Skip to main content
PMC home page
International Journal of Cardiology. Cardiovascular Risk and Prevention logoLink to International Journal of Cardiology. Cardiovascular Risk and Prevention
. 2023 Oct 12;19:200217. doi: 10.1016/j.ijcrp.2023.200217

PM2.5 and cardiovascular diseases: State-of-the-Art review

Chayakrit Krittanawong a,∗, Yusuf Kamran Qadeer b, Richard B Hayes c, Zhen Wang d,e, George D Thurston f, Salim Virani b,g, Carl J Lavie h
PMCID: PMC10585625  PMID: 37869561

Abstract

Air pollution, especially exposure to particulate matter 2.5 (PM2.5), has been associated with an increase in morbidity and mortality around the world. Specifically, it seems that PM2.5 promotes the development of cardiovascular risk factors such as hypertension and atherosclerosis, while being associated with an increased risk of cardiovascular diseases, including myocardial infarction (MI), stroke, heart failure, and arrhythmias. In this review, we seek to elucidate the pathophysiological mechanisms by which exposure to PM2.5 can result in adverse cardiovascular outcomes, in addition to understanding the link between exposure to PM2.5 and cardiovascular events. It is hypothesized that PM2.5 functions via 3 mechanisms: increased oxidative stress, activation of the inflammatory pathway of the immune system, and stimulation of the autonomic nervous system which ultimately promote endothelial dysfunction, atherosclerosis, and systemic inflammation that can thus lead to cardiovascular events. It is important to note that the various cardiovascular associations of PM2.5 differ regarding the duration of exposure (short vs long) to PM2.5, the source of PM2.5, and regulations regarding air pollution in the area where PM2.5 is prominent. Current strategies to reduce PM2.5 exposure include personal strategies such as avoiding high PM2.5 areas such as highways or wearing masks outdoors, to governmental policies restricting the amount of PM2.5 produced by organizations. This review, by highlighting the significant impact between PM2.5 exposure and cardiovascular health will hopefully bring awareness and produce significant change regarding dealing with PM2.5 levels worldwide.

1. Introduction

Air pollution has been associated with an increase in morbidity and mortality, not only in the United States, but around the world. Specifically, there have been many studies evaluating the effects of pollution on cardiovascular diseases (CVD), including myocardial infarction (MI), stroke, heart failure, and arrhythmias. PM2.5 refers to particulate matter in air that is less than 2.5 μm or less in diameter. This is significant because particulate matter that is less than 10 μm in diameter can be inhaled into the lungs and lead to adverse health effects [1]. In this review, we seek to elucidate the pathophysiological mechanisms by which exposure to particulate matter (PM2.5) can result in adverse cardiovascular outcomes, in addition to understanding the link between exposure to PM2.5 and cardiovascular events.

2. Pathophysiology

There is growing evidence to support that particulate matter such as PM2.5 is associated with cardiovascular disease. One of the mechanisms by which this may occur is through the small size, and large surface area per unit mass, of PM2.5 particles, allowing them to enter the systemic and pulmonary circulation [2,3]. A study conducted by Seaton and colleagues demonstrated that, once particulate air matter enters the pulmonary circulation, it causes inflammation which can then extend to the systemic circulation. Inflammation was measured by the release of inflammatory mediators and blood coagulation factors. The increased systemic inflammation can lead to hemostatic abnormalities, such as thrombosis or endothelial damage [4], potentially resulting in cardiovascular diseases such as stroke and myocardial infarction. A study by Kilinc and colleagues proposed a mechanism for the pro-coagulant properties of PM2.5. They found how long-term exposure to particulate matter was mediated by factor XII driven thrombin formation [5]. Another proposed mechanism for PM2.5 causing endothelial dysfunction and inflammation is through NLRP3 inflammasome activation as shown by Hu and colleagues [6].

At the cellular level, it is hypothesized that PM2.5 may exert its detrimental effects by altering the function of the mitochondria. The mitochondria is often referred to as the “powerhouse” of the cell, owing to the fact that it performs many biologically significant functions, such as ATP production, lipid metabolism, and ion regulation [7]. It has been suggested that environmental toxins can alter mitochondrial DNA and alter gene expression, as they seem to accumulate more easily in mitochondria given the high membrane lipid profile of the mitochondria [8,9]. In rat models, exposure to PM2.5 resulted in mitochondrial membrane dysfunction [10]. This dysfunction of the mitochondria can lead to cell death, which is a nidus for inflammation in different tissues. It is hypothesized that the mechanism for the inflammation is the release of mitochondrial DNA into the circulation, or via the generation of reactive oxygen species [11,12].

In terms of inflammation, it is hypothesized that particulate matter can propagate the human body's natural inflammatory response through different mediators, such as reactive oxygen species, tumor necrosis factor, c-reactive protein and IL-6 [13]. Some research has also suggested that PM2.5 may have an effect on the autonomic nervous system. Increased arrhythmias have been reported with acute exposure to PM2.5, which can lead to CVD such as heart failure [14]. Also, it has been shown that Transforming Growth Factor-Beta-containing small extracellular vesicles may promote cardiotoxicity through PM2.5 activation of macrophages [15].

A recent review conducted by Chen and colleagues sought to elucidate the various mechanisms in which PM2.5 could lead to ischemic stroke [16]. They cited a cohort study of 25,355 participants in China which found that platelet counts increased by 0.29 % for every 1 μg/m3 increase of PM2.5 exposure, with a stronger effect in male and non-DM participants [17]. In addition, a positive association between long-term PM2.5 exposure and mean platelet volume (MPV), platelet distribution width (PDW), and platelet large cell ratio (P-LCR) has been documented [18]. There is some evidence that PM2.5 exposure causes abnormal miRNA expression in endothelial cells, resulting in fragile endothelial cells [19]. Finally, PM2.5 exposure induces neuroinflammation in astrocytes and microglia, which further aggravates neuronal damage [20].

Munzel and colleagues also looked at the various mechanisms in which PM2.5 could cause CVD [21]. They believed oxidative stress to be the common denominator in the various vascular effects of PM2.5. Essentially the lung has a protective surfactant layer that includes proteins, lipids, and alveolar macrophages. PM2.5 may induce changes in the chemical structure of this surfactant layer, while promoting oxidative stress and the ability of particules to directly penetrate the lung [22].

