The coexistence of fibrin and tissue macrophages is a common finding in the histopathology of chronic lung inflammatory diseases. Human lung alveolar macrophages (LAM) obtained by lavage of healthy donors can initiate the coagulation sequence by expressing procoagulant factors. The procoagulants of LAM were in this study identified to be either thromboplastin (tissue factor) or a direct factor X activator, probably a thromboplastin/factor VII complex. LAM did not show inducible thromboplastin synthesis as did monocytes when stimulated in vitro. LAM were separated into four subpopulations by density gradient centrifugation. The specific thromboplastin activity of subpopulation cells varied inversely with their density. Low-density subpopulations of LAM released microvesicles from their surface which could be recovered in the culture medium, and which expressed procoagulant activities with the same characteristics as the LAM procoagulants. These findings suggest that alveolar macrophages and the membrane vesicles shed from their surface contribute to local fibrin deposition in the lungs by expressing procoagulant factors.