Zhang Yingying, Ji Xiaotong, Ku Tingting, Sang Nan
College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi, 030006, People's Republic of China.
Environ Toxicol. 2016 Dec;31(12):1996-2005. doi: 10.1002/tox.22200. Epub 2015 Sep 28.
SO , NO , and PM are typical air pollutants produced during the combustion of coal. Increasing evidence indicates that air pollution has contributed to the development and progression of heart-related diseases over the past decades. However, little experimental data and few studies of SO , NO , and PM co-exposure in animals exist; therefore, the relevant mechanisms underlying this phenomenon are unclear. An important characteristic of air pollution is that co-exposure persists at a low concentration throughout a lifetime. In the present study, we treated adult mice with SO , NO , and PM at various concentrations (0.5 mg/m SO , 0.2 mg/m NO 6 h/d, with intranasal instillation of 1 mg/kg PM every other day during these exposures; or 3.5 mg/m SO , 2 mg/m NO 6 h/d, and 10 mg/kg PM for 28 d). Blood pressure (BP), heart rate (HR), histopathological damage, and inflammatory and endothelial cytokines in the heart were assessed. The results indicate that co-exposure caused endothelial dysfunction by elevating endothelin-1 (ET-1) expression and repressing the endothelial nitric oxide synthase (eNOS) level as well as stimulating the inflammatory response by increasing the levels of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Additionally, these alterations were confirmed by histological staining. Furthermore, we observed decreased BP and increased HR after co-exposure. Our results indicate that co-exposure to SO , NO , and PM may be a major risk factor for cardiac disease and may induce injury to the hearts of mammals and contribute to heart disease. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1996-2005, 2016.
二氧化硫、一氧化氮和颗粒物是煤炭燃烧过程中产生的典型空气污染物。越来越多的证据表明，在过去几十年里，空气污染促使了心脏相关疾病的发生和发展。然而，关于动物同时暴露于二氧化硫、一氧化氮和颗粒物的实验数据很少，相关研究也寥寥无几；因此，这一现象背后的相关机制尚不清楚。空气污染的一个重要特征是，在整个生命周期中，低浓度的共同暴露持续存在。在本研究中，我们用不同浓度的二氧化硫、一氧化氮和颗粒物处理成年小鼠（0.5毫克/立方米二氧化硫、0.2毫克/立方米一氧化氮，每天暴露6小时，在此期间每隔一天经鼻滴注1毫克/千克颗粒物；或者3.5毫克/立方米二氧化硫、2毫克/立方米一氧化氮，每天暴露6小时，以及10毫克/千克颗粒物，持续28天）。评估了血压（BP）、心率（HR）、组织病理学损伤以及心脏中的炎症和内皮细胞因子。结果表明，共同暴露通过提高内皮素-1（ET-1）表达、抑制内皮型一氧化氮合酶（eNOS）水平导致内皮功能障碍，并通过增加环氧化酶-2（COX-2）、诱导型一氧化氮合酶（iNOS）、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）水平刺激炎症反应。此外，这些改变通过组织学染色得到证实。此外，我们观察到共同暴露后血压下降、心率增加。我们的结果表明，同时暴露于二氧化硫、一氧化氮和颗粒物可能是心脏病的主要危险因素，可能导致哺乳动物心脏损伤并促成心脏病。©2015威利期刊公司。《环境毒理学》31: 1996 - 2005，2016年。
