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EC number: 404-450-2 | CAS number: 118685-34-0 COBRATEC 435
- 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
Description of key information
Acute Oral Toxicity
The study was conducted in accordance wilth under Annex V of the EEC direcetíve 79/831/EEC, Part B Methods for determínation of toxicity, Method B1 Acute OraI Toxicity, and the OECD guideline for Testing of Chemicals No. 401 "Acute OraI Toxicity"
Key value for chemical safety assessment
Acute toxicity: via oral route
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- LD50
- Value:
- 1 400 mg/kg bw
Additional information
Acute Oral Toxicity
Mortality: There was a single male death amongst rats dosed at 0.80 g a.i/kg and deaths amongst both sexes of rat treated at 1.26 g a.i./kg and above. The majority of rats died from within six hours of dosing until Day 4. A single male, treated at the low dose Ievel, was found dead on Day 10.
Autopsy of rats that died commonly revealed no macroscopic abnormalities. The only exception was the presence of brown Iiquid within the urinary bladder of a single male dosed at 2.00 g a.i./kg.
Clinical signs: Common signs of reaction to treatment within four hours of dosing were pilo-erection, abnormal body carriage (hunched posture), abnormal gait (waddling), Iethargy, decreased respiratory rate, ptosis, pallor of the extremities, increased salivation and prostration. Other clinical signs apparent at the same time or at later intervals on Day 1 were:
- ataxia amongst rats treated at all dose levels,
- increased lachrymation amongst females dosed at 0.80 g .i./kg and in all rats treated at 1.26 and 2.00 g.a.i/kg.
Recovery of rats surviving treatment, as judged by external appearance and behaviour, was apparently complete by Days 4 and 5 (0.80 and 1.26 g a.i./kg) or Day 7 (2.00 g a.i./kg).
Delayed signs of toxicity including pilo-erection , abnormal body carriage, abnormal gait, lethargy and pallor of the extremities reappeared on Day 9 in one male dosed at 0.80 ga.i./kg and preceded death on the following day.
Bodyweight: Low bodyweight gains during the first week of the study were recorded for all surviving rats.
Single male and female rats dosed at 0.80 and 1.26 g a.i./kg and a further male treated at the high dose level showed low bodyweight, gains between Days 8 and 15.
Terminal autopsy findings were normal
Justification for selection of acute toxicity – oral endpoint
reliable study available
Justification for classification or non-classification
Acute Oral Toxicity
The acute lethal oral dose was found between 200 and 2000 mg a.i./kg bodyweight
It is concluded that butyl benzotriazol, sodium salt has to be classifiedhas harmful with risk phrase R22 (DSD) and Acute Tox. 4 with hazardous Statement H302 (CLP/GHS)
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