2,3,7,8-TCDD - A POTENT AND COMPLETE CARCINOGEN IN EXPERIMENTAL-ANIMALS

Long-term carcinogenesis studies using laboratory animals exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) have shown conclusively that this chemical is a complete carcinogen. In a series of independent studies from the first reported in 1977 to the latest in 1988, TCDD has consistently induced cancers in a variety of organs and systems. TCDD-induced neoplastic lesions occurred in each of 18 individual sex-species experiments. In rats, TCDD induced neoplasms in lung, oral/nasal cavities, thyroid and adrenal glands, and liver. In mice, TCDD caused neoplasms in the liver, subcutaneous tissue, thyroid gland, lung, and lympjopoietic system (lymphomas). In hamsters, TCDD produced squamous cell carcinomas of the facial skin. TCDD is a trans-species (rat, mouse, and hamster), trans-strain (Sprague-Dawley and Osborne-Mendel rats; B6C3F1, Swiss-Webster, and B6C mice), trans-sex, multi-site, complete carcinogen. The most potent of the identified chemical carcinogens, TCDD induced carcinogenic effects in laboratory animals with exposures as low as 0.001 ug/kg body weight/day. Proposed mechanism(s) of TCDD-induced carcinogenesis have yet to account for the many relatively rare types of tumors observed in exposed animals. In two-stage liver or skin models, TCDD exhibits considerable tumor promotion activity. With respect to carcinogenic hazards to humans, these experimental data alone indicate that TCDD should be considered for practical and public health purposes as being likely to be carcinogenic to humans; this species extrapolative conclusion gains growing support from epidemiological studies showing clear associations between exposure to dioxin and increases in cancers of the respiratory system (particularly lung), soft-tissue sarcomas, and total cancers. Other risks appear to be elevated for cancers of the testicle, thyroid gland, and other endocrine glands, largely in workers exposed to chlorophenoxy herbicides. Thus, using the collective experimental and epidemiological evidence, the prudent course of action would be to minimize to the greatest extent possible all potential exposures to this and other dioxins as well as to phenoxyacid herbicides, and where technologically and argiculturally feasible exposures should be eliminated.