Pub Date : 2002-04-01DOI: 10.1034/J.1600-0781.2002.180208_3.X
J. Breuer‐Nicham, P. Cruz, C. L. Zhang, J. Actor, D. Lewis, M. Duvic
Having reported previously that suberythmogenic doses of UVB activate HIV in human skin as shown by a 6–10 fold rise in HIV-1 gag, gene by RT-PCR and similar increments in HIV+ lymphocytes and dendritic cells by RT-PCR-ISH, we dissected the mechanisms underlying these events. Thus, we examined effects of UVB (0–200 J/m2) on HIV transcription, cell cycle distribution, and apoptosis on two Jurkat cell lines (1G5 and DC10). 1G5 and DC10 lines are identical in bearing the HIV-LTR-driven luciferase (Luc) gene, but with the latter also carrying the tat gene. Whereas lower doses of UVB (up to 50 J/m2 induced Luc expression in a UVB dose-dependent manner in DC10 cells and G2/M arrest of these cells, it produced only minimal Luc expression in 1G5 cells with no cell cycle arrest noted. By contrast. higher doses of UVB (100–200 J/m2) led to reduced Luc expression and to apoptosis in DC10 cells, but not in 1G5 cells. Our results are consistent with the concept that activation of the HIV promoter by UVB is dependent on tat. The G2/M arrest induced by lower-dose UVB may allow accumulation of HIV in activated lvmphoeytes; DNA repair may complete the cell cycle leading to proliferation of HIV+ cells. Apoptosis induced by higher-dose UVB reduced HIV transcription, but may also release viral particles from dying cells. These findings indicate that even small increments within a subelythmogenic UVB dose range can have a dramatic impact on HIV transcription, that in turn may be related to altered cell cycle programs. Thus, the precise UVB dose and other inter-current skin conditions affecting cell cycles (e.g., medications, diseases and infections other than HIV) at the time of UVB exposure may influence the net outcome of HIV activation in skin.
{"title":"003 UVB dose and cell cycle conditions influence the outcome of UVB‐induced HIV activation","authors":"J. Breuer‐Nicham, P. Cruz, C. L. Zhang, J. Actor, D. Lewis, M. Duvic","doi":"10.1034/J.1600-0781.2002.180208_3.X","DOIUrl":"https://doi.org/10.1034/J.1600-0781.2002.180208_3.X","url":null,"abstract":"Having reported previously that suberythmogenic doses of UVB activate HIV in human skin as shown by a 6–10 fold rise in HIV-1 gag, gene by RT-PCR and similar increments in HIV+ lymphocytes and dendritic cells by RT-PCR-ISH, we dissected the mechanisms underlying these events. Thus, we examined effects of UVB (0–200 J/m2) on HIV transcription, cell cycle distribution, and apoptosis on two Jurkat cell lines (1G5 and DC10). 1G5 and DC10 lines are identical in bearing the HIV-LTR-driven luciferase (Luc) gene, but with the latter also carrying the tat gene. Whereas lower doses of UVB (up to 50 J/m2 induced Luc expression in a UVB dose-dependent manner in DC10 cells and G2/M arrest of these cells, it produced only minimal Luc expression in 1G5 cells with no cell cycle arrest noted. By contrast. higher doses of UVB (100–200 J/m2) led to reduced Luc expression and to apoptosis in DC10 cells, but not in 1G5 cells. Our results are consistent with the concept that activation of the HIV promoter by UVB is dependent on tat. The G2/M arrest induced by lower-dose UVB may allow accumulation of HIV in activated lvmphoeytes; DNA repair may complete the cell cycle leading to proliferation of HIV+ cells. Apoptosis induced by higher-dose UVB reduced HIV transcription, but may also release viral particles from dying cells. These findings indicate that even small increments within a subelythmogenic UVB dose range can have a dramatic impact on HIV transcription, that in turn may be related to altered cell cycle programs. Thus, the precise UVB dose and other inter-current skin conditions affecting cell cycles (e.g., medications, diseases and infections other than HIV) at the time of UVB exposure may influence the net outcome of HIV activation in skin.","PeriodicalId":20104,"journal":{"name":"Photodermatology, Photoimmunology and Photomedicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86743170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-04-01DOI: 10.1034/J.1600-0781.2002.180208_6.X
K. Ghoreschi, M. Rcken
