Jefferey L Burgess
Adjunct Professor, Mining and Geological Engineering
Associate Dean, Research-Public Health
Professor, BIO5 Institute
Professor, Public Health
Associate Dean, Research - Mel and Enid Zuckerman College of Public Health
Primary Department
Department Affiliations
(520) 626-4918
Research Interest
Jefferey L. Burgess, MD, MS, MPH is a Professor and Division Director of Community, Environment and Policy within the University of Arizona Mel and Enid Zuckerman College of Public Health. Dr. Burgess’ research focuses on improving occupational health and safety, with a special focus on firefighters, other public safety personnel and miners. Areas of current and past research include: reduction of occupational exposures, illnesses and injuries; respiratory toxicology; environmental arsenic exposure; and hazardous materials exposures including methamphetamine laboratories. In addition to multiple research grants, Dr. Burgess is the Principal Investigator (PI) for the Centers for Disease Control and Prevention-funded Mountain West Preparedness and Emergency Response Learning Center and a joint PI for the National Institute for Occupational Safety and Health-funded Western Mining Safety and Health Resource Center. Dr. Burgess is internationally recognized for his research evaluating the health effects of firefighting and methods for reducing firefighter exposures and other hazards, including but not limited to improved respiratory protection and injury prevention. He is also internationally known for his work on mining health and safety, and is a co-PI on a large Science Foundation Arizona grant supporting mining risk management, exposure assessment and control and economic analysis of health and safety systems. A separate ongoing grant is focused on comparing exposures and health effects associated with the use of diesel and biodiesel blend fuels in underground mining. He also has carried out multiple research projects on the adverse effects of low-level arsenic exposure in drinking water and more recently has begun to evaluate exposures from dietary arsenic sources.

Publications

Kurzius-Spencer, M., Foster, K., Littau, S., Richey, K. J., Clark, B. M., Sherrill, D., Boitano, S., Caruso, D. M., & Burgess, J. L. (2015). Tracheobronchial protease inhibitors, body surface area burns, and mortality in smoke inhalation. Journal of burn care & research : official publication of the American Burn Association, 30(5), 824-31.
BIO5 Collaborators
Scott A Boitano, Jefferey L Burgess

The objective of this study was to assess tracheobronchial protease inhibitor concentrations longitudinally and determine whether initial concentrations predict subsequent lung injury and mortality in intubated burn victims. Tracheobronchial suction fluid was collected every 2 hours for 36 hours. Alpha-1-antitrypsin (AAT), secretory leukocyte peptidase inhibitor (SLPI), alpha-2-macroglobulin (A2M), and cell and differential counts were assayed. Partial pressure of oxygen in arterial blood/fraction of inspired oxygen (PaO2/FIO2) and peak airway pressure (PAP) were recorded for 72 hours. Standard statistics were used to evaluate cross-sectional relationships; random coefficient (mixed) models were used to evaluate temporal trends in marker concentrations and relation to clinical outcomes. Among 29 patients, 24 (83%) developed hypoxemia (PaO2/FIO2 35% TBSA burn (P = .010 and .033, respectively), when compared with patients with less severe burns. However, patients with increased A2M in combination with >35% TBSA burn had a 6-fold (95% CI: 1.8-20) increased relative risk of death. Tracheobronchial AAT and A2M levels were significantly lower in patients with more severe burns and increased over time. Initial SLPI levels predicted subsequent PAP. Increased early A2M in combination with extensive burn predicted early mortality.

Burgess, J. L., Kurzius-Spencer, M., Poplin, G. S., Littau, S. R., Kopplin, M. J., Stürup, S., Boitano, S., & Clark Lantz, R. (2015). Environmental arsenic exposure, selenium and sputum alpha-1 antitrypsin. Journal of exposure science & environmental epidemiology, 24(2), 150-5.
BIO5 Collaborators
Scott A Boitano, Jefferey L Burgess, Clark Lantz

Exposure to arsenic in drinking water is associated with increased respiratory disease. Alpha-1 antitrypsin (AAT) protects the lung against tissue destruction. The objective of this study was to determine whether arsenic exposure is associated with changes in airway AAT concentration and whether this relationship is modified by selenium. A total of 55 subjects were evaluated in Ajo and Tucson, Arizona. Tap water and first morning void urine were analyzed for arsenic species, induced sputum for AAT and toenails for selenium and arsenic. Household tap-water arsenic, toenail arsenic and urinary inorganic arsenic and metabolites were significantly higher in Ajo (20.6±3.5 μg/l, 0.54±0.77 μg/g and 27.7±21.2 μg/l, respectively) than in Tucson (3.9±2.5 μg/l, 0.16±0.20 μg/g and 13.0±13.8 μg/l, respectively). In multivariable models, urinary monomethylarsonic acid (MMA) was negatively, and toenail selenium positively associated with sputum AAT (P=0.004 and P=0.002, respectively). In analyses stratified by town, these relationships remained significant only in Ajo, with the higher arsenic exposure. Reduction in AAT may be a means by which arsenic induces respiratory disease, and selenium may protect against this adverse effect.

