Skin exposome
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The skin exposome refers to the totality of environmental factors, related to lifestyle and internal processes, to which a person is exposed from prenatal life until death, along with the body's biological response to these influences. This concept complements the information contained in the genome, as the genetic code alone does not explain why the skin of individuals with similar predispositions ages at different rates. The exposome includes, among others, solar radiation, air pollution, climate, tobacco smoke, diet, sleep, stress, as well as cosmetics and medications used. These factors do not act independently. They can mutually reinforce each other, leading to oxidative stress, chronic inflammation, epidermal barrier disruption, DNA damage, and accelerated degradation of the skin's extracellular matrix.
Skin exposome - what is it
The term “exposome” was introduced in environmental epidemiology as the counterpart to the genome, encompassing the full spectrum of exposures and the biological responses they induce. In dermatology, this concept refers to all factors that can influence the structure, functioning, immunity, and aging process of the skin.
The skin exposome is:
- cumulative, because the effects of multiple exposures accumulate over the years;
- dynamic, as the type and intensity of exposures change throughout life;
- individual, because the same exposure can elicit a different response depending on phototype, age, sex, genes, and health status;
- interactive, as individual factors can act additively or synergistically;
- partially modifiable, which distinguishes it from the inherited DNA sequence.
Research distinguishes three interrelated domains of the exposome:
- General external environment, encompassing climate, urbanization, socioeconomic status, and living conditions.
- Specific external exposures, such as radiation, particulate matter, tobacco smoke, diet, cosmetics, medications, and occupational factors.
- Internal environment, namely metabolism, hormonal balance, microbiome, inflammation, oxidative stress, and immune response.
The skin is a particularly useful organ for studying the exposome because it serves as the direct boundary between the body and the environment. At the same time, it responds to processes occurring inside the body. For this reason, its condition reflects both external exposures and metabolic, hormonal, and immunological health.
Skin exposome - what factors does it include
The most important recognized component of the skin aging exposome is solar radiation. UVB causes direct photochemical DNA damage, including the formation of pyrimidine dimers. UVA penetrates deeper and largely acts through reactive oxygen species. Visible light, especially high-energy blue-violet light, can exacerbate long-lasting pigmentation, particularly in individuals with darker phototypes. Infrared radiation, on the other hand, can contribute to the generation of oxidative stress and the activation of matrix metalloproteinases.
Other significant components of the exposome include:
- air pollution: PM₂,₅ and PM₁₀ particulate matter, soot, nitrogen oxides, ozone, and polycyclic aromatic hydrocarbons;
- tobacco smoke, which is a source of free radicals and toxic substances that damage fibroblasts, impair microcirculation, and accelerate collagen degradation;
- climatic factors: temperature, humidity, wind, frost, and sudden changes in environmental conditions;
- diet, including an excess of simple sugars that promotes non-enzymatic protein glycation and the formation of advanced glycation end-products, referred to as AGEs;
- alcohol, especially consumed in excess, which indirectly worsens hydration, sleep, redox balance, and inflammation control;
- sleep deprivation and sleep rhythm disorders, which can impair epidermal barrier regeneration and increase the reactivity of the stress axis;
- chronic psychological stress, acting through cortisol, neuropeptides, and inflammatory mediators;
- physical activity or lack thereof, affecting metabolism, microcirculation, and systemic inflammation;
- cosmetics, detergents, and occupational factors, which, depending on composition, dose, and method of use, can support the skin barrier or have an irritating and sensitizing effect;
- medications and hormones, including therapies affecting pigmentation, photosensitivity, sebum secretion, or skin thickness;
- skin and gut microbiome, which maintains a bidirectional relationship with immunity, metabolism, and epidermal barrier integrity.
Common consequences of many exposures are the overproduction of reactive oxygen species, activation of transcription factors AP-1 and NF-κB, and increased activity of matrix metalloproteinases, including MMP-1, MMP-3, and MMP-9. These enzymes degrade collagen and other elements of the extracellular matrix. This is accompanied by mitochondrial damage, epigenetic changes, cellular senescence, pigmentation disorders, and chronic low-grade inflammation, known as inflammaging.
