An overview of the pulmonary macrophage is provided, with particular emphasis on the origin of this cell and the adaptive mechanisms whereby the macrophagic system is able to respond to increased inhalant loads of organic and inorganic pollutants. Evidence is presented which favors an hematopoietic origin for the alveolar macrophage with a monocytic transportation compartment in the blood and an interstitial cell compartment in the lung in which cellular division and maturation may occur. Through the simple mechanism of increased cellular turnover this system of mononuclear phagocytes rapidly adapts to most inhalant challenges. In addition to its primary tasks phagocyte and destroyer of microorganisms the macrophage plays a pivotal role in the genesis of silicotic fibrosis, and it is possible that similar mechanisms may hold for a variety of cryptogenic fibroses. Paradoxically, destruction of collagen by the dual mechanisms of phagocytosis and the secretion of lytic enzymes may also occur. The relevance of this secretory function of the macrophage to the pathogenesis of destructive diseases of the lung such as emphysema remains to be determined.