Ted Schettler MD, MPH
to the Senate Committee on Environment and Public Works, Hearing on
the Government Accountability Office’s Investigation of EPA’s
Efforts to Protect Children’s Health, March 2010
Ted Schettler MD, MPH
fully referenced version of this testimony can be found here.)
you for the opportunity to submit testimony to this Committee. My
name is Ted Schettler and I am Science Director of the Science and
Environmental Health Network (SEHN). SEHN is a not-for-profit
organization working in collaboration with environmental and public
health groups, health professionals, legal scholars, ethicists,
government officials, legislators, and others seeking to protect
public health and the environment for this and future generations.
am a physician and also have training in public health and
environmental medicine. I served on the U. S. Environmental
Protection Agency’s (EPA) Endocrine Disruptor Screening and
Testing Advisory Committee (EDSTAC) from 1996-1998 and the Endocrine
Disruptor Methods Validation Subcommittee from 2001-2003.
is now 13 years since President Clinton issued executive order 13045,
establishing an interagency Task Force on Environmental Health Risks
and Safety Risks to Children and requiring every agency proposing
regulatory action to consider its impacts on children. The new report
from the Government Accounting Office contains recommendations
intended to reinvigorate EPA’s early emphasis on children. I
have been asked to comment on the US Environmental Protection
Agency’s efforts to protect children’s health from my
Vulnerability of Developing Children
to adults, developing children are uniquely susceptible to hazardous
environmental exposures. Windows of vulnerability during in utero
development, infancy, and childhood increase risks of some adverse
health outcomes resulting from exposures, often with lifelong
consequences. Among the better known examples, lead exposures that
have minimal or no discernable impacts in adults can permanently
alter brain development and function in a child. Similarly, fetal
alcohol exposures can have lifelong impacts in children, while the
same exposure in adults has only mild, transient effects.
of the reasons for this vulnerability are well understood. During
fetal, infant, and child development, cells rapidly divide, tissues
and organs are formed, and signaling mechanisms, hormone levels,
feedback loops, and their set points are established. Exposures to
hazardous chemicals as well as other environmental influences may
perturb these events through various mechanisms, with long-term
is also important to recognize that environmental exposures during
development can increase the risk of chronic, degenerative diseases
much later in life. For example, life-long cumulative exposures to
lead, including developmental exposures, increase the risk of
cognitive decline and Parkinson’s disease in people decades
later. Animal studies show that early life exposure to certain
pesticides seem to prime the brain, making it more susceptible to
further exposures in adulthood, resulting in neurodegeneration in
areas responsible for Parkinson’s disease. Indeed,
epidemiologic studies show an increased risk of Parkinson’s
disease in agricultural communities where pesticides are heavily
used. Thus, while protecting children, we are also lowering the risk
of various diseases and disabilities much later in life.
the 1990s it appeared that EPA was taking steps to address many
unique aspects of children’s environmental health. But since
then many of these efforts have fallen short. Two examples from my
own experience are illustrative.
first example has to do with the potential for some commonly
encountered chemicals to disrupt the function of hormones and other
chemical messengers that are vital to normal human development and
function. These chemicals are known as endocrine disruptors.
endocrine disruptor is “an exogenous agent or mixture of agents
that interferes with or alters the synthesis, secretion, transport,
metabolism, binding action, or elimination of hormones that are
present in the body and are responsible for homeostasis, growth,
neurological signaling, reproduction and developmental processes.”
Endocrine disruptors interfere with the body’s key signaling
pathways and can cause harm, especially during fetal and early life
disruptors gained increased public and scientific attention during
the 1990s, although the capacity for certain industrial chemicals to
mimic or otherwise interfere with hormone function was known at least
as long ago as the 1930s. For example, in 1938, scientists showed
that bisphenol A, a chemical used to make many consumer products
today, has estrogen-like properties, although its molecular structure
is quite different from naturally-occurring estrogen. The use of this
chemical is now so widespread that, according to the Centers for
Disease Control and Prevention, 93% of all Americans have residues of
bisphenol A in their urine. Recent studies link bisphenol A levels to
altered brain development, heart disease, and diabetes.
