Zhang Bin, Xu Hongbing, He Xinghou, Wang Tong, Li Mengyao, Shan Xuyang, Zhu Yutong, Liu Changjie, Zhao Qian, Song Xiaoming, Sun Yele, Zheng Lemin, Huang Wei
Department of Occupational and Environmental Health, Peking University School of Public Health, Peking University Institute of Environmental Medicine, Beijing 100191, China.
State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Toxics. 2024 Mar 19;12(3):225. doi: 10.3390/toxics12030225.
Evidence of the precise biological pathway responsible for acute cardiovascular events triggered by particulate matter (PM) exposure from anthropogenic emissions is sparse. We investigated the associations of biomarkers relevant to the pathophysiology of atherothrombosis (ceramide metabolism, pro-inflammatory response, and blood coagulation) with primary and secondary components in particulate matter with aerodynamic diameters less than 2.5 μm (PM). A total of 152 healthy participants were followed with four repeated clinical visits between September 2019 and January 2020 in Beijing. Exposure to ambient inorganic aerosols (sulfate, nitrate, ammonium, and chloride), as well as organic aerosols (OA) in PM, was measured by a real-time aerosol chemical speciation monitor, and sources of OA were performed by positive matrix factorization. We found significant increases of 101.9-397.9% in ceramide indicators associated with interquartile-range increases in inorganic aerosols and OA prior to 72 h of exposure. Higher levels of organic and inorganic aerosols in PM were associated with increases of 3.1-6.0% in normal T cells regulated upon activation and expressed and secreted relevant to the pro-inflammatory response; increases of 276.9-541.5% were observed in D-dimers relevant to coagulation. Detrimental effects were further observed following OA exposure from fossil fuel combustion. Mediation analyses indicated that ceramide metabolism could mediate the associations of PM components with pro-inflammatory responses. Our findings expand upon the current understanding of potential pathophysiological pathways of cardiovascular events posed by ambient particulates and highlight the importance of reducing primary and secondary PM from anthropogenic combustions.
关于人为排放的颗粒物（PM）暴露引发急性心血管事件的确切生物学途径的证据很少。我们研究了与动脉粥样硬化血栓形成病理生理学相关的生物标志物（神经酰胺代谢、促炎反应和血液凝固）与空气动力学直径小于2.5μm的颗粒物（PM）中的主要和次要成分之间的关联。2019年9月至2020年1月期间，在北京对152名健康参与者进行了4次重复临床随访。通过实时气溶胶化学形态监测仪测量了环境无机气溶胶（硫酸盐、硝酸盐、铵和氯化物）以及PM中的有机气溶胶（OA），并通过正矩阵分解确定了OA的来源。我们发现，在暴露前72小时内，与无机气溶胶和OA四分位间距增加相关的神经酰胺指标显著增加了101.9%-397.9%。PM中较高水平的有机和无机气溶胶与促炎反应相关的正常T细胞在激活时调节并表达和分泌增加3.1%-6.0%有关；与凝血相关的D-二聚体增加了276.9%-541.5%。在化石燃料燃烧产生的OA暴露后，进一步观察到有害影响。中介分析表明，神经酰胺代谢可以介导PM成分与促炎反应之间的关联。我们的研究结果扩展了目前对环境颗粒物引发心血管事件潜在病理生理途径的理解，并强调了减少人为燃烧产生的一次和二次PM的重要性。
