7: Skin Exposome


CHAPTER 7
Skin Exposome


Gabrielle Sore1,2 and Stephen Lynch1,2


1 L’Oréal Research and Innovation, Chevilly Larue, France


2 L’Oréal Research and Innovation, Clark, NJ, USA


Introduction


Sequencing and mapping of the human genome has provided unique insight into the origins of human physiology. However, additional factors must also be considered to fully understand numerous biological processes. In 2005, Christopher Wild identified the need to assess a person’s environmental exposure to complement genetic research [1]. He coined the term exposome to encompass all of a person’s environmental exposures from conception until death [2].


The human exposome can be divided into three overlapping domains: the general environment, the individual’s specific external environment, and the individual’s internal environment [13]. The recognition of the exposome has highlighted the need to assess the impact of environment exposure on biological processes, including identification of exposure biomarkers and indicators that could quantify environmental risk factors [2]. Exposome includes not only external factors such as diet, physical exercise, radiation, pollution, and smoking, but also those within the human body such as microbiota, inflammation, chronological aging, and oxidative stress.


This chapter will provide an overview of the most important skin exposome factors impacting skin aging and discuss the role of exposome factors in specific skin conditions such as AD, and acne. It will include some suggestions on how to limit impact of the exposome on skin.


Skin aging exposome


Skin aging combines two processes: intrinsic aging, the normal genetic processes that occur with time, and extrinsic aging, or accelerated aging, from exposure to skin exposome factors. Extrinsic environmental factors, such as sunlight, pollution, and climate trigger biological processes that accelerate aging (Figure 7.1). Self‐induced factors such as smoking and lifestyle also play a role in potentiating skin aging [5]. Importantly, skin exposome factors often act in synergy to accelerate aging. This section will focus on exposome factors directly implicated in skin aging: exposure to solar radiation, pollution, and tobacco smoking.


Solar rays


Sunlight is composed of electromagnetic rays of varying wavelength: from short wavelength ultraviolet (UV) rays to visible light (VL) to long wavelength infrared (IR) rays (Figure 7.2). The wavelength of electromagnetic radiation is inversely proportional to its frequency and energy, and proportional to its ability to penetrate the skin [6, 7]. UV radiation, with short wavelengths and high energy, can be classified by wavelength: UV‐C between 100 and 290 nm, UV‐B between 290 and 320 nm, and UV‐A between 320 and 400 nm [8, 9]. The highly reactive UV‐C radiation is filtered by the ozone layer and is generally not considered an important exposome factor.


In 1986, Kligman and Kligman popularized the term photoaging to distinguish the accelerated aging induced by sun exposure [10]. Photoaging is characterized by visible changes in the skin, such as the presence of fine and coarse wrinkles, hyperpigmentation, telangiectasia, sallowness, sagging, and rough skin texture [11]. On a molecular level, photoaging is characterized by depletion of antioxidants and damage to cellular components such as DNA, proteins, and lipids in the skin [5]. Chronic sun exposure is known to reduce collagen synthesis and degrade extracellular matrix proteins, such as collagen and elastin, that impart strength and elasticity to the skin. UV‐B, UV‐A, VL, and IR‐A have all been implicated in photoaging [5, 7].

Schematic illustration of these exposome factors have been identified to potentiate skin aging.

Figure 7.1 These exposome factors have been identified to potentiate skin aging. Exposure to sun, pollution and tobacco are now well known to trigger molecular processes that damage the skin structure, leading to the aged skin appearance. Other, less well studied factors are recognized as potentiators for skin aging. These factors have been shown to act either separately or by interacting with each other and potentiating the process.


[Source: Krutmann et al., 2017 [4]. Reproduced with permission from Elsevier.]

Schematic illustration of the solar spectrum.

Figure 7.2 The solar spectrum.


UV‐A radiation penetrates deep into the dermis and creates reactive oxygen species (ROS) which lead to oxidative stress and subsequent cellular damage. Exposure to UV‐A radiation is known to contribute to skin pigmentation and wrinkling, and trigger inflammation. In addition, UV‐A rays activate several biological pathways, including those related to cancer like cell proliferation and apoptosis [12].


About 2–5% of the total solar emission is made of UV energy. Of this, the vast majority (~95%) is UV‐A radiation [12]. About 15–20% is considered short UV‐A (320–340 nm) while the remaining 75–80% is considered long UV‐A (340–400 nm). Skin is constantly exposed to long UV‐A radiation regardless of latitude and seasonality which makes it a particularly dangerous form of radiation whose short‐ and long‐term impacts on the skin has been well described [8, 12].


