The findings, led by researchers at Duke University Medical Centre in Durham, North Carolina, indicate exposure to the food contact material may suppress the gene KCC2. This gene is vital to nerve cell function and to the development of the central nervous system.
However, respected scientists claim levels of the food contact material used in the experiments the research is based on are vastly higher than humans would ever be exposed to through their diets.
Consequently, the results, published in the journal Proceedings of the National Academy of Sciences, bear little relation to the impact of dietary levels of BPA, they say.
Referring to the work, Ian Musgrave, senior lecturer in the Faculty of Medicine at the University of Adelaide, Australia, said: “Unfortunately, its 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 through 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.”
Professor Andrew Bartholomaeus, adjunct professor of toxicology and pharmacy at the University of Canberra’s School of Pharmacy, said cells were bathed in BPA for the study. This was wildly different to the usual method of exposure in food, so could not be relied on to infer the effects of such exposure, he added.
‘Weakest form of epidemiological study’
“These types of studies are the weakest form of epidemiological study and routinely throw up associations that cannot be confirmed as real by better designed and more robust approaches,” stated Bartholomaeus. “That is, they are more likely to be irreproducible than real.”
During the early development of neurons, high levels of chloride are present in the cells. KCC2 is a chloride transporter protein, which acts to remove chloride ions from these cells.
The Duke University Medical Centre researchers claim BPA disrupts KCC2 activity by increasing the production of MECP2, a protein necessary for normal brain function. This then causes MECP2 to bind to KCC2 at a higher rate, which may help to shut it down, they postulate.
As a result, chloride levels in neurons would remain high, damaging neural circuits and hampering a developing nerve cell’s ability to move to its proper position in the brain, the study states.
Female neurons more susceptible
The effects were observed in the cortical neurons of mice, rats and humans. According to the research, female neurons were more susceptible to BPA toxicity.
This suggests possible effects could include neurodevelopmental disorders such as Rett Syndrome, an autism spectrum disorder only found in girls and characterised by mutations in the gene that produces MECP2.
“Our study found that BPA may impair the development of the central nervous system and raises the question as to whether exposure could predispose animals and humans to neurodevelopmental disorders,” states Wolfgang Liedtke, associate professor of medicine and neurology at Duke Medicine and lead author of the paper.
Source: Proceedings of the National Academy of Sciences, February 25, 2013; doi: 10.1073/pnas.1300959110; 'Bisphenol A delays the perinatal chloride shift in cortical neurons by epigenetic effects on the KCC2 promoter'.
Authors: Michele Yeo; Ken Berglund; Michael Hanna; Junjie Guo; Jaya Kittur; Maria Torres; Joel Abramowitz; Jorge Busciglio; Yuan Gao; Lutz Bimbaumer, Wolfgang Liedtke.