Search

Your search keyword '"Bromberg, Philip A."' showing total 554 results
Start Over Author "Bromberg, Philip A."
Sorry, I don't understand your search. ×
554 results on '"Bromberg, Philip A."'

3. Ozone effects on blood biomarkers of systemic inflammation, oxidative stress, endothelial function, and thrombosis: The Multicenter Ozone Study in oldEr Subjects (MOSES).

Author

Balmes, John R, Arjomandi, Mehrdad, Bromberg, Philip A, Costantini, Maria G, Dagincourt, Nicholas, Hazucha, Milan J, Hollenbeck-Pringle, Danielle, Rich, David Q, Stark, Paul, and Frampton, Mark W

Subjects
Endothelium, Vascular, Humans, Thrombosis, Inflammation, Ozone, C-Reactive Protein, Air Pollutants, Cross-Over Studies, Double-Blind Method, Inhalation Exposure, Oxidative Stress, Platelet Activation, Dose-Response Relationship, Drug, Aged, Middle Aged, Female, Male, Biomarkers, Clinical Trials and Supportive Activities, Cardiovascular, Aging, Clinical Research, Prevention, General Science & Technology
Abstract

The evidence that exposure to ozone air pollution causes acute cardiovascular effects is mixed. We postulated that exposure to ambient levels of ozone would increase blood markers of systemic inflammation, prothrombotic state, oxidative stress, and vascular dysfunction in healthy older subjects, and that absence of the glutathione S-transferase Mu 1 (GSTM1) gene would confer increased susceptibility. This double-blind, randomized, crossover study of 87 healthy volunteers 55-70 years of age was conducted at three sites using a common protocol. Subjects were exposed for 3 h in random order to 0 parts per billion (ppb) (filtered air), 70 ppb, and 120 ppb ozone, alternating 15 min of moderate exercise and rest. Blood was obtained the day before, approximately 4 h after, and approximately 22 h after each exposure. Linear mixed effect and logistic regression models evaluated the impact of exposure to ozone on pre-specified primary and secondary outcomes. The definition of statistical significance was p

Published
2019

7. Induction of Asthma and the Environment: What We Know and Need to Know

Author

Lemanske, Robert F., Gilmour, M. Ian, Neas, Lucas M., Henneberger, Paul K., Weissman, David N., Hoppin, Jane A., Dietert, Rodney R., Sly, Peter D., Geller, Andrew M., Enright, Paul L., Backus, Gillian S., Bromberg, Philip A., Germolec, Dori R., and Yeatts, Karin B.

Published
2006

8. An Integrated Imaging Approach to the Study of Oxidative Stress Generation by Mitochondrial Dysfunction in Living Cells

Author

Cheng, Wan-Yun, Tong, Haiyan, Miller, Evan W, Chang, Christopher J, Remington, James, Zucker, Robert M, Bromberg, Philip A, Samet, James M, and Hofer, Thomas PJ

Subjects
Biomedical and Clinical Sciences, Environmental Sciences, Health Sciences, Benzimidazoles, Carbocyanines, Carbonyl Cyanide m-Chlorophenyl Hydrazone, Environmental Health, Fluorescent Dyes, Hazardous Substances, Humans, Hydrogen Peroxide, Membrane Potential, Mitochondrial, Mitochondrial Diseases, Oxidative Stress, Reactive Oxygen Species, Tumor Cells, Cultured, Zinc, biosensors, confocal microscopy, hydrogen peroxide, mitochondrial dysfunction, oxidative stress, real-time imaging, ROS, Medical and Health Sciences, Toxicology, Biomedical and clinical sciences, Environmental sciences, Health sciences
Abstract

