Registration Dossier
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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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
Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 231-977-3 | CAS number: 7783-06-4
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Endpoint summary
Administrative data
Key value for chemical safety assessment
Effects on fertility
Effect on fertility: via oral route
- Endpoint conclusion:
- no study available
Effect on fertility: via inhalation route
- Endpoint conclusion:
- no adverse effect observed
- Dose descriptor:
- NOAEC
- 14 mg/m³
- Species:
- rat
- Quality of whole database:
- GLP guideline study
Effect on fertility: via dermal route
- Endpoint conclusion:
- no study available
Additional information
In a guideline study (OECD 421) with an inhalation exposure of H2S Dorman et al. (2000) determined if perinatal exposure by inhalation to H2S had an adverse effect on reproductive performance and pregnancy outcomes. Virgin male and female Sprague-Dawley rats (12/sex/group) were exposed to 0, 10, 30, or 80 ppm (0, 14, 42, or 111 mg/m3) H2S 6 hr/day, 7 days/week for two weeks prior to breeding. Exposure continued during a 2-week mating period and throughout gestational days 0-19 (GD 0-19). Evidence of copulation (vaginal plug or sperm in vaginal lavage fluid) during the 2-week mating period was considered GD 0. On postnatal day (PND) 4, litters were randomly reduced to 4 animals per sex when possible. Remaining pups were euthanized and discarded without being examined. Dams and pups were then exposed PND 5-18. Nonpregnant adult females were exposed for an additional 23-24 days following the 2-week breeding period. Adult males were exposed to H2S for 70 consecutive days. Clinical examinations were performed on all animals before and after each exposure (Dorman et al., 2000). The body weights of the F0 males and females were determined weekly throughout the study, except that female body weights were not determined weekly once evidence of mating was present. Presumed pregnant females were weighed on GD 0, 7, 14, and 20, and dams were weighed on PND 0, 4, 7, 14, and 21. Feed consumption was determined weekly in F0 males and prebreeding females. Feed consumption in presumed pregnant females was recorded for GD 0-7, 7-14, and 14-20. Dam feed consumption was recorded for PND 0-4, 4-7, 7-14, and 14-21. At the end of exposure, adult rats were euthanized and a complete necropsy was performed with emphasis on reproductive and accessory sex organs. Post-parturient animals were necropsied the day of or the day after weaning. At necropsy, the right testis from each F0 male was examined for sperm number, production, motility, and morphology.
No deaths or adverse clinical signs were observed in F0 males and females for any exposure group. There was a statistically significant decrease in feed consumption in male rats exposed to 80 ppm (111 mg/m3) H2S during the first week of the study. There was a small, but not statistically significant, decrease in body weight (5-6%) observed in F0 males and females exposed to 80 ppm (111 mg/m3) H2S that was present throughout entire exposure period. The only significant difference in organ weights was an increase in absolute and relative adrenal gland weights observed in F0 males exposed to 10 ppm (14 mg/m3) and 80 ppm (111 mg/m3) but not in the mid-dose of H2S and a decrease in the relative ovary weight of females in the 10 ppm (14 mg/m3) exposure group.
There were no statistically significant effects on reproductive performance (mating index, fertility index, postimplantation loss per litter, and number of late resorptions or stillbirths) in F0 animals. Also, the number of live pups, litter size, average length of gestation, and average number of implants per female were not affected. There were no statistically significant effects on sperm production or morphology noted in F0 males; however, a large percentage of abnormal sperm was observed in one F0 male from both the 30 (42 mg/m3) and 80 ppm (111 mg/m3) exposure groups (29 and 73%, respectively). In comparing high-exposure and control animals, there were a few histologic diagnoses with a higher incidence in the high-exposure group, including: testicular tubular degeneration, intratubular sperm stasis, tubular mineralization, sperm granulomas, and multinucleated giant cells, degenerate sperm forms in the lumen, aspermia, and oligospermia. While the incidence of testicular tubular degeneration in high-exposures was higher (42%) than the controls (17%), statistical significance was not achieved. One incidence each of sperm granuloma and unilateral necrosis of the cauda was present in the 80 ppm (111 mg/m3) exposure group. Notable histological findings in females included one each of ovarian cysts and squamous metaplasia of the endometrium in the 10 ppm (14 mg/m3) and 30 ppm (42 mg/m3) exposure groups. The olfactory neuron loss and basal cell hyperplasia observed in the male rats in this study are reported elsewhere (Brenneman et al., 2000). The study considered 12 rats/sex/group. In summary, the reproductive segment of this study did not demonstrate reproductive toxicity in either male or female rats following relatively high H2S exposure of 80 ppm (111 mg/m3) under repeated conditions (up to 70 days for males).
