The Incidence of Malignant Mesothelioma Australia

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1 American Journal of Industrial Medicine 20: (1991) The Incidence of Malignant Mesothelioma Australia in James Leigh, MB, BS, MSc, MA, PhD, Carlos F. Corvalan, MA, Ashraf Grimwood, MB, ChB, Geoffrey Berry, MA, PhD, David A. Ferguson, MD, and Rebecca Thompson From 1980 to 1985, the Australian Mesothelioma Surveillance Program, and since 1986, the Australian Mesothelioma Register, have been collecting data on all cases of malignant mesothelioma that could be ascertained in Australia. Incidence rates were calculated on 854 Program and 696 Register cases (total 1271) diagnosed in Australia between January 1, 1982 and December 31, Australia has one of the highest national rates of mesothelioma in the world (15.8 cases per million of population aged 20 years and older), and the rate is rising. The rate is far higher in males (28.3) than females (3.3). The Western Australian rate (28.9) is the highest among the states, as may be expected because of the crocidolite mine at Wittenoom; however, the largest numbers of cases occur in the more populous and industrial New South Wales. The high incidence rate, its expected continuing increase, and absence of a history of exposure to asbestos in approximately 28% of cases, demand consideration of potential environmental factors other than asbestos in the causation of this tumor, as well as continued surveillance. Key words: mesothelioma, incidence, Australia, asbestos exposure INTRODUCTION Between January 1, 1980 and December 31, 1985, the Australian Mesothelioma Surveillance Program (the Program) collected data on all known cases of malignant mesothelioma in Australia [Ferguson and Ng, 1980; Ferguson et ai., 1987]. From January 1, 1986, the Australian Mesothelioma Register (the Register) sought continued notification of cases, without the intensive data collection on each case mounted by the Program, in order to monitor the incidence, occupational associations, and geographic distribution of the disease. A parallel monitoring of incidence arising from exposure to crocidolite mining and milling at Wittenoom has been maintained by the Western Australian Mesothelioma Register [Armstrong et ai., 1984]. The need for monitoring arose because National Institute of Occupational Health and Safety, Sydney, Australia (J.L., C.F.C., A.G., D.A.F.). Department of Public Health, University of Sydney, Sydney, Australia (G.B.). New South Wales (NSW) Cancer Council, Sydney, Australia (R.T.). Address reprint requests to Dr. James Leigh, Head, Epidemiology Unit, National Institute of Occupational Health and Safety, GPO Box 58, Sydney, NSW 2001 Australia. Accepted for publication April 9, Wiley-Liss, Inc.

2 644 Leigh et al. between 1943 and 1966, Australia was a major producer of crocidolite, the type of asbestos fiber most strongly associated with onset of the tumor [Wagner et al., 1960; Wagner, 1986] and, during the 1950s, was one of the highest consumers of asbestos (mainly chrysotile) per head of population, especially in building products [Tariff Board Report on Asbestos Fibre Tariff Revision, 1955]. The asbestos cement industry used most of the imported chrysotile and amosite and a percentage of crocidolite mined at Wittenoom. Asbestos products still exist widely in the environment and remain a potential hazard. This paper is confined to one of the main aims of the Program and Register, that of tracing trends in occurrence in a country which appears to have a malignant mesothelioma incidence rate higher than that of any other country for which reasonably comparable data can be found [Ferguson et al., 1987]. METHOD The Program and later the Register actively sought notification of cases from a network of respiratory physicians, pathologists, general surgeons, medical superintendents, medical records administrators, state and territory divisions of occupational health and cancer registries, and state and commonwealth compensatory bodies. They also accepted notifications from any other source. Notifications from other than diagnosing physicians were confirmed with the treating physician. The Program Secretariat, after gaining the appropriate permissions, obtained on each case, either from the patient or next-of-kin, full occupational and environmental histories, which were analyzed by occupational hygienists. It also requested from the diagnosing pathologist slides and/or specimens on each case for circulation to the Pathology Panel appointed by the Royal College of Pathologists of Australia for confirmation of diagnosis. Wherever possible, the Secretariat obtained at postmortem lung tissue free of tumor for analysis by the Lung Fibre Counting Panel [Rogers, 1984]. The coded results from history taking, pathology diagnosis and lung fiber estimation were all forwarded to the Epidemiology Panel for computer entry and analysis. The Register used the same notification network as for the Program, without however seeking a detailed history, material for diagnosis, or lung fiber analysis and counting. Incidence rates were calculated on cases notified to the Program and Register by July 31,1990 diagnosed between 1982 and 1988 inclusive. Cases diagnosed prior to 1982 are likely to have been underreported and so were not included. Notification of some cases diagnosed in 1989 may not yet have occurred. Incidence was calculated nationally and by State and Territory using Australian Bureau of Statistics (ABS) estimated mid-year population figures for each year, for males and females aged 20 years and over [Australian Bureau of Statistics, 1987]. Cases notified to the Program and accepted by the Pathology Panel as "definite," "probable," or "possible" malignant mesothelioma were included in the calculation of incidence. A correction factor was applied to Register cases. This factor was based on the percentage of cases expected to be confirmed as mesothelioma according to the findings of the Pathology Panel on Program cases; this assumes that a similar fraction of cases would have been found not to be mesothelioma if there had been pathological review. Incidence rates were standardized to the World Standard Population aged 20 years and over using the direct method [Muir et al., 1987]. Confidence intervals of the standardized rates were

