Wang I-Jen, Karmaus Wilfried J J, Yang Chen-Chang
Department of Pediatrics, Taipei Hospital, Ministry of Health and Welfare, Taipei, Taiwan, Republic of China.
Institute of Environmental and Occupational Health Sciences, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China.
Int Arch Occup Environ Health. 2017 Apr;90(3):297-303. doi: 10.1007/s00420-017-1198-y. Epub 2017 Feb 7.
Polycyclic aromatic hydrocarbons (PAHs) are known for their carcinogenic and teratogenic properties. However, little is known about the effect of PAH on our immune and respiratory systems. Hence, we investigated associations (1) between PAH exposure and IgE levels and asthma in children and (2) between PAH exposure and the oxidative stress marker 8OHdG potentially involved in disease pathogenesis stratifying by (3) sex-based differences.
A total of 453 kindergarten children were recruited and provided samples. Urine biomarker of PAH exposure (1-OHP levels) was measured by UPLC-MS/MS and a marker of oxidative stress (8OHdG) was measured by ELISA. Serum IgE were assessed and information on asthma was collected. Associations between 1-OHP levels, 8OHdG, IgE and asthma were analyzed by multivariate linear and logistic regression. A mediation analysis was conducted to evaluate whether the risk of increased IgE and asthma related to PAH exposure is explained by 8OHdG changes.
Urine 1-OHP levels were positively related to 8OHdG levels (per ln-unit: β = 0.30kU/l, p = 0.002). Similar results were also found for 1-OHP levels with IgE levels (per ln-unit: β = 0.27 kU/l, p = 0.027). 1-OHP levels (per ln-unit) were significantly associated with asthma, with an OR (95% CI) of 1.42 (1.18-1.70). In addition, 1-OHP levels were associated with asthma. It is estimated that 35% of the effect of PAH exposure on asthma is mediated by 8OHdG levels.
Exposure to PAH may enhance oxidative stress and may induce asthma. The effect of PAH exposure on asthma may be mediated by oxidative stress.
多环芳烃(PAHs)以其致癌和致畸特性而闻名。然而,关于PAH对我们免疫系统和呼吸系统的影响知之甚少。因此,我们调查了(1)儿童PAH暴露与IgE水平及哮喘之间的关联,以及(2)PAH暴露与可能参与疾病发病机制的氧化应激标志物8-羟基脱氧鸟苷(8OHdG)之间的关联,并按(3)性别差异进行分层。
共招募了453名幼儿园儿童并采集样本。通过超高效液相色谱-串联质谱法(UPLC-MS/MS)测量PAH暴露的尿液生物标志物(1-羟基芘(1-OHP)水平),并通过酶联免疫吸附测定法(ELISA)测量氧化应激标志物(8OHdG)。评估血清IgE水平并收集哮喘相关信息。通过多变量线性和逻辑回归分析1-OHP水平、8OHdG、IgE与哮喘之间的关联。进行中介分析以评估8OHdG变化是否可以解释PAH暴露导致IgE升高和哮喘的风险。
尿液1-OHP水平与8OHdG水平呈正相关(每自然对数单位:β = 0.30kU/l,p = 0.002)。1-OHP水平与IgE水平也有类似结果(每自然对数单位:β = 0.27 kU/l,p = 0.027)。1-OHP水平(每自然对数单位)与哮喘显著相关,比值比(OR)(95%可信区间)为1.42(1.18 - 1.70)。此外,1-OHP水平与哮喘有关。据估计,PAH暴露对哮喘影响的35%由8OHdG水平介导。
PAH暴露可能会增强氧化应激并可能诱发哮喘。PAH暴露对哮喘的影响可能由氧化应激介导。