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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Toxicological information

Additional toxicological data

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Administrative data

Endpoint:
additional toxicological information
Type of information:
experimental study
Adequacy of study:
other information
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: Acceptable study report

Data source

Reference
Reference Type:
study report
Title:
Unnamed
Year:
1987
Report date:
1986

Materials and methods

Type of study / information:
Forestomach Lesion Evaluation

Test material

Constituent 1
Chemical structure
Reference substance name:
Ethyl acrylate
EC Number:
205-438-8
EC Name:
Ethyl acrylate
Cas Number:
140-88-5
Molecular formula:
C5H8O2
IUPAC Name:
ethyl acrylate
Details on test material:
- Name of test material (as cited in study report): Ethyl acrylate
- Analytical purity: no data

Results and discussion

Any other information on results incl. tables

Forestomach weights at EA doses greater than 20 mg/kg bw were increased significantly (214% at 200 mg/kg bw) relative to the vehicle control 24 hr after the last dose. This increase in the ambient weight of the organ was due to inflammation and hyperplasia. The forestomach weight was further increased in the first 6 hr following the last dose (306% of control at the 200 mg/kg bw dose) in an acute inflammatory response of the organ. The ambient NPSH concentration of the forestomach was elevated following EA dosing (reaching 198% of control at the 200 mg/kg bw dose), but was depleted immediately following dosing (reaching 12% of the control value 6 hr after the 200 mg/kg dose). By contrast, the glandular stomach did not demonstrate similar changes in organ weight or NPSH levels in response to EA dosing. Studies conducted with EA in the drinking water at the same total body burden did not result in similar increases in forestomach weight or NPSH content. The results indicate that repeated gavage dosing of EA results in a significant increase in  the detoxification capacity of the forestomach (4-fold at doses of 200 mg/kg bw) that remains insufficient to detoxify bolus EA doses greater than 50 mg/kg bw.

Applicant's summary and conclusion