Resistance to water and abrasion of a broad‐spectrum sunscreen: a prospective, open‐label study

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Abstract

Ultraviolet (UV) irradiation causes damage to the skin, such as sunburn, photoaging and skin cancer as well as immunosuppression 1. Irradiation with mainly UVB but also UVA can cause direct cellular DNA damage, triggering an inflammatory response and the production of melanin, but may also cause dipyrimidine lesions such as cyclobutane pyrimidine dimers 2. Thus, UV protection is important to prevent the damaging effects of UVB and UVA irradiation. In addition to wearing cover-up clothing, UV protection may be achieved by application of sunscreens, light-shielding substances with highly potent physical (inorganic) and/or chemical (organic) UVA- and UVB-protective filters 3. The sun-protection factor (SPF), defined as the ratio of the minimal erythema dose (MED) of sun-protected skin to the MED of non-sun-protected skin, gives a quantitative level of protection against sunburn and oedema. Sunscreens with a low SPF of 15 can prevent sunburn 4; however, the protection depends on a number of factors, such as the amount of sunscreen applied to the skin, water resistance of the sunscreen and its efficacy after abrasion. Even though several groups investigated water resistance of sunscreens (Table S1), a study evaluating the impact of water, abrasion and/or increasing UVB doses on the efficacy of a sunscreen has – to our knowledge – not yet been performed. The aim of this study was to investigate water resistance of a broad-spectrum sunscreen with a high SPF and the influence of abrasion on its efficacy in preventing sun damage in healthy volunteers (HVs). To assess the efficacy of the sunscreen, standardized protocols, which were considered most appropriate to simulate environmental exposure in daily life (i.e. taking a shower and/or abrading the skin with a towel), were applied in this prospective, open-label study. The test product, a liposomal sunscreen containing a combination of organic filters and pigments with a broad action spectrum (UVB and UVA), was applied at the amount of 2 mg/cm2 on five of six areas (1, 2, 4, 5 and 6) of uninvolved skin on the upper back of 10 HVs. After 20 min, areas 1, 2, 4, 5 and 6 were each treated with water and/or were abraded (Table S2). Area 3 was left untreated. All HVs were irradiated once on all six areas with an UVA dose of 60 J/cm2. In addition, areas 1, 2 and 3 were irradiated with the 1.5 MED of UVB and areas 4, 5 and 6 with increasing UVB doses (Table S3). Skin biopsy specimens were taken 24 h after UV irradiation from areas 3, 5 and 6, and histological and immunohistochemical analyses were performed. Additional information on "Materials and Methods" may be found in the Supporting Information (Data S1). In the untreated, UV-irradiated area 3, erythema with a mean score of 2.2 ± 0.4 (±SD) and a median of 2 (range 2–3) was observed 24 h after UV irradiation (Fig. 1a–c). The mean erythema was significantly stronger in the untreated, UV-irradiated area 3 compared to area 1 (P < 0.0001). The mean erythema in the untreated, UV-irradiated area 3 was also observed to be significantly higher compared to area 2 (P < 0.0001). None of the HVs developed erythema in area 1 or area 2. Moreover, none of the HVs showed an erythema in areas 4, 5 and 6. Therefore, no difference was observed comparing area 5 with area 1. Histological analysis of skin biopsy specimens taken from the untreated, UV-irradiated area 3 presented with a strong dermal inflammatory infiltrate and a large number of UV-damaged keratinocytes (Fig. 2a). The lymphocytic infiltrate and the number of damaged keratinocytes were significantly lower in areas 5 and 6 compared to area 3. A high expression of the cell-death marker caspase 3 was observed in the untreated, UV-irradiated area 3, which was closely associated with the UV-induced keratinocytic cell damage. Importantly, caspase 3 staining was significantly lower in areas 5 and 6 (Fig. 2b). Similar findings were observed for p53; the untreated, UV-irradiated area 3 showed a strong epidermal expression of p53, which was significantly reduced in areas 5 and 6 (Fig. 2c). In this explorative, intra-individual study, we confirmed that the use of a broad-spectrum sunscreen with a high protection factor for both UVB and UVA light prevents UV-induced erythema and hyperpigmentation in HVs as suggested in previous studies 5, 6. Most importantly, the results further demonstrated that the prevention of UV-induced damage by the application of the sunscreen was not significantly decreased – even after higher UVB irradiation doses – when the skin areas were treated with a water shower or with a water shower and consecutive towelling. Histological analysis of skin biopsies taken 24 h after sunscreen application and UV irradiation confirmed the clinical assessment. A strong dermal infiltrate was observed in sunscreen-unprotected skin after 24 h, but was absent in sunscreen-protected skin. Compared to sunscreen-unprotected skin, the number of caspase 3- and p53-positive keratinocytes was significantly lower in sunscreen-protected skin. To our knowledge, this study is the first to imitate conditions in daily life and to evaluate water resistance in combination with the influence of abrasion on the prevention of sun damage using standardized protocols in HVs. It would be interesting to confirm the results in an outdoor setting. In conclusion, this study confirms that the use of a liposomal broad-spectrum (UVA/UVB) sunscreen with a high protection factor can effectively prevent UV-induced damage in HVs, even after contact with water, abrasion and the irradiation with increased UVB doses. CSu, JW and AK were involved in research concept and design. SZ, MG and NP involved in acquisition of data. CSa, SZ, JW, AL, MG and AK were involved in analysis and interpretation of data. SZ, MG, NP and AL were involved in drafting of the manuscript. SZ, CSa, CSu, JW, AL and AK were involved in critical revision of the manuscript for important intellectual content. All authors approved the submitted and final version of the manuscript. The study was supported by Spirig Pharma AG, Egerkingen, Switzerland. Dr. Kuhn and Dr. Wenzel received honoraria from Spirig Pharma AG, Egerkingen, Switzerland, for presentations. Dr. Surber was employed by Spirig Pharma AG, Egerkingen, Switzerland. All other authors have no relevant financial interests to report. Data S1. Materials and Methods. Table S1. Investigations of the impact of abrasion and/or immersion on the efficacy of sunscreens. Table S2. Protocol overview of areas 1–6. Table S3. Applied UVA/UVB doses in healthy volunteers. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

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