Document byDJ3z8X2x8KaKx10L37LEnqZ

INT J TUBERC LUNG DIS 11(4):356-369 2007 The Union STATE OF THE ART STATE OF THE ART SERIES Occupational lung disease in high- and low-income countries Edited by M. Chan-Yeung NUMBER 3 IN THE SERIES Asbestos-related diseases of the lungs and pleura: uses, trends and management over the last century M. R. Becklake,* E. Bagatin,1* J. A. Neder * Respiratory Epidemiology and Clinical Research Unit, Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada; + Area of Occupational Health, State University of Campinas (UNICAMP), Campinas, * Jundiai School of Medicine, Jundiai, Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Diseases, Federal University of Sao Paulo (UNIFESP), Sao Paulo, SP, Brazil. S U M M ARY Asbestos is a descriptive term for a group of naturally occurring minerals known to mankind since ancient times. The main types of asbestos (chrysotile, and the amphiboles crocidolite and amosite) differ in chemical structure, biopersistence in human tissue and toxicity. Commercial exploitation, with little thought for environmental con trols, increased over the twentieth century, particularly after World War II, to accommodate globalisation and the demands of the world's burgeoning cities. As its illhealth effects, both non-malignant (fibrosis of the lungs or asbestosis; pleural effusion, plaques and thickening) and malignant (mesothelioma, lung and other cancers), became evident, public pressure rose to control its use. The last decades of the last century saw decreases in ex posure and rates of asbestosis in industrialised and in some less-industrialised countries, where pleural plaques and malignant mesothelioma are currently the most frequent manifestations of asbestos exposure. Longer follow-up of asbestos-exposed cohorts in mining and manufacturing has also strengthened the evidence of a fibre gradient in toxicity, with chrysotile exhibiting lower toxicity than the amphiboles, and amosite lower toxicity than crocidolite. The last decades of the twentieth century saw stabilisation and/or declines in mesothelioma rates in several industrialised countries. In less-industrialised countries, data on disease are sparse, exposure generally high and rates may peak in the future. Management of asbestos-related disease in the workplace requires collab oration between workers and unions (responsible for mon itoring workplace dust levels, to which they must have access) and companies (responsible for engineering con trols), reinforced by appropriate government regulations and by community support. KEY WORDS: asbestos; diseases of the lung and pleura; trends in disease; industrialised and less-industrialised countries ASBESTOS is a descriptive term for a group of natu rally occurring minerals of fibrous habit known to and used by mankind since ancient times. Table 1 lists the mineral silicates that have been found in human lung tissue, the location of the major deposits world wide, and main commercial uses and/or other sources of human exposure.1-5 Figure 1 shows the main fibre types,6 which differ in their physical and chemical properties and in the con sequences of exposure. These include non-malignant conditions (pleural plaques, effusions, diffuse pleural thickening, rounded atalectasis and asbestosis) and malignant conditions (mesothelioma, lung and other cancers). Previous articles in this series Editorial: Chan-Yeung M. Becklake M. Occupational lung disease: under-recognised, underestimated and poorly managed, even today. Int J Tuberc Lung Dis 2007; 11 (2): 119. No 1. Jeebhay M F, Quirce S. Occupational asthma in the developing and industrialised world: a review. Int J Tuberc Lung Dis 2007; 11 (2): 122-133. No 2. Blanc P D, Toren K. Occupation in chronic obstructive pulmonary disease and chronic bronchitis: an update. Int J Tuberc Lung Dis 2007; 11 (3): 251-257. THE FATE OF INHALED FIBRES The accumulation of fibres in the lungs results from exposure, deposition, clearance and retention, pro cesses that depend on exposure intensity, duration and profile.7 Long fibres clear more rapidly than short fibres, and chrysotile fibres more rapidly than amphi- Correspondence to: Margaret R Becklake, MD, Respiratory Epidemiology and Clinical Research Unit, Montreal Chest Institute, 3650 Saint-Urbain Street, Montreal, QC, Canada H2X 2P4. Tel: ( + 1) 514-934-1934, ext 32159. Fax: ( + 1) 514 843-2083. e-mail: margaret.becklake@mcgill.ca [A version in French of this article is available from the Editorial Office in Paris and from the Union website www.iuatld.org] Asbestos-related diseases of the lungs 357 Table 1 Mineral silicates that have been found in human lung tissue* Mineral: group and form Asbestos minerals Serpentine Chrysotile+ (white asbestos) Amphiboles Crocidolite (blue asbestos) Amosite (brown asbestos) Anthophyllite Location of major deposits, commercial and/other Canada (Quebec,* British Columbia, Yukon, Newfoundland) China (Szechuan Province) Russia Brazil Mediterranean countries (Cyprus, Corsica, Greece, Italy) Southern Africa (South Africa, Swaziland, Zimbabwe) South Africa (North West Cape) Western Australia (Wittenoom) South Africa (Northern Province--former Transvaal) Finland Tremolite Cummington-Grunerite Non-asbestos mineral silicates Clay minerals (usually fine-grained, powder-like) such as kaolin and bentonite Micas (usually flaky) Vermiculite (expands when heated) Zeolite (fibrous) (e.g., erionite1) Contaminates ore in some asbestos, talc, iron and vermiculate mines; also in some agricultural soils Contaminates ore in some iron mines (often not fibrous) 40 countries including China, Czechoslo vakia, Germany, Egypt, Japan, US (Georgia, North Carolina), UK (Cornwall) Australia, Kenya, South Africa, USA (Montana, Virginia) Turkey (Anatolia, Cappadocia regions); non-commercial deposits Man-made mineral fibres Glass wool and filament Rock and slag wool Produced in factories around the world As above Ceramic fibre As above Main commercial uses and/or other sources of human exposure Brake lining, ship building /repair; polishing precious stones; stone and whetstone cutting; foundry operations (mainly insulation); asbestos cement products (pipes, gutters, tiles, roofing); insulation; fireproofing; reinforced plastics (fan blades, electric switching gear); textiles; friction materials; paper and spray-on products Used in combination, mostly in cement products, also in some products listed below Filler in rubber and plastics May be removed in processing; has rural domestic use (e.g., stucco) No commercial use Functional filler in paper, plastics, bricks, cement, etc; fire clays, refractories, ceramics, lubricants Absorbents (horticulture); plasters; boards; insulation; fire resistance Houses constructed in erionite rock; soil containing fibres mixed with tremolite; sepiolite used in stucco and plaster Many uses previously reserved for asbestos Used in insulation in buildings and in car and naval construction Used in reinforced cloth, brakes, etc; high-performance ceramic fibres used in jet engines, spacecraft Note: As of 2006, 23 countries have prohibited the use of asbestos or severely restricted its use, but in most countries exceptions are allowed for some uses. A prohibition decree was adopted by the European Union in 2005. *Adapted from Table 61.3 in Cowie et al.,5 and reproduced with permission from Elsevier Saunders. This list is not exhaustive; reader should consult other sources for further information.1-5 + Accounts for over 90% of the world's production. * Currently the Jeffrey mine in Quebec, Canada, suspends its operations intermittently, depending on demand. Mining no longer in operation. 