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Updated: Aug 15, 2025

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
Published on: January 16, 2015
Progression of Smoking-Induced Emphysema in a Case with Indium Lung
Yuki Yabuuchi1,2, Tatsuya Chonan1, Taisuke Nakaizumi1,2
1Department of Medicine, Nikko Memorial Hospital.
Abstract:
Recently, it has become clear that inhaled indium-tin oxide causes emphysematous as well as interstitial changes in the lung. Here, we present a 59-year-old male ex-smoker, quitting smoking at the age of 55. He had been engaged in indium-tin oxide processing from 27 to 37 years of age, with 22 years having passed since the final exposure to indium. He was found to have a high serum indium concentration and Krebs von den Lungen-6 (KL-6). Furthermore, bilateral centrilobular emphysema was recognized in high-resolution computed tomography (HRCT). After transferring jobs to a non-indium-tin oxide section, KL-6 returned to a normal level within 4 years, whereas neither serum indium concentration nor emphysema had decreased to normal despite 22 years having passed since the exposure ended. At the age of 59, a thoracoscopic lung biopsy was performed to assess the contribution of smoking and that of indium to the lung destruction. The pathological findings demonstrated cholesterol granulomas with the accumulation of macrophages and multinucleated giant cells that had phagocytosed particles. Together with the typical findings of indium lung, fibrotic and emphysematous changes were observed. The elemental analysis of the biopsied specimens revealed excessive deposition of indium throughout the airways, interstitial spaces and alveoli. The pathological findings of this case may be the result of two kinds of pulmonary damage, i.e., smoking and indium. This report indicates that occupationally-inhaled indium could remain in the lung for as long as 22 years and continue to insult the lung tissue with inflammation caused by smoking.
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