Trichloroethylene neurotoxicity

It is estimated that concentrations of 3000 ppm cause unconsciousness in less than 10 minutes (39). Anesthetic effects have been reported at concentrations of 400 ppm after 20-min exposure. Decrease in psychomotor performance at a trichloroethylene concentration of 110 ppm has been reported in one study (33), whereas other studies find no neurotoxic effects at concentrations of 200 ppm (40—43). 

Additional animal studies of trichloroethylene following intermediate-duration oral exposure are necessary to further define dose-response relationships. Because developmental neurotoxicity appears to be a sensitive end point, a focus on this end point would be useful. Animals studies following intermediate-duration dermal exposure are necessary. These studies would indicate whether targets following dermal exposure differ compared to inhalation and oral exposure. 

Feldman RG, Mayer RM, Taub A. 1970. Evidence for peripheral neurotoxic effect of trichloroethylene. Neurology 20 599-605. 

In animal studies acetone has been found to potentiate the toxicity of other solvents by altering their metabolism through induction of microsomal enzymes, particularly cytochrome P-450. Reported effects include enhancement of the ethanol-induced loss of righting reflex in mice by reduction of the elimination rate of ethanol increased hepatotoxicity of compounds such as carbon tetrachloride and trichloroethylene in the rat potentiation of acrylonitrile toxicity by altering the rate at which it is metabolized to cyanide and potentiation of the neurotoxicity of -hexane by altering the toxicokinetics of its 2,4-hexane-dione metabolite.Because occupationally exposed workers are most often exposed to a mixmre of solvents, use of the rule of additivity may underestimate the effect of combined exposures. ... 

Bernad PG, Spyker NS Neurotoxicity and behavior abnormalities in a cohort chronically exposed to trichloroethylene (abstract). Vet Hum Toxicol 29 475, 1987 Eichert H Trichloroethylene intoxication. JAMA 106 1652-1654, 1936 Feldman RG, Mayer RM, Taub A Evidence for peripheral neurotoxic effect of trichloroethylene. Neurology 20 599-606, 1970... 

Singer R Neurotoxicity Guidebook. New York, Van Nostrand Reinhold, 1990 Smith GF The investigation of the mental effects of trichloroethylene. Ergonomics 13 580-586, 1970... 

Male preteen children are most likely to experiment with solvent inhalation. Abuse of nitrous oxide is relatively common. Toxic inhalants such as heptane, hexane, methylethylketone, toluene, and trichloroethylene may result in central and peripheral neurotoxicity, liver and kidney damage, and pulmonary disease. Sudden death has occurred following inhalation of fluorocarbons. Industrial solvents rarely cause methemoglobinemia, but this (and headaches) may occur following excessive use of nitrites. The answer is (C). 

Relevant examples of specific metabolism are toxic epoxides of benzene (hemopoietic toxicity), n-hexane 2,5-hexanedione (peripheral neurotoxic effects), metabolites of ethylene glycol efliers (reproductive toxicity), and unidentified metabolites from trichloroethylene (renal-toxic effects). It should be emphasized that only the metabohtes of these solvents are associated with toxic effects. 

There have been some reports of a peripheral neuropathy following exposure to trichloroethylene, but, in this case, sensation is first impaired around the mouth and then spreads out to involve other areas of the face. The muscles involved in swallowing may become paralysed, but this is a most uncommon manifestation of intoxication by this solvent. There is no good evidence that any of the other solvents in common use is capable of producing peripheral neuropathy, but it is known that solvents of rather low toxicity may interact with others in a mixture and either have their neurotoxicity enhanced (methyl ethyl ketone with MBK, for example) or diminished (MBK with toluene). 

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