[Academic Presentation] Air Pollution and Extrinsic Skin Aging

Article reprinted from: Chinese Journal of Dermatology and Venereology

Authors: Peng Fen, Xue Chenhong, Chen Zhou

Humans and the environment constitute an inseparable whole. As the body’s outermost organ, the skin is in direct contact with the external environment and constantly subjected to the challenges and assaults posed by environmental exposures. Consequently, skin aging is closely linked to environmental factors. Skin aging encompasses both exogenous and endogenous components: endogenous aging is genetically determined and irreversible, leading inevitably to age‑related changes that primarily result in the loss of skin functions; whereas exogenous aging—caused by environmental influences—impacts appearance and is associated with cosmetic concerns such as dryness, roughness, deep wrinkles, irregular pigmentation, and degeneration of elastic fibers. Exogenous aging also bears a strong association with numerous skin disorders, including actinic keratosis, basal cell carcinoma, and squamous cell carcinoma. It arises from the combined effects of various environmental factors and can potentially be mitigated or prevented through targeted interventions. Currently recognized contributors to accelerated exogenous skin aging include ultraviolet radiation, thermal stress, infrared exposure, sun and wind, environmental dryness, and smoking; among these, UV radiation plays a particularly pivotal role. Increasing evidence further indicates that air pollution can likewise hasten exogenous skin aging. In recent years, atmospheric particulate matter (PM) and skin aging attributable to the combustion of fossil fuels in kitchens have emerged as key research topics. This review summarizes the literature on the relationship between indoor and outdoor air pollutants and exogenous skin aging.

1. Outdoor Air Pollutants and Skin Aging

1. 1 Outdoor Air Pollutants

Outdoor air pollutants primarily include PM, ozone, carbon dioxide, nitrogen monoxide, and sulfur dioxide. PM2.5 refers to particulate matter suspended in the air with a diameter of less than 2.5 μm; it comprises smoke, soot, tiny water droplets from combustion sources, as well as particles formed through chemical reactions in the atmosphere. PM10 consists of slightly larger particles than PM2.5. In urban air pollution, the main sources of PM are transportation, forest fires, and wood combustion. Recent satellite imagery has provided global PM concentration data, revealing particularly high PM2.5 levels in northern India and China, where annual average concentrations exceed 50 µg/m³. Ozone present in the stratosphere shields the Earth from short‑wave ultraviolet radiation (UVC) and part of medium‑wave ultraviolet radiation (UVB); however, tropospheric or surface‑level ozone is a secondary pollutant, generated through photochemical reactions between ultraviolet radiation and primary pollutants in the environment. Carbon dioxide and nitrogen monoxide originate mainly from vehicle exhaust emissions, while sulfur dioxide arises primarily from the combustion of sulfur‑containing fuels. Both sulfur oxides and nitrogen oxides contribute to the formation of PM2.5 in ambient air.

1. 2 Outdoor Air Pollutants and Skin Aging

As air pollution worsens in certain regions worldwide, researchers have begun investigating its potential health impacts on humans. Studies have shown that air pollution is associated with various clinical signs of extrinsic skin aging. Vierkötter and colleagues examined the relationship between exposure to atmospheric particulate matter—primarily PM10—and skin aging. Their study included 400 Caucasian women aged 70–80, recruited from both highly industrialized urban areas and less polluted rural settings. The researchers assessed how traffic‑related soot and particulates from different environments affect skin aging, using the SCINEXA system to score the degree of skin aging. Results indicated that more than 35% of age spots were correlated with air pollutants emitted by nearby (within 100 m) busy arterial roads carrying over 10,000 vehicles per day. Age spots on the forehead and cheeks were linked to long-term exposure to soot, traffic‑derived particulates, and PM10. Each interquartile range (IQR) increase in soot levels was associated with a 20% rise in forehead and cheek age spots. Age spots are more prevalent among individuals of Indian and Southeast Asian descent, whose skin types are predominantly III or IV, and they represent a key clinical marker of premature skin aging in Asians. Another study conducted in Mexico found that residents living in heavily polluted areas exhibited significantly lower concentrations of vitamin E, squalene, and interleukin‑1 in their skin, while lactic acid levels were elevated. Squalene is an important endogenous antioxidant, whereas vitamin E serves as a major exogenous antioxidant; the observed reductions suggest that these compounds are being mobilized to counteract oxidative damage to the skin, indicating that air pollution places the skin under oxidative stress.

1. The mechanisms linking 3 PM to skin aging

Research on how the air pollutant PM contributes to skin aging is still in its early stages, and its effects on the skin may be mediated by several mechanisms.

1. 3. 1 Carrying polycyclic aromatic hydrocarbon compounds

These particulate matters can carry organic compounds such as polycyclic aromatic hydrocarbons (PAHs) into the body; these substances are highly lipophilic and readily penetrate the skin. As early as 2008, a German study demonstrated that PAHs can induce proliferation of melanocytes and skin pigmentation in mice. PAHs are potent ligands for the aryl hydrocarbon receptor (AhR), a ligand‑dependent transcription factor expressed in keratinocytes and melanocytes, and may regulate epidermal melanin production by modulating the expression of tyrosinase and tyrosinase‑related protein 2. As exogenous ligands of the AhR, PAHs activate the receptor and subsequently generate reactive oxygen species (ROS). ROS‑mediated oxidative damage affects numerous molecular targets, leading to DNA modifications, lipid peroxidation, and the release of pro‑inflammatory cytokines. A variety of endogenous and exogenous factors—such as environmental pollution, solar exposure, psychological stress, smoking, and routine metabolic processes—can generate free radicals. Evidence indicates that free radicals can disrupt gene expression, degrade collagen fibers, and promote the accumulation of elastin‑like proteins, thereby contributing to the hallmarks of skin aging.

