Children in Harm’s Way:
Toxic
Chemicals Linked to Developmental Disabilities
By Arline Kaplan © 2000 (All Rights Reserved)
Pervasive and insidious toxicological experiments are being conducted on our
nation’s children, warned authors of a recent national report issued by
the Greater Boston Physicians for Social Responsibility (GBPSR). One million
children in the United States already have blood lead levels (10 micrograms/dl
or above), which can affect their behavior and cognition. Among children examined
in one study, 92% had a metabolite of the neurotoxic pesticide, chlorpyrifos,
present in their urine. And according to Environmental Protection Agency (EPA)
estimates, 1.16 million women of childbearing age eat sufficient amounts of
mercury-contaminated fish to pose a risk of harm to their future children.
In Harm’s Way: Toxic Threats to Child Development, authored by Ted
Schettler, M.D., M.P.H., Jill Stein, M.D., Fay Reich Psy.D., and Maria Valenti,
with additions from David Wallinga, M.D., examines the contribution of toxic
chemicals to neurodevelopmental, learning and behavioral disabilities in children.
Schettler said the report, available online at www.igc.org/psr/, has both sparked
a series of requests for proposals issued by the National Institute of Environmental
Health Services (NIEHS) and will serve as the basis of day-long workshops to
be conducted at medical colleges and centers throughout the United States.
Vast quantities of neurotoxic chemicals are released into the environment each
year, the report authors said. Of the top 20 chemicals reported by the Toxics
Release Inventory as released in the largest quantities into the environment
during 1997, nearly three-quarters were known or suspected neurotoxicants. Nearly
one billion pounds of these neurotoxicants were emitted by facilities onsite
directly into the air and surface water, with the potential to be inhaled, absorbed
or otherwise ingested through our food and water supplies.
Basic toxicity information is needed, according to the report authors. An estimated
80,000 chemicals are in commercial use in the United States (U.S. Environmental
Protection Agency, 1998), with most of them being synthesized since World War
II. Yet the GBPSR report found that basic toxicity information is missing from
publicly available sources for nearly 75% of the top 3,000 high-production volume
substances (Roe et al., 1997).
Lack of Neurotoxicity Data
Neurotoxicity
data are even less available. While the EPA has had a validated, accepted guideline
for assessing a chemical’s toxicity to the nervous system in immature or
developing animals since 1991, as of December, 1998, manufacturers had submitted
results from this developmental neurotoxicity testing for only 12 chemicals
(nine pesticides and three solvents) (Makris et al., 1998). Meanwhile, in 1999,
the EPA announced a "data call-in" for 140 pesticides considered to
be neurotoxic. It requires manufacturers to conduct and submit tests of acute,
subchronic and developmental neurotoxicity to the EPA.
"We know from the few things that we do have a lot of data on, like, lead,
mercury, alcohol and nicotine, that the developing brain is extraordinarily
sensitive compared to the adult brain, and that exposures during development
can have lifelong impacts," said Schettler, a primary care physician and
science director for the nonprofit Science and Environmental Health Network.
"Yet, we are failing to require that kind of neurodevelopmental testing
in industrial chemicals before they are marketed."
Epidemic of Disabilities
This
scarcity of information about the health effects of most commonly used chemicals
combined with pervasive human exposures to many toxic chemicals and seriously
inadequate regulatory oversight combine to "create a global environmental
threat to our children," the report authors contend.
They point to "an epidemic of developmental, learning and behavioral disabilities."
Data cited in the report indicates that nearly 12 million children (17%) in
the U.S. suffer from one or more learning, developmental or behavioral disabilities.
Attention-deficit/hyperactivity disorder affects up to 6% of school children,
while learning disabilities affect up to 10%. The incidence of autism may be
as high as 2 per 1,000 children, and a California study indicated the number
of children entered into the autism registry increased by 210% between 1987
and 1998 (California Health and Human Services Agency, 1998). In Brick Township,
N.J., at least 42 children have been identified with autism, more than three
times the estimated national average of 1 in 500. The "cluster" has
prompted researchers and federal agencies to look for possible environmental
causes (Johnson, 1999).
"These disabilities are clearly the result of complex interactions among
genetic, environmental and social factors that impact children during vulnerable
periods of development," the report authors said. "Toxic exposures
deserve special scrutiny because they are preventable causes of harm."
"We have a lot of data on a relatively small number of chemical contaminants
in the ambient environment which tell us they can have an impact on brain development
and function," Schettler noted. "Some of them physicians are well
acquainted with. We tell pregnant women not to drink alcohol or smoke, because
we know that has an adverse impact on fetal brain development …But it gets
pretty thin after that in terms of what physicians are aware of. They sort of
know the lead story, but it is surprising how few are aware of the toxic effects
of mercury on brain development and the body of data that’s now emerging
on pesticides, many of them commonly used in the household and on food."
