BPA exposure from canned soup

OMG! This study is really a POS. But WTF, they got it published anyway.

Here’s the media release for this study-by-letter in the Journal of the American Medical Association:

Consuming canned soup linked to greatly elevated levels of the chemical BPA

BPA, found in soup can lining, associated with adverse health effects in humans

A new study from researchers at the Harvard School of Public Health (HSPH) has found that a group of volunteers who consumed a serving of canned soup each day for five days had a more than 1,000% increase in urinary bisphenol A (BPA) concentrations compared with when the same individuals consumed fresh soup daily for five days. The study is one of the first to quantify BPA levels in humans after ingestion of canned foods.

The findings were published online November 22, 2011, in the Journal of the Medical Association (JAMA) and will appear in the November 23/30 print issue.

“Previous studies have linked elevated BPA levels with adverse health effects. The next step was to figure out how people are getting exposed to BPA. We’ve known for a while that drinking beverages that have been stored in certain hard plastics can increase the amount of BPA in your body. This study suggests that canned foods may be an even greater concern, especially given their wide use,” said Jenny Carwile, a doctoral student in the Department of Epidemiology at HSPH and lead author of the study.

Exposure to the endocrine-disrupting chemical BPA, used in the lining of metal food and beverage cans, has been shown to interfere with reproductive development in animals and has been linked with cardiovascular disease, diabetes, and obesity in humans. In addition to the lining of food and beverage cans, BPA is also found in polycarbonate bottles (identified by the recycling number 7) and dentistry composites and sealants.

The researchers, led by Carwile and Karin Michels, associate professor in the Department of Epidemiology, set out to quantify whether canned-soup consumption would increase urinary BPA concentrations relative to eating fresh soup.

They recruited student and staff volunteers from HSPH. One group consumed a 12-ounce serving of vegetarian canned soup each day for five days; another group consumed 12 ounces of vegetarian fresh soup (prepared without canned ingredients) daily for five days. After a two-day “washout” period, the groups reversed their assignments.

Urine samples of the 75 volunteers taken during the testing showed that consumption of a serving of canned soup daily was associated with a 1,221% increase in BPA compared to levels in urine collected after consumption of fresh soup.

The researchers note that the elevation in urinary BPA concentrations may be temporary and that further research is needed to quantify its duration.

“The magnitude of the rise in urinary BPA we observed after just one serving of soup was unexpected and may be of concern among individuals who regularly consume foods from cans or drink several canned beverages daily. It may be advisable for manufacturers to consider eliminating BPA from can linings,” said Michels, senior author of the study.

What exactly is supposed to be notable in this study? As the researchers acknowledge, it is well known that canned foods contain traces of BPA, so no surprise that the participants were exposed to BPA after eating canned soup.

Apparently they understand that BPA is excreted in urine — since they analyzed urine to look for BPA — although they incorrectly state they found BPA when in fact what they found is a biologically inactive metabolite of BPA.

Apparently they also understand that BPA is rapidly metabolized and excreted — as demonstrated by numerous well conducted studies, including the Teeguarden study and recent FDA pharmacokinetic studies — since they analyzed just a few hours after ingestion, yet they say what they detected is a transient peak of yet uncertain duration.

Surely they know, but do not acknowledge, that those same studies clearly show that BPA cannot be detected in blood after oral ingestion because it is so efficiently metabolized, yet they say the effect is unknown.

They might also have estimated intake to see that it is low compared to established safe intake levels.

So we can see why this was published as a letter. If they published a complete paper, they would have had to acknowledge what they know and what is so relevant to interpret their study, in which case their study would be revealed to be the unpublishable POS that it is.

What else is notable? That CDC would waste their time on this, and put their name on the paper. Two of the three CDC authors were also on the Teeguarden paper, so they have no excuse for not knowing quite a bit about human pharmacokinetics. But they signed on anyway.

Read the JAMA “study”.

Click to obtain the Teerguarden study.

