Sunlight effects upon the skin

Ultraviolet radiation (UVR) comprises only about 5% of sunlight, with visible light and infrared radiation making up the remaining 95%. However, it is UVR which is chiefly responsible for the harmful effects of sunlight exposure. On a sunny day, UVA (315-400 nm) accounts for at least 95% of UVR, and UVB (280-315 nm) no more than 5%. UVR has acute and chronic effects on the skin.
Acute effects
Erythema (sunburn)
Sunburn or erythema can vary in intensity from mild redness to oedema, blistering and peeling. Susceptibility to sunburn and tanning depends on the skin phototype of the individual. UVB is much more effective at inducing erythema than UVA. UVB accounts for only about 5% of solar radiation but it contributes to about 80% of the erythema caused by sunlight. Experiments suggest that the synthesis and release of prostaglandin E2 (PGE2), following cyclooxygenase-2 (cox-2) gene activation, and nitric oxide within the dermis are responsible for UV-induced erythema.
Melanogenesis (tanning)
Skin colour is genetically controlled but can be enhanced by UVR exposure. Each skin phototype has a different ability to tan. Tanning and epidermal hyperplasia following UVR exposure protects against erythema and burning, but maintaining this requires repeated exposures, which can result in the chronic effects of photodamage.
Skin phototypes
Skin phototype Response to UVR exposure
I White skin, always burns, never tans (Celtic)
II White skin, burns initially, tans with difficulty
III White skin, rarely burns, tans easily
IV White skin, never burns always tans (Mediterranean)
V Brown skin (Asian)
VI Black skin
Immunosuppression
Both UVA and UVB exposure suppress cutaneous cell-mediated immunity in humans. This effect is significantly higher in skin types I/II than in types III/IV. UVR-induced immunosuppression is thought to play an important role in the emergence of skin cancer, which explains the increased risk of skin cancer in individuals with skin types I/II who have a history of repetitive and intense UVR exposure.
Chronic effects
Photoageing
Photoageing results in dry, deeply wrinkled, inelastic, leathery skin with telangiectasia, mottled pigmentation, freckling and lentigines. Repeated long-term UVR exposure, especially UVB, results in changes within the dermal connective tissue. There is elastosis and degradation and disorganization of collagen fibrils. It is thought that UVR-induced metalloproteinases (endopeptidases that degrade structural proteins) degrade the dermal matrix, which then undergoes imperfect repair.
Photocarcinogenesis
Skin cancer is the long-term result of a complex interaction between UVR exposure and genetics. Genetic factors include skin phototype, DNA repair capacity and immunocompetence. DNA damage occurs following UVR, and this is repaired by nucleotide excision repair. Repeated UV exposure together with suboptimal repair results in the clonal expansion of cells with mutated oncogenes leading to melanoma and non-melanoma skin cancer. Studies have shown that squamous cell carcinomas develop as the consequence of accumulated sun exposure, whereas melanoma and basal cell carcinomas are more dependent on specific patterns of childhood and intermittent high-dose sun exposure. Other important risk factors for the development of skin cancer include UVR-induced immunosuppression as well as immunosuppressant drugs as seen in organ transplant patients.
Photodermatoses
Photodermatoses (diseases caused by sunlight) can be divided into two main categories, those in which the sunlight has a primary role in the condition (primary photosensitivity) and those in which the sunlight acts as an exacerbating factor (secondary photosensitivity).