Abstract
EPIDEMIOLOGICAL evidence indicates that particulate matter, such as asbestos, can increase the health risk from exposure to chemical carcinogens. For example, asbestos insulation workers show an eightfold increased disposition towards lung cancer; non-smokers had only a slightly increased risk of lung cancer, whereas the smokers had a 92-fold increased risk1,2. These data indicate that 90% of the asbestos related cancers are the result of the co-carcinogenic effects of cigarette smoking and the inhalation of asbestos fibres. We have now examined one possible mechanism of co-carcinogenesis—the ability of particulate matter to increase the rate of cellular uptake of benzo[a]pyrene (BP). We used fluorescence spectroscopy to investigate the ability of two particulates, silica and asbestos, to adsorb BP, and to deliver the carcinogen to model membranes. The surface area of the asbestos sample was 60-fold less than that of our silica sample. Surprisingly the asbestos sample showed a greater ability to adsorb BP in a monomeric state than silica. Most importantly BP which is adsorbed to asbestos is more rapidly transported into membranes than BP which is adsorbed to silica. Thus increased cellular exposure to carcinogens, resulting from the presence of particulates which can adsorb and deliver these carcinogens to cells, may be involved in the process of co-carcinogenesis.
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LAKOWICZ, J., HYLDEN, J. Asbestos-mediated membrane uptake of benzo[a]pyrene observed by fluorescence spectroscopy. Nature 275, 446–448 (1978). https://doi.org/10.1038/275446a0
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DOI: https://doi.org/10.1038/275446a0
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