Yao Chen1, Yingcan Wang2, Guodong Ding3, Ying Tian4, Zhijun Zhou5, Xiumin Wang6, Lixiao Shen7, Hong Huang8. 1. MOE and Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Endocrinology and Genetic Diseases, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: chen-yao@scmc.com.cn. 2. MOE and Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Neonatology, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: wangyingcan@xinhuamed.com.cn. 3. MOE and Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Pediatrics, Shanghai East Hospital, Tong Ji University School of Medicine, Shanghai, China. 4. Department of Environmental Health, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China; MOE and Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: tianmiejp@sjtu.edu.cn. 5. School of Public Health/MOE Key Lab for Public Health Safety, Fudan University, Shanghai, China. Electronic address: zjzhou@fudan.edu.cn. 6. Department of Endocrinology and Genetic Diseases, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: wangxiumin@scmc.com.cn. 7. Department of Children Health Care, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: shenlixiao@xinhuamed.com.cn. 8. MOE and Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Environmental Health, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: huanghong@smhb.gov.cn.
Abstract
BACKGROUND: Bisphenol A (BPA) is a well-known and widely used endocrine disrupter, but data on its association with childhood reproductive development are limited. OBJECTIVES: We investigated the possible relationship between exposure to BPA and idiopathic central precocious puberty (ICPP) in school-aged girls. METHODS: We conducted a 1:1 matched case-control study in Shanghai, China, between July 2011 and September 2012. This study included 136 school-aged (6 to 9 years old) girls diagnosed with ICPP and 136 controls matched for age and body mass index (BMI). We measured the urinary BPA concentrations of all the girls and examined the association with odds of having ICPP. Laboratory examinations including serum estradiol (E2) levels, basal and gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels, bone ages (BA), and uterine and ovarian sizes were conducted in the ICPP girls. RESULTS: Median concentrations of urinary BPA in the ICPP and control groups were 6.35 and 1.17 μg/g creatinine (Cr), respectively (p < 0.001). After adjustment for confounders, compared to those with the lowest concentrations of BPA, the highest concentrations were associated with a 9.08-fold increased odds of having ICPP [odds ratio (OR) = 9.08, (95% confidence interval (CI): 2.83-29.15)]. In the ICPP group, modest negative correlation was present between urinary BPA concentrations (μg/g Cr) and peak FSH levels [β = -0.090 (95% CI: -0.178, -0.003), p = 0.044]. CONCLUSIONS: Our findings suggest that BPA exposure is associated with increased odds of having ICPP in school-aged girls, and the potential mechanism may be attributable to the relatively low FSH levels.
BACKGROUND:Bisphenol A (BPA) is a well-known and widely used endocrine disrupter, but data on its association with childhood reproductive development are limited. OBJECTIVES: We investigated the possible relationship between exposure to BPA and idiopathic central precocious puberty (ICPP) in school-aged girls. METHODS: We conducted a 1:1 matched case-control study in Shanghai, China, between July 2011 and September 2012. This study included 136 school-aged (6 to 9 years old) girls diagnosed with ICPP and 136 controls matched for age and body mass index (BMI). We measured the urinary BPA concentrations of all the girls and examined the association with odds of having ICPP. Laboratory examinations including serum estradiol (E2) levels, basal and gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels, bone ages (BA), and uterine and ovarian sizes were conducted in the ICPPgirls. RESULTS: Median concentrations of urinary BPA in the ICPP and control groups were 6.35 and 1.17 μg/g creatinine (Cr), respectively (p < 0.001). After adjustment for confounders, compared to those with the lowest concentrations of BPA, the highest concentrations were associated with a 9.08-fold increased odds of having ICPP [odds ratio (OR) = 9.08, (95% confidence interval (CI): 2.83-29.15)]. In the ICPP group, modest negative correlation was present between urinary BPA concentrations (μg/g Cr) and peak FSH levels [β = -0.090 (95% CI: -0.178, -0.003), p = 0.044]. CONCLUSIONS: Our findings suggest that BPA exposure is associated with increased odds of having ICPP in school-aged girls, and the potential mechanism may be attributable to the relatively low FSH levels.