The proposed research program involves researchers and administrative staff from five institutions: the University of California at Berkeley, University of California at San Francisco, Californi Department of Health Services, Lawrence Berkeley Laboratory and Lawrence Livermore National Laboratory. A total of twelve projects are proposed which will be supported by five cores. These projects cover a wide range of Superfund related areas and chemicals, and address the relationship between hazardous substances in the environment and their impact on human health and ecosystem viability. The research proposed has five specific goals: 1. To develop and apply biomarkers in studies of human carcinogenesis; 2. To use biomarkers to determine the causes of genetic and reproductive damage in humans and ecosystems; 3. To better understand gender and ethnic differences in susceptibility to the toxic effects of Superfund chemicals; 4. To better understand the release and transport of toxic metals and other contaminants from inactive mining sites and from various combustion processes; 5. To improve methods of remediation at sites contaminated by volatile solvents and toxic metals. Project 1 -3 will aim to develop novel biomarkers of exposure and dose to specific targets in the human body. By identifying the specific molecular targets which Superfund chemicals attack in the body it would be possible to design much better biomarkers of delivered dose to target. Project 4, on biomarkers of susceptibility, will explore the role of polymorphisms in glutathione transferases with regard to susceptibility to childhood leukemia and arsenic-induced bladder cancer. Project 5 aims to develop highly predictive biomarkers of leukemia risk with the aim of understanding the causes of leukemia in humans. Project 6 will study environmental chemical exposure of parents and children and its relationship to the development of childhood leukemia. Project 7 will continue to study the role of arsenic in producing internal cancers in humans. A new Project 8 will study the role of male-mediated genotoxicity in lowered reproductive health. Project 9 will study the multigenerational effects of environmental mutagens on ecosystem viability. Project 10 will study the transport and fate of toxic metals including arsenic at inactive mining sites. Project 11 will continue to develop new methods for site remediation using steam injection and biodegradation. Project 12 will focus on understanding the factors which influence the production of toxic intermediates during combustion processes. Together these projects should address major issues of concern at Superfund sites through basic research, and thereby improve our ability to remediate hazardous waste sites and prevent the health effects posed by them. These projects will be supported by five cores, one of which focuses on children and the environment and aims to protect children from the toxic effects of environmental chemical exposures.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Hazardous Substances Basic Research Grants Program (NIEHS) (P42)
Project #
3P42ES004705-11S1
Application #
2688726
Study Section
Special Emphasis Panel (SRC (G2))
Project Start
1995-04-01
Project End
2000-03-31
Budget Start
1997-04-01
Budget End
1998-03-31
Support Year
11
Fiscal Year
1998
Total Cost
Indirect Cost
Name
University of California Berkeley
Department
Other Health Professions
Type
Schools of Public Health
DUNS #
094878337
City
Berkeley
State
CA
Country
United States
Zip Code
94704
Bruton, Thomas A; Sedlak, David L (2018) Treatment of perfluoroalkyl acids by heat-activated persulfate under conditions representative of in situ chemical oxidation. Chemosphere 206:457-464
Schiffman, Courtney; McHale, Cliona M; Hubbard, Alan E et al. (2018) Identification of gene expression predictors of occupational benzene exposure. PLoS One 13:e0205427
Wiemels, Joseph L; Walsh, Kyle M; de Smith, Adam J et al. (2018) GWAS in childhood acute lymphoblastic leukemia reveals novel genetic associations at chromosomes 17q12 and 8q24.21. Nat Commun 9:286
Prasse, Carsten; Ford, Breanna; Nomura, Daniel K et al. (2018) Unexpected transformation of dissolved phenols to toxic dicarbonyls by hydroxyl radicals and UV light. Proc Natl Acad Sci U S A 115:2311-2316
Smith, Allan H; Marshall, Guillermo; Roh, Taehyun et al. (2018) Lung, Bladder, and Kidney Cancer Mortality 40?Years After Arsenic Exposure Reduction. J Natl Cancer Inst 110:241-249
Castriota, Felicia; Acevedo, Johanna; Ferreccio, Catterina et al. (2018) Obesity and increased susceptibility to arsenic-related type 2 diabetes in Northern Chile. Environ Res 167:248-254
Rothman, Nathaniel; Zhang, Luoping; Smith, Martyn T et al. (2018) Formaldehyde, Hematotoxicity, and Chromosomal Changes-Response. Cancer Epidemiol Biomarkers Prev 27:120-121
Yik-Sham Chung, Clive; Timblin, Greg A; Saijo, Kaoru et al. (2018) Versatile Histochemical Approach to Detection of Hydrogen Peroxide in Cells and Tissues Based on Puromycin Staining. J Am Chem Soc 140:6109-6121
Rappaport, Stephen M (2018) Redefining environmental exposure for disease etiology. NPJ Syst Biol Appl 4:30
Tachachartvanich, Phum; Sangsuwan, Rapeepat; Ruiz, Heather S et al. (2018) Assessment of the Endocrine-Disrupting Effects of Trichloroethylene and Its Metabolites Using in Vitro and in Silico Approaches. Environ Sci Technol 52:1542-1550

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