Inflammatory responses to the occupational inhalation of metal fume
Inflammatory responses to the occupational inhalation of metal fume
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DOI：
10.1183/09031936.06.00053205
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发表时间：
2006-02-01
影响因子：
24.3
通讯作者：
Shute, JK
中科院分区：
文献类型：
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作者：
Palmer, KT;McNeill-Love, R;Shute, JK
职业接触金属烟雾会导致肺炎风险可逆性增加，但具体机制尚不清楚。为了进行调查，当前作者测量了焊工和非焊工的宿主防御功能的各种标志物。从 27 名经常长期接触黑色金属烟雾的焊工和 31 名未接触黑色金属烟雾的对照中收集了诱发痰液和静脉血样本。作者测量了痰液中的细胞计数、可溶性铁和细胞铁浓度，以及白细胞介素 8、肿瘤坏死因子 α、髓过氧化物酶、基质金属蛋白酶 9、免疫球蛋白 (Ig)A、α(2)-巨球蛋白和不饱和铁结合能力的水平。对血样进行中性粒细胞活化和肺炎球菌 IgG 抗体的检测。焊工的痰液中铁水平显着升高，不饱和铁结合能力显着降低，但是，尽管铁挑战较高，但值得注意的是，没有出现炎症反应。只有血中嗜酸性粒细胞和嗜碱性粒细胞计数与熔接程度显着相关。其他几项指标也观察到了微弱的、不显着的趋势，这与中性粒细胞的低级启动一致。 总之，这些数据表明，长期接触金属烟雾会减弱对吸入颗粒物的反应。然而，缺乏可检测的局部炎症反应背后的机制需要进一步研究。
Occupational exposure to metal fume promotes a reversible increase in the risk of pneumonia, but by mechanisms which are unclear. To investigate, the current authors measured various markers of host defence function in welders and nonwelders.Induced sputum and venous blood samples were collected from 27 welders with regular long-term exposure to ferrous metal fume and 31 unexposed matched controls. In sputum, the present authors measured cell counts, the soluble and cellular iron concentration, and levels of interleukin-8, tumour necrosis factor-alpha, myeloperoxidase, matrix metalloproteinase-9, immunoglobulin (Ig)A, alpha(2)-macroglobulin and unsaturated iron-binding capacity. Blood samples were assayed for evidence of neutrophil activation and pneumococcal IgG antibodies.Welders had significantly higher iron levels and a substantially lower unsaturated iron-binding capacity in their sputum, but, despite a high iron challenge, there was a noteworthy absence of an inflammatory response. Only blood counts of eosinophils and basophils were significantly related to the extent of welding. Weak nonsignificant trends were observed for several other measures, consistent with low-grade priming of neutrophils.In conclusion, these data suggest that chronic exposure to metal fume blunts responsiveness to inhaled particulate matter. However, the mechanism behind the lack of detectable local inflammatory response requires further investigation.