**Background:** Environmental air pollution is a global health problem linked to respiratory, cardiovascular, cutaneous, and neurological diseases. The skin, as the first-line barrier, is a major target of airborne pollutants including particulate matter (PM), polycyclic aromatic hydrocarbons (PAHs), ozone (O3), cigarette smoke, and volatile organic compounds. These pollutants can directly penetrate the skin or reach it systemically after inhalation. Co-exposure with ultraviolet radiation (UVR), termed photopollution, exacerbates damage. This narrative review synthesizes current knowledge on the molecular mechanisms and clinical consequences of air pollutant effects on skin, and discusses preventive and therapeutic strategies.
**Methods:** This is a narrative review that synthesizes findings from in vitro, in vivo, and human studies. The authors discuss the physicochemical properties of pollutants (PM10, PM2.5, ultrafine PM, PAHs, O3, cigarette smoke), their cutaneous penetration routes, and molecular pathways—particularly oxidative stress and the aryl hydrocarbon receptor (AhR) signaling cascade. They review evidence linking pollutants to specific skin diseases and evaluate anti-pollution skincare approaches and AhR modulators.
**Key Results:** The paper reports that ultrafine PM (≤4 nm) can penetrate intact skin, while larger particles require barrier impairment. PM and O3 generate reactive oxygen species (ROS), deplete antioxidants (vitamin C, E, glutathione), and increase lipid peroxidation products like 4-hydroxynonenal (4HNE) and 8-iso-prostaglandin-F2α. AhR activation by PAHs (e.g., benzo(a)pyrene, BaP) induces CYP1A1, leading to ROS and mutagenic metabolites, and upregulates pro-inflammatory cytokines (IL-6, IL-8, IL-1α, IL-1β) and matrix metalloproteinases (MMP-1, MMP-3). Cigarette smoke increases MMP-1 mRNA and 4HNE levels. PM10 exposure is associated with a 52% higher relative risk of nonmelanoma skin cancer per 10 µg/m³ increase. O3 layer depletion (1% reduction) increases UVB by 2%, potentially raising melanoma incidence by 1–2% and squamous cell carcinoma by 3–4.6%. Air pollutants increase trans-epidermal water loss (TEWL), downregulate filaggrin and other barrier genes, and promote premature aging, atopic dermatitis, psoriasis, acne, melasma, and hair loss. Vitamin D synthesis is reduced by PM and O3 scattering UVB.
**Clinical Implications:** The review underscores that air pollution is a modifiable risk factor for skin diseases. Preventive strategies include protective clothing, broad-spectrum sunscreens, and antioxidant-rich topical formulations (e.g., vitamin E, ferulic acid, melatonin). Melatonin is highlighted for its potent antioxidant cascade and ability to upregulate SIRT1, reducing MMP-1/MMP-3 and NF-κB inflammation. Targeting AhR/Nrf2 with dual agonists like tapinarof (in clinical trials for atopic dermatitis and psoriasis) shows promise by reducing inflammation, upregulating barrier proteins (filaggrin, loricrin), and activating antioxidant defenses. The review emphasizes that AhR signaling has dual (Yin-Yang) effects depending on ligand and context, so modulation must be carefully targeted.