BackgroundThe mechanisms of action of many environmental agents commonly involve oxidative stress resulting from mitochondrial dysfunction. Zinc is a common environmental metallic contaminant that has been implicated in a variety of oxidant-dependent toxicological responses. Unlike ions of other transition metals such as iron, copper, and vanadium, Zn(2+) does not generate reactive oxygen species (ROS) through redox cycling.ObjectiveTo characterize the role of oxidative stress in zinc-induced toxicity.MethodsWe used an integrated imaging approach that employs the hydrogen peroxide (H2O2)-specific fluorophore Peroxy Green 1 (PG1), the mitochondrial potential sensor 5,5 ,6,6 -tetrachloro-1,1 ,3,3 -tetraethylbenzimidazolylcarbocyanine iodide (JC-1), and the mitochondria-targeted form of the redox-sensitive genetically encoded fluorophore MTroGFP1 in living cells.ResultsZinc treatment in the presence of the Zn(2+) ionophore pyrithione of A431 skin carcinoma cells preloaded with the H(2)O(2)-specific indicator PG1 resulted in a significant increase in H(2)O(2) production that could be significantly inhibited with the mitochondrial inhibitor carbonyl cyanide 3-chlorophenylhydrazone. Mitochondria were further implicated as the source of zinc-induced H(2)O(2) formation by the observation that exposure to zinc caused a loss of mitochondrial membrane potential. Using MTroGFP1, we showed that zinc exposure of A431 cells induces a rapid loss of reducing redox potential in mitochondria. We also demonstrated that zinc exposure results in rapid swelling of mitochondria isolated from mouse hearts.ConclusionTaken together, these findings show a disruption of mitochondrial integrity, H(2)O(2) formation, and a shift toward positive redox potential in cells exposed to zinc. These data demonstrate the utility of real-time, live-cell imaging to study the role of oxidative stress in toxicological responses.

Published
2010

27. Monitoring intracellular redox changes in ozone-exposed airway epithelial cells

Author

Gibbs-Flournoy, Eugene A., Simmons, Steven O., Bromberg, Philip A., Dick, Tobias P., and Samet, James M.

Subjects
Xenobiotics -- Health aspects, Oxidative stress -- Research -- Genetic aspects -- Risk factors, Toxicology -- Analysis, Environmental issues, Health
Abstract

BACKGROUND: The toxicity of many xenobiotic compounds is believed to involve oxidative injury to cells. Direct assessment of mechanistic events involved in xenobiotic-induced oxidative stress is not easily achievable. Development [...]

Published
2013

32. Additional file 1 of Cardiovascular health impacts of wildfire smoke exposure

Author

Chen, Hao, Samet, James M., Bromberg, Philip A., and Tong, Haiyan

Subjects
complex mixtures
Abstract

Additional file 1: Supplemental Table 1. Summary of epidemiological studies on wildfire smoke exposure and cardiovascular effects. Supplemental Table 2. Summary of studies on indoor and ambient biomass smoke exposure and cardiovascular effects. Supplemental Table 3. Summary of intervention and controlled human exposure studies of wood smoke exposure and cardiovascular effects. Supplemental Table 4. Summary of in vivo animal studies on wood smoke exposure and cardiovascular effects. Supplemental Table 5. Summary of in vitro studies on wood smoke exposure and biological effects related to cardiovascular system.

Published
2021
Full Text
View/download PDF

33. Ambient particulate matter induces interleukin-8 expression through an alternative NF-[Kappa]B (nuclear Factor-kappa B) mechanism in human airway epithelial cells

Author

Silbajoris, Robert, Osornio-Vargas, Alvaro R., Simmons, Steven O., Reed, William, Bromberg, Philip A., Dailey, Lisa A., and Samet, James M.

Subjects
Gene expression -- Research, Interleukin-8 -- Properties, Cellular signal transduction -- Genetic aspects, Epithelial cells -- Genetic aspects, Particles -- Health aspects, Airway (Medicine) -- Genetic aspects, Environmental issues, Health
Abstract

BACKGROUND: Exposure to ambient air particulate matter (PM) has been shown to increase rates of cardiopulmonary morbidity and mortality, but the underlying mechanisms are still not well understood. OBJECTIVE: We [...]

Published
2011

36. Diesel exhaust particulate-induced activation of Stat3 requires activities of EGFR and Src in airway epithelial cells

Author

Cao, Dongsun, Tal, Tamara L., Graves, Lee M., Gilmour, Ian, Linak, William, Reed, William, Bromberg, Philip A., and Samet, James M.

