The pooled results of the five European cities suggest a weak association of CO and PNC with AMI hospitalisations. Stronger associations were observed in the three cities that used large HDRs. Among these cities there was considerable variation in the lag times of air pollution effects. Less heterogeneous results and higher effect estimates were obtained in stratified analyses, where the associations of CO and PNC with AMI were most consistent among fatal cases (28 day fatality) <75 years of age, and during warm season.
The five cities in our study reflect different demographics, climates, and air pollution sources encountered within the European Union. In the current study, the focus was on air pollutants originating mainly from traffic in urban environments. The pooled results of the five cities suggest a weak association of CO and PNC with AMI. However, in Augsburg and Barcelona, CO and PNC were not associated with AMI. This is probably due to lower power for city‐specific analyses in these cities. In the three cities with large HDRs, there was considerable heterogeneity in results. However, the heterogeneity was reduced in stratified analyses leading to higher pooled effect estimates and providing further support for the association between the pollutants and AMI.
Many recent studies support the importance of traffic and other combustion processes as the major source of harmful particulate matter.9,10
CO and PNC both originate from combustion processes, mainly traffic in most urban environments. It is known that exposure to CO may aggravate myocardial ischaemia by reducing the oxygen carrying capacity of blood by binding to haemoglobin, and occupational studies have suggested an association between ischaemic heart disease mortality and CO exposure.27
However, given the very low ambient levels of CO in especially Stockholm and Helsinki a causal role of CO is not likely in the current study, but CO has probably acted as a proxy for traffic related particulate pollution. It has been shown that outdoor CO levels may serve as surrogates for exposure to PM2.5
, and may be poorly correlated with CO exposures.28
On the other hand, PNC might be also causally related to AMI.8
Our findings are in line with the few smaller scale studies that have evaluated associations between occurrence of AMI and traffic related air pollution. D'Ippoliti et al
found CO and NO2
to be positively associated with AMI hospitalisations in Rome, but the strongest association was observed between total suspended particles and AMI.3
Peters et al
found daily levels of both particles and gaseous pollutants to be associated with the onset of non‐fatal AMI in Boston.4
In a recent similar study in Augsburg,29
the results for daily air pollution concentrations were essentially the same. PNC was included in the latter study, but no association with AMI was found.
In our study the effects of PM10
were less clear than those of CO and PNC. The percentage increase in AMI hospitalisations for a 10 μg/m3
increase in PM10
was also lower than in a recent large study on AMI in the US: 0.3% versus 0.65%.5
However, especially in stratified analyses PM10
seemed to have an effect in the current study, too. It should be noted that the use of a few central outdoor monitors makes the comparison of effect estimates of pollutants from different sources difficult. It is likely that also in our study, for example, the spatial variability in PM10
levels has been different from the variability of more obviously traffic related pollutants like PNC and CO. However, in time series analyses the spatial variability in pollutant levels is less of a problem than possible poor temporal correlation between sites. For PM2.5
it has been shown that the levels of traffic originating mass might be very different at different sites, but still longitudinally correlating.30
We have shown in the HEAPSS study fair correlation between two monitoring sites for PNC in Barcelona, Rome, and Stockholm.16
In Helsinki, rather high longitudinal correlations have been previously reported for several monitoring sites for PNC.31
Part of the exposure to traffic originating pollutants obviously occurs while outdoors and in traffic. As the study population consisted mainly of elderly persons, the time spent outdoors has probably been lower than for general population.
We found PNC and CO to be more strongly associated with AMI among fatal cases below 75 years of age than in the whole data. In this category, there was also some evidence of PM10
effects. In the higher age group, we observed air pollution effects mainly among non‐fatal cases. Persons
75 years of age within the fatal category may be so frail that the effects of air pollution are masked by factors related, for example, to multiple comorbidities. It should also be noted that the fraction of fatal AMIs never reaching the hospital is dependent on age.32,33
Within the HEAPSS study, we have observed strong associations of out‐of‐hospital coronary deaths with PNC, PM10
, and CO in Rome.13
We observed higher pooled effect estimates for air pollution during warm season than during cold season. This is consistent with a recent large American mortality study,34
and could be due to higher exposure or better exposure assessment during the warm season because of larger proportion of time spent outdoors and higher ventilation rates. On the other hand, seasonal differences in air pollution mixture may also affect the effect estimates, and could explain the seasonal differences in lag structure. Taken together, our two types of stratified analyses demonstrate how straightforward pooling of effect estimates in multicity studies may conceal inherent differences between cities in climate, air pollution mixture, and population. One potentially important effect modifier is medication—for example, the use of statins and beta‐blockers,35,36
which might differ between cities. Unfortunately, HDRs do not include data on medication.
Recently, an association between ozone and AMI was reported in Toulouse, but no association between AMI and NO2
Thus, we decided to study the possible effects of ozone in addition to the effects of closely traffic related pollutants. However, we could not confirm the finding, as O3
was found not to be associated with AMI.
An obvious limitation in our study is the use of two different types of registers for the collection of AMI data. Nevertheless, the different practices of AMI diagnosis and registration are probably a minor limitation. Instead, the upper age limit of the AMI registers may be more problematic since it caused not only different age structure, but also different sex structure as compared to the cities with administrative hospital databases. In any case, the small number of cases alone might explain the lack of associations in Augsburg and Barcelona.
Particle number concentrations were not measured directly, but estimated using other pollutants and meteorology. We have demonstrated that the estimated concentrations correlate well with measured concentrations.17
However, due to uncertainties associated with retrospective modelling in general, the effect estimates of CO and PNC are not directly comparable. In the future, when more measurement data on the smallest fractions of particles accumulate in the five study centres and elsewhere, measured PNC can be used.
- Exposure to traffic related air pollution may increase the risk of first myocardial infarction.
- In multicity air pollution studies on hospitalisations for myocardial infarction and other cardiovascular diseases, case fatality, age of patient, and season should be considered.
- The results help the European Union and national institutions to design policies for air pollution abatement.
- Efforts to reduce population exposure to traffic originating pollution to reduce the human and economical costs paid for air pollution should be continued both in Southern and Northern Europe.
In summary, we found support for the hypothesis that exposure to traffic related air pollution increases the risk of AMI. The associations of CO and modelled PNC with AMI were most consistent among fatal hospitalised AMI patients below 75 years of age and hospitalised AMI patients 75 years of age or older with non‐fatal outcome. Associations were also stronger during the warm season than the cold season. The causal factor or factors remain to be identified