Association of ozone and particulate air pollution with out-of-hospital cardiac arrest in Helsinki, Finland: Evidence for two different etiologies

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Abstract
Out-of-hospital cardiac arrest (OHCA) has been previously associated with exposure to particulate air pollution. However, there is uncertainty about the agents and mechanisms that are involved. We aimed to determine the association of gases and particulates with OHCA, and differences in pollutant effects on OHCAs due to acute myocardial infarction (AMI) vs those due to other causes. Helsinki Emergency Medical Services provided data on OHCAs of cardiac origin (OHCA_Cardiac). Hospital and autopsy reports determined whether OHCAs were due to AMI (OHCA_MI) or other cardiac causes (OHCA_Other). Pollutant data was obtained from central ambient monitors. A case-crossover analysis determined odds ratios (ORs) for hourly lagged exposures (Lag 0–3) and daily lagged exposures (Lag 0d–3d), expressed per interquartile range of pollutant level. For OHCA_Cardiac, elevated ORs were found for PM2.5 (Lag 0, 1.07; 95% confidence interval (CI): 1.01–1.13) and ozone (O3) (Lag 2d, 1.18; CI: 1.03–1.35). For OHCA_MI, elevated ORs were found for PM2.5 (Lag 0, 1.14; CI: 1.03–1.27; Lag 0d, 1.17; CI: 1.03–1.33), accumulation mode particulate (Acc) (Lag 0d, 1.19; CI: 1.04–1.35), NO (Lag 0d, 1.07; CI: 1.01–1.13), and ultrafine particulate (Lag 0d, 1.27; CI: 1.05–1.54). For OHCA_Other, elevated ORs were found only for O3 (Lag 1d, 1.26; CI: 1.07–1.48; Lag 2d, 1.30; CI: 1.11–1.53). Results from two-pollutant models, with one of the pollutants either PM2.5 or O3, suggested that associations were primarily due to effects of PM2.5 and O3, rather than other pollutants. The results suggest that air pollution triggers OHCA via two distinct modes: one associated with particulates leading to AMI and one associated with O3 involving etiologies other than AMI, for example, arrhythmias or respiratory insufficiency.

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