Subjects
Diesel motor exhaust gas -- Health aspects, Cytokines -- Research, Biological sciences
Abstract

In vivo exposure to diesel exhaust particles (DEP) elicits acute inflammatory responses in the lung characterized by inflammatory cell influx and elevated expression of mediators such as cytokines and chemokines. Signal transducers and activators of transcription (STAT) proteins are a family of cytoplasmic transcription factors that are key transducers of signaling in response to cytokine and growth factor stimulation. One member of the STAT family, Stat3, has been implicated as a regulator of infammation but has not been studied in regard to DEP exposure. The results of this study show that DEP induces Stat3 phosphorylation as early as 1 h following stimulation and that phosphorylated Stat3 translocates into the nucleus. Inhibition of epidermal growth factor receptor (EGFR) and Src activities by the inhibitors PD-153035 and PP2, respectively, abolished the activation of Stat3 by DEP, suggesting that Stat3 activation by DEP requires EGFR and Src kinase activation. The present study suggests that oxidative stress induced by DEP may play a critical role in activating EGFR signaling, as evidenced by the fact that pretreatment with antioxidant prevented the activation of EGFR and Stat3. These findings demonstrate that DEP inhalation can activate proinflammatory Stat3 signaling in vitro. signal transducer and activator of transcription 3; epidermal growth factor receptor; reactive oxygen species; human airway epithelial cells; diesel exhaust particles

Published
2007

38. [Zn.sup.2+]-induced IL-8 expression involves AP-1, JNK, and ERK activities in human airway epithelial cells

Author

Kim, Yu-Mee, Reed, William, Wu, Weidong, Bromberg, Philip A., Graves, Lee M., and Samet, James M.

Subjects
Epithelial cells -- Research, Protein kinases -- Analysis, Particles -- Health aspects, Biological sciences
Abstract

Exposure to zinc-laden particulate matter in ambient and occupational settings has been associated with proinflammatory responses in the lung. IL-8 is an important proinflammatory cytokine in the human lung and is induced in human airway epithelial cells exposed to zinc. In this study, we examined the cellular mechanisms responsible for [Zn.sup.2+]-induced IL-8 expression. [Zn.sup.2+] stimulation resulted in pronounced increases in both IL-8 mRNA and protein expression in the human airway epithelial cell line (BEAS-2B). IL-8 promoter activity was significantly increased by [Zn.sup.2+] exposure in BEAS-2B cells, indicating that [Zn.sup.2+]-induced IL-8 expression is transcriptionally mediated. Mutation of the activating protein (AP)-1 response element in an IL-8 promoter-enhanced green fluorescent protein construct reduced [Zn.sup.2+]-induced IL-8 promoter activity. Moreover, [Zn.sup.2+] exposure of BEAS-2B cells induced the phosphorylation of the AP-1 proteins c-Fos and c-Jun. We observed that [Zn.sup.2+] exposure induced the phosphorylation of ERK, JNK, and p38 MAPKs, whereas inhibition of ERK or JNK activity blocked IL-8 mRNA and protein expression in BEAS-2B cells treated with [Zn.sup.2+]. In addition, we investigated the role of protein tyrosine phosphatases in the activation of signaling by [Zn.sup.2+] * [Zn.sup.2+] treatment inhibited ERK- and JNK-directed phosphatase activities in BEAS-2B cells. These results suggested that [Zn.sup.2+] -induced inhibition of phosphatase activity is an initiating event in MAPK and AP-1 activation that leads to enhanced IL-8 expression by human airway epithelial cells. interleukin-8; zinc; activating protein-1; c-Jun N[H.sub.2]-terminal kinase; extracellular signal-regulated kinase; mitogen-activated protein kinase phosphatase; metal; particulate matter

Published
2006

39. Induction of asthma and the environment: what we know and need to know

Author

Selgrade, Mary Jane K., Lemanske, Jr., Robert F., Gilmour, M. Ian, Neas, Lucas M., Ward, Marsha D.W., Henneberger, Paul K., Weissman, David N., Hoppin, Jane A., Dietert, Rodney R., Sly, Peter D., Geller, Andrew M., Enright, Paul L., Backus, Gillian S., Bromberg, Philip A., Germolec, Dori R., and Yeatts, Karin B.

Subjects
United States. Environmental Protection Agency, Public health, Asthma -- Development and progression, Environmental issues, Health
Abstract

The prevalence of asthma has increased dramatically over the last 25 years in the United States and in other nations as a result of ill-defined changes in living conditions in [...]

Published
2006

40. p38 and EGF receptor kinase-mediated activation of the phosphatidylinositol 3-kinase/Akt pathway is required for [Zn.sup.2+]-induced cyclooxygenase-2 expression

Author

Wu, Weidong, Silbajoris, Robert A., Whang, Young E., Graves, Lee M., Bromberg, Philip A., and Samet, James M.

