Energy input is vital in every swine operation as it directly affects production performance and overall profitability. With the increasing trend in energy prices and feed costs, the swine industry needed to find ways to improve energy use efficiency in their operations in order to reduce overall cost of production. The goals of this study were to gather benchmark information on current energy usage in swine barns through survey and energy audit, and evaluate different energy-saving measures through building simulation.<p> The results of the survey showed that the average electricity and gas cost was $6.50/head for farrow-to-finish barns, $1.70/head for grow-finish barns, $0.59/head for nursery and $1.95/head for farrow-wean barns. Significant difference (P<0.05) in energy usage within the same type of operation was observed, implying significant opportunities to improve energy use practices in some barns to reduce overall energy costs.<p> The results of the barn monitoring showed that the average daily electricity consumption during summer for farrowing, nursery, grow-finish and gestation room was 3.79 kWh/head (16 sows); 0.12 kWh/head (226 pigs); 0.14 kWh/head (551 pigs) and 0.33 kWh/head (349 sows); respectively. During winter, the average daily electricity consumption for farrowing, nursery, grow-finish and gestation room was 3.92 kWh/head (15 sows); 0.14 kWh/head (227 pigs); 0.09 kWh/head (521 pigs) and 0.22 kWh/head (322 sows); respectively. Highly negative correlation (range from -0.6 to -0.9) was observed between the fan energy consumption and gas concentration of H2S, NH3 and CO2 during summer. This implied that reducing ventilation rate was not a sound option to reduce energy consumption.<p> A simulation model was developed using the principle of heat transfer and thermodynamics to evaluate various energy-conservation measures through building simulation. Applying energy conservation strategies to lighting, creep heating, recirculation fans, exhaust fans, feed motor and heat recovery, an average annual savings of 25,957 kWh (43 kWh/sow); 47,391 kWh (79 kWh/sow); 9,872 kWh (16 kWh/sow); 118,890 kWh (198 kWh/sow); 1,846 kWh (3 kWh/sow); and 74,952 m3 (125 m3/sow) can be achieved, respectively. The outcome of this research project will help pork producers in managing the use of energy in their operations more efficiently, thereby reducing overall energy costs. Additionally, the reduction of energy use across the industry would contribute to the reduction in greenhouse gas emissions associated with energy generation.

Energy input is vital in every swine operation as it directly affects production performance and overall profitability. With the increasing trend in energy prices and feed costs, the swine industry needed to find ways to improve energy use efficiency in their operations in order to reduce overall cost of production. The goals of this study were to gather benchmark information on current energy usage in swine barns through survey and energy audit, and evaluate different energy-saving measures through building simulation.<p> The results of the survey showed that the average electricity and gas cost was $6.50/head for farrow-to-finish barns, $1.70/head for grow-finish barns, $0.59/head for nursery and $1.95/head for farrow-wean barns. Significant difference (P<0.05) in energy usage within the same type of operation was observed, implying significant opportunities to improve energy use practices in some barns to reduce overall energy costs.<p> The results of the barn monitoring showed that the average daily electricity consumption during summer for farrowing, nursery, grow-finish and gestation room was 3.79 kWh/head (16 sows); 0.12 kWh/head (226 pigs); 0.14 kWh/head (551 pigs) and 0.33 kWh/head (349 sows); respectively. During winter, the average daily electricity consumption for farrowing, nursery, grow-finish and gestation room was 3.92 kWh/head (15 sows); 0.14 kWh/head (227 pigs); 0.09 kWh/head (521 pigs) and 0.22 kWh/head (322 sows); respectively. Highly negative correlation (range from -0.6 to -0.9) was observed between the fan energy consumption and gas concentration of H2S, NH3 and CO2 during summer. This implied that reducing ventilation rate was not a sound option to reduce energy consumption.<p> A simulation model was developed using the principle of heat transfer and thermodynamics to evaluate various energy-conservation measures through building simulation. Applying energy conservation strategies to lighting, creep heating, recirculation fans, exhaust fans, feed motor and heat recovery, an average annual savings of 25,957 kWh (43 kWh/sow); 47,391 kWh (79 kWh/sow); 9,872 kWh (16 kWh/sow); 118,890 kWh (198 kWh/sow); 1,846 kWh (3 kWh/sow); and 74,952 m3 (125 m3/sow) can be achieved, respectively. The outcome of this research project will help pork producers in managing the use of energy in their operations more efficiently, thereby reducing overall energy costs. Additionally, the reduction of energy use across the industry would contribute to the reduction in greenhouse gas emissions associated with energy generation.

