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Over the last decade the medical profession around the world has conducted a major public education effort to reduce excessive ultraviolet light (UVL) exposure to decrease the incidence of skin cancer. Included in this effort has been a growing concern over the use of indoor tanning beds. Organizations such as the Council on Scientific Affairs of the American Medical Association (AMA),
have suggested that indoor tanning may be dangerous and should be discouraged. Indeed, the AMA went so far as to adopt a resolution calling for a ban on the sale and use of tanning equipment for nonmedical purposes.
Despite this effort, it appears the use of indoor tanning, both at tanning parlors and at home, continues to be more popular than ever. The indoor tanning industry estimates that 28 million Americans are tanning indoors annually at about 25,000 tanning salons around the country.
The indoor tanning industry has undertaken an aggressive campaign to assert that indoor tanning is not only safe, but healthy. Organized medicine has taken the opposite view. We will review the evidence for both the benefits and risks associated with indoor tanning.
The history and effects of indoor tanning
The tanning process is induced in skin capable of tanning by ultraviolet radiation (UVR). Sunlight reaching the earth’s surface contains both ultraviolet A (UVA) and ultraviolet B (UVB), while the ultraviolet C (UVC) portion is filtered out by the ozone layer. The content of UVB in sunlight varies seasonally, while that of UVA remains fairly constant. The majority of ultraviolet radiation in sunlight is UVA, around 90–95%, depending on time of day and year. Despite being the minority component of UVR from the sun, UVB appears to be much more potent in many of its biologic effects than UVA. In the past, most biologic effects were attributed solely to UVB, and this portion was referred to as “sunburn rays.” The effects of UVA were neglected. More recently, research has emerged showing UVA, both alone and in conjuntion with UVB, has many powerful biologic effects on the skin.
The first artificial light source used to treat humans was the carbon arc lamp developed by Niels Finsen at the turn of the century to treat tuberculosis and other infectious diseases
(Fig 1). During the 1930s and 1940s, the medical profession encouraged sun exposure as beneficial to children. Around the same time, the development of a tan for cosmetic purposes became fashionable as popularized by the French fashion designer Coco Chanel. The first generation of indoor tanning beds that appeared were principally UVB emitting, contained some UVC, and were plagued by multiple safety problems.
The development of high-intensity UVA light sources for medical purposes during the 1970s was quickly followed by their use in commercial tanning parlors. These were promoted as “safe tanning” devices because they were UVA bulbs without the harmful UVB (“sunburn rays”). The bulbs used in tanning parlors have never been pure UVA and have always provided some UVB. Furthermore, UVA by itself is not harmless.
Figure 1Multiple basal cell and squamous cell carcinomas on the leg of a patient who built his own carbon arc lamp as a teenager in the 1940s at home for tanning. The patient treated himself and charged other teenagers for use of his device. He now has multiple tumors diffusely throughout his skin.
When considering the effects of indoor tanning, it is important to consider what wavelengths are being emitted. Optically filtered high pressure mercury lamps doped with metal halides that emit within the UVA band with virtually no UVB are available but are not routinely used in tanning parlors.
Rather, the bulbs used in tanning parlors emit some UVB. In a laboratory study from 1986, bulbs commonly used in commercial tanning parlors were measured for UVB output.
Approximately 0.5% to 2.0% of total output was in the UVB range. This may seem like a trivial contribution, but for many biologic effects, such as tanning and burning, UVB is several orders of magnitude more effective than UVA. For example, the authors of the above study calculated that if a burn occurred with the bulbs measured,
the contribution of UVB in producing that burn ranged from 3.0% to 23%. In 1988, a study conducted at tanning parlors using a hand-held UV meter found UVB output to vary from 0.3 to 3.5% of the total,
in line with the laboratory study of the time. UVB is much more potent than UVA for many biologic effects, including tanning. Therefore, the current trend in indoor tanning has been to add increasing amounts of UVB back to the bulbs used in tanning parlors to better simulate natural sunlight. Manufacturers of bulbs used in indoor tanning salons now advertise this trend, such as the Interlectric Corporation,
which states “The majority of lamps used in the market today are now in the 5.0 to 9.5% UVB range. Understanding the tanning process, it is not difficult to understand why the marketplace has driven the development of lamps towards a system which more closely resembles that of natural sunlight while maintaining tanning schedules of reasonable tanning times.” Similarly, the Wolff System lamps, the leading manufacturer of indoor tanning bulbs, advertises, “Wolff System lamps emit UVA and UVB in a manner similar to natures [sic] sun.”
It would seem bulbs in current use would put this issue to rest. However, as recently as 1993 an article in Tanning Trends magazine, a leading trade publication of the indoor tanning industry, states, “Natural sunlight, however, contains a cache of the more dangerous higher concentration ultraviolet rays that are eliminated in an indoor tanning unit.”
If tanning parlors are using bulbs as the manufacturers advertise them, this is a difficult statement to support.
The biologic effects of UVR
UVR is known to have a variety of biologic effects, both beneficial and harmful. The harmful effects of UVR can be divided into acute and chronic. The most obvious acute harmful event form UVL exposure is a sunburn. Exposure to excessive UVR produces erythema with the classic signs of inflammation; warmth, pain, and swelling. It was previously believed that UVB was solely responsible for a sunburn. It has been shown that UVA by itself can cause a burn,
Such studies generated an action spectrum for erythema plotting burning versus wavelength. Radiation in the UVB portion is much more effective than the UVA range in producing a burn (Fig 2). Using data from mammalian skin cancer models, it became apparent that the action spectrum for the development of squamous cell carcinoma is essentially identical to that for human erythema.
