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Volume 114, Number 2
February 2006

Environmental Health Perspectives (EHP) is a monthly journal of peer-reviewed research and news on the impact of the environment on human health. EHP is published by the National Institute of Environmental Health Sciences and its content is free on-line. Print issues are available by paid subscription.

Environmental Health Perspectives Volume 114, Number 2, February 2006


New Thinking on Neurodevelopment

The notion that some substances in the environment can damage the
nervous system has an ancient history. The neurotoxicity of lead was
recognized more than 2,000 years ago by the Greek physician Dioscerides,
who wrote, "Lead makes the mind give way." In the intervening millennia
many other substances have been added to the list of known or suspected
neurotoxicants. Despite this accumulation of knowledge, there is still
much that isn't understood about how neurotoxicants affect the
developing brain, especially the effects of low-dose exposures. Today
researchers are taking a hard look at low-dose exposures in utero and
during childhood to unravel some of the mysteries of impaired

About 17% of school-age children in the United States suffer from a
disability that affects their behavior, memory, or ability to learn,
according to a study published in the March 1994 issue of Pediatrics by
a team from the Centers for Disease Control and Prevention (CDC). The
list of maladies includes attention deficit/hyperactivity disorder
(ADHD), autistic spectrum disorders, epilepsy, Tourette syndrome, and
less specific conditions such as mental retardation and cerebral palsy.
All are believed to be the outcome of some abnormal process that
unfolded as the brain was developing in utero or in the young child.

These disorders have an enormous impact on families and society.
According to the 1996 book Learning Disabilities: Lifelong Issues,
children with these disorders have higher rates of mental illness and
suicide, and are more likely to engage in substance abuse and to commit
crimes as adults. The overall economic cost of neurodevelopmental
disorders in the United States is estimated to be $81.5-167 billion per
year, according to a report published in the December 2001 issue of EHP

Potentially even more disturbing is that a number of epidemiologic
studies suggest that the incidence of certain disorders is on the rise.
In the United States, the diagnosis of autistic spectrum disorders
increased from 4-5 per 10,000 children in the 1980s to 30-60 per 10,000
children in the 1990s, according to a report in the August 2003 Journal
of Autism and Developmental Disorders. Similarly, notes a report in the
February 2002 issue of CNS Drugs, the diagnosis of ADHD grew 250%
between 1990 and 1998. The number of children in special education
programs classified with learning disabilities increased 191% between
1977 and 1994, according to an article in Advances in Learning and
Behavioral Disabilities, Volume 12, published in 1998.

So what is going on? The short answer is that no one really knows.
There's not even consensus on what the soaring rates actually mean.
Heightened public awareness could account for the surge in the numbers,
or it may be that physicians are getting better at diagnosing the
conditions. Some autism researchers believe the rise in that condition's
prevalence simply reflects changes in diagnostic criteria over the last
25 years. On the other hand, some scientists believe that the rates of
neurodevelopmental disease are truly increasing, and that the growing
burden of chemicals in the environment may play a role.

With that in mind, investigators are considering the effects of
gene-environment interactions. A child with a mild genetic tendency
toward a neurodevelopmental disorder might develop without clinically
measurable abnormalities in the absence of environmental "hits."
However, children in industrialized nations develop and grow up in a
veritable sea of xenobiotic chemicals, says Isaac Pessah, director of
the University of California, Davis, Center for Children's Environmental
Health and Disease Prevention. "Fortunately," he says, "most of us have
a host of defense mechanisms that protect us from adverse outcomes.
However, genetic polymorphisms, complex epistasis, and cytogenetic
abnormalities could weaken these defenses and amplify chemical damage,
initiating a freefall into a clinical syndrome."

Pessah cites the example of autism. He says susceptibility for autism is
likely conferred by several defective genes, no one of which can account
for all the core symptoms of social disinterest, repetitive and overly
focused behaviors, and problems in communication. Could multiple genetic
liabilities and exposure to a chemically complex environment act in
concert to increase the incidence and severity of the condition?

