Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV.
Department of Preventive Medicine and Public Health, Keio University School of Medicine, Tokyo, Japan.
Chest. 2012 Jun;141(6):1512-1521. doi: 10.1378/chest.11-1880. Epub 2011 Dec 29.
Reports of pulmonary fibrosis, emphysema, and, more recently, pulmonary alveolar proteinosis (PAP) in indium workers suggested that workplace exposure to indium compounds caused several different lung diseases.
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.
Ten men (median age, 35 years) who produced, used, or reclaimed indium compounds were diagnosed with interstitial lung disease 4-13 years after first exposure (n = 7) or PAP 1-2 years after first exposure (n = 3). Common pulmonary histopathologic features in these patients included intraalveolar exudate typical of alveolar proteinosis (n = 9), cholesterol clefts and granulomas (n = 10), and fibrosis (n = 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 fibrosis and one also developed emphysematous changes. Epidemiologic investigations demonstrated the potential for exposure to respirable particles and an excess of lung abnormalities among coworkers.
Occupational exposure to indium compounds was associated with PAP, cholesterol ester crystals and granulomas, pulmonary fibrosis, 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 fibrosis and emphysema, and, in some cases, premature death. Prospective studies are needed to better define the natural history and prognosis of this emerging lung disease and identify effective prevention strategies.
铟作业工人中报告有肺纤维化、肺气肿,最近又报告有肺泡蛋白沉积症(PAP),这表明工作场所接触铟化合物可引起几种不同的肺部疾病。
为了更好地了解铟肺疾病的发病机制和自然史,对所有报告病例和工作场所的临床、组织病理学、放射学和流行病学资料进行了详细、系统、多学科的分析。
10 名男性(中位年龄 35 岁)在首次接触(n=7)后 4-13 年或首次接触后 1-2 年(n=3)被诊断为间质性肺病,他们生产、使用或回收铟化合物。这些患者的常见肺部组织病理学特征包括肺泡蛋白沉积症的肺泡内渗出物(n=9)、胆固醇裂隙和肉芽肿(n=10)和纤维化(n=9)。2 例间质性肺病患者有气胸。大多数患者在停止接触后病情进展,2 例死亡。放射学数据显示,2 例 PAP 患者随后出现纤维化,1 例出现气肿性改变。流行病学调查表明,接触可吸入性颗粒和同事肺部异常的风险增加。
职业接触铟化合物与 PAP、胆固醇酯晶体和肉芽肿、肺纤维化、肺气肿和气胸有关。现有证据表明,接触铟化合物可引起一种新的肺部疾病,可能首先表现为 PAP,然后进展为纤维化和肺气肿,在某些情况下导致过早死亡。需要前瞻性研究来更好地定义这种新出现的肺部疾病的自然史和预后,并确定有效的预防策略。