However, other biologic responses to UVR, such as the development of melanoma, may not follow the erythema action spectra as was previously assumed. Determining the contribution of UVB and UVA to the development of skin cancer and other biologic effects is now being assessed.
Figure 2Action spectra for photocarcinogenesis on the hairless albino mouse (straight line) and a standardized action spectrum for UV-induced erythema in humans (dashed line).
For a biologic response to occur, the energy of photons striking the skin must be absorbed by a molecule, called a chromophore, capable of absorbing radiation of that particular wavelength. A number of subcellular targets have been shown to be capable of absorbing UVR with significant biologic consequences. Chromophores in the skin include DNA, proteins, lipids, and urocanic acid.
The mechanism for UV induced sunburn is unclear, but the absorption of photons by a chromophore is the first step. In the UVB and UVC range, the shape of the erythema action spectrum suggest that DNA is a major chromophore.
Effects of sunscreens and a DNA excision repair enzyme on ultraviolet radiation-induced inflammation, immunosuppression, and cyclobutane pyrimidine dimer formation in mice.
Clinically, a burn from UVA has a different time course than that produced by UVB exposure. A burn secondary to UVB exposure normally begins several hours after exposure, and peaks in 12 to 24 hours.
Some researchers have reported a biphasic response to UVA wherein immediate erythema is seen that fades partly or completely and is followed by a second phase of erythema.
UVA penetrates more deeply in the skin than UVB, and dermal effects may be more important. The histologic changes seen after a UVA burn are predominately dermal, while those seen with a UVB burn are epidermal.
It is possible to achieve some tanning with UVA at doses less than the MED (minimal erythema dose), which led to the claim of the “safe tan.” When indoor tanning units were principally UVA, despite tanning parlor advertisements, a burn could occur with UVA light alone. Such distinctions are less important in considering indoor tanning units currently being marketed, as these are a mixture of UVA and UVB. The important point is, burns can and do occur in indoor tanning units.
The interaction of indoor tanning and sun exposure is also an area of concern. Ultraviolet radiation, of the same or different wavelengths, is additive in producing a burn. This means that if a subminimal MED dose of UVR is given, followed sometime later by a second sub-MED dose, the energies add together and a burn can result. Although UVA and UVB produce erythema with different time course, colors, and histologic features, the effects of these different wavelengths are additive and are termed photoaddition. If a sub-MED dose of UVA is given in a tanning parlor, followed later by a sub-MED of UVB from sunlight, the energies are additive and an unexpected burn can occur.
Therefore, a visit to a tanning parlor followed by sun exposure is at least additive and can produce an unexpected burn.
Secondary adverse effects of indoor tanning
In addition to a burn, a variety of other acute adverse effects have been noted secondary to indoor tanning. Short-term adverse effects reported after indoor tanning include pruritus, xerosis, and nausea.
Conditions such as systemic lupus erythematosus, polymorphous light eruption, porphyria, and rosacea can be significantly exacerbated by exposure to indoor tanning.
Phototoxic and photoallergic reactions, usually secondary to medications, are another potential hazard. A variety of commonly used medications are photosensitizing and can produce phototoxic or photoallergic reactions.
Medicinal psoralen represents a particularly dangerous medication for the production of phototoxic reactions. Ingestion of medicinal psoralen followed by UVA tanning bed use can produce disastrous burns, such as the well-publicized case of a woman who died of massive burns in just such an event.
Psoralens in many common vegetables, such as parsley, carrot, parsnip, and celery, can also produce a phototoxic reaction. For example, a case report described a severe phototoxic burn in a woman who ate celery root before a visit to a tanning parlor.
Many acute adverse effects seem to be surprisingly common with indoor tanning. One study found erythema occurred in 22% of tanning bed subjects, pruritus in 27%, xerosis in 15%, and nausea in 4%. Other studies report similar figures, with pruritus reported in 28 to 39% of subjects,
Erythema is common following indoor tanning. We may speculate that a burn prompting a visit to a physician or the emergency room represents a serious, rather than a minor, burn. In a survey of physicians in Wisconsin it was found that 42% of responding dermatologists, 42% of ophthalmologists, and 29% of emergency department physicians had treated either a cutaneous or occular burn resulting from an indoor tanning unit within the previous year.
The Centers for Disease Control (CDC) calculated that approximately 700 visits to an emergency room were precipitated by burns from tanning beds in a single year.
These types of reports suggest serious burns are produced by indoor tanning.
The eyes represent another target for acute adverse effects from indoor tanning. Normally, the topography of the head is such that the eye is protected from direct sun exposure by the eyebrows. Measurements using a head model indicate that UVA exposure to the surface of the eye when looking directly at a UVA tanning bed could be as much as two orders of magnitude greater than when outdoors in sunlight.
A corneal burn is possible. As mentioned previously, a survey of Wisconsin ophthalmologists found 42% of responding physicians reported treating occular injuries secondary to indoor tanning devices in the preceding year.
In a survey of community emergency departments, it was reported that of 62 UV-induced corneal burns seen, 25 resulted from exposure at commercial tanning salons.
