Another Study Links BPA to Severe CAD

Reed Miller

August 20, 2012

August 20, 2012 (Exeter, United Kingdom) — Bisphenol A (BPA) exposure is higher in patients with severe coronary disease than in patients with no disease in the Metabonomics and Genomics in Coronary Artery Disease (MAGICAD) study [1]. The findings, published online August 15, 2012 in PLOS One, build on previous research suggesting a link between coronary disease and the chemical often found in food-packaging plastic, but the exact mechanism of the association remains uncertain.

Dr David Melzer (Peninsula College of Medicine and Dentistry, Exeter, UK), and colleagues compared urinary BPA (uBPA) levels with the grade of coronary stenosis measured by angiography in 591 patients in the MAGICAD study, which was primarily designed to evaluate the proton-nuclear-magnetic-resonance (1H-NMR)–based metabonomics test for coronary disease.

No disease was found in 120 of the patients, while 86 had intermediate disease, and 385 had severe disease in one to three vessels. The unadjusted median urinary BPA concentration was 1.28 ng/mL in subjects with normal coronary arteries and 1.53 ng/mL in subjects with severe coronary disease.

Adjusted for body-mass index, occupational social class, and diabetes status, uBPA concentration was significantly higher in those with severe coronary disease than in patients with no disease, (odds ratio=1.43, p=0.033) and almost significantly higher in patients with intermediate disease (OR=1.69, p= 0.061). There was no significant uBPA difference between patients with severe coronary disease and all other patients combined.

As reported by heartwire , Melzer's group previously reported that 10-year results of the UK EPIC-Norfolk cohort study showed that higher urinary concentrations of BPA metabolites are linked with a higher risk of coronary artery disease, and two analyses from the US NHANES study found an association between BPA and cardiovascular disease.

The specific mechanism linking BPA and coronary disease in humans remains unclear, but unfortunately, "future scientific work in humans is, of course, constrained by ethical limits and the practicality of repeated BPA exposure measures and long-term follow-up studies," Melzer et al explain. "Without these constraints, controlled trials would be needed to prove causation in humans, but such evidence is almost certainly beyond reach."

The authors declare no competing interests.


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