Radiation effects of Sun exposure

The sun emits electromagnetic rays comprising a continuous spectrum of short to long waves. Only a narrow range of wavelengths between 400 nm and 770 nm react with photocells in the retina and observed as the various colors of the rainbow. Beyond red (770 nm) is infrared. Heat is due to infrared radiation, which can be felt. Below violet (400 nm) are the ultraviolet (200–400 nm) and X-rays. Most short wavelengths, that can neither be seen nor felt, are filtered out by the Earth's thick atmosphere which includes ozone and water vapour. Therefore, as there is less atmosphere above mountain tops, the danger of radiation exposure is greater. The content of water vapor in the atmosphere varies, which accounts for protection from sunburn in winter, cloudy days, the early morning, or late evening sun. Glass filters out wavelengths below 320 nm, so that the closed windows of a car will protect even in a tropical desert unless one is sensitive to the longer wavelengths of ultraviolet radiation. Porphyria is, for example, a disease triggered by UVA radiation and is thus difficult to protect against by shade, cloud, or glass.
Ultraviolet radiation (UVR) is arbitrarily divided into UVC (200–280 nm), UVB (280–320), and UVA (320–400 nm). The principal effects of ultraviolet light on the skin are elastic fibre damage and cutaneous ageing, apoptosis, immunosuppression, suntan, sunburn, and carcinogenesis. While each subclass of UVR can produce all of these effects, UVC is relatively more likely to cause cancer, UVB relatively more likely to produce burning, and UVA relatively more likely to produce ageing. UVA is estimated to be 10 times less effective than UVB at producing a suntan and 100 times less effective than UVB at producing non-melanoma skin cancer. This is the basis of so-called ‘safe tanning’ using UVA light in solariums. However, high-dose UVA does cause non-melanoma skin cancer. In addition, the spectrum responsible for producing melanoma has not been established and may include UVA. UVR immunosuppression may suppress tumour surveillance and thereby enhance carcinogenesis.
The diagnosis of UVR damage is determined by recognizing the distribution of the rash as being typical of exposure. Thus the head, nose, and cheeks are principally affected, but there is often sparing below the eyebrows, under a forelock, beneath and behind the ears, and below the chin. The sides and back of the neck are picked out, but there is a sharp border to the sun damage where the collar shields the skin from sunlight. Much, of course, depends on the style of clothing as well as on the direction of irradiation. The backs of the hands and dorsum of the feet are often caught by the sun; however, there may be some tolerance of such skin previously exposed and tanned so that skin not so tolerant is clearly more prone to burning. Mediation of sunburn erythema is partly due to the generation of prostaglandins.

How to prevent skin cancer

SKIN CANCER PREVENTION
For the nonmelanoma skin cancers, the most logical approach to prevention is to limit exposure of the skin to natural and artificial sources of UV radiation. This can be achieved in numerous ways, including the use of sunscreens, the avoidance of outdoor activities during the noon hours when the amount of UV radiation in sunlight is maximal, and the use of protective clothing. Reducing the lifetime dose of UV radiation reduces the risk of skin cancer development. Because the effects of UV radiation in causing nonmelanoma skin cancers are cumulative, we would expect that reducing sunlight exposure at any age would retard the rate of tumor development.
For melanoma and perhaps even for some basal cell carcinomas, it is not clear whether this strategy would be effective because there is not a simple, direct relationship between dose of UV radiation and melanoma induction. For example, if melanoma results from childhood exposure to UV radiation, as has been suggested, reducing sunlight exposure during adult life may not be beneficial in attempting to decrease the incidence of melanoma. Obviously, more information on the dose response, wavelength dependence, and mechanism of action of UV radiation in the induction of melanomas is needed to devise effective strategies for preventing even the melanomas that are sunlight-related.

