Question marks have been raised over whether the levels of bisphenol A (BPA) that people are routinely exposed to are high enough to cause the diseases that have been linked to the controversial chemical. An analysis by Justin Teeguarden, a systems toxicologist at the Pacific Northwest National Laboratory, US, makes the bold claim that many of the animal tests that demonstrate that BPA may be a contributory factor in diseases like type 2 diabetes, obesity and heart disease have been elucidated using concentrations much greater than those ever found in humans.
BPA is ubiquitous in modern society thanks to its use in polycarbonate clear plastics, epoxy resins that line food tins and in dental sealants. Concerns have been raised about the chemical as it is thought to be an endocrine disruptor, disturbing the normal hormonal regulation of animals. As BPA products are ever present as they help to keep food fresh, anyone with a western diet will receive a daily dose of BPA. Many so-called low dose studies in animals have linked the chemical to a wide range of disorders because it can mimic the hormone oestrogen. The concentrations of BPA used in these low dose studies are meant to ape those found in people eating a fairly ordinary diet.
It is these studies that Teeguarden’s analysis takes aim at. His work took in 150 studies which measured BPA in 32,000 people’s blood and urine, as well as studies which attempted to calculate how much BPA was in their diet. These studies all came up with BPA concentrations in the pM or lower range, with the exception of one type of blood analysis that threw up concentrations a thousand times greater. It is these nM levels that many animal tests have used when establishing the dangerous effects of the chemical, he points out.
Teeguarden says that pM levels of BPA ought not to be a concern for us. This is because if the hypothesis that BPA causes harm by mimicking oestrogen is correct, then the dose of the chemical your average person receives everyday is 100 to 10,000 times lower than those needed to activate the hormone receptors. He also makes the point that the term ‘low dose’ has become somewhat debased in the BPA literature. When he looked at 130 animal studies using that term, the vast majority used BPA levels many times higher than a person would ever encounter in their diet. He says that this is more than just an academic point as it has contributed to confusion among toxicologists, epidemiologists and the general public.
Teeguarden notes that something just doesn’t add up with these studies that show up such high levels of BPA in the blood, compared with the others. This is because if you follow how much BPA someone has in their diet then these nM BPA blood concentrations seem improbable. He suggests that contamination might be a factor. ‘The canula you use to take the blood are plastic, the tubes and lines are plastic and labs are covered in dust that contains BPA,’ he says. ‘A single speck of dust containing BPA getting into a sample could put the levels off the chart.’
Richard Sharpe, an endocrinologist at the MRC Centre for Reproductive Health in the UK, says that BPA may just be an ‘innocent bystander’ in these arguments. He says that part of the problem is that many association studies looking at human populations have linked the chemical to ‘western diseases’ like type 2 diabetes. So, how can studies that suggest a strong association between diseases like obesity gel with dietary levels of BPA that may be too low to have a noticeable biological effect? Sharpe says that the old saw that correlation is not causation may hold true here. A ‘western diet’ high in fats and sugars can cause obesity and diabetes and such a diet typically comes packaged in materials that contain BPA. He says that this would be a ‘beautifully simple way’ of reconciling the available data.
Nevertheless, Teeguarden’s analysis and the suggestion that BPA is merely a marker for a bad diet are still controversial among many epidemiologists and toxicologists. Joseph Braun, an epidemiologist from Brown University, US, says that he feels that the truth lies somewhere in the middle. He accepts that the link between BPA and western diseases may just be an artefact, but thinks things are less clear cut with link between the chemical and such conditions as altered neurological development in children.
This new analysis doesn’t put an end to questions over BPA’s effects on people, as Teeguarden is the first to concede. ‘Now we have the appropriate human exposure it doesn’t mean we’re done,’ he says. ‘Now we have the concentrations to conduct studies in the range of human exposure.’
So, how can the BPA conundrum be resolved? Researchers are agreed that more high quality prospective studies are needed. But the question of how to reproduce a western-style diet without any BPA in it will be difficult to solve.