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Bisphenol A and indicators of obesity, glucose metabolism/type 2 diabetes and cardiovascular disease: A systematic review of epidemiologic research

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Bisphenol A and indicators of obesity, glucose metabolism/type 2 diabetes and cardiovascular disease: A systematic review of epidemiologic research
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  http://informahealthcare.com/txcISSN: 1040-8444 (print), 1547-6898 (electronic) Crit Rev Toxicol, Early Online: 1–30 ! 2013 Informa Healthcare USA, Inc. DOI: 10.3109/10408444.2013.860075 REVIEW ARTICLE Bisphenol A and indicators of obesity, glucose metabolism/type 2diabetes and cardiovascular disease: A systematic review of epidemiologic research Judy S. LaKind 1,2,3 , Michael Goodman 4 , and Donald R. Mattison 5,6 1 LaKind Associates, LLC, Catonsville, MD, USA,  2 Department of Epidemiology and Public Health, University of Maryland School of Medicine,Baltimore, MD, USA,  3 Department of Pediatrics, Milton S. Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA,  4 Department of Epidemiology, Emory University School of Public Health, Atlanta, GA, USA,  5 Risk Sciences International, Ottawa, Canada, and   6 McLaughlin Centrefor Population Health Risk Assessment, University of Ottawa, Ottawa, Canada Abstract Introduction : Bisphenol A (BPA), a high-volume chemical with weak estrogenic properties, hasbeen linked to obesity, cardiovascular diseases (CVD) and diabetes mellitus (DM). This reviewevaluates both the consistency and the quality of epidemiological evidence from studiestesting the hypothesis that BPA exposure is a risk factor for these health outcomes.  Methods :We followed the current methodological guidelines for systematic reviews by using twoindependent researchers to identify, review and summarize the relevant epidemiologicalliterature on the relation of BPA to obesity, CVD, DM, or related biomarkers. Each paper wassummarized with respect to its methods and results with particular attention to study designand exposure assessment, which have been cited as the main areas of weakness in BPAepidemiologic research. As quantitative meta-analysis was not feasible, the study results werecategorized qualitatively as positive, inverse, null, or mixed.  Results : Nearly all studies on BPAand obesity-, DM- or CVD-related health outcomes used a cross-sectional design and reliedon a single measure of BPA exposure, which may result in serious exposure misclassification.For all outcomes, results across studies were inconsistent. Although several studies usedthe same data and the same or similar statistical methods, when the methods varied slightly,even studies that used the same data produced different results.  Conclusion : Epidemiologicalstudy design issues severely limit our understanding of health effects associated withBPA exposure. Considering the methodological limitations of the existing body of epidemi-ology literature, assertions about a causal link between BPA and obesity, DM, or CVD areunsubstantiated. Keywords Bisphenol A, biomonitoring, BPA,cardiovascular disease, diabetes, obesity,epidemiology, systematic review History Received 6 August 2013Revised 22 October 2013Accepted 24 October 2013Published online 23 December 2013 Table of Contents Abstract ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 1Introduction ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 1Methods ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 2Overview of methodology ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 2Identification and selection of studies ... ... ... ... ... ... ... ... ... ... ... ... 3Literature review ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 3Assessment of strength of evidence from individual studies ... 4Evaluation of study results and feasibility of meta-analysis ... ... 4Results ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 4Overview of studies... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 4Studies of obesity ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 4Studies of glucose metabolism and diabetes ... ... ... ... ... ... ... ... 