Myocardial infarction has a high medical burden for families and society, and remains a worldwide public health challenge [45]. Ascertaining the risk factors of MI could provide significant information for the prevention of MI. Our meta-analysis has quantitatively examined the association between long-term exposure to ambient air pollution (PM2.5 and PM10) and MI. The pooled analysis included 22 cohort studies with more than 6.5 million people showed an inverse association between exposures to air pollutants (PM2.5 and PM10) and the risk of MI, which was consistent with previous reviews and meta-analysis [13]. However, previous meta-analysis only included studies published before 2014, while more recent studies were not included which might report lower estimates or negative results. Additionally, our meta-analysis included all cohorts studies, which data reliable, the effect of exposure can be fully and directly analyzed, and conclusions are relatively stable.
The mechanisms by air pollution exposure could contribute to the development of MI might include inflammation, induction of autophagy and down-regulation of membrane repair protein MG53. Researchers found that inflammation plays an important role in the formation of coronary atherosclerosis and aggravation of plaque instability, and air pollutants can also promote MI via promoting inflammation [46]. The second potential mechanism is induction of autophagy. Several observational studies have shown that autophagy is a normal process for cells to achieve their own metabolism and organelle renewal. Autophagy can maintain the body's metabolism to reduce damage and protect the organism. However, excessive autophagy can lead to apoptosis of cardiomyocytes and aggravate the damage of ischemic-related sites [47]. Studies have found that autophagic levels for exposure to air pollutants are significantly higher than the control group, while, the corresponding protein expression levels, MI size decreases, and myocardial cell damage decrease in Farnesoid X recertor(FXR)knock out SD rats. Therefore, it is speculated that the exposure of air pollutants promotes the development of MI through FXR-induced autophagy [48]. The third possible mechanism is down-regulation of membrane repair protein MG53.Exposure to air pollutants can affect membrane repair through down-regulating the expression of MG53 protein, and aggravates the severity of ischemia and hypoxia in MI [49].
We also found that long-term exposure to PM2.5 has a more pronounced effect than PM10 on MI risk in each 10 µg/m3 increase, which is in line with previous related researches [13]. Compared with PM10, PM2.5 can remain suspended for a longer time in the air and be inhaled into the respiratory tract and directly into the pulmonary alveoli. In addition, PM2.5 has a larger superficial area and hence absorbs more chemical constituents than PM10. Therefore, PM2.5 is probably more harmful on human health than PM10 [50, 51].
Considering the different diets, lifestyles of people, and the prevalence of MI in different regions, we also conducted subgroup analysis by region, and statistically significant differences across subgroups were found but not for PM10. In Asia, a 10 mg/m3 increase in PM2.5 exposure was positively associated with the risk of MI (RR = 1.38), which was inconsistent with previous studies. The possible reasons for the differences including inconsistency in study designs and potentially selective reporting of the results for pollutants. However, it is suggested that Asia region should pay attention to the relationship between air pollution and MI, and more works about air pollution and epidemiology remain to be done. We conducted a subgroup analysis by publication years but found the pooled result of studies before 2010 was not significantly different from that after 2010.
There are several strengths in this meta-analysis. Firstly, all the studies in our analysis were cohort studies, which is considered as stronger measure for demonstrating causation and identification of risk factors than other observational study designs [52]. Secondly,
in this comprehensive literature review, we pooled data of 22 cohort studies from several geographical regions in 1 meta-analysis, thus increasing the statistical power and allowing an investigation of regional patterns. Thirdly, sensitivity analysis and consistent results from various subgroup analyses indicated that our findings were reliable and robust, although heterogeneity existed among the included studies. Furthermore, all these studies were published in the past decade, indicating that data on both the exposure and the outcome are recent and relevant.
Some limitations in the present meta-analysis should be of concern. First of all, the heterogeneity of the included studies was significant and existed through the whole analyses. But we explored the potential heterogeneity resources by subgroup analyses and sensitivity analysis. Secondly, the number of included studies is not enough, especially for the mortality and hospital of MI and subgroup-analysis. Third, other air pollutants may have interaction with PM2.5 and PM10. A compounding effect of all these air pollutants should be examined and quantified on increasing the risk of MI.