Particulate air pollution from human activities has drawn global attention due to its potential health risks. The currently available hematological toxicology data on atmospheric fine particles is still not sufficient to explain their cause-and-effect. The complement, coagulation and kallikrein-kinin system (KKS), key components in plasma, are working in concert with each other to provide both positive and negative feedback for hematological hemostasis. Herein, we evaluated the effects of fine particulate matter exposure on crosstalk of KKS, complement and coagulation systems. Atmospheric fine particles in Beijing during wintertime were collected, extracted and characterized. Based on the physicochemical characterization of these particle samples, their potential interactions with plasma KKS zymogens were screened. Using the ex vivo, in vitro and in vivo models, fine particles were indicated to activate the plasma prekallikrein (PPK), and high-molecular-weight kininogen (HK) in a dose-dependent manner through binding with Hagmen factor XII (FXII), the initial zymogen in the KKS. Additionally, the complement and coagulation cascade activation were promoted upon fine particles exposure. More specifically, these reactions were mediated by the triggering of KKS system activation, which was demonstrated by the addition of KKS system inhibitor (aprotinin) or FXII inhibitor (CTI). The research findings provided important scientific evidences for the evaluation of health hazards from atmospheric fine particle exposure.

Fine particles regulate hematological effects through the crosstalk of KKS, complement and coagulation systems

256th National Meeting (2018)

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