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to the lifetime background mesothelioma rate, which is about 1 i n 5, 000. " At considerably higher levels of exposure than those found in public buildings, but below those observed occupationally, other epidemiological findings are relevant (1). For example, cases of mesothelioma have been observed in the vicinity of crocidolite mines, mills and factories, but not near comparable chrysotile operations. It is also clear that occasional cases of mesothelioma and possibly of radiographic abnormality can be attributed to exposure in the household of asbestos workers. The latter facts are reasonably well documented but with little or no information on fibre type or exposure intensity/duration. 5. Conclusion Whether or not the risk of malignant disease is linearly related to airborne asbestos exposure remains open to question and whether or not there is a threshold below which the excess risk is zero is probably beyond the power of science to determine. Certainly the risk of any given airborne fibre concentration is considerably greater after amphibole than commercial chrysotile exposure. The practical issue which remains is thus more philosophical and political than scientific. Asbestos cement and friction products are very valuable for building construction, water supplies, drainage and for vehicle brakes, especially in parts of the world where cost is a major consideration. Until such 10

11 time as less hazardous•but equally effective and affordable substitutes can be found, the strictly controlled use of chrysotile need entail no detectable risk. Society must therefore determine whether its resources should be directed at attempts to further reduce risks conceivably associated with the use of asbestos, a difficult and costly task, rather than concentrate on the major threats to life, health and happiness, which are all too abundant. These decisions should be taken by well-informed local people in the light of national priorities; it is unlikely that they will be the same everywhere. 6. References 1. McDonald JC. Health implications of environmental exposure to asbestos. Environ Health Perspect, 1985;fi2:319-328. 2. McDonald JC. Cancer risks due to asbestos and man-made fibres. In: Recent Results in Cancer Research, Vol 120, (ed Band P), Springer-Verlag Berlin Heidelberg 1990, pp 122-131. 3. Berry G, Newhouse ML, Antonis P. Combined effects of asbestos exposure and smoking on mortality from lung cancer and mesothelioma in factory workers. Br J Ind Med, 1985;42:12-18.

12 4. Liddell D. Epidemiological observations on mesothelioma and their implications for non-occupational exposure to asbestos. In: Proceedings of Symposium on Health Effects of Exposure to Asbestos in Buildings, December 14-16, 1988, (eds Spengler JD, dzkaynak H, McCarthy JF, Lee H), Harvard University Energy and Environmental Policy Centre, Cambridge, MA, 1989. 5. McDonald JC, McDonald AD. Epidemiology of mesothelioma. In: Mineral Fibres and Health (eds Liddell FDK, Miller K), CRC Press, Bocca Raton FLA, 1991; pp 143-164. 6. Rogers AJ, Leigh J, Berry G, Fergusson DA, Mulder HB, Ackad M. Relationship between lung cancer fiber type and concentration and relative risk of mesothelioma. Cancer, 1991;67:1912-1920. 7. Enterline PE. Extrapolation from occupational studies: a substitute for environmental epidemiology. Environ Health Perspect, 1981;42:39-44. 8. Doll R,,Peto J. Effects on health of exposure to asbestos. London, Health & Safety Commission, Her Majesty's Stationery Office, 1985. N CJ1 O E ~ 9. Hughes JM, Weill H. Asbestos exposure-quantitative -Q ~ assessment of risk. Amer Rev Resp Dis, 1986;133:5-13. fV ~ N

13 10. Vacek PM, McDonald JC. Effect of intensity in asbestos cohort exposure-response analyses. In: Occupational Epidemiology (ed Sakurai H, et al), Elsevier Science Publishers, 1990, pp 189-193. 11. Vacek PM, McDonald JC. Risk assessment using exposure intensity: an application to vermiculite mining. Brit J Ind Med, i991;48:543-547. 12. Health Effects Institute - Asbestos Research. Asbestos in public and commercial buildings, Cambridge MA, HEI.AR, 1991. 13. McDonald JC. An epidemiological view of asbestos in buildings. Toxicol Ind Health, 1999;7:187-393.

