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Original Research |

Obesity-Associated Asthma in ChildrenObesity-Associated Asthma in Children: A Distinct Entity

Deepa Rastogi, MBBS; Stephen M. Canfield, MD, PhD; Andrea Andrade, BA; Carmen R. Isasi, MD, PhD; Charles B. Hall, PhD; Arye Rubinstein, MD; Raanan Arens, MD
Author and Funding Information

From the Department of Pediatrics (Drs Rastogi, Rubinstein, and Arens and Ms Andrade) and the Department of Epidemiology and Population Health (Dr Canfield), Albert Einstein College of Medicine, Bronx; and the Department of Medicine (Dr Canfield) and Department of Epidemiology and Population Health (Drs Isasi and Hall), College of Physicians and Surgeons, Columbia University, New York, NY.

Correspondence to: Deepa Rastogi, MBBS, Joseph S. Blume Faculty Scholar, Albert Einstein College of Medicine, Children’s Hospital at Montefiore, 3415 Bainbridge Ave, Bronx, NY 10467; e-mail: drastogi@montefiore.org


Ms Andrade is currently at The American University of the Caribbean (St. Maarten, Netherland Antilles).

Funding/Support: This study was funded by a grant-in-aid from the Stony-Wold Herbert Fund, New York.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(4):895-905. doi:10.1378/chest.11-0930
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Background:  Obesity-associated asthma has been proposed to be a distinct entity, differing in immune pathogenesis from atopic asthma. Both obesity-mediated inflammation and increase in adiposity are potential mechanistic factors that are poorly defined among children. We hypothesized that pediatric obesity-associated asthma would be characterized by T helper (Th) 1, rather than the Th2 polarization associated with atopic asthma. Moreover, we speculated that Th1 biomarkers and anthropometric measures would correlate with pulmonary function tests (PFTs) in obese asthmatic children.

Methods:  We recruited 120 children, with 30 in each of the four study groups: obese asthmatic children, nonobese asthmatic children, obese nonasthmatic children, and nonobese nonasthmatic children. All children underwent pulmonary function testing. Blood was collected for measurement of serum cytokines. T-cell responses to mitogen, phorbol 12-myristate 13-acetate (PMA), or antigens tetanus toxoid or Dermatophagoides farinae were obtained by flow cytometric analysis of intracellular cytokine staining for interferon-γ (IFN-γ) (Th1) or IL-4 (Th2) within the CD4 population.

Results:  Obese asthmatic children had significantly higher Th1 responses to PMA (P < .01) and tetanus toxoid (P < .05) and lower Th2 responses to PMA (P < .05) and D farinae (P < .01) compared with nonobese asthmatic children. Th-cell patterns did not differ between obese asthmatic children and obese nonasthmatic children. Obese asthmatic children had lower FEV1/FVC (P < .01) and residual volume/total lung capacity ratios (P < .005) compared with the other study groups, which negatively correlated with serum interferon-inducible protein 10 and IFN-γ levels, respectively. PFTs, however, did not correlate with BMI z score or waist to hip ratio.

Conclusions:  We found that pediatric obesity-associated asthma differed from atopic asthma and was characterized by Th1 polarization. The altered immune environment inversely correlated with PFTs in obese asthmatic children.

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