Université Lille Nord de France, Lille, France; EA 4492, Université du Littoral-Côte d'Opale, Dunkerque, France.
Université Lille Nord de France, Lille, France; Centre Commun de Mesures, Université du Littoral-Côte d'Opale, Dunkerque, France.
Environ Res. 2015 Feb;137:256-67. doi: 10.1016/j.envres.2014.12.015. Epub 2015 Jan 16.
While the evidence for the health adverse effects of air pollution Particulate Matter (PM) has been growing, there is still uncertainty as to which constituents within PM are most harmful. Hence, to contribute to fulfill this gap of knowledge, some physicochemical characteristics and toxicological endpoints (i.e. cytotoxicity, oxidative damage, cytokine secretion) of PM2.5-0.3 samples produced during two different seasons (i.e. spring/summer or autumn/winter) in three different surroundings (i.e. rural, urban, or industrial) were studied, thereby expecting to differentiate their respective adverse effects in human bronchial epithelial cells (BEAS-2B). Physicochemical characteristics were closely related to respective origins and seasons of the six PM2.5-0.3 samples, highlighting the respective contributions of industrial and heavy motor vehicle traffic sources. Space- and season-dependent differences in cytotoxicity of the six PM2.5-0.3 samples could only be supported by considering both the physicochemical properties and the variance in air PM concentrations. Whatever spaces and seasons, dose- and even time-dependent increases in oxidative damage and cytokine secretion were reported in PM2.5-0.3-exposed BEAS-2B cells. However, the relationship between the chemical composition of each of the six PM2.5-0.3 samples and their oxidative or inflammatory potentials seemed to be very complex. These results supported the role of inorganic, ionic and organic components as exogenous source of Reactive Oxygen Species and, thereafter, cytokine secretion. Nevertheless, one of the most striking observation was that some inorganic, ionic and organic chemical components were preferentially associated with early oxidative events whereas others in the later oxidative damage and/or cytokine secretion. Taken together, these results indicated that PM mass concentration alone might not be able to explain the health outcomes, because PM is chemically nonspecific, and supported growing evidence that PM-size, composition and emission source, together with sampling season, interact in a complex manner to produce PM2.5-0.3-induced human adverse health effects.
虽然空气污染颗粒物 (PM) 对健康的不良影响的证据越来越多，但对于 PM 中哪些成分最有害仍存在不确定性。因此，为了弥补这方面知识的空白，研究了在两个不同季节（春季/夏季或秋季/冬季）和三个不同环境（农村、城市或工业）中产生的 PM2.5-0.3 样本的一些物理化学特性和毒理学终点（即细胞毒性、氧化损伤、细胞因子分泌），以期区分它们各自对人支气管上皮细胞 (BEAS-2B) 的不良影响。物理化学特性与六个 PM2.5-0.3 样本各自的来源和季节密切相关，突出了工业和重型机动车交通源的各自贡献。只有考虑到物理化学特性和空气 PM 浓度的变化，才能支持六个 PM2.5-0.3 样本的细胞毒性的空间和季节依赖性差异。无论在什么空间和季节，PM2.5-0.3 暴露的 BEAS-2B 细胞中都报告了氧化损伤和细胞因子分泌的剂量和时间依赖性增加。然而，六个 PM2.5-0.3 样本中每个样本的化学成分与其氧化或炎症潜力之间的关系似乎非常复杂。这些结果支持无机、离子和有机成分作为活性氧和随后细胞因子分泌的外源性来源的作用。然而，最引人注目的观察之一是，一些无机、离子和有机化学成分优先与早期氧化事件相关，而其他成分则与后期氧化损伤和/或细胞因子分泌相关。总之，这些结果表明，仅 PM 质量浓度可能无法解释健康结果，因为 PM 化学性质是非特异性的，并支持越来越多的证据表明 PM 大小、组成和排放源与采样季节一起以复杂的方式相互作用，产生 PM2.5-0.3 引起的人类不良健康影响。
