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Updated: May 27, 2026
04:56
Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)
Published on: August 4, 2023
Air pollution-associated procoagulant changes: the role of circulating microvesicles
J Emmerechts1, L Jacobs, S Van Kerckhoven
1Center for Molecular and Vascular Biology, Unit of Lung Toxicology, University of Leuven, Leuven, Belgium.
Journal of Thrombosis and Haemostasis : JTH
|November 10, 2011
Summary
Exposure to air pollution, specifically particulate matter (PM), increases the risk of venous thromboembolism (VTE). This study found that elevated microvesicle levels and procoagulant properties, not coagulation factors, are key contributors to VTE risk from prolonged PM exposure.
Area of Science:
- Environmental Health
- Cardiovascular Research
- Hematology
Background:
- Epidemiological studies link particulate matter (PM) air pollution exposure to increased venous thromboembolism (VTE) risk.
- The specific pathophysiological mechanisms connecting PM exposure and VTE remain incompletely understood.
Purpose of the Study:
- To elucidate the pathophysiological pathways linking particulate matter (PM) exposure to venous thromboembolism (VTE).
- To investigate associations between PM exposure and coagulation, inflammation, and circulating microvesicles in patients with diabetes.
Main Methods:
- Assessed associations between PM(2.5) and PM(10) exposure and coagulation/inflammation markers in 233 diabetes patients.
- Measured circulating microvesicles (platelet-derived, annexin V-binding, red blood cell-derived) and inflammatory markers (CRP, leukocytes, fibrinogen).
- Evaluated thrombin generation, tissue factor (TF), and coagulation times (aPTT, PT) in relation to past and current PM exposure.
Main Results:
- Current PM(2.5)/PM(10) exposure inversely correlated with platelet-derived and annexin V-binding microvesicles.
- Past PM(10) exposure (up to 1 week) associated with elevated CRP, leukocytes, fibrinogen, and TF-dependent procoagulant activity.
- Longer-term PM exposure (up to 1 year) linked to increased red blood cell-derived and annexin V-binding microvesicles, but not TF.
Conclusions:
- Increased numbers and procoagulant properties of circulating microvesicles appear to be key mediators of VTE risk.
- These microvesicle changes, rather than direct increases in coagulation factors, likely contribute to VTE development during prolonged air pollution exposure.
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