99, and ∑BDEs) but not with BDE-153 (r = 0.10). Although TT4 was not signifi- cantly associated with either of the metabo- lites, the correlation coefficients were similar in magnitude (r = 0.12–0.17) to the PBDEs. FT4 was significantly associated with BDE-47, BDE-99, and ∑BDEs (r = 0.17–0.19, p < 0.05; Figure 1) and was marginally asso- ciated with BDE-153 (r = 0.16, p = 0.06). FT4 was not associated with BDE-100 nor with the metabolites. An inverse association (r = –0.24) between TT3 and 4´-OH-BDE-49 was suggestive (p = 0.08), but nothing was significantly associated with TT3 or FT3 in linear regression analysis. R e s u l t s o f t h e m u l t i v a r i a b l e m o d e l (Table 4) show that TT4 is significantly and positively associated with BDE-47, BDE-99, BDE-100, and ∑BDEs (r = 0.32–0.50, p < 0.05), but was not significantly associ- ated with BDE 153. Logged FT4 is signifi- cantly and positively associated with BDE 47, BDE-153, and ∑BDE (r = 0.05, p < 0.05) but was not significantly associated with BDE-99 or BDE-100. These results hold equally well in logistic regression models (results not shown). In these models, PBDEs and OH-BDEs were log base 2 transformed so that their estimated odds ratios (ORs) are interpreted as the change in odds Table 3. Spearman rank correlation matrix for PBDEs (nanograms per gram lipid) and thyroid hormones with frequency of detection > 50%. 4’-OH- 6-OH- ∑OH- Variable BDE-47 BDE-100 BDE-99 BDE-153 ∑BDEs BDE-49 BDE-47 BDE PBDEsa BDE-47 BDE-100 0.80## BDE-99 0.80## 0.58## BDE-153 0.52## 0.67## 0.39## ∑BDEs 0.95## 0.85## 0.85## 0.65## 4’-OH-BDE-49 0.62## 0.47# 0.56## 0.38** 0.60## 6-OH-BDE-47 0.35** 0.44# 0.29* 0.43# 0.40** 0.62## ∑OH-BDE 0.46# 0.49## 0.39** 0.46# 0.49## 0.82## 0.93## Thyroid hormonesb TSH 0.16 0.06 0.14 –0.02 0.11 0.17 0.02 0.07 TT4 0.20* 0.20* 0.18* 0.10 0.21** 0.17 0.12 0.18 FT4 0.19* 0.09 0.17* 0.16 0.19* 0.18 0.05 0.08 TT3 0.10 0.03 0.03 0.07 0.07 –0.24 –0.09 –0.16 FT3 0.07 0.002 0.01 –0.07 0.04 –0.05 0.01 0.03 aTotal n for each of the pairwise correlations with BDE‑47, BDE‑100, BDE‑99, BDE‑153, and ΣBDEs is 137. For the phe‑ nolic metabolites, including 4’‑OH‑BDE‑49, 6‑OH‑BDE‑47, and ΣOH‑BDEs, any pairwise correlation has a total n of 57. bWhen a pairwise correlation includes a thyroid hormone and any of the non–OH‑BDEs, total n is 136. With the thyroid hormones and phenolic metabolites, total n is 56. *p < 0.05. **p < 0.01. #p < 0.001. ##p < 0.0001. 0.4 ) 0 L d / g n (T4–0.4 e e r f ln–0.8 –1.2 r = 0.19 p = 0.03 8 2 ) d i p li 0 g / g n ( 49 –2 E D B -H–4 O - ´ 4 ln –6 0 PBDEs and thyroid hormones in pregnant women aThese models report the individual BDE congener–thyroid hormone association after controlling for smoking status, maternal race, age, gestational age at blood draw, and parity. *p < 0.05. **p < 0.01. associated with a 2-fold increase in the particu- lar PBDE or OH-BDE. Adjusted ordinal logis- tic regression model ORs for normal versus low or high versus normal TT4 levels with a 2-fold increase in exposure