Abnormal dermal deposition of elastic fibers is the earliest and most striking effect of prolonged sun exposure (solar elastosis). The hyperplastic fibers are usually ascribed to ultraviolet (UV) rays. Nonetheless, other portions of the solar spectrum may play contributing roles. Heat, for example, enhances experimental UV tumorigenesis. Heat induces erythema ab igne in which the structural alterations resemble those of actinically damaged skin, including the development of premaligant and malignant lesions. In regions of high insulation, infrared radiation (IR) is a constant companion of UV. To assess the role of IR in actinic damage to the dermis, albino guinea pigs were irradiated for 45 weeks with UV-B and UV-A, with and without IR. Control animals received IR only or no irradiation at all. Unirradiated dermis contains small amounts of elastic fibers in the upper dermis with greater depositions around follicles and sebaceous glands. After irradiation with UV, the fibers became more numerous, thicker, and more twisted; IR alone produced many fine, feathery fibers. The addition of IR to UV resulted in dense matlike elastic fiber depositions that exceeded what was observed with either irradiation alone. In combination or alone UV and IR radiation produced a large increase in ground substance, a finding also seen in actinically damaged human skin. Infrared radiation, in the physiologic range, though pleasant is not innocuous.