Morphea and lichen sclerosus are inflammatory skin diseases of unknown aetiology. Morphea can be subdivided into plaque morphea, linear morphea and disabling or generalized morphea. In most patients morphea leads to superficial or deep sclerosis of the skin. The characteristic features of lichen sclerosus which often affects the genital area are edema of upper dermis, inflammatory infiltration and hyalinisation to the dermis at advanced stages. Patients with morphea or lichen sclerosus suffer especially from scar formation and morphea may lead to severe disfigurement, contractures and reduction of quality of life. Skin sclerosis seems to be the result of vascular damage, T cell activation and altered connective tissue production. Various therapies have been reported for lichen sclerosus and morphea. Whereas the topical use of ultrapotent corticosteroids is well established for genital lichen sclerosus, immunosuppressive agents are normally not successful in resolving extragenital skin sclerosis. In a retrospective study we confirmed the efficacy of phototherapy in more than 50 patients with morphea. Fourty treatments with 30 J/cm2 UVA-1 or PUVA-bath photochemotherapy resulted in a significant improvement, reduced skin thickness, as determined by high frequency ultrasound and reconstitution of functional mobility of the skin and even the underlying fasciae. In lichen sclerosus phototherapy was successful only in some patients. Thus for lichen sclerosus the use of topical corticosteroids is the first choice therapy, while phototherapy using either PUVA-bath or medium dose UVA-1 are the most effective treatments for morphea.
{"title":"006Efficacy of photochemotherapy and UVA-1 therapy in patients with morphea or lichen sclerosus","authors":"K. Ghoreschi, M. Rcken","doi":"10.1034/J.1600-0781.2002.180208_6.X","DOIUrl":"https://doi.org/10.1034/J.1600-0781.2002.180208_6.X","url":null,"abstract":"Morphea and lichen sclerosus are inflammatory skin diseases of unknown aetiology. Morphea can be subdivided into plaque morphea, linear morphea and disabling or generalized morphea. In most patients morphea leads to superficial or deep sclerosis of the skin. The characteristic features of lichen sclerosus which often affects the genital area are edema of upper dermis, inflammatory infiltration and hyalinisation to the dermis at advanced stages. Patients with morphea or lichen sclerosus suffer especially from scar formation and morphea may lead to severe disfigurement, contractures and reduction of quality of life. Skin sclerosis seems to be the result of vascular damage, T cell activation and altered connective tissue production. Various therapies have been reported for lichen sclerosus and morphea. Whereas the topical use of ultrapotent corticosteroids is well established for genital lichen sclerosus, immunosuppressive agents are normally not successful in resolving extragenital skin sclerosis. In a retrospective study we confirmed the efficacy of phototherapy in more than 50 patients with morphea. Fourty treatments with 30 J/cm2 UVA-1 or PUVA-bath photochemotherapy resulted in a significant improvement, reduced skin thickness, as determined by high frequency ultrasound and reconstitution of functional mobility of the skin and even the underlying fasciae. In lichen sclerosus phototherapy was successful only in some patients. Thus for lichen sclerosus the use of topical corticosteroids is the first choice therapy, while phototherapy using either PUVA-bath or medium dose UVA-1 are the most effective treatments for morphea.","PeriodicalId":20104,"journal":{"name":"Photodermatology, Photoimmunology and Photomedicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82482164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-04-01DOI: 10.1034/J.1600-0781.2002.180208_19.X
R. Sayre
The COLIPA Standard for solar simulators was developed to insure that SPF tested in different laboratories was not different because of the solar simulator used. Indeed for products with lower SPFs 2-10, the solar simulator standard reasonably assures similar SPFs when tested in different laboratories. For products with SPFs greater than 15, the SPF for the same product could be tested at 15 in one laboratory but as an SPF 100 in another. Differences in SPF due to solar simulator filtration will occur only for sunscreen products that exhibit absorption like cut-off filters. Products which generally absorb all UV wavelengths equally will not exhibit differences in SPF due to solar simulator filtration. In addition because of different amounts of UVA allowed within the COLIPA standard, the actual response for a given exposure may in one laboratory produce persistent pigment darkening and in another a simple sunburn. Ways to correct this flaw will be examined.
