Document ree9x8a0oQ81BBR0n5a09J7kq

\.'*p Efn^n Med I 999.56:505-513 REVIEW =505 Mesothelioma: cases associated with non-occupational and low dose exposures Gunnar Hillerdal Abstract Objectives--To estimate the importance of low dose exposure to asbestos on the risk of mesothelioma. Method*--A review of the literature. Results and conclusions--There is no evi dence of a threshold level below which there is no risk ofmesothelioma. Low level exposure more often than not contains peak concentrations which can be very high for short periods. There might exist a background level of mesothelioma occur ring in the abscence of exposure o* asbes tos, but there is no proof of this and this "natural level" is probably much lower than the 1-2/million/year which has been often cited. :Occup Environ Med 1999;54:505-513) Keywords: low exposure; asbestos; mesothelioma Department of Lung Medicine, KaroUnab* Hospital, Stockholm, Sweden Q Hilletdal Correspondence toe Dr Gunner HiUerdei, epertmcnc of Luna Medicine. Karolinska Hospital, Stockholm. Sweden. \ccepted S March 1949 Mesothelioma is an incurable disease which is almost exclusively due to inhalation of asbestos fibres. Asbestos has been extensively used in industry and construction in the 20th century, especially during and after the second world war, and even if the mineral is no longer used in most rich western countries the total world production remains high. There is a worldwide pollution with asbestos, as indicated by the finding of the mineral in samples of Greenland ice1 and on the Yorkshire Moors,1 and every dozen in the world has been exposed to some extent. Consequently, asbestos fibres can be found in most lungs at necropsy.' It is thus understandable that there is concern about the risk of mesothelioma for the general popula tion. However, it should be remembered that mesothelioma is a rare disease with incidence in industrialised countries ranging from 1 to 5/million/year among women and values for Table I Pnrpomonau morality from merodleEoma ai various cohorts Cohort .Amphibole nunen Crocidolite miners insulation worker* Patient* with asbestosts Ddazkx Cm) 1225 118 4951 29) 40 19 Dtattedut to mnothtHoma (H) Z 4 6 9 9 10 10 Reference 4 5 6 7 8 9 10 men 5-10 times higher (see table 3). Even in cohorts with a very heavy exposure to asbestos most people will die from other causes. In peo ple with certified asbestosis--that is, with a heavy exposure--up to 10% will develop mes othelioma; among insulators in the United States and Canada, also a heavily exposed group, 9.3% of the deaths have been due to this disease; and in amphibole miners in South Africa or Australia, this figure is 2-4% (table 1). Clearly, with exposure concentrations several magnitudes lower, as occurs in the gen eral population, the risk is very small, often impossible to measure. A discussion of the risks from low exposure must include the dose-response curve; the existence or non-existence of a threshold, and thus a background concentradon; and should try to define low exposure and estimate to what degree that really means a low concentration. From conflicting findings and opinions at tempts must be made to make a meaningful conclusion. The different types of asbestos seem to differ considerably in their ability to cause mesothe liomas. Chrysoole is considered by many authors to be a weak carcinogen in humans," whereas the two amphiboles crocidolite and tremoiite are much more dangerous according to many studies.'1 The third of the more important amphiboles, amhophyllite, was long considered not to cause mesothelioma, but such tumours have now been reported al though the risk seems to be small.1' There is, none the less, a minority opinion that chrysotile is in fact responsible for most of the pleural mesotheliomas in society'* or should at least be considered to carry the same risk.1' This discussion, however, falls outside the present review and is not important for the conclusions drawn here. Definition and diagnosis of mesothelioma Mesotheliomas are, by definition, tumours that arise from mesothelial cells and can thus arise from any body cavity; the pleura, the perito neum, the pericardial sac, and even the tunica vaginalis testis. Pleural mesotheliomas are the most common and pathologically the best defined ones. Pleural mesotheliomas have a male to female rate of about five to one, whereas for peritoneal tumours this ratio is l. 3 to 1 .'* Thus, either the aetiology is different, the Hiiterda! '-trie 2 Possible risk factors and mediators ,it -isk or mesatneilotna t'other than asbestos1 .LJc \>n Erionue O)romc inflammation Radiation Bervllium Vegetable fibres Hereditary* factors Immunological factors Dietarv factors 'ruses CW.vr.'f= Verv high incidence oi mesothelioma environmental exposure in Turkev Pleurai scars tuberculosis, pieunsw therapeutic pneumothorax; Single cases arter Thorotrast intection or radiotherapy; causality not proved One case in atomic bomb survivor Two doubtful cases described No proof in humans Familial cases explained b\ common asbestos exposure:) Correlation with parental cancer Rapidlv progressive cases in patients with HIV infection Provitamin A, 3-carotene mav decrease the risk Mesotheliomas in animals Simian virus 40 DNA sequences reported in mesotheliomas Rtli'ciics:! 19 20 :i 22 21 13 24-26 27 28 :o 30 31 32 diagnosis is more difficult in women, or women exposed to asbestos are more likely to develop a pentoneal than a pleural mesothelioma. In fact, one type of mesothelioma occurring almost exclusively in women is the so called multicystic mesothelioma. This tumour has a better prognosis, is more sensitive to cytostatic drugs, and seems to have no connection with exposure to asbestos.'" The pathological diagnosis of mesothelio mas requires experience, and confusion can occur with both benign pleural lesions and with metastatic pleural diseases.1' Many countries now have "mesothelioma panels", which has meant a great improvement in the diagnosis. In most national cancer registries, most likely both overdiagnosis and underdiagnosis occur. Suggested causes of mesothelioma other than mineral fibres Apart from mineral fibres, radiation (for exam ple, through the contrast medium Thorotrast) has been suggested to cause human mesothe lioma. However, in a large retrospective study of more than 250 000 women treated for mammary carcinoma, a quarter of them initially with radiotherapy, no association between radiation and mesothelioma could be found." As can be seen from table 2, other causes or