Association between short-term exposure to ambient air pollutants and biomarkers indicative of inflammation and oxidative stress: a cross-sectional study using KoGES-HEXA data.

Background: Air pollution-induced systemic inflammation and oxidative stress are hypothesized to be the major biological mechanisms underlying pathological outcomes. We examined the association between short-term exposure to ambient air pollutants and biomarkers of inflammation and oxidative stress in 2199 general middle-aged Korean population residing in metropolitan areas.

Methods: Serum levels of inflammatory cytokines (interleukin [IL]-1β, IL-6, IL-8, IL-10, and tumor necrosis factor [TNF]-α) and urinary levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured. Daily concentrations of a series of air pollutants (particulate matter [PM]₁₀, PM_2.5, SO₂, NO₂, CO, and O₃) were predicted using the Community Multiscale Air Quality modeling system, and participant-level pollutant exposure was determined using geocoded residential addresses. Short-term exposure was defined as the 1- to 7-day moving averages.

Results: The multivariable-adjusted linear models controlling for the sociodemographic, lifestyle, temporal, and meteorological factors identified positive associations of PM with IL-1β, IL-8, IL-10, TNF-α, and 8-OHdG levels; SO₂ with IL-10 levels, CO with IL-1β, IL-10, and TNF-α levels; and O₃ with IL-1β, IL-8, and 8-OHdG levels. O₃ levels were inversely associated with IL-10 levels. For each pollutant, the strongest associations were observed for the 7-day average PM and CO with IL-1β (per 10-µg/m³ increase in PM₁₀: 2.7%, 95% confidence interval [CI] = 0.6-4.8; per 10-µg/m³ increase in PM_2.5: 6.4%, 95% CI = 2.4-10.5; per 0.1-ppm increase in CO: 3.3%, 95% CI = 0.3-6.5); the 2-day average SO₂ with IL-10 levels (per 1-ppb increase in SO₂: 1.1%, 95% CI = 0.1-2.1); and the 7-day average O₃ with IL-8 levels (per 1-ppb increase in O₃: 1.3%, 95% CI = 0.7-1.9).

Conclusions: Short-term exposure to ambient air pollutants may induce oxidative damage and pro-inflammatory roles, together with counter-regulatory anti-inflammatory response.