COCO CHANEL
In the early 1920s, Coco Chanel, world-famous fashion designer, rode her yacht to the sun-soaked beaches of Cannes. The trip to Cannes and Coco's resulting sun-kissed glow have long been considered the advent of today's tanning fad. Although these tanning trends captivated the American nation, clinicians and researchers were simultaneously discovering the many deleterious effects associated with excessive sun exposure.
A study, published in 1922, became the first to elucidate a link between ultraviolet B (UV-B) light and sunburn. A few years later in 1928, the first sunscreen blend was placed on the market-It was a combination of benzyl salicylate and cinnamate, and it was designed to absorb and protect against UV-B radiation (Urbach, 2001). Ultra violet B held the spotlight for many years, and it was not until 1977 that Kumakiri, Hashimoto, and Willis (1977) proved that ultraviolet-A (UV-A) radiation could also cause negative changes in the ultrastructure of the skin. And now, 90 years following that initial sunscreen breakthrough, we are making more novel discoveries. It has most recently been shown that infrared (IR) and visible light contribute to the development of skin malignancies and extrinsic photoaging. It has even been suggested that solar aging can be attributed to the combination of four separate entities: UV radiation, visible light, IR radiation, and heat (McDaniel et al., 2015). And now you can ask ... but how?
UV RADIATION MOVES OUT OF THE SOLAR SPOTLIGHT
Solar radiation reaches the earth's surface as three separate bands-UV radiation (290-400 nm), visible light (400-760 nm), and IR radiation (760-4,000 nm) (Schroeder, Calles, & Krutmann, 2009). Of these three bands, IR radiation accounts for the majority, making up 54.3% of solar radiation. Both UV and visible lights make up the remainder of solar radiation-accounting for 6.8% and 38.9%, respectively. For years, we have focused our research efforts on the 6.8%-UV radiation. Through these efforts, we have elucidated much: UV radiation induces the formation of reactive oxygen species (ROS), peroxidizes lipid membranes, depletes antioxidants, and induces proinflammatory cytokines. This series of events then leads to a state of progressive inflammation, which then contributes to skin damage and disruption of normal skin physiology. This information is widely accepted as fact. However, most recently, UV radiation has moved out of the spotlight and our focus has shifted, appropriately, to the larger pieces of the pie: IR and visible light.
INFRARED RADIATION
Infrared radiation is made up of IR-A (760-1,400 nm), IR-B (1,400 nm-3,000 nm), and IR-C (3,000 nm-1 x 106 nm). For years, we thought of IR purely in terms of heat energy, largely discounting the more important question: How does IR radiation play a role in inducing photoaging and skin damage? The answer lies mostly in the effects of IR-A. Infrared A regulates many genes in our skin, specifically those involved in cell death, growth, and adaptations to stress (McDaniel et al., 2015).
Through its modulation of gene activity, IR-A has effects on the mitochondria in several ways. To start, IR-A increases the formation of mitochondrial ROS. These reactive species dampen the production of adenosine triphosphate (ATP) and subsequently increase the leakiness of the mitochondrial membrane. Increased ROS, decreased ATP, and increased membrane permeability all lend to the increased activation of apoptotic pathways (McDaniel et al., 2015). These pathways increase destruction of our extracellular matrix while activating matrixmetalloproteinases (MMPs), enzymes involved in the breakdown of collagen and increased elastin deposition in our skin (Schieke et al., 2002). Matrixmetalloproteinases produce some characteristic changes in IR-exposed skin including thickening of the epidermis, increase in senescent markers such as telomerase, increased angiogenesis due to increased vascular endothelial growth factor, or VEGF, expression, and redness and swelling (McDaniel et al., 2015).
