A sunburn is a radiation burn that affects primarily the skin and other tissues such as the eyes and lips. Characterized by redness, irritation, and pain, it is generally caused by prolonged and excessive exposure to a subtype of ultraviolet radiation called ultraviolet B or UVB rays.
The Sun is the primary source of UV radiation on Earth. About 10 percent of its electromagnetic radiation output is ultraviolet. However, tanning beds, incandescent lamps, gas-discharge light, welding torches, and ultraviolet LED lamps are also artificial sources.
Nevertheless, the pain and discomfort associated with sunburns, as well as the other damages and potential carcinogenic risk of overexposure to UV rays have necessitated the use of sunscreens that contain either physical or chemical blockers or absorbents and sun protective clothing.
Understanding the Mechanism of Sunburn: Specific Causes and Effects
The science behind how and why the skin and other tissues develop sunburn after exposure to ultraviolet radiation is considerably straightforward. For starters, it is important to note that UV is a form of electromagnetic radiation that sits after the visible light and before x-rays in the electromagnetic spectrum.
Electromagnetic Radiation and Photon Energy
Note that the spectrum consists of other forms of electromagnetic radiation ranging from extreme low-frequency radio waves and extreme high-frequency microwaves to x-rays and gamma radiation. These forms carry radiant or photon energy. In general, the amount of energy carried by a photon is directly proportional to its electromagnetic frequency and inversely proportional to its wavelength.
Forms with shorter wavelengths and higher frequencies essentially carry more photon energy. In other words, the amount of photon energy increases as one moves from the left to the right of the electromagnetic spectrum. An infrared light carries more energy than radio waves and microwaves. However, visible light carries more energy than infrared.
UV radiation fundamentally damages living tissues and organs because it carries more radiant or photon energy than visible light. The damage transpires at the molecular level. To illustrate further, when the skin absorbs a photon of UV, an electron that constitutes a specific skin cell enters a high energy state that disrupts molecular and cellular functions and processes.
Specific Molecular and Cellular Causes of Sunburn
A sunburn is not a simple injury akin to burns caused by exposure to heat or other hot objects. Rather, this type of radiation form is an acute cutaneous inflammatory response of the human body due to the damages caused by UVB rays. Remember that UVB is the primary culprit behind this radiation burn, and UVA does not play any role at all.
When UVB penetrates the skin, it can damage several components of the tissues and the cells. Specific damage to noncoding RNAs found in a type of skin cell called keratinocytes triggers a series of events that result in the release of tumor necrosis factor-alpha or TNF-alpha.
More specifically, UVB-damaged skin cells release the damaged noncoding RNAs. The release prompts surrounding healthy cells to release cell signaling proteins called cytokines to remove the damaged skin cells. TNF-alpha is a specific cytokine.
The release of this signaling molecule in a particular location alerts the other cells of the immune system. These immune cells and other cytokines migrate to the affected area to respond to the RNA damage by removing the affected skin cells. The study of Bernard et al. concluded that TNF-alpha is central to an inflammatory response caused by UVB damage that manifests visibly as a sunburn.
Other Mechanisms Due to Damage by UVB Irradiation
Researchers have also explored other biological, cellular, and molecular mechanisms to explain further the science behind the formation of sunburns. A dated research by Gilchrest, Soter, Stoff, and Mihm that studied the histopathology of sunburn explained that UVB exposure induces different changes occurring in different layers of the skin.
For example, in the epidermis, the damage due to radiation results in the loss of resident macrophages found in the skin called Langerhans cells and the formation of liquid-filled compartments in keratocytes. In the dermis, endothelial cells become enlarged, causing reddening, and mast cells degranulate, resulting in edema.
Other studies by B. B. Shih et al. and Lopes and McMahon explained that UVB rays are responsible for inducing the formation of DNA lesions called thymine-thymine cyclobutane dimers. The formation of these dimers triggers the body to mount a DNA repair response.
The response constitutes cell apoptosis or programmed cell death and the release of inflammatory markers such as prostaglandins, reactive oxygen species, and bradykinin. The process ultimately results in painful vasodilation and edema that translate into the classic symptoms of sunburn characterized by red and painful skin.
Furthermore, the separate studies by Bishop et al. and Dawes et al. noted that the pain and sensitivity associated with radiation burn due to UVB damage prompt the release of specific types of cytokines such as CXCL5 and activation of peripheral nociceptors. The process results in the overactivation of the pain receptors of the skin.
FURTHER READINGS AND REFERENCES
- Bernard, J. J., Cowing-Zitron, C., Nakatsuji, T., Muehleisen, B., Muto, J., Borkowski, A. W., Martinez, L., Greidinger, E. L., Yu, B. D., and Gallo, R. L. 2012. “Ultraviolet Radiation Damages Self-Noncoding RNA and is Detected by TLR3.” Nature Medicine. 18(8): 1286-1290. DOI: 1038/nm.2861
- Bishop, T., Marchand, F., Young, A. R., Lewin, G. R., and McMahon, S. B. 2010. Ultraviolet-B-Induced Mechanical Hyperalgesia: A Role for Peripheral Sensitization. Pain. 150(1): 141-152. DOI: 1016/j.pain.2010.04.018
- Dawes, J. M., Calvo, M., Perkins, J. R., Paterson, K. J., Kiesewetter, H., Hobbs, C., Kaan, T. K. Y., Orengo, C., Bennett, D. L. H., and McMahon, S. B. 2011. “CXCL5 Mediates UVB Irradiation-Induced Pain.” Science Translational Medicine. 3(90): 90ra60-90ra60. DOI: 1126/scitranslmed.3002193
- Gilchrest, B. A., Soter, N. A., Stoff, J. S., and Mihm, M. C., Jr. 1981. “The Human Sunburn Reaction: Histologic and Biochemical Studies. Journal of the American Academy of Dermatology.” 5(4): 411-422. DOI: 1016/s0190-9622(81)70103-8
- Lopes, D. M., and McMahon, S. B. 2015. “Ultraviolet Radiation on the Skin: A Painful Experience?” CNS Neuroscience & Therapeutics. 22(2): 118-126. DOI: 1111/cns.12444
- Shih, B. B., Farrar, M. D., Cooke, M. S., Osman, J., Langton, A. K., Kift, R., Webb, A. R., Berry, J. L., Watson, R., Vail, A., de Gruijl, F. R., and Rhodes, L. E. 2018. “Fractional Sunburn Threshold UVR Doses Generate Equivalent Vitamin D and DNA Damage in Skin Types I-VI but with Epidermal DNA Damage Gradient Correlated to Skin Darkness.” The Journal of Investigative Dermatology. 138(10): 2244-2252. DOI: 1016/j.jid.2018.04.015