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The Photobiology of UV Damage to Skin

A frequently recurring question within the Fluorescent Mineral Facebook Group is how UV affects the skin and eyes. At the annual NERF meeting In Nov 2013 an excellent talk and discussion on this topic was presented and documented by Howie Green. Below is a copy of Howie's writeup, published here with the author's permission. (First published in the FMS UV Waves, v44, n4)


Molecular biologist Dr. Daniel Yarosh threw out the first NERF ball at the 2013 meeting. I've been aware of Dan's work since he hosted my older son, Bryan, for summer research internships many years ago at his dermatology and skin care company, Applied Genetics Incorporated Dermatics. Dan's presence is a somewhat historic achievement for me, as I've been pursuing him as a speaker for many years, and his participation attendance brought Bryan out of the woodwork to attend his first FMS meeting. At the time of our meeting, Dan was the Senior Vice President of Basic Science Research at Estée Lauder and is now their Chief Technology Advisor, R&D. I would also suggest reading his excellent book The New Science of Perfect Skin. At our meeting, Dan described The Photobiology of UV Damage to Skin, an expanded discussion of which follows.

Dan began by illustrating the spectrum of light bombarding Earth from our sun, Sol. Ultraviolet light is the specialized designation for electromagnetic radiation with wavelengths between 100 nm and 400 nm. The energy of light is inversely proportional to its wavelength. A low-density band of ozone (O3) in the Earth's stratosphere acts as a filter absorbing higher energy UV light. Consequently, the wavelengths impinging on us include mostly UVA (320-400 nm), some UVB (280-320 nm), and a bit of UVC. Two effects of UV light, the induction of erythema (from the Greek erythros, a redness of the skin or mucous membranes, caused by dilation of superficial capillaries) and DNA damage, decay logarithmically as energy decreases (as wavelength increases) going from UVB to UVA exposure. The action spectra of these two biological endpoints overlap, leading to the obvious conclusion that both are a consequence of DNA damage. Sunburn, immunosupression of contact hypersensitivity, skin cancer, and premature aging of the skin (sun spots and collagen destruction leading to wrinkles and loss of elasticity) are other dermatologic effects of sunlight. Dan had an amazing slide of a career truck driver illustrating this phenomenon. The chronically sun-exposed left side of his face was dramatically more wrinkled than the right side.

The pathological effects on skin of UV are ALL linked to DNA damage. Sunburn is an acute effect targeting the skin and cornea, while a suntan is a delayed defense against further damage. There are two different mechanisms involved in induction of a tan by UV exposure. Oxidative stress caused by UVA exposure in turn oxidizes and rapidly darkens melanin, which is located in cells (melanocytes) of the epidermis and in the middle layer of the uvea of the eye. Melanin is the pigment primarily responsible for skin color, and ordinarily protects the skin by effectively absorbing UV light and converting it into small amounts of harmless heat. Because UVA causes melanin to be released from cells in which it is already stored, but doesn't increase melanin production (melanogenesis) significantly, this effect only cosmetic. However, without an increase in melanin production, there is little increase in protection against UVB, or protection against sunburn. In a second process, triggered primarily by UVB, there is an increase in production of melanin, which is the body's reaction to direct DNA damage from UV radiation. The tan that is created by increased melanin production, which first becomes visible about 72 hours after exposure, lasts much longer than that caused by the oxidation of existing melanin by UVA, and is actually theoretically protective against UV skin damage and sunburn, rather than being simply cosmetic. However, in order to cause true 'melanogenesis tanning' by means of UV exposure, some UVB- induced direct DNA damage must first occur.

The most serious delayed effect of UV light is skin cancer. Skin cancer is the most common form of cancer in the US, and one in five Americans will develop skin cancer in their lifetime. More than 3.5 million skin cancers in over two million people are diagnosed annually. Each cancer is designated according to the cell type from which it originates. Basal cell carcinoma, the most common skin cancer, is rarely fatal but can be disfiguring. Squamous cell carcinoma, the second most common type, is more dangerous. Melanoma, the rarest type, is cancer of the melanocytes in the skin or in the eye. Melanomas are aggressive, will spread by direct growth and metastasis, and are fatal if untreated. Of the seven most common cancers in the US, melanoma is the only one the incidence of which is increasing. Over 75.000 new cases of invasive melanoma are diagnosed annually in the US, and there are about 10,000 deaths each year from melanoma. (No statistics are available specifically for fluorescent mineral collectors.) Almost all basal cell and squamous cell cancers, and most melanomas, are a consequence of exposure to UV light from the sun. A person’s risk for melanoma doubles if he or she has had more than five sunburns in their past. The obvious interpretation is that there is no such thing as a protective pre-suntan, safe exposure in a tanning salon (97% UVA and 3% UVB), or a 'harmless' dorm room wall poster light turning Jimi Hendrix psychedelic.