3 Mesothelioma in Australia 645 calculated based on a normal approximation assuming that the number of cases in each age group was a Poisson variable [Armitage and Berry, 1987]. For a group with less than 10 cases, the factors given by Bailar and Ederer [1964], based on the exact Poisson distribution, were used. The Secretariat searched all available published sources and corresponded with overseas mesothelioma registers and panels to obtain data on incidence in other countries. In the case of personal correspondence, for the most part, incidence rates had to be calculated from information supplied on the number of cases which had occurred in the country and from the Demographic Year Book census figures or estimates of country populations [United Nations, 1986]. Australian rates were then compared with the overseas rates. RESULTS The Program received notification of 854 cases with a presumptive diagnosis of mesothelioma. Ferguson et al. [1987] reported 871 cases as being notified to the Program. Subsequently, cases found not to be mesothelioma (prior to review by the RCPA Panel) have been subtracted from the number. To July 31,1990, the Register was notified of a further 696 cases which were presumptively diagnosed between 1982 and Of the 854 Program cases, 777 have to date been reviewed by the Pathology Panel. Of these 777 cases, 746 (96%) were confirmed as malignant mesothelioma; 565 were classed as "definite" (73%),131 as "probable" (17%) and 50 as "possible" (6%). Thirty-one cases were assessed as definitely not mesothelioma. In calculations of incidence rates for the period , all the Program cases (565 cases) diagnosed between 1982 and 1985, except those rejected by the Pathology Panel, were included. The 696 Register cases were included but a correction factor of 0.96 (746/777) was applied to allow for the assumed proportion not mesothelioma. The anatomical site of the mesothelioma was available for 824 of the cases. Among 723 men, 676 (93%) had a pleural mesothelioma, 38 (5%) a peritoneal mesothelioma, and 9 had tumors in other sites. Among 101 women, 84 (83%) had a pleural mesothelioma, and 17 (17%) had a peritoneal mesothelioma. The Australian crude incidence rate per million of population aged 20 years and over increased from 12.8 in 1982 to 19.6 in 1988 (Fig. 1). The fall in incidence in 1987 can be attributed to a fall in notification rate brought about by uncertainties in the notification network following the conclusion of the Program at the end of 1985 and the establishment of the Register in The male crude rate ranged from 22.7 to 35.9 during that period, and was about seven times the female crude rate ( ). The rates in 1988 are expected to increase marginally because of delay in notification of some cases. 1 Western Australia had the highest overall incidence rates (total, male and female) of any state or territory of Australia, all the rates being half as much again as those of South Australia, which had the second highest rate (Table I; Fig. 2). However, most cases came from New South Wales and Victoria because of the prepon- IThe crude annual incidence rate per million of population 2: 20 years for 1988 is 19.6; for 1989, 23.8; for 1990, 28.8; for 1991 (to 31st May), 35.0 (approximately).

