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November 2017
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Does skin turn painlessly red well before it starts to get sunburned?

A sunburn is damage to the cells of the upper layer of the skin (epidermis) by ultraviolet light. Ultraviolet light damages the DNA of skin cells, which triggers apoptosis (programmed cell death) of these cells.

Most of the time this damage caused by UV light is either repaired by enzyme systems within cells or if not repaired, the cell is destroyed by a variety of mechanisms. When the damaged cell escapes destruction, it has the potential to turn into a skin cancer.  Sun damage to the skin is cumulative. Blistering sunburns in childhood are a risk factor for developing the most dangerous skin cancer, malignant melanoma.

The redness seen in a sunburn is from dilatation of the blood vessels and the incoming inflammation. So by the time redness is seen (2-6 hours usually), the sunburn damage has already been done. With the redness comes the discomfort, burning,and/or pain. Redness and pain are maximal at 24 hours after a sunburn. The extent and severity of the symptoms depend on the amount of exposure to ultraviolet light and the degree of damage done.

Actinic injury: Sunburn and solar erythema

The solar spectrum has been divided into different regions by wavelength. The parts of the solar spectrum important in photomedicine include UV radiation (below 400 nm), visible light (400–760 nm), and infrared radiation (beyond 760 nm). Visible light has limited biologic activity, except for stimulating the retina. Infrared radiation is experienced as radiant heat. Below 400 nm is the UV spectrum, divided into three bands: UVA, 320–400 nm; UVB, 280–320 nm; and UVC, 200–280 nm. UVA is divided into two subcategories: UVA I (340–400 nm) and UVA II (320–340 nm). Virtually no UVC reaches the earth’s surface because it is absorbed by the ozone layer above the earth.

Here is more information on the Electromagnetic Spectrum from the NASA Goddard Space Flight Center.

The minimal amount of a particular wavelength of light capable of inducing erythema on an individual’s skin is called the minimal erythema dose (MED). Although the amount of UVA radiation is 100 times greater than UVB radiation during midday hours, UVB is up to 1000 times more erythemogenic than UVA, and so essentially all solar erythema is caused by UVB. The most biologically effective wavelength of radiation from the sun for sunburn is 308 nm. UVA does not play a significant role in solar erythema and sunburn; however, in the case of drug-induced photosensitivity, UVA is of major importance.

The amount of UV exposure increases at higher altitudes, is substantially larger in temperate climates in the summer months, and is greater in tropical regions. UVA may be reflected somewhat more than UVB from sand, snow, and ice. While sand and snow reflect as much as 85% of the UVB, water allows 80% of the UV to penetrate up to 3 feet. Cloud cover, although blocking substantial amounts of visible light, is a poor UV absorber. During the middle 4–6 h of the day, the intensity of UVB is 2–4 times greater than in the early morning and late afternoon.

Clinical signs and symptoms

Sunburn is the normal cutaneous reaction to sunlight in excess of an erythema dose. UVB erythema becomes evident at around 6 h after exposure and peaks at 12–24 h, but the onset is sooner and the severity greater with increased exposure. The erythema is followed by tenderness, and in severe cases, blistering, which may become confluent (Fig. 3-12). Discomfort may be severe; edema commonly occurs in the extremities and face; chills, fever, nausea, tachycardia, and hypotension may be present. In severe cases such symptoms may last for as long as a week. Desquamation is common about a week after sunburn, even in areas that have not blistered.



After UV exposure, skin pigment undergoes two changes: immediate pigment darkening (IPD, Meirowsky phenomenon) and delayed melanogenesis. IPD is maximal within hours after sun exposure and results from metabolic changes and redistribution of the melanin already in the skin. It occurs after exposure to long-wave UVB, UVA, and visible light. With large doses of UVA, the initial darkening is prolonged and may blend into the delayed melanogenesis. IPD is not photoprotective.

