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Environmentally relevant polyethylene terephthalate (PET) microplastics induce functional and oxidative alterations in sheep placental cells In vitro
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Scientists exposed sheep placenta cells to tiny plastic particles (from PET, the plastic used in water bottles) at levels animals might realistically encounter from eating contaminated feed. The smallest plastic bits, less than 20 microns, thinner than a human hair, damaged the cells' energy production, increased cell death, and impaired their normal function, even at very low doses. While this study was done in sheep, it raises concern about how the microplastics we all encounter daily might similarly affect the placenta during human pregnancy, a critical organ for supporting a developing baby.
ABSTRACT Ruminants are among the livestock most at risk of microplastics (MPs) exposure due to the ingestion of contaminated forage, particularly with polyethylene terephthalate (PET). Yet, despite this high risk, the potential effects of microplastics on reproductive function in these species remain largely unknown. Here, we studied how environmentally relevant PET-MPs impact placental functionality and cellular responses in an in vitro sheep model. First, virgin PET was mechanically processed through progressive milling and sieving to obtain two fractions of 20–50 μm or <20 μm, which were characterised in size, distribution, and crystal structure; then ovine term placental cells were exposed to both sizes of PET-MPs for 24-48 hours. MTT revealed that the smaller PET-MPs reduced cell viability even at low concentrations (1 μg/mL), whereas the larger fraction induced cytotoxicity only at 50 μg/mL. Placental cells diminished migratory capacity in the presence of smaller PET-MPs. Oxidative stress assessment further demonstrated a reduced ability to metabolize H 2 O 2 , along with a decrease in mitochondrial membrane potential, indicating compromised mitochondrial function; additionally, apoptosis was also slightly increased following exposure to the <20 μm PETs. Overall, our findings show that PET-MPs, particularly those below 20 μm, impair multiple functional and metabolic endpoints in ovine term placental cells, highlighting the risk to reproductive health in ruminants chronically exposed to microplastic-contaminated feed.
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Researchers exposed human brain blood vessel cells to PET plastic particles (the same plastic used in water bottles) at micro and nano sizes. After three days, the cells showed reduced energy production in their mitochondria, the powerhouses of the cell, but recovered by six days. While no oxidative stress or cell death was observed, the temporary disruption of brain cell energy production raises questions about what repeated or chronic exposure might do.
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Researchers exposed pregnant rats to polystyrene microplastics at concentrations realistic for human exposure and examined effects on the placenta. They found that the microplastics accumulated in placental tissue, caused oxidative stress, triggered cell death, and reduced the expression of proteins that maintain the placental barrier. The study provides the first evidence that realistic levels of microplastic exposure can compromise the protective barrier between mother and developing offspring.
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Researchers exposed human nasal cells to nanoplastics made from real PET water bottles and found that the particles were absorbed into cells and triggered oxidative stress. The nanoplastics also disrupted mitochondrial function and activated the cell's autophagy cleanup pathway. Since the nose is the first barrier encountered when breathing in airborne plastic particles, these findings suggest that nasal tissues may be particularly vulnerable to nanoplastic exposure.
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