Chronic toxicity of heavy fuel oils to fish embryos using multiple exposure scenarios

Abstract

The chronic toxicity to rainbow trout (Oncorhynchus mykiss) embryos of heavy fuel oil (HFO) 6303, weathered HFO 6303, HFO 7102, and medium South American (MESA) crude oil was assessed by different exposure regimes. These included water accommodated fractions (WAF; water in contact with floating oil), chemically enhanced WAF (CEWAF; oil dispersed with Corexit 9500), and effluent from columns of gravel coated with stranded oil. Heavy fuel oil WAF was nontoxic and did not contain detectable concentrations of hydrocarbons, likely because the high density and viscosity of HFO prevented droplet formation. In contrast, chemically dispersed HFO and effluent from columns of stranded HFO contained measurable concentrations of alkyl polycyclic aromatic hydrocarbons (PAH), coincident with embryo toxicity. These exposure regimes enhanced the surface area of oil in contact with water, facilitating oil-water partitioning of hydrocarbons. Heavy fuel oil was consistently more toxic to fish than crude oil and the rank order of alkyl PAH concentrations in whole oil were sufficient to explain the rank order of toxicity, regardless of exposure method. Thus, the propensity of HFO to sink and strand in spawning shoals creates a long-term risk to developing fish because of the sustained release of PAHs from HFO to interstitial waters. Further, PAH monitoring is key to accurate risk assessment.

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

“…Future experiments should identify or rule out any dispersant-nujol interactions. Overall, the effect on medaka embryos of dilbit exposure corresponded to the effects of exposure of fish embryos to various crude oils (Wu et al, 2012Olsvik et al, 2011, refined oils such as heavy fuel oil (Martin et al, 2014;Incardona et al, 2011b), diesel fuel (Schein et al, 2009), and individual PAH and alkyl PAH (Incardona et al, 2006, 2011aTurcotte et al, 2011Lin et al, 2015). The greater apparent toxicity of dilbit CEWAF relative to WAF corresponded to previous observations that chemical dispersion increases the amount of oil that is bioavailable and toxic to fish embryos without any clear indications of interactive toxicity (Adams et al, 2014a).…”

“…WAF and CEWAF were prepared following the methods of Adams et al (2014a,b) and Martin et al (2014) as modified from Singer et al (2000). Briefly, WAF was prepared by adding dilbit to water at a ratio of 1:9, stirring gently for 18 h and allowing the solution to settle for 1 h. CEWAF was prepared by the same procedure, but after 18 h, Corexit ® 9500A (oil dispersant; ECOLAB/NALCO, Illinois, USA) was added to the surface layer of residual oil at a dispersant-to-oil ratio of 1:10.…”

“…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).…”

Predictive Ecotoxicology and Environmental Assessment

“…Laboratory experiments are useful in showing the relative toxicity of various oil and dispersed oil test solutions, but the preparation and characterization of laboratory exposure solutions remain a topic of discussion (Bejarano et al, 2014;Martin et al, 2014) as illustrated by the controversy about the "real world" assessment of oil dispersed as a consequence of the Deepwater Horizon accident (Coelho et al, 2013;Rico-Martínez et al, 2013). For instance, PAH monitoring is key to accurate risk assessment of petroleum (Chapter 18).…”