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Investigations on cytotoxic and genotoxic effects of laser printer emissions in human epithelial A549 lung cells using an air/liquid exposure system

✍ Scribed by Tao Tang; Richard Gminski; Mathias Könczöl; Christoph Modest; Benedikt Armbruster; Volker Mersch-Sundermann


Publisher
John Wiley and Sons
Year
2011
Tongue
English
Weight
946 KB
Volume
53
Category
Article
ISSN
0893-6692

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✦ Synopsis


Abstract

Exposure to emissions from laser printers during the printing process is commonplace worldwide, both in the home and workplace environment. In the present study, cytotoxic and genotoxic effects of the emission from five low to medium‐throughput laser printers were investigated with respect to the release of ozone (O~3~), volatile organic compounds (VOC), particulate matter (PM), and submicrometer particles (SMP) during standby and operation. Experiments were conducted in a 1 m^3^ emission chamber connected to a Vitrocell® exposure system. Cytotoxicity was determined by the WST‐1 assay and genotoxicity by the micronucleus test in human A549 lung cells. The five laser printers emitted varying but generally small amounts of O~3~, VOC, and PM. VOC emissions included 13 compounds with total VOC concentrations ranging from 95 to 280 μg/m^3^ (e.g., 2‐butanone, hexanal, m,p‐xylene, and o‐xylene). Mean PM concentrations were below 2.4 μg/m^3^. SMP number concentration levels during standby ranged from 9 to 26 particles/cm^3^. However, three of the printers generated a 90 to 16 × 10^3^‐fold increase of SMP during the printing process (maximum 294,460 particles/cm^3^). Whereas none of the printer emissions were found to cause cytotoxicity, emissions from two printers induced formation of micronuclei (P < 0.001), thus providing evidence for genotoxicity. As yet, differences in biological activity cannot be explained on the basis of the specific emission characteristics of the different printers. Because laser printing technology is widely used, studies with additional cytogenetic endpoints are necessary to confirm the DNA‐damaging potency and to identify emission components responsible for genotoxicity. Environ. Mol. Mutagen., 2012. © 2011 Wiley Periodicals, Inc.