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Lantz, R Clark
Primary Phone: (520) 6266716
Primary Phone: (520) 6266716
Ph.D., West Virginia University 1975
B.S., Juniata College 1970
- College Of Medicine
- College Of Public Health
Pulmonary Toxicology, Biological Imaging, Pathogenesis, Developmental Biology
Environmental Health Research & Expertise:
Dr. R. Clark Lantz is Professor of Molecular and Cellular Medicine, and Professor, Division of Community, Environment and Policy at the University of Arizona. Dr. has been the Deputy Director of the Southwest Environmental Health Science Center since 2000. He is intimately familiar with all aspects of the SWEHSC, having been involved with the Center since its inception. As the Deputy Director, he works closely with the Director, Dr. Lau. In the Director's absence, Dr. Lantz has represented the SWEHSC at Center Directors meetings. He is a member of the Center management team that meets weekly. He currently is Chair of the COEC Stakeholders Committee. He has served as the Director of Cellular Imaging Facility since the SWEHSC was first funded in 1993. He is also serving as the leader of the current Research Focus Group 2, Environmental Lung Diseases, where he has been successful in expanding the size and the research interactions of the group. Dr. Lantz also serves as the Deputy Director of the Arizona Superfund Research Program and is Principal Investigator of a Superfund Research Project. Dr. Lantz is heavily involved with issues related to bioinstrumentation at the University. He is the Chair of the University-wide Imaging Facilities User Committee that provides input to the Director of Biotechnology on policy and procedures related to the University imaging facilities and also evaluates University needs in imaging instrumentation and prioritizes those needs. Dr. Lantz maintains active research projects that examine the pulmonary toxicity of arsenic and uranium, especially during lung development. His most recent research has focused on the effects of water ingestion or inhalation of arsenic and other dusts on lung growth and development and on identification of arsenic and uranium induced pulmonary biomarkers. Dr. Lantz has identified several phenotypic alterations caused by the exposure to environmentally relevant levels of arsenic. A number of these phenotypic alterations have been validated in human population studies studied in Arizona and Mexico. His research has been funded from the National Institutes of Health (NIEHS, NCI) and from the USEPA. Dr. Lantz is the author of over 85 peer reviewed manuscripts. Dr. Lantz received the Career Achievement Award, Inhalation and Respiratory Specialty Section, Society of Toxicology in 2011 in recognition of his work in inhalation and respiratory toxicology.
- In utero and early childhood exposure to arsenic decreases lung function in children.
- Arsenic compromises conducting airway epithelial barrier properties in primary mouse and immortalized human cell cultures.
- Environmental arsenic exposure, selenium and sputum alpha-1 antitrypsin.
- Tanshinone I activates the Nrf2-dependent antioxidant response and protects against As(III)-induced lung inflammation in vitro and in vivo.
- Chronic arsenic exposure in nanomolar concentrations compromises wound response and intercellular signaling in airway epithelial cells.
- Sulforaphane prevents pulmonary damage in response to inhaled arsenic by activating the Nrf2-defense response.
- Arsenic toxicology: translating between experimental models and human pathology.
- Arsenic alters ATP-dependent Ca²+ signaling in human airway epithelial cell wound response.
- Pulmonary evaluation of permissible exposure limit of syntroleum S-8 synthetic jet fuel in mice.
- In utero and postnatal exposure to arsenic alters pulmonary structure and function.
- In vivo comparison of epithelial responses for S-8 versus JP-8 jet fuels below permissible exposure limit.
- Arsenic-induced decreases in the vascular matrix.
- Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells.
- Pulmonary biomarkers based on alterations in protein expression after exposure to arsenic.
- Environmental arsenic exposure and sputum metalloproteinase concentrations.
- Uranyl acetate induces hprt mutations and uranium-DNA adducts in Chinese hamster ovary EM9 cells.
- Substance P and neutral endopeptidase in development of acute respiratory distress syndrome following fire smoke inhalation.
- Vinyl acetate decreases intracellular pH in rat nasal epithelial cells. Previous years
- Enhanced activity of human IL-10 after nitration in reducing human IL-1 production by stimulated peripheral blood mononuclear cells.
- Fresh organically grown ginger (Zingiber officinale): composition and effects on LPS-induced PGE2 production.
- Role of neprilysin in airway inflammation induced by diesel exhaust emissions.
- Tissue-specific patterns of neurokinin-1 receptor (NK-1R) gene expression in mice exposed to sidestream cigarette smoke.
- Inflammatory responses in mice sequentially exposed to JP-8 jet fuel and influenza virus.
- Longitudinal decline in lung function: evaluation of interleukin-10 genetic polymorphisms in firefighters.
- Correlation between in vivo and in vitro pulmonary responses to jet propulsion fuel-8 using precision-cut lung slices and a dynamic organ culture system.
- Commercially processed dry ginger (Zingiber officinale): composition and effects on LPS-stimulated PGE2 production.
- Rapid decline in sputum IL-10 concentration following occupational smoke exposure.
- Role of oxidative stress in arsenic-induced toxicity.
- Efficacy and mechanism of action of turmeric supplements in the treatment of experimental arthritis.
- Environmental Arsenic Exposure and Urinary 8-OHdG in Arizona and Sonora.
- Arsenic and cigarette smoke synergistically increase DNA oxidation in the lung.
- A reevaluation of the threshold exposure level of inhaled JP-8 in mice.
- In Vitro Pro-inflammatory Regulatory role of Substance P in Alveolar Macrophages and Type II Pneumocytes after JP-8 Exposure.
- Turmeric extracts containing curcuminoids prevent experimental rheumatoid arthritis.
- Effects of caffeoylquinic acid derivatives and C-flavonoid from Lychnophora ericoides on in vitro inflammatory mediator production.