Halatek Tadeusz, Sinczuk-Walczak Halina, Rydzynski Konrad
Department of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, Lodz, Poland.
J Environ Sci Health A Tox Hazard Subst Environ Eng. 2008 Feb;43(2):118-24. doi: 10.1080/10934520701781178.
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(2)O(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.
对于吸入刺激性职业污染物、粉尘和烟雾的铝铸造厂工人和造船厂焊工，肺部上皮功能紊乱的情况鲜为人知。铝和锰毒性的确切机制尚不清楚，但人们认为它们可能会增强氧化应激和炎症应激，导致神经功能受损。本研究的目的是调查铝和锰暴露对神经系统的亚临床影响，并评估它们与接触神经毒性烟雾的工人中暴露和效应生物标志物之间的关系。在50名暴露于x(GM)=0.29 Al(2)O(3) mg m(-3)的铝铸造厂工人、59名暴露于x(GM)=0.16 Mn mg m(-3)的造船厂焊工以及参照组中，研究了神经和呼吸效应之间的关系。测量了血清中作为细支气管上皮功能外周标志物的抗炎、磷脂结合克拉拉细胞蛋白(CC16)。在出现主观中枢神经系统症状和异常神经生理学检查结果（脑电图和视觉诱发电位）的工人中发现了最低的CC16浓度。血清铝(Al-S)与CC16浓度之间存在强烈的负相关关系(p = 0.006)。暴露时间较短的年轻冶炼工人和焊工比工作时间较长的工人表现出更多的视觉诱发电位。亚临床神经症状(视觉诱发电位)和低CC16水平可能与铝离子与肺上皮脂质部分的内化有关，这反过来可能有助于铝离子突破血脑屏障。在年轻的锰焊工中发现的抗炎克拉拉细胞蛋白分泌受抑制和呼吸功能低下，增强了与空气中锰和锰硼暴露相关的亚临床神经毒性症状，尤其是视觉诱发电位。
