Urinary Aluminum Research Articles

Behavior of aluminum in aluminum welders and manufacturers of aluminum sulfate—impact on biological monitoring

The suitability of determining aluminum in serum or urine as a form of biological monitoring was critically assessed. Airborne and internal aluminum exposure was assessed for 12 aluminum welders in a shipyard and 5 manufacturers of aluminum sulfate. Particles were characterized with X-ray diffraction and scanning electron microscopy. Aluminum in air and biological samples was analyzed using electrothermal atomic absorption spectrometry. Basic toxicokinetic features were inferred from the data. The mean 8-hour time-weighted average concentration of aluminum was 1.1 (range 0.008-6.1) mg/m(3) for the shipyard and 0.13 (range 0.02-0.5) mg/m(3) for the aluminum sulfate plant. Welding fume contained aluminum oxide particles <0.1 microm in diameter and their agglomerates, whereas bauxite and aluminum sulfate particles ranged from 1 to 10 microm in diameter. The shipyard welders' mean postshift serum and urinary concentrations of aluminum (S-Al and U-Al, respectively) were 0.22 and 3.4 micromol/l, respectively, and the aluminum sulfate workers' corresponding values were 0.13 and 0.58 micromol/l. Between two shifts, the welders' S-Al concentration decreased by about 50% (P<0.01), but their U-Al concentration did not change (P=0.64). No corresponding temporal changes occurred among the aluminum sulfate workers. After aluminum welding at the shipyard had ceased, the median S-Al concentration decreased by about 50% (P=0.007) within a year, but there was no change (P=0.75) in the corresponding U-Al concentration. About 1% of aluminum in welding fume appears to be rapidly absorbed from the lungs, whereas an undetermined fraction is retained and forms a lung burden. A higher fractional absorption of aluminum seems possible for aluminum sulfate workers without evidence of a lung burden. After rapid absorption, aluminum is slowly mobilized from the lung burden and dominates the S-Al and U-Al concentrations of aluminum welders. For kinetic reasons, S-Al or U-Al concentrations cannot be used to estimate the accumulation of aluminum in the target organs of toxicity. However, using U-Al analysis to monitor aluminum welders' lung burden seems practical.

Biliary Function in Workers Occupationally Exposed to Aluminium Dust and Fumes

This study investigated biliary secretory function in workers occupationally exposed to aluminium dust and fumes. It included a group of 34 male workers aged (44.1+/-7.8) years and exposed up to 4.6 mg m-3 of aluminium dust and fumes in workplace air for (21.6+/-2.5) years, and a group of 30 unexposed control male workers. Serum and urine aluminium levels were measured in both groups before and after chelating treatment with 1 g deferoxamine by intramuscular injection. Biliary function was assessed by measuring gamma-glutamyl transpeptidase, alkaline phosphatase, 5-nucleotidase, cholesterol and its fractions, total and indirect bilirubin, and bile acids. We then analysed the relationship between Al exposure and biliary function. In the exposed group mean serum aluminium was significantly higher [(4.91+/-3.86) microg L-1] than in controls. The same was true for urine Al before [(1.57+/-1.93) microg L-1] and after deferoxamine [(11.51+/-14.97) microg L-1]. Total and indirect bilirubin and alkaline phosphatase were significantly higher in the exposed than in control workers, and they correlated with urine Al after the chelating treatment. Our findings suggest that chronic occupational exposure to aluminium dust and fumes leads to a significant body retention of aluminium. The impaired biliary secretion in the exposed workers manifested itself in subclinical signs of cholestasis.

