Introduction
Carbon disulfide (CS₂) is a volatile, highly flammable solvent whose vapour is toxic mainly to the nervous and vascular systems. This topic covers its occupational sources, how it is absorbed and acts, the acute and chronic clinical pictures, diagnosis, treatment and the medical expert assessment of workers exposed to it.
Etiology and sources of exposure
Pure carbon disulfide is a colourless, volatile liquid with a faintly ether-like odour, while technical grades smell strongly unpleasant. It occurs naturally in volcanic gases and in emissions from marshes and decomposing organic matter. The main occupational sources are:
- Viscose rayon and cellophane production, historically the largest source of exposure
- use as a solvent for rubber, resins, waxes, fats, sulfur and iodine
- rubber vulcanisation and manufacture of other chemicals, such as carbon tetrachloride
- production of insecticides and fumigants
- laboratory work with the solvent
Pathogenesis
The main route of entry is inhalation of vapour, with rapid absorption through the lungs. Some uptake also occurs through intact skin, which is important with liquid contact. Because the compound is lipophilic, it distributes into fatty tissues and crosses the blood-brain barrier, so the nervous system is a principal target. It is metabolised in the liver by conjugation with glutathione to dithiocarbamate-type compounds and then to thiazolidine-2-thione-4-carboxylic acid (TTCA), which is excreted in urine.
The toxic effects are thought to result from:
- binding of dithiocarbamate metabolites to copper- and zinc-containing enzymes, such as dopamine beta-hydroxylase, which disturbs neurotransmitter synthesis
- axonal degeneration of long peripheral nerves, typically starting at the distal parts
- endothelial injury and disturbed lipid metabolism, which promote atherosclerosis
- interference with iodine uptake by the thyroid, which may cause goitre