Pulmonary response after exposure to inhaled nickel hydroxide nanoparticles: Short and long-term studies in mice

Abstract

Short and long-term pulmonary response to inhaled nickel hydroxide nanoparticles (nano-Ni(OH)2, CMD = 40 nm) in C57BL/6 mice was assessed using a whole body exposure system. For short-term studies mice were exposed for 4 h to nominal concentrations of 100, 500, and 1000 mg/m3. For long-term studies mice were exposed for 5 h/d, 5 d/w, for up to 5 months (m) to a nominal concentration of 100 mg/m3. Particle morphology, size distribution, chemical composition, solubility, and intrinsic oxidative capacity were determined. Markers of lung injury and inflammation in bronchoalveolar lavage fluid (BALF); histopathology; and lung tissue elemental nickel content and mRNA changes in macrophage inflammatory protein-2 (Mip-2), chemokine ligand 2 (Ccl2), interleukin 1-alpha (Il-1α), and tumor necrosis factor-alpha (Tnf-α) were assessed. Dose-related changes in BALF analyses were observed 24 h after short-term studies while significant changes were noted after 3 m and/or 5 m of exposure (24 h). Nickel content was detected in lung tissue, Ccl2 was most pronouncedly expressed, and histological changes were noted after 5 m of exposure. Collectively, data illustrates nano-Ni(OH)2 can induce inflammatory responses in C57BL/6 mice.

Acute toxicity of nickel nanoparticles in rats after intravenous injection

“…20 Other studies involving Ni oxide nanoparticles have also reported the presence of lymphocytic infiltrates in the lung. 21 In the high dose group, foamy macrophages were observed in the alveolar spaces, which are found in various lung diseases. A study by Yuasa and Kanazawa 22 found that foamy macrophages can be derived from monocytes in the blood.…”

Exposure to nickel oxide nanoparticles induces pulmonary inflammation through NLRP3 inflammasome activation in rats

“…These observed changes may be related to the time course of different parameters and the dynamic nature of the cytokine network after NP exposure. 10 However, some studies have shown that NiONP exposure induces only mild and reversible inflammation. 33,34 Zhang et al 35 found that NiO (20 µg suspended in 50 µL of PBS) exposure induced less neutrophil cell counts, monocyte chemotactic protein-1, and IL-6 levels in BALF compared with the same amount of CuO and Cr 2 O 3 exposure in C57 BL/6 mice.…”

“…28 Inhalation is the major exposure route of Ni 2+ NPs; AMs and airway epithelial cells are the most important target cells. 10,29 Agglomerates of NiONPs have been shown to induce persistent inflammatory effects and the increased expression of cytokines, such as IL-1β and monocyte chemotactic protein-1. 30 In this study, intratracheal instillation of NiONPs resulted in persistent pulmonary inflammation, which was accompanied by neutrophil, eosinophil, and macrophage infiltration and cytokine secretion.…”

Genotoxicity and Cytotoxicity of Cadmium Sulfide Nanomaterials to Mice: Comparison Between Nanorods and Nanodots

“…Compared with their bulk counterparts, nanomaterials are often more toxic (Grassian et al, 2006;Pan et al, 2007). For example, a number of toxicological studies using rats have shown that exposure to nanodots induces greater inflammatory and cytotoxic effects than larger-sized particles at equivalent mass concentrations (Grassian et al, 2006;Gillespie et al, 2010;Rossi et al, 2010). Most nanomaterial toxicity studies have focused on nanodots (i.e., particles of various shapes with no predominant dimension, or 0D), and only a few studies have addressed the toxicity of elongated rod-like (1D) nanoparticles (Magrez et al, 2009;Song et al, 2010) or compared 1D nanomaterials with their 0D counterparts (Chithrani et al,2006;Pal et al, 2007;Ispas et al, 2009;Simon-Deckers et al, 2009).…”