Document X7D0Go6oExY3Nw2VMVX7nN4Mg

FILE NAME: Asbestos Cement Pipe and Sheet (ACPS) DATE: 1966 DOC#: ACPS011 DOCUMENT DESCRIPTION: Published Journal Article tOctober i960 I WroBAD- MLD- J - {1966)' 42' 623- and Hammond, E. C. (1965); arc to Asbestos and Meso- Med., 272, 560. fK SiusS X , : ro3 I THE IAN. Au. `J. 0931): Asbeessttoo^^; r" a Study i ' " ' " :stos Mill EPIDEMIOLOGY AND CLINICAL FEATURES . _ ' ' C. J., and Coleman, E. H. 1 t of Two Cases, Arch. Path., ` . ... . ' OF ASBESTOSIS AND RELATED DISEASES a, R. O., and McDonald,I * s a Modern Urban Hazard, ' 1 Asbestosis and the Urban I Sci., 132, !96. *;{ . T . M ., a n d P r a t t , P . c . '-=J udics of Asbestosis, Arch, P. C. Elmes, B.M., M.D., M.R.C.P. Reader in Therapeutics and Pharmacology, Institute o f Clinical Science, The Queen's University o f Belfast, Belfust 12. .,,and M archand, P .(I960); oma and Asbestos Exposure ff ; Province, Brit. J. industr. Jj onal Communication. iore, J. W. (1965): Asbestos >| ;tention in Rats, Ann. N. Y. J , and S mith, M arilyn N . I'; olonic Mucosa by Asbestos"- Microscope Study in Rats 71 Invest.. 14, 2029. - i; e, S. R. (1930): Pulmonary c. S. R. (1934): Pulmonary"! One Hundred Cases, Ibid., 2, l] is. Postgrad, med. J., 25, 631 ; JURIS0 the last 100 years many materials have been yjgd by industry for a while and then found to have unexpected harmful effects. Usually the risk ceases u'ften safety measures are adopted but sometimes jliese measures are found to be inadequate and new ones must be introduced. This has happened (ucently after the re-investigation of flax byssinosis (Carey, Elwood, McAulay, Merrett and Pemberton, 1965). . . gut with asbestos the situation is not so simple. Rowing the report in 1930 (Merewether and Price) pn the dangers of exposure to asbestos dust safety (,,easures were adopted in factories and certain porkers kept under medical surveillance. Since (hen a series of other risks have been recognised ^ ch indicate that the measures were either ,,adequate or did not cover a sufficiently wide variety of asbestos workers. Both cancer of the h,ng and mesothelioma are now recognised as jesulting from levels of exposure to asbestos which jull occur in spite o f these measures. , The summary of present knowledge about the epidemiology of asbestosis and related diseases which follows is necessarily brief and emphasises (ho# points at which our knowledge is as yet ,,complete. fte Nature and Uses of Asbestos The word asbestos is used to cover a group of fibrous silicate minerals whose chief value is that jhey have a high melting point and are non-inj^nunable. Therefore asbestos is used as strength ening r insulation where high temperatures occur, jut because it is relatively cheap and strong (the hifcs are comparable in tensile strength to steel), jdd is resistant to many chemicals and to abrasion, gbestos has many other uses. These other uses j^ u n t for the increased consumption of asbestos ,,an industrial city since 1940 (Fig. 1) (Elmes and Cade, 1965). Asbestos cement is used to protect the steel framework of modern buildings against fire, to form pipes and ducts for water, air and chemicals and to form corrugated roofing. Asbestos is incorporated in brake pads and linings and in heavy duty flooring. Soft asbestos boarding and tiles are used to give heat and sound insulation to ceilings and asbestos is sprayed on to the insides of air conditioning ducts, roofs and pipes to prevent condensation. Asbestos is spun and woven to make fire protective clothing, oven cloths, wicks for oil stoves etc. It is even used in the filters of certain types of gas mask. Three types, chrysotile, crocidolite and amosite make up the bulk of the asbestos used. Of the others such as tremolite and actinolitc only anthophyllite is of particular medical interest. Chrysotile is mined in (he greatest quantity and is mineralogically separate from the others being a pyroxene while the others are amphiboles (Table I). They were all formed early in geological history probably about 2,000 million years ago. They were produced when the original rocks were subjected to hot water under pressure. As the rock formation cooled these compound silicates crystallised out in fibrous form. The type of deposit and length of fibres depended on the condition of the parent rock. Most chrysotile asbestos was formed in cracks between shattered fragments of serpentine, a relatively hard rock. But the amphibole asbestoses were deposited in the interstices of sedimentary rocks such as banded ironstones. Harrington (1962) has demonstrated the presence of oils and waxes which suggest that organic matter must have been present when the fibres formed. These may be the cause of the fibrogcnic and carcinogenic activity of asbestos. Modes of Exposure Mining Asbestos is obtained from both open cast and 624 POSTGRADUATE MEDICAL JOURNAL Tenna? SHIPBUILDING and ASBESTOS IMPORTS. Belfast, 1906--1960- October 1966 1900 IO 2 0 3 0 4 0 50 6 0 7 0 Counnjr Horbour Citortr. F ig. 1--The dramatic increase in tonnage of asbestos imported to Belfast since 1940. (See Elmes & Wade, 1965). Narr.e Chrysotile Crocidolite " Blue" Amosite Anthophyllite TABLE 1 K inds of A sbestos in Commercial U se Formula and Geological Name Mg3 (Si2 Os) (OH) 4 Chrysotile Na2 Fe3+ + Fe2+ + + (Sig O22) (OH,F)2 Riebeckite (Mg, FeT + )7 (Sis O22) (011)2 Cummingtonite (Mg, Fe+ * )7 (Sig O22) (OH, F)2 Anthophyllite , (always mixed with Gcdrite) Estimated Total Production (1962) 3.2 million tons Including actinolite and tremolite Percentage of world production* 93 3.5 2.4 1.1** October 1.966 October 1966 ELMES: Epidemiology o f Asbestosis 625 . <k*p mines. Drilling and explosives are used when I the host rock is hard and mechanical excavation ;-s hen it is softer. The crude ore is milled to remove the host rock and the fibrous asbestos is partially leared out before it is packed into bags. Where labour is cheap some of the separation of rock {join fibre is done by hand (cobbing) by women often accompanied by their babies. Until recently - large amounts of asbestos fibre escaped into the air . from the mines and mills so that not only the miners and millers but the whole population of the mining towns and the surrounding countryside have tsen exposed. It was customary to transport asbestos from the ; mines to the factories in jute bags. This exposure ;; of a whole series of transport workers could be / ' eliminated by using sealed impervious bags. ffork in asbestos factories It was here that the danger of exposure to isbestos dust was first recognised and investigated. The asbestos is teazed out again so that the fibres tre separated