SUMMARY. Alcohol abuse is a comorbid variable that independently increases by about 3-4 times the incidence and severity of acute respiratory distress syndrome (ARDS) in patients at risk. Chronic overconsumption of alcohol causes oxidative stress in the lungs through its metabolism, and diminishes the synthesis and utilization of glutathione (GSH), which is a major antioxidant, resulting in impairment of the antioxidant ability of cells. The decreased concentration of GSH in the lungs leads to a variety of lung changes, including decrease in alveolar liquid clearance and increased protein leak across the alveolar epithelium, overexpression of transforming growth factor-β1, depression of the synthesis and secretion of surfactant phospholipids by type II alveolar epithelial cells, increased apoptosis of alveolar macrophages and loss of their phagocytic ability, and dramatic alterations in connective tissue remodelling. GSH replacement by the administration of GSH precursors such as N-acetylocysteine and procysteine has been demonstrated to minimize alcohol induced injuries More detailed studies are needed to define the mechanisms by which alcohol abuse renders the lungs susceptible to acute lung injury, in order for more specific therapeutic strategies to be developed. Pneumon 2008; 21(4):–