Association of Air Pollutant Exposure and Sinonasal Histopathology Findings in Chronic Rhinosinusitis. Issue 6 (November 2021)

• Record Type: Journal Article
• Authors: Patel, Tirth R.; Tajudeen, Bobby A.; Brown, Hannah; Gattuso, Paolo; LoSavio, Phillip; Papagiannopoulos, Peter; Batra, Pete S.; Mahdavinia, Mahboobeh
• Is Part Of: American journal of rhinology & allergy. Volume 35:Issue 6(2021)
• Page Start: 761
• Page End: 767
• Publication Date: 2021-11
• Subjects: air pollution -- chronic rhinosinusitis -- paranasal sinus disease -- eosinophilic rhinitis -- nasal polyposis -- rhinitis -- allergic rhinitis -- asthma -- aspirin exacerbated respiratory disease -- acute rhinosinusitis; Nose -- Periodicals; Allergy -- Periodicals; 616.21005
• DOI: 10.1177/1945892421993655
• Languages: English
• ISSNs: 1945-8924

Abstract

Background: Ambient air pollution is well known to cause inflammatory change in respiratory epithelium and is associated with exacerbations of inflammatory conditions such as asthma and chronic obstructive pulmonary disease. However, limited work has been done on the impact of air pollution on pathogenesis of chronic rhinosinusitis and there are no reports in the literature of how pollutant exposure may impact sinonasal histopathology in patients with chronic rhinosinusitis. Objective: This study aims to identify associations between certain histopathologic characteristics seen in sinus tissue of patients with chronic rhinosinusitis (CRS) and levels of particulate air pollution (PM2.5 ) and ground-level ozone in their place of residence. Methods: A structured histopathology report was created to characterize the tissues of CRS patients undergoing sinus surgery. An estimate for each patient's exposure to air pollutants including small particulate matter (PM2.5 ) and ground-level ozone was obtained using the Environmental Protection Agency's (EPA) Environmental Justice Screening and Mapping Tool (EJSCREEN). Mean pollutant exposures for patients whose tissues exhibited varying histopathologic features were compared using logistic regression models. Results: Data from 291 CRS patients were analyzed. Higher degree of inflammation was significantly associated with increased ozone exposure (p = 0.031). Amongst the patients with CRSwNP (n=131), presence of eosinophilic aggregates (p = 0.018) and Charcot-Leyden crystals (p = 0.036) was associated with increased ozone exposure. Conclusion: Exposure to ambient air pollutants may contribute to pathogenesis of CRS. Increasing ozone exposure was linked to both higher tissue inflammation and presence of eosinophilic aggregates and Charcot-Leyden crystals in CRSwNP patients.