The Photomedicine Society
promotes a greater understanding
of light in health and disease.

 

Archive of the 22nd Meeting of the Photomedicine Society

Thursday, February 28, 2013, 8:00 a.m. - 5:00 p.m.
Ocean Tower Ballroom 1A
Eden Roc Renaissance Miami Beach
Miami Beach, Florida, USA


PROGRAM
7:30 – 7:55 Registration
7:55 – 8:00 Opening Remarks
Sewon Kang, M.D., Baltimore, Maryland
Session 1: UVA1 Phototherapy
8:00 – 8:30 Heidi Jacobe, M.D., MSCS, Dallas, Texas
UVA1 Photoptherapy the UT Southwestern Experience
8:30 – 8:45 Ask the Expert – Moderated Discussion UVA1 Phototherapy
Abstract Session A
8:45 – 9:45 Abstract Presentations
  8:45 – 8:58
9:00 – 9:13
9:15 – 9:28
9:30 – 9:43
Murrell, D
Takeuchi, H
Menter, J
AlJasser, M
9:45 – 10:00 Break/Poster Viewing
Abstract Session B
10:00 – 11:00 Abstract Presentations
  10:00 – 10:13
10:15 – 10:28
10:30 – 10:43
10:45 – 10:58
Cole, C
Jawad, S
Lee, H
Ostewalder, U
Session 2: Keynote Address
11:00 – 11:40 Gary J. Fisher, Ph.D., Ann Arbor, Michigan
UV Signaling in Photoaging
11:40 – 12:00 Ask the Expert – Moderated Discussion of Photoaging
12:00 – 2:00 Break for Lunch
Session 3: Photoprotection
2:00 – 2:30 Steven Q. Wang, M.D., West New York, New York
The Role of Antioxidants in Photoprotection
2:30 – 3:00 Panel Discussion
Tanning Bed and Sunscreen Regulations
Moderator: Steven Q. Wang, M.D., West New York, New York
3:00 – 3:15 Break/Poster Viewing
Session 4: Use of Technology in Diagnosis of Skin Cancer
3:15 – 3:45 Nik Kollias, Ph.D., Watertown, Massachusetts
Non-invasive Diagnostics
3:45 – 4:15 Milind Rajadhyaksha, Ph.D., New York, New York
Confocal Microscopy of Skin Cancers: Technology and
Translational Research
4:15 – 4:45 Harold Rabinovitz, M.D., Miami, Florida
Update on Computer Assisted Devices for Detecting Skin Cancer
4:45 – 5:00 Ask the Experts – Moderated Discussion of the Use of
Technology in the Diagnosis of Skin Cancer

The presentations were the following, in order of presentation
(Click on each title to see the abstract and its authors.)

  1. Dedee Murrell1, Stephen Shumack2, Lynda Spelman3, Joann See4, Daniel Hewit5, Peter Foley6, Hans Christian Wulf7, Diana Marie Rubel8.
    1 Premier Specialists, Kogarah, Australia
    2 St George Dermatology and Skin Cancer Center, Kogarah, Australia
    3 Specialist Connect, Woolloongabba, Australia
    4 Central Sydney Dermatology, Sydney, Australia
    5 Skin and Cancer Foundation, Westmead, Australia
    6 Skin and Cancer Foundation, Carlton, Australia
    7 Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark
    8 Woden Dermatology, Phillip, Australia

    Conventional photodynamic therapy (c-PDT) using LED lamps, is approved for the treatment of actinic keratoses (AK). Although it provides high rate of AK clearance with a good cosmetic outcome it is time consuming and usually associated with pain.

    Clinical studies performed in Scandinavia have shown that natural-daylight photodynamic therapy (NDL-PDT) with methyl-aminolevulinate cream provides similar AK clearance rates as c-PDT, induces much less pain, and simplifies the procedure. With NDL-PDT the photosensitizer is activated immediately upon its formation, whereas, with c-PDT the photosensitizer accumulates for 3 hours under occlusion and then is activated by the lamp.

