Very low embryonic crude oil exposures cause lasting cardiac defects in salmon and herring.

Although not clearly dose-dependent, the effect of oil exposure was highly significant (ANOVA P = 0.0012) with salmon from all oil treatments having shorter outflow tracts relative to controls (all P values < 0.005) except for the lowest ΣPAH exposure (9.8 μg/L).

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Analysis in fixed sections from 5–6 individuals for each treatment group showed a trend of increased cardiomyocyte width related to oil exposure with a mean (±s.e.m.) in controls of 4.03 ± 0.05 μm and ranging from 4.16 ± 0.05 to 4.24 ± 0.05 μm across oil-exposed groups ( Fig. 4B ).

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While measurements of the outflow tract angle had greater variability, there was a clear trend that mirrored the effect on bulbus arteriosus length ( Fig. 3D ).

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