Urinary Aluminum Concentrations Research Articles

Prenatal aluminum exposure is associated with increased newborn mitochondrial DNA copy number

Aluminum is a widely distributed metal that has been reported to have embryotoxicity and fetotoxicity in animal studies. However, there has been no study of the association between prenatal aluminum exposure and newborn mitochondrial DNA copy number (mtDNAcn). We aimed to investigate the effect of prenatal aluminum exposure on newborn mtDNAcn. A total of 762 mother-newborn pairs were recruited between November 2013 and March 2015 in Wuhan city, China. We measured maternal urinary aluminum concentrations at three trimesters of pregnancy. Relative mtDNAcn was measured in DNA extracted from umbilical cord blood samples. We used generalized estimating equations to assess the relationship between prenatal aluminum exposure and newborn mtDNAcn. The geometric means of creatinine corrected aluminum concentrations were 31.0 μg/g Cr (95% CI: 27.6, 34.7), 40.9 μg/g Cr (95% CI: 35.7, 46.8) and 58.4 μg/g Cr (95% CI: 51.2, 67.4) for the first, second and third trimesters, respectively. After adjustment for potential confounding factors, a doubling of maternal urinary aluminum concentrations during the second and third trimesters was related to 3.16% (95% CI: 0.88, 5.49) and 4.20% (95% CI: 1.64, 6.81) increases in newborn mtDNAcn, respectively, while the association between maternal urinary aluminum concentration during the first trimester and newborn mtDNAcn was not significant (percent difference: 0.70%, 95% CI: −2.25, 3.73). Prenatal aluminum exposure during the second and third trimesters was positively associated with newborn mtDNAcn. Further studies are essential to elucidate on the potential health consequences of newborn mtDNAcn.

A study of the association between urinary aluminum concentration and pre-clinical findings among aluminum-handling and non-handling workers.

BackgroundAluminum is considered to be a relatively safe metal for humans. However, there are some reports that aluminum can be toxic to humans and animals. In order to estimate the toxicity of aluminum with respect to humans, we measured the aluminum concentration in urine of aluminum-handling and non-handling workers and investigated the relationships between their urinary aluminum concentrations and pre-clinical findings.MethodsTwenty-three healthy aluminum-handling workers and 10 healthy non-aluminum-handling workers participated in this study. Their medical examinations, which were otherwise unremarkable, included the collection of urine and blood. Urinary aluminum levels were analyzed using ICP analysis. As pre-clinical tests, we measured KL-6, SP-D, TRCP-5b, IL-6, and IL-8 in blood and δ-ALA and β2-microglobulin in urine. These were considered to be lung, bone, kidney and inflammation markers. Moreover, we measured 8-OHdG in urine as an oxidative DNA damage marker.ResultsThe aluminum concentration in urine ranged from 6.9 to 55.1 μg/g cre (median: 20.1 μg/g cre) in the aluminum-handling workers and from 5.6 to 15.6 μg/g cre (median: 8.8 μg/g cre) in the non-aluminum-handling workers, with a significant difference between them. In the pre-clinical findings, there were no significant differences between these two groups except in the case of δ-ALA. However, there were no significant relationships between aluminum concentration and the pre-clinical findings, work years, age or 8-OHdG in the aluminum-handling workers.ConclusionsWhile the excretion of aluminum in urine was elevated in aluminum-handling workers, our findings suggest that low-dose aluminum is not directly harmful to humans, at least when workers’ urinary aluminum concentration is below 55 μg/g cre.

Human biomonitoring of aluminium after a single, controlled manual metal arc inert gas welding process of an aluminium-containing worksheet in nonwelders.

Several existing field studies evaluate aluminium welding works but no thoroughly controlled exposure scenario for welding fume has been described yet. This study provides information about the uptake and elimination of aluminium from welding fumes under controlled conditions. In the Aachen Workplace Simulation Laboratory, we are able to generate welding fumes of a defined particle mass concentration. We exposed 12, until then occupationally unexposed participants with aluminium-containing welding fumes of a metal inert gas (MIG) welding process of a total dust mass concentration of 2.5 mg/m(3) for 6 h. Room air filter samples were collected, and the aluminium concentration in air derived. Urine and plasma samples were collected directly before and after the 6-h lasting exposure, as well as after 1 and 7 days. Human biomonitoring methods were used to determine the aluminium content of the samples with high-resolution continuum source atomic absorption spectrometry. Urinary aluminium concentrations showed significant changes after exposure compared to preexposure levels (mean t(1) (0 h) 13.5 µg/L; mean t(2) (6 h) 23.5 µg/L). Plasma results showed the same pattern but pre-post comparison did not reach significance. We were able to detect a significant increase of the internal aluminium burden of a single MIG aluminium welding process in urine, while plasma failed significance. Biphasic elimination kinetic can be observed. The German BAT of 60 µg/g creatinine was not exceeded, and urinary aluminium returned nearly to baseline concentrations after 7 days.