Visible light (VL) comprises wavelengths ranging from 400 to 740 nm and accounts for about 47% of solar radiation. Although VL is of a relatively low energy, it is capable of penetrating deep into the skin. Evidence suggests that VL plays a fundamental role in hyperpigmentation, particularly in individuals with deeper skin phototypes (Fitz type III–VI) where persistent pigment darkening has been observed following VL exposure [13, 14]. It is believed that lower the wavelength, higher the energy portion of VL (blue‐violet light from 400 to 500 nm) is responsible for the pigmentation induced by VL. Studies have shown that physiological doses comparable to 90–150 minutes of midday summer sun exposure are capable of inducing a lasting pigmentation [14]. Recently, a unique mechanism involving activation of melanogenesis via the opsin 3 photoreceptor has been described [15].


IR rays accounts for approximately 51% of total solar energy. Only the shortest wavelengths, IR‐A (770–1400 nm) have sufficient energy and skin penetration to cause significant damage. IR radiation is known to upregulate the production of matrix metalloproteinases (MMPs), enzymes that facilitate the degradation of extracellular matrix proteins [4, 7]. The earliest biological event that occurs after IR‐A radiation in human fibroblasts is an increase in the intra‐mitochondrial production of ROS. There is a shift in the glutathione equilibrium to its oxidized state. The discovery of this mitochondrial signaling response caused by IR‐A has a direct clinical impact because it indicates that the use of antioxidants may be an effective strategy to help protect the skin against effects from IR‐A [16, 17].


Air pollution


Air pollution is a growing concern worldwide and plays a major role in the emerging environmental crisis. Airborne pollutants, predominantly from human activities – industrialization, urbanization, and increased combustion of fossil fuels – modify our environment and severely impact human health [18]. The concentration of pollutants may vary daily, seasonally, with geographical location, and according to human activity [19]. Pollutants include airborne particulate matter (PM), gases (CO2, CO, SO2, NO, NO2, and NO x2), and volatile organic compounds that are present in the atmosphere from a variety of sources [1820]. In general, topical exposure to pollutants harms the skin by increasing oxidative stress that modifies lipid, DNA, and protein function [18, 21, 22]. Exposure to pollution decreases skin quality, but also exacerbates existing skin conditions, such as AD and acne [18, 20, 22, 23]. Systemic exposure to pollution through inhalation is unavoidable in urban areas and its cutaneous impact is highly probable since some pollutants present in plasma could be delivered to skin by the blood flow, post inhalation. In fact, aggravation of skin diseases such as atopy or eczema during peaks in pollution suggests that the skin surface is not the sole mechanism for such exacerbation [18].


In general, pollutants have been implicated in the evolution of wrinkles and formation of pigmented spots which are the most prominent visible signs of premature aging [19, 20, 24]. A study performed on women in two Chinese cities differently polluted revealed that people who live in a highly polluted area have some facial features, including various types of wrinkles and pigmentations, that show signs of accelerated aging [25].


Photopollution refers to the exposome resulting from the synergistic combination of sunlight and pollution. The photochemical reactions of pollutants in the presence of heat and UV radiation generate pollutants, such as ozone and activated polycyclic aromatic hydrocarbons (PAHs). It is reported that ozone levels increase during summer as a result of these photochemical reactions [20]. Ozone is a powerful oxidant that can affect the skin in several ways including oxidizing lipids and proteins, and depleting antioxidants such as tocopherol (vitamin E) and ascorbic acid (vitamin C) [18, 23]. PAHs, constituents of pollution, are activated upon sunlight exposure [18, 26]. PAHs usually absorb light in the UV‐A range, but some that contain at least five aromatic rings can absorb in the visible range. Once activated, these intermediates react with oxygen producing highly unstable ROS that can damage DNA, as well as oxidize lipids and proteins.


Smoking


Tobacco smoke is a complex mixture composed of solid and gaseous phases. Polycyclic aromatics, heterocyclic amines, and nitrosamines, among other mutagens and carcinogens, are present in the solid phase. The gas phase contains numerous toxic gases, including carbon dioxide, carbon monoxide, and hydrogen cyanide [27].


The most common visible sign of tobacco smoking is accelerated aging. The “smoker’s face” has a dull grey complexion with increased skin wrinkling [27, 28]. This dull complexion is due to decreased facial blood flow, increased concentration of hemoglobin, and increased melanin production. Tobacco smoking is also implicated in numerous skin disorders, including contact and AD, pustular psoriasis, palmoplantar pustulosis and skin cancer [27]. Smoking accelerates skin aging by decreasing expression of collagen I and III and increasing the expression of certain MMPs that degrade extracellular matrix proteins, including collagens and elastin [4, 27]. In addition, smoking promotes oxidative stress and increases melanin production leading to degraded skin texture and hyperpigmentation [4, 28, 29].


Additional factors


Diet: Cutaneous signs such as dermatitis, cheilite, perleche, alopecia, and depigmentation have been observed during certain nutritional deficiencies, which highlights a link between nutrition and skin [30, 31]. There is some evidence that dietary factors and nutritional supplements may influence skin aging, but the exact extent to which nutrition contributes to skin aging is currently not fully understood [3234].

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Nov 13, 2022 | Posted by in Dermatology | Comments Off on 7: Skin Exposome
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