Porter D W, Ramsey D, Hubbs A F, Battelli L, Ma J, Barger M, Landsittel D, Robinson V A, McLaurin J, Khan A, Jones W, Teass A, Castranova V
National Institute for Occupational Safety and Health, Health Effects Laboratory Division, Morgantown, WV 26505, USA.
J Environ Pathol Toxicol Oncol. 2001;20 Suppl 1:1-14.
Previous studies have determined that alpha-quartz (crystalline silica) can cause pulmonary inflammation, damage, and fibrosis. However, the temporal relationship between silica inhalation and pulmonary inflammation, damage, and fibrosis has not been fully examined. To address this gap in our knowledge of silica-induced pulmonary fibrosis, a chronic inhalation study using rats was designed. Specifically, rats were exposed to a silica aerosol (15 mg/m3 silica, 6 h/d, 5 d/wk, 116 d), and measurements of pulmonary inflammation, damage, and fibrosis were monitored throughout the study. We report (1) data demonstrating that the silica aerosol generation and exposure system produced a consistent silica aerosol of respirable size particles; (2) the time course of silica deposition in the lung; (3) calculations that demonstrate that the rats were not in pulmonary overload; (4) histopathological data demonstrating time-dependent enhancement of silica-induced alveolitis, epithelial hypertrophy and hyperplasia, alveolar lipoproteinosis, and pulmonary fibrosis in the absence of overload; and (5) biochemical data documenting the development of lipidosis, lung damage, and fibrosis.
以往的研究已经确定，α-石英（结晶二氧化硅）可导致肺部炎症、损伤和纤维化。然而，吸入二氧化硅与肺部炎症、损伤和纤维化之间的时间关系尚未得到充分研究。为了填补我们在二氧化硅诱导的肺纤维化知识方面的这一空白，设计了一项使用大鼠的慢性吸入研究。具体而言，将大鼠暴露于二氧化硅气溶胶（15毫克/立方米二氧化硅，每天6小时，每周5天，共116天），并在整个研究过程中监测肺部炎症、损伤和纤维化的测量值。我们报告：（1）数据表明二氧化硅气溶胶生成和暴露系统产生了大小可吸入的一致二氧化硅气溶胶；（2）二氧化硅在肺部沉积的时间进程；（3）计算结果表明大鼠不存在肺部过载；（4）组织病理学数据表明在无过载情况下，二氧化硅诱导的肺泡炎、上皮肥大和增生、肺泡蛋白沉积症以及肺纤维化随时间增强；（5）生化数据记录了脂质沉积、肺损伤和纤维化的发展情况。