and particles of rock etc., removed. The next process depends upon whether the fibre is lo be woven into a textile or mixed with some binding material for the fabrication of boards, pipes etc. The textile procedures are similar to those used in the wool and cotton industries, carding being the dustiest. In the fabrication of hoard and cement products there was a considerable jzard when the product was cut and trimmed or machined. JJo special effort was made to suppress dust in these factories and the dust was everywhere in them. Although all workers, even the clerks in the jjhces, were exposed, some jobs were worse than others. Where forced ventilation was used the dusty air was often discharged unfiltered producing high levels of air pollution close to the factories. . The protection of workers at certain scheduled processes from asbestos dust became compulsory under the Government regulations which followed the publication of the Merewether report (Merewether and Pr.ce, 1930). The workers also jume under compulsory medical supervision and there was an incentive for the relatives to ask for an tuiopsy wheh a death occurred. Cleaning up the itry dusty processes and filtering the effluent of the exhaust ventilation systems also reduced the general air pollution of the factory- and its environment. Although measurements of the dust concentrations ^erestarted at this time they are technically difficult. They may not detect the smallest fibres, and these pay be as harmful and be disseminated more widely than the larger fibres. OKof asbestos goods The products o f the asbestos factories are not usually supplied direct to the public but arc used in the manufacture of factories, houses, power units, ships, cars, domestic stoves etc., by a variety of skilled tradesmen with their helpers. These men sometimes use powdered material which they mix and apply on the spot or they use prefabricated blocks, quilts etc., which require cutting, sawing or shaping to make them fit. The materials are usually rough-finished when they leave the factory and release some dust when handled by storemen and transport workers. Insulation workers have been using asbestos goods in this way for a long time. More recently building workers, interior decorators and many others have started to use them. Others (electricians, plumbers, fitters, paint ers etc.) may work in the same confined space as insulators and become exposed to the same dust or may create dust cutting or drilling asbestos material in the course of their own work. .Most asbestos materials are coated with paint or sandwiched between other materials so that they do not present a continuing risk until the building or installation is demolished. But asbestos roofing I and brake linings must cause some general atmos- I pheric pollution and certain uses such as the lining of air condition ducts with soft asbestos and the use of unsealed ceiling tiles cause continuous, pollution of the air o f office and factory buildings where people work all day. A simple industrial history will not necessarily -- reveal exposure to asbestos when this has occurred. \ A careful description of the type of work and the I materials encountered at work will often help but I there remains the unpredictable exposures, which will only be revealed by chance. A woman of 53 (Fig. 2) was recently investigated following a spontaneous pneumothorax. She had been increas ingly breathless and been under observation by the Chest Clinic because of pulmonary fibrosis for several years. The findings were compatible with asbestosis but the patient denied occupational exposure. A few days later she told the house physician that she had helped her husband build two asbestos bungalows in 1947-8. She had held I the sheets while her husband sawed them up and 1 they lived in one of the bungalows for about two \ years before painting over the asbestos sheets 1 lining the walls and ceilings. The husband was a | deck-hand on a long-haul merchantman and also had no `occupational' exposure to asbestos. X-rays taken when he was next in port revealed a similar extensive fibrosis although he was still able to work. Similar unexpected sources of exposure can be revealed by retrospective investigation of patients dying of asbestosis or its complications. Newhouse and Thompson (1965) describe the wife who brushed the asbestos dust ofT her husband's clothes when he came home in the evenings. 626 POSTGRADUATE MEDICAL JOURNAL October 1966 Oclot, 1931 and 1949 no less than 31 T, had active tuber r culosis at ncciopsy computed with only 4 healed lesions found in 71 nectopsies earned out between 1957 and 1964 on cases from the same source (Table 2) (Smither, 1965). This difference in exposure and absence of complicating tuberculosis results in a more insidious onset of symptoms which may start 20 or 30 years after first exposure to asbestos and may even develop yeais after the exposure has ceased. ' i Symptoms The first symptoms arc breathlessness on exertion and productive cough. The breathlessness is relatively severe compared with the accompanying cough and spit and is not associated with upper i respiratory infections or adverse weather conditions. But when 50 asbestos workers were carefully Fig. 2--Woman aged 53 who helped her husband build two asbestos bungalows 18 years befoie. Her husband shows similar changes. Diffuse fibrosis with linear markings in the lower zones. Pleural thickening with loss of clear demarcation of diaphragms. The scarring or 'large opacities' in the middle and upper zones may represent inactive tuberculosis. The Diseases Related to Asbestos Exposure Asbestosis Many descriptions of asbestosis appeared in the matched wulh controls recently both severe cough and more than minimal sputum production were significantly mote frequent. 1 Bain in the chest is emphasised in the early literature, but our patients more often complain of a 'tightness' than a pain. This is unrelated to effort and comes and goes unpredictably. Sometimes it may be described as a pain by the younger and more apprehensive asbestos worker who may show no definite evidence of asbestosis. Severe gnawing pain suggests the development of some complication Clubbing and H arts: As in other conditions of Fig. 3-- f t f I n o u literature between 1924 and 1933. Descriptions insidious onset associated with clubbing of the such as those of Seiler (1928), Cooke (1927), Oliver fingers only the occasional patient is aware of t (1927) and Wood (1928) refer to fibrosis resulting from a level of dust exposure far in excess of those experienced now. There have been two changes since, the disease now comes on more slowly and there has been a virtual disappearance of con comitant tuberculosis. In Wycrs' series (Wyers', Clubbing docs not seem to occur in the absence of significant chest disese and is not invariably present when the chest disease is severe. Warts are common in people who handle asbestos and arc liable to have cuts or abrasions of their hands. 