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• W3046888079 abstract "Vol. 128, No. 7 Science SelectionOpen AccessBisphenol Exposure and Type 2 Diabetes: New Evidence for a Potential Risk Factoris accompanied byExposure to Bisphenol A and Bisphenol S and Incident Type 2 Diabetes: A Case–Cohort Study in the French Cohort D.E.S.I.R. Nate Seltenrich Nate Seltenrich Search for more papers by this author Published:30 July 2020CID: 074006https://doi.org/10.1289/EHP6637AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit AbstractThe plasticizer bisphenol A (BPA), used in can linings, thermal paper, and polycarbonate plastics,1,2 has been associated with a wide range of health outcomes, including type 2 diabetes.3 Numerous experimental4 and population-based5,6 studies over the last decade have explored the BPA–diabetes relationship. Now a longitudinal study published in Environmental Health Perspectives, examining not just BPA but also its widely used substitute bisphenol S (BPS), adds to the evidence.7 The study found positive associations between incidence of diabetes and exposure to both BPA and BPS, independent of traditional risk factors.It is well established that eating a healthful diet and staying active can protect against type 2 diabetes, given that obesity and a sedentary lifestyle are by far the greatest predictors of this disease.8 But even in individuals without these known risk factors, exposure to endocrine disruptors such as BPA and BPS may set the stage for diabetes. Image: © iStockphoto/Kosamtu.The research included 755 individuals followed over 9 years as part of the French cohort Data from an Epidemiological Study on the Insulin Resistance Syndrome (D.E.S.I.R.).8 The participants, who were diabetes-free when recruited, provided urine samples at enrollment (between 1994 and 1996) and again 3 years later. The authors estimated participants’ exposure to BPA and BPS based on urine metabolites of these bisphenols.A total of 201 D.E.S.I.R. participants received diabetes diagnoses during the 9-year follow-up period, but the risk was not equally distributed. The authors estimated that participants in the second and third quartiles of estimated BPA exposure were more than twice as likely to develop diabetes as those in the lowest quartile. Participants with the highest estimated exposures were at increased risk as well, but less so than more moderately exposed individuals. The analysis also suggested that participants with any urine BPS metabolites were nearly three times as likely to develop diabetes compared with participants with no detectable exposure.“I think this paper is particularly good because it’s longitudinal and there are very few [such papers on bisphenols],” says Angel Nadal, a professor at Spain’s Miguel Hernandez University. Nadal, who was not involved in the current study, has researched the physiological link between BPA exposure and diabetes since 2006.9 In 2018 he co-led an experimental study in which low doses of BPA triggered an insulin response (a predictor of type 2 diabetes) in a small group of men and women.10Human and animal studies have shown that BPA is metabolized in the body within a day, or potentially sooner.11,12 This means that urine levels may fluctuate dramatically depending on recent food consumption and other activities, making single measurements of urinary BPA an unreliable predictor of past exposures. “Having a couple of samples that have been measured makes a stronger connection between BPA exposure and type 2 diabetes,” Nadal says.The mechanisms through which BPA and BPS exposure may affect diabetes risk are complex and not fully understood, but certainly plausible, according to Fanny Rancière, the study’s first author and an associate professor at Paris Descartes University in France. “Several biological pathways through which BPA could affect the development of diabetes have been identified,13 such as insulin resistance and pancreatic beta-cell dysfunction,” she says.Rancière points out that there is a smaller body of literature for BPS. “However,” she adds, “a recent systematic review14 of experimental studies concluded that BPS has endocrine-disrupting effects similar to those of BPA, which is not surprising given the similarity between their chemical structures.”Other endocrine-disrupting chemicals besides BPA and BPS have been associated with diabetes incidence in other studies,13,15 says senior author Dianna Magliano. “Make no mistake, the best way to get diabetes is to put on weight and become obese,” she says. “But [certain endocrine disruptors] do have some association by themselves, independent of obesity and diet and whether you smoke or not and whether you exercise.”The pattern of associations with BPA suggests a nonmonotonic dose response, with the highest estimated diabetes risk among those who were moderately exposed. However, the authors note that the trend might also be a chance finding. Nonmonotonic dose responses may be a hallmark of hormone-mimicking chemicals, such that effects of very low levels are consistent with effects of endogenous hormones. On the other hand, high exposures could cause overwhelmed cell receptors to down-regulate or desensitize.16University of Illinois at Chicago associate professor Robert Sargis, coauthor of a review of the link between endocrine-disrupting chemicals and type 2 diabetes,17 says the team’s findings illustrate the need for safer products. “With BPA finally getting attention and companies starting to recognize that people are attuned to its adverse effects, the