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How Plastic We've Become
Our bodies carry residues of kitchen plastics
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Our bodies carry residues of kitchen plastics

By Janet Raloff

Web edition: January 17, 2008

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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Antonia M. Calafat

Division of Laboratory Sciences

National Center for Environmental Health

Centers for Disease Control and Prevention

4770 Buford Hwy., NE

Mailstop F53

Atlanta, GA 30341


Steven G. Hentges

Polycarbonate/BPA Global Group

American Chemistry Council

1300 Wilson Boulevard

Arlington, VA 22209


Frederick S. vom Saal

105 Lefevre Hall

Division of Biological Sciences

University of Missouri

Columbia, MO 65211

Calafat, A.M., et al. 2008 Exposure of the U.S. Population to Bisphenol A and 4-tertiary-Octylphenol: 2003–2004. Environmental Health Perspectives 116(January):39. doi:10.1289/ehp.10753


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Morgan, K. 2003. Wrong number: Plastic ingredient spurs chromosomal defects. Science News 163(April 5):213. Available to subscribers at [Go to].

Raloff, J. 2007. Clearly concerning. Science News 172(Sept. 29):202-204. Available at [Go to].

______. 2007. Bad for baby: New risks found for plastic constituent. Science News 172(Aug. 11):84. Available at [Go to].

______. 1999. What's coming out of baby's bottle? Science News Online (July 24). Available at [Go to].

______. 1997. Dental sealant safety reconsidered. Science News 152(Nov. 22):324. Available at [Go to].

______. 1997. A pollutant that can alter growth. Science News 152(October 18): 255. Available at www.sciencenews.org/pages/pdfs/data/1997/152-16/15216-18.pdf.

______. 1996. Estrogenic agents leach from dental sealant. Science News 149(April 6):214. Available at www.sciencenews.org/pages/pdfs/data/1996/149-14/14914-08.pdf.

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______. 1993. Plastics may shed chemical estrogens. Science News 144(July 3):12.

Comments (4)

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  • I think this is one of signs that we should go back to more organic and recycled stuff being used.
    It's because of our fast paced culture that needs to have everything NOW that we use so much plastic. The biggest threat in my opinion is the microwave and the containers we use to heat food in, I bet they contain this chemical substance and I get I already have some in me because of the bad habit of using microwave every day.
    The BPA-based products should definitely not be used around foods, I agree.
    --
    Krys from [Link was removed]
    Krystian Szas Krystian Szas
    Nov. 27, 2009 at 6:47am
  • Genetic disorders are often caused by sperm DNA that has double strand breaks, copy number variations, point mutations and imprinting mutations that have to do with advancing paternal age. Men need to know about their biological clock and father babies in their 20s and very early



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    Dec. 26, 2009 at 10:42pm
  • Was very useful article. Thank you. [Link was removed]
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    Jan. 10, 2010 at 7:21pm
  • CHOP used to be an acronym for Cyclophosphamide, drugs starting in H and O and prednisone but they changed the two middle drugs and kept the acronym (and added -R for rituxan). I had this for diffuse large B-cell lymphoma (NHL) in summer-fall 2003, after losing 20 lb of mostly muscle (down to 93 lb). I gained back 30 during and after chemo. Before starting chemo I was too weak to sit up but got progressively stronger during chemo as I regained muscle, except for periods of weakness for a copule of days after the 5 days of prednisone, which prevents muscle growth. My partner dragged me out for walks starting about a week after my first therapy, at first a slow progression to the curb and back (the porch step was a problem), then we made it to the near corner, the far corner, the nearby orchard a few houses away where I sat as he picked windfalls, eventually around the block, to the pharmacy 1/4 mile away (a 'milestone') and after four months I made it to town 1 mile away, rested at the only placeopen Christmas day
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    Jan. 12, 2010 at 5:08pm
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