YOU ARE NOW CONNECTED TO THE TOXLINE (1981 FORWARD, NON-ROYALTY) FILE. ==SILICA, FUSED AND SILICOSIS== 1 AUTHOR Guo WX AUTHOR Li GH AUTHOR Zheng SQ AUTHOR Lin ZN TITLE Effects of silica on serum phospholipid, lipid peroxide and morphological characteristics of rat lung. SOURCE Biomed Environ Sci; VOL 8, ISS 2, 1995, P169-75 ABSTRACT The effects of instilled silica have been studied on the serum-phospholipid (PL), lipid peroxide (LPO) and histopathology of rat lung up to 140 days from the first day of instillation. Silica induced relatively higher serum-PL throughout the experiment. The level of LPO also increased appreciably. They presented positive linear correlation. The early lesion was acute alveolitis with silica particles. These lesions became silicotic nodules on the 30th day, which then were enlarged gradually and fused by fibrosis. Alveolar macrophages (AM) were activated and surface structure was damaged. These results indicate that instilled silica can induce lipid peroxidation of cell membrane and selective accumulation of lung PL. 2 AUTHOR Ratney RS TITLE The Threshold Limit Value for Various Forms of Amorphous Silica SOURCE Proceedings of the VIIth International Pneumoconioses Conference, Part II. Pittsburgh, Pennsylvania, August 23-26, 1988. NIOSH, U.S. Department of Health and Human Services, DHHS (NIOSH) Publication No. 90-108 Part II, pages 1134-1135, 9, 1990 SOURCE references ABSTRACT A brief review was presented of the chemical and physical structure of silica (7631869), crystalline silica, amorphous silica, fused silica, and elemental silicon (7440213). Precipitated silica and silica gel have been considered the prototypical nuisance dusts. Silica gel injected intratracheally in rats has not been demonstrated to cause fibrosis and neither have inhalation exposures. Macrophage accumulations and mild proliferation of reticulin fibers were observed. In a group of 165 workers exposed to precipitate silica estimated to be near or below 10mg/m3 for an average of 8.6 years, no serial changes in pulmonary function or chest radiographs were observed. Fumed silica and silica fume display entirely different toxicities. Fumed silica appeared to be only slightly more toxic than precipitated silica and silica gel. However, several studies have indicated that silica fume produced a unique complex of acute and chronic effects which were reversible after exposure ceased. Brief high exposures to silica fume produced symptoms of metal fume fever which have been observed to persist up to three months. Chronic exposure produced X-ray and pulmonary function evidence of silicosis. The threshold limit value (TLV) for fumed silica has been set at 10mg/m3. While no value has been established for silica fume, a TLV of 0.2mg/m3 was suggested. The author concludes that additional uses of fused quartz (14808607) in modern technology make it important to gather more solid toxicological data on this material as well. 3 AUTHOR Mastromatteo E TITLE Silica, Silicosis, and Cancer: A Viewpoint from a Physician Employed in Industry SOURCE Silica, Silicosis, and Cancer: Controversy in Occupational Medicine, D. F. Goldsmith, D. M. Winn, C. M. Shy, Editors; New York, New York, Praeger Publishers, Cancer Research Monographs, Vol. 2, pages 491-503, 33 references, 19861986 ABSTRACT Information on the two forms of silica (crystalline and amorphous) from the point of view of an industrial physician was presented. For crystalline silica, topics included occupational exposures, silicosis, mixed dust pneumoconiosis, occupational exposure limits to crystalline silica, and lung cancer. For amorphous silica, topics included health effects, and occupational exposure limits. The author concluded from his review that silicosis and its sequelae remain the major health risks from exposure to crystalline silica. Amorphous silica in the form of precipitated silica and silica-gels containing less than 1 percent quartz may be regarded as nuisance dusts. The health effects of fumed amorphous silica (7631869) require additional study. Although there have been conflicting recommendations with respect to occupational exposure limits, the author recommends limits of 100 micrograms/cubic meter (microg/m3) for respirable quartz (14808607) and fused silica, 50microg/m3 for cristobalite (14464461) and tridymite (15468323), and 10microg/m3 for amorphous silicas containing less than 1 percent quartz. The author states that there are inadequate epidemiologic or experimental data to conclude that exposure to crystalline silica by itself is associated with increased risk of any form of cancer. 4 AUTHOR Uber CL AUTHOR McReynolds RA TITLE Immunotoxicology Of Silica SOURCE CRC Critical Reviews in Toxicology, Vol. 10, No. 4, pages 303-319, 84 references, 19821982 ABSTRACT The immunotoxicology of silica (7631869) is reviewed. The epidemiological aspects of exposure to silica are summarized. The pathogenesis of silica related diseases is discussed. The development of silicotic lesions depends on inhaling non combined forms of particulate silica of respirable size. The particles are ingested by alveolar macrophages and incorporated into a membrane bound vesicle called a phagosome. The phagosome is then merged with a lysosome. The membranes of these vesicles fuse together forming a single bound vesicle containing both phagocytized material and activated lysosomal enzymes known as a phagolysosomes. Phagocytized silica disrupts lipoprotein membranes by an unknown mechanism. It has been suggested that this phenomenon represents the starting point of the tissue reactions that result in silicosis. The effects of silica on human immunological competence are reviewed. Experimental silicosis in animal models is discussed. Such models have shown that silica is a selective macrophage toxin in all species. Interspecies variations occur with respect to the morphology of pulmonary lesions induced by silica. Aberrations of both humoral and cellular immune responses have been observed in guinea-pigs, rats, and mice following silica exposure. These aberrations involve humoral, cellular, and regional immunity, and increased susceptibility to pulmonary infections, especially tuberculosis.