Ultraviolet Exposure

In our environment, it is very important to protect our skin from oxidative stress. No matter how diligent we are with sun cream, you can’t be assured of full protection, so it's important to look at the effects of UV, warning signs and how we can maintain a healthy skin.

Ask us a question
  • This field is for validation purposes and should be left unchanged.

UVR14Australasia has one of the highest rates of skin cancer in the world attributable of several factors: altitude, proximity to the equator, and the fact that its population loves to be outdoors. In a study carried out by the Australian Institute of Health and Welfare, during the past ten years, skin cancer occurred in about 4.3 percent in men and about 1.8 per cent in women.1 There are about 400,000 new cases of non-melanoma (NMSC) skin cancer diagnosed in Australia and is considered the most common form. Projections as of 2008 indicated that around 434,000 persons would be diagnosed with skin cancer. Many outdoor workers are highly susceptible to overexposure and pose a higher risk. Skin damage from the sun is normally irreversible and is accumulative with each exposure.1 Great efforts have been made to educate and inform labourers to take extra precaution when working in direct sunlight. The Australian Cancer Council has published numerous guidelines for cancer control and prevention.

Origins and susceptibility for cancer

Through a process of natural selection, the human body has the ability to adapt to varying environmental conditions to ensure survival. This process, however takes thousands of years for the evolutional process to create features and biological responses required for optimal health and survival. Australian Aborigines arrived around 51,000 years ago and gradually acquired the traits necessary that allowed for them to adapt to their surroundings through the skin darkening providing adequate filtering for UVB that is necessary for vitamin D synthesis.

Not all people living in Australasia had the opportunity to adapt to their surroundings. During the 17th and 18th centuries, Great Britain emptied out their overcrowded prisons and sent them to Sydney Cove where the new inhabitants settled in very primitive conditions. Furthermore, there was an influx of displaced Europeans after World War II including countries such as The Netherlands and Italy. Given their European origins, new populations were not prepared for the dry, hot and barely habitable climate of Australia. The fair skin of new emigrants soon became susceptible to over exposure to UV. As a result, the rate of cancer in Australasia is the highest in the world. At least two out of three people will be diagnosed with skin cancer by the age of 70. When fair skin people move to an area in the world such as Australia, they end up with the propensity for sun burning with deep, irreversible damage to cell DNA. Risks for skin cancer accelerates especially when there is red hair and freckles.

Risk of Exposure

  • Sunlight – UV radiation is the most important risk for any type of skin.
  • Severe blistering sunburns: Just one severe blistering sun increases the risk for cancer.
  • Lifetime sun exposure: The total hours of sun exposure over a lifetime.
  • Tanning: While a tan has a slightly lower the risk of sunburn, even people who tan well without sunburning first still have a higher risk due to lifetime exposure.
Fig. 5 Keratoacanthoma
Low-grade subtype of squamous cell carcinoma. Occurs in sun-exposed skin – hands or face
Additionally, there are a few rare types of cancer that affects the skin and include Merkel cell lesions, Kaposi sarcoma, and cutaneous lymphoma.
Pre Cancerous Lesions from overexposure to UV based on lifetime hours
Actinic Keratosis can develop into squamous cell carcinoma (SCC) UVR8 UVR7
Fig. 9 Dysplastic Nevi
30% of population has moles called dysplastic nevi. Family history of melanoma at high risk for developing melanoma at an early age. Congenital nevi in photo are major risk factors for melanoma and appear before age of 10.


Basal and Squamous Cell Skin Cancer

UVR5Risk factors for acquiring skin cancer varies from individual to individual. Each type of cancer also has its own risk factors that are controllable such as smoking, overexposure to UV, and genetics. UV radiation from the sun is a natural phenomenon. Moreover, artificial UV coming from tanning beds and UV lamps pose a high risk. There is a greater risk for skin cancer with longer exposure to UV including the onset of melanoma. The amount of exposure varies depending upon where one lives. Normally the closer to the equator from which a person originates, the darker the skin since it contains more melanin. Additionally, childhood exposure is also a factor for determining the probability of getting skin cancer later in life. There are several risk factors that are associated with basal and squamous cancer:

