European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery · 2025
Air Pollution, Genetic Susceptibility, and Risk of Symptomatic Peripheral Arterial Disease: A Cohort Study of the UK Biobank.
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Li Chenshu, Qiu Peng, Guo Hongbin, Ying Xiaoliang, Liu Kailang, Sun Pin, Wu Hai, Zhan Yanqing, Wang Ruihua, Zhou Zhen
Аннотация
OBJECTIVE: This study aimed to investigate the relationship between exposure to various air pollutants and the risk of symptomatic peripheral arterial disease (PAD) and to explore whether the association is modified by genetic predisposition to PAD.
METHODS: A prospective cohort study was conducted using data from the UK Biobank. The analysis included individuals without a history of PAD at baseline and with available data for air pollutants and covariables. Data from 1 June to 17 July 2024 were analysed. Exposures of interest included nitrogen dioxide, total nitrogen oxides, and particulate matter with an aerodynamic diameter of < 2.5 μm, 2.5 - 10 μm, and < 10 μm. Symptomatic PAD was identified through International Classification of Diseases code, operation code, and self report. Multivariable Cox proportional hazards models were used for outcome analysis. Subgroup analysis was performed by the levels of genetic susceptibility to PAD.
RESULTS: This study included 377 163 participants. The mean standardised age was 56.19 ± 8.1 years and 52.3% (n = 197 404) were women. The cohort was predominantly White (94.8%; n = 357 375). Over a median follow up duration of 15.21 years (interquartile range 14.44, 15.88), 5 715 new cases of symptomatic PAD were recorded. A positive association was observed between exposure to all air pollutants and the risk of symptomatic PAD (all p values < .050). No significant interaction between genetic risk, as determined by the PAD polygenic risk score, and any air pollutant was observed in relation to PAD risk.
CONCLUSION: The findings revealed a significant association between exposure to air pollutants and a heightened risk of symptomatic PAD, regardless of an individual's genetic risk. These findings reinforce the current consensus that enhancing air quality is crucial for mitigating the prevalence of PAD and other cardiovascular diseases.
METHODS: A prospective cohort study was conducted using data from the UK Biobank. The analysis included individuals without a history of PAD at baseline and with available data for air pollutants and covariables. Data from 1 June to 17 July 2024 were analysed. Exposures of interest included nitrogen dioxide, total nitrogen oxides, and particulate matter with an aerodynamic diameter of < 2.5 μm, 2.5 - 10 μm, and < 10 μm. Symptomatic PAD was identified through International Classification of Diseases code, operation code, and self report. Multivariable Cox proportional hazards models were used for outcome analysis. Subgroup analysis was performed by the levels of genetic susceptibility to PAD.
RESULTS: This study included 377 163 participants. The mean standardised age was 56.19 ± 8.1 years and 52.3% (n = 197 404) were women. The cohort was predominantly White (94.8%; n = 357 375). Over a median follow up duration of 15.21 years (interquartile range 14.44, 15.88), 5 715 new cases of symptomatic PAD were recorded. A positive association was observed between exposure to all air pollutants and the risk of symptomatic PAD (all p values < .050). No significant interaction between genetic risk, as determined by the PAD polygenic risk score, and any air pollutant was observed in relation to PAD risk.
CONCLUSION: The findings revealed a significant association between exposure to air pollutants and a heightened risk of symptomatic PAD, regardless of an individual's genetic risk. These findings reinforce the current consensus that enhancing air quality is crucial for mitigating the prevalence of PAD and other cardiovascular diseases.