Silicon carbide

Endpoint summary

Description of key information

In conclusion, the present investigation confirmed that SiC itself, along with SiC commercial products, has none or only a limited toxicological potential on the cellular level.

Additional information

Available data indicate the absence of pulmonary damage after intratracheal instillation of high dose (5 mg/100 ml MRV) of SiC in rats (Vaughan et al., 1993).

Bruch et al. (1993) examined the effects of various dusts (SiC (F 1200), corundum and quartz (DQ12)) with a grain diameter < 3 µm on guinea pig alveolar macrophages (H₂O₂release) and CBF1-mice bone marrow macrophages (TNF-αrelease). The various dusts were studied at doses ranging from 20 to 60 µg/10⁶cells. After 16 hours incubation, the results showed a complete inhibition of stimulation of H₂O₂with 60 µg Quartz, and about 40 % at the lower dose of 20 µg. By contrast, corundum and SiC had no effect on H₂O₂release, similar to the untreated cells. Release of TNF-αassessed by growth inhibition of L-929 cells did not differ from controls with doses of SiC up to 50 µg/well of SiC, whereas 10 µg/well of quartz led to a significant effect.

The same authors (Bruch and Rehn, 1996) then tested with comparable procedures two different SiC dusts; F 1200 (as previously) with 2.26 µm mean aerodynamic diameter and NF2 with 1.14 µm mean aerodynamic diameter. Positive control was quartz (DQ12), the negative one corundum. Cell cytotoxicity measured by lactate dehydrogenase (LDH) activity showed no significant difference in doses ranging from 20 to 180 µg/10⁶guinea pig alveolar macrophages (AM) for two SiC or corundum dusts, whereas quartz reduced cell viability even in low doses. In contrast to the results obtained for cell viability, marked differences between the two SiC samples could be measured in the H₂O₂release as a measure for cell damage. Macrophages burdened with NF2 or quartz exert a significant and dose dependant reduction in H₂O₂release. In contrast the F 1200 samples did not show this effect, as corundum. Moreover, side-to-side comparison each fraction of sample NF2 is more toxic than sample F 1200. The authors concluded that different grain size distribution alone could not solely explain the differences. The biopathogenicity of in vitro NF2 SiC seems to consider the possible differences for the tested varieties of SiC.

Using the vector-model, a new in vitro testing concept based on the knowledge of the primary reactions of alveolar macrophages activated by the phagocytosis of dust particles, Bruch and colleagues assessed the biological activity of SiC products on the market (Bruch et al., in press). Particular attention was given to the presence of SiC cleavage fragments (CFs) in SiC commercial products. No SiC whiskers and no crystalline silica were detected in the respirable fractions from the commercial products. Average CF concentrations varied from 17 to 493 10⁶/g of particles in the five respirable fractions of SiC grains. The in vitro doses used of 15, 30, 60 and 120 µg dust per 10⁶AM correspond to a lung exposure of approximately 0.15 to 2,4 mg dust/rat lung via intratracheal instillation, relevant to thein vivosituation. The results showed that SiC commercial products induced a very low level of biological activity in the vector model comparable to the electrocorundum. However, in the mid and the top dose range an isolated secretion of reactive oxygen species (ROS) was observed for some samples. This increase was not related to the contents of cleavage fragments. Moreover, the isolated ROS response at higher exposure levels could not be related to in vivo toxic effects. The decrease in ROS response after heat-treatment of SiC commercial products suggested that macrophage activation is mediated by strong interactions between the surface of the particle and some cell membrane components. In conclusion, the present investigation confirmed that SiC itself, along with SiC commercial products, has none or only a limited toxicological potential on the cellular level.