(302g) Effect of Combustion Particle Size on Pathologically Important Responses in Lung Cells

Authors: 
Kelly, K., University of Utah
Kaur, K., University of Utah
Mohammadpour, R., University of Utah
Jaramillo, I., University of Utah
Paine, R., University of Utah
Reilly, C., University of Utah
Ghandehari, H., University of Utah
Numerous studies have demonstrated associations between combustion-derived particulate matter (cdPM) and adverse human health outcomes. cdPM is a significant contributor to fine and ultrafine PM levels, particularly in urban areas. However, understanding the relationship between cdPM and its health effects is complicated by cdPM’s complex nature: a dynamic mixture of particles and condensed material with different sizes, shapes, and chemical compositions that is generated from a range of sources. Furthermore, several confounding factors make comparing results from various studies difficult, including particle sources and for cdPM: fuel composition, engine age, combustion conditions, lubricants, and sampling methods. For example, experimental and epidemiological studies about the effect of various PM size fractions (PM10, PM2.5 and PM1) provide somewhat conflicting results. As particle size diameter decreases, its relative surface area increases, which in turn increases the bioavailability of atoms or molecules leading to, for example, increased pro-inflammatory effects. This study focuses on directly testing the effect of cdPM size on biological responses in lung cells.

The cdPM is generated from a premixed flat-flame burner combusting a jet-fuel surrogate at an equivalence ratio of 2.1. A nitrogen shroud and a glass housing minimize atmospheric effects. The sample is diluted, thermally denuded, and size separated using a differential mobility analyzer. Three different cdPM size fractions are examined (with particle diameters of 25, 45, and 65 nm) for their effect on oxidative potential, cell viability, cellular uptake, inflammatory response, cytochrome P450 (CYP) 1 A1 and 1 B1 mRNA induction, and the activation of transient receptor potential Ankyrin-1 (TRPA1). The biological outcomes are evaluated in A 549 human alveolar basal epithelial cells, with the exception of the TRPA1, which is evaluated in TRP over-expressing HEK293 cells. These results are a step towards understanding some of the interactions between understanding the links between combustion particle aging and health effects.