Registration Dossier

Data platform availability banner - registered substances factsheets

Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Description of key information

No data are available for the repeated dose oral and inhalation toxicity of chloro(dimethyl)vinylsilane, therefore good quality data for the analogue of the hydrolysis product have been read-across to address the potential for systemic toxicity. In a 28-day repeated dose oral toxicity study in rats with trimethylsilanol, conducted in accordance with OECD 407 but lacking Functional Observation Battery examinations, the NOAEL was determined to be 250 mg/kg bw/day (Ramm and Bomhard, 1986). At the highest dose level, 750 mg/kg bw/day, adverse effects included increased relative liver weight in females and small deposits of brown pigment in the bile ducts of 4/5 males. Minimal bile duct proliferation was also observed in one male in the high dose group. In a repeated dose inhalation study  with trimethylsilanol conducted according to OECD 422 and in compliance with GLP (Fleeman, 2008), there were no adverse effects at any test concentration up to 600 ppm (ca. 2210 mg/m3).
In a 4-week inhalation study conducted specifically to assess respiratory tract changes and local toxicity, dichloro(dimethyl) silane was administered to rats at 5 or 25 ppm resulting in concentration-related effects in the nasal cavity indicative of a local irritant effect. The local effects noted at 25 ppm (resulting in 50ppm HCl on hydrolysis) were considered to be generally comparable to the group receiving hydrogen chloride at 50 ppm in the same study.
For local effects a good quality study on hydrogen chloride is available. In a 90-day repeated dose inhalation study, rats and mice (Toxigenics, 1983), were exposed to test concentrations of 0, 10, 20 and 50 ppm hydrogen chloride gas (HCl). Treatment was whole-body exposure for 6 hour per day, 5 days per week. The NOAEC for systemic effects was determined to be 20 ppm (approximately 30 mg/m3) based on decreased body weight following exposure to 50 ppm. A NOAEC could not be established as irritation/corrosion was observed at every concentration.

Key value for chemical safety assessment

Repeated dose toxicity: via oral route - systemic effects

Endpoint conclusion
Endpoint conclusion:
adverse effect observed
Dose descriptor:
250 mg/kg bw/day
Study duration:

Repeated dose toxicity: inhalation - systemic effects

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed
Dose descriptor:
2 210 mg/m³
Study duration:

Repeated dose toxicity: inhalation - local effects

Endpoint conclusion
Endpoint conclusion:
adverse effect observed
Dose descriptor:
15 mg/m³
Study duration:

Repeated dose toxicity: dermal - systemic effects

Endpoint conclusion
Endpoint conclusion:
no study available

Repeated dose toxicity: dermal - local effects

Endpoint conclusion
Endpoint conclusion:
no study available

Additional information

There are no adequate long term repeated dose toxicity data on chloro(dimethyl)vinylsilane or its hydrolysis product, dimethyl(vinyl)silanol, so good quality data for the related monosilanol, trimethylsilanol (1066-40-6), and the hydrolysis product, hydrogen chloride, have been used to assess the potential for adverse effects following exposure to chloro(dimethyl)vinylsilane.

It is considered not to be either ethical or technically feasible to perform repeated dose toxicity testing with chloro(dimethyl)vinylsilane by any route of exposure due to its known corrosive properties, which will dominate the toxicity profile of this substance. Following repeated oral dosing, the corrosive nature of the product could affect the lining of the stomach, giving rise to hyperplasia and a subsequent reduced food intake. This would confound the interpretation of any systemically driven effects. A guideline-compliant repeated-dose inhalation study should elicit systemic toxicity at the highest test concentration. Since the local corrosive effects of chloro(dimethyl)vinylsilane would be significant a valid inhalation study according to the relevant guidelines is technically not feasible. It is also unlikely that any systemic effects would be seen at dose levels made sufficiently low to prevent the known corrosive effects and/or distress in the test species. In the case of chloro(dimethyl)vinylsilane this concentration would need to be less than 49.3 mg/m3(based on a NOAEC for local effects of less than 10 ppm for HCl; see section on inhalation below for further details of testing with HCl). This has been confirmed in a 28-day inhalation study with another chlorosilane, dichloro(dimethyl)silane (WIL Research, 2014) in which there were no effects of treatment on clinical signs, body weight or food consumption that would indicate a systemic effect. Furthermore, the histopathology in the study indicated that the effects in the upper respiratory tract were similar to HCl. It is therefore concluded that HCl will determine the inhalation toxicity profile of chloro(dimethyl)vinylsilane.

