Revenues from consumer electronics are at an all-time high, leading to an increased demand for indium-tin oxide (ITO) to produce touch screens and plasma and liquid crystal displays. Composed of 90% indium oxide (In2O3) and 10% tin oxide (SnO2) by weight, ITO is synthesized under conditions of high heat via a process known as sintering. Concerns have arisen over the health of workers in the ITO industry, as severe pulmonary toxicity and increased levels of indium in blood have been associated with occupational exposure to ITO. In the current study, murine macrophage (RAW 264.7) and epidermal (JB6/AP-1) cells were used to differentiate between the toxicological profiles of sintered ITO (SITO) and an unsintered ITO (UITO) mixture. We hypothesized that sintering would play a key role in free radical generation and cytotoxicity. Cells were treated with either 50 microg/ml, 150 microg/ml or 250 microg/ml of ITO and various endpoints were measured over time. Exposure of cells to both UITO and SITO caused a time and dose dependent decrease on the viability of cells. Intracellular ROS generation was inversely related to the concentration of both UITO and SITO, a direct reflection of the decreased number of viable cells observed at higher concentrations. Electron paramagnetic resonance, used to measure free radical generation, showed significantly increased hydroxyl radical generation in cells treated with UITO versus those treated with SITO. This is different from observed LDH release, which showed that SITO caused significantly increased damage to the cell membrane compared to UITO. Our results delineate the need for a better understanding of the mechanisms of toxicity and free radical production associated with workplace exposure to indium, allowing for earlier disease detection and improved health amongst workers.
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