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The wavelength dependence for UVA-induced cumulative damage was investigated in human skin. Epidermal changes (stratum corneum thickening, viable epidermal thickening sunburn cell production), as well as dermal alterations (lysozyme deposition, inflammation), were used as indices of cumulative photoperturbation. UVA wavelengths between 320 nm and 345 nm were more effective than longer wavelengths (360-400 nm) in inducing viable epidermal thickening. Similarly, the shorter wavelengths (320-345 nm) elicited more sunburn cells, although these differences did not reach statistical significance. All UVA bands were equally effective in inducing the dermal markers. At equal fluences, wavelengths > 400 nm produced no measurable cutaneous alterations. These findings suggest that (i) chronic epidermal and dermal damages have different spectral dependence and (ii) the action spectrum for dermal damage in the UVA is broad, extending up to 400 nm, and is different from the acute erythema spectrum in humans.

Daily exposures to relatively small suberythemogenic fluences of UVA (50-200 kJ/m2) for 8 days resulted in cumulative morphological skin alterations indicative of early tissue injury. Histologically, irradiated skin revealed epidermal hyperplasia, inflammation and deposition of lysozyme along the dermal elastic fiber network. Sunburn cells were also present within the epidermis. These changes were quantified by image analysis and were found to be related to the cumulative UVA fluence. A long UVA waveband (UVAI, 340-400 nm) was as effective as a broad UVA band (320-400 nm), suggesting that these changes are induced by longer UVA wavelengths.