Plasma and Urinary Aluminum Concentrations in Severely Anemic Geophagous Pregnant Women in the Bas Maroni Region of French Guiana: A Case-Control Study

The clays consumed by geophagous individuals contain large quantities of aluminum, a known neurological and hematological toxin. This is the first study to evaluate the risk of aluminum poisoning in geophagous individuals. Blind determinations of plasma and urinary aluminum concentrations were carried out in 98 anemic geophagous pregnant women and 85 non-anemic non-geophagous pregnant women. Aluminum concentrations were significantly higher (P < 0.0001) in the geophagous anemic women than in the controls, with odds ratios of 6.83 (95% confidence interval [CI] = 2.72-19.31) for plasma concentrations (13.92 ± 14.09 μg/L versus 4.95 ± 7.11 μg/L) and 5.44 (95% CI = 2.17-14.8) for urinary concentrations (92.83 ± 251.21 μg/L versus 12.11 ± 23 μg/L). The ingested clay is the most likely source of this overexposure to aluminum. If confirmed, the clinical consequences of this absorption for pregnant women and their offspring should be explored.

Decrements in cognitive performance in metal inert gas welders exposed to aluminium.

OBJECTIVES: Often little has been discovered of the cognitive functions affected by occupational toxins because many functions cooperate to produce the single performance scores typically reported from neuropsychological tests. To...

Speciation and bioavailability of aluminium in drinking water

The form of aluminium in water abstracted for potable supply, in water after treatment, and in water delivered to consumers' taps, has been examined using techniques based on size and chemical reactivity. Speciation in water is compared with that in tea. Although the concentration of the metal in tea is an order of magnitude larger than that in water, its relative contribution to dietary intake depends on the degree of absorption. Bioavailability is examined, using human subjects, via the determination of aluminium concentrations in both serum and urine, after the ingestion of various test drinks. Aluminium in water after treatment was found to be in a more chemically labile form than the metal present in most raw waters. Speciation in tea is dominated by high molecular weight, organically complexed forms. A slight increase in urinary aluminium concentrations was observed after consumption of both a spiked mineral water and tea. This increase was small with respect to the quantity of aluminium ingested, suggesting relatively low bioavailability from both sources.

Effect of aluminum mobilization on hemoglobin during the first six months after transplantation

We prospectively monitored 38 patients for the first six months following successful renal cadaver allograft transplantation. Hemoglobin increased from a mean of 8.2 +/- 0.3 g/dl to 13.4 +/- 0.3 g/dl (SEM), P < 0.001, plasma aluminum decreased from 1.3 +/- 0.2 mumol/liter to 0.46 +/- 0.04 mumol/liter, P < 0.001, and urinary aluminum excretion which peaked at one week post-transplant, 5.5 +/- 1.3 mumol/24 hr decreased to 1.8 +/- 0.3 mumol/24 hr, P < 0.001. Prior to transplantation 22 patients had been prescribed aluminum-containing phosphate binders. Following transplantation this group had persistently greater plasma aluminum and urinary aluminum concentrations which were sustained throughout the study period, compared with those not given aluminum containing medicaments. Hemoglobin and iron status were similar in the two groups prior to transplantation, although red blood cell volume was smaller in those given aluminum-containing phosphate binders, 89 +/- 0.9 fl (fentoliters) versus 95 +/- 1.6 fl, P < 0.05. However, the percentage increase in hemoglobin following transplantation was greater in the group not given aluminum preparations, 34 +/- 4% versus 7 +/- 5% at one month, 69 +/- 7% versus 37 +/- 7% at three months, and 80 +/- 8% versus 56 +/- 8% at six months respectively, all P < 0.05. This study suggests that aluminum mobilization following successful renal transplantation may reduce the rate of hemopoiesis.

Aluminium mobilization following renal allograft transplantation may have an immunomodulatory role by reducing the incidence of graft rejection

Urinary aluminium excretion was prospectively monitored during the first year following first cadaver renal allograft transplantation in 79 consecutive patients. Plasma and urinary aluminium concentrations steadily declined with time. Thirty-five patients had 0-1 episodes of acute graft rejection compared to 44 with two or more rejections; more of the former group had been prescribed aluminium-containing phosphate binders (74% versus 56%, P < 0.02), and following transplantation this group had a persistently greater urinary aluminium excretion, suggesting a greater aluminium body burden. There were no significant differences in terms of gender distribution, blood transfusion, or HLA matching between the groups, thus suggesting that either the subsequent mobilization of aluminium body stores following transplantation and/or the accumulation of aluminium in the reticulo-endothelial system prior to transplantation may have had an immunomodulatory effect in reducing the incidence of renal allograft rejection.

