Dioxin-induced chloracne

Industrial workers involved in chlorinated aromatic production including chlorophenol suffered dioxin-induced chloracne 2,3). Chloracne and other serious health disturbances have been attributed to polychloro-dibenzo-p-dioxins in workers involved in manufacturing 2,4,5-T 4, 5). Dioxins are toxic to chick embryos, guinea pigs, rabbits, and monkeys 6, 7, 8, 9, 10). 

Chemical Acne Many chemical compounds induce skin lesions that are similar to acne. Oils, tar, creosote, and several cosmetic products induce chemical acne. These compounds induce keratinization of the sebaceous glands of the skin, obstruction of the glands, and formation of acne. Chloracne is a specific skin lesion that is induced by chemical compounds that are structurally similar to 2,5,7,8-tet-rachloro dibenzo-p-dioxin (TCDD). Chloracne is slow to heal and difficult to... 

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. 

Acne, characterized by skin eruptions commonly known as blackheads or whiteheads plus a variety of pustules, cysts, and pits on the skin surface, can be caused by exposure to chemicals. The most notable kind of chemically induced acne is chloracne, resulting from exposure to chlorinated hydrocarbons. Of these, the most notorious is dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) ... 

In 1956 a chemist synthesized a powerful chloracnegic agent, 2,3,7,8-tetrabromodibenzo-p-dioxin (TBDD). He initially contracted chloracne, a chemically induced acne, after an initial synthesis. The toxicity of this compound was unknown but the chemist did not use a chemical hood or personal protective equipment during this work. Later that same year he synthesized 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and this work resulted in a very severe case of chloracne—he was hospitalized for evaluation and later released. He recovered from the two incidents and was in good health in 1991. At that time the chemist volunteered to have his blood sampled for the measurement of TBDD in the blood sample itself and also in the blood adjusted for its lipid content—an indication of the compound in his fat tissues. The analysis revealed that the concentration of TBDD in blood lipids in 1991 was 625 parts per trillion. The concentration of TCDD in blood lipids was 16 parts per trillion. Based on this observation as well as other measurements, the initial body burden of halogenated dioxins in 1956 was estimated to have been between 13,000 and 150,000 parts per trillion. 

Induction of chloracne in humans after exposure to dioxin and related compounds is supported by studies in laboratory animals. Rabbits, monkeys, and hairless mice have all proved useful in investigating this response. In addition, cellular systems provide a research tool in elucidating the chloracne response at the cellular level. Keratinocytes, the principal cell type in the epidermis, have been used as an in vitro model for studies of TCDD-induced hyperkeratosis, a feature of chloracne, in human- and animal-derived cell cultures. The response in these systems is analogous to the hyperkeratinization observed in vivo as a part of chloracne [181]. 

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