We found an association between ambient fine particle concentrations and out-of-hospital cardiac arrests in New York City. For an increase of 10 μg/m3
, there was a 4%–10% increase in the number of arrests. This study indicates that the consequences of air pollution can be acute and severe. Since an out-of-hospital arrest is usually fatal, with approximately 5% of patients surviving to hospital discharge, an increase in cardiac arrests can be considered an increase in cardiac fatalities. The likelihood of being resuscitated from an out-of-hospital cardiac arrest in large metropolitan areas is among the lowest, with survival ranging from about 1% to 3% (24
A number of previous studies have linked short-term exposure to PM with the development of acute ischemic heart disease and dysrhythmia. The possible pathobiologic mechanisms include increased platelet aggregation and clotting potential (26
), inflammatory mediators, and C-reactive protein (27
). PM is associated with dysregulation of the cardiac autonomic nervous system, including increased heart rate and reduced heart rate variability (28
). Among individuals at high risk for sudden death with implanted defibrillators, an increased frequency of recorded ventricular dysrhythmias occurs with increasing ambient pollution (29
). Short-term exposure to PM is also associated with myocardial infarction, and the risk for an acute infarction increases with greater exposure (31
The data that implicate PM as a risk factor for acute coronary ischemia support our findings of PM2.5
as a risk for cardiac arrest, since sudden cardiac arrest most typically occurs in individuals with underlying ischemic heart disease (33
). Those with known coronary artery disease, as well as elderly individuals, are more likely to have ST depression when stressed on higher pollution days (PM2.5
or black carbon), suggesting that those most vulnerable to developing ischemia are impacted more by pollution (34
). Additional evidence comes from a controlled study in which men with established coronary heart disease developed acute cardiac ischemia after a brief exposure to dilute diesel exhaust (35
There are conflicting findings in the literature on whether pollution increases the risk of sudden death. Similar to our findings, an analysis in Rome, Italy, of 5,144 cases found associations between PM indices (estimated particle number concentration and particles with an aerodynamic diameter of ≤10 μm, or PM10
) and out-of-hospital cardiac deaths (12
). The link between pollution and particle number concentration was stronger in the elderly. While the particle number concentration was indirectly estimated in that study, it is considered a good surrogate of ultrafine particles (which are produced mostly by local traffic) (36
). Additional support comes from 2 other studies where deaths that occurred outside of hospitals (all-cause mortality) were more strongly associated with air pollution than deaths in hospitals (37
). A study of sudden death from Indianapolis, Indiana, did not find associations between daily PM2.5
and cases (n
= 1,374) but did report associations between the hourly data of PM2.5
exposure and the cardiac arrests witnessed by bystanders (n
= 511) (13
). Since both cardiac arrest and PM2.5
likely have diurnal patterns, such analysis may have more accurate exposure characterization but at the same time may also reflect temporal confounding not present in the daily data.
In contrast, 2 studies of 362 and 1,206 cases from the Seattle, Washington, area that examined out-of-hospital sudden death showed no associations between fine particles (as measured by nephelometer) and cardiac arrests (10
). Associations between fine particles and the onset of acute myocardial infarction (5,793 cases) were evaluated in King County, Washington (39
), and, in contrast to other reports evaluating acute myocardial infarction, no association was found (31
). Since health effects are known to vary by PM composition (and therefore by region), a possible explanation for the lack of association between fine particles and cardiac arrest in the Seattle area may be the local PM composition, which is lower in sulfate and transition metal content than northeast US cities (11
). Further support for region-specific health effects is found in a study of PM2.5
-mortality associations in 27 US cities (40
), where PM2.5
was associated with all-cause mortality in Manhattan (i.e., New York County, the only New York City county analyzed in that study) but not in Seattle.
We found that significant associations between fine particles and out-of-hospital cardiac arrests appear to be found mainly in the warm season. This is consistent with several analyses of PM and all-cause mortality in which the strongest associations were found in summer (40
). The reasons are not known, but there are several possible explanations. The stronger association in the warm season may be related to the higher penetration rate of outdoor PM into indoors (44
). In addition, among studies of specific PM components and mortality in Phoenix, Arizona (45
), and Washington, DC (46
), sulfate-related PM showed the strongest associations among the source-apportioned PM components. One possible explanation is that sulfate particles are more harmful; another potential explanation is that a higher warm-weather rate of photochemical conversion from sulfur dioxide to sulfuric acid may make transition metals more water soluble and therefore more bioavailable to cells (47
We also analyzed cardiac arrests relative to changes in ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide but found that these gaseous pollutants’ associations with cardiac arrest were weaker than that for PM2.5
. In our study, ozone was not significantly associated with out-of-hospital cardiac arrest. This contrasts with the positive and significant association other studies found with ozone for all-cause or circulatory mortality in New York City (9
). One possible explanation is that our study is far smaller in terms of daily counts (~4.4 cardiac arrest/day) compared with daily mortality for all-cause (~180/day) or circulatory mortality (~87/day), limiting its statistical power. Nitrogen dioxide was also not significantly associated with cardiac arrest in our analysis, but the magnitude of risk estimate for the warm season was similar to the trend of increased risk found in Rome (12
). In the Rome study, carbon monoxide was significantly associated with cardiac deaths but in our study was not. The lack of associations for carbon monoxide and sulfur dioxide in our study may be due in part to the expected larger exposure misclassification for these pollutants compared with PM2.5
, ozone, or nitrogen dioxide (17
), as representativeness of exposures relevant to the residents for these local combustion sources may vary from city to city.
In using both time-series and case-crossover designs, the risk estimates in our study results from case-crossover analysis were slightly less significant, which was expected. The time-stratified referent day sampling scheme (the same day of week in the same month/year) in the case-crossover method we applied effectively uses 12 degrees of freedom/year, as compared with 7 degrees of freedom/year for time-series design, to adjust for season/temporal trends and may explain the slightly smaller risk estimates in the case-crossover result. A recent study compared time-series, case-crossover, and extended Cox regression designs in an analysis of a cohort of myocardial infarction survivors in 5 European cities to assess the probability of recurrent hospitalizations (49
). These methods gave similar results, and findings suggested that time-series analysis might also be most practical. Since time-series analysis involves selection of degrees of freedom for temporal adjustment, case-crossover analysis provides an alternative to ensure that the result is not dependent on model specifications. However, a recent study that discussed the equivalency of these 2 methods pointed out that the case-crossover analysis does not account for overdispersion of the Poisson variance (23
). Thus, while the 2 methods may produce generally similar results, they may be used as model-checking methods for each other.
Among study limitations, the derivation of this data set comes from only cases treated by paramedics of the Fire Department of New York City and not by voluntary ambulance crews. Though the data set represents the majority of calls within the 5 boroughs, the New York City 911 system comprises not only the Fire Department of New York City but also a number of voluntary hospital ambulance systems, representing 65% and 35% of the available paramedic units, respectively. We do not suspect the data would be biased based on whether a municipal or a voluntary ambulance crew responded to the call, especially since our endpoint was cardiac arrest and not death. In addition, we did not follow patients to either admission to or discharge from the hospital. For large cities, however, because an out-of-hospital cardiac arrest almost always results in death, the arrest endpoint is nearly equivalent and, regardless, represents a substantial cardiac event.
In conclusion, fine particles are associated with an increased risk of sudden out-of-hospital cardiac arrests. These observations are supported by previous data linking ischemic heart disease and dysrthymias with PM. Since few individuals survive an out-of-hospital cardiac arrest, controlling air pollution may be a preventable means to decrease cardiovascular mortality.