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ne working in ;hing in this s degree in oads to the .nee of the extend over jndon School E7HT. Ann. oecup. Hyg. Vol. 16. pp. 97-107. Pergamon Press 1973. Printed in Great Britain t \ l ASBESTOS IN THE WORK PLACE AND THE' COMMUNITY Muriel L. Newhouse T.U.C. Centenary Institute of Occupational Health, London School of Hygiene and Tropical Medicine, Kcppel St-,, London, WCIE 7HT Abstract--The fibrogenic properties of asbestos dust were detected early, later knowledge accumulated about the carcinogenic properties of the mineral and a hazard of bronchial carcinoma and mcsothelial tumours was recognised. Mortality studies have measured the effect of exposure on working populations. Recent analysis of data from a cohort of asbestos factory workers shows that even with low to moderate exposure there is excess mortality from cancer of the lung and pleura and other cancers, after more than 25 years' observation. The mesothelioma rate increases both with severity and length of exposure. Occurrence of these and other tumours appears to be dose- related. The markers of a community effect of asbestos dust in the environment are the occurrence of mcsothelial tumours in neighbourhoods of a source of asbestos dust, and the presence of asbestos bodies or calcified asbestos pleural plaques in the general population. Conditions giving rise to neighbourhood mesothelial tumours may not now occur, but the importance of adequate control \ all countries where asbestos is mined or manufactured is stressed. * INTRODUCTION Although asbestos with its fire-resistant qualities has been known since ancient times its commercial exploitation dares 'only from the last twenty years of the nine teenth century. Chrysotile asbestos was first used in textile factories, a little later South African crocidolite and amosite were imported and used for manufacture of textiles, in cement products! and an ever-expanding list of objects. Anthophyllite asbestos is mined and used principally in Finland. The fibrogenic properties of asbestos were soon recognised. In the early part of the century there were increasing numbers of reports of pulmonary fibrosis among workers, culminating in the well-known Home Office Survey conducted by Merewether and Price (1930) who found approximately a third of a population of factory workers were suffering from pulmonary fibrosis. There is ample anecdotal information about the dusty conditions in the first factories, in the early days. Elderly workers will tell of clouds of dust, which even obscured visibility. \ After the introduction of the regulations of 1931, dust sampling was undertaken ' ' in some factories for some processes both in the United Kingdom and in the United States but, due to the multiplicity of instruments used and the various methods of recording observations,, the figures are confusing and difficult to compare. Never theless, without doubt the reguiarions caused a very marked improvement in factory conditions. The recognised tumours associated with asbestos exposure are the mesothelioma of pleura and peritoneum, broncuiai carcinoma, and possibly cancer of stomach and bowel. Case reports of lung cancer in asbestos workers date from the time in the 1930s when this was still a comparatively uncommon disease. The association 97 A 50010248 \ * ,. : ' "j 1 ! -^" r j>~~Tr~vfr~,ViniiSffw<*ifrfii nr W-.- vV--^c^T-^c^Yd^--a*^ ^ 98 Muriel L. Newhouse between the mesothelial tumour and exposure to asbestos was not recognised till much later when Wagner et al. (1960) published their repoit on the South African series of 33 patients with this tumour, 32 had had contact with crocidoiite asbestos. -. ASBESTOS IN THE WORK PLACE Mortality studies have been widely used to measure the effect of asbestos exposure in working populations. Doll (1965) and Knox et al. (1968) studied a textile factory in the north of England. Selikoff et al. (1970) have made a long-term mortality study of New York insulators and Macdonald et al. (1971) studied the mortality of chrysotile asbestos mine workers in Canada. Personal studies have been made of an East London asbestos factory (Newhouse, 1969; Newhouse et al., 1972). This factory, a heavy user of crocidoiite asbestos, as well as of amosite and chrysotile, kept a unique file of all employees. These records gave both personal details and details of jobs while