Document peQKO4eQpD8KgzOkZqb3O8xdj

q.j.C.z COMMENTS UV JOHNS-MANVI LLE CORPORATION UN THE JUNE 1, 1978 "DRAFT REPORT - ASSESSMENT OF POTENTIAL ENVIRONMENTAL HEALTH HAZARD ASSOCIATED WITH AIRBORNE MINERAL FIBERS EMITTED DURING TACONITE ORE PROCESSING" BY PHILIP M. COOK, Ph.D. Initially, the title of the draft report leads the reader to believe that the report will provide an assessment of the potential environmental health hazards associated with airborne mineral fibers emitted during taconite ore processing. However, the report is no more than a collection of references from which the implication is made that there may be a health hazard as sociated with such emissions. In addition, it is incongruous why an individual with Dr. Cook's background was chosen to prepare a document of this nature. Dr. Cook's training as a physical in organic chemist in no way prepares or qualifies him to evaluate potential health hazards that might be present. Furthermore, it is likely that Dr. Cook is not without bias in his assessment of this situation, since he was the principal technical advisor to the federal government during portions of the Reserve Mining trial in 1973- This incidentally took place only one year after Dr. Cook received his doctorate from the University of Wisconsin. Set forth below are comments relating to specific paragraphs of Dr. Cook's draft report. ~ Page 1, paragraph 1. In essence, this paragraph is an allencorr.passing statement which implies that any type or level of exposure to asbestos fibers can lead to an increased risk of disease. Dr. Cook makes no attempt whatsoever to place the various types of exposure, i.e. occupational, para-occupational, and non-occupational in proper perspective as far as exposure levels and potential and actual risk of disease are concerned. Manifestations of asbestos-related diseases have not been associated with low level exposures to asbestos fibers, as is implied by Dr. Cook. The occurrence of asbestos-related diseases is dose related in terms of fiber levels and years of exposure. There is increasing evidence to indicate that even in para-occu pational situations, those who have developed asbestos diseases did receive high doses to fibers. The first paragraph erroneously implies that household exposures to asbestos have been minimal in the dose-relationship concept. It is likely that these exposures were substantial. As recognized by Selikoff and others, the impregnation of drapes, rugs, furniture, etc. with asbestos fibers and the constant resuspension of fibers in the respirable range creates an exaggerated hazard. These household exposures provide an opportunity for repetitively high, short peak exposures due to the shaking out of v;ork clothes. Lacking specific dust counts UCC 007446 over the appropriate time period, any conclusion that these exposures were minimal is totally unacceptable. Once asbestos is carried home by the workmen, it accumulates in the home; and its presence in the home is likely to become permanent. For example, it gets into the rugs, from which it becomes resuspended by movements such as brushing and walking. In consequence, family members are getting a 21)-hour a day, 7-day a week exposure, relatively speaking, rather than an interval exposure. Further more, in the home environment, an exaggerated opportunity is present for co-factors to be operating, such as smoking and other household pulmonary insults. At the New York Academy of Sciences June 1978 Science Week Con ference, E. Cuyler Hammond, reported on a study which he conducted with Dr. Selikoff and others which was aimed at finding out if exposure to small amounts of asbestos will lead to any long-term harmful effects. This study traced the fates of .5,550 men who lived in the community near an asbestos plant in Paterson, New Jersey between 1942 and 1954. The researchers stated that it was safe to assume that people living in that community were exposed to asbestos. Samples of settled dust collected from the attics of houses near the factory still contained appreciable numbers of amosite asbestos fibers. However, the researchers failed to find any unusual incidence of cancer among these asbestos-exposed people. This is evidence that a low-level exposure, to asbestos has not led to any increased incidence of malignancies. Page 1, paragraph 2. The unqualified statements in paragraph 1 are followed in the second paragraph by a greatly over-simplified statement on risk assessment by Dr. Cook, which in contrast .in cludes a statement which implies that fiber concentrations are important in relationship to the risk of disease. As Dr. Cook has noted, the physical, chemical, and morphological properties of fibers are extremely important in comparing incidence of disease from one location to another. However, it is extremely important that other factors, which may have influenced the occurrence of disease, also be taken into account. An example of this is the relatively large difference in the incidence of disease which is found in miners and millers of asbestos fiber, as compared with insulation workers, which indicates that co factors may play an important part. Page 1, paragraph 3- We are at a loss to appreciate the relevance of the reference in the third paragraph to the study by Kleinfeld, et al, on exposures to asbestos in the talc mining and milling industry. These were not exposures to short "asbestos-like" fibers of the type encountered in taconite operations, but repre sented exposures to fibers of the type which have been shown in other situations to be capable of producing disease when present in high enough concentrations. While it is agreed that occu pational exposures to tremolite and anthophylite of sufficient dose and duration can produce