  • Fair skin – risk higher in whites than dark-skin
  • Older age – risk of basal and squamous cell cancer. Sun exposure has been longer.
  • Men – two times more likely than women to have basal cell cancers and 3 times more likely to have squamous cell cancer
  • Chemicals – exposure to arsenic and heavy metals (insecticides) sometimes found in creeks and water reservoirs. Exposure to industrial pollutants, coal, paraffin, and certain oils may increase risks.
  • History of skin cancer – chance of reoccurrence is higher.
  • Long-term or severe skin problems – scars from burns, and other skin damage
  • Psoriasis treatments – Some people with long-lasting inflammatory skin disease are treated with UV treatments that can increase their risk of getting squamous cell skin cancer.
  • Family genetic traits: Xeroderma pigmentosum: A rare disease that interferes with the skin to repair sun damage. Increases the susceptibility to cancer. Basal cell nevus syndrome: Present at birth and rare. Causes some individuals to have basal cell cancers.
  • Weakened immune system – individuals are prone to develop non-melanoma skin cancer. Transplant patients often take medications that weaken the immune system in order to prevent organ rejections.
  • HPV Infection – human papilloma virus causes warts in the genital and anus areas.
  • Smoking – risk factor in squamous cells but not necessarily a risk for basal cell cancer
  • Genetics – certain individuals who carry what is known as the “red head” gene (MCR1) can be very susceptible to UV damage.

Basal cell carcinoma begins in the basal layer of the skin. Sun exposed skin – the face – is the most prominent place for this cancer.

Squamous cell skin cancer begins in the squamous (epithelial) cells. In people with dark skin, squamous cell skin cancer is the most common type and it’s usually found in places that are not the sun, such as the legs or feet.12 Fair skin individuals can have squamous cell skin cancers on parts of the skin that have been in the sun – head, face, ears, and neck.12


This form of cancer begins in the melanocytes. It may begin as a mole (skin melanoma) and can also begin in pigmented tissues such as the eye or the intestines. Melanoma begins in the melanocytes and can appear on any skin surface. It can be found on the head and neck, or between the shoulders and the hips in men. In women, it can be found on the lower legs or between the shoulders and the hips.

Spreading Cancer Cells – Metastasis

Skin cancer can invade normal tissues nearby and it can also spread throughout the body. Melanoma is most likely the one that will spread. When they do, they break away from the original growth and enter the vascular or lymph system and into the lymph nodes. This allows them to spread to other tissues and begin to form new tumors.

UVR – Ultra Violet Radiation

UVR3Our planet and its inhabitants certainly require the energy from the sun in order to survive. UV radiation is part of the electromagnetic (light) spectrum. Since UVR wavelengths are shorter than visible light, it is invisible to the naked eye. Over exposure to ultra violet radiation and the awareness of the changes occurring in the earth’s atmospheric ozone layers are certainly influential indicators that provide information for potential cancer risk. Residing in high-risk areas can easily lead the way to genetic mutations and irreversible cell damage. Exposure to sunlight automatically activates the melanocytes to begin the process of filtering ultra violet rays in order to protect the underlying skin structures. Overexposure to UVR breaks down chemical bonds in the cells that leads to oxidative stress and destroys nucleic components and cell membranes. It can cause cataracts, suppress the immune system, and produce mutations leading to skin cancers. Overexposure interferes with the DNA and can eventually lead to oxidative stress in the cells and destroy nucleic components and cell membranes. Premature ageing is a result along with the risk for skin cancer.

Wavelengths of UVR comes in three forms: UVA, UVB, and UVC each of which filters through the earth’s atmos¬phere (ozone layer) at varying degrees.