4 646 Leigh et al. 40 u e C Males Persons Females I d r ate nce i r / /' I ~ *- 201 I~~~.~ o Year of diagnosis Fig. 1. Australian crude incidence rates of malignant mesothelioma per million of population aged ~20 years, by sex, inclusive. derance of the Australian population and industry on the eastern seaboard. More than 60% of Australia's population is in New South Wales and Victoria (Fig. 3). In all 854 Program cases, data are available for the state or territory of all known exposure to asbestos. In all Program cases and in the 696 Register cases to July 31, 1988, data are also available for cases in which exposure occurred at the crocidolite mining town of Witte noom in Western Australia; 64 (7.5%) ofthe 854 Program cases and 27 (5.5%) of the 492 Register cases, overall 91 (6.8%) of 1,346 cases, had a direct occupational or environmental exposure at Wittenoom. Among 776 Program cases coded for asbestos exposure, Western Australia had the highest proportion of notified cases with exposure to asbestos in the same state and the lowest proportion of unexposed cases. Almost 70% of cases with first exposure in Western Australia received that exposure at Wittenoom (Table II). The relatively high incidence rate in South Australia, not a higwy industrialized state, was attributable mainly to that state having the highest proportion of cases first exposed overseas and the third highest proportion first exposed in another state or territory. About half had their exposure in the state or territory of notification, and about one in ten of exposed cases had an exposure overseas before migrating to Australia. Generally, about 28% of Program cases gave no history of exposure. For the combined sexes, the highest average annual crude incidence rate for the 7 years combined (61.3) occurred in the group aged years (Table III). Among males and females overall, the rate increased with age up to 79 years and then declined. Generally, incidence rates increased each year within age groups. Comparison of the Australian incidence rate has been made with some countries

5 ustralian Standardized " " a a a rateconfidence " a a limits Males 647 rate Mesothelioma in Australia Mesothelioma Territory Register* 95% *Australian mesothelioma incidence rates per million of population aged 2:20 years inclusive. afewer than 10 cases. that have in the past been major consumers of asbestos (Table IV). The Australian national rate (15.8) is the highest of those countries listed. However, the white South African male incidence rate (32.9) is higher than the Australian male rate (28.0) and the female colored South African rate (13.9) and the female white South African rate (8.9) [Zwi et ai., 1989] are higher than the Australian female rate (3.6). The national incidence rate for South Africa is not given. The rates for Northern Ireland (14.7) [Langlands, 1987], Norwegian males (13.0) [Mowe et ai., 1990], Dutch males (20.9) [Meijers et ai., 1990], and the expected national rate for South Africa are the only national rates to approach that for Australia in overall incidence. In some regions, incidence rates approach those of some states of Australia, for example, Rotterdam and Flushing [Planteydt, 1979] and some regional death rates in Great Britain [Jones et ai., 1988]. However, comparability cannot be strict because of differences in research parameters and methods, varying population and age bases, exclusion or underreporting of cases of mesothelioma of the peritoneum, pericardium, and tunica

6 648 Leigh et al. S ta 60 n 50 d a r d i z e d 40 ~ Males i n c i d e n c e r a t e o WA SA NSW QLD VIC TAS ACT NT State or territory of Australia Persons _ Females Fig. 2. Australian standardized incidence rates of malignant mesothelioma per million of population 2':20 years, by state and sex, inclusive. vaginalis, limitation to occupational asbestos exposure (compensation claims), differences in time period and in standards of histological confirmation, and use of standardized and nonstandardized rates. DISCUSSION Monitoring of malignant mesothelioma by the Program and Register has confirmed that Australia has an overall incidence rate apparently higher than that of other countries that have been major producers and/or consumers of asbestos and that the rate is rising. This rise has been continuous since 1947 [Musk et ai., 1989]. Certainly the rate is outstanding and in Western Australia far exceeds the experience of any other country or region, with the exception of Karain, Turkey, where exposure was to erionite [Baris et ai., 1981]. However, the circumstances there are hardly comparable. It would be expected that the South African national incidence rate would be of a magnitude similar to that of Australia. Although the male and female national death rates for Great Britain are lower than the Australian incidence rates, some of the former's regional death rates [Jones et ai., 1988] approach those of some of the states of Australia. Australia has a lower percentage of peritoneal cases reported than in Great Britain [Jones et ai., 1988] or South Africa [Zwi et ai., 1989]. The percentage of peritoneal cases is greater in females than in males which is consistent with trends from other studies [Zwi et ai., 1989; Jones et ai., 1988]. The extent to which the Australian pre-eminence in rates internationally and to which the rising rate over the period in Australia represent a genuine excess and secular increase in

