UVB Radiation Causes Both Vasodilation and Erythema
Yes, UVB radiation from sunlight directly causes vasodilation followed by erythema (sunburn) through distinct but overlapping inflammatory mechanisms.
Temporal Sequence of Vascular and Inflammatory Responses
Vasodilation occurs first, well before visible erythema appears. Research demonstrates that vasodilation can be detected immediately or very shortly after UVB exposure, even before erythema becomes visible to the eye 1. The so-called "latent period" between UV exposure and visible sunburn is actually an artifact of visual detection limitations—vascular changes begin much earlier 1.
Early Phase (0-4 hours post-exposure):
- Vasodilation initiates within minutes to hours after UVB exposure, detectable by reflectance instruments before any visible redness 1
- Cutaneous vascular conductance does not increase significantly above baseline for the first 4-6 hours, despite ongoing vascular changes 2
- This early vasodilation is independent of visible erythema and represents the initial inflammatory response 2
Peak Erythema Phase (24-96 hours):
- Visible erythema typically peaks at 24 hours but can continue developing until 96 hours or later 3
- The British Journal of Dermatology confirms that PUVA-induced erythema shows a delayed response with broad erythemal peak between 96-144 hours 3
- Maximum erythema development occurs at 4-8 hours post-UVB exposure in most clinical observations 3
Molecular Mechanisms Underlying These Responses
Vasodilatory Mediators:
UVB triggers sequential release of potent vasodilatory prostaglandins. The inflammatory cascade produces PGE₂, PGF₂α, and PGE₃ within the first 24-48 hours, which directly cause dermal blood vessel dilation and accompany clinical erythema 4. This occurs through COX-2 upregulation peaking at 24 hours post-exposure 4.
Inflammatory Cell Recruitment:
- Leukocyte chemoattractants (11-, 12-, and 8-HETE) are elevated from 4-72 hours, driving neutrophil influx at 24 hours 4
- CD3+ lymphocyte infiltration and 12-/15-LOX expression increase from 24-72 hours 4
- These overlapping sequential profiles regulate the progression and eventual resolution of sunburn 4
DNA Damage and Cellular Injury:
UVB causes direct DNA damage including cyclobutane pyrimidine dimers and (6-4) photoproducts, triggering membrane phospholipid hydrolysis and release of polyunsaturated fatty acids that fuel eicosanoid production 5. This molecular damage accumulates in keratinocytes and other skin cells, leading to characteristic morphological changes and eventual apoptosis if damage is irreparable 6.
Endothelial Dysfunction Beyond Visible Erythema
A critical but often overlooked consequence: UVB attenuates nitric oxide-mediated vasodilation in cutaneous microvasculature, independent of visible erythema 2. This represents vascular dysfunction that occurs separately from sunburn and may persist beyond the visible inflammatory phase 2.
Clinical Implications and Common Pitfalls
Protection Strategies:
- Broad-spectrum sunscreen (SPF ≥30) prevents both vasodilation and erythema when applied before UVB exposure 3, 2
- The CDC recommends minimizing sun exposure during peak UV hours (10 AM-4 PM, especially 11 AM-1 PM) 3, 7
- Interestingly, sweat on the skin may provide some protection against UVB-induced vascular dysfunction 2
Phototherapy Considerations:
- Erythema is the most common acute adverse effect of therapeutic UVB, occurring in 9.8-32.4% of treatments 3
- Treatment intervals should be no less than 2-3 days to account for delayed erythema peaking at 96 hours 3
- Fair-skinned individuals with red/blond hair who burn easily face the highest risk 7
Critical Caveat:
Do not apply sunscreen before therapeutic phototherapy sessions, as this creates areas of differential UV tolerance that can cause burning on subsequent treatments if inadvertently exposed 3. However, sunscreen with SPF 30 should be applied on non-treatment days and after phototherapy 3.