15Studies of CVD and markers of cardiovascular health ... ... ... ... 18Feasibility of conducting a meta-analysis ... ... ... ... ... ... ... ... ... ... 24Discussion ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 24Conclusions and suggestions for future research... ... ... ... ... ... ... ... 26Declaration of interest ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 27Supplementary material... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 27References ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 27 Introduction Environmental obesogen is a term that has been coinedto describe ‘‘ . . . chemicals that inappropriately alter lipidhomeostasis and fat storage, metabolic setpoints, energybalance, or the regulation of appetite and satiety to promotefat accumulation and obesity’’ (Kirchner et al., 2010). It hasbeen hypothesized that exposure to obesogens can causean array of medical conditions that result in increased risk for obesity, type 2 diabetes mellitus (DM) and cardiovasculardisease (CVD) (Cameron, 2010). The marine antifoulingchemical tributyl tin and the synthetic estrogen diethylstil-bestrol are commonly cited as obesogens, but a growingnumber of environmental chemicals have been postulatedto have effects on the endocrine system that could ultimatelylead to metabolic syndrome (MetS) (which includes patho-logical factors such as insulin resistance (IR), hyperinsuline-mia, abdominal obesity, impaired glucose tolerance, DM  , microalbuminuria, high level of triglycerides (TG), low levelof high-density lipoprotein (HDL) cholesterol, elevatedblood pressure, and proinflammatory and prothrombotic Address for correspondence: Judy S. LaKind, LaKind Associates, LLC,106 Oakdale Avenue, Catonsville, MD 21228, USA. Tel.:  þ 1 410 7888639. Fax:  þ 1 410 788 8639. E-mail: lakindassoc@comcast.net    C  r   i   t   i  c  a   l   R  e  v   i  e  w  s   i  n   T  o  x   i  c  o   l  o  g  y   D  o  w  n   l  o  a   d  e   d   f  r  o  m    i  n   f  o  r  m  a   h  e  a   l   t   h  c  a  r  e .  c  o  m    b  y   6   9 .   1   4   3 .   9   1 .   2   3   3  o  n   0   1   /   0   6   /   1   4   F  o  r  p  e  r  s  o  n  a   l  u  s  e  o  n   l  y .  state [Pacholczyk et al., 2008]) and related adverse healthoutcomes (Holtcamp, 2012).As noted by Diamanti-Kandarakis et al. (2009), ‘‘Thereis a gap in knowledge about the mechanisms by which EDCs[endocrine disruptors] act as ‘obesogens’, particularly inhow these processes develop.’’ One complicating factor isthat diet is likely the predominant the route of exposurefor many of the chemicals that have been implicated asobesogens. This raises the question: Is obesity (andassociated morbidities) due to increased intake of foodsthat happen to contain these chemicals, or are the chemicalsthemselves causing increases in weight and associatedmorbidities? Sharpe & Drake (2013) suggested that afocus on epidemiologic investigations might yield fruitfulinformation in two regards: first, epidemiologic researchprovides information that is focused on actual levels of human exposures in contrast to toxicological studies whichfrequently use much higher dosing regimens; second, suchresearch might allow one to tease out the contribution of factors such as diet to development of obesity and relatedillnesses. In this systematic review, we focus on the first of these issues by examining the currently available epidemio-logic evidence as it relates to bisphenol A (BPA) andobesity, DM, and CVD.BPA, or 2,2 0 - bis -4-hydroxyphenyl-propane, is a high-volume chemical used in the manufacturing of polycarbonateplastic and epoxy resins, which are then used for makingbottles, food storage containers, and dental sealants (Arnichet al., 2011; Calafat et al., 2005). Biomonitoring data indicatethat most people have detectable levels of conjugated BPA,and to a lesser extent, unconjugated BPA (the bioactivemonomer) in urine, with diet considered the primary sourceof exposure in the general population (Calafat et al., 2008;Kang et al., 2006; LaKind & Naiman, 2008; LaKind et al.,2012a, 