Proper eye protection is absolutely essential for indoor tanning, and Food and Drug Administration (FDA) guidelines mandate that protective goggles be provided to tanning salon patrons.
US Food and Drug Administration. The darker side of tanning: Skin cancer, eye damage, skin aging, allergic reactions. Rockville, MD: Public Health Service, 1987; HHS Publication No. (FDA) 87-8270.
Chronic effects secondary to indoor tanning are delayed, long-term adverse effects that may not be apparent for many years. Simple cause and effect relationships, such as a burn shortly following exposure, are harder to demonstrate. Rather, we must sift through a wealth of clinical and epidemiologic studies, animal studies, and in vitro laboratory studies to move toward a conclusion.
The eye is a target for chronic damage as well as acute corneal burn. As outlined in “The Eyes Have It” in this issue, the conjunctivae, lens, and retina are all targets for chronic photodamage.
Pitts DG, Cullen AP, Hacker PD, et al. Ocular ultraviolet effects from 295 to 400 nm in the rabbit eye. Washington, DC: National Institute for Occupational Safety and Health; DHEW publication No. 77-175.
US Food and Drug Administration. The darker side of tanning: Skin cancer, eye damage, skin aging, allergic reactions. Rockville, MD: Public Health Service, 1987; HHS Publication No. (FDA) 87-8270.
Photoaging is one chronic adverse effect not readily apparent to young tanners. The clinical, histological, and physiological changes in chronically sun exposed skin (photoaging) are separate and distinct from those changes occurring as a result of longevity (intrinsic aging).
Intrinsic aging, which seems to occur in every tissue in the body, has a relatively modest impact on the skin. With the passage of time the vasculature may become more prominent, and the skin remains smooth and unblemished with only a mild thinning and loss of elasticity. In contrast, chronically sun exposed skin shows profound clinical, histological, and functional changes superimposed on the intrinsic process. Photoaged skin is clinically characterized by skin that is coarse, dry, deeply wrinkled, inelastic, leathery, yellowish, and telangiectatic, with uneven pigmentation and brown spots. Histologically, the changes of photoaged skin are strikingly different than those of intrinsic aging.
These changes are outlined in Dr. Cockerell’s paper in this issue.
Experimental evidence indicates UVR is responsible for photoaging. In a mouse model, both UVA and UVB can produce wrinkling, elastosis, collagen damage, and an increase in glycosaminoglycans.
These studies indicate that UVB is more effective in inducing the changes of photoageing in mouse skin. However, it was noted that skin sagging in the albino mouse was seen only with UVA irradiation, with a peak at 340 nm.
The extrapolation of animal studies to humans requires caution. First, most studies use the hairless mouse. These mice have much thinner epidermis than humans and a relative lack of epidermal melanin that makes them much more sensitive to UVR. Furthermore, the short life-span of experimental mice necessitates high-dose exposure for short periods of time. For humans, low-dose exposure over long periods of time is more relevant in understanding photoaging. Finally, variations of wavelength, dosing schedule, and fluence of UV irradiation must be accounted for. In particular, dosing schedule is an important consideration. A large dose given to human skin at one time can result in a burn, while multiple small doses may produce a tan. The goal of any indoor tanning parlor is to produce a tan while avoiding a burn. Studies utilizing human skin and multiple low dose exposures of UVL better approximate what people may experience with indoor tanning. Lowe and colleagues
exposed different areas of human skin to one MED of solar simulated light (UVA and UVB), one MED of UVA, and a sub-MED dose of UVA twice a week for 24 weeks. All treatment protocols, including the sub-MED dose, produced both epidermal and dermal changes consistent with photoaging. All treatment regimes produced a thickening of the viable epidermis and stratum corneum and produced vascular dilation and a perivascular inflammatory infiltrate, as well as alterations in dermal elastin content. In a similar study
a 0.5 MED dose of UVA was compared to a 0.5 MED dose of solar simulated light, each given daily to human volunteers five days per week for 28 total doses. Again, both produced changes consistent with photoaging. Interestingly, the UVA regime produced greater cumulative damage than solar simulated irradiation as evidenced by greater cumulative erythema during the first week of treatment, epidermal hyperplasia and stratum corneum thickening, depletion of epidermal Langerhans’ cells, dermal inflammatory infiltrates, and evidence of elastin degradation. Both studies indicate that relatively small, sub-MED doses of UVA and UVB produce changes consistent with photoaging, and that at the doses given UVA may actually exceed UVB in producing these changes. Most importantly, these studies suggest photoaging occurs with repetitive small UVR doses, similar to that with indoor tanning. In addition to the obvious cosmetic disfigurement produced by photoaging, carcinogenesis is a concern as most skin cancers arise in photoaged skin.
The mechanism of UVR-induced photoaging is now becoming elucidated. An in vivo study of human skin revealed UVR induced three metalloprotinases capable of degrading the dermal collagen matrix.
The metalloprotinases are a family of proteolytic enzymes that specifically degrade collagens, elastin, and other proteins in connective tissue and bone.
A single sub-MED exposure of UVR induced the three metalloprotinases studied (collagenase, gelatinase, and stromelysin-1). In addition, biochemical evidence of collagen degradation was noted. Other studies have noted the expression of the elastin gene is markedly activated in cells in sun damaged dermis.
