Abstract
Background and ObjectivesExposure to traffic is an established risk factor for the triggering of myocardial infarction (MI). Particulate matter, mainly emitted by diesel vehicles, appears to be the most important stressor. However, the possible influence of benzene from gasoline-fueled cars has not been explored so far.Methods and ResultsWe conducted a case-crossover study from 2,134 MI cases recorded by the local Coronary Heart Disease Registry (2000–2007) in the Strasbourg Metropolitan Area (France). Available individual data were age, gender, previous history of ischemic heart disease and address of residence at the time of the event. Nitrogen dioxide, particles of median aerodynamic diameter <10 µm (PM10), ozone, carbon monoxide and benzene air concentrations were modeled on an hourly basis at the census block level over the study period using the deterministic ADMS-Urban air dispersion model. Model input data were emissions inventories, background pollution measurements, and meteorological data. We have found a positive, statistically significant association between concentrations of benzene and the onset of MI: per cent increase in risk for a 1 µg/m3 increase in benzene concentration in the previous 0, 0–1 and 1 day was 10.4 (95% confidence interval 3–18.2), 10.7 (2.7–19.2) and 7.2 (0.3–14.5), respectively. The associations between the other pollutants and outcome were much lower and in accordance with the literature.ConclusionWe have observed that benzene in ambient air is strongly associated with the triggering of MI. This novel finding needs confirmation. If so, this would mean that not only diesel vehicles, the main particulate matter emitters, but also gasoline-fueled cars –main benzene emitters–, should be taken into account for public health action.
Highlights
The effects of traffic-related air pollution on cardiorespiratory mortality have been consistently established since the late 1980s [1]
All these pollutants were well correlated, as expected: Pearson’s r for daily mean concentrations (Table 3) were in the range reported in the literature, the lowest being 20.16 (O3 and PM10) and the highest being 0.73 (NO2 and PM10), all statistically significant, in agreement with results reported in the literature [19,20]
Using a proven, robust case-crossover design, we observed associations (Table 4) between classically studied traffic-related pollutants (PM10, NO2, carbon monoxide (CO) and ozone) and outcomes that were within the range reported in the literature [3], non-significant for the study population as a whole, due to our limited sample size
Summary
The effects of traffic-related air pollution on cardiorespiratory mortality have been consistently established since the late 1980s [1]. Further studies investigated the association between exposure to traffic and the onset of myocardial infarction (MI), one of the most frequent causes of death. Since the publication of the seminal paper by Peters et al (2001) [2], which shows an association between exposure to traffic and the onset of myocardial infarction (MI), many studies have been published on the issue. The latest review and meta-analysis to date considered the association between short-term exposure to traffic-related air pollutants and subsequent MI risk [3]. Exposure to traffic is an established risk factor for the triggering of myocardial infarction (MI). The possible influence of benzene from gasoline-fueled cars has not been explored so far
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