Sunburn Pathophysiology: From UV Damage to Long-Term Skin Cancer Risk

Stepwise Mechanism

1. UV Absorption: UVB (290–320 nm) absorbed by DNA, proteins; UVA (320–400 nm) penetrates deeper, generates ROS.
2. Direct DNA Damage: Cyclobutane pyrimidine dimers (CPDs), 6-4 photoproducts → mutations if unrepaired.
3. Inflammatory Cascade: Keratinocytes release cytokines (IL-1, TNF-α, IL-6), prostaglandins, chemokines → vasodilation, neutrophil infiltration.
4. Clinical Signs: Erythema (2–6h), edema, pain, heat; blistering if severe (epidermal necrosis).
5. Resolution: Desquamation (peeling) as damaged keratinocytes shed; apoptosis of mutated cells.

Long-Term Consequences

• Photoaging: Collagen/elastin degradation → wrinkles, solar elastosis.
• Actinic keratosis: Precancerous scaly plaques.
• Skin cancer: BCC, SCC (cumulative UV); melanoma (intermittent intense burns, especially childhood).
• Immune suppression: Local and systemic, reducing tumor surveillance.

Prevention Hierarchy

1. Avoid peak sun (10 AM–4 PM)
2. Protective clothing (UPF 50+), wide-brim hat, UV-blocking sunglasses
3. Broad-spectrum SPF 30+ sunscreen, reapplied 2-hourly
4. Seek shade; avoid tanning beds

Treatment of Acute Sunburn

• Cool compresses, colloidal oatmeal baths
• NSAIDs (ibuprofen) early for inflammation
• Hydration, topical aloe/soy
• Do not pop blisters; topical antibiotic if ruptured
• Seek care if fever, extensive blistering, signs of infection