ArticleJournal of thoracic disease2026
Occupational asbestos exposure and lung cancer: contemporary research trends, exploratory genetic evidence, and global burden from 1990 to 2021.
Article in Journal of thoracic disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Asbestos exposure is a confirmed risk factor for lung cancer, but its causal relationship with different subtypes and its global disease burden remain poorly characterized. This study aims to comprehensively evaluate the association between occupational asbestos exposure and lung cancer through multidimensional analysis, integrating bibliometric analysis, mendelian randomization, and Global Burden of Disease data to identify research trends, explore potential subtype-specific associations, and characterize global disease burden patterns. Methods: This study included a bibliometric analysis of publications from the Web of Science Core Collection on asbestos-related lung cancer. Mendelian randomization was performed using OpenGWAS data to investigate whether asbestos exposure is differentially associated with specific lung cancer subtypes. Global Burden of Disease 2021 data were analyzed to estimate the asbestos-related lung cancer burden by age and sex. Future burden was projected using the Bayesian age-period-cohort model. Results: Bibliometrics revealed fluctuating publication trends, with a thematic shift toward molecular mechanisms. Mendelian randomization analysis identified a suggestive causal relationship between asbestos exposure and lung adenocarcinoma [odds ratio (OR) =4.901, 95% confidence interval (CI): 1.150-20.881, P=0.03], but no significant causal links were observed with overall lung cancer or other subtypes. None of the instrumental variables demonstrated horizontal pleiotropy or heterogeneity. Global Burden of Disease analysis showed a higher asbestos-related lung cancer burden in males and older populations, with the greatest attributable burden in high socio-demographic index regions. Projections indicate a continued decline in global burden by 2036. Conclusions: The mendelian randomization results offer genetic evidence supporting a specific causal role of asbestos in lung adenocarcinoma development. Despite a decline in burden due to control policies, ongoing exposure in developing countries and legacy asbestos in buildings remain serious challenges. Future research should focus on larger genetic studies and analysis tailored to subtypes, while global efforts need to prioritize a comprehensive asbestos ban, improved screening for high-risk groups, and enhanced international cooperation to eliminate asbestos-related diseases.
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