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AMERICAN JOURNAL OF INDUSTRIAL MEDICINE 41:188-201 (2002) Malignant Mesothelioma in Australia, 1945-2000 James Leigh, mb, bs, ma, msc, md, PhD,1 Patricia Davidson,1 Leigh Hendrie, ba, mph,2 and Dale Berry2 Background Australia has maintained a total national malignant mesothelioma case register since 1980. There has been a marked increase in the incidence of mesothelioma in the last 20 years. Currently 450--600 cases are notified annually in a population of 20 million. While the history of the Wittenoom (Western Australia) crocidolite mine and its aftermath is well known, these cases comprise only 5% of the total. This study describes the incidence of mesothelioma in Australia from 1945 to 2000. Methods Using register data, time trends in mesothelioma incidence were calculated. Analyses of incidence are reported by age, sex, anatomical site, and state of notification. Associations with occupational and environmental asbestos exposure histories are described. Lung fiber content measurements were made on a subset of cases. Results Australia has had 6,329 cases of mesothelioma from 1 January 1945 to 31 December 2000. (A further 620 cases were notified in the periodfrom 1 January 2001 to 31 October 2001.) Annual incidence rates for Australia per million population > 20 years (1997) were: male, 59.8; female, 10.9; total, 35.4. Incidence rates have been continually increasing and are the highest reported national rates in the world. While Western Australia has the highest rate (1997 total rate, 52.8), most cases arise from the two most populous eastern states, New South Wales and Victoria. In 88% (male 90%, female 61%) of cases, a history of asbestos exposure was obtained. Exposures occurred in a wide variety of occupational and environmental circumstances. In 80% of cases with no history of exposure, TEM lung asbestos fiber counts > 200,000 fibers > 2 pm length per gm dry lung were obtained, suggesting unrecognized exposure. Conclusions Australia's high incidence of mesothelioma is related to high past asbestos use, of all fiber types, in a wide variety of occupational and environmental settings. The number of cases in total is expected to be about 18,000 by 2020, with about 11,000 yet to appear. Am. J. Ind. Med. 41:188-201, 2002. 2002 Wiley-Liss, Inc. KEY WORDS: malignant mesothelioma; incidence; Australia; asbestos exposure; future predictions Abbreviations used: NSW, New South Wales; VIC, Victoria; QLD, Queensland; TAS, Tasmania; SA, South Australia; WA, Western Australia; ACT, Australian Capital Territory; NT, NorthernTerritory. 'Center for Occupational and Environmental Health, Department of Public Health and Community Medicine, University of Sydney Sydney, NSW Australia National Occupational Health and Safety Commission, Sydney, NSW Australia The views expressed in this article are those of the authors and do not necessarily reflect those of the National Occupational Health and Safety Commission. Dr James Leigh works as a Director 'Correspondence to: Dr James Leigh, Center for Occupational and Environmental Health, Department of Thoracic Medicine, Concord Hospital 2139, NSW Australia. E-mail: jleigh@bigpond.com Accepted 30 November 2001 2002 Wiley-Liss, Inc. D0l10.1002/ajim.10047 INTRODUCTION Asbestos was mined in Australia for over 100 years and Australia was the world's highest user per capita of asbestos in the 1950's. Given the ecological relationship between per capita asbestos consumption and mesothelioma incidence [Takahashi et al., 1999], it is no surprise that in the last twenty years of the 20th century, Australia has had the world's highest reported incidence of malignant mesothe lioma. Australia has one of the world's most complete national surveillance systems for mesothelioma and this has Malignant Mesothelioma in Australia 189 been in operation since 1980. We will describe the history of asbestos use and the incidence of mesothelioma in Australia as a whole, rather than concentrating on the well-known Wittenoom crocidolite mining operation and township in Western Australia [Musk et al., 1992]. This study updates and enhances previous reports [Leigh et al., 1991b, 1997, 1998; Leigh, 1994]. History of Asbestos Production