The skin exposome includes external and internal factors, their interactions, and the response of the human body to these factors leading to biological and clinical signs of skin aging.6 However, studying the exposome in its entirety is challenging because it is highly variable and dynamic.14 The exposome factors of skin aging can be broadly categorized as solar radiation: UVR, visible light (VL), and infrared (IR) radiation; air pollution; tobacco; nutrition, cosmetics, and other lesser-known factors.6 Most factors of skin exposome are solar radiation and air pollution. Biological responses to exposome factors can cause physiological adaptations, such as metabolic changes, protein modifications, DNA mutations and others.15 Most skin disorders are highly influenced by exposure to exposome factors.14

Air pollutants that can cause extrinsic skin aging mostly include gases such as ground-level ozone, and PM, a complex mixture of solids and liquid particles suspended in the air. PM can be formed in two main ways: directly emitted from a source like vehicle exhaust, construction activities, wildfires (primary PM) or formed in the atmosphere via complex chemical reactions between gas precursors such as volatile organic compounds (VOCs) and the presence of solar radiation (secondary PM).16,17 PMs are categorized based on its diameter: PM2.5 (fine particles; diameter ≤2.5μm) and PM10 (coarse particles; diameter ≤10μm). Air pollutants interact with the body, either via skin contact, inhalation or ingestion.18 Air pollutants affect the human skin through four different ways: generating ROS, triggering inflammation, impacting skin microbiota, and activating hydrocarbon receptor (AhR).19 The activation of AhR – a transcription factor – can lead to hyperpigmentation, wrinkles, skin cancer and worsening of several dermatoses such as acne, atopic dermatitis and psoriasis.11

Exposure to ozone causes changes in the stratum corneum (SC), the outermost layer of the epidermis. It reduces SC-associated antioxidants, leading to an oxidative stress response. This oxidative stress response reaches the deeper layers of the skin, including the dermis, affecting collagen metabolism, leading to wrinkle formation.20

Repeated exposure of the skin to PM even at non-toxic concentrations increases the production of ROS, which in turn leads to the secretion of cytokines and cellular dysfunction. This can break down the lipid barrier of the epidermis, decrease the number of cutaneous microbial species, trigger inflammatory skin diseases, and induce melanogenesis via AhR activation.21 A study showed that one-unit increase in PMs was associated with a 20% increase in lentigines on the forehead and cheeks and in wrinkles of the nasolabial fold. The risk of lentigines was higher after increased exposure to PM2.5 than after increased exposure to PM10.22 PM2.5 are highly lipophilic and penetrate the skin easily vs the PM10 particles that stay at the surface of the skin.23 Regarding skin cancer, an epidemiological study shows that an increment of 10μg/m3 PM10 in the air increases 52% relative risk of developing non-melanoma skin cancers.24 AhR may play a role in inducing skin cancer; AhR-deficient mice exposed to PM did not develop keratinocyte carcinomas whereas those AhR positive developed keratinocyte carcinomas via CYP1A1 expression.25

In addition to PM, other air pollutants have been shown to have an impact on skin health.26 Studies indicate that high levels of environmental factors including polycyclic aromatic hydrocarbons (PAHs), VOCs, heavy metals, and gases such as CO, NOx, SO, and O3, can impair the skin's barrier function. Both the concentration and duration of exposure are significant. These pollutants are linked to various skin issues, including aging, inflammatory diseases, acne, hair loss, and skin cancers, with responses varying by pollutant characteristics.27

The relationship between pollution and skin aging was evaluated in a cohort of 389 patients aged 30–74 who planned to undergo laser treatment. Researchers used the VISIA Complexion Analysis System to assess skin conditions alongside levels of various air pollutants, including CO, non-methane hydrocarbons (NMHC), nitrogen oxides (NO, NO2, NOx), PM2.5 and PM10, O3, and SO2. Findings revealed a strong correlation between NMHC exposure and issues such as skin texture, enlarged pores, and brown spots. Conversely, exposure to ozone was associated with better skin texture and pore scores. Notably, brown spots were negatively associated with several pollutants, particularly in individuals older than 45 years.28

Moreover, we already know that increased NO2 concentrations characterize traffic-related air pollution. Although the effects of NO2 on skin health have not been previously explored, the relationship between environmentally induced lung and skin aging prompted an assessment of NO2 exposure and lentigo development.29 Data from the extended SALIA population and an independent Han Chinese cohort were analyzed. Results indicated a significant correlation between NO2 exposure and increased lentigines on the cheeks in both cohorts. Specifically, a 10μg/m3 increase in NO2 correlated with a 25% increase in lentigines in SALIA participants and a 24% increase in Chinese women >50 years.26

