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University of Colorado Denver


Alison Bauer, Ph.D. (2000), University of Colorado

Environmental, Occupational and Cancer Research

Bauer Laboratory Research Interests

Role of environmental and occupational exposures in respiratory disease, including chronic inflammation and carcinogenesis

  • Constituents of 2nd and 3rd-hand cigarette smoke (eg. polycyclic    aromatic hydrocarbons, PAHs)
  • Contaminants of particulate air pollution and soil (eg. vanadium pentoxide  (V2O5)  PAHs)

Role of the innate immune system in pulmonary neoplastic and non-neoplastic diseases

  • Toll-like receptor 4 (TLR4) and additional innate immune markers in  pulmonary neoplasia
  • TLR4 and heat shock protein 70 (Hsp70) in ozone induced lung injury and inflammation

Prevention of respiratory diseases through chemoprevention



 Current Projects


Environmental and Occupational Research

Investigating the role of PAHs in respiratory diseases induced by 2nd-hand smoke and other environmental exposures

Secondhand smoke (2nd-hand) is associated with many diseases including respiratory diseases, such as chronic obstructive pulmonary disease (COPD), childhood and adult asthma, and lung cancer.[1,2] In certain occupations in the U.S., 2nd-hand smoke exposure was or still is greater than many occupations, such as flight attendants and casino workers.[3-7] Little is currently known about the human health effects of thirdhand (3rd-hand) smoke, components of 2nd-hand smoke that persist on walls, carpets and other areas in indoor environments, and contain PAHs, such as fluoranthene, among other cigarette components.[10]However, based on multiple assessments of 3rd-hand smoke constituents[7,10-14], inhalation of these toxicants should not be overlooked. Unfortunately, due to the latency of many chronic pulmonary diseases, individuals exposed to 2nd-and 3rd-hand smoke can observe effects years after exposure. Thus, the effects of these exposures are a real concern for human health at all ages.

    Our current research focuses on the most abundant PAHs in 2nd-hand and 3rd-hand smoke, the low molecular weight fractions, particularly the two-four-ringed PAHs (such as fluoranthene)[15-17]and their role in pulmonary inflammation and tumor promotion (see Osgood et al, (2013).[18]For example, cell-cell communication is inhibited by many of these toxicants. In addition, many of these LMW PAH species are also considered U.S.E.P.A. priority PAHs based on their potential for human exposure and abundance at hazardous waste sites, among others.

Investigating the role of V2O5 as a lung tumor promoter

Vanadium pentoxide (V2O5) exposure occurs both occupationally in industries such as the manufacturing of steel and aluminum, mining, petroleum production and refining, and welding, as well as environmentally as a component of particulate matter, and has been associated with respiratory conditions in humans and pulmonary inflammation and carcinogenesis in rodents.[19] We previously demonstrated that V2O5 can function as a lung tumor promoter in mice in a strain dependent manner.[20] Current studies focus on innate immune pathways and oxidative stress in response to V2O5.



Basic Cancer Research

The role of toll-like receptor 4 in mouse pulmonary neoplasia

More people will succumb to lung cancer this year than any other type of cancer. Lung adenocarcinoma (AC), a subtype of non-small cell lung carcinoma, is increasing at a faster rate than any other type of lung neoplasia, is the most common among nonsmokers, and is rarely detected early. Chronic inflammatory lung diseases predispose the lung to neoplasia. However, activation of certain innate immune pathways may confer protection against lung AC development. For example, several epidemiology studies observed significant decreases in lung cancer risk in those individuals exposed to endotoxin, such as farm and textile workers.[21-26]Toll-like receptor 4 (TLR4), an innate immune receptor, is the primary receptor that binds endotoxin (lipopolysaccharide; LPS)[27], thus TLR4 is likely involved in the protective effects of exposure to endotoxin. While the observation linking lung neoplasia to endotoxin is intriguing, there is a major gap in our understanding of how this protection is elicited. Our long-term goal is to determine if TLR4 and associated molecular events are involved in the underlying mechanisms that govern this association between the innate immune system and lung carcinogenesis, which may provide novel preventive, diagnostic, and therapeutic strategies for a disease that severely lacks in identifiable biomarkers.