and Use in Australia Between 1880 and 1889, approximately 47 tonnes of amphiboles were mined at Jones' Creek, near Gundagai, New South Wales, and between 1890 and 1899, about 35 tonnes of chrysotile was mined at Anderson's Creek, Tasmania. South Australia was the first State to mine croci dolite at Robertstown in 1916. Over the 20th century, there was a gradual increase in asbestos production, with more chrysotile than amphiboles mined until 1939. With the commencement of mining at Wittenoom, Western Australia, in 1937, crocidolite domi nated production, until final closure in 1966. New South Wales, the first State to mine asbestos, also produced the largest tonnages of chrysotile (until 1983) as well as smaller quantities of amphiboles (until 1949). With the closing of the crocidolite mine at Wittenoom in 1966, Australian asbestos production declined to a pre-1952 level. Exports declined from 1967. Imports of chrysotile also started to decline. The earliest records of asbestos imports date from 1929. The main sources of raw asbestos imports were Canada (chrysotile) and South Africa (crocidolite and amosite). About twice as much chrysotile was imported as was mined and half as much crocidolite was imported as was mined. After Wittenoom was closed, a small amount (122 tonnes) of crocidolite was mined in South Australia. In New South Wales, the chrysotile mine at Baryulgil continued production. In 1971, the chrysotile deposits at Woodsreef near Barraba, New South Wales began to be exploited and exports of asbestos fiber expanded as production increased. This operation was open-cast with dry milling. Australian production of asbestos fiber decreased in 1981 because of the drop in world demand for asbestos and the increased operating costs at the Woodsreef mine. This mine ceased production in 1983 when the dry milling plant could not meet dust control regulations. Details of Australian asbestos production and imports are shown in Tables I and II. Australian asbestos (crocidolite and chrysotile) was exported to the USA, Japan, UK, and Europe. In particular, Wittenoom crocidolite was ex ported to the USA and Europe [The Colonial Sugar Refining Company Limited, 1956]. In addition to imports of asbestos fiber, Australia also imported many manufactured asbestos goods, including TABLE I. Asbestos Production in Australia*, 1880-1983 Years (10) 1880-1889 1890-1899 1900-1909 1910-1919 1920-1929 1930-1939 1940-1949 1950-1959 1960-1969 1970-1979 1980-1983 Crocidolite (tonnes) -- -- -- 22 18 422 5,619 63,227 86,566 -- -- Chrysotile (tonnes) -- 20 61 580 3,577 1,151 2,967 11,511 8,855 394,361 160,408 Amosite (tonnes) 26 -- 21 23 54 51 750 1 -- -- -- Total (tonnes) 26 20 80 625 3,649 1,624 9,338 74,739 95,421 394,361 160,408 Total 155,874 583,491 926 740,291 `Based on figures supplied by Bureau of Mineral Resources [Hughes, 1978], asbestos cement products, asbestos yarn, cord and fabric, joint and millboard, friction materials and gaskets. The main sources of supply were the United Kingdom, USA, Federal Republic of Germany, and Japan. Apparent consumption of asbestos, the difference between production and imports, and export is shown in Table III and Figure 1. This gives a crude estimate of overall exposure. However the export process itself, bagging, transport, and wharf labor caused much exposure. In Australia, over 60% of all production and 90% of all consumption of asbestos fiber was by the asbestos cement manufacturing industry [Hughes, 1978]. From about 1940 to the late 1960's, all three types of asbestos were used in this industry, crocidolite then being phased out. Amosite use in this industry continued until about 1983. Chrysotile was used until about 1987. Much of this industry output remains in service today in the form of TABLE II. Asbestos Imports Prior to1930 Until 1983 in Australia(in tonnes)* Year Chrysotile Amosite Crocidolite 19??