A new BPA claims that exposure to realistic levels of BPA during pregnancy increases “biochemical markers for oxidative stress,” which are “associated with insulin resistance and inflammation, which are risk factors for diabetes and other metabolic disorders as well as cardiovascular disease.”
A careful reading of the paper and comparison with the scientific literature reveals:
- The effects observed in this study are actually biochemical markers. These markers in themselves do not demonstrate the adverse health effects claimed in the study and the media reports cited below
- The human study portion of the paper is an epidemiology study in which BPA levels in human urine, collected during pregnancy, are compared to biochemical marker levels. As is typical in such a study, it is not possible to conclude that BPA is the cause of any difference observed in the levels of any biomarkers measured in the study. Higher BPA levels were statistically associated with increased 3-nitrotyrosine (a marker of oxygen stress) and with elevated levels of the free fatty acid palmitic acid, a possible marker of metabolic distress.
- In the animal studies, the doses tested do not represent realistic levels of human exposure. For instance, the lowest dose tested in this study was an oral dose of 50 micrograms per kilogram body weight per day (50 µg/kg bw/d) in the rat study. This is more than 58 times higher than the highest estimated human exposure level (0.857 µg/kg bw/d) from the just published European Food Safety Agency (EFSA) Opinion (http://www.efsa.europa.eu/en/efsajournal/doc/3978.pdf).
- The study claims a concordance of results from studies using human epidemiology, and laboratory studies of sheep, rats and mice. However, a review of the results indicates that the human results and animal results in fact were not concordant. For instance, the mouse results were the closest to the human results but while the mouse was the only animal to change the same biomarker for oxidative stress (3-nitrotyrosine), the changes in the free fatty acids pattern was completely different from the pattern in humans.
In short, the study did not demonstrate adverse effects, the human study did not demonstrate cause and effect, the laboratory animal study did not test BPA at realistic human exposure concentrations and the claim that the results from human and animal studies are in concordance is based on the authors’ interpretation of the results more than on exact agreement between the set of results.
News reports on the study follow:
University of Michigan
1/20/2015
BPA exposure during pregnancy causes oxidative stress in child, mother
http://www.uofmhealth.org/news/archive/201501/bpa-exposure-during-pregnancy-causes-oxidative-stress-child
Medscape
1/20/2015
Endocrine Disruptor BPA Increases Fetal Oxidative Stress
http://www.medscape.com/viewarticle/838387
Medical Xpress
1/20/2015
BPA exposure during pregnancy causes oxidative stress in child, mother
http://medicalxpress.com/news/2015-01-bpa-exposure-pregnancy-oxidative-stress.html
Someboy has noticed!
“The chemical bisphenol A, used to stiffen some plastic food containers, poses no health risk to consumers of any age, including unborn children, at current levels of exposure, ” according to the European Food Safety Authority (EFSA), Europe’s equivalent of the US’ FDA. EFSA found that exposure to BPA was “considerably under” the safe level known as the “tolerable daily intake”, or TDI.
http://www.reuters.com/article/2015/01/21/us-health-europe-bisphenola-idUSKBN0KU1JV20150121
Given the degree of institutionalized chemophobia present in Europe where the Registration, Evaluation, Authorisation and Restriction of Chemicals (REACH) has been in place for 8 years, and GMOs are treated as the devil’s own poison, the evidence concerning health effects of BPA must be far from damning.