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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 research centers

Our Research Centers

Get involved in our research centers, where you can join a research project or help translate findings into practice and policy.
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our faculty

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.
Meet our alumni

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.

Thu
2/23
EOH Journal Club
EOH Journal Club - Spring 2017 - Hsiu-Chi/Shawn Ting EOH Journal Club
EOH Journal Club - Spring 2017 - Hsiu-Chi/Shawn Ting
Thu 2/23 11:00AM - 12:00PM
Bridgeside Point - 339

EOH Journal Club Seminar - Spring 2017

Date: Thursday February 23, 2017

Time: 11am - 12pm

Presenter: Hsiu-Chi/Shawn Ting

Paper: ACSL4 dictates ferroptosis sensitivity by shaping cellular lipid composition

Authors: Doll S, Proneth B, Tyurina YY, Panzilius E, Kobayashi S, Ingold I, Irmler M, Beckers J, Aichler M, Walch A, Prokisch H, Trümbach D, Mao G, Qu F, Bayir H, Füllekrug J, Scheel CH, Wurst W, Schick JA, Kagan VE, Angeli JP, Conrad M.

Abstract: Ferroptosis is a form of regulated necrotic cell death controlled by glutathione peroxidase 4 (GPX4). At present, mechanisms that could predict sensitivity and/or resistance and that may be exploited to modulate ferroptosis are needed. We applied two independent approaches-a genome-wide CRISPR-based genetic screen and microarray analysis of ferroptosis-resistant cell lines-to uncover acyl-CoA synthetase long-chain family member 4 (ACSL4) as an essential component for ferroptosis execution. Specifically, Gpx4-Acsl4 double-knockout cells showed marked resistance to ferroptosis. Mechanistically, ACSL4 enriched cellular membranes with long polyunsaturated ω6 fatty acids. Moreover, ACSL4 was preferentially expressed in a panel of basal-like breast cancer cell lines and predicted their sensitivity to ferroptosis. Pharmacological targeting of ACSL4 with thiazolidinediones, a class of antidiabetic compound, ameliorated tissue demise in a mouse model of ferroptosis, suggesting that ACSL4 inhibition is a viable therapeutic approach to preventing ferroptosis-related diseases.

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Thu
2/23
EOH Seminar Series
GPCR Dysfunction in Alzheimer's Disease EOH Seminar Series
GPCR Dysfunction in Alzheimer's Disease
Thu 2/23 12:00PM - 1:00PM
Bridgeside Point

Thu
3/2
EOH Journal Club
EOH Journal Club - Spring 2017 - Qiao Lin EOH Journal Club
EOH Journal Club - Spring 2017 - Qiao Lin
Thu 3/2 11:00AM - 12:00PM
Bridgeside Point - 339

EOH Journal Club Seminar - Spring 2017

Date: Thursday March 2, 2017

Time: 11am - 12pm

Presenter: Qiao Lin

Paper: Combating multidrug-resistant Gram-negative bacteria with structurally nanoengineered antimicrobial peptide polymers

Authors: Lam SJ, O'Brien-Simpson NM, Pantarat N, Sulistio A, Wong EH, Chen YY, Lenzo JC, Holden JA, Blencowe A, Reynolds EC, Qiao GG.

Abstract: With the recent emergence of reports on resistant Gram-negative 'superbugs', infections caused by multidrug-resistant (MDR) Gram-negative bacteria have been named as one of the most urgent global health threats due to the lack of effective and biocompatible drugs. Here, we show that a class of antimicrobial agents, termed 'structurally nanoengineered antimicrobial peptide polymers' (SNAPPs) exhibit sub-μM activity against all Gram-negative bacteria tested, including ESKAPE and colistin-resistant and MDR (CMDR) pathogens, while demonstrating low toxicity. SNAPPs are highly effective in combating CMDR Acinetobacter baumannii infections in vivo, the first example of a synthetic antimicrobial polymer with CMDR Gram-negative pathogen efficacy. Furthermore, we did not observe any resistance acquisition by A. baumannii (including the CMDR strain) to SNAPPs. Comprehensive analyses using a range of microscopy and (bio)assay techniques revealed that the antimicrobial activity of SNAPPs proceeds via a multimodal mechanism of bacterial cell death by outer membrane destabilization, unregulated ion movement across the cytoplasmic membrane and induction of the apoptotic-like death pathway, possibly accounting for why we did not observe resistance to SNAPPs in CMDR bacteria. Overall, SNAPPs show great promise as low-cost and effective antimicrobial agents and may represent a weapon in combating the growing threat of MDR Gram-negative bacteria.

