Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2024 Dec 7:zwae390.
doi: 10.1093/eurjpc/zwae390. Online ahead of print.

Air Pollution, Genetic Susceptibility, and the Risk of Ventricular Arrhythmias: A prospective cohort study in the UK Biobank

Yun-Jiu Cheng  1 , Chen Zhu  2 , Hai Deng  1 , Yang Wu  3   4 , Hui-Qiang Wei  1 , Wei-Dong Lin  1 , Wulamiding Kaisaier  3   4 , Runkai Li  3   4 , Yili Chen  3   4 , Yugang Dong  3   4 , Xian-Hong Fang  1 , Yi-Jian Liao  5 , Shu-Lin Wu  1 , Hong-Tao Liao  1 , Yu-Mei Xue  1 , Zexuan Wu  3   4
Affiliations

Air Pollution, Genetic Susceptibility, and the Risk of Ventricular Arrhythmias: A prospective cohort study in the UK Biobank

Yun-Jiu Cheng et al. Eur J Prev Cardiol. .

Erratum in

Abstract

Aims: Both genetic and environmental factors contribute to the development of ventricular arrhythmias (VAs). However, the extent to which genetic susceptibility modifies the effects of air pollutants on the risk of VAs remains poorly understood.

Methods: This study included 491,305 participants without VAs at baseline from UK Biobank. Exposure to ambient air pollutants, including particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2) and nitrogen oxides (NOX), was estimated through land use regression modelling. The associations between air pollutants and the incidence of VAs were then investigated using a Cox proportional hazards model adjusted for covariates. Additionally, we established a polygenic risk score (PRS) for VAs and assessed the joint effect of genetic susceptibility and air pollution on incident VAs.

Results: During a median follow-up of 14.3 years, 4,333 participants were diagnosed with VAs. Increased long-term exposure to PM2.5, PM10, NO2 and NOx was significantly associated with higher risks of VAs, with hazard ratios (HR) per quintile increase of 1.07 (95% confidence interval, 95% CI: 1.03-1.11), 1.07 (1.03-1.11), 1.10 (1.06-1.14) and 1.08 (1.05-1.12) for each pollutant respectively. Notably, there were significant additive interactions between air pollutants and genetic risk. Participants with both high genetic risk and high exposure to air pollution exhibited the greatest risk of VAs, with the highest HRs observed for PM2.5 (HR, 4.51; 95% CI, 3.66-5.56), PM10 (HR, 4.28; 95% CI, 3.52-5.22), NO2 (HR, 4.90; 95% CI, 3.97-6.03), and NOx (HR, 4.56; 95% CI, 3.72-5.60), respectively.

Conclusions: Long-term exposure to air pollution is associated with an increased risk of VAs, especially in individuals with a high genetic risk.

Keywords: PM10; PM2.5; UK biobank; air pollution; genetic susceptibility; sudden cardiac arrest; sudden cardiac death; ventricular arrhythmias.

Plain language summary

In a large prospective cohort study involving 491,305 participants from the UK Biobank, we found significant associations between long-term exposure to PM2.5, PM10, NO2, and NOx, and an increased risk of developing ventricular arrhythmias (VAs). Individuals with high genetic risk and high exposure to air pollution exhibited the greatest risk of VAs, highlighting significant additive interactions between air pollutants and genetic predisposition. This study underscores the importance of considering both environmental and genetic factors in the assessment of VA risks, providing novel insights into the synergistic effects of air pollution and genetic susceptibility.

PubMed Disclaimer

Comment in

LinkOut - more resources