The Teerguarden abstract is below:

Twenty-Four Hour Human Urine and Serum Profiles of Bisphenol A during High-Dietary Exposure

Justin G. Teeguarden*,1, Antonia M. Calafat†, Xiaoyum Ye†, Daniel R. Doerge‡, Mona I. Churchwell‡, Rudy Gunawan* and Morgan K. Graham*
+ Author Affiliations

*Fundamental and Computational Sciences, Pacific Northwest National Laboratory, Richland, Washington 99352
†Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia 30341
‡Division of Biochemical Toxicology, National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson, Arkansas 72079
↵1To whom correspondence should be addressed at Fundamental and Computational Sciences, Pacific Northwest National Laboratory, 902 Battelle Boulevard, Richland, WA 99352. Fax: (509) 376-9449. E-mail: justin.teeguarden@pnl.gov.
Received April 18, 2011.
Accepted June 10, 2011.

Abstract

By virtue of its binding to steroid hormone receptors, bisphenol A (BPA, the unconjugated bioactive monomer) is hypothesized to be estrogenic when present in sufficient quantities in the body, raising concerns that widespread exposure to BPA may impact human health. To better understand the internal exposure of adult humans to BPA and the relationship between the serum and urinary pharmacokinetics of BPA, a clinical exposure study was conducted. Blood and urine samples were collected approximately hourly over a 24-h period from 20 adult volunteers who ingested 100% of one of three specified meals comprising standard grocery store food items for breakfast, lunch, and dinner. The volunteers’ average consumption of BPA, estimated from the urinary excretion of total BPA (TOTBPA = conjugated BPA + BPA), was 0.27 μg/kg body weight (range, 0.03–0.86), 21% greater than the 95th percentile of aggregate exposure in the adult U.S. population. A serum time course of TOTBPA was observable only in individuals with exposures 1.3–3.9 times higher than the 95th percentile of aggregate U.S. exposure. The TOTBPA urine concentration Tmax was 2.75 h (range, 0.75–5.75 h) post-meal, lagging the serum concentration Tmax by ∼1 h. Serum TOTBPA area under the curve per unit BPA exposure was between 21.5 and 79.0 nM•h•kg/μg BPA. Serum TOTBPA concentrations ranged from less than or equal to limit of detection (LOD, 1.3 nM) to 5.7 nM and were, on average, 42 times lower than urine concentrations. During these high dietary exposures, TOTBPA concentrations in serum were undetectable in 83% of the 320 samples collected and BPA concentrations were determined to be less than or equal to LOD in all samples.

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3 responses to “BPA exposure from canned soup

  1. chuck in st paul

    ““Previous studies have linked elevated BPA levels with adverse health effects. …” – in mice, a poor analog
    “Exposure to the endocrine-disrupting chemical BPA, …”
    “…[BPA] is hypothesized to be estrogenic …”

    Not proven in humans. There are to date no published and vetted human studies or trials for BPA actual bad effects on the human system, just rats and mice (exposed to ridiculous amounts). I’m sure that somewhere on Earth someone was adversely affected by BPA, but so far “Where’s Waldo” has failed to find them.

  2. What was the BPA level in the canned soup itself? I’d like to know how much was retained and how much was in the urine. If it mostly passes through with little absorption then this would be even more of a non-issue.

  3. Your notes on the limitations of this study are sound. However, your tone seems prematurely dismissive. To Chuck in St. Paul’s objection, in addition to data in experimental models, here are now several human studies finding associations between BPA exposure and adverse health effects, in adults and especially in developing children; eg:

    Melzer D, Rice NE, Lewis C, Henley WE, Galloway TS. Association of urinary bisphenol a concentration with heart disease: evidence from NHANES 2003/06. PLoS One. 2010 Jan 13;5(1):e8673. PubMed PMID: 20084273; PubMed Central PMCID: PMC2800195.

    Braun JM, Yolton K, Dietrich KN, Hornung R, Ye X, Calafat AM, Lanphear BP. Prenatal bisphenol A exposure and early childhood behavior. Environ Health Perspect. 2009 Dec;117(12):1945-52. Epub 2009 Oct 6. PubMed PMID: 20049216; PubMed Central PMCID: PMC2799471.