{"title":"019 The COLIPA Standard for solar simulators failed to standardize sunscreen SPFS","authors":"R. Sayre","doi":"10.1034/J.1600-0781.2002.180208_19.X","DOIUrl":"https://doi.org/10.1034/J.1600-0781.2002.180208_19.X","url":null,"abstract":"The COLIPA Standard for solar simulators was developed to insure that SPF tested in different laboratories was not different because of the solar simulator used. Indeed for products with lower SPFs 2-10, the solar simulator standard reasonably assures similar SPFs when tested in different laboratories. For products with SPFs greater than 15, the SPF for the same product could be tested at 15 in one laboratory but as an SPF 100 in another. \u0000 \u0000 \u0000 \u0000Differences in SPF due to solar simulator filtration will occur only for sunscreen products that exhibit absorption like cut-off filters. Products which generally absorb all UV wavelengths equally will not exhibit differences in SPF due to solar simulator filtration. \u0000 \u0000 \u0000 \u0000In addition because of different amounts of UVA allowed within the COLIPA standard, the actual response for a given exposure may in one laboratory produce persistent pigment darkening and in another a simple sunburn. Ways to correct this flaw will be examined.","PeriodicalId":20104,"journal":{"name":"Photodermatology, Photoimmunology and Photomedicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83961217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-04-01DOI: 10.1034/J.1600-0781.2002.180208_5.X
S. Collins, S. Ahmadi, G. Murphy
Topical photodynamic therapy (PDT) involves selective photosensitization of a target tissue by means of a topical agent, which is then activated by light to effect an oxygen dependent cytotoxic reaction. Premalignant and malignant skin conditions including actinic keratosis, squamous cell carcinoma in situ (Bowen's disease), and superficial basal cell carcinoma (BCC) have been effectively treated with PDT. A number of studies support the use of topical PDT in the treatment of acne, warts, psoriasis and T-cell lymphoma. There are many case reports and small series, with varying results, in a wide variety of other non-malignant applications. We report our experience of topical PDT over a 3 year period. We selected patients to participate in an open study of ALA-PDT on the basis of failure of, or unsuitability for conventional therapy. One hundred and ten patients participated in the study, with a mean age of 73 years. One hundred and twenty-nine lesions were treated, which consisted of 95 lesions of Bowen's disease, 21 superficial BCC's, nine patients with multiple actinic keratosis and four with porokeratosis. Patients were assessed at 3, 6 and 12 month intervals. Clearance and recurrence rules, adverse events and patient preference (where lesions had been treated previously) were recorded, Clearance rates for actinic keratosis, Bowen's disease and BCC were 87.5%, 84%, and 57%, respectively. Seventy-four percent of patients had a single treatment. Fourteen percent had two, and the remainder had up to four treatements in total. Though topical PDT has not proven to be superior to conventional methods, it is well tolerated with excellent cosmetic results. It is of particular value in the treatment of large lesions, in those with poorly vascularised skin, and in areas of diffuse actinic damage. Careful patient selection, prior debulking of lesions, and newer more selective agents with enhanced penetration, promise to further improve outcome.
{"title":"005 Topical photodynamic therapy in dermatology – 3 years experience at Beaumont Hospital","authors":"S. Collins, S. Ahmadi, G. Murphy","doi":"10.1034/J.1600-0781.2002.180208_5.X","DOIUrl":"https://doi.org/10.1034/J.1600-0781.2002.180208_5.X","url":null,"abstract":"Topical photodynamic therapy (PDT) involves selective photosensitization of a target tissue by means of a topical agent, which is then activated by light to effect an oxygen dependent cytotoxic reaction. Premalignant and malignant skin conditions including actinic keratosis, squamous cell carcinoma in situ (Bowen's disease), and superficial basal cell carcinoma (BCC) have been effectively treated with PDT. A number of studies support the use of topical PDT in the treatment of acne, warts, psoriasis and T-cell lymphoma. There are many case reports and small series, with varying results, in a wide variety of other non-malignant applications. \u0000 \u0000 \u0000 \u0000We report our experience of topical PDT over a 3 year period. We selected patients to participate in an open study of ALA-PDT on the basis of failure of, or unsuitability for conventional therapy. One hundred and ten patients participated in the study, with a mean age of 73 years. One hundred and twenty-nine lesions were treated, which consisted of 95 lesions of Bowen's disease, 21 superficial BCC's, nine patients with multiple actinic keratosis and four with porokeratosis. Patients were assessed at 3, 6 and 12 month intervals. \u0000 \u0000 \u0000 \u0000Clearance and recurrence rules, adverse events and patient preference (where lesions had been treated previously) were recorded, Clearance rates for actinic keratosis, Bowen's disease and BCC were 87.5%, 84%, and 57%, respectively. Seventy-four percent of patients had a single treatment. Fourteen percent had two, and the remainder had up to four treatements in total. \u0000 \u0000 \u0000 \u0000Though topical PDT has not proven to be superior to conventional methods, it is well tolerated with excellent cosmetic results. It is of particular value in the treatment of large lesions, in those with poorly vascularised skin, and in areas of diffuse actinic damage. Careful patient selection, prior debulking of lesions, and newer more selective agents with enhanced penetration, promise to further improve outcome.","PeriodicalId":20104,"journal":{"name":"Photodermatology, Photoimmunology and Photomedicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84722304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-04-01DOI: 10.1034/j.1600-0781.2002.180208_22.x
