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EC number: 203-564-8 | CAS number: 108-24-7
- 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
Short description of key information on bioaccumulation potential result:
A similar systemic toxicology profile should apply to acetic anhydride and acetic acid since acetic anhydride is rapidly and completely transformed to acetic acid. In contrast at the point of initial contact, each substance should require a specific assessment of local effects.
Key value for chemical safety assessment
Additional information
Although no toxicokinetic studies (human or non-human) are directly available for acetic anhydride it is known that this substance, like many acid anhydrides, readily hydrolyses within an aqueous environment to produce, in this case, acetic acid.
Rate
calculations derived from first principles have considered the maximum
rate of hydrolsis of acetic anhydride by water in air at both 20 and 40oC
with resulting half-life values of 6.5 and 2.8 minutes, respectively
(personal communication with Pete Wilson, BP Chemicals, 1998).
The half-life of the hydrolysis has been measured for several acid
anhydrides, at an initial concentration 2mM, in carbonate buffer at
pH7.4 (Brown et al., 1978). For acetic anhydride these authors reported
a half-life of about 3 minutes (182 seconds). The half-life of the
hydrolysis is likely to reduce as the pH of the environment increases.
Within the context of mammalian toxicology therefore one might consider that even if some acetic anhydride were absorbed systemically as the intact molecule, it would quickly hydrolyse in vivo (pH=7.4) to acetic acid and therefore the systemic toxicity of acetic acid should be relevant to acetic anhydride. A consequence of these considerations is that, at a sufficiently high concentration, acetic anhydride will induce local effects at the site of initial contact, but any systemic effects are more likely to be mediated by the natural product, acetic acid. Therefore the disposition of acetic acid in vivo is critical to understanding the systemic toxicity of acetic anhydride.
Absorption of Acetic Acid
Acetic acid, itself, is absorbed from the gastrointestinal tract. Absorption of acetic acid from the pylorus-ligated stomach of rats over a 6 hour period showed a log-dose response; approximately 100% was absorbed at a dose of 20 mg/rat, this decreased to approximately 30% when the dose was increased to 420 mg/rat (Hertling et al., 1956). The proportion of ionised (acetate) relative to non-ionised (acetic acid) is pH dependent. When either acetic acid or sodium acetate is orally administered to rats, the pH within the environment of the stomach is low (about pH=2 in rat) and the absorbed material is likely to be the same (acetic acid) whether acetic acid or the sodium salt was administered. Following absorption from the gut to the blood, the pH of which is 7.4, the vast majority of the absorbed material will be then be present as acetate, irrespective of which form was administered.
Metabolism
Following the rapid hydrolysis of acetic anhydride, acetic acid is formed. In blood (pH=7.4) only 0.23% of the acid will be non-ionised and capable of crossing lipid barriers. The ionized form, acetate, has a central role in normal intermediary metabolism; it reacts with coenzyme A before entering the citric acid cycle as acetyl-coenzyme A (Acetyl-CoA). Acetyl-CoA is utilised in the mitochondrial citrate cycle or channeled into other endogenous processes such as fatty acid synthesis. The capacity of the cycle in man is approximately 640 mg acetate/kg/day (Simoneau et al., 1994).
Rats given radiolabelled acetate in diet excreted approximately 50% of the radiolabel as CO2 (Lunberg, 1988; cited by Health Council of the Netherlands, 2004). Humans given 120 mg acetate/kg bw in a drink converted about 80% to CO2 within 90 minutes (~ 0.5 mg acetate/kg bw removed per minute) (Smith et al., 2007).
Excretion
The elimination half life of acetate from the blood of dogs administered sodium acetate intravenously (3-6 mmol/kg) was 3-5 minutes (Freundt, 1973). In rabbits, acetate was rapidly eliminated from blood following intravenous administration (0.5-1 g sodium acetate/kg bodyweight), mean residence time (MRT) and dose normalised AUC increased with dose indicating saturable elimination kinetics. The elimination of acetate from blood was best described by a two compartment open model with Michaelis-Menten elimination kinetics (Fujimiya et al., 1999).
Citations
Brown NA et al. (1978) The relationship between acylating ability and teratogenicity of selected anhydrides and imides. Toxicol & Appl Pharmacol V45 p361
Health Council of the Netherlands (2004): Committee on Updating of Occupational Exposure Limits. Acetic acid; Health-based Reassessment of Administrative Occupational Exposure Limits. The Hague: Health Council of the Netherlands, 2000/15OSH/113.
Lundberg P (1988): Consensus report for acetic acid. In: Scientific basis for Swedish Occupational Standards IX. Arbete och Hälsa 32 pp132-7
Simoneau S et al (1994) Measurement of Whole Body Acetate Turnover in Healthy Subjects with Stable Isotopes. Biological Mass Spectrometry, V23, pp 430 -433
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