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.

 

Tyurina finds genetic engineering could open possibilities for Parkinson’s patients

MEDICIAL LIFE SCIENCES -  A t...
Tyurina finds genetic engineering could open possibilities for Parkinson’s patients

MEDICIAL LIFE SCIENCES -  A team of researchers including EOH's Yulia Tyurina unveiled the most promising strategies in applying genetic engineering. The noble method can help study the role of cellular processes in the disease progression, develop new treatment methods and drugs, and estimate thei... (09/16/2019)

Praekunatham promoted to chief of Epidemiology and Public Health Emergency Response

Hirunwut Praekunatham (EOH, '...
Praekunatham promoted to chief of Epidemiology and Public Health Emergency Response

Hirunwut Praekunatham (EOH, '18) was recently promoted to chief of the Epidemiology and Public Health Emergency Response unit under the new Division of Occupational and Environmental Diseases in Thailand. Praekunatham's responsibilities include surveillance of environmental/occupational diseases at... (09/09/2019)

EOH alumna Lauren Chubb is looking beyond what the eye can see to keep miners safe.

PITT MAGAZINE - Lauren Chubb,...
EOH alumna Lauren Chubb is looking beyond what the eye can see to keep miners safe.

PITT MAGAZINE - Lauren Chubb, DrPH, MPH (EOH ’16, ’13) occasionally dons a hard hat to see the results of her work in the lab. Her team at the National Institute for Occupational Safety and Health's Mining Program has developed software to analyze respirable dust samples in just a few minutes, rath... (08/05/2019)

Stacy finds correlation between obesity in mothers, childhood cancer risk in children

SPECIALTY PHARMACY TIMES - A ...
Stacy finds correlation between obesity in mothers, childhood cancer risk in children

SPECIALTY PHARMACY TIMES - A new studying has found a correlation between children born to pre-pregnancy body-mass index (BMI) and the likelihood of developing childhood cancer, even after correcting for known risk factors, such as newborn size and maternal age. "My hope is that this study can be, ... (07/23/2019)

Hill, Fabisiak talk to KDKA radio about asthma and the Clairton Coke Works

KDKA RADIO – The Clairton Cok...
Hill, Fabisiak talk to KDKA radio about asthma and the Clairton Coke Works

KDKA RADIO – The Clairton Coke Works is one of the biggest emitters of air pollutants in the area and there is a lot of anecdotal evidence about poor health in that area. EOH’s Jim Fabisiak and Brandy Hill (EOH ‘21) talk about their work and the importance of scientific investigation learning about... (07/03/2019)

 

Thu
10/17
EOH Journal Club
Muscle-generated BDNF is a sexually dimorphic myokine that controls metabolic flexibility EOH Journal Club
Muscle-generated BDNF is a sexually dimorphic myokine that controls metabolic flexibility
Thu 10/17 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Heng Bai

Paper: Muscle-generated BDNF is a sexually dimorphic myokine that controls metabolic flexibility

Authors: Xiuying Yang, Daniel Brobst, Wing Suen Chan, Margaret Chui Ling Tse,  Oana Herlea-Pana, Palak Ahuja, Et. Al.

Abstract: The ability of skeletal muscle to switch between lipid and glucose oxidation for ATP production during metabolic stress is pivotal for maintaining systemic energy homeostasis, and dysregulation of this metabolic flexibility is a dominant cause of several metabolic disorders. However, the molecular mechanism that governs fuel selection in muscle is not well understood. Here, we report that brain-derived neurotrophic factor (BDNF) is a fasting-induced myokine that controls metabolic reprograming through the AMPK/CREB/PGC-1 pathway in female mice. Female mice with a muscle-specific deficiency in BDNF (MBKO mice) were unable to switch the predominant fuel source from carbohydrates to fatty acids during fasting, which reduced ATP production in muscle. Fasting-induced muscle atrophy was also compromised in female MBKO mice, likely a result of autophagy inhibition. These mutant mice displayed myofiber necrosis, weaker muscle strength, reduced locomotion, and muscle-specific insulin resistance. Together, our results show that muscle-derived BDNF facilitates metabolic adaption during nutrient scarcity in a gender-specific manner and that insufficient BDNF production in skeletal muscle promotes the development of metabolic myopathies and insulin resistance

Thu
10/24
EOH Journal Club
Maternal vitamin C regulates reprogramming of DNA methylation and germline development EOH Journal Club
Maternal vitamin C regulates reprogramming of DNA methylation and germline development
Thu 10/24 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Qi Wei

Paper: Maternal vitamin C regulates reprogramming of DNA methylation and germline development

Authors: Stephanie P. Ditroia, Michelle Percharde, Marie-Justine Guerquin, estelle Wall, evelyne Collignon, Kevin t. ebata, Kathryn Mesh, Swetha Mahesula, Michalis Agathocleous, Diana J. Laird, Gabriel Livera & Miguel Ramalho-Santos