the 1950s, 1960s, and early 1970s the potent synthetic estrogen
diethylstilbestrol was purposely given to many pregnant women with
the unfounded promise that it would help to prevent miscarriages and
promote healthier pregnancies. Tragically, fetal exposure to DES
resulted in abnormalities of reproductive tract development in
females and males and a sharply increased risk of reproductive tract
cancers in women decades later. Thus, we learned through uncontrolled
human experimentation that certain chemicals could profoundly alter
development, with consequences that were often not apparent at birth
and might only become manifest decades later.
the 1980s and 1990s exposures of wildlife to industrial chemicals and
their health effects were increasingly reported in the scientific
literature. Reproduction and development of birds, amphibians,
reptiles, and mammals have been affected by exposure to
endocrine-disrupting chemicals. Fish in numerous rivers, including
the Potomac, have disrupted sexual development—specifically,
feminized male fish. When this finding was first noted in England in
the 1990s, it was considered unusual. It is now recognized as a
widespread, pervasive phenomenon.
on findings in wildlife and laboratory animal studies, many
scientists are concerned that the increasing incidence of cancer of
the testis, prostate, and breast; birth defects of the male
reproductive tract; lower sperm counts; behavioral disorders;
diabetes; and a wide range of other abnormalities in humans may
result, at least in part, from exposures to endocrine-disrupting
recent report shedding new light on a puzzling observation that has
baffled scientists for years is illustrative. Many studies find a
higher incidence of testicular cancer and male reproductive tract
abnormalities in Danish men than in nearby Finland. Finnish boys have
larger testes and higher sperm counts than Danish boys. Reasons for
these differences have been unclear. Recently, scientists analyzed
the breast milk of 68 women from the two countries for 121 different
chemicals and found significantly higher levels in the milk of the
Danish women. The chemicals tested for included flame retardants,
pesticides, phthalates, polychlorinated biphenyls, dioxins, and
furans. These chemicals are commonly identified in biomonitoring
studies around the world, including in the US. Their concentration in
breast milk is a good indicator of fetal exposures during pregnancy.
This kind of study cannot definitively establish a causal
relationship between the different levels of these industrial
chemicals in mothers in Denmark and Finland and the patterns of male
reproductive tract abnormalities in the two countries. But a causal
relationship is plausible, based on what we know about the effects of
many of these chemicals in laboratory animal studies. Current
environmental exposures also include hundreds if not thousands of
chemicals that were not tested for in this study that may also be
part of the problem.
of growing concern about endocrine-disrupting chemicals, in 1996 the
EPA created the Endocrine Disruptor Screening and Testing Advisory
Committee (EDSTAC) in response to a Congressional mandate in the Food
Quality Protection Act and authorization in the Safe Drinking Water
Act Amendments of 1996.
laws specified that EPA:
a screening program, using appropriate validated test systems and
other scientifically relevant information, to determine whether
certain substances may have an effect in humans that is similar to an
effect produced by a naturally occurring estrogen, or other such
endocrine effect as the Administrator may designate.”
laws required EPA to develop a screening program by August 1998, to
implement the program by August 1999, and to report on the program’s
progress by August 2000. Unfortunately, EPA is now about a decade
served on the EDSTAC. The committee included representatives from
industry, government, environmental and public health groups, and
academia. We were charged with developing consensus-based
recommendations for a screening program that would provide EPA the
necessary information to make regulatory decisions about endocrine
effects of chemicals.
committee delivered a final report by the statutory deadline of
August 1998. It included a groundbreaking priority-setting,
screening, and testing approach that encompasses the universe of
chemicals in use today, evaluates a range of human health and
ecological effects, and recommends a feasible, health-protective
approach. The committee:
that problems with endocrine disruption go beyond estrogen, and also
called for screening of chemicals for interference with male
androgens and thyroid hormone.
the use of new technologies to rapidly pre-screen numerous chemicals
to see if they interact with hormone receptors in vitro (in
the “test-tube”). The committee recommended that this
technology be used to rapidly evaluate the ten thousand most widely
used chemicals within one year.
a computer-based tracking system allowing information about health
effects and exposure to be collected in one place to facilitate
prioritization. That database didn’t exist then, and it
doesn’t exist today.