Delayed tanning is induced by the same wavelengths of UVB that induce erythema, begins 2–3 days after exposure, and lasts 10–14 days. Delayed melanogenesis by UVB is mediated through the production of DNA damage and the formation of cyclobutane pyrimidine dimers (CPD). Therefore, although UVB-induced delayed tanning does provide some protection from further solar injury, it is at the expense of damage to the epidermis and dermis. Hence, tanning is not recommended for sun protection. Commercial sunbed-induced tanning, while increasing skin pigment, does not increase UVB MED, and is therefore not protective for UVB damage.

An individual’s inherent baseline pigmentation, ability to tan, and the ease with which he/she burns are described as his/her “skin type.” Skin type (See Table below) is used to determine starting doses of phototherapy and sunscreen recommendations, and reflects the risk of development of skin cancer and photoaging.

Skin types (phototypes)
Skin type Baseline skin color Sunburn and tanning history
I White Always burns, never tans
II White Always burns, tans minimally
III White Burns moderately, tans gradually
IV Olive Minimal burning, tans well
V Brown Rarely burns, tans darkly
VI Dark brown Never burns, tans darkly black

Exposure to UVB and UVA causes an increase in the thickness of the epidermis, especially the stratum corneum. This increased epidermal thickness leads to increased tolerance to further solar radiation. Patients with vitiligo may increase their UV exposure without burning by this mechanism.


Once redness and other symptoms are present, treatment of sunburn has limited efficacy. The damage is done and the inflammatory cascades are triggered. Prostaglandins, especially of the E series, are important mediators. Aspirin (ASA) and nonsteroidal anti-inflammatory drugs (NSAIDs), including indomethacin, have been studied, as well as topical and systemic steroids.

Medium potency (class II) topical steroids applied 6 h after the exposure (when erythema first appears) give a small reduction in signs and symptoms. Since oral NSAIDs and systemic steroids have been tested primarily prior to or immediately after sun exposure, there is insufficient evidence to recommend their routine use, except immediately after solar over-exposure. Therefore treatment of sunburn should be supportive, with pain management (using acetaminophen, ASA, or NSAIDs), plus soothing topical emollients or corticosteroid lotions. In general, a sunburn victim experiences at least 1 or 2 days of discomfort and even pain before much relief occurs.


Sunburn is best prevented. Use of the UV index, published daily by the National Weather Service for many US cities and found in newspapers, facilitates taking adequate precautions to prevent solar injury. Numerous educational programs have been developed to make the public aware of the hazards of sun exposure. Despite this, sunburn and excessive sun exposure continue to occur in the US and Western Europe, especially in white persons under the age of 30, among whom more than 50% report at least one sunburn per year. Sun protection programs have four messages:

  • Avoid midday sun
  • Seek shade
  • Wear protective clothing
  • Apply a sunscreen

The period of highest UVB intensity, between 9 am and 3–4 pm, accounts for the vast majority of potentially hazardous UV exposure. This is the time when the angle of the sun is less than 45° or when a person’s shadow is shorter than his/her height. In temperate latitudes it is almost impossible to burn if these hours of sun exposure are avoided.

Trees and artificial shade provide substantial protection from UVB. Foliage in trees provides the equivalent of sun protection factor (SPF) 4–50, depending on the density of the greenery. Clothing can be rated by its ability to block UVB radiation. The scale of measure is the UV protection factor (UPF) (analogous to SPF in sunscreens). Although it is an in vitro measurement, as with SPF, it correlates well with the actual protection the product provides in vivo.

In general, denser weaves, older, washed clothing, and loose-fitting clothing screen UVB more effectively. Wetting a fabric may substantially reduce its UPF. Laundering a fabric in a Tinosorb-containing material (SunGuard) will add substantially to the UPF of the fabric. Hats with at least a 4-inch brim all around are recommended.

