Two-and 13-week Inhalation Toxicities of Indium-tin Oxide and Indium Oxide in Rats: Kasuke NagaNo, et al. Japan Bioassay Research Center, Japan Industrial Safety and Health AssociationObjectives: Two-and 13-week inhalation toxicities of indium-tin oxide (ITO) and indium oxide (IO) were characterized for risk assessments of workers exposed to ITO. Methods: F344 rats of both sexes were exposed by inhalation to ITO or IO aerosol for 6 h/day, 5 day/wk for 2 wk at 0, 0.1, 1, 10 or 100 mg/m 3 or 13 wk at 0, 0.1or 1 mg/m 3 . An aerosol generator and inhalation exposure system was constructed. Results: Blood and lung contents of indium were elevated in a dose-related manner in the ITO-and IO-exposed rats. ITO and IO particles were deposited in the lung, mediastinal lymph node and nasal-associated lymphoid tissue. Exposures to ITO and IO induced alveolar proteinosis, infiltrations of alveolar macrophages and inflammatory cells and alveolar epithelial hyperplasia in addition to increased lung weight. ITO affected the lung more severely than IO did. Fibrosis of alveolar wall developed and some of these lesions worsened at the end of the 26-week post-exposure period. Conclusions: Persistent pulmonary lesions including alveolar proteinosis and macrophage infiltration occurred after 2-and 13-week inhalation exposures of rats to ITO and IO. Fibrosis of alveolar wall developed later. These lesions occurred after ITO exposure at the same concentration as the current occupational exposure limit in the USA and at blood indium levels below the biological exposure index in Japan for indium. (J Occup Health 2011; 53: 51-63)

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tion. Conclusions: All six printing workers with cholangiocarcinoma were exposed to very high levels of 1,2-DCP for a long term. (J Occup Health 2014; 56: 332−338)

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565Kenichi YAMADA, et al.: Exposure levels in printers with cholangiocarcinoma (3rd) which suggests that ink did not contribute to the development of cholangiocarcinoma. (J Occup Health 2015; 57: 565−571)

average exposure concentrations were 84 to 440 ppm. Conclusions: Our findings suggest that DCM may contribute to the development of cholangiocarcinoma in humans. (J Occup Health 2015; 57: 245−252) Key words: 1,2-dichloropropane, Cholangiocarcinoma, Dichloromethane, Environment, PrinterIn May 2012, five employees (including former employees) of an offset proof-printing plant in Osaka, Japan, were reported to have developed intrahepatic or extrahepatic bile duct cancer (cholangiocarcinoma) 1) . Subsequently, other individuals who developed cholangiocarcinoma were identified from the employees of this plant, with the total number of cases reaching 17 by the end of 2012 2) . All workers who developed cholangiocarcinoma were recognized by the Ministry of Health, Labour and Welfare (MHLW) as having developed an occupational disease. It is suspected that the cancer developed due to high-level, long-term exposure to 1,2-dichloropropane (1,2-DCP) 3,4) . After this incident became widely known through the mass media, workers who developed cholangiocarcinoma at other printing plants filed workers' compensation claims, with the total number of such workers reaching 70 (excluding the aforementioned 17) as of March 2014 5) . By April 2014, 13 of the 70 workers were recognized as having developed an occupational disease. We previously reported that six of these 13 printing workers had experienced long-term exposure to very high concentrations of 1,2-DCP 6). The present study aimed to identify the chemicals that the remaining seven workers were exposed to, and estimate the levels of chemical exposure using mathematical models. This study was approved by the Ethics Committee of Osaka City University. In several Japanese printing plants, printing workers have suffered from cholangiocarcinoma. 1,2-dichloropropane (1,2-DCP) is considered to be a causative agent, and whether or not other chemicals also contribute to the development of this disease has not been conclusively determined. This study aimed to identify the chemicals used by seven printing workers who developed cholangiocarcinoma, as well as to estimate the levels of chemical exposure among them. Methods: Information was obtained from the Ministry of Health, Labour and Welfare, Japan, to identify chemicals used by printing workers who developed cholangiocarcinoma and to estimate chemical exposure concentrations. Working environment concentrations of the chemicals in the printing rooms were estimated using a well-mixed model, and exposure concentrations during the ink removal operation were estimated using a near-field and far-field model. Shift time-weighted averages of exposure concentrations were also calculated. Results: Four of the seven printing workers were exposed to both 1,2-DCP and dichloromethane (DCM). The estimated maximum exposure concentrations for each of the four workers were 230 to 420 ppm for 1,2-DCP and 58 to 720 ppm for DCM, and the estimated shift average exposure concentrations were 0 to 210 ppm for 1,2-DCP and 15 to 270 ppm for DCM. The remainin...

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