employed. A cohort of male workers who started work at the factory any time between the implementation of the Asbestos Regulations of 1931 in April 1933 and the closure of the factory in 1968, and a smaller cohort of women who were first employed between 1936 and 1942, were established. The war?time.period was chosen for the women because regulations during the war simplified the difficult task of establishing whether women who had changed their name on marriage were alive or dead. The mortality experienced by the workers was assessed by comparing the number of observed deaths with the number of deaths that would be expected in a similar population of England and Wales using the man years method of Case and Lea (1955). Degree of dust exposure was categorised either as low-moderate (non-production workers and those working with low proportions of asbestos in the product were in this category) or as severe (a category which described openers, disintegrators and production workers in both scheduled and unscheduled jobs). The analysis of mortality has now been extended to 31 March, 1970. Among the men no excess mortality was found in the group with low-moderate exposure and short periods of employment at the factory (Table 1), but in those with longer Table 1. Mortality of male workers wrrH low-moderate exposure to asbestos, less than 2 yr in job Follow-up years No. of men 10-14 734 Obs. Exp. All causes Cancer of lung_and pleura (162, 163) Other cancers Respiratory disease excluding cancer Other unspecified Pleural mesothelioma Peritoneal mesothelioma 29 1 8* 6 14 0 0 22-2 1-8 3-1 3-3 14-0 *P<00S. 15-19 583 Obs. Exp. 15 23-0 1 1-9 2 3-1 3 3-4 9 14-6 0 0 20-24 365 Obs. Exp. 13 16-2 1 1-2 1 20 2 2-5 9 10-5 0 1 25+ . ' 179 ' ' Obs. Exp. 13s 13-4 3 1-2 1 1-8 2 2-0 7 8-4 1 0 500'i0?49 I'l'J 1til1 iirntfiniirii i~r rf ccognised till iouth African te asbestos. ' ` ' ` Asbestos in the work place and the community 99 periods of exposure (Table 2) and more than 25 yr of observation in the cohort there is a significant excess of mortality from cancer, which was not seen in the earlier study where there was a shorter period at risk in the cohort. Among the male <tos exposure rcxtile factory :rm mortality the mortality . (Newhouse, >lite asbestos, oyees. These A cohort of .plementation .he factory in 936 and 1942, =e regulations nen who had cperienced by aths with the England and dust exposure .hose working ) or as severe >rkcrs in both 970. Among rate exposure e with longer Table 2. Mortality or male workers with low-moderate exposure to asbestos, more than 2 yr in job Follow-up years No. of men All causes Cancer of lung and pleura (162, 163) Other cancers Respiratory diseases excluding cancer Other unspecified Pleural mesothelioma Peritoneal mesothelioma 10-14 479 Obs. Exp. 17 19-1 3 1*6 2 2'6 I 2'9 11 11-9 0 0 15-19 374 Obs. Exp. 15 18-4 2 1-6 1 2-5 3 2-8 9 11-5 0 0 20-24 228 Obs. Exp. 13 " 9-6 2 0-9 1 1-3 2 1-4 8 5-9 0 1 25497 Obs. Exp. 16t 7-8 3* 0-7 8t 1-0 3 1-2 2 4-9 2 2 P< 0-05. t/'COOI. :/><oooi. workers with severe exposure (Tables 3 and 4) whether they were employed for short or longer periods, excess mortality from lung cancer is already apparent in the group followed, up-for-15 yr or longer: The relative risk of carcinoma of lung is .highest in those with long and severe exposure. Among the women workers, who were followed till 31 December, 1968, there was only a small group of 126 with low-moderate exposure, but there was a signi ficant excess of lung cancer (Obs. 2, Exp. 0-3, P<0-05). The experience of the severely exposed women, who were predominantly textile workers, is shown in ^OS, LESS THAN Table 3. mortality of male workers with severe exposure to asbestos dust, less than 2 yr IN JOB 254 179 Obs. Exp. 13 13-4 3 1-2 1 1-8 2 20 7 8-4 I 0 Follow-up years No. of men 10-14 845 Obs. Exp. 15-19 708 Obs. Exp. 20-24 540 Obs. Exp. 254324 Obs. Exp. All causes Cancer of lung and 23 17-6 25 18-3 25f 13-0 32f 18-5 -. pleura (162, 163). - - 2. 1-5 7t 1-8 3 1-3 8t 2-0 1 Other cancers I 2-4 4 2-6 8+ 1-9 6 2-7 Respiratory diseases excluding cancer 3 2-8 2 ' 2-5 2 1-7 5 2-4 Other unspecified 17 10-9 12 II-4 12 81 13 11-4 Pleural mesothelioma 0 1 03 Peritoneal mesothelioma 0 1 1 2 tPcO-01. tP<0-001. 