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Surgery and Cosmetics

Ellen Marmur, MD

New Developments in Sun Protection

Ellen Marmur

Tuesday, June 06, 2006

Skin cancer is increasing in incidence in all ages and skin types. Despite the warnings, the popularity of sunbathing and tanning salons is rising, and skin cancer is a major public health concern. In the past, carcinogenesis of the skin was mainly attributed to ultraviolet B (UVB) radiation and most sun-protection measures were geared toward blocking UVB rays. Skin cancer research has recently revealed the importance of UVA exposure in skin cancer and premature photoaging. Now that we know UVA is just as dangerous as UVB, new developments are focused on UVA protection, immune protection, and public awareness.

Ultraviolet Radiation

Less than 5% of the sunlight that reaches the earth's surface is UV radiation (UVR). The other components of sunlight are visible light and infrared radiation, which are not considered harmful to humans. Ultraviolet radiation is composed of UVA, UVB, and UVC wavelengths. UVC rays are high-energy, short wavelengths that can burn and tan the skin at extremely high elevations but are almost completely absorbed by the stratospheric ozone layer. UVB rays are longer, lower-energy wavelengths comprising about 2% of the UV radiation on the earth's surface. These UVB rays vary with time and season and are the major cause of sunburns. Sunburned skin is a leading risk factor for melanoma and non-melanoma skin cancers. UVA rays are the longest, lowest-energy wavelengths and comprise nearly 98% of the UV radiation on the earth. On a cloudy day or behind glass windows, UVB is significantly reduced but UVA is not.

U.S. Food and Drug Administration (FDA) testing for sun protection factor (SPF) specifies an application dose of 2 mg/cm² to the entire body surface area (except for the skin area covered by a bathing suit), or around 1 fluid ounce to cover an average adult. The application cream is rubbed in until no visible residue remains. Then the test area is exposed to UVR from 290 nm to 400 nm (covering both UVA and UVB wavelengths). However, the SPF is a measure of the MED (minimal erythemal dose), or sunburn, which is largely due to UVB. Therefore, sunscreens today reflect the protection from UVB but not UVA. A universal classification and standard method to measure UVA protection has been recommended to the FDA.

Regulations and Marketing

Strict safety regulations apply to UV filters, the chemicals in sunscreens and sunblocks. They must be found to be nontoxic, non-allergenic, photostable, and effective. Before a new filter can be marketed in the United States as an over-the-counter drug, it must undergo considerable testing in clinical trials, costing millions of dollars. European UV filters are listed as cosmetics and often are available first while costly safety and allergy testing is undertaken in the United States. Chemicals listed as cosmetics are not required to undergo the same level of testing and enter the market more rapidly.

The current trend in marketing sunscreen is to advertise a higher and higher number SPF. It is true that increasing from SPF 15 to SPF 30 provides better sun protection, from approximately 90% to 95% coverage respectively. But whether increasing from SPF 30 to SPF 40 or 50 provides more clinically relevant protection is unknown. Using a sunscreen with a very high number may lead to a false hope of complete protection and subsequent overexposure to harmful photodamage. For this reason, Australia set an official upper limit of SPF 30 to sunscreens.

The Ideal Sunscreen

The ideal sunscreen will block both UVA and UVB for long periods of time. It will be waterproof, sweat proof, and cosmetically elegant. Sunscreens contain organic compounds that absorb UVR, converting it into heat (infrared) or fluorescence (visible light). Sunblocks contain organic or inorganic compounds (such as titanium dioxide or zinc oxide) that scatter or reflect UVR. These mechanisms help protect the epidermal and dermal cells from photocarcinogenic DNA damage. Many excellent sun protection products contain a mixture of sunscreen and sunblock.

Table 1


Types of UVR Wavelengths
(nm)
 
UVC 200-290 Absorbed by the ozone layer of the stratosphere
UVB 290-320 High energy
- causes sunburn
- intensity changes with seasons, time, cloud cover
- can cause delayed skin pigmentation
UVA 320-400 Low energy
- always present independent of cloud cover or glass
- photobiological effects are cumulative
- long-term effects include pigmentation, DNA damage
- can penetrate deep into dermis and beyond
Visible light 400-700 Not harmful to human skin
Infrared 700-3000 Intense heat damages human skin

 

Limitations of Sunscreens

Sunscreens today are limited by several factors. Each chemical in sunscreen covers only a portion of the spectrum of UVR. Most sunscreens today absorb UV rays in the region of 300 nm (UVB). The most commonly used organic UVB filters are cinnamic acid esters, methylbenzylidene camphor, and a water-soluble benzimidazole. In contrast to UVB sunscreens, there are very few UVA sunscreens. Avobenzone (Parsol 1789) effectively blocks UVA and UVB but is photo-unstable, making its efficacy diminish quickly in sunlight. By virtue of the mechanism of absorbing UVR and converting it into heat or light, ingredients in sunscreens are eventually consumed, requiring frequent reapplication to the skin.

Sunblocks are mainly limited by poor cosmesis. UV filters such as titanium dioxide or zinc oxide are microfine physical blockers of UVR but leave an inelegant, chalky residue on the skin. Other UV filters wash off the skin too easily, making them impractical for recreational sun exposure.

