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Exposure dose and type of asbestos is needed for relating lung diseases.
Asbestos Literature Does Not Support Study Conclusions
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John H. Lange, Environmental and Occupational Consultant Envirosafe
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john.pam.lange{at}worldnet.att.net John H. Lange
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The paper by Ohar et al., 2004 (1), reports on relationships of asbestos diseases and pulmonary function. This is certainly an important question. What is not mentioned, although there is an assertion to asbestos exposure, is that a dose-response relationship exists for asbestos and related diseases (e.g. mesothelioma) (2). It has also been shown that there is a threshold exposure dose for the asbestos diseases as well (3,4). Simply classifying persons by occupation does not provided information on exposure and the type of asbestos to which they were exposed. It has also been recognized (4,5), by at least some, that chrysotile has a low potential in causing asbestos related diseases? Thus, the type of asbestos is important. There are also a large number of other materials that can results in the “asbestos” diseases as well, including mesothelioma (6). Studies that attempt to relate asbestos exposure with disease need to include information on exposure and the type of asbestos (7). Failure to include this information can be misleading in a relationship of asbestos and disease. References 1. Ohar J, Sterling DA, Bleecker E, Donohue J. (2004). Changing patterns in asbestos-induced lung disease. Chest. 125: 744-753. 2. Rodelsperger K, Woitowitz H-J, Bruckel B, Arhelger R, Pohlabein H, Jockel K-H. (1999). Dose-response relationship between amphibole fiber lung burden and mesothelioma. Cancer Detection and Prevention. 23: 183- 193. 3. Ilgren EB. (2001). Health Risks from Exposures to Asbestos and Inorganic Metals due to Collapse of the World Trade Center: An Environmental Residential Survey. Indoor Built Environment 2001; 10: 361- 383. 4. Liddell FD, McDonald AD, McDonald JC (1997) The 1891-1920 birth cohort of Quebec chrysotile miners and millers: development from 1904 and mortality to 1992. Ann Occup Hyg. 41:13-36. 5. Bernstein DM, Chevalier J, Smith P (2003) Comparison of Calidria chrysotile asbestos to pure tremolite: inhalation biopersistence and histopathology following short-term exposure. Inhalation Toxicol 15: 1387- 1419. 6. Lange JH. (2004). There are other non-asbestos causes of mesothelioma. American Journal of Epidemiology (accepted) (letter) 7. Lange JH. (2004). A study on the type and amount of asbestos in floor tile and mastic. Bull Environ Cont Tox (accepted). |
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Lawrence Martin, Physician Case Western University School of Medicine
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larry.martin{at}adelphia.net Lawrence Martin
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Several articles in the asbestos literature, including some published in Chest, argue against the findings of Ohar et al (1). In their study a large number of subjects with a small opacity profusion reading of “1/0” were accepted as having asbestosis. However, there are several reasons for small opacities on chest x-ray other than asbestos (2-5), so not all “1/0” readings in exposed workers indicate asbestosis. As one author has written, “The clinical diagnosis of asbestosis in this century requires more than a chest radiograph” (6). Ohar et al also noted that “pleural abnormalities were the only abnormality in 54% of subjects with low ILO scores.” However, they didn’t account for numerous other conditions that are known to cause or mimic pleural shadows, and that can be misconstrued as asbestos-related pleural disease (7-9). As for lung cancer, 67 subjects (out of 3140 with “asbestos disease”) had this diagnosis, and only 1 of these was a never smoker. Yet all 67 cases of lung cancer were accepted by the authors as “asbestos-induced.” There is considerable debate in the literature about the role of asbestos in causing lung cancer in the absence of true asbestosis (10-13), the diagnosis of which was not really confirmed because of the low profusion scores. The authors state that their cohort of patients was “drawn from trade unions, television, and newspaper advertisements,” and “recruited from legal cases,” i.e., workers who were solicited for purpose of filing asbestos claims. When chest x-rays from a similar cohort were reviewed objectively (by physicians uninvolved with the legal process), there was a very small concordance with the original interpretations (14). One plaintiff B-reader has written a letter indicating concern with the way these “screening chest x-rays” on solicited workers are handled and interpreted. He found that “in some of the screenings, the worker’s’ X-ray had been ‘shopped around’ to as many six radiologists until a slightly positive reading was reported by the last one of them,” and also that there is a higher payment to the B-reader for a reading of “1/0” than of “0/1” (15). For a large study on asbestos screening x-rays to have validity, the films should be read blindly, i.e., in a way so that the exposure history and legal claim status are unknown to the B-reader. Given the methods used by Ohar, et al, and omission of references to suggest other causes for the x-ray abnormalities, it is difficult to accept their conclusion that there is a changing pattern in asbestos-induced lung disease.
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