These studies show that ultraviolet irradiation is the major cause of photoaging. Since decades of UV exposure may be necessary before skin changes are evident to the naked eye, those seeking a cosmetic tan are often unconcerned with this long-term consequence.
The development of skin cancer represents perhaps the greatest potential risk from tanning, either indoor or outdoor. The incidence of the three most common skin cancers, basal cell carcinoma, squamous cell carcinoma, and melanoma, is increasing rapidly
and has reached near epidemic proportions. The association of UVL exposure with the development these three skin cancers is strong. The association of sunlight with the development of skin cancer was first appreciated by Unna late in the last century.
Since that time, a wealth of epidemiologic, clinical, and laboratory studies have supported this association. Multiple epidemiologic studies, comprehensively reviewed elsewhere,
led to the conclusion that sun exposure causes skin cancer. The main observations are that skin cancer is more frequent in fair-skinned sun sensitive people, that skin cancer occurs more often in sun exposed areas of the body, that the incidence of skin cancer in susceptible populations increases in geographic locations with high ambient solar irradiance, and that skin cancer is more frequent in skin that shows signs of photodamage (photoaging). The UV portion of sunlight is implicated in the huge increase in the incidence of skin cancer in patients with xeroderma pigmentosa. These patients have a deficiency in repair of UVR-induced DNA damage.
Mechanisms of skin cancer formation
Laboratory studies have provided important information about the mechanisms involved in the development of skin cancer. Squamous cell carcinoma is the best studied as this type of cancer can be induced in a variety of experimental animals. Findlay first suggested a causal relationship between UVL and skin cancer in 1928, when he induced skin cancer in mice exposed to a quartz mercury vapor lamp.
Since then, multiple studies using multiple animal models have shown UVR induces skin cancers, typically squamous cell carcinoma. Early studies by Roffo in 1934,
using sunlight filtered through window glass (and hence depleted of UVB) suggested UVA did not cause squamous cell carcinoma in experimental animals. However, further studies using high output UVA lamps, such as those used in tanning parlors, clearly demonstrate UVA alone can induce skin cancer in experimental animals.
The dose response curve plotting wavelength versus tumor formation in albino mice (squamous cell carcinoma) closely approximates the action spectrum for UV-induced erythema in humans
Sunlight contains one to two orders of magnitude more UVA than UVB. Based on the action spectrum for tumor development in animals and differences in epidermal transmission in humans, it has been estimated that UVA contributes about 10–20% of the carcinogenicity of the sun.
The idea of “safe” tanning with no carcinogenic risk with high output UVA bulbs is not supported by these studies. Furthermore, the tanning industry seems to be abandoning the “UVA only” tanning bed.
The mechanisms of UVR-induced skin cancer formation are now being elucidated. The development of cancer is thought to involve multiple steps, and UVR has multiple effects on the skin that may contribute to this process. First, both UVA and UVB are capable of directly inducing DNA mutations in vitro and in human skin.
It has been proposed that UVR is also mutagenic indirectly, and produces other cellular damage, by producing activated oxygen species generated by endogenous photosensitizers.
Different (direct and indirect) mechanisms for the induction of DNA-protien crosslinks in human cells by far and near ultraviolet radiation (290 and 405 nm).
Animal studies have indicated a possible interaction with indoor tanning and subsequent sun exposure. In several studies, UVB induced tumor production was enhanced by prior, simultaneous, or subsequent exposure to UVA to a degree greater than simple addition.
at variance with the majority of studies. The South American opossum has a DNA repair system that is activated by UVA and visible light, hence UVA/visible light exposure after solar exposure lowers the incidence of skin cancer formation in this animal.
It does not seem humans have this photoactivated DNA repair system, and hence this finding is not relevant to humans. Furthermore, the temporal pattern is also somewhat irrelevant to humans; people do not visit the tanning parlor after a day at the beach. In sum, exposure at a tanning parlor may actually enhance the carcinogenicity of sun exposure.
Most animal studies involve only squamous cell carcinoma. Unfortunately, there is not a good animal model for basal cell carcinoma. It cannot be induced in mice (the most common laboratory model) and only rarely induced in other animals.
There is a platyfish-swordtail hybrid model of melanoma. While phylogenetically further away from humans than mice, these studies provide useful information indicating UVA as a much more potent inducer of melanoma than UVB, in contrast to tanning, burning, and development of squamous cell carcinoma.
High dose exposure to UVR in experimental animals is not the same as the use of tanning beds by human beings. The short lifespan of experimental animals necessitates high dose exposure over short periods, a pattern unlikely to be experienced by indoor tanners. At high doses, the thermal effects of UVA become important.
The albino mouse is a favored laboratory model. These mice have little protective melanin and hence are quite UVR sensitive. Studies using albino mice are complimentary with human epidemiologic studies in arriving at a conclusion about the risks of indoor tanning. Large, controlled epidemiologic studies are now becoming available, evaluating the effects of indoor tanning. Caution must be applied in interpreting such studies, as there is great variability in wavelengths emitted and dosing schedules used with various indoor tanning units. Indoor tanners may differ in their behavior in other aspects of their lives, confounding such studies. For example, a survey on tanning habits revealed tanning bed users were more likely than nonusers to tan outdoors as well.