    Yang YJ, Hong YC, Oh SY, Park MS, Kim H, Leem JH, Ha EH. Bisphenol A exposure is associated with oxidative stress and inflammation in postmenopausal women. Environ Res. 2009 Aug;109(6):797-801. Epub 2009 May 22. PubMed PMID: 19464675.

    Lang IA, Galloway TS, Scarlett A, Henley WE, Depledge M, Wallace RB, Melzer D. Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults. JAMA. 2008 Sep 17;300(11):1303-10. Epub 2008 Sep 16. PubMed PMID: 18799442.

    Sugiura-Ogasawara M, Ozaki Y, Sonta S, Makino T, Suzumori K. Exposure to bisphenol A is associated with recurrent miscarriage. Hum Reprod. 2005 Aug;20(8):2325-9. Epub 2005 Jun 9. PubMed PMID: 15947000.

    Li DK, Zhou Z, Miao M, He Y, Qing D, Wu T, Wang J, Weng X, Ferber J, Herrinton LJ, Zhu Q, Gao E, Yuan W. Relationship between urine bisphenol-A level and declining male sexual function. J Androl. 2010 Sep-Oct;31(5):500-6. Epub 2010 May 13. PubMed PMID: 20467048.

    Meeker JD, Calafat AM, Hauser R. Urinary bisphenol A concentrations in relation to serum thyroid and reproductive hormone levels in men from an infertility clinic. Environ Sci Technol. 2010 Feb 15;44(4):1458-63. PubMed PMID: 20030380; PubMed Central PMCID: PMC2823133.

    Kandaraki E, Chatzigeorgiou A, Livadas S, Palioura E, Economou F, Koutsilieris M, Palimeri S, Panidis D, Diamanti-Kandarakis E. Endocrine disruptors and polycystic ovary syndrome (PCOS): elevated serum levels of bisphenol A in women with PCOS. J Clin Endocrinol Metab. 2011 Mar;96(3):E480-4. Epub 2010 Dec 30. PubMed PMID: 21193545.

    Li D, Zhou Z, Qing D, He Y, Wu T, Miao M, Wang J, Weng X, Ferber JR, Herrinton LJ, Zhu Q, Gao E, Checkoway H, Yuan W. Occupational exposure to bisphenol-A (BPA) and the risk of self-reported male sexual dysfunction. Hum Reprod. 2010 Feb;25(2):519-27. Epub 2009 Nov 10. PubMed PMID: 19906654.

    It’s important therefore to get to the root of these associations, and ongoing studies on absorption, distribution, metabolism, and excretion are part of that investigation. The fact that BPA appears in the urine largely as the glucuronide metabolite, and that BPA aglycone seems indetectable in serum, doesn’t necessarily mean that there are no biological effects: as one example, human beta-glucuronidase (which can strip the aglycone of the glucuronide moiety) is widely dispersed in the body, and individual cells exposed to the apparently-inactive glucuronide might hydrolyze the glycosidic bond, converting them back into free, active BPA locally and leading to absorption of the biologically active moiety without measurably affecting serum levels. Studies like Teeguarden’s (or Michel’s) do not address such possibilities.

    It’s six decades since the evidence for tobacco causing lung cancer became highly convincing, and we still don’t know what the role of different mechanisms are in that effect (eg, the role of specific carcinogenic compounds in tobacco, vs. polycyclic aromatic hydrocarbons and other generic products of the combustion of *any* organic compound, vs. the irritant and heat effects in inflaming the lung tissue, vs. the effects of the radionuclide content of tobacco (lead-210 and polonium-210).

    Lack of clear mechanism does not refute a causal connection, and doesn’t rebut epidemiological associations. Research like Michel’s and Teeguarden’s is part of teasing out any possible causal connection, and *both* should be welcomed as part of the evidence base (along with rodent data) — but certainly, pharmacokinetic studies aren’t by themselves enough to prove or disprove causality.

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