A second possibility is that these polymorphisms affect the metabolism of ethanol and acetaldehyde by microorganisms (bacteria and yeast) residing in the human oral cavity. Such organisms, which can metabolise ethanol into acetaldehyde, are being increasingly recognised as important contributors to alcohol-related UADT cancer risk, owing in large part to the pioneering studies of Salaspuro and colleagues [10]. Yokoyama and colleagues [11] have shown that in a Japanese population, individuals who were homozygous for the less active ADH1B R48 allele had significantly higher salivary ethanol and acetaldehyde levels that those with at least one ADH1B H48 allele.
