Exploring the relationships between prenatal phthalate exposure and neonatal thyroid function: A prospective cohort study
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Updated: May 16, 2025

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Zhaoying Xiong1, Gaga Mahai1, Aizhen Wang2
1School of Environmental Science and Engineering, Hainan University, Haikou 570208, China; Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Abstract:
Previous studies have reported the thyroid disruptive effects of prenatal phthalate exposure; however, evidence on the impact of prenatal phthalate alternative exposure on neonatal thyroid function is still limited. We aimed to investigate the associations between prenatal exposure to phthalates and phthalate alternatives (individually and as a mixture) and neonatal thyroid function, based on longitudinal data from the Wuhan Healthy Baby Cohort Study. We measured concentrations of phthalate and phthalate alternative metabolites (mPAEs) in urine samples, provided by 1202 mothers at three trimesters, and neonatal thyroid stimulating hormone (TSH) levels in heel-prick blood samples. The results suggested higher levels of some mPAEs, particularly monomethyl phthalate (MMP) and mono-2-ethyl-5-Carboxypentyl terephthalate (MECPTP), were associated with increased neonatal TSH. Interquartile range (IQR) increases of mPAEs were associated with an increase in TSH ranging from 8.21 % to 13.5 %, and the associations were more likely to occur in girls. Quantiles g-computation models revealed that joint exposure to phthalates was significantly associated with increased TSH in three trimesters, MEOHP and MMP were the most predominant contributors to the positive associations. The research results imply that prenatal phthalate exposure may interfere with thyroid hormone homeostasis, which warrants further replication.
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