Introduction

There are benefits and risks to sunlight exposure of the skin. Our skin utilizes ultraviolet light to produce vitamin D and provides protection against the harmful effects of the sun’s ultraviolet light (UVL). Fair skin more easily synthesizes vitamin D but is more vulnerable to sun-induced skin cancer, compared with darker skin which is better suited for accommodating intense sunlight.¹ However, there is no such thing as a “safe” suntan. This review discusses ultraviolet A (UVA) and ultraviolet B (UVB) light induced skin reactions and various aspects of sun protection with sunscreen.

UVA and UVB Light-Induced Skin Reactions

• Sunburn is produced largely by UVB exposure. Most other photosensitive reactions, such as idiopathic, phototoxic and photoallergic reactions, as well as sun rashes and the aggravation of existing conditions, are predominantly produced by UVA exposure.
• The types of UVL reactions can be categorized as short- and long-term effects (Table 1).
• Short-term effects of UVL include sunburn and idiopathic reactions to UVL (polymorphous light eruption – PLE).
• PLE is an itchy rash seen within hours of sun exposure. It may last for days, in contrast to solar urticaria which develops within minutes of exposure and lasts for hours only.1
• Further short-term effects are phototoxic and photo-allergic skin reactions, caused by a number of drugs and chemicals (e.g. tetracyclines and thiazides) which can produce either a phototoxic or photo-allergic reaction.¹
• Many pre-existing conditions are triggered by UV radiation. Some of the significant ones include: rosacea; seborrheic dermatitis; melasma; discoid and systemic lupus; dermatomyositis; herpes simplex; viral exanthema; pemphigus; Darier’s disease; and porphyria.
• Long-term effects of UVL include photodamage and actinic keratosis, photo-aging and skin cancer.
• The primary environmental cause of skin cancers and aging of the skin is UVA and UVB radiation from the sun.^2-5 Its damaging effects are cumulative, so daily protection throughout life is important.^5-6
• Given the aging “baby boomer” population, an increase in the incidence of skin cancer is likely to occur but will not be limited to this cohort.
• The rate of melanoma in young Caucasian women (<44 years) has increased 6.1% annually, which may reflect recent trends in indoor tanning, such as by tanning beds that use mainly UVA light.⁷

Sunscreen Application is One of the Necessary Measures for Photo-Protection

• Photoprotection should be encouraged to prevent both immediate and long-term adverse effects of excessive sun exposure.
• Minimizing skin exposure to the sun, including wearing protective clothing and seeking shade, remain the most effective means of avoiding sun-induced skin cancer.
• Because being in the sun provides a great sense of well-being, it is important to mitigate its harmful effects through the regular use of sunscreens.
• Sunscreens are either:
  1. physical (absorb and reflect sunlight) and are made of inorganic particles such as zinc oxide or titanium dioxide;
  2. chemical organic substances (absorb light energy) such as cinnamates (octinoxate), benzophenone (oxybenzone) salicylates (octisalate), octocrylene, ensulizone (phenylbenzimidazole sulfonic acid) and avobenzone (butyl methoxydibenzoylmethane).
• Sunscreen is available as a lotion, spray, gel or other topical product that absorbs or scatters and reflects part of the sun’s UV radiation on the skin to help prevent photodamage.^2-4
• Originally developed to block UVB light to prevent sunburn, sunscreens inadvertently left the user unprotected against the negative effects of increased UVA exposure.
• Recent technological advances have produced a new generation of full spectrum UVA stable sunscreens, which, when used regularly, are likely to help reduce the risk of photo-aging and skin cancer.⁸
• Avobenzone is likely the most effective broad spectrum UVA sunscreen.⁹ However, by itself it is unstable when exposed to sunlight. Consequently, several different companies developed systems to stabilize it.¹⁰ A combination of diethyl 2,6-naphthalate, avobenzone and oxybenzone has been formulated under the name Helioplex™ (Neutrogena®/Johnson & Johnson) (Figure 1).¹¹
• Another example is Ecamsule (Mexoryl™ SX, L’Oreal), a benzylidene derivative, which has a peak absorption in the UVA spectrum at 345nm.
• Many of the chemicals effective in UVA protection automatically raise the sun protection factor (SPF) value of the vehicle, as they also protect against the UVB part of the spectrum.
• An ideal sunscreen should block the whole spectrum of UVL.

Figure 1: Avobenzone spectrum of protection compared with physical screens.

Sun Protection Factor

• The SPF is a measure of the protectiveness of a sunscreen against the sun’s UV rays.
• Approximately 80% of sunburn comes from the UVB rays in sunlight and 20% is attributable to the UVA range.
• SPF is based on determining the minimum erythema dose (MED), defined as the smallest amount of energy required for triggering the erythema, in areas of sunscreen protected and unprotected skin.^12,13
• Studies have shown that protection against sunburn with sunscreen is directly related to SPF levels.¹⁴ The protection provided is related to the amount of sunscreen applied to the skin.¹² The SPF is calculated using 2 mg/cm² (an equivalent of two tablespoons) of sunscreen applied to the area of interest. If the unprotected skin burns in 10 minutes, properly applied sunscreen at SPF 15 will provide protection against sunburn for 150 minutes (2 ½ hours).
• The protection provided by sunscreen is related to the amount of product applied as well as the correct selection of the sunscreen.¹² Most people apply only 25-50% of the correct amount of sunscreen required, which means they do not have the level of SPF protection indicated on the label. Application of an adequate amount of sunscreen is by far the most important factor influencing efficacy.¹²

Adherence to Sunscreen Use

• Sunscreen compliance is, in part, related to the degree of individual awareness of the cumulative nature of sun damage, balanced against the desire to have a sun tan.
• The initial consideration when choosing a sunscreen should be sunburn prevention, using a sunscreen that offers broad spectrum UV protection.
• Good UVA protectors also tend to increase the SPF because they are broad spectrum. Choosing a cream, lotion, stick, gel or spray that feels good on the skin is critical for good adherence: it is unreasonable to expect that sunscreens will be used if they do not feel comfortable.
• Generally speaking, the lighter feeling sunscreens tend to be more popular. Physical blocks tend to give a white appearance to the skin and are not as protective with respect to UVA as organic screens. However, developments including micronization of the particles and nanotechnology have improved these types of sunscreens.¹⁵
• Daily use of sunscreen is important in people at high risk of skin cancer. At sufficient SPF levels, sunscreens are effective in protecting the skin from actinic keratoses and squamous cell carcinomas.⁸
• Daily use of sunscreens is also important for people who want to maintain youthful looking skin.

Potential Issues When Using Sunscreen

• A burning or stinging sensation upon application is the most frequent complaint with sunscreen application.
• Contact urticaria may develop on application of sunscreen in some individuals.
• Irritant dermatitis and allergic contact dermatitis to fragrances and preservatives may occur.
• While it has long been thought that sunscreens are the most common source of photo-allergy, this has been disputed of late.¹⁶
• Acne may be induced or exacerbated by sunscreens.¹⁶
• Individuals with oily skin need oil-free, alcohol-based gels or lighter lotions.
• The US Food & Drug Administration recently issued a warning regarding flammability of alcohol-based sunscreens, based on reports of burn incidents. The agency recommends that while applying and wearing sunscreen products labeled as flammable the wearer does not smoke and should avoid open flames from lighting cigarettes, lit cigarettes, grilling, candles or sparking materials.

Some Controversies Around Sunscreens

• There are claims that avobenzone and oxybenzone may be linked to breast cancer because of their estrogenic effects. Despite the fact that benzene rings are proficient at neutralizing free radicals they are also mutagenic.¹⁷ It should be noted that these estrogenic effects are hundreds of times weaker than those associated with soy. ¹⁷
• Controversy also exists regarding retinyl palmitate (also benzene ring) and an increased risk of skin cancer. This increase was seen in albino mice when retinyl palmitate was used at significantly high doses and combined with UV light. Experience over several decades has shown a skin cancer protective effect with the use of vitamin A products.¹⁸
• There is some concern around the use of nanotechnology in physical sunscreens related to their systemic absorption. However, it appears that the particles stick together in what is called “agglomeration,” preventing systemic absorbption.¹⁶

Vitamin D and Sunscreens

• UVB is needed for vitamin D production in the skin. While there are conflicting reports, it is thought that sunscreens, applied for intended use (according to the manufacturer’s instructions) will not be sufficient to prevent vitamin D production in most people.
• People with ethnically dark skin and the elderly are more at risk for reduced vitamin D production with the use of sunscreens.
• Additionally, obese individuals who experience fat malabsorption may also be at greater risk of reduced vitamin D absorption, as they are less able to absorb oral vitamin D. ²⁰

The 5 Sun Protection Commandments

1. Choose sunscreen with SPF 30 or more that is cosmetically acceptable to you.
2. Apply 15 minutes prior to heading outdoors and re-apply every 2 hours when exposed.
3. Use daily if you have a risk of skin cancer or have a photosensitive condition.
4. Choose a water resistant product during recreational activity.
5. Wear broad-brimmed hats plus proper sunglasses.

Conclusion

While sun exposure does have negative effects on the skin, modern sunscreens are safe and effective in preventing sunburn, photodamage and skin cancer. However, it must be noted that the SPF is essentially a laboratory number: in real world experience people do not typically apply the same quantity of sunscreen on the skin as is used in laboratory tests. This causes confusion and means that the protection offered is in fact less than appears on the product label. To some extent, this shortfall may be compensated for by using a higher SPF sunscreen. With respect to safety concerns around sunscreens, they have yet to be scientifically proven. Therefore, regular sunscreen use should be mandatory for those with a personal or family history of skin cancer light-induced dermatoses, or connective tissue disease. Further, individuals with fair skin should also be advised on the risk of cumulative sun exposure and the benefits of sunscreen use.

References

1. Lim WL, Jlm Hawk. Photodermatologic disorders. Chapter 87. Dermatology textbook Bolognia et al 3rd edition.
2. Schalka S, et al. Photodermatol Photoimmunol Photomed. 2009;25(4): 175-180.
3. Schalka S, et al. An Bras Dermatol. 2011;86(3):507-515.
4. Nicolaidou E, et al. et al. J.Cosmet Dermatol. 2006;5(4):322-327.
5. Dennis LK, et al. Ann. Intern. Med. 2003;139(12):966-978.
6. Moyal D, et al. J. Am Acad Dermatol. 2008;58(5 Suppl 2): S149–S154.
7. Little EG, et al. Dermatol Clin. 2012;30(3):355-361
8. Naylor MF, et al. Arch dermatol. 1997;133(9):1146-1154
9. Shaath NA. Photochem Photobiol Sci. 2010;9(4):464-469.
10. Cole C. Photodermatol Photoimmunol Photomed. 2001;17(1): 2-10
11. Cole C, et al. Comparison of photoprotection efficacy and photostability of broad spectrum sunscreens. Presented at: The 64th Annual Meeting of the American Academy of Dermatology; San Francisco, CA; March 3-7, 2006. Poster #P2617.
12. Faurschou A, et al. Br. J. Dermatol. 2007;156(4):716–719
13. Bissonnette R, et al. J. Am Acad Dermatol. 2000;43(6):1036-1038.
14. Ou-Yang H, et al. J Am Acad Dermatol. 2012; 67(6):1220-1227.
15. Lodén M, et al. Br. J. Dermatol. 2011; 165(2):255-262.
16. Shaw T, et al. Dermatitis. 2010; 21(4):185-198.
17. Wang SQ, et al. Arch Dermatol. 2011;147(7):865-866.
18. Shapiro SS, et al. J Drugs Dermatol. 2013;12(4):458-463.
19. Diehl JW, et al. Dermatol Ther. 2010;23(1):48-60
20. AAD recommendations (Dermatology Daily–AAD July 8, 2013). Personal communication to author July 8, 2013.

Key Words: cosmetics, photoprotection, SPF, sun protection factor, sunscreen, UV, ultraviolet light

Sunscreens are perceived as gooey, sticky, uncomfortable products that are difficult to apply and distasteful to wear. This accounts for dismal compliance when dermatologists ask patients to use daily sunscreen. Since the time delay between accumulated sun exposure and skin cancer can be more than 20 years, patients do not receive a short-term benefit from photoprotection. Any marketing genius will tell you that compliance requires both self-perceived short- and long-term benefits in order to reinforce positive behavior. This insight into the human psyche led skin care companies to develop the concept of the “multifunctional cosmetic,” which by definition delivers several benefits in one bottle. Currently, popular multifunctional cosmetics include sunscreen-containing moisturizers and facial foundations.

