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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Toxicity to reproduction

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Administrative data

extended one-generation reproductive toxicity - basic test design (Cohorts 1A, and 1B without extension)
Data waiving:
study scientifically not necessary / other information available
Justification for data waiving:
the extended one-generation reproductive toxicity study does not need to be conducted because there are no results from available repeated dose toxicity studies that indicate adverse effects on reproductive organs or tissues, or reveal other concerns in relation with reproductive toxicity
Reason / purpose for cross-reference:
data waiving: supporting information

RDT oral (OECD TG 408), rat: NOAEL local = 40 mg/kg bw/day, NOAEL systemic = 40 mg/kg bw/day

Endpoint conclusion:
adverse effect observed
Dose descriptor:
40 mg/kg bw/day
Study duration:
Quality of whole database:
The available information comprises an adequate and reliable study, and is thus sufficient to fulfil the standard information requirements set out in Annex VIII-IX, 8.6, of Regulation (EC) No 1907/2006.
Endpoint conclusion:
no study available
Endpoint conclusion:
adverse effect observed
Dose descriptor:
15 mg/m³
Study duration:
Quality of whole database:
The study was well documented and meets generally accepted scientific principles, and conducted in compliance with GLP. The relevance of these data for hazard assessment of dichloro(diphenyl)silane is discussed in the endpoint summary.
Endpoint conclusion:
no study available
Endpoint conclusion:
no study available

Oral route

A reliable subchronic study in rats according to OECD TG 408 and in compliance with GLP is available by the oral route for dichloro(diphenyl)silane (BSL, 2021). Based on the results of a dose-range finding study (BSL, 2019) male and female Wistar rats were administered the test substance at dose levels of 10, 40 and 125 mg/kg bw/day for 90 days. The control group received the vehicle dried and deacidified corn oil. A recovery group was included in the control and high dose group and observed for a period of 28 days following the last administration.

No test item-related mortality was observed during the treatment and recovery periods and no adverse clinical findings were found during the observation period, weekly detailed clinical observation and functional observation and ophthalmoscopy in the last week of the treatment period or recovery period. There were no test item-related effects on body weight development and food consumption in any of the dose groups when compared to controls in both males and females. No test item-related adverse effects were observed in haematology, coagulation and urinalysis parameters in any of the dose groups. Furthermore, no test item-related effects were observed for thyroid hormone analysis. In correlation to the histopathological findings in the liver and kidneys, the changes observed in mean ASAT, creatinine and potassium were considered to be test item-related in the high-dose group. Fertility parameters in males were not affected by treatment with the test item and no test item-related effects on the testicular histomorphology were observed. No test item-related changes were observed on the estrous cycle in all dose groups at the end of the treatment and recovery periods. There were no macroscopic changes that could be attributed to treatment with the test item. Test item-related organ weight increases were observed in the liver and kidneys in the mid-dose and high-dose groups at the end of the treatment period. At the end of the recovery period, there were no statistically significant differences in the liver and kidney weights of both sexes.

Histological findings related to treatment with the test item were seen in several organs of the high-dose group (kidney, urinary bladder, liver, adrenal glands, jejunum, stomach and nasal cavity).

There was diffuse vacuolation of the proximal tubular cells in both sexes of the high-dose group in the kidney. This vacuolation caused tubular cell hypertrophy in most of the affected animals. These findings were not associated with further evidence of degenerative changes, and therefore were deemed not to be of an adverse nature, but an adaptive response to an increased demand of tubular functions such as transcellular transport and metabolism.

In the urinary tract, there was also diffuse, simple urothelial hyperplasia in the urinary bladder and was observed in both sexes in the high-dose group. In some affected cases, edema and/or mononuclear cell infiltration in the submucosa/lamina propria were also involved in the lesions.

In the stomach, there was increased incidence and/or severity of inflammation and reactive changes in the forestomach of both sexes at the high dose. The findings consisted of multifocal inflammatory cell infiltration, submucosal edema, and focal to multifocal hyperplasia of the squamous epithelium with hyperkeratosis. In a single case (one male), there was also ulceration. These effects were considered to be the lesions caused by the corrosive or irritative properties of the test item.

The histological findings that were considered to be related to the physiocochemical properties of the test item were also observed in the nasal cavity of both sexes of the high-dose group. The findings consisted of regenerated olfactory and/or respiratory epithelium, accompanied by mucosal to submucosal mixed inflammatory cell infiltration in some cases. The cause of nasal cavity lesions was deemed to be a consequence of incidental influx or retrograde uptake of the test item formulation.

