{"title":"铟肺旁气肿:追踪慢性暴露的病理足迹。","authors":"Chihiro Inoue, Atsuko Amata, Tatsuya Chonan, Yoshinori Kawabata, Yosuke Matsuno, Takashi Suzuki","doi":"10.1620/tjem.2024.J017","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":23187,"journal":{"name":"Tohoku Journal of Experimental Medicine","volume":null,"pages":null},"PeriodicalIF":1.7000,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Paraseptal Emphysema in Indium Lung: Tracing the Pathological Footprints of Chronic Exposure.\",\"authors\":\"Chihiro Inoue, Atsuko Amata, Tatsuya Chonan, Yoshinori Kawabata, Yosuke Matsuno, Takashi Suzuki\",\"doi\":\"10.1620/tjem.2024.J017\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Indium lung is an occupational lung disease caused by exposure to indium-tin-oxide (ITO) dust. 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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. 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引用次数: 0
摘要
铟肺是一种因接触铟锡氧化物(ITO)粉尘而引起的职业性肺病。与其他职业性肺病相比,铟肺的潜伏期较短,即使在工作环境改善后,呼吸状况仍会继续恶化。无论是否有吸烟史,通过计算机断层扫描(CT)获得的胸部图像上都能看到主要影响胸膜下区域的副肺气肿。然而,铟肺气肿的发病机制仍不清楚。因此,我们重新评估了之前报道的三例铟肺的病理变化。在吸烟者和非吸烟者中都观察到了副肺气肿。随着时间的推移,副肺气肿病例的阻塞性呼吸功能损害逐渐加重。许多肺泡壁遭到破坏,与是否存在气肿性改变或纤维化无关。此外,与石棉沉滞症(最常见的职业性肺病)或由吸烟引起的慢性阻塞性肺病的常见病例相比,铟肺中支气管炎的发病率较低。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(肺气肿的三大主要原因)。此外,纳米级的 ITO 不易滞留在上呼吸道,很容易到达胸膜下肺泡。此外,ITO 可能会继续在肺泡水平造成持续的组织损伤,有可能导致肺气肿。还需要进一步研究,通过与其他职业性肺病进行比较,阐明铟肺的详细发病机制。
Paraseptal Emphysema in Indium Lung: Tracing the Pathological Footprints of Chronic Exposure.
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.
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