Abstract
Chronic alcohol consumption that begins during adolescence produces a deleterious effect on different organs, liver, skin, lung, pancreas, brain, among others. At the lung level, alcohol metabolites specifically affect apical cilia, type II alveolar epithelial cells, macrophages, and the blood-air membrane. Constituting the alcoholic lung phenotype, which increases the risk of developing lung infections, direct damage, exacerbated symptoms and causes an increase in mortality in many other lung diseases. Similarly, this toxicity is associated in people with genetic susceptibility, with the appearance of lung cancer. Acetaldehyde is the main metabolite of alcohol that produces cellular oxidative stress and produces the subsequent damage involved in the pathogenesis of many lung diseases, including acute lung injury, asthma, acute pulmonary edema, and COPD. Additionally, inflammatory oxidants produced by the acetaldehyde alters several important stages of the natural or innate response at the bronchial and pulmonary levels to pathogens and injuries, and alters the epithelial barrier, predisposing the lungs to bronchitis, pneumonia, and tuberculosis. Therefore, it is of fundamental importance to implement preventive measures and promote awareness of the damage that alcohol produces in adolescents, and in the population with chronic alcohol consumption.