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EC number: 240-934-8 | CAS number: 16893-85-9
- 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
Endpoint summary
Administrative data
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
- Bioaccumulation potential:
- low bioaccumulation potential
Additional information
Oral uptake
Due to the acidic and aqueous conditions in the stomach, fluoride ions, which are liberated from disodium hexafluorosilicate , are present in the form of hydrogen fluoride and then behave as fluoride from any other inorganic source. Hydrogen fluoride easily penetrates biological membranes by passive diffusion both in stomach and intestines (NIWL, 2005; WHO, 2002). However, the presence of fluoride-binding cations, such as Ca2+, can reduce the absorption of fluoride
Available information suggests that ingested Na2SiF6acts similarly to NaF from a biological point of view, although no reliable information regarding percentages of fluoride in blood coming from Na2SiF6have been found. However, if analogous metabolism for NaF and Na2SiF6is assumed, read-across from NaF will be possible. Nonetheless, metabolism of Na2SiF6by dermal or inhalation route have not been reported. Thus, the extent of absorption via dermal and inhalation route cannot be specified.
Absorption in animals
Inhalation:There are no toxicokinetic investigations concerning inhalation exposure in animals.
Dermal:There are no toxicokinetic investigations concerning dermal exposure in animals.
Oral:A study carried out on rats compared absorption/ elimination of fluoride using NaF and Na2SiF6as source. This study reported that rats which ingested Na2SiF6absorbed more fluoride than those which ingested NaF. However, rats which ingested Na2SiF6excreted by urine more fluoride than those which ingested NaF, so that the percentage retained was almost identical (Ohio Agric ExpStat 1935; 558: 59–60).
It has been noted that more F-from silicofluoride treated water was eliminated in urine of young male rats than from sodium fluoride treated water (Kick et al., 1935). Female rats were fed sodium fluoride treated water or silicofluoride treated water for 4 months before their urine was tested. No difference was found for fluoride intake, excretion, and retention. It has been stated that levels of F-exposures affects calcium-dependent processes, including those associated with neural as well as kidney functions (Borke and Whitford, 1999). This is consistent with the damage found in squirrel monkeys exposed to silicofluoride treated water at 1–5 ppm F-for 18 months (Manocha et al., 1975). The same F-levels harmful rat kidney phospholipid cell membranes has been found to be associated with dental fluorosis (Guan et al., 2000).
The physiological effects of NaF and Na2SiF6have been extensively studied in chronic fluorine toxicosis manifested by the characteristic effects of fluorine on rats’ incisor teeth. Comparing NaF, Na2SiF6and Na3AlF6at levels of 14-16 ppm fluorine, chronic fluorine intoxication in rats occurred to the same extend from all of them (Public Health Rep 1950:1175–86).
A comparative study of the rate of retention and paths of excretion of fluorine when fed to rats as NaF, Na2SiF6and CaF2showed that there was no difference between NaF and Na2SiF6regarding the percentage of fluoride retained in the rat’s body, although there were differences in the paths of excretion (urine or feces). (Public Health Rep 1950:1175–86).
McClure (1950) studied the physiological effects of different fluoride salts when ingested. No different effects on the growing rats of NaF and Na2SiF6became apparent. No different percentages of fluoride in the ash of the bones and teeth which could be attributed to the source of fluoride used were observed, i. e., the percentage of fluoride retained from NaF and Na2SiF6are not significantly different.
The study reported the rate of retention and paths of excretion of fluorine coming from NaF, CaF2and Na2SiF6in rats. (Fluoride in animal nutrition. Ohio Agricultural Experiment Station Bulletin 558, November 1935, cited in Public Health Rep 1950:1175–86).No difference can be observed between NaF and Na2SiF6. Although the percent of excretion depends on the path of excretion, the balance of fluoride is similar. Fluoride is mainly deposited in bones and teeth.
Fluoride compounds with low solubility, such as calcium fluoride, magnesium fluoride and aluminium fluoride, are poorly absorbed. Fluoride is mainly absorbed in the form of hydrogen fluoride, which has a pKa of 3.45. That is, when ionic fluoride enters the acidic environment of the stomach lumen, it is largely converted into hydrogen fluoride (Whitford & Pashley, 1984). Most of the fluoride that is not absorbed from the stomach will be rapidly absorbed from the small intestine. Either natural fluoride compounds or those added to drinking water yield fluoride ions, which are almost completely absorbed from the gastrointestinal tract. Thus, fluoride in drinking-water is generally bioavailable.
Respect to toxicokinetics, absorption of any inorganic fluoride is thought to be a passive process according toEuropean Union risk Assessment Report Hydrogen Fluoride, 2001 and the fate or the effects of that uptake are independent of the inorganic fluoride source. After oral, inhalatory or dermal exposure to fluoride, it can be found in all tissues in the body. Sequestration takes place in bone tissue in which about half of the absorbed fluoride is deposited. The major route for excretion is via the urine. In humans half-lives are in the range of 2 to 9 hr for plasma and in the range of 8 to 20 years for fluoride in bone deposits.
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