Alcohol use, and misuse, has been a part of human culture for thousands of years. In the modern medical era, a great deal of attention has been justifiably focused on elucidating the mechanisms underlying the psychological and biological addiction to alcohol. However, a significant percentage, if not the majority, of alcohol-related morbidity and mortality occurs in individuals who do not meet the formal diagnostic criteria for alcohol use disorders. For example, many serious medical consequences of chronic alcohol ingestion can occur in individuals who do not have signs or symptoms of alcohol dependence. There is now clear evidence that even in otherwise healthy-appearing individuals who chronically consume excessive amounts of alcohol, alveolar macrophage immune capacity is impaired and, as a consequence, these individuals are at significantly increased risk of pneumonia. This brief review summarizes some of the key mechanisms underlying this phenomenon and proposes a hypothetical scheme by which alcohol interferes with zinc bioavailability within the alveolar space and thereby dampens macrophage function.