UV-A vs UV-B radiation on the skin
UV-A (320-400 nm)
Aging and tanning rays
95% of UV radiation that reaches us on earth is UV-A. Unlike UV-B, UV-A is not absorbed by ozone. UV-A penetrates earth’s ozone layer, clouds, smog, and 70-90% of that UV-A can penetrate through home and auto glass.
UV-A rays are pretty constant. During all daylight hours throughout the entire year.
UV-A radiation causes INDIRECT, oxidative damage
UV-B penetrates to the epidermis (skins surface layer), but UV-A penetrates further to the dermis and can damage components within those skin cells. UV-A’s longer wavelength enables it to enter the skin’s dermis, and although UV-A radiation is less energetic than UV-B, excessive amounts of UV-A can generate reactive oxygen species (ROS), e.g. hydroxyl radical and singlet oxygen, within skin cells, which can cause oxidative damage to (i.e. steal electrons from) lipids, proteins and nucleic acids (chains of nucleotides that store genetic information), including DNA and RNA . Out of the sun, humans are not usually exposed to UV wavelengths > 294 nm, and human cells have inherent systems to protect against oxidant damage from exposure to higher UV wavelengths of sunlight, including antioxidant systems glutathione-glutathione peroxidase and thioredoxin and DNA repair mechanisms, but prolonged exposure can overwhelm these systems.
Unlike UV-B, which alerts us to its DNA damage by causing sunburn, UV-A’s damage is pain-free and has no other warning signals, making us oblivious to the damage being wrought by ROS.
- UV-A photons are tanning rays. UV-A oxidizes pre-existing melanin from melanocytes (skin’s melanin-producing cells), which in turn immediately creates the tan color in the skin; tanning beds use UV-A (some also use UV-B). Excessive amounts of UV-A can cause sunburn. Only broad-spectrum suntan lotions absorb or block UV-A rays.
- Can cause some skin cancers. UV-A can cause oxidative stress leading to cancerous mutations when naturally protective mechanisms are overwhelmed. E.g. 92% of malignant melanoma is caused by indirect DNA damage;
- UV-A can break down vitamin D in your skin. previously formed from exposure to UV-B rays.
- UV-A is known for causing premature aging. UV-A can cause photo-aging by damaging collagen and elastin fibers and destroying vitamin A in skin. Actinic (or solar) elastosis is an accumulation of abnormal elastin (elastic tissue) in the skin’s dermis layer (and in the conjunctiva of the eye), as a result of prolonged / excessive sun exposure.
Excited Chromophore* (UV-A + Chromophore ) + 3O2 → Chromophore + 1O2 (singlet oxygen)
1O2 + Intact DNA → 3O2 + Damaged DNA
UV-B (280-320 nm)
Vitamin D-making Rays
5% of the UV rays reaching earth. Most UV-B absorbed by ozone layer, water vapor, oxygen and carbon dioxide.
UV-B ray intensity is affected by various factors
- Latitude. Most of the US is between 30° and 45°latitude, which for several months a year, has insufficient UV-B sunlight to produce optimal D level:
30° (N and S). Insufficient UV-B 2-6 months of the year, even at midday; only Florida and S. Texas are below 30°N in mainland US
40°. Insufficient UV-B during 6-8 months of the year; includes Oregon, Idaho, Wyoming, Nebraska, Iowa, S. Dakota, N. Illinois, Wisconsin, N. Indiana, Michigan, Ohio, Pennsylvania, New York and the New England States;
45° (far N or S). Even summer sun is too weak. Includes most of Washington, Montana, N. Dakota, and northernmost parts of Minnesota, Wisconsin and Maine;
- Altitude. UV-B is stronger at higher altitudes;
- Glass. Only ~5% of UV-B goes through glass;
- Ozone layer, clouds, smog or fog. Full cloud cover decreases UV-B ~50%; stratospheric ozone depletion increases;
- Time of day / Sun’s position in sky – More UV-B rays reach earth at midday than in the morning or evening. When the sun is high in the sky around noon, its rays have a shorter distance to travel through the Earth’s ozone layer to reach the surface of the Earth, which reduces absorption by the ozone layer and increases amount of penetration. Conversely, when the sun’s rays are at an oblique angle early and late in the day, they have a further distance to travel through the ozone layer and have reduced intensity than when rays hit directly. When the sun goes down toward the horizon, UV-B is filtered out much more than UV-A
UV-B penetrates only as far as the outer layer of the skin, called the epidermis.
