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EC number: 242-670-9 | CAS number: 18917-91-4
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Basic toxicokinetics
Administrative data
- Endpoint:
- basic toxicokinetics
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: By a European authority peer-reviewed data
Data source
Referenceopen allclose all
- Reference Type:
- other: governmental assessment report
- Title:
- Safety of aluminium from dietary intake - Scientific Opinion of the Panel on Food Additives, Flavourings, Processing Aids and Food Contact Materials (AFC)
- Author:
- EFSA - European Food Safety Authority
- Year:
- 2 008
- Bibliographic source:
- The EFSA Journal (2008) 754, 1-34
- Reference Type:
- other: governmental assessment report
- Title:
- STATEMENT OF EFSA - On the Evaluation of a new study related to the bioavailability of aluminium in food
- Author:
- EFSA - European Food Safety Authority
- Year:
- 2 011
- Bibliographic source:
- EFSA Journal 2011;9(5):2157
Materials and methods
- Principles of method if other than guideline:
- review of several in vivo studies: oral bioavailability of Al from Aluminium salts
Test material
- Reference substance name:
- Aluminium salts
- IUPAC Name:
- Aluminium salts
Constituent 1
Results and discussion
Applicant's summary and conclusion
- Conclusions:
- Interpretation of results (migrated information): other: According to the EFSA evaluations, using data from a wide set of different aluminium compounds, the bioavailability of Al after oral intake is below 1%
According to the EFSA evaluations, using data from a wide set of different aluminium compounds, the bioavailability of Al after oral intake is at the highest 0.3 %. - Executive summary:
The European Food Safety Authority - EFSA - reviewed in its Scientific Opinion on Safety of aluminium from dietary intake (2008) the absorption, distribution and excretion of aluminium from oral (dietary) intake. The data were rereviewed in view of new data three years later an EFSA published a statement On the Evaluation of a new study related to the bioavailability of aluminium in food in 2011.
According to EFSA evaluation 2008:
“It has been suggested that acid digestion in the stomach would solubilise most of the ingested aluminium compounds. In acidic aqueous solutions with pH <5, the aluminium ion exists mainly as Al+3, e.g. hydrated Al3+ (Al(H2O)6)3+). By passing from the stomach to the intestines the increase in pH results in the formation of complexes of aluminium with hydroxide and finally the formation of insoluble aluminium hydroxide at neutral pH. Therefore, as the pH is neutralised in the duodenum the aluminium ion is gradually converted to aluminium hydroxide and the majority is then expected to precipitate in the intestine, with subsequent faecal excretion, leaving only a minor fraction available for absorption.
Although the water solubility of aluminium compounds appears to be one of the major factors affecting their bioavailability, it is not possible to extrapolate from solubility in water to bioavailability. Additionally, due to available dietary ligands that may either increase (e.g. citrate, lactate, and other organic carboxylic acid complexing agents, fluoride), or decrease the absorption (such as phosphate, silicon, polyphenols) the bioavailability of any particular aluminium compound can be markedly different depending on the presence or absence of particular food and beverages in the intestines.
Available studies indicate that the oral bioavailability of aluminium in humans and experimental animals from drinking water is in the range of 0.3%, whereas the bioavailability of aluminium from food and beverages generally is considered to be lower, about 0.1%. However, considering the available human and animal data, it is likely that the oral absorption of aluminium from food can vary at least 10-fold depending on the chemical forms present in the intestinal tract.
Except for sodium aluminium phosphate (SALP), acidic, none of the aluminium compounds authorised as food additives in the EU have been studied for bioavailability. The bioavailability of aluminium from SALP, acidic, when incorporated in a biscuit, was found to be about 0.1 % in the rat. However, the Panel noted that in the FEEDAP opinion on Zeolite, a form of sodium aluminium silicate used in animal feed, it was stated that sodium aluminium silicate may be partly hydrolysed in the digestive tract, mainly in the abomasum (because of the low pH value) resulting in release of aluminium and silicate ions. Thus, in an unpublished study in cows, an increase of the aluminium serum level from 13μg/l before treatment to 85μg/l during a three-week administration of 600 g Zeolite per day was reported.
This finding on sodium aluminium silicate in cows is in line with the suggestion by some authors that acid digestion in the stomach would solubilise most of the ingested aluminium compounds to the monomolecular species Al+3 (e.g. hydrated Al(H2O)6)3+). The Panel therefore noted that other insoluble aluminium-containing food additives that previously have been considered not to be absorbed from the gut can be expected to behave similarly.
After absorption, aluminium distributes unequally to all tissues in humans and accumulates in some. The total body burden of aluminium in healthy human subjects has been reported to be approximately 30–50 mg/kg bw. Normal levels of aluminium in serum are approximately 1–3μg/L. About one-half of the total body burden of aluminium is in the skeleton, and about one-fourth is in the lungs (from accumulation of inhaled insoluble aluminium compounds). Reported normal levels in human bone tissue range from 5 to 10 mg/kg. Aluminium has also been found in human skin, lower gastrointestinal tract, lymph nodes, adrenals, parathyroid glands, and in most soft tissue organs. In rats accumulation of aluminium was higher in the spleen, liver, bone, and kidneys than in the brain, muscle, heart, or lung. It has also been reported that aluminium can reach the placenta and fetus and to some extent distribute to the milk of lactating mothers. Aluminium levels have been found to increase with ageing in a number of tissues and organs (bone, muscle, lung, liver, and kidney) of experimental animals.
