• 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2020-03
  • 2020-07
  • 2020-08
  • 2021-03
  • br Consistent with national biomonitoring


    Consistent with national biomonitoring data (Centers for Disease Control and Prevention, 2015), lipid-normalized serum concentrations were highest for BDE-47, followed by BDE-153, and BDE-100 (geo-metric means = 14.1 ng/g, 5.3 ng/g, and 2.6 ng/g, respectively). Sta-tistically significant positive correlations (p < 0.001) were observed between all congeners. Serum levels of BDE-100 and BDE-47 were highly correlated (r = 0.89) while BDE-153 was less strongly correlated with the other congeners (r = 0.54 for BDE-100; r = 0.36 for BDE-47). Serum PBDE and lipid concentrations for cases and controls are pre-sented in Table 2. Median concentrations of the BDE congeners did not statistically differ between cases and controls. Total Lipids were
    Table 2
    Serum concentration of PBDEs and total PSB 1115 among 902 breast cancer cases and 936 controls.a
    DFd LODe
    Serum concentrationb,c
    Mean Median Minimum Maximum p-Valuef
    a Data presented only for the BDE congeners with detection frequencies (DF) ≥ 75%.
    b Concentration expressed in ng/mL for BDE congeners and mg/mL for total lipids.
    c Distributions for the BDE congeners based on measured and imputed values where samples below the limit of detection (LOD) were estimated by single imputation from a log-normal probability, based on method suggested by Lubin et al. (2004).
    d DF = detection frequency for BDE congener. e LOD = average limit of detection for BDE congener. f p-Value from the Wilcoxon rank sum test for differences in medians by case-control status.
    Table 3
    Association of invasive breast cancer risk with serum PBDE concentrations among 1838 study participants.
    PBDE serum concentration # cases # controls Crudea,b p-Valuec Fully adjusteda,d p-Valuec
    Q1 (lowest quartile)
    Q1 (lowest quartile)
    Q1 (lowest quartile)
    a OR = odds ratio; CI = confidence interval. b Crude ORs adjusted for matching design variables of age at baseline enrollment, race/ethnicity, study collection site, and total serum lipids. c For the categorical analysis, the p-values represent a test for linear trend with quartiles of PBDE modeled as a 4-level ordinal variable; for the continuous BDE term, the p-value represents the p-value of the Wald-statistic for the b-coefficient for the BDE congener modeled as a continuous term. d Fully adjusted ORs adjusted for age at baseline enrollment, race/ethnicity, study collection site, total serum lipids, date of blood draw, season of blood draw, body mass index, physical activity, family history of breast cancer, parity/age at first full-term pregnancy, menopausal status/hormone therapy use at blood draw, and pork consumption.
    The ORs for breast cancer associated with serum concentrations of PBDEs from the crude and fully-adjusted multivariable logistic regres-sions are presented in Table 3.
    No statistically significant associations were observed for any of the three congeners, regardless of whether the serum concentrations were modeled as continuous or as ordinal terms. All ORs were close to 1.0 and 95% confidence intervals included 1.0. Estimates generated from the crude and fully-adjusted models did not substantially differ. Stratification of the data by menopausal status yielded risk estimates for the post-menopausal women similar to those for the full study popu-lation and no statistically significant effects were observed (Supplemental Table S2). While the pattern of risk appeared somewhat different among the small number of women (n = 147) who were pre-or peri-menopausal, none of the ORs significantly differed from one. Likewise, stratification by tumor hormone responsiveness did not reveal any statistically significant associations between PBDEs and breast cancer risk (Supplemental Table S3). With few exceptions, stratification by categories of BMI and changes in body weight generally yielded si-milarly null results (Supplemental Tables S4 and S5). Analyses within additional subsets of the study population (including parous women who had breastfed, women who had never used menopausal hormone therapy, and among women who entered menopause or experienced their first full-term pregnancy during peak human population ex-posures) demonstrated similar patterns of risk and did not yield sta-tistically significant findings (data not shown).