Leila J Mady1, Hannah L Schwarzbach2, John A Moore1, Robert M Boudreau3, Ellen Kinnee, Zan M Dodson, Thomas J Willson4, Jane E Clougherty, Stella E Lee1. 1. Department of Otolaryngology, University of Pittsburgh, Pittsburgh, PA. 2. University of Pittsburgh School of Medicine, Pittsburgh, PA. 3. Graduate School of Public Health, Department of Epidemiology, University of Pittsburgh, Pittsburgh, PA. 4. Uniformed Services University of the Health Sciences, Department of Otolaryngology, San Antonio Military Medical Center, San Antonio, TX.
Abstract
BACKGROUND: Little is known about the role of environmental exposures in the pathophysiology of chronic rhinosinusitis (CRS). In this study, we measured the impact of air pollutants (particulate matter 2.5 [PM2.5 ] and black carbon [BC]) on CRS with nasal polyposis (CRSwNP) and CRS without nasal polyposis (CRSsNP). METHODS: Spatial modeling from pollutant monitoring sites was used to estimate exposures surrounding residences for patients meeting inclusion criteria (total patients, n = 234; CRSsNP, n = 96; CRSwNP, n = 138). Disease severity outcome measures included modified Lund-Mackay score (LMS), systemic steroids, number of functional endoscopic sinus surgeries (FESS), and 22-item Sino-Nasal Outcome Test (SNOT-22) score. PM2.5 and BC exposures were correlated with outcome measures. RESULTS: Mean PM2.5 and BC findings were not significantly different between CRSwNP and CRSsNP patients or patients with and without asthma. Among those with CRSsNP, PM2.5 was significantly associated with undergoing FESS. For each unit increase in PM2.5 , there was a 1.89-fold increased risk in the proportion of CRSsNP patients who required further surgery (p = 0.015). This association was not identified in CRSwNP patients (p = 0.445). BC was also significantly associated with SNOT-22 score in the CRSsNP group. For each 0.1-unit increase in BC, there was a 7.97-unit increase in SNOT-22 (p = 0.008). A similar, although not significant, increase in SNOT-22 was found with increasing BC in the CRSwNP group (p = 0.728). CONCLUSION: Air pollutants correlate with CRS symptom severity that may be influenced by exposure levels, with a more pronounced impact on CRSsNP patients. This study is the first to demonstrate the possible role of inhalant pollutants in CRS phenotypes, addressing a critical knowledge gap in environmental risk factors for disease progression.
BACKGROUND: Little is known about the role of environmental exposures in the pathophysiology of chronic rhinosinusitis (CRS). In this study, we measured the impact of air pollutants (particulate matter 2.5 [PM2.5 ] and black carbon [BC]) on CRS with nasal polyposis (CRSwNP) and CRS without nasal polyposis (CRSsNP). METHODS: Spatial modeling from pollutant monitoring sites was used to estimate exposures surrounding residences for patients meeting inclusion criteria (total patients, n = 234; CRSsNP, n = 96; CRSwNP, n = 138). Disease severity outcome measures included modified Lund-Mackay score (LMS), systemic steroids, number of functional endoscopic sinus surgeries (FESS), and 22-item Sino-Nasal Outcome Test (SNOT-22) score. PM2.5 and BC exposures were correlated with outcome measures. RESULTS: Mean PM2.5 and BC findings were not significantly different between CRSwNP and CRSsNP patients or patients with and without asthma. Among those with CRSsNP, PM2.5 was significantly associated with undergoing FESS. For each unit increase in PM2.5 , there was a 1.89-fold increased risk in the proportion of CRSsNP patients who required further surgery (p = 0.015). This association was not identified in CRSwNP patients (p = 0.445). BC was also significantly associated with SNOT-22 score in the CRSsNP group. For each 0.1-unit increase in BC, there was a 7.97-unit increase in SNOT-22 (p = 0.008). A similar, although not significant, increase in SNOT-22 was found with increasing BC in the CRSwNP group (p = 0.728). CONCLUSION: Air pollutants correlate with CRS symptom severity that may be influenced by exposure levels, with a more pronounced impact on CRSsNP patients. This study is the first to demonstrate the possible role of inhalant pollutants in CRS phenotypes, addressing a critical knowledge gap in environmental risk factors for disease progression.
Authors: Anika Kaura; Rishi Shukla; Abigail Lamyman; Robert Almeyda; Mark Draper; Pablo Martinez-Devesa; Ali Qureishi Journal: Turk Arch Otorhinolaryngol Date: 2020-12-01
Authors: Christopher J Hill; Charles D Meyer; James E McLean; Danielle C Anderson; Yajing Hao; Feng-Chang Lin; Adam J Kimple; Gregory G Capra Journal: J Occup Environ Med Date: 2022-06-09 Impact factor: 2.306
Authors: Zhenyu Zhang; Nicholas R Rowan; Jayant M Pinto; Nyall R London; Andrew P Lane; Shyam Biswal; Murugappan Ramanathan Journal: JAMA Netw Open Date: 2021-05-03