Air pollution interacts with past episodes of bronchiolitis in the development of asthma

Authors


  • Edited by: Thomas Bieber

Correspondence

Soo-Jong Hong, Department of Pediatrics, Childhood Asthma and Atopy Center, Research Center for Standardization of Allergic Diseases, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Poongnap-Dong, Songpa-Gu, Seoul 138-736, Korea.

Tel.: 822 3010 3379

Fax: 822 473 3725

E-mail: sjhong@amc.seoul.kr

Abstract

Background

Exposure to ambient air pollution and bronchiolitis are risk factors for asthma. The aim of this study was to investigate the effect of air pollution on the development of asthma in children with past episodes of bronchiolitis.

Methods

A prospective 2-year follow-up survey consisting of parental responses to the International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire, and allergy evaluations were conducted in 1743 children with a mean age of 6.8 years. Recent 5-year exposure to air pollution was estimated using a geographic information system.

Results

Higher exposure to ozone was associated with airway hyper-responsiveness (PC20 ≤ 16 mg/ml) at enrollment (odds ratio [OR] = 1.60, 95% CI [confidence interval] = 1.13–2.27) and with new episodes of wheezing during the 2-year period (OR = 1.92, 95% CI = 0.96–3.83). Past episodes of bronchiolitis were associated with both current wheezing and physician-diagnosed asthma. When the two factors were combined, the prevalence of bronchial hyper-reactivity (OR = 2.96, 95% CI = 1.41–6.24) and new wheezing (OR = 4.17, 95% CI = 0.89–19.66) as well as current wheezing and physician-diagnosed asthma was even greater (P for trend <0.05 for all). In children with both risk factors, lung function was significantly decreased, with atopic children being particularly vulnerable.

Conclusion

In children, the interaction between air pollution and past episodes of bronchiolitis resulted in a greater prevalence of asthma and pointed to an association with bronchial hyper-reactivity and decreased lung function. These results suggest mechanisms underlying the development of asthma.

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