The suppression of silica (7631869) and kaolin (1318747) cytotoxicity by lecithin (8002435) and a component of pulmonary surfactants was investigated. Hemolysis caused by native dusts and those treated with dipalmitoyl lecithin was examined in sheep blood erythrocytes incubated for 1 hour with dusts at concentrations from enzyme release studies were carried out using macrophages harvested from male Sprague-Dawley-rats, incubated for 2 hours with native dust or lecithin treated silica or kaolin at 1mg/ml concentrations. Effects of varying the lecithin/kaolin dust ratio from 0.01 to 1.33mg lecithin/mg kaolin on erythrocyte hemolysis were also examined. Some cells were treated with lecithin prior to incubation with 1mg/ml kaolin and lysosomal enzyme release was followed. Incubation of silica or kaolin with lecithin suppressed dust induced cytotoxicity almost entirely. Incubation with native dusts caused linear, dose dependent hemolysis, approaching 20 and 50 percent, respectively, for silica and kaolin concentrations of 1mg/ml. Native silica induced 440 percent increases in lactate-dehydrogenase (LDH), beta-glucuronidase (Gl) increases of 350 percent, and beta-N- acetylglucosaminidase (NAG) increases of 340 percent of control values. Native kaolin induced LDH, Gl, and NAG increases of 570, 600, and 570 percent, respectively. Lecithin treatment suppressed the dust induced enzyme release almost entirely. The lecithin/kaolin ratio directly affected percent of hemolysis. Native kaolin induced 44.8 percent hemolysis, no hemolysis was seen with a lecithin/kaolin ratio of 1.33, and intermediate ratios produced intermediate ratio dependent hemolysis values. Lecithin treatment of macrophages reduced enzyme release significantly from that produced by native kaolin in untreated macrophages: Gl and NAG release were reduced from 19.7 and 28.9 percent with native kaolin in untreated macrophages to 15.3 and 23.6 percent in lecithin treated macrophages. The authors conclude that surface modification of minerals with different adsorption properties by pulmonary surfactants generally lessens their prompt adverse effects.