Chrysotile fibers exert a marked hemolytic activity on suspensions of washed sheep erythrocytes, but amphibole asbestiform minerals such as crocidolite, amosite, tremolite, and anthophyllite possess only negligible hemolytic properties. The minimal hemolytic concentration of chrysotile asbestos is dependent on the openness of the fibers as characterized by the air permeability surface area and decreases with increasing surface area. This fact was also observed in the evaluation of hemolysis of fibrous, nonasbestiform minerals, e.g., sepiolite and nemalite. Chrysotile hemolysis can be inhibited by disodium ethylenediaminetetraacetic acid (EDTA) and by certain acidic polymers particularly by polystyrene sulfonates, carboxymethylcellulose ether sodium salt (CMC), and the pyran-copolymer NSC 46015. These substances are not effective as inhibitors of silica (quartz) hemolysis, whereas polyvinylpyridine-N-oxide (PVPNO), a very potent antagonist of silica hemolysis, interferes with chrysotile only at high concentrations. The hemolytic action of chrysotile can be markedly reduced by repeated treatment with red blood cells. The mechanism of asbestos hemolysis cannot yet be satisfactorily interpreted. There is a marked correlation of hemolytic potency with the surface area and the degree of opening of the fibers which may be influenced by the action of the antagonistic polymers. The role of the magnesium hydroxide surface characteristic for chrysotile is not yet elucidated, because magnesium hydroxide is not hemolytic, although nemalite, a natural fibrous magnesium hydroxide, and a lightly burned magnesium oxide are active hemolytic agents.