1 In one of three epidemics of mesothelioma in Turkish villages, erionite was implicated; in the other two, tremolite or chrysotile were implicated. bole fibres.5 Fibres of less than 3 ^ are phagocytosed by activated macrophages, which then drain via lym phatics to the pleural surface and eventually into the pleural space.5 How fibres transmigrate to the parietal pleura to produce plaques is not known. Longer fibres are partly phagocytosed, usually by several macro phages, and become the core of asbestos bodies, so called because of their association with asbestos expo sure and their ready identification on light microscopy. In the lungs of exposed individuals, the number of un coated (bare) fibres exceeds the number of coated fibres (asbestos bodies) by from 5000 to 10000 times.5 Most, but not all, coated fibres contain asbestos, usually an amphibole. The presence of more than one coated fibre has been accepted for many years8 and challenged9 as necessary for the pathological diagnosis of asbestosis, even in a subject with an appropriate exposure history. Asbestos bodies found in sputum or bronchoalveolar lavage (BAL) reflect high tissue levels.10 They are more commonly found after recent exposure than after re mote exposure, and after exposure to amphiboles than after exposure to chrysotile.11 DIAGNOSTIC EVALUATION OF ASBESTOS-RELATED DISEASES Clinical features Breathlessness, the most common respiratory symp tom associated with asbestosis, is usually of insidious onset and first noted on exertion.12,13 Symptoms should 358 The International Journal of Tuberculosis and Lung Disease Figure 1 Different types of asbestos fibres (a, chrysotile; b, crocidolite; c, amosite; d, anthophyllite) as seen by transmission electron microscopy (UICC reference material). Reproduced from De Vuyt and Gevenois, Figure 9.2, page 144, with permission from Elsevier.6 UICC = International Union Against Cancer. thus be objectively quantified using a validated ques tionnaire. Other features include non-productive cough and mid-to-late inspiratory crackles that persist after cough.14 Haemoptysis should prompt further assess ment for malignancy or concurrent infection by tuber culosis, using sputum cytology and bronchoscopy. Oppressive chest pain, especially on exertion, was re ported in up to 70% of heavily exposed workers in an Indian asbestos mill,15 and in 43% of a Western Aus tralian cohort of 1280 subjects who had worked on or lived near a crocidolite mine.16 Extensive crackles, clubbing and/or cyanosis are associated with increased risk for asbestos-related mortality.14 Imaging Conventional chest X-ray A standardised system for obtaining and classifying postero-anterior chest X-rays for the presence and pro fusion of parenchymal opacities and pleural changes was published in 1980 (International Classification of Radiographs of Pneumoconiosis, International La bour Office [ILO]),1 and updated in 2003.17 The orig inal films and reading sheets for the presence and pro fusion of parenchymal opacities were retained, and those for pleural and other disease (chest wall, vascu lar, etc.) considerably expanded. Profusion scores de rived from epidemiological surveys have been found to correlate with mortality and functional impair ment in asbestosis.18-20 High-resolution computed tomography High-resolution computed tomography (HRCT) has displaced conventional chest X-rays for the clinical evaluation of asbestos-exposed subjects because it is more sensitive for detecting asbestosis.21-24 Abnor malities that characterise asbestosis on HRCT include thickened intra- and inter-lobular lines, subpleural cur vilinear lines, subpleural `dotlike' opacities, parenchy mal bands, small cystic spaces, patchy areas of groundglass change and honeycombing in advanced disease (Figures 2-5).25 By contrast, conventional chest X-rays are appropriate for screening asbestos-exposed popu lations for the extent of pleural lung abnormalities.21 Other imaging methods Digital enhancement of chest radiographs improves their sensitivity and specificity in identifying pleural involvement in a clinical context.26 Ultrasound may be useful in locating pleural fluid. Magnetic resonance imaging (MRI) can be of value in identifying rounded atelectasis and in distinguishing parietal lesions (chest wall and/or pleural) from fluid accumulation.26 Positronemission tomography (PET), especially when used in association with HRCT, is useful for differentiating be nign from malignant effusions and for staging patients with known pleural mesothelioma (Figure 5).26 Sputum analysis and bronchoalveolar lavage Identification of asbestos bodies may help in assessing exposed individuals for asbestosis. However, sputum analyses for asbestos bodies miss almost half the occu pationally exposed individuals in whom asbestos bodies are found on BAL.10 Asbestos bodies recovered on BAL are also useful in the clinical diagnosis of paren chymal involvement: the amphibole burden in the lungs correlates better with amphibole recovery on BAL than chrysotile burden with chrysotile recovery.27 Pulmonary function tests Established asbestosis may be, but is not invariably, as sociated with a restrictive lung function profile.5 With less advanced radiological disease, forced vital capac ity (FVC) and diffusing capacity are usually reduced, and flow at low lung volumes may also be reduced, con sistent with asbestos-related small airway disease.28 A substantial proportion of workers (up to 50% in some studies) exhibit a mixed or obstructive lung function profile,29 consistent with the parallel development of airways and parenchymal effects of working in dusty occupations contaminated by mineral dusts contain ing asbestos.5 Pulmonary gas exchange disturbances, re flected by reduced diffusing capacity of the lung for car bon monoxide (DLCO) and widening alveolar-arterial oxygen difference at rest and exercise, are more sen sitive indices of dysfunction than ventilatory impair Asbestos-related diseases of the lungs 359 ment.30 Cardiopulmonary exercise testing may be use ful in disability evaluations. Many subjects with circumscribed pleural plaques have normal lung function at rest but develop short ness of breath during exercise.31 Controversy exists as to whether pleural plaques are associated with venti latory dysfunction,22,32 while diffuse pleural thicken ing usually, but not always, leads to significantly re duced vital capacity and diffusing capacity.33 BENIGN ASBESTOS-RELATED DISEASE Pleural plaques Pleural plaques are circumscribed, discrete areas of fi brous tissue and have long been considered markers of asbestos exposure (Figure 2). Histologically, they are characterised by acellular deposits of collagen on the parietal pleura.28 With the improvement of environ mental controls in workplaces, an increasing number of workers are seen in whom pleural plaques are the only manifestation of asbestos exposure. In one study of 110 construction insulators, all currently working, over half exhibited isolated pleural plaques, reported short ness of breath on exertion and had an average decrease in forced expiratory volume in one second (FEV1) and FVC of 200 and 300 ml, respectively.34 These reductions could not be attributed to radiographic and/or subradio graphic fibrosis, evidence that isolated pleural plaques may reduce ventilatory function significantly.34 Diffuse pleural thickening Diffuse pleural thickening is characterised by fibrosis of the parietal pleura which frequently extends to vis ceral pleura. The 1980 ILO Classification for Chest Radiographs for Pneumoconiosis states that pleural thickening should be considered as diffuse `only in the Figure 2 A 55-year-old non-smoking asymptomatic male who worked for 10 years (1968-1978) in the asbestos cement indus try. Chest radiography (top) on the right shows calcified pleural plaques en face and on the diaphragm, and blunting of the costophrenic angle. On the left it also shows calcified pleural plaques en face and on the diaphragm. The HRCT scan (bot tom) shows a calcified pericardial plaque on the right and calci fied parietal and pericardial plaques on the left. HRCT = highresolution computed tomography. Figure 3 A 44-year-old non-smoking asymptomatic male with an 18-year history of exposure to asbestos in the asbestos ce ment industry. Top: Chest radiograph revealed ill-defined, small patchy opacifications on the right lower lobe: a diaphragmatic plaque was also suspected. Bottom: A sagittal reconstruction of the thorax CT scan (with contrast) shows a rounded atelectasis in the left lower lobe and a partly calcified diapraghmatic pleu ral plaque on the right. CT = computed tomography. 