Human Skin: Pollution's Unseen Gateway To Our Bodies

Air pollution is the contamination of outdoor (ambient) and indoor (household) environments by any chemical, physical, or biological agent that modifies the natural characteristics of the atmosphere. Nearly all (90%) of the world’s population experience daily pollution. In 2019, air pollution was considered by the World Health Organization to be the biggest environmental health risk to humans, responsible for killing more than 7 million people prematurely every year.

Air pollution affects many organ systems such as cardiovascular, pulmonary, central nervous, reproductive, and integumentary systems.

There is also evidence that air pollution affects the skin. Skin interfaces with the atmosphere. Studies show that pollutants gain entrance to the skin by direct accumulation on the skin surface, absorption via the hair follicles, inhalation, ingestion, and circulation of pollutants in plasma that diffuse into deeper dermal tissues.

The skin disorders associated with pollution include acne, hyperpigmentation, atopic dermatitis, and psoriasis.

Skin is a target of environmental stressors

Airborne pollution is defined as contamination by any chemical, physical, or biological agent from biogenic, anthropogenic, or mixed origins that modifies the natural characteristic of the atmosphere.

The skin is a complex, multifunctional organ with the capacity to maintain cutaneous and overall body homeostasis, electrolyte and fluid balance, and thermoregulation. It operates as a fully functional and independent neuroendocrine biofactory producing hormones, neuropeptides, and neurotransmitters. The skin also serves as a source of hormones and as a target for their activities.

The skin, together with the lungs, is the main target organ affected by the harmful insults of air pollution. Billions of people are still exposed to unhealthy ambient air, and the mixture of pollutants could affect skin physiology either directly by transcutaneous absorption or indirectly by their systemic distribution after inhalation or ingestion.

The skin is also a target of another physical stressor represented by UV radiation (UVR). UVR is the most harmful environmental factor that affects skin biology, contributing to photodamage on chronically sun-exposed areas, thus accelerating the physiological ageing process and increasing skin cancer risk.

The impact of air pollution on skin health and diseases has been well established. The skin is targeted by pollutants, either by direct accumulation on the skin surface or by indirect distribution by the systemic route after pollutant inhalation or ingestion.

Airborne pollutants can penetrate the skin via nanoparticles and generate quinones, which are redox-cycling chemicals that produce reactive oxygen species (ROS). This increase in the amount of ROS and free radicals within the cell and its mitochondria overcomes the skin's innate antioxidant defences, including depletion of enzymatic and nonenzymatic antioxidant capacities. The ROS and free radicals interact with the lipid-rich plasma membrane, initiating a lipid peroxidation reaction that unleashes proteolytic activity, causing further tissue injury. This cascade in turn triggers an increase of metalloproteinases, resulting in inflammation and metabolic impairments. Oxidative stress initiates complex biological processes resulting in genetic damage, activation of transcription factors such as activator protein 1 and nuclear factor-κB and signaling pathways such as extracellular signal-regulated kinases, c-Jun N-terminal kinases, and p38 mitogen-activated protein kinases, involved in cell growth and differentiation and in the degradation of the connective tissue of the dermis.

The effects of pollutants on the skin can be amplified by the deleterious synergy between pollution and sunlight. Repeated and frequent exposure to high levels of these pollutants may have deleterious effects on the skin, which include association with or causation of premature ageing, photodamage, solar lentigines, melasma, and increased incidences of atopic dermatitis, psoriasis, skin cancers, and acne.

Acne, hyperpigmentation, atopic dermatitis, and psoriasis have been shown to be influenced by air pollution. It is important for pollution to be added as a risk factor for these skin disorders and for a discussion to be had on mitigating its negative effects on patients.

Pollutants can be detected in the blood

The skin is exposed to a mixture of harmful air pollutants, which can affect its physiology and are responsible for cutaneous damage. Some polycyclic aromatic hydrocarbons are photoreactive and could be activated by ultraviolet radiation (UVR). Therefore, such UVR exposure would enhance their deleterious effects on the skin.

Air pollution also affects vitamin D synthesis by reducing UVB radiation, which is essential for the production of vitamin D3, tachysterol, and lumisterol derivatives. Ambient air pollutants, photopollution, blue-light pollution, and cigarette smoke compromise cutaneous structural integrity, can interact with human skin microbiota, and trigger or exacerbate a range of skin diseases through various mechanisms.

Generally, air pollution elicits an oxidative stress response on the skin that can activate the inflammatory responses. The aryl hydrocarbon receptor (AhR) can act as a sensor for small molecules such as air pollutants and plays a crucial role in responses to (photo)pollution. On the other hand, targeting AhR/Nrf2 is emerging as a novel treatment option for air pollutants that induce or exacerbate inflammatory skin diseases.

