They are everywhere: so called ‘present organic pollutants’, or POPs for short.   Since almost all the everyday items that make modern life so much easier emerged from a chemical factory, its not surprising that environmental contamination with organic chemicals is increasing all the time – even ‘environmentally aware’ Western countries.  But maybe it will surprise you to learn they are in your food as well.

New data, published in the Journal of the American Medical Association last week, showed that eating canned soup increased exposure to the compound Bisphenol A (BPA).  Since BPA is a component of many plastics, and is found in lots of food packaging and particularly in cling film, its been known to find its way into food for many years.

In response to the latest study, suggesting that canned food, as well as plastic-wrapped food, can be contaminated with BPA (since modern tin cans, as well as not being made of tin, also have a plastic inner lining), the Food Standards Agency in the UK moved quickly to quell fears:  “Our current advice is that BPA from food contact materials does not represent a risk to consumers” they said.

But is that true?

A British Heart Foundation funded project at the Universities of Exeter and Cambridge have been using the Total Scientific biomarker platform to investigate this question in some detail.  And while the results are not yet conclusive, there is certainly no reason to be complacent.  If the Food Standards Agency had said “There is presently no conclusive evidence that BPA from food contact materials represents a risk to consumers” they would have been correct – but the absence of evidence is certainly not the same thing as the absence of risk.  A more cautious approach is almost certainly warranted.

BPA is an organic compound classified as an ‘endocrine disruptor’: that is, a compound capable of causing dysfunction to hormonally regulated body systems. More than 2.2 million metric tonnes of BPA are produced worldwide each year for use mainly as a constituent monomer in polycarbonate plastics and epoxy resins. Widespread and continuous human exposure to BPA is primarily through food but also through drinking water, dental sealants, dermal exposure and inhalation of household dusts. It is one of the world’s highest production volume compounds and human biomonitoring data indicates that the majority (up to 95%) of the general population is exposed to BPA, evidenced by the presence of measurable concentrations of metabolites in the urine of population representative samples.

In 2008, our collaborator Professor David Melzer in Exeter published the first major epidemiological study to examine the health effects associated with Bisphenol A. They had proposed that higher urinary BPA concentrations would be associated with adverse human health effects, especially in the liver and in relation to insulin, cardiovascular disease and obesity. In their human study higher BPA concentrations were associated with cardiovascular diagnoses (with an Odds Ratio per 1SD increase in BPA concentration  of 1.39, 95% CI 1.18-1.63; p=.001 with full adjustment).  Higher BPA concentrations were also associated with diabetes (OR per 1SD increase in BPA concentration, 1.39;95% CI 1.21-1.60;p<.001) but not with other common diseases.

What that study did not do, however, was determine whether increased exposure to BPA was causing the increase in cardiovascular disease, or was an association due to some confounding factor.

Using our MaGiCAD cohort, these researchers have attempted to replicate these previously published associations, and using the prospective component of MaGiCAD should allow a first indication of whether any observed associations are actually causal.  If exposure to BPA really does increase the risk of heart disease, the implications for safety assessment of BPA and other POPs is significant: we may have to re-evaluate our use of BPA and introduce tighter controls on existing and new chemicals to which people are commonly exposed.

The problem is that it is really difficult to detect a weak, but significant, association between a common exposure and a highly prevalent disease, such as coronary heart disease.  Worse still, because the exposure is so common, even a relatively small increase in risk among those exposed could contribute a significant fraction of the population burden of heart disease, the biggest cause of death in the UK today.  And with every possibility that it is chronic low dose exposure over decades that is responsible for any damaging effects, it is difficult to envision how we could determine whether such POPs are safe enough to justify their use – at least until the harms they cause are detected decades after their widespread adoption.

Indeed, past history shows that chemicals can be very widely used before their harmful effects become known.  The insecticide DDT, or the carcinogenic food dyes such as Butter Yellow are good examples.  It is easy to assume in the 21^st Century that our regulations and controls are good enough to prevent a repeat of these mistakes.

But the emerging data on BPA suggests that this is no time to be complacent.  Just because of the sheer scale of the exposure over so many years, it is far from impossible that BPA has caused more illness and death than any other organic pollutant.

The results from our studies, and other parallel studies by the same researchers, have just been submitted for scientific journals for peer review.  It is only appropriate that the results are released in this way, after rigorous scrutiny by the scientific community (in so far as peer review is ever rigorous).  But those results, when made public, will only add to the concern being expressed about BPA.  There may not yet be a conclusive answer as to the safety of BPA, but it is already time to ask just how much evidence will be needed before it is time to act to reduce our exposure.  Do we need to prove beyond all doubt that it is harmful, or will a “balance of probabilities” verdict suffice?

This is more a question of public policy than epidemiology.  A previous government was willing to ban beef on the bone when the evidence of risk to the population from that route was negligible.  Society needs to make some clear and consistent decisions when to act.  Ban passive smoking, allow cigarettes and alcohol, ban cannabis, allow BPA contamination but ban T-bone steaks.  Sometimes it seems like the decisions made to protect us have very little to do with the evidence at all.

What this study definitely has done, however, is expand still further the range of questions that have been investigated using our biomarker platforms.  Biomarkers may find the bulk of their applications in disease diagnostics and in clinical trials of new therapeutics, but the work on BPA proves that they are also very well suited to complex epidemiological investigations.  Biomarkers, it seems, can do almost everything – except inform the decision about what measures to take in response to the knowledge gained.  Sadly, the politicians are not very good at that either.