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All Journal Majalah Obstetri dan Ginekologi
Sri Sulistyowati
Department of Obstetrics and Gynecology, Medical Faculty of Sebelas Maret University, Dr. Moewardi Hospital, Solo, Surakarta
Health Professions Medicine & Pharmacology

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Placental micro- and nanoplastic contamination: A systematic review of eco-exposome pathways to preterm birth and neonatal outcomes I Nyoman Hariyasa Sanjaya; Wiku Andonotopo; Muhammad Adrianes Bachnas; Julian Dewantiningrum; Mochammad Besari Adi Pramono; Ryan Saktika Mulyana; Evert Solomon Pangkahila; Muhammad Ilham Aldika Akbar; Cut Meurah Yeni; Dudy Aldiansyah; Nuswil Bernolian; Anak Agung Gede Putra Wiradnyana; Adhi Pribadi; Sri Sulistyowati; Milan Stanojevic; Asim Kurjak
Majalah Obstetri & Ginekologi Vol. 34 No. 1 (2026): April
Publisher : Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/mog.V34I12026.70-83

Abstract

HIGHLIGHTS First comprehensive synthesis of human and mechanistic evidence linking placental micro- and nanoplastic (MNP) contamination to preterm birth and neonatal outcomes. Quantitative human studies demonstrate higher placental MNP burdens in preterm versus term pregnancies. Molecular pathways identified include oxidative stress, ferroptosis-driven syncytiotrophoblast senescence, trophoblast invasion impairment, inflammatory signaling, endocrine disruption, and epigenetic modifications. Clinical and policy relevance: Findings support the need for standardized biomonitoring, maternal exposure mitigation, and the integration of eco-exposome considerations into perinatal care.   ABSTRACT Objective: To systematically review emerging evidence on micro- and nanoplastic (MNP) contamination of the human placenta, explore molecular pathways underlying placental dysfunction, and evaluate associations with preterm birth and neonatal outcomes. Materials and Methods: Following PRISMA 2020 guidelines, literature searches (in PubMed, Web of Science, and Scopus) and grey sources were conducted through July 2025. Inclusion criteria comprised studies detecting MNPs in the human placenta or fetal compartments, mechanistic experiments using human placental models, or reviews addressing pregnancy outcomes. Methodological quality was assessed using AMSTAR-2, ROBIS, or the Newcastle–Ottawa Scale. Data were synthesized into three evidence domains: human biomonitoring, molecular pathways, and clinical implications. Results: Twenty studies met the inclusion criteria. MNPs were consistently detected in the human placenta, amniotic fluid, cord blood, and meconium, with higher burdens in preterm versus term placentae. Mechanistic studies demonstrated oxidative stress, ferroptosis-mediated syncytiotrophoblast senescence, impaired trophoblast invasion, inflammatory responses (IL-6, TNF-α, NLRP3 activation), endocrine disruption (altered ß-hCG and progesterone signaling), and epigenetic modifications. These pathways converge to impair nutrient and oxygen exchange and immune tolerance, increasing the risks of preterm birth, fetal growth restriction, low birth weight, and neonatal respiratory and metabolic vulnerability. Conclusion: Micro- and nanoplastic contamination of the human placenta is increasingly documented and biologically plausible as a contributor to preterm birth and neonatal morbidity. These findings support urgent investigation of exposure mitigation, standardized biomonitoring, and the integration of eco-exposome risks into perinatal clinical practice and policy.
Perinatal exposure to ultraprocessed foods and its impact on maternal gut dysbiosis, placental inflammation, and neonatal immune programming: A systematic review I Nyoman Hariyasa Sanjaya; Wiku Andonotopo; Muhammad Adrianes Bachnas; Julian Dewantiningrum; Mochammad Besari Adi Pramono; Ryan Saktika Mulyana; Evert Solomon Pangkahila; Muhammad Ilham Aldika Akbar; Cut Meurah Yeni; Dudy Aldiansyah; Nuswil Bernolian; Anak Agung Gede Putra Wiradnyana; Adhi Pribadi; Sri Sulistyowati; Milan Stanojevic; Asim Kurjak
Majalah Obstetri & Ginekologi Vol. 33 No. 3 (2025): December
Publisher : Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/mog.V33I32025.236-248

Abstract

HIGHLIGHTS Perinatal ultraprocessed food (UPF) exposure disrupts maternal gut microbiota composition, increasing pro‑inflammatory taxa and systemic endotoxemia. Placental immune activation and oxidative stress represent key mediators linking maternal diet to fetal immune and metabolic programming. Neonatal outcomes include altered regulatory T‑cell development, Th2 immune skewing, allergic sensitization, and early metabolic risk. Integrated dietary counseling, microbiota‑targeted interventions, and public health policies are urgently needed to mitigate transgenerational immune health risks.   ABSTRACT Objective: To synthesize and critically evaluate evidence linking perinatal exposure to ultraprocessed foods (UPFs) with maternal gut dysbiosis, placental inflammation, and neonatal immune programming, and to identify translational implications for perinatal care. Materials and Methods: A systematic narrative review was conducted following PRISMA 2020 guidelines, without PROSPERO registration. Literature searches of major databases (2000–March 2025) identified 1,845 records. After screening and eligibility assessment, 20 studies were included. Study quality was appraised using validated tools, and data were synthesized thematically into evidence domains covering maternal microbiota, inflammatory pathways, placental changes, and neonatal immune outcomes. Results: Maternal UPF consumption was associated with gut dysbiosis characterized by reduced microbial diversity, increased pro-inflammatory taxa, and systemic endotoxemia. Elevated inflammatory biomarkers including lipopolysaccharide, interleukin‑6, tumor necrosis factor‑a, and C‑reactive protein were frequently reported. Limited placental studies revealed increased innate immune activation and oxidative stress. Neonatal immune alterations included regulatory T cell suppression, T helper 2 skewing, increased allergic sensitization, and metabolic programming changes. Evidence strength was highest for maternal gut dysbiosis and immune programming but limited for direct placental mechanisms. Translational opportunities include dietary counseling, microbiota-targeted interventions, and public health strategies aimed at improving maternal diet quality. Conclusion: Perinatal exposure to UPFs adversely impacts the maternal gut–placenta–fetal immune axis. Integrated dietary interventions and population-level nutrition policies are urgently needed to mitigate downstream transgenerational immune risk.
Co-Authors Adhi Pribadi Anak Agung Gede Putra Wiradnyana Asim Kurjak Cut Meurah Yeni Dudy Aldiansyah Evert Solomon Pangkahila I Nyoman Hariyasa Sanjaya Julian Dewantiningrum Milan Stanojevic Mochammad Besari Adi Pramono Muhammad Adrianes Bachnas Muhammad Ilham Aldika Akbar Nuswil Bernolian Ryan Saktika Mulyana Wiku Andonotopo