42 per cent ofj group of 100 insulators had these at the time of ( past. Thv hyperkert this centr disappear years. 1949) collected at an east London factory between examination and a further 26 had had them in ,k f Physical s TABLE 2 . t The m. cyanosis, rales hear Post Mortem F indings in A sbestos Factory W orkers fingers. 1 3) with d ( A m u Smiu iir 1965) six were c and 13 h 1931 -49 1957 - 64 frequent e Number of cases Age at death Tuberculosis Carcinoma of lung Primary pleural malignancy Primary peritoneal malignancy Other abdominal malignancy 115 40.8 36 17 1 0 7 lesions inactive 71 " 56 4* 26 2 13 7 Cough (oik Spit ("Durn Brcathlessn Oubbing o Warts . Cyanosis . Basal 'dry'  October 1966 October 1966 EL MES: Epidemiology o f Asbestosis 627 id active tuberonly 4 healed cd out between e same source id absence of more insidious 20 or 30 years md may even ceased. less on exertion eathlessness is accompanying ted with upper tlier conditions, were carefully h sexere cough iroduction were d in the early ten complain of related to effort '. Sometimes it mnger and more i may show no severe gnawing ne complication, r conditions of lubbing of the is aware of it. l the absence of variably present irts are common re liable to have 2 per cent of a at the time of had them in the 757 - 64 71 56 4* 26 2 13 7 Fig. 3--Pipe coverer (insulation worker) for 16 years; died at 65 years of carcinoma of the stomach. No metastasis found in the lung at post mortem. Diffuse fibrosis with linear markings in the middle and lower lobes. Loss of clear outline of both diaphragms. The scarring in the right upper zone was not tuberculous. Flo. 4--Pipe coverer (insulation worker) for 26 years; died at the age of 71 sears of cor pulmonale. Ill addition to the dilluse fibrosis there is extensive calcification of pleural plaques more marked on the left than the right. There is some generalised plcuial thickening and a loss of clear demarcation of both diaphragms and pericardium. past. They start as a lump in the skin which becomes hyperkeratotic and a central white area appears. If lliis centre is picked out with a pin the lesion will disappear but otherwise it will persist for months or years. physical sign* The main features of the more severe case are cyanosis, restricted chest movement, kyphosis, fine rales heard over the lung bases and clubbing of the fingers. In a group of 21 insulation workers (Table 3) with definite asbestosis w'ho were still at work, xvvere cyanosed, 7 showed clubbing of the fingers 13 had basal rales. The signs became more frequent and marked as the disease progresses and when definite signs of right heart failure appear the men are unable to work and are unlikely to survive the next acute respiratory illness. The rales and clubbing together present a pattern which it is easy to distinguish from chronic bronchitis. The rales have a characteristic fine " dry" character which is persistent in spite of deep breathing or coughing. They are often mistaken for a rub and are so described in the earlier literature. These signs are of no value in distinguishing asbestosis from other forms of chronic interstitial fibrosis with clubbing of the fingers. But with restriction of chest move ment, kyphosis (loss of height) and cyanosis they are useful in the detection and assessment of asbestosis in workers on whom serial examinations TABLE 3 S ymptoms and Signs in Early A sbestosis in 21 W orking Men with D i:itnitl Radiological C hanges Cough (other than `in mornings only') .. 14 Spit ^During the day' as well as `in mornings') 10 greathlessness (M.R.C. grade 2 or more) . . 4 Clubbing of the fin g e r s........................................... 7 Warts .............................................................. 16 6 a l `dry' rales.............................................. 13 628 POSTGRADUATE MEDICAL JOURNAL October October 1966 are carried out. For instance in this survey of phragm or pericardium they are rounded, but o; fibres. These are nc insulation workers it was found that the 21 men with definite pulmonary fibrosis averaged l i inches the chest wall they are guttate and lie along the li^i tion. If the sputum of the ribs usually from the mid-axillary antiformin and the shorter (making allowance for age) than those with forward. They are not easy to sec on X-ray unt; contrast or with tl no evidence of pulmonary fibrosis. they begin to calcify. When calcified plaques ha^ asbestos bodies sh a characteristic appearance with clear cut margin polarised light ma; X-ray changes and a bilateral distribution (as in Fig. 4) they asbestos fibres Tl The changes which result from exposure to asbestos can occur with other forms of chronic probably diagnostic of asbestos exposure. The,! cates current ex may appear before the parenchymal changes indicate exposure i diffuse fibrosis involving the pleura. Localised have been used by Kiviluoto (1965) to plot t|*i Neither can be coi areas of damage resulting from tuberculosis or intercurrent infections give rise to an irregular environmental area of asbestos exposure in Finlani[ patient has asbesto In the Belfast series of dead asbestos worktrl X-ray changes or tl scarring in the upper or midzone (Figs. 2 and 3). Linear markings in the periphery appear first in the lower zones. They run out into the pleura and with increasing change join to produce a honeycomb or cystic appearance at the base. There is loss of the clear-cut margin between lung and pleura over the diaphragm and pericardium. By the time this appearance has developed at the bases, linear markings are usually apparent over the whole lung there were 13 with plaques out of the 87 for whorj chest X-rays were available. In a survey of l(U living pipe coverers of varying ages in the same arql six showed plaques and the only one under 40 yejJ of age had been exposed in childhood. t Plaques are very common in and around tl,r anthophyllite mining areas in Finland and j# workers in Eastern Germany using anthophylliJ and other fibres. In South Africa they are st^?