Superoxide Release from Macrophages upon Exposure to Biomass Burning Aerosols, Plastic Combustion PM, Secondary Organic Aerosols, and Brake Wear Particles
KASEY EDWARDS, Rizana Salim, Ting Fang, Caitlyn Cruz, Sukriti Kapur, Sachin S. Gunthe, James Smith, Sergey Nizkorodov, Manabu Shiraiwa, University of California, Irvine
Abstract Number: 484
Working Group: Aerosol Exposure
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 five hours after initial exposure of cells to PM suspensions by applying a chemiluminescence assay combined with electron paramagnetic resonance spectroscopy. Limonene SOA was found to induce the largest amount of superoxide release, with an activation dose of 500 µg/mL. Naphthalene SOA, toluene SOA, and biomass burning aerosol showed minor enhancement of superoxide production, but had lower activation doses from 0.1-1 µg/mL. Plastic combustion 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 dose for plastic combustion PM was found to be between 10-100 µg/mL. Brake wear PM, on the other hand, led to immediate suppression of cellular superoxide release. Determining the activation dose and resulting cellular superoxide production of different types of PM provide critical insights for their relative inflammatory responses.