The compound Bisphenol A (BPA) has been commonly used in making hard, clear plastics, such as plastic bottles, since 1957. The compound is a precursor to the line of polycarbonate plastics such as Lexan and these compounds are used in the construction industry wherever transparent domes and walls are needed, since it has low scratch resistance. Polycarbonates are also used in electronics because of their hardness and low conductivity and also are used for making CDs and DVDs. You will also find Lexan in your food processor work bowl, of course.
The process for making polycarbonates was discovered in 1953 at Bayer by Hermann Schnell and independently at General Electric by Daniel Fox, who is considered the “father of Lexan.” The similar Bayer product is called Makrolon. The process for making the polymer from BPA amounted to reacting it with phosgene, (Cl-C=O-Cl). The two chlorines were displaced by the OH groups of BPA forming new bonds between BPA molecules.
But it wasn’t until about 2008 that people began to express concerns about the potential toxicity of BPA and the resulting polycarbonates. The question, then, is whether there is actually any evidence that BPA is harmful in our food and packaging. Currently we find it used in lining soup and soda cans and this might be on concern if BPA showed siginificant danger.
Critics have called BPA an “estrogen disruptor,” which seems to mean that it at least weakly mimics the effect of actual estrogens. Of course many natural and synthetic compounds do this, including soy, but we really have little evidence that this is somehow dangerous. It just sounds that way. One particularly difficult problem for proponents of the endocrine disruptor hypothesis is the idea that Parcelsus dictum that “the dose makes the poison” does not apply. They believe there is strong evidence that very low doses cause reactions that are not amplified (or even observed) in the presence of larger doses. This is called a “nonmonotonic response” and was reviewed by Vandenberg in 2012.
However, in Entine’s extensive review of BPA research in Forbes, he notes that most independent scientists remain unconvinced that this effect exists.
The CDC reports that traces of BPA have been found in the urine of most adults and children, but the measurement methods are so sensitive, that the traces are almost surely too small to matter.
Back in 2008, L. Earl Gray, Jr, the senior reproductive biologist at the EPA testified before Congress on the BPA and phthalates. His group reviewed over 700 studies on the effects of BPA, finding some possible low dose effects but no indication that effects increased with dosage. He noted that while BPA is an estrogen mimetic, it is about 10,000 less potent than estradiol, an important human estrogen.
He also noted that the studies of low dose effects are not repeatable across laboratories and these low dose effects are not necessarily adverse effects. His panel tentative conclusion was at best that there might be “some concern” for neural and behavioral effects and much less concern for other effects.
The Teeguarden Study
But the most significant study of BPA was carried out in 2011 by Teeguarden’s group at Pacific Northwest Laboratories, along with workers at the CDC and the FDA. This study, which we have reviewed before, monitored human volunteers for 24 hours while they were fed standard grocery store items whose packaging would contain BPA.
They found that while BPA was excreted in the urine on the order of 0.27 µg/kg, 21% greater than even the highest amount people might encounter, there was no detectable BPA in the blood serum in 83% of the samples, and in the rest the amount detected was less than or equal to the lower limit of detection.
In other words, there was essentially no BPA in the bloodstream of any of the subjects: it was all excreted. This means than concern for BPA in our diet is simply not an issue: it never remains in the body!
Petition to the FDA by the NRDC
Nonetheless, despite this conclusive evidence, the Natural Resources Defense Council petitioned the FDA to ban the use of BPA in food packaging based on earlier references they cited. The FDA very carefully considered every single piece of research they cited and in March of 2012 issued what might be considered a “stinging denial.” They conclude
Although FDA is not persuaded by the data and information in your petition to initiate rulemaking to revoke the food additive approvals for BPA, FDA will continue in its broader and more comprehensive review of emerging data and information on BPA.
The Baker Study
In 2012, Michael Baker of UC San Diego published an interesting molecular modeling study describing how BPA could act as estrogens do. This was not a paper that asserted that such dangers exist, but that if it was found they did, this is how the molecules might interact. Essentially Baker and his coworkers created 3-dimensional models of BPA and its metabolites and potential receptor molecules in the body, showing how they might interact like a “lock and key.” They did not assert that this actually happens, and admitted in interviews that they were not aware of Teeguarden’s work published the previous year.
Nonetheless, the popular press jumped all over this modeling study, claiming that it showed the dangers of BPA and its metabolites. It didn’t.
In 2014, K Barry Delclos and coworkers from the FDA published a rat experiment where they dosed pregnant rats and then their offspring with several different small dosages of BPA (2.5–2700 μg/kg ), and with two very large doses (100,000 to 300,000 µg/kg per day). Only the huge doses, which were expected to have adverse effects. There were no effects at any of the lower doses.
No effect means no effect
Despite blizzards of work and hundreds of papers, there has been no research showing that BPA is dangerous. The FDA is still right to approve its use. You can all relax. Read the Teeguarden study. It is easily readable and quite reassuring. The alarmism is indeed BS! The FDA's position is that the small quantities of BPA found in foods are safe.
- L N Vandenberg, et. al. “Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses,” Endocr Rev. 2012 Jun;33(3):378-455. 1.usa.gov/1l71h1E
- Jon Entine, “Bisphenol A (BPA) found not harmful yet again,” Forbes, 10/31/12. onforb.es/1jVNrz8
- L. Earl Gray, Jr. Testimony before the Committee on energy and commerce Subcommittee on Commerce, trade, and consumer protection United states House of Representatives. 1.usa.gov/1gysxpo
- Justin Teeguarden, et. el., “Twenty-Four Hour Human Urine and Serum Profiles of Bisphenol A during High-Dietary Exposure,” Toxicological Sciences 123 (1), 48-57. bit.ly/Nnt8yw
- Sarah Janssen, MD, PhD, “FDA/OC Letter to Natural Resources Defense Council – Petition Denial,” 1.usa.gov/1hrUSeL
- Michael A Baker, “3D Models of MBP, a Biologically Active Metabolite of Bisphenol A, in Human Estrogen Receptor α and Estrogen Receptor β,” PLOS One, October 4, 2012. bit.ly/1iVRIRH
- K.Barry Delclos, et. al. , “Toxicity Evaluation of Bisphenol A Administered by Gavage to Sprague Dawley Rats From Gestation Day 6 Through Postnatal Day 90,” Toxicol. Sciences, 14 Feb, 2014. bit.ly/1iVbLnM