contributing factors have also been suggested. Viruses can cause mesotheliomas in animals, but this has not been described in humans. DNA sequences associated with Simian virus 40 (SV 40) transforming factors have been reported inr a high proportion of mesothelio mas from some countries.1' This suggests that there is a connection between SV40, which was a contaminant of live polio vaccines in 1959-61, and later development of mesothe lioma. Thus, SV 40 might be a cofactor to asbestos in some patients with mesothelioma , but the results have not been confirmed and are still disputed. In summary, then, as far as is known today, factors other than mineral fibres can only explain a very small proportion of mesothelio mas, and can for practical purposes be disregarded. Thus, a malignant mesothelioma can be regarded either as caused by asbestos or belonging to a normal background level--that is a spontaneously occurring tumour. The rela tive uiuiportance of these two factors has been debated and will be further explored in this review. Incidence of mesothelioma There is a large variation in the incidence of mesothelioma in different countries and in most places a steadily rising number of cases with time. In table 3, the incidence or mortality from mesotheliomas in different countries at various times can be seen. As mortality for practical puprposes is the same as the inci dence for this disease, both figures have been used in the table. Some of the differences between the countries are probably due to diagnostic difficulties, but most of the varia tions can be explained by the use of asbestos in the particular society some decades earlier. Dose-response and latency time Most researchers agree that there is a positive dose-response curve for mesothelioma--the heavier the exposure to asbestos, the greater the risk. This is found in cohort studies as well as in analyses of amphibole asbestos fibres in the lungs.45-" It was realised early that time since first exposure was of great importance, and therefore the "cubic residence-time model" was suggested by Doll and Peto in their report in 1985": I (T) = c x F x (T4-(T-D)4 Where, I (T)=incidence at the time T after exposure; c=a constant depending on the process, F=intensity of exposure, and D=duration of exposure. This equation has been used in many studies with an acceptable fit for normal occupational exposure concen trations . F in the equation is the total exposure--a combination of fibre concentra tions and exposure time--usually measured in fibre-years. (1 fibre-year = a mean of 1 fibre/ml air for 1 working year). Thus, the doseresponse curve is supposed to be linear, but the result is heavily influenced by the time factor. Unfortunately, the exact value of F is often uncertain, even in well defined highly exposed cohorts. The equation is thus rarely useful especially with low doses, in which F is usually a crude guess only. As can be seen from table 1, even with heavy exposure only up to 10% of a cohort will die from mesothelioma--so the for mula is not applicable in these cases either. With very heavy exposure, most patients will die from pulmonary insufficiency due to asbestosis before there has been sufficient time to develop a mesothelioma. Even more troublesome is the time factor T, which quickly becomes very important in this equation. If the equation is correct, the risk . JCtWU: ..Jf v rtn Ant-' .4 V ino- von s.d2Jirc. F-ance ; ,.i' X. U'cu . : v- L States vi'JiP Bn j : -.-nd .-ji U.i a r k r.id<*m :>.rnarfc \ inivvYin 'Nature. France 'u ,-ji Brra r Vw'irJlu .j.'.-j; Bruj.ft i:cai Bn;j r " ia >/*/u :>i1 : uvi'k arcus ,-ivr (one -`72 4 7n- -ui : : *? m : -sH-'l : >. Jt-w4 ' *2 ~o : :**45 ; 047-)| !m44 ;: ;' ' i !: : ' .i * > - ;l 12 o i:: i: 5 !4 " l -> 4 2' 7 24 * 1.) 5 W0 14 4 2 2 > *v !2 4: :v : :s is \2 '0 * (> \ \3 i4 14 4.S >4 o "o U 40 >5 .0 42 15 40 4) 10 40 44 would increase steeply with time, making early childhood exposure of great importance.'" However, there are clear indications that mineral fibres clear from the lung, albeit with different half lifes for the different types of asbestos. Chrysotile has the shortest half life, and crocidolite is generally accepted to have the longest. The half life of crocidolite has been estimated to 7-8 years. ' This clearing of fibres would, at least theoretically, tend to actually decrease the risk of mesothelioma and other diseases with time. In conclusion, the value of the cubic residence-time formula is in practice low and it should not be used for extrapolations, at least not at the extreme ends of exposure. The latency time varies in different cohorts, and is dependent on how long a cohort is followed up. In 370 necropsy cases from Italy, latency time could be calculated in 312." Latency time was also dependent on exposure, varying from 29.6 years for insulators (with the highest exposure) to 51.7 in women with domestic exposure. The threshold value and the background concentration There have been strong arguments for the existence of a threshold value (a minimal expo sure required for development of a mesothelioma).""' In most studies, several patients with mesothelioma do not report any occupational or other exposure to asbestos," 'MB and thus there seems to be a small spontaneous basal or background inci dence of the tumour. In a large study from England, consisting of 185 cases and 159 con trols who were very carefully interviewed, 5% of the cases (and 27% of the controls) seemed not to have any kind of exposure to asbestos." This included domestic and even residential exposure. However, it is of course possible that some of these background cases might in fact be due to occupational, domestic, or even envi ronmental exposure, unknown to (or forgotten by) the patients themselves. There ate authors who claim that the presumed background level must be very low, and retrospective searches for the tumour in the medical literature yield no convincing cases of mesothelioma before 1046. although ,u.h negative evidence is of questionable vj.ue. McDonald and McDonald, in a recent review, estimated the background level to be 1 2 million/year; they came to this figure by extrapolating backwards from epidemiological studies from various countries.': Malignant mesothelioma can occur :n children, " and such cases can be considered as proof of non-asbestos (spontaneous) aetiology, as the latency time with necessity must be \crv short in these cases. Asbestos fibres have, how ever, been reported in the lungs of children, even in stillborn ones, ` showing