Chemical contaminants found at Superfund sites and in their leachates may play a significant role in the causation of human disease and in the deterioration of ecosystem health. Thus, such disease and ecological degradation is preventable to the extent that such factors can be identified and either removed from the environment or counteracted. Recognition of this possibility requires intensified efforts to identify the causal factors, to determine those conditions which modulate their bioavailabilities, to elucidate their mechanisms of action and to formulate appropriate measures for blocking or reversing their effects. The purpose of this Program is to provide training to prepare scientists for active and productive careers in environmental toxicology with interdisciplinary emphases on environmental engineering, bioremediation, ecology, and biomedical research. The objective is to prepare the trainees to plan, conduct, and interpret toxicological studies which are appropriate to specific scientific issues regarding the fate and effects of Superfund contaminants on human and wildlife populations. The scope of this program is broad. For example, trainees will be provided with backgrounds enabling them to study genetic and epigenetic factors which impact variation in susceptibilities to environmentally-induced disease in humans and in fish by metals and aromatic hydrocarbons and to understand those factors which influence bioavailabilities of these contaminants in ecosystems. The program provides for two predoctoral (Ph.D.) And four internship positions.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Hazardous Substances Basic Research Grants Program (NIEHS) (P42)
Project #
1P42ES010344-01
Application #
6335597
Study Section
Special Emphasis Panel (ZES1-MAO-A (G2))
Project Start
2000-06-01
Project End
2005-03-31
Budget Start
Budget End
Support Year
1
Fiscal Year
2000
Total Cost
$164,078
Indirect Cost
Name
New York University
Department
Type
DUNS #
City
New York
State
NY
Country
United States
Zip Code
10016
Niu, Yingmei; DesMarais, Thomas L; Tong, Zhaohui et al. (2015) Oxidative stress alters global histone modification and DNA methylation. Free Radic Biol Med 82:22-8
Brocato, Jason; Hernandez, Michelle; Laulicht, Freda et al. (2015) In Vivo Exposures to Particulate Matter Collected from Saudi Arabia or Nickel Chloride Display Similar Dysregulation of Metabolic Syndrome Genes. J Toxicol Environ Health A 78:1421-36
Brocato, Jason; Chen, Danqi; Liu, Jianli et al. (2015) A Potential New Mechanism of Arsenic Carcinogenesis: Depletion of Stem-Loop Binding Protein and Increase in Polyadenylated Canonical Histone H3.1 mRNA. Biol Trace Elem Res 166:72-81
Brocato, Jason; Costa, Max (2015) SATB1 and 2 in colorectal cancer. Carcinogenesis 36:186-91
Brocato, Jason; Wu, Fen; Chen, Yu et al. (2015) Association between sleeping hours and cardiometabolic risk factors for metabolic syndrome in a Saudi Arabian population. BMJ Open 5:e008590
Brocato, Jason; Chervona, Yana; Costa, Max (2014) Molecular responses to hypoxia-inducible factor 1? and beyond. Mol Pharmacol 85:651-7
Brocato, Jason; Fang, Lei; Chervona, Yana et al. (2014) Arsenic induces polyadenylation of canonical histone mRNA by down-regulating stem-loop-binding protein gene expression. J Biol Chem 289:31751-64
Brocato, Jason; Costa, Max (2013) Basic mechanics of DNA methylation and the unique landscape of the DNA methylome in metal-induced carcinogenesis. Crit Rev Toxicol 43:493-514
Arita, Adriana; Muñoz, Alexandra; Chervona, Yana et al. (2013) Gene expression profiles in peripheral blood mononuclear cells of Chinese nickel refinery workers with high exposures to nickel and control subjects. Cancer Epidemiol Biomarkers Prev 22:261-9
Passantino, Lisa; Muñoz, Alexandra B; Costa, Max (2013) Sodium metavanadate exhibits carcinogenic tendencies in vitro in immortalized human bronchial epithelial cells. Metallomics 5:1357-67

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