7 Mesothelioma in Australia 649 /\ \ \ Wlttenoom Mine Northern Territory (0.9%) I R 5.8 Queensland (16.2%) IR 14.3 (8.9%) IR 28.9 South Australia (8.7%) IR 19.5 Aust Capital Territory (1.6%) IR 10.1 \; V (2.8%) TasmaniaIR 4.6 Fig. 3. State and territory proportion (%) of national population of Australia and standardized lllcloence rates (IR) of malignant mesothelioma per million of population aged 2:20 years, inclusive. incidence, or rather a more complete reporting, owing to enhanced awareness of the tumor and of the Program and Register, is not clear. The continuity of the increase since 1947, however, supports a real effect. The incidence rates across states and territories of Australia are not uniform. The high rate in Western Australia is due in large part to the number of cases exposed occupationally and/or environmentally at the Wittenoom crocidolite mine, most of whom have remained resident in that state; in 53% of asbestos exposed cases in that state, exposure occurred at Wittenoom. The high rate in South Australia was increased mainly by migration of cases from other states (14.3%) and from overseas (15.6%). The degree of migration has not been as great for other states or territories except Queensland and Tasmania. Queensland is a state that tends to receive postretirement migration from southern states. Previous analysis indicates that the relatively high New South Wales rate is probably due to: (1) the asbestos product manufacture that occurred there; (2) use of the product from the 1930s to 1960s; and (3) the fact that it is the most heavily industrialized state, with widespread use of asbestos in lagging, thermal insulation, soundproofing, and packing [Ferguson et al., 1987]. The overall increase in incidence rate with age up to 79 years and then decline may have been a cohort effect in that very aged people were past the time of risk of exposure when major use of asbestos escalated during the late 1940s and 1950s. Overall, the female incidence rate of 3.3 per million aged ~20 years was higher

8 650 Leigh NSWc QLD TAS SAb VIC No. of Program cases (n=77) (n=94) (n=386) = Ill) et 13) al. (n=97) Wittenoom Asbestos territory, excluding Exposure* exposures TABLE II. Notifications to Australian Mesothelioma Surveillance State Program of diagnosis Coded for *Proportion (%) of cases (n = 778) by place of first exposure to asbestos and state or territory of residence at time of diagnosis. adocumented first exposure to asbestos, irrespective of type, severity, or regularity. bcases from Northern Territory are included with South Australia. ccases from Australian Capital Territory are included with New South Wales. TABLE III. Notifications to Australian Mesothelioma Surveillance Program and Australian Mesothelioma Register* :::: Ten-year age groups *Australian age-specific crude incidence rates by age at diagnosis and sex, than would be expected on the basis of almost exclusively male occupational exposure to asbestos during the 1940s to 1960s [McDonald and McDonald, 1977]; 24% of women had some form of exposure to asbestos compared to 75% in males. This relatively high incidence with relatively low exposures may be due to women with no elicited exposure having received exposures environmentally, for example by living adjacent to primary asbestos production or cohabiting with a primary asbestos production worker. Owing to differences in time and age periods and in criteria of case collection, comparison of incidence rates from different countries is of dubious validity. For example, in some countries, such as Germany, mainly cases with asbestos exposure are notified, as in compensation cases [Otto, 1986]; and in some countries peritoneal mesothelioma has been relatively underreported [Bignon et al., 1979; Bignon, personal communication, 1986] although such is also thought to be the case in Australia. Generally, high rates, both overall and in males and females, tend to occur in

