Environmental Health Sciences
The Department of Environmental Health Sciences (EHS) identifies and explores common biological and environmental pathways that contribute to a broad range of diseases in an effort to develop applicable prevention and intervention strategies. Our graduate level EHS programs prepare students for professional roles in which they will apply the highest quality performance of mechanism-based and evidence-based research to help detect, prevent and control adverse influences of the environment on human health, while communicating the complex interactions between genetic variation and environmental stressors.
The EHS department advocates for research-led teaching, so students are able to get the most up-to-date information as we share our passion for the field. Our interdisciplinary faculty of physicians, chemists, toxicologists, cancer scientists, molecular biologists, environmental/water resource scientists and other public health scientists give great breadth to our teaching and research, which also provides students with an excellent opportunity to help reduce risk and improve public health at the local and global level upon graduation.
Note: Environmental Health Sciences was formerly known as the Department of Environmental and Occupational Health (EOH). A name change went into effect at the end of 2017.
Master's Level Overview (MPH)
MPH, Concentration in Environmental Health Sciences
With the target of launcing in the fall of 2018, we revamped the Master of Public Health (MPH) degree with a concentration in Environmental Health Sciences to provide a broad overview of the field of EHS. The concentration will cover topics such as environmental toxicology, risk assessment, health and safety and environmental disasters, while allowing students to tailor studies to meet specific needs/interests through a wide range of electives delivered by faculty in cutting-edge scientific settings.
MPH, Concentration in Brain, Behavior and the Environment
With the target of launching in the fall of 2018, we revamped the Master of Public Health (MPH) degree with a concentration in Brain, Behavior and the Environment. The concentration is a branch of Environmental Health Sciences that incorporates neurotoxicology, neuroscience, imaging, psychology and psychiatry, alongside environmental exposures. This focus is officially recognized by FIU as an Emerging Preeminent Program and will be taught by top researchers from Stempel College’s faculty roster.
PHC 6945 (Practicum in Public Health) and PHC 6930C (Integrative Seminar in Public Health/culminating experience) are both required for all MPH students.
The practicum may be taken after completing a minimum of 30 hours, including all core courses. The practicum may be waived if the student has at least three years of relevant practice experience working in a public health setting. The waiver request is prepared and submitted by the student through their faculty advisor and department chair. If the practicum requirement is waived, the student will need to substitute three additional approved hours so that the total curriculum hour requirement of 45 is met. MPH students are expected to complete PHC 6930C Integrative Seminar in Public Health during their last semester in the program.
Doctoral Level Overview (Ph.D.)
Our department’s areas of research interests include cancer, cardiopulmonary disease, neurodegenerative disease, cognition and behavior, along with the emerging area of environmental health impacts, which encompasses new health threats caused by climate change. Doctoral projects are encouraged in these areas.
Ph.D. in Public Health, Concentration in Environmental Toxicology
With the target of launcing in the fall of 2018, we revamped the Ph.D. degree in public health with a concentration in Environmental Toxicology to offer advanced and highly specialized training of doctoral students who focus on research.
Ph.D. in Public Health, Concentration in Brain, Behavior and the Environment
With the target of launching in the fall of 2018, we revamped the Ph.D. degree in public health with a concentration in Brain, Behavior and the Environment that incorporates neurotoxicology, neuroscience, imaging, psychology and psychiatry, as well as environmental exposures. This focus is officially recognized by FIU as an Emerging Preeminent Program and will be taught by top researchers from Stempel College’s faculty roster.
Funding your education
At Stempel College, we understand that academic success can be affected by financial aid and funding opportunities. Our students have access to myriad funding options by degree level (bachelor’s, master’s, doctoral) and by academic discipline (Public Health, Dietetics & Nutrition, Social Work). It’s important to understand the basics of applying for financial aid and the additional resources available to you as a Stempel College student. For more, please visit Funding Your Education in our website’s “Student Life” section.
Everything you need to know about applying for your preferred degree level or certificate in our various academic programs can be located by using the “Apply Now!” search tool below. For example, you can select your preferred degree level and unit/concentration in the drop-down fields. Alternatively, you can leave the search term field blank to conduct a search of the college’s entire academic repertoire.
Name of Lab:
Oxidative Stress Group
Environmental Health Sciences
Subject area description:
The lab focuses on oxidative stress and genomic instability, from basic mechanisms to translational application of validated biomarkers. It concentrates on the formation and repair of damage to nuclear/mitochondrial DNA, the nucleotide precursor pools and DNA adductomics such as: (i) the totality of adducts in cellular DNA and urine; and (ii) the genome-wide mapping of damage.
