Tan now…pay later. That sun-kissed smile comes at a price.
Beside its effect on photoaging, IR is linked to photocarcinogenesis. Recent studies have shed light on the basic molecular processes, such as cellular signal transduction and gene expression triggered by exposure to IR radiation. This previously unrecognized molecular IR response shows that IR radiation is capable of interfering with cellular functions. This new information provides a molecular basis for biological effects of IR on human skin.6
Dermatologists have harnessed the power of infrared light.
Recent evidence indicates that IR and heat may induce premature skin aging, just like UV radiation including: (a) IR exposure of human skin stimulates the expression of MMP-1 and decreases type I procollagen expression in vivo. Acute IR irradiation also increases new, leaky vessel formation and induces inflammatory cellular infiltration and (b) Heat energy, which increases skin temperature, also increases MMP-1, -3, and -12, and modulates elastin and fibrillin synthesis, resulting in the development of solar elastosis. Acute heat shock in human skin stimulates new vessel formation, recruits inflammatory cells and causes oxidative DNA damage.7 Cho and associates stated that the number of mast cells in sun-exposed facial skin is always significantly higher than that of sun-protected buttock skin from the same individual. On the other hand, the effect of IR on dermal cell prevalence remains unclear. Tryptase expression (the most abundant granule-derived serine proteinase in mast cells used as a marker for mast cell activation) was also clearly up-regulated by IR treatment in human skin in vivo.7 Based on these observations, it can be concluded that IR and heat are important physical stimuli that may result in aging in human skin. IR generates heat and increases skin temperature during sun exposure. Repeated and prolonged exposure to heat insufficient to produce a burn can cause a cutaneous lesion, described as erythema ab igne, which is characterized clinically by reticular hyperpigmentation and telangiectasia, and histologically by the basophilic degeneration of connective tissue and elastic fiber alterations, which are similar to those observed in photoaged skin.7
IR can produce wrinkles. Studies show that repetitive IRA irradiation produces significant wrinkle formation in hairless mice.8 Chronic IR exposure can cause pronounced elastosis in mouse skin, which mimics UV damage. The effects of chronic IR exposure on skin aging were investigated, especially on the development of skin wrinkles, in a hairless mouse model. Kim and associates found chronic IR-induced skin wrinkles in hairless mice after 15 weeks of exposure and that IR-augmented, UV-induced wrinkle formation from 5 weeks post-UV/IR treatment. Although IR was less effective than UV at producing wrinkles, it was found in this study that chronic IR treatment can produce wrinkling in its own right, and augment wrinkle formation by UV.7
IR is different from UV and must be treated as such. IRA exposure led to down regulation of collagen de novo synthesis. According to Krutmann, et. al., “The IRA-induced up regulation of MMP-1 was different from that induced by UV at the mechanistic level, since it involves the formation of mitochondrial reactive oxygen species (ROS) and the subsequent initiation of a retrograde signaling response (i.e. from the mitochondria to the nucleus) in human skin.”9 The presence of IRA, its biophysical properties, and the fact that it acts differently from UV, points to the necessity of including specific IRA-directed strategies in modern sunscreens.1,9
IR is not all bad. Infrared radiation is used very successfully in cosmetic dermatological procedures. Equipment used by dermatologists (i.e., Fraxel, Nd:Yag, Fotofacial, Smoothbeam) involves IR laser damage to the skin in a controlled manner to induce a wound healing response and affects no more than 5-10% of the skin. These lasers emit a precise wavelength with a variance of +/- 20nm targeting the water molecules in the skin that denature collagen and cause cell death, thereby inducing a wound healing response. It is evident that Infrared radiation has both dangers and benefits, but its attributes will be useless if its dangers are ignored.
