Tuesday, 16 June 2009 15:10

Rays of Hope

Written by   Diana L. Howard Ph.D.

Solar Risks
Our love affair with the sun may finally be coming to an end. After years of romancing the sun, we are now more than ever dealing with the long term effects of our affair: wrinkles, hyperpigmentation, premature aging – not to mention a repressed immune system and the potential for skin cancer are all consequences of sunlight exposure. According to the Skin Cancer Foundation, skin cancer is the most common form of cancer in the U.S. with one million new cases diagnosed every year. One in five Americans will develop skin cancer; 90 percent of these cancers will be the result of exposure to ultraviolet (UV) radiation from the sun.

The risk of exposure is so alarming the National Institutes of Health (NIH) added UV radiation to its list of “human carcinogens” in 2002. With the threat of premature aging and the ultimate insult, skin cancer, it is apparent that the best defense is to limit one's exposure to the sun and protect the skin with sunscreen at all times.

What is Sunlight?
Very simply, it is electromagnetic radiation composed of varying wavelengths of energy. From the short cosmic rays to the very long radio waves, the range is often called the electromagnetic spectrum. Sandwiched in between X-radiation and visible light is UV radiation. While visible light constitutes about 35 percent of the spectrum, ultraviolet (UV) rays comprise only five percent; the latter spans the spectrum from 200 to 400nm in length. (Note: nm is the abbreviation for nanometers, the unit of measure used to denote the energy level of the radiation.) Within the UV range, there are the longer UVA rays constituting 320 to 400nm wavelengths, the shorter UVB rays at 290 to 320nm, and the very short UVC rays from 200 to 290nm. As skin care professionals, we must concern ourselves primarily with the UVA and UVB range of radiation. Fortunately, the ozone layer in our stratosphere filters out the UVC radiation, making it less problematic. Unless of course, we destroy the ozone layer, which appears to be what is occurring over Australia; this may account for the higher incidence of skin cancer in that region.

Electromagnetic Spectrum:
High Energy/short waves    
Low Energy/long waves

UVC
200 to 290nm 

UVB
290 to 320nm

UVA
320 to 400nm

Visible
400 to 700nm

According to the World Health Organization, UV radiation levels rise by about 10 to 21 percent for every 1,000 feet of altitude, and reflection from water, snow, sand, or concrete can magnify the effect by up to 80 percent. Unbeknownst to most people, UVA rays penetrate glass and are present even on cloudy, foggy days. UVA rays are 1,000 times more prevalent than UVB rays, which are 1,000 times stronger than UVA rays.
When we are exposed to sunlight, a portion of the radiation is reflected off the skin and some is absorbed. Wavelengths of less than 320nm (UVB and UVC) are mostly reflected or absorbed by the layers of the epidermis while the longer rays, 320nm or more (UVA), are more inclined to enter into the dermis. The UVB rays, with their higher energy level, tend to cause burning and damage to DNA, while the lower energy UVA rays generate excess free radicals, damage cell membranes, suppress the immune system, and cause photoaging of skin. All forms of UV radiation can induce skin cancer.
The amount of radiation reflected off the skin is influenced by the amount of melanin in the skin. If the skin is light, more radiation (60 percent) is reflected; for darker skin, less (25 percent) is reflected, allowing more UV rays to penetrate the tissue. However, once the rays penetrate into the epidermis where there is more melanin present, the energy of the rays is absorbed and given off as heat. For this reason, darker skin is afforded more protection and only allows about five percent of the UVA radiation to penetrate down into the dermis. In lighter skin, with less protective melanin to absorb the ray’s energy, more radiation (about 15 percent) penetrates down into the dermis. Once these rays reach the dermis serious damage may occur.