Beyond these direct effects of IR-A, the heat energy associated with IR has been shown to increase the expression of even more MMPs, including MMP3 and MMP12 (Schieke et al., 2002). Heat energy increases the temperature of our skin and causes premature aging. The effects of heat energy have been attributed mainly to IR-B and IR-C-IR that confines itself primarily to the epidermis. Heat associated with IR increases the expression of tropoelastin while decreasing fibrillin-1 expression, leading to a buildup of elastotic materials in the dermis (McDaniel et al., 2015). Infrared radiation shifts our body's delicate balance of ROS and antioxidants in favor of these destructive ROS, contributing to expedited aging.
HOW CAN WE PROTECT OUR SKIN FROM THIS IR DAMAGE BY RESULTING ROS?
For years, we have been hyperaware of the deleterious effects of UV radiation, scrambling to protect ourselves from this meager 6.8% of the solar radiation that reaches the earth in the form of UV radiation. But now we must focus our efforts on the remaining 93.2%. We pose the question-How can we protect ourselves from damage incurred by these wavelengths? The answer lies in the common pathway for both UV and IR damage: the generation of oxidative stressors via ROS. Most modern-day sunscreen protect against UV-A and UV-B with chemicals such as cinnamates, oxybenzones, camphor derivatives, para-aminobenzoic acid derivatives, and salicylates. Cinnamates are the earliest sunscreen ingredients and are effective at absorbing UV-B (Roelandts, 1998). Another commonly used ingredient is oxybenzone, and its popularity has increased because it is non-water-soluble and improves the stability of sunscreen. Terephthalylidene-dicamphor sulfonic acid (Mexoryl SX) is another commonly used sunscreen ingredient and also the first photostable sunscreen, absorbing mostly within the UV-A range. Drometrizole trisiloxane (Mexoryl XL) was the first broad-spectrum sunscreen active against UV-A and UV-B (Hughes, Martin, Lewis, & Stone, 2005). Most recently, strategies for the advancement of these sunscreens blends have been proposed and sunscreens have been developed to include more antioxidants, with the goal of neutralizing many of the ROS, as well as promoting repair (Rai, Shanmuga, & Srinivas, 2012). SkinMedica, an Allergan Company in Irvine, CA, has created a new "superscreen" called Total Defense + Repair (TD + R). This superscreen acts to protect against UV-A, UV-B, IR-A, and associated heat damage. Its efficacy has been proven in vitro, ex vivo, as well as through clinical testing.
In vitro studies have shown that tissues treated with TD + R have a decreased number of sunburn cells, as well as decreased formation of cyclobutane pyrimidine dimers. In addition to in vitro studies, a "proof-of-concept" clinical study was conducted to assess the clinical utility of TD + R. Subjects were selected, and two areas on their back were selected for testing-one area was treated with TD + R, and the other served as the untreated control. Patients were then exposed to an IR source for 30 min, and skin temperature was recorded at each 30-min interval. All sites treated with TD + R were protected from IR heat accumulation in comparison with the untreated control sites. Further clinical studies showed that TD + R used on subjects with moderate facial photodamage had a notable improvement in wrinkles and skin tone after just 4 weeks of daily use (McDaniel et al., 2015).
A recent novel approach for sun protection has been the addition of antioxidants or DNA repair enzyme such as photolyase in the sunscreen. Photolyase, a DNA repair enzyme, converts deleterious cyclobutane dimers formed in response to UV radiation to monomers, thereby decreasing DNA damage and inducing DNA repair. When used in combination with other chemical and physical blockers, the addition of photolyase to the sunscreen proven to decrease the number of actinic keratosis and nonmelanoma skin cancers in a particular skin field (Puviani, Barcella, & Milani, 2013).
WHAT NOW?
Our evolved understanding of IR radiation and the synergistic role it plays alongside UV and visible light has created a paradigm shift in how we view the sun and, more importantly, how we protect against it. It is imperative that we continue to develop sunscreens with a blend of SPF ingredients, as well as antioxidants. Infrared radiation, while potentially benign at first glance, carries an armamentarium of photodamaging capabilities. As research and IR understanding continue to evolve, antioxidant superscreens may be our greatest protection against this damage.
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