Background: Previous studies have suggested that exposure to air pollution may increase stroke risk, but the results remain inconsistent. Evidence of more recent studies is highly warranted, especially gas air pollutants. Methods: We searched PubMed, Embase, and Web of Science to identify studies till February 2020 and conducted a meta-analysis on the association between air pollution (PM_2.5, particulate matter with aerodynamic diameter less than 2.5 μm; PM₁₀, particulate matter with aerodynamic diameter less than 10 μm; NO₂, nitrogen dioxide; SO₂, sulfur dioxide; CO, carbon monoxide; O₃, ozone) and stroke (hospital admission, incidence, and mortality). Fixed- or random-effects model was used to calculate pooled odds ratios (OR)/hazard ratio (HR) and their 95% confidence intervals (CI) for a 10 μg/m³ increase in air pollutant concentration. Results: A total of 68 studies conducted from more than 23 million participants were included in our meta-analysis. Meta-analyses showed significant associations of all six air pollutants and stroke hospital admission (e.g., PM_2.5: OR = 1.008 (95% CI 1.005, 1.011); NO₂: OR = 1.023 (95% CI 1.015, 1.030), per 10 μg/m³ increases in air pollutant concentration). Exposure to PM_2.5, SO₂, and NO₂ was associated with increased risks of stroke incidence (PM_2.5: HR = 1.048 (95% CI 1.020, 1.076); SO₂: HR = 1.002 (95% CI 1.000, 1.003); NO₂: HR = 1.002 (95% CI 1.000, 1.003), respectively). However, no significant differences were found in associations of PM₁₀, CO, O₃, and stroke incidence. Except for CO and O₃, we found that higher level of air pollution (PM_2.5, PM₁₀, SO₂, and NO₂) exposure was associated with higher stroke mortality (e.g., PM₁₀: OR = 1.006 (95% CI 1.003, 1.010), SO₂: OR = 1.006 (95% CI 1.005, 1.008). Conclusions: Exposure to air pollution was positively associated with an increased risk of stroke hospital admission (PM_2.5, PM₁₀, SO₂, NO₂, CO, and O₃), incidence (PM_2.5, SO₂, and NO₂), and mortality (PM_2.5, PM₁₀, SO₂, and NO₂). Our study would provide a more comprehensive evidence of air pollution and stroke, especially SO₂ and NO₂.

Inflammation and the coagulation cascade are considered to be the potential mechanisms of ambient particulate matter (PM) exposure-induced adverse cardiovascular events. Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-8 (IL-8), and fibrinogen are arguably the four most commonly assayed markers to reflect the relationships of PM with inflammation and blood coagulation. This review summarized and quantitatively analyzed the existing studies reporting short- and long-term associations of PM2.5(PM with an aerodynamic diameter ≤2.5 μm)/PM10 (PM with an aerodynamic diameter≤10 μm) with important inflammation and blood coagulation markers (TNF-α, IL-6, IL-8, fibrinogen). We reviewed relevant studies published up to July 2020, using three English databases (PubMed, Web of Science, Embase) and two Chinese databases (Wang-Fang, China National Knowledge Infrastructure). The OHAT tool, with some modification, was applied to evaluate risk of bias. Meta-analyses were conducted with random-effects models for calculating the pooled estimate of markers. To assess the potential effect modifiers and the source of heterogeneity, we conducted subgroup analyses and meta-regression analyses where appropriate. The assessment and correction of publication bias were based on Begg's and Egger's test and "trim-and-fill" analysis. We identified 44 eligible studies. For short-term PM exposure, the percent change of a 10 μg/m3 PM2.5 increase on TNF-α and fibrinogen was 3.51% (95% confidence interval (CI): 1.21%, 5.81%) and 0.54% (95% confidence interval (CI): 0.21%, 0.86%) respectively. We also found a significant short-term association between PM10 and fibrinogen (percent change = 0.17%, 95% CI: 0.04%, 0.29%). Overall analysis showed that long-term associations of fibrinogen with PM2.5 and PM10 were not significant. Subgroup analysis showed that long-term associations of fibrinogen with PM2.5 and PM10 were significant only found in studies conducted in Asia. Our findings support significant short-term associations of PM with TNF-α and fibrinogen. Future epidemiological studies should address the role long-term PM exposure plays in inflammation and blood coagulation markers level change.

Evidence of more recent studies should be updated to evaluate the effect of long-term exposure to particulate matter (PM) on blood pressure and hypertension. Studies of long-term effects of PM₁, PM_2.5 and PM₁₀ on blood pressure (SBP, DBP, MAP), hypertension were searched in Pubmed, Web of Science and Embase before May, 2021. Meta-analysis of 41 studies showed that exposure to PM₁, PM_2.5 was associated with SBP (1.76 mmHg (95%CI:0.71, 2.80) and 0.63 mmHg (95%CI:0.40, 0.85), per 10 μg/m³ increase in PM), all three air pollutants (PM₁, PM_2.5, PM₁₀) was associated with DBP (1.16 mmHg (95%CI:0.34, 1.99), 0.31 mmHg (95%CI:0.16, 0.47), 1.17 mmHg (95%CI:0.24, 2.09), respectively. As for hypertension, PM₁, PM_2.5 and PM₁₀ were all significantly associated with higher risk of hypertension (OR=1.27 (95%CI:1.06, 1.52), 1.15 (95%CI:1.10, 1.20) and 1.11 (95%CI:1.07, 1.16). In conclusion, our study indicated a positive association between long-term exposure to particulate matter and increased blood pressure, hypertension.

Health effects induced by heavy metal components of particulate matter need further research. A total of 32 healthy volunteers were recruited to walk for 4 h in two different exposure scenarios in Wuhan from May 1 to Jun 30, 2019. Metabolomics technology was used to identify serum cardiovascular-related metabolites disturbance, and the health risk assessment model was employed to assess the non-carcinogenic and carcinogenic risks associated with airborne heavy metals. The results showed that the average mass concentrations of Co, Ni, Cd, Cu, Ag and Ba in PM₁₀ from May 1 to Jun 30, 2019 were 0.22, 0.49, 11.53, 2.23, 34.47 and 4.19 ng/m³, respectively, and were 0.86, 128.47, 291.85, 291.94, 98.55 and 422.62 ng/m³ in PM_2.5, respectively. Healthy young adults briefly exposed to heavy metals were associated with serum cardiovascular-related metabolites disturbance, including increased SM(d18:1/17:0) and Sphingomyelin, and decreased GlcCer(d16:1/18:0) and Galabiosylceramide, simultaneously accompanied by activation of the sphingolipid metabolism pathway. Non-carcinogenic and carcinogenic risks of airborne heavy metals via the inhalation route were observed, Ni and Cd most influenced to potential health risks. Findings indicated exposure to increment of heavy metals may increase health risks by causing cardiovascular-related metabolites disturbance via activating the sphingolipid metabolism pathway.