The purpose of this thesis is to examine applications of thermal and laser-based methods to monitor airborne particulates in underground coal mines. Specifically, coal and mixed mineral mine dust, as well as, diesel particulate matter (DPM). These particulates have historically, and continue to have, significant health impacts on underground miners. Chapters 1 and 2 of this thesis concentrate on using a novel method of thermogravimetric analysis (TGA) to characterize respirable coal and mixed mineral mine dust and presents the results of this method being applied to samples collected in Appalachia coal mines. Appalachia has been a geographic "hotspot" for the rise in occupational lung disease amongst underground coal miners, which began in 1990's after decades of steady decline. This has led researchers to propose there could be something unique about the respirable dust composition in Appalachia coal mines, which resulted in the surge of lung disease cases; however, the knowledge base regarding the actual composition of respirable coal mine dust is limited. The results of this thesis show that most of the mass fraction of respirable Appalachia coal mine dust is not coal, but rather carbonates and non-carbonate minerals (i.e. silica and silicates). These findings are significant as many researchers now suspect silica and silicates to be the true culprit in the occupational lung disease of coal miners. DPM presents an additional occupational health hazard to underground coal miners where diesel equipment is used and is difficult to monitor due to its complex nature. In underground metal/non-metal mines, airborne DPM is regulated and monitored using carbon surrogates. However, due to the potential interference from coal-sourced carbon, DPM in coal mines is monitored only by taking samples at the tailpipe of each piece of equipment. This thesis aims to investigate the potential for a laser-based instrument, the FLIR Airtec, to be used in underground coal mines. In particular, what effect the coal dust will have on the instrument, as it measures DPM by way of elemental carbon (EC). The results of this study show that while the Airtec will not over-estimate coal-sourced EC, there could be some sampling artifacts associated with its operation in coal mines, which may inhibit its effectiveness. / Master of Science

The purpose of this thesis is to examine the potential of a novel method for analysis and characterization of coal mine dust. Respirable dust has long been an industry concern due to the association of overexposure leading to the development occupational lung disease. Recent trends of increased incidence of occupational lung disease in miners, such as silicosis and Coal Workers Pneumoconiosis, has shown there is a need for a greater understanding of the respirable fraction of dust in underground coal mines. This study will examine the development of a comprehensive standard methodology for characterization of respirable dust via thermogravimetric analysis (TGA). This method was verified with laboratory-generated respirable dust samples analogous to those commonly observed in underground coal mines. Results of this study demonstrate the ability of the novel TGA method to characterize dust efficiently and effectively. Analysis of the dust includes the determination of mass fractions of coal and non-coal, as well as mass fractions of coal, carbonate, and non-carbonate minerals for larger respirable dust samples. Characterization occurs through the removal of dust particulates from the filter and analysis with TGA, which continuously measures change in mass with specific temperature regions associated with chemical changes for specific types of dust particulates. Results obtained from the verification samples reveal that this method can provide powerful information that may help to increase the current understanding of the health risks linked with exposure to certain types of dust, specifically those found in underground coal mines. / Master of Science

