Arguments presented by third parties

Asbestosis

1. 
   Dr. Henderson asserts that: "[T]he amphibole varieties of asbestos appear to be substantially more pathogenic than chrysotile for the induction of asbestosis and mesothelioma." According to Dr. Henderson, "[A]sbestosis is a dose-dependent disorder with a threshold effect [...] There is widespread agreement that asbestosis in general is a consequence of high intensity exposure (or lower intensity but more prolonged exposure)."
   
2. 
   INSERM also supports the existence of a threshold for asbestosis,⁶⁴ and according to INSERM, current low-level exposures to chrysotile pose no threat of asbestosis: "les expositions actuellement relevées dans les industries directement utilisatrices d'amiante devraient conduire à la disparition des cas d'asbestose confirmée (Doll et Peto, 1985)."⁶⁵ It is clear, therefore, that asbestosis is not relevant to this dispute.
   

2. Lung Cancer

1. 
   Dr. Musk believes that lung cancer risks are more than ten times greater in the case of amphiboles than in the case of chrysotile asbestos. Dr. de Klerk suggests the difference may be up to 50-fold.
   
2. 
   Dr. Henderson states that the "greater carcinogenicity of the amphiboles [...] appears not to extend to the induction of lung cancer"⁶⁶ but he admits that "chrysotile is implicated in one of the lowest rates of asbestos-associated lung cancer (in Quebec chrysotile miners and millers)."⁶⁷ Dr. Henderson's reluctance to conclude the greater carcinogenicity of amphiboles seems to be caused by the results of Dr. Dement's study of the Charleston, South Carolina asbestos textile industry.⁶⁸
   
3. 
   The Charleston data has recently been revisited by Bruce Case, André Dufresne, A.D. McDonald, J.C. McDonald and Patrick Sébastien in a study released in Maastricht in October 1999 at the VII^th International Symposium on Inhaled Particles, a symposium attended by some of the world's leading experts. This study shows that a significant amount of crocidolite and amosite fibres was found in the textile workers' lungs. This analysis sheds new light on the issue and explains the extreme results of the original study by Dr. Dement⁶⁹ and the subsequent study by Dr. Stayner.⁷⁰ These studies of textile workers exposed to crocidolite and amosite can thereby no longer be used to demonstrate the risks associated with chrysotile fibres.
   
4. 
   The seminal findings of Case et al. may cause Dr. Infante to reconsider his view – based principally on the studies by Dement and by Stayner – that "chrysotile may be more potent in causing lung cancer."
   

3. Mesothelioma

51. 
    On the relative risks of mesothelioma, Dr. Henderson observes that: "[T]here is general though not universal agreement of a differential potency between the amphiboles versus [chrysotile] for mesothelioma induction." He believes amphiboles may be greater than 60 times more likely than chrysotile to induce mesothelioma.⁷¹ Drs. Musk and de Klerk estimate that the potency of amphiboles may be 100 times greater. And although Dr. Infante also concedes that "amphiboles may be more potent in causing mesothelioma", he fails to conclude from this that a distinction exists between chrysotile and amphibole fibres.
    
52. 
    This distinction is also emphasized in pathology medical reference books:
    

2. Other Diseases

   1. 
      Dr. de Klerk links other asbestos-related diseases such as pleural plaques and pleural thickening more with amphiboles than with chrysotile: "[P]leural plaques appear to be more common among anthophyllite workers than others while crocidolite workers have more diffuse pleural thickening, and benign asbestos pleurisy also seems to be more common after crocidolite exposure." Dr. Henderson also raises the issue of types of fibres in dealing with parietal pleural plaques.
      

