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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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: 231-901-9 | CAS number: 7778-39-4
- 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
![](https://echa.europa.eu./o/diss-blank-theme/images/factsheets/A-REACH/factsheet/print_toxicological-information.png)
Toxicity to reproduction
Administrative data
- Endpoint:
- screening for reproductive / developmental toxicity
- Remarks:
- based on test type (migrated information)
- Type of information:
- migrated information: read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- supporting study
- Study period:
- 2006
- Reliability:
- 4 (not assignable)
- Rationale for reliability incl. deficiencies:
- other: Data from review article
Cross-reference
- Reason / purpose for cross-reference:
- reference to same study
Data source
Reference
- Reference Type:
- review article or handbook
- Title:
- Unnamed
- Year:
- 2 006
Materials and methods
- Principles of method if other than guideline:
- Data from review article
- GLP compliance:
- no
- Limit test:
- no
Test material
- Reference substance name:
- Sodium dioxoarsenate
- EC Number:
- 232-070-5
- EC Name:
- Sodium dioxoarsenate
- Cas Number:
- 7784-46-5
- IUPAC Name:
- sodium dioxoarsenate(1-)
- Reference substance name:
- Arsenic
- EC Number:
- 231-148-6
- EC Name:
- Arsenic
- Cas Number:
- 7440-38-2
- IUPAC Name:
- arsine
- Reference substance name:
- Arsine
- EC Number:
- 232-066-3
- EC Name:
- Arsine
- Cas Number:
- 7784-42-1
- IUPAC Name:
- arsine
- Details on test material:
- - Name of test material (as cited in study report): Inorganic arsenic and structural analogues including arsenite and arsenic trioxide
Constituent 1
Constituent 2
Constituent 3
Test animals
- Species:
- other: rats and mice
- Strain:
- other: Swiss albino mice; CD-1 mice; Wistar rats
- Sex:
- male/female
Administration / exposure
- Route of administration:
- other: oral: gavage or drinking water; intraperitoneal
- Vehicle:
- water
- Details on mating procedure:
- No data
- Analytical verification of doses or concentrations:
- not specified
- Duration of treatment / exposure:
- Not applicable
- Frequency of treatment:
- Not applicable
- Details on study schedule:
- Not applicable
- No. of animals per sex per dose:
- Not applicable
Results and discussion
Overall reproductive toxicity
- Reproductive effects observed:
- not specified
Any other information on results incl. tables
A review article was published by Wang et al. (2006) describing the reproductive and developmental effects of arsenic and analogues.
Male reproductive toxicity:
Arsenite given through drinking water or by i.p. injection interferes spermatogenesis and lowers levels of testosterone and gonadotrophin causes male reproductive toxicity; these results suggest that arsenic may act on the brain or pituitary as well as directly on the germ cells (Chinoy et al., 2004; Pant et al., 2001, 2004; Sarkar et al., 2003).
- Male mice exposed to sodium arsenite in drinking water at up to 533.90μmol/L for 35 days showed reproductive toxicity without clinical effects. AsIII-treated mice did not show changes in body weight, testes weight, or accessory sex organ weights. However, at 533.90μmol/L, the activity of 17β-hydroxysteroid dehydrogenase (HSD) was decreased and conversely, the activities of lactate dehydrogenase (LDH) andγ-glutamyltranspeptidase (γGT) were increased in the testes. LDH was used as a marker of Leydig cell function, andγGT as a marker of Sertoli cell function. AsIII-treated mice also showed decreases in sperm count and motility along with an increase in abnormal sperm (Pant et al., 2001).
- Swiss albino mice were given sodium arsenite at 53.39μmole/L (equivalent to 4 ppm arsenic) via drinking water for 365 days, causes decreased testicular weights, sperm count and sperm motility and the percentage of abnormal sperm was increased. It also affects the activities of marker testicular enzymes which ultimately causes damage to germ cells (Pant et al., 2004).
- Sodium arsenite was administered to Wistar rats via i.p. injections at 4, 5, or 6 mg/kg/day for 26 days. At 5 and 6 mg/kg/day, relative testicular weight, accessory sex organ weights and epididymal sperm counts were decreased. Arsenic induced low levels of LH and FSH might be the trigger of suppressed testosterone synthesis, leads to increased spermatid degeneration (Sarkar et al., 2003).
- Male Swiss mice were administered with arsenic trioxide orally at 0.5 mg/kg for 30 days, affects the spermatogenesis, cholesterol metabolism and testicular testosterone level. Co-exposures to arsenic and fluoride (NaF) found that the recovery from arsenic and fluoride-induced effects can be facilitated by ascorbic acid, calcium, and vitamin E, which suggests that arsenic and fluoride induced reproductive toxicity was at least in part mediated by oxidative stress (Chinoy et al., 2004).
Female reproductive toxicity:
In female mice and rats, inorganic arsenic suppresses ovarian steroidogenesis, prolongs diestrus, and degenerates ovarian follicular and uterine cells. It also increases meiotic aberrations in oocytes, and decreases cleavage and pre implantation development (Chattopadhyay et al., 2001; Navarro et al., 2004; Zhang et al., 2000).
- Female Wistar rats gavaged with 10 mL of 0.4 ppm sodium arsenite daily for 28 days, causes uterine and ovarian toxicity, prolonged diestrous (due to low estradiol), decreased relative ovarian and uterine weights and affects the neuroendocrine regulation of female sex hormones (decreased LH, FSH, and estradiol). Decreased FSH level may contribute to the degeneration of ovarian follicles. It also causes uterine cell degeneration may be due to low ovarian estradiol and/or increased production of reactive oxygen species after arsenic treatment. The primary cause of AsIIItoxicity in the female reproductive system could be arsenic induced changes in the levels of catecholamines in the brain, which lowers gonadotrophin synthesis and secretion (Chattopadhyay et al., 2001, 2003).
- Female CD-1 mice were injected with 0, 8, or 16 mg/kg sodium arsenite i.p. every 2 days for a total of 7 injections over 14 days followed by injections of equine and human chorionic gonadotrophins overlapping the end of AsIII treatment to induce superovulation. AsIII induces oocyte meiotic aberrations and could subsequently decrease oocyte fertilization, preimplantation development, and embryo viability. Some of these arsenic effects on oocytes were observed at 8 mg/kg, which was a previously established maternal no-observed-adverse-effect level (NOAEL) (Navarro et al., 2004).
Applicant's summary and conclusion
- Conclusions:
- In conclusion, exposure to inorganic arsenic and analogues via oral or intraperitoneal route has shown adverse effects on reproduction in mice and rats.
- Executive summary:
A review article was published by Wang et al. (2006) describing the reproductive and developmental effects of arsenic and analogues. Exposure to inorganic arsenic and analogues through drinking water or by i.p. injection causes male reproductive toxicity by interfering spermatogenesis and lowering levels of testosterone and gonadotrophin. This suggested that arsenic may act on the brain or pituitary as well as directly on the germ cells. (Chinoy et al., 2004; Pant et al., 2001, 2004; Sarkar et al., 2003). In female mice and rats, inorganic arsenic suppresses ovarian steroidogenesis, prolongs diestrus, and degenerates ovarian follicular and uterine cells. It also increases meiotic aberrations in oocytes, and decreases cleavage and pre implantation development (Chattopadhyay et al., 2001; Navarro et al., 2004; Zhang et al., 2000).
In conclusion, exposure to inorganic arsenic and analogues via oral or intraperitoneal route has shown adverse effects on reproduction in mice and rats.
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.
![ECHA](/o/diss-blank-theme/images/factsheets/A-REACH/factsheet/echa_logo.png)