Skin Can Be Protected
Skin damage from oxidative stress triggered by UV radiation, IR radiation, smoking, pollution or other environmental conditions, increases MMPs in fibroblasts and keratinocytes. This causes a degradation of dermal matrix components (i.e. collagen), inferior repair of matrix damage, DNA mutations leading to wrinkle formation, photodamage and ultimately skin cancer. The use of antioxidants induces a powerful protective barrier, preserves skin’s genetic inheritance and neutralizes free radicals. Readily available today are protocols that deliver efficient antioxidants directly to the skin.
A lifetime of sunshine can lead to face full of wrinkles.
Ascorbic acid for example, the gold standard among antioxidants, must be un-ionized to get into the skin. Its pH must be acidic (below 3.5) and in concentrations that are significant (above 10%) to be effective against the UV and IR damage.10 Most formulations on the market do not fit these criteria for effective antioxidant protection. Armed with this clinical evidence about the damaging effects of solar radiation, the use of a broad-spectrum sunscreen product with efficient UVB and photostabilized UVA filters is a user’s first line of defense. Moreover, a powerful antioxidant regimen that adequately penetrates the skin delivered in reasonable effective concentration is highly recommended.
In the future, additional ingredients that provide a line of defense from both the UV and IR spectrum will be formulated in all standard sunscreen products. Designing new sun safety products that can address these new revelations from research will improve significantly the protection we currently provide to the consumer.
1. Krutmann J., Morita A., and Chung J., “Sun Exposure: What Molecular Photo Dermatology Tells Us about Its Good and Bad Sides” J. Invest. Dermatol. (2012) 132: 976–984.
2. Schieke S, Stege H, Kurten V , Grether-Beck S,Sies H and Krutmann J. (2002) “Infrared-A radiation-induced matrix metalloproteinase 1 expression is mediated through extracellular signal regulated kinase 1/2 activation in human dermal fibroblasts.” J. Invest. Dermatol. 119:1323–9.
3. Schroeder P.,Lademann J., Darvin M.,BruhnkeS. and Krutmann J. (2008)” Infrared radiation-induced matrix metalloproteinase in human skin: implications for protection.” J Invest Dermatol 128:2491–7.
4. Kim MS, Kim YK, Cho KH and Chung JH. (2006) “Regulation of type I procollagen and MMP-1 expression after single or repeated exposure to infrared radiation in human skin.” Mech. Ageing Dev. 127:875–82
5. Schroeder P,Calles C,Benesova T,Macaluso F, andKrutmann J. (2010) “Photoprotection beyond ultraviolet radiation—effective sun protection has to include protection against infrared A radiation-induced skin damage.” Skin Pharmacol. Physiol. 23:15–7
6. Schiek, S., Schroeder,P. and Krutmann, J., “Cutaneous effects of Infrared radiation”, Photodermatol. Photoimmunol. Photomed. (2003), 19: 228-34.
7. Cho S,Shin MH,Kim YK,Seo JE,Lee YM,Park CH,Chung JH. , “Effects of Infrared radiation and heat on human skin aging in vivo”, J. Invest. Dermatol. Symposium Proceedings (2009), 14: 15-19.
8. Kim HH,Lee MJ,Lee SR,Kim KH,Cho KH,Eun HC and Chung JH. (2005) “Augmentation of UV-induced skin wrinkling by infrared irradiation in hairless mice.” Mech. Ageing Dev. 126:1170–7.
9. P. Schroeder, C. Calles, Dipl.-Biol, J. Krutmann, “Prevention of Infrared-A Radiation Mediated Detrimental Effects in Human Skin”, Skin Therapy Letter (2009).
10. Pinnel, S. et al.,(2001) Dermatol. Surg., 27:137-142
Dr. Nadim Shaath is the president of Alpha Research & Development, Ltd. in White Plains, NY. He has over 30 years of experience as chairman of the chemistry department at SUNY-Purchase and the CEO of Kato Worldwide. Recently he formed a consulting company serving the cosmetic industry called ShaathMeadows Corporation (SMC) with laboratories in New York, New Jersey, Texas, Florida and Egypt.