Document NEq0napmMxe84YBqBonQvy7yQ

CORRESPONDENCE rablc excess sotilc-asbeslg opinions fe exposure. EPA's view hcory is unhrysotile aslstrate an in- oscs.: These ;hold for safe ssible reason letect an inloses, even if r), is that the used was in safe exposure in practice. OSTAS, PH.D. UUDO, Ph.D. use dc Madrid Madrid, Spain M.D., Ph.D. Teresa Herrera Coruna, Spain 90,247:1017. I) M^J919S9fii33S: ? power ::1s iWWWWT:hbchav- I the report by the low rate of n the asbestosarticle size and lowever, ample stile mills of the lions of respirace" of cause of e processing fa: to asbestosis.2 sestosis is virtu- Furthermore, :ancer was 2.52 pected deaths), agents were rcr and asbestosis, haled chrysotile rspirable. ihnique and the ration-Nadonal alth method of of these mills, lowed that fiber 5 fibers per milThe mean levels r of air.3 Again, roonntnaKsafits and at riooJ^^PI^?'yysotiieferent size distri butions in the work environments; there are important dif ferences in the physical and chemical properties of fibers as well.3'4 There are also considerable data on chrysotile's deg radation in a biologic host and subsequent detoxification.4 phe existence of a threshold cannot be proved, but a change in the exposure - response slope at low doses must certainly take place.5 Arthur M. Langer, Ph.D. Brooklyn College of the Cirv University of New York Brooklyn, NY 11210 Editors note: Dr. Langer has served as an expert witness in asbestos litigation during the past five years. t. Landrigan PI. Asbestos -- still a carcinogen. N Engl J Med 1998;338: 1618-9. 2. Nicholson W], SelikotTIJ, Seidman H, Lilis R, Formby P. Long-term mortality experience of chrysotile miners and millers in Thetford Mines, Quebec. Ann N Y Acad Sci 1979;330:11-21. 3. Langer AM, Nolan RP. The properties of chrysotile asbestos as determi nants of biological activity: variations in cohort experience and disease spec tra related to mineral properties. Accomplishments Oncol 1986;1(2):30-51. 4. Langer AM, Nolan RP, Addison J. Physico-chemical properties of as bestos as determinants of biological potential. In: Liddell D, Miller K, eds. Mineral fibers and health. Boca Raton, Fla.: CRC Press, 1991:211-28. 5. Bern' G. Mesothelioma incidence and time since exposure to asbestos. In: Gibbs GW, Dunnigan }, Kido M, Higashi T, cds. Health risks from exposure to mineral fibres: an international perspective. North York, Oat.: Captus Press, 1991:40-8. To the Editor: Landrigan is wrong in concluding that "a more than sevenfold mortality rate . . . from pleural can cer in mining areas, as compared with nonmining areas, corroborates an enormous body of literature showing that Canadian chrysotile . . . is a potent carcinogen." This mortality rate (seven cases) is entirely explained by the few cases among women in the area who had occupational ex posure to amphiboles in the manufacture of gas masks,1 the repair of burlap bags that contained imported fibers,2 and possibly, in one case, the tremolitc brought home on miners' clothes.2 Seven such women received workers' compensation in Quebec during the period of the study by Camus et al. Indeed, there is now a scientific consensus that chrysotile asbestos is not a cause of malignant meso thelioma, even among chrysotile-asbestos miners and mill ers.1 Reasonable caution should continue to be used in ex posing workers or bystanders to chrysotile, but if the levels of exposure currently recommended by the Occupational Safer\- and Health Administration and the National Insti tute for Occupational Safety and Health can be main tained, public health workers can concentrate their work n lung cancer where it belongs: on smoking. With respect to women in the mining area, it has been established that the content of chrysotile and tremolitc in the lungs is directly proportional to the number of years lived in the mining region and inversely proportional to the distance between the place of residence and the mining re s'011'2 In fact, these women were exposed to levels of chrysotile as high as 1 fiber per milliliter of air as recently as one month in 1984.2 Bruce W. Case, M.D. McGill University Montreal, QC H3A 2B4. Canada Editor's note: Dr. Case has served as an expert witness in asbestos litigation during the past five years. 1. McDonald AD, Case BW, Churg A, et al. Mesothelioma in Quebec chrvsotiic miners and millers: epidemiology and aetiology. Ann Occup Hvg 1997;41:707-19. 