There are healthy effects of UV light on skin. For example, photons of UVB, especially 295-297 nm, catalyze the synthesis of vitamin D3 from cholesterol in skin. This accounts for about 90% of our vitamin D requirement, most of the rest coming from dietary absorption from irradiated milk and cold water fish. Interestingly, there is also some speculation that endorphin release accompanying sun tanning results in an 'addiction-like' pleasurable sense of well-being.

To understand the mechanism of DNA damage and repair, a biochemistry primer is helpful. Our genes are comprised of DNA (deoxyribonucleic acid), which encodes the genetic instructions for the cellular functioning. Most DNA molecules consist of two biopolymer strands coiled around each other in a structure described as a double helix. Each DNA strand is comprised of four types of nucleotides, each made of a nitrogen-containing nucleobase, a sugar (deoxyribose), and a phosphate group. The nucleotide monomers are joined to each other by covalent phosphodiester bonds between the sugar of one nucleotide and the phosphate of the next, and form the outer backbone of the double helix. The nucleobase of each nucleotide is either a purine (adenine or guanine) or a pyrimidine (thymine or cytosine) (abbreviated A, G, T, or C.) The nucleobases of each polynucleotide strand point toward the inside of the molecule, and are joined to a nucleobase of the opposite polynucleotide strand by relatively weak hydrogen bonds, forming the double-stranded DNA helix. The nucleobase pairs are stacked like rungs of a ladder. Only certain neucleobases in the double helix are compatible with each other; normally A only pairs with T and C only pairs with G. This specificity of base pairing results in both strands being complimentary, each the predictable counterpart of the other.

The DNA that makes up the human genome can be subdivided into information bytes called genes. The human genome contains about 21,000 genes. Each gene encodes a unique protein that performs a specialized function in the cell. Unlike the sugar-phosphate backbone, the sequence of nucleobase pairs is unique for each gene, the 'meaning' of which is encoded in the specific sequence of the four bases. Since genes are hundreds to thousands of nucleotides long, the variety of possible base pair sequences is virtually unlimited. Cells use the two-step process of transcription and translation to read each gene and produce the string of amino acids that makes up a protein. The basic rules for translating a gene into a protein are laid out in the Universal Genetic Code. This is the sequence of nucleotides in DNA that serves as instructions for synthesizing proteins. The genetic code is based on an 'alphabet' consisting of sixty four triplets of nucleobases called codons. The order in which codons are strung together determines the order in which the amino acids for which they code are arranged in a protein.

In order for an organism to grow, cell division must take place. When a cell divides the daughter cells must have the same genetic information as the parent cell. Each parent molecule is comprised of two complimentary strands of DNA. This feature of DNA enables the precise copying of genes necessary for inheritance. During replication the two strands separate like a zipper, and because of the base-pairing rules, each original strand serves a template that determines the order of nucleotides which plug in to form the 'new' complimentary UV Waves July-August 2014 4 strand. After replicating, each new DNA molecule consists of one original strand and one new strand, and is identical to the parent molecule.

Please spend a few minutes watching the animations of all of these genetic topics on the website of the DNA Learning Center of the Cold Spring Harbor Laboratory. Go to

