Biological Aspects of Aluminium in Food and Water Supply
This report was produced for the Urban Water Research Association of Australia, a now discontinued research program.
Report No UWRAA 201
The literature reviewed for this report indicates that the putative link between aluminium intake and Alzheimer’s disease appears to be weak if it exists at all, but it remains open to scientific debate and further investigation.
If in the future, research demonstrates an association between aluminium intake and adverse health effects, then there are a number of population sub-groups who would most likely be at higher risk than the “normal, healthy, adult” population. These sub-groups include infants [particularly low birth weight infants], children, the elderly and people with renal impairment. That is, those people who are likely to have increased absorption and/or decreased excretion of aluminium, and those who have a low body mass.
Aluminium in the diet comes from foods, food additives, storage and cooking materials and drinking water. Drinking water contributes generally less than 10% to the total daily intake of aluminium. However, other sources of aluminium in the diet are more under discretionary control. Pharmaceutical agents such as aluminium-containing antacids and buffered analgesics potentially contribute substantial amounts of aluminium to the total body burden. There is thought to be dermal aluminium absorption from antiperspirants. Occupational exposure to aluminium can cause very high inhaled intakes, but is controlled by occupational health and safety regulations.
There is evidence that the composition of the diet, particularly the citrate content, can significantly increase the bioavailability of ingested aluminium. It has been suggested, on the basis of one small study in rats, that the aluminium in alum-treated drinking water may be more readily bioavailable than aluminium derived from other dietary sources and may be retained in brain tissue, but greater absorption of aluminium from drinking water in humans has not been demonstrated.
There are no well-validated methods for measuring the bioavailability of aluminium in humans, nor for determining total body burden of aluminium and its storage sites in live human beings. Our knowledge about the dynamics of aluminium metabolism in humans is largely inferred from the results of studies in rats. Analytical techniques used in human aluminium balance studies are not sufficiently 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 forms of ingested aluminium are converted to the highly soluble form (or forms) when exposed 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 more bioavailable to humans than other forms of aluminium in foods could bed discounted.
The question for public bodies whose practices with respect to aluminium may have an impact on public health, such a as Australia’s water authorities, is where does the balance of evidence lie? There is possibly a link between very high levels of occupational exposure to aluminium and cognitive decline. However, at lower levels of aluminium intake, there is no clear evidence of a public health problem, but there is much public speculation about the dangers of aluminium.
Potentially molecular biologists will discover the aetiology of Alzheimer’s disease, and perhaps of cognitive decline, in the next few years.