eMedicine Specialties > Pediatrics: General Medicine > Dermatology

Sunburn

Author: Lyn Guenther, MD, Professor, Department of Medicine, Division of Dermatology, University of Western Ontario, London, Canada
Coauthor(s): Benjamin Barankin, MD, FRCPC, Dermatologist, Private Practice, Toronto; Julie Powell, MD, Assistant Professor of Pediatrics, Director, Department of Pediatrics, Division of Dermatology, Ste-Justine Hospital, University of Montreal, Quebec, Canada
Contributor Information and Disclosures

Updated: Nov 5, 2007

Introduction

Background

A sunburn is an intense, delayed, transient inflammatory response caused by acute overexposure to ultraviolet radiation (UVR) in sunlight, primarily ultraviolet B (UV-B). UVR accounts for 5% of the total energy reaching the earth's surface. UVR is composed of ultraviolet A ([UV-A], 320-400 nm), UV-B (290-320 nm), and ultraviolet C ([UV-C], 200-290 nm). UV-A is further divided into UV-A II (320-340 nm) and UV-A I (340-400 nm). Sunlight contains the entire UVR spectrum, but only UV-A and UV-B reach the earth's surface. Approximately 95-98% of the solar UVR at the earth's surface is UV-A. UV-A can penetrate glass; UV-B cannot.

Unlike UV-A, all UV-C and approximately 90% of UV-B is filtered by the ozone layer; therefore, no UV-C and only 10% of UV-B reaches the earth. Exposure to UV-C may result from welding arcs, bactericidal lamps, and mercury arc lamps. The depth of UVR skin penetration depends on the wavelength; longer wavelengths have deeper penetration. Approximately 90% of UV-B is absorbed by the epidermis, whereas 50% of UV-A reaches the basal layer or deeper.

Since the 1920s, a tanned appearance has been a symbol of health and wealth, often indicating the ability to travel to sunny areas. Outdoor recreational activities have led to increased sun exposure and, thus, increased risk of sunburn. In 1996, 79% of Canadians reported an average of at least 30 minutes daily exposure to the summer sun, 32% reported 1-2 hours, and 28% reported 2 or more hours.1 A 1996 US survey of adults older than 18 years showed that 83% had at least 1 hour of weekday exposure during the summer, and 93% had more than 1 hour of weekend exposure; most of this exposure occurred between 10 am and 4 pm.2

A tan is the skin's response to injury produced by UVR; a safe tan is not possible.

Approximately 25% of an individual's estimated lifetime sun exposure occurs during childhood and adolescence, 50% by age 40 and 75% by age 60.

Use of artificial tanning beds and sun lamps has become common, particularly by women, but artificial tanning devices are associated with the same risks as exposure to UVR from sunlight. Over the past 10 years, the idea that a tan is healthy has gradually lost favor because sun exposure has become strongly associated with skin cancer, immunosuppression, cataract formation, and photoaging. Blistering sunburns, particularly during childhood, significantly increase an individual's subsequent risk of developing cutaneous melanoma.

Ozone layer thickness varies with the seasons. The layer above North America is thickest in late winter and thinnest in late summer and early fall. The ozone layer has been decreasing. Reactive nitrogen compounds (eg, nitrous oxide, nitrogen dioxide), halogens (eg, chlorine, bromine), and hydrogen compounds can destroy the ozone layer. Nitrogen gases from various sources (eg, supersonic aircraft, air pollution, fertilizers, microorganisms); chlorofluorocarbons (CFCs), which are used as refrigerants and in aerosols, extruded foam, and solvents; and bromine-containing halons, which are used in fire extinguishers, contribute to ozone layer depletion.

Buildup of greenhouse gas (eg, carbon dioxide) traps heat near the earth's surface, cools the stratosphere, and increases ozone loss. A 1% decrease in ozone results in a 1-2% increase in UV-B and a consequent 2% increase in skin cancers. Clouds and air pollution have little effect on UVR because as much as 80% of UVR penetrates. UVR also penetrates 1-m depths of water.

UVR exposure increases 4% for each 300-m rise in altitude. Reflection from sand, pavement, snow, and water also increases UVR exposure. Humidity increases susceptibility to sunburn. The equator receives the greatest amount of UVR throughout the year.

