Overexposure to UV‑B radiation not only can cause sunburn but also some forms of skin cancer. However, the degree of redness and eye irritation (which are largely not caused by UV‑A) do not predict the long-term effects of UV, although they do mirror the direct damage of DNA by ultraviolet.
All bands of UV radiation damage collagen fibers and accelerate aging of the skin. Both UV‑A and UV‑B destroy vitamin A in skin, which may cause further damage.
UVB radiation can cause direct DNA damage. This cancer connection is one reason for concern about ozone depletion and the ozone hole.
The most deadly form of skin cancer, malignant melanoma, is mostly caused by DNA damage independent from UV‑A radiation. This can be seen from the absence of a direct UV signature mutation in 92% of all melanoma. Occasional overexposure and sunburn are probably greater risk factors for melanoma than long-term moderate exposure. UV‑C is the highest-energy, most-dangerous type of ultraviolet radiation, and causes adverse effects that can variously be mutagenic or carcinogenic.
In the past, UV‑A was considered not harmful or less harmful than UV‑B, but today it is known to contribute to skin cancer via indirect DNA damage (free radicals such as reactive oxygen species). UV‑A can generate highly reactive chemical intermediates, such as hydroxyl and oxygen radicals, which in turn can damage DNA. The DNA damage caused indirectly to skin by UV‑A consists mostly of single-strand breaks in DNA, while the damage caused by UV‑B includes direct formation of thymine dimers or cytosine dimers and double-strand DNA breakage. UV‑A is immunosuppressive for the entire body (accounting for a large part of the immunosuppressive effects of sunlight exposure), and is mutagenic for basal cell keratinocytes in skin.
UVB photons can cause direct DNA damage. UV‑B radiation excites DNA molecules in skin cells, causing aberrant covalent bonds to form between adjacent pyrimidine bases, producing a dimer. Most UV-induced pyrimidine dimers in DNA are removed by the process known as nucleotide excision repair that employs about 30 different proteins. Those pyrimidine dimers that escape this repair process can induce a form of programmed cell death (apoptosis) or can cause DNA replication errors leading to mutation.
As a defense against UV radiation, the amount of the brown pigment melanin in the skin increases when exposed to moderate (depending on skin type) levels of radiation; this is commonly known as a sun tan. The purpose of melanin is to absorb UV radiation and dissipate the energy as harmless heat, protecting the skin against both direct and indirect DNA damage from the UV. UV‑A gives a quick tan that lasts for days by oxidizing melanin that was already present and triggers the release of the melanin from melanocytes. UV‑B yields a tan that takes roughly 2 days to develop because it stimulates the body to produce more melanin.