-1930 1930-1940 1940-1949 1950-1959 1960-1969 1970-1979 1980-1983 -- -- -- 186,855 329,129 388,003 64,672 -- -- -- 107,509 81,432 87,901 8,338 -- -- -- 2,778 -- -- -- Other -- -- -- 16,938 24,112 79,683 4,188 Total 2,568 51,554 139,987 314,080 434,673 555,587 77,198 Total 968,659 285,180 2,778 124,921 1,575,647 `Based on figures supplied by Bureau of Mineral Resources [Hughes, 1978], 190 Leigh et al. TABLE III. Asbestos--Apparent Consumption* in Australia Year 1880-1889 1890-1899 1900-1909 1910-1919 1920-1929 1930-1939 1940-1949 1950-1959 1960-1969 1970-1979 1980-1985 Production (tonnes) 26 20 82 625 3,649 1,624 9,338 74,739 95,421 394,361 160,408 Imports (tonnes) -- -- -- -- 2,568 51,554 139,987 314,080 434,674 555,587 104,324 Exports (tonnes) -- -- -- -- -- 1,196 2,410 51,413 44,703 45,523 9,786 Apparent consumption (tonnes) 26 20 82 625 6,217 51,982 146,915 337,406 485,392 704,425 154,946 Total 740,293 1,602,774 455,031 1,888,036 *Based on figures provided by Bureau of Mineral Resources [Hughes, 1978], "fibro" houses and water and sewerage piping. By 1954, Australia was fourth in the world in gross consumption of asbestos cement products, after the USA, UK, and France, and was clearly first on a per capita basis. After World War II to 1954, 70,000 asbestos cement houses were built in the State of New South Wales alone (52% of all houses built). In Australia as a whole, until the 1960's, 25% of all new housing was clad in asbestos cement. Australia still imports about 1,500 tonnes a year of chrysotile fiber, and about $A13.5 m worth of asbestos products a year, over half as friction material, but also fabricated yarn, fabric, jointing, gaskets, millboard, and asbestos cement products [Victorian Occupational Health and Safety Commission, 1990; NOHSC, 1999]. However, a phase out of new (chrysotile) asbestos use by 2003 is in place. Handling of asbestos in place and removal operations are subject to a strict National Code of Practice. A series of regulations adopted in the late 1970's and early 1980's by the Australian states and territories now impose exposure limits of 0.1 fiber/ml for crocidolite, amosite, and mixtures (all states and territories) and 0.1 (ACT), 0.5 (NSW,VIC) or 1.0 fiber/ml (SA, WA, NT, QLD, TAS) for chrysotile (TWA 8 hr membrane filter method light microscopy, WHO fibers). The chrysotile limit is currently under review. Exposures in the past were very high in some indus tries and jobs. For example, up to 25 million particles per cubic foot were documented in asbestos pulverizors and disintegrators in the asbestos cement industry [Roberts and Whaite, 1952]. High concentrations of fibers in mining occupations were also recorded (up to 600 fibers/ml) in baggers at Wittenoom [Major, 1968]. With this background, it was almost certain that Australia would suffer a mesothelioma epidemic of a severe nature. The first reported case, from Wittenoom, was in 1962 [McNulty, 1962]. Three more cases were reported from Victoria in 1966 [Riddell, 1966], two from Queensland in 1968 [Mortimer and Campbell, 1968], and an additional nine from Victoria in 1969 [Milne, 1969]. FIGURE1. Asbestos consumption in Australia (1900-1985). Malignant Mesothelioma in Australia 191 METHODS Australian Mesothelioma Surveillance Program The Australian Mesothelioma Surveillance Program (the Program, as it hnally became known) endeavored to correct most of the weaknesses identified in the 1960's and 70's in other such surveillance schemes throughout the world, viz., under-reporting of cases, uncertain diagnosis, poor elucidation of the role of occupational and environ mental asbestos exposure, and less than comprehensive coverage [Ferguson et al., 1987]. The Program began on 1 January 1980 after preli minary work from 1977. Formal voluntary notification of cases was actively sought from a network of respiratory physicians, pathologists, general and thoracic surgeons, medical superintendants, medical records administrators, State and Territory departments of occupational health, cancer registries, compensation authorities, or any other source. Notifications from other than the diagnosing physician were confirmed with him/her. After gaining the appropriate consents, a complete occupational and envi ronmental history was obtained for each case, either from the patient or next-of-kin, by a specially trained interviewer. The history taking was non-directive, but included specific questions on asbestos exposure. These histories were coded by two occupational hygienists, who naturally could not be blinded to case status. They also discussed cases together and were thus