the
cancellation of pesticides. The striking absence of
36
this link, knowing that alternatives are available, in
the Kid-Safe Chemicals Act, which we’ll talk about
later, is troubling to me. Risk assessment without
safer substitutes is bad policy in the 21st century.
Finally, we must join together to effect a transformation at this historic time. Science can and should
inform this transformation and drive home the
urgency of embracing green practices.
Philip Landrigan, MD, MSc, Director of the
Children’s Environmental Health Center,
Mount Sinai School of Medicine
Knowing all that we know about pesticides, what
are the strategies that we as a society can adopt to
reduce exposures? I tend to think that control of a
toxic exposure such as pesticides ought to proceed
on three levels. There are steps that need to be
taken at the national level having to do with pesticide registration standard setting; there are steps
that need to be taken at the state or the city level;
and there are steps that people can take in their
own homes, pursuing the maxim that a parent is
the CEO in their own home and there are things
they can do, sometimes alone, sometimes in partnership with city and national authorities.
In that last vein about control of pesticides at
the most local level, in the home, I’d like to tell you
about something we did a few years ago a couple of
miles from here in East Harlem. We basically
undertook a very rigorous evaluation in the East
Harlem community to see if integrated pest management could be successful in a mostly poor, 90%
minority community. We partnered with two
neighborhood health centers that are about ten
blocks apart in East Harlem. We introduced IPM to
the parents who were attending one, and a very
vigorous fire-safety and accident-prevention program to parents in the other. After a year we introduced everything to everyone. For the first year we
followed the two groups of parents to see whether
IPM could make a difference. When a mom who
was pregnant came in to the clinic for her prenatal
care we offered to provide her IPM. If she agreed
we sent a handyperson out to the home to teach
the mom and the family about how to clean up
food residues. The person also spent a couple of
hours closing cracks and crevices in the apartment,
the portals through which the cockroaches entered
the apartment.
We evaluated levels of pesticides in the homes
that participated in the IPM program and compared
them to levels of pesticides in the homes that
received conventional pesticide spraying. We also
engaged in the wonderfully salubrious exercise of
conducting roach censuses, which we did by taking
a sticky pad about the size of this piece of paper and
sticking it under the sink once a month for 24 hours
and actually doing a body count and seeing how
many roaches accumulated.
We found three things. First, the homes that
swore off chemical pesticides and went to integrated pest management decreased their indoor contamination by chemical pesticides by 90%. Second,
in homes that went to IPM there was a 50% reduction in the numbers of roaches as actually counted
compared to the homes that used traditional pest
control, which had no reduction in roach counts. I
think all the traditional pesticides do is chase the
roaches from one apartment to another. It’s like the
coming and going of the tide. Finally, there was virtually no cost difference between the two. There
was a one-time $25 cost per unit to bring the
handyperson in to do the repairs, and then after
that the costs were equal. So it works. It’s doable. It
was the model that the City adopted when they
embarked on the larger program that Dan Kass presented this morning. It’s something that I commend
to you and wish you well with.
Robin Whyatt, DrPH, Professor and Deputy Director,
Columbia Center for Children’s Environmental Health,
Mailman School of Public Health
Phthalates are ubiquitous, and virtually everybody
in the United States is exposed daily to multiple
phthalates. They’re used as plasticizers to make
plastic soft. They’re also very sticky chemicals so
they’re used to hold scent and are in all kinds of
scented products. There are phthalates in virtually
all perfumes. They’re used in time-released pills, in
pesticide formulations, household cleaners, nail
polish, hairspray, air fresheners, tablecloths, floor
tiles, shower curtains, raincoats, baby pants, upholstery in both home and car, synthetic leather, floor
files, food wraps, raincoats, carpets, and that’s just
to name a few sources. So you can see why we all
have so much exposure to them.
So what are we going to do about it? Well,
first there’s some good news. In August 2008,
Congress passed the Product Safety Improvement
Act that banned six phthalates from children’s toys
(defined as toys for children ages birth through 12
years). There has also been a lot of state action
taken and recently proposed. Industries in the
United States have also taken steps to remove
phthalates from products. SC Johnson recently
announced that they would remove phthalates
from their fragrance products and, equally exciting to me, they also said that they were going to
start listing the ingredients on their air care and
home cleaning products. Phthalates are not listed
in any products at this point. That’s true of most of
the endocrine disruptors.
Despite this good news, we have a long way to
go. First, the ban that was just passed on children’s
toys does nothing about exposures during pregnancy, a window of major susceptibility. Regulation of
phthalates in the United States is a real mishmash,
with multiple agencies and very little coordination
among them. The FDA is responsible for regulation
of phthalates in cosmetics and also in medications
with time-release properties. EPA regulates phthalates in pesticides. The Consumer Product Safety
Commission is responsible for regulating phthalates
in children’s toys and in other consumer products.
And while there are alternatives to phthalates,
there are enormous data gaps. That brings me to my
two solutions. First, we need to amend the Toxic
Substances Control Act. I think that’s desperately
needed and overdue. I think we should make it comparable to the European Union (EU) Registration,
Evaluation, Authorisation and Restriction of
Chemicals (REACH) regulation. In fact, most of the
companies that are selling products in the United
States are also selling them in the European market.
One of the reasons that the US ban on phthalates in
toys was successful was because the companies that
were affected had already removed the phthalates
from these toys because a ban had already been
passed in Europe.
These are global markets that affect each
other, so I think the two statutes should be comparable. REACH is an EU regulatory initiative on
chemicals and their safe use. It is based on the precautionary principle, and shifts the burden away
from requiring regulatory agencies to make the
case that a compound is harmful in order to
remove it from the market. Instead, it requires the
industries to make the case that the compound is
safe as a condition of registration. It also requires
testing of chemicals. REACH is only addressing
high-production chemicals. But it’s still an enormous step forward.
Second, we need to require labeling of ingredients on consumer products. At this point, if you
want to avoid phthalates in products, there’s no way
for you to tell whether a shampoo, hair spray, soap
or other product that you’re picking up off the shelf
contains phthalates as part of the ingredients.
37
Gina Solomon, MD, MPH, Senior Scientist,
Natural Resources Defense Council (NRDC)
It’s interesting and challenging to pull together the
threads of discussion today and to bring the science
out into the public policy arena. Jay Feldman talked
about exposure reduction, and the importance of
reducing exposure before all the scientific evidence
is complete. That was done in California in 2005
when research came out of Sweden showing PBDE
(polybrominated diphenyl ether) flame retardants
“The ultimate solution isn’t just a chemical-by-chemical
approach, and it’s not an approach that focuses on targeting
companies and doing consumer product campaigns. It’s an
approach that changes the whole system that governs the
way that chemical policy is put together at the federal level
in this country.”
in breast milk. Studies from the US, including from
California, soon followed, showing that these chemicals increased logarithmically over time. A dramatic
increase means that, whether or not there are health
effects right now, at some point there will be a problem. Concern was compounded by the fact that
these chemicals looked structurally very much like
PCBs. So there was legislation passed to ban PBDEs
in California. That was a good decision, since newer
science has confirmed the toxicity of the PBDEs.
That legislative success was followed the next
year by the realization that, well, okay, that’s great,
we pat ourselves on the back, but now what? What
chemicals are coming out to replace these chemicals? What chemicals are being added to consumer
products instead? This is something that policy
advocates in environmental health have faced for
many years. We call the problem “whack a mole”—
when you finally club some toxic chemical down,
something else pops up to replace it. That was the
impetus for the creation of the California
Biomonitoring Program, which has focused on trying to identify new emerging contaminants. It
focused initially on emerging flame retardants,
which include chemicals like tetrabromo-bisphenol-A and chlorinated tris, which was banned for
use in children’s sleepwear in the 1970s because it is
carcinogenic. Tris was only banned in sleepwear,
and now is turning up in sofa cushions and all kinds
of other things. Monitoring and detecting chemicals
in the environment and in people can be an important trigger for action.
