The Importance Of Sunscreen: Scientific Sunscreen Guide Part I.

Daily sunscreen use is on the rise as people begin to realize just how damaging UV radiation can be for the skin. However, there is still plenty of confusion regarding how to choose a sunscreen with good UV protection. What exactly is the importance of sunscreen? Is a moisturizer with added SPF ok? Are physical sunscreens better than chemical? How do you know whether a sunscreen is broad-spectrum? Are higher SPFs always better? How do you know how good a sunscreen is at protecting against UVA damage? Do you need to worry about visible light or infra-red? Should you wear sunscreen indoors?

These are just a small selection of the hundreds of possible questions that may go through your head when trying to decide on a sunscreen.

Hopefully, after reading this three-part guide, you will have a better idea of the importance of sunscreen, how sunscreens work, how UV protection is measured, and how to make an informed decision when choosing a sunscreen.

If you’re not too fussed about the ‘how’s’ and the ‘why’s’, and would rather just be given a list of good sunscreens to choose from – check out Part III – The Best Sunscreens With High UVA Protection.

However, if you love a bit of science and need to know how and why things work – carry on reading…

A Quick Recap Of Skin Anatomy

The skin is the largest organ of the body and our first line of defense against the environment and its various pollutants. It also plays a role in regulating body temperature and is responsible for preventing excess water loss from the body. It consists of three main layers – the epidermis, the dermis, and the subcutaneous layer (or hypodermis)^[1].

Epidermis

The epidermis continually produces a protective layer of skin cells, a process known as epidermal desquamation (also referred to as skin cell turnover). This is an active process that occurs without our knowledge. In fact, it is estimated that a billion skin cells are shed from the surface of the skin every day due to this continuous process.

The epidermis is made up of four layers – the basal layer, the spinous (squamous cell) layer, the granular layer, and the stratum corneum (cornified layer) ^[1].

In the basal layer, the skin cells are initially attached to a basal membrane where they rapidly multiply before detaching from the membrane and moving outward through the spinous layer and the granular layer until they are eventually shed by the stratum corneum ^[2].

Within a four-week period, the basal cell is created, developed, and shed from the skin’s surface.

Melanocytes, the cells that produce melanin, are found in the epidermis and hair follicles. The transfer of melanin to keratinocytes (skin cells that makes up 80% of the cells in the epidermis) from melanocytes determines the skin’s color and is involved in protecting skin cells from UV radiation ^[3].

Dermis

The dermis makes up the bulk of the skin and is responsible for its pliability, elasticity, and tensile strength. There are two distinct sections in the dermis; the adventitial dermis (papillary and periadnexal dermis) and the reticular dermis. The papillary dermis borders the epidermis, while the reticular dermis borders the subcutaneous tissue.

The main component of the dermis is collagen, which represents 70% of the skins total dry weight. Collagen bundles are thicker in the reticular dermis than in the adventitial dermis and, along with elastic connective tissue, form the majority of the dermal matrix. Matrix remodeling enzymes regulate dermal matrix turnover and degrade collagen fibers in order for them to be replaced by new fibres.

The dermis also contains the nerves and blood vessels, while sweat glands, hair follicles, and sebaceous glands are found in the dermal-epidermal junction(a porous membrane that holds the epidermis and dermis together and allows the exchange of cells and fluids between the two) ^[1].

Subcutaneous Layer

The subcutaneous layer is made up of fat cells and stores energy for the body. It varies in thickness depending on the skin site. For example, the subcutaneous layer is thinnest on the eyelids and thickest on the soles of the feet ^[1].

Why Is This Relevant?

The key point to take away from this is that the epidermis contains a number of cells that can be affected by UV radiation; basal cells, squamous cells, and melanocytes. While the dermis is mainly made up of collagen and elastin.

Solar Radiation And The Types of UV Radiation

The radiation produced by the sun (solar radiation) that is able to reach our skin is mainly made up of:

• Infrared radiation (780-5000nm wavelength; approximately 53% of solar radiation).
• Visible light (400-780nm wavelength; approximately 39-44% of solar radiation).
• UV radiation (290-400nm wavelength; 3-7% of solar radiation) ^[4].

UV radiation can be further broken down into UVA (340-400nm), UVB (290-320nm), and UVC (200-290nm). UVC rays are the shortest of the three types of UV rays and are entirely absorbed by the atmosphere. This means that they are unable to reach our skin in order to damage it ^[5].

However, UVA and UVB rays are able to penetrate the skin and cause damage. A general rule of thumb is that UVA rays cause Aging and UVB rays cause Burning but, as you can imagine, it’s not quite as simple as that.