The mechanism by which UV light causes DNA damage begins with the absorption of a photon of UV light by its chromophore. A chromophore is defined as the part of a molecule which absorbs certain wavelengths of light and transmits or reflects others, determining various optical properties such as color. The chromophore can be thought of as being analogous to the activator of fluorescence in minerals. The physical chemistry of the activators is central to our scientific study of fluorescent minerals. For example, the NERF meeting of 2012 included a presentation exploring the relationship between the structure and chemistry of activator systems in apatite group minerals and their fluorescent properties. A second talk described how UV light is absorbed by diamonds at defects called luminescence centers, causing fluorescence that is an identifying characteristic of different diamond types, as well as an aid in the detection of synthetic diamonds. As will be discussed later, our current meeting included a discussion of a special example of the interaction of UV light and an activator system, namely the phenomenon of tenebrescence in sodalite and tugtupite. Presentations in prior NERF meetings have also extended the analogy to biological systems. We've studied how various wavelengths light are absorbed by the chromophore of retinal opsin proteins, and subsequent mechanisms of signal transduction which result in color vision and in mood regulation (UV light has no mood regulatory effects). In past years, presentations have defined how UV and blue light are absorbed by light-sensitive fluorescent proteins in sea animals, the chromophores of which are structurally similar to opsin proteins, and which then undergo similar conformational chemical changes. We have studied the bioluminescence and biofluorescence of various fluorescent proteins in marine animals, and of one specific protein, green fluorescent protein (GFP). GFP has had a dramatic enough effect on medical science to have earned its discoverers the Nobel Prize in Chemistry in 2008.

The C=C double bonds of the aromatic ring structure of the nitrogenous DNA nucleobases, especially the pyrimidine bases, absorb UV light in the range of 260 nm most efficiently. There is little UV light of this wavelength in the ordinary sunlight that reaches our troposphere, but DNA can absorb UVB well also. As a molecule of DNA absorbs UVB, it does so by adding the energy at that wavelength to the vibrational energy of the molecule at a particular bond. When the vibration at that bond is already occurring at that wavelength or a harmonic of it, it absorbs the energy and begins to vibrate more strongly. The atoms on either end of the bond get farther apart as a result of the stronger vibration. With greater separation, the bond is more easily broken, allowing for a reaction with neighboring bases. If the neighboring base on the same strand is another pyrimidine, the UV-modified base forms a direct covalent bond with it instead of with the corresponding base on the complimentary strand.

The result of this cross-linking is an abnormal, tight four-carbon cyclobutane ring, the most commonly formed type being between two neighboring thymine bases. In many instances replication can proceed correctly in spite of this mutation. However, since there are four possible nucleobases, normal base pairing occurs with a chance frequency of only 1 in 4, and replication is frequently arrested. It is estimated that 50-100 DNA-damaging reactions occur during every second of exposure to sunlight. This direct DNA damage caused by UVB is the primary cause of melanoma in humans, but more frequently causes sunburn, basal cell cancer, and squamous cell cancer.

Indirect DNA damage occurs when a photon, usually UVA, is absorbed in the human skin by a UV Waves July-August 2014 5 chromophore that does not have the ability to convert the energy into harmless heat very quickly. Several natural molecules perform this internal conversion very quickly, reducing the unstable excited-state lifetime of the chromophore. This can be a crucial property for enabling photoprotection by molecules such as melanin, which has an internal conversion rate (a few femtoseconds, 10−15s) that is many orders of magnitude faster than an unstable UV-excited chromophore, or any man-made molecule for that matter. Molecules that have a long-lived excited state have a high probability for reaction with other molecules, generating dangerous free radicals and reactive oxygen species (ROS). These unstable chemical species can reach and react with intact DNA throughout the body by diffusion, causing oxidative damage to the DNA of any organ (unlike direct DNA damage, which affects only areas directly exposed to UVB light). That indirect DNA damage can occur remotely is indicated by the fact that malignant melanoma can be found in places that are not directly illuminated by the sun, in contrast to basal cell carcinoma and squamous cell carcinoma, which appear only on directly exposed locations on the body. Free radicals and ROS can cause damage to proteins, DNA, and cell membranes, 'scavenging' their electrons by oxidation, in turn causing a chain reaction of further oxidative damage. It is important to note that indirect DNA damage does not result in any clinically apparent warning signal or pain, like a sunburn.

