Document 2q6rLXJLvKnZbrV9DBoDqkZ96

22628 Federal Register / Vol. 51, No. 119 / Friday, June 20, 1986 / Rules and Regulations . . . it'ie much easier to generate dust clouds.from amphiboles [than from chrysolilej.. So,. . . people who Were exposed lo amphiboles in the past almost certainly were exposed to very high levels [compared to the levels of chrysolite to which people were exposed) (Tr. 7/9, p. 35). Using a similar line of argument, Dr. Hans Weill of Tulane University suggested that epidemiologic studies show a fiber-specific risk differential because "it is likely . . . that a cloud of asbestos dust contains a higher proportion of respirable 'carcinogenic' Fibers if crocidolite is present. . Crocidolite might therefore be more likely to be deposited in the deep ' portion of the lung and migrate more easily to the pleural surfaces" (Ex. 99. pp. 17-18). Although the higher levels of amphiboles to which workers were exposed in the past may partly explain the different findings between epidemiologic and animal studies, physical differences between chrysolite and the amphiboles that affect the ability of the lung to clear fiber particles may also have led to these different findings. A number of studies have shown that chrysolite is more rapidlycleared from the lung than are the amphiboles (Exs. 84-171, 84-175, 64-178,. 84-202, 312). For example, Clyseth. et al. (Ex. 312) examined the asbestos content of lung tissue samples taken from asbestos cement workers who had died of pleural mesothelioma or lung cancer. Although more than 90 percent of the fibers used by the workers were chrysotile, 86 to 69 percent of the fibersfound In the lung tissues were amosite, crocidolite, and anthophyllite.The differential lung retention of various Fiber types has also been demonstrated in animals. Castleman (Ex. 121) discussed a study by Wagner [1982) that found that animals exposed to chrysotile fibers developed lung cancer even though a smaller amount of chrysotile was retained in the lung compared to similar tests with amphiboles. He suggested that "chrysotile fibers engaged in a process that led to cancer before removal and decomposition of , . . [the Fibers] occurred" (Ex. 121, p. 2). Dr. Weill believed that "these differences in tissue persistence may wholly of partially explain the observations [that exposure to amphiboles are associated with a higher prevalence of-mesothelioma] in human . . -. populations . . . Non-confirmation . of fiber type differences in animal experiments may be related to the much shorter life span ... [of experimental animals, which would not allow] the effects of varying tissue persistence to carcinogen than amphiboles when be expressed" (Ex. 99, p. 18). administered by inhalation or Dr. Davis also testified that the intrapleural injection, thus conflicting differential lung retention of chrysotile with the findings of human epidemiology and the amphiboles may account for the studies. Rulemaking participants have conflicting results of human and animal suggested several reasons for the studies, albeit by a different mechanism. discrepancy: (1) Exposures to He explained this view as follows: amphiboles in the past were much [I suggest) that chryBotile or sufficient chrysotile is able to remain in the lung tissue for two or three years. Enough of it (to induce higher than exposures to chrysotile, (2) chrysotile Fibers break up and are more easily cleared from the lung than are cancer) will stay for the (entire) life span of amphiboles, effectively reducing the the rat. That means it can exert its maximum effect in the rat, and it means that the rat results showing chrysotile as being [more] hazardous are genuine.' I believe that chrysotile is largely removed from human lungtissue during the much longer 20,30, [or] 40-year tumor induction period that you have got to have in human residence time of chrysotile in the human lung, and (3) the break-up of chrysotile fibers into individual fibrils occurs more readily than for amphibole fibers, thus increasing the effective dose of chrysotile in animals. Dr. Davis explained at the hearing that the net beings. I think that if that wasn't the case, effect of these biological mechanisms is then all the epidemiological evidence would be showing that chrysotile was the nastiest of the dusts" (Tr. 7/9, p. 36). Several rulemaking participants (Ex9. 84-256,99. Tr. 7/9, p. 39) expressed the opinion that chrysotile fibers, which are composed of several hundred smaller unknown: "... Is one fiber ... of amphibole more dangerous than one Tiber. . . of chrysotile? There, I . . . (have) to point out that our evidence cannot answer this with certainty. On the one side, you have almost certainly the greater harmful potential of chrysotile fibrils, are easily broken apart in the and the greater durability of the lung as the result of magnesium leaching amphiboles. ... I could imagine that one from the Fibers. The magnesium loss fiber of each in human beings will end up reduces the structural strength and length of the fiber, facilitating removal of the Fiber by phagocytosis. This process occurs to a lesser extent with the amphiboles, which contain a smaller roughly the same harmfulness, or that might not be the case. It may be that the greater durability of amphiboles will still give a tittle bit of an edge. I have no definite data on this, and nobody else has." (Tr. 7/9. p. 65) quantity of magnesium. Although this OSHA agrees with Dr. Davis that may explain why chrysotile is more epidemiological and animal evidence,. easily cleared from the lung, it also takentogether. fail to establish a effectively increases the dose, in terms definitive risk differential for the various of the numbep of fibers, that reaches the . types of asbestos Tiber. Accordingly, lung. Dr. Davis explaihed this OSHA has. in its Quantitative Risk possibility: Assessment (see Section V) and in the "Now 1 believe what happens--and we have evidence of this--Is that chrysotile ' deposited in lung tissue quite rapidly establishment of a permissible exposure limit (see Section X) recognized that all types of asbestos fiber have the same separates out into its individual fibrils. So if fibrogenic and carcinogenic potential. you think you have deposited one Fiber in the lung tissue, six weeks later you have actually got 100. which potentially at least are the same length, but are very, very much thinner. Now I think this certainly explains some of the very hlghjiarmful potential df chrysotile in our animal experiments. We are actually . Evidence for a Differential Risk by Fiber Size and Aspect Ratio: Several studies contained in the rulemaking docket suggest that Fiber dimension is an important determinant-in asbestosrelated disease development. Stanton el giving the animals. . . many more fibers al. (Exs. 84-193,84-195) studied the even when we are trying to use equal doses - effects of various sizes of fibrous (of chrysotile and amphiboles]" (Tr. 7/9.X. materials, including all forms of pp. 38-39). asbestos, implanted in the pleura of rats To summarize the data on risk and found that some fibrous glasses and differential by asbestos fiber type, all asbestos fiber types produced human epidemiological studies have malignant lumors. The most suggested that occupational exposure to carcinogenic fibers were 0.25 urn or less amphiboles is associated with a greater in diameter and greater than 8 um in risk of mesothelioma than is exposure to length. Fibers less than 8 um in length chrysotile. No clear risk differential for appeared to be engulfed and digested by lung cancer or other asbestos-related phagocytes. However, fibers that were disease has been demonstrated by 1.5 um or less in diameter and longer epidemiological studies. Animal than 4 um (an aspect ratio of experiments, however, have indicated approximately 3) also showed a higher that chrysotile is a more potent correlation with carcinogenicity. Wright GLEASON-000876