TABLES AND FIGURES Source Table 1 Exposure-response for lung cancer in McDonald (1) male cohorts where exposure estimates Table 3 were made for each subject individually Table 2 Lung cancer and smoking in asbestos Berry etal (3) workers Table 8 Table 3 Estimated lifetime risks per million McDonald (1) population from non-occupational Table 4 exposure to asbestos Table 4 Lifetime risk estimates for populations McDonald (13) exposed to chrysotile only Table 4 Figure 1 Standardized mortality ratio (SMR) by McDonald (2) exposures to asbestos fibres. Exposure- Figure 2 response relationships from 11 studies Figure 2 Concentrations of chrysotile and McDonald & amphibole fibres more than 8µm in length McDonald (5) in lung tissue at autopsy f rom Figure 3 mesothelioma cases and controls Figure 3 Relationship of loge (odds ratio) to Rogers e al (6) l og30 ( f i bre concentrati on i n l ung ) for Fi gure 1 total uncoated fibres by light microscopic analysis

Table 1 i'abl e 2 Study Type of Fiber Number in Total Lung cancer expected Refatsve slope per no. industn' Study Plate t)'pe cohort deathf csxes m(xf•yr I itiinin= and MeDona)d (ii) Quebec ChrysoUle 10.939 3,291 18.1 0.164 2 mdling Cenenl Henderson and U.S. Chrysoule 1,075 781 23.3 0.353 manufacture Enterline (t3) CrIK1dOI1te Amosite 3 Cement producta Wei)) (t6) New Orleans Chrysotile 5,615 601 49.2 0.658 Crocido6te 4 Te=t;l« nemeslt (rm S. carolina &ysoc>7e 768 191 7.5 6.896 5 Textiks MeDonald (3i) S. Carolina Gvy:att7e 2,543 857 29.6 5.863 S Mainly te:tt7e: McDonald (st) Feru>:Ylrania Chrywt;ie 4,137 1,392 50.5 5.101 Amosite 7 Frietion products Berry and New• En=land Goeido(ite t3+rysotik 9,113 1,640 139.5 'etfeetively seav' house {50 Ctoeidafite a Friction products 1deDoaald (tt) Connecticut Clvysot+7e 3.641 1,267 49.1 'effectively zero' 9 Cesnent pnldncts F'utkelsttin Gtt) Oetsrio cuysotik 536 138 5.4 not calculated Cracidolite Nonsmokers Sraokers' xelative _~ R l i ti Rd uba=os ffe 95% d f Study Obarxd Scpocu+d e at ve cisk Observed £:peded a ve risk e ct (NS3) eon enea + limiu (1) fasulatioa wotkers, 0 0.05 0 24 2.93 i.1 0 0-5.0 New York and New lcrsey. i963-71" (2) Insu(ato% iJSA and 4 0.7 S.7 268 S1A 53 1.1 0.3-2t; CAnada,1967-76r' ' (3) Amaite factory ~ S 0.2 25.0 45 9.6 4.7 SJ Lf-t 22 w_orkers, 1%1-77" (4) Faetory workers 1 0.2 S.0 14 1.9 7.4 0.7 0.1-3.4 (woroeni uK. 19G0•-7o' (5) Factory wxkers. 4 0.55 7.3 75 31.02 24 3.0 0.t-7.5 UK, 1971-•80 Asyesta uposure (61 Miners and millers. Canada. 1951-75 nse-toauot data" Yes No ± Yes No t Lun= nncer .17 6 131 69 Controls 93 103 10 274 240 1.7 1.3 0.7-5.4 Combined studiac - - - - - - I E I.1-2.E Lung cancer Mesotheliolna "'able 3 Enteriine (M 2 1U(I" Scllneidernlan 4iS) 3-32 4-24 Nicholson (40) 12-18 6-24 NRC Committee (46) Smokers, mak 64-320 Smokers, female 23-120 Nonsmokers, male 6-29 9-46 Nonsmokers, female 3-15 'This figure should probably have been about 50 (see text). Populaticn(n) Oonoentration Duration Attributable cases f/mi) (yr) Ltr-q cancer Mesothelictrg Total Asbestos calerot 0.5 20 26 5 31 workes•s(10,000) 40 51 6 57 able 4 Scteool chi ldren 0 million) 0.001 6 0.6 0.9 1.5 0.003 1.9 2.6 4.5 eased on Hugttes and 4+lei 11 (1986)

Figure 1 Figure 2 Lung cancer SMR f-100 tYmres/q 1'10 r1 Grulacire : (?rsrabi]it7 Scale) t 20 30 40 50 60 70 $0 !0 !S !8 1 f 1 1 1 1 1 1 1 i ; ,~~Casu CI2) I Curlati.e S (troia/ilicq Sule) 20 )0 40 50 60 70 80 !0 !S !6 ~ i / 1 1 1 1 1 1 f f i Relstive risk (odds ratio) (loge scale ) U1 O © -J 0 Figure 3 2J 4-0 4•5 5-0 5•5 6•0