RACHEL: Children In Harm's Way [Hg, Pb, Pesticides, TCDD, PCB]
Gary.Greenberg at Duke.Edu
Sun Nov 26 08:28:36 EST 2000
Environmental Research Foundation
(Moderator Note: ERF is an advocacy organization, routinely alarmed
about potential new claims of environmental health dangers. Their
well-written editorials are presented to the OEM-L forum in an effort to
provoke intellectual discussion, not as an endorsed point of view. For
contrast, see the newsletters posted from ACSH. -G)
. RACHEL'S ENVIRONMENT & HEALTH WEEKLY #712 .
. ---November 23, 2000--- .
. HEADLINES: .
. CHILDREN IN HARM'S WAY .
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CHILDREN IN HARM'S WAY
by Rachel Massey*
A new report by a group of physicians says that millions of children in
the U.S. exhibit learning disabilities, reduced IQ and destructive,
aggressive behavior because of exposures to toxic chemicals.
"Neurodevelopmental disabilities are widespread, and chemical exposures
are important and preventable contributors to these conditions," the
report says (pg. 117).
Titled IN HARM'S WAY, the report was written by physicians Ted Schettler
and Jill Stein and two of their colleagues and was published by Greater
Boston Physicians for Social Responsibility in partnership with the
Clean Water Fund. IN HARM'S WAY links toxic exposures during early
childhood, or even before birth, to lifelong disabilities including
attention disorders, reduced IQ and poorly-controlled aggression.
IN HARM'S WAY reviews scientific and medical information on a range of
toxins to which most or all American children are exposed, and draws
links to the rising number of children diagnosed each year with abnormal
brain development or function. The report is a call to action for
everyone interested in children's welfare and the future of our society.
To avert brain damage in growing numbers of children, we have to reclaim
our government from corporate special interests, the report concludes.
Developmental disabilities such as autism, attention deficit
hyperactivity disorder (ADHD), dyslexia and uncontrollable aggression
currently affect an estimated 12 million children under age 18 in the
U.S. -- almost one child in five. Furthermore, the incidence of some of
these disabilities appears to have increased dramatically in recent
decades. For example, nationwide, the number of children classified with
learning disabilities and placed in special education programs increased
191% between 1977 and 1994. The number of children taking the drug
Ritalin to combat attention deficit hyperactivity disorder (ADHD) has
approximately doubled every 4 to 7 years since 1971. Experts estimate
that autism rates have risen from around 4 per 10,000 in the early 1980s
to between 12 and 20 per 10,000 in the 1990s. According to a recent
article in US NEWS AND WORLD REPORT, the number of children in New York
classified with learning disabilities rose 55 percent between 1983 and
Some argue that reported disabilities are increasing because of improved
diagnosis and rising expectations as children are required to learn more
complicated skills at younger ages. But many parents, teachers, and
physicians who work with children think these explanations are only
partially correct because "they can not imagine that such disabilities
escaped notice in the past," the report says. (pg. 11)
Experts may argue about the exact number of children suffering from
individual disorders, but the undisputed reality is that huge numbers of
children currently suffer with serious developmental disabilities and
they are exposed to many toxic chemicals that are known to produce such
disabilities. "We believe we can no longer ignore the mounting evidence
that chemical exposures contribute to the epidemic of developmental
disabilities," the report says. (pg. 9)
IN HARM'S WAY walks us through a sampling of neurotoxic substances to
which many or all American children are exposed -- metals (lead,
mercury, manganese); nicotine; pesticides; persistent organochlorine
compounds (e.g., dioxin and PCBs); solvents, including alcohol;
fluoride; and food additives -- and reviews existing human and animal
data on developmental effects of these chemicals. These effects can vary
dramatically depending on the exact timing of exposures. Tiny exposures
that would have no noticeable effect at most stages of development can
produce devastating permanent damage if they occur during a "window of
vulnerability" when certain organs are developing rapidly. (pg. 9)
Here is a sampling of the toxins that can misdirect the development of a
-- Lead exposure in infants and children is associated with attention
deficit, aggression, and reduced IQ. Blood lead levels below those
labeled "safe" by U.S. Environmental Protection Agency (EPA) are
associated with learning problems, and no threshold has been identified
below which adverse effects do not occur. Young monkeys exposed to lead
show symptoms including heightened distractability and inappropriate
responses to stimuli. One million American children currently live with
blood lead levels above the threshold recognized by EPA as affecting
behavior and cognition. Millions more would be added to this list if
EPA's threshold were updated to take account of the most current science
on the effects of lead in children.
-- At low doses, mercury exposure can produce impairments in language
ability, attention, and memory; at high doses it can cause mental
retardation, vision problems, and problems walking. Mercury enters the
environment through waste incinerators and coal-burning power plants. It
bioaccumulates in fish in its most toxic form, methylmercury (see REHW
#597). The EPA estimates that 1.16 million women of childbearing age
"eat sufficient amounts of mercury-contaminated fish to pose a risk of
harm to their future children." (pg. 64)
-- Many pesticides kill insects by exerting a toxic effect on cells in
the nervous system. Not surprisingly, such pesticides can disrupt the
development and functioning of the human nervous system by the same
mechanisms. Animal studies show that neurotoxic pesticides can produce
permanent changes in brain structure and functioning when exposures
occur on a single critical day of development. For example, some effects
occurred in newborn mice if exposures occurred on day 10 of development,
but not if exposures occurred on day 3 or 19. (pg. 82) Short-lived
"pulse" exposures may have devastating developmental effects and yet can
be difficult or impossible to identify after the fact (see REHW # 648).
