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PLAINTIFF'S EXHIBIT Cancer Produced by Nonoccupafionai Asbestos Exposure In the United States Philip 1. Enierline University ot Pim* rgh # there Is considerable evidence ot asbestos fibers in the genera) en> firooment, and asbestos fibers can be found In the lungs of most adults in urban areas ot the western world. Concentrations in large urban r-ots appear to average around 3 og/ms of air and In rural areas around 0.1 nfl/m5 ot air. For tho entire U.S. population It can be es timated that the average population tsposuro le 1.S ng/m*. Based m the results of case control and other studies, H Is estimated that about a third ot the 1900 or so ca - m of malignant mesothelioma that occur In the U.S. each year appear to be related to this type ot nsnoccupetlonal asbestos esposure. This is s ICetlme risk Of 100 per million population. Lung cancer caused by asbestos In the general environment can be estimated from linear extrapolations ot doseresponse dele arising from occupational studies. Using data from a study of retired asbestos products workers H Is estimated that the lifetime risk ot lung cancer due to continuous asbestos exposure at 1.s ng/m1 la 2 per million. Possibla causes for a titty-told difference between lung cancer and mesotheliomas caused by nonoceupational exposure lo asbestos are discussed. These estimates an compered with estimates derived tram e recent report commissioned by the West German government. Coated fibers have been found in the lungs of residents of urban areas of the western world for nearly20 years now. The meaning of this for human health remains os unclear today as it vas when the phenomenon was discovered At first, it was believed that ail of the fibers were asbestos but it was soon realized that many were not Nevertheless, a sufficiently large proportion have been positively identified as asbestos to warrant the descriptive term "asbestos bodies". The discovery of asbestos bodies in human lungs has led to a careful examination of the air in urban areas and the con clusion that all urban areas are polluted with asbestos fibers.1 The source of these fibers appears to be primarily asbestos building products. Table 1 summarizes levels of asb^toa found in U.S. cities based on 24 h samples from each city.3 On av al***. tbs conc*MJ*i)Dj> in far** urban ansa appears W be about. 3, ng/m3, rsngitig from 0.09 to 70 ng/so3. fr> tuts! and in small urban areas of the U.S., asbestos concentrations are much lower--around 0.1 ng/m5.3 Weighting these concen trations by number of people in large urban as compared with other areas gives sn average outdoor asbestos exposure level of around l.S ng/m3. I SSJ-A *<< Cw>t*IA<nu* 318 Thu is an attempt to estimate the number of cancers tl are likely to be produced by asbestos among the nonoccup tionally exposed populations in the U.S., thatis, the popul Hons exposed to asbestos at the estimated average outdc background level of 1.5 ng/ro* of air. Not included in this t fcimate it cancer caused bv nonoccupationai indoor air poll tion. Only two of the health effects of asbestos will be co sidered: malignant mesotheliomas and lung cancers. Mali nant mesotheliomas produced by background levels of a bestos will be estimated directly from reports on the sumbe of these cases and their probable asbestos exposures, whi lung cancers will be estimated by extrapolation from lur cancers produced by asbestos in occupational environment Studies which attempted to estimate the overall impact < occupavional asbestos exposures on the cancer problem in t'r U.S. will first be reviewed, as these demonstrate some of tf problem* encountered in the estimation of health effects; background levels. Table I. Concentrations of asbestos in urban areas of the US. Asbestos concentration ng/mJ <1 1-2 2-6 6-10 10-20 20-60 60-100 Mean Median Ml Sinai Number of samples 61 50 45 12 8 1 2 3.58 1.57 Batielle Institute Number of samples 27 33 42 22 l 2 0 3.62 2.29 Table II and Figure 1 summarize six studies that estimate the contribution of occupational asbestos exposures to annua *ficcr (ssidtnct in the U.S.