Key result
PM2.5 exposure linked to ~16% higher acute cerebrovascular event risk in AF patients.
Why the study?
Patients with nonvalvular atrial fibrillation are at increased risk of cerebrovascular events, yet no prior reports had addressed their susceptibility to air pollution exposure and its impact on event incidence.
Does exposure to air pollution (PM2.5, NO₂, B(a)P, and SO₂) increase the risk of acute cerebrovascular events in patients with nonvalvular atrial fibrillation?
Cohort (n=20,757)
Does exposure to air pollution (PM2.5, NO₂, B(a)P, and SO₂) increase the risk of acute cerebrovascular events in patients with nonvalvular atrial fibrillation?
Short-term increases in ambient air pollutants (PM2.5, B(a)P, SO₂, and NO₂) significantly elevate the risk of ischemic stroke, TIA, and stroke-related death in patients with nonvalvular atrial fibrillation, particularly among women and the elderly.
Background Patients with nonvalvular atrial fibrillation (NVAF) are at increased risk of cerebrovascular events; however, to date, there are no reports addressing the susceptibility of this patient population to air pollution (AP) exposure and its impact on these events’ incidence. The aim of our study was to assess the impact of exposure to AP in an AF cohort. Methods The adult population of the Podlaskie Voivodeship in Poland in 2014 was included in the study. A cohort of patients with NVAF was identified and followed for 6 years through the end of 2019. Poisson regression was used to evaluate the association between exposure to AP and the risk of the primary and secondary endpoints [Figure 1]. AP exposure was defined as a daily increase of 10 µg/m³ for PM2.5 and NO₂ and 1 µg/m³ for benzo(a)pyrene [B(a)P] and SO₂. Results The final study cohort included 20,757 NVAF patients [median age 75 years (IQR 66-81); 52.9% women]. The most common comorbidities were hypertension (86.9%), heart failure (63.7%), and chronic coronary syndrome (36.5%). The median CHA₂DS₂-VASc and HAS-BLED scores were 4 and 2, respectively. Over a 6-year follow-up, a total of 3,139 primary endpoints were observed: 2,370 ischemic strokes (IS), 782 transient ischemic attacks (TIA), and 733 IS-related deaths. Increase of PM2.5, SO2 and B(a)P were associated with increased risk of primary endpoint in the overall AF cohort, with higher effects in elderly and in women [Figure 2]. For PM2.5, the same pattern was observed for TIA (overall: RR 1.155; 95% CI 1.049–1.272; p=0.003; ≥65 years: RR 1.163; 95% CI 1.049–1.289; p=0.004; women: RR 1.158; 95% CI 1.027–1.305; p=0.016), while for IS, a significant association was present only in elderly. Exposure to NO₂ increased risk of TIA in the overall cohort (RR 1.171; 95% CI 1.016–1.349; p=0.029) and in elderly (RR 1.211; 95% CI 1.044–1.404; p=0.011). Exposure to both SO₂ and B(a)P were associated with increased risks of IS and TIA in the overall cohort, elderly, and women, with effect estimates ranging from RR 1.026 to 1.045 for SO₂ (p≤0.029) and from RR 1.062 to 1.095 for B(a)P (p≤0.015). Notably, NO₂ was the only pollutant significantly associated with increased IS-related mortality, and this effect was observed exclusively in women (RR 1.217; 95% CI 1.010–1.465; p=0.039). PM2.5 and B(a)P showed stronger effects on the primary endpoint in elderly and women (all pinteraction<0.001). Conclusions Exposure to AP, particularly PM2.5, B(a)P, and SO₂, is associated with an increased risk of acute cerebrovascular events in patients with AF. Women and elderly individuals appear to be especially vulnerable phenotypes. Patients with AF should monitor smog forecasts and limit exposure during periods of elevated AP, and highlighting the need for system-level interventions and public health policies to reduce ambient AP and associated cerebrovascular risk in this population.Study design.Air pollution and primary endpoint risk.
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Święczkowski et al. (2026) conducted a cohort in Nonvalvular atrial fibrillation (NVAF) (n=20,757). Air pollution exposure (PM2.5, NO2, B(a)P, SO2) was evaluated on Composite of ischemic stroke (IS), transient ischemic attack (TIA), and IS-related deaths (RR 1.155, 95% CI 1.049-1.272, p=0.003). Air pollution exposure (PM2.5, SO2, B(a)P) increased acute cerebrovascular events in AF patients, with PM2.5 raising TIA risk (RR 1.155; 95% CI 1.049-1.272; p=0.003).
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