In Harm's Way
report examines the contribution of toxic chemicals to neurodevelop-mental,
learning, and behavioral disabilities in children. These disabilities are
clearly the result of complex interactions among genetic, environmental and
social factors that impact children during vulnerable periods of development.
Toxic exposures deserve special scrutiny because they are preventable causes of
is estimated that nearly 12 million children (17%) in the United States
under age 18 suffer from one or more learning, developmental, or behavioral
deficit hyperactivity disorder (ADHD), according to conservative estimates,
affects 3 to 6% of all school children, though recent evidence suggests the
prevalence may be as high as 17%. The number of children taking the drug
Ritalin for this disorder has roughly doubled every 4-7 years since 1971 to
reach its current estimate of about 1.5 million.
disabilities alone may affect approximately 5-10% of children in public
number of children in special education programs classified with learning
disabilities increased 191% from 1977-1994.
1% of all children are mentally retarded.
incidence of autism may be as high as 2 per 1000 children. One study of
autism prevalence between 1966 and 1997 showed a doubling of rates over that
time frame. Within the state of California, the number of children entered
into the autism registry increased by 210% between 1987 and 1998.
trends may reflect true increases, improved detection, reporting or record
keeping, or some combination of these factors. Whether new or newly recognized,
these statistics suggest a problem of epidemic proportion.
Animal and human studies demonstrate that a variety of chemicals commonly encountered in industry and the home can contribute to developmental, learning, and behavioral disabilities.
Developmental neurotoxicants are chemicals that are toxic to the developing brain. They include the metals lead, mercury, cadmium, and manganese; nicotine; pesticides such as organophosphates and others that are widely used in homes and schools; dioxin and PCBs that bioaccumu-late in the food chain; and solvents, including ethanol and others used in paints, glues and cleaning solutions. These chemicals may be directly toxic to cells or interfere with hormones (endocrine disruptors), neurotransmitters, or other growth factors.
in blood lead levels during infancy and childhood are associated with
attention deficits, increased impulsiveness, reduced school performance,
aggression, and delinquent behavior.
on learning are seen at blood lead levels below those currently considered
Large fetal exposures to methylmercury cause mental retardation, gait and visual disturbances.
fetal exposures, such as those resulting from regular maternal fish
consumption, have been implicated in language, attention, and memory
impairments that appear to be permanent.
many other metals, some manganese is essential as a catalyst in several
critically important enzymatic processes. However, several studies report a
relationship between excessive childhood levels of manganese exposure and
hyperactivity or learning disabilities.
born to women who smoke during pregnancy are at risk for IQ deficits,
learning disorders, and attention deficits.
born to women who are passively exposed to cigarette smoke are also at risk
for impaired speech, language skills, and intelligence.
Monkeys exposed to dioxin as fetuses show
evidence of learning disabilities.
and animals exposed to low levels of PCBs as fetuses have learning
exposed to PCBs during fetal life show IQ deficits, hyperactivity, and
attention deficits when tested years later.
tests of pesticides belonging to the commonly-used organophosphate class of
chemicals show that small single doses on a critical day of development can
cause hyperactivity and permanent changes in neurotransmitter receptor
levels in the brain.
of the most commonly used organophosphates, chlorpyrifos (Dursban),
decreases DNA synthesis in the developing brain, resulting in deficits in
pyrethroids, another commonly used class of pesticides, also cause permanent
hyperactivity in animals exposed to small doses on a single critical day of
exposed to a variety of pesticides in an agricultural community in Mexico
show impaired stamina, coordination, memory, and capacity to represent
familiar subjects in drawings.
to organic solvents during development may cause a spectrum of disorders
including structural birth defects, hyperactivity, attention deficits,
reduced IQ, learning and memory deficiencies.
little as one alcoholic drink a day by a mother during pregnancy may cause
her offspring to exhibit impulsive behavior and lasting deficits in memory,
IQ, school performance, and social adaptability.
and limited human studies show that exposures to common chemicals like
toluene, trichloroethylene, xylene, and styrene during pregnancy can also
cause learning deficiencies and altered behavior in offspring, particularly
after fairly large exposures.
deluge of highly technical information has created communication gaps within
the field of child development.
pyrethroids cause permanent
recent explosion of research in the many sciences related to child
development has produced a glut of highly technical information not readily
understood by those outside the field in which the research was performed.
communication gap has resulted, dividing fields of research and separating
the domains of research, clinical practice, and the public.
and cognition can be described using clinical disorders, such as ADHD or
Asperger’s syndrome, which are categorical and qualitative. Alternatively,
behavior and cognition can be described using abilities/traits, such as
attention and memory, which are continuous and quantitative.
