Oxidation of acetaldehyde molecules adsorbed on Na- and Mg-Wyoming montmorillonite at room temperature (20-25°C) and in N2 atmosphere has been studied by I.R. spectroscopy, A comparison between clay-acetic acid complex and that prepared from acetaldehyde is given. The influence of the nature of the saturating cation as well as the clay pretreatment on this oxidation process are discussed and reaction pathways are proposed. Acetic acid directly adsorbed on the clay surface is almost removed at 110°C, while that produced from the oxidation of the adsorbed acetaldehyde appears to be strongly held. Within a temperature range 180-230°C, the fixed acetic acid molecules dissociate to acetate form; then occurs an interaction of the acetate and the residual acid with the lattice OH of the clay at 200–300°C. This interaction involves the loss of the structural OH and deposition of carbon on the clay surfaces. The thermal decomposition of the residual complex is almost completed at 500–600°C

Some of the seed-evolved volatiles, which were mainly composed of methanol, acetaldehyde, ethanol and acetone, caused the loss of seed germinability during storage. In general, the deleterious effects of the volatiles increased with increasing RH and temperature during storage. Acetaldehyde had the strongest deleterious effect regardless of RH and temperature, while ethanol caused seed deterioration only at high RHs. Acetone was slightly deleterious to some species, while methanol was almost inert in most seeds. Various aldehydes applied during storage showed some toxicity to seed germinability, which decreased, except for 3-methylbutanal, with increasing molecular size, suggesting that the endogenous volatile compounds with an aldehyde group cause seed deterioration. On the other hand, the contents of volatile compounds in seeds were higher when they were stored at 44% RH (water sorption zone 2), than when stored at 12% RH (water sorption zone 1). Acetaldehyde, the most deleterious volatile, was more abundantly accumulated within the seeds stored at −3.5°C than at 23°C. Based on these facts, it is suggested that endogenous volatiles, especially acetaldehyde, may be an important factor that accelerates seed deterioration which often occurs under lower RHs and/or temperatures throughout long-term storage.

Chronic alcohol consumption is a major risk factor for cancer of upper aero-digestive tract (oro-pharynx, hypopharynx, larynx and oesophagus), the liver, the colo-rectum and the breast. Evidence has accumulated that acetaldehyde is predominantly responsible for alcohol-associated carcinogenesis. Acetaldehyde is carcinogenic and mutagenic, binds to DNA and protein, destroys the folate molecule and results in secondary cellular hyper-regeneration. Acetaldehyde is produced by mucosal and cellular alcohol dehydrogenase, cytochrome P450 2E1 and through bacterial oxidation. Its generation and/or its metabolism is modulated as a result of polymorphisms or mutations of the genes responsible for these enzymes. Acetaldehyde can also be produced by oral bacteria. Smoking, which changes the oral bacterial flora, also increases salivary acetaldehyde. Cigarette smoke and some alcoholic beverages, such as Calvados, contain acetaldehyde. In addition, chronic alcohol consumption induces cytochrome P450 2E1 enxyme activity in mucosal cells, resulting in an increased generation of reactive oxygen species and in an increased activation of various dietary and environmental carcinogens. Deficiencies of riboflavin, Zn, folate and possibly retinoic acid may further enhance alcohol-associated carcinogenesis. Finally, methyl deficiency as a result of multiple alcohol-induced changes leads to DNA hypomethylation. A depletion of lipotropes, including methionine, choline, betaine and S-adenosylmethionine, as well as folate, results in the hypomethylation of oncogenes and may lead to DNA strand breaks, all of which are associated with increased carcinogenesis.

Breast cancer is a multifactorial disease that is triggered by gene–environment interactions. Epidemiological research has identified alcohol consumption as a significant non-hormonal-related and consistent risk factor, and is thus a preventable cause of breast cancer. The reasons why alcohol drinking increase breast cancer risk are unclear, and several hypotheses exist. The perturbation of estrogen metabolism and response appears to one mechanism underlying the association. Alcohol consumption also increases breast density in postmenopausal women and affects sex steroid levels. Other plausible mechanisms include: (1) mutagenesis by acetaldehyde, which is a metabolite of ethanol; (2) by enhancing the susceptibility of the mammary gland to carcinogenesis by affecting DNA repair, stimulating cell proliferation or altering mammary gland structural development; (3) influencing the disposition and function of essential nutrients or dietary factors considered cancer protective (e.g. affecting folate and one-carbon metabolism pathways); (4) inducing genome instability and DNA damage; and (5) inducing oxidative damage via ethanol or estrogen metabolism. To better understand the etiological nature of the effect of alcohol on breast carcinogenesis, further studies at the cellular and molecular levels on the interaction between ethanol and other risk factors, estrogen, carcinogens are needed.