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Silicic acid, lithium salt belongs to the soluble silicates and is an inorganic white powder with a SiO2/Li2O molar ratio of 2.8 - 6.3 (molecular weight 198.1 - ≤ 408.3). No definite water solubility value for silicic acid, lithium salt can be stated, since only lithium but not silicic acid, lithium salt was dissolved in water (see IUCLID section 4.8: Affolter, 2010; Paulus, 2010). In the test item silicic acid, lithium salt (MR: 4.8), a lithium content of approx. 3.66% was measured (see IUCLID section 4.8: Paulus, 2010). In general, partition coefficients (octanol/water) log Pow cannot be determined for inorganic substances. However, Dermwin v2.01 estimated a log Pow value of -4.46 for silicic acid, lithium salt. Soluble silicates are totally insoluble in n-octanol and have no bioaccumulation potential (CEES, 2008).

 

There were no studies available for assessment, in which the toxicokinetic properties of silicic acid, lithium salt were investigated. However, toxicokinetic studies were performed with the structural analogue substances disodium metasilicate, silicic acid, sodium salt and sodium metasilicate nonahydrate. The toxicokinetic profile of lithium is well characterized since lithium is used therapeutically for bipolar disorders.

 

Absorption, Distribution and Excretion

Perorally administered sodium metasilicate nonahydrate (average daily dose of silicon of 0.1 g/kg bw for the first six weeks, 0.2 g/kg bw for the next six weeks and 0.4 g/kg bw for the last six weeks) resulted in a significantly increase of serum and tissue (liver, kidney, lung and aorta) silica levels compared to the control animals. When guinea pigs were orally administered radiolabeled sodium [31Si]metasilicate, the majority of silica was quickly absorbed and excreted in urine, although a significant amount remained in the tissues (Haneke, 2002). Several 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 (Benke and Osborn, 1979; King et al., 1933; King and McGeorge, 1938, Sauer et al., 1959). Ingested silicates are also excreted to a lesser extent via the faeces.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.

 

Lithium ions are readily absorbed, e.g. after an oral dose of a diluted lithium chloride solution the serum lithium concentrations peaked at 30-60minutes and plateau levels were reached at 12-24 hours. Absorption of lithium salts through the skin is very low.

Lithium is not protein bound and after ingestion it slowly equilibrates between the extracellular and intracellular spaces in humans. The distribution in tissues is unevenly: at steady-state the concentration in liver, erythrocytes and cerebrospinal fluid and brain is lower than in serum, while it is higher in kidneys, thyroid and bone. Lithium crosses the human placenta and can be taken up by infants through breast milk.

Excretion of lithium is predominantly by the kidney and approx. 80% of lithium is reabsorbed by the proximal renal tubule and 20% is excreted in the urine. Factors that decrease the glomerular filtration rate or increase proximal tubular reabsorption of sodium will decrease the clearance of lithium (Lagerkvist and Lindell, 2002; Opresko, 1995; Aral and Vecchio-Sadus, 2008).

 

Metabolism

Silicic acid, lithium salt is not metabolized to any appreciable extent.

 

 

References

Haneke, K.E. (2002): Sodium Metasilicate, Anhydrous [6834-92-0], Sodium Metasilicate Pentahydrate [10213-79-3], and Sodim Metasilicate Nonahydrate [13517-24-] – Review of Toxicological Literature, Prepared for National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, http://ntp.niehs.nih.gov/ntp/htdocs/Chem_Background/ExSumPdf/sodiummetasilicate.pdf

Lagerkvist, B.J. and Lindell, B. (2002) The Nordic Expert Group for Criteria Documentation of Health Risks from Chemicals- 131. Lithium and lithium compounds, National Institute for Working Life, Stockholm, Sweden, ISBN 91-7045-659-3, http://www.inchem.org/documents/kemi/kemi/ah2002_16.pdf

Aral, H. and Vecchio-Sadus, A. (2008) Toxicity of lithium in humans and the environment – A literature review. Ecotoxicology and Environmental Safety 70:349-356

Opresko, D.M. (1995) Toxicity Summary for Lithium. Prepared for Oak Ridge Reservation. Environmental Restoration Program, Oak Ridge National Laboratory, Oak Ridge, TN, USA