In recent years, reactions to the sun’s rays have become increasingly common, which is not only related to the ever-expanding number of photosensitizers in the environment, but also to the obsession with sunbathing.

Sunlight emits a wide spectrum of radiation energy, extending from radiowaves through infrared, visible, and ultraviolet (UV) light, to X-rays. Visible light has relatively harmless wavelength range between 400–800 nm. However, this is not true for individuals with photosensitivity disorders, such as porphyria, solar urticaria and polymorphous light eruption. Infrared light ranges from 800 to 1800 nm. It is the UVA and UVB wavelengths (290–400 nm) that cause most cutaneous reactions. Wavelengths <220 nm are absorbed by atmospheric gases, including oxygen and nitrogen, and those <290 nm are absorbed by the atmospheric ozone layer. The remaining middle-wavelength (UVB, 290–320 nm) and long-wavelength (UVA1, 340–400 nm; UVA2, 320–340 nm) UV radiation can reach Earth and be absorbed by biological molecules, thereby damaging them. The skin is quite effective at protection from UV penetration, but the depth of penetration depends upon the wavelength. UVA easily reaches the deeper dermis, whereas UVB is absorbed in the epidermis and little reaches the upper dermis.

Ultraviolet light also reaches the skin through reflection from the snow (80–85%), the sand (17–25%), the water (5%, but up to 100% when the sun is directly overhead), as well as sidewalks and the ground. Ultraviolet exposure also increases by 4% for every approximately 300 metres elevation above sea level. What we should remember is that on a bright, cloudy day with thin cloud cover, it is possible to receive 60–85% of the amount of UV radiation present on a bright clear day. Furthermore, hats provide only a moderate degree of protection, and surfaces with reflectivity increase sunlight exposure to a large extent.

Tanning and sunburn reactions

The visible short-term effects of exposure to ultraviolet radiation include sunburn and tanning. Sunburn development declines markedly with increasing wavelength. UVA light at 360 nm is 1000-fold less effective in causing a sunburn, or skin erythema, than UVA light at 300 nm. This indicates that UVB light is largely responsible for sunburn, with peak induction up to one day (6–24 hours) after sun exposure. Sunburns gradually fade during the next 3–5 days, as the skin starts to desquamate. The severity of reactivity to UVB light ranges from a mild asymptomatic erythema to a more intense reaction, including redness and tenderness, pain, oedema, and, less frequently, vesiculation and bulla formation, particularly the day after the first appearance of the sunburn. In case of extensive area with sunburn, constitutional symptoms may include nausea, malaise, headache, fever, chills, or even delirium. Sunburns during childhood correlate with a higher risk of developing melanocytic nevi, as well as UV-induced skin cancers.

Tanning is also dependent on the wavelength and it is biphasic. Immediate pigment darkening results primarily from exposure to UVA light. It is caused by alteration and redistribution of melanin, and fades within 6 to 8 hours. Delayed tanning usually results from exposure to UVB and peaks at about 3 days after exposure. Fair skin (type II) is only able to tan with UVB dosages that cause at least some degree of sunburn, whereas darker skin types (type III and higher) can tan significantly without burning. Sunburn causes apoptosis (cell death) of keratinocytes or, if the dosage is high enough, it induces cell cycle arrest, allowing the cell to undergo repair of their DNA template before proliferating. In addition to this, sunburn depletes the protective Langerhans cells, it can cause epidermal thickening (which reduces exposure of the basal keratinocytes to UV radiation) as a protective mechanism, it stimulates release of inflammatory cytokines, and it induces the formation of antioxidative enzymes (which reduce oxidative DNA damage). The tan induced by UVB involves increased melanin synthesis, increased numbers of melanocytes, and increased transfer of melanosomes to keratinocytes.

Table 1 – Skin types and photosensitivity

Skin type Reactivity to sun Examples


I Very sensitive: always burn easily and severely, tan little or not at all Individuals with fair skin; blond or red hair, blue or brown eyes, and freckles
II Very sensitive: usually burn easily, tan minimally or lightly Individuals with fair skin; red, blond, or brown hair; and blue, hazel, or brown eyes
III Moderately sensitive: burn moderately, tan gradually and uniformly Average white individuals
IV Moderately sensitive: burn minimally, tan easily Individuals with dark brown hair, dark eyes, and white or light brown skin
V Minimally sensitive: rarely burn, tan well and easily Brown-skinned (Middle Eastern and Hispanic) individuals
VI Deeply pigmented: almost never burn, tan profusely Blacks and others with heavy pigmentation


The long-term effects of chronic sun exposure include photo-aging, photo-carcinogenesis, and immunosuppression. Given its potential to penetrate more deeply into the dermis, UVA light is thought to play a particularly important role in photo-aging. UVA, but not UVB, is able to penetrate through window glass. Thus, individuals who sit in offices exposed to UVA through windows or drive cars extensively, can show significant asymmetry in UVA damage on the face. UVA light is also the light used in indoor tanning, a practice prevalent particularly among older female adolescents. This practice promotes skin damage, leading to an increased risk of skin cancer and photodamage, but no increased protection against sun exposure. The danger of using tanning facilities has led to legislation to control use by minors and limitations of exposure in several states. In addition, many facilities now offer ‘safe’ tanning, in which an artificial tan is produced by dihydroxyacetone (DHA). DHA is a sugar that interacts with the stratum corneum proteins to produce a brown pigment called melanoidins. The brown colour resists washing, but provides minimal and transient sun protection.

Prevention of sunburn depends primarily on the utilization of measures that reduce exposure to strong sunlight. This is especially important for fair-skinned individuals, particularly blue-eyed persons, redheads, blonds, and those with freckles who withstand actinic exposure poorly, burn easily, and, over the years, tend to suffer chronic effects of light exposure. Prophylactic measures to reduce the impact of harmful UV rays include timing of outdoor activities to avoid peak UV light exposure between 10 a.m. and 3 p.m. in the warmer seasons of the year; wearing broad-rimmed hats, sun protective clothing, and sunglasses; and staying in the shade. Light-textured materials such as T-shirts (especially when wet) give only partial protection. Clothes with a tighter weave are commercially available (e.g.,,,, or clothes can be laundered with a chemical that provides sun protection (SunGuard).

Sunscreens occupy an important position in the management of UV light exposure. The lifetime use of sunscreen and sun-avoidance has been calculated to reduce the lifetime risk of developing UV-induced skin cancer by 78%. The most common misconception (particularly among teenagers) is the belief that certain sunscreens can induce or promote a suntan. Sunscreens are topical preparations designed to protect the skin from the effects of UV light. The most common sunscreen components and their absorbance capacity are listed in Table 2. These inorganic sunscreens (titanium dioxide and zinc oxide) protect skin by reflecting and scattering UV and visible light (290–700 nm). These so-called ‘inorganic’ sunscreens frequently contain one or both of these agents. Organic sunscreens absorb light at particular wavelengths into specific chemical UV filters, and re-emit the energy as insignificant quantities of heat. Newer organic sunscreen components now absorb in both the UVA and UVB spectrum, thus providing protection against the damaging effects of the broad spectrum of UV light. These newer sunscreens are photostable (in contrast to avobenzone), and include bis-ethylhexyloxyphenol methoxyphenol triazine (anisotriazine, Tinosorb S), drometrizole trisiloxane (silatriazole or Mexoryl XL), methylene-bis-benzotriazolyl tetramethylbutylphenol (Tinosorb M), and terephthalylidene dicamphor sulfonic acid (Mexoryl SX). Ideally, organic sunscreens should be applied 20–30 min before the onset of sun exposure, so that there is adequate time to bind to the stratum corneum and show effectiveness; the inorganic sunscreens can be applied immediately before sun exposure. Sunscreens should be reapplied after swimming, periods of excessive perspiration, frequent washing, or showering. Oral sunscreens containing antioxidants (e.g., lycopene, vitamins C and E) and botanicals (e.g., polyphenols, such as green tea and flavonoids, such as genistein) are now commercially available. They provide some protection against acute sun damage, but they are not as effective as topical sunscreens in preventing sunburns, their long-term protective effects are not clear, and they should not replace other forms of photoprotection for children.

Table 2 — Common sunscreen filters and protection from UV radiation

Sunscreen filter Wavelength protection
Organic sunscreens
 PABA group UVB
 Padimate O
 Salicylate UVB
 Cinnamate UVB
 Benzophenone UVB, some UVA
 Avobenzone (Parsol 1789) UVA
 Bis-ethylhexyloxyphenol methoxyphenol triazine UVA and UVB
 Drometrizole trisiloxane UVA and UVB
 Methylene-bis-benzotriazolyl tetramethylbutylphenol UVA and UVB
 Terephthalylidene dicamphor sulfonic acid UVA and UVB
Inorganic sunscreens
 Titanium dioxide UVA and UVB
 Zinc oxide UVA and UVB


Traditionally, protection against UVB light has been rated based on the sun protective factor (SPF). The SPF rating can be determined by dividing the least amount of time it takes to produce erythema on sunscreen-protected skin by the time it takes to produce the same erythema without sunscreen protection. Thus, individuals using a sunscreen with an SPF of 15 who normally burn following unprotected sun exposure, can theoretically stay out 15 times longer before getting the same degree of erythema. It should be recognized, however, that this SPF rating is only a reflection of protection against sunburn from UVB light and does not measure protection from the non-erythema effects, especially from UVA light, including immune suppression, photo-aging, and skin cancer. Thus, sunscreens that protect against exposure to UVA light should be chosen in addition to the SPF rating of the sunscreen. A new 4-star grading system has been proposed by the FDA to rate UVA-based on in vitro and in vivo testing.

