AAAR 32nd Annual Conference
September 30 - October 4, 2013
Oregon Convention Center
Portland, Oregon, USA
Abstract View
Commercial Charbroiling Emission Induces Inflammatory Response in Human Bronchial Epithelial Cells: The Role of Oxidative Stress and p38 MAPK
NING LI, Keisha Williams, Nicholas Gysel, Nachamari Rivera-Rios, Georgios Karavalakis, Michigan State University
Abstract Number: 639 Working Group: Health Related Aerosols
Abstract Commercial charbroiling emissions (CCE) are a significant source of ambient particulate matter (PM). Cooking meat on under-fired charbroilers emits significant amount of PM containing almost exclusively organic compounds, including carcinogenic polycyclic aromatic hydrocarbons which have also been associated with the pro-oxidative, pro-inflammatory and toxic effects of diesel exhaust particles. Currently, little is known about the respiratory effects of CCE. To better understand the effect of these emissions on restaurant workers health, as well as neighboring communities, we investigated whether compounds contained in the organic extracts of commercial charbroiling meat-derived emission had the ability to induce an inflammatory response in human airway epithelial cells, and if this effect was mediated through the generation of oxidative stress. PM2.5 samples collected during meat cooking processes on a commercial-grade under-fired charbroiler were sequentially extracted with water followed by methanol to obtain an aqueous PM suspension (AqPM) and organic extract (OE) respectively. Using human bronchial epithelial cell line (BEAS-2B) and primary normal human bronchial epithelial cells (NHBE) we showed that at non-toxic concentrations, OE, but not the AqPM, strongly induced the expression of antioxidant enzyme heme oxygenase-1, a highly sensitive marker of oxidative stress. The production of IL-6 and IL-8 was also significantly up-regulated by OE and this response could be effectively inhibited by the presence of antioxidant (N-acetyl cysteine), nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activator (sulforaphane), and p38 MAPK inhibitor (SB203580). Our results indicate that organic chemicals associated with PM2.5 emitted from commercial charbroiled meat cooking are capable of inducing oxidative stress and inflammatory responses, which involved the activation of Nrf2- and p38 MAPK-mediated signaling pathways. Further research is needed to better characterize the ability of charbroil cooking emissions to generate inflammatory response, and to assess the resulting adverse health effects on workers in the restaurant industry.