Meeting Abstract
Several years after the 1989 Exxon Valdez oil spill, the Pacific herring (Clupea pallasi) population of Prince William Sound crashed and never recovered. Despite finding that larvae are sensitive to very low concentrations of polycyclic aromatic hydrocarbons (PAHs), the connection between oil spills and delayed mortality at the population level has yet to be established. The developing heart is the primary target of crude oil toxicity and a strong hypothetical starting point for a cascade of events leading to reduced recruitment at the population level. To establish this, we evaluated larval cardiac morphology and growth through metamorphosis in addition to juvenile cardiorespiratory performance. Herring embryos were exposed to 0 to 5.1 ppb ∑PAHs from 24 hours post fertilization to 10 days and subsequently reared in clean sea water. Concentrations were maintained by a dispersion generator which injected microdroplets of Alaskan North Slope crude oil into the exposure system. Cardiac morphology was assessed weekly by video microscopy through metamorphosis, approximately 80 days post hatch. At near-detection limit concentrations, we observed cardiac edema and altered ventricular shape. This was accompanied by reduced cardiorespiratory performance in juveniles. Ongoing studies relate cardiorespiratory performance, growth, and infectious disease resistance which are strong determinants of population-dynamics. Therefore, larval cardiotoxicity and reduced juvenile performance at least partially explain the delayed mortality observed after the Exxon Valdez oil spill. This work is part of a larger collaboration to evaluate the relationship between larvae and juvenile physiology and population decline.