360 The International Journal of Tuberculosis and Lung Disease presence of and in continuity with, an obliterated costophrenic angle'.1,17 Thickness of at least 3 mm is required in the 2003 ILO classification for reporting pleural thickening.17 Involvement of the visceral pleura is suggested by the presence of fibrous strands extending into the parenchyma (`crow's feet').32 Benign pleural effusion Pleural effusions may occur early or late after the onset of asbestos exposure. They may last several months, be exudative and are often haemorrhagic. While most are asymptomatic, some present with fever and severe pleuritic pain. The clinical course is variable, and re currence can occur on the same or the opposite side.24,32 A blunted costophrenic angle or diffuse pleural thick ening are often the residua of acute pleural effusions. Diagnosis is usually by exclusion: fluid cytology is use ful for distinguishing benign from malignant effusions. Rounded atelectasis Rounded atelectasis (shrinking pleuritis, Blesovsky's syn drome or folded lung) develops from infolding of thick ened visceral pleura with collapse of the intervening lung parenchyma (Figure 3). These lesions may be multiple and frequently resemble masses.28,32 A classic `comet sign' can be seen on HRCT or plain films. Histological examination shows folded and fibrotic visceral pleura with atelectasis and variable amounts of chronic lung inflammation. The sudden appearance of rounded atelectasis may follow acute pleuritis with effusion. Asbestosis Asbestosis is characterised by pulmonary parenchymal fibrosis, in the presence of an exposure history of ap propriate duration, latency (usually two decades) and intensity. Histologically, the term asbestosis refers to interstitial fibrosis caused by the deposition of asbes tos fibres in the lung.24 Clinical features include breath lessness, inspiratory crackles and pulmonary func tion abnormalities (a restrictive or mixed restrictiveobstructive pattern, decreased DLCO and, in advanced cases, pulmonary gas exchange disturbances during exertion). The ILO classification remains the pre ferred tool to identify subjects with asbestosis:1,17 a profusion of irregular opacities at the level of 1/0 is commonly used as the threshold to indicate disease.24 Figure 4 Chest radiograph and HRCT of two ex-workers from the asbestos cement industry with mild and advanced asbestosis (left and right, respectively). More extensive changes are seen on the HRCT scan (bottom) than on the chest X-ray (top), including paren chymal bands, honeycombing and traction bronchiectasis. Note that the opacities are mostly nodular, suggestive of silicosis but com patible with exposure in the asbestos cement industry. HRCT = high resolution computed tomography. Asbestos-related diseases of the lungs 361 HRCT is often useful in clarifying the exact nature of uncharacteristic or complex abnormalities seen on conventional chest X-ray (Figure 4). MALIGNANT ASBESTOS-RELATED DISEASE Malignant mesothelioma Malignant mesothelioma is a hard white tumour that characteristically encases the lung.35 In its early stages it may appear as white nodules studding the pleura and diaphragm. There is some evidence that these tumours start on the parietal surface. Histologically, there are three cell types: epithelial (Figure 5), mixed cell and sarcomatous, distinguished by histochemical reaction.35 The median survival time for these cell types is 18, 11 and 8 months, respectively. Lung cancer Asbestos-related lung cancers were first considered to be scar cancers.24 This changed as more data became available on the fibre burden in workers with other types of asbestos-related disease. For example, fibre concentrations in lungs of Quebec chrysotile miners and millers dying of asbestosis were shown to be on average over two-fold higher than in those dying of lung cancer (30 vs. 13 million chrysotile fibres per gram of dry lung tissue).5 All lung cancer cell types have been associated with asbestos exposure, further supporting the concept of exposure playing a direct role in their genesis, independent of smoking.36 Other asbestos-related cancers Other asbestos-related cancers include laryngeal can cer, for which evidence of a causal association is con sidered reasonably strong,35 and oesophageal cancer, for which the evidence is suggestive. For other can cers, such as ovarian cancer, renal cancer and lym phoma, the evidence is less conclusive, although the possibility that these rare tumours may be caused by asbestos should not be dismissed.36 Figure 5 A 63-year-old non-smoking male who worked for 5 years in the asbestos cement industry (1960-1965) presented with a 3-month history of breathlessness and chest pain. A. Chest radiograph showed extensive opacification of the low er left lung fields. B. HRCT scan revealed a pleural effusion with increased pleural thickness. C. A combined F-18 fluorodeoxyglucose (FDG) PET/CT scan showed increased local soft tissue re tention of the tracer, which is highly suggestive of malignancy. An open biopsy confirmed the diagnosis of epithelial mesothe lioma. (Courtesy of Prof M Terra-Filho, Division of Respiratory Diseases, University of Sao Paulo, Brazil.) HRCT = high-resolution computed tomography; PET = positron emission tomography; CT = computed tomography. EPIDEMIOLOGY OF ASBESTOS-RELATED DISEASES Recent trends in industrialised countries Trends in mesothelioma mortality in men have been analysed in a number of industrialised countries, to assess the status of the current mesothelioma epi demic and predict its future course37 (Table 2). In Britain, death certified as malignant mesothe lioma rose steeply in men by birth cohort from 1893 to 1948, then fell.38 Despite the fall, the authors of the study predict that the rate will continue to rise until about 2020, based on the assumption that the profile of deaths will not change over the next two decades.38 This assumption does not account for improved ex posure controls in workplaces in the last two decades 362 The International Journal of Tuberculosis and Lung Disease Table 2 Mesothelioma incidence in men: recent trends in selected studies carried out in industrialised countries (by year) First author, year, reference Peto J, 199538 Peto J, 199939 Kjaergaard J, 200040 Hemminki K, 20034 Ulvestad B, 200342 Source Periods compared Rates UK Health & Safety Register WHO database (1992) Danish Cancer Register Swedish Cancer Registry Norway Cancer Register 1943-1948 1948-1953 1953-1958 (age cohorts) 1998 2018 (birth cohort 1945-1950) 1943-1947 1983-1987 1988-1992 1991-1995 1996-2000 1965-1999 RR 1.00 RR 0.79 RR 0.46 5000/year ~9000/year (6 countries ) 0.10/100 000 py 1.30/100 000 py 1.31/100 000 py 1.82/100 000 1.79/100 000 Rates rose to 16.6/million py Montanaro F, 200343 European Cancer Registries Leigh J, 200344 Pelluchi C, 200445 Australian Registry, 1945-2002 WHO database (2003) 1978-1987 1988-2007 (21 countries) 1999 (data for age >20 years) 1970-1974 1985-1989 Increase (significant) Deceleration started 53.3/million/year ~8750 deaths ~9550 deaths Weill H, 200446 SEER (NCI) USA 1973-1990 1990-1997 Increase (significant) Down slope (non-significant) Authors' comments Despite falling rates, annual deaths are unlikely to peak before 2010 and more likely to peak in the 2020s Highest risks for men born around 1945-1950. Asbestos use in Europe peaked in 1970s, remained high till the 1980s Rates peaked in the 1940-1944 age cohort. Effect of exposure regulation unlikely to occur before 2010-2015 Incidence stable, flattened earlier in younger cohorts Cohort-specific rates for men born up to ~1935 increased, then seemed to stabilise Incidence still rising in some countries, deceleration has started in others. Time trend increase restricted to age >50 years, suggesting exposure controls in 1970s have been effective Data from France, Italy and Germany suggest mesothelioma deaths are levelling off Outcome was age-adjusted incidence. Peak exposure was in the 1960s UK = United Kingdom; RR = risk ratio; WHO = World Health Organization; py = person-years; SEER = Surveillance, Epidemiology and