  • UVA (320-400nm) accounts for about 90-95 per¬cent of terrestrial radiation reaching the earth’s surface. It is estimated that 10 to 12 times more UVA than UVB reaches the earth’s surface at sea level. Unlike UVB, UVA can easily penetrate window glass, clouds and retains the same energy level all day long, year round. It triggers a tanning effect. There is a slight risk for erythema; however, the longer rays penetrate into the epidermal and dermis causing DNA damage to both keratinocytes and fibroblasts.16 It is a primary factor in ageing and wrinkling since its accumulative effect leads to the destruction of collagen and elastin networks as well as diminishes/destroys vitamin A.16 UVA also compromises the immune system.16
  • UVA is the predominant ray found in tanning beds. People who use them are 2.5 times more susceptible to developing squamous cell carcinoma and 1.5 more times likely to develop basal cell carcinoma. First exposure for a young person increases the risk for melanoma by 75 percent.16
  • UVR2UVB (280-320nm) is considered to be the most destructive form of UV yet amounts to about 10% of the UV radiation. It penetrates into the epidermis creating an erythemic response (sun burn), plays a contributory role in tanning and photoageing, and increases risk for skin cancer.16 UVB’s intensity is the highest between 10AM and 4PM from spring into summer decreasing into the fall and winter months. UVB induces the formation of melanin and is essential for the formation of vitamin D.
  • UVC (100-200nm) is absorbed completely by the earth’s atmosphere. It is, however, artificially manufactured for germicidal lamps. Accidental contact can cause burns such as on the skin or in the cornea of the eye.

The Vitamin D Factor – Yes we need some exposure

UVR1There are biological requirements for the body to manufacture vitamin D. A controlled amount of UVB must infiltrate the skin in order for the body to catalyze vitamin D. Season, time of day, the length of daylight, atmospheric conditions (clouds, flog, smog) and application of sunscreen can all affect an individual’s actual exposure rate for the correct synthesis of vitamin D. Most individuals will receive adequate levels of sun exposure when they spend time outdoors. A few minutes of exposure during UV peak time periods between 10AM to 3PM on the arms, face, and hands is all that is required to ensure vitamin D synthesis. In winter, the southern regions of Australia are less intense; people may require about two to three hours of sunlight. Individuals who are at higher risk for vitamin D deficiencies include those with very dark skin, the elderly in residential care or people who are housebound, factory workers and others.18

Sun protection is normally required when the UV index is 3 or above. Sun intensity varies regionally throughout Australia since UV radiation is higher in northern states than southern states. We recommend that you refer to the Cancer Council of Australia web site and print their on-line brochure, How much sun is enough? Getting the balance right: Vitamin D and sun protection.

What is vitamin D?

Vitamin D is a group of fat-soluble secosteroids. Approximately 90% of this vitamin is normally synthesized in the basal and spinosum layers of the skin as well as in the kidneys from a cholesterol-like precursor chemical (7-dehydroxholesterol)., the remaining 10% of vita¬min D comes from our nutrition (fatty fish, egg yolks). Vitamin D is converted into two sequential forms. Its benefits are far reaching for our health. The amount of exposure is dependent upon our geographical location and we have to adjust the duration of time spent out in the sun accordingly. Geographical latitude does not consistently predict that a person will receive enough UV duration for vitamin D synthesis.

  • Vitamin D3 (cholecalciferol) is required for the intestines to absorb calcium and phosphorus from food for bone growth and repair. Calcium is required for proper heartbeat, bone growth and repair.
  • Vitamin D is important for our immune system by promoting the production of cathelicidin, an effective defender against fungal, bacterial, and viral infections.
  • Vitamin D affects neuromuscular function, inflammation, and influences the action of many regulating genes for the regeneration, differentiation, and apoptosis of cells.24
  • Women who have had prolonged vitamin D deficiencies during their developing years have a higher risk of pelvic deformities that prevent normal delivery of babies.24
  • Conversely, excessive ultra violet radiation causes the break down of folic acid (or folate, a B vita¬min).23 Deficiencies in folic acid can lead to anemia and creates risk for miscarriage in pregnant women. Folic acid is required for DNA replication during cell mitosis. It is theorized that our ability to produce melanin was selected in our early ancestors to help preserve the body’s folic acid supply and deter the risk for cancer.

Inhabitants of northern latitudes with lighter skin tones have less skin shielding pigmentation in order for the skin to receive adequate UVB radiation for the production of vitamin D. A darker skin type moving into a northern region may not be able to receive enough UVB. They can have a potential issue with developing rickets in children and osteoporosis in adults. In contrast, the lighter skin types moving to regions closer to the equator are highly susceptible to developing cell damage and skin cancer.

