Sunburn and mechanisms of protection 33 Figure 1. Action spectrum for just perceptible erythema in fair-skinned human subjects back skin, readings at 7-8 and 24 h. The 100K level at 260 nm represents a mean MED of 4.3 mJcm -•, standard deviation 1.4. 100, 250 260 2,0 2[0 go ' 310 WAVELENGTH (rim) monochromator (Rank-Hilger, D330 with D335 grating) with a 450 W Xenon arc source (Osram, XBO 450 W). The half-maximum bandwidth used was 2.6 nm, giving minimal dispersion around the selected wavelength. Readings of the reactions were made at 7-8 h and 24 h after the exposures. The minimum dose required to produce a reaction, whether observed at 7-8 h or 24 h, was taken as the minimal erythema dose (MED). The action spectrum is plotted from the reciprocal of the MED at each wavelength and is a relative effectiveness curve. It is typical of the various action spectra published in the past (3) and resembles those of Cripps and Ramsay (16) and Nakayama et al. (17). Problems have arisen with regard to the shape of the action spectrum in the wavelength region below 285 nm which were foreshadowed in the work of Hausser and Vahle (18). In the action spectra published before that of Everett, Olson and Sayre (19) the wavelength region around 260 nm, although shown to have a peak of activity, was less effective than the 290-nm region. Where the reaction observed is a minimally perceptible erythema, it is obvious from Fig. I that the shorter wavelengths are, in fact, more effective. Moreover, the trough in the action spectrum at 280 nm is much deeper in the earlier publications. Explanations for these discrepancies were proposed by Everett et al. (19) and by Berger, Urbach and Davies (20) and these are elegantly discussed by Leun (21). A minimal erythema produced by 260-nm radiation may develop by 8 h but fade before 24 h. Thus, for erythema readings at 24 h only, a higher dose is required for the shorter wavelengths' reactions and the activity of this wavelength region will appear to be relatively low. More- over, the gradation of erythema redness produced by the two wavelength regions with increasing dose is different. While the intensity of the 260-rim reaction increases slowly and reaches a low plateau level, that for longer wavelengths increases rapidly to a much higher plateau level. If some degree of erythema other than the minimally perceptible is chosen as the end point for plotting an action spectrum, as was the case in the earlier studies, the longer wavelengths will again appear to be more effective. The trough in the action spectrum at 280 nm has always been ascribed to the filtering effects of the stratum corneum. This may be true as the trough is deeper in action spectra obtained with forearm skin with a relatively thick corneum, than in those obtained with back skin. The prolonged arguments about the effects of uvr wavelengths not present in natural sunlight may appear superfluous. However, these shorter wavelengths are a prominent part of uvr photobiology, particularly in the investigations of cellular mechanisms of uvr damage. Nucleic acids have major absorption peaks in this wavelength region as do proteins through the aromatic amino acid constituents. Also, the total action spectrum

34 B. oe. Johnson for erythema has allowed interesting theoretical treatments of the mechanisms involved in the sunburn reaction (22, 13). Leun (13) concludes that the uvr erythema is brought about by a dermal reaction to all effective wavelengths, the shorter wavelengths being more active, and that a more superficial reaction to the 290-300 nm region results in the formation of a diffusible mediator for erythema, this action being superimposed upon the dermal one to produce a double peak action spectrum. Although most of the incident radiation between 250 and 320 nm is absorbed in the epidermis, at least 1 •o may reach the dermis (23). The penetration of the longer uvr wavelengths is significantly greater than that of the 260-nm region and it appears more likely that the shorter wavelengths would act at a more superficial level. However, the theoretical treatment of uvr erythema published by Leun (13), Ramsay and Challoner (24) notwithstanding, has not been re- pudiated and at this time, the mechanisms suggested fit well with the majority of the experimental data. All the published action spectra show similar features for uvr beyond 290-295 nm, i.e. a rapid fall off in effectiveness so that for all practical purposes, 320 nm and longer wavelength radiation are ineffective, confirming the filtering action of window glass. As the intensity of uvr in natural sunlight falls rapidly from 330 nm to almost zero at 290 nm, the most active wavelength region in natural sunlight will be at a higher value than that shown in Fig. 1. Schulze (25) has computed the most effective wavelength as around 307 nm using the data of a 'standard' erythema action spectrum and the solar radiation measurements of Bener (26). This peak of effectiveness would be moved further into the long-wavelength uvr in geographical locations in which a more rapid fall-off of intensity with decreasing wavelength occurs. As the gradation of severity of reaction increases so markedly with increasing dose at these wavelengths, it is not surprising that a severe sunburn may result from exposure to natural sunlight which appears to be very little beyond a minimal erythema dose. In fair-skinned individuals in Dundee, latitude 56.5N, back skin exposed to 20 min of mid-day June sunlight may show no reaction. A 30-min exposure, however, may resbit in an intense erythema accompanied by tender- ness and oedema. MECHANISMS FOR THE REACTIONS Erythema is the most easily observed component of the sunburn reaction and has there- fore been the most ardently studied. Mild erythema is a manifestation of vasodilatation in the superficial venous plexus of the papillary dermis. More intense erythema, accom- panied by increased skin temperature, reflects arterial and arteriolar dilatation and increased blood flow (24, 27). With very high doses of uvr, vascular stasis may occur (28). Despite the intensive studies of the reaction, the nature and location of the primary molecular target for uvr damage to skin remain unknown. A direct effect of uvr on isolated blood vessels has been described (29) but the immediate contraction observed seems to have little relevance for the delayed onset, persistent erythema observed in irradiated skin. The effects of direct damage to blood vessels in the skin are seen in the photosensitised reac- tion obtained in the disease Erythropoietic Protoporphyria in which excess protopor- phyrin production in the red blood cells leads to abnormal skin reactions to 400-rim radiation. The vascular endothelium is partially destroyed and perivascular deposits of a mucoid substance are laid down as the endothelium is repaired (30). There is no evidence of a similar process in the sunburn reaction and only when excessively high doses of uvr, in particular uv-A, are used, is endothelial damage observed (31).