Chronic inflammation that has been observed for malignant and non-neoplastic lung diseases of smokers has been attributed to the numerous and diverse particulate ('tar')-phase and gas-phase chemicals in mainstream smoke, most of which arise from the burning of tobacco. The primary cell-mediator of lung inflammation is the macrophage. Most probably, inflammation is promoted also from some of the more than 50 other cell types of the lung. Cured tobacco in diverse types of cigarettes is known to harbor a plethora of bacteria (Gram-positive and Gram-negative), fungi (mold, yeast), spores, and is rich in endotoxin (lipopolysaccharide). Reviewed herein are recent observations of the authors' team and other investigators that support the hypothesis that lung inflammation of long-term smokers may be attributed in part to tobacco-associated bacterial and fungal components that have been identified in tobacco and tobacco smoke.