Most studies have examined a possible relationship between indoor tanning and melanoma. In the area of nonmelanoma skin cancer, there is one case control study where use of sunlamps was statistically significantly associated with the development of squamous cell carcinoma,
Long-term use of oral methoxypsoralen and UVA radiation (PUVA) for therapeutic purposes has been associated with an increased risk for squamous cell carcinoma,
Members of the Photochemotherapy Follow-up Study Genital tumors among men with psoriasis exposed to psoralens and ultraviolet A radiation (PUVA) and ultraviolet B radiation.
although indoor tanners are unlikely to take oral psoralens.
The possibility of melanocytic proliferations induced by tanning beds is more convincing. Lentiginous melanocytic proliferations that demonstrate some of the cytologic atypia and architectural features seen in dysplastic nevi have been seen after the use of tanning beds.
These lesions are analogous to the well-described “PUVA lentigines.” A possible association of tanning bed use and melanoma comes from case reports of cutaneous melanoma developing in patients with frequent tanning bed use,
reported a statistically significant increased risk of melanoma in patients receiving PUVA photochemotherapy, particularly in those receiving more than 250 treatments. Case-control studies evaluating cosmetic indoor tanning and melanoma have provided variable results. Earlier studies found little, or statistically insignificant, association between indoor tanning and melanoma.
As with any epidemiologic studies, the problems of unspecified dosage and wavelengths is present; furthermore, the latent period after exposure may have been inadequate. The results from the PUVA/melanoma study indicate a latent period of at least 15 years may be required before a significant increase in melanoma risk is detected.
have a more rigorous design than earlier studies. Of particular note in these four studies was that a dose-response association was observed; risk increased with increasing exposure. The risks of indoor tanning remain controversial; however, these risks were sufficiently compelling for the AMA to call for an interstate ban on tanning beds.
Given the risks outlined above, we may ask are there benefits from indoor tanning that outweigh the adverse consequences? First, people visit indoor tanning parlors to achieve a socially desirable tan. The belief that a tan is attractive is a fairly recently acquired opinion in our society,
UVR produces two types of tanning: immediate and delayed. Immediate tanning is the development of a darker, bronze coloring that appears during irradiation and is maximal immediately afterwards. This color fades in minutes to hours. UVA and visible light (400–700 nm) preferentially produce this reaction.
The exact mechanism is unknown, but it could result from the rearrangement of preexisting melanin in the skin. Possible mechanisms include the rearrangement of melanosomes within keratinocytes, extension of melanocytic dendrites, or the oxidation of melanin by oxygen radicals.
Immediate tanning fades so rapidly that it is of no cosmetic benefit. Delayed tanning refers to a persistent change in color which develops days after exposure. Delayed tanning is the result of increased production and transfer of melanosomes to keratinocytes. UVB is much more effective than UVA in inducing delayed tanning, but UVA alone can induce delayed tanning in doses less than the MED.
This feature of UVA led to the use of high output principally UVA sunlamps for a “safe tan.” It is important to emphasize that UVA is not particularly efficient at inducing delayed tanning, therefore, the trend in indoor tanning is to use bulbs with greater UVB content.
Not all people are capable of developing a tan. Those with Type I and II skin are at greatest risk for skin cancer and by definition are poor tanners. In a survey of tanning parlor users in England, 15.2% were self-reported to be Type I skin, and 27.8% Type II.
Fully 98% of these indoor tanners (all skin types combined) reported the development of at least some tan after indoor tanning. (This is a biased group because only those satisfied with indoor tanning would continue to be clients.) A similar survey of American indoor tanners revealed 5% were Type I and 7% were Type II.
These phototypes are just the groups that would get little cosmetic benefit and be at greatest risk for carcinogenesis. In a controlled study of 33 volunteers, Devgun et al.
found 10 whole body exposures to UVA tanning bed over a two-week period produced some tanning in only 20 subjects (60%). Tanning did not correlate with skin type as determined by history, pointing out personal history may not be an accurate way to determine skin type. Subjects did report they tanned better in sunlight than with the tanning bed. In another study, UVA tanning beds were utilized to deliver three exposures per week for four weeks, and at least a mild tan was induced in all subjects;
however, a deep tan was difficult to achieve. It seems for many patrons of indoor tanning, the cosmetic benefit is very small. These poor tanners are presumably just the people at most risk for deleterious effects of UVR.
A second reason for indoor tanning is to protect against subsequent sunburn. Many patrons of indoor tanning parlors visit before vacation to develop a “base tan” and avoid an unpleasant burn. The indoor tanning industry has taken this notion a step further. In trade publications they state that burns, not tanning, cause skin cancer. They argue that since a tan helps to reduce burning, indoor tanning is actually preventive. Tanning Trends magazine, a trade publication, writes, “Moderate tanning has never been linked scientifically to skin cancer. In fact, by helping people tan with a reduced incidence of sunburn, indoor tanning may reduce your risk of ever contracting skin cancer.”
Manufacturers of indoor tanning devices are regulated by the FDA and the Federal Trade Commission; operators cannot market these devices for any purpose other than cosmetic tanning and are subject to confiscation and fines if claims are made about safety or health benefits.
The indoor tanning industry cannot advertise this supposed benefit of indoor tanning, but they may try to reach the public through the media.
