I must say that I have never previously heard a study described as “majestically scientific.”  But the British do have a way with words. And those were the words that Dr. Richard Sharpe of the University of Edinburgh’s Human Reproductive Sciences Unit used in his analysis of a paper entitled “24 Hour Human Urine and Serum Profiles of Bisphenol A During High Dietary Exposure.” That’s quite a compliment from one of the world’s leading experts on “endocrine disruption.”
Back in 1993 Sharpe was actually the first scientist to suggest in a landmark paper in the British medical journal The Lancet, that exposure during pregnancy to hormone-like chemicals could lead to developmental problems in the offspring. Since that time, his research has focused on male reproductive health and the role that environmental chemicals may play in the increasing incidence of testicular cancer, low sperm count and low testosterone levels. Like most researchers in the field, Sharpe was open to the possibility that bisphenol A (BPA), a chemical widely used in the production of polycarbonate plastics and epoxy resins, and which exhibits clear estrogen-like behavior, could be a problem. After all, the chemical was showing up, albeit in trace amounts, in most everyone’s urine!
But it was University of Missouri professor Fred vom Saal’s finding of abnormal prostate growth and decreased sperm production in rats, at doses far lower than what was considered to be safe, that catapulted bisphenol A from obscurity onto the public stage. Vom Saal’s work, coupled with reports of female oysters acquiring male characteristics when exposed to the estrogenic detergent breakdown product nonylphenol, and penis deformities in Florida alligators linked to environmental contaminants captured the both the media’s and scientists’ attention. Grants became available and research on bisphenol A mushroomed to the extent that it may now well be the most studied chemical ever, with over 4500 research papers devoted to it. One would think that would be enough to eliminate all confusion, but alas, such is not the case.
Reproducibility is one of the cornerstones of scientific research. But try as they might, other scientists were unable to reproduce the prostate problems in rats. Vom Saal argued that they were using the wrong breed of animals, or that the studies absolving bisphenol A were funded by chemical companies and therefore could not be trusted. Actually, various breeds of animals were used, and furthermore, if subtle differences between closely related species have such a significant effect on bisphenol A metabolism, then how can we drawn any inference about humans? And as far as studies are concerned, the relevant question is not the source of funding, but whether the data is robust enough to pass peer review.
The debate about bisphenol A quickly took on an acrimonious nature with accusations of “flawed studies,” a usual euphemism for poor work, flying back and forth. But virtually all regulatory agencies came to the conclusion that there was no evidence of any harm to humans, although some, such as Health Canada, exercised the “precautionary principle” and banned polycarbonate baby bottles. That sat well with Dr. vom Saal who commented: “The science is clear and the findings are not just scary, they are horrific. Why would you feed a baby out of a clear, hard plastic bottle-it’s like giving a baby a birth control pill?” Well, the truth is that the science is not clear, and a comparison with the birth control pill is absurd. The estrogenic potential of the amount of bisphenol A that enters our body through our daily diet is about 50,000 times less than that of one birth control pill.
This is not to say that there is no legitimate controversy concerning bisphenol A. Some researchers have detected blood levels they claim are comparable to those that cause problems in animals, but these studies have been criticized because they do not mesh with what is known about the amount of BPA ingested, how the chemical is metabolized, and the amount that shows up in the urine. Contamination of samples by traces of BPA in laboratory equipment has been offered as a likely explanation. To truly evaluate the effects of bisphenol A, it is imperative to determine blood levels accurately. And this is where the current “majestic” research comes in.”
The study was carried out jointly by a U.S. Department of Energy lab, the Centers for Disease Control and the FDA, not exactly fly-by-night operations. Twenty subjects consumed a diet of mostly processed foods that had been in contact with bisphenol A, as in can liners. According to calculations, this put them in the highest possible category of oral exposure to BPA. Blood samples were taken every hour over a 24 hour period, a type of investigation that had never been done before. Furthermore, the samples were sent for analysis of bisphenol A to two independent laboratories that were thoroughly experienced in preventing contamination. In a nutshell, the biologically active bisphenol A levels in the blood throughout the day were below the detection capabilities of the most sophisticated instruments available! This remarkably meticulous study casts doubt on previously detected blood levels by others.
“Beautifully designed and executed,” was Professor Sharpe’s comment about the study. His interpretation is that the majority of effects observed in animal studies can now be seen as probably not relevant to humans because they involved much higher BPA blood levels. Humans would have to be thousands of times more sensitive to BPA than rats to experience developmental issues, a very unlikely scenario.
