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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Neurotoxicity

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Administrative data

Description of key information

Propyl acetate
Rat, inhalation, motoneuronal EC37: ca. 27.5 mg/L (Frantik et al. 1994)
Mouse, inhalation, motoneuronal EC30: ca. 26 mg/L (Frantik et al. 1994)

Key value for chemical safety assessment

Effect on neurotoxicity: via oral route

Endpoint conclusion
Endpoint conclusion:
no study available

Effect on neurotoxicity: via inhalation route

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed

Effect on neurotoxicity: via dermal route

Endpoint conclusion
Endpoint conclusion:
no study available

Additional information

Propyl acetate

Groups of 4 male albino SPF-Wistar rats or 4 female H strain mice were exposed individually for 4 hours to a range of propyl acetate concentrations (analytically determined; Frantik et al. 1994). Measurement of any potential neurotoxic effect started within one minute after removal from exposure. A short electrical impulse (0.2 sec, 50 Hz, 180 V) was applied through ear electrodes. The duration of tonic extension of the hindlimbs in exposed and control rats was measured. All animals were given three control tests at weekly intervals prior to the first exposure. The concentration which resulted in a 37% (EC37) decrease in  rat hindlimb extension during electrically-induced seizure events was 6600 ppm (+/- 1200 ppm) or 27.522 mg/L (+/- 5.004 mg/L), while the concentration which resulted in a 30% (EC30) decrease in  mouse hindlimb extension during electrically-induced seizure events was 6200 ppm (+/- 830 ppm) or 25.854 mg/L (+/- 3.461 mg/L)

Justification for classification or non-classification

Taken together all available data for propyl acetate, there were no irreversible subchronic neurotoxic effects in doses without systemic toxicity. Therefore no classification is required.