Facial Dermatoses in E-Cigarette Users and the Role of Nicotine-Induced Oxidative Stress

Facial dermatoses in e-cigarette users arise from nicotine-induced oxidative stress, inflammatory signaling, and barrier dysfunction, contributing to an increased prevalence of acneiform eruptions, perioral dermatitis, and rosacea exacerbations. E-cigarette aerosols contain nicotine, volatile organic compounds, and reactive oxygen species (ROS) that disrupt cutaneous homeostasis by impairing antioxidant defense mechanisms and promoting lipid peroxidation in the epidermis. Nicotine exposure induces mitochondrial dysfunction in keratinocytes and sebocytes, leading to dysregulated sebum production, enhanced Cutibacterium acnes colonization, and increased susceptibility to inflammatory acne. Additionally, nicotine-mediated vasoconstriction and endothelial dysfunction reduce dermal microcirculation, compromising oxygen delivery and delaying wound healing, while heightened expression of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α further amplifies cutaneous inflammation. Perioral dermatitis in e-cigarette users may result from a combination of vaporized chemical irritants, barrier disruption, and dysbiosis, paralleling the effects seen with traditional cigarette smoking but with unique patterns of dermal exposure. Emerging evidence also suggests an association between chronic e-cigarette use and exacerbations of rosacea, possibly linked to nicotine’s role in neurovascular dysregulation. Identifying the dermatologic consequences of e-cigarette use reinforces the need for targeted patient counseling, oxidative stress mitigation strategies, and further research into the long-term cutaneous effects of vaping.