*-* Fivs out oflb* six nmnj *r< m relatively close agreement, whereas the U.S. government' estimate that 13-18% of all cancer is the result of occupations asbestos exposure is quite different The only other estiraati of this magnitude was by Dr. Irving Selikoff, who estimate' 40,000 cancer deaths per year caused by occupational exposun to asbestos, or about 10% of all cancer deaths.10 The U.S. government report has had a great impact or world opinion about asbestos since it was announced in I97i toimal of tho Air Pollution Control Assoc`atio< 006269 Table If- Annual number ofcancer deaths in the U.S, due to oct upjtmnal exposure to asbtstoa--various estimates._ Source Exposed Annual Percent of population number of all i J ,S. alive 1980 cancer deaths cancer deaths McDonald* (198114 Htgpnson (1979)5 EnterimeU981l* Nicholson rt al 11981) 7.600,000 9,200.000 Hogan and Hoel 7-8,000.000 <19811* U.S Govt (19781* 7-10,000.000 3,330 4,000 4,084 8,500 12.000 58-75,000 <1% 1% 1% 2% 13-18% " tJ.S. and Canada. and received extensive press coverage throughout the world. In its J979 report to the Congress. HEW listed this report as a significant accomplishment during the year 1978.*1 If the finding that 13-18% of all cancer is due to occupational ex posures to asbestos were credible, clearly the banning of ail asbestos should be considered. There is little support for the government document, however, as Table !I suggests. In fact, partly as the result of this estimate. Congress commissioned n study that included an evaluation of the importance of oc cupational exposure to asbestos. The study concluded that asbestos may cause about 5% of ail present day lung cancer.12 inasmuch as lung cancer constitutes about 20% ofall cancer, this suggests that asbestos-caused lung cancer accounts for about U'o of all cancers--a finding which tends to support most cf the estimates shown in Table II. Author example, in 1976 a group of government investigator* reported-' on the effect* of very low human exposures to aibestiform fif" bers among workers at a gold mine at Lead, SD.13 They t* ported a threefold excess in respiratory cancer and suggested, that this was due to very low fiber exposures. A second study of workers from the tame mine by researchers from McGill University showed essentially no excess in respiratory cancar.*4 The U.S. government commissioned a third study by a private research group. This study found no excess in res piratory cancer among these same workers.15 One method for estimating lung cancer caused by low dose environmental exposure is-by extrapolation from effects of exposure at higher levels.14 An estimate of lung cancer caused by nonoccupationai exposure was prepared (using the 1981 Enterline estimate from Table II), assuming a general popu lation exposure of l.S ng/m3 and that 1 ng contains 40 fibers of asbestos greater than 5pm in length, seen by the optical microscope.4 The number of lung cancers at 1.5 ng/m3 was estimated by a simple linear extrapolation from the experience in a tingle British study by Peto, et ol. of the dose-response relationship between asbestos and lung cancer in a population: of asbestos textile workers.12 These estimates of asbestoscaused lung cancer are shown in Table III. Table III. Annual number of cancer deaths in the U S. caused byexposure to asbestos Type of exposure and cancer Occupational exposure Lung cancer Mesothelioma Other cancer Nonoccupationai exposure Lungcancer Mesothelioma Annual number of cancer deaths 4034 2501 333 2150 361 28 333 Percent of all U.S. cancer deaths 1 <0.1 F^ur* 1. (Estimates of the p*rc*nt*$e of alt canear due to occupational etposir* to asbestos m tie U $ at I960 (McOonftJd estimate reflects U S ana Canada). While there are very large differences in the cancer deaths shown in Table H. there is not much disagreement on the size of the occupationally exposed population. The reasons for the differences in the estimates of health effects ore twofold: (It a difference of opinion as to the intensity of exposures received by various groups of workers, and (2) a difference of opinion as to the appropriate dose-response relationship for asbestos and cancer. When dealing with the health effects ofoutdoor background asbestos concentrations, there are too few