Document 2ZgJ3nzrXakMgoz93eRL9zyb

i QHeeuAfJ THc^Acif Sozx^f CHj office') UNION CARBIDE CORPORATION OLD RlDGEBURY ROAD. DANIBURY. CT Q6B 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 flonmalignant 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 product ion 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 023609 Dt. 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 are 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 ate detected so that they can be kept under nore 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 UCC 023610 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 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 sane use to you if you decide to draft a response to Dr. Franzlau and Dr. Lilis. Best wishes for 1987. Sincerely HCL/tt 1657A Hilton C. Lewinsohn, M.D UCC 023611 *02 17