How UV Rays Impact the Skin
When UV rays penetrate the skin, they generate ROS (Reactive Oxygen Species) or free radicals that wreak havoc on cellular material. ROS not only alter DNA but they may damage the membranes surrounding the cells, destroy enzymes and proteins required for cellular metabolism, and impact protein building blocks, the amino acids. Any of these reactions can result in the formation of sun-induced skin cancers.
Likewise, exposure to UV radiation also triggers the formation of matrix metalloproteinase (MMPs) enzymes (e.g. collagenase, elastase, etc.) that breakdown structural proteins of the dermis; at the same time when the MMPs are stimulated, collagen synthesis is shut down, cell proliferation and differentiation cease, and biosynthesis of extracellular matrix materials in the dermis stop. We now know that topical application of retinol (vitamin A) has been demonstrated to reverse the effects that UV radiation imparts on these metabolic activities.
As our body attempts to repair the damage triggered by the UV rays, our cells release by-products of this assault and repair process. Initially, the skin's inflammatory response is seen as a sunburn or redness (erythema), which results from dilation of blood vessels in the dermis. Erythema generally appears two to six hours after exposure to sunlight. The degree of redness is an indication of damage to the tissue. For this reason erythema is also used as a measure of the effectiveness of a sunscreen to absorb the burning UVB rays; this is designated as its sun protection factor or SPF.
Exposure to ultraviolet radiation triggers an immediate signal to the melanocyte to make melanin and transfer the melanosomes (packets of melanin) to the adjacent cells. As a result, skin becomes darker or tan. Tanning may be the result of exposure to both UVA and UVB rays, although it appears that UVB rays are more effective in producing this response.
Aside form tanning, exposure to sunlight can cause premature photo aging of skin, non-cancerous disorders, and skin cancer. It is believed that the majority of age-associated symptoms seen on our skin are the result of exposure to sunlight. Whether it is wrinkling of the skin that is attributed to cross-linking of collagen fibers, loss of elasticity, thinning, dilated spider veins (telangiectasia), hyper- or hypopigmentation, all of these manifestations of photoaged skin can be attributed to exposure to UV radiation.
Non-cancerous disorders of the skin resulting from UV exposure include actinic keratosis, solar lentigines (liver spots), and solar elastosis. While not carcinogenic, many of these disorders can be precursors to skin cancer and should be monitored by a dermatologist.
And of course, the ultimate insult to skin is the formation of skin cancer. These are usually the result of years of UV exposure and can result in squamous cell carcinoma, basal cell carcinoma, and melanomas. As skin care professionals, whenever you see any suspicious lesion or skin disorder, you should refer your clients to a medical doctor for immediate attention and diagnosis.

Protect the Skin
While limiting our exposure to the sun’s radiation is the most obvious measure, it isn’t always the most practical. Utilizing sunscreens not only helps prevent premature photodamage and aging of skin, it is essential to ensure the health and integrity of the body's largest organ. The physical sunscreens, often called inorganic sunscreens, include zinc oxide and titanium dioxide; they work by reflecting harmful UV rays. Chemical sunscreens, often called organic sunscreens, function by absorbing damaging UV radiation. Physical sunscreens are favored by those with sensitive skin and those who tend to break out from repeated use of chemical sunscreens. Their popularity has also risen as a result of newer technology that has resulted in a smaller particle size, making them more aesthetically pleasing to use; the opaque white creams often associated with lifeguards in the 60s are now replaced with more translucent sunscreens that lack the geisha-girl white appearance when applied to the skin.
In the U.S. sunscreen products offering a SPF of greater than 4 are classified as over-the-counter (OTC) drugs and are governed by the USA FDA Monograph on Sunscreens, which currently limits the number of sunscreen agents that we may use. While criticized by many as being too restrictive and out of date, one could also argue that in view of the high incidence of sensitivity toward sunscreen ingredients, this new drug application process does prevent the marketing of products containing ingredients that may have not been thoroughly evaluated. Nevertheless, the painfully slow pace of this approval process has even prompted some legislators in Washington DC to demand the FDA respond in a more timely fashion.

Ultraviolet Rays and Sunscreen Ingredients
The list of commonly used sunscreens that protect against UVA and UVB rays are noted in Figure 1. Cosmetic formulators use combinations of sunscreens to broaden the range of the spectrum that they protect against, hence the name, broad spectrum sunscreens.

