Abstract
BackgroundAlthough classified as metal oxides, cobalt monoxide (CoO) and lanthanum oxide (La2O3) nanoparticles, as representative transition and rare earth oxides, exhibit distinct material properties that may result in different hazardous potential in the lung. The current study was undertaken to compare the pulmonary effects of aerosolized whole body inhalation of these nanoparticles in mice.ResultsMice were exposed to filtered air (control) and 10 or 30 mg/m3 of each particle type for 4 days and then examined at 1 h, 1, 7 and 56 days post-exposure. The whole lung burden 1 h after the 4 day inhalation of CoO nanoparticles was 25 % of that for La2O3 nanoparticles. At 56 days post exposure, < 1 % of CoO nanoparticles remained in the lungs; however, 22–50 % of the La2O3 nanoparticles lung burden 1 h post exposure was retained at 56 days post exposure for low and high exposures. Significant accumulation of La2O3 nanoparticles in the tracheobronchial lymph nodes was noted at 56 days post exposure. When exposed to phagolysosomal simulated fluid, La nanoparticles formed urchin-shaped LaPO4 structures, suggesting that retention of this rare earth oxide nanoparticle may be due to complexation of cellular phosphates within lysosomes. CoO nanoparticles caused greater lactate dehydrogenase release in the bronchoalveolar fluid (BALF) compared to La2O3 nanoparticles at 1 day post exposure, while BAL cell differentials indicate that La2O3 nanoparticles generated more inflammatory cell infiltration at all doses and exposure points. Histopathological analysis showed acute inflammatory changes at 1 day after inhalation of either CoO or La2O3 nanoparticles. Only the 30 mg/m3 La2O3 nanoparticles exposure caused chronic inflammatory changes and minimal fibrosis at day 56 post exposure. This is in agreement with activation of the NRLP3 inflammasome after in vitro exposure of differentiated THP-1 macrophages to La2O3 but not after CoO nanoparticles exposure.ConclusionTaken together, the inhalation studies confirmed the trend of our previous sub-acute aspiration study, which reported that CoO nanoparticles induced more acute pulmonary toxicity, while La2O3 nanoparticles caused chronic inflammatory changes and minimal fibrosis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0155-3) contains supplementary material, which is available to authorized users.
Highlights
Classified as metal oxides, cobalt monoxide (CoO) and lanthanum oxide (La2O3) nanoparticles, as representative transition and rare earth oxides, exhibit distinct material properties that may result in different hazardous potential in the lung
Nanoparticles CoO nanoparticles were purchased from SkySpring Nanomaterials (Houston, TX) and La2O3 nanoparticles were purchased from Nanostructured & Amorphous Materials, Inc. (Houston, TX)
The mass median aerodynamic diameters of the CoO and La2O3 nanoparticles were determined by a cascade impactor (MOUDI Models 110-R, MSP Corp, Shoreview, MN), which fractionates the particles into 10 size ranges from 56 nm to 18 μm
Summary
Classified as metal oxides, cobalt monoxide (CoO) and lanthanum oxide (La2O3) nanoparticles, as representative transition and rare earth oxides, exhibit distinct material properties that may result in different hazardous potential in the lung. A number of transition metal oxide nanoparticles exhibit semi-conductor properties in which the material band gap plays a role in electron transfer to and from biological redox components. This can lead to the generation of adverse health effects due to the generation of oxygen radicals and oxidative stress [2]. La2O3 (and other rare earth oxide) nanoparticles exhibit non-oxidative surface reactivity that may come into play in a biological environment with the possibility to generate hazard through complexation of cellular phosphate groups in the lysosome [6]. This study addresses how phosphate complexation of La nanoparticles in the acidic environment of the phagolysosome can induce lysosomal membrane damage, activation of the NRLP3 inflammasome, and IL1β production [6]
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