Absence of genotoxicity following pulmonary exposure to metal oxides of copper, tin, aluminum, zinc, and titanium in mice
Claudia Torero Gutierrez (National Research Centre for the Working Environment, University of Copenhagen)
Niels Hadrup (National Research Centre for the Working Environment, Technical University of Denmark (DTU))
Charis Loizides (The Cyprus Institute)
Iosif Hafez (The Cyprus Institute)
George Biskos (The Cyprus Institute, TU Delft - Civil Engineering & Geosciences)
Martin Roursgaard (University of Copenhagen)
Anne Thoustrup Saber (National Research Centre for the Working Environment)
Peter Møller (University of Copenhagen)
Ulla Vogel (Technical University of Denmark (DTU), National Research Centre for the Working Environment)
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Abstract
Inhalation of nanosized metal oxides may occur at the workplace. Thus, information on potential hazardous effects is needed for risk assessment. We report an investigation of the genotoxic potential of different metal oxide nanomaterials. Acellular and intracellular reactive oxygen species (ROS) production were determined for all the studied nanomaterials. Moreover, mice were exposed by intratracheal instillation to copper oxide (CuO) at 2, 6, and 12 μg/mouse, tin oxide (SnO2) at 54 and 162 μg/mouse, aluminum oxide (Al2O3) at 18 and 54 μg/mouse, zinc oxide (ZnO) at 0.7 and 2 μg/mouse, titanium dioxide (TiO2) and the benchmark carbon black at 162 μg/mouse. The doses were selected based on pilot studies. Post-exposure time points were 1 or 28 days. Genotoxicity, assessed as DNA strand breaks by the comet assay, was measured in lung and liver tissue. The acellular and intracellular ROS measurements were fairly consistent. The CuO and the carbon black bench mark particle were potent ROS generators in both assays, followed by TiO2. Al2O3, ZnO, and SnO2 generated low levels of ROS. We detected no increased genotoxicity in this study using occupationally relevant dose levels of metal oxide nanomaterials after pulmonary exposure in mice, except for a slight increase in DNA damage in liver tissue at the highest dose of CuO. The present data add to the body of evidence for risk assessment of these metal oxides.
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