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Bisphenol A and the risk of cardiometabolic disorders: a systematic review with meta-analysis of the epidemiological evidence

Identifieur interne : 000B58 ( Pmc/Curation ); précédent : 000B57; suivant : 000B59

Bisphenol A and the risk of cardiometabolic disorders: a systematic review with meta-analysis of the epidemiological evidence

Auteurs : Fanny Rancière [France] ; Jasmine G. Lyons ; Venurs H. Y. Loh ; Jérémie Botton [France] ; Tamara Galloway [Royaume-Uni] ; Tiange Wang [République populaire de Chine] ; Jonathan E. Shaw ; Dianna J. Magliano

Source :

RBID : PMC:4472611

Abstract

Bisphenol A (BPA) is suspected to be associated with several chronic metabolic diseases. The aim of the present study was to review the epidemiological literature on the relation between BPA exposure and the risk of cardiometabolic disorders. PubMed and Embase databases were searched up to August 2014 by two independent investigators using standardized subject terms. We included observational studies (cohort, case–control and cross-sectional studies) carried out in children or adults, measuring urinary BPA (uBPA), including at least 100 participants and published in English. The health outcomes of interest were diabetes, hyperglycemia, measures of anthropometry, cardiovascular disease (CVD) and hypertension. Data were extracted and meta-analyzed when feasible, using a random-effects model. Thirty-three studies with sample size ranging from 239 to 4811 met the inclusion criteria, including five with a prospective design. Twelve studies reported on diabetes or hyperglycemia, 16 on anthropometry, 6 on CVD and 3 on hypertension. Evidence for a positive association between uBPA concentrations and diabetes, overweight, obesity, elevated waist circumference (WC), CVD and hypertension was found in 7/8, 2/7, 6/7, 5/5, 4/5 and 2/3 of the cross-sectional studies, respectively. We were able to conduct outcome-specific meta-analyses including 12 studies. When comparing the highest vs. the lowest uBPA concentrations, the pooled ORs were 1.47 (95 % CI: 1.21–1.80) for diabetes, 1.21 (95 % CI: 0.98–1.50) for overweight, 1.67 (95 % CI: 1.41–1.98) for obesity, 1.48 (95 % CI: 1.25–1.76) for elevated WC, and 1.41 (95 % CI: 1.12–1.79) for hypertension. Moreover, among the five prospective studies, 3 reported significant findings, relating BPA exposure to incident diabetes, incident coronary artery disease, and weight gain. To conclude, there is evidence from the large body of cross-sectional studies that individuals with higher uBPA concentrations are more likely to suffer from diabetes, general/abdominal obesity and hypertension than those with lower uBPA concentrations. Given the potential importance for public health, prospective cohort studies with proper adjustment for dietary characteristics and identification of critical windows of exposure are urgently needed to further improve knowledge about potential causal links between BPA exposure and the development of chronic disease.

Electronic supplementary material

The online version of this article (doi:10.1186/s12940-015-0036-5) contains supplementary material, which is available to authorized users.