How do SPFs Work?
A product designated with an SPF 2 protects your skin from 50 percent of the UVB rays, so you can stay in the sun twice as long before burning. For example, if you burn in 10 minutes use of an SPF of 2 will extend the time before burning to 20 minutes (SPF 2 times 10 minutes). Other factors like activity (e.g. sweating or swimming), amount of sunscreen applied, and frequency of application must also be factored into determining how long one can stay in the sun before burning.
If the SPF is increased to 8, it blocks 87.5 percent of the rays, leaving 12.5 percent to penetrate and burn your skin. An SPF 8 means you can stay in the sun SPF 8 times 10 or 80 minutes before burning. An SPF 15 blocks 93.33 percent of UVB and some UVA rays and an SPF 30 blocks 96.6 percent of UVB and some UVA rays.
An important point to consider is that in order to achieve the extra sun protection, (e.g. going from a SPF 15 to 30) the concentration of sunscreen ingredient in the product has to be doubled. Considering many individuals are prone to breakouts and irritation with regular use of chemical sunscreens, this can be a problem; therefore, we recommend that these individuals use the physical sunscreens to avoid any issues or opt for the lower SPF (e.g. SPF 15) and apply more frequently.
One of the biggest problems is that individuals do not apply an adequate amount of sunscreen to provide the expected SPF protection. For your face you must use a teaspoon and for the body use one ounce (two tablespoons)! Any less and you are not providing the designated SPF for UVB protection. Remember, SPF is only a measure of UVB protection. As of now there is no accepted means of measuring UVA protection. Hopefully when the new Sunscreen Monograph is accepted and implemented, it will include a protocol and means of measuring UVA protection as well. At that time, labeling requirements for sunscreens will also change.
For the best protection, one should apply sunscreen 30 minutes before exposure and again 30 minutes after exposure. After that, repeat application every two hours. If you are very active and sweating, reapply more frequently. Even water resistant sunscreens should be reapplied after swimming. The Skin Cancer Foundation considers SPFs of 15 or higher acceptable UVB protection.
One of the biggest concerns in the U.S. is the limitation of sunscreens that provided UVA protection. In 1996 avobenzone, one of the newest UVA filters, was finally approved for use. More recently, scientists have been concerned about stability issues regarding avobenzone. After one hour of UV exposure, avobenzone tends to break down. While one could argue that in sun exposure you should be reapplying every hour anyway, this has led research scientist to develop complexes that stabilize avobenzone. Known as “quenchers,” most are patented and their use highly regulated. Mexoryl, approved for use in the U.S. only recently, is a patented combination of ecamsule, avobenone, and octocrylene designed to stabilize avobenzone.
Another important fact to consider is that sunscreens only protect against 55 percent of the ROS that form as a result of UV exposure. Remember, ROS or free radicals lead to inflammation and premature aging of skin. Studies at the University of Illinois Fluorescence Dynamics Lab conducted by Dr. Kerry Hanson demonstrated that when sunscreens are combined with antioxidant vitamins E and C, they quench the ROS and provide enhanced photoprotection of the skin. More specifically, using both antioxidants with a sunscreen SPF 8 increased the ability of the product to reduce ROS from 84.7 percent to 91.7 percent. To ensure adequate protection against UV-induced ROS, look for sunscreens that incorporate antioxidants or new UV smart booster technology to provide enhanced photoprotection.
I am often asked if there is any evidence to warrant the use of sunscreens. In fact, there is strong evidence that sunscreens do protect against the development of precancerous actinic keratosis (AK) and squamous cell carcinomas (SCC). Studies in the U.S. and Australia demonstrated that regular sunscreen use resulted in fewer AK and SCC. As for proof that sunscreens reduce premature photo aging, just look at identical twins where one was raised in a sunny location like southern California, while the twin was raised in Minnesota. The proof is staring you in the face.
In many respects the state of sunscreens in the U.S. is in its infancy. Even if raw material suppliers hasten their research and development schedules to produce new and better sunscreens the bottleneck will ultimately be the FDA and its snail pace approval process. Until someone can streamline the process, at least there is a ray of hope that the current sunscreens available will provide some protection and that we as professional skin therapists can continue our effort to educate consumers as to the importance of using sunscreens year round.

References:
www.skincancer.org/skin-cancer-facts
Voorhees, J. et al Archiv Derm. 2007 143:606-612
Haywood et al (2003) J. Investigative Dermatology 121:862-868
www.skincancer.org

As Vice President of Technical Development for The International Dermal Institute and Dermalogica, Dr. Diana Howard travels the world as a researcher and speaker, sharing her knowledge of ingredient technology, with a special emphasis on how ingredients impact the structure and function of skin. Dr. Howard earned her doctorate degree from The University of California Los Angeles where she specialized in plant biochemistry. For more than 29 years, Dr. Howard’s interest in research on skin and the development of novel ingredient complexes has made her an invaluable asset to many of the major cosmetic companies. www.dermalinstitute.com, This email address is being protected from spambots. You need JavaScript enabled to view it.

 

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