ADDITIVE INTERACTIONS BETWEEN PAIRS OF POLYBROMINATED DIBENZO-P-DIOXIN, DIBENZOFURAN, AND BIPHENYL CONGENERS IN A RAINBOW-TROUT EARLY-LIFE STAGE MORTALITY BIOASSAY

Use of fish-specific toxic equivalency factors (TEFs) to estimate the risk that exposure to polybrominated dibenzo-p-dioxins (PBDDs), dibenz ofurans (PBDFs), and biphenyls (PBBs) pose to fish early life stage su rvival depends on validation of the hypothesis that these chemicals ac t additively to produce mortality. A rainbow trout early life stage bi oassay was used to determine how pairs of PBDD, PBDF, and PBB congener s 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-tetrabromodibenzo-p-dioxin (2,3,7,8-TBDD)/1,2,3,7,8-penta bromodibenzop-dioxin (1,2,3,7,8-PBDD); 2,3,7,8-TBDD/1,2,3,7,8-pentabro modibenzofuran (1,2,3,7,8-PBDF); 1,2,3,7,8-PBDD/2,3,4,7,8-pentabromodi benzofuran (2,3,4,7,8-PBDF); and 2,3,4,7,8-PBDF/3,3',4,4'-tetrabromobi phenyl (3,3',4,4'-TBB). Graded doses of each congener alone, or graded doses of fixed ratios of paired congeners were injected into newly fe rtilized rainbow trout eggs. In all cases, interactions between congen er pairs were additive as tested by a probit model. Isobolographic ana lysis also supported the hypothesis that the PBDD, PBDF, and PBB conge ners act additively. Thus, the use of fish-specific TEFs to convert fi sh tissue concentrations of individual PBDD, PBDF, and PBB congeners t o TCDD equivalents (TEs) and then adding the TEs contributed by the va rious 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) a nd lowest-observed-effect level (LOEL) for early life stage mortality, the risk that complex mixtures of these polybrominated chemicals in e ggs pose to sac fry survival can be estimated. (C) 1996 Academic Press , Inc.