End Results Programme of the National Cancer Institute, USA. of the twentieth century, nor for differences in meso thelioma risk associated with the different fibre types (chrysotile less than amphiboles, and amosite less than crocidolite). A 1999 analysis of the European mesothelioma epi demic among men suggests that the rate will double between 1995 and 2018, then decline, with the great est risk being seen in the cohort of men born between 1945 and 1950.39 Asbestos use in Western Europe was high until 1980. These projections are based on a simple age-birth cohort model from 1970 to 1989 for six countries (Britain, France, Germany, Italy, Nether lands and Switzerland), which together include about three-quarters of Western Europe.39 In Denmark, incidence rates of malignant meso thelioma in men peaked in the 1940-1944 cohort, then decrease in the 1950-1954 cohort.40 The authors of this study expect a further increase to occur and that the effect of banning imports in 1979 will only be come evident between 2010 and 2015. A 2002 report based on an analysis of the Swed ish Cancer Registry suggests that mesothelioma inci dence in men has levelled off in that country.41 Agestandardised incidence rates fell from 1.82 per 100 000 population in 1991-1995 to 1.79/100 000 in 1996 2000; this occurred some 17 years after a drastic re duction in asbestos imports to Sweden.41 Sweden is thus among the first countries to show a levelling-off in mesothelioma incidence. An age-period-cohort model was used to analyse time trends for pleural mesothelioma in men in Nor way.42 From 1965 to 1999, the annual number rose to 16.6 million person-years (py), after which rates seemed to stabilise. Importation of asbestos was banned in 1982, although imports fell for several years prior to that date. The authors consider that the delayed pe riod effect of the ban is likely to have its greatest effect around 2010.42 Geographic and temporal variations in mesothe lioma incidence in men in Europe were examined in a 2003 report.43 Data were extracted from 118 general cancer registries in 25 countries. Annual rates varied widely between countries, from about 8% in Britain and the Netherlands to less than 1% in Spain. Tem poral rates also varied widely between countries, in creasing significantly for all countries (except Denmark) between 1978 and 1987, and decelerating in the follow ing 10 years in all countries except England and France. The authors expect the decline to continue over the next decade, given the decrease in asbestos exposure and the recent European Union ban on its use.43 Time trends in malignant mesothelioma for the pe riod 1945-2002 were the focus of a study in Austra lia.44 Incidence rates for men aged >20 years were Asbestos-related diseases of the lungs 363 53.3/million--according to the author, the highest re ported in the world. In 90% of cases with no history of exposure, lung fibre counts longer than 2 ^ exceeded 200 000/g of dry lung tissue, implying unrecognised exposure. The author attributes Australia's high inci dence of mesothelioma to high past usage of all fibre types in many settings, and expects rates to rise until 2020.44 In response to reports that incidence rates of meso thelioma in several European countries were levelling off, an update on the mesothelioma epidemic in West ern Europe was carried out using the 2003 World Health Organization (WHO) mortality database.45 The authors conclude that all data for the most recent pe riod for France, Germany and Italy were lower than predicted, suggesting that mesothelioma deaths may be levelling off in much of Europe.45 Trends in mesothelioma incidence in the United States were the focus of a 2004 publication, based on data gathered by the Surveillance, Epidemiology and End Results (SEER) programme of the National Can cer Institute of the National Institutes of Health.46 For rates in men, a highly significant change in the upward trend was observed in the early 1990s. The authors note that the high risk for mesothelioma is prominently influenced by amphibole asbestos, usage of which peaked in the 1960s and then declined. A gradual decline in US mesothelioma cases can be ex pected, thus reducing the ill-health and economic bur den of this lethal asbestos-related tumour.46 Recent trends in less-industrialised countries Asbestos production and consumption is growing in many less-industrialised countries.47 Of the six lead ing producers, five are considered less industrialised (Table 3). However, the literature on the epidemiology of asbestos-related diseases in these countries is sparse. Russia and Kazakhstan These two republics from the former Soviet Union are today the leading producers of asbestos (Table 3). A 1999 Finnish-American-Russian project set out to develop a comprehensive health and exposure surveil lance plan for Siberian asbestos miners. In a prelimi- Table 3 Asbestos production by country (per 1000 tons) Russia China Kazakhstan Canada Brazil Zimbabwe Other countries World total 2000 752 350 179 320 209 152 88 2050 2004 875 355 347 200 195 150 110 2232 2005* 875 360 350 240 195 100 80 2200 Source: US Geological Survey, Mineral Commodity Summaries. * Estimated. nary report, the authors fund that pulmonary chrysotile concentrations in 47 unselected autopsies (24 chrysotile workers and 23 long-term residents of Asbest Town) were about the same as those reported pre viously in Canadian chrysotile miners and millers.48 However, the mean concentration of tremolite fibres was less by at least one order of magnitude. More recently, an update on trends in the Russian Federation was presented at the International Con ference on Chrysotile, held in Montreal, Canada, in 2006.49 Russia is currently the world's largest pro ducer and consumer of chrysotile asbestos, and Sverdlovk province is the most industrialised region of the Russian Federation and the site of the Bazhenovskoye mine, the world's largest chrysotile asbestos deposit.49 Mesotheliomas have been diagnosed in 32 of 66 mu nicipal locations of Sverdlovsk province. In areas of asbestos industrial facilities, mesothelioma incidence ranges from 4.3 cases/million (chrysotile asbestos), to 7.1/million in the Sysert area (anthophyllite-asbestos province of Urals), to 27.1/million for crocidolite as bestos. Mesothelioma-related mortality in Asbest Town, excluding cases with occupational exposure, was 1.4/ million. In Sukhoy Log City and Beloyarskiy village, where factories producing asbestos cement and card board are located, there is no excess mesothelioma incidence.49 China China is the world's third leading producer of asbestos (Table 3): 95% of the Chinese production is chrysotile. In many mines and manufacturing sites, air con tamination exceeds the national standard of 2 mg/m3 of total dust. Amphibole fibres (mainly tremolite) were also found in all of 10 bulk samples from six chrysotile mines: this finding may explain the excess rate of lung cancer and mesothelioma among Chinese chrysotile workers.50 Much of the recent Chinese literature relates to en vironmental exposure to crocidolite in surface soil of a rural county, Da-Yao (south-western region). Since 1988, three large epidemiological studies have been con ducted in this area (Table 4).51-53 These studies, sum marised in a 2003 report,54 showed a progressive in crease in the annual mortality rate for mesothelioma, from 85/million (1977-1983) to 178/million (1987 1993) to 365/million (up to 2003). No mesotheliomas were found in the populations living in areas where crocidolite was not known to exist in the environ ment. However, as commercial use of crocidolite was banned only in 1984, the incidence of mesothelioma is expected to peak in this area and other areas of China in the next few years.54 Brazil Brazil is the world's fifth leading producer of asbestos (Table 3). Large-scale mining and milling activities 364 The International Journal of Tuberculosis and Lung Disease Table 4 Mesothelioma incidence in men: recent trends in selected studies carried out in less-industrialised countries (by country and most often by year) First author, year, reference Country Asbestos