Exposure from chrysotile textile materials

Exposure from chrysotile textile materials

1. 
   Table 14 represents a reproduction of Table 7 in EHC 203 for exposure estimates in the South Carolina chrysotile textile plant (1930-1975) before and after controls on exposure levels. As can be seen from this Table, the application of controls on exposure levels produced a significant reduction of exposure, and currently available control technology allows even lower levels to be attained (EHC 203).
   
2. 
   EHC 203 refers to a study in Japan which reported a geometric mean concentration of 0.1‑0.2 f/ml in the period 1984-1986, for asbestos spinning. From published studies, it seems clear that asbestos textile workers are at greater risk for asbestosis (historically) and lung cancer than mesothelioma. EHC 203 also gives the following comments:
   

3. 
   On p. 114, EHC 203 goes on to discuss other consequences of exposures sustained during textile manufacture:
   

The most recent update of the Charleston study by Dement et al. (1994) demonstrated an overall lung cancer SMR of 1.97 (126 observed) and an overall SMR for non-malignant respiratory diseases ... of 3.11 (69 observed). The data for white males, for which data were more complete, demonstrated an overall lung cancer SMR of 2.34 for those achieving at least 15 years of latency. The risk of lung cancer was found to increase rapidly in relation to cumulative exposure. Data for the entire cohort demonstrated an increase in the lung cancer risk of 2-3% for each fibre/ml-year of cumulative chrysotile exposure. Two mesotheliomas were observed among this cohort and an additional mesothelioma was identified among plant workers, occurred after the study follow-up period. Analyses of an overlapping cohort from the same factory ... provided similar results.

4. 
   From the foregoing discussion, it is plain that these risks apply to occupational circumstances, and not to non-occupational situations. It is my perception that there is debate among experts over the carcinogenicity of chrysotile released from or associated with friction products and textiles respectively.
   

5. 
   Exposure to chrysotile asbestos through the manufacturing and downstream manipulation of friction products and textiles carries with it the risks associated with exposure to asbestos, most notably, lung cancer, asbestosis and mesothelioma. This is mostly an occupational issue except for consumers, who do their own brake replacement which would put them at risk of developing these diseases.
   
6. 
   Epidemiological studies of workers involved in the manufacturing of friction products demonstrate an elevated risk of lung cancer (McDonald et al. 1994). Other investigators have not observed an excess of lung cancer in the manufacturing of chrysotile and cricidolite containing friction products, but have identified cases of mesothelioma related to both types of asbestos used to produce these products (Berry and Newhouse, 1983). Cases of mesothelioma also have been reported among car mechanics who serviced brakes containing chrysotile fibres only and were exposed to levels estimated to be below 1 f/cc-year cumulative exposure (Woitowitz and Rodelsperger, 1991). Epidemiological study results indicate a high risk of disease related to chrysotile textiles. See my responses to Questions 4(a)-4(c).
   

7. 
   It is my opinion that there is a risk of disease from the release of chrysotile fibres from friction materials (as in brakes and clutches) or textiles (as in asbestos blankets and suits). In general the risk will be dependent on the degree of exposure (as above) and is therefore likely to be greater in people with occupational rather than non-occupational exposure. Fibres released from friction materials may be shorter than from other sources. These fibres may clear more rapidly from the lungs and possibly be related to lower risks but I am not aware of any direct data on this.
   

8. 
   In terms of risks to human health, epidemiological evidence is clear that, for a given quantity (intensity and duration) of exposure, chrysotile imparts less risk than amphibole fibres.
   

9. 
   YES — a clear distinction should be made between chrysotile and the amphibole forms of asbestos. On a fibre-for-fibre basis, amphiboles such as crocidolite and amosite are substantially more carcinogenic for the mesothelium than chrysotile. This potency differential is to some extent confounded by the far greater usage of chrysotile both now and historically (> 95 per cent of world asbestos production). In addition, it is worth reiterating that Canadian chrysotile on average contains trace quantities of fibrous tremolite (an amphibole).
   