500^0250 t i jr 3 V$ '3 4 a *;i 3t \ 1 1 ~w ~~rr * ir--ilriiiirt 100 Muriel L. Newhouse Table 4. Mortality of male workers with severe exposure to asbestos dust, more than 2 yr in job Follow-up years No. of men All causes Cancer of lung and pleura (162, 163) Other cancers Respiratory diseases excluding cancer Other unspecified Pleural mesothelioma Peritoneal mesothelioma 10-14 482 Obs. Exp. 18 22-5 3 2-1 5 3-2 4 3-6 6 13-7 0 0 15-19 414 Obs. Exp. 40f 21-9 16t 2-0 6 3-1 6 3-3 12 13-5 1 2 20-24 281 Obs. Exp. 32i 13-8 iot 1-2 4 1-8 7t 2-1 11 8-7 1 3 25+ 127 Obs. Exp. 24t 12-6 n 1-1 8t 1-7 3 1-9 6 7-9 0 2 fPcOOl. tP <0-001. Table 5. There is marked excess of cancer, both of lung and pleura and of other sites. As among the males, excess of mortality from chronic respiratory diseases which includesrasbestosis, is only seen in those with severe and long exposure. Table 5. Mortality of women workers with severe exposure to asbestos dust No. of women All causes Cancer of lung and pleura (162, 163 Other cancers " ' Respiratory disease excluding cancer Other unspecified Pleural mesothelioma Peritoneal mesothelioma Less than 2 yr in job 557 Obs. Exp. 55 49-9 6t 1-0 16 12-4 10 7-4 23 29-1 3 3 More than 2 yr in job 239 Obs. Exp. 56t 24-5 14t 0-5 17t 6-1 at 3-6 14 14-3 3 2 tP<001. fFcO-OOl. The number of deaths from pleural and peritoneal tumours in each exposure category are indicated in the tables. By relating the number of deaths due to these tumours to the number of ycars-at risk in the cohort, excluding the period before the tenth year during which there is no observable excess mortality from any cause, a `mesothelioma rate' was obtained (Tabie 6). It will be seen that the rate increases both with severity of exposure and with length of exposure in the job. If the excess annual death rat?s, both for lung cancer and other cancers, are calculated (Table 7) a similar progression is observed. These figures suggest that the risk of mesothelial tumours as well as of bronchogenic lung cancer is strongly related to both the degree and the length of exposure to asbestos dust, and that 509*0Z5l L  Ti~if ^ ^ JliiiLTiii `irr 'ljr iW7iSilSlW,~1~'Tl`T^ V more than 2 yr 25-r 127 Obs. Exp. 24t 12-6 7t 1-1 at 1-7 3 1-9 6 7-9 0 2 | i I 1 i tjt t | } and of other dory diseases \posure. TO ach exposure due to these <>d before the any cause, a rate increases r cancers, are i suggest that cr is strongly lust, and that t.. me--- Asbestos in the work place and the community 101 Table 6. Number of deaths (n) and mesothelioma rate (r) per 100,000 subject-years (j>) after more than 10 years' follow-up Length of employment Men Women less than 2 yr more than 2 yr less than 2 yr more than 2 yr Low-moderate n sy r Exposure Severe n sy r n i 7899 5 4926 0 931 0 640 25 8 102 9 --6 --5 11193 5851 7176 3538 71 4 154 4 84 -- 141 -- Laggers sy r 2550 1530 -- -- 157 261 -- -- Table 7. Excess annual death rates for cancer among male workers per 100,000 subject YEARS AFTER MORE THAN 10 YEARS' FOLLOW-UP Length of employment Less than 2 yr More than 2 yr Exposure Low-moderate Severe Lung cancer Other cancer Lung cancer Other cancer -2 2S 119 84 105 92 506 227 although there may be no critical level where the cancer risk can be confidently said to be eliminated, strict control of factory hygiene and dust suppression may minimise the risk. - ASBESTOS IN THE ENVIRONMENT The evidence that asbestos dust can cause biological effects in the community rests on, firstly, the development of mesothelial tumours in persons with no occupa tional or other exposure to asbestos except residence near a source of asbestos dust, such as mine, factory or dockyard, secondly, the demonstration of asbestos bodies in the lungs of members of the general public, and thirdly, radiological evidence in the community living in the vicinity of a mine or large commercial user of asbestos of those pleural changes which are commonly associated with asbestos exposure. Eleven of Wagner's (1960) series of 33 patients with mesothelial tumours in the Cape Province of South Africa had had no occupational exposure, but had been bom and lived some-years on'the asbestos mine fields. Among the London Hospital series of 76 cases (Newhouse and Thompson, 1965) 11, significantly more than in the. control series, had had no occupational or other contact with asbestos but had lived 1 ' within half a mile of an asbestos factory. In these instances, exposure occurred usually more than thirty years before death, and it may have been considerable. A patient suffering`from a peritoneal mesothelioma