Exposure to various particles and fibers can result in lung inflammation that may progress to fibrosis, even lung cancer for which there is no effective clinical treatment now. The mechanism involved in pulmonary injury has not been well defined ; however, most current evidence implicates a central role for alveolar macrophages (AM) in this process. Also apoptosis or programmed cell death is regarded as a mechanism which is related with the pulmonary fibrosis. We propose that the cytotoxic potential of various particles may be evaluated by measuring lactic dehydrogenase (LDH) from particle co-cultured supernatant and theses particles may induce the characteristics of apoptosis, DNA ladder. We analyzed rat AM culture media which was incubated for 3 days with the same concentration (10 ug/ml) of silica(Si), chrysotile(Ch), crocidolite(Cr), ceramic fiber(CF), rock wool(RW) and glass wool (GW). And each particles (50ug/cm(2)) was incubated with A549 (pneumocyte in tracheal epithelium) cell lines for 24 hours to confirm the DNA ladder. Additionally, silica induced apoptosis in vivo was confirmed by electromicroscopic observation. The results were as follows; 1. Silica, asbestos and man-made mineral fibers (MMMF) co-cultured with AM showed the increase of LDH significantly with the time interval of 24, 48, 72 hours except for ceramic fiber in 48 and 72 hours and crocidolite in 72 hours. 2. Silica, asbestos and man-made mineral fibers (CF, GF) showed the characteristics of apoptosis, DNA ladder, which was induced by incubating A549 cell with each particles for 24 hours in vitro 3. Apoptotic alveolar macrophage was observed the findings of zeiosis (membrane blebbing), condensation of nuclear chromosome and many vacuoles in cytoplasm, electomicroscopically.