EPA to accept nominations from the public of chemicals or chemical
mixtures for expedited testing. This would allow workers or
impacted communities to press for more information about chemicals
to which they are exposed.
EPA missed deadline after deadline and became bogged down in an
endless set of validation exercises that remain unfinished. Many of
the recommendations were discarded. Finally, a decade late, EPA
implemented an extremely scaled-down version of the program when it
issued the first test orders in October 2009. Only 67 chemicals are
on the list for this first round of screening – mostly
pesticides, including a number of chemicals that are already
well-known endocrine disruptors. Meanwhile tens of thousands of
chemicals in consumer products, food, water, and air have not been
tested for endocrine-disrupting properties.
2009 the Endocrine Society evaluated the science on endocrine
disruptors and concluded:
evidence for adverse reproductive outcomes (infertility, cancers,
malformations) from exposure to endocrine-disrupting chemicals is
strong, and there is mounting evidence for effects on other endocrine
systems, including thyroid, neuroendocrine, obesity and metabolism,
and insulin and glucose homeostasis.”
Endocrine Society is comprised of over 14,000 research scientists and
physicians from over 100 countries. This statement has since been
endorsed by the American Medical Association, which is joining the
Endocrine Society in calling for decreased public exposure to
endocrine-disrupting chemicals. The American Chemical Society just
issued a similar statement with additional recommendations for: “More
rapid advancement of the congressionally mandated effort by the EPA,
called the Endocrine Disruptor Screening Program (EDSP).”
a result of EPA’s failure to implement a strong endocrine
disruptor screening program, the Endocrine Disruption Prevention
Act was introduced in Congress in 2009. This act would authorize
a new research program at the National Institute of Environmental
Health Sciences (NIEHS) to identify endocrine-disrupting chemicals,
using the most current science. It would establish an independent
panel of scientists to oversee research and develop a prioritized
list of chemicals for investigation. If the panel determined that a
chemical presented endocrine-disrupting concerns, it would compel the
federal agencies with established regulatory authority to report to
Congress and propose next steps within six months. NIEHS has the
capacity to carry out such a research program if provided with
appropriate resources. But EPA remains the regulatory authority
responsible for protecting children from environmental threats.
have focused here on endocrine-disrupting chemicals, but my concerns
about human exposures to industrial chemicals are not limited to
those with endocrine-disrupting properties. Well-known flaws in the
Toxic Substances Control Act (TSCA) have allowed tens of thousands of
untested industrial chemicals to stay on the market and new ones to
be brought to market with limited or no toxicity information. These
include chemicals to which workers and people in the general
population, including pregnant women and children, are regularly
EPA Office of the Inspector General’s (OIG) report, released in
February 2010, and previous GAO reports clearly describe these
problems. Not only are basic safety data lacking, but whatever
limited information is submitted to the agency is frequently
accompanied by requests to protect it from public disclosure. The OIG
report concludes that the agency’s process is “predisposed
to protect industry information rather than to provide public access
to health and safety studies.” Physicians and other healthcare
professionals do not have access to the data they need in order to
appropriately advise patients, and workers and communities remain
ignorant of the potential hazards of the chemicals to which they may
TSCA reform is essential in order to protect developing children and
people of all ages from the impacts of exposure to hazardous
chemicals in consumer products, food, water, and air.
impacts of industrial chemicals, including pesticides, on brain
development and function
area of concern to bring to your attention is the failure of EPA to
require adequate evaluation of the impacts of industrial chemicals,
including pesticides, on brain development and function in children.