A brief interlude for fluorescent mineral collectors: that DNA absorbs UV light has a fortunate consequence for us. Nucleic acid gel electrophoresis is a common analytic technique used to identify, quantify, and purify nucleic acid fragments. As such, it is used in forensics, molecular biology, genetics, microbiology, and biochemistry. Study samples are loaded into wells of a viscous gel and are subjected to an electric field. Due to the net negative charge in its sugar-phosphate backbone, DNA migrates toward the anode. Shorter DNA fragments will travel more rapidly, whereas the longest fragments will remain closest to the origin in the gel, resulting in separation based on size. When adequate migration has occurred, DNA fragments can be stained with a fluorescent dye like ethidium bromide, which intercalates between bases of DNA. The chromatographic effects are analyzed quantitatively by visualizing the gel with UV light and a gel imaging device, and the intensity of the band of interest is measured and compared against standard markers loaded on the same gel. The viewing device is a UV transilluminator, which works by emitting UVB light through a viewing surface which filters out other wavelengths. Because these standard Hoya 325c filters are only used with UVB, little solarization occurs- essentially a functionally new filter. About fifteen years ago I first noticed an electrophoresis transilluminator on eBay, and adapted it for glowhound use with the advice of my mentor, NERF Mark Cole of Unless challenged, I claim to be the fluorescent mineral hobbyist pioneer in the use of this technology. I now have 22 display cases of fluorescent minerals in my basement, each with a transilluminator powered by 240w of SW passing through a Hoya 325c filter at least 8" x16". NB: in deference to Dan's message, all visitors are shielded from UV exposure by either glass or Marine Vinyl.

Back to the story: it is important to distinguish between DNA damage and mutation, the two major types of error in DNA. DNA damage and mutation are fundamentally different. Two types of damage can occur. Endogenous damage can occur as a result of normal metabolic byproducts generating ROSs. As described above, examples of exogenous DNA damage are UVB-induced structural abnormalities, cyclobutane pyrimidine dimers (CPDs), and free radical damage from exposure to UVA. As many as one hundred thousand individual sites of DNA damage occur in each cell each day. Fortunately there are many different enzyme pathways by which DNA repair can occur, provided redundant information, such as the undamaged sequence in the complementary DNA strand, is available for copying. However, when the rate of damage exceeds the cell's repair capacity, cells can enter into a state of irreversible dormancy (senescence) or can undergo a process of programmed cell death called apoptosis. Senescence and apoptosis are frequently protective to the organism. In contrast to DNA damage, a mutation is a change in the base sequence of the DNA, which cannot be recognized by enzymes once the base change is present in both DNA strands. Therefore, a mutation cannot be repaired, and may cause alterations in basic DNA functions like protein formation and function. Common types of mutations are insertions (the addition of an extra nucleotide), deletion (the deletion of a nucleotide), and substitution (the incorrect placement of a nucleotide.) When a cell replicates a mutation is inherited by the daughter cells. In UV Waves July-August 2014 6 rapidly dividing cells like skin cells, unrepaired DNA damage that does not kill the cell, thereby blocking replication, will tend to cause replication errors and thus mutation. Most mutations are deleterious to a cell's survival. However, mutations sometimes provide a survival advantage for a cell at the expense of neighboring cells. Thus, DNA damage in frequently dividing cells can give rise to mutations, which is a prominent cause of cancer. This risk is greatly magnified when mutations inactivate genes coding for tumor suppression enzymes and DNA repair enzymes.

An important gene involved in both tumor suppression and DNA repair is the p53 gene, so important that it is nicknamed "the guardian of the genome". In its anti-cancer role, p53 can induce an arrest in cellular functioning, allowing time for DNA repair to take place, or initiate apoptosis, which prevents mutated genes from being replicated.

A variety of repair mechanisms have evolved to restore lost genetic information resulting from DNA damage, most consisting of enzymes for damage recognition and repair. The most efficient mechanisms use the undamaged complimentary strand of DNA as a template for correction of the damaged strand. Dan described two 'excision repair' mechanisms that reverse damage in humans. A mechanism called dark repair, or base excision repair, efficiently repairs damage caused by oxidative DNA damage. A sequence of enzymatic reactions recognize and remove a damaged base and a few surrounding bases, catalyze resynthesis of the missing part, and repair the nick in the chain. Nucleotide excision repair (NER) is a distinct process in which helix-distorting CPDs and up to 30 nucleotides are excised by the enzyme photolyase and the whole chunk is then repaired. A third mechanism not found in humans is photoreactivation. This is termed light repair because it requires the energy of absorbed blue light to proceed. An animated depiction of these two processes can be viewed at 1/animation_quiz_5.html.

Xeroderma pigmentosum (XP) is a genetic disorder of DNA repair mechanisms in which the ability to repair damage caused by UV light is impaired. XP involves both sexes and all races, with an incidence of 1:250,000 in the United States. Affected individuals suffer from severe photosensitivity following minimal exposure to UV light, and are extremely vulnerable to the development of skin cancer, with a 50% incidence by age 8. Individuals with XP are about 3,000 times more likely to develop skin cancer than are individuals without the disorder. Malignant melanoma and squamous cell carcinoma are the two most common causes of death. XP can result from a defect in any one of seven DNA repair genes. One of the most frequent is an autosomal recessive genetic defect of NER enzymes, resulting in an inability to repair carcinogenic CPDs. An examination of the expression of the tumor suppression gene p53 in the majority of tumors from XP patients revealed mutations characteristic of UV exposure. Dan's research with DNA repair enzymes has made a promising impact on the fight against skin cancer in XP patients. A bacterial enzyme, T4 endonuclease V, repairs damaged DNA in vitro. The problem was how to deliver the enzyme to the site of the damage in the nucleus of the skin cell. Dan's lab solved this problem by enclosing the enzyme in a fat bubble called a T4N5 liposome, which penetrates into the skin cell with the repair enzyme functionally intact. When applied topically in a lotion to XP patients, these liposomes accelerated the removal of CPDs compared with placebo, cutting the time for repair of 50% of damaged DNA sequences from 24h to 6h. In a subsequent prospective clinical study of XP patients, topical treatment with T4N5 liposome lotion lowered the rate of precancerous lesions and basal cell carcinomas compared with placebo lotion by 68% and 30% respectively! In addition, there seemed to be a continuation of benefit after discontinuation of treatment, implying that T4N5 removal of CPDs reversed a fundamental and common source of these cancers.

Although further study is required, it is also possible that T4N5 lotion might function as a “morning after” lotion for anyone who has just suffered severe sunburn, hopefully reducing DNA damage and the risk of future skin cancer. In the long-term, T4N5 application may restore p53 gene tumor suppression function and exert a lasting chemopreventative effect. Perhaps the largest commercial market of all is the potential for T4N5 lotion to reverse the effects of photoaging secondary to sunlight exposure.

A more familiar example of impaired DNA repair is in the breast cancer early onset genes BRCA1 and BRCA2. These are tumor suppression genes UV Waves July-August 2014 7 found in all humans, the protein products of which are BRCA1 and BRCA2 (no italics). BRCA1 and BRCA2 are normally expressed in breast cells, where they help repair damaged DNA or destroy cells if DNA cannot be repaired. If BRCA1 or BRCA2 itself is abnormal due to a BRCA mutation, damaged DNA is not repaired properly, and this increases the risk for breast cancer.

Cancer treatments such as chemotherapy and radiation therapy work by overwhelming the capacity of targeted cells to repair DNA damage, resulting in cell death. Cancer cells, which are typically the most rapidly dividing, are preferentially affected. The undesirable consequence is that other non-cancerous but rapidly dividing cell populations, such as progenitor cells in the gut, skin, and hematopoietic system are also affected. This accounts for side effects such as hair loss and interference with blood cell production, which may lead to anemia and increased vulnerability to infection. Efficient cancer treatments attempt to localize the DNA damage to cells and tissues affected with cancer. This may be accomplished either by physical means, such as concentrating radiation in the region of the tumor, or by biochemical means which exploit features unique to cancer cells. One such example is the treatment of thyroid cancer using radioactive iodine, which is absorbed by cancerous and normal thyroid cells only.

Another medical use of UV is in the treatment of psoriasis. Psoriasis is relatively common, affecting 2-4% of the population, and was probably what was mistaken for leprosy in the Old Testament. It is a chronic, non-contagious immune-mediated inflammatory disease that occurs in genetically vulnerable individuals, primarily affecting skin and in some cases, joints. Normally, skin cells grow gradually and flake off about every 4 weeks, and new skin cells grow to replace the outer layers of the skin as they shed. However, in psoriasis, new skin cells proliferate in days rather than weeks, resulting in thick patches called plaques which are itchy, tender, and unsightly. Although early concepts of the pathogenesis of psoriasis focused primarily on this skin cell hyperproliferation, dysregulation of the immune system triggering hyperproliferation is now recognized as a critical event in this disease. This evolving knowledge of the role of the immune system in psoriasis has had a significant impact on treatment development. Many new and emerging therapeutic agents target specific immunologic aspects of psoriatic disease.

