Epidemiological studies have associated particulate air pollution with reduced cognitive performance (Zhang et al., 2018), development of diseases in the pulmonary and cardiovascular systems (Devlin et al., 2014;Schwarze et al., 2006;Seaton et al., 1995), and dementia (H. Chen et al., 2017). The biological mechanisms behind higher risk of cardio-respiratory diseases in an air-polluted urban environment have been studied and associated with ultrafine particles (Leitte et al., 2012;Miller et al., 2017;Penttinen et al., 2001). The size, morphology, and chemical composition of particles are critical in gauging detrimental effects to human health. Conventional air pollution indices classify and monitor PM as a function of its aerodynamic diameter: Exposure to PM 0.1 (≤0.1 μm), often referred to as ultrafine particles (UFPs), is of increasing focus and concern because of UFPs potential adverse health implications, as small particles can exert higher toxicity than larger particles (Ohlwein et al., 2019). UFPs can be drawn into the body via ingestion (Calderón-Garcidueñas et al., 2020), skin (Araviiskaia et al., 2019), olfactory transport, and through the lungs, entering the alveoli and penetrating biological membranes, effectively translocating to almost all organs (