Acute Effects of Air Pollution on Pulmonary Function, Airway Inflammation, and Oxidative Stress in Asthmatic Children
OBJECTIVE: In this study we investigated acute effects of air pollution on pulmonary function and airway oxidative stress and inflammation in asthmatic children.
METHODS: We studied 182 children with asthma, 9-14 years of age, for 4 weeks. Daily ambient concentrations of sulfur dioxide, nitrogen dioxide, ozone, and particulate matter < or = 2.5 microm in aerodynamic diameter (PM(2.5)) were monitored from two stations. Once a week we measured spirometry and fractional exhaled nitric oxide (FeNO), and determined thiobarbituric acid reactive substances (TBARS) and 8-isoprostane--two oxidative stress markers--and interleukin-6 (IL-6) in breath condensate. We tested associations using mixed-effects regression models, adjusting for confounding variables.
RESULTS: Interquartile-range increases in 3-day average SO2 (5.4 ppb), NO2 (6.8 ppb), and PM(2.5) (5.4 microg/m3) were associated with decreases in forced expiratory flow between 25% and 75% of forced vital capacity, with changes being -3.1% [95% confidence interval (CI), -5.8 to -0.3], -2.8% (95% CI, -4.8 to -0.8), and -3.0% (95% CI, -4.7 to -1.2), respectively. SO2, NO2, and PM(2.5) were associated with increases in TBARS, with changes being 36.2% (95% CI, 15.7 to 57.2), 21.8% (95% CI, 8.2 to 36.0), and 24.8% (95% CI, 10.8 to 39.4), respectively. Risk estimates appear to be larger in children not taking corticosteroids than in children taking corticosteroids. O3 (5.3 ppb) was not associated with health end points. FeNO, 8-isoprostane, and IL-6 were not associated with air pollutants.
CONCLUSION: Air pollution may increase airway oxidative stress and decrease small airway function of asthmatic children. Inhaled corticosteroids may reduce oxidative stress and improve airway function.
History
Publication title
Environmental Health PerspectivesVolume
117Issue
4Pagination
668-674ISSN
0091-6765Department/School
Menzies Institute for Medical ResearchPublisher
Us Dept Health Human Sciences Public Health SciencePlace of publication
Natl Inst Health, Natl Inst Environmental Health Sciences, Po Box 12233, Res Triangle Pk, USA, Nc, 27709-2233Rights statement
Copyright unknownRepository Status
- Open