Neurotoxicants Threaten Childhood Development

Arline Kaplan / Psychiatric Times v.18, i.3 Mar01

Pervasive and insidious toxicological experiments are being conducted on our nation's children, warned authors of a national report issued by the Greater Boston Physicians for Social Responsibility (GBPSR). One million children in the United States already have blood lead levels of 10 mgrams/dL or above, which can affect their behavior and cognition. Among children examined in one study, 90% had a metabolite of the neurotoxic pesticide chlorpyrifos present in their urine. And, according to U.S. 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 told Psychiatric Times that the report, available online at www.igc.org/psr/, has sparked requests from the National Institute of Environmental Health Services for proposals and will serve as the basis of day-long workshops to be conducted at medical colleges and centers throughout the United States beginning in April.

Vast quantities of neurotoxic chemicals are released into the environment each year, the report authors explained. 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 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. According to the GBPSR, an estimated 80,000 chemicals are in commercial use in the United States. Since most of them have been synthesized since World War II, they are relatively new to the human environment in the evolutionary time frame. Yet the report found that basic toxicity information is missing from publicly available sources for nearly 75% of the top 3,000 high-production volume substances.

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 for only 12 chemicals (nine pesticides and three solvents). Meanwhile, in August 1999, the EPA announced a "data call-in" for 140 pesticides considered to be neurotoxic. This requires manufacturers to conduct and submit tests of acute, subchronic and developmental neurotoxicity.

"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."

This scarcity of information combined with pervasive human exposures to many toxic chemicals and seriously inadequate regulatory oversight 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 indicate that nearly 12 million children (17%) in the United States suffer from one or more learning, developmental or behavioral disabilities. Attention-deficit/hyperactivity disorder and learning disabilities affect up to 6% and 10%, respectively, of schoolchildren. The incidence of autism may be as high as two per 1,000 children; in Brick Township, N.J., at least 42 children have been identified with autism, more than three times the estimated national average of one in 500. This 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 wrote. "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. While physicians are familiar with the adverse effects associated with some chemicals (e.g., alcohol and nicotine), it is unclear how much they are aware of other dangers. "They sort of know the lead story," he said, "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 ofthe 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 the 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."

The report summarizes 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, xylene, styrene and others 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 and gait and visual disturbances (e.g., Grandjean et al., 1997). The authors also note several studies that report a relationship between excessive childhood levels of manganese exposure and hyperactivity or learning disabilities. Similarly, children exposed to a variety of pesticides in an agricultural community in Mexico showed impaired stamina, coordination, memory and capacity to represent familiar subjects in drawing (Figure) (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 (e.g., Bellinger et al., 1987).

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 impulsiveness, aggressiveness and dysfunctional social behavior [Rice, 1998]."

By translating and then disseminating neurodevelopmental toxicity research, the report authors hope that physicians and other health care professionals will incorporate the knowledge into their clinical practices.

"For psychiatrists, just like other health care providers who deal with children and families, 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. "Protecting Your Child From Toxic Threats to Brain Development: Personal Guidelines for Children, Parents and Future Parents," available online at www.igc.org/psr/protect-child.htm, discusses ways to reduce risks.

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, parents 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." While he doesn't believe society should halt progress, he asserts, "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…[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." Schettler said 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.

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.

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.

Rice DC (1998), Developmental lead exposure: neurobehavioral consequences. In: Handbook of Developmental Neurotoxicology, Slikker W Jr, Chang LW, eds. San Diego: Academic Press.

source: http://www.mhsource.com/pt/p010301a.html 20jan02

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