Summary Comments by Dr. Henderson

Summary Comments by Dr. Henderson

101. 
     In-place asbestos is widely distributed in industrialized societies and much includes mixtures of chrysotile and amphiboles — although chrysotile has been the predominant type of asbestos used throughout Western Europe for many years (about 94-97%).
     
102. 
     Lung cancer and mesothelioma are the most important bio-hazards from asbestos in place and the continued use of asbestos.
     
103. 
     Because of the prolonged lag-time between exposure and the subsequent development of either lung cancer or mesothelioma, most mesotheliomas in the 1990s and beyond can be attributed to exposures sustained decades before; the mesothelioma "epidemic" predicted for Europe over the next three decades can be attributed to exposures before, during and after the 1960s and 1970s, especially to one or more of the amphibole varieties.
     
104. 
     For the amphibole forms of asbestos and mixtures of asbestos types, a linear dose-response relationship has been found at high levels of exposure; a dose-response relationship with an increase of the relative risk of mesothelioma to > 2.0 has also been observed at low levels of exposure, in the order of 0.5-1.0 fibre-year (which overlaps with non-occupational environmental exposures). No lower threshold dose for mesothelioma induction has been delineated for the amphiboles.
     
105. 
     Chrysotile also has the capacity to induce mesothelioma, although it is less mesotheliomagenic than the amphiboles (my estimate is 1/10^th-1/30^th).
     
106. 
     Commercial Canadian chrysotile on average contains trace quantities of tremolite, including fibrous tremolite (< 1%).
     
107. 
     Tremolite — a non-commercial amphibole — also has the capacity to induce mesothelioma.
     
108. 
     The carcinogenicity of Canadian chrysotile may be attributable to the trace tremolite content, but it is not possible to separate the dose-response effects for the chrysotile and the tremolite.
     
109. 
     At high levels of exposure to Canadian chrysotile, a linear dose-response relationship has been observed.
     
110. 
     To the best of my knowledge, there are no epidemiological or observational data on dose-response effects of chrysotile only at low levels of exposure.
     
111. 
     No lower threshold dose for the carcinogenic effects of chrysotile has been identified (EHC 203).
     
112. 
     To the best of my knowledge, there are no observational data on the potential carcinogenic effects of inhaled chrysotile when superimposed upon a pre-existing burden of amphiboles ± chrysotile in lung tissue.
     
113. 
     Although the amphiboles are far more potent than chrysotile for mesothelioma induction, this differential in carcinogenicity may be less obvious or absent for lung cancer induction, but this is still the subject of some dispute; chrysotile is associated with a low risk of lung cancer among Canadian chrysotile miners and millers, but the highest risk for lung cancer induction has been observed for South Carolina asbestos textile workers who used Canadian chrysotile almost exclusively.
     
114. 
     A linear dose-response relationship has also been observed for the risk of lung cancer versus cumulative asbestos exposure. Although some authorities favour a linear no-threshold model for lung cancer induction, others suggest that a threshold may exist, but this has not been delineated in numerical terms.
     
115. 
     In contrast, asbestosis is a dose-dependent non-cancerous disorder, with clear evidence of a threshold effect, although the threshold may be lower than previously supposed, at least for histological asbestosis; there is no risk of asbestosis at low levels of chrysotile exposure.
     
116. 
     Although reduction of airborne asbestos fibre concentrations in the mining and manufacturing industries has been achieved, it is too early to evaluate the effects of these reduced exposures, because no epidemiological data are available; however, with reduction of cumulative exposures, a reduction in the incidence of both asbestos-related mesothelioma and asbestos-related lung cancer can be expected.
     
117. 
     The risks from low-level occupational exposure to chrysotile, or from occasional peak concentrations, have not been delineated but are predictably small.
     
118. 
     Carcinogenic hazards from ultra-low levels of atmospheric chrysotile fibres (e.g. simple occupancy of public buildings) appear to be minuscule, negligible or undetectable.
     
119. 
     Therefore, health concerns over chrysotile dust exposure narrow down to a workplace issue.
     
120. 
     There is evidence of an increased incidence of mesothelioma among, say, brake mechanics in Australia exposed to chrysotile derived from brake blocks and lining.
     
121. 
     With the reductions of airborne fibre concentrations in the asbestos mining, milling and manufacturing industries, construction trades workers constitute the group of workers at greatest risk from exposure to asbestos-cement products (e.g. builders, builders' labourers, carpenters, electricians, plumbers and roofing workers). This group constitutes a large, disparate and non-cohesive workforce for which controlled use of asbestos is not achievable, for the reasons discussed earlier in this report.
     
122. 
     Therefore, chrysotile asbestos should not be used in building materials, because of the hazards imposed by installation, maintenance and removal operations (EHC 203); these risks may be compounded for some groups by catastrophic events affecting buildings — e.g. fires (with a burst of asbestos fibres into the atmosphere and the necessity for clean-up operations), and other disasters.
     
