Increased salivary acetaldehyde levels in heavy drinkers and smokers: a microbiological approach to oral cavity cancer

The pathogenetic mechanisms behind alcohol-associated carcinogenesis in the upper digestive tract remain unclear, as alcohol is not carcinogenic. Howe ver, there is increasing evidence that a major part of the tumour-promoting action of alcohol might be mediated via its first, toxic and carcinogenic metabolite acetaldehyde. Acetaldehyde is produced from ethanol in the epith elia by mucosal alcohol dehydrogenases, but much higher levels derive from microbial oxidation of ethanol by the oral microflora, In this study we inv estigated factors that might alter the composition and quantities of the or al microflora and, consequently, influence microbial acetaldehyde productio n. Information about dental health, smoking habits, alcohol consumption and other factors was obtained by a questionnaire from 326 volunteers with var ying social backgrounds and health status, e.g. oral cavity malignancy. Par affin-induced saliva was collected and the microbial production of acetalde hyde from ethanol was measured. Smoking and heavy drinking were the stronge st factors increasing microbial acetaldehyde production. Whether poor denta l status may alter local acetaldehyde production from ethanol remained unan swered. Bacterial analysis revealed that mainly Grampositive aerobic bacter ia and yeasts were associated with higher acetaldehyde production, Increase d local microbial salivary acetaldehyde production due to ethanol among smo kers and heavy drinkers could be a biological explanation for the observed synergistic carcinogenic action of alcohol and smoking on upper gastrointes tinal tract cancer. It offers a new microbiological approach to ethanol-ass ociated carcinogenesis at these anatomic sites.