Chloracne polychlorinated biphenyls causing

TCDD is the most potent inducer of chloracne. This has been well known since the accident in Seveso, Italy, in 1976 in which large amounts of TCDD were distributed in the environment subsequent to an explosion in a factory that produced a chlorophenoxy herbicide, 2,4,5-T. TCDD is an impurity produced during the production of 2,4,5-T. The most common long-term effect of TCDD exposure was chloracne. Exposed individuals also suffered increased excretion of porphyrins, hyper-pigmentation, central nervous system effects, and liver damage and increased risk of cancer was a long-term consequence of the exposure. In addition to TCDD, polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans, and polychloronaphthalens cause chloracne as well as other effects typical of TCDD. 7i... 

Chloracne was first reported by Von Bettman in 1897. In 1899, Herxheimer used the term chloracne to describe four cases of severe acne resulting from environmental contact with electrolytically produced potassium hypochlorite. Since that time, various chloracnegenic chemicals have been identified. Chlo-ronapthalenes and polychlorinated biphenyls (PCBs) were the causative agents in the pre-World-War-II era. Since then, trace contaminants formed during the manufacture of PCBs and other polyhalogenated compounds, especially herbicides, have been the major causes of chloracne. These include polyhalogenated dibenzofurans, polychlorinated dibenzo-p-dioxins and chlorinated azo- and azoxy benzenes. 

Dioxins are prominent members of the class of polychlorinated hydrocarbons that also includes diben-zofuran, biphenyls and others. Dioxins are highly toxic environmental contaminants. Like others small planar xenobiotics, some dioxins bind with high affinity to the arylhydrocarbon (Ah) receptor. Dioxins activate the receptor over a long time period, but are themselves poor substrates for the enzymes which are induced via the Ah-receptor. These properties of the dioxins and related xenobiotics may be important for the toxicity of these compounds. Dioxins like 2,3,7,8-tetrachloro-p-dibenzodioxin can cause persistent dermatosis, like chloracne and may have other neurotoxic, immunotoxic and carcinogenic effects. 

Although drugs such as acetaminophen bind to AhR, the majority of AhR agonists or antagonists are environmental chemicals. Polychlorinated diben-zodioxins such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), dibenzofu-rans, biphenyls, and a number of other chemicals are widespread pollutants in aquatic ecosystems. These compounds cause a high reproductive and developmental toxicity, which is mediated via binding to the AhR. Thus they pose a serious threat to many populations of mammals, birds, and fish. Various adverse effects—including structural malformations, reduced fertility, tumor promotion, immunotoxicity, and skin disorders like chloracne—have been observed [139]. 

---