Tanning Risk

Ultraviolet (UV) radiation is the most prominent and universal cancer-causing agent in our environment. The US Department of Health and Human Services, Public Health Service, National Toxicology Program Report on Carcinogens (cancer-causing agents) states that UV solar radiation, and use of sun lamps and sun beds are "known to be a human carcinogen." . Some scientists have suggested recently that there may be an association between UVA radiation (the type of radiation that makes up most of the radiation in tanning beds) and malignant melanoma, the most dangerous form of skin cancer. There is persuasive evidence that each of the three main types of skin cancer, basal cell carcinoma (BCC), squamous cell carcinoma (SCC) and melanoma, is caused by sun exposure. Women who visited a tanning parlor at least once a month were 55% more likely to later develop melanoma than women who didn't artificially suntan. Those who used sun lamps to tan while in their 20s had the greatest later risk, about 150% higher than similarly aged women who shunned tanning beds.

Exposure to ultraviolet radiation induces two of the most common DNA mutations known in cellular biology. Those include cyclobutane–pyrimidine dimers (CPDs) and 6–4 photo products (6–4PPs) and their Dewar valence isomers. Cells have developed a number of repair mechanisms to counteract the DNA damage caused by ultraviolet radiation and other toxins. In human cells, a repair process is initiated after DNA damage is detected in which the damaged DNA is removed before it is replicated. As humans age, their cellular repair mechanisms make more errors because they have accumulated years of oxidative stress from daily life. Over time, it is more difficult for the cell to find and destroy aberrant DNA. The replication of damaged DNA leads to cancer, and exposure to UV radiation sets a process in motion that can take decades to ultimately cause skin cancer Similarly, most people who smoke cigarettes do not get lung cancer until decades of use have passed. Most critically, if a mutation occurs within a gene that regulates cell division, the cell becomes prone to malignancy. For example, squamous cell carcinoma (a type of skin cancer) is caused by a UVB induced mutation in the p53 gene.

Exposure to UV radiation has a detrimental effect on the immune system. Exposure causes changes in antigen presentation by Langerhans cells and macrophages. Also, the activities of natural killer cells and T cells is reduced. Last, cytokine regulation is disrupted by UV exposure. Ultraviolet radiation exposure may facilitate the growth of skin neoplasms and the spreading of skin-associated infections due to stimulation of suppressor T cells.

While the dangers of UVB are widely recognized the dangers of UVA are less understood. UVA is less likely to burn the skin, and it has been called the "bronzing light." However, it is clearly associated with inducing aging changes in the skin and in promoting the development of skin cancer. This is because UVA penetrates the skin more deeply than UVB, and therefore causes damage on a deeper level. Most aging of skin is due to UVA rays destroying collagen and connective tissue beneath the superficial layer of the skin. UVB rays do not reach as far below the skin. Excessive exposure to UVA radiation will cause premature aging, including wrinkles, sunspots, and loss of skin elasticity.

One study conducted amongst a college student population found that awareness of the risks of tanning beds did not deter the students from using them.

Although rare, it is possible for tanning beds to be a vector for infections of pubic lice, also known as crabs. If the surface of the bed is not properly cleaned or if towels provided by the salon are not washed in hot water, crab lice can survive for several days on these surfaces. Crab lice are difficult to see on the acrylic of a dimly lit tanning bed, and they are not killed by anti-bacterial or anti-viral cleaning agents used in salons. They can only be killed by physical removal or by the use of insecticides such as pyrethrin.

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