ReportNo WSAA 201

December 1996




Theliterature reviewed for this report indicates that the putative link betweenaluminium intake and Alzheimer’s disease appears to be weak if it exists atall, but it remains open to scientific debate and further investigation.


If inthe future, research demonstrates an association between aluminium intake andadverse health effects, then there are a number of population sub-groups whowould most likely be at higher risk than the “normal, healthy, adult”population. These sub-groups include infants [particularly low birth weightinfants], children, the elderly and people with renal impairment. That is,those people who are likely to have increased absorption and/or decreasedexcretion of aluminium, and those who have a low body mass.


Aluminiumin the diet comes from foods, food additives, storage and cooking materials anddrinking water. Drinking water contributes generally less than 10% to the totaldaily intake of aluminium. However, other sources of aluminium in the diet aremore under discretionary control. Pharmaceutical agents such asaluminium-containing antacids and buffered analgesics potentially contributesubstantial amounts of aluminium to the total body burden. There is thought tobe dermal aluminium absorption from antiperspirants. Occupational exposure toaluminium can cause very high inhaled intakes, but is controlled byoccupational health and safety regulations.


Thereis evidence that the composition of the diet, particularly the citrate content,can significantly increase the bioavailability of ingested aluminium. It hasbeen suggested, on the basis of one small study in rats, that the aluminium inalum-treated drinking water may be more readily bioavailable than aluminiumderived from other dietary sources and may be retained in brain tissue, butgreater absorption of aluminium from drinking water in humans has not beendemonstrated.


Thereare no well-validated methods for measuring the bioavailability of aluminium inhumans, nor for determining total body burden of aluminium and its storagesites in live human beings. Our knowledge about the dynamics of aluminiummetabolism in humans is largely inferred from the results of studies in rats.Analytical techniques used in human aluminium balance studies are notsufficiently sensitive to detect minute amounts of aluminium retention which,over a lifetime, could lead to a critical body burden.


Reiberet al’s (1995) theory that all formsof ingested aluminium are converted to the highly soluble form (or forms) whenexposed to the low pH of the stomach is yet to be proven. If it were confirmed,then the hypothesis that the aluminium in drinking water is somehow morebioavailable to humans than other forms of aluminium in foods could bediscounted.


Thequestion for public bodies whose practices with respect to aluminium may havean impact on public health, such a as Australia’s water authorities, is wheredoes the balance of evidence lie? There is possibly a link between very highlevels of occupational exposure to aluminium and cognitive decline. However, atlower levels of aluminium intake, there is no clear evidence of a public healthproblem, but there is much public speculation about the dangers of aluminium.


Potentiallymolecular biologists will discover the aetiology of Alzheimer’s disease, andperhaps of cognitive decline, in the next few years.


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