There is an exception to finding darker skin types in colder regions, in particular the Polar Regions. Inuit people (Eskimos) actually have moderate to heavy skin pigmentation that deters vitamin D production. However, their diet of fish and sea mammal blubber adequately supplements their body with vitamin D.24

Skin colour provides a protective regulating factor that is closely tied to human health, light absorption, and the ability to synthesize vitamin D as well as other biochemical responses. During recent years, vitamin D deficiency has become a growing health concern. People spend less time outdoors and many have replaced quality nutrition with fast foods, sugar, artificial sweeteners, soda pop, and other refined products.

dermaviduals® and sun protection – Choosing efficient filters

There are international standards for UVB and UVA protection. Sunscreen products are supposed to cover both the relevant wavelength ranges of UVA and UVB, however, there is no 100% protection. Awareness of their effect is important in understanding how they work. There are two different types of filters: physical and chemical. The duration time for protection will vary dependent upon several factors including one’s ability to burn or tan, the type of sun filter, geographical location, and more.

Mineral (titanium dioxide, zinc oxide)

These filters stay on the surface of the skin and they are gentle for children and diseased skin. They do not penetrate the skin but rather scatter and reflect the light.


UVR4Chemical filters work by absorbing UVR. Depending upon their chemical structure, penetration rates will vary. When a filter molecule absorbs photon energy (UV) it moves them into what is called an “excited state”. This excited state should only be temporary, since it begins to create thermal energy (heating). When this occurs there is a tendency for the formation of oxidative stress (free radicals). Examples of chemical filters include octylcrylene, avobenzone, octinoxate, oxybenzone, octyl methoxycinnamate, etc. Some of these can cause photosensitivity, irritations, and be allergenic. Moreover, chemical stability is a significant issue. When chemical filter ingredients are combined with additives such as emulsifiers, preservatives and perfume, these substances may cause instabilities and undesirable side effects.26 Photo stability of the filters is a significant issue, which means that it will not break down when exposed to light. Avobenzone, for example is highly unstable.

SPF/PPD – Sun Protection Factors

When assessing a sunscreen, it should protect against both UVA and UVB. Instead of looking primarily at the SPF number, it is more accurate to know the SPF and PPD. SPF is the sun protection factor and measures how well it protects against UVB. PPD (persistent pigment darkening) measures how well a sunscreen protects against UVA. SPF protects against sunburns, while PPD guards against photoageing.21 Be aware that regulations may vary from country to country however, each has government web sites regarding sun protection and recommendations to a particular region.

Quite simply, the SPF is the amount of time of sun exposure it takes to create erythema (redness) on the skin. Lighter skin types (Celtic) normally have about 10-15 minutes of exposure time before becoming red. This time will also vary for each person dependent upon his or her genetic traits. Darker skin types have a longer exposure time.

The SPF increases along with the concentration of the UVB filters in the sun cream. For example if erythema occurs in 10 minutes then:

10 minutes x 15 SPF = 150 or 2.5 hours of protection

20 minutes x 15 SPF = 300 minutes or 5 hours of protection

A 30 SPF is calculated the same.

What about higher SPFs?

Sun filters with an SPF of 15 provide 93.3% of protection for the skin. Those with 30 SPF provide 96.7% protection and are considered higher in protection.27 The rate of individual erythemic reaction is also dependent upon the time of year, the altitude, atmospheric conditions (fog, pollution, snow, water), and the proximity to the equator. Don’t be fooled thinking that higher SPFs (50+ for example) are going to provide more protection. In essence, you are just adding on more chemicals and the potential for irritation.

Dosage – How much to apply and how often?

An adult body requires about 6 teaspoons (36 grams) of sunscreen applied on the whole body.27 Keep in mind that clothing and hats add to your sun protection. With the exception of just a few minutes for vitamin D synthesis, avoid being in strong sunlight between the hours of 10AM – 4PM during hot seasons. It is also recommended that you reapply product after water sports, sweating, and during long outdoor exposure. Be mindful that when remaining in strong sunlight for hours, the skin additionally receives a dose of infrared radiation to the body. The skin and body overheats and causes dehydration and thermal reaction in the skin issues, especially in small children. Avoid direct sun exposure for babies and small children.

Applying sunscreens and moisturisers – A layering affect

Many people like the idea of purchasing moisturisers with the SPF combined in the product. We recommend that you purchase a separate moisturiser and sunscreen. Apply your sunscreen on top of the moisturiser. This layering affect offers greater protection. Moisturisers should contain anti-oxidants that boost the effect of the sunscreen. This layering technique provides an ultimate protection from UVA and UVB. It is more effective than an SPF factor contained within.

