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The Environmental and Occupational Health (EOH) Department has a sound reputation as a leader in training students to...

  • Identify agents that affect health
  • Study the long-term effects of environmental and occupational health risks
  • Determine the molecular mechanisms of toxic agents that contribute to the development of certain illnesses and diseases.

Environmental health specialists help find ways to promote healthier environments and minimize risks that increase the incidence of respiratory, cardiovascular, and musculoskeletal diseases, asthma, lower respiratory infections, road traffic injuries, poisonings, and drownings.
Occupational health specialists study all aspects of health and safety in the workplace. From exposure to toxins on the job, to workplace violence and lifting injuries, occupational hazards create an enormous health burden, unnecessary pain and suffering, and economic loss in the workplace.

Find a research program for your interests

Many EOH faculty members collaborate with basic sciences and clinical investigators throughout other departments at Pitt Public Health, and the University of Pittsburgh schools of medicine and engineering. Students and faculty perform studies on the principles and practice of environmental health ranging from basic research at the cellular and molecular level to applied translational studies of human disease, population exposure, and public health studies.

In addition, faculty and students work with local governmental organizations, such as the Allegheny County Health Department, the Pittsburgh Office of the U.S. Department of Labor, Occupational Safety and Health Administration, and the Allegheny County Sanitary Authority to study and improve the environmental health of southwestern Pennsylvania.

Pursue a career in environmental and occupational health

Doctoral degree graduates are prepared to work in laboratory-based academic settings as faculty or postdoctoral fellows and become prominent members of government agencies and independent industries. Recent graduates have obtained fellowships at top-tier academic institutions, positions with
the National Institutes of Health, the Environmental Protection Agency, and in firms conducting chemical and environmental risk assessment.

Master's degree graduates play prominent roles as environmental/occupational health practitioners in various settings, including industry, hospitals, government agencies, and private practice.

Degrees

The EOH Department offers two degrees in the environmental health sciences, providing a broad theoretical and practical education for positions in academia, industry, or government. The multiple tracks provide flexibility in acquiring advance training in toxicology, environmental biophysics, molecular and cellular pathobiology, risk assessment, and exposure science.

Our professional degree program allows students to earn concentrations in environmental health or risk assessment and apply these concepts to public health practice.

 

Fabisiak comments on the region's cancer risk related to air pollution

ENVIRONMENTAL HEALTH NEWS - A...
Fabisiak comments on the region's cancer risk related to air pollution

ENVIRONMENTAL HEALTH NEWS - Around one in three Americans gets a cancer diagnosis during their lifetime. "If someone chooses to smoke, most of the risk will only impact them," said James Fabisiak. "When we think about air pollution, on the other hand, the risk is smaller than smoking but that risk ... (12/18/2018)

Travis Lear awarded predoctoral fellowship F31 award

Travis Lear (EOH '20) has bee...
Travis Lear awarded predoctoral fellowship F31 award

Travis Lear (EOH '20) has been awarded an F31 predoctoral fellowship from the NHLBI. His project will focus on the molecular mechanisms of dysregulated inflammation in the lung, which is the cause of several lung diseases and a major cause of morbidity and mortality in critically-ill patients.  (12/13/2018)

Sahu and Ambrosio find longevity protein rejuvenates muscle healing in old mice

UPMC - New research, develope...
Sahu and Ambrosio find longevity protein rejuvenates muscle healing in old mice

UPMC - New research, developed largely from Amrita Sahu's (EOH) thesis work, implicates the so-called “longevity protein” Klotho, both as culprit and therapeutic target to the inability for skeletal muscle to hear after injury as we get older. “We found that we were able to rescue, at least in part... (11/27/2018)

Kagan, Wenzel, Bayir partner to better understand cell death and ferroptosis

PITT MED - Cells die—that’s j...
Kagan, Wenzel, Bayir partner to better understand cell death and ferroptosis