-- One pesticide exposure study examined children in two Mexican
communities. The two communities were very similar in ethnic composition
and culture, but one community practiced chemical-intensive agriculture
while the other used few farm chemicals. Children in the community with
chemical-intensive agriculture scored substantially lower on measures of
memory, physical stamina and coordination, and had trouble with ordinary
children's activities such as drawing a simple picture of a person.
(pgs. 82-83) Children in the pesticide-exposed group also displayed more
aggressive behavior than their unexposed counterparts (see REHW #648).
-- Dioxins and polychlorinated biphenyls (PCBs) are organochlorine
compounds that bioaccumulate in fatty tissue and are found at
significant levels in human breast milk. Both animal and human studies
show strong links between these pollutants and developmental disorders.
Monkeys exposed before birth to dioxin in the range of human breast milk
contamination levels were impaired in their ability to reverse a learned
behavior in response to new stimuli. Young monkeys exposed to PCBs at
levels typically found in human breast milk showed retarded learning as
well as abnormally repetitive behavior. Studies of human children have
found lowered IQs associated with PCB exposure in the womb, and a study
of babies whose mothers ate PCB-contaminated fish from Lake Ontario
found impaired development including abnormal reflexes and startle
responses. (pgs. 76-79) These are just a few of the studies covered in
IN HARM'S WAY.
Government officials set "safe" exposure levels based on individual
chemicals. But in the real world children are exposed to many chemicals
simultaneously. Such multiple exposures can be far more damaging than
exposure to single chemicals. For example, one study found that certain
combinations of pesticides produce changes in thyroid levels that are
not observed when the chemicals are tested individually, and thus the
combination may produce unexpected developmental effects (see REHW
#648). Proper thyroid levels are essential for brain development. Other
studies reveal that exposure to a combination of mercury and PCBs, two
pollutants that accumulate in fish, can produce even greater effects on
neurological development than either pollutant alone. (pg. 67)
Under our current regulatory system, industrial chemicals need not be
tested for toxicity before they are marketed. (pg. 108) EPA estimates
that somewhere between 2400 and 4000 industrial chemicals now on the
market are neurotoxic. (pg. 107) However, this number is "highly
speculative" (pg. 107) because most chemicals in commercial use have not
been tested for neurotoxicity. EPA's Toxics Release Inventory (TRI) --
which covers just 625 out of 80,000 industrial chemicals -- reported
that nearly a billion pounds of known neurotoxins were released directly
into air and water in 1997. (pg. 103) Pesticides must be tested before
marketing, but not for toxicity to the nervous system. Of 890 pesticide
"active ingredients" EPA believes 140 are neurotoxins. Some 20 million
U.S. children under age 5 eat an average of 8 different pesticides on
their food each day. (pg. 106)
The authors of IN HARM'S WAY point out that there is no reason to delay
protecting our children; we don't need more scientific information
before taking precautionary action. "We should not need to identify with
certainty exactly how much and through what mechanism a neurotoxic
pesticide impairs brain development before coming to the conclusion that
public health is not protected when the urine of virtually every child
in this country contains residues of these chemicals. ... We do not need
to exhaustively understand the mechanism by which methylmercury
interferes with normal fetal brain development before concluding that it
is not acceptable for freshwater and many ocean fish to be sufficiently
contaminated with mercury to threaten developing brains. We know how to
reduce the environmental releases of mercury so that fish are once again
safe to eat regularly. We can modify manufacturing practices so that
lead use in products goes steadily down instead of up. We can eliminate
or modify outmoded technologies that produce the dioxin that
contaminates fetuses and breast milk. We know how to do these things."
In order to do these things, we have to take back control of our
regulatory system. As things stand now, corporations that benefit
financially by exposing children to toxic substances are accepted --
even by most environmentalists -- as valid "stakeholders" in the process
that determines "safe" levels of exposure. As a result, we have failed
to protect our children from industrial poisons. As the authors of IN
HARM'S WAY put it, "The role of special interests in the regulation of
environmental chemicals is an important matter for public debate, as it
has direct relevance to the neurological development of children now and
in the future." (pg. 121) In sum, our current regulatory system is like
a trial in which the criminal defendant gets to serve on the jury. If we
want to have children who can play, think and learn normally, we will
have to change corporations and our government so that protecting brain
development comes ahead of protecting profits.
* Rachel Massey is a consultant to Environmental Research Foundation.
 Ted Schettler, Jill Stein, Fay Reich, Maria Valenti, and David
Wallinga, IN HARM'S WAY: TOXIC THREATS TO CHILD DEVELOPMENT (Cambridge,
Mass.: Greater Boston Physicians for Social Responsibility [GBPSR], May
2000). Available on the web at http://www.igc.org/psr/ or as a paper
copy from GBPSR in Cambridge, Mass.; telephone 617-497-7440.
 Sheila Kaplan and Jim Morris, "Kids At Risk," US NEWS AND WORLD
REPORT Vol. 128, No. 4 (June 19, 2000), pgs. 47-53.
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