Familial aggregation of malignant mesothelioma in former workers and residents of Wittenoom, Western Australia.

Clustering of cases of malignant mesothelioma within families has often been observed, but disentangling genetic and exposure effects has not been done. Former workers and residents exposed to crocidolite at Wittenoom, Western Australia, where many families shared exposure to asbestos, have had high rates of mesothelioma. Our study aimed to estimate the additional risk of mesothelioma in relatives, after allowance for common exposure to crocidolite. More than 11,000 former asbestos workers and residents from Wittenoom have been followed up in cancer and death registries. Levels of exposure for all members of the Wittenoom cohorts have been estimated previously. Relationships between family members of all mesothelioma cases were established from questionnaires, birth and death certificates. Expected numbers of cases of mesothelioma were estimated by fitting a Weibull survival model to all data, based on time from first asbestos exposure, duration and intensity of exposure and age. For each family group, the earliest case was considered the index case. Predicted risk was estimated for each subject from the time of diagnosis of the index case. Familial risk ratios were estimated by dividing observed cases by the sum of risks of all same degree relatives of index cases. There were 369 family groups with at least one case of mesothelioma and a further 25 cases of mesothelioma among relatives in the same families, with 12.9 expected. The risk ratio for blood relatives was 1.9 (95% confidence interval [CI] = 1.3-2.9, p = 0.002). These findings suggest an important, but not large, genetic component in mesothelioma, similar to many other cancers.

All-cause mortality and cancer incidence among adults exposed to blue asbestos during childhood.

BACKGROUND: There are few data on the long-term health outcomes of exposure to asbestos in childhood. This study investigated cancer and mortality of adults exposed to blue asbestos as children. METHODS: Data linkage to relevant health registries was used to identify cancers and mortality in a cohort of adults (n = 2,460) that had lived in an asbestos mining town during their childhood (<15 years). RESULTS: There were 217 (93 female) incident cancers and 218 (70 female) deaths among the cohort. Compared with the Western Australian population females had elevated mesothelioma, ovarian and brain cancers, and increased "all cause" and "all cancer" mortality. Males had elevated mesothelioma, leukemia, prostate, brain, and colorectal cancers, and excess mortality from "all causes," "all cancers," circulatory disease, diseases of the nervous system, and accidents. CONCLUSION: Exposure to blue asbestos in childhood is associated with an increased risk of cancer and mortality in adults.

Effects of asbestos and smoking on gas diffusion in people exposed to crocidolite.

OBJECTIVE: To examine the effects of asbestos exposure and tobacco smoking on the level and rate of change of the diffusing capacity of the lung for carbon monoxide (DLCO). DESIGN AND PARTICIPANTS: A cohort study of 934 people (including both mine workers and town residents) exposed to crocidolite (blue asbestos) at the asbestos mines and in the town of Wittenoom, Western Australia, between 1943 and 1966. DLCO measurements were taken during a follow-up period from 1992 to 2002. MAIN OUTCOME MEASURES: Baseline levels of DLCO and change in levels over time. RESULTS: 2980 DLCO measurements were done on 934 people (of whom 818 were men and 724 were workers) who underwent a median of 2 (range, 1-17) measurements during the follow-up period. Radiographic asbestosis at baseline and asbestos exposure at a younger age were associated with lower DLCO values. The average rate of decline in DLCO was 0.33 (95% CI, 0.31-0.35) units per year, plus an additional decrement of 0.22 (95% CI, 0.12-0.32) units per year if the participant had radiographic asbestosis at the beginning of the follow-up period. Compared with never-smokers, current smokers and ex-smokers had lower DLCO at baseline, but smoking status did not affect the change in DLCO during the follow-up period. CONCLUSIONS: Our results confirm a continuous deleterious effect of crocidolite on DLCO, especially on people with asbestosis. Smoking was associated with lower DLCO levels, but was not a significant predictor of rate of change in DLCO. Smoking status did not affect the relationships between crocidolite exposure and the level or rate of change of DLCO in this population.