10. 
    It is my perception that there is broad agreement among experts that the amphiboles are more potent carcinogens for the mesothelium than chrysotile.
    

11. 
    For purposes of assessing disease risk from exposure to asbestos fibres, I see no basis for making a distinction between chrysotile and amphibole asbestos. Several high quality epidemiological studies of workers exposed to chrysotile asbestos demonstrate an elevated risk of death from lung cancer, asbestosis and mesothelioma. The risk of death from lung cancer and asbestosis related to chrysotile exposure appears to be similar to that from exposure to other forms of asbestos. Although epidemiological study suggests that the risk of death from mesothelioma from chrysotile exposure may be less than the mesothelioma risk from amphibole asbestos, it is somewhat difficult to make this comparison. Many of the studies of workers exposed to amphibole asbestos go back further in time and less information is available on the quantitative aspects of exposure. Thus, the role of error in exposure estimation on the perceived difference is difficult to determine. On the other hand, some experimental inhalation studies demonstrate that chrysotile asbestos may be more potent than other forms of asbestos in the induction of mesothelioma (and lung cancer) in relation to the amount of dust deposited in the lungs (Wagner et al., 1974). In any event, the attributable risk of respiratory diseases from exposure to asbestos is going to be heavily weighted by lung cancer and asbestosis. So, even if exposure to chrysotile asbestos would result in a slightly lower relative risk of death from mesothelioma, the overall risk of the asbestos related diseases combined, i.e., lung cancer, asbestosis, mesothelioma, decrements in pulmonary function, will not be perceptively different for chrysotile as compared to the amphiboles. Thus, a distinction should not be made between chrysotile asbestos and amphibole asbestos. In my opinion, exposure to all forms of asbestos results in a significant disease burden to society.
    
12. 
    I believe that there is a need to distinguish chrysotile asbestos from amphiboles based on the epidemiological data at least.
    

13. 
    The properties are the same: size, shape and durability in the lung, that is fibres have to be of certain size and shape to be deposited in the lungs and have to stay there long enough to produce a response. Since most of the body's responses to fibres appear to be stochastic in nature, the additional features are of course the intensity and duration of exposure as outlined above. All the types of asbestos differ according to these properties, the main difference with chrysotile is that it is less durable in lung tissue than amphibole fibres: it is more soluble and the fibres tend to break more readily into smaller fibrils, it also tends to be more curly rather than dead straight in shape.
    

14. 
    As discussed already, the pathogenicity of asbestos appears to reside in the physical properties and biopersistence of the fibres, summarized as the 3 Ds — namely dose, fibre dimensions and durability (bio-persistence). All commercial asbestos has the capacity to induce asbestosis, lung cancer, mesothelioma and other pleural abnormalities (e.g., parietal pleural fibrous plaques, benign asbestos pleuritis with effusion, and diffuse pleural fibrosis). Chrysotile and the amphiboles have different potencies in generating these disorders: for example, the amphibole varieties of asbestos appear to be substantially more pathogenic than chrysotile for the induction of asbestosis and mesothelioma, whereas the differential is not sustained for the induction of lung cancer, for which chrysotile is associated with one of the lowest lung cancer rates (in Quebec chrysotile miners and millers) and the highest rate of lung cancer (South Carolina asbestos textile workers, who used Canadian chrysotile).
    
15. 
    Asbestosis: There is good evidence that asbestosis 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) than mesothelioma not associated with asbestosis, so that the concentration of asbestos bodies and uncoated asbestos fibres within the lung tissue of asbestotics is considerably higher than the concentrations encountered in mesothelioma patients without asbestosis and in individuals with parietal pleural plaques. In addition, some studies have shown that the severity of asbestosis and its liability to progression are related to the asbestos body and fibre concentration in lung tissue. In the past, asbestosis as a consequence of high-dose exposure was a progressive disorder leading to progressive respiratory insufficiency and death, whereas many cases of asbestosis encountered during the 1980s and 1990s represent milder and static forms of the disease.
    