not independent. The diagnosing pathologist was requested to provide slides and or tissue specimens. These were circulated among a pathology panel for con firmation of diagnosis. Post-mortem examination was acti vely sought for in every case in order to confirm diagnosis and to obtain lung tissue free of tumor for lung fiber content analysis. Occupational and environmental exposure was classi fied as definite, probable, and possible, based on the sub jective opinions of the two hygienists. Further grading of intensity of exposure was also very subjective in many cases and duration depended on historical recollection. Year of presumptive diagnosis was the year in which mesothelioma was first suspected clinically. Year of de finitive diagnosis was the year when pathology panel diagnosis was finalized. The panel of five members of the Royal College of Pathologists of Australasia reported individually on the diagnosis as definite, probable, possible and not mesothelioma. The level of consensus was good, with exact agreement or disagreement of only one category in 94% of cases. A scoring system of 1 (definite), 0.75 (probable), 0.5 (possible), 0 (not mesothelioma) was used and the definitive score taken as the score nearest the mean of five. Panel members also classified mesothelioma cell type as epithelial, sarcomatous, mixed, or not agreed. Lung fiber content was assessed by a local modification of a sodium hypochlorite digestion and filter method. Both light and transmission electron microscopy (TEM) (with energy dispersive x-ray analysis) were used. Fibers were counted by asbestos type and length, but not diameter. All fiber lengths were recorded, but because of uncertainties about filter contaminants by < 2 pm fibers, only fibers > 2 pm (TEM) or > 5 pm (LM) were considered in analyses. These methods gave a sensitivity, corresponding to one fiber counted, of 15,000 fibers/g dry lung (LM) and 200,000 fibers/g dry lung (TEM). Assuming a Poisson distribution of fibers in the counting units, the upper limit of the 95% confidence interval for the population mean, given a zero count obtained, is 3.69. Thus the TEM "detection limit'' is about 740,000 fibers/g [Rogers, 1984]. Reports on lung fiber content levels were sometimes used for medico legal purposes in a fallacious way in that counts were reported as being "within the normal range'' as if this excluded an occupational asbestos exposure and liability. The "normal'' range was in fact taken from urban hospital patients without mesothelioma, and where fibers were counted, exposure obviously had been received (and not always environmental only as judged by fiber length distribution. It must have sometimes been from occupa tional sources, but no work histories were available). It was not realized until later that these patients should be treated as non-cases (referents) in a case-referent study. Detailed analyses of Program data relating lung fiber content, cell type, tumor site, and survival [Leigh et al., 1991a]; lung fiber type and content to risk [Rogers et al., 1991, 1994]; and clinical studies [Driscoll et al., 1993] have been previously reported. Australian Mesothelioma Register From 1 January 1986, a less detailed notification system has operated, with a short questionnaire occupational and environmental exposure history (followed up assiduously with up to four letters per case); no pathology panel diag nosis and only sporadic lung fiber counts. In the case of NSW and WA (60% of all Australian notifications), histories are obtained from direct detailed questioning by compen sation authorities or cancer registries. Only histologically confirmed cases are accepted and full reconciliation with all state cancer registries and compensation authorities is carried out. This is now known as the Australian Meso thelioma Register, but is a continuation of the Program. Incidence rates are periodically calculated on cases notified to the Register. An annual report series is produced [NOHSC, 1989-2001]. Cases accepted by the pathology panel in the Program as definite, probable or possible are included. In this report, incidence rates have been cal culated up to the end of 1997 only, due to a possible 2-year delay in notification experienced, while