It was fabulous to get phthalates out of chil-
38
dren’s toys, and that legislation moved initially from
the city of San Francisco to statewide California in a
bill sponsored by the Breast Cancer Fund, to a federal bill. But what’s replacing the phthalates in toys?
We need to stay ahead of the curve. Policy
approaches that can support science, by moving
biomonitoring ahead and better understanding
chemical toxicity, are good approaches.
There’s a third approach that’s been used quite
a lot in public policy: consumer campaigns to educate the public about alternatives. Robin mentioned
some of NRDC’s work on air fresheners. We were
trying to figure out where all these phthalates in
people were coming from. Since we knew that
phthalates are in fragrances, we decided to take a
look at air fresheners, and yes, we found phthalates.
And yes, some change has happened as a result.
Walgreen’s immediately pledged to take phthalates
out of their air fresheners. SC Johnson recently followed suit. But that kind of approach has problems
because there are still plenty of air fresheners on the
market that have phthalates. Most don’t list their
ingredients. Air fresheners are one source of phthalates but there’s still a panoply of other sources. If we
have to go hunting under every rock, just looking
blindly for the sources of exposure, it’s going to take
us way too long to protect families and kids.
The ultimate solution isn’t just a chemical-bychemical approach, and it’s not an approach that
focuses on targeting companies and doing consumer product campaigns. It’s an approach that
changes the whole system that governs the way that
chemical policy is put together at the federal level
in this country. True reform gives people the information they need to protect themselves, but also
phases out bad actor chemicals and improves the
way chemicals are assessed so that there is no
longer the need to gather huge amounts of information before any action can be taken. Real chemical policy reform may be just around the corner,
and scientists should support it.
Erik Olson, Director of Chemical and Food Safety
Programs, The Pew Charitable Trusts
Someone earlier said that this has been a historic
conference, and I have to agree with that. I think
that no one who listened to Lisa Jackson or Linda
Birnbaum today could fail to be impressed with
how much the leadership of the country has
changed and how important it is to have senior government officials talking about the issues in a way
that indicates that they are going to listen to the science. It’s really impressive to hear them make com-
mitments about moving forward with the toxicchemical policy agenda.
I believe we’ve actually made some significant
progress. But what we have not made progress on,
or as much progress as we need to, is on this huge
mountain of evidence that’s been accumulating.
The research that we saw presented this morning is
really compelling. It’s very rare that you see an
intervention, a policy intervention, tracked, and
you see direct, immediate impacts from that. That’s
what I think that Dursban (chlorpyrifos) study
showed, and that’s why I quote it so often when I’m
up on the Hill. It’s very similar to what happened
when we phased out lead in gasoline, where you
saw almost immediate benefits in terms of blood
lead levels. Here you see almost immediate benefits
to the pregnant women and to their children who
no longer were being exposed to this chemical.
That is compelling stuff, and I think we really need
to be supporting that kind of research because it
feeds into the policy arena very effectively, and it’s
hard to deny that it’s important.
So that’s the good side of the story. I want to
talk about the bad side of the story, and how bad
our toxic chemical policy is just briefly. For those of
you who are interested in this I would commend to
your attention a couple of GAO (Government
Accountability Office) reports that were done in the
last couple of years. They provide information
about the 1976 law called the Toxic Substances
Control Act, or what our former colleague Al
Meyerhoff used to call the Toxic Chemical
Conversation Act, because it only required ongoing
conversations and no action. That law has essentially been a failure. What we know is that there are
now 82,000, plus or minus, chemicals in commerce. Guess how many of those EPA has been able
to regulate under the Toxic Substances Control Act?
Five out of 82,000. This is according to GAO. The
last one that was regulated under that act was in
1990—19 years ago, according to GAO. Fewer than
200 chemicals out of 82,000 have been required to
be tested under this law, according to GAO. EPA has
assessed fewer than 2% of the chemicals that are in
the inventory. Even if you look at the most highly
produced chemicals, the high-production-volume
chemicals of which over a million pounds are made
a year, according to GAO, 7% have even the six basic
toxicity studies, so 93% do not. Now maybe that’s
changed slightly in the last couple of years, but the
bottom line is that we don’t know much about the
chemicals that are in virtually everything in this
room, that we’re all being exposed to and our kids
are being exposed to, almost every day.
This highlights the need for comprehensive
reform of the Toxic Substances Control Act. We
need to be able to take effective regulatory action.
First, we need a systematic review of all new and
existing chemicals. We can’t grandfather existing
chemicals, which the previous law did. Secondly, we
need to look at the entire spectrum of health
effects. We need to look at cancer, developmental
effects, immunotoxicity, endocrine effects, and so
on. We can’t limit ourselves just to one or two
effects. Third, we absolutely have to have a standard
that protects children and vulnerable populations.
We’ve learned from the Food Quality Protection Act,
a law passed in 1996, that when you have a relatively
tough standard, if there are people willing to sue
EPA and be watchdogs on it, you can actually make
progress. And that’s what happened. Dursban
(chlorpyrifos) didn’t magically disappear; it took
very difficult and sustained work and a tough standard in the law. Fourth, we need to reverse the burden of proof so that the chemical industry is
responsible for proving the safety of their chemicals. Fifth, we need to make sure that public health
effects data is made public, that there is a right to
know in the public, and that this information is
“We need to reverse the burden of proof so that the chemical
industry is responsible for proving the safety of their chemicals.”
shared and not claimed as confidential. Lastly, we
need to improve our exposure information. We
need to have more biomonitoring data and an
effective program that ensures that we know what
our children are being exposed to, and what we are
all being exposed to.
I think all of those components are in the KidSafe Chemicals Act, which was introduced in the
previous Congress by Congressman Waxman and
Congresswoman Solis, who’s now in our Cabinet,
and by Senator Lautenberg and Senator Boxer and
others, that I hope will be improved and reintroduced in not too long a period. I think that’s the
kind of reform we’re going to need. It’s not going to
be enacted this week or next month, but it’s the
kind of reform we have to seriously discuss. I think
we actually have to go beyond where Europe is at
this point and reach for the stars.
39
Speakers and Panelists
Rohit T. Aggarwala, PhD is Director of the
New York City Mayor’s Office of Long-Term
Planning and Sustainability. This office was
charged with the creation of PlaNYC: A
Greener, Greater New York, a comprehensive
sustainability plan consisting of 127 separate
initiatives to green New York City. Dr.
Aggarwala is now charged with implementing the plan and supporting other efforts
related to the sustainability of New York City.
Under his leadership the City has begun
implementing over 90% of the 127 initiatives
in PlaNYC, including regulations to make the
City’s taxicabs and black car fleets clean,
planting a million trees throughout the five
boroughs and overseeing the investment of
$80 million a year to reduce City government’s greenhouse gas. A native of
Manhattan, NY, Dr. Aggarwala holds BA,
MBA, and PhD degrees from Columbia
University, as well as a master’s from Queens
University in Ontario. Prior to joining the
Bloomberg administration for the City,
Aggarwala was a management consultant at
McKinsey & Company. During the Clinton
Administration, he worked at the Federal
Railroad Administration.
John M. Balbus, MD, MPH is the Chief Health
Scientist for Environmental Defense Fund
(EDF). He has authored studies and lectures
on global climate change and health, transportation-related air pollution, the toxic
effects of chemicals, and regulatory
approaches to protecting susceptible subpopulations. Recent publications include the
Climate Change Science Program’s Synthesis
and Assessment Product 4.6, for which he
was a chapter co-author, and the EDF Report
“Are We Ready? Preparing for the Public
Health Challenges of Climate Change.” Dr.
Balbus is a member of the EPA Science
Advisory Board, the National Research
Council’s Board on Environmental Studies
and Toxicology and the EPA Children’s Health
Protection Advisory Committee. He received
his AB degree in Biochemistry from Harvard
University, his MD from the University of
Pennsylvania, and his MPH from the Johns
Hopkins School of Public Health.
