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Environmental and Occupational Health
environmental and occupational health

Environmental and Occupational Health

Who's Making Sure
Our Environment
Isn't Making Us Sick?
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Our Faculty

Meet the faculty who will teach and mentor you, and learn about the innovative research projects they're directing.
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our alumni

Our Alumni

Read about what our graduates are doing in the environmental and occupational health field.
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Environmental and Occupational Health

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. Our doctorate-level professional degree program in environmental health sciences provides education for those who aspire to high-level administration or decision-making leadership positions.

 

Kagan and Bayir unlock clues to cell death

PITTSBURGH POST-GAZETTE - “Bet...
Kagan and Bayir unlock clues to cell death

PITTSBURGH POST-GAZETTE - “Better treatments for traumatic brain injury and acute kidney injuries are desperately needed,” stated Hulya Bayir HULYA BAYIR (EOH). VALERIAN KAGAN (EOH), the study’s senior author, was key in discovering the protein’s important role in the cell-death process. (10/19/2017)

Goldstein says we can’t be short-sighted on weather disasters intensified by global climate change

THE HILL - Emeritus dean and e...
Goldstein says we can’t be short-sighted on weather disasters intensified by global climate change

THE HILL - Emeritus dean and environmental professor BERNARD GOLDSTEIN comments that, as we help communities affected by recent weather disasters, it's time to talk about our national responsibility to fund restoration of areas likely to be repeatedly impacted in the future. “Would it not be better,... (09/09/2017)

NIH awards five-year R01 support to EOH’s Di for antibiotics research

The NIH has just announced a f...
NIH awards five-year R01 support to EOH’s Di for antibiotics research

The NIH has just announced a five-year award to Y. PETER DI of the Department of Environmental and Occupational Health (EOH) for his group’s research on developing a new class of antibiotics. Di also serves as the director of the Inhalation Exposure Facility and president of theChinese American Lung... (08/15/2017)

Contaminants in Pittsburgh's drinking water worry D.C. environmental group, but not local experts

WESA 90.5 - Lead isn't the onl...
Contaminants in Pittsburgh's drinking water worry D.C. environmental group, but not local experts

WESA 90.5 - Lead isn't the only potential water contaminant Pittsburgh residents should worry about, according to researchers at the nonprofit Environmental Working Group. Of potential concern are chemicals called trihalomethanes, though they don't worry Pitt researchers including EOH's AARON BARCHO... (07/28/2017)

On health effects, blame the trucks, not the fracking?

WESA 90.5 - WVU’s Mike McCawle...
On health effects, blame the trucks, not the fracking?

WESA 90.5 - WVU’s Mike McCawley studies the spike in diesel truck traffic as a potential contributor to health impacts associated fracking. EOH’s JIM FABISIAK isn’t surprised, as diesel exhaust is a known carcinogen, adding “We also know that it contributes probably significantly to many of the othe... (07/28/2017)

 

Thu
10/26
EOH Journal Club
EOH Journal Club - Fall 2017 - Meghan Matlack EOH Journal Club
EOH Journal Club - Fall 2017 - Meghan Matlack
Thu 10/26 11:00AM - 12:00PM
Bridgeside Point - 339

EOH Journal Club Seminar - Fall 2017
Date: Thursday October 26, 2017
Time: 11am - 12pm
Presenter: Meghan Matlack

Paper:  Reduced biological effect of e-cigarette aerosol compared to cigarette smoke evaluated in vitro using normalized nicotine dose and RNA-seq-based toxicogenomics

Authors: Linsey E. Haswell, Andrew Baxter, Anisha Banerjee, Ivan Verrastro, Jessica Mushonganono, Jason Adamson, David Thorne, Marianna Gaça & Emmanuel Minet

