Review and Evaluation of the Potential Health Effects of Oxidic Nickel Nanoparticles

Abstract

The exceptional physical and chemical properties of nickel nanomaterials have been exploited in a range of applications such as electrical conductors, batteries, and biomaterials. However, it has been suggested that these unique properties may allow for increased bioavailability, bio-reactivity, and potential adverse health effects. Thus, the purpose of this review was to critically evaluate data regarding the toxicity of oxidic nickel nanoparticles (nickel oxide (NiO) and nickel hydroxide (Ni(OH)2) nanoparticles) with respect to: (1) physico-chemistry properties; (2) nanomaterial characterization in the defined delivery media; (3) appropriateness of model system and translation to potential human effects; (4) biodistribution, retention, and clearance; (5) routes and relevance of exposure; and (6) current research data gaps and likely directions of future research. Inhalation studies were prioritized for review as this represents a potential exposure route in humans. Oxidic nickel particle size ranged from 5 to 100 nm in the 60 studies that were identified. Inflammatory responses induced by exposure of oxidic nickel nanoparticles via inhalation in rodent studies was characterized as acute in nature and only displayed chronic effects after relatively large (high concentration and long duration) exposures. Furthermore, there is no evidence, thus far, to suggest that the effects induced by oxidic nickel nanoparticles are related to preneoplastic events. There are some data to suggest that nano- and micron-sized NiO particles follow a similar dose response when normalized to surface area. However, future experiments need to be conducted to better characterize the exposure–dose–response relationship according to specific surface area and reactivity as a dose metric, which drives particle dissolution and potential biological responses.

Hematobiochemical, Oxidative Stress, and Histopathological Mediated Toxicity Induced by Nickel Ferrite (NiFe2O4) Nanoparticles in Rabbits

“…These histopathological changes in the liver and other visceral tissues might be due to the accumulation of nickel ferrite nanoparticles [76,78]. Furthermore, different histopathological changes in kidneys and spleen of rats exposed to higher doses of oxidic nickel nanoparticles have also been observed [76,78]. In contrast to our results, no histopathological changes in the spleen, heart, brain, and kidneys were reported in Wistar rats exposed to nickel-containing nanoparticles [79].…”

“…In contrast to our results, no histopathological changes in the spleen, heart, brain, and kidneys were reported in Wistar rats exposed to nickel-containing nanoparticles [79]. Moreover, various microscopic changes in the brain of rats due to nickel oxide nanoparticles like gliosis, necrosis, spongy changes, and hyperemia were observed [78].…”

“…However, different earlier studies have observed various histopathological alterations in the liver (increased liver weight, binucleated hepatocytes, increased akaryotic hepatocytes, hepatic sinus disappearance, cellular edema, and focal areas of necrosis) in rats treated with oxidic nickel nanoparticles [76,77]. These histopathological changes in the liver and other visceral tissues might be due to the accumulation of nickel ferrite nanoparticles [76,78]. Furthermore, different histopathological changes in kidneys and spleen of rats exposed to higher doses of oxidic nickel nanoparticles have also been observed [76,78].…”

LncRNA MEG3 restrained pulmonary fibrosis induced by NiO NPs via regulating hedgehog signaling pathway‐mediated autophagy

“…30 In occupational or industrial environments, workers were most often exposed to NiO NPs through inhalation. 2 Therefore, the potential harm of NiO NPs to pulmonary toxicity has attracted much attention. NiO NPs promoted lung inflammatory damage in rats and mice by enhancing cytotoxicity and inducing the overproduction of ROS and inflammatory cytokines.…”

LncRNA MEG3amelioratesNiOnanoparticles‐induced pulmonary inflammatory damage via suppressing the p38 mitogen activated protein kinases pathway

“…In natural conditions, inhalation of NiO NPs caused acute inflammatory reactions, and chronic effects were only observed at high dosages or long periods 43 . However, most extant studies focused on acute animal experiments and indicators were not extensive 12,13 .…”