How Plastic We’ve Become
Our bodies carry residues of kitchen plastics
In the 1967 film classic The Graduate, a businessman corners Benjamin Braddock at a cocktail party and gives him a bit of career advice. “Just one word…plastics.”
Although Benjamin didn’t heed that recommendation, plenty of other young graduates did. Today, the planet is awash in products spawned by the plastics industry. Residues of plastics have become ubiquitous in the environment—and in our bodies.
A federal government study now reports that bisphenol A (BPA)—the building block of one of the most widely used plastics—laces the bodies of the vast majority of U.S. residents young and old.
Manufacturers link BPA molecules into long chains, called polymers, to make polycarbonate plastics. All of those clear, brittle plastics used in baby bottles, food ware, and small kitchen appliances (like food-processor bowls) are made from polycarbonates. BPA-based resins also line the interiors of most food, beer, and soft-drink cans. With use and heating, polycarbonates can break down, leaching BPA into the materials they contact. Such as foods.
And that could be bad if what happens in laboratory animals also happens in people, because studies in rodents show that BPA can trigger a host of harmful changes, from reproductive havoc to impaired blood-sugar control and obesity (SN: 9/29/07, p. 202).
For the new study, scientists analyzed urine from some 2,500 people who had been recruited between 2003 and 2004 for the National Health and Nutrition Examination Survey (NHANES). Roughly 92 percent of the individuals hosted measurable amounts of BPA, according to a report in the January Environmental Health Perspectives. It’s the first study to measure the pollutant in a representative cross-section of the U.S. population.
Typically, only small traces of BPA turned up, concentrations of a few parts per billion in urine, note chemist Antonia M. Calafat and her colleagues at the Centers for Disease Control and Prevention. However, with hormone-mimicking agents like BPA, even tiny exposures can have notable impacts.
Overall, concentrations measured by Calafat’s team were substantially higher than those that have triggered disease, birth defects, and more in exposed animals, notes Frederick S. vom Saal, a University of Missouri-Columbia biologist who has been probing the toxicology of BPA for more than 15 years.
The BPA industry describes things differently. Although Calafat’s team reported urine concentrations of BPA, in fact they assayed a breakdown product—the compound by which BPA is excreted, notes Steven G. Hentges of the American Chemistry Council’s Polycarbonate/BPA Global Group. As such, he argues, “this does not mean that BPA itself is present in the body or in urine.”
On the other hand, few people have direct exposure to the breakdown product.
Hentges’ group estimates that the daily BPA intake needed to create urine concentrations reported by the CDC scientists should be in the neighborhood of 50 nanograms per kilogram of bodyweight—or one millionth of an amount at which “no adverse effects” were measured in multi-generation animal studies. In other words, Hentges says, this suggests “a very large margin of safety.”
No way, counters vom Saal. If one applies the ratio of BPA intake to excreted values in hosts of published animal studies, concentrations just reported by CDC suggest that the daily intake of most Americans is actually closer to 100 micrograms (µg) per kilogram bodyweight, he says—or some 1,000-fold higher than the industry figure.
Clearly, there are big differences of opinion and interpretation. And a lot may rest on who’s right.
Globally, chemical manufacturers produce an estimated 2.8 million tons of BPA each year. The material goes into a broad range of products, many used in and around the home. BPA also serves as the basis of dental sealants, which are resins applied to the teeth of children to protect their pearly whites from cavities (SN: 4/6/96, p. 214). The industry, therefore, has a strong economic interest in seeing that the market for BPA-based products doesn’t become eroded by public concerns over the chemical.
And that could happen. About 2 years after a Japanese research team showed that BPA leached out of baby bottles and plastic food ware (see What’s Coming Out of Baby’s Bottle?), manufacturers of those consumer products voluntarily found BPA substitutes for use in food cans. Some 2 years after that, a different group of Japanese scientists measured concentrations of BPA residues in the urine of college students. About half of the samples came from before the switch, the rest from after the period when BPA was removed from food cans.
By comparing urine values from the two time periods, the researchers showed that BPA residues were much lower—down by at least 50 percent—after Japanese manufacturers had eliminated BPA from the lining of food cans.
Concludes vom Saal, in light of the new CDC data and a growing body of animal data implicating even low-dose BPA exposures with the potential to cause harm, “the most logical thing” for the United States to do would be to follow in Japan’s footsteps and “get this stuff [BPA] out of our food.”
Kids appear most exposed
Overall, men tend to have statistically lower concentrations of BPA than women, the NHANES data indicate. But the big difference, Calafat says, traces to age. “Children had higher concentrations than adolescents, and they in turn had higher levels than adults,” she told Science News Online.
This decreasing body burden with older age “is something we have seen with some other nonpersistent chemicals,” Calafat notes—such as phthalates, another class of plasticizers.
The spread between the average BPA concentration that her team measured in children 6 to 11 years old (4.5 µg/liter) and adults (2.5 µg/L) doesn’t look like much, but proved reliably different.
The open question is why adults tended to excrete only 55 percent as much BPA. It could mean children have higher exposures, she posits, or perhaps that they break it down less efficiently. “We really need to do more research to be able to answer that question.”
Among other differences that emerged in the NHANES analysis: urine residues of BPA decreased with increasing household income and varied somewhat with ethnicity (with Mexican-Americans having the lowest average values, blacks the highest, and white’s values in between).
There was also a time-of-day difference, with urine values for any given group tending to be highest in the evening, lowest in the afternoon, and midway between those in the morning. Since BPA’s half-life in the body is only about 6 hours, that temporal variation in the chemical’s excretion would be consistent with food as a major source of exposure, the CDC scientists note.
In the current NHANES paper, BPA samples were collected only once from each recruit. However, in a paper due to come out in the February Environmental Health Perspectives, Calafat and colleagues from several other institutions looked at how BPA excretion varied over a 2-year span among 82 individuals—men and women—seen at a fertility clinic in Boston.
In contrast to the NHANES data, the upcoming report shows that men tended to have somewhat higher BPA concentrations than women. Then again both groups had only about one-quarter the concentration typical of Americans.
The big difference in the Boston group emerged among the 10 women who ultimately became pregnant. Their BPA excretion increased 33 percent during pregnancy. Owing to the small number of participants in this subset of the study population, the pregnancy-associated change was not statistically significant. However, the researchers report, these are the first data to look for changes during pregnancy and ultimately determining whether some feature of pregnancy—such as a change in diet or metabolism of BPA—really alters body concentrations of the pollutant could be important. It could point to whether the fetus faces an unexpectedly high exposure to the pollutant.
If it does, the fetus could face a double whammy: Not only would exposures be higher during this period of organ and neural development, but rates of detoxification also would be diminished, vom Saal says.
Indeed, in a separate study, one due to be published soon in Reproductive Toxicology, his team administered BPA by ingestion or by injection to 3-day-old mice. Either way, the BPA exposure resulted in comparable BPA concentrations in blood.
What’s more, that study found, per unit of BPA delivered, blood values in the newborns were “markedly higher” than other studies have reported for adult rodents exposed to the chemical. And that makes sense, vom Saal says, because the enzyme needed to break BPA down and lead to its excretion is only a tenth as active in babies as in adults. That’s true in the mouse, he says, in the rat—and, according to some preliminary data, in humans.
Vom Saal contends that since studies have shown BPA exhibits potent hormonelike activity in human cells at the parts-per-trillion level, and since the new CDC study finds that most people are continually exposed to concentrations well above the parts-per-trillion ballpark, it’s time to reevaluate whether it makes sense to use BPA-based products in and around foods.
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