Document 2qKypd53kBj5ayxq4ajM9BQo5
590 I. T. Hodgson and A. Oamton
environmental asbestos pollution in an asbestos textile fac tory. Annuls uf Occupational Hygiene 29. 305-335. Piolatto. G,, Negri. E.. La Vecchia. C.. Pira. 6.. Oecarli. A. and Peto, i. (1990) An update of cancer mortality among chrysolite asbestos miners in Baiangero. nonhem Italy. Bri tish Juuntul of Industrial Medicine 47. 810-SI4. Rddelspcrger. K.. Woiiowiiz, H. -J.. BrUckel. B.. Arihelger, R.. Pohlabein. H. and idckel. K. -H. (1999) Dose response relationship between amphibole fiber lung burden and meso thelioma. Cancer Detection and Prevention 23. 183-193. Rogers. A. (1990) Cancer monalily and exposure to crocidolitc. British Journal of Industrial Medicine 47. 28b. Rogers. A.. Leigh. J.. Berry. 0.. Ferguson. 0. A.. Mulder, H. B. and Ackud. M. (1991) Relationship between lung asbestos fibre type and concentration and relative risk of mesotheli oma. Cuncer (17. 1912-1920. Ross iter. C. E. and Coles, R. M. (1980) KM Dockyard. Devonport: 1947 monality study. In Biological Effects of Minertd Fibres. Scientific Publication no. 30. ed. J. C. Wager, pp. 713-721. IARC. Lyon. Slbastien. P.. McDonald. J. C., McDonald. A. O.. Case. B. and Harley. R. (1989) Respiratory cancer in chrysolite textile and mining industries: exposure inferences from lung analysis. British Journal of Industrial Medicine 46. 180--137. Scidman. H. and Selikoff. I. ). (1990) Decline in death rates among asbestos insulation woken 1967-1986 associated with diminuation of work exposure to asbestos. Annuls of New York Academy of Science 609. 30(3-318. Seidman. H., Selikoff, I. /. and Gelb, S. K. (1986) Mortality experience of amosite asbestos factory workers: doseresponse relationships 5 to 40 yean after oaset of short-term work exposure. American Journal ofIndustrial Medicine 10. 479-514. Sluis-Cremer. G. fC.(l99l) Asbestos disease at low exposures after long residence times. Annals of New York Academy of Science 643. 182-193. Sluis-Cremer, G. K.. Liddell. F. D. K.. Logan. W. P. D. and BezuidenhouL B. N. (1992) The mortality of amphibole minen in South Africa. 1946-30. British Journal of Indus trial Medicine 49. 566-575. Smith, A. H. and Wright. C. C. (1996) Chrysolite asbestos is the main cause of pleural mesothelioma. American Journal of Industrial Medicine 30. 252-266. Stanton. M. F.. Layard, M.. Tegeris, A.. Miller, E- May. M.. Morgan, E. and Smith, A. (1981) Relation of panicle dimen sion to carcinogenicity in amphibole asbestos and other fibrous materials. Journal of the National Cancer (nxriture 67. 965-975. Stayner. L. T- Daakovlc, D. A. and Lemen. R. A. (1996) Occu pational exposure to chrysotile asbestos and cancer risk: a review of the amphibole hypothesis. American Journal of Public Health 86. 179-186. Stayner, L.,`Smith. R., Bailer. i,, Gilbert. S.. Steenlond, K., Dement. ).. Brown, D. and Lemen. R. (1997) Exposureresponse analysis .of risk of respiratory disease associated with occupational exposure to chrysolite asbestos. Occu pational and Environmental Medicine 54. 646-665. Talcott. 1. A.. Thurber. W. A- Kantor, A. F.. Gaensler. & A.. Danohy, J. F., Ammon. K. A. and Li, F. P. (1989) Asbestos-' associated diseases in a cohort of cigarette-filter workers. New England Journal of Medicine 321, 1220-1223. Thomas. H. F.. Benjamin. 1. T,, Elwood, P. C. and Sweetium. P. M. (1982) Further follow-up study of workers from an asbestos cement factory. British Journal of Industrial Medi
cine 39. 273-276. Vainio, H. and Bofetta. P. (1994) Mechanisms of (he combined
effect of asbestos and smoking in the aetiology of lung can cer. Scandinavian Journal of Work Environment and Health 20. 235-242. Weill. H. (1994) Biological effects: asbestos cement manufac turing. Annnls of Occupational Hygiene 38. 533-538.
Appendix A
-|
EXTRACTED COHORT DATA
The details of extracted data is shown in Tables 12 and 13. with explanatory notes in Tables 14 and 15.
SUMMARISING MORTALITY AND EXPOSURE
MEASURES - THE CHOICE OF FOLLOW UF
PERIOD IN RELATION TO EXPOSURE PERIOD
LUNG CANCER For most of the studies considered in this review,
mortality was reported for the period 20 or more years from first exposure. The reason for this is that it is assumed that this represents a period in which the effect of exposure will be fully expressed. Deaths Observed Fn the period immediately following first exposure will be unaffected by that exposure, and the effect of exposure will become progressively more apparent as follow up time increases. Comparisons of observed and expected deaths that include periods immediately after first exposure wiLkintroduce some downward bias to the assessed risk'level.
Evidence on the levels of excess in different per iods after exposure suggests that between 10 or 20 and about 40 yr from exposure the lung cancer r.' is reasonably stable. Beyond 40 or 45 yr follow there may be some decline ,in risk, but the extent to which this may have diluted recorded lung cancer risk in these cohorts seems limited (for example, there is very little difference between the US/Canada insu lators lung cancer SMR calculated over all follow up from 20 yr and one restricted to the period between 20 and 40 yr). No adjustment for differences in maxi mal follow up between cohorts has therefore been applied.
The impact of follow up less than 10 yr being included in the reported results, and the related prob lem of choosing on average exposure appropriate to the observed mortality needs to be considered. If observed and expected mortality from observauons less than 10 yr from first exposure ore uninformative of the possible effects of the exposure the inclusion of such observations in the reported results for a cohort, will dilute any actually occurring effect Pro vided there is a reasonable amount of informative fol low up on every cohort member this dilution effect can probably be ignored, since the observed and expected deaths generated from the early (uninformative) follow up will be outweighed for ail individuals by their later observations. But if a high proportion of a cohort generates mainly uninforma tive follow up. reported overall results may be seri ously distorted. This can happen if recruitment to. cohort continues to the end of follow up. Subject, starting within 10 yr of the end of follow up will con tribute no informative mortality data.