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

Abstract

BackgroundSecondhand 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. MethodsWe 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. ResultsDuring 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). ConclusionObjectively measured greater SHS exposure expressed by urine cotinine might be associated with 1.6-fold higher risk of incident AF in never smokers.