The Acute Effects of Fine Particulate Matter Constituents on Blood Inflammation and Coagulation

Abstract

Limited evidence is available on the effects of various fine particulate matter (PM) constituents on blood inflammation and coagulation. We examined the associations between 10 constituents and 10 circulating biomarkers in a panel of 28 urban residents with four repeated measurements in Shanghai, China. Based on the linear mixed-effect models, we fitted the single-constituent models, the constituent-PM joint models, and the constituent-residual models to evaluate the associations between PM constituents and eight inflammatory biomarkers (fibrinogen, C-reactive protein, monocyte chemoattractant protein-1, tumor necrosis factor-α, interleukin-1b, intercellular adhesion molecule-1, P-selectin, vascular cell adhesion molecule-1) and two coagulation biomarkers (plasminogen activator inhibitor-1 and soluble CD40 ligand). We found robust associations of organic carbon (OC), elemental carbon (EC), nitrate (NO), and ammonium (NH) with at least 1 of 8 inflammatory markers. On average, an interquartile range increase in the four constituents corresponded to increments of 50%, 37%, 25%, and 26% in inflammatory biomarkers, respectively. Only sulfate (SO) or NH was robustly associated with coagulation markers (corresponding increments: 23% and 20%). Our results provided evidence that some constituents in PM (OC, EC, NO, SO, and NH) might play crucial roles in inducing systematic inflammation and coagulation, but their roles varied by the selected biomarkers.

Harmful impact of air pollution on severe acute exacerbation of chronic obstructive pulmonary disease: particulate matter is hazardous

“…26 In addition to acute damage, PM enters the body and causes abnormal inflammatory responses and coagulopathy. 9 Recent study shows that PM 2.5 contributes to abnormal airway inflammation through various signaling pathways, such as epidermal growth factor receptor (EGFR), mitogen-activated protein kinase (MAPK), nuclear factor (NF)-kB and the interleukin pathway. 27 – 29 Also, PM 2.5 affects the fractional concentration of exhaled nitric oxide (FeNO), which can lead to airway inflammation in COPD patients.…”

“…PM is thought to cause direct damage to the lungs, bronchi and skin 6 , 7 as well as an abnormal inflammatory response and coagulopathy, resulting in various diseases. 8 , 9 PM can have a more harmful impact on patients with pulmonary diseases, such as COPD. 10 However, studies regarding the harmful effects of PM on COPD and acute exacerbation of COPD (AECOPD) are lacking.…”

Particulate Matter Air Pollution: Effects on the Cardiovascular System

“…Exposure to PM has been shown to induce a prothrombotic state, which may play a role in its ability to cause arterial thrombotic (myocardial infarction, ischemic/thrombotic cerebrovascular events) and venous thrombotic events (deep venous thrombosis) ( 81 , 82 ). Exposure to PM induces the production of fibrinogen, and other factors that play a role in hemostasis including Von Willebrand factor, sCD62P, and sCD40L ( 65 , 83 – 85 ). In addition to prothrombotic pathways, antifibrinolytic pathways are also activated by PM exposure.…”

Functional human 3D microvascular networks on a chip to study the procoagulant effects of ambient fine particulate matter

“…3,4 And PM induced coagulation abnormalities are very likely responsible for many kinds of cardiovascular disease. 5,6 The precise pathway explaining how PM disrupts the coagulation function has, however, not yet been entirely determined. Recent studies have increasingly focused on ambient ne particulate matter (FPM).…”