Document Rpvm8z4wy1bk5mLXaN9Vz71kz

(a.'MF REVIEW Vi* ill 505 Mesothelioma: cases associated with non-occupational and low dose exposures Gunnai Hillerdai Abstract Objectives-To estimate the importance of low dose exposure to asbestos on the risk of mesothelioma. Afethods-A review of the literature. Results and conchisions-There is no evi dence of a threshold level below which there is no risk of mesothelioma. 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 of 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 Eitedron Med 1999;56:505-513) Keywords: low exposure; asbestos; mesothelioma Department o/Lung Medicine, Karolinska Hospital, Stockholm, Sweden G Hillerdai Correspondence to: Dr Gunnai Hillerdai, Department td Lung Medicine, Karolinska Hospital, Stockholm, Sweden. Accepted s March rasa 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 ifthe 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 ofthe mineral in samples of Greenland ice'and on the Yorkshire Moors,- and every citizen 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 I to 5/million/year among women and values for Tsbte 1 Proportionate morietityfront inoedheiioina hi various cohorts SO,,,, Amphibole miners Crocidolite miners Insulation workers Patients with asbestosis D.i/dts (n) 1225 1 Iff 4951 283 40 50 Deaths cfe, w uusmheNiuua ?S5) 2 4 G 9 9 ft! 19 Ralcrewe 4 5 0 7 8 9 to 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% ofthe 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 concentration; 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. Chrysotile is considered by many authors to be a weak carcinogen- in humans," whereas the two amphiboles crocidolite and tremolite are much more dangerous according to many studies." The third of the more important amphiboles, anthophyilite, was long considered not to cause mesothelioma, but such tumours have now been reported al though the risk seems to be small." 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." 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 tunics 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 1.5 to 1." Thus, either the aetiology is different, the 512 (T Ki-lJ 'e2*l Table 2 Possible risk factors and stediators ofrisk oftnesothetlotaa (other than Bsiesios) Firei Erionitc Chronic inflammation Radiation Beryllium Vegetable fibres Hereditary factors Immunological factors Dietary factors Viruses CO Very high Incidence of mesothelioma environmental exposure in 'lurkey Pleural scars (tuberculosis, pleurisy, therapeutic pneumothorax) Single cases after Thorctrast injection or radiotherapy; causality not proved One case in atomic bomb survivor Two doubtful cases described No proof In humans Familial cases (explained by common asbestos exposure?) Correlation with parental cancer Rapidly progressive cases in patients with HIV infection Provitamin A, 0-carotene may decrease the risk Mesotheliomas In animals Simian virus 40 DNA sequences reported In mesotheliomas 19 20 21 22 23 19 24-26 27 2829 3031 32 diagnosis is more difficult in women, or.women exposed to asbestos are more likely to develop a peritoneal 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." 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 ofniesothelioina 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 in 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 itnnportance 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 lun8s- - 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': 1 (T) = c x F x (T4-Cr-D)4 Where, I (T)=incidence at the time T after exposure; c=a constant depending on the process, ^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 erode guess only. As can be seen from table 1, even with heavy exposure only up to [Offiv 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 fhe equation is correct, the risk ,9 fesollrchoara Table 3 lacidereee or rtrortalftJ, ojtrtesothelforraa in trariotts aattnri.es and areas oar time (/ nilliAit inhabitants 13,ear) Comary or area United States North America Nahtes-SBint-Nazaire,. France Texas Selected cities. United States United States .Barcelona, Spain Great Britain Finland Great Britain Nantes-Saint-Nazaire, France United Kingdom Denmark Nantes-Saint-Nazaire, France Great Britain Australia Great Britain Great Britain Australia liar 1 96B-81 1972 1956-74 1976-80 I97fli 1986 1983-90 1 96S-71 1990-94 1972-76 1975-84 1983 1978-80 1985-92 1968-71 1982-88 1982-86 1987-91 1994 Aisle 2A 2.8 S.2 5.8 4.4-11.1 7-13 8.4 10 12.6 17.2 ns 14.7 19.4 20.7 283 30.5 44,0 493 F71fdlC 0.8 0.7 0.2 2.1 1.2-3.8 1-2 4.7 IS 2.9 2.8 0.8 3.2 7.0 4.0 4.3 33 4.9 6.4 4.8 Reference 33 34 35 36 37 38 39 40 41 40 35 16 42 35 40 43 40 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-tithe formula is in practice low and it should not be used for extrapolations, at least not at the extreme ends ofexposure. 