Prothrombotic Biomarkers Are Not Altered by Wood Smoke: A Pilot Controlled Exposure Study

ABSTRACT Inhalation of wood smoke (WS) has been associated with increased risk of cardiovascular events, including heart attacks and strokes, both of which are caused in part by the thrombotic occlusion of blood vessels. To characterize the effects of WS on levels of established, circulating prothro...

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Published inFASEB bioAdvances Vol. 7; no. 7; pp. e70038 - n/a
Main Authors Dobson, Dre' Von A., Holle, Lori A., Tatsumi, Kohei, Rebuli, Meghan E., Mackman, Nigel, Wolberg, Alisa S., Jaspers, Ilona
Format Journal Article
LanguageEnglish
Published United States John Wiley & Sons, Inc 01.07.2025
John Wiley and Sons Inc
Wiley
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Summary:ABSTRACT Inhalation of wood smoke (WS) has been associated with increased risk of cardiovascular events, including heart attacks and strokes, both of which are caused in part by the thrombotic occlusion of blood vessels. To characterize the effects of WS on levels of established, circulating prothrombotic biomarkers, healthy human subjects at rest were exposed to WS (500 μg/m3) or filtered air for 2 h. Plasma samples were then used to assess markers of endogenous procoagulant activity: cellular activation (tissue factor‐positive extracellular vesicles, TF + EVs), thrombin‐antithrombin complexes (TAT), fibrin formation/breakdown (D‐dimer), and thrombin generation potential. No significant differences in TF + EVs, TATs, D‐dimer, or thrombin generation parameters were detected between WS‐ or filtered air‐exposed individuals. Although females had significantly higher TATs and D‐dimers, and slightly but non‐significantly shorter thrombin generation lag times than males, there were no significant differences between WS‐ or air‐exposed males or females in any measurements. These data suggest that acute WS exposure does not increase prothrombotic biomarkers in plasma. Matched plasma samples from healthy volunteers collected before and after controlled woodsmoke exposure showed no differences in prothrombotic markers.
Bibliography:Funding
This study was supported by funding from the National Institutes of Health (R01HL126974 to ASW, F32HL176084 to DAD, R01ES013611 to IJ).
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Funding: This study was supported by funding from the National Institutes of Health (R01HL126974 to ASW, F32HL176084 to DAD, R01ES013611 to IJ).
ISSN:2573-9832
2573-9832
DOI:10.1096/fba.2025-00125