Registration Dossier

Administrative data

Link to relevant study record(s)

Description of key information

Experimental toxicokinetics study was not available on n-hexyl acrylate. A read-across is proposed between N-hexyl acrylate and N-Butyl acrylate for repeated dose systemic and reproductive/developmental effects. This read-across is justified in attachements per relevant endpoint study record. Based on the chemical and physical state, a low absorption is expected after oral route, dermal route or inhalation.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

Information on absorption, distribution, metabolism and excretion may be deduced from the physicochemical properties, according to the REACH guidance document R7.C (2012).

Both substances share similar physical chemical properties:



N-hexyl acrylate

N-butyl acrylate

Molecular Weight

156.22 g/mol

128.17 g/mol

Melting Temperature

 -48 °C

-64.6 °C

Boiling Temperature

 190°C at 1013.25 hPa

147 °C at 1013.25 hPa



g/cm3at 20°C


g/cm3at 20°C

Water Solubility

57.4 mg/L at 20°C

1.7 g/L at 20°C

Vapor Pressure

130 Pa at 20 ± 1°C

500 Pa at 22.2°C

Partition coefficient

4.2 at 40°C


2.38 at 25°C




Based on the physicochemical characteristics of n-hexyl acrylate, a higher log Kow equal to 4.2 and a low molecular weight, a low oral absorption is expected. The assumption of a low oral absorption is confirmed by data on acute oral toxicity where no mortalities were observed at doses > 2,000 mg/kg (LD50 22.9 g/kg bw in rats).


Dermal absorption of n-hexyl acrylate is expected to be slowed due to binding to skin of the acrylate group and the low water solubility. This is supported by the low toxicity observed in acute dermal testing (LD50 = 4.98 g/kg). However n-hexyl acrylate is a moderate skin sensitizer based on the guinea pig maximization test.


According to the value of vapor pressure (130 Pa at 20°C) both substances are considered to be slightly volatile. Low absorption by inhalation of N-hexyl acrylate is expected at the maximum attainable concentration due to the low values of vapor pressure, log Kow and water solubility.



As a small molecule, a wide distribution of n-hexyl acrylate is expected. No specific test data was found on metabolism of n-hexyl acrylate.


Evidence from other types of acrylates suggests that hydrolysis of the ester bond is likely to occur, producing acrylic acid which is further biotransformed to carbon dioxide and the corresponding alcohol. Alternative bio-elimination pathways include conjugation with Glutathione (GSH) by Glutathione-S-transferase. Detoxification by hydrolysis is supported by studies in which the toxicity of various acrylate esters was enhanced following the inhibition of carboxyl esterase by tri(ortho-toyl)phosphate (TOTP) (Silver et al. 1978; Silver 1981). Additionally, following inhalation or at high exposure levels, carboxylesterase-mediated hydrolysis may be saturated and residual intact ester may reach systemic circulation and influence systemic toxicity through binding with macromolecules.


The major routes of excretion for both substances from the systemic circulation are the urine (due to the low molecular weight) and the exhaled air (of the hydrolysis products).