Date Awarded


Document Type


Degree Name

Doctor of Philosophy (Ph.D.)


Virginia Institute of Marine Science


Morris H. Roberts, Jr


Spot, Leiostomus xanthurus, were exposed to suspended sediments (&\approx&20 mg/L) contaminated with polycyclic aromatic hydrocarbons (PAH) in a laboratory flow-through system to evaluate the applicability of hepatic ethoxyresorufin O-deethylase (EROD) induction as an indicator of PAH exposure. PAH sources tested were coal-tar creosote (CTC), a low molecular weight fraction of creosote (LMWF), and a high molecular weight fraction of creosote (HMWF). A standard 96-h acute toxicity test was conducted to ensure that PAH concentrations tested in induction studies were sub-acutely toxic. The 96-h LC50 for spot was 1740 &\mu&g PAH/L (95% confidence interval = 1480-2060 &\mu&g PAH/L). The lowest concentration producing an observable effect in 96 h was 560 &\mu&g PAH/L; no effects were observed for spot exposed to 250 &\mu&g PAH/L for 96 h. Induction of hepatic EROD activity occurred rapidly in fish exposed to high environmentally realistic concentrations of CTC or the HMWF, but not the LMWF. Maximal induction (30-fold) occurred in fish exposed for 48 h to 150 &\mu&g PAH/L. Induction was concentration-dependent up to 150 &\mu&g PAH/L; at 320 &\mu&g PAH/L induction was 14-fold. EROD activity decreased upon further exposure; by day 7, EROD activity was not significantly different than that on day 0. EROD activity in fish exposed to 16 &\mu&g PAH/L was not consistently higher than that in control fish. Spot exposed to at least 70 &\mu&g PAH/L from CTC or the HMWF experienced severe fin erosion, epidermal lesions, and mortality beginning a few days after maximal EROD induction occurred. No relationship between EROD induction and whole animal responses is implied, only that EROD induction did precede any high order effects. These results indicate complications to the use of EROD activity as a sensitive, reliable indicator of PAH exposure. The toxicity of CTC may inhibit or interfere with continued induction of EROD activity, but neither the toxicity nor inducing capability is associated with the LMWF. The lack of exposure-dependent EROD induction indicate there could be difficulties in interpreting field studies, where fish have unknown exposure histories.



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