Research Concentrations in Environmental Medicine

Available for Spring 2014 (revised 12-20-13)

Kevin Cromar
Cumulative risk assessment of environmental risk factors impacting health in urban environments

Environmental health risks do not occur in isolation; rather, many diverse environmental risks are constantly impacting public health.  Cumulative risk assessments are designed to account for and prioritize these risks.  Working under the direction of Dr. Cromar, and in conjunction with the EPA, students will pilot a Community, Cumulative Risk Assessment Tool (CCAT) to assess and prioritize chemical and non-chemical risk factors impacting health in an urban environment, specifically New York City.  Results of the project will be used to inform cumulative risk assessment practices used by the EPA as well as be disseminated to local policymakers that deal with environment, community, and health issues.


Lung Chi Chen
Cardiovascular effects of ambient air pollution

Dr. Chen's lab is investigating the cardiovascular effects of ambient air pollution using various animal models of cardiovascular disease. After inhalation exposure of ambient particles, changes in blood pressure, ECG tracing, atherosclerosis, vascular function, glucose/insulin tolerance are monitored using telemetry or ultrasound imaging systems. We are focused on the mechanisms of these cardiometabolic effects of ambient air pollution such as systemic inflammation, autonomic nervous system regulation, and lipid oxidation, and energy utilization. We are also interested in the influence of diet, genetic factor, and the compositions of ambient particle on these effects


Max Costa
Epigenetic effects of environmental carcinogens

Dr. Costa is investigating the changes in epigenetic programs in human (PBMCs and nasal scrapings) exposed occupationally to Ni and  Arsenic in the drinking water.  DNA methylation of tumor suppressor genes, changes in gene expression, as well as cytokine and chemokine levels in serum are being studied. Similar studies are being conducted in human Cell culture systems using carcinogenic metals such as Ni, As and Cd. In addition the epigenetic effects of ssUVR on human dermal fibroblasts and keratinacytes is being investigated with an emphasis on those changes that are persistent and inherited.


Wei Dai
Mechanisms of genome instability during cell division

Dr. Dai's laboratory is interested in molecular mechanisms by which environmental carcinogens and toxicants induce genomic instability during cell division, leading to malignant transformation and tumorigenesis. Extensive research over the past two decades has revealed the existence of important surveillance mechanisms (referred to as cell cycle checkpoints) that regulate cell cycle progression. These checkpoints monitor specific cell cycle–related processes and block cell cycle progression until these processes are completed with high fidelity. Cell cycle checkpoint failures often result in genomic instability, a condition from which cells with an advantage for tumor growth will be selected. At present, Dr. Dai's laboratory studies functions of several important cell cycle regulators including Plk1, BubR1, and Sgo1 in the regulation of cell survival and cell division, as well as in the maintenance of genomic stability and suppression of tumor formation. His research group also attempts to understand how environmental toxicants including arsenic, nickel, chromium, and UV cause carcinogenesis by perturbing functions of cell cycle checkpoint components, thereby deregulating cell cycle control and causing genomic instability.  


Terry Gordon
Air pollution and susceptibility to pulmonary and cardiovascular effects

The Gordon lab is focused on the study of the interplay of the adverse effects of air pollution and the susceptibility factors that modify documented pulmonary and cardiovascular effects.  The majority of our studies are done in mouse models utilizing inhaled nanoparticles or ambient particulate matter.  In addition, there are research opportunities to study the adverse effects of environmental pollutants in human panel studies and in epidemiology cohort studies.  Recently, we have begun to examine the expanding use of alternate tobacco products, such as hookah smoking, in adolescents and young adults in the NYC metropolitan area.


Gabriel Grunig
The immune response in pulmonary hypertension

In the Grunig laboratory, we are interested in understanding the pathogenesis of pulmonary hypertension associated with autoimmune or infectious diseases and how the environment affects the expression of these diseases.  The immune response plays a critical role for the remodeling of the lung's vasculature and for the development of changes in the right heart.  We are using mouse model studies to look at molecular mechanisms with particular focus on cytokines and micro-RNA with the goal to identify new molecular markers of the disease and new targets for therapy.  Dr. Grunig is trained as a veterinarian, has a PhD in immunology from Cornell University, and postdoctoral training in translational pulmonary medicine and immunology. During a concentration, a student would be able to choose between projects that involve primarily analytical work, e.g. literature review and data analysis, or primarily bench work combined with analytical work using for example immunohistochemistry, qPCR, ELISA assays; or primarily microsurgery work by being involved in terminal animal catheterization studies of the right heart and the lungs. An important goal of the work during the concentration would be to give the student the opportunity for professional networking (e.g. by attending seminars and a conference), and to be a co-author of a manuscript.


