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Re-published by Environmental Assistance with permission from Environmental Data Services Ltd (ENDS). Originally published in The ENDS Report, Issue 297, 1999. For further information see www.endsreport.com
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The toxicity of aluminium and its role in dementia


Aluminium is one of the most abundant elements in the earth's crust but most of it is locked away in minerals such as alumino-silicates. Free, biologically available aluminium is a relative rarity in natural ecosystems. In freshwaters, the metal is toxic to fish at the levels permitted in drinking water, although its bioavailabilty depends on pH and other compounds present.

The chemistry of aluminium is complex. At a high pH it is precipitated and unavailable, while with elements such as silicon or fluorine it forms complexes which reduce its toxicity.

Aluminium appears to be particularly toxic in acid conditions as the Al 3+ ion. Many of the environmental problems associated with acid rain are due to aluminium ions leaching from upland soils which lack elements such as calcium and magnesium.

Speaking at the Craigavon conference, Dr Chris Exley of Keele University explained that fish chronically exposed to aluminium accumulate it in their brains. The metal can be found around blood vessels and nerve cell membranes and in plaques similar to those found in many kinds of dementia. He concluded: "Aluminium is very toxic in high concentrations and there should be no doubt that it will make people very ill."

Professor John Savory of the University of Virginia explained that there was "no doubt at all" of aluminium's neurotoxicity. Hundreds of kidney dialysis patients had died from a syndrome first described in 1972 involving progressive dementia.

The cause was now recognised to be high levels of aluminium in the blood over several years. Another line of evidence was that those occupationally exposed to the metal, such as welders and foundry workers, developed neurological symptoms such as memory loss and poor co-ordination.

One positive link between aluminium and Alzheimer's disease was the discovery of elevated levels of the metal attached to protein tangles inside nerve cells. These neuro-fibrillary tangles are a characteristic feature of the disease and are also found in many other dementias.

Animal experiments
Rabbits injected with aluminium into their spinal fluid develop an Alzheimer's-like dementia within several days, Professor Savory explained. They develop behavioural abnormalities followed by paralysis of the hind limbs, and their brains show the characteristic neuro-fibrillary tangles. While any direct link to Alzheimer's is controversial, the effect has proved a useful model to help understand dementias.

Professor Savory has shown that aged rabbits are more susceptible to the toxic effects of aluminium and develop more protein tangles than young animals. Chelation therapy - a technique which reduces the aluminium circulating in the tissues - is capable of breaking down the tangles, suggesting that the metal may play a role in preventing cell metabolism from breaking down the tangles. The experiment has parallels in humans, where chelation has proved effective in stopping the progressive deterioration which is a feature of Alzheimer's.

Professor Daniel Perl of the Mount Sinai Medical Centre in New York told the meeting of his investigations into neuro-fibrillary tangles which showed that the lesions contained five to ten times the level of aluminium in healthy tissue.

A further link between aluminium and dementia could be found in areas of the western Pacific such as the island of Guam, where the inhabitants are particularly prone to two dementing illnesses. Both are age-related and involve the production of neuro-fibrillary tangles in the brain.

Genetic factors for the illnesses appear unlikely as immigrants are susceptible. However, an important factor may be the island's unusual soils, which are high in leachable aluminium and low in magnesium and calcium. Further studies are needed to investigate intakes of aluminium from drinking water and food. Whatever the cause, lengthy exposure appears necessary, and the latency period may be as long as 40 years. Some Guam natives who had emigrated to the US mainland in early adulthood have since fallen prey to the illness.

Professor Perl concluded that aluminium's role in the formation of neuro-fibrillary tangles is far from understood. However, it appears that the metal may be essential for the formation of the tangles and that the structures could not be broken down by the body. He speculated that aluminium could be an intracellular "tanning mechanism" - binding to the proteins and preserving them. However, he cautioned that aluminium is "not a simple toxin?[Effects] may be more to do with what you drank in childhood than what you are drinking this afternoon."

Epidemiological studies
The Craigavon conference included a presentation by Dr Virginie Rondeau of the medical research institute Inserm, based in Bordeaux.

Dr Rondeau's cohort study of 3,777 ageing people in the Gironde and Dordogne area of south-west France is the latest in a series of investigations into the relationship between aluminium and Alzheimer's disease. Each individual's brain function was assessed using psychometric tests and an examination by a neurologist at the start of the study. Subjects were interviewed subsequently after three, six and eight years. Data on aluminium levels in drinking water were incorporated into the study in 1991-94.

During the study, 253 cases of dementia were diagnosed, of which 182 were identified as Alzheimer's Disease. Some 95% of the supplies came from groundwaters or springs, and the levels of aluminium were rather low - averaging 9µg/l with a range of 1-459µg/l.

However, the amount of cognitive impairment shown by the cohort was related to concentrations of aluminium and silicon and the pH of the supply. The risk ratio for aluminium levels over 100µg/l was significantly elevated at 2.14 - while silica levels of more than 11,250µg/l were associated with a lower risk of dementia of 0.73. However, the study was unable to demonstrate a dose-response relationship between aluminium and dementia.

Canadian research
The study lends support to the findings of Professor Donald McLachlan of Toronto University, a lifelong investigator of aluminium toxicity.

Laboratory-confirmed cases of Alzheimer's disease in Ontario were found to be more common in areas where aluminium levels in drinking water were elevated, and the risk of Alzheimer's increased with rising average aluminium concentrations. For people exposed to levels averaging 100µg/l, the risk of the disease was increased 2.5 times compared to controls - while for levels exceeding 175µg/l the risk was 8.1 times higher.

Professor McLachlan concluded that cutting aluminium in drinking water to minimal levels would reduce cases of the disease by about 40%, while reduction to below 100µg/l would reduce incidence by 23%. He has recommended that concentrations of the metal in drinking water be kept below 50µg/l and the pH at about 7.9.

Other epidemiological studies have failed to find a link between aluminium in water and Alzheimer's. A study published by the Environmental Epidemiology Unit in Southampton in 1997 is one example. The research failed to find any association between cases referred to eight neuro-radiology centres in England and Wales and patients' exposure to aluminium or silicon in drinking water. This was despite the availability of drinking water data for many cases since age 25 years.

Professor McLachlan attributes failures to find a link to the diversity of drinking water supplies and the varying toxicity of different forms of aluminium.

In 1993, the eminent physician Professor Sir Richard Doll concluded that "cognitive impairment and, more specifically Alzheimer's disease, tend to be associated with residence in areas where drinking water is acid and the aluminium content is high." There still seems no good reason to write off that conclusion.



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