Aluminium toxicokinetics: An updated MiniReview

This MiniReview updates and expands the MiniReview of aluminium toxicokinet ics by Wilhelm et al. published by this journal in 1990. The use of Al-26, analyzed by accelerator mass spectrometry, now enables determination of Al toxicokinetics under physiological conditions. There is concern about alumi nium in drinking water. The common sources of aluminium for man are reviewe d. Oral Al bioavailability from water appears to be about 0.3%. Food is the primary common source. Al bioavailability from food has not been adequatel y determined. Industrial and medicinal exposure, and perhaps antiperspirant use, can significantly increase absorbed aluminium. Inhalation bioavailabi lity of airborne soluble A appears to be about 1.5% in the industrial envir onment. Al may distribute to the brain from the nasal cavity, but the signi ficance of this exposure route is unknown. Systemic Al bioavailability afte r single underarm antiperspirant application may be up to 0.012%. All intra muscularly injected Al, e.g. from vaccines, may eventually be absorbed. Al distributes unequally to all tissues. Distribution and renal excretion appe ar to be enhanced by citrate. Brain uptake of Al may be mediated by Al tran sferrin and Al citrate complexes. There appears to be carrier-mediated effl ux of Al citrate from the brain. Elimination half-lives of pears have been reported in man, probably reflecting release from bone. Al elimination is p rimarily renal with 2% excreted in bile. The contribution of food to absorb ed Al needs to be determined to advance our understanding of the major comp onents of Al toxicokinetics.