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The potential for delayed mortality following short‐term episodic pollution events was evaluated by exposing cladocerans (Ceriodaphnia dubia) and rainbow trout (Oncorhynchus mykiss) to zinc (Zn) in various 1‐ to 48‐h and 1‐ to 96‐h exposures, respectively, followed by transferring the exposed organisms to clean water for up to 47 h for C. dubia and up to 95 h for trout for additional observation. For C. dubia, 1‐h exposures of up to 3790 µg Zn/L never resulted in mortality during the actual Zn exposures, but by 48 h, a 1‐h exposure to 114 µg/L, a concentration similar to the present US national water quality acute criterion for the test water conditions, ultimately killed 70% of C. dubia. With C. dubia, the speed of action of Zn toxicity was faster for intermediate concentrations than for the highest concentrations tested. For rainbow trout, pronounced delayed mortalities by 96 h only occurred following ≥8‐h exposures. For both species, ultimate mortalities from Zn exposures ≤8 h mostly presented as delayed mortalities, whereas for exposures ≥24 h, almost all ultimate mortalities presented during the actual exposure periods. With Zn, risks of delayed mortality following exposures to all concentrations tested were much greater for the more sensitive, small‐bodied invertebrate (C. dubia) than for the less sensitive, larger‐bodied fish (rainbow trout). These results, along with previous studies, show that delayed mortality is an important consideration in evaluating risks to aquatic organisms from brief, episodic exposures to some substances. Environ Toxicol Chem 2021;40:2484–2498. © 2021 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC. This article has been contributed to by US Government employees and their work is in the public domain in the USA., Rainbow trout could withstand extreme Zn pulses of 1 to 3 h, with few subsequent deaths. Few Ceriodaphnia dubia died during 1‐ to 3‐h Zn pulses, but after 48 h, most were dead. Time to effects decreased as expected as rainbow trout were exposed to increasing Zn concentrations. Not so with C. dubia: time to effects was fastest in intermediate Zn exposures, with longer survivals in higher Zn exposures.

In recent studies, a high incidence of amphibian mortality and malformation has been reported in the field, suggesting that toxic and/or bioactive agents are present in the environment of the affected amphibians. This study provides evidence for this hypothesis, because it applies to several affected ponds in Minnesota and Vermont, USA. Three developmental bioassays were carried out on samples from three reference and three test sites in Minnesota and one reference and three test sites, in Vermont. The bioassays utilized Xenopus as a model system, measuring altered developmental patterns during the first 4 d of development (frog embryo teratogenesis assay-Xenopus [FETAX]), hind-limb development over a 30-d period, and tail length resorption over a 14-d period. Strong correlations were observed among the results for all three in vitro bioassays, as well as between adverse developmental effects in vitro and in the field.

Water samples from several ponds in Minnesota were evaluated for their capacity to induce malformations in embryos of Xenopus laevis. The FETAX assay was used to assess the occurrence of malformations following a 96-hr period of exposure to water samples. These studies were conducted following reports of high incidences of malformation in natural populations of frogs in Minnesota wetlands. The purpose of these studies was to determine if a biologically active agent(s) was present in the waters and could be detected using the FETAX assay. Water samples from ponds with high incidences of frog malformations (affected sites), along with water samples from ponds with unaffected frog populations (reference sites), were studied. Initial experiments clearly showed that water from affected sites induced mortality and malformation in Xenopus embryos, while water from reference sites had little or no effect. Induction of malformation was dose dependent and highly reproducible, both with stored samples and with samples taken at different times throughout the summer. The biological activity of the samples was reduced or eliminated when samples were passed through activated carbon. Limited evidence from these samples indicates that the causal factor(s) is not an infectious organism nor are ion concentrations or metals responsible for the effects observed. Results do indicate that the water matrix has a significant effect on the severity of toxicity. Based on the FETAX results and the occurrence of frog malformations observed in the field, these studies suggest that water in the affected sites contains one or more unknown agents that induce developmental abnormalities in Xenopus. These same factors may contribute to the increased incidence of malformation in native species.

Accumulation of the polychlorinated terphenyl formulation Aroclor 5432 in aquatic species has previously been reported. Polychlorinated terphenyls (PCTs) are structurally similar to polychlorinated biphenyls (PCBs), and were used in related applications. However, their biological effects have not been thoroughly studied. Effects of PCT mixtures on levels of hepatic cytochrome P4501A (P4501A) and associated ethoxyresorufin O-deethylase (EROD) activity in the mummichog (Fundulus heteroclitus), a common estuarine fish, were assessed here. Fish were injected intraperitoneally with PCT formulations Aroclor 5432, Aroclor 5460, or the PCB formulation Aroclor 1254, at doses of 0.32 to 100 mg/kg body weight. Elevated levels of P4501A and EROD activity were detected in fish injected with Aroclor 5432 and Aroclor 1254 doses of 32 and 100 mg/kg. Induction resulting from Aroclor 5432 was greater than that caused by equivalent doses of Aroclor 1254. Treatment with Aroclor 5460 did not result in significant induction. Because commercial PCT mixtures contain small amounts of PCBs, the PCB components may have contributed to the induction observed for Aroclor 5432. This work represents the first report of hepatic cytochrome P4501A induction caused by Aroclor 5432 in teleosts and, similar to work in mammalian systems, suggests that the effects of this mixture may bemore » at least partially mediated through Ah receptor binding.« less

Polychlorinated terphenyls (PCTs) are structurally similar to polychlorinated biphenyls (PCBs) and have been used in analogous applications. Aroclor 5432, a PCT formulation whose congeners contain predominantly two to five chlorines, was detected in sediments and oysters from a saltmarsh creek and an adjacent Chesapeake Bay tributary, Back River. Reports of the occurrence of Aroclor 5432 are virtually nonexistent, although sporadic reports of the more highly chlorinated PCT formulation Aroclor 5460 have been published. Capillary gas chromatography with electrolytic conductivity detection was used for quantitation. Identifications were confirmed by both electron ionization and negative chemical ionization mass spectrometry. Sediment concentrations detected were as high as 250,000 {mu}g/kg (dry-weight basis). Oysters collected from these areas contained up to 35,000 {mu}g/kg. This value is equivalent to 6,300 {mu}g/kg, on a wet-weight basis, and exceeds the applicable US limit for PCBs in edible shellfish by more than a factor of 3.