Sunscreen or simulated sweat minimizes the impact of acute ultraviolet radiation on cutaneous microvascular function in healthy humans.

NEW FINDINGS: What is the central question of this study? Are ultraviolet radiation (UVR)-induced increases in skin blood flow independent of skin erythema? Does broad-spectrum UVR exposure attenuate NO-mediated cutaneous vasodilatation, and does sunscreen or sweat modulate this response? What are the main findings and their importance? Erythema and vascular responses to UVR are temporally distinct, and sunscreen prevents both responses. Exposure to UVR attenuates NO-mediated vasodilatation in the cutaneous microvasculature; sunscreen or simulated sweat on the skin attenuates this response. Sun over-exposure may elicit deleterious effects on human skin that are separate from sunburn, and sunscreen or sweat on the skin may provide protection. ABSTRACT: Exposure to ultraviolet radiation (UVR) may result in cutaneous vascular dysfunction independent of erythema (skin reddening). Two studies were designed to differentiate changes in erythema from skin vasodilatation throughout the 8 h after acute broad-spectrum UVR exposure with (+SS) or without SPF-50 sunscreen (study 1) and to examine NO-mediated cutaneous vasodilatation after acute broad-spectrum UVR exposure with or without +SS or simulated sweat (+SW) on the skin (study 2). In both studies, laser-Doppler flowmetry was used to measure red cell flux, and cutaneous vascular conductance (CVC) was calculated (CVC = flux/mean arterial pressure). In study 1, in 14 healthy adults (24 ± 4 years old; seven men and seven women), the skin erythema index and CVC were measured over two forearm sites (UVR only and UVR+SS) before, immediately after and every 2 h for 8 h post-exposure (750 mJ cm-2 ). The erythema index began to increase immediately post-UVR (P < 0.05 at 4, 6 and 8 h), but CVC did not increase above baseline for the first 4-6 h (P ≤ 0.01 at 6 and 8 h); +SS prevented both responses. In study 2, in 13 healthy adults (24 ± 4 years old; six men and seven women), three intradermal microdialysis fibres were placed in the ventral skin of the forearm [randomly assigned to UVR (450 mJ cm-2 ), UVR+SS or UVR+SW], and one fibre (non-exposed control; CON) was placed in the contralateral forearm. After UVR, a standardized local heating (42°C) protocol quantified the percentage of NO-mediated vasodilatation (%NO). The UVR attenuated %NO compared with CON (P = 0.01). The diminished %NO was prevented by +SS (P < 0.01) and +SW (P < 0.01). Acute broad-spectrum UVR attenuates NO-dependent dilatation in the cutaneous microvasculature, independent of erythema. Sunscreen protects against both inflammatory and heating-induced endothelial dysfunction, and sweat might prevent UVR-induced reductions in NO-dependent dilatation.

Radon progeny activity in sweat following radon exposure in a warm and humid environment.

The objective was to evaluate whether activity of radon progenies can be detected in sweat following speleotherapeutic radon exposure (40 kBq/m3) in a warm (38 degrees C) and humid (relative humidity > 70%) environment. A group of 11 male patients with spondyloarthropathy (n = 6) or non-inflammatory rheumatic diseases (n = 5) underwent a 1-h treatment in the gallery of the Gasteiner Heilstollen, and 20 min after leaving the treatment area radon progeny activity was measured in sweat by utilizing a special filter set. The results suggest that radon is discharged with sweat, causing a significant activity of radon and radon progenies on the skin. This finding may be important from a clinical point of view, since specialists experienced in radon therapy have repeatedly emphasized the importance of the degree of radioactivity on the skin for the effectiveness of treatment. It has even been claimed that the skin is the major target for radon therapy, possibly because of the influence on Langerhans' cell function.

Radiation response of murine eccrine sweat glands.

Following irradiation of the left-hind feet of mice, we measured the ability of the eccrine glands to secrete sweat following stimulation by pilocarpine. Silicone elastomer impression moulds of the foot pads gave repeatable, detailed localization of sweat ducts by retaining the impression of each emerging sweat droplet. Loss of gland function occurred rapidly following irradiation (within 2 weeks) and the rate of loss was dose-dependent, being over three times greater following a dose of 13.0 Gy than after 6.8 Gy. There was a dose-dependent nadir of function at around 8 weeks, followed by a gradual recovery that was complete by about 30 weeks after irradiation, leaving a dose-dependent residual functional deficit. Eccrine sweat glands are very radiosensitive organs compared with the epidermis. A single dose of 13 Gy resulted in complete loss of eccrine gland function at 8 weeks whilst about 23 Gy would be required to elicit transient moist desquamation, in oxygen-breathing mice. Substantial sparing was seen when two doses were split by intervals of up to 24 h.