C. R. Taylor, A. Taneja, S. Gupta, A. Racette, P. Asawanonda, M. Trehan
The excimer 308 nm laser has recently been FDA-approved in the United States for the treatment of psoriasis. Our center was the first to study this device systematically for this indication. Investigations to date have included an initial dose-response study, a high-dose as well as a medium-dose one. Collectively, these results were analyzed and remission periods were reviewed. The rapidity of clearing as well as the severity of side-effects showed a clear dose-response relationship. Even thick plaques responded. The treatment process itself is quick and painless, allowing the operator to cover a palm-sized area in just a minute. The laser is easy to use and there are no disfiguring purpura. By selectively focusing on lesional skin, overall cutaneous ultraviolet burden is minimized. Localized tanning is another side-effect to be anticipated. Obviously, blistering doses show limited applicability as the sole treatment for extensive disease. Moreover, the long-term risks associated with blistering directly on plaques of psoriasis themselves, while not clearly established, seem unlikely to be favorable. On the other hand, sub-blistering doses appear to be extremely well-tolerated. Wound care, except in the cases of blistering doses, is minimal. In short, the 308 nm excimer laser offers a novel targeted treatment modality for localized psoriasis, even when the plaques are quite thick.
{"title":"022 308 excimer laser treatment of psoriasis","authors":"C. R. Taylor, A. Taneja, S. Gupta, A. Racette, P. Asawanonda, M. Trehan","doi":"10.1034/j.1600-0781.2002.180208_22.x","DOIUrl":"https://doi.org/10.1034/j.1600-0781.2002.180208_22.x","url":null,"abstract":"The excimer 308 nm laser has recently been FDA-approved in the United States for the treatment of psoriasis. Our center was the first to study this device systematically for this indication. Investigations to date have included an initial dose-response study, a high-dose as well as a medium-dose one. Collectively, these results were analyzed and remission periods were reviewed. The rapidity of clearing as well as the severity of side-effects showed a clear dose-response relationship. Even thick plaques responded. The treatment process itself is quick and painless, allowing the operator to cover a palm-sized area in just a minute. The laser is easy to use and there are no disfiguring purpura. By selectively focusing on lesional skin, overall cutaneous ultraviolet burden is minimized. Localized tanning is another side-effect to be anticipated. Obviously, blistering doses show limited applicability as the sole treatment for extensive disease. Moreover, the long-term risks associated with blistering directly on plaques of psoriasis themselves, while not clearly established, seem unlikely to be favorable. On the other hand, sub-blistering doses appear to be extremely well-tolerated. Wound care, except in the cases of blistering doses, is minimal. In short, the 308 nm excimer laser offers a novel targeted treatment modality for localized psoriasis, even when the plaques are quite thick.","PeriodicalId":20104,"journal":{"name":"Photodermatology, Photoimmunology and Photomedicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75595058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-04-01DOI: 10.1034/J.1600-0781.2002.180208_15.X
D. Moyal
Sunscreens are designed to protect against sunburn and their efficacy is indicated by the so-called sun protection factor (SPF). However this index may be inadequate to provide a relevant measurement of protection against other biological damages induced by UV such as immunosuppression. We measured in human volunteers the ability of two broad spectrum SPF 15 sunscreens, with different UVA protection levels, to prevent the fall in local delayed type hypersensitivity (DTH) response to recall antigens (Multitest Pasteur/Merieux) after acute solar simulated UV exposure. We first determined the UVR-dose needed to induce a significant reduction of DTH response in different groups of 15 volunteers. Two minimal erythernal dose (MED) were found to be the minimal immunosuppressive dose. This dose induced a 36% average fall in immune DTH response. The lower doses tested (0.5 and 1 MED) were ineffective. Sunscreen treated groups were exposed to a dose equal to 2 MED × SPF of the products. The DTH response was not lowered in the group treated by the product having the highest UVA protection. Conversely the DTH response was significantly reduced by 55.7% in the group treated with the low UVA protection sunscreen. These data suggest that sun protection factor may not be sufficient to predict the ability of sunscreens to protect the immune system. A measurement of UVA protection may also be necessary as UVA seems to have a low contribution to erythema but strongly affects immune response.
