Solano-Lopez Claudia, Zeidler-Erdely Patti C, Hubbs Ann F, Reynolds Steven H, Roberts Jenny R, Taylor Michael D, Young Shih-Houng, Castranova Vincent, Antonini James M
Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, 26505, USA.
Toxicol Pathol. 2006;34(4):364-72. doi: 10.1080/01926230600815122.
It has been suggested that welding fume (WF) exposure increases lung cancer risk in welders. Epidemiology studies have failed to conclude that WF alone causes lung cancer and animal studies are lacking. We examined the course of inflammation, damage, and repair in the lungs of A/J mice, a lung tumor susceptible strain, caused by stainless steel WF. Mice were exposed by pharyngeal aspiration to 40 mg/kg of WF, silica, or saline. Bronchoalveolar lavage (BAL) was performed 24 hours, 1 and 16 weeks to assess lung injury and inflammation and histopathology was done 1, 8, 16, 24, and 48 weeks postexposure. Both exposures increased inflammatory cells, lactate dehydrogenase and albumin at 24 hr and 1 week. At 16 weeks, these parameters remained elevated in silica-exposed but not WF-exposed mice. Histopathologic evaluation at 1 week indicated that WF induced bronchiolar epithelial hyperplasia with associated cellular atypia, alveolar bronchiolo-alveolar hyperplasia (BAH) in peribronchiolar alveoli, and peribronchiolar lymphogranulomatous inflammation. Persistent changes included foci of histiocytic inflammation, fibrosis, atypical bronchiolar epithelial cells, and bronchiolar BAH. The principle changes in silica-exposed mice were histiocytic and suppurative inflammation, fibrosis, and alveolar BAH. Our findings that WF causes persistent bronchiolar and peribronchiolar epithelial changes, suggest a need for studies of bronchiolar changes after WF exposure.
有人提出，接触焊接烟尘（WF）会增加焊工患肺癌的风险。流行病学研究未能得出仅WF就能导致肺癌的结论，且缺乏动物研究。我们研究了不锈钢WF对A/J小鼠（一种肺肿瘤易感品系）肺部炎症、损伤和修复的过程。通过咽部吸入法使小鼠接触40毫克/千克的WF、二氧化硅或生理盐水。在接触后24小时、1周和16周进行支气管肺泡灌洗（BAL）以评估肺损伤和炎症，并在接触后1周、8周、16周、24周和48周进行组织病理学检查。两种接触在24小时和1周时均增加了炎症细胞、乳酸脱氢酶和白蛋白。在16周时，这些参数在接触二氧化硅的小鼠中仍然升高，但在接触WF的小鼠中没有。1周时的组织病理学评估表明，WF诱导细支气管上皮增生并伴有细胞异型性，细支气管周围肺泡出现肺泡细支气管肺泡增生（BAH），以及细支气管周围淋巴肉芽肿性炎症。持续变化包括组织细胞性炎症灶、纤维化、非典型细支气管上皮细胞和细支气管BAH。接触二氧化硅的小鼠的主要变化是组织细胞性和化脓性炎症、纤维化和肺泡BAH。我们的研究结果表明WF会导致细支气管和细支气管周围上皮持续变化，这表明需要对接触WF后的细支气管变化进行研究。
