大气细颗粒物是指大气中直径≤2.5 μm的颗粒物,也称为PM2.5,是大气污染的主要成分之一.PM2.5成分复杂,粒径小,表面积大,可携带大量的化学物质、细菌和病毒等到达肺泡并在肺泡中沉积,通过血液循环到达全身各个系统,严重危害人类健康.氧化应激和炎症反应损伤是PM2.5致呼吸系统损伤的重要机制之一,本文从人群流行病学、体内实验和体外实验3个部分综述PM2.5致呼吸系统氧化应激和炎症反应损伤机制的主要研究进展.人群流行病学的研究结果表明,PM2.5与哮喘、慢性阻塞性肺病等呼吸系统疾病的发病率密切相关.在动物实验中主要体现在气道损伤,引发哮喘和肺组织等器官损伤,细胞损伤机制主要包括细胞信号通路改变,各种类型的DNA损伤、免疫损伤、细胞自噬和细胞凋亡等.%Fine particles,less than 2.5 micrometer in diameter (PM2.5),are the main components of inhalable particles.Because of their relatively small size and large surface area,PM2.5 can absorb and retain chemicals,bacteria,viruses and other toxic substances,penetrate deeply into the respiratory tract and easily reach the alveolar ducts,exerting adverse effects on the lungs.PM2.5 can also be absorbed into the bloodstream through alveolar capillaries,causing serious damage to human health.The biological effects produced by PM2.5 are frequently attributed to the oxidative stress induced by intracellular reactive oxygen species alterations and abnormal release of inflammatory mediators closely involved in the development of lung diseases.This review discusses the research advances in relationships between PM2.5 exposure and inflammatory responses and oxidative stress based on experimental researches,in vivo and in vitro studies.Recent epidemiologic investigations have shown associations between increased incidence of respiratory diseases and lung cancer from exposure to low levels of various forms of respirable fibers and particulate matter.In vivo experiments have disclosed the association between PM2.5 exposure and the exacerbation of asthma,bronchitis,chronic obstructive pulmonary disease,and other lung damages.Cell damage mechanisms mainly include alterations of cell signaling pathways,DNA damage,immune injury,autophagy and apoptosis.
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