Respiratory cancer in chrysotile textile and mining industries: exposure inferences from lung analysis.

Abstract

In an attempt to explain the much greater risk of respiratory cancer at the same cumulative exposure in asbestos textile workers in Charleston, South Carolina, than in Quebec miners and millers, both exposed to chrysotile from the same source, 161 lung tissue samples taken at necropsy from dead cohort members were analysed by transmission electron microscopy. Altogether 1828 chrysotile and 3270 tremolite fibres were identified; in both cohorts tremolite predominated and fibre dimensions were closely similar. Lung fibre concentrations were analysed statistically (a) in 32 paired subjects matched for duration ofemployment and time from last employment to death and (b) in 136 subjects stratified by the same time variables. Both analyses indicated that the Quebec/ Charleston ratios for chrysotile fibre concentration in lung tissue were even higher than the corresponding ratios of estimated exposure intensity (mpcf). After allowance for the fact that regression analyses suggested that the proportion oftremolite in dust was probably 2 5 times higher in Thetford Mines, Quebec, than in Charleston, the results from both matched pair and stratification analyses of tremolite fibre concentrations in lung were almost the same as for chrysotile. It is concluded that neither fibre dimensional differences nor errors in estimation of exposure can explain the higher risks of lung cancer observed in asbestos textile workers. The possible co-carcinogenic role of mineral oil used in the past in asbestos textile plants to control dust provides an alternative hypothesis deserving consideration. exposures of the past were seldom documented. This difficult exercise has been attempted in nine industrial populations.2 Among these were the chrysotile miners and millers of Quebec34 and the chrysotile textile workers of Charleston, South Carolina.5 Linear relations between excess mortality from respiratory cancer and cumulative exposure in these two populations (fig 1) illustrate the problem considered in the present report. In both cohorts cumulative exposures (mpcf.y) were calculated from impinger data, all that were available for the past. Cumulative exposures as high as 2000 mpcf.y were recorded in the Quebec cohort, 10 times higher overall than exposures in Charleston. Figure 1 shows that, for the same cumulative exposure, the risk of respiratory cancer was about 50 times higher in Charleston. These estimates of risk were essentially corroborated by independent studies in the Charleston plant' and in Quebec.9 Studies in two other textile plants, one in the United States and another in the United Kingdom, gave similar results.'1 "The large difference in risk between mining and 180

Persistence of Natural Mineral Fibers in Human Lungs: An Overview

“…In this regard it is striking that the two studies demonstrating an exposure correlation for chrysotile (Table 2) both come from a group oftextile workers, suggesting that there may be something special about the fibers to which these workers are exposed. This suggestion has also been raised in regard to the high incidence of carcinoma in the same population (11).…”

“…Essentially identical results (25,26). However, no information is avail-remote [ (29) However, some reports do demonstrate lung chrysotile burdens that are proportional to exposure (4,11), providing evidence against the idea ofdeposition failure.…”

“…The issue of persistence in animal models is discussed at length elsewhere in these proceedings. Table 1 lists published studies that supply information on the relative proportion of chrysotile and amphiboles found in lung samples (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16). The preparative methods, types of electron microscope, and counting rules used in studies differ markedly, and these differences undoubtedly affect the results.…”

Asbestos Tissue Burden Study on Human Malignant Mesothelioma.

“…The current Occupational and Health Administration (OSHA) method by light microscopy counts asbestos fibers that are longer than 5 µm in length with on aspect ratio of larger than 3 to 1, assuming that all fibers shorter than 5 µm are not carcinogenic. Further, even on the electron microscopic level, using the same assumption, some investigators have neglected to count short asbestos fibers (≤ 5 µm) in their tissue burden studies 12,[15][16][17][18][19] . However, our previous studies revealed that the majority of asbestos fibers in human lung and mesothelial tissues taken from mesothelioma patients did not fit Stanton's hypothetical dimensions; less than 2% of chrysotile fibers and less than 10% of amosite fibers in these tissues fit with Stanton's criteria.…”

Air Pollution with Asbestos in Several Cities in Romania

“…They have been classified as markers of exposure, markers of effect, and markers of susceptibility (NAS/NRC 1989). Principal biomarkers of exposure to asbestos fibers include the detection and counting of fibers or asbestos bodies in bronchoalveolar lavage fluid samples (De Vuyst et al 1982, 1997Dumortier et al 1990Dumortier et al , 1998Roggli et al 1994a;Sebastien et al 1988a;Teschler et al 1994;, Tuomi et al 1991b),sputum samples (McDonald et al 1988(McDonald et al , 1992Sebastien et al 1988b), or in autopsied or surgically resected lung tissue samples (Case 1994;Churg 1982;Churg and Warnock 1981;Churg and Wright,1994;Churg et al 1993;de Klerk et al 1996;Dodson et al,1999;Dufresne et al 1995Dufresne et al , 1996aDufresne et al , 1996bSebastien et al 1989). Asbestos bodies are collections of fibers (usually of length >8 μm) with a protein -iron coating (also known as ferruginous bodies) that, when observed in lung tissue sections in conjunction with fibrosis, have been proposed to be used in the diagnosis of asbestosis (Churg 1989;.…”