Secondhand tobacco smoke exposure, urine cotinine, and risk of incident atrial fibrillation: The multi-ethnic study of atherosclerosis

Background: Secondhand tobacco smoke (SHS) exposure may reduce heart rate variability and lead to atrial fibrillation (AF); however prior study findings have not been confirmed using objective measures for both SHS and AF events. Methods: We prospectively examined the association between SHS exposure and incident AF in 5731 participants, ages of 45–84 years and free of known AF and other cardiovascular diseases (CVD) at baseline (2000−2002), who were followed through 2015 in the Multi-Ethnic Study of Atherosclerosis (MESA). SHS weekly exposure time was identified by self-report. Urine cotinine was collected in a cohort subset of 3237 current non-smoking cohort participants. AF events were identified using Medicare claims, hospital records, and 12‑lead electrocardiographic findings. A multivariable Cox proportional hazards regression analysis was used with simultaneous adjustment for demographic factors, educational level, health insurance status, active smoking status, tobacco pack-years, traditional CVD risk factors, depressive symptoms and medications. Results: During a median follow-up of 14.0 years, 856 and 452 AF events were identified in the overall and the cohort subset, respectively. No association of SHS exposure time or urine cotinine with incident AF was observed. However, a higher AF risk with greater urine cotinine (8.53–442.0 ng/mL) compared with lower urine cotinine (≤7.07 ng/mL) was observed in never smokers [hazard ratios (HR) and 95% confidence intervals: 1.60 (1.16, 2.19)], but not in former smokers [HR: 0.88 (0.63, 1.23)] (p-value for multiplicative interaction: 0.009 and for additive interaction: 0.017, respectively). Conclusion: Objectively measured greater SHS exposure expressed by urine cotinine might be associated with 1.6-fold higher risk of incident AF in never smokers.