TY - JOUR
T1 - Biologic mechanisms of environmental tobacco smoke in children with poorly controlled asthma
T2 - Results from a multicenter clinical trial
AU - Lang, Jason E.
AU - Dozor, Allen J.
AU - Holbrook, Janet T.
AU - Mougey, Edward
AU - Krishnan, Sankaran
AU - Sweeten, Shawn
AU - Wise, Robert A.
AU - Teague, W. Gerald
AU - Wei, Christine Y.
AU - Shade, David
AU - Lima, John J.
N1 - Funding Information:
Baylor College of Medicine, Houston, Tex: N. A. Hanania (principal investigator), M. Sockrider (co-principal investigator), L. Bertrand (principal clinic coordinator), M. Atik, L. Giraldo, B. Flores (coordinators) Columbia University–New York University Consortium, New York, NY: J. Reibman (principal investigator), E. DiMango, L. Rogers (co-principal investigators), C. Cammarata, and K. Carapetyan (clinic coordinators at New York University), J. Sormillon, and E. Simpson (clinic coordinators at Columbia University) Duke University Medical Center, Durham, NC: L. Williams (principal investigator), J. Sundy (co-principal investigator), G. Dudek (principal clinic coordinator), R. Newton, and A. Dugdale (coordinators) Emory University School of Medicine, Atlanta, Ga: W. G. Teague (principal investigator), A. Fitzpatrick, S. Khatri (co-principal investigators), R. Patel (principal clinic coordinator), J. Peabody, E. Hunter, and D. Whitlock (coordinators) Illinois Consortium, Chicago, Ill: L. Smith (principal investigator), J. Moy, E. Naureckas, A. Prestridge (co-principal investigators), J. Hixon (principal clinic coordinator), A. Brees, and J. Judge (coordinators) Indiana University, Asthma Clinical Research Center, Indianapolis, Ind: M. Busk (principal investigator), P. Puntenney (principal clinic coordinator), N. Busk, and J. Hutchins (coordinators) University of Pennsylvania, Philadelphia, Pa: F. Leone (principal investigator) and M. Hayes-Hampton (principal clinic coordinator) National Jewish Health, Denver, Colo: R. Katial (principal investigator), M. Krawiecz (co-principal investigator), and H. Currier (principal clinic coordinator) Nemours Children's Clinic–University of Florida Consortium, Jacksonville, Fla: J. Lima (principal investigator), K. Blake (co-principal investigator), J. Lang (co-principal investigator), D. Schaeffer (investigator), A. Santos (principal coordinator), and M. McRae (coordinator) Hofstra University School of Medicine (formerly North Shore–Long Island Jewish Health System), New Hyde Park, NY: J. Karpel (principal investigator), R. Cohen (co-principal investigator), and R. Ramdeo (principal clinic coordinator) Northern New England Consortium (formerly Vermont Lung Center at the University of Vermont), Colchester, Vt: C. G. Irvin (principal investigator), A. E. Dixon, D. A. Kaminsky (co-principal investigators), R. Colletti (GI consultant), S. M. Burns, L. M. Bourassa, S. E. Lang, L. V. Griffes (coordinators), R. Pratt, K. B. Nakos, and K. J. Girard The Ohio State University Medical Center/Columbus Children's Hospital, Columbus, Ohio: J. Mastronarde (principal investigator), K. McCoy (co-principal investigator), J. Parsons (co-investigator), J. Drake (principal clinic coordinator), R. Compton, L. Raterman, and D. Cosmar (coordinators) Maria Fareri Children's Hospital at Westchester Medical Center and New York Medical College, Valhalla, NY: A. Dozor (principal investigator), S. Krishnan (co-principle investigator), and I. Gherson (principal clinic coordinator) University of Alabama at Birmingham, Birmingham, Ala: L. B. Gerald (principal investigator), W. C. Bailey, R. Grad (co-principal investigators), S. Erwin (principal clinic coordinator), A. Kelley, and D. Laken (coordinators) University of Miami, Miami–University of South Florida, Tampa, Fla: A. Wanner (principal investigator, Miami), R. Lockey (principal investigator, Tampa), E. Mendes (principal clinic coordinator for University of Miami), S. McCullough (principal clinic coordinator for University of South Florida), M. Grandstaff-Singleton, and D. Miller (coordinators) University of Minnesota, Minneapolis, Minn: M. N. Blumenthal (principal investigator), G. Brottman, J. Hagen (co-principal investigators), A. Decker, D. Lascewski, S. Kelleher (principal clinic coordinators), K. Bachman, C. Quintard, and C. Sherry (coordinators) University of Missouri, Kansas City School of Medicine, Kansas City, Mo: G. Salzman (principal investigator), C. Dinakar, D. Pyszczynski (co-principal investigators), and P. Haney (principal clinic coordinator) St. Louis Asthma Clinical Research Center: Washington University, St. Louis, Mo: M. Castro (principal investigator), L. Bacharier, K. Sumino (co-investigators), J. Tarsi (principal coordinator), and B. Patterson (coordinator) University of California San Diego, Calif: S. Wasserman (principal investigator), J. Ramsdell (co-principal investigator), P. Ferguson, K. Kinninger, and T. Greene (clinic coordinators) Chairman's Office University of Alabama, Birmingham, Ala (formerly at Respiratory Hospital, Winnipeg, MB, Canada): W. Bailey and N. Anthonisen (research group chair) Data Coordinating Center, Johns Hopkins University Center for Clinical Trials, Baltimore, Md: R. Wise (center director), J. Holbrook (deputy director), E. Brown (principal coordinator), D. Amend-Libercci, K. Barry, M. Daniel, A. Lears, G. Leatherman, C. Levine, D. Nowakowski, N. Prusakowski, S. Rayapudi, S. Roettger, A. Thurman, D. Shade, E. Sugar, and C. Wei Esophageal pH Probe Quality Control Center, Children's Center for Digestive Healthcare