There are two points to consider about this claim. First, does indoor tanning provide protection against sunburn from subsequent sun exposure? Second, what is the pattern of UVR exposure that contributes to skin cancer? Does prolonged low-dose exposure (tanning) contribute to skin cancer formation or does only intermittent high-dose exposure (burning) cause skin cancer? Several studies have addressed the issue of whether an “indoor tan” is protective against a subsequent burn. Devgun et al.
Comparative protection efficiency of UVA and UVB induced tans against erythema and formation of endonuclease sensitive sites in DNA by UVB in human skin.
found UVA tanning did not protect at all against subsequent UVB-induced erythema, but a UVB-induced tan was protective. These authors noted that a UVB-induced tan results in pigment dispersed throughout the epidermis, whereas UVA-produced pigment is primarily confined to the basal layer. UVB tanning was also associated with significant thickening of the stratum corneum and epidermis; UVA tanning did not produce significant thickening, which may explain why a UVB tan was protective and a UVA was not. However, these investigators also found that both UVA and UVB tans afforded equally significant protection against subsequent UVB-induced DNA damage. Because a UVA tan still allows UVB to penetrate the skin and induce erythema, some mechanism of the UVA tan other than blocking UVB transmission must afford protection against DNA damage.
There is one study that reports very large doses of UVA produced a tan that was protective against subsequent UVB exposure.
found that UVA-induced tan protected against subsequent UVA-induced dermal damage. This study is only relevant to further exposure in a UVA tanning bed and not sunlight. These investigators reported a significant point: The UVA tan itself produced dermal inflammation and vessel thickening. In other words, the UVA exposure did protect against further UVA exposure, but the skin seemed to be damaged in acquiring that protection. In sum, the majority of studies suggest that a tan acquired with indoor tanning provides little protection for subsequent sun exposure; and the acquisition of that minimally protective skin may be damaging to the skin.
Melanin protects the skin from many harmful effects of UVR. The incidence of both melanoma and nonmelanoma in darkly pigmented races is low.
The low incidence of the adverse consequences of solar radiation are seen in people who have constitutive dark skin; they are born that way. Tanning is an acquired melanization in response to UV irradiation, presumably to protect against further damage. This raises an important point; if tanning is a protective response, then UVR damage may be the signal that induces a tan. In other words, damage must occur to acquire a tan. There is now experimental evidence that DNA damage is a signal that induces tanning. Eller et al.
added DNA fragments to cultured human epidermal cells and observed the production of melanin. Tanning was induced in vivo when DNA fragments were applied to guinea pig skin. These results suggest UVR-induced DNA damage is a signal that produces tanning. Current thought on multistage carcinogenesis is that persistent DNA damage (mutations) is an important step in the cancer development process.
Implications of patterns of sun exposure in skin cancer
The evidence that UVR causes skin cancer is overwhelming and convincing. Even the indoor tanning industry admits UVR causes skin cancer, although only when delivered as a burn. What is the evidence about UVR exposure patterns and skin cancer? As previously mentioned, the wealth of epidemiologic studies indicate sun exposure causes skin cancer. However, these studies do not address the pattern of sun exposure responsible. The pattern of exposure is an important consideration when evaluating the potential risk of indoor tanning. Epidemiologic studies of sun exposure patterns are difficult, as subjects may be asked to recall sun exposure habits from as long as 40 years ago. In the development of squamous cell carcinoma, such epidemiologic studies suggest a somewhat linear relationship; the greater the cumulative exposure, the greater the incidence of squamous cell carcinoma throughout life.
The development of squamous cell carcinoma is correlated with chronic low-dose exposure, such as that experienced by outdoor workers, and is not correlated with brief intense exposure during vacations.
Chronic low-dose exposure as the etiology is further supported by the almost exclusive appearance of squamous cell carcinoma on chronically sun-exposed skin (face and hands), and its development in skin with signs of chronic photodamage. Melanoma seems to follow a different pattern; rather than cumulative exposure, there is evidence to suggest intermittent exposure is important in the induction of melanoma. This hypothesis is suggested by the observations that melanoma occurs as commonly in women as in men (although men are more likely to work outdoors and have greater cumulative sun exposure), occurs in sites not typically exposed to chronic sun but rather intermittently exposed (the back in men, the lower legs in women), has a relative peak in middle life (which is not expected if cumulative sun exposure is responsible), and is more common in indoor workers than outdoor workers and in those of higher socioeconomic status.
This hypothesis is not proven. For example, it is reported that melanoma is more common in non-sun-exposed skin as support for this hypothesis; however, when surface area is taken into account, melanoma is located in the chronically exposed areas,
in a pattern similar to squamous cell carcinoma. Furthermore, photoaging (evidence of cumulative, chronic sun damage) has been strongly associated with the risk of melanoma in a study from Western Australia.
Recent epidemiologic studies have suggested that the development of basal cell carcinoma may resemble that of melanoma rather than squamous cell carcinoma. Basal cell carcinoma resembles squamous cell carcinoma in that the vast majority are seen on chronically sun exposed skin, with 85% occurring on the head and neck alone.
Surprisingly however, chronically exposed hands rarely develop basal cell carcinoma. The development of basal and squamous cell carcinomas is strongly correlated with photodamaged skin, a sign of chronic exposure.
