Bisphenol A, commonly known as BPA, is in the news, again. BPA has been around for decades in a multitude of consumer products. Should it be of concern to you?
History and Use
The first report of BPA dates back to 1905, when Thomas Zincke of the University of Marburg, Germany, described its synthesis from phenol and acetone. Its commercial production did not arrive until the 1950s, when it was found to be a good starting material for the then newly developed polycarbonate plastic materials and epoxy resins. Since then, a variety of other uses of BPA have made it a large-scale production compound, used worldwide for many different purposes. To mention just a few of such: additive for many different types of synthetic polymers, such as the materials lining common food tin cans, dental sealants, paints and inks, and almost any synthetic material found in a plethora of articles.
More recently, concern has arisen about BPA’s presence in human serum and urine samples. One source was thought to be its occurrence in clear polycarbonate bottles that are widely used as water and beverage containers. The presence of BPA in the latter was mainly due to incomplete reaction of BPA with other substances to create the polymer.
Toxicological & Environmental Effects
There are literally thousands of scientific papers and media reports about BPA. The American Chemistry Council, an umbrella organization for chemical companies, has a whole website dedicated to BPA [1]. Furthermore, over the years, many governments and international agencies have reviewed it for the purpose of assessing its safety for use in the food industry.
The toxicology of BPA has been extensively studied by industry, government and academic research groups. Both short and long term exposure tests, including several reproduction studies, multi-generation exposure studies and a cancer bioassay were undertaken. None of these studies showed that BPA would cause any adverse toxic effects from exposure through the use of common consumer products. For example, even in the long-term studies, lasting approximately two years, mice fed with diets containing 1,000 mg (BPA)/kg (food) or more, showed no toxicological effects. The same is the case for any environmental effects resulting from the disposal of BPA containing products. Those instances where “feminization” of fish and similar effects were observed in field studies were most likely due to the presence of synthetic estrogen derivatives in effluents from sewage systems.
BPA is also known to degrade rapidly under common environmental conditions. It only resists degradation under anoxic (oxygen deprived) conditions, such as found in anoxic sediments or in some landfill sites.
Endocrine Disruptors
Then, approximately ten years ago, a new concern arose based on certain field observations, but not related to any specific substance. That concern was about so-called “endocrine disruptors”, that is substances that have low-level effects on important hormonal systems. In subsequent work, BPA was found to have a very low affinity to the “estrogen receptor”, an important mammalian hormonal regulator. Suddenly, BPA was of concern, once again.
So, what are the facts and do we need to be concerned in terms of any endocrine effects of BPA?
Endocrine Effects
The estimated dietary intake of BPA from food contact with polycarbonate plastic and epoxy resin, based on the results of multiple migration studies with consistent results, has a No Effect Level (NOEL) of less than 0.000118 mg/kg (body weight) per day [1].” That means, for a 75 kg (165 lb) person, a daily intake NOEL limit of approximately 0.009 mg/person. In comparison, the current exposure limit set by the US EPA is 3.75 mg/person.
The “relative binding affinity” (RBA) of BPA to the mammalian estrogen receptor, relative to the reference compound 17beta-estradiol (E2), is approximately 10^(-4), or 1/10,000 of that of E2 [2]. The RBA is what determines any compound’s effectiveness as an endocrine disruptor.
Multiplying the maximum daily intake (using the NOEL) by the RBA, results in an exposure limit of 0.0000009 mg E2-equivalent per average-weight person per day.
To put that potential exposure to BPA from food intake into perspective: Many physicians prescribe estrogen supplements (either natural E2 or synthetic derivatives of E2) for women in order to alleviate menopausal symptoms or loss of bone density. Such prescriptions typically contain doses of 0.05 to 0.3 mg (E2)/person and day, or even higher.
Also the male human body has levels of E2 which are comparable to that of the female body. But males also produce testosterone, which counteracts the effect of estrogen.
Therefore, the potential estrogenic effects from BPA are approximately six orders of magnitude lower than from natural or drug exposure to E2.
The level of BPA anyone is exposed through ingestion of food or drinks which have been in contact with containers containing traces of BPA is neglible. No toxicological effects of any sort, even with chronic exposure could normally arise from that, nor any endocrine system disrupting effects.
Summary
No doubt, there will be more studies on BPA, and more reviews. But to this date, none of the numerous studies and reviews undertaken have been able to unequivocally find any problem with its current uses and, most likely, more studies and reviews will not change that.
[1] American Chemistry Council;
bisphenol-a.org
[2] TerraTox - Steroids database,
terrabase-inc.com