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).1'-" In most studies, several patients with mesothelioma do not report any occupational or other exposure to asbestos," s " 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 ofexposure to asbestos." This included domestic and even residential exposure. However, it is ofcourse 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 theulselves. There are 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 nlesotllelioma before 1946," although such negative evidence is of questionable value. McDonald and McDonald, in a recent review, estimated the background level to be 1-2/ trillion/year; they came to this figure by extrapolating backwards from epidemiological studies from various countries." Malignant mesothelioma can occur in children," and such cases can be considered as proof of non-asbestos (spontaneous) aetiology, as the latency time with necessity must be very 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 hulran 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 ofonly 5 years.'" Mesotheliomas also occur in animals, from baboons" and domestic dogs" "' to fish." Dogs ate exposed environmentally to asbestos just like their human masters, which might explain some of the tuniours," 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 nonoccupational 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," oil refineries," electrical industry," jewellery workers," sugar refineries," 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." 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. 508 Hillerdal Non-occupational exposure to asbestos URBAN AIR POLLUTION DOMESTIC EXPOSURE The air in cities contains a very low concentra The family of an asbestos worker could be tion of asbestos. Near to construction or exposed to considerable amounts of asbestos demolition work the concentrations are higher. brought home on-his working clothes, which all It has been suggested that the air of London too often it was the duty of the wife or daugh during the blitz was heavy with asbestos. ter to clean. Pleural thickening, calcifications, Asbestos is also released on braking, and close and pulmonary fibrosis have been described in to a motorway the fibre concentrations in the such cases, as Well as mesotheliomas. ' ' air will be higher than the background, but still well below the industrial threshold values. A AIR POLLUTION FROM ASBESTOS MINES, risk not often appreciated is in dumps. In the FACTORIES, DOCK YARDS, ETC ..vicinity of a waste disposal site the concentra Asbestos mines used to be great environmental tion of asbestos fibres can be 10-1000 times nuisances. They could be seen from a distance above the background concentration." because of the dust cloud. Asbestos fibres can Drinking water can contain asbestos or spread over a distance many kilometres from a asbestiform fibres from natural sources or pol mine, and the tailings from the mines were lution. The use of asbestos cement pipes can used for paving roads, parking areas, play cause a considerable number of fibres in the grounds, etc. In the crocidolite mining areas in drinking water. Small amounts of asbestos can South Africa, the incidence of mesotheliomas be found in some wines, beers, liquors, and was increased to at least 10 times that expected other beverages, probably deriving from the fil even among women, proving a non- tration process. Fibres that are ingested will to occupational exposure. However, whether some extent also enter the blood stream as seen some of this exposure was domestic (see later) from animal experiments." In humans, there is not clear." are few reports. However, when amphibole Another example is the formerly active fibres were found in drinking water from Lake crocidolite mine at Wittenoom, Western Aus Superior, a very small portion could be traced tralia. At least 5000 people lived in the in urine," and when chrysotile occurred in the township of Wittenoom without working in the drinking water, very small amounts were again mines, and in 1993 27 cases of mesothelioma found in urine." However, most ingested min had occurred among these people........It has eral fibres will never be absorbed but will be been estimated that 1.1 % of child residents and cleared in the normal way, and the harmful 1.9 % of the female residents of Wittenoom effects ofasbestos in drinking water or drinks is have died or will die from mesothelioma, probably minuscule (and much smaller than Nvheteas among the workforce this figure would the risk of drinking the alcohol). be 6%. Even if ingested asbestos is not dangerous, it Around the chrysotile mines in Quebec, has to be realised that it is only a very small Canada, there have been at least 53 occupa portion of the tap water that we actually drink. tional mesotheliomas from the mines, nine Most of it is used for other purposes. Once the domestic, and two with general environmental water has dried after washing, cleaning, taking exposure only." In the nearby t6wns, the lungs showers etc the asbestos fibres will spread