Habitat damage resulting from oil contamination is underestimated by acute toxicity assays. Nearshore substrates oiled by spills may become persistent pollution sources of toxic polycyclic aromatic hydrocarbons (PAH). Recent findings resulting from research following the Exxon Valdez oil spill include: ( 1) PAHs are released from oil films and droplets at progressively slower rates with an increasing molecular weight, leading to greater persistence of larger PAHs; ( 2) eggs from demersally-spawning fish species accumulate dissolved PAHs released from oiled substrates, even when the oil is heavily weathered; and (3) PAHs accumulated by embryos from aqueous concentrations of < 1 μg/L can lead to adverse sequelae appearing at random over the lifespan of an exposed cohort, probably as a result of damage during early embryogenesis. Polycyclic Aromatic Hydrocarbons (PAH) can be a slow-acting poison, and toxic effects may not manifest until long after exposure. These considerations have important policy implications regarding protection of fish natal and rearing habitats.