With regard to the dermal route, due to the known corrosive effects of chloro(dimethyl)vinylsilane appropriate H-phrases and P-statements are included in the labelling, but repeated skin contact is unlikely to occur. Any accidental skin contact is expected to cause severe local effects but would be unlikely to cause any systemic effects.



The following discussion justifies the use of the conclusion 'no hazard identified' for humans exposed via the environment. Oral exposure is only relevant for the assessment of exposure via the environment as there are no consumer uses of this substance.

There are no adequate repeated dose toxicity data on chloro(dimethyl)vinylsilane so good quality data for the related monosilanol, trimethylsilanol (1066-40-6) have been used to assess the general systemic oral toxicity of chloro(dimethyl)vinylsilane. Local effects from the hydrolysis product, hydrogen chloride (HCl) are not addressed by these data (see section on local effects below).

Chloro(dimethyl)vinylsilane is very unstable in the presence of water and will hydrolyse very rapidly to dimethyl(vinyl)silanol and hydrogen chloride in the presence of moisture (see Section The hydrolysis half-life is less than 1 minute at 25°C and pH 4, 7 and 9. Most, if not all of this hydrolysis will have occurred before absorption into the body. Therefore the use of hydrolysis product data is considered appropriate in the assessment of the repeated dose toxicity profile of chloro(dimethyl)vinylsilane.

In general, due to the very rapid hydrolysis of chloro(dimethyl)vinylsilane, relevant environmental exposure would not be to the parent substance but to the hydrolysis products, dimethyl(vinyl)silanol and HCl. At environmentally-relevant concentrations, the silicon-containing hydrolysis product would be present predominantly as monomeric silanol. However, the assessment of the potential level of human risk via the environment is done by first calculating a Derived-No-Effect-Level (DNEL) for the General Population for the relevant route(s) e.g. oral and theoretically in some cases, inhalation. The route of choice for studies most relevant to exposure via the environment is the oral route, since direct exposure to the general population to chlorosilanes or silanols via air emissions from industrial sites is negligible.

Toxicity data for the silicon-containing hydrolysis product are read-across from the related substance, trimethylsilanol. However, the doses and concentrations used in the toxicity studies are not relevant for the environmental exposure assessment. This is because the silanols undergo condensation reactions at the high concentrations that can occur internally in test animals. This means that what the animals are actually exposed to in toxicity studies is not only the monomer, which would be present in the environment, but also to the dimer (assuming that the behaviour in the GI tract follows the in vitro chemical behaviour). Therefore, any observed effects could be due to exposure to the dimer and would then not be relevant for exposure via the environment, where low concentrations mean that condensation is not significant.

A toxicity study conducted at doses and concentrations low enough to ensure exposure to monomer only i.e. minimal condensation reactions occurring, would almost certainly not result in any systemic toxicological effects.

Dimethyl(vinyl)silanol undergoes condensation reactions in solution to give siloxane dimers (.1,1,3,3 -tetramethyl-1,3 -divinyldisiloxane, CAS 2627 -95 -4). A dynamic equilibrium is established and under certain conditions an insoluble product is formed. The overall rate and extent of condensation is dependent on nominal loading, temperature, and pH of the system, as well as what else is present in the solution. The condensation reactions of monosilanols may be modelled as an equilibrium between monomer and dimer. The reactions are reversible unless the dimer concentration exceeds its solubility; in this case, the dimer forms a separate phase, driving the equilibrium towards the dimer. For dimethyl(vinyl)silanol, a solution at 100 mg/l is predicted to contain >99% monomer, with small amounts of dimer. At loadings above about 250 mg/l the concentration of the dimer of the silanol hydrolysis product is predicted to exceed its solubility, resulting in formation of a separate phase. 

