Scientists have known about the existence of infrared radiation (IR) as long as they have known about the existence of ultraviolet (UV). Links between UV light and sunburn were reported since the 1920s and the first sunscreen containing a UV-filtering agent was commercialised by Eugene Schueller (the French founder of L’Oréal) in 1936. Contrary to IR radiation that was associated with skin damage and premature ageing only recently.
In terms of energy, IR represents 54% of global radiation (versus 7% for UVs).1 One third of all IR energy penetrates the skin, but with disparities. Sixty-five per cent of IR-A deeply penetrates the dermis, even reaching the hypodermis, whereas IR-B only marginally penetrates the dermis and IR-C remains in the epidermis, heating it extensively due to water molecules.2,3 IR has some benefits, which are used in medicine. Some systems have been developed that help improve healing and diminish joint pain and pain caused by trauma, and there are even systems that help reduce wrinkles. These systems directly use the heating capacity of IR either at the surface or deep within.
Generally considered harmless, chronic IR exposure under painless conditions (without thermal injury) nevertheless causes some skin disturbances, such as erythema, hyperpigmentation and neovascularisation.4 Kim et al.5 demonstrated that, although a single IR radiation dose stimulates procollagen synthesis in human skin, repeated exposure represses the synthesis of TGF-β and simultaneously induces MMP-1 formation. Moreover, Kim demonstrated accelerated wrinkle formation as well as dermal angiogenesis in mice that were repeatedly irradiated (5 times a week for 15 weeks).1 Other systems that do not filter as much demonstrate the thermal denaturation of collagen fibres under the effect of IR-A and IR-B starting at 52°C.6,7
Schroeder et al.8 used an IR-A system (760 nm-1440 nm) to demonstrate that a significant exposure led to a decrease in endogenous skin antioxidant levels and a parallel increase in type I matrix metalloproteinases (MMP-1). The latter are known to play a role in photo-induced UVA and UVB ageing by destroying collagen I, collagen III and elastic fibres. These effects are linked to the increased formation of reactive oxygen species (ROS) in the
mitochondria when exposed to IR-A, since mitochondrial cytochrome c oxidase can serve as an IR chromophore.9 Krutmann and Schroeder10 believe that ROS created in this way are added to those linked to the poorly-functioning proteins that have undergone mutations due to UV exposure. This leads to a decrease in ATP production by the cells’ energy-producing mitochondria, an increase in cellular ageing and the loss in mitochondrial water that precedes senescence.11
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