Despite the uncertainties, many scientists believe it would be wise to
err on the side of caution when it comes to a research agenda. As Martha
Herbert, a pediatric neurologist at Harvard Medical School, puts it,
"Even though we may have neither consensus nor certainty about an autism
epidemic, there are enough studies coming in with higher numbers that we
should take it seriously. Environmental hypotheses ought to be central
to research now. The physiological systems that have been harmed by
environmental factors may also point to treatment targets, and this
might be a great way to help the children."

The Parade of Neurotoxicants
Among the most intensely studied neurotoxicants are metals (lead,
mercury, and manganese), pesticides, polychlorinated biphenyls (PCBs),
and polybrominated diphenyl ethers (PBDEs). A number of these compounds
were identified as neurotoxicants when individuals were exposed to high
doses during occupational accidents or childhood poisonings. Scientists
are now exploring the potential consequences of low-dose exposures,
especially to children and fetuses. Epidemiologic studies play a central
role, and these are often complemented by experimental work on animals
and cell cultures. These days, researchers are looking not only at
associations between toxicants and disease, but also at the underlying
cellular and molecular mechanisms.

Lead. Studies dating to the 1970s show that children exposed to lead
have deficits in IQ, attention, and language. In response, the CDC
revised its limits for acceptable blood levels of the metal in several
steps, from 60 micrograms per deciliter (g/dL) in the 1960s to the
current level of 10 g/dL, set in 1991. But many scientists think that
limit is still too high. A study reported in the September 2005 issue of
EHP found that there were significant effects on a child's IQ even when
blood lead concentrations were below 10 g/dL. Upon the July 2005
release of the Third National Report on Human Exposure to Environmental
Chemicals by the CDC, Jim Pirkle, deputy director for science at the
CDC's Environmental Health Laboratory, stated, "There is no safe blood
[lead] level in children."

Several groups have also found evidence that lead exposure may shape a
child's social behavior. An article in the May 2000 issue of
Environmental Research reports a strong correlation, dating back to
1900, between violent crime and the use of lead-based paint and leaded
gasoline. The research complements studies by Herbert Needleman, a
professor of psychiatry and pediatrics at the University of Pittsburgh
School of Medicine, who found that bone lead levels in young males were
correlated with aggression and criminality. "Lead is significantly
associated with a risk for delinquency," says Needleman. His research
appeared in the November-December 2002 issue of Neurotoxicology and
Teratology and the 7 February 1996 issue of JAMA.

Another new area of research links early lead exposure to changes in the
aging brain. Nasser Zawia, an associate professor of pharmacology and
toxicology at the University of Rhode Island, Kingston, and his
colleagues found increased expression of amyloid precursor protein (APP)
and its product, -amyloid (which is a hallmark of Alzheimer disease),
in aging rats that were exposed to lead shortly after birth. In
contrast, old rats that were exposed to lead did not show an increased
expression of APP and -amyloid. The work, published in the 26 January
2005 issue of The Journal of Neuroscience, suggests that early exposure
to lead can "reprogram" gene expression and regulation later in life.
According to Zawia, preliminary research also shows that "monkeys
exposed to lead as infants exhibit similar molecular changes as well as
exaggerated Alzheimer's pathology."

Mercury. The current Environmental Protection Agency (EPA) reference
dose for methylmercury (an organic, toxic form of mercury) is 0.1
micrograms per kilogram per day (g/kg/day). Humans are exposed to
methylmercury primarily through consumption of contaminated fish; a good
70% of this contamination comes from anthropogenic sources such as
emissions from coal-fired power plants. High-level exposure to
methylmercury in the womb is linked to a number of impairments,
including mental retardation, cerebral palsy, seizures, deafness,
blindness, and speech difficulties. An article in the May 2005 issue of
EHP puts the economic cost to the United States of methylmercury-induced
toxicity (in terms of lost productivity) at $8.7 billion annually.

The effects of low-dose exposures are not so apparent. Two large
epidemiologic studies of fishing populations in the Faroe Islands and
the Seychelles have produced conflicting results regarding low-dose
effects. Both studies sought to examine the association between
methylmercury exposure and neurodevelopment in children whose mothers
ate contaminated seafood during pregnancy.

