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Various societal trends can be linked to the increased exposure to sunlight. I think a major reason is that, around the mid-1900s, Americans started finding time, access, and money to discover outdoor recreation. Steady income, infrastructure, and a doctor’s orders to exercise encouraged families to pursue many new outdoor activities like water sports, swimming, and vacationing at the beach. These trends–and likely others–created the need for protection against the sun’s rays. Therefore, this decades-old research topic is pretty new, though we’ve learned quickly. With this article, I hope I’ve provided at least a partial view of what’s been learned regarding the mechanisms of sunburns, and that, with it, you might be better able to prevent and treat them.

Recommendation: Determine how important sun exposure is to you. If it’s important to you, for example because of a sport you play, or your desire to look tan, at least understand the basics of how sunlight effects your skin. This is especially important if you’re fair-skinned or have family history of skin cancer. As always, you should talk to your doctor (or dermatologist) about anything you read here before adjusting your normal activities.

This article will provide a partial view of what’s been learned regarding the mechanisms which cause sunburns and how to prevent and treat them. As usual, we’ll first give a basic background and get deeper into the science as we proceed. We’ll barely discuss skin cancer and Vitamin D, as covering each of those topics would require a full-length article to be written.

The basic science: what’s a sunburn and why is it harmful?

Simply put: any change in the color of your skin due to sunlight is a sign of damage. Furthermore, plenty of research shared here suggests that your skin is damaged even before you get a sunburn or tan. And don’t think you need to tan to get adequate Vitamin D–healthy skin makes plenty of Vitamin D from natural sunlight before it changes color, especially if you’re fair-skinned.

“Sunburn cells” (SC) are “severely UVB-damaged single standing cells that undergo programmed cell death in favor of the surrounding tissue. In this context induction of apoptosis following UVB exposure appears to be a protective mechanism, getting rid of damaged cells that bear the risk of becoming malignant.” ((Independent contribution of three different pathways to ultraviolet-B-induced apoptosis (2002)))

Beyond increasing risk of skin cancer, the repeated inflammation from chronic exposure to UV radiation causes negative aesthetic effects. UV radiation generates reactive oxygen species (ROS) that inhibit the skin’s enzymatic and nonenzymatic antioxidant defense systems. ((Ultraviolet Radiation: A Hazard to Children and Adolescents (2011)))

This contributes to wrinkles, or sun damaged skin:

A basic diagram of this process is seen here:

When it comes to moderate sunlight exposure, research clearly shows the benefits of UV light. ((Beneficial effects of UV radiation other than via vitamin D production)) ((UV Radiation and the Skin (2013))) Some research has suggested only UVB can produce Vitamin D which we won’t get into. ((Ultraviolet Radiation: A Hazard to Children and Adolescents (2011))) However, there is recent evidence that UVA can, though less effectively. ((Vitamin D levels after UVB radiation: effects by UVA additions in a randomized controlled trial (2013))) But when we’re overexposed to sun, UVB (280–315 nm) is more carcinogenic than UVA (315-400) “because of its ability to damage DNA, to disrupt tumour-suppressor pro-apoptotic signalling pathways, and to suppress immune responses.” ((Life and Death Signaling Pathways Contributing to Skin Cancer)) ((Sunburn cell: Regulation of death and survival of the keratinocyte (2005))) The general rule is: the longer the wavelength, the less energy it has to affect our cells (beneficially or harmfully).

How to prevent sunburns

When it comes to preventing skin damage, it must be noted that we can prevent sunburns, but we can’t prevent skin cancer, per se. It’s better to think about how we can avoid increasing our risk of getting it–i.e. by reducing acute, chronic, and intense sun exposure. Interestingly, other risk factors like age, race, and family history are actually more strongly associated with melanoma than the risk factor “number of sunburns”. However, which of the four can you control? Health organizations like the American Cancer Society, the Centers for Disease Control and Prevention, etc. have recommended ways to reduce risk via skin damage. These include:

1.Do not burn; avoid suntanning and tanning beds.
2.Wear protective clothing and hats.
3.Seek shade.
4.Use extra caution near water, snow, and sand. (They reflect UV light)
5.Apply sunscreen.
6.Wear sunglasses.” ((Ultraviolet Radiation: A Hazard to Children and Adolescents (2011)))

As you can see, the most effective prevention is pretty straight-forward. While there are nuances of the science behind sunburns, these basic behaviors get the job done. Beyond that, don’t spend more time in the sun than your sport/activity requires. Keep in mind that the hours of 10 to 4pm are the strongest UV rays that will hurt us. Finally, plan to get sun when the “UV index” is low. This index is a prediction of tomorrow’s UV intensity. Each day, your local weather predicts the next day’s intensity of UV light based on the sun’s position, clouds, ozone, and other atmospheric info. 0 to 2 is minimal; 3 to 4 is low; 5 to 6 is moderate; 7 to 9 is high; and 10 or higher is very high. Find it for your city at www.weather.com or in your daily newspaper.

