Canadian chrysotile (white asbestos) could be a paradigm for those agents that are successfully exploited commercially long after they have been found to be lethal. Mining started in the late 1870s, and reports of disability and death followed in Britain (1898), in France (1906), and Italy (1908), but it was not until 1955 that Canada acknowledged asbestosis in its asbestos miners and millers. Even when shortly after asbestos was shown to be carcinogenic, Canadian Public Relations experts assisted by their scientists exculpated chrysotile by deeming other agents to have been causal.
The PR techniques that have been successfully used in the defense of chrysotile are reviewed, to forewarn scientists involved in formulating public health policy for similar agents, as to the tricks that will be played on them.
Primary prevention carried out today can reduce the disease incidence in the future decades. The present disease panorama is the consequence of past asbestos exposure mainly before the 1970s. The peak incidence of asbestos-induced diseases will be reached around 2010 in Finland. The number of asbestos-related premature deaths is at present annually about 150 which exceeds the figure of fatal work accidents. Asbestos-related cancer will increase still for 15-20 years and reach its maximum, about 300 cases, in 2010, and will start to decrease after that. More than 20,000 asbestos-exposed workers have participated in the medical screening and follow-up. The termination of exposure, antismoking campaigns, improved diagnostics and careful attention to compensation issues, as well as other potentials for prevention, were the central issue of the Asbestos Program of the Finnish Institute of Occupational Health. An important objective of research work is to improve early diagnostics, and thereby treatment prospects, in case of asbestos-induced cancers.
One prospective epidemiologic study of asbestos cement workers with radiological small opacities has been cited as a rationale for attributing excess lung cancer to asbestosis. This approach could have considerable practical value for disease attribution in an era of decreasing exposure. However, a recent International Agency for Research on Cancer review concludes that the mechanism of production of asbestos-related lung cancer are unknown. Asbestosis, therefore, cannot be a biologically effective dose marker of lung cancer susceptibility. Asbestosis nonetheless would be useful in identifying asbestos-attributable lung cancer cases if it could be proven an infallible exposure indicator. In this study, we tested this hypothesis in the chrysotile miners and millers of Quebec, Canada. We examined exposure histories, autopsy records, and lung fiber content for 111 Quebec chrysotile miners and millers. If the hypothesis of an asbestosis requirement for lung cancer attribution were accurate, we would expect as asbestosis diagnosis to separate those with lung cancer and high levels of exposure from those with lower levels of exposure in a specific and sensitive manner. This is the first such study in which historical job-based individual estimates based on environmental measurements, lung fiber content, exposure timing, and complete pathology records including autopsies were available for review. We found significant excesses of lung tremolite and chrysotile and estimated cumulative exposure in those with lung cancer and asbestosis compared to those with lung cancer without asbestosis. However, when the latter were directly compared on a case-by-case basis, there was a marked overlap between lung cancer cases with and without asbestosis regardless of the measure of exposure. Smoking habits did not differ between lung cancer cases with and without asbestosis. In regression models, smoking pack-years discriminated between those with the without lung cancer, regardless of asbestosis status. Most seriously, the pathologic diagnosis of asbestosis itself seemed arbitrary in many cases. We conclude that although the presence of pathologically diagnosed asbestosis is a useful marker of exposure, the absence of this disease must be regarded as one of many factors in determining individual exposure status and disease causation.
Cites: Br J Ind Med. 1980 Feb;37(1):11-247370189
Cites: Br J Ind Med. 1987 Feb;44(2):96-1003814551
Cites: Arch Environ Health. 1987 Jul-Aug;42(4):185-912821933
Cites: Br J Ind Med. 1989 Mar;46(3):180-72539184
Cites: Br J Ind Med. 1989 Aug;46(8):537-402550049
Cites: Am J Ind Med. 1996 Oct;30(4):398-4068892544
Cites: Br J Ind Med. 1993 Dec;50(12):1073-818280638
Cites: Ann Occup Hyg. 1994 Aug;38(4):503-18, 410-17978972