Acute Exposure to Air Pollution Triggers Atrial Fibrillation
What is the role of exposure to acute air pollution as an acute trigger of atrial fibrillation (AF) in patients with continuous monitoring of atrial arrhythmias through implantable devices over an extended period of follow-up?
This was a prospective study of 176 patients with dual-chamber implantable cardioverter-defibrillators (ICDs) followed for an average of 1.9 years. ICD data were interrogated for electrograms of atrial and ventricular events when patients were followed with either a clinic visit or by telephone; these arrhythmias were later reviewed and interpreted by an electrophysiologist blinded to air quality. The authors restricted the analyses to AF lasting 30 seconds or longer. The association of AF onset with components of air quality—ambient fine particulate matter (PM2.5), black carbon (BC), sulfate, particle number (PNC), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone—in the 24 hours prior to the arrhythmia were examined using a case-crossover analysis. Associations with mean air pollution for the prior 2, 6, 12, and 48 hours were examined in sensitivity analyses.
The odds of AF increased by 26% (95% confidence interval, 8-47%) for each 6.0 µg/m3 increase in PM2.5 in the 2 hours preceding the onset of AF (p = 0.004). There was effectively no association with mean over the previous 48 hours. Similar patterns were observed for BC, NO2, and PNC.
The authors concluded that aspects of air pollution and, in particular, particulate matter, which include direct motor vehicular emissions, were associated with increased odds of onset of AF within hours following exposure.
Previous studies have established associations between air pollution and cardiovascular health. This prospective analysis, with its limitations aside, extends these findings by demonstrating that air pollution is an acute trigger of AF. As the authors indicate and of particular concern, the higher odds of AF were observed at air quality levels well under ambient air quality standards prescribed by the Environmental Protection Agency (EPA). Indeed, the risk of AF following acute exposure to air pollution may be even higher in cities with particularly high levels of air pollution, as the average PM2.5 during the study period was <60% of the current EPA annual average standard of 15 µg/m3.
Keywords: Soot, Cities, Follow-Up Studies, United States Environmental Protection Agency, Heart Conduction System, Particulate Matter, Nitrogen Dioxide, Transcription Factors, Carbon, Ozone, Sulfur Dioxide, Vehicle Emissions, United States, Defibrillators, Implantable
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