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EC number: 202-873-5 | CAS number: 100-63-0
- 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
Additional information
Non-human data:
Several in vitro studies assessing the genotoxic potential of phenylhydrazine were available:
Phenylhydrazine and phenylhydrazine hydrochloride were investigated in a number of Ames tests, in a variety of strains, and in the presence and absence of exogenous metabolic activation using up to 1000 ug phenylhydrazine or phenylhydrazine hydrochloride per plate (Shimizu et al., 1978; Tosk et al., 1979; De Flora, 1981; Parodi et al., 1981; Levin et al., 1982; Malca-Mor & Stark, 1982; Rogan et al., 1982; De Flora et al., 1984a,b; Wilcox et al., 1990; Muller et al., 1993). Study quality was high and standard methodology used. There is some variability in the findings, with positive results have been obtained in Salmonella typhimurium strains TA97, TA100, TA102, TA1537, and TA1538 in the absence of exogenous metabolic activation. In addition, positive results were obtained in the presence of metabolic activation in TA98 and TA1535.
Some investigators reported that the mutagenic action is slightly decreased by the presence of exogenous metabolic activation (Parodi et al., 1981; Malca-Mor & Stark, 1982; De Flora et al., 1984a,b).
However, one study reports an increase in mutagenic activity in the presence of metabolic activation (Rogan et al., 1982).
Phenylhydrazine was also positive in a number of other, less well validated bacterial assays (using S. typhimurium strains such as TA2638, TP138, BA9, and BA13), in the presence and absence of exogenous metabolic activation (De Flora et al., 1984b; Ulitzur et al., 1984; Ruiz-Rubio et al., 1985; Levi et al., 1986; Muller et al., 1993).
Phenylhydrazine was not tested in an in vitro chromosomal aberration assay. In a mammalian cell gene mutation assay in V79 cells, with and without metabolic activation, a positive result was reported for phenylhydrazine (Kuszynski et al., 1981). However, the study quality was low as there were several deficiencies in the reporting.
In unscheduled DNA synthesis assays in rat and mouse primary hepatocytes, concentrations of 0.0144 – 144 mg phenylhydrazine hydrochloride/litre were assessed (Mori et al., 1988). Although toxicity was measured, no details were given, and quantitative data were not reported. A positive result was obtained in both cell types, although the effect was small.
Phenylhydrazine was tested in a micronucleus assay in vitro using primary mouse bone marrow cells (Suzuki, 1985). Bone marrow cells from the femur were exposed to 1–50 g phenylhydrazine/mL for 30 min, in the presence and absence of metabolic activation. A total of 1500 polychromatic erythrocytes (PCEs) per concentration were scored for the presence of micronuclei. There was no measure of cytotoxicity. The percentage of micronucleated PCEs was statistically significantly increased, in the presence of S9 only, at phenylhydrazine concentrations of 5 ug/ml and greater in a concentration-related manner.
Several in vivo studies assessing the genotoxic potential of phenylhydrazine were available.
BALB/c mice were administered a single intraperitoneal injection of phenylhydrazine, and the incidence of micronucleated PCEs in the bone marrow measured at 24 and 48 h (Suzuki, 1985). Phenylhydrazine was reported positive in this test. However, in view of the poor reporting, no firm conclusions were drawn.
Groups of 11–12 female BALB/c mice were given a single intraperitoneal injection of 50 mg phenylhydrazine/ kg body weight in saline (Steinheider et al., 1985). Blood smears of tail vein blood were prepared at 24-h intervals for 7 or 11 days, and reticulocytes and micronuclei in normochromatic erythrocytes (NCEs) and PCEs were counted. There was no reporting of toxicity. Phenylhydrazine caused a statistically significant increase in the reticulocyte count on days 2–4 postinjection and in PCEs on day 3. There was a statistically significant increase in the incidence of micronucleated PCEs at 24 h post-injection (from 1 to 4.7 per 1000) and in micronucleated NCEs at 48 h post-injection (from 0.7 to 2.3 per 1000). However, similar increases in micronucleated NCEs were also seen following bleeding of the animals and splenectomy. The increase in micronuclei seen following phenylhydrazine treatment was considered due to stimulation of erythropoiesis, at least partly, because of the haemolysis induced by phenylhydrazine, thus leading to more errors of nuclear expulsion; hence, the results do not necessarily indicate a direct genotoxic action of phenylhydrazine.
In a study on DNA damage and repair groups of 7–12 mice were given a single intraperitoneal injection of either 85 or 170 mg phenylhydrazine/ kg body weight and killed 1 and 6 h, respectively, after treatment (Parodi et al., 1981). In addition, six mice were given a series of five daily intraperitoneal injections of 7.6 mg phenylhydrazine/kg body weight and sacrificed 6 h after the last injection. Control animals were injected with saline only. DNA damage was assessed by measurement of the alkaline elution rate of single-strand DNA from liver and lung tissue extracts. A statistically significant change in the elution rate of liver and lung DNA was seen in all groups of treated animals compared with controls, except in the case of lung tissue DNA from mice given a single dose of 85 mg phenylhydrazine/kg body weight. Phenylhydrazine is considered to give a positive result in this assay for DNA damage.
Finally, the formation of DNA adducts (N7-methylguanine and a trace of O6-methylguanine) in the liver was demonstrated in rats receiving 65 mg phenylhydrazine/kg body weight by oral gavage (Mathison et al., 1994).
Human data:
No data available
Short description of key information:
Phenylhydrazine was investigated for genotoxicity in a number of in vitro (Ames test, unscheduled DNA synthesis assay, micronucleus assay) and in vivo (micronucleus assay, formation of DNA adducts) assays. In summary, phenylhydrazine was considered genotoxic.
Endpoint Conclusion:
Justification for classification or non-classification
Based on genotoxicity results obtained and according to Directive 67/548/EEC (DSD) and Regulation 1272/2008/EC (CLP), phenylhydrazine was classified as mutagen ( cat 3, R68; cat 2, H341).
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