ArticleToxicological sciences : an official journal of the Society of Toxicology2026
Effects of urban PM2.5 on primary sinonasal epithelial cells in individuals with chronic rhinosinusitis.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- The primary cilium as a compartmentalized signaling hub in tissue immunity and homeostasis.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
7 authors.
Funding
Abstract
Fine particulate matter (PM2.5), airborne particles with an aerodynamic diameter of ≤2.5 µm, a major air pollutant, has been implicated in sinonasal inflammatory diseases such as chronic rhinosinusitis (CRS) even at levels below national air quality standards. PM2.5 is thought to exacerbate CRS by compromising the epithelial barrier, impairing mucociliary clearance, and promoting inflammation. However, evidence linking PM2.5 exposure to sinonasal epithelial remodeling remains limited. This study investigated the effects of environmentally relevant doses of urban PM2.5 organic extract (PM2.5 OE) on primary sinonasal epithelial cell cultures derived from individuals with and without CRS. We hypothesized that PM2.5 OE exposure would induce transcriptional changes indicative of mucociliary remodeling, reduce transepithelial resistance, and increase inflammatory cytokine production. Primary nasal epithelial cells from healthy (N = 8) and CRS subjects (N = 10) were differentiated in an air-liquid interface, followed by acute (24-h) and subacute (5-day) exposure to an environmentally relevant dose of PM2.5 OE (9 μg/ml; 1.34 µg/cm2) or the vehicle control. PM2.5 OE exposure did not significantly alter these outcomes, regardless of disease status. Instead, variation was primarily driven by biological sex and CRS, with male CRS samples exhibiting downregulation of cilia assembly pathways. Cytokine production from unexposed cultures demonstrated sex-specific differences, with female-derived cultures displaying a more pro-inflammatory profile, highlighting intrinsic immune variability. These findings underscore the importance of biological sex and disease status when evaluating environmental exposures, suggesting that longer exposures may be necessary to fully capture PM2.5 OE-induced effects. This work highlights the need to investigate the crosstalk between environmental exposures and individual-specific factors influencing CRS disease progression.
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Registered trials
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