Ample scientific evidence confirms the unique susceptibility of the
developing brain to chemical exposures that can disrupt one or more
of a number of biologic processes that must proceed in an orderly
fashion as brain architecture and chemistry are established
throughout pregnancy, infancy, and childhood.
mercury, polychlorinated biphenyls (PCBs), arsenic, ethyl alcohol,
and toluene are recognized causes of neurodevelopmental disorders. A
large body of experimental and human epidemiologic evidence shows
diverse, long-lasting impacts of these substances on the ability of
children to learn, remember, pay attention, and behave appropriately.
The effects can occur after relatively low-level exposures that have
no discernable effects in adults.
that reduce exposures to these substances have been successful. For
example, the removal of lead from gasoline resulted in a sharp
decline in average blood levels in children throughout the US. Even
so, the economic consequences of lower IQ resulting from lead levels
in children in the US today are conservatively estimated to be in
excess of $40 billion annually. That figure does not take into
account costs to society incurred by responding to special
educational needs and disruptive or criminal behavior.
these well-studied substances are the exception. The large majority
of industrial chemicals have never been evaluated for their potential
impact on the developing brain of children. This is true even for
those chemicals known to be toxic to the nervous system more
the Federal Insecticide, Fungicide, and Rodenticide Act, the EPA has
the authority to require pesticide registrants to provide data about
the impacts of their chemicals on the developing brain. But these
data are not part of the core requirement, and the agency may decide
on a case-by-case basis whether to require their submission.
Historically, the EPA has always been reluctant to exercise this
authority, even when a food-use pesticide was known to have nervous
system toxicity as the mechanism whereby it killed pests.
are a group of pesticides that are notorious nervous system
toxicants. They disrupt nerve impulse transmission and can cause a
plethora of symptoms. In the 1990s and early 2000s after EPA issued a
data call-in, registrants slowly delivered developmental
neurotoxicity data on various organophosphates. These data finally
led to some restrictions, including a phaseout of
chlorpyrifos-containing products for home and garden use.
Chlorpyrifos is among the organophosphate pesticides known to
adversely impact the developing brain of children as well as
laboratory animals. But chlorpyrifos remains in widespread
agricultural use in the US today. About 8 million pounds are applied
to US crops annually. Children in farming communities are regularly
exposed to this and other organophosphate neurotoxins. It is
difficult to imagine the justification for continued use of
chlorpyrifos in agriculture.
we thought that we were finally going to see more regular
requirements for neurodevelopmental testing of neurotoxic pesticides,
we were sadly disappointed in 2007 when EPA registered the fumigant
methyl iodide (MeI) for agricultural use without knowing what it
might do to the developing brain of a fetus, infant, or child.
was proposed as a substitute for methyl bromide, a fumigant that is
supposed to be phased out under the Montreal Protocol because it
depletes stratospheric ozone. MeI is an extremely toxic chemical that
must be handled with extraordinary care in the laboratory setting. It
is damaging to DNA, causing mutations, and is listed on the
California Proposition 65 list as “known to the State of
California to cause cancer.” But here I want to consider
impacts of MeI on the developing brain.
iodide is highly likely to be a developmental neurotoxicant, with
long-lasting impacts on the brain of fetuses, infants, and young
children at levels of exposure lower than those that cause damage to
the adult brain. This concern is based on several lines of evidence.
to scientific reports, adults who have been accidentally exposed to
MeI may develop “symptoms of irritability, headache diplopia,
nystagmus, lethargy, somnolence, slurred speech, ataxia, dysmetria,
and visual disturbances. . . . These symptoms may progress to
paralysis, convulsions, coma, and death. If recovery occurs, the
acute neurologic symptoms may . . . give way to late neuropsychiatric
sequelae such as behavioral disturbances, and cognitive deficits,
psychoses, and emotional lability.”
mechanism(s) by which MeI exerts its neurotoxic effects are not
completely understood. However, it is clear that glutathione (GSH)
depletion is an important contributor in the causal pathway leading
to neurotoxicity. Glutathione is a naturally occurring antioxidant
that enables the body to cope with toxic substances that cause
oxidative stress. Several studies conclude that glutathione depletion
alone leads to neurotoxicity.