UV-B photons can be DIRECTLY absorbed by:
- DNA
- Chromosomes: present in skin cells.
- Melanin (Chromophores)
- Essential fatty acids (present in skin cell membranes). Omega-3 fatty acids mitigate skin damage caused by UV-B
Beneficial effects of UV-B
UV-B helps skin produce vitamin D3 – a potent defense against melanoma in the epidermis. Melanoma cells convert vitamin D3 to its active form CALCITRIOL, which triggers growth inhibition and apoptotic cell death. (Conversely, research shows that increased UV-A exposures together with inadequately maintained cutaneous vitamin D3 levels will promote melanoma)
- The body’s production of ACTIVE VITAMIN D (CALCITRIOL) from D3 is affected by certain factors: sufficient dietary fat is required; trans fats are inhibitory, as are certain medical conditions, e.g. parathyroid gland or kidney diseases.
Vitamin D – “The Sunshine Vitamin”
Increases MELANIN production (commonly known as a suntan). UV-B stimulates melanocytes (certain skin cells) to produce melanin, a brown protein pigment metabolized from tyrosine, that protects against overexposure to UV-B radiation by absorbing UV energy and dissipating it as harmless heat and also colors the skin. The tan resulting from increasing melanin production takes about two days to develop but is longer-lasting and less harmful than the one obtained from UV-A.
UV-B stimulates production of Melanocyte Stimulating Hormone (MSH). Important in weight loss and energy production.
UV-B rays can cause DIRECT damage
UV-B causes DIRECT photodamage when absorbed by DNA nucleobases (the 5 fundamental units of the genetic code – adenine (A), cytosine (C), guanine (G), thymine (T), urasil (U). A, C, G and T are in DNA). DNA is able to efficiently transform >99.9% of the photons into harmless heat (via a photochemical process called internal conversion), but the remaining <0.1% create an excited state that can cause a disruption in the DNA strand (thymine base pairs next to each other in genetic sequences bond together into thymine dimers), which reproductive enzymes cannot copy, potentially leading to mutations.
Prolonged UV-B exposure can cause DNA damage leading to:
- Sunburn. Damage from the untransformed <0.1% UV-B is able to cause sunburn, a painful warning signal that DNA damage from UV-B is occurring to cells. No such warning is generated from UV-A’s INDIRECT damage.
- Premature aging
- Increased risk of basal and squamous cell carcinomas and melanoma cancers (8% of melanoma attributed to UV-B radiation).
Naturally protective mechanisms against oxidative stress caused by UV radiation
The skin pigment melanin is a natural “sunscreen”. Melanin, the primary color determinant of skin, hair and eyes, is produced by melanocytes (cells found in the basal layer of the epidermis, eyes, hair, also inner ear, and brain) by UV-B radiation. Melanin is derived from the non-essential amino acid tyrosine.
Melanin is transferred into melanosomes, organelles of the skin’s epidermal cells, where it efficiently absorbs both UV-A and UV-B rays and turns them into harmless heat, thereby protecting nuclear DNA / RNA from potential UV-promoted mutations. Melanin is also able to neutralize reactive oxygen species (ROS) providing a protection from oxidative stress.
Melanin is composed of a chromophore (and attached protein) and when UV-A rays excite a chromophore that is unable to quickly convert UV-photon energy into harmless heat, ROS are produced.
Studies show that melanin-rich, dark-skinned people have less incidence of UV-induced DNA damage in skin. However, when those with darker skin are diagnosed with melanoma, it is often at a later stage than fairer skinned people, is more deadly and most is in areas which are not usually exposed to the sun, such as the soles of the feet, palms, inside the mouth and under the nails (where it is more prevalent on the big toe, thumb and index finger, and on the dominant hand).
DNA repair mechanisms
- Nucleotide excision repair
Antioxidants:
- Adequate vitamin D levels (dietary or formed in the skin by UV-B rays).
- The adequate presence in the skin of other antioxidants. E.g. vitamin A /retinol, vitamin C, resveratrol and other polyphenols, vitamin B3, vitamin E, CoQ10, and astaxanthin can neutralize ROS.
Essential fats (omega-3 and omega-6)
