Sunburn is a form of skin damage caused by overexposure to ultraviolet (UV) radiation from the sun. It results in red, painful skin that feels hot to the touch. But why does sunburn cause redness specifically? The reddening is caused by increased blood flow to the skin as part of the body’s inflammatory response to UV damage. When skin cells are bombarded by too much UV radiation, it causes oxidative damage and inflammation. The inflammatory response prompts blood vessels near the surface of the skin to dilate and become leaky, which allows more blood to flow into the area, causing reddening.
What causes sunburn?
Sunburn is caused by overexposure to UVB and UVA rays from sunlight. UVB rays penetrate the top layers of skin and are the primary cause of sunburn. UVA rays penetrate deeper into the skin and contribute to skin aging. Here’s an overview of how sunburn develops:
– UV rays damage skin cells – The DNA in skin cells absorbs UV photon energy, causing damage to the DNA structure. This generates free radicals that can kill skin cells.
– Inflammation triggered – Damaged skin cells release inflammatory mediators including prostaglandins, cytokines, and histamine. This triggers an inflammatory response.
– Blood vessels dilate – Inflammatory mediators prompt blood vessels in the skin to expand and become leakier. This allows more blood to flow into the sunburned area.
– Redness and pain – Increased blood flow causes reddening. Inflammation and nerve irritation leads to pain and tenderness.
So in summary, sunburn is an inflammatory reaction to direct UV damage of skin cells and structures. The inflammatory response is what causes the characteristic red color.
UVB rays cause most sunburn
UVB rays in sunlight are the primary cause of sunburn because they penetrate the top layers of the epidermis where they are readily absorbed by DNA. UVB has a shorter wavelength than UVA, so it is absorbed by DNA rather than passing deeper into skin. UVB causes direct DNA damage that generates free radicals and kills keratinocytes. This triggers the inflammatory reaction.
While both UVA and UVB contribute to sun damage, UVB induces more reddening and sunburn pain. However, UVA penetrates deeper and can still cause some inflammation and vasodilation. The sun’s UVB rays are most intense between 10am and 4pm.
Oxidative damage triggers inflammation
When UVB radiation is absorbed by DNA, it causes adjacent molecules to lose electrons, forming free radicals. These highly reactive molecules then damage other cell components like proteins and lipids. The oxidative damage directly kills skin cells and triggers the inflammatory response.
Inflammatory mediators released in response to this free radical damage include:
– Cytokines like interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α)
– Vasodilators like prostaglandins and histamine
– Proteinases that allow inflammatory factors to spread
These substances increase blood flow, fluid leakage, and stimulate pain nerve fibers, causing the red, swollen, painful burn.
Why does increased blood flow cause redness?
The characteristic redness of sunburn is caused by increased blood flow to the inflamed area. Here’s a closer look at why augmented blood flow leads to skin reddening:
– More blood vessels dilate – Inflammatory mediators prompt tiny blood vessels (capillaries) near the skin’s surface to expand and fill with more blood. This is known as vasodilation.
– Blood vessels get “leaky” – Inflammation makes capillaries more permeable so fluid leaks out into the tissue. This allows more red blood cells to enter the area.
– Light absorption changes – When there are more red blood cells in the swollen tissue, it changes light absorption. Red blood cells contain hemoglobin that absorbs green/yellow light, making the skin appear red.
– Blood pools near skin – Gravity causes more blood to pool in capillaries of the head, shoulders and upper skin when standing upright after sun exposure. This accentuates the redness.
So in summary, inflammatory mediators make capillaries dilate and become more permeable, allowing a greater volume of red blood cells to enter the sunburned skin. The extra red blood cells alter light absorption to make the skin appear red.
Vasodilation and plasma leakage
Inflammation induces vasodilation – enlargement of blood vessels – which allows greater blood flow to the area. Specific mediators involved in sunburn vasodilation include:
– Nitric oxide: This gas is released by UV-damaged skin cells and causes surrounding blood vessels to relax and dilate.
– Prostaglandins: These lipid molecules are synthesized from arachidonic acid in cell membranes damaged by UV exposure. Prostaglandins strongly promote vasodilation and plasma leakage.
