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EC number: 201-861-7 | CAS number: 88-85-7
- 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
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
Additional information
Animal data indicates that dinoseb is readily absorbed and metabolised via oral and dermal as well as parenteral routes of administration (Bandal et al. 1972, Hall et al. 1992, Shah et al. 1990). Signs of systemic toxicity, and deaths, were in fact observed early after dosing in the available acute oral and dermal studies. Absorbed dinoseb is extensively metabolised, and distributed throughout the body. The metabolite profile is similar in rats treated by the dermal route or injected i.v. (Hall et al. 1992). Dinoseb reaches the embryo in pregnant mice although the placenta acts as an efficient barrier leading to concentrations of 2.5% of those of maternal plasma levels. A similarly efficient barrier exists for the brain, where levels of radioactivity comparable to those noted in the embryo were observed (Gibson et al. 1972). Metabolic pathway involves oxidation of the side chain and reduction of a nitro group, and, mainly in rabbits, conjugation with glucuronic acid (Ernst and Bar 1964). Excretion is almost complete within 72 hrs, with urine being the main route of excretion (more than 70% in dermally treated adult rats - Hall et al. 1992; approx. 65% after a single oral dose in rats, a little less, ca. 40% in mice - Bandal et al. 1972). Less than 3% of unchanged dinoseb could be detected in the 24-h urine of treated rats and rabbits (Ernst and Bar 1964), and detection of dinoseb in urine from dermally or i.v. treated rats was minimal (Hall et al. 1992). Toxicokinetic data in mice and pregnant mice showed that Tmax in the embryo was much shorter when dinoseb was administered via intraperitoneal injection than by oral administration (8 minutes compared to 12 hours), with radioactivity (associated to dinoseb or its metabolites) already detectable in the embryo within 1 minuteafter i.p. injection, but not earlier than 30 minutes following oral administration. In the mothers, dinoseb administered i.p. was absorbed 40 times faster than after oral administration (Gibson et al. 1972). Differences in kinetics were considered to be a possible cause of the differences in findings in teratogenicity studies using different routes of exposure. Dinoseb was found to cause specific teratogenic effects (microphthalmia) in rats and rabbits by dietary and dermal routes of exposure for the mothers (Giavini et al. 1986, Johnson et al. 1988), or transient nephropathies following i.p. injection on days 11-13 of pregnancy (McCormack et al. 1980). These effects were not seen following single daily doses by oral gavage (Giavini et al. 1986).
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