Manual of Dermatologic Therapeutics
7th Edition
© 2007 Lippincott Williams & Wilkins
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33
Sun Reactions and Sun Protection
Janine D’Amelio Miller
I. Definition and Pathophysiology
The sun radiates a broad system of energy that may be categorized in terms of the wavelength of the electromagnetic waves. This radiation reaching the earth’s surface may be broadly subdivided into (i) infrared (range 800 to 1,700 nm), felt as heat or a sensation of warmth, (ii) visible (range: 400 to 800 nm), the energy that stimulates the retina, and (iii) ultraviolet (UV) (290 to 400 nm), wavelengths shorter than the visible range.
  • Ultraviolet radiation (UVR) can be subdivided into three bands.
    • Ultraviolet A (UVA) radiation (320 to 400 nm, long wavelength) can be further divided into UVAI (340 to 400 nm) and UVAII (320 to 340 nm). UVA causes immediate pigment darkening of preformed melanin and may play an additive role in assisting ultraviolet B (UVB) (see subsequent text) in causing sunburn or aging. In the presence of some drugs (psoralens, antibiotics such as doxycycline, sulfonamides, phenothiazides, chlorothiazides, sulfonylureas, and others), UVA may induce severe phototoxicity (sunburn and blistering). UVA can cause skin cancers in mice, induce deoxyribonucleic acid (DNA) damage through production of photoproducts, and suppress the immune system (1).
    • UVB radiation (290 to 320 nm, middle wavelength) acutely causes erythema and edema, followed by stimulation of melanocytes to make new melanosomes, thereby causing pigment darkening and a tan. Chronic exposure induces most of the changes commonly attributed to aging and carcinogenesis.
    • Ultraviolet C (UVC) radiation (200 to 290 nm) from sunlight is absorbed by the ozone layer in the atmosphere and does not reach the earth’s surface. This radiation kills bacteria, can cause mild conjunctivitis or sunburn, and is used in operating-room germicidal lamps.
      Approximately two thirds of the total daily UVR reaches the earth between 10 a.m. and 2 p.m. Midday UVR is 10% UVB and 90% UVA, because little UVA is filtered by the atmosphere. Cloud cover can reduce the total amount of radiation by 50%. Water also reduces the penetration of ultraviolet light (UVL) by 50%. Snow and ice reflect 80% of the radiation, whereas sand reflects 20% and grass, 2.5%. A breeze will alter an individual’s perception of total UV exposure as the skin is cooled. The more hydrated the skin becomes (such as after swimming), the less the reflection of UV light and, subsequently, increased absorption. Window glass blocks UV radiation below 320 nm, thereby providing protection against UVB. Tinted windows can offer increased protection against UVA (2,3).
      UVR induces genetic damage by covalent induced mutations and chromosome damage, which inactivates tumor suppressor genes such as p53. Both UVA and UVB induce DNA damage indirectly through the generation of reactive oxygen free radicals. UVB is a more potent inducer of these reactive species than UVA, although 96% of the UV spectrum is UVA. Blue light in the range of 400 to 450 nm can contribute to DNA damage. UVL also suppresses the immune system with altered response to antigens, release of immunosuppressive factors such as interleukins, and inhibition of natural killer cells.
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Ozone Layer
The ozone layer has been diminishing during the last 20 years, primarily from the release of chlorofluorocarbon compounds into the atmosphere. As a consequence, more UVB can now reach the earth’s surface. In general, each degree increase in latitude corresponds to a 3% increase in UVR reaching the earth, and every 1,000 meters above sea level corresponds to a 10% increase in UVR (4,5). The impact of climate changes caused by the stratospheric ozone depletion on skin cancer incidence still remains uncertain (6). Ozone depletion might result in an increased incidence of ocular changes, leading to cataracts, the development of cutaneous melanoma, and the incidence of basal and squamous cell carcinomas (7,8).
