Several neurological effects have been attributed to aluminum intoxication. In weanling rats, dietary aluminum fed at high levels to their dams has been demonstrated to delay brain maturation. This effect has not been described in man.

Aluminum-induced impairment of cognitive function following the occupational exposure of gold miners to inhaled aluminum, the exposure of members of the general public to ingested aluminum sulfate, and, recently, exposure of workers and ex-workers in the aluminum industry has been claimed but not proven. No convincing evidence has been produced to either support or refute the existence of neurological effects at low levels of aluminum uptake. However, there is sufficient evidence that such effects may occur in man at some levels of uptake. For example, dialysis patients exposed to lower than average levels of aluminum sometimes demonstrate disturbed cerebral function compared to controls.

In one study of dialysis patients, correlations were sought between cognitive function and exposure to aluminum in both dialysis source water and administered oral gut phosfate binders. The results of the study were confusing since it found negative correlations between the cognitive measures and source water aluminum but positive correlations with the level of orally administered phosfate binder. Again, in a gold miner study, some results indicated cognitive impairment, whereas others were less conclusive. It has been noted that most studies performed to date are flawed, because they have failed to include normal aging controls. Attempts to improve cognitive scores by chelation therapy have met with very limited success.

The most important neurological effects produced by aluminum occur at large body burdens. These include ataxia, dysarthria, dysphagia, myoclonia, convulsions, and dementia. Epidemiological studies have shown that aluminum-induced encephalopathy (dialysis dementia) was absent at dialysis centers using water with aluminum concentrations less than 50 mgl-1. In contrast, encephalopathy was common in those that employed water with aluminum concentrations greater than 200 mgl-1. At these centers, the prevalence of the disease increased significantly with increasing cumulative exposure to aluminum and was often a direct cause of death. In terminal cases, facial grimacing, myotonic spasms, and dysphagia interfere with eating and lead to inhalation pneumonia and death. The recorded concentrations of aluminum in the brains of such patients are highly variable, but values of 15-100 mgkg-1 are typical. Experience has shown that chelation therapy with desferrioximine is effective in reversing neurological effects in renal patients.

The mechanisms of encephalopathy are not clear. Most evidence suggests that aluminum likely crosses the blood-brain barrier by a transferrin-mediated mechanism. Imaging secondary ion mass spectrome-try has shown aluminum to be deposited within the brain cortex as focal deposits at sites known to be rich in transferrin receptors. These sites, corresponding to the distribution of pyramidal neurones, have a high demand for iron in the synthesis of respiratory chain enzymes. It is suggested that damage at these sites results in the neuropathy.

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