With regards to developmental effects from H2S exposure, there were no statistically significant increases in structural malformations. Observed malformations included kinked tail, agenesis of the tail, anophthalmia, small rear legs and body, frontal bone defects, hypognathia, and skin lesion characterized by detachment of the skin and dermis. However, none of these effects was dose-related. There were no significant differences in pup weight gain or development (pinnae detachment, surface righting, incisor eruption and negative geotaxis, vaginal patency, preputial separation, and eyelid separation). Surface righting was also equivalent across exposure groups. There were no treatment-related effects on motor activity, acoustic startle response, passive avoidance observed, or FOB. Terminal body and organ weights in all exposure groups were comparable to controls. Although a wide variety of gross observations were noted, they were not considered treatment-related by the investigators. Microscopic examination of six levels of the brain from pups from the control and high-dose group failed to demonstrate any histologic abnormalities.
Therefore the NOAEC for the reproductive and developmental toxicity was 80 ppm (111 mg/m3).
Short description of key information:
In a GLP study Dorman et al. (2000) examined the effects on
reproductive performance of an inhalation exposure to H2S. In this
combined systemic- and reproduction toxicity study according to OECD 421
Groups of 12 male and 12 female Sprague-Dawley rats were exposed to
hydrogen sulfide at 0, 10, 30, or 80 ppm 6 h/day, 7 days/week for 2
weeks before breeding. Exposures continued during a 2-week mating period
and then on GD 0-19. Exposure of the dams and pups (eight rats per
litter after culling) resumed from PND 5 to PND 18. Adult male rats were
exposed on 70 consecutive days.
Offspring were evaluated on the basis of motor activity, passive
avoidance, a functional observational battery, acoustic startle
response, and neuropathology. There were no deaths and no
treatment-related adverse clinical signs in parental males or females.
There were no significant effects on reproductive performance of the
parental rats as assessed by the number of females with live pups,
average gestation length, and average number of implants per pregnant
female.
There were no statistically significant effects on reproductive
performance (mating index, fertility index, postimplantation loss per
litter, and number of late resorptions or stillbirths) in F0 female
animals. Also, the number of live pups, litter size, average length of
gestation, and average number of implants per female were not affected.
No treatment-related effects in pups were noted in growth, development,
or behavioral tests.
No effect on fertility and no other effects were noted at any
concentration. The results of this study suggests that H2S is neither a
reproductive toxicant nor a behavioral developmental neurotoxicant in
the rat.
Therefore the NOAEC for the reproductive and developmental toxicity was
80 ppm (111 mg/m3).
Justification for selection of Effect on fertility via inhalation
route:
Key study
Effects on developmental toxicity
Description of key information
In a combined systemic- and reproduction toxicity study according to OECD 421 Groups of 12 male and female rats were exposed to H2S in concentratins of 0, 10, 30 and 80 ppm in the breathing air 6 hours per day on 7 days per week.
There were no deaths and no adverse physical signs observed in F0 male or female rats. There were no statistically significant effects on the reproductive performance of the F0 rats as assessed by the number of females with live pups, litter size, average length of gestation,and the average number of implants per pregnant female.
No relevant gross abnormalities were observed at necropsy in the brain, spinal cord, or peripheral nerves of any pup. Exposue to H2S did not affect pup growth, development, or performance on any of the behavioral tests. The results of this study suggests that H2S is neither a reproductive toxicant nor a behavior develomental neurotoxicant. So the NOAEC for the reproductive and developmental toxicity was 80 ppm (111 mg/m3).
In the histopathologic examination a significant increase in nasal lesions, such as olfactory neuron loss and basal cell hyperplasia, were observed following exposure to 30 and 80 ppm H2S. So the no-observed adverse effect level with respect to systemic toxicity was 10 ppm (14 mg/m³).
Effect on developmental toxicity: via oral route
- Endpoint conclusion:
- no study available
Effect on developmental toxicity: via inhalation route
- Endpoint conclusion:
- no adverse effect observed
- Dose descriptor:
- NOAEC
- 111 mg/m³
- Species:
- rat
- Quality of whole database:
- reliable. Above NOAEC of 111 mg/m3 is for the reproductive and developmental toxicity.
Effect on developmental toxicity: via dermal route
- Endpoint conclusion:
- no study available
Additional information
With respect to the data on the toxicity to reproduction of H2S a GLP combined systemic- and reproduction toxicity study according to OECD 421 is availiable. From this study the systemic toxicity as well as the different parts of reproduction toxicity: fertility, developmental toxicity and peri- and postnatal toxicity, can be evaluated.
All the other studies reported in literature were not performed according to a guideline and used a much shorter exposition time per day as the study of Dorman et al. (2000). Therefore their results are not comparable to the guideline study and these studies are judged as "not reliable" or as "not assignable" and the results of these studies are not used for the evaluation of the toxicity of H2S.
Justification for selection of Effect on developmental
toxicity: via inhalation route:
key study
Justification for classification or non-classification
According to the available data and CLP/DSD criteria, no classification is warranted for reprotoxic effects.
Additional information
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.