Superoxide Release from Macrophages upon Exposure to Secondary Organic Aerosols, Biomass Burning, Plastic Combustion, and Brake Wear Particles

KASEY EDWARDS, Ting Fang, Rizana Salim, Caitlyn Cruz, Sukriti Kapur, Sachin S. Gunthe, James Smith, Sergey Nizkorodov, Manabu Shiraiwa, University of California, Irvine

     Abstract Number: 566
     Working Group: Health-Related Aerosols

Abstract
Oxidative stress induced by reactive oxygen species (ROS) is a key process for adverse health effects upon respiratory deposition of particulate matter (PM). Alveolar macrophages can release large amounts of superoxide upon phagocytosis of PM through a process called the respiratory burst. The release of cellular ROS should depend on both PM composition and dose, but the dose-response relationship for various types of PM remains unclear. Here, we quantify cellular superoxide generation by macrophage cells exposed to secondary organic aerosols (SOA) derived from ॱOH oxidation of limonene, toluene, and naphthalene, as well as primary organic aerosols (POA) from biomass burning, brake wear, and pyrolysis of five different types of plastics. We quantified cellular superoxide production over the span of four hours after initial exposure of cells to PM suspensions by applying a chemiluminescence assay combined with electron paramagnetic resonance spectroscopy. We additionally identified the activation threshold, or the dose in which cellular superoxide production was altered compared to unexposed cells. Limonene SOA was found to induce the largest amount of superoxide release but had the largest activation threshold of 500 µg mL-1. Naphthalene SOA, toluene SOA, and biomass burning aerosol showed minor enhancement of superoxide production but had lower activation thresholds from 0.1-1 µg mL-1. Plastic burning PM showed a varied response depending on the type of plastic, with polyethylene terephthalate (PET) and high-density polyethylene (HDPE) having the highest observed superoxide production. The activation threshold for plastic combustion PM was found most often to be between 10-100 µg mL-1. Brake wear PM, on the other hand, led to suppression of cellular superoxide release beyond a dose of 5 µg mL-1. Determining the activation threshold and resulting cellular superoxide production of different types of PM provide critical insights for their relative inflammatory responses.