UVA rays account for the majority (95%) of UV radiation, are relatively constant all year round, and can penetrate deeper into the skin due to their longer wavelength. In the dermis, UVA rays can cause damage to DNA and break down collagen and elastin. This damage is usually an accumulative effect and invisible to the naked eye. UVA rays are also able to pass freely through glass.

UVB rays account for less than 5% of total UV radiation and are stronger in the summer. Due to their shorter wavelength, UVB rays are only able to penetrate the epidermis and are not able to pass through glass. In the epidermis, UVB rays cause DNA damage that causes an inflammatory response and is visible almost immediately as sunburn ^[5].

UVA rays are still able to cause sunburn but the dose required is one-thousand times that of UVB rays ^[6].

How Do UVA & UVB Rays Damage DNA?

As mentioned earlier, UV radiation makes up the minority of solar radiation yet it causes the most damage. This is due to the fact that shorter wavelengths of light/radiation have more energy than longer wavelengths. For this reason, UVA rays have less energy than UVB rays.

This energy is transferred to light-absorbing molecules in the skin called chromophores. In human skin, especially the epidermis, there are several key naturally-occurring chromophores that absorb UV radiation – DNA, urocanic acid, amino acids, and melanin ^[7].

When UV radiation is absorbed by DNA it can cause damage that can lead to genetic mutations. Usually, our cells correct this damage seconds after it has occurred, however, if the damage goes uncorrected, the genetic information may be permanently mutated^[8].

One of the key cell regulators that can end up mutated as a result of DNA damage is the p53 tumor-suppressor gene which, as you may have guessed from the name, prevents the formation of tumors.  If the key regulatory genes fail, cells with mutated genes can multiply uncontrollably and eventually result in skin cancer ^[9].

In fact, mutations in the p53 tumor-suppressor gene have been found in more than 90% of all squamous cell carcinoma (SCC) skin cancers and in approximately 50% of all basal cell carcinoma (BCC) skin cancers ^[9].

UVA and UVB rays damage DNA in slightly different ways. Due to UVAs longer wavelength and lower energy, it is not directly absorbed by DNA. Instead, it is absorbed by other, non-DNA, chromophores and causes the production of reactive oxygen species (ROS; a type of free radical). It is the ROS that then damage DNA rather than UVA itself ^[10].

In contrast, UVB radiation is directly absorbed by DNA ^[9], which suggests that it plays a larger role in the development of skin cancers than UVA radiation ^[11].

How Does UV Radiation Affect Melanin?

There are three main steps involved in the increase in skin pigmentation after exposure to UV radiation – immediate pigment darkening (IPD), persistent pigment darkening (PPD), and delayed tanning or delayed pigment darkening (DT/DPD) ^[12].

IPD is a temporary darkening of pigment that occurs within minutes of UV exposure. It initially appears as a greyish color before fading to a brown color over a period of minutes to days and is a result of melanin oxidization and melanosome redistribution. It doesn’t appear to have any protective effect from UV radiation and is particularly activated by UVA rays.

PPD follows IPD and is a longer phase of tanning that appears brown in color. Similarly to IPD, PPD is thought to be caused by melanin oxidization and is more strongly activated by UVA than UVB. However, PPD lasts at least 3-5 days. (PPD can be used to test the protection factor that sunscreens offer against UVA radiation).

The last phase of tanning (DPD) is caused by an increase in melanin production, an increase in the number and activity of melanocytes, and increased transfer of melanosomes. DPD can be caused by either UVA or UVB and is first noticeable 2-3 days after sun exposure and usually lasts for at least 3-4 weeks before beginning to fade. DPD caused by UVB radiation seems to have a photoprotective effect while DPD caused by UVA radiation does not ^[12].

Melanin absorbs both UV radiation and visible light. When melanin is transferred from melanocytes to keratinocytes, it can create a ‘cap’ (a supranuclear melanin cap) above the cell’s nucleus (where the DNA is stored). These melanin caps can reduce UV transmission to DNA by absorbing the majority of UV radiation before it is able to reach the cell’s nucleus. This is concentration-dependent in that the more melanin present in the ‘cap’, the more UV radiation is absorbed by the melanin and the less UV radiation is able to cause DNA damage ^[13].

Because darker skin contains more melanin, darker-skinned individuals have a higher natural protection from UV-induced DNA damage as more melanin is available to absorb UV light before it is able to damage DNA. However, melanin itself only offers a sun protection factor (SPF) of about 1.5-4. Specifically, darker skin only appears to allow 7.4% of UVB and 17.5% of UVA to penetrate, while fairer skin allows 24% of UVB and 55% of UVA to penetrate ^[12].

