Meeting Abstract
Polycyclic aromatic hydrocarbons (PAHs) are the major toxic component of petrochemicals. PAH exposure causes a syndrome of abnormalities, many of which are downstream sequelae of diminished cardiac function. Failure to inflate the swim bladder is a common developmental outcome of PAH exposure, and has been linked to heart defects, but may occur by other mechanisms as well. Here, we review multiple mechanisms by which oil may affect swim bladder inflation or function. A lack of circulation due to diminished cardiac function causes failed development and non-inflation. However, EC50 data indicate that swim bladder non-inflation can be a more sensitive outcome than diminished cardiac function, especially for some particular PAH. Because initial inflation occurs by surface gulping in physostomes and many physoclists, inflation failure can also occur due to the presence of a surface film or the inability to complete swim-up behavior and reach the surface. Non-inflation could also result from failed maintenance of swim bladder volume following initial air gulping, due to damage to the rete mirabile. Functional studies of swim bladder function in adults following PAH exposure are lacking. Thus, there are many potential mechanisms of swim bladder failure in response to oil or PAH exposure, and some could lead to sub-lethal chronic effects.
