Document 659knV2pMeRJbdmDj3wNbMgk6

Sch\vcrk/Riester/Hes$|gl >nary disease and somisfjv; pleural fluid in generahSi. 765-795 (1960). .||| C J.; Maklad, N. F, ana|| nic evaluation of pleuran&14; 135-140 (1975). wka, P., and Lypacewic^ pleural effusion by ultra^H techniques. Chest 7Q:i S. L.; Chikos, P. M., and ;onic evaluation of radiohe chest. Am. J. Roentg^r i JUgR, and Reid, J. M.: ij^^Jtetection and local: fusion. J. Am. med. Ass. .'iTkv /, R. A.: Problems in the V nography for the evalua- ' acities. Radiology 126: Case Report from the Thoracic Services Boston University Medical School Respiration 39; 229-240 (1980) y Asbestos-Related Disease from Household Exposure1 Gary R. Epler, Muiris X. Fitz Gerald, Edward A. Gaensler and Charles B. Carrington Thoracic Services and Evans Memorial Department of Clinical Research, Deparments of Medicine and Surgery, Boston University Medical Center, Boston, Mass., and the Department of Pathology, Stanford University School of Medicine, Palo Alto, Calif. " Key Words. Asbestosis Asbestos effusion Pleural plaques Pleural calcification Mesothelioma ess, W.: Ultrasonic diffe- 1 eural effusion from sub- ' itudinal scans of the right irtance of recognizing the y 123: 155-158 (1977). .. embirek, H.: Sonographitose supra- und infradia-' Fortschr. Gcb. Rontg-" 319-322 (1979). nson, J. C,; Gosink, B. B., Itrasound in diagnosis, loter^Mk loculatcd pleural K^Ps2.- 50-53 (1975). ' eshi, M., and Hassani, N.:... and aspiration of loculat- Respiration 34: 36-38 sonic evaluation of intra in. Ultrasound 4: 269-273 1979 aruar 1980 itiitsklinik, n Abstract. The importance of nonoccupational asbestos exposure has been emphasized recently. To illustrate this problem, we report 4 persons with asbestos-related disease from household exposure. There were 2 wives of asbestos workers, who cleaned their husbands' work clothes. One developed a mesothelioma and the other plaques, calcification, benign asbestos pleural effusion and subpleural parenchymal fibrosis. 2 men were exposed as children while playing in a cellar room which was also used for their father's muffler repair be iness. At ages 27 and 33, they had pleural and diaphragmatic calcifications. * Y The lungs and pleura react to asbestos in several ways. This fibrous silicate causes as bestosis, that is, a chronic interstitial pneu monia and it is associated with lung cancer. Pleural complications include plaque forma tion, calcification, diffuse thickening, effu sion, and malignant mesothelioma. These disorders may result not only from `inplant' direct or indirect exposure, but also from 'out-of-plant1 neighborhood or household 1 Supported in part by Research Training Grant HL-07035, Program Project Grant HL-19717 and Career Award HL-1173, all from the National Heart, Lung, and Blood Institute, US Public He?.?th Service, exposure. We describe 4 cases of asbestosrelated disease in family members of asbes tos workers. Case Reports Case 1 A 60-year-old woman was evaluated in Sep tember, 1973, because of acute, severe back pain. She had anorexia and weight loss of 2 months' dur ation, there was no dyspnea, cough, or hemopty sis, and she had never smoked cigarettes. She took intermittent medication for hypertension. Al though there was no pulmonary disease in her family, two sisters had breast carcinoma. Since 1933, she had worked in a shoe shop, a woolen mill, a clothing factory and an electronic firm. Fig, 1. a Overpenetrated chest roentgenogram of case 1, a 60-year-old woman. There is a 10-cm mass which, in the lateral view, proved to be be hind the heart. Thoracotomy revealed an inopera- ble mesothelioma (fig. 2). b This roentgenog. is of her 55-year-old husband. It shows diffuse, linear, irregular opacities suggesting asbestosis. On examination the blood pressure was 180/110. No rales were heard, a soft systolic mur mur was