move has been to replace it with other bisphenols. And what this paper underscores is that the replacement compounds aren’t always better,” says Sargis, who was not involved in the current study. “Companies take pride in putting ‘BPA-free’ on their label, which is admirable in part, but it may be misrepresenting a risk that is highly relevant.”Nate Seltenrich covers science and the environment from the San Francisco Bay Area. His work on subjects including energy, ecology, and environmental health has appeared in a wide variety of regional, national, and international publications.References1. National Institute of Environmental Health Perspectives.2019. Bisphenol A (BPA). [Website.] Updated 5 March 2020. https://www.niehs.nih.gov/health/topics/agents/sya-bpa/index.cfm [accessed 17 July 2020]. Google Scholar2. Bernier MR, Vandenberg LN. 2017. Handling of thermal paper: implications for dermal exposure to bisphenol A and its alternatives. PLoS One 12(6):e0178449, PMID: 28570582, 10.1371/journal.pone.0178449. Crossref, Medline, Google Scholar3. Rancière F, Lyons JG, Loh VHY, Botton J, Galloway T, Wang T, et al.2015. Bisphenol A and the risk of cardiometabolic disorders: a systematic review with meta-analysis of the epidemiological evidence. Environ Health 14(1):46, PMID: 26026606, 10.1186/s12940-015-0036-5. Crossref, Medline, Google Scholar4. Alonso-Magdalena P, Quesada I, Nadal A. 2011. Endocrine disruptors in the etiology of type 2 diabetes mellitus. Nat Rev Endocrinol 7(6):346–353, PMID: 21467970, 10.1038/nrendo.2011.56. Crossref, Medline, Google Scholar5. Duan Y, Yao Y, Wang B, Han L, Wang L, Sun H, et al.2018. Association of urinary concentrations of bisphenols with type 2 diabetes mellitus: a case-control study. Environ Pollut 243(pt B):1719–1726, PMID: 30408859, 10.1016/j.envpol.2018.09.093. Crossref, Medline, Google Scholar6. Lang IA, Galloway TS, Scarlett A, Henley WE, Depledge M, Wallace RB, et al.2008. Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults. JAMA 300(11):1303–1310, PMID: 18799442, 10.1001/jama.300.11.1303. Crossref, Medline, Google Scholar7. Rancière F, Botton J, Slama R, Lacroix MZ, Debrauwer L, Charles MA, et al.2019. Exposure to bisphenol A and bisphenol S and incident type 2 diabetes: a case–cohort study in the French cohort D.E.S.I.R. Environ Health Perspect 127(10):107013, PMID: 31663775, 10.1289/EHP5159. Link, Google Scholar8. Balkau B, Lange C, Fezeu L, Tichet J, de Lauzon-Guillain B, Czernichow S, et al.2008. Predicting diabetes: clinical, biological, and genetic approaches: data from the Epidemiological Study on the Insulin Resistance Syndrome (DESIR). Diabetes Care 31(10):2056–2061, PMID: 18689695, 10.2337/dc08-0368. Crossref, Medline, Google Scholar9. Alonso-Magdalena P, Morimoto S, Ripoll C, Fuentes E, Nadal A. 2006. The estrogenic effect of bisphenol A disrupts pancreatic β-cell function in vivo and induces insulin resistance. Environ Health Perspect 114(1):106–112, PMID: 16393666, 10.1289/ehp.8451. Link, Google Scholar10. Stahlhut RW, Myers JP, Taylor JA, Nadal A, Dyer JA, vom Saal FS. 2018. Experimental BPA exposure and glucose-stimulated insulin response in adult men and women. J Endocr Soc 2(10):1173–1187, PMID: 30302422, 10.1210/js.2018-00151. Crossref, Medline, Google Scholar11. Vandenberg LN, Hauser R, Marcus M, Olea N, Welshons WV. 2007. Human exposure to bisphenol A (BPA). Reprod Toxicol 24(2):139–177, PMID: 17825522, 10.1016/j.reprotox.2007.07.010. Crossref, Medline, Google Scholar12. Stahlhut RW, Welshons WV, Swan SH. 2009. Bisphenol A data in NHANES suggest longer than expected half-life, substantial nonfood exposure, or both. Environ Health Perspect 117(5):784–789, PMID: 19479022, 10.1289/ehp.0800376. Link, Google Scholar13. Sargis RM, Simmons RA. 2019. Environmental neglect: endocrine disruptors as underappreciated but potentially modifiable diabetes risk factors. Diabetologia 62(10):1811–1822, PMID: 31451869, 10.1007/s00125-019-4940-z. Crossref, Medline, Google Scholar14. Rochester JR, Bolden AL. 2015. Bisphenol S and F: a systematic review and comparison of the hormonal activity of bisphenol A substitutes. Environ Health Perspect 123(7):643–650, PMID: 25775505, 10.1289/ehp.1408989. Link, Google Scholar15. Ruiz D, Becerra M, Jagai JS, Ard K, Sargis RM. 2018. Disparities in environmental exposures to endocrine-disrupting chemicals and diabetes risk in vulnerable populations. Diabetes Care 41(1):193–205, PMID: 29142003, 10.2337/dc16-2765. Crossref, Medline, Google Scholar16. Zoeller RT, Brown TR, Doan LL, Gore AC, Skakkebaek NE, Soto AM, et al.2012. Endocrine-disrupting chemicals and public health protection: a statement of principles from The Endocrine Society. Endocrinology 153(9):4097–4110, PMID: 22733974, 10.1210/en.2012-1422. Crossref, Medline, Google Scholar17. Bonini MG, Sargis RM. 2018. Environmental toxicant exposures and type 2 diabetes mellitus: two interrelated public health problems on the rise. Curr Opin Toxicol 7:52–59, PMID: 29392186, 10.1016/j.cotox.2017.09.003. Crossref, Medline, Google ScholarFiguresReferencesRelatedDetailsRelated articlesExposure to Bisphenol A and Bisphenol S and Incident Type 2 Diabetes: A Case–Cohort Study in the French Cohort D.E.S.I.R.30 October 2019Environmental Health Perspectives Vol. 128, No. 7 July 2020Metrics About Article Metrics Publication History Manuscript received6 December 2019Manuscript accepted18 December 2019Originally published30 July 2020 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days." @default.
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