Abstract: Development is often assumed to be hardwired in the genome, but several lines of evidence indicate that it is susceptible to environmental modulation with potential long-term consequences, including in mammals1,2. The embryonic germline is of particular interest because of the potential for intergenerational epigenetic effects. The mammalian germline undergoes extensive DNA demethylation3–7 that occurs in large part by passive dilution of methylation over successive cell divisions, accompanied by active DNA demethylation by TET enzymes3,8–10. TET activity has been shown to be modulated by nutrients and metabolites, such as vitamin C11–15. Here we show that maternal vitamin C is required for proper DNA demethylation and the development of female fetal germ cells in a mouse model. Maternal vitamin C deficiency does not affect overall embryonic development but leads to reduced numbers of germ cells, delayed meiosis and reduced fecundity in adult offspring. The transcriptome of germ cells from vitamin-C-deficient
 embryos is remarkably similar to that of embryos carrying a null mutation in Tet1. Vitamin C deficiency leads to an aberrant DNA methylation profile that includes incomplete demethylation of key regulators of meiosis and transposable elements. These findings reveal that deficiency in vitamin C during gestation partially recapitulates loss of TET1, and provide a potential intergenerational mechanism for adjusting fecundity to environmental conditions

Thu
10/31
EOH Journal Club
Electronic cigarettes disrupt lung lipid homeostasis and innate immunity independent of nicotine EOH Journal Club
Electronic cigarettes disrupt lung lipid homeostasis and innate immunity independent of nicotine
Thu 10/31 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Emily Nicholls

Paper: Electronic cigarettes disrupt lung lipid homeostasis and innate immunity independent of nicotine

Authors: Matthew C. Madison, … , David B. Corry, Farrah Kheradmand

Abstract: Electronic nicotine delivery systems (ENDS) or e-cigarettes have emerged as a popular recreational tool among adolescents and adults. Although the use of ENDS is often promoted as a safer alternative to conventional cigarettes, few comprehensive studies have assessed the long-term effects of vaporized nicotine and its associated solvents, propylene glycol (PG) and vegetable glycerin (VG). Here, we show that compared with smoke exposure, mice receiving ENDS vapor for 4 months failed to develop pulmonary inflammation or emphysema. However, ENDS exposure, independent of nicotine, altered lung lipid homeostasis in alveolar macrophages and epithelial cells. Comprehensive lipidomic and structural analyses of the lungs revealed aberrant phospholipids in alveolar macrophages and increased surfactant-associated phospholipids in the airway. In addition to ENDS-induced lipid deposition, chronic ENDS vapor exposure downregulated innate immunity against viral pathogens in resident macrophages. Moreover, independent of nicotine, ENDS-exposed mice infected with influenza demonstrated enhanced lung inflammation and tissue damage. Together, our findings reveal that chronic e-cigarette vapor aberrantly alters the physiology of lung epithelial cells and resident immune cells and promotes poor response to infectious challenge. Notably, alterations in lipid homeostasis and immune impairment are independent of nicotine, thereby warranting more extensive investigations of the vehicle solvents used in e-cigarettes.

Fri
11/1
EOH Seminar Series
Environment/diet interaction in fatty liver diseases EOH Seminar Series
Environment/diet interaction in fatty liver diseases
Fri 11/1 1:00PM - 2:00PM
A719 Public Health

Thu
11/7
EOH Journal Club
TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer’s Disease EOH Journal Club
TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer’s Disease
Thu 11/7 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Yi Lu

Paper: TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer’s Disease

Authors: Ana Griciuc, Shaun Patel, Anthony N. Federico, ..., Joseph El Khoury, Marco Colonna, Rudolph E. Tanzi

Abstract: The microglial receptors CD33 and TREM2 have been associated with risk for Alzheimer’s disease (AD). Here, we investigated crosstalk between CD33 and TREM2. We showed that knockout of CD33 attenu-ated amyloid beta (Ab) pathology and improved cognition in 5xFAD mice, both of which were abro-gated by additional TREM2 knockout. Knocking out TREM2 in 5xFAD mice exacerbated Ab pathology and neurodegeneration but reduced Iba1+ cell numbers, all of which could not be rescued by addi-tional CD33 knockout. RNA-seq profiling of microglia revealed that genes related to phagocytosis and signaling (IL-6, IL-8, acute phase response) are upre-gulated in 5xFAD;CD33 and downregulated in 5xFAD;TREM2 mice. Differential gene expression in 5xFAD;CD33 microglia depended on the pres-ence of TREM2, suggesting TREM2 acts downstream of CD33. Crosstalk between CD33 and TREM2 in-cludes regulation of the IL-1b/IL-1RN axis and a gene set in the ‘‘receptor activity chemokine’’ cluster. Our results should facilitate AD therapeutics target-ing these receptors.