Following dosing by oral gavage, partitioning will occur between the dose vehicle and the aqueous environment in the stomach.

Mass dosed                            =        Body weight (in kg) x dose level (in mg/kg bw day)


Dose Concentration                 =        mass dosed/volume


This represents an upper limit of the concentration as some of the substance is expected to adsorb to fatty tissue or remain dissolved in the dose vehicle (until this is broken down)

For a study conducted at a dose level of 10 mg/kg bw/day and assuming a body weight of 300 g, the total amount dosed is therefore 3 mg, into an estimated aqueous volume of 1.5 ml in the rat stomach. The concentration in water is therefore up to 2000 mg/l. At such a concentration, condensation is already an important factor.

Body weight                            =        300 g  =        0.3 kg

Total amount dosed                 =        3 mg

Estimated aqueous volume       =        1.5 ml

Dose concentration                  =        2000 mg/l


At a typical upper dose level of 1000 mg/kg bw/day the corresponding concentration would be 200 000 mg/l.

Body weight                            =        300 g   =        0.3 kg

Total amount dosed                 =        300 mg

Estimated aqueous volume       =        1.5 ml

Dose concentration                  =        200 000 mg/l


Based on a condensation limit of 250 mg/l, the maximum dose level that could be used in practice to ensure exposure mainly to monomeric dimethy(vinyl)silanol is approximately 1.25 mg/kg bw/day or less.

Body weight                            =        300 g  =        0.3 kg

Total amount dosed                 =        0.375 mg

Estimated aqueous volume       =        1.5 ml

Dose concentration                  =        250 mg/l


Therefore, any in vivo study relevant to humans via the environment (MvE) would have to be conducted at doses that would not result in any useful toxicological information and as such would not be ethical to conduct from an animal usage perspective. This ethical point has been confirmed by third parties in the recent consultations required for the trichlorosilane legal action (Case No. A-017 -2015) . Therefore, it is reasonable to conclude that testing for the MvE endpoint only would not be ethical. In REACH terms, this could equates to a conclusion of no hazard for MvE.


In an oral gavage study conducted to OECD test guideline 407 with trimethylsilanol, groups of Wistar rats (5/sex/dose) were given daily doses of either 0 (castor oil vehicle only), 80, 250 or 750 mg/kg bw/day for 28 days (Ramm and Bomhard, 1986). Clinical observations, food and water intake, body weights, organ weights, clinical chemistry, haematology, and histopathology were all recorded. Toxicologically relevant adverse effects (reduced body weight gain, reduced alkaline phosphatase, reduced glucose (males), increased liver weights (females), and increased adrenal weights (males), and minor deposits in the bile ducts) were observed at the highest dose of 750 mg/kg bw/day. The NOAEL was 250 mg/kg bw/day, as effects observed at this or the lower dose of 80 mg/kg bw/day, were not dose-dependent and often values were within the normal range for historical controls.



As has already been described above, chloro(dimethyl)vinylsilane is a corrosive substance that is decomposed by water, producing dimethyl(vinyl)silanol and HCl, and the systemic effects of chloro(dimethyl)vinylsilane would be secondary to local corrosion. For local effects it is appropriate to read across results of a 90 -day inhalation toxicity study on HCl, which demonstrates the severe corrosive effects of HCl in the respiratory tract.

In a 90-day repeated dose inhalation study in rats and mice (Toxigenics, 1983), 31 males and 21 females of each species/strain were exposed to test concentrations of 0, 10, 20 and 50 ppm hydrogen chloride gas (HCl). Treatment was whole-body exposure for six hour per day, 5 days per week. Fifteen males and 10 females from each group were sacrificed after four exposures and the nasal turbinates, trachea, lung and gross lesions were examined microscopically. In general, all animals in the high dose group showed adverse findings after 4-days exposure.