Historically, phototherapy in the form of sunlight was used to treat psoriasis. Subsequently, special UV lamps have been developed for this application. One such lamp uses narrow band UVB light (NBUVB) with a specific wavelength of 311- 313 nm. A major mechanism of NBUVB is the induction of DNA damage in the form of CPDs. This is therapeutic because the formation of CPDs interrupts the pathological rapid division of skin cells characteristic of psoriasis. The activity of many types of immune cells found in the skin is also effectively suppressed by NBUVB treatment. Another treatment, psoralen and UVA phototherapy (PUVA), combines the oral or topical administration of psoralen with exposure to UVA. Psoralen intercalates into DNA, and on exposure to UVA can form covalent cross-links between pyrimidine nucleobases on opposite DNA strands, inhibiting the abnormally rapid production of the cells in psoriatic skin and inducing apoptosis. PUVA therapy has considerable clinical efficacy. One unfortunate a side effect of PUVA treatment may be a higher risk of squamous cell skin cancer.

At this point in the program, I wasn't too sure who was at greater risk for catalepsy- the audience when contemplating their extent of lifetime UV exposure, or Dan after realizing such a cohort as we fluoresophiles exists (and we didn't even discuss potential damage secondary to SW UV exposure)! To review, after a sunburn 100,000 separate loci of DNA damage to EACH skin cell occur, ten-fold more causing direct rather than indirect damage. A good estimate is that half of this damage is repaired each day, mostly in the evening and overnight. This timing is particularly advantageous because it follows peak sunlight exposure and precedes morning, when most cell division occurs. Our capacity for DNA repair decreases with age at an approximate rate of 0.06%/yr. The inference is that repeated daily exposure to UV light in sunlight results in significant residual unrepaired damage. In other words, if a person lives long enough, the development of skin cancer would be inevitable.

At any rate, while not wasting his time recommending the abstinence that any sane fluorescent mineral collector should contemplate, Dan offered helpful suggestions. I suspect that he had some sense of our group's cumulative UV exposure, and factoring in the photoaging inherent as a result of UV Waves July-August 2014 8 that exposure, figured we were actually quite a bit younger than we look, and thus worth saving.

Some common sense tips; avoid sun exposure between 10 a.m. and 2 p.m., when UVB emission is at the maximum. Top down protection is essential, but clothing really only offers partial protection, the benefit of which is proportional to the tightness of the weave. The American Association of Dermatology (AAD) recommends that a "broad spectrum" sunblock (both UVA and UVB protection) with a sun protection factor (SPF) of at least 15 be applied daily to all sun exposed areas, and reapplied every two hours. Statistics suggest that regular daily use of sunblock with an SPF of 15 higher reduces the risk of developing squamous cell carcinoma by 40% and melanoma by 50%. However, Dan noted that on the basis of recent clinical trials, sunblock with SPF 30 provided significantly better protection than sunblock with SPF15. Be aware that many medicines induce photosensitivity, as do essential citrus oils applied topically during a facial. Dermatologic self-examination is estimated to convey a 50% decrease in skin cancer mortality. While the potential benefits of regular dermatologic checkups are obvious, the cost-effectiveness is controversial.

Sun protection works by filtering and/or reflecting UVA and UVB radiation. Many people use the words sunscreen and sunblock interchangeably. Technically, however, these are two entirely different forms of sun protection. Sunscreen, the more commonly used type of sun protectant, filters the sun's UV rays -- keeping most rays out, but letting some in. On the other hand, sunblock physically reflects the sun's rays from the skin, blocking the rays from penetrating the skin. The SPF rating indicates how long sun protection remains effective on the skin. A user can determine how long his sun protection will be effective by multiplying the SPF factor by the length of time it takes for him or her to suffer a burn without protection. For instance, if a user normally develops sunburn in 10 minutes without wearing a sunscreen, sun protection with an SPF of 15 will protect for 150 minutes. The active ingredients of sun protection can be divided into chemical versus physical agents. Chemical sunscreens are usually aromatic molecules which work by absorbing high energy UV light and releasing it at a lower, safer energy. As a precaution, many commercially available sunscreens contain antioxidants that help protect against any ROS that are a consequence of this sunscreen action. Physical sunblocks reflect or scatter UV radiation before it reaches the skin. Some sun protection products combine both chemical and physical mechanisms. Two types of physical sunblocks that are available are zinc oxide (available in unrefined form at the Sterling Hill Mining Museum on the Mine Run Dump) and titanium dioxide. Both provide broad spectrum UVA and UVB protection and are gentle enough for everyday use. Because physical blocking agents are not chemically active, they rarely cause the skin irritation that a chemical sunscreen with PABA might, and are thus especially useful for individuals with sensitive skin. Most chemical sunscreens are composed of several active ingredients because no single chemical ingredient blocks the entire UV spectrum. Instead, most chemicals only block a narrow region of the UV spectrum. Therefore, by combining several chemicals, broad spectrum protection is achievable. Most chemical agents used in sunscreens work in the UVB region, offering protection against basal cell and squamous cell cancers caused by direct DNA damage, but not against melanoma. Only a few chemicals block the UVA region, so the best recommendation is that a sunscreen also contain either a physical blocking agent or avobenzone.

