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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

No experimental toxicokinetic study is available on tetrahydrofurfuryl acrylate. However, as per REACH guidance document R7.C (2014), information on absorption, distribution, metabolism and excretion may be deduced from the physicochemical properties.
Based on the toxicological data and the physicochemical properties, the absorption of tetrahydrofurfuryl acrylate is expected to be moderate by oral route, dermal route and by inhalation.

Key value for chemical safety assessment

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

Additional information

No experimental toxicokinetic study is available on tetrahydrofurfuryl acrylate. However, as per REACH guidance document R7.C (2014), information on absorption, distribution, metabolism and excretion may be deduced from the physicochemical properties, including:

-Mean molecular weight: 156 g/mol

-Water solubility: 79.1 g/L (soluble)

-Partition coefficient Log Kow: 0.81

-Vapour pressure: 319 Pa (slighlty volatile)



The moderate values of log Kow (between -1 and 4) and water solubility (79 g/L) of tetrahydrofurfuryl acrylate are favorable for an oral absorption. Indeed, the oral LD50 is of 928 mg/kg bw after one single administration of tetrahydrofurfuryl acrylate by gavage in rats, indicating a good oral absorption. An oral absorption is expected to be moderate for tetrahydrofurfuryl acrylate.

With a solubility of 79.1 g/L, dermal absorption is anticipated to be moderate. A Log Kow of 0.81 and a low molecular weight (156 g/mol) suggest a moderate dermal absorption. The acrylates are known to bind to skin components, and this binding decreases their dermal absorption. Indeed, the dermal absorption of tetrahydrofurfuryl acrylate is anticipated to be moderate. Tetrahydrofurfuryl acrylate is considered to be skin corrosive and skin sensitizer.

Based on ta moderate value of the vapour pressure (319 Pa), tetrahydrofurfuryl acrylate is considered to be slightly volatile. Moreover, the absorption by inhalation can be expected to be moderate for tetrahydrofurfuryl acrylate based on the values of water solubility and log kow.



No specific data is available on the distribution or metabolism of tetrahydrofurfuryl acrylate. No organ toxicity was showed in the studies.

No specific metabolism data is available on THFA. However, the metabolism of the (meth)acrylate esters is known. Indeed, hydrolysis of (meth)acrylate esters results in the formation of its unsaturated acid and alcohol (THF alcohol in the case of THFA and THFMA). The toxicity of acrylate esters is theorized to involve alkylation of critical cellular nucleophiles via the Michael addition. Acrylic acid, except under conditions of extremely low pH, is not electrophilic. Therefore, carboxylesterase-mediated hydrolysis of acrylates is a detoxification mechanism as the unsaturated acid produced is not electrophilic under physiological conditions (McCarthy TJ et al. 1997). After ester hydrolysis, acrylic acid enters the intermediary metabolism and is efficiently degraded to carbon dioxide as the metabolic end product (Linhart I et al. 1994).

Several publications are available to show this carboxylesterase-mediated hydrolysis on (meth)acrylate esters:

·        N-butyl acrylate is rapidly absorbed and metabolized in male rats (75% was eliminated as CO2, approximately 10% via urine and 2% via feces) after oral administration. The major portion of n-butyl acrylate was hydrolyzed by carboxyesterase to acrylic acid and butanol and eliminated as CO2. A smaller portion was conjugated with endogenous GSH to be subsequently excreted as mercapturic acids in the urine (SIDS 2005).

·        The disposition of ethyl acrylate was found to be very similar to that of acrylic acid and is probably a function of the rapid enzymatic hydrolysis of the ester moiety. The carboxylesterase enzymes which catalyze this reaction are widely distributed in both the soluble and membrane fractions of the tissues, and provide an efficient metabolic route for many organic esters. The rate of excretion of carbon dioxide is virtually identical to that of acrylic acid, suggesting a rapid rate of absorption and incorporation of ethyl acrylate into the same metabolic pathway as acrylic acid. However, a second metabolic pathway for ethyl acrylate is clearly evident in the increased urinary excretion of radioactivity. A corresponding change was noted in the analysis of specific urinary metabolites, which provided evidence for the reaction of glutathione with the parent compound. No urinary metabolites derived from the oxidative metabolism of ethyl acrylate to an epoxide were detected (DeBethizy 1987).

A physiologically based pharmacokinetic and pharmacodynamics model has been developed to describe the absorption, distribution, and metabolism of orally doses ethyl acrylate. The model describes the metabolism of ethyl acrylate in 14 tissues based on in vitro metabolic studies conducted with tissue homogenates. The routes of metabolism included in the model are carboxylesterase-

·        catalyzed ester hydrolysis, conjugation with glutathione and binding to protein. The very rapid metabolism predicted by the model was consistent with the observation that ethyl acrylate was metabolized too rapidly in vivo to be detected by common analytical techniques for tissue metabolite analysis (Frederick CB et al. 1992).

·        Methyl methacrylate is rapidly degraded to methacrylic acid and methanol after oral exposure (Bereznowski 1995). It was demonstrated that methyl methacrylate is metabolized to methacrylic acid in vivo and in vitro (Corkill 1976, Crout 1979). It was found that methyl methacrylate is hydrolysed both in human and rat serum due to serum nonspecific carboxylesterase (Bereznowski 1995).


Using purified porcine liver carboxylesterase, the enzymatic hydrolysis of several acrylate esters was characterized (McCarthy TJ et al. 1997). The results of this study indicate that alpha-methyl substitution appears to have a minor effect in the enzymatic hydrolysis of acrylates, and suggest that the relative toxicity of acrylates is not due to differences in carboxylesterase-mediated hydrolysis.


Moreover, the OECD QSAR Toolbox was used to predict the liver metabolism and the hydrolysis (acidic) of THFA. With this software, the acidic hydrolysis of (meth)acrylate esters in to raw materials [THF alcohol + (meth)acrylic acid] is confirmed.

The simulation of liver metabolism showed 4 metabolites for THFA.

-tetrahydrofurfuryl alcohol (CAS 97-99-4) ; one of the raw materials

-acrylic acid (CAS 79-10-7) the second raw material of THFA

-tertahydro-2-furancarboxylic acid (CAS 16874-33-2): substance registered but no toxicological data are available. The GHS classification for the human health is: Acute tox 4 (oral), Skin Corr.1B, Eye Dam 1. It is the same classification than THFA.

-a non-identified structure; probably not stable.



Due to the moderate water solubility and the low molecular mass, the excretion of THFA in the urines is expected to be high.