Inoue Chihiro, Amata Atsuko, Chonan Tatsuya, Kawabata Yoshinori, Matsuno Yosuke, Suzuki Takashi
Department of Anatomic Pathology, Tohoku University Graduate School of Medicine.
Department of Medicine, Nikko Memorial Hospital.
Tohoku J Exp Med. 2024 May 30;263(1):51-54. doi: 10.1620/tjem.2024.J017. Epub 2024 Mar 15.
Indium lung is an occupational lung disease caused by exposure to indium-tin-oxide (ITO) dust. Compared to other occupational lung diseases, indium lung has a shorter latency period and the respiratory status continues to worsen even after exposure to the work environment improves. Paraseptal emphysema which affects mainly the subpleural area is seen on chest images obtained via computed tomography (CT), regardless of the smoking history. However, the pathogenesis of emphysema in indium lung is still unclear. Therefore, we re-evaluated the pathology of three previously reported cases of indium lung. Paraseptal emphysema was observed in both smokers and nonsmokers. Obstructive respiratory impairment worsened over time in the cases with paraseptal emphysema. Many alveolar walls were destroyed independent of the presence or absence of emphysetamous changes or fibrosis. Moreover, bronchiolitis was found to be less common in indium lung than in asbestosis (the most common occupational lung disease) or common cases of chronic obstructive pulmonary disease caused by smoking. It has been shown that ITO causes protease anti-protease imbalance, oxidant-antioxidant imbalance, and continuous, abnormal inflammation (the three major causes of emphysema). In addition, nano-sized ITO is less likely to be trapped in the upper airways and may easily reach the subpleural alveoli. Furthermore, ITO may continue to cause sustained tissue injury at the alveolar level potentially resulting in emphysema. Further studies are needed to elucidate the detailed pathogenesis of indium lung by comparing it with other occupational lung diseases.
铟肺是一种因接触铟锡氧化物(ITO)粉尘而引发的职业性肺病。与其他职业性肺病相比,铟肺的潜伏期较短,即便脱离工作环境后,呼吸状况仍会持续恶化。通过计算机断层扫描(CT)获取的胸部影像显示,无论有无吸烟史,铟肺患者主要表现为累及胸膜下区域的间隔旁肺气肿。然而,铟肺中肺气肿的发病机制仍不清楚。因此,我们对之前报道的3例铟肺病例的病理情况进行了重新评估。吸烟者和非吸烟者均出现了间隔旁肺气肿。间隔旁肺气肿患者的阻塞性呼吸功能障碍随时间推移而加重。许多肺泡壁遭到破坏,与是否存在肺气肿样改变或纤维化无关。此外,与石棉肺(最常见的职业性肺病)或吸烟所致的慢性阻塞性肺疾病常见病例相比,细支气管炎在铟肺中较少见。研究表明,ITO会导致蛋白酶 - 抗蛋白酶失衡、氧化剂 - 抗氧化剂失衡以及持续的异常炎症(肺气肿的三大主要病因)。此外,纳米级ITO不太可能滞留在上呼吸道,可能很容易到达胸膜下肺泡。再者,ITO可能会在肺泡水平持续造成持续性组织损伤,进而引发肺气肿。需要通过与其他职业性肺病进行比较,进一步研究以阐明铟肺详细的发病机制。