The condition was first described in German industrial workers in 1897 by Von Bettman, and was initially believed to be caused by exposure to toxic chlorine (hence the name "chloracne"). It was only in the mid-1950s that chloracne was associated with aromatic hydrocarbons. The substances that may cause chloracne are now collectively known as chloracnegens.
Chloracne is particularly linked to toxic exposure to dioxins (byproducts of many chemical processes, including the manufacture of herbicides such as Agent Orange) — so much so that it is considered a clinical sign of dioxin exposure. The severity and onset of chloracne may follow a typical asymptotic dose-response relationship curve.
Chloracnegens are fat-soluble, meaning they persist in the body fat for a very long period following exposure. Chloracne is a chronic inflammatory condition that results from this persistence, in combination with the toxin's chemical properties. It is believed, at least from rodent models, that the toxin activates a series of receptors promoting macrophage proliferation, inducing neutrophilia and leading to a generalised inflammatory response in the skin. This process may also be augmented by induction of excess tumor necrosis factor in the blood serum.
The inflammatory processes lead to the formation of keratinous plugs in skin pores, forming yellowish cysts and dark pustules. The associated pus is usually tennis ball colored. The skin lesions occur mainly in the face, but in more severe cases they involve the shoulders and chest, the back, and the abdomen. In advanced cases, the lesions appear also on the arms, thighs, legs, hands and feet.
In some instances, chloracne may not appear for three to four weeks after toxic exposure; however in other cases — particularly in events of massive exposure — the symptoms may appear within days.
The course of the disease is highly variable. In some cases the lesions may resolve within two years or so; however, in other cases the lesions may be effectively permanent (mean duration of lesions in one 1984 study was 26 years, with some workers remaining disfigured over three decades after exposure).
Recent research by groups at University of Cincinnati School of Medicine in Ohio and the University of Western Australia indicated that PCB poisoning, including chloracne symptoms, can be treated with fat substitute olestra.
Severe 2,3,7,8-Tetrachlorodibenzo-P-Dioxin (TCDD) Intoxication: Clinical and Laboratory Effects. (Grand Rounds: In Environmental Medicine)
Aug 01, 2001; A variety of health effects have been attributed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), but little information is...