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Exposure scenario: Another important factor determining the toxic effects of PM2.5 and possible mechanisms involved

机译：暴露场景：决定PM2.5毒性影响和涉及的可能机制的另一个重要因素

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摘要

Worsening air pollution is a serious threat to public health in many urban and heavily industrialized areas. Particle size and chemical composition are well known determinants of the pathological response to air pollution. In addition, pathological responses may depend on the exposure profile (or scenario) of air pollution. For instance, we previously demonstrated that repeated exposure to low levels of fine airborne particulate matter (PM2.5) induced distinct epigenetic changes compared to acute high-doses exposure. In the present study, we evaluated the differential pathological responses of BEAS-2B human bronchial epithelial cells to two distinct PM2.5 exposure scenarios: 24-h exposure to high-doses PM2.5 (0, 6, 12, 24, 48, 96 mu g/cm(2)) and 10 days' repeated exposure to low levels of PM2.5 (0, 1.5, 3, 6 mu g/cm(2)). Acute exposure to high concentrations of PM2.5 caused ROS burst, marked DNA damage, dysfunction of the endoplasmic reticulum (ER) stress response, autophagy and necrotic cell death. In contrast, repeated low levels of PM2.5 led to sustained low-grade ROS accumulation, milder DNA damage, ER stress/unfolded protein response (UPR), S-phase arrest, apoptosis, and autophagy. Notably, most cells surviving repeated low-level exposure showed a series of abnormal adaptive responses, such as inhibition of mitochondria biogenesis and epigenetic dysregulation. These results indicate that different PM2.5 exposure scenarios induce distinct forms cytotoxicity and adaptive response. In addition to particle size and chemical composition, exposure scenario may be a critical factor determining the toxic health effects of PM2.5. (C)2017 Elsevier Ltd. All rights reserved.
机译：在许多城市和工业化程度很高的地区，日益严重的空气污染严重威胁着公共健康。粒径和化学组成是对空气污染的病理反应的众所周知的决定因素。此外，病理反应可能取决于空气污染的暴露状况（或情景）。例如，我们先前证明，与急性高剂量暴露相比，反复暴露于低水平的细颗粒空气悬浮颗粒物质（PM2.5）会引起明显的表观遗传变化。在本研究中，我们评估了BEAS-2B人支气管上皮细胞对两种不同PM2.5暴露情况的不同病理反应：高剂量PM2.5（0、6、12、24、48， 96μg/ cm（2））和10天反复暴露于低水平的PM2.5（0、1.5、3、6μg/ cm（2））。急性暴露于高浓度PM2.5会引起ROS破裂，明显的DNA损伤，内质网应激反应功能障碍，自噬和坏死细胞死亡。相反，反复低水平的PM2.5导致持续的低水平ROS积累，较轻的DNA损伤，ER应激/未折叠蛋白反应（UPR），S期停滞，细胞凋亡和自噬。值得注意的是，大多数在反复低水平暴露下存活的细胞表现出一系列异常的适应性反应，例如抑制线粒体的生物发生和表观遗传异常。这些结果表明，不同的PM2.5暴露场景会诱导不同形式的细胞毒性和适应性反应。除了粒径和化学成分外，暴露情况可能是决定PM2.5毒性健康影响的关键因素。 （C）2017 Elsevier Ltd.保留所有权利。

著录项

  • 来源
    《Environmental Pollution》 |2017年第7期|412-425|共14页
  • 作者

    Zhou Wei; Tian Dongdong; He Jun; Zhang Li; Tang Xiuli; Zhang Lijun; Wang Yimei; Li Lizhong; Zhao Jun; Yuan Xiaoyan; Peng Shuangqing;

  • 作者单位

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

    Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    PM2.5; Exposure scenario; Toxic effects; Cellular responses; Autophagy;

    机译：PM2.5;接触情景;毒性作用;细胞反应;自噬;

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