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2064318 
Technical Report 
Neurotoxicity of Aluminum 
Marquis, JK 
1989 
NIOSH/00193365 
T 
0 
289-298 
eng 
The neurotoxicity of aluminum (7429905) was reviewed. The major sources of human exposure to aluminum were listed, including drinking water, residues in food, cooking utensils, food and beverage packaging, antacid preparations, antiperspirant formulations, and acidic substances leaching into groundwater. Pathological conditions that have been associated with aluminum exposure included dialysis encephalopathy, Parkinsonian dementia of Guam, Alzheimer's disease, and osteomalacia. It was noted that the apparent association of aluminum exposure with neurotoxicity requires careful evaluation since aluminum is the third most abundant element on the earth and has been generally regarded as safe. The transport of aluminum across biological membranes was discussed. Studies in rats have shown that aluminum increases the permeability of the blood/brain barrier to small peptides and that aluminum may be able to form complexes with lipids. In-vivo studies of aluminum neurotoxicity have shown that intraventricular injections of aluminum cause altered neurotransmitter uptake in isolated synaptosomes and decrease acetylcholinesterase (AChE) and choline-acetyltransferase activities in the brain and spinal cord that can be correlated with areas of neurofibrillary degeneration. Brain dopamine concentrations and AChE activity were decreased and brain dopamine-beta-hydroxylase and phenyl-N-methyl-transferase activities were altered in rats given aluminum in their diet. In-vitro studies have shown that aluminum alters dopamine uptake, decreases glucose utilization, and decreases calcium influx into rat brain synaptosomes. Aluminum altered membrane fluidity and phospholipid constituents in isolated membranes. The effects of aluminum on AChE activity were discussed. Aluminum-chlorohydrate (12042910) at 1 to 5 millimolar has been shown to stimulate purified bovine caudate nuclear AChE, but noncompetitively inhibit it at higher concentrations. The author concludes that the ability of aluminum to inhibit AChE is hard to reconcile with the notion that aluminum is a causative agent for Alzheimer type senile dementias. Data are insufficient to create an adequate working biochemical model for aluminum neurotoxicity.