present, and left periumbilical tenderness was detected. Her chest roentgenogram revealed a mediastinal mass (fig. la). A thoracic aneurysm was suspected and an exploratory thoracotomy was performed immediately. An inoperable tumor was found. She was readmitted 2 months later with left-sided weakness and died. Autopsy re vealed a mesothelioma involving the left pleural surface, left lung, liver, abdominal cavity and brain. The tumor consisted of large cells which were frequently elongated or spindle-shaped and sometimes more rounded so as to suggest a biphasic pattern (fig. 2). The nuclei were quite pleo morphic and had coarse chromatin and some con tained one or occasionally two very prominent eosinophilic nucleoli. The uninvolved pleura had hyaline plaques (fig. 3a). In the lung there were scattered asbestos bodies, but no diffuse intersti tial pneumonia or fibrosis (fig. 3b, c). Because of these findings, a detailed exposure history was ob tained from her husband. He was a machine oper- ator in an asbestos product factory for 23 years and we had seen him annually as part of a respir atory survey. His examination revealed physi:_ogic and roentgenographic evidence of minimal as bestosis with progression in 1977 (fig. lb). The family lived on a farm 23 km from the factory, and the wife had never been in the plant. However, she had brushed white dust from herhusband's work clothes twice weekly for many years. Case 2 ' A 56-year-old woman saw her family physician in September, 1971, because of dyspnea while climbing stairs or performing housework during the previous 6 months. There was no chest pain> hemoptysis, cough or sputum. In 1957 a tubercu lin test had been positive, but the chest roentgeno gram was normal. She had smoked one pack of cigarettes daily since age 18, had no chronic medi cal problems, and did not take medication. From 1942 to 1949, she packed munitions fr an arms company and then worked in a wool 12.77 roentgenogram shows diffuse, : asbestosis. Fig. 2. Microphotographs of the mesothelioma of case 1. a Low-power view showing elongated or spindle-shaped cells arranged in interwoven bundles, b Higher magnification. The tumor cells are irregularly polygonal in shape, have abundant cytoplasm, and simulate an undifferentiated carci- ry for 23 years part of a respirealed physiologof minimal as* 1 (fig. lb). The omjie factory, iMc plant. ! (Ium from her eekly for many family physician dyspnea while ouscwork during is no chest pain, 1957 a tubcrcuchcst rocntgenoked one pack of no chronic medidication. ed munitions for ked in a woolen inill for 2 years. From 1951 to 1956, she worked for a rubber shoe company. Talc was used in the m: tufacturing process; but, as an inspector, she worked in a separate area at the end of the line. Since then she had been employed in a hospital food service department. Her chest roentgenogram revealed linear, ir regular opacities in the lung bases and minimal bi lateral pleural effusions. Therefore, she was ad mitted to a community hospital. The physical ex amination was recorded as normal. Evaluations for connective tissue diseases and tuberculosis were negative. A left thoracentesis yielded 3 ml of bl.od-tinged fluid with a total protein of 3g/ 109 ml, a sugar of 42 ml/100 ml, and a white blood cell count of 1,300, mostly polymorpho nuclear leukocytes. A thoracotomy was performed to establish a definite diagnosis. The lung was adherent to the chest wall, and the pleura was 4-5 cm thick in some places. The biopsy showed alveolar wall hyPerccllularity, subpleural interstitial fibrosis and scattered asbestos bodies (fig. 4). We first saw her in July, 1974, for disability evaluation. Dyspnea had persisted and a dry cough had developed. Physical examination re vealed bilateral, fine, crackling rales. The chest film now showed linear irregular opacities that were graded 1/1 by the 1LO U/C classifica tion [1] (fig. 5a). Additionally, both costophrenic angles were blunted, and she had a long medias tinal calcification parallel to the right heart bor der. Physiologic studies showed a forced vital ca pacity (FVC) of 2.071 or 73% of the predicted value. The forced expired volume in 1 sec (FEV,) was 1.63 1, thus there was no evidence of airflow obstruction with an FEV,/FVC of 79%. The expi ratory reserve volume of 0.741 and residual vol ume of 1.24 1 were normal. Gas exchange was ab normal: the single breath diffusing capacity was low, 14.5 ml/min/mm Hg or 68% predicted, and steady state studies showed an elevated alveolararterial oxygen pressure difference P(A-a)02 of 49 mm Hg at rest and 45 mm Hg during exercise. Normally the steady state diffusing capacity (Dss) is 15 ml/min/mm Hg at rest and doubles to 30 iaensler/Carrington ^l Asbestos-Related Disease from Household Exposure 233 ly thickened al[arrows) (b). HE. I''ig- 4. Lung biopsy of case 2 at low magnificat>on (a) shows minimal pleural thickening, alvsolar wall hypercellularity and some fibrosis reSemhling organizing chronic pneumonia. Many air > spaces contain large macrophages. At higher mag nification (b, c), isolated asbestos bodies are scat tered throughout the lung. HE. ) 234 Epler/Fitz Gerald/Gnensler/Cnrrington ^sbestos-Rela Fig. 5. a Chest roentgenogram of case 2, a 56-year-old woman. There are diffuse linear opac ities at both lung bases with blunting of the costophrenic angles as well as plaques and diffuse pleural thickening. A mediastinal calcification is indicated by arrows, b This roentgenogram is of her 58-year-old husband. There are diffuse linear opacities and honeycombing indicative o' ad vanced asbestosis. A blunting of the right ccstophrenic angle and diffuse pleural thickening were the first indications of a mesothelioma of which he died 6 months later. He had worked in an as bestos fireproofing factory since 1939. , ; Ftg. 6. a R old man. Cab leaves and rot sated by arrc with exercice, her Dss was 14.6 at rest but only increased to 18.9 with exercise. Review of her environmental history revealed that her husband had worked in an asbestos pro duct factory beginning in 1939. He developed se vere asbestosis (fig. 5b) and died of a pleural me sothelioma 28 years later in 1967. The wife's only contact with asbestos occurred while cleaning her husband's work clothes. Periodically these were so laden with white powder that dusting had to be performed outside the house. Case 3 ) A 33-year-old shipyard worker was seen by us in 1978 during an industrial respiratory survey. Review of the chest roentgenograms revealed cal cifications over both diaphragms and well-defined rounded plaques on both lateral chest walls (fig. 6a). He had come to the shipyard 13 years earlier in 1965 as a pipefitter, but remained only 4 months. He then worked in a machine shop else where without contact with asbestos for 5 years, and then for 6 years in several jewelry sh_ :s. In 1976, he returned to the shipyard as a iagger, when he was exposed only to fiberglass. His physi cal examination and pulmonary function studies were normal. Case 4 The 27-year-old brother of case 3 was also seen during the survey in 1978. His chest roent genogram showed a 3-mm calcification on the left diaphragm, a longer hairline calcification on the right diaphragm and a 4-cm calcification on the left chest wall (fig. 6b). Review of his preeniplol' ment chest roentgenogram revealed the same le sions. He began working at the shipyard in 1975 as a Iagger using only fiberglass. His physical examina tion and pulmonary function studies were norrnalWe discussed the radiographic findings '*'b the two brothers pointing out that, in case 4 the preemployment film at age 24 had shown calcifi* ( cations, and plaques and cr thbnths' expos: lljatl^e chat Patio^Pe ol bad acquired had been I (erTor 20 yea. a Iagger P4nt. He had -^/f from th *inaH businc bafflers with .