that asbestos fibres spread in the human body and even pen etrate through the placenta. Even if a latency time of only a few years is extremely rare in mesothelioma related to asbestos," it can occur. There are some published examples of latency times of only 5 years." Mesotheliomas also occur in animals, from baboons' and domestic dogs'* to fish. Dogs are exposed environmentally to asbestos just like their human masters, which might explain some of the tumours,'*w r; but in fish it would be difficult to blame asbestos for the tumour. Thus, as in other animals, there is probably a background level of spontaneous mesothelio- . mas in humans. Levels of exposure Although many authors write about low-level exposure to asbestos, there is rarely a definition of this term. In fact, in many articles low level exposure seems to be synonymous to nonoccupaiional exposure, which, as described later, is certainly not true in many cases. Occu pational as well as non-occupational exposure can be anything from very heavy to very low. Occupational exposure to asbestos It must be realised that occupational exposure to asbestos occurs or has occurred not only in the "classic" industries, such as asbestos mines and factories, shipyards, Insulating business, asbestos cement industry, building and con struction etc, but also in very many other occu pations and trades. Examples are pulp and paper industry,7' oil refineries, ' electrical industry," jewellery workers,'' sugar refineries,77 and cigarette filter workers. * Sea men and fishermen can have been exposed to asbestos used as insulation in their boats. In the reprocessed textile industry, bags heavily con taminated with asbestos could be reused for various other purposes, for instance covering heaps of rags; in an Italian investigation of such an industry, mesotheliomas and lung cancer were found to be fairly common among rag sorters.7' Given the extensive use of the mineral, many people have been occupationally exposed to asbestos. This exposure can have been only brief but perhaps intense during that short period. In many or most instances the workers have no idea of the exposure and it can be impossible or almost impossible to elucidate it. Also, the level of exposure is often very difficult to estimate, should the information be avail able. i08 HiUerdai Noii-occupational exposure to asbestos DOMESTIC EXPOSURE The family of an asbestos worker could be exposed to considerable amounts of asbestos brought home on his working clothes, which all too often it was the duty of the wife or daugh ter to clean. Pleural thickening, calcifications, and pulmonary fibrosis have been described in such cases, as well as mesotheliomas. MR POLLUTION FROM ASBESTOS .MINES, FACTORIES, DOCK YARDS, ETC Asbestos mines used to be great environmental nuisances. They could be seen from a distance because of the dust cloud. Asbestos fibres can spread over a distance many kilometres from a mine, and the tailings from the mines were used for paving roads, parking areas, play grounds, etc. In the crocidolite mining areas in South Africa, the incidence of mesotheliomas was increased to at least 10 times that expected even among women, proving a nonoccupational exposure. However, whether some of this exposure was domestic (see later) is nut clear."' Another example is the formerly active crocidolite mine at Wittenoom, Western Aus tralia. At least 5000 people lived in the township of Wittenoom without working in the mines, and in 1993 27 cases of mesothelioma had occurred among these people."**" It has been estimated that 1.1% of child residents and 1.9 % of the female residents of Wittenoom have died or will die from mesothelioma, whereas among the workforce this figure would be 6%." Around the chrysodle mines in Quebec, Canada, there have been at least 53 occupa tional mesotheliomas from the mines, nine domestic, and two with general environmental exposure only." In the nearby towns, the lungs of residents who have never worked in the mines have a fibre concentration which is 10 times higher than that of the average Canadian." Mesotheliomas have also been reported from the surroundings of asbestos factories*1 and in people living near dockyards. However, the risk from residential exposure is probably low. In a large study from England, this factor ac counted for only 3% ofall the identified cases." CONSUMER GOODS Asbestos has been introduced into various goods used by the public. Examples are wall paints and speckling and jointing compounds. Another is a hand held hair drier, of which 13 million were sold in the United States and which has been described as a "small asbestos spray gun"." In commercially produced Kent filter cigarettes, crocidolite was used in the fil ters from 1952-6. The sale of these cigarettes was 11.7 billion, and in the commercials the health effects of this filter was emphasised.'* '* Once asbestos is introduced into a home, it will spread to all rooms and is almost impossi ble to remove even with a vaccum cleaner. It will easily be disturbed into the air from the slightest movement, and sedimentation is very slow."' URBAN AIR POLLUTION The air in cities contains a very low concentra tion of asbestos. Near to construction or demolition work the concentrations are higher. It has been suggested that the air of London during the blitz was heavy with asbestos. Asbestos is also released on braking, and close to a motorway the fibre concentrations in the air will be higher than the background, but still well below the industrial threshold values. A risk not often appreciated is in dumps. In the vicinity of a waste disposal site the concentra tion of asbestos fibres can be 10-1000 times above the background concentration.9' Drinking water can contain asbestos or asbestiform fibres from natural sources or pol lution. The use of asbestos cement pipes can cause a considerable number of fibres in the drinking water. Small amounts of asbestos can be found in some wines, beers, liquors, and other beverages, probably deriving from the fil tration process. Fibres that are ingested will to some extent also enter the blood stream as seen from animal experiments.92 91 In humans, there are few reports. However, when amphibolc fibres were found in drinking water from Lake Superior, a very small portion could be traced in urine,94 and when chrysotile occurred in the drinking water, very small amounts were again found in urine." However, most ingested min eral fibres will never be absorbed but will be cleared in the normal way, and