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Nanosilver induces minimal lung toxicity or inflammation in a subacute murine inhalation model.

Stebounova LV, Adamcakova-Dodd A, Kim JS, Park H, O'Shaughnessy PT, Grassian VH, Thorne PS - Part Fibre Toxicol (2011)

Bottom Line: In contrast to published in vitro studies, minimal inflammatory response or toxicity was found following exposure to nanosilver in our in vivo study.Dissolution studies showed that nanosilver did not dissolve in solutions mimicking the intracellular or extracellular milieu.However, longer term exposures with higher lung burdens of nanosilver are needed to ensure that there are no chronic effects and to evaluate possible translocation to other organs.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Chemistry, University of Iowa, Iowa City, IA 52242, USA.

ABSTRACT

Background: There is increasing interest in the environmental and health consequences of silver nanoparticles as the use of this material becomes widespread. Although human exposure to nanosilver is increasing, only a few studies address possible toxic effect of inhaled nanosilver. The objective of this study was to determine whether very small commercially available nanosilver induces pulmonary toxicity in mice following inhalation exposure.

Results: In this study, mice were exposed sub-acutely by inhalation to well-characterized nanosilver (3.3 mg/m³, 4 hours/day, 10 days, 5 ± 2 nm primary size). Toxicity was assessed by enumeration of total and differential cells, determination of total protein, lactate dehydrogenase activity and inflammatory cytokines in bronchoalveolar lavage fluid. Lungs were evaluated for histopathologic changes and the presence of silver. In contrast to published in vitro studies, minimal inflammatory response or toxicity was found following exposure to nanosilver in our in vivo study. The median retained dose of nanosilver in the lungs measured by inductively coupled plasma-optical emission spectroscopy (ICP-OES) was 31 μg/g lung (dry weight) immediately after the final exposure, 10 μg/g following exposure and a 3-wk rest period and zero in sham-exposed controls. Dissolution studies showed that nanosilver did not dissolve in solutions mimicking the intracellular or extracellular milieu.

Conclusions: Mice exposed to nanosilver showed minimal pulmonary inflammation or cytotoxicity following sub-acute exposures. However, longer term exposures with higher lung burdens of nanosilver are needed to ensure that there are no chronic effects and to evaluate possible translocation to other organs.

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A. Powder X-ray diffraction patterns for nanosilver with patterns shown for three reference compounds including Ag, AgO and AgO2. B. X-ray photoelectron spectrum for nanosilver. C. TEM image of nanosilver and D. particle primary diameter count distribution from TEM images.
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Figure 2: A. Powder X-ray diffraction patterns for nanosilver with patterns shown for three reference compounds including Ag, AgO and AgO2. B. X-ray photoelectron spectrum for nanosilver. C. TEM image of nanosilver and D. particle primary diameter count distribution from TEM images.

Mentions: The results of particle characterization are summarized in Figure 2 and Table 1. The XRD patterns in Figure 2A compare the nanosilver results with metallic silver and silver oxide (Ag2O, AgO) reference spectra and demonstrate that the nanoparticles are metallic silver with no detectable silver oxide. Surface composition was also examined using XPS (Figure 2B) to test for the presence of an oxide surface layer. Peaks in the Ag3d, Ag3p, O1s, and C1s regions of the photoelectron spectrum were identified. The Ag3d doublet at 368.2 eV and 374.2 eV is consistent with silver in the Ag0 oxidation state. The O1s region does not show any oxygen peaks below 530 eV attributable to AgO or Ag2O, but there is a peak due to CO32- at 530.7 eV. There are also unique peaks at 287.3 and 288.7 eV which we attribute to C=O and CO32-, respectively. In summary, the XPS data indicate the presence of adventitious carbon, some carbon-oxygen functionality, likely due to the use of polyvinylpyrrolidone (PVP) during synthesis to control particle size, and Ag2CO3 on the surface of the nanosilver, but no evidence of a silver oxide coating. This coating accounts for up to 17% of the nanoparticle mass, as determined by ICP analysis and corresponds to a coating thickness of approximately 0.7 nm. A presence of PVP on Ag nanoparticles surface diminishes the propensity of nanoparticles towards aggregation [40] and shows a minimal effect on the Ag nanoparticles toxicity against prokaryotic bacteria [12]. The specific surface area of nanosilver was determined to be 3 ± 2 m2/g using multi-point BET analysis and is lower than the manufacturer's specified specific surface area of 10 ± 1 m2/g.


