Studies after the Exxon Valdez oil spill demonstrated that fish embryos exposed to low levels of PAHs in weathered crude oil develop a syndrome of edema and craniofacial and body axis defects.
Additionally, delayed mortality also occurred in the absence of external malformations, as indicated by the reduced oceanic survival of pink salmon exposed to weathered crude oil as embryos and released as smolts (Heintz et al.
A previous analysis showed that micromolar concentrations of individual tricyclic PAHs representing the homologous series most abundant in weathered crude oil (fluorene, dibenzothiophene, and phenanthrene) caused a syndrome of edema and craniofacial and body axis defects after dose-dependent cardiac dysfunction that was first observed at about 36 hpf (Incardona et al.
Embryonic cardiac dysfunction and the weathered crude oil syndrome.
Grossly, all embryos exposed to weathered crude oil showed dorsal curvature of the body axis; mild to moderate pericardial edema was seen in OGE-exposed embryos (Figure 4B,D), and yolk sac edema was seen in WAF-exposed embryos (data not shown).
The key finding is that the complex PAH mixture that comprises weathered crude oil caused early cardiac dysfunction similar to effects of model tricyclic PAHs, rather than a syndrome that arises later during the larval period, such as that associated with pyrene or TCDD exposure.
As we observed for chrysene, injection of AhR2-MO blocked the epidermal induction of CYP1A by weathered crude oil, leaving the vascular induction intact (Figure 5I).
We did not assess whether the finfold defects resulting from weathered crude oil exposure required a functional AhR pathway.
Similarly, because chrysene had no overt toxicity in AhR1/AhR2 double or CYP1A morphants, neither unmetabolized chrysene nor CYP1A-derived metabolites are likely to contribute to the embryotoxicity of weathered crude oil.
The effects of weathered crude oil exposure have little in common with pyrene or TCDD toxicity and instead overlap to a surprising degree with those of individual tricyclic PAHs.