Student Research: Eva Browne
Polybrominated diphenyl ethers (PBDEs), a class of brominated flame retardants, are added to consumer products including electronics, polyurethane foam, and plastics. These chemicals persist in the environment and have been bioaccumulating in human and wildlife tissues over the past twenty years. Of particular concern in the Pacific Northwest are the PBDE congener residues in Chinook salmon from the Puget Sound, which are among the highest in salmonids, and are dominated by lower molecular weight congeners, in particular, BDE 47. However, PBDE congener production and use are dominated by the higher brominated compound, BDE 209, suggesting that the high levels of the lower brominated congeners in Puget Sound salmon may be due to environmental or biological debromination. Using in vitro incubations, we determined the capacity of Bhinook liver subcellular fractions to debrominate BDE 99, a congener readily debrominated by common carp, into lower molecular weight PDBEs. Relative to carp, Chinook microsomal fractions were inefficient at debrominating BDE 99 converting about 3% of BDE 99 to BDE 49 at a slow rate of less than 2 pmol/hour/mg protein. Carp microsomal fractions rapidly converted BDE 99 to BDE 47. This data indicates the differences in debromination capacity as well as debromination products between teleost species. However, these metabolism studies do not explain the high concentrations of tetra brominated BDEs found in Chinook salmon from the Puget Sound.
In addition to metabolism studies, in situ caging studies in a historically polluted waterway in Seattle, WA were employed to determine the effect of urbanization on the expression of hepatic genes implicated in PBDE metabolism and/or important in chemical biotransformation. This waterway has undergone remediation efforts in the last decade. Quantitative PCR assays were developed for a suite of seven different genes with functions involving biotransformation, PBDE debromination, and/or protecting against cell injury. These molecular endpoints were assayed in juvenile Chinook salmon caged in 3 sites within the waterway for 9 days (along with respective controls kept in the hatchery) and interpreted along with analytical chemistry data from the sites. The PCR studies did not indicate any statistically significant site-related differences in gene expression in caged fish relative to controls. The lack of significant effects may have been associated with exposure concentrations in salmon below those modulating hepatic gene expression. The results of this project strongly suggest that relatively high concentrations of BDE 47 in Chinook salmon are a result of environmental degradation processes or recalcitrance of BDE 47 in urbanized waterways, as opposed to hepatic metabolism, and have implications regarding the use of molecular biomarkers in characterizing the effects of remediation on salmon injury.