Halatek Tadeusz, Sinczuk-Walczak H, Rydzynski K
Department of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, 8 Teresy St. P.O. Box 199, 90-950 Łódź, Poland.
J Inorg Biochem. 2005 Sep;99(9):1904-11. doi: 10.1016/j.jinorgbio.2005.06.027.
The relationship between respiratory and neurological effects of exposure to aluminium (Al) was investigated in a group of foundry workers exposed to Al at concentrations below the threshold limit value (TLV) binding in Poland (2.0 mg Al2O3 m(-3)). Neurological and neurophysiological parameters indicated subclinical effects of Al exposure on the nervous system. The measurement of serum anti-inflammatory Clara cell protein (CC16) was employed as a peripheral marker of the lung epithelium function. There was a strong inverse relationship between serum Al (Al-S) and CC16 concentrations (p = 0.006). The lowest CC16 concentrations were found in serum of workers characterised by subjective symptoms of the central nervous system (CNS) and abnormal results of neurophysiological examinations (EEG and VEP). Low serum CC16 concentrations and enhanced Al and iron (Fe) levels were also observed in the younger age group of workers with the subjective CNS symptoms and abnormal VEP results, which suggests that Fe is implicated in strengthening of the neurotoxic Al potential. The results of our study support the hypothesis that subclinical neurological symptoms (especially abnormal VEP) are most likely associated with internalisation of Al ions with lipid fractions of the lung epithelium, which in turn may help Al ions overcome the blood-brain barrier. Low serum CC16 concentrations (<10 microg L(-1)) were noted in workers with the abnormal results of neurological (CNS) and neurophysiological (EEG and VEP) examinations as well as with Al body burden manifested by urinary excretion (Al-U) below 60 microg L(-1) and Al-S concentration of 2 microg L(-1). This concentration may be considered as a threshold allowable biological concentration of aluminium.
在波兰，对一组暴露于低于阈限值（TLV）（2.0 mg Al2O3 m(-3)）的铝（Al）环境中的铸造工人，研究了铝暴露的呼吸和神经效应之间的关系。神经学和神经生理学参数表明铝暴露对神经系统有亚临床效应。血清抗炎克拉拉细胞蛋白（CC16）的测量被用作肺上皮功能的外周标志物。血清铝（Al-S）和CC16浓度之间存在强烈的负相关关系（p = 0.006）。在有中枢神经系统（CNS）主观症状且神经生理学检查（脑电图和视觉诱发电位）结果异常的工人血清中，发现CC16浓度最低。在有主观CNS症状且视觉诱发电位结果异常的年轻工人组中，也观察到血清CC16浓度低以及铝和铁（Fe）水平升高，这表明铁与增强铝的神经毒性潜力有关。我们的研究结果支持以下假设：亚临床神经症状（尤其是异常的视觉诱发电位）最有可能与铝离子通过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。在神经学（CNS）和神经生理学（脑电图和视觉诱发电位）检查结果异常以及尿排泄（Al-U）低于60 μg L(-1)且Al-S浓度为2 μg L(-1)表明有铝体内负荷的工人中，发现血清CC16浓度低（<10 μg L(-1)）。该浓度可被视为铝的阈值允许生物浓度。
