0
Article Tier 2 Environmental Sources Human Health Effects Policy & Risk Reproductive & Development Sign in to save

Polystyrene microplastics and di-2-ethylhexyl phthalate co-exposure: Implications for female reproductive health

Environmental Science and Ecotechnology 2024 42 citations

AI summary Read the abstract

When rats were exposed to both polystyrene microplastics and the common plasticizer DEHP together, they developed significantly more ovarian damage -- including increased cystic follicles, fibrosis, and hormone imbalance -- than from either substance alone. The combined exposure activated a specific signaling pathway (TGF-beta1/Smad3) linked to ovarian fibrosis and may increase the risk of polycystic ovary syndrome, raising concerns about real-world co-exposure in women.

Polymers
Body Systems
Models

Microplastics and phthalates are prevalent and emerging pollutants that pose a potential impact on human health. Previous studies suggest that both microplastics and phthalates can adversely affect the reproductive systems of humans and mammals. However, the combined impact of these pollutants on the female reproductive system remains unclear. Here we show the impacts of exposure to polystyrene microplastics (PS-MPs) and di-2-ethylhexyl phthalate (DEHP) on female Sprague-Dawley rats' reproductive systems. We find that co-exposure to PS-MPs and DEHP results in a marked increase in cystic and atretic follicles, oxidative stress, fibrosis, and dysregulation of serum sex hormone homeostasis in the ovaries of the rats. Proteomic analysis identified differentially expressed proteins that were predominantly enriched in signaling pathways related to fatty acid metabolism and tight junctions, regulated by transforming growth factor β1 (TGF-β1). We further confirm that co-exposure to DEHP and PS-MPs activates the TGF-β1/Smad3 signaling pathway, and inhibiting this pathway alleviates oxidative stress, hormonal dysregulation, and ovarian fibrosis. These results indicate that exposure to the combination of microplastics and phthalates leads to a significant increase in atretic follicles and may increase the risk of polycystic ovary syndrome (PCOS). Our study provides new insights into the reproductive toxicity effects of microplastics and DEHP exposure on female mammals, highlighting the potential link between environmental pollutants and the occurrence of PCOS. These findings highlight the need for comprehensive assessments of the reproductive health risks posed by microplastic pollution to women and contribute to the scientific basis for evaluating such risks.

More Papers Like This

Article Tier 2

Polystyrene-microplastics and DEHP co-exposure induced DNA damage, cell cycle arrest and necroptosis of ovarian granulosa cells in mice by promoting ROS production

AI summary Read the abstract

Researchers found that co-exposure to polystyrene microplastics and DEHP (a common plastic additive) caused more damage to mouse ovarian cells than either pollutant alone, triggering excessive oxidative stress that led to DNA damage, cell cycle arrest, and cell death. These findings suggest that microplastics combined with their chemical additives may pose a synergistic threat to female reproductive health.

Article Tier 2

Polystyrene nanoparticles enhance the adverse effects of di-(2-ethylhexyl) phthalate on male reproductive system in mice

AI summary Read the abstract

Researchers investigated the combined reproductive toxicity of polystyrene nanoparticles and the plasticizer DEHP in male mice over 35 days. The study found that co-exposure to nanoparticles and DEHP produced enhanced adverse effects on sperm quality and testicular tissue compared to either substance alone, suggesting nanoplastics may amplify the endocrine-disrupting effects of plasticizers.

Article Tier 2

Co-exposure to polystyrene microplastics and lead aggravated ovarian toxicity in female mice via the PERK/eIF2α signaling pathway

AI summary Read the abstract

Researchers found that combined exposure to polystyrene microplastics and lead caused more severe ovarian damage in female mice than either pollutant alone. The study showed that co-exposure activated endoplasmic reticulum stress through the PERK/eIF2-alpha signaling pathway, leading to increased cell death in ovarian tissue, but these effects could be alleviated with stress inhibitor or antioxidant treatment.

Article Tier 2

Co-exposure to polystyrene nanoplastics and di(2-ethylhexyl) phthalate: Effects and mechanistic insights into hepatic lipid metabolism in mice

AI summary Read the abstract

In mice, exposure to tiny plastic particles (nanoplastics) combined with a plastic chemical called DEHP caused more liver fat buildup and liver damage than either alone. Tests in liver cells showed this involved a specific stress pathway, and blocking that pathway reduced the fat buildup caused by the combined exposure.

Article Tier 2

Maternal co-exposure to polystyrene microplastics and DEHP impairs thyroid function in adult rat offspring

AI summary Read the abstract

When pregnant rats were exposed to microplastics and DEHP (a common plastic-softening chemical found in food packaging and personal care products) together, their offspring showed worse thyroid problems than exposure to either substance alone, including disrupted thyroid hormone levels and changes in gut bacteria linked to thyroid function. This matters because it suggests real-world plastic pollution, which almost always involves multiple chemicals mixing together, may pose bigger risks to developing babies than studies testing one chemical at a time have shown, and effects may differ between males and females.

Research digests by email

When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.

Email me about

Share this paper