Comparative study on the pulmonary toxicity of indium hydroxide, indium-tin oxide, and indium oxide following intratracheal instillations into the lungs of rats

Akiyo Tanaka, Miyuki Hirata, Nagisa Matsumura, Kazunori Koga, Masaharu Shiratani, Yutaka Kiyohara

研究成果: 著書/レポートタイプへの貢献会議での発言

1 引用 (Scopus)

抄録

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 In2O3particles, 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 In203-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.

元の言語英語
ホスト出版物のタイトルPlasma Processing and Diagnostics for Life Sciences
編集者E.R. Fisher, M. Kong, K.D. Weltmann, M. Shiratani
出版者Materials Research Society
ページ8-13
ページ数6
ISBN(電子版)9781510806078
DOI
出版物ステータス出版済み - 1 1 2015
イベント2014 MRS Fall Meeting - Boston, 米国
継続期間: 11 30 201412 5 2014

出版物シリーズ

名前Materials Research Society Symposium Proceedings
1723
ISSN(印刷物)0272-9172

その他

その他2014 MRS Fall Meeting
米国
Boston
期間11/30/1412/5/14

Fingerprint

Indium
Tin oxides
toxicity
indium oxides
lungs
tin oxides
rats
hydroxides
Toxicity
indium
Rats
Oxides
hydroxide ion
indium oxide
indium tin oxide
indium(III) hydroxide
Rat control
body weight
Flat panel displays
flat panel displays

All Science Journal Classification (ASJC) codes

  • Materials Science(all)
  • Condensed Matter Physics
  • Mechanics of Materials
  • Mechanical Engineering

これを引用

Tanaka, A., Hirata, M., Matsumura, N., Koga, K., Shiratani, M., & Kiyohara, Y. (2015). Comparative study on the pulmonary toxicity of indium hydroxide, indium-tin oxide, and indium oxide following intratracheal instillations into the lungs of rats. : E. R. Fisher, M. Kong, K. D. Weltmann, & M. Shiratani (版), Plasma Processing and Diagnostics for Life Sciences (pp. 8-13). (Materials Research Society Symposium Proceedings; 巻数 1723). Materials Research Society. https://doi.org/10.1557/opl.2015.21

Comparative study on the pulmonary toxicity of indium hydroxide, indium-tin oxide, and indium oxide following intratracheal instillations into the lungs of rats. / Tanaka, Akiyo; Hirata, Miyuki; Matsumura, Nagisa; Koga, Kazunori; Shiratani, Masaharu; Kiyohara, Yutaka.

Plasma Processing and Diagnostics for Life Sciences. 版 / E.R. Fisher; M. Kong; K.D. Weltmann; M. Shiratani. Materials Research Society, 2015. p. 8-13 (Materials Research Society Symposium Proceedings; 巻 1723).

研究成果: 著書/レポートタイプへの貢献会議での発言

Tanaka, A, Hirata, M, Matsumura, N, Koga, K, Shiratani, M & Kiyohara, Y 2015, Comparative study on the pulmonary toxicity of indium hydroxide, indium-tin oxide, and indium oxide following intratracheal instillations into the lungs of rats. : ER Fisher, M Kong, KD Weltmann & M Shiratani (版), Plasma Processing and Diagnostics for Life Sciences. Materials Research Society Symposium Proceedings, 巻. 1723, Materials Research Society, pp. 8-13, 2014 MRS Fall Meeting, Boston, 米国, 11/30/14. https://doi.org/10.1557/opl.2015.21
Tanaka A, Hirata M, Matsumura N, Koga K, Shiratani M, Kiyohara Y. Comparative study on the pulmonary toxicity of indium hydroxide, indium-tin oxide, and indium oxide following intratracheal instillations into the lungs of rats. : Fisher ER, Kong M, Weltmann KD, Shiratani M, 編集者, Plasma Processing and Diagnostics for Life Sciences. Materials Research Society. 2015. p. 8-13. (Materials Research Society Symposium Proceedings). https://doi.org/10.1557/opl.2015.21
Tanaka, Akiyo ; Hirata, Miyuki ; Matsumura, Nagisa ; Koga, Kazunori ; Shiratani, Masaharu ; Kiyohara, Yutaka. / Comparative study on the pulmonary toxicity of indium hydroxide, indium-tin oxide, and indium oxide following intratracheal instillations into the lungs of rats. Plasma Processing and Diagnostics for Life Sciences. 編集者 / E.R. Fisher ; M. Kong ; K.D. Weltmann ; M. Shiratani. Materials Research Society, 2015. pp. 8-13 (Materials Research Society Symposium Proceedings).
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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 In2O3particles, 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 In203-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.",
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N2 - 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 In2O3particles, 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 In203-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.

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