Antonini J M, Krishna Murthy G G, Brain J D
Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA.
Exp Lung Res. 1997 May-Jun;23(3):205-27. doi: 10.3109/01902149709087368.
Possible mechanisms were examined whereby welding fumes may elicit injury and inflammation in the lungs. The effects of different welding fumes on lung macrophages and on the in vivo production of two inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1 beta), were assessed. Fume was collected during flux-covered manual metal are welding using a stainless steel consumable electrode (MMA-SS) and gas metal are welding using a mild steel electrode (GMA-MS). For the in vitro study, bronchoalveolar lavage was performed on untreated rats to recover lung macrophages, and the effects of the welding fumes on macrophage viability and respiratory burst were examined. In vivo, additional rats were intratracheally instilled with the welding fumes at a dose of 1 mg/100 g body weight. These rats were lavaged 1, 14, and 35 days postinstillation, and indicators of lung damage (cellular differential, albumin. TNF-alpha and IL-1 beta release, and lactate dehydrogenase and beta-n-acetyl glucosaminidase activities) were measured. In vitro, the MMA-SS fume was more cytotoxic to the macrophages and induced a greater release of reactive oxygen species as measured by the respiratory burst compared to the GMA-MS fume. In vivo, evidence of lung damage was observed for both fumes 1 day postinstillation. By 14 days, lung responses to the GMA-MS fume had subsided and were not different from the saline vehicle control group. Significant lung damage was still observed for the MMA-SS group at 14 days, but by 35 days, the responses had returned to control values. One day after the instillations, both welding fumes had detectable levels of TNF-alpha and IL 1 beta within the lavage fluid. However, the MMA-SS particles caused a significantly greater release of both cytokines in the lavage fluid than did the GMA-MS group. The results demonstrate that MMA-SS fume caused more pneumoloxicity than GMA-MS. This increased response may reflect enhanced macrophage activation, the increased production of reactive oxygen species, as well as secretion of TNF-alpha and IL-1 beta.
研究了焊接烟尘可能导致肺部损伤和炎症的潜在机制。评估了不同焊接烟尘对肺巨噬细胞以及两种炎性细胞因子——肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）体内产生的影响。使用不锈钢消耗电极进行药皮焊条手工电弧焊（MMA-SS）以及使用低碳钢电极进行气体保护金属电弧焊（GMA-MS）时收集烟尘。在体外研究中，对未处理的大鼠进行支气管肺泡灌洗以获取肺巨噬细胞，并检测焊接烟尘对巨噬细胞活力和呼吸爆发的影响。在体内实验中，给另外的大鼠经气管内注入剂量为1mg/100g体重的焊接烟尘。在注入后1天、14天和35天对这些大鼠进行灌洗，并测量肺损伤指标（细胞分类、白蛋白、TNF-α和IL-1β释放以及乳酸脱氢酶和β-N-乙酰氨基葡萄糖苷酶活性）。在体外，与GMA-MS烟尘相比，MMA-SS烟尘对巨噬细胞的细胞毒性更大，并且通过呼吸爆发测量显示其诱导的活性氧释放更多。在体内，注入后1天观察到两种烟尘都有肺损伤的迹象。到14天时，对GMA-MS烟尘的肺部反应已消退，与生理盐水载体对照组无差异。在14天时，MMA-SS组仍观察到明显的肺损伤，但到35天时，反应已恢复到对照值。注入后1天，两种焊接烟尘在灌洗液中均可检测到TNF-α和IL-1β水平。然而，MMA-SS颗粒在灌洗液中引起的两种细胞因子释放均明显高于GMA-MS组。结果表明，MMA-SS烟尘比GMA-MS烟尘引起更多的肺毒性。这种增强的反应可能反映了巨噬细胞活化增强、活性氧产生增加以及TNF-α和IL-1β的分泌增加。
