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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Endpoint:
additional ecotoxicological information
Type of information:
experimental study
Adequacy of study:
other information
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
test procedure in accordance with national standard methods with acceptable restrictions
Remarks:
Acceptable, well documented publication

Data source

Reference
Reference Type:
publication
Title:
Comparing the Potency of Chemicals with Multiple Modes of Action in Aquatic Toxicology: Acute Toxicity Due to Narcosis versus Reactive Toxicity of Acrylic Compounds.
Author:
Freidig AP et al.
Year:
1999
Bibliographic source:
Environ. Sci. Technol. 33: 3038-3043

Materials and methods

Type of study / information:
Acute fish toxicity due to narcosis versus reactive toxicity of acrylic compounds

Test material

Constituent 1
Chemical structure
Reference substance name:
Isobutyl acrylate
EC Number:
203-417-8
EC Name:
Isobutyl acrylate
Cas Number:
106-63-8
Molecular formula:
C7H12O2
IUPAC Name:
isobutyl acrylate

Results and discussion

Any other information on results incl. tables

A series of acrylates and methacrylates was used to illustrate a strategy to compare the importance of two modes of action and thereby identify the predominant cause of acute fish toxicity.

Acrylic compounds are known to be Michael acceptors and may therefore react with glutathione, causing GSH-depletion in vivo, but acrylates may also act by a nonspecific mechanism (narcosis).

The model presented in this publication was validated with four model compounds (i.e. ethyl acrylate, acrolein, acrylonitrile, acrylamide) and an in vivo study (GSH depletion in rainbow trouts exposed to ethyl acrylate at near-lethal concentrations). The model includes specific, physiological information of the target site but excludes kinetic processes and organ specificity. For the modes of action mentioned above, toxic ratios were calculated and compared for all chemicals in the series (including isobutyl acrylate).

 

Among others, isobutyl acrylate is a strong Michael acceptor and has a TR reactivity (toxic ratio = TR) which is close to one and its TR narcosis does not exceed 0.1, it is therefore highly probable that it shares the acute toxic effect of GSH depletion and acute toxicity is not caused by narcosis.

 

Applicant's summary and conclusion