Ultraviolet Radiation — Skin Cancer Risk Factor

Ultraviolet radiation occupies the electromagnetic spectrum between visible light and X-rays. It is divided into three subtypes based on wavelength: UVA, UVB, and UVC. UVC is largely absorbed by Earth's ozone layer, but UVA and UVB reach the surface and penetrate human skin.

UVB rays primarily damage the outer skin layers, causing sunburn and direct structural breaks or mutations in DNA. UVA rays penetrate more deeply, generating reactive oxygen species that cause indirect genetic damage and premature ageing. Accumulated DNA damage over time can prompt skin cells to grow uncontrollably.

Recognising UV radiation as a primary carcinogen empowers you to take meaningful preventive measures. Protecting your skin with broad-spectrum sunscreen, protective clothing, and shade significantly reduces your cancer risk. For patients already treated for skin cancer, strict UV protection helps prevent disease recurrence or the development of second primary tumours.

UV exposure is not measured through a blood test. Instead, clinicians assess cumulative UV damage by examining skin changes such as actinic keratoses, solar elastosis, and freckling. When a suspicious lesion is biopsied, genetic profiling often reveals a characteristic 'UV signature'—specific DNA mutation patterns such as C-to-T transitions.

UV radiation is directly linked to cutaneous malignant melanoma, the most aggressive skin cancer. It is also the primary driver for non-melanoma skin cancers, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), as well as rarer conditions such as Merkel cell carcinoma.

Tumours caused by extensive UV radiation often carry a high tumour mutational burden (TMB). Because these tumours produce many abnormal proteins, they frequently respond well to immune checkpoint inhibitors like pembrolizumab or nivolumab. Early non-melanoma lesions may be managed with surgical excision, cryotherapy, or topical therapies like 5-fluorouracil.