    The results of a multi-center, randomized, investigator-blinded, controlled, intra-individual Australian noninferiority study comparing NDL-PDT and c-PDT with methyl aminolevinulate cream for the treatment of mild AK in 100 patients are presented below.

    At week 12 after a single NDL-PDT session, the lesion complete response rate with NDL-PDT was non-inferior to c-PDT (89% vs 93%). The maximal pain, as assessed by subjects was significantly lower with NDL-PDT compared to c-PDT (mean pain 0.8 vs 5.7 on an 11 point scale). There were fewer subjects with related adverse events with NDL-PDT compared to c-PDT (38% vs 55%).

    In conclusion, NDL-PDT with methyl-aminolevinulate cream was not inferior to c-PDT and significantly less painful.

  2. Premature aging in Hutchinson Gilford progeria syndrome (HGPS) is caused by a mutation of the LMNA gene that activates a cryptic splice site. This results in expression of a truncated form of Lamin A, called progerin. Accumulation of progerin in the nuclei of HGPS cells impairs nuclear functions and causes abnormal nuclear morphology.

    As accumulation of progerin has also been described during normal intrinsic aging, we hypothesized that accumulation of progerin with abnormal nuclear shapes (HGPS-like phenotype) may in addition be accelerated by extrinsic agents, in particular by ultraviolet light, and contribute to photoaging of the skin. We therefore exposed cultured neonatal and aged fibroblasts to single or repeated doses UVA and UVB and assessed cells for induction of a HGPS-like phenotype.

    UVA induced progerin protein and mRNA expression and HGPS-like abnormal nuclear shapes in all cells, in young and in aged cells, but more in the latter. This induction of progerin is mediated by UVA-induced alternative splicing of the LMNA transcript, as mRNA expression of Lamin A was not induced.

    So far, alternative splicing of other genes has been reported after exposure to UVC, but not after exposure to UVA. As we found the induction of progerin only after exposure to UVA, but not after exposure to UVB, we hypothesized that UVA-induced oxidative damage may mediate the alternative splicing of the LMNA pre-mRNA. This was confirmed by a complete inhibition of UVA-induced progerin mRNA by incubation with the singlet oxygen-quencher sodium azide (5 mM, not toxic, no effect on baseline progerin mRNA).

    In summary, we describe induction of the aging-associated progerin with altered nuclear morphology by UVA through formation of oxidative damage and subsequent alternative splicing. Our data represent a novel mechanism by which UVA mediates photoaging of the skin. The data also indicate that at least some aspects of photoaging should be regarded as a process of damage-accelerated intrinsic agiing.

  3. Julian Menter, LaToya Freeman, and Otega Edukuye
    Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, GA

    Statement of Purpose Type I collagen has several post-translational fluorescent molecules, that are unstable to UV radiation, as evidenced by fluorescence “fading” on exposure to UV rays. Knowledge of the kinetics and temperature dependence of photochemical fluorescence fading can eventually lead to a better understanding of in vivo phenomena such as “photoaging” and UV carcinogensis.

    Methods “Old”” (Lot#121) and “new” (Lot#159) Type I Calf – Skin collagen at 0.5 at, pH 7.4, were exposed to a UVC hand lamp, T = 8°, 20° and 40 ° C in thermostatted cuvettes. Fluorescence spectra and intensities were recorded on a PE – 650 - 40 Spectrofluorometer at excitation/emission wavelength pairs correspond roughly to tyrosine and its post translational products. Reciprocal normalized fluorescence intensity vs. time were plotted on each sample.

    Results Fluorescence spectral properties of both samples significantly differed, whereas other properties (e.g. electrophoresis, appearance) were not sensitive to age and temperature. The older lot #121 spectra were more reminiscent of oxidized samples. Preliminary temperature dependence data suggests a non–linear Arrhenius Plot for both samples, with lot #121 fading roughly 10-fold faster than lot #159

    Summary of Conclusions ® “Aged” collagen appears much more photolabile than “newer” collagen. Owing to the slow turnover (15 years) of skin collagen, this suggests that considerable collagen degradation could occur by “natural” aging processes alone.

