Author:

• Nathan Krah

Deputy Editor:

• Adriene Pavek

Faculty Reviewers:

• Chloe Ekelem
• Julia A Curtis

Publish date: Posted on March 8, 2020October 23, 2023
Last updated: October 23, 2023

Keywords #

sunburn
sun avoidance
sunscreen
UVA
UVB
skin cancer
melanoma
SPF

Diagnosis #

Sunburn is an acute inflammatory process of the skin that results from excessive exposure to ultraviolet (UV) radiation. Sunburn is usually secondary to increased sun exposure but may also be caused by artificial sources of UV light, such as tanning beds and acrylic nail-curing lamps.  Clinical presentations typically range from mild cases with minor skin erythema to severe cases with painful erythema and coexisting edema, vesiculation, and blistering.  Severe sunburn induces increased production of local prostanoids and bradykinin, which cause tissue swelling. Increased pain sensitivity is mediated by chemokines, such as CXCL5, from immune cells infiltrating the area which activate resident nerve fibers.[4]

Susceptibility to sunburn varies among individuals and is determined by the ability of melanin to protect keratinocyte DNA, which correlates to traits such as skin, eye and hair color. Individuals with Fitzpatrick type I skin (fair skin prone to freckling and often associated with blonde or red hair) are most susceptible to UV-induced sun damage, while darker skin tones (Fitzpatrick type IV-VI) typically require higher doses of UV radiation to demonstrate erythema or burn.[11]

Importantly, sunburn and cumulative lifetime UV exposure are the most important modifiable risk factors for the development of skin cancers, including melanoma. Both UVA and UVB exposure can cause DNA damage, however only UVB radiation causes sunburn, likely through an interferon-dependent mechanism.[8,10] UVB radiation damages DNA by causing pyrimidine dimers (thymine) and subsequent double-strand breaks. UVA radiation damages DNA by creating free radicals, which cause single strand DNA breaks.  Either mechanism of DNA damage can induce replication errors, which propagate mutations if the apoptotic response (programmed cell death) is evaded. Accumulation of these mutations, especially in specific genes like BRAF, ultimately leads to pre-malignant behavior of melanocytes. [5] Other noteworthy physiologic consequences of UVA exposure include damage to collagen fibers and elastic fibers which accelerate the appearance of aging of the skin.

Key Concepts #

• Sunburn is a clinical diagnosis; it is an acute inflammatory response within the skin to excessive UV radiation.
• Fair skin, light-colored eyes, and light hair color have been associated with higher risk for sunburn.
• As UV radiation causes DNA damage, sunburn increases the risk for all types of skin cancer, including melanoma.
• Sunburn is self-resolving, but symptomatic treatment options include cold compresses, NSAIDs, aloe vera based gels. Severe burns may require parenteral fluid replacement and pain control.
• Prevention of sunburn should be encouraged for all patients. Strategies include avoiding direct sun exposure between 10 am and 2 pm, wearing wide-brimmed hats and long sleeves, and application of broad spectrum, sun protection factor (SPF) 50 (or greater) sunscreen in all sun-exposed areas.
• Despite recent controversy about systemic absorption of sunscreen ingredients, the American Academy of Dermatology and Federal Drug Administration continue to recommend sunscreen use, as the benefits of skin cancer prevention presumably outweigh the unidentified harms of ingredient absorption.

Epidemiology #

Sunburn is common and mild cases rarely require medical care, making the incidence difficult to accurately measure. One recent study analyzed data from the National Health Interview Survey (a cross-sectional, nationally representative sample of the adult US civilian population) and found that over a third of adults experienced an average of 2.4-2.6 sunburns a year (34.2%, 37%, and 34.1% in 2005, 2010, and 2015, respectively).[7] In this study, non-Hispanic white adults >18 years of age, were most likely to experience sunburn and the percentage of individuals reporting sunburn decreased as age increased.[7] These results suggest that education about long-term sun damage, especially to young adults with fair (Fitzpatrick type-1 & 2) skin, would be highest yield in prevention of morbidity.

Clinical Features #

• Mild erythema
• Local edema, vesiculation, blistering in sun-exposed areas

Differential Diagnoses #

The differential diagnosis for sunburn is narrow but there are important considerations if appropriate for the clinical context:

• Phototoxic reactions caused by medications, such as tetracyclines, amiodarone, retinoids, fluoroquinolones, 5-Fluorouracil, furosemides, thiazides, NSAIDs, and vinblastine.
• Photoallergic type IV hypersensitivity; this could be precipitated by medications and present with intense pruritis (unlike phototoxic reactions).
• Phytophotodermatitis – UV radiation causes damage after the skin has come into contact with a photosensitizer, such as meadow grass or lime juice.
• Solar urticaria – characterized by UV-induced wheals that appear within minutes of sunlight exposure.

Other systemic diseases that have skin manifestations exacerbated by sunlight, such as systemic lupus erythematosus, dermatomyositis and rosacea should be kept in mind.

Treatment #

Sunburn is a self-limiting medical problem and will resolve with time and supportive care. Mainstays of therapy focus on symptom/pain relief. The American Academy of Dermatology (AAD) recommends treating sunburn as early as possible through 6 mechanisms:

1. Avoidance of further sun exposure. If the patient must be in the sun, cover the sun-burned areas with clothing.
2. Application of cool water to the burned areas to help control pain. Follow with moisturizer to trap moisture in the skin.
3. Use a moisturizer containing aloe vera to help soothe the affected area. Avoid treating the affected area with numbing medications, such as benzocaine, as this can further irritate the skin.
4. Ibuprofen and other NSAIDs can help alleviate swelling and discomfort.[6]
5. Stay hydrated by drinking more water, as sunburn draws fluid out of the body.
6. If the skin blisters, leave them intact. The blister roof acts as a sterile band-aid and can help with healing.

