Skin cancer becomes more common after age 60 primarily because of the cumulative effects of ultraviolet (UV) radiation exposure over many years, combined with natural changes in the skin and immune system that occur with aging. The risk increases as the skin’s ability to repair DNA damage declines, and the protective mechanisms that shield skin cells from harmful mutations weaken.
Over a lifetime, repeated exposure to sunlight and other sources of UV radiation causes damage to the skin’s DNA. This damage accumulates slowly, often without immediate symptoms, but over decades it can lead to mutations in skin cells that trigger uncontrolled growth, resulting in skin cancers such as basal cell carcinoma, squamous cell carcinoma, and melanoma. Older adults have had more time to accumulate this damage, which explains why skin cancer rates rise significantly after age 60.
In addition to cumulative sun exposure, aging skin undergoes structural and functional changes that increase vulnerability to cancer. The skin’s outer layer thins, and the number of immune cells that patrol the skin to detect and destroy abnormal cells decreases. This reduced immune surveillance means that mutated cells are less likely to be eliminated before they develop into cancer. The skin also loses elasticity and its ability to repair itself efficiently, making it easier for precancerous lesions to progress.
Certain precancerous conditions, like actinic keratosis, become more common with age. These rough, scaly patches on sun-exposed areas are caused by long-term UV damage and can develop into squamous cell carcinoma if untreated. Older adults are more likely to have these lesions due to decades of sun exposure, especially if they worked outdoors or had limited sun protection in their youth.
Genetics and skin type also play roles. People with lighter skin, freckles, red or blond hair, and blue or green eyes have less natural protection against UV radiation and are more prone to skin damage and cancer. A family history of skin cancer further increases risk. Additionally, some genetic mutations that impair the skin’s ability to repair UV damage or regulate cell growth become more impactful with age.
Immune system changes with aging, known as immunosenescence, reduce the body’s ability to fight off cancer cells. Older adults may also have other health conditions or take medications that suppress immune function, further increasing skin cancer risk.
Environmental and lifestyle factors throughout life contribute too. Outdoor work or hobbies without adequate sun protection, history of sunburns, and use of tanning beds all add to cumulative UV damage. Even if sun exposure was moderate, the long latency period of skin cancer means it often appears many years later.
Emerging research suggests that changes in the skin’s microbiome—the community of microorganisms living on the skin—may also influence skin cancer risk in older adults. Certain microbial patterns have been linked to higher risk of squamous cell carcinoma, although the exact role of these microbes is still being studied.
In summary, skin cancer is more common after age 60 because of the combined effects of lifelong UV exposure causing DNA damage, age-related decline in skin repair and immune defense, the presence of precancerous lesions, genetic predispositions, and other health factors. The damage that may have been invisible or manageable in youth accumulates and manifests as skin cancer in older age, making vigilance and protective measures important throughout life.
