In a new study published online on January 30, 2015 in the peer-reviewed journal Environment International, Lorber and colleagues estimate dietary exposure of the adult U.S. population to bisphenol A (BPA, CAS 80-05-7) from food survey data (Lorber et al. 2015). The researchers then compare their exposure estimates to total intake of BPA back-calculated from urinary biomonitoring data collected through the National Health and Nutrition Examination Survey (NHANES).
Methods. The team of researchers previously measured BPA in foods sold in Dallas, U.S. (Schecter et al. 2010). BPA was detected in 63 out of 105 samples. Only a single positive result was from a non-canned sample. The current study builds upon the earlier one by adding 116 food samples from the same region. Samples included a variety of fresh, frozen and canned foods. BPA measurements were performed using High Resolution Gas Chromatography Low Resolution Mass Spectrometry (HRGC/LRMS). To assess dietary exposure to BPA, the authors used a combined set of 204 samples (infant formula and pet food samples from Schecter et al. 2010 were not included). The daily BPA exposure was first calculated using a “forward” approach, which combines data on BPA concentrations in food with daily food consumption rates. Exposure estimates calculated in this manner were then compared with the daily BPA intake determined from NHANES urinary BPA concentrations by backward calculations (“backward” approach). Furthermore, samples were categorized into broad food types, namely, vegetables, fruit, dairy, meat, fruit juices and fish. For each category, samples were further separated into “canned” and “all other”. Then, for each category, the fraction of total consumption stemming from canned food was determined (“fraction canned”). This approach allowed the authors to estimate the amount of total BPA exposure from canned foods and non-canned foods.
Results and discussion. BPA was detected in 70% of canned samples, but only in 6% of non-canned foods. Measured BPA concentrations ranged from 0.24 ng/g ww in a fresh peach to 149.0 ng/g ww in canned cut green beans. Measured concentration data from both sampling rounds were consistent. Mean adult dietary intake of BPA was estimated to be 12.6 ng/kg/day, of which 12.4 ng/kg/day (98%) was from canned foods. For NHANES cycles between 2005 and 2010, the total BPA intake representing a central tendency (median as well as mean) ranged from 30 to 70 ng/kg/day, thus was markedly higher compared to the forward modeling approach intake. The authors provide possible explanations for this difference:
First, the BPA concentrations measured in this study may not be adequately representative of typical U.S. canned foods. They were found to be generally lower in comparison to BPA concentrations detected in canned foods in six other worldwide food surveys, including three in North America. It is nevertheless possible that the lower concentrations may be partly due to differences in analytical methodologies between the various studies. Researchers from the U.S. Food and Drug Administration (FDA) surveyed foods in the Washington D.C. metropolitan area, U.S. (Noonan et al. 2011). Noonan and colleagues highlighted that BPA concentrations in the first round of sampling of the current study are lower than their measured concentrations and identified differences in analytical protocols that might explain the difference.
Second, not all canned products that might contain BPA, particularly canned beverages such as soft drinks, were sampled. In 2007, researchers from Health Canada analyzed 69 canned soft drinks sold on Canadian market and detected BPA in all samples (Cao et al. 2009). Later in 2013, the European Food Safety Authority (EFSA) published data on the occurrence of BPA in canned beverages from several European countries (EFSA, 2013). BPA was found in over 50% of the samples in the various studies considered by EFSA.
Third, the biomonitored intake estimates represent aggregate exposure i.e. exposure via all pathways and sources, unlike the forward-based intake estimates. Therefore, it is possible that there are other important dietary and particularly also non-dietary sources that were not considered in the current exposure assessment. For instance, thermal paper has been previously shown to be a source of BPA dermal exposure (FPF reported).
Conclusions. The authors conclude that the BPA levels in the canned foods tested greatly exceeded non-canned concentrations. This finding is consistent with other studies and underscores the importance of canned foods in the overall exposure of adults to BPA. Further, BPA intake estimates in this study are well below the currently set government benchmarks. However, as the authors point out, BPA is a known endocrine disrupting chemical (EDC). It can interact not only with multiple estrogen receptors, but also with several other nuclear and membrane-bound receptors. The safe levels established by FDA and EFSA nevertheless do not currently consider such cumulative exposures to multiple EDCs and thus their potential health risks. Finally, the researchers highlight that BPA must be replaced with caution, as several of its alternatives may pose health risks similar to BPA.
Cao, X.L. et al. (2009). “Levels of bisphenol A in canned soft drink products in Canadian markets.” Journal of Agricultural and Food Chemistry 57, 1307–1311.
Lorber, M. et al. (2015). “Exposure assessment of adult intake of bisphenol A (BPA) with emphasis on canned food dietary exposures.” Environment International 77, 55–62.
Noonan, G.O. et al. (2010). “Concentration of bisphenol A in highly consumed canned foods on the U.S. market.” Journal of Agricultural and Food Chemistry 59, 7178–7185.
Schecter, A. et al. (2010). “Bisphenol A (BPA) in U.S. food.” Environmental Science & Technology 44, 9425–9430.