Plasma and urine aluminium concentrations in healthy subjects after administration of sucralfate [see comments

1. Sucralfate (basic sucrose aluminium sulphate), a topical intestinal agent, was administered in suspension or granule form to 25 healthy subjects at a total dose of 4 g day-1 for 21 days. Aluminium in plasma and 24 h urine samples was assayed before, during and after administration of sucralfate by inductively coupled plasma optical emission spectrometry. 2. Sucralfate produced significant increases in plasma and urine aluminium concentrations. On average, plasma aluminium increased from about 2 micrograms 1-1 to more than 5 micrograms 1-1 and 24 h urine aluminium increased from less than 5 micrograms to more than 30 micrograms. Both plasma and urine aluminium concentrations decreased rapidly after sucralfate was stopped. However, urinary aluminium concentrations remained higher than normal 5 and 10 days after discontinuation of sucralfate administration. Moreover subjects receiving sucralfate granules had significantly higher average urinary excretion of aluminium than subjects receiving the suspension. 3. The small but significant increase in plasma and urine aluminium following sucralfate administration in therapeutic doses may reflect intestinal absorption of aluminium. Although such absorption would appear to be moderate in healthy subjects, it is suggested that aluminium-based treatments should be used only intermittently, especially in patients with renal disorders.

Differential Effect of Steroids and Chloroquine on the Intestinal Absorption of Aluminium and Calcium

In rats with normal renal function the intestinal absorption of aluminium appears to be partly vitamin D dependent. To further characterise the similarities between the absorption of aluminium and calcium we investigated the effects of dihydroxylated vitamin D metabolites, prednisolone, and chloroquine (CQ) in Sprague-Dawley rats with normal or reduced renal function. The latter agents interfere with lysosomal functions and have been reported to reduce the intestinal absorption of calcium, whereas vitamin D metabolites may stimulate the absorption of both aluminium and calcium. To assess the intestinal absorption of aluminium we monitored urinary aluminium excretion and serum aluminium concentrations following an oral load of 410 mumol aluminium. Calcium absorption was calculated from the differences between an orally administered dose of 45calcium and faecal excretion. In vitamin-D-deficient rats cholecalciferol and calcitriol augmented urinary aluminium excretion to a similar degree subsequent to an oral load whereas 24R,25(OH)2D3 was without an apparent effect. In vitamin-D-replete rats with normal renal function CQ (225 mg/kg i.p.; 3 days) as well as prednisolone (25 mg/kg; 7 days) significantly reduced calcium absorption (% dose) (CQ: 39 +/- 5%, prednisolone: 42 +/- 3%, control: 58 +/- 11%). In contrast neither drug reduced urinary aluminium excretion (CQ: 519 +/- 92, prednisolone: 494 +/- 137, control: 469 +/- 187 nmol/5 days) or the postload increase in serum aluminium following oral exposure. When aluminium was administered intravenously recovery of aluminium was comparable between treatment groups and controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence of aluminum loading in infants receiving intravenous therapy.

To investigate the possibility that premature infants may be vulnerable to aluminum toxicity acquired through intravenous feeding, we prospectively studied plasma and urinary aluminum concentrations in 18 premature infants receiving intravenous therapy and in 8 term infants receiving no intravenous therapy. We also measured bone aluminum concentrations in autopsy specimens from 23 infants, including 6 who had received at least three weeks of intravenous therapy. Premature infants who received intravenous therapy had high plasma and urinary aluminum concentrations, as compared with normal controls: plasma aluminum, 36.78 +/- 45.30 vs. 5.17 +/- 3.1 micrograms per liter (mean +/- S.D., P less than 0.0001); urinary aluminum:creatinine ratio, 5.4 +/- 4.6 vs. 0.64 +/- 0.75 (P less than 0.01). The bone aluminum concentration was 10 times higher in infants who had received at least three weeks of intravenous therapy than in those who had received limited intravenous therapy: 20.16 +/- 13.4 vs. 1.98 +/- 1.44 mg per kilogram of dry weight (P less than 0.0001). Creatinine clearances corrected for weight did not reach expected adult values until 34 weeks of gestation. Many commonly used intravenous solutions are found to be highly contaminated with aluminum. We conclude that infants receiving intravenous therapy have aluminum loading, which is reflected in increased urinary excretion and elevated concentrations in plasma and bone. Such infants may be at high risk for aluminum intoxication secondary to increased parenteral exposure and poor renal clearance.

Exposure and urinary excretion of aluminum during welding.

The exposure and urinary excretion of aluminum was studied among three previously unexposed volunteers and six welders exposed to welding fumes containing aluminum. The aluminum concentrations in air and urine were determined. The urinary aluminum concentrations rose rapidly in volunteers exposed only for 1 d and returned to the preexposure levels with an estimated half-time of about 8 h. The welders were monitored for one workweek. During the subsequent weekend a decrease in the urinary concentrations occurred in the three welders exposed for two years or less, but such a decrease was not observed among welders exposed for more than 15 years. The urinary concentrations of aluminum were dependent partly on the level of current exposure and partly on the duration of exposure. The data suggest that welders exposed to welding fumes containing aluminum may retain some of the inhaled metal fume for extended periods of time.