^..cellar roc ' -.W^d with she ^ructed a i The chii i-5i father h .gening phy;^F>. his che; plaque indicative of adof the right costo-al thickening were ithclioma of which d worked in an as* : 1939. i'ig. 6. a Roentgenograms of case 3, a 33-yearold man. Calcifications over both diaphragmatic leaves and rounded plaques on the right are indi cated by arrows, b An enlarged section of the chest roentgenogram of case 4, his 27-year-old brother. A tiny diaphragmatic calcification and a thin 4 cm long calcification on the left chest wall are indicated by arrows. ;bcstos for 5 years, il jewelry shops. In pyard as a 1agger, ibergiass. His physi* iry function studies cations, and in case 3, at age 33 there were plaques and calcifications with possibly minimal 4 mo V:hs' exposure only 13 years ago. We suggested that these changes could not be the result of occu pation. The older brother then explained that they had acquired asbestos disease from their father who had been employed at the shipyard as a lag- ^ 6er for 20 years and, for 22 years before that, had rf case 3 was also been a lagger and asbestos worker at a chemical 78. His chest roent- plant. He had brought home asbestos sheets and cification on the left `fluff from the chemical plant and he established calcification on the calcification on the a small business at home for repairing burned-out mufiers with asbestos sheets. For this purpose, w of his preemploy- 'he cellar room where the children played was vented the same le* filled with sheets and blocks. Furthermore, he had e shipyard in 1975 as constructed a tree house from these asbestos mate His physical examina- rials. The children played there for many years. studies were normal* The father had no respiratory symptoms and aphic findings with screening physiologic studies were normal. How t that, in case 4 the ler, his chest roentgenogram showed bilateral 4 had shown calcifi- Pleural plaques. Discussion The dangers of indirect exposure to haz ardous dust within the workplace are well known. The possibility of exposure outside of a plant, so-called neighborhood or house hold exposure, probably was first recog nized .in connection with beryllium [2]. More recently the importance of neighbor hood exposure to asbestos has been empha sized. Mesothelioma was related to asbestos exposure by Wagner et al. [3] in 1960. This study contained one patient with household exposure, the daughter of an asbestos min er, and 14 neighborhood cases, that is, per sons who lived near the mine or who, as I1 .`.,irt: " '( d [ Asbestos-Rel; 236 Epler/Fitz Gerald/Gaensler/Carringt0j, Table I. Neighborhood- and Household-exposed cases of mesothelioma js hemorrhr phic marke. Authors Country Year Total Exposures plaques or none occupa neigh- house- asbestos worker or un tional borhood hold in household known The diagno; by fluid cyt more often, formed. Thi Wagner et at. [3] South Africa 1960 33 i 17 14 1 father Newhouse and Thompson [4] England 1965 83 32 31 11 9 husband:5 sister: 3 daughter: 1 Lieben and Pistawka [5] USA 1967 42 21 10 8 3 father: 2 Milne [6] Australia 1969 15 4 10 sons: I 0 1 father Champion [7] Rubino et at. {8] Canada Italy 1971 2 1972 54 0 43 1 5 0 1 father 3 3 wife: 1 relatives: 2 McDonaldand McDonald [9] Canada 1973 71 40 26 0 5 father: 3 mor, causin. progression tion of vise continuous ; ance^^o ir_ chog^P oj cell types a comatous o; ferential dia Lillington [10] USA Greenberg and LloydDavies [11] England Anderson etaL [12] USA Wliitwellet at. [13] Vianna and Rolan [14] England USA Edge and Choudhury [15] Li et at. [16] England USA 1974 2 0 1 1974 246 65 167 1976 4 0 0 1977 100 1978 52 11 30 88 6 1978 50 1 4S 1978 2 0 0 husband: 1 I other two. I 0 1 husband | tablished to 13 1 brother 0 4 father: 3 195 