For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
23
views
123
references
 Top references
cited by
41
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
1 collections
    0
    shares
      200
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      International expert consensus on the management of allergic rhinitis (AR) aggravated by air pollutants : Impact of air pollution on patients with AR: Current knowledge and future strategies

      research-article
      Author(s): a , ∗ , b , c , d , j , e , f , g , h , i , j , k , l , m , n , o , p , q , r , s , t , u , v , w , x , y , z , s
      Publication date (Electronic):
      Journal: The World Allergy Organization Journal
      Publisher: World Allergy Organization
      Keywords: Allergic rhinitis, Occupational rhinitis, Air pollution, Climate change, Air pollutants, Indoor air quality, Oxidative stress, Antioxidant enzymes, AP, Activator protein, AER, Allergic eosinophilic rhinitis, AR, Allergic rhinitis, ARE, Antioxidant response element, CO, Carbon monoxide, CFS, Chronic fatigue syndrome, COPD, Chronic obstructive pulmonary disease, DAMP, Damage-associated molecular patterns, DEP, Diesel exhaust particles, ECAT, Elemental carbon attributable to traffic, ECP, Eosinophil cationic protein, GSH-Px, Glutathione peroxidase, HVAC, Heating, ventilation and air conditioning, HO, Hemeoxygenase, HEPA, High efficiency particulate air, HDM, House dust mites, IAP, Indoor air pollution, IAQ, Indoor air quality, INS, Intranasal steroids, LDH, Lactate dehydrogenase, MSQPCR, Mold specific quantitative PCR, MCP, Monocyte chemotactic protein, NOx, Nitric oxides, NO2, Nitrogen dioxide, NAR, Non allergic rhinitis, Nrf2, Nuclear factor erythroid-2 related factor, NF-κβ, Nuclear factor kappa β, OAP, Outdoor air pollution, O3, Ozone, PON, Paraoxonase, PM, Particulate matter, PAMP, Pathogen-associated molecular patterns, RNS, Reactive nitrosative species, ROS, Reactive oxygen species, SO2, Sulphur dioxide, SOD, Superoxide dismutase, TLR, Toll like receptor, TOS, Total oxidative status, TRAP, Traffic related air pollutants, TNF, Tumor necrosis factor, UFP, Ultra-fine particles, VOCs, Volatile organic compound

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Allergic rhinitis affects the quality of life of millions of people worldwide. Air pollution not only causes morbidity, but nearly 3 million people per year die from unhealthy indoor air exposure. Furthermore, allergic rhinitis and air pollution interact. This report summarizes the discussion of an International Expert Consensus on the management of allergic rhinitis aggravated by air pollution. The report begins with a review of indoor and outdoor air pollutants followed by epidemiologic evidence showing the impact of air pollution and climate change on the upper airway and allergic rhinitis. Mechanisms, particularly oxidative stress, potentially explaining the interactions between air pollution and allergic rhinitis are discussed. Treatment for the management of allergic rhinitis aggravated by air pollution primarily involves treating allergic rhinitis by guidelines and reducing exposure to pollutants. Fexofenadine a non-sedating oral antihistamine improves AR symptoms aggravated by air pollution. However, more efficacy studies on other pharmacological therapy of coexisting AR and air pollution are currently lacking.

          Related collections

          Most cited references123

          • Record: found
          • Abstract: found
          • Article: not found

          Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines-2016 revision.

          Arnav Agarwal, Claus Bachert, Sinthia Z Bosnic-Anticevich … (2018)
          Allergic rhinitis (AR) affects 10% to 40% of the population. It reduces quality of life and school and work performance and is a frequent reason for office visits in general practice. Medical costs are large, but avoidable costs associated with lost work productivity are even larger than those incurred by asthma. New evidence has accumulated since the last revision of the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines in 2010, prompting its update.
          Article 0 comments Cited 518 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Clearing the air: a review of the effects of particulate matter air pollution on human health.

