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Review
. 2015 Dec;27(6):724-35.
doi: 10.1097/MOP.0000000000000286.

Air pollution and allergic diseases

Eric B Brandt  1 , Jocelyn M Biagini Myers, Patrick H Ryan, Gurjit K Khurana Hershey
Affiliations
Review

Air pollution and allergic diseases

Eric B Brandt et al. Curr Opin Pediatr. 2015 Dec.

Abstract

Purpose of review: Exposure to traffic-related air pollutants (TRAPs) has been implicated in asthma development, persistence, and exacerbation. This exposure is highly significant because increasingly large segments of the population worldwide reside in zones that have high levels of TRAP, including children, as schools are often located in high traffic pollution exposure areas.

Recent findings: Recent findings include epidemiologic and mechanistic studies that shed new light on the impact of traffic pollution on allergic diseases and the biology underlying this impact. In addition, new innovative methods to assess and quantify traffic pollution have been developed to assess exposure and identify vulnerable populations and individuals.

Summary: This review will summarize the most recent findings in each of these areas. These findings will have a substantial impact on clinical practice and research by the development of novel methods to quantify exposure and identify at-risk individuals, as well as mechanistic studies that identify new targets for intervention for individuals most adversely affected by TRAP exposure.

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Conflict of interest statement

Conflict of interest: The authors have declared that no conflict of interest exists.

Figures

Figure 1
Figure 1. Mechanistic insights into DEP effects on asthma pathogenesis
Lung epithelial cells recognize polycyclic aromatic hydrocarbons present in diesel exhaust particles (DEP) via the aryl hydrocarbon receptor (AhR), promoting cytochrome P450 family 1 A1 (CYP1A1) mediated detoxification. Failure to detoxify results in oxidative stress and release of repair cytokines (amphiregulin, TGFα), which signal through the epidermal growth factor receptor (EGFR), p38 mitogen-activated protein kinase and NF-κB to induce secretion of chemokines, as well as cytokines involved in TH17 and TH2 differentiation (TSLP). DEP promotes allergic airway inflammation by upregulating the expression of the Jagged1/Notch1 pathway in dendritic cells (DC) in an AhR dependent manner in concert with allergens.
Figure 2
Figure 2. Overview
More accurate assessment of TRAP exposure will enable the design of epidemiologic and mechanistic studies aimed at discovery of biomarkers to identify the individuals most at-risk from the harmful effects of TRAP exposure and the design of novel targeted interventions.
See this image and copyright information in PMC

References

    1. HEI Panel on the Health Effects of Traffic-Related Air Pollution. Traffic-Related Air Pollution: A Critical Review of the Literature on Emissions, Exposure, and Health Effects. Boston, MA: Health Effects Institute; 2010.
    1. Acciani TH, Brandt EB, Khurana Hershey GK, Le Cras TD. Diesel exhaust particle exposure increases severity of allergic asthma in young mice. Clin Exp Allergy. 2013;43(12):1406–18. - PMC - PubMed
    1. Takahashi G, Tanaka H, Wakahara K, Nasu R, Hashimoto M, Miyoshi K, et al. Effect of diesel exhaust particles on house dust mite-induced airway eosinophilic inflammation and remodeling in mice. Journal of pharmacological sciences. 2010;112(2):192–202. - PubMed
    1. Brandt EB, Kovacic MB, Lee GB, Gibson AM, Acciani TH, Le Cras TD, et al. Diesel exhaust particle induction of IL-17A contributes to severe asthma. The Journal of allergy and clinical immunology. 2013;132(5):1194–204. e2. - PMC - PubMed
    1. Appatova AS, Ryan PH, LeMasters GK, Grinshpun SA. Proximal exposure of public schools and students to major roadways: a nationwide US survey. J Environ Plann Man. 2008;51(5):631–46.

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