Tobacco smoke and the pulmonary alveolar macrophage.

The pulmonary alveolar macrophage (PAM) has been shown by numerous investigators to be responsible for maintaining sterility of the lower respiratory tract (4, 8). This key host defense cell must interact with and destroy invading microorganisms, as well as inactivate and remove various non-viable particulates to which the lung is exposed. Perhaps the most common particulate in this class is tobacco smoke, a complex chemical aerosol comprised of over 3,000 separate gaseous, liquid and solid components. The lung is the primary target organ affected by tobacco smoke and the first line of resistance to the inhaled smoking products is the alveolar macrophage. Failure on the part of this phagocyte to deal effectively with this environmental inhalant could conceivably lead to an increased susceptibility to microbial infection, as well as an altered pulmonary integrity. We have investigated, therefore, the effects of tobacco smoke on the structure, function, and metabolism of alveolar macrophages harvested by bronchopulmonary lavage from rats previously exposed to carefully quantified dosages of tobacco smoke for periods of 30–180 consecutive days.