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EC number: 200-858-8 | CAS number: 75-29-6
- 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
In the GLP compliant, key bacterial reverse mutation assay (equivalent to OECD guideline 471), IPC was tested at doses of 0, 8, 40, 200, 1000, or 5000 µg/plate in Salmonella typhimurium strains TA 98, TA 100, TA 1535, and TA 1537 both in the absence and presence of exogenous metabolic activation [rat liver S9 (compound used to induce cytochrome P450 enzymes was not reported)] (Creutziger, 1989). The experiment was conducted in quadruplicate and an independent repeat experiment was performed. Acetone was used as the vehicle and positive controls were included in all incubations. No cytotoxicity was observed at any IPC concentration and no increases in the reverse mutation rate were noted in any strain either in the absence or presence of metabolic activation. Incubation with positive control substances in the absence or presence of metabolic activation resulted in anticipated increases in reverse mutation rates.
In a key, GLP compliant mammalian chromosome aberration test (according to OECD guideline 473), IPC was tested at doses of 0, 30, 300, or 800 µg/mL in human peripheral blood lymphocytes in the absence or presence of exogenous metabolic activation (Aroclor 1254-induced rat liver S9) (Heidemann, 1990). Incubations at each concentration were done in duplicate; however, an independent repeat experiment was not performed. Dimethyl sulphoxide (DMSO) was used as the vehicle control and ethylmethanesulfonate and cyclophosphamide were used as the positive control compounds in the absence and presence of metabolic activation, respectively. No cytotoxicity was observed and no chromosome damage was noted at any IPC concentration either in the absence or presence of metabolic activation. Incubations with the positive control compound resulted in anticipated increases in chromatid damage.
In a key, GLP compliant mammalian gene mutation assay (according to OECD guideline 476), IPC was tested at doses of 0, 80, 200, 400, or 800 µg/mL in the absence or presence of exogenous metabolic activation (Aroclor 1254-induced rat liver S9) in Chinese hamster lung fibroblast (V79) cells (Heidemann, 1990). The experiment was conducted in duplicate and an independent repeat experiment was performed. DMSO was used as the vehicle and ethylmethanesulfonate and 7,12-dimethylbenz[a]anthracene were used as the positive control compounds in the absence and presence of metabolic activation, respectively. Cytotoxicity was not observed and increases in the mutant frequency were not noted at any IPC concentration either in the absence or presence of metabolic activation. Incubation with positive control substances in the absence or presence of metabolic activation resulted in anticipated increases in the mutation frequencies.
In a key, GLP compliant in vivo micronucleus assay (according to OECD guideline 474), IPC was administered via intraperitoneal (IP) injection to male and female NMRI mice at a single dose of 2,000 mg/kg body weight (Korn, 1989). Corn oil was used as the vehicle and cyclophosphamide was administered via IP injection as the positive control compound. Animals were sacrificed 24, 48, or 72 hours after administration of the test article or controls (5 to 15 mice/sex/dose). No deaths were reported; however, sedation and piloerection were observed following test article administration. Statistically significant increases in the number of micronucleated polychromatic erythrocytes were not noted following IPC administration. The positive control compound caused anticipated increases in micronucleated polychromatic erythrocytes.
In a GLP compliant in vivo unscheduled DNA synthesis assay (equivalent to OECD guideline 486), IPC was orally administered to male Wistar rats at doses of 0, 100, 330, or 1000 mg/kg body weight (5 males/dose) (Fautz, 1990). Polyethylene glycol 400 was used as the vehicle and orally administered 2-acetylaminofluorene was used as the positive control compound. Following a post-exposure period of 12 to 14 hours, 1 rat receiving 1000 mg/kg body weight died; however, no clinical signs of toxicity were noted. In addition, no increases in the average nuclear grain count were observed at any IPC concentration. Administration of the positive control compound resulted in an anticipated increase in the average nuclear grain count.
Short description of key information:
The genetic toxicity of isopropyl chloride (IPC) has been assessed in 3 in vitro studies (including a bacterial reverse mutation assay) as well as in 2 in vivo studies (a micronucleus assay and an unscheduled DNA synthesis assay). Negative results were reported in all studies.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
The submission substance produced negative results in both in vitro and in vivo genetic toxicity studies. As a result, the substance does not meet the criteria for classification according to Regulation (EC) No 1272/2008, Annex I section 3.5.
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