2011; Mahalingaiah et al., 2008). Whether the generalpopulation has detectable levels of BPA in serum is a subjectof strenuous debate (Calafat et al., 2013), although a recentstudy of individuals with high dietary exposure found nounconjugated BPA in serum above the limit of detection(Teeguarden et al., 2011).Because of widespread exposure to BPA and the fact thatBPA has estrogenic properties, potential human health effectsat low-level exposures have attracted considerable attention(Goodman et al., 2009; Melnick et al., 2002). As biologicallyplausible effects of estrogenic compounds may involvevarious organs and tissues, the adverse health endpointsostensibly linked to BPA could include a wide range of diseases and conditions. Although much of the concernregarding BPA toxicity pertains to reproductive health andchildren’s development (Braun & Hauser, 2011; Golub et al.,2010; Hauser & Sokol, 2008; Goodman et al., 2006, 2009;Meeker, 2010), more recently attention has shiftedtowards possible metabolic effects of BPA, which arehypothesized to increase the risk for obesity, CVD and DM(Alonso-Magdalena et al., 2011; Thayer et al., 2012).For these outcomes, the proposed mechanism of BPA action is activation of estrogen receptor- a , whichregulates the function of pancreatic  b -cells (Livingstone &Collison, 2002; Ropero et al., 2008). It is hypothesizedthat BPA may promote excessive insulin signaling andultimately IR, leading to elevated risks of DM, hypertension(HTN), and dyslipidemia (Alonso-Magdalena et al., 2006;Nadal et al., 2009).The current weight-of-the-evidence (WOE) debate aboutendocrine effects of environmental chemicals, including BPA,is focused primarily (although not exclusively) on the resultsof   in vitro  experiments and studies using  in vivo  animalmodels (European Food Safety Authority, 2010; Hengstleret al., 2011; Rhomberg et al., 2012; Talsness et al., 2009;Thayer et al., 2012; Vandenberg et al., 2012). In contrast,comprehensive evaluations of epidemiological data pertainingto BPA effects are scarce (Dash et al., 2006; Tang-Peronardet al., 2011), and to our knowledge, only one previous review(Braun et al., 2011a) critically assessed the association of BPA with CVD and DM (in addition to other endpoints)in human population studies.Epidemiological studies of BPA represent a rapidlyexpanding field with multiple papers evaluating variousendpoints published each month. Whereas the previouslycited review (Braun et al., 2011a) identified only two relevantreports linking BPA to DM or CVD (Lang et al., 2008;Melzer et al., 2010) and one for body mass index (Wolff et al.,2007), more than 40 additional relevant studies are nowavailable. Thus, a new assessment of epidemiological evi-dence addressing this issue is warranted. In the currentreview, we systematically evaluate both the consistency andthe quality of the epidemiological evidence from studiestesting the hypothesis that BPA is a risk factor for obesity,CVD, and/or DM. Methods Overview of methodology In conducting this study, we followed the guidelines of thecurrent methodological literature on systematic reviews(Moher et al., 2009; Shea et al., 2007; Sutton et al., 1998).In particular, we cross checked our study methods against the‘assessment tool of multiple systematic reviews’ (AMSTAR)guidelines (Shea et al., 2007), which represent an extensionof the previously published instruments (Delaney et al.,2007; Moher et al., 1999). The AMSTAR tool includesthe following 11 items: (1) an  a priori  statement of researchquestions and inclusion/exclusion criteria; (2) duplicateliterature searches by two or more co-authors; (3) the use of at least two electronic search engines followed by a supple-mental search of reviews, textbooks, and secondary referenceswith key words and Medical Subject Headings (MESH)reported in the methods section; (4) specification of statusof publication (e.g. gray literature, defined as reports that arenot published in peer-reviewed journals or scientific mono-graphs) as inclusion/exclusion criterion; (5) a list of studiesexcluded from the review; (6) a summary of study charac-teristics that met the inclusion criteria; (7) a formal assess-ment of strength of limitations of individual studies;(8) consideration of strength of evidence in drawing conclu-sions; (9) whenever possible pooling of study results in aquantitative meta-analysis accompanied by a test for hetero-geneity; (10) assessment of publication bias; and (11) a 2  J.S. LaKind et al.  