In order to be effective, adequate amounts of sunscreen must be applied to all UV-exposed areas and the sunscreen must be reapplied every few hours. It is critical that individuals continue sensible sun protection by means other than sunscreens and not increase their exposure because of sunscreen availability.

The degree to which a person sunburns or tans depends on genetic factors and the natural protection of the skin. Skin types, accordingly, are ranked from skin type I, the most sensitive, to skin type VI, the least sensitive to sun damage (Table 1). Since sun damage begins in children and is cumulative, it is strongly recommended that everyone adopt a program of sun protection and daily sunscreen use, preferably with an SPF of 15 or greater, from infancy on. Individuals with extreme photosensitivity should use sunscreens with levels of SPF 30 or higher. For black-skinned individuals, who already have protective melanin levels, sunscreens with an SPF of 6 or 8 may be adequate, but black skin can burn as well, and the increased melanin is not totally protective.

Considerable media attention has focused on the need for UV-induced vitamin D synthesis in the skin as a rationale for sun exposure. In fact, UV exposure that stimulates vitamin D3 production in the skin is inseparable from UV exposure that is carcinogenic. Although sunscreens do markedly reduce the capacity of skin to produce vitamin D (and greater vitamin D deficiency has been linked to darker skin colour), sunscreen use has not been linked with deficiency, and oral administration of vitamin D likely suffices. The American Academy of Paediatrics has recently recommended increasing the minimum daily intake of vitamin D for infants, children and adolescents to 400 IU/day, beginning shortly after birth. Patients who require strict photoprotection as treatment should be monitored for possible vitamin D deficiency and provided dietary supplementation.

Treatment of sunburn consists of cool compresses or cool tub baths in colloidal oatmeal, baking soda, or cornstarch; topical formulations with pramoxine or menthol; mild topical corticosteroid formulations; an emollient cream; and systemic preparations with analgesic and anti-inflammatory properties, such as NSAIDs. When symptoms are severe, a short course of systemic corticosteroids (oral prednisone, or its equivalent, in dosages of 1 mg/kg per day, with tapering after a period of 4–8 days) will abort severe reactions and afford added relief.

Certain disorders predispose individuals to the adverse effects of ultraviolet light. For example, children with alopecia totalis, just as adults with androgenetic alopecia and balding at the vertex, have a higher risk of developing skin cancer at the exposed site if not protected. Patients with diminished or absent melanin, as in oculocutaneous albinism, or with defective DNA repair mechanisms, as in xeroderma pigmentosum (see below) have an increased tendency to develop UV-induced DNA damage and cutaneous malignancy. Individuals with nevoid basal cell carcinoma syndrome, which predisposes to the early onset of numerous basal cell carcinomas, have mutations in the PTCH gene, a gene that can also be mutated by UV light exposure in sporadic basal cell carcinomas. Sunlight can also exacerbate or trigger certain dermatoses, among them acne, herpes simplex infection, lupus, dermatomyositis, Darier disease, pemphigus, and bullous pemphigoid.

About the author:

Christofer Tzermias

Specialised in the UK (Oxford & London) and in North America (New York & San Diego) in the field of LASER Dermatology, Dr Tzermias, has been providing dermatological state-of-the-art treatments using cutting-edge LASER and Energy based Devices for over 20 years. He has been Director of Interventional and LASER Dermatology Department at the Athens Medical Center for over 18 years and for the last 9 years is the Scientific Director of IQ - Intensive Quality Dermatology & Cosmetic Surgery Clinics, which at the 2017 Healthcare Awards won the ‘Innovation Award for Innovative Services’ for their pioneering contributions. Since 2018, IQ Dermatology & Cosmetic Surgery Clinics has also been operating in London, UK and in Muscat, Oman. Dr Tzermias is a Fellow of the world-renowned American Society for LASER Medicine and Surgery (ASLMS), a Founder Member of the European Society LASER Dermatology (ESLD), the Vice President of the ‘Open Health Alliance’ and he is also on the Board of Directors of Elitour - Greek Medical Tourism Council.

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