awaiting confirmed 192 Leigh et al. diagnosis and reconciliation with the state cancer registries. Incidence rates for 1998 are available in the Australian Mesothelioma Report for 2001 [NOHSC, 2001]. RESULTS Incidence of Mesothelioma in Australia From 1 January 1980 to 31 December 2000, a total of 5,671 notihcations had been received by the Program and Register. Between 1945 and 1979, there were 658 cases (535 male, 123 female) in Australia [Musk et al., 1989]. Thus the total number of mesotheliomas in Australia from 1945 -2000 inclusive is 6,329. (An additional 620 noti hcations have been received in the period 1 January 2001 to 31 October 2001.) Notihcations show a continuing up ward trend in both males and females (Fig. 2). The notihcations prior to 1982 were probably the result of initial slow acceptance of a new Program and are artihcially low (1980:16, 1981:104), although a smooth curve of in creasing incidence starting from the early 1960's has since been demonstrated by retrospective search (Fig. 3). The Australian population has increased from 14.5 million in 1980 to 20 million in 2001. Mesothelioma incidence rates in persons over 20 years of age have increased from 11.8 per million per year in 1982 to 35.4 per million per year in 1997 (males and females combined) (59.8 per million per year (males) and 10.9 per million per year (female)). Figure 4 shows incidence rates by time and sex. If the 1981 hgure is accepted, it can be claimed that mesothelioma incidence rates have increased four- to hvefold in 19 years in Australia. Both male and female rates have increased, but the male rate is over hve times the female rate. These are the highest reported incidence rates in the world [Hillerdal, 1999; Peto et al., 1999; Takahashi et al., 1999; Kjellstrom and Smartt, 2000] and equal to the Australian (NSW) incidence rates of liver cancer and in mortality terms, equal to the mortality rates of kidney cancer in males and uterine cancer in females [New South Wales Cancer Council, 2000]. Mesothelioma is no longer a "rare disease'' . Figure 5 shows age-specihc incidence for males and females (> 20 years) for the year 1997. Incidence increases with age up to 80 year and then falls, consistent with a cohort effect in that the oldest persons may have missed the heaviest exposure era from 1950-1970. The occurrence of cases in the < 40 year age groups indicates that exposure can occur in children. Figures 6 and 7 show age-specihc incidence trends over time for males and females. Generally the time trend of increasing incidence is restricted to age groups over 50 from 1986 onwards, suggesting that oc cupational exposure controls introduced from the 1970's have been effective. Table IV shows notihcations by state up to 31 December 2000. uuu 450 - 400 - A 350 - Males L 300 8 250 - ...A"'*' A ..-'' ` 1 200 - . - A* * A 150 - .''' A A A /-'''A * A .--' 100 50 - a . - ' '. ' ' .' Females ...... ' ......... ............... 0 -j t 1 1 | | | | | |1 1 1 "| | -------------1-------------1-------------1-------------1-------------1-------------1-------------1------------ 1979 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 2001 Year of Notification FIGURE 2. Australian Mesothelioma Register Notifications (1979-2000) (by sex). Malignant Mesothelioma in Australia 193 Western Australia has the highest incidence (1997 rates: total 52.8 per million/year; male 96.2, female 9.4), but contributes only 15% of the total cases. Wittenoom contributes only 5% of the Australian cases, yet is certainly the most publicized and best known internationally. Most of the cases come from the two most populous and indus trialized states, New South Wales and Victoria (Table IV). In 93.2% of all Program cases, the mesothelioma was pleural in site with 6.5% peritoneal and 0.3% in other sites. Among males, 94.3% were pleural, 5.3% peritoneal; among women, 86.3% pleural, 13.7% peritoneal. These proportions have been generally maintained in Register cases although the female peritoneal proportion has dropped to 10.4%. Of the cases that underwent pathology panel review 96% were conhrmed as mesothelioma (73% dehnite, 17% probable, and 6% possible). The most common occupational expo sures were repair and maintenance of asbestos materials (18%), shipbuilding (11%), asbestos cement production (7%), asbestos cement use (7%), railways (6%), Wittenoom crocidolite mining/milling (6%), insulation manufacture/ FIGURE 4. Time trend of annual incidence rate (per million population > 20 years) of mesothelioma in Australia by sex (1982-1997). 