However, retrospective epidemiologic studies on sun exposure patterns suggest a more complex relationship to sun exposure and basal than that of squamous cell carcinoma. Epidemiologic studies suggest the development of basal cell carcinoma does not correlate with lifetime cumulative sun exposure,
as has been commonly believed. Further analysis does show a positive correlation with recreational sun exposure during the teenage years and the subsequent development of basal cell carcinoma later in life.
A large retrospective study of basal cell carcinoma found that it was correlated with recreational, rather than occupational (intermittent vs. continual) sun exposure.
The sum of these studies suggests the development of basal cell carcinoma at low total doses of sunlight; after about 10,00 to 35,000 cumulative life-time hours of sun exposure, the incidence peaks then plateaus with no further increase in basal cell carcinoma with increasing sun exposure.
This phenomenon varied by skin type. This plateau is reached at relatively low total exposure levels in subjects with a poor ability to tan, and risk may even decrease at very high exposure levels; good tanners showed increasing risk with increasing total exposure in a manner more similar to the development of squamous cell carcinoma.
These epidemiologic studies suggest the risk for the development of squamous cell carcinoma increases with increasing chronic low-dose exposure, while the exposure pattern for melanoma and basal cell carcinoma remain somewhat unclear. In the case of basal cell carcinoma, it has been suggested that after relatively low total doses of sunlight, a plateau in the incidence is reached, but this does not suggest that only “burns” cause basal cell carcinoma.
Animal studies have provided some information about dose-time interactions and the development of skin cancer. Simulated solar radiation is more carcinogenic for the development of squamous cell carcinoma in experimental animals when given in many small doses compared to the same amount of energy given in a few large doses.
The South American opossum Monodelphid domestica is capable of developing melanocytic tumors and has been used as an animal model for melanoma. Studies with this animal suggest multiple low doses of UVR are more effective than high doses in inducing melanoma.
While it is clear UVR causes all three types of skin cancer, in the case of melanoma and basal cell carcinoma it remains unclear what pattern of exposure is most carcinogenic. As pointed out, it is not known whether burning or tanning is more carcinogenic. Even if burns are more carcinogenic than tanning (which is not true for the development of squamous cell carcinoma), with current knowledge it is not reasonable to encourage tanning to prevent carcinogenic sunburns. As previously mentioned, patrons can, and frequently do, burn themselves at indoor tanning parlors, and indoor tanning provides little protection against burns from the sun. The people most likely to develop skin cancer, fair-skinned Type I and II individuals, are by definition poor tanners and will not derive much increase in pigmentation at the tanning parlor. Most importantly, the tanning process itself, in the absence of burning, injures the skin.
Potential benefits of UVL exposure
Psychologic benefit is often sited by indoor tanners as a reason for visiting a tanning parlor. In one survey of tanning parlor patrons, fully 83% reported feeling relaxed while indoor tanning.
When exposed to sunlight, infrared radiation is mainly responsible for the warm glow we feel on the skin, while visible light seems to have a positive effect on mood.
Stern RS. The effects of sunlight on the young and elderly. Proceedings of the National Conference on Environmental Hazards to the Skin, October 1992. Schaumburg, IL: American Academy of Dermatology, 1994:37–41.
DeLeo VA. Tanning salons. Proceedings of the National Conference on Environmental Hazards to the Skin, October 1992. Schaumburg, IL: American Academy of Dermatology, 1994:37–41.
It seems possible we may be able to derive the positive effects of visible light while avoiding the deleterious effects of UVR with adequate UVR sunscreens.
Treatment of dermatologic conditions is a real benefit of indoor tanning. A variety of dermatologic conditions respond to UV therapy. Patients visit commercial tanning parlors as treatment for skin conditions such as psoriasis, eczema, and acne.
Phototherapy in medical use typically consists of UVB lamps or UVA lamps plus psoralen, while commercial tanning parlors utilize principally UVA bulbs with a small amount of UVB with no psoralen, and thus are inherently less therapeutic. Despite this limitation, in one study of psoriaisis treated at a commercial tanning parlor, a reduction in the psoriasis area severity index of 35% was seen.
Treatment was reasonably safe with mild burning in 35% and pruritis in 15%. These results are not as impressive as the results that can be achieved with UVB or PUVA therapy. Most medical therapies and medications have potential side effects: the adversity of these side effects is weighed against the benefit of therapy. As previously mentioned, long-term therapeutic use of PUVA is associated with the development of squamous cell carcinoma
Members of the Photochemotherapy Follow-up Study Genital tumors among men with psoriasis exposed to psoralens and ultraviolet A radiation (PUVA) and ultraviolet B radiation.
so phototherapy is not risk-free. The higher therapeutic efficacy of medical phototherapy (as opposed to a commercial tanning parlor), in a professional and controlled environment allows the patient to receive the greatest benefit at the lowest risk.
The formation of Vitamin D3 in the skin under the influence of UVB represents another potential benefit. Recently, the indoor tanning industry has promoted the idea that indoor tanning prevents internal malignancies by elevating serum vitamin D. The implication of such a claim is that tanning is healthy and that the medical establishment is sadly mistaken in urging tanning avoidance. This idea is not new and was suggested by epidemiologists more than 20 years ago,
but only recently has the indoor tanning industry promoted on the idea. The original epidemiologic observation was that colon and breast cancer have lower incidence in southern latitudes.
