<p>Air Pollution and Allergic Rhinitis: Role in Symptom Exacerbation and Strategies for Management</p>

Abstract

This article reviews the current understanding of the role of air pollution in both the symptom exacerbation and rising prevalence of allergic rhinitis (AR) for the development of future AR therapeutics and management strategies. We discuss the epidemiological evidence for this relationship through birth cohort studies, the economic impact of AR, and the influence of air pollution through the lens of the exposome framework of allergic disease development. This is followed by a discussion on the influence of diesel exhaust and diesel exhaust particles (DEP) from motor vehicle emissions and their implication in the rising prevalence of allergic disease and allergic sensitization through triggering inflammatory signalling pathways that exacerbate AR symptoms. Finally, a summary is provided of clinical trials assessing the influence of air pollution on AR with a depiction of currently available therapies and management strategies. Future directions in the development of AR modalities given the air pollution-mediated symptom exacerbation are challenged with unfolding the complex gene-environment interaction product of heterogenous AR presentation.

Effect of fexofenadine hydrochloride on allergic rhinitis aggravated by air pollutants

“…the dose-dependent deleterious effects of pollen exposure were magnified by air pollutant exposure) [ 29 ]. While a growing body of evidence supports a link between allergic diseases and air pollution [ 3 , 30 ], other studies show mixed results [ 31 , 32 ]. M ö lter et al [ 32 ] found no significant association between asthma prevalence and exposure to selected air pollutants in a meta-analysis of five European birth cohorts.…”

“…Pharmacological options for the treatment of allergic rhinitis are well established, but additional research is needed on the efficacy of conventional pharmacotherapy in patients exposed to air pollution [ 26 ]. A review of the studies investigating allergic rhinitis symptoms aggravated by air pollutants showed that fexofenadine HCl is the only allergic rhinitis medication with demonstrated efficacy and tolerability for the management of DEP-aggravated symptoms [ 26 , 30 ]. DEP exposure has been shown to trigger numerous pro-inflammatory signalling pathways other than histamine-mediated ones [ 30 ].…”

“…A review of the studies investigating allergic rhinitis symptoms aggravated by air pollutants showed that fexofenadine HCl is the only allergic rhinitis medication with demonstrated efficacy and tolerability for the management of DEP-aggravated symptoms [ 26 , 30 ]. DEP exposure has been shown to trigger numerous pro-inflammatory signalling pathways other than histamine-mediated ones [ 30 ]. DEP increases circulating neutrophils, eosinophils, and cytokines, and induces the expression of adhesion molecules as intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) which are critical for T cell activation [ 9 , 21 ].…”

Intranasal levels of lead as an exacerbation factor for allergic rhinitis in humans and mice

“…There have been a variety of quantitative allergotoxicologic studies [44][45][46] in which the effects of total suspended particles including particulate matter with diameter <2.5 mm on allergic rhinitis were examined. Although there have been qualitative allergotoxicologic studies 46,47 on the effects of components in total suspended particles on allergic rhinitis, the amount of information about the components that exacerbate allergic rhinitis is insufficient.…”

An Exploratory Study of the Relationships Between Diesel Engine Exhaust Particle Inhalation, Pulmonary Inflammation and Anxious Behavior

“…Based on these disadvantages, heavy casualties may occur. In the long term, lifetime DEP inhalation from air pollution may cause significant pathological alterations, such as asthma [29,30], allergic reactions [31], and cardiac pressures [32]. Moreover, DEP exposure to neuronal cells elevates neuronal oxidative stress and inflammation [33], as well as neurotoxicity [34].…”