School of Public Health, Key Lab of Public Health Safety of the Ministry of Education and NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai, 200032, China.
School of Public Health, Key Lab of Public Health Safety of the Ministry of Education and NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai, 200032, China; Shanghai Key Laboratory of Meteorology and Health, Shanghai, 200030, China.
Environ Res. 2019 Oct;177:108620. doi: 10.1016/j.envres.2019.108620. Epub 2019 Aug 1.
Few epidemiological studies have evaluated the respiratory effects of personal exposure to nitrogen dioxide (NO), a major traffic-related air pollutant. The biological pathway for these effects remains unknown.
To evaluate the short-term effects of personal NO exposure on lung function, fractional exhaled nitric oxide (FeNO) and DNA methylation of genes involved.
We conducted a longitudinal panel study among 40 college students with four repeated measurements in Shanghai from May to October in 2016. We measured DNA methylation of the key encoding genes of inducible nitric oxide synthase (NOS2A) and arginase (ARG2). We applied linear mixed-effect models to assess the effects of NO on respiratory outcomes.
Personal exposure to NO was 27.39 ± 23.20 ppb on average. In response to a 10-ppb increase in NO exposure, NOS2A methylation (%5 mC) decreased 0.19 at lag 0 d, ARG2 methylation (%5 mC) increased 0.21 and FeNO levels increased 2.82% at lag 1 d; and at lag 2 d the percentage of forced vital capacity, forced expiratory volume in 1 s and peak expiratory flow in predicted values decreased 0.12, 0.37 and 0.67, respectively. The model performance was better compared with those estimated using fixed-site measurements. These effects were robust to the adjustment for co-pollutants and weather conditions.
Our study suggests that short-term personal exposure to NO is associated with NOS2A hypomethylation, ARG2 hypermethylation, respiratory inflammation and lung function impairment. The use of personal measurements may better predict the respiratory effects of NO.
很少有流行病学研究评估个人接触二氧化氮（NO）对呼吸的影响，而 NO 是一种主要的与交通有关的空气污染物。这些影响的生物学途径仍不清楚。
评估个人 NO 暴露对肺功能、呼出气一氧化氮分数（FeNO）和涉及的基因 DNA 甲基化的短期影响。
我们在 2016 年 5 月至 10 月期间在上海进行了一项纵向队列研究，纳入了 40 名大学生，共进行了 4 次重复测量。我们测量了诱导型一氧化氮合酶（NOS2A）和精氨酸酶（ARG2）的关键编码基因的 DNA 甲基化。我们应用线性混合效应模型来评估 NO 对呼吸结果的影响。
个人 NO 暴露的平均值为 27.39±23.20 ppb。NO 暴露增加 10 ppb，NOS2A 甲基化（%5 mC）在滞后 0 天减少 0.19，ARG2 甲基化（%5 mC）增加 0.21，FeNO 水平增加 2.82%在滞后 1 天；在滞后 2 天，用力肺活量、1 秒用力呼气量和预计峰流速的百分比分别减少 0.12、0.37 和 0.67。与固定点测量估计的模型性能相比，该模型的性能更好。这些影响在调整了共污染物和天气条件后仍然稳健。
我们的研究表明，短期个人接触 NO 与 NOS2A 低甲基化、ARG2 高甲基化、呼吸炎症和肺功能损害有关。使用个人测量可能更好地预测 NO 的呼吸影响。