Linda S. Birnbaum, PhD, DABT, ATS, is
Director of the NIEHS and the National
Toxicology Program (NTP). Prior to her
appointment as NIEHS Director, Dr.
Birnbaum was a senior advisor at the
Environmental Protection Agency (EPA),
where she has served for 16 years as director
of the Experimental Toxicology Division. She
is a board certified toxicologist and has
served as a federal scientist for nearly 29
years—the first 10 of those at NIEHS — first as
a senior staff fellow at the NTP, then as a
principal investigator and research microbiologist, and finally as a group leader for the
Institute’s Chemical Disposition Group. The
40
author of more than 600 peer-reviewed
publications, book chapters, abstracts and
reports, Dr. Birnbaum’s research focuses on
the pharmacokinetic behavior of environmental chemicals; mechanisms of actions of
toxicants, including endocrine disruption;
and linking of real-world exposures to
effects. She is also an adjunct professor in
the School of Public Health, the Toxicology
Curriculum, and the Department of
Environmental Sciences and Engineering at
the University of North Carolina, Chapel
Hill, as well as in the Integrated Toxicology
Program at Duke University. Dr. Birnbaum
earned her MS and PhD in microbiology
from the University of Illinois, Urbana.
Cecil D. Corbin-Mark, MPhil, is the Deputy
Director of WE ACT for Environmental Justice.
He is the former Vice-President of his neighborhood association, and the former Chair of
the Landmarks Preservation Committee of his
Community Planning Board. Mr. Corbin-Mark
either currently sits on, or has in the past served
on, the following environmental boards, coalitions and committees: New York Jobs with
Justice, Center for Environmental Health,
Urban Wet Weather FACA for the EPA, the New
York State DEC Urban Air Toxic Committee,
New York State Cumulative Risk Assessment
Work Group, New York City DEP Water Quality
Citizen Advisory Committee, Manhattan Solid
Waste Advisory Board, Clean Air Network,
Association for Clean Water Action, Clean
Products/Clean Production Network,
Environmental Justice Fund, Organization of
Waterfront Neighborhoods, the NYC
Environmental Education Advisory Council. He
is also a member of the Steering Committee for
the Northeast Environmental Justice Network.
He received his undergraduate degree in political science at Hunter College, CUNY, and his
graduate degree in political science at Oxford
University in the United Kingdom.
Jay Feldman, MS, Executive Director of
Beyond Pesticides, is a cofounder of the
organization and has served as its director
since 1981. Mr. Feldman has helped to build
Beyond Pesticides’ capacity to assist local
groups and impact on national pesticide and
alternatives policy. He has tracked specific
chemical effects, regulatory actions, pesticide
law, and safe pest management. Publications
include numerous Beyond Pesticides’ publications, including Taking Toxics Out of Health
Care, Ending Toxic Dependency, Safer Schools, The
Schooling of State Pesticide Laws, Pole Pollution,
Poison Poles, Voices for Pesticide Reform, A Failure
to Protect, Safety at Home, and Unnecessary Risks,
and numerous articles on pesticides and
schools, food safety and agriculture, farmworker protection, landscape management,
children and related issues. Mr. Feldman
provides testimony regularly before the US
Congress. He is the author of the School
Environment Protection Act; co-author,
Organic Farming Act, and contributor to the
Organic Foods Production Act. He has a master’s in Urban and Regional Planning from
Virginia Polytechnic Institute and a BA from
Grinnell College.
Linda P. Fried, MD, MPH, Dean and DeLamar
Professor of the Mailman School of Public
Health, introduced keynote speaker Lisa
Jackson. Dr. Fried is a leader in the fields of
epidemiology and geriatrics, and has dedicated her career to the science of healthy
aging, particularly the prevention of frailty
and disability, and the design of generative
health-promoting roles for older adults. Dr.
Fried co-founded Experience Corps, a community-based senior volunteer program that
both serves the academic success of public
school children and is a health promotion
program for older adults. Dr. Fried is the
recipient of numerous awards, including the
APHA Archstone Award, the Maxwell Pollack
Award of the Gerontological Society of
America, and the American Geriatrics
Society’s Henderson Award for career contributions to research on aging. Previously,
Dr. Fried served as the Mason F. Lord
Professor of Geriatric Medicine at Johns
Hopkins University and held joint appointments in the Bloomberg School of Public
Health and the School of Nursing. She
directed The Johns Hopkins Medical
Institutions’ Center of Excellence for Aging
Research, the Center on Aging and Health,
and the Division of Geriatric Medicine and
Gerontology. Dr. Fried received her MD
from Rush Medical College in Chicago and
her MPH from Johns Hopkins.
Michel Gelobter, PhD, is the founder of
Cooler, Inc., a for-profit, social venture that
provides easy ways for consumers and retailers to address the global warming impact of
goods and services. Dr. Gelobter brings over
25 years of experience working on climate
change, and led the national think-tank,
Redefining Progress, in designing the world’s
most aggressive climate legislation, signed
into California law in August 2006. He has
been a Congressional Black Caucus Fellow
with the US House of Representatives Energy
and Commerce Committee; Director of
Environmental Quality for the City of New
York, and an Assistant Commissioner for its
Department of Environmental Protection;
and founder and director of the
Environmental Policy Program at Columbia
University’s School of International and
Public Affairs. He serves on the Advisory
Board of Vice-President Al Gore’s Alliance
for Climate Protection, and the Board of the
Natural Resources Defense Council among
others. He earned his PhD, MS, & BS in
Energy and Resources from UC Berkeley and
is an alumnus of Deep Springs College.
Speakers and Panelists
Lisa P. Jackson, Administrator of the US
Environmental Protection Agency, leads a
staff of approximately 18,000 professionals
dedicated to protecting the public health and
environment of all Americans. She was nominated to lead the Agency by President Barack
Obama on Dec. 15, 2008 and confirmed by
the Senate on Jan. 23, 2009. She is the first
African American to serve in that position.
Administrator Jackson lists among her priorities reducing greenhouse gas emissions,
improving air quality, managing chemical
risks, cleaning up hazardous waste sites, and
protecting America’s water. Before becoming
EPA’s Administrator, Jackson served as Chief
of Staff to New Jersey Governor Jon S.
Corzine. Prior to that, she was appointed by
Governor Jon S. Corzine to be Commissioner
of the state’s Department of Environmental
Protection (DEP) in 2006. While
Commissioner, Jackson was known for her
advocacy for reducing greenhouse gases,
aggressively addressing pollution, and having
an open and honest dialogue with stakeholders in the public policy process. She was also
noted for ensuring that underserved communities received fair environmental protection under the law. Jackson joined N.J. DEP in
2002, serving as Assistant Commissioner for
Compliance and Enforcement followed by
Land Use Management before becoming
Commissioner. Prior to joining N.J. DEP, she
worked for 16 years as an employee of the US
EPA. Jackson is a summa cum laude graduate
of Tulane University’s School of Chemical
Engineering and earned a master’s degree in
chemical engineering from Princeton
University.
Daniel Kass, MSPH, is Assistant Commissioner
for the Bureau of Environmental Surveillance
and Policy at the NYC Department of Health
and Mental Hygiene, which provides epidemiologic, analytic, policy analysis and other services, promotes public awareness of environmental health, and works on a variety of
urban environmental concerns. Mr. Kass also
serves as the Principal Investigator on the
agency’s Environmental Public Health
Tracking grant, a CDC effort to enhance environmental surveillance. Mr. Kass oversees
New York City’s Local Law 37 pesticide use
reduction program, and has worked since
1998 to promote and evaluate safer pest control in urban settings. Mr. Kass was formerly
Director of Evaluation for the NYC Childhood
Asthma Initiative and Deputy Director for
Environmental & Occupational Disease
Epidemiology. Before joining the Department,
he founded and directed the Hunter College
Center for Occupational and Environmental
Health. In 2008, he and other staff at BESP
received the US EPA Regional Children’s
Environmental Health Champion Award for
their work in understanding and preventing
exposures to methylmercury. He earned a ScB
degree from Brown University and MSPH
degree from the UCLA School of Public
Health, and completed doctoral studies at
NYU’s Wagner School.