Skin exposome - what is its contribution to aging compared to genes
Skin aging is the result of the overlap between intrinsic aging and extrinsic aging. The former results from the passage of time, genetic predispositions, hormonal changes, telomere shortening, mitochondrial dysfunction, and the gradual exhaustion of the regenerative capacity of cells. The latter is a consequence of the impact of the exposome, primarily solar radiation, tobacco smoke, and pollution.
There is no single scientifically justified percentage value defining the contribution of genes and the environment to the overall process of skin aging. The proportions depend on the analyzed trait, age, phototype, anatomical region, and exposure history. The popular claim that external factors account for 80–90% of skin aging is an oversimplification and should not be applied to all skin characteristics.
Twin studies show that:
- genes and the environment may have a similar contribution to shaping perceived age, wrinkles, pigment spots, and visible signs of photodamage;
- approximately 40% of the variation in perceived age in one large twin population was associated with non-genetic factors;
- the heritability of individual parameters varies greatly: it has been estimated at around 44% for the melanin index, around 21% for sebum secretion, and around 11–13% for skin hydration;
- tobacco smoking, intense sun exposure, and lack of photoprotection can cause marked differences in appearance even in identical twins.
Genes determine, among other things, phototype, pigmentation properties, connective tissue structure, and the efficiency of DNA repair mechanisms. The exposome, on the other hand, influences the extent to which these predispositions are manifested. The environment can also modify gene expression through DNA methylation, histone modifications, and the regulation of non-coding RNAs. Therefore, the modern model of skin aging is based on the genome–exposome interaction, rather than a simple opposition of genes versus the environment.
Skin exposome - how to limit it
The exposome cannot be completely eliminated. However, exposures with the best-documented effects can be reduced, and the skin's protective capacity can be strengthened.
Basic management includes:
- daily broad-spectrum photoprotection, an adequate amount of product, and reapplication during prolonged outdoor exposure;
- limiting sun exposure during peak hours, using protective clothing, headwear, and shade;
- complete avoidance of tanning beds;
- not smoking tobacco and avoiding passive smoke exposure;
- gentle skin cleansing after contact with pollutants, without disrupting the epidermal barrier;
- using barrier-restoring products containing, among others, ceramides, cholesterol, and physiological fatty acids;
- a diet based on vegetables, fruits, whole grain products, valuable protein sources, and unsaturated fatty acids;
- limiting excessive simple sugars, alcohol, and highly processed foods;
- regular sleep, physical activity, and treating chronic inflammatory and metabolic diseases;
- dermatological consultation in the case of new or changing pigmented lesions, non-healing erosions, or signs of advanced photodamage.
Topical retinoids, vitamin C, and other antioxidants can support prevention or the reduction of some changes, but they do not replace sun protection. The selection of a retinoid should take into account skin tolerance, contraindications, and the risk of irritation.
Treatments available at Ambasada Urody that may be considered to reduce the visible consequences of the exposome include:
- ClearLift laser rejuvenation as well as 2940 and CO₂ ablative fractional lasers, targeted at skin remodeling, improving its texture, and reducing selected signs of photoaging;
- laser removal of hyperpigmentation and light therapies used for pigmented lesions and uneven skin tone;
- chemical peels, supporting controlled epidermal renewal and the reduction of superficial hyperpigmentation;
- Dermapen 4.0 and microneedle mesotherapy, utilizing controlled microneedling to induce repair processes;
- microneedle radiofrequency, whose thermal action stimulates collagen remodeling and improves skin tightness;
- HIFU, acting with focused ultrasound on deeper-lying supporting structures;
- needle mesotherapy and biorevitalizing procedures, supporting hydration and improving skin quality;
- platelet-rich plasma PRP, concentrated growth factors CGF, and autologous therapies, used to stimulate regenerative processes;
- tissue stimulators, such as Juvelook, Profhilo, polynucleotides, polylactic acid, amino acid preparations, Karisma, and skin profiloplasty, selected depending on the predominant issue;
- botulinum toxin and fillers, which can correct specific wrinkles or volume loss, but do not eliminate the biological causes of exposome-related aging.
These treatments reduce selected consequences of past damage, but they do not "remove the exposome" and do not replace prevention. The procedure should be selected after assessing the phototype, type of lesions, active skin diseases, medications taken, and the risk of post-inflammatory pigmentary disorders. Special caution is required in individuals with melasma, darker phototypes, and a tendency to hyperpigmentation.
