The epidemiological pattern of chloracne has changed much since the first cases occurred in the early years of the twentieth century when they arose from the manufacture of chlorine and hydrochloric acid by an electrolytic process in tar-lined towers. During the 1920s, the predominant causes  were halogen waxes, mixtures of chlorinated  naphthalenes  and biphenyls  which  had many industrial applications.  During the Cutaneous manifestations Chloracne  The distribution of chloracne lesions is of diagnostic  importance.  The  most sensitive areas are below and to the outer side of and behind the ear; these may show persistent lesions years after more extensive chloracne has faded. The cheeks, forehead and neck are also  frequently involved and the genitalia, both penis and  scrotum,  are sensitive regions. With increasing toxicity and exposure  the lesions  affect other sites. Axillary lesions  are only commonly seen in those patients where ingestion is the only,  or major, route of absorption.

  The basic lesion of chloracne is the comedone and, in the least severe examples, these may be the only lesions present . In all but the mildest cases small, pale  yellow cysts, from pinhead to lentil size  mingle  with  the  comedones  and, in  the worst cases,  comedones - some no larger than pinpoints  may involve every follicle.

  In the most severe cases inflammatory lesions begin to appear and with them the  larger cysts  come to resemble that of severe cystic acne but with much less inflammation. However some, at times extensive, scarring may arise .  Such gross lesions are most often seen on the back of the neck, trunk and buttocks.

  While most cases have  cleared within  four years, some of the severest may still have lesions present after thirty years but  usually only in the  malar  region and behind the ears.

  Histological examination reveals eventual disappearance of the sebaceous glands due to squamous metaplasia of sebaceous-forming cells.

  Scarring, absent in the mildest cases, varies  from a fine  pitting, like atrophoderma vermiculata,  to extensive  lesions of the sort following severe cystic acne. Pigmentation  Pigmentation   is  largely confined to the face but may, in the worse cases, extend more widely and so severely as to cast  doubt  upon the patient's racial origin.

Hypertrichosis and follicular hyperkeratosis  Hypertrichosis and follicular hyperkeratosis, which are rare, may be secondary to the hepatic porphyria caused by TCDD. Erythema   The   temporary  erythematous  changes which may occasionally be associated with the onset of chloracne  have been the subject  of confusion in the literature and  wrongly ascribed to  photosensitivity. Hyperhidrosis, mainly of the palms  and soles, is rare. Ophthalmic changes Conjunctivitis, usually mild, has  often been noted in severe poisoning with chloracnegens but has only been seen in an extreme  form in Japanese victims whose meibomian glands were converted into squamous cysts filled with a cheesy keratinous material. Systemic effects Hepatic changes  Liver damage does occur uncommonly. This is usually related to dose  and route of absorption. Lipid and porphyria metabolism changes   Cholesterol levels, although variable,  are usually normal as are high-density lipoprotein  cholesterol levels.

The only consistent abnormality in human subjects is  a raised triglyceride level  which may be  due to  a  decrease in removal of  plasma triglyceride  or to a decrease in plasma  lipoprotein lipase activity.  Porphyria of the hepatic type has  been  described only twice so far in human poisoning, each time from TCDD. Pulmonary symptoms   Acute pulmonary changes are frequent and persistent bronchitis may be a feature. Neurological symptoms   The reported  symptoms of central nervous system involvement are subjective and so  are difficult to evaluate,  but  a  combination  of headache, fatigue, irritability, insomnia, impotence and loss of libido have  occurred. Peripheral neuritis is uncommon but may cause lower limb pains of disabling severity. Carcinogenicity  Well-controlled lifetime feeding studies on rats and mice with  TCDD  and  the two most toxic hexachlordioxin isomers have revealed that malignant tumours can be induced.  Skin painting suggested that ioxins may be complete carcinogens, i.e. initiators and promotors. Mortality In the more recent  episodes, mortality is  extremely uncommon. The  actual  cause  of  death  from chloracnegens is  unknown, but even when the  minimum lethal dose is greatly increased, the time to date, e.g. 14-21 days, remains unchanged.