Patrick Kinney, ScD, is Associate Professor
and the Director of the program in climate
and health at the Mailman School of Public
Health. Dr. Kinney’s teaching and research
address issues at the intersection of global
environmental change, human health, and
policy, with an emphasis on the public
health impacts of climate change and air
pollution. His work in the 1990s on air
quality and environmental justice in
Northern Manhattan and the South Bronx
led to important new insights into the
impacts of diesel vehicle emissions on local
air quality. He has carried out numerous
studies examining the human health effects
of air pollution, including studies of the
effects of ozone and/or particulate matter
on lung health and on daily mortality in
large cities. More recently, he developed a
new interdisciplinary research and teaching program at Columbia examining the
potential impacts of climate change on
human health. Dr. Kinney earned his doctorate at the Harvard School of Public
Health, where he studied the effects of air
pollution on lung function in children as
part of the Harvard Six Cities Air Pollution
and Health Study.
Philip J. Landrigan, MD, MSc, the Ethel Wise
Professor and Chair of the Department of
Community and Preventive Medicine at Mt.
Sinai, is a pediatrician, epidemiologist, and
internationally recognized leader in public
health and preventive medicine. He has
been a member of the faculty of Mount
Sinai School of Medicine since 1985, Chair
of the Department of Community and
Preventive Medicine since 1990, and he is
the Director of the Mt. Sinai Children’s
Environmental Health Center. He served
for 15 years as an Epidemic Intelligence
Service Officer and medical epidemiologist
at the Centers for Disease Control and
Prevention (CDC) and the National Institute
for Occupational Safety and Health
(NIOSH). He has also chaired committees at
the National Academy of Sciences (NAS).
The NAS report that he directed on pesticides and children’s health was instrumental in securing passage of the Food Quality
Protection Act, the only environmental law
in the United States that contains explicit
provisions for the protection of children. In
1997-1998, Dr. Landrigan served as Senior
Advisor on Children’s Health to the
Administrator of the US EPA and was
instrumental in helping to establish a new
Office of Children’s Health Protection at
EPA. He has published more than 500 scientific papers and 5 books. Dr. Landrigan
received his undergraduate degree from
Boston College, his medical degree from
Harvard Medical School, a Diploma of
Industrial Health from the University of
London, and a Masters of Science in
Occupational Medicine degree from the
London School of Hygiene and Tropical
Medicine.
Brian Lehrer is host of “The Brian Lehrer
Show,” WNYC Radio’s daily call-in program,
covering politics and life, locally and globally.
The show airs weekdays from 10 a.m. to noon
on WNYC 93.9 FM, AM 820 and wnyc.org.
“The Brian Lehrer Show” was recognized with
a 2007 George Foster Peabody Award for
“Radio That Builds Community Rather Than
Divides.” Time Magazine has called Lehrer’s
show “New York City’s most thoughtful and
informative talk show.” He also hosts a weekly
television program on CUNY-TV, “Brian
Lehrer Live” featuring issue-oriented web
video. In addition to the Peabody, Lehrer has
won numerous awards, including four
Associated Press New York Broadcasters “Best
Interview” Awards since 2000. He has hosted
his eponymous program, originally called
“On The Line,” since its inception in 1989.
Prior, he was an anchor and reporter for the
NBC Radio Networks, and an award-winning
author and documentary producer. Lehrer
holds master’s degrees in public health from
Columbia University and journalism from
Ohio State University and a bachelor’s in
music and mass communications from the
State University of New York at Albany.
Rachel L. Miller, MD, FAAAAI is an Associate
Professor of Medicine and Environmental
Health Sciences (in Pediatrics) at New
York–Presbyterian Hospital/Columbia
University Medical Center. She is also Deputy
Director of Columbia Center for Children’s
Environmental Health (CCCEH). As Director
of the CCCEH Asthma Project, her research
focuses on mechanisms for the onset of asthma. Her clinical work specializes in the treatment of asthma and allergies. A major
emphasis of her research is the role of prenatal and early postnatal exposure in later pediatric and adolescent asthma risk. Additional
areas of research include identifying novel
genetic by environment interactions and epigenetic by environment interactions important to the onset of asthma. She received her
undergraduate degree from Harvard
University, and her medical degree from New
York University.
Erik D. Olson is the Director of Chemical and
Food Safety Programs at the Pew Charitable
Trusts. He was deputy staff director and general counsel of the Senate Committee on
Environment and Public Works until
November 2008, and has 25 years of experience in environmental policy and consumer
advocacy. Mr. Olson is responsible for consumer product safety, including efforts to
improve food safety, overhaul toxic chemical
regulatory programs to better protect children and other vulnerable people, and
establish safeguards for emerging risks in
consumer products. During his Senate
tenure, he worked on environmental issues
and on health threats from toxic chemicals,
playing a key role in major environmental
legislation and hearings on global warming,
toxic chemicals, children’s environmental
health, clean air, drinking water, clean water
41
and environmental justice, among other
issues. He also helped to negotiate the lead
and phthalates provisions enacted in the
Consumer Product Safety Improvement Act
of 2008, and the green buildings and green
schools provisions of the Energy
Independence and Security Act of 2007.
Prior to his Senate work, Erik worked for 15
years at the Natural Resources Defense
Council, where he held various positions
including advocacy center director, public
health program director and a senior attorney. He previously served as counsel for the
National Wildlife Federation’s environmental
quality program for five years, and as an
attorney for EPA’s Office of General Counsel,
working on hazardous waste and water
issues. He graduated from the University of
Virginia School of Law, and from Columbia
College of Columbia University.
Frederica P. Perera, DrPH, is a Professor at the
Mailman School of Public Health, where she
serves as Director of the Columbia Center
for Children’s Environmental Health and of
the Disease Investigation Through
Specialized Clinically-Oriented Ventures in
Environmental Research (DISCOVER)
Center. Dr. Perera pioneered the field of
molecular epidemiology, beginning with
studies of cancer and is now applying molecular techniques within studies of pregnant
women and their children. Her areas of specialization include prevention of environmental risks to children, molecular epidemiology, cancer prevention, environment-susceptibility interactions in cancer, developmental damage, asthma, and risk assessment. She is the author of over 200 publications and has received numerous honors,
including: First Irving J. Selikoff Cancer
Research Award, The Ramazzini Institute
(1995); Newsweek, The Century Club Award
(1997); First Children’s Environmental Health
Award, The Pew Center for Children’s Health
and the Environment (1999); Distinguished
Lecturer, National Cancer Institute,
Occupational and Environmental Cancer
(2002); Doctoris Honoris Causa, Jagiellonian
University, Krakow, Poland (2004);
Children’s Environmental Health Excellence
Award, US Environmental Protection Agency
(2005); and CEHN (Children’s
Environmental Health Network) Award
(2008). Dr. Perera received her undergraduate degree from Harvard University and her
master’s and doctoral degrees in public
health from Columbia University.
Virginia Rauh, ScD, MSW, is a Professor of
Clinical Population and Family Health at the
Mailman School of Public Health, and
Deputy Director of Columbia Center for
Children’s Environmental Health. Dr. Rauh
has been working in the field of perinatal
epidemiology since 1982. Her expertise is in
the area of low birth weight and preterm
delivery, particularly with respect to socioeconomically disadvantaged and minority
populations. At the Columbia Center for
42
Children’s Environmental Health her work
focuses on the adverse impact of exposure
to air pollutants, including second hand
smoke and pesticides; pregnancy and child
health; and the susceptibility of disadvantaged populations to environmental hazards. She is working with other Columbia
faculty to study the effects of the World
Trade Center disaster on pregnant women
and newborns. Dr. Rauh is currently principal investigator for the Manhattan Site of
the National Children’s Study. She is the primary instructor for the Child Health course
within the Heilbrunn Department of
Population and Family Health. She holds an
MSW from Smith College and an ScD from
Harvard University.
