The Effects of Photochemical Aging of Combustion Particles with Secondary Organic Aerosol Interactions on Cellular Toxicity

REUBEN ATTAH, Kamaljeet Kaur, Kerry Kelly, University of Utah

     Abstract Number: 166
     Working Group: Health-Related Aerosols

Abstract
Fine particulate matter (PM 2.5) is associated with numerous adverse health effects, such as pulmonary and cardiovascular diseases and premature death. Primary organic combustion particles and secondary organic aerosol (SOA) derived from the oxidation of anthropogenic VOCs are significant components of ambient particulate matter. Atmospheric aging induces changes in their chemical composition. However, the impact of these changes on human health is poorly understood. This study aims to understand how the atmospheric aging of primary combustion particles and its interaction with secondary organic aerosols affects biological responses. Combustion particles were produced by combusting a jet-fuel surrogate in the flat-flame burner and photochemically oxidized in a potential aerosol mass (PAM) oxidation flow reactor. SOA was produced by the oxidation of toluene vapor in the PAM reactor. The PAM simulated atmospheric aging of 10 days by exposing the combustion particles and combustion particles coated with SOA to OH radicals in the presence of 245nm ultraviolet light, humidity, and ozone. The O3/OH and HO2/OH ratios in the PAM reactor were similar to atmospheric values. The particle size distribution, molecular structure, and composition of soot and SOA particles were characterized by SMPS, FTIR, and GCMS, respectively. Monocultures of human epithelial cells A549 and co-cultures of A549 and THP-1 macrophages grown under submerged conditions were exposed to the three particle types at concentrations of 25μg/cm2 6μg/cm2 and 1.5μg/cm2. After an 8-hour exposure, cytotoxicity, xenobiotic metabolism (CYP 1A1), and pro-inflammatory biomarkers, IL-8 and TNF-α, were evaluated. The monoculture of A549 cells demonstrated a higher IL-8 response to aged combustion particles than to fresh combustion particles suggesting that oxidized species at the particle surface strongly contribute to PM2.5 inflammatory response.