PITT MED - Cells die—that’s just part of life. But there’s always a reason. Pitt scientists are figuring out how to keep programmed cell death in check. EOH's VALERIAN KAGAN and SALLY WENZEL and other colleagues including EOH's HULYA BAYIR, are partnering to better understand “the reason” for ferro... (10/09/2018)

Goldstein profiled in Risk Analysis

RISK ANALYSIS - Before joinin...
Goldstein profiled in Risk Analysis

RISK ANALYSIS - Before joining Pitt Public Health in 2001, BERNARD GOLDSTEIN, EOH professor and former dean, obtained his medical degree from NYU. In 1980, he was recruited by Rutgers Medical School to help with the increase in public and political concerns about environmental pollution. Later, he ... (10/01/2018)

 

Fri
2/15
EOH Seminar Series
Divorcing EPA from Academia EOH Seminar Series
Divorcing EPA from Academia
Fri 2/15 1:00PM - 2:00PM
A719 Public Health

Presented by Bernard D. Goldstein, dean emeritus and professor emeritus of environmental and occupational health. 

Thu
2/21
EOH Journal Club
Exposure to Secondhand Smoke and Arrhythmogenic Cardiac Alternans in a Mouse Model EOH Journal Club
Exposure to Secondhand Smoke and Arrhythmogenic Cardiac Alternans in a Mouse Model
Thu 2/21 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Emma Yi Lu

Paper: Exposure to Secondhand Smoke and Arrhythmogenic Cardiac Alternans in a Mouse Model

Authors:  Zhen Wang, Lianguo Wang, Srinivas Tapa, Kent E. Pinkerton, Chao-Yin Chen, and Crystal M. Ripplinger

Abstract:

BACKGROUND: Epidemiological evidence suggests that a majority of deaths attributed to secondhand smoke (SHS) exposure are cardiovascular related. However, to our knowledge, the impact of SHS on cardiac electrophysiology, Ca2þ handling, and arrhythmia risk has not been studied.

OBJECTIVES: The purpose of this study was to investigate the impact of an environmentally relevant concentration of SHS on cardiac electrophysiology and indicators of arrhythmia.

METHODS: Male C57BL/6 mice were exposed to SHS . Hearts were excised and Langendorff perfused for dual optical mapping with voltage- and Ca2þ-sensitive dyes.

RESULTS:At slow pacing rates, SHS exposure did not alter baseline electrophysiological parameters. With increasing pacing frequency, action potential duration (APD), and intracellular Ca2þ alternans magnitude progressively increased in all groups. At 4 and 8 wk, there were no statistical differences in APD or Ca2þ alternans magnitude between SHS and FA groups. At 12 wk, both APD and Ca2þ alternans magnitude were significantly increased in the SHS compared to FA group (p<0 :05). SHS exposure did not impact the time constant of Ca2þ transient decay (s) at any exposure time point. At 12 wk exposure, the recovery of Ca2þ transient amplitude with premature stimuli was slightly (but nonsignificantly) delayed in SHS compared to FA hearts, suggesting that Ca2þ release via ryanodine receptors may be impaired.

CONCLUSIONS: In male mice, chronic exposure to SHS at levels relevant to social situations in humans increased their susceptibility to cardiac alternans, a known precursor to ventricular arrhythmia

Thu
3/7
EOH Journal Club
Inhibition of Mevalonate Pathway Prevents Adipocyte Browning in Mice and Men... EOH Journal Club
Inhibition of Mevalonate Pathway Prevents Adipocyte Browning in Mice and Men...
Thu 3/7 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Heng Bai

Paper: Inhibition of Mevalonate Pathway Prevents Adipocyte Browning in Mice and Men by Affecting Protein Prenylation

Authors:  Miroslav Balaz, Anton S. Becker, Lucia Balazova, ..., Matthias Johannes Betz, Irene A. Burger, Christian Wolfrum

Abstract:

Through genetic and pharmacological in vivo and in vitro approaches, Balaz et al. show that the mevalonate pathway is important for adipocyte browning. The importance of this pathway is supported by a retrospective clinical study and a small volunteer trial with fluvastatin. The authors identify geranylgeranyl pyrophosphate as the key mevalonate intermediate driving adipocyte browning.

