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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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Particles found inside alveolar macrophages were identified using TEM-EDS as silver (A, B).
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Figure 7: Particles found inside alveolar macrophages were identified using TEM-EDS as silver (A, B).

Mentions: No pathologic changes were found in Ag-exposed animals or sham-exposed mice. No signs of inflammatory cell infiltrate, alveolitis, perivasculitis, lymphoid agglomerates, epithelial damage, granulomas, giant cells or fibrosis were observed. Particle-laden macrophages were found in the BAL fluid of nanosilver-exposed mice as well as in the lung parenchyma immediately after the last exposure as shown using dark field microscopy (Figures 6A) and also by TEM-EDS of BAL macrophages (Figure 7A, B). Three weeks post exposure there was still evidence of silver particles in macrophage phagosomes (Figures 6C). However, there was a higher percentage of macrophages (76%) found in BAL fluid of mice necropsied at 0 wk post exposure as compared to mice necropsied 3 wks post exposure (28%).


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)

Particles found inside alveolar macrophages were identified using TEM-EDS as silver (A, B).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 7: Particles found inside alveolar macrophages were identified using TEM-EDS as silver (A, B).
Mentions: No pathologic changes were found in Ag-exposed animals or sham-exposed mice. No signs of inflammatory cell infiltrate, alveolitis, perivasculitis, lymphoid agglomerates, epithelial damage, granulomas, giant cells or fibrosis were observed. Particle-laden macrophages were found in the BAL fluid of nanosilver-exposed mice as well as in the lung parenchyma immediately after the last exposure as shown using dark field microscopy (Figures 6A) and also by TEM-EDS of BAL macrophages (Figure 7A, B). Three weeks post exposure there was still evidence of silver particles in macrophage phagosomes (Figures 6C). However, there was a higher percentage of macrophages (76%) found in BAL fluid of mice necropsied at 0 wk post exposure as compared to mice necropsied 3 wks post exposure (28%).

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