Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6063049 | Journal of Allergy and Clinical Immunology | 2014 | 8 Pages |
Abstract
Despite attempts and some successes to improve air quality over the decades, current US national trends suggest that exposure to outdoor and indoor air pollution remains a significant risk factor for both the development of asthma and the triggering of asthma symptoms. Emerging science also suggests that environmental exposures during the prenatal period and early childhood years increase the risk of asthma. Multiple mechanisms mediate this risk because a wide range of deleterious air pollutants contribute to the pathogenesis of asthma across a variety of complex asthma phenotypes. In this review we will consider the role of altered innate and adaptive immune responses, gene-environment interactions, epigenetic regulation, and possibly gene-environment-epigene interactions. Gaining a greater understanding of the mechanisms that underlie the effect of exposure to air pollution on asthma, allergies, and other airway diseases can identify targets for therapy. Such interventions will include pollutant source reduction among those most exposed and most vulnerable and novel pharmaceutical strategies to reduce asthma morbidity.
Keywords
PAHDEPDAMPGSTMYD88CCCEHPAMPTLRPM10TregPM2.5FOXP3β2ARAHRColumbia Center for Children's Environmental HealthNOxAir pollutiondamage-associated molecular patternpathogen-associated molecular patternOzoneInnate immunityadaptive immunityAirway hyperreactivityToll-like receptorforkhead box P3diesel exhaust particleparticulate matterDendritic cellRegulatory T Epigenetic regulationMechanismsNO2Nitrogen dioxidePolycyclic aromatic hydrocarbonmyeloid differentiation primary response gene 88Single nucleotide polymorphismSNPBlack carbonglutathione-S-transferaseβ2-adrenergic receptor
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Authors
Rachel L. MD, David B. MD,