type/ exposure site Mesothelioma rates, fibre level in lung Authors' comments Tossavainen A, 200048 Russia (Asbest Town) Autopsy material on 24 chrysotile workers and 23 Town residents Chrysotile workers: chrysotile, 0.8-50.6 f/g amphibole, 0.1-1.9 f/g Town residents: chrysotile, 0.1-14.6 f/g amphibole, 0.1- 0.7 f/g Lung chrysotile levels in Russia about the same as in Canadian miners, but tremolite levels less by an order of magnitude Kashansky S V, 200649 Russia (Swerdlovsk Region) Chrysotile mine Bashenofskuye Amphibole mine Crocidolite mine Asbest Town 4.3/million 7.1/million 27.1/million 1.4/million In Swerdlovsk province, trend towards reduction in mesothelioma incidence Tossavainen A, 200150 China Chrysotile mine dust (10 bulk samples from 6 mines) Lung fibre levels in 7 deceased miners were: anthophyllite, 71% chrysotile, 10% tremolite, 9% All 10 bulk samples contained tremolite, one contained anthophyllite. Lung fibre levels show faster clearance of chrysotile vs anthophyllite Liu X, 199051 China (South West) Crocidolite ubiquitous in soil in Da-Yao county Of 2175 local residents studied, 16 had asbestosis and 232 pleural plaques Crocidolite had been widely used for road pavements, stoves and wall paint Luo S O, 199752* China Crocidolite (Da-Yao Region) 178/million/year Cohort study (n = 4598) of villagers; lung cancer RR = 2.14 Zhou Y, 199853* China Crocidolite (Da-Yao Region) 1987-1995 = 79 cases 1996-1999 = 87 cases Estimated mesothelioma rate for Da-Yao county, 24/million/year Case series from a single hospital Luo S, 200354 China Crocidolite in the soil (Da-Yao Region) of Da-Yao county, South West China Mesothelioma mortality: 1984-1995 85/million/year 1996-1999 178/million/year to 2003 365/million/year in a population of 68 000 Commercial use of crocidolite banned since 1984. As mesothelioma latency is ~30-40 years, the ban had little effect in the 1990s Zwi A B, 198960 South Africa (1976-1984) Case registry by medical Mesothelioma incidence Rates among the highest for a practitioners, institutions 32.9, 95%CI 22.7-46.4, national population; likely an standardised rates/million underestimate; legislated controls population aged >15 years/year fewer in South Africa than in many countries Sluis-Cremer G K, South Africa 199261 Crocidolite and amosite mines (1945-1955) Mesothelioma incidence crocidolite, 44.6/100 000 py amosite, 7.8/100 000 py Crocidolite more dangerous than amosite. Crocidolite-induced mesothelioma seen after only 1-15 years exposure Kielkowski D, 200062 South Africa Crocidolite mining/milling. Cause-specific mortality, Birth cohort of white mesothelioma, 32.9/million py residents (1916-1936) Exposure environmental as well as occupational. Given the long latency, mesothelioma rates likely to increase over next 10 years until 2010 Mutetwa B, 200663 Zimbabwe Two chrysotile mines: Shibanie, Gaths Between 1970 and 2001, 36 mesothelioma cases identified; exposure information scanty or non-existent Mines use an action level of 0.5 f/cm3 vs. a WHO level of 1.0 f/cm3. In 2004, 94.5% of Shibanie samples were <0.3 f/cm3 SzeszeniaDabrowska N, 199864 Poland (rural southeast region) Factory using chrysotile from 1985 (for roofing, siding), and crocidolite from 1987 (for pressure pipes) In a cohort of 1526 asbestos cement workers followed 1959-1996: SMR for mesothelioma: 80-fold excess SMR for colon cancer: 3-fold excess The very high risk for mesothelioma exhibited by this cohort attributed to non-occupational exposure (use of asbestos cement waste for surfacing farmyards, roads, paths, sports fields, buildings) Gaafar R M, 200565 Egypt 14 asbestos factories; two surrounded by residential areas 1989-1999, 148 cases 2000-2003, 635 cases (an increase of cases diagnosed in 3 Cairo hospitals from 0.47% to 1.3%) Residential exposure experienced by 64.7% (mainly in Shobra El Khaymah, and in Helwan, El-Maasara and surrounding areas) Emri S, 200466 Turkey (south-east region) Tremolite, chrysotile and anthophyllite; also erionite in Cappadocia Estimated incidence of mesothelioma in the SE region 43/million, and 996/100 000 in erionite villages Environmental exposure from stucco, paint and whitewash on walls, floors, ceilings, etc., comparable to occupational exposure (continued) Asbestos-related diseases of the lungs 365 Table 4 (Continued) First author, year, reference Country Asbestos type/ exposure site Mesothelioma rates, fibre level in lung Authors' comments Dutta M, 200367 Murlidhar V, 200568 Joshi T K, 200469 India, West Jharkhand Abandoned chrysotile mine dump in Roro hills Survey of 252 subjects (45% ex-miners) from 14 villages showed: 17.5% had breathing difficulties, 7.1% had haemoptysis. Careless closure of the mine resulted in waste slipping down into paddy fields .In each monsoon waste runs off into villages and paddy fields India (Mumbai) Factory making textiles, brake/clutch linings, asbestos fibre Of 181 workers examined, asbestosis diagnosed in 22%. Prevalence of asbestosis less than expected, suggesting a 'healthy' worker effect India Exposure to asbestos Except in the mining sector, occurs in mining, milling mesothelioma is not a notifiable and manufacturing sectors occupational disease in India. Asbestos use not regulated in factories or construction In India, most manufactured products are consumed domestically. Local production has decreased due to large-scale imports from Canada * Article in Chinese but with English abstract. f/g = fibre per gram; RR = risk ratio; CI = confidence interval; py = person-years; f/cm3 = fibres per cm3; WHO = World Health Organization; SMR = standard ised mortality rates. started in the early 1940s. A single company has been responsible for asbestos exploration (primarily chrysotile) in Brazil: from 1940 to 1967 in the north-east state of Bahia, and thereafter in the central state of Goias. In a retrospective study of 3634 past and present workers, radiographic abnormalities and lung func tion impairment declined significantly (three to five fold) over time as exposure was progressively reduced from between 16 and 19 fibres/cm3 to approximately 1 fibre/cm3 (in asbestos grinding, drilling, mixing and sacking operations).55 Another important source of occupational expo sure to asbestos in Brazil is the fibre-cement industry. In a cross-sectional study of 828 compensation claim ants with long-term exposure, the authors found a prevalence of 8.9% for asbestosis and 29.7% for pleu ral thickening.56 Pleural thickening was also indepen dently associated with chronic bronchitis and short ness of breath. Less is known about the malignant effects of asbes tos exposure. In a retrospective study conducted in the state of Rio de Janeiro, 83 cases of pleural mesothe lioma were identified among death certificates coded as pleural tumours.57 However, their asbestos expo sure could not be retrospectively ascertained. South Africa South Africa has a long history of asbestos mining; chrysotile, amosite and crocidolite deposits have all been exploited. Blue asbestos (crocidolite) was identi fied in the Northern Cape by explorers in the early 1800s.58 The link between asbestos and mesotheli oma was first reported in a case-series from the North western Cape.59 Mining peaked in the late 1970s, with more than 20 000 miners being then employed in the industry.58 A study in the 1980s suggested that there had been a steady increase in annual mesothelioma incidence in white males aged >15 years from 27.6/ million in 1976 to 40.5/million in 1984 (Table 4).60 A 1992 study showed a high incidence (44.6/100 000 py) in a cohort of 1800 white men exposed only to crocidolite at work, compared to a much lower incidence (7.8/100 000 py) in a cohort of 1810 white men ex posed only to amosite at work.61 Respective propor tional mortality rates for mesothelioma for the two cohorts were 11.9% and 1.7%. The incidence of mesothelioma in black workers is likely to have been much higher. In a birth cohort study of white men, residents of Prieska, a small town close to a crocidolite mine productive from 1893 to the late 1960s, cause-specific mortality for mesothelioma was 32.9 (95% confidence interval 22.7-74.6) per