UVB rays can only penetrate through the epidermal or outer layer of the skin, resulting in DNA mutation and deformity caused by chemical changes. These mutations are clinically related to specific signs of photoageing such as wrinkling, an increase in elastosis and collagen damage resulting in sagging, textural changes and an overall dull, aged appearance.
Upon exposure to UVB rays, melanin, a pigment that gives the skin its color tone is produced, UVB will result in the formation of freckles and dark marks, both of which are signs of photoageing. With persistent exposure to UVB rays, signs of photoageing might appear and precancerous lesions or skin cancer can develop.
UVA rays on the other hand are able to penetrate deeper into the skin. Thus, in addition to the epidermal layer becoming damaged, the dermal layer will also be damaged. The dermis is the second most important layer of the skin and is made up of collagen, elastin, and the extrafibrillar matrix which provides structural support to the skin. With constant UVA exposure, the size of the dermis will be reduced, causing the epidermis to start sagging Due to the presence of blood vessels in the dermis, UVA rays can cause dilated or broken blood vessels which are most commonly visible on the nose and cheeks. UVA can also damage DNA indirectly through the generation of reactive oxygen species (ROS). These ROS damage cellular DNA as well as lipids and proteins.