Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.
Neurotoxicology. 2009 Nov;30(6):915-25. doi: 10.1016/j.neuro.2009.09.006. Epub 2009 Sep 25.
Serious questions have been raised by occupational health investigators regarding a possible causal association between neurological effects in welders and the presence of manganese (Mn) in welding fume. Male Sprague-Dawley rats were exposed by inhalation to 40 mg/m(3) of gas metal arc-mild steel (MS) welding fume for 3 h/day for 10 days. Generated fume was collected in the animal chamber during exposure, and particle size, composition, and morphology were characterized. At 1 day after the last exposure, metal deposition in different organ systems and neurological responses in dopaminergic brain regions were assessed in exposed animals. The welding particles were composed primarily of a complex of iron (Fe) and Mn and were arranged as chain-like aggregates with a significant number of particles in the nanometer size range. Mn was observed to translocate from the lungs to the kidney and specific brain regions (olfactory bulb, cortex, and cerebellum) after MS fume inhalation. In terms of neurological responses, short-term MS fume inhalation induced significant elevations in divalent metal ion transporter 1 (Dmt1) expression in striatum and midbrain and significant increases in expression of proinflammatory chemokines (Ccl2, Cxcl2) and cytokines (IL1beta, TNFalpha) in striatum. In addition, mRNA and protein expression of glial fibrillary acidic protein (GFAP) was significantly increased in striatum after MS fume exposure. However, the 10-day MS welding fume inhalation did not cause any changes in dopamine and its metabolites or GABA in dopaminergic brain regions nor did it produce overt neural cell damage as assessed by histopathology. In summary, short-term MS welding fume exposure led to translocation of Mn to specific brain regions and induced subtle changes in cell markers of neuroinflammatory and astrogliosis. The neurofunctional significance of these findings currently is being investigated in longer, more chronic welding fume exposure studies.
职业健康调查人员提出了一些严重的问题，他们怀疑焊工神经效应与焊接烟尘中锰（Mn）的存在之间可能存在因果关系。雄性 Sprague-Dawley 大鼠通过吸入方式暴露于 40mg/m³的气体保护金属电弧-低碳钢（MS）焊接烟尘中，每天 3 小时，共 10 天。在暴露期间，在动物室中收集产生的烟尘，并对其粒径、组成和形态进行了表征。在最后一次暴露后的 1 天，评估了暴露动物不同器官系统中的金属沉积和多巴胺能脑区的神经反应。焊接颗粒主要由铁（Fe）和 Mn 的复合物组成，并排列成链状聚集物，其中大量颗粒处于纳米尺寸范围。观察到 Mn 从肺部转移到肾脏和特定的脑区（嗅球、皮层和小脑），在吸入 MS 烟尘后。就神经反应而言，短期 MS 烟尘吸入会导致纹状体和中脑中二价金属离子转运蛋白 1（Dmt1）的表达显著升高，纹状体中促炎趋化因子（Ccl2、Cxcl2）和细胞因子（IL1beta、TNFalpha）的表达也显著增加。此外，MS 烟尘暴露后，纹状体中的神经胶质纤维酸性蛋白（GFAP）的 mRNA 和蛋白表达显著增加。然而，10 天的 MS 焊接烟尘吸入并未导致多巴胺及其代谢物或多巴胺能脑区中的 GABA 发生任何变化，也未通过组织病理学评估产生明显的神经细胞损伤。总之，短期 MS 焊接烟尘暴露导致 Mn 转移到特定脑区，并诱导神经炎症和神经胶质增生的细胞标志物发生微妙变化。目前正在进行更长期、更慢性的焊接烟尘暴露研究，以调查这些发现的神经功能意义。
