American Association for Aerosol Research - Abstract Submission

AAAR 38th Annual Conference
October 5 - October 9, 2020

Virtual Conference

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Biomass Burning Aerosol Components Impair Mitochondrial Functioning to Induce Toxicological Response in Lung Cell Lines

FARIA KHAN, Karina Kwapiszewska, Alicia M. Romero, Nasir Jalal, Krzysztof Rudzinski, Jason Surratt, Rafal Szmigielski, ICHF, PAS, Warsaw, Poland

     Abstract Number: 334
     Working Group: Health-Related Aerosols

Abstract
Wildfires, biofuel combustion, and wood burning emit 10-15 Tg/yr of organic carbon (OC) into the atmosphere globally. The UV-light absorbing component of OC termed as “brow carbon” (BrC) contains a group of poorly characterized nitrated aromatic compounds (NACs). These NACs are important secondary products of urban biomass burning aerosol (BBA) involving nitrogen oxides (NOx) as key reactants. The present work assesses the inhalation toxicological effects of one primary marker of BB burning (levoglucosan) and six NACs including nitrated phenols (2-nitrophenol, 3-nitrophenol, and 4-nitrophenol), nitrocatechol, nitroguaiacol, and nitro-salicylic acid. Two in vitro lung cells models were used to assess the exposure effects of BBA: A549 (alveolar epithelial carcinoma cells) and BEAS-2B (bronchial epithelial normal cells). Acute toxicity effects occurred in both cell lines at 24- and 48-hours after exposure to solutions containing 100-200µg/mL of substances tested. The cellular and sub cellular organelle toxicity effects were more predominant in the BEAS-2B cell lines than in the A549 cell lines. A high number of apoptotic cells were observed after 24 hours, and late apoptotic cells at 48-hours as determined through flow cytometric analysis. The increase in cellular and mitochondrial reactive oxygen species (ROS) buildup was detected through confocal imaging and flow cytometry. The latter was the main reason for cellular death after exposure to BBA mixture. A decreased tetramethylrhodamine (TMRM) signal was also observed for the BBA treated cells, which indicates the impaired mitochondrial membrane potential as a major mechanism of induced toxicity in lung cells. The study highlights the potential inhalation effects of NACs in urban settings and raises the importance of controlling their emission rates for improved health conditions and decreased pulmonary diseases associated burden.