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In 2006, the Joint Food and Agriculture Organization/World Health Organization Expert Committee on Food Additives (JECFA) re-evaluated the toxicology of aluminium. JECFA reduced its Provisional Tolerable Weekly Intake (PTWI) of aluminum from all sources, including food additives.Aluminium has not been labelled as being carcinogenic, but, “aluminium production” has been classified as carcinogenic to humans by the International Agency for Research on Cancer (IARC) (for further explanation, please see Effects on Humans, Effects from Occupational Exposure, Cancer).

Many countries have set occupational limits for exposure to aluminium dust and aluminium oxide. For non-occupational environments, limits have been set for intake in foods and drinking water.

Uses of Aluminium and its compounds

Aluminium oxides are used as food additives and in the manufacture of, for example, abrasives, refractories, ceramics, electrical insulators, catalysts, paper, spark plugs, light bulbs, artificial gems, alloys, glass and heat resistant fibres.

Aluminium hydroxide is used widely in pharmaceutical and personal care products. Food related uses of aluminium compounds include preservatives, fillers, colouring agents, anti-caking agents, emulsifiers and baking powders; soy-based infant formula can contain aluminium. Natural aluminium minerals especially bentonite and zeolite are used in water purification, sugar refining, brewing and paper industries.

Food is one of the major intake source of aluminium, followed by drinking water. When considering bioavailability, namely the fraction that is actually taken up into the blood stream, food is again the primary uptake source for individuals not occupationally exposed. However, chronic use of antacids, buffered aspirins and other medical preparations would likely constitute the major uptake source, even when exposed at work.

Effect on Humans
The toxicity of Al has been extensively reviewed by the World Health Organization, for the US Department of Health and Human Services, and most extensively by a multi-national group led by Daniel Krewski (WHO 1997; ATSDR 2008; Krewski et al. 2007).

When hemodialysis was initially extensively used, some patients developed a progressive encephalopathy that was fatal within 6 months. Dialysis (associated) encephalopathy (aka: dialysis dementia) is characterized by dyspraxia, dysarthria, emotional changes, trembling, ataxia, myoclonus, and fatal convulsions. It is associated with elevated levels of Al in the brain, and serum Al > 80 μg/L (Nieboer et al. 1995).

Dialysis encephalopathy was due to Al contamination of the dialysis fluids and administration. Exposure to lower levels of Al than those that caused Al-induced encephalopathy can produce a low turnover bone disease and a microcytic anemia.

Aluminum-induced bone disease Aluminum-induced low-turnover bone disease is manifest anemia.

Studies conducted in some species of experimental animals suggest that various aluminum compounds, when added to the diet or to drinking water at high enough levels, are capable of causing adverse effects related to reproduction, neurological behaviour and neurological development.

Aluminum is often suggested as a possible cause of Alzheimer’s disease; although, to date research results that suggest an association between high aluminum accumulation in the body and Alzheimer’s disease are not considered conclusive.


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