registry brother-in-law; 1 l or 69% as le 0 1 father ( one-half of 6 10 01 02 husband:9 father: 1 husband father 1 few survive l radical surgt [ tomy has bet I with untreat V not increase l radiak^ als children, had played on the mine dumps. Since then, several cases of mesothelioma in spouses, siblings and children of asbestos workers have been documented throughout the world (table I) [3-16], There are some indications that both the occurrence of me sothelioma and the latent period, that is, the duration between first exposure and diagno sis, are dose-related [4, 13]. The interval between first exposure and death was short est, averaging 29 years, for a group of heavily-exposed factory workers and long est, 49 years, for presumably minimally ex posed persons living in factory neighbor hoods [4]. The fact that mesothelioma can result from neighborhood exposures sug I 1 fl gests that the threshold is low. It is possible 1 occurred in that, rather than a real threshold, the very lowest doses simply have so long a latent I in 1 case in. I series of sue period that it exceeds man's normal life 1 tnanifestatior span. Although the latent period almost in Been confirn variably is very long, the duration of expo the world [2 sure may have been as brief as 3 weeks, but fusion' by ft Iaveraged 20 years [4, 6, 11]. confirmation The clinical features of mesothelioma films, no evu are now well described [3-16]. Ther ap [ Wh effusion | m 3 years. pears to be no correlation with cigarette smoking. Because effusion occurs in over .vjxers, we 90% and may be massive, rapid onset of Asbesti shortness of breath is common. The effusion Infestation 'Gaensler/Carringtoj! ^sbestos-Related Disease from Household Exposure 237 is hemorrhagic in only 15/o. Roentgenogra- phic markers-of asbestos -exposure,, such-as plaques or calcification, are seen in 60%. w The diagnosis sometimes can be established >use- asbestos worker by fluid cytology or pleural needle biopsy; Id in household -t: more often, exploratory thoracotomy is per formed. This sometimes may spread the tu father husband:5 sister: 3 m daughter: 1 S; father: 2 sons:1 father ; father ire: 1 atives: 2 `ather: 3 husband:2 husband brother father: 3 brother-in-law: l mor, causing increased pain and more rapid progression [15]. Grossly, there is permea tion of visceral and parietal surfaces by a continuous layer of tumor, but this appear ance also may be caused by primary bron chogenic or metastatic tumor. Histologic cell types are classified as epithelial, sar comatous or, as in our case 1, mixed. Dif ferential diagnosis is not a problem with the mixed cell types, but may be difficult in the other two. For example, a UICC panel, es tablished to verify the diagnoses, reviewed 19: registry cases and considered only 134, or o9/o as `definite' [11]. Prognosis is poor: father . one-half of patients die within 1 year and husband:9 father: 1 husband father ! tew survive more than 3 years. Although ^ radical surgery such as pleuro-pneumonec- tomy has been encouraged [17], comparison with untreated series suggests that it does , not increase survival. Chemotherapy and radiation also have not altered mortality. >d exposures suglow. It is possible hr^feld. the very : s^nong a latent nan's normal life : period almost in duration of e.xpoief as 3 weeks, but l]of mesothelioma [3-16]. Ther apion with cigarette m occurs in over ve, rapid onset of tmon. The effusion -ienign asbestos-related, effusion, which occurred in our case 2, was first described in 1 case in 1962 [18]. Since we reported a series of such patients in 1971 [19], this > manifestations of asbestos exposure has been confirmed in many cases throughout die world [20, 21], We defined `asbestos ef fusion' by four criteria: definite exposure, cor urination by thoracentesis of serial chest films, no evidence of any disease