防晒霜是用来防止晒伤的，其功效由所谓的防晒系数(SPF)来表示。然而，该指数可能不足以提供对紫外线引起的其他生物损伤(如免疫抑制)的保护的相关测量。我们在人类志愿者中测量了两种具有不同UVA防护水平的广谱SPF 15防晒霜在急性太阳模拟紫外线照射后防止局部延迟型超敏反应(DTH)对召回抗原(Multitest Pasteur/Merieux)的反应下降的能力。我们首先确定了不同组15名志愿者显著降低DTH反应所需的uvr剂量。最小红热剂量(MED)为最小免疫抑制剂量。该剂量诱导免疫DTH应答平均下降36%。低剂量试验(0.5和1 MED)无效。防晒霜处理组暴露于等于2 MED × SPF产品的剂量。在使用具有最高UVA保护的产品的组中，DTH反应并未降低。相反，在使用低UVA防护防晒霜的组中，DTH反应显着降低了55.7%。这些数据表明，防晒系数可能不足以预测防晒霜保护免疫系统的能力。测量UVA的保护也可能是必要的，因为UVA似乎对红斑的贡献很低，但强烈影响免疫反应。
{"title":"015 Two broadspectrum SPF 15 sunscreens offer different protection against UV induced depression of delayed type hypersensitivity response in humans","authors":"D. Moyal","doi":"10.1034/J.1600-0781.2002.180208_15.X","DOIUrl":"https://doi.org/10.1034/J.1600-0781.2002.180208_15.X","url":null,"abstract":"Sunscreens are designed to protect against sunburn and their efficacy is indicated by the so-called sun protection factor (SPF). However this index may be inadequate to provide a relevant measurement of protection against other biological damages induced by UV such as immunosuppression. \u0000 \u0000 \u0000 \u0000We measured in human volunteers the ability of two broad spectrum SPF 15 sunscreens, with different UVA protection levels, to prevent the fall in local delayed type hypersensitivity (DTH) response to recall antigens (Multitest Pasteur/Merieux) after acute solar simulated UV exposure. We first determined the UVR-dose needed to induce a significant reduction of DTH response in different groups of 15 volunteers. \u0000 \u0000 \u0000 \u0000Two minimal erythernal dose (MED) were found to be the minimal immunosuppressive dose. This dose induced a 36% average fall in immune DTH response. The lower doses tested (0.5 and 1 MED) were ineffective. Sunscreen treated groups were exposed to a dose equal to 2 MED × SPF of the products. The DTH response was not lowered in the group treated by the product having the highest UVA protection. Conversely the DTH response was significantly reduced by 55.7% in the group treated with the low UVA protection sunscreen. \u0000 \u0000 \u0000 \u0000These data suggest that sun protection factor may not be sufficient to predict the ability of sunscreens to protect the immune system. A measurement of UVA protection may also be necessary as UVA seems to have a low contribution to erythema but strongly affects immune response.","PeriodicalId":20104,"journal":{"name":"Photodermatology, Photoimmunology and Photomedicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82960227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-04-01DOI: 10.1034/J.1600-0781.2002.180208_4.X
C. Cole, F. Natter, E. Ruvolo, N. Issachar
Standard methods for measuring the sunburning protection of sunscreens (SPF) are globally established. In vivo methods of determining UVA protectiveness of sunscreens have been reduced to either a Persistent Pigment Darkening (PPD) or Protection Factor A (PFA-either persistent pigment darkening or erythema endpoints) test protocols. Both of these techniques require human exposure to UVA radiation that can be time consuming and do not benefit the human subject. Validated methodologies that would minimize the UVA exposure, or could be performed in vitro would simplify the determination of UVA protectiveness and assist product optimization. Diffuse reflectance spectroscopy of sunscreens on human skin was utilized to evaluate a series of seven model sunscreen systems that were previously evaluated in vivo by both PPD and PFA testing. Correlation of the values found with this technique correlated highly with the in vivo test results, with 1:1 correspondence of protection values. Separately, an in vitro test model was assessed on these same model sunscreens. Sunscreen was applied to roughened surface quartz plates, and the absorbance of the sunscreens was measured before and after UV exposure. The absorbance was mathematically forced to fit the in vivo SPF value and the UVA protectiveness was calculated using both erythema and pigment darkening action spectra. The in vitro predictions of UVA was highly correlated with the in vivo PPD and PFA values. It was determined that preirradiation of the sunscreen samples is needed to accurately predict the protection provided by sunscreens that are not photostable. Both of these techniques provide new ways to accurately predict sunscreen UVA protectiveness.
