Sunlight: Positive and Negative Effects

Sunlight is electromagnetic energy, and the solar spectrum has a wavelength that ranges from 200 to 1800 nanometers (nm). Three different types of light can be distinguished: visible light, which can be seen with the naked eye; infrared light, which is invisible and responsible for the sensation of heat; and ultraviolet light, which, with its various wavelengths, can induce skin pigmentation.

The effects of light on the body vary, as does the way it is absorbed. Visible light (37%) is not harmful to health and does not damage the skin. It may sometimes cause temporary glare and a sensation of momentary blindness. Light is also very important for regulating certain bodily functions, such as the sleep-wake cycle, the circadian rhythm of hormones, and the stimulation of serotonin production, an important neurotransmitter involved in various functions, especially those related to behavior.

Infrared rays (60%) primarily produce thermal effects. They can be artificially reproduced and used for therapeutic purposes. Most of them are absorbed by the atmosphere. Their most important feature is the transmission of heat to the outer layer of the skin (stratum corneum). Therefore, excessive absorption can damage the skin, causing hyperthermia and symptoms ranging from vasodilation to skin dehydration.

Ultraviolet (UV) radiation can have both positive and negative effects. It contributes to the synthesis of vitamin D, a substance necessary for bone development and protection against conditions such as rickets, osteomalacia, and osteoporosis. UV rays are also highly effective in the treatment of skin conditions such as psoriasis and atopic dermatitis.

Among the possible negative effects are:

• Sunburn caused by excessive or improper exposure

• Skin spots

• Skin aging characterized by wrinkles, furrows, and loss of skin elasticity

• Skin cancer – UV rays are strongly linked to the development of oncological skin diseases, including the frequent occurrence of keratotic lesions with epithelial damage, which can represent the initial stage of possible carcinomatous evolution.
  

Ultraviolet (UV) radiation, characterized by short wavelengths, is divided into UVC (200–290 nm), UVA (320–400 nm), and UVB (290–320 nm). They have the following characteristics:

• UV-C (100–280 nm):Fortunately, they do not reach the Earth's surface because they are filtered by the atmospheric ozone layer. They have extremely high energy levels. In recent decades, atmospheric pollution has led to the widening of the ozone hole, increasing the risk that we may become more easily exposed to the harmful effects of these rays in the future.

• UV-A (320–400 nm):They are the least energetic rays (energy is inversely proportional to the wavelength), but they can penetrate deep into the dermis, where they can damage collagen and elastin. These UV-A rays stimulate the maturation process of melanin present in melanosomes; therefore, they are responsible for the immediate pigmentation of the skin, which appears during sun exposure and fades within 2–3 hours. Since they penetrate deeper, they are more strongly linked to the formation of skin tumors, photoaging, photoimmunosuppression, and phototoxicity and photoallergy phenomena.

• UV-B (280–320 nm):They are responsible for the immediate and visible effects of solar radiation on the skin because they stimulate melanogenesis and cause tanning, which continues even after exposure. They are also the main rays responsible for immediate damage, such as sunburn (erythema) or skin redness.
  

When the skin is exposed to the sun, various biological protection processes are activated. Our body is able to protect itself through several mechanisms, mainly involving melanin, urocanic acid, and thickening of the stratum corneum:

• The stratum corneum begins to thicken (hyperkeratosis) due to increased mitosis of the basal cells of the epidermis, aiming to protect the skin from UV radiation.

• There is an increase in β-carotene, an antioxidant molecule that acts as a neutralizer of oxygen free radicals and as a membrane stabilizer.

• Sweating is activated, along with the production of urocanic acid, a molecule derived from the deamination of histidine, which can absorb UVA rays and thus protect the skin.

• The enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH) are activated, functioning as scavengers of reactive oxygen species (ROS).

• DNA repair and replication mechanisms are triggered.

• The main self-protection mechanism against UV rays is activated: pigmentation, or tanning.
  

However, when sun exposure is excessive, the body's physiological responses become insufficient, and solar rays can cause harmful effects. The most common acute damage is acute erythema caused by vasodilation of the microcirculation in the papillary dermis and the production of inflammatory substances by keratinocytes.

On the other hand, repeated, long-term sun exposure (photoaging) can lead to:

• Solar elastosis – Thinning of the skin, which loses its elasticity.

• Irregular distribution of melanin pigment, leading to the formation of pigment spots.

• Loss of the skin's ability to retain water, resulting in rough and dry skin. This leads to skin aging, including deep wrinkles and sun-induced freckles (solar lentigines).

