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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.
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页码:250 / 258
页数:9
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