The main carrier of Al3+ in plasma is the iron binding protein transferrin. Studies have demonstrated that about 89% of the Al3+ in plasma is bound to transferrin and about 11% to citrate. Cellular uptake of aluminium in organs and tissues is believed to be relatively slow and most likely occurs from the aluminium bound to transferrin by transferrin-receptor mediated endocytosis. There are two routes by which aluminium might enter the brain from the blood: 1) through the blood brain barrier (BBB) and 2) through the choroid plexuses into the cerebrospinal fluid of the ventricles within the brain and then into the brain. Aluminium has been shown to rapidly enter the brain extracellular fluid and the cerebrospinal fluid, with smaller concentrations in these than in the blood.
The distribution of aluminium may be modulated by several factors. Although citrate and fluoride have been shown to reduce tissue accumulation of aluminium and increase its renal excretion in experimental animals, this only occurs when the aluminium concentration exceeds the transferring metal binding capacity. This will seldom happen in humans. The iron status is negatively correlated with aluminium accumulation in tissues and animal experiments have shown that calcium and magnesium deficiency may contribute to accumulation of aluminium in the brain and bone.
Following ingestion in humans, absorbed aluminium from the blood is eliminated primarily by the kidneys, presumably as the citrate, and excreted in the urine. Unabsorbed aluminium is excreted in the faeces. Excretion via the bile constitutes a secondary, but minor route. The two most recent studies in humans that had normal renal function, did not consume any specific diet, took no medications containing aluminium, and had no other special exposure to aluminium, reported urine levels of aluminium of 3.3 (median) and 8.9μg/l (mean), respectively.
Multiple values have been reported for the elimination half life of aluminium in humans and animals, suggesting that there is more than one compartment of aluminium storage from which aluminium is eliminated.
Within the first day after receiving a single injection of 26Al citrate, approximately 59% of the dose was excreted in the urine of six subjects. At the end of 5 days, it was estimated that 27% of the dose was retained in the body. However, when 26Al levels were monitored for more than 3 or 10 years in a single subject that received the injection, half-lives of approximately 7 years and 50 years were estimated.
Initial half-lives of 2 – 5 hours were reported in rats, mice, rabbits and dogs after intravenous injection of soluble aluminium salts. When the sampling time was prolonged the half-life of aluminium in rabbits was estimated to be 113, 74, 44, 42, 4.2 and 2.3 days in spleen, liver, lung, serum, kidney cortex, and kidney medulla, respectively. A second half-life in the kidney greatly exceeded 100 days. In rats, the whole organism elimination half-life was estimated to be 8 to 24 days in serum, kidney, muscle, liver, tibia and spleen.
Aluminium persists for a very long time in the rat brain following intraveneous injection of very small doses of 26Al. A half-life of 150 days has been reported. However, this estimate is not expected to have a high degree of accuracy as brain samples were not obtained for at least 3 half-lives. Based on calculations for offspring of rats that were given 26Al injections daily from day 1 to 20 postpartum and thereafter examined on days 40, 80, 160, 320 or 730 postpartum, elimination half-lives of approximately 13 and 1635 days in the brain were suggested. Half-lives of 7 and 520 days were suggested for parietal bone. For liver and kidneys half-lives were suggested to be 5 and 430 days and 5 and 400 days, respectively. In blood the values were 16 and 980 days.
There is little published information on allometric scaling of aluminium elimination rates that can be used to extrapolate these results from the rat to the human. For aluminium in the brain 150 days is approximately 20% of, and 1365 days exceeds, the rat’s normal life span. For comparison, the whole-body half-life of aluminium in the human was estimated to be 50 years.”
The study discussed in the EFSA Statement 2011 confirmed the bioavailability data reviewed in the Scientific Opinion 2008 and extended them to further aluminium containing substances (aluminium citrate, - chloride, - nitrate, - sulphate, - hydroxide, - oxide, and - metal, sodium aluminium phosphate, acidic and basic, sodium aluminium silicate, powdered pot electrolyte and Allura Red AC aluminium lake (FD&C red 40 aluminium lake) were tested):
" […] the mean bioavailability of the soluble aluminium salts ranged between 0.05% and 0.21%. Among the soluble aluminium salts, aluminium sulphate had the highest bioavailability. The bioavailability of the insoluble aluminium hydroxide, aluminium oxide and powdered pot electrolyte was somewhat lower (range 0.02-0.04%). In contrast the bioavailability of the insoluble Allura Red AC aluminium lake (FD&C red 40 aluminium lake) and sodium aluminium silicate were 0.09 and 0.12%, respectively."
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