• Cellular alterations such as mutations – From solar or actinic keratoses to epithelial tumors. This is a hypertrophic alteration specific to sun-exposed skin, with signs of proliferative disorder that, depending on the genetic mutation, may give rise to neoplasia.
  

From a histopathological perspective, the most significant damage occurs at the level of the dermis, where UVA rays are able to penetrate. The alterations affect both the components of the extracellular matrix and the dermal cells. The dermis becomes altered, takes on a yellowish color, increases in thickness, and makes the skin less elastic and lacking in tone. Collagen fibers are degraded, leading to severe depletion of fibrillar proteins and a significant alteration of elastic fibers in both their components and three-dimensional structure.

Obviously, cells are also involved in this process, with an increase in fibroblasts, histiocytes, and mast cells, which in turn secrete inflammatory mediators that promote fibroblast proliferation. Melanocytes become scattered along the basal membrane, and blood vessels become more tortuous and appear more dilated. Most of these disorders are due to both the increased production of free radicals (reactive oxygen species, ROS) induced by UVA rays and direct damage to nucleic acids (DNA and RNA) caused by UVB rays. The latter are more responsible than UVA rays for the onset of skin cancers other than melanoma, such as basal cell carcinoma and squamous cell carcinoma.

Recently, data has been collected on the direct damage caused by UVA rays associated with increased production of oxidative species (free radicals), which cause immunosuppression, oxidative DNA damage, and the induction of specific mutations in oncogenes—phenomena directly linked to the pathogenesis of melanoma.

It has been documented that sporadic sun exposure in early life is the most dangerous. Free radicals produced by UVA rays attack the structure of the cell membrane of the basal cells of the epidermis, causing oxidation of membrane amino acids, lipid-lipid and lipid-protein crosslinking, disulfide bonds, and protein cleavage. All these reactions alter permeability, leading to cell death and subsequent early signs of aging. For these reasons, it is essential to ensure adequate protection of the skin and its appendages.

Prevention: These are primarily practical recommendations:

• Use sunscreen with a sun protection factor (SPF) > 30 and water resistance. In the evening, before going to bed, apply oil-based creams with high moisturizing, soothing, anti-inflammatory, and antibacterial properties.

• Avoid sun exposure during the central hours of the day (10 AM to 2 PM).

• Be cautious of reflected sunlight from snow, sand, water, etc.

• Wear protective clothing: shirts, t-shirts, pants, hats, and always wear certified sunglasses.
  

EYE CARE: Prolonged exposure of the eyes to sunlight, particularly intense ultraviolet light, can promote the formation of cataracts, while high levels of high-energy visible light can be linked to age-related macular degeneration.

• Ensure an adequate intake of vitamin D, including through dietary supplements.

• Follow a diet rich in fruits and vegetables. It is advisable to add dietary supplements with antioxidant properties. The substances taken orally aim to protect cells and their DNA from the attack of free radicals.

• Avoid artificial tanning (tanning beds) due to their carcinogenic risk.

• Have an annual skin check and consult a dermatologist in case of bleeding lesions or changes in color and shape.
  

Bibliografia

• Hughes MC, Williams GC, Baker P, Green AC; "Sunscreen and Prevention of Skin Aging, a Randomized Trial". Ann Int Med 2013; 158(11):781-790

• Stern RS. Prevalence of a history of skin cancer in 2007: results of an incidence-based model. Arch Dermatol. 2010 Mar;146(3):279-8

• The International Agency for Research on Cancer Working Group on artificial ultraviolet (UV) light and skin cancer. The association of use of sunbeds with cutaneous malignant melanoma and other skin cancers: A systematic review. International Journal of Cancer: 2006 March 1;120:1116–1122

• Holloway L. Atmospheric sun protection factor on clear days: its observed dependence on solar zenith angle and its relevance to the shadow rule for sun protection. Photochem Photobiol 1992;56:229-34

• Xu S et al. Sunscreen Product Performance and Other Determinants of Consumer Preferences JAMA Dermatol. Published online July 06, 2016. doi:10.1001/jamadermatol.2016.2344

• Lindqvist PG et al. Avoidance of sun exposure as a risk factor for major causes of death: a competing risk analysis of the Melanoma in Southern Sweden cohort J Int Med 2016 online: DOI: 10.1111/joim.12496

• Lindqvist PG. On elucidating a possible link between vitamin D and venous thromboembolism–finding a piece of the puzzle.

• S.Lautenschlager, H.C.Wulf, M.R.Pittelkow “Photoprotection” Lancet 2007; 370:528-37).

• Amgad A. Awad El.Gied, Abdelkareem M.Abdelkareem and Elnazeer. Hamedelniel: Investigation of cream and ointment on antimicrobial activity of Mangifera indica extrac.