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Thu
3/9
EOH Journal Club
EOH Journal Club - Spring 2017 - Shuo Cao EOH Journal Club
EOH Journal Club - Spring 2017 - Shuo Cao
Thu 3/9 11:00AM - 12:00PM
Bridgeside Point - 339

EOH Journal Club Seminar - Spring 2017

Date: Thursday March 9, 2017

Time: 11am - 12pm

Presenter: Shuo Cao

Paper: Structural and transcriptomic response to antenatal corticosteroids in an Erk3-null mouse model of respiratory distress

Authors: Pew BK, Harris RA, Sbrana E, Guaman MC, Shope C, Chen R, Meloche S, Aagaard K.

Abstract:
BACKGROUND:
Neonatal respiratory distress syndrome in preterm infants is a leading cause of neonatal death. Pulmonary insufficiency-related infant mortality rates have improved with antenatal glucocorticoid treatment and neonatal surfactant replacement. However, the mechanism of glucocorticoid-promoted fetal lung maturation is not understood fully, despite decades of clinical use. We previously have shown that genetic deletion of Erk3 in mice results in growth restriction, cyanosis, and early neonatal lethality because of pulmonary immaturity and respiratory distress. Recently, we demonstrated that the addition of postnatal surfactant administration to antenatal dexamethasone treatment resulted in enhanced survival of neonatal Erk3-null mice.

OBJECTIVE:
To better understand the molecular underpinnings of corticosteroid-mediated lung maturation, we used high-throughput transcriptomic and high-resolution morphologic analysis of the murine fetal lung. We sought to examine the alterations in fetal lung structure and function that are associated with neonatal respiratory distress and antenatal glucocorticoid treatment.

STUDY DESIGN:
Dexamethasone (0.4 mg/kg) or saline solution was administered to pregnant dams on embryonic days 16.5 and 17.5. Fetal lungs were collected and analyzed by microCT and RNA-seq for differential gene expression and pathway interactions with genotype and treatment. Results from transcriptomic analysis guided further investigation of candidate genes with the use of immunostaining in murine and human fetal lung tissue.

RESULTS:
Erk3(-/-) mice exhibited atelectasis with decreased overall porosity and saccular space relative to wild type, which was ameliorated by glucocorticoid treatment. Of 596 differentially expressed genes (q < 0.05) that were detected by RNA-seq, pathway analysis revealed 36 genes (q < 0.05) interacting with dexamethasone, several with roles in lung development, which included corticotropin-releasing hormone and surfactant protein B. Corticotropin-releasing hormone protein was detected in wild-type and Erk3(-/-) lungs at E14.5, with significantly temporally altered expression through embryonic day 18.5. Antenatal dexamethasone attenuated corticotropin-releasing hormone at embryonic day 18.5 in both wild-type and Erk3(-/-) lungs (0.56-fold and 0.67-fold; P < .001). Wild type mice responded to glucocorticoid administration with increased pulmonary surfactant protein B (P = .003). In contrast, dexamethasone treatment in Erk3(-/-) mice resulted in decreased surfactant protein B (P = .012). In human validation studies, we confirmed that corticotropin-releasing hormone protein is present in the fetal lung at 18 weeks of gestation and increases in expression with progression towards viability (22 weeks of gestation; P < .01).

