Bio: Dr. Qunwei Zhang, MD, MPH, PhD, is a tenured Professor at the School of Public Health and Information Sciences, University of Louisville, USA. He has a long‐term interest in studying the health effects of various environmental and occupational agents including engineered nanoparticles, ambient PM, cigarette smoke, etc. He has been exploring the genetic, epigenetic, and carcinogenic effects of metal nanoparticles such as nickel and cobalt nanoparticles. He has published more than 100 articles in peer‐reviewed journals, reviews, and book chapters on these topics. Dr. Zhang received research grant awards from the National Institutes of Health (NIH), American Heart Association (AHA), American Lung Association (ALA), Health Effects Institute (HEI), Kentucky Science & Engineering Foundation (KSEF), Kentucky Lung Cancer Research Program (KLCRP), etc. He also received a Walter A. Rosenblith New Investigator Award from HEI in 2006. He has served as an ad hoc or regular grant reviewer for Medical Research Council (MRC) of United Kingdom, National Institutes of Health (NIH, USA), California Tobacco‐Related Disease Research Program (TRDRP), National Natural Science Foundation of China (Phase II), and Qatar Research, Development and Innovation (QRDI) Council. As a member of the IARC Working Group, he participated in the preparation of Volume 131 of the IARC Monographs “Cobalt, Antimony Compounds, and Weapons-grade Tungsten Alloy” (2023). He is the Editor of “Nanotoxicology Methods and Protocols”, which is part of the book series: Methods in Molecular Biology (MIMB, volume 1894).

Abstract: Metal nanoparticles, such as Nano-Ni and Nano-Co, have been increasingly used in industrial and biomedical fields, thus, their potential adverse health effects cannot be ignored. We explored metal nanoparticles-induced genotoxic and carcinogenic effects, including DNA damage and mutation, DNA repair defect, and cell transformation as well as the potential underlying mechanisms. We found that exposure to Nano-Ni or Nano-Co, but not Nano-TiO2, caused DNA damage both in vitro and in vivo, which was reflected by increased phosphorylation of DNA damage response-associated proteins such as ATM, p53, and gH2AX. Exposure to Nano-Co, but not Nano-Ni, induced a much higher mutant frequency as compared to controls in the genomic DNA of gpt delta transgenic mice, and most common mutation was G:C to T:A transversion, which may be explained by Nano-Co-induced increased formation of 8-OHdG. However, Nano-Ni exposure induced HIF-1α nuclear accumulation, miR-210 up-regulation, and down-regulation of homologous recombination repair gene RAD52. Knocking out HIF-1α or inhibition of miR-210 ameliorated Nano-Ni-induced RAD52 down-regulation. Long-term low-dose Nano-Ni exposure led to cell malignant transformation, which was significantly reduced by augmentation of RAD52 expression. Combined effects of Nano-Ni-induced DNA damage and DNA repair defects through HIF-1α/miR-210/RAD52 pathway likely contribute to Nano-Ni-induced genomic instability and cell transformation.