Abstract
A multitude of recent studies have documented the detrimental effects of crude oil exposure on early life stages of fish, including larvae and embryos. While polycyclic aromatic hydrocarbons (PAHs), particularly alkyl PAHs, are often considered the main cause of observed toxic effects, other crude oil derived organic compounds are usually overlooked. In the current study, comprehensive two-dimensional gas chromatography coupled to mass spectrometry was applied to investigate the body burden of a wide range of petrogenic compounds in Atlantic haddock (Melanogrammus aeglefinus) and cod (Gadus morhua) embryos that had been exposed to sublethal doses of dispersed crude oil. Several groups of alkylated monoaromatic compounds (e.g. alkyl tetralins, indanes and alkyl benzenes), as well as highly alkylated PAHs, were found to accumulate in the fish embryos upon crude oil exposure. To investigate the toxicity of the monoaromatic compounds, two models (1-isopropyl-4-methyltetralin and 1-isopropyl-4-methylindane) were synthesized and shown to bioaccumulate and cause delayed hatching in developing embryos. Minor developmental effects, including craniofacial and jaw deformations and pericardial edemas, were also observed at the highest studied concentrations of the alkylindane.
Highlights
The main toxic responses observed in crude oil exposed fish early life stages (ELS) include mortality, cardiotoxicity and morphogenetic defects (Brette et al, 2014; Incardona and Scholz, 2016; Sørhus et al., 2015a), but the toxicological mechanisms are still not fully understood
New observations suggest that the presence of crude oil droplets leads to more severe effects than if only the water-soluble fraction (WSF) is present (González-Doncel et al, 2008; Khursigara et al, 2017)
Several groups of petrogenic monoaromatic compounds were identified in cod and haddock embryos after exposure to dispersed crude oil
Summary
The main toxic responses observed in crude oil exposed fish ELS include mortality, cardiotoxicity and morphogenetic defects (Brette et al, 2014; Incardona and Scholz, 2016; Sørhus et al., 2015a), but the toxicological mechanisms are still not fully understood. It was hypothesized that this was caused by direct interaction with crude oil droplets adhering to the chorion of the exposed embryos, causing a secondary exposure pathway (Hansen et al, 2018) by allowing direct transfer of crude oil compounds from the droplets to the eggs This way, water solubility becomes less important for bioavailability and significant accumulation of high log KOW compounds becomes feasible. This secondary pathway has been demonstrated to cause increased internal body burden of embryotoxic PAHs and alkyl PAHs in haddock eggs (Sørensen et al, 2017), leading to much more severe effects than in exposed cod eggs that are less affected by oil adhesion (Hansen et al, 2018)
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