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Objectives: This is the second of two parallel longitudinal studies investigating Al exposure and neurobehavioral health of Al welders over 4 years. While the first published study in the trail and truck construction industry examined the neurobehavioral development of Al welders from age 41-45 in the group mean (Kiesswetter et al. in Int Arch Occup Environ Health 81:41-67, 2007), the present study in the automobile industry followed the development from 35 to 39. Although no conspicuous neurobehavioral developments were detected in the first study, which furthermore exhibited the higher exposure, it cannot be excluded that exposure effects appear in earlier life and exposure stages., Methods: The longitudinal study is based on a repeated measurement design comprising 4 years with three measurements in 2 years intervals. 92 male Al welders in the automobile industry were compared with 50 non-exposed construction workers of the same industry and of similar age. The repeated measurements included total dust in air, and Al pre- and post-shift plasma and urine samples. Neurobehavioral methods comprised symptoms, verbal intelligence, logic thinking, psychomotor behavior, memory, and attention. The computer aided tests came from the Motor Performance Series and the European Neurobehavioral Evaluation System. The courses of neurobehavioral changes were analyzed with multivariate covariance-analytical methods considering the covariates age, indicators of 'a priori' intelligence differences (education or markers of 'premorbid' intelligence), and alcohol consumption (carbohydrate-deficient transferrin in plasma). Additionally, the interrelationship, reliability and validity of biomonitoring measures were examined., Results: The mean environmental dust load during welding, 0.5-0.8 mg/m(3), and the mean internal load of the welders (pre-shift: 23-43 microg Al/g creatinine in urine; 5-9 microg Al/l plasma) were significantly lower than in the parallel study. Under low exposure, the stability of biomonitoring measures was reduced, but the Al load differed significantly between Al welders and referents. It could not be shown that the development of neurobehavioral performances over the 4-year period differed between both groups. Mainly, markers of premorbid intelligence and age were related to neurobehavioral performance differences but not Al exposure., Conclusions: The biomonitoring and neurobehavioral results are in line with the results of the first published study. The repeated measurement models of both studies showed no adverse neurobehavioral effects of Al welding. A modular lifetime-oriented research concept is outlined aiming at the investigation of sequential periods of exposure life with special focus on the biologically most sensitive phases like first exposure and old age.

Objectives: Previous cross sectional studies on potential neurotoxic effects of long-term aluminium exposures by aluminium welders lack clear interpretable results for methodological reasons. The present longitudinal study examined on the one hand the reliability and representativity of Al-biomonitoring as indicator of individual long-term exposure and on the other hand the long-term changes of neurobehavioural performance in Al welders in relation to Al exposure and neurobehavioural performance changes of a non-exposed control group., Methods: The longitudinal study compared repeatedly measured exposure data and neurobehavioural data of 20, initially 44, male Al welders in the train and truck construction industry with data of a control group of similar age on the basis of three investigations over a period of 4 years. The repeated measurements of exposure included total dust in air as well as Al in pre- and post-shift plasma and urine samples. Neurobehavioural methods comprised symptoms, verbal intelligence, logic thinking, psychomotor behaviour, memory, and attention. Computer-aided tests from the Motor Performance Series (MLS) and the European Neurobehavioural Evaluation System (EURO-NES) were used. The characteristics of the biomonitoring data and the relationship to neurobehavioural data were examined with methods of correlation and regression analysis. The courses of neurobehavioural changes were analysed with multivariate covariance-analytical methods (MANCOVA) considering the covariates age, indicators of 'a priori' intelligence differences (education or 'premorbid' intelligence), and alcohol consumption (carbohydrate-deficient transferrin in plasma, CDT)., Results: The mean total dust load during welding, near to the routinely worn ventilated helmets, was in the range of 5-8 mg/m(3). The biomonitoring data of the welders (pre-shift: 88-140 microg Al/g creatinine in urine; 13-16 microg Al/l plasma) showed a high long-term stability but also sensitivity to acute shift dependent exposure changes. The Al welders who had been working in this profession at an average of 15 years showed no significantly increased symptom levels compared with the control group. Explorative regression and covariance analyses revealed neither a correlation between biomonitoring and performance variables nor a significant difference between Al-exposed and controls in the performance courses during the 4 years period. Explorative modelling indicated that the structure of neurobehavioural outcomes could be determined by possible indicators of intellectual 'a priori' (premorbid) differences between subjects but not by their exposure information., Conclusions: Compared to studies in the literature this study is characterized by relatively high and non-confounded Al exposure of the welders, a repeated-measurement design, and multivariate analyses. However, the long-term stable interindividual differences of internal Al exposure were not related to interindividual differences in neurobehavioural performances. Additionally, the lack of processual changes of neurobehavioural performances during the observation phase and the insignificant group differences do not make it very probable that degenerative processes caused by Al had happened before study onset or stopped just at this time point.

To evaluate an adequate strategy for biological monitoring of aluminium (Al), a group of 62 Al welders (age in 1999: 23-51 years, median 35 years) was surveyed annually from 1999 to 2003 by determination of pre- and post-shift Al in urine and plasma. Biomonitoring was supplemented by personal air measurements of the total dust concentration. The welders' internal exposure was compared to the exposure of 60 non-exposed assembly workers (age in 1999: 21-51 years, median: 36 years) who were surveyed in 1999, 2001 and 2003. Having a nearly constant dust exposure, median concentrations of Al in urine (Al in plasma) of the welders decreased from 40.1 microg/g to 19.8 microg/g creatinine (8.7 to 4.6 microg/l). For the control group the median levels of Al in urine (plasma) ranged from 4.8 microg/g to 5.2 microg/g creatinine (2.4-4.3 microg/l) indicating a higher sensitivity for the marker Al in urine. No systematic differences have been found between pre- and post-shift internal exposure. This might be caused by the slow elimination kinetics and low systemic bioavailability of Al. A correlation analysis did not yield close relationships between dust exposure, Al in plasma and Al in urine underlining the importance of biomonitoring for assessment of Al exposure.

