Neurotoxicology and Behavior

Abstract

Neurotoxicity is important to consider as a component of occupational and environmental safety and health programs. The failure to do so has contributed to a number of tragic cases in which workers, consumers of manufactured products, and people exposed in the environment were irreparably harmed by exposure to industrial compounds that proved toxic to the nervous system. The National Institute for Occupational Safety and Health (NIOSH) has listed neurotoxic disorders as one of the ten leading occupational problems in the United States. Many of the most severe environmental, industrial, and commercial human health disasters attributable to chemical exposure have involved neurotoxic effects. In Detroit, Michigan, in 1934, for example, an automotive redesign required grinding large amounts of excess lead solder from each car. Inhalation of the resulting lead dust produced between 2,700 and 4,000 cases of lead poisoning whose symptoms ranged from mild gastrointestinal upset to severe neurological deficits, including peripheral neuropathy and encephalopathy. As many as 12 people may have died. In another case that occurred during the Prohibition Era, a single batch of the popular ethanol-based elixir “Ginger Jake” was adulterated with tri-o-cresylphosphate (TOCP). This batch was then distributed throughout the southeastern and midwestern United States. As many as 50,000 people suffered peripheral neuropathy caused by degeneration of the large, long axons in the peripheral nerves of the legs and spinal cord. In a food contamination episode, 459 people were killed and more than 6,500 became ill in Iraq from methylmercury which was applied as a fungicide to seed grain intended for planting, but which was instead ground into flour and cooked into bread. Methylmercury was also the cause of environmental poisonings in Minamata Bay, Japan, in which industrial effluent discharged into the Bay bioconcentrated in the food chain and eventually led to exposure of thousands of inhabitants who consumed seafood from the bay. The effects on Minamata children exposed in utero were particularly severe. Since that time methlymercury poisoning has been referred to as “Minamata disease.” Fortunately, catastrophic disasters are relatively rare occurrences that typically involve exposures to high concentrations of neurotoxic compounds. A more common concern in occupational and environmental settings is exposure to lower levels of potentially neurotoxic compounds, for long periods of time. It is important to consider neurotoxicity in long-term, low-level exposure situations. Many occupational and environmental exposure standards have been established on the basis of effects on the nervous system. There is also concern that subtle neurotoxic damage might not be evident at the time of exposure due to the plasticity and functional reserve capacity of the nervous system but may become manifest later. Damage inflicted long ago may become evident as individuals age or undergo other stresses. Alternatively, low-level exposure to neurotoxic compounds may cause a progressive accumulation of damage that becomes apparent only over an extended period of time. The possibility that there could be a latent period between exposure to neurotoxic compounds and the time at which functional impairments become evident should be considered. Keywords: Neurotoxicology; Occupational exposure standards; Neurobehavioral effects; Nervous system; Neurotoxic outcomes; U.S. EPA neurotoxicity guidelines; Metals; Solvents; Pesticides; Prevention