            Jonathan Anderson, Josef G. Thundiyil, Andrew Stolbach (2012)
            The World Health Organization estimates that particulate matter (PM) air pollution contributes to approximately 800,000 premature deaths each year, ranking it the 13th leading cause of mortality worldwide. However, many studies show that the relationship is deeper and far more complicated than originally thought. PM is a portion of air pollution that is made up of extremely small particles and liquid droplets containing acids, organic chemicals, metals, and soil or dust particles. PM is categorized by size and continues to be the fraction of air pollution that is most reliably associated with human disease. PM is thought to contribute to cardiovascular and cerebrovascular disease by the mechanisms of systemic inflammation, direct and indirect coagulation activation, and direct translocation into systemic circulation. The data demonstrating PM's effect on the cardiovascular system are strong. Populations subjected to long-term exposure to PM have a significantly higher cardiovascular incident and mortality rate. Short-term acute exposures subtly increase the rate of cardiovascular events within days of a pollution spike. The data are not as strong for PM's effects on cerebrovascular disease, though some data and similar mechanisms suggest a lesser result with smaller amplitude. Respiratory diseases are also exacerbated by exposure to PM. PM causes respiratory morbidity and mortality by creating oxidative stress and inflammation that leads to pulmonary anatomic and physiologic remodeling. The literature shows PM causes worsening respiratory symptoms, more frequent medication use, decreased lung function, recurrent health care utilization, and increased mortality. PM exposure has been shown to have a small but significant adverse effect on cardiovascular, respiratory, and to a lesser extent, cerebrovascular disease. These consistent results are shown by multiple studies with varying populations, protocols, and regions. The data demonstrate a dose-dependent relationship between PM and human disease, and that removal from a PM-rich environment decreases the prevalence of these diseases. While further study is needed to elucidate the effects of composition, chemistry, and the PM effect on susceptible populations, the preponderance of data shows that PM exposure causes a small but significant increase in human morbidity and mortality. Most sources agree on certain "common sense" recommendations, although there are lonely limited data to support them. Indoor PM exposure can be reduced by the usage of air conditioning and particulate filters, decreasing indoor combustion for heating and cooking, and smoking cessation. Susceptible populations, such as the elderly or asthmatics, may benefit from limiting their outdoor activity during peak traffic periods or poor air quality days. These simple changes may benefit individual patients in both short-term symptomatic control and long-term cardiovascular and respiratory complications.
            Article 0 comments Cited 373 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Perennial allergen sensitisation early in life and chronic asthma in children: a birth cohort study.

