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Inhalation Toxicology
International Forum for Respiratory Research
Volume 25, 2013 - Issue 11
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Research Article

Toxicological effects of PM0.25–2.0 particles collected from a photocopy center in three human cell lines

, , , , , & show all
Pages 621-632 | Received 03 Apr 2013, Accepted 09 Jul 2013, Published online: 17 Sep 2013
 

Abstract

Printing devices such as photocopiers and printers emit predominantly nanoparticles, which may aggregate with time to form PM0.25–2.0 particles. To date, there are no reports on cytotoxic or genotoxic effects of PM0.252.0 particles emitted from photocopiers. This study's objective was to investigate the ability of PM0.252 fraction emitted from photocopiers, to induce pro-inflammatory cytokines, DNA damage and apoptosis in different human-derived cell lines. Three cell types, i.e. a THP-1 line, primary human nasal and small airway epithelial cells, were used. The airborne PM0.252.0 size fraction collected from a photocopy center was characterized for its physicochemical and morphological properties, dispersed in culture media and cells were treated with 30, 100 or 300 µg/ml doses. Levels of 13 cytokines and chemokines in the culture medium harvested at 6 and 24 h of treatment were measured using Luminex cytokine kits. In cells harvested at the same timepoints, DNA damage in cells was studied by Comet assay, and apoptosis was measured by cytofluorimetry using an Annexin V staining kit. The results indicate that in THP-1 cells, several cytokines (IL-6, IL-8, TNFα and IL-1β) were significantly elevated. Only IL-8 was significantly elevated in the primary nasal and small airway cells. Cells exposed to PM0.252.0 underwent apoptosis in a dose-dependent manner, but no significant differences were found in the extent of DNA damage at either timepoint. Airborne PM0.252.0 collected at one photocopier center was capable of inducing several pro-inflammatory cytokines and apoptosis, but no genotoxicity, in all cell lines suggesting a role for PM0.252.0 in our previously documented airway inflammation in human volunteers. Further toxicological evaluations of these particles across different toner manufacturers are warranted.

Acknowledgements

We would like to thank Dr Sharvan Sehrawat for his critical input during the manuscript preparation and the photocopy center employees for their support during sampling for airborne particles. Authors would also like to thank John Martin for his help with gravimetric analysis of samples and during field sampling campaigns.

Notice of Correction

The version of this article published online ahead of print on 17 September 2013 contained a number of additional references in error. These have been removed for this version.

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