This lack of awareness may be related to the fact that many of the studies have
been conducted within the science of developmental neurotoxicology, said co-author
Stein, who is an instructor in adolescent medicine at Harvard Medical School,
a practicing physician and co-chair of the Human Health and the Environment
Project.
"[Developmental neurotoxicology] is a branch of neuroscience, but it uses
a language of its own, so its [research] is not readily available to many people
for whom the information is of interest," said Stein. One of the report’s
goals, she explained, is "to summarize and transfer this very technical
body of scientific literature to health care professionals and the public."
The information transfer problem is compounded, Schettler said, because educators,
researchers, health care providers and others are not communicating with one
another. Clinicians, for example, are talking about syndromes and diagnostic
categories, while toxicologists are in the laboratory looking at traits, such
as attention deficits, IQ deficits and impulsive behaviors that emerge from
exposures to chemicals. For understanding etiology and prevention, Schettler
believes it is useful to think in terms of traits and abilities.
"When you start to do the testing of kids with mercury exposures in utero,
you find you can identify specific attention deficits or memory problems or
problems with language skills, those are the ones that seemed to show up at
the lowest levels of exposure for mercury. Now that is worth noting without
trying to say, ‘ Well does this kid have a syndrome we can name?’
You can then start to get correlations between the animal data and the human
data and …get a better handle on what are the traits that emerge from various
levels of exposure at various times during development. Later, it might be useful
to package them up into diagnostic categories, but to start there is to create
barriers to understanding between disciplines that have not been very helpful."
Metals, Pesticides, Solvents, PCBs
The
report summarizes what is known about the neurodevelopmental toxicity of metals
(e.g., lead, mercury, cadmium and manganese); pesticides (e.g., organophosphates
commonly used in homes and schools); some solvents (e.g. ethanol used in paints,
glues and cleaning solutions); dioxin and polychlorinated biphenyls (PCBs) that
bioaccumulate in the food chain; and nicotine. It also explores controversies
over the potential neurodevelopmental toxicity of compounds intentionally added
to drinking water and food (e.g., fluoride and certain food additives). It specifically
focuses on how neurotoxic chemicals contribute to developmental delays, hyperactivity,
memory loss, attention deficit, learning disabilities and aggressive behavior.
For example, the report cites studies showing that large fetal exposures to
methylmercury cause mental retardation, gait and visual disturbances (Grandjean
et al., 1997; Harada, 1978). The authors also note that several studies report
a relationship between excessive childhood levels of manganese exposure and
hyperactivity or learning disabilities (Crinella et al., 1998). Children exposed
to a variety of pesticides in an agricultural community in Mexico show impaired
stamina, coordination, memory and capacity to represent familiar subjects in
drawing (Guillette et al., 1998). Children exposed to PCBs during fetal life
showed IQ deficits, hyperactivity and attention deficits when tested years later
(Jacobson and Jacobson, 1996).
Other studies reported adverse neurodevelopment impacts resulting from fetal
or infant exposures to lead, including lowered intelligence and hyperactivity
(Bellinger et al., 1987; Pihl and Parkes, 1977).
Currently, researchers have the most information regarding links between chemicals
and learning, intelligence, attention and memory, as that has been the focus
of research, said Stein.
"But increasingly, we find relationships emerging between more emotional
and behavioral issues [and exposures to chemicals]," she said. "I
think we are going to find there may be a toxic, and therefore, preventable
contribution to disorders which are distinctly psychiatric."
She cited the progression of lead research as an example.
"When lead first emerged as a problem, which was actually in the early
1900s, we focused on the most apparent problems—coma, encephalopathy and
death from lead toxicity. Over the course of several decades, it was found that
lower doses of lead could cause IQ problems. More recently, the literature begins
to review a strong relationship between lead and attention problems, specifically
attention-deficit/hyperactivity disorder, and also with impulsiveness, aggressiveness
and dysfunctional social behavior (Needleman et al., 1996; Rice, 1998).
By translating and then disseminating neurodevelopmental toxicity research,
the report authors hope that physicians and other health professionals will
incorporate the knowledge into their clinical practices.
"There are many ways this information is relevant and useful," Stein
said. "When children, for example, come in with attention or learning problems,
it is a good idea for them to be screened for exposures that may be contributing
to these kinds of problems….It is worth thinking about ongoing lead or
pesticide exposure in kids who are having problems."
