Received for publication March 5, 2001, and accepted for publication September 13, 2001. Abbreviations: EPA, US Environmental Protection Agency; NIOSH, US National Institute for Occupational Safety and Health; 2,4,5-T, trichlorophenoxyacetic acid; 2,3,7,8-TCDD, tetrachlorodibenzo-p-dioxin; VA, US Department of Veterans Affairs. 1 ENVIRON International Corporation, Arlington, VA. 2 Solutia Inc., St. Louis, MO. 3 National Center for Environmental Assessment, US Environmental Protection Agency, Washington, DC. 4 Center for Environmental and Occupational Health, School of Public Health, MCP Hahnemann University, Philadelphia, PA. Correspondence to Dr. Joseph Rodricks, ENVIRON International Corporation, 4350 N. Fairfax Drive, Suite 300, Arlington, VA 22203 (e-mail: jrodricks@environcorp.com). Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8TCDD)) and related congeners (polychlorinated dibenzo-pdioxins, referred to generally as dioxins) are among the most widely known and perhaps feared environmental contaminants. The laboratory findings of extreme potency of dioxin as a carcinogen and its documented widespread presence in the environment have raised concern that it contributes to the population’s burden of cancer. As understanding of dioxin’s interactions with cells has grown, the list of possible health effects has expanded (1). Risks of dioxin exposure have been presented to the public in dramatic ways— its potency as a carcinogen, the evacuation of Times Beach, Missouri, and the exposure of the military in Vietnam to dioxin-contaminated defoliants—and it has become one of the most feared environmental carcinogens as a result. The resulting need to characterize the risks of dioxin for risk management purposes has challenged laboratory scientists and epidemiologists. Following the observation that dioxin is extremely potent in animal bioassays, researchers turned to finding the mechanism for its action. Dioxin is now thought to be toxic through its interaction with the aryl hydrocarbon (Ah) receptor, raising the possibility that it may increase risk for cancers of multiple sites and for other diseases through this mechanism (2). Complementary support for dioxin as a human carcinogen has been sought using epidemiologic approaches with two broad purposes: 1) validating the animal findings for carcinogenicity; and 2) quantifying the exposure-response relation. Human data on quantitative cancer risk have been needed to address the uncertainty inherent in using exposure-response estimates from animal studies in quantitative risk assessment. The epidemiologic evidence has been considered in several distinct policy-making settings in the United States and elsewhere. This case study focuses on two: the use of epidemiologic evidence in quantitative risk assessment and its use in identifying conditions for compensation among veterans exposed to herbicides in the Vietnam conflict. The limited role played by epidemiologic findings in the fashioning of current regulatory and public health policies contrasts sharply with the approach for compensation of Vietnam veterans for adverse health effects associated with their exposures to the dioxin-containing herbicide Agent Orange. For this exposure, the committees formed by the Institute of Medicine, National Academy of Sciences to assess the scientific evidence on Agent Orange chose to focus on the epidemiologic data, as they were mandated to determine if associations could be found with adverse outcomes (3).
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