- Nuclear DNA base excision repair
- Nuclear DNA nucleotide excision repair
- Formation and repair of nuclear DNA Inter-strand crosslinks
- Cellular antioxidant capacity
- Mitochondrial DNA damage and repair
- Nuclear and mitochondrial DNA adductomics for the genome-wide mapping of damage and repair
- Cellular DNA adductomics
- Nuclear DNA damage in peripheral blood mononuclear cells (pin prick of blood)
- Biomarkers of oxidative stress in extracellular matrices e.g. urine, serum or plasma:
- 8-oxo-7,8-dihydroguanosine – derived from RNA/GTP pool
- 8-oxo-7,8-dihydro-2’-deoxyguanosine – derived from DNA/dGTP pool
- Urinary DNA adductomics
Dr. Mahsa Karbaschi, postdoctoral fellow
Hadi Abdulwahed, doctoral candidate
Yunhee Ji, doctoral candidate
Yenny Diaz, doctoral candidate
Jesenia Perez, MARC U-STAR student
Jessica Cobb, undergraduate student
Dr. Mu-Rong Chao (Chung Shan Medical University, Taiwan)
Dr. Chiung Hu (Chung Shan Medical University, Taiwan)
Dr. John Anetor (University of Ibadan, Nigeria)
Dr. Gloria Anetor (University of Ibadan, Nigeria)
Name of lab:
Parkinson’s Disease Research Laboratory
Environmental Health Sciences (EHS)
Subject area description:
The long-term goal of this laboratory is to study the pathogenic mechanisms induced by environmental toxicants, genetic mutations and gene-environment interactions in Parkinson’s disease (PD) with the ultimate goal of developing disease-modifying therapeutics for this brain disorder.
Overall, the research projects in this laboratory address the following fundamental questions:
- Gene-environment interactions: Do mutations linked to PD render dopamine neurons more susceptible to environmental toxicants?
- Glia-neuron interactions: How do glial cells contribute to the vulnerability of dopamine neurons in PD?
- Dynamin related protein (Drp1) is classically known as a mitochondrial fission protein. However, Dr. Tieu’s research team has recently discovered that blocking Drp1 alleviates autophagic inhibition, independent of its mitochondrial function. Rigorous studies are being conducted to investigate whether blocking Drp1 would reduce the spread and aggregation of toxic proteins, neuroinflammation, mitochondrial and autophagic impairment. The ultimate goal is to determine whether this protein can be targeted for PD treatment.
To address these questions, Dr. Tieu’s laboratory utilizes innovative and transdisciplinary approaches from a team of accomplished investigators with relevant established track-records, a wide range of chemical and genetic tools, high standard techniques and innovative experimental models for molecular target manipulations with functional studies at cellular, circuit and whole animal levels.
Hary Estrada (Lab manager / Research Technician II)
Zhangqiuzi Fan (Postdoctoral Research Associate)
Afzaal Mohammed (Postdoctoral Research Associate)
Yanhao Lai (Postdoctoral Research Associate)
David Villanueva (PhD candidate)
Ritishka Kapoor (PhD candidate)
Andres Makarem (MSc candidate)
Name of lab:
Brain, Behavior and the Environment Laboratory
Environmental Health Sciences (EHS)
Subject Area Description
The overall research focus of the Brain, Behavior, and the Environment laboratory is to understand the role of environmental pollutants on neurological and neurodegenerative diseases and mental health. Our work uses behavioral, cellular and molecular approaches, ranging from studies using primary culture of brain cells to the application of brain imaging technologies. Major projects include:
Effects of early life lead (Pb2+) exposure on cognitive function and molecular mechanisms:
Our laboratory was one of two research labs that initially showed that Pb2+ is a potent inhibitor of the NMDA receptor. This initial finding was followed by a series of studies showing that early life Pb2+ exposure disrupts the normal ontogeny of NMDA receptor subunits in the hippocampus leading to impairments of synaptic plasticity in the form of long-term potentiation and deficits in spatial learning. This work also showed that early life Pb2+ exposure impairs adult neurogenesis in the hippocampus. Our lab was the first to show that environmental enrichment can reverse the Pb2+-induced deficits in spatial learning and normalize the deficits in NMDA receptor subunits. This worked formed the basis for developing a working model of the molecular mechanisms by which Pb2+ exposure alters synapse development and function. During the last five years, our work has shown that early life Pb2+ exposure may be a risk factor for mental disorders, specifically schizophrenia, as well as substance abuse.
Environmental enrichment reverses cognitive and molecular deficits induced by developmental lead exposure. Guilarte TR, Toscano CD, McGlothan JL, Weaver SA (2003) Annals of Neurology 53: 50-56.
Chronic exposure of mutant DISC1 mice to lead produces sex-dependent abnormalities consistent with schizophrenia and related mental disorders: a gene-environment interaction study. Abazyan B, Dziedzic J, Hua K, Abazyan S, Yang C, Mori S, Pletnikov MV, Guilarte TR (2014) Schizophrenia Bulletin 40: 575-84.
Early life lead exposure recapitulates the selective loss of parvalbumin-positive GABAergic interneurons and subcortical dopamine system hyperactivity present in schizophrenia. Stansfield KH, Ruby KN, Soares BD, McGlothan JL, Liu X, Guilarte TR (2015) Translational Psychiatry 5e522.
