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Ambient air pollution, genetic risk and telomere length in UK biobank



Telomere length (TL) is a biomarker of genomic aging. The evidence on the association between TL and air pollution was inconsistent. Besides, the modification effect of genetic susceptibility on the air pollution-TL association remains unknown.


We aimed to evaluate the association of ambient air pollution with TL and further assess the modification effect of genetic susceptibility.


433,535 participants with complete data of TL and air pollutants in UK Biobank were included. Annual average exposure of NO2, NOx, PM10 and PM2.5 was estimated by applying land use regression models. Genetic risk score (GRS) was constructed using reported telomere-related SNPs. Leukocyte TL was measured by quantitative polymerase chain reaction (qPCR). Multivariable linear regression models were employed to conduct associational analyses.


Categorical exposure models and RCS models both indicated U-shaped (for NO2 and NOx) and L-shaped (for PM10 and PM2.5) correlations between air pollution and TL. In comparison to the lowest quartile, the 2nd and 3rd quartile of NO2 (q2: −1.3% [−2.1%, −0.4%]; q3: −1.2% [−2.0%, −0.3%], NOx (q2: −1.3% [−2.1%, −0.5%]; q3: −1.4% [−2.2%, −0.5%]), PM2.5 (q2: −0.8% [−1.7%, 0.0%]; q3: −1.3% [−2.2%, −0.5%]), and the third quartile of PM10 (q3: −1.1% [−1.9%, −0.2%]) were inversely associated with TL. The highest quartile of NO2 was positively correlated with TL (q4: 1.0% [0.0%, 2.0%]), whereas the negative correlation between the highest quartile of other pollutants and TL was also attenuated and no longer significant. In the genetic analyses, synergistic interactions were observed between the 4th quartile of three air pollutants (NO2, NOx, and PM2.5) and genetic risk.

Impact statement

Our study for the first time revealed a non-linear trend for the association between air pollution and telomere length. The genetic analyses suggested synergistic interactions between air pollution and genetic risk on the air pollution-TL association. These findings may shed new light on air pollution’s health effects, offer suggestions for identifying at-risk individuals, and provide hints regarding further investigation into gene-environment interactions.

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Fig. 1: Association curve of air pollutants and telomere length.
Fig. 2: The association of air pollutants with telomere length, stratified by GRS categories.

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Data availability

All data are available on the aforementioned public repository and are accessible with permission from the corresponding data committee. No restrictions on data availability other than those imposed by the corresponding data committee.


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We are grateful to all the staff and participants in the UK Biobank for their contributions to this study. This research has been conducted using the UK Biobank resource under application number 69741.

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Authors and Affiliations



YHT and LXT conceived and designed the study. DKL prepared the data. LXT conducted the data analysis and drafted the manuscript. YHT, BBS and JNW revised the manuscript. All authors agreed on the final version of the manuscript and take responsibility for its content.

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Correspondence to Binbin Su or Yaohua Tian.

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The authors declare no competing interests.

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UK Biobank received ethical approval from the North West Multi-centre Research Ethics Committee (REC reference: 16/NW/0274).  

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Tang, L., Li, D., Wang, J. et al. Ambient air pollution, genetic risk and telomere length in UK biobank. J Expo Sci Environ Epidemiol (2023).

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