were 1.42 [95% confi- dence interval (CI), 1.08–1.86, p = 0.01] for BDE-47; 1.37 (95% CI, 1.01–1.84, p = 0.04) for BDE-100; 1.25 (95% CI, 1.00–1.57, p = 0.05) for BDE-99; and 1.45 (95% CI, 1.04–2.01, p = 0.03) for ∑BDEs. Likelihood ratio tests of the proportionality of odds assumption did not find evidence to reject the hypothesis that the odds were the same across outcome categories. For each 2-fold increase in BDE-47, the odds of having low FT4 decreased by 40% (OR = 0.60; 95% CI, 0.39–0.93, p = 0.02) and by 49% for ∑BDEs (OR = 0.51; 95% CI, 0.27–0.97, p = 0.04). Although PBDEs (Table 4) and OH-BDEs (data not shown) were not associated with TT3 modeled as a continuous variable, high TT3 levels (178 ng/dL) were positively asso- ciated with BDE-47 (OR = 1.30; 95% CI, 1.00–1.69, p = 0.04) and inversely associated with 4´-OH-BDE-49 (OR = 0.51; 95% CI, 0.30–0.86, p = 0.01) and ∑OH-BDEs (OR = 0.72; 95% CI, 0.48–1.07, p = 0.10). Discussion The PBDE levels and congener distributions in this pregnancy cohort were similar to levels reported among the general U.S. popula- tion in the 2003–2004 National Health and Nutrition Examination Survey (NHANES) (Sjodin et al. 2008). This similarity was unex- pected, because PBDEs have been phased out from use since 2004, and there was a 4- to 7-year time gap between the sample collec- tions for the two cohorts. One might expect to see declining levels of PBDEs in human tissues over the preceding 4–7 years. Our data suggest that levels are stable; however, some caveats must be noted with this comparison. The NHANES study observed higher PBDE levels in non-Hispanic blacks relative to non- Hispanic whites, and decreasing PBDE levels with age; therefore, levels may be comparable because our cohort was composed primarily of non-Hispanic black females ages 18–22 years. Geometric mean BDE-47 levels in NHANES (2003–2004) for 12- to 19-year- olds (28.2 ng/g lipid), 20- to 39-year-olds ln BDE-153 0.12 (–0.35 to 0.58) 0.05* (0.006 to 0.09)* 0.03 (–0.08 to 0.14) 0.01 (–0.04 to 0.07) –0.02 (–0.04 to 0.01) 0 2 4 ln ΣBDEs (ng/g lipid) 6 2 4 ln ΣBDEs (ng/g lipid) 6 Figure 1. Correlations observed between PBDEs and FT4 (A), and between PBDEs and OH‑BDE‑49 ( B), in serum. Table 4. Multiple linear regression with TT4 and FT4 and BDEs and total BDE, controlling for maternal characteristics [β (95% CI)].a Dependent variable Thyroid hormone (n = 136) TT4 ln FT4 ln TSH ln TT3 ln FT3 ln BDE-47 0.42 (0.05 to 0.78)* 0.05 (0.01 to 0.08)** 0.07 (–0.02 to 0.16) 0.04 (–0.01 to 0.08) 0.01 (–0.01 to 0.03) ln BDE-99 0.32 (0.02 to 0.63)* 0.02 (–0.009 to 0.05) 0.04 (–0.04 to 0.11) 0.01 (–0.03 to 0.05) 0.003 (–0.01 to 0.02) Environmental Health Perspectives • volume 119 | number 10 | October 2011 r = 0.60 p < 0.001 8 Explanatory variables ln BDE-100 0.41 (0.003 to 0.82)* 0.02 (–0.02 to 0.06) 0.01 (–0.09 to 0.11) 0.001 (–0.05 to 0.05) 0.0004 (–0.02 to 0.02) ln ∑BDEs 0.50 (0.06 to 0.94)* 0.05 (0.01 to 0.09)* 0.06 (–0.04 to 0.17) 0.02 (–0.03 to 0.08) 0.01 (–0.02 to 0.04) 1457