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Evaluation of the pulmonary toxicity of PSNPs using a Transwell-based normal human bronchial epithelial cell culture system
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Researchers used a Transwell air-liquid interface cell culture system to assess how polystyrene nanoplastics affect human bronchial epithelial cells, finding that even ultralow, non-cytotoxic doses triggered inflammatory signaling (NF-κB, NLRP3), while higher doses induced apoptosis and autophagy — suggesting nanoplastics pose a pulmonary health risk at ambient exposure levels.
To reduce the nanoplastics (NPs) toxicity assessment error, we established a Transwell-based bronchial epithelial cell exposure system to assess the pulmonary toxicity of polystyrene NPs (PSNPs). Transwell exposure system was more sensitive than submerged culture for toxicity detection of PSNPs. PSNPs adhered to the BEAS-2B cell surface, were ingested by the cell, and accumulated in the cytoplasm. PSNPs induced oxidative stress and inhibited cell growth through apoptosis and autophagy. A noncytotoxic dose of PSNPs (1 ng/cm) increased the expression levels of inflammatory factors (ROCK-1, NF-κB, NLRP3, ICAM-1, etc) in BEAS-2B cells, whereas a cytotoxic dose (1000 ng/cm) induced apoptosis and autophagy, which might inhibit the activation of ROCK-1 and contribute to reducing inflammation. In addition, the noncytotoxic dose increased the expression levels of zonula occludens-2 (ZO-2) and α1-antitrypsin (α-AT) proteins in BEAS-2B cells. Therefore, in response to PSNP exposure, a compensatory increase in the activities of inflammatory factors, ZO-2, and α-AT may be triggered at low doses as a mechanism to preserve the survival of BEAS-2B cells. In contrast, exposure to a high dose of PSNPs elicits a noncompensatory response in BEAS-2B cells. Overall, these findings suggest that PSNPs may be harmful to human pulmonary health even at an ultralow concentration.
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Researchers exposed bronchial epithelial cells to europium-doped polystyrene nanoplastics to assess cytotoxicity in a model of the human airway. The nanoplastics caused dose-dependent cell death and inflammatory signaling, supporting concerns about respiratory health effects from inhaled plastic particles.
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Researchers tested polystyrene nanoplastics on two types of human lung cells and found that the particles caused cell damage, oxidative stress, and inflammation-related gene changes at relatively low concentrations. Using a co-culture model that mimics the lung's layered structure, they showed that nanoplastics can trigger immune responses even in cells not directly exposed. The study suggests that inhaled nanoplastics may pose respiratory health risks through both direct toxicity and inflammatory signaling.
Cytotoxicity analysis of polystyrene nanoplastics in the bronchial epithelial cell line BEAS-2B
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Researchers assessed cytotoxicity and inflammatory responses in human bronchial epithelial cells exposed to polystyrene nanoplastics doped with the rare earth element europium. Nanoplastic exposure triggered cell death and pro-inflammatory signaling in a dose-dependent manner, with implications for inhalation risk assessment.
Internalization and toxicity: A preliminary study of effects of nanoplastic particles on human lung epithelial cell
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Researchers studied the effects of polystyrene nanoplastic particles on human lung cells and found that the particles were internalized by the cells and caused dose-dependent toxicity. The nanoplastics triggered oxidative stress, inflammation, and disrupted normal cell function. The findings suggest that inhaling airborne nanoplastics may pose risks to respiratory health.
Pulmonary hazards of nanoplastic particles: a study using polystyrene in in vitro models of the alveolar and bronchial epithelium
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