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Comparative Study on the Pulmonary Toxicity of Indium Hydroxide, Indium-Tin Oxide, and Indium Oxide Following Intratracheal Instillations into the Lungs of Rats

Published online by Cambridge University Press:  09 February 2015

Akiyo Tanaka
Affiliation:
Department of Environmental Medicine, Graduate School of Medical Sciences, Kyushu University, EC Building 2F, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan
Miyuki Hirata
Affiliation:
Department of Environmental Medicine, Graduate School of Medical Sciences, Kyushu University, EC Building 2F, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan
Nagisa Matsumura
Affiliation:
Department of Environmental Medicine, Graduate School of Medical Sciences, Kyushu University, EC Building 2F, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan
Kazunori Koga
Affiliation:
Department of Electronics, Graduate School of Information Science and Electrical Engineering, Kyushu University, 744 Motooka, Nishi-ku, Fukuoka 819-0395, Japan
Masaharu Shiratani
Affiliation:
Department of Electronics, Graduate School of Information Science and Electrical Engineering, Kyushu University, 744 Motooka, Nishi-ku, Fukuoka 819-0395, Japan
Yutaka Kiyohara
Affiliation:
Department of Environmental Medicine, Graduate School of Medical Sciences, Kyushu University, EC Building 2F, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan
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Abstract

We studied the pulmonary toxicity of indium hydroxide (In(OH)3), which is produced during a recycling process of indium-tin oxide (ITO), in comparison with that of ITO or indium oxide (In2O3), two raw materials of flat panel displays. One hundred and forty-four male Wistar rats were intratracheally given equivalent doses of 10 mg/kg indium as In(OH)3, ITO, or In2O3 particles, twice a week, for a total of 5 times for 2 weeks. Control rats were given distilled water as a vehicle. After 3 weeks, these rats were serially euthanized, and toxicological effects were determined. Body weight gain was significantly suppressed in the In(OH)3-treated rats compared to that in the control group, but not in the ITO- or In2O3-treated rats. Relative lung weights in all the indium-treated groups significantly increased compared to those in the control group throughout the observation period. Furthermore, lung weights in the In(OH)3 group were significantly higher than those in either the ITO or In2O3 group. Blood indium levels in the In(OH)3-treated rats were much higher, 70- to 200-fold, than those in the In2O3- or ITO-treated rats at each time point. Although the lung indium content decreased gradually during the observation periods, the content in the In(OH)3 group was significantly higher than that in either the ITO or In2O3 group. A histopathological analysis revealed foci indicating a slight to severe pulmonary inflammatory response, including exudation to alveolar spaces, were present in all the indium-treated groups. Interstitial fibrotic proliferation was seen only in the In(OH)3-treated rats. The severity of these lesions in the In(OH)3-treated rats was greater than that in either the ITO- or In2O3-treated rats.

The results of our study clearly demonstrated that In(OH)3 particles caused severe pulmonary toxicity when repeated intratracheal instillations were performed in rats. Furthermore, the toxic potency of In(OH)3 in the lung was much higher than that of ITO and In2O3. Accordingly, the toxicity of In(OH)3 particles should be considered in addition to that of ITO and In2O3 particles when indium exposure occurs.

Type
Articles
Copyright
Copyright © Materials Research Society 2015 

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References

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