Document YDYzdJjEY3djK69Ny0oqv5mDN

QrteeiciVfi Ttfo^Aac CHj o?ftce) UNION CARBIDE CORPORATION old PIOGEBURY ROAD. DANBURY. CT QBB 1 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 "The Diagnosis of Nonmalignant Diseases Related to Asbestos." I would comment 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. Vie 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 ezizov UCC 009406 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. I 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 ace 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 radiologically 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 mote 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 ILO 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 ' Vigny UCC 009407 Dc. 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 plaques 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 Dr. Franzlau and Dr. Lilis. Best wishes for 1987. Sincerely HCL/tt 16 57A Hilton C. Lewinsohn, M.D UCC 009408 fc0217b PULMONOLOGY SERVICES. INC. 1153 CENTRE STREET BOSTON. MASSACHUSETTS 02130 TELEPHONE 617-522-SBOO December 31, 1986 To: Committee Members Prom: Raymond L. H. Murphy, M.D Re: Attached .i'w!: m7 H. C. LEWINSOHN, MJ). Raymond L. H. Murphy. Jr.. M. D. I received this letter from Dr. Reuben Chernlack. If you have any comments, please let me know. Sincerely, :-2 t~f- Raymond L.H. Murphy, t33v) RLHM/dt UCC 009409 A 02 176 O* TM| <11* IMMUNITY O* *1*4 TOtk. THE MOUNT SINAI MEDICAL CENTER OST ('.LIST AVI- I I I V'i' Cl At ! \! 'A > okk \ V iwOu Mount Sinai School of Medic tno * Tlic Mount Sinai Hospital 7&V \ i; \Mcm}$intu,' Hsvtbjl November 22. 1986 . Reuben Chernieck, M.D. Editor American Review of Respiratory Disease National Jewish Center for Immunology and Raspiratory Medicine - 1400 Jackson Street Denver, Colorado 80206 I'.m imnmrnta, Sciences l.ahomtorv i-'urrtnunjis Hasu' Sciences Huiitiing m Last m2 sm-et \eu \ork. \rit I ork lu02v iJIJi ti.iii-Hl 73 Daar Sir: Th racant consensus statement by the Ad Hoc Committee of Scientific Assembly on Environmental and Occupational Health*1* (the Committee) regarding the diagnosis of nonmalignant asbestos-related disease had the stated purposes of summarizing "the current state of knowledge while pointing out cleas where additional information is necessary", and to "summarize [the] present knowledge on the diagnosis of nonmalignant asbestos-related pulmonary disease". Unfortunately, the desired clarification of this complex issue was not achieved, and in some instances additional confusion was generated. The following are comments on some of the important issues raised. The statement, "World production of asbestos has dropped markedly since the mid 1970's" is misleading, and engenders a false sense of security regarding the trend of asbestos impact on worker health. The decrease in world production of asbestos since the all-time peak of 1973 is probably attributable to the world-wide recession of the mid-1970's*2). The impact of environmental 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 China), and many industrialized nations have maintained or expanded their production and use of asbestos from 1978 through 1905*23). More significantly, the U.5. 4Bureau of Nines predicts a k 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. ' AQ2 177 UCC 009410 I The section entitled "Benign Pleural Abnormalities Associated with Asbestos*' is confusing. The tern 'pleural plaques' hoe been used to describe circumscribed pleural fibrosis. Diffuse pleural fibrosis, which by definition is extensive and involves the costopnremc angles, does nor fit the term 'pleural plaques'. Throughout this section 'pleural fibrosis', which is the pathologic process underlying both the circumscribed pieural abnormalities <pleurai plaques) and the diffuse pleural thickening, is only mentioned once. This is a significant choice of terminology since it obscures the relationship between the 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 separate the fibrogenicity for the pleura from that for the pulmonary parenchyma, and to include only the latter in the definition of asbestosis, disappears. Thus, the definition of asbestosis chosen by the Committee is 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, and prognosis". Although such differences exist, it is an arbitrary and illogical distinction. Numerous examples could be given of diseases in which manifestations with different clinical features and prognosis are included within the usually accepted definition. Some examples ere tuberculosis, rheumatic fever, silicosis, and rheumatoid arthritis. Under "Exposure History" it is stated that "particular attention should be paid to occupations in which direct contact with asbestos has occurred". No clarification of the meaning of "direct contact" is provided, end many readers may infer that the Committee intended to imply personal handling of asbestos during a worker's occupation. If this is the case, this recommendation is 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 asbestosis have had exposure by virtue of working in areas where only a small fraction of employees personally handled asbestos. This applies to tha shipbuilding and ship repair industry and the construction industry with its many trades. The spraying of asbestos 