The correlation was not perfect, with Japan (in northern latitudes) being a notable exception. This geographic observation has been expanded to include ovarian cancer
and was then used to generate two conclusions. First, people residing in southern latitudes receive greater exposure to UVB, and second, as a result of increased UVB exposure, these people have increased serum vitamin D. Neither of these conclusions are necessarily true, as lifestyle, work habits, recreation, and skin type will all effect cutaneous exposure and reaction to UVB. More importantly, many cancers are known to exhibit geographic variations in incidence in ways that do not correlate with sun exposure. Even small geographic variations, such as within Japan
have been shown to result in variations in the incidence of a variety of cancers, suggesting multiple environmental factors affect the development of cancer in unknown ways. In the case of comparing cancer rates between countries in southern latitudes with those in northern latitudes, multiple differences exist between the populations in question, such as genetic variations between racial groups; variances in diet, lifestyle, chemical exposure; and a variety of other factors in addition to presumed sun exposure. For example, a high fat diet has been suggested as a risk for the development of breast cancer.
Do these factors vary as one moves towards the equator? To extrapolate a geographic variation in cancer rates to the conclusion that vitamin D prevents cancer is an unsupported speculation.
Vitamin D has been studied for a possible effect on cancer. Vitamin D is an essential vitamin required for bone integrity and calcium homeostasis. Synthesis of Vitamin D begins in the skin when UVB converts 7-dehydrocholesterol to previtamin D3 and then to vitamin D3. Vitamin D3 can also be acquired orally in food. Vitamin D3, whether made in the skin or ingested orally, is next hydroxylated in the liver and then again in the kidney to produce the active form 1,25 diyhdroxy vitamin D. Vitamin D is generally believed to be principally acquired through casual sun exposure,
Influence of season and latitude on the synthesis of vitamin D3 Exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 systhesis in human skin.
However, a study in Australia compared regular sunscreen use (SPF 17) vs. placebo in healthy active subjects. This study showed that no one in the study group became Vitamin D deficient as a result of regular sunscreen use.
In a more recent study, patients with xeroderma pigmentosa who practiced rigorous sun avoidance were found to have vitamin D levels within the normal range.
Vitamin D levels can be maintained without intentional tanning.
Laboratory studies have shown that many tumor cell lines in culture, such as breast cancer lines, colon cancer lines, and melanoma lines, express a vitamin D receptor.
If increased serum levels are indeed protective against the development of some internal malignancies, then the simple dietary manipulation of oral supplimentation with vitamin D would be a tremendously simple and effective public health measure. Unfortunately, studies using oral supplementation have not shown such a benefit. For example, epidemiologic studies on dietary prevention of colon cancer with vitamin D have been disappointing
We know that UVR causes skin cancer and photoaging, while a possible protective role for elevated serum vitamin D is uncertain. While UVB will elevate serum vitamin D, so will oral supplementation. To advocate indoor tanning as healthy and protective against cancer seems ill advised at this point. California Suncare, a company that manufactures tanning lotions (accelerators, not sunscreens) used for indoor tanning, was cited by the FTC for making just such a claim in their advertising. This company, which makes products to enhance tanning, advertised that tanning reduces the risk of colon and breast cancer, reduces the risk of skin cancer, prevents bone disorders, lowers elevated blood pressure and cholesterol, treats AIDS and seasonal affective disorder, enhances the immune system, and is not harmful to the skin. In a settlement with the FTC, the company will not make any claims about “health” benefits of tanning, and is required to place a prominent cautionary statement in future advertisements and on their products stating, “CAUTION: Tanning in sunlight or under tanning lamps can cause skin cancer and premature skin aging—even if you don’t burn.”
Organized medicine and the indoor tanning industry are clearly at odds on the risks and benefits of indoor tanning. A significant effort has been undertaken both in this country and around the world to educate the public about the dangers of excessive UVR exposure. This educational effort has been successful; surveys show the public is increasingly aware that UVR causes skin cancer.
There is every reason to believe the indoor tanning industry will continue with an aggressive campaign claiming indoor tanning is not only safe but healthy. Physicians can and should play a major role in educating the public and regulating the indoor tanning industry, both at the state and national level.
Effects of sunscreens and a DNA excision repair enzyme on ultraviolet radiation-induced inflammation, immunosuppression, and cyclobutane pyrimidine dimer formation in mice.
US Food and Drug Administration. The darker side of tanning: Skin cancer, eye damage, skin aging, allergic reactions. Rockville, MD: Public Health Service, 1987; HHS Publication No. (FDA) 87-8270.
Pitts DG, Cullen AP, Hacker PD, et al. Ocular ultraviolet effects from 295 to 400 nm in the rabbit eye. Washington, DC: National Institute for Occupational Safety and Health; DHEW publication No. 77-175.
Different (direct and indirect) mechanisms for the induction of DNA-protien crosslinks in human cells by far and near ultraviolet radiation (290 and 405 nm).
Comparative protection efficiency of UVA and UVB induced tans against erythema and formation of endonuclease sensitive sites in DNA by UVB in human skin.
Stern RS. The effects of sunlight on the young and elderly. Proceedings of the National Conference on Environmental Hazards to the Skin, October 1992. Schaumburg, IL: American Academy of Dermatology, 1994:37–41.
DeLeo VA. Tanning salons. Proceedings of the National Conference on Environmental Hazards to the Skin, October 1992. Schaumburg, IL: American Academy of Dermatology, 1994:37–41.
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