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Association of air pollution exposure and genetic susceptibility with increased risk of thoracic aortic aneurysm and dissection

Nature Cardiovascular Research (2025)Cite this article

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Abstract

Thoracic aortic aneurysm and dissection (TAAD) represent a serious health threat, yet the role of air pollution exposure on its development has been underexplored. Here we investigate the relationships between air pollutants and TAAD incidence. In a Cox’s proportional hazards model, hazard ratios (95% confidence intervals) of TAAD for an interquartile range increase in air pollutants were 2.15 (1.96, 2.35) for particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5; per 2.15 μg m−3 increase), 1.76 (1.61, 1.92) for PM10 (per 2.99 μg m−3 increase), 1.45 (1.34, 1.58) for NO2 (per 6.97 μg m−3 increase) and 1.40 (1.29, 1.51) for NOx (per 11.58 μg m−3 increase). These estimates remained consistent when using inverse probability weighting and generalized propensity score methods. Furthermore, this study revealed potential joint effects and interactions between air pollutants and genetic susceptibility on TAAD risk, especially the multiplicative and additive interactions between PM2.5 and genetic susceptibility. Air pollution exposure is associated with an increased TAAD risk and genetic susceptibility modifies this association.

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Fig. 1: Associations of air pollutants exposure with the risk of incident TAAD.
Fig. 2: The joint associations of long-term PM2.5 and PM10 exposure and genetic risk with the risk of incident TAAD.
Fig. 3: The joint associations of long-term NO2 and NOx exposure and genetic risk with the risk of incident TAAD.

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Data availability

Data from the UK Biobank are available upon application. The UK Biobank is an open research resource, available after submission of a research plan via the website (https://www.ukbiobank.ac.uk). Air pollution data (2006–2021) were provided by DEFRA (https://uk-air.defra.gov.uk).

Code availability

Codes utilized for analyses have been made available through the GitHub repository at https://github.com/MoooDylan/Ma_TAAD_air-pollution.

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Acknowledgements

This work was supported by the National Natural Science Foundation of China (grant no. 824B2102) and the Opening Project of Hubei Key Laboratory of Ischemic Cardiovascular Disease (grant no. SZ202402). We thank all the staff and participants of the UK Biobank and DEFRA for their hard work and dedication in collecting the underlying data.

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Authors and Affiliations

  1. Ministry of Education Key Laboratory of Environment and Health, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

    Yudiyang Ma, Jianing Wang, Linxi Tang, Feipeng Cui, Lei Zheng, Meiqi Xing & Yaohua Tian

  2. Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

    Yudiyang Ma, Jianing Wang, Linxi Tang, Feipeng Cui, Lei Zheng, Meiqi Xing & Yaohua Tian

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Contributions

Y.H.T. and Y.D.Y.M. contributed to the conception and design of the study, advised on all statistical aspects and interpreted the data. Y.D.Y.M., J.N.W., L.X.T., F.P.C., L.Z., M.Q.X. and Y.H.T. performed the literature search and the analyses. All authors critically reviewed this and previous drafts; all approved the final version of the manuscript; and all approved the final draft for submission, with final responsibility for publication. The corresponding author attests that all the listed authors meet authorship criteria and that no others meeting the criteria have been omitted.

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Correspondence to Yaohua Tian.

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Extended data

Extended Data Fig. 1 Distribution of the GPS for the high and low air pollutants exposure groups.

Abbreviations: GPS, generalized propensity score; PM2.5, particulate matter with diameter <2.5 μm; PM10, particulate matter with diameter <10 μm; NO2, nitrogen dioxide; NOx, nitrogen oxides.

Source data

Extended Data Fig. 2 Mean absolute correlation for Cox proportional hazards model and weighted Cox proportional hazards model.

Covariate balance was evaluated using mean AC, with AC < 0.1 indicating good balancing for covariates included in the analyses. Abbreviations: AC, absolute correlation; PM2.5, particulate matter with diameter <2.5 μm; PM10, particulate matter with diameter 10 μm; NO2, nitrogen dioxide; NOx, nitrogen oxides; BMI, body mass index; TDI, Townsend deprivation index.

Source data

Extended Data Fig. 3 Associations of long-term PM2.5, PM10, NO2, and NOx exposure with the risk of TAAD in the UK Biobank examined using the Fine-Gray proportional sub-distribution hazards model.

Cumulative incidence curves were plotted using the cumulative incidence function as implemented in the ‘cmprsk’ R package. Abbreviations: PM2.5, particulate matter with diameter <2.5 μm; PM10, particulate matter with diameter <10 μm; NO2, nitrogen dioxide; NOx, nitrogen oxides; TAAD, thoracic aortic aneurysm and dissection.

Source data

Extended Data Fig. 4 Associations of PRS with the risk of TAAD in the UK Biobank examined using the Fine-Gray proportional sub-distribution hazards model.

Cumulative incidence curves were plotted using the cumulative incidence function as implemented in the ‘cmprsk’ R package. Abbreviations: PRS, polygenic risk score; TAAD, thoracic aortic aneurysm and dissection.

Source data

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Ma, Y., Wang, J., Tang, L. et al. Association of air pollution exposure and genetic susceptibility with increased risk of thoracic aortic aneurysm and dissection. Nat Cardiovasc Res (2025). https://doi.org/10.1038/s44161-025-00719-w

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