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J D Repko

Publications and source records attributed to J D Repko.

4 recordsLinked to original sources
PubMed1981

Neurotoxicity of methyl chloride.

Methyl chloride is encountered in the chemical industry as a methylating agent in the production of butyl rubber, tetramethyl lead, and other products as well as a blowing agent for some polystyrene foams. It is a potent CNS depressant whose principal route of absorption is by inhalation, although it can be absorbed through the skin. Symptoms of the neurotoxicity include headache, drowsiness, giddiness, ataxia, convulsion, and coma. This review focuses on the human case reports of acute and chronic exposures as well as some of the more important inhalation studies conducted with animals. The chemical and physical properties and the more important industrial uses are also discussed.

Animals↗
PubMed1979

Behavioral, neurological, and toxic effects of methyl chloride: a review of the literature.

A large number of reports have been devoted to the physiologic and toxic effects of methyl chloride, many of which are based on case histories involving occupational exposure. The detrimental actions of methyl chloride on the central and peripheral nervous systems are well established effects. It is a moderately severe narcotic and potentially severe nerve poison. Chronic intoxication is associated with damage to the central nervous system (CNS), kidneys, liver, bone marrow, cardiovascular system, respiratory system, and intestinal tract. The signs and symptoms range from the more severe medical dysfunctions such as cardiac irregularities, respiratory paralysis, nerve degeneration, and severe convulsions to the more subtle clinical observations such as CNS depression, nervousness and emotional instability, insomnia and anorexia, ataxia, blurred vision, light-headedness, nausea, dizziness, narcosis, and disorientation. The behavioral correlates of these and other neurotoxic effects of methyl chloride suggest that a gradual behavioral degradation occurs. Pharmacodynamic studies have shown the compound to be rapidly absorbed by the blood with most authors attributing the toxicity to an enzyme-catalyzed methylation reaction in the body. Despite the fact that several investigators have attempted to correlate such biological responses of methyl chloride with its toxicity, the present knowledge of the problem still lacks a detailed mechanism of action. Until such mechanisms are verified, adequate methods to assess subclinical neurological and behavioral changes must be effectively developed.

Animals↗