Sunburn is usually the result of excessive exposure to UVB radiation but may be a response to excessive UVC from artificial light sources or UVA in the presence of a topical or systemic photosensitizing agent. It is seen most commonly after exposure to the sun but may also follow exposure to sunlamps or occupational light sources (welding arcs [250 to 700 nm], photoengraving [250 to 700 nm], bactericidal or cold quartz lamps [254 nm]). UVB is not screened out by thin clouds on overcast days but is fully absorbed by window glass and is partially absorbed in the smoke and smog around large cities. The epidermis reflects 10% of the UVB rays, and 20% will penetrate to the dermis. UVA penetrates deeper and has more effect on the dermis, markedly accentuating UVB damage. A great deal of UVL reaches the skin through reflection from snow, sand, or sidewalks; hats and umbrellas provide only moderate protection.
Skin Types and Natural Protection
Our own natural sun-protective mechanisms include the thickness of the epidermis, natural antioxidants, melanin, urocanic acid (natural UV absorber), DNA repair mechanisms, and Fas ligand signaling. Transplantation patients are an example of what can happen in nonmelanoma skin when there is a combination of immunosuppression and prior mutations of the p53 gene. Tolerance to sunlight is based on the amount of melanin in the skin and an individual’s genetic capacity to produce melanin following exposure to the sun, that is, a suntan. On the basis of the response to the first 30-minute exposure to summer sun and the tan that develops in persons with white skin, sun-reaction skin types can be classified as follows:
  • Skin type I: always burns easily, never tans.
  • Skin type II: usually burns easily, tans minimally.
  • Skin type III: burns moderately, tans gradually.
  • Skin type IV: burns minimally, tans readily.
  • Skin type V: rarely burns, tans profusely, and occurs in heavily pigmented individuals such as darker Mediterraneans, Mongolians, and Indians.
  • Skin type VI: never burns, darkly pigments, and occurs in blacks.
People with type I and II skin often have light skin color and blue eyes, may have red scalp hair, and may or may not have freckling. However, some persons with darker hair and blue or green eyes have type I and II sun reactions. People with type I and II skin will exceed their sunburn threshold tolerance in 10 to 20 minutes of noontime temperate summer sunlight. Three to eight times the minimal erythema dose (MED) will produce a moderate to severe burn.
A number of genetic (e.g., xeroderma pigmentosum), metabolic (e.g., pellagra and porphyria cutanea tarda), neoplastic (e.g., actinic keratosis, basal cell carcinoma), connective-tissue (e.g., lupus erythematosus), immunologic (e.g., solar urticaria, drug photoallergy), and idiopathic (e.g., hydroa aestivale, polymorphous light eruption) diseases may be caused or exacerbated by light exposure. In a large study that evaluated patients with photosensitive disorders, 26% had polymorphous light eruption, 17% had chronic actinic dermatitis, 8% had photoallergic contact dermatitis, 7% had systemic phototoxicity to therapeutic agents, and 4% had solar urticaria. The most frequent allergic agents were fragrances, sunscreens, and antimicrobial agents (9).
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Evidence is increasing that UVL is responsible for the development of at least 10% of all cataracts and macular degeneration. Pingueculae and pterygium appear on the conjunctival surface of the eye and are more prevalent in geographic areas close to the equator. The lower eyelid, the most anatomically exposed area of the eye, is at risk for both melanoma and nonmelanoma skin cancers.
Ultraviolet Index
The UV Index is a program that informs the public about the amount of harmful UVL reaching the earth on a particular day and is a recognized part of the weather report in many cities. The SunWise program, which lists the UV Index and has developed programs for the education of the public, notably children, can be accessed on the Environmental Protection Agency (EPA) web site at http://www.epa.gov. The National Meteorological Center determines the index daily; a recommendation for fair-skinned individuals who burn easily and tan minimally is as follows:
  • 0 to 2: Minimal. One hour of unprotected exposure may produce UV damage in people with sun-sensitive skin.
  • 3 to 4: Low. Sunburn may occur within 30 to 60 minutes of unprotected exposure.
  • 5 to 6: Moderate. Significant risk of skin damage and sunburn in only 20 to 30 minutes of unprotected exposure.
  • 7 to 9: High. Unprotected skin may burn in 10 to 20 minutes.
  • 10 to 15: Very high. Burning will occur in <10 minutes without protection.