One female high dose mouse was found dead on study day 12, and four low dose male mice were found dead on study day 92. In addition, one high dose female mouse was sacrificed in extremis on study day 20. One high dose female Sprague-Dawley rat was found dead on study day 4. However, the study authors noted that the deaths did not appear to be related to exposure to HCl. Clinical signs were consistent with the irritant/corrosive properties of HCl (appendage, tail or lip injury in the form of toe missing/swollen/open/gelatinous, scabbed/deformed/lesion, crusty nose, tissue mass, mouth injury, scabbed nose, crusty muzzle, red stained fur, nasal discharge, crusty eye, poor coat quality); some of the observed injuries may have been mechanical and not related to test material exposure.

Ninety days exposure to 50 ppm HCl resulted in decreased body weights in all four strains after four exposures. Following 90 days of exposure B6C3F1 male and female mice and male Sprague-Dawley rats exposed to 50 ppm had biologically significant decreases in body weight.

After four days of exposure there were statistically significant decreases in food consumption for high dose male Sprague-Dawley rats and male Fischer 344 rats. After 90 days high dose mice had the largest reduction in food consumption. The rats did not show a consistent reduction in food consumption that could be deemed exposure-related.

There were no treatment-related effects on the haematology, clinical chemistry or urinalysis parameters that were examined.

Decreased liver weights were observed in high dose male and female mice and Fischer 344 female rats. The authors noted that this might have been due to the overall reduced body weights.

Animals exposed to all concentrations of HCl had minimal to mild rhinitis, which occurred in the anterior portion of the nasal cavity and was dose and time related. Mice also developed varying degrees of cheilitis with accumulations of haemosiderin-laden macrophages involving the perioral tissues at 50 ppm. At all exposure concentrations mice developed oesinophilic globules in epithelial cells lining the nasal turbinates after 90 days of exposure. The No Observed Adverse Effect Concentration (NOAEC) for systemic effects was determined to be 20 ppm (approximately 30 mg/m3) based on decreased body weight following exposure to 50 ppm. No NOAEC for local effects was established as irritant/corrosive effects were observed at all dose levels tested.

Since the NOAEC for local effects following exposure of rodents to HCl in the above study was unknown but less than 10 ppm, it can be concluded that a concentration of less than 49.3 mg/m3 of chloro(dimethyl)vinylsilane would need to be tested in order to avoid the local effects of the HCl hydrolysis product. 

Similar local effects were noted for the group administered HCl in the 4 -week dichloro(dimethyl)silane inhalation study (WIL, 2014).This study compared the effects of dichloro(dimethyl)silane at 5 or 25 ppm (equivalent to 10 and 50 ppm HCl after the rapid hydrolysis. I

n this 4-week repeated dose study (WIL, 2014) inhalation administration of dichloro(dimethyl)silane at targeted concentrations of 5 or 25 ppm (26 or 132 mg/m3) or hydrogen chloride at 50 ppm to rats for 5 days per week for 4 weeks resulted in subacute inflammation, hyperplasia and/or hyperkeratosis of the squamous epithelium and mucous cell hyperplasia of the respiratory epithelium in the anterior nasal cavity, with a clear dose-relationship in incidence and severity between the 5 and 25 ppm dichloro(dimethyl)silane groups for the majority of findings. Exposure to 25 ppm (132 mg/m3) dichloro(dimethyl)silane or 50 ppm hydrogen chloride was also associated with interstitial edema and respiratory epithelial degeneration within the anterior nasal cavity and acute inflammation in the larynx. Generally the incidence and severity of effects were similar in the 25 ppm dichloro(dimethyl)silane and 50 ppm hydrogen chloride groups, or greater in the hydrogen chloride group. The incidence and severity of the effects in the hydrogen chloride exposed group were generally comparable to those noted in the 90-day inhalation study with hydrogen chloride (Toxigenics, 1983). Overall, the histopathology observations in the nasal cavity did not suggest a greater irritant effect for the 25 ppm dichloro(dimethyl)silane group compared with the 50 ppm HCl group.



