Abstract

Aerosols, also known as particulate matter (PM), strongly influence the climate and pose considerable risks to human health. As short-lived climate forcers, aerosols alter the Earth’s radiative budget by absorbing and scattering incident solar radiation, thereby affecting global and regional temperatures, atmospheric circulation, cloud formation, and precipitation patterns. From a public health perspective, exposure to particulate matter, particularly fine and ultrafine particles, has been associated with a wide range of adverse outcomes, including respiratory diseases, neurodegenerative disorders, and premature mortality. In addition, aerosols can transport pathogens and represent a critical pathway for the transmission of airborne infectious diseases. Despite contributing to only a small fraction of the total atmospheric aerosols, bioaerosols are important determinants of indoor air quality and the associated human exposure. In urban areas, the climatic and health impacts of aerosols are of particular concern because of the large population exposed to elevated PM pollutant concentrations. Urban aerosols comprise a complex mixture of particles originating from diverse sources, ranging from anthropogenic emissions, such as fossil fuel combustion, industrial activities, and biomass burning, to natural sources, such as biogenic, secondary atmospheric processing, and wildfires. Given the rapid pace of urbanization and growth of urban populations worldwide, understanding the optical properties and health impacts of urban aerosols is essential for developing effective regulatory and mitigation strategies to reduce the aerosol-related environmental and public health burdens. Light-absorbing organic aerosols, commonly referred to as brown carbon (BrC), are among the dominant light absorbers in the atmosphere. Conventional understanding of BrC limits its absorption to ultraviolet-blue regions of the spectrum and associates its sources predominantly with biomass burning. Recently, the discovery of dark BrC (d-BrC) in biomass burning emissions has spurred a reassessment of BrC’s contribution to global radiative forcing. Unlike the more commonly reported weakly absorbing BrC, d-BrC exhibits strong absorption extending into the near-infrared wavelengths. However, despite the prevalence of anthropogenic BrC emission sources globally, the occurrence and climatic significance of d-BrC in urban environments remain underexplored. In Study (1), we present observational evidence of d-BrC aerosols in Southeast Texas, a hub for petrochemical industries located at the intersection of continental and marine airmasses. Combined real-time and offline measurements revealed that over 80% of aerosol light absorption at blue and near-infrared wavelengths was attributable to non-black carbon aerosols, with d-BrC identified as a dominant contributor. Particle-scale electron energy-loss spectroscopy corroborated the strong absorptivity of these d-BrC aerosols, characterized by imaginary refractive indices of ~0.11 at 550 nm and ~0.06 at 1047 nm. The observed d-BrC particles were likely emitted as primary aerosols from non-biomass burning sources, particularly traffic-related emissions. These findings provide compelling evidence for the presence and climatic importance of d-BrC in urban atmosphere, extending its relevance beyond biomass burning and wildfire emissions, and highlight the need to incorporate d-BrC into regional and global aerosol-climate models. Beyond its climatic impacts, ambient air pollution has received increasing attention from its associative role in accelerating the development of neurodegenerative disorders, such as Alzheimer’s disease (AD). Fine and ultrafine particulate matter, defined as particles with aerodynamic diameters less than 2.5 and 0.1 micrometers (PM2.5 and PM0.1), respectively, are of major concern because the small sizes enable them to deposit deeply into respiratory tract upon inhalation and facilitate their translocation into the brain. In Study (2), we investigated the effects of acute PM exposure on the early development of AD using in vivo mouse models. We developed a whole-body mouse exposure chamber with a custom-designed aerosol-dispenser inlet to rapidly establish and maintain uniform particle concentrations throughout the chamber, particularly at the mouse nose level. The chamber was integrated with high-temporal-resolution in vivo microdialysis, enabling continuous monitoring of the hippocampal amyloid-beta (Aβ) peptide level, a pathological hallmark of AD, while ensuring unrestricted mouse movement and thereby minimizing stress-related interference. Chamber characterization showed that particle number concentration reached steady state within 7-8 minutes of aerosol introduction and remained spatially uniform. Using this platform, APP/PS1 mice were exposed to pyrolyzed wood-derived organic particles (Pyrosol), representative of biomass burning emissions, and copper oxide nanoparticles (CuO), representative of vehicle brake-wear emissions, through five 2-hour inhalation exposures over three days. Hourly microdialysis measurements revealed that Pyrosol induced a rapid increase in Aβ40 levels, reaching more than three-fold of baseline level within 2 hours of the first exposure, but the responses declined over time. In contrast, the CuO produced a delayed but persistent Aβ40 rise, reaching ~3.5 times the baseline level after the fourth exposure (~33 hours). These results demonstrate the capability of the whole-body chamber-microdialysis platform to capture time-resolved neurobiological responses to inhaled pollutants and reveal that short-term PM exposures can disrupt Aβ homeostasis, providing mechanistic insight into air pollution-associated AD risks. In Study (3), we examined the neurotoxicity potential of a broader range of common urban fine and ultrafine PM constituents using in vitro mouse-derived Neuro-2a cells, focusing on cell viability and mitochondrial membrane potential (MMP). A diverse set of pollutants–including carbonaceous particles (black carbon), organic matter (9,10-phenanthrenequinone), transition metal compounds (copper (Cu), iron (Fe), zinc (Zn), and manganese (Mn) species), and inorganic salts (sulfates, nitrates, and ammonium)–was tested across graded concentrations to derive dose-response relationships and lethal concentrations corresponding to 50% cell death (LC50). Results showed large variability in neuronal cytotoxicity across different urban aerosol chemical compositions, with 9,10-phenanthrenequinone (9,10-PQN) exhibiting the strongest neurotoxicity, while the inorganic sodium sulfate (Na2SO4) showed minimal toxicity. For the transition metal compounds, insoluble metal oxides (CuO, Fe3O4, ZnO) showed higher toxicity than their soluble counterparts. The MMP measurements revealed that mitochondrial dysfunction often occurred at relatively high cell viability, suggesting it can serve as an early indicator of neuronal stress preceding overt cell death. Importantly, not all cytotoxic pollutants strongly reduced MMP, indicating that different PM constituents follow distinct mechanisms of neuronal injury. This study highlights strong composition-dependent neurotoxicity and mechanistic diversity of PM constituents, and emphasizes the need for composition- and emission source-specific regulatory and mitigation strategies to alleviate the health risks of atmospheric PM. In Study (4), motivated by the lack of standardized methods for sampling virus-laden aerosols in indoor environments, we evaluated the effects of different bioaerosol aerosolization and sampling methods on the structural integrity of airborne viruses. Using filamentous influenza A virus-like particles (VLPs) as a safe surrogate, we compared three nebulizers–Collison, Blaustein Atomization Modules (BLAM), and jet nebulizers–and three bioaerosol samplers–liquid spot sampler (LSS), SKC BioSampler, and wet cyclone. The BLAM and jet nebulizers preserved 12–21 % of filamentous structures, whereas the Collison nebulizer reduced the filament recovery to ∼10 % due to its higher-shear aerosolization mechanism. Among the samplers, the condensation-based LSS achieved the highest filament retention (~30%), whereas SKC BioSampler and wet cyclone sampler retained only ∼10 % and ∼7 % of filamentous VLPs, respectively, because of their higher flowrates, shear forces, and impaction stresses. Furthermore, we also investigated the influence of relative humidity (RH) on viral structure integrity. An elevated RH level (85 %) improved filament retention by ∼20 % compared with dry conditions (25% RH). These findings demonstrate that commonly used bioaerosol aerosolization and sampling techniques can substantially alter the viral morphology, potentially affecting the viability and infectivity of sampled viruses. This highlights the necessity for gentler methodologies to improve the accuracy of laboratory studies and environmental monitoring of airborne pathogens. Collectively, the research presented in this dissertation advances our understanding of the impacts of aerosols on climate, neurodegenerative disease risks, and airborne pathogen sampling. These findings contribute to improving the accuracy of aerosol-climate models, provide insights for developing regulatory and mitigation strategies to address environmental health risks, and inform approaches for monitoring airborne pathogens.

Committee Chair

Rajan Chakrabarty

Committee Members

Jenna Ditto; Joseph Puthussery; Lu Xu; Michael Vahey

Degree

Doctor of Philosophy (PhD)

Author's Department

Energy, Environmental & Chemical Engineering

Author's School

McKelvey School of Engineering

Document Type

Dissertation

Date of Award

7-28-2026

Language

English (en)

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