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Air pollution, climate and cardiac arrest
  1. Neal Chatterjee
  1. Electrophysiology Section, Division of Cardiology, University of Washington, Seattle, Washington, USA
  1. Correspondence to Dr Neal Chatterjee, University of Washington, Seattle, WA 98195-0005, USA; nchatter{at}cardiology.washington.edu

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Sudden cardiac death (SCD) refers to a sudden or unexpected death or arrest attributable to a cardiovascular cause. SCD is estimated to account for 15%–20% of global mortality and the majority of these deaths are out-of-hospital cardiac arrests (OHCAs).1 Despite secular improvements, the incidence of SCD and OHCA remains high and public health strategies to mitigate its risk are critical.

Air pollution and meteorological factors have long been associated with adverse health outcomes.2 Particular matter (PM) with an aerodynamic diameter of 2.5 µm or less (PM2.5) has been of specific interest as these particles are estimated to be small enough to reach pulmonary alveoli.3 Elevations in PM2.5 have been associated with increased cardiovascular mortality and morbidity, including ventricular arrhythmia and heart failure.4 5 In addition to air pollution, meteorological factors such as temperature variability have also been linked to cardiovascular mortality, with emerging evidence that air pollution and meteorological perturbations may act synergistically to increase OHCA risk.6

In this issue of Heart, Kim and colleagues7 present a time-series analysis of approximately 39 000 OHCAs in Korea, between 2012 and 2016. Time-series analyses use daily measures of health outcomes, in this instance OHCA, and regress against exposures of interest, which in this study included 13 meteorological factors and PM2.5. In time-series analyses, the population serves as its own control with minimal confounding, as relevant demographic and comorbidity factors are unlikely to change over a short time span. Meteorological and pollution indices were measured (hourly) at 77 stations across Korea and …

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Footnotes

  • Twitter @Nchatterjeemd

  • Contributors I am the sole author of this work.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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