asbestos disease, we do not see how this is relevant for inclusion in an assessment of the potential environmental health hazards associated with airborne mineral fibers emitted during taconite ore processing. A Z'Q 3 r` ' UCC 007447 -3- Reference is then made to two studies or the Momestake miners who have been exposed to cummingtonite-grunerite fibers of relatively short dimensions. The first paper reports the research efforts of Drs. Gillam, Dement, Lemen, Wagoner, and their associates at NIOSH. The authors of this study reported an excess of both lung cancer and pneumo coniosis in this population. They attributed the excess to the presence of a form of asbestos in cummingtonite-grunerite ore. The NIOSH group totally dismissed the possibility that this excess- was caused by other potential lung cancer hazards present in the mine, such as diesel exhaust, arsenic and radon daughters. Cigarette smoking habits were ignored. The increase in fibrosis was erroneously attributed to asbestos, rather than to free crystalline silica, known to be present in the mine in substantial quantities. The Gillam, et al paper is fatally flawed due to its failure to understand the problems inherent in studying a small cohort. The authors' claim of excessive rates in the asbestos-related malignant and non-ir.alignant disease categories is clearly based on poor and incomplete data analyses. Even if the claim were based on valid analyses, data to incriminate asbestos, rather than one or a com bination of other coexisting materials in the causation of cancer, are entirely lacking. To ascribe the excess of non-malignant respiratory disease to asbestos and ignore the known exposure to high levels of free crystalline silica in the past, confirmed by the frequent diagnosis of silicosis on the death certificates, borders on irresponsibility. To ignore the potential for carcino genic and co-carcinogenic effects resulting from the mixed exposure to silica dust, arsenic fumes and particles, blasting powder fumes and radon daughters, and to arbitrarily ascribe all of their excess of cancer to asbestos particles Is manifestly irresponsible and has no justification in the methodology of science. As a result of the serious concerns raised by Johns-Manville and others regarding the NIOSH methodology and conclusions, this study is currently being repeated by NIOSH. As Dr. Cook properly notes, a subsequent study by McDonald of a much larger cohort from the same mine indicates no excess of respiratory cancer deaths. The McDonald study has greater scientific credibility due to its inclusion of a much larger population sample. Finally, it should be noted that neither NIOSH or the McDonald study found any excess of mesothelioma or gastrointestinal tumors. Since the McDonald study did not find any excess incidence of bronchogenic cancer, mesothelioma, or gastrointestinal tumors, and since the Homestake Mine environment included fibers virtually all of which were less than 5 micrometers in length, one can con clude that long-term exposure to amphibole fibers with such physical dimensions, at least at the dose levels reported, does not induce the development of asbestos-related disease. A208G? UCC 007448 -n- -Page 1, paragraphs 4 and 5- In these two paragraphs, Dr. Cook Implies that It is extremely difficult to extrapolate from the known biological activity of chrysoti le and various amphibole fibers to minerals which may be similar but not identical in crystalline form or chemical composition. While this may be true, based on the work of Dr. Stanton and others, it is the physical dimensions of the fiber.that is of primary importance, whereas subtle differences in chemistry and physics are of secondary importance. Page 2, paragraph 1. In the first paragraph of the second page. Dr. Cook refers to the work of Dr. Stanton and characterizes his findings by stating that "fibers less than or equal to 1.5 /* in diameter and greater than 8 /* in length yielded the highest probability of pleural sarcomas." Dr. Cook has characterized ' Dr. Stanton's findings in a rather incomplete manner, as Dr. Cook's characterization leaves one with the impression that fibers less than 8 micrometers in length can yield tumors in these animal studies. However, such a characterization is not supported by the. findings of Dr. Stanton and others. For example, Stanton's fibrous glass studies show a high correla tion between the probability of tumor production and the size of fibers; the probability rising as the numbers of fibers thinner than 1.5 microns and longer than 8.0 microns is increased. Stanton's data show that the low tumor yield group and especially the zero yield group were treated with glass fibers that were either virtually 100Z less than 8 microns in length or were thicker than 1.5 microns. In reporting the results of his studies, Stanton stated: "The results of these experiments raised at least two points that merit discussion, the relationship of fiber dimension to mechanisms of carcinogenesis and the relevance of findings to human exposure. An earlier paper proposed that the fibers at the lower range of optical visibility (i.e. diameters <1.5/**) that were exceptionally short (i.e. lengths < 5/t) might account for the carcinogenicity of several types of glass and asbestos fibers (1). This hypothesis was not supported by subsequent data (2), which along with that of the present report indicates that the fine diametered fibers that are very long, are carcinogenic and probably become more carcinogenic as their length increases. The negligible carcinogenicity of short fibers is perhaps related to the histological observation that virtually all coarse and fine diametered fibers with lengths of 8y^or less are efficiently entrapped by