I’m going to take a break from my planned blogging of the WHO Endocrine Disrupting Chemicals Report to talk about this paper “Bisphenol A delays the perinatal chloride shift in cortical neurons by epigenetic effects on the Kcc2 promoter”, just published in the Proceedings of the National Academy of Sciences.
Why? The paper illustrates some of the issues with the WHO report, and the perils of trying to make otherwise valid scientific research “relevant”. Let’s start with the press release.
“DURHAM, N.C. – Environmental exposure to bisphenol A (BPA), a widespread chemical found in plastics and resins, may suppress a gene vital to nerve cell function and to the development of the central nervous system, according to a study led by researchers at Duke Medicine”
We have met bisphenol A before. It is an endocrine disrupting chemical, which mimics the structure of the hormone oestrogen.
However, it’s a very weak mimic, and is rapidly broken down in the environment and in our bodies. While BPA is used to make plastics that are used for drink bottles and food storage, our exposure to this chemical is minuscule.
Now, back to the paper. Will environmental exposure to BPA do what the press release says?
This is a very interesting study, unfortunately, it’s linkage to environmental exposure to bisphenol A is misleading, in that the concentrations used in this study are hundreds to thousands of times higher than humans would be exposed to that the maximal permissible level of BPA in food. Thus, this study, while it throws light on aspects of gene regulation, is not relevant to human exposure to this chemical.
In the first part of the study, cultured nerve cells were exposed to “relatively” low levels of BPA. When I say relatively, these levels are inn the nanomolar range (ie very tiny). But even these tiny levels are around 100 times greater than the blood levels expected from exposure to the highest permitted levels of BPA.
Also, direct exposure of these cells to BPA does not reflect the levels (or conditions) that brain cells in the body would be exposed to.
In the second part of the study female mice were fed BPA containing food and the effects on the brain of the offspring were studied. In terms of human exposure, the concentrations of BPA fed were 1000 times higher than the maximal permitted level of human exposure, so again not relevant to human exposure.
Put it this way, for a pregnant woman to get the same dose BPA the pregnant mice were getting, they would have to eat well over 2000 cans a day, every day, for months, of the foods Choice found to have the highest levels of BPA in them. This would be a heroic feat under any circumstances, and you would have other issues just from consumption of this much food alone.
While the study establishes that it’s possible to manipulate how genes are switched on in the developing brain, and that some of these genes may have a significant effect on processes relevant to brain function, the concentrations of BPA in this study are well beyond that which would be experienced by humans.
Trying to pitch the study as being environmentally relevant distorts the actual research and creates unnecessary panic. The authors should have a severe talk to their PR department.