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Fig. S1. Mean and SEM for three independent assays showing relative ER binding activity for a strong positive (17β-E2), a weak positive (19-norethindrone), and a negative control (octyltriethoxysilane).

Fig. S2. (A) Representative binding dose–response curves showing the binding of [3H]17β-E2 to the ER during the saturation binding experiment; (B) representative scatchard plot illustrating the binding of [3H]17β-E2 to the ER.

Fig. S3. Representative dose–response curve showing the relative transcriptional activity for proficiency chemicals in the ERTA assay. Relative transcriptional activity was based on the response of these compounds compared to 1 nM 17β-E2, the PC. Cytotoxicity was observed with corticosterone treatment at 10−4 M; therefore, this data point was omitted from data analysis.

Fig. S4. Representative dose–response binding curve for a strong positive (R1881) and a weak positive (dexamethasone) in the androgen receptor binding assay.

Fig. S5. Representative dose–response curve showing enzyme inhibition by the positive control, 4-hydroxyandrostenedione, in the aromatase assay.

Fig. S6. Average response curves for a positive test material used in the human recombinant aromatase assay. Data points represent the mean of three replicates, error bars represent the SD, and dashed lines represent the 95% CI of the best fit curve (solid line). There was a statistically significant difference in the logIC50 and Hill slope values of the three runs in this aromatase assay (p = 0.0011 and 0.0329, respectively); however, biologic meaningfulness of this difference was negligible.

Fig. S7. Dose–response curves for proficiency chemicals in the steroidogenesis assay. These figures illustrate forskolin-induced increases in T and E2 production and PRO-induced decreases in TST and E2 production in the H295R cells.

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