Abstract: Electronic cigarettes (e-cigarettes) use has increased globally and could potentially offer a lower risk alternative to cigarette smoking. Here, we assessed the transcriptional response of a primary 3D airway model acutely exposed to e-cigarette aerosol and cigarette (3R4F) smoke. Aerosols were generated with standard intense smoking regimens with careful consideration for dose by normalizing the exposures to nicotine. Two e-cigarette aerosol dilutions were tested for equivalent and higher nicotine delivery compared to 3R4F. RNA was extracted at 24 hrs and 48 hrs post exposure for RNA-seq. 873 and 205 RNAs were differentially expressed for 3R4F smoke at 24 hrs and 48 hrs using a pFDR < 0.01 and a [fold change] > 2 threshold. 113 RNAs were differentially expressed at the highest dose of e-cigarette aerosol using a looser threshold of pFDR < 0.05, 3 RNAs exceeded a fold change of 2. Geneset enrichment analysis revealed a clear response from lung cancer, inflammation, and fibrosis associated genes after 3R4F smoke exposure. Metabolic/biosynthetic processes, extracellular membrane, apoptosis, and hypoxia were identified for e-cigarette exposures, albeit with a lower confidence score. Based on equivalent or higher nicotine delivery, an acute exposure to e-cigarette aerosol had a reduced impact on gene expression compared to 3R4F smoke exposure in vitro.
Thu
10/26
EOH Seminar Series
Transitioning regulatory immune cell thereapy to the clinic in organ transplantation EOH Seminar Series
Transitioning regulatory immune cell thereapy to the clinic in organ transplantation
Thu 10/26 12:00PM - 1:00PM
Bridgeside Point - 540

Thu
11/2
EOH Journal Club
EOH Journal Club - Fall 2017 - Shawn Ting EOH Journal Club
EOH Journal Club - Fall 2017 - Shawn Ting
Thu 11/2 11:00AM - 12:00PM
Bridgeside Point - 339

EOH Journal Club Seminar - Fall 2017

Date: Thursday November 2, 2017

Time: 11am - 12pm

Presenter: Shawn/Hsiu-Chi Ting

Paper:  PEBP1 Wardens Ferroptosis by Enabling Lipoxygenase Generation of Lipid Death Signals

Authors: Sally E. Wenzel, Yulia Y. Tyurina, Jinming Zhao, ..., Ivet Bahar, Hulya Bayır, Valerian E. Kagan

Abstract: Ferroptosis is a form of programmed cell death that
is pathogenic to several acute and chronic diseases
and executed via oxygenation of polyunsaturated
phosphatidylethanolamines (PE) by 15-lipoxygenases
(15-LO) that normally use free polyunsaturated
fatty acids as substrates. Mechanisms
of the altered 15-LO substrate specificity are enigmatic.
We sought a common ferroptosis regulator
for 15LO. We discovered that PEBP1, a scaffold
protein inhibitor of protein kinase cascades,
complexes with two 15LO isoforms, 15LO1 and
15LO2, and changes their substrate competence
to generate hydroperoxy-PE. Inadequate reduction
of hydroperoxy-PE due to insufficiency or dysfunction
of a selenoperoxidase, GPX4, leads to
ferroptosis. We demonstrated the importance of
PEBP1-dependent regulatory mechanisms of ferroptotic
death in airway epithelial cells in asthma,
kidney epithelial cells in renal failure, and cortical
and hippocampal neurons in brain trauma. As master
regulators of ferroptotic cell death with profound
implications for human disease, PEBP1/15LO complexes
represent a new target for drug discovery.

