The toxicity of the proposed asbestos substitute wollastonite (13983170) was studied in-vivo and in-vitro. Kenolit-A-60 (KA60), Kenolit-N (KN), or Kenolit-ASB-3 (ASB3) varieties of Indian wollastonite, or chrysotile (12001295) dusts were incubated with suspensions of human erythrocytes. The extent of hemolysis was determined. Female albino rats were administered 5 milligrams KA60, KN, ASB3, or chrysotile intratracheally. Ninety days later they were killed and the lung tissues were examined for histopathological changes, collagen, phospholipids, mucopolysaccharides, and sialic- acid. Lung microsomal and cytosolic fractions were prepared and assayed for ascorbic-acid, glutathione, hexosamine, cytochrome-P-450 (P450), benzo(a)pyrene-hydroxylase (BaPOHase), epoxide-hydratase (EH), and glutathione-S-transferase (GST). In-vitro, the extent of hemolysis induced by chrysotile, KA60, KN, and ASB3 was 72.16, 43.37, 41.19, and 35.28%, respectively. KA60 caused a significant increase in lung collagen, phospholipid, and sialic-acid content. All dusts induced mild to moderate interstitial fibrosis. KA60 also induced peribronchiolar fibrosis. All dusts significantly increased lung weight. KA60 caused large increases than KN, ASB3, or chrysotile. All dusts increased microsomal P450 content, chrysotile and KA60 having the largest effect. Chrysotile and KA60 induced large increases in BaPOH and EH activity. Chrysotile caused a significant decrease in GST activity. KA60 caused a slight decrease in GST activity. KN and ASB3 increased GST activity. Chrysotile and KA60 significantly decreased ascorbic-acid content and chrysotile decreased glutathione content. Chrysotile, KA60, and KN significantly increased the extent of lipid peroxidation, chrysotile and KA60 showing the strongest effect. The authors conclude that Indian wollastonites are less toxic than chrysotile.