associated with effusion, and no malignant tumor withm 3 years. In longitudinal studies of 931 "orkers, we found a prevalence of 3-5% [22], Asbestos effusion, like other pleural manifestations, may develop after minimal > exposure. However, in contrast to these oth ers,-it-occurs-early, that-is, within 10 years of first exposure. Effusions are bilateral or recurrent in 50%, and sanguinous in one- third. Most are transient and require no therapy. With severe residual thickening, there may be physiologic abnormalities and then decortication may relieve the restric tion if there is no underlying parenchymal disease,......... . ................ Pleural plaques and calcifications are the most common manifestations of asbestos exposure. They may be seen after slight or very brief contact, but always with a latent period of at least 15 and more commonly 30-40 years [23-25]. Eventually, they may be seen in one-half or more of all roentgen ograms of asbestos-exposed workers, while in unexposed populations they are exceed ingly rare, about 0.03% among 10,000 rou tine radiographs [26]. These lesions also can occur from `neighborhood' exposure in persons living near asbestos mines or facto ries [24-27], in agricultural workers tilling soil containing asbestoform minerals [28] and in those unknowingly using asbestos- containing paints [29]. `Household' or family exposure as a cause of plaques is il lustrated by all 4 of our cases and has been reported by others [12, 26, 30, 31]. It ap pears to be more important than `neighbor hood' exposure because of the higher fre quency among family members compared with those living near plants; exposure from workers' clothes may be greater than that from the atmosphere [26]. For example, in a radiographic and clinical survey in Ham burg, among 92 persons with plaques or cal cifications, the cause could be traced to oc cupational exposure in 34, to domestic con tacts in 22 and to environmental exposure in only 21; and 5 had no exposure history [26], In another large study of 326 house- 238 hold members of asbestos workers, 7 had calcifications and 42 had pleural thickening [12]. Calcifications are readily recognized, most often oh the diaphragm, while uncalci fied plaques are difficult to see, especially if they are eri face in the posteroanterior view. Mediastinal calcifications, as in case 2, are rare, while involvement of the pericardium is not uncommon. Plaques are not precancerous lesions nor do they cause functional impairment, since they are situated on the chest wall and diaphragm, do not involve the lungs, and the pleural space remains free. For these reasons plaques and calcifi cations should not be regarded as a com pensable disease [26], However, they are important epidemiologic markers. No treat ment is indicated; however, because of inad equate occupationals and environmental history or because of failure to review older roentgenograms, some patients are unneces sarily operated upon. Asbestosis is defined as a pneumoconio sis, that is, a chronic interstitial pneumonia and fibrosis due to dust inhalation. Like all asbestos-related disease it is dose-related, but the dose required for recognizable mani festations certainly is larger than that re quired to produce pleural-based disorders. Therefore, asbestosis resulting from `outof-plant' neighborhood or household expo sure is unlikely. For example, in patients with mesothelioma related to neighborhood or household exposure, lung tissue, when available, did not show asbestosis (table I), though often it contained asbestos bodies (fig. 3). However, in a radiographic study of household contacts, 2 or 0.6% were said to have definite signs of asbestosis [12], Clinical, radiographic or physiologic mani festations of asbestosis in our experience are never seen less than 10 years after onset of exposure. Dyspnea is the most