Evaluation of aluminium concentrations in samples of chocolate and beverages by electrothermal atomic absorption spectrometry

Literature regarding the biochemistry of aluminum and eight similar ions is reviewed. Close and hitherto unknown similarities were found. A hypothetical model is presented for the metabolism, based on documented direct observations of Al3+ and analogies from other ions. Main characteristics are low intestinal absorption, rapid urinary excretion, and slow tissue uptake, mostly in skeleton and reticuloendothelial cells. Intracellular Al3+ is probably first confined in the lysosomes but then slowly accumulates in the cell nucleus and chromatin. Large, long-lived cells, e.g., neurons, may be the most liable to this accumulation. In heterochromatin, Al3+ levels can be found comparable to those used in leather tannage. It is proposed that an accumulation may take place at a subcellular level without any significant increase in the corresponding tissue concentration. The possible effects of this accumulation are discussed. As Al3+ is neurotoxic, the brain metabolism is most interesting. The normal and the lethally toxic brain levels of Al3+ are well documented and differ only by a factor of 3-10. The normal brain uptake of Al3+ is estimated from data on intestinal uptake of Al3+ and brain uptake of radionuclides of similar ions administered intravenously. The uptake is very slow, 1 mg in 36 years, and is consistent with an assumption that Al3+ taken up by the brain cannot be eliminated and is therefore accumulated. The possibility that Al3+ may cause or contribute to some specific diseases, most of them related to aging, is discussed with the proposed metabolic picture in mind.

Aluminum ion is bound to at least one of the two specific iron binding sites of serum transferrin and also to serum albumin, as shown by in vivo competition studies with 67-Ga, gel filtration chromatography and ultraviolet difference spectroscopy. Binding of aluminum to transferrin requires CO2 and therefore involves a specific iron site. Samples of commercial transferrin contained large amounts of aluminum. Aluminum may cause anemia by entering pathways of iron distribution and metabolism.

Comparisons of maps and correlation and regression analysis indicate a geographical association between aluminium (Al) in drinking water and registered death rates with dementia (coded from death certificates as the underlying or a contributory cause of death) in Norway. High levels of Al in drinking water are in most cases related to acid precipitation. In general, correlations between aggregate environmental measurements and mortality are a weak source of evidence for risk factors for disease, however, and interpretations regarding cause-and-effect relationships should therefore be made with great care. The major uncertainty probably relates to the use of registered death rates with dementia as a measure of incidence rates of Alzheimer's disease. The dementia rates are correlated with population density, and it is possible that the association between AI and dementia might be due to differences in diagnosis and reporting of dementia. Thus, the present study can only be regarded as introductory, and further epidemiological studies are needed to help elucidate the role of AI in Alzheimer's disease. The results provide little evidence of an association between AI in drinking water and Parkinson's disease or amyotrophic lateral sclerosis.