Polychlorinated Biphenyls and Polychlorinated Dioxins-Furans in Lake Trout and Whitefish Composite Samples from Commercial Fisheries in Lakes Erie, Huron, and Superior.

Polychlorinated biphenyls (PCBs; sum of 36 congeners) and polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs; sum of 17 2,3,7,8-substituted congeners) were measured in 93 composite samples prepared from individual lake trout (Salvelinus namaycush) and whitefish (Coregonus clupeaformis) samples collected from Lake Erie, Lake Huron, and Lake Superior. All samples had detectable concentrations of PCBs and PCDD/Fs; maximum PCB concentrations in both trout (750 ng g-1 whole weight [ww]) and whitefish (210 ng g-1 ww) were found in composites from fish collected from Lake Huron. The maximum toxic equivalent concentration was found in a lake trout composite sample from Lake Huron (53 pg g-1 ww). PCB and PCDD/F congener profiles were comparable to patterns observed in fishes collected from other regions of Canada, although concentrations were above those found in other regions. A positive correlation was found between PCB concentrations determined using the historical Aroclor equivalency method and those determined using the sum of the congeners measured (r2 = 0.871; Spearman correlation r = 0.917) or using the six indicator PCB congeners (28, 52, 101, 138, 153, and 180; r2 = 0.850; Spearman correlation r = 0.935). PCBs were the dominant contributor to the overall toxic equivalent concentrations in the fish composite samples tested. These findings provide insight into PCB and PCDD/F concentrations in two commercially important fish species over a discrete time period.

Toxicologic effects of 28-day dietary exposure to the flame retardant 1,2-dibromo-4-(1,2-dibromoethyl)-cyclohexane (TBECH) in F344 rats.

The brominated flame retardant TBECH is used as an additive to delay ignition and inhibit fires in construction materials and consumer goods. Trends in human exposure are not clear, although humans may be exposed to TBECH via indoor dust and air. In birds and fish there is some evidence of disruption in endocrine and reproductive parameters due to TBECH. In vitro studies indicate that TBECH is an androgen receptor agonist. In this study rats were exposed to 0, 10, 50, 250, 1250 or 5000mg/kg technical TBECH for 28days in diet, corresponding to 0, 0.9, 4.2, 21.3, 98.0 or 328.9mg TBECH/kg bw/d in males and 0, 0.8, 3.9, 19.4, 91.7 or 321.4mg TBECH/kg bw/d in females. Dose-dependent increases in α- and ß- TBECH were detected in serum, liver and adipose. Rats in the 5000mg/kg group lost weight rapidly and were euthanized after 15-18days. At study termination rats displayed dose-dependent clinical and histopathological changes consistent with mild hepatic and renal inflammation. In male rats, evidence of gender-specific alpha2u-globulin nephropathy was not considered predictive of renal toxicity in humans. Frank immunosuppression or inappropriate immunostimulation were not apparent, nor was there a primary effect of TBECH on adaptive immunity. Some evidence of hormone disruption was observed, including changes in serum testosterone levels in males and changes in serum T3 and T4 levels in females. Apparent increases in thyroid follicular cell hypertrophy and hyperplasia in male and female rats were not statistically significant. Benchmark dose (BMD) modelling indicated that clinical changes indicative of mild nephrotoxicity and increased blood monocyte numbers indicative of inflammation and tissue damage were the most sensitive outcomes of TBECH exposure that could be modelled. Preliminary evidence of hormone disruption supports the need for rodent studies using more sensitive models of growth, development and reproduction.