Sunscreen-containing Moisturizers

Sunscreen-containing moisturizers have dramatically improved photoprotection compliance. These products can provide moisturization by decreasing transepidermal water loss through creation of an environment that is optimal for barrier repair. Through the use of occlusive agents such as dimethicone, petrolatum, and mineral oil, as well as the use of humectants such as glycerin, propylene glycol, and hyaluronic acid, a therapeutic moisturizer can aid in the restoration of the corneocyte and intercellular lipid organization. In addition, a sunscreencontaining moisturizer can deliver effective ultraviolet B (UVB) and ultraviolet A (UVA) photoprotection, thereby contributing to the prevention of sunburn, photoaging, and skin cancer simultaneously. Through the inclusion of active ingredients such as retinol, niacinamide, and/or green tea, additional antiaging benefits may be achieved. In short, one bottle of sunscreencontaining moisturizer can be designed to moisturize the skin, repair the barrier, stop sunburn, prevent skin cancer, minimize photoaging, and potentially reverse oxidative insults.

Most sunscreen-containing moisturizers are formulated at a sun protection factor (SPF) between 15 to 30. SPF 15 products can be designed with little UVA photoprotection and they may or may not be labeled as broad spectrum. SPF 30 products must contain both UVB and UVA photoprotective ingredients and are therefore preferred. This logic encouraged the American Academy of Dermatology to restate its sun protective recommendations and raise the minimum recommended SPF to 30. For most formulations, SPF 30 is a nice compromise between photoprotection and aesthetics. Once the SPF raises much above 30, the product becomes sticky. Many highly effective sunscreen filters, such as octocrylene, are thick oils and increasing their concentration in the final formulation leads to poor aesthetics.¹ Yet, for casual limited sun exposure, SPF 30 provides excellent daily photoprotection.²

Sunscreen-containing Facial Foundations

If a sunscreen-containing moisturizer is tinted to match the skin, it can then be classified as a facial foundation. Facial foundations are another category of multifunctional cosmetics that can be helpful in encouraging sun protection compliance. There are four basic facial foundation formulations: oil-based, water-based, oilfree, and water-free forms. The most popular facial foundations are liquid oil-in-water emulsions containing a small amount of oil in which the pigment is emulsified with a relatively large quantity of water. The primary emulsifier is usually a soap, such as triethanolamine or a nonionic surfactant. The secondary emulsifier, present in smaller quantity, is usually glyceryl stearate or propylene glycol stearate.

Facial foundations are designed to color, blend, and camouflage the underlying skin and create an illusion of perfect complexion beauty. The ability of a foundation to conceal or cover the underlying skin is known as “coverage.” Higher coverage products deliver better photoprotection while lower coverage products deliver less photoprotection. In this case, the photoprotection is due to inorganic filters in the formulation, which commonly include titanium dioxide, zinc oxide, talc, kaolin and precipitated chalk. Even coloring agents, such as iron oxide, can function as inorganic filters.

Sheer coverage foundations with minimal titanium dioxide are almost transparent and have an SPF around 2 while moderate coverage foundations are translucent and have an approximate SPF of 4 to 5. Thick, waterproof cream facial foundations that are used for camouflage purposes or post-surgically completely obscure the underlying skin and have an unlimited SPF because they function as a total physical block. For persons with severe photosensitive facial skin disease, such as lupus, these waterproof cream facial foundations offer superior photoprotection.

In addition to the normal photoprotective constituents of a facial foundation, other inorganic and organic filters can also be added. The most commonly added organic filter is octyl methoxycinnamate. It is an excellent UVB filter with no aesthetic issues and limited allergenicity.¹ It may be combined with other filters, such as oxybenzone, to increase coverage in the UVA range.^3,4 Some of the newer facial foundations even add avobenzone that has been photostabilized with octocrylene and oxybenzone. Selecting the proper mixture of sunscreen ingredients is key to providing superior photoprotection and aesthetics while offering a high broad spectrum SPF.

New sunscreen-containing facial foundation formulations are available in a variety of forms: liquid, mousse, water-containing cream, soufflé, anhydrous cream, stick, cake, and shake lotion. Liquid formulations are most popular because they are the easiest to apply, provide sheer to moderate coverage, and create a natural appearance. As previously mentioned, they contain mainly water, oils, and titanium dioxide. To this basic formulation, sunscreen filters can be added. For most patients, this type of sun protection through a facial cosmetic is the best way to increase compliance.

Other formulations of facial foundations can also be created. If the liquid is aerosolized, a foam foundation known as a mousse is produced. A cream foundation has the additional ingredient of wax, which makes a thicker, occlusive, more moisturizing formula. These thicker cream facial foundations also deposit more pigment on the skin surface and obscure more of the underlying skin. Cream formulations typically offer better photoprotection than liquids. Whipping the cream produces a soufflé foundation. Finally, an anhydrous cream with no water in its formulation provides enhanced occlusion and exceptional long-lasting coverage. These products resist water removal better and can be used with greater success in persons who need superior photoprotection when perspiring heavily.

There are three final forms of facial foundation that have been adapted for sun protection. These include stick, cake, and powder facial foundations. Adding more wax to the cream facial foundation results in a stick that can be stroked across the face. These facial foundation sticks are also water-free and provide water resistant photoprotection. This is in contrast to the cake and powder facial foundations that are dusted over the face. A cake foundation is a compressed powder consisting of talc, kaolin, precipitated chalk, zinc oxide, and titanium dioxide compressed into a cake that is applied to the skin with a sponge. If the ingredients are not compressed into a cake, they can be left loose in a jar with a brush attached to one end. This loose powder facial foundation is sometimes called a mineral makeup.

Mineral makeup are some of the newest sun protective cosmetics. They are dusted onto the face and can be just easily dusted off the face. Powders do not provide water resistance characteristics, making them only appropriate for day wear with casual sun exposure. Also, the powder does not provide an even film over the face, allowing for uneven photoprotection. For the patient with serious sun protection needs, it is best to apply a sunscreencontaining moisturizer followed by a mineral makeup. The moisturizer will allow the powder to stay in place and offer increased photoprotection due to layering. It is important to note that the SPF rating of the powder and the moisturizer are not additive. For example, an SPF 15 sunscreen-containing moisturizer and an SPF 15 mineral makeup do not combine to confer SPF 30 photoprotection. Each product application will make a more even sun protective film, allowing closer approximation of the SPF 15 rating.

Multifunctional SPF Rated Cosmetics

Multifunctional SPF rated cosmetics are increasing in the marketplace. Lipsticks, lip balms, facial serums, and eye creams are all commercially available formulations that can possess an SPF rating. Increasing patient compliance with sun protection through the inclusion of sunscreen filters in many commonly used facial products can be a synergistic effect. Patients do not wish to purchase or use multiple products that are expensive and time consuming to apply. The multifunctional cosmetic is an important dermatologic advance. This trend is expected to continue with extensions to male skin care, such as sunscreencontaining after shave preparations. Sunscreen filters are also finding their way into hair care products that claim to prevent color fading. Protection from UV exposure improves color purity and retention, lengthening the time a hair dye can be worn until repeat dyeing is required.⁵ This is a positive trend for dermatology as it reinforces our safe sun message to our patients.

Conclusion

With the widespread emergence of sunscreen-containing moisturizers, foundations, and various lip treatments, it is apparent that the cosmeceutical industry has embraced the importance of photoprotection. These multifunctional products have the potential to encourage patient adherence to regimented sunscreen use by facilitating ease of application, thus minimizing the need for any significant behavioral modification, particularly during the morning routine.

References

1. Draelos ZD. Photoprotection in colored cosmetics. In: Lim HW, Draelos ZD (eds). Clinical guide to sunscreens and photoprotection. New York: Informa Healthcare USA, (2008).
2. Draelos ZD. Sunscreens and hair photoprotection. Dermatol Clin 24(1): 81-4 (2006 Jan).
3. Steinberg D. Regulatory review: sunscreens. Cosmet Toiletries 121(11):41-6 (2006 Nov).
4. Caswell M. Sunscreen formulation and testing. Cosmet Toiletries 119(9):49-58 (2001 Sep).
5. Wakefield G, Stott J, Duggan A. UVA skin protection: issues and new developments. Cosmet Toiletries 122(2):57-62 (2007 Feb).

ABSTRACT
Key to the management of photodermatoses is photoprotection, which includes seeking shade; wearing photoprotective clothing, wide brimmed hats, and sunglasses; and applying sunscreens. The process of selecting the most effective sunscreen depends on identification of the wavelengths of photons that are responsible for inducing the sensitivity reaction, which can be determined through assessment of patient history or by phototesting. Sunscreens with sun protection factor (SPF) >30 that incorporate photostable or photostabilized ultraviolet A (UVA) filters (labeled as “broad spectrum” in the US) are usually the appropriate choice for adequate photoprotection.

Key Words:
photodermatoses, photoprotection, photosensitivity disorders, sunscreen, UVA, UVB

Photodermatoses are a group of diseases involving abnormal cutaneous reactions to solar radiation. They include immunologically mediated photosensitive disorders, drug or chemical induced photosensitivity reactions, DNA repair-deficiency photodermatoses, and photoaggravated dermatoses.¹ While these diseases have different pathophysiologic mechanisms, not all of which have been clearly defined, photoprotection is an integral part of their management. Photoprotection includes seeking shade, wearing photoprotective clothing, a wide brimmed hat, and sunglasses, as well as applying broad spectrum sunscreens with sun protection factor (SPF) >30.^1-3

Choice of Sunscreen Protection

The method by which the clinician chooses the most effective sunscreen for each patient depends on identification of the photon wavelength responsible for inducing the sensitivity reaction, i.e., the action spectrum.³ This can often be ascertained through the determination of minimal erythema dose to ultraviolet B (UVB) (280-320 nm) (MED-B) and ultraviolet A (UVA) (320-400 nm) (MED-A), and though the induction of lesions by UV or visible light (400-700 nm).^2,3 The fact that window glass filters out UVB, but not longwave UVA, also helps to determine the action spectrum of the patient’s photosensitivity disorder.

In the United States, UVB and UVA filters are categorized into organic and inorganic filters (Table 1). While there are many excellent UVB filters, there are only a limited number of organic UVA filters available in the US, namely the benzophenones (oxybenzone, dioxybenzone, and sulisobenzone), butyl methoxydibenzoylmethane (commonly known as avobenzone), and methyl anthranilate.^1,3 All, with the exception of avobenzone, are primarily protective only against UVA-2 (320-340 nm). The absorption of avobenzone extends into UVA-1 (340-400 nm).^1,3 However, because avobenzone is photolabile, degradation occurs rapidly upon exposure to sunlight. In the past few years, technology has been developed to photostabilize avobenone. This can be achieved by combining it with photostable UV filters, such as octocrylene, salicylates, or oxybenzone; in some products non-UV filter photostabilizing compounds, such as diethylhexyl 2,6-naphthalate (DEHN), diethylhexyl syringylidene malonate (Oxynex® ST), or caprylyl glycol are also used.¹ Ecamsule (Mexoryl™ SX) is a photostable organic short UVA filter (with maximum absorbance at 344 nm) that was approved by the US FDA in 2006 only as a component of certain sunscreen products.⁴ The approved inorganic sunscreens or physical blockers are titanium dioxide and zinc oxide, which offer protection from UVB to visible ranges. They are used in micronized form to improve cosmetic acceptability.^1,3 However, it should be noted that the micronized form protects only in the UVB and UVA spectrums, but not in the visible range.

The SPF value for sunscreens reflects the ability of the product to protect against UV-induced erythema, which is primarily the effect from UVB exposure, and to a lesser extent from UVA-2. While there are rating systems used in many other countries to grade the protectiveness of sunscreens against UVA, currently, the FDA has not yet finalized the revised rating system that will be implemented in the US. Consumers should look for sunscreens that provide “broad spectrum” protection, which would indicate that the formulations contain UVA filters. However, as noted above, since many UVA filters do not cover longwave UVA (UVA-1), and not all sunscreens incorporate a photostabilized UVA-1 filter (i.e., avobenzone), the current UVA rating system used in the US reveals significant shortcomings.

Sunscreens and Photodermatoses

Herein, the use of sunscreens in the management of photodermatoses (polymorphic light eruption and solar urticaria) and photoaggravated dermatosis (lupus erythematosus) is outlined.

Polymorphic Light Eruption (PMLE)

PMLE is the most common photodermatosis, with prevalence as high as 10-20%, typically starting during the second and third decades of life.^1,3,5,6 Lesions develop within hours of sun exposure, usually resolve in a few days, and do not scar. PMLE is generally most severe in the spring or early summer and a genetic predisposition appears to be a likely risk factor.^5,6 The pathogenesis is thought to be attributable to the failure of normal UV-induced immunosuppression, which results in enhanced reactivity to UV triggered photoallergens in the skin.^1,5,6 Photoprovocation tests have shown that PMLE was induced by UVA in 59% to 94.2% of cases, and UVB in 23% to 40%.^6-9 Induction by a combination of UVA and UVB was observed in 18% to 90% of patients, depending on the methodology used in the photoprovocation tests.^6,7,9 Because most sunscreens protect predominantly against UVB, and therefore, fail to prevent PMLE,^6-9 the need to study sunscreens with high UVA protection, through the use of photostable UVA filters, was fostered.^8,9 In a retrospective study of 133 patients with PMLE, the complete follow-up information on photoprotection was available for 79 subjects. The data revealed that the use of a sunscreen with a mean SPF of 14 did not prevent skin lesions in 88% of these patients.⁷ Another study using a sunscreen with high SPF and high UVA-PF (UVA protection factor), containing photostable UV filters (Tinosob® M, Tinosorb® S) and photostabilized avobenzone, showed that it protected against the development of lesions in 69% of subjects with PMLE after standardized photoprovocation.⁸

Other trials have compared the efficacy of two sunscreens with similar SPF, but different levels of UVA protection. In an indoor, bilateral comparison study, 14 volunteers used a product with SPF 60 and UVA-PF 15 (containing avobenzone, Mexoryl™ SX, Eusolex®, and micronized titanium dioxide) on one side of the chest, and the other side received another product with SPF 50 and UVA-PF 4 that contained titanium dioxide and zinc oxide. Following photoprovocation, only two subjects developed new PMLE on the side treated with the higher UVA-PF sunscreen, while 14 subjects developed new lesions on the other side.⁴ In an outdoor study, 16 female subjects susceptible to PMLE were exposed daily to sunlight for 7 days after using two products with similar SPF 60+, but different UVA-PF values on each half of the body. Fifteen subjects experienced eruptions with the photounstable lower UVA protection (UVA-FP 4) product, compared with only four patients exhibiting eruptions with the photostable high UVA (UVA- PF 28) sunscreen.⁴

Solar Urticaria (SU)

SU is an uncommon photodermatosis, often occurring
in the third decade of life and demonstrating a female
preponderance.^9,11,12 Urticaria is a mast cell-mediated
disease that can develop within minutes after exposure to
sunlight.^9,11,12 The action spectrum includes UVA, UVB, and
visible light.⁹

Because there is no sunscreen product available that
adequately protects against visible light, photoprotection
in SU induced by visible light can only be achieved with
physical measures, such as clothing, which in one study
resulted in symptomatic control in 84% of patients.⁹ Broad
spectrum high SPF sunscreens are helpful for SU that is
triggered by UVA and/or UVB.

Lupus Erythematosus (LE)

LE is the most common photoaggravated dermatosis.^13,14 Following UV exposure, skin lesions develop within days or up to weeks after and can persist for months.¹⁴ Tumid LE is the most photosensitive subset, followed by subacute cutaneous LE, systemic LE, and discoid LE. Sunlight exposure can even induce systemic disease activity.¹⁴ Provocative phototesting by Kuhn et al. produced characteristic skin lesions in 175 of 323 LE patients; 42% were reactive to only UVB and 34% to UVA only.¹³ Of the patients receiving combination UVA + UVB irradiation, 53% exhibited positive photosensitivity reactions.

The study performed by Stege et al.¹⁵ tested the efficacy of three distinct sunscreens to prevent the UV radiation-induced generation of skin lesions in photosensitive LE patients by employing a standard provocative phototest.¹⁵ The 11 patients developed LE-specific skin lesions upon photoprovocation with a combination of UVA and UVB radiation. The same group was tested with three different sunscreens. The most effective was a product with high SPF and high UVA-PF (UVB filter: octocrylene; UVA filters: Mexoryl™ SX, Mexoryl™ XL, avobenzone, and titanium dioxide), which protected 11 of 11 patients. Five patients were protected by a product with similar SPF, but medium UVA-PF (UVB filters: Eusolex® 6300, Parsol® MCX, Uvinul® T150, Neohelipan®; UVA filter: avobenzone; titanium dioxide) and only three by a product with the lowest SPF and lowest UVA-PF (UVB filters: Eusolex® 6300, Parsol® MCX, Uvinul® T150; UVA filter: avobenzone; titanium dioxide). While several of the filters used in the study are not commercially available in the US, this trial does indicate that sunscreens with high SPF and high UVA-PF are necessary for the management of patients with photosensitive LE.¹⁵

Conclusion

Sunscreens are an integral component of photoprotection in the management of photodermatoses. UV filters are broadly categorized into organic UVB and UVA filters, and inorganic filters. The efficacy of sunscreens has been well documented in PMLE, solar urticaria, and lupus erythematosus.

References

1. Draelos ZD, Lim HW, Rougier A. Sunscreens and photodermatoses. In: Lim HW, Draelos ZD (eds). Clinical guide to sunscreens and photoprotection. New York: Informa Healthcare, p83-8 (2008).
2. Van den Keybus C, Laperre J, Roelandts R. Protection from visible light by commonly used textiles is not predicted by ultraviolet protection. J Am Acad Dermatol 54(1):86-93 (2006 Jan).
3. Deleo V. Sunscreen use in photodermatoses. Dermatol Clin 24(1):27-33 (2006 Jan).
4. Fourtanier A, Moyal D, Seite S. Sunscreens containing the broad-spectrum UVA absorber, Mexoryl SX, prevent the cutaneous detrimental effects of UV exposure: a review of clinical study results. Photodermatol Photoimmunol Photomed 24(4):164-74 (2008 Aug).
5. Gonzalez E, Gonzalez S. Drug photosensitivity, idiopathic photodermatoses, and sunscreens. J Am Acad Dermatol 35(6):871-85 (1996 Dec).
6. Honigsmann H. Polymorphous light eruption. Photodermatol Photoimmunol Photomed 24(3):155-61 (2008 Jun).
7. Mastalier U, Kerl H, Wolf P. Clinical, laboratory, phototest and phototherapy findings in polymorphic light eruptions: a retrospective study of 133 patients. Eur J Dermatol 8(8):554-9 (1998 Dec).
8. Schleyer V, Weber O, Yazdi A, et al. Prevention of polymorphic light eruption with a sunscreen of very high protection level against UVB and UVA radiation under standardized photodiagnostic conditions. Acta Derm Venereol 88(6):555-60 (2008).
9. Beattie PE, Dawe RS, Ibbotson SH, et al. Characteristics and prognosis of idiopathic solar urticaria: a cohort of 87 cases. Arch Dermatol 139(9):1149-54 (2003 Sep).
10. Kullavanijaya P, Lim HW. Photoprotection. J Am Acad Dermatol 52(6):937-58 (2005 Jun).
11. Uetsu N, Miyauchi-Hashimoto H, Okamoto H, et al. The clinical and photobiological characteristics of solar urticaria in 40 patients. Br J Dermatol 142(1):32-8 (2000 Jan).
12. Faurschou A, Wulf HC. Synergistic effect of broad-spectrum sunscreens and antihistamines in the control of idiopathic solar urticaria. Arch Dermatol 144(6):765-9 (2008 Jun).
13. Kuhn A, Sonntag M, Richter-Hintz D, et al. Phototesting in lupus erythematosus: a 15-year experience. J Am Acad Dermatol 45(1):86-95 (2001 Jul).
14. Sanders CJ, Van Weelden H, Kazzaz GA, et al. Photosensitivity in patients with lupus erythematosus: a clinical and photobiological study of 100 patients using a prolonged phototest protocol. Br J Dermatol 149(1):131-7 (2003 Jul).
15. Stege H, Budde MA, Grether-Beck S, et al. Evaluation of the capacity of sunscreens to photoprotect lupus erythematosus patients by employing the photoprovocation test. Photodermatol Photoimmunol Photomed 16(6):256-9 (2000 Dec).

ABSTRACT
Human skin is increasingly exposed to sunlight. In order to achieve complete protection against the cumulative detrimental effects from sun exposure, topical strategies must shield against the range of solar wavelengths that can damage the skin. Importantly, the harm sustained by the skin is not limited to that caused by the ultraviolet (UV) portion of the light spectrum, but also includes the adverse effects inflicted by near infrared energy. Consequently, in an attempt to provide the necessary broad spectrum coverage, innovative research continues through the exploration of new compounds and novel combinations of chemical and physical UV filters with molecules that are capable of interfering with and/or preventing the deleterious effects of infrared A (IRA) radiation. Existing examples of infrared-protective active agents include mitochondrially targeted antioxidants of synthetic or natural origin.

Key Words:
infrared, IRA, photoaging, sunscreens, skin protection, UVA, UVB, ultraviolet

Adverse Skin Effects from Solar Radiation

Despite some positive and health promoting effects from
sunlight, it is apparent that high acute, chronic low dose,
and/or unprotected exposure have several detrimental
effects, including premature skin aging and the development
and progression of cancer.¹ For many years the focus of
research, and therefore for protective strategies, has been
centered on the ultraviolet (UV) part of sunlight, i.e.,
ultraviolet B (UVB) (290-320 nm) and ultraviolet A (UVA)
(320-400 nm), because their relatively high photon energy
causes macroscopic skin changes that are visible even after
a short duration of exposure. However, UV radiation only
accounts for approximately 7% of the sun’s energy,² which
underlines the necessity to consider the detrimental effects
from other parts of the sunlight spectrum. Accordingly, we
and others identified infrared A (IRA) (760-1440 nm) as a
damaging environmental factor to skin through its ability
to engender alterations in gene expression of skin cells at
multiple points,³ resulting in accelerated skin aging^4,5 and
contributing to the development of cancer.⁶

It is well known that the most effective protection against
UV radiation is sun avoidance, e.g., by limiting exposure, or
at least direct exposure during peak times, and by wearing
appropriate clothing. However, in Western civilizations the
level of sun exposure continues to rise, e.g., for recreational
reasons and due to increased life expectancy.

Complete Photoprotection Considers All Relevant Parts of the Solar Spectrum

Taking into account recent findings, it is evident that effective
photoprotection must provide more than UV coverage, but
rather it should protect against IRA as well. It is estimated
that about one-third of solar energy is comprised of IRA,
which is capable of deep skin penetration.²

Multipronged Approach to Complete Photoprotection

Modern topical photoprotection integrates both primary
protective factors (e.g., organic or inorganic light filtering
agents) that absorb or reflect UV radiation and secondary
factors (e.g., antioxidants, osmolytes, and DNA repair
enzymes) that can disrupt the photochemical cascade
triggered by UV-penetration, thereby limiting skin damage.

Primary Photoprotection

Primary photoprotection is achieved by using physical and/
or chemical UV filtering agents, which have been key active
components in commercially available sunscreens for more
than 60 years. The most frequently used physical UV filters
are the inorganic micropigments, zinc oxide and titanium
dioxide.

Most chemical filters absorb UV energy across a relatively
narrow or specific wavelength range, converting UV
radiation to longer wavelength photons. Due to the limited
absorption spectrum of any single ingredient, a combination
of sunscreen actives is required to yield both UVA and UVB
protection, but the degradation of some UVA filters by
sunlight presents formulary challenges. However, in recent
years, tremendous progress has been made in developing
more photostable UV filters, such as ecamsule (Mexoryl™
SX) and drometrizole trisiloxane (Mexoryl™ XL) and by
formulating efficient combinations, such as avobenzone
combined with diethylhexyl 2,6-naphthalate and oxybenzone
(Helioplex™). Concerning UV filters used in commercially
available products, it should be noted that there are
differences between approved agents in the European Union
when compared with the US, as the US FDA has been more
conservative in sanctioning new chemical sunscreens. As for
protection against other parts of the light spectrum (other
than UV), these chemical compounds do not provide any
benefit beyond their UV specificity.

Secondary Photoprotection

Secondary photoprotection involves the use of active agents
to interfere with or counteract the inherent photochemical
processes that can induce DNA damage in skin cells.
Secondary photoprotection may be achieved by an extremely
heterogeneous and constantly growing group of molecules
that are termed “actives”. Examples of such actives include
antioxidants, osmolytes, and DNA repair enzymes7,8 (e.g.,
photolyase and T4 endonuclease V).

Antioxidants that are typically used in sunscreens and
other cosmetic products are comprised of vitamins and
polyphenols. Prime examples of vitamins formulated in
sunscreens are water soluble vitamin C and lipophilic
vitamin E. The term “polyphenols” refers to compounds that
possess at least 2 adjacent hydroxyl groups on a benzene ring.
Natural polyphenols (e.g., flavonoids and procyanidins) are
present in numerous foods and have been demonstrated to
provide protective properties through topical application.9,10
In addition, antioxidants have also been shown to protect
against IRA. Accordingly, significant importance resides with
molecules that are targeted toward mitochondria, because
of their central role in IRA-induced adverse effects.3,5,11,12
However, it should be noted that the precise mechanism of
action of topically applied actives remain to be elucidated;
there is a need to fully understand their effects at both cellular
and molecular levels prior to supporting their therapeutic
benefits as photoprotective agents.

Osmolytes are small molecules that control and stabilize the
cellular environment by regulating hydration and responses
to stress conditions. Osmolytes (compatible organic solutes)
are not only utilized by cells to control cell volumes, but they
have been identified as integral parts of the cellular defence
against environmental noxae. The osmolytes taurine13
and ectoine14 have been demonstrated to protect against
detrimental UV effects and are amalgamated into several
commercially available sunscreens.

Conclusion

Complete topical photoprotection can only be obtained if a
sunscreen formula defends against UVB, UVA, and IRA.
Whether additional wavelengths contribute to skin damage
is currently not known. In order to achieve as near complete
broad spectrum protection as is possible, a sunscreen must
combine multiple therapeutic approaches that incorporate
both essential elements of primary and secondary
photoprotection.

References

1. Krutmann J, Gilchrest BA. Photoaging of skin. In: Gilchrest BA, Krutmann J (eds). Skin aging. New York: Springer, p33-44 (2006).
2. Kochevar IE, Taylor CR, Krutmann J. Fundamentals of cutaneous photobiology and photoimmunology. In: Wolff K, Goldsmith LA, Katz S, et al. (eds). Fitzpatrick’s dermatology in general medicine, 7th ed. New York: McGraw-Hill, p797-808 (2008).
3. Calles C, Schneider M, Macaluso F, et al. Infrared A radiation influences the skin fibroblast transcriptome: mechanisms and consequences. J Invest Dermatol (In press 2010).
4. Schroeder P, Pohl C, Calles C, et al. Cellular response to infrared radiation involves retrograde mitochondrial signaling. Free Radic Biol Med 43(1):128-35 (2007 Jul 1).
5. Schroeder P, Lademann J, Darvin ME, et al. Infrared radiationinduced matrix metalloproteinase in human skin: implications for protection. J Invest Dermatol 128(10):2491-7 (2008 Oct).
6. Jantschitsch C, Majewski S, Maeda A, et al. Infrared radiation confers resistance to UV-induced apoptosis via reduction of DNA damage and upregulation of antiapoptotic proteins. J Invest Dermatol 129(5):1271-9 (2009 May).
7. Dong KK, Damaghi N, Picart SD, et al. UV-induced DNA damage initiates release of MMP-1 in human skin. Exp Dermatol 17(12):1037-44 (2008 Dec).
8. Yarosh DB, O’Connor A, Alas L, et al. Photoprotection by topical DNA repair enzymes: molecular correlates of clinical studies. Photochem Photobiol 69(2):136-40 (1999 Feb).
9. Allemann IB, Baumann L. Botanicals in skin care products. Int J Dermatol 48(9):923-34 (2009 Sep).
10. Krutmann J, Yarosh D. Modern photoprotection of human skin. In: Gilchrest BA, Krutmann J (eds). Skin aging. New York: Springer, p103-12 (2006).
11. Krutmann J, Schroeder P. Role of mitochondria in photoaging of human skin: the defective powerhouse model. J Investig Dermatol Symp Proc 14(1):44-9 (2009 Aug).
12. Schroeder EK, Kelsey NA, Doyle J, et al. Green tea epigallocatechin 3-gallate accumulates in mitochondria and displays a selective antiapoptotic effect against inducers of mitochondrial oxidative stress in neurons. Antioxid Redox Signal 11(3):469-80 (2009 Mar).
13. Rockel N, Esser C, Grether-Beck S, et al. The osmolyte taurine protects against ultraviolet B radiation-induced immunosuppression. J Immunol 15;179(6):3604-12 (2007 Sep).
14. Buenger J, Driller H. Ectoin: an effective natural substance to prevent UVA-induced premature photoaging. Skin Pharmacol Physiol 17(5):232-7 (2004 Sep-Oct).

ABSTRACT
Sunscreens have been around for more than 70 years. Designed originally to protect against sunburn, recognition of the various harmful effects of ultraviolet (UV) radiation has broadened the use of sunscreens. The addition of effective UVA sunscreen agents has enabled claims beyond protection against sunburn to include prevention of idiopathic photodermatosis, actinic keratoses, skin cancer, and photoaging. This article will review some of the recent advances in photoprotection, including the development of sunscreen formulations offering higher and broader protection against solar radiation.

Key Words:
sunscreens, photoprotection, ultraviolet A, ultraviolet B, UVA, UVB, sun protection factor, SPF

Protection Against Ultraviolet A (UVA) Radiation

Rating UVA Protection

The almost universal use of the sun protection factor (SPF) has lured many consumers into thinking that a higher SPF means a better sunscreen. Because SPF is mostly an indicator of UVB protection, it is difficult for consumers and physicians to compare the UVA protection afforded by sunscreens.¹ For many years, some countries have been using UVA labeling systems that can provide guidance on both UVA and UVB protection that is offered by sunscreens. Other countries, like the US and Canada, have been slower to introduce guidelines for UVA protection labeling.

Modifications to Sunscreen Labeling

The US FDA recently proposed inclusion of a 4 star grading system in conjunction with a descriptor (i.e., low, medium, high, and highest) to rate UVA protection.2 This star rating system will depend on results of both in vitro and in vivo UVA testing. According to the agency, UVA ratings would be based on 2 tests: one would measure the sunscreen’s ability to reduce UVA penetration and the second would measure the product’s ability to prevent tanning. The test that yields the lowest level of UVA protection would determine the number of stars that the sunscreen would receive. This will help consumers and physicians identify the level of UVA protection provided by the different sunscreens. Other modifications include making minor changes to UVB testing procedures to improve accuracy, increasing the maximum sunburn protection factor from SPF 30+ to SPF 50+, and sanctioning the use of new combinations of active ingredients.²

Avobenzone and Photostability

Protection against UVA radiation was revolutionized by the introduction of butyl methoxydibenzoylmethane (avobenzone) in the late 1980s and early 1990s. This was the first organic sunscreen agent that provided some protection for mid- to long-range UVA rays. However, the degradation of some UVA filters, such as avobenzone, by sunlight, prompted the need to stabilize the formulation in order to prevent the loss of efficacy. Upon absorption of UV radiation, the avobenzone molecule can transform into a molecule that no longer absorbs UVA radiation. In formulations where avobenzone is not photostable, UVA protection decreases with the time spent under the sun. This has been shown to occur after as little as 60-90 minutes of sun exposure.³


A number of different companies have developed systems to stabilize avobenzone in the final formulations. For example, a combination of avobenzone and 2-ethylhexyl ester (octocrylene) has been shown to achieve a photostable product.4 The addition of diethylhexyl 2,6-naphthalate also makes avobenzone photostable.⁵ The combination of diethylhexyl 2,6-naphthalatate, avobenzone and oxybenzone is known under the commercial name of Helioplex™ and it is present in UltraSheer® and Age Shield® sunscreens (Neutrogena®/Johnson & Johnson). The addition of
Tinosorb S® (Ciba Specialty Chemicals) has also been shown to photostabilize avobenzone.⁶ Confirmation of avobenzone’s photostability in a given formulation is difficult unless the sunscreen’s chemical stability has been studied and the results are published in a peer reviewed journal. In the absence of such studies, physicians can get indirect evidence of the photostability of a given formulation from UVA protection factor determination with methods such as persistent pigment darkening (PPD).

PPD evaluates pigmentation present at 2 hours after the end of exposure to different UVA fluences. Because UVA exposures for these methods are rather lengthy, a sunscreen formulation with unstable avobenzone will have a lower protection factor than a similar formulation with stabilized avobenzone.

Recently Introduced Organic UVA Sunscreen Agents

A number of UVA sunscreen agents have been introduced in the past few years. Unfortunately, their availability varies widely from country to country. For example, in the US and Canada, sunscreen agents are considered to be drugs. Sunscreen manufacturers must therefore submit a new drug application when they want to incorporate a new agent into a formulation. This explains why ecamsule (terephthalylidene dicamphor sulphonic acid [Mexoryl SX™, L’Oréal]) was only recently introduced in the US in 2006, whereas, this agent has been available in most other regions of the globe for more than 10 years. Mexoryl SX™ is a photostable chemical sunscreen agent that offers mid-range UVA protection.7 When combined with avobenzone, UVA protection is enhanced. Sunscreen products that contain Mexoryl SX™, and are available in the US, include Anthelios SX™ Daily Moisturizing Cream (SPF 15), Anthelios™ 15 Sunscreen Cream (SPF 15) and Anthelios SX™ 40 Sunscreen Cream (SPF 40, to be introduced in 2008).

Dometrizole trisiloxane (Mexoryl XL™) is another recently introduced organic sunscreen agent offering mid-range UVA protection. The addition of Mexoryl XL™ to Mexoryl SX™ has been shown to increase UVA protection in a synergistic manner, which may be attributable to its 2 phase component. Mexoryl XL™ was introduced in Canada in 2006. It has not yet been approved in the US, but has been available worldwide for many years in different sunscreens made by L’Oréal. In Canada, Mexoryl XL™ can be found in sunscreens sold under different brands including Anthelios™, Ombrelle™, Vichy™ and Biotherm™ (L’Oréal).

Bemotrizinol and bisoctrizole (Tinosorb S® and Tinosorb M®
respectively, Ciba Specialty Chemicals) are organic compounds that also provide broad-spectrum UV protection. Tinosorb S® has been shown to increase photostability of avobenzone.6 Tinosorb S® and Tinosorb M® are mid-range photostable sunscreen agents that have been used in Europe for many years, but they are not yet approved in the US. These UV filters have recently been introduced in Canada and are formulated in Minesol® SPF 60 products (RoC®/Johnson & Johnson).

Protection Against Visible Light

The effect of visible light on the skin has received very little attention, compared with UV radiation. The role of visible light, viewed as both physiologic and pathologic phenomena, and its effects on the skin are probably less important than the role of UV radiation. However, visible light sensitivity is an important phenomenon in diseases such as porphyria, solar urticaria, and other idiopathic photodermatoses, such as polymorphous light eruption. Patients who undergo photodynamic therapy treatments also become sensitive to visible light for a few days because of the accompanying topical medications, such as aminolevulinic acid and methylaminolevulinate, or for a few weeks due to systemic agents like porfimer sodium. A recent study by Mahmoud, et al. suggested that visible light exposure can increase pigmentation in patients with skin phototype IV to VI.8 Protection against visible light might be important for darker skinned patients who have pigmentary disorders such as post-inflammatory hyperpigmentation and melasma. Further research on the effects of visible light is definitely needed.

Organic sunscreen agents usually offer no protection against visible light, as their absorption spectrum is limited to UVB and UVA wavebands. Inorganic sunscreen agents, such as iron oxide, titanium dioxide, and zinc oxide can offer some visible light protection. However, the spectral protection of these agents varies according to their particle size. Larger particles of titanium dioxide and zinc oxide can protect in the visible range. Earlier formulations containing physical blocking agents tended to leave a white/pasty film on the skin, but with the advent of smaller-sized particles, modern physical sunscreens have made improvements in their effect on cosmetic appearance. Iron oxide is another physical UV blocking agent; however, it has the unique advantage of being closer to the natural skin color of phototype II and III individuals. The difference in visible light protection afforded by high SPF sunscreens with inorganic sunscreen agents was illustrated in a recent study that compared 2 inorganic sunscreens containing titanium dioxide, zinc oxide, and iron oxide for their ability to protect against blue light sensitivity induced by aminolevulinic acid application.9 The sunscreen containing 3.2% iron oxide (Avène Compact, Pierre Fabre Dermo-Cosmétique) offered a protection factor of 22:1 (i.e., the ratio of the lower blue light fluence that induced erythema on sunscreen protected skin to the lower blue light fluence that induced erythema on skin that was unprotected). Whereas the sunscreen with a lower concentration of 0.3% iron oxide offered only a protection factor of 2:1.

Systemic Absorption of Sunscreening Agents

Until recently, systemic exposure to sunscreen agents had also received relatively little attention in the medical literature. Agents such as benzophenones and octyl-methoxycinnamate can be detected in plasma and urine after topical application of sunscreen products.10 Unfortunately, most of these studies were conducted with non-commercial sunscreen formulations or were performed at significantly higher doses than what the average consumer uses. Additional research is definitely needed to explore the absorption of active agents contained in commercial sunscreens used under normal conditions. Furthermore, studies assessing the risks (or benefits) of systemic absorption of various sunscreen agents in adults, children, and pregnant women are also warranted.

Sunlight, Vitamin D and Sunscreens

Over the past few years there has been considerable media coverage about the influence of vitamin D and sun exposure on various diseases, including different types of cancer. The incidence of and mortality from many cancers have been reported to be reduced with decreasing latitude.11 Holick hypothesized that this reduction is related to higher vitamin D production from increased sun exposure.11 Vitamin D synthesis is a UVB phenomenon and sunscreens are usually very effective in protecting against UVB. Few prospective studies on the role of vitamin D and sun exposure in cancer prevention have been published. Additional studies are necessary to address issues such as the optimal amount of vitamin D needed to have beneficial effects and the role of oral vitamin D intake versus vitamin D synthesis following sun exposure.

Sun avoidance and the adequate use of high SPF and high UVA protection sunscreens on all exposed skin areas may still be appropriate for a kidney transplant patient who already has had multiple invasive squamous cell carcinomas. However, the situation is different for a healthy phototype IV indoor worker living in Canada who has no personal or familial history of skin cancer and takes part in no outdoor activities. Based on the current retrospective and prospective studies, physicians should individualize the sun protection advice that they give to their patients and discuss whether additional benefits can be derived from oral vitamin D supplementation. The Canadian Cancer Society issued a statement in 2007 recommending that Canadian adults should consider taking 1000 IU of vitamin D daily. This was based on evidence suggesting that vitamin D could reduce the risks of breast, colorectal, and prostate cancers.

Conclusion

Many sunscreens now offer very good broad-spectrum protection in both the UVA and UVB ranges. In many countries, changes in labeling guidelines will make it easier for consumers and physicians to evaluate the level of UVA protection afforded by sunscreens. However, further research is needed in many areas including the role of visible light, the risks of systemic absorption of sunscreen agents, and the role of vitamin D and sun exposure in preventing cancers and other diseases.

References

1. Bissonnette R, Allas S, Moyal D, et al. Comparison of UVA protection afforded by high sun protection factor sunscreens. J Am Acad Dermatol 43(6):1036-8 (2000 Dec).
2. Department of Health and Human Services, Food and Drug Administration. Federal Register, 21 CRF Parts 347 and 353 Sunscreen Drug Products for Over-the-Counter Human Use; Proposed Amendment of Final Monograph; Proposed Rule. Vol. 72, No. 165 (2007 August 27).
3. Gonzalez H, Tarras-Wahlberg N, Stromdahl B, et al. Photostability of commercial sunscreens upon sun exposure and irradiation by ultraviolet lamps. BMC Dermatol 7:1 (2007).
4. Gaspar LR, Maia Campos PM. Evaluation of the photostability of different UV filter combinations in a sunscreen. Int J Pharm 307(2):123-8 (2006 Jan 13).
5. Cole C, Chu M, Finkey MB, et al. Comparison of photoprotection efficacy and photostability of broad spectrum sunscreens. Presented at: The 64th Annual Meeting of the American Academy of Dermatology; San Francisco, CA; March 3-7, 2006. Poster #P2617.
6. Chatelain E, Gabard B. Photostabilization of butyl methoxydibenzoylmethane (Avobenzone) and ethylhexyl methoxycinnamate by bis-ethylhexyloxyphenol methoxyphenyl triazine (Tinosorb S), a new UV broadband filter. Photochem Photobiol 74(3):401-6 (2001 Sep).
7. Moyal D. Prevention of ultraviolet-induced skin pigmentation. Photodermatol Photoimmunol Photomed 2004;20(5):243-7 (2004 Oct).
8. Mahmoud BH, Hexsel C, Lim H, et al. Impact of long wavelength UVA and visible light on melanocompetent skin. Presented at: The 66th Annual Meeting of the American Academy of Dermatology; San Antonio, TX; February 1-5, 2008. Poster #P2420.
9. Bissonnette R, Nigen S, Bolduc C, et al. Protection afforded by sunscreens containing inorganic sunscreening agents against blue light sensitivity induced by aminolevulinic acid. Dermatol Surg. In press 2008.
10. Janjua NR, Kongshoj B, Andersson AM, et al. Sunscreens in human plasma and urine after repeated whole-body topical application. J Eur Acad Dermatol Venereol 22(4):456-61 (2008 Apr).
11. Holick MF. Vitamin D deficiency. N Engl J Med 357(3):266-81 (2007 Jul 19).

ABSTRACT
Ultraviolet (UV) radiation is a carcinogen that also compromises skin appearance and function. Since the UV action spectra for DNA damage, skin cancer, and vitamin D photosynthesis are identical, and vitamin D is readily available from oral supplements, why has sun protection become controversial? First, the media and, apparently, some researchers are hungry for a new message. They have also drawn attention to the emerging evidence of possible vitamin D benefits other than for bone health. Second, the controversy is fueled by a powerful special interest group: the tanning industry. This industry does not target the frail elderly or inner-city ethnic minorities, which are the groups at greatest risk of vitamin D deficiency, but rather fair-skinned teenagers and young adults, who are at highest risk of UV photodamage. Third, evolution does not keep pace with civilization. When nature gave humans the appealing capacity for cutaneous vitamin D photosynthesis, life expectancy was less than 40 years of age; long-term photodamage was not a concern, and vitamin D deficiency, with its resulting skeletal abnormalities (rickets), was likely to be fatal in early life. This article briefly reviews the “pseudo-controversy”, as well as the data supporting a revision of the recommendations for vitamin D supplementation. It concludes with a suggested message for patients, many of whom are understandably confused by recent media coverage of the topic.

Key Words:
vitamin D, photosynthesis, sun protection

The media and certain elements within the biomedical research community have created a “controversy” regarding the allegedly conflicting goals of skin cancer prevention through sun protection on the one hand, and achieving optimal vitamin D homeostasis on the other. I will attempt to distinguish this pseudo-controversy from the true controversy surrounding the rather poorly documented health benefits of very high vitamin D levels, however achieved.

The somewhat elusive basis of the pseudo-controversy lies in the often unstated assumption that vitamin D levels, specifically, levels of the inactive prehormone 25-hydroxyvitamin D [25(OH)D], which is measured in serum, are best achieved from increased ultraviolet (UV) exposure to enhance photosynthesis of vitamin D within the irradiated epidermis. This assumption has framed discussions in the popular press and on the internet, even though all intervention studies that suggest a benefit for increasing the conventional “normal” or “sufficient” 25(OH)D level in specific population groups have examined the effect of oral vitamin D supplements, not increased exposure to sun or other UV sources.¹

This formulation of the debate also fails to acknowledge that the major motivation for sun exposure in the population at large is not for improved general health, but rather, it is to attain the cosmetic and lifestyle goal of tanning, at least for people genetically capable of tanning. Thus, reports continue on the “debate” between professional groups with primary interests in skin health versus those who specialize in endocrinologic health, even though often no such debate exists. These deliberations can create confusion among the general public regarding recommended health behaviors.

The Pseudo-Controversy

In recent years, numerous newspaper reporters, freelance journalists, and television news anchors have reported on a “medical controversy” that pits the unwanted effects of acute sunburn, photoaging, and skin cancer against both well-established and postulated benefits of vitamin D photosynthesis. Simplistically stated, these articles and reports ask if the public should maximize vitamin D levels (measured as the biologically inactive storage form of 25(OH)D in serum)² through intentional UV exposure to reduce their risk of internal cancers, hypertension, diabetes, multiple sclerosis, and a litany of other disorders that some attribute to “insufficient” vitamin D levels.³

By framing the issue in this way, the media reports ignore the fact that people can obtain ample vitamin D levels from a combination of diet, supplements, and incidental protected sun exposure,^1,4-7 and that, to date, most intervention studies suggesting a benefit of increased 25(OH)D levels have used oral supplements, not UV exposure.^1,2,8

Reports often cite low or low normal levels of vitamin D in darkly pigmented individuals, such as inner-city minority groups, or among the frail elderly in order to justify promoting unprotected sun exposure. However, these at-risk groups have inefficient cutaneous vitamin D photosynthesis.

In darkly pigmented people melanin absorbs UV photons that generate vitamin D,⁹ and the thinned epidermis of the elderly appears to contain less 7-dehydrocholesterol, which is the cell membrane constituent that UVB converts to pre-vitamin D.^10,11 As well, population groups most attracted to sunbathing, i.e., healthy Caucasian teenagers and young adults, including many fair-skinned individuals who tan poorly,¹² are at lowest risk of vitamin D insufficiency, yet at greatest risk of long-term photodamage.

What is Vitamin D Insufficiency?

It is virtually impossible to find a definition of this recently coined term in the literature. It loosely refers to levels of 25(OH)D above those classically associated with bone disease and below those found in various observational or epidemiologic studies to be statistically associated with a higher risk of the studied disorder, for example, cancer. These upper cut-off values vary enormously from study to study and author to author, from perhaps 50nmol/L to 150nmol/L, often 75-80nmol/L.¹

A recent study¹³ of 93 healthy young adults who were recruited from the University of Hawaii and a Honolulu skateboard shop, questioned the frequently suggested serum 25(OH)D “sufficiency” cut-off value of 75nmol/L. The investigators based recruitment of this convenience sample of prototypic “surfer dudes” (mean age 24 years, mean body-mass index 23.6 kg/m2) on a self-reported minimum outdoor sun exposure of 15 hours (mean 29 hours) per week during the preceding 3 months; 40% reported never using sunscreen and the group overall reported an average of 22.4 hours per week of unprotected sun exposure. All were clinically tanned. Nevertheless, the group’s mean 25(OH)D level, measured by 2 standard techniques (high-performance liquid chromatography and radioimmunoassay), was 79nmol/L, and 51% had a level below the suggested 75nmol/L cut-off for “sufficiency”.¹³ These data suggest that a public health goal of >75nmol/L for the entire population might be unachievable through sun exposure.

Regardless of the cut-off used, the great majority of people with insufficient 25(OH)D levels have no detectable disease or health problem and, statistically, they probably never will. On an individual basis, there is no detectable benefit from a high 25(OH)D level and, conversely, no harm from a lower level. Even more curious, in many instances the statistical associations on which the “insufficient” status is based are not measured 25(OH)D levels, but instead presumptive correlates such as insolation (i.e., the amount and intensity of incident UV irradiation) in the general geographic region of residence. In fact, latitude, altitude, season, cloud cover, smog, and other variables affect insolation, which is generally high near the equator and low near the poles; and lifestyle choices introduce enormous variation in sun exposure, even among individuals in identical climates.

The True Controversy

The real controversy is whether increasing a person’s conventionally normal serum 25(OH)D level has health benefits, as some epidemiologic studies have suggested, but prospective randomized studies, with the one exception noted below, have not confirmed. A thorough discussion of the quality and consistency of the epidemiologic and observational data available through 2005, which some interpreted to support a health benefit of serum 25(OH)D levels far above those associated with normal skeletal maintenance, is available elsewhere1 and is beyond the scope of this editorial. However, because prevention of colorectal cancer is often cited as the best established benefit of unconventionally high 25(OH)D levels, a brief discussion of this example is instructive. Several much-referenced reports link colorectal cancer incidence^14-16 to “low” vitamin D levels within the conventional normal range or to a presumptive proxy, i.e., little sun exposure, usually based on residence in a poorly insolated area, as noted above. Although other epidemiologic or observational studies of similar size and design (grade B, level 2 or 3 in the hierarchy of evidence-based medicine)¹⁷ found no statistical relationship or even an inverse relationship between sun exposure and colorectal cancer or closely related diseases,^18-22 the popular media coverage of the topic has selectively and prominently cited the positive reports at the suggestion of interviewed “experts.”

