Registration Dossier

Administrative data

Link to relevant study record(s)

Description of key information

Short description of key information on bioaccumulation potential result: 
Half life of 2-butoxyethyl acetate (deacylation to parent glycol ether 2-butoxyethanol) 0.96mins
Short description of key information on absorption rate:
QSAR data

Key value for chemical safety assessment

Absorption rate - dermal (%):
30
Absorption rate - inhalation (%):
65

Additional information

There is very little specific toxicokinetic information available for this substance. However, in vitro hydrolysis studies show the half life of 2 -butoxyethyl acetate (2BA) in rat plasma to be of the order of 1 -5 minutes for conversion to the parent glycol ether 2 -butoxyethanol (2BE), with evidence that the half life increases with increasing concentration. Once hydrolyzed, the kinetics for the glycol ether derived from the acetate are identical to that observed following administration of the glycol ether itself. The toxicological databases for systemic effects for the glycol ether and its acetate are essentially toxicologically equivalent. The possible exception to this is effects on the upper respiratory tract, where the hydrolysis product is acetic acid. However, no lesions in this area were reported in the inhalation study data available, which may reflect the relatively low volatility of the substance. The toxicological equivalence of these two compounds 2BE and 2BA is consistent with the demonstration of rapid hydrolysis of the glycol ether acetate to the glycol ether and acetic acid in vitro, and subsequent metabolism of the glycol ether via common metabolic pathways.

The available information on metabolism supports the use of the toxicological database for 2 -butoxyethanol as a surrogate for the systemic toxicity of 2 -butoxyethyl acetate.

There is no dermal absorption data available for 2 -butoxyethyl acetate. However, there is experimental data available for the primary in vivo metabolite 2 -butoxyethanol (2BE) which indicate that under semi-occlusive conditions, dermal uptake of pure 2BE is between 20 and 30 % of the administrated dose.

Discussion on bioaccumulation potential result:

There is very little specific toxicokinetic information available for this substance. However, an in vitro hydrolysis showed the half life of 2 -butoxyethyl acetate in rat plasma to be of the order of 1 -5 minute for conversion to the parent glycol ether 2 -butoxyethanol, withe evidence that the half life is concentration dependent (increasing with increasing concentration.) Once hydrolyzed, the kinetics for the glycol ether derived from the acetate are identical to that observed following administration of the glycol ether itself. The toxicological databases for systemic effects for the glycol ether and its acetate are essentially toxicologically equivalent. The possible exception to this is effects on the upper respiratory tract, where the hydrolysis product is acetic acid. However, no lesions in this area were reported in the inhalation study data available, which may reflect the relatively low volatility of the substance. The toxicological equivalence of these two compounds is consistent with the demonstration of rapid hydrolysis of the glycol ether acetate to the glycol ether and acetic acid in vitro, and subsequent metabolism of the glycol ether via common metabolic pathways.

Based on data from similar substances, a respiratory uptake of 65% is deemed appropriate.

Discussion on absorption rate:

There is no dermal absorption data available for 2 -butoxyethyl acetate. QSAR data for 2 -butoxyethyl acetate indicates that it will have a lower rate than the parent glycol ether 2 -butoxyethanol, which is known to have a dermal uptake of around 30% of total dose. It seems to be a conservative approach to assume a similar level of dermal uptake for 2 -butoxyethyl acetate (the assumption used in the EU risk assessment.)