Document KJJ06pna7jNaM5mZ8M67qezNw

F/ ,, ftr/eftciVfi "Ttfcx?Acic So&ezf CHj office) UNION CARBIDE CORPORATION QLD RIOGESURY fROAO. DANBURY. CT 0601 7 January 12, 1987 Dr. Raymond L. H. Murphy Pulmonary Services, Inc. 1153 Centre Street Boston, Massachusetts 02130 Dear Dr. Murphy: Re: Letter to Reuben Cherniak, M.D. from Drs. Franzlau and Lilis I have read the above-mentioned letter with interest and reviewed the writers' comments on the ATS statement on "Tbe Diagnosis of Nonmalignant Diseases Related to Asbestos." I would comnent as follows on the letter and these comments represent my personal viewpoint and should in no way be construed as an expression of Union Carbide's opinions: Paragraph 2, Page 1: Franzblau and Lilis' attempt to discredit a perfectly reasonable comment on the state of world production of asbestos by alleging that the decline is due to economic factors rather than health factors. This may be so, but nowhere in the ATS document is there an attempt to "engender a false sense of security." By quoting the statement out of context, Franzblau and Lilis are the ones who are attempting to be misleading! The ATS statement is quite definite that "The cumulative production of asbestos, however, continues to increase." Franzblau and Lilis acknowledge this. It is my opinion that the health hazards of asbestos are probably the best known of all the occupational lung disorders and that throughout the world preventive control measures now exist. If there is no safe exposure level, then Franzblau and Lilis are justified in their comments on the expanded use of asbestos in third world countries or countries with managed economies. It remains to be seen whether the permissible exposure levels in countries other than the United States are more or less effective in preventing the non-malignant diseases related to asbestos and whether, in fact, the current PEL in the U.S. is justified. I find Franzblau and Lilis' comments on page 2, paragraph 1, confusing. We have stated in the concensus document that: "Microscopically, plaques are seen to be laminated collagenous connective tissue, acellular, with few inflammatory or fibrocytic nuclei; many are covered by a thin layer of regular and well-differentiated mesothelial cells. Capillaries are rare. Elastic staining shows intact lamellae beneath the plaque in continuity with the surrounding normal paretal pleural connective tissue, suggesting that plaques are extrapleural and develop between the latter and its covering layer of mesothelial cells." Franzblau and Lilis imply ulterior motives in separating UCC 009406 cz Dr. R.L.H. Murphy -2- January 12, 1987 the description of pleural plaques from that of pleural thickening and thereby display their ignorance of the differences in site and appearances of these two lesions. 1 can but conclude that they would wish to include three separate pathological processes into a single diagnosis on the basis that they are all due to the fibrogenic properties of asbestos. This is illogical since asbestosis is used specifically to describe bilateral diffuse interstitial pulmonary fibrosis and through common usage is an accepted diagnostic term. By adding the words asbestos-related before pleural plaques or pleural thickening, the etiological diagnosis can still be made and there is no loss of its significance. Franzblau and Lilis are surely aware that pleural plaques can be discovered without evidence of pulmonary fibrosis and pleural thickening usually accompanies pulmonary fibrosis. In the former instance, a diagnosis of asbestosis cannot be made since pulmonary fibrosis has not been demonstrated, whereas in the latter the primary diagnosis is most likely asbestosis with pleural thickening present as a complicating factor. On the subject of "Exposure History' I can only say that the writers' comments ate fatuous and pedantic and if they took the trouble to read the entire section and did not merely attempt to infer double meanings from the choice of certain of our words, they would realize the correctness of our comments. If, as they tell us they are experienced "in evaluating effects of asbestos exposure," they should be familiar with the term "direct contact" as opposed to "casual" or "indirect contact." These terms are referred to in the section. The issue as to whether a radiographic diagnosis of asbestosis requires a profusion of