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EC number: 604-669-5 | CAS number: 149021-58-9
- 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
- Bioaccumulation potential:
- no bioaccumulation potential
Additional information
No reliable studies concerning toxicokinetics, metabolism and distribution were identified for 2-propylheptyl acrylate. However, data from the structural analogues 2-ethylhexyl acrylate, and ethyl acrylate were considered for the assessment and read across approach was performed.
Toxicokinetics, metabolism, and distribution
There are no guideline studies on toxicokinetics, metabolism and distribution of 2 -ethylhexyl acrylate. Nonetheless, an assessment of the toxicokinetic behaviour of the substance can be made based on a variety of publications, primarily by Sapota (1988, 1990). 14C-2-EHA (labelled on the vinyl carbons) was administered p.o. and i.p. to rats at a dose of 100 mg/kg bw, respectively (Sapota 1988). The highest specific radioactivity was found three hours after i.p. administration in liver and kidneys, followed by spleen, lung, brain, adipose tissue and blood. The 14C levels decreased continuously in all tissues except in the adipose where radioactivity remained nearly constant (0.7%) for 72 hours. After oral dosing about 50% of the radioactivity was eliminated via the expired air and about 38% via the urine within the first 24 hours. A small portion of 2-EHA (about 1% of the dose) was excreted via the faeces. No specific studies have been carried out on the metabolism of 2-EHA. However a variety of studies on rats have indicated that short-chain acrylates such as ethylacrylate undergo the following metabolic reactions: carboxylesterase catalyzed hydrolysis of the ester function to release acrylic acid and alcohol (De Bethizy et al. 1987; Frederick et al. 1992). The half-life of ethylacrylate-hydrolysis in rat liver (in vitro) was approximately 2 seconds. In 13 other tissues it was as much as 15 minutes (Frederick et al. 1992). The acrylic acid is decarboxylated and degraded to carbon dioxide (Gut et al. 1988; Sapota 1988). Only a small part of approx. 2% (varies with the route of administration) of the administered 2-EHA was conjugated to glutathione and excreted as thioether (Gut et al. 1988; Vodicka et al. 1990).
Discussion on bioaccumulation potential result:
No reliable studies concerning toxicokinetics, metabolism and distribution were identified for 2-propylheptyl acrylate. However, data from the structural analogue 2-ethylhexyl acrylate (EHA) were considered for the assessment.
The distribution and excretion of 2-ethylhexyl [2,3-14C]-acrylate following intraperitoneal (i.p.) and oral (p.o.) administration to male Wistar rats at a dose of 100 mg/kg body weight was investigated by Sapota (1988). The radioactivity was absorbed rapidly and completely, independent of the route of administration.14C found in the tissues was mainly associated with liver, kidneys and lung. Loss of 14C from these tissues occurred fairly rapidly, with the exception of the rats given EHA intraperitoneally.
EHA underwent rapid metabolism and excretion with expired air (78% after i.p. and 51% of the dose after p.o. administration) and urine (10% after i.p. and 41% of the dose after p.o. administration). Only a small portion was excreted via faeces (3% after i.p. and 1% of the dose after p.o. administration). In all cases more than 90% of radioactivity had been excreted up to 72 hours after administration. Most of the radioactivity found in the expired air was quickly exhaled within the first 3 hours after administration of the acrylate. 14C in the expired air was probably present as 14CO2. At 72 hours after a single intraperitoneal administration of EHA, the total radioactivity present in the examined tissues amounted to approx. 1% of the dose, but in the fat and sciatic nerve the specific radioactivity was still relatively high. In a second study, [14C]-2-ethylhexyl acrylate was given to adult male Wistar rats intravenously (i.v.) and intraperitoneally (i.p.) at a dose of 10 mg/kg bw (Gut et al. 1988). The elimination of radioactivity from blood was bi-exponential, irrespective of the route of administration or the age (weight) of the rats. The first phase half-lives after i.v. and i.p. administration in 4-month-old rats were 30 and 60 min, in 7-month-old rats 115 and 130 min, respectively. The corresponding values for the slow-phase were 5 and 6 h, and 14 and 14 h. Elimination of radioactivity from tissues followed a pattern similar to that seen for blood. More than half of the administered radioactivity was exhaled as carbon dioxide. Exhalation of unchanged [14C]-EHA accounted for only 0.05% (i.v.) and 0.3% (i.p.) of the initial dose, respectively. The radioactivity excreted in the urine within the first 24 h post-treatment accounted for 7% (i.p.) and 14% (i.v.) of the initial dose, respectively. Only 2% was excreted as thioethers.
Exposure of male Wistar rats to 2-ethylhexyl acrylate vapours at different concentrations for 6 hours increased the absolute amounts of urinary thioether excretion in a dose-dependent manner (Vodicka et al. 1990). Most pronounced non-protein-SH depletion was observed in the liver, less in blood and moderate in brain and lungs. The authors suggested that GSH depletion may participate in acute lethal and biochemical toxic effects of acrylic acid esters. However, the portion of the acrylate ester metabolised to thioethers was low (3-8% of the inhaled dose). With increasing concentrations of inhaled EHA, the metabolised proportion of EHA decreased slightly (8.0% at 250 mg/m3, 5.5% at 500 mg/m3 and 3.0% at 1000 mg/m3).
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