Prevention: To prevent sunburn and potential sequelae, such as skin cancer, the AAD suggests avoiding direct skin exposure to sunlight (seeking shade) between 10 am and 2 pm, in addition to wearing protective clothing, such as a wide-brimmed hat, long sleeves, pants, and sunglasses.[3] Whenever possible the AAD recommends application of a broad-spectrum, water-resistant sunscreen with SPF 30 or higher on sun-exposed skin.

While sun avoidance and protective clothing are relatively intuitive, choosing which sunscreen to use can be overwhelming. The AAD officially recommends broad-spectrum sunscreen, as this designation ensures that patients are protected from both UVA- and UVB -induced photodamage. SPF is a function of UV energy (millijoules) required to induce minimal erythema, the higher the SPF the more UVB must be applied to the skin to reach minimal erythema. SPF is often misinterpreted as the amount of time required for UVB to induce erythema/burn, however multiple factors such as time of day, fairness of skin, and thickness of layer applied affect the SPF needs of each individual. Regardless of SPF, it is very important to apply sunscreen correctly – in a thick layer and repeatedly every two hours.

 

Sunscreens can be categorized into physical or chemical blockers. Physical sunscreens contain either titanium dioxide or zinc oxide, molecules that deflect and scatter UV radiation away before it reaches skin cells. Chemical sunscreens contain UV filters, such as oxybenzone, that absorb UV radiation. Unlike physical creams, chemical sunscreens do not leave a chalky or white residue on the skin, which many patients find more cosmetically appealing.

Recent studies conducted by the Food and Drug Administration (FDA) received media attention for showing that when chemical sunscreen is used at maximal recommended dosage, active ingredients, such as avobenzone, oxybenzone, octocrylene, and ecamsule are absorbed through the skin, leading to systemic levels above the FDA’s threshold for patient safety. [9] While this preliminary data is intriguing, it does not provide evidence of physiologic harm associated with absorption of these ingredients. Data from animal models, however, indicate possible health risks, such as endocrine disruption associated with avobenzone and oxybenzone.[12] There is also ongoing research regarding effects of the sunscreen ingredient, oxybenzone, on coral reefs. Some studies have shown a deleterious effect on coral health.[13]

Slide Viewer #

https://utahderm.med.utah.edu/image-viewer/

References #

1. Adamson AS, and Shinkai, K. (2020) Systemic Absorption of Sunscreen: Balancing Benefits with Unknown Harms. JAMA. 323(3):223-224. PMID: 31961400
2. American Academy of Dermatology: “How to Treat Sunburn.” (https://www.aad.org/public/everyday-care/injured-skin/burns/treat-sunburn). Accessed 3/19/2020.
3. American Academy of Dermatology: “Prevent Skin Cancer.”

(https://www.aad.org/public/diseases/skin-cancer/prevent/how). Accessed 3/19/2020.

4. Dawes JM, Calvo M, Perkins JR, Paterson KJ, Kiesewetter H, Hobbs C, Kaan TK, Orengo C, Bennett DL, and McMahon SB. (2011) CXCL5 mediates UVB irradiation-induced pain. Science Translational Medicine. 3(90): 90ra60. PMID: 21734176.
5. Davies H et al., (2002) Mutation of the BRAF gene in human cancer. Nature 417, 949-954.
6. Edwards EK, Horwitz SN, Frost P. (1982) Reduction of the erythema response to UV light by nonsteroidal anti-inflammatory agents. Arch Dermatol Res 272:263
7. Holman, DM. et al. (2019) Sunburn prevalence among US adults, National Health Interview Survey 2005, 2010, and 2015. J Am Acad Dermatol. 80(3): 817-820. PMID: 30744879
8. Khan AQ, Travers JB, Kemp MG. (2019) Roles of UVA radiation and DNA damage response in melanoma pathogenesis. Environ Mol Mutagen. 59 (5): 438-460.
9. Matta MK, Zusterzeel R, Pilli NR, et al.  (2019) Effect of sunscreen application under maximal use conditions on plasma concentration of sunscreen active ingredients: a randomized clinical trial. JAMA. 321(21): 2082-2091.
10. Terui T, Tagami H. (2000) Mediators of inflammation involved in UVB erythema. J Dermatol Sci, 23 Suppl 1:S1
11. Wolff K, Johnson R, Saavedra A (2013). Fitzpatrick’s color atlas and synopsis of clinical dermatology(7th ed.). New York: McGraw-Hill Medical.
12. Yeager DG, Lim HW. (2019) What’s new in photoprotection: a review of new concepts and controversies.Dermatol Clin. 37(2):149-157.
13. Wijgerde T, van Ballegooijen M, Nijland R, van der Loos L, Kwadijk C, Osinga R, Murk A, Slijkerman D. Adding insult to injury: Effects of chronic oxybenzone exposure and elevated temperature on two reef-building corals. Sci Total Environ. 2020 Sep 1;733:139030. doi: 10.1016/j.scitotenv.2020.139030. Epub 2020 May 4. PMID: 32446051.