phagocytes. Many of the smallest particles are transported to regional lymph nodes, but even those that are not seem completely sequestered within the cytoplasmic limits of macrophages and foreign-body giant cells at th- site of implantation. Similar . observations have been made with chrysotile fibers in vitro (8)." A2030c ^Stanton, M. F., Laynard, M. , Miller, M. , May, M., West, E. : Carcino genicity of Fibrous Glass: Pleural Response in the Rat in Relation to Fiber Dimension. J. Nat'I. Cancer Inst. , 58:587-603 (1977). UCC 007449 - lJ - Using fibrous glass samples of unusual specJflclty placed directly into the pleura of hamsters, Smith has obtained information quite similar to that reported by Stanton. Smith confirms Stanton's findings as to the strong relationship between length of the fibers and tumor development. However, Smith found no tumors with a sample in which 98% of the fibers were 10 microns or less in length. Animal studies by Pott, Wagner, Davis and others have also reported the induction of mesothelioma following the introduction of long, thin, durable fibers of various kinds into the pleura or peritoneal cavities. All of these researchers have induced tumors in animals by this method using a variety of durable fibers such as asbestos, fibrous glass, ceramic fibers, aluminum whiskers, and other materials, whenever sufficient numbers of long, very thin fibers were intro duced. All of these researchers have been unable to induce tumors when only short and/or thick fibers are introduced. In the middle of the first paragraph, Dr. Cook implies that long fibers, which have carcinogenic potential, have greatly diminished abilities to reach target tissue. This inference by Dr. Cook is contrary to findings of long fibers in both animals and man in all areas of the lung following inhalation exposures to-long fibers. On the other hand, short fibers are quickly removed from the lung by the mucociliary and macrophage system. The only case where Dr. Cook's inference could be true is in the case of long chrysotile fibers which are curly and present a larger cross-section. This, larger cross-section causes the fibers to be trapped in the bronchial system, rather than permitting them to "penetrate to the distal portions of the lung. Page 2, paragraph 2. In this paragraph. Dr. Cook continues with his short fiber hypothesis. With regard to the study by Pott, Hugh and Friedrichs referred to by Dr. Cook, it has now been established that the sample used in that experiment contained a sufficient quantity of long fibers (greater than 10 micrometers in length) to induce mesothelioma. This, together with the massive doses of fibers which were used, can easily account for the tumors which were found in the animals. The reference to the work of Bignon, presented at the National Bureau of Standards in 1977, is another example of the presence of short fibers in the target tissue, with the unfounded presumption that they were responsible for the disease. This is extremely poor logic, in that the mere presence of an agent does not necessarily mean that it was responsible for biological changes. Again, the significance of the presence of long fiber in the pleural tissue of these workers is neglected by Dr. Cook. Page 2, paragraph 3- In the third paragraph. Dr. Cook refers to the work now being carried out by Dr. Pelekar using amphibole fibers obtained from the Reserve Mining Company. First of all, the fact that these fibers cause hemolosis of sheep erythrocytes UCC 007450 A : 08 rV-/ jJ b and depress the activity of rabbit alveolar macrophages in no way can be related to their biological activity in the whole animal. There have been many attempts to make such blanket corre lations, but they have failed. Dr. Cook does correctly state that the cytotoxic effect in in vitro tests have not been associated with carcinogenesis. Unfortunately, Dr. Cook fails t'o note that the fiber samples being used in these tests are not at all representative of the fibers which are emitted from the Reserve Mining Company's taconite processing plant. These fibers were produced from a geological curiosity found' by IITRI personnel during a very thorough explora tion of the Reserve Mining pit. This sample represents an almost asbestiform occurrence of the mineral cummingtonite, which is normally carried through the processing system. It was ground to produce a sample which contained fibers, 85% of which were less than 5 micrometers in length. The remaining 15% contained fibers up to 100 micrometers in length. By comparison, the airborne fibers from Reserve's taconite processing plant contained probably less than 1% of fibers greater than 5 micrometers in length. To the best of our knowledge, there are no reports of fibers in excess of 10 micrometers in length. Therefore, the fibers being tested by EPA, as referred to by Dr. Cook, are not representative of actual human exposure to amphibole fibers emitted-from the Reserve Mining Company's taconite processing operations. Since these fibers are not representative of human exposures, the data which ultimately will be forthcoming from these tests will not be useful in assessing the potential environmental health hazard associated with airborne mineral fibers-emitted during taconite ore processing at the Reserve Mining Company's operations or else where. It is interesting to note that Dr. Cook only refers to Reserve Mining's taconite operations as if there were no other taconite processing operations in this country. Based on the title of his draft report, one assumes he would have examined emissions from other taconite operations. Page 2, paragraph 4. In the final paragraph on page 2, Dr. Cook refers to two. studies in which minerals other than asbestos have produced mesothelioma. However, neither of these studies are supportive of Dr. Cook's short fiber hypothesis, since in both studies sufficient concentrations of long, thin fibers were present to produce mesotheliomas.