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A1300 - Ambient Vapor- and Particle-Phase Air Pollutants Simultaneously Collected at the Same Location in Southern California Promote Allergic Sensitization by Targeting Different Immune Responses
Author Block: N. Li1, R. Lewandowski1, D. Sidhu1, J. Wagner1, P. Akbari1, A. Eiguren-Fernandez2, J. Harkema1, A. Cho2, J. Froines2; 1Pathobiology, Michigan State University, East Lansing, MI, United States, 2University of California Los Angeles, Los Angeles, CA, United States.
Rationale: Contribution of volatile and semi-volatile organic chemicals to air pollutant-associated asthma pathogenesis and exacerbation is poorly understood. Although ambient air pollution includes chemicals in both the vapor- and particle-phases most health effects studies have focused on particulate matter (PM). While it has been established that exposure to ambient PM is a complicating risk factor for asthma, the health effects of vapor-phase air pollutants and their combined effects with PM have not been investigated. We tested the hypothesis that vapor-phase air pollutants would act as an adjuvant to promote allergic sensitization and this effect would be further enhanced in the presence of PM.
Methods: Ambient PM and matching vapor-phase air samples (vapor) were simultaneously collected at the same location in San Bernadino, CA. After analysis of samples' chemical properties we used a mouse asthma model to determine the adjuvant effects of PM, vapor and the combination of PM and vapor on allergic sensitization to ovalbumin (OVA). Mice were sensitized by three intranasal instillations of OVA with or without air pollutant(s) over a 7-day period and challenged with OVA aerosol two weeks later. Necropsy was performed 48 hrs after the last OVA challenge for endpoint analyses.
Results: PM and vapor-phase samples had strong pro-oxidant and electrophilic activities, respectively. PM, vapor and the combination of PM and vapor all exerted potent adjuvant effects on OVA sensitization. This was evidenced by eosinophil and neutrophil influx and marked morphological changes in the lung and increased OVA-specific antibody levels in the blood. Comparison of in vivo responses between the mice sensitized by OVA alone and those sensitized by OVA plus air pollutant(s) revealed that PM, vapor and PM plus vapor promoted allergic sensitization by targeting different immune responses. As an adjuvant while PM alone had a strong effect in causing neutrophil influx, vapor alone was a potent inducer of eosinophilic lung inflammation. Exposure to the combination of PM and vapor during sensitization led to the highest levels of OVA-specific antibodies in the systemic circulation.
Conclusions: Our results suggest that air pollutants contribute to allergic airway inflammation by targeting different immune-regulatory pathways, which is determined by air pollutants' chemical composition and reactivity. These findings indicate the importance of conducting multi-pollutant research in order to fully understand the health effects of ""real-life"" air pollution.