Crit Rev Toxicol, Early Online: 1–30    C  r   i   t   i  c  a   l   R  e  v   i  e  w  s   i  n   T  o  x   i  c  o   l  o  g  y   D  o  w  n   l  o  a   d  e   d   f  r  o  m    i  n   f  o  r  m  a   h  e  a   l   t   h  c  a  r  e .  c  o  m    b  y   6   9 .   1   4   3 .   9   1 .   2   3   3  o  n   0   1   /   0   6   /   1   4   F  o  r  p  e  r  s  o  n  a   l  u  s  e  o  n   l  y .  statement of sources of support (Shea et al., 2007). With theexception of items 9 and 10, which are contingent on thefeasibility of a formal meta-analysis, the AMSTAR checklistis applicable to any systematic review. Identification and selection of studies Electronic data sources including PubMed and EMBASEwere used to conduct the initial literature search. Usingkeywords ‘‘BPA,’’ ‘‘bisphenol A,’’ ‘‘toxicity,’’ ‘‘humans,’’‘‘health,’’ ‘‘health outcomes,’’ ‘‘obesity’’, ‘‘overweight’’,‘‘DM, ’’ ‘‘diabetes,’’ ‘‘epidemiology,’’ ‘‘heart disease(s),’’‘‘CVD(s),’’ ‘‘myocardial infarction (MI),’’ ‘‘heart attack,’’‘‘coronary disease(s),’’ ‘‘coronary heart disease(s) (CHD),’’‘‘coronary artery disease(s) (CAD),’’ and ‘‘epidemiology’’as well as various combinations of these keywords, weselected articles that investigated the health effects associatedwith BPA exposures in humans. Secondary references of retrieved articles were reviewed to identify publications notcaptured by the electronic search. Additional literaturesearches were conducted to identify pertinent reports andtextbook chapters that were not published in the peer-reviewed literature. As many studies did not focus specificallyon obesity, CVD or DM, but still contained relevant data, anattempt was made to retrieve all epidemiological studiesof BPA and health. These articles were then reviewed toextract information pertaining to the present research ques-tion. The complete list of epidemiological studies retrievedand considered for inclusion is provided in the Supplementarymaterial.The search and selection of relevant studies was conductedindependently by two study authors (J.L. and M.G.) withall disagreements resolved by consensus. The criteria forinclusion into the review were as follows:(1) Studies of human populations with different levels of exposure to BPA as measured in biological samples.(2) Outcomes of interest that fall into five broad categories:(a) Indicators of overweight or obesity: body massindex (BMI), waist circumference (WC), bodyweight (BW), fat mass (FM), fat-free mass(FFM), hip circumference (HC), waist-hip ratio(WHR), and % body fat (%BF).(b) Conditions that reflect impaired glucose metabol-ism: DM and IR.(c) Biomarkers of glucose metabolism: circulatinglevels of fasting glucose (FG), insulin (I), glycosy-lated hemoglobin (HbA1C), and other indicatorssuch as measures of   b -cell function (BCF).(d) Conditions that constitute CVD: MI, CHD, orCAD, HTN, angina, stroke, any CVD (all CVDcombined), or other miscellaneous conditions thataffect cardiac or vascular health status such as thepresence of plaques on carotid artery ultrasoundor peripheral artery disease (PAD).(e) Biomarkers of cardiovascular health: blood levelsof total cholesterol (TC), low-density lipoproteins(LDL), HDL, and TG; measured diastolic andsystolic blood pressures (DBP and SBP, respect-ively), and other miscellaneous indicators of cardiovascular function such as Framingham Risk Score (FRS) or heart rate variability (HRV).(3) The association between BPA exposure and any of theabove outcomes either was assessed by the publicationauthors or could be assessed based on the informationprovided in the publication.