Faruqui Nilofar, Orell Sofie, Dondi Camilla, Leni Zaira, Kalbermatter Daniel M, Gefors Lina, Rissler Jenny, Vasilatou Konstantina, Mudway Ian S, Kåredal Monica, Shaw Michael, Larsson-Callerfelt Anna-Karin
Department of Chemical & Biological Services, National Physical Laboratory, Teddington TW11 0LW, UK.
Lung Biology, Department of Experimental Medical Sciences, Lund University, 221 84 Lund, Sweden.
Int J Mol Sci. 2025 Jan 20;26(2):830. doi: 10.3390/ijms26020830.
Particulate matter (PM) is a major component of ambient air pollution. PM exposure is linked to numerous adverse health effects, including chronic lung diseases. Air quality guidelines designed to regulate levels of ambient PM are currently based on the mass concentration of different particle sizes, independent of their origin and chemical composition. The objective of this study was to assess the relative hazardous effects of carbonaceous particles (soot), ammonium nitrate, ammonium sulfate, and copper oxide (CuO), which are standard components of ambient air, reflecting contributions from primary combustion, secondary inorganic constituents, and non-exhaust emissions (NEE) from vehicular traffic. Human epithelial cells representing bronchial (BEAS-2B) and alveolar locations (H441 and A549) in the airways, human lung fibroblasts (HFL-1), and rat precision-cut lung slices (PCLS) were exposed in submerged cultures to different concentrations of particles for 5-72 h. Following exposure, cell viability, metabolic activity, reactive oxygen species (ROS) formation, and inflammatory responses were analyzed. CuO and, to a lesser extent, soot reduced cell viability in a dose-dependent manner, increased ROS formation, and induced inflammatory responses. Ammonium nitrate and ammonium sulfate did not elicit any significant cytotoxic responses but induced immunomodulatory alterations at very high concentrations. Our findings demonstrate that secondary inorganic components of PM have a lower hazard cytotoxicity compared with combustion-derived and indicative NEE components, and alveolar epithelial cells are more sensitive to PM exposure. This information should help to inform which sources of PM to target and feed into improved, targeted air quality guidelines.
颗粒物（PM）是环境空气污染的主要成分。接触PM与多种不良健康影响相关，包括慢性肺部疾病。目前旨在规范环境PM水平的空气质量指南是基于不同粒径的质量浓度制定的，而不考虑其来源和化学成分。本研究的目的是评估碳质颗粒（烟灰）、硝酸铵、硫酸铵和氧化铜（CuO）的相对有害影响，这些都是环境空气中的标准成分，反映了一次燃烧、二次无机成分和车辆交通非尾气排放（NEE）的贡献。在浸没培养中，将代表气道中支气管（BEAS-2B）和肺泡位置（H441和A549）的人上皮细胞、人肺成纤维细胞（HFL-1）和大鼠精密切割肺切片（PCLS）暴露于不同浓度的颗粒中5至72小时。暴露后，分析细胞活力、代谢活性、活性氧（ROS）形成和炎症反应。CuO以及在较小程度上的烟灰以剂量依赖的方式降低细胞活力，增加ROS形成，并诱导炎症反应。硝酸铵和硫酸铵未引起任何显著的细胞毒性反应，但在非常高的浓度下诱导免疫调节改变。我们的研究结果表明，与燃烧衍生成分和指示性NEE成分相比，PM的二次无机成分具有较低的细胞毒性危害，并且肺泡上皮细胞对PM暴露更敏感。这些信息应有助于确定应针对哪些PM来源，并为改进的、有针对性的空气质量指南提供参考。