Peggy Shepard is the Executive Director and
co-founder of WE ACT for Environmental
Justice, also known as West Harlem
Environmental Action. Founded in 1988 in
West Harlem, WE ACT works to build community power to improve environmental
health, policy and protection in communities
of color. She is a recipient of the 2008 Jane
Jacobs Lifetime Achievement Award from the
Rockefeller Foundation, the 10th Annual
Heinz Award for the Environment, and the
Dean’s Distinguished Service Award from the
Columbia Mailman School of Public Health
in 2004. WE ACT is a nationally recognized
organization in the field of community-based
participatory research in partnership with
the Mailman School of Public Health at
Columbia University. Ms. Shepard is a member of the National Children’s Study Federal
Advisory Committee to the National
Institutes of Health. Ms. Shepard served as
guest editor of an Environmental Health
Perspectives monograph, Advancing
Environmental Justice Through Community-Based
Participatory Research, April 2002, and is coauthor of “Promoting Environmental Health
Policy Through Community Based
Participatory Research: A Case Study from
Harlem, New York,” published in the Journal
of Urban Health, Bulletin of the New York
Academy of Medicine, Jan. 2006.
Sandra Steingraber, PhD, is an ecologist,
author and cancer survivor. Dr. Steingraber is
currently a Distinguished Visiting Scholar at
Ithaca College. She is the author of PostDiagnosis, a volume of poetry, and co-author
of a book on ecology and human rights in
Africa, The Spoils of Famine. She has taught
biology at Columbia College, Chicago, held
visiting fellowships at the University of
Illinois, Radcliffe/Harvard, and Northeastern
University, and served on President Clinton’s
National Action Plan on Breast Cancer. Dr.
Steingraber is an internationally recognized
expert on the environmental links to cancer
and human health. Dr. Steingraber’s highly
acclaimed book, Living Downstream: An Ecologist
Looks at Cancer and the Environment presents
cancer as a human rights issue. Her new
work, Having Faith: An Ecologist’s Journey to
Motherhood, explores the intimate ecology of
motherhood. Most recently, she has contributed to What We Do Now, an anthology of
individual manifestos outlining a series of
passionate new ideas for living. Dr.
Steingraber has won many awards for her
work. Several interviews with Dr. Steingraber
have appeared in The Chicago Tribune, USA
Today, The Cleveland Plain Dealer, on National
Public Radio, “The Today Show,” and “Now”
with Bill Moyers. She received her doctorate
in biology from the University of Michigan
and master’s degree in English from Illinois
State University.
Gina Solomon, MD, MPH, is a Senior Scientist
at the Natural Resources Defense Council
(NRDC) and an Associate Clinical Professor of
Medicine at the University of California at
San Francisco (UCSF) where she is also the
Director of the Occupational and
Environmental Medicine Residency Program
and the Associate Director of the UCSF
Pediatric Environmental Health Specialty
Unit. Her work has included over 40 scientific papers, book chapters, and reports on air
pollution, pesticides, global warming, and
other environmental and occupational
threats to health. Dr. Solomon serves on the
US EPA Science Advisory Board Drinking
Water Committee, the National Toxicology
Program Board of Scientific Counselors, and
the California Scientific Guidance Panel for
biomonitoring. Dr. Solomon attended medical school at Yale University and received her
postgraduate training in internal medicine,
public health, and occupational and environmental medicine at Harvard University.
Robin M. Whyatt, DrPH, is Professor of
Clinical Environmental Health Sciences at
the Mailman School of Public Health and is
Deputy Director of the Columbia Center for
Children’s Environmental Health. Her
research focus is on the effects of environmental exposures on women and children,
including the developing fetus. Dr. Whyatt’s
particular focus is on the extent of exposure
to non-persistent pesticides (organophosphates, carbamates and pyrethroids) and
phthalates during pregnancy among this
minority cohort. She is also collaborating
with the Centers for Disease Control on the
validation of biomarkers of prenatal exposures to contemporary-use chemicals. She
has served on a number of federal committees, including the National Academy of
Science Committee on Human
Biomonitoring for Environmental Toxicants,
for the US EPA on children’s environmental
health issues including considerations of
developmental changes in behavior and
anatomy when assessing exposures to children, and on a framework for assessing
health risks of environmental exposures to
children. She also served as co-chair of the
chemical exposures workgroup for the
National Children’s Longitudinal Cohort
Study. She received her MPH and DrPH from
Columbia University.
CCCEH Key Findings & Interventions
For a comprehensive list and the full text of all CCCEH publications, please visit: www.ccceh.org/papers.html
Mothers & Newborns Study,
Northern Manhattan / South Bronx
The Center’s largest study focuses on 725 AfricanAmerican and Latino women and their children
whose health is monitored from birth through
eleven years of age. Exposure beginning in the
womb to polycyclic aromatic hydrocarbons (PAH)
from traffic-related air pollution, pesticides in common home pest-control products, and pest allergens
in the home can result in asthma and other respiratory symptoms, delays in cognitive development,
and changes at the molecular level that could
increase children’s cancer risk. These pollutants can
cross the placenta and expose the developing fetus
to chemical contamination. Children are more vulnerable to environmental exposures than adults
because their bodies are still developing, and they
are less able to clear toxins from their systems.
Exposures of concern in this study include
PAH in ambient air pollution, secondhand smoke,
pesticides, endocrine-disrupting chemicals such as
phthalates and bisphenol-A, and indoor pest allergens. PAH are a group of chemicals released into the
air during the incomplete burning of fossil fuels
such as gasoline, diesel, coal, and other organic
substances. Secondhand smoke gets into the air
when tobacco products are burned in cigarettes,
cigars, and pipes. This smoke contains thousands of
toxic chemicals, many of which are known to be
cancer-causing. Harmful pesticides can be inhaled
following the use of spray pesticides indoors, and
young children also have greater exposure because
they spend more time on the floor where pesticides
are commonly applied. Plastics and other consumer
products contain chemicals that mimic or block
natural hormones and thus are capable of disrupting early development. Exposure to pest allergens
from cockroaches, dust mites, and rodents can
cause serious allergic and asthmatic reactions.
Following is a summary of key findings from the
Center’s research study:
Exposure
• All pregnant women in the study and their babies
are exposed to multiple common pollutants that
can harm fetal and child development, affect respiratory health, or increase cancer risk. Exposures
include air pollution, pesticides used in homes,
and secondhand smoke [1-3].
• PAH from air pollution were detected in 100% of
the personal air samples [4].
• There was widespread phthalate exposure during
pregnancy among the study participants.
Phthalates were detected in 99%-100% of maternal
personal air samples. Levels of exposure were
generally higher among CCCEH cohort women
than among women of reproductive age (18-40
years) sampled through the National Health and
Nutrition Examination Survey (NHANES) [5].
Fetal Growth and Neurobehavioral Development
CCCEH research has shown that prenatal exposures
to PAH, pesticides, and secondhand smoke are
linked to reduced fetal growth and developmental
problems in children. These findings have important implications for health and learning ability
because early developmental delays and attentional/behavioral problems such as AttentionDeficit/Hyperactivity Disorder (ADHD) can affect
later school performance.
PAH
• Prenatal exposure to PAH reduced birth weight
and head circumference in African-American
babies born to women who were more highly
exposed to the air pollutants [4]. Several studies
have reported that reduction in head circumference at birth or during the first year of life corre-
1. Perera FP, Rauh V, etal. Effects of transplacental exposure to environmental pollutants on birth outcomes in a multi-ethnic population. Environmental Health Perspectives, 111(2): 201-5, February 2003.