CONCLUSION:
Characterization of whole transcriptome gene expression revealed glucocorticoid-mediated regulation of corticotropin-releasing hormone and surfactant protein B via Erk3-independent and -dependent mechanisms, respectively. We demonstrated for the first time the expression and temporal regulation of corticotropin-releasing hormone protein in midtrimester human fetal lung. This unique model allows the effects of corticosteroids on fetal pulmonary morphologic condition to be distinguished from functional gene pathway regulation. These findings implicate Erk3 as a potentially important molecular mediator of antenatal glucocorticoid action in promoting surfactant protein production in the preterm neonatal lung and expanding our understanding of key mechanisms of clinical therapy to improve neonatal survival

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Thu
3/16
EOH Journal Club
EOH Journal Club - Spring 2017 - Chai-Hsin/Aaron Liu EOH Journal Club
EOH Journal Club - Spring 2017 - Chai-Hsin/Aaron Liu
Thu 3/16 11:00AM - 12:00PM
Bridgeside Point - 339

EOH Journal Club Seminar - Spring 2017

Date: Thursday March 16, 2017

Time: 11am - 12pm

Presenter: Chai-Hsin/Aaron Liu

Paper: Combined inhibition of DDR1 and Notch signaling is a therapeutic strategy for KRAS-driven lung adenocarcinoma

Authors: Ambrogio C, Gómez-López G, Falcone M, Vidal A, Nadal E, Crosetto N, Blasco RB, Fernández-Marcos PJ, Sánchez-Céspedes M, Ren X, Wang Z, Ding K, Hidalgo M, Serrano M, Villanueva A, Santamaría D, Barbacid M.

Abstract:
Patients with advanced Kirsten rat sarcoma viral oncogene homolog (KRAS)-mutant lung adenocarcinoma are currently treated with standard chemotherapy because of a lack of efficacious targeted therapies. We reasoned that the identification of mediators of Kras signaling in early mouse lung hyperplasias might bypass the difficulties that are imposed by intratumor heterogeneity in advanced tumors, and that it might unveil relevant therapeutic targets. Transcriptional profiling of Kras(G12V)-driven mouse hyperplasias revealed intertumor diversity with a subset that exhibited an aggressive transcriptional profile analogous to that of advanced human adenocarcinomas. The top-scoring gene in this profile encodes the tyrosine kinase receptor DDR1. The genetic and pharmacological inhibition of DDR1 blocked tumor initiation and tumor progression, respectively. The concomitant inhibition of both DDR1 and Notch signaling induced the regression of KRAS;TP53-mutant patient-derived lung xenografts (PDX) with a therapeutic efficacy that was at least comparable to that of standard chemotherapy. Our data indicate that the combined inhibition of DDR1 and Notch signaling could be an effective targeted therapy for patients with KRAS-mutant lung adenocarcinoma.

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Arsenic work by EOH's Barchowsky cited as top paper of 2016

ENVIRONMENTAL FACTOR - The NIE...
Arsenic work by EOH's Barchowsky cited as top paper of 2016

ENVIRONMENTAL FACTOR - The NIEHS journal signaled out work by AARON BARCHOWSKY and co-authors as one of the top 25 "Papers of the Year" among 2,700 research papers funded by the National Institute of Environmental Health Sciences. The research, published in Stem Cells, found that chronic exposure ... (02/16/2017)

EOH's Bernard Goldstein receives 2017 Society of Toxicology Public Communications Award

Congratulations to Dr. Bernard...
EOH's Bernard Goldstein receives 2017 Society of Toxicology Public Communications Award

Congratulations to Dr. Bernard D. Goldstein, dean emeritus, on receiving the Society of Toxicology's 2017 Public Communications Award! (02/14/2017)

APHA declares 2017 the Year of Climate Change and Health

What we don’t always understa...
APHA declares 2017 the Year of Climate Change and Health

What we don’t always understand is how climate change is impacting our health, right now! We are seeing rising rates of climate-related health issues like asthma and allergies, respiratory disease, cholera, Zika, malaria, and dengue – just to name a few. The good news is that when people understan... (01/05/2017)

Three Pitt Public Health researchers recognized with 2017 Toxicology Awards

Three Pitt Public Health resea...
Three Pitt Public Health researchers recognized with 2017 Toxicology Awards

Three Pitt Public Health researchers will be honored at the March awards ceremony of the 2017 Society of Toxicology (SOT), which recognizes excellence in advancing the science of toxicology. (01/05/2017)

Rosemarie Ramos (EOH '03, '05)

My positive experience at Pit...
Rosemarie Ramos (EOH '03, '05)

My positive experience at Pitt Public Health has had a lifelong impact on me as a public health professional. It’s given me the self-confidence to contribute to improvements in population health and health equity.   (12/22/2016)
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