Trace aluminium determination in biological samples after microwave digestion followed by solid phase extraction with l-methionine on controlled pore glass

Aluminium is an element found in biological samples at low concentrations and aluminum-related neuropathological diseases in human beings have been reported. For this reason the determination of Al in this type of samples requires the development of enrichment methods capable of improving the instrumental detection for this analyte. l-methionine immobilized on controlled pore glass (CPG) was tested for the retention of aluminium. This adsorbent material was packed in a conical minicolumn and connected to an on-line flow injection system. An inductively coupled plasma optical emission spectrometer associated to an ultrasonic nebulization system (USN-ICP OES) was used for aluminium detection. Al(III) was retained at pH 12.5 and removed from the column with 20% (v/v) HNO 3. The precision of the preconcentration method was evaluated by passing a measured volume of aluminium standard solution (1 μg L − 1 ) through the minicolumn and repeating this procedure five times. The relative standard deviation (RSD) was 2.5%, calculated with the peak heights obtained. A total enhancement factor of 1600 was attained for a sample volume of 10 mL (10-fold for the ultrasonic nebulization system and 160-fold for the preconcentration methodology). The detection limit (DL), calculated as the amount of Al required to yield a net peak equal to three times the standard deviation of the blank solution, was 25 ng L − 1 . The proposed system was successfully applied to the determination of aluminium in urine, hair, and saliva samples, which were pretreated using a microwave digestion methodology with the introduction of a digestion program for saliva. The average aluminium levels found in urine, hair, and saliva samples were 5.5 μg L − 1 , 19 μg g − 1 and 93 μg L − 1 respectively.

Elevated urinary aluminium in current and past users of illicit heroin

The use of illicit heroin is associated with aberrant neurology of unknown aetiology and various psychiatric illnesses. Aluminium, which is a proven neurotoxin, is present in significant amounts in illicit heroin and may also be volatilized and inhaled following the vaporization of heroin off aluminium foil ('Chasing the Dragon'). The purpose of this study was to establish if the use of illicit heroin was associated with an increase in the body burden of aluminium. We have used graphite furnace atomic absorption spectrometry to measure the aluminium and iron contents of the urine of current and past users of illicit heroin and used these data to estimate body burdens of aluminium. Urinary excretion of aluminium is the most effective non-invasive indicator of the body burden of aluminium and was found to be significantly (P < 0.001) higher in users of illicit heroin, range 14-3382 nmol/mmol creatinine (mean +/- SD; 222 +/- 491 nmol/mmol creatinine), than in a normal non-drug abusing control population, range 23-74 nmol/mmol creatinine (mean +/- SD; 43 +/- 19 nmol/mmol creatinine). Exposure to aluminium from the use of illicit heroin may be of particular significance because the urinary excretion of iron, another major contaminant of illicit heroin, in users (mean +/- SD; 53 +/- 63 nmol/mmol creatinine) was not significantly different (P > 0.05) from the control population (mean +/- SD; 38 +/- 18 nmol/mmol creatinine). We have shown for the first time that the use of illicit heroin may be a significant contributor to the body burden of aluminium. Further research will be required to determine if adventitious aluminium has a role in heroin use-related neuropathology and neurology.

Short report: plasma aluminium concentration and 24-hour urinary aluminium excretion before, during and after treatment with sucralfate

Ten dyspeptic patients were treated with 1 g sucralfate q.d.s. for six weeks. The plasma aluminium concentration and 24-h urinary aluminium excretion were measured at 3-weekly intervals before, during and after treatment with sucralfate. Compared with before treatment, there were significant rises in the median plasma aluminium concentration at 3 and 6 weeks during treatment with sucralfate (6 micrograms/L to 13 and 12 micrograms/L). The median 24-h urinary aluminium excretion rose significantly from a pretreatment level of 20 micrograms to 71 and 78 micrograms after 3 and 6 weeks of treatment; the significant increase of urinary aluminium excretion persisted for three weeks after cessation of treatment (52 micrograms/24 hours), but thereafter urinary excretion was not significantly different from pretreatment. The results are consistent with significant absorption and tissue accumulation of aluminium during standard treatment with sucralfate in individuals with normal renal function.

