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Effects of different micro- and nanoplastic polymers on steroidogenesis in a feto-placental in vitro model
Summary
Scientists built a lab model of the placenta to test what happens when tiny plastic particles—like those found in bottled water and food packaging—come into contact with it. They found that several common plastic types can cross the placental barrier and disrupt hormone production, including hormones important for a healthy pregnancy. While this is a lab study (not proof of harm in real pregnancies), it raises real questions about whether the microplastics we're all exposed to daily could affect babies during development.
BACKGROUND: Micro- and nanoplastics (MNPs) have been detected in human placenta, though their impact on steroidogenesis during pregnancy remains unknown. Existing in vitro placental models are limited in capturing both barrier function and maternal-fetal steroidogenic interactions. METHOD: A Transwell tri-culture model was developed, consisting of BeWo b30 (apical) and HUVEC cells on the insert and H295R cells at the bottom (basolateral). Fluorescently-labelled (F) polymers were added apically: commercially PS (50 nm, 200 nm and 1000 nm) and custom-made PMMA (340-740 nm), PVC (2140-5700 nm), PA6,6 (280-640 nm) and PET (1460-5200 nm). Translocation from apical to basolateral side was measured after 72 h, and uptake assessed by confocal microscopy. Mitochondrial activity, steroid hormone levels and gene expression of steroidogenic enzymes were also evaluated. RESULTS: F-PS translocation was size-dependent, with the highest observed for F-PS50 nm (4.4%). F-PMMA showed the highest translocation (10.7%), followed by F-PVC (6.5%) and F-PET (4.2%), while F-PA could not be reliably quantified. In the tri-culture, 19 steroid hormones were detected apically and 18 basolaterally. PS1000 nm and PS50 nm (10 μg/mL) decreased 17-hydroxy-dihydroprogesterone (17-OH-DHP) by 36% and 29%, respectively. PET, PMMA, PA6,6, and PVC (10 μg/mL) reduced apical etiocholanolone by 23-25%. PET (1 μg/mL) reduced it by 22%. PS1000 nm (1 μg/mL) lowered apical 17β-estradiol by 14%. CYP17 expression decreased after PS200 nm and PS1000 nm exposure; other polymers showed no effect. CONCLUSIONS: This in vitro model demonstrates that MNPs cross the placental barrier and alter steroidogenesis, raising concerns about their potential endocrine-disrupting effects during pregnancy.