Registration Dossier
Registration Dossier
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EC number: 216-823-5 | CAS number: 1675-54-3
Endpoint summary
Administrative data
Link to relevant study record(s)
Description of key information
Short description of key information on bioaccumulation potential result:
Following dermal application to mice, only 20% of the dose was eliminated in the feces and 3% in the urine. Most (66%) of the dose remained on the application area and its covering foil. Conversely, following oral administration to mice, 80% of the administered 14C material was eliminated in the feces and 11% in the urine. Urine and fecal metabolite profiles derived from dermal application and oral dosing were essentially similar.
In studies on oral vs. IV dosing, little of the orally administered 14C-BADGE was absorbed unchanged. Consistent with this, 4 hr after oral administration less than 10% of the radioactivity in the plasma represented unchanged 14C-BADGE. 14C-BADGE was not stable in simulated gastric fluid and degradation of 14C-BADGE in the stomach or during its initial transit through the liver could account for the route dependent differences observed in the fate of 14C-BADGE.
The metabolic inactivation of BADGE was studied in subcellular fractions of human, C3H mouse and F344 rat liver and lung. BADGE was chemically stable and resistant to aqueous hydrolysis but was rapidly hydrolysed by EH in cytosolic and microsomal fractions of liver and lung. Microsomal EH is more efficient than cytosolic EH in hydrolysis of BADGE and human microsomes are more efficient than rodent microsomes. BADGE, which is more lipophilic was a poor substrate for GST. In general, rodents are more efficient in GSH conjugation than humans.
Key value for chemical safety assessment
- Bioaccumulation potential:
- low bioaccumulation potential
Additional information
Absorption following dermal exposure to BADGE is low, with most of the dose (66%) remaining at the application site and/or its covering. Oral absorption of 14C-BADGE is high, but further studies indicate that the material is not stable in gastric fluid and is likely degraded either in the stomach or first-pass toxicokinetics through the liver. Metabolite profiles indicate rapid degradation by epoxide hydrolases in liver and lung, and comparative toxicokinetic studies indicate that human microsomes are more efficient in degrading BADGE than rodent microsomes. Metabolism occurs by ring-opening of the two epoxide rings to form diols. This metabolite (the bis-diol of BADGE) is excreted in both free and conjugated froms and is further metabolized to various carboxylic acids. The high activity of epoxide hydratase towards BADGE suggests that glyceraldehyde and not glycidaldehyde is formed in vivo. No bisphenol A is formed during metabolism.
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