The ability of silicates to generate hydroxyl radicals (OHs) and induce hemolysis was studied in-vitro. One milligram (mg) dust samples of the pneumoconiosis causing silicates minusil-5 (14808607), kaolin (1318747), and diatomite (68855549), the nonfibrogenic dusts fiberglass, wollastonite (13983170), talc (14807966), and tremolite (14567738), and amosite (12172735), crocidolite (12001284), and chrysotile (12001295) were incubated with hydrogen-peroxide and dimethyl-sulfoxide in the presence or absence of ascorbic-acid and the OH scavenger dimethylthiourea. Production of OHs was determined by monitoring the formation of methane. A similar experiment was performed with samples that had been preincubated with the trivalent-iron chelators deferoxamine and transferrin. Suspensions containing 2 percent erythrocytes were incubated with 0 or 1mg per milliliter amosite, minusil, or kaolin. The extent of hemolysis was assessed by determining the extent of lipid peroxidation by measuring the amount of malondialdehyde formed. Minusil, kaolin, diatomite, amosite, chrysotile, and crocidolite generated significant quantities of OH when ascorbic- acid was present. The nonfibrogenic dusts did not generate OHs. Dimethylthiourea prevented OH formation by the silicates, amosite, crocidolite, and chrysotile. Deferoxamine and transferrin significantly inhibited production of OHs. Normalizing the amount of fibrogenic silicates to a 10 centimeter square surface showed that they and amosite, crocidolite, and chrysotile had equivalent OH producing activity. Amosite, kaolin, and minusil caused appreciable erythrocyte hemolysis which was significantly inhibited by DIDS, NPG, catalase, and deferoxamine. The authors conclude that fibrogenic silicates function as Fenton catalysts to generate OHs from hydrogen-peroxide and ascorbic-acid. Asbestos and silicates may cause pneumoconiosis through an oxidant mediated process that catalyzes the production of OHs in the lung.