The lipid accumulation in the lamina propria mucosa of the jejunum was observed in both sexes at the high-dose. The minimal centrilobular hepatocellular hypertrophy in itself was considered to be of an adaptive nature but not adverse. Meanwhile, in the liver of the high-dose group, there was both an increased incidence and severity of hepatocellular fatty change in multifocal or patchy manner. Increased or increased tendency of liver weights recorded in mid-dose and/or high-dose groups were considered to be associated with these findings most likely of a metabolic nature in the liver. In addition, the incidence and/or severity of fatty change in the zona fasciculata of the adrenal gland were increased in both sexes at the high-dose. Thus, the effects on lipid biosynthesis and/or metabolism were suggested.
All findings mentioned above, whether systemic or local, primary or secondary to the treatment-related effects, recovered or showed signs of recovery after a 28-day withdrawal period.

Under the conditions of this oral 90-day repeated dose toxicity study in rats the NOAEL for local (forestomach) and systemic toxicity (liver) was established at 40 mg/kg bw/day.

Inhalation route

Dichloro(diphenyl)silane (CAS 80-10-4) is a highly moisture-sensitive liquid that hydrolyses rapidly in contact with water (measuredhalf-life of 6 to 10 seconds at pH 4, 7 and 9 at 1.5°C) to diphenylsilanediol and hydrogen chloride (HCl). Hydrolysis is complete within few minutes.

In a 90-day repeated dose inhalation study in rats and mice (Toxigenics, 1984), 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. 15 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. 90-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 urinalyis 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.

With regard to the inhalation route of exposure, a guideline-compliant repeated-dose inhalation study should elicit systemic toxicity at the highest test concentration. Since the local corrosive effects of chlorosilanes 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. This hypothesis has been confirmed in a 28-day inhalation study with a chlorosilane, dichloro(dimethyl)silane (CAS 75-78-5, WIL, 2014). In this 4-week repeated dose study 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 (75 mg/m³) 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. There was a clear dose-relationship in incidence and severity between the 26 or 132 mg/m³ dichloro(dimethyl)silane groups for the majority of findings. Exposure to 132 mg/m³ dichloro(dimethyl)silane or 75 mg/m³ hydrogen chloride was also associated with interstitial oedema 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 132 mg/m³ dichloro(dimethyl)silane and 75 mg/m³ 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 132 mg/m³ dichloro(dimethyl)silane group compared with the 75 mg/m³ hydrogen chloride group.

It is therefore concluded that hydrogen chloride will dominate the inhalation toxicity profile of chlorosilanes. Based on these conclusive data, repeated dose animal studies via the inhalation route with chlorosilanes are not considered to be ethically justifiable.

The available acute inhalation toxicity studies with chlorosilanes all meet the criteria for classification as either acutely toxic or harmful (LC50 below 20 mg/L with deaths occurring minutes after start of exposure). The local effects and mortalities observed in the studies can be attributed to hydrogen chloride (hydrolysis of the parent chlorosilanes would occur rapidly when inhaled, even if a mixture of parent and hydrolysis products were present in air) (Jean et al. 2006). The mortalities associated with the severe corrosive nature of chlorosilanes (rather than a systemic effect) have been confirmed by the findings from studies for at least fourteen chlorosilanes, which were performed according to the respective OECD guideline. In these studies, severe corrosive effects were observed even after short exposure times (e.g. 1 hour). The most common observations were respiratory irritation (labored breathing, rales, gasping and necrosis of the nose), dermal irritation, ocular effects (corneal opacities, lacrimation) as well as red/brown staining around the snout and/or eyes and scabs on snout. Substances causing these effects include the following: dichloro(methyl)(vinyl)silane (CAS 124-70-9), dichloro(dimethyl)silane (CAS 75-78-5), dichloro(methyl)silane (CAS 75-54-7), trichloro(vinyl)silane (CAS 75-94-5), chlorotri(3-methyl-propyl)silane (CAS 13154-25-1) or trichloro(methyl)silane (CAS 75-79-6). Most of the above mentioned indicators of toxicity showed marked resolution in those animals which survived to the end of the recovery period. Macroscopic observation of the animals also revealed lung injury (consolidation, haemorrhage, congestion, and ectasia), red or dark red discoloration of the lungs, fluid-filled pleural and thoracic cavities and trachea, periocular and perinasal encrustations and eye abnormalities. Substances causing the above macroscopic observations include the following: dichloro(dimethyl)silane (CAS 75-78-5), dichloro(methyl)(vinyl)silane (CAS 124-70-9), trichloro(vinyl)silane (CAS 75-94-5), dichloro(methyl)silane (CAS 75-54-7), trichloro(propyl)silane (CAS 141-57-1), chlorotrimethylsilane (CAS 75-77-4), chlorodimethylsilane (CAS 1066-35-9) or dichlorosilane (CAS 4109-96-0).The typical effects associated with exposure to corrosive substances were observed in the acute studies.

Overall, 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.

The available oral repeated dose toxicity data of the registered substance do not meet the criteria for classification according to Regulation (EC) No. 1272/2008, and are therefore conclusive but not sufficient for classification.

Data source

Materials and methods

Results and discussion

Applicant's summary and conclusion