International forum of allergy & rhinology · 2025
Inflammatory Effects of Microplastics and Nanoplastics on Nasal Airway Epithelial Cells.
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Kahan Maayan S, Nguyen Hoang C B, Madhusudanan Pallavi, Mitchell Margaret B, Huang Di, Bleier Benjamin S, Amiji Mansoor M, Workman Alan D
Аннотация
BACKGROUND: Microplastics and nanoplastics (MNPs) have emerged as ubiquitous environmental contaminants; these particles have been detected in mucus and irrigation fluids, and at greater concentrations in patients with sinusitis and allergic rhinitis. Emerging evidence at other mucosal surfaces, including the gut and lung, suggests that MNPs exacerbate epithelial barrier dysfunction and induce inflammatory responses. Despite their relevance, the impact of inhaled plastics on the nasal epithelium, the initial point of contact for airborne plastics, remains underexplored.
METHODS: Submerged RPMI 2650 nasal epithelial cultures and air-liquid interface (ALI) cultures of primary human nasal epithelial cells were dosed with polystyrene (PS) MNPs, with a focus on the effects of 100 nm nanoplastics and surface charge alterations. Analyses of secreted cytokines, transcriptomic changes, epithelial integrity, and histologic appearance were performed.
RESULTS: Note that 100 nm PS nanoplastics caused transcriptomic inflammatory and oxidative stress pathway activation in RMPI 2650 submerged cultures, with conserved inflammatory gene signatures in the ALI exposure model as well. Dose-dependent elevations in IL-8 and TNFα were observed after ALI exposure to 1 µm PS microplastics, and 100 nm PS nanoplastics elicited early elevations in IL-6, IL-8, and TNF, with more pronounced effects from amine-modified particles, while no cytotoxicity, barrier disruption, or type-2 alarmin induction was observed. Scanning electron microscopy revealed ciliary disruption and particle adherence.
CONCLUSIONS: PS MNPs cause inflammatory cytokine responses in nasal epithelial cells over even a short timeframe, in addition to ciliary blunting and transcriptional evidence of significant inflammation and stress response. This sinonasal model can help answer critical questions about the pathogenicity of plastic exposures.
METHODS: Submerged RPMI 2650 nasal epithelial cultures and air-liquid interface (ALI) cultures of primary human nasal epithelial cells were dosed with polystyrene (PS) MNPs, with a focus on the effects of 100 nm nanoplastics and surface charge alterations. Analyses of secreted cytokines, transcriptomic changes, epithelial integrity, and histologic appearance were performed.
RESULTS: Note that 100 nm PS nanoplastics caused transcriptomic inflammatory and oxidative stress pathway activation in RMPI 2650 submerged cultures, with conserved inflammatory gene signatures in the ALI exposure model as well. Dose-dependent elevations in IL-8 and TNFα were observed after ALI exposure to 1 µm PS microplastics, and 100 nm PS nanoplastics elicited early elevations in IL-6, IL-8, and TNF, with more pronounced effects from amine-modified particles, while no cytotoxicity, barrier disruption, or type-2 alarmin induction was observed. Scanning electron microscopy revealed ciliary disruption and particle adherence.
CONCLUSIONS: PS MNPs cause inflammatory cytokine responses in nasal epithelial cells over even a short timeframe, in addition to ciliary blunting and transcriptional evidence of significant inflammation and stress response. This sinonasal model can help answer critical questions about the pathogenicity of plastic exposures.