Lone Tree Council Meeting

Monday, November 17th, 2003

7pm GreenPoint Nature Center For all the news and updates on Dow Chemical's contamination of our watershed.

At Monday's meeting we will be showing a video by Dr. Linda Birnbaum, EPA, world renowned expert on the human health effects of dioxin.

Environmental Health Perspectives Volume 111, Number 4, April 2003

[ Citation in PubMed ] [ Related Articles]

Cancer and Developmental Exposure to Endocrine Disruptors

Linda S. Birnbaum1 and Suzanne E. Fenton2

1Experimental Toxicology and 2Reproductive Toxicology Divisions, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USAAbstract
Developing organisms have increased susceptibility to cancer if they are exposed to environmental toxicants during rapid growth and differentiation. Human studies have demonstrated clear increases in cancer after prenatal exposure to ionizing radiation, and there is suggestive evidence that brain tumors and leukemia are associated with parental exposures to chemicals. Animal experiments have demonstrated increased tumor formation induced by prenatal or neonatal exposure to a variety of chemicals, including direct-acting carcinogens and drugs. Recently, natural estrogens have been classified as known human carcinogens. Prenatal exposure to natural and synthetic estrogens is associated with increases in breast and vaginal tumors in humans as well as uterine tumors in animals. Synthetic halogenated chemicals increase liver tumors after early life-stage exposure. Recently, a prototypical endocrine-disrupting compound, 2,3,7,8-tetrachlorodibenzo-p-dioxin, has been shown to be a developmental toxicant of the mammary gland in rodents. Dioxin alters multiple endocrine systems, and its effects on the developing breast involve delayed proliferation and differentiation of the mammary gland, as well as an elongation of the window of sensitivity to potential carcinogens. Implications of these new findings suggest that causes of endocrine-related cancers or susceptibility to cancer may be a result of developmental exposures rather than exposures existing at or near the time of tumor detection. Key words: animal models, atrazine, carcinogenesis, childhood cancers, development, dioxin, endocrine disrupters.