sideration of epidemiologic and experimental findings for known carcinogens have demonstrated that site-specificity is not necessarily the rule across species. Documentation of persistence of fibers at a target site would represent important evidence in support of biologic plausibility. Although inhaled asbestos fibers clearly pass by the tissues in question in this report, either directly or by swallowing secretions following clearance from the respiratory tract, investigations on fiber persistence in the target organs with definitive findings proved to be unfortunately sparse. Consequently, the epidemiologic data did, in large part, influence the committee’s decision-making for these five sites.

The inference of causality for laryngeal cancer reflects the consistency of the evidence from a substantial number of both worker cohorts and general-population case-control studies, an indication of greater risk among more highly exposed persons, and the finding of an association with exposure in studies that addressed potential confounding by tobacco-smoking and alcohol consumption. In considering biologic plausibility, the committee noted that the epithelium of the larynx is similar to the respiratory epithelium lining the conducting airways of the lung. Inhaled fibers pass through the larynx and may deposit there; although fiber deposition and persistence in the larynx have not been studied extensively, there are reports of fibers and asbestos bodies being recovered from laryngeal tissues.

For all the sites for which the evidence was classified as suggestive, the case-control information was less abundant than for laryngeal cancer. For stomach and colorectal cancers, there actually were a few more informative cohorts, but fewer than half as many cohorts provided data on pharyngeal cancer as had on laryngeal cancer. The committee’s review found less consistency among the findings of the individual studies for these sites and there was only limited indication of exposure-response relationships. Asbestos fibers could pass through the lumen of the pharynx, stomach, and colon and rectum, but it is uncertain how fibers might interact with the presumed target for carcinogenesis, the cells of the epithelium. Despite sporadic reports of asbestos bodies or fibers being recovered from stomach and colon tissue, information was lacking on the fiber doses received by target cells in the gastrointestinal epithelium. Relevant animal evidence was available from feeding studies, which showed the induction of colon polyps in rats but not the production of malignancy.

The evidence was most sparse for cancer of the esophagus, for which the designation was inadequate. There was a suggestion of an exposure-response relationship from the available cohort studies, but the summary estimate of 0.99 for any asbestos exposure was indicative of no association. Only three case-control studies were identified, and investigation of potential confounding was limited. Animal-feeding studies did not show production of esophageal cancers.



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