    Acknowledgements This work was funded in part by GRANTS: MBRS #GM08248, RCMI #8G12MD007602, and DOD # 911 NF – 10 – 1 0448. There are no conflicts of interest.

  4. Mohammed AlJasser1, Sunil Kalia1, Jianhua Zhao1, Hequn Wang1, Richard I. Crawford2, Harvey Lui1, David McLean1
    1Department of Dermatology and Skin Science, University of British Columbia, Photomedicine Institute, Vancouver Costal Health Research Institute, Vancouver, British Columbia, Canada
    2Department of Pathology and Laboratory Medicine, University of British Columbia and Vancouver General Hospital, Vancouver, British Columbia, Canada

    Background Amongst different individuals, there appears to be greater inter-individual differences in color of palm creases as compared to overall palm color. Perhaps surprisingly, the specific morphologic basis for the darker color of palm creases is unknown. The objective of this study is to determine the origin of palm crease pigmentation.

    Methods The palm creases of patients with vitiligo involving the hand were assessed, using digital photography, dermoscopy, Wood’s light, and near infrared (NIR) imaging. Reflectance confocal microscopy (RCM) and two punch biopsies were performed in one patient.

    Results Four patients with vitiligo involving the palm were evaluated, and the findings were similar in all patients. Digital photography and dermoscopy showed complete loss of crease pigmentation within depigmented patches. Wood’s light examination demonstrated prominent accentuation of the color of the unaffected creases compared to the surrounding normal non-crease skin. In the affected creases, there was a complete loss of pigmentation under Wood’s light. A bright linear white signal was detected within normal creases and absent in the contiguous affected creases on NIR imaging. The RCM showed brighter signals within keratinocytes in the normal crease when compared to both the normal surrounding non-crease skin and vitiligo-involved crease. Histology revealed increased epidermal melanin within the normal crease with no increase in melanocyte density as compared to normal non-crease skin.

    Conclusion The preliminary results of this study show evidence of increased melanin in the palm crease which is probably responsible for its darker color. However, there does not seem to be an increase in the number of melanocytes within crease skin.

  5. Eduardo Ruvolo Jr, Lucas Santos, Susan Daly and Curtis Cole

    In the past 35 years many different in vitro methodologies have been developed and published to assess the substantivity and water resistance of sunscreen products but there is no method with good correlation with the in vivo measurements.

    Two sunscreen products were used to examine the reproducibility water resistance in sunscreen products in a Round Robin test involving 9 different clinical laboratories around the world. Products were tested according with the ISO 24444, Cosmetics-Sun protection test methods-in vivo determination of Sun Protection Factor (SPF) with addition of a water immersion step after product application. The individual water resistance retention was calculated based on the SPF values before and after water immersion. The same sunscreen products were tested by measuring the sun protection factor in vivo using DRS technique before and after the immersion of the subject forearm in water bath using different water conductivity.

    Water conductivity (but not water hardness) appears to be a key determinant of sunscreen retention on skin. A range of water conductivity values needs to be set to assure repeatability of testing outcomes.

  6. Sarah Jawed, B.A.1, Tatiana Drovetskaya, Ph.D2, Gustavo Vazquez2, Stephen W. Dusza, DrPH1, Steven Q. Wang, M.D.1
    1Memorial Sloan-Kettering Cancer Center, New York, NY, USA
    2BASF Corporation, Tarrytown, NY, USA

    Purpose To evaluate the efficacy of human hair as a protective agent and determined the level of UV protection in relationship to hair loss. Lastly, to analyze the difference in the UV protection offered by brown versus blonde hair.