Abilities/traits cluster into disorders in various ways and are emerging as
an important bridge among the scientific disciplines focusing on child
Although genetic factors are important, they should not be viewed in isolation.
exposed to levels of dioxin that exceed adult
genes may be susceptible to or cause individuals to be more susceptible to
environmental “triggers.” Particular vulnerability to a chemical exposure
may be the result of a single or multiple interacting genes. For example:
for certain enzymes can influence how chemicals are metabolized or stored in
the body, or increase a person’s susceptibility to a chemical. For
example, a gene coding for the enzyme, delta aminolevulinic acid dehydratase
(ALA-D), can influence lead metabolism, bone storage of lead, and blood lead
genes increase susceptibility to organophosphate pesticides. One, carried by
4% of the population, results in lower levels of acetylcholinesterase, the
target enzyme of organophosphates. The other, carried by 30-40% of the
population, results in reductions in paroxonase, an enzyme that plays an
important role in breaking down organophosphate pesticides.
reactions to infections is another important gene-environment interaction.
For example, studies suggest that “PANDAS” (pediatric autoimmune
neuropsychiatric disorders associated with streptococcal infection), that
may affect patients with obsessive compulsive disorder, Tourette’s
syndrome and tics, result from streptococcal antibodies that cross react
with critical brain structures in genetically susceptible children.
are not merely a potential threat to children. In some instances, adverse
impacts are seen at current exposure levels.
to EPA estimates, about 1.16 million women in the U.S. of childbearing years
eat sufficient amounts of mercury-contaminated fish to risk damaging brain
development of their children.
infants are exposed to levels of dioxin that exceed adult exposures by as
much as a factor of 50. Dioxin exposures of this magnitude have been shown
to cause abnormal social behavior in monkeys exposed before birth through
the maternal diet. (While breast milk contaminants may compromise some of
the cognitive benefits of breast feeding, breast milk remains strongly
preferred over infant formula due to numerous important benefits to infant
exposure to PCBs at ambient environmental levels adversely affects brain
development, causing attention and IQ deficits, which remain detectable
years later and may be permanent.
that appear to have trivial effects on an individual have profound impacts
when applied across populations. For example, a loss of 5 points in IQ is of
minimal significance in a person with an average IQ. However a shift of 5 IQ
points in the average IQ of a population of 260 million increases the number
of functionally disabled by over 50% (from 6 to 9.4 million), and decreases
the number of gifted by over 50% (from 6 to 2.6 million).
quantities of neurotoxic chemicals are released into the environment each
the top 20 chemicals reported by the Toxics Release Inventory as released in
the largest quantities into the environment in 1997, nearly three-quarters
are known or suspected neurotoxicants. They include methanol, ammonia,
manganese compounds, toluene, phosphoric acid, xylene, n-hexane, chlorine,
methyl ethyl ketone, carbon disulfide, dichloromethane, styrene, lead
compounds, and glycol ethers. Over a billion pounds of these neurotoxic
chemicals were released directly on-site by large, industrial facilities
into the air, water, and land.
quantities of neurotoxic chemicals are also used in industrial processes and
incorporated into products. For example, according to 1997 data from the
Massachusetts Toxics Use Reduction Act, over half of the top twenty
chemicals in use (over 500 million pounds), and half of those incorporated
into products in Massachusetts, are known or suspected neurotoxicants.
of lead in manufacturing increased 77% in Massachusetts between 1990-1997.
additional 1.2 billion pounds of registered pesticide products are
intentionally and legally released each year in the United States.
contamination of our waterways is so widespread that 40 states have issued
one or more health advisories warning pregnant women or women of
reproductive age to avoid or limit fish consumption. Ten states have issued
advisories for every lake and river within the state’s borders.
releases often lead to human exposures with potential for harm. Dispersion
of these chemicals is global.
million children in the US exceed the currently accepted threshold for blood
lead level exposure that affects behavior and cognition (10 micrograms/dl).
