Silicon nanowires (NW) are manufactured for use as bio-sensors, gas sensors, and field effect transistors for various circuit applications. The goal of these studies was to assess the potential pulmonary toxicity of silicon NW using an in vivo model. Single-crystal silicon NW were synthesized by the vapor-liquid-solid method in an ultrahigh vacuum-chemical vapor deposition chamber with silane as the silicon precursor and gold as the catalyst (approximately20-30 nm Diameter x approximately15 microm Length, with a 20 nm gold nanoparticle catalyst at one end). NW were isolated, suspended in a physiologic dispersion medium (DM, phosphate-buffered saline + 0.6 mg/ml rat serum albumin + 0.01 mg/ml dipalmitoyl phosphocholine), and sonicated. On day 0, Sprague-Dawley rats were intratracheally-instilled with the NW in DM at a dose of 10, 25, 50, 100, or 250 microg or DM alone (control). Rats were humanely sacrificed 1, 3, and 7 days post-exposure and the right lung was lavaged. The lavage fluid and cells were analyzed for indicators of lung injury and inflammation. On days 1 and 3, there was a dose-dependent increase in lung injury, indicated by elevations in lactate dehydrogenase and albumin in lavage fluid. There was also a dose-dependent increase in inflammation indicated by the presence of neutrophils in the lung on day 1, which persisted on day 3 in the rats treated with the highest dose. In addition to neutrophils, there were also significant increases in alveolar macrophages, lymphocyte, and eosinophil influx into the lungs. Macrophage uptake of NW was observed in cells recovered at all time points and this uptake was paralleled by increased oxidant production in these cells. These initial lung injury and inflammatory responses resolved by day 7. To summarize, the NW were found to induce a transient lung injury and inflammation accompanied by cellular oxidant production. Studies are ongoing to assess long-term pulmonary responses to NW as well as to assess lung distribution and clearance of NW over time.
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