In 2006, a prospective, randomized, placebo-controlled trial (grade A, level 1 for medical decision making)17 of vitamin D supplementation (400 IU/day) for 7 years or longer involving more than 36,000 post-menopausal women found no relationship between colorectal cancer risk (incidence or mortality; tumor grade, stage, or size) and supplement use, total vitamin D intake, or amount of sun exposure (crudely and indirectly calculated, as in the positive epidemiologic studies).⁸ Although the investigators found an inverse correlation with baseline serum 25(OH)D levels, they found no indication that increasing initially low vitamin D levels by supplementation reduced cancer risk over the subsequent 7 years.⁸ An accompanying editorial²³ and the investigators themselves noted that 7 years of supplementation might be too short, the subjects might have received a dose of vitamin D that was too low, they might have had a lifestyle that was too healthy, or they might have been too young (62 years on average) to develop this cancer in large numbers. In brief, the authors concluded that no result is ever definitively negative. Yet, less than 2 months later, the media prominently covered a far less definitive, multivariable model study that statistically inversely linked the risk of cancer, including colorectal cancer, to 6 indirect historical measures of sun exposure and presumptively correlated vitamin D levels,²⁴ with no reference to the “gold-standard” negative colorectal cancer study.⁸

Most recently, the American Journal of Clinical Nutrition published a 4-year randomized, prospective blinded study of 1,179 presumptively healthy postmenopausal Caucasian women in rural Nebraska who were followed for 4 years while taking a calcium (Ca) supplement (n=445), a Ca plus vitamin D (Ca-D) supplement (n=446), or a placebo only (n=288).² This study was designed to assess bone fracture risk, but data were also analyzed to assess cancer incidence.² The women were interviewed by a study nurse every 6 months and, if they reported a new diagnosis of nonskin cancer, their medical records were reviewed. Fifty women with a newly diagnosed cancer (19 with breast cancer, 3 with colon cancer, and 28 with other cancers) were identified, 13 in year 1 and 37 in years 2-4, representing 6.9% of the placebo group and 3.8% and 2.9% of the Ca and Ca-D groups, respectively, which indicated a significantly reduced relative risk of 0.4 for the Ca-D group. The vitamin D dose (1,000 IU/day) was higher than the current RDA of 400-600 IU/day, depending on age, and increased the average 25(OH)D level in all groups from approximately 71 to 96nmol/L in the Ca-D group by the end of year 1. For the initial and control groups, 25(OH)D levels are of interest in that they are very close to the commonly recommended “sufficient” level of 25(OH)D of =75nmol/L and the average 25(OH)D level of 79nmol/L observed in a population of healthy, tanned young men in Hawaii with a self-reported unprotected sun exposure of 22.4 hours/week.¹³ The article does not report the 25(OH)D levels of the 50 women who developed cancer vs. the 1,129 who did not, either at baseline or during supplementation; nor does it report data for the original primary endpoint, bone fracture incidence.² The apparent protective effect of high dose Ca-D supplementation on cancer risk is certainly of interest, however, and confirmatory studies are eagerly awaited.

Irrelevance of Both Controversies to Sun Protection

A neglected but critical point is that the “true” optimal level of 25(OH)D for musculoskeletal health, cancer prevention, or any of the other claimed benefits is irrelevant to the proven value of sun protection. Whatever this optimal level, ample vitamin D can be obtained from diet, supplements, and incidental sun exposure.^1,4-7 Intentional unprotected sun exposure to increase vitamin D photosynthesis is not only unnecessary, but also inefficient for those at highest risk of vitamin D deficiency.^9-11 The groups most responsive to the media’s unprotected sun exposure message are those who have the statistically lowest risk of vitamin D deficiency: healthy fair-skinned adolescents and young adults. Indeed, surveys in the US show that more than 70% of tanning bed users are Caucasian women aged 16-49 years12 and 95% of all users exceed the exposure levels recommended by the US FDA²⁵ for maximizing vitamin D photosynthesis. The demographics and exposure habits of the sunbathing public are similar to those of tanning bed users, although the average age is probably even younger and exposures even greater. The safe-sun message promulgated by dermatologists and the American Academy of Dermatology does not target dark-skinned individuals, who already have excellent endogenous sun protection in the form of epidermal melanin. Moreover, the groups at demonstrated risk of vitamin D deficiency have not embraced the “UV advantage” message,³ perhaps because this message does not target them.

The interest among the media and public in the pseudo-controversy is nevertheless real and persistent. Why? The sun protection message is old, dating back at least 23 years,²⁶ and its intended audience views it as wimpy, like the “buckle up” seatbelt message. Real men, and rebellious, fun-loving, and spontaneous adolescents do not wear sunscreen (or seatbelts). Moreover, many people, especially teenagers, want to sunbathe to acquire a “sexy” tan, not to reduce their risk of age-associated disease decades later.²⁷ In addition, relaxing in the sun and making one’s own vitamin D have a back-to-nature holistic appeal for many individuals. It is therefore not surprising that the print and electronic media continue to cover the pseudo-controversy: it sells. However, press releases crafted by representatives and employees of the USD $5 billion/year indoor tanning industry^28,29 have greatly facilitated the media’s natural tendency to pursue a “new” and controversial story, especially if it is one their audience wishes to hear.

The indoor tanning industry’s concern for the public health would be more credible if its coverage of the issues were more balanced, and a decade or so of extolling the virtues of UVA lamps (not the UVB lamps that it now touts as “healthful”) had not preceded the current campaign.^30-32 Before publication of the epidemiologic studies questioning the adequacy of conventional vitamin D recommendations, the industry argued strenuously that indoor tanning was superior to natural sun exposure precisely because people could tan with less UVB exposure (and, of course, less vitamin D photosynthesis).³³ Indeed, a review of the industry’s public positions over the 30 years of its dramatic growth in annual revenues34 reveals a series of opportunistic, contradictory positions. There can be no doubt that the goal of the tanning industry is to sell tanning sessions, not to safeguard the public’s health.

One Dermatologist’s Recommendation to Patients

Common sense and overwhelming medical/scientific literature support the fact that fair-skinned people benefit from regular, lifelong, safe sun practices. Moreover, people who wear high-sun protection factor (SPF) sunscreen in season, probably synthesize vitamin D maximally in exposed areas during incidental sun exposure.³⁵ Although some have claimed that sunscreens block all UV (and hence, all vitamin D photosynthesis³⁶) this is not the case. By definition, sunscreens allow continuous transmission of a fraction of erythemogenically weighted incident UV photons equal to 1/SPF of the total (e.g., 1/15th or 7% for an SPF 15 product). Moreover, studies have shown that sunscreen users customarily apply half or less of the FDA-stipulated amount of product required to generate the stated level of protection (2mg/cm2) and hence achieve far less protection.³⁷ If people require 2-8 minutes of unprotected summer sun exposure to maximize their cutaneous vitamin D synthesis,3 they could accomplish this in approximately 10-20 minutes of exposure after applying an SPF 15-30 sunscreen in the customary manner.^37,38 Most critically, regardless of one’s complexion, or the extent of UV exposure, daily oral vitamin D supplementation can completely compensate for the lack of cutaneous vitamin D photosynthesis.¹ Of note, those rare individuals with compromised absorption of orally-administered vitamin D should be advised to use intramuscular injections or very high-dose oral supplements.

Despite the above considerations, many patients ask their dermatologist to recommend a “safe” or “prudent” amount of sun exposure. Such recommendations must be individualized, as the risk-benefit ratio varies enormously within the population. Moderate or even generous sun exposure might have little effect on a darkly pigmented person’s risk of subsequent photoaging and skin cancer while promoting higher 25(OH)D levels; but even quite modest exposure could promote development of precancerous and cancerous lesions in already-photodamaged fair skin without increasing the already maximized vitamin D photosynthesis. A rule of thumb might be that any sunburn dose is too much by a factor of at least 3, as maximal vitamin D synthesis is achieved after approximately one-third of a minimal erythema dose.³⁹

Individuals who never sunburn or who live in climates that never allow them to sunburn are relatively “safe” from the damaging effects of unprotected sun exposure. People with complexions or living circumstances associated with the possibility of frequent sunburns probably have no “safe”, minimum unprotected exposures. Such unprotected exposures would only be a few minutes in length, but in the course of their routine activities, this higher-risk group would almost certainly exceed the prudent exposure time on a daily basis.
Although the much discussed epidemic of vitamin D insufficiency has been linked by some to the overuse of sunscreens, there is little or no evidence that this is the case, even if such an epidemic exists. Those population groups most likely to be vitamin D deficient (and presumably insufficient, if that term is accepted) are indeed unlikely to use sunscreens at all; these groups include inner city dark-skinned minorities, frail elderly who are often home-bound or institutionalized, and Middle Eastern women who wear the bourka, and therefore expose very little skin to the sun.

Strong evidence suggests that many individuals in these groups derive at least a musculoskeletal benefit from vitamin D supplementation, although they infrequently consult a dermatologist in this regard. Strong evidence also suggests that long-term oral vitamin D supplementation at doses up to 10 times the current RDAs are safe,^4,40 and many endocrinologists and nutritionists now suspect that the RDAs are too low. Therefore, it seems quite reasonable to recommend to all older patients who practice sun safety and to anyone even remotely concerned about vitamin D “sufficiency” that he/she take 1,000 IU of vitamin D daily, especially in the winter months. Routine measurement of the serum 25(OH)D level does not seem warranted, as the test is expensive and the “normal” or “optimal” range is debatable; in any case, the treatment for “low” levels is supplementation at this dose.

References

1. Wolpowitz D, Gilchrest BA. The vitamin D questions: much do you need and how should you get it? J Am Acad Dermatol 54(2):301-17 (2006 Feb).
2. Lappe JM, Travers-Gustafson D, Davies KM, et al. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr 85(6):1586-91 (2007 Jun).
3. Holick MF, Jenkins M. The UV Advantage. ibooks, Incorporated (2004).
4. Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr 69(5):842-56 (1999 May).
5. Boucher BJ. Sunlight “D”ilemma. Lancet 357(9260):961 (2001 Mar 24).
6. Calvo MS, Whiting SJ, Barton CN. Vitamin D intake: a global perspective of current status. J Nutr 135(2):310-6 (2005 Feb).
7. Utiger RD. The need for more vitamin D. N Engl J Med 338(12):828-9 (1998 Mar 19).
8. Wactawski-Wende J, Kotchen JM, Anderson GL, et al. Calcium plus vitamin D supplementation and the risk of colorectal cancer. N Engl J Med 354(7):684-96 (2006 Feb 16).
9. Clemens TL, Adams JS, Henderson SL, et al. Increased skin pigment reduces the capacity of skin to synthesise vitamin D3. Lancet 1(8263):74-6 (1982 Jan 9).
10. Bell NH. Vitamin D metabolism, aging, and bone loss. J Clin Endocrinol Metab 80(4):1051 (1995 Apr).
11. Need AG, Morris HA, Horowitz M, et al. Effects of skin thickness, age, body fat, and sunlight on serum 25-hydroxyvitamin D. Am J Clin Nutr 58(6):882-5 (1993 Dec).
12. Swerdlow AJ, Weinstock MA. Do tanning lamps cause melanoma? An epidemiologic assessment. J Am Acad Dermatol 38(1):89-98 (1998 Jan).
13. Binkley N, Novotny R, Krueger D, et al. Low vitamin D status despite abundant sun exposure. J Clin Endocrinol Metab 92(6):2130-5 (2007 Jun).
14. Garland CF, Garland FC, Gorham ED. Can colon cancer incidence and death rates be reduced with calcium and vitamin D? Am J Clin Nutr 54(1 Suppl):193S-201S (1991 Jul).
15. Garland CF, Garland FC, Gorham ED. Calcium and vitamin D. Their potential roles in colon and breast cancer prevention. Ann N Y Acad Sci 889:107-19 (1999).
16. Holick MF. Vitamin D: Photobiology, metabolism, mechanism of action, and clinical applications. In: Favus M, editor. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 4th ed. Philadelphia: Lippincott Williams & Wilkins; p92-8 (1999).
17. Bigby M, Szklo M. Evidence-based dermatology. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, editors. Fitzpatrick’s Dermatology in General Medicine. 6th ed. New York: McGraw-Hill; p2301-11 (2003).
18. Grau MV, Baron JA, Sandler RS, et al. Vitamin D, calcium supplementation, and colorectal adenomas: results of a randomized trial. J Natl Cancer Inst 95(23):1765-71 (2003 Dec 3).
19. Tuohimaa P, Tenkanen L, Ahonen M, et al. Both high and low levels of blood vitamin D are associated with a higher prostate cancer risk: a longitudinal, nested case-control study in the Nordic countries. Int J Cancer 108(1):104-8 (2004 Jan 1).
20. Gross MD. Vitamin D and calcium in the prevention of prostate and colon cancer: new approaches for the identification of needs. J Nutr 135(2):326-31 (2005 Feb).
21. Hartman TJ, Albert PS, Snyder K, et al. The association of calcium and vitamin D with risk of colorectal adenomas. J Nutr 135(2):252-9 (2005 Feb).
22. Majewski S, Skopinska M, Marczak M, et al. Vitamin D3 is a potent inhibitor of tumor cell-induced angiogenesis. J Investig Dermatol Symp Proc 1(1):97-101 (1996 Apr).
23. Forman MR, Levin B. Calcium plus vitamin D3 supplementation and colorectal cancer in women. N Engl J Med 354(7):752-4 (2006 Feb 16).
24. Giovannucci E, Liu Y, Rimm EB, et al. Prospective study of predictors of vitamin D status and cancer incidence and mortality in men. J Natl Cancer Inst 98(7):451-9 (2006 Apr 5). 25. use: are we exceeding Food and Drug Administration limits? J Am Acad Dermatol 49(4):655-61 (2003 Oct).
25. Hornung RL, Magee KH, Lee WJ, et al. Tanning facility use: are we exceeding Food and Drug Administration limits? J Am Acad Dermatol 49(4):655-61 (2003 Oct).
26. Robinson JK, Rigel DS, Amonette RA. Trends in sun exposure knowledge, attitudes, and behaviors: 1986 to 1996. J Am Acad Dermatol 37(2 Pt 1):179-86 (1997 Aug).
27. Geller AC, Brooks DR, Colditz GA, et al. Sun protection practices among offspring of women with personal or family history of skin cancer. Pediatrics 117(4):688-94 (2006 Apr).
28. Demierre MF. Time for the national legislation of indoor tanning to protect minors. Arch Dermatol 139(4):520-4 (2003 Apr).
29. Dellavalle RP, Parker ER, Cersonsky N, et al. Youth access laws: in the dark at the tanning parlor? Arch Dermatol 139(4):443-8 (2003 Apr).
30. Westerdahl J, Ingvar C, Masback A, et al. Risk of cutaneous malignant melanoma in relation to use of sunbeds: further evidence for UV-A carcinogenicity. Br J Cancer 82(9):1593-9 (2000 May).
31. US Department of Health and Human Services, Public Health Service, National Toxicology Program. Exposure to sunlamps or sunbeds. In: Report on carcinogens. 11th ed. (2005).
32. Spencer JM, Amonette RA. Indoor tanning: risks, benefits, and future trends. J Am Acad Dermatol 33(2 Pt 1):288-98 (1995 Aug).
33. Levine JA, Sorace M, Spencer J, et al. The indoor UV tanning industry: a review of skin cancer risk, health benefit claims, and regulation. J Am Acad Dermatol 53(6):1038-44 (2005 Dec).
34. Albert MR, Ostheimer KG. The evolution of current medical and popular attitudes toward ultraviolet light exposure: part 3. J Am Acad Dermatol 49(6):1096-106 (2003 Dec).
35. Gilchrest BA. Sun exposure and vitamin D sufficiency. J Natl Cancer Inst 2008: in press.
36. Matsuoka LY, Ide L, Wortsman J, et al. Sunscreens suppress cutaneous vitamin D3 synthesis. J Clin Endocrinol Metab 64(6):1165-8 (1987 Jun).
37. Bech-Thomsen N, Wulf HC. Sunbathers’ application of sunscreen is probably inadequate to obtain the sun protection factor assigned to the preparation. Photodermatol Photoimmunol Photomed 9(6):242-4 (1992 Dec).
38. Pinnell SR. Cutaneous photodamage, oxidative stress, and topical antioxidant protection. J Am Acad Dermatol 48(1):1-19 (2003 Jan).
39. Holick MF, MacLaughlin JA, Clark MB, et al. Photosynthesis of previtamin D3 in human skin and the physiologic consequences. Science 210(4466):203-5 (1980 Oct 10).
40. Hollis BW. Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake recommendation for vitamin D. J Nutr 135(2):317-22 (2005 Feb).

