Key result
Air pollutant exposure linked to ~1% higher incident arrhythmia risk per 10 μg/m3.
Why the study?
The metabolic mechanisms underlying the association between air pollution and cardiac arrhythmia remain poorly understood.
Does exposure to air pollutants increase the risk of cardiac arrhythmias in individuals without baseline arrhythmia?
Cohort (n=449,068)
Does exposure to air pollutants increase the risk of cardiac arrhythmias in individuals without baseline arrhythmia?
Effect estimate: HR 1.015 to 1.257 per 10 μg/m3
Exposure to air pollution is prospectively associated with increased risks of cardiac arrhythmias, a relationship that is partially mediated by perturbations in lipid, ketone body, and amino acid metabolism.
Air pollution exposure was associated with arrhythmia risk via metabolic pathways; extends mechanistic understanding in large cohorts but remains hypothesis-generating.
Background Air pollution is an established modifiable risk factor for cardiac arrhythmia, yet the metabolic mechanisms underlying this association remain poorly understood. This study aimed to elucidate how air pollutants promote arrhythmias through metabolic pathway perturbations. Methods We conducted a prospective analysis of 449,068 UK Biobank participants without baseline arrhythmia. Exposures to PM 2.5 , PM 10 , NO 2 , and NO x were assessed using land use regression models. Plasma metabolomic profiling including 170 metabolites via 1H-NMR was performed at baseline. Elastic net regression, Cox proportional hazards models, and mediation analysis were employed to identify pollutant-associated metabolic signatures, quantify their mediating effects, and characterize pathway enrichment across different kinds of arrhythmias. Results During a median follow-up of 16.31 years, a total of 47,381 arrhythmia cases were identified. All four pollutants were prospectively associated with increased arrhythmia risk (hazard ratios ranged from 1.015 to 1.257 per 10 μg/m 3 ). The derived metabolomic signatures significantly mediated these associations between different air pollutants and arrhythmia (mediation proportions: PM 2.5 -related, 11.19%; PM 10 -related, 5.19%; NO 2 -related, 7.44%; NO x -related, 9.82%). Pathway enrichment analysis consistently identified lipid metabolism, ketone body metabolism, and amino acid metabolism as core affected pathways. Notably, compared to atrial fibrillation and supraventricular tachycardia, the ketone body metabolic pathway appeared to account for a larger proportion of the association with intraventricular block. Conclusions This study suggests that air pollution increases arrhythmia risk through distinct, subtype-specific metabolic perturbations, providing novel insights into the metabolic pathways linking environmental pollutants to different arrhythmia subtypes.
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Wu et al. (2026) conducted a cohort in arrhythmia (n=449,068). Air pollution (PM2.5, PM10, NO2, NOx) was evaluated on arrhythmia (HR 1.015 to 1.257 per 10 μg/m3). Exposure to air pollutants was associated with increased risk of incident arrhythmia (HRs 1.015 to 1.257 per 10 μg/m3), which was mediated by specific metabolic pathway perturbations.
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