The answer lies in understanding how light interacts with skin; more specifically the invisible spectrum of light, ultraviolet (UV) light (200-400nm in wavelength) and its subtypes: UVA emits between 400-320nm, UVB emits between 320-280nm and UVC between 280-200nm.
A traditional tanning bed works by emitting UVA and a small percentage of UVB light.
UV at these wavelengths (particularly UVB) induces damage in the skin which, in turn, responds by activating a barrier of protective melanin in skin; the so-called ‘tanning response’ (for a more in-depth view of this process, see our Technology Update on the tanning response and our article on Tanning). UVA also causes what’s known as ‘immediate pigmentary darkening’ – altering existing melanin within skin cells within minutes to make the skin appear visibly darker (this process doesn’t – however – stimulate more melanin in the skin).
Other (less visible) short, medium and long term responses by the skin to UV light are known to be responsible for causing certain types of non-melanoma skin cancer and have been proven to be significant factors in contributing to melanoma, the deadliest skin cancer.
When UV impacts upon skin, it penetrates to various levels. UVB, being a short wavelength, cannot penetrate deeply and so impacts upon surface levels of the skin. Here, UVB helps to activate melanin, but also causes damage to skin cells and, more specifically, to DNA within skin cells. This damage (known medically as photodamage or dimer formation) causes the chemical bonds that hold DNA together to break.
Exposing skin to sunlight for an hour causes around 80,000 dimers per skin cell. While our bodies are able to repair much of this damage or kill off the mutated cells, sometimes an overload of UVB will lead to damage going unrepaired and mutated (damaged) cells accumulating. Too much accumulation causes cancerous growth; skin cancer.
Compared to UVB, UVA penetrates much deeper into the skin and creates an imbalance by causing reactive oxygen species (ROS) to tissues of the skin. Accumulated ROS can also damage DNA in cells by altering their chemical structure, as well as damaging enzymes which are important for the protective responses created in the body; processes known as ‘oxidative stress’. The body has mechanisms to absorb ROS – including antioxidants like vitamin E and vitamin C – but too much exposure to UVA light creates an imbalance in skin and leads to oxidative stress, which can in turn contribute to skin cancer creation and proliferation. (You can read more about these processes here).
This damage to cells is not only caused by an intensity of UV but also the total amount of UV to which the skin is exposed. What this means is that an hour of exposure at the same UV intensity – whether it is in an hour long block or four 15 minutes sessions – can still cause the same level of cellular damage to the skin.
Cellular damage is known to play a role in skin cancers but also in melanoma formation, although there are several processes which are still being researched to determine exactly how this cellular damage leads to cancer. What we do know, however, is that there is a significant correlation between exposing unprotected skin to UV light on a regular, intense basis and the incidence of melanoma. Research specifically focused on tanning beds has even led to the declaration by the World Health Organization that tanning beds, like cigarettes, are a known carcinogen to humans.
So, in short and simply put, excessive chronic exposure to UV light, whether it is from the sun or a tanning bed, can contribute to cellular damage, which in turn may lead to an increased risk of skin cancer and melanoma formation. As the body of research around the UV-cancer link grows, expect to see even more regulations put in place.
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