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Vitro Pulmonary Toxicity of Metal Oxide Nanoparticles
Citation:
SNYDER, R. J. AND K. L. DREHER. Vitro Pulmonary Toxicity of Metal Oxide Nanoparticles. Presented at Society of Toxicology (SOT) Annual Meeting, Washington, DC, March 06 - 10, 2011.
Impact/Purpose:
An integrated multi-tier testing strategy (www.epa.gov/nanoscience/) was implemented to address these challenges allowing for the rapid screening/prioritization of engineered-nanomaterials and ultimately identify alternative tests predictive of their toxicity.
Description:
The diversity of engineered-nanomaterials and their applications as well as potential unknown health effects of these novel materials are significant challenges to assessing the health risks of nanotechnology. An integrated multi-tier testing strategy (www.epa.gov/nanoscience/) was implemented to address these challenges allowing for the rapid screening/prioritization of engineered-nanomaterials and ultimately identify alternative tests predictive of their toxicity. This research represents Tier 2 -in vitro toxicity assessment of 8 metal oxide nanoparticles (NPs). Human bronchial epithelial airway cell line (BEAS2B) was exposed for 24 or 48 h to various concentrations (6 -100 ug/ml) of 6 Ti02 or 2 Ce02 NPs obtained from a variety of commercial sources and differing in size and crystal structure. The effect which NPs had on cell cytotoxicity was measured using both the WST -1 assay and LDH release. The ability of NPs to induce cellular reactive oxygen stress (ROS) was measured at 2h post-exposure by DCFH fluorescent intensity. Ti02 and Ce02 NPs had no significant dose-dependent effect on the BEAS2B cell cytotoxicity when examined using the WST -1 assay. Differential cell cytotoxicity amongst the various Ti02 and Ce02 NPs [Ce02(15nm) > Ti02(32nm/anatase-rutile) > Ce02(70nm) > Ti02(200nm/anatase) = Ti02(10nm/anatase) = Ti02(30nm/anatase-rutile) > Ti02(25nm/anatase) > Ti02(250nm/rutile)] was detected by LDH release as early as 24h postexposure. BEAS2B cellular ROS was induced in differential and dose-dependent manner by all Ti02 NPs [Ti02(25nm/anatase) = Ti02(250nm/rutile) > Ti02(30nm/anatase-rutile) = Ti02(10nm/anatase) = Ti02(32nm/anatase-rutile) = Ti02(200nm/anatase) > Ce02(70nm) = Ce02(15nm)]. Ce02 NPs did not induce ROS in BEAS2B cells at any size or dose. The results demonstrate that differential toxicity of various Ti02 and Ce02 NPs was detected by in vitro pulmonary toxicity testing. Metal oxide NP BEAS2B cell cytotoxicity was found not to be dependent on size alone and did not correlate with the ability to induce ROS. This abstract does not necessarily reflect EPA policy.