Exposure to high concentrations of crude oil produces a lethal syndrome of heart failure in fish embryos. Mortality is caused by cardiotoxic polycyclic aromatic hydrocarbons (PAHs), ubiquitous components of petroleum. Here, we show that transient embryonic exposure to very low concentrations of oil causes toxicity that is sublethal, delayed, and not counteracted by the protective effects of cytochrome P450 induction. Nearly a year after embryonic oil exposure, adult zebrafish showed subtle changes in heart shape and a significant reduction in swimming performance, indicative of reduced cardiac output. These delayed physiological impacts on cardiovascular performance at later life stages provide a potential mechanism linking reduced individual survival to population-level ecosystem responses of fish species to chronic, low-level oil pollution.

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The 1989 Exxon Valdez disaster exposed embryos of pink salmon and Pacific herring to crude oil in shoreline spawning habitats throughout Prince William Sound, Alaska. The herring fishery collapsed four years later. The role of the spill, if any, in this decline remains one of the most controversial unanswered questions in modern natural resource injury assessment. Crude oil disrupts excitationcontraction coupling in fish heart muscle cells, and we show here that salmon and herring exposed as embryos to trace levels of crude oil grow into juveniles with abnormal hearts and reduced cardiorespiratory function, the latter a key determinant of individual survival and population recruitment. Oil exposure during cardiogenesis led to specific defects in the outflow tract and compact myocardium, and a hypertrophic response in spongy myocardium, evident in juveniles 7 to 9 months after exposure. The thresholds for developmental cardiotoxicity were remarkably low, suggesting the scale of the Exxon Valdez impact in shoreline spawning habitats was much greater than previously appreciated. Moreover, an irreversible loss of cardiac fitness and consequent increases in delayed mortality in oil-exposed cohorts may have been important contributors to the delayed decline of pink salmon and herring stocks in Prince William Sound.The year 2014 marked the 25 th anniversary of the 1989 Exxon Valdez oil spill in Prince William Sound, Alaska. At the time, the spill was the largest in U.S. history, with extensive oiling of shoreline spawning habitats for Pacific herring (Clupea pallasi) and pink salmon (Oncorhynchus gorbuscha), the two most important commercial fish species in the Sound. Herring larvae sampled in proximity to oil were visibly abnormal 1 , and mortality rates were higher for pink salmon embryos at oiled sites 2 . The herring fishery collapsed 3-4 years after the spill 3,4 when the cohort spawned in oiled areas would have reached reproductive maturity 5 . The contribution of the spill to the herring population collapse, if any, was never determined and remains controversial.In the early 1990s little was known about the effects of low-level crude oil exposures on fish early life stages. In the ensuing years, the syndrome of developmental defects and mortality documented in field-collected herring and salmon larvae was linked to polycyclic aromatic hydrocarbons (PAHs), an abundant fraction of most crude oils [6][7][8] . Subsequent research using the zebrafish model showed that the etiology of the syndrome was a disruption of embryonic cardiac function and morphogenesis 9,10 . This cardiotoxicity was specifically attributed to three-ringed PAHs 9,10 , and it was further shown that normal-appearing zebrafish embryos surviving trace crude oil exposures grow into adults with malformed hearts and reduced cardiorespiratory performance 11 . It is now established that crude oils from different geological sources disrupt heart development 12,13 in a diversity of fish species 14,15 , by a mechanism

Returning adult salmon represent an important source of energy, nutrients, and biochemicals to their natal streams and may therefore have a quantitative effect on the energy levels of stream‐resident salmonids. We tested this hypothesis by constructing simulated streams for coho salmon Oncorhynchus kisutch to which we added 0, 1, and 4 carcasses/m2 (0, 0.71, and 2.85 kg wet mass/m2) of pink salmon O. gorbuscha. After 60 d we evaluated the lipid class and fatty acid composition of rearing coho salmon from the simulated streams; the lipid content and triacylglycerols of the coho salmon increased with increasing carcass density whereas phospholipids decreased. Increased amounts of triacylglycerols accounted for most of the lipid increase. In addition to increasing in concentration, the fatty acid composition of the triacylglycerols also changed with carcass density. Triacylglycerols of juvenile coho salmon from the control streams had significantly higher omega‐3 : omega‐6 ratios as a result of fivefold and sixfold increases in the concentrations of eicosapentanoic and docosahexanoic fatty acids, respectively. These data demonstrate an immediate nutritional benefit resulting from the introduction of salmon carcasses in juvenile coho salmon rearing habitat and indicate the utility of fatty acid and lipid class analysis for examining the effects of marine‐derived nutrients on juvenile salmonids.

Abstract-Low-density polyethylene membranes, typically filled with triolein, have been previously deployed as passive environmental samplers designed to accumulate nonpolar hydrophobic chemicals from water, sediments, and air. Hydrocarbons in such samplers, known as semipermeable membrane devices (SPMDs), diffuse through pores in the membranes and are trapped in the central hydrocarbon matrix, mimicking uptake by living organisms. Here, we describe laboratory and field verification that lowdensity polyethylene membrane devices (PEMDs) without triolein provide reliable, relatively inexpensive, time-integrated hydrocarbon sampling from water. For comparison, polynuclear aromatic hydrocarbon (PAH) uptake in SPMDs and pink salmon eggs also was studied. Total concentrations of PAH accumulated by PEMDs were highly correlated with concentrations in water (r 2 Ն 0.99) and linear over the range tested (0-17 g/L). Higher-molecular-mass PAH preferentially accumulated in PEMDs and in pink salmon eggs, but the source of oil in PEMDs remained identifiable. Accumulations of PAH were highly similar to those in SPMDs. The PEMDs retained approximately 78% of accumulated total PAH for 40 d in clean water. Thus, a simple plastic membrane can be conveniently used for environmental monitoring, particularly during situations in which contaminant concentrations are low (in the parts-per-billion range), variable, and intermittent.

We deployed semipermeable membrane devices (SPMDs) on beaches for 28 days at 53 sites in Prince William Sound (PWS), Alaska, to evaluate the induction potential from suspected sources of cytochrome P450 1A (CYP1A)-inducing contaminants. Sites were selected to assess known point sources, or were chosen randomly to evaluate the region-wide sources. After deployment, SPMD extracts were analyzed chemically for persistent organic pollutants (POPs) and polycyclic aromatic hydrocarbons (PAH). These results were compared with hepatic CYP1A enzyme activity of juvenile rainbow trout injected with the same extracts prior to clean-up for the chemical analyses. Increased CYP1A activity was strongly associated with PAH concentrations in extracts, especially chrysene homologues but was not associated with POPs. The only apparent sources of chrysene homologues were lingering oil from Exxon Valdez, asphalt and bunker fuels released from storage tanks during the 1964 Alaska earthquake, creosote leaching from numerous pilings at one site, and PAH-contaminated sediments at Cordova Harbor. Our results indicate that PWS is remarkably free of pollution from PAH when nearby sources are absent as well as from pesticides and PCBs generally.

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