in of residents who have never worked in the the air. Such amounts are small but not mines have a fibre concentration which is 10 insignificant and will add to the normal times higher than that of the average background exposure." Canadian." Mesotheliomas have also been reported from ASBESTOS IN PLACE = BUILDINGS CONTAINING the surroundings of asbestos factories" and in ASBESTOS people living near dockyards. However, the risk A mixture containing asbestos was popular from residential exposure is probably low. In a after the second world war for spraying on ceil large study from England, this factor ac ings and walls for insulation and decoration. counted for only 3% of all the identified cases." This was used well into the 1960s. There is now a public danger because ofthe plaster fall CONSUMER GOODS ing down from natural wear and tear, vandal Asbestos has been introduced into various ism, or "artistic" carving in schools, etc. In goods used by the public. Examples are wall many industrial buildings, asbestos was also paints and spackling and jointing compounds. used for spraying on the underside of the roof, Another is a hand held hair drier, of which 13 and with natural wear and tear (and for million were sold in the United States and instance birds building nests!)" there is now which has been described as a "small asbestos release of fibres to the surroundings. Asbestos spray gun"." In commercially produced Kent was also extensively used in walls or around filter cigarettes, crocidolite was used in the fil plumbing for insulation purposes, in cement to ters from 1952-6. The sale of these cigarettes strengthen it, or just as a cheap filler. was 11.7 billion, and in the commercials the In a modem city, asbestos can often be found health effects of this filter was emphasised." [p in many places; in the cellar, where steam pipes Once asbestos is introduced into a home, it are insulated; in storage or laundry rooms; in will spread to all rooms and is almost impossi air conditioning sets; in theatres, museums, ble to remove even with a vaccum cleaner. It restaurants, etc."' Whenever there is damage to will easily be disturbed into the air from the any construction or machine that contains slightest movement, and sedimentation is very asbestos, the possibilities of exposure, some slow.' times even fairly high, is there. 1 i.t ,.tntha.t(; 509 Table 4 Reported tuesothelionta cases afler**posure to "asbestos In place" Occupation r exptsare School teachers Attended school Office clerk Female office worker Asbestos insulation at home Cotnntents 9/487 patients with tncsotficlioirta I case each 4 cases 6/262 patients with noesodtelionta Reference 99 100-103 104 102 102 105 J 06 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 wa]]s'"-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 of asbestos, but these results are not undisputed and there is a probable overdiagno sis, as control groups are missing." 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 ofthe houses the risk will disap pear when this procedure is stopped, but due to the long latency time this will take many decades.1- 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 bom in these places and living there in their childhood and youth now have moved to other places, taking with them not only the plaques but also the risk of mesothelioma.'" 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 to 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 the 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."= 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 f/ml. Measurements from working places in the 1960= 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 ablerion-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 Table 5 Local deposits ofmineralfibres (asbestos or erionite), occurrence o/plaques, and ofntalignanr tDesothelloma Country or axes Afghanistan Austria Bulgaria Corsica Cyprus Czechoslovakia Finland Greece: Metsovg SW Aride*, Macedonia New Caledonia i2 South Africa Turkey irssn Type offibre Tremolite Trentolite Anthophyllite Tremolite ' Tremolite Tremolite Unknown * Anthophyllite Tremolite AmosJtc crocidolite Tremolite Erionite Unknown ofPlaques (7o iumrigated inhabitants) _ S3 2,8 women 5.6 men 4M1 (>50 y) 2.7-6* 63-9.0 46.9 24.2 {>49 y) 2.5-6.6 1.3-25 65 Locally high Afcswhelionta risk (rllO*/ _ Not increased Not Increased High High -- Not increased 2811 140(1985-94) High 8Ja 3001 Fifth High Conaneot Case report only Vineyard and field workers Tobacco growers General pollution General pollution Farmers White washing houses White washing houses Population around raise White washing houses Farmers Referenu 108 109 110 111112 1ii1s3114 116 117 118 119-121 123 123 1Z4 4125 126-128 19* 128, 129 130 r12 cascsJJdS 900 inhabitants/10 y. 