A total of 79
288 myocardial infarctions with time of event available were recorded in MINAP within the 15 conurbations during 2003–6 (table 1). Overall, 34
566 (44%) of the events were ST elevation myocardial infarctions, though the proportion was notably higher in Kingston-upon-Hull. Time of myocardial infarction was most commonly based on the time of symptom onset (n=58
594, 74%), time of call for help (n=6887, 9%), or time of arrival at hospital (n=13
144, 17%). Of the 79
288 events, 70
331 (89%) were confirmed by at least one recorded electrocardiogram (for ST elevation myocardial infarction) or raised troponin or creatine kinase levels.
Table 1 Characteristics of myocardial infarctions and local levels of air pollutants in 15 conurbations in England and Wales. Values are medians (interquartile range) unless stated otherwise
Table 1 shows the median hourly pollution levels overall and within conurbations. We excluded 4931 events (6.2%) from the multi-pollutant model because of missing pollution data; for single pollutant models, the number of events excluded ranged from 1952 (2.5%) to 2447 (3.1%) depending on the pollutant (further details in web appendix). Correlations between pollutant pairs were positive with the exception of ozone, which was negatively correlated with other pollutants. Correlations were weaker in summer (r<0.5 in all cases) compared with other seasons (table 2).
Table 2 Correlation coefficients between exposure variables (temperature and air pollutants) measured in 15 conurbations in England and Wales. Values are overall correlations (correlations for summer*/other seasons)
Effects of pollutants on myocardial infarction risk in single and multi-pollutant models
When the five pollutants under investigation were modelled in separate single pollutant models, there was evidence at the shortest lag term (1–6 hours) of a raised risk of myocardial infarction associated with higher PM10 and NO2 levels, though effect estimates at longer lags were in the protective direction (table 3 and fig 1). A 10 µg/m3 increase in PM10 level was associated with a 1.2% (95% confidence interval 0.3% to 2.1%) increase in myocardial infarction risk 1–6 hours later, but in subsequent lag periods the risk was reduced so that over 1–72 hours there was no overall risk increase (cumulative change in risk −0.8% (−1.8% to 0.2%)). Similarly for NO2, a 10 µg/m3 increase was associated with a 1.1% (0.3% to 1.8%) increase in risk 1–6 hours later, but no net risk increase over 72 hours (cumulative change in risk −0.4% (−1.2% to 0.4%)). There was little evidence of any detrimental effect of CO, ozone, or SO2 in single pollutant models; indeed, for CO the net effects over 1–72 hours were in the protective direction.
Table 3 Estimated excess risk of myocardial infarction associated with increased levels of pollutants at five time lags in single and multi-pollutant models*
Fig 1 Estimated excess risk of myocardial infarction associated with increases in air pollutants (with five lag terms covering 0–72 hours) from a single pollutant model (separate models for each of the pollutants adjusted for temperature (five (more ...)
In the multi-pollutant model containing all five pollutants, the immediate effect of NO2 persisted, and there remained weak evidence of an independent effect of PM10, though the confidence interval just included the null (P=0.05) (table 3). After adjustment for other pollutants, there was a suggestion of a positive association between higher ozone levels and myocardial infarction risk at 1–6 hours lag, but this was more than cancelled out over the longer term, with some evidence of a protective association over 72 hours (−1.2% (−2.1% to −0.2%) change in risk per 10 µg/m3 increase in ozone). For CO, both the shortest lag effect and the cumulative effect were in the protective direction (−1.3% (−2.3% to −0.2%) change in risk per 0.1mg/m3 increase, over 72 hours). Of note, in two pollutant models (web table A in appendix), the appearance of both a detrimental effect of ozone at lag 1–6 hours and an apparently protective association between CO and myocardial infarction risk at lag 1–6 hours seemed to be driven by adjustment for NO2, with which both ozone and CO are strongly correlated in opposite directions (r=−0.58 and 0.61 respectively).
Effect modification by age, prior coronary heart disease, and smoking
For NO2, the pattern of a raised risk of myocardial infarction associated with 1–6 hour lagged pollution levels followed by a reduced risk associated with 7–12 hour lagged levels seemed to be restricted to intermediate age groups, with little evidence of any such pattern in those aged <60 or ≥80 years (Pinteraction=0.002, fig 2). A similar pattern was observed visually for PM10, but there was little statistical evidence of effect modification for this or other pollutants after allowing for multiple testing. We found weak evidence that the effects of NO2 were also more pronounced among those with prior coronary heart disease (Pinteraction=0.007, web fig A in appendix), but no evidence of any effect modification by smoking status (web fig B, Pinteraction>0.73 for each pollutant).
Fig 2 Estimated excess risk of myocardial infarction associated with increases in air pollutants (with five lag terms covering 0–72 hours) from a single pollutant model (see fig 1 for details) stratified by age group. Pinteraction=0.05, 0.54, (more ...)
Pollution effects by season and the role of hourly temperature
Web figure C shows the associations between pollution and myocardial infarction by season (summer v other seasons). Effect estimates for the short lag effects of NO2 and myocardial infarction risk were larger in the autumn–spring periods compared with summer, whereas we observed the opposite pattern for PM10. However, there was little evidence that these or other variations by season were any greater than expected by chance (Pinteraction>0.33 for each pollutant). Web figure D shows the effects of adjusting for hourly (as well as daily) temperature in the nine conurbations where these data were available. Effect estimates were similar before and after adjustment for hourly temperature.
Sensitivity of pollutant effects to key model specifications
Our findings seemed robust with regard to (i) restricting analysis to those cases with a recorded time of symptom onset; (ii) restricting to those with corroborative evidence confirming the myocardial infarction diagnosis; (iii) using robust standard errors to allow for any clustering by conurbation; (iv) altering the strategy for selecting control days; (v) matching control days on, rather than adjusting for, day of the week; and (vi) relaxing the assumption of linearity when adjusting for temperature effects. The results of analyses (i) to (iii) are presented in web table B.
For each sensitivity analysis, all confidence intervals included the original effect estimates from our main single pollutant models. For PM10 and NO2, the estimated excess risk associated with a 10 µg/m3 increase at lag 1–6 hours in the six sensitivity analyses ranged from 0.9% to 1.3% and from 0.5% to 1.2% respectively, compared with our original estimates of 1.2% (95% confidence interval 0.3% to 2.1%) and 1.1% (0.3% to 1.8%) respectively. The patterns of effects at longer lags and for other pollutants were also consistent across models. As expected, confidence intervals estimated from the sensitivity analyses were generally wider, since the analyses involved the inevitable reduction in power associated with excluding events (analyses i and ii), calculating robust standard errors (analysis iii), and using smaller case-control sets (analyses iv and v).