The toxic effects of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) to fathead minnow (Pimephales promelas), channel catfish (Ictalurus punctatus), lake herring (Coregonus artedii), medaka (Oryzias latipes), white sucker (Catastomus commersoni), northern pike (Esox lucius), and zebrafish (Danio danio) were observed during early life‐stage development after waterborne exposure of fertilized eggs. Species sensitivity based on TCDD‐Cegg (TCDD concentration in eggs) was determined by effects observed over a 32‐d period for all species except lake herring in which a 100‐d period was used. Signs of TCDD toxicity, including edema, hemorrhaging, and craniofacial malformations were essentially identical to those observed in salmonids following TCDD egg exposure and preceded or accompanied mortality most often during the period from hatch through swim‐up. The no‐observed‐effect concentrations and lowest‐observed‐effect concentrations, based on significant decreases in survival and growth as compared to the controls, ranged from 175 and 270 pg/g for lake herring to 424 and 2,000 pg/g for zebrafish, respectively. Shapes of concentration–response curves, expressed as TCDD‐Cegg versus percent mortality, were similar for all species and were consistently steep suggesting that the mechanism of action of TCDD is the same among these species. The LCegg50s (concentrations in eggs causing 50% lethality to fish at test termination) ranged from 539 pg/g for the fathead minnow to 2,610 pg/g for zebrafish. Comparisons of LCegg50s indicate that the tested species were approximately 8 to 38 times less sensitive to TCDD than lake trout, the most sensitive species evaluated to date. When LCegg50s are normalized to the fraction lipid in eggs (LCegg,l50s), the risk to early life stage survival for the species tested ranges from 16‐ to 180‐fold less than for lake trout.

Abstract-The toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to fathead minnow (Pimephales promelas), channel catfish (Ictalurus punctatus), lake herring (Coregonus artedii), medaka (Oryzias latipes), white sucker (Catastomus commersoni), northern pike (Esox lucius), and zebrafish (Danio danio) were observed during early life-stage development after waterborne exposure of fertilized eggs. Species sensitivity based on TCDD-C egg (TCDD concentration in eggs) was determined by effects observed over a 32-d period for all species except lake herring in which a 100-d period was used. Signs of TCDD toxicity, including edema, hemorrhaging, and craniofacial malformations were essentially identical to those observed in salmonids following TCDD egg exposure and preceded or accompanied mortality most often during the period from hatch through swim-up. The no-observedeffect concentrations and lowest-observed-effect concentrations, based on significant decreases in survival and growth as compared to the controls, ranged from 175 and 270 pg/g for lake herring to 424 and 2,000 pg/g for zebrafish, respectively. Shapes of concentration-response curves, expressed as TCDD-C egg versus percent mortality, were similar for all species and were consistently steep suggesting that the mechanism of action of TCDD is the same among these species. The LC egg 50s (concentrations in eggs causing 50% lethality to fish at test termination) ranged from 539 pg/g for the fathead minnow to 2,610 pg/g for zebrafish.Comparisons of LC egg 50s indicate that the tested species were approximately 8 to 38 times less sensitive to TCDD than lake trout, the most sensitive species evaluated to date. When LC egg 50s are normalized to the fraction lipid in eggs (LC egg,ᐉ 50s), the risk to early life stage survival for the species tested ranges from 16-to 180-fold less than for lake trout.

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Abstract-Adult brook trout (Salvelinus fontinalis) were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with a contaminated trout pellet diet to determine the effects of TCDD on reproduction, to document tissue-specific TCDD distribution, and to establish the maternally derived dose of TCDD to the F 1 generation. Five treatment groups and a control were exposed to achieve targeted whole body TCDD concentrations of 0, 75, 150, 300, 600, and 1,200 pg TCDD per gram fish. Net dietary assimilation of TCDD was estimated to be 89% of the applied dose, and the distribution of TCDD generally followed the distribution of lipids in liver, gonad, fat, blood, and muscle. Depuration could not be measured over 81 d, but a hypothetical depuration rate was estimated to be 0.002 d Ϫ1 assuming 100% dietary assimilation. The concentration of TCDD in ovaries and spawned eggs was estimated to be 61 and 39% of the whole body TCDD concentrations, respectively. Survival, growth, gonadal development, and egg production were not affected in any treatment. The onset of spawning was delayed by 13 d in the highest treatment group, suggesting that TCDD might have affected ovulation. Otherwise, the adult life stage was not as sensitive to TCDD as the early life stage.

Recent reports concerning the lethal effects of solar ultraviolet-B (UV-B) (290-320 nm) radiation on amphibians suggest that this stressor has the potential to impact some amphibian populations. In this study embryos and larvae of three anuran species, Rana pipiens, Rana clamitans and Rana septentrionalis, were exposed to full-spectrum solar radiation and solar radiation filtered to attenuate UV-B radiation or UV-B and ultraviolet-A (UV-A) (290-380 nm) radiation to determine the effects of each wavelength range on embryo and larval survival. Ambient levels of solar radiation were found to be lethal to all three species under exposure conditions that eliminated shade and refuge. Lethality was ameliorated by filtration of UV-B radiation alone, demonstrating that ambient UV-B radiation is sufficient to cause mortality. Although several studies have qualitatively demonstrated the lethality of UV-B to early life stage amphibians this study demonstrates that the larval life stages of the three species tested are more sensitive than the embryonic stages. This suggests that previous reports that have not included the larval life stage may underestimate the risk posed to some anuran populations by increasing UV-B exposure. Furthermore, this study reports quantitative UV-B dosimetry data, collected in conjunction with the exposures, which can be used to begin the assessment of the impact of environmental changes which increase UV-B exposure of these anurans.