Environment and Breast Cancer: Science Review
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This article is not a primary breast cancer epidemiology research report. It is provided as a supplementary resource for interpreting the epidemiological literature.
Dioxin revisited: developments since the 1997 IARC classification of dioxin as a human carcinogen
Steenland, K., Bertazzi, P., Baccarelli, A., Kogevinas, M. Environ Health Perspect. 2004. 112:13, 1265-8.
Topic area
Environmental pollutant - Dioxin
Environmental pollutant - Dioxin
Study design
Review
Review
Abstract
In 1997 the International Agency for Research on Cancer (IARC) classified 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; the most potent dioxin congener) as a group 1 carcinogen based on limited evidence in humans, sufficient evidence in experimental animals, and extensive mechanistic information indicating that TCDD acts through a mechanism involving the aryl hydrocarbon receptor (AhR), which is present in both humans and animals. The judgment of limited evidence in humans was based primarily on an elevation of all cancers combined in four industrial cohorts. The group 1 classification has been somewhat controversial and has been challenged in the literature in recent years. In this article we review the epidemiologic and mechanistic evidence that has emerged since 1997. New epidemiologic evidence consists primarily of positive exposure-response analyses in several of the industrial cohorts, as well as evidence of excesses of several specific cancers in the Seveso accident cohort. There are also new data regarding how the AhR functions in mediating the carcinogenic response to TCDD. The new evidence generally supports the 1997 IARC classification.
In 1997 the International Agency for Research on Cancer (IARC) classified 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; the most potent dioxin congener) as a group 1 carcinogen based on limited evidence in humans, sufficient evidence in experimental animals, and extensive mechanistic information indicating that TCDD acts through a mechanism involving the aryl hydrocarbon receptor (AhR), which is present in both humans and animals. The judgment of limited evidence in humans was based primarily on an elevation of all cancers combined in four industrial cohorts. The group 1 classification has been somewhat controversial and has been challenged in the literature in recent years. In this article we review the epidemiologic and mechanistic evidence that has emerged since 1997. New epidemiologic evidence consists primarily of positive exposure-response analyses in several of the industrial cohorts, as well as evidence of excesses of several specific cancers in the Seveso accident cohort. There are also new data regarding how the AhR functions in mediating the carcinogenic response to TCDD. The new evidence generally supports the 1997 IARC classification.
Author address
Rollins School of Public Health, Emory University, Atlanta, Georgia 30306, USA. nsteenl@sph.emory.edu
Rollins School of Public Health, Emory University, Atlanta, Georgia 30306, USA. nsteenl@sph.emory.edu