'Occurrence in local area. 51 0 ffdLvdrl Table 6 Fibre concentrations in air and lungs toith mart-occupational exposure to asbestos 7-PC 0j-agnOStaV Fibres in air Fibcis In lrtt;es . (IxIO'lg drv tissue) Reference Domestic exposure (paraoccupational) Near asbestos mines, factories, etc: In Wlttenoom: When mine operating After closure of mine Farmers near mine in Canada Local asbestos findings: Greece: In the yard of an abandoned house In a newly whitewashed roots Corsica New Caledonia: While sweeping floor . Road dust clouds Asbestos In place: .Teacher's aid Female office worker 0.5 0,01-11,21 0.01 0,02*17.9 70 0.06-0,07 5,3-319,5 0.0040 1.2-26.8 21111 0.0043 31 (t'EM) 11 1D2 48 m 123 114 124,125 102 103 "39 ng/m' (100 times higher then controls). TEM. - transmission electron microscopy. Fibres in the lungs ofpatients 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 46 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 .Inesotlielioma, which was significant.'" In this study (which has unfortunately only been pub lished in German) as in many others, the mean number of fibres in die 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.2' 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 unexposed group can be found in the world. where whitewashing occurs, low values are There is no proof of a threshold value-that is, reported when there is no disturbance, but in a a minimal lower limit below which asbestos newly whitewashed roots and while sweeping ' fibres cannot cause the tumour-and thus it is 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: <0.001 fibres/ml), but once deterioration takes place values can go up to 15 fibres/nil, and when being removed there can be even higher values. In schools in the United States, the 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 incidence ofmesothelioma in a group with such background exposure with the incidence in a truly non-exposed group. mean concentration was estimated to be 0.003 This is not possible, as no such group can be fibres/ml, and in federal buildings 0.006."' found. Thus, with so called non-occupational expo sure, the typical exposure is a low or very low, almost unmeasurable, background concentra tion, but occasional high exposure when there It is nevertheless possible that there is a background level of mesothelioma,-that is, that the tumour can occur even in the complete 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 loxv- exposure from history alone is an impossibility probably much<l case/million people/year. in most cases; but secondly, and perhaps more This figure comes from studies of industrial importantly, that any person living or working ised countries, where background exposure to in (or even temporarily visiting) buildings asbestos is unavoidable. What the true figure is where asbestos has been used in construction can only be guessed. 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. In most studies, there is a clear dose-response relation between expqpijre and the number of fibres in the lungs." t= " " What, then, are the consequences for the public health? From the studies of non- occupational 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 are also necessary whenever rebuilding or tear ing down of structures containing asbestos to avoid asbestos pollution ofthe environment. If 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." ! Larger AM. Inorganic particles in human tissue and their association with neoplastic disease. Environ Health krsuect L 97-5 ;9:22 9-3 3. 2 Gloag D. Asbestos fibres and the environment BAfj 1981; 282:623-6. 1 Churg A. Fiber counting and analysis in the diagnosis of asbestos-related disease. Hunt Pathol 1982;13:381-92. 4 Sluts-Cremes GK, Liddell FDK, Logan WDP, er al. The mortality of amphibole miners in South Africa, 1946-80. Brj lad Med 1992;49:566-75- 5 Cookson WOCMj GlancyJJ, de Klerk NH. et al. Benign and malignant pleural effusions in former Wittenaom miners and millers. AustNZ,7Afed 1985;15:731-7. 6 Rogers A, Nevfll M. Occupational and environmental mes otheliomas due to crocidolite mining activities in Wittenoora. Western Australia. Scared j Wcrft Envinru Health 199541:259-64. 7 Selikoff U, Seidman H. Asbestos-associated deaths among insulation workers in the United States and Canada, 196787..4nrt2Y TAcad Sci 1991;643:1-14. 8 Berry G. Mortality ofworkers certified by pneumoconiosis mearcaJ panels as having asbestosis. Brj lad Med,I981;3B: ^ Navratil M. Schicksal von Patienten mit Asbestose in Verlaufeiner 25jiihrigen praventiven Gesundheitsplege. Zouralban Arbeiuruedizin and Arbeilsschraz I979;29:25964. I 0 Courts It, Gilson JC. Mortality in cases of asbestosis diagnosed by a pneumoconiosis panel. Thorax 1987;42: 11 Gibbs AR, Griffiths DM, Pooley FD, et al. Comparison of fibre types and size distributions in Lung tissues ofparaoc- cupatiottal and occupational cases of malignant mesothe lioma. Br y Ind Aled 1990;47:621-6. 11 Rogers A, Leigh J, Beny G, et al. Relation between lung asbestos fiber type and concentration and relative risk oT mesothelioma. A case-control study. Cancer 1991;67:191220. . 