Pulmonology Service, Medicine Department, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación en Red de Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III (ISCIII), Madrid, Spain; Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Barcelona, Spain.
Centro de Investigación en Red de Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III (ISCIII), Madrid, Spain; Pulmonology Department-Muscle Research and Respiratory System Unit (URMAR), Institut Hospital del Mar d'Investigacions Mèdiques (IMIM)-Hospital del Mar, Department of Experimental and Health Sciences (CEXS), Universitat Pompeu Fabra, Parc de Recerca Biomèdica de Barcelona (PRBB), Barcelona, Spain.
Sci Total Environ. 2019 Feb 20;652:1129-1138. doi: 10.1016/j.scitotenv.2018.10.188. Epub 2018 Oct 15.
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 complex mixture 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.
暴露于空气污染物与哮喘严重程度的增加和已存在哮喘的恶化有关。然而,环境污染是否会导致哮喘仍然是一个有争议的问题。本综述分析了柴油机排气颗粒(DEP)与哮喘之间可能存在因果关系的现有科学证据,DEP 是柴油机排气复杂混合物的固体部分。影响哮喘表达和发展的机制很复杂。在儿童中,长时间暴露于 DEP 等污染物可能会增加哮喘的发病率。在成年人中,这种因果关系不太清楚,可能是由于进行的研究存在异质性。也有证据表明 DEP 可以通过生理机制引起哮喘。细胞反应与 DEP 之间最常描述的相互作用是诱导肺部氧化应激和炎症,以及激活支气管上皮细胞的受体,如 toll 样受体或 Th2 和 Th17 细胞因子的增加,这些通常协调哮喘反应。其他机制则通过表观遗传变化、肺部微生物组的改变或 DEP 与环境抗原的相互作用来增强其活性,从而发挥间接作用。然而,尽管有这些证据,仍需要更多的研究来评估污染的有害影响——不仅是短期内以恶化率增加的形式,而且是中长期内,因为它可能是疾病的一个潜在诱因。