(Originally posted on bcotoronto.com on Mar 8th, 2012)
There is a lot of fear and uncertainty around the chemical known as BPA, or Bisphenol A. I would like to clear this up a little by leading you through the research this week. BPA is found in approximately 90% of the general populous (1, 2) at extremely low concentrations (2, 3) so understanding what we are exposed to and the risks involved is very important. It has been known for a long time that BPA mimics estrogen in the body and so is known as an Endocrine (hormone system) Disruptor. Its effect was originally thought to be minimal (3) but now research has started to explore the implications of exposure to this chemical.
For every hormone in the body there is a receptor on the cellular membranes of targeted tissues within the body. This allows these signal molecules to have their effect. For very versatile hormones there is more than one receptor type throughout the body so that subtle chemical changes can alter the effect. Estrogen has two different receptor types and BPA interacts with both giving a very wide range of effects throughout the body (1, 4, 5, 12). Some evidence suggests that BPA actually works at the genetic level and alters the organization of DNA determining what genes are used (“epigenetics”) (1, 5).
Exposure of a fetus in the womb has been linked to multiple conditions mainly originating around neurological development. BPA effects dopamine (an important neurological signalling hormone) nerve connections in the developing brain and causing mental developmental disorders, diminished gender differentiation within the structures of the brain (6, 7, 12, 13). As well, an association with delayed sexual maturation has been shown. Specifically in animal studies on males early BPA exposure has been shown to decrease prostate development at low levels and increase the risk of prostate cancer at higher doses (1).
Issues with infertility were a common claim among the papers I found but it was contested often as well. None of the reviews cited any articles to support these claims except one that showed a correlation between BPA exposure and decreased seamen quality through disruption of the connections between the sperm producing cells (8).
Despite the well established link between increased estrogen levels in the body and increased risk of breast and ovarian cancer there is no research suggesting that BPA has any such activity. Along the same lines, other known Endocrine Disruptors have been shown to increase the risk of diabetes and obesity by inducing hyperglycemia but no such evidence has been found regarding BPA although fetal exposure was linked to predisposition to weight gain later in life (9). Due to BPA’s effects on dopamine-using (“dopaminergic”) nerves it has been hypothesised that it could cause or contribute to degenerative neurological diseases such as Parkinson’s but this has not yet been investigated (6).
There are many other claims about conditions such as heart disease and liver dysfunction being associated with BPA in the news but no such information was covered in the reviews that came from the search I performed.
On the other side of the debate there was one major review article out of Germany that came up in my search of the literature where the authors proposed that the quality of the research being performed is not enough to lead to any solid conclusions about the effect of BPA (3). They suggest that the currently (as of 2010) tolerable intake levels recommended by most governments is below the level where any adverse effects have been confidently shown (3). This view sets itself against the majority of the research but it is extremely well written and the arguments are well thought out and very thorough. There is one thing about the article that is a little suspicious. Three of the nine authors reported a potential conflict of interest with the content of the review article. One is an employee of a BPA producer but from a different department. One is an employee of the Bavarian Health and Food Safety Authority and has published research about BPA many times previously and the final potential conflict was from a former department head at the Federal Institute for Risk Assessment in Germany. So to me it looks like one conflict to promote BPA and two to regulate it. This may colour your attitude towards this review which is a decision you have to make on your own. Personally, I think this article is very important and well worth reading.
The environmental work group also did a large review of the literature in 2007 and had something different to say about the results. They cited twenty separate articles that found harmful results at or lower doses of BPA than the Canadian government has deemed tolerable and twenty-three at or lower than the United States limit (10).
In Canada, BPA is officially on the list of known industrial toxins (10) but has not been banned. As of 2008 the tolerable daily intake of BPA was 25 µg (micrograms [http://en.wikipedia.org/wiki/Microgram])/kg of body weight (3) and the Canadian government had taken small steps to limiting BPA exposure in infants in March 2010. They banned baby bottles that contain any BPA and they, “…work[ed] to develop and implement codes of practice to reduce levels of BPA in infant formula as low as reasonably achievable.” (3) I don’t know about you but this seems a little backwards to me. Why ban the container that has BPA but the actual food substance that goes in the container can still have it?
