Ultraviolet A or UVA and Ultraviolet B or UVB are forms of electromagnetic radiation and examples of an electromagnetic wave critical to understanding and addressing the negative effects of prolonged and excessive exposure to sunlight on the skin and overall human health.
Both are specific subtypes of ultraviolet radiation. The Sun is their main source on Earth. However, artificial sources include incandescent light bulbs, gas-discharge lamps, excimer laser, and UV light-emitting diodes, among others.
The formulation of sunscreens is based primarily on utilizing the properties of active ingredients that can neutralize UVA and UVB. Take note that these two affect the skin and human bodies differently. Ideal sunscreens should provide broad-spectrum protection.
The Different Ways UVA and UVB Rays Damage the Skin and Affect Health
Basics of UV Damage
Electromagnetic radiation is fundamentally a stream of mass-less particles called photons. Each photon carries photon energy. Within the electromagnetic spectrum, the amount of energy carried by a photon is directly proportional to its electromagnetic frequency and inversely proportional to its wavelength.
Subtypes of UV radiation have shorter wavelengths and higher frequencies than visible light and other forms of electromagnetic radiation that precede them within the electromagnetic spectrum. Hence, they carry more photon energy. It is for this reason that exposure to UVA and UVB rays can be harmful to tissues.
When a photon of UV is absorbed into the skin, it excites a particular electron that constitutes a specific skin cell. An electron at a high-energy state disrupts internal cellular functions and processes such as cellular integrity, repair, replication, and metabolism. Damage from UV exposure essentially transpires at the molecular level.
UVA vs. UVB Damage
To understand why the effects of UVA and UVB differ, note that the different subtypes of ultraviolet radiation are classified according to their wavelengths, frequencies, and the photon energy they carry. For example, UVA rays have wavelengths ranging from 315-400nm while UVB rays have wavelengths ranging from 280-315nm.
Damages from UVA and UVB rays overexposure have different mechanisms because they have different wavelengths. UVA rays penetrate deeper into the skin because of their longer wavelengths while UVB rays affect mostly the outer layer of the skin and do not penetrate deeply beyond other layers because they have medium wavelengths.
It is also worth mentioning that irradiation from Ultraviolet B is more damaging to the surface of the skin because specific rays carry more photon energy than Ultraviolet A rays. The difference between UVA rays and UVB rays fundamentally centers on their different wavelengths, which translate further to the different amount of photon energy they carry.
Below are the specific characteristics and effects of excessive exposure to Ultraviolet A rays:
Photoaging Due to Collagen Breakdown
Photo-accelerated aging or photoaging is premature aging of the skin resulting from years of cumulative damages due to repeated exposure to sunlight. Visible signs include wrinkling and sagging, sallowness and hyperpigmentation, dryness and roughness, and loss of skin tone.
UVA rays penetrate deep into the dermis and induce damages that trigger an overproduction of elastin that in turn, prompts the production of enzymes called matrix metalloproteinases. The condition is called elastosis. Matrix metalloproteinases are responsible for breaking down collagen.
Elastosis essentially replaces collagen with elastin. Collagen provides strength and rigidity. Elastin provides elasticity. Both are important in maintaining the firmness and tightness, as well as the overall youthful appearance of the skin.
Depletion of Retinol or Vitamin A
Ultraviolet A radiation alters the ability of the skin cells called keratinocytes and melanocytes to recognize and metabolize retinoic acid and synthesize it to retinol or Vitamin A. Repeated exposure to this radiation results in epidermal retinol depletion.
Vitamin A is critical to the production of collagen fibers, as well as the formation of healthy blood vessels that supply the skin with nutrition. Note that Vitamin A provides protection against UVB rays. Hence, retinol depletion is also responsible for collagen loss and photoaging, as well as for increasing risks from UV radiation exposure.
The retinol depletion caused by UVA rays is largely independent from oxidative stress. Studies suggest that they set off photochemical reactions whenever they penetrate the dermis and affect particular cellular components.
Formation of Cataracts
The lenses in human eyes are clear. Cells in these lenses contain proteins properly aligned to let light through. Cataracts reduce the transparency of these cells and the overall transparency of the lens. A person with a cataract sees faded colors, blurry or double vision, halos around light, and trouble seeing at night.