9 Mesothelioma in Australia 651 countries, provinces, states or cities known for their shipbuilding, general manufacturing and asbestos cement manufacturing. In the countries or regions with high incidence, such as Australia, British Columbia [Churg, 1985], England, Scotland, and Wales [Jones et al., 1988], Netherlands [Planteydt, 1979; Zambon et al., 1983; Meijers et al., 1990], Norway [Mowe and Gylseth, 1986; Mowe et al., 1990], Switzerland [Ruttner, 1987], and Connecticut [Lewisohn et al., 1980], but excluding Denmark [Andersson and Olsen, 1985], the male rate was 5-9 times the female rate. Where both earlier and more recent data were available for a region, the later rates were always higher. The rates for some countries therefore, such as Canada, Finland, and the United States, could be expected to have risen since the periods listed. Trends in the United States show an increase from 1973 to 1980, especially among older persons [Spirtas et al., 1986]. Information on the incidence rates of South Africa (a major crocidolite producer) is not given in Table IV, as the number of mesothelioma cases for the whole population was not available. The question arises, then, whether Australia's incidence rate is really one of the highest in the world and, if so, why? Some factors possibly contributing to the high Australian rate include the following: efficient reporting due to awareness of the disease and promotion of the Program and Register; widespread use of crocidolite in asbestos manufacturing, shipbuilding, railway, and metal fabrication and construction industries [Ferguson et al., 1987]; poor industrial hygiene record [Layman, 1983]; the post-world War II building boom, which saw more than 50% of housing construction in Australia being of asbestos cement sheeting [Layman, 1983], leading to Australia's position as the fourth largest consumer of asbestos cement products and the highest per capita user of asbestos in the world during the 1950s [Tariff Board of Asbestos Fibre Tariff Revision, 1955]; and the crocidolite mine at Wittenoom, which has been directly associated with 91 of the 1,346 cases collected by the Program and Register. Clearly, fiber type from this region is a major factor as it has been shown to have physical properties different from and likely to be more hazardous than those of crocidolite mined elsewhere [Timbrell et al., 1988]. Lung fiber content estimations show that about 60% of cases are also exposed to chrysotile and amosite [Rogers et al., 1991]. In about 28% of cases in the Program, there was no historical record of asbestos exposure despite intensive search. However, only about 7% of cases have lung fiber counts below the transmission electron microscope detection limit [Leigh et al., 1991]. This difference is presumably attributable to environmental exposure. Since there is also a dose-response relationship for asbestos-related mesothelioma [Rogers et al., 1991], the low-level lung fiber contents are not necessarily evidence of causality. Consideration therefore, needs to be given to other possible contributory factors to the high Australian incidence rate. With the large amounts of asbestos still in the environment, regular monitoring should occur to ensure safe work and domestic environments. A detailed analysis of the occupational and industrial asbestos exposure of Program cases is in preparation. ACKNOWLEDGMENTS We wish to thank the following people for their contribution to the work of the Program and Register. Dr. Theo Constance, Dr. Phillip W. Allen, Professor A. Harold Attwood, Dr. Douglas W. Henderson, Dr. Keith Shilkin, and Dr. Richard H. Steele of the Royal College of Pathologi~ls of Australasia Pathology Panel; Dr.

10 anada Quebec Republic) 245 yr - - I TABLE Greenberg IV. Churg Bignon Asbestos McDonald Donna Nurminen ~70h ~79h Otto ~45 Bignon ~90 ~54 ~67 EXp",d (%) 0.03 Females" 0,9 0,3g International c 4, ,Og ,3 0, (%) Males" incidence" et 11986] [ al [1986] and 3.4g J and , ~ [19791 Andersson Lloyd Reference McDonald 93 Incidence , >20 Davies Years 1975 and yr " Jones Zambon McDonald 11977J of Olsen Cont" Mesothelioma: et al. et and al J [ , McDonald JCountry, ) McDonald State, Province, and McDonald City and 4.4 Scotland Hist

