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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

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.
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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.

Join the entire Pitt Public Health community in support of the second Day of Giving on Pitt’s Founder’s Day, February 28, 2018. 

Participation is the primary goal, so every gift counts! 

Support today....

 

Goldstein on the EU's distortion of public health and effects on US agricultural produce

THE HILL - The European Union...
Goldstein on the EU's distortion of public health and effects on US agricultural produce

THE HILL - The European Union's unclear definitions of the Precautionary Principles allows them to ban trade of goods such as beef previously treated with growth hormones and GMO grains without demonstration that such goods cause any health risks. EOH's BERNARD GOLDSTEIN says, "The US is not withou... (01/31/2018)

EPI's Adibi to address 2018 One Health One Community Symposium at Phipps

EPI's JENNIFER ADIBI has been...
EPI's Adibi to address 2018 One Health One Community Symposium at Phipps

EPI's JENNIFER ADIBI has been announced as a featured speaker for the 2018 One Health One Community Symposium at Phipps Conservatory.  Taking Place on March 7 & 8, this year's event will center on the theme "Health Impacts: Chemicals of Concern in the Environment," with a special focus on endocrine... (01/19/2018)

Goldstein advises Dow Chemical on sustainability

SUSTAINABLE BRANDS - The Dow C...
Goldstein advises Dow Chemical on sustainability

SUSTAINABLE BRANDS - The Dow Chemical Company counts EOH's BERNARD GOLDSTEIN among its 8-member Sustainability External Advisory Council (SEAC),  the first of its kind in the petrochemical industry. The council has a significant influence on Dow’s approach to sustainability and environment, health a... (12/20/2017)

Kagan helps find mechanism of dendritic cell needed for antitumor immune response

DRUG TARGET REVIEW - A team in...
Kagan helps find mechanism of dendritic cell needed for antitumor immune response

DRUG TARGET REVIEW - A team including EOH researcher VALERIAN KAGAN has revealed the mechanism causing defective function of tumour-associated dendritic cells, explaining why they’re ineffective in inducing antitumor immune responses and effective cancer treatment. The findings could lead to new str... (12/15/2017)

Goldstein comments on new study findings: Low birth weights linked to fracking sites

STATE IMPACT - Infants born to...
Goldstein comments on new study findings: Low birth weights linked to fracking sites

STATE IMPACT - Infants born to mothers who live very close to natural gas fracking sites have a higher risk of low birth weight, according to a new peer-reviewed study published Wednesday in the journal Science Advances . In response to the findings, EOH professor emeritus BERNARD GOLDSTEIN noted t... (12/13/2017)

 

Mon
2/26
EOH Lecture
Mitigating Climate Change by Transitioning to a Renewable Resource-Based Economy - Steven Cohen Mitigating Climate Change by Transitioning to a Renewable Resource-Based Economy - Steven Cohen EOH Lecture
Mitigating Climate Change by Transitioning to a Renewable Resource-Based Economy - Steven Cohen
Mon 2/26 2:00PM - 3:00PM
William Pitt Union - Assembly Room

Dr. Steven Cohen of the Earth Institute at Columbia University will discuss how to address the global climate crisis by taking on political, organizational, and financial challenges as we transition economies from fossil fuels to renewable resources. Reserve a seat online for this free lecture in the Pitt Honors College Climate Change Series.

Thu
3/1
EOH Journal Club
EOH Journal Club - Spring 2018 - Heng Bai EOH Journal Club
EOH Journal Club - Spring 2018 - Heng Bai
Thu 3/1 11:00AM - 12:00PM
Public Health 4140, Young Seminar Room

EOH Journal Club Seminar - Spring 2018
Date: Thursday March 1, 2018
Time: 11am - 12pm
Presenter: Heng Bai

Paper: Declining exposures to lead and cadmium contribute to explaining the reduction of cardiovascular mortality in the US population, 1988–2004

Authors: Adrian Ruiz-Hernandez, Ana Navas-Acien, Roberto Pastor-Barriuso, Ciprian M Crainiceanu, Josep Redon, Eliseo Guallar, Maria Tellez-Plaza

Abstract:

Background
Lead and cadmium exposures have markedly declined in the USA following the implementation of large-scale public health policies and could have contributed to the unexplained decline in cardiovascular mortality in US adults. We evaluated the potential contribution of lead and cadmium exposure reductions to explain decreasing cardiovascular mortality trends occurring in the USA from 1988–94 to 1999–2004.

