RT Journal Article
SR Electronic
T1 Toxicity assessment of spark-generated, airborne copper oxide nanoparticles in lung epithelial cells
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP P1489
VO 44
IS Suppl 58
A1 Peter Thorne
A1 Xuefang Jing
A1 Jae Hong Park
A1 Andrea Adamcakova-Dodd
A1 Thomas Peters
A1 Sarah Perry
YR 2014
UL http://erj.ersjournals.com/content/44/Suppl_58/P1489.abstract
AB Background: Copper oxide nanoparticles (CuONPs) are of great interest in nanotoxicology due to widespread use and significant toxicity.The aim of this study was to evaluate and compare the toxicity of CuONPs in human primary cells and in a commonly-employed cancer cell line. We investigated the consequences of CuONPs exposure using an in vitro air-liquid interface system.Methods: Human Bronchial Epithelial Cells (HBEC) and A549 cells were exposed to clean air or spark-generated CuONPs for 2 or 4 h. Cellular doses of Cu were assessed by inductively coupled plasma mass spectrometry. Outcome measures included cell viability, cytotoxicity (lactate dehydrogenase [LDH]), oxidative stress (reactive oxygen species [ROS]) and inflammation (interleukin [IL]-8).Results: The number median diameterand concentration of CuONPswere 9.2 nm and 3.5×107 particles/cm3. Compared with control, CuONPs significantly reduced cell viability, increased LDH release and elevated levels of ROS and IL-8 in a dose dependent manner. 4 hr exposure to CuONPs resulted in 63% loss of viability, 1.9-fold increase of ROS and 290% LDH release over controls in A549 cells; whereas HBEC had 15% viability loss, 2.7-fold ROS increase and 165% LDH release (all p<0.001 compared with A549); IL-8 was comparable in two cell types. N-acetylcysteine reduced the cell viability loss from 63% to 16% (p<0.001) and decreased ROS level from 190% to 132% (p<0.001).Conclusion: Spark-generated CuONPs exposure induced cytotoxicity, oxidative stress and inflammation in both cell types in a dose dependent manner. A549 cells were more susceptible to CuONPs effects than primary HBEC. Antioxidant treatment reduced CuONPs-induced cytotoxicity.