Ethyl alcohol as a cocarcinogen with special reference to the aerodigestive tract: a cytogenetic study.

Although prior to its metabolic conversion alcohol has no mutagenic activity, an interaction of alcohol with tobacco in carcinogenesis of the head and neck region is well characterized. In a recent ecogenetic case control study of these cancers we documented an interaction between alcohol use and in vitro mutagen-induced chromosome damage in cancer risk. The present report evaluates the in vitro genotoxicity of five mutagens (including cigarette smoke condensate) tested in conjunction with 2% and 4% ethanol in human lymphoid cell lines. Ethanol alone did not exert a demonstrable clastogenic effect, as measured by the frequency of chromatid breaks per cell. However, the clastogenic potential of all mutagens increased when ethanol was added concurrently with the mutagens, and there was a dose-dependent potentiation of clastogenicity by ethanol, with a threshold dose between 0.5% and 1.0%. Preliminary experimental results strongly indicate that ethanol, at relatively high doses, inhibits DNA and chromosome repair systems. These data support the epidemiologic evidence of an interaction between alcohol and mutagens in carcinogenesis and suggest that alcohol may have co-carcinogenic properties.