Sunlight effects upon the skin

Ultraviolet radiation (UVR) comprises only about 5% of sunlight, with visible light and infrared radiation making up the remaining 95%. However, it is UVR which is chiefly responsible for the harmful effects of sunlight exposure. On a sunny day, UVA (315-400 nm) accounts for at least 95% of UVR, and UVB (280-315 nm) no more than 5%. UVR has acute and chronic effects on the skin.
Acute effects
Erythema (sunburn)
Sunburn or erythema can vary in intensity from mild redness to oedema, blistering and peeling. Susceptibility to sunburn and tanning depends on the skin phototype of the individual. UVB is much more effective at inducing erythema than UVA. UVB accounts for only about 5% of solar radiation but it contributes to about 80% of the erythema caused by sunlight. Experiments suggest that the synthesis and release of prostaglandin E2 (PGE2), following cyclooxygenase-2 (cox-2) gene activation, and nitric oxide within the dermis are responsible for UV-induced erythema.
Melanogenesis (tanning)
Skin colour is genetically controlled but can be enhanced by UVR exposure. Each skin phototype has a different ability to tan. Tanning and epidermal hyperplasia following UVR exposure protects against erythema and burning, but maintaining this requires repeated exposures, which can result in the chronic effects of photodamage.
Skin phototypes
Skin phototype Response to UVR exposure
I White skin, always burns, never tans (Celtic)
II White skin, burns initially, tans with difficulty
III White skin, rarely burns, tans easily
IV White skin, never burns always tans (Mediterranean)
V Brown skin (Asian)
VI Black skin
Immunosuppression
Both UVA and UVB exposure suppress cutaneous cell-mediated immunity in humans. This effect is significantly higher in skin types I/II than in types III/IV. UVR-induced immunosuppression is thought to play an important role in the emergence of skin cancer, which explains the increased risk of skin cancer in individuals with skin types I/II who have a history of repetitive and intense UVR exposure.
Chronic effects
Photoageing
Photoageing results in dry, deeply wrinkled, inelastic, leathery skin with telangiectasia, mottled pigmentation, freckling and lentigines. Repeated long-term UVR exposure, especially UVB, results in changes within the dermal connective tissue. There is elastosis and degradation and disorganization of collagen fibrils. It is thought that UVR-induced metalloproteinases (endopeptidases that degrade structural proteins) degrade the dermal matrix, which then undergoes imperfect repair.
Photocarcinogenesis
Skin cancer is the long-term result of a complex interaction between UVR exposure and genetics. Genetic factors include skin phototype, DNA repair capacity and immunocompetence. DNA damage occurs following UVR, and this is repaired by nucleotide excision repair. Repeated UV exposure together with suboptimal repair results in the clonal expansion of cells with mutated oncogenes leading to melanoma and non-melanoma skin cancer. Studies have shown that squamous cell carcinomas develop as the consequence of accumulated sun exposure, whereas melanoma and basal cell carcinomas are more dependent on specific patterns of childhood and intermittent high-dose sun exposure. Other important risk factors for the development of skin cancer include UVR-induced immunosuppression as well as immunosuppressant drugs as seen in organ transplant patients.
Photodermatoses
Photodermatoses (diseases caused by sunlight) can be divided into two main categories, those in which the sunlight has a primary role in the condition (primary photosensitivity) and those in which the sunlight acts as an exacerbating factor (secondary photosensitivity).

Melanocyes and Melanin

Most people's skin darkens when exposed to UV light, giving them more protection when it is needed. This is the physiological purpose of sun tanning.
Freckles and moles are formed where there is a localized concentration of melanin in the skin.
So what is Melanin?
Melanin has a photoprotective role.
It is produced by melanocytes, through a process called melanogenesis. Melanocytes are cells located in the bottom layer of the skin's epidermis. Although human beings generally possess a similar concentration of melanocytes in their skin, the melanocytes in some individuals and ethnic groups more frequently or less frequently express the melanin-producing genes, thereby conferring a greater or lesser concentration of skin melanin.
Once made, melanin is moved along arm-like structures called dendrites in a special container called a melanosome which is shipped to the keratinocytes. Melanosomes are vesicles or packages of the chemical inside a plasma membrane. The melanin is in organelles called "melanosomes", that are organized as a cap protecting the nucleus of the keratinocyte.
Because melanin is an aggregate of smaller component molecules, there are a number of different types of melanin with differing proportions and bonding patterns of these component molecules. Both pheomelanin and eumelanin are found in human skin and hair, but eumelanin is the most abundant melanin in humans.
Eumelanin is found in hair and skin, and colors hair grey, black, yellow, and brown. In humans, it is more abundant in peoples with dark skin. There are two different types of eumelanin. The two types are black eumelanin and brown eumelanin. Black eumelanin is the darkest, brown eumelanin is lighter than black eumelanin. black eumelanin is in mostly non-Europeans and aged Europeans, while brown eumelanin is in mostly young Europeans. A small amount of black eumelanin in the absence of other pigments causes grey hair. A small amount of brown eumelanin in the absence of other pigments causes yellow (blond) color hair.
Pheomelanin is also found in hair and skin and is both in lighter skinned humans and darker skinned humans. But in general women have more pheomelanin than men, and thus women's skin is generally redder than men's. Pheomelanin imparts a pink to red hue and, thus, is found in particularly large quantities in red hair. Pheomelanin is particularly concentrated in the lips, nipples, glans, and vagina. Pheomelanin also may become carcinogenic when exposed to the ultraviolet rays of the sun.
Melanocytes insert granules of melanin into specialized cellular vesicles called melanosomes. These are then transferred into the other skin cells of the human epidermis. The melanosomes in each recipient cell accumulate atop the cell nucleus, where they protect the nuclear DNA from mutations caused by the ionizing radiation of the sun's ultraviolet rays. When ultraviolet rays penetrate the skin and damage DNA; fragments from damaged DNA will trigger melanogenesis and cause the melanocyte to produce melanosomes, which are then transferred by dendrite to the top layer of keratinocytes.
People whose ancestors lived for long periods in the regions of the globe near the equator generally have larger quantities of eumelanin in their skins. This makes their skins brown or black and protects them against high levels of exposure to the sun, which more frequently results in melanomas in lighter skinned people.