chronic pleuritic pain in four patients with asbestos ... · fuse and circumscribed pleural...

British Journal of Industrial Medicine 1990;47:147-153

Chronic pleuritic pain in four patients with asbestosinduced pleural fibrosis

A Miller

AbstractFour patients occupationally exposed to asbes-tos, each suffering at least eight years of dis-abling, persistent, and often bilateral pleuriticpain are described. Radiographic evidence ofpleural disease ranged from plaques seen onlyon computed tomography to typical bilateralplaques or diffuse thickening to extensive dif-fuse and circumscribed pleural fibrosis andcalcification. There was no history or evidenceof acute pleuritis or pleural effusion in threepatients. Intermittent pleural friction rubshave been present in all four; one patientshowed pleural uptake of gallium-67. Exten-sive workups including repeated pulmonaryventilation-perfusion scans and cardiac cath-eterisation have not yielded other diagnoses toexplain the pain. It is proposed that persistentpleuritic pain be added to the manifestations ofbenign asbestos induced pleural disease.

Two types of chronic asbestos induced pleuralfibrosis are well described-namely, circumscribed(plaques) and diffuse,' the latter generally a residualof inflammatory pleural effusions."3 Althoughintense inflammation may be evident on histologicalexamination in asbestos induced chronic diffusepleural fibrosis,4 clinical symptoms are not those ofactive inflammation. Pleuritic pain is notable by itsabsence. Indeed, unless experiencing recurrenteffusions, patients are asymptomatic or notice short-ness of breath attributable to ventilatory insuffi-ciency45 (or underlying asbestosis of the lung). Thepleura seems to behave differently from the pericar-dium; chronic recurrent or persistent pain, or both, isa feature ofmany forms of pericarditis but is not seenin chronic pleuritis of diverse aetiologies.

In a practice that includes many patients withasbestos induced pleural fibrosis I have noted a fewwho complain of continuing chest pain or discomfortthat is not clearly pleuritic. I have also encountered

four patients with documented benign asbestosinduced pleural disease who have persistent pain ofclearly pleuritic nature variably accompanied byother manifestations of pleural inflammation includ-ing friction rub and positive gallium scan.

Case reportsPATIENT 1 (date of birth 13 December 1919)This man came to me in October 1979 because ofpersistent chest pain of several months duration.This pain varied in intensity, was left or right sided,or both, anterior or posterior, or both, but neverrelented completely and was exacerbated by inspira-tion, cough, and movement. He was dyspnoeic onclimbing one and a half flights of steps.He had experienced a right sided spontaneous

pneumothorax on 4 April 1976 that required decom-pression with a pleural tube. After this he beganto experience anterior pleuritic pain radiating tothe shoulders. On 8 November 1976 he suffereda recurrence of the right pneumothorax whichcould not be expanded by pleural suction, and athoracotomy was performed. Subpleural apical blebsmeasuring up to 0 5 cm in diameter were resected as awedge and oversewn and the parietal pleura wasstripped. Parietal pleura showed "a white, firm,plaque measuring 2 x 1 x 0-2 cm." On microscopicexamination the pleura showed "fibrosis and chronicinflammation"and the lung "patchy, marked inter-stitial fibrosis" (fig 1). No connection was madebetween this patient's occupational history (seebelow) and these findings ofa typical asbestos pleuralplaque and interstitial pulmonary fibrosis.The chest pain continued, now associated with

dyspnoea and friction rub. A diagnosis ofpericarditiswas entertained but not supported by electro-cardiograms. The pain and the rub cleared withprednisone treatment but recurrent episodes of painresponded to prednisone less well and the localisationof the pain changed to that described above.

Occupational historyThe patient had been an iron worker and boiler-maker, beginning work at the first of severalshipyards in 1938. He had to remove asbestosinsulation from ceilings, walls, and pipes and hemixed asbestos cements used on boilers. In 1952 a

Division of Pulmonary Medicine, Department ofMedicine, Mount Sinai School ofMedicine, Box 1232,New York, New York 10029, USAA Miller

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Figure I Resected lung tissuefrom patient I (haematoxylin and eosin stain) showing alveolar septalfibrosis and likelyferruginous body.

