Fractional exhaled nitric oxide in healthy non‐asthmatic 7‐year olds and prenatal exposure to polycyclic aromatic hydrocarbons: Nested regression analysis
Authors:
- Wieslaw JedrychowskiWJWieslaw Jedrychowski
- Elzbieta MrozEMElzbieta Mroz
- Elzbieta FlakEFElzbieta Flak
- Ryszard JacekRJRyszard Jacek
- Agata SowaASAgata Sowa
- 15 May 2012
- journal article
- research article
- Published by Wiley in Pediatric Pulmonology
- Vol. 47 (11) , 1131-1139
Abstract
The main goal of the study was to assess possible association between transplacental exposure to genotoxic PAH compounds assessed by the cord blood PAH–DNA adducts and fractional exhaled nitric oxide (FeNO) measured in healthy non‐asthmatic children at the age of 7 years. The subjects included the subsample of 89 children who took part in the ongoing population based birth cohort study in Krakow and attended FeNO testing. The effect of transplacental PAH exposure was adjusted for potential confounders, such as maternal allergy and children's specific atopy to common domestic allergens.Results: FeNO values were significantly elevated in children with higher prenatal PAH exposure (gmean = 7.7 ppb; 95% CI: 5.8–10.2 ppb) compared with those at low exposure level (gmean = 3.8 ppb; 95% CI: 2.3–6.3) (P = 0.011). Children with maternal allergy had also significantly higher mean FeNO values (gmean = 13.7 ppb, 95% CI: 8.8–21.4 ppb) compared with the subjects whose mothers denied allergy (gmean = 5.6 ppb, 95% CI: 4.3–7.3 ppb) (P = 0.012). Similarly, FeNO values in atopic children were higher (gmean = 11.2 ppb; 95% CI: 3.8–32.8 ppb) than in non‐atopic individuals (gmean = 6.0 ppb; 95% CI: 4.7–7.7 ppb, P = 0.079). The results of the nested multivariable linear regression analysis showed that both maternal allergy and sensitization of children to domestic aeroallergens jointly explained 10.4% of FeNO variance, however, the additional 10.9% was determined by prenatal PAH exposure.Conclusion: FeNO is more than a marker useful for screening atopy or symptomatic bronchial inflammation and may also be a proxy for cytokine deregulation and “allergic response” phenotype possibly established in fetal period due to transplacental PAH exposure. Preliminary results of our study should encourage more studies on intrauterine PAH exposure and later respiratory symptoms. Pediatr Pulmonol. 2012. 47:1131–1139.Keywords
Funding Information
- International Center for Research in Biomedicine, Luxembourg
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