The short- and long-term associations of particulate matter with inflammation and blood coagulation markers: A meta-analysis

Abstract

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 PM 2.5 (PM with an aerodynamic diameter ≤2.5 μm)/PM 10 (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/m 3 PM 2.5 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 PM 10 and fibrinogen (percent change = 0.17%, 95% CI: 0.04%, 0.29%). Overall analysis showed that long-term associations of fibrinogen with PM 2.5 and PM 10 were not significant. Subgroup analysis showed that long-term associations of fibrinogen with PM 2.5 and PM 10 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.

Effects of particulate matter on hospital admissions for respiratory diseases: an ecological study based on 12.5 years of time series data in Shanghai

“…Second, PM 2.5 induction of a local or systematic inflammatory reaction is the major pathologic basis for the onset and progression of several related diseases [ 38 ]. Evidence from a meta-analysis [ 39 ] also showed that PM exposure increased the levels of fibrinogen and TNF-α.…”

The Association of White Blood Cells and Air Pollutants—A Population-Based Study

“…Fine particles (PM 2.5 , with a diameter smaller than 2.5 μm) and ultrafine particles (UFP, with a diameter smaller than 0.1 μm) can reach the alveoli deep inside the lungs, and even penetrate through the epithelia into the bloodstream [ 23 , 27 , 28 ]. The inhaled pollutants cause epithelium injuries and activate the immune system to launch a cascading inflammation response [ 22 , 23 , 29 , 30 ].…”

Effects of PM Exposure on the Methylation of Clock Genes in A Population of Subjects with Overweight or Obesity

“…Exposure to excessive concentrations of air pollutants has been implicated in the etiology and/or worsening of several pathological conditions, ranging from cardiovascular and neurological diseases to cancer [1][2][3]. It is now generally recognized that one of the main pathological mechanisms elicited by airborne pollutants, including particulate matter (PM), is based on the activation of a systemic inflammatory cascade [4,5]. After inhalation, fine PM deposits throughout the respiratory tract and damages the airway epithelium.…”