million py.62 The authors point out that, given its long latency, the mesothelioma-related mortality can be expected to increase throughout the current decade. Zimbabwe Zimbabwe ranks sixth in the order of world produc tion, and produced 152 000 tons of chrysotile asbes tos in 2004 (Table 3), of which 83% was exported. Chrysotile is mined at the Shibanie and Gaths mines, which employ approximately 5000 persons and sup port more than 20 000 persons in the mining towns of Zvishawe and Moshawa.63 Chrysotile manufacturing also supports over 1500 persons; over 60 000 families depend on downstream industries, as do 300 000 in the construction industry, which uses asbestos cement prod ucts in housing, water reticulation, sanitation and ir rigation. The mines use an action level of 0.5 fibres/cm3, against a WHO level of 1 fibre/cm3. In 2000, 94% of samples from Shibanie mine were <0.3 fibres/cm3 (Table 4). Thirty-six mesothelioma cases were identi fied between 1970 and 2001; however, exposure infor mation was scanty or non-existent in the case files reviewed.63 The author of this study concludes that chrysotile is a low-cost product, as safe as any of the substitutes available, and can be mined safely using today's technology.63 366 The International Journal of Tuberculosis and Lung Disease Other less-industrialised countries In a 1998 Polish report on 1526 workers in an asbes tos cement factory, standardised mortality ratio (SMR) analysed using the man-year, method identified 16 cases of pleural mesothelioma; four cases had a short exposure/latency period (Table 4).64 Additional inves tigations revealed that available asbestos-cement waste had been used for road surfacing. Asbestos was used in Egypt from 3000 to 2000 bc to embalm the bodies of the Pharoahs.65 Of the 14 fac tories in the country today, one began operation in 1927 before people lived in the area but is now sur rounded by residential areas exhibiting a high rate of mesothelioma. Case series from two Cairo hospitals have documented an increase in mesothelioma rates from 148 cases in 1989-1999 to 635 cases in 2000 2003 (Table 4).65 A 2004 study from Turkey estimated the incidence of malignant pleural mesothelioma at 43/million in the south-east part of the country.66 Also, 996/100 000 inhabitants of villages in Cappadocia use erionite in their homes as a whitewash or stucco for walls, floors and roofs, and as a substitute for baby powder. A sur vival advantage was shown for asbestos-induced ver sus erionite-induced mesothelioma (Table 4).66 In India, exposure to asbestos occurs in mining/ milling, the asbestos-cement industries, civil construc tion and electro-mechanical appliances.67-69 Domes tic production has decreased due to large-scale impor tation from Canada. India is also a high consumer of asbestos, and most products manufactured are used in the country.69 A recent (2005) study found a prev alence of 22% for asbestosis among 181 workers of an asbestos composite mill in Mumbai.68 The authors note that fewer than 30 cases in the country have re ceived compensation for asbestosis. In an observa tional study in the small town of Roro, Eastern India, the impact on the environment and the community of careless closure of an asbestos mine in 1983 was exam ined.67 With each monsoon, the waste from the dump runs off into fields, villages and streams. The older age groups who worked in the mines in the past re ported shortness of breath and haemoptysis (Table 4). CLINICAL MANAGEMENT, EXPOSURE CONTROL AND PREVENTION Clinical management of asbestos-related disease is no different from clinical management of these conditions in the absence of a history of asbestos exposure.5 How ever, because asbestos-related disease is work-related or potentially work-related, physicians should make the appropriate notification of disease according to the jurisdiction in their local practice area. Advice concerning continuing employment in a job with con tinuing exposure should be based on our knowledge of its impact on the natural history of asbestos-related disease and the risk of developing new disease after leaving a job that involved exposure,5 including chronic airflow limitation (chronic obstructive pulmo nary disease).29 No treatment (medical or surgical) has been shown to influence the clinical course of asbestosis, which appears to be more resistant than other forms of pulmonary fibrosis, perhaps because the agent (particularly if it is an amphibole) persists in the lung after exposure ceases.5 For individuals with a past exposure history, there is encouraging news.5 Only a small minority of those exposed are likely to show changes on X-ray, and only a small minority of those with X-ray changes are likely to develop clinical evidence of disease.5 Smoking ces sation is likely to benefit an individual with past ex posure more than one without because of the multi plicative interaction between smoking and asbestos. For non-malignant pleural disorders, the evidence is now reasonably strong that subjects with pleural fi brosis (pleural effusion seems to be a step in the de velopment of pleural fibrosis) are at greater risk for developing asbestosis.5 Advice against continuing in a job involving asbestos exposure (even in workplaces that respect the exposure limits) is probably sound, although it may be difficult for workers to accept, es pecially if it comes late in their working careers when retraining is not easy to find or undertake. Exposure control is key to prevention, and is impor tant in the management of asbestos-related disease. The last decades of the twentieth century saw work place dust levels decline and work practices improve (e.g., laundering of work clothes on-site) in many in dustrialised countries and some less-industrialised countries.5 There was also a decline in rates of nonmalignant and malignant asbestos-related disease in many industrialised and some less-industrialised coun tries: the study from Brazil63 is an example of how, with decreasing exposure, radiological markers de creased and lung function levels improved. A ban on asbestos was introduced to control the worldwide epidemic of asbestos-related disease,5 mainly in industrialised countries without asbestos mining and milling activities.47 By contrast, in less-industrialised countries, which account for the bulk of the world's use of asbestos, there is concern about the lack of af fordable and equally effective substitutes. It has been argued that chrysotile has made it possible for many around the world, particularly those in low-income countries, to have clean, safe water supplies and af fordable housing.63 This could change with the further development of waste plant-fibres, coupled with evi dence that they are as effective as chrysotile (particu larly in cement, friction and insulation products).70 Clearly, wherever chrysotile is used, management of this workplace hazard requires collaboration between workers, unions (responsible for monitoring dust levels in the workplaces, to which they must have access) and companies (responsible for engineering controls within its operation and in the surrounding environ Asbestos-related diseases of the lungs 367 ment), that is supported by appropriate government regulation, including laws on cleaning up dumps fol lowing the closure of mines and/or factories, and always with community support. References 1 Lesage M. ILO international classification of radiographs of pneumoconioses. In: Stellman J M, ed. International Labour Office. Encyclopaedia of occupational health and safety. 4th ed. Part II. Respiratory system. Geneva, Switzerland: ILO, 1997: pp 10.33-10.38. 2 Liddell D, Miller K. Mineral fibres and health. Boca Raton, FL, USA: CRC Press, 1991: p 381. 3 Selikoff I, Lee D H K. Asbestos and disease. New York, NY, USA: New York Academic Press, 1978: p 549. 4 Rom W N. Asbestos related diseases. In: Rom W N, ed. Envi ronmental and occupational medicine. 3rd ed. Philadelphia, PA, USA: Lippincott-Raven, 1998: 349-376. 5 Cowie R L, Murray J, Becklake M R. Pneumoconioses. Chap ter 61. In: Mason R J, Broaddus V C, Murray J T, Nadel J A, eds. Murray and Nadel's textbook of respiratory medicine, 4th ed. Vol. 2. Philadelphia, PA, USA: Elsevier Saunders, 2005: pp 1748-1782. 