- Page 3 paragraph 1. We are assuming that in the first sentence of this paragraph, Dr. Cook is referring to the amphibole fibers which were specially obtained for EPA's studies. However, as pre viously indicated, these fibers are not representative of actual human exposure to taconite emissions. Dr. Cook is correct in noting that at this time there is no evidence of fibrosis in Reserve employees with more than 20 years' employ ment. Dr. Cook further notes that these studies cannot be extended to conclude that increased risk of lung cancer and mesothleioma is UCC 007451 aC'Ob ; o absent. While Ur. Cook is correct In this regard, ho attributes this solely to the low exposures to fibers. While Dr. Cook may be correct, he totally ignores the possibility that the fibers to which the Reserve employees were exposed are too short to induce fibrosis. Dr. Cook also fails to note that in other populations occupationally exposed to asbestos for periods of less than 20 years, an excess incidence of both lung cancer and mesothelioma have been reported. It is irresponsible for Dr. Cook to fail to even consider the possibility that the dimensions of the fibers to which the Reserve employees are exposed are such as to render them biologically inactive, regardless of the level of exposure. Page 3, paragraph 2. In the second paragraph on page 3, Dr. Cook is guilty of not being objective about his work. In effect, he is saying that anyone who gets results which agree with him is doing good work, whereas others are using "inferior analytical techniques." There is considerable debate still going on regard ing the reproducability of analyses of environmental fiber concen trations. EPA is well aware of the problems in this area, and has reached the conclusion that it is impossible to regulate fiber emissions into the air without a reliable analytical method. Experts in this field generally agree that the Environmental Sciences Laboratory at Mt. Sinai in New York and Dr. Cook's labora tory in Duluth generally obtain higher fiber counts..than other laboratories. Regardless of the accuracy of Dr. Cook's reported findings, we are unable to determine the relevance of the state-, ments he makes in this paragraph to an assessment of potential environmental health hazards associated with airborne mineral fibers emitted during taconite ore processing. Page 3, paragraph 3- In the last paragraph on page 3, Dr. Cook makes the statement that "the dose response equation for humaninhaled fiber exposure is not well established..." To the con trary, the data do show a dose-response relationship with regard to asbestos exposures, even though the precise level at which there v/ill be no adverse impact on morbidity and mortality is not known. However, we believe that a critical review of the best available evidence indicates that a time-weighted average health standard of 2 F/cc will not have any adverse impact on the morbidity or mortality of individuals occupationally exposed to asbestos. As Dr. Cook recognizes, the amphibole fiber concentrations in the air near the taconite processing facility at Silver Bay, Minnesota are far less than the current OSHA permissible exposure level of 2 F/cc. Dr. Cook then goes on to imply that there may indeed be a health hazard due to the consideration of such factors as 2iJ-hour per day exposure, etc. However, there is no foundation upon which to even base an implication of a possible hazard. Two paragraphs earlier, Dr. Cook notes that there is no evidence of fibrosis in Reserve Mining Company employees with more than 20 years' employment Yet, most of these individuals received a 2^-hour per day exposure, if one includes the time spent at home and otherwise in the UCC 007452 A008 ' 1 neighborhood of the facility. The literature, if showing nothing else, shows that background concentrations of asbestos are un related to any increase of disease. In addition, there is no evidence of any excess disease from non-occupational and non-para- occupational exposures to asbestos. As we previously indicated, Cuyler Hammond's recently delivered paper at the New York Academy of Sciences meeting reported no. unusual incidence of cancer among people who lived in neighborhoods near an asbestos plant in Paterson, New Jersey, while at the same time the employee popu lation at that plant have exhibited a high incidence of asbestosrelated disease. Page The last page contains many citations from the original Reserve Mining trial and the decision from the U.S. Circuit Court of Appeals. While these may represent findings by the District Court and Appeals Court, they cannot be taken as scientifically factual. It is disturbing to think that EPA, or any other govern ment agency, would even consider making health hazard assessments based on court decisions, rather than scientifica data. Since when has our Judicial system become the source of complex scientific determinations? In summary, we have read with interest this as well as previous publications of Dr. Cook. In manuscripts that describe his analytical studies and other research, we respect his qualifi cations. We are at a loss, however, to understand or appreciate his qualification to prepare a critical review or assessment of a situation in which "Environmental Health Hazard" is the shibboleth by which regulatory action is proposed-r. Equally astounding is our information that Roy Albert has used this Draft Report as the basis for the conclusion that a health hazard has been demonstrated incidental to taconite ore processing. UCC 007453 c ubu 1 o