Biological effects of asbestos fibers were reviewed in relation to the polyclonal activation of human lymphocytes and to the release of free radicals from human neutrophils in Vitro. Chrysotile, crocidolite, and amosite asbestos activate CD4⁺ T lymphocytes polyclonally, followed by activationinduced cell death (a type of apoptosis). The activation is HLA class II dependent, and certain Vβ repertoire, e.g. Vβ 5.3, are detected among the fractionated T cells with a high Ca⁺⁺ level that had been stimulated by asbestos fibers. These observations support the possibility that asbestos acts as a superantigen, and that asbestos stimulate lymphocytes repeatedly in vivo. It has been reported that asbestos-induced cytotoxicity can be suppressed by the scavengers of superoxide or hydroxyl radical. Some of these scavengers such as dimethylsulfoxide (DMSO) or retinoic acid are known as inducers of cell differentiation. The biological functions of DMSO for cell differentiation of HL-60 cells to neutrophils are suppressed by co-culturing of crocidolite asbestos, because DMSO reacts with the hydroxyl radical released after the stimulation with crocidolite and spent itself. Superoxide dismutase (SOD) inhibited the effects of crocidolite, reacting rapidly with •O^-₂ before the secondary release of OH. It seems to be probable that asbestos fibers, especially crocidolite, suppress the tissue cell differentiation by releasing free radicals and by wasting inducers of cell differentiation as radical scavengers.