Science of Skin

Tanning

TanTanning is the skin's response to damage caused by ultraviolet (UV) radiation. The overall effect is an increase in the protective pigment, eumelanin (henceforth referred to as melanin), which helps to shield skin cells from further UV exposure. The most common source of a tan is solar radiation, though the UV radiation emitted by solariums also induces a tanning response. Historically speaking, tanning rose to popularity in the mid-1920’s. More recently, many people still prefer a tan for cosmetic purposes, despite a growth in knowledge of the dangerous consequences of UV exposure. Young people, young women in particular, have become the target of government anti-skin cancer campaigns due to their affinity for sunbathing and solarium use to acquire a tan.

The history of tanning

Throughout history, many cultures including the Greeks and Romans have prized pale skin. In Europe, prior to the 1900’s, a tan was considered undesirable; it indicated poverty and a life of manual labour under the sun. The wealthy and privileged stayed indoors, used skin-lightening cosmetics and covered themselves with hats and parasols. Early in the 20th century, however, industrialisation reversed the situation. With the working class banished to mines or factories and the prosperous free to enjoy the outdoors, tanning came into style. This was aided by a notorious accident, in which the French fashion designer Coco Chanel became unintentionally tanned during a cruise. Her influence catapulted tanning to popularity almost overnight and deep bronzed skin became regarded as a fashion necessity. In addition, sunbathing (initially a pastime associated with nudism) became well accepted by the 1930’s and the beach became a common holiday destination.

Many people, particularly in Western societies, still see tanned skin as a sign of leisure and beauty. This trend toward tanning has continued with the advent of solariums. With increasing awareness of the dangers associated with UV tanning, many people opt for a cosmetic solution, using any of the multitudes of self-tanning products available on the market to achieve their aesthetic desires.

Mechanisms of tanning

Melanin is the black/brown pigment produced in the skin by cells called melanocytes. It gives the skin its colour, or pigmentation, and protects skin cells from damage by filtering photons of UV radiation which reach the skin. The basal, or constitutive, skin color designates a genetically determined amount of melanin present in an individual’s skin, in the absence of any additional influences, such as UV exposure. The facultative skin colour is an induced level of increased melanin content in an individual’s skin, as a result of solar radiation, hormones or other environmental factors. The induction of facultative skin pigmentation following UV exposure is commonly known as the tanning reaction. There are three distinctive phases of tanning, depending on the time the reaction takes to occur. The immediate pigment darkening (IPD) and the persistent pigment darkening (PPD) reactions occur very quickly, while the delayed tanning reaction (DTR) takes several days to develop.

Immediate and persistent pigment darkening (IPD and PPD)

Immediate and persistent pigment darkening (IPD and PPD), are the skin's earliest responses when exposed to UV radiation; these response are much stronger to UVA than to UVB, in particular wavelengths of 340 nm.  IPD’s effect is immediate (within minutes of UV exposure), yet temporary, darkening of the skin. IPD in lightly pigmented skin may appear as blue or grey mottled patches, whereas darker skin tones tend to develop a deeper IPD tan. PPD takes more time to occur (within hours of  UV exposure), persists several days and develops as a tan to brown colour. As little new melanin is produced within the few days after UV exposure, researchers believe that the reactions at a molecular level involve the redistribution of preexisting melanosomes (the melanin producing factories) within skin cells and the chemical alteration (oxidation and/or polymerization) of existing melanin or melanogenic precursors. It is thought that the purpose of IPD and PPD tanning is to take up and disperse UV radiation in the shallow layers of skin to avoid deeper damage.

Delayed tanning reaction (DTR)

The more familiar DTR tan develops more slowly than IPD and PPD and arises in the days following UV exposure. The length of time taken for a tan to develop and last depends on the duration, intensity and type of UV exposure. While both UVA and UVB radiation generate tanning responses, the pigmentation stimulated by UVA radiation persists longer than that induced by UVB.

The delayed tanning reaction is activated by signals sent by skin cells in response to genetic damage caused by UV radiation. There are several cellular mechanisms responsible for the visible changes seen in tanned skin. First of all, melanin in the skin is rearranged, bringing it closer to the surface. Secondly, the shape of the pigment and its location within the cell change to better protect the skin. Finally, the function of skin melanocytes is altered. Upon exposure of human skin to UV radiation, a network of physiological factors within the skin is activated. These initiate various signaling pathways in the melanocytes which affect melanin production (melanogenesis), proliferation and survival.

Melanin synthesis (melanogenesis)

aMSH-signalling-pathway
Figure 1. The signalling pathway that takes place in melanocytes as part of the tanning response.

Exposure to UV radiation stimulates the production and release of a hormone, alpha melanocyte stimulating hormone (α-MSH), by skin keratinocytes. α-MSH binds to a receptor (melanocortin 1 receptor or MC1R) on the surface of the skin melanocytes and activates a series of chemical reactions, or signaling cascade, known as the cAMP/PKA pathway.