11 Puget Sound Netherlandsi P1anteydt ].4 2.5f 3.6f I] [1979] Meijers 14.7g g 1980-]984 et al. [1990] Meijers 20.9f 1O.8f j Langlands Wright Hinds I-linds Ruttner j Mowe Baris loom ~ k 70h 82h g II g [1978] Iet and ] et Ial. Colored 11987] Gylseth White [1984] [ ;() 85% Lewisohn [ g ' females ] et Hinds McDonald al. Zwi et [19781 [1978] 11978] 100 al. et ~40 al. and [1989] ~20 [1990] McDonald mall I1Person-years. kmales of ipleural 'Per gcalculated Demographic hoccupational imajority [United estimates thousand. exposed 93 with mesothelioma Nations, ofp1anteydt from cases. occupational to Year exposure Planteydt country erionite figures 1986]. Book [] only. 987] populations only. fibers. I] provided census exposure. 979] figures using Kanton Karain Walcheren of Zurich 1sland)

12 654 Leigh et ai. Thomas Ng, World Health Organisation, Geneva, and Mr. Gersh Major, Consulting Occupational Hygienist, both of whom were instrumental in the development of the Program; Mrs. Sally Andreas, the original Registrar of the Program; Dr. Joyce Ford of the NSW Cancer Registry; Dr. Julian Lee, The Thoracic Society of Australia's representative; all the colleagues throughout Australia who participated in the Australian Mesothelioma Surveillance Program, particularly the state occupational health division medical officers, the state department of health community nurses, and private clinicians and pathologists. The Program has received support from the National Health and Medical Research Council, the NSW Workers' Compensation (Dust Diseases) Board and various other donors, and has been fully funded by the National Occupational Health and Safety Commission since REFERENCES Andersson M, Olsen JH (1985): Trend and distribution of mesotheliomas in Denmark. Br J Cancer 51: Armitage P, Berry G (1987): "Statistical Methods in Medical Research," 2nd Ed. Oxford: Blackwell, pp Armstrong BK, Musk AW, Baker JE, Hunt JM, Newall CC, Henzel! HR, Blunsdon BS, Clarke-Hundey MD (1984): Epidemiology of malignant mesothelioma in Western Australia. Med J Aust 141: Australian Bureau of Statistics (1987): Estimated resident population by sex and age: States and territories of Australia. June 1981 to June Canberra (Catalogue No ). Bailar JC, Ederer F (1964): Significant factors for the ratio of a Poisson variable to its expectation. Biometrics 20: Baris YI, Simonato L, Saracci R, Skidmore JW (1981): Malignant mesothelioma and radiological chest abnormalities in two villages in Central Turkey. Lancet 1: Bignon J (1986): French Mesothelioma Register, Centre Hospitalier Intercommunal, 40. Ave de Verdun, Creteil Cedex, France. Personal communication. Bignon J, Sebastien P, Di Menza L, Payan H (1979): French Mesothelioma Register. Ann NY Acad Sci 330: Churg A (1985): Malignant mesothelioma in British Columbia. Cancer 55: Donna A (1987): Italian Representative of CEC Mesothelioma Panel. Personal communication. Ferguson D, Ng TG (1980): Australian Mesothelioma Register. Med J Aust 1: Ferguson DA, Berry G, Jelihovsky R, Andreas SB, Rogers AJ, Chung Fung S, Grimwood A, Thompson R (1987): The Australian Mesothelioma Surveillance Program Med J Aust 147: Greenberg M, Lloyd Davies TA (1974): Mesothelioma Register Br J Ind Med 31: Hinds WM (1978): Mesothelioma in the United States. J Occup Med 20: Jones RD, Smith DM, Thomas PG (1988): Mesothelioma in Great Britain. Scand J Work Environ Health 14:145-i52. Langlands JHM (1987): Register of Mesothelioma-Northern Ireland. Respiratory Investigation Centre, Belfast City Hospital, 93 Lisburn Road, Belfast BT 9 7 AB. Personal communication. Layman L (1983): Work and worker's responses at Wittenoom, Community Health Studies 7:1-18. Leigh J, Rogers AJ, Ferguson DA, Mulder HB, Ackad M, Thompson R (1991): Lung asbestos fiber content and mesothelioma cell type, site and survival. Cancer 68: Lewisohn HC, Meigs JW, Tete MJ, Flannery JT (1980): The influence of occupational and environmental asbestos on the incidence of malignant mesothelioma in Connecticut. In Wagner JC (ed): "Biological Effects of Mineral Fibres." Lyon: IARC Sci Pub 39 pp McDonald JC, McDonald AD (1977): Epidemiology of mesothelioma from estimated incidence. Prevent Med 6: Meijers JMM, Planteydt HT, Swaen GMH (1990): Asbestos exposure and pleural mesotheliomas in the