The primary environmental cause of aging of the skin and most skin cancers is ultraviolet (UV) light from the sun. Its
damaging effects are cumulative, so daily protection throughout life is important. In the US, most people will get < 25% of
their lifetime UV dose by 18 years of age. By the age of 60, they have absorbed 80% of their lifetime dose.¹ The predominant
acute biologic damage, as well as chronic damage risks, such as elastosis and squamous cell carcinoma, are associated with
the UVB portion of the solar spectrum over UVA in a ratio of 4:1.²

Chronic UVA exposure can occur by several scenarios:

• Tanning beds (some promote UVA-only radiation)
• Exposure to the sun using a UVB-absorbing sunscreen
• UVA exposure through windows (only UVB rays are blocked)

People may be unaware that they are unprotected from the damaging effects of UVA under these circumstances.

Sun Protection

A 2003 survey by the American Academy of Dermatology reported regular sunscreen use by 47% of women and 33%
of men.³ There is general consensus among experts that daily, year-round, broad-spectrum photoprotection of at least sun
protection factor (SPF) 15 is a key component of a sun-safe strategy to reduce cumulative lifetime exposure to UV light.

Sun Protection Factor

• The SPF number indicates how much longer one can stay out in the sun before burning compared with no protection.
• An SPF of 15 means that theoretically one can stay out without burning, 15 times longer than with no protection. However, this should not be used to encourage prolonged sun exposure.
• The level of UV filtration is not proportional to the SPF. The amount of UV transmission is 1/SPF so with an SPF of 2, 50% of UVB light is transmitted. An SPF of 30, will block out 97% of UVB light (1/30 transmitted).
• SPF relates to UVB protection only. However, higher SPF sunscreens tend to provide more UVA protection.
  • While UVA rays don’t cause sunburn, they penetrate deeper into skin and cause photoaging, cutaneous immunosuppression, and can cause some skin cancers.
• There is no universally accepted rating to determine how good a sunscreen is at blocking UVA rays, although several measures have been proposed.⁴

Sunscreens

Sunscreens are divided into two broad categories:

1. Inorganic or physical blockers, which:

• reflect back and scatter the UV and visible light.
• are regarded as nontoxic and stable and do not penetrate below the stratum corneum.
• are esthetically less acceptable.

2. Organic or chemical agents, which:

• work through electron excitation and grounding, thus changing light energy into heat energy.
• are divided into UVA, UVB, and broadband absorbers.

The ideal sunscreen would:

• provide superior efficacy with broad-spectrum coverage, photostability, and high substantivity.
• have an appealing feel and smell and apply easily, uniformly coating the skin surface.
• not cause irritant or allergic contact dermatitis.
• be sold at a reasonable cost.⁵

New Generation Sunscreens

• Newer sunscreens combine ingredients that will protect the skin from both UVA and UVB rays and are available in creams, gels, lotions, sprays, and sticks.
• New generation sunscreens are more esthetically pleasing.
• The need for broad-spectrum, photostable filters has led to the development of new agents, including ecamsule and drometrizole trisiloxane, which provide both UVB and UVA protection.
• Degradation of some UVA filters by sunlight requires chemical stabilization to prevent loss of efficacy.
• An advanced formulation that incorporates the photolabile filter avobenzone, provides protection throughout the UVA range, and is combined with diethylhexyl 2,6-naphthalate (DEHN) and oxybenzone to achieve a photostable product. DEHN is a non-UV filter that stabilizes avobenzone by accepting energy absorbed by avobenzone during UVA exposure, while oxybenzone both enhances photostability and provides additional UVA protection.
  • This technology yields protection that is reported to be comparable to that of drometrizole trisiloxane, which provides efficient UVA coverage and photostability.⁶

Sunscreen Application

• Experts recommend that sunscreen be applied 15-30 minutes before going outdoors and reapplied every 2 hours or after swimming/ heavy exertion.
• The recommended dose is 2mg/cm² of skin, or 30ml (2 tablespoons) for the whole body. However, the actual dose being used is believed to be much lower.
• Application of an adequate amount of sunscreen is by far the most important factor influencing efficacy.

Sunscreens and Cancer

• Sunscreens, at sufficient SPF levels, are effective in protecting the skin from actinic keratoses and squamous cell carcinomas.⁷
• They have not been shown to reduce the incidence of a first basal cell carcinoma, but they may prolong the time to develop a second lesion.
• Dennis, et al., looked at sunscreen use and the risk for melanomas, and found no association between these two factors.⁸

The Vitamin D Controversy

• The UV action spectra for DNA damage leading to skin cancer and for vitamin D photosynthesis are virtually identical.⁹
• Nash, et al., analyzed the risks/ benefits of sunscreens on vitamin D by estimating its production, based on measures of sunlight exposure and determining the impact of an SPF 15 sunscreen on vitamin D levels in humans. The study found that the combination of diet and sunlight, even with daily use of an SPF 15 sunscreen, provides adequate intake of vitamin D.¹⁰

Conclusion

The new generation of sunscreens serve an important role in overall skin protection from the sun. However, they should be
used in conjunction with other sun protection measures such as sun protective clothing, hats, and sunglasses.

References

1. Godar DE, et al. Photochem Photobiol 77(4):453-7 (2003 Apr).
2. Cole C. Photodermatol Photoimmunol Photomed. 17(1):2-10 (2001 Feb).
3. American Academy of Dermatology. 2005 Skin Cancer Survey Fact Sheet. URL: www.aad.org.
4. Chen T, et al. Comprehensive evaluation of sunscreen protection beyond SPF and PF values. Presented at the 66th Annual Meeting of the American Academy of Dermatology, February 2008, San Antonio, TX. P2404.
5. Palm MD, et al. Derm Ther 20(5):360-76 (2007 Sep-Oct).
6. Rigel D, et al. Photostability of UVA/UVB sunscreens under extreme tropical sun exposure. Presented at the 64th Annual Meeting of the American Academy of Dermatology, March 2006, San Francisco, CA. P2623.
7. Naylor MF, et al. Arch Dermatol 131(2):170-5 (1995 Feb).
8. Dennis LK, et al. Ann Intern Med 139(12):966-78 (2003 Dec 16).
9. Wolpowitz D, et al. J Am Acad Dermatol 54(2):301-17 (2006 Feb).
10. Nash JF, et al. J Am Acad Dermatol 52(3):161 (2005 Mar).
11. Drealos Z. Am J Clin Dermatol 3(5):317-8 (2002).

The skin has evolved to protect us from the harmful effects of ultraviolet light. Sunscreens were first developed to prevent sunburns by blocking UVB; they allowed us to prolong our time in the sun, but that resulted in increased exposure to UVA. Most modern sunscreens
attempt to block the whole spectrum of UV light, however not all so-called broad spectrum sunscreens protect skin from the whole range of UVA.

A Comparison on UVA and UVB

Long-term Effects on the Skin

Most of us know that sun exposure has immediate positive and negative effects on the skin. The medium and longer term effects are negative. Positive effects include a sense of warmth, pleasure and Vitamin D production.

Photosensitive Rashes

These occur only when activated by UV light. Most of them are brought on by UVA. Photosensitive rashes (detailed below) can be thought of as:

1 – Idiopathic reactions to UV light
(Polymorphous light eruption – PLE)

The timing of the onset of the rash in relation to sun exposure and its duration, as well as the type of reaction produced on the skin, is key to making the diagnosis. As always there is some variation.

2 – Phototoxic and photoallergic skin reactions

There are a number of drugs and chemicals that can produce a reaction in the skin. These can be either phototoxic or photoallergic reactions.

3 – UV aggravation of existing conditions

There are many pre-existing conditions that are aggravated by sunshine. Some of the important light aggravated conditions are:

Polymorphous Light Eruption

Sun Exposure Causes
Rash starts within hours of exposure and lasts for days even with no further sunshine. Solar urticaria is seen within minutes of exposure. Rash can be seen in the form of papules, papulovesicles or plaques, hence the term polymorphous. Plaques are less commonly seen.		Polymorphous light eruption (PLE) Mostly caused by UVA Occurs in early spring or summer, and often during vacation periods Is mostly symmetrical, red papules and plaques. Occurs in exposed areas but not necessarily all the exposed areas Occurs in 10%-20% of the population May be confused for allergic reaction to sunscreen Skin tends to be less reactive to sun as the summer progresses. The type of rash tends to remain constant for each patient.		Treatment of PLE Sun avoidance and protection with broad spectrum sunscreen (UVA and UVB) Topical steroids and antihistamines UVA and UVB light therapy may help some at the start of the season, which can harden the skin and prevent the reaction. Hydroxychloroquine, 400mg daily for 2 weeks in the spring or before a vacation may help

Photoxic vs. Photoallergic Reactions

Phototoxic drugs or chemicals

• Sunburn-like
• Usually seen within hours
• Usually caused by UVA

Includes tetracyclines, sulfa, amioderone, fursomide, naproxen, piroxicam, chlorpromazine, ciprofloxacin, thiazides

Photoallergic reactions

• An eczema like reaction. Can be thought of as a delayed hypersensitivity type reaction.
• Causes: Sunscreens, fragrances/aftershave (like musk ambrette, sandalwood oil), chlorhexidine

Phytophotodermatitis

• A special type of reaction to topical contact with a sensitizer called psoralen contained in a number of plants.
• UVA plus psoralen will produce a blistering reaction often seen in streaks; a brown pigmentation is produced
• which may last for months.
• Plants containing psoralen are responsible including lime, yarrow, cow parsley, celery, lemon, fig

Photoprotection

Should be encouraged to prevent the immediate, medium and long-term ill effects of excessive sun exposure. Some sun exposure is desirable for vitamin D production.

Two ways to encourage photoprotection:

1. Sun avoidance

• Avoid the sun between 10am and 3pm.
• Try to stay in the shade.
• Wear protective, tightly woven clothes and a broad brimmed hat.

2. Sun protection

• Use a Broad-spectrum sunscreen in a sufficientquantity.
• SPF = the ratio of minimal erythema dose (MED) of protected skin/MED of unprotected
• skin. This is a crude biological measure.
• The SPF factor is calculated using 2mg/cm2 of sunscreen. Most people apply only 25-50% of this.
• Reapply sunscreen every 2 hours; UVL causes some chemical sunscreens to become inactive over time.

