Exposure to Bisphenol A ‘hard to avoid’ in everyday life
86 per cent of UK students aged between 17 and 19 years have traces of Bisphenol A (BPA), a chemical compound used to make plastics, in their body, an Engaged Research public engagement project in collaboration with the University of Exeter has found. Manneken Pis image credit David Kenny.
2018 Research Abstract
Objective
Bisphenol A (BPA) has been associated with adverse human health outcomes and exposure to this compound is near-ubiquitous in the Western world. We aimed to examine whether self-moderation of BPA exposure is possible by altering diet in a real-world setting.
Design
An Engaged Research dietary intervention study designed, implemented and analysed by healthy teenagers from six schools and undertaken in their own homes.
Participants
A total of 94 students aged between 17 and 19 years from schools in the South West of the UK provided diet diaries and urine samples for analysis.
Intervention
Researcher participants designed a set of literature-informed guidelines for the reduction of dietary BPA to be followed for 7 days.
Main outcome measures
Creatinine-adjusted urinary BPA levels were taken before and after the intervention. Information on packaging and food/drink ingested was used to calculate a BPA risk score for anticipated exposure. A qualitative analysis was carried out to identify themes addressing long-term sustainability of the diet.
Results
BPA was detected in urine of 86% of participants at baseline at a median value of 1.22 ng/mL (IQR 1.99). No effect of the intervention diet on BPA levels was identified overall (P=0.25), but there was a positive association in those participants who showed a drop in urinary BPA concentration postintervention and their initial BPA level (P=0.003). Qualitative analysis identified themes around feelings of lifestyle restriction and the inadequacy of current labelling practices.
Conclusions
We found no evidence in this self-administered intervention study that it was possible to moderate BPA exposure by diet in a real-world setting. Furthermore, our study participants indicated that they would be unlikely to sustain such a diet long term, due to the difficulty in identifying BPA-free foods.
Discussion
Exposure to the EDC BPA is ubiquitous, with growing evidence that it may be associated with adverse health outcomes. Here, 94 researcher participants aged 17–19 years designed and undertook a quantitative and qualitative engaged research project designed to assess the potential for reduction of personal exposure to BPA through moderation of diet, which would have utility in a ‘real-world’ setting. We conclude that the ‘real-world’ diet designed to reduce BPA exposure had no effect on creatinine-adjusted urinary BPA concentrations in our cohort over a period of 7 days in our dataset.
Although concentrations of urinary BPA in our study cohort were slightly lower at the outset of the study than in others, measurable concentrations were present in the vast majority of our participants. Participants were unable to achieve a reduction in their urinary BPA over the 7-day trial period, despite good compliance to supplied guidelines. Avoidance of BPA was not easily achieved on an individual level in our study population, with qualitative analysis indicating that participants experienced feelings of restriction and difficulties in sourcing BPA-free food due to inadequate labelling of foods and food packaging. This suggests that the intervention would be difficult to sustain in the longer term.
This work represents the largest group of unrelated participants in a high exposure demographic to date, since previous work has focused on families and related individuals, who may share common sources of BPA. Although other population demographics such as young children may have higher concentrations of BPA than our chosen study population, it would not have been possible to do the sort of engaged research project that we envisaged in this group. Our intervention is a ‘real-world’ diet, designed to a set of guidelines (such as reduction in the usage of tinned foods or foods with high levels of processing), rather than the strict, prescribed diets that have been used in other studies, which suggested that it was possible for participants to reduce their urinary BPA excretion by approximately 60% in a period of just 3 days. In our self-designed, self-administered study this was unachievable. This may reflect the difficulty in identifying and sourcing foods free of BPA in the current commercial environment. Finally, the qualitative thematic analysis has given an indication that adherence to even a ‘real-world’ BPA reduction diet with fewer restrictions and more choice over the longer term was unlikely in our study population due to difficulties in identifying foodstuffs likely to contain less BPA.
BPA has a terminal half-life of 6 hours. Spot samples may therefore not be as accurate as continuous sampling strategies (24 hours urine collection). However, recent studies suggest that despite its short half-life, measurable BPA remains present for up to 43 hours postfasting, indicating non-food exposures or accumulation in body tissues such as fat. We identified no impact of time of sample collection on BPA concentrations in our sample set, in either creatinine-adjusted or unadjusted data, indicating that our measurements were not influenced by time since the last meal. Spot sampling as used here may therefore represent an acceptable compromise and remains a practical option in the community setting. The large variability in urinary BPA within an individual sampled at different times may also have reduced our ability to observe an effect. This could be facilitated by the use of multiple sampling or pools of multiple urines, but was not feasible within the confines of our study.
Calculating an accurate BPA risk score is challenging. Data were self-reported, and foodstuffs are not labelled for BPA content. It is difficult to generalise across food types and large variations in BPA concentrations occur between different products of the same food type or even different lots of the same product. Foods that were free of BPA-containing packaging (as far as it was possible to tell) may have been highly processed or contain food items from a variety of sources. Highly processed and ‘fast’ food has previously been demonstrated to be a source of BPA. A study of the temporal trends seen in composite food samples found no change in the overall BPA content of the food, despite large reduction in the BPA content of some individual food items, illustrating the difficulties in effectively excluding BPA from a varied diet. Participants may therefore have changed BPA-containing foods for other, perceived healthier choices, which may still contain BPA by virtue of processing.
BPA enters foodstuffs by leaching from polycarbonate or epoxy resin after manufacture, or by hydrolysis of the polymer itself. The migration rate of BPA increases with higher temperatures, and with time and use, for example, repeated use of polycarbonate water bottles. Exposure to BPA can also occur through routes other than food, including dust ingestion and dermal absorption and this was not taken into account in our study. A study of volunteers who purposefully handled thermal receipts showed an increase in urinary BPA excretion of up to 84%, and their BPA levels took longer to return to pre exposure levels, suggesting a difference in the bioavailability of BPA through skin and oral routes. It is also possible that some manufacturers may have voluntarily reduced the amount of BPA-containing food packaging compared with their previous usage, given the attention that EDCs have received in the media. However, measurable levels of BPA were still detected in the majority of participants in our study, which suggests that there may be other, non-dietary, sources of BPA, and that exposure to BPA remains an issue. We may also have been underpowered to detect subtle changes in urinary BPA, given the heterogeneity in food choice; detection of such effects may need thousands of participants. Finally, our study, like other studies of its type, does not take account of interindividual differences in the metabolism and excretion of BPA arising from differences in genetic background between people. BPA is metabolised primarily by uridine 5′-diphospho-glucuronosyltransferases, and altered activity polymorphisms of these enzymes have been reported.
Emerging evidence suggests that that BPA may be linked to several chronic human health conditions, suggesting that continued study of the human health effects of BPA exposure is justified. The opinion of the European Food Safety Authority (EFSA), is that while uncertainty over the human health effects of BPA exists, caution should be exercised in ingestion of BPA. Our data suggest that in our study population, it is unlikely that participants could moderate their own BPA exposure in the long term by self-directed modification of diet in a ‘real-world’ setting, and furthermore, participants would have been reluctant to adopt such a lifestyle change in the longer term due to the restrictions in dietary choice and the effects on day-to-day life. Most of these barriers appear to arise from the pervasiveness of BPA in our food chain, and inadequate labelling of foods packaged in BPA-containing substances. We propose that until a definitive assessment of the health risks of BPA is available, informed choice over whether or not to consume BPA and similar chemicals in foodstuffs should be facilitated by better labelling.
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