16. 
    Churg [234] points out that:
    

17. 
    To some extent, this differential in potency may reflect fibre dimensions and the generation of oxidants, but a more likely explanation is the faster clearance of chrysotile from lung tissue than any of the amphiboles. However, Churg's comments seem to apply to Quebec chrysotile miners and millers in particular; in contrast, the study reported by Green et al. [191], which reported histological asbestosis at relatively low cumulative exposures was carried out on South Carolina asbestos textile workers who also worked with Canadian chrysotile (please see following discussion).
    
18. 
    There is also evidence that long fibres are implicated in the development of asbestosis, but this may reflect in part the anatomical distribution of long versus short fibres in lung tissue. For example, some studies have shown that short fibres in the vicinity of 1 µm in length have a biological potency similar to that of the longer fibres for initiation of the inflammatory changes implicated in the development of asbestosis, but they do not penetrate the walls of bronchi or bronchioles to the same extent as the longer fibres, to reach the alveolar interstitium. Another study related the development of asbestosis to the total surface area of deposited fibres, rather than to particular lengths of fibres.
    
19. 
    The effect of dose: There is good evidence that the inhaled dose of asbestos affects: (i) the development of the disease itself; (ii) the latency period between exposure and the onset of the disease; and (iii) the severity and progression of disease.
    
20. 
    Fibre burden studies on human lung tissues show that patients with asbestosis in general have higher tissue burdens than patients with asbestos-related diseases other than asbestosis. Accordingly, Mossman and Churg [202] state that:
    

21. 
    The Ontario Royal Commission [235] noted that asbestos exposures < 25 fibre-years would be unlikely to produce clinical asbestosis (about ≤ 1 per cent of individuals exposed at this level may develop clinical or radiological asbestosis), whereas Browne [236] considered that the minimum dose required to produce clinical asbestosis was in the range of 25-100 fibre-years.
    

22. 
    In an autopsy study of South Carolina asbestos textile workers who used Canadian chrysotile — the same group studied by Dement et al. [171, 172, 237-241] and McDonald et al. [161, 242] — Green et al. [191] showed that histological asbestosis was usually present at ≥ 20 fibre-years of exposure, and a few cases were observed at 10-20 fibre-years. Thimpont and de Vuyst [243] reported that around 50 per cent of specimens of lung tissue removed because of lung cancer showed low-grade airway and interstitial fibrosis with asbestos bodies, when the asbestos body concentration was ≥ 5000 per gram dry lung tissue.
    
23. 
    These different threshold doses are not inconsistent with each other, because they deal with identification of asbestosis by different modalities (i.e. clinical/radiological asbestosis versus histological asbestosis). In this respect, histological examination is generally considered to represent the most sensitive and specific technique for the diagnosis of asbestosis, followed in descending order by high-resolution CT scanning, conventional CT scans and chest X-rays (which will fail to detect asbestosis in about 20 per cent of cases, especially low-grade asbestosis). In other words, early (grade I) asbestosis may be undetectable by clinical investigations.
    
24. 
    Latency interval: there is also evidence that the latency period between first exposure to asbestos and the subsequent diagnosis of asbestosis is roughly inversely proportional to the exposure level, so that short latencies are encountered with high exposures (e.g. the Wittenoom cohort).
    
25. 
    Mossman and Churg [202] also state that:
    

1. 
   There are two additional points that are worth emphasis:
   

• 
  There appears to be considerable variation among individuals in their propensity to develop asbestosis (or variation in the latency intervals for equivalent exposures). For example, I have seen cases where there was a high content of amphibole asbestos in lung tissue (up to 100 million fibres per gram dry lung tissue or more), in the absence of histological asbestosis — at the time when the fibre burden analysis was carried out — whereas other cases had clinical asbestosis with much lower tissue fibre burdens. Of course, one caveat about this situation concerns latency, whereas another relates to the time when the fibre burden analysis was carried out, which is different from the time when the disease was developing.
  