Methods
Prospective study in 15 421 adults ≥40 years old who had participated in the National Health and Nutrition Examination Survey 1988–94 or 1999–2004. We estimated the amount of change in cardiovascular mortality over time that can be independently attributed to the intermediate pathway of changes in blood lead and urine cadmium concentrations.

Results
There was a 42.0% decrease in blood lead and a 31.0% decrease in urine cadmium concentrations. The cardiovascular mortality rate ratio [95% confidence intervals (CIs)] associated with a doubling of metal levels was 1.19 (1.07, 1.31) for blood lead and 1.20 (1.09, 1.32) for urine cadmium. The absolute reduction in cardiovascular deaths comparing 1999–2004 to 1988–94 was 230.7 deaths/100 000 person-years, in models adjusted for traditional cardiovascular risk factors. Among these avoided deaths, 52.0 (95% CI 8.4, 96.7) and 19.4 (4.3, 36.4) deaths/100 000 person-years were attributable to changes in lead and cadmium, respectively.

Conclusions
Environmental declines in lead and cadmium exposures were associated with reductions in cardiovascular mortality in US adults. Given the fact that lead and cadmium remain associated with cardiovascular disease at relatively low levels of exposure, prevention strategies that further minimize exposure to lead and cadmium may be needed.
Thu
3/15
EOH Journal Club
EOH Journal Club - Spring 2018 - Antonella Marrocco EOH Journal Club
EOH Journal Club - Spring 2018 - Antonella Marrocco
Thu 3/15 11:00AM - 12:00PM
Public Health 4140, Young Seminar Room

EOH Journal Club Seminar - Spring 2018
Date: Thursday March 15, 2018
Time: 11am - 12pm
Presenter: Antonella Marrocco

Paper: NF-κB Restricts Inflammasome Activation via Elimination of Damaged Mitochondria 

Authors: Zhong Z, Umemura A, Sanchez-Lopez E, Liang S, Shalapour S, Wong J, He F, Boassa D, Perkins G, Ali SR, McGeough MD, Ellisman MH, Seki E, Gustafsson AB, Hoffman HM, Diaz-Meco MT, Moscat J, Karin M.

Abstract: Nuclear factor κB (NF-κB), a key activator of inflammation, primes the NLRP3-inflammasome for activation by inducing pro-IL-1β and NLRP3 expression. NF-κB, however, also prevents excessive inflammation and restrains NLRP3-inflammasome activation through a poorly defined mechanism. We now show that NF-κB exerts its anti-inflammatory activity by inducing delayed accumulation of the autophagy receptor p62/SQSTM1. External NLRP3-activating stimuli trigger a form of mitochondrial (mt) damage that is caspase-1- and NLRP3-independent and causes release of direct NLRP3-inflammasome activators, including mtDNA and mtROS. Damaged mitochondria undergo Parkin-dependent ubiquitin conjugation and are specifically recognized by p62, which induces their mitophagic clearance. Macrophage-specific p62 ablation causes pronounced accumulation of damaged mitochondria and excessive IL-1β-dependent inflammation, enhancing macrophage death. Therefore, the "NF-κB-p62-mitophagy" pathway is a macrophage-intrinsic regulatory loop through which NF-κB restrains its own inflammation-promoting activity and orchestrates a self-limiting host response that maintains homeostasis and favors tissue repair.

Thu
3/22
EOH Journal Club
EOH Journal Club - Spring 2018 - Shuo Cao EOH Journal Club
EOH Journal Club - Spring 2018 - Shuo Cao
Thu 3/22 11:00AM - 12:00PM
Public Health 4140, Young Seminar Room

EOH Journal Club Seminar - Spring 2018
Date: Thursday March 22, 2018
Time: 11am - 12pm
Presenter: Shuo Cao

Paper: Inactivating mutations and hypermethylation of the NKX2-1/TTF-1 gene in non-terminal respiratory unit-type lung adenocarcinomas

Authors: Matsubara D, Soda M, Yoshimoto T, Amano Y, Sakuma Y, Yamato A, Ueno T, Kojima S, Shibano T, Hosono Y, Kawazu M, Yamashita Y, Endo S, Hagiwara K, Fukayama M, Takahashi T, Mano H, Niki T.