     We previously demonstrated that TLR4-deficient mice (BALBLps-d ) were significantly more sensitive to lung tumor promotion and pulmonary inflammation at both early and advanced stages of disease than the Tlr4-wild-type mice (BALB/c) using a two stage initiation/promotion model.[28,29] Our current studies, funded by the American Cancer Society (RSG-10-162-01-LIB; AKB), focus on the importance of several innate immune receptors and pathways. More specifically, we are currently investigating the role of cell-cell communication using novel methodologies and growth factor pathways, such as epidermal growth factor (EGF).




Carla-Maria Alexander, PhD






Kalpana Velmurugan, PhD







Ross Osgood, PhD Candidate





Dr. Brad Upham, Department of Pediatrics and Human Development, Michigan State University, East Lansing, MI;

Dr. John Volckens, Department of Radiological and Environmental Health Sciences, Colorado State University and Colorado School of Public Health, Fort Collins, CO;

Dr. Charles Henry, Department of Chemistry, Colorado State University, Fort Collins, CO;

Dr. Christopher Evans, Department of Medicine, Division of Pulmonary Sciences, University of Colorado Denver, Aurora, CO;

Dr. Seyed Javad Moghaddam, Department of Pulmonary Medicine, M.D. Anderson Cancer Center, Houston, TX;

Dr. Linda Sargent, Molecular Genetics Laboratory, National Institute for Occupational Safety and Health, Morgantown, West Virginia;

Dr. Steven Kleeberger, Laboratory of Respiratory Biology, Environmental Genetics Group, National Institute of Environmental Health Sciences, RTP, NC;


Dr. Pavel Babica, Masaryk University, Research Center for Toxic Compounds in the Environment, Brno, Czech Republic;

Dr. Iva Sovadinova, Masaryk University, Research Center for Toxic Compounds in the Environment, Brno, Czech Republic;


