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Kilin?et al. Particle and Fibre Toxicology 2011, 8:12 http://www.particleandfibretoxicology.com/content/8/1/LETTER TO THE EDITOROpen AccessThe procoagulant effects of fine particulate matter in vivoEvren Kilin?*, Holger Schulz2,4*, Gerhardus JAJM Kuiper1, Henri MH Spronk1, Hugo ten Cate1, Swapna Upadhyay7, Koustav Ganguly7, Tobias Stoeger4, Manuela Semmler-Bhenke4, Shinji Takenaka4, Wolfgang G Kreyling4,6, Mike Pitz3, Peter Reitmeir5, Annette Peters3, Oliver Eickelberg4, H Erich Wichmann2,Abstract Inhalation of fine particulate matter (<2.5 m; fine PM) has been shown to increase the risk for cardiovascular events. In this letter, we reappraise the role of tissue factor (TF) antigen and we also summarize changes in measured coagulation proteins in humans and rodents by other studies with fine PM. By considering all studies including ours, we conclude that monitoring the overall coagulation state by measuring capacity assays such as thrombin generation, and quantification of TF activity would be more suitable than determining single coagulation proteins (such as TF antigen) in order to better PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/20618955 assess the systemic prothrombotic effects of fine PM. Blood coagulation markers and fine PM exposure studies Evren Kilin? Gerhardus JAJM Kuiper, Henri MH Spronk, Hugo ten Cate Earlier 2-Chloro-5,6-dihydro-7H-cyclopenta[b]pyridin-7-one epidemiologic and experimental studies have shown that fine particulate matter (<2.5 m; fine PM) inhalation is associated with arterial and venous thrombosis, as well as an increased risk for cardiovascular death [1]. Several studies have addressed the possible mechanisms involved in PM-related arterial and venous thrombosis, although the recently published work by Emmerechts et al. could not establish a direct effect of intratracheal PM instillation on induction of venous thrombosis in mice PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/13867361 [2]. Tissue factor (TF) is expressed in subendothelial cells upon injury, or on the surface of cells like monocytes, macrophages and neutrophils. A small amount of TF is necessary to form a complex with factor VIIa to produce thrombin via the extrinsic pathway of coagulation [3]. Since PM is also related to endothelial damage and* Correspondence: e.kilinc@maastrichtuniversity.nl; schulz@helmholtzmuenchen.de Contributed equally 1 Department of Internal Medicine, 5-Tetramethyl-2-(2-methyl-5-nitrophenyl)-1 Laboratory for Clinical Thrombosis Dimethyl 4-iodopyridine-2,6-dicarboxylate and Haemostasis, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, P.O. Box 616, UNS 50: Box 8, 6200 MD, Maastricht, The Netherlands 2 Institute of Epidemiology I, Helmholtz Zentrum M chen, German Research Center for Environmental Health, Ingolstaedter Landstrasse 1, D85764, Neuherberg/Munich, Germany Full list of author information is available at the end of the articleactivation of platelets and macrophages upon short term in vivo exposure [1], the measurement of TF in blood may be considered as a marker of cell damage. A recent publication in this journal, addressed the effects of ambient fine PM in spontaneously hypertensive rats (SHRs) following intratracheal instillation at varying concentrations. Surprisingly, an early decrease in lung specific tissue factor (TF) antigen was.