interviewed recently, recalled playing with handfuls of asbestos on waste ground near a factory as a small boy, some forty years before he developed his turpour. Thompson (1965) examined the lungs of an unselected series of autopsies in Cape Town, while a parallel investigation was carried out in Miami. In both cities asbestos bodies were found in basal lung smears in approximately 30 per cent of the male lungs and 20 per cent of the female. Similar observations have now been made in the United States, Europe and the United Kingdom. The highest counts are found in occupationally-exposed men (Ashcroft, 1968) with lesser numbers in women 50010252 102 Muriel L. Newhouse 3 and rural dwellers. If the newer techniques of electron microscopy are used, chrysotile asbestos fibres or fibrils can be identified in nearly all the lungs of adult urban dwellers (Langer et al., 1971). It was an investigation in Finland that drew attention to widespread presence of calcification of the pleura in communities exposed to asbestos dust. Kjviluoto (1965) found several hundred persons with radiological evidence of pleural calcifica tion among rural people living in the vicinity of two open cast anthophyllite asbestos 1 mines. In Bulgaria, Burlikoff and Michailova (1970) found calcified pleural plaques among peasants cultivating tobacco in areas where the natural rock contained a considerable proportion of anthophyllite asbestos. In an attempt to define the quantity of asbestos dust in air in urban areas Selikoff et al. (1972) using high volume samplers and electron microscopy techniques quantified the asbestos content of air near building sites in Manhattan where asbestos I spraying was being undertaken. Measurable but minute amounts of asbestos were detected, the maximum concentration downwind of the source was 80 x 10~9 g/m3. A recent report of an Advisory Committee on Asbestos Cancers (1973) states 4 that at present there is no evidence of lung damage from fibrosis by the low levels of asbestos exposure encountered by the general public in urban areas. Nor do they find evidence.for an increased risk of cancer resulting from asbestos contamina- ' tion of water, beverages or food. However in the past asbestos pollution from crocidolite mines and factories using crocidolite has resulted in the occurrence of mesothelial tumours in the neighbour hood-populations. These conditions probably do not now arise in developed coun 3 tries, but asbestos products, particularly asbestos cement piping, are very widely ' used and many countries are developing their own manufacturing industries. It isimportant that there is wide knowledge of the asbestos hazard and that all users of asbestos, whether in mining or milling, ship building and repairing or manufacturing; practise scrupulous industrial hygiene and control of effluvia and waste products. REFERENCES Advisory Committee on Asbestos Cancers (1973) Report to the Director of the International Agency for Research on Cancer. Ann. occup. Hyg. 16, 9. 1 Ashcroft, T. (1968) Br. med.J. 1, 614 Burlikoff, T. and Michailova, L. (1970) Envir. Res. 3, 443. Case, R. A. M. and Lea, A. J. (1955) Br. J. prev. soc. Med. 9,62. doll, R. (1955) Br.J. ind. Med. 12, 81. Kiviluoto, R. (1965) Ann. M. Y. Acad. Sci. 132, 235. Knox, J. F., Holmes, S., Doll, R. and Hill, I. D. (1968) Br. J. ind. Med. 25, 293. ' Langer, A. M., Baden, V. and Hammond, E. (1971) Inhaled Particles--HI (Edited by Walton^ \ W. H.), Vol. 2 p. 683, Unwin, Old Woking, Surrey. Macdonald, J. C., Macdonald, A. D,, Gibbs, G. W,, Siematycki, J. and Rossiter, C. E. (1971) Ardts. envir. Hlth 22, 677. , Merewether; E. R. A. and Price, C. W. (1930) Report on the effect of asbestos dust in the lungs. K.M.S.Ol, London. Newhouse, M. L. (1969) Br. J. ind. Med. 26, 294. Newhouse, M. L. and Thompson, H. (1965) Br. J. ind. Med. 22, 261. Newhouse, M. L., Berry, G., Wagner, J. C. and Turok, M. E. (1972) Br. J. ind. Med. 29, 134. Selikoff, I. J., Hammond, E. C. and Churg, J. (1970) Pneumoconiosis: Proceedings ofthe International Conference, Johannesburg 1969 (Edited by Shapiro, H. A., p. 180. Oxford University Press, Cape Town. Selikoff, I. J., Nicholson, W. J. and Langer, A. M. (1972) Archs envir. Hlth 25, I. Thompson, J. G. (1965) Ann. N.Y. Acad. Sci. 132, 196. Wagner, J. C.. Sleggs, C. A. and Marchand, P. (1960) Br. J. ind. Med. 17, 260. i 50010,753 e ntujijigjum | ikjB1* t <( ii i -- mi i`T^