US EPA

1973937 

Journal Article 

HEXACHLOROBENZENE POISONING IN TURKEY 

Peters, HA 

1976 

Yes 

Federation Proceedings
ISSN: 0014-9446 

FEDERATION AMER SOC EXP BIOL 

BETHESDA 

35 

12 

2400-2403 

English 

823051 

WOS:A1976CF61500018 

http://://WOS:A1976CF61500018
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The epidemic proportions of the hexachlorobenzene induced porphyria are outstanding and demonstrate that the usual genetically determined metabolic lesion can be induced by exposure to organochlorine compounds. The author notes that compounds related to HCB such as 2,4 D and 2,4,5 T are increasingly utilized in our environment and are also capable of inducing porphyria. With human tissue levels of HCB increasing measurably throughout the world, the effect of low chronic doses of these compounds must be considered. Storage in body fat and the transmission of these compounds through maternal milk as exemplified by the Turkish cases of HCB induced porphyria raise questions as to genetic damage to progeny. Peters and coworkers fed HCB to rats and after several days exposed them to ultraviolet light, with the result that hemorrhagic bullae developed over the head, ears, and nose. When other rats were fed HCB plus oral EDTA, they did not demonstrate any response to ultraviolet light challenge. Additional persistence of the induced chemical lesion in Turkish patients with HCB induced porphyria is currently being investigated in Turkey. Future studies of this poisoned population might include evaluation of body iron storage, the effect on uroporphyrinogen synthetase in the blood, and the persistence of the abnormal porphyrin excretion in the urine and feces. The outcome of cirrhotic changes as well as rheumatoid arthritic changes in distal phalanges noted in some patients with HCB induced porphyria should be determined. Finally, the longterm therapeutic effect of chelation therapy on the treated patients with HCB induced porphyria should be of interest.