This thesis investigates the uptake, transport and excretion of toxic aluminium, with reference to it's speciation, in the human body. The long-lived isotope 26Al (t½= 7.16 X 10e5 years), of negligible natural abundance and low radiological hazard, made an ideal physiological tracer. Measurement by Accelerator Mass Spectrometry eliminated the insufficient detection limits and isobaric interference, due to the biologically abundant 26Mg, encountered by conventional decay techniques. Chapter One outlines basic aluminium chemistry, metabolism and the relevant biomedical literature on aluminium toxicity. The second Chapter briefly outlines the different analytical techniques employed with emphasis on the applications of, and 26Al measurement by Accelerator Mass Spectrometry. The preparation of biological samples, including development work, is also discussed. Chapter Three monitors blood and urine 26Al within one human over a period of one year post ingestion. A proposed kinetic model is included in the data analysis and a projected value for aluminium retention for the individual's life-span. The distribution of 26Al between the low and high molecular weight fractions of plasma was determined by an ultrafiltration technique. Chapter Four details a human uptake study (n = 5) on the effect of natural and artificial solutions of dissolved silicate on the uptake and excretion of 26Al. Whilst no substantial effect of silicate on the uptake of aluminium was found there was some evidence of altered renal clearance. Chapter Five is a continuation of Chapter Four. It exploits the theory of Dr. J.P. Powell that the silicon speciation is critical [Taylor, 1997 #582]. Oligomeric silicate reduced the uptake of 26Al significantly in comparison to monomeric silicate. Finally Chapter Six investigated the 26A1 protein binding using ion exchange chromatography. Transferrin was found to be major 26Al transport protein.