Url:
DOI: 10.1186/s12940-015-0036-5
PubMed: 26026606
PubMed Central: 4472611

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Fanny Rancière
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Jasmine G. Lyons
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Venurs H. Y. Loh
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Jonathan E. Shaw
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Dianna J. Magliano
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<p>Bisphenol A (BPA) is suspected to be associated with several chronic metabolic diseases. The aim of the present study was to review the epidemiological literature on the relation between BPA exposure and the risk of cardiometabolic disorders. PubMed and Embase databases were searched up to August 2014 by two independent investigators using standardized subject terms. We included observational studies (cohort, case–control and cross-sectional studies) carried out in children or adults, measuring urinary BPA (uBPA), including at least 100 participants and published in English. The health outcomes of interest were diabetes, hyperglycemia, measures of anthropometry, cardiovascular disease (CVD) and hypertension. Data were extracted and meta-analyzed when feasible, using a random-effects model. Thirty-three studies with sample size ranging from 239 to 4811 met the inclusion criteria, including five with a prospective design. Twelve studies reported on diabetes or hyperglycemia, 16 on anthropometry, 6 on CVD and 3 on hypertension. Evidence for a positive association between uBPA concentrations and diabetes, overweight, obesity, elevated waist circumference (WC), CVD and hypertension was found in 7/8, 2/7, 6/7, 5/5, 4/5 and 2/3 of the cross-sectional studies, respectively. We were able to conduct outcome-specific meta-analyses including 12 studies. When comparing the highest vs. the lowest uBPA concentrations, the pooled ORs were 1.47 (95 % CI: 1.21–1.80) for diabetes, 1.21 (95 % CI: 0.98–1.50) for overweight, 1.67 (95 % CI: 1.41–1.98) for obesity, 1.48 (95 % CI: 1.25–1.76) for elevated WC, and 1.41 (95 % CI: 1.12–1.79) for hypertension. Moreover, among the five prospective studies, 3 reported significant findings, relating BPA exposure to incident diabetes, incident coronary artery disease, and weight gain. To conclude, there is evidence from the large body of cross-sectional studies that individuals with higher uBPA concentrations are more likely to suffer from diabetes, general/abdominal obesity and hypertension than those with lower uBPA concentrations. Given the potential importance for public health, prospective cohort studies with proper adjustment for dietary characteristics and identification of critical windows of exposure are urgently needed to further improve knowledge about potential causal links between BPA exposure and the development of chronic disease.</p>
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<pmc article-type="research-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">Environ Health</journal-id>
<journal-id journal-id-type="iso-abbrev">Environ Health</journal-id>
<journal-title-group>
<journal-title>Environmental Health</journal-title>
</journal-title-group>
<issn pub-type="epub">1476-069X</issn>
<publisher>
<publisher-name>BioMed Central</publisher-name>
<publisher-loc>London</publisher-loc>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">26026606</article-id>
<article-id pub-id-type="pmc">4472611</article-id>
<article-id pub-id-type="publisher-id">36</article-id>
<article-id pub-id-type="doi">10.1186/s12940-015-0036-5</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Review</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Bisphenol A and the risk of cardiometabolic disorders: a systematic review with meta-analysis of the epidemiological evidence</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" equal-contrib="yes">
<name>
<surname>Rancière</surname>
<given-names>Fanny</given-names>
</name>
<address>
<email>fanny.ranciere@inserm.fr</email>
</address>
<xref ref-type="aff" rid="Aff1"></xref>
<xref ref-type="aff" rid="Aff2"></xref>
<xref ref-type="aff" rid="Aff3"></xref>
</contrib>
<contrib contrib-type="author" equal-contrib="yes">
<name>
<surname>Lyons</surname>
<given-names>Jasmine G.</given-names>
</name>
<address>
<email>jasmine.lyons@bakeridi.edu.au</email>
</address>
<xref ref-type="aff" rid="Aff3"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Loh</surname>
<given-names>Venurs H.Y.</given-names>
</name>
<address>
<email>venurs.loh@bakeridi.edu.au</email>
</address>
<xref ref-type="aff" rid="Aff3"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Botton</surname>
<given-names>Jérémie</given-names>
</name>
<address>
<email>jeremie.botton@inserm.fr</email>
</address>
<xref ref-type="aff" rid="Aff1"></xref>
<xref ref-type="aff" rid="Aff2"></xref>
<xref ref-type="aff" rid="Aff4"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Galloway</surname>
<given-names>Tamara</given-names>
</name>
<address>
<email>t.s.galloway@exeter.ac.uk</email>
</address>
<xref ref-type="aff" rid="Aff5"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Wang</surname>
<given-names>Tiange</given-names>
</name>
<address>
<email>wtg@live.cn</email>
</address>
<xref ref-type="aff" rid="Aff6"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Shaw</surname>
<given-names>Jonathan E.</given-names>
</name>
<address>
<email>jonathan.shaw@bakeridi.edu.au</email>
