Sun Damage

UVB rays work at the surface of the skin, where they reach the DNA of epidermal cells. In the short term this causes sunburn. Over years, small errors accumulate in the cells' instruction manual, including in the melanocytes that make pigment, which can begin producing colour continuously in one spot rather than evenly.

This continuous pigment production is the origin of solar lentigines, the flat brown sun spots sometimes wrongly called age spots. Unlike freckles, which are genetic and fade in winter, lentigines come from a fixed local increase in pigment activity. They are acquired through exposure and no longer fade when the sun is gone.

UVA rays penetrate deeper, into the dermis where the skin's structure lives. More penetrating than UVB, present year-round and able to pass through glass, they generate free radicals that fragment collagen, degrade elastin and switch on enzymes that digest the skin's supporting framework. This is the root of texture change and lost firmness.

The skin has a memory: each exposure leaves a fraction of damage the skin cannot fully repair. A tan itself is already a defence reaction, the skin making pigment to shield its cells. The damaged elastic fibres build into solar elastosis, the thickened, leathery texture seen in midlife as the sum of every exposure since childhood.

Sun damage is not only a summer-beach concern. In Canada, snow strongly reflects UV back onto the skin, and UVA passes through clouds and windows all year. Think of a poster left for years behind a shop window: the colours fade in patches and the paper grows brittle, not in a day, but by the silent addition of each day of light.