Abstract
Children are widely viewed as the population subgroup that is most vulnerable to the toxicities that result from exposure to environmental chemicals. Their enhanced vulnerability is due to a variety of behavioral and physiologic factors. For many chemicals, the central nervous system (CNS) is the most sensitive target organ. In general, the impacts depend on a chemical’s mode of action, the dose, and the stage of development at which exposure occurs. This paper surveys the toxicology of environmental chemicals, specifically the impacts on children’s intellectual development. It focuses on metals (or metalloids), including mercury, lead, arsenic, fluoride, as well as on pesticides, air pollution, synthetic organic chemicals, and endocrine disruptors. The final section discusses issues germane to estimating the global burden of disease associated with exposures to neurotoxic environmental chemicals.
Original abstract online at http://pm.amegroups.com/article/view/4617/html
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Sex-Specific Neurotoxic Effects of Early-Life Exposure to Fluoride: a Review of the Epidemiologic and Animal Literature.
Purpose of Review: A growing body of evidence suggests adverse neurodevelopmental effects of early-life exposure to fluoride that may differ depending on timing of exposure and sex of the exposed. We conducted a literature search to identify the animal and human epidemiologic studies that examined sex-specific neurodevelopmental differences in response
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The effects of high levels of fluoride and iodine on intellectual ability and the metabolism of fluoride and iodine.
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The relationship of a low-iodine and high-fluoride environment to subclinical cretinism in Xinjiang.
Cretinism in iodine-deficiency areas is well known, yet the milder forms of somatic and psychomotor maldevelopment and thyroid dysfunction caused by iodine deficiency may be more difficult to detect. DeQuervain, in 1936, called this milder form "semi-cretinism," while in 1980 Laggasse used the term "cretinoidism." It was formally named "subclinical
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Vitamin A deficiency: An oxidative stress marker in sodium fluoride (NaF) induced oxidative damage in developing rat brain
Fluoride induced oxidative stress through depletion in levels of various anti-oxidants such as glutathione, superoxide dismutase (SOD), fat soluble vitamins (D and E) with increased levels of lipid peroxidation (LPO) and fluoride aggravate the damage in rodents as well as in humans. Vitamins A, a fat soluble vitamin possess antioxidant
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An Evaluation of Neurotoxicity Following Fluoride Exposure from Gestational Through Adult Ages in Long-Evans Hooded Rats.
At elevated levels, fluoride (F-) exposure has been associated with adverse human health effects. In rodents, F- exposure has been reported to induce deficits in motor performance and learning and memory. In this study, we examined Long-Evans hooded male rats maintained on a standard diet (20.5 ppm F-) or a low
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