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Learning and Developmental
Disabilities and Toxic Chemical Exposures

lockerThe role of environmental factors — particularly toxic chemical exposures — in the onset, trajectory, and overall incidence of a number of diseases and disabilities is often overlooked. While adverse health outcomes are the result of a complex interplay of multiple factors, including heredity, gene-environment interaction, nutrition, and socioeconomic status, both laboratory and human studies indicate that toxic chemical exposures may play a role. Scientific evidence implicates environmental exposures as discernable contributors to adverse health outcomes, such as cancer, neurodegenerative diseases, reproductive health problems, and learning and developmental disabilities.

It is important to note that both the dosage and the timing of exposure have significant roles in determining potential health outcome. The presence of environmental chemicals in the human body does not necessarily imply that they are causing adverse health effects.

Below is a list of the chemicals included in this study and some of the health outcomes that have been associated with exposure to them. This list serves as a quick reference and a shorthand introduction to the chemical fact sheets found in Appendix B. For many of these chemicals, it is not possible to prove that they are responsible for adverse health outcomes in humans. Information regarding the neurotoxicity or developmental neurotoxicity of these chemicals is often from laboratory experiments, typically with animal subjects. Conclusive human epidemiological studies are rare. The scientific community must rely on the weight of evidence that these chemicals can alter development or disrupt normal brain function. For some chemicals, the weight of evidence is strong enough for the scientific community to accept a causal relationship; for others this strong connection has yet to be established, and may never be. Regardless, precaution dictates that we take action to reduce and eliminate harmful exposures.

Information about these chemicals was gathered from primary research and review articles. The actions of these chemicals, suspected of disrupting normal neurological development or functioning, are included with citations. In cases where there is a lack of human data, animal studies are used to provide evidence of adverse effects. While toxicity research conducted on animals is not conclusive, animal toxicological studies have been shown to help predict human health impacts.31

The following chemicals are known or suspected to adversely affect human health, and specifically neurodevelopment. The weight of evidence for adverse outcomes varies with each chemical, and is represented below.

Bisphenol A

Animal: BPA has estrogenic activity and as such alters both sexual development and neurobehavior.32,33 BPA blocked the receptors for estradiol in the hippocampus and prefrontal cortex of rodents and non-human primates.34 BPA was found to reduce nerve cell density in certain parts of the mouse brain.35 A study of mice found that prenatal exposure to BPA produced memory impairments.36
Human: Prenatal BPA exposure is associated with altered behavior in two-year old children, especially females.37
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Human: Prenatal exposure to lead is associated with premature births, reduced growth, learning difficulties and decreased IQ.38,39 Exposures to lead are also associated with neuropsychiatric disorders such as attention deficit hyperactivity disorder (ADHD) and antisocial behavior.40,41 There is also evidence that lead damages brain tissue.42,43 Research shows that there is no safe level of exposure to lead in children. Early exposure to lead has been reported to lead to juvenile delinquency.44
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Human: Reported neurobehavioral effects of mercury exposure include altered motor function and memory, as well as learning disabilities.45 Developing fetuses and children are particularly vulnerable to impairment of the developing central nervous system, as well as pulmonary and nephrotic damage.46,47,48
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Organochlorine pesticides

Animal: Exposure to organochlorine pesticides has been associated with permanent behavioral changes, and altered androgen levels in rats.49,50
Human: Exposure to organochlorine pesticides has been associated to decreased psychomotor function and mental function, including memory, attention, and verbal skills in children.51,52,53 Much of this research was carried out in children raised in agricultural areas with exposures that are higher than in non-agricultural areas.
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Animal: Numerous studies on rodents suggest that neonatal exposure to PBDEs permanently affects learning and memory functions, impairs motor activity, and is associated with aberrations in spontaneous motor behavior and hyperactivity.54,55,56
Human: Prenatally exposed children demonstrated impaired fine motor skills and attention.57 Elevated levels of PBDEs 47, 99, and 100 in umbilical cord blood were correlated with lower scores on multiple developmental tests in children.14 These studies evaluated effects at typical exposure levels for the U.S. population.
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Animal: Maternal perchlorate exposure was associated with a reduction of iodine in breast milk and a reduction in neonatal thyroid hormone levels in rats.58
Human: High doses of perchlorate cause changes in iodine uptake but not thyroid hormones in otherwise healthy individuals.59 Women with low iodine levels were likely to have decreased T4 when exposed to perchlorate.60 Research suggests that maternal perchlorate exposure during pregnancy could potentially cause abnormal development through hypothyroidism.61
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Animal: Adult mice that were prenatally exposed to PFOA and PFOS displayed decreased spontaneous behavior, increased hyperactivity, and lack of habituation to a new environment.62
Human: PFOA and PFOS exposure in utero has also been associated with small reductions in birth weight in newborn babies at typical exposure levels for the U.S. population.63,64
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Animal: Triclosan disrupts thyroid hormone function in rats65,66 and disrupts normal physical development in frogs.67 Triclosan disrupts normal estrogen transportation pathways in sheep placenta.68
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