Science News, September 13th, 2008

POPULAR PLASTICS CHEMICAL POSES FURTHER THREAT

[Rachel's introduction: Studies show that a common chemical in plastics, known as BPA or Bisphenol-A, may increase heart attacks and type 2 diabetes. The U.S. Food and Drug Administration says it's entirely safe.]

By Rachel Ehrenberg

The rap sheet for bisphenol A [BPA], a chemical commonly found in food and water containers, baby bottles and the lining of aluminum cans, just keeps getting longer. But the chemical still has friends at the FDA.

A new study examining the effects of bisphenol A in human fat tissue finds that the chemical suppresses a hormone that protects people from heart attacks and type 2 diabetes. Bisphenol A doses examined in the study are typical of what is found in human blood.

The study, to be published in Environmental Health Perspectives, appeared online on August 14, a day before the Food and Drug Administration released a draft assessment of bisphenol A that decrees the chemical safe at current exposure levels.

"I do not understand why the governments of the United States and Europe put money into studying pollutants like bisphenol A and then later don't listen to what scientists have found," comments Angel Nadal, of the Spanish Biomedical Research Network in Diabetes and Associated Metabolic Disorders in Alicante, Spain. "They are using a last century approach to toxicology."

Hundreds of studies have documented bisphenol A's ability to meddle with the development and function of a wide range of tissues. The chemical, which is the starter material for many plastics and epoxy resins, has a number of adverse health effects in lab animals, including reproductive problems, certain cancers and asthma.

Human breast fat cells taken from a surgical patient were exposed to bisphenol A. The amount of adiponectin, a protective hormone released by these cells, plummeted with exposure. The dose of bisphenol A that had the strongest effect is the same as levels commonly found in human blood.Nira Ben-JonathanThe FDA responded to requests for comment on the research with an e-mail stating "FDA is in a legally mandated peer review process so we are not going to comment on the scientific points regarding individual pieces of data prior to that review process."

Bisphenol A naturally leaches from food and beverage containers, and human exposure to the chemical is widespread. A 2005 National Center for Environmental Health analysis detected bisphenol A in the urine of 95 percent of the study's participants.

In the body, bisphenol A mimics the hormone estrogen, presumably by attaching to the same cellular sensor molecules that natural estrogens stimulate. But the chemical's precise mode of action remains a puzzle, says Nira Ben-Jonathan, an endocrinologist at the University of Cincinnati in Ohio, who led the new study. "It's really still enigmatic, no one can put their finger on how it works," she says.

Recently, evidence has accumulated that estrogen-sensing molecules, or receptors, play an important role in metabolic disorders. Mutant mice that don't have certain estrogen receptors eat more, become obese and become resistant to insulin, says Nadal. Estrogen receptors also seem to be involved in the body's management of insulin in the liver and skeletal muscle. So it is not surprising that something like bisphenol A, which also interacts with these receptors, might interfere with metabolism, he says.

In the new study, Ben-Jonathan's team collected fat tissue surgically removed from people having breast reduction, tummy tucks and gastric bypass surgery at Christ Hospital in Cincinnati. The researchers exposed some of the tissue to estradiol, a natural form of human estrogen, and some to bisphenol A. Both treatments suppressed the release of the protective hormone adiponectin. Adiponectin is secreted by fat cells and protects against the suite of conditions that can result in heart attacks and type 2 diabetes.

"These findings provide the molecular basis for bisphenol A being implicated in both obesity and potentially the associated disease that is now being detected in children and adolescents -- type 2 diabetes," comments Frederick vom Saal, a specialist in endocrine disruptors from the University of Missouri in Columbia.

Even though the baseline levels of the protective adiponectin varied greatly from person to person, the work nicely demonstrates that low doses of bisphenol A influence the fat cells' output of adiponectin, says Nadal.

"The paper is important," he says.

A study of mice by Nadal and colleagues, published in April in PLoS ONE, found that bisphenol A makes the pancreatic cells known as beta cells crank up their insulin output. This work follows research by Nadal, who is also affiliated with the Institute of Bioengineering at the Universidad Miguel Hernandez de Elche in Alicante, and other scientists that demonstrated that low doses of bisphenol A made mice insulin-resistant.

The new study by Ben-Jonathan and colleagues is especially notable because it uses relevant doses and human tissues, says Nadal.

Suggested Reading:

Raloff, J. 2007. Clearly concerning. Science News 172 (Sept. 29):13. Available at link.

Harder, B. 2006. Boyish Brains: Plastic chemical alters behavior of female mice. Science News 169(May 6):276. Available at link.

______. 2006. Diabetes from a plastic? Estrogen mimic provokes insulin resistance. Science News 169(Jan. 21):36. Available at link.

Bisphenol A research investigation from Milwaukee Journal Sentinel link

Citations & References:

Draft assessment of bisphenol A on FDA docket link

Hugo, E.R.... and N. Ben-Jonathan. In press. Bisphenol A at environmentally relevant doses inhibits adiponectin release from human adipose tissue explants and adipocytes. Environmental Health Perspectives. doi:10.1289/ehp.11537

Alonso-Magdalena, P.... and A. Nadal. 2008. Pancreatic insulin content regulation by the estrogen receptor ERa. PLoS ONE 3:e2069. doi:10.1371/journal.pone.0002069

Calafat, A.M., et al. 2005. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Environmental Health Perspectives 113(April):4. Available at link. doi: 10.1289/ehp.7534 Archive o

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