- on X-ray is due to e Respiratory Jiinct groups of asbestos v, able controls there : result from :-- (i) Low total lun (ii) Low vital c airways obsti and there are usually some localised scars (" lung both in the blue asbestos and in the amosite minii Low pulmor opacities" as defined by the I.L.O. classification of 1958). The early changes do not reproduce well but all the films (Figs. 2 - 6 ) show easily recognisable linear shadowing with loss of the clear-cut line of the pleura. An adaption of the I.L.O. classification of X-ray changes in pneumoconiosis to make it applicable to asbestosis is at present under discussion (U.l.C.C. Report, 1965). This will enable the findings of different groups to be compared. Pleural thickening, as opposed to the loss of clear demarcation between lung and pleura, can take two forms. The first is a diffuse thickening with ill-defined margins which is most marked over the lower lobes and is related in severity to the parenchymal change. The second is the formation areas (Sluis-Cremer, 1965). The incidence in t| ehrysotile mining areas of Quebec varies from mir^ to mine (Cartier, 1965). Although mesotheliorry have developed in patients with calcified plaqu^ they are not necessarily associated. Mesothelion&f are unknown both in Finland, and in the amosJ areas of South Africa where plaques are qu|J common (Table 4). t Laboratory tests No test, short of lung biopsy, is diagnostic, asbestosis, but some tests results support t| diagnosis:-- Sputum: The sputum is mucoid unless there complicating bronchial infection. There are specific cytological changes but malignant cells r; Low diffusin; Williams and 1-1ug malities in diffusing before X-ray change Belfast insulation w diffusion test is less sc of early evidence of i There is a large i tests and each may t <jf diseases. Therefor the detection of ear! ease unless serial rea available (Bader, B 1965; Hunt, 1965). feet is the best estii of plaques which are circumscribed areas of hyaline fibrous tissue in the parietal pleura. On the dia be found before there is other evidence of carcinoi The sputum may contain both asbestos bodies ffce Complications o r _ The pattern of mo TABLE 4 'asbestos workers ha: *ork have improved, G eographical R elationship Between Plaques and M esotheliomas put into the sacks amosite in the mills (Schepers, 1965) sc Area Fibre Plaques Frequency of Mesotheliomas asbestos board in the enclosed and subject Finland E. Germany S. Africa S. Africa Quebec mines and \ related textile millsJ Insulation Workers: New York Belfast Anthophvllite Anthophyllite and other fibres Crocidolite Amosite Chrysotile Mixed Mixed Common Common Common Common / Sometimes rare \ \ Sometimes common j Common Common None 6 since 1957 Common None Rare Common Common . In some factorie: L fibrosis used to occut ^ men who have \ ^'without any detect | fibro is. Heavily ex "work in the factorie complications of asb F they were stll! at wor jftcr a short period --t fcarcinoma o f the Ii . October 1966 . October 1966 FLMLS: Epidemiology o f Asbestosis 629 are rounded, but on and lie along the line ,he mid-axillary line to sec on X-ray until :alcified plaques have ith clear cut margins ts in Fig, 4) they are ;tos exposure. They ichymal changes and 0 (1965) to plot the s exposure in Finland, ad asbestos workers it of the 87 for whom In a survey of 100 ages in the same area ily one under 40 years tildhood. 1 in and around the in Finland and in y using anthophyllite Africa they are seen in the amosite mining The incidence in the ebec varies from mine hough mesotheliomas with calcified plaques :iated. Mesotheliomas d, and in the amosite re plaques are quite opsy, is diagnostic of results support the nucoid unless there is ?tion. There are no ut malignant cells may evidence of carcinoma, h asbestos bodies and y of Mesotheliomas - None 6 since 1957 Common None Rare , Common Common (jbre$- These are not easy to see on direct examina tion. If the sputum is first treated with " Fuso!" or jntiformin and the sediment examined by phase gjjntrast or with the substage condenser lowered asbestos bodies show up clearly (Gloyne, 19.12). polarised light may be needed to recognise the jsbestos fibres. The presence of fibres only in dicates current exposure and asbestos bodies indicate exposure in the recent or distant past. Neither can be considered proof either that the patient has asbestosis in the absence of definite X-ray changes or that the pulmonary fibrosis seen on X-ray is due to exposure to asbestos. Respiratory function tests: When applied to groups of asbestos workers compared with comparjble controls there are clear-cut differences. These result from:-- () Low total lung volume. () Low vital capacity without evidence of airways obstruction. (i) Low pulmonary compliance. (v) Low diffusing capacity (transfer factor). Williams and Hugh-Jones (1960) reported abnor malities in diffusing capacity for carbon dioxide before X-ray changes in factory workers. But in gelfast insulation workers the carbon monoxide diffusion test is less sensitive than X-rays in detection ofearly evidence of asbestosis. There is a large range of normal for all these jjsts and each may be made abnormal by a variety 0fdiseases. Therefore the tests are of little value in he detection of early asbestosis in the individual jjse unless serial readings over previous years are available (Bader, Bader, Tierstein and Selikoff, 965; Hunt, 1965). The extent of the diffusion defect is the best estimate of disability. The Complications of Asbestosis The pattern of morbidity and mortality amongst jsbestos workers has changed as the conditions of svork have improved. Just as children are no longer put into the sacks to stamp down the fibrous jmosite in the mills in the South African mines (Schepers, 1965) so the machinery for cutting jsbestos board in the modern factory is automated, tnclosed and subjected to exhaust ventilation. In some factories where crippling pulmonary fibrosis used to occur in less than 10 years, there arc now men who have worked continuously since 1933 without any detectable evidence of pulmonary fibro is. Heavily exposed workers were unable to i0rk in the factories for long enough for the late c0mplicalions of asbestos exposure to appear while hey were still at work. But those who left the work after a short period of exposure lived to develop carcinoma o f the lung and mesothelioma of the pleura. These cases have only recently been brought to light by studies in which the fate of workers w-ho left factories before 1933 arc being traced (New house, 1966). The second factor which delayed the recognition of the malignant complications was the long interval between first exposure and the deselopment of malignancy. The asbestos industry had started on a small scale at the end of the last century and continued to employ small numbers of men and women until the