Respiratory effects of short-term exposure to ozone in a panel of healthy elderly

Background Air pollution is a major public health problem widely concerned. In recent years, the growing concentration of ozone (O₃) in association with human health effects cannot be ignored.

Objective This study aims to investigate acute adverse human respiratory effects of O₃ and to determine whether glutathione S-transferase-theta 1 (GSTT1) gene modifies those effects.

Methods Healthy and retired teaching staff of Xinxiang Medical College who met the inclusion criteria were enrolled in the study, and were followed up five times (once every four weeks) from December 2018 to April 2019. Detection indicators were lung function indicators, including forced vital capacity (FVC), forced expiratory volume in one second (FEV₁), and peak expiratory flow (PEF); airway inflammation indicators, such as fractional exhaled nitric oxide (FeNO), interleukin-8 (IL-8), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in nasal samples; and oxidative stress indicator, namely 8-epi-prostaglandin F2 alpha (8-epi-PGF2α). Daily average concentrations of individual exposure were calculated by hourly concentration of O₃ and meteorological factors recorded by fixed monitoring sites. Linear mixed-effect model was used to analyze the relationship between O₃ concentration (lag0-lag4 and lag01-lag04) and respiratory effects, and then the potential modifying effects of GSTT1 polymorphism were studied by stratification analysis.

Results A total of 32 elderly healthy volunteers were enrolled in the study, with an average age of (63.53±5.76) years and an average body mass index (BMI) of (26.30±3.36) kg·m^-2. There were 20 cases (62.5%) with GSTT1 gene expression, 32 cases (100%) with GSTM1 gene expression, and 32 cases (100%) with GSTP1 gene expression. The O₃ concentration was 18.96-60.92 μg·m^-3, and the average concentration was (36.91±13.88) μg·m^-3; the temperature was (6.10±6.77)℃; the relative humidity was (43.92±9.50)%. The average concentrations of four biological indicators (IL-1β, IL-8, TNF-α, and 8-epi-PGF2α) of the study subjects were (179.61±126.67), (49.67±38.19), (0.49±0.31), and (41.64±20.94) μg·L^-1, respectively; the average concentration of FeNO was (28.10±9.96) ppb; the values of lung function indicators (FVC, FEV₁, FEV₁/FVC, PEF, and MV) were (2.49±0.53) L, (2.15±0.47) L, (0.87±0.06) L·s^-1, (4.19±1.54) L·s^-1, and (7.78±2.75) L, respectively. For every 10 μg·m^-3 increase in O₃ concentration in the single-pollutant model, the IL-1β level at lag3 increased by 79.36% (95% CI: 1.86%-156.85%); except for the O₃+PM_2.5 model, the other dual-pollutant models are not statistically significant. Genetic stratification analysis results showed that the change of airway inflammation indicator FeNO in GSTT1 (+) population was higher than that in GSTT1 (-) population.

Conclusion Elevated IL-1β levels could be caused by acute O₃ exposure in the elderly. GSTT1 gene deletion aggravates O₃-induced airway inflammation.