ScholarWorks@숙명여자대학교

초록

Due to steady increase of childhood asthma, exposures to air toxics including PAHs have been thought as an etiology for the asthma. PAHs-involvement in airway inflammation, such as IgE production, is the potential mechanism of the PAHs-induced asthma. Cytochrome P450s (CYPs), particularly, CYP1A1 is a known enzyme to metabolize PAHs and to be induced by PAHs. The CYP1A1 expression has been emphasized as an biomarker for PAHs-exposure. The present study was performed to clarify the etiology of childhood asthma with PAHs-exposure using mRNA expression of CYP1A1. The study subjects were Korean children who were asthma patients (cases) or other hospital controls (N = 20; age, 3~16; boys, 56%). As results, we detected expression of the CYP1A1 in all peripheral blood specimens which were collected from the subjects. Moreover, we found approx. 300 fold-higher expression of the CYP1A1 in the cases than that in the controls (p⁄0.01). When we considered age which was related to asthma, the above significant trend was somewhat diluted, however, the relation between asthma and the CYP1A1 expression was stronger than that between asthma and age (chi square, 7.99 vs. 3.34). Therefore, our study supports that PAHs induce or worse childhood asthma and suggests application of expression of the CYP1A1 as an initiation or progress biomarker for PAHs-induced childhood asthma.

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