first World War. A large popu lation did not reach the length of exposure or age for cancer until 1940 - 50. Since 1931 all workers in the scheduled occupa tions in Great Britain have been registered and kept under medical supervision. Their deaths are reported to the coroner and a postmortem is usually carried out so from (hat time the cause of death amongst workers who were already in certain jobs in the asbestos industry is fairly accurate ly known. It was not until the figures for 1947 were published (H.M.S.O. 1949) that an undue incidence (13%) of death due to cancer of the lung was noticed. Amongst the men there were no cases of cancer of the lung under the age of 45 but above that age they amounted to 22 out of 76 with a peak incidence in the 55 - 64 age group. .Detailed studies on one asbestos textile factory has confirmed the high incidence of cancer of the lung (Knox, Doll and Hill, 1965) but indicate that only workers exposed to the heavy dust concentrations before 1933 were at risk. Although workers taken on after that date in that factory appear to run no greater risk of developing cancer of the lung than other sections of the population, the national figures still show' a rising incidence. Nearly 50% of deaths in workers with certified asbestosis in the 1961-3 period were due to intrathoracic tumours (Buchanan, 1965). Studies from another asbestos factory (Smither, 1965) reveal a similar change in pattern (see Table 2). Tuberculosis has been replaced by primary carcinoma of the lung and by mesothelial tumours of the pleura and peritoneum. In Dresden the causes of death for asbestos workers have been recorded separately since 1952 (Jacob and Anspach, 1965). There were no cases of intrathoracic tumours among 18 deaths in the first year but in the next two five-year periods the incidence was 19% and 29% of 47 and 85 deaths respectively. One-fifth of these intrathoracic tumours were mesotheliomas of the pleura. The duration of e'xposure for these cases varied between two and 42 years (average 14.2 years) and the average latent period for all intrathoracic tumours was 30.7 years and for mesothelioma was 31.8 years. The epidemiology and pathogenesis of these two tumours, cancer of the lung and mesothelioma, is  -- !*$ t J ! I ! ' W 1 ! a -Vt<M ...&_i*-$*&3* R lS ^ t* ;!'V .f safe-v -? 630 POSTGRADUATE MEDICAL JOURNAL October 1966 still under investigation in relation to asbestos exposure. Cancer o f the lung This appears to occur in workers exposed to any type of asbestos fibre but statistics are xery fiagmentary. It has been obserxed in all mining areas, but little accurate information is available to compare with the general population allowing for factors such as smoking and atmospheric pollution. Finland is a country xvith a high tate for cancer of the lung anyxxay and in all countries the rapidly rising incidence which has been attributed to cigarette smoking makes all such statistics difficult to interpret. The factory populations (Knox, Doll and Hill, 1965; Smither, 1965; Jacob and Anspach, 1965) already mentioned show an incidence of pulmonary or pleural neoplasms of the order of 30% amongst men exposed to dusty conditions which arc not sufficiently severe to cause death due to pulmonary fibrosis and respiratory failure in more than 20%. This risk of cancer of the lung amongst workers exposed to factory conditions before any effort at dust suppression has been estimated as 15 times that expected. The conditions under which insulators work have only changed gradually over the years. Part of this change has been due to the introduction of pre fabricated materials which arc easier and less dusty to handle. More recently materials which do not contain asbestos have been used. Although masks have been supplied for certain very dusty jobs such as limpet spraying no deliberate effort has been made to reduce the dustiness of this type of work. In Belfast all insulators oxer 50 years of age and 30 years of exposure so far examined show definite exidence of pulmonary damage whereas only about 3()",, of men between the ages of 30-40 or with 10-19 years of exposure show such evidence This suggests a degtee of exposure less than that which existed in some of the factories before 1933 but more than that described by Knox and others (1965) following that date. 107 deaths in insulators in Belfast since 1940 haxe been investigated so far. The causes of death are given in Tabic 5. There is a moderately high incidence of non-malignant respiratory deaths but it is not far m excess of that expected as in the fitst half of the period tuberculosis was still relatively common. It has not been easy to differentiate betxvcen deaths due to cancer of the lung and those due to pleural mesothelioma where no autopsy material has been preserved. They haxe been classified together and arc about five times the expected. There litis been no definite change in pattern of deaths amongst insulation workers over the years j (see Fig. 6) apart from the disappearance of ~2 pulmonary tuberculosis. The age of death, pro portion of cases xvith pulmonary fibrosis and proportion with cancer have all remained the same suggesting a constant level of exposure at least until 10-15 years ago. ' Hammond, Selikoff and Churg (1965) have found an incidence of intrathoracic tumours in insulation workers seven times the expected and also a high rate of gastrointestinal neoplasms. The peak mortality due to lung cancer for men in all reported series of asbestos workers is between 55 and 60 years of age and the only clinical difference between these and other lung cancers is a higher proportion TABLE 5 C ause of D eath in Insulation W orkers Belfast 1940 - 65 Total: 107 Mean A ge: 55.3 T 11.25 Y ears Cause Observed Expected* Malignant :-- Intrathoracic neoplasms Abdominal neoplasms Other neoplasms Non-Maugnant :-- Pulmonary disease Cardiac and circulatory Other causes Unknown 28 5.3 15 9.0 4 6.7 31 25.6 21 37.1 5 21.3 3 "" This is a rough estimate based on the Registrar General's distribution of deaths in the age group 45 - 64 in the year 1951 (H.M.S.O. 1953). StJk a TNbst m m m Tm z- October 1966 1 ' i 50 years of age and imined show definite 1 whereas only about s of 30 - 40 or with . low such evidence, osurc less than that actories before 1933,. c by Knox and others C ' deaths in insulators , i investigated so far. in Table 5. There is ; of non-malignant far in excess of that ie period tuberculosis I has not been easy due to cancer of the mesothelioma where , (reserved. They have : : about five times the change in pattern of tkers over the years e disappearance of age o f death, prolonary fibrosis and II remained the same >f exposure at least irg (1965) have found umours in insulation ;ted and also a high ' iplasms. The peak , ir men in all reported between 55 and 60 . xiI difference between ; a higher proportion October 1966 4030- ELMES: epidemiology o f Asbcstosis 631 Distribution of Deaths by Year of Death. 