Kurzius-Spencer, M., Foster, K., Littau, S., Richey, K. J., Clark, B. M., Sherrill, D., Goodman, R. B., Boitano, S., & Burgess, J. L. (2015). Tracheobronchial markers of lung injury in smoke inhalation victims. Journal of burn care & research : official publication of the American Burn Association, 29(2), 311-8.
BIO5 Collaborators
Scott A Boitano, Jefferey L Burgess

Although smoke inhalation injury victims frequently develop severe hypoxemia and are at increased risk of acute respiratory distress syndrome (ARDS), no early prognostic tests are currently available. The objectives were to determine early longitudinal changes in tracheobronchial fluid inflammatory markers and assess the value of initial concentrations as predictors of subsequent lung injury. Partial pressure of arterial oxygen (Pao2) and the fraction of inspired oxygen (Fio2) were recorded approximately every 6 hours from intubated smoke inhalation victims admitted to a regional burn center. Tracheobronchial suction fluid was collected every 2 hours and assayed for interleukins (IL-1beta, -8, and -10), tumor necrosis factor-alpha, transforming growth factor-beta1, soluble Fas ligand (sFasL), and complement factor 5a. Temporal trends in marker concentrations during 36 hours and the relations between initial concentrations and lowest Pao2/Fio2 or ARDS within 72 hours were assessed using random coefficients modeling and cross-sectional analysis. In 21 subjects with tracheobronchial samples collected within 6.5 hours of intubation, 14 (66.7%) developed acute hypoxemia (Pao2/Fio2 200 (P = .042) during 72 hours. In smoke inhalation victims, tracheobronchial IL-1beta and IL-8 increase rapidly and high initial IL-8 may predict improved oxygenation.

Olsen, C. E., Liguori, A. E., Zong, Y., Lantz, R. C., Burgess, J. L., & Boitano, S. (2008). Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells. American journal of physiology. Lung cellular and molecular physiology, 295(2), L293-302.
BIO5 Collaborators
Scott A Boitano, Jefferey L Burgess, Clark Lantz

As part of the innate immune defense, the polarized conducting lung epithelium acts as a barrier to keep particulates carried in respiration from underlying tissue. Arsenic is a metalloid toxicant that can affect the lung via inhalation or ingestion. We have recently shown that chronic exposure of mice or humans to arsenic (10-50 ppb) in drinking water alters bronchiolar lavage or sputum proteins consistent with reduced epithelial cell migration and wound repair in the airway. In this report, we used an in vitro model to examine effects of acute exposure of arsenic (15-290 ppb) on conducting airway lung epithelium. We found that arsenic at concentrations as low as 30 ppb inhibits reformation of the epithelial monolayer following scrape wounds of monolayer cultures. In an effort to understand functional contributions to epithelial wound repair altered by arsenic, we showed that acute arsenic exposure increases activity and expression of matrix metalloproteinase (MMP)-9, an important protease in lung function. Furthermore, inhibition of MMP-9 in arsenic-treated cells improved wound repair. We propose that arsenic in the airway can alter the airway epithelial barrier by restricting proper wound repair in part through the upregulation of MMP-9 by lung epithelial cells.

Lantz, R. C., Lynch, B. J., Boitano, S., Poplin, G. S., Littau, S., Tsaprailis, G., & Burgess, J. L. (2007). Pulmonary biomarkers based on alterations in protein expression after exposure to arsenic. Environmental health perspectives, 115(4), 586-91.
BIO5 Collaborators
Scott A Boitano, Jefferey L Burgess, Clark Lantz

Environmental exposure to arsenic results in multiple adverse effects in the lung. Our objective was to identify potential pulmonary protein biomarkers in the lung-lining fluid of mice chronically exposed to low-dose As and to validate these protein changes in human populations exposed to As.