Subjects
Phosphatidylinositol -- Analysis, Epithelial cells -- Analysis, Epithelial cells -- Growth, Company growth, Biological sciences
Abstract

Cyclooxygenase 2 (COX-2) expression is induced by physiological and inflammatory stimuli. Regulation of COX-2 expression is stimulus and cell type specific. Exposure to [Zn.sup.2+] has been associated with activation of multiple intracellular signaling pathways as well as the induction of COX-2 expression. This study aims to elucidate the role of intracellular signaling pathways in [Zn.sup.2+]-induced COX-2 expression in human bronchial epithelial cells. Inhibitors of the phosphatidylinositol 3-kinase (PI3K) potently block [Zn.sup.2+]-induced COX-2 mRNA and protein expression. Overexpression of adenoviral constructs encoding dominant-negative Akt kinase downstream of PI3K or wild-type phosphatase and tensin homolog deleted on chromosome 10, an important PI3K phosphatase, suppresses COX-2 mRNA expression induced by [Zn.sup.2+]. [Zn.sup.2+] exposure induces phosphorylation of the tyrosine kinases, including Src and EGF receptor (EGFR), and the p38 mitogen-activated protein kinase. Blockage of these kinases results in inhibition of [Zn.sup.2+]-induced Akt phosphorylation as well as COX-2 protein expression. Overexpression of dominant negative p38 constructs suppresses [Zn.sup.2+]-induced increase in COX-2 promoter activity. In contrast, the c-Jun N[H.sub.2]-terminal kinase and the extracellular signal-regulated kinases have minimal effect on Akt phosphorylation and COX-2 expression. Inhibition of p38, Src, and EGFR kinases with pharmacological inhibitors markedly reduces Akt phosphorylation induced by [Zn.sup.2+]. However, the PI3K inhibitors do not show inhibitory effects on p38, Src, and EGFR. These data suggest that p38 and EGFR kinase-mediated Akt activation is required for [Zn.sup.2+]-induced COX-2 expression and that the PI3K/Akt signaling pathway plays a central role in this event. zinc; airway epithelial cell; signal transduction

