Sensitivity of shovelnose sturgeon (Scaphirhynchus platorynchus) and pallid sturgeon (S. albus) early life stages to 3,3′,4,4′,5-pentachlorobiphenyl and 2,3,7,8-tetrachlorodibenzo-P-dioxin exposure

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The aquatic food web of the Great Lakes has been contaminated with polychlorinated biphenyls (PCBs) since the mid-20th century. Threats of PCB exposures to long-lived species of fish, such as lake sturgeon (Acipenser fulvescens), have been uncertain because of a lack of information on the relative sensitivity of the species. The objective of the present study was to evaluate the sensitivity of early-life stage lake sturgeon to 3,3',4,4',5-pentachlorobiphenyl (PCB-126) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure. Mortality, growth, morphological and tissue pathologies, swimming performance, and activity levels were used as assessment endpoints. Pericardial and yolk sac edema, tubular heart, yolk sac hemorrhaging, and small size were the most commonly observed pathologies in both TCDD and PCB-126 exposures, beginning as early as 4 d postfertilization, with many of these pathologies occurring in a dose-dependent manner. Median lethal doses for PCB-126 and TCDD in lake sturgeon were 5.4 ng/g egg (95% confidence interval, 3.9-7.4 ng/g egg) and 0.61 ng/g egg (0.47-0.82 ng/g egg), respectively. The resulting relative potency factor for PCB-126 (0.11) was greater than the World Health Organization estimate for fish (toxic equivalency factor = 0.005), suggesting that current risk assessments may underestimate PCB toxicity toward lake sturgeon. Swimming activity and endurance were reduced in lake sturgeon survivors from the median lethal doses at 60 d postfertilization. Threshold and median toxicity values indicate that lake sturgeon, like other Acipenser species, are more sensitive to PCB and TCDD than the other genus of sturgeon, Scaphirhynchus, found in North America. Indeed, lake sturgeon populations in the Great Lakes and elsewhere are susceptible to PCB/TCDD-induced developmental toxicity in embryos and reductions in swimming performance. Environ Toxicol Chem 2017;36:988-998. Published 2016 Wiley Periodicals Inc. on behalf of SETAC. This article is a US government work and, as such, is in the public domain in the United States of America.

Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 70%

Section: Fish Culturementioning

confidence: 99%

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Sensitivity of lake sturgeon (Acipenser fulvescens) early life stages to 2,3,7,8-tetrachlorodibenzo-P-dioxin and 3,3′,4,4′,5-pentachlorobiphenyl

Tillitt

Buckler²,

Nicks

et al. 2016

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“…This suggests that up-regulation of CYP1A in liver explants could be predictive of in vivo responses of regulatory relevance, such as embryo lethality. Embryos of Atlantic sturgeon (Acipenser oxyrinchus), shortnose sturgeon (Acipenser brevirostrum), shovelnose sturgeon (Scaphirhynchus platorynchus), and pallid sturgeon (Scaphirhynchus albus) have been shown to differ significantly in their sensitivity to exposure to TCDD [14,33]. However, nothing is currently known regarding sensitivity of embryos of white sturgeon or lake sturgeon to TCDD or other dioxin-like compounds.…”

Section: Relative Sensitivity Of Fishes To Dioxin-like Compounds In Vmentioning

confidence: 99%

“…However, current WHO TEFs for fishes are based almost entirely on embryo-lethality studies with a single common laboratory test species, the rainbow trout (Oncorhynchus mykiss). Differences in concentrations of TCDD that cause embryo lethality among fishes vary by more than 200-fold [14][15][16][17][18][19][20][21], whereas relative potencies for some dioxin-like compounds are predicted to vary by more than 80-fold based on in vitro activation of AhRs [9][10][11][12][13]. Although the use of different methods and endpoints used to assess relative potencies of dioxin-like compounds to fishes complicate direct comparisons among studies conducted to date, relative potencies for rainbow trout likely differ from relative potencies of other fishes, and therefore, current WHO TEFs based solely on rainbow trout might not be protective of the diversity of fishes.…”

Section: Introductionmentioning

confidence: 99%

Cross-species comparison of relative potencies and relative sensitivities of fishes to dibenzo-p-dioxins, dibenzofurans, and polychlorinated biphenyls in vitro

Eisner

Doering

Beitel

et al. 2015

Dioxin-like compounds of varying toxicities are found in complex mixtures. The toxic equivalency factor (TEF) approach was developed based on the potency of a dioxin-like compound relative to the potency of 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) to streamline risk assessment. One limitation of the TEF approach is uncertainty regarding differences in the relative potency of dioxin-like compounds among different species. Relative potencies among fishes are limited, relative to relative potencies among birds and mammals, and TEFs for fishes are based entirely on the model species, rainbow trout (Oncorhynchus mykiss). An in vitro liver explant assay was used to characterize species-specific responses with regard to up-regulation of CYP1A transcript after exposure to 6 dioxin-like compounds in rainbow trout, white sturgeon (Acipenser transmontanus), lake sturgeon (Acipenser fulvescens), and northern pike (Esox lucius). Differences in sensitivities were observed among species after exposure to dioxin-like compounds. The relative potencies developed from liver explants of rainbow trout were comparable to relative potencies developed from embryo toxicity assays. Differences in relative potencies between species with the least and greatest relative potencies were up to 40-fold. To compare relative potencies among species, concentrations of dioxin-like compounds in fish eggs in the Fraser River and in Lake Ontario were used to calculate toxic equivalency quotients (TEQs) determined from TEFs or TCDD equivalents determined from relative potencies. The TEQs underestimated TCDD equivalents for white sturgeon, lake sturgeon, and northern pike, indicating uncertainty in application of TEFs to diverse fishes.

Predicting Early Life Stage Mortality in Birds and Fishes from Exposure to Low-Potency Agonists of the Aryl Hydrocarbon Receptor: A Cross-Species Quantitative Adverse Outcome Pathway Approach

Doering

Dubiel

Wiseman

2020

Dioxin-like compounds (DLCs) cause early life stage mortality of vertebrates through activation of the aryl hydrocarbon receptor (AhR). A prior study developed a cross-species quantitative adverse outcome pathway (qAOP) which can predict full dose-response curves of early life stage mortality for any species of bird or fish exposed to DLCs using the species-and chemical-specific 50% effect concentration (EC50) from an in vitro AhR transactivation assay with COS-7 cells. However, calculating a reliable EC50 for input into this qAOP requires the maximal response of the concentration-response curve to be known, which is not always possible for low-potency agonists, such as some polychlorinated biphenyls (PCBs). To enable predictions for these low-potency agonists, the present study revised this qAOP to use the effect concentration threshold (EC Threshold) from the in vitro AhR transactivation assay as input. Significant linear relationships were demonstrated between EC Threshold and the dose to cause 0, 10, 50, or 100% mortality among early life stages of 3 species of birds and 7 species of fish for 4 DLCs: 2,3,7,8-tetrachlorodibenzo-p-dioxin, PCB 126, PCB 77, and PCB 105. These 4 linear relationships were combined to form the revised qAOP. This qAOP using the EC Threshold enables prediction of experimental dose-response curves for lower-potency agonists to within an order of magnitude on average, but the prior qAOP using EC50 predicts experimental dose-response curves for higher-potency agonists with greater accuracy.