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Administrative data

Description of key information

No data on the repeated dose toxicity of reaction mass of potassium methylsiliconate are available, therefore data on trimethoxy(methyl) silane have been read-across. Exposure to trimethoxy(methyl) silane (MTMS) was associated with organ weight and/or histomorphological changes in males (liver, thymus, thyroid, duodenum, jejunum, and red blood cell) and females (liver, thyroid, duodenum, jejunum, and adrenal gland) at dose levels at or above 250 mg/kg bw/day. A marked increase in prothrombin time was observed for males at 250 and 1000 mg/kg bw/day whereas females were unaffected. Exposure was also associated with increased blood platelet concentration for males and females at 1000 mg/kg bw/day. These data support a NOAEL for the toxicity phase of the study of 50 mg/kg bw/day. There were several instances of urinary bladder hyperplasia; the study authors considered these to be the result of a reaction to a foreign body in the form of amorphous material.
There is also a 90-day inhalation study on trimethoxy(methyl) silane. Based on the increased incidence of grossly observed urinary bladder calculi along with the kidney dilation at the 400 ppm exposure level, the NOAEL for trimethoxy(methyl) silane vapor administered six hours per day, five days per week for a 90-day interval via whole-body inhalation exposure to male and female Sprague-Dawley rats, was 100 ppm (equivalent to 557.14 mg/m3).

Key value for chemical safety assessment

Repeated dose toxicity: via oral route - systemic effects

Endpoint conclusion
Dose descriptor:
NOAEL
50 mg/kg bw/day

Repeated dose toxicity: inhalation - systemic effects

Endpoint conclusion
Dose descriptor:
NOAEC
557.14 mg/m³

Additional information

No data on the oral repeated dose toxicity of reaction mass of potassium methylsiliconate are available. Reaction mass of potassium methylsiliconate is a multi-constituent substance containing methylsilanetriolate, dimers and oligomers of methylsilanetriolate, and potassium hydroxide. In contact with water the substance is dissolving. The resulting aqueous solution is only stable at high pH. As the pH is lowered, polymerisation occurs. Under comparable conditions of concentration and pH methylsilanetriolate is equivalent to the parent acid, methylsilanetriol.

The surrogate substance, trimethoxy(methyl)silane (CAS 1185-55-3), hydrolyses in contact with water at pH 7 (half-life approx. 2 hours), producing methanol and methylsilanetriol. Under acidic conditions, such as in the stomach following oral ingestion, hydrolysis is very rapid. Since potassium ions will not contribute to any systemic toxicity effect, and methanol does not contribute any significant repeated dose toxicity to rodents at the dose levels tested (*see below), and both substances share the same silanol product it is considered appropriate to read across the available data on trimethoxy(methyl)silane. Dimers and oligomers of methylsilanetriol are expected have lower toxicity than the corresponding monomer, therefore use of data on MTMS represents a worst-case interpretation.

Local irritant or corrosive effects due to the high pH of an aqueous solution of the registered substance are not addressed by the read-across data. It should be noted that at a concentration of 100 ppm (the NOAEC for MTMS), significant local effects would be expected, therefore the local NOAEC of an aqueous solution of so

lid phase potassium methylsilanetriolate is expected to be lower than the systemic NOAEC read-across from MTMS.

*Methyltrimethoxysilane (MTMS) hydrolyses to give methylsilanetriol and methanol. For the oral route, a NOAEL of 500 mg/kg was determined for methanol in a study to which reliability could not be assigned. This was based on fairly minor effects at 2500 mg/kg; there was stated to be increased liver weights, with increased liver enzymes. These liver effects were also observed for MTMS, but in females only, and not the same enzymes. Therefore, from the limited information on oral ingestion of methanol, there is no reason to think that the effects for MTMS were caused by methanol. For the inhalation route, the NOEL for methanol was 0.13 mg/l (10 ppm) based on slight body weight and organ weight changes, but even effects at 1000 ppm were not considered to be toxicologically relevant. Effects for MTMS occurred at doses of 400 ppm and above, and were more significant than those of methanol. Therefore, the effects of MTMS cannot be attributed to methanol.

Justification for classification or non-classification

The available data do not suggest that reaction mass of potassium methylsiliconate should be classified for effects following repeated exposure.