Epidemiological studies provide definite evidence that alcohol drinking is an independent risk factor for laryngeal cancer. This risk increases with the amount of alcohol consumed: in a meta-analysis of 20 studies conducted in North America, Europe, Japan and Korea the multivariate relative risks were about 2 for 50 g ( approximately 4 drinks)/day and about 4 for 100 g/day compared to nondrinkers, in the absence of evidence of a threshold. Genetic polymorphisms in the alcohol-metabolizing enzyme aldehyde dehydrogenases have been found to be associated with upper aerodigestive tract cancer, including the larynx. Further, the risk increases by concomitant tobacco smoking, each agent approximately multiplying the effect of the other. In the absence of smoking, the relative and absolute risks are small for moderate alcohol consumption, but there is an increased risk for elevated alcohol consumption. After stopping drinking, some fall in risk becomes apparent only in the long term. The supraglottis is more closely related to alcohol consumption, as compared to the glottis/subglottis. In various populations, the most commonly used alcoholic beverage appears to be the one most strongly associated with laryngeal cancer risk, suggesting that no meaningful difference exists for different types of alcoholic beverages.
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