Department of Occupational Health and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China.
Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China; Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, China.
J Hazard Mater. 2022 Jan 5;421:126760. doi: 10.1016/j.jhazmat.2021.126760. Epub 2021 Jul 27.
Large amounts of epidemiological evidence have confirmed the atmospheric particulate matter (PM) exposure was positively correlated with the morbidity and mortality of respiratory diseases. Nevertheless, its pathogenesis remains incompletely understood, probably resulting from the activation of oxidative stress, inflammation, altered genetic and epigenetic modifications in the lung upon PM exposure. Currently, biomarker investigations have been widely used in epidemiological and toxicological studies, which may help in understanding the biologic mechanisms underlying PM-elicited adverse health outcomes. Here, the emerging biomarkers to indicate PM-respiratory system interactions were summarized, primarily related to oxidative stress (ROS, MDA, GSH, etc.), inflammation (Interleukins, FE, CC16, etc.), DNA damage (8-OHdG, γH2AX, OGG1) and also epigenetic modulation (DNA methylation, histone modification, microRNAs). The identified biomarkers shed light on PM-elicited inflammation, fibrogenesis and carcinogenesis, thus may favor more precise interventions in public health. It is worth noting that some inconsistent findings may possibly relate to the inter-study differentials in the airborne PM sample, exposure mode and targeted subjects, as well as methodological issues. Further research, particularly by -omics technique to identify novel, specific biomarkers, is warranted to illuminate the causal relationship between PM pollution and deleterious lung outcomes.
大量的流行病学证据证实,大气颗粒物(PM)暴露与呼吸道疾病的发病率和死亡率呈正相关。然而,其发病机制尚不完全清楚,可能是由于 PM 暴露后肺部氧化应激、炎症、遗传和表观遗传改变的激活。目前,生物标志物研究已广泛应用于流行病学和毒理学研究,这有助于理解 PM 引起的不良健康后果的生物学机制。本文总结了新兴的用于指示 PM-呼吸系统相互作用的生物标志物,主要与氧化应激(ROS、MDA、GSH 等)、炎症(白细胞介素、FE、CC16 等)、DNA 损伤(8-OHdG、γH2AX、OGG1)和表观遗传调节(DNA 甲基化、组蛋白修饰、microRNAs)有关。已鉴定的生物标志物阐明了 PM 引起的炎症、纤维化和致癌作用,因此可能有利于更精确地进行公共卫生干预。值得注意的是,一些不一致的发现可能与空气中 PM 样本、暴露模式和目标人群的研究差异以及方法学问题有关。需要进一步的研究,特别是通过组学技术来识别新的、特定的生物标志物,以阐明 PM 污染与肺部有害后果之间的因果关系。