3. CV risk

PM2.5 is associated with many clinical risk factors for cardiovascular disease, such as hypertension. Studies have shown that both acute and chronic exposure to PM2.5 levels can result in elevated blood pressure and hypertension [23,24]. Liang and colleagues examined 22 studies and found that there was an increase in systolic and diastolic blood pressure per 10 μg/m^3 of PM2.5 by 1.393 mmHg and 0.895 mmHg respectively [25]. There are many proposed mechanisms by which PM2.5 can lead to hypertension. One suggested mechanism is via the generation of reactive oxygen species which leads to impairment in nitric oxide (NO) mediated vasodilation. This lack of NO mediated vasodilation leads to vasoconstriction of blood vessels and thus hypertension [26,27]. In addition, it has been suggested that PM2.5 exposure can result in increased levels of endothelin-1, which is a known vasoconstrictor and can lead to endothelial dysfunction [28,29].

PM2.5 also may have an association with diabetes mellitus, which is an established risk factor for cardiovascular disease. He and colleagues found that for every 10 μg/m^3 increase in PM2.5 levels, there was a 25 % increased risk of developing diabetes mellitus with long term exposure to PM2.5 levels [30]. Similarly, Chilian-Herrera and colleagues found that there was an association with increased PM2.5 levels and development of diabetes mellitus in individuals living in Mexico City [31]. What was interesting about this study was that it seemed to suggest that in areas with PM2.5 levels that exceed the guidelines set by the WHO (WHO guidelines recommend an annual PM2.5 Air Quality Guidance level of 5ug/m^3), individuals living in those areas were more likely to develop diabetes mellitus. In terms of the mechanism behind PM2.5 exposure and development of diabetes mellitus, it is hypothesized that the cause may be insulin resistance secondary to oxidative damage, inflammation, and endothelial dysfunction [[32], [33], [34]].

Finally, it is hypothesized that PM2.5 levels is associated with hyperlipidemia. Li and colleagues in China found that reductions in PM2.5 levels were correlated with a decrease in LDL-C and total cholesterol levels [35]. Likewise, McGuinn and colleagues found that among cardiac catheterization patients residing in North Carolina, increases in PM2.5 levels were associated with an increase in lipoprotein concentrations [36]. Similarly, Zhang and colleagues found how PM2.5 leads to altered lipid metabolism which can then result in the development of atherosclerosis [37]. The specific mechanism for PM2.5 alteration of lipid metabolism seems to be caused by disturbances to the lipolysis and fatty acid oxidation pathways [38].

4. PM2.5 and MI

PM2.5 exposure has also been shown to cause myocardial infarctions (MI). A large meta-analysis conducted by Farhadi and colleagues analyzed 26 studies that evaluated the association between short term exposure to PM2.5 and the risk of developing myocardial infarction [39]. They found a 2 % increased risk of myocardial infarction with each 10 μg/m^3 exposure to PM2.5 (RR = 1.02; 95 % CI 1.01–1.03; P ≤ 0.0001). Similarly, Madrigano and colleagues sought to show that not only short term, but long term exposure to PM2.5 can be associated with MI. The study they conducted was a case-control study looking at residents living in Massachusetts who had developed MI between 1995 and 2003. This study found that long term exposure to PM2.5 was associated with an increased odds of MI [40]. An interesting study was conducted by Liao and colleagues, that sought to understand the cardiovascular effect of PM2.5 exposure on individuals with prior CVD history compared to individuals with no CVD history. They found that among individuals with prior stroke or MI, that these individuals were at increased risk of developing MI even when PM2.5 levels were less 12 μg/m^3 [41]. This study highlights the importance of developing strict regulations in regards to PM2.5 levels worldwide in order to prevent the development of CVD. Confounding due to social determinants of health which frequently co-exist with hier levels of PM2.5 cannot be totally excluded to be at least partly responsible for the observed associations in these studies.

5. PM2.5 and stroke

PM2.5 exposure has also been associated with stroke. Rhinehart and colleagues sought to evaluate the risk of stroke in patients with Atrial Fibrillation who were exposed to PM2.5 levels. They found that for every 1 standard deviation increase in PM2.5 levels, there was an 8 % increased risk of developing ischemic stroke [42]. Interestingly, O'Donnell and colleagues in Ontario, Canada looked at patient's hospitalized with ischemic stroke and who lived within 50 km of a PM2.5 monitor. They found no significant association with short-term PM2.5 exposure and risk of developing ischemic stroke. However, when they stratified patient's based on risk factors, they found that in individuals with diabetes mellitus that there was an 11 % increase risk of ischemic stroke [43]. This again highlights the significance of adverse CVD outcomes for individuals with CVD risk factors who are exposed to PM2.5. A large systematic review and meta-analysis of 16 cohort studies that included over 2.2 million individuals found that long-term exposure to PM2.5 levels was associated with stroke. Yuan and colleagues found that the pooled hazard ratio (HR) for each 5 μg/m3 increment in PM2.5 was 1.11 (95 % CI: 1.05, 1.17) (CI for confidence interval) for incidence of stroke and 1.11 (95 % CI:1.05, 1.17) for mortality from stroke [44]. Likewise, in China, Yang and colleagues found that for every 10 μg/m^3 increase in PM2.5 levels, there was a 31 % increased risk of stroke mortality [45].

6. PM2.5 and heart failure

PM2.5 exposure has also been shown to be associated with heart failure. Shah and colleagues sought to evaluate the association between PM2.5 levels and development of heart failure and heart failure mortality. They evaluated 35 studies and found that increases in particulate matter exposure was associated with heart failure hospitalization or death. They hypothesized that an average reduction of PM2.5 levels by 3.9 μg/m^3 in the US would result in 7978 fewer heart failure hospitalizations a year and would save the U.S. healthcare system a third of a billion dollars in expenses [46]. Similarly, a study in China sought to evaluate the role of PM2.5 exposure and heart failure in 26 large Chinese cities. They found that an interquartile range increase in PM2.5 levels was associated with a 1.3 % risk of heart failure hospitalizations [47]. Likewise, Wang and colleagues sought to understand the relationship between long term exposure to particulate matter and incidence of heart failure. They analyzed 432,530 patients from 2006 to 2010 and followed them until 2018. The hazard ratio [95 % confidence interval (CI)] of HF for a 10 μg/m3 increase in PM2.5 was 1.85 (1.34–2.55). These results indicated that long term exposure to PM2.5 was associated with an increased risk of heart failure [48]. Furthermore, Zhang and colleagues also provided more evidence for PM2.5 and increased risk of heart failure. In an analysis of 35 studies, for long-term exposure, the growing risk of HF was significantly associated with each 10 μg/m3 increase in PM2.5 (OR = 1.196, 95% CI: 1.079–1.326; I2 = 76.8%) [49].

