PreventionEpidemiologyN/A (epidemiology)

UV radiation and skin cancer

Ultraviolet radiation; UVR; UVA; UVB; sunlight and skin cancer

Ultraviolet radiation from natural sunlight and artificial sources is classified by the WHO/IARC as a Group 1 carcinogen — sufficient evidence for carcinogenicity in humans. UVA (315–400 nm) penetrates deeply and is the principal driver of photoageing, immunosuppression and BCC; UVB (280–315 nm) drives most direct DNA damage (cyclobutane pyrimidine dimers), erythema and cSCC. Melanoma risk is driven principally by intermittent intense exposure and childhood sunburn; cSCC by cumulative lifetime exposure; BCC by both. Understanding UV biology underpins photoprotection, sunbed counselling and the management of immunosuppressed patients.

CurrentLast reviewed 15 May 2026

UVA vs UVB — biology

  • UVB (280–315 nm) — absorbed by stratum corneum and upper epidermis; principal cause of erythema (sunburn), direct DNA damage (cyclobutane pyrimidine dimers, 6-4 photoproducts), p53 mutations and squamous-cell carcinoma initiation. Variable across seasons and time of day.
  • UVA (315–400 nm) — penetrates dermis; predominantly indirect oxidative damage via reactive oxygen species. Drives photoageing, immunosuppression, melanoma initiation, basal-cell carcinoma. Far more abundant than UVB and present at high levels year-round, including through window glass and on cloudy days.
  • UVC (100–280 nm) — almost entirely absorbed by the ozone layer; not relevant to natural exposure.

UV and cancer types

  • cSCC — cumulative lifetime UV dose drives risk; chronic sun-exposed sites (head, neck, forearms, dorsal hands).
  • BCC — both intermittent intense and cumulative exposure; site-related (head and neck dominant).
  • Melanoma — intermittent intense exposure, sunburn in childhood and adolescence are dominant; truncal lesions in men, lower-limb in women.
  • Merkel cell carcinoma — chronic UV-damaged skin + MCPyV interaction.
  • Lentigo maligna / actinic keratoses — chronic cumulative damage.

UV-induced immunosuppression

  • UV exposure suppresses cutaneous and systemic immunity through Langerhans-cell depletion, regulatory T-cell induction and cytokine modulation.
  • Contributes to skin cancer development and may impair tumour immune surveillance.
  • Particularly relevant to organ transplant recipients who are already pharmacologically immunosuppressed — UV protection in OTRs reduces non-melanoma skin cancer incidence substantially.

UV index and UK exposure

  • UV Index (UVI) — open-ended scale; UK summer typically peaks at 6–8 (high).
  • UVI ≥ 3 — sunscreen recommended; UVI ≥ 6 — additional protection (shade, clothing, hat).
  • UV does not need to feel hot to cause damage — overcast days can deliver up to 80% of clear-day UV.
  • Snow, sand and water reflect UV — exposure is intensified.
  • UK Met Office and many weather apps provide daily UVI forecasts.

IARC classification and policy

  • UV radiation is an IARC Group 1 carcinogen — same category as tobacco, asbestos, ionising radiation.
  • Solar radiation, broad-spectrum UV, sunbeds — all Group 1.
  • UK policy — Sunbeds (Regulation) Act 2010 (under-18s banned); ongoing campaigns on photoprotection.

References

  1. IARC Monograph 100D. Radiation — UV (solar and equipment). 2012.
  2. WHO. Ultraviolet radiation and human health. Fact sheet; 2017.
  3. Public Health England / UK Health Security Agency. UV index and health information. GOV.UK; accessed 18 May 2026.

Spot a correction?

If any clinical statement, citation or link on this page needs updating, please email admin@skinoncology.net with the page name, the proposed correction and the supporting source.