6 De Vuyst P, Gevenois P A. Asbestosis. In: Hendrick D J, Burge P S, Beckett W S, Churg A, eds. Occupational disorders of the lung: recognition, management and prevention. Edinburgh, UK: WB Saunders, Elsevier Science, 2002: p 144. 7 Copes R, Thomas D, Becklake M R. Temporal patterns of ex posure and nonmalignant pulmonary abnormality in Quebec chrysotile workers. Arch Environ Health 1985; 40: 80-87. 8 Craighead J E, Abraham J L, Churg A, et al. The pathology of asbestos-associated diseases of the lungs and pleural cavities: diagnostic criteria and proposed grading schema. Report of the Pneumoconiosis Committee of the College of American Pa thologists and the National Institute for Occupational Safety and Health. Arch Pathol Lab Med 1982; 106: 544-596. 9 Becklake M R. Asbestos criteria. [Letter to the editor] Arch Pathol Lab Med 1984; 108: 93. 10 De Vuyst P, Jedwab J, Dumortier P, et al. Asbestos bodies in bronchoalveolar lavage. Am Rev Respir Dis 1982; 126: 972 976. 11 Case B W, Sebastien P. Environmental and occupational expo sures to chrysotile asbestos: a comparative microanalytic study. Arch Environ Health 1987; 42: 185-191. 12 McDonald J C, Becklake M R, Fournier-Massey G, Rossiter C E. Respiratory symptoms in chrysotile asbestos mine and mill workers of Quebec. Arch Environ Health 1972; 24: 358-363. 13 Brodkin C A, Barnhart S, Anderson G, Checkoway H, Omenn G S, Rosenstock L. Correlation between respiratory symptoms and pulmonary function in asbestos-exposed workers. Am Rev Respir Dis 1993; 148: 32-37. 14 Ross R. The clinical diagnosis of asbestosis in this century re quires more than a chest radiograph. Chest 2003; 124: 1120 1128. 15 Mukherjee A K, Rajmohan H R, Dave S K, Rajan B K, Kakde Y, Rao S R. An environmental survey in chrysotile asbestos mill ing processes in India. Am J Ind Med 1992; 22: 543-551. 16 Mukherjee S, de Klerk N, Palmer L J, Olsen N J, Pang S C, Musk A W. Chest pain in asbestos-exposed individuals with benign pleural and parenchymal disease. Am J Respir Crit Care Med 2000; 162: 1807-1811. 17 International Labour Office. International classification of radio graphs of pneumonconiosis. Geneva, Switzerland: ILO, 2003. 18 Lilis R, Miller A, Godbold J, Chan E, Selikoff I J. Radiographic abnormalities in asbestos insulators: effects of duration from onset of exposure and smoking. Relationships of dyspnea with parenchymal and pleural fibrosis. Am J Ind Med 1991; 20: 1-15. 19 Miller A, Lilis R, Godbold J, Wu X. Relation of spirometric function to radiographic interstitial fibrosis in two large work forces exposed to asbestos: an evaluation of the ILO profusion score. Occup Environ Med 1996; 53: 808-812. 20 Lee Y C, Singh B, Pang S C, de Klerk N H, Hillman D R, Musk A W. Radiographic (ILO) readings predict arterial oxygen de saturation during exercise in subjects with asbestosis. Occup Environ Med 2003; 60: 201-206. 21 Gevenois P A, De Vuyst P, Dedeire S, Cosaerte J, Van de Weyer R, Sturyven J. Conventional and high-resolution CT in asymp tomatic asbestos exposed workers. Acta Radiol 1994; 35: 226 229. 22 Harkin T J, McGuinness G, Goldring R, et al. Differentiation of the ILO boundary chest roentgenograph (0/1 to 1/0) in asbestosis by high-resolution computed tomography scan, alveo litis, and respiratory impairment. J Occup Environ Med 1996; 38: 46-52. 23 Neri S, Boraschi P, Antonelli A, Falaschi F, Baschieri L. Pulmo nary function, smoking habits, and high resolution computed tomography (HRCT) early abnormalities of lung and pleural fibrosis in shipyard workers exposed to asbestos. Am J Ind Med 1996; 30: 588-595. 24 American Thoracic Society. Diagnosis and initial management of nonmalignant diseases related to asbestos. Am J Respir Crit Care Med 2004; 170: 691-715. 25 Lynch D A, Gamsu G, Aberle D R. Conventional and high res olution computed tomography in the diagnosis of asbestosrelated diseases. Radiographics 1989; 9: 523-551. 26 Copley S, Hansell D M. Imaging. In: Hendrick D J, Burge P S, Beckett W S, Churg A, eds. Occupational disorders of the lung: recognition, management and prevention. Edinburgh, UK: WB Saunders, Elsevier Science, 2002: pp 483-502. 27 Teschler H, Friedrichs K H, Hoheisel G B, et al. Asbestos fibers in bronchoalveolar lavage and lung tissue of former asbestos workers. Am J Respir Crit Care Med 1994; 149: 641-645. 28 Churg A. Non neoplastic induced asbestos-related disease. In: Churg A, Green F H Y, eds. Pathology of occupational lung disease. 2nd ed. Baltimore, MD, USA: Williams and Wilkins, 1998: pp 277-338. 29 Becklake M R. Occupational exposures: evidence for a causal association with chronic obstructive pulmonary disease. Am Rev Respir Dis 1989; 140 (Suppl): S85-S91. 30 Sette A, Neder J A, Nery L E, et al. Thin-section CT abnormal ities and pulmonary gas exchange impairment in workers ex posed to asbestos. Radiology 2004; 232: 66-74. 31 Shih J F, Wilson J S, Broderick A, et al. Asbestos-induced pleu ral fibrosis and impaired exercise physiology. Chest 1994; 105: 1370-1376. 32 Cugell D W, Kamp D W. Asbestos and the pleura: a review. Chest 2004; 125: 1103-1117. 33 Kee S T, Gamsu G, Blanc P. Causes of pulmonary impairment in asbestos-exposed individuals with diffuse pleural thicken ing. Am J Respir Crit Care Med 1996; 154: 789-793. 34 Bourbeau J, Ernst P, Chrome J, Amstrong B, Becklake M R. Re lationship between respiratory impairment and asbestos-related pleural abnormality in an active workforce. Am Rev Respir Dis 1990; 142: 837-842. 35 Churg A. Neoplastic induced asbestos-related disease. In: Churg A, Green F H Y, eds. Pathology of occupational lung disease. 2nd ed. Baltimore, MD, USA: Williams and Wilkins, 1998: pp 339-391. 36 Gong M N, Christiani D. Lung cancer. In: Hendrick D J, Burge P S, Beckett W S, Churg A, eds. Occupational disorders of the lung: recognition, management and prevention. Edinburgh, UK: WB Saunders, Elsevier Science, 2002: pp 305-326. 37 Hodgson J T, Darnton A. The quantitative risks of mesothe lioma and lung cancer in relation to asbestos exposure. Ann Occup Hyg 2000; 44: 565-601. 38 Peto J, Hodgson J T, Matthews F E, Jones J R. Continuing 368 The International Journal of Tuberculosis and Lung Disease increase in mesothelioma mortality in Britain. Lancet 1995; 345: 535-539. 39 Peto J, Decarli A, La Vecchia C, Levi F, Negri A. The European mesothelioma epidemic. Br J Cancer 1999; 79: 666-672. 40 Kjaergaard J, Andersson M. Incidence rates of malignant me sothelioma in Denmark and predicted future number of cases among men. Scan J Work Environ Health 2000; 26: 112-117. 41 Hemminki K, Xinjun L, Mesothelioma incidence seems to have leveled off in Sweden. Int J Cancer 2003; 103: 145^6. 42 Ulvestad B, Kjaerheim K, Moller B, Andersen A. Incidence trends of mesothelioma in Norway, 1965-1999. Int J Cancer 2003; 107: 94-98. 43 Montanaro F, Bray F, Gennaro V, et al. Pleural mesothelioma incidence in Europe: evidence of some deceleration in the in creasing trends. Cancer Causes Control 2003; 14: 791-803. 44 Leigh J. Malignant mesothelioma in Australia, 1945-2002. Int J Occup Environ Health 2003; 9: 206-217. 45 Pelucchi C, Malvezzi M, La Vecchia C, Levi F, Decarli A, Negri E. The mesothelioma epidemic in Western Europe: an update. Br J Cancer 2004; 90: 1022-1024. 46 Weill H, Hughes J M, Churg A M. Changing trends in US meso thelioma incidence. Occup Environ Med 2004; 61: 438-441. 47 Kazen-Allen L. Asbestos and mesothelioma: worldwide trends. Lung Cancer 2005; 49S1: S3-S8. 48 Tossavainen A, Kovalevsky E, Vanhala E, Tuomi T. Pulmonary mineral fibers after occupational and environmental exposure to asbestos in the Russian chrysotile industry. Am J Ind Med 2000; 37: 327-333. 49 Kashansky S V. Prevalence of mesothelioma in various sites in Russia: differences in the exploitation of asbestos fibre types and in the products manufactured. [Abstract] Presented at the International Conference on Chrysotile. Montreal, QC, Can ada: Chrysotile Institute, May 23-24, 2006. 50 Tossavainen A, Kotilainen M, Takahashi K, Pan G, Vanhala E. Amphibole fibres in Chinese chrysotile asbestos. Ann Occup Hyg 2001; 45: 145-152. 