Sun protection based on corneotherapy

It is essential to begin skin correction as soon as absolutely possible after sun exposure. Not only should a sunscreen contain UV filters, but also other barrier mimicking ingredients that support and/or prevent further damage during exposure. It should be free of preservatives, emulsifiers, colour, and fragrance. Appropriate moisturising ingredients include amino acids that mimic the NMF (natural moisturising factor). Photo damaged skin must be protected in order to avoid accumulative damage. Non-compliance to this results in injured cells both in the epidermis and dermis.

Condition Recommended dermaviduals® – actives

Condition Recommended dermaviduals® – actives
Inflammation Evening Primrose Oil Nanoparticles, Linseed Oil Nanoparticles, Novrithen, Echinacea Extract, Aloe Vera, d-Panthenol, liposomal concentrate of phosphatidylcholine (linoleic acid, choline) and Boswellia.
Tyrosinase inhibitors
Liposomal vitamin C supports the collagen forming enzymes by permeating the vitamin C derivatives into the skin where they are hydrolyzed by enzyme reactions.21 Vitamin C liposomes are also beneficial to hyperpigmentation. Tyrosinase inhibitors that are great preventative agents toward pigmentation include vegetable extracts of mallow, mint, cowslip, lady’s mantle, veronica (used in dermaviduals® Whitening Serum) balm and yarrow. GM Glucan aids cellular protection from both UVA and UVB rays.
Actinic Keratosis Boswellia extract: inhibits the natural enzyme 5-lipoxygenase which plays a major role in the formation of inflammation.Boswellia nanoparticles: help accelerate the apoptosis (cell death) process and have anti-tumour effects; encapsulated in phosphatidylcholine.

In our environment, it is very important to protect our skin from oxidative stress. Anti-oxidant vitamins such as vitamin A, C and E play a pivotal role in skin defence. CM Glucan, Grape Seed Extract and Green Tea Extract also provide important protective and anti-oxidant capabilities. The polyphenols in Caffeine Extract are protectors that also need to be considered when choosing active ingredients to arm our skin with the actives essential for adequate protection, as SPF alone is not considered as total protection. Rather, SPF used as a separate layer to anti-oxidant vitamins, provides the most appropriate armoury to protect our skin against ultra violet radiation.


