Health effects of tremolite. Now and in the future.
Although tremolite asbestos has been well characterized since 1916, appreciation of its role in disease induction is relatively recent. It has always been understood that the morphology of tremolite is complex, and part of the slowness in recognizing it as a hazard has been definitional in nature. Reduced to simple terms the questions are, when is tremolite "asbestos-like," when is it an innocuous amorphous particle, do these forms occur together, with what confidence can they be separated for regulatory purposes, and what is the spectrum of disease potential for varying exposure? A brake on regulation is partially due to a convergence of opinion of unlikely and unintentional allies: industries producing tremolite-containing materials and some epidemiologists resisting attribution of risk to tremolite on the grounds that its known effects--pleural plaques, asbestosis, lung cancer and mesothelioma--are principally due to chrysotile, which is often contaminated with fibrous tremolite. The latter group concentrate their skepticism on internal-dose biomarker studies associating lung tremolite content with mesothelioma (but not so clearly with lung cancer or asbestosis). They ignore the basic carcinogenic quality of fibrous tremolite, shown in both animal and epidemiological studies. Evidence from the Quebec chrysotile/tremolite mining districts suggests that very low concentrations of tremolite in ambient air can be translated into high concentrations in lung, even in those without occupational exposure. Disease incidence, especially for mesothelioma, seems also to be associated with tremolite air and lung content. The risk associated with tremolite has been demonstrated in Corsica, Cyprus, the United States, and Canada. Of particular importance is an apparent increase in the proportion of mesothelioma risk attributable to tremolite, since the fibers heretofore most responsible for that disease--commercial amphiboles--have been or are being severely regulated or completely eliminated in production and use. Further, amosite and crocidolite, while still a concern, form a small fraction of "asbestos-in-place": most of this material is chrysotile and we do not really know to what degree it is contaminated with tremolite. The available evidence suggests that bulk analysis or airborne fiber analysis will not answer this question, and perhaps only animal bioaccumulation assay is sufficient. Until we know more, it seems prudent for public health to avoid dispersing chrysotile/tremolite into the environment, and, where we can, to regulate all tremolite "fibers" conservatively.
Case
B W
BW
Center for Environmental Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pennsylvania 15261.
D000818:Animals; D017636:Asbestos, Amphibole; D002273:Carcinogens; D006801:Humans; D008175:Lung Neoplasms / Q000139:chemically induced* / Q000453:epidemiology; D008654:Mesothelioma / Q000139:chemically induced* / Q000453:epidemiology; D008906:Mining; D009784:Occupational Diseases / Q000139:chemically induced* / Q000453:epidemiology; D010316:Particle Size; D012824:Silicic Acid / Q000633:toxicity*
D017636:Asbestos, Amphibole; D002273:Carcinogens; D012824:Silicic Acid; C005846:tremolite