data on the intensity of exposure to cause much disagreement. The main problem is to calculate the response likely at very low exposure levels. Attempts to directly measure the amount of lung cancer produced by low doses of asbestos have been unsuccessful. For April 1983 Volume 33, No. 4 Also shown is malignant mesothelioma caused by asbestos exposure. This was calculated as follows: There are abo-'t 1000 new malignant mesotheliomas in the U.S. uach year with a male-female ratio of 3:1, or about 750 males and 250 females.14 McDonald and McDonald estimate that for males with mesothelioma, 53% are the result of an occupational asbestos exposure.4 From their study it also appears that no more than 5% of females with a malignant mesothelioma have this as the mult of an occupational asbestos exposure. Thus, there are 397 males and 13 females out of the 1000 malignant meso theliomas reported each year whose mesotheliomas were caused by occupational asbestos exposure This it a slight upward revision of the 333 reported in 1981 (Table III), since it is based on data not available in 1981. By subtraction, there are 353 males and 237 females whose mesotheliomas were caused by something other than occupational exposure to asbestos. What percent of this total 590 are caused by the average outdoor asbestos level of l.S ng/m3 of air? There is evidence that fibers other than asbestos cause malignant mesothelio mas.19 There is also evidence that nonoccupationai exposures to asbestos cause malignant mesotheliomas.50 The previously estimated 333 malignant mesotheliomas caused by nonoc cupationai asbestos exposure--a little over half the 590 nonoccupationally crused malignant mesotheliomas4---is consistent with an estimate made by McDonald and Mc Donald in 1981.4 This will continue to be used as a best esti mate. rince the estimate of nonoccupationai lung cancer shown in Table 111 was made, some assumptions in the study upon which it was based have been revised. Apparently, exposure 318 008270 ***^rtr** ebeaenbecauxe it u thaoniyatudy feM7$hhi*torM!pasure data were available gjggfjaedJji^JUjarj. the currently acceptable method of reporting iaKtoa. concentration*. Moreover, it appeared to be well known and well accepted) and was one of three selected for inclusion in the dose-responsa section of the report by the Advisory Committee on Asbes tos.22 It has now been reported, however, that the fiber ex posures in this study were probably *bc-jt3 times higher than originally thought. Ifso, this would make the estimate of lung cancer deaths in Table III around 9 or 10 rather than 28. This has little effect on the overall estimate of 361. In 2981, the effects of asbestos fibers emitted by hair dryers with asbestos-containing heat shields on lung cancer mortality were reported.16 This estimate was based on a linear extrap olation from a study of lung cancer among retired U.S. as bestos products workers.23 Figure 2 shows the dose-response relationship between asbestos concentration expressed as million particles per cubic foot (mppcf) and excess lung cancer expressed as Standardized Mortality Ratios (SMR). SMR are the ratio of observed to expected deaths times 100 and are a commonly used measure of excess deaths in epidemiologic studies. From these data, lung cancer deaths that would result from continuous exposure to very iow levels of airborne as bestos can be estimated. Some results from the 1981 report are shown in Table IV, expressed as lifetime risk of lung cancer resulting from con tinuous asbestos exposure per million people exposed. In preparing this table, asbestos concentrations expressed, as were converted to fibers per cubic centimeter if/ce) of sur b'- assuming i mppcf * 2 f/cc. Also, as in Table III. 1 ng of asbestos was assumed to contain 40 fibers of asbestos greater than 5m in length as counted by the optical method. The rationale for these conversions appears in the 1981 report. Lifetime lung cancers were calculated assuming that lung cancer starts 20 yr after the beginning of exposure and that an av erage lifetime is TO yr. so that the effective exposure period is 50 yr. The effect of hair dryers appears on the first line followed by the effect of