The bioavailability and metabolism of aluminium compounds in man.

Considerable concern has been expressed regarding the possible toxicity of A1 in the body. In particular, many workers have speculated that this metal may be an important causative agent in Alzheimer’s disease (e.g. McLachlan, 1991) as this disease is characterized by a dementia that is similar to dialysis dementia which is known to be caused by the accumulation of A1 in the brain (Alfrey et al. 1976). It has been claimed that this speculation is supported by the results of a number of epidemiology studies linking the incidence of Alzheimer’s disease with exposure to A1 in drinking water. However, the power of these studies was generally low and the best of them, a French study, failed to demonstrate a link (Michel et al. 1991). Moreover, analytical studies conducted at the Harwell Laboratory (in collaboration with the Newcastle Medical Research Council (MRC) group) which use SIMS to demonstrate the presence of A1 in brain tissues, show no consistent difference between the levels of this metal in normal and diseased brain tissues. Similar results have been obtained elsewhere and, although some groups still claim to be able to detect high levels of Al in the brain of dementia patients, most workers now agree that this metal is unlikely to be implicated in the causation of Alzheimer’s disease. However, A1 is toxic at high concentrations within the body. The occurrence of dialysis dementia in renal patients, who accumulated high levels of A1 due to its presence in the water used for dialysis is well documented, as are the occurrence of Al-induced bone disease (Klein et al. 1982; Visser & Van de Vyver, 1985) and microcytic anaemia (Elliott & McDougall, 1978) and the suppression of parathyroid hormone excretion (CournotWitmer et al. 1981). The occurrence of these ‘high-level effects’ has been reviewed by many authors including by De Broe & Van de Vyver (1985), Van de Vyver & Visser (1990) and Ward (1991). In addition, impaired brain function has been claimed at lower concentrations in the body, for example as a result of the occupational exposure of gold miners to inhaled Al, McIntyre powder (Rifat et al. 1990), and in members of the general public following the Camelford accident in the UK (Edwardson, 1992). Also, dietary Al, as lactate, albeit at high levels, has been demonstrated to delay brain maturation in weanling rats (H. M. Wisniewski, personal communication) and to cause learning difficulties in young mice