Heart in the midst of smog: the impact of air pollution on atrial fibrillation triggering (EP-PARTICLES Study)

Abstract Background Atrial fibrillation (AF) is the most common arrhythmia and environmental conditions are one of its risk factors. With the ever-increasing burden of air pollution and the concomitant rise in atrial fibrillation cases, understanding and addressing this nexus holds significant implications for both clinical management and public health interventions. Aim To assess the relationship between air pollution and the occurrence of acute AF episodes. Material and methods The spatio-temporal analysis was performed on the EP-PARTICLES cohort constructed of residents of Eastern Poland (N= 8,077,671). Data on hospitalizations for 2011-2020 were obtained from regional departments of the National Health Fund. In the statistical analysis, a time series Poisson regression models were used. Results are presented as % increases of admissions - % IR, 95% confidence intervals - 95% CI. Results During the 10-year period, 311,645 hospitalizations due to AF were reported, including 252,566 acute admissions which were included in the final analysis. Each 10 µg/m3 increment of PM2.5 and NO2 concentration, 1 µg/m3 of SO2 and 10 ng/m3 of BaP concentration on the day of exposure resulted in a 1.13% (0.70%−1.55%), 1.65% (1.05%−2.26%), 0.11% (0.01%−0.21%), and 0.3% (0.04%−0.55%) increase in acute AF admissions, respectively. This effect persisted for up to 4 days and was more pronounced in women and older population. A 10 mg/m3 increase in PM2.5 increased AF admissions by 1.5% (95%CI 1.010-1.020) in less urbanized areas vs. 0.4% (0.996-1.012) in the highly urbanized ones. In a single-pollutant model, the relative risk in daily AF cases change per 10 μg/m3 increase in PM2.5 was 1.1%. This effect remained significant at the same level after the adjustment to BaP (1.011, 1006-1016), SO2 (1.011, 1.007-1.016), and NO2 (1.007, 1.003-1.012) in the two-pollutant model. PM2.5 showed a significantly stronger effect on AF during the days in which PM2.5 concentrations did not exceed WHO standards resulting in a 5.1% increase in AF admissions, in contrast to days when the norms were exceeded resulting in a 0.8% increase. Non-linear effects in the exposure-response functions were observed with steeper slopes of the pollutant-outcome associations in the lower ranges of exposures, which were far below the WHO air quality guidelines for daily mean of PM2.5 (15 mg/m3) and NO2 (10µg/m3). For the PM2.5 zero-emission scenario, we estimated 5,873 avoidable AF admissions (95% CI 3,679 to 8,047), as for NO2 - 3,295 avoidable AF admissions (2,108-4,477). Conclusions Air pollution, especially PM2.5 and NO2, acts as a triggering factor and is associated with acute AF incidents. The greater increase in acute AF episodes at pollutant concentrations below the WHO norms suggests that there is no safe level of pollution and any reduction in exposure, even at low levels, is crucial for effective cardiac prevention. Graphical abstract