The leader of the Faroe Islands study, Philippe Grandjean, an adjunct
professor of environmental health at the Harvard School of Public
Health, and his colleagues reported in the November 1997 issue of
Neurotoxicology and Teratology that 7-year-old Faroese children had
significant cognitive deficits and neurological changes after prenatal
exposure to methylmercury. Grandjean's team followed up on the children
at age 14. According to a report in the February 2004 issue of The
Journal of Pediatrics, the children continued to have problems,
including neurological changes and decreased nervous control of the

In contrast, the authors of the Seychelles study found little evidence
of lasting harm on a cohort of 66-month-old children, according to their
report in the 26 August 1998 issue of JAMA. A follow-up study, published
in the 17 May 2003 issue of The Lancet, similarly found no lasting
effects on language, memory, motor skills, or behavioral function when
the children were 9 years old.

The different outcomes of the two studies are puzzling because the
children of both populations appeared to be exposed to similar amounts
of methylmercury. Several explanations have been proposed, including the
possibility that genetic differences between the populations may alter
their relative predispositions to harm from mercury exposure. The source
of methylmercury is also different in the two populations. The Faroese
are exposed primarily through the consumption of pilot whale meat,
whereas the Seychelles population relies heavily on ocean fish.
According to Gary Myers, a professor of neurology and pediatrics at the
University of Rochester Medical Center and one of the principal
investigators of the Seychelles study, whale meat contains many other
contaminants (including PCBs) besides methylmercury. "There is also
evidence," he says, "that the effects of concomitant PCB and mercury
exposure are synergistic."

Researchers continue to look at whether there is a danger from
methylmercury at the levels of exposure achieved by fish consumption.
Another layer of uncertainty was added with findings published in the
October 2005 issue of EHP showing that fish consumption during pregnancy
appeared to boost infant cognition--but only as long as mercury intake,
as measured in maternal hair, wasn't too high.

The question of whether low levels of mercury are harmful has also
manifested itself in a controversy over the use of vaccines containing
thimerosal, a preservative. Although thimerosal was removed from many of
these vaccines in 2001, children that were immunized before that date
could have received a cumulative dose of more than 200 g/kg of mercury
with the routine complement of childhood vaccinations, according to a
study in the May 2001 issue of Pediatrics. Thimerosal is nearly half
ethylmercury by weight. Because ethylmercury is an organic form of
mercury, there is some suspicion that it acts like methylmercury in the
brain, although research published in the August 2005 issue of EHP
suggests that the two forms differ greatly in how they are distributed
through and eliminated from the brain. Developing countries continue to
use pediatric vaccines that contain thimerosal. In the United States,
thimerosal is still present in influenza vaccines, which the CDC
recommends be given to pregnant women and children aged 6-23 months.

Advocacy groups, such as SafeMinds, have suggested that the decades-long
rise in the diagnosis of autism is related to the presence of thimerosal
in vaccines. In May 2004, however, the Institute of Medicine (IOM)
issued a report, Immunization Safety Review: Vaccines and Autism,
stating that several epidemiological studies published since 2001
"consistently provided evidence of no association" between
thimerosal-containing vaccines and autism. However, the IOM's report has
been severely criticized by a number of advocacy groups, including the
National Autism Association, for relying too heavily on a specific set
of epidemiologic data while dismissing clinical evidence and other
epidemiologic studies that showed evidence of a link.

Despite the assurances of the IOM, some scientists continue to explore
the mechanisms underlying the potential neurotoxic effects of
thimerosal. In the January 2005 issue of NeuroToxicology, S. Jill James,
a professor of pediatrics at the University of Arkansas for Medical
Sciences, and her colleagues report that the neuronal and glial cell
toxicity of methylmercury and ethylmercury (as dosed via thimerosal) are
both mediated by the depletion of the antioxidant peptide glutathione.
Of the two cell types, neurons were found to be particularly susceptible
to ethylmercury-induced glutathione depletion and cell death, according
to James, and pretreatment of the cells with glutathione reduced these
effects. Other studies by James and her colleagues, reported in the
December 2004 issue of the American Journal of Clinical Nutrition,
showed that autistic children had lower levels of glutathione compared
to normal controls, and may therefore have had a significant reduction
in the ability to detoxify reactive oxygen species.

