Effect of Soot and Coal Fly Ash Particles on Human Lung Cells



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Soot and coal fly-ash (CFA) are common anthropogenic aerosol particles emitted into the atmosphere. Their sources include vehicular/aircraft engines and industrial emissions. Millions of people are exposed directly or indirectly to these particles, as they work or live nearby coal power plants and airports. Both airborne CFA and soot are classified under carbon based PM2.5. These particles are small in size and can penetrate deeply into human lungs causing deleterious health outcomes, such as cardiovascular problems, lung cancer, adverse birth outcomes, and damage to the central nervous system, some of which may be fatal. The coal fly ash particles are a complex amalgam of different elements and minerals. Even though CFA is a major pollutant worldwide, there are very few studies which coherently characterize its toxicity based on its constituents. The pure toxicity of isolated soot particles is also not clearly understood. Its impact is predominantly known in the context of diesel engine exhaust due to the carcinogenic nature of vehicular emissions. Most of the in-vitro studies on the health impact of soot are done with ambient particulate matter and represent toxicity due to secondary pollutants like poly-aromatic hydrocarbons and heavy metals. There is very limited data on the toxic effects of isolated soot particles. This project investigated the impact of CFA and soot particles on human lung epithelial cells (A549). The CFA samples were obtained from three coal power plants in the United States while the soot samples were prepared in the laboratory. The cells were exposed to six different concentrations (0, 150, 200, 600, 900, and 1200 μg ml-1) for 24 hours and changes in cell viability for each concentration was assessed via cell population assay. The primary aims were to understand the impact of these particles on cell death, examine their dose dependent effects on cell viability, analyze the difference between their toxicities, as well as identify the constituents and physicochemical characteristics of an anthropogenic particle that make it toxic. The results showed significant (P < 0.05) toxicity for both the CFA and soot particles at all exposure concentrations compared to the control (no exposure). Further, a dosage-dependent trend in toxicity was observed. The CFA particles were sourced from the ambient environment and their particle toxicity was predominantly related to their constituent metal content and particle sizes. A higher cell death was found with increase in concentration of smaller particles (< 1 μm) and higher proportion of constituent metals such as calcium, selenium, and mercury in the CFA matrix. The soot particles were prepared in the laboratory from a propane flame and were relatively free from secondary pollutants. The relatively more hydrophilic black soot particles showed higher cell death at all concentrations in comparison to the more hydrophobic brown soot particles. The soot particles were significantly less toxic in comparison to CFA particles, mainly at higher concentrations. The cell death at highest concentration in the most toxic CFA (Missouri) sample was six times higher than that in brown soot. Thus, smaller size particles with higher amounts of constituent metals were responsible for higher toxicity of all carbon-based anthropogenic particles yet for pure, synthesized soot particles the physical properties such as solubility were a primary determinant of cell viability.

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Soot, particulate matter, in vitro toxicity of particulate matter, cell viability, Coal fly ash, coal power plants, a549 human lung epithelial cells, air pollution