17 metre fall aboard ship left him comatose for threeweeks, fractured his right arm and leg, and detached aretina. He then stopped smoking his one pack ofcigarettes a day. After seven years of rehabilitation,he returned to work as an inspector of rolling stockfor the New York City subways, working as such forthe next ten years without exposure to asbestos. Hewas placed on light duty in 1979 but could notcontinue working in 1980 because of the pleuriticpain and dyspnoea.On examination he was a chronically ill white man

who appeared to be his stated age of 59 and hadobvious chest pain. This was exacerbated by deepbreath, cough, and movement of his torso or arms.Right thoracotomy and anterior thoracotomy scarswere present, as were fine inspiratory basal rales.There was no finger clubbing.

Chest radiographs from 1979 to 1986 showed onlyblunting of the right costophrenic angle (attributableto his thoracotomy) and a calcific plaque over theright upper lobe coded as Al on the ILO scale. Theparenchyma was normal (0/0) as were the heart andhila.The histological slides from his wedge resection

were now sent to the Mount Sinai School ofMedicine. Dr Yasunosuke Suzuki reported "advan-ced pulmonary asbestosis" with interstitial fibrosis

and calcification and associated calcific pleuralplaque. There were many ferruginous bodies, free orwithin macrophages, both intra-alveolar and inter-stitial.

It was apparent that asbestosis could explain hisprogressive dyspnoea and rales, despite the paucityof radiographic findings, and it seemed possible thatan active asbestos induced pleuritis might explain hischronic pleuritic pain and intermittent friction rub.

After failure of a wide variety of analgesics andnon-steroidal anti-inflammatory agents to bringrelief, the patient was admitted to the Mount SinaiSchool of Medicine in January 1980 for furtherevaluation. Haematological and chemical profiles,erythrocyte sedimentation rate, antinuclear antibodystudies, and latex fixation were normal. Two galliumscans were made over a ten day interval and showedpersistent uptake in both apices, hila and bases, readas "pleural localisation, rule out mesothelioma." Themitral and aortic valves were normal on echo-cardiography. On right heart catheterisation, allpressures were normal, cardiac output was 6 1/minand there was no evidence ofpericardial constriction.Computed tomography of the chest showed multiplesites of pleural thickening (more on the left) that didnot correlate with the areas of gallium uptake andquestionable evidence of interstitial fibrosis.

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Chronic pleuritic pain in four patients with asbestos induced pleuralfibrosis

Complete pulmonary function tests showed only a

slight decrease in diffusing capacity (6 89 mmol/min/kPa or 20 6 ml/min/mm Hg, 69% of predicted6) andan increase in physiological dead space (VD/VT 0-49)at rest. For consistency, the same predictive equa-

tions have been used for all studies on all patients,even if they had not been published when the testswere performed. Full lung volumes by plethys-mography, spirometry (including FEF2,.75.),maximum voluntary ventilation, and dynamic com-

pliance at basal respiratory rate were normal; the vitalcapacity was 4 40 1 (83% of predicted).'The PaO2 varied from 71 to 77 mm Hg at rest

(minimally reduced), did not fall with two minutes ofstep up exercise, and rose appropriately on inhalationof 100% 02. Small airways disease was suggested bya decrease in FEF75.. and frequency dependence ofcompliance. The increase in dead space ventilationand slight decrease in diffusing capacity were consis-tent with interstitial lung disease, despite the normallung volumes and compliance and the absence ofradiographic findings.The evaluation during this period in hospital

confirmed both bilateral pleural plaque formationnot apparent on conventional radiography and an

active pleural inflammation capable of taking up

Ga-67 citrate. The chest pains could not beattributed to mitral valve prolapse or pericarditis.Evidence of interstitial lung disease from the pul-monary function and radiographic studies was lessstriking than from the histological lesions.The course over the next six years has not changed.

