Exposure of laboratory mice to domestic cooking gas: implications for toxicity.

The ability of domestic cooking gas to induce hepatotoxicity and clastogenicity in mice was studied. The mice were exposed to domestic gas for twenty-one days at doses of 100 mg/kg, 200 mg/kg and 300 mg/kg respectively. The positive control group of mice were given sodium arsenite intraperitoneously at a dose of 2.5 mg/kg body weight. While the negative control group had only distilled water, sodium arsenite significantly (p < 0.05) induced the formation of micronucleated polychromatic erythrocytes (mPCEs), serum and liver gamma glutamyl transferase (gammaGT) and alkaline phosphatase (AP) activities respectively as compared with the observations made in the negative control group. Similarly, the domestic gas significantly (p<0.05) induced mPCEs formation, serum and liver, gammaGT and AP activities. The degree of induction was in the order of 100 mg/kg < 200 mg/kg < 300 mg/kg. However, when compared with the positive control group, the domestic cooking gas at the tested doses was not as potent as sodium arsenite in its ability to induce enzyme activity and mPCEs formation. Limited histopathological analysis of liver samples from treated and untreated mice showed distended blood vessels, necrosis and hepatocellular degeneration in the groups treated with high doses of domestic gas or sodium arsenite as compared with the untreated group. Our findings suggest that the domestic cooking gas has some degree of clastogenic and hepatotoxic activities in mice. Health risks may therefore be associated with long-term occupational and/or domestic exposure in humans.