Document mqxY583aM3LLBZeQe3OdvQwY4

584 I. T. Hodgson and A. Damion This review has presented evidence suggesting that this may not be the case. Uncertainty about the slopes of exposure-response lines has an increasing impact by 0.054P,.. For women with typical past smoking habits the figure would be 0.028PL. Table 11 makes statements about the lifetime risks with increasing distance from the observed range. of exposures accumulated over short (up to 5 yr) per Also the strength of qualitative arguments such as iods from age 30. The factors given in Table 10 can those advanced in the HSE review (Meldrum, 1996), be used to apply the mesothelioma estimates to other in favour of a threshold for the lung cancer effect ages at exposure. The lung cancer estimates are based increase as exposure falls. on 1997 male lung cancer rates. They are not sensi All the above implies that simply to present a table tive to age at exposure. of risk estimates--or even risk ranges--for different For the lung cancer risk due to chrysotile two prin cumulative exposures cannot capture the changing cipal figures are given: a best estimate and a cautious balance of the different kinds of uncertainty. Table estimate. A risk estimate derived from the Carolina 11 gives a verbal assessment of risk at a range of cohort is also given, with the qualification that this representative cumulative exposures. No estimates might be arguable in 'exceptional circumstances'. have been given for lifetime risks lower than l in These exceptional circumstances cannot be defined 100 000, and this level is referred to as 'insignificant'. with any certainly since the features of exposure at A lifetime risk of l in 100000 corresponds to an this plant responsible for the very high lung cancer annual risk well below 1 in a million, which HSE has risks there are not known. Exposure to textile grade suggested (Health and Safety Executive, 1999) as a (i.e. long fibre) chrysotile is presumably necessary, "guideline for the boundary between the broadly but does not seem to be sufficient, since other textile acceptable and tolerable regions (of fatal risk to an plants have recorded much lower exposure-specific individual]." It is also well below the level at which risk (even with additional exposure to amphibole it is suggested that mesothelioma would occur in the fibre). The spraying of the taw fibre with mineral oil absence of asbestos exposure: a clear majority of the (as a dust suppression measure) has teen suggested very few mesotheliomas that would occur at this level as a possible explanation. This hypothesis seems to would not be caused by asbestos. be supported by a case-control study of lung cancers Mesothelioma risks in the observed cohorts have at Carolina (though the relevant results have not teen been expressed as a percentage (PM) of total expected fully repotted), and by observations from another mortality in order to standardise observations from asbestos textile plant (Rochdale), where men first different follow up configurations. To make predic employed after oil spraying was introduced had three tions of risk this measure must be converted back into times the exposure-specific risk of those first absolute terms, and this is done using the average employed in earlier periods (though still lower than male life table discussed in Appendix A. For the Carolina risk). exposures starting at age 30 the excess mortality esti The main uncertainties in this picture relate to the mate /m is applied to the total expected mortality effects of chrysotile, particularly at low doses. The from age 40 to age 79 (allowing a 10 yr minimum application of these estimates in the assessment of a latency, and truncating risk at age 80). The life table particular risk situation will depend on the purposes predicts that about 70% of survivors to age 30 will of that particular assessment, and the extent to which die between the ages of 40 and 80. Absolute risk esti a precautionary approach is appropriate. mates can therefore be derived from the PM value for a given exposure by multiplying by a factor of 0.7. _ Lung cancer risks have been expressed as a percent DISCUSSION age excess of expected lung cancer mortality. The There have been a number of papers (Cullen, 1998: major determinant of this underlying lung cancer risk Stayner r a/., 1996; Nicholson and Landrigan, 1996; is smoking--especially cigarette smoking--and the Smith and Wright, 1996), in the literature recently number of asbestos-related lung cancers will be affec which directly or indirectly consider whether there ted by the prevalence of smoking in the exposed are differences in potency between the fibre types as population. Currently (in 1997) about 9.5% of male causes of mesothelioma and lung cancer. The claim deaths between the ages of 40 and 79 Ore due to lung that there are important differences is often described cancer. For women the figure is 7%, reflecting differ as `the amphibole hypothesis'. In its strongest form ences in past smoking. Total survival to age 80 is this has been said to claim that pure chrysotile (i.e. lower in men than in women, and combining data for without any associated tremolite fibre) would present survival and proportionate mortality from lung cancer little or no carcinogenic risk. At the other extreme, it it can be predicted that for 1000 30-yr-old men 54 has teen argued (Smith and Wright. 1996), that there will die of lung cancer between the ages of 40 and is virtually no difference between the risks presented 79. For women the number is 28. Thus for a popu by the different fibre types. Most commentators (e.g. lation with the past smoking habits of British men Doll and Pcto, 1985; Hughes and Weill, 1986; Health aged 6(H- (the ages at which most lung cancers occur), Effects Institute, 1991) have considered that the the lung cancer risk from asbestos exposure is given amphibole fibre types are more dangerous, parti-