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Harmful effects of true-to-life nanoplastics derived from PET water bottles in human alveolar macrophages.
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Researchers tested nanoplastics derived from actual PET water bottles on mouse lung immune cells, focusing specifically on cells that had internalized the particles. Even though the nanoplastics were taken up by 100% of cells at the highest dose, they did not cause outright cell death. However, they did trigger significant increases in reactive oxygen species and shifted the immune cells toward a pro-inflammatory state, suggesting that inhaled nanoplastics from everyday plastic products could promote chronic lung inflammation.
The increasing presence of secondary micro/nanoplastics (MNPLs) in the environment requires knowing if they represent a real health concern. To such end, an important point is to test representative MNPLs such as the denominated true-to-life MNPLs, resulting from the degradation of plastic goods in lab conditions. In this study, we have used polyethylene terephthalate (PET) NPLs resulting from the degradation of PET water bottles. Since inhalation is an important exposure route to environmental MNPLS, we have used mouse alveolar macrophages (MH-S) as a target cell, and the study focused only on the cells that have internalized them. This type of approach is novel as it may capture the realistic adverse effects of PETNPLs only in the internalized cells, thereby mitigating any biases while assessing the risk of these MNPLs. Furthermore, the study utilized a set of biomarkers including intracellular reactive oxygen species (ROS) levels, variations on the mitochondrial membrane potential values, and the macrophage polarization to M1 (pro-inflammatory response) and M2 (anti-proinflammatory response) as possible cellular effects due to PETNPLs in only the cells that internalized PETNPLs. After exposures lasting for 3 and 24 h to a range of concentrations (0, 25, 50, and 100 μg/mL) the results indicate that no toxicity was induced despite the 100% internalization observed at the highest concentration. Significant intracellular levels of ROS were observed, mainly at exposures lasting for 24 h, in an indirect concentration-effect relationship. Interestingly, a reduction in the mitochondrial membrane potential was observed, but only at exposures lasting for 24 h, but without a clear concentration-effect relationship. Finally, PETNPL exposure shows a significant polarization from M0 to M1 and M2 subtypes. Polarization to M1 (pro-inflammatory stage) was more marked and occurred at both exposure times. Polarization to M2 (anti-inflammatory stage) was only observed after exposures lasting for 24 h. Due to the relevance of the described biomarkers, our results underscore the need for further research, to better understand the health implications associated with MNPL exposure.
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Effects of true-to-life PET nanoplastics using primary human nasal epithelial cells
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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.
Distinct pro-inflammatory responses to pristine and microbially contaminated PET nanoplastics in a human alveolar cell co-culture
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Scientists tested how tiny plastic particles from recycled PET bottles (the plastic used in water bottles) affect lung cells, and found that plastic contaminated with bacteria triggered a much stronger inflammatory response than clean, uncontaminated plastic particles. This suggests that germs riding along on plastic waste—not necessarily the plastic itself—may be a bigger driver of lung irritation, which is especially relevant for workers in recycling and waste facilities who breathe in plastic dust regularly. The plastic didn't kill the cells in either case, but the findings suggest that future safety testing on microplastics
Respirable polyethylene terephthalate microplastics modulate airway inflammation and immune responses in murine allergen co-exposure models
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Scientists exposed mice to tiny plastic particles from PET (a common plastic in bottles and polyester clothing) and found the particles stuck around in the lungs for two weeks and triggered inflammation, especially when combined with allergens like ragweed pollen. This suggests breathing in these ultra-small plastic fragments could worsen allergic reactions or immune responses, though this was tested in mice at controlled doses, so more research is needed before we know exactly what this means for people breathing in everyday microplastics.
Polyethylene terephthalate nanoparticles effect on RAW 264.7 macrophage cells
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Researchers exposed mouse immune cells to PET nanoplastics (tiny particles from plastic bottles and containers) and found the cells easily absorbed them, triggering mild oxidative stress and switching on several genes linked to immune defense and cell maintenance, providing early evidence of how nanoplastics may affect human immune function.
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When rats breathed in tiny plastic particles (the same polyethylene used in plastic bags and bottles) over several weeks, their lungs showed inflammation, tissue damage, and elevated markers linked to disease — even at the lowest doses tested. This suggests there may be no truly "safe" amount of inhaled plastic particles, though more research is needed to know exactly what this means for humans, since we're regularly exposed to microplastics in air, dust, and everyday products.
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