194 Leigh et al. FIGURE 5. Age-specific incidence rates of mesothelioma in Australia (1997) (male and female). installation (4%), wharf laboring (3%), power stations (3%), boilermaking (2%), para-occupational, hobby, and environ mental (15%). When the earlier cases classed as "no history of exposure" were reviewed, it was found that 57 of the 203 so classihed actually had history of some exposure recorded. Thus only 19% had no known history. Moreover, of this "no known history" group, 81% had hber counts > 200,000 hbers/gm dry lung detected in the lungs, 30% with more than 106 hbers/g > 2 pm including "long" (> 10 pm) hbers suggesting that nearly all cases have been exposed. Past exposure is not always recognized as such and this is more likely to be the case in females. Indeed even absence of hbers in the lungs does not negate exposure as hbers may have initiated mesothelioma and then been cleared before FIGURE 6. Age-specific incidence of mesothelioma in Australia(1986--1997) (male). Malignant Mesothelioma in Australia 195 Incidence per million Females Year of Diagnosis FIGURE 7. Age-specific incidence of mesothelioma in Australia (1986-1997) (female). TABLE IV. Mesothelioma Notifications in Australia(1980-2000) 1980 1981 1982 1983 1984 1985 1986 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 ALL % NSW VIC QLD WA SA TAS NT ACT Total 15 1 0 0 0 0 0 51 3 18 22 5 5 0 90 20 9 0 20 2 0 53 23 26 46 19 6 0 76 38 20 26 14 1 1 71 39 27 30 19 1 0 46 34 38 32 18 2 1 54 40 26 28 32 0 0 57 28 45 23 36 1 0 124 25 35 44 22 3 0 111 82 43 26 25 1 0 105 44 46 66 55 10 0 117 45 40 37 39 3 1 99 34 42 47 25 5 0 151 41 74 32 30 8 0 124 89 49 33 43 11 1 87 157 53 127 30 4 1 107 32 64 82 24 5 0 160 84 65 66 21 80 252 113 73 79 20 7 0 168 106 99 47 60 7 0 2,118 1,078 892 893 557 90 5 37.3 19.0 15.7 15.7 9.8 1.6 0.1 0 16 0 104 1 142 0 173 2 178 2 189 1 172 2 182 2 192 1 254 1 289 2 328 1 283 0 252 1 337 3 353 4 463 4 318 1 405 7 551 3 490 38 5,671 0.7 100 NSW, New South Wales; VIC.Victoria; QLD, Queensland; WA.Western Australia; SA, South Australia; TAS.Tasmania; NT, Northern Territory; ACT, Australian Capital Territory. 196 Leigh et al. TABLE V. Asbestos Exposures as Documented in the Australian Mesothelioma Register (1 January1986-31 October 2000) Circumstances of exposure Acoustic engineer Air-conditioning Aircraft Armed forces/wartime Armed forces/peacetime Asbestos bagging (not Wittenoom) Asbestos bags--handled which had contained asbestos Asbestos clothing--worn Asbestos covers for cooking Asbestos dwelling/fence-built/renovated Asbestos dwelling--lived in Asbestos products--lived near Asbestos products factory--worked near Asbestos mine--worked/lived near (not Wittenoom) Asbestos product handled in the workplace Asbestos product manufacturer--worked Asbestos product--part of workplace or surroundings Asbestos tailings--played on as a child Asbestos/orproductsworker--lived with/washed clothes Bakery (ovens) Boilermaker/cleaner/attendant/installer/welder Brake linings--made/repaired Brewery Bricklayer Brickworks Builder/Builder's laborer Carpenter/joiner Cement factory worker Chemical engineer Civil engineer Concreting Construction worker Demolition Design engineer Diesel engineer Dockyard worker Electrical engineer Electrical fitter Electrical mechanic Electrician Electroplater Engineer Fireproofing Firedoors Firefighter Fitter/turner Foundry Furnace Glassworks/glaziers Exposed (with no other exposure)(single) 1 12 11 28 6 8 8 9 3 70 29 11 11 12 42 106 26 8 42 3 79 58 1 15 8 185 224 20 1 7 5 12 5 2 -- 40 5 15 3 55 -- 26 5 5 5 51 6 6 6 Exposed (with other exposures) (multiple) -- 14 3 16 2 4 -- 4 -- 13 8 2 -- 6 8 36 9 4 6 -- 54 19 -- 4 3 40 42 1 -- -- 3 2 2 1 1 23 7 4 -- 12 1 1 -- -- 3 20 2 -- -- Total exposures 1 26 14 44 8 12 8 13 3 83 37 13 11 18 50 142 35 12 48 3 133 77 1 19 11 225 266 21 1 7 8 14 7 3 1 63 12 19 3 67 1 27 5 5 8 71 8 6 6 TABLE V. (Continued) Circumstances of exposure Industrial chemist