small opacities of 1/1 or greater is one which cannot presently be resolved. This is certainly the appearance which is tadiologically unequivocally acceptable and I suppose the quality of the film and the experience of the X-ray reader are less likely to affect recognition of abnormality at this level of profusion. Nevertheless, Franzblau and Lilis have a point when they suggest that a reading of 1/0 indicates the presence of radiographic abnormalities. It is important that patients be made aware of abnormalities as soon as they are detected so that they can be kept under more intensive surveillance and guard against factors likely to aggravate their condition. With regard to the comments on the omission of pleural abnormalities from the final summary, I do not find justification for these remarks. Pleural lesions are commented on and to describe them would not serve any real purpose since the IIO U/C classification which we refer to provides adequate guidance on the diagnostic features. It would appear that the writers of the letter reserve the real motives for their concerns to the last sentence of their letter and that is that by differentiating between the pulmonary fibrotic effects of asbestos exposure and the extra-pulmonary effects they will have difficulty in justifying their expert evidence in lawsuits based mainly on pleural lesions (the commonest asbestos-related lesion) rather than on disabling pulmonary fibrosis (or asbestosis). perhaps we were remiss in our ttiznv UCC 009407 Dr. R.L.H. Murphy -3- January 12, 1987 document in not defining asbestosis as a disabling form of pulmonary fibrosis resulting from exposure to asbestos, defining pleural plagues as benign and non-disabling lesions and indicating that diffuse pleural thickening could aggravate either of the former conditions. I hope my impassioned comments are of some use to you if you decide to draft a response to Dt. Franzlau and Dr. Lilis. Best wishes for 1987. Sincerely HCL/tt 1657A Hilton C. Lewinsohn, M.D UCC 009408 M3 2 Wo pulmonology SERVICES. INC. 1SS CENTRE STREET DSTON. MASSACHUSETTS C2130 TiumoNi stT-saa-ssDO December 31, 1986 To: Committee Members Prom: Raymond L. H. Murphy, M.D. Re: Attached CgivED J/u! ; mj a & LEW1NS0HN, M.D. Raymond L. H. Murphy, Jb.. M. D. I received this letter from Dr. Reuben Chemiack. If you have any comments, please let me know. Sincerely, Raymond L.H. Murphy, M.D. RLHM/dt UCC 009409 A02176 THE MOUNT SINAI MEDICAL CENTER ON; C,INI/H I I II VY I'! \l ! N! \V i ufck \ \ IlKO'* Of 1MI CiT* UmtfVttMTV nww rut* .Mount Sinai School <>t Medit ino Ilic Mount Sinai HiNpitat November 22, 1966 Reuben Chernieck, M.D. Editor American Review of Rsapiratory Dieeae' National Jewieh Center for Immunology and Respiratory Medicine .. 1400 Jackson Street Denver, Colorado 60206 i.'ii trnnm>'ntn. S'`imi'Cs LQftamiOrv Cummins Horn* Scrcnti's tu tasi in2 Street \eu VorJt. \eu York Iu029 ijtji 7v> Dear Sir: The recent consensus stateaent by the Ad Hoc Coaeittee of Scientific Asseably on Environaental and Occupational Health** * (the Coaaittee) regarding the diagnosis of nonmalignant asbestos-related disease had the stated purposes of sumaarizing "the current state of knowledge while pointing out e.eas where additional inforaation is necessary", and to "suaaarize [the) present knowledge on the diagnosis of nonaalignant asbestos-related pulaonary disease". Unfortunately, the desired clarification of this complex issue was not achieved, and in soae instances additional confusion was generated. The following are consents on eons of the iaportant issues raised. The stateaent, "World production of asbestos has dropped markedly since the aid 1970's" is misleading, and engenders a false sense of security regarding the trend of asbestos iapact on worker health. The decrease in world production of asbestos since the all-tiae peak of 1973 is probably attributable to the world-wide recession of the mid-1970's*2). The impact of environsental and health concerns on asbestos utilization is only a phenomenon of Western industrialized countries, specifically the United States. Third world countries, countries with managed economies (the Soviet Union, eastern Europe, Peoples Republic of Chins), and many industrialized nations hove maintained or expanded their production and use of asbestos from 1978 through 1985*2*3). More significantly, the U.5. Bureau