Audience discussion focused on three topics related to UV exposure. The first question was how to weigh the benefit of protection against sunlight compared to the risk that that protection would be at the expense of lower vitamin D production. Dan was vehement in pointing out that medical decisions always are a balance of putative benefits and risks. In this case, adequate vitamin D levels can be achieved by ingesting milk or fish, and by oral vitamin D supplementation, and therefore there is absolutely no justification for the risk of UV exposure for this indication.

The second topic discussed was the dangerous ophthalmologic effects of UV and short blue visible light of 400-440 nm, neither of which are essential for sight or circadian rhythm regulation. An acute clinical effect of UV exposure is photokeratitis of the cornea and conjunctiva (the inside of the eyelids and the 'whites' of the eyes). This is an inflammatory photochemical response akin to sunburn. Many fluoresophiles use ketorolac eyedrops as a short-term remedy. Both UV and blue visible light contribute to cataract formation in the lens and age-related macular degeneration in the retina. The lens only transmits light from 300-1400 nm UV Waves July-August 2014 9 through to the retina. The dominant damage mechanism for exposure times greater than 10 seconds is a photochemical blue-light hazard (photoretinitis), resulting in the production of free radicals which damage both photoreceptors and the retinal pigmented epithelium (RPE - a layer of cells on the outer surface of the retina, which supports the photoreceptors’ function). For shorter exposure times, a thermal hazard dominates at the site of exposure, causing the denaturation of retinal proteins. In addition, as mentioned above, UV-induced DNA damage to melanocytes in the eye can lead to melanoma of the eye.

The final topic was of a case report involving a woman diagnosed with stable Systemic Lupus Erythematosus (SLE) and a known history of photosensitivity. She became delirious and febrile to 104oF after several visits to a tanning salon. SLE is a chronic, systemic autoimmune disease affecting at least 1.5 million Americans, the severity of which ranges from mild to life-threatening. Fortunately, with good medical care, most people with lupus can lead a full life. Please go to for more information. Lupus can result in pain, inflammation, and damage to any part of the body (skin, joints, heart, lungs, brain, kidneys, or blood vessels). Lupus is a complex disorder that most likely results from a combination of processes and factors. Normally, environmental factors such as viruses, exposure to certain chemicals or medicines, or the UV component of sunlight trigger inflammatory or immune activity. This immune activation may begin as an appropriate response to the external stimulus itself or to the byproducts of the interaction between the trigger and the affected body part. But because of a combination of genetic factors, the immune system of an individual with lupus cannot distinguish between 'self' and these foreign 'invaders' or byproducts. This results in the production of antibodies, which ordinarily dispose of body waste and protect against infection, but which in this case mistakenly destroy healthy tissue in an inappropriate, self-perpetuating, and dangerous immune response. The exact combination of genes that predispose individuals to SLE may differ somewhat from patient to patient. However, common pathways may be impaired clearance of both immune-triggering stimuli and the detritus resulting from the body's normal apoptotic processes.

While it is established that UVB can trigger the cutaneous manifestations of lupus, there is growing evidence that UVA can also be dangerous. The tanning salon process uses UV that is about 85% UVA and 15% UVB. Therefore in addition to the UVB-induced direct DNA damage resulting in tanning, indirect DNA damage also occurs. After UVA exposure, the body recognizes the photoproduct of UVA with its own DNA as foreign, inducing an immune system reaction with resulting autoantibody production and cellular toxicity. This will trigger inflammation systemically, which explains the clinical manifestations reported in the case discussed. Fortunately, despite being delirious and on a respirator, the patient recovered after several weeks of treatment with high doses of corticosteroids. It's not known whether she resumed visits to the tanning salon or whether she received a refund.

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