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3. The physiology and pathology of sunburns and suntans


3a. Sunburns and suntans

The skin is the largest organ in the body covering 20 square feet (1.8 m2) in the average sized adult (AAD, 2006). It varies in thickness from 1 to 3 mm and provides a waterproof protective coating for the internal organs. The skin contains a large blood supply and nerve network (Dorlands, 1981). It offers protection from invasion of bacteria, viruses, and parasites, and it is a living armor, because it is self repairing (heals). The skin through the sweat glands help regulate body temperature with evaporation of sweat for cooling. Blood vessels in the skin contract to shift blood flow to deep areas of the body to conserve heat, or they dilate to allow superficial blood flow to radiate heat from the body.

The skin is composed of three layers – the epidermis, the dermis, and the hypodermis or subcutaneous tissue (fatty tissue) (figure 6). Below the skin are muscles or bone. The top layer of the epidermis consists of dead cells that are constantly being shed. The epidermis has no blood vessels or nerves. One of the specialized cells in the epidermis is the melanocyte which contains melanin a dark pigment. Melanin is a yellow-black pigment derived through a series of oxidation steps from the amino acid tyrosine. The dermis and lower layers of the epidermis are the active portions of the skin with a multitude of cell types and functions. As the epidermis cells age, they are gradually transported to the exterior where they eventually die. There is a rich blood and nerve supply in the dermis (Gardner, 1963).

The skin is subject to three types of burns as illustrated by figure 6. These most commonly result form thermal injury in a fire, but they can also be obtained by chemical and radiation injuries, such as a sunburn. First degree burns represent a reddening or erythema that mainly affects the epidermis. They heal rapidly. Second degree burns are deeper and more painful. They include destruction of a portion of the dermis and often included severe blistering which is a healing protective effect. Second degree burns take longer to heal, and they are subject to infection. They typically do not produce scars. Third degree burns are severe injuries which destroy the entire thickness of a portion of the skin. If they are widespread over the body, they are life-threatening with a high mortality rate. Third degree burns require extensive prolonged treatment and are subject to severe infections and severe scarring. Curiously, third degree burns often initially do not cause much pain as all the nerve fibers have been destroyed by the burn. Most sunburns represent first and second degree burns, but third degree burns are possible, and prolonged sun exposure can even lead to death from a sunburn.



First Burn

Figure 6. The composition of the skin and the three types of burns. From: Medline (2004).


The erythema or skin redness produced by a sunburn occurs as fast as 30 minutes after exposure. Its cause is unknown, but it involves a long sequence of inflammatory5 reactions with microscopic and macroscopic changes in the skin. Less intense exposure to ultraviolet radiation results in an increase in skin pigmentation (suntan). This takes place in two stages. First, there is an immediate pigment darkening in the skin, perhaps from oxidation and redistribution of the skin pigment melanin. Next, there is a delayed response of at least 24 to 72 hours in which there is increased synthesis of melanin in the epidermis. Repeated exposure to UVR results in further skin thickening and melanin production (Foster, 2005). The melanin absorbs the UVR and provides a protective effect. Darker skinned individuals have more melanin in their skin and are thus more resistant to the ill effects of ultraviolet exposure. This is presumably a long term genetic response to exposure of their ancestors to increased sunlight.

The principle cause of sunburn is UVB radiation which accounts for 85% of the effect. However, UVA comprises the majority of the ultraviolet radiation reaching the Earth’s surface at midday. It therefore accounts for a significant amount of the immediate and long term effects of ultraviolet radiation. The minimal single dose of UVR measured as energy per unit area needed to produce redness at an exposed place is known as the minimal erythema dose or MED. Moderate to severe sunburns are produced by 3 to 8 MEDs (Foster, 2005). When compared with white skinned individuals, moderately pigmented races require 3 to 5 time more UVR exposure to cause erythema, while blacks can be up to 30 times mores resistant to the effects of UVR. Tanning increases the resistance to burning by a factor of only 2 to 3. Moist skin allows more penetration of UVR, and the UVR exposure increases 4% for every 300 m increase in altitude (Foster, 2005).


3b. Consequences of chronic Sun exposure – wrinkles, cancer, cataracts

A light skinned individual may not take more than a 15 minute exposure prior to suffering a sunburn (Medline Plus, 2004). The consequence of exceeding a MED is a sunburn. Long term exposure to the Sun at levels not producing a sunburn leads to protective tanning and further darkening of the skin. Tans project an active, healthy appearance. However, long term exposure to the Sun has a variety of unpleasant consequences, including wrinkles, skin aging, skin cancer, and cataracts.