Nanosilver induces minimal lung toxicity or inflammation in a subacute murine inhalation model.

Stebounova LV, Adamcakova-Dodd A, Kim JS, Park H, O'Shaughnessy PT, Grassian VH, Thorne PS - Part Fibre Toxicol (2011)

A. Powder X-ray diffraction patterns for nanosilver with patterns shown for three reference compounds including Ag, AgO and AgO2. B. X-ray photoelectron spectrum for nanosilver. C. TEM image of nanosilver and D. particle primary diameter count distribution from TEM images.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3040688&req=5

Figure 2: A. Powder X-ray diffraction patterns for nanosilver with patterns shown for three reference compounds including Ag, AgO and AgO2. B. X-ray photoelectron spectrum for nanosilver. C. TEM image of nanosilver and D. particle primary diameter count distribution from TEM images.
Mentions: The results of particle characterization are summarized in Figure 2 and Table 1. The XRD patterns in Figure 2A compare the nanosilver results with metallic silver and silver oxide (Ag2O, AgO) reference spectra and demonstrate that the nanoparticles are metallic silver with no detectable silver oxide. Surface composition was also examined using XPS (Figure 2B) to test for the presence of an oxide surface layer. Peaks in the Ag3d, Ag3p, O1s, and C1s regions of the photoelectron spectrum were identified. The Ag3d doublet at 368.2 eV and 374.2 eV is consistent with silver in the Ag0 oxidation state. The O1s region does not show any oxygen peaks below 530 eV attributable to AgO or Ag2O, but there is a peak due to CO32- at 530.7 eV. There are also unique peaks at 287.3 and 288.7 eV which we attribute to C=O and CO32-, respectively. In summary, the XPS data indicate the presence of adventitious carbon, some carbon-oxygen functionality, likely due to the use of polyvinylpyrrolidone (PVP) during synthesis to control particle size, and Ag2CO3 on the surface of the nanosilver, but no evidence of a silver oxide coating. This coating accounts for up to 17% of the nanoparticle mass, as determined by ICP analysis and corresponds to a coating thickness of approximately 0.7 nm. A presence of PVP on Ag nanoparticles surface diminishes the propensity of nanoparticles towards aggregation [40] and shows a minimal effect on the Ag nanoparticles toxicity against prokaryotic bacteria [12]. The specific surface area of nanosilver was determined to be 3 ± 2 m2/g using multi-point BET analysis and is lower than the manufacturer's specified specific surface area of 10 ± 1 m2/g.

Bottom Line: In contrast to published in vitro studies, minimal inflammatory response or toxicity was found following exposure to nanosilver in our in vivo study.Dissolution studies showed that nanosilver did not dissolve in solutions mimicking the intracellular or extracellular milieu.However, longer term exposures with higher lung burdens of nanosilver are needed to ensure that there are no chronic effects and to evaluate possible translocation to other organs.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Chemistry, University of Iowa, Iowa City, IA 52242, USA.

ABSTRACT

Background: There is increasing interest in the environmental and health consequences of silver nanoparticles as the use of this material becomes widespread. Although human exposure to nanosilver is increasing, only a few studies address possible toxic effect of inhaled nanosilver. The objective of this study was to determine whether very small commercially available nanosilver induces pulmonary toxicity in mice following inhalation exposure.

Results: In this study, mice were exposed sub-acutely by inhalation to well-characterized nanosilver (3.3 mg/m³, 4 hours/day, 10 days, 5 ± 2 nm primary size). Toxicity was assessed by enumeration of total and differential cells, determination of total protein, lactate dehydrogenase activity and inflammatory cytokines in bronchoalveolar lavage fluid. Lungs were evaluated for histopathologic changes and the presence of silver. In contrast to published in vitro studies, minimal inflammatory response or toxicity was found following exposure to nanosilver in our in vivo study. The median retained dose of nanosilver in the lungs measured by inductively coupled plasma-optical emission spectroscopy (ICP-OES) was 31 μg/g lung (dry weight) immediately after the final exposure, 10 μg/g following exposure and a 3-wk rest period and zero in sham-exposed controls. Dissolution studies showed that nanosilver did not dissolve in solutions mimicking the intracellular or extracellular milieu.

Conclusions: Mice exposed to nanosilver showed minimal pulmonary inflammation or cytotoxicity following sub-acute exposures. However, longer term exposures with higher lung burdens of nanosilver are needed to ensure that there are no chronic effects and to evaluate possible translocation to other organs.

Show MeSH
Related in: MedlinePlus