4 Toxic Threats to Your Child’s Development
Animal tests show that small, single doses of organophosphates [class of pesticides] on a critical day of development can cause hyperactivity and permanent changes in neurotransmitter receptor levels in the brain. Some pyrethroids, another class of commonly used pesticides, cause permanent hyperactivity in animals exposed to small doses on a singe critical day of development.
Mercury 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.
According 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.
Exposure to organic solvents during development may cause a spectrum of disorders, including structural birth defects, hyperactivity, attention deficits, reduced IQ, learning and memory deficiencies.
Of the 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… Over a billion pounds of these neurotoxic chemicals were released directly on-site by large, industrial facilities into the air, water, and land.
Children exposed to a variety of pesticides in Mexico show impaired stamina, coordination, memory, and capacity to represent family subjects in drawings.
Certain genes may … cause individuals to be more susceptible to environmental “triggers.” Two 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.
Children exposed to PCBs during fetal life show IQ deficits, hyperactivity, and attention deficits when tested years later.
A recent five-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.
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. Multi-chemical exposures often interact to magnify damaging effects or cause new types of harm.
Developmental neurotoxicants are chemicals that are toxic to the developing brain. They include: metals like lead, mercury, cadmium, and manganese; nicotine; pesticides such as organophosphates and others that are widely used in homes and schools; dioxin and PCBs that bioaccumulate in the food chain; 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.
- Lead: Associated with attention deficits, increased impulsiveness, reduced school performance, aggression, and delinquent behavior. Effects on learning are seen at blood lead levels below those currently considered “safe.”
- Mercury: Large fetal exposures to methylmercury cause mental retardation, and gait and visual disturbances. Smaller 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.
- Manganese: 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.
- Nicotine: Children born to women who smoke during pregnancy are at risk for IQ deficits, learning disorders, and attention deficits. Children born to women who are passively exposed to cigarette smoke are also at risk for impaired speech, language skills, and intelligence.
More Important Facts
The number of children known to be affected by developmental disabilities is staggering and appears to be increasing.
The historical record clearly reveals that our scientific understanding of the effects of toxic exposure 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.
Although our understanding is incomplete, we are now certain that complex interactions among genetic and environmental factors play extremely important roles. It is no longer in keeping with the state of scientific understanding to attribute the bulk of these developmental disabilities to genetic inheritance.
Animal studies of lead, mercury, and PCBs each underestimated the levels of exposure that cause effects in humans by 100 to 10,000 fold. Regulatory decisions that rely largely on toxicity testing in genetically similar animals… will continue to fail to reflect threats to the capacities and complexity of the human brain, as well as important gene-environment interactions.
Inuit 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.
The failure of the regulatory system to protect public health can often be traced to the influence of vested economic interests upon the regulatory process.
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.
Excerpted with permission from In Harm’s Way, a report by the Greater Boston Physicians for Social Responsibility. Some sections have been summarized for space.