HUMAN HEALTH RISK ASSESSMENT FOR ALUMINIUM, ALUMINIUM OXIDE, AND ALUMINIUM HYDROXIDE http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782734/pdf/nihms33559.pdf
Aluminum and Alzheimer’s Disease – Effects on Laboratory Mammals and In Vitro Test Systems, Neurotoxicity, Alzheimer’s Disease, studies reported aluminium may affect levels of cholesterol, which has been suggested in numerous studies as a potential modulator or Alzheimer-type amyloid formation.
Aluminum and Dementia: In a study of 20 AD subjects aged 65 to 76 , the blood aluminium was significantly greater at 60 minutes than in control subjects (104 vs. 38 μg/L).In the older subjects, the increase in blood aluminium levels was greater, but not statistically different, in the controls than in patients, in contrast to the younger subjects. Based on greater serum and urine aluminium patients with dementia appear to absorb more aluminium from the diet than healthy subjects.
Gilbert-Barness et al. (1998) reported the case of a 9-year-old female who was found not to be progressing developmentally at the age of 2 months. At the age of 4 months the child was diagnosed with a neurodegenerative disorder with severe mental retardation. The patient’s condition progressively worsened, resulting in death at the age of 9 years. Autopsy revealed CNS cortical atrophy, small basal ganglia, and hypomyelination of the spinal cord, cerebral cortex, subcortex and cerebellar white matter. Following autopsy it was discovered that the mother had taken an average of 75 Maalox® tablets (containing 200 mg of aluminium hydroxide per tablet) each day during the pregnancy. These results suggested that the high levels of aluminium intake by the mother, during critical periods of the foetus’ brain development, resulted in neurological damage to the infant.
Increased oral aluminium absorption has been suggested in Alzheimer’s disease (AD) and Down’s subjects.
Tissue aluminium concentration increases with age. Some studies have reported that the aluminium concentration in the bulk brain samples, neurofibrillary tangles (NFT) and plaques was higher in AD subjects than controls.
Serum aluminium > 30 μg/L in dialysis patients has been associated with osteomalacia and related disorders and > 80 μg/L associated with encephalopathy.
Aluminium may be able to enter the brain from the nasal cavity by a direct route, bypassing systemic circulation, but convincing evidence is lacking. Absorption of aluminium from intramuscularly (i.m.) injected aluminium hydroxide and aluminiun phosphate adjuvants is significant, and may eventually be complete. Tissue aluminium concentration increases with age. The form of aluminium most often presented to tissues outside of the blood stream is expected to be bound to Tf. In brain, aluminium is prone to dissociate from Tf as a soluble citrate salt. Most cells of the central nervous system (CNS) express Tf receptor, and thus receptor-mediated uptake would be one mechanism by which aluminium could enter cells of the brain. Free flow endocytosis of aluminium citrate could be an alternative route of uptake.
Conclusions—This report synthesizes data from relevant studies on potential health effects of exposure to aluminium to quantify risk using the four-step process specified by the National Research Council: 1) hazard identification, 2) exposure assessment, 3) dose-response assessment, and 4) risk characterization. Hazard identification qualitatively identifies adverse effects by route of exposure, and determines whether those effects are likely in humans at some level of exposure, perhaps much greater than exposure levels experienced in the population of interest. It is important to note that the identification of effects that can be caused by aluminium says nothing about how likely those effects are at exposure levels in human populations. That probability depends on the level of exposure and the dose-response relationship.
Exposure assessment, dose-response assessment, and risk characterization were conducted for those effects for which the evidence was judged to be either strong or modest.
HUMAN HEALTH RISK ASSESSMENT FOR ALUMINIUM, ALUMINIUM OXIDE, AND ALUMINIUM HYDROXIDE Daniel Krewski1,2, Robert A Yokel3, Evert Nieboer4, David Borchelt5, Joshua Cohen6, Jean Harry7, Sam Kacew2,8, Joan Lindsay9, Amal M Mahfouz10, and Virginie Rondeau11