  1. Templeton, S. Skin Cancer… Australia’s Curse. Retrieved from http://www.webwombat.com.au/lifestyle/health/skinc1.htm
  2. Non-melanoma skin cancer: general practice consultations, hospitalization and mortality. News release, AIHW. 15 October 2008. Retrieved from http://www.aihw.gov.au/publication-detail/?id=6442468158
  3. O’Neil, D. (2011) Human Biological Adaptability: An introduction to Human Responses to Common Environmental Stresses. Behavioral Sciences Dept. Palomar College, San Marcos, California. Retrieved from http://anthro.palomar.edu/adapt/adapt_4.htm
  4. Jablonski, N. (2006). Skin: A Natural History. University of California Press, Berkley.
  5. Immigration to Australia. Wikipedia Retrieved from http://en.wikipedia.org/wiki/Immigration_to_Australia
  6. Sun Smart. Skin Cancer. Retrieved from http://www.sunsmart.com.au/skin_cancer
  7. National Cancer Institute (NIH) Melanoma and Other Skin Cancers: Risk Factors. Booklet NIH Publication No. 10-7625. Retrieved from http://www.cancer.gov/cancertopics/wyntk/skin
  8. General practice consultations, hospitalisation and mortality. Australian Institute of Health and Welfare and Cancer Australia. September 2008. Catalogue No. CAN 39. Retrieved from http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=6442454591
  9. DiChiara, T. (March 2009) Pictures, Part IV: Non-Cancerous and Pre-Cancerous Skin Lesions http://skincancer.about.com/od/symptoms/ss/noncancerous_8.htm
  10. Risk Factors for Skin Cancer: What Causes Basal and Squamous Cell Skin Cancer. Retrieved from http://www.cancer.org.au/Search.htm?search=sun%20statistics
  11. American Cancer Society. (2010) Overview: Skin Cancer – Basal and Squamous Cell. Retrieved from http://www.cancer.org/Cancer/SkinCancer-BasalandSquamousCell/index
  12. National Cancer Institute (NIH) Types of Skin Cancers. Booklet NIH Publication No. 10-7625. Public domain. Retrieved from http://www.cancer.gov/cancertopics/wyntk/skin
  13. National Cancer Institute (NIH) Melanoma and Other Skin Cancers. Booklet NIH Publication No. 10-7625. Retrieved from http://www.cancer.gov/cancertopics/wyntk/skin
  14. Understanding UVA and UVB. http://www.skincancer.org/prevention/uva-and-uvb/understanding-uva-and-uvb
  15. Lautenschläger, H. (2010) Sun Protection: on the efficiency of UV filters. Kosmetische Praxis (2), 10-13.
  16. Understanding UVA and UVB. http://www.skincancer.org/prevention/uva-and-uvb/understanding-uva-and-uvb
  17. Dietary Supplement Fact Sheet: Vitamin D. National Institutes of Health, Office of Dietary Supplements. Retrieved from http://ods.od.nih.gov/factsheets/vitamind-HealthProfessional/
  18. Vitamin D. Cancer Council Australia. http://www.cancer.org.au//cancersmartlifestyle/SunSmart/VitaminD.htm
  19. Vitamin D. http://www.cancer.org.au/cancersmartlifestyle/SunSmart/VitaminD.htm
  20. Cancer Council of Australia. http://www.cancer.org.au/File/Cancersmartlifestyle/How_much_sun_is_enough_FINAL2012.pdf
  21. O’Neil, D. (2011) Human Biological Adaptability: An introduction to Human Responses to Common Environmental Stresses. Behavioral Sciences Dept. Palomar College, San Marcos, California. Retrieved from http://anthro.palomar.edu/adapt/adapt_4.htm
  22. Holick, M.F. (1995) “Environmental factors that influence the cutaneous production of vitamin D 1-3”. Am J Clin Nutr 1995:61 (supple):638S
  23. Black History: Modern scientific explanation of human biological variation – Race. Retrieved from http://www.britannica.com/blackhistory/article-234690
  24. Black History: Modern scientific explanation of human biological variation – Skin Color Adaptation Retrieved fromhttp://www.britannica.com/blackhistory/article-234690
  25. Holick, M.F. (1995) “Environmental factors that influence the cutaneous production of vitamin D 1-3”. Am J Clin Nutr 1995:61 (supple):638S
  26. Lautenschläger, H. (2010) Sun protection: on the efficiency of UV filters.
  27. How to Choose the Right Sunscreen. Retrieved from http://www.skinacea.com/sunscreen/choose-right-sunscreen.html


  1. Figure 1: Sunburn from a 5-hour exposure – Wikipedia (public)
  2. Figure 2: Squamous cell SCC – National Cancer Institute Visuals Online – Public Domain, http://visualsonline.cancer.gov/searchaction.cfm?q=basal+cell+carcinoma&from=&to=&sort=datecreated
  3. Figure 3: Basal Cell Carcinoma – National Cancer Institute (NCI) Visuals Online – Public Domain
  4. Figure 4: Melanoma – NCI Visuals Online – Public Domain
  5. Figure 5: Keratoacanthoma – Wikipedia (public)
  6. Figure 6: Melanoma – Foot – NCI Public Domain (Photographer – Kelly Nelson)
  7. Figure 7: Actinic Keratosis – Ask Skin Cancer Guide.com http://www.skincancerguide.com/images/content/ak04_lg.jpg
  8. Figure 8: Actinic Keratosis –
  9. Figure 9: Dysplastic nevi sourced from National Cancer Institute at NIH. http://www.cancer.gov/cancertopics/factsheet/Risk/moles
  10. Figure 10: Normal and cancer skin cells sourced from
  11. Figure 11: UV Spectrum (public)
  12. Figure 12: UV Skin Penetration (public)
  13. Figure 13: UV Alert Chart – Cancer Council of Australia
  14. Figure 14: Sun Screen Application


This dossier has been prepared on behalf of dermaviduals Australia and New Zealand as a reference that relates to various skin conditions. In no way does it replace the advice of your medical practitioner or a dermatologist. All views represent the research and findings of the writer in conjunction with derma aesthetics.

Ask us a question

  • This field is for validation purposes and should be left unchanged.