Can atrial fibrillation be caused or triggered by air pollution? An epidemiological perspective

Abstract

Atrial fibrillation, the most prevalent sustained cardiac arrhythmia in clinical practice, was designated as an epidemic some 20 years ago. The aging population, improved survival after myocardial infarction and heart failure, and higher awareness and initiatives to enhance detection were among the factors contributing to increasing hospital admission rates for atrial fibrillation, which then seemingly leveled off after the turn of the millennium. Atrial fibrillation carries major clinical and economic implications, and is associated with increased rates of death, stroke and other thromboembolic events, heart failure incidence and hospitalizations, degraded quality of life, reduced exercise capacity, and left ventricular dysfunction. Several recognized risk factors for atrial fibrillation were previously identified, including advanced age, male sex, hypertension, diabetes mellitus, coronary artery disease, heart failure, sleep apnea, sedentary lifestyle, smoking and obesity. Recent risk scores predicting atrial fibrillation development have been proposed, showing moderate discriminatory power (C-statistic 0.75). Notably, these risk scores were based entirely on clinical data, to the exclusion of social and environmental determinants. Air pollution is increasingly recognized as a contributor to cardiovascular disease risk, including cardiac arrhythmias. A few studies have previously suggested a triggering effect of exposure to air pollution on acute exacerbation of atrial fibrillation. Evidence for a long-term (i.e. chronic) effect of air pollution exposure on atrial fibrillation incidence is even more scarce. In the context of a need to better understand the possible environmental determinants of atrial fibrillation in the population and with the recognition that short-term and long-term exposure to air pollution may have different effect, Kwon and colleagues provide a unique and important extension of existing research on the association between exposure to air pollution and atrial fibrillation. In this issue of the European Journal of Preventive Cardiology, they conduct an analysis of both shortand long-term effects of air pollution on atrial fibrillation in Seoul, Korea. For short-term exposure, the association between daily concentrations of air pollution and daily counts of emergency atrial fibrillation admissions was examined (time-series analysis). Hourly concentrations of fine particulate matter <2.5 mm in aerodynamic diameter (PM2.5), PM10, carbon monoxide, sulfur dioxide, nitrogen dioxide and ozone were collected from 27 monitoring stations located in Seoul. Various models were constructed, for each pollutant, according to lag periods of 0–5 days post exposure. Between 2007 and 2015, 1137 episodes of an emergency visit for atrial fibrillation were identified. For long-term exposure, a cohort design was used (median follow-up, 8 years). During this period, among 124,010 subjects (free of atrial fibrillation at baseline) who had resided in Seoul since 2007, 1903 participants developed incident atrial fibrillation. By applying an elegant statistical analysis, the authors concluded there was a differential effect between short-term and long-term exposure to air pollution on atrial fibrillation. A 10 -mg/m increase in PM2.5 level was associated with a significant increase (relative risk, 1.045; 95% confidence interval, 1.002–1.089) in admissions for atrial fibrillation at lag day 3. In contrast, long-term exposure to any air pollutants, including PM2.5, was not associated with the development of new-onset atrial fibrillation. The authors interpreted the results as evidence for lack of chronic effect of exposure to air pollution on atrial remodeling, which is thought to be a key factor in