Ultraviolet index

The UV index was introduced in 1994 to forecast UVR intensity. UV index ratings and associated risks, based upon the estimated extent of exposure required to cause sunburn in a fair-skinned person, are as follows:

  • 0-2 - Minimal risk (1-h exposure required to sunburn)
  • 3-4 - Low risk (20-min exposure required to sunburn)
  • 5-6 - Moderate risk (<15-min exposure required to sunburn)
  • 7-9 - High risk (<10-min exposure required to sunburn)
  • 10 or more - Extreme risk (<5-min exposure required to sunburn)

Additional information about the US Environmental Protection Agency's UV monitoring program is available at the UV-Net Web site.

Measurements of sunburn and skin protection

The unit of measurement for sunburn is the minimal erythema dose (MED), defined as the minimum UV-B exposure required to produce a clearly marginated erythema in an irradiated site following a single exposure. Sunscreens are rated with a sun protection factor (SPF) number, a number that primarily reflects the sunscreen's protection from UV-B. No standard measurement exists for UV-A photoprotection. SPF numbers are calculated by dividing the MED with sunscreen applied by the MED without sunscreen. Note that this degree of protection is determined under ideal laboratory conditions and may be considerably less with thin application and outdoor use. No internationally accepted test for UVA protection has been recognized.

Pathophysiology

UV-B radiation causes most sunburn reactions and is 1000 times as erythemogenic as UV-A. UV-B is also most likely to induce and promote DNA damage.

UV-A causes approximately 15% of sunburn reactions but causes most phototoxic drug reactions.

UV-A and UV-B are absorbed by chromophores, which resonate at the same wavelength as UVR and become excited and then subsequently degraded. The chromophores for wavelengths less than 300 nm are the nucleic, amino, and urocanic acids. Melanin is the chromophore for longer wavelengths.

The DNA in epidermal keratinocytes absorbs UVR, resulting in pyrimidine dimer formation.

Cells with damaged DNA can repair the damaged DNA or they can be eliminated through P53 gene–dependent sunburn cell (apoptotic keratinocyte) formation. Sunburn cell formation depends on Fas ligand, a proapoptotic protein induced by DNA damage. UVR may cause P53 gene mutations, resulting in diminished surveillance against UVR-induced cancer. Many cytokines and inflammatory mediators are synthesized and released, probably because of DNA damage.

UVR causes increased synthesis and release of arachidonic acid metabolites (eg, prostaglandin E2 [PGE2], prostaglandin D2 [PGD2], prostaglandin F2 a [PGF2 a ], 12 hydroxyeicosatetraenoic acid [12-HETE]), cytokines (eg, interleukin [IL]-1, IL-6, IL-8, IL-10, IL-12, tumor necrosis factor [TNF]-a), adhesion molecules, histamines, kinins, substance P, calcitonin gene–related peptide, and nitric oxide.

Reactive oxygen species can induce membrane lipid peroxidation and destruction.

Alcohol consumption is associated with greater body surface area sunburned, greater initial pain, and increased likelihood of developing blisters.

Frequency

United States

A 1996 national survey of US adults reported that 39% had experienced a sunburn that year; the mean number of sunburns per adult was 1.75.2 A telephone survey of 503 continental US households during the summer of 1997 found that 13% of children had sunburned during the week or weekend prior to the survey contact, as had 9% of their parents during the prior weekend.3 A 2003 continental US survey showed that 39% of respondents had at least one sunburn in the previous year, 26% had 2 or more, 15% had 3 or more, and 9% had 4 or more.4 Sunburn was more common in individuals who were smokers or who consumed a lot of alcohol.

International

A 1996 Canadian national survey showed that half of the population had experienced at least one sunburn during the summer months, one third reported 2 or more sunburns, and 13% reported 4 or more sunburns.1 A mild sunburn (ie, erythema with sensitivity) was reported by 40% of Canadians, moderate sunburn (ie, erythema with sensitivity and peeling) was reported by 28%, and blistering sunburn every summer was reported by 4%.

Sunburns are more common in those who use sun beds than in those who do not. Twenty-five percent of Italian salon users and 44% of Swedish salon users had salon-induced sunburns.5,6

Mortality/Morbidity

Sunburns, for the most part, are a symptomatic nuisance that results in pruritic and tender erythematous skin. In the long term, sunburns are associated with nonmelanoma skin cancer (NMSC) and malignant melanoma, which can add to morbidity and shorten the lifespan. Severe sunburns infrequently require the attention of a burn unit, and more rarely, result in death.