– Histamine: Stored in mast cells of the skin, histamine release also prompts vasodilation and fluid leakage when triggered by inflammation.
In addition to relaxing blood vessels, inflammatory mediators make capillaries more permeable. This plasma leakage results in fluid buildup in the sunburned tissue, which helps red blood cells move into the area and contribute to reddening.
Light absorption by hemoglobin
Once increased blood flow brings more red blood cells into sunburned skin, this alters light absorption in the swollen tissue.
Red blood cells contain abundant hemoglobin proteins that give blood its red color. Hemoglobin strongly absorbs light in the green-yellow wavelength ranges while reflecting back red light.
When there are extra red blood cells in the sunburned area, it causes enhanced absorption of green/yellow light. This leaves predominantly red light to be reflected back, making the skin appear red.
Other factors that influence sunburn redness
While vasodilation primarily drives sunburn redness, some other factors can influence the severity of reddening including:
UV exposure time
The longer the skin is exposed to UV radiation, the more severe the sunburn damage and inflammation will be. Brief intense exposure and accumulated longer duration exposure both increase sunburn redness.
UV exposure pattern
If the skin is exposed to some UV radiation over consecutive days rather than a one-time burn, this allows sunlight-induced pigments called melanins to accumulate in the skin. Melanins help protect against UV so may reduce redness somewhat.
Skin pigmentation
People with lighter skin have less protective melanin pigment. Those with fair skin often experience more severe burning and redness as they have less inherent UV protection.
Blood pressure
People with high blood pressure tend to experience more severe inflammatory responses. Hypertension can prolong sunburn redness.
Skin hydration
Well-hydrated skin tends to sunburn less severely than very dry skin. Keeping skin moisturized may help limit inflammation.
Genetics
Genetic variances affect skin sensitivity to UV. Red haired people commonly sunburn more readily due to MC1R gene variants.
Medications
Some drugs like nonsteroidal anti-inflammatories (NSAIDs), antibiotics, and birth control pills can make skin more sun sensitive. Thisresults in easier sunburning.
The role of melanin
Melanin pigments play an important role in skin color and protecting against sunburn. But melanin takes time to accumulate after sun exposure. Here’s an overview:
Melanin and skin color
Melanin is produced by melanocytes – pigment producing cells in the skin’s epidermis. Melanin protects skin by absorbing and scattering UV rays.
There are two types of melanin – eumelanin which appears brown or black, and pheomelanin which appears reddish-yellow. People with dark skin have more eumelanin while those with fair skin have more pheomelanin.
Tanning response
When skin is regularly exposed to moderate UV radiation, this stimulates melanin production in a process called tanning. The extra melanin builds up to help block UV and prevent sunburn. But it takes days for substantial melanin accumulation to occur.
Initial sunburn
If someone with pale skin gets intense UV exposure before melanin has built up, they will sunburn. The redness occurs because there is not enough melanin present in the skin to prevent inflammation.
Repeated tanning
With repeated UV exposure over weeks, melanin deposits in the skin create a tan. This offers more protection against sunburn. However, melanin only blocks about 50% of UV rays, so sunburn can still happen.
So in summary, melanin offers natural sun protection, but it takes time to accumulate. A tan helps limit sunburn but does not completely prevent it.
The role of keratinocytes in sunburn
Keratinocytes are a main type of cell found in the epidermis – the outermost layer of skin. Here is how keratinocytes are involved in sunburn:
Absorption of UV
Keratinocytes in the stratum basale of the epidermis are located closest to the melanocytes producing melanin. These basal keratinocytes absorb the bulk of incoming UV radiation.
DNA damage
Once UV rays are absorbed by keratinocytes, the UV energy damages the DNA inside these cells. This stimulates release of inflammatory mediators.
Cell suicide
The UV radiation penetrating keratinocytes can directly kill the cells by damaging their DNA. This process of cell death is called apoptosis.
Inflammatory mediators
Keratinocytes release cytokines, histamine, and prostaglandins when their DNA is damaged by UV exposure. This triggers the inflammatory response.