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 worked (as electricians, carpenters, welders, etc.) in such areas. In the summary section it is stated that a number of "necessary" conditions have to be present for a diagnosis of asbestosis 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 1L0 classification of 1/1 or greater as a cut-off for a diagnosis of asbestosis. The ILO guidelines do not specify a threshold of parenchymal opacities for the diagnosis of A02178 UCC 009411 aebeetoeie, and do "not imply legal definitions of pneumoconiosis for compensation purposes, nor set nor imply a level at which compensation is payable"***. The choice of the above mentioned cut-off is therefore somewhat arbitrary. In our opinion the Comsittee has decided upon a threshold which is too restrictive. We believe that an ILO classification of 1/0 is more appropriate. By the choice of "1" for the numerator, a clinician or radiologist is indicating that he/she has interpreted a particular film to be abnormal, although "0", or normal, was a consideration in the deliberations. With a level of 1/1 as a cut-off, the Comsittee appears to encourage practitioners to tell patients with a suitable exposure history and latency, small opacities with profusion 1/0, end no pleural disease, that they have no evidence of asbestos-related disease. From the perspective of patient care, and also, we believe, for the purposes of workers' compensation and liability, 1/1 is too restrictive. It is well known that the PA chest x-ray is not the most sensitive test for interstitial fibrosis, and that as many os 10* of pathologically proven cases of asbeetosie will have "normal" chest x-rays <0/0 or 0/1 ILO classification)*5*. An important omission in ths consensus document is the complete abeence of pleural abnormalities from ths final aussary of diagnostic critsria for asbastosis. From its titls ("Ths Diagnosis of Nonmalignant Dissasss Raloted to Asbastoa"), ona would anticipate that tha guidelines would hslp the reader in tha diagnosis of both pleural and parenchymal asbestosrsletsd diseass. As noted above, the omission of pleural disease from tha diagnostic criteria of asbeatoais waa by design; ths dsfinition of asbestosis was chossn to excluds plsural abnormalitiss. Ths isprsssion givsn is that such findings are irrslsvsnt to ths diagnosis of nonmalignant asbaatoa-ralatsd disease. Although benign pleural disease results m significant functional impairment only when extensive*6*, the goal is tha definition of criteria for tha diagnosis of nonmalignant asbestoa-relatsd diseass, and not the dsgree (or lack thersof) of functional impairment. In addition, the well accepted concept that pleural plaques ere a marker of esbeetos exposure*7* is not given the focus end attention it deserves. Should a patient with an appropriate exposure end latency, calcified pleural plaauaa, and "normal" parenchyma (0/0 or 0/1 1L0 claeaification) be told that he has no evidence of biologic effects of esbestos exposure? In the development of diegnostic criteria one must begin by outlining the goals of such an endeavour, particularly since all nonmalignant asbestosrelated conditions are untreatable, except, for symptomatic relief. Of utmost importance to clinicians should be their responsibility to their patients, end in this case the advice, prognostic information, paliative therapy, and motional support which can be offered. As noted in the consensus document, asbestos and asbestos-related disease have become significant public health and public policy issues. Obviously, physicians have en important role to play in these situations. Numerous physicians ore, and will continue to be, 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 and reproducible UCC 009412 *02 17.9 criteria for defining and diagnosing the disease under study. Although a restrictive definition of a disease say have an attraction for some, we believe that the Comittee has forsulated diagnostic criteria for nonmalignant asbestos-related disease which are too restrictive from the perspectives of patient cars, workers' compensation, third-party liability, public Health and public policy. Alfred Franzblau, H Ruth Lilis, H.D. Mount Sinai Medical Center Division of Environmental and Occupational Medicine 10 East 102 Street Mew York, Mew York 10029 REFERENCES 1. Murphy RL (chairman), Becklake MR, et al. The Diagnosis of Nonmalignant Diseases Related to Asbestos. As Rev Respir Dis 1966; 134:363 366. 2. Clifton RA. Asbestos. Bureau of Mines Minerals Yearbook, Volume I, Metals and Minerals. 1962. 3. Clifton RA. Asbestos in 1965. Bureau of Hines Mineral Commodity Summaries-1966, preliminary report. 1966. 4. International Labour Organization. Guidelines for the use of ILO International Classification of Radiographs of Pneumoconioses. Revised Edition, 1960. International Labour Office, Geneva. 5. Epler GR, McLoud TC. Gaensler EA. Hikus JP, Carrington CB. Normal Chest Roentgenograms in Chronic Diffuse Infiltrative Lung Disease, NEJM 1976s 296J934-939. 6. Hiller A, Tieretein AS. 5elikoff I. Ventilatory Failure due to Asbestos Pleurisy. Am J Had 1963:75:911-919.7 7. Craighead JE (chairman), Abraham JL, et al. The Pathology of AsbestosAssociated Diseases of the Lung and Pleural Cavities: Diagnostic Criteria and Proposed Grading Schema. Arch Pathol Lab Had 1962:106:544-596. UCC 009413