[Advances on the toxicology and molecular mechanisms of different components of ambient fine particulate matter].

Ambient fine particulate matters (PM2.5) refer to particulate matters with an aerodynamic diameter less than or equal to 2.5 μm. PM2.5 enter the body through the target organ-lung, and can induce a variety of adverse health effects (such as cardiovascular diseases, diabetes, respiratory diseases, neurodegenerative diseases and adverse birth outcomes). PM2.5 are known to have complex compositions (including water-soluble/-insoluble components and biological components), diverse sources and capacity of secondary transformation. Numerous epidemiological and toxicological studies indicated that different components of PM2.5 may induce adverse health effects through different biological mechanisms. In adddition, co-exposure of different components and their interaction should also be considered. Thus here we have systematically reviewed studies in recent years about the toxicological effects and underlying mechanisms of different components of ambient fine particulate matters, including inflammatory response, oxidative stress, endoplasmic reticulum stress, activation of the NF-κB signaling pathway and so on. The information may give some insights into the prevention and treatment of adverse health effects caused by exposure to different components of PM2.5.大气细颗粒物（PM2.5）是指空气动力学直径小于或等于2.5 μm的颗粒物，经由靶器官肺脏进入机体，可诱发多种不良健康效应（如心血管疾病、糖尿病、呼吸系统疾病、神经退行性疾病和不良出生结局等）。PM2.5具有组成的复杂性（可溶性/非可溶性成分和生物成分等）、来源的多样性和二次转化等特性，大量的流行病学和毒理学研究提示PM2.5的不同组成在诱发不良健康效应时所涉及的毒理学作用机制存在差异。另外，PM2.5作为载体，还存在多组分间的混合暴露和联合效应。本文对近几年大气细颗粒物不同成分暴露所涉及的毒理学作用机制及不同组分间的联合效应进行了较为系统的阐述，主要包含炎症反应、氧化应激、内质网应激、核因子κB（NF-κB）信号通路的激活等，为PM2.5不同组分暴露所引发的不良健康效应的防治提供依据。.