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Boston, Massachusetts: A new study (1) evaluating the link between air pollution and atrial fibrillation (AF) demonstrated that acute exposure to air pollutants was associated with AF. This study showed that AF events were likely when there was prior exposure to fine particle mass with likelihood increasing with increase in prior exposure to fine particle mass.
Air pollution is associated with increased risk of sudden cardiac death, myocardial infarction, heart failure and stroke. Studies have shown that air pollution can increase the incidence of ventricular arrhythmias and atrial premature beats. This new study evaluated whether acute exposure to air pollution was a trigger for AF.
Patients with (1) dual chamber ICD, (2) residing within 50 Km radius of Harvard Supersite air quality monitoring station and (3) who were followed for at least 90 days were included in the study. Patients (a) younger than 18 years, (b)with chronic AF, or (c) who were being followed at Tufts Medical Center were excluded from the study. ICD interrogation was performed every 3 months. AF episodes lasting greater than 30 seconds were included for analysis. Hourly measurements of fine particle mass (PM2.5), black carbon (BC), PNC (number of particles per cm3), sulfate (SO4), sulfur dioxide (SO2), nitrogen dioxide (NO2) and ozone (O3) in Boston metropolitan area were collected. This study was designed in a case-crossover manner. Case period was defined as subject’s exposure before the onset of AF varying in duration from 2 hours to 48 hours (2 hr, 4 hr, 8hr, 24hr, and 48 hr) before AF. Control period was the identical duration of subject’s exposure on the same weekday and hour in the same calendar month. Therefore each subject was his/her own control. Air pollutant levels during case and control periods were compared and odds of AF with air pollution exposure were calculated.
A total of 1,143 patients were screened of which 843 patients were excluded. Of the remaining 300 patients, 176 patients were followed for more than 90 days. ICD interrogation of these 176 patients revealed 328 AF episodes in 49 patients (mean number of AF events: 6.7). Air pollutant exposure of 49 patients alone was used for analysis as this was a case crossover design.
Mean PM2.5 during study period extending from September 2006 to March 2010 was 8.4 µg/m3 (currently accepted EPA standard: 35 µg/m3). The odds of AF increased by 14% with each 5 µg/m3 increase in 24 hour PM2.5 exposure. Increased odds of PM2.5 (26%) and BC (16%) were observed for case/control period of 2 hours but there was no significant difference for case/control period of 24 hours( PM2.5 : 14 %, p=0.12; BC: 6%, p=0.47) prior to the event. There was no significant difference in exposure to NO2, PNC, sulfate, SO2, NO2 and O3(for any duration of case/control period). In those living closer than 26 km from air pollution monitoring site, stronger association was demonstrated with PM2.5, BC and NO2 (only for case/control period of 2 hour). No association of air pollution exposure and AF was demonstrated for 24 hour and 48 hour case/control period for any air pollutants (PM2.5, BC, NO2, PNC, sulfate, SO2, NO2 and O3.
This is an interesting study which demonstrates that acute exposure to fine particle mass is associated with AF. This observational study demonstrates association and not causal relationship between air pollutants and AF. There was no association between average exposure of air pollutants for 24 hours preceding the event and AF. There was correlation only for 2 hour average exposure levels of fine particle mass and AF. This was a dose dependant association i.e., the AF event was more likely with higher levels of prior exposure to fine particle mass. This association might be due to chance or a true causality. Further studies in animals are required to demonstrate whether air pollutants cause AF.
Reference: 1. Link MS, Luttmann-Gibson H, Schwartz J, Mittleman MA, Wessler B, Gold DR, et al. Acute exposure to air pollution triggers atrial fibrillation. Journal of the American College of Cardiology. 2013;62(9):816-25. Epub 2013/06/19. doi: 10.1016/j.jacc.2013.05.043. PubMed PMID: 23770178; PubMed Central PMCID: PMCPMC3752319.
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