7. PM2.5 and cardiac arrhythmias

PM2.5 exposure is associated with many different types of cardiac arrhythmias, but the most notable one seems to be atrial fibrillation. Lee and colleagues found in a study conducted in Taiwan that there was a 22 % increased risk of atrial fibrillation in patients exposed to an interquartile increase of 26.2 μg/m^3 in same day PM2.5 levels [50]. Wang and colleagues conducted a robust systematic review and meta-analysis of 16 observational studies including over 10 million individuals and found that PM2.5 levels had an adverse effect of causing atrial fibrillation among elderly individuals. Specifically, they found an increased odds of 11 % of atrial fibrillation per 10 μg/m^3 of PM2.5 levels, and that the risk of atrial fibrillation was increased in areas that were exposed to a PM2.5 level of greater than 25 μg/m^3 [51]. Likewise, it is hypothesized that individuals with high risk of cardiovascular deterioration are at an increased risk of developing atrial fibrillation when exposed to increased PM2.5 levels. Gallo and colleagues found this to be true as they evaluated patients with devices (CRT, pacemakers) and found that exposure to PM2.5 was associated with developing atrial fibrillation in these patients [52]. There is also some evidence that PM2.5 exposure can lead to ventricular arrhythmias as well. Data taken from the Penn State Child Cohort study and analyzed by He and colleagues found that a 10 μg/m3 increment in PM2.5 was associated with a 5 % (95 % CI, 1%–10 %) increase in premature ventricular contraction counts within 2 h after exposure [53]. In addition, there was some evidence provided by the European Society of Cardiology that PM2.5 exposure is related to the development of ventricular arrhythmias [54].

8. PM2.5 and CVD mortality

There have been many studies that have sought to analyze the relationship between PM2.5 levels and cardiovascular mortality. In general, it is hypothesized that the increasing level and duration of exposure to PM2.5, the greater the risk of cardiovascular mortality there is. One study suggested that five percent of myocardial infarctions are caused by exposure to PM2.5 levels since millions of people around the globe are continuously affected. In the United States, the National Institutes of Health-AARP found that long term exposure to PM2.5 levels (in the range of 8–12 μg/m^3) increased cardiovascular disease related mortality by a relative 10 % [55]. Likewise, in China a meta-analysis of 59 studies found that for every 10 μg/m^3 increase in PM2.5 levels there was an 0.63 % increase in cardiovascular mortality. However, it should be noted that the PM2.5 levels ranged from 39 to 177 μg/m^3 [56]. In addition, there have been studies in Canada that have shown that even relatively minimal levels of PM2.5 levels are associated with cardiovascular disease [57,58]. Given that exposure to PM2.5 and other particulate matter occurs throughout an individual's lifetime, it is plausible to support that the mechanism behind the cardiovascular mortality also occurs slowly throughout an individual's lifetime. One of the mechanisms proposed is that PM2.5 level exposure throughout a person's lifetime facilitates the development of atherosclerosis and thus predisposes individuals to cardiovascular disease [59]. Finally, Liu and colleagues analyzed daily mortality (total, cardiovascular, and respiratory) and air pollution data from 205 cities in 20 countries/regions. They found that a 10 μg/m3 increase in PM2.5-10 concentration on lag 0–1 day was associated with increments of 0.51 % (95 % confidence interval [CI], 0.18%–0.84 %), 0.43 % (95 % CI, 0.15%–0.71 %), and 0.41 % (95 % CI, 0.06%–0.77 %) in total, cardiovascular, and respiratory mortality, respectively. This suggested that short term exposure to particulate matter resulted in increased mortality [60].

9. Variability in effects as a function of particle size, source, and composition

Some PM2.5 health effects research has evaluated the variability in CVD health impacts as a function of fine particle size, source, and composition. For example, Thurston and colleagues, considering the large and well characterized ACS cohort, found that fossil fuel combustion PM2.5 (e.g., from coal burning and traffic) had a larger ischemic mortality effect per μg/m3 than PM2.5 from other sources, such as windblown soil and biomass (wood) burning [61]. Kazemiparkouhi et al. found confirmatory variations in CVD mortality effects from PM2.5 exposure as a function of emission source in the nationwide Medicare population [62]. With regard to composition, Weichenthal and colleagues recently found that PM2.5 enriched in both sulfur and transition metals lead to greater particulate oxidative potential, consistent with PM2.5 of fossil fuel combustion origins [63]. With regard to size, submicrometer, and especially ultrafine particulate matter (<0.1 μm in diameter) have been found to have among the most toxic particulate matter [64,65].

10. Strategies to reduce PM2.5 exposure

Given the significant cardiovascular adverse outcomes associated with both short and long term exposure to PM2.5, measures need to be undertaken to limit exposure. Carlsten and colleagues provided some suggestions on how best to do so [66]. One such measure that could be undertaken is to wear facemasks in high pollution cities [67]. However, the effectiveness of facemasks is limited by factors such as facial hair, facial structure and type of mask used [68]. Another recommendation that could be implemented is for pedestrians to avoid taking travel routes that would expose themselves to heavy road-air pollution. It seems that the highest particle concentrations are often found in congested areas such as traffic interesections, partly due to the significant automobile exhaust present there [69]. This would exposure individuals to lower amount of particulate matter, as was found in a study that looked at particulate exposure for cyclists biking in crowded intersections as compared to off road intersections [70]. Another recommendation would be to design cars that decrease the amount of toxic emissions. As the shift to more electric based vehicles is ongoing, one strategy to minimize exposure to the toxic fumes of cars would be to keep windows rolled up in traffic. A study found that while in traffic, opening car windows increased in-car cabin black carbon and UFP concentrations by 2–4-fold versus driving with windows closed [71].

11. Conclusion

In this review, we sought to illustrate the mechanism behind how PM2.5 results in adverse cardiovascular outcomes. Primarily, it is hypothesized that PM2.5 functions via 3 mechanisms: increased oxidative stress, activation of the inflammatory pathway of the immune system, and stimulation of the autonomic nervous system. These pathways promote endothelial dysfunction, atherosclerosis, and systemic inflammation that can thus lead to CVD such as heart failure, MI, stroke, and arrhythmias. This review found evidence that both short-term and long-term exposure to PM2.5 levels is associated with CVD outcomes such as mortality, stroke, heart failure, MI, and cardiac arrhythmias. Future studies are needed, and consensus opinion is warranted to try and elucidate an approach to minimize PM2.5 levels in areas that are densely inhabited by humans. In general, it is hypothesized that the lower the level of PM2.5 and the less time exposed, the lower the risk of developing cardiovascular complication. Nevertheless, given the lack of strict guidelines, it is imperative to have an expert consensus regarding what type and level of PM2.5 components constitute safe vs. unsafe exposures to PM2.5 levels, given the overwhelming evidence that particulate matter contributes to CVD morbidity and mortality.

Funding source(s) related to this manuscript

None.

Author's access

All authors had access to the data and a role in writing the manuscript.

