CoO and La2O3 nanoparticle-induced pulmonary response in mice after whole-body inhalation exposure
Public Domain
-
2016/02/07
-
Details
-
Personal Author:Andrew, Michael E. ; Battelli L ; Castranova, Vincent ; Chen BT ; McKinney W ; Mercer R ; Mihalchik A ; Porter, Dale ; Qian Y ; Shaffer J ; Sisler JD ; Wolfarth M
-
Description:Metal oxide nanoparticles have the unique property of semi-conduction and can serve as conduits for electron transfer between aqueous reactants. Studies have shown that these semi-conducting properties may be responsible for generating adverse health effects. Two metal oxide nanoparticles with different semi-conductor properties, cobalt monoxoide (CoO) and lanthanum oxide (La2O3) may pose different toxicological potentials in vivo and in vitro. Our previous in vitro study showed that CoO nanoparticles induce a more potent toxicological response in human small airway epithelial cells than La 2O3 nanoparticles. The current study determined CoO and La2O3 metal oxide nanoparticles-induced pulmonary response in mice after whole-body inhalation exposure. Mice were exposed to 10 or 30 mg/m 3, for 6 h per day over 4 days and were examined at 1, 7 and 56 days post exposure. Both CoO and La 2O3 nanoparticles were present in the lung at 1, 7 and 56 days post exposure; however, CoO caused greater lactate dehydrogenase, macrophages, lymphocytes, neutrophils and eosinophils in the bronchoalveolar fluid compared to La2O3 nanoparticles at both doses and all post exposure time points. Histopathological results show that there was acute pulmonary inflammation at 1 day post-exposure for both nanoparticles; however, no chronic fibrotic response was observed. Mice exposed to CoO had higher levels of proinflammatory cytokine expression compared to mice exposed to La 2O3 nanoparticles. Taken together, the results demonstrate that CoO nanoparticles induce more overall acute pulmonary toxicity when compared to La2O3 nanoparticles. Moreover, this study starts to fills the gap between in vivo and in vitro nanoparticle-induced toxicity studies and risk assessment. [Description provided by NIOSH]
-
Subjects:
-
Keywords:
-
Publisher:
-
Document Type:
-
Genre:
-
Place as Subject:
-
CIO:
-
Division:
-
Topic:
-
Location:
-
NIOSHTIC Number:nn:20048487
-
Citation:Fibrosis: from basic mechanisms to targeted therapies joint with the meeting on stromal cells in immunity, February 7-11, 2016, Keystone, Colorado. Silverthorne, CO: Keystone Symposia, 2016 Feb; :104
-
CAS Registry Number:
-
Federal Fiscal Year:2016
-
NORA Priority Area:
-
Peer Reviewed:False
-
Source Full Name:Fibrosis: from basic mechanisms to targeted therapies joint with the meeting on stromal cells in immunity, February 7-11, 2016, Keystone, Colorado
-
Collection(s):
-
Main Document Checksum:urn:sha-512:3cd00feceefb20bed0108442c9de10162d8a27e6ba1542e6b524b673c04953f6f38e60102f06c3cb2ae97cd623b0e011a8e91aec539929ab3cfa6f7fc9179405
-
Download URL:
-
File Type:
ON THIS PAGE
CDC STACKS serves as an archival repository of CDC-published products including
scientific findings,
journal articles, guidelines, recommendations, or other public health information authored or
co-authored by CDC or funded partners.
As a repository, CDC STACKS retains documents in their original published format to ensure public access to scientific information.
As a repository, CDC STACKS retains documents in their original published format to ensure public access to scientific information.
You May Also Like