Early neurotoxic effects of inhalation exposure to aluminum and/or manganese assessed by serum levels of phospholipid-binding Clara cells protein.

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.