INTRODUCTION
The skin is the most exposed organ to the environment. Solar radiation, pollutants, and fluctuations in temperature are all environmental factors that can impact skin. These environmental exposures are part of the exposome and are known to accelerate skin aging.1 Solar radiation is likely the most damaging environmental exposure and is estimated to be responsible for 80% of skin aging seen on the face of Caucasian patients.2 Chronic sun exposure causes an increase in epidermal thickness, pigment heterogeneity, deposition of elastotic material, degradation of collagen, and formation of ectatic blood vessels.2 The phenotype of photoaging includes mottled hyperpigmentation, lentigines, coarse wrinkling, telangiectasia, sallowness, dryness, and roughness.3 In addition, chronic UV exposure causes mutagenesis resulting in the formation of actinic keratoses and skin cancers.4 Thus, preventing sun exposure is important for maintaining skin health and a youthful appearance.
The solar spectrum is a wide range of electromagnetic energies emitted by the sun. The UV component includes UVC (100-290 nm), UVB (290-320 nm), and UVA (320-400 nm). UVC is absorbed completely by the ozone layer, whereas UVB and UVA reach the earth’s surface.5 UVB is almost completely absorbed by the epidermis with very little reaching the dermis. UVB exposure increases stratum corneum (SC) thickness and compromises barrier function by altering SC lipids.6,7 UVB is responsible for sunburn and damages DNA directly resulting in cyclobutane pyrimidine dimers (CPDs) or 6,4-photoproducts that induce mutagenesis and skin cancer.4 UVA penetrates down to the level of the dermis and is a major contributor to photoaging. UVA is absorbed by various chromophores in the skin resulting in the generation of reactive oxygen species (ROS).8 ROS cause oxidation of DNA, nucleic acids, proteins, lipids, and organelles, such as mitochondria, and contributes to photoaging and photocarcinogenesis.9 ROS also activate redox-sensitive transcription factors, including activator protein 1 (AP-1) and nuclear factor kappa beta.10 AP-1 is responsible for the production of matrix metalloproteinases (MMPs) that degrade dermal collagen, and nuclear factor kappa beta triggers pro-inflammatory cytokines that contribute to skin aging, so-called inflammaging.
There is also evidence that longer wavelengths of light outside the UV spectrum contribute to skin aging.11-16 Studies have demonstrated that visible light (VL) (400-700 nm) can induce immediate pigment darkening and sustained skin pigmentation.12,13 It is also of interest that VL induces erythema and tanning in darker skin types but does not have this effect in lighter skin.14 VL also increases ROS, proinflammatory cytokines, and MMP expression in the skin.15,16 Thus, VL potentiates the detrimental effects of UV on skin aging. Infrared (IR) also plays a role in skin aging. IR is divided into IRA (799-1400 nm), IRB (1400-3000 nm), and IRC (3000 nm-1 mm).11 IRA, also called near infrared (NIR), is the most energetic and penetrates deeply into the skin, reaching the deep dermis and subcutaneous layer.17 IRA exposure increases MMPs and decreases collagen synthesis in lightly pigmented skin, while in darker skin, IRA increases melanin production but has little effect on dermal matrix proteins.18 IRA induces changes in the skin similar to photoaging including deposition of elastotic material and angiogenesis.17 IRA is also known to increase mitochondrial ROS production disrupting the electron transport chain and accelerating skin aging.19-21
The role of pollutants in skin aging is now well recognized.22-28 In urban areas, levels of ozone, or O3, can reach toxic concentrations, especially during the summer months.23 Ozone does not penetrate the stratum corneum but causes damage by inducing oxidative stress in the SC via the formation of lipid peroxidation products.24 Ozone exposure depletes the skin of antioxidants and results in a reduction in collagen I and collagen III. In 2 large cohorts of elderly German patients, O3 exposure was shown to be associated with increased facial wrinkling but not brown spots, and this was independent of sun exposure.25 Particulate matter (PM) is the principal component of air pollution and contains polycyclic aromatic hydrocarbons (PAHs), metals, and inorganic and organic toxins.22 PAHs induce aryl hydrocarbon receptor signaling and gene expression in human epidermal keratinocytes.26 A recent study demonstrated that exposure to traffic-related air pollution was associated with an increase in the formation of lentigines in Caucasian and Asian populations.27 Thus, it appears that increases in ground-level ozone are associated with wrinkling, while PM produces pigmentation seen in extrinsic skin aging.28
Although broad-spectrum sunscreens are effective against UV light, they do not confer protection against VL, IR, or pollutants. Therefore, more advanced skin regimens are required for comprehensive environmental protection. In addition, consumers desiring a more youthful appearance seek products that can repair existing environmental damage. In this study, a 6-step skincare regimen (RATIONALE Essential Six, Victoria, Australia), including daily protection and repair formulations, was tested in patients with mild-to-moderate photoaging. Each product has been carefully formulated with ingredients curated to provide optimal environmental protection and repair (Table 1).
