Congener-specific hepatic levels of PCDD/Fs and PCBs were also compared among samples of YOY tomcod from multiple sites in the HR estuary extending from RM 1 to RM 120, including Newark Bay (Yuan et al., 2001; Ikonomou et al., 2004). YOY fish (4-7 months old) were used with the anticipation that their vagility was less than that of adults, their hepatic contaminant and CYP1A1 mRNA levels would reflect localized conditions, and congener-specific signatures could be used to micro-map bioavailable pollutant levels and perhaps identify their sources.
The expectation of a gradient from upriver sources to New York City in hepatic PCB levels in tomcod from the main stem HR was not observed. The lowest levels of PCBs were observed at the most upriver sites and the highest levels at RM 37 (Ikonomou et al., 2004). Surprisingly, levels of PCBs at sites within Newark Bay were as high as those at the most contaminated site in the main stem HR and congener patterns were similar to those in the main stem HR.
Hepatic levels of PCDD/Fs were highest in tom-cod from two sites in the Newark Bay complex, almost certainly resulting from their transport from the single herbicide manufacturing facility on the lower Passaic River. Ratios of total PCDDs to total PCDFs and congener-specific analyses of both indicated that there are different sources in the main stem HR compared to Newark Bay and the likely absence of exchange of tomcod between the two waterways.
Levels of CYP1A1 mRNA expression were also quantified in YOY tomcod from forty sites in the HR estuary to evaluate the correspondence between hepatic CYP1A1 and hepatic concentrations of PCBs, PCDD/Fs and to determine the utility of gene expressionin evaluating the microgeographic distribution of contaminants within the estuary (Yuan et al., 2001). Significant spatial heterogeneity in CYP1A1 mRNA levels was observed among
sites with levels of gene expression differing maximally by twenty-three to thirty-four-fold. Although levels of PCBs and PCDD/Fs and CYP1A1 mRNA were highest in tomcod from the Newark Bay complex, there was little relationship between hepatic contaminants and hepatic CYP1A1 mRNA in tomcod from sites in the main stem HR. Based on these results and controlled laboratory experiments which demonstrated impaired CYP1A1 in-ducibility by PCBs and TCDD, it was hypothesized that high levels of CYP1A1 in environmentally exposed tomcod from the HR is due to PAHs or other contaminants not measured.
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