Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 215-199-1 | CAS number: 1312-76-1
There are no experimental studies available in which the toxicokinetic properties of silicic acid, potassium salt (CAS 1312-76-1) were investigated. Therefore, whenever possible, toxicokinetic behaviour was assessed taking into account the available information on physicochemical and toxicological characteristics of silicic acid, potassium salt according to “Guidance on information requirements and chemical safety assessment Chapter R.7c: Endpoint specific guidance (ECHA, 2012)”.
Silicic acid, potassium salt (CAS 1312-76-1) is composed of oligomers of the tetrahedral orthosilicate anion SiO4 with potassium cations as counter ion. The connectivity of silicon atoms in terms of Si-O-Si bonds varies depending on the concentration of potassium cations: the more K+, the less Si-O-Si bonds are formed and vice versa. Therefore, the connectivity of silicon atoms in potassium silicate varies depending on the mixing ratio of the silicon source (quartz sand) and the potassium source (potash or KOH). The resulting molecular structures are described in terms of molar ratios (SiO2:K2O). Molar ratios (MR) of commercial silicic acid, potassium salt typically vary between 1.5 and 5.The higher the molar ratio, the less potassium ions are present in the silica network and consequently the less alkaline the silicates are.
Potassium silicate glasses (lumps) are produced by direct fusion of precisely measured portions of pure silica sand (SiO2) and potash (K2CO3) at temperatures above 1000°C. Solutions of soluble silicates ("waterglass") may be produced either by dissolving the soluble silicate lumps in water at elevated temperatures (and partly at elevated pressure) or by hydrothermally dissolving a reactive silica source (mainly silica sand) in potassium hydroxide solution.
Silicic acid, potassium salt is an amorphous glass melt (lumps) with a three-dimensional structure. Following further processing it can be used as aqueous solution or spray-dried powder with ca. 20% of residual water.The anhydrous solid dissolves extremely slowly at ambient conditions. The lumps can be solubilised only at elevated temperature and pressure, whereas spray-dried solutions readily dissolve in water. Aqueous solutions are infinitely miscible with water. However, since the aqueous solution is characterised by dynamic polymerisation/hydrolysis equilibrium of monomeric SiO2 (aq.), oligomeric silicate ions and polysilicate ions, determination of quantitative water solubility is strongly pH-dependent. The vapour pressure of silicic acid, potassium salt has not been measured, but the vapour pressures for three solid sodium silicates are available: 0.0103 hPa at 1175 °C (MR 1.0, disodium metasilicate), 0.0031 hPa at 1165 °C (MR 2.0) and 0.0016 hPa at 1172 °C (MR 3.0). The vapour pressures are extremely low and thus not relevant at ambient temperatures.As sodium and potassium silicates only differ from each other by their counter ions, it is unlikely that the vapour pressures for potassium silicates vary significantly from those determined for the respective sodium silicates.The partition coefficient n-octanol/water is also not relevant, as alkali silicates are ionisable inorganic compounds which are not soluble in alcohol.
Silicic acid, potassium salt is member of the soluble silicates category. In general, the category members are structurally very similar and the biological properties are mainly governed by their intrinsic alkalinity. As the members of the soluble silicates category exhibit a similar toxicological profile, data on disodium metasilicate (CAS 6834-92-0) and silicic acid, sodium salt (CAS 1344-09-8) can be used whenever no toxicological data are available for silicic acid, potassium salt.
Absorption and distribution
Two acute oral toxicity studies have been conducted in rats using silicic acid, potassium salt with molar ratios of 2.47 and 2.25, respectively. However, in both studies only limited details were reported. In the study of Durando (2004), female rats were administered silicic acid, potassium salt (30%, MR = 2.47) at the dose level of 5000 mg/kg bw. No effects on body weight were observed and all animals were active and healthy throughout the experiment. At necropsy, no gross abnormalities were found. Therefore, the LD50 was considered to be > 5000 mg/kg bw. In another study referred to by Spanjers and Til (1981), male and femals rats were administered the test substance (MR =2.25) in dose levels of 3300–6864 mg/kg bw. In a dose dependent manner, deaths occurred between 2 hours and 2 days after dosing. Number of deaths at each dose: 1 at dose 3300 mg/kg bw, 2 at dose 3960 mg/kg bw, 2 at dose 4752 mg/kg bw, 3 at dose 6864 mg/kg bw. Clinical symptoms observed consisted of sedation and signs of discomfort within few hours after treatment. Later on sluggishness and unconsciousness were frequently observed. The effects were reversible in the recovery period of the surviving animals. No treatment-related gross alterations were noted. The LD50 was calculated to be 5700 mg/kg bw.
