Environmental concentration of spray paint particulate matters causes pulmonary dysfunction in human normal bronchial epithelial BEAS-2B cell

被引:15
|
作者
Chen, Yi-Chun [1 ,2 ]
Lin, Chia-Hua [1 ]
Lung, Shih-Chun Candice [3 ]
Chen, Ku-Fan [2 ]
Wang, Wen-Cheng Vincent [3 ]
Chou, Cheng-Tai [1 ]
Lai, Chia-Hsiang [4 ]
机构
[1] Natl Formosa Univ, Dept Biotechnol, Huwei Township 63208, Yunlin, Taiwan
[2] Natl Chi Nan Univ, Dept Civil Engn, Nantou, Taiwan
[3] Acad Sinica, Res Ctr Environm Changes, Taipei 11529, Taiwan
[4] Cent Taiwan Univ Sci & Technol, Dept Safety Hlth & Environm Engn, Taichung 40601, Taiwan
关键词
Paint; Particulate matter; Inflammation; BEAS-2B; Chronic obstructive pulmonary disease; LONG-TERM EXPOSURE; OXIDATIVE STRESS; AIR-POLLUTION; SIGNALING PATHWAY; BARRIER FUNCTION; POTENTIAL ROLE; COPD PATIENTS; LUNG; TOXICITY; ALPHA(1)-ANTITRYPSIN;
D O I
10.1016/j.psep.2019.04.013
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
In addition to airborne particulate matter (PM), exposure to spray paint PMs (SPPMs) may also be associated with pulmonary dysfunction. In this study, we employed human normal bronchial epithelial BEAS-2B cells to elucidate the association between pulmonary toxicity and different sizes of SPPMs (SPPM10-3.2, SPPM3.2-1 and SPPM1) under realistic environmental concentrations in a spray paint factory. Results indicated that all SPPMs (20-100 mu g/cm(2)) induced significant decreases in cell viability (> 70% compared to the control), except for low-dose SPPM10-3.2 (20 and 50 mu g/cm(2)). Almost all SPPMs (20 mu g/cm(2) and 100 mu g/cm(2)) induced oxidative stress (2-4 times that of the control), which increased the production of proinflammatory cytokines (1.5-4.5 times that of the control) as well as increased alpha 1-antitrypsin expression (3-4.5 times that of the control). Moreover, we found that almost all SPPMs induced pulmonary epithelial barrier dysfunction (0.77-0.11 times that of the control) through the depletion of zonula occludens proteins (0.8-0.65 times that of the control). In conclusion, smaller SPPMs induced more severe adverse pulmonary adverse effects. Exposure to SPPM1 was a potential major risk factor for pulmonary epithelial barrier dysfunction. Our evidence demonstrates that exposure to SPPMs, especially SPPM1, may increase the risk of pulmonary dysfunction. (C) 2019 Institution of Chemical Engineers. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:250 / 258
页数:9
相关论文
共 50 条
  • [41] Gene expression changes in human bronchial epithelial cells (BEAS-2B) and human pulmonary alveolar epithelial cells (HPAEpiC) after interaction with Cladosporium sphaerospermum
    Lo, Sing Gee
    Wong, Shew Fung
    Mak, Joon Wah
    Choo, Khi Khi
    Ng, Kee Peng
    MEDICAL MYCOLOGY, 2020, 58 (03) : 333 - 340
  • [42] Culture conditions profoundly impact phenotype in BEAS-2B, a human pulmonary epithelial model
    Zhao, Fei
    Klimecki, Walter T.
    JOURNAL OF APPLIED TOXICOLOGY, 2015, 35 (08) : 945 - 951
  • [43] BEAS-2B cells, a human bronchial epithelial cell line, produce C-C chemokine, MDC and TARC
    Arima, M
    Yoshida, N
    Cheng, G
    Eda, F
    Hirata, H
    Honda, K
    Fukushima, F
    Fukuda, T
    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2001, 107 (02) : S47 - S47
  • [44] Effects of radon on miR-34a-induced apoptosis in human bronchial epithelial BEAS-2B cells
    Wu, Jing
    Sun, Bin
    Zhang, Shuyu
    Zhang, Jie
    Tong, Jian
    Nie, Jihua
    Li, Jianxiang
    JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES, 2019, 82 (16): : 913 - 919
  • [45] Toxicogenomic study of toxic mechanism on methotrexate, amiodarone, nitrofurantoin and carbamazepine in human bronchial epithelial (BEAS-2B)
    Song, Mee
    Kim, Youn-Jung
    Ryu, Jae-Chun
    MOLECULAR & CELLULAR TOXICOLOGY, 2007, 3 (04) : 51 - 51
  • [46] TWEAK ENHANCES TGF-β-INDUCED EPITHELIAL-MESENCHYMAL TRANSITION IN BEAS-2B HUMAN BRONCHIAL EPITHELIAL CELLS
    Itoigawa, Yukinari
    Harada, Norihiro
    Harada, Sonoko
    Katsura, Yoko
    Matsuno, Kei
    Ishimori, Ayako
    Nagashima, Osamu
    Makino, Fumihiko
    Ito, Jun
    Atsuta, Ryo
    Takahashi, Kazuhisa
    RESPIROLOGY, 2013, 18 : 97 - 97
  • [47] Adverse pulmonary impacts of environmental concentrations of oil mist particulate matter in normal human bronchial epithelial cell
    Lai, Chia-Hsiang
    Chen, Yi-Chun
    Lin, Kun-Yi Andrew
    Lin, Yi-Xian
    Lee, Tsung-Han
    Lin, Chia-Hua
    SCIENCE OF THE TOTAL ENVIRONMENT, 2022, 809
  • [48] Combined cytotoxicity of co-exposure to aldehyde mixtures on human bronchial epithelial BEAS-2B cells
    Zhang, Sen
    Zhang, Jingni
    Chen, Huan
    Wang, An
    Liu, Yong
    Hou, Hongwei
    Hu, Qingyuan
    ENVIRONMENTAL POLLUTION, 2019, 250 : 650 - 661
  • [49] Ambient Vapor Samples Activate the Nrf2-ARE Pathway in Human Bronchial Epithelial BEAS-2B Cells
    Shinkai, Yasuhiro
    Nakajima, Syun
    Eiguren-Fernandez, Arantza
    Di Stefano, Emma
    Schmitz, Debra A.
    Froines, John R.
    Cho, Arthur K.
    Kumagai, Yoshito
    ENVIRONMENTAL TOXICOLOGY, 2014, 29 (11) : 1292 - 1300
  • [50] Transcriptomic analyses of human bronchial epithelial cells BEAS-2B exposed to brominated flame retardant (tetrabromobisphenol A)
    Wu, Shijin
    Zhu, Zhenzhen
    Chen, Jialin
    Wu, Mei
    Qiu, Lequan
    ENVIRONMENTAL TOXICOLOGY, 2019, 34 (06) : 742 - 752