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Cancer Causes & Control

, Volume 25, Issue 12, pp 1587–1593 | Cite as

Urinary bisphenol A-glucuronide and postmenopausal breast cancer in Poland

  • Britton TrabertEmail author
  • Roni T. Falk
  • Jonine D. Figueroa
  • Barry I. Graubard
  • Montserrat Garcia-Closas
  • Jolanta Lissowska
  • Beata Peplonska
  • Stephen D. Fox
  • Louise A. Brinton
Original paper

Abstract

Purpose

Concerns regarding a possible link between bisphenol A (BPA) and breast cancer have been mounting, but studies in human populations are lacking. We evaluated the association between the major urinary BPA metabolite [BPA-glucuronide (BPA-G)] and postmenopausal breast cancer risk in a large population-based case–control study conducted in two cities in Poland (2000–2003); we further explored the association of BPA-G levels with known postmenopausal breast cancer risk factors in our control population.

Methods

We analyzed creatinine-adjusted urinary BPA-G levels among 575 postmenopausal cases matched on age and study site to 575 controls without breast cancer using a recently developed assay. Odds ratios and 95 % confidence intervals were used to estimate the association between urinary BPA-G level and breast cancer using conditional logistic regression. Among controls, geometric mean BPA-G levels were compared across categories of breast cancer risk factors using linear regression models.

Results

There was no indication that increased BPA-G was associated with postmenopausal breast cancer (p-trend = 0.59). Among controls, mean BPA-G was higher among women reporting extended use of menopausal hormones, a prior screening mammogram, and residence in Warsaw. Other comparisons across strata of postmenopausal breast cancer risk factors were not related to differences in BPA-G.

Conclusions

Urinary BPA-G, measured at the time of diagnosis, is not linked to postmenopausal breast cancer.

Keywords

Breast cancer Bisphenol A-glucuronide Postmenopausal Case–control 

Notes

Acknowledgments

This research was supported by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics and by contracts from the Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Department of Health and Human Services.

Conflict of interest

The authors declare that they have no actual or potential competing financial interests.

Supplementary material

10552_2014_461_MOESM1_ESM.pdf (27 kb)
Supplementary material 1 (PDF 27 kb)
10552_2014_461_MOESM2_ESM.pdf (26 kb)
Supplementary material 2 (PDF 27 kb)
10552_2014_461_MOESM3_ESM.pdf (908 kb)
Supplementary material 3 (PDF 909 kb)

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Copyright information

© Springer International Publishing Switzerland (outside the USA) 2014

Authors and Affiliations

  • Britton Trabert
    • 1
    Email author
  • Roni T. Falk
    • 1
  • Jonine D. Figueroa
    • 1
  • Barry I. Graubard
    • 1
  • Montserrat Garcia-Closas
    • 2
  • Jolanta Lissowska
    • 3
  • Beata Peplonska
    • 4
  • Stephen D. Fox
    • 5
  • Louise A. Brinton
    • 1
  1. 1.Division of Cancer Epidemiology and Genetics, Department of Health and Human ServicesNational Cancer Institute, National Institutes of HealthBethesdaUSA
  2. 2.The Institute of Cancer ResearchLondonUK
  3. 3.Department of Cancer Epidemiology and PreventionCancer Center and M. Sklodowska-Curie Institute of OncologyWarsawPoland
  4. 4.Department of Environmental EpidemiologyNofer Institute of Occupational MedicineLodzPoland
  5. 5.Protein Characterization Laboratory, Cancer Research Technology ProgramLeidos Biomedical Research, Inc., Frederick National Laboratory for Cancer ResearchFrederickUSA

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