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

Abstract

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.

Health effects and arsenic species in urine of copper smelter workers

“…[32] A similar picture is observed in welders occupationally exposed by inhalation to gases and dusts from welding fumes containing Mn or in aluminum smelter workers exposed to dusts containing aluminum, and in copper smelter workers exposed to arsenic. [33,34] Exposure to arsenic causes significant changes in the kidneys. In this study we observed increased urinary levels of low molecular weight protein β 2 M and RBP, and the increase was statistically significant in Furnace Department workers ( Table 2).…”

Uptake and intracellular distribution of various metal ions in human monocyte-derived dendritic cells detected by Newport Green™ DCF diacetate ester

“…The fluorescence signal of metal ion treated cells, particularly in the context of Ti(III), sufficiently increased to a level where we could be sure that any background fluorescence from native metal ion complexes was essentially insignificant. In addition, a significant increase of the fluorescent signal was seen for Al, Cr(III), Mo, Ni and Ti(IV), all metals that have been reported to be either neurotoxic or nominated to play a role in chronic nervous diseases (Campbell et al, 2004;Halatek et al, 2008;Smorgon et al, 2004;Song et al, 2008;Wang et al, 2008;Wu et al, 2008).…”

“…Sudden, acute intoxication with high metal concentrations causes usually significantly correlated, unequivocal neurotoxic symptoms, as described for Cr, cobalt (Co) and lead (Pb) (Gobba, 2003;Halatek et al, 2008;Kumar, 2001;Pecze et al, 2005;Song et al, 2008). Little is known about long-term exposure to lower 0165-0270/$ -see front matter © 2008 Elsevier B.V. All rights reserved.…”

Noninvasive measurement of aluminium in human bone: Preliminary human study and improved system performance

“…Although such a pattern is not always seen [8], it remains controversial as to whether aluminium is necessarily a causative agent in the development of Alzheimer's disease [9]. However, there continue to be reports in which impaired cognitive function is associated with industrial exposure to aluminium [10][11][12][13]. Although a link between aluminium and Alzheimer's disease is debatable, there is clear evidence that aluminium can cause severe encephalopathy in patients being dialysed for kidney disease [14].…”

“…Aluminium can be measured in a person's plasma (or serum) [16] and urine [13], but this will reflect short term exposure, which is certainly valuable, but not well suited to assessing whether cumulative exposure could be causally related to specific health effects. The presence of aluminium can be clearly demonstrated by taking a biopsy and using the appropriate staining technique [17,18].…”