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Administrative data

Link to relevant study record(s)

Description of key information

Butyl acrylate is rapidly absorbed, distributed and excreted after oral application or intravenous injection. In vitro and in vivo, BA is rapidly and completely metabolized.

Key value for chemical safety assessment

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

Additional information

In vitro:

Butyl acrylate was tested for relative rates of hydrolysis by a representative mammalian esterase (Porcine hepatic esterase). At concentrations of 0.2, 0.5 and 2.0 mM, conversion rates ranged between 54 - 69 μmol/min/mg protein (4 - 33 %) after 2 minutes, and 43 - 72 μmol/min/mg protein (10 - 68 %) after 5 minutes of incubation at 37°C (BASF AG, 2001). Thus, BA was rapidly hydrolysed by hepatic esterase activity under in-vitro conditions.

Recent investigations on the in vitro metabolism of butyl acrylate after incubation with S9 fraction of rat liver as well as with blood and plasma of rats have demonstrated that the elimination is very rapidly (BASF SE, 2015). The cleavage of the ester and formation of acrylic acid is the predominant metabolic step after incubation with S9, while after incubation with blood and plasma butyl acrylate reacts mainly with GSH. Acrylic acid occurred to a lesser extent under these test conditions. These results are in line with findings published in the literature (Miller et al., 1981; deBethizy et al., 1987, Linhart et al., 1994).

In a study by Dow Chemical (1979), the disappearance of butyl acrylate in rat blood in vitro and the conversion of butyl acrylate to acrylic acid in rat liver homogenate and blood was determined. Butyl acrylate disappeared rapidly when added to rat blood in vitro with a half time of 7.7 min. Butyl acrylate was hydrolyzed to acrylic acid in the liver in vitro at a rate of 26 nmoles/min and in blood at a rate of 4.6 nmoles/min.

In a study by Stott (1985), the in vitro activity of carboxylesterase was determined in mouse nasal mucosa, liver, kidney, lung, and blood and in nasal mucosa of rat, rabbit, and dog. The specific activity of nasal carboxylesterase in mice was found to be equivalent to that of the liver and greater than that of the kidney, lung or blood. Mice and dogs were found to have similar nasal carboxylesterase activities which were slightly higher than that found in rats and about six-fold higher than that found in rabbits. These data suggest that extensive hydrolysis of acrylate esters occurs in the nasal mucosa of animals exposed to these materials.

In vivo:

After oral administration (gavage), Butyl [2,3-14C]-acrylate was rapidly absorbed and metabolized in male Fischer 344 rats (75 % was eliminated as CO2, approximately 10 % via urine and 2 % via faeces). The major portion of butyl acrylate was hydrolysed 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 (Sanders, 1988).

After i.v. administration, the labelled butyl acrylate was rapidly absorbed and metabolized. The acrylate moiety was metabolized primarily to CO2, accounting for elimination of up to 45 % of the administered radiolabel. The second major route of elimination was in urine, with only trace amounts in faeces and as volatiles (Sanders, 1988). No parent compound was detected in any urine, bile, or tissue extract samples by HPLC analysis. The two major metabolites in urine after both oral and intravenous routes of exposure were identified as N-acetyl-S-(2-carboxyethyl)cysteine and N-acetyl-S-(2-carboxyethyl)cysteine-S-oxide (Sanders, 1988).

Thus, after oral and i.v. administration, butyl acrylate (BA) is rapidly absorbed and metabolized in male rats. The major portion of BA was hydrolysed by carboxyesterase to acrylic acid and butanol. The subsequent metabolism follows that for acrylic acid, and involves metabolism to carbon dioxide via the propionate degradation pathway (acrylic acid --> 3-hydroxypropionic acid --> malonyl semialdehyde --> acetyl S CoA --> tricarboxylic acid cycle --> CO2). Metabolism of butanol proceeds via the alcohol and aldehyd dehydrogenase pathway. A smaller portion of the administered BA was conjugated with endogenous GSH to be subsequently excreted as mercapturic acids in the urine.

In a study by Sapota (1991), 36 male Wistar rats were administered 100 mg/kg bw of BA-14C (about 435 kBq/rat) intraperitoneally or by oral gavage. Urine, faeces, blood and expired air was collected. Animals were killed 0.5, 4, 8, 12, 24 and 48 h after administration of the test compound. Liver, kidneys, lungs, brain, spleen, heart, stomach, a fragment of sciatic nerve and a section of fat from the abdomen were collected for determination of radioactivity. Most of 14C found in tissues was associated with the liver and kidneys. The level of 14-C associated with most of the examined tissues remained unchanged, at least for the first 8 - 12 hours, followed by its fairly rapid loss. The expired air was found to be the main route of excretion of 14C. More than 70 - 80% of the given dose of 14C was eliminated in this way during 24 hours following the administration of butyl acrylate. 14C was also excreted in considerable amount (17 - 21 %) in urine, mainly during the first 24 hours, and partly during the following day and night. After 48 hours the total amount of the excreted 14C reached almost 100%.


- BASF SE (2015). Bachelor thesis Kertsin Roos, unpublished data, Testing laboratory: BASF SE, Experimental Toxicology and Ecology,67056 Ludwigshafen, Germany. Report date: 2013.

- deBethizy JD, Udensky JR, Scribner HE, Frederick CB (1987). The disposition and metabolism of acrylic acid and ethyl acrylate in male Sprague Dawley rats, Fund. Appl. Toxicol., 8, 549-561.

- Linhart I, Vosmanska M, Smejkal J (1994). Biotransformation of acrylates. Excretion of mercapturic acids and changes in urinary carboxylic acid profile in rat dosed with ethyl and 1-butyl acrylate, Xenobiotika, 24, 1043-1052.

- Miller RR, Ayres JA, Rampy LW, McKenna MJ (1981). Metabolism of acrylate esters in rat tissue homogenates, Fund. Appl. Toxicol., 1, 410-414.