Increased urine aluminum levels found in patients with MS

Increased urine aluminum levels found in patients with MS

Non-invasive therapy to reduce the body burden of aluminium in Alzheimer's disease

There are unexplained links between human exposure to aluminium and the incidence, progression and aetiology of Alzheimer's disease. The null hypothesis which underlies any link is that there would be no Alzheimer's disease in the effective absence of a body burden of aluminium. To test this the latter would have to be reduced to and retained at a level that was commensurate with an Alzheimer's disease-free population. In the absence of recent human interference in the biogeochemical cycle of aluminium the reaction of silicic acid with aluminium has acted as a geochemical control of the biological availability of aluminium. This same mechanism might now be applied to both the removal of aluminium from the body and the reduced entry of aluminium into the body while ensuring that essential metals, such as iron, are unaffected. Based upon the premise that urinary aluminium is the best non-invasive estimate of body burden of aluminium patients with Alzheimer's disease were asked to drink 1.5 L of a silicic acid-rich mineral water each day for five days and, by comparison of their urinary excretion of aluminium pre-and post this simple procedure, the influence upon their body burden of aluminium was determined. Drinking the mineral water increased significantly (P<0.001) their urinary excretion of silicic acid (34.3 +/- 15.2 to 55.7 +/- 14.2 micromol/mmol creatinine) and concomitantly reduced significantly P=0.037) their urinary excretion of aluminium (86.0 +/- 24.3 to 62.2 +/- 23.2 nmol/mmol creatinine). The latter was achieved without any significant (P>0.05) influence upon the urinary excretion of iron (20.7 +/- 9.5 to 21.7 +/- 13.8 nmol/mmol creatinine). The reduction in urinary aluminium supported the future longer-term use of silicic acid as non-invasive therapy for reducing the body burden of aluminium in Alzheimer's disease.

Elevated urinary excretion of aluminium and iron in multiple sclerosis

Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system of as yet unknown aetiology. A consensus of opinion has suggested that the disorder is the result of an interplay between environmental factors and susceptibility genes. We have used a battery of analytical techniques to determine if the urinary excretion of i) markers of oxidative damage; ii) iron and iii) the environmental toxin aluminium and its antagonist, silicon, are altered in relapsing remitting (RRMS) and secondary progressive MS (SPMS). Urinary concentrations of oxidative biomarkers, MDA and TBARS, were not found to be useful indicators of inflammatory disease in MS. However, urinary concentrations of another potential marker for inflammation and oxidative stress, iron, were significantly increased in SPMS (P<0.01) and insignificantly increased in RRMS (P>0.05). Urinary concentrations of aluminium were also significantly increased in RRMS (P<0.001) and SPMS (P<0.05) such that the levels of aluminium excretion in the former were similar to those observed in individuals undergoing metal chelation therapy. The excretion of silicon was lower in MS and significantly so in SPMS (P<0.05). Increased excretion of iron in urine supported a role for iron dysmetabolism in MS. Levels of urinary aluminium excretion similar to those seen in aluminium intoxication suggested that aluminium may be a hitherto unrecognized environmental factor associated with the aetiology of MS. If aluminium is involved in MS then an increased dietary intake of its natural antagonist, silicon, might be a therapeutic option.

Aluminosis – Detection of an almost forgotten disease with HRCT

The aim of this study was to investigate whether it is possible to detect high-resolution computed tomography (HRCT) findings in aluminium powder workers, which are consistent with early stages of aluminosis.62 male workers from 8 departments of two plants producing aluminium (Al) powder were investigated using a standardized questionnaire, physical examination, lung function analysis, biological monitoring of Al in plasma and urine, chest X-ray, HRCT and immunological tests.Chronic bronchitis was observed in 15 (24.2%) of the workers, and four workers (6.5%) reported shortness of breath during exercise. HRCT findings in 15 workers (24.2%) were characterized by ill-defined centrilobular nodular opacities. Workers with ill-defined centrilobular nodular opacities had a lower vital capacity than workers who had no such HRCT-findings (90.9 % pred. vs. 101.8 % pred., p = 0.01). Biological monitoring in plasma and urine revealed higher internal exposure to Al in affected workers (33.5 μg/l plasma to 15.4 μg/l plasma, p = 0.01) and (340.5 μg/g creat. to 135.1 μg/g creat., p = 0.007). Years of exposure and concentration of aluminum in urine and plasma appear to be the best predictors for HRCT findings. Age and decreased vital capacity show borderline significance.We conclude that aluminosis is still relevant in occupational medicine. With HRCT it is possible to detect early stages of aluminosis and biological monitoring can be used to define workers at high risk.

