Hydrocarbons hepatotoxic effects

Trichloroethylene may occur in drinking water along with other chlorinated hydrocarbons, so effects of these chemicals in combination are of interest to public health. Hepatotoxicity, as measured by plasma enzyme activity, was increased synergistically in rats by oral administration of carbon tetrachloride combined with trichloroethylene (Borzelleca et al. 1990). In addition, synergistic effects were implicated in a 3-day study in... 

Heptanone is known to potentiate the nephrotoxic and hepatotoxic effects of halogenated hydrocarbons. 

A study of petrochemical workers exposed to a mixture of benzene (2.13), toluene (2.73), and xylene (3.15), each below its TLV (and total VOCs below all three individual TLVs) produced hepatotoxic effects. No reason for the observed effect was offered, but it was concluded that exposure to low level aromatic hydrocarbon mixtures can cause liver damage. 43 ... 

Exposures to hydrocarbon mixtures have been shown to produce hepatotoxic effects. JP-8 jet fuel is a complex mixture of hydrocarbons, including the following volatile compounds ... 

Coke oven emissions are complex mixtures of hydrocarbons, including benzene and polynuclear aromatic compounds heavy metals including arsenic, beryllium, and cadmium and other particulates and vapors. In a study of coking workers in Taiwan, it was found that liver function profiles were altered by exposures to coke oven emissions and that exposure to even low levels of these emissions was hepatotoxic. The authors of the study suggest that the adverse hepatotoxic effects are caused by a mixture of chemicals rather than by any one identifiable speciesJ36 ... 

It seems possible that the general adverse hepatotoxic effects of halothane can slow the normal rate of phenytoin metabolism. One suggested explanation for the increased adverse effects on the liver is that, just as in animals, pre-treatment with phenobarbital and phenytoin increases the rate of drug metabolism and therefore the hepatotoxicity of halogenated hydrocarbons, including carbon tetrachloride and halothane. As well as increased metabolism, the halothane-rifampicin interaction might also involve additive hepatotoxicity. 

The hepatotoxicity of 1,1,1-trichloroethane is quite low compared to other chlorinated hydrocarbons, including 1,1,2-trichloroethane. The relatively low toxicity of 1,1,1-trichloroethane may be due to its relatively low metabolism rate, since the more hepatotoxic halocarbons are extensively metabolized. Whether the mild effects of repeated 1,1,1 -trichloroethane exposure are evoked by the parent compound or the limited quantities of metabolites produced is not known, however. The available data indicate that the acute effects on the central nervous and the cardiovascular systems are caused by 1,1,1-trichloroethane and not its metabolites. The interference of 1,1,1-trichloroethane with membrane-mediated processes, due to lipophilicity, may be responsible for the acute effects on these systems several cellular and biochemical processes appear to be affected by... 

Table 19.6.5. Lesions produced by halogenated aliphatic hydrocarbons. [Adapted, by permission, from Zimmerman HJ, Hepatotoxicity The Adverse Effects of Drugs and Other Chemicals on the Liver, Appleton-Century-Crofts, New York, 1978],...

---