@article{lagier_manzo_dye_2013, title={Diesel exhaust particles induce aberrant alveolar epithelial directed cell movement by disruption of polarity mechanisms}, volume={76}, number={2}, journal={Journal of Toxicology and Environmental Health. Part A}, author={LaGier, A. J. and Manzo, N. D. and Dye, J. A.}, year={2013}, pages={71–85} }
 @article{manzo_lagier_slade_ledbetter_richards_dye_2012, title={Nitric oxide and superoxide mediate diesel particle effects in cytokine-treated mice and murine lung epithelial cells - implications for susceptibility to traffic-related air pollution}, volume={9}, journal={Particle and Fibre Toxicology}, author={Manzo, N. D. and LaGier, A. J. and Slade, R. and Ledbetter, A. D. and Richards, J. H. and Dye, J. A.}, year={2012} }
 @article{manzo_slade_richards_mcgee_martin_dye_2010, title={Susceptibility of Inflamed Alveolar and Airway Epithelial Cells to Injury Induced by Diesel Exhaust Particles of Varying Organic Carbon Content}, volume={73}, ISSN={["1087-2620"]}, DOI={10.1080/15287390903566625}, abstractNote={Exposure to traffic-related ambient air pollution, such as diesel exhaust particles (DEP), is associated with adverse health outcomes, especially in individuals with preexisting inflammatory respiratory diseases. Using an analogous novel in vitro system to model both the healthy and inflamed lung, the susceptibility of epithelial cells exposed to DEP of varying organic carbon content was studied. Murine LA-4 alveolar type II-like epithelial cells, as well as primary murine tracheal epithelial cells (MTE), were treated with exogenous cytokines (tumor necrosis factor [TNF] α + interleukin [IL]-1 β + interferon [IFN] γ) to model a mild inflammatory state. Epithelial cells were subsequently exposed to DEP of varying organic carbon content, and the resultant cytotoxic, cytoprotective, or antioxidant cell responses were inferred by changes in lactate dehydrogenase (LDH) release, heme oxygenase-1 (HO-1) expression, or glutathione levels, respectively. Data showed that exposure of healthy LA-4 cells to organic carbon-rich DEP (25 μg/cm2; 24 h) induced adaptive cytoprotective/antioxidant responses with no apparent cell injury. In contrast, exposure of inflamed LA-4 cells resulted in oxidative stress culminating in significant cytotoxicity. Exposure of healthy MTE cells to organic carbon-rich DEP (20 μg/cm2; 24 h) was seemingly without effect, whereas exposure of inflamed MTE cells resulted in increased epithelial solute permeability. Thus, surface lung epithelial cells stressed by a state of inflammation and then exposed to organic carbon-rich DEP appear unable to respond to the additional oxidative stress, resulting in epithelial barrier dysfunction and injury. Adverse health outcomes associated with exposure to traffic-related air pollutants, like DEP, in patients with preexisting inflammatory respiratory diseases may be due, in part, to similar mechanisms.}, number={8}, journal={JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES}, author={Manzo, Nicholas D. and Slade, Ralph and Richards, Judy H. and McGee, John K. and Martin, Linda D. and Dye, Janice A.}, year={2010}, pages={565–580} }
 @article{lagier_manzo_carll_jaskot_slade_richards_winsett_farraj_dye_2008, title={A Hyperlipidemic Rabbit Model Provides New Insights into Pulmonary Zinc Exposure Effects on Cardiovascular Health}, volume={8}, ISSN={["1530-7905"]}, DOI={10.1007/s12012-008-9028-9}, abstractNote={This study ascertains the effects of zinc, a major component of particulate matter, on pulmonary and systemic endpoints using hyperlipidemic rabbits to model diet-induced human atherosclerosis. New Zealand White rabbits were fed a normal or cholesterol-enriched diet and then were intratracheally instilled 1x/week for 4 weeks with saline or 16 microg/kg of zinc, equal parts sulfate and oxide. Physiologic responses, blood after each exposure, and terminal bronchoalveolar lavage (BAL) were assessed. Rabbits fed a cholesterol-rich diet developed hyperlipidemia and had consistently higher circulating leukocyte counts than rabbits fed normal chow. Within minutes after zinc instillation, saturation of peripheral oxygen was decreased in hyperlipidemic rabbits and heart rate was increased in hyperlipidemic rabbits with total serum cholesterol levels greater than 200 mg/dl. Total circulating leukocytes levels were increased 24 h after the first zinc instillation, but upon repeated exposures this effect was attenuated. After repeated zinc exposures, BAL fluid (BALF) N-acetylglucosaminidase activity was increased regardless of hyperlipidemic state. Hyperlipidemic rabbits had an increase in BALF-oxidized glutathione and a decrease in serum nitrite. The study elucidates mechanisms by which the zinc metal component of PM drives cardiovascular health effects, as well as the possible susceptibility induced by hyperlipidemia. Furthermore, the study exemplifies the benefits of monitoring circulatory physiology during exposure as well as after exposure.}, number={4}, journal={CARDIOVASCULAR TOXICOLOGY}, author={LaGier, Adriana J. and Manzo, Nick D. and Carll, Alex P. and Jaskot, Richard H. and Slade, Ralph and Richards, Judy H. and Winsett, Darrell W. and Farraj, Aimen K. and Dye, Janice A.}, year={2008}, month={Dec}, pages={195–206} }