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Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

Toxicokinetics of Mullite constituents

Summary of Aluminium toxicokinetics


In experimental animals, absorption of aluminium via the gastrointestinal tract is usually less

than 1%. The main factors influencing absorption are the chemical structure, solubility and pH.

Organic complex forming compounds, notably citrate, increase absorption.

Aluminium absorption may interact with calcium and iron transport systems.

Aluminium, once absorbed, is distributed in most organs within the body, with accumulation occurring mainly in bone at high dose levels.

To a limited but as yet undetermined extent, aluminium passes the blood–brain barrier and is also distributed to the fetus. Aluminium is eliminated effectively in urine.


In humans, aluminium and its compounds appear to be poorly absorbed, although the rate and extent of absorption have not been adequately studied. The mechanism of gastrointestinal absorption has not yet been fully elucidated. Variability results from the chemical properties of the element and the formation of various chemical species, which is dependent upon the pH, ionic strength, presence of competing elements (e.g. silicon), and presence of complex forming agents within the gastrointestinal tract (e.g. citrate). The urine is the most important route of aluminium excretion.


Steady state serum to whole blood aluminium concentrations are approximately equal. Slightly above 90% of plasma aluminium is associated with transferrin (Tf), ca. 7 to 8% with citrate, and less than 1% with phosphate and hydroxide.

Normal plasma aluminium concentration is believed to be 1 to 2μg/L. Normal tissue aluminium concentrations are greater in lung (due to entrapment of particles from the environment) than bone than soft tissues.

Approximately 60, 25, 10, 3 and 1% of the aluminium body burden is in the bone, lung, muscle, liver and brain, respectively.

Higher concentrations are observed in uraemia and they are still higher in dialysis encephalopathy.


Tissue aluminium concentration increases with age. Some studies have reported that the aluminium concentrations in bulk brain samples, neurofibrillary tangles (NFT) and






plaques were higher in AD subjects than controls. Other studies have found no difference.Hair aluminium concentration has been described but its value as an indicator of aluminium body burden has not been demonstrated.


More than 95% of aluminium is eliminated by the kidneys and ca. 2% in bile.

Occupational aluminium exposure increases urinary aluminium concentrations more than in plasma concentration above their normal levels.


Depending on the type and route of exposure, aluminium clearance has been characterized to obviously have multiple half-times and is therefore estimated in hours, days and years. Most of the Aluminium was eliminated within the first week; the terminal half-life probably represents less than 1% of the injected aluminium.


1) Background document for development of WHOGuidelines for Drinking-water Quality,



    ALUMINIUM HYDROXIDE“,Daniel Krewski, Robert A Yokel, Evert Nieboer, David

   Borchelt, Joshua Cohen, Jean Harry7, Sam Kacew, Joan Lindsay, Amal M Mahfouz,

   Virginie Rondeau; available at:



Summary of Silicon toxicokinetics



Distribution and metabolism


Silicon is a component of serum, being present in the form of non proteinbound orthosilicic acid. Its metabolic pathways are only partially understood. Silicic acid is thought to be the form present in blood.


The highest silicon levels, among human tissues, are found in the walls of the aorta, tendons, aponeuroses and skin. In dialysis patients silicon has been found in the liver, spleen and lung.


In rats given intra-cardiac injections of 31silicon labelled silicic acid, one hour after dosing the highest levels were found in the kidney, liver and lungs with moderate amounts being found in bone, skin, muscle, testes and spleen. The levels then began to decline when measured 2 and 4 hours after dosing Brain tissue contained negligible amounts of silicon suggesting active exclusion by the blood-brain barrier.


Silicon can be detected in small areas of ossifying bone during the early stages of mineralisation. The silicon content of young osteoid tissue increases markedly, together with that of calcium, but at more advanced stages of bone formation, when calcification sets in, the silicon content decreases again to trace levels. The element is located within the mitochondria of the osteoblast.


It has been shown that silicon concentrations in human arteries decrease with increasing age and with the onset of atherosclerosis. Several reports have independently confirmed a decline in silicon with age in some animal tissues, but ist causes and possible relevance to the ageing process remain unknown.





The kidneys play the main role in silicon excretion. It is excreted in urine in the form of the orthosilicic anion bound mainly with magnesium or calcium cations. Significant correlations

were observed between creatinine clearance and silicon levels in serum and urine. Renal clearance was 82-96 ml/min suggesting high renal filterability.


In patients suffering from chronic renal failure, urinary silicon excretion was decreased and serum silicon levels increased. Silicon excretion was not increased in 391 patients with renal stones compared to 370 healthy controls and no relationship with calcium or oxalate excretion was apparent.


Elimination of radiolabelled silicic acid in a human volunteer indicated two simultaneous first-order processes with half lives of 2.7 and 11.3 hours respectively. Elimination was essentially complete after 48 hours and was equivalent to 36% of the dose given. 90% of the absorbed silicon was rapidly eliminated and was probably retained in the extracellular fluid volume while the slowly eliminated silicon could represent intra-cellular silicon.


Silicon is also excreted, in smaller quantities, via the faeces.




Expert Group on Vitamins and Minerals Secretariat, August 2002, available at: