Melody J. Eide, MD, MPH, Department of Dermatology, Henry Ford Hospital, 3031 West Grand Boulevard, Suite 800, Detroit, MI 48202, or email: firstname.lastname@example.org.
Indoor tanning has become increasingly popular over the past decades, despite evidence of an increased risk of melanoma and, possibly, nonmelanoma skin cancer. Tanning bed proponents cite the health benefits of vitamin D to support indoor tanning, including concerns that reduced vitamin D levels or certain vitamin D receptor polymorphisms may be associated with increased incidence of various cancers, including cutaneous melanoma. However, most tanning devices primarily emit ultraviolet A, which is relatively ineffective in stimulating vitamin D synthesis. Health benefits can be fully dissociated from the ultraviolet exposure risks with vitamin D supplementation, although optimal levels remain to be established. Indoor tanning represents an avoidable risk factor for skin cancer, and education of the general public as well as the enactment and stricter enforcement of indoor tanning legislation are a public health imperative.
Skin cancer is the most common of all cancers in the United States. In 2009, it is estimated that there will be more than 1 million new cases of nonmelanoma skin cancer and around 70,000 new cases of melanoma skin cancer (1). Although melanoma accounts for a small fraction of skin cancers, it is responsible for about 73% of skin cancer deaths (2). Incidence rates of both melanoma and nonmelanoma skin cancer have continued to rise over the past decades, especially in young women (3–6).
Traditionally, solar radiation has been the main source of human exposure to ultraviolet (UV) radiation, which is subdivided into UVA, UVB, and UVC. Multiple epidemiological studies have established a causal association between exposure to solar radiation and skin cancer, and solar radiation is classified as “carcinogenic to humans” by the International Agency for Research on Cancer (IARC), a World Health Organization (WHO) agency that classifies carcinogens (7).
In the recent decades, indoor tanning booths have emerged as another source of UV radiation. The indoor tanning business has been one of the fastest growing industries in the United States, with $5 billion in estimated annual revenue (8). Proponents of the tanning industry have promoted the health benefits of stimulation of vitamin D production by tanning bed use. In 2008, the tanning industry published an advertisement in The New York Times claiming that “the benefits of moderate exposure to sunlight outweigh the hypothetical risks” and that “there is no compelling scientific evidence that tanning causes melanoma”(9). In2009, the WHO and IARC classified tanning bed exposure as “carcinogenic to humans.” With evidence showing that tanning bed exposure before age 30 years increases the risk of melanoma by 75%, the IARC placed tanning beds in the highest risk category, alongside other Group I carcinogens including asbestos, cigarettes, and arsenic (7).
This article will review the demographics and trends in the use of indoor tanning devices as well as the current evidence concerning tanning and skin cancer risk. We will also discuss the proposed benefits of tanning, in relation to vitamin D production, and the concept of “moderate tanning,” which is the position supported by the tanning industry.
The indoor tanning industry
Demographics and trends of indoor tanning
Over the last four decades, the availability of, and access to, indoor tanning has increased dramatically. The first commercial tanning center in the United States opened in Arkansas in the 1970s (10). Over the next few decades, indoor tanning became increasingly popular, and in 2006, the mean tanning facility number across 116 large US cities was estimated to be 41.8 facilities per city (11). The mean tanning facility density, computed as the number of indoor tanning facilities in the city plus those in a 3-mi buffer zone divided by the city's total population, was estimated to be 11.8 per 100,000 persons. Significantly higher facility densities are found in cities with higher percentage of whites and lower UV index scores, as seen in multivariate analysis. There is also evidence to suggest that tanning facilities are more concentrated in geographic areas with higher proportions of teenagers and females aged 15–29 years (12).
Use of indoor tanning facilities continues to rise, with the highest reported use in young adult women (13,14). In 1988, as few as 1% of American adults reported using indoor tanning facilities, and by 2007, that percent reporting use had increased to 27% (15). A recent large cross-sectional study examined indoor tanning prevalence among almost 30,000 US adults participating in the 2005 National Health Interview Survey (13). The National Health Interview Survey study found that indoor tanning rates were higher among individuals who were young, white, and female. Rates of indoor tanning varied from 20.4% for those aged 18–29 years to 7.8% for those over 65 years of age. In the multivariate analysis, the most important factors associated with higher indoor tanning rates among those younger than 50 years were being female, being white, having a higher education level, having a moderate-to-high tanning ability, reporting more past-year sunburns, and not staying in the shade when outside. Other studies have similarly found the use of indoor tanning equipment most prevalent among younger females (14).