2. 
   Drs. de Klerk and Musk agree that the existing epidemiological data show no excess health risks at low-level chrysotile exposures. Dr. Henderson is not aware of exposure-response data for low-level exposures. Dr. Infante again relies heavily on Stayner's study, a study on one single cohort of textile workers now known to be based on textile workers exposed to amphiboles as well as to chrysotile.⁷³ Newhouse and Sullivan studied exposures to chrysotile in the manufacturing setting: "[I]t is concluded that with good environmental control, chrysotile asbestos may be used in manufacture without excess mortality."⁷⁴
   
3. 
   Thomas et al. concluded similarly for an asbestos cement factory: "[T]hus the general results of this mortality survey suggest that the population of the chrysotile-cement factory studied are not at any excess risk in terms of total mortality, all cancer mortality, cancers of the lung and bronchus, or gastrointestinal cancers."⁷⁵
   
4. 
   There is clearly no increased risk of lung cancer in the friction products manufacturing industry at levels below 356 f/ml‑years. This means that there was no chrysotile‑related increase in lung cancer risk for persons exposed to the equivalent of up to 8.9 f/ml for 40 years. Even if we allowed a 10-fold protection factor this would be 0.9 f/ml for 40 years for lung cancer.⁷⁶ More recently in 1997, McDonald et al. concluded from the analysis of a cohort of 10,000 asbestos workers with average exposures to 45 f/ml over 20 years that: "[...] from the point of view of mortality [...] exposure in this industry to less than 300 mpcf.years [approximately 45 f/ml over 20 years] has been essentially innocuous."⁷⁷ This unequivocal data comes from the longest term study of the largest group of chrysotile workers ever conducted. A review of eight studies of cohorts exposed to chrysotile only led its authors to conclude: "[T]he evidence for chrysotile shows that for lung cancer and mesothelioma there exist levels of exposure below which risks are for practical purposes zero."⁷⁸
   

5. 
   According to Dr. Henderson, whether a threshold exists generally is a much-debated issue. For the case at hand, i.e. low-level exposure to chrysotile, Dr. Henderson states that: "[I]f a threshold exists, it must lie somewhere in this area, between no exposure, low-level environmental exposure, and low-level occupational exposure." He also points out that, although no threshold has been identified, "at the same time, no increase in risk of mesothelioma has been identified at very low-levels of exposures." Drs. Musk and de Klerk agree that the epidemiological data show an absence of risk at low exposure levels, but are unwilling to commit to the existence of a threshold. If there is agreement that low level exposures show no increased health risk, admitting the existence of a threshold is academic.
   
6. 
   The extreme difficulty of proving a threshold scientifically is echoed by the European Communities' DG XXIV Report:
   

7. 
   The corollary to the proof of a threshold is the proof of the absence of a threshold. The proof that no threshold exists would need to explain the absence of an excess risk of lung cancer or mesothelioma in chrysotile-only cohorts, as well as the lack of any chrysotile-related increase in lung cancer mortality in workers exposed to less than 900 f/ml-years in the 10,000 miners and millers studied in Quebec.⁸⁰  Dr. Henderson does acknowledge the existence of a threshold for asbestosis in his answer to Question 3: "Asbestosis is a lung dependent disorder with a threshold effect [...] There is widespread agreement that asbestosis in general is a consequence of high intensity exposure (or lower intensity but more prolonged exposure)." INSERM also supports the existence of a threshold for asbestosis:
   

8. 
   Why could there not be a threshold for other asbestos-related diseases? Dr. de Klerk asserts that:
   

9. 
   Some experts advising the EC believe there is a threshold for diseases other than asbestosis:
   

10. 
    This links to Dr. de Klerk's observation that: "[T]he smaller the effect that needs to be demonstrated, the larger the study needs to be." Dr. Infante, who dismisses the Panel's question as "moot", points out that "it is not possible to determine thresholds from epidemiological studies because of the lack of statistical power to distinguish that the risk is virtually zero." Canada argues – epidemiological data in hand – just that low-level exposures to chrysotile pose a risk that is "virtually zero": "un risque indétectable". Dr. Infante uses Stayner's data once again to claim that the chrysotile data fit with a linear no‑threshold model. With the new analysis on the Charleston cohort data discussed above, this argument does not hold.⁸⁴
    

11. 
    Drs. de Klerk and Musk agree that there is epidemiological data indicating no increased risk at low-level exposures, but the experts believe the linear model may be appropriate. However, "[W]hether or not it is a valid method is unknown."⁸⁵ According to international experts from the Health Effects Institute-Asbestos Review (HEI-AR), such as Julian Peto, David G. Hoel and W. Nicholson, the linear model is not used for its validity, but precisely because it tends to overestimate risk.⁸⁶ Dr. de Klerk shares this view and states that the model provides a "conservative estimate."
    