2. Case BW. Biological indicators of chrvsotiic exposure. Ann Occup Hvg 1994;38:503-18. To the Editor: Landrigan misleads readers with the state ment, "Clinical and epidemiologic studies have established incontrovcrtibly that asbestos causes cancer of the lung, malignant mesothelioma of the pleura and peritoneum, cancer of the larynx, and certain gastrointestinal cancers." To prove his point, he cites only one report. The cohort cited by Landrigan is only one of many asbestos-exposed cohorts described in the medical literature. That cohort has an atypical pattern of lung cancer, as compared with other cohorts. Our review of mortality from gastrointesti nal cancer in occupational-cohort studies1 has shown that there is little evidence that asbestos causes gastrointestinal cancer. Similarly, there is a body of literature that indicates that there is no increased risk of laryngeal cancer.2'3 Lan drigan presents a biased view of the literature in an at tempt to discredit the interesting and valuable contribu tion of Camus et al. Robert W. Morgan, M.D., S.M.Hyg. Michael Goodman, M.D., M.P.H. Exponent Health Group Menlo Park, CA 94025 Editor's note: Drs. Morgan and Goodman have served as expert witnesses in asbestos litigation during the past five years. 1. Morgan RW, Folurt DE, Wong O. Asbestos and gastrointestinal cancer a review of the literature. West J Med 1985;143:60-5. 2. Armstrong BK, de Klerk NH, Musk AW, Hobbs MS Mortality in min ers and millers of crocidoiite in Western Australia. BrJ Ind Med 1988;4S: 5-13. 3. Ncwhouse ML, Bern1 G, Wagner JC. Mortality of factory workers in east London 1933-80. Br J Ind Med 1985;42:4-11. The authors reply: To the Editor: Some of the correspondents attribute to us inferences we did not make. We did not conclude that chrysotile asbestos is not carcinogenic, nor did wc discuss the regulatory implications of our findings. We observed that the EPA's model greatly overestimated the risk of deaths from asbestos-induced lung cancer in our study population and that the model "may also overestimate the risk ... in other populations with nonoccupational ex posure." In the absence of any other published validation of the EPA's model in a population with nonoccupational exposure to asbestos, and given the fact that the model was based on a number of unverified and conservative as sumptions, this statement seemed fairly restrained to us. With regard to Demiroglu's letter, the much higher rates of lung cancer and mesothelioma in the populations of some Turkish villages than in our study population are generally attributed to exposure to crionitc (fibrous zeo lite) rather than chrysotile asbestos.1 Sokas misunderstood WVo|ume 339 NurJ o'< defEeXnHdIBaInTt^ HWBUI0007863 The Nor England Journal of Medicine the following aspects of our study: 2142 was the number of deaths, not the size of the population; there were deaths from asbestosis and mesothelioma in the control popula tion; and both the control and the exposed populations consisted predominantly of small-town French-Canadian housewives with similar socioeconomic status and lifestyle. Furthermore, we presented some data on smoking habits and argued that confounding could not have accounted for the large discrepancy between the EPA model's predic tion and the observed relative risk of lung cancer. We agree with Costas ct al. that the study had low statis tical power to detect small risks; this was conveyed by the wide confidence intervals for our risk estimates. Our study would, however, have detected a relative risk as large as that predicted by the EPA's model. Churg's suggestion that the cases of pleural cancer and asbestosis were attributable to occupational rather than nonoccupational exposure is a possibility that will be explored in our ongoing research. There are many possible explanations for the EPA mod el's overestimation of the risk of lung cancer in Quebec's chrvsotile-mining towns. Our report offered six for consid eration, and the correspondents' letters and Landrigan's editorial added others. At this time, all the explanations are speculative. We tend to disagree with the hypothesis that asbestos fibers in the air of mining towns were too large to be respirable, because, among other things, the main source of asbestos pollution in the mining towns was not the mines but the mills, which involved air-intensive processes designed to retain larger fibers and expel smaller ones. Michel Camus, Ph.D. Jack Siemiatycki, Ph.D. University of Quebec Laval, QC HA7 4Z3, Canada 1. Simonato L, Baris R, Saracc: R, Skidmore J, Winkclmann R. Relation of environmental exposure to cnonite fibres to risk of respiratory cancer. In: Bignon J, Pcto J, Saracci R, eds. Non-oecupational exposure to mineral fibres. Lvon, France: International Agency for Research