The pains, variably associated with a pleural rub,have never abated and on several occasions were so

severe on one side or the other as to bring him tovarious hospital emergency rooms to rule outpneumothorax or pulmonary embolism. Repeatedattempts to relieve the pain with non-steroidal anti-inflammatory drugs and steroids have been unsuc-

cessful. Dyspnoea has persisted. He was readmittedto the Mount Sinai Hospital in October 1982 becauseof these symptoms and blood streaking. Fibreopticbronchoscopy showed no endobronchial lesions;transbronchial biopsy showed interstitial fibrosis andferruginous bodies. The FVC and TLC were lower,3 88 1 (67% of predicted) and 5 61 1 (680% ofpredicted), respectively, whereas the DLCOSB was

unchanged (6 35 mmol/min/kPa; 19-0 ml/min/mmHg).On physiological re-evaluation in February 1987,

the FVC was 3 40 1 (decreased from 1982), FEV,2-82 1, FEV1/FVC 0 83, FEF2575O 2-98 1/sec (93% ofpredicted),7 but the DLCOSB was now 462 mmol/

min/kPa (13 8 ml/min/mm Hg), 49% of predicted.6Results on incremental exercise testing were: maxi-mum 02 consumption 1-19 I/min (51% of predicted),maximum ventilation 88 1/min (78% of predicted),8normal heart rate response, considerably increased

ventilatory response, excessive dead space ventila-tion without the expected fall on exercise (VD/VT 0 47at rest and 0-45 at VO2 1 0 1), and slight exerciseinduced hypoxaemia (PaO2 69 mm Hg, alveolararterial difference 40 mm Hg). These abnormalitiesare characteristic of interstitial fibrosis.

PATIENT 2 (date of birth 19 June 1932)This man was seen in October 1988. He beganexperiencing chest pains in 1981. He was admitted tohospital in 1982 with severe chest pain to "rule outpulmonary infarction" and was discharged takingmuscle relaxants. He has continued to experiencebilateral, primarily right sided, anterior chest painincreasing with cough, deep breathing, sneeze,straining, and certain motions. Cardiac catheterisa-tion in 1986 was normal. He is dyspnoeic on walkingone block rapidly.

Past history includes allergic rhinitis (withnegative sinus films) treated by immunotherapy,upper gastrointestinal haemorrhage in 1986, andchronic back syndrome but no pleurisy orpneumonia. He has never smoked.

Occupational historyThe patient was exposed to asbestos insulation as abystander from 1951 to 1954 and as a maintenancemechanic in nylon and mylar plants, removing oldinsulation, cutting asbestos blocks, and mixing andapplying asbestos cements from 1954 to 1981.On examination, the patient changed position with

obvious pain in the right chest that increased on deepbreathing. A pleural friction rub was heard on theright, greater anteriorally.The ECG was normal but chest radiographs in

1988 showed bilateral calcified diaphragmaticplaques and calcified chest wall plaques coded as R B,1 en face 2 and L en face 2 (fig 2). The parenchymawas normal except for a small area of atelectasis in theleft costophrenic angle. The earliest film in 1969showed a left diaphragmatic plaque and right chestwall plaque Al. Computed tomography in 1982showed only pleural thickening.Pulmonary function results were available from

1979 to 1988. Spirometric efforts were associatedwith chest pain. The FVC decreased gradually from5-62 1 in 1979 to 4-39 1 in 1986 and more steeply to3-081 (61% of predicted)7 in 1988, with correspond-ing FEV, values 3-76 1, 3 19 1, and 2-44 1 (61% ofpredicted) and FEVI/FVC ratios 0-67,0 65, and 0-79.The FRC, RV, TLC, and DLCOSB have been normal.The maximum voluntary ventilation in 1988 wasborderline, 87 1/min, 79%, of predicted.8 Theseresults are consistent with a progressive restrictiveimpairment of chest cage type; earlier evidence ofslight airways obstruction is no longer detectable.The chest pains have persisted despite treatment

