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Inhalation Toxicology
International Forum for Respiratory Research
Volume 23, 2011 - Issue 9
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Research Article

Amorphous silica coatings on magnetic nanoparticles enhance stability and reduce toxicity to in vitro BEAS-2B cells

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Pages 532-543 | Received 26 Apr 2011, Accepted 27 May 2011, Published online: 05 Aug 2011
 

Abstract

Background: Nanoparticles are being rapidly assimilated into numerous research fields and consumer products. A concurrent increase in human exposure to such materials is expected. Magnetic nanoparticles (MNPs) possess unique and beneficial features, increasing their functionality and integrative potential. However, MNP toxicity characterization is limited, especially in regards to the human respiratory system. This study aimed to assess the in vitro effects of airborne MNPs on BEAS-2B cells. Uncoated iron oxide was compared with two amorphous silica-coated MNPs, hypothesizing the coatings reduced toxicity and increased particle stability.

Method: BEAS-2B cells were cultured at an air–liquid interface and exposed to airborne MNPs using a fabricated exposure device. Indices of cytotoxicity, inflammatory response, oxidative stress, and iron homeostasis were monitored postexposure via cell viability assays and qRT-PCR. Concentrations of soluble iron-associated with different MNPs were also examined before and after contact with several aqueous organic and inorganic acids.

Results: The silica-coated MNPs had reduced soluble iron concentrations. This result indicates that the silica coating provides a barrier to and prevents the mobilization of soluble iron from the particle to the cell, thereby reducing the risk of oxidative stress or alterations of iron homeostasis. Cells exposed to MagSilica50 and MagSilica50–85® showed little to no indications of cytotoxicity or induction of inflammatory response/oxidative stress at the examined delivery concentrations.

Conclusion: MNPs coated with amorphous silica are protected from acidic erosion. Correspondingly, the particle stability translates into reduced cytotoxicity and cellular influence on human airway epithelial cells.

Acknowledgments

This work was supported by grants from the Health Effects Institute (4786-RFPA09-5/10-2) and the National Science Foundation (ATM-0852747) to the University of Florida.

Declaration of interest

The authors report no declarations of interest.

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