Handling Editor: D Levy

References

  • 1.California Air Resources Board. “Inhalable Particulate Matter and Health (PM2.5 and PM10) | California Air Resources Board.” Ca.gov, California Air Resources Board, ww2.arb.ca.gov/resources/inhalable-particulate-matter-and-health. Accessed 8 September. 2023.
  • 2.Nemmar A., Hoet P., Vanquickenborne B., Dinsdale D., Thomeer M., Hoylaerts M.F., Vanbilloen H., Mortelmans L., Nemery B. Passage of inhaled particles into the blood circulation in humans. Circulation. 2002;105:411–414. doi: 10.1161/hc0402.104118. [DOI] [PubMed] [Google Scholar]
  • 3.Nemmar A., Vanbilloen H., Hoylaerts M.F., Hoet P.H.M., Verbruggen A., Nemery B. Passage of intratracheally instilled ultrafine particles from the lung into the systemic circulation in hamster. Am. J. Respir. Crit. Care Med. 2001;164:1665–1668. doi: 10.1164/ajrccm.164.9.2101036. [DOI] [PubMed] [Google Scholar]
  • 4.Seaton A., MacNee W., Donaldson K., Godden D. Particulate air pollution and acute health effects. Lancet. 1995;345:176–178. doi: 10.1016/S0140-6736(95)90173-6. [DOI] [PubMed] [Google Scholar]
  • 5.Kilinç E., Van Oerle R., Borissoff J.I., Oschatz C., Gerlofs-Nijland M.E., Janssen N.A., Cassee F.R., Sandström T., Renné T., Ten Cate H., Spronk H.M. Factor XII activation is essential to sustain the procoagulant effects of particulate matter. J. Thromb. Haemostasis. 2011 Jul;9(7):1359–1367. doi: 10.1111/j.1538-7836.2011.04280.x. PMID: 21481175. [DOI] [PubMed] [Google Scholar]
  • 6.Hu T., Zhu P., Liu Y., Zhu H., Geng J., Wang B., Yuan G., Peng Y., Xu B. PM2.5 induces endothelial dysfunction via activating NLRP3 inflammasome. Environ. Toxicol. 2021;36:1886–1893. doi: 10.1002/tox.23309. [DOI] [PubMed] [Google Scholar]
  • 7.Boovarahan S.R., Kurian G.A. Mitochondrial dysfunction: a key player in the pathogenesis of cardiovascular diseases linked to air pollution. Rev. Environ. Health. 2018;33:111–122. doi: 10.1515/reveh-2017-0025. [DOI] [PubMed] [Google Scholar]
  • 8.Byun H.-M., Panni T., Motta V., Hou L., Nordio F., Apostoli P., Bertazzi P.A., Baccarelli A.A. Effects of airborne pollutants on mitochondrial DNA Methylation. Part. Fibre Toxicol. 2013;10:18. doi: 10.1186/1743-8977-10-18. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Meyer J.N., Leung M.C.K., Rooney J.P., Sendoel A., Hengartner M.O., Kisby G.E., Bess A.S. Mitochondria as a target of environmental toxicants. Toxicol. Sci. 2013;134:1–17. doi: 10.1093/toxsci/kft102. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Xu Z., Xu X., Zhong M., Hotchkiss I.P., Lewandowski R.P., Wagner J.G., Bramble L.A., Yang Y., Wang A., Harkema J.R., et al. Ambient particulate air pollution induces oxidative stress and alterations of mitochondria and gene expression in brown and white adipose tissues. Part. Fibre Toxicol. 2011;8:20. doi: 10.1186/1743-8977-8-20. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Breda C.N.D.S., Davanzo G.G., Basso P.J., Câmara N.O.S., Moraes-Vieira P.M.M. Mitochondria as central hub of the immune system. Redox Biol. 2019;26 doi: 10.1016/j.redox.2019.101255. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Murphy M.P. How mitochondria produce reactive oxygen species. Biochem. J. 2009;417:1–13. doi: 10.1042/BJ20081386. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.van Eeden S.F., Tan W.C., Suwa T., Mukae H., Terashima T., Fujii T., Qui D., Vincent R., Hogg J.C. Cytokines involved in the systemic inflammatory response induced by exposure to particulate matter air pollutants (PM10) Am. J. Respir. Crit. Care Med. 2001;164:826–830. doi: 10.1164/ajrccm.164.5.2010160. [DOI] [PubMed] [Google Scholar]
  • 14.Liao D., Duan Y., Whitsel E.A., Zheng Z.-J., Heiss G., Chinchilli V.M., Lin H.-M. Association of higher levels of ambient criteria pollutants with impaired cardiac autonomic control: a population-based study. Am. J. Epidemiol. 2004;159:768–777. doi: 10.1093/aje/kwh109. [DOI] [PubMed] [Google Scholar]
  • 15.Hu X., Chen M., Cao X., Yuan X., Zhang F., Ding W. TGF-β-Containing small extracellular vesicles from pm2.5-activated macrophages induces cardiotoxicity. Front Cardiovasc Med. 2022;9 doi: 10.3389/fcvm.2022.917719. PMID: 35872905; PMCID: PMC9304575. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Chen Z., Liu P., Xia X., Wang L., Li X. The underlying mechanism of PM2.5-induced ischemic stroke. Environ Pollut. 2022 Oct 1;310 doi: 10.1016/j.envpol.2022.119827. Epub 2022 Jul 30. PMID: 35917837. [DOI] [PubMed] [Google Scholar]
  • 17.Hehua Z., Qing C., Yuhong Z. Association between ambient particulate matter exposure and platelet counts in adults: a retrospective cohort study. Environ. Sci. Pollut. Res. Int. 2021 Jun;28(24):31268–31275. doi: 10.1007/s11356-021-12865-2. Epub 2021 Feb 18. PMID: 33599925. [DOI] [PubMed] [Google Scholar]
  • 18.Hou J., Duan Y., Liu X., Li R., Tu R., Pan M., Dong X., Mao Z., Huo W., Chen G., Guo Y., Li S., Wang C. Associations of long-term exposure to air pollutants, physical activity and platelet traits of cardiovascular risk in a rural Chinese population. Sci. Total Environ. 2020 Oct 10;738 doi: 10.1016/j.scitotenv.2020.140182. Epub 2020 Jun 12. PMID: 32594998. [DOI] [PubMed] [Google Scholar]
  • 19.Wang Y., Zou L., Wu T., Xiong L., Zhang T., Kong L., Xue Y., Tang M. Identification of mRNA-miRNA crosstalk in human endothelial cells after exposure of PM2.5 through integrative transcriptome analysis. Ecotoxicol. Environ. Saf. 2019 Mar;169:863–873. doi: 10.1016/j.ecoenv.2018.11.114. Epub 2018 Nov 29. PMID: 30597786. [DOI] [PubMed] [Google Scholar]
