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      Maternal Urinary Bisphenol A during Pregnancy and Maternal and Neonatal Thyroid Function in the CHAMACOS Study

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          Abstract

          Background: Bisphenol A (BPA) is widely used in the manufacture of polycarbonate plastic bottles, food and beverage can linings, thermal receipts, and dental sealants. Animal and human studies suggest that BPA may disrupt thyroid function. Although thyroid hormones play a determinant role in human growth and brain development, no studies have investigated relations between BPA exposure and thyroid function in pregnant women or neonates.

          Objective: Our goal was to evaluate whether exposure to BPA during pregnancy is related to thyroid hormone levels in pregnant women and neonates.

          Methods: We measured BPA concentration in urine samples collected during the first and second half of pregnancy in 476 women participating in the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study. We also measured free thyroxine (T 4), total T 4, and thyroid-stimulating hormone (TSH) in women during pregnancy, and TSH in neonates.

          Results: Associations between the average of the two BPA measurements and maternal thyroid hormone levels were not statistically significant. Of the two BPA measurements, only the one taken closest in time to the TH measurement was significantly associated with a reduction in total T 4 (β = –0.13 µg/dL per log 2 unit; 95% CI: –0.25, 0.00). The average of the maternal BPA concentrations was associated with reduced TSH in boys (–9.9% per log 2 unit; 95% CI: –15.9%, –3.5%) but not in girls. Among boys, the relation was stronger when BPA was measured in the third trimester of pregnancy and decreased with time between BPA and TH measurements.

          Conclusion: Results suggest that exposure to BPA during pregnancy is related to reduced total T 4 in pregnant women and decreased TSH in male neonates. Findings may have implications for fetal and neonatal development.

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          Most cited references45

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          A structural approach to selection bias.

          The term "selection bias" encompasses various biases in epidemiology. We describe examples of selection bias in case-control studies (eg, inappropriate selection of controls) and cohort studies (eg, informative censoring). We argue that the causal structure underlying the bias in each example is essentially the same: conditioning on a common effect of 2 variables, one of which is either exposure or a cause of exposure and the other is either the outcome or a cause of the outcome. This structure is shared by other biases (eg, adjustment for variables affected by prior exposure). A structural classification of bias distinguishes between biases resulting from conditioning on common effects ("selection bias") and those resulting from the existence of common causes of exposure and outcome ("confounding"). This classification also leads to a unified approach to adjust for selection bias.
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            Epidemiologic Evaluation of Measurement Data in the Presence of Detection Limits

            Quantitative measurements of environmental factors greatly improve the quality of epidemiologic studies but can pose challenges because of the presence of upper or lower detection limits or interfering compounds, which do not allow for precise measured values. We consider the regression of an environmental measurement (dependent variable) on several covariates (independent variables). Various strategies are commonly employed to impute values for interval-measured data, including assignment of one-half the detection limit to nondetected values or of “fill-in” values randomly selected from an appropriate distribution. On the basis of a limited simulation study, we found that the former approach can be biased unless the percentage of measurements below detection limits is small (5–10%). The fill-in approach generally produces unbiased parameter estimates but may produce biased variance estimates and thereby distort inference when 30% or more of the data are below detection limits. Truncated data methods (e.g., Tobit regression) and multiple imputation offer two unbiased approaches for analyzing measurement data with detection limits. If interest resides solely on regression parameters, then Tobit regression can be used. If individualized values for measurements below detection limits are needed for additional analysis, such as relative risk regression or graphical display, then multiple imputation produces unbiased estimates and nominal confidence intervals unless the proportion of missing data is extreme. We illustrate various approaches using measurements of pesticide residues in carpet dust in control subjects from a case–control study of non-Hodgkin lymphoma.
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              Parent bisphenol A accumulation in the human maternal-fetal-placental unit.

              Bisphenol A (BPA), an endocrine disruptor, is employed in the manufacture of a wide range of consumer products. The suggestion that BPA, at amounts to which we are exposed, alters the reproductive organs of developing rodents has caused concern. At present, no information exists concerning the exposure of human pregnant women and their fetuses to BPA. We therefore investigated blood samples from mothers (n = 37) between weeks 32 and 41 of gestation. Afer the births, we also analyzed placental tissue and umbilical cord blood from the same subjects. We developed a novel chemical derivatization-gas chromatography/mass spectrometry method to analyze parent BPA at concentrations < 1 micro g/mL in plasma and tissues. Concentrations of BPA ranged from 0.3 to 18.9 ng/mL (median = 3.1 ng/mL) in maternal plasma, from 0.2 to 9.2 ng/mL (median = 2.3 ng/mL) in fetal plasma, and from 1.0 to 104.9 ng/g (median = 12.7 ng/g) in placental tissue. BPA blood concentrations were higher in male than in female fetuses. Here we demonstrate parent BPA in pregnant women and their fetuses. Exposure levels of parent BPA were found within a range typical of those used in recent animal studies and were shown to be toxic to reproductive organs of male and female offspring. We suggest that the range of BPA concentrations we measured may be related to sex differences in metabolization of parent BPA or variable maternal use of consumer products leaching BPA.
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                Author and article information

                Journal
                Environ Health Perspect
                Environ. Health Perspect
                EHP
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                1552-9924
                04 October 2012
                January 2013
                : 121
                : 1
                : 138-144
                Affiliations
                [1 ]Center for Children’s Environmental Health Research, School of Public Health, University of California, Berkeley, Berkeley, California, USA
                [2 ]Division for Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA
                Author notes
                Address correspondence to J. Chevrier, Center for Environmental Research and Children’s Health (CERCH), School of Public Health, University of California, Berkeley, 1995 University Ave., Suite 265, Berkeley, CA 94704-7392 USA. Telephone: (510) 642-8917. Fax: (510) 642-9083. E-mail: chevrier@ 123456berkeley.edu
                Article
                ehp.1205092
                10.1289/ehp.1205092
                3553432
                23052180
                4a34007b-8163-42bf-b340-a5add3e84ae7
                Copyright @ 2013

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, properly cited.

                History
                : 13 February 2012
                : 25 September 2012
                Categories
                Research

                Public health
                bisphenol a,endocrine disruption,neonates,pregnancy,thyroid hormone
                Public health
                bisphenol a, endocrine disruption, neonates, pregnancy, thyroid hormone

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