In an inhalation study conducted according to OECD 422 with trimethylsilanol (Fleeman, 2008), three groups of Crl: CD(SD) rats, each group consisting of 10 males, 10 toxicity phase females and 10 reproductive phase females, were exposed via whole-body inhalation to vapour atmospheres of the test article, trimethylsilanol, 6 hours/day, 7 days/week. F0 toxicity phase females were exposed for 28 consecutive days. One F0 toxicity phase female in the 300 ppm group was found dead but there were no mortalities in the 600 ppm group. Therefore, this mortality at 300 ppm was not attributed to test article exposure. All other toxicity phase females and all F0 males survived to the scheduled necropsies. There were no test article-related macroscopic findings or effects on organ weights. There were no remarkable clinical observations noted at any exposure level. Mean body weights, body weight gains and food consumption for males and females at all exposure levels were similar to the control group for all phases. There were no test article-related effects on FOB parameters. Test article-related effects were limited to changes in haematology (lower eosinophil and lymphocyte counts for males) and serum chemistry (higher alanine aminotransferase for males and toxicity phase females) at 600 ppm. These changes occurred in the absence of correlating histologic changes and were not considered adverse. Therefore, under the conditions of this screening study, an exposure level of 600 ppm was considered to be the no-observed-adverse-effect concentration (NOAEC) for systemic toxicity of trimethylsilanol when administered via whole-body inhalation exposure to Crl: CD(SD) rats.

A supporting study for repeated dose inhalation toxicity with the read-across substance trimethylsilanol was also available, which reports a NOAEL of >= to 300 ppm, based on CNS/behavior-related clinical signs of hypoactivity (males) and impaired equilibrium (females) and macroscopic findings of diffusely pale lungs in the 600 ppm group (Weinberg, 2007). The study exposed the rats six hours per day, daily and was conducted according to a protocol similar to OECD guideline 412).



CAS Number



Chemical Name



Si hydrolysis product


Not applicable

Molecular weight



log Kow(parent)

Not measurable


log Kow(silanol hydrolysis product)


Not applicable

Water sol (parent)

Not measurable

995 mg/l

Water sol (silanol hydrolysis product)

3700 mg/l

Not applicable

Vapour pressure (parent)

9500 Pa at 20oC

1290 Pa at 20oC

Vapour pressure (silanol hydrolysis product)


250 Pa at 25oC

Not applicable


Hydrolysis t1/2at pH 7 and 25°C

<1 minute

Not applicable


Hydrolysis t1/2at pH 2 and 37°C

 <1 minute  Not applicable

Chloro(dimethyl)vinylsilane hydrolyses very rapidly in contact with moisture and therefore any systemic exposure to the substance would relate only to hydrolysis products.

(c) Similar toxicokinetics

The only potential route for oral exposure applicable to chloro(dimethyl)vinylsilane is for humans exposed via the environment. As explained above, exposure would be predominantly to monomeric silanol and it is not feasible to conduct a meaningful study for this endpoint. Nevertheless, the available repeated dose toxicity data for an analogous monosilanol (trimethylsilanol) are included for completeness.

For the inhalation route, dimethyl(vinyl)silanol and trimethylsilanol have similar molecular weight and log Kowvalues, indicating that systemic uptake in the respiratory tract is similar. The higher vapour pressure of trimethylsilanol means that the available inhalation study was conducted at a concentration higher than could be achieved with the hydrolysis product of the registration substance and thus represents a worst case in terms of exposure concentration.

The critical effect following dermal exposure to chloro(dimethyl)vinylsilane is corrosion and therefore significant systemic exposure is not expected since appropriate measures are in place to prevent local effects (see Section 9 of the CSR).

(d) Acute toxicity

Although an acute oral toxicity study is available for the registration substance (LPT, 2002), it is not appropriate to directly compare the results of this study with the available data for trimethylsilanol due to the potential for confounding effects due to the corrosive nature of the chlorosilane.

The available oral toxicity study for trimethylsilanol (Bayer, 1985), reports an LD50for trimethylsilanol of 3.5 ml/kg bw (2835 mg/kg bw based on a density of 0.81 g/cm3) in rats. There was a general deterioration in the animals' health, including anaesthesia, lateral position, ruffled fur. All surviving animals appeared symptom-free after ten days.