and infants normally have lower levels of glutathione in their
tissues than young adults. (Glutathione levels also decline in older
people.) Lower baseline levels of glutathione would be anticipated to
increase susceptibility to a neurotoxicant like MeI whose mechanism
of action depends, at least in part, on glutathione depletion. For
that reason alone, it can be predicted that the developing brain is
more vulnerable to MeI neurotoxicity than the fully developed adult
brain. Beyond that, however, impacts of oxidative stress differ in
the developing brain because of unique developmental events without
counterparts in the adult.
rationale for not requesting developmental neurotoxicity testing was
based on the assumption that protecting against exposures sufficient
to cause thyroid effects would also protect against impacts in the
developing brain. That is, they assumed that the only mechanism by
which MeI could adversely impact the developing brain was through
decreasing thyroid hormone levels or, alternatively, that other
mechanisms would have a higher exposure threshold than that necessary
to cause thyroid impacts. These are untested hypotheses for which
there is no evidence.
the California Department of Pesticide Regulation
carried out its own risk assessment of MeI and sent it out for
external review by a Scientific Review Committee (SRC). In its final
report, the SRC said: “The lacunae in our knowledge
about methyl iodide are particularly wide and deep in relation to key
aspects of its potential toxicity such as neuro- and other
developmental effects, neuro-toxicity beyond the development stage
(in particular, following chronic exposure), and mechanisms of
is a description of the existing data gaps pertaining to this
dangerous, highly toxic chemical. EPA had the authority to require
neurodevelopmental testing before registration but didn’t,
despite concerns voiced by numerous scientists.
more quickly to implement the Endocrine Disruptor Screening Program
for chemicals in consumer products, air, food, and water, using
current, up-to-date scientific methods. Evaluation should include
commonly encountered mixtures as identified in environmental media
(air, water, food) and biomonitoring studies. If NIEHS becomes the
institution in which the endocrine-disrupting properties of
chemicals are evaluated, EPA must then promptly respond to the
findings with health protective interventions.
developmental neurotoxicity testing of MeI and suspend its
registration until data gaps are filled and risks have been
require neurodevelopmental toxicity testing of pesticides proposed
for registration or continued use when they are known or suspected
to be toxic to the nervous system.
should pass comprehensive chemical regulatory policy reform.
Effective reform should:
Initiate Action on the Worst Chemicals:
Persistent, bioaccumulative toxicants (PBTs) are uniquely hazardous.
Any such chemical to which people could be exposed should be phased
out of commerce.
Basic Information for All Chemicals:
Manufacturers should be required to provide basic information on the
health hazards associated with their chemicals, how they are used,
and the ways that the public or workers could be exposed.
the Most Vulnerable: Chemicals
should be assessed against a health standard that explicitly
requires protection of the most vulnerable subpopulations. That
population is likely to include children, but it could also be
workers, pregnant women, or another vulnerable group.
the Best Science and Methods: The
National Academy of Sciences’ recommendations for reframing
risk assessment at the EPA should be adopted. Regulators should
expand development and use of information gleaned from
“biomonitoring” for setting priorities.
Industry Responsible for Demonstrating Chemical Safety:
Chemical manufacturers should be responsible for evaluating and
demonstrating the safety of their products.
Environmental Justice: Effective
reform should contribute substantially to reducing the
disproportionate burden of toxic chemical exposure placed on people
of color, low-income people, and indigenous communities.
Government Coordination: The EPA
should work effectively with other agencies such as the Food and
Drug Administration that have jurisdiction over some chemical
exposures. The ability of the states to enact stricter chemical
policies should be maintained and state/federal cooperation on
chemical safety encouraged.
Safer Alternatives: There should be
national support for basic and applied research into green chemistry
and engineering, and policies should favor chemicals and products
that are benign over those that are hazardous.
the Right to Know: The public,
workers, and the marketplace should have full access to chemical
safety data and information about the way in which government safety
decisions are made.
should also adopt legislation establishing the Endocrine Disruption
Prevention Program so that 1) environmental chemicals can be screened
for endocrine-disrupting properties using the most current science in
a timely manner and 2) regulatory agencies are obligated to take
action to protect public health based on the best available science.