James says the abnormal profile "suggests that these children may have
an increased vulnerability to pro-oxidant environmental exposures and a
lower threshold for oxidative neurotoxicity and immunotoxicity."
Speaking at the XXII International Neurotoxicology Conference in
September 2005, she presented evidence that multiple genetic
polymorphisms affecting glutathione pathways may interact to produce a
chronic metabolic imbalance that could contribute to the development and
clinical symptoms of autism. Her paper in the American Journal of
Clinical Nutrition reported that low glutathione levels in many autistic
children were reversible with targeted nutritional intervention, but the
ramifications of this finding are still unclear.

Manganese. As an essential nutrient, manganese is required for normal
development; the reference dose for manganese is 0.14 mg/kg/day. Chronic
occupational exposure to high levels of this metal is associated with
manganism, a condition reminiscent of Parkinson disease that is
characterized by tremors, rigidity, and psychosis. The illness is seem
primarily among miners.

Animal studies published in the August 2005 issue of Neurotoxicology by
David Dorman, director of the division of biological sciences at the
CIIT Centers for Health Research in Research Triangle Park, North
Carolina, suggest that the fetus is protected to a certain extent from
maternally inhaled manganese. According to Dorman, children are exposed
to manganese primarily by ingesting it, but he knows of no link between
childhood exposure to manganese and later Parkinson disease.

Nevertheless, because manganese affects the adult brain, people suspect
that the developing brain may be even more susceptible to harm from this
metal, and recent research has unveiled a new cause for concern: In the
January 2006 issue of EHP, child psychiatry professor Gail Wasserman and
colleagues from Columbia University reported that Bangladeshi children
who drank well water with high concentrations of naturally occurring
manganese had diminished intellectual function. The researchers noted
that the bioavailability of manganese in water is higher than that of
manganese in food. They also pointed out that about 6% of U.S. wells
have a high enough manganese content to potentially put some children at
risk for diminished intellectual function.

The cellular and molecular mechanisms of manganese neurotoxicity are not
well understood. The dopaminergic system in the basal ganglia, which is
affected in Parkinson disease, may be involved, but this hypothesis is
controversial. Toms Guilarte, a professor of molecular neurotoxicology
at the Johns Hopkins Bloomberg School of Public Health, described
research on these systems in nonhuman primates at the XXII International
Neurotoxicology Conference. According to Guilarte, unpublished
positron-emission tomography studies of the basal ganglia show that
"manganese does appear to have an effect on dopaminergic neurons."
Guilarte found that the more manganese the animals received, the less
dopamine was released through the actions of amphetamine (which is used
to induce the release of the neurotransmitter). "This does not mean that
manganese causes Parkinson's disease, merely that it has an effect on
those neurons," he says. This is the first report of an in vivo effect
on dopamine release by manganese.

PCBs, PBDEs, and pesticides. Many chemicals raise concerns because of
their persistence in the environment and their tendency to bioaccumulate
in animal tissues. They are typically synthetic molecules that were
designed for use in everyday products, such as electrical equipment,
computers, furniture, and pesticides.

PCBs appear to be present in all parts of the food chain, and humans are
exposed to these molecules primarily through the ingestion of animal
fat. The toxicity of these chemicals was first recognized after mass
poisonings in Japan in 1968 and Taiwan in 1979. Children born to women
who had ingested contaminated cooking oil in Taiwan had a number of
developmental abnormalities, including psychomotor delay and lower
scores on cognitive tests, according to a report in the 15 July 1988
issue of Science.

Since those earlier observations, several studies have described a
connection between prenatal exposure to PCBs and delayed cognitive
development and lower IQ. For example, a study in the 10 November 2001
Lancet reports those infants and young children exposed to PCBs through
breast milk scored lower on tests of psychomotor and mental development.
The mothers were exposed to normal background levels of PCBs in Europe.
In response to such studies, the U.S. Food and Drug Administration set
tolerance levels for PCBs in a number of consumer products, such as milk
and manufactured dairy products (1.5 parts per million), poultry (3.0
parts per million), and baby food (0.2 part per million).

