In an inhalation study (Wagner et al, 1974) chrysotile, caused as many mesotheliomas as did crocidolite in an inhalation study.
The authors fail to impose quality control standards to their study, as required when dealing with hetrogeneous data sets and as demonstrated by Lenters et al (2011) in their meta-analysis, which included only studies adequately controlled for exposure.
Mc Cormack et al (2012) further state that figures showing mesotheliomas related to chrysotile asbestos exposure may be erroneously over-reported, but give no explanation for their statement that ‘the lung cancer excess depends critically on the rates on which the SMR is based’.
Such an effect would be true for all asbestos types, including the amphibole and mixed exposure cohorts, especially given the inadequate coding scheme for mesothelioma and under-reporting due to a variety of country-to-country reporting errors (Delgermaa et al, 2011) over the time frames covered by the cited epidemiology studies of Mc Cormack et al (2012).
Until recently, the coding for mesothelioma was unspecific until the implementation of the International Classification of Diseases-10 in 1994, which gave mesothelioma its own specific codes.
The relative lack of biopersistence of chrysotile asbestos in lung tissue can hardly be grounds for concluding that chrysotile asbestos does not cause mesothelioma, given the translocation and biopersistence of chrysotile in target sites of mesothelioma occurrence (Sebastien et al, 1980; Dodson et al, 1990; Suzuki and Yuen, 2001; Suzuki et al, 2005).