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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Specific investigations: other studies

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Administrative data

Link to relevant study record(s)

Description of key information

Additional information

Abstracts of specific studies which do not follow standard test procedures indicate:

  • Observations following the repeated administration of 2 -EH to rats and mice included increased liver weight, peroxisome proliferation, and changes (induction) of enzymes involved in Phase I and Phase II drug metabolism
  • 2 -EH is a peroxisome proliferator in rodents (rats and mice), but not in other species including humans. This effect is therefore not relevant for the assessment of human health effects.
  • 2 -EH is hepatotoxic. Impairment of the mitochondrial energy supply is the underlying toxic mechanism.
  • Degeneration of testes and Sertoli cells were not associated with 2 -EH, but with MEHP, which is generated following the administration of DEHP.
  • 2-EH administered to cells of mouse Leydig tumour cell line, MA-10, did not reveal any reduction of steroidogenic potential of the cells (no reduction of progesterone production or gene expression of key steroidogenic enzymes). Whereas DEHP, MEHP and 2-ethylhexanal significantly disrupt the steroidogenesis in MA-10 cells.
  • 2 -EH was found to have an impact on maternal-embryonic zinc metabolism (decrease of embryonic Zn uptake).