12. 
    The limits of the linear model and the conditions under which extrapolations are made must be clearly set out. Extrapolations from high-level exposures and exposures to amphiboles should not be taken at face value to ban chrysotile in today's context of low-level chrysotile-only exposures. Canada's critical view of the linear model is supported by a 1999 report by the Australian National Industrial Chemicals Notifications and Assessments Scheme (NICNAS) cited by Dr. Henderson:
    

13. 
    Not only does the linear model provide a worst-case scenario, it provides a grossly exaggerated estimate of risk when "confounding factors", as Dr. Henderson calls them, are so clearly present. INSERM made extrapolations from high-level amphibole exposures to mixed fibre type exposures, as well as from exposures in the textile industry and during the installation of low-density products such as flocking.⁸⁸ Amphiboles are much more potent than chrysotile, and the risks in the textile industry cannot be compared with the risks in the high-density chrysotile products, as Dr. Henderson points out in citing Boffetta: "[I]n general, the risk of lung cancer ... is highest in studies of asbestos textile workers."⁸⁹
    
14. 
    Another important consideration is the human biological defence mechanisms that are naturally much more effective at low-levels of exposure, i.e. clearance, biopersistence and DNA repair mechanisms.⁹⁰ Given these mechanisms, the reasoning behind the threshold model is both intuitively and scientifically sound, as well as epidemiologically validated. To illustrate this, consider the following illustration: the effect of 50 fibres in the lungs will be more than five times the effect of ten fibres.
    
15. 
    According to Sir Richard Doll, who first demonstrated the link between asbestos and lung cancer (as well as between smoking and lung cancer), "[W]e have no real ground for postulating that a linear relationship for lung cancer can be extrapolated back to the levels of dose with which we are concerned in non-occupational settings."⁹¹ Ames and Gold are of the same view: "[l]inear extrapolation from the maximum tolerated dose in rodents to low-level exposure in humans has led to grossly exaggerated forecasts in mortality." ⁹² Fournier and Efthymiou are even more categorical: "[L]inear extrapolation to zero is an unscientific methodology whose social consequences are so immense that it warrants unconditional elimination."⁹³ INSERM acknowledges the limits of the linear model's application when it states that it provides nothing more than food for thought: "cette extrapolation ne crée pas une information scientifiquement certaine, elle représente une aide à la réflexion en matière de maîtrise de risque."⁹⁴
    
16. 
    As Dr. de Klerk points out, "how one extrapolates risk assessment outside the range of available data is more of a societal decision than a scientific one."
    

17. 
    Situations where there is no increased risk at low levels of exposure have been used by Stayner et al. to establish NOAELs [i.e. no observable adverse effect levels] for silica. A similar model is used for asbestosis. Canada believes that the use of such a model is warranted for other asbestos-related diseases, particularly since it has been acknowledged by Dr. Musk and Dr. de Klerk that epidemiological data exists to justify such an approach.
    

18. 
    We concur with Dr. Henderson's view that "[t]his question iterates the issue of a threshold exposure." Canada nonetheless notes the use by Dr. Infante of a 1992 study by Bégin et al. to demonstrate the risks related to "background levels" is erroneous. As has been pointed out by Canada in its factual arguments,⁹⁵ this study is based on exposures to a mix of chrysotile and amphiboles in the manufacturing and construction industry, and therefore is not relevant to exposures from the current uses of chrysotile.
    

1. 
   Clearly the answers given by the four experts are based on their concept of what is meant by controlled use. It is also evident that the controlled use concept as espoused by Canada was not the approach that resulted in their answers. We must therefore respectfully disagree with the answers given by the experts in respect of controlled use of chrysotile and high-density chrysotile containing products. The fact that they agreed that controlled use of chrysotile and high-density chrysotile products is feasible at some points of the life cycle, but not in others, suggests that they are not far from the view of Canada. The only difference is that Canada believes that the experts misunderstand the controlled use principle and that, as properly understood and implemented, use can be controlled throughout the full life cycle of high-density chrysotile containing products. The basis for our view, with supporting evidence, is set out below.⁹⁶
   

1. 
   
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