    Methods Baseline UV transmissions of five blonde and five brown hair samples were measured using a photospectrometer, and the degree of UV protection is expressed as ultraviolet protection factor (UPF). Following the initial, nine sequential hair reductions were performed for each hair sample and resulting UV transmission was then measured after each hair reduction treatment.

    Results The UPF of blonde and brown hair samples in the highest density quartile (34 to 51 g/cm2) was 1898 and 2000, respectively. The UPF of blonde and brown hair in the lowest density quartile (6 to 14 g/cm2) was 6 and 16, respectively. UPF begins to decrease significantly with 20% of hair loss in both brown and blonde hair samples, and the rate of decrease in UPF accelerates with additional hair loss. Our study showed that UPF dropped to below 16 when there is approximately 13 and 9.5g/cm2 hair density for blonde and brown hair, respectively. The median critical wavelength (CW) for blonde and brown hair samples were above 380 nm and did not change with respect to sequential hair reduction.

    Conclusion High density hair inherently provides superior, uniformed, and broad spectrum UV protection for the scalp that exceeds that of sunscreen and hats. The degree of UV protection decreases dramatically with progressive hair loss.

  7. Heajung Lee, Melvin Chiu
    Division of Dermatology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA

    Repair of UV-induced DNA damage has shown circadian rhythmicity in mice, as mice exposed to UVB radiation in the morning developed skin cancers at a faster rate and at higher frequency compared to mice exposed to the same UV dose in the evening.

    Narrowband UVB (NBUVB) phototherapy is a widely used treatment modality in dermatology. We aimed to determine if time of day of exposure contributes to possible carcinogenicity in patients receiving NBUVB.

    Patients at highest risk of developing skin cancer (age >50, skin types I-III) who received NBUVB between 2006-2012 were identified and grouped based on the time of day of their phototherapy treatments (before 10AM [n=46] and after 2PM [n=42]). Patients in the morning and evening groups were analyzed starting at 3 months from their first treatment date for subsequent diagnoses of skin cancer. Additionally, two matched controls were identified for each cancer patient on the basis of age, sex, and skin type.

    During 177 person-years of follow-up, incident skin cancer occurred in 2 morning patients (2 per 100 person years) and 5 evening patients (6.3 per 100 person-years) (p=.19). Median follow-up durations were 21.5 (AM) and 17.1 (PM) months; there was no significant difference in age, cumulative UVB dose, or duration of follow-up between the two groups (p>.43). Mean time of exposure was 12:54PM and 11:43AM in those with and without skin cancers, respectively (p=.25).

    There was a non-statistically significant trend toward a higher incidence of skin cancer in patients who received the majority of their phototherapy after 2PM compared to those exposed in the morning and later average treatment times in those who developed skin cancer compared to their matched cancer-free controls. With the current data, we were unable to find a definite association between time of day of NBUVB treatment and skin cancer. Future studies with larger sample size and longer follow-up are needed to detect a true difference with adequate power.

  8. Osterwalder U1, He Q1, and Wang SQ2
    1BASF PCN, Monheim, Germany
    2 Memorial Sloane–Kettering Cancer Center, New York, NY, USA

    In sun protection, the notion of sun protection factor (SPF) is well established. Since UVA I radiation (i.e., 340-400nm) is less erythemogenic than UVB (290-320nm) and UVA II (320-340nm) radiation, an additional metric for the assessment of the protection against UVA radiation is required. The in vitro metric Critical Wavelength (CW) is an early UVA metric that has just recently been adopted in the USA in 2011. The CW is defined as the wavelength at which 90% of the total area under the absorbance curve resides, with the absorption measures across the UV spectrum from 290 to 400nm. CW ≥ 370nm is required for the broad-spectrum claim.

    The first objective is to quantify amount of UVA absorption provided by sunscreens that meet the FDA criterion of CW ≥370nm. Second objective is to convert the CW metric into UVA-protection factor value, an index that is more relevant for the public.

