The multidisciplinary Environmental and Integrative Toxicological Sciences (EITS) Training Program at MSU produces scientists having a base knowledge in environmental toxicology coupled with research expertise gained in a biomedical basic science graduate program. Pre-doctoral trainees must meet the full Ph.D. requirements of their partnering biomedical doctoral program and complete the coursework, research and interactive aspects of the EITS Doctoral Program administered through the Center for Integrative Toxicology (CIT). The dual nature of the training is recognized in the biomedical science-environmental toxicology title of the degree awarded (e.g., Ph.D. in "Biochemistry and Molecular Biology-Environmental Toxicology"). Graduates of the program are well equipped to conduct research and interact with other scientists in the course of solving complex environmental toxicological problems that require collaborative, multidisciplinary approaches. Twenty-three training faculty members conduct pre-doctoral training in eight basic science Ph.D. programs (Pharmacology/Toxicology, Genetics, Biochemistry and Molecular Biology, Food Science, Cell and Molecular Biology, Comparative Medicine and Integrative Biology, Microbiology and Molecular Genetics, Neuroscience). Added to the basic biomedical science-based education and environmental toxicology research training are didactic, toxicology-oriented courses and other requirements of the EITS Program. This coursework and less formal multidisciplinary interactions and activities provided by the CIT impart a wider scope of knowledge than is available within basic science programs alone. Research topics for trainees span various organ systems and encompass gene-environment interactions and the role of environmental factors in disease susceptibility and progression. There is an integrative biology emphasis to the research training, which emphasizes whole animal, cell-based, molecular and genomic methodologies to understand mechanisms of toxicity in a collaborative atmosphere. The postdoctoral training program involves not only conducting research in the laboratories of the training faculty but also gaining additional environmental toxicology experience and career- building training by following an individual development plan (IDP) and through participation in CIT and University-wide activities. This application is for support of seven pre-doctoral and two postdoctoral trainees, thereby continuing a highly effective multidisciplinary and interactive training program that combines formal and informal approaches to prepare graduates for leadership roles in research in the field of environmental toxicology.

Public Health Relevance

Exposure to various agents in the environment can cause illness directly or exacerbate disease caused by other factors. Reducing the impact of such exposures on human health and devising effective interventions requires public health officials and scientists trained in several areas, including scientists equipped to study and understand mechanisms by which chemical agents cause or exacerbate illness. This Program employs an excellent, research-intensive faculty experienced in doctoral and postdoctoral training in a collaborative environment to train scientists to address toxicological mechanisms of environmental concern.

National Institute of Health (NIH)
Institutional National Research Service Award (T32)
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Environmental Health Sciences Review Committee (EHS)
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Shreffler, Carol K
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Michigan State University
Schools of Veterinary Medicine
East Lansing
United States
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Turley, Alexandra E; Zagorski, Joseph W; Rockwell, Cheryl E (2015) The Nrf2 activator tBHQ inhibits T cell activation of primary human CD4 T cells. Cytokine 71:289-95
Poulsen, Kyle L; Olivero-Verbel, Jesus; Beggs, Kevin M et al. (2014) Trovafloxacin enhances lipopolysaccharide-stimulated production of tumor necrosis factor-? by macrophages: role of the DNA damage response. J Pharmacol Exp Ther 350:164-70
Mochizuki, Akie; Pace, Aaron; Rockwell, Cheryl E et al. (2014) Hepatic stellate cells orchestrate clearance of necrotic cells in a hypoxia-inducible factor-1?-dependent manner by modulating macrophage phenotype in mice. J Immunol 192:3847-57
Flannery, Brenna M; Amuzie, Chidozie J; Pestka, James J (2013) Evaluation of insulin-like growth factor acid-labile subunit as a potential biomarker of effect for deoxynivalenol-induced proinflammatory cytokine expression. Toxicology 304:192-8
Fullerton, Aaron M; Roth, Robert A; Ganey, Patricia E (2013) 2,3,7,8-TCDD enhances the sensitivity of mice to concanavalin A immune-mediated liver injury. Toxicol Appl Pharmacol 266:317-27
O'Brien, Kate M; Allen, Katryn M; Rockwell, Cheryl E et al. (2013) IL-17A synergistically enhances bile acid-induced inflammation during obstructive cholestasis. Am J Pathol 183:1498-507
Fullerton, Aaron M; Roth, Robert A; Ganey, Patricia E (2013) Pretreatment with TCDD exacerbates liver injury from Concanavalin A: critical role for NK cells. Toxicol Sci 136:72-85
Jia, Cuihong; Hayoz, Sebastien; Hutch, Chelsea R et al. (2013) An IP3R3- and NPY-expressing microvillous cell mediates tissue homeostasis and regeneration in the mouse olfactory epithelium. PLoS One 8:e58668
Sparkenbaugh, Erica M; Ganey, Patricia E; Roth, Robert A (2012) Hypoxia sensitization of hepatocytes to neutrophil elastase-mediated cell death depends on MAPKs and HIF-1?. Am J Physiol Gastrointest Liver Physiol 302:G748-57
Johnson, Frank O; Yuan, Yukun; Hajela, Ravindra K et al. (2011) Exposure to an environmental neurotoxicant hastens the onset of amyotrophic lateral sclerosis-like phenotype in human Cu2+/Zn2+ superoxide dismutase 1 G93A mice: glutamate-mediated excitotoxicity. J Pharmacol Exp Ther 338:518-27

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