Ruth H. Allen,1 Michelle Gottlieb,2 Eve Clute,3 Montira J. Pongsiri,4 Janette Sherman,5 and G. Iris Obrams1
1Extramural Epidemiology and Genetics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland; 2Health, Environment, and Development Program, World Resources Institute, Washington, DC; 3School of Public Health, University of Hawaii, Honolulu, Hawaii; 4School of Forestry and Environmental Studies, Yale University, New Haven, Connecticut; 5Department of Sociology, Western Michigan University, Kalamazoo, Michigan
Only 30% of all breast cancer can be explained by known risk factors. Increases in breast cancer incidence rates in Hawaii over the past few decades cannot be attributed solely to improvements in screening and detection. Avoidable environmental factors may contribute to a proportion of the unexplained cases. Emerging evidence on endocrine disruption suggests that environmental chemicals may play a role in the development of breast cancer. Agricultural chemicals, including endocrine disruptors, have been used intensively in Hawaii's island ecosystem over the past 40 years leaching into groundwater, and leading to unusually widespread occupational and general population exposures. This paper discusses breast cancer patterns in Hawaii in the context of documented episodes of exposure to two endocrine-disrupting chemicals, chlordane/heptachlor and 1,2-dibromo-3-chloropropane (DBCP), at levels that sometimes exceeded federal standards by several orders of magnitude. In light of this history, detailed geographic-based studies should be undertaken in Hawaii to elucidate the potential role of environmental factors in the development of breast cancer and other diseases. -- Environ Health Perspect 105(Suppl 3):679-683 (1997)
Key words: breast cancer, exposure assessment, Hawaii, endocrine disruption, chlordane/heptachlor, DBCP
This paper was presented in part at the Workshop on Hormones, Hormone Metabolism, Environment, and Breast Cancer held 28-29 September 1995 in New Orleans, Louisiana. Manuscript received at EHP 22 July 1996; manuscript accepted 18 December 1996.
This research was supported by pilot funds from the Long Island Breast Cancer Study Project (LIBCSP) and a Greater Leadership Opportunity (GLO) Program Award to RHA. The GLO Award from the U.S. Environmental Protection Agency, Office of Pesticide Programs, during 1994 to 1995 enabled R.H. Allen to work at the National Cancer Institute, under the general direction of G.I. Obrams, Director, Extramural Epidemiology and Genetics Program, Division of Cancer Epidemiology and Genetics, and Director, LIBCSP. A grant from the Jennifer Altman Fund partially supported this work.
Address correspondence to Dr. R.H. Allen, Extramural Epidemiology and Genetics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6130 Executive Boulevard., Room 531N, Bethesda, MD 20892-7105. Telephone: (301) 496-1609. Fax: (301) 402-4279. E-mail:allenr@epndce.nci.nih.gov
Abbreviations used: DBCP, 1,2-dibromo-3-chloropropane; DD, mixture of 1,3-dichloropropene and 1,2-dichloropropane; hER, human estrogen receptor; PCBs, polychlorinated biphenyls; Telone, 1,3-dichloropropane.
Last Update: April 10, 1997