the harmful effects of asbestos in drinking water or drinks is probably minuscule (and much smaller than the risk of drinking the alcohol). Even if ingested asbestos is not dangerous, it has to be realised that it is only a very small portion of the up water that we actually drink. Most of it is used for other purposes. Once the water has dried after washing, cleaning, taking showers etc the asbestos fibres will spread in the air. Such amounts are small but not insignificant and will add to the normal background exposure.9* ASBESTOS IN PLACE * BUILDINGS CONTAINING ASBESTOS A mixture containing asbestos was popular after the second world war for spraying on ceil ings and walls for insulation and decoration. This was used well into the 1960s. There is now a public danger because of the plaster fall ing down from natural wear and tear, vandal ism, or "artistic" carving in schools, etc. In many industrial buildings, asbestos was also used for spraying on the underside of the roof, and with natural wear and tear (and for instance birds building nests!)97 there is now release of fibres to the surroundings. Asbestos was also extensively used in walls or around plumbing for insulation purposes, in cement to strengthen it, or just as a cheap filler. In a modem city, asbestos can often be found in many places: in the cellar, where steam pipes are insulated; in storage or laundry rooms; in air conditioning sets; in theatres, museums, restaurants, etc." Whenever there is damage to any construction or machine that contains asbestos, the possibilities of exposure, some times even fairly high, is there. ***** * < . .ipdiii * S*.no,'l rci.rers trt (ended *crii*nl Oftice uierK remaic .v.-ocer r'>-.4i!t'n Ji :u'rne +tU'r sxpoiure 'o ".i.restos in place" He .\rdnci ** > 48" patients with mevithfimma 44 : wjse each : 00-101 t cases `04 i.is : :o: patients w,th rrev'thetmma !-'5 106 It has been claimed that up to 1000 prema ture deaths from lung cancer or mesothelioma will occur in the future among school children from schools where asbestos was used in the walls"--calculations which, however, had to be built on extrapolations and assumptions. Sev eral case reports have been published on patients with mesothelioma, in which the only exposure to asbestos that was reported was "in place" (table 4). From various cohorts with such exposure, significant increases in radio logical findings from the lungs--such as pleural plaques--have also been reported, indicating exposure ot asbestos, but these results are not undisputed and there is a probable overdiagno sis, as control groups are missing.107 ENVIRONMENTAL MESOTHELIOMAS FROM LOCAL DEPOSITS OF FIBROUS .MINERALS "Endemic pleural plaques" were first described from Finland and since then many such findings have been reported. In these areas, there are small local pockets of asbestos which sometimes have been quarried, often for generations, for some local use. The most common use is whitewashing of houses with tremolite, which has resulted in an extremely high incidence of mesothelioma in some villages (table 5). When the exposure is due to whitewashing of the houses the risk will disap pear when this procedure is stopped, but due to the long latency time this will take many decades. A non-asbestos fibre, the zeolite erionite, has been found in some Turkish villages. Roads, buildings, etc, can contain this fibre in small amounts. Erionite is even more dangerous than crocidolite and the incidence of mesotheliomas in these unfortunate villages is extremely high. Endemic plaques are of interest also in other countries, as many people born in these places and living there in their childhood and youth now have moved to ocher places, taking with them not only the plaques but also the risk of mesothelioma.1'1 Concentrations of exposure OCCUPATIONAL CONCENTRATIONS The concentration of exposure which the first workers exposed to asbestos have experienced can only be guessed. Estimated or recreated values from the past suggest fibre concentra tions from 25 up co occasional values of 1000 2000 fibres;ml. With his own recalculations, Harries in 1970 estimated the fibre concentra tions in the dockyard in 1951 as follows: sprayed asbestos insulation 171-322 fibres,cc; stripping asbestos 334; sweeping 353; adjacent passage 83; and in the passageway to che shower 25. Bagging debris 564; pipe lagging 194-200; removal of pipe lagging 171. Snap samples showed values to up to 1000-2000 fibres/cc.112 These values are similar to the ones published by McMillan in 1983, who recreated values from the past: engine room 88; delag ging in boilers room 171; bagging debris 353 fiml.'" Measurements from working places in the' 1960s often showed peak doses of 20 fibres, ml and much less in more recent years. Where asbestos is still used, many countries have adopted a concentration of 1-2 fibres/ml as the upper legal concentration of exposure. These figures should be compared with the few avail able non-occupational measurements (table 6). A problem with the legal concentration is that most asbestos use today occurs in developing countries, many of which have adopted stand ards which they cannot enforce. As a result, actual exposures may be much higher than the standard in these countries. NON-OCCUPATIONAL CONCENTRATIONS The fibre concentrations in domestic exposure might in fact be as high as in occupational exposure. Brushing clothes might give peaks of & 100 fibres/ml." Ordinary vacuum cleaning is not effective in removing asbestos fibres, which TabUS Local depotta of mirunifibrm fasbatoi or tnomu), occurrence of piaqius, and of malignant maot/utioma Country or ana TfptjjUn Afghanistan Austria Bulgaria Corsica Cyprus Czechoslovakia Finland Greece: Vtetsovo Tremolite Tremotan Aruhophytlrt* Tremolite Tremotit* Tremolite Unknown Anthophyllite Tremolite SW Andes, Macedonia New Caledonia *2 South Africa Turkey USSR Araosite croadolite Tremolite Gnonite Unknown * 12 cue* 145 OOO inhabitants/10 y. {Occurrence m local area. Ptaquu (% of immtigamt inhabitants) ___ 53 2.8 women 5 6 men 41 (>50 v) 2 7-6 6 6.5-9 0 46.9 24 2 :>40 v) 2.5-6.6 1.2-25 65 Locally high Msunkotioma rub (yulGfiy) ___ Not increased Not iocmaaed High High -- Sot increased 280 140(1985-04) High a.3m 300f High High Cotmmm Case report only Vineyard sad field workers Tobacco growers General pollution General pollution Fanners White washing houses White washing houses Population around mine White washing bouses Farmers Referenc 108 109 no ill 112 113 114 115 116 117 118 119-121 122 123 124 125 4 126-128 19, 128, 129 130 Hitterjjt Ijr'. * Fibre joncentrattons m Jir and lunqs cmih non-oecupationai exposure to asbestos ! ". r Ib.'J.VIY D`>!nesfv exposure paraoccypaijonaJ} Near asbestos mines, lactones, etc: In \X irttfn.'om: Wh*r 'rime operating \ier .;*'sure of mine Kirmer % near mine m Canada L-. -4I asbestos findings Greece ir ard of an abandoned house Jr jtv -1% room Or-oca New Caledonia- Whiie seeping flot"- R >ad oust clouds Asbcw- n place; fvacher s aid F'-rnaic otTice workT /ibw nr jtr 05 001-021 0 01 0.02 !?.