Data on the ability of silica (14808607) to directly generate radicals as well as stimulate radical production in alveolar macrophages were presented and summarized. Results of previous studies indicated lung and parenchymal damage and tissue scarring from exposure to crystalline silica, resulting in fibrosis. The cytotoxicity exerted by crystalline silica was suggested to be a direct consequence of toxic interactions between quartz particles and cell membranes, or silica induced production of oxidant species by pulmonary phagocytes. Sandblasting, silica flour milling, rock drilling, and tunneling occupations were associated with high risks of pulmonary fibrosis. Studies have shown the generation of free radicals on the surface of the cleavage planes from the grinding or fracturing of quartz particles during such operations. Silica induced activation have resulted in the production of superoxide, hydrogen-peroxide (H2O2), and nitric-oxide (NO) and other oxidant species with the ability to damage lung cells. Data have indicated that oxidant injury was significant in the pathogenesis of silicosis. Reactive oxygen species were shown to be derived from direct hydroxyl radical generation from freshly fractured silica or from superoxide, H2O2, and NO produced by silica exposed alveolar macrophages. Further evidence indicated the decisive role of oxygen species from recruited blood leukocytes in the development of silica induced lung injury. Tetrandrine was noted to effectively block the ability of quartz to stimulate oxidant release from pulmonary phagocytes.
NIOSH-Author; Silica-dusts; Dust-exposure; Dust-inhalation; Lung-irritants; Respiratory-system-disorders; Cytotoxic-effects; Lung-cells; Mining-industry; Toxic-effects; Free-radical-generation; Immune-reaction;
Author Keywords: silicosis; silica radicals; alveolar macrophages; oxygen radicals; nitric oxide; fibrosis; tetrandrine