New Products

Like avobenzone (Parsol 1789), three new products claim to have broad-spectrum UVB/UVA protection but with better photostability. Terephthalylidene dicamphor sulfonic acid (TDSA, Mexoryl®SX, Chimex SA, Le Thillay, France), is a broad-spectrum UVB/UVA filter. It has a maximum absorption at 345 nm. A second Mexoryl chemical, drometrizole trisiloxane (DT, Mexoryl®XL), is a broad-spectrum UVB/UVA filter with 2 peaks of absorption: at 303 nm and 344 nm. It is widely marketed in Europe and Canada but not yet approved in the United States. It prevents immediate and persistent pigmentation (tanning from UVA) plus erythema (sunburn from UVB). Unlike Parsol 1789, there are no reports in the literature indicating that Mexoryl causes photocontact dermatitis. Tinosorb M is a similar product developed by the Swiss. Finally, there is now a U.S. product called Helioplex. Helioplex complies with FDA regulations and protects the skin from UV while remaining photo-stable. It is available in Neutrogena Ultra Sheer products.

Genistein is an interesting compound that is not yet available on the market as a broad-spectrum sunscreen. It is a soybean isoflavone with a wide range of anticarcinogenic properties. Genistein has been taken orally to prevent many types of cancers. It is a potent antioxidant and phytoestrogen found naturally in fermented soy products like soy sauce. Clinical studies indicate that genistein has antiphotocarcinogenic and antiphotoaging effects for both UVA and UVB. Genistein blocks UVB-induced sunburns in humans as well as psoralen-UVA (PUVA)-induced molecular damage in mice. In addition, when applied after UVB exposure, genistein provides significant comfort and slightly reduces erythema or sunburn.

Lastly, immunity-driven technology is a future direction in skin cancer prevention and treatment. We know that UV exposure causes immunosuppression via multiple mechanisms in the skin including via urocanic acid. Any exposure to the sun disables the immune system's ability to fight skin cancer. Childhood sun damage causes cumulative damage to DNA. The DNA mutations formed during childhood tanning or burning may cause skin cancers in adulthood, especially with more and more sun exposure. Products with immune protection factor (IPF) contain DNA-repair enzymes and antioxidants that may reduce mutations and enable the immune system to combat photodamage. Dimericine® (T4N5 Liposome Lotion, AGI Dermatics) is a drug engineered to deliver the DNA repair enzyme T4 endonuclease V into cells of the skin. In clinical testing in xeroderma pigmentosum (XP), a genetic disease predisposing to skin cancer, Dimericine reduced the incidence of pre-malignant actinic keratosis and basal cell carcinoma. If topical IPFs prove to be safe but only moderately effective, systemic medications targeted at immunomodulation of the skin to fight skin cancer may become the wave of the future.

Promoting Sun Protection in Other Ways

Perhaps as important as the new research on broad-spectrum UVA plus UVB sunscreens is the heightened effort by public health organizations and private companies to promote sun protection:

  • Sun-protective clothing is becoming popular, offering tightly woven, colored, chemically coated, comfortable styles that have an SPF of 30 or more. Children's swimwear is looking more like surf wear, covering more of the body like a wetsuit
  • There are a number of entertaining and educational school-based programs such as SCIPS (Skin Cancer Information and Prevention Service), which is run by a group of medical students who arrange for school-wide assemblies to teach children about sun protection
  • Advertisements for eye protection advise to protect the eyes from sun-induced cataracts and even melanoma
  • At a ski resort in Alta, Utah, the only warning sign off the highest tram at 11,000 feet is not about broken bones but about sunscreen

Future immunomodulators may provide the most potent protection, but at this time mainstream awareness plus new scientific developments in sun protection will hopefully bring the rising incidence of skin cancer to a halt. Meanwhile, complete avoidance of tanning salons, frequent and generous application of SPF 30, and staying out of the midday sun are still the best protection against photodamage.

References

  1. Han J, Colditz GA, Samson LD, et al. Polymorphisms in DNA double-strand break repair genes and skin cancer risk. Cancer Res. 2004 May 1;64(9):3009-13.
  2. Kozmin S, Slezak G, Reynaud-Angelin A, et al. UVA radiation is highly mutagenic in cells that are unable to repair 7,8-dihydro-8-oxoguanine in Saccharomyces cerevisiae. Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13538-43.
  3. http://www.fda.gov/ohrms/dockets/dailys/00/Sep00/090600/c000573_10_Attachment_F.pdf
  4. Schmidt T, Ring J, Abeck D. Photoallergic contact dermatitis due to combined UVB (4-methylbenzylidene camphor/octyl methoxycinnamate) and UVA (benzophenone-3/butyl methoxydibenzoylmethane) absorber sensitization. Dermatology. 1998;196(3):354-7.
  5. Berne B, Ros AM. 7 years experience of photopatch testing with sunscreen allergens in Sweden. Contact Dermatitis. 1998 Feb;38(2):61-4.
  6. Wei H, Saladi R, Lu Y, et al. Isoflavone genistein: photoprotection and clinical implications in dermatology. J Nutr. 2003 Nov;133(11 Suppl 1):3811S-3819S.
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