Indoor Tanning
The use of indoor tanning beds in the United States is a $2 billion per year industry. Dermatologists and others have expressed concern with the lack of regulation of this industry. The sunlamps (usually UVA wavelengths) in these tanning units emit 26 times more damaging UVL than the equivalent amount of sunlight. This dose can produce erythema and melanogenesis but does not provide the protection of a naturally occurring tan, because there is no thickening of the stratum corneum and the pigmentation is restricted to the basal layer.
The major concern regarding tanning beds is the carcinogenic effect of multiple doses of UVL. One systematic review of the current literature found a significantly increased risk of cutaneous melanoma subsequent to sunbed/sunlamp exposure (10). Also, a recent study evaluated the link between keratinocyte carcinomas and sunlamp usage, finding that the use of tanning devices may contribute to the incidence of nonmelanoma skin cancers (11). Additionally, polymorphous light eruption occurs in 10% to 13% of patrons. Other concerns are exacerbation of systemic lupus erythematosus, porphyria, and rosacea and the induction of phototoxic and photoallergic reactions (12).
Solar UV radiation and exposures to sun lamps and sunbeds are now listed as known human carcinogens. All sun-tanning products must now contain a package warning that says: “This product does not contain a sunscreen and does not protect against sunburn. Repeated exposure of unprotected skin while tanning may increase the risk of skin aging, skin cancer, and other harmful effects to the skin even if you do not burn.”
Reactions to Excess Ultraviolet Exposure
I. Subjective Data
  • A mild sunburn will be tender to the touch and cause a hot, taut, drawn feeling. Symptoms usually peak in 16 to 24 hours.
  • Severe burns are accompanied by intense pain, inability to tolerate contact with clothing and sheets, and constitutional symptoms, including nausea, tachycardia, chills, and fever. This constellation of symptoms is what the lay public calls “sun poisoning.”
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II. Objective Data
  • The earliest sign of a burn is a pink to scarlet hue of the skin and mild edema. The more severe the burn, the earlier it will be evident. Sun exposure will cause immediate erythema, which then fades. A delayed erythema appears in 2 to 4 hours, peaks at 14 to 20 hours, and lasts 24 to 72 hours.
  • This burn may progress to a vivid erythema, intense edema, and blistering.
  • Peeling follows as a consequence of increased epidermal turnover during the repair response, usually a week or more after the burn.
  • Hyperpigmentation is seen because of UVB-induced new pigment formation and offers some protection against further sunburn. This is evident as immediate pigment darkening of preformed melanin (2 to 24 hours) and delayed tanning, reflective of new pigment formation (4 to 7 days).
  • UVA reactions follow a slower time course; erythema becomes evident as late as 48 hours, and the reaction may become more severe for several days.
  • UVC reactions are seldom severe; overexposure to short-wave UVL rarely leads to blistering but can lead to conjunctivitis and keratitis.
III. Assessment
The patient’s history will usually be adequate to explain the clinical picture. It is important to be certain that there are no predisposing or underlying factors (drug administration, topical application of photosensitizers, or systemic illnesses such as lupus or porphyria).
IV. Therapy
Mild Sunburn
  • Apply cool tap water or Burow’s solution compresses for 20 minutes three to four times a day or more frequently.
  • A topical corticosteroid spray, lotion, cream, or gel may reduce inflammation and pain.
  • Use emollients (Eucerin, Lubriderm, Nivea, petrolatum) to soothe and relieve dryness.
  • Most proprietary over-the-counter (OTC) burn remedies contain local anesthetics (benzocaine, dibucaine, or lidocaine), antiseptics, emollients, and fragrant materials. There is little need for any of these ingredients in the care of a sunburn, and only 20% benzocaine (Americaine) has been demonstrated to be effective. The vehicles of “anesthetic” sprays, creams, and lotions may be cooling and the ointments lubricating, thereby lessening the symptoms, but this must be weighed against the hazard of becoming sensitized, especially to benzocaine. Because burns are intrinsically self-healing, it is mandatory that the therapy be less noxious than the problem.
  • Aspirin, indomethacin, and ibuprofen in usual doses can help relieve the discomfort.
Severe Sunburn
  • Patients should call immediately if they are overexposed to sunlamps or to sunlight, because it is easier and more effective to abort severe inflammation than to treat an already established reaction. A short course of systemic corticosteroids may reduce potentially severe sunburn; prednisone 40 to 60 mg or its equivalent should be administered daily for 3 days and then discontinued. Some studies have been unable to confirm that prednisone suppresses sunburn, but the clinical impression still remains that it may often be useful.
