Role of Surface Chemistry in the Toxicological Properties of Manufactured Nanoparticles
|Principal Investigator||Prabir Dutta|
|Institution||The Ohio State University|
|Relevance to Implications||High|
|Class of Nanomaterial||Engineered Nanomaterials|
|Broad Research Categories||
|Anticipated Total Funding||$400,000.00|
|Anticipated End Year||2007|
The objectives of this program are to verify two hypotheses: 1) the quantifiable differences in surface reactivity of nanoparticles, as measured by acidity, redox chemistry, metal ion binding and Fenton chemistry as compared with micron-sized particles of similar composition cannot be explained by the increase in surface area alone, and 2) the oxidative stress and inflammatory response induced by nanoparticles upon interaction with macrophages and epithelial cells depends on their surface reactivity. The basis of these hypotheses is that nanoparticles contain a significantly higher number of broken bonds on the surface that provide different reactivity as compared to larger particles.
The experimental approach focuses on three classes of manufactured nanoparticles: catalysts (aluminosilicates), titania, and carbon. For the catalysts and titania samples, nanoparticles (<100nm) and micron-sized particles of similar bulk composition will be studied. For carbon, carbon black and single-walled carbon nanotubes are chosen. Nanoparticles of aluminosilicates and titania will be synthesized, whereas the other particles will be obtained from commercial sources. Characterization will involve electron microscopy, surface area, surface and bulk composition.
Reactivity of well characterized particles in regardsto their acidity, reaction with antioxidants simulating the lung linig fluid, coordination of iron, and Fenton chemistry will be carried out using spectroscopic methods. Particular attention will be paid to surface activation as may exist during manufacturing and processing. In-vitro oxidative stress and inflammatory responses upon phagocytosis of the particles by macrophages and pulmonary epithelial cells will form the toxicological/biological end points of the study. Methods include gene array techniques, assays for reactive oxygen species, and adhesion molecules on endothelial cells.
(Project budget is an estimate only, based on available data)