Is 2,3,7,8-TCDD (dioxin) a carcinogen for humans?

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has suddenly become the focal point of controversy over the relationship of chemical waste to human health. Specific concern exists regarding its potential association with human malignancy. Subcellular, cellular, and whole-animal experiments suggest that TCDD exerts much of its activity by inducing enzymes that protect the intact organism from the assault of environmental contamination. TCDD is a potent inducer of aryl hydrocarbon hydroxylase, although wide variations between species do exist. Conventional tests for mutagenicity have produced conflicting results. Animal experiments have shown the development of tumors following chronic low level ingestion of TCDD. The human evidence regarding the potential carcinogencity of TCDD comes from occupational, military and environmental exposures. Several studies have come out of Sweden suggesting an association between sarcoma and exposure to herbicides. Although there is little solid evidence that 2,3,7,8-TCDD produces substantial chronic disability or premature death in man, a significant body of experimental evidence for its carcinogenicity makes it likely that a small number of human malignancies may be due to its action. Since 2,3,7,8-TCDD is an unwanted contaminant it could be eliminated with little measurable consequence.

Molecular Probes, Chemosensors, and Nanosensors for Optical Detection of Biorelevant Molecules and Ions in Aqueous Media and Biofluids

“…962 TCDD is a known human carcinogen and a potent endocrine disruptor that has a long half-life in humans due to its lipophilicity. 963,964 Common examples of man-made water pollution come from the textile, cosmetics, leather, food, pharmaceutical, paint, and paper industries. Many toxic dyes such as methylene blue, rhodamine B, methyl orange, congo red, methyl red, and crystal violet, used by these industries often end up, accidentally or not, in freshwater.…”

“…The “Seveso disaster” is a well-known case of man-made pollution in which a polychlorinated dibenzo- p -dioxin, namely 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), was released into the air and soil as a result of a factory explosion . TCDD is a known human carcinogen and a potent endocrine disruptor that has a long half-life in humans due to its lipophilicity. , Common examples of man-made water pollution come from the textile, cosmetics, leather, food, pharmaceutical, paint, and paper industries. Many toxic dyes such as methylene blue, rhodamine B, methyl orange, congo red, methyl red, and crystal violet, used by these industries often end up, accidentally or not, in freshwater .…”

How the AHR Became Important in Cancer: The Role of Chronically Active AHR in Cancer Aggression

“…By 1974, it was known that mice of disparate genetic backgrounds exhibited different sensitivities to the environmental chemical 2,3,7,8-tetrachlorodibenzo(p)dioxin (TCDD) and that these differences were likely due to polymorphisms in this unidentified “induction” receptor [ 4 , 5 , 6 ]. With mounting evidence that TCDD is a type 1 carcinogen in animals and humans [ 7 , 8 ] came the realization that the carcinogenicity of at least some environmental chemicals might not require mutagenesis but might be by this postulated receptor. With the biochemical purification in 1988 of the aryl hydrocarbon receptor (AHR) [ 9 ], the sequencing in 1991 of the AHR’s highly conserved N-terminal sequence [ 10 ], and the cloning of the AHR gene in 1992 [ 11 , 12 ], came a better understanding of the AHR’s environmental ligand reactivity and its contribution to the induction of hydroxylases that generate mutagenic intermediates.…”