Be wary of relying on cloud cover for protection. Clouds block more heat than they do UVB light, meaning you might feel cool in the shade, but you’re still absorbing radiation. Also, the amount and intensity of UVB radiation varies. Summer is more dangerous than winter and the hours of 10am to 4pm are more intense than morning or late afternoon. Geography matters, too; as your altitude and proximity to the equator rise, so does UVB intensity. Air pollution and humidity also affect UVB intensity. UVA is more consistent, though. One publication explains, “in contrast to the variability of UVB radiation, UVA radiation is relatively constant throughout the day and the year.” Finally, don’t think you’re safe underwater, as UV radiation can reach a depth of 60cm. ((Ultraviolet Radiation: A Hazard to Children and Adolescents (2011))) and ((Changes in biologically active ultraviolet radiation reaching the Earth’s surface (2003)))

One last note on UVA vs UVB radiation and tanning–“IPD” and “PPD” are immediate and persistent pigment darkening, respectively. They differ from “DTR” (delayed tanning reaction). UVA radiation is mainly responsible for IPD and PPD by “photooxidation of melanin precursors” which are naturally found in skin. I found that these reactions “take place within a few minutes or hours but are mostly reversible, so that the tanning of the skin diminishes within a few days”. DTR, on the other hand, arm, leg, cheek…(sun pun)…is caused by UVB radiation. Normally, “pigment formation takes place in the basal layer and is based on the proliferation of specific enzymes, especially tyrosinase. The melanocytes are stimulated to form melanin, which is transported to KCs to protect the cell nuclei in particular. With the movement of the epidermis cells, the pigment also moves towards the skin surface. The formation of the suntan takes several days and lasts for a few weeks.” ((Shining Light on Skin Pigmentation: The Darker and the Brighter Side of Effects of UV Radiation (2012)))

Wouldn’t it be nice if our IPD/PPD pre-vacation tan protected us from the Florida sun?! According to one study, that base tan (from the extra radiation you’re soaking up) provides an SPF of 3–and that’s only if it’s natural sunlight. An identical “UVA-only” tan (from a tanning bed) provides even less protection: around 1.3 SPF. ((Tanning beds, skin cancer, and vitamin D: an examination of the scientific evidence and public health implications (2010))) This surprised me, though, as apparently tanning beds emit waves in a similar ratio to the natural sunlight we receive (about 95% UVA). ((UVB and UVA irradiances from indoor tanning devices (2011))) I would’ve thought differently about tanning beds. I also would’ve assumed artificial tanning lotions or “bronzers” helped protect our skin from sun; the same study taught me otherwise. The chemical reaction on your skin which creates this spray tan provides zero protection against UV radiation, as opposed to the melanin in naturally darker skin. Though, many of those products do contain sunblock, which must be reapplied as normal.

Technically there’s no such thing as a “healthy tan”

Clearly, when it comes to radiation, any change in skin color indicates damage. Like many people, I thought tanning was fine, as long as I didn’t burn. However, tanners who don’t burn simply experience less acute inflammation in response to natural sunlight. While “natural tanners” enjoy more protection from melanin, oxidative damage is still the cause of the tan.

The sun damages hair cells similarly. The same UVA radiation that causes ageing skin is responsible for the bleach-blonde hair color after repeated sun exposure. ((The health benefits of natural skin UVA photoprotective compounds found in botanical sources (2015)))

One report says it best:

“Based on the tanning pathway, it appears that UV-mediated DNA damage can occur in the absence of tanning. However, tanning does not occur without preceding DNA damage…” ((Tanning beds, skin cancer, and vitamin D: an examination of the scientific evidence and public health implications (2010)))

Another explains, “The UV radiation exposure necessary for tumorigenesis may be below the threshold needed to induce inflammation, suggesting that tanners are at a risk of skin cancer even if they do not suffer any side effects such as sunburns.” Also, a month of Monday-Friday exposure to solar radiation (280-400 nm) and UVA (320–400 nm) below the amount needed for immediate sunburn caused “…a greater cumulative erythema response in the first week of treatment, epidermal hyperplasia and stratum corneum thickening, depletion of Langerhans cells, dermal inflammatory infiltrates, and deposition of lysozyme on elastin fibers. This suggests that similar exposures from indoor tanning can contribute to long-term actinic damage even in the absence of sunburns. This, again, challenges the idea of a safe tan.”