How Does UV Radiation Age Skin?

UV radiation is responsible for approximately 80% ^[14] to 90% ^[15] of facial skin aging. This is due to the generation of reactive oxygen species (ROS) by UV radiation, particularly by UVA radiation. UV-light-induced ROS activate the transcription factors that regulate matrix metalloproteinases (MMPs) leading to an increase in MMPs. MMPs are enzymes that degrade matrix proteins such as collagen and elastin. This means that increases in MMPs lead to the destruction of collagen and elastin. Because of this, the destruction of collagen is considered a trademark of premature aging due to UV exposure (photoaging/photodamage) ^[16].

As mentioned earlier, UVA rays are able to penetrate into the dermis (where collagen and elastin reside) which is why the association between premature aging and UVA is stronger than the association between premature aging and UVB.

The Importance Of Sunscreen

Sunscreens work in combination with biological photoprotection (melanin production) by absorbing or scattering UV rays and preventing them from reaching DNA and other skin components that are prone to damage from UV radiation ^[17].

Sunscreens can be organic (chemical), inorganic (physical), or a combination of the two. Chemical sunscreen filters are absorbed into the skin where they act as exogenous (external) chromophores. This means that the chemical filter molecule absorbs UV radiation instead of the naturally occurring chromophores (e.g. melanin and DNA). As it has no biological purpose, the chemical filter dissipates the energy it absorbs from UV radiation in the form of heat. Chemical filters can offer protection against the UVA and/or UVB spectrums.

Physical sunscreens act as a barrier on top of the skin and, like chemical filters, display broad absorption across the UVA and UVB spectrums. However, they also scatter the incoming UV radiation away from the skin. The absorption and scattering efficiency of physical sunscreen filters largely depends on the particle properties (e.g. diameter, surface, coating, etc.) ^[18].

Because of their scattering properties, physical sunscreens are considered photostable. However, if chemical filter molecules are unable to dissipate the energy from absorbed UV radiation fast enough, they may lose their photoprotective qualities and become unstable.

Basically, the chemical filter absorbs a photon of light and becomes energized. If it is unable to lose this energy, it is not able to absorb the next photon of light. This means that the second photon of light may be absorbed by DNA or melanin instead, which defeats the object of the chemical filter in the first place.

Some chemical filters are more stable than others and those that are unstable can be stabilized when combined with other chemical filters.

Sunscreen Filters

Here is a chart containing some of the common chemical and physical sunscreen filters with information on their absorbance spectrum and photostability:

* = May Have Health Risks (Read More). Sources = [19] & [20]

Summary

While UV radiation only accounts for a small percentage of total solar radiation, it is by far the most damaging. This is due to the fact that shorter wavelengths of light contain more energy than longer wavelengths. This also means that UVA rays have less energy than UVB rays. 

This energy is transferred to light-absorbing molecules in the skin called chromophores. Chromophores that absorb light in the UV spectrum include DNA and melanin. When UV radiation is absorbed by DNA it causes damage that can lead to genetic mutations. If this damage is not corrected by the cells natural defenses, mutated cells can multiply rapidly and eventually result in skin cancer.

UVA and UVB rays damage DNA in different ways. UVB rays are directly absorbed by DNA which is why they are more closely associated with skin cancer. UVA rays, on the other hand, cause indirect DNA damage through the generation of free radicals. It is these free radicals that cause the DNA damage rather than the UVA rays themselves.

Melanin acts as a natural defense against UV radiation by creating a ‘cap’ above the cell’s nucleus. As melanin absorbs UV radiation, it reduces the transmission of UV rays into the nucleus to be absorbed by DNA. The more melanin contained within skin, the better the skins natural protection. An increase in melanin production in response to UV radiation is called ‘tanning’ and consists of three separate stages:

• Immediate Pigment Darkening (IPD) is temporary, happens almost immediately, and has no protective effect. It is caused by melanin oxidization and melanosome redistribution.
• Persistent Pigment Darkening (PPD) follows IPD but lasts at least 3-5 days and is caused by melanin oxidization. It is particularly activated by UVA radiation.
• Delayed Pigment Darkening (DPD) is the last phase of tanning, is caused by an increase in melanin production, and lasts a couple of weeks. DPD caused by UVB seems to have a protective effect, unlike DPD caused by UVA.

Finally, UV radiation is responsible for 80-90% of facial skin aging. This is due to the fact that it causes the generation of free radicals that activate enzymes that degrade collagen and elastin. As collagen and elastin are contained within the dermis, and as UVA can penetrate the dermis, the premature aging associated with UV radiation is predominantly due to UVA.