Objectives: The neurotoxicity of occupational exposure to aluminium (Al)-containing welding fumes has been discussed with controversial results. The aim of the longitudinal study was to examine a group of Al welders for significant central nervous changes in comparison with a non-exposed cohort., Methods: A group of 98 Al welders (mean age 37 years) in the car-body construction industry, with a median of 6 years of occupational exposure to Al welding fumes, and an education-matched, gender-matched, age-matched control group of 50 car-production workers (mean age 36 years) at the same plant, were included in this longitudinal study. Two cross-sectional studies were done in 1999 and 2001. In the second cross-sectional study 97 welders and 50 controls could be examined. The examination programme consisted, for example, of a standardised anamnesis, focussing on occupational history, education, illnesses, medication, accidents and current alcohol consumption, a physical examination that included neurological status, and the assessment of Al concentration in plasma and urine. The neurobehavioral methods included a symptom questionnaire, modified Q16, and computerised and non-computerised tests: psychomotor performance (steadiness, line tracing, aiming, tapping), verbal intelligence (WST), simple reaction time, digit span, block design (HAWIE), symbol-digit substitution, digit span, switching attention (European neurobehavioral evaluation system, EURO-NES), and standard progressive matrices. The data were analysed by multivariate analysis of covariance (MANCOVA) for repeated measurements with covariates age, education, and carbohydrate-deficient transferrin in plasma (CDT). RESULTS. The median Al urine concentration (mean preshift/postshift) was 52.4 microg/g creatinine (2001) and 57.6 microg/g creatinine (1999). Median respirable air dust was 0.67 mg/m(3) (2001) and 0.47 mg/m(3) (1999). Welders and controls did not report significantly more symptoms in the modified Q16. Furthermore, no significant differences in psychomotor performance and other neurobehavioral tasks, except for reaction time, were seen between welders and non-welders. Regression analyses reveal a significant relationship between reaction time and Al excretion in urine that was confounded by other factors., Conclusions: At present the outcome for reaction time has to be interpreted as a single result. However, as the modified Q16 questionnaire and the rest of the psychomotor performance showed no significant changes, the next cross-sectional study, in 2003, will provide further information on which a final conclusion can be based.

Two cross-sectional studies were conducted at a German aluminum (Al) powder plant to evaluate possible nervous system effects from occupational Al exposure. The investigation included biological monitoring, a neuropsychological test battery, and event-related P300 potentials. Neurophysiologic findings in workers chronically exposed to Al dust did not differ from non-Al-exposed controls from the same plant. The authors suggest that chronic exposure to Al dust, at the levels documented in this study, does not induce measurable cognitive decline.

Objective: The aim of this case study was to investigate the suitability of high-resolution computed tomography (HRCT) for detecting early stages of lung fibrosis induced by aluminium (Al) dust., Methods: A 40-year-old worker was studied who had worked as a stamper for 14 years in a plant producing aluminium powder and had been exposed to high levels of aluminium dust during this time. The investigation included the collection of general data on health and details on occupational history, immunological tests, a physical examination, lung function analysis, biological monitoring of Al in plasma and urine, chest X-rays and HRCT., Results: For many years the man has suffered from an exercise-induced shortness of breath. Lung function analysis revealed a reduction of the vital capacity to 57.5% of the predicted value. The Al concentration in plasma was 41.0 micrograms/l (upper reference value 10 micrograms/l) and in urine 407.4 micrograms/l upper reference value 15 micrograms/l, biological tolerance (BAT) value 200 micrograms/l[ at the time of diagnosis. Chest X-ray showed unspecific changes. HRCT findings were characterised by small, centrilobular, nodular opacities and slightly thickened interlobular septae. Exposure to other fibrotic agents could be excluded., Conclusions: HRCT was more sensitive than chest X-rays for detecting this early stage of Al-dust-induced lung disease. The suitability of HRCT in the surveillance of workers highly exposed to aluminium powder should be evaluated in further studies. Biological monitoring can be used to define workers at high risk.

Within the framework of a cross-sectional study, we investigated 61 employees in an aluminium powder factory to see if aluminium had an influence on bone mineral content using the non-invasive method of bone density measurement. Thirty-two workers had been employed for, on average, 151 months in the area of aluminium powder production. Twenty-nine employees in the same factory, who had not been engaged in the production of aluminium powder, served as controls. The groups differed significantly in the concentrations of aluminium in urine and plasma. The bone mineral content, which was determined in the lumbar spine by means of photon absorptiometry showed no significant difference between the groups. The bone density value amounted to 1.00 g/cm2 for those exposed and 1.02 g/cm2 for the control group (median values). No correlation could be determined between the values obtained from the biological monitoring of the plasma or the duration of exposure and the bone density values. To summarise, using osteodensitometry as the method of investigation here, no influence could be detected for an occupational exposure to aluminium powders on the mineral salt content of the skeletal system in the area of the lumbar spine.

Within the framework of a transverse study, the mental performance of a group of subjects exposed to aluminium over many years (n = 32; aluminium powder industry) was compared with that of a structurally similar control group (n = 30). Neuropsychological and electrophysiological tests revealed no signs of cognitive performance, despite aluminium burdening. Aluminium levels in plasma and urine were elevated.