Unraveling Potential Causative Components for the Deleterious Effect of Atmospheric Fine Particulate Matter on Red Blood Cells

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Abstract
Atmospheric fine particulate matter (PM2.5) poses threats to the cardiovascular system. Red blood cells (RBCs) are the most abundant cells in blood, which are actively involved in multiple hematological diseases, such as blood clot formation and thrombosis. Exploring how PM2.5 with spatiotemporal heterogeneity influences the hematological system by targeting RBCs would help gain insights into the deleterious effects of PM2.5 and provide clues for finding the causative components therein. Herein, the PM2.5 samples collected from 3 urban sites in Beijing (i.e., Chaoyang, Shunyi, and Yanqing districts) during 4 seasons of 2022 were studied for their toxicities to mouse RBCs, and the main contributing components were further explored through chemical analysis and correlation measure. The results showed that exposure to PM2.5 samples decreased adenosine triphosphate (ATP) levels and increased phosphatidylserine (PS) externalization of RBCs, causing cell morphological deformity. The Pearson correlation analysis showed that the aromaticity of the dissolved organic matter (DOM) in PM2.5 samples was positively correlated with PS exposure of RBCs, showing that the lignin-like compounds were the potential contributors. The negative correlation of zeta potentials of PM2.5 samples with PS exposure of RBCs showed the particle-derived bioactivities of this airborne pollutant. The simulative test based on artificial nanomaterials of carbon black (CB) and oxidized CB (OCB) confirmed the crucial role of particulate carbon in PM2.5-induced effects on RBCs, and soot with a certain oxidation degree was, thus, recognized as another contributor, given its ubiquitous existence in PM2.5 samples. This study, for the first time, revealed PM2.5-induced PS exposure of RBCs, and the causative components of DOM and soot were unraveled. Considering the inevitable contact of airborne PM2.5 with RBCs in the blood circulatory system, the findings obtained herein would help bridge the gap between PM2.5 exposure and the risk of cardiovascular diseases, like thrombogenesis.
Funding Information
  • National Key Research and Development Program of China (2023YFC3708302)
  • National Natural Science Foundation of China (22176203, 22193050)
  • Chinese Academy of Sciences (XDB0750300)

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