Professor and Associate Head

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Address: POB 245044
Tucson, AZ 85724-5044
Phone: (520) 626-6716
E-Mail: lantz@email.arizona.edu

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Research Interests

Exposure to environmental toxicants alters lung structure and function and leads to chronic lung disease, including cancer. Current investigations are examining the effects of exposure to environmentally relevant doses of arsenic and uranium. Arsenic is a naturally occurring metalloid found in water, soil and air. Exposure to inorganic arsenic occurs worldwide through environmental (contaminated drinking water, air, food and domestic fuel sources) and occupational exposures (smelting industries, pesticide production). In addition to its association with non-malignant diseases, arsenic is of major worldwide health concern because of its carcinogenic potential in humans. Epidemiologic studies have associated arsenic exposure with an increased risk of multiple human cancers including lung, skin, bladder, kidney, liver and stomach cancers.

 Our current research is focusing on two models to examine the effects of arsenic in the lung. One model relies on exposure to arsenic during lung development, both in utero and postnatally. We have previously shown that exposure of pregnant female rats to 500 ppb as arsenic until embryonic day 18 resulted in altered expression of extracellular matrix genes. In addition, genes involved in vascular development also appear to be targets. Alterations in gene expression are currently being correlated with alterations in structure and lung function. In addition, alterations in protein levels and sites of expression are being determined.

A second model relies on chronic 4 to 8 week exposure of adult mice to arsenic in drinking water. We have evaluated alterations in mRNA and protein levels from animals exposed to 50 ppb. Again, extracellular matrix genes are among the classes of genes that are altered by this exposure. In addition, alterations in elastin and collagen deposition are being determined to link gene expression changes with phenotypic structural alterations in the lung. Data are also being analyzed using an annotated data base to identify pathways and transcriptional regulators that may be affected by the exposure to arsenic.

Research is also on going to identify protein alterations in lung lining fluid as biomarkers of exposure and effect prior to the development of cancer following exposure to arsenic. This study uses the technology of proteomics to evaluate and identify biomarkers of chronic environmental exposure to arsenic by evaluating large numbers of proteins simultaneously. We are comparing alterations in protein expression in exposed human populations in Arizona and Mexico, human cell lines, and in vivo rodent studies. Patterns of alterations in protein expression, both common and unique to these different test systems, will be identified.

Finally, in collaboration with Northern Arizona University, we are evaluating the chemical genotoxicity of uranium. In addition to its radioactive effects, uranium may also have adverse health effects because of its interactions with cellular macromolecules. We are currently evaluating the toxicity of the uranium based on solubility and oxidative states.

Selected Publications

Wong SS, Thomas A, Barbaris B, Lantz RC, Witten ML. Jun 2009. Pulmonary evaluation of permissible exposure limit of syntroleum S-8 synthetic jet fuel in mice. Toxicol Sci, 109:312-20

Lantz RC, Chau B, Sarihan P, Witten ML, Pivniouk VI, Chen GJ. Feb 2009. In utero and postnatal exposure to arsenic alters pulmonary structure and function. Toxicol Appl Pharmacol, 235:105-13

Petrick JS, Blachere FM, Selmin O, Lantz RC. May 2009. Inorganic arsenic as a developmental toxicant: in utero exposure and alterations in the developing rat lungs. Mol Nutr Food Res, 53:583-91

Wong SS, Vargas J, Thomas A, Fastje C, McLaughlin M, Camponovo R, Lantz RC, Heys J, Witten ML. Dec 2008. In vivo comparison of epithelial responses for S-8 versus JP-8 jet fuels below permissible exposure limit. Toxicology, 254:106-11