Pediatric Gastroenterology, Hepatology, and Nutrition, (formerly at Emory University School of Medicine, Atlanta, Ga): B. Gold (center director) Data and Safety Monitoring Board, San Francisco, Calif: S. Lazarus (chair), W. Calhoun, M. Cloutier, B. McWilliams, A. Rogatko, and C. Sorkness Project Office, American Lung Association, New York, NY: E. Lancet (project officer), N. Edelman (scientific consultant), and S. Rappaport Project Office, National Heart, Lung, and Blood Institute, Bethesda, Md: V. Taggart (project officer) and G. Weinmann (DSMB secretary, airway branch chief) ALA Scientific Advisory Committee, New York, NY: E. N. Schachter (chair), L. A. Baggott (vice-chair), W. C. Bailey, A. L. Brannen II, M. Castro, B. W. Christman, A. Chuang, R. M. Donaldson, C. Holloway, T. A. Mahr, J. A. Neubauer, J. M. Samet, E. R. Swenson, D. J. Upson, D. J. Weiss, and R. Wise
Funding Information:
This research project was independent of any commercial funder (with the exception of support listed in the title page footnote). As the lead and corresponding author, J. E. Lang had access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. This research was performed by the American Lung Association Asthma Clinical Research Centers (ALA-ACRC). The members of the ALA-ACRC research group for the trial were as follows:
PY - 2013/3
Y1 - 2013/3
N2 - Background: Environmental tobacco smoke (ETS) negatively affects children with asthma. The prevalence of ETS exposure among children with poor asthma control may be changing. Importantly, the mechanisms by which ETS worsens asthma control are poorly understood. Objective: We describe how ETS affects gastroesophageal reflux (GER), respiratory infections, and leukotriene production among children with poor asthma control. Methods: We analyzed data from 306 children between 6 and 17 years of age with poorly controlled asthma enrolled in a 6-month clinical trial. We evaluated prevalence and determinants of ETS exposure by interview, questionnaire, and urinary cotinine and the association of ETS exposure on leukotriene production, respiratory infections, GER, lung function, and asthma control. We used multivariable linear, logistic, and Poisson regressions to assess outcomes. Results: ETS prevalence estimates ranged from 6% to 30%. Children with domestic indoor exposure had worse asthma control (c-Asthma Control Test, 17.8 vs 21.5; P = .04), worse FEV1 % predicted (84.1 vs 90.7; P = .02), and a trend for increased mean urinary leukotriene E4. ETS from any setting was associated with increased symptomatic respiratory infections (adjusted incidence rate ratio: 1.30; P = .02). However, children exposed to ETS did not have symptoms or pH probe results, suggestive of heightened GER. Conclusions: Domestic smoking exposure was associated with both higher rates of symptomatic respiratory infection and poorer asthma control despite generally intensive controller therapy. ETS exposure is common among asthmatic children with poor control and may worsen asthma control by promoting respiratory infections. Further investigation is required to elucidate ETS mechanisms in poor asthma control.
AB - Background: Environmental tobacco smoke (ETS) negatively affects children with asthma. The prevalence of ETS exposure among children with poor asthma control may be changing. Importantly, the mechanisms by which ETS worsens asthma control are poorly understood. Objective: We describe how ETS affects gastroesophageal reflux (GER), respiratory infections, and leukotriene production among children with poor asthma control. Methods: We analyzed data from 306 children between 6 and 17 years of age with poorly controlled asthma enrolled in a 6-month clinical trial. We evaluated prevalence and determinants of ETS exposure by interview, questionnaire, and urinary cotinine and the association of ETS exposure on leukotriene production, respiratory infections, GER, lung function, and asthma control. We used multivariable linear, logistic, and Poisson regressions to assess outcomes. Results: ETS prevalence estimates ranged from 6% to 30%. Children with domestic indoor exposure had worse asthma control (c-Asthma Control Test, 17.8 vs 21.5; P = .04), worse FEV1 % predicted (84.1 vs 90.7; P = .02), and a trend for increased mean urinary leukotriene E4. ETS from any setting was associated with increased symptomatic respiratory infections (adjusted incidence rate ratio: 1.30; P = .02). However, children exposed to ETS did not have symptoms or pH probe results, suggestive of heightened GER. Conclusions: Domestic smoking exposure was associated with both higher rates of symptomatic respiratory infection and poorer asthma control despite generally intensive controller therapy. ETS exposure is common among asthmatic children with poor control and may worsen asthma control by promoting respiratory infections. Further investigation is required to elucidate ETS mechanisms in poor asthma control.
KW - Asthma
KW - Children
KW - Environmental tobacco smoke
KW - Gastroesophageal reflux
KW - Leukotriene
KW - Respiratory infection
KW - Spirometry
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UR - http://www.scopus.com/inward/citedby.url?scp=84877984588&partnerID=8YFLogxK
U2 - 10.1016/j.jaip.2012.11.006
DO - 10.1016/j.jaip.2012.11.006
M3 - Article
C2 - 24565456
AN - SCOPUS:84877984588
SN - 2213-2198
VL - 1
SP - 172-180.e2
JO - Journal of Allergy and Clinical Immunology: In Practice
JF - Journal of Allergy and Clinical Immunology: In Practice
IS - 2
ER -