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Tuesday, February 21, 2012

Bisphenol: Urinary Concentration and Risk of Future Coronary Artery Disease


Urinary Bisphenol: A Concentration and Risk of Future Coronary Artery Disease in Apparently Healthy Men and Women

  1. David Melzer1*
  2. Nicholas J. Osborne2
  3. William E. Henley3;
  4. Ricardo Cipelli4
  5. Anita Young5
  6. Cathryn Money5
  7. Paul McCormack5;
  8. Robert Luben6
  9. Kay-Tee Khaw6
  10. Nicholas J. Wareham7;
  11. Tamara S. Galloway4
+Author Affiliations
  1. 1 Peninsula Medical School, University of Exeter, Exeter, United Kingdom;
  2. 2 Peninsula College of Medicine & Dentistry, University of Exeter, Exeter, United Kingdom;
  3. 3 University of Plymouth, Plymouth, United Kingdom;
  4. 4 University of Exeter, Exeter, United Kingdom;
  5. 5 Brixham Environmental Laboratory, Brixham, United Kingdom;
  6. 6 University of Cambridge, Cambridge, United Kingdom;
  7. 7 Medical Research Council Epidemiology Centre, London, United Kingdom
  1. * Corresponding author; email: david.melzer@pms.ac.uk

Abstract

Background—The endocrine disrupting chemical Bisphenol A (BPA) is widely used in food and beverage packaging. Higher urinary BPA concentrations (uBPA) were cross-sectionally associated with heart disease in NHANES 2003/04 and NHANES 2005/6, independent of traditional risk factors.
Methods and Results—We included 758 incident coronary artery disease (CAD) cases and 861 controls followed for 10.8 yrs from the European Prospective Investigation of Cancer - Norfolk UK. Respondents aged 40-74 yrs and free of CAD, stroke or diabetes provided baseline spot urine samples. uBPA concentrations (median value 1.3 ng/ml) were low. Per standard deviation (4.56ng/ml) increases in uBPA concentration were associated with incident CAD in age, sex and urinary creatinine adjusted models (n=1919, OR=1.13 95% CI 1.02 to 1.24, p=0.017). With CAD risk factor adjustment (including education, occupational social class, BMI category, systolic blood pressure, lipid concentrations and exercise) the estimate was similar but narrowly missed two-sided significance (n=1744 OR=1.11 95% CI: 1.00 to 1.23, p=0.058). Sensitivity analyses with the fully adjusted model, excluding early CAD (<3 year follow up); those with BMI>30; abnormal renal function; or adjusting additionally for vitamin C; C-reactive protein; or alcohol consumption, all produced similar estimates and all showed associations at p≤0.05.
Conclusions—Associations between higher BPA exposure (reflected in higher urinary concentrations) and incident CAD during over ten years of follow-up showed similar trends to previously reported cross-sectional findings in the more highly exposed NHANES respondents. Further work is needed to accurately estimate the prospective exposure response curve and to establish the underlying mechanisms.

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