all nonoccupational expo sures. Tabic IV. Lifetime lung cancer deaths resulting from various levels of asbestos exposure per million exposed- ______________________________ Level of exposure (ng/m`l Equivalent fibers cc 05 am tong) Lung cancer deaths i ,-i. '' 6 1-5 5 SO soo 5.000 50.000 0.000037 0.00006 0.0002 0.002 0.02 0.2 2 0.85 2,08 4.6 46.06 4606 4.606 463160 For a U.S. population of 225 million. Table IV suggests 225 X 2.08. or <68 lifetime deaths from lung cancer due to nonoccupational asbestos exposure at 1.5 ng/m\ whereas Table 111 suggests 28 X 70. or 1960 lifetime asbestos lung cancers related to nonoccupational asbestos exposure at 1.5 ng/m-'. If the exposure estimate upon which Table HI was based are off by a factor of 3, however, these estimates are much closer <653 vs. 468). For malignant mesothelioma. Table III suggests a lifetime risk of 333 X 70 or 23.310 cases for a U.S. population of 225 million It is plausible that the original estimates of fiber exposure in the British study of asbestos textile workers were indeed too low. The British study estimated an average fiber count fot asbestos textile operations of around 12 f/cc prior to 1950.17 320 _ /, ;t' tfV-r-'.- `J'y - y.t< I CO + o For retired workers, from a Johns ManviUe asbestos prodi plant in the Ui, average worker exposure was 10 rnppc , If thisis converted to f/cc by assuming i mppcf 3 f/cc ti this jivesan average exposure of30 f/cc. In a textile operat reported m by Nicholson, historic fiber counts were estims at 80 f/cc.2* It seems likely, therefore; that exposures in .British study could have averaged 36 f/cc rather than i 2 i and that the estimates of U-S. lung cancer deaths showr Table II should be lowered by a factor of 3. One important assumption in Tables 111 and IV wonce the conversion of ng to fibers seen by the optical me;r. Many fibra cannot be seen by the optical method. Moreo-. fiber size determines tl i conversion factor. The converfactor of 40. usedin estimating nonoccupationaiiy caused !_ cancer in Tables III and IV, is perhaps high. For example conversion factor of 30 was used in EPA's water quality d ument.a Bmckman recommends 20.26 To the extent that conversion factor is high, it overstates lung cancer cases caua by nonoccupational asbestos exposure. It is difficult to judge the validity of the estimates shov in f. bles JJI end IV. There have been only a few attempts estimate the health effects of asbestos exposure on he gene: population. In 1977, Brockman reported on the developme of criteria for setting an asbestos air standard for the state Connecticut and concluded that 30 ng/m3 would be a sa level.2* It was estimated that at this level, a minimum of 1 mesotheliomas would be produced on a nationwide basis. Th level was justified as one that results in about the sair number of deaths as train mishaps and about Vio the year! fatalities from airplane accidents. Only a minimum numbi of mesothelioma deaths was calculated on the grounds thrthis would be difficult to criticize as being too stria. An uppi limit can be calculated from the data and appears to be aboi 10,000. Extensive detailson the manner in which these est: mates were made are not given. In 1981, Schneiderman, et al were commissioned by th West German government to prepare a report on the risk- b exposure to tow levels of asbestos in the general environ ment,-" Their report provides a basis for calculating the life time risk of asbestos exposures at low levels, provided sum conversion of ng to fillers can be made. The concluding tabl in their report, labeled "Risk assessments for the genera population..apparently is related to the risk for a workin population exposed 8 h/dav, five days/week. These risks ca be converted to continuous exposure, however, by dividing b 0.24. since working time is 241* of total time. It can then b Journal of the Air Pollution Control Associate 008271 calculated that the lower limit of lifetime Halt oflung rtnCtr for a population exposed to l f/cc for i yr i* 0.0015. The ltrtiftsr limit of risk for exposure to 1.5 ng/ro3 with 36 yr effective ex posure (assumed by Schneiderman, et of.