Institute of Environmental Science, Shanxi University, Wucheng Road 92#, Taiyuan, 030006, Shanxi Province, People's Republic of China.
State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong, SAR, China.
Environ Sci Pollut Res Int. 2018 Jan;25(2):1742-1751. doi: 10.1007/s11356-017-0558-1. Epub 2017 Nov 3.
Chalk teaching is widely used in the world due to low cost, especially in some developing countries. During teaching with chalks, a large amount of fine chalk dust is produced. Although exposure to chalk dust is associated with respiratory diseases, the mechanism underlying the correlation between chalk dust exposure and adverse effects has not fully been elucidated. In this study, inflammation and its signal pathway in rat lungs exposed to fine chalk dust were examined through histopathology analyses; pro-inflammatory gene transcription; and protein levels measured by HE staining, RT-PCR, and western blot analysis. The results demonstrated that fine chalk dust increased neutrophils and up-regulated inflammatory gene mRNA levels (TNF-α, IL-6, TGF-β1, iNOS, and ICAM-1), and oxidative stress marker (HO-1) level, leading to the increase of inflammatory cell infiltration and inflammatory injury on the lungs. These inflammation responses were mediated, at least in part, via p38 and extracellular regulated proteinase (ERK) mitogen-activated protein kinase (MAPK) signaling mechanisms. In contrast, N-acetyl-L-cysteine (NAC) supplement significantly ameliorated these changes in inflammatory responses. Our results support the hypothesis that fine chalk dust can damage rat lungs and the NAC supplement may attenuate fine chalk dust-associated lung inflammation.
chalk 教学由于成本低，在世界范围内被广泛使用，尤其是在一些发展中国家。在使用 chalks 进行教学时，会产生大量的细 chalk 粉尘。尽管接触 chalk 粉尘与呼吸道疾病有关，但 chalk 粉尘暴露与不良影响之间的关联机制尚未完全阐明。在这项研究中，通过组织病理学分析、促炎基因转录和 HE 染色、RT-PCR 和 western blot 分析测量的蛋白水平，研究了细 chalk 粉尘暴露对大鼠肺部的炎症及其信号通路。结果表明，细 chalk 粉尘增加了中性粒细胞并上调了促炎基因 mRNA 水平（TNF-α、IL-6、TGF-β1、iNOS 和 ICAM-1）和氧化应激标志物（HO-1）水平，导致肺部炎症细胞浸润和炎症损伤增加。这些炎症反应至少部分是通过 p38 和细胞外调节蛋白激酶（ERK）丝裂原激活蛋白激酶（MAPK）信号机制介导的。相比之下，N-乙酰-L-半胱氨酸（NAC）补充显著改善了这些炎症反应的变化。我们的结果支持以下假设，即细 chalk 粉尘会损害大鼠肺部，NAC 补充可能会减轻细 chalk 粉尘相关的肺部炎症。
