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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Main Authors: Dre' Von A. Dobson, Lori A. Holle, Kohei Tatsumi, Meghan E. Rebuli, Nigel Mackman, Alisa S. Wolberg, Ilona Jaspers
Format: Article
Language:English
Published: Wiley 2025-07-01
Series:FASEB BioAdvances
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Online Access:https://doi.org/10.1096/fba.2025-00125
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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.
ISSN:2573-9832