The solar spectrum is a wide range of electromagnetic energies emitted by the sun. The UV component includes UVC (100-290 nm), UVB (290-320 nm), and UVA (320-400 nm). UVC is absorbed completely by the ozone layer, whereas UVB and UVA reach the earth’s surface.5 UVB is almost completely absorbed by the epidermis with very little reaching the dermis. UVB exposure increases stratum corneum (SC) thickness and compromises barrier function by altering SC lipids.6,7 UVB is responsible for sunburn and damages DNA directly resulting in cyclobutane pyrimidine dimers (CPDs) or 6,4-photoproducts that induce mutagenesis and skin cancer.4 UVA penetrates down to the level of the dermis and is a major contributor to photoaging. UVA is absorbed by various chromophores in the skin resulting in the generation of reactive oxygen species (ROS).8 ROS cause oxidation of DNA, nucleic acids, proteins, lipids, and organelles, such as mitochondria, and contributes to photoaging and photocarcinogenesis.9 ROS also activate redox-sensitive transcription factors, including activator protein 1 (AP-1) and nuclear factor kappa beta.10 AP-1 is responsible for the production of matrix metalloproteinases (MMPs) that degrade dermal collagen, and nuclear factor kappa beta triggers pro-inflammatory cytokines that contribute to skin aging, so-called inflammaging.
There is also evidence that longer wavelengths of light outside the UV spectrum contribute to skin aging.11-16 Studies have demonstrated that visible light (VL) (400-700 nm) can induce immediate pigment darkening and sustained skin pigmentation.12,13 It is also of interest that VL induces erythema and tanning in darker skin types but does not have this effect in lighter skin.14 VL also increases ROS, proinflammatory cytokines, and MMP expression in the skin.15,16 Thus, VL potentiates the detrimental effects of UV on skin aging. Infrared (IR) also plays a role in skin aging. IR is divided into IRA (799-1400 nm), IRB (1400-3000 nm), and IRC (3000 nm-1 mm).11 IRA, also called near infrared (NIR), is the most energetic and penetrates deeply into the skin, reaching the deep dermis and subcutaneous layer.17 IRA exposure increases MMPs and decreases collagen synthesis in lightly pigmented skin, while in darker skin, IRA increases melanin production but has little effect on dermal matrix proteins.18 IRA induces changes in the skin similar to photoaging including deposition of elastotic material and angiogenesis.17 IRA is also known to increase mitochondrial ROS production disrupting the electron transport chain and accelerating skin aging.19-21
The role of pollutants in skin aging is now well recognized.22-28 In urban areas, levels of ozone, or O3, can reach toxic concentrations, especially during the summer months.23 Ozone does not penetrate the stratum corneum but causes damage by inducing oxidative stress in the SC via the formation of lipid peroxidation products.24 Ozone exposure depletes the skin of antioxidants and results in a reduction in collagen I and collagen III. In 2 large cohorts of elderly German patients, O3 exposure was shown to be associated with increased facial wrinkling but not brown spots, and this was independent of sun exposure.25 Particulate matter (PM) is the principal component of air pollution and contains polycyclic aromatic hydrocarbons (PAHs), metals, and inorganic and organic toxins.22 PAHs induce aryl hydrocarbon receptor signaling and gene expression in human epidermal keratinocytes.26 A recent study demonstrated that exposure to traffic-related air pollution was associated with an increase in the formation of lentigines in Caucasian and Asian populations.27 Thus, it appears that increases in ground-level ozone are associated with wrinkling, while PM produces pigmentation seen in extrinsic skin aging.28
Although broad-spectrum sunscreens are effective against UV light, they do not confer protection against VL, IR, or pollutants. Therefore, more advanced skin regimens are required for comprehensive environmental protection. In addition, consumers desiring a more youthful appearance seek products that can repair existing environmental damage. In this study, a 6-step skincare regimen (RATIONALE Essential Six, Victoria, Australia), including daily protection and repair formulations, was tested in patients with mild-to-moderate photoaging. Each product has been carefully formulated with ingredients curated to provide optimal environmental protection and repair (Table 1).