The German review also pointed out that the half-life (the amount of time needed for 50% of a sample to degrade) of BPA within the body is 2 hours (3) and so it does not build up within our system like other environmental toxins do. It may not last long but 2 hours is definitely enough time to have some physiological effect.
There is no central, reliable source of information on the sources of BPA in the environment and our diets so what I have done is find as many sites with lists of BPA sources and compiled them, eliminating items that only appear on one or two sites. BPA is a common constituent in plastics (4, 11, 13) which is why it has such a varied presence in our daily lives. My list of sources of BPA is as follows:
-Epoxy resin lining the inside of food cans
-Plastic Bottles (specifically those marked with the Recyclable #3 or #7 codes)
-Lining on the lids of glass jars
-Plastic children’s toys
-Recycled cardboard in pizza boxes
-Plastic food processors and blenders
-Toilet paper made from recycled BPA containing paper
-Thermal Paper (the paper used in receipt printing). There is some evidence that skin absortion may be a significant additional source of BPA exposure (14).
-Wine fermented in plastic lined vats
There really is an overwhelming amount of research out there suggesting negative effects of BPA at a myriad of different exposure levels but the major review opposing the claims of BPA toxicity at regulated tolerances is very well argued and convincing. BPA seems to be becoming a fairly ubiquitous substance in our daily lives so here is my advice. Caution! Limit your exposure as much as possible so that when you are exposed without your knowledge, it won’t be a strain on your system. The German review may be right, but I would rather be the guy saying, “Oops” when they are proven right rather than when they are proven wrong. As well, be extra cautious with exposure of children and during pregnancy as the endocrine and neurological systems of children and unborn infants are much more sensitive to disruption.
Thanks for reading,
1. Taylor JA, Richter CA, Ruhlen RL, vom Saal FS. Estrogenic environmental chemicals and drugs: mechanisms for effects on the developing male urogenital system. J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):83-95.
2. Bushnik T, Haines D, Levallois P, Levesque J, Van Oostdam J, Viau C.Lead and bisphenol A concentrations in the Canadian population. Health Rep. 2010 Sep;21(3):7-18.
3. Hengstler JG, Foth H, Gebel T, Kramer PJ, Lilienblum W, Schweinfurth H, Völkel W, Wollin KM, Gundert-Remy U. Critical evaluation of key evidence on the human health hazards of exposure to bisphenol A. Crit Rev Toxicol. 2011 Apr;41(4):263-91.
4. Myers DE, Hutz RJ. Current status of potential bisphenol toxicity in dentistry. Gen Dent. 2011 Jul-Aug;59(4):262-5.
5. Kundakovic M, Champagne FA. Epigenetic perspective on the developmental effects of bisphenol A. Brain Behav Immun. 2011 Aug;25(6):1084-93.
6. Masuo Y, Ishido M. Neurotoxicity of endocrine disruptors: possible involvement in brain development and neurodegeneration. J Toxicol Environ Health B Crit Rev. 2011;14(5-7):346-69.
7. Braun JM, Hauser R. Bisphenol A and children’s health. Curr Opin Pediatr. 2011 Apr;23(2):233-9.
8. Wong EW, Cheng CY. Impacts of environmental toxicants on male reproductive dysfunction. Trends Pharmacol Sci. 2011 May;32(5):290-9.
9. Tang-Péronard JL, Andersen HR, Jensen TK, Heitmann BL. Endocrine-disrupting chemicals and obesity development in humans: a review. Obes Rev. 2011 Aug;12(8):622-36.
10. The Environmental Work Group. Bisphenol A: Toxic Plastics Chemical in Canned Food
11. Rubin BS. Bisphenol A: an endocrine disruptor with widespread exposure and multiple effects. J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):27-34.
12. Golub MS, Wu KL, Kaufman FL, Li LH, Moran-Messen F, Zeise L, Alexeeff GV, Donald JM. Bisphenol A: developmental toxicity from early prenatal exposure. Birth Defects Res B Dev Reprod Toxicol. 2010 Dec;89(6):441-66.
13. Erler C, Novak J. Bisphenol a exposure: human risk and health policy. J Pediatr Nurs. 2010 Oct;25(5):400-7.
14. Geens T, Goeyens L, Covaci A. Are potential sources for human exposure to bisphenol-A overlooked? Int J Hyg Environ Health. 2011 Sep;214(5):339-47.
Sites with lists of BPA sources