The report authors are also developing patient handouts on toxic chemical exposure.
One, "Protecting Your Child From Toxic Threats to Brain Development: Personal
Guidelines for Children, Parents and Future Parents," is posted on the
following website: www.igc.org/psr/protect-child.htm. It discusses ways to reduce
risks from pesticides, lead, chemicals that accumulate in food, and household
products, among others.
What Needs To Be Done
When
asked what should be done on a national level to protect our children, Schettler,
recommended three first steps.
"We need to require neurodevelopmental evaluations of industrial and other
chemicals before marketing. For those that are on the market, they need to be
tested," he said.
"Secondly, we have to get the medical community, teachers and others aware
of the fact that exposures [to toxic chemicals] during brain development can
have a lifelong impact on how the brain functions, and we know enough about
many of these to take action to mitigate exposures now.… It doesn’t
mean that we stop modern society in its tracks and resist all development, but
it does mean that there comes a point when evidence is sufficient to take precautionary
action to mitigate exposure while we are still coming to a more complete understanding
of what the harms might be.
"Then, of course, we need further research, which is what the government
agencies are beginning to fund more of…to get a better body of knowledge
about exactly how and in what ways the brain is vulnerable to exposures, so
we have a better idea of how to pre-empt those from the outset," he said,
acknowledging that government agencies are beginning to fund more research.
References
Bellinger D, Leviton A, Waternaux C et al. (1987), Longitudinal analysis
of prenatal and postnatal lead exposure and early cognitive development. N Engl
J Med 316(17):1037-1043.
California Health and Human Services Agency, Department of Development Services
(1999), Changes in the Population of Persons with Autism and Pervasive Developmental
Disorders in California’s Developmental Services System: 1987 Through 1998.
A Report to the Legislature, March 1, 1999. Available at www.autism.com/ari/dds/dds.html.
Accessed Jan. 11.
Crinella FM, Cordova EJ, Ericcson JE (1998), Manganese, aggression, and attention-deficit/hyperactivity
disorder. Neurotoxicol 19(3):468-469.
Grandjean P, Weihe P, White RF et al. (1997), Cognitive deficit in 7-year-old
children with prenatal exposure to methylmercury. Neurotoxicol Teratol 19(6):417-428.
Guillette EA, Meza MM, Aquilar MG et al. (1998), An anthropological approach
to the evaluation of preschool children exposed to pesticides in Mexico. Environ
Health Perspect 106(6):347-353.
Harada
H (1978), Congenital Minamata disease: interauterine methylmercury poisoning.
Teratology 18(2):285-288.
Jacobson JL, Jacobson SW (1996), Intellectual impairment in children exposed
to polychlorinated biphenyls in utero. N Engl J Med 335(11):783-789 [see comment].
Johnson LA (1999), Study opens on autism in N.J. The Detroit News, Jan. 21.
Makris S, Raffaele K, Sette W, Seed J (1998), A retrospective analysis of twelve
developmental neurotoxicity studies submitted to the U.S. EPA Office of Prevention,
Pesticides, and Toxic Substances, draft 11/12/98.
Needleman HL, Reiss JA, Tobin MJ et al. (1996), Bone lead levels and delinquent
behavior. JAMA 275(5):363-369 [see comments].
Pihl RO, Parkes M (1977), Hair element content in learning disabled children.
Science 198(4313):204-206.
Rice DC (1998), Developmental lead exposure: neurobehavioral consequences. In:
Handbook of Developmental Neurotoxicology, Slikker W, Chang LW, eds. San Diego:
Academic Press.
Roe D, Pease W, Florini K, Silbergelt E (1997), Toxic Ignorance: the Continuing
Absence of Basic Health Testing for Top-Selling Chemicals in the United States.
New York: Environmental Defense Fund.
U.S. Environmental Protection Agency (1998), Office of Prevention, Pesticides
and Toxic Substances. Endocrine Disruptor Screening and Testing Advisory Committee.
Final Report. Washington, D.C.
(AK102)
Viewers, Your Help Is Needed:
I am a freelance medical journalist. Some of the articles posted on this Web site were originally written for health care professionals, but I believe patients/consumers may also find value in the articles. Many of us who have chronic or life-threatening health problems become experts on them. For that reason, I have kept the rights to electronically post these articles.
Additionally, I am developing new stories specifically for this site. It is my intention to offer you high-quality, well-researched information. Because this site accepts no advertising, your financial support is needed to continue this user-sponsored service.
I welcome your comments, suggestions and financial help. You can send voluntary contributions to, or contact me at:
HealthRising
Arline Kaplan
P.O. Box 3644
Costa Mesa , CA 92628