Results and Discussion

Technical Note DOER-C8

July 1999

RESULTS AND DISCUSSION

Toxic Equivalency. The 2,3,7,8-TCDD congener is the most potent of the 17 PCDD/PCDFs

containing the 2,3,7,8-chloro substitution pattern, which is a requirement for AhR binding and for

toxicity. For that reason, the concentrations of the other congeners measured in chemical analyses

are normalized to 2,3,7,8-TCDD using toxic equivalency factors (TEFs). Toxic equivalents (TEQ)

of the mixture are equal to the sum of the concentrations of individual congeners (i) multiplied by

their potencies (TEFi) relative to 2,3,7,8,-TCDD.

TEQ = Σ(PCDDi TEFi) + Σ(PCDFi TEFi)

(1)

Hence, the TEQ of a PCDD/PCDF mixture can be treated as though it were the concentration of

2,3,7,8-TCDD. In addition to these, EPA recognizes 13 coplanar PCBs as having dioxin toxic

equivalents.1

Coplanar PCBs and some PAHs bind with the AhR similarly to dioxins, but with less strength and

less potency to effect gene transcription. TEFs for PCBs and PAHs relative to 2,3,7,8,-TCDD were

developed at Columbia Analytical Services, Inc. (CAS), Carlsbad, CA, using the transgenic 101L

human hepatoma cells. The CAS TEFs for PCBs and PAHs were included in TEQ calculations for

the NYDMMP GC/MS analysis comparisons with TEQs measured in the 101L assay (Equation 2).

TEQ = Σ(PCDDi TEFi) + Σ(PCDFi TEFi) +

(2)

Σ(PCBi TEFi) + Σ(PAHi TEFi)

Additivity is assumed in the calculation and is a conservative assumption because it is known that

some PCB mixtures exhibit nonadditive (antagonistic) interactions (Safe 1994).

NYDMMP Sediments. Results for the SA/SG-cleaned sediment extracts obtained with the

P450RGS and EROD assays were plotted individually against the GC/MS chemical analysis data

as shown in Figures 1A and 1B, respectively. The TCDD TEQs for the NYDMMP sediment GC/MS

data were calculated using PCDD/PCDF and PCB analyses but not PAH analyses, with the

assumption that all PAHs were removed by the SA/SG cleanup. Dioxin activity in 2 of the 10

extracts was not detectable with the EROD assay. These two data points were arbitrarily assigned

a TEQ of one-tenth the limit of detection (LOD) of the assay. The LOD for the P450RGS assay

was 26.8 pg g-1, which was about one-half that of the EROD assay (51.3 pg g-1). The two cell-based

assays are compared in Figure 2. Although neither assay correlated with the GC/MS data (r2 =

0.240 for P450RGS, r2 = 0.082 for EROD), the correlation between the two assays was good (r2 =

0.610). Furthermore, the distribution of data points between assays suggests a similar pattern in the

two. The P450RGS assay produced a slightly higher response to the cleaned extracts than did the

EROD assay.