Serum Clara Cell Protein as an Indicator of Pulmonary Impairment in Occupational Exposure at Aluminum Foundry

Although some of the exposures in aluminum (Al) smelting have been well characterized, and respiratory disorders in aluminum production workers are well known, the relationship between internal aluminum loads and appropriate lung biomarkers have not been elucidated. The aim of our work was to carry out a comprehensive investigation in workers employed in the Aluminum Foundry Casting Department with special reference to currently existing hygiene standards, known as threshold limit values (TLV) based on aluminum effects on the respiratory system. The measurement of serum anti-inflammatory Clara cell protein (CC16) was employed as a peripheral marker of the lung epithelium function. A group of 50 casting smelters, 5 locksmiths, 11 sawyers and auxiliary workers exposed to dust containing 14% of aluminum, and a group of 42 controls were examined. Respiratory function tests were performed and forced volume capacity (FVC), forced expiratory volume in 1 s (FEV1), forced expiratory volume in the first percent (FEV1%), forced expiratory flows in 50% VC (FEV50), and markers of foundry workers' exposure and body burden, Al concentration in the breathing zone, blood and urine, biomarkers of the effects of exposure, concentration of CC16 and hyaluronic acid (HA) in serum were determined in all examined workers. Additional measurements comprised determinations of serum iron (Fe) levels, myeloperoxidase (MPO), eosinophil cationic protein (ECP), immunoglobulin E (IgE), glutathione S-transferase (GST), and superoxide dismutase (SOD) activity in erythrocytes. The group of casting smelters was characterized by the highest levels of aluminum in urine (Al-U) (43.7 microg L(-1)), high levels of MPO, ECP and IgE, high SOD activity, low CC16 levels, and low activity of GST. Lower Al-U excretion was observed in locksmiths (35.2 microg L(-1)) and sawyers (21.7 microg L(-1)). Serum CC16 proved to be the most sensitive biomarker, showing high inverse relationship with serum Al (Al-S) concentrations in casting smelters (p = 0.006). The study showed that in conditions of occupational exposure, dusts containing Al2O3 < 1 mg m(-3) cause changes in the respiratory system and biomarkers in serum, especially in CC16, connected with altered functioning of this system. Changes in concentrations of the examined biomarkers and also in respiratory parameters of the study subjects were observed when Al-U concentration was > 40 microg L (-1).

Effect of Aluminum Exposure on Pteridine Metabolism

Occupational and environmental aluminum (Al) exposure cause serious health problems by interaction with biological systems. Al is one of the most documented metals because its cellular targets are unclear biochemical processes and membranes of organisms. The major aim of the present study was to investigate the alteration of serum and urine aluminum in occupational exposure and to observe whether the metal exposure could cause any changes in pteridine-pathway-related critical compounds such as urinary neopterin and biopterin and blood dihydropteridine reductase (DHPR). In this study, determination of the metal concentrations was carried out in Al-exposed workers (n=23) and healthy volunteers (n=18) by using atomic absorption spectrometer. DHPR enzyme activity and levels of neopterin and biopterin were detected by spectrophotometric and high-performance liquid chromatographic methods, respectively. It was found that occupational exposure to the metal led to a statistically significant increase in serum Al levels compared to the controls (p<0.05). At the same time, urinary neopterin and biopterin concentrations of the exposed group were higher than nonexposed subjects (both p<0.05). The correlations among Al levels and DHPR activity, magnesium concentration in serum and urine, working years, smoking status, and age were evaluated.

