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HERO ID
6793272
Reference Type
Journal Article
Title
Diesel exhausts particles: Their role in increasing the incidence of asthma. Reviewing the evidence of a causal link
Author(s)
Munoz, X; Barreiro, E; Bustamante, V; Lopez-Campos, JL; Gonzalez-Barcala, FJ; Cruz, MJ; ,
Year
2019
Is Peer Reviewed?
1
Journal
Science of the Total Environment
ISSN:
0048-9697
EISSN:
1879-1026
Publisher
ELSEVIER
Location
AMSTERDAM
Page Numbers
1129-1138
PMID
30586799
DOI
10.1016/j.scitotenv.2018.10.188
Web of Science Id
WOS:000454418500104
Abstract
Exposure to air pollutants has been correlated with an increase in the severity of asthma and in the exacerbation of pre-existing asthma. However, whether or not environmental pollution can cause asthma remains a controversial issue. The present review analyzes the current scientific evidence of the possible causal link between diesel exhaust particles (DEP), the solid fraction of the complexmixture of diesel exhaust, and asthma. The mechanisms that influence the expression and development of asthma are complex. In children prolonged exposure to pollutants such as DEPs may increase asthma prevalence. In adults, this causal relation is less clear, probably because of the heterogeneity of the studies carried out. There is also evidence of physiological mechanisms by which DEPs can cause asthma. The most frequently described interactions between cellular responses and DEP are the induction of pulmonary oxidative stress and inflammation and the activation of receptors of the bronchial epithelium such as toll-like receptors or increases in Th2 and Th17 cytokines, which generally orchestrate the asthmatic response. Others support indirect mechanisms through epigenetic changes, pulmonary microbiome modifications, or the interaction of DEP with environmental antigens to enhance their activity. However, in spite of this evidence, more studies are needed to assess the harmful effects of pollution - not only in the short term in the form of increases in the rate of exacerbations, but in the medium and long term as well, as a possible trigger of the disease. (C) 2018 Elsevier B.V. All rights reserved.
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