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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

There are no in vivo or in vitro data on the toxicokinetics of dichlorosilane. The following summary has therefore been prepared based on physicochemical properties of the substance itself and its hydrolysis products. Dichlorosilane is an inorganic gas at standard temperature and pressure and is very unstable in the presence of moisture. It will rapidly hydrolyse (half-life approximately 5 seconds at pH 4, 7 and 9 and 25°C (analogue read-across)) generating HCl and silanediol. The Si-H bonds of silanediol is expected to react rapidly to produce hydrogen and monosilicic acid. At concentrations above about 100 -150 mg/l (measured as SiO2 equivalents), condensation products of silanediols and monosilicic acid can also form. At concentrations >100 -150 mg/l of SiO2, monomeric monosilicic acid condenses into insoluble colloidal particles of polysilicic acid (silica sol) or a highly cross-linked network (silica gel). These forms of polysilicic acid are equivalent to synthetic amorphous silica. Before absorption into the body, most or all hydrolysis will have occurred and therefore, relevant systemic exposure is limited to the hydrolysis products.


Relevant inhalation exposure would be to the hydrolysis products (hydrolysis would occur rapidly when inhaled, even if a mixture of parent and hydrolysis products were present in air). The substance would also hydrolyse rapidly in contact with moist skin. The resulting HCl hydrolysis product would be severely irritating or corrosive.




Significant oral exposure is not expected for this corrosive substance. Should it occur then gastrointestinal absorption of insoluble silica will be insignificant as compared to the absorption of the soluble species (Carlisle, 1986).



The high water solubilities of silanediol and monosilicic acid might lead to some of this hydrolysis product being retained in the mucous of the lungs. Damage to membranes caused by the corrosive nature of the HCl hydrolysis product might enhances the uptake. Absorption of the insoluble condensation products is not expected.



The molecular weights of the parent and hydrolysis products favour absorption across the skin. However, the very high water solubilities (1E+06 mg/l and 1E+06; which are theoretical values and do not take into account the condensation reaction) and low predicted log Kow values (-1.5 and -4) of the initial hydrolysis product, silanediol and monosilicic acid, respectively, suggest that it is too hydrophilic to cross the lipid rich stratum corneum. Since the other hydrolysis product, HCl is corrosive to the skin, damage to the skin might increase penetration.

Absorption of the insoluble condensation products is not expected.

There are no reliable studies to check for signs of dermal toxicity, and skin irritation/corrosion studies did not report any signs of systemic toxicity.



All absorbed material is likely to be in the form of the hydrolysis products, silanediol, monosilicic acid and hydrogen chloride. Silanediol and monosilicic acid are small molecules, and therefore have potential to be widely distributed, but their hydrophilic nature will limit their diffusion across membranes (including the blood-brain and blood-testes barriers) and its accumulation in fatty tissues. Human blood contains 1 mg SiO2/l of monosilicic acid (Iler RK, 1979). Hydrogen and chloride ions will enter the body's natural homeostatic processes.



Dichlorosilane is rapidly hydrolysed generating HCl and silanediol, which will then further hydrolyse to monosilicic acid, both will then condense to give an amorphous precipitate. There is no data regarding the metabolism of silanediol. Silicon is an essential trace element participating in the normal metabolism of higher animals. It is required in bone, cartilage and connective tissue formation as well as participating in other important metabolic processes. The silicon is present almost entirely as free soluble monosilicic acid (Carlisle, 1986).



The low molecular weight and high water solubility of silanediol suggest that it is likely to be rapidly eliminated via the kidneys in urine. There is therefore no evidence to suggest that this substance will accumulate in the body. Any hydrogen produced as a result of the hydrolysis of silanediol to monosilicic acid would be exhaled.