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
  • [1] Morphologically and karyotypically atypical cells of 'normal' human bronchial epithelial cell line (Beas-2B)
    Lee, Younsu
    Ryu, Young-Joon
    ULTRASTRUCTURAL PATHOLOGY, 2023, 47 (06) : 470 - 477
  • [2] Oxidative stress of silica nanoparticles in human bronchial epithelial cell, Beas-2B
    Eom, Hyun-Jeong
    Choi, Jinhee
    TOXICOLOGY IN VITRO, 2009, 23 (07) : 1326 - 1332
  • [3] β-Hexachlorocyclohexane Drives Carcinogenesis in the Human Normal Bronchial Epithelium Cell Line BEAS-2B
    Rubini, Elisabetta
    Minacori, Marco
    Paglia, Giuliano
    Altieri, Fabio
    Chichiarelli, Silvia
    Romaniello, Donatella
    Eufemi, Margherita
    INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2021, 22 (11)
  • [4] Adherence of Streptococcus pneumoniae to human bronchial epithelial cells (BEAS-2B)
    Adamou, JE
    Wizemann, TM
    Barren, P
    Langermann, S
    INFECTION AND IMMUNITY, 1998, 66 (02) : 820 - 822
  • [5] Expression of CC-chemokine receptors in the human bronchial epithelial cell line BEAS-2B
    Shahabuddin, S
    Plitt, J
    Stellato, C
    Beck, LA
    Barnette, MS
    Brawner, M
    Schleimer, RP
    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2000, 105 (01) : S379 - S379
  • [6] TRANSFORMED HUMAN BRONCHIAL EPITHELIAL-CELLS (BEAS-2B) ALTER THE GROWTH AND MORPHOLOGY OF NORMAL HUMAN BRONCHIAL EPITHELIAL-CELLS INVITRO
    ALBRIGHT, CD
    JONES, RT
    HUDSON, EA
    FONTANA, JA
    TRUMP, BF
    RESAU, JH
    CELL BIOLOGY AND TOXICOLOGY, 1990, 6 (04) : 379 - 398
  • [7] Gene expression profiling of human bronchial epithelial (BEAS-2B) cells treated with nitrofurantoin, a pulmonary toxicant
    Kim, Youn-Jung
    Song, Mee
    Ryu, Jae-Chun
    MOLECULAR & CELLULAR TOXICOLOGY, 2007, 3 (04) : 222 - 230
  • [8] Identification of genes induced by carbamazepine in human bronchial epithelial BEAS-2B cells
    Song M.
    Kim Y.-J.
    Ryu J.-C.
    Toxicology and Environmental Health Sciences, 2011, 3 (2) : 106 - 113
  • [9] Cytotoxicity of Copper Nanoparticles in Cultured Human Bronchial Epithelial Cells (BEAS-2B)
    Park, Eun-Jung
    Park, Kwangsik
    TOXICOLOGICAL RESEARCH, 2005, 21 (04) : 303 - 307
  • [10] Cytotoxicity and autophagy dysfunction induced by different sizes of silica particles in human bronchial epithelial BEAS-2B cells
    Li, Qiuling
    Hu, Hejing
    Jiang, Lizhen
    Zou, Yang
    Duan, Junchao
    Sun, Zhiwei
    TOXICOLOGY RESEARCH, 2016, 5 (04) : 1216 - 1228