Our skin, draped around us, forms a bridge between the inside of our body and the outside. As the largest organ in the human body, weighing up to 9 kg, the skin plays important roles in protecting us, while maintaining an effective communication between us and the outside. Despite its crucial role, we do not regard the skin as an important organ in the human body. The brain and heart are more readily thought of in this context. Such thoughts could, perhaps, be why we do not invest as much care into our skin, for instance by abstaining from wearing sunscreen.

Without our skin we would, quite literally, evaporate. The waterproof epidermis, the skin’s outermost layer, controls water flow in and out of the skin. Not only does the skin protect us from the outside world and help to maintain homeostasis, but the skin also enables us to communicate, and be part of our surroundings. The epidermis also contains the majority of our touch receptors, each one serving a specific purpose, ranging from the detection of pain (nociceptors) to changes in the outside temperature (thermoreceptors). These touch receptors are linked to different areas of the brain through neurons. Once a receptor on the skin is stimulated, a cascade of neurons relays the signal to the brain. The brain then imposes a response to the stimulus: for instance, in the cold, blood vessels contract to keep an individual warm - this is the reflex commonly known as goosebumps. Interestingly, the brain pays disproportionate attention to each part of the body, the hands, lips and feet being the most sensitive.

The dermis is the layer that lies below the epidermis, as its name suggests. Its main role is to sustain the epidermis, by supplying it with oxygen and nutrients. The dead cells from the dermis are what later forms the epidermis. The fatty bottom layer, the subcutaneous tissue, keeps the skin attached to our muscles and tendons. It also acts as an insulating layer, which contributes to maintaining our regular body temperature.

“Sun damage truly becomes harmful when mutations in the cell’s DNA inhibit its apoptotic [cell death] mechanism.”

Although human skin has evolved to help us sense and protect ourselves from the outside, it remains a relatively vulnerable organ. This susceptibility to damage is mainly due to sun exposure, which causes about 90% of ageing, with characteristics such as wrinkling and loss of elasticity, as well as the majority of skin diseases. Although the phrase “sunburns cause cancer” is repeated every summer, it also tends to be a fact to which we do not pay enough attention.

In fact the sun emits, amongst others, ultraviolet or UV radiation. These rays, not visible to the human eye, can infiltrate the dermis and epidermis and cause damage to their underlying skin cells. The ozone layer can prevent certain types of harmful UV rays from penetrating the atmosphere, however the phenomenon of ozone depletion has damaged this property. Studies have directly linked ozone depletion to increased rates of skin cancer.

While low doses of UV radiation help maintain a healthy immune system by promoting Vitamin D production, higher exposure can be harmful to the skin in two ways: either by causing direct damage to skin cells or by acting as a mutagen, causing changes in the cell’s DNA sequence. More precisely, UV rays cause two adjacent thymine base pairs to abnormally bond to each other, and to form what is known as a thymine dimer. This dimer affects the shape of the entire DNA molecule by locally preventing it from adopting its helical shape. DNA is crucial in processes such as cell division and protein formation, meaning that these mutations can obstruct the proper functioning of the entire cell.

In many cases, thymine dimerisation can be fixed by nucleotide excision repair. When too many such mutations occur, the cell’s DNA is damaged beyond repair. A process known as apoptosis, or programmed cell death, is triggered. As the cell dies, blood vessels dilate to bring immune cells, which dispose of the dead cell, to the area. This process is what causes the redness, swelling and burning sensation felt during a sunburn. Sun damage truly becomes harmful when mutations in the cell’s DNA inhibit its apoptotic mechanism. When apoptosis is inhibited, cells do not die but rather proliferate, with the possibility of them eventually leading to cancer.

There are many genetic factors that influence one’s danger of UV-mediated skin disease. The polymorphisms of certain genes, such as MC1R and where one’s skin lies on the Fitzpatrick scale (a numerical classification of skin color) are all factors. Despite our genetic predispositions, everyone’s skin needs protection from sun damage, albeit to varying extents. The most effective way of doing so, besides staying inside, is by applying sunscreen. Sunscreen works by blocking and absorbing UV rays that would otherwise come into contact with our skin. It contains physical particles, namely metals such as titanium dioxide or zinc. Physical particles reflect the UV rays, making them “bounce off” the skin. Sunscreen also contains chemical particles, which absorb UV frequencies before they can come into contact with our skin. They usually release the energy in the form of heat. These molecules can be broken down by sunlight, hence the need to reapply sunscreen regularly.

Sunscreens have different Sun Protection Factors (SPF). Their values normally vary from 15 to 50, indicating the increase in the amount of Sun exposure that it takes UV rays to cause a sunburn, versus when the product is not being used. For instance, an SPF of 50 means that it takes 50 times more solar energy to get a sunburn compared to when it is not being used.

Whether tanning in the park on a moderately cloudy British summer day, or on the beach on a Greek island, we will all increase our sun exposure in the coming months. Understanding how best to protect our skin is vital if we are to preserve our long-term health.