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Updated: Sep 10, 2025

Impact Assessment of Repeated Exposure of Organotypic 3D Bronchial and Nasal Tissue Culture Models to Whole Cigarette Smoke
Published on: February 12, 2015
Secondhand tobacco smoke and risk of atrial fibrillation: An observational epidemiologic and gene-environment
Tae-Min Rhee1, Kyung-Yeon Lee2, JungMin Choi3
1Department of Internal Medicine, Seoul National University Hospital, Seoul, Republic of Korea; Department of Internal Medicine, Seoul National University Hospital Healthcare System Gangnam Center, Seoul, Republic of Korea.
Background:
The relationship between secondhand tobacco smoke (SHS) and the risk of incident atrial fibrillation (AF) remains controversial.
Objective:
This study aimed to evaluate the long-term risk of AF associated with SHS exposure and assess potential gene-environment interactions using extensive population-based data.
Methods:
We performed a nationwide population-based cohort study using the UK Biobank database. Participants were categorized into SHS-exposure and nonexposure groups. The primary outcome was the risk of incident AF. We also evaluated the synergistic effect of SHS exposure and the polygenic risk score of AF.
Results:
During a median follow-up of 12.5 years, AF occurred in 23,471 (5.9%). The SHS-exposure group (median exposure 0.5 [0.5-1.5] h/wk) was younger and predominantly male. The risk of AF was significantly higher in the SHS-exposure group (multivariable-adjusted hazard ratio 1.06; 95% confidence interval 1.02-1.09; P = .002) than the nonexposure group, suggesting a dose-dependent manner (adjusted hazard ratio of the severe SHS-exposure group 1.11; 1.04-1.18; P = .001). The risk of AF was higher in the SHS-exposure group regardless of the exposure location (home, outside, or workplace). When SHS exposure was combined with the high genetic risk of AF, a significant additive interaction was observed on the risk of AF (synergy index of SHS exposure with the third tertile of AF polygenic risk score 1.13; 1.05-1.21; P = .024).
Conclusion:
Exposure to SHS is a significant predictor of an increased risk of AF, with a synergistic effect when combined with genetic predisposition. Minimizing SHS exposure, especially in individuals with a heightened genetic susceptibility to AF, may potentially reduce the future risk of AF.
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