| The Biological Speciation and Toxicokinetics of Aluminum Emily DeVoto
1
and Robert A. Yokel
2
1
Department of Environmental Sciences and Engineering, School of Public Health, University of North Carolina at Chapel Hill
2
Division of Pharmacology and Experimental Therapeutics, College of Pharmacy and Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40536-0082 USA Abstract
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 tissues. 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. Key words : absorption, aluminum, citrate, equilibrium modeling, NMR, pharmacokinetics, plasma, speciation, transferrin, uremia. Environ Health Perspect 102:940-951 (1994) http://ehpnet1.niehs.nih.gov/docs/1994/102-11/devoto.html Address correspondence to E. DeVoto, Department of Epidemiology, CB 7400, UNC-Chapel Hill, Chapel Hill, NC 27599 USA. This work was made possible by EPA Cooperative Agreement 818558. We acknowledge the advice and assistance of Louise Ball, James McKinney, and Mark Shuman. Although this paper was funded by the U.S. Environmental Protection Agency and has been submitted to the agency's peer and policy review, it does not necessarily reflect the views of the agency, and no official endorsement of any kind should be inferred. Received 5 October 1993 ; accepted 3 August 1994.
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