Physics of Infrared Radiation, Natural and Artificial Sources, Experimental Infrared A Irradiation Doses Solar radiation is filtered by the atmosphere and when it finally hits human skin, it includes photons of 290-4,000 nm in wavelength. This portion of the electromagnetic spectrum is divided into three major bands: ultraviolet (UV) radiation (290-400 nm), visible light (400-760 nm) and infrared (IR) radiation (760-4,000 nm), with IR radiation being further divided into IRA (760-1,440 nm), IRB

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... (1,440-3,000 nm) and IRC (3,000-1 mm). Concerning the impact of the three major bands, approximately 54% of the solar energy reaching the human skin is IR radiation, while UV radiation only accounts for 7% of the energy [1] . Within IR radiation, roughly 30% of the total solar energy is IRA which penetrates deeply into the human skin [1] . Most of the IRA radiation load of human skin is of solar origin, but in recent years artificial IRA sources are used increasingly. Besides therapeutic approaches the use of IRA for nontherapeutic, i.e., wellness and lifestyle, purposes is steadily rising [2] . The question which IRA doses are of physiological relevance has been addressed in a recent discussion [3] ; therefore, some facts on that matter will be presented here as well. Human dermal fibroblasts withstand IRA doses up to at least 1,200 J/cm 2 [4] ; the gene-regulatory effects can Abstract Solar radiation is well known to damage human skin, for example by causing premature skin ageing (i.e. photoageing). We have recently learned that this damage does not result from ultraviolet (UV) radiation alone, but also from longer wavelengths, in particular near-infrared radiation (IRA radiation, 760-1,440 nm). IRA radiation accounts for more than one third of the solar energy that reaches human skin. While infrared radiation of longer wavelengths (IRB and IRC) does not penetrate deeply into the skin, more than 65% of the shorter wavelength (IRA) reaches the dermis. IRA radiation has been demonstrated to alter the collagen equilibrium of the dermal extracellular matrix in at least two ways: (a) by leading to an increased expression of the collagen-degrading enzyme matrix metalloproteinase 1, and (b) by decreasing the de novo synthesis of the collagen itself. IRA radiation exposure therefore induces similar biological effects to UV radiation, but the underlying mechanisms are substantially different, specifically, the cellular response to IRA irradiation involves the mitochondrial electron transport chain. Effective sun protection requires specific strategies to prevent IRA radiation-induced skin damage.