13.0 Silicon Carbide 13.0.1 CAS Number: [409-21-2]
Carborundum; carbolon; silicon monocarbide; silicon carbide, 98.8% 13.0.3 Trade Name: NA
13.0.4 Molecular Weight: 40.097
13.0.5 Molecular Formula: SiC
In recent years, a crystalline form of silicon carbide, known as silicon carbide whiskers, has become an important industrial material. A silicon carbide whisker is a single crystal of silicon carbide that has a cylindrical shape, an aspect ratio of greater than 3, and a diameter of less than 5 mm (167).
Color: Yellow to green to bluish black iridescent crystals (149).
Silicon carbide, also known by the trade name Carborundum, has been manufactured and used as an abrasive material for more than a century. It combines desirable properties of hardness and thermal resistance. It is produced by heating high-grade silica sand with finely ground carbon at 2400°C in an electric furnace (178). In its powdered or granular form, it has been used as the abrasive material in "empty" paper and wheels. It is used as an abrasive in sandblasting and engraving. It has been incorporated into ceramics and glass and especially into refractory ceramic materials.
In silicon carbide, whiskers are used to impart strength and increased thermal resistance to structural materials that are used at high temperatures. Composite ceramics containing silicon carbide whiskers have been used in manufacturing sandblasting nozzles, rocket motor nozzles, heat shields for reentry vehicles, and parts for nuclear reactor fuel assemblies.
13.3.3 Workplace Method The recommended method for determining workplace exposures to silicon carbide is NIOSH Method #0500 for total dust and Method #0600 for respirable dust (31).
13.4.1 Experimental Studies 188.8.131.52 Chronic and Subchronic Toxicity Silicon carbide whiskers accumulated in a dose-related manner in lung tissue during the exposure period and resulted in a significant increase in lung weight for the rats in the highest exposure group compared to controls. The whiskers were most concentrated at the bifurcations of the alveolar ducts and respiratory bronchioles. Most whiskers were either engulfed by alveolar macrophages or located intracellularly in the interstitial tissues. Whiskers also accumulated in the bronchial and mediastinal lymph nodes. Whiskers were present in the interstitial lung tissue and lymph nodes after the 26-week recovery period. Histopathologically, there was evidence of inflammation in both the alveoli and in the lymph nodes. Bronchiolar, alveolar, and pleural thickening, focal pleural fibrosis, and reactive lymphoid hyperplasia were observed in treated rats, and the incidence and severity were dose-related. At the end of the 26-week recovery period, inflammation and lymph node hyperplasia regressed but there was an increased incidence of alveolar and pleural thickening accompanied by a dose-related incidence of adenomatous hyperplasia of the lungs. Despite the relatively short exposure period in this study, the changes seen are consistent with early pulmonary responses to fibrogenic and carcinogenic mineral fibers, such as asbestos, and some of these changes were not reversible. Lapin et al. also noted that no "no-effect level" was demonstrated in their study and that lower exposure levels would need to be examined to detect such a level (167).
In vitro and in vivo studies of silicon carbide whiskers deposited on the ciliated epithelium of the respiratory system indicated that the whiskers were swept to the nonciliated regions by ciliary action (143). There they penetrated the epithelial layers and caused cell damage and death. The cytotoxicity observed was similar to that of asbestos. Intrapleural injections of 20 mg of silicon carbide whiskers once a month for three months caused a 47.7% incidence of pleural mesotheliomas in rats compared to a 34.1% incidence in rats treated with UICC chrysolite asbestos (168).
184.108.40.206 Epidemiology Studies Silicon carbide dust has been considered relatively inert when inhaled. However, in recent years, a number of publications have appeared, suggesting that inhalation of silicon carbide during its manufacture or use as an abrasive may result in pneumoconiosis, Individual cases were described in reports by Funahashi et al. (169), De Vuyst et al. (170), and Hayashi and Kajita (171). Peters et al. (172) found radiographic abnormalities and altered pulmonary function in 171 men employed in the manufacture of silicon carbide. Osterman et al. (173) and Gauthier et al. (174) studied workers from this same plant and also reported decrements in pulmonary function, increased respiratory symptoms, and radiographic changes related to the duration of exposure. Elding et al. (175), on the other hand, found no increases in total mortality, cancer mortality, or mortality from nonmalignant respiratory diseases among 521 men who manufactured abrasive materials using silicon carbide. Interpretation of the results from the studies by Peters et al. (172) and Osterman et al. (173) is complicated by the fact that workers involved in the manufacture of silicon carbide are also exposed to sulfur dioxide and polycyclic aromatic hydrocarbons. Furthermore, the particulate matter to which they were exposed contained small quantities of quartz and cristobalite (176). Durand et al. (177) examined chest radiographs of 200 workers at a Quebec silicon carbide manufacturing plant. Twenty-eight had abnormal radiographs providing clinical evidence of pneumoconiosis, half of which were typical of pure silicosis. Examination of these workers over a seven-year period indicated that the condition did not progress. These same authors examined the particulate materials to which these workers were exposed and conducted experiments in sheep designed to identify the agent that might cause the conditions that were seen (178). They discovered that the particulate matter in the air of the plant contained silicon carbide in both particulate and fibrous form. In the sheep model, silicon carbide particles were no more active than inert materials such as latex beads and graphite powder. The silicon carbide fibers, on the other hand, had fibrogenic activity comparable to that of crocidolite and chrysotile asbestos fibers. They concluded that workers in silicon carbide manufacturing plants may be exposed to silicon carbide fibers, which can contribute to the induction of interstitial lung disease. 13.5 Standards, Regulations, or Guidelines of Exposure
NIOSH has a standard of 10 mg/m (total); 5 mg/m (resp). OSHA has a standard of 15 mg/m total
(<1% silica) and 5 mg/m (resp) (149). These standards and guidelines reflect the traditional view of this material as relatively innocuous. Silicon carbide whiskers in particular and perhaps silicon carbide dust also may be more biologically active than is reflected by these numbers. Occupational exposure should be minimized while additional information is being developed. The ACGIH TLV has a
TWA of 10 mg/m which is the value for particulate matter containing no asbestos and <1% crystalline silica. There is concern that it is carcinogenic for humans, but not enough data exists for a definite determination. The critical effect is on the lungs (155).
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