13 Kadalainen A, Meuiman LO, Pukkala E. Four cases of mesothelioma among Finnish aothophyllite miners. Occap Euyuvon Health 199451:212-15. 14 Smith AH, Wright CC. Chrysotile asbestos is the main c'laiutseiof rpleural mesothelioma. Ant a Ind Aled 1996':30: 15 Stayner IT, Dankovic DA, Lenten RA. Occupational expo sure to chrysotile asbestos and cancer risk: a review ofthe amphibole hypothesis. Am j Public Heahh 1995;86:179-86. 16 Jones RD, Smith Dl\4, Thomas PG. Mesothelioma in Great Britain in 1963-83. Scaudj Irbrk Environ Health 1933;14: 145-52. 17 Weiss SW.Tavassoli FA. Multicystic mesothelionra. An - analysis ofpathologic findings ana biologic behaviour in 37 , cases. Am.j Sure Pathol 1988;12:737-46. I SIfillerdal G.Malignant mesothelioma 1982: review of4710 published cases.BrjO/s Chest 1983;77:321-43. 19 Basis Yl,sinhonato L, Artvinli M, et al. Epidemiological and environmental evidence of the health effects of exposure to crionite fibers: a four-year study in the Cappadocian region ofTurkey. IntJCanoer [ 987;39:10-17. 20 Hilleidal G, Bergh J. Malignant mesothelioma secondary to chronic inflammation and old scars. Two new cases and review ofthe literature. Cancer 1985;55:1963-72. 21 Cavazza A, Travis LB, Travis WD, et ah Post-irradiation malignant mesothelioma. Cancer 1996;77:1379-85. 22 Neugut Al, Ahsan H, Amman KH. Incidence of maligDant pleural mesothelioma after thoracic radiotherapy. Cancer 1997;80:943-50. 23 Mizuki M, Yukishige K, Abe Y, et al. A case ofmalignant pleural mesothelioma following exposure to atomic radia tion in Nagasaki. Respirology lw7;2:201-5. 24 MArtensson Gr Larsson s Zettergren L Malignant mesothelioma in two pain: ofsiblings; is there a hereditary predisposing factor? Enrj Respir Dis 1984;65:179-84. 25 Dawson A, Gibbs A, Browne K, et al. Familial mesothelioma: details of 17 cases with histapa,holagic findings and mineral analysis. Caacr 1992:70:1183-7. 26 Hirvonen A, Pelin KJammilclhto L. et al. Inherited GSM I and NAT2 defects as concurrent risk modifiers in asbestosrelated human malignant nhesutheliunha. Cancer Rc$ 1995;55:2981-3. 27 Huncbarek M, Kelsey K, Muscat J, et al. Parental cancer and genetic predisposition in malignant ^kural mesothelioma; a case-control study. Cancer Lett 1996:102: 205-8. 28 Belding CA, Wolf PL, Haghighi P. AIDS and malignant misotbeliohna: [g there a connection? Chest 199.3:103: 1268-9. 29 Idemyor V, Cherubin CE. Rapidly progressive mesothe lioma in an HIV-positive patient. Ann Phartaaconier 19?2;26:429. 30 Schifirihan M, Pickle LW, Fontham E, et al. Case-control study of diet and mesothelioma in Louisiana CancerR.es 198S;48:29IM5. 31 Muscat JE, Huncharck M. Dietary intake and the risk of malignant mesothelioma. Brj Cattur 1996;73:1122-5. S(enton SC. Asbestos, Simian virus 40 and malignant mes othelioma. Thorax 1997;52{suppl 3):552-7. 33 Emerline PE, Henderson VL. Geographic patterns for pleu ral rihesothelionha deaths in the United States, 1968-8l..j Nail Cancer last 1987;79:31-7. 34 McDonald AD, McDonald JC. Malignant mesothelioma in North America. Cancer 1930;46:1650-6. 35 Chailleux.E, Pioche D, Chopra S, et al. Epidemiologic rfu mesutlhetiome pleural malin dans la region de J-Jantes- Saint-Nazaire. Evolution 1956-92. Rev Afal Respir 1995; 12:353-7. H 36 Weiss NS, Martin J, Suarez I, et aLRcview ofmesothelioma incidence and mortality in Texas. Texas A4ed 1988;84:44-8. 37 Hinds MW Mesothelioma in the United States. Incidence iuthe l97Qs.jOccupMedl978-2Q:469-7L 38 Spirtas R, Beebe GW, Coinnelly RR. Recent trends in mes othelioma incidence in the United States. Arn ; ind Med 1986;9:397-407. ,J . . 39 Grupo de Estudio del Mesotelioma en Barcelona. Mortali- dadpor mesotelioma pleural en la provincia de Barcelona. Medfclin (Bare) 1993;101:565-9. 40 Peto J, Hodgson IT, Matthews FE, et al. Continuing increase Id mesothelioma mortality in Britain. Lancer 1995:345; 535-9. 41 Kadalainen A, Pukkala E, Mattson K et al, Trends in mes othelioma incidence and occupational mesodhefiomas ^ Finland in 1960-95. Scandl Wort Environ Health I997;23: 266-70. 42 Andersson M, Olsen H. Trend and distribution ofmesothe lioma in Denmark. Bi jCancer 1985;51:699-705. 43 Leigh J, Corvalin CF, Grimwood A, etal. The incidence of malignant mesothelioma in Australia 1982-8. Ant .j Ind Afed199140:643-55. ' 44 Leigh J, Hull B, Davidsson P. Australian mesothelioma register report The incidence of mesothelianta in Australia 1992-4. J^reyl:95fetinal lnstitute of Occupational Health and 45 McDonald JC, Armstrong B, Case B, et al. Mesothelioma and asbestos fiber type, Evidence from lung tissue analyses. Cancer 1989i63:1544-7. 46 Roggli VI, pfate pc, Brody AR. Asbestos content of lung tissue in asbestos related diseases: a study of 110 cases. Br v Ind Aid 1986;43:18-28. 47 Churg A, Wright JL, Vedal S. Fiber burden and patterns of asbestos-related disease in chrysotile miners and millers. Am Rev Respir Dis 1993;148:25-31. 