{"title":"004 Validation of in vivo and in vitro methods to measure UVA protectiveness of sunscreen","authors":"C. Cole, F. Natter, E. Ruvolo, N. Issachar","doi":"10.1034/J.1600-0781.2002.180208_4.X","DOIUrl":"https://doi.org/10.1034/J.1600-0781.2002.180208_4.X","url":null,"abstract":"Standard methods for measuring the sunburning protection of sunscreens (SPF) are globally established. In vivo methods of determining UVA protectiveness of sunscreens have been reduced to either a Persistent Pigment Darkening (PPD) or Protection Factor A (PFA-either persistent pigment darkening or erythema endpoints) test protocols. Both of these techniques require human exposure to UVA radiation that can be time consuming and do not benefit the human subject. Validated methodologies that would minimize the UVA exposure, or could be performed in vitro would simplify the determination of UVA protectiveness and assist product optimization. Diffuse reflectance spectroscopy of sunscreens on human skin was utilized to evaluate a series of seven model sunscreen systems that were previously evaluated in vivo by both PPD and PFA testing. Correlation of the values found with this technique correlated highly with the in vivo test results, with 1:1 correspondence of protection values. Separately, an in vitro test model was assessed on these same model sunscreens. Sunscreen was applied to roughened surface quartz plates, and the absorbance of the sunscreens was measured before and after UV exposure. The absorbance was mathematically forced to fit the in vivo SPF value and the UVA protectiveness was calculated using both erythema and pigment darkening action spectra. The in vitro predictions of UVA was highly correlated with the in vivo PPD and PFA values. It was determined that preirradiation of the sunscreen samples is needed to accurately predict the protection provided by sunscreens that are not photostable. Both of these techniques provide new ways to accurately predict sunscreen UVA protectiveness.","PeriodicalId":20104,"journal":{"name":"Photodermatology, Photoimmunology and Photomedicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85594960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-04-01DOI: 10.1034/J.1600-0781.2002.180208_8.X
I. Man, R. Dawe, J. Ferguson, S. Ibbotson
We examined the characteristics of TL-01 UVB erythema and determined the optimal starting dose prior to TL-01 phototherapy, Twenty-eight subjects were recruited. Eight test sites on each subject's back were irradiated with a TL-01 dose series (50-550 mJ/cm2). Erythema was recorded visually and with a reflectance device at 4, 8, 12, 24, 48 and 72 h in 19 subjects and at 12, 15, 18, 21 and 24 h in nine subjects. Dose-response curves were constructed and the D0.025 (equivalent to the visual minimal erythema dose [MED]) and the maximum slope determined. Erythema was evident at 4 h in the 19 subjects tested. The lowest median MED occurred at 12 h (170 mJ/cm2) and this was significantly lower that at 24 h (median 200 mJ/cm2; P = 0.019). the majority of subjects were at maximal erythema at 12 h (22/28) and 15 h (8/9). MED reading at 24 h (MED24 h) would miss peak erythema in 15/28 subjects. If, as is commonly practiced, 70% of the MED24 h was given, 10/28 subjects would have received a first treatment dose that would be equal to or exceed the lowest MED. If 50% of the MED24 h was given, only 2/28 would develop erythema (P = 0.0078, 95% Cl [10-46.5%]). From the dose-response data, D0.025 at 12 h was significantly lower than at 24 h (P = 0.0019). The slope of the erythemal dose-response curve remained constant from 8 to 48 h. Maximal TL-01 UVB erythema occurs at 12 h. Our data suggest that the optimal first TL-01 treatment dose is 50% of the MED24 h.
