Exposure to air pollution is associated with the onset of symptomatic arrhythmia within a few hours, new data indicate.
In a nationwide case–crossover study of almost 200,000 people in China, an increase in nitrogen dioxide (NO2) concentration was associated with an 11.4% increase in the risk for atrial flutter. Sulfur dioxide (SO2) and carbon monoxide (CO) also were associated with increased risk for atrial fibrillation, atrial flutter, and supraventricular tachycardia (SVT) within 24 hours of exposure.
“Our study provides novel evidence that hourly exposures to air pollutants may immediately trigger the episodes of multiple types of arrhythmia,” senior author Renjie Chen, PhD, professor of public health at Fudan University in Shanghai, China, told Medscape Medical News. “We further found the risks were still present even at very low air pollution levels.”
The data were published today in the Canadian Medical Association Journal.
Researchers at more than a dozen institutions in China conducted a retrospective study of 190,115 patients in the Chinese Cardiovascular Association Database with acute onset of symptomatic arrythmia between 2015 and 2021. Only data collected from 2025 hospitals with chest pain centers certified by the National Chest Pain Center Program in 322 cities were included in the analysis.
The study used a time-stratified, case–crossover design to evaluate the association between hourly exposure to ambient air pollution and the onset of arrhythmia symptoms. This approach “has been widely used in epidemiological studies of air pollution,” according to the investigators.
The researchers captured hourly concentrations of the following six pollutants:
Data were obtained from the National Urban Air Quality Real-time Publishing Platform. The researchers calculated concentrations of PM2.5–10 by subtracting the concentrations of PM2.5 from those of PM10 at the same station. They calculated the odds of arrhythmia onset using the interquartile range increase in the concentration of air pollutants — the difference between the 75th and 25th percentiles of increase in concentration.
Among the study population, 96,133 had atrial fibrillation, 5300 had atrial flutter, 41,613 had overall premature beats and 47,069 had SVT. Average age was 64 years.
The investigators calculated 24-hour concentrations of 34.4 μg/m3 for PM2.5, 25.5 μg/m3 for PM2.5–10, 27.5 μg/m3 for NO2, 8.9 μg/m3 for SO2, 0.7 mg/m3 for CO, and 59 μg/m3 for O3. The average 24-hour temperature was 17.5 °C (63.5 °F).
An interquartile range increase in PM2.5, NO2, SO2, and CO in the first 24 hours after exposure was associated with significantly higher odds of atrial fibrillation (1.7% to 3.4%), atrial flutter (8.1% to 11.4%), and SVT (3.6% to 8.9%). Exposure to PM2.5–10 was associated with significantly increased odds of atrial flutter (8.7%) and SVT (5.4%). Exposure to O3 was associated with higher odds of SVT (3.4%).
The researchers conducted a supplemental analysis to account for other potential exposures that patients encountered. “Specifically, in addition to single-pollutant models, we fit pairwise two-pollutant models to control for potential confounding of another pollutant, and the results were still robust,” said Chen.
Healthcare professionals can use this information when managing patients at risk for arrhythmias. “When encountering a day of apparent air pollution, cardiologists or public health professionals may provide alertness for arrhythmia patients to reduce the risk of symptom exacerbations,” said Chen. “Some effective intervention measures may include using air purifiers indoors and wearing a respirator outdoors.”
The findings emphasize the importance of addressing air pollution as a public health concern and taking necessary measures to reduce exposure to harmful pollutants, said Chen. “The present study also emphasizes the need for incorporating air pollution reduction into the prevention and intervention strategies for arrhythmia patients.”
Commenting on the study for Medscape, Adrian Baranchuk, MD, professor of medicine at Queen’s University in Kingston, Ontario, and president-elect of the Interamerican Society of Cardiology, praised its methodology because it analyzed multiple pollutants and evaluated air pollution exposure within a specific time point. The researchers “did a terrific job of eliminating some of the classic confounders,” he added.
Nevertheless, “the results of this study are difficult to conceptualize from a cardiac electrophysiology perspective, and this is where I think we find the weakest point of this contribution,” said Baranchuk, who has studied the social determinants of atrial fibrillation, including air pollution.
Although air pollution is a well-known trigger of atrial fibrillation, even in people with normal cardiac rhythm, atrial flutter and SVT are less prone to external triggers and more closely linked to anatomical factors. “The explanation in the paper of how air pollution was more associated with the two arrhythmias that do require an anatomical substrate is weak,” said Baranchuk.
The finding regrading atrial flutter and SVT “is interesting,” he added, “but this needs to be explained in a different manner and not be inserted as one more finding in the study.”
The study received funding support from the National Key Research and
Development Program, Shanghai Committee of Science and Technology, the National Natural Science Foundation of China, and the Shanghai Clinical Research Center for Interventional Medicine . Chen and Baranchuk reported no relevant financial relationships.
CMAJ. Published May 1, 2023. Full text
Richard Mark Kirkner is a medical journalist based in the Philadelphia area.