Sunlight can cause premature skin aging. It is estimated exposure to UVA or UVB may account for up to 90% of the symptoms of premature aging, such as easy bruising and excessive wrinkles (Brannon, 2006). This is greatly accelerated by exposure to the Sun in fair skinned individuals.  A tanned youth may turn into a very wrinkled old man or woman.  UVA does leak through the atmosphere and is considered a major cause of skin damage.  UVA apparently penetrates deeper into the skin and is more constant than UVB during the day.  UVA is not filtered by glass (Brannon, 2006). UVC would even be more harmful to the skin, but is not a factor for sunburn, suntan, or the long term effects of the Sun, because it is completely absorbed by the atmosphere and does not cause skin damage.  Both UVA and UVB are responsible for long term damage to the skin and probably for the long term systemic effects of exposure to excessive sunlight (ADD, 2006; Brannon, 2006).

Long term exposure to the Sun with repeated burns increase one's likelihood of getting a skin cancer. In the United States over one-half of all new cancers are skin cancers with more than one million cases diagnosed per year (AAD, 2006). There are three main types of skin cancers: basal cell carcinoma, squamous cell carcinoma, and melanoma.  Basal cell and squamous cell carcinomas account for 79% and 15%, respectively, of these new cases. Basal cell carcinoma and squamous cell carcinoma have better than a 95% cure rate if found early. They are locally aggressive but only rarely metastasize (spread to distant organs) late in the course of the disease. The risk factors for these cancers are fair skin, advancing age, and male sex (Ferrini, 1998). Five or more sunburns doubles one’s risk of a developing a skin cancer (ADD, 2006).

Five per cent of new skin cancers are melanomas, and 1% are miscellaneous rare malignancies. Melanoma is an aggressive malignancy with 7770 deaths in the US attributed to it in 2005 (ADD, 2006). Older white males have the highest mortality rate from melanoma. The highest incidence of melanoma is found in Australia, and the second highest incidence is in the U.S. in Arizona, where there are large numbers of fair skinned individuals receiving too much exposure to the Sun. The American Academy of Dermatology (AAD) considers tanning salon exposure as harmful as outdoor Sun exposure (ADD, 2006). Some dermatologists would go so far as to say there is no such thing as a safe tan, because a tan is the skin’s response to an injury, and every time you tan, you accumulate more damage to the skin.

It is well known that intense ultraviolet light can produce temporary damage to the retina of the eyes from the unprotected viewing of welding or from prolonged exposure to sunlight reflecting off snow. Acute exposure to excessive ultraviolet light can also produce photokeratitis, an inflammation of the cornea and iris, and photoconjunctivitis, an inflammation of the membranes that line the eyelids and the white surfaces of the eye (WHO, 2006).

Cataracts represent the clouding of the lens with crystalline formation and impairment of vision. They are caused by many factors, including trauma, “aging”, and congenital diseases. There is an association between long term UVB exposure and cataract formation (AgingEye, 2006). The World Health Organization (WHO) estimates as many as 20% of cataracts may be due to UV radiation (WHO, 2006). The most effective protection of the eyes from UVB radiation is to limit one’s exposure to the midday Sun and to use sunglasses with UV radiation protection. Lens color or tint is not indicative of the UV blocking ability of a pair of sunglasses (AgingEye, 2006). Fortunately, most modern spectacles made of plastics or polycarbonate absorb much of the UVA radiation and almost all of the UVB radiation. Skiers should be especially cautious in selecting their sunglasses due to the highly reflective nature of snow and ice. Also, skiers should use fully wraparound sunglasses to prevent UVR from entering the eye at oblique angles.

The immune system may be harmed through prolonged exposure to UVR by changing the activity and distribution of the cells participating in the immune response (WHO, 2006). This has not been proven in humans, but experimental studies in rodents show UVR can suppress immune responses and make rodents more susceptible to infections. Further research needs to be done in this regard.

The mechanisms for the damaging effects of UVR are unknown. It is known UVA is not energetic enough to modify the cellular DNA bases, but it may play an important role in the formation of cellular carcinogenic oxygen radicals. However, wavelengths in the mid UVB region can directly attack cellular DNA. The UVR is absorbed by the double bond in pyrimidine bases in DNA opening up the bond and allowing it to react with other molecules. Such reactions are common, and each cell in the skin might experience 50-100 such reactions during a second of sunlight exposure (Goodsell, 2001). Most of these are corrected within seconds after they happen using a cellular process known as “nucleotide excision repair.” Interestingly, rodents show a weakened nucleotide excision repair mechanism (Goodsell, 2001). This might be a factor in their seeming sensitivity to immune deficiency after exposure to UVR.