7,8-Dihydroxyflavone rescues lead-induced impairment of vesicular release: A novel therapeutic approach for lead-intoxicated children. Zhang XL, McGlothan JL, Miry O, Stansfield KH, Loth MK, Stanton PK, Guilarte TR (2018) Toxicological Sciences 161: 186-195.
Translocator Protein 18 kDa (TSPO): A Molecular Biomarker of Brain Injury & Inflammation:
Our laboratory has performed pioneering work in the validation and application of Translocator Protein 18 kDa (TSPO) as a biomarker of brain injury and inflammation. TSPO is currently being used in clinical and preclinical neuroimaging studies in major research institutions around the world. In the normal brain neuropil, TSPO levels are almost non-detectable, but following brain injury, TSPO levels increase markedly in microglia and astrocytes and this effect depends on the type and severity of the injury. More recent work in the lab relates to the function of TSPO in glial cells, specifically microglia and astrocytes. This work has recently shown that TSPO ligands induce reactive oxygen species production in microglia and this effect may be associated with the activation of NADPH oxidase. Further work has shown the utility of TSPO to detect inflammation in other organs systems besides the brain, for example myocardial inflammation.
Translocator protein 18 kDa (TSPO): molecular sensor of brain injury and repair. Chen MK, Guilarte TR (2008) Pharmacology & Therapeutics 118:1-17.
TSPO finds NOX2 in microglia for redox homeostasis. Guilarte TR, Loth MK, Guariglia SR (2016) Trends in Pharmacological Sciences 37: 334-343.
Imaging of glial cell activation and white matter integrity in brains of active and recently retired National Football League players. Coughlin JM, Wang Y, Minn I, Bienko N, Ambinder EB, Xu X, Peters ME, Dougherty JW, Vranesic M, Lee M, Cottrell C, Sair HI, Sawa A, Munro CA, Nowinski CJ, Dannals RF, Lyketsos CG, Kassiou M, Guilarte TR, Pomper MG (2017) JAMA-Neurology 74: 67-74.
TSPO in diverse CNS pathologies and psychiatric disease: a critical review and a way forward. Guilarte TR (2018) Pharmacology & Therapeutics 194: 44-58.
Behavioral and Molecular Effects of Chronic Manganese Exposure in Non-Human Primates:
Our laboratory has been studying the effects of chronic manganese exposure on neurological health in non-human primates. This work, in collaboration with Dr. Jay Schneider (Thomas Jefferson) and Dr. Dean Wong (Johns Hopkins), utilizes behavioral, neuroimaging and neuropathological endpoints to determine the mechanisms of manganese-induced parkinsonism. This research was the first to show that manganese-induced parkinsonism differs from idiopathic Parkinson’s disease in that manganese-induced parkinsonism does not involve degeneration of dopamine neuron cell bodies in the substantia nigra pars compacta, but in fact, it is related to a marked inhibition of dopamine release in the dorsal striatum. We propose that the marked inhibition of striatal dopamine release by manganese in conjunction with degeneration of cells intrinsic to the basal ganglia (cholinergic interneurons) will form the basis for the movement abnormalities documented in humans and experimental animals. Using this same non-human primate model, our lab was the first to show that chronic manganese exposure results in beta-amyloid aggregation and neurodegeneration in the frontal cortex. This effect was associated with impairment of working memory and paired-associative learning in these same animals.
Nigrostriatal dopamine system dysfunction and subtle motor deficits in manganese-exposed non-human primates. Guilarte TR, Chen MK, McGlothan JL, Verina T, Wong DF, Zhou Y, Alexander M, Rohde CA, Syversen T, Decamp E, Koser AJ, Fritz S, Gonczi H, Anderson DW, Schneider JS. (2006) Exp Neurol 202: 381-90.
Increased APLP1 expression and neurodegeneration in the frontal cortex of manganese-exposed non-human primates. Guilarte TR, Burton NC, Verina T, Prabhu VV, Becker KG, Syversen T, Schneider JS. (2008) J Neurochem 105: 1948-59.
Chronic manganese exposure impairs visuospatial associative learning in non-human primates. Schneider JS, Williams C, Ault M, Guilarte TR. (2013) Toxicol Lett 221: 146-51.
PET imaging of dopamine release in the frontal cortex of manganese-exposed non-human primates. Guilarte TR, Yeh CL, McGlothan JL, Perez J, Finley P, Zhou Y, Wong DF, Dydak U, Schneider JS. (2019) J Neurochem 150: 188-201.
Jennifer McGlothan Dziedzic,
Research associate and lab manger
Dr. Diana Azzam,
Research assistant professor
Dr. Damaris Albores-Garcia,
Dr. Monica Rodriguez-Silva,
Dr. Elena Cubedo Gil,
Undergraduate research assistant