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.

Swine barn air is a heterogeneous mixture of dust, bacteria and irritant chemicals including ammonia and hydrogen sulphide. Gram-negative bacteria are commonly found in swine barn air and significantly contribute to pulmonary disease in unprotected swine barn workers, through the endotoxin moiety, lipopolysaccharide (LPS). Toll-like Receptor-4 is the ligand for LPS. It is found on many cell types including monocytes, macrophages, neutrophils, endothelial cells, and to a lesser extent, epithelial cells. The severity and outcome of acute lung injury following barn air exposures depends upon the balance between epithelial and vascular endothelial repair mechanisms, including angiogenesis. Vascular Endothelial Growth Factor (VEGF) is an endothelial mitogen produced by mesenchymal and alveolar Type II epithelial cells and by activated bronchial airway epithelial cells. Research investigating the role of cytokines in angiogenesis has shown that close proximity of immune cells and endothelial cells modulates the production of various compounds that regulate vascular function. Given that LPS is the ligand for TLR4 there appeared to be a role for TLR4 in angiogenesis, particularly following endotoxin exposure. To determine whether this was occurring, we examined whether exposure to swine barn air alters vascular density in the lungs and the role of TLR4 using a murine model. Toll-like Receptor-4 wild-type (C3HeB/FeJ) and TLR4 mutant (C3H/HeJ) mice were obtained and exposed to swine barn air for 1-, 5-, or 20-days for 8 hours/day. Wild-type animals showed a 127% increase in vascular density after 20-days barn air exposure. Vascular Endothelial Growth Factor-A protein levels were decreased by 0.62-fold after one-day swine barn air exposure in wild-type animals, indicating that VEGF-A is being used as a pro-angiogenic mitogen. Transcription of VEGF-A mRNA was increased in wild-type animals after all swine barn air exposure periods. The receptor VEGFR-1 showed increased mRNA transcription over all time points. These effects were only observed in TLR4 wild-type animals, indicating that these effects are mediated by TLR4. Further, VEGF-A and VEGFR-1 appear to be involved in the manifestation of TLR4-induced angiogenesis in the lung.

Swine barn air is a heterogeneous mixture of dust, bacteria and irritant chemicals including ammonia and hydrogen sulphide. Gram-negative bacteria are commonly found in swine barn air and significantly contribute to pulmonary disease in unprotected swine barn workers, through the endotoxin moiety, lipopolysaccharide (LPS). Toll-like Receptor-4 is the ligand for LPS. It is found on many cell types including monocytes, macrophages, neutrophils, endothelial cells, and to a lesser extent, epithelial cells. The severity and outcome of acute lung injury following barn air exposures depends upon the balance between epithelial and vascular endothelial repair mechanisms, including angiogenesis. Vascular Endothelial Growth Factor (VEGF) is an endothelial mitogen produced by mesenchymal and alveolar Type II epithelial cells and by activated bronchial airway epithelial cells. Research investigating the role of cytokines in angiogenesis has shown that close proximity of immune cells and endothelial cells modulates the production of various compounds that regulate vascular function. Given that LPS is the ligand for TLR4 there appeared to be a role for TLR4 in angiogenesis, particularly following endotoxin exposure. To determine whether this was occurring, we examined whether exposure to swine barn air alters vascular density in the lungs and the role of TLR4 using a murine model. Toll-like Receptor-4 wild-type (C3HeB/FeJ) and TLR4 mutant (C3H/HeJ) mice were obtained and exposed to swine barn air for 1-, 5-, or 20-days for 8 hours/day. Wild-type animals showed a 127% increase in vascular density after 20-days barn air exposure. Vascular Endothelial Growth Factor-A protein levels were decreased by 0.62-fold after one-day swine barn air exposure in wild-type animals, indicating that VEGF-A is being used as a pro-angiogenic mitogen. Transcription of VEGF-A mRNA was increased in wild-type animals after all swine barn air exposure periods. The receptor VEGFR-1 showed increased mRNA transcription over all time points. These effects were only observed in TLR4 wild-type animals, indicating that these effects are mediated by TLR4. Further, VEGF-A and VEGFR-1 appear to be involved in the manifestation of TLR4-induced angiogenesis in the lung.