By Themis Halka
Sunscreen, the smelly cream or oil that reminds us of summer holidays and beaches, has become a multi-billion-dollar market over the last fifty years. Cosmetic industries exploit the popular sun care field to keep creating new products that fit the numerous customer’s exigences. Although sunscreen largely pursues aesthetic goals, we must remember it is a necessary precaution for our healthcare.
Sun protection lotions have existed since antiquity and the first synthetic chemical sun protection was created in the late 1920s. Yet it wasn’t until the 1970s that the sun care mass market started to expand. In fact, until then, tanning was very fashionable, a long-lasting trend initiated by Coco Chanel in the French Riviera, and the dangers of this ‘healthy glow’ weren’t well-known (Rupert 2018). Sun protection stopped simply being a luxury and fashionable product to become a necessary precaution when the relation between sun exposure and skin cancer became public knowledge.
The sun’s effect on our skin is due to UV light that can cross the atmosphere. We differentiate two types of UV that have different effects on our skin: UVA and UVB. UVA, which accounts for 95% of UV light on Earth, was for a long time used in tanning beds, until it was discovered to be responsible for skin ageing. UVB, on the other hand, is the main cause of burnings, but is also our principal source of vitamin D (The Skin Cancer Foundation 2019). While UVB can’t cross glass, UVA can’t be stopped, which explains why, when looking at a truck driver that has spent his life on a road, it strikes us that one side of his face seems more aged than the other due to always being exposed to UVA light (Lyman 2019). Thus, a first consequence of sun exposure, particularly to UVA, is the feared acceleration of skin-ageing.
These UV rays both contribute to tanning but have further consequences on our skin’s health. UVA mainly penetrate deep into the dermis, and though it can also hit the outer layers of our skin and participate in the development of cancer, UVB are mainly responsible for its emergence. In fact, UVB are stopped by the epidermis, their energy being absorbed as they slice the DNA of the outermost skin cells (Lyman 2019). UV radiations induce two classes of DNA lesions: cyclobutane pyrimidine dimers and 6,4 photoproducts, that both distort DNA structure by creating bends that prevent transcription and replication (Clancy 2008).
Fortunately, a single sunburnt won’t irremediably lead to cancer, as cells possess elaborated repair systems. To face damaged DNA, the cell can use its excision repair system, that will extract the damaged nucleotides and replace them with new bases (Clancy 2008). However, if they do repair damaged DNA, most of the time these repair mechanisms aren’t 100% efficient and sometimes DNA isn’t repaired. This makes the DNA particularly sensible and if further mutated could give birth to cancer. On that subject, moles are to be watched and carefully protected from sun exposure, as it is estimated 20 to 40 percent of melanomas form within existing moles (Cymerman et al. 2015).
Sun exposure would cause irremediable DNA damages all the time if it wasn’t for our melanocytes. Melanocytes are specialised cells located at the bottom of our epidermis, that produce the substance responsible for tanning: melanin. Melanin disarms the UV ray by liberating a proton to counter it, transforming it into harmless heat. Thus, when lastingly exposed to sunlight, melanocytes start to produce melanin in big quantities so that it can keep protecting our skin’s DNA from permanent damage, which induces tanning (Naoi et al. 2017). However, melanin can’t indefinitely absorb all UV radiation and a suntan isn’t a sufficient protection against sunlight, providing a sun protection factor of only 3, compared to a minimum of 15 for efficient sunscreens (Lyman 2019).
Melanin, therefore, isn’t enough, as sunburns painfully remind us. Sunburns are to be prevented at any cost, as they are the sign our melanocytes have been overwhelmed and couldn’t protect us from all the dangerous radiations. If reddening and usual sunburns don’t significantly increase the risk of developing cancer later in life, it is not the case for blistering sunburns. Research suggests that a blistering sunburn in childhood increases the risk of melanoma later in life by 50% (Dennis et al. 2008). Melanoma is a type of skin cancer strongly linked to sun exposure, that must be taken seriously, as it can be lethal if not detected early, due to its high probability of metastasizing (The Skin Cancer Foundation 2018). Thus, sunburns can have a lifelong impact on our health and must be prevented at any cost. Fortunately, this ‘at any cost’ can be achieved rather easily by using sunscreen, hats and caps.
Sun protection is therefore a necessity to prevent UV rays from altering our skin’s functions, and the correct use of sunscreen can minimise skin-ageing and especially sunburns, as well as damages in our DNA that could lead to melanoma. To have an adequate protection against UV light, an average-sized adult must cover his skin with 35-45mL of sunscreen, i.e. between 6 and 8 teaspoons of broad-spectrum (for both UVA and UVB) sunscreen. The SPF, sun-protection factor, must be at least 15, meaning it will take 15 times longer for the skin to redden than with no sunscreen. SPF only accounts for UVB; for UVA, a 1-5-star system indicates the protection (Lyman 2019).
Cosmetic firms now offer hundreds of different sunscreens, specialised for adolescent’s oily skins or mum’s anti-ageing. These special features can seem important, yet the priority must be given to the sun protection offered by the cream, which is the most important for your health, your skin, and will have the best long-term effect on wrinkles too.
Rupert C., 2018. The story of sun cream. Available from : https://blog.sciencemuseum.org.uk/the-story-of-sun-cream/ [Accessed 14th November 2020]
The Skin Cancer Foundation. (2019). UV Radiation – The Skin Cancer Foundation. [online] Available at: https://www.skincancer.org/risk-factors/uv-radiation/ [Accessed 14th November 2020]
Lyman M., The remarkable Life of the Skin, 2019, pp.70-78.
Clancy S., 2008. DNA damage & repair : mechanisms for maintaining DNA integrity. Nature Education 1(1):103. Available from : https://www.nature.com/scitable/topicpage/dna-damage-repair-mechanisms-for-maintaining-dna-344/ [Accessed 14th November 2020]
Cymerman R. M., Wang K., Murzaku E. C., Penn L. A., Osman I., Shao Y., Polsky D.. De novo versus Nevis-associated melanoma: differences in associations with prognostic indicators and survival. American Society of Clinical Oncology, 2015.
Naoi M., Maruyama W. and Riederer P. (2010). Melanin. Encyclopedia of Movement Disorders, pp.169–171
Dennis L. K., Vanbeek M. J., Freeman L. E. B., Smith B. J., Dawson D. V., Coughlin J. A.. Sunburns and risk of cutaneous melanoma : does age matter ? A comprehensive meta-analysis. Annals of epidemiology, 18(8), 2008, pp.614-27.
The Skin Cancer Foundation. (2018). Melanoma – The Skin Cancer Foundation. [online] Available at: https://www.skincancer.org/skin-cancer-information/melanoma/ [Accessed 14th November 2020]