Document Znn5xREmEkO1v4aGEv3J09BnL

I INTERNAL CORRESPONDENCE 51933 UNION CARBIDE CORPORATION OLD RIDGEBURY ROAD, DANBURY, CT D6B17 To (Nemo) Div.Bion Location Area Medical Directors Contract Physicians Copy to Dow oneineting Doot. Aren subject August 8, 1983 Corporate Medical/HS&EA Danbury, P2594 Asbestos Related Diseases Because asbestos related diseases both with and without asbestosis are a cause of considerable concern and confusion, I have attached an execellent article written by D. Davies that appeared in the July 16, 1983 issue of the BRITISH MEDICAL JOURNAL. Davies has distilled a great deal of information into a succinct description of when compensability may be indicated. His comments on lung cancer are especially interesting. The fact that only a small percentage of pleural plaques (15% reported by Hourihane) are detectable during a lifetime by usual chest radiographs gives one concern. If our chest x-ray examin ations are of poor quality and are poorly interpreted, we could be accused of exercising inadequate "reasonable" care in our detection efforts. Hilton has been working with you to try to up grade our chest x-ray examinations and interpretations.I I appreciate that Dr. Hilton Lewinsohn called this article to my attention. Hilton is our resident expert on asbestosis and asbestos related diseases so if you have any questions or problems give him a call on extension 8-421-5214. Thomas A. Lincoln, M.D. Corporate Medical Director TAL:ems enclosure UCC 008440 1W value and importance? Once the questions are identified it may be easier to choose the forum in which to answer them. Deputy Editor, BMJ Tony Smith 'Anonymous. Does Britain need an academy of medicine ? Br Med J 1979pi:16U. 1 Godber G. An institute of health ? The Tima Health Supplement 1982 Feb 19:9 (col 1-4). ' British Medical Association. The medical effects of nuclear tear. The report of the British Medical Association's Board of Science and Education. Chichester: John Wiley and Sons, 1983. Asbestos related diseases without asbestosis Asbestosis and mesothelioma are prescribed diseases under the Industrial Injuries Scheme and entitle the patient or his dependants to compensation. The term asbestosis should be used only to denote fibrosis within the lungs. The three other non-malignant conditions associated with exposure to asbestos are pleural plaque, pleural effusion, and diffuse pleural thickening. The Industrial Injuries Council now recommends that, when it reaches a certain extent, the last of these should also be prescribed.1 Pleural plaques develop in the parietal pleura, seldom cause disability, and are not to be prescribed. Pleural effusions may be transient but some are chronic and may recur.2 No pre scription is proposed for these, but, under the new proposals, if they cause sufficient bilateral thickening of the pleura an application to a pneumoconiosis medical panel would lead to certification. Diffuse pleural thickening associated with exposure to asbestos has become increasingly recognised.3 4 Both pleural layers are affected and restrict the expansion of the lung. Histological examination shows only non-specific fibrosis, and, as with effusions, the diagnosis depends on excluding other causes such as tuberculosis and other infections, collagen diseases, trauma, chronic uraemia, and drug induced fibrosis.3 With such exclusions, the Industrial Injuries Council is satisfied that bilateral diffuse pleural thickening in asbestos workers is likely to be industrial and recommends that dis ablement benefit should be awarded when the thickening is bilateral, is over 5 mm thick, and extends over more than a quarter of the chest wall. The prescription of this condition will be welcomed, though some may be dissatisfied that the disease has to be so extensive to allow certification. Nevertheless, the committee suggests that this requirement should be reviewed in the light of experience. The report also considers cancer of the lung in asbestos workers. At present this condition is not prescribed, but when it occurs in association with asbestosis it is considered to be a sequel and benefit is payable. Claims which have been rejected during life may be successful after death because necropsy may disclose previously undiagnosable mild asbestosis. The council now lecommends prescription of lung cancer in patients with asbestosis and in certain other circumstances. In doing so it had to consider how to take account of smoking habits and the amount of exposure which would justify certification. The problem