Exposure and inhalation risk assessment in an aluminium cast-house

To date the exposure, absorption and respiratory health effects of cast-house workers have not been described since most studies performed in the aluminium industry are focused on exposure and health effects of potroom personnel. In the present study, we assessed the external exposure and the absorbed dose of metals in personnel from the aluminium cast house. This was combined with an evaluation of respiratory complaints and the lung function of the personnel. 30 workers from an aluminium casting plant participated and 17 individuals of the packaging and distribution departments were selected as controls. The exposure was assessed by the quantification of total inhalable fume with metal fraction and by the determination of urinary aluminium, chromium, beryllium, manganese and lead concentration. Carbon monoxide (CO), carbon dioxide (CO2), aldehydes and polyaromatic hydrocarbons and man-made mineral fibres concentration were assessed as well. In order to evaluate their respiratory status each participant filled out a questionnaire and their lung function was tested by forced spirometry. Total inhalable fume exposure was maximum 4.37 mg m(-3). Exposure to the combustion gases, man-made mineral fibres and metal fume was well below the exposure limits. Beryllium could not be detected in the urine. The values of aluminium, manganese and lead in the urine were all under the respective reference value. One individual had a urinary chromium excretion above the ACGIH defined biological exposure index (BEI) of 30 microg g(-1) creatinine. There was no significant difference in any of the categories of the respiratory questionnaire and in the results of the spirometry between cast house personnel and referents (Chi-square, all p > 0.05). Exposure in cast houses seem to be acceptable under these conditions. However, peak exposure to fumes cannot be excluded and the potential risk of chromium and beryllium exposure due to the recycling of aluminium requires further attention.

Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine

Reference values for environmental pollutants related to the German population are established continuously by the Human Biomonitoring Commission of the German Federal Environmental Agency. The reference values for arsenic, cadmium, lead, mercury and platinum in blood or urine were derived from the German Environmental Survey 1998 (adults aged 18 – 69 years). The reference value for lead in blood was lowered for females from 90 to 70 μg/l and for males from 120 to 90 μg/l, while the values for cadmium of 1.0 and for mercury of 2.0 μg/l in blood remained unchanged. For cadmium in urine the reference value was lowered from 1.5 to 0.8 μg/l and for mercury in urine from 1.4 to 1.0 μg/l. New reference values were derived for arsenic (15 μg/l) and platinum in urine (0.01 μg/l). Additionally, for nickel in urine a new reference value of 3.0 μg/l based on data from the literature was established. Reference values for estimation of the selenium status were summarized from the literature. For aluminium in blood or urine no reference values were derived and the use of human biomonitoring to estimate aluminium exposure in environmental medicine is not recommended.

Aluminum Contamination of Parenteral Nutrition and Aluminum Loading in Children on Long‐Term Parenteral Nutrition

ABSTRACTBackgroundChildren who are receiving parenteral nutrition are at risk of aluminum overload, which may contribute to such side effects as osteopenic bone disease. The aim of the present study is to determine the aluminum contamination of parenteral nutrition solutions and their components, and to assess the aluminum status of children on long‐term parenteral nutrition.MethodsAluminum concentrations were determined by graphite furnace absorption spectroscopy in components and in final parenteral nutrition solutions. The urinary aluminum excretion and plasma aluminum concentration were determined in 10 children on long‐term parenteral nutrition.ResultsThe mean aluminum concentration in the administered parenteral nutrition solutions was 1.6 ± 0.9 μmol × l−1(mean ± standard deviation (SD)). The resulting mean aluminum daily intake of the 10 patients was 0.08 ± 0.03 μmol × kg−1 × day−1.ConclusionsCompared to two previous studies performed in 1990 and in 1995 in our hospital, the aluminum contamination of parenteral nutrition solutions and the daily aluminum intake of the children seemed to decrease. However, the plasma aluminum concentration and daily urinary aluminum excretion of the children still remain above normal standards. The children had no clinical symptoms of bone disease but aluminum accumulation in tissue can not be excluded. To prevent this iatrogenic toxicity, the aluminum contamination of parenteral nutrition should be assessed regularly.