Sunbed Tan

• Very popular, producing good, even colour.
• Contain dihydroxyacetone (DHA); reacts with amino acids containing keratin. DHA concentration varies from 2%-6%; higher numbers give a darker colour.
• DHA has an SPF of 2%-3%. Some have a low SPF screen added that lasts only a few hours.
• Coloured skin does not provide protection against photodamage.
• Bronzers are dyes that are added to the skin; can be washed off.
• Beta-carotene, tyrosine, tanning accelerators such as psoralen are not recommended.

Sunscreen Use

• Broad spectrum only should be used.
• SPF related to UVB protection only; does not provide a reference to UVA protection.
• All sunscreens have UVB protection; reflected in the SPF.
• If skin sunburns in 10 minutes, properly applied sunscreen at SPF 15 means skin will burn in 150 minutes.
• Physical screens reflect light; chemical screens absorb UV, converting energy into heat
• SPF15 blocks 87.5% of UVB and SPF 50 blocks 98% of UVB.

Sunscreen Choices

Sunscreen with full spectrum UVA protection contains:

Avobenzone (Parsol 1789), Mexoryl Sx, and Zinc oxide working together. The first two have slightly different peaks of protection. Titanium Dioxide, Dioxybenzone Methyl anthranilate and Octocrylene provide UVA protection, but not along the whole spectrum. Some recommended general sunscreens: Ombrelle® 30, 45, 60, cream and lotion. (This broad spectrum sunscreen was pioneered in Canada); Anthelios® 30, 45, 60; Neutrogena® Heathy Defense Sunblocks 30, 45 with parsol.

Special sunscreens:
Lip protection: SCC is more commonly seen in men and women who don’t wear lipstick:
Ombrelle® Lip Balm SPF30; RoC Minesol® Lipstick SPF 20; Neutrogena Stick 30; Antherpos ® SPF 50. For joggers these can also be used above the eyebrows to prevent the screen from entering the eyes. Can also be used on the nose.

Spray for athletes, or for people with hairy or oily skin: Ombrelle® Sport Spray 15; Coppertone ® Sport 15 and 30; Neutrogena® Healthy Defense Spray 30.

ABSTRACT
ROSASOL Cream is a novel topical formulation of 1% metronidazole in a vehicle containing sunscreens (SPF 15). This product has demonstrated efficacy in the treatment of inflammatory lesions, erythema, and telangiectasiae associated with rosacea.

Key Words:
metronidazole, sunscreens, inflammatory lesions, erythema, telangiectasia, rosacea

ROSASOL Cream (Stiefel Canada) was issued a Notice of Compliance by TPP – Canada in October 2000, for the treatment of inflammatory lesions (papules and pustules), erythema, and telangiectasia associated with rosacea. This new formulation combines 1% metronidazole in a cream vehicle containing the sunscreens Parsol 1789 and MCX, as well as cyclomethicone and phenyl trimethicone. The latter ingredients have been shown to reduce potential irritation associated with the use of sunscreens in rosacea patients.¹ The sunscreens were formulated to provide SPF 15.

Development was based on the importance of sun protection in the management of rosacea,^2,3 and the demonstrated efficacy of topical metronidazole (see Table 1).

Table 1: Randomized placebo-controlled trials of topical metronidazole in treatment of rosacea.
*Indicates statistical significance at 0.05 level
**A reduction in inflammatory lesions and a significant decrease in telangiectasiae were seen by week 4.
There was a significant decrease in erythema by week 8.

Mechanism of Action

Current evidence suggests that the mechanism of action of metronidazole in rosacea is via inhibition of release of neutrophil-induced inflammatory mediators such as reactive oxygen species.⁹ Parsol 1789 and MCX are broad-spectrum sunscreens that are effective in both UVB and UVA wavelengths.

Table 2: Dosage and Cost (CDN) of drugs used to treat rosacea, and of SPF 15 sunscreen. Formulary prices are from La Regie de l’assurance maladie (2001 Apr) and the Ontario Drug Benefit Formulary (2001 Mar).

Pivotal Clinical Trial

A Canadian multi-center double-blind randomized trial of 120 patients against sunscreen vehicle demonstrated that ROSASOL Cream applied twice daily was significantly more effective in the treatment of rosacea.⁴ At the end of 12 weeks of treatment, mean reductions for ROSASOL Cream (in comparison to placebo) were:

• inflammatory lesions by 70% (placebo: 23%, P = 0.005)
• erythema scores by 41% (placebo: 27%, P = 0.021)
• telangiectasia scores by 17% (placebo: 4%, P = 0.043).

ROSASOL Cream was well tolerated with the majority of patients noting a reduction in itching, dryness and stinging over the course of the 12-week study.

Adverse Effects

The 37 adverse events attributed to ROSASOL Cream in the Canadian double-blind study occurred at the site of application and consisted of stinging (13 cases), erythema (8 cases), itching (5 cases) and dryness (4 cases). All patients recovered completely without sequelae.⁴

Conclusion

ROSASOL Cream, a topical product containing 1% metronidazole with sunscreens, is efficacious and well-tolerated in treatment of rosacea. In addition to improving the inflammatory and vascular clinical manifestations of this condition, it also provides the additional benefit of photoprotection in this combined product.

References

1. Nichols K, Desai N, Lebwohl MG. Effective sunscreen ingredients and cutaneous irritation in patients with rosacea. Cutis 61(6):344–6 (1998 Jun).
2. Greaves MW. Flushing and flushing syndromes, rosacea and perioral dermatitis. In: Champion RH, Burton JL, Burns DA, Breathnach, eds. Rook/Wilkinson/Ebling Textbook of Dermatology, 6th Edition. Oxford: Blackwell Science ch 46 (1998).
3. Plewig G, Kligman AM. Acne and Rosacea. Berlin, Springer-Verlag p 433 and 439 (1993).
4. Tan JKL, Girard C, Krol A, et al. Metronidazole 1% cream with sunscreen SPF 15 in treatment of rosacea. Data on file Stiefel Canada (1999). In preparation for publication.
5. Bitar A, Bourgouin J, Dore N, et al. A Double-blind randomized study of Metronidazole (Flagyl) 1% cream in the Treatment of Acne Rosacea: A placebocontrolled study. Drug Invest 2(4):242–8 (1990).
6. Bjerke JR, Nyfors A, Austad J, et al. Metronidazole (Elyzol) 1% cream v. placebo cream in the treatment of rosacea. Clin Trials J 26(3): 187–94 (1989).
7. Bleicher PA, Charles JH, Sober AJ. Topical metronidazole therapy for rosacea. Arch Dermatol 123(5):609–14 (1987 May).
8. Gamborg Nielsen P. Treatment of rosacea with 1% metronidazole cream. A double–blind study. Br J Dermatol 108(3):327–32 (1983 Mar).
9. McLellan KJ, Noble S. Topical metronidazole: A review of its use in rosacea. Amer J Clin Dermatol 1(3):191–9 (2000 May–June).
10. Jorizzo JL, Lebwohl M, Tobey RE. The efficacy of metronidazole 1% cream once

A review of the American Academy of Dermatology’s (AAD) National Skin Cancer Screening Program indicates that middle-aged and older men are not detecting melanoma in its early stages when it is most curable because they are the least likely to perform monthly skin self-examinations or visit a dermatologist regularly.

Melanomas are characterized by the uncontrolled growth of pigment-producing cells. They may suddenly appear without warning, but can also develop from or near a mole. They can occur anywhere on the body, but are found most frequently on the upper backs of men and women, or on the calves of women.

The study included 242,374 screenings conducted between 1992 and 1994, as part of the AAD’s National Skin Cancer Screening Program*. Overall, 3,476 individuals were given a presumptive diagnosis of melanoma or possible melanoma. However, melanoma was more than three times as common among middleaged and older men than among all those screened. This group of men comprised more than 44% of patients

ABSTRACT
Over the past century, tanned skin shifted from being unpopular to becoming the height of fashion. However, the past decade has again seen white skin become fashionable as more and more people become aware of the dangers of spending too much time in the sun. Even so, having tanned skin is still popular and probably will be for some time to come. This article will focus on cosmetic products that are designed to simulate tanning of the skin by coloring or staining the skin without sun exposure. 

Key Words:
self-tanning creams, sunscreens

Despite extensive evidence that sun exposure induces premature cutaneous aging and skin cancer, patients continue to find tanned skin cosmetically desirable. Tanning booths are frequented by people of all ages from adolescent to mature patients and the industry is presently thriving in all regions of the United States. However, brown skin was not always fashionable. Wealthy females of the mid-to-late 1800s shunned sun exposure to the point of carrying parasols and spending extensive time indoors to distinguish themselves from farm labor who displaued deeply tanned skin from hours of working outdoors. As machinery replaced farm workers and indoor work behind a desk or in a factory became the norm, white skin became a sign that an individual did not have the luxury of spending time in the sun or vacationing in a sunny location. Therefore, as the work activities shifted indoors, a tan became fashionable.

Perhaps some of the education provided by dermatologists regarding sun avoidance is reaching fashion circles, as a review of the chic look for fall 1990 was white skin. Currently, the trendy makeup fashion is a powdered, matte, white face with vivid red lips and dark hair, but it is hard to imagine that “the tan” will loose its fashion desirability quickly.

Cosmetic products that imitate a summer tan fall into several categories: self-tanning creams, bronzing gels, bronzing powders and tinted moisturizers.

Self-Tanning Creams

Self-tanning creams, sold at both mass merchandisers and cosmetic counters, have become extremely popular because they produce a golden skin color overnight without sun exposure. These products are not new, but have seen a resurgence of popularity. This is because the new formulations produce a more natural golden color while the older products dyed the skin a somewhat unusual orange color. The golden color is quite acceptable on persons with blonde or light brown or light brown hair who tend to have golden hues to their skin, but it is not attractive on Mediterranean individuals with an olive complexion, or extremely fair persons with pink skin tones.

The active ingredient is 3-5% dihydroxyacetone incorporated into a glycerin and mineral oil base to form a white cream that turns the stratum corneum golden. A chemical reaction actually occurs between the keratin protein of the skin and the sugar component of the self-tanning cream. The resulting byproduct is a brown color that stains the skin. Formulations are available for the face and body, but most do not incorporate a sunscreen, nor is the golden skin color protective against actinic damage. Allergic contact dermatitis from use of the product is infrequent, but may be due to the incorporated fragrance or preservative.

The color is not permanent and is lost as the stratum corneum desquamates. Thus continues use is necessary. The major disadvantage of the product is that it stains all contacted skin surfaces including the palms of the hands, if it is not removed, and will produce deeper staining of the follicular ostia, seborrheic keratosis, actinic keratosis, porokeratosis and icthotic skin. Many patients are not aware that they have these skin conditions until the self-tanning cream highlights the irregularity.

Self-tanning creams cost from $15-$40 (US) for a 4-6oz tube and provide approximately 10-12 complete leg applications. Products are marketed to both men and women.

Dermatologists should ask patients about the use of a self-tanning cream before making the diagnosis of carotenemia from the appearance of yellow palms, or expressing undue concern of a lesion that has changed color. This may simply represent a stained stucco keratosis. Other than this confusion, self-tanning creams are safe and an excellent alternative to a tan from hours spent in the sun.

Bronzing Gel

Bronzing gels are pigmented polymers that are spread over the skin to simulate the appearance of a tan. They provide transparent color. Some products actually stain the skin, while others are removed with one washing, and still others incorporate a sunscreening agent in the formulation. Products are marketed through both male and female cosmetic lines and have become surprisingly popular with men.

Bronzing Powders

Bronzing powders are identical in formulation to face powders except for the addition of different pigments. The powder is stroked from a compact with a powder sponge or puff and applied to the body. The product is usually dusted down the central face, neck and shoulders to simulate a tan. The powder is easily removed by rubbing and provides slight physical sun protection due to the titanium dioxide in most formulations.

Tinted Moisturizers

Some moisturizers contain pigment that provides a sheer tanned appearance in addition to possessing emollient qualities.

Technically, it is impossible to separate a tinted moisturizer from a sheer, moisturizing facial foundation. Usually a facial foundation contains titanium dioxide to provide coverage to underlying cutaneous pigment defects whereas a tinted moisturizer does not, but the distinction is slight. Tinted moisturizers may or may not possess a chemical sunscreen.

Conclusion

Dermatologists may wish to familiarize themselves with cosmetics designed to simulate a tan for those patients who insist on displaying bronze skin. The cosmetics may or may not contain a sunscreening agent, but the color produced is not protective. Certainly, a cosmetic tan is safe alternative for patients who use a tanning booth or worship the sun.

References

1. Draelos ZK, Cosmetic in Dermatology. Edinburgh, Churchill Livingstone, 1990. Pp 25-30.