2. Whyatt RM, Rauh VA, et al. Prenatal insecticide exposures, birth weight and length among an urban minority cohort. Environmental
Health Perspectives, 112(10):1125-32, 2004.
3. Perera FP, Rauh V, et al. Molecular evidence of an interaction between prenatal environmental exposures on birth outcomes in a
multiethnic population. Environmental Health Perspectives, 112(5):626-30, 2004.
4. Perera FP, Rauh V, et al. Effects of transplacental exposure to environmental pollutants on birth outcomes in a multi-ethnic population. Environmental Health Perspectives, 111(2): 201-5, February 2003.
5. Adibi JJ, Whyatt RM, et al. Characterization of phthalate exposure among pregnant women assessed by repeat air and urine samples. Environmental Health Perspectives, 116(4):467-73. April 2008.
43
lates with poorer cognitive functioning and school
performance in childhood.
• Children with high prenatal exposure to PAH had
significantly lower test scores at age 3 on the
Bayley test for cognitive development and were
more likely to be developmentally delayed [6].
• Prenatal exposure to PAH at levels encountered in
NYC air can adversely affect child IQ scores at 5
years of age. After adjustment for potential confounders, highly exposed children had full-scale
and verbal IQ scores that were 4.31 and 4.67 points
lower compared to less exposed children. These
reductions are similar to the effects of low-level
lead exposure [7].
Pesticides
• Prenatal exposure to two household pesticides,
chlorpyrifos and diazinon, which transfer easily
from the mother to her fetus, reduced birth
weight by an average of 6.6 ounces—the equivalent
of weight reduction seen in babies born to women
who smoked [8].
• Children prenatally exposed to high levels of
chlorpyrifos were significantly more likely than
children exposed to low levels to experience delay
in both psychomotor and cognitive development,
and to show symptoms of attentional disorders,
ADHD, and pervasive personality disorder at age 3.
Although the EPA banned residential use of chlorpyrifos in 2001, this pesticide is still widely used in
agriculture [9].
• Pyrethroid insecticides appear to be replacing the
organophosphorus insecticides like chlorpyrifos
and diazinon for residential pest control among
the cohort. Levels of permethrin, a common
pyrethroid insecticide, and piperonyl butoxide, a
pyrethroid synergist, have increased in personal
air samples collected during pregnancy. Also following the 2000-2001 EPA restrictions, both
reporting of cockroaches in the home and use of
spray pesticides during pregnancy have increased.
Insect resistance to pyrethroids may be one possible explanation for these trends [10].
Secondhand Smoke
• Children prenatally exposed to secondhand
smoke—especially children experiencing material
hardship (unmet basic needs of food, clothing, and
housing)—had significantly reduced scores on tests
of cognitive development at two years of age [11].
Phthalates
• Prenatal exposure to the phthalate DEHP was associated with shorter gestation. Gestational age was
shorter by 1.1 days for each log-unit increase in
metabolite concentrations and averaged 5.1 days
less among the most exposed. Given inconsistencies with prior findings in other study populations, additional research is warranted [12].
Asthma Risk
Childhood asthma in urban communities is a serious disease that accounts for a significant proportion of emergency room visits, hospitalizations, and
deaths. Asthma is a chronic disease of the lungs and
airways that causes difficulty breathing, and occurs
most commonly in people who become sensitized
to certain allergens in our environment. Different
people with asthma react to different triggers.
Common triggers include air pollution, diesel
exhaust, environmental tobacco smoke, cockroach
particles, dust mites, cat or dog dander, and mold.
These exposures may also contribute to the early
development of the disease.
• Over half the babies in the study have been born
with an immune response to cockroach proteins
that may increase the risk of asthma in certain
children [13].
6. Perera FP, Rauh VA, et al. Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the
first three years of life among inner-city children. Environmental Health Perspectives, 114(8):1287-92, August 2006.
7. Perera FP, Li Z, et al. Prenatal Airborne Polycyclic Aromatic Hydrocarbon Exposure and Child IQ at Age 5. Pediatrics, published
online July 20, 2009.
8. Whyatt RM, Rauh VA, et al. Prenatal insecticide exposures, birth weight and length among an urban minority cohort. Environmental
Health Perspectives, 112(10):1125-32, 2004.
9. Rauh VA, Garfinkel R, et al. Impact of prenatal chlorpyrifos exposure on neurodevelopment in the first three years of life among
inner-city children. Pediatrics, 2006.
10. Williams M., Rundle, A., et al. Changes in pest infestation levels, self-reported pesticides use and permethrin exposure during
pregnancy following the 2000-01 US EPA restriction of organophosphates, Environmental Health Perspectives, Vol 116, 1681-8, 2008.
11. Rauh VA, Whyatt RM, et al. Developmental effects of exposure to environmental tobacco smoke and material hardship among
inner-city children. Journal of Neurotoxicology and Teratology, 26(3):373-85, 2004.
12. Whyatt RM, Adibi JJ, et al. Prenatal di(2-ethylhexyl) phthalate exposure in relation to length of gestation among a cohort of innercity mothers and their newborns. Pediatrics, in press.
44
13. Miller RL, Chew G, et al. Prenatal exposure, maternal sensitization, and sensitization in utero to indoor allergens in an inner-city
cohort. American Journal of Respiratory and Critical Care Medicine, 164(995-1001), 2001.
• Pest infestation, allergen levels, and pesticide use
are higher among women and babies living in the
most deteriorated housing [14].
• Combined prenatal exposure to airborne PAH and
postnatal secondhand smoke results in the
increased likelihood of respiratory symptoms at
one and two years of age that may be associated
with increased asthma risk [15].
• In the Center’s evaluation of the New York City
Housing Authority’s intervention to reduce toxic
pesticide use in public housing, high cockroach
and mouse allergen levels were significantly associated with asthma prevalence among children
and adults [16].
• Developing antibodies to cockroach and mouse
proteins is associated with a greater risk for
wheeze, hay fever, and eczema in preschool children as young as three years of age [17].
• CCCEH has linked epigenetic alterations associated with prenatal exposure to PAH in cord blood
with parental report of asthma by age 5.
Epigenetic changes may disrupt the normal functioning of genes by affecting how they are
expressed, but do not cause structural changes or
mutations in the genes [18].
Cancer Risk
This study is finding that exposure to air pollution
during pregnancy is associated with genetic damage
in babies before they are even born. This type of
genetic damage has been generally associated with
increased cancer risk later in life.
• Approximately 40% of babies in the study were
born with DNA damage associated with PAH. In
other studies such damage has been tied to an
increased risk of cancer. Of particular concern,
newborns had higher (approximately 10-fold) levels of adducts than mothers per unit of estimated
exposure, indicating greater fetal susceptibility
and potential risk from these pollutants [19].
• Prenatal exposure to PAH was linked to structural
changes in babies’ chromosomes. Such genetic
alterations have been related in other studies to
increased risk of cancer in children and adults
[20].
Interventions and Impact on Policy
• From its inception, the Center has worked in partnership with, and provided data to, a Community
Advisory Board of health service and environmental advocacy organizations in Northern Manhattan
and the South Bronx, including WE ACT for
Environmental Justice (WE ACT). With WE ACT,
the Center developed the Healthy Home Healthy
Child (HHHC) community education campaign in
2000. The campaign provides families, physicians,
and their patients with practical tips for reducing
harmful environmental exposures and protecting
children’s health, and information on clean air
campaigns in the community. HHHC has also provided training workshops for community leaders
and health professionals.
• CCCEH data on the health effects of air pollution
have been used by local and national groups to
support clean air policies in New York City. From
1998 to 2006, PAH levels from personal monitoring of pregnant mothers in the cohort decreased
significantly over time [21].