PBDEs are widely used as flame retardants in consumer products. The
effects of PBDEs on humans is not clear, but animal toxicity studies
described in volume 183 (2004) of Reviews of Environmental Contaminants
and Toxicology show that PBDEs can cause permanent learning and memory
impairments, hearing deficits, and behavioral changes. There is a
growing concern about PBDEs because they appear to be accumulating in
human tissues. Andreas Sjdin, a toxicologist at the CDC, and colleagues
found a trend toward increasing concentrations of PBDEs in human serum
taken from sample populations in the southeastern United States from
1985 through 2002, and in Seattle, Washington, from 1999 through 2002.
This report appears in the May 2004 EHP. Several studies have also
discovered PBDEs in human breast milk. The current EPA reference dose
for PBDEs is 2 mg/kg/day.

As for pesticides, it's been suggested by zoologist Theo Colborn of the
University of Florida that every child conceived today in the Northern
Hemisphere is exposed to these chemicals from conception through
gestation and beyond. Some pesticides appear to be more harmful than
others, and so the reference dose varies somewhat from one compound to

The effects of pesticides on the developing brain have been investigated
in human epidemiologic studies and in laboratory experiments with
animals. Vincent Garry, a professor of environmental medicine at the
University of Minnesota, and his colleagues found that children born to
applicators of the fumigant phosphine were more likely to display
adverse neurological and neurobehavioral developmental effects. The
herbicide glyphosate was also linked to neurobehavioral effects,
according to the same report, which appeared in the June 2002 issue of
EHP Supplements. Another epidemiologic study, reported in the March 2005
issue of NeuroToxicology, showed that women who were exposed to
organophosphate pesticides in an agricultural community in California
had children who displayed adverse neurodevelopmental effects, and that
higher levels of pesticide metabolites in maternal urine were associated
with abnormal reflexes in the women's newborn children.

Many PCBs, PBDEs, and pesticides are the subject of the 2001 Stockholm
Convention on Persistent Organic Pollutants, which became international
law in May 2004. The goal of the treaty is to "rid the world of PCBs,
dioxins and furans, and nine highly dangerous pesticides," according to
the United Nations Environment Programme. Implementation of the treaty
has significant practical challenges, however, including the difficulty
of eliminating one persistent pollutant without creating another (for
example, when burning PCBs yields by-products such as dioxins and

Not Immune to Harm
Exposure to a neurotoxicant may not be the only way to disrupt the
natural growth of the brain. Scientists are now looking at the subtle
physiological effects of immunotoxicants and infectious agents on
biological events during development.

It turns out that mothers who experience an infection during pregnancy
are at a greater risk of having a child with a neurodevelopmental
disorder such as autism or schizophrenia. For example, prenatal exposure
to the rubella virus is associated with neuromotor and behavioral
abnormalities in childhood and an increased risk of schizophrenia
spectrum disorders in adulthood, according to an article in the March
2001 issue of Biological Psychiatry. Rubella has also been linked to
autism: some 8-13% of children born during the 1964 rubella pandemic
developed the disorder, according to a report in the March 1967 Journal
of Pediatrics. The same study also noted a connection between the
rubella virus and mental retardation.

Some epidemiologic studies have found an increased risk of schizophrenia
among the children of women who were exposed to the influenza virus
during the second trimester of pregnancy, according to a report in the
February 2002 Current Opinion in Neurobiology. In the August 2004
Archives of General Psychiatry, Ezra Susser, head of epidemiology at
Columbia University's Mailman School of Public Health, and his
colleagues reported that the risk of the mental disorder was increased
sevenfold if the schizophrenic patient's mother had influenza during her
first trimester of pregnancy. A prospective birth cohort study in the
April 2001 Schizophrenia Bulletin found that second trimester exposure
to the diphtheria bacterium also significantly increased the risk of

How might infectious agents cause these disorders? According to John
Gilmore, a professor of psychiatry at the University of North Carolina
at Chapel Hill, maternal infections during pregnancy can alter the
development of fetal neurons in the cerebral cortex of rats. The
mechanism is far from clear, but signaling molecules in the mother's
immune system, called cytokines, have been implicated. Speaking at the
XXII International Neurotoxicology Conference, Gilmore described in
vitro experiments showing that elevated levels of certain
cytokines--interleukin-1, interleukin-6 and tumor necrosis factor-alpha
(TNF-)--reduce the survival of cortical neurons and decrease the
complexity of neuronal dendrites in the cerebral cortex. "I believe that
the weight of the data to date indicates [that the maternal immune
response] can have harmful effects," says Gilmore.