Is this the final word on BPA? No. The final word in science is that there is rarely a final word. Undoubtedly, those who look on BPA as the chemical from Hell, are scrambling to poke holes in this new study. They may point out that it is not oral, but rather skin exposure to BPA that causes a rise in blood levels. Cash register ink is often made with BPA and paper currency that is in contact with receipts may become contaminated. Indeed almost all currency that has been investigated had traces of BPA, but the amounts were so small that researchers estimate exposure from such sources to be about ten times less than from house dust which also contains trace levels of BPA. And of course house dust BPA exposure would have been noted in the “majestic study.” A wagging finger may also be pointed at a recent study that found an association between higher blood levels of BPA and lower estrogen levels in the blood of women whose eggs were being harvested for in vitro fertilization. The implication is that this could have an adverse effect on the eggs. The health of the eggs was not investigated and the study has not been reproduced so any further conclusion is inappropriate.
I suspect that most readers have not heard of the “majestic study” I’ve been discussing. Isn’t it amazing how any news that implicates bisphenol A as a potentially harmful substance makes headlines but accounts of its safety get swept under the rug? Should a study show some sort of association between feeding some rodent an inordinate amount of bisphenol A and some hormonal change, it gets trumpeted in the press. Never mind that the study can’t be reproduced by other researchers. Or should there be a possible link between occupational exposure to bisphenol A and impaired sexual function, you can be sure that the headline writers will be at the ready with their clever quips. Never mind that such exposure has no relevance for the general population. But when a major organization such as the German Society of Toxicology comes out with a peer-reviewed article in a prestigious journal, the Critical Reviews in Toxicology, declaring that BPA poses no substantive risk, there is nary a mention. Except perhaps some bluster in the Huffington Post about all the members of the German panel being allied to the plastics industry, which is blatantly untrue.
Neither do I recall seeing headlines when the Food and Drug Administration in the U.S. reviewed the chemical in 2010 and concluded that it was safe at current low levels of exposure. Or when the European Food Safety Association examined over 800 studies and concluded that BPA was not harmful. Indeed after some 50 years of use and thousands of studies there is no evidence that bisphenol A harms human health. Of course it is true that the absence of evidence of harm is not evidence of the absence of harm. Given the fact that this chemical does have hormone-like properties and in test tube experiments and in animal trials can have some endocrine disruptive effects, the possibility of subtle effects on humans cannot be ruled out. This would seem to be especially the case during early development. If BPA is to cause any harm it is most likely to do so if exposure is in utero or during infancy.
It is almost dogma that scientific papers wrap up with the statement that “more studies are needed.” But, as blasphemous as that may sound, perhaps with BPA, enough is enough. After years and years of research and buckets of money spent, we have learned that if there is any danger it is vanishingly small, otherwise it would have been noted. Indeed that is the conclusion that Dr. Richard Sharpe has now come to. Here is what he says: “Fundamental, repetitive work on bisphenol A has sucked in hundreds of millions of dollars and it looks increasingly like an investment with nil return. All it has done is to show that there is a huge price to pay when initial studies are adhered to as being correct when the second phase of scientific peer review, namely, the inability of other laboratories to repeat the initial studies says otherwise.” He references a study in the journal Toxicological Sciences that showed complete absence of effect of a rage of bisphenol A exposures on reproductive development, function and behavior in female rats. The results of this study are robust and unequivocal and counter previous more circumspect studies that spawned the BPA fear. The press, however, didn’t pick up this story.
It may never be possible to tease out the effects, if there are any, of BPA on human health because the fact is that our bodies are awash in both natural and synthetic compounds that are potential endocrine disruptors. Soy, flax, wine, nuts and beer all contain such and then there are various plasticizers, pesticides and disinfectants. One can argue that finding substitutes for BPA in food applications is an appropriate application of the precautionary principle. Maybe. But the evidence to support it is pretty flimsy. Professor Sharpe, who you’ll remember was once on the anti-BPA bandwagon, now believes that the supposed risk of BPA was arrived at based on faulty studies. He opines: As scientists we all like our ideas and hypotheses to be proved correct; yet there is equal merit in being proved wrong.” The evidence now suggests that the notion that bisphenol A is a chemical from hell is wrong. The time has perhaps come to put estrogenic concerns about this chemical on the back burner. Of course that back burner needs to be monitored for flare-ups.
