Identification of compounds in heavy fuel oil that are chronically toxic to rainbow trout embryos by effects‐driven chemical fractionation

Abstract

The present study isolated and identified compounds in heavy fuel oil 7102 (HFO 7102) that are bioavailable and chronically toxic to rainbow trout embryos (Oncorhynchus mykiss). An effects-driven chemical fractionation combined the chemical separation of oil with toxicity testing and chemical analyses of each fraction to identify the major classes of compounds associated with embryo toxicity. Toxicity was assessed with 2 exposure methods, a high-energy chemical dispersion of oil in water, which included oil droplets in test solutions, and water accommodated fractions which were produced by oiled gravel desorption columns, and which did not contain visible oil droplets. Fractions of HFO with high concentrations of naphthalenes, alkanes, asphaltenes, and resins were nontoxic to embryos over the range of concentrations tested. In contrast, fractions enriched with 3- to 4-ringed alkyl polycyclic aromatic hydrocarbons (PAHs) were embryotoxic, consistent with published studies of crude oils and individual alkyl PAHs. The rank order of fraction toxicity did not vary between the exposure methods and was consistent with their PAH content; fractions with higher-molecular weight alkyl PAHs were the most toxic. Exposure of juvenile trout to most fractions of HFO induced higher activities of cytochrome P450 enzymes, with a rank order of potency that varied with exposure method and differed somewhat from that of embryotoxicity. Induction reflected the bioavailability of PAHs but did not accurately predict embryotoxicity.

Diluted bitumen causes deformities and molecular responses indicative of oxidative stress in Japanese medaka embryos

“…The malformations evident as BSD in embryonic and juvenile fish exposed to oil have been attributed largely to the toxic effects of 3-to 5-ringed PAH, including alkyl-phenanthrenes (Adams et al, 2014b;Incardona et al, 2006Incardona et al, , 2011aFallahtafti et al, 2012;Turcotte et al, 2011), although the myriad of compounds comprising dilbit may include unknown constituents that contributed to embryotoxicity. Here, we present the first report of similar malformations in Japanese medaka hatchlings exposed to dilbit.…”

“…Of particular importance are the effects on the early developmental stages of fish species, which seem particularly vulnerable due to their inability to avoid oil exposure, and their high sensitivity to toxicity (Carls et al, 2000). The embryo toxicity of crude and refined oils is well established (e.g., Martin et al, 2014;Schein et al, 2009;Carls et al, 2000) and has been linked to the concentrations of 3-to 5-ringed alkyl polycyclic aromatic hydrocarbons (alkyl PAHs) that can partition from oil droplets into water at toxic concentrations (Adams et al, 2014b;Bornstein et al, 2014;Hodson et al, 2007). Phenotypic responses include an exposure-dependent increase in the prevalence of signs of blue-sac disease (BSD; including edemas, heart malformations, craniofacial malformations, and fin erosion) and impairment of development (He et al, 2012;Farwell et al, 2006).…”

The influence of heart developmental anatomy on cardiotoxicity-based adverse outcome pathways in fish

“…2). These effects range from outright embryonic heart failure and mortality at relative high PAH exposures (Adams et al, 2014a;Adams et al, 2014b;Esbaugh et al, 2016;Incardona et al, 2014;Incardona et al, 2013;Jung et al, 2013;Jung et al, 2015;Madison et al, 2015;Martin et al, 2014;McIntyre et al, 2016a;McIntyre et al, 2016b;Sørhus et al, 2015), to more subtle effects on heart shape and delayed impacts on cardiovascular performance at lower concentrations (Hicken et al, 2011;Incardona et al, 2015). These latter, protracted physiological impacts likely contributed to the delayed mortality and poor population recruitment previously observed both in 1) mark-recapture studies with pink salmon (Oncorhynchus gorbuscha) exposed to crude oil during embryogenesis (Heintz, 2007;Heintz et al, 2000) and 2) the losses of wild pink salmon spawned in shoreline habitats that were oiled in the aftermath of the 1989 Exxon Valdez disaster (Rice et al, 2001).…”

Retene causes multifunctional transcriptomic changes in the heart of rainbow trout ( Oncorhynchus mykiss ) embryos

“…It has been found in sedimenting particles and the sediment surface layer in lake areas contaminated by treated pulp and paper mill effluents, and in municipal landfill soil (Leppanen and Oikari, 1999,Leppanen and Oikari, 2001,Legler et al, 2011. As an alkylphenanthrene, retene is representative of the compounds in petroleum products that cause dioxin-like developmental toxicity in fishes (Adams et al, 2014). Retene is an AhR agonist, and it causes BSD in early life stages of zebrafish, medaka, and rainbow trout (Oncorhynchus mykiss) (Billiard et al, 1999,Kiparissis et al, 2003,Scott et al, 2011.…”