Document wDObm7bGNeoap30KM54xwgZGQ

PULMONOLOGY SERVICES. INC. 1153 CENTRE STREET BOSTON. MASSACHUSETTS 02130 TlUMONI 617-522*5600 December 31, 1986 To: Committee Members From:: Raymond L. H. Murphy, M.D Re: Attached J /i i I . mi H. a IEWINSOHN, Mi). Raymond _ M. Murphy. Ur.. M. D. PLAINTIFF'S EXHIBIT UC-2580 I received this letter from Dr. Reuben Cherniack. If you have any comments, please let me know. Sincerely, -----------< a <-> Raymond L.H. Murphy, M.D. RLHM/dt UCC 023612 A U 2 1 76 < 1MC <T l.lNVfft`SITf O* NIVi, TOtt. THE MOUNT SINAI MEDICAL CENTER ONI- CAM AVI- t ! I VY !'! -V. ! V`A lUkK M iimC-j Mount Sinai School of Mcilmnc- Tlic Mourn Sinai Hospital | MountSinai.' V-. Hwtal A. 'A ,, ' November 22, 1986 Reuben Chernisck, K.D. Editor American Review of Respiratory Disease National Jewish Center for Immunology and Respiratory Medicine - 1400 Jackson Street Denver, Colorado 80206 l.rt imnmentn. Sciences i.a*Ktrntorv t.'umnnns Hxsic Sciences 10 ICast /,f- street >>t York. Nri York f002y i J!It b5i<-*il73 Dear Sir: The recent consensus stotement by the Ad Hoc Committee of Scientific Assembly on Environmental and Occupational Heolth*^* <the Committee) regarding the diagnosis of nonmalignant asbestos-related disease hod the stated purposes of summarizing "the current state of knowledge while pointing out aleas where additional information is necessary", and to "summarize Itne) 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 6ince the all-time peak of 1975 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 Chine), and many industrialized nations hove maintained or expanded their production and use of asbestos from 1978 through 1985(23>^ More significantly, the U.5. Bureau of Mines predicts a 4* annual increase in use of asbestos in the United States from 1985 through 1990*3*. A6 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 on increasing rote. A02177 UCC 023613 The section entitled "Benign Pieuxal Abnormalities Associated with Asbestos" is confusing- The term 'pleural plagues' has been used to describe circumscribed pleural fibrosis. Diffuse pleural fibrosis, which by definition is extensive and involves the coetophrenic angles, does not. fit the ter* `pleural plaques'. Throughout thi6 section 'pleural fibrosis', which is the pathologic process underlying both the circumscribed pieural abnormalities (pieurai 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 tne 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 are 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". Ho clarification of the meaning of "direct contact" is provided, and 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 the 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 <es electricians, carpenters, welders, etc.) in such areas. In the summary section it is stated that a number of "necessory" conditions have to be present for a diagnosis of asbestosis to be considered. Specifically, m the absence of a pathologic specimen, a patient must have an appropriate history of exposure and latency intervol. We agree with these criteria. However, the subsequent "clinicol 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 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 A 02 1 7.1 UCC 023614 asbestosis, 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 Committee has oecided upon a threshold which is too restrictive. We believe that an ILO claesification 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 Committee appears to encourage practitioners to tell patients with a suitable exposure history and latency, small opacities with profusion 1/0, and no pleural disease, that they have no evidence of asoestos-related disease. From the perepective of patient care, and also, we believe, for the purposes of workers' compensation and liobility, 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 as 10* of pathologically proven cases of asbestosis will have "normal" chsst x-rays <0/0 or 0/1 ILO classification)^). An important omission in the consensus document is the complete absence of pleural abnormalities from ths final summary of diagnostic criteria for aebeetosis. From its title ("The Diagnosis of Nonmalignant Diseases Related to Asbestos"), one would anticipate that the guidelines would help the reader in the diagnosis of both pleural and parenchymal asbestosrelated disease. As noted above, the omission of pleural disease from the diagnostic criteria of asbestosis was by design: the definition of asbeetosis was chosen to exclude pleural abnormalities. The impression given is that such findings are irrelevant to the diegnosis of nonmalignant asbestos-related disease. Although benign pleural disease results in significant functional impairment only when extensive44*), the goal is the definition of criteria for the diagnosis of nonmolignant asbestos-related diseose, and not the degree (or lack thereof) of functional impairment. In addition, the well accepted concept that pleural plaques are a marker of aabestom exposure47) is not given the focus and attention it deserves. Should a patient with an appropriate exposure and latency, calcified pleural plaques, and "normal" parenchyma (0/0 or 0/1 ILO classificotion) be told that he has no evidence of biologic effects of asbestos exposure? In the development of diagnostic 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, and in this case the advice, prognostic information, paliative theropy, and emotional 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 an important rcle to play in these situations. Numerous physicians are, and will continue to be, enmeshed in the legal conflicts resulting from workers' compensation cloims ond third-party liobility suits. Finally, the epidemiologic study of diseases, including asbestos-related conditions, requires that investigators have valid and reproducible UCC 023615 4 02 t / %+ V 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 Cosaittee has forsulateo diagnostic criteria for nonselignant eebestoe-related disease which are too restrictive fros the perspectives of patient care, workers' compensation, third-party liability, public health and public policy. Mount Sinai Medical Center Division of Environmental and Occupational Medicine 10 East 1C2 Street Mew York, New York 10029 REFERENCES 1. Murphy RL (chairman), Becklake MR, et al. The Diagnosis of Nonmolignont Diseases Related to Asbestos. As Rev Respir Die 1966; 134:363368. 2. Clifton RA. Asbestos. Bureau of Mines Minerals Yearbook, Volume I, Metals and Minerals. 1982. 3. Clifton RA. Asbestos in 1985. Bureau of Mines Mineral Commodity Summaries-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, McLoud TC. Gaensler EA, Miku6 JP, Carrington CB. Normal Chest Roentgenograms in Chronic Diffuse Infiltrative Lung Disease. NEJH 1978; 298:934-939. 6. Miller A, Tierstein AS, Selikoff I. Ventilatory Failure due to Asbestos Pleurisy. Am J Med 1983;75:911-919. 7. Craighead JE (chairman), Abraham JL, et el. The Pathology of AsbestosAssociated Diseases of the Lung and Pleural Cavities: Diagnostic Criteria and Proposed Grading Schema. Arch Pathol Lab Med 1982;106:544-596. UCC 023616 ^ 'i 6 0