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EC number: 244-617-5
CAS number: 21850-44-2
Short description of key information on bioaccumulation potential result: One publication is available: "Absorption, distribution, metabolism, and excretion of intravenously and orally administered tetrabromobisphenol A[2,3-dibromopropyl ether] in male Fischer-344 rats", by Knudsen, G.A., Jacobs, L.M., Kuester, R.K., Sipes, I.G. (Toxicology 237 (2007) 158-167).
Studies regarding the absorption, distribution, metabolism, and
excretion of TBBA-DBPE were conducted. Male Fischer-344 rats were dosed
with TBBA-DBPE (20mg/kg) by oral gavage or IV administration. Following
a single oral administration of TBBA-DBPE, elimination of [14C]
equivalents in feces was extensive and rapid (95% by 96 hours).
Following repeated daily oral doses for 5 or 10 days, route and rate of
elimination was similar to single administration of TBBA-DBPE. After IV
administration, fecal excretion of [14C] equivalents was much
slower (27% of dose eliminated by 36h, 71% by 96h). Urinary elimination
was minimal (<0.1%) following oral and IV administration. A single peak
that co-eluted with the standard of TBBA-DBPE was detected in extracts
of whole blood following oral or IV administration. TBBA-DBPE
elimination from the blood was slow. Kinetic constants following IV
dosing were: t1/2b:
24.8h; CLb: 0.1mL/min. Kinetic constants following oral
dosing were: t1/2a:
2.5h:13.9h; CLb :4.6mL/min.
Systemic bioavailability was 2.2%. Liver was the major site of
disposition following oral or IV administration. After oral
administration, 1% of the dose was eliminated in bile in 24h as
metabolites. Inin vitro experiments utilizing hepatocytes or
liver microsomal protein, no detectable metabolism of TBBA-DBPE
occurred. These data indicate that TBBA-DBPE is poorly absorbed from the
gastrointestinal tract. Compound which is absorbed is sequestered in the
liver, slowly metabolized, and eliminated in the feces.
The results of these studies show that the likelihood of systemic
exposure following ingestion of [14C] TBBA-DBPE is low. Additionally,
disposition in liver tissue was minimal, and metabolite formation was
slow. Consequently, it was determined that the probability of formation
of the carcinogenic moiety DBP was low.
In summary, these data show that TBBA-DBPE was poorly absorbed across
the gut lumen following oral administration. However, that which was
absorbed was rapidly sequestered in the liver, was slowly metabolized
and finally eliminated in the bile for fecal excretion.
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