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Asthma is a chronic inflammatory respiratory disease influenced by genetic and environmental factors. Emerging evidence suggests that microplastics and nanoplastics (NPs) pose significant health risks. When inhaled, these tiny particles can accumulate in the lungs, triggering inflammation, oxidative stress, and other disruptions in pulmonary function. This study investigates the role of polyvinyl chloride (PVC) NPs, which are extensively used in products such as packaging, medical devices, and construction materials, in asthma pathogenesis. Using an ovalbumin (OVA)‐induced murine asthma model, it is demonstrated that PVC NPs exposure exacerbates airway hyperresponsiveness, increases inflammatory cell infiltration, and elevates inflammatory cytokine levels in the lungs. Further mechanistic studies reveal that PVC NPs suppress Ribonuclease H1 (RNASEH1), leading to RNA–DNA hybrid loop (R‐loop) accumulation and activation of the Cyclic GMP‐AMP Synthase (cGAS)‐Stimulator of Interferon Genes (STING) inflammatory pathway. The critical involvement of this pathway is confirmed using STING‐deficient mice, where pathway inhibition alleviates the inflammation exacerbated by PVC NPs exposure. These findings provide new insights into the potential role of NPs pollutants in modulating immune responses through R‐loop formation, linking PVC NPs to asthma pathogenesis. This study highlights the importance of addressing environmental exposure to NPs in asthma prevention and management and identifies potential molecular targets for therapeutic intervention. Polyvinyl chloride (PVC) nanoplastics (NPs) are shown to aggravate allergic airway inflammation in asthma by triggering R‐loop accumulation and activating the cGAS‐STING pathway in macrophages. This study reveals a novel immunotoxic mechanism linking environmental plastic exposure to asthma pathogenesis and highlights potential molecular targets for mitigating nanoplastic‐induced respiratory inflammation.

Polyvinyl chloride (PVC) is commonly employed as mulch in agriculture to boost crop yields. However, its toxicity is often overlooked. Due to its chemical stability, resistance to degradation, and the inadequacy of the recycling system, PVC tends to persist in farm environments, where it can decompose into microplastics (MPs) or nanoplastics (NPs). The radish (Raphanus sativus L.) was chosen as the model plant for this study to evaluate the underlying toxic mechanisms of PVC NPs on seedling growth through the integration of multi-omics approaches with oxidative stress evaluations. The results indicated that, compared with the control group, the shoot lengths in the 5 mg/L and 150 mg/L treatment groups decreased by 33.7% and 18.0%, respectively, and the root lengths decreased by 28.3% and 11.3%, respectively. However, there was no observable effect on seed germination rates. Except for the peroxidase (POD) activity in the 150 mg/L group, all antioxidant enzyme activities and malondialdehyde (MDA) levels were higher in the treated root tips than in the control group. Both transcriptome and metabolomic analysis profiles showed 2075 and 4635 differentially expressed genes (DEGs) in the high- and low-concentration groups, respectively, and 1961 metabolites under each treatment. PVC NPs predominantly influenced seedling growth by interfering with plant hormone signaling pathways and phenylpropanoid production. Notably, the reported toxicity was more evident at lower concentrations. This can be accounted for by the plant’s “growth-defense trade-off” strategy and the manner in which nanoparticles aggregate. By clarifying how PVC NPs coordinately regulate plant stress responses via hormone signaling and phenylpropanoid biosynthesis pathways, this research offers a scientific basis for assessing environmental concerns related to nanoplastics in agricultural systems.

The total mass of individual synthetic polymers present as microplastic (MP < 2 mm) pollutants in the sediments of interconnected aquatic environments was determined adopting the Polymer Identification and Specific Analysis (PISA) procedure. The investigated area includes a coastal lakebed (Massaciuccoli), a coastal seabed (Serchio River estuarine), and a sandy beach (Lecciona), all within a natural park area in Tuscany (Italy). Polyolefins, poly(styrene) (PS), poly(vinyl chloride) (PVC), polycarbonate (PC), poly(ethylene terephthalate) (PET), and the polyamides poly(caprolactame) (Nylon 6) and poly(hexamethylene adipamide) (Nylon 6,6) were fractionated and quantified through a sequence of selective solvent extractions followed by either analytical pyrolysis or reversed-phase HPLC analysis of the products of hydrolytic depolymerizations under acidic and alkaline conditions. The highest concentrations of polyolefins (highly degraded, up to 864 µg/kg of dry sediment) and PS (up to 1138 µg/kg) MPs were found in the beach dune sector, where larger plastic debris are not removed by the cyclic swash action and are thus prone to further aging and fragmentation. Surprisingly, low concentrations of less degraded polyolefins (around 30 µg/kg) were found throughout the transect zones of the beach. Positive correlation was found between polar polymers (PVC, PC) and phthalates, most likely absorbed from polluted environments. PET and nylons above their respective LOQ values were found in the lakebed and estuarine seabed hot spots. The pollution levels suggest a significant contribution from riverine and canalized surface waters collecting urban (treated) wastewaters and waters from Serchio River and the much larger Arno River aquifers, characterized by a high anthropogenic pressure. Graphical abstract

Thermal analysis of micro- and nanoplastics (MNPs) is a well-established complementary method to spectroscopic techniques, enabling simultaneous quantification of synthetic polymers at trace levels. However, pyrolysis is complex and prone to interferences. As the MNP composition in environmental samples is unknown, pyrolytic signals attributed to specific homopolymers often contain degradation products from copolymers and formulations, sharing the same polymer building blocks. Thus, results need to be reported as polymer clusters (C-). However, depending on marker specificity, residual organic matrix like natural polymers, especially refractory substances, and even unrelated synthetic polymers, can compromise quantification. Polyvinyl chloride (PVC), a common polymer, is a prominent example. Its thermal degradation mainly yields chlorine-free, partially alkylated aromatics dominated by benzene and naphthalene derivatives, which lack specificity. This study evaluated the applicability of PVC pyrolysis markers, including naphthalene and methylnaphthalene, across diverse (chlorinated) synthetic and natural polymers, including soot. All polymers released these markers. Alternative indicators like dihydro- and tetrahydronaphthalene showed slightly improved but still insufficient specificity. Thus, no definitive C-PVC marker was identified. Semi-quantitative estimates of C-PVC may be feasible in less complex or well-characterized environments. Its accurate quantification in complex matrices, where residual organic matrix is unavoidable, even after severe pretreatment, remains problematic. This requires critical reassessment of C-PVC data in environmental and biological samples. If organic residues cannot be fully excluded, thermal C-PVC. quantification should be avoided or supported by complementary methods. As a compromise, a broader C-PVC* cluster that includes refractory polymers like soot or black carbon, is suggested, provided other organics (e.g. natural fibers) have been effectively removed during preprocessing. Graphical Abstract