Associations between air pollution, accelerated biological aging, and oral inflammatory diseases: evidence from the UK Biobank cohort
4 affiliations
- 1Department of Dentistry, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology
- 2Medical Big Data and Bioinformatics Research Centre, First Affiliated Hospital of Gannan Medical University
- 3Ganzhou Key Laboratory of Environment and Health, Gannan Medical University
- 4Gannan Subcenter for Medical Genomics, National Genomics Data Center
Abstract
Background: The relationships between air pollution exposure and incident risk of oral inflammatory diseases (OIDs) and roles of accelerated biological aging remain unclear.
Methods: In 348,247 adults from the UK Biobank, the individual levels of air pollutants, including particulate matter (PM) (PM 2.5 , PM ₁₀ , PM 2.5–10, and PM 2.5 absorbance ), nitrogen dioxide (NO ₂ ), nitric oxides (NO x ), and air pollution score (multiple air pollutants exposure), were estimated. The associations between air pollution exposure and incident risk of OIDs were assessed. The mediation roles of the Klemera–Doubal method biological age (KDM-BA) acceleration and the phenotypic age (PhenoAge) acceleration were evaluated.
Results: During the median follow-up of 16.49 years, a total of 3,967 incident OIDs were documented. Each one standard deviation increment in PM 2.5 , PM ₁₀ , PM 2.5–10, PM 2.5 absorbance , NO ₂ , NO x , and air pollution score was significantly associated with 8%, 4%, 3%, 5%, 10%, 8%, and 8% increments in incident risk of OIDs, respectively (all p < 0.05). All air pollutants except PM 2.5–10 were significantly and positively associated with KDM-BA acceleration, and all air pollutants were significantly and positively associated with PhenoAge acceleration (all p < 0.05). KDM-BA acceleration mediated the associations between all air pollution (except PM 2.5–10 ) and incident risk of OIDs, with mediation proportion ranging from 1.21 to 5.42%. PhenoAge acceleration mediated the associations between all air pollutants and incident risk of OIDs, with mediation proportion ranging from 8.52 to 16.65%.
Conclusion: Air pollution may contribute to increased incident risk of OIDs, and premature aging may play an important role in the pathogenic process.
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BibTeX
@article{zhan2026associations,
title = {{Associations between air pollution, accelerated biological aging, and oral inflammatory diseases: evidence from the UK Biobank cohort}},
author = {Hui Zhan and Dong Liu and You Guo and Wei Liu},
journal = {Frontiers in Public Health},
year = {2026},
month = oct,
doi = {10.3389/fpubh.2026.1869182},
url = {https://www.frontiersin.org/articles/10.3389/fpubh.2026.1869182/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Associations between air pollution, accelerated biological aging, and oral inflammatory diseases: evidence from the UK Biobank cohort
AU - Hui Zhan
AU - Dong Liu
AU - You Guo
AU - Wei Liu
PY - 2026
DA - 2026/10/27
JO - Frontiers in Public Health
DO - 10.3389/fpubh.2026.1869182
UR - https://www.frontiersin.org/articles/10.3389/fpubh.2026.1869182/full
AB - Background: The relationships between air pollution exposure and incident risk of oral inflammatory diseases (OIDs) and roles of accelerated biological aging remain unclear. Methods: In 348,247 adults from the UK Biobank, the individual levels of air pollutants, including particulate matter (PM) (PM 2.5 , PM ₁₀ , PM 2.5–10, and PM 2.5 absorbance ), nitrogen dioxide (NO ₂ ), nitric oxides (NO x ), and air pollution score (multiple air pollutants exposure), were estimated. The associations between air pollution exposure and incident risk of OIDs were assessed. The mediation roles of the Klemera–Doubal method biological age (KDM-BA) acceleration and the phenotypic age (PhenoAge) acceleration were evaluated. Results: During the median follow-up of 16.49 years, a total of 3,967 incident OIDs were documented. Each one standard deviation increment in PM 2.5 , PM ₁₀ , PM 2.5–10, PM 2.5 absorbance , NO ₂ , NO x , and air pollution score was significantly associated with 8%, 4%, 3%, 5%, 10%, 8%, and 8% increments in incident risk of OIDs, respectively (all p < 0.05). All air pollutants except PM 2.5–10 were significantly and positively associated with KDM-BA acceleration, and all air pollutants were significantly and positively associated with PhenoAge acceleration (all p < 0.05). KDM-BA acceleration mediated the associations between all air pollution (except PM 2.5–10 ) and incident risk of OIDs, with mediation proportion ranging from 1.21 to 5.42%. PhenoAge acceleration mediated the associations between all air pollutants and incident risk of OIDs, with mediation proportion ranging from 8.52 to 16.65%. Conclusion: Air pollution may contribute to increased incident risk of OIDs, and premature aging may play an important role in the pathogenic process.
SN - 2296-2565
ER -