Published
2005

43. Contributeurs

Author

Runge, Marschall S., primary, Greganti, M. Andrew, additional, Adimora, Adaora A., additional, Alattar, Maha, additional, Aris, Robert M., additional, Bae-Jump, Victoria Lin, additional, Baggstrom, Maria Q., additional, Barritt, A. Sidney, additional, Bassim, Marc K., additional, Bates, Toby, additional, Beaven, Anne W., additional, Berger, Robert G., additional, Berkowitz, Lee R., additional, Bernard, Stephen A., additional, Blau, William S., additional, Boggess, John F., additional, Bowman, Mary C., additional, Brecher, Mark E., additional, Bromberg, Philip A., additional, Brown, Sue A., additional, Brown, Vickie, additional, Bryson, Paul C., additional, Buckmire, Robert A., additional, Bullitt, Elizabeth, additional, Burkhart, Craig, additional, Busby-Whitehead, M. Janette, additional, Buse, John B., additional, Bynum, Debra L., additional, Carey, Lisa A., additional, Carey, Timothy S., additional, Carson, Culley C., additional, Chang, Patricia P., additional, Chaudhary, Sanjay, additional, Clemmons, David R., additional, Coghill, James M., additional, Colindres, Romulo E., additional, Connolly, AnnaMarie, additional, Copeland, Benjamin J., additional, Correll, Todd, additional, Denu-Ciocca, Cynthia J., additional, Devetski, Thomas S., additional, DeWalt, Darren A., additional, Diaz, Luis A., additional, Donohue, James F., additional, Dooley, Mary Anne, additional, Dostou, Jean M., additional, Drossman, Douglas A., additional, Dupree, Carla Sueta, additional, Eapen, Rose J., additional, Ebert, Charles S., additional, Erdem, Nurum F., additional, Eron, Joseph J., additional, Falk, Ronald J., additional, Farmer-Boatwright, Mary Katherine, additional, Fasy, Elizabeth A., additional, Finkel, Alan G., additional, Finn, William F., additional, Fitzgerald, David P., additional, Ford, Carol A., additional, Forneris, Catherine A., additional, Fowler, Amy M., additional, Fowler, W. Craig, additional, Fowler, Wesley Caswell, additional, Fried, Michael W., additional, Gabriel, Don A., additional, Galvin, Shannon, additional, Gangarosa, Lisa M., additional, Garbutt, James C., additional, Gay, Cynthia, additional, Gaylord, Susan A., additional, Gettes, Leonard S., additional, Ghio, Andrew J., additional, Gilmore, John H., additional, Godley, Paul A., additional, Goldberg, Lee R., additional, Goldberg, Richard M., additional, Goldenberg, Matthew N., additional, Goldstein, Brian P., additional, Greenwood, Robert S., additional, Grimm, Ian S., additional, Grossman, Steven H., additional, Gwyther, Robert E., additional, Haggerty, John J., additional, Harris, Russell P., additional, Heizer, William D., additional, Henderson, Ashley G., additional, Henke, David C., additional, Hill, Michael A., additional, Hinderliter, Alan L., additional, Hinn, Albert R., additional, Hladik, Gerald A., additional, Hoffman, Hal M., additional, Hosseinipour, Mina C., additional, Howard, James F., additional, Huang, David Y., additional, Huang, Xuemei, additional, Hutto, Burton R., additional, Isaacs, Kim L., additional, Israel, Bruce F., additional, Ivester, Thomas S., additional, Jacobe, Heidi T., additional, Jacobson, Peter Lars, additional, Jantac, Lukas, additional, Jawanda, Jaspaul S., additional, Johnson, Sandra M., additional, Jonas, Beth L., additional, Jordan, Joanne M., additional, Juliano, Jonathan J., additional, Kahn, Kevin A., additional, Kaplan, Andrew H., additional, Key, Nigel S., additional, Kim, William Y., additional, Kizer, John S., additional, Klein, Caroline M., additional, Klemmer, Philip J., additional, Kölln, Karen, additional, Koruda, Mark J., additional, Kurz, James E., additional, LaCour, Jeffrey, additional, Ladha, Alim M., additional, Leight, W. Derek, additional, Leone, Peter A., additional, Lindsey, B. Anthony, additional, Madanick, Ryan D., additional, Mandelkehr, Lawrence K., additional, Mann, J. Douglas, additional, Markovic-Plese, Silva, additional, Marshall, Allen F., additional, Mattern, William D., additional, Mayer, Celeste M., additional, Meredith, Travis A., additional, Miller, William C., additional, Mitchell, Beverly S., additional, Moll, Stephan, additional, Morgan, Douglas R., additional, Morrell, Dean S., additional, Muñoz, M. Cristina, additional, Nachman, Patrick H., additional, Nelson, Kelly C., additional, Nester, Carla M., additional, Nicholas, Linda M., additional, Ohman, E. Magnus, additional, O'Neil, Bert H., additional, Ontjes, David A., additional, Orlowski, Robert Z., additional, Parsons, Daniel J., additional, Patel, Dhavalkumar D., additional, Patterson, Cam, additional, Patterson, Kristine B., additional, Peppercorn, Amanda, additional, Pillsbury, Harold C., additional, Rathmell, W. Kimryn, additional, Reuland, Daniel S., additional, Ringel, Yehuda, additional, Rivera, M. Patricia, additional, Rosebrock, Craig N., additional, Rosenberg, Pinchas, additional, Roubey, Robert A.S., additional, Rubenstein, David S., additional, Runge, Susan Riggs, additional, Russo, Mark, additional, Rutala, William A., additional, Sanders, William E., additional, Sanoff, Hanna K., additional, Sanoff, Scott L., additional, Scarlett, Yolanda V., additional, Schwarz, Emily J., additional, Senior, Brent A., additional, Serody, Jonathan S., additional, Shaheen, Nicholas J., additional, Shea, Thomas C., additional, Sheahan, Richard G., additional, Shockley, William W., additional, Shrestha, Roshan, additional, Sickbert-Bennett, Emily E., additional, Sickel, Micah J., additional, Sikich, Linmarie, additional, Simpson, Ross J., additional, Smith, Sidney C., additional, Socinski, Mark A., additional, Sparling, P. Frederick, additional, Stinchcombe, Thomas E., additional, Stouffer, George A., additional, Tarrant, Teresa K., additional, Taylor, Mark, additional, Thomas, Michael J., additional, Thomas, Nancy E., additional, Thorpe, John M., additional, Tilley, Stephen L., additional, Ting, Jenny P., additional, Tomsick, Robert S., additional, van der Horst, Charles M., additional, Vaughn, Bradley V., additional, Vick, Pamela G., additional, Vissers, Robert J., additional, Voorhees, Peter M., additional, Wang, Tracy Y., additional, Watson, Lea C., additional, Weber, David J., additional, Wehbie, Robert S., additional, Weissler, Mark C., additional, Wells, Ellen C., additional, Whang, Young E., additional, Willis, Park W., additional, Winfield, John B., additional, Winzelberg, Gary S., additional, Wohl, David A., additional, Wong, Leslie P., additional, Wu, Diem N., additional, and Zacks, Steven, additional