This signaling cascade begins with G proteins coupled to the MC1R receptor; these proteins activate an enzyme located within the membrane of the melanocyte, adenylate cyclase (AC). AC converts energy containing molecules within the cell, known as ATP (adenosine triphosphate), into cyclic adenosine monophosphate (cAMP). The cAMP molecules then activate the protein kinase A (PKA), which subsequently activates, by phosphorylation (addition of a phosphate group to), a protein called CREB (cAMP-responsive element). The CREB protein is a transcription factor, meaning that it binds to a specific sequence of DNA and regulates the expression of genes in that region. Activated CREB promotes the transcription of a protein called MITF (microphthalmia-associated transcription factor).  The MITF protein, in turn, binds to and increases the transcription of several other genes. These include the MC1R genes and the genes responsible for the production of the melanogenic enzymes; tyrosinase, TRP1 and TRP2.

Melanogenesis
Figure 2. Melanogenesis - the synthesis of new melanin in the skin.

These enzymes cause increased production of melanin (eumelanin) within melanosomes; the cellular factories which synthesise melanin. The melanin is then transported from the melanosomes to the keratinocytes. The pigmentation produced by this process confers some protection of the skin against subsequent sun exposure, as the melanin absorbs part of the incoming UV radiation.

Health effects associated with tanning

Exposure to UV radiation poses multiple risks to human health. The most immediate and noticeable among these is the redness and erythema (inflammation) of sunburn that may also be followed by scarring. Less obvious, are the long-term effects of UV damage such as photoaging. Photoaging, which presents as wrinkled, discoloured or sagging skin, is caused by damage to collagen fibres and the degeneration of skin cells and surrounding blood vessels. Perhaps the most severe danger associated with UV exposure is the increased risk of skin cancer due to skin cell damage. The World Health Organization estimates that, worldwide, skin cancer is responsible for 66,000 deaths each year. UV radiation is also capable of inducing ocular (eye) damage. Of the 12-15 million annual cases of blinding cataracts, it is estimated that 20% are caused, or exacerbated, by UV exposure. There is also mounting evidence that UV radiation can cause immunosupression, which subsequently increases the chance of infection and disease. As their reduced pigmentation provides less natural protection, light-skinned individuals are more susceptible to skin damage by UV radiation.

Sunburn
Figure 5. Sunburn caused by UV radiation.
Melanoma
Figure 3. Melanoma, the most lethal form of skin cancer.
Wrinkled skin
Figure 4. Wrinkled skin, a symptom of photoaging.

The UV radiation responsible for the tanning reaction also, importantly, stimulates the production vitamin D. Vitamin D, which is essential for good health, is manufactured in the skin upon exposure to UVB wavelengths of light. However, due to the health risks associated with UV exposure, most physicians recommend dietary changes or medically-supervised supplementation to boost levels of vitamin D where incidental sun exposure is insufficient. Vitamin D deficiency affects bone condition (causing rickets in children and osteomalacia in adults) and neuromuscular funtion. It has been implicated as playing a role in a number of diseases including: diabetes mellitus; some forms of internal cancer (particularly breast, colon and colorectal); hypertension; mental illness (including depression and Seasonal Affective Disorder); autoimmune diseases; metabolic disorders; muscle weakness and cardiovascular disease.

Attitudes on tanning

According to studies, the greatest motivation for a tan is appearance. One 2007 U.S. survey indicated that 81% of participants believed that people look better with a tan. Other reasons commonly given for deliberately seeking a tan include enhanced confidence and ‘feeling healthier’. A small number of people claim that tanning improves their acne or that they wish to attain an underlying tan to protect their skin in situations of extreme UV. The most common reason given for avoidance of tanning is the detrimental effects related to UV exposure and the consequences this may have on physical appearance (i.e. skin scarring or photoaging). It has been revealed that the years of adolescence and young adulthood are pivotal in determining such attitudes on tanning and one’s approach to sun protection.

Related posts on the CLINUVEL Blog

Resources

American Academy of Dermatology

References

  • Chin, L, 2003, ‘The genetics of malignant melanoma: lessons from mouse and man’, Nature Reviews Cancer, 3:559-570.
  • Mighall, R, 2008, A history of tanning, accessed 15th July 2010, .
  • Miller, A.J & Tsao, H, 2009, ‘New insights into pigmentary pathways and skin cancer’, British Journal of Dermatology, 162(1):22-28.
  • Miyamura, Y et al., 2006, ‘Regulation of human skin pigmentation and responses to ultraviolet radiation’, Pigment Cell Research, 20:2-13.
  • Mosher, C.E & Danoff-Burg, S, 2010, ‘Addiction to Indoor Tanning: Relation to Anxiety, Depression, and Substance Use’, Archives of Dermatology, 146(4):412-417.
  • Robinson, J.K et al., 2008, ‘Indoor Tanning Knowledge, Attitudes, and Behaviour Among Young Adults From 1988-2007’, Archives of Dermatology, 144(4):484-488.
  • Routaboul , C, Denis, A & Vinche, A, 1999, ‘Immediate pigment darkening: description, kinetic and biological function’, European Journal of Dermatology, 9(2):95-99.
  • Suh, K.S et al., 2007, ‘A long-term evaluation of erythema and pigmentation induced by ultraviolet radiations of different wavelengths’, Skin Research and Technology, 13(4):360-368.
  • Tadokoro, T et al., 2005, ‘Mechanisms of Skin Tanning in Different Racial/Ethnic Groups in Response to Ultraviolet Radiation’, Journal of Investigative Dermatology, 124:1326 -1332.
  • World Health Organization, n.d, Health effects of UV radiation, accessed 15th July 2010, .

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