{"title":"008 The time‐course of TL‐01 UVB erythema","authors":"I. Man, R. Dawe, J. Ferguson, S. Ibbotson","doi":"10.1034/J.1600-0781.2002.180208_8.X","DOIUrl":"https://doi.org/10.1034/J.1600-0781.2002.180208_8.X","url":null,"abstract":"We examined the characteristics of TL-01 UVB erythema and determined the optimal starting dose prior to TL-01 phototherapy, Twenty-eight subjects were recruited. Eight test sites on each subject's back were irradiated with a TL-01 dose series (50-550 mJ/cm2). Erythema was recorded visually and with a reflectance device at 4, 8, 12, 24, 48 and 72 h in 19 subjects and at 12, 15, 18, 21 and 24 h in nine subjects. Dose-response curves were constructed and the D0.025 (equivalent to the visual minimal erythema dose [MED]) and the maximum slope determined. \u0000 \u0000 \u0000 \u0000Erythema was evident at 4 h in the 19 subjects tested. The lowest median MED occurred at 12 h (170 mJ/cm2) and this was significantly lower that at 24 h (median 200 mJ/cm2; P = 0.019). the majority of subjects were at maximal erythema at 12 h (22/28) and 15 h (8/9). MED reading at 24 h (MED24 h) would miss peak erythema in 15/28 subjects. If, as is commonly practiced, 70% of the MED24 h was given, 10/28 subjects would have received a first treatment dose that would be equal to or exceed the lowest MED. If 50% of the MED24 h was given, only 2/28 would develop erythema (P = 0.0078, 95% Cl [10-46.5%]). From the dose-response data, D0.025 at 12 h was significantly lower than at 24 h (P = 0.0019). The slope of the erythemal dose-response curve remained constant from 8 to 48 h. Maximal TL-01 UVB erythema occurs at 12 h. Our data suggest that the optimal first TL-01 treatment dose is 50% of the MED24 h.","PeriodicalId":20104,"journal":{"name":"Photodermatology, Photoimmunology and Photomedicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84511575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-04-01DOI: 10.1034/J.1600-0781.2002.180208_16.X
R. Sayre, J. Dowdy
An examination of the UV emission by fluorescent and tungsten lamps often used for lighting in the home, office or school indicates a considerable amount of UV radiation load for unsuspecting individuals. The amount of UV exposure from non-solar sources would appear to be potentially as great as 1/2–2/3 MEDs daily or 150 MED yearly. This is interesting as it exceeds the generally often-quoted levels of expected UV accumulated from sunlight exposure during normal daily activities. Of possibly greater significance is the fact that this exposure contains wavelengths not present in sunlight reaching the earth's surface. Fluorescent lamps, activated by excited mercury wavelengths, emit significant amounts of short radiation < 290 nm, including clearly detectable 254 nm lines. Similarly, the common tungsten bulbs, even low 60 Watt bulbs, emit detectable UV radiation as short as 280 nm. Wavelengths this short do not represent a detectable risk from outdoor exposure. It would appear plausible that concern about the increasing risk of melanoma due to UV in sunlight exposure may be misplaced. Individuals at greatest risk include doctors, nurses, school teachers, lawyers and office workers and not farmers, fishermen, or construction workers. The indoor office workers would receive vastly greater exposure from artificial lighting, especially at non-solar wavelengths, than would similar outdoor workers.
