Inflammatory and oxidative stress responses of healthy adults to changes in personal air pollutant exposure.

Exposure to air pollutants has been associated with respiratory and cardiovascular mortality, but the underlying molecular mechanisms remain inadequately understood. We aimed to examine molecular-level inflammatory and oxidative stress responses to personal air pollutant exposure. Fifty-three healthy adults aged 22-52 were measured three times for their blood inflammatory cytokines and urinary malondialdehyde (MDA, an oxidative stress biomarker) within 2 consecutive months. Pollutant concentrations monitored indoors and outdoors were combined with the time-activity data to calculate personal O3, PM2.5, NO2, and SO2 exposures averaged over 12 h, 24 h, 1 week, and 2 weeks, respectively, prior to biospecimen collection. Inflammatory cytokines and MDA were associated with pollutant exposures using linear mixed-effects models controlling for various covariates. After adjusting for a co-pollutant, we found that concentrations of proinflammatory cytokines were significantly and negatively associated with 12-h O3 exposures and significantly but positively associated with 2-week O3 exposures. We also found significant and positive associations of proinflammatory cytokines with 12-h and 24-h NO2 exposures, respectively. However, we did not find clear associations of PM2.5 and SO2 exposure with proinflammatory cytokines and with MDA. The removal of an O3-generating electrostatic precipitator in the mechanical ventilation systems of the offices and residences of the subjects was associated with significant decreases in IL-1β, IL-2, IL-6, IL-8, IL-17A, and TNF-α. These findings suggest that exposure to O3 for different time durations may affect systemic inflammatory responses in different ways.