Children are particularly sensitive to the acute effects of ultraviolet exposure. Most of the non-melanoma skin cancers are in fair skinned individuals who tend to burn. However, dark skinned people do develop skin cancers, and they are also susceptible to the long term effects of UV radiation on the eye and the immune system (WHO, 2006).


3c. Sun protection

The best Sun protection is to stay out of the Sun, but that is not always possible or desirable. Swimming, skiing, walking, tennis, soccer, and lying in a hammock often include exposure to the Sun. Keeping the exposure to proper intervals, wearing as much protective clothing as is practical, and using sunscreens will prevent sunburns and may obviate or lessen the long term detrimental effects of Sun exposure.


Physical inorganic sunscreens, such as opaque zinc oxide and titanium oxide, reflect both UVA and UVB. The organic or chemical sunscreens are non-opaque and absorb UVA, UVB, or both by directly absorbing the UVR and dissipating it as heat. The Sun Protection Factor (SPF) is an experimentally determined number that relates how well a protective agent works relative to no protection in the midday Sun.  An agent with SPF of 15 will delay a burn by a factor of 15 over no protection at all. It filters 92% of the UVB (Ferrini, 1998). The SPF mainly measures UVB protection. There is no good way to estimate UVA protection. Because of their differing wavelengths, UVA and UVB change their relative proportions reaching the ground as the day progresses. UVA is less absorbed by a thicker atmosphere and is less affected by the atmosphere in the early morning and late afternoon, while the absorption and scattering of UVB is more intense due to its shorter wavelength. UVB more easily penetrates the thinner atmosphere in the midday, and it increases its proportion in the UV spectrum relative to UVA in the midday (Ferrini, 1998).

A dark tan on a white skin only offers a SPF of 4. Sunscreens are not intended to increase one’s exposure to the Sun. They are intended to increase protection during unavoidable exposures (WHO, 2006). Sunscreens at levels of SPF of 15 and above are quite effective against sunburn if applied properly and regularly (AAD, 2006). Sunscreens come in a large variety of ointments, creams, gels, lotions, sprays, and wax sticks. They are all labeled with SPF numbers, and they have a variable resistance to being washed off by water.

While sunscreens are protective against sunburns, it is a hotly contested issue as to whether they protect against the long term effects of chronic UVR exposure, mainly skin cancer (Ferrini, 1998). The majority of the data seems to favor them offering some protection against basal cell and squamous cell carcinoma. The data is quite mixed regarding any protection against melanoma. In fact, there is some evidence to suggest the incidence of melanoma increases with sunscreen usage, possibly from carcinogenic effects of the sunscreens themselves or possibly from the sunscreens permitting one to have a longer exposure to sunlight without suffering a sunburn. Until the role of sunscreens can be better assessed, it is best they be used to protect one against excess Sun exposure for activities in the Sun that can not be avoided, but they should not be used to extend one’s Sun exposure.

In the United States the Ultraviolet (UV) Index is reported daily.  It offers an analysis of UV light levels on a scale of 1 to 11+ (worse).  The UV Index is a forecast of the amount of ultraviolet radiation expected to reach the Earth's surface when the Sun is high in the sky.  It depends on the Sun's elevation, the cloud cover, and the amount of ozone in the atmosphere.  Special care is supposed to be taken when the index is 5 or higher.  For US cities, the UV Index information is available daily from a number of web sites (NOAA, 2006). The UV Index conforms with the international guidelines for UV reporting established by WHO.

WHO defines a Global Solar UV Index (UVI). The UVI is a forecast of the maximum amount of UV radiation expected to reach the Earth’s surface at Solar noon. For the midday Sun at noon close to the equator, the UVI can reach 20, while summertime values in mid Northern latitudes rarely exceed 8 (WHO, 2006). The Australian Government through the Bureau of Meteorology maintains a SunSmart UV Alert web page for a daily guide to Sun protection (SunSmart, 2006). It is based on the WHO Global Solar UV Index. According to SunSmart, when the UV Index reaches 3, sensible Sun protection is warranted; this level of Sun exposure also makes it unlikely one would suffer from Vitamin D deficiency6.

 

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Notes

[5] Inflammation is a term used since ancient times to describe a combination of redness, swelling, pain, and heat in an area subject to physical, chemical, or infectious injury.  It is part of the body’s response to injury, and it is the first part of the healing mechanism.  It is mediated through a complex system of chemicals released from injured cells, chemicals and cells brought to the injured area via the blood stream, and cells that make their own way to the injured area through cellular locomotion. 

[6] Vitamin D consists of a complex group of hormones that help regulate body levels of calcium and phosphorus which in turn controls the mineralization of bone.  Individuals with adequate exposures to sunlight do not require dietary vitamin D.  Lack of vitamin D leads to various childhood and adult diseases, such as rickets.

 

 

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