Particulate matter exposure is associated with increased inflammatory cytokines and eosinophils in chronic rhinosinusitis
Rory J. Lubner, Kolin E. Rubel, Rakesh K. Chandra, Justin H. Turner, Naweed I. Chowdhury
Abstract
Abstract Background Chronic rhinosinusitis (CRS) is thought to result from complex interactions between the host immune system, microbiota, and environmental exposures. Currently, there is limited data regarding the impact of ambient particulate matter ≤2.5 μm in diameter (PM 2.5 ) in the pathogenesis of CRS, despite evidence linking PM 2.5 to other respiratory diseases. We hypothesized that PM 2.5 may result in differential cytokine patterns that could inform our mechanistic understanding of the effect of environmental factors on CRS. Methods We conducted an analysis of data prospectively collected from 308 CRS patients undergoing endoscopic sinus surgery. Cytokines were quantified in intraoperative mucus specimens using a multiplex flow cytometric bead assay. Clinical and demographic data including zip codes were extracted and used to obtain tract‐level income and rurality measures. A spatiotemporal machine learning model was used to estimate daily PM 2.5 levels for the year prior to each patient's surgery date. Spearman correlations and regression analysis were performed to characterize the relationship between mucus cytokines and PM 2.5. Results Several inflammatory cytokines including IL‐2, IL‐5/IL‐13, IL‐12, and 21 were significantly correlated with estimated average 6, 9, and 12‐month preoperative PM 2.5 levels. These relationships were maintained for most cytokines after adjusting for age, income, body mass index, rurality, polyps, asthma, and allergic rhinitis (AR) ( p < .05). There were also higher odds of asthma (OR = 1.5, p = .01) and AR (OR = 1.48, p = .03) with increasing 12‐month PM 2.5 exposure. Higher tissue eosinophil counts were associated with increasing PM 2.5 levels across multiple timeframes ( p < .05). Conclusions Chronic PM 2.5 exposure may be an independent risk factor for development of a mixed, type‐2 dominant CRS inflammatory response.