Additive interactions between pairs of polybrominated dibenzo-p-dioxin, dibenzofuran, and biphenyl congeners in a rainbow trout early life stage mortality bioassay.

Abstract Use of fish-specific toxic equivalency factors (TEFs) to estimate the risk that exposure to polybrominated dibenzo- p -dioxins (PBDDs), dibenzofurans (PBDFs), and biphenyls (PBBs) pose to fish early life stage survival depends on validation of the hypothesis that these chemicals act additively to produce mortality. A rainbow trout early life stage bioassay was used to determine how pairs of PBDD, PBDF, and PBB congeners interact to produce 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD)-like toxicity associated with sac fry mortality. The congener pairs tested were 2,3,7,8-tetra- bromodibenzo- p -dioxin (2,3,7,8-TBDD)/1,2,3,7,8-pentabromodi- benzo p -dioxin (1,2,3,7,8-PBDD); 2,3,7,8-TBDD/1,2,3,7,8-penta- bromodibenzofuran (1,2,3,7,8-PBDF); 1,2,3,7,8-PBDD/2,3,4,7,8-pentabromodibenzofuran (2,3,4,7,8-PBDF); and 2,3,4,7,8-PBDF/3,3′,4,4′-tetrabromobiphenyl (3,3′,4,4′-TBB). Graded doses of each congener alone, or graded doses of fixed ratios of paired congeners were injected into newly fertilized rainbow trout eggs. In all cases, interactions between congener pairs were additive as tested by a probit model. Isobolographic analysis also supported the hypothesis that the PBDD, PBDF, and PBB congeners act additively. Thus, the use of fish-specific TEFs to convert fish tissue concentrations of individual PBDD, PBDF, and PBB congeners to TCDD equivalents (TEs) and then adding the TEs contributed by the various congeners to give the total TCDD equivalents concentration (TEC) in the tissue is supported by these results. By comparing the TEC in feral fish eggs to the fish egg TCDD no-observed-effect level (NOEL) and lowest-observed-effect level (LOEL) for early life stage mortality, the risk that complex mixtures of these polybrominated chemicals in eggs pose to sac fry survival can be estimated.