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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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SEM-EDS mapping of nanosilver aerosols deposited on TEM grid during the exposure. The colored dots represent the elemental map for Ag at the expected characteristic X-ray energy for Ag and show, based on size, the presence of silver nanoparticle agglomerates.
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Figure 4: SEM-EDS mapping of nanosilver aerosols deposited on TEM grid during the exposure. The colored dots represent the elemental map for Ag at the expected characteristic X-ray energy for Ag and show, based on size, the presence of silver nanoparticle agglomerates.

Mentions: SEM-EDS of the particles collected on TEM grids in the whole body chamber showed nanosilver aerosol between 50 and 100 nm detected at the characteristic X-ray energy for Ag (Figure 4). The size distributions of Ag nanoparticle aerosols measured during exposure using an SMPS show that the nanosilver aerosols have a GM mobility diameter of 79 nm and GSD of 1.5 (Table 1). These measurements show that mice were exposed to agglomerates of nanosilver that were larger than the primary nanoparticles.


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)

SEM-EDS mapping of nanosilver aerosols deposited on TEM grid during the exposure. The colored dots represent the elemental map for Ag at the expected characteristic X-ray energy for Ag and show, based on size, the presence of silver nanoparticle agglomerates.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: SEM-EDS mapping of nanosilver aerosols deposited on TEM grid during the exposure. The colored dots represent the elemental map for Ag at the expected characteristic X-ray energy for Ag and show, based on size, the presence of silver nanoparticle agglomerates.
Mentions: SEM-EDS of the particles collected on TEM grids in the whole body chamber showed nanosilver aerosol between 50 and 100 nm detected at the characteristic X-ray energy for Ag (Figure 4). The size distributions of Ag nanoparticle aerosols measured during exposure using an SMPS show that the nanosilver aerosols have a GM mobility diameter of 79 nm and GSD of 1.5 (Table 1). These measurements show that mice were exposed to agglomerates of nanosilver that were larger than the primary nanoparticles.

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