  • 20.Kang Y.J., Tan H.Y., Lee C.Y., Cho H. An air particulate pollutant induces neuroinflammation and neurodegeneration in human brain models. Adv. Sci. 2021 Nov;8(21) doi: 10.1002/advs.202101251. Epub 2021 Sep 24. PMID: 34561961; PMCID: PMC8564420. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.Münzel T., Gori T., Al-Kindi S., Deanfield J., Lelieveld J., Daiber A., Rajagopalan S. Effects of gaseous and solid constituents of air pollution on endothelial function. Eur. Heart J. 2018 Oct 7;39(38):3543–3550. doi: 10.1093/eurheartj/ehy481. PMID: 30124840; PMCID: PMC6174028. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22.Pöschl U., Shiraiwa M. Multiphase chemistry at the atmosphere-biosphere interface influencing climate and public health in the anthropocene. Chem. Rev. 2015 May 27;115(10):4440–4475. doi: 10.1021/cr500487s. Epub 2015 Apr 9. PMID: 25856774. [DOI] [PubMed] [Google Scholar]
  • 23.Cai Y., Zhang B., Ke W., Feng B., Lin H., Xiao J., Zeng W., Li X., Tao J., Yang Z., et al. Associations of short-term and long-term exposure to ambient air pollutants with hypertension. Hypertension. 2016;68:62–70. doi: 10.1161/HYPERTENSIONAHA.116.07218. [DOI] [PubMed] [Google Scholar]
  • 24.Yang B.-Y., Qian Z., Howard S.W., Vaughn M.G., Fan S.-J., Liu K.-K., Dong G.-H. Global association between ambient air pollution and blood pressure: a systematic review and meta-analysis. Environ. Pollut. 2018;235:576–588. doi: 10.1016/j.envpol.2018.01.001. [DOI] [PubMed] [Google Scholar]
  • 25.Liang R., Zhang B., Zhao X., Ruan Y., Lian H., Fan Z. Effect of exposure to PM2.5 on blood pressure. J. Hypertens. 2014;32:2130–2140. doi: 10.1097/HJH.0000000000000342. discussion 2141. [DOI] [PubMed] [Google Scholar]
  • 26.Brook R.D., Rajagopalan S., Pope C.A., Brook J.R., Bhatnagar A., Diez-Roux A.V., Holguin F., Hong Y., Luepker R.V., Mittleman M.A., Peters A., Siscovick D., Smith S.C., Jr., Whitsel L., Kaufman J.D. American heart association council on epidemiology and prevention, council on the kidney in cardiovascular disease, and council on nutrition, physical activity and metabolism. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American heart association. Circulation. 2010 Jun 1;121(21):2331–2378. doi: 10.1161/CIR.0b013e3181dbece1. Epub 2010 May 10. PMID: 20458016. [DOI] [PubMed] [Google Scholar]
  • 27.Courtois A., Prouillac C., Baudrimont I., Ohayon-Courtes C., Freund-Michel V., Dubois M., Lisbonne-Autissier M., Marthan R., Savineau J.P., Muller B. Characterization of the components of urban particulate matter mediating impairment of nitric oxide-dependent relaxation in intrapulmonary arteries. J. Appl. Toxicol. 2014 Jun;34(6):667–674. doi: 10.1002/jat.2909. Epub 2013 Jul 23. PMID: 23881823. [DOI] [PubMed] [Google Scholar]
  • 28.Calderón-Garcidueñas L., Villarreal-Calderon R., Valencia-Salazar G., Henríquez-Roldán C., Gutiérrez-Castrellón P., Torres-Jardón R., Osnaya-Brizuela N., Romero L., Torres-Jardón R., Solt A., Reed W. Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants. Inhal. Toxicol. 2008 Mar;20(5):499–506. doi: 10.1080/08958370701864797. PMID: 18368620. [DOI] [PubMed] [Google Scholar]
  • 29.Lund A.K., Lucero J., Lucas S., Madden M.C., McDonald J.D., Seagrave J.C., Knuckles T.L., Campen M.J. Vehicular emissions induce vascular MMP-9 expression and activity associated with endothelin-1-mediated pathways. Arterioscler. Thromb. Vasc. Biol. 2009 Apr;29(4):511–517. doi: 10.1161/ATVBAHA.108.176107. Epub 2009 Jan 15. PMID: 19150882; PMCID: PMC4103743. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.He D., Wu S., Zhao H., Qiu H., Fu Y., Li X., He Y. Association between particulate matter 2.5 and diabetes mellitus: a meta-analysis of cohort studies. J Diabetes Investig. 2017 Sep;8(5):687–696. doi: 10.1111/jdi.12631. Epub 2017 May 3. PMID: 28122165; PMCID: PMC5583950. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31.Chilian-Herrera O.L., Tamayo-Ortiz M., Texcalac-Sangrador J.L., Rothenberg S.J., López-Ridaura R., Romero-Martínez M., Wright R.O., Just A.C., Kloog I., Bautista-Arredondo L.F., Téllez-Rojo M.M. PM2.5 exposure as a risk factor for type 2 diabetes mellitus in the Mexico City metropolitan area. BMC Publ. Health. 2021 Nov 13;21(1):2087. doi: 10.1186/s12889-021-12112-w. PMID: 34774026; PMCID: PMC8590776. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 32.Rao X., Montresor-Lopez J., Puett R., Rajagopalan S., Brook R.D. Ambient air pollution: an emerging risk factor for diabetes mellitus. Curr. Diabetes Rep. 2015 Jun;15(6):603. doi: 10.1007/s11892-015-0603-8. PMID: 25894943. [DOI] [PubMed] [Google Scholar]
  • 33.Xu X., Yavar Z., Verdin M., Ying Z., Mihai G., Kampfrath T., Wang A., Zhong M., Lippmann M., Chen L.C., Rajagopalan S., Sun Q. Effect of early particulate air pollution exposure on obesity in mice: role of p47phox. Arterioscler. Thromb. Vasc. Biol. 2010 Dec;30(12):2518–2527. doi: 10.1161/ATVBAHA.110.215350. Epub 2010 Sep 23. PMID: 20864666; PMCID: PMC3065931. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34.Faiz A.S., Rhoads G.G., Demissie K., Lin Y., Kruse L., Rich D.Q. Does ambient air pollution trigger stillbirth? Epidemiology. 2013 Jul;24(4):538–544. doi: 10.1097/EDE.0b013e3182949ce5. PMID: 23676263. [DOI] [PubMed] [Google Scholar]
  • 35.Li J., Yao Y., Xie W., Wang B., Guan T., Han Y., Wang H., Zhu T., Xue T. Association of long-term exposure to PM2.5 with blood lipids in the Chinese population: findings from a longitudinal quasi-experiment. Environ. Int. 2021 Jun;151 doi: 10.1016/j.envint.2021.106454. Epub 2021 Mar 3. PMID: 33676285. [DOI] [PubMed] [Google Scholar]
