Objective
Large quantities of epidemiological studies manifest that indoor and outdoor air pollutants may trigger and aggravate asthma symptoms, whose mechanism, however, has not been completely made clear yet. As shown by the result of the experiment in which in-vitro cells and animals are exposed to high-density air pollution, the triggering effect of air pollution on asthma is associated with inflammatory reaction, IgE expression and regulation pathways. However, there is a lack of evidence from population studies to support that association. This study plans to conduct continuous monitoring over indoor and outdoor air pollutants facing the asthmatic children from Beijing with a view to carry out an overall assessment of their exposure to air pollutants. Meanwhile, biomarkers which are directly reflecting airway inflammation as well as the signal molecules which are related to IgE expression and regulation are monitored. The next step is to establish an exposure-effect relationship to explore the trigger effect of air pollutants on childhood asthma.
Methods
1. Questionnaires were used to collect general information (including age, drug use, indoor home decoration, passive smoking, diet during the study, indoor mildew, allergic history, history of diseases and family heredity history) in 60 asthmatic children (males, Han nationality, aged 5 to 14 years)from Beijing who were recruited into this study.
2. A comprehensive evaluation was conducted on their exposure levels of air pollutants by continuous monitoring of indoor PM2.5, black carbon, benzene, toluene, xylene and formaldehyde in their houses and collecting monitoring data with respect to PM2.5, PM10, NO2and SO2at air quality monitoring sites near their houses. Benzene, toluene and xylene were measured by two-stage thermal desorption-gas chromatography (GC), formaldehyde by AHMT spectrophotometry, mass concentration of PM2.5by gravimetric method, black carbon in PM2.5by multi-wavelength absorption spectroscopy. The concentration data of ambient outdoor air pollutants were available from the real-time air quality publishing platform of Beijing Municipal Environmental Monitoring Center.
3. Exhaled FeNO of asthmatic children were taken as biomarkers reflecting their airway inflammation. FeNO was measured by electrochemical method (off-line monitoring).
4. Trigger effect of air pollution on IgE signaling pathway of asthmatic children was investigated by determining signal molecules of two signaling pathways related to IgE expression and regulation in peripheral serum. Signal molecules were determined by ELISA.
5. Confounding factors were controlled by stratification analysis and multiple linear regression model, and a comprehensive analysis was conducted of the triggering effect of air pollution on children asthma.
Results
1. During the research, as for subjects, concentrations of indoor PM2.5, BC, formaldehyde, benzene, toluene, m-, p-and o-xylenes were 55.3±29.9 μg/m3, 3.8±1.4 μg/m3,62.2±42.7 μg/m3, 13.1±15.9 μg/m3, 18.7±16.7 μg/m3, 7.9±7.9 μg/m3and 3.1±5.0 μg/m3, respectively. The7-day weighted average concentrations of outdoor PM2.5, PM10, SO2and NO2were 101.3±87.6μg/m3, 152.8±88.4μg/m3, 48.6±39.8 μg/m3and 63.1±27.7μg/m3, respectively. There was a significant correlation between 7-day weighted average concentrations of indoor and outdoor PM2.5 simultaneously (r=0.697, P<0.001), with a indoor/outdoor PM2.5concentration ratio (I/O ratio) of 0.86±0.39 (P25-P75ranging from 0.62 to 1.01).
2. After adjusting for such influencing factors as age, types of asthma, and season, analysis of all subjects found that FeNO was significantly positively correlated with either benzene in indoor air, or PM2.5, SO2and NO2 in ambient outdoor air. Separate analysis of subjects untreated with inhaled corticosteroids (ICSs) found that FeNO was significantly positively correlated with PM2.5, SO2and NO2 in ambient outdoor air, while this correlation was not significant in the ICS-treated group.
3. In serum, there was a significantly positive correlation between signal molecules in the two regulatory pathways of IgE expression. After adjusting for such influencing factors as age, types of asthma, and passive smoking. No effect of air pollutants on level of signaling molecule was observed in this study.
Conclusion
Monitoring results of indoor and outdoor air pollutants show that, at a high level of exposure to air pollutants, exposure of asthmatic children to indoor and outdoor air pollutants may cause or aggravate the airway inflammation. Administration of ICSs can control or attenuate the airway inflammation caused by air pollutants in asthmatic children, while the level of signaling molecule in the regulatory pathway of IgE expression in serum may not be an ideal marker for reflecting the trigger effect of air pollution on children asthma. / published_or_final_version / Public Health / Master / Master of Public Health
| Identifer | oai:union.ndltd.org:HKU/oai:hub.hku.hk:10722/206933 |
| Date | January 2014 |
| Creators | Lin, Xia, 林夏 |
| Publisher | The University of Hong Kong (Pokfulam, Hong Kong) |
| Source Sets | Hong Kong University Theses |
| Language | English |
| Detected Language | English |
| Type | PG_Thesis |
| Rights | The author retains all proprietary rights, (such as patent rights) and the right to use in future works., Creative Commons: Attribution 3.0 Hong Kong License |
| Relation | HKU Theses Online (HKUTO) |
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