Inflammatory responses in the mother may not be the only route to
modifying the fetal brain. The University of California, Davis, Center
for Children's Environmental Health and Disease Prevention is conducting
a large study of autistic children in California called CHARGE
(Childhood Autism Risks from Genetics and the Environment), which
suggests that the child's immune system may also be involved. According
to Pessah, the study principal investigator, children with autism appear
to have a unique immune system. "Autistic children have a significant
reduction in plasma immunoglobulins and a skewed profile of plasma
cytokines compared to other children," he says. "We think that an immune
system dysfunction may be one of the etiological cores of autism."

He continues, "We know that many of the things that kids are exposed to
these days are immunotoxicants. . . . We have evidence that ethylmercury
and thimerosal alter the signaling properties of antigen-presenting
cells, known as dendritic cells, at nanomolar levels." Since each
dendritic cell can activate 250 T cells, any dysregulation will be
magnified, he says. "Add to that a genetic abnormality in processing
immune information, and there could be a problem."

Such problems might extend to the central nervous system. The brains of
individuals who have a neurodevelopmental disorder also show evidence of
inflammation. In the January 2005 issue of the Annals of Neurology,
Carlos Pardo, an assistant professor of neurology and pathology at the
Johns Hopkins University School of Medicine, and his colleagues report
finding high levels of inflammatory cytokines (interleukin-6,
interleukin-8, and interferon-) in the cerebrospinal fluid of autistic
patients. Glial cells, which serve as the brain's innate immune system,
are the primary sources of cytokines in the central nervous system. So
it may not be surprising that Pardo's team also discovered that glia are
activated--showing both morphological and physiological changes--in
postmortem brains of autistic patients.

The recognition that the immune system is involved in neurodevelopmental
disorders is changing people's perceptions of these conditions.
"Historically, scientists have focused on the role of neurons in all
kinds of neurological diseases," Pardo says, "but they have generally
been ignoring the [glia]." He adds, "In autism, it could be that the
[glia] are responding to some external insult, such as an infection, an
intrauterine injury, or a neurotoxicant."

According to Pardo, it's still not clear whether the neuroimmune
responses associated with autism contribute to the dysfunction of the
brain or whether they are secondary reactions to some neural
abnormality. "John Gilmore's work [showing that cytokines can be harmful
to brain cells] is quite interesting and important," he says. "However,
in vitro studies may produce results that don't reflect what occurs
under in vivo conditions. Cytokines like TNF- may be beneficial for some
neurobiological functions at low concentrations, but may be extremely
neurotoxic at high concentrations."

Lending Brain Power to Exposure Assessment
The medical and scientific communities recognize the colossal challenges
involved in identifying the ultimate causes of neurodevelopmental
disorders. This is complicated by the sheer numbers of potential
exposures involved. More than 67% of the nearly 3,000 chemical compounds
produced or imported in amounts exceeding 1 million pounds per year have
not been examined with even basic tests for neurotoxicity, according to
Toxic Ignorance, a 1997 analysis by Environmental Defense.

In the past few years, several large projects have been proposed, and
funding by the NIH has been increased. For example, the NIH boosted its
support for autism research from $22 million in 1997 to $100 million in
2004. In 2001, the NIEHS and the EPA jointly announced the creation of
four new children's environmental health research centers (including the
one at the University of California, Davis), which focus primarily on
neurodevelopmental disorders. More recently, the proposed
multibillion-dollar National Children's Study, which is cosponsored by
the Department of Health and Human Services and the EPA, has been
designed to follow nearly 100,000 children over the course of 21 years.
The investigators plan to study the effects of environmental factors on
children's growth and development, including impacts on learning,
behavior, and mental health. Study investigators hope to enroll the
first participants in early 2007.

