Pulmonary Toxicity Induced by Intratracheal Instillation of Coarse and Fine Particles of Cerium Dioxide in Male Rats

Toya, Tadao; Takata, Ayako; Otaki, Noriko; Takaya, Mitsutoshi; Serita, Fumio; Yoshida, Katsumi; Kohyama, Norihiko

doi:10.2486/indhealth.48.3

Cited by 31 publications

(24 citation statements)

References 27 publications

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“…Other studies have shown that intratracheal exposure of CeO 2 induced pulmonary inflammation and small granulomas in both rats (Toya et al, 2010) and mice (Park et al, 2010), and that exposure of mice to CeO 2 through head and nose inhalation caused chronic inflammatory responses (Srinivas et al, 2011). Our previous studies have demonstrated that CeO 2 exposure induced pulmonary phospholipidosis, activated alveolar macrophage (AM) production of inflammatory cytokines, and induced fibrogenic and extracellular membrane (ECM) mediator production leading to pulmonary fibrosis (Ma et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Effects of amorphous silica coating on cerium oxide nanoparticles induced pulmonary responses

Mercer

Barger

et al. 2015

Toxicology and Applied Pharmacology

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Recently cerium compounds have been used in a variety of consumer products, including diesel fuel additives, to increase fuel combustion efficiency and decrease diesel soot emissions. However, cerium oxide (CeO2) nanoparticles have been detected in the exhaust, which raises a health concern. Previous studies have shown that exposure of rats to nanoscale CeO2 by intratracheal instillation (IT) induces sustained pulmonary inflammation and fibrosis. In the present study, male Sprague–Dawley rats were exposed to CeO2 or CeO2 coated with a nano layer of amorphous SiO2 (aSiO2/CeO2) by a single IT and sacrificed at various times post-exposure to assess potential protective effects of the aSiO2 coating. The first acellular bronchoalveolar lavage (BAL) fluid and BAL cells were collected and analyzed from all exposed animals. At the low dose (0.15 mg/kg), CeO2 but not aSiO2/CeO2 exposure induced inflammation. However, at the higher doses, both particles induced a dose-related inflammation, cytotoxicity, inflammatory cytokines, matrix metalloproteinase (MMP)-9, and tissue inhibitor of MMP at 1 day post-exposure. Morphological analysis of lung showed an increased inflammation, surfactant and collagen fibers after CeO2 (high dose at 3.5 mg/kg) treatment at 28 days post-exposure. aSiO2 coating significantly reduced CeO2-induced inflammatory responses in the airspace and appeared to attenuate phospholipidosis and fibrosis. Energy dispersive X-ray spectroscopy analysis showed Ce and phosphorous (P) in all particle-exposed lungs, whereas Si was only detected in aSiO2/CeO2-exposed lungs up to 3 days after exposure, suggesting that aSiO2 dissolved off the CeO2 core, and some of the CeO2 was transformed to CePO4 with time. These results demonstrate that aSiO2 coating reduce CeO2-induced inflammation, phospholipidosis and fibrosis.

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Section: Introductionmentioning

confidence: 99%

Effects of amorphous silica coating on cerium oxide nanoparticles induced pulmonary responses

Mercer

Barger

et al. 2015

Toxicology and Applied Pharmacology

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“…Therefore, most toxicological studies on REEs have focused on the evaluation of cerium compounds. However, lanthanum is also used in significant amounts (4-7), but only a few comparative toxicity studies of lanthanum and other REEs have been conducted. For example, Palmer et al .…”

Section: Introductionmentioning

confidence: 99%

Toxicity of Two Different Sized Lanthanum Oxides in Cultured Cells and Sprague-Dawley Rats