Aluminum contamination of parenteral nutrition and aluminum loading in children on long-term parenteral nutrition.

Children who are receiving parenteral nutrition are at risk of aluminum overload, which may contribute to such side effects as osteopenic bone disease. The aim of the present study is to determine the aluminum contamination of parenteral nutrition solutions and their components, and to assess the aluminum status of children on long-term parenteral nutrition. Aluminum concentrations were determined by graphite furnace absorption spectroscopy in components and in final parenteral nutrition solutions. The urinary aluminum excretion and plasma aluminum concentration were determined in 10 children on long-term parenteral nutrition. The mean aluminum concentration in the administered parenteral nutrition solutions was 1.6 +/- 0.9 micromol x l(-1)(mean +/- standard deviation (SD)). The resulting mean aluminum daily intake of the 10 patients was 0.08 +/- 0.03 micromol x kg(-1) x day(-1). Compared to two previous studies performed in 1990 and in 1995 in our hospital, the aluminum contamination of parenteral nutrition solutions and the daily aluminum intake of the children seemed to decrease. However, the plasma aluminum concentration and daily urinary aluminum excretion of the children still remain above normal standards. The children had no clinical symptoms of bone disease but aluminum accumulation in tissue can not be excluded. To prevent this iatrogenic toxicity, the aluminum contamination of parenteral nutrition should be assessed regularly.

Direct determination of aluminium in serum and urine by electrothermal atomic absorption spectrometry using ruthenium as permanent modifier

Ruthenium (Ru), thermally deposited on a integrated platform graphite furnace, was investigated as a permanent modifier for the determination of Aluminum (Al) in blood serum and urine by electrothermal atomic absorption spectrometry (ETAAS). The platform was treated with 500 μg of Ru as previously described. The pyrolysis and atomization temperatures for each material were of 1300 and 2300 °C, for serum sample and of 1000 and 2400 °C, for urine. The characteristic mass were of 31 and 33 pg for Al in serum sample and urine, respectively (recommended of 31 pg for Al in nitric acid 0.2% (v/v)). For this reason, the calibration was made with aqueous solutions for both the samples. Calibration curves presented r of 0.99145 and 0.99991 for serum and urine, respectively. With the optimized temperatures, being analyzed eight spiked blood serum samples, the recovery was between 95.90 and 113.50%. Two certified urines samples were analyzed with good agreement between experimental and reference values. In both the samples the R.S.D. were <5% ( n=3). The detection limit ( k=3, n=10) was of 0.40 μg of Al per liter for both the samples. The absorption pulses obtained were symmetrical, with very low background and without interferences. The life time of the tube-platform was higher than 600 cycles of atomizations for both the urine and serum samples.

Further studies on the interrelationship of aluminum and silicon in patients receiving aluminum hydroxide therapy for dyspepsia and factors that relate to the solubilization of aluminum

AbstractIt is known that the intake of aluminum‐containing antacids is related to increases in serum concentration and the urinary output of aluminum, and that silicon intake as orthosilicic acid may facilitate renal excretion of aluminum. However, how either the amount of antacid ingested or the therapy period affects these and the subsequent interrelationship of aluminum and silicon has not been fully investigated. In addition, factors that affect the solubility of aluminum hydroxide need further clarification. A study of 122 patients with dyspepsia who were receiving aluminum hydroxide therapy and 144 healthy controls confirmed that, in the patients, serum and urine aluminum (0.39 ± 0.21 and 2.02 ± 2.0 μmol/L, mean ± 1 SD, respectively) were slightly but significantly increased (P &lt; 0.05) compared with the controls (0.21 ± 0.13 and 1.55 ± 0.89). However, there was no evidence of any association between these changes and the amount ingested or the therapy period. Urine silicon although increased in the patients (716 ± 488 μmol/L) compared with the controls (472 ± 333 μmol/L) was not affected by the amount or time of therapy but was just significantly correlated with the urine (r = +0.19, P = 0.03) and serum aluminum (r = +0.13, P = 0.05) in the combined groups. Thus, the renal excretion of silicon and aluminum may in some part be interdependent. Studies into factors that affect the solubility of aluminum from aluminum hydroxide indicated that at a pH &gt; 3.5 the solubility of aluminum reduced significantly. However, addition of 5 or 20 mmol/L phosphate had no significant effect. With a synthetic food, solubility of aluminum was markedly increased even at the elevated pH 5.5. Thus, the pH, as well as the chemical complexity of the mixture, is an important factor in affecting solubilization of aluminum. The potential of increased exposure to aluminum could be dependent on co‐ingestion with food components and may explain the increased risk to renal failure patients on aluminum‐containing phosphate binders. J. Trace Elem. Exp. Med. 15:9–19, 2002. © 2002 Wiley‐Liss, Inc.

