Abstract

Over two‐fifths of the world’s population uses solid biomass fuels such as animal dung, plastic, rubber or wood for the purpose of cooking and the heating of their homes. In some instances, especially in underdeveloped regions of the world, biomass smoke exposure can disproportionately impact women and children of color, as they are more than likely to be performing cooking duties and being exposed to this type indoor air pollution. Poor ventilation of homes can also contribute to poorer health outcomes associated with biomass smoke exposure. These individuals exposed to biomass smoke and particulate matter are also more likely to be suffer from negative health outcomes such as repeated, acute lower respiratory infections (ALRI) and asthma. The mechanisms by which biomass smoke exposure contributes to these pathologies of the lung remain largely unknown. The purpose of this research was to determine the general effects of woodsmoke on lung airway epithelial cells (A549). In this project, we are modeling the effects biomass smoke exposure using solubilized wood smoke. Biomass smoke is believed to have a significant impact on the innate immune system and the epithelial cells than line airways. To determine the pro‐inflammatory effects of woodsmoke, we used the polymerase chain reaction (PCR) to assess the expression of many pro‐inflammatory genes. Results thus far show that treated A549 cells displayed an increase in COX‐2 expression with increasing concentrations of woodsmoke. This induction of iNOS, TGF‐beta, and HO‐1 gene expression was also observed. The cytotoxicity of woodsmoke on A549 cells was also assessed using the lactate dehydrogenase assay (LDH) assay. Future studies are aimed at determining the impact of woodsmoke on cytokine secretion in A549 cells and whether smoke exposure is capable of inducing oxidative stress in these cells.Support or Funding InformationUniversity of Richmond’s Integrated and Inclusive Science Program

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