There is growing concern over the use of indoor tanning facilities by adolescents. Two cross-sectional population-based surveys focusing on US youths aged 11–18 years and their primary caregivers were conducted in 1998 (n= 1196) and 2004 (n= 1613) to assess the use of indoor tanning in adolescents and the correlates of this behavior (16). The prevalence of indoor tanning use by adolescents changed little from 1998 to 2004 (10–11%). Multivariate analysis identified older age (aged 16–18 years), female sex, positive attitudes toward a tan, having a parent/guardian who used indoor tanning within the previous year, and parental permission to use indoor tanning as significantly associated with indoor tanning use. This is consistent with findings from previous studies (17–19). Other significant risk factors for indoor tanning use by adolescents include residence in the Midwest or South, attending a rural high school, substance use, and dieting (17).
Public health measures to reduce tanning bed use by adolescents have been proposed. More than 30 states have considered or adopted legislation to require parental permission for minors to use indoor tanning. Of interest, state legislation restricting access to indoor tanning was not found to be significantly associated with indoor tanning use, likely because of noncompliance with regulation enforcement (16).
Types of indoor tanning equipment
A wide variety of indoor tanning devices exist, including sunlamps, sunbeds, and tanning booths. Before 1980, tanning devices emitted greater amounts of UVB. It was subsequently felt that a UVA-induced tan was safer than one from UVB. Hence, since the 1980s, most equipments emit mainly UVA, with less than 5% in the UVB range (20,21). The Food and Drug Administration (FDA) does not regulate the relative amounts of UVA and UVB in tanning devices, although it does limit acceptable amounts of UVC (22). The UV output and spectral characteristics of tanning devices in the market vary widely, with factors including design (e.g., the number and types of fluorescent tubes, the presence of high-pressure UV lamps, the materials composing the filters, and the distance from the device to the skin), power, and tube aging (21).
Multiple studies have shown concerning evidence that tanning bed patrons are receiving much higher doses of UV radiation than they would from summer sun exposure. Summer solar noon output in Washington, DC, is estimated to be 48 W/m2 UVA and 0.18 W/m2 erythemally weighted UVB (20). In contrast, in a study in North Carolina, UV output in standard tanning facility beds was found to be much higher, with a mean of 192.1 W/m2 UVA and 0.35 W/m2 erythemally weighted UVB (23). In a study by the FDA, for a typical tanner (20 sessions at two minimal erythema dose (MED)/session), the annual UVA doses from commonly used fluorescent sunlamps were 0.3–1.2 times that received from the sun. For a frequent tanner (100 sessions at four MED/session), the annual UVA doses from fluorescent sunlamps were 1.2–4.7 times that received from the sun and 12 times for recently available, high-pressure sunlamps (20).
Another study in Switzerland found that sunbed emission spectra are similar to the sun spectrum in the UVB range, but reach values 10–15 times higher in the UVA range (24). An average erythema-effective irradiance of 0.33 W/m2 was determined for sunbeds. This corresponds to a UV index of 13, which is significantly higher than the UV index of 8.5 of the high summer sun at noon at intermediate latitudes. In such a sunbed, the MED threshold of a person with skin type II is reached after 12.6 minutes (250 J/m2), and that of a person with skin type III after 17.7 minutes (350 J/m2). As visitors of tanning salons with skin types II and III spend, on average, 20 minutes in sunbeds, overexposure to UV radiation is very likely (25).
Motivation for indoor tanning
There are several factors that motivate individuals to attempt to tan their skin. Although the Indoor Tanning Association (ITA) uses the health benefits of vitamin D as justification for indoor tanning, studies show that most indoor tanners do not visit tanning facilities for health benefits. Their main motivations reported include a desire to achieve an attractive tan, and for warmth, light, and relaxation (25,26). In one survey, reasons for using a sunbed included to get a tan or a “top-up tan” (i.e., to extend the tanned appearance before the next full sunbed treatment) in 24%, to get a pre-vacation tan in 13%, and to look or feel good in 39% (27).
There have been several studies that suggest the addictive nature of tanning. A small, randomized controlled trial of opioid antagonism in frequent and infrequent tanners tested whether or not opioid blockade produces withdrawal symptoms in frequent tanners. Results demonstrated that four of eight frequent tanners exhibited withdrawal symptoms consisting of nausea and jitteriness when given an opioid antagonist before UV exposure. This effect was not observed in any of the infrequent tanners (28). Tanners also often report difficulty quitting indoor tanning, and there was a statistically significant positive correlation between frequency of use and difficulty quitting indoor tanning (29). Furthermore, a survey study of 145 beachgoers found that 26% met tanning-modified CAGE (Cut down, Annoyed, Guilty, Eye-opener) criteria and that 53% met tanning-modified Diagnostic and Statistical Manual, Fourth Edition, Text Revision diagnosis for substance-related disorder with respect to UV light tanning (30).
UV carcinogenesis pathway
UV irradiation causes DNA damage that can lead to carcinogenesis. Sunburn is primarily caused by UVB (31). UVB is also far more effective at inducing inflammation than UVA, and in murine studies, it has been estimated to be 1000–10,000 times more effective for inducing skin cancer (32,33). In the past, UVB was considered the only carcinogenic part of the solar spectrum, through the generation of cyclobutane pyrimidine dimers (CPDs) that cause C → T and CC → TT mutations, also known as UVB fingerprint mutations (34). Recent evidence suggests that radiation in the UVA range can also trigger DNA damage via cyclobutane pyrimidine dimer formation and C → T mutations (35,36). Normally, p53, a tumor-suppressor gene, is upregulated by sunlight exposure, leading to increased DNA repair, cell cycle arrest, and apoptosis of damaged keratinocytes. However, p53 itself is also susceptible to mutagenesis, and sunlight-induced p53 mutations have been found in skin precancers and even in sun-exposed skin, rendering these cells apoptosis resistant (37). In vitro studies have confirmed that chronic UVA exposures at environmentally relevant doses can induce malignant transformation of human keratinocytes associated with acquired apoptotic resistance. Malignant transformation was established by the production of aggressive squamous cell carcinomas (SCCs) after inoculation of cells into nude mice (38).
The tanning pathway
As shown in FIG. 1, when UV light damages DNA, this leads to activation of the tumor-suppressor gene p53 in keratinocytes through the displacement of negative regulators such as mouse double minute 2 (MDM2) (39). Activation of p53 induces transcription of a host of target genes, including the pro-opiomelanocortin (POMC) gene and a group of proinflammatory cytokines. The transcription of POMC in sun-exposed keratinocytes leads to an increased release of alpha-melanocyte-stimulating hormone, which is a cleavage product of POMC. The alpha-melanocyte-stimulating hormone (α-MSH) then signals to melanocytes via the melanocortin 1 receptor (MC1R). This results in increased melanogenesis, melanocytic differentiation, and transfer of melanosomes to keratinocytes, which, together, are responsible for the tanning response. This pathway also produces β-endorphin, another POMC derivative, which potentially contributes to the addictive potential of tanning (40).
There is evidence that p53 plays a critical role in UV-induced skin darkening. In a key study by Cui and colleagues, it was found that the absence of p53, as in knockout mice, is associated with absence of the tanning response (40). If signaling further downstream in the tanning pathway through the MC1R receptor is disrupted, tanning also does not occur. This is seen in red-haired individuals who have loss of function polymorphisms of MC1R and burn in response to sun exposure without tanning.
The safe tan
There has been debate about the role of tanning beds as a means of obtaining a “safe tan,” a phrase felt by many dermatologists to be an oxymoron. The ITA states that “moderate tanning, for individuals who can develop a tan, is the smartest way to maximize the potential benefits of sun exposure while minimizing the potential risks associated with either too much or too little sunlight”(8). However, there is evidence to suggest that UV-mediated tanning occurs secondary to DNA damage, and therefore carries an inherent carcinogenic risk (40,41). Based on the tanning pathway, it appears that UV-mediated DNA damage can occur in the absence of tanning. However, tanning does not occur without preceding DNA damage, thus casting doubt over the possibility of a safe or moderate tan.
Furthermore, several animal models provide evidence that skin tumors, both epithelial and melanoma, can form after exposure to UV radiation (42–45). The UV radiation exposure necessary for tumorigenesis may be below the threshold needed to induce inflammation, suggesting that tanners are at a risk of skin cancer even if they do not suffer any side effects such as sunburns. In particular, UVA at doses several hundred-fold too low to be inflammatory can induce skin cancers in animal models and at least contribute to photocarcinogenesis in human skin grafted on to immunodeficient mice (46).
Human studies also provide evidence of UV-induced cutaneous damage. One study in human subjects examined the effects on human skin of equal suberythemal doses (0.5 MED) of solar-simulated radiation (290–400 nm) and UVA (320–400 nm) daily, 5 days a week, for 28 days. Of interest, UVA induced greater cumulative changes than solar-simulated radiation. These changes included a greater cumulative erythema response in the first week of treatment, epidermal hyperplasia and stratum corneum thickening, depletion of Langerhans cells, dermal inflammatory infiltrates, and deposition of lysozyme on elastin fibers. In contrast, a single short-term dose of UVA did not elicit these changes. These findings are important as, first, they demonstrate the cumulative nature of UVA-induced injury after repeated exposure to relatively low doses. Second, they also highlight that the spectral dependence for cumulative damage does not parallel the action spectrum for acute injury. This suggests that similar exposures from indoor tanning can contribute to long-term actinic damage even in the absence of sunburns. This, again, challenges the idea of a safe tan (47).
One common misconception of tanners is that a tan affords protection against further UV damage. In one survey, 17% gave a pre-vacation tan to prevent sunburn as the reason for using a sunbed (27). In individuals who tan easily, UVA first leads to immediate pigment darkening via the oxidation of preexisting melanin. Immediate pigment darkening has no photoprotective effect against UV-induced skin redness or DNA damage (48). Delayed tanning occurs subsequently via melanin synthesis, with variations dependent on tanning ability and the UV spectrum of the tanning device. Of note, it was found that a UVB-induced tan, such as one obtained from sunbathing, confers only minimal photoprotection, equivalent to a sunscreen with a sun protection factor of 3. A visually identical UVA-induced tan, such as one from a sunbed, provides even less protection, with a sun protection factor of around 1.3 (49). Tanners with this misconception may spend a longer time in the sun, thus further increasing the risk for skin cancer.
Indoor tanning and skin cancer risk
Accumulation of compelling scientific evidence requires significant investigation and time. Initial studies on the carcinogenic effects of indoor tanning were inconclusive (50). Tanning bed proponents, including the ITA, used the lack of scientific evidence that tanning bed use was associated with melanoma to support the acceptance of indoor tanning. However, a recent landmark study by the WHO's IARC Working Group confirms the association between indoor tanning and melanoma (21). This is a meta-analysis of 19 reports evaluating indoor tanning behavior and malignant melanoma risk and other skin cancers, and includes a total of 7355 cases. Ever-use of indoor tanning equipment was associated with an increased risk of melanoma (relative risk (RR) 1.15, 95% confidence interval (CI) 1.00–1.31), although there was no consistent evidence of a dose-response relationship. Of note, based on seven of the included reports, first exposure to indoor tanning before 35 years was associated with a concerning 75% increased risk of developing melanoma (RR 1.75, 95% CI 1.35–2.26). The present study provides the most extensive evidence to date of the risk of melanoma associated with indoor tanning and supports that young adults should be discouraged from using indoor tanning equipments.
Evidence regarding tanning bed use and nonmelanoma skin cancers has also been examined. The IARC meta-analysis studied the risk of nonmelanoma skin cancers (21). They found that based on three studies, ever-use of indoor tanning equipment was associated with an increased risk of SCCs (RR 2.25, 95% CI 1.08–4.70), but they did not find sufficient evidence to support an association with basal-cell carcinomas (BCCs).
Although more investigation is necessary, there are studies suggesting an association between indoor tanning and BCC. Karagas and colleagues designed a population-based, case-control study that included 603 BCC case patients, 293 SCC case patients, and 540 controls (51). Karagas et al. found that any use of tanning devices was associated with odds ratios of 2.5 (95% CI 1.7–3.8) for SCC and 1.5 (95% CI 1.1–2.1) for BCC, which persisted after adjustment for history of sunburns, sunbathing, and sun exposure. Similar to melanoma, there was a trend for highest risk of BCC and SCC among those who began using tanning devices earlier, including before age 20 years, before 1975, or 20 or more years before being diagnosed with skin cancer, although these trends were not statistically significant. Another study also found that young women with a BCC had, on average, almost twice as many lifetime tanning salon visits as matched controls (52).
The vitamin D controversy
Vitamin D and cancer
Vitamin D insufficiency has received increasing attention in terms of health risks, including cancer susceptibility. Most experts agree that the optimal serum 25-hydroxyvitamin D3 is at least 80 nmol/L. However, the optimal level to be recommended for all adults remains to be determined (53). There have been an increasing number of studies that suggest reduced serum 25-hydroxyvitamin D3 levels are associated with an increased incidence and an unfavorable outcome of various types of cancers. A wide range of cancers, including colorectal, prostate, breast carcinoma, and non-Hodgkin's lymphoma, have been associated with vitamin D deficiency, although the evidence is not conclusive (54).
Of particular interest, recent studies have shown a possible association between serum 25-hydroxyvitamin D3 levels and melanoma prognosis. One study in Europe examined serum 25-hydroxyvitamin D3 levels in 205 patients with malignant melanoma and 141 healthy controls, and found the serum 25-hydroxyvitamin D3 levels were significantly reduced in stage IV melanoma patients (median = 32.7 nmol/L) as compared with stage I melanoma patients (median = 40.9 nmol/L) (p= 0.0006) (55). There was a trend toward a greater tumor thickness of the primary cutaneous melanoma in patients with serum 25-hydroxyvitamin D3 less than 25 nmol/L (2.6 mm) as compared with those with serum levels > 49.9 nmol/L (1.5 mm) (p= 0.08), as well as earlier distant metastatic disease (median 24.4 months vs. 29.5 months, p= 0.6). However, it should be noted that there was a high prevalence of vitamin D deficiency in both the melanoma group (78%) and the control group (63%), and, importantly, when all melanoma patients were considered as a whole, there was no significant difference in the serum 25-hydroxyvitamin D3 levels (median = 35.7 nmol/L in melanoma patients and 38.9 nmol/L in the control group, p= 0.4). This highlights the fact that most individuals with vitamin D deficiency are healthy without a detectable disease.
Another British study also sought to determine the relationship between vitamin D levels and melanoma relapse. A retrospective pilot study of 271 melanoma patients found that non-relapsing patients had a higher mean 25-hydroxyvitamin D3 level than patients with recurrence (p= 0.3) (56). A subsequent prospective cohort of 872 patients was assembled, with a median follow-up of 4.7 years. The group found that higher serum 25-hydroxyvitamin D3 levels at diagnosis was associated with both lower Breslow thickness (p= 0.002) and better survival from melanoma, independent of Breslow thickness. The adjusted hazard ratio for relapse-free survival was 0.79 (95% CI 0.64–0.96, p= 0.01) for a 20-nmol/L increase in serum level.
Vitamin D supplementation has also been associated with decreased relapse. Regular intake of supplemental vitamin D can lead to higher serum levels and has been associated with a trend toward decreased risk of melanoma relapse (odds ratio = 0.6, 95% CI 0.4–1.1, p= 0.09) (56). A meta-analysis also found a significant protective effect for cutaneous melanoma with vitamin D intake (summary RR 0.63, 95% CI 0.42–0.94) (57).
In an effort to explain this association, research has focused on vitamin D receptor (VDR) polymorphisms, as VDR is the crucial mediator for the cellular effects of vitamin D and also interacts with other cell-signaling pathways that influence cancer development (58). A recent meta-analysis was performed looking at the association between the most studied VDR FokI and BsmI polymorphisms and the risk of prostate, breast, colorectal, and skin cancer. The study found a significant 30% increase in skin cancer risk and 14% increase in breast cancer risk for carriers of FokI ff compared with the wild-type FF genotype, and a significant 17% decrease of prostate cancer risk for BsmI Bb in comparison with bb carriers (59).
Another meta-analysis found a similar positive association of the FokI f allele with cutaneous melanoma (summary RR = 1.13, 95% CI 1.01–1.25). Compared with the FF wild-type genotype, the summary RR for cutaneous melanoma was 1.21 (95% CI 1.03–1.42) and 1.21 (95% CI 0.95–1.54) for the FokI Ff and ff genotypes, respectively. The BsmI B allele, however, showed a statistically significant negative association with cutaneous melanoma (summary RR = 0.84, 95% CI 0.75–0.94). The summary RR was 0.78 (95% CI 0.65–0.92) and 0.75 (95% CI 0.59–0.95) for Bb and BB genotypes, respectively, in comparison with the wild-type bb genotype. Findings were similar when nonmelanoma skin cancers were included (57). These findings are also supported by other studies (56,60).
Compared with the F allele, the f allele results in a VDR protein that is less effective, and thus, may increase cancer risk especially at lower serum vitamin D levels (59). Further study of the vitamin D pathway and its influence on pathogenesis and progression of malignant melanoma and other malignancies is warranted. Additional studies are also needed to establish optimal serum levels for these patients.
Indoor tanning and vitamin D levels
Studies have examined the association of indoor tanning use with vitamin D levels. Although one study found that sunbed use increased serum 25-hydroxyvitamin D3 levels, the study was confounded by the fact that the tanners also stayed out in the sun significantly longer (61). As mentioned, although the action spectrum for vitamin D synthesis is predominantly in the UVB range, peaking at around 300 nm, most indoor tanning devices emit mainly UVA (62). A recent randomized controlled trial found that although tanning devices emitting less than 1.5% UVB do lead to increases in serum 25-hydroxyvitamin D3 levels, the increase reaches a plateau after only four sunbed sessions of 6 minutes (63). The increase is dependent on the UVB radiation dose, with sunlamps emitting 1.4% UVB leading to more than double the average increase in serum levels compared with sunlamps emitting 0.5% UVB. However, increasing the UVB dose and exposure time led to increasing side effects, such as erythema and polymorphous light eruption.
Skin phenotype influences the response to UV radiation. Individuals with Fitzpatrick type I to II skin burn readily and tan minimally, and would achieve maximal vitamin D photosynthesis within less than 10 minutes of midday spring or summer sun exposure in New York or Boston (62). In contrast, those with darker skin types burn less and tan more, but also photosynthesize limited amounts of vitamin D because of UV absorption by melanin (64). Thus, those at highest risk of photodamage, which includes white females who are most likely to go to tanning salons, are in fact at the lowest risk of vitamin D insufficiency.
Indoor tanning, skin cancer, and vitamin D
In June 2009, the IARC published a special report reviewing human carcinogens. Of note, the Working Group raised the classification of UV-emitting tanning devices to Group 1, “carcinogenic to humans,” based on data that strongly link tanning devices to increased risk of melanoma of the skin and ocular melanoma (7).
In contrast, although there are data to suggest the association of vitamin D with incidence and outcomes of various cancers, including melanoma, no clear causal relationship has been established, and optimal serum levels remain to be defined. Given the relative inefficiency of UVA-emitting tanning devices in increasing serum vitamin D levels, especially in those most at risk of vitamin D deficiency, indoor tanning is not recommendable as a way to achieve optimal vitamin D levels in the general public.
Furthermore, a sufficient vitamin D level can be established with 5–30 minutes of midday sun exposure twice a week to the face, arms, legs, or back; a healthy diet; or oral supplements. The American Academy of Dermatology currently recommends a daily total dose of 1000 IU of vitamin D for those at risk of vitamin D insufficiency or those who regularly and properly practice photoprotection (65).
Indoor tanning regulation
The FDA regulates equipment specifications, exposure schedules, use of eyewear, and warning statements. Current FDA tanning bed warnings include the increased risk of skin cancer and premature aging (22). The FDA has recommended exposure schedules for first-time users based on skin type, suggesting that exposure be limited to no more than 0.75 MED three times the first week, followed by a gradual increase to maintenance doses of a maximum of 4.0 MED delivered weekly or biweekly (66). However, in San Diego, only 6% complied with these maximum tanning frequency recommendations (67). In North Carolina, 95% of patrons exceeded recommended limits and 33% began tanning at the maximum doses recommended for maintenance indoor tanning (23). In one survey, 58% of users reported burns from indoor tanning, which was significantly associated with the frequent use of indoor tanning, greater or equal to six sessions within the past year (16). Previous studies have also reported that indoor tanning causes burns and erythema in 18–55% of users (68–70).