Blistering
In severe sunburn, fluid-filled blisters can form between layers of keratinocytes or underneath these cells. Blistering indicates extensive cell damage.
So in summary, keratinocytes in the outermost skin absorb incoming UV rays which damages their DNA. The inflammatory mediators released when keratinocytes are damaged induce sunburn redness and pain.
The stages of sunburn
Sunburn develops in progressive stages as inflammation unfolds and skin attempts to heal. Here are the key stages:
Initial exposure
During initial UV exposure that exceeds skin tolerance, DNA damage occurs but no visible changes are apparent immediately. It takes hours for inflammation to ramp up.
Early onset erythema
1 to 12 hours after sun exposure ends, skin starts to turn pink from inflammation-induced vasodilation and blood pooling.
Peak redness & pain
Vasodilation and inflammation peak at 12-24 hours post exposure. Redness and pain are most pronounced during this stage.
Late phase reactions
24 to 72 hours after sun overexposure, inflammatory mediators taper off and skin starts to heal. Peeling of damaged skin occurs.
Resolution & tanning
Skin gradually returns to normal over 4-7 days. Some darkening of skin may occur as melanin production is stimulated.
So sunburn develops progressively, with the worst redness and pain 1-2 days after initial UV overexposure. Healing takes place over several days.
Sunburn vs suntan
Although sunburn and suntan appear similar, they have some important differences:
| Sunburn | Suntan |
|---|---|
| – Caused by acute UV overexposure – Damages DNA – Triggers inflammation – Red, painful skin – Blistering can occur – Peeling skin after |
– Caused by repeated UV exposure – Stimulates melanin production – Gradual darkening of skin – Not painful – No blistering or peeling |
So in summary:
– Sunburn is an acute inflammatory reaction to excessive UV radiation that damages DNA and skin cells.
– Suntan is a gradual process where repeated UV exposure stimulates melanin pigment production and darkens skin color as a protective response.
Preventing sunburn
Sunburn can be prevented by taking the following precautions when skin will be exposed to sunlight:
Limit time in midday sun
Avoid being outdoors without sun protection between 10am and 4pm when UV rays are strongest.
Wear protective clothing
Cover your body with tightly-woven, full length clothing when feasible. Wear a broad brimmed hat.
Apply broad spectrum sunscreen
Use a broad spectrum sunscreen with a minimum SPF 30 at least 15 minutes before sun exposure. Reapply every 2 hours.
Seek shade
Stay in the shade under trees, umbrellas or canopies whenever possible.
Wear UV blocking sunglasses
Sunglasses prevent sunburn of the eyes, lids and surrounding skin. Ensure they offer full UVA/UVB protection.
Avoid reflective surfaces
Water, sand, snow and other surfaces can reflect up to 85% of UV rays and increase likelihood of sunburn.
Treating sunburn
If sunburn occurs, the following methods can help ease discomfort during healing:
Cool baths or compresses
Take lukewarm baths or apply cool compresses to help relieve heat and pain. Do not use ice directly on skin.
Moisturizing aloe vera
Apply aloe vera gel liberally to sunburned skin to moisturize and soothe inflammation.
Over-the-counter pain medication
Anti-inflammatories like ibuprofen can help reduce swelling, pain and discomfort from a sunburn.
Topical hydrocortisone
Applying an over-the-counter hydrocortisone cream can decrease skin inflammation.
Drink extra fluids
Drink ample water and electrolyte drinks to stay hydrated as fluid loss occurs from plasma leakage.
Moist wound healing
Cover severe blistering sunburns with non-stick gauze and antibacterial ointment to prevent infection.
Conclusion
In summary, sunburn is caused by DNA damage and inflammation from overexposure to UV radiation in sunlight. Increased blood flow prompted by inflammatory mediators causes the characteristic red color as more blood fills vessels near the skin. While melanin and tanning offer some sun protection with repeated UV exposure, they do not completely prevent sunburn. Using sunscreen, protective clothing, and avoiding peak midday sun can help prevent sunburn. Treating sunburn involves cooling, moisturizing, pain relief, and wound care for severe blistering reactions. Understanding the physiology behind sunburn allows us to prevent and manage this common, painful phenomenon.
