The Center for Environmental Health serves to nucleate and support interdisciplinary research programs bridging environmental analysis with human health through both basic and applied research. The center cultivates external grant proposal development in Environmental Health Sciences.

Indiana University Center of Environmental Health is engaged in:

1. Comparison of Acrylonitrile (ACN)-induced oxidative DNA damage in rat astrocytes and Normal Human Astrocytes.

Our previous work has shown that acrylonitrile causes oxidative stress, including the increased level of free radicals, lipid peroxidation, oxidative DNA damage and the modulation of antioxidant defense in cultured rat astrocytes, rat brain cortex and rat white blood cells. The current project is to compare the response of rat astrocytes and Normal Human Astrocytes upon the exposure to acrylonitrile. These studies will help in predicting the possibility of ACN to produce brain tumors in humans.

2. Genetic polymorphism and prostate cancer.

Studies have shown that genetic polymorphisms of certain genes are involved in prostate cancer and its progression. This project is examining relationships of polymorphisms selected genes, including oxidative stress related genes, and the occurrence and progression of prostate cancer. This study will also investigate the interaction between genetic predisposition and environmental factors, such as smoking, diet, etc.

3. Investigating the role of the Kupffer cell activation on the tumor promotion stage of hepatocarcinogenesis.

Kupffer cells are the resident macrophages in the liver. Upon activation, Kupffer cells produce an array of biologically active products including reactive oxygen species, cytokines, eicosanoids etc which have an impact on hepatocyte growth regulation. The role of Kupffer cells in toxicity of chemicals like acetaminoiphen, carbon tetrachloride, alcohol etc. has been well studied. But not much is known about the role of Kupffer cells in hepatocarcinogenesis. We are investigating the role of Kupffer cells in the tumor promotion stage of hepatocarcinogenesis using diethylnitrosamine (DEN) as a tumor initiator in conjunction with treatment by various tumor promoters' results in the activation of Kupffer cells. This activation is accompanied by the release of cellular growth regulatory signaling molecules that are believed to produce an increase in preneoplastic, initiated hepatocytes. Additionally knock out mice will be employed to understand the contribution of various mediators released from activated Kupffer cells in cell proliferation induced by tumor promoters.

4. Evaluating the potential of inhaled 1,3-Dichloropropene (1,3-D) to promote the development of lung tumors in male B6C3F1 mice.

1,3 -D is an agricultural soil fumigant used to control the growth of nematodes. Previous studies have suggested that 1,3-D may function as a tumor promoter.