Sunscreens and Photoaging: A Review of Current Literature

Linna L. Guan; Henry W. Lim; Tasneem F. Mohammad

Disclosures

Am J Clin Dermatol. 2021;22(6):819-828. 

In This Article

Electromagnetic Radiation and Photoaging

Solar UV radiation (UVR) consists of UVA (320–400 nm), UVB (280–320 nm), and UVC (100–280 nm). UVA is further categorized as UVA1 (340–400 nm) and UVA2 (320–340 nm). UVC is the shortest wavelength and considered the most damaging type of UVR. However, it is completely absorbed by the ozone and does not reach the earth's surface.[6]

UVB is the major portion of UVR that induces sunburns or UV-induced erythema. It is known to be significantly more erythemogenic than UVA.[6] For example, for skin phototype I, the minimal erythema dose for UVB is 20–40 mJ/cm2, whereas that for UVA is 20–40 J/cm2. Although UVB accounts for approximately 6% of all UVR that reaches the earth's surface, it is more cytotoxic than UVA, causing direct DNA damage through photon absorption in the form of cyclobutane pyrimidine dimers (CPDs) or 6,4-photoproducts that eventually induce mutagenesis and skin cancers.[7,8] UVB has been shown to be highly associated with the development of squamous cell carcinomas.[9] Additionally, even suberythemal doses of UVB have been shown to induce CPD formation and therefore increased p53 expression as cells undergo apoptosis or repair.[10] UVB has also been shown to induce matrix metalloproteinases (MMPs), reactive oxygen species (ROS), and elastases involved in photoaging.[11]

UVB is predominantly absorbed by the skin's epidermis, whereas UVA has a longer wavelength and therefore deeper dermal penetration, making it the primary driver of photoaging.[12] Although UVA is lower in energy than UVB, it is approximately 20 times more abundant in the earth's atmosphere and is not blocked by glass.[13] The ratio of UVB/UVA varies by season.[14] Studies of UVA on skin models demonstrated that UVA caused the induction of apoptosis in dermal fibroblasts and increased MMP levels, which are enzymes involved in collagen degradation.[12,15] Additionally, repeat exposure to UVA on in vivo human skin induced elevated markers of photoaging, such as ferritin and lysozyme, which are involved in the oxidative stress response and elastin degradation, respectively.[16] In a study looking at asymmetric UVA exposure of the face, chronic exposure to UVA significantly affected the clinical level of wrinkling and roughness of the skin.[17] Furthermore, in a study of 22 participants exposed to multiple sessions of low-dose UVA1, increasing levels of MMP-1 and MMP-3 were observed in a dose-dependent response in the dermis, further highlighting the role of UVA in collagen breakdown and photoaging.[13] In skin of color, UVA has been shown to induce irregular spotty pigmentation associated with photoaging.[12]

However, the effects of UVA and UVB are not always distinct, as overlapping cutaneous biologic effects have been observed. UVA has been shown to induce CPDs through ROS generated by photo-activation of UVA-absorbing molecules (chromophores) in the skin such as riboflavin, porphyrins, and heme-containing proteins.[18] Similarly, UVB has also been shown to induce dermal fibroblast senescence.[19]

There is increasing evidence that infrared light (IR; 700 nm–1 mm) and VL (400–700 nm), predominantly in the blue light range (380–455 nm), play a role in photodamage and photoaging. Studies have demonstrated that VL can independently generate ROS, proinflammatory cytokines, and MMP-1 expression and potentiate the effects of UVR.[20–23] Effects of photoaging have also been observed with irradiation of skin within the UV/VL boundary region (385–405 nm), demonstrating differential expression of genes involved in inflammation, oxidative stress, and photoaging when compared with nonirradiated skin.[24] Likewise, in vivo skin irradiated with IR and VL has shown significantly increased MMP-1 and MMP-9 expression and decreased type I procollagen expression, implicating IR and VL light in the degradation of dermal collagen.[25] Moreover, studies have demonstrated that there is a synergistic relationship between even small amounts of UVA1 and VL in the induction of increased and prolonged pigmentation.[21,26] This suggests that VL and IR may play a significant but underreported role in photoaging and dyspigmentation.

Although the exact mechanisms are not yet fully understood, increasing literature indicates a need for photoprotection against the broad spectrum of electromagnetic radiation (UV, VL, and IR) to prevent photoaging.

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