Cheilitis caused by contact allergy to anethole in spearmint flavoured toothpaste.

A 63-year-old woman presented with a 6-year history of persistent cheilitis. Minimal improvement was achieved with therapeutic measures. Patch testing was positive to anethole, a flavouring used in her toothpaste. Her cheilitis resolved after cessation of the flavoured toothpaste. This case demonstrates the importance of considering contact allergy to toothpaste flavours in patients with cheilitis.

Sunlight-induced immunosuppression in humans is initially because of UVB, then UVA, followed by interactive effects.

Solar-simulated ultraviolet radiation (ssUV) suppresses immunity in humans. The ultraviolet B (UVB) waveband is recognized as immunosuppressive; however the relative significance of UVA to ssUV immunosuppression is unknown. We created dose and time-response curves for UVB-, UVA-, and ssUV-induced suppression of memory immunity to nickel in humans. UVB caused immunosuppression within 24 h. UVA immunosuppression required 48 h and was normalized by 72 h. UVB alone accounts for ssUV immunosuppression at 24 h, but both UVB and UVA contributed at 48 h. By 72 h neither waveband accounted for ssUV immunosuppression. An interaction between these wavebands was therefore the major contributor. To confirm this dose-response curves were used to determine immune protection factors (IPF) for sunscreens with nickel challenge 72 h following ssUV. A sunscreen with good UVA protection had an IPF twice that of a poor UVA protector, despite providing similar protection from sunburn. Thus UVA was a major contributor to ssUV-induced immunosuppression at 72 h but only with the cooperation of UVB. Hence, UVB initiates immunosuppressive signals within 24 h, followed by UVA at 48 h, then an interaction between UVB and UVA. By 72 h following ssUV exposure, neither UVB nor UVA, but an interaction between them is the major cause of sunlight-induced immunosuppression.

The suppression of immunity by ultraviolet radiation: UVA, nitric oxide and DNA damage.

We have examined the mechanism by which solar-simulated ultraviolet radiation (ssUV) suppresses memory immunity to nickel in allergic humans. In initial studies, we used inbred mice to determine the contribution of different wavebands to sunlight-induced immunosuppression. We found that low dose UVA can enhance memory, medium dose UVA (half the amount in one minimum erythemal dose of ssUV) is immunosuppressive, but higher doses protect from UVB. This is genetically dependent, as it is not observed in all mouse strains. UVA caused a similar dose-related change in recall immunity in humans. ssUV dose responses determined the limits of protection provided by sunscreens from immunosuppression in humans. Immune protection factors calculated from these data correlated with UVA protection, but not with sun protection factor, showing that in commercial sunscreens that provide good UVB protection, UVA protection limits prevention of immunosuppression. N(G)-monomethyl-l-arginine acetate (l-NMMA) was used to inhibit nitric oxide (NO) production and T4N5 liposomes containing T4 endonuclease V to enhance DNA repair. Sub-erythemal ssUV caused a dose-related local suppression of recall immunity to nickel in humans. l-NMMA and the liposomes protected the nickel reaction, suggesting that NO and DNA damage are mediators of UV-induced immunosuppression in humans.

Objective measurement of minimal erythema and melanogenic doses using natural and solar-simulated light.

Very little information exists on the amount of natural and artificial UV light required to cause sunburn and tanning in individuals with very pale skin who are at the greatest risk of developing skin cancer. We have investigated minimal erythema dose (MED) and minimal melanogenic dose (MMD) in a group of 31 volunteers with Fitzpatrick skin types I and II using an Oriel 1000 W xenon arc solar simulator and natural sunlight in Sydney, Australia. We measured the erythemal and melanogenic responses using conventional visual scoring, a chromameter and an erythema meter. We found that the average MED measured visually using the artificial UV source was 68.7 +/- 3.3 mJ/cm2 (3.4 +/- 0.2 standard erythema doses [SED]), which was significantly different from the MED of sunlight, which was 93.6 +/- 5.6 mJ/cm2 (P < 0.001) (11.7 +/- 0.7 SED). We also found significant correlations between the solar-simulated MED values, the melanin index (erythema meter) and the L* function (chromameter). The average MMD (obtained in 16 volunteers only) using solar-simulated light was 85.6 +/- 4.9 mJ/cm2, which was significantly less than that measured with natural sunlight (118.3 +/- 8.6 mJ/cm2; P < 0.05). We mathematically modeled the data for both the chromameter and the erythema meter to see if we were able to obtain a more objective measure of MED and differentiation between skin types. Using this model, we were able to detect erythemal responses using the erythema index function of the erythema meter and the a* function of the chromameter at lower UV doses than either the standard visual or COLIPA methods.

Prevention of immunosuppression by sunscreens in humans is unrelated to protection from erythema and dependent on protection from ultraviolet a in the face of constant ultraviolet B protection.

Sunscreens have been advocated as an important means of preventing skin cancer. Ultraviolet radiation induced immunosuppression is recognized as an important event in skin cancer development, yet the effectiveness of sunscreens in protecting the human immune system from ultraviolet radiation (i.e. ultraviolet radiation) is still unclear. The only currently accepted method of sunscreen rating is the sun protection factor system based on the prevention of erythema. We determined immune protection factors for six commercially available sunscreens using a nickel contact hypersensitivity model in humans. Both sun protection factor and immune protection factor testing was performed using the same solar simulated ultraviolet radiation source and dose-responses were used to determine endpoints both with and without sunscreens. We found that the immune protection factor did not correlate with the sun protection factor; however, immune protection factor was significantly correlated to the ultraviolet A protective capability of the sunscreens, indicating that sunscreen protection from ultraviolet A is important for the prevention of ultraviolet immunosuppression, when there is constant ultraviolet B protection. We recommend that sunscreens should be rated against their immune protective capability to provide a better indication of their ability to protect against skin cancer.

The importance of using broad spectrum SPF 30+ sunscreens in tropical and subtropical climates.

BACKGROUND/PURPOSE: To evaluate the Sun Protection Factors (SPF) of six sunscreens sold in Australia, using an ultraviolet (UV) spectrum which mimics sunlight as closely as possible, and by using volunteers with a range of skin types to reflect the Australian population. METHODS: Open prospective study. Seventy-five volunteers of skin types 1-3 were tested in a dermatology research laboratory in a major metropolitan teaching hospital in Sydney, Australia in the years 2000-2001. Sunscreen SPF's were measured using a solar simulator and procedures which complied with the Australian Standard. RESULTS: Sun Protection Factors, as measured by a solar simulator more approximating to natural sunlight than commercial simulators, and using individuals of skin type 1-3, were shown to be approximately between 50% and 80% of their labelled value. Sunscreen application method can also affect SPF measurement. CONCLUSION: For a number of reasons, Sun Protection Factors are often overestimated. In addition, many individuals use less than half the amount of sunscreen recommended. Those living in tropical or subtropical climates should be encouraged to use only broad spectrum SPF 30+ sunscreens to achieve adequate protection from the sun.