Updating the toxic threshold in keeping with the results of the most recent
studies would further lower this threshold, resulting in the addition of
millions children to the roles of those impaired by lead exposure.
metabolite of the pesticide chlorpyrifos is present in the urine of over 80%
of adults and 90% of children from representative population samples.
mothers in the Arctic, far from sources of industrial pollution, have some
of the highest levels of PCBs in their breast milk as a result of a diet
rich in marine mammal fat.
historical record clearly reveals that our scientific understanding of the
effects of toxic exposures is not sufficiently developed to accurately
predict the impact of toxicants, and that our regulatory regime has failed
to protect children.
As testing procedures advance, we learn that lower and lower doses are harmful.
historical record shows that “safe thresholds” for known neurotoxicants have
been continuously revised downward as scientific knowledge advances. For
example, the initial “safe” blood lead level was set at 60
micrograms/deciliter (ug/dl) in 1960. This was revised down to 10 ug/dl in 1990.
Current studies suggest that lead may have no identifiable exposure level that
is “safe.” The estimated “toxic threshold” for mercury has also
relentlessly fallen, and like lead, any level of exposure may be harmful. Such
results raise serious questions about the adequacy of the current regulatory
regime, which, by design, permits children to be exposed up to “toxic
thresholds” that rapidly become obsolete.
Most chemicals are not tested for their general toxicity in animals or humans,
not to mention toxicity to a child’s developing brain specifically.
75% of the top high production and volume chemicals have undergone little or no
toxicity testing. However, the EPA estimates that up to 28% of all chemicals in
the current inventory of about 80,000 have neurotoxic potential. In addition:
tests for developmental neurotoxicity have been submitted to EPA for only 12
chemicals - nine pesticides and three solvents – as of December 1998.
for developmental neurotoxicity is not required even in the registration or
re-registration of pesticides, one of the strictest areas of chemical
c. Even when regulated, the risks from chemical exposure are estimated for one chemical at a time, while children are exposed to many toxicants in complex mixtures throughout development. Multiple chemical exposures often interact to magnify damaging effects or cause new types of harm.
the exception of pesticides used on the food supply, current regimes regulate
only one chemical at a time and do not take into account the potential for
interactions. Since real world exposures are to multiple chemicals, current
regulatory standards, based on single chemical exposures, are inherently
incapable of providing adequate margins of safety.
studies in humans and in the laboratory show that PCBs and mercury interact
to cause harm at lower thresholds than either substance acting alone.
recent 5-year pesticide study suggests that combinations of commonly used
agricultural chemicals, in levels typically found in groundwater, can
significantly influence immune and endocrine systems, as well as
neurological function, in laboratory animals.
Animal studies generally underestimate human vulnerability to neurotoxicants.
studies of lead, mercury and PCBs each underestimated the levels of
exposures that cause effects in humans by 100-10,000-fold.
decisions that rely largely on toxicity testing in genetically similar
animals under controlled laboratory conditions will continue to fail to
reflect threats to the capacities and complexity of the human brain as well
as important gene-environment interactions.
our children from preventable and potentially harmful exposures requires a
precautionary policy that can only occur with basic changes in the
inability of the current regulatory system to protect public health is not
surprising, considering the disproportionate influence of special interests
in the regulatory process. When there is evidence for serious, widespread
and irreversible harm, as described in this report, residual scientific
uncertainties should not be used to delay precautionary actions. Actions
should include reduction and or elimination of exposures as well as further
scientific investigation of developmental neurotoxicity.
Learning, behavior, and developmental disabilities in children are clearly the result of complex interactions among chemical, genetic and social-environmental factors that influence children during vulnerable periods of development. This report focuses on the role of toxic exposures since they are a preventable cause of harm. The cognitive and behavioral characteristics that result from these interacting influences can be described as traits or abilities, such as attention or memory, which can be measured quantitatively using a variety of neuropsychological tests. Aggregates of these traits are often described using diagnostic labels that identify clinical syndromes, such as attention deficit/hyperactivity disorder, autism or learning disability. Such labels are useful for the purpose of providing clinical interventions. However, traits are generally better suited to research since they can be readily defined, quantitatively measured, and are more amenable to animal models. As a result, a large body of scientific data has begun to describe the effects of chemicals or other influences on neurodevelopment in terms of effects on traits, rather than on clinical syndromes associated with diagnostic labels. In addition, traits provide a common denominator between different fields of research, and allow us to acknowledge influences on the neurocognitive function of “normal” populations, as well as on those with diagnostic labels.
Full Report and Executive Summary are available for pdf download at: http://www.preventingharm.org/harmswayreadmore.html
[ Pesticide Poisoning Site Map ] * [ Get Set Site Map ]