Ultraviolet (UV) radiation is a segment of the electromagnetic spectrum characterized by wavelengths shorter than visible light. This radiation is naturally emitted by the sun and is categorized into three main types based on wavelength: UVA, UVB, and UVC. Ultraviolet B (UVB) light is defined by its intermediate wavelength and high energy, which enables it to induce significant photochemical reactions upon reaching the Earth’s surface and interacting with biological tissues. The effects of UVB on human health are complex, spanning from beneficial biochemical processes to detrimental cellular damage.
Defining the Wavelength
The UVB spectrum encompasses wavelengths ranging from approximately 280 to 315 nanometers (nm). This medium-wave radiation is a fraction of the solar UV light that penetrates the atmosphere. Unlike the shortest UVC rays, which are entirely blocked, and the longest UVA rays, which pass through almost unimpeded, most UVB is absorbed by the stratospheric ozone layer.
The amount of UVB that reaches the ground is highly dependent on factors like the angle of the sun, altitude, and ozone concentration. Consequently, UVB intensity is greatest near the equator, at high altitudes, and during summer months around midday. Upon contact with the skin, UVB light is largely absorbed by the epidermis, the outermost layer, and penetrates only minimally into the deeper dermis.
The Role in Vitamin D Production
The constructive effect of UVB light involves initiating the synthesis of Vitamin D3 in the skin. This process begins when a precursor molecule, 7-dehydrocholesterol (7-DHC), is exposed to UVB photons. The energy causes the B-ring of the 7-DHC molecule to break, resulting in the formation of pre-vitamin D3.
Pre-vitamin D3 undergoes a temperature-dependent rearrangement, known as thermal isomerization, converting it into Vitamin D3 (cholecalciferol). This Vitamin D3 is transported via the bloodstream to the liver. In the liver, it undergoes its first hydroxylation step to become 25-hydroxyvitamin D, the major circulating form used to assess Vitamin D status.
The efficiency of this synthesis pathway is influenced by several external and personal factors. Latitude, time of day, and season determine the intensity of UVB radiation reaching the skin’s surface. For example, at higher latitudes, the sun’s angle during winter months is too low for sufficient UVB photons to penetrate the atmosphere and enable production.
A person’s skin pigmentation also plays a significant role in determining synthesis rates. Melanin, the pigment responsible for skin color, acts as a natural absorber of UV radiation, effectively competing with 7-DHC for UVB photons. Individuals with darker skin pigmentation require longer exposure times to synthesize the same amount of Vitamin D3 compared to those with lighter skin. The process is self-regulating, as continued exposure to UV light can convert pre-vitamin D3 into inactive byproducts, preventing excessive Vitamin D production.
Acute and Chronic Skin Damage
Despite its constructive role, uncontrolled exposure to UVB light is a significant cause of both immediate and long-term tissue damage. The most common acute reaction is sunburn, or solar erythema, which is an inflammatory response to overexposure. UVB is recognized as the most effective waveband for inducing this redness in human skin.
Sunburn results from direct injury to the DNA within epidermal cells, particularly the keratinocytes. This damage triggers an inflammatory cascade, involving the release of mediators such as histamine and various cytokines. The resulting biological response includes vasodilation, which causes the characteristic visible redness that typically peaks around 24 hours after exposure. Cells that sustain irreparable DNA damage are programmed to undergo apoptosis, or cell death, appearing microscopically as “sunburn cells.”
On a chronic level, the danger of cumulative UVB exposure stems from its ability to directly alter the structure of DNA. The radiation is absorbed by the pyrimidine bases (thymine and cytosine) in the DNA strand. This absorption causes adjacent pyrimidines to bond together abnormally, forming photoproducts, primarily cyclobutane pyrimidine dimers (CPDs) and (6-4) photoproducts.
These dimers physically distort the DNA helix, disrupting the processes of replication and transcription. While the body possesses repair mechanisms, errors or failure to repair the damage can lead to permanent gene mutations. These mutations, often referred to as a “UV signature,” are implicated in the development of non-melanoma skin cancers, such as basal cell carcinoma and squamous cell carcinoma.
Cumulative UVB exposure also contributes significantly to photoaging, characterized by wrinkles and a loss of skin elasticity. The radiation breaks down the structural proteins in the dermis, specifically collagen and elastin fibers. This degradation compromises the skin’s supportive scaffolding, leading to the formation of fine lines and a leathery texture over time.
Clinical Phototherapy Uses
In a controlled medical setting, UVB light is intentionally utilized as a therapeutic tool, a practice known as phototherapy. This clinical application focuses on treating various chronic inflammatory skin conditions. Narrowband UVB (NB-UVB) therapy is the most common approach, using a precise wavelength band around 311 to 312 nm.
This narrow band is selected because it delivers the desired therapeutic effect while minimizing the wavelengths that cause sunburn and deep DNA damage. The mechanism of action involves the light suppressing overactive localized immune responses in the skin. NB-UVB effectively manages conditions like psoriasis, which is characterized by rapid skin cell growth, by modulating the activity of immune cells and slowing down the excessive proliferation of skin cells.
NB-UVB is also a treatment option for vitiligo, a condition resulting in the loss of skin pigment. In this case, the light can stimulate the remaining melanocytes—the pigment-producing cells—to encourage repigmentation in the white patches. Treatment protocols typically involve exposing the affected areas to the light source several times a week in short, controlled sessions.