There is considerable evidence that alveolar macrophages play a pivotal role in the pathogenesis of asbestosis (Kagan 1985, Kagan 1988), since these phagocytic cells are a notable feature of histologic lesions at sites of asbestos deposition in the lungs (Davis 1963, Brody et al. 1981, Oghiso et al. 1984). Multinucleated giant cells also are a prominent component of the macrophage response to inhaled asbestos (Kagan et al. 1983a, Kagan 1988). Conceivably, the accumulation of alveolar macrophages in evolving asbestotic lesions may reflect a localized tissue response to the release of asbestos-induced pulmonary chemoattractants. Support for this concept is provided by experimental studies which have demonstrated that inhalation of, asbestos fibers can evoke the release of chemotactic stimuli for alveolar macrophages (Kagan et al. 1983b, Warheit et al. 1985). Asbestos inhalation also is associated with enhanced expression of immune- associated (la) surface antigens on alveolar macrophages and with augmented production of the immunostimulatory monokine, interleukin-1 (Hartmann et al. 1984a, Hartmann et al. 1984b). Since the surface expression of la antigens on macrophages is a useful morphologic correlate of macrophage activation (Garrett et al. 1984, Kunkel et al. 1984), these findings collectively suggest that contact with asbestos fibers may induce alveolar macrophages to become functionally activated.