Calciumsilicat

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

30 [mg/m3]

330 [mg/m3]

2000 [mg/m3]

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical. [http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=13983-17-0]

Results from studies in 1981 on 46 men exposed to wollastonite for an average of 21.5 yr (10-41 yr) in a Finnish quarry have been reported ... Chronic bronchitis was found in 11/46 workers (including 3/15 nonsmokers). Chest radiographs showed small irregular parenchymal opacities (grade 1/0 or 1/1) in seven, pleural thickening only (grade >/= a,3) in six men and both lung and pleural changes in seven; among the 138 referents, five had pulmonary fibrosis only, six had pleural thickening only, and one had both lung and pleural changes. Differences in smoking habits did not account for these changes.

The hemolytic and cytotoxic characteristics of wollastonite were assessed in an in-vitro study using human red blood cells and compared to results for chrysotile. Red blood cell cultures were established from blood samples donated by healthy volunteers. Hemolytic studies were conducted by incubating cell cultures in 0.2% dust suspensions of wollastonite or chrysotile at 37 degrees-C for 20 minutes. Hemoglobin content was determined spectrophotometrically at 545 nanometers. Peroxidative damage of polyunsaturated fatty acids was assessed by the formation of malonaldehyde (MDA) after incubation of either intact cell suspensions or hemolysate supernatant with varying concentrations of wollastonite or chrysotile. A dose and time dependent response was observed in the percentage of cell lysis with treatment of the dust suspensions; however, chrysotile was more effective in inducing hemolysis than wollastonite. Wollastonite was shown to induce the cytotoxic effects seen with chrysotile to a lesser degree: lipid-peroxidase stimulation in intact cells and hemolysate supernatant and a concentration dependent increase in MDA formation. The addition of vitamin-E, glutathione, and bovine serum albumin demonstrated a reduction of the cytotoxicity induced by wollastonite and chrysotile. The authors conclude that wollastonite is less toxic than chrysotile, and that the reduced toxicity seen in the in-vitro study can be extrapolated to in-vivo situations.

The incidence of fibrosis of the lung and pleura was studied in workers with long term exposure to wollastonite, a fibrous silicate material. Subjects of the study were 49 workers (40 men and nine women) in a Finnish limestone and wollastonite mine and mill. Mean exposure of the workers was 25 years. Mean concentrations of total dust in the mine and mill varied in 1981 from 0.3 to 67 mg/cu m, and fiber level ranged from 5.1 to 33 fibers/cubic centimeter, (f/cm3), determined by phase contrast optical microscopy. The average respirable fraction contained 15% wollastonite and 3% quartz. Later dust measurements revealed fiber concentrations ranging from 0.04 to 3.4f/cu m for wollastonite mining and milling. The subjects underwent a physical examination, and work histories and symptoms of chronic bronchitis were recorded. Chest radiographs were performed, and spirometry and diffusion capacity were measured. Four workers underwent high resolution computed tomography and bronchoalveolar lavage. Lung tissue specimens (autopsy samples) were available for two workers. Mineral fibers and asbestos bodies were analyzed from the bronchoalveolar lavage fluid and lung tissue specimens, and the tissue was analyzed for lung fibrosis. Two workers were found to have small irregular lung opacities, but high resolution computed tomography revealed no parenchymal fibrosis in those workers. Nine workers, five of whom had been exposed to asbestos, had pleural plaques. Multivariate logistic regression analyses revealed no association of plaques with the duration of wollastonite or asbestos exposure. Wollastonite fibers or bodies were not found in any of the four workers who underwent bronchoalveolar lavage, nor in either of the workers whose lung tissue specimens were available. The authors conclude that no evidence was found that long term exposure to wollastonite causes parenchymal fibrosis of the lung and pleura. They further conclude that the findings indicate that wollastonite fibers are poorly retained in human lungs.

Wollastonite

Group 3: Not classifiable as to its carcinogenicity to humans

Volume Sup 7: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, 1987; 440 pages; ISBN 92-832-1411-0 (out of print)

1997

1996

Wollastonite was evaluated for mutagenicity in the Salmonella/microsome preincubation assay using the standard protocol approved by the National Toxicology Program. Wollastonite was tested at doses of 0, 1.0, 3.3, 10, 33, 100, 333, 1000, 3333, and 10,000 ug/plate in four Salmonella typhimurium strains (TA98, TA100, TA1535, and TA1537) in the presence and absence of Aroclor-induced rat or hamster liver S9. Wollastonite was negative in these tests and the highest ineffective dose level tested (not producing a precipitate) in any Salmonella tester strain was 1000 ug/plate.

The toxicity of wollastonite to LLC-MK2 (monkey kidney) cells was found to be comparable to that of asbestos minerals. Following exposure to 5 mg/ml, cell survival was approximately 50% ...

/Researchers/ investigated the effects of Finnish wollastonite ... on rat alveolar macrophages. ... After exposure to 25 ug/ml wollastonite, cell viability was reduced by 15% and LDH release increased by 125% within 24 hr ... In exposed cultures, wollastonite was more toxic than titanium dioxide but less toxic than UICC crocidolite; its effect on LDH release was similar to that of titanium dioxide but smaller than that of crocidolite.

The cytotoxic effects of wollastonite samples on lipid peroxidation and glutathione depletion were studied in an in-vitro model using hepatocytes from male albino-rats. Cell suspensions were incubated with 100 micrograms of the wollastonite samples kemolit-ASB-3, kemolit-N, and kemolit-A-60 and with chrysotile for comparison. Malondialdehyde (MDA) formation, an index of lipid peroxidation, and intracellular glutathione (GSH) content were estimated using optical density measurements. A significant increase in MDA formation was seen after incubation of hepatocytes for 3 hours with wollastonites and chrysotile, but less lipid peroxidation was observed with wollastonites than with chrysotile. Intracellular GSH was depleted to a significant degree in all treated cells compared with controls, and chrysotile treatment resulted in higher depletion than did wollastonite treatments. A comparison of lipid peroxidation and GSH in the presence and absence of methionine indicated a significant inhibition of MDA in the presence of methionine, while intracellular GSH increased in the presence of methionine. It as concluded that chrysotile is more toxic than wollastonites. These results support the theory that GSH deficient hepatocytes undergo lipid peroxidation rapidly enough to destroy the cells.

For more Non-Human Toxicity Excerpts (Complete) data for WOLLASTONITE (7 total), please visit the HSDB record page.