Scientists also see the need for designing better studies. In
neurodevelopmental studies, as in any other field, the quality of a
study is only as good as all of its parts. Jean Harry, head of the NIEHS
Neurotoxicology Group, says, "You can have a valid assessment of
behavior, but in the absence of good exposure data, a causative
association with environmental factors will be compromised."

In a bid to address the difficulties faced by epidemiologic studies
that look for neurodevelopmental effects from in utero chemical
exposure, a working group of 20 experts gathered in September 2005 under
the auspices of the Penn State Hershey Medical Center, coincident with
the XXII International Neurotoxicology Conference. The goal of their
day-long session was to develop a scheme of best practices for the
design, conduct, and interpretation of future investigations, as well as
the practical inclusion of new technologies, such as imaging.

At one point in the dialogue, the group recognized that perhaps the
greatest challenge in these studies was determining how to evaluate in
utero exposures to environmental chemicals. "Quite often the very nature
of epidemiological studies limits the ability to perform accurate
exposure assessments," says Harry, who was part of the expert group.
"Such exposures may have occurred in the distant past, they may have
been unknown, or they may have been in conjunction with many other

The group therefore recommended that actual measurements, even if
indirect, are better than methods based on subject recall. It also
recommended that a well-defined hypothesis should form the foundation of
in utero studies for assessing neurodevelopmental outcomes. "[These and
other] conclusions will move the science forward by describing methods
that should improve interstudy comparisons, and they offer ways in which
research results should be reported to the scientific and medical
communities," says Judy LaKind, an adjunct associate professor of
pediatrics at the Hershey Medical Center and a member of the workshop
steering committee. The complete workshop report will be published in an
upcoming issue of NeuroToxicology.

Imagining the Big Picture
The challenges of addressing neurodevelopmental disorders are more than
scientific. The difficulties come together at a crossroads where the
communication of knowledge, the treatment of patients, and theregulation of
potentially toxic chemicals meet. Says Herbert,
"Evidence-based medicine has not yet developed standards for assessing,
or practices for treating, the impacts of chronic, multiple low-dose
exposures." Rather than waiting, she says, patients and parents of
patients are turning to alternative medicine to address their concerns.

That's not always a good thing, especially when patients and parents may
be misinformed. Kathy Lawson, director of the Healthy Children Project
at the Learning Disabilities Association of America, says there is a
disconnect between scientific knowledge and the public's awareness of
ways to reduce the incidence of some disorders. "In my visits to various
organizations, I've discovered that people are completely unaware that
there is a connection between environmental toxicants and their health,"
she says. "Even pediatricians often don't know about these things," she

Educating the public is only part of the solution. Elise Miller,
executive director of the nonprofit Institute for Children's
Environmental Health, thinks that federal regulatory agencies do not
adequately protect children's health. "The Toxic Substances Control Act,
which was passed thirty years ago, needs a major overhaul to ensure
neurotoxicants and other chemicals are prioritized, screened, and tested
properly," she says. "Currently, there are too many chemicals on the
market and in the products we use every day for which there is no
toxicity data."

Some politicians agree with these sentiments. In July 2005, Senator
Frank R. Lautenberg (D-NJ) introduced the Child, Worker, and Consumer
Safe Chemicals Act, which initially calls for chemical manufacturers to
provide health and safety information on the chemicals used in certain
consumer products, among them baby bottles, water bottles, and food
packaging. If passed into law, the bill, coauthored by Senator James
Jeffords (I-VT), would require all commercially distributed chemicals to
meet the new safety measures by 2020.

The human brain is often touted as the most complex structure in the
known universe. The developmental process that produces this remarkable
entity may also be among the most delicate in nature. As one scientist
put it, "The brain doesn't like to be jerked around." That kind of
fragility makes it difficult for scientists to untangle genetic
influences from what often may be subtle environmental assaults. Even
so, the catalogue of harmful environmental agents will undoubtedly
continue to grow as scientists learn more about the interactions between
the developing brain and its environment. The hope is that enough good
minds will use that catalogue to create a future with healthier brains
and more peace of mind for parents and society alike.             


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