Abstract: The major driver mutations of lung cancer, EGFR mutations and EML4-ALK fusion, are mainly detected in terminal respiratory unit (TRU)-type lung adenocarcinomas, which typically show lepidic and/or papillary patterns, but are rarely associated with a solid or invasive mucinous morphology. In order to elucidate the key genetic events in non-TRU-type lung cancer, we carried out whole-exome sequencing on 43 non-TRU-type lung adenocarcinomas based on morphology (17 acinar, nine solid, and two enteric adenocarcinomas, and 15 adenocarcinomas with a mucinous morphology). Our analysis identified mutations in TP53 (16/43, 37.2%), KRAS (13/43, 30.2%), and NKX2-1/TTF-1 (7/43; 16.3%) as the top three significantly mutated genes, while the EGFR mutation was rare (1/43, 2.3%) in this cohort. Eight NKX2-1/TTF-1 mutations (five frameshift, two nonsense, and one missense) were identified, with one case harboring two distinct NKX2-1/TTF-1 mutations (one missense and one frameshift). Functional assays with the NK2 homeobox 1 (NKX2-1)/thyroid transcription factor 1 (TTF-1) mutants revealed that none of them retain the activity as a transcriptional factor. Histologically, invasive mucinous adenocarcinomas accounted for most of the NKX2-1/TTF-1 mutations (five cases), as well as one enteric and one acinar adenocarcinoma. Immunohistochemistry showed that the cohort was largely divided into TTF-1-postive/hepatocyte nuclear factor 4-α (HNF4-α)-negative and TTF-1-negative/HNF4-α-positive groups. NKX2-1/TTF-1 mutations were exclusively found in the latter, in which the gastrointestinal markers, mucin 5AC and cytokeratin 20, were frequently expressed. Bisulfite sequencing revealed that the NKX2-1/TTF-1 gene body was highly methylated in NKX2-1/TTF-1-negative cases, including those without the NKX2-1/TTF-1 mutations. The genetic or epigenetic inactivation of NKX2-1/TTF-1 may play an essential role in the development and aberrant differentiation of non-TRU-type lung adenocarcinomas.
Thu
3/29
EOH Journal Club
EOH Journal Club - Spring 2018 - Meghan Matlack EOH Journal Club
EOH Journal Club - Spring 2018 - Meghan Matlack
Thu 3/29 11:00AM - 12:00PM
Public Health 4140, Young Seminar Room

EOH Journal Club Seminar - Spring 2018
Date: Thursday March 29, 2018
Time: 11am - 12pm
Presenter: Meghan Matlack

Paper: Blockade of dengue virus infection and viral cytotoxicity in neuronal cells in vitro and in vivo by targeting endocytic pathway

Authors: Min-Ru Ho, Tsung-Ting Tsai, Chia-Ling Chen, Ming-Kai Jhan, Cheng-Chieh Tsai,  Yi-Chao Lee, Chun-Han Chen & Chiou-Feng Li

Abstract: Dengue virus (DENV) infection in neuronal cells was speculated to trigger neuropathy. Herein, we determined the blockade of DENV infection by targeting endocytic pathways in vitro and in vivo. In DENV-infected mouse brains, we previously showed that viral proteins are expressed in neuronal cells around the hippocampus with accompanying neurotoxicity. DENV caused infection, including entry, double-stranded (ds)RNA replication, protein expression, and virus release, followed by cytotoxicity in the mouse neuronal Neuro-2a cell line. Pharmacologically blocking clathrin-mediated endocytosis of the DENV retarded viral replication. Targeting vacuolar-type H+-ATPase (V-ATPase)-based endosomal acidification effectively blocked the DENV replication process, but had no direct effect on viral translation. Blockade of the clathrin- and V-ATPase-based endocytic pathways also attenuated DENVinduced neurotoxicity. Inhibiting endosomal acidification effectively retarded DENV infection, acute viral encephalitis, and mortality. These results demonstrate that clathrin mediated endocytosis of DENV followed by endosomal acidification-dependent viral replication in neuronal cells, which can lead to neurotoxicity.

© 2018 by University of Pittsburgh Graduate School of Public Health

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