Description, Causes and Risk Factors:

An acne-like eruption due to occupational contact, by inhalation or ingestion or through the skin, with certain chlorinated compounds (naphthalenes and diphenyls) used as insulators, insecticides, fungicides, and herbicides, including Agent Orange.

Chloracne is a skin condition that looks like common forms of acne that affect teenagers. At present, chloracne is the only well established long-term effect of exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or dioxin, the contaminant found in one of the ingredients of Agent Orange.

It is important to note that skin disorders are among the most common health problems experienced by combat forces. Because of the environment and living conditions, veterans developed a variety of skin problems, ranging from bacterial and fungal infections to a condition known as "tropical acne." However, the only skin disorder consistently reported to be associated with Agent Orange and other herbicides is Chloracne.

The appearance of chloracne and its clinical severity does not correlate with the blood levels of dioxins. Pathogenesis of chloracne remains largely unclear. An "aryl hydrocarbon receptor (AhR)"-mediated signaling pathway affecting the multipotent stem cells in the pilosebaceous units is probably the major molecular mechanism inducing Chloracne.

Most of the effects of TCDD in humans and animals appear to be mediated by the AhR signaling pathway. AhR was previously found to be expressed and activated in human keratinocytes and skin ?broblasts as well as in human sebaceous glands and human immortalized SZ95 sebocytes. In the skin lesions of chloracne patients exposed to dioxin, there was an activation and up-regulation of phosphorylated-epidermal growth factor receptor (p-EGFR), phosphorylated-mitogen-activated protein kinase, and CK17 in all chloracne tissues but not in the controls, while transglutaminase 1 showed distinct distribution patterns. Furthermore, an increase in the dioxin-independent transcriptional activity of the AhR has recently been demonstrated in a Drosophila model to be also responsible for the in vivo dioxin toxicity.

The speci?c histologic changes of chloracne can be rationally explained by the hypothesis based on stem-cell theory. Downstream molecular targets of AhR are versatile including in?uence of classical xenobiotic metabolizing enzymes (such as CYP1A1 and CYP1A2), interleukin-1 beta, TGFs (tumor growth factors), c-Myc, EGFRs, and B lymphocyte-induced maturation protein-1.

The real prevalence of chloracne among Vietnamese civilians & American soldiers caused by Agent Orange (containing phenoxyl herbicide contaminated with dioxins) is unknown. After the World War II, several episodes of large-scale dioxin poisoning (Ludwigshafen/Germany, Amsterdam/Netherlands, Fukuoka/Japan, Seveso/Italy, and Changhua/Taiwan) were reported each with more than 100 victims.



The first sign of chloracne may be excessive oiliness of the skin. This is accompanied or followed by the appearance of numerous blackheads. In mild cases the blackheads may be limited to the area around the eyes extending along the temples to the ears. In more severe cases blackheads may appear in many places on the body, especially over the malar (or cheek bone) area, other facial areas, behind the ears, and along the arms. The blackheads are usually accompanied by fluid-filled cysts and by an increased or darker growth of body hair. The skin may become thicker and flake or peel. In severe cases, the acne may result in open sores and permanent scars. The condition fades slowly after exposure. Minor cases may disappear altogether, but more severe cases may persist for years after the exposure.


Physicians, even dermatologists, sometimes have difficulty in distinguishing chloracne from other more common skin disorders. While chloracne may be a sensitive indicator of exposure to dioxins in some people, it may not be in other individuals who had equal or greater exposure to dioxins.

Histopathology is essential for a definite diagnosis, which exhibits atrophy or absence of sebaceous glands as well as infundibular dilatation or cystic formation of hair follicles, hyperplasia of epidermis, and hyperpigmentation of stratum corneum.


Chloracne is resistant to all the available treatment modalities used to treat acne. The aim of treatment is to lower or to eliminate the accumulated dioxins in the body at the very beginning of intoxication, e.g., by using dioxin-chelating substances such as synthetic dietary fat substitutes. The problem of dioxin contamination and its potential health hazards should be taken seriously in the wave of industrial globalization in the twenty-first century. Clinicians, especially dermatologists, are in the forefront of early diagnosis of dioxin intoxication.

Some individual reports showed that Altinac &Retinova, dermabrasion, and light electrodesiccation may be useful in the treatment of Chloracne.

Recently, a synthetic dietary fat substitute, known as olestra, could bind to chloracnegens and accelerate their fecal excretion. A further study has showed that combined dietary olestra and caloric restriction causes a 30-fold increase in the rate of excretion of labeled compound, which may be a prospective therapeutic method in the future.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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