Acute effects of air pollution on pulmonary function, airway inflammation, and oxidative stress in asthmatic children.
BACKGROUND
Air pollution is associated with respiratory symptoms, lung function decrements, and hospitalizations. However, there is little information about the influence of air pollution on lung injury.


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.


CONCLUSIONS
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.
Liu
Ling
L
Healthy Environments and Consumer Safety Branch, Health Canada, Ottawa, Ontario, Canada. ling_liu@hc-sc.gc.ca
Poon
Raymond
R
Chen
Li
L
Frescura
Anna-Maria
AM
Montuschi
Paolo
P
Ciabattoni
Giovanni
G
Wheeler
Amanda
A
Dales
Robert
R
D000293:Adolescent; D000305:Adrenal Cortex Hormones / Q000032:analysis; D000393:Air Pollutants / Q000633:toxicity*; D001249:Asthma / Q000378:metabolism / Q000503:physiopathology*; D002648:Child; D004784:Environmental Monitoring; D005260:Female; D006801:Humans; D019570:Inhalation Exposure / Q000032:analysis; D008168:Lung / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D009569:Nitric Oxide / Q000032:analysis; D009585:Nitrogen Dioxide / Q000633:toxicity; D018384:Oxidative Stress; D010126:Ozone / Q000633:toxicity; D052638:Particulate Matter / Q000633:toxicity; D011014:Pneumonia / Q000378:metabolism*; D013458:Sulfur Dioxide / Q000633:toxicity
D000305:Adrenal Cortex Hormones; D000393:Air Pollutants; D052638:Particulate Matter; D013458:Sulfur Dioxide; D009569:Nitric Oxide; D010126:Ozone; D009585:Nitrogen Dioxide