Industrial engineer Instrument technician Insulation Jeweller Laboratory technician Laborer Lagger Lagging in workplace Laundry/dry cleaners Linesman Locksmith Machine fitter Machine inspector Machine operator Machinist Maintenance carpenter Maintenance electrician Maintenance engineer Maintenance fitter Maintenance mechanic Maintenance worker Marine engineer Mechanical engineer Mechanical fitter Metal fabrication Metal trades Metallurgy Moulder Navy/merchant navy Oil refinery Painter/decorator Panel beater Papermill Patternmaker Pipes--handled/cut/stored/drilled Plasterer Plumbing Powerstation worker Pressure pack manufacturer Printing Radiographer Railways Renovations/maintenance/lagging in workplace Roofing Sheetmetal Ships--building/repairing/on Shop fitter Site visits/inspections Malignant Mesothelioma in Australia 197 Exposed (with no other exposure)(single) 4 2 1 18 6 6 33 31 24 14 9 1 3 2 1 3 3 2 3 13 3 12 9 5 7 2 3 1 4 160 7 37 9 3 6 24 16 56 86 1 10 2 101 21 16 14 75 1 8 Exposed (with other exposures) (multiple) -- -- -- 4 2 2 15 16 4 5 4 -- 1 -- 3 -- 1 1 1 4 2 3 7 -- 3 -- 1 -- -- 64 2 8 1 2 3 5 7 27 51 -- -- -- 49 5 4 11 57 -- 7 Total exposures 4 2 1 22 8 8 48 47 28 19 13 1 4 2 4 3 4 3 4 17 5 15 16 5 10 2 4 1 4 224 9 45 10 5 9 29 23 83 137 1 10 2 150 26 20 25 132 1 15 198 Leigh et al. TABLE V. (Continued) Circumstances of exposure Smelting Steelworks Storeman Stoves Sugar mill Tannery Telephone technician Tiler Toolmaker Trades assistant Transporting asbestos Transporting asbestos product Tire factory Waterside worker Weighing trucks Welder Whitewash--Greece/Cyprus Wine making (filters) Wittenoom (former mining area in Western Australia) Wood machinist Asbestos exposure Single Multiple Possible No apparent asbestos exposure No response to questionnaire Total cases from1/1/86 to 31/10/2000 Proportion of respondents with asbestos exposure Exposed (with no other exposure)(single) 1 13 15 2 6 2 6 11 4 17 14 15 10 94 1 22 4 1 193 3 Exposed (with other exposures) (multiple) 8 4 3 1 2 3 6 2 4 13 9 1 51 Summary of asbestos exposures 2,608 400 274 457 1,099 4,838 |7| = 88% Total exposures 1 21 15 2 10 2 9 12 6 20 20 17 14 107 1 31 5 1 244 3 death [Becklake and Case, 1994]. The shortest duration of exposure was 16 hr (waterside worker loading crocidolite hber [Musk et al., 1991]). Three percent of cases had exposure of less than 3 months. According to history assess ment of exposure of the first 530 cases by the two hygienists, most cases (55%) had mixed amphibole-chrysotile expo sure, 13% amphibole only, 7% amphibole, plus possible chrysotile, 6% chrysotile, with possible amphibole, and 4% chrysotile only, with 15% unknown fiber type [Grimwood, 1988]. Mean latency from first exposure to presumptive diagnosis was 37.4 years [Ferguson et al., 1987]. The range of latencies was 4-75 years. In the cases reported since 1 January 1986, when less detail of history of exposure was sought, 89.9% of males responding to questionnaire and 61.2% of females gave a history of asbestos exposure (overall 86.4%) (non-response 22% males, 30% females). The pattern of exposure history is changing, and more product, domestic, environmental and para-occupational exposure is apparent, compared to the older traditional industries. Table V shows the circum stances of exposure in cases from 1986-2000. This is a combination of occupation and industry or domestic or environmental circumstance. Exposure occurred in a wide range of occupations and industries and non-occupational settings. Some common exposure histories were: repair and maintenance of asbestos materials (13%), shipbuilding (3%), asbestos cement production (4%), railways (3%), powerstations (3%), boilermaking (3%), Wittenoom (5%), wharf labor (2%), para-occupational, hobby, environmental (4%), carpenter (4%), builder (6%), navy (3%), plumber 2%), brake linings (2%), and multiple (12%). CONCLUSIONS The high and increasing incidence of mesothelioma in Australia is due to high asbestos use in the past, combined Malignant Mesothelioma in Australia 199 with poor hygiene practice, relatively high amphibole use in asbestos cement products, carcinogenic potency of chrysotile, and excessive focus on Wittenoom to the exclusion of other more common exposures. There