Combined methodologies for measuring exposure of rainbow trout (Oncorhynchus mykiss) to polycyclic aromatic hydrocarbons (PAHs) in creosote contaminated microcosms

Semipermeable membrane devices (SPMDs), RTL-W1 and H4IIE cell line-derived 2,3,7,8-TCDD equivalents (TEQs) and hepatic 7-ethoxyresorufin O-deethylase (EROD) activity were used to show that following 28-days in creosote-dosed microcosms, rainbow trout (Oncorhychus mykiss) were exposed to biologically -active polycyclic aromatic hydrocarbons (PAHs), despite the fact that PAHs were not detected at high concentrations in the trout tissue. Rainbow trou t and SPMDs were exposed to creosote at doses of 0, 5, 9, 17, 31 and 56 muL /L in microcosms. Total PAH concentration in SPMDs increased with creosote dose (r(2) = 0.910, p < 0.05). In contrast, concentrations of PAHs in rainb ow trout liver extracts did not increase with creosote dose, likely due to metabolism of these compounds. SPMD TEQs derived using both cell line bioas says (BD-TEQs) or toxic equivalent factors (TEFs; CD-TEQs) increased with c reosote dose, revealing that more Ah receptor-active compounds were accumul ated at higher creosote doses. Trout TEQs were lower than SPMD TEQs and did not increase with creosote dose. TEQs were essentially the same whether de termined with RTL-WI or H4IIE, suggesting that the predictive value of the two cell lines was equal. Hepatic EROD activity increased with creosote dos e (r(2) = 0.827, p < 0.05) and was correlated with BD-TEQs in SPMDs (r(2) = 0.811, p < 0.05) but not with BD-TEQs in rainbow trout liver. This indicat ed that EROD-inducing compounds were taken up by rainbow trout bur not main tained in tissues. Overall the three technical approaches were effective in evaluating exposure of rainbow trout to PAHs, compounds whose concentratio ns are typically difficult to estimate due to metabolism.