Reviews and feature articleThe severity-dependent relationship of infant bronchiolitis on the risk and morbidity of early childhood asthma
Section snippets
Study design and population
To estimate the association of bronchiolitis during infancy with the development of early childhood asthma, we conducted a population-based retrospective birth cohort study of more than 90,000 term, non–low birth weight infants enrolled in TennCare within the first month of life (1995-2000, the TABS). Only children born between 1995 and 2000 were included because all children were followed to 5.5 years by using the years for which data were available. In 1994, TennCare replaced the federal
Results
A total of 90,341 term healthy children were included in the cohort. Forty-nine percent of the children were girls; the children were white (56%), black (39%), and Hispanic (2%; Table I). The median EGA was 40 weeks, and the median birth weight was 3289 g. Overall, 26% of children had mothers who smoked during pregnancy. Eighteen percent of children had at least 1 health care visit for bronchiolitis during infancy, and children were classified into the following groups: no visit (82%),
Discussion
Although the association of viral lower respiratory tract infection during infancy and subsequent childhood wheezing is well established, this study addresses important gaps in our knowledge regarding the relationship of bronchiolitis severity on early childhood asthma risk and asthma morbidity. To our knowledge, this is the first study to demonstrate the dose-response relationship between the severity of infant bronchiolitis and the increased odds of both early childhood asthma and increased
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Supported in part by NIH U01 HL 072471 (T.V.H.), the Thrasher Research Fund (T.V.H.), NIH KO1 AI070808 (K.N.C.), NIH K24 AI 077930 (T.V.H.), NIH F32 HL 086048 (P.W., T.V.H.), and the Parker B. Francis Research Foundation (K.N.C.).
Disclosure of potential conflict of interest: K. N. Carroll has received research support from the National Institutes of Health/National Institute of Allergy and Infectious Diseases and the Parker B. Francis Foundation. P. Wu has received research support from the National Institutes of Health and the Thrasher Research Fund. T. Gebretsadik has received research support from the National Institutes of Health/National Institute of Allergy and Infectious Diseases. M. R. Griffin has received research support from MedImmune, Pfizer, the Center for Disease Control and Prevention, and the Agency for Healthcare Research and Quality. T. V. Hartert has served as a speaker for and on the Advisory Board for Merck and has received research support from the National Institutes of Health and the Thrasher Research Fund. The rest of the authors have declared that they have no conflict of interest.