Maximum contaminant levels are used to control potential health hazards posed by chemicals in drinking water, but no primary national or international limits for aluminum (Al) have been adopted. Given the differences in toxicological profiles, the present evaluation derives total allowable concentrations for certain water-soluble inorganic Al compounds (including chloride, hydroxide, oxide, phosphate and sulfate) and for the hydrated Al silicates (including attapulgite, bentonite/montmorillonite, illite, kaolinite) in drinking water. The chemistry, toxicology and clinical experience with Al materials are extensive and depend upon the particular physical and chemical form. In general, the water solubility of the monomeric Al materials depends on pH and their water solubility and gastrointestinal bioavailability are much greater than that of the hydrated Al silicates. Other than Al-containing antacids and buffered aspirin, food is the primary source of Al exposure for most healthy people. Systemic uptake of...

Total allowable concentrations of monomeric inorganic aluminum and hydrated aluminum silicates in drinking water.

This review discusses recent literature on the chemical and physiological factors that influence the absorption, distribution, and excretion of aluminum in mammals, with particular regard to gastrointestinal absorption and speciation in plasma. Humans encounter aluminum, a ubiquitous yet highly insoluble element in most forms, in foods, drinking water, and pharmaceuticals. Exposure also occurs by inhalation of dust and aerosols, particularly in occupational settings. Absorption from the gut depends largely on pH and the presence of complexing ligands, particularly carboxylic acids, with which the metal can form absorbable neutral aluminum species. Uremic animals and humans experience higher than normal body burdens of aluminum despite increased urinary clearance of the metal. In plasma, 80-90% of aluminum binds to transferrin, an iron-transport protein for which receptors exist in many tissue. The remaining fraction of plasma aluminum takes the form of small-molecule hydroxy species and small complexes with carboxylic acids, phosphate, and, to a much lesser degree, amino acids. Most of these species have not been observed in vivo but are predicted from equilibrium models derived from potentiometric methods and NMR investigations. These models predict that the major small-molecule aluminum species under plasma conditions are charged and hence unavailable for uptake into tissues.

/pdf/the-biological-speciation-and-toxicokinetics-of-aluminum-572maua2of.pdf

The biological speciation and toxicokinetics of aluminum.

In the present study, an attempt has been made to investigate the distribution of aluminum in different regions of brain and body organs of male albino rats, following subacute and acute aluminum exposure. Aluminum was observed to accumulate in all regions of the brain with maximum accumulation in the hippocampus. Subcellular distribution of aluminum indicated that there was maximum localization in the nucleus followed by cytosolic, microsomal, and mitochondrial deposition. Elution profile of cytosolic proteins on G-75 Sephadex column revealed a substantial amount of aluminum bound to high-mol-wt protein fraction. Aluminum was also seen to compartmentalize in almost all the tissues of the body to varying extents, and the highest accumulation was in the spleen.

Distribution of aluminum in different brain regions and body organs of rat

Dementias: the role of magnesium deficiency and an hypothesis concerning the pathogenesis of Alzheimer's disease.

General.- Historical survey of aluminum-related diseases.- Chemistry of aluminum.- The metabolism of aluminum.- Intestinal absorption of aluminum.- Aluminum determination in biological samples.- Quality control of aluminum measurements.- Pathophysiology.- Pathophysiologic mechanisms of aluminum toxicity: Aluminum-induced bone disease.- Aluminum encephalopathy: Experimental vs human.- Alzheimer's disease: Aluminum and fibrinous proteins.- Aluminum interaction with macromolecules and membranes.- Cellular and subcellular localization of aluminum: Histochemistry.- Cellular and subcellular localization of aluminum.- Experimental models of aluminum toxicity.- Clinical.- Sources of aluminum.- Unusual sources of aluminum.- Experimental aluminum induced bone disease.- Aluminum induced bone disease: Clinical features.- Aluminum induced bone disease: Histology.- Dialysis encephalopathy.- Other clinical syndromes associated with aluminum. Microcytic anemia, joint pain, severe infections, liver dysfunction.- Aluminum toxicity in childhood.- Occupational exposure to aluminum and its compounds and their health effects.- Diagnosis.- The Diagnosis of aluminum toxicity.- Treatment.- Deferoxamine therapy of aluminum toxicity in dialysis patients.- Alternative phosphate binders for aluminum hydroxide.- Risk factors for aluminum toxicity and its prevention.- Index of subjects.

Aluminum and Renal Failure

Role of plasma aluminum in the detection and prevention of aluminum toxicity.

In a region with a relatively low incidence of aluminum toxicity water, dialysis fluid and plasma aluminum were monitored in hemodialysis patients before and after the introduction of reverse osmosis (RO) water. Before the use of RO water, there was a close correlation between plasma and dialysis fluid aluminum with exposure to aluminum being reflected equally by either water, dialysis fluid or plasma aluminum. Patients with clinical manifestations of aluminum toxicity were characterised by a plasma aluminum consistently greater than mumol/l and a dialysis fluid aluminum consistently greater than 1 mumol/l. No evidence of clinical toxicity was found in patients in whom the plasma aluminum was maintained up to 5 mumol/l. Following the introduction of RO water, the dialysis fluid aluminum was able to be maintained less than 1 mumol/l, the plasma aluminum fell and no new cases of clinical toxicity were identified over the following five years. An effect of aluminum hydroxide dosage on plasma aluminum could be identified only in patients in whom the dialysis fluid aluminum was less than 1 mumol/l. Plasma aluminum was found to be a poor guide to bone stores but appeared to correlate better with the presence of bone toxicity than total bone aluminum. Regular monitoring of dialysis fluid and plasma aluminum is recommended as a means of detecting exposure to aluminum as well as the source of exposure and as a guide to the risk of clinical toxicity.

What is the value of plasma/serum aluminum in patients with chronic renal failure?

Epidemiology of Aluminium Toxicity in a ‘Low Incidence’ Area

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Role of plasma aluminum in the detection and prevention of aluminum toxicity.

What is the value of plasma/serum aluminum in patients with chronic renal failure?

Epidemiology of Aluminium Toxicity in a ‘Low Incidence’ Area