  • 36.McGuinn L.A., Schneider A., McGarrah R.W., Ward-Caviness C., Neas L.M., Di Q., Schwartz J., Hauser E.R., Kraus W.E., Cascio W.E., Diaz-Sanchez D., Devlin R.B. Association of long-term PM2.5 exposure with traditional and novel lipid measures related to cardiovascular disease risk. Environ. Int. 2019 Jan;122:193–200. doi: 10.1016/j.envint.2018.11.001. Epub 2018 Nov 13. PMID: 30446244; PMCID: PMC6467069. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 37.Zhang J., Liang S., Ning R., Jiang J., Zhang J., Shen H., Chen R., Duan J., Sun Z. PM2.5-induced inflammation and lipidome alteration associated with the development of atherosclerosis based on a targeted lipidomic analysis. Environ. Int. 2020 Mar;136 doi: 10.1016/j.envint.2019.105444. Epub 2020 Jan 11. PMID: 31935561. [DOI] [PubMed] [Google Scholar]
  • 38.Yang S., Chen R., Zhang L., Sun Q., Li R., Gu W., Zhong M., Liu Y., Chen L.C., Sun Q., Liu C. Lipid metabolic adaption to long-term ambient PM2.5 exposure in mice. Environ Pollut. 2021 Jan 15;269 doi: 10.1016/j.envpol.2020.116193. Epub 2020 Nov 30. PMID: 33302088. [DOI] [PubMed] [Google Scholar]
  • 39.Farhadi Z., Abulghasem Gorgi H., Shabaninejad H., Aghajani Delavar M., Torani S. Association between PM2.5 and risk of hospitalization for myocardial infarction: a systematic review and a meta-analysis. BMC Publ. Health. 2020 Mar 12;20(1):314. doi: 10.1186/s12889-020-8262-3. PMID: 32164596; PMCID: PMC7068986. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.Madrigano J., Kloog I., Goldberg R., Coull B.A., Mittleman M.A., Schwartz J. Long-term exposure to PM2.5 and incidence of acute myocardial infarction. Environ. Health Perspect. 2013 Feb;121(2):192–196. doi: 10.1289/ehp.1205284. Epub 2012 Nov 29. PMID: 23204289; PMCID: PMC3569684. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41.Liao N.S., Sidney S., Deosaransingh K., Van Den Eeden S.K., Schwartz J., Alexeeff S.E. Particulate air pollution and risk of cardiovascular events among adults with a history of stroke or acute myocardial infarction. J. Am. Heart Assoc. 2021;10(10) doi: 10.1161/JAHA.120.019758. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 42.Rhinehart Z.J., Kinnee E., Essien U.R., Saul M., Guhl E., Clougherty J.E., Magnani J.W. Association of fine particulate matter and risk of stroke in patients with atrial fibrillation. JAMA Netw. Open. 2020 Sep 1;3(9) doi: 10.1001/jamanetworkopen.2020.11760. PMID: 32930777; PMCID: PMC7492916. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 43.O'Donnell M.J., Fang J., Mittleman M.A., Kapral M.K., Wellenius G.A. Investigators of the Registry of Canadian Stroke Network. Fine particulate air pollution (PM2.5) and the risk of acute ischemic stroke. Epidemiology. 2011 May;22(3):422–431. doi: 10.1097/EDE.0b013e3182126580. PMID: 21399501; PMCID: PMC3102528. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 44.Yuan S., Wang J., Jiang Q., He Z., Huang Y., Li Z., Cai L., Cao S. Long-term exposure to PM2.5 and stroke: a systematic review and meta-analysis of cohort studies. Environ. Res. 2019 Oct;177 doi: 10.1016/j.envres.2019.108587. Epub 2019 Jul 15. PMID: 31326714. [DOI] [PubMed] [Google Scholar]
  • 45.Yang X., Zhang L., Chen X., Liu F., Shan A., Liang F., Li X., Wu H., Yan M., Ma Z., Dong G., Liu Y., Chen J., Wang T., Zhao B., Liu Y., Gu D., Tang N. Long-term exposure to ambient PM2.5 and stroke mortality among urban residents in northern China. Ecotoxicol. Environ. Saf. 2021 Apr 15;213 doi: 10.1016/j.ecoenv.2021.112063. Epub 2021 Feb 24. PMID: 33636465; PMCID: PMC8150861. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 46.Shah A.S., Langrish J.P., Nair H., McAllister D.A., Hunter A.L., Donaldson K., Newby D.E., Mills N.L. Global association of air pollution and heart failure: a systematic review and meta-analysis. Lancet. 2013 Sep 21;382(9897):1039–1048. doi: 10.1016/S0140-6736(13)60898-3. Epub 2013 Jul 10. PMID: 23849322; PMCID: PMC3809511. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 47.Liu H., Tian Y., Song J., Cao Y., Xiang X., Huang C., Li M., Hu Y. Effect of ambient air pollution on hospitalization for heart failure in 26 of China's largest cities. Am. J. Cardiol. 2018 Mar 1;121(5):628–633. doi: 10.1016/j.amjcard.2017.11.039. Epub 2017 Dec 11. PMID: 29304993. [DOI] [PubMed] [Google Scholar]
  • 48.Wang M., Zhou T., Song Y., Li X., Ma H., Hu Y., Heianza Y., Qi L. Joint exposure to various ambient air pollutants and incident heart failure: a prospective analysis in UK Biobank. Eur. Heart J. 2021 Apr 21;42(16):1582–1591. doi: 10.1093/eurheartj/ehaa1031. PMID: 33527989; PMCID: PMC8060055. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 49.Zhang D., Chen W., Cheng C., Huang H., Li X., Qin P., Chen C., Luo X., Zhang M., Li J., Sun X., Liu Y., Hu D. Air pollution exposure and heart failure: a systematic review and meta-analysis. Sci. Total Environ. 2023 May 10;872 doi: 10.1016/j.scitotenv.2023.162191. Epub 2023 Feb 11. PMID: 36781139. [DOI] [PubMed] [Google Scholar]
  • 50.Lee H.H., Pan S.C., Chen B.Y., Lo S.H., Guo Y.L. Atrial fibrillation hospitalization is associated with exposure to fine particulate air pollutants. Environ. Health. 2019;18:117. doi: 10.1186/s12940-019-0554-7. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 51.Wang F., Ahat X., Liang Q., Ma Y., Sun M., Lin L., Li T., Duan J., Sun Z. The relationship between exposure to PM2.5 and atrial fibrillation in older adults: a systematic review and meta-analysis. Sci. Total Environ. 2021 Aug 25;784 doi: 10.1016/j.scitotenv.2021.147106. Epub 2021 Apr 15. PMID: 34088062. [DOI] [PubMed] [Google Scholar]
