Ambient air pollution, lung function, and airway responsiveness in asthmatic children - 05/02/16
, Antonella Zanobetti, PhD c, Brent A. Coull, PhD d, Steve Melly, MS c, Dirkje S. Postma, MD, PhD b, e, H. Marike Boezen, PhD a, b, Judith M. Vonk, PhD a, b, Paul V. Williams, MD f, Gail G. Shapiro, MD f, †, Edward F. McKone, MD, MS g, Teal S. Hallstrand, MD, MPH h, Jane Q. Koenig, PhD i, Jonathan S. Schildcrout, PhD j, Thomas Lumley, PhD k, Anne N. Fuhlbrigge, MD, MS l, Petros Koutrakis, PhD c, Joel Schwartz, PhD c, Scott T. Weiss, MD, PhD l, Diane R. Gold, MD, MPH c, l, ⁎ for the
Childhood Asthma Management Program Research Group
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.
Le texte complet de cet article est disponible en PDF.Key words : Asthma, ambient air pollution, airway hyperresponsiveness, inhaled corticosteroids, lung function
Abbreviations used : AHR, CAMP, CO, FVC, ICS, IQR, NO2, SO2
Plan
| Supported by the National Institutes of Health (NHLBI P01 HL083069, U01 HL075419, U01 HL65899, R01 HL 086601; NIEHS P01 ES09825, R21 ES020194, P30 ES000002), the US Environmental Protection Agency (RD 83241601, RD 83479801), and the International Initiative for Environment and Public Health Cyprus Program of HSPH. The contents of this publication are solely the responsibility of the grantee and do not necessarily represent the official views of the US Environmental Protection Agency. Further, the US Environmental Protection Agency does not endorse the purchase of any commercial products or services mentioned in the publication. The CAMP trial and CAMP Continuation Study were supported by contracts NO1-HR-16044, 16045, 16046, 16047, 16048, 16049, 16050, 16051, and 16052 with the NHLBI and General Clinical Research Center grants M01RR00051, M01RR0099718-24, M01RR02719-14, and RR00036 from the National Center for Research Resources. The CAMP Continuation Study/phases 2 and 3 were supported by grants U01HL075232, U01HL075407, U01HL075408, U01HL075409, U01HL075415, U01HL075416, U01HL075417, U01HL075419, U01HL075420, and U01HL075408 from the NHLBI. The National Jewish Health site was also supported in part by Colorado CTSA grant UL1RR025780 from NCRR/NIH and UL1TR000154 from NCATS/NIH. |
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| Disclosure of potential conflict of interest: B. A. Coull has received research support from the United States Environmental Protection Agency and the National Institutes of Health (NIH). D. S. Postma has received research support from AstraZeneca and Chiesi and has consultant arrangements with AstraZeneca, Boehringer Ingelheim, Chiesi, GlaxoSmithKline, Nycomed, and TEVA. P. V. Williams has received research support from the National Heart, Lung, and Blood Institute (NHLBI). T. S. Hallstrand has received research grants from the NIH, has served as a consultant for Amgen and TEVA Pharmaceuticals, and has received lecture fees from Merck & Co. A. N. Fuhlbrigge has received research support from the NHLBI and has received personal fees from GlaxoSmithKline, Merck, Icon Medical Imaging, and the Lovelace Respiratory Research Institute. J. Schwartz has received research support from the NIH. D. R. Gold has received research support from the United States Environmental Protection Agency and the NIH (5 P01 HL 083069-05 NIH/NHLBI/P01; NIEHS PO1 ES-09825, US EPA RD-83241601, and US EPA grant RD 83479801; and the International Initiative for Environment and Public Health Cyprus). The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 137 - N° 2
P. 390-399 - février 2016 Retour au numéro
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