• 
  In addition to high fibre burdens, the severity and progression of asbestosis can be
  

27. 
    Mesothelioma: Please see discussion in Section C.1.(f) to(h).
    
28. 
    Lung cancer: Please see discussion in Section C.1.(i).
    
29. 
    Other asbestos-related pathology: The effect of dose is less clear for the induction of parietal pleural fibrous plaques than for other asbestos-related disorders. There is evidence that the frequency and extent of plaques are dose-related, so that plaques tend to be more extensive with higher exposures. However, plaques can also follow trivial exposures to asbestos and asbestos-like minerals, so that the frequency of asbestos-related pleural plaques appears to correlate more closely with duration since exposure than the level of exposure. Plaques are known to be endemic in Finland, apparently as a consequence of very low-level exposure to asbestos-like fibres in the general environment; on the other hand, in societies where plaques are not endemic — e.g. North America, Western Europe and Australia — about 80-90 per cent of radiologically well-defined plaques are a consequence of occupational exposure to asbestos. In such societies, pleural plaques also represent a useful tissue marker for prior asbestos exposure. At the same time, it is also worth emphasising that parietal pleural plaques by themselves do not predispose to any other asbestos-related disorder, the liability being related to inhaled dose and fibre types.
    

30. 
    The key properties of the pathogenicity of amphiboles and chrysotile fibres, although not known for certain, are thought to be related to the physical characteristics of the fibres, namely the diameter, length, aspect ratio of length to diameter, surface area and perhaps surface charge of the fibres. Toxicological data suggest that long thin asbestos fibres may be relatively more potent than other asbestos fibres in their ability to induce asbestos related diseases. There is also experimental evidence, however, that shorter fibres can produce asbestos related diseases, though not in as great a magnitude. Any manipulation of these fibres that results in their diameter becoming thinner may provide a relatively greater contribution to the associated pathology and a greater toxic response than if the fibres were not manipulated in any way. The issue of solubility has been raised in terms of asbestos fibres and their capability to cause disease. The role of solubility with asbestos fibres and disease potential, however, is not so clear because chrysotile asbestos seems to have the same overall potency as other forms of asbestos, yet chrysotile fibres appear to be relatively more soluble than amphibole fibres.
    

31. 
    It is my opinion that the key characteristics determining the pathogenicity of asbestos for asbestosis, lung cancer, mesothelioma and other diseases are determined by the physical and chemical characteristics of the asbestos. The physical characteristics include length, diameter and "straightness" of the fibres. The chemical properties determine the durability of the fibres.
    

32. 
    Comparisons between chrysotile and the amphiboles in their capacity to produce mesothelioma and lung cancer have been extensive, for the other diseases, much less so. There is some in vitro and in vivo evidence that amphiboles, particularly crocidolite, are more fibrogenic than chrysotile, but there is no clear epidemiological evidence on this. Pleural 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. Historically, asbestosis occurred commonly after heavy exposure to all types of asbestos. For mesothelioma, it is thought that for a given cumulative exposure, chrysotile is between one tenth and one hundredth as potent as crocidolite. There is some controversy over the relative capacity of amosite and crocidolite, but amosite seems to carry about one tenth of the risk of crocidolite. For lung cancer, amosite and crocidolite seem to have similar capacities, with chrysotile weighing in around one tenth to one fiftieth of this.
    