Solar radiation is the major external factor related to skin aging. Up to 80% of skin aging is caused by sun exposure.30 Sun-exposed areas such as the face and neck appear prematurely aged vs unexposed skin. Clinical features of aging due to sun exposure include wrinkles, dullness, changes in pigmentation, laxity, roughness, and telangiectasia.31 Solar radiation that raises earth's surface includes electro-magnetic rays of different wavelengths. These include UVR (UVB and UVA), VL, and IR. They arrive at the earth's surface in different proportions and penetrate the skin to different levels. Skin aging occurs due to daily exposure to non-extreme, low doses of these solar waves. The most energetic radiation – UVB (290–315nm) – only penetrates up to the epidermis. It mainly causes erythema, photo-immunosuppression and cutaneous cancer. Additionally, it increases the production of epidermal matrix metalloproteinase (MMP)-1, which disseminates into the dermis where it breaks down collagen, contributing to skin aging.2 UVA (315–400nm) is the main radiation responsible for photoaging. It penetrates up to the dermis and has direct effects on dermal fibroblasts.32,33 Both UVB and UVA contribute to acquired skin pigmentation and skin cancer.31 Regarding skin cancer, while UVB causes direct damage to DNA, UVA causes indirect damage to DNA by forming ROS.34 UVR is a recognized carcinogen, responsible for more than 50% of all tumors. It causes almost 65% of malignant melanomas and 90% of keratinocyte carcinomas.31 VL (400–700nm) is the wavelength that can be detected by the human eye. One of the VL wavelengths with more biologic effects is the blue-violet light (BL) also known as high-energy visible light (≈400–500nm). It produces ROS and induces MMP-1 expression contributing to skin aging.6,35 OPN3 receptors detect BL and increase the synthesis of tyrosinase and dopachrome tautomerase involved in melanogenesis and hyperpigmentation.

The impact of BL is higher in subjects with darker skin tones (ITA <28°); hence, protection vs BL is specially recommended in them.36,37 IR (700nm–1mm) damages the skin; IR-A penetrates deeply, generating mitochondrial ROS, increasing MMP-1, reducing collagen production, promoting angiogenesis, and raising mast cell numbers.38

Humans are not exclusively exposed to a single exposome factor. While many studies examine the impact of solar radiation or air pollution on the skin of aging individually, few assess their combined effect.30 In this regard, solar radiation converts volatile organic compounds (VOC), found in the air, into secondary organic aerosols that contribute to PM formation, particularly PM2.5.19 Additionally, the combined effect of UVA radiation and ozone can synergistically induce more oxidative stress in human skin.39

In preclinical studies, the combination of UVA and diesel PMs (DPM) induced significant cytotoxic and genotoxic damage through the photoactive production of singlet oxygen, which was not observed with either UVA or DPM extracts alone.40 Furthermore, other in vitro data have demonstrated that PAHs, found in PM, in combination with UVA significantly increases skin damage and aging in the skin.41 UVA along with air pollutants considerably increases the risk of skin cancer.34 Clinically, an analysis of 799 Caucasian women in Germany suggested that facial lentigines are the consequence of an interplay between UVR and PMs.42 A recent study compared a similar population from two Chinese cities located at the same latitude (thus receiving approximately the same sun exposure) but exposed to different atmospheric pollution levels. It was found that people living in a higher polluted environment for many years had a higher prevalence of hyperpigmented lesions as well as higher severity of wrinkles.43

However, pollution could have in some circumstances a photoprotective effect reducing UV irradiance due to the presence of O3, NO2, SO2 and scattering particulates in the troposphere.44 More research is needed to elucidate the mechanisms of UV and pollution interaction.45 However, all existing evidence leads to the conclusion that the combination of solar radiation plus air pollution can have synergistic effects increasing their detrimental cutaneous effects. Hence, combined anti-pollution and photoprotective strategies should be implemented.

Cosmetic ingredients can help protect the skin from air pollution mainly by forming a protective film (film-forming), neutralizing ROS (antioxidants) and decreasing AhR expression. Some active ingredients with scientific evidence are listed below:

• 1.

  Film-forming agents: One novel film-forming agent is Alteromonas ferment extract, an exopolysaccharide derived from marine microorganisms. It creates a protective film on the skin, reducing the adherence of PM2.5 and improving skin barrier function. A study showed that after 56 days of daily use, Alteromonas ferment extract significantly improved skin hydration, firmness, and elasticity.47 Other film-forming agents are extracts from Kappaphycus alvarezii and Caesalpinia spinosa.48,49

• 2.

  Antioxidant ingredients: Several categories of ingredients can act as antioxidants including vitamins, plant-derived compounds, and microorganism-derived substances.

