Inhalation of SiO 2 particles causes a granulomatous inflammatory response that progresses to interstitial fibrosis as well as systemic immune deficits ( 1– 5). Silicosis occurs as the result of exposure through occupation (e.g., construction, mining), recreation (e.g., pottery), or environment (e.g., soil). Silicosis is a progressive, disabling, and often-fatal lung disease resulting from the inhalation of crystalline silica (SiO 2) particles over prolonged periods of time.
Silicon dioxide, also known as silica, is one of the most common elements on earth, yet its inhalation can result in acute lung injury and ongoing inhalation can result in permanent lung damage due to deposition of particles in the lung. Collectively, our data suggest that SiO 2 exposure alters AM phenotype, which in turn affects their ability to uptake and respond to bacterial lipoproteins. Furthermore, SiO 2 exposure decreased uptake of fluorescently labeled Pam 2CSK 4 and Pam 3CSK4, resulting in reduced secretion of IL-1β, but not IL-6. Interestingly, these responses were dependent on interactions between SiO 2 and the class A scavenger receptor CD204, but not MARCO. Alveolar and bone marrow-derived macrophages downregulate TLR2 expression following acute SiO 2 exposure (e.g., 4 h). Because recognition and clearance of inhaled particulates and microbes are largely mediated by pattern recognition receptors (PRRs) on the surface of AM, we hypothesized that exposure to SiO 2 limits the ability of AM to respond to bacterial challenge by altering PRR expression. Numerous studies have examined the relationship between alveolar macrophages (AMs) and crystalline silica (SiO 2) using in vitro and in vivo immunotoxicity models however, exactly how exposure to SiO 2 alters the functionality of AM and the potential consequences for immunity to respiratory pathogens remains largely unknown.
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She has been a long time member of the Society for Hispanic Professional Engineers and the Society for the Advancement of Chicanos and Native Americans in Science. Beamer has served as Academic Councilor on the Board of the International Society of Exposure Science. Beamer is also involved field sampling and exposure modeling projects aimed at understanding children's exposures to pesticides in agricultural communities and metals near hazardous waste sites. Currently she is using this laboratory to measure the concentration of tricholoethylene in breastmilk and water contaminants in Nogales. Beamer has built a laboratory to characterize exposure and risk of water-borne contaminants. As an expert in micro-activity patterns she is examining the activity patterns of older children and utilizing them to estimate dust ingestion.
She is currently using GIS techniques to assess the risk of wheezing from exposure to traffic pollutants in early childhood. Beamer is using both computer modeling and laboratory techniques in her research. The central motivation behind her research is in the development of tools that can help provide more robust exposure and dose estimates and improve the demonstration of a relationship between measured environmental concentrations and resulting health effects, particularly amongst children and underserved populations. Beamer, Ph.D., joined the College of Public Health in 2007 as an assistant professor in Environmental Health Sciences.
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