Environmental Stressors on Skin Aging. Mechanistic Insights

Abstract

The skin is the main barrier that protects us against environmental stressors (physical, chemical, and biological). These stressors, combined with internal factors, are responsible for cutaneous aging. Furthermore, they negatively affect the skin and increase the risk of cutaneous diseases, particularly skin cancer. This review addresses the impact of environmental stressors on skin aging, especially those related to general and specific external factors (lifestyle, occupation, pollutants, and light exposure). More specifically, we have evaluated ambient air pollution, household air pollutants from non-combustion sources, and exposure to light (ultraviolet radiation and blue and red light). We approach the molecular pathways involved in skin aging and pathology as a result of exposure to these external environmental stressors. Finally, we reflect on how components of environmental stress can interact with ultraviolet radiation to cause cell damage and the critical importance of knowing the mechanisms to develop new therapies to maintain the skin without damage in old age and to repair its diseases.

Keywords: air pollutant; inflammation; oxidative stress; photo-pollution; skin aging.

Figure 1

Effects of air pollution and ultraviolet radiation (UVR) on the skin. A simplified representation of the effects of epidermal keratinocyte effects of particulate matter (PM), polycyclic aromatic hydrocarbons (PAH), ozone (O₃), and UVR. The AhR binds to PM, PHA, O3, and UVR adducts. After ligand binding, AhR translocates to the nucleus and induces the transcription of cytochrome P450 (CYP 1A1, CYP 1B1). CYP 1A1 generates toxic and reactive intermediates of xenobiotics, increasing ROS. In addition to the canonical AhR pathway, the activation of AhR affects NF-κB pathways. NF-κB induces an increase of proinflammatory cytokines and MMP and decreases TGF-β, and I collagen synthesis. ROS also induces NF-κB activation. Among the next targets of the pollutants are the proinflammatory mediators (COX and PGE2). Pollutants induce the production of NALP3a. NALP3 stimulates caspase-1 to promote proinflammatory cytokines. In epidermal KC, AhR activation results from the absorbance of UVB radiation by tryptophan (Trp). Trp induces the generation of 6-formylindolo[3,2-b]carbazole (FICZ). FICZ is a high-affinity ligand for AhR. ROS induced by pollutants alters lipids, proteins, and DNA. Also, oxidative stress causes overexpression of MMP in the ECM and collagen degradation.

Figure 2

Skin responses to air pollutions (particulate matter, PM; polycyclic aromatic hydrocarbons PAH; and ozone, O₃) and ultraviolet radiation.