According to a 1999 survey of Galveston (Texas) beachgoers, 16% of 56 sunburned beachgoers missed work (average 1.89 days) within the previous year because of sunburn.7

Race

White people are more susceptible to sunburn, although people of all races may experience sunburn with prolonged exposure.

Sunburns occur most frequently in persons with skin phototype (SPT) 1 or 2 (ie, individuals with light skin who have difficulty tanning). Type 1 phototypes are fair skinned and often have freckles, burn easily, and never tan. Individuals with type 5 (ie, brown skin) and 6 (ie, black skin) are less likely to sunburn but can burn with prolonged UVR exposure.

SPTs are genetically determined but are also based in part on individuals' histories of sun exposure and reactions. SPT is based on a person's own estimate of sunburning and tanning; therefore, patients should be asked if they tan easily. A negative response to this question from a white person implies an SPT 1 or SPT 2 designation (25% of the US population), whereas affirmative responses imply designations of SPT 3 or SPT 4.

Sex

Males typically experience more sunburns, use fewer sun protective measures, and tend to be less informed about skin malignancies and UV indices than women.

In the 1996 Canadian national survey, 57% of the men reported at least one sunburn in the summer, compared to 49% of the women.1 Men reported longer sun exposure; 35% had an average of at least 2 hours exposure daily in the summer, compared with 21% of the women. Most outdoor workers responding to this survey were men.

No difference has been observed in the anatomic distribution of painful sunburns in men and women.

Age

Although sunburn occurs in people of all ages, incidence of sunburns increases from childhood to adolescence. The highest prevalence of multiple sunburns in the summer occurs in individuals aged 15-24 years.

Clinical

History

Patients with sunburn have a history of excessive sun exposure from outdoor recreation or work and, less frequently, a history of concomitant ingestion of oral medications or application of topical agents.

  • All individuals develop sunburns from large doses of UVR, although persons with darker skin burn less frequently.
  • Individuals with blue or green eye color, lighter skin, and those who tan poorly and freckle easily are more prone to sunburn.
  • If the patient has received the threshold dose of UVR, delayed skin erythema in exposed areas occurs in 2-6 hours, peaks at 15-36 hours, and resolves within 72-120 hours.
  • Individuals with fair skin (eg, SPT 1 and 2) may have a history of immediate transient flush.
  • The trunk, neck, and head burn at lower UVR doses than upper limbs; upper limbs burn more readily than lower limbs.
  • According to the 1996 Canadian National Survey, the area most commonly sunburned was the back and shoulders; followed by the arms and legs; then face, scalp and neck, and chest.1
  • Erythema following UV-A exposure from sun beds begins immediately, peaks at approximately 8 hours, and persists 24-48 hours.

Physical

  • Confluent erythema and warmth are present in exposed areas.
  • Edema, pain and tenderness, and pruritus may occur as a result of moderate-to-severe sun exposure.
  • Vesiculation occurs in severe cases of sunburn and may require a week or longer to resolve.
  • Complications due to secondary infection are infrequent.
  • Scaling or peeling occurs a few days following exposure.
  • Nausea, abdominal cramping, weakness and malaise, fever, chills, and headache may also occur, most often with severe sunburn.
  • Patients with severe sunburn may have a rapid pulse rate.

Causes

Although exposure to UV-B light causes most sunburns, use of tanning salons and home tanning devices have made UV-A–induced sunburn increasingly common.

