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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

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There are no data on the toxicokinetics of tripotassium propylsilanetriolate.

The following summary has therefore been prepared based on validated predictions of the physicochemical properties of the substance itselfand using this data in algorithms that are the basis of many computer-based physiologically based pharmacokinetic or toxicokinetic (PBTK) prediction models. The main input variable for the majority of these algorithms is log Kow so by using this, and other where appropriate, known or predicted physicochemical properties of tripotassium propylsilanetriolate reasonable predictions or statements may be made about its potential absorption, distribution, metabolism and excretion (ADME) properties.

The substance as registered is stable only as an alkaline aqueous solution at approximately pH >14.Tripotassium propylsilanetriolate is the potassium salt of propylsilanetriol. In solution tripotassium propylsilanetriolate will be completely dissociated to propylsilanetriolate and three free potassium ions. Under comparable conditions of concentration and pH, propylsilanetriolate is equivalent to the parent acid propylsilanetriol, therefore exposure to this substance will be discussed as representative of the parent substance in terms of potential ADME properties.

Potential human exposure can occur via inhalation, as an aerosol, or dermal routes. However, due to the very high pH of the parent solution, severe irritant or corrosive effects are likely to be the most significant factors when exposure occurs.



Significant oral exposure is not expected for this corrosive substance.

However, should it occur, and excepting the fact that the primary limiting factor will be the corrosive nature of the solution, oral exposure to humans may be relevant for propylsilanetriol.When oral exposure takes place it is necessary to assume that except for the most extreme of insoluble substances, that uptake through intestinal walls into the blood takes place. Uptake from intestines can be assumed to be possible for all substances that have appreciable solubility in water or lipid. Other mechanisms by which substances can be absorbed in the gastrointestinal tract include the passage of small water-soluble molecules (molecular weight up to around 200) through aqueous pores or carriage of such molecules across membranes with the bulk passage of water (Renwick, 1993).

As propylsilanetriol is very water soluble (1E+06 mg/l) and has a molecular weight of approximately 121 it meets both of these criteria, so should oral exposure occur it is reasonable to assume systemic exposure will occur also. 


The fat solubility and therefore potential dermal penetration of a substance can be estimated by using the water solubility and log Kowvalues. Substances with log Kowvalues between 1 and 4 favour dermal absorption (values between 2 and 3 are optimal) particularly if water solubility is high.

Although the water solubility (1E+06 mg/l) of propylsilanetriol is favourable for absorption, the predictedlog Kow of -1.4 is not, so it is considered too hydrophilic to cross the lipid-rich stratum corneum. Therefore dermal uptake is likely minimal.

However, since the parent solution with a pH of 14 will be severely corrosive to the skin damage to the skin may result in increased penetration. There are no studies to check for signs of dermal toxicity.


There is a QSPR to estimate the blood:air partition coefficient for human subjects as published by Meulenberg and Vijverberg (2000). The resulting algorithm uses the dimensionless Henry coefficient and the octanol:air partition coefficient (Koct:air) as independent variables.

Using these values for propylsilanetriol results in a very high blood:air partition coefficient (approximately 2E+09:1) so significant uptake would be expected into the systemic circulation. However, the high water solubility of propylsilanetriol may lead to some of it being retained in the mucus of the lungs so this may limit absorption.

As with dermal exposure, damage to membranes caused by the corrosive nature of the parent solution may enhance the uptake. There are no studies to check for signs of inhalation toxicity.


For blood:tissue partitioning a QSPR algorithm has been developed by De Jongh et al. (1997) in which the distribution of compounds between blood and human body tissues as a function of water and lipid content of tissues and the n-octanol:water partition coefficient (Kow) is described. Using this value for propylsilanetriol, predicts that should systemic exposure occur, distribution would be minimal with tissue:blood partition coefficients of less than 1 for all tissues (zero for fat).

Table 1: tissue:blood partition coefficients


Log Kow















Potassium ions will enter the body's natural homeostatic processes.


There are no data regarding the metabolism of tripotassium propylsilanetriolate or propylsilanetriol.


A determinant of the extent of urinary excretion is the soluble fraction in blood. QPSR’s as developed by De Jonghet al. (1997) using log Kowas an input parameter, calculate the solubility in blood based on lipid fractions in the blood assuming that human blood contains 0.7% lipids.

Using this algorithm, the soluble fraction ofpropylsilanetriolin blood is > 99% suggesting it is likely to be effectively eliminated via the kidneys in urine and accumulation is very unlikely.