  • 52.Gallo E., Folino F., Buja G., Zanotto G., Bottigliengo D., Comoretto R., Marras E., Allocca G., Vaccari D., Gasparini G., Bertaglia E., Zoppo F., Calzolari V., Nangah Suh R., Ignatiuk B., Lanera C., Benassi A., Gregori D., Iliceto S. Daily exposure to air pollution particulate matter is associated with atrial fibrillation in high-risk patients. Int. J. Environ. Res. Publ. Health. 2020 Aug 19;17(17):6017. doi: 10.3390/ijerph17176017. PMID: 32824908; PMCID: PMC7504134. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 53.He F., Yanosky J.D., Fernandez-Mendoza J., Chinchilli V.M., Al-Shaar L., Vgontzas A.N., Bixler E.O., Liao D. Acute impact of fine particulate air pollution on cardiac arrhythmias in a population-based sample of adolescents: the Penn state Child cohort. J. Am. Heart Assoc. 2022 Sep 20;11(18) doi: 10.1161/JAHA.122.026370. Epub 2022 Sep 14. PMID: 36102241; PMCID: PMC9683666. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 54.Newby D.E., Mannucci P.M., Tell G.S., Baccarelli A.A., Brook R.D., Donaldson K., Forastiere F., Franchini M., Franco O.H., Graham I., Hoek G., Hoffmann B., Hoylaerts M.F., Künzli N., Mills N., Pekkanen J., Peters A., Piepoli M.F., Rajagopalan S., Storey R.F. ESC working group on thrombosis, European association for cardiovascular prevention and rehabilitation; ESC heart failure association. Expert position paper on air pollution and cardiovascular disease. Eur. Heart J. 2015 Jan 7;36(2):83–93b. doi: 10.1093/eurheartj/ehu458. Epub 2014 Dec 9. PMID: 25492627; PMCID: PMC6279152. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 55.Lim S.S., Vos T., Flaxman A.D., Danaei G., Shibuya K., Adair-Rohani H., Amann M., Anderson H.R., Andrews K.G., Aryee M., Atkinson C., Bacchus L.J., Bahalim A.N., Balakrishnan K., Balmes J., Barker-Collo S., Baxter A., Bell M.L., Blore J.D., Blyth F., Bonner C., Borges G., Bourne R., Boussinesq M., Brauer M., Brooks P., Bruce N.G., Brunekreef B., Bryan-Hancock C., Bucello C., Buchbinder R., Bull F., Burnett R.T., Byers T.E., Calabria B., Carapetis J., Carnahan E., Chafe Z., Charlson F., Chen H., Chen J.S., Cheng A.T., Child J.C., Cohen A., Colson K.E., Cowie B.C., Darby S., Darling S., Davis A., Degenhardt L., Dentener F., Des Jarlais D.C., Devries K., Dherani M., Ding E.L., Dorsey E.R., Driscoll T., Edmond K., Ali S.E., Engell R.E., Erwin P.J., Fahimi S., Falder G., Farzadfar F., Ferrari A., Finucane M.M., Flaxman S., Fowkes F.G., Freedman G., Freeman M.K., Gakidou E., Ghosh S., Giovannucci E., Gmel G., Graham K., Grainger R., Grant B., Gunnell D., Gutierrez H.R., Hall W., Hoek H.W., Hogan A., Hosgood H.D., 3rd, Hoy D., Hu H., Hubbell B.J., Hutchings S.J., Ibeanusi S.E., Jacklyn G.L., Jasrasaria R., Jonas J.B., Kan H., Kanis J.A., Kassebaum N., Kawakami N., Khang Y.H., Khatibzadeh S., Khoo J.P., Kok C., Laden F., Lalloo R., Lan Q., Lathlean T., Leasher J.L., Leigh J., Li Y., Lin J.K., Lipshultz S.E., London S., Lozano R., Lu Y., Mak J., Malekzadeh R., Mallinger L., Marcenes W., March L., Marks R., Martin R., McGale P., McGrath J., Mehta S., Mensah G.A., Merriman T.R., Micha R., Michaud C., Mishra V., Mohd Hanafiah K., Mokdad A.A., Morawska L., Mozaffarian D., Murphy T., Naghavi M., Neal B., Nelson P.K., Nolla J.M., Norman R., Olives C., Omer S.B., Orchard J., Osborne R., Ostro B., Page A., Pandey K.D., Parry C.D., Passmore E., Patra J., Pearce N., Pelizzari P.M., Petzold M., Phillips M.R., Pope D., Pope C.A., 3rd, Powles J., Rao M., Razavi H., Rehfuess E.A., Rehm J.T., Ritz B., Rivara F.P., Roberts T., Robinson C., Rodriguez-Portales J.A., Romieu I., Room R., Rosenfeld L.C., Roy A., Rushton L., Salomon J.A., Sampson U., Sanchez-Riera L., Sanman E., Sapkota A., Seedat S., Shi P., Shield K., Shivakoti R., Singh G.M., Sleet D.A., Smith E., Smith K.R., Stapelberg N.J., Steenland K., Stöckl H., Stovner L.J., Straif K., Straney L., Thurston G.D., Tran J.H., Van Dingenen R., van Donkelaar A., Veerman J.L., Vijayakumar L., Weintraub R., Weissman M.M., White R.A., Whiteford H., Wiersma S.T., Wilkinson J.D., Williams H.C., Williams W., Wilson N., Woolf A.D., Yip P., Zielinski J.M., Lopez A.D., Murray C.J., Ezzati M., AlMazroa M.A., Memish Z.A. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012 Dec 15;380(9859):2224–2260. doi: 10.1016/S0140-6736(12)61766-8. Erratum in: Lancet. 2013 Apr 13;381(9874):1276. Erratum in: Lancet. 2013 Feb 23;381(9867):628. AlMazroa, Mohammad A [added]; Memish, Ziad A [added]. PMID: 23245609; PMCID: PMC4156511. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 56.Lu F., Xu D., Cheng Y., Dong S., Guo C., Jiang X., Zheng X. Systematic review and meta-analysis of the adverse health effects of ambient PM2.5 and PM10 pollution in the Chinese population. Environ. Res. 2015 Jan;136:196–204. doi: 10.1016/j.envres.2014.06.029. Epub 2014 Nov 25. PMID: 25460637. [DOI] [PubMed] [Google Scholar]