</address>
<xref ref-type="aff" rid="Aff3"></xref>
</contrib>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Magliano</surname>
<given-names>Dianna J.</given-names>
</name>
<address>
<phone>+61 3 8532 1826</phone>
<email>dianna.magliano@bakeridi.edu.au</email>
</address>
<xref ref-type="aff" rid="Aff3"></xref>
</contrib>
<aff id="Aff1">
<label></label>
Inserm, U1153, Epidemiology and Biostatistics Sorbonne Paris Cité Research Centre (CRESS), Early Origin of the Child’s Health and Development (ORCHAD) Team, Villejuif, France</aff>
<aff id="Aff2">
<label></label>
Univ Paris Descartes, UMR1153, Paris, France</aff>
<aff id="Aff3">
<label></label>
Department of Clinical Diabetes and Epidemiology, Baker IDI Heart and Diabetes Institute, Level 4, 99 Commercial Road, Melbourne, VIC 3000 Australia</aff>
<aff id="Aff4">
<label></label>
Faculty of Pharmacy, Univ Paris-Sud, Châtenay-Malabry, France</aff>
<aff id="Aff5">
<label></label>
Department of Biosciences, University of Exeter, College of Life and Environmental Sciences, Exeter, UK</aff>
<aff id="Aff6">
<label></label>
Shanghai Clinical Center for Endocrine and Metabolic Diseases, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China</aff>
</contrib-group>
<pub-date pub-type="epub">
<day>31</day>
<month>5</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>31</day>
<month>5</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="collection">
<year>2015</year>
</pub-date>
<volume>14</volume>
<elocation-id>46</elocation-id>
<history>
<date date-type="received">
<day>5</day>
<month>1</month>
<year>2015</year>
</date>
<date date-type="accepted">
<day>25</day>
<month>5</month>
<year>2015</year>
</date>
</history>
<permissions>
<copyright-statement>© Rancière et al. 2015</copyright-statement>
<license license-type="open-access">
<license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0">http://creativecommons.org/licenses/by/4.0</ext-link>
), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (
<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/publicdomain/zero/1.0/">http://creativecommons.org/publicdomain/zero/1.0/</ext-link>
) applies to the data made available in this article, unless otherwise stated.</license-p>
</license>
</permissions>
<abstract id="Abs1">
<p>Bisphenol A (BPA) is suspected to be associated with several chronic metabolic diseases. The aim of the present study was to review the epidemiological literature on the relation between BPA exposure and the risk of cardiometabolic disorders. PubMed and Embase databases were searched up to August 2014 by two independent investigators using standardized subject terms. We included observational studies (cohort, case–control and cross-sectional studies) carried out in children or adults, measuring urinary BPA (uBPA), including at least 100 participants and published in English. The health outcomes of interest were diabetes, hyperglycemia, measures of anthropometry, cardiovascular disease (CVD) and hypertension. Data were extracted and meta-analyzed when feasible, using a random-effects model. Thirty-three studies with sample size ranging from 239 to 4811 met the inclusion criteria, including five with a prospective design. Twelve studies reported on diabetes or hyperglycemia, 16 on anthropometry, 6 on CVD and 3 on hypertension. Evidence for a positive association between uBPA concentrations and diabetes, overweight, obesity, elevated waist circumference (WC), CVD and hypertension was found in 7/8, 2/7, 6/7, 5/5, 4/5 and 2/3 of the cross-sectional studies, respectively. We were able to conduct outcome-specific meta-analyses including 12 studies. When comparing the highest vs. the lowest uBPA concentrations, the pooled ORs were 1.47 (95 % CI: 1.21–1.80) for diabetes, 1.21 (95 % CI: 0.98–1.50) for overweight, 1.67 (95 % CI: 1.41–1.98) for obesity, 1.48 (95 % CI: 1.25–1.76) for elevated WC, and 1.41 (95 % CI: 1.12–1.79) for hypertension. Moreover, among the five prospective studies, 3 reported significant findings, relating BPA exposure to incident diabetes, incident coronary artery disease, and weight gain. To conclude, there is evidence from the large body of cross-sectional studies that individuals with higher uBPA concentrations are more likely to suffer from diabetes, general/abdominal obesity and hypertension than those with lower uBPA concentrations. Given the potential importance for public health, prospective cohort studies with proper adjustment for dietary characteristics and identification of critical windows of exposure are urgently needed to further improve knowledge about potential causal links between BPA exposure and the development of chronic disease.</p>
<sec>
<title>Electronic supplementary material</title>
<p>The online version of this article (doi:10.1186/s12940-015-0036-5) contains supplementary material, which is available to authorized users.</p>
</sec>
</abstract>
<kwd-group xml:lang="en">
<title>Keywords</title>
<kwd>Bisphenol A</kwd>
<kwd>Cardiovascular disease</kwd>
<kwd>Diabetes</kwd>
<kwd>Epidemiology</kwd>
<kwd>Hyperglycemia</kwd>
<kwd>Hypertension</kwd>
<kwd>Meta-analysis</kwd>
<kwd>Obesity</kwd>
<kwd>Overweight</kwd>
<kwd>Systematic review</kwd>
</kwd-group>
<custom-meta-group>
<custom-meta>
<meta-name>issue-copyright-statement</meta-name>
<meta-value>© The Author(s) 2015</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
</record>

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