{"title":"016 Daily non-solar UV exposure","authors":"R. Sayre, J. Dowdy","doi":"10.1034/J.1600-0781.2002.180208_16.X","DOIUrl":"https://doi.org/10.1034/J.1600-0781.2002.180208_16.X","url":null,"abstract":"An examination of the UV emission by fluorescent and tungsten lamps often used for lighting in the home, office or school indicates a considerable amount of UV radiation load for unsuspecting individuals. The amount of UV exposure from non-solar sources would appear to be potentially as great as 1/2–2/3 MEDs daily or 150 MED yearly. This is interesting as it exceeds the generally often-quoted levels of expected UV accumulated from sunlight exposure during normal daily activities. \u0000 \u0000 \u0000 \u0000Of possibly greater significance is the fact that this exposure contains wavelengths not present in sunlight reaching the earth's surface. Fluorescent lamps, activated by excited mercury wavelengths, emit significant amounts of short radiation < 290 nm, including clearly detectable 254 nm lines. Similarly, the common tungsten bulbs, even low 60 Watt bulbs, emit detectable UV radiation as short as 280 nm. Wavelengths this short do not represent a detectable risk from outdoor exposure. \u0000 \u0000 \u0000 \u0000It would appear plausible that concern about the increasing risk of melanoma due to UV in sunlight exposure may be misplaced. Individuals at greatest risk include doctors, nurses, school teachers, lawyers and office workers and not farmers, fishermen, or construction workers. The indoor office workers would receive vastly greater exposure from artificial lighting, especially at non-solar wavelengths, than would similar outdoor workers.","PeriodicalId":20104,"journal":{"name":"Photodermatology, Photoimmunology and Photomedicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88473283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-04-01DOI: 10.1034/J.1600-0781.2002.180208_14.X
D. Moyal, A. Chardon
A variety of in vitro and in vivo methods have been proposed to evaluate the UVA efficacy of sunscreens. Diffuse reflectance spectroscopy (DRS) is a recent approach that allows measuring sunscreen protectiveness in the UVA portion of the spectrum. FDA representatives have shown a marked interest for the development of this alternative method. The absorption spectrum of the product is obtained by measuring the change in skin reflection due to the product. From this absorption spectrum the UVA efficacy of a sunscreen product can then be calculated for an appropriate UV source and a given skin response action spectrum. One major advantage of this test method is that the UVA protection is determined directly on human skin, thus accounting for sunscreen/skin surface and emulsion interactions encountered in vivo, but not in vitro. Both DRS and in vivo persistent pigment darkening (PPD) method were used to compare the UVA efficacy of various UVA sunscreens (such as oxybenzone, avobenzone, ecamsule and zinc oxide at different concentrations) and of marketed products. A significant correlation was found between DRS and PPD results only for photostable products. To get a correlation with PPD results with photo-unstable products, a pre-exposure of the products applied on skin was found necessary before performing the DRS measurements. The DRS method allows evaluating both the UVA absorption spectrum of the products and their broadness of absorption and can thus be considered as a powerful tool for the in-vivo evaluation of sunscreen UVA protective efficacy.
{"title":"014 In-vivo determination of UVA sunscreen efficacy using diffuse reflectance spectroscopy","authors":"D. Moyal, A. Chardon","doi":"10.1034/J.1600-0781.2002.180208_14.X","DOIUrl":"https://doi.org/10.1034/J.1600-0781.2002.180208_14.X","url":null,"abstract":"A variety of in vitro and in vivo methods have been proposed to evaluate the UVA efficacy of sunscreens. Diffuse reflectance spectroscopy (DRS) is a recent approach that allows measuring sunscreen protectiveness in the UVA portion of the spectrum. FDA representatives have shown a marked interest for the development of this alternative method. The absorption spectrum of the product is obtained by measuring the change in skin reflection due to the product. From this absorption spectrum the UVA efficacy of a sunscreen product can then be calculated for an appropriate UV source and a given skin response action spectrum. One major advantage of this test method is that the UVA protection is determined directly on human skin, thus accounting for sunscreen/skin surface and emulsion interactions encountered in vivo, but not in vitro. Both DRS and in vivo persistent pigment darkening (PPD) method were used to compare the UVA efficacy of various UVA sunscreens (such as oxybenzone, avobenzone, ecamsule and zinc oxide at different concentrations) and of marketed products. A significant correlation was found between DRS and PPD results only for photostable products. To get a correlation with PPD results with photo-unstable products, a pre-exposure of the products applied on skin was found necessary before performing the DRS measurements. The DRS method allows evaluating both the UVA absorption spectrum of the products and their broadness of absorption and can thus be considered as a powerful tool for the in-vivo evaluation of sunscreen UVA protective efficacy.","PeriodicalId":20104,"journal":{"name":"Photodermatology, Photoimmunology and Photomedicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90610120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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