Suntans, sunburns, and premature skin aging can all be caused by overexposure to cancer-causing ultraviolet A and ultraviolet B (UVA and UVB) rays.
Both types of rays damage the skin cells’ DNA, prompting melanocytes (skin cells in the top layer of skin, the epidermis) to produce more melanin, the pigment that gives our eyes and skin their color.
UVA oxidizes the existing melanin, causing immediate pigment darkening. [Figure 1] UVB causes inflammation, which releases new melanin to neighboring epidermal cells, and in about 72 hours, this leads to further tanning that lasts much longer than the UVA-triggered tanning. All of this melanin production signals that DNA damage has already occurred: it is a far from perfect attempt by the body to protect the skin from further damage. Nonetheless, the damage from repeated UV exposures keeps accumulating and can ultimately lead to skin cancer.
Comparison Chart
What is a Sunless Tan?
With sunless tanning, no such damage occurs. The “tan” from most sunless tanners comes from the coloring agent dihydroxyacetone (DHA), a simple carbohydrate. DHA binds to the proteins on the skin’s surface, forming brownish melanin-like molecules called “melanoids” that make the skin appear tan. Unlike UV, DHA does not penetrate beyond the skin surface. As can be seen in Figure 1, it is active only in the stratum corneum, the epidermis’s protective outermost layer of dead skin cells. Antioxidants such as caffeic acid phenethyl ester (CAPE) may be added to the self-tanner1,2 to mitigate the artificial-looking orange or yellow color DHA can produce on the skin and achieve a more natural tone.3
Source: Skin Cancer Society