`i 0 06-0 67 Ftben i/f '/* /(T i Jr\ nut. . 5 3-31* 5 0 W4 R<-fi i; 102 4# 1 2-268 ; >4 123 21*11 114 124. 125 >0043 3? fTEM: 102 103 * ^ is tr. 1 no rimes ngfter -.ban controls; TEM = transmission electron microscopy Fibres in the lungs of patients with non-occupational mesothelioma As has been mentioned, asbestos fibres can be found in the lungs of the general population without any known exposure. In Germany, the upper normal limit was estimated to be 300 000 fibres-'g dry lung. In a large study of 324 malignant mesotheliomas, from which 4b lung samples were available, it was found that even at a fibre concentration of 100 000-200 000 fibres/g, there was a fivefold increased risk of mesothelioma, which was significant.1" In this study (which has unfortunately only been pub lished in German) as in many others, the mean number of fibres in the lungs of patients with malignant mesothelioma is much higher than the normal values, but there are usually patients with values that lie within the normal level." can remain for years in the house and be Discussion airborne again whenever disturbed. Thus, Any asbestos fibre found in a lung must have domestic exposure is not low exposure. been inhaled. As far as is known, no truly Environmental concentrations in the villages where whitewashing occurs, low values are reported when there is no disturbance, but in a newly whitewashed room and while sweeping floors, the concentrations can be quite consid erable (table 6). With asbestos in place, as long as the asbes tos is undisturbed the concentrations in the air are very low (zero or hardly measurable: SO.001 fibres/ml),but once deterioration takes place values can go up to 15 fibres/ml, and when being removed there can be even higher values. In schools in the United States, the mean concentration was estimated to be 0.003 fibres/ml, and in federal buildings 0.006.1" unexposed group can be found in the world. There is no proof of a threshold value--that is, a minimal lower limit below which asbestos fibres cannot cause the tumour--and thus it is plausible that even such low exposure can cause mesothelioma (even if the risk is extremely low). Patients with mesothelioma whose lungs show fibre concentrations within the normal range cannot be dismissed as back ground cases,--that is, not due to asbestos. The only way to prove such a hypothesis would be to compare the inddence of mesothelioma in a group with such background exposure with the incidence in a truly non-exposed group. This is not possible, as no such group can be found. Thus, with so called non-occupational expo It is nevertheless possible that there is a sure, the typical exposure is a low or very low, background level of mesothelioma,--that is, almost unmeasurable, background concentra that the tumour can occur even in the complete tion, but occasional high exposure when there absence of asbestos (or erionite) fibres. How is a disturbance of some kind. It follows, firstly, ever, the data reviewed here indicate that if so, that retrospective estimation of cumulative this background level must be very low-- exposure from history alone is an impossibility probably much <1 case/million people.year. in most cases; but secondly, and perhaps more importantly, that any person living or working in (or even temporarily visiting) buildings where asbestos has been used in construction or otherwise might well have been exposed to high concentrations of airborne asbestos fibres once or many times in their lives, and in most instances unknowingly. This includes most of us! A better way of estimating lifelong exposure might be analysis of fibres in the lungs, but as already mentioned fibres do clear from the lungs. How big the differences in clearance are between people is unknown. Thus, the correla tion between lifetime cumulative exposure and fibre concentrations in the lungs is not excellent, but the findings from the lungs prob ably give a better estimation of exposure than even a careful retrospective analysis of the patient's history, at least in low grade exposure. This figure comes from studies of industrial ised countries, where background exposure to asbestos is unavoidable. What the true figure is can only be guessed. What, then, are the consequences for the public health? From the studies of nonoccupational exposures it seems probable that the occasional high level exposure situations are the ones that are most important. Although the background, hardly measurable, concentra tions of fibres in the air cannot be completely dismissed, the cumulative risk of these expo sures is probably minor--and what is more, there is no way to reduce these concentrations. It is the high concentration situations which should be avoided. By knowing where asbestos occurs, such risks could be identified. Any source of pollution by asbestos which releases significant amounts of fibres should be elimi nated as soon as it is discovered, using correct equipment and techniques. Correct techniques In most studies, there is a dear dose-response are also necessary whenever rebuilding or tear relation between exposure and the number of ing down of structures containing asbestos to fibres in the lungs." " avoid asbestos pollution of the environment. If .VftJi the asbestos is well contained and not dis turbed, it is usually better to leave it in place. In many instances, encapsulation is also better than removal. : Langer AM. Inorganic particles >n human tissue and their .issocMQon with neoplastic disease. Environ Health Ptnpect 1474,9:229-3). 2 Gioag 0. Asbestos fibres and the environment. 8MJ 1981; 2S2.623-6. 3 Churg A. Fiber counting and analysis n the diagnosis of asbestos-related disease. Hum Pathoi 1982;13:381-92. 4 Sluis-Cremer GK, Liddell FDK, Logan WDP, n ai. The mortality of amphibole miners in South Africa, 1946-80. Brjind Med 1992;49:566-75. 5 C>okson WOCM,GlaiKv JJ, d< KJerk NH, a/ Benign and malignant pleural effusions in former Wittenoom miners and millers. Ausi SZJMed 1985;15:731-7. 