Salaspuro recently

summarized all of this evidence and estimated that the mutagenic amount of acetaldehyde in saliva falls between 50 and 150 μM [46]. Linderborg et al. [31] indicated that the oral and upper digestive tract mucosa is exposed to a much higher acetaldehyde concentration after ingestion of calvados (i.e., 20-50 times higher than those considered to be mutagenic), which is consistent with our results. Conclusions Because alcohol use significantly increases Selleck LEE011 salivary acetaldehyde above endogenous levels (even if the alcohol is not contaminated, as in the case of vodka), we ascertain that a “”biological threshold”" is clearly exceeded during alcohol consumption. The observations of the present study and the suggested molecular mechanisms could conceivably explain the increased oral cancer risk associated with alcohol use seen in epidemiological Niraparib price studies [6]. Salivary acetaldehyde concentrations in the range associated with sister chromatid exchange and Cr-PdG formation are clearly achievable. Highly contaminated beverages could present a higher cancer risk than beverages Saracatinib purchase with none or very low concentrations of acetaldehyde (for example, see Linderborg et al. [31]). Currently only limited and inconclusive epidemiological evidence exists to confirm this beverage specificity, however. From the 56 studies

on oesophageal cancer summarized by IARC [6], the influence of the type of alcoholic beverage consumed was examined in several studies. Consumption of beer or hard liquor led to a higher relative risk than consumption of wine [47–52], whereas two studies [53, 54] also found an excess risk for wine drinkers. Most of the studies that investigated types of alcoholic beverage showed no substantial difference in risk [6]. This probably derives from the fact that the most commonly consumed beverage groups on a population scale (i.e., beer, wine and white spirits) are typically low in acetaldehyde content. It would be also challenging to design an epidemiological study that could consider the acetaldehyde content, when even the ethanol amount is often difficult to measure in retrospect [55] and international data Non-specific serine/threonine protein kinase on acetaldehyde

content of alcoholic beverages are very limited [4]. Currently, the acetaldehyde content of most alcoholic beverage types is not regulated. The recent IARC evaluation of acetaldehyde associated with alcohol consumption as a “”group 1″” carcinogen has not yet been implemented in international risk assessments (e.g., by JECFA or EFSA). Until such assessments become available, we would currently recommend the implementation of the ALARA principle (“”as low as reasonably achievable”") [56]. In the case of spirits, which were linked to very high short-term acetaldehyde concentrations in our study, avoidance of acetaldehyde contamination is relatively easy if the first distillation fractions are discarded [4]. Acknowledgements This article is dedicated to our late colleague and friend Eva-Maria Sohnius.