Chuanshu Huang
Molecular mechanisms underlying environmental carcinogens, cancer metastasis and anti-cancer drugs

Exposure of cells to environmental carcinogens results in activation of transcription factors and regulation of their target genes through signal transduction pathways, which have been characterized as tumor promotion and progression stages of carcinogenesis.  Elucidation of those signal transduction pathways will, therefore, not only define the central scientific hunt in cancer biology and open an unprecedented window into the nature of cancer, but also will be necessary for cancer prevention and therapy as well. As a result, my research addresses fundamental questions concerning the responses of mammalian cells to environmental carcinogens at the level of protein kinases, transcription factors and their target genes, as well as the protein modification both in vitro and in vivo. We also investigate the gene expression and protein modification, and protein-protein interaction leading to cancer invasion and metastasis, as well as identify novel anti-cancer compounds from natural products and their anticancer mechanisms. 

Current and future research interests in this research field are described as follows: 1), elucidate the novel scenario for the contribution of XIAP to the modulating RhoGDI SUMOylation, F-actin polymerization, cancer cellular migration and invasion accounts for XIAP-mediated cancer metastasis in individuals with various types of cancer. Such information enables us to further explore the potential utilization of XIAP as a prognostic marker and plausible specific target for treatment of metastatic cancers. Thus, we will further elucidate the molecular basis underlying the XIAP RING domain deletion knockin mice resistant to BBN-induced invasive invasive bladder cancer development. We will also use XIAP RING domain as a specific target for screen and indetification of new anti-cancer small molecules for potential application to metastatic cancer thereapy; 2), identify isorhapontigenin (ISO) as a major active compound for the anti-cancer activity of Gnetum Cleistostachyum by downregulation of XIAP expression and induction of cancer cell apoptosis through specific targeting of Sp1 pathway, and cast new light on the treatment of the cancer patients with XIAP overexpression. We are working on elucidating deep insight mechanisms responsible for its anti-cancer, and making its drugdable by modification of ISO chemical structure; 3), identify novel signaling pathways triggering cellular apoptosis in cell responses to environmental stress, such as, we identify a novel signaling pathway of p85α/NFAT3/TNFα for mediating cell apoptosis upon UV radiation. Our most recently studies also characterize a novel pro-apoptotic pathway of IKKβ/NF-κB p50/GADD45α/JNK in cellular response to arsenite; 4), demonstrating role of the transcription factor NFAT in environmental carcinogenic response; 4), elucidating molecular mechanisms of carcinogenic effect of arsenite exposure; 6), initiating finding of crucial role of PI-3K/Akt pathway in carcinogenic responses and as a target for chemoprevention; 7), identifying a novel function of XIAP acting as a modulator of RhoGDI sumoylation, by which XIAP mediates cancer cell motility and metastasis. 


George Thurston
Exposures and Human Health Effects of Air Pollution

In this concentration, students will aid in the collection and analyses of individual-level air pollution and health effects monitoring in urban locales with high air pollution exposures, such as hookah bars (second-hand and smoking exposures), running paths along roadways, subways, etc.  Dr. Thurston's lab has identified associations between ambient air pollution and adverse human health effects at both the individual and community level. In these analyses, we have considered cohorts of individual subjects and their responses to ambient pollution, as well as citywide and nationwide population health characteristics (e.g., hospital admissions counts) and their aggregate associations with air pollution. Our past studies have included both healthy and asthmatic children at summer camps in the northeastern United States, as these children are often outdoors and active during summer air-pollution episodes, as well as children with asthma in the South Bronx.  In the aftermath of 9/11, we also monitored the air pollution levels at the NYU Downtown Hospital near Ground Zero until the fires were extinguished.


Judith Zelikoff
Early life environmental exposure and later life disease susceptibilities

Our laboratory evaluates the effects and underlying mechanisms of environmental exposure during prenatal development and its influence on disease susceptibility later in life including tumor susceptibility, cardiovascular risk factors, immunosuppression, and adverse effects on reproductive health. Our work focuses on inhaled nanomaterials such as gold, cadmium and silver, as well as ambient particulate matter and alternative smoked and smokeless tobacco products. A student interested in doing a concentration study in this laboratory would utilize prenatally exposed mouse offspring and evaluate immunological alterations associated with tumor surveillance. Chemoprotective studies using the same model can/will include the addition of special 'tea extracts' from Nigeria that is touted to have "cancer preventative" properties.