The chronic effects of ultraviolet (UV) radiation are photoaging and photocarcinogenesis.
Photoaging is greatly influenced by the amount of melanin, its composition, and its distribution.
In darker skin of color, photoaging is typically not evident until the fifth or sixth decade.
Photoaging in Asians presents more often as pigmentary changes and less often as wrinkling.
Hispanics are an extremely heterogeneous group with widely varied photoaging phenotypes.
Because of the protective effects of melanin, individuals with skin of color are less prone to develop UV-associated skin cancers compared with fair-skinned individuals.
CHRONIC EFFECTS OF ULTRAVIOLET RADIATION
Photoaging and photocarcinogenesis are the primary long-term effects of chronic ultraviolet (UV) radiation (UVR) on skin.
Photoaging, or dermatoheliosis, is distinct from intrinsic aging. Intrinsic skin aging is due to the passage of time, whereas photoaging results from damage to the skin from UVR superimposed on intrinsically aged skin. Intrinsically aged skin appears lax, dry, and pale with fine wrinkles and is prone to the development of benign neoplasms. In contrast, photoaged skin is coarser, rougher, leathery, inelastic with deep wrinkles, and telangiectatic. In addition, pigmentary changes consist of persistent constitutive hyperpigmentation, irregular hyperpigmentation, reticular hyperpigmentation (poikiloderma of Civatte), guttate hypomelanosis, freckling, and/or solar lentigines. Open comedones (Favre-Racouchot syndrome), sebaceous hyperplasia, and erosive pustulosis may also be present in photodamaged skin. Irregular hyperpigmented macules (“sunburn freckles”) can develop as early as several months after a sunburn. Repeated exposure to suberythemogenic UVR has the potential to change the morphology of acquired melanocytic nevi with increased size, darker color, and dermoscopic patterns that simulate melanoma in situ.1 Photoaged skin loses resilience and elasticity and has increased fragility and decreased capacity for wound healing. Histologically, there can be acanthosis or atrophy, loss of polarity, cellular atypia in the epidermis, and increased melanin in keratinocytes, especially in skin of color. In the dermis, reduced anchoring fibrils, loss of mature collagen, basophilic collagen degeneration, elastosis, increased ground substance, and, in skin of color, increased number of large, densely melanin-packed melanophages may be seen.2 Additionally, there is an increase in the numbers of mast cells, histiocytes, fibroblasts, and mononuclear cells, although in the epidermis, there are decreased numbers of Langerhans cells.3
Both UVA and UVB can induce photoaging. However, UVA plays a more significant role due to its greater average depth of penetration into the dermis, increased abundance in terrestrial sunlight (5% UVB, 95% UVA), and persistent irradiance throughout the day and year. Studies also demonstrated that exposure of human skin to suberythemogenic doses of UVA alone resulted in stratum corneum thickening, Langerhans cell depletion, and dermal inflammatory infiltrates with deposition of lysozyme on the elastic fibers. This suggests that frequent casual exposure to sunlight containing primarily UVA eventually may result in dermal collagen and elastin damage, contributing to photoaging. UVA increases the cross-linking of collagen fibers, rendering dermal collagen ...