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Figure 2 Chest radiographs, posteroanterior, patient 2;(A), made in 1988, shows bilateral diaphragmatic andchest wall plaques which have progressed since (B), madein 1976. Lb.with analgesics, anti-inflammatory agents, anxio-lytics, and muscle relaxants. Although he was assig-ned to light duty, he had to stop working early in 1988and no longer engages in previous activities, such as

fishing or lawn mowing. Psychiatric and psycho-logical (Minnesota multiphasic personality inven-tory) evaluations yielded a diagnosis of "psychologicfactors (either depressive disorder or adjustmentdisorder with mixed anxiety and depression) con-

tributing to a physical condition-chronic pain(DSM-III-R316-0)." Hypochondriacal neuroses,conversion disorder, and malingering were notthought to be present.

PATIENT 3 (date of birth 21 August 1909)This man was referred by a cardiologist in September1987 for left and, less frequently, right anteriorpleuritic pain over the past ten years. The pain had atfirst come on once a week but was now present eachday, lasting all day. The pain was increased by a deepbreath and by movement and was neither exertionalnor radiating. It was difficult to evaluate dyspnoeabecause of limited activity due to pain.

Past history included a myocardial infarction in1974, aortic stenosis, and single vessel coronarydisease confirmed at cardiac catheterisation in 1982and an episode of congestive heart failure in Septem-ber 1986, which included new bilateral pleuraleffusions and peripheral oedema responding todiuretic treatment. On gated blood pool scan, the leftventricle was enlarged and hypokinetic, with dys-kinesia of the apex consistent with a large apical

aneurysm. The ejection fraction was 260. Thepatient had smoked one pack of cigarettes a day butswitched to a pipe in 1962 and discontinued alltobacco in 1986.

Occupational historyHe was a plumber's helper (1925-9) and then aplumber (1929-41, 1945-72), occasionally mixingand applying asbestos cements, installing pipesaround asbestos insulated boilers, and workingalongside insulators. From 1940 to 1945, he was apipefitter foreman at several shipyards and powerplants, working in boiler rooms and frequentlyremoving asbestos insulation.On examination, chest expansion was normal;

pleural rubs were heard anteriorally on both sides. Agrade 3/6 systolic "sea gull" murmur at the apexradiated to the left axilla and a grade 3/6 systolicmurmur at the aortic area radiated to the neck. Fingerclubbing was not present. The ECG showed an oldanteroseptal infarct, left anterior hemiblock, andpremature atrial and ventricular beats.

Chest radiographs showed extensive bilateral cal-cific pleural thickening, both diffuse and circum-scribed (RC3, en face 2, L C2, en face 3), withblunting of both costophrenic angles and calcifica-tion of both diaphragms and the left mediastinalpleura (fig 3). As well as could be discerned, the lungfields were s/t, 0/1, and the heart was not enlarged.Computed tomography confirmed the pleural abnor-malities described above and the normal cardiac

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Chronic pleuritic pain infour patients with asbestos induced pleural fibrosis

Figure 3 Chest radiograph, posteroanterior, patient 3,

showing extensive bilateral calcified pleural thickening of the

chest wall, diaphragm, and mediastinum.

contours and absence of interstitial fibrosis. Gallium

scan was technically unacceptable.On spirometric testing, the VC was 2361 (770o of

predicted), FEV, 2-25 1 (940" of predicted), FEV,/FVC 0 95, FEF2575. 3-08 1/sec (1319o of predicted)7and maximum voluntary ventilation 69 1/min (750oof predicted).8 The vital capacity was unchangedfrom values a year earlier, at which time the (N2washout) functional residual capacity was 3-12 1(1030/ of predicted), the residual volume 2 25 1(104% of predicted), and total lung capacity 4-43(92%// of predicted).9 Results suggested a minimalrestrictive impairment.The patient was advised to continue his diltiazem

and diuretic regimen. Manipulating the route,schedule, and dosage of nitrate treatment did notaffect his pleuritic pain. Repeated attempts toameliorate the pain with aspirin, various non-

steroidal agents, and prednisone were unsuccessful.