common tend to rem symptom, and fine, end-inspiratory crackles exposure mr (rales), are heard in over 65% of patients development [32], Physiologic abnormalities include de foregoing it creased vital capacity and abnormal gas ex {sure historic; change documented by low diffusing capaci posed, for c ty and elevated P(A-a)0, during exercise. neighborhooi Significant obstruction is no more common even more di than in control populations matched for age, sex and smoking habits [33]. The urual radiographic abnormalities consist of linear or irregular opacities that are most marked Reference at the lung bases and often obscure the car diac and diaphragmatic outline. Histologi cally, asbestosis is characterized by a usual interstitial pneumonia and fibrosis that mav proceed to honeycombing. After a latency period of 10-15 years, both the severitv oE the lesions and their rate of progression are dose-related. Usually, there is progression y even if the workers are removed from fur ther exposure. Death often has been attrib uted to cardiorespiratory failure. However, in recent years it has become apparent that I 20-50% of those asbestos workers who smoke die of bronchogenic carcinoma [13, 2 Eiscnbud, man. L._ T Non-occup icol. 31: 28. 3 Wagner, J, P.: Diffuse exposure ir Br. J. ind, i 4 Newhouse, lioma of pi posure to : ind. Med. 2 5 Lieben, J. ; 34], > A diagnosis of an occupationally or envi ronmentally related disease generally is based on adequate history taking. This task is especially difficult in relation to asbestos asbestos e 559-563 (H 6 Milne, J.: " 11 ssoi asl s in (1969). for several reasons. First, there are over 7 Champion, 1,000 asbestos-containing products, that, t sothelioma until recently were not labeled as to content so that workers in secondary industries of ten were not aware of exposure. Second, be cause of the long latency period, exposure 0 Rev. resp E ARubino, G. (Palestro, G lioma in N rind. Med. : often occurred in the distant past and has .[^McDonald, been forgotten. Third, asbestos-related rmiologic sv manifestations may result from brief or min imal exposure. Finally, job descriptions such as `plasterer', `fireman' or `engineer , ada. Can. r. hlLillington, lioma. Ne ::(1974). are often misleading, because official title5 h;_Greenberg, the most common^ tend to remain the same while hazardous inspiratory crackle^ exposure may change dramatically with the :r 65/o of patieni? development of new technologies. From the nalities include def foregoing it is apparent that eliciting expo d abnormal gas eP sure histories from persons, peripherally, ex >w diffusing capacjl? posed, for example, from those living in 3* during exercise^ neighborhoods or from family members, is . no more comnjc^ even more difficult. .tions matched for bits [33], The usual' es consist of linear it are most marked References en obscure the caroutline. Histologi- ( cte^Hl by a usual 1 ILO U/C 1971 international classification of radiographs of the pneumoconioses. Med. Radiogr, Phoiogr. 4S: 67-76 (1972). d fibrosis that may tg. After a latency 30th the severity of ; of progression are rere is progression * removed from furen has been attrib/ failure. However, come apparent that stos workers who nic carcinoma [13, upationally or envisease generally is :y Miring. This task rell^Pi to asbestos ' 1 Eisenbud, M.; Wanta, R. C.; Dustan, C.; Stead man, L. T.; Harris, W. B., and Wolf, B. S.: Non-occupational berylliosis. J. ind. Hyg. Tox icol. 31: 2S2-294 (1949), 3 Vagner, J. C.; Sleggs, C. A., and Marchand, P. i'.: Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province. Br. J. ind. Med. 17: 260-271 (1960). 4 Newhouse, M. L. and Thompson, H.: Mesothe lioma of pleural and peritoneum following ex posure to asbestos in the London area. Br. J. ind. Med. 22: 261-269 (1965). 