Robert Clark Lantz, PhD

Professor, Cellular and Molecular Medicine
Investigator, Center for Toxicology
Professor, BIO5 Institute
Professor, Public Health
Major Areas of Research Interest: 

Pulmonary alveolar macrophages (PAM), cells that reside in the airways and airspaces of the lung, are the first line of defense against foreign inhaled material. Because of its ability to move, phagocytize particles and initiate inflammatory responses, PAM serves a pivotal role in the pathogenesis of lung disease. Current investigations are concentrating on the ability of various toxicant and infectious agents to alter PAM function.

Because PAM have been shown to be a heterogeneous population, we have adapted and developed techniques that permit functional analysis to be performed on single cells. Using digital image analysis, alterations in production of antibacterial oxygen radicals are evaluated in individual cells. These techniques provide information not only on the average cellular response but also on the variability of the response between cells.

Exposure to environmental toxicants alters lung structure and function and leads to impairment of the pulmonary defense mechanisms in the lung. Current investigations are examining the effects of arsenic exposure, acute smoke inhalation and environmental tobacco smoke on PAM function. Arsenic exposure has been found to alter PAM function following both in vivo and in vitro exposure. Inhibition of production of superoxide and of inflammatory mediators, such as tumor necrosis factor, are obtained at --M concentrations of arsenic. Inhibition effects are dependent upon both the oxidative state of the arsenic and on the physical state of the arsenic compounds. Current investigations are examining possible intracellular sites of action of the arsenic.

Acute inhalation of complex smoke, as would be experienced in a fire, leads to respiratory failure. This respiratory distress does not occur instantaneously, but becomes present only several hours after smoke inhalation. PAM activation may play a role in the respiratory distress. We have found that immediately following smoke inhalation, PAM function is suppressed. However, 3 hours after smoke inhalation, PAM function is enhanced. We have postulated that the enhanced activation of PAM is producing lung injury which is contributing to the respiratory failure. Current investigations are examining the mediators that are produced by PAM during this time of activation and are evaluating the ability of therapeutic drugs to delay and/or inhibit the onset of respiratory failure.

Environmental tobacco smoke (ETS) exposure, especially to neonates, has the potential to alter lung structure and function. We are currently investigating the effects of ETS on septal formation during neonatal lung development. The effect of ETS on growth factors, alveolar macrophages and alveolar epithelial type II cells is being examined as possible sites of ETS toxicity.

NIH High School Student Research Program: 

-Margie Uswandi, Dobson High School, Mesa, 1992
-Jennifer Celaya, Sabino High School, 1995
-Vanessa Estrada, Pueblo High School, 1997
-Peter S. Madrigal, Tucson High Magnet School, 1999

NIH K-12 Science Teacher Program: 

-Sharon Goldwasser, Baboquivari Junior/Senior High School, 1992

Tuesday, March 6, 2018