was also a reluctance to recognize the causal signihcance of low occupational and non-occupational exposures and a tendency to ignore or discredit the warnings of scientists, the late Irving J. Selikoff among others. It is now apparent that nearly all human mesothelioma cases result from asbestos or erionite exposure, which may be of very small magnitude. Other proposed risk factors or co-factors, such as radiation and inflammatory lung con ditions are supported only by anecdotal evidence at best. Indeed a recent very large study of mesothelioma after radiotherapy for breast cancer in US nurses is convincingly negative [Neugut et al., 1997]. The case for SV40 virus involvement as a co-factor is still unproven. While there is a dose-response relationship with asbestos exposure, a threshold has not been identified although recent studies have shown it to be less than 0.15 fiber year/ml [Rodelsperger et al., 2001]. If there is a "background incidence rate", it has been estimated to be much less than 1 per million per year [Hillerdal, 1999]. The studies relating lung fiber content and type to mesothelioma risk showed that for Australia as a whole, the greatest risk of mesothelioma was associated with exposure to crocidolite > 10 pm in length. It was difficult to assess the risks associated with chrysotile alone, due to almost universal assessed mixed exposure to amphibole and chrysotile, and the possibility of differential clearance effects. However, in a subset of cases and referents with only chrysotile found in the lungs a significant doseresponse trend was found. The expected total number of mesothelioma cases in Australia from 1945 to 2020 is estimated to be about 18,000, based on models by Berry [1991] and de Klerk et al. [1989] for Wittenoom, extrapolated for Australia as whole (assuming Wittenoom contributes 5% of cases), and direct extrapolation from the best fit to the empirical incidence curve, constrained to have a maximum value at 2010, following a 40 year latency from the time of maximum exposure (1970) (Fig. 8). This will create a heavy clinical and compensation load. Cases will arise from a large vari ety of occupations and workforces and environmental and para-occupational circumstances. Although classic cohorts related to insulation work and crocidolite mining will have the highest risks, occupations such as carpenters, builders, plumbers, and electricians, because of numbers emplo yed, will generate similar case loads. The risk in brake mechanics is also elevated [WTO, 2000], consistent with chrysotile only causation. With asbestos related lung cancer estimated to occur at a ratio of 2:1 to mesothelioma [Barroetavena et al., 1996], the expected future case load of asbestos related cancer can be expected to be of the order of 30,000-40,000 by 2020. This prediction is consistent, on a population and asbestos consumption adjusted basis, with those made for Europe [Burdorf et al., 1998; Peto et al., 1999], USA, and Japan [Consensus Report, 2000]. The various Australian state, territory, and federal government preventive, clinical, and compensatory autho rities are now developing a national strategy for dealing 200 Leigh et al. with this problem. The elements of this strategy are the phasing out of all new use of asbestos in Australia by the end of 2003, strict control of demolition and removal operations involving asbestos containing materials, screen ing programs for high risk asbestos exposed groups using spiral CT, support programs for victims of asbestos-related disease, research into better clinical treatments, prophy laxis programs where indicated, and uniform compensation standards based on the principles of the Helsinki criteria Consensus Report [2000]. REFERENCES Barroetavena MC, Teschke K, Bates DV. 1996. Unrecognized asbestos-induced disease. Am J Ind Med 29:183-185. Becklake MR, Case BW. 1994. Fiber burden and asbestos-related lung disease: determinants of dose-response relationships (editorial). Am J Resp Crit Care Med 150:1488-1492. Berry G. 1991. Prediction of mesothelioma, lung cancer, and asbestosis in former Wittenoom asbestos workers. Br J Ind Med 48:793-802. Burdorf A, Swuste PHJJ, Looman CWN. 1998. 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