PATIENT 4 (date of birth 4 October 1940)He was first reviewed at Mount Sinai Hospital on 21June 1982. He had been admitted to St ThomasHospital, Nashville, Tennessee, in April 1978 forchills and dyspnoea that had begun one monthearlier. He was treated with antibiotics and steroidsand was admitted to hospital again five months laterfor persistence of these symptoms. Fibreopticbronchoscopy including biopsy was normal.Adhesions were noted on open pleural biopsy; histo-logical examination showed fibrous tissue with

infiltration of mature lymphocytes around smallblood vessels. Because of a positive tuberculin test(second strength), the patient was treated withisoniazid which was discontinued after three weeksbecause of hepatitis.

In March 1979 the patient noted left pleuritic pain,fever, malaise, and dyspnoea, with a rub on physicalexamination and a large left pleural effusion. Thefluid was exudative; pleural biopsy showed fibrosiswith "dense infiltration of histiocytes, lymphocytes,and eosinophils" and mesothelial proliferation. Afterthree thoracenteses, fluid was no longer present butpleuritic pain, rubs, and fluid reappeared within twoweeks, requiring a chest tube. A third pleural biopsyshowed similar findings. Results of bacterial, viral,fungal, and mycobacterial cultures and stains werenegative and right and left sided pleural effusionscaused by asbestos were diagnosed.

Occupational historyThe patient had been an asbestos insulator since 1963(at age 23), working in constructing power plants andremoving old insulation.He could return to work despite the persistent

exertional dyspnoea, right pleuritic pain requiringcodeine, chills, and fever. Pleural friction rubs wereheard throughout this period. On review at theMount Sinai Hospital, chest radiographs from 1980to 1982 showed bilateral diffuse pleural thickening(A 2, face on 1), and irregular small opacities coded as1/1.Because of the persistent pain of the right chest,

xylocaine was injected into the chest wall on severaloccasions, and in February 1984 intercostal nerveblocks were performed. Pain was unrelieved and inApril 1984 the right intercostal nerves were sur-gically interrupted. On this admission, breath soundsand resonance were diminished at the right base anda rub was present.The stabbing pleuritic component of the patient's

chest pain was no longer present; he discontinuedpain medication and gained weight. Bronchoscopywas performed on 28 February 1986 because ofhaemoptysis. Biopsy showed chronic bronchitis,denuded mucosa, and goblet cell hyperplasia; lungparenchyma showed numerous macrophages and"mild interstitial fibrosis."By October 1986, however, the pain had increased

in severity, was unresponsive to transcutaneouselectrical nerve stimulation (TENS), and requirednarcotics. On 3 November 1986, the patient under-went T3-T9 laminectomy, right T,, ganglio-nectomies, and DREZ lesioning of the T,, dorsalroot entry zones at Vanderbilt University Hospital inNashville. Pain in the distribution of the 12thintercostal nerve persisted and was relieved only witha block of this nerve; ganglionectomy was thenperformed. Pain persists above T, and pain and

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muscle spasm below T12. Nevertheless, the patientcontinues to work as a union official. He has beenunable to stop smoking his usual daily pack ofcigarettes.Pulmonary function test results are available from

1978 to 1988, showing little change in lung volumesbut significant decrease in DLCOSB during this tenyear span: FVC 4 0 (1978) to 3 50 1 (1988; 650o ofpredicted), FEV, 3-18 to 2-66 1 (61°o of predicted),FEVI/FVC 0 79 to 0-76, FEF2575' 3-46 to 2-72 1/sec(720o of predicted),7 TLC 587 to 6/02(84°o of

predicted), RV 2-62 to 2-52 1 (110io of predicted),9PaO296 to 97 Torr and DLCOSB 8-76 mmol/min/kPa(26 2 ml/min/mm Hg) to 5-85 mmol/min/kPa (17-5ml/min/mm Hg, 540°o of predicted). These resultsare consistent with a moderate restrictive impairmentwith loss of diffusing capacity.

DiscussionThese four patients have in common theiroccupational exposure to asbestos, unequivocalevidence of asbestos related disease, and persistent,often bilateral, pleuritic pain. They are unlike in howthey manifest their asbestos related disease clinically,in that patient 1 has no specific evidence of pleural or

parenchymal disease on plain films (despite strikinghistological abnormalities of both tissues), patient 2has typical pleural plaques, patient 4 typical diffusethickening and small irregular opacities, whereaspatient 3 has extensive diffuse and circumscribedpleural disease. Thorough physiological evaluationin patients 1 and 4 showed gas exchange abnor-malities -of interstitial fibrosis; all have slight tomoderate restrictive impairment.

Other causes for chest pain in the three patientswithout a history of acute pleuritis or effusion haverepeatedly been ruled out during the long periodsthey have been under observation. The first patient'stwo episodes of spontaneous pneumothorax (andsubsequent surgical intervention), both on the sameside, do not explain the bilateral manifestations, nordo consequences of his injuries 24 years before theonset of pain. Similarly, the heart disease shown inpatient 3 does not explain his progressive pleuriticpain. All three patients have undergone cardiaccatheterisation, coronary angiography, and repeatedpulmonary ventilation perfusion scans.No explanation can be offered for the persistence

of the pleuritic pain in these four patients. Such painhas not been described in the many patients who havecome to medical attention with asbestos inducedpleural plaques or, indeed, in those with diffusepleural fibrosis and calcification of asbestos induced,tuberculous, traumatic, or pyogenic aetiology.Recurrent, often bilateral, pleuritic pain has beendescribed in acute asbestos induced pleurisy, inassociation with exudative effusions. Patient 4

had characteristic asbestos related acute pleuraleffusions early in his course. Probably patient 3 hadsimilar effusions that caused his diffuse pleuralthickening, although the onset of his pain was notrelated to these. There is no evidence that patients 1and 2 had such effusions, although they may wellhave occurred and not come to medical attention. Inany event, these two patients do not have diffusepleural thickening which may result from sucheffusions.

Persistent pleuritic or poorly characterised chestwall pain is characteristic ofmesothelioma, which hasbeen ruled out by the long periods ofobservation, thecomputed tomography, and the biopsies.There are few, and limited, descriptions of persis-

tent pleuritic pain without coexisting effusion.Robinson and Musk noted that three of their 22patients with asbestos induced effusions had pain upto eight years after resolution of the effusions.'4Eisenstadt cited a patient with pleuritic pains for 12years before the advent of mesothelioma, in whomnecropsy showed benign asbestos induced pleuraldisease in those portions of the thorax not affected bythe malignancy.'0 Quite reasonably, he concludedthat "these pains must have been caused by a benignprocess preceding the malignancy."

Gaensler and Kaplan noted that asbestos inducedpleural effusions may be "followed by continuedchest pain," and cited several cases in which painpersisted in the absence of effusions, in one casedespite repeated intercostal nerve blocks and "resec-tion of the costal arch."3There have been few reports of gallium scans in

benign asbestos pleural disease. Teirstein andcolleagues noted that three of 16 patients had positivescans; these had exuberant diffuse pleuritis.'5 Thepositive scans and intermittent rubs in patient 1 whohas only plaques on computed tomography and blandhistology on biopsy, the occasional rubs in patient 2,and the persistent rubs in patient 4 suggest thatinflammatory activity may be present despite quies-cent features.The sequelae of benign asbestos induced pleural

disease include recurrent exudative pleural effusionas well as minor'"'8 and occasionally major45 impair-ments of ventilatory function. A rare syndrome ofpersistent pleuritic pain that may be associated withother markers of active inflammation such as frictionrubs and uptake of67-gallium should be added to thislist.

I thank my colleagues in the division of environ-mental and occupational medicine- Drs Stephen MLevin and Steven B Markowitz, for referring patient3 and providing their material on patient 4.

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I International classification of radiographs of pneumoconioses.Geneva: International Labour Office, 1980.

2 Epler GR, McLoud TC, Gaensler EA. Prevalence and incidenceof benign asbestos pleural effusion in a working population.JAMA 1982;247:617-22.

