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Administrative data

Link to relevant study record(s)

Description of key information

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential
Absorption rate - oral (%):
Absorption rate - inhalation (%):

Additional information


Acetic acid 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).

Dermal absorption from a 10% solution was studied in an in vitro study using human female skin and was 43% (Buist et al., 2010). As this was an in vitro, enclosed system where evaporation/run off would not occur, the absorption value is likely to be higher than that reflected in normal exposure scenarios

No data on the absorption of acetic acid via the inhalation route is available. Therefore a value of 100% has been assumed.

The proportion of ionised (acetate) relative to unionised (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 pH2 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. Consequently, studies with acetate salts (e.g. sodium acetate) orally administered and studies with sodium acetate, intravenously administered, contribute to the overall assessment of systemic toxicity of acetic acid and have been considered within this document as key or supporting studies rather than read-across to a structural analogue.

For sodium acetate the situation is relatively simple as sodium (simultaneously formed) is also ubiquitous in mammals and therefore the sodium released may not influence the toxicology significantly.  However, the situation becomes rather complex when the moiety, simultaneously released during the formation of acetate, be it a metal counter ion or indeed an organic molecule, exhibits significant toxicity in its own right.  Such information has been considered, but therefore excluded in the assessment of the toxicology of acetic acid presented in this submission.


In blood (pH ~7.4), only 0.23% of acetic acid will be non-ionised and capable of crossing lipid barriers, this will limit distribution into extra-vascular tissues. Sodium acetate was administered to anaesthetised dogs by intravenous infusion to maintain a constant plasma concentration (22 µmol/ml acetate) for a 60 minute period; during this time, acetate diffused slowly into cerebral spinal fluid only reaching concentrations approximately 20x lower than in plasma (Freundt, 1973). 


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) ), representing some 45 g/day (SCOEL, 2012). 

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).


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).


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