33. 
    See my response to Question 3(b).
    

34. 
    The quantitative risk of dying from lung cancer as a result of exposure to chrysotile asbestos is at least as great as that from exposure to other forms of asbestos. Quantitative risk assessments based on several epidemiological studies indicate a very high risk of lung cancer (potency) among workers exposed to chrysotile asbestos. The cohort study by Dement et al., first published in 1983 and updated in 1994 contains one of the best estimates of worker exposure to chrysotile accompanied by the estimates of relative risk (RR) for lung cancer and asbestosis. In this study, the investigators determined conversion ratios from the available industrial hygiene data by evaluating sampling results from surveys that used the impinger method to measure dust in million particles per cubic foot (MPPCF), and membrane filter samples that allowed for the counting of fibre concentrations. For early exposure periods, the investigators converted one MPPCF to the equivalent of 3 f/cc > 5 um in length for all areas except for preparation where a conversion factor of 8 fibres for every MPPCF was used. In my opinion, this study is the strongest in its methodology for estimating asbestos exposure among cohort members. Quantitative risk assessment based on data for the entire cohort estimates an increase in the RR of lung cancer ranging from 2-3 per cent for each fibre/cc-year of cumulative chrysotile exposure. To my knowledge, this is the highest estimated risk of lung cancer among asbestos exposed workers that has been corroborated by other investigators, i.e., the same population was also studied by McDonald et al., (1983) and the results are remarkably similar. Studies of lung cancer risk among chrysotile asbestos textile workers from two additional occupational cohorts by McDonald et al., (1982) and Peto et al., (1985) also provide similar results. Using data from the McDonald et al., (1983) study and a conversion factor of 6 fibres per MPPCF, Peto et al., (1985) estimated an increase in the RR of lung cancer among chrysotile textile workers to be 1.25 per cent per fibre/cc-year of exposure. From their own study of Rochdale textile workers, Peto et al., (1985) estimated the excess lung cancer risk to range from 0.5-1.5 per cent per f/cc-year of cumulative exposure depending upon whether the estimate was based on the entire cohort or on those employed in 1951 or later, respectively. These estimates are of surprisingly similar magnitude given that they are from epidemiological studies that incorporated retrospective exposure estimation that had to rely upon the conversion of measurements from particles to fibres per cc. Thus, three separate populations of chrysotile asbestos textile workers demonstrate remarkably similar elevated risks of lung cancer and therefore add to the confidence of the estimates of excess lung cancer risk per unit of fibre exposure that these studies demonstrate.
    
35. 
    Studies of workers exposed to chrysotile in several industries demonstrate a significantly elevated risk of lung cancer. Studies of workers exposed to a combination of chrysotile and cricidolite, or to chrysotile only in cement production (Hughes et al., 1987) indicate a virtually identical excess risk of mortality from lung cancer. In a study of workers exposed to crocidolite in mining, de Klerk et al., (1989) estimate an elevated relative risk of lung cancer of 1 per cent per f/cc-year of exposure. Essentially, the excess relative risk for lung cancer indicated in all of these studies is close to about 1 per cent per fibre per cc-year of exposure (Stayner et al., 1997). The risk of lung cancer from chrysotile asbestos exposure is at least as great as the risk of lung cancer associated with amphibole asbestos exposure.
    
36. 
    Analyses based on the study by McDonald et al. (1993) indicates a much lower dose response for lung cancer in relation to chrysotile asbestos in mining and milling as compared to the risk estimates from other studies, particularly chrysotile textile workers. I suspect, however, that the fibre exposure from this study may be overestimated, particularly among the portion of the cohort that is comprised of miners and that a fair amount of misclassification took place in the amount of fibre exposure estimated for individual cohort members.
    
37. 
    Gibbs and Lachance (1972) who published the initial exposure estimates for this population of workers stated that their cumulative dust concentrations for the cohort members may have been far from their actual experience. Subsequent dose response analysis of this cohort applied only a single conversion factor to estimate fibre exposures from the dust count data for the entire cohort. In the study of Siberian chrysotile miners and millers (Tossavainen et al., 1999), those involved in mining experienced average exposures of 0.08 f/cc, while those involved in two separate mills experienced average exposures of 3.62 f/cc (ranges of average exposures for different milling operations 0.37‑6.21 f/cc) and 0.65 f/cc (range of average exposures 0.20-1.26 f/cc). The gravimetric sampling results indicate a 5-fold difference in average exposure for miners versus millers, while the sampling results for fibre exposures (the exposure of concern) indicate a 45-fold difference in average exposure concentrations between miners and millers. Taking into consideration the variation within mining and milling jobs, the difference between exposures to workers involved in these jobs would be even greater. The large difference in the fibre exposures between miners and millers that was observed in the Tossavainen et al. (1999) study adds further support to my concern that applying a single conversion factor from dust samples in estimating chrysotile fibre exposures for miners and millers is the most likely explanation for the slope of the dose response for lung cancer in the McDonald et al. study being so different from the slope for lung cancer based on the studies of chrysotile textile workers. Stayner et al. (1996) provide a summary of data indicating that the lung cancer risk from exposure to chrysotile in either experimental animals or in humans is similar to the risk from exposure to amphibole asbestos in these species.
    