1940 -44 . 1945 -49- 1950 -54 1955 -5 9 . I960 -64 . NonMalignant apparen unrelated lo asbestos. f : : I Pul m o n a ry Jfibrosis . co n trib u to ry. I Malignant. IO - zo o ~ Mean Age. 50-7 Hran Exposure 16 (Years) ' Fig. 5--The increasing number of deaths relating to successive five year periods may be due to increasingly efficient case finding rather than a change in the death rate among insulation workers. TABLE 6 Mesotheliomas and Exposure to Asbestos Examples of Retrospective Studies Sojrce . Expected* 5.3 9.0 6.7 25.6 37.1 21.3 ie age group 45 - 64 in ' London Mewhouse & Thompson (1965) Belfast Elmes & Wade (1965) Liverpool Owen (1965) South A frica Wagner, Sleggs & Marchand (1960) Total .. . Total Cases 76 Controls 76 Cases 42 Controls 42 Cases 17 Controls 0 Cases 33 Controls 0 Cases 168 Direct 31 8 8 2 7 14 60 36% Exposure Casual Environmental or Domestic 0 9 0 1 24 0 7 0 6 0 5 13 35 22 21% 13% None 36 67 10 3 4 1 51 30% 632 POSTGRADUATE MEDICAL JOURNAL October 1966 F ig. 6--Pipe coverer (insulation worker) for 26 years; died of a primary carcinoma of tlie lung aged 66 years. Linear marking and small opacities in the middle and lower zones. Loss of clear demarcation of the diaphragm and pericardium. The peripheral tumour in the left upper lobe is indistinguishable radiologically from a mesothelioma. of lower lobe tumours (Jacob and Anspach, 1965). The symptoms, signs and X-ray changes of cancer of the lung are too well known to require description here. Fig. 6 shows the chest film of an insulation worker with both asbestosis and a primary cancer of the lung. In all the cases of proven primary carcinoma of the lung in the Belfast scries there was histological evidence of asbestosis, but this was not always obvious on X-ray. Mesothelioma Epidemiology: This tumour has been the subject of considerable research and comment since McCaughey (1958) described a series of cases in Belfast and Wagner and others (1960) related an even larger series to environmental exposure to blue asbestos. The histological evidence relating mesothelioma to the inhalation or ingestion of asbestos is very impressive. When a history of exposure to asbestos is looked for in cases of mesothelioma it can usually be found (Table 6). But in only a third of cases is this exposure of the sort of intensity that might ! i r t u ir tl b y t th Fig. 7--Pipe coverer (insulation worker) for nearly 30 years; died at 44 years of a mesothelioma of the left pleura. The tumour is visible above the level of the left basal effusion. There is a partial collapse of the right lower lobe. Pulmonary fibrosis, though present, is not sufficient to sho* in the reproduction. cause asbestosis or carcinoma of the lung. ln another third of the cases there is an apparently trivial exposure at work or in the home environment The environmental exposure ranged from playinj on the slag heaps outside an asbestos mine up to the age o f seven years in a woman who died of a mesothelioma at the age of 35 (Wagner, Sleggs and Marchand, 1960) to the woman who developed j mesothelioma at 63 years and who used to was! out her daughter's overalls when the latter worker in an asbestos factory (Newhouse and Thompson. 1965). Casual exposure at work ranged frorr. occasionally having to remove the remains o! lagging from machinery which was being dismantle; for servicing, to the repairing of hessian bags sorrt of which had been used for asbestos (Owen, 1965] The relatively large group (30"/) with no histor, of exposure can be accounted for in three ways:- 1. Occupational exposure which the patient ha; forgotten or in which he was unaware of th* nature of the materials handled. 2. Environmental or domestic exposure of win'd the patient was unaware. 3. No exposure at all. In (I) and (2) one would expect to find asbest;, bodies or fibres in the lungs. In a retrospect!,; study of 20 patients dying with asbestos bodies ] id in 0 ar A1 ar an fre fac so Ih; ex I wo ex! exp inc am ma ( occ chi dur yea bet exp pul Pie 1 J inc wei Bey be adr se\ rou sur of bot pat firs ' October 1966 October 1966 ELMES: Epidemiology o f Asbestosis 633 the lungs the source of exposure was only found in |4 (Elmes and Wade, 1965). This deficit could iccount for all the mesotheliomas for whom no history of exposure is obtained. Nevertheless there remains the possibility from epidemiological studies that a small proportion of mesotheliomas occur in patients who have never been exposed to asbestos. - Because of the trivial exposures recorded in a \ third of the cases and the increasing and manifold use to which asbestos has been put we can expect an increasing number of mesotheliomas at least over the next 40 years. (In the London series the interval between first exposure and death varied between 29 years for factory exposure and 48 years for environ mental exposure. For the Belfast group as a whole the interval was 43 y ears 13). ` Numerous cases of mesothelioma have been identified amongst people u'ho have lived or worked jn blue asbestos mining areas in South Africa (Table 4) and cases have been reported from the area around the crocidolite mines in Western Australia. No cases have been reported from around the amosite mines in South Africa or the worker) for nearly 30 a mesothelioma of the - is visible above the ,ion. There is a partial wer lobe. Pulmonary s not sufficient to show jnthophyllite mines in Finland and only two cases from the Quebec chrysotile mining area. Much factory work entails exposure to mixed dusts but 50 far the evidence from the factories indicates hat frequency of mesotheliomas may vary with the jxtent to which blue asbestos is used. In insulation ^rkers it is usually impossible to identify the jjient to which individual workers have been la of the lung. In i jxposid to individual types of asbestos. The ere is an apparently - ucidence of mesothelioma amongst these workers ie home environment. | and amongst other workers exposed to the same ranged from playing jnaterials is relatively high. asbestos mine up to Clinical features o f mesothelioma: This tumour oman who died o f a ^ r s in either sex and people exposed during (Wagner, Sleggs and uldhood may develop it earlier than those exposed ian who developed a urjng adult life. The age of onset varies from 31 d who used to wash' -ar$ to 83 years and the