• CCCEH estimated the economic burden of one
aspect of developmental delays associated with
prenatal secondhand smoke exposure—Early
Intervention Services—to be over $50 million per
14. Rauh V, Chew G, et al. Deteriorated housing contributes to high cockroach allergen levels in inner-city households. Environmental
Health Perspectives, 110 (suppl.2):323-327, 2002.
15. Miller RL, Garfinkel R, et al. Polycyclic aromatic hydrocarbons, environmental tobacco smoke, and respiratory symptoms in an
inner-city birth cohort. Chest, 136, 1071-78, 2004.
16. Chew G, Carlton E, et al. Determinants of cockroach and mouse exposure and associations with asthma among families and the
elderly living in New York City public housing. Annals of Allergy, Asthma and Immunology, 2006.
17. Donohue KM, Al-alem U, et al. Anti-cockroach and anti-mouse IgE are associated with early wheeze and atopy in an inner-city
birth cohort. Journal of Allergy and Clinical Immunology, 122(5):914-20, November 2008.
18. Perera F, Tang W-Y, et al. Relation of DNA Methylation of 59-CpG Island of ACSL3 to Transplacental Exposure to Airborne
Polycyclic Aromatic Hydrocarbons and Childhood Asthma. PLoS ONE 4(2): e4488. February 2009.
19. Perera FP, Rauh V, et al. Molecular evidence of an interaction between prenatal environmental exposures on birth outcomes in a
multiethnic population. Environmental Health Perspectives, 112(5):626-30, 2004.
20. Bocskay KA, Tang D, et al. Chromosomal aberrations in cord blood are associated with prenatal exposure to carcinogenic polycyclic aromatic hydrocarbons. Cancer Epidemiology, Biomarkers & Prevention, 14(2):506-11, February 2005.
21. Narvaez R., Hoepner L, et al. Spatial and temporal trends of polycyclic aromatic hydrocarbons and other traffic-related airborne
pollutants in New York City, Environmental Science and Technology, 42:7330-35, 2008.
45
year for New York City Medicaid births and $99
million per year for all New York City births [22].
• Governmental regulations such as the 2000-2001
EPA restrictions on residential use of the
organophosphorous insecticides, chlorpyrifos and
diazinon, have positive impacts on children’s
health. These regulations significantly reduced use
of and exposure to these compounds during pregnancy [23].
• Despite a regulatory ban on residential use of
chlorpyrifos, agricultural applications continue in
the US and abroad. In September 2008, at a public
hearing of the EPA’s Scientific Advisory Panel,
Federal Insecticide, Fungicide and Rodenticide Act
(“Scientific Issues Associated with Chlorpyrifos
and PON1”), the Panel unanimously recommended
that EPA accept the epidemiologic evidence that
chlorpyrifos may act as a neurotoxicant in human
beings. The panel cited CCCEH data as epidemiologically sound and recommended that the Agency
attempt to use the cohort data to inform the risk
assessment process.
• CCCEH conducted a pilot intervention using
Integrated Pest Management (IPM) to reduce pest
infestations and residential insecticide exposures
among pregnant women living in New York City.
Residential IPM is a pest-control method that minimizes exposure to toxic pesticides in the home
through the use of lower-toxicity pesticides, such
as sticky traps, bait stations, and gels; cleaning;
and repairing leaks and holes. Insecticides measured in indoor air samples and in maternal cord
blood decreased significantly after the intervention. These pilot data suggest that IPM is an effective strategy for reducing pest infestation levels
and the internal dose of insecticides during pregnancy [24].
• CCCEH has collaborated with the New York City
Housing Authority (NYCHA) and the New York
City Department of Health (NYCDOH) in the
development, implementation, and evaluation of
Integrated Pest Management (IPM) interventions
in public housing. The evaluation has shown that
IPM is more effective than the conventional use of
more toxic pesticides in reducing levels of cockroach and cockroach allergens in apartments [25].
• WE ACT incorporates Center findings into regular
education seminars, promotes health events, and
supports and translates institutional research for
the education of Northern Manhattan residents.
The organization developed a citywide network,
Our Housing is Our Health, which is comprised of
several organizations collaborating to empower
communities to mitigate health effects of environmental exposures related to poor-quality housing.
WE ACT has also organized a number of briefings,
presentations, case-studies for publication, and
testimony to public interest groups and government agencies.
• Other recent impacts of WE ACT’s work in New
York City, informed in part by CCCEH research,
include:
— The introduction of the Asthma Free Housing Act
by Public Advocate Betsy Gotbaum and City
Council member Rosie Mendez in April 2008. The
bill seeks to improve indoor air quality in the
homes of NYC asthma sufferers;
— The coordination of the inaugural taskforce
meetings on rodent control with NY State Senator
Bill Perkins; and
— The organization of several successful community
workshops throughout Northern Manhattan on topics ranging from lead poisoning to pest infestation.
22. Miller T, Rauh VA, et al. The economic impact of early life environmental tobacco smoke exposure: early intervention for developmental delay. Published Online, Environmental Health Perspectives, July 11, 2006.
23. Whyatt RM, Rauh VA, et al. Prenatal insecticide exposures, birth weight and length among an urban minority cohort.
Environmental Health Perspectives, 112(10):1125-32, 2004.
24. Williams MK, Barr DB, et al. An intervention to reduce residential insecticide exposure during pregnancy among an inner-city
cohort. Published Online, Environmental Health Perspectives, July 27, 2006.
25. Kass D, McKelvey W, et al. Effectiveness of an integrated pest management intervention controlling cockroaches, mice, and allergens in New York City public housing. Environmental Health Perspectives, 117(8): 1219-1225, 2009.
46
Glossary of Terms
Glossary of Terms
Allergen: Any substance that induces an allergy: common allergens include pollen, grasses, dust, and some
medications.
Attention-Deficit/Hyperactivity Disorder: One of the
most common childhood disorders that can continue
through adolescence and adulthood. Symptoms
include difficulty staying focused and paying attention, difficulty controlling behavior, and hyperactivity
(over-activity).
Autism Spectrum Disorder (ASD): A developmental and
behavioral syndrome that consists of certain combinations of characteristically autistic traits.
Biomarker: A component in a biological substance
(blood, DNA, saliva, breast milk, hair, etc.) used to
indicate exposure to, or early biological effect of, an
environmental chemical, or susceptibility to disease.
Bisphenol-A (BPA): An industrial chemical used to
make polycarbonate plastic resins, epoxy resins, and
other products.
Carbamates: A group of chemical pesticides.
Cell proliferation: Cell growth and multiplication.
Chloropyrifos: An organophosphate pesticide widely
used before an EPA ban on household use in 2001.
Cholinesterase inhibition: An action that prevents the
breakdown of the neurotransmitter acetylcholine by
acetylcholinesterase, so that high levels of acetylcholine accumulate at reactive sites, increasing the
action of this neurotransmitter.
Chromosome aberrations: Any change in the normal
structure or number of chromosomes. This may result
in physical or mental abnormalities.
Climate change: Modification of Earth’s climate over
time brought about as a result of changes in the
atmosphere as well as interactions between the atmosphere and various other geologic chemical, biological,
and geographic factors within the Earth system.
Cohort: Group of people participating in a research
study.
Community-based participatory research (CBPR): A collaborative approach to research that equitably
involves community and academic investigators in the
research process and recognizes the unique strengths
that each brings, particularly with the goal of achieving social change, to improve health outcomes and
eliminate health disparities.
Cord blood: Blood from a newborn’s umbilical cord.
When analyzed, cord blood can indicate allergens and
other substances to which an infant was exposed
before birth.
Developmental disorder (or disability): A delay or problem in a child’s development involving the brain or
nervous system. These include learning disabilities,
Attention Deficit/Hyperactivity Disorder (ADHD), and
other behavioral and cognitive dysfunctions.
Diesel particulate filter (DPF): A device designed to
remove diesel particulate matter or soot from the
exhaust gas of a diesel engine.