6 Rogers A, NevrU M. Occupaaonai and environmental mes otheliomas due to croctdolite mining activities in Witte noom, Western Australia. Scand J 'Xbrk Envxron Health ,995;21:259-64. 7 Selikotf I], Seidman H. Asbestos-associated deaths among insulaoon workers in the United States and Canada, 1967 87. Ann N Y Acad Set 1991 ;643:1-14. 3 Berry G. Mortality of workers certified by pneumoconiosis medical panels as having asbestosts. BrJ Ind Med 1981,38: 130-7 4 Navraoi M. scfticfcsai von Paoenten mic Asbestose in Veriauf einer 25jihrigen prkvenaven Gesundhenapflege. Ztntraibaa Arbatsmedizin und Arbeusschuu 1979:29:259 64. 10 Courts II, Gilson JC. Mortality in cases of asbescosis diagnosed by a pneumoconiosis panel. Thorax 1987;4J: 111-6. 11 Gibbs AR, Griffiths DM, Pooley FD, it ai. Comparison of fibre types and size distributions tn lung tissues of paraoccupaoonai and occupational cases of malipunc mesothe lioma. BrJ Ind Mid 1990;47:621-6. 12 Rogers A, Leigh J, Berry G, et ai. Relation between lung asbestos fiber type and concentration and relative risk of mesocheboma. A cate-control study* Conor 1991 ;67:1912- 20. 13 Kariaiaincn A, Meurman LO Pufckaia E. Four cases of mesothelioma among Finnish anthophyUite miners. Ocatp Emnoron Health 1994;51:212-15. 14 Smith AM, Wrighs CC. Chrysottfa wfamci m tha mam cause of pleural mesothelioma. Am J Ind Med 1996J9: 252-66. 15 Stayncr LT, Danfcovic DA, Leman RA Occupational expo sure to chryaoblc asbestoc and cancer risk: a review of the amphibole hypothesis. Am J Public Health 1995;86:179-86. 16 Jones RD, Smith DM, Thomas PC. Mesothelioma in Crete Britain in 1968-83. ScandJ flbnfc Emnrom Health 19W;l4; 145-52. 17 Wens SW, Tavmuoh FA Mulbcysoc mesothelioma. An anaiysia of pathologic findings and biologic behaviour in 37 cases. AmJSarg Pathoi 1988;12:737-46. 18 HiBerdalC. Mahmuuumeaocheikiaka 1982: review of 4710 published cases. BrJ Du Chest 1983;77:321-43. 19 Bans Yl, Sononaco L Artvinh M, er aL Epidemiological and environmental evidence of the health effects of exposure to eriooite fibers: a four-yesr study in the Cappadocian region of Turkey. InsJ Cancer 1987^9:10-17. 20 Hilierdal G, Bergfa J. Malignant mtsoebehoma secoodary to chronic **o--and old scars. TWo new cases and review of the literature, Canon 1985;55:1968-72. 21 Cavazza A TVsvis LB> Ttaris WD, ee aL Post-irradiaboa nnlipaant mnnrhilinnua ^micr 1996;77:1379-85. 22 Neugut AX, Ahsan H, Anonan KH. {cadence of imHgnenr pleural mcsochehoma after thoracic radiotherapy. Corner 1997^8948-50. 23 Mizula M, YuJoahigt K, Abe Y,tfd.A case of malignant pleural tMsocfteboma following exposure to atomic radin don in Nigaiehi Respentagy 1997;2:201-5. 24 Mirtensoon G, Larsson S Zenergren L. Malignant mesatheHrens in two pain of siblings: is there a hereditary predispociag boor? curj Respr Dts 1984;65:179-84. 25 Dawson A Gibbs A Browne K, et aL Fumtial mesothelioma: details of 17 cases with histopathologic findings and mineral analysis. Cancer 1992;76:1183-7. 26 Hiivunen A A Tkmrnikhto L, et aL Inherited GSMl and NAT2 defects as concurrent risk modifiers in asbestosrelated human --tp-- tnesodreHome, Cancer An 1995;55:2981-3. 27 Huocharek M, Kelsey A Muscat J, et aL Parental cancer and genetic prediaposiooo in malignant pleuni mesothelioma: a case-control study. Cancer Leu 1996;162: 205-8. 28 Behliug CA Wblf PL, Haghighi P. AIDS and malignant mesothelioma: it there a connection? Cheez 1993;169t 1268-9. 29 Idemyor V, Cberubm CE. Rapidly ptogressive mesothe lioma in an HIV-poaadvc ptneztc. Arm Pharmacoeker 199206:429. 30 ScfuAma M, Pickle LW, FocMham B, et eL Caaa rniwvnl study of diet and mesothelioma in Louisiana. Cancer Ret 1988;48:2911-15. 31 Muscat JB, Hunchaiek M. Dietary intake and die rid: of malignant mesothelioma. BrJ Cancer 1996;73:1122-5. 32 Stenton SC. Asbestos, Simian virus 40 and mshgiam me,>ihJion*. Thorax I907;i2(*uppl 3>S52-T. 33 Enterline PE, Henderson VX. Geographic patterns tor plu ral mesothelioma deaths in the United States. i} \\ul Cancer Inst l987;79'31-7 34 McDonald AD. McDonald JC. Malignant mesothelioma in North America. Cancer 1980;46:1650-6 15 Chaitteux E. Pioche D. Chopra S, et M. Epidemiology iu mcsntheliome pleural malin dans la region de Nantes- Samt-Nazaire. Evolution 1956-92. Rev Mai Respir 1^45; 12:353--7 36 Weiss NS. Martin J, Suarez L, ec ai. Review of mesothelioma incidence and mortality in Texas. Texas Med 1988;84:44-8 37 Hinds MW Mesothelioma in the United States. Incidence m the 1970s. 7 Occup Med 1978;20:469-71. 38 Spirtas R, Beebe GW, Coinncily RR. Recent trends in mes othelioma incidence tn the United States. Am J Ind Med 1986;9:397-407. 39 Gnipo de Esrudio del Mesotelioma en Barcelona. Mortali- dad por mesotelioma pleural en la provincia de Barcelona. MedCtin(Barc) 1993;101:565-9 40 Peto J Hodgson JT, Matthews FE, et ai. Continuing increase in mesothelioma mortality in Britain. Lancet 1995J45; 335-9. 41 Karjaiainen A, Pukfcala E, Mattson K. et ai. Trends in mes othelioma incidence and occupational mesotheliomas m Finland in 1960-95. Scand J Vtbrh Environ Health 1997.23: 266-70. 42 Andersson M, Olsen H. Trend and distribution of mesothe lioma ut Denmark. BrJ Cancer 1985;51:699-705. 43 Leigh J, Corvalan CF. Grimwood A, tt ai. The incidence of malignant mesothelioma in Australia 1082-8. Am J Ind Med 1991;20:643-55. 44 Leigh /Hull B, Davidsson P. Australian mesothelioma register report. The incidence of mesothelioma m Australia /992-4. Sydnev: Naoonal Institute of Occupational Health and Safety, 1996. 44 McDonald JC, Armstrong B, Case B, *t ai. Mscthelioma and asbestos fiber type. Evidence from lung tissue analyses. Cancer 1989;63:1544-7. 46 Roggii VL, Pratt PC, Brody AR. Asbestos content of lung tissue in asbestos related diseases: a study of 110 cases. BrJ Ind Med 1986;43:18-28. 47 Churg A Wright JL, Vedal S. Fiber burden and patterns of - asbestoa-retaced dneaac in chrysonk miners and millers. Am Rev Respo Do 1993;148:25-31. 48 Hansen J, de Klerk NH, Musk AW, et aL Environmental exposure to crocidoiite and mesothelioma. Exposure- response telabonahipt. Am J Respir Cm Com .Vfatf 1998;157:66-75. 49 DoB R, Peto J. Effects on health cfexposure to asbestos. A report to the Health and Sqkty Commission. London: The Staoon- ery Office, 1985. 50 LandnguiPJ. A population ofchildren at risk ofexposure to asbestos m place. Amt H Y Acad Set 1991;643:283-6. 51 de Klerk NH, Musk AW, Williams V, #r oi. Comparison* of memures of exposure to asbestos in former crocidoiite workers from Wittenoom Gorge, W Australia. Am J Ind Med 199646:579-87. 