The increased risk of skin cancer, especially with early use of tanning devices, coupled with the increasing prevalence of indoor tanning in adults and adolescents, all point toward the need for interventions and regulations on indoor tanning use, in particular, for minors. The WHO has recommended a complete ban on indoor tanning for anyone under the age of 18 years. The IARC states, “policymakers should strongly consider enacting measures, such as prohibiting minors and discouraging young adults from using indoor tanning equipment, in order to protect the general population from additional risk for melanoma and squamous cell skin cancer”(21). Currently, around 30 states have considered or adopted legislation to regulate the use of tanning facilities by minors. Most states require written parental consent to tan for minors, and some states require that a parent accompany minors or impose a minimum age at which adolescents are allowed to use indoor tanning facilities, generally age 14 years.
Although an electronic survey found that most indoor tanning facility operators believed that minimum age (92%) and parental consent (80%) regulations for indoor tanning should be required, in practice, compliance with youth access laws is low (71). In Minnesota and Massachusetts, laws require parental permission for those younger than 16 or 18 years of age, respectively, for indoor tanning. In one study in these two states, 81% of 200 indoor tanning businesses sold a session to 15-year-old girls who tried to purchase a tanning session without parental consent, on at least one of two tries (72). In North Carolina, only 13% of facilities complied with a required guardian consent form for youths, whereas 43% of facilities complied with parental consent regulations in San Diego (67,73).
Other aspects of indoor tanning, including customer notification of risks, UV exposure control, equipment standards, facility operations, operator training and responsibilities, sanitation, enforcement/legal issues, and penalties for violations, are also regulated at the state level (74). However, enforcement of state indoor tanning laws leaves much to be desired. In 2008, one study surveyed contacts, mostly state or local city health agencies' employees, who were knowledgeable about, and responsible for, enforcement practices in 28 states with tanning legislation at the time (75). The study found that at least 32% of the cities did not inspect indoor tanning facilities for compliance with the state law, and another 32% conducted inspections less than annually. Slightly less than half of the cities gave citations to tanning facilities that violated the state law.
The provision of informed consent by indoor tanning facility operations has also been found to be inadequate. In a survey of 400 facilities in four states, 87% advised patrons of the potential risk of sunburn from indoor tanning, but in three of four states, less than half of facility operations informed patrons about the risk of skin cancer and premature aging (76). Similarly, only 19% of North Carolina tanning facilities provided consumers with a statement outlining the risks of UV tanning, and only 17 and 32% of San Diego facility operators stated that sunburn and skin cancer were a risk, respectively (67,73). It is clear that future evaluations of indoor tanning legislation need to measure not only the written law, but also its implementation and enforcement.
In one survey of Chicago beachgoers, knowledge of limiting tanning to help prevent melanoma increased from 1988 (25%) to 1994 (88%), but then decreased in 2007 (67%), possibly because of increase in the attitude that having a tan looks better. In the same time frame, use of indoor tanning beds increased from 1988 (1%) to 2007 (27%) (15).
Given mounting evidence of the risks of tanning bed use, education of the general public, in particular by physicians, is critical. Only 15% of respondents in a survey in 2007 reported ever talking to a doctor about indoor tanning, although physicians, especially dermatologists, were considered the most trusted information source (15). Patients should also be counseled about non-UV means to obtain recommended serum vitamin D levels, and further studies need to be performed to address the role of vitamin D in the pathogenesis of various cancers, as well as to establish optimal serum levels. Lastly, legislation to expand regulation of the tanning industry, especially with regard to access by minors, is crucial. Although having such legislation in place is the first step, it is clear from various studies that mechanisms to enforce these regulations need to be addressed as well in order to reduce the burden of skin cancer on society. With respected public health organizations such as the WHO warning of the dangers of indoor tanning, especially before the age of 30 years old, it is hoped that public awareness and recognition of associated health risks will increase and tanning bed use will ultimately decline.