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Air pollutants may be environmental risk factors in chronic rhinosinusitis disease progression
Author(s) -
Mady Leila J.,
Schwarzbach Hannah L.,
Moore John A.,
Boudreau Robert M.,
Willson Thomas J.,
Lee Stella E.
Publication year - 2018
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.22052
Subject(s) - medicine , chronic rhinosinusitis , asthma , nasal polyps , air pollutants , sinusitis , pathophysiology , endoscopic sinus surgery , pollutant , gastroenterology , surgery , air pollution , chemistry , organic chemistry
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 [PM 2.5 ] 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. PM 2.5 and BC exposures were correlated with outcome measures. Results Mean PM 2.5 and BC findings were not significantly different between CRSwNP and CRSsNP patients or patients with and without asthma. Among those with CRSsNP, PM 2.5 was significantly associated with undergoing FESS. For each unit increase in PM 2.5 , 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.