These authors contributed equally to this study.
Air pollution-associated procoagulant changes: the role of circulating microvesicles
Article first published online: 4 JAN 2012
© 2011 International Society on Thrombosis and Haemostasis
Journal of Thrombosis and Haemostasis
Volume 10, Issue 1, pages 96–106, January 2012
How to Cite
EMMERECHTS, J., JACOBS, L., VAN KERCKHOVEN, S., LOYEN, S., MATHIEU, C., FIERENS, F., NEMERY, B., NAWROT, T.S. and HOYLAERTS, M.F. (2012), Air pollution-associated procoagulant changes: the role of circulating microvesicles. Journal of Thrombosis and Haemostasis, 10: 96–106. doi: 10.1111/j.1538-7836.2011.04557.x
- Issue published online: 4 JAN 2012
- Article first published online: 4 JAN 2012
- Accepted manuscript online: 8 NOV 2011 10:04AM EST
- Received 14 June 2011, accepted 31 October 2011
- air pollution;
Summary. Background: Epidemiological studies suggest an association between exposure to particulate matter (PM) in air pollution and the risk of venous thromboembolism (VTE). Objectives: To investigate the underlying pathophysiological pathways linking PM exposure and VTE. Patients and methods: We assessed potential associations between PM exposure and coagulation and inflammation parameters, including circulating microvesicles, in a group of 233 patients with diabetes. Results: The numbers of circulating blood platelet-derived and annexin V-binding microvesicles were inversely associated with the current levels of PM2.5 or PM10, measured on the day of sampling. Recent past exposure to PM10, up to 1 week prior to blood sampling, estimated at the patients’ residential addresses, was associated with elevated high-sensitivity C-reactive protein (CRP), leukocytes and fibrinogen, as well as with tissue factor (TF)-dependent procoagulant changes in thrombin generation assays. When longer windows of past exposure were considered, up to 1 year preceding blood sampling, procoagulant changes were evident from the strongly increased numbers of red blood cell-derived circulating microvesicles and annexin V-binding microvesicles, but they no longer associated with TF. Past PM exposure was never associated with activated partial thromboplastin time (aPTT), prothrombin time (PT), or factor (F) VII, FVIII, FXII or D-dimers. Residential distance to a major road was only marginally correlated with procoagulant changes in FVIII and thrombin generation. Conclusions: Increases in the number of microvesicles and in their procoagulant properties, rather than increases in coagulation factors per se, seem to contribute to the risk of VTE, developing during prolonged exposure to air pollutants.