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Neurotoxicity following acute inhalation of aerosols generated during resistance spot weld-bonding of carbon steel

机译:碳钢电阻点焊过程中急性吸入气溶胶后产生的神经毒性

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Welding generates complex metal aerosols, inhalation of which is linked to adverse health effects among welders. An important health concern of welding fume (WF) exposure is neurological dysfunction akin to Parkinson's disease (PD). Some applications in manufacturing industry employ a variant welding technology known as "weld-bonding" that utilizes resistance spot welding, in combination with adhesives, for metal-to-metal welding. The presence of adhesives raises additional concerns about worker exposure to potentially toxic components like Methyl Methacrylate, Bisphenol A and volatile organic compounds (VOCs). Here, we investigated the potential neurotoxicological effects of exposure to welding aerosols generated during weld-bonding. Male Sprague-Dawley rats were exposed (25 mg/m(3) targeted concentration; 4 h/day X 13 days) by whole-body inhalation to filtered air or aerosols generated by either weld-bonding with sparking (high metal, low VOCs; HM) or without sparking (low metal; high VOCs; LM). Fumes generated under these conditions exhibited complex aerosols that contained both metal oxide particulates and VOCs. LM aerosols contained a greater fraction of VOCs than HM, which comprised largely metal particulates of ultrafine morphology. Short-term exposure to LM aerosols caused distinct changes in the levels of the neurotransmitters, dopamine (DA) and serotonin (5-HT), in various brain areas examined. LM aerosols also specifically decreased the mRNA expression of the olfactory marker protein (Omp) and tyrosine hydroxylase (Th) in the olfactory bulb. Consistent with the decrease in Th, LM also reduced the expression of dopamine transporter (Slc6a3; Dat), as well as, dopamine D2 receptor (Drd2) in the olfactory bulb. In contrast, HM aerosols induced the expression of Th and dopamine D5 receptor (Drd5) mRNAs, elicited neuroinflammation and blood-brain barrier-related changes in the olfactory bulb, but did not alter the expression of Omp. Our findings divulge the differential effects of LM and HM aerosols in the brain and suggest that exposure to weld-bonding aerosols can potentially elicit neurotoxicity following a short-term exposure. However, further investigations are warranted to determine if the aerosols generated by weld-bonding can contribute to persistent long-term neurological deficits and/or neurodegeneration.
机译:焊接会产生复杂的金属气溶胶,其吸入与焊工之间的不利健康影响有关。焊接烟雾(WF)暴露对健康的重要关注是类似于帕金森氏病(PD)的神经功能障碍。制造业中的某些应用采用了一种称为“焊接”的变体焊接技术,该技术利用电阻点焊与粘合剂相结合进行金属到金属的焊接。粘合剂的存在引起了人们对工人暴露于潜在毒性成分(例如甲基丙烯酸甲酯,双酚A和挥发性有机化合物(VOC))的担忧。在这里,我们调查了暴露于焊接过程中产生的焊接气溶胶的潜在神经毒理作用。通过全身吸入将雄性Sprague-Dawley大鼠暴露于(25 mg / m(3)目标浓度; 4 h /天X 13天)暴露于过滤空气或通过焊接结合产生火花的气溶胶(高金属,低VOC) ; HM)或无火花(低金属;高VOC; LM)。在这些条件下产生的烟雾显示出复杂的气溶胶,其中既包含金属氧化物颗粒又包含VOC。 LM气溶胶比HM气溶胶含有更多的VOC,而HM气溶胶主要包含超细形态的金属颗粒。在所检查的各个大脑区域中,短期暴露于LM气雾剂会导致神经递质,多巴胺(DA)和血清素(5-HT)的水平发生明显变化。 LM气雾剂还特异性降低嗅球中嗅觉标记蛋白(Omp)和酪氨酸羟化酶(Th)的mRNA表达。与Th的减少一致,LM还降低了嗅球中多巴胺转运蛋白(Slc6a3; Dat)以及多巴胺D2受体(Drd2)的表达。相比之下,HM气雾剂诱导Th和多巴胺D5受体(Drd5)mRNA的表达,引起嗅球中神经炎症和血脑屏障相关变化,但并未改变Omp的表达。我们的发现揭示了LM和HM气雾剂在大脑中的不同作用,并表明暴露于焊缝气雾剂可能会在短期暴露后引起神经毒性。但是,需要进行进一步的研究以确定通过焊接结合产生的气溶胶是否会导致长期的长期神经功能缺损和/或神经变性。

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