on Cancer, 1989: 398-405. " i | an excess risk of pleural cancer in the absence ot lung can- ' cer in these women is explained by a well-characterized difference in the dose-response relation between asbestos exposure and these two types of tumor.2 Morgan and Goodman are highly selective in their reading of the literature on the risk of gastrointestinal and larvn. geal cancer in persons exposed to asbestos. The Interna-' tional Agency for Research on Cancer considers chrvsotik asbestos a cause of gastrointestinal as well as laryngeal can. cer.3 Also, contrary to Morgan and Goodman's interprets tion, the study they cite by Nevvhouse et al.4 found dose- related excess mortality' for both these cancers. Case is inaccurate in his claim that chrysotile asbestos from Canada is not a cause of mesothelioma, and his as sertion that there is a scientific consensus on this point is not true.5 Also, he is disingenuous in his one-sided quest for factors other than chrysotile that would explain away the observed sevenfold excess of mesotheliomas among women in the chrysotile-asbestos-mining areas of Quebec Experimental as well as epidemiologic studies have shown conclusively that Canadian chrysotile is fully capable of causing malignant mesothelioma,' and the International Agency for Research on Cancer acknowledges that chryso-. tile is a cause of mesothelioma.3 Philip J. Landrjgax, M.D. Mount Sinai School of Medicine New York, NY 10029 1. McDonald AD, Fry JS, Woolley Al, McDonald J. Duse exposure and mortality in an American chrvsotile textile plant. Br J Ind Med 1983;40: 361-7. 2. Iwatsubo Y, Pairon JC, Boutin C, ct al. Pleural mesothelioma: dose- response relation at low levels of asbestos exposure in a French populationbased case-control study. Am J Epidemiol 1998;148:133-42. 3. Monographs on evaluation of the carcinogenic risk of chemicals to man. . Vo!. 14. Asbestos. Lyon, France: International Agency for Research on Cancer, 1977. 4. Newhousc ML, Bern G, Wagner JC. Mortality of factory workers in east London 1933-80, Br J Ind Med 1985;42:4-11. 5. Asbestos, asbestosis, and cancer: the Helsinki criteria for diagnosis and attribution. Scand J Work Environ Health 1997;23:311-6. To the Editor Langer ignores the pivotal point that the size distribution of airborne asbestos fibers in the mining areas of Quebec is very different from that encountered in any setting in the United States. This disparity' provides the most plausible explanation for the difference in the risk of lung cancer in these two environments. In Quebec, exposure to asbestos involves crude, unprocessed asbestos, and many of the fibers arc too large to be taken into the alveoli. In contrast, the asbestos in American industries, schools, and office buildings has been carded, spun, and woven. In these high-energy manufacturing processes, fi ber bundles are broken, and millions of shorter, thinner, respirable fibers are created. It is probably this difference in the size distribution of fibers that accounts for the 10- fold to 50-fold difference in the risk of lung cancer report- . ed between miners in Quebec and asbestos-mill workers i in South Carolina.1 I To be sure, there are respirable asbestos fibers in the .; Quebec mining townships. Although relatively few in | number, they are responsible for the excess mortality from 1 "pleural cancer" (probably mesothelioma) and asbestosis ! observed among women there. The apparent paradox of 1 Endometriosis in the Thoracic Aorta To the Editor: Manifestations of endometriosis in thorac ic organs are very rare.1-2 We describe a case of endometri osis in the thoracic aorta. After an uneventful pregnancy, a 28-vcar-old woman delivered a healthy girl by elective cesarean section. The procedure was complicated by severe, intractable hyper tension. No cause was found for the severe hypertension, which was still present several weeks after delivery, A chest x-ray film and computed tomographic scan obtained postoperativelv showed a pscudoaneurysm of the descending aorta with a maximal diameter of 9 cm in the area of a patch repair of a coarctation, which had been performed 16 years earlier. During her first pregnancy at the age of 24, which had also resulted in cesarean section, the patient had hypertension but no signs of gestosis. Arterial hypertension resolved without treatment after delivery. A chest x-ray film was normal at that time. VVe operated on the patient three weeks after the second cesarean section. Intraoperatively, we found a rupture of the suture line of the distal part of the patch, with a false 1002 O etober 1, 1998 HWBUI0007864