of the contribution of smoking to lung cancer in asbestos workers has been disposed of neatly. Studies in the United States in bsulation workers have shown that the relative risks of developing lung cancer are: non-exposed non-smokers 1; asbestos exposed non-smokers 5; non-exposed smokers 11; asbestos exposed smokers 53. Because exposure bcreases the risk by a factor of five in both smokers and non-smokers the council recommends that smoking should be disregarded. Cancer of the lung in asbestos workers may be divided into two broad types. Firstly, peripheral adenocarrinoma, which is unrelated to smoking and accepted as bebg due to asbestos exposure. The second is squamous, undifferentiated, and small-cell cancer arising in proximal airways, certainly related to smoking but only doubtfully related to asbestos. Perhaps wisely, the council makes no attempt to distinguish between these and recommends prescription irrespective of type. Most authorities accept that the risk of lung cancer is increased only when there has been heavy exposure to dust. Reasonable estimates of exposure may be made for people working in circumscribed places such as asbestos factories, but this may be impossible for, say, shipyard workers or engineers with intermittent exposure in various jobs, particularly b the distant past. Faced by this difficulty the council has made an ingenious proposal that the presence of other indicators of asbestos exposure should justify certification. It recommends prescrip tion when primary cancer of the lung is accompanied by one or more of the following features: asbestosis, bilateral diffuse pleural thickenbg, and bilateral pleural plaques. Asbestosis provides clear evidence of heavy exposure, but, though bilateral diffuse pleural thickenbg and bilateral pleural plaques are lbked with exposure to asbestos, the relation is less definite and more capricious,7 Moreover, pleural disease and asbestosis are also poorly correlated, for the former may appear b lightly exposed people such as the wives of asbestos workers and residents b the virinity of asbestos mbes and factories. Given a minimum exposure to dust, the development ofpleural calcification, which facilitates the diagnosis of plaques, is probably mainly determbed by age, usually takbg over 20 years from the first exposure. 9 Only some 15% of plaques are detectable during life,10 but this proportion might be higher if oblique x ray views were used b addition to th* routine ones.11 Hence probably the people who are certified during life will not be all those who have plaques but only the mbority b whom they are demonstrable. The case for necropsies b people who have had bdustrial exposure to asbestos and die of lung cancer is clear. The council's aim has been to identify people with sufficient exposure to dust to justify certification if they develop lung cancer. Workable regulations are difficult to devise, but the proposals favour those with pleural x ray shadows which may be the result of light exposure b the distant past and discrimbate agabst those with much heavier exposure who, for unknown reasons, do not develop pleural lesions or have not had time to do so. The council has decided agabst specifybg a duration and degree of exposure as a qualifybg condition because it considers this to be arbitrary and lackbg b scientific validity. Even so, the criteria of pleural lesions that it proposes are probably a less than satisfactory bdex and, though the extension of prescription will be welcomed--even if requires legislation--probably many will find that the details of the proposals which are now before the Secretary of State for Health are unsatisfactory. D Davies Consultant Chest Physician, City Hospital, Nottingham NG5 1PB UCC 008441 MUTISM. MEDICAL JOURNAL VOLUME 287 16 JULY 1983 1 Industrial Injuries Advisory Council. Asbestcn-related dittos* without asbestosis. London: HMSO. 1982. (Cmnd 8750.) * Gaensler EA, Kaplan AI. Asbestos pleural effusion- Aim Intern Med 1971;74:178-91. ' Sheers G. Asbestos-associated disease in employees of Devonport dock yard. Ann NY Acad Sd 1979;330:281-7. * Hillerdal G. Non-malignant asbestos pleural disease. Thorosc 1981 ^6: 669-75. * Albelda SM, Epstein DM, Gefter WB, Miller WT. Pleural thickening: its significance and relationship to asbestos dust exposure. Am Rev Respir Dis 1982;126:621-4. * Hammond EC, Selikoff IL_ Scidman H. Asbestos exposure, cigarette smoking and death rates. Ann NY Acad Sd 1979;330:473-90. ' Gibbs GW. Etiology of pleural calcification; a study of Quebec chrysotile asbestos miners and millers. Arch Environ Health 1979;34:76-82. * Rossi ter CE, Bristol LJ, Cartier PH, ei of. Radiographic changes in chryso tile asbestos mine and mill workers in Quebec. Arch Environ Health 1972;24:388-400. * Jones JSP, Sheers G. Pleural plaques. In: Bogorski P, Timbrell V, Gilson JC, Wagner JC, eds. Biological effects of asbestos. Lyon: 1ARC, 1973. (IARC Scientific Publication No 8.) 