mode for most series lies ten the latter worked jttween 55 and 65 years. Other evidence of asbestos ouse and Thompson, jjposure (clubbing of the fingers, asbestos warts, work ranged front; pjmonary fibrosis and basal rales) is often absent. ove the rem ains of was being dismantled ' inal cases of hessian bags some > Mode o f onset: This usually starts with gradually sbestos (Owen, 1965). greasing pain or breathlessness, taking several 30%) with no history ^ics before the patient seeks medical advice, for in three w ays:-, ^ause of this insidious onset the condition may which the patient had j found accidentally. One patient recently was c was unaware of the fitted to hospital with a fall, another with handled, ptre influenza and yet another was submitted to stic exposure of which pjiine chest X-rays as part of an occupational .jvey. Only on direct questioning was the history jfpain or breathlessness elicited. The onset of xpect to find asbestos s. In a retrospective ith asbestos bodies in ptli symptoms is sometimes so gradual that the client is unable to say which symptom started (, The pain is described as a heavy feeling and confined to the affected side of the chest at first and then radiates to the shoulder and epigastrium. It becomes more severe, a "dull toothache'' little influenced by respiration on movement unless there is a secondary fiozen shoulder. In a few cases breathlessness comes on in a matter of hours or 2 - 3 days, and in these cases there is usually a large pleural cfTusion which is sometimes bloody. But even in these cases there is seldom much evidence on examination of a shift of the mediastinum to the opposite side. As the tumour extends around the lung there is restriction of movement on that side with a shrinking down of the whole of that side of the chest and a pulling over the heart and mediastinum to the affected side. Tumour may become palpable in the supraclavicular fossa and between the ribs but seldom grows through the chest wall unless it is along the track of a thoracentesis needle, through a thoracotomy wound, at the site of a fractured rib or through an area of chest wall damaged by deep X-ray therapy. X-ray appearances (see Fig. 7) are indistinguish able in most cases from a simple pleural effusion with or without some degree of pulmonary fibrosis. The actual tumour may not be visible until the fluid is aspirated when it usually shows up as a lumpy area in the pleura which also shows some degree of thickening all round the lung. Rib destruction appears late and local lymph node enlargement is rarely apparent on X-ray. Diagnosis: This can often be made on clinical grounds after the exclusion of other causes of persistent pleural effusion in the middle-aged or elderly and the failure to find a distant primary malignancy. It is difficult to verify the diagnosis. The fluid, when clear, is often unusually viscous, but frequently contains fresh or altered blood. Cytological examination of the fluid may reveal cells strongly suggestive of mesothelioma but the diagnosis should not be based on this alone (Klempman, 1962; Naylor, 1963). The presence of hyaluronic acid (Harrington, Wagner and Smith, 1963) is also strongly suggestive but may occur with other malignant lesions of the pleura. The presence of blood interferes with this test. Especially in the absence of free fluid the diagnosis can only be verified by biopsy, but there is a variation in the histological appearance in different parts of a single tumour. There are often extensive areas of fibrous tissue which are indistinguishable from chronic inflammatory disease. Therefore needle biopsy, and even limited surgical biopsy, may fail to provide the pathologist with sufficient material to make the correct diagnosis. An open thoracotomy must be performed and pieces of tissue from different areas taken. To avoid tumour growing through the thoracotomy wound Thompson 634 POSTGRADUATE MEDICAL JOURNAL October 1966 October (1965) advocates the instillation of nitrogen mustard into the pleural cavity at the end of procedure. Treatment: Neither radical surgery nor radio therapy can improve the prognosis and both may encourage direct extension of the tumour through the chest wall. Palliative treatment should be restricted to removal of the pleural fluid to relieve breathlessness and instillation of nitrogen mustard into the space if the accummulation of fluid is rapid. Pain due to infiltration of the chest wall and vertebrae does not usually respond to radiation or systemic cytotoxic drugs; it is usually too extensive for treatment by regional nerve root section. Course and prognosis: Patients seldom survive more than a year from the time the diagnosis is established. The survival from onset of symptoms or from the earliest X-ray changes may be consider ably longer but four years is probably the maximum. Apart from increasing pain and breathlessness the patients usually remain in good health until invasion of the mediastinal tissue interferes with nutrition and they lose weight. Death is usually due to restriction of ventilation but intercurrent chest infection may complicate the terminal illness. Peritoneal cases The onset is even more insidious than in the pleural cases. The symptoms may mimic any form of abdominal neoplasm, presenting as upper or lower gastrointestinal tract obstruction with or without pain. Sometimes painless ascites is the presenting feature. The diagnosis can usually only be established by laparotomy and adequate biopsy but occasionally cytology of the fluid may be sufficient. Weight loss occurs earlier than in the pleural lesion but the interval between diagnosis and death is the same. No treatment is of any value except that the rapid re-accumulation of ascitic fluid can be checked by local nitrogen mustard therapy. Summary and Conclusions Pulmonary fibrosis due to exposure to asbestos dust in factory workers has become uncommon and when it occurs is less severe than it was before the introduction of dust suppression measures in 1932- 33. However there remain occupations which were not covered by the Merewether report which can cause sufficiently severe fibrosis to lead to death before the retiring age. Insulation workers are a group in which this is likely to occur but the spreading use of asbestos in the building industry may be leading to similar levels of exposure among occupational groups where this hazard has not existed before. An increase in the number of such cases can only be prevented by constant vigilance on the part of the medical profession in identifying this as a cause ! of diffuse pulmonary fibrosis in individual cases and bringing