In the currently accepted concept of porphyria cutanea tarda (PCT), the disease is classified into two types: an acquired type which follows liver damage, and an hereditary type which appears in younger individuals, presumably without exposure to hepatotoxic substances. However, the validity of this classification has not been determined conclusively.
Awareness of the number of substances capable of inducing PCT by impairing liver function has been growing steadily; barbiturates, alcohol, allylisopropylacetylcarbamide (Sedormid), lead, and griseofulvin are but a few. In 1959 and 1960 an epidemic of PCT in Turkey, which affected thousands of individuals, resulted from ingestion of wheat pretreated with hexachlorobenzene, commonly used on seed wheat because of its fungicidal action.
In the June issue of the Archives of Dermatology1 Bleiberg et al report an outbreak of chloracne and PCT among workers in a factory which manufactures herbicides. Of 29 patients exhibiting features of chloracne, 11 were excreting