The studies on potassium silicate fit well into the toxicity pattern of the sodium silicates: Inverse correlation of acute oral toxicity of soluble silicates to the molar ratio SiO2/Na2O. Toxicity decreases in rats with increasing molar ratio from LD50 of 500 mg/kg bw for molar ratio 0.5 to 8650 mg/kg bw for 3.38.
With regard to the dose administered and the effects observed, systemic bioavailability of the test substance is considered to play only a minor role. This is confirmed by oral repeated dose toxicity studies with the silicic acid, sodium silicate or disodium metasilicate ranging from 90 to 180 days and performed in rats and mice. While in rats no treatment-related effects on gross pathology and histopathology were noted with disodium metasilicate (Ito et al., 1975), a reduced pituitary glands weight was observed at 716 - 892 mg/kg bw/day after treatment for 90 days in female mice (Saiwai et al., 1980). From the available 90 d repeated dose toxicity studies a NOAEL of 227 - 237 mg/kg bw/day and of 260-284 mg/kg bw/day was derived for rats and mice, respectively. Silicic acid, sodium salt, had a NOAEL (180 days) of 159 mg/kg bw/day for rats (Smith et al., 1973). For the repeated dose toxicity studies conducted with rats, the NOAELs correspond to the highest tested dose level.
In the acute inhalation toxicity study, male and female rats were exposed to 2.06 ± 0.19 mg/L silicic acid, potassium salt (30%, MR = 2.47) (Durando, 2004). All animals survived exposure to the test atmosphere and gained body weight over the 14 -day period. During exposure, animals showed hunched posture and hypoactivity. However, upon removal from the exposure chamber, all animals recovered from the above clinical signs and appeared healthy and active over the 14 -day observation period. At necropsy, no gross abnormalities were noted. The LC50 was > 2.06 mg/L. The data are in line with the very low vapour pressure for sodium silicates, indicating that inhalation is not considered to be a significant route of exposure for silicic acid, potassium salt.
The mean particle size for powders (MR 3.2) is 220-320 µm (PQ Corporation, 2009, unpublished data). Furthermore, in commercial granular products, 96-98% of the particles are > 200 µm and therefore, silicic acid, potassium salt is essentially non inhalable.
Due to the hygroscopic properties and the ready solubility in water, the majority of particles, if inhaled, will be retained and dissolved by mucus in the upper respiratory tract. Thus, effects would be restricted to local corrosive/irritant effects, due to the intrinsic alkalinity of silicic acid, potassium salt. Also based on the hygroscopic properties, anhydrous silicic acid, potassium salt tends to aggregate in the presence of moisture.
In the acute dermal toxicity study of Durando (2004), the test substance (MR = 2.47, 30%) was applied on the skin of male and female rats. All animals survived, gained weight and appeared healthy and active. Apart from the dermal irritation (erythema) and alopecia noted at the application site of five animals (4 females and 1 male) between days 1 and 8, there were no other signs of toxicity. No gross lesions were observed at final necropsy in any animal. The LD50 was > 5000 mg/kg bw.
In addition, acase report demonstrated that a fifty-seven year old dyer was regularly exposed at work to 20% sodium silicate solution (CAS 1344-09-8) of unknown molar ratio. The man had recurrent ulcerative lesions on his left hand over a period of two years. The ulcers were associated with chronic eczematous changes resulting from primary irritant contact dermatitis to sodium silicate, as indicated by a positive patch test. The man also had another type of cutaneous reaction to sodium silicate, contact urticaria. An immediate wheal and flare reaction was seen fifteen minutes after the application of sodium silicate to a scratch test site. Such a response was not seen in healthy control subjects.
As also demonstrated for the section “irritation/corrosion”, potassium silicate can be irritating to corrosive to the skin depending on the molar ratio and the concentration. Therefore, effects would predominantly occur if not be restricted to local corrosive/irritant effects, due to the intrinsic alkalinity of potassium silicate.
From the chemical structure of silicic acid, potassium salt, it can be deduced that it is not metabolised in-vivo. By calculating potential metabolites via OECD QSAR toolbox v.3.2 (2013), this assumption is confirmed: metabolites were generated neither by the liver metabolism simulator nor by the skin metabolism simulator nor by the microbial metabolism simulator. Based on this information, it is considered to be very unlikely that silicic acid, potassium salt will be metabolised in-vivo. Repeated dose toxicity studies via the oral route performed in rats and mice also support the hypothesis that there are no toxic metabolites of silicic acid, potassium salt in-vivo.