48 Hansen J, de Merk brli. Musk AW, etal. Environmental exposure to crocidolite and Mesothelioma. Exposure- response relationships. Arn .i Respir Crit Care'Aled 1998;157:69-75. J . 49 Doll R, Peto J. 8liects oa health ufexposure to asbestos. A report to the Health and Safety C<ulrunssMU. London: The Station ery Office, 1985. 50 Landrigan PJ. A population ofchildren at risk ofexposure to asbestos in place. Ann NFApad So 1991 ;643:283-6. 51 de Klerk'NH, Musk AW Williams V, er al. Comparisons of measures of exposure to asbestos in former crocidolite workers from Wittcnoom Gorge, W Australia. Arn .j Ind Afed 1996;30:579-87. 52 Bianchi C, Giaxelli L, Garedi G, et al. Latency periods in asbestos-related mesothelioma ofthe pteura. Ear Y Cancer Prcv 1997;6:162-6. 53 Browne K. Asbestos-related mesothelioma: epidemiological evidence for asbestos as a promoter. Arch Environ Health 1983;38:261-6. 54 Ilgren EB, Wagner JC. Background incidence of mesothelioma: animal and human evidence. Regal Toxicol Pbarmaad 1991;13:133-49. 55 Ilgren EB, Browne K. Asbestos-related mesothelioma: evidence for a threshold in animals and humans. Regul 7oxieol Phamracol 1991;13:116-32. 56 Ashcroft T. Epidemiological and quantitative relationships between mesothelioma and asbestos on Tyneside, j Cltn Pathol 1973;26:832-40. 57 Clhellini e, Fomaciai G, Merler E, er al. Pleural malignant mesothelioma ip Tuscany, Italy (1970-88): II. Identifica tion of occupational exposure to asbestos. Am i Ind Afed 1992,49:599. 58 Spirtas R, Heinemann EF, Bernstein L, et al. Malignant mesothelioma: attributable risk of asbestos exposure. Uccup Emriran a fed 1994;51:804-1]. 59 Howel D, Arblaster L, Swinburne L, et al. Routes of asbes tos.exposure and the development ofmesothelioma m an English region, Occup Envirou A led 1997;54:493-9. 60 fates DH, Corrin B, Stidolph PN, et al. Malignant mesothelioma in south east England: clinicopathological experience of 272 cases. Thorax 1997;52:507-12._ 61 Mats; EJ, Yokoi T Absenoe of evidence for a significant background incidence ofdiffuse malignant mesothelioma apart from asbestos exposure. AnnN YAcadSci 1991:643: 196-294. 62 McDonald JC, McDonald AD. The epidemiology of mesothelioma in historical context. Eur Respir 7 1996;9: 1932-42. 63 Fraire AE, Cooper S, Greenberg SD, et al. MesothheJioma of childhood. Cancer 3988;62:83S-47. 64 Haque AK.KanzME Asbestos bodies in children's lungs. -Arch Pariiol Lab A4,d 1938;112:514-18. 65 Haque AK, Vrazel DM, Burau K, et al. Is there transplacen tal transfer of asbestos? A study of 40 stillborn infants. Ped Pathol Lab Mod 1996;16:877-92. . 66 Booth SJ, Weaver EJM. Malignant pleural mesothelioma five years after domestic exposure to blue asbestos. Lancet 1986-1:435. ' Ifillordal 67 Fortman JD, Manaligod JR, Bennett B7;_Malignant mesothelioma in an olive baboon (Papio anubis), Lao Arti- n;al Sci 1993;43:503-5. 68 Qlickman LT, Domanski LM, Maguire TG, et al. Mesothe- lionta i a pet dogs associated with exposure of their owners to asbestos. EirmrouRes 1983;32:305-13. 69Harbison ML, Godleski JJ..Malignant mesothelioma in urban dogs. Ki Pathol 1983;20:53MO. 70 Smith DA, Hill FW Metastatic malignant mesothelioma in a dog. C Comp Partial 1989;100:97-r01. 71 Herman RL. Mesothelionia in rainbow trout, Saltuo gaird- neri Richardson.IbumalofFish Diseases 1985;8:373-6. 72 Mirabella F. Studio epidemiologies del mesoteliotna spontaneo camno: sun possible milita' in riferimento alia patologia umana. Med Lavoie 1987;78:28-32. 73 Jarvholm B, Malker H, Malker B, et al. Pleural mesothe lioma and asbestos exposure in the pulp and paper industries: a new risk group identified by linkage ofofficial register, Ant fhid Aged 1988;13:561-7.. _ 74 Finkelstein MM. Asbestos-associated cancers in tire Ontario refinery and petrochemical sector. Ant j' LtdAfed 1996:30: 610-15. 75 Inhbemori E, Goldberg M, Bonenfant S, et al. Occupational respiratory cancer ana exposure to asbestos: a case-control study in a cohort of workers in the electricity and gas industry. Antj bid Med 1995;28:339-52. 76 Kent DG, Hanley KT, Roggli VL. Malignant mesothelioma in the jewelry industry, Antj Lidded 1992;21:409-16. 77 Maltoni C, Pinto C, Valenti D, et al. Mesotheliomas follow ing exposure to asbestos used in sugar refineries: report of I fhauan cases. In; AMehlman, A Upton, eds. Advances in modems environmental toxicology. VoIXXJL The identification and control ofetwiroDinedtalaml occupational diseases: hazards and risks of chemicals in the oil refining indusLry.Prinectean, NJ: Princeton Scientiftc,`l994:629-34. 78 Talcott JA, T urbeF WA, Kantor AF, ct al. Asbeatos- . associated disease in a cohort of cigarette-filter workers. N EngUMed 1690^21:1220-3. 79 Quinn MM, KriebeJ D, Buiatti E, et al. An asbestos hazard in the reprocessed textile industty. Am f hid Med 19S7;11: 255-67. ^ 80 Kane MJ, Cliahinina All, Holland JF. Malignant mesothe lioma in young adults. Cancer 1990;65:1449-55. SI Maghani C, Terracini B, Ivaldi C, el al. A cohort study on mortality among wives ofworkers in the asbestos cement industry in Casale Monferrato, Italy. Br i Ittd Med 1993;59:779-84. J` 82 Schneider J, WoitowiV. HJ. Tumors linked to para- occupational exposure to airborne asbestos, hidoor Built Enominmentl 9Sfe;5:67-75. 