哮喘
医学
过敏
环境卫生
被动吸烟
呼出气冷凝液
烟草烟雾
免疫学
作者
Qingbin Liu,Wei Wang,Jing Wei
标识
DOI:10.1080/09603123.2018.1506569
摘要
Indoor air pollution is associated with childhood asthma but the molecular mechanism remains unclear. We aimed to explore the relationship between indoor air pollution and pediatric asthma, and the potential molecular mechanism. The serum level of miR-155 was measured by real-time qPCR in 180 Chinese children with asthma caused by air pollution (an asthma group). Meanwhile, 180 healthy subjects were selected as a control group. HCHO, NO2, and particles (PM10, PM2.5, and PM1) were measured. Univariate and multivariate logistic regression were analyzed to assess the relationship between air pollutants and asthma risk. A rank correlation test was used to explore the relationship between serum level of miR-155 and the level of PM2.5 or HCHO. Serum level of miR-155 was higher in the asthma group than the control group (p < 0.001). The history of childhood allergy, breastfeeding, environmental tobacco smoke, PM2.5, and HCHO were significantly different between two groups (p < 0.05). Serum level of miR-155 was closely associated with the levels of indoor PM2.5 and HCHO in the asthma group (p < 0.05) but not in the control group (p > 0.05). Indoor air pollution aggravates the asthma in Chinese children and induces the changes in the serum level of miR-155. Abbreviation: DEP: Diesel exhaust particles; PAHs: Polycyclic aromatic hydrocarbons; THBS1: thrombospondin 1; ISAAC: International Study of Asthma and Allergies in Childhood; PFTs: Pulmonary Function Tests; FEV1: The first second of forced expiration; EDTA, ethylenediaminetetraacetic acid; RT-qPCR, Reverse transcription quantitative real-time PCR; ETS: environmental tobacco smoke; PAEs: phthalate esters.
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