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EC number: 268-952-1 | CAS number: 68155-26-0
- 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
Link to relevant study record(s)
Description of key information
Absorption, Distribution, Metabolism and Excretion
In Vitro
Dodecanamide, N,N-bis(2-hydroxyethyl)- (CASRN 120-40-1)
Human liver slices and liver slices from diethylhexyl phthalate-(DEHP) induced and untreated male F344 rats were incubated with [14C]lauramide DEA.23Lauramide DEA “partitioned well” into the human liver slices and the liver slices from DEHP-induced and untreated rats.Approximately 70% of the radioactivity absorbed into the slices in 4 h. The absorbed radioactivity was present mostly as lauramide DEA. In the media from the human, rat, and DEHP-induced rat liver slice incubations, 32, 18, and 43% of the radioactivity, respectively, was present in the form of metabolites. The analytes present in the incubation media included half-acid amides, parent lauramide DEA, and three other metabolites that are products of ω- and ω-1 to 4 hydroxylation.
The in vitro metabolism of [14C]lauramide DEA, randomly labeled on the diethanolamine moiety, was examined in liver and kidney microsomes from rats and humans to determine the extent of hydroxylation, and to determine the products
formed.24Incubation of lauramide DEA with liver microsomes from control and DEHP-treated rats produced two major high performance liquid chromatography peaks that were identified as 11-hydroxy- and 12-hydroxy-lauramide DEA. Treatment with DEHP increased the 12-hydroxylation rate 5-fold, while the 11-hydroxylase activity was unchanged.
Upon comparison of lauramide DEA hydroxylation rates using human liver microsomes from the rates measured using rat liver and kidney microsomes, the lauramide DEA 12-hydroxylase activity in human liver microsomes was similar to the activity in liver microsomes from control rats. The 12-hydroxylase activity in liver microsomes was 3 times greater than that observed in rat kidney microsomes.
Oral
Non-Human
Dodecanamide, N,N-bis(2-hydroxyethyl)- (CASRN 120-40-1)
Three male F344 rats were dosed orally with [14C]lauramide DEA that was randomly labeled on the diethanolamine moiety, 16-18μCi/dose, and that was formulated with an appropriate amount of unlabeled lauramide DEA and water to give delivery of the target dose in a volume of 5 ml/kg bw.23After oral dosing with 1000 mg/kg [14C]lauramide DEA, approximately 10, 60, and 79% of the dose was recovered in the urine after 6, 24, and 72 h, respectively.
Approximately 4% of the dose was recovered in the tissues after 72 h, with almost 3% found in adipose tissue and 1.3% in the liver. At 6 h, no diethanolamine, diethanolamine metabolites, or unchanged lauramide DEA were present in the urine; only very polar metabolites were found. The researchers postulated that the metabolites were carboxylic acids, and that the acid function was formed
from the lauryl chain.
Dermal
Non-Human
Dodecanamide, N,N-bis(2-hydroxyethyl)- (CASRN 120-40-1)
Groups of four male B6C3F1mice and four F344 rats were dosed dermally with [14C]lauramide DEA that was randomly labeled on the diethanolamine moiety.23The vehicle was ethanol.A non-occlusive application was made to a 0.5 sq. in. area of mouse skin and to a 1 sq. in. area of rat skin. At the end of the study, the excised skin was rinsed with ethanol.
Absorption was calculated from the total disposition of radioactivity in the tissues, urine, feces, and dose site. In mice dosed with 5-800 mg/kg [14C]lauramide DEA, 50-70% of the applied radioactivity was absorbed at 72 h, and absorption was similar
for all the doses. Approximately 32-55% of the radioactivity was excreted in the urine. In rats dosed with 25 or 400 mg/kg lauramide DEA, 21-26% of the radioactivity penetrated the skin in 72 h, and 3-5% was recovered at the application site. Approximately
20-24% of the radioactivity was recovered in the urine. The tissue/blood ratio was greatest in the liver and kidney.
Lauramide DEA and the half-acid amide metabolites were detected in the plasma, with maximum levels found 24 h after dosing.
The researchers also examined the effects of repeated administration lauramide DEA on absorption and excretion. Lauramide DEA, 25 mg/kg/day, was applied to 5 rats, 5 times/wk, for 3 wks. The rate of absorption of lauramide DEA did not vary much at the different collection time points, and the amounts excreted were similar at each collection period.
Intravenous
Non-Human
Dodecanamide, N,N-bis(2-hydroxyethyl)- (CASRN 120-40-1)
Three male B6C3F1mice and four F344 rats were dosed intravenously (i.v.) with [14C]lauramide DEA that was randomly labeled on the diethanolamine moiety, 3-5μCi and 16-17μCi, respectively, and that was formulated to deliver a target dose in a volume of 4 ml/kg in mice and 1 ml/kg in rats.23The dose for mice was 50 mg/kg and the dose for rats was 25 mg/kg.In B6C3F1mice, lauramide DEA was quickly metabolized and eliminated. At 24 h after dosing, approximately 95% of the dose was excreted, with 90% found in the urine; the highest concentrations and total amounts of the lauramide DEA were in adipose tissue. In F344 rats, 50% of the dose was excreted in the urine within the first 6 h, and more than 80% was excreted in the urine by 24 h. The rats were killed at 72 h after dosing, and only 3% of the dose was recovered in the tissues; 1% of the dose was in the adipose tissue and 0.67% was found in the liver.
Key value for chemical safety assessment
- Bioaccumulation potential:
- no bioaccumulation potential
Additional information
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