  • 57.Crouse D.L., Peters P.A., van Donkelaar A., Goldberg M.S., Villeneuve P.J., Brion O., Khan S., Atari D.O., Jerrett M., Pope C.A., Brauer M., Brook J.R., Martin R.V., Stieb D., Burnett R.T. Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: a Canadian national-level cohort study. Environ. Health Perspect. 2012 May;120(5):708–714. doi: 10.1289/ehp.1104049. Epub 2012 Feb 7. PMID: 22313724; PMCID: PMC3346774. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 58.Pinault L.L., Weichenthal S., Crouse D.L., Brauer M., Erickson A., Donkelaar A.V., Martin R.V., Hystad P., Chen H., Finès P., Brook J.R., Tjepkema M., Burnett R.T. Associations between fine particulate matter and mortality in the 2001 Canadian census health and environment cohort. Environ. Res. 2017 Nov;159:406–415. doi: 10.1016/j.envres.2017.08.037. Epub 2017 Sep 18. PMID: 28850858. [DOI] [PubMed] [Google Scholar]
  • 59.Brook Robert D., Rajagopalan Sanjay. Particulate matter air pollution and atherosclerosis. Curr. Atherosclerosis Rep. 2010;12:291–300. doi: 10.1007/s11883-010-0122-7. [DOI] [PubMed] [Google Scholar]
  • 60.Liu C., Cai J., Chen R., Sera F., Guo Y., Tong S., Li S., Lavigne E., Correa P.M., Ortega N.V., Orru H., Maasikmets M., Jaakkola J.J.K., Ryti N., Breitner S., Schneider A., Katsouyanni K., Samoli E., Hashizume M., Honda Y., Ng C.F.S., Diaz M.H., la Cruz Valencia C., Rao S., Palomares A.D., Pereira da Silva S., Madureira J., Holobâc I.H., Fratianni S., Scovronick N., Garland R.M., Tobias A., Íñiguez C., Forsberg B., Åström C., Vicedo-Cabrera A.M., Ragettli M.S., Guo Y.L., Pan S.C., Milojevic A., Bell M.L., Zanobetti A., Schwartz J., Gasparrini A., Kan H. Coarse particulate air pollution and daily mortality: a global study in 205 cities. Am. J. Respir. Crit. Care Med. 2022 Oct 15;206(8):999–1007. doi: 10.1164/rccm.202111-2657OC. PMID: 35671471. [DOI] [PubMed] [Google Scholar]
  • 61.Thurston G.D., Burnett R.T., Turner M.C., Shi Y., Krewski D., Lall R., Ito K., Jerrett M., Gapstur S.M., Diver W.R., Pope C.A. Ischemic heart disease mortality and long-term exposure to source-related components of U.S. Fine particle air pollution. Environ. Health Perspect. 2016 Jun;124(6):785–794. doi: 10.1289/ehp.1509777. Epub 2015 Dec 2. PMID: 26629599; PMCID: PMC4892920. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 62.Kazemiparkouhi F., Honda T., Eum K.D., Wang B., Manjourides J., Suh H.H. The impact of Long-Term PM2.5 constituents and their sources on specific causes of death in a US Medicare cohort. Environ. Int. 2022;159 doi: 10.1016/j.envint.2021.106988. [DOI] [PubMed] [Google Scholar]
  • 63.Weichenthal S., Lavigne E., Traub A., Umbrio D., You H., Pollitt K., Shin T., Kulka R., Stieb D.M., Korsiak J., Jessiman B., Brook J.R., Hatzopoulou M., Evans G., Burnett R.T. Association of sulfur, transition metals, and the oxidative potential of outdoor PM2.5 with acute cardiovascular events: a case-crossover study of Canadian adults. Environ. Health Perspect. 2021 Oct;129(10) doi: 10.1289/EHP9449. Epub 2021 Oct 13. PMID: 34644144; PMCID: PMC8513754. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 64.Schwarz M., Schneider A., Cyrys J., Bastian S., Breitner S., Peters A. Impact of ambient ultrafine particles on cause-specific mortality in three German cities [published online ahead of print, 2023 mar 6] Am. J. Respir. Crit. Care Med. 2023 doi: 10.1164/rccm.202209-1837OC. 10.1164/rccm.202209-1837OC. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 65.Xu R., Wei J., Liu T., Li Y., Yang C., Shi C., Chen G., Zhou Y., Sun H., Liu Y. Association of short-term exposure to ambient PM1 with total and cause-specific cardiovascular disease mortality. Environ. Int. 2022 Nov;169 doi: 10.1016/j.envint.2022.107519. Epub 2022 Sep 16. PMID: 36152364. [DOI] [PubMed] [Google Scholar]
  • 66.Carlsten C., Salvi S., Wong G.W.K., Chung K.F. Personal strategies to minimise effects of air pollution on respiratory health: advice for providers, patients and the public. Eur. Respir. J. 2020 Jun 4;55(6) doi: 10.1183/13993003.02056-2019. PMID: 32241830; PMCID: PMC7270362. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 67.Rajper S.A., Ullah S., Li Z. Exposure to air pollution and self-reported effects on Chinese students: a case study of 13 megacities. PLoS One. 2018;13 doi: 10.1371/journal.pone.0194364. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 68.Cherrie J.W., Apsley A., Cowie H., Steinle S., Mueller W., Lin C., Horwell C.J., Sleeuwenhoek A., Loh M. Effectiveness of face masks used to protect Beijing residents against particulate air pollution. Occup. Environ. Med. 2018 Jun;75(6):446–452. doi: 10.1136/oemed-2017-104765. Epub 2018 Apr 9. PMID: 29632130; PMCID: PMC5969371. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 69.Goel A., Kumar P. A review of fundamental drivers governing the emissions, dispersion and exposure to vehicle-emitted nanoparticles at signalised traffic intersections. Atmos. Environ. 2014;97:316–331. doi: 10.1016/j.atmosenv.2014.08.037. [DOI] [Google Scholar]
  • 70.Hatzopoulou M., Weichenthal S., Dugum H., Pickett G., Miranda-Moreno L., Kulka R., Andersen R., Goldberg M. The impact of traffic volume, composition, and road geometry on personal air pollution exposures among cyclists in Montreal, Canada. J. Expo. Sci. Environ. Epidemiol. 2013 Jan-Feb;23(1):46–51. doi: 10.1038/jes.2012.85. Epub 2012 Aug 22. PMID: 22910003. [DOI] [PubMed] [Google Scholar]
  • 71.Carvalho A.M., Krecl P., Targino A.C. Variations in individuals' exposure to black carbon particles during their daily activities: a screening study in Brazil. Environ. Sci. Pollut. Res. Int. 2018;25:18412–18423. doi: 10.1007/s11356-018-2045-8. [DOI] [PubMed] [Google Scholar]

Articles from International Journal of Cardiology. Cardiovascular Risk and Prevention are provided here courtesy of Elsevier

RESOURCES