Indium oxide (In2O3) nanoparticles induce progressive lung injury distinct from lung injuries by copper oxide (CuO) and nickel oxide (NiO) nanoparticles.
Indium is an essential element in the manufacture of liquid crystal displays and other electronic devices, and several forms of indium compounds have been developed, including nanopowders, films, nanowires, and indium metal complexes. Although there are several reports on lung injury caused by indium-containing compounds, the toxicity of nanoscale indium oxide (In2O3) particles has not been reported. Here, we compared lung injury induced by a single exposure to In2O3 nanoparticles (NPs) to that caused by benchmark high-toxicity nickel oxide (NiO) and copper oxide (CuO) NPs. In2O3 NPs at doses of 7.5, 30, and 90 cm(2)/rat (50, 200, and 600 µg/rat) were administered to 6-week-old female Wistar rats via pharyngeal aspiration, and lung inflammation was evaluated 1, 3, 14, and 28 days after treatment. Neutrophilic inflammation was observed on day 1 and worsened until day 28, and severe pulmonary alveolar proteinosis (PAP) was observed on post-aspiration days 14 and 28. In contrast, pharyngeal aspiration of NiO NPs showed severe neutrophilic inflammation on day 1 and lymphocytic inflammation with PAP on day 28. Pharyngeal aspiration of CuO NPs showed severe neutrophilic inflammation on day 1, but symptoms were completely resolved after 14 days and no PAP was observed. The dose of In2O3 NPs that produced progressive neutrophilic inflammation and PAP was much less than the doses of other toxic particles that produced this effect, including crystalline silica and NiO NPs. These results suggest that occupational exposure to In2O3 NPs can cause severe lung injury.
Laboratory of Toxicology, Department of Medicinal Biotechnology, School of Natural Resources and Life Sciences, Dong-A University, 840 Hadan-2dong, Saha-gu, Pusan, 604-714, Korea.
Jiyoung
J
Jeong
Laboratory of Toxicology, Department of Medicinal Biotechnology, School of Natural Resources and Life Sciences, Dong-A University, 840 Hadan-2dong, Saha-gu, Pusan, 604-714, Korea.
Jeongeun
J
Kim
Department of Microbiology and Immunology, Institute of Endemic Disease, Seoul National University College of Medicine, Seoul, Korea.
Seung Hyeok
SH
Seok
Laboratory of Toxicology, Department of Medicinal Biotechnology, School of Natural Resources and Life Sciences, Dong-A University, 840 Hadan-2dong, Saha-gu, Pusan, 604-714, Korea. wcho@dau.ac.kr.
Wan-Seob
WS
Cho
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002478:Cells, Cultured; D003300:Copper / Q000633:toxicity*; D016207:Cytokines / Q000378:metabolism; D005260:Female; D007204:Indium / Q000008:administration & dosage / Q000633:toxicity*; D019394:Ki-67 Antigen / Q000378:metabolism; D055370:Lung Injury / Q000139:chemically induced*; D016676:Macrophages, Alveolar / Q000187:drug effects; D053768:Metal Nanoparticles / Q000008:administration & dosage / Q000737:chemistry / Q000633:toxicity*; D009532:Nickel / Q000008:administration & dosage / Q000633:toxicity*; D010743:Phospholipids / Q000378:metabolism; D011014:Pneumonia / Q000139:chemically induced; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism
D016207:Cytokines; D019394:Ki-67 Antigen; D010743:Phospholipids; D017382:Reactive Oxygen Species; D007204:Indium; C047711:indium oxide; D003300:Copper; D009532:Nickel; C028007:nickel monoxide; C030973:cupric oxide
Fibrosis; In2O3; Indium oxide; Neutrophilic inflammation; Pharyngeal aspiration; Pulmonary alveolar proteinosis