Abstract

Biomass smoke is a common component of indoor air pollution that affects millions of people worldwide. Indoor air pollution has been demonstrated to induce inappropriate activation of the immune system and pro‐inflammatory responses. In some underdeveloped regions of the world, individuals are especially susceptible to the negative health effects associated with biomass smoke exposure and indoor air pollution. In many cases, which citizens’ homes do not have the proper air filtration, are they are therefore disproportionately affected by indoor air pollution exposure. Individuals chronically exposed to indoor air pollution often suffer from recurring upper respiratory infections and exacerbated asthma. The mechanisms that lead to these negative health outcomes are mostly unknown, but are thought to be mediated by activated cells of the innate immune system. The purpose of this research was to examine the impacts of woodsmoke on macrophages, a key mediator of innate immunity. RAW 264.7 macrophages were challenged with woodsmoke to and assessed for pro‐inflammatory responses. We hypothesized that an increasing concentration of woodsmoke would be damaging to the macrophages and would result in higher levels of cytokine production and release in nitric oxide. Multiple assays were performed to measure cytotoxicity, cytokine production and nitric oxide release. Some of the cytokines that were measured include MIP‐2 and TNF‐alpha, both of which are upregulated during inflammatory responses in macrophages. The LDH assay was used to assess the cytotoxicity of woodsmoke in treated macrophages. Our results thus far demonstrate, the following exposure to wood smoke, the release of MIP‐2 and TNF‐alpha was significantly increased following wood smoke exposure. Furthermore, the wood smoke exposure induced minimal amounts of cellular toxicity.Support or Funding InformationUniversity of Richmond’s Integrated and Inclusive Science Program

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