Pacific herring (Clupea pallasii), a cornerstone of marine food webs,
generally spawn on marine macroalgae
in shallow nearshore areas that are disproportionately at risk from
oil spills. Herring embryos are also highly susceptible to toxicity
from chemicals leaching from oil stranded in intertidal and subtidal
zones. The water-soluble components of crude oil trigger an adverse
outcome pathway that involves disruption of the physiological functions
of cardiomyocytes in the embryonic herring heart. In previous studies,
impaired ionoregulation (calcium and potassium cycling) in response
to specific polycyclic aromatic hydrocarbons (PAHs) corresponds to
lethal embryolarval heart failure or subtle chamber malformations
at the high and low ends of the PAH exposure range, respectively.
Sublethal cardiotoxicity, which involves an abnormal outgrowth (ballooning)
of the cardiac ventricular chamber soon after hatching, subsequently
compromises juvenile heart structure and function, leading to pathological
hypertrophy of the ventricle and reduced individual fitness, measured
as cardiorespiratory performance. Previous studies have not established
a threshold for these sublethal and delayed-in-time effects, even
with total (∑)PAH exposures as low as 29 ng/g of wet weight
(tissue dose). Here, we extend these earlier findings showing that
(1) cyp1a gene expression provides an oil exposure
metric that is more sensitive than typical quantitation of PAHs via
GC–MS and (2) heart morphometrics in herring embryos provide
a similarly sensitive measure of toxic response. Early life stage
injury to herring (impaired heart development) thus occurs below the
quantitation limits for PAHs in both water and embryonic tissues as
a conventional basis for assessing oil-induced losses to coastal marine
ecosystems.