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Multi-Omics Analysis Reveals the Toxicity of Polyvinyl Chloride Microplastics toward BEAS-2B Cells
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Researchers used advanced gene and metabolite analysis to reveal how PVC microplastics damage human lung cells. Exposure altered the expression of 530 genes and nearly 4,000 metabolites, particularly disrupting fat metabolism pathways and activating inflammatory stress responses. These findings are important because airborne PVC microplastics are common in indoor and outdoor environments, and the study reveals specific biological pathways through which inhaled microplastics could contribute to lung disease.
Polyvinyl chloride microplastics (PVC-MPs) are microplastic pollutants widely present in the environment, but their potential risks to human lung health and underlying toxicity mechanisms remain unknown. In this study, we systematically analyzed the effects of PVC-MPs on the transcriptome and metabolome of BEAS-2B cells using high-throughput RNA sequencing and untargeted metabolomics technologies. The results showed that exposure to PVC-MPs significantly reduced the viability of BEAS-2B cells, leading to the differential expression of 530 genes and 3768 metabolites. Further bioinformatics analyses showed that PVC-MP exposure influenced the expression of genes associated with fluid shear stress, the MAPK and TGF-β signaling pathways, and the levels of metabolites associated with amino acid metabolism. In particular, integrated pathway analysis showed that lipid metabolic pathways (including glycerophospholipid metabolism, glycerolipid metabolism, and sphingolipid metabolism) were significantly perturbed in BEAS-2B cells following PVC-MPs exposure. This study provides new insights and targets for a deeper understanding of the toxicity mechanism of PVC-MPs and for the prevention and treatment of PVC-MP-associated lung diseases.
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Integration of transcriptomics and metabolomics reveal cytotoxic mechanisms of Polyethylene terephthalate microplastics in BEAS-2B cells
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Researchers exposed human lung cells to PET microplastics and used combined gene and metabolite analysis to uncover the mechanisms of toxicity. They found that the microplastics disrupted lipid metabolism and activated cell death pathways, reducing cell viability over time. The study suggests that inhaled PET microplastics could pose risks to respiratory health by triggering harmful molecular changes in lung tissue.
Polyamide and polyvinyl chloride microplastics induce cytotoxicity and cytokine release in primary normal human bronchial epithelial cells
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Scientists exposed lung cells from human airways to tiny plastic particles (from nylon and PVC, two common plastics) to see how they'd react, similar to what might happen when we breathe in airborne microplastics. The smallest particles caused cell damage and triggered inflammation-related signals, with PVC causing harm at lower doses than nylon—suggesting the type and size of plastic particles we inhale may matter for lung health. This is early-stage lab research, so more studies are needed to confirm what this means for people breathing in real-world air.
Polypropylene nanoplastic exposure leads to lung inflammation through p38-mediated NF-κB pathway due to mitochondrial damage
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This study found that polypropylene nanoplastics, one of the most common types of plastic particles, can cause lung inflammation by damaging mitochondria (the energy-producing parts of cells) and triggering inflammatory signaling pathways. These findings suggest that breathing in tiny plastic particles could contribute to lung disease through a specific chain of cellular damage.
A single-cell perspective on polyethylene microplastic toxicity: linking fibroblast reprogramming to immune microenvironment alterations in the lung
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Scientists exposed rats' lungs to polyethylene microplastics (a common plastic found in air pollution) over time and used advanced cell-tracking technology to see exactly what happens inside lung tissue. They found that these plastic particles trigger immune cells to release signals that push scar-tissue-forming cells into overdrive, leading to thickened, scarred lung tissue and disrupted immune function. Since microplastics are already known to accumulate in human lungs, this research helps explain a possible mechanism behind plastic-related lung damage and points to specific molecules that could one day be targeted to prevent or treat it.
Polypropylene microplastic exposure leads to lung inflammation through p38-mediated NF- κB pathway due to mitochondrial damage
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Researchers found that instilling polypropylene microplastic particles into mouse lungs caused dose-dependent increases in inflammatory cell counts, reactive oxygen species, and pro-inflammatory cytokines, with lung tissue analysis revealing the particles triggered inflammation via mitochondrial damage activating the p38-mediated NF-kB signaling pathway.
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