A Bayesian approach to assess interaction between known risk factors: the risk of lung cancer from exposure to asbestos and smoking

Wraith, Darren; Mengersen, Kerrie

doi:10.1177/0962280206075525

Cited by 13 publications

(5 citation statements)

References 44 publications

(76 reference statements)

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“…Our findings on lung cancer are, therefore, unlikely due to uncontrolled confounding from smoking. We were, however, unable to assess the combined effect of tobacco smoking and asbestos [54, 76].…”

Section: Discussionmentioning

confidence: 99%

Cumulative asbestos exposure and mortality from asbestos related diseases in a pooled analysis of 21 asbestos cement cohorts in Italy

et al. 2019

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Background Despite the available information on cancer risk, asbestos is used in large areas in the world, mostly in the production of asbestos cement. Moreover, questions are raised regarding the shape of the dose response relation, the relation with time since exposure and the association with neoplasms in various organs. We conducted a study on the relationship between cumulative asbestos exposure and mortality from asbestos related diseases in a large Italian pool of 21 cohorts of asbestos-cement workers with protracted exposure to both chrysotile and amphibole asbestos. Methods The cohort included 13,076 workers, 81.9% men and 18.1% women, working in 21 Italian asbestos-cement factories, with over 40 years of observation. Exposure was estimated by plant and period, and weighted for the type of asbestos used. Data were analysed with consideration of cause of death, cumulative exposure and time since first exposure (TSFE), and by gender. SMRs were computed using reference rates by region, gender and calendar time. Poisson regression models including cubic splines were used to analyse the effect of cumulative exposure to asbestos and TSFE on mortality for asbestos-related diseases. 95% Confidence Intervals (CI) were computed according to the Poisson distribution. Results Mortality was significantly increased for ‘All Causes’ and ‘All Malignant Neoplasm (MN)’, in both genders. Considering asbestos related diseases (ARDs), statistically significant excesses were observed for MN of peritoneum (SMR: men 14.19; women 15.14), pleura (SMR: 22.35 and 48.10), lung (SMR: 1.67 and 1.67), ovary (in the highest exposure class SMR 2.45), and asbestosis (SMR: 507 and 1023). Mortality for ARDs, in particular pleural and peritoneal malignancies, lung cancer, ovarian cancer and asbestosis increased monotonically with cumulative exposure. Pleural MN mortality increased progressively in the first 40 years of TSFE, then reached a plateau, while peritoneal MN showed a continuous increase. The trend of lung cancer SMRs also showed a flattening after 40 years of TSFE. Attributable proportions for pleural, peritoneal, and lung MN were respectively 96, 93 and 40%. Conclusions Mortality for ARDs was associated with cumulative exposure to asbestos. Risk of death from pleural MN did not increase indefinitely with TSFE but eventually reached a plateau, consistently with reports from other recent studies. Electronic supplementary material The online version of this article (10.1186/s12940-019-0510-6) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Cumulative asbestos exposure and mortality from asbestos related diseases in a pooled analysis of 21 asbestos cement cohorts in Italy

et al. 2019

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“…A synergistic effect between tobacco smoke and asbestos in the causation of lung cancer 12,13) may also explain this result. The prevalence of male smokers has generally decreased in Europe during the last decade, whereas the smoking rate remains high in many Asian countries 14) .…”

Section: Discussionmentioning

confidence: 99%

Variations of Lung Cancer Risk from Asbestos Exposure: Impact on Estimation of Population Attributable Fraction

et al. 2013

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The purpose of this study is to investigate the potential impact of differing lung cancer risks in study populations on estimating population attributable fraction (PAF) from asbestos exposure. Studies were identified via a MEDLINE search up to September 2009 and from the reference lists of publications about asbestos exposure and lung cancer risk. Relative risk estimates were extracted from 160 studies and meta-relative risks were calculated according to randomeffect models. Hypothetical PAFs were calculated based on the meta results and on the difference exposure scenarios. The risks for lung cancer from asbestos exposure were variable according to the region as well as other study characteristics. The risk estimates proved higher in Asian countries (RR=3.53), in studies with 500 or fewer subjects (RR=2.26), and papers published in the 1990s or earlier (RR=1.91), than did those for European or North American countries, studies with more than 500 subjects, and papers published in the 2000s, respectively. The differences in PAFs between Asian and North American studies were 15.5%, 30.3%, and 36.2% when the exposure prevalence was 10%, 30%, and 50%, respectively. This study suggested that it is important to apply appropriate lung cancer estimates to each study population when calculating PAF from asbestos exposure.

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“…If the latter were not available, crude relative risks were calculated from the numbers of subjects and person-years reported in the tables. Additive (S) and multiplicative interaction indexes (V) between each infection and cigarette smoking status and their 95% confidence intervals (95% CI) were calculated for each study (22). …”

Section: Methodsmentioning

confidence: 99%

Interaction between Cigarette Smoking and Hepatitis B and C Virus Infection on the Risk of Liver Cancer: A Meta-analysis

Chuang

Lee

Hashibe

et al. 2010

Cancer Epidemiology, Biomarkers &Amp; Prevention

127

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Introduction Chronic infection with HBV and HCV as well as cigarette smoking are established risk factors of hepatocellular carcinoma (HCC), but it is unclear whether an interaction exists between these factors in causing hepatocellular carcinogenesis. We conducted a meta-analysis to evaluate the interaction of HBV and HCV infection and cigarette smoking on the risk of HCC. Methods We systematically searched the PUBMED and the China National Knowledge Infrastructure (CNKI) databases. A total of 16 eligible publications were identified. Cigarette smoking, and chronic HBV and HCV infections were dichotomized into present or absent. Additive (S) and multiplicative interaction indexes (V) between smoking and each of the two infections and their 95% confidence intervals (95% CI) were calculated for each study and then combined in a meta-analysis. Results We found a more than additive interaction between HBV infection and cigarette smoking (S=1.44, 95% CI=1.00–2.06; 9 studies) and a more than multiplicative interaction (V=1.60, 95% CI=1.16–2.20; 6 studies) between HCV infection and cigarette smoking. No publication bias was detected. Conclusion Smoking appears to interact with both HBV and HCV in determining HCC risk. A pooled analysis of individual subject data, with appropriate adjustment with other risk factors is warranted to confirm these results. Impact Chronic carriers of HBV and HCV are suggested to avoid smoking.

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A Bayesian approach to assess interaction between known risk factors: the risk of lung cancer from exposure to asbestos and smoking

Cited by 13 publications

References 44 publications

Cumulative asbestos exposure and mortality from asbestos related diseases in a pooled analysis of 21 asbestos cement cohorts in Italy

Cumulative asbestos exposure and mortality from asbestos related diseases in a pooled analysis of 21 asbestos cement cohorts in Italy

Variations of Lung Cancer Risk from Asbestos Exposure: Impact on Estimation of Population Attributable Fraction

Interaction between Cigarette Smoking and Hepatitis B and C Virus Infection on the Risk of Liver Cancer: A Meta-analysis

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