(4) Publication appeared in English prior to 1 June 2013(end of literature search). Literature review Each study that met the inclusion criteria was examinedindependently by the same two co-authors (J.L. and M.G.)who conducted the literature search. The data from each studywere tabulated, and the resulting summary tables were againcross-checked with disagreements resolved by consensus.Information extracted from each study for the purposes of thisreview included:(1) Description of the study population: size, composition,source, and location.(2) Study design: cohort, cross-sectional, case-control, orother.(3) BPA exposure categorization: type of specimen, numberof samples, and the type of variable (e.g. ordinal, binary,or continuous) used in the analysis.(4) Endpoints of interest (see inclusion criteria).(5) Statistical approach and covariates included in the model.(6) Results: Effect estimate (e.g. an odds ratio [OR] forbinary endpoints, or a linear regression coefficient ordifference between two means for continuous endpoints),and a measure of precision (e.g. a 95% confidenceinterval [CI] or a standard deviation [SD]). If themeasures of precision were not reported, a  p  value wasrecorded. When the result was reported in a qualitativefashion, the corresponding text was extracted from thesrcinal and reproduced verbatim.(7) Description of study-specific BPA levels: units, measuresof central tendency, quantile (e.g. tertile or quartile)cutoffs, or range.For those studies that did not report effect estimates ormeasures of precision, where possible the appropriate resultswere calculated from the data provided in the publications.For example, some studies did not report the results in termsof ORs, but did provide information necessary to reconstructthe two-by-two tables. In those instances, the ORs werecalculated by one of the authors (M.G.) using cross-productsof counts, and the Taylor series approach (Kleinbaum, 2004).In some studies, means and standard errors (or SDs) forcontinuous endpoints (e.g. LDL or FG) in different BPAexposure groups were reported, but the publication did notinclude an assessment of differences of those means usingstatistical tests. If the data also included sample sizes for eachexposure group, we used a  t  -test to calculate differences and95% CIs for different exposure levels using the lowestcategory (e.g. the first tertile) as a reference. The distributionassumptions were based on the data reported in the srcinalpapers. If a study reported medians and interquartile ranges,the distribution was assumed to be skewed and a parametrictest was deemed inappropriate. All additional calculations DOI: 10.3109/10408444.2013.860075  Bisphenol A and indicators  3    C  r   i   t   i  c  a   l   R  e  v   i  e  w  s   i  n   T  o  x   i  c  o   l  o  g  y   D  o  w  n   l  o  a   d  e   d   f  r  o  m    i  n   f  o  r  m  a   h  e  a   l   t   h  c  a  r  e .  c  o  m    b  y   6   9 .   1   4   3 .   9   1 .   2   3   3  o  n   0   1   /   0   6   /   1   4   F  o  r  p  e  r  s  o  n  a   l  u  s  e  o  n   l  y .  were performed using OpenEpi statistical software (Sullivanet al., 2009). Assessment of strength of evidence fromindividual studies Although the strength of evidence provided by any epidemio-logical study depends on multiple factors including overalldesign, selection of participants, ability to minimize exposureand outcome misclassification, and control for confounders(Vandenbroucke et al., 2007), a subset of those factors areparticularly relevant for studies of short-lived chemicals suchas BPA. An important limitation of epidemiological studies of BPA noted by other researchers is the use of measurementsof BPA in serum (Koch et al., 2012; Teeguarden et al., 2011).As BPA comes from sources such as plastics (includinglabware), only its conjugated form (present primarily in urine)is considered by many researchers to be a valid exposurebiomarker because the conjugate is not affected by outsidecontamination of samples (Calafat et al., 2013). In addition,because BPA has a short half-life in both urine and serumsamples, reliance on a single spot sample to characterize long-term exposure leads to random error and increases potentialfor exposure misclassification (Ye et al., 2011; this isaddressed in greater detail in the Discussion section).Perhaps