What are the effects of pollution on the skin?

Indeed, chronic exposure to increasing amounts of all these forms of pollutants compromises the integrity of the skin. They exert their harmful effects by inducing oxidative stress in the skin tissues, with an overproduction of free radicals and reactive oxygen species, the peroxidation of polyunsaturated fatty acids, and a depletion of the enzymatic antioxidant capacity (glutathione peroxidase, superoxide dismutase, catalase, etc.) and non-enzymatic (vitamin C, vitamin E), which damage the barrier function of the epidermis. The main atmospheric pollutants that affect the skin are polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds, nitrogen oxides, airborne fine particles, ozone and heavy metals.

Regardless of the route of entry, either directly through the absorption of atmospheric pollutants via the skin (transdermal route) or through hair follicles, or indirectly through the absorption of particles by the lungs which are then transported by the blood to the skin, this disruption leads to the development of various skin issues, as soon as the skin's normal defence potential is exceeded. Indeed, cells can no longer rid themselves of free radicals, thus slowing down the skin's repair mechanisms. Result : a whole series of inflammatory reactions is triggered and skin disorders can appear, sparing no skin type.

• An accelerated ageing.

  Several studies have demonstrated that exposure to atmospheric pollutants contributes to accelerating the appearance of skin ageing signs by penetrating the deep layers of the skin, notably the formation of more pronounced wrinkles and elastosis. One of the main mechanisms through which ambient particles exert their harmful effects is the imbalance between the defence system and an excessive production of free radicals. They are thus responsible for a slowdown in cellular renewal, lipid peroxidation, damage to the stratum corneum, and degradation of collagen and elastin fibres, which are vital elements of the extracellular matrix, following an upregulation of matrix metalloproteinases (MMPs).

• A dulling of the complexion.

  It has been demonstrated that carbon monoxide binds to haemoglobin, altering its conformation and reducing its ability to transport oxygen. Indeed, this decrease in skin oxygenation can lead to a loss of radiance. Furthermore, repeated exposure to these aggressors can trigger oxidative events that may disrupt the normal functioning of keratinocytes. The skin then regenerates more slowly and dehydrates more easily.

• A loss of skin texture uniformity.

  Environmental pollution can also lead to acneiform eruptions, characterised by comedones and cysts, by acting at different levels. A study reported that ozone, along with long UVA rays and cigarette smoke rich in polycyclic aromatic hydrocarbons, are powerful oxidising agents of squalene, an unsaturated lipid present in the sebum (10 - 15%) produced by the cells of the sebaceous glands (sebocytes) which is highly sensitive to oxidative processes due to the presence of six non-conjugated carbon double bonds. However, such a biochemical modification induces the formation of oxidised squalene by-products, mainly peroxidised forms, which then lead to an increase in comedones or even inflammatory acne.

  Furthermore, when oxidised, the elemental composition of oxidised squalene reveals an oxygen content of around 25%. This high value is likely to regulate the oxygen tension within the follicular canal, a critical factor in the survival and development of the resident anaerobic skin flora. Similarly, another study has shown that ambient air pollution can induce an abundance of Malassezia spp., commensal fungi on the skin, which could lead to a dysbiosis of the skin ecosystem and result in certain skin disorders.

• A weakened and irritated skin.

  Several studies suggest that air pollution induces an inflammatory response in the epidermis, which can disrupt epidermal differentiation and, consequently, affect the skin's immune barrier. Indeed, the reactive oxygen species generated promote the maturation of pro-inflammatory mediators (IL-18 and IL-1β) in keratinocytes, leading to the accumulation of neutrophils and other phagocytic cells that in turn generate free radicals, thus creating a vicious cycle. They are also capable of increasing the expression of NF-kB, a transcription factor that regulates the expression of pro-inflammatory cytokines in epidermal cells. Pollutants also attack the lipids of skin cell membranes making the skin more reactive and sensitive, which increases the risk of developing redness and sensitivities.

• A loss of skin hydration.

  Pollution can lead to a dysfunction of the skin's protective barrier. For instance, fine airborne particles negatively impact the expression of hydrophobic epidermal lipids, including cholesterol sulphate, phospholipids, sphingomyelin, and glucosylceramides, which are key components of the barrier function. They also affect the expression of claudin-1, a significant protein that contributes to the integrity of tight junctions and are also capable of destroying keratin proteins that protect the skin from dehydration. On the other hand, exposure to ozone results in the formation of aldehydes and ozonation products of lipids, following the oxidation of unsaturated fatty acids in the upper layers of the epithelium (horny layer), damaging the barrier function of the epidermis. Studies have even shown that it can cause a depletion in tocopherol (vitamin E) and vitamin C, as well as an increase in malondialdehyde, a by-product of lipid peroxidation, leading to an impairment of the barrier function.

• A loss of skin tone uniformity.

  Several ethnically diverse cohort studies (Caucasians and Asians) have revealed that skin exposure to atmospheric pollutants (black carbon particles, polycyclic aromatic hydrocarbons and heavy metals) is significantly correlated with the formation of more lentigines on the face and back of the hands. The activation of aryl hydrocarbon receptors (AhR) in melanocytes could provide a mechanistic explanation for these epidemiological observations.

  Indeed, fine particles laden with organic chemicals, such as PAHs, which are highly lipophilic and easily penetrate the skin, would induce the proliferation of melanocytes associated with an increase in the transcription of genes involved in the synthesis de novo of melanin, and thus of skin pigmentation. This melanin synthesis would serve to protect the skin against oxidative stress induced by air pollution and therefore represents a skin defence strategy, given that eumelanin has antioxidant properties.