A sunscreen’s efficacy in blocking the UVB (sunburn-inducing) radiation is expressed as an SPF. This is the ratio of the number of MEDs of radiation required to induce erythema through a film of sunscreen (2 mg/cm2), compared with unprotected skin. Most persons apply sunscreens in too thin a film, so the actual “applied SPF” is about half that on the label. Sunscreening agents include UV-absorbing chemicals (chemical sunscreens) and UV-scattering or blocking agents (physical sunscreens).

Available sunscreens, especially those of high SPFs (>30), usually contain both chemical sunscreens (such as p-aminobenzoic acid [PABA], PABA esters, cinnamates, salicylates, anthranilates, benzophenones, benzylidene camphors such as ecamsule [Mexoryl], dibenzoylmethanes [Parsol 1789, in some products present as a multicompound technology Helioplex], and Tinosorb [S/M]) and physical agents (zinc oxide or titanium dioxide). They are available in numerous formulations, including sprays, gels, emollient creams, and wax sticks. Sunscreens may be water-resistant (maintaining their SPF after 40 min of water immersion) or waterproof (maintaining their SPF after 80 min of water immersion).

For skin types I–III (see Table above), daily application of a sunscreen with an SPF of 30 in a facial moisturizer, foundation, or aftershave is recommended. For outdoor exposure, a sunscreen of SPF 30 or higher is recommended for regular use. In persons with severe photosensitivity and at times of high sun exposure, high-intensity sunscreens of SPF 30+ with inorganic blocking agents may be required.

Application of the sunscreen at least 20 min before and 30 min after sun exposure has begun is recommended. This dual application approach will reduce the amount of skin exposure by two- to three-fold over a single application. Sunscreen should be reapplied after swimming or vigorous activity or toweling. Sunscreen failure occurs mostly in men, due to failure to apply it to all the sun-exposed skin, or failure to reapply sunscreen after swimming. Sunscreens may be applied to babies (under 6 months) on limited areas. Vitamin D supplementation may be recommended with the most stringent sun-protection practices.

Photoaging and cutaneous immunosuppression are mediated by UVA as well as UVB. For this reason, sunscreens with improved UVA coverage have been developed (Parsol 1789, Mexoryl, Tinosorb). The UVA protection does not parallel the SPF on the label. If UVA protection is sought, a combination sunscreen with inorganic agents and UVA organic sunscreens (identified by name in the list of ingredients) is recommended.


  • Baron ED, Stevens SR: Sunscreens and immune protection.  Br J Dermatol  2002; 146:933.
  • Diffey BL, Diffey JL: Sun protection with trees.  Br J Dermatol  2002; 147:385.
  • D’Souza G, et al: Mexoryl.  Plast Reconstr Surg  2007; 120:1071.
  • Duteil L, et al: A randomized, controlled study of the safety and efficacy of topical corticosteroid treatments of sunburn in healthy volunteers.  Clin Exp Dermatol  2002; 27:314.
  • Faurschaou A, et al: Topical corticosterids in the treatment of acute sunburn.  Arch Dermatol  2008; 144:620.
  • Hatch KL, et al: Garments as solar ultraviolet radiation screening materials.  Dermatol Clin  2006; 24:85.
  • Iuternschlager S, et al: Photoprotection.  Lancet  2007; 370:528.
  • Lim HW, et al: Sunlight, tanning booths and vitamin D.  J Am Acad Dermatol  2005; 52:868.
  • Lowe NJ: An overview of ultraviolet protection, sunscreens, and photo-induced dermatoses.  Dermatol Clin  2006; 24:9.
  • Medeiras VL, et al: Sunscreens in the management of photodermatoses.  Skin Therapy Lett  2010; 15:1.
  • Moehrle M, et al: UV exposure in cars.  Photodermatol Photoimmunol Photomed  2003; 19:175.
  • Palm MD, et al: Update on photoprotection.  Dermatol Ther  2007; 20:360.
  • Thieden E, et al: Sunburn related to UV radiation exposure, age, sex, occupation and sun bed use based on time-stamped personal dosimetry and sun behaviour diaries.  Arch Dermatol  2005; 141:482.

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