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Exposure to microplastics during pregnancy and fetal liver function
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Researchers detected microplastics in the placentas of nearly 90% of over 1,000 pregnant women and found that higher placental microplastic levels were linked to elevated liver enzymes in umbilical cord blood. This suggests that microplastics crossing the placenta may affect fetal liver function before birth, raising concerns about the health effects of prenatal plastic exposure.
Emerging evidence suggests that in-utero exposure to microplastics (MPs) may have physiological consequences for fetal development, yet human data remain limited. This study investigates the association between placental microplastic exposure and umbilical liver enzyme levels as markers of fetal hepatic function. A prospective cohort study was conducted in Shenyang, China, including 1057 pregnant women. Placental microplastic quantification was performed using LD-IR chemical imaging, targeting polyvinyl chloride (PVC), polypropylene (PP), and polybutylene succinate (PBS). Umbilical cord blood was collected at delivery, and liver enzyme levels alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT) were analyzed using biochemical assays. Associations were assessed via multivariable regression models adjusting for maternal and socioeconomic confounders. Mixture effects were examined using Bayesian Kernel Machine Regression (BKMR) and quantile g-computation (g-comp). Placental microplastics were detected in most samples (PVC: 88.4 %, PP: 88.8 %, PBS: 89.1 %), with a median total MPs of 12 particles per 10 g of tissue (IQR: 8). Higher placental PVC particles was significantly associated with increased ALP levels (β = 28.07, 95 % CI: 6.65-49.49, p = 0.01). PP exposure correlated positively with ALT (β = 0.63, 95 % CI: 0.01-1.25, p = 0.05) and AST (β = 3.42, 95 % CI: 0.87-5.96, p = 0.01). Both PP and total MPs burden exhibited strong associations with GGT elevation (p < 0.01). Mixture analysis revealed significant overall effects on ALP (β = 30.04, 95 % CI: 11.15-48.92, p < 0.01), AST (β = 7.30, 95 % CI: 4.33-10.27, p < 0.01), and GGT (β = 22.98, 95 % CI: 7.49-38.46, p < 0.01), with ALT showing a suggestive positive trend. Our findings provide novel evidence that placental MP exposure is associated with altered fetal liver enzyme levels, particularly ALP, AST, and GGT, indicating potential impacts on hepatic function. These results underscore the need for further investigation into the underlying mechanisms and long-term health implications of prenatal MP exposure.
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