For more than 20 years, public debate about the safety of of bisphenol A (BPA) has lingered in the food-packaging world. You can’t go through a sports store without noticing the “BPA-free” labels on almost every reusable water bottle on display. A near-constant stream of newspaper and blog headlines has linked BPA to anything and everything that ails us.
The question of BPA’s safety has also plagued regulatory agencies, which must look beyond the headlines to the data that produced them. Not surprisingly, the study results and headlines do not always match up.
But now we have a new study that represents the most comprehensive evaluation to date of BPA absorption in the human body. It shows that the body quickly metabolizes and excretes BPA ingested orally, from a food that most of us routinely eat from a can: soup.
To understand the study’s importance, it helps to understand how we asses the effects that chemicals have on the human body. Toxicologists take a lot of factors into account when they evaluate whether something is harmful to humans. For starters, every substance is toxic at some level of exposure. You can die from drinking too much water, for example — but water is not generally recognized as a “toxic” substance.
Evaluations of a given substance’s toxicity rely on two broad areas. The determination of what amount results in harm is called a hazard assessment. An exposure assessment relates to the amounts people are being exposed to. Taking those into consideration together gives you a measure of the danger to humans: the risk assessment.
Another way to think of this is to look at the risk from a hole in the ground. The depth of the hole, and the danger it poses, is considered the hazard: The hole can be as shallow as a few inches or as deep as the Grand Canyon. Your proximity represents your exposure. The hole may be the Grand Canyon — but if you’re in Florida, the risk is nil. On the other hand, if you’re standing on a tiny crack in the pavement, your exposure is high, but to a very small hazard. What regulators look for are situations where people are standing next to a very large hole.
Anyone who has followed the BPA facts over the years is well aware that there are more than enough studies to contribute to the hazard assessment. Those are the studies that make all the headlines.
What may surprise you, however, is that the exposure assessment is really just now being fully understood.
An important part of determining exposure levels to a substance is understanding what happens to that substance once it enters the body: how it gets in, where it goes and how fast it is degraded and removed. This is called pharmacokinetics. And recent work on BPA pharmacokinetics has shown the truly low levels of BPA that exist in the body after ingestion — a critical consideration in regulatory agencies’ risk assessments.
It has been known for some time that when BPA is ingested, it is quickly metabolized by intestinal and liver cells to an inactive form — no biological activity — and excreted in urine after about three to six hours. What was at question was the level of active BPA entering the bloodstream.
That question was definitively answered back in 2011 by researchers from the Pacific Northwest National Laboratory (PNNL), Justin Teeguarden, and a team from the FDA’s National Center for Toxicological Research. In their study, volunteer participants were checked into a clinic to control their diets and other activities. They were fed a diet high in BPA content, and the level of exposure was determined through evaluation of their urine output.
Obtained via state-of-the-art detection techniques from the Centers for Disease Control and Prevention and the U.S. Food and Drug Administration, the results showed that at no time was active BPA measured in the blood of participants.
What was most interesting about the publication of this work in the Journal Toxicological Sciences, besides its positive implications for BPA-based packaging, was the backlash it caused in the antichemicals camp, including a letter published in a subsequent issue of the journal. The most remarkable claim the letter’s authors made was that the test subjects were exposed to less BPA than came out in their urine, which violates the most fundamental concept of mass balance: What goes in can’t be less than what comes out. In general, the authors’ arguments fell so far outside the realm of possibility that the journal responded by introducing a new editorial policy requiring Letters the Editor be sent for peer review to prevent future outlandish claims to be made in their journal.
Fast-forward to 2015, when Teeguarden and the PNNL group looked deeper into the pharmacokinetics of BPA, seeking to determine if any active BPA could get into the bloodstream from direct absorption from the oral cavity. Human participants were fed tomato soup with BPA that was isotopically labeled, making it easy to trace and measure. Levels of BPA in the soup were approximately 1,000 times the amount you would normally find in a can.
The results of this 2015 study, published in Toxicology and Applied Pharmacology were consistent with the 2011 study. Only extremely low levels of active BPA could be found in the bloodstreams of the participants; in other words, even with extremely high doses, the participants were able to effectively metabolize more than 99.9 percent of ingested BPA. Additionally, the level of active BPA absorbed directly through the oral cavity was nil.
The anti-BPA crowd has cried foul again. In new attacks, they claim that because blood was drawn from the arm — versus a vein closer to the mouth — oral cavity absorption wasn’t properly measured. They also say the soup didn’t have enough fat to make the BPA soluble. Once again, these criticisms are of no merit and are sometimes refuted by the critics’ own work (in this case, a study in dogs that dissolved BPA in water and alcohol; fats are not needed to dissolve a water-soluble compound).
The new Teeguarden study is the most complete evaluation of BPA absorption in the human body to date and was designed to observe any significant absorption from the oral cavity. What cannot be denied is that all of the criticisms levied at the 2011 study have now been addressed. The group that criticized the 2011 paper should publicly acknowledge that their claims were unfounded. The data supplied by both the 2011 and 2015 studies, as well as previous studies in 2002 and 2005 — plus preliminary data from a human study conducted by the National Institute of Environmental Health Sciences — should confirm the quick metabolism and excretion of BPA, not only to regulatory scientists but to even the most ardent BPA critics.
The simple facts cannot be denied: Ingested BPA is swiftly and efficiently metabolized and excreted in urine. Active BPA is not measurable in the bloodstreams of humans exposed to doses relevant to actual human exposure in foods. If a substance is not in the bloodstream, it will not reach a target organ and do harm.
Dr. John M. Rost is Chairman of the North American Packaging Alliance, Inc.