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Effects of Endocrine Disrupting Chemicals on Fetal Weight: Exposure Monitoring Among Mothers with Gestational Diabetes Mellitus and Their Fetuses
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Researchers measured exposure to endocrine-disrupting chemicals — BPA, MEP, and PFOA — in mothers with gestational diabetes and their fetuses, finding that GDM-related dietary changes reduced fetal BPA transfer but that higher maternal BPA levels were still positively associated with fetal birthweight, indicating persistent metabolic vulnerability.
Gestational diabetes mellitus (GDM) requires lifestyle changes that may alter exposure to endocrine-disrupting chemicals (EDCs). This study aimed to assess maternal and fetal exposure to EDCs-including bisphenol-A (BPA), monoethyl phthalate (MEP), and perfluorooctanoic acid (PFOA)-during the COVID-19 pandemic and to evaluate their association with fetal birthweight. Maternal urine (second and third trimester) and paired cord blood samples were analyzed from 58 GDM and 118 non-GDM pregnancies using UPLC-MS/MS. Significant correlations were found between maternal urine and cord blood levels of BPA and MEP. Cord blood BPA levels were significantly lower in GDM mothers (0.35 vs. 0.72 μg/L, p < 0.05), suggesting reduced exposure due to dietary interventions. However, maternal urinary BPA levels in GDM pregnancies were positively associated with fetal birthweight (β = 2.69, p < 0.05), indicating increased susceptibility to obesogenic effects. PFOA was present in all cord blood but only 41% of maternal urine samples. These findings underscore the dual impact of GDM-related lifestyle changes: reduced EDC transfer to the fetus, yet persistent metabolic vulnerability.
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The relationship between emerging contaminants and gestational diabetes mellitus: a review
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Researchers reviewed evidence linking exposure to emerging contaminants — including microplastics, PFAS, and phthalates — to gestational diabetes mellitus, finding that endocrine-disrupting chemicals may impair insulin sensitivity and glucose regulation during pregnancy through multiple hormonal pathways.
Prenatal Dietary Exposure to Endocrine Disruptors and Its Lasting Impact on Offspring Health
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This narrative review examines how prenatal dietary exposure to endocrine-disrupting chemicals (EDCs) — including bisphenols, phthalates, and pesticides — can cross the placenta and alter fetal hormonal programming, with lasting effects on children's immune, metabolic, neurological, and reproductive health. The review highlights epigenetic reprogramming and oxidative stress as key mechanisms and calls for targeted interventions to reduce maternal EDC exposure.
Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus
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This review synthesizes epidemiological, animal, and cellular evidence linking bisphenols and phthalates from plastic pollution to altered glucose regulation and diabetes mellitus risk. Both compounds disrupt β-cell physiology through changes in insulin secretion, mitochondrial function, and gene expression, with epidemiological studies confirming associations with diabetes prevalence.
Endocrine disruptor load in pregnancy and the thyroid–glucose axis: A mixture-aware systematic review and meta-analysis with mechanistic integration and a conceptual framework for the Pregnancy Disruptor Exposure Score
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This review of 39 studies found that pregnant women exposed to common chemicals like plastics-related compounds (phthalates, bisphenols), PFAS ("forever chemicals"), and metals tend to show disrupted thyroid function and blood sugar control together—not just one or the other—and the effects looked stronger when researchers studied these chemicals as real-world mixtures rather than one at a time. Since thyroid and blood sugar regulation are both critical for a healthy pregnancy and baby's development, this suggests everyday chemical exposures may compound each other's effects, though evidence on newer concerns like microplastics is
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Endocrine-disrupting chemicals found in plastics—including bisphenols, phthalates, and PFAS—act as obesogens by interfering with adipogenesis pathways, gut microbiota, and hormonal appetite regulation, contributing to the global rise in obesity and metabolic syndrome. This review reinforces that plastic-associated chemical exposures carry systemic metabolic health risks beyond physical microplastic particle ingestion.
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