Despo Ierodiakonou1, Antonella Zanobetti2, Brent A Coull3, Steve Melly2, Dirkje S Postma4, H Marike Boezen5, Judith M Vonk5, Paul V Williams6, Gail G Shapiro6, Edward F McKone7, Teal S Hallstrand8, Jane Q Koenig9, Jonathan S Schildcrout10, Thomas Lumley11, Anne N Fuhlbrigge12, Petros Koutrakis2, Joel Schwartz2, Scott T Weiss12, Diane R Gold13. 1. University of Groningen, Department of Epidemiology, University Medical Center Groningen, Groningen, The Netherlands; Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, Groningen, The Netherlands. Electronic address: d.ierodiakonou@euc.ac.cy. 2. Environmental Epidemiology and Risk Program, Harvard T.H. Chan School of Public Health, Boston, Mass. 3. Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Mass. 4. Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, Groningen, The Netherlands; University of Groningen, Department of Pulmonology, University Medical Center Groningen, Groningen, The Netherlands. 5. University of Groningen, Department of Epidemiology, University Medical Center Groningen, Groningen, The Netherlands; Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, Groningen, The Netherlands. 6. Department of Pediatrics, School of Medicine, University of Washington, Seattle, Wash. 7. Department of Respiratory Medicine, St Vincent University Hospital, Dublin, Ireland. 8. Department of Pulmonary and Critical Care, School of Medicine, University of Washington, Seattle, Wash. 9. Department of Environmental Health, School of Medicine, University of Washington, Seattle, Wash. 10. Department of Biostatistics, School of Medicine, Vanderbilt University, Nashville, Tenn. 11. Department of Statistics, University of Auckland, Auckland, New Zealand. 12. Channing Laboratory, Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Boston, Mass. 13. Environmental Epidemiology and Risk Program, Harvard T.H. Chan School of Public Health, Boston, Mass; Channing Laboratory, Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Boston, Mass. Electronic address: diane.gold@channing.harvard.edu.
Abstract
BACKGROUND: Although ambient air pollution has been linked to reduced lung function in healthy children, longitudinal analyses of pollution effects in asthmatic patients are lacking. OBJECTIVE: We sought to investigate pollution effects in a longitudinal asthma study and effect modification by controller medications. METHODS: We examined associations of lung function and methacholine responsiveness (PC20) with ozone, carbon monoxide (CO), nitrogen dioxide, and sulfur dioxide concentrations in 1003 asthmatic children participating in a 4-year clinical trial. We further investigated whether budesonide and nedocromil modified pollution effects. Daily pollutant concentrations were linked to ZIP/postal code of residence. Linear mixed models tested associations of within-subject pollutant concentrations with FEV1 and forced vital capacity (FVC) percent predicted, FEV1/FVC ratio, and PC20, adjusting for seasonality and confounders. RESULTS: Same-day and 1-week average CO concentrations were negatively associated with postbronchodilator percent predicted FEV1 (change per interquartile range, -0.33 [95% CI, -0.49 to -0.16] and -0.41 [95% CI, -0.62 to -0.21], respectively) and FVC (-0.19 [95% CI, -0.25 to -0.07] and -0.25 [95% CI, -0.43 to -0.07], respectively). Longer-term 4-month CO averages were negatively associated with prebronchodilator percent predicted FEV1 and FVC (-0.36 [95% CI, -0.62 to -0.10] and -0.21 [95% CI, -0.42 to -0.01], respectively). Four-month averaged CO and ozone concentrations were negatively associated with FEV1/FVC ratio (P < .05). Increased 4-month average nitrogen dioxide concentrations were associated with reduced postbronchodilator FEV1 and FVC percent predicted. Long-term exposures to sulfur dioxide were associated with reduced PC20 (percent change per interquartile range, -6% [95% CI, -11% to -1.5%]). Treatment augmented the negative short-term CO effect on PC20. CONCLUSIONS: Air pollution adversely influences lung function and PC20 in asthmatic children. Treatment with controller medications might not protect but rather worsens the effects of CO on PC20. This clinical trial design evaluates modification of pollution effects by treatment without confounding by indication.
BACKGROUND: Although ambient air pollution has been linked to reduced lung function in healthy children, longitudinal analyses of pollution effects in asthmatic patients are lacking. OBJECTIVE: We sought to investigate pollution effects in a longitudinal asthma study and effect modification by controller medications. METHODS: We examined associations of lung function and methacholine responsiveness (PC20) with ozone, carbon monoxide (CO), nitrogen dioxide, and sulfur dioxide concentrations in 1003 asthmatic children participating in a 4-year clinical trial. We further investigated whether budesonide and nedocromil modified pollution effects. Daily pollutant concentrations were linked to ZIP/postal code of residence. Linear mixed models tested associations of within-subject pollutant concentrations with FEV1 and forced vital capacity (FVC) percent predicted, FEV1/FVC ratio, and PC20, adjusting for seasonality and confounders. RESULTS: Same-day and 1-week average CO concentrations were negatively associated with postbronchodilator percent predicted FEV1 (change per interquartile range, -0.33 [95% CI, -0.49 to -0.16] and -0.41 [95% CI, -0.62 to -0.21], respectively) and FVC (-0.19 [95% CI, -0.25 to -0.07] and -0.25 [95% CI, -0.43 to -0.07], respectively). Longer-term 4-month CO averages were negatively associated with prebronchodilator percent predicted FEV1 and FVC (-0.36 [95% CI, -0.62 to -0.10] and -0.21 [95% CI, -0.42 to -0.01], respectively). Four-month averaged CO and ozone concentrations were negatively associated with FEV1/FVC ratio (P < .05). Increased 4-month average nitrogen dioxide concentrations were associated with reduced postbronchodilator FEV1 and FVC percent predicted. Long-term exposures to sulfur dioxide were associated with reduced PC20 (percent change per interquartile range, -6% [95% CI, -11% to -1.5%]). Treatment augmented the negative short-term CO effect on PC20. CONCLUSIONS: Air pollution adversely influences lung function and PC20 in asthmatic children. Treatment with controller medications might not protect but rather worsens the effects of CO on PC20. This clinical trial design evaluates modification of pollution effects by treatment without confounding by indication.
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