Abstract
Limited information is available on risk of peritoneal mesothelioma after asbestos exposure, and in general on the risk of cancer after cessation of asbestos exposure. We updated to 2013 the follow‐up of a cohort of 1083 female and 894 male textile workers with heavy asbestos exposure (up to 100 fb/mL), often for short periods. A total of 1019 deaths were observed, corresponding to a standardized mortality ratio (SMR) of 1.68 (95% confidence interval [CI]: 1.57–1.78). SMRs were 29.1 (95% CI: 21.5–38.6) for peritoneal cancer, 2.96 (95% CI: 2.50–3.49) for lung cancer, 33.7 (95% CI: 25.7–43.4) for pleural cancer, and 3.03 (95% CI: 1.69–4.99) for ovarian cancer. For pleural and peritoneal cancer, there was no consistent pattern of risk in relation to time since last exposure, whereas for lung cancer there was an indication of a decline in risk after 25 years since last exposure. The findings of this unique cohort provide novel data for peritoneal cancer, indicating that – as for pleural cancer – the excess risk does not decline up to several decades after cessation of exposure.
Highlights
The incidence of mesothelioma rises as function of the third or fourth power of time since first asbestos exposure [12], after taking into account time since cessation of exposure
We reported the mortality follow-u p to 2004 of a cohort of heavily exposed asbestos textile workers employed between 1946 and 1984, in which we observed 315 cancer deaths compared to 153.9 expected, including 39 deaths from peritoneal cancer, 36 deaths from pleural cancer, and 109 deaths from lung cancer [14, 15]
Using an updated follow-up of this unique cohort of textile workers heavily exposed to asbestos, we were able to address the role of stopping exposure separately on pleural and peritoneal cancer
Summary
The incidence of mesothelioma rises as function of the third or fourth power of time since first asbestos exposure (latency) [12], after taking into account time since cessation of exposure. The other determinants of mesothelioma incidence are average exposure to asbestos (linear relationship), and type of asbestos, with stronger potency of amphiboles than chrysotile [3]. The influence of other time-related aspects such as age at first exposure and duration of exposure appears to be largely or totally explained by latency [12]. These models linking asbestos exposure to mesothelioma incidence have been developed and validated mainly on the basis of results for the pleural form of the disease, since most available cohort studies include a small number of peritoneal mesothelioma [2]. In that analysis there was no difference in the SMR of pleural and peritoneal cancer between workers who had stopped exposure below age 30, and those who had continued exposure after age 40 [15]
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