Occupational exposure to endotoxin-rich swine barn air induces respiratory diseases and loss of lung function. Barn exposure induces recruitment of pulmonary intravascular monocytes/macrophages (PIMMs) and subsequent increased host sensitivity to <i>Escherichia coli</i> LPS challenge. Therefore, to further clarify the biology of PIMMs we examined the role of recruited PIMMs in a rat <i>Escherichia coli</i>-induced lung inflammation model. Following sepsis, lung inflammation was induced with recruitment of PIMMs and subsequently, <i>Escherichia coli</i> LPS challenge exacerbated the lung inflammation with localization of multiple inflammatory cytokines in PIMMs to suggest their possible involvement in modulating lung inflammation in this model.<p> In order to delineate mechanisms of barn air induced lung dysfunction, a rat model of occupational exposure was characterized to show that one and five exposures to the barn environment induced acute lung inflammation and increased airway hyperresponsiveness (AHR). Following 20 exposures, AHR was dampened to indicate adaptive responses. Barn air contains high levels of endotoxin which led us to investigate its role in lung inflammation and AHR. Exposure of mice with either a functional TLR4 (WT) or non-functional TLR4 (mutants) to barn air revealed dependence of lung inflammation but not AHR on a functional TLR4.<p> I investigated whether exposure to barn air alters host responses to a subsequent microbial challenge. Following one day barn exposure and <i>Escherichia coli</i> LPS challenge, lung inflammation was exacerbated with increased granulocytes and IL-1β levels compared to one day barn exposed rats without <i>Escherichia coli</i> LPS challenge. However, increased granulocytes and IL-1β levels in barn exposed and <i>Escherichia coli</i> LPS challenged rats were not different from control rats treated with <i>Escherichia coli</i> LPS indicating a lack of priming effect of barn exposure. However, above results are suggestive of an underlying risk of increased lung inflammation following secondary microbial infection in naïve barn workers.<p> Lastly, I investigated the expression and activity of novel signalling molecules called <i>N</i>-myristoyltransferase and calcineurin in barn air and <i>E. coli</i> LPS induced lung inflammation models. Following one day barn exposure, increased protein expression but not activity of <i>N</i>-myristoyltransferase and calcineurin was shown. However, there is a need to identify the specific role of these two molecules in barn air induced lung inflammation. To conclude, animal models of barn exposure are useful tools to understand mechanisms of lung inflammation and AHR. However, there is still a need to examine endotoxin-independent nature of AHR and roles of other molecules of the innate immune system in regulating barn air induced effects.

Occupational exposure to endotoxin-rich swine barn air induces respiratory diseases and loss of lung function. Barn exposure induces recruitment of pulmonary intravascular monocytes/macrophages (PIMMs) and subsequent increased host sensitivity to <i>Escherichia coli</i> LPS challenge. Therefore, to further clarify the biology of PIMMs we examined the role of recruited PIMMs in a rat <i>Escherichia coli</i>-induced lung inflammation model. Following sepsis, lung inflammation was induced with recruitment of PIMMs and subsequently, <i>Escherichia coli</i> LPS challenge exacerbated the lung inflammation with localization of multiple inflammatory cytokines in PIMMs to suggest their possible involvement in modulating lung inflammation in this model.<p> In order to delineate mechanisms of barn air induced lung dysfunction, a rat model of occupational exposure was characterized to show that one and five exposures to the barn environment induced acute lung inflammation and increased airway hyperresponsiveness (AHR). Following 20 exposures, AHR was dampened to indicate adaptive responses. Barn air contains high levels of endotoxin which led us to investigate its role in lung inflammation and AHR. Exposure of mice with either a functional TLR4 (WT) or non-functional TLR4 (mutants) to barn air revealed dependence of lung inflammation but not AHR on a functional TLR4.<p> I investigated whether exposure to barn air alters host responses to a subsequent microbial challenge. Following one day barn exposure and <i>Escherichia coli</i> LPS challenge, lung inflammation was exacerbated with increased granulocytes and IL-1β levels compared to one day barn exposed rats without <i>Escherichia coli</i> LPS challenge. However, increased granulocytes and IL-1β levels in barn exposed and <i>Escherichia coli</i> LPS challenged rats were not different from control rats treated with <i>Escherichia coli</i> LPS indicating a lack of priming effect of barn exposure. However, above results are suggestive of an underlying risk of increased lung inflammation following secondary microbial infection in naïve barn workers.<p> Lastly, I investigated the expression and activity of novel signalling molecules called <i>N</i>-myristoyltransferase and calcineurin in barn air and <i>E. coli</i> LPS induced lung inflammation models. Following one day barn exposure, increased protein expression but not activity of <i>N</i>-myristoyltransferase and calcineurin was shown. However, there is a need to identify the specific role of these two molecules in barn air induced lung inflammation. To conclude, animal models of barn exposure are useful tools to understand mechanisms of lung inflammation and AHR. However, there is still a need to examine endotoxin-independent nature of AHR and roles of other molecules of the innate immune system in regulating barn air induced effects.