  • Topical care of established severe sunburns entails almost continuous cool compresses, topical steroids and emollients, a cradle for bed linens, analgesics as needed, and careful surveillance for bacterial superinfection. Application of a class I topical steroid b.i.d. for 3 days within 48 hours of the burn can provide symptomatic relief but does not repair damage to the skin. Topical 5% indomethacin in combination with the class I steroid can provide additional benefit.
  • Some fair-skinned individuals may increase their tolerance of UVL through systemic administration of psoralen compounds. These drugs will increase the capacity of the skin
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    to produce melanin after sun exposure and will also result in retention of melanin granules in a thickened stratum corneum. Two hours before sun exposure, trioxsalen (Trisoralen) 30 mg should be taken, and exposure during the first week should be increased gradually. Use of this medication without subsequent exposure to light will be ineffective.
Photoprotection
Sunscreen has been shown to prevent ultraviolet-induced DNA damage, cutaneous immunosuppression, and the generation of T suppressor cells. Application of sunscreens does decrease the risk for development of nonmelanoma skin cancers and actinic keratoses; its effect on the prevention or development of melanoma is controversial.
Sun-protective topical medications are available as sunscreens, which contain multiple chemical substances and physical blockers. Chemical sunscreens, more recently termed organic by the U.S. Food and Drug Administration (FDA), block the penetration of UV radiation by acting as filters and by absorbing and reflecting UVL. The physical or nonchemical sunscreens scatter or reflect UV radiation. Most sunscreens are good protective agents against UVB and short-wave UVA; however, complete protection against long-wave UVA has not yet been achieved (13).
In 1997, Congress requested the FDA to create new regulations and recommendations on the prevention and treatment of sunburn. The result was the most recent FDA monograph of sunscreens containing requirements for formulation and simplified labeling (14). This new monograph listed 16 ingredients that companies can use in sunscreen products (see subsequent text). Other changes included labeling any sunscreen greater than a sun protection factor (SPF) of 30 with an “SPF 30 plus.” The terms “waterproof” and “all-day protection” were dropped, replacing them with “water resistant” and “very water resistant.”
Sunscreen Ultraviolet Light Absorption
Most sunscreens have their peak absorption in the UVB range between 290 and 320 nm. Of the commonly used sunscreen agents, only the benzophenones and anthranilates have substantial absorption in the UVA range, from 320 to 400 nm. Newer sunscreens with padimate O and Parsol 1789 provide some increased UVA absorption but less UVB photoprotection. Parsol 1789 is a chemical with a major absorption peak at 360 nm, in the UVA range. Many photosensitizing drugs are activated at 360 nm.
Specific Agents
Product Percent (%) Absorbance
Aminobenzoic acid Up to 15 UVB
Avobenzone 2 to 3 UVAI
Cinoxate Up to 3 UVB
Dioxybenzone Up to 3 UVB, UVAII
Ensulizole Up to 4 UVB
Homosalate Up to 15 UVB
Meradimate Up to 5 UVAII
Octocrylene Up to 10 UVB
Octinoxate Up to 7.5 UVB
Octisalate Up to 5 UVB
Oxybenzone Up to 6 UVB, UVAII
Padimate O Up to 8 UVB
Sulisobenzone Up to 10 UVB, UVAII
Titanium dioxide 2 to 25 Physical
Trolamine salicylate Up to 12 UVB
Zinc oxide 2 to 20 Physical
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Physical blockers or “chemical-free” sunscreens contain small particles that scatter, reflect, or absorb in the UV and visible range. Because some of the energy is absorbed, secondary oxygen radicals can be formed. Coating the particles with silicone absorbs these free radicals and is the basis of a product called Z-cote. The physical blockers include the following:
  • Zinc oxide
  • Titanium dioxide
  • Iron oxide
  • Kaolin
Sun Protection Factor
The SPF value is defined as the dose of UVR required to produce one MED on protected skin after the application of 2 mg/cm2 of product divided by the UVR required to produce one MED on unprotected skin. The SPF usually ranges from 2 (minimal protection) to 30+ (highest protection). SPF 2 gives 50% protection, SPF 15 produces 93% protection, and SPF 34 gives 97% protection. Some have recommended that SPF be changed to Sunburn Protection Factor, because it is a misconception that application of sunscreen will offer protection against sun-induced skin damage. The use of higher SPF sunscreens appears to increase the duration of recreational sun exposure, giving these individuals a false sense of security.
