Short-Term Exposure to Ambient Air Pollution and Cardiovascular Events
Patients with cardiovascular disease share many modifiable and non-modifiable risk factors including ethnicity, family history, hypertension and smoking [25-27]. One of the key differences between these risk factors and environmental air pollution is that exposure to pollutants is, for many, unavoidable. Therefore whist the individual risk estimates for exposure to ambient air pollution are relatively small compared to other cardiovascular risk factors, since the exposure can be assumed to be 100 %, the overall population attributable risk is significant [25].
In the early 1980s, Knox et al. proposed that air pollution was a means by which weather conditions could contribute to the relationship between weather conditions and stroke [28]. Later that decade, indoor coal fumes were highlighted as a risk factor for stroke, independent of age, blood pressure and cigarette smoking [29]. Schwartz et al. (1994) looked at the relationship daily PM recordings and cause of death in the US between 1973 and 1980. They noticed an weak, but sizeable (RR = 1.19) association between PM and stroke, discussing the findings in relation to those of the London smog episode in 1952 [30]. Subsequently, there has been a plethora of studies considering these associations with more recent data; these are reviewed in detail elsewhere [31]. Of note, though, Dominici et al. investigated the effect of short-term increases in particulate pollution and risk of admission from cardiopulmonary disease across one of the largest cohorts, involving 204 US counties [19]. The study showed that a reduction of 10 pg/m3 of PM25 concentrations would reduce approximately 1 in 10 stroke admissions. Diesel exhaust is likely to be a prominent contributor to the effects of urban PM on stroke in Europe [32].
Meta-analysis of ecological studies has already shown a consistent effect of both gaseous and particulate air pollution and adverse cardiac events [17, 23, 33, 34]. A recent meta-analysis has now shown that both incident stroke and mortality form stroke is associated with both gaseous and particulate pollutants [18] (Fig. 1). Across 103 studies evaluating short-term exposure to air pollution involving 6.2 million incident strokes or stroke deaths, there was a 1.1 % increment in the risk of stroke per 10 ^g/m3 increment in PM25 levels. The associations were strongest on the day of the event and showed a close temporal relationship between exposure and outcome [18]. Interestingly, exposure to PMj0 showed weaker associations with stroke hospitalisation and mortality compared to PM25 consistent with observations from other meta-analyses for stroke [35] and long-term exposure studies [24]. The underlying reasons explaining these differences remain unclear, especially when compared to associations with other pathologies like heart failure where the adverse effects of the larger particles was more striking. These differences in particle size and adverse stroke events likely reflect differences in particle composition. However,
Fig. 1 Meta-analysis of the association of air pollutants and stroke worldwide, stratified by time lag (days). Adapted from Shah et al. 2015 [18] mechanistic pathways will also be an influence, with larger particles exerting local pulmonary effects, whereas fine or ultra-fine particles cause additional systemic cardiovascular effects through alternative means [10]. The adverse effect of larger particles in patients with heart failure was more striking, possibly reflecting indirect biological pathways such as the adverse effect of sympathetic nervous activation on the failing heart [10, 33]. The effect estimates noticed for particulate matter were consistent with meta-estimates observed for coronary artery disease [17], although a recent study in Germany suggests that the effect size of PM could be greater for stroke than coronary artery disease [36]. Of concern, a recent study performed in Stockholm found associations for both PM10 and NOx with stroke that, while the effect size was small, occurred at low levels of these pollutants [37], confirming previous studies demonstrating these associations at PM levels below that suggested by the US Environmental Protection Agency [38, 39].
