Evidence of an oxidative mechanism for the hemolytic activity of silica particles.

The formation of reactive oxygen species resulting from the interaction of silica dust particles with red blood cell membranes was investigated; particularly, the effect of surface hydroxyl (silanol) group concentration on the rate of formation of such reactive oxygen species was investigated. The rate of formation was measured indirectly through the effect of catalase, a hemoprotein peroxidase, on silica-induced hemolysis. It was found that the addition of exogenous catalase to erythrocytes markedly reduces the hemolysis caused by silica particles. Furthermore, the amount of catalase required for deactivation of silica per unit area of particle surface is lower for fumed silica particles and calcined crystalline particles than for uncalcined, crystalline silica, suggesting a correlation between the concentration of OH groups at the silica particle surface and its potential for generation of H2O2. The addition of albumin, a copper chelator, also decreases hemolysis. These results suggest that the hemolysis caused by silica particles is at least partly related to the formation of H2O2 at the particle surface and its subsequent reaction with Cu+ ions. The relationship between the concentration of surface silanol groups on the silica surface and the amount of catalase required to decrease hemolysis may also provide a method for testing potential fibrogenicity of respirable dusts.