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J Environ Sci (China). 2017 Dec;62:100-114. doi: 10.1016/j.jes.2017.08.018. Epub 2017 Sep 8.

Mesoporous carbon nanomaterials induced pulmonary surfactant inhibition, cytotoxicity, inflammation and lung fibrosis.

Author information

1
State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China; University of Chinese Academy of Sciences, Beijing 100049, China.
2
Department of Mechanical Engineering, University of Hawaii at Manoa, Honolulu, HI 96822, USA.
3
Beijing Key Laboratory of Bioprocess Beijing Advanced Innovation Center for Soft Matter Science, Engineering Beijing Laboratory of Biomedical Materials, Beijing University of Chemical Technology, Beijing 100029, China.
4
State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China.
5
Department of Mechanical Engineering, University of Hawaii at Manoa, Honolulu, HI 96822, USA. Electronic address: yzuo@hawaii.edu.
6
State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China; University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address: sjliu@rcees.ac.cn.

Abstract

Environmental exposure and health risk upon engineered nanomaterials are increasingly concerned. The family of mesoporous carbon nanomaterials (MCNs) is a rising star in nanotechnology for multidisciplinary research with versatile applications in electronics, energy and gas storage, and biomedicine. Meanwhile, there is mounting concern on their environmental health risks due to the growing production and usage of MCNs. The lung is the primary site for particle invasion under environmental exposure to nanomaterials. Here, we studied the comprehensive toxicological profile of MCNs in the lung under the scenario of moderate environmental exposure. It was found that at a low concentration of 10μg/mL MCNs induced biophysical inhibition of natural pulmonary surfactant. Moreover, MCNs at similar concentrations reduced viability of J774A.1 macrophages and lung epithelial A549 cells. Incubating with nature pulmonary surfactant effectively reduced the cytotoxicity of MCNs. Regarding the pro-inflammatory responses, MCNs activated macrophages in vitro, and stimulated lung inflammation in mice after inhalation exposure, associated with lung fibrosis. Moreover, we found that the size of MCNs played a significant role in regulating cytotoxicity and pro-inflammatory potential of this nanomaterial. In general, larger MCNs induced more pronounced cytotoxic and pro-inflammatory effects than their smaller counterparts. Our results provided valuable information on the toxicological profile and environmental health risks of MCNs, and suggested that fine-tuning the size of MCNs could be a practical precautionary design strategy to increase safety and biocompatibility of this nanomaterial.

KEYWORDS:

Environmental exposure; Fibrosis; Inflammation; Mesoporous carbon nanomaterials; Pulmonary surfactant

PMID:
29289281
DOI:
10.1016/j.jes.2017.08.018
[Indexed for MEDLINE]

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