Environmental and occupational medicine, second edition. Rom WN, ed. Boston, MA: Little, Brown and Company, 1992 Jan; :345-358
Silicon (7440213) induced pulmonary disease was discussed in this review. Occupations including sandblasting, mining or tunneling, milling, pottery, glassmaking, foundry work, quarry work, and abrasive work have been found to pose a high risk to workers for silicosis. Pathological changes in the lungs of patients with chronic silicosis have included fibrosis of the visceral pleura and hyalinized intrapulmonary nodules along with the presence of birefringent material in the periphery. Progressive massive fibrotic lesions have resulted from the coalescence of the silicotic nodules. Acute silicosis has been distinguished by the presence of proteinaceous material in the alveoli along with hypertrophic type- II pneumocytes and a minimal amount of fibrosis. Studies have suggested that the fibrogenic effect of silica (14808607) may be due to the release of inflammatory mediators by silica activated alveolar macrophages. The clinical presentation, diagnosis, and natural history of silicosis were described and discussed.
NIOSH-Cooperative-Agreement; Silicon-compounds; Silica-dusts; Silicate-miners; Pulmonary-system-disorders; Physiopathology; Occupational-exposure; Risk-factors
Environmental and occupational medicine, second edition
Center to Protect Workers' Rights