13 Mesothelioma in Australia 655 Netherlands-Trends and geographical patterns rd Int Cong Occup Health 610 (abst). Mowe G, Andersen A, Osvoll P (1990): Malignant mesothelioma in Norway registered by the Cancer Registry and notified to the Labour Inspection between rd Int Congr Occ Health: 611 (abst). Mowe G, Gylseth B (1986): Occupational exposure and regional variation of malignant mesothelioma in Norway, Am J Ind Med 9: Muir C, Waterhouse J, Mack T, Powell J, Whelan S (1987): "Cancer Incidence in Five Continents. Vol. 5." Lyon: IARe. Musk AW, Dolin PJ, Armstrong BK, Ford JM, de-klerk NH, Hobbs MS (1989): The incidence of malignant mesothelioma in Australia Med J Aust 150: Nurminen M (1975): The epidemiologic relationship between pleural mesothelioma and asbestos exposure. Scand J Work Environ Health 1: Otto H (1986): Pathologisches Institut der Stodt Kliniken, Beurhausstr. 40, 6400 Dortmund I, Federal Republic of Germany. Personal communication. Planteydt HT (1979): Netherlands Mesothelioma Register. Ann NY Acad Sci 330: Planteydt HT (1987): Netherlands Mesothelioma Register. Streeklaboratorium, Zeeland, Molenwater 47, 4331SC Middelburg, Netherlands. Personal communication. Rogers AJ (1984): Determination of mineral fibre in human lung tissue by light microscopy and transmission electron microscopy. Ann Occup Hyg 28:1-12. Rogers AJ, Leigh J, Berry G, Ferguson DA, Mulder HB, Ackad M, (1991): Relationship between lung asbestos fiber type and concentration and relative risk of mesothelioma. A case-control study. Cancer 67: Ruttner JR (1987): Zurich Pneumoconiosis Research Group. Institute of Pathology, University Hospital, CH-8091, Zurich. Personal communication. Spirtas R, Beebe GW, Connelly RR, Wright WE, Peters JM, Sherwin RP, Henderson BE, Stark A, Kovasznay BM, Davies JNP, Vianna NJ, Keehn RJ, Ortega LG, Hochholzer L, Wagner JC (1986): Recent trends in mesothelioma incidence in the United States. Am J Ind Med 9: , Tariff Board Report on Asbestos Fibre Tariff Revision (1955): Appendix B Summary of Evidence. Canberra: Government Printing Office, September 1955, pp 16. Timbrell V, Ashcroft T, Goldstein B, Heyworth F, Meurman LO, Randall REG, Reynolds JA, Shilkin KB, Whitaker D (1988): Relationships between retained amphibole fibres and fibrosis in human lung tissue specimens. Ann Occup Hyg (suppl 1), 32: United Nations Department ofinternational Economic and Social Affairs, Statistical Office. (1986): 1986 Demographic Year Book. United Nations, New York, pp Wagner JC (1986): Mesothelioma and mineral fibers. Cancer 57: Wagner JC, Sleggs CA, Marchand P (1960): Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province. Br J Ind Med 17: Wright WE, Sherwin RP, Dickson EA, Bernstein L, Fronn J, Henderson BE (1984): Malignant mesothelioma: Incidence, asbestos exposure and reclassification of histopathology. Br J Ind Med 41: Zambon P, Simonato L, Mastrangelo G, Saia B, Chieco-Bianchi L (1983): Age characteristics of mesothelioma incidence in the general population of the Province of Padova Tumori 69: Zwi AB, Reid G, Landau SP, Kielkowski D, Sitas F, Becklake MR (1989): Mesothelioma in South Africa : incidence and case characteristics. Int J EpidemioI18: