Abstract
ASBESTOS is well documented as a carcinogen and cocarcinogen in man and experimental animals, and malignancy may appear after exposure to small amounts. In people who have worked with asbestos insulation there has often been a lag of 20 yr between the first exposure and the development of neoplasia. Among these workers a high incidence of carcinoma of the lung and a high frequency of the rare neoplasm mesothelioma has been reported1. The risk of death from lung cancer is 92 times greater for an asbestos worker who smokes than for someone who is statistically comparable and neither smokes nor works with asbestos. The additive effect of smoking and exposure to asbestos is much greater than that of either factor alone, indicating a cocarcinogenic effect2. Exposure to asbestos is not confined to the occupational environment, for asbestos is present in the air of 49 cities in the USA, in some talcum powders and gypsum spackles and in about 400 industrial products3. As the initial in vivo response to asbestos involves uptake by host macrophages4, we have quantified the effects of standard Union Internationale centre le Cancer (UICC) reference samples of amosite and chrysotdle B asbestos in vitro on the P388D1 line of malignant cells. These cells have macrophage-like characteristics5, but, unlike fresh culture systems, they are capable of reproduction and make long term experimentation possible. We found that asbestos toxicity could be measured as a function of the percentage of cells associated with fibres. Chrysotile was more toxic per unit weight than amosite because it had more fibres per unit weight that could become associated with cells.
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WADE, M., LIPKIN, L., TUCKER, R. et al. Asbestos cytotoxicity in a long term macrophage-like cell culture. Nature 264, 444–446 (1976). https://doi.org/10.1038/264444a0
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DOI: https://doi.org/10.1038/264444a0
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