Toxicity

The toxicity of carbon disulphide has been extensively studied. Research initially concentrated on its neurological effects and it was only later that the cardiovascular effects of carbon disulphide became apparent. Exposure is almost exclusively confined to occupational situations and chronic exposure has been extensively studied from an industrial hygiene perspective.

Historically, literature on the toxicity of carbon disulphide comes from its use in the cold vulcanisation of rubber and in the manufacture of viscose rayon, the incidence of poisoning roughly paralleling its industrial use in various countries. The toxicity of carbon disulphide first became apparent in the 1800s when it was used for cold vulcanisation of rubber in Europe. This process was never in common use in the US (where the heat cure method of rubber vulcanisation was favoured). In the US occupational exposure to carbon disulphide appeared with the viscose rayon manufacturing industry and practically all epidemiological studies to date have been conducted on viscose rayon workers.

In 1856, Delpech, a physician in Paris, presented the first study on the effects of carbon disulphide. He described a variety of nervous system and mental disorders, and reported that workers typically had an early stage of excitation followed by a period of depression, and he termed the syndrome 'carbon disulphide neurosis'. Towards the end of the nineteenth century and in the beginning of the twentieth century reports began to appear in the German literature. A landmark paper by Laudenheimer describing 50 cases of carbon disulphide 'insanity' resulted in the occupational exposure limit being reduced from several hundred to less than 30 ppm. As a result of this reduction it was said that the general morbidity among rubber workers during the early 1900s declined by 75% and their mental disorders by 86% (Gordy and Trumper, 1938; Davidson and Feinleib, 1972; Spyker et al., 1982). Due to further improved working and hygiene conditions in the industrial environment, adverse effects from carbon disulphide exposure are now less frequent and less pronounced. Recent studies have concluded that the current TLV of 10 ppm is sufficient to protect workers from the neurotoxic (DeFruyt et al., 1998) and cardiovascular (Franco et al., 1982; Drexler et al., 1996) effects of carbon disulphide.

Toxicity from acute exposure to carbon disulphide is rare and most adverse effects have been reported from chronic exposure. Carbon disulphide is a potent neurotoxin and is narcotic at high concentrations. Target organs are the central and peripheral nervous systems, including the optic and auditory nerves, the liver, heart, testes and skin. Less pronounced are the toxic effects of carbon disulphide on the pancreas, kidney, the haematopoietic system and the hormonal regulatory system. At high concentrations carbon disulphide is embryotoxic. Epidemiological studies of workers in the viscose rayon industry have shown that the main toxic effects are on the neurological system (both central and peripheral) and the cardiovascular system (coronary heart disease and ECG changes). Ocular effects are also widely reported (alterations in the retinal microvasculature and impaired colour discrimination) and liver and kidney damage can occur (WHO, 1979; BUA, 1991; Gehring et al., 1991; Feldman, 1999).

Carbon disulphide is formed in the body from degradation of other sulphur xenobiotics such as disulfiram and this presents a potential source of minor exposure to carbon disulphide (Dalvi, 1988). Disulfiram is converted enzymatically to carbon disulphide. Carbon disulphide is known to cause neurofilamentous distal axonopathy in animals. Similar changes in human nerve tissue after disulfiram administration, suggest that carbon disulphide is the toxic agent (Ansbacher et al., 1982).

There is a huge amount of literature on carbon disulphide toxicity spanning over a century and it has been the subject of many studies. For a comprehensive review see Beauchamp et al. (1983).

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