52 Biaochi C, Giarelli L, Garndi G, <t oi. Latency periods in asbestoe-rdeted mesothelioma of the pleura. Ear J Cancer Aav 1007^:162-6. 53 Browne K. Asbestoa-reiattd mesotheboma: epidemiological evidence for asbestoa ai a promoter. Arch Enuren Health 1983;38:26t-6, 54 llgm EB, WkgDer JC. Background incidence of mesothelioma: animal and human evidence. Regul Toxtcol Pharmacol 1901;13:133-49. 55 Dgrea EB, Browne A Aabescoa-related mesothelioma: evidence for a threshold in animals and humans. Rigid Task* Pharmacol 1991;13:116-32, 56 Ashcroft T. EpidetniofogicaJ and quantitative reiaoonahips between mewchdioma and asbestoa on Tyneside. J C/m fbehal 107348:832-40. 57 CK^iBm E, Fornadat G, Metier E et d. Pleural maitgnam mesothelioma in Tbscany, Italy (1970-88): Cl. Identifies- don of occupational exposure to asbestos. Am J Ind Med 1992,4*599. 58 Spinas A Hooemaan EF, Bernstein L, et ai. Malimant nuaoihalinms strnbmabls risk ofasbestoa exposure. Oeeup Encmrn Med 199441:604-11. 59 Howel D, Arblaatcr L Swinburne L,etai. Routes of asbes toa exposure and the development of mesothelioma in an English region. Ocaep Emhrom Med 1997;54:403-9. 60 Yma DH, Corn B, Stidolph PN, et eL Malignant mesomelsona in south esst England: diaicopatholocical expcncace of272 cues. Thorax 1997;52:507-12. 61 Mark EJ )fokoi T. Absence of evidence for a significant background incidence of diftisa malimant mesothelioma apart from asbestos expoaure. Amt N YAcad Set 1991,643: 196-204. 62 McDonald JC, McDonald AD. The epidemiology of nitiothelioma in historical context. Ear Respir J 1996;* 1932-42. 63 FraireAB, Cooper S, Greenberg SB, esaL Mesothelioma of childhood. 1988*62:838-47. 64 Haqu, AK. Kam MF. Atboto* bodw in childRo'i lunfi. 65 Hiqu* AX. Vnxl DM, Bunu K, <t <X. Is (hoe tnnsplmcenlil imufti Ilf iitiminT ft iiiiiIt nf 1ft HillTnT infinr ~~l htMLAMti 1996;16:877-92. 66 Boeik SI, Amt EJM. Mdi(Mm pteunl mootbcUom, 8m yon alter domnne eapomr to Muc aabotos. Loan l6^:43S. 512 HiUerdai 67 Foreman JD. Manaligod JR, Bennett BT Malignant mesothelioma in an olive baboon (Papm anubis) Lab AmmaiSct 1993,43:503-3. 68 GUckmaa LT, Domanski LM, Maguire TG, ti ai Mesothe- Uoma in pet dogs associated with exposure of their owners to asbestos. Ertvmm Ret 1983,32.305-13 69 Hartnsoa ML, Godlcslu JJ. Malignant mesothelioma in urban dogs. Vit Pathol 198340:531-40 70 Smith DA, HU) FW Metastaoc malignant mesothelioma in a dog. J Comp PtuM 1989;100:97-101 71 Herman RL- Mesothelioma m rainbow trout, Salmo gaudrn Richardson. JWm/ cf FuM Duui 1985,8 37 3-0 72 MirabeUa F Studio eptdenuologico del mesotelioma spontaoeo canmo: sua possibile uohta' in nfenmenio alia patologu umana. MtdLavoro 1987,78:28-32 73 Jarvholm B, Malker H, Milker B, ti ai Pleural mesothe lioma and asbestos exposure in the pulp and paper industries: a new nsk group tdenofied by linkage of official registers. Am J ind Mad 1988;13:561-7 74 Finkelstein MM. Asbestos-associated cancers in the Ontario refinery and petrochemical sector. Am J Ind Mod 1996;30: 610-15. 75 Imbernon E, Goldberg M, Boncnfam S, ai. Occupaoonal respiratory cancer and exposure to asbestos: a case-coauoi study m a cohort of workers in the electricity and gas industry. Am J Ind Mod 19954*339-52 76 Kern DG, Hanley KT, Roggli VL. Malignant mesothelioma in the jewelry industry. Am J Ind Mod 199241:409-16. 77 Maltont C, Pinto C, Valenti D, ti ai. Mesotheliomas follow ing exposure to asbestos used in sugar refineries: report of 11 Italian cases. In: A Mehlman, A Upton, eds. Advances in modtm emhronmeruai toxicology. Vol XXII. Tkt tdenoficazson andcontrol ofenvironmental and occupationaldiseases: hazards and nshs of chemicals m the od rtfimng industry. Prinecteon, NJ: Pnnceton Scientific, 1994:629-34 78 Talcott JA, Thurbcr WA, Kantor AJF, et ti. Asbestos- aiaodated disease in a cohort of cigarette-filter workers. N EngiJ Mod 1090421:1220-3. 79 Quinn MM, Kriebel D, Butara E, tt ai. An asbestos hazard in the reprocessed textile industry Am J Ind Mod 1987;ll: 255-67. ' 30 Kaoc MJ, Chahmina AP, Holland JF. Malignant mesoebe- Uoma tn young adults. Cancer 1990;65:1449-55. 81 Magnani C, Temdni B, Ivakb C, et ai .K cohort study on mortality among wives of workers in the asbestos cement industry in Ornate Mooferraco, Italy. Br J Ind Mod 19934*779-84. 82 Schneider J, Woitcwiu HJ. Tumors linked to para- occupational exposure to airborne asbestos. Indoor Built Emhrmmem 1996;5:67-75. 83 Botha JL Irwig LM, Strebel PM. Excess mortality from stomach cancer, king cancer, and asbestoses and/or mesothelioma in croddoltte mining districts in South Africa. Am J Epidemmd 1986;123:30-40. 84 Musk AW, de Klerk N, Ecctes JL,et ai. Wirtenoom, Western Australia: a modern industrial disaster. Am J Ind Mod 199241:735-47. 85 Haringtoo JS. Mesotfaahoma among workers in the Quebec chrvsodte mining usd milling industry. Am J Ind Mod 1992;22:925-6. 86 Cburg A. Lung asbestos content in long-term residents of a chrysodle mining town. Am Rev Respir Dis 1986;134:125- 7 87 Ham E, Dalquen P, Bohlig H, tt ai. Katamnesdsche Unter- suchungen xur Genese des Mesotelioms. Bericht uber 150 Fill* aus dem Hamburger Raum. lnumnnonaUs Archtv fitr Arbouxmodmn 197443:15-37. 88 Smith RJ. Briefing. Science 1979;204:285. 89 Longo WE, Rigler MW, Slade J. Croadolne asbestos fibers in smoke from original Kent cigarettes. Cancer Res 1995;55:2232-5. 90 Moorcroft JS, Duggan MJ. Rat* of d*dia* of asbestos fibre concentration in room air. Ann Occup Hyg 1984,28:453-7. 91 5uta BE, Levine RJ. Noo-occupaoonaJ asbestos emissions and nmnames In: L Micabete, SS Chissick, eds. Asbestos. Vol 1. Dimmitmi. apphcattcmi, and hazards. New York: John Wiley, 1979:171-205. 92 Cunningham HM, Moodie CA, Lawrence GA, tt ai. Chronic effects of ingested asbestos in rats. Arch Envtron Comum Teoncel 1977;6:507-13. 93 Sfbaaitea P, Masse R, Bignon J. Recovery of ingested asbes tos fibers from the gastrointestinal tvmph in rats. Emnron Ret 198042401-16. 94 Cook MP, Olsoa GF. Ingested mineral fibers: elimination m human urine. Science 1979404:195-8. 95 Boarman H. Use of quantitative analysis of urine to assess exposure to asbestos fibers in drinking water in the Puget Sound area. Environ HoaUh Penpoct 1983;53:131-9. 96 Webber JS, Syrotynski S, King MV. Asbestos-contaminated dnnking water its impact on household sir mtnm Res 1988;46:153-67. 97 Greenberg M. Malignant mesothelioma in paper mill workers: where might the asbestos have come from? Am J Ind Mod 199640:641. 98 Molloy LB. Asbestos in place in metropolitan New York. Ann .V Y Acad Sci 1991;643:614-21 . 