83 Botha JL, (twig LIA, Stiebel PM. Excess mortality from stomach cancer, lung cancer, and asbestosis and/or mesothelioma in crocidolite mining districts in South Africa. AmJ Epidemiol 1986;123:30-40, 84 Musk AW, de Klerk N, Eccles JL, et al. Wittenoom, Western Australia: a modem industrial disaster. Am jf hid Aged 1992;21:735-47. - 85 Harington JS. Mesothelioma among workers in the Quebec ^9^22 ^ industry. Am 3 Ltd Med 86 Churg A. Lung asbestos content in long-term residents of a chiysotile mining town. Am Rro Respir Dis 19B6;134:125- 87 Hain E, Dalquen P, Bolilig If, et at. Katamuestische Untersuchungen zurGenesedes Mcsotclioms. Bericht fiber 150 Falls aes dem Hamburger Raum. Internationales Arabia, fib Arbeiismedirirt 1974;33:15-37. 88 Smith Rj. Briefing. Science l979;204:285. 89 Longo WE, Rigler MCir, Slade J. Crocidolite asbestos fibers in smoke from original Kent cigarettes. Cancer Res 1995;55:2232-5. 90 Moorcroft JS, Duggan MJ, Rate of decline of asbestos fibre concentration in room air. Aun CKcup Hyg 1984;28:453-7. 91 Seta BE, Levine rj, Non-occupational asbestos emissions and exposures. In: L Micahels, SS Chissick, eds. Asbestos. Vol 1, Properties, applications, and hazards. New York: John Wiley* 1979:171-205. - 92 Cunningham HM Moudie CA, Lawrence GA, et al. Chronic effects ofingested asbestos in rats. Arch Environ Couiant Toeicol 1977io:507-13. 93 Sebastien l', Masse R, Bignon J. Recovery of ingested asbes tos fibfers front the gastrointestinal lymph in rats. DiviroiT Resl980;22:20]-Ux JK 94 Cook MP, Olson GF, Ingested mineral Fibers; elimination in human urine. Science 1979;204:195-8. 95 Boatman H. Use of quantitative analysis of urine to assess exposure to asbestos fibers in drinking water in the Puget Sound area. Envinni Health Perspecr 1983;53:131-9. 96 YCehbeT JS, Syrotynski S, King MV Asbestos-contaminated dnnkin^ wafer^ its intact on household air. Eirviron Res 97 Greenberg M, Malignant mesothelioma in paper mill workers: where might die asbestos have collie from? Ant Ind.lled 1996;3Q:64L 98 Mollov.LB. Asbestos in place in metropolitan New York. Ann WTlAcadSci 1991*643:614-21. - 99 Anderson HA, Hamahan 1 ScliirmerJ, ei al. Mesotlielionia among employees with! likely contact with in-place asbestos-contauung building materials. Anit N Y Acad Sci 1991 ;643;550-72. 100 Dodspn RF, O'Sullivan M, Cons C. Technique dependent variations in asbestos burden as illustrated in a case of nonoccupational mesothelioma. Aiuj IndAfed 1993;24:235-40. 101 Huncharek M. Occult asbestos exposure. AJit I Ltd Med 1991;20:713-14. 102 Roggli VL., Longo WE. Mineral fiber content of lung tissue in patients with environmental exposures: household ' contacts v building occupants. Aun N Y Acad Sci 1991;643:511-18. 103 Srebro S, Roggli VL. Asbestos-related disease associated with asbestiform tremolite, Am j (rid Med I994,26,8Q919. ' ' 104 Lilienfeld DE. Asbestos-associated pleural mesothelioim in school teachers: a discussion of four cases. Artu/V l'Acad Sri 1991;643:454-8. 105 SteinRC, Kitajewska JY,Kirkham jb, etal. Pleural mesothelioma resulting from exposure to amosite asbestos in a building. Respir Med 1989;83:237-9. 106 Dodoli D, Del Novo M, Fiumalbi C, et al. Environmental n household exposures lo asbestos and occurrence ofpleural mesothelioma.Are, dudMed 1992;21:681-7. 109 Hillerdal G. Pleural plaques; incidence and epidemiology, expoaed workers and the general population. Indoor Built Eirviroturreru 1997;6:86-95. 108 Voisio C, Marin 1, Brochard P, et al. Environmental airborne tremolite asbestos pollution and pleural plaques in Afghanistan. Chest 1994;106:974-6. 109 Neuburger M, Griindorfer W, Haider M, et al. Urawelt- bedingte endemische Pleuraplaques, Zentrblatt furBakieriologte andH3giatlerAbrer7 Original 1978;167:391-404. 110 Neuburger M, Kundi M, Fried! HP. Environmental asbes tos exposure and cancer mortality. Arch Environ Health 1984;39:261-5. i 11 Burilkov T, Babadjov L. Em Bcitrag zum endemischen Auflreten doppelsertiger Pleuraverkalkungen. Praxis fair Pitertntologie 1970;24:433-8. 112 Zolov C, Bourilkov T, Babadjov L. Pleural asbestosis in agricultural workers. EimironRCS 1967;1:287-92. 113 Rey F, Boutin C, SteinbauerJ, ei al. Environmental pleural plaques in an asbestos exposed population of Northeast Corsica. Fur Respir31993j6:978-82r 114 Rey F, Viallat JR, Boutin C, el al. Les rnesotheliames envi- ronnementaux ea Corse du nord-est. Rev Mai Respir 1993; 10:339-45. 115 McConnochie K, Simonato L, Mavrides P, et al. Mesothe lioma in Cyprus: the role of tremolite. Thorax 1987;43: 342-7. 116 Marsova M. Beitrag ztir Atiologie des Pleuraverkalkungen. ZeirschrifrfurTuherlnjlose 1964;321:329-34. 