Dioxins: Chemical contaminants that are formed during combustion processes such as waste incineration,
forest fires, and backyard trash burning, as well as
during some industrial processes. They are associated
with cancer, and reproductive and developmental
problems, and an increased risk of heart disease and
diabetes.
DNA adduct: This forms as a result of DNA binding to a
genotoxic chemical. It reflects exposure to specific
carcinogens, and is a marker of cumulative unrepaired DNA damage.
DNA methylation: The chemical modification of DNA
involving the addition of a methyl group (a combination of one carbon atom and three hydrogen atoms).
This methylation has the potential to alter gene
expression without changing the underlying DNA
sequence.
Ecosystem: A system formed by the interaction of a
community of organisms with their environment.
Endocrine disruptor: Substance that can mimic or disrupt the action of naturally occurring hormones with
effects on development and reproduction.
Endometriosis: The presence of uterine lining in other
pelvic organs, especially the ovaries, characterized by
cyst formation, adhesions, and menstrual pains.
Environmental justice: The fair treatment and meaningful involvement of all people regardless of race,
color, national origin, or income with respect to the
development, implementation, and enforcement of
environmental laws, regulations, and policies.
Environmental pollutant: Substance present in the
environment (indoor or outdoor) that can have a negative effect on health and development. Common pollutants include pesticides, polycyclic aromatic hydrocarbons (PAH) produced by combustion of organic
materials, particulate matter (also from fossil fuels
and other combustion including diesel exhaust), environmental tobacco smoke, lead, and mercury.
Environmental tobacco smoke (ETS): Smoke generated
from the burning end of a cigarette, pipe, or cigar, and
smoke that is exhaled by smokers.
47
Epigenome: Collection of chemical modifications
throughout the human genome (i.e. genetic materials)
that influence gene expression.
Neurodevelopmental disorder: An impairment of the
growth and development of the brain or central nervous system.
Epigentic changes: Heritable alternations in gene
expression that do not change the DNA sequence.
Neuroendocrinology: The study of the anatomical and
physiological interactions between the nervous and
endocrine systems.
Genetic susceptibility: An inherited increase in the risk
of developing a disease.
Global warming: An increase in the Earth’s average
atmospheric temperature caused by an accumulation
of greenhouse gases.
Greenhouse gases: Gases that trap heat in the atmosphere, such as carbon dioxide and ozone. Some greenhouse gases occur naturally; others are created and
emitted solely through human activities.
In utero: In the uterus; unborn.
Hypospadias: A developmental anomaly of the urethra
in which a part of the urethral canal is open on the
undersurface of the penis or on the perineum.
Integrated pest management (IPM): A safer, low-toxicity
approach to keeping homes free of pests and toxic pesticides. Examples of IPM methods include: sealing pest
entry points in the home with caulking compounds
and/or metal screens; using low-toxicity, citrus-based
cleaning products to remove food debris and grease
stains; and placing glue traps, gels and bait stations for
cockroaches and sticky traps for mice throughout the
kitchen, bathroom, and any problem areas.
Intelligence quotient (IQ): The ratio of tested mental age
to chronological age, usually expressed as a quotient
multiplied by 100.
Longitudinal birth-cohort studies: Typically long-term
observational studies; often following mothers during
pregnancy and/or babies from birth through several
stages of the developmental.
Magnetic resonance imaging (MRI): The use of a nuclear
magnetic resonance spectrometer to produce electronic images of specific atoms and molecular structures in solids, especially human cells, tissues, and
organs.
Metabolites: Biological by-products of metabolism.
Often used as a biomarker to confirm exposure to
environmental factors.
Molecular epidemiology: A science that focuses on the
contribution of potential genetic and environmental
risk factors, identified at the molecular level, to the
etiology, distribution and prevention of disease within
families and across populations.
48
Neurotoxic pesticides: Pesticides that alter the normal
functioning of the nervous system.
Organophosphate: Any of several organic compounds
containing phosphorus, some of which are used as
fertilizers and pesticides.
Ozone: An unstable form of oxygen found naturally in
the stratosphere and troposphere. At ground level it is
considered an air pollutant having harmful effects
upon the respiratory system.
Particulate matter (PM): The summation of airborne
molecules, both solid and liquid, that remain suspended in air. These molecules vary in toxicity due to their
size (e.g., PM10, PM2.5) and/or composition.
Pesticides: Chemicals used to kill pests, especially insects.
Phthalates: Chemicals used to soften plastics in many
consumer products, including children’s toys, plastic
containers, and personal care products. Phthalates can
seep out of these products, and studies have shown
that phthalates can disrupt the endocrine system,
which is the body’s system of regulating hormones.
Polybrominated diphenyl ethers (PBDE): A potentially
toxic bioaccumulating flame retardant substance
found in many household products (e.g., electronics,
furniture).
Polychlorinated biphenyl (PCB): Any of a family of very
stable industrial compounds used as lubricants, heattransfer fluids, and plasticizers. The manufacture and
use of PCBs has been restricted since the 1970s
because they are very harmful to humans and the
environment.
Polycyclic aromatic hydrocarbons (PAH): A carcinogenic
organic molecule produced from the burning of organic substances such as coal, garbage, oil, and cigarettes.
Pyrethroid: Any of several synthetic compounds similar to pyrethrin, used as an insecticide.
Risk assessment: An estimate of the likelihood of
adverse effects that may result from exposure to certain health hazards.
Toxic Substances Control Act (TSCA): A federally-managed law that gives EPA broad authority to regulate the
manufacture, use, distribution in commerce, and disposal of chemical substances.
We would like to thank the women and children participating in CCCEH studies.
We would also like to thank the following individuals:
CCCEH Key Investigators: H. Andrews, S. Chillrud, K. Donohue, D. Evans, R. Garfinkel, I. Goldstein, J. Herbstman,
L. Hoepner, P. Kinney, S.A. Lederman, G. Lovasi, R. Miller, M. Orjuela, M. Patel, M. Perzanowski, F. Perera, V. Rauh,
A. Rundle, B. Sheares, P. Shepard, D. Tang, R. Whyatt, S. Wang, M. Williams.
Mothers & Newborns and Sibling Study Research Workers: F. Arias, G. Badia, L. Calero, D. Diaz, B. Plaza, M. Reyes, C. Tobon.
CCCEH Staff & Technicians: K. Bernabe, S. Chu, T. Dasgupta, A. Divjan, S. Edwards, E. Evans, C. DeLeon, F. Hafeeez,
D. Holmes, S. Hsu, L. Hua, F. Hua, I. Ibrahimagic, X. Jin, I. Jung, A. Just, K. Kern, M. Kurzon, K. Lane, J. Li, C. Lin, H. Lu,
R. Martinez, S. Mehta, K. Moors, B. Obeng, M. Rosa, A. Schneider, I. Suen, A. Tse, J. Yu, L. Qu, M. Quaratino, J. Yu, M. Yung,
N. Velez de Villa, W. Wang, H. Zhang, D. Zhu.
WE ACT: O. Dotson-Newman, P. Shepard.
CUMC Genetics Lab: D. Warburton, C. Cujar, T. Tubo, X. Liu.
NCI: S. Chanock.
University of Cincinnati: S.M. Ho, W. Tang.
CDC: D. Barr, T. Bernert, A. Calafat, L. Needham, R. Schleicher, A. Sjodin.
NIEHS: D. Bell, G. Pittman.
Institute for Cancer Research, London: A. Ford, M. Greaves, D. Phillips.
Jagiellonian University in Krakow: W. Jedrychowski.
Children’s Hospital of Chongqing Medical University: T-Y Li.
Conference Photographer: J. Ramirez.
Conference Report: K. Lane, S. Mehta; designed by A. Garland.
COLUMBIA CENTER
FOR CHILDREN’S
ENVIRONMENTAL
HEALTH
MAILMAN SCHOOL OF PUBLIC HEALTH
Columbia University
www.ccceh.org
printed on recycled paper

Translating Science to Policy - Columbia Center for Children`s

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