most importantly, the use of cross-sectional design,which does not permit assessment of the temporal relationbetween exposure and disease, is a particularly importantissue in studies of BPA (Braun et al., 2011a; Dash et al., 2006;Koch et al., 2012; Vo¨lkel et al., 2002). Whereas blood or urinelevels of BPA reflect exposures that occurred just hours ago,most health outcomes of interest are chronic conditions thattake years or even decades to develop.These considerations were used to assess the strengthof evidence from each study included in the current review.The studies received one point for fulfilling each of thefollowing criteria: (1) longitudinal data collection (e.g. cohortdesign); (2) use of urinary measures of BPA rather than serummeasures; and (3) evaluation of two or more samplescollected over time. Thus, the total number of possiblepoints ranged from 0 to 3. Evaluation of study results and feasibility of meta-analysis Qualitatively, all study results were categorized as ‘‘positive’’if the measures of association were in the hypothesizeddirection and statistically significantly different from the nullwhen comparing the highest to the lowest exposure category,and if there was evidence of a significant trend. The result wasconsidered ‘‘null’’ if the associations were not statisticallysignificant, and ‘‘inverse’’ if the results were significant,but were opposite to the hypothesized direction. The result was‘‘mixed’’ if in the presence of several analyses, some of theresults were significant but others were not, and/or if category-specific estimates were not supported by the test for trend.The quantitative study results were also recorded andonce all relevant data were compiled, we attempted to dividethe entire body of the literature into reasonably homogenousgroups of studies in order to assess the feasibility of conducting a meta-analysis. For each group of studies,in order to conduct a meta-analysis, the individual studiesmust have (i) the same or similar exposure categorization(e.g. quantiles versus continuous; or if continuous, with versuswithout log-transformation), (ii) the same outcome (e.g. DMversus FG or MI versus any CVD), and (iii) the same orsimilar measure of association (e.g. risk [or odds] ratiosversus linear    -coefficients). We then assessed the feasibilityand appropriateness of a meta-analysis using current recom-mendations by the Cochrane Collaboration (Higgins andGreen, 2011) to determine if the reported results are suitablefor pooling. Results Overview of studies We identified 93 epidemiological studies reporting on theassociation between BPA and various health endpoints inhumans (Supplementary material). Of those, 45 studies metthe criteria for inclusion in the current review (Tables 1–3).Of the 45 studies, 20 (44%) were conducted in the US(Bhandari et al., 2013; Bloom et al., 2011; Carwile et al.,2011; Harley et al., 2013; Lang et al., 2008; Melzer et al.,2010; Mok-Lin et al., 2010; LaKind et al., 2012b;Padmanabhan et al., 2008; Shankar & Teppala, 2011, 2012;Shankar et al., 2012a,b; Silver et al., 2011; Teppala et al.,2012; Trasande et al., 2012; Wolff et al., 2007, 2008, 2010;Yolton et al., 2011), nine studies were conducted in China(Duan et al., 2013; Li et al., 2012, 2013; Ning et al., 2011;Wang et al., 2012a,b,c, 2013; Zhao et al., 2012), six in SouthKorea (Bae et al., 2012; Hong et al., 2009; Kim & Park, 2013;Kim et al., 2012; Yang et al., 2006, 2009), two in the UK (Melzer et al., 2012a,b), two in Sweden (Lind & Lind, 2011;Olse´n et al., 2012), two in Japan (Takeuchi et al., 2002, 2004)and one each in France (Fe´nichel et al., 2012), Italy (Gallowayet al., 2010), Taiwan (Chou et al., 2011), and Greece(Kandaraki et al., 2011). Not all studies represented inde-pendent data sources. Eleven US studies used data from theNational Health and Nutrition Examination Survey(NHANES), and all were based, at least in part, on the2003/2004 survey (i.e. some researchers pooled data from twoor more surveys, so for example, NHANES 2003/2008represents pooled data from the 2003/2004, 2005/2006, and2007/2008 surveys) .  