The Unsolved Relationship of Alcohol and Asthma

thermore, high intakes of alcohol increase serum-specific IgE sensitization to cross-reactive carbohydrate determinants that may interfere with serum IgE determinations for the diagnostic evaluation of allergic patients [11] . Alcoholic drinks are commonly reported as triggers of hypersensitivity reactions of the skin and airways. In Asian populations these reactions are often particularly severe, resulting in alcohol-induced asthma and “Oriental flushing syndrome”. The high risk of alcohol-induced reactions in these populations is due to a high frequency of a genetically determined decreased activity of acetaldehyde dehydrogenase 2 (ALDH2) that metabolizes acetaldehyde, the metabolite of alcohol [12] . Persons with this genetic variant develop asthma and flushing following the intake of alcohol, and these reactions are believed to be mediated through the immunological effects of acetaldehyde that peak following alcohol intake in individuals with a genetically determined low capacity to metabolize acetaldehyde [13] . Experimental studies seem to suggest that acetaldehyde has a histamine-releasing effect on mast cells in the airways and that this effect could represent the mechanism underlying the effects of alcohol on airways in ALDH2-deficient humans [14–18] . It has been assumed that the above mechanisms do not play a role in Caucasians where the ALDH2 slow-metabolizing variant is rare [19] . In spite of this, alcoholic drinks Alcoholic drink consumption is a common lifestyle habit throughout the world. It is well known that a high consumption of alcohol increases the risk of several types of cancer. In contrast, alcohol’s effects on the immune and respiratory systems are less recognized. Alcohol consumption induces a strong suppression of the allergen-specific Th1-dependent response that renders alcoholics at markedly increased risk of respiratory bacterial infections such as tuberculosis [1] and pneumococcal disease [2] . Alcohol induces Th2 skewing of the immune response in terms of increased levels of Th2 cytokine and a marked increase in levels of serum total IgE [3, 4] . The increased levels of serum total IgE consistently observed in alcoholics decreases following alcohol abstinence [5] , supporting the idea that alcohol’s increasing effect of serum total IgE is causal. Furthermore, Danish birth cohort studies found that maternal alcohol consumption during pregnancy was associated with increased levels of total IgE in the cord blood of the newborn child [6] and the risk of atopic dermatitis in early infancy [7] , suggesting that alcohol influences the fetal immune system. A few epidemiological studies have suggested that increasing consumption of alcohol increases the risk of IgE sensitization against inhalant allergens, a well-documented biomarker of allergic respiratory disease, but studies have not been consistent [8–10] . FurPublished online: December 14, 2016