The action spectra for delayed erythema and melanogenesis in Caucasian human skin are determined for wavelengths between 250 and 435 nm. The untanned skin of very fair volunteers was observed after single exposures to a range of fluences of monochromatic radiation. At wavelengths longer than 300 nm the two action spectra are indistinguishable, and at wavelengths shorter than 300nm. they are of similar shape despite a distinct separation. This suggests a common or similar chromophore for initiation of the vascular and pigmentary responses to UV. A broad minimum in the action spectra occurs near 280 nm, a maximum near 296 nm, and for wavelengths longer than 300 nm, increasingly larger fluences of radiation are required to induce delayed erythema and melanogenesis. Between 304 and 334 nm both action spectra exhibit a rapid decrease of almost three orders of magnitude. In contrast, between 334 and 405 nm the spectra decrease by only one order of magnitude, and there is a suggestion of a small maximum at or near 365 nm. Different chromophores, sites of damage, or response mechanisms may be responsible for induction of delayed erythema at these longer wavelengths. After spectral corrections for the optical effects of the stratum corneum, the shape and magnitude of the action spectra are grossly consistent with a mechanism in which DNA is the primary chrornophore initiating the response pathways for wavelengths less than 313 nm. Whatever the actual basis for these action spectra may be, they are of practical significance in predicting skin response to sources of ultraviolet radiation.

Using a monochromator the action spectrum for ultraviolet phototherapy of psoriasis was determined for radiation between 254 and 313 nm and compared to the action spectrum for erythema of uninvolved adjacent skin. Daily exposures of different doses of 254, 280, 290, 296, 300, 304 and 313 nm radiation were observed. Wavelengths of 254, 280, 290 nm were erythemogenic but not therapeutic even at 10 to 50 times the minimal erythema dose. At the other wavelengths studied, the 2 action spectra were similar. In general, fixed daily doses cleared at lower cumulative dose than did incrementally increased daily doses. The small number of suberythemogenic exposure doses required suggests that monochromatic radiation may have advantages over broadband sources.

The buttock skin of clinically normal human subjects was subjected to approximately 2.5 minimal erythema doses of ultraviolet A irradiation. Deep red erythema developed during irradiation, faded slightly within the next few hours, increased to maximum intensity between 9-15 h, and decreased gradually thereafter although still persisting strongly at 48 h. Suction blister exudates were obtained at 0, 5, 9, 15, 24, and 48 h after irradiation as well as suction blister exudates from a contralateral control site and assayed for arachidonic acid, prostaglandins D2 and E2, and the prostacyclin breakdown product 6-oxo-prostaglandin F1 alpha by gas chromatography-mass spectrometry, and for histamine by radioenzyme assay. Increased concentrations of arachidonic acid and prostaglandins D2, E2, and 6-oxo-prostaglandin F1 alpha were found maximally between 5-9 h after irradiation, preceding the phase of maximal erythema. Elevations of histamine concentration occurred 9-15 h after irradiation, preceding and coinciding with the phase of maximal erythema. At 24 h, still at the height of the erythemal response, all values had returned to near control levels. Hence increased concentrations of arachidonic acid and its products from the cyclooxygenase pathway, and of histamine, accompany the early stages up to 24 h. A causal role in production of the erythema seems likely for these substances although other mediators are almost certainly involved.