3 Gaensler EA, Kaplan Al. Asbestos pleural effusion. Ann InternMed 1971;74:178-91.

4 Miller A, Teirstein AS, Selikoff IJ. Ventilatory failure due toasbestos pleurisy. Am J Med 1983;75:91 1-9.

5 McGavin CR, Sheers G. Diffuse pleural thickening in asbestosworkers: disability and lung function abnormalities. Thorax1 984;39:604-7.

6 Miller A, Thornton JC, Warshaw R, Anderson HA, TeirsteinAS, Selikoff IJ. Single breath diffusing capacity in a represen-tative sample of the population of Michigan, a large industrialstate. Predicted values, lower limits ofnormal and frequenciesof abnormality by smoking history. Am Rev Respir Dis1983;127:270-7.

7 Miller A, Thornton JC, Warshaw R, Bernstein J, Selikoff IJ,Teirstein AS. Mean and instantaneous expiratory flows, FVCand FEV,: prediction equations from a probability sample ofMichigan, a large industrial state. Bull Eur Physiopathol Respir1986;22:589-97.

8 Bass H. The flow volume loop: normal standards and abnor-malities in chronic obstructive pulmonary disease. Chest1973;63: 171-6.

9 Goldman HI, Becklake MR. Respiratory function tests. Normal

values at median altitudes and the prediction ofnormal results.Am Rev Respir Dis 1959;79:457-67.

10 Eisenstadt HB. Asbestos pleurisy. Dis Chest 1964;46:78-81.11 Eisenstadt HB. Benign asbestos pleurisy. JAMA 1965;192:

419-21.12 Mattson S-B. Monosymptomatic exudative pleurisy in persons

exposed to asbestos dust. Scand J Respir Dis 1975;56:263-72.13 Chahinian P, Hirsch A, Bignon J. Les pleurisies asbestosiques

non tumorales. Revue Francaise des Maladies Respiratoires1973;1:5-39.

14 Robinson BWS, Musk AW. Benign asbestos pleural effusion:diagnosis and course. Thorax 1981;36:896-900.

15 Teirstein AS, Chahinian P, Goldsmith SJ, Sorek M. Galliumscanning in differentiating malignant from benign asbestos-related pleural disease. Am J Ind Med 1986;9:487-94.

16 Becklake MR, Fournier-Massey G, McDonald JC, ShemiatyckiJ, Rossiter CE. Lung function in relation to chest radiographicchanges in Quebec asbestos workers. Bull Physiopathol Respir1 970;6:637-59.

17 Zitting A, Huuskonen MS, Alanko I, Mattson T. Radiographicand physiologic findings in patients with asbestosis. Scand JWork Environ Health 1978;4:275-83.

18 Jarvholm B, Sanden A. Pleural plaques and respiratory function.Am J Ind Med 1986;10:419-26.

Accepted 14 August 1989

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All manuscripts submitted to the Br J Ind Medshould conform to the uniform requirements formanuscripts submitted to biomedical journals(known as the Vancouver style)The Br J Ind Med, together with many other

international biomedical journals, has agreed toaccept articles prepared in accordance with theVancouver style. The style (described in full inBr Med J, 24 February 1979, p 532) is intended tostandardise requirements for authors.

References should be numbered consecutivelyin the order in which they are first mentioned inthe text by Arabic numerals above the line oneach occasion the reference is cited (Manson'confirmed other reports2 - ...). In future refer-ences to papers submitted to the Br J Ind Medshould include: the names of all authors if there

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International Steering Committee of Medical Editors. Uni-form requirements for manuscripts submitted to biomedicaljournals. Br Med J 1979:1:532-5.

2 Soter NA, Wasserman Si. Austen KF. Cold urticaria: releaseinto the circulation of histamine and eosino-phil chemo-tactic factor of anaphylaxis during cold challenge. N EnglJ Med 1976;294:687-90.

3 Weinstein L. Swartz MN. Pathogenic properties of invadingmicro-organisms. In: Sodeman WA Jr. SodemanWA. eds. Pathologic physiology. mechanismsof disease. Philadelphia: W B Saunders. 1974:457-72.

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