117 KLviluoto R. Pleural calcification as a roentgenologic sign of non-occupational endemic anthophyllite asbestosis. Actor Radial 196U;(supp1 194), 118 Raunio V Occurrence of unusual pleural calcification in Finland. Studies on atmospheric pollution caused by asbestos. Aunales de Medicirta hitema Feiudae 1966: 55(suppl 47). 1 119 Constantopoulos SH, Malamou-Mitsi VD, Goudevenos JA, et al. High incidence ofmalignant pleural mesodielionna in neighbouring villages of Northwestem Greece. Respira tion 1987;51:266-71. I 20 Bazas T, Oakes D, Gilson JC, er al. Pleural calcification in northwest Greece. Euviron Res 1985;38:239-47. 121 Longer AM, Nolan RP, Constantopoulos SH, et al. Associ ation ofMetsovo lung and pleural mesothelioma with exposure to tremolitc-containing whitewash. Lancet 1987;t: 122 Sakellariou EC, Maianiou-Mitsi V, Haritou a, et a/. Malignant pleural mesothelioma from non-occupational exposure in Metsovo (north-west Greece): slow end of an epidemjc? Ettr Respirf 1996;9:1206-10. 123 Sichletidis L, Daskalopoulou E, Chipros D, ei al. Five cases ofpleural mesothelioma with endemic pleural calcifications in a rural area in Greece, MedLairro 1992;83:259-65. 124 Qqldberg P, Luce Dr Billon-Gallant MA, et al. Role poten tial de rexpositiou environnementale et doraestique a la tremolite darts le cdiicer de la plevre cn Nouvelle Caledcnue. Rev Epidetniol Saari R^l 1995-43:444-50 125 Luce D, Brochard i;Quenel P, er al. Malignant pleural mesothelioma associated with exposure to tremolite. Lancer 1994;ii:1777. 126 Basis YI, Sahin AA, Ozesmi M, a al. An outbreak ofpleu- (Jt mesothelioma and chronic fibrosing pleurisy in die vill^eofKarain/U^ijp in Anatolia. Thorax 197833:181-92, 127 Basis YI, BilirN. Artvinli M, etal. An epidemiological study in an Anatolian village environmentally exposed to tremolite asbestos. Brj hid bled 1988;45:838-40. 128 Selcuk Z,, C6plu L, Einri S, et al. Malignant pleural mesothelioma due to environmental mineral fmer exposure in Turkey. Analysis of 135 cases. Chest !992;102;790-6. 129 Artvinli m, Baris Yd. Environmental fiber-induced plcuro- putmonary diseases in an Anatolian village: an epiaemiologicstudy. Arch Eiroiron Health 1982;37:177-81. 130 Ginzburg EA, SilovaMV, Komeieva MJ, etal.Rdntgenolo- gie des nichtberufs-bedineien Ashestoseder Pleura. Radiologia Diagnosrica 1973;14:307-12. 131 Boman G, Schubert V, Svane B, etal, Malignant mesothe lioma in Turkish immigrants to Sweden. Scant -i fl'ink Eiviiyn Health I982;8:ld&-12. 132 Harries PG. The effects and control ofdiseases associated Leith exposure to asbestos in a naval dacktv/id (MD Thesis}. Alverstoke, Gosport, UK: Institute ofi4avaf Medicine. 1970. 133 McMillan GHG. The jscaldf ofwdders in navaJ dockyards, j Occup Med 1983;25:727-30. 134 ChurgA. Analysis of lung asbestos content. Bra'(rid Med 1991;48:649-52. .Ucsuhrluntts 513 135 U S Environmental Protection Agency. EP.4 study on asbes tos containing materials as public bullijTugf. Washington, DC: US6PAl 1986. 136 Woitowitz HJ, Hillerdal Q, Calavrezos A, et al. Risiko-urtd EinfJms/akforen des diffusen maligueU AftSOl6elioni5 (DAM). Scfir/teureifte d&r BunaesaustaJttt'XA rbeitsscfiuis. Bonn; BfA, 1993. (Fb69B0 i 37 Murai Y, Kitagawa M. Asbestos fiber analysis in 27 malig nant mesotheliomacases. AntilndAied 1992;22:193-207, 138 Tuomi 1\ Segerberg-KonUinen M, Tammiiebto L, et al. Mineral fiber concentration in lung tissue of mesothelioma patients in Finland. Atnj tud Msa 1989;16:247-54, 139 Tuomi T, Huuskoneo M, Tammiiebto C, et al. Relative risk of mesothelioma associated with different levels of exposure to asbestos. Scand I Ilitrk Eutdros Health 1991;17:404^8. 140 Sakai K, Hisanaga N, Huang J, et al. Asbestos and non-asbestos filer content in lung tissue oflapanese patients with malignant mesothelioma. Cancer 1994;73:1825-35. 1*11 Dodson RF, O'Sullivan M, Com CJ. Analysis of asbestos fiber burden in Iude tissue from mesothelioma patients. Ultastruct Pathol 1997;21:321-36. 142 Ferguson D. Low-level asbestos: the priorities are wrong. AffedlAust 1990;152:617-18, Occupational and Environmental Medicine - ht1p://www.nccenvmeH .r,nm Visitors to the world wide web can now access Occupational and Environmental Medicine either through the BMJ Publishing Group's home page (http://www.bmjpg.com) or directly by using its individual URL (http://www.occenvmed.com). There they will find the following: Current contents list for the journal Contents lists of previous issues Members of the editorial board Subscribers' information Instructions for authors Details of reprint services. A hotlink gives access to: BMJ Publishing Group home page British Medical Association website Online books catalogue BMJ Publishing Group books. The web site is at a preliminary stage and there are plans to develop it into a more sophisticated site. Suggestions from visitors about features they would like to see are welcomed. They can be left via the opening page of the BMJ Publishing Group site or, alternatively, via the journal page, through "about this site".