Similarly, three Chinese studies (Li et al.,2012; Ning et al., 2011; Wang et al., 2012c) were based on thesame data as were both Swedish studies. All but four studies(Bae et al., 2012; Harley et al., 2012; Mok-Lin et al., 2010;Yolton et al., 2011) relied in a single measurement of BPAexposure. The following sections review the available litera-ture according to the main outcomes category: (1) indicatorsof obesity, (2) DM and measures of glucose metabolism, and(3) CVD and markers of cardiovascular health. In each of these three sections, we begin the review with the studies thatprovide the strongest evidence. Studies of obesity Table 1 and Figure 1 describe studies that evaluatedthe association between BPA and indicators of obesity.Nine studies (Bloom et al., 2011; Chou et al., 2011;Fe´nichel et al., 2012; Kandaraki et al., 2011; Kim et al., 4  J.S. LaKind et al.  Crit Rev Toxicol, Early Online: 1–30    C  r   i   t   i  c  a   l   R  e  v   i  e  w  s   i  n   T  o  x   i  c  o   l  o  g  y   D  o  w  n   l  o  a   d  e   d   f  r  o  m    i  n   f  o  r  m  a   h  e  a   l   t   h  c  a  r  e .  c  o  m    b  y   6   9 .   1   4   3 .   9   1 .   2   3   3  o  n   0   1   /   0   6   /   1   4   F  o  r  p  e  r  s  o  n  a   l  u  s  e  o  n   l  y .  Table 1. Summary of studies evaluating the association between BPA and indicators of obesity. Reference Study population; country Design BPA exposure characterization Outcome(s) Results BPA concentrationsBhandari et al.(2013)2200 6–18 year old participantsin 2003/2008 NHANES,pooled in a single analysis;USCross-sectional One-time total (free and con- jugated) urinary BPA; spotsamples; quartiles; log-transformed continuousObesity defined as BMI  95th%ile for age and genderBMI, mean change (95% CI):Q1: ref Q2: 0.82 (0.19–1.45)Q3: 0.52 (  0.19 to 1.23)Q4: 1.17 (0.50–1.84)  p -trend ¼ 0.0056log BPA: 0.30 (0.05–0.55)Obesity, OR (95% CI):Q1: ref Q2: 2.35 (1.56–3.53)Q3: 1.78 (1.13–2.79)Q4: 2.55 (1.65–3.95)  p -trend ¼ 0.0022log BPA: 1.25 (1.09–1.43)Quartiles, ng/mL:Q1: 5 1.5Q2: 1.5–2.7Q3: 2.8–5.4Q4: 4 5.4Bloom et al. (2011) 44 women undergoing IVF; US Cross-sectional One-time (unconjugated) serumBPA; continuous; log-transformedBMI Correlation coefficient (  p ):   0.12 (0.44) ng/mL serum:Mean (SD): 7.22 (14.15)Min: 0.0025th %ile: 0.52Median: 2.5375th %ile: 6.31Max: 67.36Carwile et al.(2011)2747 participants in 2003/2006NHANES, pooled in asingle analysis; USCross-sectional One-time total (free and con- jugated) urinary BPA; spotsamples; quartilesObesity: BMI  30kg/m 2 Overweight: BMI25.0–29.9kg/m 2 Elevated WC:   102cm in menor   88cm in womenContinuous BMI and WCOverweight; OR (95% CI):Q1: 1.0 (ref)Q2: 1.66 (1.21–2.27)Q3: 1.26 (0.85–1.87)Q4: 1.31 (0.80–2.14)Obesity; OR (95% CI):Q1: 1.0 (ref)Q2: 1.85 (1.22–2.79)Q3: 1.60 (1.05–2.44)Q4: 1.76 (1.06–2.94)Elevated WC; OR (95% CI):Q1: 1.0 (ref)Q2: 1.62 (1.11–2.36)Q3: 1.39 (1.02–1.90)Q4: 1.58 (1.03–2.42)BMI,     (95% CI)Q1: 0 (ref)Q2: 1.48 (0.46–2.51)Q3: 1.69 (0.62–2.76)Q4: 1.56 (0.25–2.87)  p -trend ¼ 0.18WC,     (95% CI)*:Q1: 0 (ref)Q2: 3.98 (1.2–6.8)Q3: 3.64 (1.4–5.9)Q4: 3.93 (0.9–7.0)*Estimated from Figure 1 of Carwile et al. m g/g creatinine:GM ¼ 2.0525th %ile: 1.1875th %ile: 3.33Quartiles, ng/mL:Q1:   1.1Q2: 1.2–2.3Q3: 2.4–4.6Q4:   4.7Chou et al. (2011) 97* mother/infant pairs fromobstetrics and gynecologyclinic, Taiwan*  N   reported as 97 or 60Cross–sectional ana-lysis of birth cohortdataOne-time maternal blood BPA;sampled at time of cordblood sampling; binary:high versus low using geo-metric mean of 2.51ng/mLas cutoff; continuous;tertilesPregnant women BMI Spearman correlation coefficient:BPA, total:   0.08T1:   0.01T2:   0.21T3:   0.48**  p 5 0.05Maternal; ng/mL:range: 0.3–29.4GM: 2.5Mean  SD: 5.4  6.3Tertiles; ng/mL:T1: 0.3–3.38T2: 3.38–7.04T3 4 7.04 ( continued  ) D OI    :  1   0   . 3  1   0   9   /   1   0  4   0   8  4  4  4   .2   0  1   3   . 8   6   0   0   7   5   B  i    s   p h   e n o l   A  a n d   i    n d   i    c a t   or  s   5   Critical Reviews in Toxicology Downloaded from informahealthcare.com by 69.143.91.233 on 01/06/14For personal use only.
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