Published
2011
Full Text
View/download PDF

45. Contributors

Author

Runge, Marschall S., primary, Greganti, M. Andrew, additional, Adimora, Adaora A., additional, Alattar, Maha, additional, Aris, Robert M., additional, Bae-Jump, Victoria Lin, additional, Baggstrom, Maria Q., additional, Barritt, A. Sidney, additional, Bassim, Marc K., additional, Bates, Toby, additional, Beaven, Anne W., additional, Berger, Robert G., additional, Berkowitz, Lee R., additional, Bernard, Stephen A., additional, Blau, William S., additional, Boggess, John F., additional, Bowman, Mary C., additional, Brecher, Mark E., additional, Bromberg, Philip A., additional, Brown, Sue A., additional, Brown, Vickie, additional, Bryson, Paul C., additional, Buckmire, Robert A., additional, Bullitt, Elizabeth, additional, Burkhart, Craig, additional, Busby-Whitehead, M. Janette, additional, Buse, John B., additional, Bynum, Debra L., additional, Carey, Lisa A., additional, Carey, Timothy S., additional, Carson, Culley C., additional, Chang, Patricia P., additional, Chaudhary, Sanjay, additional, Clemmons, David R., additional, Coghill, James M., additional, Colindres, Romulo E., additional, Connolly, AnnaMarie, additional, Copeland, Benjamin J., additional, Correll, Todd, additional, Denu-Ciocca, Cynthia J., additional, Devetski, Thomas S., additional, DeWalt, Darren A., additional, Diaz, Luis A., additional, Donohue, James F., additional, Dooley, Mary Anne, additional, Dostou, Jean M., additional, Drossman, Douglas A., additional, Dupree, Carla Sueta, additional, Eapen, Rose J., additional, Ebert, Charles S., additional, Erdem, Nurum F., additional, Eron, Joseph J., additional, Falk, Ronald J., additional, Farmer-Boatwright, Mary Katherine, additional, Fasy, Elizabeth A., additional, Finkel, Alan G., additional, Finn, William F., additional, Fitzgerald, David P., additional, Ford, Carol A., additional, Forneris, Catherine A., additional, Fowler, Amy M., additional, Fowler, W. Craig, additional, Fowler, Wesley Caswell, additional, Fried, Michael W., additional, Gabriel, Don A., additional, Galvin, Shannon, additional, Gangarosa, Lisa M., additional, Garbutt, James C., additional, Gay, Cynthia, additional, Gaylord, Susan A., additional, Gettes, Leonard S., additional, Ghio, Andrew J., additional, Gilmore, John H., additional, Godley, Paul A., additional, Goldberg, Lee R., additional, Goldberg, Richard M., additional, Goldenberg, Matthew N., additional, Goldstein, Brian P., additional, Greenwood, Robert S., additional, Grimm, Ian S., additional, Grossman, Steven H., additional, Gwyther, Robert E., additional, Haggerty, John J., additional, Harris, Russell P., additional, Heizer, William D., additional, Henderson, Ashley G., additional, Henke, David C., additional, Hill, Michael A., additional, Hinderliter, Alan L., additional, Hinn, Albert R., additional, Hladik, Gerald A., additional, Hoffman, Hal M., additional, Hosseinipour, Mina C., additional, Howard, James F., additional, Huang, David Y., additional, Huang, Xuemei, additional, Hutto, Burton R., additional, Isaacs, Kim L., additional, Israel, Bruce F., additional, Ivester, Thomas S., additional, Jacobe, Heidi T., additional, Jacobson, Peter Lars, additional, Jantac, Lukas, additional, Jawanda, Jaspaul S., additional, Johnson, Sandra M., additional, Jonas, Beth L., additional, Jordan, Joanne M., additional, Juliano, Jonathan J., additional, Kahn, Kevin A., additional, Kaplan, Andrew H., additional, Key, Nigel S., additional, Kim, William Y., additional, Kizer, John S., additional, Klein, Caroline