In case you weren’t suspicious of tanning beds yet, here’s a final data point (though they’re specifically referring to “frequent” tanners):

“In terms of biological activity, the intensity of UVA radiation produced by large, powerful tanning units may be 10 to 15 times higher than that of the midday sun. Frequent indoor tanners may receive 1.2 to 4.7 times the annual dose of UVA than is received from the sun, in addition to doses from sun exposure.” ((Ultraviolet Radiation: A Hazard to Children and Adolescents (2011)))

A short description of “SPF”

Image from thebeautyproof.com

The sun protection factor of a sunscreen refers to its ability to protect our skin against UVB radiation. An SPF-2 sunscreen applied at recommended thickness 15-30 minutes prior to going in the sun will block approximately 50% of UVB radiation. I found it would take 1 oz (30 ml) of sunscreen to adequately cover all sun-exposed areas of an average adult wearing a bathing suit. According to the source of this info, for most users, proper application and reapplication are more important factors than using a product with a higher SPF. ((Sunblocks/Sunscreens and Skin Protection)) But, if you are diligent and use it as directed, SPF-10 blocks 90%, SPF-15 blocks 94%, and SPF-30 blocks 97%.

Also, note that not all clothing is equal in sun protection. Clothes are assigned a “UPF” rating to measure their protective ability. I couldn’t find a lot of specifics on UPF or how it converts to SPF, but I was surprised to find that a standard cotton T-shirt might provide very little protection. Also assumed is that clear glass protects against sunburns–while this depends on the type of glass, note that clear glass only blocks UVB light (and shorter wavelengths). UVA passes through, putting fair-skinned people at slight risk in their homes and cars.

One last area of interest regarding sunblock is toxicity. Since this article is about sunburns and not chemical toxicity, I won’t dive into that subject, fully. The caution does exist, though–especially for mothers who are nursing. Basically, we know chemicals are absorbed and may have affects in nursing infants at levels found in mothers who use common sunscreen/cosmetics. One study calls for research on how chemicals in sunscreen may react with skin, stating,

“Due to the chemical structure of the most common organic UV filters and their known photodegradation products, various reactions, for example with protein structures of the skin, are conceivable but not yet sufficiently investigated.” ((Photoprotection in changing times – UV filter efficacy and safety, sensitization processes and regulatory aspects (2014)))

What’s the best treatment for sunburn?

If you do get burnt, there are a few things you can do to relieve the pain, support healing, and prevent future damage. The American Academy of Dermatology lists 6 steps to take to treat your sunburn:

1. Take frequent cool baths or showers to help relieve the pain.

As soon as you get out of the bathtub or shower, gently pat yourself dry, but leave a little water on your skin. Then, apply a moisturizer to help trap the water in your skin. This can help ease the dryness.

2. Use a moisturizer that contains aloe vera or soy to help soothe sunburned skin.

If a particular area feels especially uncomfortable, you may want to apply a hydrocortisone cream that you can buy without a prescription. Do not treat sunburn with “-caine” products (such as benzocaine), as these may irritate the skin or cause an allergic reaction.

3. Consider taking aspirin or ibuprofen to help reduce any swelling, redness and discomfort.

4. Drink extra water. A sunburn draws fluid to the skin’s surface and away from the rest of the body.

Drinking extra water when you are sunburned helps prevent dehydration.

5. If your skin blisters, allow the blisters to heal.

Blistering skin means you have a second-degree sunburn. You should not pop the blisters, as blisters form to help your skin heal and protect you from infection.

6. Take extra care to protect sunburned skin while it heals.

Wear clothing that covers your skin when outdoors. Tightly-woven fabrics work best. When you hold the fabric up to a bright light, you shouldn’t see any light coming through. ((How to treat sunburn))

Regarding treatment with drugs, the sunburn response involves multiple pathways of repair, so drugs targeted for sunburn treatment should reflect this. COX (cyclooxygenase) and LOX (lipoxygenase) are enzymes kept in balance by the body. The activity of each in response to UV radiation leads to different products (e.g. PGE2 vs 12-HETE). Thus, COX-inhibition may contribute to more inflammation, instead of less, as it shifts the ratio in favor of LOX products. ((COX inhibition enhances inflammatory immune cell infiltration in UV-irradiated human skin: implications for the treatment of sunburn (2015))) If you’re prescribed a COX-2 inhibitor for your sunburn, ask your doc if he or she has any insight on a corresponding LOX inhibitor (e.g. a green tea-derived product) to balance the inflammatory response.

Finally, certain botanical products have been and will continue to be tested. Reviews of aloe have explained why it’s able to prevent and treat sunburns. As expected, it has to do with natural antioxidants. ((Evaluation of biological properties and clinical effectiveness of Aloe vera: A systematic review (2015))) and ((Anti-inflammatory and antioxidant effects of Aloe saponaria Haw in a model of UVB-induced paw sunburn in rats (2014))) The flower Viola tricolor or “heartsease” has also been shown to have similar benefits. ((Antiinflammatory effects of Viola tricolor gel in a model of sunburn in rats and the gel stability study (2013)))

The specific mechanisms which cause the sunburn response (erythema)

It might not be obvious, but the life of a skin cell (aka “keratinocyte”) can be hard. In a schizophrenic way, our skin cells are cyclically encouraged toward apoptosis and anti-apoptosis to delay death until the time is just right. After birth, the keratinocyte is carefully guided toward programmed death, to occur at a specific time and place which benefit the organ as a whole. Keratinocytes must live long enough to differentiate, but must die soon enough to maintain a protective outer layer of dead cells. Thus, while apoptosis (programmed cell death) in response to sunburn is a vital part of maintaining healthy skin, overall, it also plays an important role in the life of all keratinocytes at some point. The outermost layer of skin (stratum corneum) is made of dead cells which underwent apoptosis at specific times and locations along their journey to the surface. Maintaining healthy skin is a complex, highly regulated process.

When a keratinocyte is exposed to UV radiation, ROS are formed via inflammation and advanced glycation endproduct (AGE) formation caused by acute and chronic exposure to DNA-damaging UV light. These are the primary causes of tissue damage. ((Glycyrrhizic acid prevents ultraviolet-B-induced photodamage: a role for mitogen-activated protein kinases, nuclear factor kappa B and mitochondrial apoptotic pathway (2016))) ((Increased matriptase zymogen activation by UV irradiation protects keratinocyte from cell death (2016))) That first study from 2016 found clear indication of damage due to the “mitogen-activated protein kinases, nuclear factor kappa B and mitochondrial apoptotic pathways”. It also claims that, “UV-B-induced DNA damage (via p53), death receptor activation (via TNF-α, Fas, activating caspase 8) and ROS generation initiate a cascade of events leading to apoptotic sunburn cells in the epidermis”.

The second study explains that UVA has the ability to increase ROS formation, justifying avoidance of more than just UVB light. Unlike the direct damage UVB causes, UVA indirectly leads to DNA damage via ROS activity, but it’s mechanism might not be as well understood as that of UVB. ((UVA-induced DNA double-strand breaks result from the repair of clustered oxidative DNA damages (2012))) One reason is that UVA rays are too weak to break covalent bonds, so it must cause DNA damage indirectly via different molecules in the cell. Conversely, UVB rays directly break bonds in DNA. Whether caused by UVA or UVB, DNA damage, known here as “photolesions”, disrupts vital genetic mechanisms (DNA transcription and replication). ((UV Radiation and the Skin (2013)))

The specific mechanisms of cellular response to UV radiation are not fully understood. For example, while the p53 gene seems to inhibit certain anti-apoptotic proteins, I didn’t see certain evidence that this is in response to UVA or UVB, specifically. Further, even cells that don’t have p53 undergo UV-related apoptosis and p53 protection of cells only applies to differentiated keratinocytes (not basal cells). Thus, there’s possibly more at play in this process.

As one review explains,

“On the contrary, it is becoming increasingly apparent that UV induced signal transduction pathways are enormously complex and the final outcome of the intricate network of cellular signaling pathways vary significantly, depending on the cellular background and the wavelength and the dose of UV radiation.” ((Ultraviolet radiation-induced apoptosis in keratinocytes: On the role of cytosolic factors))

The conclusion of that review was that multiple pathways and genes are likely involved in the sunburn response. In fact, the research team suggested that some genes expressed in response to UV radiation might only be expressed due to “aberrant signaling” caused by overall cellular stress. In other words, they know the expression of genes is correlated with radiation, but they can’t predict which genes will be expressed.

