Document Type


Date of Degree Completion

Spring 2018

Degree Name

Master of Science (MS)



Committee Chair

Anne Johansen

Second Committee Member

Dion Rivera

Third Committee Member

Tim Sorey


Fine atmospheric particulate matter (PM2.5) emitted during the combustion of fossil and biomass fuels is known to adversely affect human health. While the underlying mechanisms are thought to be driven by the generation of reactive oxygen species (ROS), specific particle characteristics responsible for this detrimental effect are not well understood. In this research, the quantitative determination of the biologically relevant antioxidant, glutathione (GSH), was optimized for use as an indicator of oxidative stress to shed light on relevant particle characteristics. This was accomplished via fluorescent spectroscopy for GSH determination by way of reaction with o-phthalaldehyde (OPA), a fluorescent marker. Physicochemical properties of particles were studied using Scanning Electron Microscopy (SEM), laser particle size analyzer, Inductively Coupled Plasma Mass Spectrometry (ICP-MS), and Thermal Gravimetric Analysis (TGA) to determine particle morphology, aqueous particle surface area and diameter, trace metal content, and volatile organic content, respectively. These physical and chemical properties were correlated with the oxidative capacity of particles in reaction with GSH. Results show that the fluorometric analysis of GSH is relatively simple to employ to study particle toxicity and that different particles display unique oxidative capacity, which cannot be directly correlated to any one of the measured parameters. The pseudo first order rate constant, k’, for heat-treated samples was correlated to total transition metals and the loss of mass after heat treatment to 700 ˚C with an R2 value of 0.708. It is thought that elemental carbon (EC) drives particle toxicity. This research contributes to the analytical determination of particle toxicity and helps increase our understanding of the mechanisms that control their adverse effects.