Bisphenol A – half of the story

Bisphenol A might be contributing to obesity (Photo: Malingering)

Bisphenol A might be contributing to obesity (Photo: Malingering)

We have written about bisphenol A before. Bisphenol A is mainly used in combination with other chemicals to manufacture polycarbonate plastics and resins used as food contact materials but can also be found in carbonless copy paper and thermal point-of-sale receipt paper. It is clear that bisphenol A is an endocrine disruptor at high doses but there are also some indications that it might be equally effective at very low doses. It has been proposed that the latter might even be one explanation of many to the obesity epidemic. According to this theory exposure to bisphenol A might induce epigenetic changes turning on obesity genes. Question is do we need to take action to remove bisphenol A from the food supply?

Let’s look at the process to arrive at a plausible answer to that question.

When assessing potential risks to public health posed by a food hazard it is necessary to have detailed knowledge of the expected toxicological effects of the hazard, the amount needed to be consumed to cause such effects and the expected population exposure to the hazard. There might also be other sources than the diet to be considered when calculating exposure. It might sound a bit complex and of course in most cases a lot of scientific data need to be gathered and assessed to draw reliable conclusions. But at the end it is still only a straight forward mathematical calculation using the critical dose and the estimated exposure as inputs.

But what inputs to use? Scientific facts evolve over time both on the toxicological side and the exposure side. A range of new scientific findings have been or are about to be published covering low-dose effects of bisphenol A. They are currently being evaluated by the European Food Safety Authority (EFSA) so this side of the equation is still uncertain. In the meantime, EFSA has published a revised exposure assessment providing half of the story needed to complete a risk assessment of bisphenol A.

EFSA previously calculated exposure to bisphenol A in 2006 using rough estimates of its presence in food and very basic food consumption information. This might be acceptable in case such conservative estimates are far lower than the expected dose of  toxicological concern. However, it didn’t include attempts to estimate exposure from non-food sources that could have been considerable. Now EFSA has published a refined exposure assessment using accurate data on the amount of bisphenol A present in food and detailed food consumption information provided by many European Union member countries. On top of that, EFSA also included exposure from non-food sources, thus combining data from oral, inhalation and dermal routes in the final results. Exposure modelling involved the assessment of chronic exposure to bisphenol A through diet, thermal paper, air, dust, toys, cosmetics, and dental sealants.

The new exposure estimates were much lower than the estimates of 2006. In the previous assessment, high exposure was up to 5,300 ng/kg bodyweight per day in toddlers and up to 11,000 ng/kg bodyweight per day in infants aged 3 months. This should be compared with the current estimates of up to 857 ng/kg bodyweight per day for toddlers and up to 495 ng/kg bodyweight per day for infants of 1-5 days.

Thermal paper not considered before was the second highest contributor to exposure in all population groups above 3 years of age. However, diet was found to be the major source of bisphenol A exposure in all population groups so this was not an important shortcoming of the previous exposure assessment.

Cashier a risk group still to be considered (Photo: Dan Goorevitch)

Cashiers a risk group still to be considered (Photo: Dan Goorevitch)

To check the accuracy of the calculations, total exposure to bisphenol A was also estimated using urinary biomonitoring data. Biomonitoring estimates based on urinary bisphenol A concentrations were in good agreement with modelled bisphenol A exposures from all sources, suggesting that no major exposure sources had been missed for the modelled exposure assessment.

There is a slight caveat in the presented data. Estimates of dermal exposure to bisphenol A were associated with considerable uncertainty and didn’t include cashiers as a particular group at risk because of lack of data. This might be rectified when an ongoing study on dermal exposure in cashiers sponsored by the National Institute of Environmental Health Sciences in the USA under the National Toxicology Program is published.

And of course, despite the considerable lowering of the exposure estimates for bisphenol A, we will not know if those levels still pose a risk to public health until the toxicological evaluation has been completed.

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