Aluminum body burden

The major population at risk for aluminum loading and toxicity consists of individuals with renal failure. In a study by Alfrey (1980), 82% of nondialyzed uremic patients and 100% of dialyzed uremic patients had an increased body burden of aluminum. The decreased renal function and loss of the ability to excrete aluminum, ingestion of aluminum compounds to lessen gastrointestinal absorption of phosphate, the aluminum present in the water used for dialysate, and the possible increase in gastrointestinal absorption of aluminum in uremic patients can result in elevated aluminum body burdens. The increased body burdens in uremic patients has been associated with dialysis encephalopathy (also referred to as dialysis dementia), skeletal toxicity (osteomalacia, bone pain, pathological fractures, and proximal myopathy), and hematopoietic toxicity (microcytic, hypochromic anemia). Pre-term infants may also be particularly sensitive to the toxicity of aluminum due to reduced renal capacity (Tsou et al. 1991)... 

Flora SJS, Dhawan M, Tandon SK. 1991. Effects of combined exposure to aluminum and ethanol on aluminum body burden and some neuronal, hepatic and hematopoietic biochemical variable in the rat. Hum Exp Toxicol 10 45-48. 

Chronic renal failure/dialysis During sucralfate administration, small amounts of aluminum are absorbed. Concomitant use with other aluminum-containing products may increase the total body burden of aluminum. Patients with chronic renal failure or receiving dialysis have impaired excretion of absorbed aluminum, and aluminum is not dialyzed. Aluminum accumulation and toxicity have occurred. 

Aluminum occurs normally in the body tissues of humans (Ganrot 1986). The total body burden of aluminum in healthy human subjects is approximately 30-50 mg (Allfey 1981, 1984 Allfey et al. 1980 Coumot-Witmer et al. 1981 Ganrot 1986 Hamilton et al. 1972/73 Tipton and Cook 1963). Of the total body burden of aluminum, about one-half is in the skeleton, and about one-fourth is in the lungs (Ganrot 1986). Most of the aluminum detected in lungs is probably due to accumulation of insoluble aluminum compounds that have entered the body via the airways (Ganrot 1986). Most of the aluminum in other parts of the body probably originates from food intake. 

In rabbits given a single intravenous dose of aluminum lactate, aluminum concentrations did not increase above controls in the cerebellum, white brain tissue, hippocampus, spinal cord, adrenal glands, bone, heart, testes, or thyroid (Yokel and McNamara 1989). Treated animals did have significant increases of aluminum in the liver, serum, bile, kidneys, lungs, and spleen. The liver of exposed rabbits had over 80% of the total body burden of aluminum. Persistence of aluminum in the various tissues, organs, and fluids varied. Estimated half-times of aluminum were 113, 74, 44, 42, 4.2, and 2.3 days in the spleen, liver, lungs, serum, renal cortex, and renal medulla, respectively. The kidneys of treated rabbits also demonstrated a second half-time which exceeded 100 days. 

Reliable monitoring data for the levels of aluminum in contaminated media at hazardous waste sites are needed so that the information obtained on levels of aluminum in the environment can be used in combination with the known body burdens of aluminum to assess the potential risk of adverse health effects in populations living in the vicinity of hazardous waste sites. 

Rifat SL, Eastwood MR, McLachlan DRC, et al Effect of exposure of miners to aluminium powder. Lancet 336 1162-1165, 1990b Riihimaki V, Hanninen H, Akila R, et al Body burden of aluminum in relation to central nervous system function among metal inert-gas welders. Scand J Work Environ Health 26 118-130, 2000... 

Many types of biological specimens can be analyzed for aluminum. Tissue and bone have been suggested as the specimens of choice to evaluate the true body burden [23-2S]. Since these specimens are not obtainable on a regular basis, blood aluminum levels have been analyzed to reflect a subject s aluminum burden [26-28], Most of these methods use serum or plasma as intUcator specimen. The monitoring of aluminum levels in these specimens is considered to be the most appropriate approach to ensure that aluminum toxicity problems do not develop in individual uremic or renal dialysis patients [27]. Urine samples have been analyzed for aluminum content for the biological monitoring of occupationally exposed persons. 

Exley C, Swarbrick L, Gherardi RK, Authier FJ. A role for the body burden of aluminum in vaccine-associated macro-phagic myofasciitis and chronic fatigue syndrome. Med Hypotheses 2009 72(2) 135-9. 

Historically, aluminum has not been considered an important toxicant. With the total body burden of aluminum less than 30 mg, it was thought that the skin, gastrointestinal tract, emd lungs were effective barriers in excluding environmentfil aluminum from interned entry. ... 

Dihydropteridine reductase is an important enzyme in the synthesis of several important neurotransmitters, such as tyrosine and acetyl choline. They found that erythrocyte levels of dihydropteridine reductase activity were less than predicted values, and correlated with plasma aluminum levels (Altmann et ah, 1987). After treatment with desferrioxamine, red cell dihydropteridine reductase activity levels doubled. Although brain levels of dihydropteridine reductase activity were not evaluated, it was suggested that high brain aluminum levels might lead to decreased availability of dihydropteridine reductase in the brain. It has been suggested that the mere presence of an increased body aluminum burden has an adverse effect on overall mortality (Chazan et al, 1988). More specifically, an increased body aluminum burden (estimated by the desferrioxamine infusion test) has been associated with memory impairment and increased severity of myoclonus with decreased motor strength (Sprague et al., 1988). 

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