Although the general public is starting to wear sunscreen on a daily basis, studies have shown that they do not use sunscreen correctly. If a patient uses only half of the recommended amount of sunscreen, the SPF can be reduced by as much as a power of two (therefore, an SPF 15 would become an SPF 4 and an SPF 30 would become an SPF 8). The use of a higher SPF can partially compensate for underapplication. For a sunscreen to be effective, a layer of 0.5 mm should be applied. This is about a quarter of most standard-sized bottles of sunscreen when applied to the entire body. Reapplication every 20 to 90 minutes is necessary to keep most sunscreens effective, depending on the formulation and the activity level of the person (15). The American Academy of Dermatology recommends, regardless of skin type, a broad-spectrum sunscreen with an SPF of at least 15 to be worn year round.
Water-resistant labeling indicates that the SPF is maintained after two 20-minute immersions in water. Very water-resistant labeling can be used if the SPF is maintained after four 20-minute immersions. Therefore, neither of these labels translates into protection that can last for the entire afternoon at the pool with one application.
Ultraviolet Protection Factor
The protection achieved by wearing fabrics is expressed as the “Ultraviolet Protection Factor” (UPF), which was coined in Australia in 1996 (16). Depending on material, stitch, color, moisture content, and chemical additives, clothing can provide a range of protection. Fabrics with tighter weaves, darker colors, synthetic fibers, and loose fit typically provide the greatest protection. Materials that are light in color, loosely woven, natural fibers, or material stretched tightly over the skin provide the least protection. When clothing becomes wet, it usually results in a reduction, but may result in an increase in SPF, depending on the particular fabric (17). For these reasons, clothing is usually overestimated in its protectiveness, and in one study it was estimated that 33% of summer clothing had a UPF <15, compared with the recommended UPF of >30 (18).
Method of Use
The term substantivity refers to a product’s ability to remain effective under the stress of prolonged exercise, sweating, and swimming. Para-aminobenzoic acid (PABA) esters may be more effective than PABA in ethanol, and cream-based vehicles may, in some cases, be more resistant to removal than those in alcohol bases. Whatever product is used, it should be applied 15 to 30 minutes before exposure and reapplied generously several times during exposure, particularly after swimming or sweating. Application of sunscreen is variable,
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with one study showing that 60% of people missed an application to the posterior neck, 35% skipped the anterior neck, and 32% did not cover the ears. The average person applies only one-half or less of the recommended amount of sunscreen.
Vehicle
  • Lotions have low viscosity, spread easily, and are nongreasy. Lotions usually contain an SPF of 15 or less.
  • The products with a higher SPF have more sunscreen oil and have a heavier, greasy consistency. The addition of silicone liquids has decreased the greasiness and increased the water-resistant nature of the high SPF sunscreens.
  • Men, acne-prone patients, and individuals with oily skin prefer oil-free gels. Water-based gels are ideal for individuals who plan on exercising, but can only incorporate water-soluble sunscreens, therefore limiting the SPF. Hydroalcoholic gels can achieve a higher SPF, but none of these products are waterproof. It is sometimes more difficult to obtain uniform application of gel sunscreens compared with lotions.
  • Dry lotions (anhydrous) are for athletes who experience eye stinging.
  • Sticks contain lipid-soluble sunscreens and are effective for protection of limited areas such as the nose, under the eyes, and the ears. These products are the most water resistant and can be helpful in applying sunscreen to critical areas of the face in uncooperative children. They are too occlusive for general application.
  • Aerosols and sprays are a new delivery system, but problems with skip areas and uneven distribution of product decrease their level of protection.
  • Nonchemical or physical blockers and sun-protective clothing are suitable for patients with sensitive skin, individuals who are intolerant to sunscreens, and babies <6 months old.
