There are studies on microplastic toxicity already. These are linked directly in the OP article:
Even at low concentrations (1–30 µg/ml), photoaged microspheres at 1 and 5 µm in diameter exerted more pronounced biological responses in the A549 cells than was caused by pristine microspheres. High-content imaging analysis revealed S and G2 cell cycle accumulation and morphological changes, which were also more pronounced in A549 cells treated with photoaged microspheres, and further influenced by the size, dose, and time of exposures. Polystyrene microspheres reduced monolayer barrier integrity and slowed regrowth in a wound healing assay in a manner dependent on dose, photoaging, and size of the microsphere. UV-photoaging generally enhanced the toxicity of polystyrene microspheres in A549 cells
Maternal exposure to microplastics and nanoplastics has been shown to result in fetal growth restriction in mice. [...] Maternal exposure to both microplastics and nanoplastics resulted in evidence of placental dysfunction that was highly dependent on the particle size. The umbilical artery blood flow increased by 48% in the microplastic-exposed group and decreased by 25% in the nanoplastic-exposed group compared to controls (p < 0.05). The microplastic- and nanoplastic-exposed fetuses showed a significant decrease in the middle cerebral artery pulsatility index of 10% and 13%, respectively, compared to controls (p < 0.05), indicating vasodilation of the cerebral circulation, a fetal adaptation that is part of the brain sparing response to preserve oxygen delivery. Hemodynamic markers of placental dysfunction and fetal hypoxia were more pronounced in the group exposed to polystyrene nanoplastics, suggesting nanoplastic exposure during human pregnancy has the potential to disrupt fetal brain development, which in turn may cause suboptimal neurodevelopmental outcomes.
PS-MPs can decrease transepithelial electrical resistance by depleting zonula occludens proteins. Indeed, decreased α1-antitrypsin levels in BEAS-2B cells suggest that exposure to PS-MPs increases the risk for chronic obstructive pulmonary disease, and high concentrations of PS-MPs can induce these adverse responses. While low PS-MP levels can only disrupt the protective pulmonary barrier, they may also increase the risk for lung disease. Collectively, our findings indicate that PS-MP inhalation may influence human respiratory health.
Even at low concentrations (1–30 µg/ml), photoaged microspheres at 1 and 5 µm in diameter exerted more pronounced biological responses in the A549 cells than was caused by pristine microspheres. High-content imaging analysis revealed S and G2 cell cycle accumulation and morphological changes, which were also more pronounced in A549 cells treated with photoaged microspheres, and further influenced by the size, dose, and time of exposures. Polystyrene microspheres reduced monolayer barrier integrity and slowed regrowth in a wound healing assay in a manner dependent on dose, photoaging, and size of the microsphere. UV-photoaging generally enhanced the toxicity of polystyrene microspheres in A549 cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10176241/
Maternal exposure to microplastics and nanoplastics has been shown to result in fetal growth restriction in mice. [...] Maternal exposure to both microplastics and nanoplastics resulted in evidence of placental dysfunction that was highly dependent on the particle size. The umbilical artery blood flow increased by 48% in the microplastic-exposed group and decreased by 25% in the nanoplastic-exposed group compared to controls (p < 0.05). The microplastic- and nanoplastic-exposed fetuses showed a significant decrease in the middle cerebral artery pulsatility index of 10% and 13%, respectively, compared to controls (p < 0.05), indicating vasodilation of the cerebral circulation, a fetal adaptation that is part of the brain sparing response to preserve oxygen delivery. Hemodynamic markers of placental dysfunction and fetal hypoxia were more pronounced in the group exposed to polystyrene nanoplastics, suggesting nanoplastic exposure during human pregnancy has the potential to disrupt fetal brain development, which in turn may cause suboptimal neurodevelopmental outcomes.
https://pubmed.ncbi.nlm.nih.gov/37724921/
PS-MPs can decrease transepithelial electrical resistance by depleting zonula occludens proteins. Indeed, decreased α1-antitrypsin levels in BEAS-2B cells suggest that exposure to PS-MPs increases the risk for chronic obstructive pulmonary disease, and high concentrations of PS-MPs can induce these adverse responses. While low PS-MP levels can only disrupt the protective pulmonary barrier, they may also increase the risk for lung disease. Collectively, our findings indicate that PS-MP inhalation may influence human respiratory health.
https://pubmed.ncbi.nlm.nih.gov/31727530/
(TL;DR; they are affecting our bodies for the worse, even as feti)