This chapter considers the effects of ultraviolet B (UVB) and ultraviolet A (UVA) on normal human skin with regard to clinical manifestations, histopathologic alterations, and biochemical events. The acute responses of normal human skin to ultraviolet irradiation are a form of inflammation. The acute responses can be elicited by ultraviolet C (UVC), UVB, and UVA radiation. Evidence suggests that DNA is the chromophore for erythema induced by UVB; the chromophore for erythema induced by UVA is unknown. UVB, the major source of sunburn erythema, is the most efficient waveband in eliciting erythema in human skin. Cutaneous suction blister aspirates, serum, skin biopsy specimens, and keratinocyte cultures have been used to study inflammatory mediators, cytokines, and adhesion molecules after exposure to UVB. Dyskeratotic cells, characteristic of UVB-induced erythema reactions, were absent. Pigment responses to UVA, but not to UVB, can be abolished by making the skin hypoxic during exposure. UVB radiation causes the epidermis to thicken.