Study supports connection between BPA and heart disease

A previously reported link between exposure to the plastics chemical bisphenol A and heart disease stands, reports a new study published online January 12 in PLoS ONE.

Added to previous work, the finding provides a third prong of evidence implicating the chemical in cardiovascular and metabolic problems, notes Richard Stahlhut of the Center for Reproductive Epidemiology at the University of Rochester in New York. “It’s becoming a coherent picture that really does fit together,” says Stahlhut, who was not involved in the research. “If these all connect, we really do have a problem.”

Researchers analyzed data from the 2005–2006 National Health and Nutrition Examination Survey, or NHANES, conducted by the U.S. Centers for Disease Control and Prevention. NHANES uses physical examinations, clinical and lab tests, and personal interviews to get a snapshot of the health and nutritional status of the U.S. population. The new analysis of 2005–2006 data reveals an association between concentrations of bisphenol A in urine and risk of cardiovascular disease, a link also detected in the 2003–2004 NHANES data.

“We now have two completely separate samples with completely different people,” says study coauthor David Melzer, an epidemiologist at the Peninsula Medical School in Exeter, England. The new work shows that the previous finding of a link “wasn’t a blip,” Melzer says. “It does need to be investigated.”

Human exposure to bisphenol A is widespread. The chemical is a building block of polycarbonate plastics and is common in the epoxy linings of canned food. It also mimics estrogen. Numerous studies have found that BPA interferes with development and function in a range of tissues.

The NHANES link to cardiovascular disease is a third line of evidence implicating the chemical in metabolic and heart problems, Stahlhut says. A 2008 study examining human fat tissue found that BPA suppresses a hormone that protects people from heart attacks and type 2 diabetes. A separate group of researchers reported that year that, in mice, BPA spurs pancreatic cells known as beta cells to crank up their insulin output.

Pooling data from NHANES 2003–04 and 2005–06 on a total of 2,605 people with known BPA levels, researchers identified 159 people who reported being diagnosed with cardiovascular disease. Based on this data, the team predicts that among 60-year-old men with relatively high BPA levels (falling within the top third of the population), about 10 percent would develop cardiovascular disease, compared with 7 percent of men whose BPA levels were in the lowest third, says Melzer. Only 5.2 percent of men in the middle tier of exposure would be expected to have cardiovascular disease. This increased risk at the upper and lower ends of the exposure range is not uncommon for compounds that interact with hormones. Rather than causing a more straightforward response that increases with the dose of the chemical, such compounds can trigger different metabolic pathways and feedback loops at different doses.

Despite ample evidence of BPA’s effects, its mode of action still isn’t entirely clear, and recent research suggests that all routes of exposure aren’t nailed down. While it’s known that the chemical leaches from food and beverage containers, recent work by Stahlhut and others points to sources of nonfood exposure, such as household dust. Carbonless cash register receipts, the kind used for credit card purchases, are also under investigation.

While reinforcing the link to cardiovascular disease, the new analysis did report lower overall levels of BPA in the urine of Americans than found in earlier NHANES data, a drop from a mean of 2.49 nanograms per milliliter to 1.79 nanograms per milliliter.

Stahlhut cautions that there is still a lot about BPA that warrants investigation. Chlorinated BPA is detectable in the fat tissue of women and children, scientists from Spain reported in 2007 and 2008. “This plus this, plus this, means we better chase this,” Stahlhut says.