Effects of personal nitrogen dioxide exposure on airway inflammation and lung function

Few epidemiological studies have evaluated the respiratory effects of personal exposure to nitrogen dioxide (NO₂), a major traffic-related air pollutant. The biological pathway for these effects remains unknown.

To evaluate the short-term effects of personal NO₂ 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 NO₂ on respiratory outcomes.

Personal exposure to NO₂ was 27.39 ± 23.20 ppb on average. In response to a 10-ppb increase in NO₂ 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 NO₂ 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 NO₂.