Adverse Effects
PABA may stain clothing yellow, especially after exposure to the sun. Contact dermatitis develops occasionally from the use of PABA, PABA esters, benzophenones, and cinnamates; glyceryl PABA is the most common cause. Although rarely reported, allergy to a component of the sunscreen vehicle may certainly occur. Patients allergic to benzocaine, procaine, paraphenylenediamine, and sulfonamides may have allergic reactions to PABA.
General Guidelines for Sunscreen Use
  • Select a sunscreen with SPF 15 to 30 that has both UVA and UVB protection.
  • Apply sunscreen 15 to 30 minutes before exposure and allow to dry; reapply every 1 to 2 hours during outdoor activities.
  • Select a water-resistant sunscreen for beach or outdoor activities associated with perspiring.
  • Reapply sunscreen after swimming or exercising.
  • All children should be protected from excessive sun exposure through avoidance of midday sun and use of sun-protective clothing and sunscreens.
  • Children <6 months of age should have sunscreen applied to the exposed areas; titanium dioxide–containing sunscreens are safe and are less likely to irritate the skin. Sun-protective clothing and avoidance are strongly recommended in this age-group.
  • To minimize eye stinging, use a sport gel formula and avoid the benzophenones.
  • For maximum eye protection, pick wrap-around sunglasses that fit close to the forehead and absorb up to 400 nm in the UVA, UVB, and blue light range. Polarizing lenses help cut the glare from reflective surfaces but do not add UV blocking properties. The Skin Cancer Foundation has a Seal of Recommendation for sunglasses that meet its criteria to block 99% of UVA and UVB.
  • Lipstick sunscreens are generally available but often overlooked as part of a sun protection program. Frequent application is also helpful in decreasing the potential for activation of herpes labialis.
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Parents and children should be educated regarding the importance of sun protection. The American Academy of Pediatrics (AAP) has determined that limited sunscreen use in infants is acceptable if no other method of sun protection is available. Adverse effects of sunscreens in infants younger than 6 months of age have not been reported. The AAP still recommends that infants be kept out of direct sunlight and that they be covered with sun-protective clothing.
It has been estimated that use of sunscreen during the first 18 years of life would reduce the incidence of nonmelanoma skin cancers by 78% over one’s lifetime. Chronic use of sunscreen does alter vitamin D synthesis; a normal diet should compensate for this.
Dihydroacetone
Dihydroacetone (DHA), the active ingredient in skin “tanning” or “bronzing” products, produces a brown-orange staining of the stratum corneum; there is no stimulation of melanin pigmentation. There is some photoprotection against long-wave UVA and visible light. Recently, it has been shown that DHA, in addition, offers a modest SPF in humans (19). However, self-tanning creams only offer an SPF of 3 to 4, this protection is only present for several hours after application of the product, and does not last for the duration of the tan (20). Some products now include a sunscreen with SPF 15 or higher. Most products contain a concentration of 3% to 5% DHA; higher concentrations will result in a deeper color that may look unnatural. The color fades with normal epidermal desquamation over 5 to 7 days.
  • Lightly exfoliate the skin before application.
  • Apply every 2 to 3 hours until the desired skin color is achieved.
  • Different application techniques include sprays, wipes, and application by hand.
  • Wash the hands well to prevent staining.
  • Elbows, knees, and ankles take up the chemical unevenly and require less product.
  • Freckles will take up more of the color as will hair and nails.
  • Fabrics may become stained on contact with the product before drying.
  • The lotion must be applied every 3 to 5 days to maintain the color.
Future Directions in Sunscreen Development
  • Experimental studies have shown that it is possible to encapsulate endonucleases into liposomes. These enzymes recognize and repair the structural defects in the DNA induced by UVL. Topical treatment with these liposomes containing T4 endonuclease V has been found to protect human skin in vivo from ultraviolet-induced upregulation of interleukin-10 and tumor necrosis factor-α. Therefore, correcting ultraviolet-induced skin damage with DNA repair enzymes may provide a new avenue for photoprotection.
  • 2-Furildioxime, an iron binder chelator, is capable of decreasing the free radicals formed by UVL exposure and appears to offer some degree of photoprotection.