Lim¹

2015

Toxicological Research

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In recent years, the use of both nano- and micro-sized lanthanum has been increasing in the production of optical glasses, batteries, alloys, etc. However, a hazard assessment has not been performed to determine the degree of toxicity of lanthanum. Therefore, the purpose of this study was to identify the toxicity of both nano- and micro-sized lanthanum oxide in cultured cells and rats. After identifying the size and the morphology of lanthanum oxides, the toxicity of two different sized lanthanum oxides was compared in cultured RAW264.7 cells and A549 cells. The toxicity of the lanthanum oxides was also analyzed using rats. The half maximal inhibitory concentrations of micro-La2O3 in the RAW264.7 cells, with and without sonication, were 17.3 and 12.7 times higher than those of nano-La2O3, respectively. Similar to the RAW264.7 cells, the toxicity of nano-La2O3 was stronger than that of micro-La2O3 in the A549 cells. We found that nano-La2O3 was absorbed in the lungs more and was eliminated more slowly than micro-La2O3. At a dosage that did not affect the body weight, numbers of leukocytes, and concentrations of lactate dehydrogenase and albumin in the bronchoalveolar lavage (BAL) fluids, the weight of the lungs increased. Inflammatory effects on BAL decreased over time, but lung weight increased and the proteinosis of the lung became severe over time. The effects of particle size on the toxicity of lanthanum oxides in rats were less than in the cultured cells. In conclusion, smaller lanthanum oxides were more toxic in the cultured cells, and sonication decreased their size and increased their toxicity. The smaller-sized lanthanum was absorbed more into the lungs and caused more toxicity in the lungs. The histopathological symptoms caused by lanthanum oxide in the lungs did not go away and continued to worsen until 13 weeks after the initial exposure.

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“…Animal studies have reported that particle matter 2.5 (PM2.5), including ultrafine particle, and diesel particles have an influence on organs such as brain and testis, which are not open to direct exposure [2][3][4][5][6] , and a low dose of particles induces pulmonary inflammation 6,7) ; these results lead to concern that manufactured nanomaterial, may have similar biological effects. The lung is a target organ of nanoparticle exposure, and reports have described workers showing severe pulmonary inflammation and fibrosis due to inhalation exposure to nanoparticles 8) .…”

Section: Introductionmentioning

confidence: 99%

Investigation of Gene Expression of MMP-2 and TIMP-2 mRNA in Rat Lung in Inhaled Nickel Oxide and Titanium Dioxide Nanoparticles

et al. 2011

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In order to investigate whether or not dispersed nanoparticles have an effect of inflammation and fibrosis on animals, we developed a nanoparticle generation system and examined the gene expression of matrix metalloproteinase (MMP) and tissue inhibitor matrix proteinase (TIMP) in rat lung containing inhaled nickel oxide (NiO) or titanium dioxide (TiO 2 ) nanoparticles. In both experiments, Wistar male rats were exposed to NiO or TiO 2 nanoparticles for 4 wk (6 h/day). The geometric mean diameters of NiO and TiO 2 in the chamber were 139 ± 12 nm and 51 ± 9 nm, respectively. The average concentration of the particle number of NiO and TiO 2 was 1.0E+05 /cm 3 and 2.8E+05 /cm 3 , respectively. At 4 d, 1 and 3 months after the end of the inhalation, the rats exposed to these particles were sacrificed and the gene expressions of MMP-2, TIMP-2 and type I collagen were measured using RT-PCR. Pathological finding revealed that there was minimum inflammation with nickel oxide only at 4 d and no change with titanium oxide. However, there were no changes of the gene expression of MMP-2, TIMP-2, and type I collagen in either the NiO or TiO 2 exposure groups. In this study, inhalation of nickel oxide and titanium dioxide nanoparticles did not induce the gene expression of MMP-2 and TIMP-2 mRNA in rat lungs.

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Pulmonary Toxicity Induced by Intratracheal Instillation of Coarse and Fine Particles of Cerium Dioxide in Male Rats

Cited by 31 publications

References 27 publications

Effects of amorphous silica coating on cerium oxide nanoparticles induced pulmonary responses

Effects of amorphous silica coating on cerium oxide nanoparticles induced pulmonary responses

Toxicity of Two Different Sized Lanthanum Oxides in Cultured Cells and Sprague-Dawley Rats

Investigation of Gene Expression of MMP-2 and TIMP-2 mRNA in Rat Lung in Inhaled Nickel Oxide and Titanium Dioxide Nanoparticles

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