In an acute inhalation study (WIL, 2007), the reported 4 hour LC50of trimethylsilanol was 3151 ppm (11.8 mg/l) in rats. Significant clinical observations for the surviving animals included decreased respiration, shallow respiration, rales, hypoactivity, prostration, ataxia, lacrimation of the eyes, partial closure of the eyes, decreased defecation, decreased urination, opacity of the eyes.

In comparison, acute oral and inhalation have been included for a number of alkoxysilane substances which contain vinyl groups, as shown in the table below, which indicate that the presence of the vinyl group in place of methyl does not lead to any enhanced acute systemic toxicity and in fact trimethylsilanol may be regarded as a worst case.

CAS Number






Chemical name






Hydrolysis product

Not applicable





Acute oral LD50(rat)

3.5 ml/kg (2835 mg/kg)

3575 mg/kg

 No data

7.34 ml/kg males; 7.46 ml/kg females.

>5000 mg/kg

Acute inhalation LC50(rat)

11.8 mg/l

43.1 mg/l

>5 mg/l

2773 ppm (16.9 mg/l)


(e) Discussion of repeated systemic toxicity of the non-silanol hydrolysis product

In a 90-day repeated inhalation study with HCl, no serious adverse systemic effects were observed in rats and mice exposed up to 50 ppm (ca. 70 mg/m3) for 6 hours per day, 5 days per week. The only significant adverse finding relating to systemic toxicity was decreased body weight at the highest dose level. Local effects on the nasal turbinates of mice were observed at all dose levels tested (10, 20 and 50 ppm). Testing with HCl at higher test concentrations is neither ethically nor technically feasible since severe corrosive effects would lead to discomfort and distress in the test animals. The author of this CSR considers that the apparent systemic effects at 50 ppm in the study were most likely secondary to local corrosive effects at this dose level.

Following uptake of HCl, hydrogen and chloride ions will enter the body’s natural homeostatic processes and significant systemic effects are unlikely.

(f) Discussion of local inhalation toxicity of HCl and chlorosilanes

No long-term toxicity studies are available for the registration substance, chloro(dimethyl)vinylsilane. A non-standard acute inhalation study (Dow Corning, 1969) is available. In this study, all 5 animals exposed to saturated vapour died within 27 minutes. Significant ocular and respiratory irritation was observed after 3 minutes of exposure.

Comparison of the acute inhalation toxicity of chlorosilanes to that of hydrogen chloride showed a correlation between toxicity (LC50) and the amount of HCl generated by the chlorosilanes (Jean et al., 2006).

In a 4-week inhalation study (WIL, 2014) conducted specifically to assess respiratory tract changes and local toxicity, dichloro(dimethyl) silane was administered to rats at 5 or 25 ppm resulting in concentration-related effects in the nasal cavity indicative of a local irritant effect. The local effects noted at 25 ppm (resulting in 50ppm HCl on hydrolysis) were considered to be generally comparable to the group receiving hydrogen chloride at 50 ppm in the same study.

Given the comparability of existing results for chlorosilanes and HCl, and the rapid hydrolysis of chlorosilanes in the atmosphere, the effects of HCl dominate local toxicity on the respiratory tract and therefore data for HCl can be used to assess the local repeated-dose toxicity of chlorosilanes.

Justification for selection of repeated dose toxicity via oral route - systemic effects endpoint:
The selected study is the only relevant oral repeated dose study available. It was conducted in accordance with an appropriate OECD test guideline and in compliance with GLP. However, the study did not include the full Functional Observation Battery examinations required by the guideline.

Justification for selection of repeated dose toxicity inhalation - systemic effects endpoint:
The key study is conducted to OECD test guideline, in compliance with GLP and of the available inhalation studies it tested the longest duration of exposure.

Justification for selection of repeated dose toxicity inhalation - local effects endpoint:
The selected study is a reliable 90-day repeated inhalation study with hydrogen chloride. The effects observed in this test reflect local effects that would be caused by chlorosilanes which rapidly hydrolyse to produce hydrochloric acid.

Justification for classification or non-classification

Based on the available read across data from trimethylsilanol (an analogue of the silanol hydrolysis product), and hydrogen chloride, chloro(dimethyl)vinylsilane does not require classification for repeated dose toxicity according to Regulation (EC) 1272/2008.