Dataset Information

The effects of hourly differences in air pollution on the risk of myocardial infarction: case crossover analysis of the MINAP database.

ABSTRACT:

Objectives

To investigate associations between air pollution levels and myocardial infarction (MI) on short timescales, with data at an hourly temporal resolution.

Design

Time stratified case crossover study linking clinical data from the Myocardial Ischaemia National Audit Project (MINAP) with PM(10), ozone, CO, NO(2), and SO(2) data from the UK National Air Quality Archive. Pollution effects were investigated with delays (lags) of 1-6, 7-12, 13-18, 19-24, and 25-72 hours in both single and multi-pollutant models, adjusted for ambient temperature, relative humidity, circulating levels of influenza and respiratory syncytial virus, day of week, holidays, and residual seasonality within calendar month strata.

Setting

Population based study in 15 conurbations in England and Wales.

Subjects

79,288 diagnoses of myocardial infarction recorded over the period 2003-6.

Main outcome measures

Excess risk of myocardial infarction per 10 µg/m(3) increase in pollutant level.

Results

In single pollutant models, PM(10) and NO(2) levels were associated with a very short term increase in risk of myocardial infarction 1-6 hours later (excess risks 1.2% (95% confidence interval 0.3 to 2.1) and 1.1% (0.3 to 1.8) respectively per 10 μg/m(3) increase); the effects persisted in multi-pollutant models, though with only weak evidence of an independent PM(10) effect (P = 0.05). The immediate risk increases were followed by reductions in risk at longer lags: we found no evidence of any net excess risk associated with the five pollutants studied over a 72 hour period after exposure.

Conclusions

Higher levels of PM(10) and NO(2), which are typically markers of traffic related pollution, seem to be associated with transiently increased risk of myocardial infarction 1-6 hours after exposure, but later reductions in risk suggest that air pollution may be associated with bringing events forward in time ("short-term displacement") rather than increasing overall risk. The well established effect of air pollution on cardiorespiratory mortality may not be mediated through increasing the acute risk of myocardial infarction, but through another mechanism.

SUBMITTER: Bhaskaran K

PROVIDER: S-EPMC3176903 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundIn studies showing associations between ambient air pollution and myocardial infarction (MI), data have been lacking on the inherent spatial variability of air pollution. The aim of this study was to determine whether the long-term spatial distribution of air pollution influences short-term temporal associations between air pollution and admission to hospital for MI.MethodsWe identified adults living in Calgary who were admitted to hospital for an MI between 2004 and 2012. We evaluated associations between short-term exposure to air pollution (ozone [O3], nitrogen dioxide [NO2], sulfur dioxide [SO2], carbon monoxide [CO], particulate matter < 10 μm in diameter [PM10] and particulate matter < 2.5 μm in diameter [PM2.5]), and hospital admissions for MI using a time-stratified, case-crossover study design. Air Quality Health Index (AQHI) scores were calculated from a composition of O3, NO2 and PM2.5. Conditional logistic regression models were stratified by low, medium and high levels of neighbourhood NO2 concentrations derived from land use regression models; results of these analyses are presented as odds ratios (ORs) with 95% confidence intervals (CIs).ResultsFrom 2004 to 2012, 6142 MIs were recorded in Calgary. Individuals living in neighbourhoods with higher long-term air pollution concentrations were more likely to be admitted to hospital for MI after short-term elevations in air pollution (e.g., 5-day average NO2: OR 1.20, 95% CI 1.03-1.40, per interquartile range [IQR]) as compared with regions with lower air pollution (e.g., 5-day average NO2: OR 0.90, 95% CI 0.78-1.04, per IQR). In high NO2 tertiles, the AQHI score was associated with MI (e.g., 5-day average OR 1.13, 95% CI 1.02-1.24, per IQR; 3-day average OR 1.13, 95% CI 1.04-1.23, per IQR).InterpretationOur results show that the effect of air pollution on hospital admissions for MI was stronger in areas with higher NO2 concentrations than that in areas with lower NO2 concentrations. Individuals living in neighbourhoods with higher traffic-related pollution should be advised of the health risks and be attentive to special air quality warnings.

Project description:IntroductionTraffic-related air pollution can trigger myocardial infarction (MI). However, the hourly hazard period of exposure to nitrogen dioxide (NO2), a common traffic tracer, for incident MI has not been fully evaluated. Thus, the current hourly US national air quality standard (100 ppb) is based on limited hourly-level effect estimates, which may not adequately protect cardiovascular health.ObjectivesWe characterized the hourly hazard period of NO2 exposure for MI in New York state (NYS), USA, from 2000 to 2015.MethodsFor nine cities in NYS, we obtained data on MI hospitalizations from the NYS Department of Health Statewide Planning and Research Cooperative System and hourly NO2 concentrations from the US Environmental Protection Agency's Air Quality System database. We used city-wide exposures and a case-crossover study design with distributed lag non-linear terms to assess the relationship between hourly NO2 concentrations over 24 h and MI, adjusting for hourly temperature and relative humidity.ResultsThe mean NO2 concentration was 23.2 ppb (standard deviation: 12.6 ppb). In the six hours preceding MI, we found linearly increased risk with increasing NO2 concentrations. At lag hour 0, a 10 ppb increase in NO2 was associated with 0.2 % increased risk of MI (Rate Ratio [RR]: 1.002; 95 % Confidence Interval [CI]: 1.000, 1.004). We estimated a cumulative RR of 1.015 (95 % CI: 1.008, 1.021) for all 24 lag hours per 10 ppb increase in NO2. Lag hours 2-3 had consistently elevated risk ratios in sensitivity analyses.ConclusionsWe found robust associations between hourly NO2 exposure and MI risk at concentrations far lower than current hourly NO2 national standards. Risk of MI was most elevated in the six hours after exposure, consistent with prior studies and experimental work evaluating physiologic responses after acute traffic exposure. Our findings suggest that current hourly standards may be insufficient to protect cardiovascular health.