M., additional, Klemmer, Philip J., additional, Kölln, Karen, additional, Koruda, Mark J., additional, Kurz, James E., additional, LaCour, Jeffrey, additional, Ladha, Alim M., additional, Leight, W. Derek, additional, Leone, Peter A., additional, Lindsey, B. Anthony, additional, Madanick, Ryan D., additional, Mandelkehr, Lawrence K., additional, Mann, J. Douglas, additional, Markovic-Plese, Silva, additional, Marshall, Allen F., additional, Mattern, William D., additional, Mayer, Celeste M., additional, Meredith, Travis A., additional, Miller, William C., additional, Mitchell, Beverly S., additional, Moll, Stephan, additional, Morgan, Douglas R., additional, Morrell, Dean S., additional, Muñoz, M. Cristina, additional, Nachman, Patrick H., additional, Nelson, Kelly C., additional, Nester, Carla M., additional, Nicholas, Linda M., additional, Ohman, E. Magnus, additional, O'Neil, Bert H., additional, Ontjes, David A., additional, Orlowski, Robert Z., additional, Parsons, Daniel J., additional, Patel, Dhavalkumar D., additional, Patterson, Cam, additional, Patterson, Kristine B., additional, Peppercorn, Amanda, additional, Pillsbury, Harold C., additional, Rathmell, W. Kimryn, additional, Reuland, Daniel S., additional, Ringel, Yehuda, additional, Rivera, M. Patricia, additional, Rosebrock, Craig N., additional, Rosenberg, Pinchas, additional, Roubey, Robert A.S., additional, Rubenstein, David S., additional, Runge, Susan Riggs, additional, Russo, Mark, additional, Rutala, William A., additional, Sanders, William E., additional, Sanoff, Hanna K., additional, Sanoff, Scott L., additional, Scarlett, Yolanda V., additional, Schwarz, Emily J., additional, Senior, Brent A., additional, Serody, Jonathan S., additional, Shaheen, Nicholas J., additional, Shea, Thomas C., additional, Sheahan, Richard G., additional, Shockley, William W., additional, Shrestha, Roshan, additional, Sickbert-Bennett, Emily E., additional, Sickel, Micah J., additional, Sikich, Linmarie, additional, Simpson, Ross J., additional, Smith, Sidney C., additional, Socinski, Mark A., additional, Sparling, P. Frederick, additional, Stinchcombe, Thomas E., additional, Stouffer, George A., additional, Tarrant, Teresa K., additional, Taylor, Mark, additional, Thomas, Michael J., additional, Thomas, Nancy E., additional, Thorpe, John M., additional, Tilley, Stephen L., additional, Ting, Jenny P., additional, Tomsick, Robert S., additional, van der Horst, Charles M., additional, Vaughn, Bradley V., additional, Vick, Pamela G., additional, Vissers, Robert J., additional, Voorhees, Peter M., additional, Wang, Tracy Y., additional, Watson, Lea C., additional, Weber, David J., additional, Wehbie, Robert S., additional, Weissler, Mark C., additional, Wells, Ellen C., additional, Whang, Young E., additional, Willis, Park W., additional, Winfield, John B., additional, Winzelberg, Gary S., additional, Wohl, David A., additional, Wong, Leslie P., additional, Wu, Diem N., additional, and Zacks, Steven, additional

Published
2009
Full Text
View/download PDF

48. Do Ambient Ozone or Other Pollutants Modify Effects of Controlled Ozone Exposure on Pulmonary Function?

Author

Rich, David Q., primary, Thurston, Sally W., additional, Balmes, John R., additional, Bromberg, Philip A., additional, Arjomandi, Mehrdad, additional, Hazucha, Milan J., additional, Alexis, Neil E., additional, Ganz, Peter, additional, Zareba, Wojciech, additional, Thevenet-Morrison, Kelly, additional, Koutrakis, Petros, additional, and Frampton, Mark W., additional

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results