1. 3. 2 Directly enters the skin

Particulate matter can penetrate the skin through follicular openings, wounds, and an impaired skin barrier, directly triggering allergic reactions, oxidative stress, and inflammatory responses [5, 18]. 1.3.3 Synergistic Effects of Pollutants with Other Factors Such as Sunlight It is well known that under natural light, the skin is subjected to the combined effects of ultraviolet and infrared radiation, leading to damage to collagen and elastin fibers. Recent studies have demonstrated that high concentrations of air pollutants can exponentially accelerate the skin‑aging process induced by solar exposure. The interaction between UVA radiation and environmental pollutants such as particulate matter (PM) and polycyclic aromatic hydrocarbons (PAHs) can effectively hasten exogenous skin aging. The MC1R gene, which determines hair and skin color in humans, has been shown—through the Elf‑akir A study involving 524 French women—to confer a sixfold higher risk of severe skin aging in individuals carrying two loss‑of‑function MC1R variants (R151C, R160W, R142H, D294H, I155T, D84E) compared with those homozygous for the wild‑type alleles. Among these, carriers of R142H, R151C, or D84E exhibited the highest risk. This research further confirmed that mutant MC1R alleles not only markedly exacerbate age‑related skin aging but also, to some extent, promote skin aging caused by environmental pollution.

1. The Mechanisms Linking Ozone to Skin Aging

Currently, there are relatively few studies investigating the relationship between ozone and skin aging. Stratospheric ozone absorbs and scatters ultraviolet radiation; a reduction in its concentration increases the amount of UV radiation—particularly UVB—that reaches the Earth’s surface, thereby posing significant risks to the skin. In contrast, tropospheric ozone is a highly reactive molecule that acts directly on the skin’s surface, readily oxidizing molecules in the stratum corneum. In vitro experiments have shown that even at ozone concentrations comparable to those found in ambient air pollution, epidermal levels of vitamins E and C can be depleted, while malondialdehyde—a lipid peroxidation product—accumulates in the epidermis. Malondialdehyde elevates hydrogen peroxide levels and reduces ATP concentrations in epidermal keratinocytes, enhances the release of IL‑1α, and upregulates pro‑inflammatory markers such as COX‑2, heat‑shock proteins (HSP32, HSP70, HSP27), NF‑κB, and matrix metalloproteinases (MMPs). Moreover, oxidative stress induced by ozone can lead to DNA damage.

2 Indoor Air Pollution and Skin Aging

The primary sources of indoor pollution are smoking and the combustion of fossil fuels in kitchens.

2. 1 Smoking

Smoking is not only harmful to health but also contributes to ambient air pollution. Numerous studies have shown that smoking is an independent risk factor for skin aging. It is associated with upper‑lip wrinkles, photo‑induced elastin degradation, telangiectasia, and skin laxity; in 40‑year‑olds with a long smoking history, skin appearance often resembles that of 70‑year‑olds who have never smoked, underscoring the premature aging effects of tobacco use. Tobacco is a complex mixture of pollutants, akin to air pollution, which can disrupt collagen metabolism. A reduction in collagen leads to diminished skin tension, accelerating skin aging and promoting wrinkle formation. Moreover, smoking elevates levels of elastin and matrix metalloproteinases. Recent research has identified high‑mobility group box 1 (HMGB1) protein in the cytoplasm of epidermal keratinocytes in mice; increased HMGB1 correlates negatively with collagen content, suggesting its role in collagen loss. In mouse epidermal keratinocytes exposed to secondhand smoke for four weeks, HMGB1 levels were significantly higher than in control groups. In 2015, Suzaynn introduced the concept of “thirdhand smoke,” whereby polycyclic aromatic hydrocarbons (PAHs), nicotine, cotinine, and tobacco‑specific nitrosamines released during smoking persist on indoor surfaces or on cotton fabrics worn by individuals—often at concentrations up to ten times higher than in unexposed settings—forming thirdhand smoke. These residues can enter the body via skin contact or inhalation, causing systemic harm.

2. 2 Kitchen Fossil Fuels

Recently, Li and colleagues investigated the relationship between kitchen cooking fumes and skin aging in Chinese individuals. They recruited women aged 30 to 90 from Pingding (northern China) and Taizhou (southern China), using the SCINEXA system to assess the degree of skin aging. The results indicated that combustion of fossil fuels in kitchens increases the risk of facial wrinkles by 5%–8% and dorsal hand wrinkles by 74%. Although the mechanisms underlying how fossil fuel combustion accelerates skin aging remain poorly understood, such combustion generates polycyclic aromatic hydrocarbons (PAHs), including benzo[a]pyrene (BaP), which is produced by the incomplete combustion of fossil fuels and can persist in air, food, and water. A 2009 mouse study demonstrated that exposure to BaP induces oxidative DNA damage, leading to the formation of 8‑hydroxydeoxyguanosine (8‑OHdG) and hydrogen peroxide (H₂O₂). Moreover, mice exposed simultaneously to BaP and UVA exhibited oxidative DNA damage levels 14 times higher than those observed in mice exposed to BaP or UVA alone.

3. Summary and Outlook

Indoor and outdoor air pollutants, like ultraviolet radiation, can accelerate skin aging and contribute to the development of extrinsic aging signs. Because extrinsic skin aging linked to air pollution is associated with oxidative stress, both oral and topical antioxidants may serve as effective strategies to counteract pollution‑induced aging. Topical application of antioxidant‑infused barrier creams and thorough nighttime facial cleansing can minimize direct contact between air pollutants and the skin. Following cleansing, using products containing antioxidants to nourish the skin can help delay the onset of extrinsic skin aging caused by air pollution.

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