The study outcomes with regard to the basis of serum immunochemistry biomarkers and HRCT indicate that exposure to hardly soluble indium compound dust may represent a risk for interstitial lung damage.

The production of indium-tin oxide has increased, owing to the increased manufacture of liquid-crystal panels. It has been reported that interstitial pneumonia occurred in two indium-processing workers; therefore, the present study aimed to evaluate whether interstitial pulmonary disorders were prevalent among indium workers. The study was carried out in 108 male workers in the indium plant where the two interstitial pneumonia patients mentioned above were employed, and included high-resolution computed tomography (HRCT) of the lungs, pulmonary function tests and analysis of serum sialylated carbohydrate antigen KL-6 and the serum indium concentration. Significant interstitial changes were observed in 23 indium workers on HRCT and serum KL-6 was abnormally high (>500 U x mL(-1)) in 40 workers. Workers with serum indium concentrations in the highest quartile had significantly longer exposure periods, greater HRCT changes, lower diffusing capacity of the lung for carbon monoxide and higher KL-6 levels compared with those in the lowest quartile. The serum indium concentration was positively correlated with the KL-6 level and with the degree of HRCT changes. In conclusion, the results of the present study indicated that serum KL-6 and high-resolution computed tomography abnormalities were prevalent among indium workers and that these abnormalities increased with the indium burden, suggesting that inhaled indium could be a potential cause of occupational lung disease.

Indium is a relatively rare element that has had limited use for decades as a metal, in alloys, and for electronics applications. During the past 15 years, global demand for indium has increased several-fold, driven by the novel use of indium-tin oxide (ITO) thin fi lms in the production of fl at-panel displays (such as liquid crystal displays [LCDs]), touch screens, and other electronic devices. 1,2 ITO is a sintered ceramic material typically consisting of 90% indium oxide (In 2 O 3 ) and 10% tin oxide (SnO 2 ). Exposures to indium metal and indium compounds (including indium hydroxide [In(OH) 3 ], indium oxide, and ITO) may occur during ITO production, ITO use for the creation of thin fi lms, and reclamation. The bulk of the ITO industry is located in Japan, with some activity in the United States, China, Taiwan, and South Korea. 3 As of May 2010, 10 clinical cases of lung disease in indium workers from three countries (Japan, United States, and China) had been reported. 2 Seven cases were described as interstitial lung disease (ILD) characterized by pulmonary fi brosis with or without emphysema. Three cases were described as pulmonary alveolar proteinosis (PAP). Individually, these 10 case reports left unclear why some workers developed ILD and others developed PAP, and the relationship, if any, between these distinct pulmonary disease processes.Background: Reports of pulmonary fi brosis, emphysema, and, more recently, pulmonary alveolar proteinosis (PAP) in indium workers suggested that workplace exposure to indium compounds caused several different lung diseases. Methods: To better understand the pathogenesis and natural history of indium lung disease, a detailed, systematic, multidisciplinary analysis of clinical, histopathologic, radiologic, and epidemiologic data for all reported cases and workplaces was undertaken. Results: Ten men (median age, 35 years) who produced, used, or reclaimed indium compounds were diagnosed with interstitial lung disease 4-13 years after fi rst exposure (n 5 7) or PAP 1-2 years after fi rst exposure (n 5 3). Common pulmonary histopathologic features in these patients included intraalveolar exudate typical of alveolar proteinosis (n 5 9), cholesterol clefts and granulomas (n 5 10), and fi brosis (n 5 9). Two patients with interstitial lung disease had pneumothoraces. Lung disease progressed following cessation of exposure in most patients and was fatal in two. Radiographic data revealed that two patients with PAP subsequently developed fi brosis and one also developed emphysematous changes. Epidemiologic investigations demonstrated the potential for exposure to respirable particles and an excess of lung abnormalities among coworkers. Conclusions: Occupational exposure to indium compounds was associated with PAP, cholesterol ester crystals and granulomas, pulmonary fi brosis, emphysema, and pneumothoraces. The available evidence suggests exposure to indium compounds causes a novel lung disease that may begin with PAP and progress to include fi brosis and emphysema, and, in som...

Causal Relationship between Indium Compound Inhalation and Effects on the Lungs: Makiko NAKANO, et al. Department of PreventiveMedicine and Public Health, School of Medicine, Keio University-Background: Recent case reports and epidemiological studies suggest that inhalation of indium dust induces lung damage. Objectives: To elucidate the dose-dependent effects of indium on the lungs and to prove a causal relationship more clearly. Methods: A baseline observation was conducted on 465 workers currently exposed to indium, 127 workers formerly exposed to indium and 169 workers without indium exposure in 12 factories and 1 research laboratory from 2003 to 2006. Indium in serum (In-S) was determined as an exposure parameter, and its effects on the lungs were examined. Results: The means of In-S in the current, former and no exposure workers were 8.35, 9.63 and 0.56 ng/ml, respectively. The current and former exposure workers had significantly higher levels of KL-6, and showed significant dose-dependent increases in KL-6, SP-D, and SP-A. Current exposure workers with In-S of 3 ng/ml or above demonstrated a significant increase of KL-6 in both GM and prevalence exceeding the reference value. Approximately a quarter of the former exposure workers had interstitial changes as seen on chest HRCT. In-S of exposed workers who had been working before improvements of the working environment (Group Bef) and those who started working after improvements (Group Aft) were 12.29 and 0.81 ng/ml, respectively. Adjusted odds ratios indicated 87%, 71% and 44% reductions among Group Aft workers who exceeded the reference values of KL-6, SP-D and SP-A, respectively. Conclusion: Dosedependent lung effects due to indium exposure were shown, and a decrease of indium exposure reduced the lung effects. An In-S value of 3 ng/ml may be a cut-off value which could be used to prevent early effects on the lungs. (J Occup Health 2009; 51: 513-521)