ArticleAllergy, asthma & immunology research2019
Short-term Haze Exposure Predisposes Healthy Volunteers to Nasal Inflammation.
Article in Allergy, asthma & immunology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 20 citations in OpenAlex.
- Air pollution may increase the sleep apnea severity: A nationwide analysis of smart device-based monitoring.Innovation (Cambridge (Mass.)) · 2023Article
- The risk factors for urinary incontinence in female adults with chronic cough.BMC pulmonary medicine · 2022Article
- Intranasal budesonide for rhinitis during a high airborne pollution period: a randomized controlled trial.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2022Article
- Budesonide repairs decreased barrier integrity of eosinophilic nasal polyp epithelial cells caused by PMClinical and translational allergy · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
purposeThis study aimed to investigate the impact of short-term haze exposure on nasal inflammation in healthy volunteers.
methodsThirty-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
resultsMild 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 PM2.5 significantly increased release of IL-1β, IL-4, IL-5, IL-8 and IL-10 from PBMCs.
conclusionsShort-term haze exposure may lead to nasal inflammation and hypersensitivity in healthy subjects predominantly by Th2 cytokine-mediated immune responses.
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