of Mines predicts a 4k annual increase in use of asbestos in the United States from 1985 through 1990*3). As the authors of the consensus document suggest, the asbestos materials currently in the environment will present hazards as they deteriorate and are disturbed during repair, replacment, and removal. The cumulative burden is not only growing, but at an increasing rate. A02177 UCC 009410 The section entitled "Benign Pleural Abnormalities Associated with Asbestos" is confusing. The ters 'pleural plaques' has been used to describe circumscribed pleural fibrosis. Diffuse pleural fibrosis, which by definition is extensive and involves the costopnremc angles, does not fit the term 'pleural plaques'. Throughout this section 'pleural fibrosis', which is the pathologic process underlying both the circumscribed pleural abnormalities <pleural plaques) and the diffuse pleural thickening, is only mentioned once. This is a significant choice of terminology since it obscures ths relationship bstween ths fibrotic changes which can occur in both the pleura and parenchyma. Once it is recognized that asbestos is fibrogenic for the pleura, the reason to seperats ths fibrogsnicity for ths pleura from that for the pulmonary parenchyma, and to include only the latter in the definition of eebeatosis. disappears. Thus, the definition of aebeetoaie chosen by the Committee ia artificially restrictive. The justification offered for the exclusion of pleural abnormalities is that "there are differences between pleural and parenchymal fibrosis in epidemiology, clinical features, end prognosis". Although such differences exist, it is sn arbitrary end illogical distinction. Numerous sxamples could be given of diseases in which manifestations with different clinical faaturaa and prognosis are included within the usually accepted definition. Some examples are tuberculosis, rheumatic fever, silicosis, end rheumatoid arthritis. Under "Exposure History" it is stated that "particular attention should be paid to occupations in which direct contact with osbeatoe has occurred". No clarification of the meaning of "direct contact" ia provided, and many readers may infer that the Committee intended to imply personal handling of asbestos during s worker's occupation. If this is the case, this recommendation re not only confusing but also misleading. It is well known to those who have experience in evaluating effects of asbestos exposure that many, and possibly a majority, of patients recently and currently presenting with eebeetoeie have had exposure by virtue of working in arses where only a smell fraction of employees personally handled asbestos. This applies to ths shipbuilding and ship repair industry and the construction industry with its many trades. The spraying of aebeetoe on steel beams is mentioned in the next paragraph, and is an excellent example of a hazardous exposure for workers who had no "direct contact" with asbestos, i.e. who did not spray, but who worksd (as electricians, carpenters, welders, etc.) in such ereos. In the summary section it is stated that a number of "necessary" conditions have to be present for a diagnosis of eebeetoeie to be considered. Specifically, in the absence of a pathologic specimen, a patient must have an appropriate history of exposure and latency interval. We agree with these criteria. However, the subsequent "clinical criteria" raise a number of significant questions. First, the Committee has chosen a radiographic appearance of small opacities corresponding to an ILO classification of 1/1 or greetsr as a cut-off for a diagnosis of ssbestosis. The ILO guidelines do not specify a threshold of parenchymal opacities for the diagnosis of A02178 UCC00941I eabestosis. and do "not imply legal definitions of pneusocomosia for compensation purposes, nor set nor iaply a lava! at which compensation ia payable"**1. Tha choica of thw abova mentioned cut-off ia therefore womewhat arbitrary* In our opilliOR thl CoillttM hit QlCldld UP0I1 d threshold which i* too raatrictiva. Wa beiiava that an ILO classification of 1/0 is aorw appropriate. By tha choica of "l" for tha nuaarator, a clinician or radiologist is indicating that ha/sha has interpreted a particular filn to ba abnoraal, although "0", or noraai, was a consideration in the deliberations. With a level of 1/1 as a cut-off. tha Coaaittae appears to encourage practitioners to tell patients with a suitable exposure history and latency, saall opacities with profusion 1/0. and no pleural disease, that they have no evidence of asbestos-related disease. From the perepective of patient care, end also, we believe, for the purpoeee of workers' coapensation and liability. 