Pollutants induce an oxidative stress response in the skin

Human skin is one of the main targets of pollutants, which can reach both the superficial and deeper skin layers through transcutaneous and systemic routes. Many environmental pollutants are oxidants or contribute to the production of reactive oxygen species (ROS), which are believed to alter apoptotic pathways that may be involved in the pathogenesis of several skin disorders.

ROS are highly reactive molecules that can damage lipids, proteins, and macromolecules such as DNA and RNA. They are generated from the surface of particles where polycyclic aromatic hydrocarbons (PAH) and nitro-PAH are adsorbed. Additionally, transition metals such as iron, copper, chromium, and vanadium can catalyze Fenton's reaction, producing a highly reactive hydroxyl radical that can induce oxidative DNA damage.

Oxidative stress occurs when there is an imbalance between ROS formation and individual antioxidant activity. This stress can lead to mitochondrial damage and the activation of inflammatory cells, including neutrophils, eosinophils, and monocytes. It can also increase the number of macrophages capable of generating ROS and reactive nitrogen species.

Initially, when oxidative stress is relatively low, the body induces a series of antioxidant and detoxification enzymes, such as catalase, superoxide dismutase, and glutathione S-transferase, to counteract ROS formation and protect against adverse biological outcomes. However, prolonged or severe oxidative stress can overwhelm these defense mechanisms, leading to cellular damage and potentially contributing to skin disorders and other pathologic processes.

Pollution is associated with skin ageing

The skin is one of the main targets of environmental pollutants, which reach the superficial and deeper skin layers by transcutaneous and systemic routes. While the skin acts as a biological barrier against pro-oxidative air pollutants, prolonged exposure to high levels of pollutants can induce alterations in skin homeostasis and has been associated with ageing and inflammatory skin conditions such as eczema.

There is now epidemiological evidence that exposure to traffic-related air pollution, including PM, NO2, and ground-level O3, is associated with pigment spots and wrinkle formation. An increase in PM2.5 absorbance (soot) and traffic particles was associated with more pigment spots on the forehead and cheeks. The association between NO2 concentrations and pigment spots has been observed in individuals over 50 years old in Germany and China.

Additionally, indoor air pollution from cooking with solid fuels may accelerate skin ageing, particularly in Chinese women. The skin may be affected by environmental pollutants concentrating at its surface, and studies of specific populations with high levels of dermal uptake, such as coke oven workers, have indicated that dermal uptake is a direct route of pollutant contamination.

The exposure time window is also relevant, with more severe outcomes at certain ages, such as childhood and advanced age. Moreover, air pollution exposure during pregnancy may cause adverse effects on fetal growth and development.

Pollution is linked to inflammatory skin diseases

Yes, pollution is linked to inflammatory skin diseases.

Air pollution is a growing threat to human health worldwide. The skin is one of the main targets of pollutants, which reach the superficial and deeper skin layers by transcutaneous and systemic routes.

Pollutants may activate cell metabolism and inflammatory processes. In normal human epidermal keratinocytes exposed to O3, activation of the aryl hydrocarbon receptor (AHR) induced the expression of several cytochrome P450 genes, including CYP1A1. AHR activation and increased CYP1A1 expression have also been reported after exposure to B[a]P, PM2.5 and water-soluble tobacco smoke extracts.

Activation of the AHR pathway has also been implicated in the pathology of atopic dermatitis in humans. The neurotrophic factor Artemin (ARTN) has been identified as the missing link between pollution and AHR-CYP1A1 in an atopic dermatitis mouse model. This prospective study also showed that epidermal CYP1A1 and ARTN messenger ribonucleic acid (RNA) levels were significantly higher in human skin samples from patients with atopic dermatitis (N = 20) than in those from patients with contact dermatitis (N = 5) or from healthy subjects (N = 20). AHR-dependent elevated expression of CYP1A1 and ARTN was also detected in NHEKs and HaCaT cells exposed to diesel exhaust particles. Pollutants may therefore exacerbate atopic dermatitis symptoms via direct activation of AHR and subsequent ARTN overexpression.

Activation of the AHR pathway in NHEKs by PM or B[a]P has been linked to the induction of proinflammatory molecules, such as interleukin-8 and cyclooxygenase-2 via the production of reactive oxygen species (ROS) involved in oxidative stress processes.

Oxidative stress responses were also observed in HaCaT cells exposed to concentrated air particles and in primary human keratinocytes exposed to cigarette smoke condensate or diesel particulate extract. Clinical evidence for an oxidative stress response occurring in humans after exposure to pollutants comes from two prospective clinical studies comparing the impact of pollution on subjects living in Mexico City and Cuernavaca or in urban and rural areas of Shanghai. Among several biochemical changes in sebum and the stratum corneum, vitamin E, squalene and ATP levels decreased. In contrast, oxidized protein levels were augmented, indicating that skin antioxidant molecules were depleted in subjects exposed to elevated pollution levels. These studies show that pollutants induce an oxidative stress response in human skin.

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