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The environmentally induced skin aging process is called premature or extrinsic skin aging.1
Unlike intrinsic skin aging, the extrinsic skin aging process is characterized by striking morphologic and physiologic changes and its prominent manifestations are coarse wrinkles, solar elastosis and pigment irregularities.1,2
For decades, it was thought that extrinsic skin aging resulted largely from exposure to UV radiation, and the terms extrinsic and photoaging were used as synonyms.
There is, however, growing evidence that other environmental factors may contribute to skin aging:
A relationship between air pollution and skin aging was first shown in the SALIA study (Study on the Influence of Air pollution on Lung function, Inflammation and Aging – 402 Caucasian women aged 68 to 79 living in the industrialized Ruhr area or in the rural area of Borken, Germany – results published in 2010).2,3
A significant association was found between traffic-related airborne particles and signs of extrinsic skin aging, especially pigment spots and wrinkles, in particular nasolabial folds.1,2 A correlation was also found between increase of NO2 and increase of pigment spot formation.2
The results also confirmed that UV exposure is significantly associated with a more pronounced occurrence of pigmented spots.2
The SALIA study provided epidemiological evidence that traffic-related PM presents an important environmental factor contributing to extrinsic skin aging in humans.2
Exposure to traffic-related air pollution including PM, NO2 and ground-level ozone (O3) is associated with pigmented spot and wrinkle formation in Caucasians and East Asians, and preliminary evidence suggests that at least some of these effects may be mediated via Aryl hydrocarbon Receptors (AhR) signalling in human skin.
A major mechanism by which ambient PM exerts its damaging effects is through the generation of oxidative stress, an important contributor to extrinsic skin aging.1,2
Furthermore, particles can serve as carriers for organic chemicals and metals that are capable of localizing and generating Reactive Oxygen Species (ROS) directly in mitochondria, leading to skin aging by mitochondrial damage.1,2
It was also suggested that the skin-aging pathway may be induced by polycyclic aromatic hydrocarbons (PAHs), which are adsorbed on the surface of suspended PM in urban air and are able to activate the xenobiotic metabolism via the AhR.1,2
Studies on the effects of O3 previously showed that regular contact with O3 depletes antioxidants from the stratum corneum.5 O3 also increases lipid peroxidation and protein oxidation in mouse skin.6,7 In vitro, O3 activates AhR in cultured keratinocytes, thereby providing a potential mechanism.8
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