A BEI has not been established for carbon tetrachloride by the ACGIH. Measurement of carbon tetrachloride and its metabolites in expired air has been the most convenient way to determine exposure (ATSDR, 1994). Carbon tetrachloride can also be detected by gas chromatography in blood and serum, which may also be used as an indicator of exposure. Any detectable blood concentration indicates exposure, but concentrations do not correlate well with adverse health effects (ATSDR, 1992b).

Carbon tetrachloride has been studied extensively and most of the present understanding of metabolism by the liver and toxic effects on the liver by other agents has resulted from these studies. For a comprehensive view of the hepatic mechanisms and effects see Plaa (1986). Carbon tetrachloride is a CNS depressant and a mild anaesthetic agent. It can cause fatal damage to the liver and/or kidneys in both acute and chronic exposure. After acute exposure hepatic and/or renal dysfunction, may be delayed in onset for several days. CNS depression does not always precede the onset of nephrotoxicity or hepatotoxicity. Diverse effects on other organs are likely to be secondary to CNS, liver or kidney damage (ATSDR, 1992a). Carbon tetrachloride is no longer used as a solvent because of awareness of the risk of hepatorenal toxicity and the ready availability of less hazardous solvents. It is used primarily as a chemical intermediate (Reid, 2001).

Carbon tetrachloride causes fatty degeneration of the liver and centrilobular necrosis (Recknagel et al., 1989, Chyker et al., 2000). Biochemical evidence of hepatic injury often includes greatly elevated activities of transaminases and a variety of other hepatic enzymes in plasma. The main histological abnormalities include hepatic steatosis and hepatic centrilobular necrosis. As hepatic injury develops, signs of renal damage may also be observed and may dominate the clinical picture; renal failure is the most frequent cause of death.

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