Associations of short-term PM2.5 exposures with nasal oxidative stress, inflammation and lung function impairment and modification by GSTT1-null genotype: A panel study of the retired adults

PM₂.₅ (particulate matter ≤2.5 μm in aerodynamic diameter) is a major urban air pollutant worldwide. Its effects on the respiratory system of the susceptible population have been less characterized. This study aimed to estimate the association of short-term PM₂.₅ exposure with respiratory outcomes of the retired adults, and to examine whether these associations were stronger among the subjects with GSTT-null genotype. 32 healthy subjects (55–77 years) were recruited for five follow-up examinations. Ambient concentrations of PM₂.₅ were monitored consecutively for 7 days prior to physical examination. Pulmonary outcomes including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV₁), peak expiratory flow (PEF), and fractional exhaled nitric oxide (FeNO), and nasal fluid concentrations of 8-epi-prostaglandin F2 alpha (8-epi-PGF2α), tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8) and IL-1β were measured. A linear mixed-effect model was introduced to evaluate the associations of PM₂.₅ concentrations with respiratory outcomes. Additionally, GSTT1 genotype-based stratification was performed to characterize modification on PM₂.₅-related respiratory outcomes. We found that a 10 μg/m³ increase in PM₂.₅ was associated with decreases of 0.52 L (95% confidence interval [CI]: -1.04, -0.002), 0.64 L (95% CI: -1.13, -0.16), 0.1 (95% CI: -0.23, 0.04) and 2.87 L/s (95% CI: -5.09, -0.64) in FVC, FEV₁, FEV₁/FVC ratio and PEF at lag 2, respectively. Meanwhile, marked increases of 80.82% (95% CI: 5.13%, 156.50%) in IL-8, 77.14% (95% CI: 1.88%, 152.40%) in IL-1β and 67.87% (95% CI: 14.85%, 120.88%) in 8-epi-PGF2α were observed as PM₂.₅ concentration increased by 10 μg/m³ at lag 2. Notably, PM₂.₅-associated decreases in FVC and PEF and increase in FeNO were stronger among the subjects with GSTT1-null genotype. In summary, short-term exposure to PM₂.₅ is associated with nasal inflammation, oxidative stress and lung function reduction in the retired subjects. Lung function reduction and inflammation are stronger among the subjects with GSTT1-null genotype.