Is your soup poisoning you? In a recent study subjects who ate canned vegetable soup had markedly increased levels of BPA in their urine compared to those who ate freshly prepared soup. We are constantly bombarded with alarmist warnings about the dangerous chemicals in the products we use. Especially BPA (Bisphenol A) and phthalates. Beware plastic bottles! Beware rubber ducks! And now, beware canned soup! BPA and phthalates are classified as endocrine disruptors. They have been discussed before on SBM here and here. BPA has been accused of causing everything from obesity to prostate cancer. Phthalates have been accused of causing everything from breast cancer to reduced anogenital distance in baby boys (the significance of this is unknown: there is not even any standard for what the normal distance is).
In the book Slow Death by Rubber Duck
Using a variety of test methods, the authors determined individual “body burdens,” or the toxic chemical load we carry. The innocuous rubber duck, for example, offers a poison soup of phthalates that “permeate the environment and humans.” From other products and food we also have a collection of chemicals shorthanded as PFCs, PFOAs, PSOSs, and PCBs. None of them are good, and they are everywhere…
Is this science or irresponsible fear-mongering? What does the best evidence tell us? Should we be afraid of our canned soup and rubber ducks?
Phthalates and BPA are ubiquitous and unavoidable. They are widely used in the manufacture of plastics, medical devices, and many consumer products. How dangerous are these and other common chemicals in our environment? Does it mean anything to have a high level of a chemical in our urine if the chemical is rapidly eliminated from the body and didn’t cause any harm while it was there? When does intelligent concern become irrational fear?
The canned soup study was reported in a “Research Letter” rather than as a typical peer-reviewed journal article. It was single-blind and its sole purpose was to measure “total BPA and conjugated species” in the urine. It did not even attempt to investigate whether there was any effect on the subjects’ health. The researchers themselves noted that the elevation of urinary BPA was transient and that further research is needed. They found the highest levels ever reported outside of occupational exposure, which raises questions. If levels this high are confirmed in other studies, that still doesn’t tell us whether such transient levels have any clinical significance.
I won’t attempt to cover the vast body of research on endocrine disruptors; but for those who are interested, Wikipedia provides useful compilations of studies on the health effects of phthalates and BPA. To summarize: research by chemical companies has generally shown no risk; studies elsewhere have raised many concerns, but results are inconsistent and inconclusive and often based on animal experiments with no confirmation in humans. The World Health Organization (WHO) and government agencies in various countries have concluded that current use is not risky, but a few groups have disagreed. Canada banned BPA in baby bottles as a precautionary measure.
What Do the Measurements Mean?
Measurement of these chemicals in urine is problematic. Nearly all the BPA found in the urine is in the form of metabolites. Trace levels of BPA found in some samples may be due to degradation of metabolites back to BPA after collection. It makes a difference which metabolite is chosen. One-time measurement is not likely to reflect overall exposure. Excretion varies by time of day and other confounding factors. These compounds are rapidly excreted from the body and may not stay around long enough to cause any problems. BPA is rapidly and completely metabolized into glucuronide, which is not estrogenic and is rapidly excreted in the urine. Even premature infants can metabolize it at the low levels involved. Rodents have a different metabolism. They excrete BPA through bile into the gut where it can be reabsorbed and has a longer half-life. Studies using IV administration are inapplicable to oral consumption.
Kamrin reviewed and analyzed all the available data in his 2009 article “Phthalate Risks, Phthalate Regulation, and Public Health: A Review.” He concluded that “the risks are low, even lower than originally thought, and that there is no convincing evidence of adverse effects on humans… [so] phthalate regulations that have been enacted are unlikely to lead to any marked improvement in public health.”
He says, “Early high-dose studies in animals suggested that phthalates might induce liver cancer in humans, but careful consideration of the mechanism of action, peroxisome proliferation, led to the conclusion that animal studies are not relevant for humans.” Animal studies can alert us to possible problems in humans, but they can also create false alarms. For instance, aspirin causes congenital defects in mice, but it has no such effects in humans.
Do combined exposures to multiple phthalates increase risk? He argues that they probably don’t, because individual exposures are so small that the total doesn’t approach effect levels, there is no evidence of additive effects in humans, and not all phthalates affect the body in the same way.
Epidemiological evidence is inconsistent and not persuasive. Adults and neonates who have been exposed to high levels of the phthalate DEHP from medical procedures do not exhibit the adverse effects seen in animals.The lowest levels at which adverse effects occur in sensitive animals are much higher than the doses to which humans are exposed.
There is further reassurance in a 2010 article by Witorsch and Thomas. They reviewed endocrine disruptors in personal care products and concluded “although select constituents exhibit interactions with the endocrine system in the laboratory, the evidence linking personal care products to endocrine disruptive effects in humans is for the most part lacking.”
Should We Be Worried?
We were once blissfully unaware of the trace amounts of all these things in our bodies. Our improving technology enables us to measure them and worry about them. My interpretation of the evidence on endocrine disruptors like phthalates and BPA is that the risks are still theoretical and unproven, that drastic measures are not warranted without more evidence, and that we need to keep an open mind and evaluate any new evidence as it comes along. As we do that, we need to keep a couple of things in mind:
- We are not mice. Concerns from animal experiments can’t be automatically extrapolated to humans. Human studies are required.
- We can’t protect ourselves from every conceivable risk. Trying to eliminate one risk often results in other, unforeseen ones. Banning BPA and phthalates would result in substituting other compounds that are more costly, may not work as well, and have not been as well tested for safety. BPA-free products are marketed for what they are not, not for what they are.
In my opinion, current evidence might be sufficient to justify banning phthalates and BPA for mice, but not for men. I’m not going stop eating canned food, and I’m not about to throw my rubber ducky away. I’m with Ernie.
This article was originally published in the Science-Based Medicine Blog