In addition, studies with disodium metasilicate in mice did not induce chromosome aberrations in the bone marrow and did not alter cell proliferation in the auricular lymph nodes using the local lymph node assay (Ito et al, 1986; Saiwai et al., 1980; Karrow et al., 2002). No indication has therefore been found that toxic metabolites are formed in-vivo.
Moreover, studies on genetic toxicity in-vitro were all negative with disodium metasilicate (Ames test) or with silicic acid, sodium silicate (MR=3.3; 36% active ingredient; gene mutation and chromosome aberration in V79 cells), indicating that there is also no evidence of reactivity under the in-vitro test conditions (BASF SE 2012; Schulz, 2006; Wollny 2009).
The toxicokinetic studies on rats, guinea pigs, cats and dogs showed that the excretion of silicon dioxide with the urine was markedly increased after exposure (oral, inhalation or intravenous injection) to silicates. The excretion rate was independent of the doses applied indicating that the limiting factor is the rate of production of soluble or absorbable silicon dioxide in the gastrointestinal tract.
Since silicic acid, potassium salt is a polar substance and water soluble, its elimination mainly occurs by the kidneys. In the excretion study of Sauer et al. (1959), sodium metasilicate pentahydrate was administered to guinea pigs by the oral route. Urinary silicon levels were measured after a single dose or after repeated doses (4 doses) of sodium metasilicate pentahydrate (equivalent to 80 mg SiO2). The excretion rates were neither precisely determined nor were detailed dose-response data obtained. Within 8 days, 60% of the silica administered as a single dose and 96% of the silica administered as repeated doses was excreted. The urinary excretion was apparently limited by restricted absorption from the gastrointestinal tract.
Therefore, the excretion rate was independent of the doses applied indicating that the limiting factor is the rate of production of soluble or absorbable silicon in the gastrointestinal tract.
Markedly increased and rapid urinary excretion of silica was also observed when various “soluble silicates” were administered to rats (oral, Benke and Osborn, 1979), dogs (oral and intravenous, King et al., 1933) and cats (oral, intraperitoneal and inhalative, King and McGeorge, 1938). Benke and Osborne (1979) determined urinary excretion levels of silicon after single oral administration ofsodium silicate (analytical amount of silicon: 25.9%). The dose levels were 40 and 1000 mg/kg bw. Urine was collected in periods of 0 – 24, 24 – 48, 48 – 72 and 72 – 96 hours after dosing.The rats excreted urinary silicon in excess of background levels. The urinary silicon excretion increased rapidly after dosing and the majority of silicon was excreted during the first 24 hours. For sodium silicate, a half life of 24 hours was determined with a first-order excretion kinetic. The amount of silicon excreted in urine increased with the dose level, but when expressed as percentage of dose, the urinary silicon excretion decreased with increasing dose (18.9% of silicon dose recovered in urine at the low dose and 2.8% at the high dose). The fact that the increase in urinary excretion was not in direct proportion to the increase in dose may have been due to the saturation of some processes, related either to the absorption or to the excretion of silicon. Similar findings were reported by King et al. (1933), who administered silicic acid to dogs and found that increasing the dose caused a smaller fraction of the silicon to be excreted in urine. Benke and Osborne (1979) proposed that an acid mediated hydrolysis in the gastrointestinal tract is responsible for forming soluble or absorbable forms of silicon and that, therefore, lower silicon doses are not excreted more rapidly.
Silicon is an essential ultratrace element participating in the normal metabolism of the mammalian body. It is required in bone, cartilage and connective tissue formation as well as participating in other important metabolic processes. Also, potassium is an essential element of the mammalian body. The salt of the metal ion is a natural constituent of the regular human diet.
Taking into account all available data, the biological properties of silicic acid, potassium salt are mainly governed by its intrinsic alkalinity. Silicic acid, potassium salt was shown to possess a low systemic toxicity and is therefore expected to have only a low potential to accumulate in biological systems.
Literature (not cited in IUCLID):
ECHA (2012) Guidance on information requirements and chemical safety assessment Chapter R.7c: Endpoint specific guidance
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
Welcome to the ECHA website. This site is not fully supported in Internet Explorer 7 (and earlier versions). Please upgrade your Internet Explorer to a newer version.
Close Do not show this message again