Bisphenol A (BPA) is an endocrine disruptor that in animal studies can bind to the thyroid hormone receptor and affect thyroid function. Relevant epidemiologic studies are limited and results are inconsistent. We explored the relationship between urinary BPA and thyroid function in a Chinese population.
The study population included 3394 subjects age 40 years or older who were enrolled in a population-based study from Songnan Community, Baoshan District, Shanghai, China, from June through August 2009. We analyzed the association between urinary BPA and thyroid function using multivariate linear regression. Participants were further divided according to thyroid function status, and logistic regression was applied to determine the relationship between urinary BPA and thyroid function.
Each one-quartile increase in BPA was related to an increase of 0.068 pmol/l (95% confidence interval = 0.065– 0.071) in free triiodothyronine and a 0.084 μIU/ml decline (−0.099 to −0.069) in thyroid-stimulating hormone (TSH) in men. For women, there was a 0.10 pmol/l (0.09 to 0.11) increase in free triiodothyronine and a 0.13 μIU/ml decline (−0.14 to −0.11) in TSH. High urinary BPA level was associated with increased thyroid function (adjusted odds ratio= 1.71 [1.26 to 2.32]).
Our results support previous reports of associations between BPA exposure and altered thyroid hormones in animal models and epidemiologic studies. Because our study is cross-sectional, no causal relationships can be established.
From the aKey Laboratory for Endocrine and Metabolic Diseases of Ministry of Health, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, E-Institute of Shanghai Universities, Shanghai, China; bShanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolism, Rui-jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; cJohns Hopkins University School of Medicine, Baltimore, MD.
Submitted 27 March 2012; accepted 30 November 2012; posted 18 January 2013.
Supported by the grants from the Key Laboratory for Endocrine and Metabolic Diseases of Ministry of Health [1994DP131044], the Sector Funds of Ministry of Health , the National Key New Drug Creation and Manufacturing Program of Ministry of Science and Technology [2012ZX09303006-001], National Nature Science Foundation of China [81170739, 81170719, 81222008], Science and Technology Commission of Shanghai Municipality [11DJ1400200], 863 Project [2012AA02A509], and Shanghai New Excellent Youth Program [XYQ2011009].
T.W. and J.L. contributed equally to this work.
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Correspondence: Guang Ning, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Department of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Rui-Jin 2nd Road, Shanghai 200025, China. E-mail: firstname.lastname@example.org.