123. 
     Substitutes for chrysotile are available for many applications (e.g. cellulose fibres, para-aramid fibres and polyvinyl alcohol); evidence indicates that these fibres are less bio-persistent than chrysotile and, therefore, national health authorities (EHC 203, NICNAS 99) have recommended phasing out or prohibition of chrysotile whenever safer substitute materials are available.
     
124. 
     Therefore, from a perspective of caution and prudence for occupational health and safety, it follows that chrysotile should either:
     
     1. 
        Be restricted to only a few and well-defined applications so that it is inaccessible to the great majority of workers and is available for use by only small and cohesive specialized worker groups that can be trained effectively in its controlled use (e.g. analogous to nuclear fuels); in effect, this means that chrysotile should not be used in building products (e.g. high-density fibro-cement materials such as asbestos-cement sheets) or friction products.
        

1. 
   It should be made inaccessible to everyone, by prohibition, unless the alternatives pose equal or greater hazards and equal or greater problems with control.
   
1. 
   These views are also expressed in EHC 203, wherein it is stated:
   

b) Where safer substitute materials for chrysotile are available, they should be considered for use.

c) Some asbestos-containing products pose particular concern and chrysotile use in these circumstances is not recommended These uses include friable products with high exposure potential. Construction materials are of particular concern for several reasons. The construction industry workforce is large and measures to control asbestos are difficult to institute. In-place building materials may also pose risk to those carrying out alterations, maintenance and demolition" … [p 144]

d) The combined effects of chrysotile and other insoluble respirable particles needs further study.

1. 
   NICNAS 99 sets out a similar set of recommendations:
   

• 
  "Chrysotile is a known human carcinogen.
  
• 
  Prudent OHS [occupational health & safety] policy and public health policy favours the elimination of chrysotile wherever possible and practicable.
  
• 
  The main exposure to Australian workers arises from manufacture, processing and removal of friction products and gaskets. Home mechanics are also exposed during 'do-it-yourself' replacement of brake pads/shoes. ... . In Australia, chrysotile is no longer used in high density materials such as chrysotile-cement.
  
• 
  Current overseas experience with the phasing out of chrysotile products indicates that a range of alternatives is available to suit the majority of uses. Good OHS practice dictates that use of chrysotile products should be restricted to those uses where suitable substitutes are not available, and alternatives should continue to be sought for remaining uses".
  

127. 
     Whether the objective of removal of chrysotile from the workplace and the general environment is achievable by enforcement of controlled use for a few restricted applications — or by prohibition — is essentially a societal question and a public health policy issue. For the reasons discussed in this report, a complete ban is more certain to accomplish this objective (paragraph iii.124(b)). Therefore, as a cautious and prudent approach to national occupational health policy, a complete ban is neither unreasoned nor unreasonable; on the balance of prevailing scientific evidence and uncertainties discussed in this report, such a policy seems defensible and, arguably, justifiable as a national health measure. Perhaps it is best to let Bradford Hill have the last words:
     

4. Endnote by Dr. Henderson

1. 
   Wishing to add two further pertinent references after completing his Report, Dr. Henderson attached the following Endnote. These references²⁷ deal with the following:
   
2. 
   Clearance of chrysotile fibres from human lung tissue: In the past, the kinetics of chrysotile clearance from lung tissue have been investigated mainly in experimental models using rodents. In an autopsy study published in 1999, Finkelstein and Dufresne [1] investigated clearance of chrysotile from the lung tissue of 72 Quebec chrysotile miners and millers in comparison to 49 control subjects, using regression analyses, with the following findings:
   

• 
  There was a significant association between the duration of occupational exposure and the tissue burdens of chrysotile and tremolite.
  
• 
  The concentration of chrysotile decreased with time after exposure ceased but the concentration of tremolite did not.
  
• 
  The clearance rate varied inversely with the length of chrysotile fibres. For fibres > 10 µm in length - i.e. fibre lengths in the reported range for carcinogenicity - the clearance half-time was estimated to be eight years. In other words, the tissue bio‑persistence of chrysotile fibres in this study seems substantially more prolonged than in rodent experiments, and presumably corresponds to persistent high chrysotile fibre concentrations for many years after cessation of occupational exposure in humans, as discussed in paragraphs 5.112 - 5.113. It is also notable that the concentration of 6,250,000 chrysotile fibres mentioned in those paragraphs (for an individual but by no means unusual patient) is probably above the level at which Rogers et al. [2] identified an odds ratio for mesothelioma of > 8.5 (even allowing for differences in fibre size between the two different laboratories), and even the duration of 16 years after exposure stopped (as opposed to its commencement: 24 years) falls into the lag-time range lung cancer induction by asbestos.
  
• 
  Studies like this suggest that clearance mechanisms can be overwhelmed and break down at occupational levels of exposure in humans, with the existence of a long-term sequestered fraction of chrysotile fibres.
  

1. 
   Mesothelioma rates in men and women in Sweden: attached to this Endnote is a recent paper by Jarvholm et al. [3] on trends in mesothelioma incidence in Sweden, which re-emphasizes some of the points made earlier in this report.
   

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