Thu
11/9
EOH Journal Club
EOH Journal Club - Fall 2017 - Shuo Cao EOH Journal Club
EOH Journal Club - Fall 2017 - Shuo Cao
Thu 11/9 11:00AM - 12:00PM
Bridgeside Point - 339

EOH Journal Club Seminar - Fall 2017
Date: Thursday November 9, 2017
Time: 11am - 12pm
Presenter: Shuo Cao

Paper: TLR4 signaling induces TLR3 up-regulation in alveolar macrophages during acute lung injury

Authors: Ding X, Jin S, Tong Y, Jiang X, Chen Z, Mei S, Zhang L, Billiar TR, Li Q

Abstract: Acute lung injury is a life-threatening inflammatory response caused by severe infection. Toll-like receptors in alveolar macrophages (AMΦ) recognize the molecular constituents of pathogens and activate the host's innate immune responses. Numerous studies have documented the importance of TLR-TLR cross talk, but few studies have specifically addressed the relationship between TLR4 and TLR3. We explored a novel mechanism of TLR3 up-regulation that is induced by LPS-TLR4 signaling in a dose- and time-dependent manner in AMΦ from C57BL/6 mice, while the LPS-induced TLR3 expression was significantly reduced in TLR4-/- and Myd88-/- mice and following pretreatment with a NF-κB inhibitor. The enhanced TLR3 up-regulation in AMΦ augmented the expression of cytokines and chemokines in response to sequential challenges with LPS and Poly I:C, a TLR3 ligand, which was physiologically associated with amplified AMΦ-induced PMN migration into lung alveoli. Our study demonstrates that the synergistic effect between TLR4 and TLR3 in macrophages is an important determinant in acute lung injury and, more importantly, that TLR3 up-regulation is dependent on TLR4-MyD88-NF-κB signaling. These results raise the possibility that bacterial infections can induce sensitivity to viral infections, which may have important implications for the therapeutic manipulation of the innate immune system.


Thu
11/16
EOH Journal Club
EOH Journal Club - Fall 2017 - Brandy Hill EOH Journal Club
EOH Journal Club - Fall 2017 - Brandy Hill
Thu 11/16 11:00AM - 12:00PM
Bridgeside Point - 339

EOH Journal Club Seminar - Fall 2017
Date: Thursday November 16, 2017
Time: 11am - 12pm
Presenter: Brandy Hill

Paper: Influence of Age and Eosinophilic Esophagitis on Esophageal Distensibility in a Pediatric Cohort

Authors: Menard-Katcher C, Benitez AJ, Pan Z, Ahmed FN, Wilkins BJ, Capocelli KE, Liacouras CA, Verma R, Spergel JM, Furuta GT, Muir AB.

Abstract: OBJECTIVES:
Sequelae of eosinophilic esophagitis (EoE) include food impaction and esophageal stricture. Duration of inflammation is a predicted risk factor; however, complications remain unpredictable. Studies using the functional lumen imaging probe (FLIP) have demonstrated decreased distensibility of the esophagus in adult patients with EoE. As the impact of inflammation on the developing esophagus is unknown, we investigated esophageal distensibility in a pediatric cohort to determine the effect of age, ongoing inflammation, and fibrotic features on distensibility.
METHODS:
We conducted a prospective observational study at two tertiary pediatric institutions. Subjects underwent FLIP evaluation during endoscopy to determine distensibility of the esophagus. During stepwise distension, simultaneous intrabag pressure and 16 channels of cross-sectional areas were measured. The minimal diameter at maximal esophageal distention at an intrabag pressure of 40 mm Hg was identified. Distensibility was compared between EoE and non-EoE subjects and between clinical variables within the EoE cohort. Potential confounding variables were identified.
RESULTS:
Forty-four non-EoE and 88 EoE subjects aged 3-18 years were evaluated. Age positively correlated with esophageal distensibility in the non-EoE cohort, but this trend was not observed in the EoE population. Subjects with EoE had reduced distensibility even after adjusting for age. Active inflammation (eosinophils >15 eos/high-power field), histological lamina propria fibrosis, and various features of a fibrotic phenotype (stricture, food impaction, circumferential rings on endoscopy) were associated with decreased distensibility within the EoE cohort. FLIP was safe, feasible, and well tolerated.
CONCLUSIONS:
These findings suggest that remodeling occurs in the pediatric EoE population, warranting early diagnosis and initiation of therapy prior to the onset of disease complications.

© 2017 by University of Pittsburgh Graduate School of Public Health

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