  • Severe sunburns often result after falling asleep at the beach or under a UV lamp or from prolonged exposure at swimming areas.
  • Both outdoor work and outdoor recreational activities are risk factors for sunburn.
  • Sunburn is common when residents of northern latitudes have prolonged sun exposure while vacationing in southern latitudes or near the equator.
  • Outdoor exposure on cloudy days may provide people a false sense of protection. As much as 80% of UVR penetrates clouds.
  • Reflective surfaces such as sand, snow, water, and cement may contribute to sunburn development.
  • Increased humidity reduces the threshold for erythema caused by UVR.
  • Medical treatments that expose patients to UV-B and UV-A may cause a sunburn reaction.
  • UV-C exposure from welding arcs, bactericidal lamps, and mercury arc lamps may cause sunburn.
  • The degree of sunburn depends on the duration and intensity of exposure, patient's skin type or complexion, and previous conditioning of the skin.
  • The unit of measurement of a sunburn is the MED, defined as the minimum UV-B exposure required to produce a clearly marginated erythema in an irradiated site following a single exposure. MED is expressed as mJ/cm2.
  • Phototoxic reactions resulting in a sunburn reaction usually occur in the UV-A range and can be caused by topical and systemic agents. In contrast to photoallergic reactions, phototoxic reactions may occur after the initial exposure and do not affect areas of the body that were protected from light.
  • Topical agents causing phototoxic reactions include the following:
    • Bergamot oil (5-methoxypsoralen)
    • Coal tar derivatives
      • Acridine
      • Anthracene
      • Fluoranthene
      • Naphthalene
      • Phenanthrene
      • Pyridine
      • Thiophene
    • Dyes or pigments
      • Acriflavine
      • Anthraquinone
      • Cadmium sulfate
      • Eosin
      • Methylene blue
      • Rose bengal
      • Toluidine blue
    • Methoxsalen
    • Plants (furocoumarins)
      • Leguminosae family
      • Moraceae family - Figs
      • Rutaceae family - Bergamot orange, gas plant, lemon, lime
      • Umbelliferae family - Angelica, anise, bishop weed, celery, cow parsley, dill, fennel, giant hogweed, wild parsnip, wild carrot
    • Retinoids (after continued use)
      • Adapalene
      • Tazarotene
      • Vitamin A acid
    • Tar
  • Systemic agents causing phototoxic reactions include the following:
    • Antimicrobials
      • Ceftazidime
      • Griseofulvin
      • Quinolones - Ciprofloxacin, nalidixic acid, norfloxacin, ofloxacin
      • Sulfonamides
      • Tetracyclines - Doxycycline, tetracycline
      • Trimethoprim
    • Antineoplastic agents
      • Dacarbazine
      • 5-Fluorouracil
      • Vinblastine
    • Antimalarials - Quinine
    • Cardiac medications
      • Amiodarone
      • Quinidine
    • Diuretics
      • Furosemide
      • Hydrochlorothiazide
    • Hematoporphyrin
    • Hypolipidemics
      • Clofibrate
      • Atorvastatin
    • Nonsteroidal anti-inflammatory drugs (NSAIDs)
      • Diclofenac
      • Ibuprofen
      • Indomethacin
      • Ketoprofen
      • Naproxen
      • Piroxicam
      • Sulindac
      • Tiaprofenic acid
    • Psoralens
      • Methoxsalen
      • Trioxsalen
    • Antipsychotics
      • Alprazolam
      • Chlordiazepoxide
      • Chlorpromazine
      • Desipramine
      • Imipramine
      • Perphenazine
      • Prochlorperazine
      • Thioridazine
      • Trifluoperazine
    • Retinoids
      • Acitretin
      • Isotretinoin
    • Sulfonylureas - Tolbutamide
    • Sulfites

More on Sunburn

Overview: Sunburn
Differential Diagnoses & Workup: Sunburn
Treatment & Medication: Sunburn
Follow-up: Sunburn
Multimedia: Sunburn
References
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Further Reading

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Keywords

sunburn, sun burn, acute sun damage, acute sunburn reaction, erythema solare, tanning, sun sensitivity, ultraviolet radiation, UVR, ultraviolet B, UV-B, ultraviolet A, UV-A, UV-A I, UV-A II, ultraviolet C, UV-C, ultraviolet index, ozone layer, ozone loss, greenhouse gas, skin protection, skin protection factor, SPF, minimal erythema dose, MED, sunscreen

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Contributor Information and Disclosures

Author

Lyn Guenther, MD, Professor, Department of Medicine, Division of Dermatology, University of Western Ontario, London, Canada
Lyn Guenther, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, Canadian Dermatology Association, Canadian Medical Association, College of Physicians and Surgeons of Ontario, International Society for Dermatologic Surgery, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Society for Investigative Dermatology, and Society for Pediatric Dermatology
Disclosure: L'Oreale Consulting fee Consulting

Coauthor(s)

Benjamin Barankin, MD, FRCPC, Dermatologist, Private Practice, Toronto
Benjamin Barankin, MD, FRCPC is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, Canadian Dermatology Association, Canadian Medical Association, International Society of Dermatology, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Julie Powell, MD, Assistant Professor of Pediatrics, Director, Department of Pediatrics, Division of Dermatology, Ste-Justine Hospital, University of Montreal, Quebec, Canada
Disclosure: Nothing to disclose.

Medical Editor

Kevin P Connelly, DO, Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University; Medical Director, Paws for Health Pet Visitation Program
Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Nothing to disclose.

Managing Editor

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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