  1. Osgood RS, Upham BL, Hill T, Helms KL, Velmurugan K, Babica P, Bauer AK. Polycyclic aromatic hydrocarbon-induced signaling events relevant to inflammation and tumorigenesis in lung cells are dependent on molecular structure. PLoS One. 2013; 8(6):e65150.
    View in: PubMed
  2. Bauer AK, Hill T, Alexander CM. The Involvement of NRF2 in Lung Cancer. Oxid Med Cell Longev. 2013; 2013:746432.
    View in: PubMed
  3. Bauer AK, Cho HY, Miller-Degraff L, Walker C, Helms K, Fostel J, Yamamoto M, Kleeberger SR. Targeted deletion of Nrf2 reduces urethane-induced lung tumor development in mice. PLoS One. 2011; 6(10):e26590.
    View in: PubMed
  4. Bauer AK, Rondini EA, Hummel KA, Degraff LM, Walker C, Jedlicka AE, Kleeberger SR. Identification of Candidate Genes Downstream of TLR4 Signaling after Ozone Exposure in Mice: A Role for Heat-Shock Protein 70. Environ Health Perspect. 2011 Aug; 119(8):1091-7.
    View in: PubMed
  5. Backus GS, Howden R, Fostel J, Bauer AK, Cho HY, Marzec J, Peden DB, Kleeberger SR. Protective role of interleukin-10 in ozone-induced pulmonary inflammation. Environ Health Perspect. 2010 Dec; 118(12):1721-7.
    View in: PubMed
  6. Bauer AK, Kleeberger SR. Genetic mechanisms of susceptibility to ozone-induced lung disease. Ann N Y Acad Sci. 2010 Aug; 1203:113-9.
    View in: PubMed
  7. Rondini EA, Walters DM, Bauer AK. Vanadium pentoxide induces pulmonary inflammation and tumor promotion in a strain-dependent manner. Part Fibre Toxicol. 2010; 7:9.
    View in: PubMed
  8. Bauer AK, Fostel J, Degraff LM, Rondini EA, Walker C, Grissom SF, Foley J, Kleeberger SR. Transcriptomic analysis of pathways regulated by toll-like receptor 4 in a murine model of chronic pulmonary inflammation and carcinogenesis. Mol Cancer. 2009; 8:107.
    View in: PubMed
  9. Dahl M, Bauer AK, Arredouani M, Soininen R, Tryggvason K, Kleeberger SR, Kobzik L. Protection against inhaled oxidants through scavenging of oxidized lipids by macrophage receptors MARCO and SR-AI/II. J Clin Invest. 2007 Mar; 117(3):757-64.
    View in: PubMed
  10. Cho HY, Morgan DL, Bauer AK, Kleeberger SR. Signal transduction pathways of tumor necrosis factor--mediated lung injury induced by ozone in mice. Am J Respir Crit Care Med. 2007 Apr 15; 175(8):829-39.
    View in: PubMed
  11. Bauer AK, Dixon D, DeGraff LM, Cho HY, Walker CR, Malkinson AM, Kleeberger SR. Toll-like receptor 4 in butylated hydroxytoluene-induced mouse pulmonary inflammation and tumorigenesis. J Natl Cancer Inst. 2005 Dec 7; 97(23):1778-81.
    View in: PubMed
  12. Recio L, Bauer A, Faiola B. Use of genetically modified mouse models to assess pathways of benzene-induced bone marrow cytotoxicity and genotoxicity. Chem Biol Interact. 2005 May 30; 153-154:159-64.
    View in: PubMed
  13. Dwyer-Nield LD, Srebernak MC, Barrett BS, Ahn J, Cosper P, Meyer AM, Kisley LR, Bauer AK, Thompson DC, Malkinson AM. Cytokines differentially regulate the synthesis of prostanoid and nitric oxide mediators in tumorigenic versus non-tumorigenic mouse lung epithelial cell lines. Carcinogenesis. 2005 Jul; 26(7):1196-206.
    View in: PubMed
  14. Bauer AK, Malkinson AM, Kleeberger SR. Susceptibility to neoplastic and non-neoplastic pulmonary diseases in mice: genetic similarities. Am J Physiol Lung Cell Mol Physiol. 2004 Oct; 287(4):L685-703.
    View in: PubMed
  15. Faiola B, Bauer AK, Fuller ES, Wong VA, Pluta LJ, Abernethy DJ, Mangum JB, Everitt JI, Recio L. Variations in Prkdc and susceptibility to benzene-induced toxicity in mice. Toxicol Sci. 2003 Oct; 75(2):321-32.
    View in: PubMed
  16. Bauer AK, Faiola B, Abernethy DJ, Marchan R, Pluta LJ, Wong VA, Gonzalez FJ, Butterworth BE, Borghoff SJ, Everitt JI, Recio L. Male mice deficient in microsomal epoxide hydrolase are not susceptible to benzene-induced toxicity. Toxicol Sci. 2003 Apr; 72(2):201-9.
    View in: PubMed
  17. Bauer AK, Faiola B, Abernethy DJ, Marchan R, Pluta LJ, Wong VA, Roberts K, Jaiswal AK, Gonzalez FJ, Butterworth BE, Borghoff S, Parkinson H, Everitt J, Recio L. Genetic susceptibility to benzene-induced toxicity: role of NADPH: quinone oxidoreductase-1. Cancer Res. 2003 Mar 1; 63(5):929-35.
    View in: PubMed
  18. Kisley LR, Barrett BS, Bauer AK, Dwyer-Nield LD, Barthel B, Meyer AM, Thompson DC, Malkinson AM. Genetic ablation of inducible nitric oxide synthase decreases mouse lung tumorigenesis. Cancer Res. 2002 Dec 1; 62(23):6850-6.
    View in: PubMed
  19. Kisley LR, Barrett BS, Dwyer-Nield LD, Bauer AK, Thompson DC, Malkinson AM. Celecoxib reduces pulmonary inflammation but not lung tumorigenesis in mice. Carcinogenesis. 2002 Oct; 23(10):1653-60.
    View in: PubMed
  20. Malkinson AM, Radcliffe RA, Bauer AK. Quantitative trait locus mapping of susceptibilities to butylated hydroxytoluene-induced lung tumor promotion and pulmonary inflammation in CXB mice. Carcinogenesis. 2002 Mar; 23(3):411-7.
    View in: PubMed
  21. Malkinson A, Radcliffe R, Bauer A, Dwyer-Nield L, Kleeberger S. Quantitative trait loci that regulate susceptibility to both butylated hydroxytoluene-induced pulmonary inflammation and lung tumor promotion in CXB recombinant inbred mice. Chest. 2002 Mar; 121(3 Suppl):82S.
    View in: PubMed


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