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Bisphenol A and phthalates are widely detected in human urine, blood, breast milk, and amniotic fluid. Both bisphenol A and phthalates have been suggested as playing a role in obesity epidemics. Exposure to these chemicals during fetal development, and its consequences should be concerning because they can cross the placenta. Thus, this study aimed to assess the association between prenatal exposure to bisphenol A and phthalates, and cord blood metabolic-related biomarkers. Maternal serum was used during the first trimester, to determine prenatal exposure to bisphenol A and phthalates. Levels of metabolic-related biomarkers in the cord blood were also determined. Linear regression models were applied to the 365 participants with both, exposure and biomarker assessments, adjusted for maternal age, pre-pregnancy body mass index, parity, education, and sex of the child. The level of bisphenol A was negatively associated with the leptin level (β = −0.06, 95% confidence interval [CI]: −0.11, −0.01), but was positively associated with the high-molecular-weight adiponectin level, with marginal significance (β = 0.03, 95%CI: 0.00, 0.06). The mono-isobutyl phthalate (MiBP), mono-n-butyl phthalate (MnBP), mono-(2-ethylhexyl) phthalate (MEHP), and summation of MEHP and MECPP to represent DEHP exposure (ΕDEHPm) levels were inversely associated with the leptin levels (β=−0.14, 95%CI: −0.27, −0.01; β = −0.12, 95%CI: −0.24, 0.00 with marginal significance; β=0.08, 95%CI: −0.14, −0.03; and β = −0.09, 95%CI: −0.16, −0.03, respectively). The present study provided some evidence that prenatal exposure to bisphenol A and certain phthalates may modify fetal adiponectin and leptin levels.Early pregnancy exposure to bisphenol A, DBP and DEHP was observed.Maternal bisphenol A level was negatively associated with cord leptin level.Early pregnancy exposure to DEHP and DBP may decrease cord leptin levels.