Another issue beyond skin cancer and ageing is generally impaired immune function. One report explains that, “UV light can alter and damage the Langerhans cells (LCs) embedded between KCs in the epidermis. LCs normally identify exogenous substances through their surface profile, activate resting T lymphocytes and therefore initiate a specific immune response against the exogenous substances.” ((Photoprotection in changing times – UV filter efficacy and safety, sensitization processes and regulatory aspects (2014)))

Promising developments and conclusion

While this perspective is based on a reasonable amount of evidence to-date, new topics of research are underway. They will, perhaps, allow us enhanced protection against UV radiation. These include circadian rhythms, drugs, and botanicals/natural products. Here’s a brief glimpse at what the future may bring.

Circadian rhythms may provide a way to hack our body’s defense against sunburns. One study found that “sunburn apoptosis, inflammatory cytokine induction, and erythema” were higher when the skin of mice was exposed to early morning or afternoon UV radiation. ((The Circadian Clock Controls Sunburn Apoptosis and Erythema in Mouse Skin (2014))) Note: mice are nocturnal; thus their circadian rhythms would flip the effects we’d expect in humans. That is, we might be better off getting morning sun than afternoon sun.

In either case, circadian rhythm does seem to play a significant role. Why? They explain:

“The early morning is when DNA repair is at a minimum, thus the acute responses likely are associated with unrepaired DNA damage… Among the proteins that are regulated by the clock is XPA (Xeroderma Pigmentosum complementation group A), which is one of the six core factors that are required for removing UV photoproducts from DNA.”

Since I don’t want this to turn into an in-depth examination of circadian rhythms, I will take it as given that their control of DNA repair/replication is well-documented. Further, they add that the human tumor suppressing gene p53 (involved in sunburn response) is also on a circadian clock.

Other aspects of skin found to follow rhythms include “hydration and transepidermal water loss (TEWL), capillary blood flow, sebum production, temperature, surface pH, keratinocyte proliferation rates, and even the visibility of facial rhytides (wrinkles)”. ((Biological Rhythms in the Skin (2016)))

Certain chemicals in drugs are known to cause sensitivity to UV radiation. “Chemical photosensitivity refers to an adverse cutaneous reaction that results when certain chemicals or drugs are applied topically or taken systemically at the same time that a person is exposed to UVR or visible radiation. Phototoxicity is a form of chemical photosensitivity that does not depend on an immunologic response; the reaction can occur on first exposure to an agent. Most phototoxic agents are activated in the range of 320 to 400 nm (the UVA range). Drugs associated with phototoxic reactions include those commonly used by adolescents, such as nonsteroidal anti-inflammatory agents; tetracyclines and tretinoin; other medications such as phenothiazines, psoralens, sulfonamides, and thiazides; and para amino benzoic acid (PABA) esters.” ((Ultraviolet Radiation: A Hazard to Children and Adolescents (2011)))

Because plants need to have natural defenses against radiation, certain antioxidants have been tested for their ability to protect us against the sun. Potentially beneficial antioxidants are found in a huge variety of sources. Cocoa, aloe, chamomile, soy, pomegranate, garlic, ginger, tangerine, chickpeas, passion fruit, peanuts, coffee, tea, oats, corn, and wheat were all listed in a 2015 review of published research on dozens of compounds shown to protect against inflammation and UV radiation (mostly UVA). ((The health benefits of natural skin UVA photoprotective compounds found in botanical sources (2015))) The demand for natural products seems to be growing rapidly, so these products will likely have plenty of consumers, whether they’re in supplements ((Supplementation with tomato-based products increases lycopene, phytofluene, and phytoene levels in human serum and protects against UV-light-induced erythema (2005))), whole-foods ((Skin protection against UV light by dietary antioxidants (2014))), or directly applied to skin. ((Nondenatured Soy Extracts Reduce UVB-induced Skin Damage via Multiple Mechanisms (2008)))

I think we can safely conclude that the sun’s radiation is able to damage our skin in non-cancerous or aesthetic ways. Therefore, it’s prudent to spend some time planning to avoid sunlight unnecessarily–this requires evaluating how important certain activities are to you (and to your loved ones). Obviously, if you have a passion for surfing, surf! You may make the assessment that tans and burns are worth it. Still, this guidance is meant to inform those who might value the long-term health of their skin more than certain activities which increase exposure. As with everything related to health, it’s best to identify your own priorities!