TL;DR: The conclusion that EVO caused significant damage to herring in PWS is supported and previous demonstration by the laboratory that most malformed or precocious larvae die corroborates the decreased larval production measured after the spill.
Abstract: Pacific herring eggs were exposed for 16 d to weathered Alaska North Slope crude oil. Exposure to an initial aqueous concentration of 0.7 parts per billion (ppb) polynuclear aromatic hydrocarbons (PAHs) caused malformations, genetic damage, mortality, and decreased size and inhibited swimming. Total aqueous PAH concentrations as low as 0.4 ppb caused sublethal responses such as yolk sac edema and immaturity consistent with premature hatching. Responses to less weathered oil, which had relatively lower proportions of high molecular weight PAH, generally paralleled those of more weathered oil, but lowest observed effective concentrations (LOECs) were higher (9.1 ppb), demonstrating the importance of composition. The LOEC for more weathered oil (0.4 ppb) was similar to that observed in pink salmon (1.0 ppb), a species with a very different development rate; by inference, other species may be similarly sensitive to weathered oil. Our methods simulated conditions observed in Prince William Sound (PWS) following the Exxon Valdezoil (EVO) spill. Biological effects were identical to those observed in embryolarval herring from PWS in 1989 and support the conclusion that EVO caused significant damage to herring in PWS. Previous demonstration by our laboratory that most malformed or precocious larvae die corroborates the decreased larval production measured after the spill. Keywords—Herring larvae Morphological damage Genetic damage Polynuclear aromatic hydrocarbons Exxon Valdez oil spill
TL;DR: In this paper, a group of federal, state, academic and industry representatives from North America and Europe have been working toward standardizing both biological and analytical methods used to produce acute toxicity estimates of complex mixtures such as oil, dispersants and dispersed oil.
TL;DR: It is shown that environmentally realistic exposures to crude oil cause specific dose-dependent defects in cardiac function in all three species, with circulatory disruption culminating in pericardial edema and other secondary malformations.
Abstract: The Deepwater Horizon disaster released more than 636 million L of crude oil into the northern Gulf of Mexico. The spill oiled upper surface water spawning habitats for many commercially and ecologically important pelagic fish species. Consequently, the developing spawn (embryos and larvae) of tunas, swordfish, and other large predators were potentially exposed to crude oil-derived polycyclic aromatic hydrocarbons (PAHs). Fish embryos are generally very sensitive to PAH-induced cardiotoxicity, and adverse changes in heart physiology and morphology can cause both acute and delayed mortality. Cardiac function is particularly important for fast-swimming pelagic predators with high aerobic demand. Offspring for these species develop rapidly at relatively high temperatures, and their vulnerability to crude oil toxicity is unknown. We assessed the impacts of field-collected Deepwater Horizon (MC252) oil samples on embryos of three pelagic fish: bluefin tuna, yellowfin tuna, and an amberjack. We show that environmentally realistic exposures (1–15 µg/L total PAH) cause specific dose-dependent defects in cardiac function in all three species, with circulatory disruption culminating in pericardial edema and other secondary malformations. Each species displayed an irregular atrial arrhythmia following oil exposure, indicating a highly conserved response to oil toxicity. A considerable portion of Gulf water samples collected during the spill had PAH concentrations exceeding toxicity thresholds observed here, indicating the potential for losses of pelagic fish larvae. Vulnerability assessments in other ocean habitats, including the Arctic, should focus on the developing heart of resident fish species as an exceptionally sensitive and consistent indicator of crude oil impacts.
TL;DR: In this article, the authors show that polynuclear aromatic hydrocarbons (PAH) accumulation in embryo tissues during direct contact and effluent exposure experiments were not significantly different, indicating that PAH accumulation was mediated by aqueous transport.
Abstract: We incubated pink salmon embryos under three exposure conditions, direct contact with oil-coated gravel, effluent from oil-coated gravel, and direct contact with gravel coated with very weathered oil (VWO). Embryo mortalities and polynuclear aromatic hydrocarbon (PAH) accumulation in embryo tissues during the direct-contact and effluent exposure experiments were not significantly different, indicating that PAH accumulation was mediated by aqueous transport. Mortality rates for embryos exposed initially to a total PAH concentration (TPAH) of 1.0 ppb were significantly higher than controls when the PAH were derived from VWO. The same aqueous TPAH concentration failed to increase mortality rates when the PAH were derived from less weathered oil, indicating that toxicity of effluents from the VWO was primarily associated with the larger PAH. We conclude that water quality standards for TPAH above 1.0 ppb may fail to protect fish embryos. Further, pink salmon embryos incubating in Prince William Sound after the Exxon Valdez oil spill may have accumulated lethal concentrations of PAH from interstitial water that was contaminated when it percolated through oil reservoirs located upstream from salmon redds.
TL;DR: In this paper, the authors examined petroleum hydrocarbons in oil mousse collected from the sea surface and salt marshes, and in oil deposited in sediments adjacent to the wellhead after the Deepwater Horizon (DWH) oil spill.
Abstract: The oil released during the Deepwater Horizon (DWH) oil spill may have both short- and long-time impacts on the northern Gulf of Mexico ecosystems. An understanding of how the composition and concentration of the oil are altered by weathering, including chemical, physical and biological processes, is needed to evaluate the oil toxicity and impact on the ecosystem in the northern Gulf of Mexico. This study examined petroleum hydrocarbons in oil mousse collected from the sea surface and salt marshes, and in oil deposited in sediments adjacent to the wellhead after the DWH oil spill. Oil mousses were collected at two stations (OSS and CT, located 130 and 85 km away from the wellhead, respectively) in May 2010, and two sediment samples from stations SG and SC, within 6 km of the wellhead, in May 2011. We also collected oil mousse from salt marshes at Marsh Point (MP), Mississippi, 186 km away from the wellhead in July 2010. In these samples, n-alkanes, polycyclic aromatic hydrocarbons (PAHs), alkylated PAHs, BTEX (collective name of benzene, toluene, ethylbenzene and p-, m-, and o-xylenes), C3-benzenes and trace metals were measured to examine how the oil was altered chemically. The chemical analysis indicates that the oil mousses underwent different degrees of weathering with the pattern of OSS < CT < MP. This pattern is consistent with the projected oil mousse movement from the accident site to salt marshes. Also, the contents of trace metals Al, V, Cr, Fe, Mn, Ni, Co, Cu, As and Pb in the oil mousse generally increased along the way to the salt marshes, indicating that these trace metals were perhaps aggregated into the oil mousse during the transport. Petroleum hydrocarbon data reveal that the oil deposited in sediments underwent only light to moderate degradation one year after the DWH oil spill, as supported by the presence of short-chained n-alkanes (C10–C 15), BTEX and C 3-benzenes. The weathering of oil in sediment may result from biological degradation and dissolution, evidenced by the preferential loss of mid-chained n-alkanes C16–C 27, lower ratios of n-C 17/Pr and n-C 18/Ph , and preferential loss of PAHs relative to alkylated PAHs.