Ultraviolet A radiation can result in cataract formation. More specifically, photons of UVA rays can clump the proteins in the lens due to oxidative stress. The clumping reduces the transparency of the lens because it prevents light to pass through.
The human body has a mechanism for preventing this clumping through a special set of proteins called chaperones. However, repeated oxidative stress due to different trigger and risk factors, such as repeated exposure to UV radiation, can outperform this natural mechanism, thus resulting in the formation of cataracts.
Role in Skin Cancer Formation
UVA rays that penetrate the skin can cause indirect damages to the DNA of skin cells. To explain further, irradiation produces unstable hydroxyl and oxygen molecules with a missing electron. These unstable molecules are collectively called free radicals.
Electrons are found in pairs. Free radicals scavenge for missing electrons from other molecules. Scavenging for electrons essentially damages the cells at the molecular level. The damage can also affect cellular genetic material or DNA. Altered DNA can lead to replication errors and cell mutations.
The body normally responds to damaged DNA and cells either through repair or by removing them completely via an immune response. However, a buildup of DNA errors and cellular mutations can go out of control. Overexposure to UVA rays has been linked to basal cell carcinoma and squamous cell carcinoma.
The following the specific characteristics and effects of excessive exposure to Ultraviolet B rays:
Radiation Burn Called Sunburn
A noteworthy difference between UVA and UVB rays is that the latter are responsible for sunburns. A sunburn is a radiation burn that affects the skin and other living tissues. Classical signs of this condition include redness, irritation, pain, and discomfort.
Remember that sunburns and other radiation burns are different from direct burns or injuries caused by contact or exposure to fire or hot objects. They are a form of acute cutaneous inflammatory response resulting from UVB radiation penetrating the skin and damaging its cellular and molecular components such as RNAs and DNAs.
A damaged skin cell prompt nearby skin cell to release cytokines that in turn, would result in the migration of immune cells and production of more signaling proteins to the affected area. The process can transpire in both the epidermis and the dermis. The classical signs of sunburns are fundamentally a product of this immune response.
Formation of Malignant Melanoma
Ultraviolet B radiation is also primarily responsible for most incidents of the most dangerous type of skin cancer called malignant melanoma. Specifically, melanoma develops from melanocytes, a type of skin cell that produces the brown pigment called melanin. Those with low levels of melanin have a high risk of developing this type of skin cancer.
Compared to UVA rays, exposure to UVB rays can cause direct damage to the DNA. The damage transpires because irradiation distorts the shape of the DNA. Unfixed distortions can lead to a buildup of genetic errors and cellular mutations. Melanoma can develop if these mutations affect melanocytes.
Note that melanoma is the most dangerous type of skin cancer because it tends to spread to other parts of the body if not detected and treated early and properly. The metastatic nature of this cancer transpires if the affected melanocytes grow deeper into the skin to reach the blood vessels and lymphatics, and spread further to various organs.
Also Responsible for Retinol Depletion
Similar to UVA radiation, UVB radiation also alters the capability of skin cells to metabolize retinoic acid and convert them into retinol or Vitamin A. Depletion due to UVB exposure is based primarily on oxidative stress.
The oxidative stress resulting from the production of free radicals induces specific damages to skin cells and their cellular or molecular components. Specific damages to specific areas or components inhibit the ability of the skin to synthesize Vitamin A. Further depletion of retinol occurs with the damaging effects of UVA radiation.
Remember that Vitamin A is essential in collagen production. Hence, retinol depletion due to UVB radiation indirectly causes premature skin aging. In addition, Vitamin A provides protection against this subtype of ultraviolet radiation. Further depletion makes the skin more vulnerable to the other harmful effects of irradiation.
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
- Andersson, E., Rosdahl, I., Törmä, H., and Vahlquist, A. 1999. “Ultraviolet Irradiation Depletes Cellular Retinol and Alters the Metabolism of Retinoic Acid in Cultured Human Keratinocytes and Melanocytes.” Melanoma Research. 9(4): 339-346. DOI: 1097/00008390-199908000-00001
- 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
- Sorg, O., Tran, C., Carraux, P., Didierjean, L., Falson, F., and Saurat, J.-H. 2002. “Oxidative Stress-Independent Depletion of Epidermal Vitamin A by UVA.” Journal of Investigative Dermatology. 118(3): 513-518. DOI: 1046/j.0022-202x.2002.01674.x