38. 
    With regard to asbestosis, Stayner et al. (1997) published a dose response analysis based upon the updated study of chrysotile textile workers by Dement et al. (1994). Their analysis indicates an excess risk of 2 deaths from asbestosis per 1000 employees exposed to 0.1 f/cc for an occupational lifetime exposure of 45 years, or 0.2 per cent from a cumulative exposure of 4.5f/cc-years. Two additional studies estimate similar risks of death from asbestosis in relation to cumulative chrysotile exposure. The study by Berry et al. (1979) estimates a risk of 1 per cent for those categorized as "probably having asbestosis" among chrysotile textile workers who were exposed to an estimated range of 0.3 f/cc to 1.1 f/cc for 40 years, or a cumulative exposure of 12-44 f/cc-years. For those categorized as "certified asbestosis" a 1 per cent excess risk of death was associated with 63 f/cc-years of exposure. Huang (1990) estimates a risk of asbestosis of 1 per cent associated with 22 f/cc-years of exposure during the manufacturing of chrysotile textile and friction products. Data from Dement et al. (1994) allow for an estimate of 2 per cent asbestosis associated with 22.5 f/cc-years of exposure. Studies of workers exposed to a mixture of chrysotile and crocidolite asbestos in the manufacture of cement products have demonstrated an elevated the risk of "certified asbestosis" of 1 per cent associated with 10 f/cc-years of exposure (Finkelstein 1982). Finkelstein was of the opinion that he identified a 1 per cent excess risk of asbestosis related to a lower cumulative dose of asbestos exposures than Berry et al. (1979) because of the longer period of follow-up of the cohort which gave more time for the asbestosis to clinically manifest itself.
    
39. 
    I am not aware of evidence that similar cumulative exposures to amphibole forms of asbestos will result in a greater risk of asbestosis. Thus, it is difficult to make any distinction in potency between the amphiboles and chrysotile asbestos in relation to asbestosis.
    
40. 
    Chrysotile exposures related to numerous jobs and occupations has been associated with mesothelioma through epidemiological studies and case reports. In some situations, standby exposure only was associated with mesothelioma. Based on epidemiological studies, the potency of chrysotile to induce mesothelioma may be less than that from other forms of asbestos. However, the rarity of mesothelioma in the general population and the difficulty in determining asbestos exposure levels experienced by cohort members decades before measurements were taken, coupled with conversion of dust counts in particles to fibres per cc, make it difficult to determine differences in potency estimates with regard to the various forms of asbestos and mesothelioma. Based on toxicological study results, in terms of the quantity of dust deposited and retained in the lungs, chrysotile may be more potent than other forms of asbestos in the induction mesothelioma and fibrosis (Wagner et al., 1974). The population attributable risk of contracting mesothelioma from chrysotile, however, will be greater than from other forms of asbestos because of the much greater potential for exposure to chrysotile.
    
41. 
    I have not seen any quantitative data related to decrements in lung function for either chrysotile and amphibole asbestos. On the basis of mortality from asbestosis, I assume there is little difference in lung function related to the various forms of asbestos.
    
42. 
    In summary to this question, in evaluating the epidemiological evidence, I see no basis for concluding that the overall disease potential from exposure to the amphiboles is any different than that from exposure to chrysotile asbestos with the possible exception that amphiboles may be more potent in causing mesothelioma and chrysotile may be more potent in causing lung cancer. Studies in experimental animals demonstrate the ability of chrysotile asbestos as well as the amphiboles to induce fibrosis, lung cancer and mesothelioma. From a public health standpoint, in terms of quantification of disease, it would be extremely difficult to make any distinction between exposure to the amphiboles and chrysotile asbestos fibres.
    

43. 
    Broadly it is my understanding that the relative pathogenicity of the different fibres for the various diseases is different (see Table)
    

44. 
    There have been several epidemiological studies that have shown no increased risk for low levels of exposure to chrysotile, particularly in friction products industries.
    