51 Liu X, Luo S, Wang Z, et al. An investigation of crocidolite contamination and mesothelioma in a rural area of China. Biomed Environ Sci 1990; 3: 156-165. 52 Luo S O, Mu S H, Zhan C. A retrospective cohort study (1987 1995) of malignant neoplasm in a country contaminated with crocidolite. Chin J Ind Hyg Occup Dis 1997; 15: 272-276. 53 Zhou Y, Luo S, Song Y, et al. A clinical-pathologic analisis of 47 cases of mesothelioma resulted from environmental expo sure to crocidolite. Chin J Ind Hyg Occup Dis 1998; 16: 169 170. [Chinese] 54 Luo S, Liu X, Mu S, Tsai S P, Wen C P. Asbestos related diseases from environmental exposure to crocidolite in Da-yao, China. I. Review of exposure and epidemiological data. Occup Environ Med 2003; 60: 35-42. 55 Bagatin E, Neder J A, Nery L E, et al. Non-malignant conse quences of decreasing asbestos exposure in the Brazil chrysotile mines and mills. Occup Environ Med 2005; 62: 381-389. 56 Algranti E, Mendonca E M, DeCapitani E M, Freitas J B, Silva H C, Bussacos M A. Non-malignant asbestos-related diseases in Brazilian asbestos-cement workers. Am J Ind Med 2001; 40: 240-254. 57 Pinheiro G A, Antao V C, Monteiro M M, Capelozzi V L, Terra-Filho M. Mortality from pleural mesothelioma in Rio de Janeiro, Brazil, 1979-2000: estimation from death certificates, hospital records, and histopathologic assessments. Int J Occup Environ Health 2003; 9: 147-152. 58 McCulloch J. Asbestos blues: labour, capital, physicians and the state in South Africa. Bloomington, IN, USA: James Currey and Indiana University Press, 2002. 59 Wagner J C, Sleggs C A, Marchand P. Diffuse pleural mesothe lioma and asbestos exposure in the North-Western Cape prov ince. Br J Ind Med 1960; 17: 260-271. 60 Zwi A B, Reid G, Landau S P, Kielkowski D, Sitas F, Becklake M R. Mesothelioma in South Africa, 1976-84: incidence and case characteristics. Int J Epidemiol 1989; 18: 320-329. 61 Sluis-Cremer G K, Liddell F D, Logan W P, Bezuidenhout B N. The mortality of amphibole miners in South Africa, 1946-80. Br J Ind Med 1992; 49: 566-575. 62 Kielkowski D, Nelson G, Rees D. Risk of mesothelioma from exposure to crocidolite asbestos: a 1995 update of a South Af rican mortality study. Occup Environ Med 2000; 57: 563 567. 63 Mutetwa B. Chrysotile asbestos and asbestos in Zimbabwe. Presented at the International Conference on Chrysotile. Mon treal, QC, Canada: Chrysotile Institute, May 23-24, 2006. 64 Szeszenia-Dabrowska N. Environmental exposure to asbestos in asbestos cement workers: a case of additional exposure from indiscriminate use of industrial wastes. Int J Occup Med Environ Health 1998; 11: 171-177. 65 Gaafar R M, Eldin N H A. Epidemic of mesothelioma in Egypt. Lung Cancer 2005; 49 (Suppl 1): S17-S20. 66 Emri S, Demir A U. Malignant pleural mesothelioma in Tur key, 2000-2002. Lung Cancer 2004; 45 (Suppl 1): S17-S20. 67 Joshi T K, Gupta R K. Asbestos in developing countries: mag nitude of risk and its practical implications. Int J Occup Med Environ Health 2004; 17: 179-185. 68 Murlidhar V, Kanhere V. Asbestosis in an asbestos composite mill at Mumbai: a prevalence study. Environ Health 2005; 4: 1-7. 69 Dutta M, Sreedhar R, Basu A. The blighted hills of Roro, Jharkhand, India: a tale of corporate greed and abandonment. Int J Occup Environ Health 2003; 9: 254-259. 70 Cartheman B. `Controlled use' of asbestos. Int J Occup Environ Health 2003; 9: 294-298. L'amiante est un terme descriptif concernant un groupe de mineraux existant dans la nature et connus par l'humanite depuis l'antiquite. Les principaux types d'amiante (chrysotile, et les amphiboles crocidolite et amosite) sont differents en ce qui concerne la structure chimique, la biopersistance dans les tissus humains et la toxicite. Une exploitation commerciale, ne prenant guere les problemes environnementaux en consideration, a augmente au cours du dernier siecle, particulierement apres la deuxieme guerre mondiale, pour repondre a la globalisation et aux besoins des cites en expansion dans le monde. Au fur et a mesure que ses effets de sante, qu'ils soient nonmalins (fibrose pulmonaire ou asbestose, epanchement, RESUME plaques ou epaississement de la plevre) ou malins (mesotheliome, cancer du poumon et autres cancers), sont devenus evidents, la pression du public pour le controle de son utilisation s'est accrue. Les dernieres decennies du siecle dernier ont vu une decroissance de l'exposition et des taux d'asbestose dans les pays industrialises et dans quelques pays moins industrialises ou les plaques pleurales et les mesotheliomes pleuraux sont actuellement les manifestations les plus frequentes de l'exposition a l'amiante. Un suivi plus prolonge des cohortes exposees a l'amiante dans les mines ou les manufactures a egalement renforce les preuves d'un gradient dans la toxicite des fi bres, les chrysotiles montrant une toxicite plus faible que Asbestos-related diseases of the lungs 369 les amphiboles et l'amosite plus faible que la crocidolite. Dans les dernieres decennies du siecle dernier, on a ob serve une stabilisation et/ou une decroissance des taux de mesotheliome dans plusieurs pays industrialises. Dans les pays moins industrialises, les donnees sur la maladie sont mediocres, l'exposition generalement elevee et les taux pourraient connaitre leur sommet a l'avenir. La prise en charge des maladies liees a l'amiante au niveau des lieux de travail exige une collaboration entre les travailleurs, les syndicats (responsables du suivi des taux de poussieres dans les lieux de travail, auxquels ils doivent avoir acces), et les societes (responsables des controles de la technique) ; ces actions doivent etre renforcees par des reglements gouvernementaux appropries et par le soutien de la collectivite. Amianto es un termino descriptivo que agrupa minerales que se encuentran naturalmente y que el hombre conoce desde tiempos muy antiguos. Los principales tipos de fibras de amianto (el crisolito y las formas anfibolicas crocidolita y amosita) difieren con respecto a su estructura qmmica, su persistencia en los tejidos humanos y su toxicidad. La explotacion comercial, con escasa consideracion de las regulaciones medioambientales, aumento du rante el siglo pasado, en particular despues de la Segunda Guerra Mundial, con el proposito de adaptar la globali zation a la demanda de las ciudades en expansion a traves del mundo. Cuando fueron evidentes sus efectos perjudiciales sobre la salud, tanto benignos (fibrosis pulmonar o asbestosis ; derrame, placas y engrosamiento pleurales) como malignos (mesotelioma, cancer de pulmon y otros tipos de cancer), se acrecento la presion publica por una regulation de la utilizacion del amianto. En los ultimos decenios del siglo pasado tuvo lugar una disminucion de la exposicion y de la incidencia de asbestosis en los pa^ses industrializados y en algunos menos industrializados, donde las placas pleurales y el mesotelioma maligno constituyeron las manifestaciones mas fre- ___________________________________________ RE S U M E N cuentes de la exposicion al amianto. Asimismo, el seguimiento a mas largo plazo de cohortes expuestas al amianto en la industria minera y manufacturera ha consolidado las pruebas sobre un gradiente de toxicidad de las fibras, segun el cual la toxicidad del amianto crisolito es infe rior a la de las formas anfibolicas y entre ellas, la amosita es menos toxica que la crocidolita. En los ultimos decenios del siglo pasado se observo una estabilizacion o una disminucion de la incidencia de mesotelioma en varios pa^ses industrializados. En pa^ses menos industrializados, los datos sobre esta enfermedad son escasos, la exposicion suele ser alta y su incidencia puede alcanzar puntos maximos en el futuro. El control de las enfermedades causadas por el amianto en el puesto de trabajo precisa la colaboracion entre los trabajadores, los sindicatos (encargados de supervisar los datos sobre la con centration de polvo en los lugares de trabajo, a los cuales tienen que tener acceso) y las empresas (que tienen a su cargo los controles tecnicos) reforzada por reglamentaciones gubernamentales apropiadas y por el apoyo de la comunidad.