Thu
3/21
EOH Journal Club
Dysfunctional CD8 T Cells Form a Proliferative, Dynamically Regulated Compartment... EOH Journal Club
Dysfunctional CD8 T Cells Form a Proliferative, Dynamically Regulated Compartment...
Thu 3/21 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Pattra Chun-On

Paper: Dysfunctional CD8 T Cells Form a Proliferative, Dynamically Regulated Compartment within Human Melanoma

Authors:  Hanjie Li, Anne M. van der Leun, Ido Yofe, Yaniv Lubling, ..., Ton N. Schumacher, Amos Tanay, Ido Amit

Abstract:
Single-cell analysis of melanoma tumor immune infiltrates reveals a separation between bystander cytotoxic T cells and a population that displays a continuous progression from a transitional toward a dysfunctional state that is associated with active proliferation and tumor reactivity.

Thu
3/28
EOH Journal Club
Maternal phthalate exposure promotes allergic airway inflammation over 2 generations EOH Journal Club
Maternal phthalate exposure promotes allergic airway inflammation over 2 generations
Thu 3/28 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Nicole Shuangjia Xue

Paper: Maternal phthalate exposure promotes allergic airway inflammation over 2 generations through epigenetic modifications

Authors: Susanne Jahreis, PhD, Saskia Trump, PhD, Mario Bauer, MD, Tobias Bauer, PhD,c Loreen Th€urmann, MSc, Ralph Feltens, PhD, Qi Wang, PhD, Lei Gu, PhD, Konrad Gr€utzmann, PhD, Stefan R€oder, PhD, Marco Averbeck, MD, Dieter Weichenhan, PhD, Christoph Plass, PhD, Ulrich Sack, MD, Michael Borte, MD, Virginie Dubourg, MSc, Gerrit Sch€u€urmann, PhD, Jan C. Simon, MD, Martin von Bergen, PhD, J€org Hackerm€uller, PhD,h Roland Eils, PhD, Irina Lehmann, PhD, and Tobias Polte, PhD

Abstract:
Background: Prenatal and early postnatal exposures to environmental factors are considered responsible for the increasing prevalence of allergic diseases. Although there is some evidence for allergy-promoting effects in children because of exposure to plasticizers, such as phthalates, findings of previous studies are inconsistent and lack mechaistic information.

Objective: We investigated the effect of maternal phthalate exposure on asthma development in subsequent generations and their underlying mechanisms, including epigenetic alterations.

Methods: Phthalate metabolites were measured within the prospective mother-child cohort Lifestyle and Environmental Factors and Their Influence on Newborns Allergy Risk (LINA) and correlated with asthma development in the children. A murine transgenerational asthma model was used to identify involved pathways.


Results: In LINA maternal urinary concentrations of mono-nbutyl phthalate, a metabolite of butyl benzyl phthalate (BBP), were associated with an increased asthma risk in the children. Using a murine transgenerational asthma model, we demonstrate a direct effect of BBP on asthma severity in the offspring with a persistently increased airway inflammation up to the F2 generation. This disease-promoting effect was mediated by BBP-induced global DNA hypermethylation in CD41 T cells of the offspring because treatment with a DNA-demethylating agent alleviated exacerbation of allergic
airway inflammation. Thirteen transcriptionally downregulated genes linked to promoter or enhancer hypermethylation were identified. Among these, the GATA-3 repressor zinc finger protein 1 (Zfpm1) emerged as a potential mediator of the enhanced susceptibility for TH2-driven allergic asthma.

Conclusion: These data provide strong evidence that maternal BBP exposure increases the risk for allergic airway inflammation in the offspring by modulating the expression of genes involved in TH2 differentiation through epigenetic alterations. (J Allergy Clin Immunol 2018;141:741-53.)

© 2019 by University of Pittsburgh Graduate School of Public Health

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