45. 
    So far as I am aware, there are no exposure-response data for such levels of exposure.
    
46. 
    For example, EHC 203 states the following:
    

"Overall, the available toxicological data provide clear evidence that chrysotile fibres can cause fibrogenic and carcinogenic hazards to humans. The data, however, are not adequate for providing quantitative estimates of the risk to humans. This is because there are inadequate exposure-response data from inhalation studies, and there are uncertainties concerning the sensitivities of the animal studies for predicting human risk" [EHC 203, p.7].

"There is evidence that fibrous tremolite causes mesothelioma in humans. Since commercial chrysotile may contain fibrous tremolite, it has been hypothesized that the latter may contribute to the induction of mesotheliomas in some populations exposed primarily to chrysotile. The extent to which the observed excesses of mesothelioma might be attributed to the fibrous tremolite content has not been resolved" [EHC 203, p 8-9].

"Epidemiological studies that contribute to our understanding of the health effects of chrysotile conducted to date and reviewed in this monograph have been on populations mainly in the mining or manufacturing sectors and not in construction or other user industries. This should be borne in mind when considering potential risks associated with exposure to chrysotile" [EHC 203 , p 137].

47. 
    One means of determining the risk from low exposure levels for carcinogens is to estimate the risk from studies where exposure information is of reasonably good quality and the estimates of risk were made using sound epidemiological principles and methodology. Once these studies have been identified, an appropriate way to determine quantitative risk from low exposure levels is to use all of the available data in a particular study and to estimate dose response. As mentioned in my response to Question 3(c) above, several studies of workers exposed to chrysotile asbestos can be used to estimate risk from low levels of exposure. The studies mentioned above, which represent three separate populations of chrysotile textile workers demonstrate an excess relative risk of lung cancer ranging from 0.5-3 per cent for each fibre/cc-year of exposure. Risk assessment based on the study of South Carolina chrysotile textile workers (Stayner et al., 1997) indicates that individuals exposed to 0.1 f/cc‑year for an occupational lifetime of 45 years, e.g., 4.5 f/cc-years cumulative exposure to chrysotile, have an elevated risk of 5 extra deaths from lung cancer and 2 extra deaths from asbestosis per 1000 workers. Dose response for mesothelioma could not be estimated because there were too few deaths from this cause in the study.
    
48. 
    Epidemiological study results and case reports indicate that a large number of jobs which entail occasional peak exposures to chrysotile asbestos have resulted in workers being diagnosed with mesothelioma. Furthermore, mesothelioma has been diagnosed among household contacts of asbestos cement workers (Magnani et al., 1992; Ascoli et al., 1996), among individuals living near chrysotile mining and milling operations (Began et al., 1992), or living in houses constructed with asbestos cement (Ascoli et al., 1996), or who were exposed to low cumulative amounts of chrysotile asbestos from brake lining work (Woitowitz and Rodelsperger, 1991), or from standby exposure as bakers (Ascoli et al., 1996). This information contributes to the evidence that very low exposure to all forms of asbestos can induce cancer. These observations of mesothelioma should be considered as sentinel events for the pathologies other than mesothelioma that are more difficult to identify among large populations that experience relatively more remote exposure to chrysotile asbestos. In my opinion, these studies constitute high level risk from low levels of exposure to chrysotile asbestos.
    

49. 
    It my understanding there are epidemiological studies which do not show a statistically increased risk of disease from low levels of exposure to chrysotile. However, the absence of demonstrating an increased risk does not mean that there is not some risk as it is not possible to prove a negative and a threshold has not been demonstrated for any carcinogen (nor in my opinion is it biologically likely that one exists).
    

50. 
    It is extraordinarily difficult to demonstrate lack of an effect, or a threshold effect, in epidemiological studies because of the ubiquitous problems of bias, confounding and chance. In particular, the smaller effect that needs to be demonstrated, the larger the study needs to be, both in population size and follow-up time and such studies can rarely be done, even with animals.
    

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