1/1 is too restrictive. It is wsll known that the PA chest x-ray is not the aost sensitive test for interstitial fibrosis, and that aa aany aa 10X of pathologically provan caeas of asbestosis will have "noraai** cheat x-rays (0/0 or 0/1 ILO classification)*5), An iaportant omission in the consensus document is the coaplete absence of pleurel abnormalities froa the final suaaary of diagnostic criteria for esbastosis. Froa its title ("The Diagnosis of Nonmalignant Diseases Related to Asbestos'*), one would anticipate that tha guidelines would help the reader in the diagnosis of both pleural and parenchymal asbestosrelated disease. As noted above, the osission of pleural disease froa tha diagnostic criteria of asbostoaia was by design; the definition of asbaetoeis waa chosen to exclude pleural abnormalities. The impression given ia that such findings arm irralevsnt to tha diagnosis of nonmalignant asbastos-ralatad diaaaaa. Although banign pleural dieaaea rasults in significant functional iapairssnt only when extensive*61. the goal ia the definition of criteria for the diagnosis of nonmalignant asbestos-related disease, end not the degree (or lack thereof) of functional impairment. In addition, the well accepted concept that pleural plaques are a marker of asbestos exposure*?1 is not given the focus end attention it deserves. Should a patient with an appropriate exposure and latency, calcified pleural plaques, and "normal" parenchyma (0/0 or 0/1 ILO classification) be told that he has no evidence of biologic effects of ssbsstos exposure? In the development of diagnostic criteria one suet begin by outlining the goals of such an endeavour, particularly since all nonaalignant ambestosrelated conditions are untraatable, except, for symptomatic reliaf. Of utmost importance to clinicians should be their responsibility to their patients, and in this case the advice, prognostic information, paliative therapy, and emotional support which can ba offered. As noted in the consensus docuaent, asbestos and asbestos-related disease have become significant public health and public policy isaues. Obviously, physicians have an important role to ploy in these situations. Numerous physicians ere, and will continue to ba, enmeshed in the legal conflicts resulting from workers' compensation claims and third-party liability suits. Finally, the epidemiologic study of diseases, including asbestos-related conditions, requires that investigators have valid end reproducible UCC 009412 *02179 criteria for defining and diagnoeing the disease under study. Although a restrictive definition of a disease *ay have an attraction for soee. we believe that the Coaaittee has formulated diagnostic criteria for nonealignent asbestos-related disease which are too restrictive froe the perspectives of patient care, workers' compensation, third-party liability public health and public policy. Alfred Franzblau, H Ruth Lilis, H.D. Mount Sinai Medical Center Diviaion of Environsantal and Occupational Madicine 10 Eaat 102 Street New York, New York 10029 REFERENCES 1. Murphy RL (chairman). Becklake HR, et al. The Diagnosis of Nonmalignant Diseases Related to Asbestos. Am Rev Respir Dim 1986; 134:363368. 2. Clifton RA. Asbestos. Bureau of Hines Minerals Yearbook, Volume I, Ratals and Minerals. 1982. 3. Clifton RA. Asbestos in 1985. Bureau of Hines Mineral Commodity Sumnaries-1986. preliminary report. 1986. 4. International Labour Organization. Guidelines for the use of ILO International Classification of Radiographs of Pneumoconioses. Revised Edition, 1980. International Labour Office, Geneva. 5. Epler GR, HcLoud TC, Gaensler EA, Hikus JP, Carrington CB. Normal Chest Roentgenograms in Chronic Diffuse Infiltrative Lung Disease, NEJM 1978; 298:934-939. 6. Hiller A. Tierstein AS, Selikoff I. Ventilatory Failure due to Asbestos Pleurisy. Am J Had 1983:75:911-919. 7. Craighead JE (chairman), Abraham JL, et al. The Pathology of AsbestosAssociated Diseases of the Lung end Pleural Cavities: Diagnostic Criteria and Proposed Grading 5chema. Arch Pathol Lab Had 1982:106:544-596. UCC 009413