99 Anderson HA, Hanrahan L, Schirmcr J, et ai. Mesothelioma among employees with likely contact with in-place asbestos-containing building materials. Ana A V Acad Set 1991;643:550-72. 100 Dodson RF, O'SuOrvan M, Com C Technique dependent variations ui asbestos burden as illustrated in a case of nonoccupational mesothelioma. Aw .7 fed Med 1993;24:235-10. 101 Huncharek M. Occult asbestos exposure. Am J Ind Med 1991;20:713-14 102 Roggli VL, Longo WE. Mineral fiber content of lung tissue in patients with environmental exposures: household contacts t; building occupants. Ann S Y Acad Sa 1991;645:511-18. 103 Srebro S, Roggli VL. Asbestos-related disease associated with ssbesuform tremolite. Am J Ind Med 1994,26:809 19 104 Lilienfeld DE. Asbestos-associated pleural mesothelioma in school teachers: s discussion of four esses. Ann N YAcad Sa 1991;043:454-8. 105 Stein RC, Kitajewska JY, Kirkham JB, ei ai. Pleural mesothelioma resulting from exposure to amotite asbestos in s building. Respir Med 1989;83:237-9. 106 Dodoli D, Del Nevo M, Fiumalbi C, ex ai. Environmental household exposures to asbestos and occurrence of pleural mesothelioma. Am J Ind Mod 199241:681-7. 107 Hilterdal G. Pleural plaques: incidence and epidemiology, exposed workers and the general population. Indoor Built Environment 1997;6:86-95. 108 Vcusin C, Marin I, Brochard P, et ai. Environmental airborne tremolite asbestos pollution and pleural plaques in Afghanistan. Chest 1994;106:974-6. 109 Neuburger M, Grundorfer W, Haider M, et ai. Urowelt- bedmgte endemnche Pleunplsques. Zentrbiast fur Bakten- oiofte tend Hyftine,Abmi Original 1978;167:391-404. 110 Neuburger M, Kundi M, Friedl HP. Environmental asbes tos exposure and cancer mortality. Arch Emnron Health 19844*261-5. 111 Burilkov T, Btbadjov L. Ein Bestng rum endcnuschen Auftreten doppeteeitiger Pteunverkatkungcn. Praxis fur Pneumoiogu 197044:433-8. 112 Zotov C, Bourilkov T, Babadjov L. Pleural asbestosu in tgnculrural workers. Environ Res 1967;1:287-92. 113 Rey F, Boutin C, Steinbauer J, et ai. Environmental pleural plaques in an asbestos exposed population of Northeast Corsica. Bur Respir3 19934 978-82. 114 Rey F, Vlaltet JR, Boutin C, t ai. Les mesothebomes env>- ronnementaux en Cone du nord-est. Rev Mai Rasper 1993; 10:339-45. 115 McConnochie K, Simonato L Mavrktes P, et ai. Mesothe lioma in Cyprus: the rote of tremolite. Thorax 1987,43: 342-7. , 116 Martova M. Befttag *ur Ackdogie der Pteuraverkalfcungen. ZeuschnfifAr Tuberkolose 1964;121:329-34. 117 Kiviluoto R. Pleural calcification as a roentgenologic sign of non-occupabonal endemic anthopbyUite asbestoais. Acta Radioi 1960;(Mppl 194). 118 Raumo V. Occurrence of unusual pleural calcification in Finland. Studies on atmospheric pollution caused by asbestos. Anmsdes de Modecma Interna Fenmae 1966; 55(tupp( 47). 119 Constaatopouios SH, Malamou-Mitsi VD, Goudevenot JA, et aL Higfr incidence of malignant pleural mesotheliotna in neighbouring villages of Northwestern Greece. Resptra- non 1987;51:266-71. 120 Bazas T, Oakes D, Gilson JC, <r aL Pleural calcification in northwest Greece. Environ Res 1985;38:239-47. 121 Linger AM, Nolan RP, Consuntopoulos SH, et ai. Ascoo- soon of Metiovo lung and pleural mesothelioma with exposure to tremobte-contatrung whitewash. Lancet 1987;i: 965-7. 122 Sakellanou K, Malamou-Mitsi V, Haritou A, et ai. Malignant pleural mesothelioma from oon-occupanonal exposure in Metsovo (north-west Greece): stow end of an epidemic? Eser ResptrJ 1996;9:1206-10. 123 Sichlehdis L, Daskalopoulou E, Chiocos IX tt ai. Five cases ofpleural mesothelioma with endemic pleural calcifications in a rural area in Greece. Mod Lavoro 1992;83:259~45. 124 Goldberg P, Luce D, BiUon-Galland MA, et ai. Role poten- bel de ^exposition enviroanementalc et domesbque i la tremolite dans le cancer de It plevre en NouveUe Caledome. Rov Epidemiol Same PeM 1995;43:444-50. 125 Luce D, Brochard P,Quenel P, <i ai. Malignant pleural mesothelioma associated with exposure to tremolite. Lancet 1994^:1777. 126 Baris YI, Sahm AA, Oxesnai M, et ai. An outbreak of pleu ral mesothelioma and chronic fibrosing pleurisy in the vil lage of Karain/Urgup in Anttoba. Thorax 1978;33:181-92. 127 Baris YI, Biter N, Artvinte M, et ai. An epidemioioficaJ study in an Anatolian village environmentally exposed to tremolite asbestos. BrJ bad Mod 198*45:838^40. 128 Selcuk Z, C6pKl L, Emri S, it ai. Militant pleura) mesothelioma due to environmental mineral fiber exposure m Turkey. Aaalysit of 135 cases. Chost 1992;102;790-6. 129 Anvinii M, Barit YX. Environmental fiber-induced pleuro- pulmonary diseases in an Anatolian village: an epidemio logic study. Arch Environ Hoahh 1982;37:177-8). 130 Ginzburg EA Silova MV, Kornejcva MJ, et ai. Rontgenolo gic der nichtberufs-bedingten Asbestos# der Pleura. Radio- iogta Diagnoshca 1973;14:307-12. 131 Boman G, Schubcn V, Svaae B, ex ai. Malignant mesothe lioma in Turkish immigrants to Sweden. Scand J Work Environ Health 19824:108-12. 132 Harries PG. The effects and control of diseases associated vnth exposure to asbestos m a naval dockyard [MD Thesis). Alver- stoke, Gosport, UK: Instmite**of Navtl Medicine, 1970. 13 3 McMillan GHG. The health ofwelders in navel dockyards. 3 Occup Mod 198345:727-30. 134 Churg A. Analysis of lung asbestos content. BrJ ind Med 1991;48:649-52. r \ii%otne(io*"a 515 1 L' S Environmental Protection Agency. EP.4 ttudv on j<t- ..* .dufumm? materials m puoi<< puddings. Washington, DC: LSEPA, 1<J86. 36 Woitowuz HJ-, Hilierdal G. CaUvre20S A, it m. Rmko-und EtttfitiSS/akrorfn Jes Jiffmen maugnen Mesotkehoms 'DMM). S^hnttenmne Mr QunddianiiMt fur Arbextsschuts. Bonn: BA, 199 3 ,Fb<>98 ) 137 Murai Y, Kitagawa M Asbestos fiber analysis m 27 malig nant mesothelioma cases .4 J hui Med 1992;22:193-207. 138 Tuomi T, Segerberg-Kontnnen M, Tammiiehto L, <t j{. Minerai fiber concentration m iung tissue of mesothelioma patients in Finland. Am J Ind MeJ i 980.46,2'47~54. I JO Tuomi T, Huuskoncn M, Tammiiehto L. *t M. Relative risks of mesothelioma associated with different ,<vei$ A exposure to asbestos. Scand J lfork Environ H*m:H tO0l;t? 404~8. 140 SaJcai K, Hisanags N. Huang /, <ti J. .Asbestos jnd non-asbestos fiber content in lung tissue of Japanese pauents wuh malignant mesothelioma. Cancer 19Q4;7V. IS25--\S 141 Dodson RF. O'Sullivan .M, Corn CJ. .Analysis of asbestos fiber burden m lung tissue from mesothelioma patients. Utasirua Pathol l W .21:521-36. 142 Ferguson D. Low-level asbestos: the pnonues are wrong. MedJAust 1990i!J2:617-ia. 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