首页> 外文期刊>Journal of Environmental Science and Health. A, Toxic/Hazardous Substances & Environmental Engineering >Early neurotoxic effects of inhalation exposure to aluminum and/or manganese assessed by serum levels of phospholipid-binding Clara cells protein
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Early neurotoxic effects of inhalation exposure to aluminum and/or manganese assessed by serum levels of phospholipid-binding Clara cells protein

机译:通过血清磷脂结合的克拉拉细胞蛋白水平评估吸入暴露于铝和/或锰的早期神经毒性作用

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Little is known on the disturbances of lung epithelium function in aluminum casting smelters and shipyard welders exposed by inhalation to irritant occupational pollutants, dust and fumes. The exact mechanism of aluminum and manganese toxicity is not known, but it is thought that they may potentiate oxidative and inflammatory stress, leading to impaired neurological function. The aim of the study was to investigate the subclinical effects of aluminum and manganese exposure on the nervous system and to assess their relationship to the biomarkers of exposure and effect in workers exposed to neurotoxic fumes. The relationship between the neurological and respiratory effects was investigated in 50 workers at aluminum casting smelters exposed to x_(GM) = 0.29 Al_2O_3 mg m~(-3), and 59 shipyard welders exposed to x_(GM) = 0.16 Mn mg m~(-3), and the reference group. Serum anti-inflammatory, phospholipid-binding Clara cell protein (CC16) as a peripheral marker of the bronchiolar epithelium function measured. The lowest CC16 concentrations were found in workers showing subjective CNS symptoms and abnormal neurophysiological findings: EEG and visual evoked potentials. A strong inverse relationship was found between serum Al (Al-S) and CC16 concentrations (p = 0.006). Younger smelter workers and welders, with a shorter exposure duration, presented a higher number of VEPs than the workers employed for a longer period of time. The sub-clinical neurological symptoms (VEP) and low CC16 level can be associated with an internalization of Al ions with lipid fractions of the lung epithelium, which in turn may help Al ions overcome the blood-brain barrier. The inhibited secretion of anti-inflammatory Clara cell protein and low respiratory performance in younger Mn welders was found to enhance subclinical neurotoxic symptoms, especially VEPs, related to exposure to airborne Mn and Mn-B.
机译:对于铝制冶炼厂和造船厂焊工因吸入暴露于刺激性职业污染物,粉尘和烟雾而引起的肺上皮功能障碍知之甚少。铝和锰毒性的确切机理尚不清楚,但据认为它们可能增强氧化和炎性应激,从而导致神经功能受损。这项研究的目的是调查铝和锰暴露对神经系统的亚临床影响,并评估它们与暴露的生物标志物的关系以及对暴露于神经毒性烟雾的工人的影响。在暴露于x_(GM)= 0.29 Al_2O_3 mg m〜(-3)的铝铸造冶炼厂的50名工人和暴露于x_(GM)= 0.16 Mn mg m〜的59个船厂焊工中,研究了神经和呼吸作用之间的关系。 (-3)和参考组。血清抗炎,磷脂结合的克拉拉细胞蛋白(CC16)作为细支气管上皮功能的外周标志物被测量。在具有主观中枢神经系统症状和异常神经生理学发现(脑电图和视觉诱发电位)的工人中发现最低的CC16浓度。发现血清Al(Al-S)与CC16浓度之间存在强烈的反比关系(p = 0.006)。暴露时间较短的年轻冶炼厂工人和焊工所呈现的VEP数量比长期雇用的工人更高。亚临床神经症状(VEP)和低CC16水平可能与Al离子与肺上皮脂质成分的内在化有关,这反过来又可以帮助Al离子克服血脑屏障。在年轻的锰焊工中,抗炎性克拉拉细胞蛋白的分泌受到抑制,呼吸功能低下,可增强亚临床神经毒性症状,尤其是与暴露于空气中的Mn和Mn-B有关的VEP。

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