*3) can be calculated if ng are convened to fibers. Using the conversion factor of40 gives O.OOOOS f/cc. The risk is therefore (0.00006M36K0.001S). or 0.00000324 Since the U.S. population is about 225 million this mean* a lift time excess of 729 lung cancer deaths due to nonoccupational asbestos exposure (0.00000324K225 million). Tables in the fichneiderman, et at. report also show upper lirniu. with the upper limit of their lung cancer estimates simply 10 times the lower. Therefore, the upper limit of lung cancer deaths due to nonoccupational asbestos exposure i* 7290. These estimates of 729 and 7290 contrast with the above estimates of 428 and 653. The Schneiderraan, it at. report also permits an estimate of lifetime risk for malignant mesotheli oma. This is 0.0033 (tower limt) for 1 yr exposure at 1 f/cc. For exposure at 1.5 ng/m3, assuming 20 yr effective exposure (assumed by Schneiderman. et at.), this is a lifetime lower limit of 891 cases. The upper limit is 5.400 cases. This con trasts with a lifetime excess of70 X 333, or 23,310, calculated from Table 111. One nf the reasons for the higher lung cancer estimates in the Sc hneiderman. et at. report is that they found reasons to reject the results of four epidemioli ->:ic studies which gave risks' of less than !* for I yr exposure at 1 f/cc. This included all three studies used in the dose-response section of the report issued by the Advisory Committee on Asbestos.*2 Rather, they relied on dose-response data compiled in 1981 by Nichclson, some of which were previously unpublished.*4 Of the five studies they found acceptable, three were from Selikoffs laboratory in New York City, one of which yielded a doseresponse relationship based on only 2 lung cancer deaths.*4 Neither of the others was designed to study dose-response. For one. only duration of exposure was measured for each worker, while for the other, workers could only be subdivided by time since first exposure, since duration of exposure was unknown. The fourth study** provides very few data on exposure and was described by Nicholson as containing "only sketchy in formation" *4 The authors of that study only discuss "possible exposure levels" with no details on how these were deter mined. The fifth study, a study of asbestos textile workers by Dement, et al, appears to be a good one with well documented exposure levels.*9 Numbers of lung cancer cases were relatively small, however, and the results of this study are quite unlike anything observed elsewhere. Lung cancer response per unit dose was ver" high It was 88 times greater than a similarly documented but much larger study of asbestos miners.* Discussion The above calculations lead to estimates of lifetime risks due to nonoccupational asbestos exposure of 100 per million for malignant mesotheliomas and 2 per million for lung can cers. This is a fifty-fold difference in favor of mesothelioma and is quite unlike contrast* observed in studies of occupa tionally exposed populations, fr. occupationally exposed populations, the excess favors lung cancer, with the ratio of excess lung cancer to mesotheliomas around 2 or 3 4 Using a different set of assumptions, the Schneiderman, et at study gives estimates of a lifetime excess due to nonoccupational exposure of 4-24 per million for mesothelioma and 3-30 per million for excess lung cancers.*7 This also differs from the 2 or 3 ratio of lung cancers to mesotheliomas in occup:. ,<onally exposed populations. Is it reasonable to suppose that nonoccupetiona! asbestos exposures produce more mesotheliomas than lung cancers while occupational exposures produce more lung cancer than mesotheliomas'' One reason for an excess of mesotheliomas in nonoccupationally exposed populations may be the much earlier age at first exposure and an unusual mesothelioma risk associated with exposure at an early age. This is because the April 1983 Volume 33. No. 4 ;PUKWII by which axbesiia prisdd<rmefbtis*libmat xeems io bh different frora the process by which asbestos causa* lung ameers. Peto, et al. feel that in the production ofmeaothtli* oiniii, asbestos acts at an early stage in a multistage process believed to produce cancer.31 As a result, they feel that mesotheliomas are manifest only many years after first ex posure, and that