them to the notice of the factory inspector- ) ate. One of the difficulties here is the lack of clinical features to distinguish asbestosis from other forms of dilfuse fibrosis. When the source of exposure is not obvious open biopsy of the lung may be necessary to establish the ctm.se and initiate investigation for sources of exposure. Carcinoma of the lung resulting from exposure ' to asbestos appears to be common in patients whose exposure to the dust was insufficiently long or intense to cause crippling fibrosis. There is evidence that the risk may have been eliminated by the application of thorough dust suppression under factory conditions. But there may be many other workers handling asbestos who are still at risk as ' has been shown for insulation workers. The nature age of onset and course of cancer of the lung secondary to asbestos exposure does not appear to differ greatly from cases arising in the general population. A rapidly increasing number of cases of mesothe- . lioma of the pleura and peritoneum have been recognised in the last 10 years. It is an invariably fatal tumour for which there is no satisfactory palliative treatment. There is an association between exposure to asbestos and the development ( of this tumour. The degree of exposure in many : cases is slight and indicates that many people may ' by now have had sufficient exposure either in the course of their work, hobbies or in the home. As there is no evidence of another factor operating jn the initiation of this tumour it seems likely that increasing numbers of cases will arise in the next . 30 years. Prevention of further cases beyond that date depends on the restriction of use and greater 1. I precautions in the handling of all types of asbestos f C fibre now. It is possible that the elimination of ' one type of fibre (crocidolite) from commercial use t might reduce the incidence of the tumour very considerably. Badik, : Seliko ii. Several A. >'. B uchan, v Int rat hi 507. C arey. G Me r k it i. Flax W CARIltR, Asbesto Ir.dust. C artier. i A'. Y. A i C ook i\ W J,, ii, 10 E lmes, P. between in Belfa: G loyne, S 1351. H ammond, Neopiasi States v Neopiasi H arking r< Containi Asbestos H arrinctc (1963): 1 Fluids ol Brit. J. e. H unt. R. 830 Emp N. Y. Aca h .m .s .o . ( of Facto h .m .s .o , h .m .s .o . Registrar H.M.S.O. J aco b, G ., plasia am Acad. Sci. Kiviluoto, Further ( occupatioi 235. In writing this article I have drawn on information which has become available as a result of research woff i done in the Department of Therapeutics and Pharma, cology by Professor O. L. Wade, Dr. Jean H. M Langlands and Dr. W. F. M. Wallace as well as mysdf . some of which has not yet been published. This worfc is part of a collaborative study of the problem of asbestos t . exposure organised by Dr. J. C. Gilson. Director of the ~ M.R.C. Pneumoconiosis Research Unit at Cardiff. Tt* i. Biological Effects of Asbestos were discussed at an ' International Symposium held in New York under thj c ' auspices of the New York Academy of Sciences j October 1964. For convenience 1have quoted references ; to the proceedings of this Symposium although muchef 7 the work has also been published elsewhere. 4-' . . .. " t October 1966 ELMES: Epidemiology o f Asbestosis 635 ` October 1966 | g this as a cause ' I victual cases and 1 tetory inspector- I ie lack of clinical | om other forms j REFERENCES BadER. M. E., Badir, R. A., Tiiksiiin, A. S., and Selikoff, j, (]965): Pulmonary Function in Asbestosis. Several Tests in a Long Term Prospective Study, Ann. fry. Acad. Sci.. 132. 391. Buchanan, W. D. (1965): Asbestosis and Primary Intrathoracic Neoplasms, Ann. N. V. Acad. Sci., 132, e of exposure is ' I may be necessary | investigation for > from exposure ` .n patients whose iciently long or There is evidence minated by the ppression under / be many other c still at risk as ccrs. The nature, icer of the lung ies not appear to ; in the general " cases of mesotherteum have been t is an invariably ; no satisfactory an association the development -xposure in many ; nany people may ' mre either in the " in the home. As ` ictor operating in seems likely that arise in the next cases beyond that if use and greater" types of asbestos ; he elimination of - 507. Carey, G. C. R., Elwood, P. C,, McCallay, I. R., Merrett, J. D,, and P exu iert o n , J. (1965): Byssinosis in Flax Workers in Northern Ireland. Belfast: H.M.S.O. Cartier, P. (1955): Some Clinical Observations of Asbestosis in Mine and Mill Workers, A.M.A. Arch. Indust. Health. II. 204. C artier P. (1965): Discussion on Pleural Plaques, Ana. IIJ. Acad. Sci., 132, 387. Cooke W. E. 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Nat t or, B. (1963): The Exfoliative Cytology of Diffuse Malignant Mesothelioma. J. Path. Baer., 86. 293. N lvvhdusi, M. L., and 1iiompson, H. (1965): Mcsolheli- oma of the Pleura and Peittoneum following Exposure to Asbestos in the London Area, Brit. J. industr. Med., 22, 261. N lvvhousf, M. L. (1966): Personal Communication. O liver, Sir T. (1927): Clinical Aspects of Pulmonary Asbestosis, Brit. med.J., 1, 1026. O wi.n, W. G. (1965): Mcsnthclial Tumours and Ex posure to Asbestos Dust, Ann. N. Y. Acad. Sci., 132, 674. St it t it, II. E. (1928): A Case of Pneumoconiosis: the Result of Inhalation of Asbestos Dust, Btit. mcd. J., ii, 982. ScHipiRS, A. W. H. (1965): Discussion on `Human Exposure to Asbestos: Community Studies,' Ann. N. Y. Acad. Sci., 132, 246. Sl.lJIs-Cltl Ml R, G. K. (196)5): Asbestosis in South Africa -- Certain Geographical and Environmental Con siderations, Ann. N. Y. Acad. Sci., 132, 215. Smithir, W. J. (1965): Secular Changes in Asbestosis in an Asbestos Factory, Ann. N.Y. Acad. Sci., 132, 166. Thompson, V. C. (1965): Clinical Aspects of Diffuse Mcsothelial Tumours, Proc. Thor. Soc., Thorax, 20, 286. U.I.C.C. International U nion against C ancer (1965): Report and Recommendations of the Working Group on Asbestos and Cancer, Ann. N. Y. Acad. Sci., 132, 706. Wagner, J. C., Sleggs, C. A., and Marchand, P. (1960): Diffuse Mesothelioma and Asbestos Exposure in the North West Cape Province, Brit. J. industr. Med., 17, 260. Williams, R., and H ugh-Jones, P. (I960): Lung Function Changes in Asbestosis, Thorax, 15, 109. Wood, W. B. (1928): Pulmonary Asbestosis, Tubercle (Edinb)., 10, 353. Wyers, H. (1949): Asbestosis, Postgrad, med. J., 25, 631. v iwn on information ult of research work eutics and Pharma- , Dr. Jean H. M. cc as well as myself iblished. This work problem of asbestos son. Director of the Jnlt at Cardiff. The re discussed at an lew York under the ;my of Sciences in ve quoted references m although much of