              Sabina Illi, Erika von Mutius, Susanne Lau … (2006)
              Reduced lung function is a feature of chronic asthma, which becomes apparent at school age. Unknown factors between birth and school age determine the progressive loss of pulmonary function in children with persistent asthma. We investigated the role of allergic sensitisation and allergen exposure early in life. The German Multicentre Allergy Study followed 1314 children from birth to 13 years of age. We regularly interviewed parents about their child's asthma and measured IgE levels. Allergen exposure was assessed at age 6 months, 18 months, and at 3, 4, and 5 years; lung function was assessed at 7, 10, and 13 years; post-bronchodilator response at 10 and 13 years; and a bronchial histamine challenge was done at 7 years. 90% of children with wheeze but no atopy lost their symptoms at school age and retained normal lung function at puberty. By contrast, sensitisation to perennial allergens (eg, house dust mite, cat and dog hair) developing in the first 3 years of life was associated with a loss of lung function at school age. Concomitant exposure to high levels of perennial allergens early in life aggravated this process: forced expiratory volume in 1 s (FEV1) to forced vital capacity (FVC) ratio was 87.4 (SD 7.4) for those sensitised and with high exposure compared with 92.6 (6.0) for those not sensitised, p<0.0001; and maximal expiratory flow at 50% (MEF50) 86.4 (25.1) for sensitised and with high exposure compared with 101.5 (23.2; p=0.0031) for those not sensitised. Such exposure also enhanced the development of airway hyper-responsiveness in sensitised children with wheeze. Sensitisation and exposure later in life had much weaker effects and sensitisation to seasonal allergens did not play a part. The chronic course of asthma characterised by airway hyper-responsiveness and impairment of lung function at school age is determined by continuing allergic airway inflammation beginning in the first 3 years of life. However, children with a non-atopic wheezing phenotype lose their symptoms over school age and retain normal lung function at puberty.
              Article 0 comments Cited 118 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Robert Naclerio
                Journal
                Journal ID (nlm-ta): World Allergy Organ J
                Journal ID (iso-abbrev): World Allergy Organ J
                Title: The World Allergy Organization Journal
                Publisher: World Allergy Organization
                ISSN (Electronic): 1939-4551
                Publication date PMC-release: 03 April 2020
                Publication date Collection: March 2020
                Publication date (Electronic): 03 April 2020
                Volume: 13
                Issue: 3
                Electronic Location Identifier: 100106
                Affiliations
                [a ]Johns Hopkins School of Medicine, Baltimore, MD, USA
                [b ]Department of Allergy & Immunology, Hospital Quironsalud Bizkaia- Bilbao, Spain
                [c ]INSERM U 1168, VIMA: Ageing and Chronic Diseases Epidemiological and Public Health Approaches, Villejuif, France
                [d ]University Versailles St-Quentin-en-Yvelines, France
                [e ]Humanitas University & Research Hospital, Milano, Italy
                [f ]Division of Respiratory and Allergic Diseases, High Specialty Hospital A. Cardarelli, Napoli, Italy; School of Specialization in Respiratory Diseases University Federico II Naples, Italy
                [g ]Pediatric Respiratory Medicine Division, Complexo Hospital de Clinicas, UFPR, Curitiba, Brazil
                [h ]Dept. of Pediatrics, Nippon Medical School, Tokyo, Japan
                [i ]UNC Center for Environmental Medicine, Asthma, and Lung Biology; Division of Allergy, Immunology and Rheumatology, Dpt. of Pediatrics UNS School of Medicine, USA
                [j ]Allergy-Centre-Charité, Charité–Universita¨tsmedizin Berlin, Berlin, Germany
                [k ]Medicine & Ophthalmology Hackensack Meridian School of Medicine at Seton Hall University Nutley, New Jersey, USA
                [l ]Institute for Immunological Research, University of Cartagena, Cartagena de Indias, Colombia
                [m ]Centre de Bioclimatology, University de Florence, Florence, Italy
                [n ]SOS Allergy and Immunology, Prato - USL Toscana Centro, Italy
                [o ]Fundación Hospital Universitario Metropolitano de Barranquilla, Barranquilla, Colombia
                [p ]Federal University of Paraná, Brazil
                [q ]Department of Botany, Ecology and Plant Physiology, University of Córdoba, Spain
                [r ]San Francisco Centro de Especialistas Médicos Monterrey NL, Mexico
                [s ]Department of Otolaryngology- Head and Neck Surgery, Eye and Ear University Hospital, Beirut, Lebanon
                [t ]Alexander's University Hospital Clinic of Allergy & Asthma, Bulgaria
                [u ]Alergia e Inmunología, Hospital Italiano Regional del Sur, Bahía Blanca-Buenos Aires, Argentina
                [v ]Department of Clinical and Experimental Medicine, Università; di Parma, Parma, Italy
                [w ]Allergy Asthma and Immunology, Emek Medical Center, Afula, Israel
                [x ]Rappaport Faculty of Medicine Technion, Israel Institute of Technology, Haifa, Israel
                [y ]Department of Plant Science, Faculty of Science, Mahidol University, Bangkok, Thailand
                [z ]Systems Biology of Diseases Research Unit, Faculty of Science, Mahidol University, Bangkok, Thailand
                Author notes
                [∗ ]Corresponding author. rnacler1@ 123456jhmi.edu
                Article
                Publisher ID: S1939-4551(20)30009-0 Publisher ID: 100106
                DOI: 10.1016/j.waojou.2020.100106
                PMC ID: 7132263
                PubMed ID: 32256939
                SO-VID: c5474f0f-376d-4cc0-beee-1464931aa656
                Copyright © © 2020 The Authors
                License:

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 21 February 2019
                Date revision received : 17 January 2020
                Date accepted : 23 January 2020
                Categories
                Subject: Article

                ScienceOpen disciplines: Immunology
                Keywords: allergic rhinitis,occupational rhinitis,air pollution,climate change,air pollutants,indoor air quality,oxidative stress,antioxidant enzymes,ap, activator protein,aer, allergic eosinophilic rhinitis,ar, allergic rhinitis,are, antioxidant response element,co, carbon monoxide,cfs, chronic fatigue syndrome,copd, chronic obstructive pulmonary disease,damp, damage-associated molecular patterns,dep, diesel exhaust particles,ecat, elemental carbon attributable to traffic,ecp, eosinophil cationic protein,gsh-px, glutathione peroxidase,hvac, heating, ventilation and air conditioning,ho, hemeoxygenase,hepa, high efficiency particulate air,hdm, house dust mites,iap, indoor air pollution,iaq, indoor air quality,ins, intranasal steroids,ldh, lactate dehydrogenase,msqpcr, mold specific quantitative pcr,mcp, monocyte chemotactic protein,nox, nitric oxides,no2, nitrogen dioxide,nar, non allergic rhinitis,nrf2, nuclear factor erythroid-2 related factor,nf-κβ, nuclear factor kappa β,oap, outdoor air pollution,o3, ozone,pon, paraoxonase,pm, particulate matter,pamp, pathogen-associated molecular patterns,rns, reactive nitrosative species,ros, reactive oxygen species,so2, sulphur dioxide,sod, superoxide dismutase,tlr, toll like receptor,tos, total oxidative status,trap, traffic related air pollutants,tnf, tumor necrosis factor,ufp, ultra-fine particles,vocs, volatile organic compound
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: allergic rhinitis, occupational rhinitis, air pollution, climate change, air pollutants, indoor air quality, oxidative stress, antioxidant enzymes, ap, activator protein, aer, allergic eosinophilic rhinitis, ar, allergic rhinitis, are, antioxidant response element, co, carbon monoxide, cfs, chronic fatigue syndrome, copd, chronic obstructive pulmonary disease, damp, damage-associated molecular patterns, dep, diesel exhaust particles, ecat, elemental carbon attributable to traffic, ecp, eosinophil cationic protein, gsh-px, glutathione peroxidase, hvac, heating, ventilation and air conditioning, ho, hemeoxygenase, hepa, high efficiency particulate air, hdm, house dust mites, iap, indoor air pollution, iaq, indoor air quality, ins, intranasal steroids, ldh, lactate dehydrogenase, msqpcr, mold specific quantitative pcr, mcp, monocyte chemotactic protein, nox, nitric oxides, no2, nitrogen dioxide, nar, non allergic rhinitis, nrf2, nuclear factor erythroid-2 related factor, nf-κβ, nuclear factor kappa β, oap, outdoor air pollution, o3, ozone, pon, paraoxonase, pm, particulate matter, pamp, pathogen-associated molecular patterns, rns, reactive nitrosative species, ros, reactive oxygen species, so2, sulphur dioxide, sod, superoxide dismutase, tlr, toll like receptor, tos, total oxidative status, trap, traffic related air pollutants, tnf, tumor necrosis factor, ufp, ultra-fine particles, vocs, volatile organic compound

                Comments

                Comment on this article

                scite_

                Similar content200

                See all similar

                Cited by38

                See all cited by

                Most referenced authors2,230

                See all reference authors