If BPA exposure is so low, why should we be worried?

In response to my earlier post about bisphenol A in soda and beer, reader Skeptic had an insightful comment:

As someone involved in environmental health myself, I have been following the BPA controversy from north of the 49th parallel with some interest. I have often wondered whether the actual data supports regulation of BPA. The first study you cite, for example, hides this line in its discussion: “Thus, median and 95th percentile intake estimates were approximately two to three orders of magnitude below the current health-based guidance value. This result is similar to that given by Ye et al. (2009) for a cohort of Norwegian women, with the estimated average daily intakes of BPA reported to be about three orders of magnitude lower than the RfD and TDI.”

What is your take?

It’s a valid point. Industry and regulatory agencies argue that exposure to BPA is well below recommended limits—so why should we be concerned? I think there are several issues here. First, as we’re discovering more day by day, BPA is everywhere: receipts, reusable water bottles, food storage containers, canned beans and produce, soda, beer. Who knows where else! So yes, a study might conclude that average exposure to BPA through one particular route might be well below recommended daily exposure limits, but that’s not taking into account the myriad other sources we’re being bombarded with on a daily basis.

To be fair, though, studies in the past have assessed BPA levels in human urine, and they have found average levels to be quite low. So let’s assume that we are being exposed to BPA at levels below the recommended exposure limits (which for the US and Europe is .05 mg of BPA per kg of body weight per day). I still don’t think we’re out of the danger zone, because there’s evidence to suggest that we should be questioning the exposure limit itself. For one thing, the EPA doesn’t know what happens to animals (let alone humans) who are exposed to .05 mg/kg of BPA per day. They’ve never tested it. They arrived at this limit by testing what happened to rats exposed to 5 mg/kg per day; then they divided by 100 and assumed that the resulting level would be absolutely safe. As Laura Vandenberg, a BPA expert and biologist at Tufts University explained to me a few months ago, “the way that traditional toxicology is done is by looking at a whopping dose of something and then guessing what would happen at a lower dose. That’s how the safe level of BPA was set.”*

And there is evidence to suggest that BPA affects the body at doses below .05 mg/kg per day. In 2007, 38 researchers from institutions including Harvard, Tufts, the University of Texas, and even the EPA published a consensus statement in which they discussed, among other things, the handful of studies suggesting that BPA elicits biological effects at doses much lower than the EPA “safe level.” As Vandenberg explained to me, “the animal literature shows links between BPA and mammary cancer, prostate cancer, infertility, changes in the female reproductive tract, etcetera—we’re talking about studies that show those effects below what the EPA says is safe.” BPA affects hormones, and it could well be that hormone dose-response curves are not linear (i.e., you can’t necessarily assume that if a lot of a substance has a big effect, a little of it will have a small effect). In fact, many compounds have been found to elicit unexpectedly big effects at tiny doses—sometimes they even have opposite effects at low versus high doses—and some researchers argue that regulatory agencies are relying on highly outdated (and more notably, undertested) dose-response models.

Worse, despite the fact that there is evidence to suggest that BPA harms the body at very low doses, agencies all but ignore these findings. In September, for instance, the European Food Safety Authority (EFSA) announced that it saw no reason to include new studies in its BPA exposure limit assessment; to date, the EFSA relies on only two studies that were conducted in rats. (I’m not sure which two studies they are, but if they’re the same two the US relies on, then it’s important to note that they are extremely flawed.) Today there are hundreds of studies published on BPA, but the EFSA says it didn’t consider these other studies because they “had shortcomings.” It’s unclear exactly what the agency means by that, but my guess is that it has something to do with the fact that academic researchers conduct studies differently than regulatory agencies do, a problem (highlighted in this excellent Nature news feature by Brendan Borrell) that is one of the key reasons regulatory and academic scientists cannot seem to agree on the BPA issue.

So, in a nutshell: we shouldn’t ignore BPA because we’re exposed to so little of it (if, indeed, we are exposed to so little of it). The research that exists on the chemical suggests that it affects the body at teeny tiny exposure levels—levels well below what the EPA and EFSA deem to be safe. What we really need is for agencies to acknowledge these studies and consider them in their safety assessments alongside the very few studies they have relied on for years. The science on BPA is moving forward in great leaps and bounds, but regulatory agencies simply aren’t evolving alongside it—and that’s putting everyone’s health at risk.

*Added 3:30pm, 10/19: For more on the (lack of) validity of using of high-dose testing to predict low-dose effects, see this 2009 paper published in Environmental Health Perspectives.


Lakind JS, & Naiman DQ (2010). Daily intake of bisphenol A and potential sources of exposure: 2005-2006 National Health and Nutrition Examination Survey. Journal of exposure science & environmental epidemiology PMID: 20237498

VOMSAAL, F., AKINGBEMI, B., BELCHER, S., BIRNBAUM, L., CRAIN, D., ERIKSEN, M., FARABOLLINI, F., GUILLETTEJR, L., HAUSER, R., & HEINDEL, J. (2007). Chapel Hill bisphenol A expert panel consensus statement: Integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure Reproductive Toxicology, 24 (2), 131-138 DOI: 10.1016/j.reprotox.2007.07.005

Calabrese EJ (2009). Getting the dose-response wrong: why hormesis became marginalized and the threshold model accepted. Archives of toxicology, 83 (3), 227-47 PMID: 19234688

Myers, J., Zoeller, R., & vom Saal, F. (2009). A Clash of Old and New Scientific Concepts in Toxicity, with Important Implications for Public Health Environmental Health Perspectives DOI: 10.1289/ehp.0900887

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