10 Hourihane DO'B, Lcssof L, Richardson PC. Hyaline and calcified pleural plaques as an index of exposure to asbestos. A study of radiological and pathological features of 100 cases with a consideration of epidemiology. Br MedJ 1966;i: 1069-74. 11 Fletcher DE, Edge JR. The early radiological changes in pulmonary and pleural asbestosis. Clin Radiol 1970;21:355-65. Difficulties with knees gan ifill the the s is . be hat ave it it :ecl is 165 laxity of the ligament--and 18 of the patients eventually decided that their symptoms werjmot severe enough to justify surgical reconstruction. The greater problem is th^fnterior cruciate. After years of discussion authorities still^annot agree. This difference of opinion was highlighted adtun in theJournal of Bone and Joint Surgery in February oW this year. Hughston and Barrett reported that rupture Of the anterior cruciate did not in itself contribute to instabilro of the knee.1 They believe that the instability which occurs in knees with this lesion is related to damage to the cajiyue, other ligaments and muscles, and the medial meniscus./n their hands careful evaluation and repair of the damagediftructures produced knees stable enough to withstand vigoipus sport, whether or not the anterior cruciate was ruptured^They emphasised the prime importance pf the medial mentis as a stabilising structure. By contj/st, Noyes ei al described the disability in 103 patients wth chronic laxity of the anterior crucial^ ligament uncomplicated by other major deficiencies or prdnous recon structed procedures.3 They showed that damajfe to this ligamenwras detected in only seven of the 103 Mtients initially, inciting those examined by orthopaedic surgeons. They found : if untreated an isolated anterior cruciay lesion would lead Itially to a lower sporting achievement/id later to reinjury, lamage to the meniscus, and eventuallwo osteoarthrosis. The average orthopaedic surgeon Mds such a wide diver gence of opinion difficult to understariQ. He should have found comfort in the sensible editorial in the same journal, though the author, Robert Larson, could no/reconcile the differences.4 He did, however, attempt to givVsome guidelines on manage ment based on his beliefthat alhfhe structures play a part in the stability of the joint; none is /[ important, all depend on each other. Thus to re-establisy stability all damaged structures should be identified, reputed, or augmented. Larson argues that repair should be u/iertaken urgently after injury, but acknowledges that thi&^ipproach requires accurate and early^ diagnosis. The anterioff cruciate itself, he believes, should nc be repaired but augmented, for experience has shown rirat repair is difficult apd produces poor results. He think^hat repair of the knee^vith chronic injuries should be appneached with caution, few judicious advice to the patient majrobviate surgery, esjjedpiy if he is taught to develop his Jfamstrings and quadric^K and lower his athletic requirem^ns. In those patients whdfe knees are so unstable as to interfe^ with normal life--or thpe who want to engage in sporting OTivities at a high standardise joint should be carefully ^sessed and the appropAte repairs and augmentation unOTtaken. In tjfe light of all this conflicting evidMce, what is the key ? the answer is a superspeciahn service for the few paints who are crippled by the linage to their knee, or raps a better diagnostic servic/for the acutely damaged knee, or perhaps both. C D R Lightowler Consultant Orthopaedic Surgeon,, Essex Nuffield Hospital, Brentwood CM15 8EH 't>ari^ DJ,'Tuaey RJ. Tftc long-term results of unrepaired tears of the posterior cruciate lig^ient. J Bone Joint Surg 1982 ;64B :92-4. * Hughston JC, Banja GR. Acute anteromedial rotatory instability. Long-term resuli/of surgical repair. J Bone Joint Surg 1983;65A:14553. * Noyes FR, M^fir PA, Matthews DS, Butler DL. The symptomatic anterior crrfCiate-deficient knee. Part 1; the long-term functional disability/] athletically active individuals. J Bone Joint Surg 1983; SA: 15/62, * LarsonJltL. The knee--the physiological joint. J Bone Joint Surg 1983; B5AP43-4. tew UCC 008442 hy.