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Conclusions

The extensive scientific literature related to asbestos fiber types relevant to industry and mesothelioma was reviewed. Human exposures to various amphibole fiber types have been linked to mesothelioma, but this article concerns the hypothesis of the existence of a causal association of mesothelioma with exposure to chrysotile fibers without contamination with amphiboles. The following points are addressed:

1. The use of scientific method requires the development and testing of hypotheses.

2. Epidemiology tests hypotheses about exposures potentially toxic to humans. The results of these tests to date indicate:

a. Epidemiological studies show amphiboles cause mesothelioma in humans.

b. In workers exposed to both chrysotile and amphibole, there are fewer mesothelioma cases than in studies of amphiboles alone.

c. cases of mesothelioma in cohorts where no amphibole exposure was identified do not demonstrate chrysotile is the cause of mesothelioma.

3. Epidemiological review of cohorts does not support the hypothesis that exposures to chrysotile fibers, uncontaminated by amphiboles, cause mesothelioma.

4. As indicators of exposure to asbestos, fiber burden studies of mesothelioma cases can generate hypotheses. They cannot replace analytical epidemiology, which is required to assess better exposure-outcome associations and infer causation.

5. Patient reports, case series, and ecological surveys do not provide independent scientific evidence for chrysotile causing mesothelioma.

6. Regulatory decisions about chrysotile reflect policy and are based not only on scientific results and conclusions concerning mesothelioma.

Conclusions regarding causation of mesothelioma from chrysotile uncontaminated by identified amphiboles must be based on the application of the scientific method. Observations, hypothesis generation, hypothesis testing, and replication of results (i.e., the scientific method) are the accepted process steps for deriving conclusions about a theory. The basis for determining whether chrysotile asbestos causes mesothelioma should rest primarily on the results of analytic epidemiological studies. Most cohort studies that have been published have the potential for concomitant amphibole fiber exposures. Epidemiological studies investigating mesothelioma risk from exposures of cohort members to chrysotile asbestos fibers not known to be contaminated with amphiboles do not justify a conclusion of causality at this time. Whenever mesothelioma cases have been observed in cohort studies, the presence of amphiboles has not been ruled out. Although the causal hypothesis has been studied intensively for cohorts primarily exposed to chrysotile, the number of mesotheliomas observed has been far fewer than those where amphibole exposures occurred, and the possibility of unidentified amphibole exposures remains in these few individual cases where only exposure to chrysotile asbestos was identified for the entire cohort. Hopefully, risk communications and public policy can be improved by thorough medical review of the literature of human studies spanning most of the last century.