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Fractional exhaled nitric oxide in healthy non-asthmatic 7-year olds and prenatal exposure to polycyclic aromatic hydrocarbons: Nested regression analysis

机译:健康的7岁非哮喘患者和产前暴露于多环芳烃的部分呼出气一氧化氮:嵌套回归分析

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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.
机译:该研究的主要目的是评估在脐带血PAH-DNA加合物评估的胎盘暴露于遗传毒性PAH化合物与在7岁健康非哮喘儿童中测得的呼出气一氧化氮(FeNO)之间的可能联系。受试者包括89名儿童的子样本,这些儿童参加了正在进行的克拉科夫基于人口的出生队列研究并参加了FeNO测试。调整了胎盘PAH暴露的影响以适应潜在的混杂因素,例如母亲过敏和儿童对常见的家庭过敏原的特应性过敏。结果与低暴露水平(gmean = 3.8 ppb; 95%CI:2.3-6.3)相比,高PAH暴露(gmean = 7.7 ppb; 95%CI:5.8-10.2 ppb)的儿童中的FeNO值显着升高( P = 0.011)。与母亲拒绝过敏的受试者(gmean = 5.6 ppb,95%CI:4.3-7.3 ppb)相比,患有母体过敏的孩子的平均FeNO值也更高(gmean = 13.7 ppb,95%CI:8.8-21.4 ppb)( P = 0.012)。同样,特应性儿童的FeNO值较高(gmean = 11.2 ppb; 95%CI:3.8-32.8 ppb),高于非特应性个体(gmean = 6.0 ppb; 95%CI:4.7-7.7 ppb,P = 0.079)。嵌套多元线性回归分析的结果表明,母亲过敏和儿童对家庭空气过敏原的敏感性共同解释了FeNO变化的10.4%,但是,另外的10.9%是由产前PAH暴露确定的。结论FeNO不仅是用于筛查特应性或症状性支气管炎症的标志物,而且还可能是细胞因子失调和因经胎盘PAH暴露而在胎儿期可能建立的“过敏反应”表型的替代物。我们研究的初步结果应鼓励对宫内PAH暴露和以后的呼吸道症状进行更多的研究。小儿科薄荷油。 2012. 47:1131-1139。

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