Association of umbilical cord blood phthalate levels with neonatal growth parameters in term pregnancies

Prenatal exposure to endocrine-disrupting chemicals (EDCs), including di(2-ethylhexyl) phthalate (DEHP) and bisphenol A (BPA), has been associated with altered fetal growth. Umbilical cord blood provides a direct indicator of fetal exposure and may offer advantages over maternal urinary biomarkers. To examine the associations between cord blood concentrations of DEHP metabolites and BPA and neonatal anthropometric measures in term pregnancies. This cross-sectional study included 84 singleton term mother–infant pairs. Cord blood DEHP metabolites and BPA were quantified using liquid chromatography–tandem mass spectrometry (LC–MS/MS). Birth weight, length, and head circumference were measured at delivery and expressed as sex- and gestational age–adjusted z-scores. Multivariable linear regression models adjusted for maternal age, pre-pregnancy body mass index, parity, smoking status, infant sex, gestational age and maternal occupation were applied. Exposure–response patterns were further explored using quartile-based analyses and restricted cubic spline models. DEHP metabolites were detected in 92.0% and BPA in 90.4% of cord blood samples. Higher ΣDEHP concentrations were associated with lower birth weight (β = − 0.24 SD), birth length (β = − 0.15 SD), and head circumference (β = − 0.11 SD; all p < 0.05). BPA exhibited a non-linear, threshold-type association, as confirmed by restricted cubic spline analyses, with lower birth weight and length observed only at higher exposure levels. No significant sex-specific interactions were identified. Higher prenatal DEHP exposure, assessed using umbilical cord blood, was associated with modest yet consistent differences in neonatal growth parameters among term infants, whereas BPA demonstrated weaker and non-linear associations. These findings should be interpreted within an observational framework and do not imply causality. These findings underscore the relevance of prenatal exposure to common endocrine-disrupting chemicals for early human growth.