  • The topical application of antioxidants such as vitamin C (L-ascorbic acid) and E (α-tocopherol), caffeine, isoflavones, green tea (polyphenols), ferulic acid, caffeic acid, cadmium, and cistus has been advocated, but more studies regarding efficacy and penetration of the skin are needed (21). The two most studied of these are vitamin C and vitamin E. Studies have shown that use of these agents, both orally and topically, has significantly decreased the MED from sun exposure.
  • White particulate pigments (Ciba Specialty Products), somewhat like the physical blockers, are being adapted from the clothing industry and appear to offer a broad range of photoprotection.
References
1. Nghiem DX, Kazimi N, Clydesdale G, et al. Ultraviolet a radiation suppresses an established immune response: implications for sunscreen design. J Invest Dermatol 2001;117(5):1193–1199.
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2. Johnson JA, Fusaro RM. Broad-spectrum photoprotection: the roles of tinted auto windows, sunscreens and browning agents in the diagnosis and treatment of photosensitivity. Dermatology 1992;185(4):237–241.
3. Hampton PJ, Farr PM, Diffey BL, et al. Implication for photosensitive patients of ultraviolet A exposure in vehicles. Br J Dermatol 2004;151(4):873–876.
4. Rigel DS, Rigel EG, Rigel AC. Effects of altitude and latitude on ambient UVB radiation. J Am Acad Dermatol 1999;40(1):114–116.
5. Winkler P, Trepte S. Ozone decline and UV increase. Gesundheitswesen 2004;66(suppl 1):S31–S36.
6. Autier P. Skin cancers and environmental factors. Rev Med Brux 1998;19(4):A346–A350.
7. de Gruijl FR, Longstreth J, Norval M, et al. Health effects from stratospheric ozone depletion and interactions with climate change. Photochem Photobiol Sci 2003;2(1):16–28.
8. Kripke ML. Impact of ozone depletion on skin cancers. J Dermatol Surg Oncol 1988;14(8):853–857.
9. Fotiades J, Soter NA, Lim HW. Results of evaluation of 203 patients for photosensitivity in a 7.3-year period. J Am Acad Dermatol 1995;33(4):597–602.
10. Gallagher RP, Spinelli JJ, Lee TK. Tanning beds, sunlamps, and risk of cutaneous malignant melanoma. Cancer Epidemiol Biomarkers Prev 2005;14(3):562–566.
11. Karagas MR, Stannard VA, Mott LA, et al. Use of tanning devices and risk of basal cell and squamous cell skin cancers. J Natl Cancer Inst 2002;94(3):224–226.
12. Spencer JM, Amonette RA. Indoor tanning: risks, benefits, and future trends. J Am Acad Dermatol 1995;33(2 Pt 1):288–298.
13. Pustisek N, Lipozencic J, Ljubojevic S. A review of sunscreens and their adverse reactions. Acta Dermatovenerol Croat 2005;13(1):28–35.
14. Sunscreen drug products for over-the-counter human use; final monograph. Food and Drug Administration, HHS. Final rule. Fed Regist 1999;64(98):27666–27693.
15. Diffey BL. When should sunscreen be reapplied? J Am Acad Dermatol 2001;45(6):882–885.
16. Georgouras KE, Stanford DG, Pailthorpe MT. Sun protective clothing in Australia and the Australian/New Zealand standard: an overview. Australas J Dermatol 1997;38(suppl 1):S79–S82.
17. Gambichler T, Hatch KL, Avermaete A, et al. Influence of wetness on the ultraviolet protection factor (UPF) of textiles: in vitro and in vivo measurements. Photodermatol Photoimmunol Photomed 2002;18(1):29–35.
18. Gambichler T, Rotterdam S, Altmeyer P, et al. Protection against ultraviolet radiation by commercial summer clothing: need for standardised testing and labelling. BMC Dermatol 2001;1(1):6.
19. Faurschou A, Wulf HC. Durability of the sun protection factor provided by dihydroxyacetone. Photodermatol Photoimmunol Photomed 2004;20(5):239–242.
20. Draelos ZD. Self-tanning lotions: are they a healthy way to achieve a tan? Am J Clin Dermatol 2002;3(5):317–318.
21. Dreher F, Maibach H. Protective effects of topical antioxidants in humans. Curr Probl Dermatol 2001;29:157–164.
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