where exposure to asbestos starts at an early age, mesotheliomas will constitute a high proportion of as bestos ref .ted cancer deaths. On the other hand, in the pro duction of asbestos lung cancers there is considerable evidence to suj, ,est that asbestos acts at a late stage in a multistage process. As a result, lung cancers occur more quickly than mesotheliomas, so that even where exposure starts at age 30 or 40 theie is time for lung cancers to be manifest before deaths due to other causes intervene. Mesotheliomas may, therefore, be the predominant asbestos cancer related to nonoccupational exposures simply because of the early age at which these exposures start, whereas lung cancer is the predominant cancer in occupationally exposed populations due to the older age at which exposure starts and a lack of time for mesotheliomas to be fully expressed. Whether this is a sufficient explanation for a fifty-fold ex cess in mesotheliomas relative to iung cancers may be ques tioned. Given the w*ll established role ofasbestos in the eti ology ofmesotnelioraas, andthe exposure ofnearly the entire D.S. population to asbestos, it seems likely that nonoccupa tional exposure causes at least a third of the mesotheliomas that occur in the U.S. each year and perhaps more. Therefore, the estimate of a lifetime risk of 100 per million due to nonoccupational asbestos exposure seems conservative and the true risk may, in fau, be higher than this. On the other hand, the estimate of a lifetime risk of 2 per million for lung cancer could be low. The dose-response relationship may not be linear at low doses, as supposed, or perhaps the response per unit dose is greater than was assumed. No one has seri ously proposed a dow-response relationship that is curvilinear downward, as would be needed to increase response at low dose. There are, however, studiis that give a larger response for lung cancer pc unit dose than the one used. The highest re sponse yet reported was in the study by Dement, et a/.*4 If this had been used, instead of th study of retired asbestos work ers,* then the lifetime risk of asbestos lung cancers resulting from nonoccupationr! asbestos exposure would heve been 40 per million instead of 2. This reduces the apparent mesothe- lioma-iung cancer discrepancy butdoes not eliminate it. There does not appear to be any reasonable set of assumptions that would yield, for the nonoccupationally exposed population, the 2-3 excess iung cancers per mesothelioma observed in occupationally exposed populations. The issue, thereto, 'oes no* appear to be whether the ratic of mesotheliomas to lung cancers caused by background levels of asbestos exceeds 1, but rather, by how much it exceeds 1. References 1. P. Sebastien. M. A. Billon. C. Dufour. A. Gaudichet, G. Bonnaud. S. Bignon. "Levels of asbestos air pollution m some environmental situations," Ann, /V Y, Acad Set. 330:401 (19791 2. W. J. Nicholson. A. N. Rohl, R. N. Sawyer, E. J. Swoszowski, J. D. Todaro. "Comrot of Sprayed Asbestos Surfaces in School Buildings: A Feasibility Study." Report to the Nat:onal Institute of Environmental Health Science*. New York. June 15.1978. 3. R. J. Thompson. G. B. Morgan, "Determination of Asbestos in Ambient Air," in Proceedings of International Symposium on Identification and Measurement of Environmental Pollutants, D. Hoffman, ed . National Research Council of Canada, Ottawa, Ontario, tPTl. 4. J. C. McDonald. A. D, McDonald, "Mesothelioma as an Index of Asbestos Impact," in Banbury Report 9, Quantification of Oc cupational Cancer R. Peto. M Schneiderman. yds . Cold Spring Harbor Laboratory. Cold Spring Harbor. NY. 1981. p. 73. 5. J. Higginson. "Proportion of cancer due to occupation," Pre ventive Medicine, S: 180 119801. to. P E. Enterline. "Proportion of Cancer Due to Exposure to As bestos.