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.
Keywords: Air pollutant exposure; Inflammation; O(3) exposure; Oxidative stress; Temporal-dependent response.
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