PHOTOSENSITIVITY 87 Of the newer sulfonamide derivatives, the diuretics and oral hypo- glycemic sulfonamides are capable of producing an appreciable number of photosensitivity reactions. In some instances, chemically related compounds, such as the local anesthetics (procaine group), hair dye components, such as p- phenylene diamine, and the drug and sunscreen, p-aminobenzoic acid, will induce photosensitivity reactions. Moreover, the same patient, because of cross-sensitivity mechanisms, may show photosensitization to all of these. Derivatives are also potentially active, as for example, monoglycerol p-aminobenzoate (5). Demethylchlortetracycline (Declomycin), a member of the tetra- cycline family, produces reactions in as high as 25% of users exposed to sunlight. In a clinical study by Cahn and Levy (6), 600 mg. daily re- sulted in an incidence of 15-25% phototoxicity 450 mg. daily resulted in 3% reaction, while 300 mg. resulted in 0-1% reaction. This observation is important since in phototoxic reactions the chemical not only must be present in the skin but must be present in adequate concentration, for even great amounts of sunlight would not produce phototoxicity in pa- tients having less than threshold concentration of drug. Of paramount interest to the cosmetic chemist is the effect of certain topical agents in producing photosensitivity. If the agent is of plant origin, a variety of names may be found in the literature to confuse the issue, such as "perfume" dermatitis, Berloque dermatitis, meadow grass dermatitis, phytophotodermatitis, fig dermatitis, and dermatitis bullosa striata pratensis. The photosensitizers are furocoumarins, of which there are more than 20 naturally occurring derivatives (5). These sub- stances are used in many perfumes and colognes and, after being exposed to sunlight on the skin, may initiate the development of patchy areas of redness and blistering, with subsequent scaling and hyperpigmentation. The eruption usually appears about the face and neck, symmetrically distributed. Photosensitization is caused by radiation between 3100 and 3700 A (7). Promethazine hydrochloride (Phenergan) may cause photosensitiza- tion when topically applied or ingested (8). Coal tar has long been noted for its photosensitizing properties when applied to the skin. The ability of coal tar to photosensitize is of appreciable consequence in in- dustrial medicine. Workers coming into contact with the crude tar or its distillates frequently develop varying degrees of reaction on the af- fected skin surfaces, with a marked tendency to develop hyperpigmenta-

88 JOURNAL OF THE SOCIETY OF COSMETIC CHEMISTS tion. This sensitizing principle is used in the Goeckerman treatment of psoriasis, employi•_g coal tar and an ultraviolet lamp or natural sunlight. The sensitizing ra•_ge is 3900 to 5000 A. Sunscreens may act as photosensitizers in man, and it has been proven that monoglycerol p-aminobenzoate could be a contact photo- sensitizer (9). Other reports have followed, describing the esters of p-aminobenzoic acid as photosensitizers. Later, it was noted that the sunscreening preparation digallolyl trioleate could sensitize the skin to ultraviolet light (10). Recently, a persistent light reactor was found to have positive photopatch tests to both of these agents (11). Certain antiseptics may produce photosensitivity reactions. Four well-known bactericidal agents are tetrachlorosalicylanilide (TCSA), bithionol, tribromosalicylanilide (TBS), and hexachlorophene. Contact and contact photodermatitis from TCSA has occurred in hundreds of in- dividuals (12). Recently, the bactericidal agent bithionol used in a number of soaps, shampoos, cosmetics, and acne preparations was found to be a contact photosensitizer. TBS is rarely a primary contact photosensitizer, and as yet hexachlorophene has not been proved to be a primary contact photosensitizer. However, cross-sensitization may exist between all of these antiseptic agents (12-15). 8. Photoallergy represents a qualitatively altered reaction to specific bands of light, as a rule in the sunburn spectrum. These imply an antigen-antibody reaction, therefore an incubation period. Certain drugs (ingested) may cause an eczematous, urticarial, or papular re- sponse after exposure to sunlight, for example, sulfonamides, gold, and quinidine and some phenothiazine derivatives. There is also a class of patients who have chronic polymorphous light eruption, a disease char- acterized by papular and plaque-like dermatitis of exposed parts of the body, occurring each spring and summer after exposure of sunlight and resembling lupus erythematosus clinically (16). What is the role of porphyrins in sensitizing the skin to sunlight? Photosensitization by the porphyrins is produced by wavelengths of light between 3000-4500 A principally and to a lesser extent by visible radia- tions extending to about wavelength 6500 A. Except in the disease porphyria, either the erythropoietic or the hepatic type, it has not been shown that the porphyrins have a role in any of the other skin diseases associated with sunlight sensitivity.