Short-term Haze Exposure Predisposes Healthy Volunteers to Nasal Inflammation
10.4168/aair.2019.11.5.632
- Author:
Mu XIAN
1
;
Kuiji WANG
;
Hongfei LOU
;
Yang WANG
;
Luo ZHANG
;
Chengshuo WANG
Author Information
1. Beijing Institute of Otolaryngology, Department of Otolaryngology Head and Neck Surgery, Beijing TongRen Hospital, Capital Medical University, Beijing, China. dr.luozhang@139.com, wangcs830@126.com
- Publication Type:Original Article
- Keywords:
Air pollution;
particulate matter;
nasal inflammation;
cytokines;
neuropeptides
- MeSH:
Air Pollution;
Airway Resistance;
Cytokines;
Healthy Volunteers;
Humans;
Hypersensitivity;
Inflammation;
Interleukin-10;
Interleukin-4;
Interleukin-5;
Interleukin-8;
Interleukins;
Nasal Cavity;
Nerve Growth Factor;
Neuropeptide Y;
Neuropeptides;
Nitric Oxide;
Particulate Matter;
Peptides;
Respiratory System;
Substance P
- From:Allergy, Asthma & Immunology Research
2019;11(5):632-643
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: This study aimed to investigate the impact of short-term haze exposure on nasal inflammation in healthy volunteers. METHODS: Thirty-three healthy university students were assessed for nasal symptoms, nasal patency, upper and lower respiratory tract nitric oxide (NO) as well as inflammatory mediators and neuropeptides in nasal secretions before and after a 5-day haze episode. Peripheral blood mononuclear cells (PBMCs) were stimulated with particulate matter with an aerodynamic diameter of less than 2.5 μm (PM(2.5)), and cytokines in the supernatants were examined. RESULTS: Mild nasal symptoms were reported by some participants during the haze episode. Objective measures of nasal patency demonstrated that nasal airway resistance was significantly increased from baseline levels, while nasal cavity volume and minimum cross-sectional area were significantly decreased. Similarly, the levels of nasal and exhaled NO, eotaxin, interleukin (IL)-5, chemokine (C-C motif) ligand 17, IL-8, substance P, nerve growth factor and vasoactive intestinal peptides in nasal secretions were significantly increased from baseline values following the haze episode. In contrast, the levels of interferon-γ, IL-10, transforming growth factor-β and neuropeptide Y were significantly decreased. Incubation with 0.1-10 μg/mL PM(2.5) significantly increased release of IL-1β, IL-4, IL-5, IL-8 and IL-10 from PBMCs. CONCLUSIONS: Short-term haze exposure may lead to nasal inflammation and hypersensitivity in healthy subjects predominantly by Th2 cytokine-mediated immune responses.
