Crawford Judith A, Sanyal Soma, Burnett Bryan R, Wiesenfeld Stephen L, Abraham Jerrold L
Department of Pathology, SUNY Upstate Medical University, Syracuse, New York, USA.
Meixa Tech, Cardiff, California, USA.
Am J Ind Med. 2024 Mar;67(3):179-199. doi: 10.1002/ajim.23561. Epub 2024 Jan 24.
With increasing reports of accelerated and acute silicosis, PMF, and autoimmune disease among coal miners and silica-exposed countertop workers, we present previously incompletely-described pulmonary pathology of accelerated silicosis and correlations with mineralogy, radiography, and disease progression in 46 Texas oilfield pipe sandblasters who were biopsied between 1988 and 1995.
Worker examinations included pulmonary function tests, chest X-ray (CXR), high-resolution computed tomography (HRCT), and Gallium-67 scans. Quantitative mineralogic analysis of pulmonary parenchymal burden of silica, silicates, and metal particles used scanning electron microscopy with energy dispersive x-ray spectroscopy (SEM EDS).
Workers had clinical deterioration after <10 years exposure in dusty workplaces. Although initial CXR was normal in 54%, Gallium-67 scans were positive in 68% of those with normal CXR, indicating pulmonary inflammation. The histology of accelerated silicosis is diffuse interstitial infiltration of macrophages filled with weakly birefringent particles with or without silicotic nodules or alveolar proteinosis. Lung silica concentrations were among the highest in our database, showing a dose-response relationship with CXR, HRCT, and pathologic changes (macrophages, fibrosis, and silicotic nodules). Radiographic scores and diffusing capacity worsened during observation. Silica exposure was intensified, patients presented younger, with shorter exposure, more severe clinical abnormalities, higher lung particle burdens, and more rapid progression in a subset of patients exposed to recycled blasting sand.
Accelerated silicosis may present with a normal CXR despite significant histopathology. Multivariable analyses showed silica, and not other particles, is the driver of observed radiologic, physiologic, and histologic outcomes. Eliminating this preventable disease requires higher physician, public health, and societal awareness.
随着煤矿工人和接触二氧化硅的台面工人中加速型和急性矽肺、进行性大块纤维化（PMF）及自身免疫性疾病的报告日益增多，我们展示了1988年至1995年间接受活检的46名得克萨斯州油田管道喷砂工人中加速型矽肺先前未被完整描述的肺部病理学特征，以及其与矿物学、放射学和疾病进展的相关性。
对工人的检查包括肺功能测试、胸部X线（CXR）、高分辨率计算机断层扫描（HRCT）和镓-67扫描。使用扫描电子显微镜和能量色散X射线光谱仪（SEM EDS）对肺实质中二氧化硅、硅酸盐和金属颗粒的负担进行定量矿物学分析。
工人在接触粉尘工作场所不到10年后临床症状恶化。虽然最初54%的CXR正常，但CXR正常者中68%的镓-67扫描呈阳性，表明存在肺部炎症。加速型矽肺的组织学表现为弥漫性间质浸润，巨噬细胞充满弱双折射颗粒，伴有或不伴有矽结节或肺泡蛋白沉积症。肺二氧化硅浓度在我们的数据库中处于最高水平，与CXR、HRCT和病理变化（巨噬细胞、纤维化和矽结节）呈剂量反应关系。在观察期间，放射学评分和弥散能力恶化。在接触回收喷砂的一部分患者中，二氧化硅暴露加剧，患者发病年龄更小，接触时间更短，临床异常更严重，肺颗粒负担更高，疾病进展更快。
尽管有显著的组织病理学表现，但加速型矽肺的CXR可能正常。多变量分析表明，二氧化硅而非其他颗粒是观察到的放射学、生理学和组织学结果的驱动因素。消除这种可预防的疾病需要提高医生、公共卫生和社会的认识。