The influence of fluoride ingestion on urinary aluminum excretion in humans.

Fluoride (F) and aluminum (Al) are both ingested daily in water, foods, and pharmaceuticals. Owing to the strong chemical affinity between F and Al, these elements can interact in biological systems. The purpose of the present study was to investigate the influence of F ingestion on Al excretion in humans. Six healthy volunteers ingested 100 ml of distilled water at 6:00 a.m. on day 1 (control period) and the same volume of sodium fluoride solution containing 5 mg of F at 6:00 a.m. on day 2 (test period). A schedule for meals and for blood and urine collection was followed for the two successive days. The concentration of F was measured with an F-electrode, and Al was determined by ion-pair RP-HPLC with its complexation with 8-quinolinol. The mean concentration of serum F peaked within 30 minutes after ingestion of F and rapidly decreased thereafter, reaching baseline 24 hours later. In control period, there was no increase of Al concentration in serum in 24 hours. In test period, Al concentration in serum did not increase significantly compared with those in control serum. Although some variation was observed among subjects, cumulative amounts of F and Al excreted in urine during the test period were significantly higher than those during the control period. The results suggest that absorbed F enhanced urinary Al excretion and that the Al in urine may be, at least in part, derived from endogenous tissues.

Direct and simultaneous determination of copper, chromium, aluminum, and manganese in urine with a multielement graphite furnace atomic absorption spectrometer.

A simple method was developed for the direct and simultaneous determination of copper, chromium, aluminum, and manganese in urine using a multielement GFAAS (Perkin-Elmer SIMAA6000). Pd was used as the chemical modifier along with a special purge gas (5% H2 in Ar). A simple calibration curve method can be used (with 1:1 dilution). A standard reference material (Seronorm Trace Elements Urine) was used to find the optimal temperature program and to confirm the accuracy of the technique. The analyzed values were within 90-110% of the certified values. The relative standard deviations were 1.7, 1.5, 1.6, and 1.5% for these four elements and the detection limits were 0.08 microg L(-1) for Cu, 0.05 microg L(-1) for Cr, 0.06 microg L(-1) for Al, and 0.06 microg L(-1) for Mn. The recoveries of Cu, Cr, Al, and Mn from real urine samples were 100 +/- 5%, except for Cu (80%). The found values of Cu, Cr, Al, and Mn in a real urine sample were 14.3, 0.78, 18.9, and 0.06 microg L(-1), respectively. Scanning electron micrographs were used to investigate the physical form of Pd on the surface of the platform in the graphite furnace. Use of 5% H2 in Ar as the purge gas resulted in smaller and more uniformly distributed Pd particles (Pd particle diameters 0.4-0.6 microm using 5% H2 in Ar compared to 0.4-1.2 microm using pure Ar), increasing the effect of the Pd chemical modifier and promoting the efficiency of atomization.

Effects on the nervous system in different groups of workers exposed to aluminium

OBJECTIVETo investigate possible neurotoxic effects in groups of aluminium pot room and foundry workers, aluminium welders, and a small group of workers exposed to aluminium in the production of flake...