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环境浓度油雾颗粒物质对正常人支气管上皮细胞的肺部影响。

Adverse pulmonary impacts of environmental concentrations of oil mist particulate matter in normal human bronchial epithelial cell.

机构信息

Department of Biotechnology, National Formosa University, Yunlin 63208, Taiwan.

Department of Environmental Engineering, National Chung Hsing University, Taichung 40227, Taiwan.

出版信息

Sci Total Environ. 2022 Feb 25;809:151119. doi: 10.1016/j.scitotenv.2021.151119. Epub 2021 Oct 29.

Abstract

Airborne oil mist particulate matter (OMPM) is generated during industrial processes such as metalworking and may be associated with pulmonary dysfunction. In this study, we employed the normal human bronchial epithelial BEAS-2B cell line to elucidate the association between pulmonary toxicity and OMPM of 2.5-10 μm, 1.0-2.5 μm and <1.0 μm particle sizes (OMPM, OMPM and OMPM). We measured OMPM concentrations at a precision machinery factory to estimate lung deposition rates and select realistic environmental concentrations for testing. All OMPMs (1-50 μg/cm) significantly decreased BEAS-2B cell viability (>38% of control), except for low-dose OMPM (1 μg/cm). OMPM and OMPM, but not OMPM, induced oxidative stress (1.5-4-fold increase compared with the control) and increased the production of proinflammatory cytokines (1.5-3-fold). However, only OMPM induced pulmonary epithelial barrier dysfunction via depletion of zonula occludens (0.65-0.8-fold) and α1-antitrypsin proteins (0.65-0.8-fold). In conclusion, a higher risk of lung disease was associated with smaller particle size OMPM. Exposure to OMPM may be a potential risk factor for chronic obstructive pulmonary disease. The evidence also demonstrates that occupational exposure to OMPM may cause pulmonary disease at very low concentrations.

摘要

空气中油雾颗粒物质(OMPM)在金属加工等工业过程中产生,可能与肺部功能障碍有关。在这项研究中,我们采用正常的人支气管上皮 BEAS-2B 细胞系来阐明肺毒性与 2.5-10μm、1.0-2.5μm 和<1.0μm 粒径(OMPM、OMPM 和 OMPM)的 OMPM 之间的关联。我们测量了精密机械厂的 OMPM 浓度,以估计肺部沉积率并选择现实环境浓度进行测试。所有 OMPM(1-50μg/cm)都显著降低了 BEAS-2B 细胞活力(超过对照的 38%),除了低剂量 OMPM(1μg/cm)。OMPM 和 OMPM 但不是 OMPM 诱导了氧化应激(与对照相比增加了 1.5-4 倍)并增加了促炎细胞因子的产生(增加了 1.5-3 倍)。然而,只有 OMPM 通过封闭蛋白(0.65-0.8 倍)和α1-抗胰蛋白酶蛋白(0.65-0.8 倍)的耗竭诱导了肺上皮屏障功能障碍。总之,与较小粒径的 OMPM 相关的肺部疾病风险更高。暴露于 OMPM 可能是慢性阻塞性肺疾病的潜在危险因素。该证据还表明,职业性暴露于 OMPM 可能在非常低的浓度下导致肺部疾病。

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