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EC number: 932-389-6 | CAS number: -
- 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
The mutagenic potential of Cyhalothrin was assessed in a bacterial reverse mutation assay (Trueman 1981).
The test item Cyhalothrin was found to be not mutagenic in the bacterial reverse mutation assay (Ames test) with the tester strains TA1535, TA1537, TA1538, TA98, and TA100 with or without metabolic activation using S9 mix from Aroclor1254 induced rat liver.
There are three supporting studies that indicate no genetic toxicity activity for cyhalothrin.
A microbial mutagenicity study (Hideo Fukuda, 1983): in the recassay using Bacillus subtilis H17 and M45 strains cyhalothrin induced no inhibition zone at all in these strains even at the highest dose level (100% V/V, undiluted concentrate 20μl/disc). In addition, reverse mutation tests with and without a metabolic activation system from the liver using Escherichia coli WP2 strain and five strains of Salmonella typhimurium TA series were conducted, and cyhalothrin proved negative in the tests.
It has been concluded that cyhalothrin is negative in the microbial mutagenicity study conducted under the testing conditions employed in this study because cyhalothrin induced no inhibition zone at all in the two tester strains at all dose levels in the rec-assay and it showed no mutagenicity at all in the reverse mutation tests.
A micronucleus test on mouse (Randall, 1989): Cyhalothrin has been evaluated for its ability to induce micronuc1eated polychromatic erythrocytes in the bone marrow of C57BL/6JfCD-l/Alpk mice. Cyhalothrin was given as a single oral dose to groups of five male mice at dose levels of 13.5 or 21.6mg/kg and to groups of five female mice at dose levels of 15.5 or 24.8mg/kg; these being 50% and 80% of the median lethal dose as determined over a four day period. Bone marrow samples were taken for analysis 24, 48 and 72 hours after dosing.
An examination of the incidence of micronucleated polychromatic erythrocytes showed a negative response for cyhalothrin at both of the dose levels tested. The positive control substance, cyclophosphamide dosed at 65mg/kg, gave significantly increased frequencies of micronucleatect polychromatic erythrocytes at the 24 hour sampling time, thus demonstrating the sensitivity of the test system to a known clastagen. It is therefore concluded that cyhalothrin is not clastagenic in this assay.
An Oral (gavage) dominat lethal study in the male mouse (Lorraine, 1981): three groups of proven, male mice were dosed with Cyhalothrin, by gavage, at dose levels of 1, 5 or 10 mg/kg daily for 5 consecutive days. They were then sequentially mated with virgin, female mice (2females/male/week) for 8 weeks.
Two control groups were employed. The negative control group consisted of proven, male mice given 10 ml/kg maize oil (the vehicle), by gavage, over the same period and similarly mated.
The positive control group consisted of proven, male mice dosed once with Cyclophosphamide (200 mg/kg), by intraperitoneal injection, and similarly mated.
At the dose levels studied there was no evidence of an increase in the frequency of dominant lethal mutations following treatment, for 5 consecutive days, with Cyhalothrin. Therefore, the highest “no effect” level established in this study was 10 mg/kg/ day Cyhalothrin. Treatment with Cyclophosphamide at 200 mg/kg elicited dominant lethal mutations during the first 3 weeks of the mating period and male mortality and low fertility during the last 2 weeks of the mating period and therefore demonstrates the susceptibility of the strain of mouse used to a known mutagen.
Short description of key information:
not mutagenic, bacterial reverse mutation assay (Ames test), equivalent or similar to OECD Guideline 471, Trueman 1981
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
The available data on genotoxicity are adequate for the risk assessment, classification and labelling.
As the results available are "negative", the substance does not meet the criteria for classification under the Directive 2001/59/EC, Annex VI, 4.2.2 as well as the criteria in the Regulation (EC) No. 1272/2008, Annex I, Part 3, 3.5.
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