Occupational asbestos exposure and lung cancer: contemporary research trends, exploratory genetic evidence, and global burden from 1990 to 2021

Our plain-English summary of Occupational asbestos exposure and lung cancer: contemporary research trends, exploratory genetic evidence, and global burden from 1990 to 2021, by Y. Chen, C. Gao, X. Lou, et al (Journal of Thoracic Disease, 2026).

The study

• Authors: Y. Chen, C. Gao, X. Lou, Z. Han, L. Shao, T. Feng, S. Miao, L. Wu
• Journal: Journal of Thoracic Disease
• Published: 2026;18(9):1034
• Read it: PubMed · Publisher · Free full text

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.

© AME Publishing Company.

In plain English

This study combined three analyses of occupational asbestos exposure and lung cancer. A count of 478 publications from 2008 to 2025 found yearly output of 18 to 35, with recent topics centred on prevention and cell-level cancer mechanisms. Using genetic data from European populations (a method called Mendelian randomization), the authors reported a suggestive association between asbestos exposure and lung adenocarcinoma (odds ratio 4.901, 95% CI 1.150 to 20.881, P=0.03). They found no significant association with lung cancer overall (odds ratio 2.110, 95% CI 0.738 to 6.031) or with small cell or squamous cell lung cancer. In Global Burden of Disease 2021 estimates, asbestos-related lung cancer death rates rose with age and were higher in males. The attributable burden increased with socio-demographic index, mainly in Western Europe and Australasia. Projected age-standardized death rates fell between 2021 and 2036, from 7 to 5 per 100,000 in males and from 0.89 to 0.68 in females. The authors concluded the genetic results suggest a potential causal relationship with adenocarcinoma. They noted European-only genetic data, limited statistical power and no external validation.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Combined study: a bibliometric analysis of published literature, a two-sample Mendelian randomization analysis using public genetic association (GWAS) data, and a secondary analysis of Global Burden of Disease 2021 estimates with projections to 2036 using a Bayesian age-period-cohort model
• Who was studied: Three data sources. (1) 478 documents (395 articles and 83 reviews) from the Web of Science Core Collection, 2008 to 2025. (2) GWAS summary data from European populations: 1,262 exposure cases and 75,195 controls; 29,863 lung cancer cases and 55,586 controls; 11,245 lung adenocarcinoma cases and 54,619 controls; 2,791 small cell lung carcinoma cases and 20,580 controls; 7,704 squamous cell lung cancer cases and 54,763 controls. (3) Global Burden of Disease 2021 estimates for people aged 20 and older, 1990 to 2021, across 21 GBD regions and 5 socio-demographic index regions.
• Exposure: Occupational asbestos exposure; no fiber types were specified. In the genetic analysis, the exposure trait was 'worked with materials containing asbestos: often'. In the Global Burden of Disease analysis, asbestos-related lung cancer was defined as tracheal, bronchus and lung cancer burden attributable to occupational exposure to asbestos.
• Main results:
  • Lung adenocarcinoma, genetic analysis: suggestive association with asbestos exposure, odds ratio 4.901 (95% CI 1.150 to 20.881, P=0.03) by the main inverse variance weighted method, using 84 genetic variants. This was after two outlier variants were removed because the initial set of 86 showed heterogeneity (Q=108.251, P=0.045).
  • Overall lung cancer, genetic analysis: no significant causal association, odds ratio 2.110 (95% CI 0.738 to 6.031, P=0.16).
  • Small cell lung cancer, genetic analysis: no significant causal association, odds ratio 8.910 (95% CI 0.549 to 144.543, P=0.12).
  • Squamous cell lung cancer, genetic analysis: no significant causal association. No odds ratio is given in the article text.
  • Global Burden of Disease estimates, 2021: the death rate from asbestos-related lung cancer increased with age and was higher in males than in females in the same age group. The authors reported that the burden in 2021 had increased compared with 1990.
  • Across the five socio-demographic index regions, the impact of asbestos on lung cancer DALYs grew with socio-demographic index, mainly affecting Western Europe and Australasia for both sexes.
  • Projected global age-standardized death rate for males: from 7 per 100,000 in 2021 to 5 per 100,000 by 2036, a decline of approximately 28.6%.
  • Projected global age-standardized death rate for females: from 0.89 per 100,000 in 2021 to 0.68 per 100,000 in 2036, a decline of nearly 23.6%.
  • Bibliometric analysis: annual publications from 2008 to 2025 ranged from 18 to 35. Recent research hotspots were asbestos prevention and research on asbestos-induced carcinogenesis at the cellular level.
• The authors' conclusion: The authors concluded that the Mendelian randomization approach suggested a potential causal relationship between occupational asbestos exposure and lung adenocarcinoma, while no causal link was found with overall lung cancer or other subtypes. They also concluded that the burden is projected to continue declining through 2036, consistent with the expected impact of asbestos restrictions.
• Limitations the authors state:
  • The bibliometric analysis was restricted to publications from 2008 onward, so earlier studies were not included.
  • The genetic analysis mainly used data from European populations, which limits how far the findings apply to other populations.
  • Statistical power was limited because the subtype-specific genetic datasets were smaller, and the genetic instruments were proxies of modest strength.
  • Burden estimates depend on cancer registry quality. The Global Burden of Disease data cannot separate lung cancer from tracheal and bronchus cancers or analyze histological subtypes.
  • Global Burden of Disease figures are model-derived approximations, not direct registry counts, and uncertainty is higher in regions with weaker surveillance.
  • The study examined asbestos exposure only, without considering interactions with other risk factors.
  • The genetic findings were not independently validated in another cohort or dataset.

Topics

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Lung Cancer, Lung Adenocarcinoma, Odds Ratio, confidence interval.

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