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Micro- and nanoplastic (MNPs) exposure at single-cell resolution impaired placental function and cellular dynamics
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Researchers performed single-cell transcriptomic analysis of placentas from pregnant women exposed to micro- and nanoplastics, finding that MNP exposure altered trophoblast, macrophage, and fibroblast subpopulations, suggesting impaired placental function through disruption of cell communication and immune regulation.
The placenta is crucial for a successful pregnancy, acting as a protective barrier for fetal health. Growing evidence suggests that pregnant women are widely exposed to micro- and nanoplastics (MNPs), which have been implicated in placental dysfunction associated with pregnancy complications and adverse offspring outcomes. To investigate this, we characterized MNPs-induced placental cellular dynamics at the single-cell level. Our analysis of placental tissue identified 14 major cell types, including trophoblasts and immune cells. Comparative transcriptomics between control and MNPs-exposed groups revealed significant alterations in subpopulations of trophoblasts, macrophages, and fibroblasts, indicating an adaptive response to toxic stress. Specifically, we observed a marked upregulation of genes related to endoplasmic reticulum stress and xenobiotic clearance in trophoblasts, and of ECM remodeling pathways in fibroblasts. This was supported by the integration of metabolomic and proteomic data, which detailed the accompanying molecular cascades. We propose that while these processes represent an attempt to maintain placental homeostasis, prolonged or high-level MNP exposure may overwhelm such compensatory mechanisms, ultimately leading to dysfunction. Consequently, our study provides a foundational resource for understanding the cellular mechanisms of MNP-induced placental toxicity and establishes a basis for future research into protective strategies against environmental reproductive toxicants.
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Researchers systematically reviewed 20 studies detecting micro- and nanoplastics in human placental tissue, cord blood, and amniotic fluid, finding higher MNP burdens in preterm versus term placentae and identifying oxidative stress, ferroptosis, impaired trophoblast invasion, and inflammatory signaling as converging molecular pathways linking placental MNP contamination to preterm birth and neonatal morbidity.
Multi-omics integration reveals human placental molecular signatures associated with microplastics exposure
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Scientists studied human placenta tissue and found that higher levels of microplastics were linked to changes in genes, proteins, and metabolism, including signs of immune stress, oxidative damage, and problems with mitochondria (the energy-producing parts of cells). This is early evidence that microplastics may disrupt how the placenta functions, which matters because a healthy placenta is essential for delivering nutrients and oxygen to a developing baby. More research is needed to confirm whether these changes actually harm pregnancy outcomes, but the findings raise real questions about how everyday plastic exposure could affect maternal and fetal health
Placental Micro- and Nanoplastic Contamination: A Systematic Review of Eco-Exposome Pathways to Preterm Birth and Neonatal Outcomes
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This systematic review examined evidence that micro- and nanoplastics have been found in human placentas and may be linked to preterm birth. The particles appear to cause inflammation, oxidative stress, and disruption of placental function through multiple molecular pathways, raising concerns about the impact of plastic pollution on pregnancy outcomes and newborn health.
Nano-scale dangers: Unravelling the impact of nanoplastics on human trophoblast invasion
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Researchers exposed human trophoblast cells — which form the placenta — to 40 nm and 200 nm polystyrene nanoparticles and found that the smaller particles reduced expression of invasion-related proteins (integrins, N-cadherin, matrix metalloproteinase-2) and impaired cell migration, suggesting nanoplastics may interfere with early placental development.
Gestational exposure to micro- and nanoplastics leads to poor pregnancy outcomes by impairing placental trophoblast syncytialization
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Researchers found that exposing pregnant mice to micro- and nanoplastics led to increased embryo loss, reduced embryonic weight, and smaller placentas. The plastic particles impaired a critical process called syncytialization, where placental cells fuse together to form a functional barrier, by activating a stress-response signaling pathway. The study suggests that prenatal microplastic exposure could disrupt placental development and contribute to poor pregnancy outcomes.
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