* in Banbury Report 9, Quantification of Occupational 321 0uS272 w."xfife&iwa. from Occupational Asbestos: Exposure Projects-18#0-20QO." in Banbury Repart 9, Quantification of Occupational Cancer R. Psrlo. M. Srhneiderman. ed*.. Cold Spring Harbor Laboratory, Cold Spring Harbor. NY. 19S1. p. 87. M. 0. Hogan, D. G. Hoei, "Estimated cancer risk associated with occupational asbestos exposure." Risk Analytic 1:87 (1981). K. Bridbord, P. DeCouile, J. F. Fraumani. D. G. Hoel, R. N. Hoover, D. P. Rail. U. Safliotti, M. A. Schneiderman,A. C. Upton. "Estimate*ai the Fraction ofCancer in the United Sute* Related to Occupational Factors," National Cancer Institute, Washington, DC. September 1978. JO. 1. Selikoff, Generic Cancer Policy Hearings, U.S. Occupational Safety and Health Administration, Washington, DC, June 1,1978. laiimvnt, U. "Health United States." publication no. (PHS1 80-1232, U.S. Dept, of Health. Education, and Welfare. 1979. 12. R. Doll. R. Prto. The Causes of Cancer, Osford University Press. Oxford. England, 1981. 13. J D. Gillam, J. M. Dement, R. A. Lemen. J. K. Wagoner. V. E. Archer. H. P. Blejer. "Mortality patterns among hard rock gold miners exposed to an esbestilbrm mineral," Ann. N.Y. Acad. Set., 271:336(1976). 14. J. C. McDonald. G. W. Gibbs. F. D. K. Liddell. A. D. McDonald. Mortality after long exposure to cummingtonite-frunerite. Am. Ret- Rcspiral. Diseases 118:271 (1978). 15. S. D. Kaplan. W. R. Gaffev. "Miners Exposed to Amphibole Mineral: A Retrospective Cohort Mortality Study." report: Na tional Institute for Occupational Safety and Health. Cincinnati, OH. 1981. 16. P. E. Enterline. "Extrapolation from occupational studies: a substitute for environmental epidemiology," Environ. Health Perspectives 42:39 (1981). 17. J.Peto.R. Doll.S. V.Howard.L. J.Kinlen.H.C.Lewinsohn."A mortality study among workers in an English asbestos factory," Br. J. Ind. Med. 34:169 (19771. 18. A. 0. McDonald. J. C. McDonald. "Malignant mesothelioma in North America." Cancer 44:1650 (19601. 19. Y. 1. Baris, M. Artvinii. A. A. Sabin. "Environmental mesotheli oma in Turkrv. health hazards ofasbestos exposure." Ann A". Y. Arad Sri. 330:42311979). 20 J C. Wagner. C. A. Sleggs. P. Marchan, "Diffuse pleural meso thelioma and asbestos exposure in the Northwestern Cape Province."Br J. Ind Mrd 17:260(1960). 21 J Petu. "Lung Cancer Mortality in Relation to Measure Dust Levels m an Asbestos Textile Factory." in Biological Effects of Mineral Fibres. Vol. ii. J. C. Wagner, ed.. International Agency for Ke-earch on Cancer. Lyon. France, 1980, p. 82S. 22, Advisory Committee on Asbestos, report to the Health & Safety Commission. He* Majesty's Stationery Office, London. 1979. 23 V L Hendersun. P. E. Enterline, "Asbestos exposure: factors associated with excess cancer and respiratory disease mortality." Ann S Y Acad Set. 330; 117 (19791, Ehvirmmanu(f5w|i^feiii;ww; 35. "Ambient Wtur Qdufity Criteria for Asbestos# U.S: Environ mantai ProtacUoB Agency, Office of Water Regulations and 28, L. Bruckman, "A Study of Airborne Asbestos Fibers in Con necticut,'' in Proceedings a( the Workshop on Asbestos: Defini tions ~nd Measurement Methods, National Bureau ofStandards 3978, pp. 179-190. 27. M. S. Schneiderman. I. C. T. Nisbet, S. M. Brett, "Assessment of Risks Posed by Exposure to Low Levels of Asbestos in the General Environment," in Health Hazards Posed by Asbestos K. Aurand. W.-S. Kieraki. ed*., Federal BureauofHealth, Federal Republic of Germany, 1981. 28. M. L. Newhouse. G. Berry, "Patterns of disease among long-term asbestoswotkets inthe United Kingdom," Ann. N.Y. Acad. Sa 330:53(1979). 29. J. M. Dement, R. L. Harris. M. J, Symons. C. Shy. Estimates of Dose-Response for Respiratory Cancer Among Chrysolite As bestos Textile Workers." Ann. Occupational Hyg., to be pub lished. 30. 3. C. McDonald, F- D. K. Liddell. "Mortality in Canadian miners and millers exposed to chrysolite," Ann. N.Y. Acad. Sci. 330:1 (1979). 31. J. Peto, H. Seidmen. I. J. Selikoff. "Mesothelioma mortality in asbestos workers: implications for models of carcinogenesis and risk assessment," Br. J. Cancer 4S: 121 (1982). Dr. Enterline is a Professor and Chairman. Department of Biostatics, and Associate Director. Center for Environmental Epidemiology, Graduate School of Public Health. University ofPittsburgh. Pittsburgh. PA 15261. This paper was submit ted for editorial review on June 2, 1982: the revised manu script was received on February 14,1983. j \ ____________________________ ____________________ __________________ ! 322 Journal ot trie Air Pollution Control Associatior 008273