  • 2.1

    Vitamins: Topical vitamin C is a potent antioxidant that increases collagen synthesis and reduces the expression of matrix metalloproteinases (MMPs), increasing collagen levels.50 It can reduce pigmentation by inhibiting tyrosinase activity, prevent UV-induced erythema, and maintain skin hydration.50 Vitamin E is another important antioxidant that decreases MMP-1 levels and reinforces skin barrier.50 Topical niacinamide (vitamin B3) has been shown to improve the appearance of aging facial skin by reducing hyperpigmentation, pore size, and redness.51,52 It also offers benefits in preventing photo-immunosuppression and photo-carcinogenesis. Niacinamide improves skin barrier function, decreases sebum production, and is well tolerated.51,52 An in vitro study showed that continuous exposure for 3 days to 30pmol/cm2 of benzo(a)pyrene (BaP) and squalene monohydroperoxides, as surrogate environmental stressors, led to significant reductions in cell viability, increased inflammation, and rise in pigmentation in reconstructed human skin equivalents. Niacinamide pretreatment (5mmol/L) effectively reduced these effects, likely by supporting NAD+-dependent detoxification pathways.53 Medical literature does not contain studies specifically examining the protective effects of the other vitamins individually vs pollution-related skin aging. However, their capacity to mitigate oxidative stress – regardless of the source – suggests that such effects may be inferred. Future research should focus on this area of investigation.

  • 2.2

    Plant-derived compounds: Ginger oil from Zingiber officinale possesses antioxidant and anti-inflammatory properties. It has been shown to reduce UVB-induced erythema and wrinkle formation.54 In preclinical studies, Zingiber montanum has proven capable of inhibiting ROS formation, increase type I procollagen synthesis and decrease MMP (1, 3 and 9) expression and elastase activity.55 Another plant-derived antioxidant active is Polypodium leucotomos (PL). An aqueous PL leaf extract reduced oxidative stress and inhibited melanogenic pathway activation in keratinocyte and melanocyte cells exposed to BaP pollutants and UVA.56 In a study of cultured keratinocytes exposed to PM2.5, PL reduced inflammation and generation of new melanocytes.57

  • 2.3

    Microorganism-derived compounds: Ectoine, a metabolite produced by a halophilic bacterium, reinforces the skin barrier and suppresses inflammatory processes.58 In UVA-irradiated keratinocytes, it suppresses α-MSH-stimulated melanogenesis and activates the antioxidant Nrf2 pathways having a skin-whitening effect.59Porphyridium cruentum, a red microalga, produces a high amount of sulfated polysaccharides (SPs) that interfere with ROS formation and inhibit elastase activity, preserving elastin and collagen.60K. alvarezii, another seaweed extract, has demonstrated antioxidant, photoprotective, and anti-inflammatory properties.61

  • 2.4

    Other anti-pollution ingredients: Melatonin acts as an antioxidant by scavenging ROS (direct antioxidant) and increasing the levels of endogenous antioxidant enzymes (indirect antioxidant)62; additionally, it has been demonstrated that topical melatonin 12.5% protect vs UVB-induced erythema.63 Coenzyme Q10 (Q10) is an important endogenous coenzyme whose levels decrease with age and exposomal factors exposure. Topical Q10 can penetrate the skin and exert antioxidant effects, benefiting both elderly individuals with Q10 deficiency and people of all ages seeking protection due to oxidative stress.64 Moreover, Q10 decreases PM-induced inflammation by enhancing the cellular oxidative status, suppressing pro-inflammatory NF-kB, and improving the levels of the antioxidant and anti-inflammatory regulators Nrf2 and SIRT1 in human dermal fibroblasts.65

• 3.

  Aryl-receptor inhibitors: Another way to counteract the effect of pollution on the skin is through the blockade of the AhR. Deschampsia antarctica is a polyextremophile Gramineae native to Antarctica whose aqueous extract has shown to counteract the pollutant-induced AhR activation in the keratinocytes.66 A night cream containing melatonin, carnosine and Helichrysum italicum extract reduced the expression levels of AhR by 96% in human skin explants exposed to a mixture of PAH and heavy metals for 1.5h vs the control group.67

In addition to cosmetics, oral supplements can also mitigate the harmful effects of exposome. Carotenoids reduce UVA-induced oxidative stress and pigmentation, and UVB-induced erythema.7 However, humans cannot synthesize carotenoids on their own and dietary supplementation is necessary.55,68,69 Ferulic acid found in tissues of plants has antioxidant and anti-inflammatory effects on the skin.69 Green tea is rich in polyphenols which scavenge ROS, enhance immunity and decrease MMPs.70 Another useful active ingredient is the extract of the Mesoamerican fern P. leucotomos (PL). It has been demonstrated that oral treatment with PL extracts reduced the harmful effects of UVB irradiation, including the appearance of sunburn cells, DNA damage, and inflammation.71 It also protects vs VL, particularly from hyperpigmentation.72–74 In a study with 22 individuals irradiated with UVB, UVA, and VL, oral PL extract showed suppressive effects on UVB-induced erythema within 2h of administration.75

The mechanism of action and administration route of different anti-pollution ingredients are shown in Table 1.