5 Lieben, J. and Pistawka, H.: Mesothelioma and asbestos exposure. Archs envir. Hlth 14: "59-563 (1967). 6 Milne, J.: Fifteen cases of pleural mesothe lioma associated with occupational exposure to asbestos in Victoria. Med. J. Aust. //: 669-273 (1969). -st, there are over I 7 Champion, P.: Two cases of malignant me tg products, that, ' sothclioma after exposure to asbestos. Am. tbclcd as to content tdary industries ofposure. Second, be y period, exposure Rev. resp Dis. 103: 821-826 (1971). 8 Rubino, G. F.; Scansetti, G.; Donna, A., and Palcstro, G.: Epidemiology of pleural mesotheioma in North-western Italy (Piemont). Br. J. md. Med. 29: 436-442 (1972). stant past and has 9 McDonald, A. D. and McDonald, J. C.: Epide- l, asbestos-related niiologic surveillance of mesothelioma in Can : from brief or min , job descriptions man' or `engineer' cause official titles ada. Can. med. Ass. J. 109: 359-362 (1973). '0 Lillington, G. A.: Conjugal malignant mesothe lioma. New Engl. J. Med 291: 583-584 (1974). U Greenberg, M. and Lloyd Davies, T. A,: Me sothelioma register 1967-1968. Br. J. ind. Med. 31: 91-104 (1974). 12 Anderson, H. A.; Lilis, R.; Daum, S. M., et al.: Household-contact asbestos neoplastic risk, Ann. N. Y. Acad. Sci. 271: 311-323 (1976). 13 Whitwell, F.; Scott, J., and Grimshaw, M.: Re lationship between occupations and asbestos-fi ber content of. the lungs in patients with pleu ral mesothelioms, lung cancer and other dis eases. Thorax 32: 377-386 (1977). 14 Vianna, N. J. and Polan, A. K.: Non-occupa tional exposure to asbestos and malignant me sothelioma in females. Lancet i: 1061-1063 (1978). 15 Edge, J. R. and Choudhury, S. L.: Malignant mesothelioma of the pleura in Barrow-in-Fur ness. Thorax 33: 26-30 (1978). 16 Li, F. P.; Lokich, J.: Lapey, J., et al.: Familial mesothelioma after intense asbestos exposure at home. Am. med. Ass. 240: 467 (197S). 17 Aisner, J. and Wiernik, P. H.: Malignant me sothelioma. Chest 74: 43SM44 (1978). 18 Eisensladt, H. B.: Pleural asbestosis. Am. Practnr Dig. Treat. 13: 573-578 (1962). 19 Gaensler, E. A. and Kaplan, A. I.: Asbestos pleural effusion. Ann. intern Med. 74: 178-191 (1971). 20 Elder, J. L.: A study of 16 cases of pleurisy . with effusion in ex-miners from Wittcnoon Gorge. Aust. N. Z. 1. Med. 2: 328-329 (1972). 21 Chretieu, J.; Chahinian, P. H.; Hirsch, A. et Nebut, M.: Pleuresies non tumorales de l'asbeste. Rev. fr. Mai. respir. 4: suppl. 2, pp. 87-92 (1976). 22 Eplcr, G. R. and Gaensler, E. A.: Asbestos ef fusion. Chest 72: 399 (1977). 23 Jacob, G. and Bohlig, H.: Die rontgenologischen Komplikationen der Lungenasbcstose. Fortschr. Rbntgenstr. S3: 515-525 (1955). C.: Hyaline and calcifiea pleural plaques as an Sci. 132: 235-239 (1965). 24 Kiviluoto, R.: Pleural calcification ns a roent genologic sign of non-occupational endemic anthophyllitc-asbestosis. Acta radio!., suppl. 194, pp. 1-67 (1960). 25 SelikoCf, K. J.: The occurrence of pleural cal cification among asbestos insulation workers. Ann. N. Y. Acad. Sci. 132: 351-367 (1965). 26 Dalqucn, P.; Hinz, I. und Dabbert. A. F.: Pleuraplaques, Asbestosc und Asbestexposition, eine epidcmiologische Studie aus dent Hamburger Raum. Pneumonologie 143: 23-42 (1970). 27 Hourihane, D.; Lessof, L., and Richardson, P. C.: Hyaline and calcifide pleural plaques as an index of exposure to asbestos. Br. med. J. t: 1069-1974(1966). 28 Zolov, C.; Bourilkov, T., and Babadjov, L.: Pleural asbestosis in agricultural workers. En viron. 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SO East Concord Street, Boston, MA 02113 (USA) ^ Respiration i 1 ia.: Meehan. # Thoracit Andre Del I I?) Chest Service Key^%rds Abstract* V : strapping. In ; . chest wall du: . those observec t Volume and c | Pst (L) at FRC I given transtho average chest v are shown to 1 elastic work ol due to the wot & wquired i^ver fl. ihlntroductior *In I960, Ca ..Section of the strapping p ; ^oil of the It