References

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2. Fuchs, E. (2008). ‘Skin stem cells: rising to the surface’, J Cell Biol., 180(2), 273. Available at: http://jcb.rupress.org/content/180/2/273
3. Cichorek, M., Wachulska, M., Stasiewicz, A. & Tyminska, A. (2013). ‘Skin melanocytes: biology and development’, Postepy Dermatol Alergol., 30(1), 30-41. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834696/
4. Frederick, J., Snell, H. & Haywood, E. (1989) ‘Solar ultraviolet radiation at the earth’s surface’, Photochem Photobiol, 50, pp. 443–450. https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1751-1097.1989.tb05548.x
5. Palm, M. & O’Donoghue, M. (2007). ‘Update on photoprotection’, Dermatologic Therapy, 20(5), 360-376. Available at: https://onlinelibrary.wiley.com/doi/full/10.1111/j.1529-8019.2007.00150.x
6. Parrish, J., Jaenicke, K. & Anderson, R. (1982). ‘Erythema and melanogenesis action spectra of normal human skin’, Photochem Photobiol., 36(2), 187-191. Available at: https://www.ncbi.nlm.nih.gov/pubmed/7122713/
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9. Seebode, C., Lehmann, J. & Emmert, S. (2016). ‘Photocarcinogenesis and skin cancer prevention strategies’, Anticancer Research, 36(3), 1371-1378. Available at: http://ar.iiarjournals.org/content/36/3/1371.full
10. Scharffetter-Kochanek, K., Wlaschek, M., Brenneisen, P., Schauen, M., Blaudschun, R. & Wenk, J. (1997). ‘UV-induced reactive oxygen species in photocarcinogenesis and photoaging’, Biol Chem., 378(11), 1247-1257. Available at: https://www.ncbi.nlm.nih.gov/pubmed/9426184?dopt=Abstract
11. Kumar, R., Deep. G. & Agarwal, R. (2016). ‘An overview of ultraviolet B radiation-induced skin cancer chemoprevention by silibinin’, Curr Pharmacol Rep, 1(3), 206-215. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4471873/
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13. Kobayashi, N., Nakagawa, A., Muramatsu, T. et al. (1998). ‘Supranuclear melanin caps reduce ultraviolet induced DNA photoproducts in human epidermis’, J Invest Dermatol., 110(5), 806-810. Available at: https://www.sciencedirect.com/science/article/pii/S0022202X15400855
14. Baumann, L. (2007). ‘Skin ageing and its treatment’, J Pathol., 211(2), 241-251. Available at: https://www.ncbi.nlm.nih.gov/pubmed/17200942
15. Farage, M., Miller, K., Elsner, P. & Maibach, H. (2008). ‘Intrinsic and extrinsic factors in skin ageing: a review’, Int J Cosmet Sci., 30(2), 87-95. Available at: https://www.ncbi.nlm.nih.gov/pubmed/18377617
16. Pandel, R., Poljsak, B., Godic, A. & Dahmane, R. (2013). ‘Skin photoaging and the role of antioxidants in its prevention’, ISRN Dermatology, Article ID 930164, 11 pages. Available at: https://www.hindawi.com/journals/isrn/2013/930164/
17. Baker, L. & Stavros, V. (2016). ‘Observing and understanding the ultrafast photochemistry in small molecules: Applications to sunscreens’, Science Progress, 99(3). Available at: https://journals.sagepub.com/doi/abs/10.3184/003685016X14684992086383
18. Barker, L., Marchetti, B., Karsilli, T., Stavros, V. & Ashfold. (2017). ‘Photoprotection: extending lessons learned from studying natural sunscreens to the design of artificial sunscreen constituents’, Soc. Rev., 46, pp. 3770-3791. Available at: https://pubs.rsc.org/en/content/articlehtml/2017/cs/c7cs00102a
19. Lionetti, N. & Rigano, L. (2017). ‘The new sunscreens among formulation strategy, stability issues, changing norms, safety and efficacy evaluations’, Cosmetics, 4(2), pp. 15. Available at: https://www.mdpi.com/2079-9284/4/2/15/htm
20. Osterwalder, U. & Herzog, B. (2010). ‘The long way towards the ideal sunscreen – where we stand and what still needs to be done’, Photochemical and Photobiological Sci., 9(4), 470-481. Available at: https://www.researchgate.net/publication/42768818_The_long_way_towards_the_ideal_sunscreen_-_Where_we_stand_and_what_still_needs_to_be_done