    The basic data for in vitro measurements on sunscreens comes from the transmission measurement of a (monochromatic) beam of UV radiation (i.e., 290 to 400nm) through a Poly(methyl methacrylate) (PMMA) plate with and without sunscreen. The monochromatic protection factor is defined as the reciprocal value of the transmission, 1/T.

    15 sunscreen samples with SPF between 15 and 60 were measured. CW values were between 370 and 380 nm. Transmissions T in the UVA I range are much higher than in the UVB and UVA II range. Thus, the UVA I protection factor PF-UVAI is much lower, in general about 10 to 35% of the SPF value.

    Sunscreens that meet the FDA criterion of 370nm still permit high amount of UVA-I transmission, ranging from 10% to 40% depending on the SPF and CW values. Transmission data can be readily converted to protection factors, i.e., PF-UVAI, a concept that may be more relevant to the public. Compared to the SPF, UVA I protection factors are much lower.

  9. Knobler R, Tanew A, Jantschitsch C, Just U
    Dept of Dermatology, University of Vienna, Austria

    Extracorporeal photochemotherapy (ECP, Photopheresis) is an FDA-approved therapy for cutaneous T-cell lymphomas (CTCL), graft-versus-host disease (GvHD), organ transplant rejection, systemic sclerosis, and other T-cell-mediated diseases.

    Morphea (localized scleroderma) is a skin disorder with significant morbidity. There is no standard therapeutic approach proven to be consistently effective to substantially modify the course of the disease.

    Recent publications indicate that ECP can be applied for changing in a positive manner the course of generalized deep morphea.

    Eleven patients (age 21-65a, female:7, male:4) with therapy resistent localized scleroderma were included in this prospective single center clinical study. ECP was performed every two weeks for a total of six months. Clinical examination as well as high-frequency ultrasound evaluation of skin involvement was performed before initiating the treatment as well as after the 6-months-treatment regime.

    In 7 of 11 patients there was a marked decrease in skin induration. One patient with uncontrolled disease progression prior to ECP showed no further progression after starting the ECP treatment. In one patient the symptoms of generalized morphea increased despite treatment.

    Present data of this ongoing study confirms published literature that the use of ECP in refractory localized scleroderma is a seemingly viable treatment option with no noticeable side effects. Further extension of this clinical study and additional research into the clinical and immunological mechanisms of action of this therapy should provide important information to define its true value in the treatment of morphea.

  10. Christian Oresajo, Margarita Yatskayer, Angelike Galdi, Peter Foltis, Sreekumar Pillai

    UV-irradiation of the skin causes oxidative stress, leading to inflammatory reactions and premature skin aging. Sunscreens absorb UV on the skin surface and provide photo protection. Antioxidants provide protection by quenching reactive oxygen species generated by UV. Antioxidants and sunscreens can thus complement each other in providing photo protection to human skin.

    The aim of the study was to evaluate and compare the photoprotective benefits of a formulation containing an antioxidant complex consisting of a Cassia alata leaf extract and Oxynex®-ST), a photo stabilizing polymer with antioxidant functionality (Product A) to that of a formulation containing both the antioxidant complex and sunscreen (Product B) on normal healthy volunteers using biomarkers of skin damage.

    Ten (10) subjects were treated with the 2 products and the placebo (Product C) on the lower back for four (4) consecutive days. On Day 4, the three test sites and a control site received solar-simulated UV-irradiation equivalent to 5 times the MED (Minimal Erythemal Dose). On Day 5, digital images were taken and four-millimeter (4-mm) punch biopsies were collected from the four irradiated sites, and a control site (untreated, non-irradiated) for immunohistochemistry.

    Product A provided significant photoprotection as did Product B in mitigating UV-induced erythema in human skin. 5xMED demonstrated significant damage as assessed by thymine dimer formation, MMP-9 and p53 protein expression. All of these changes were significantly attenuated by Product A and Product B. Product B was most protective, followed by Product A. Product C showed very minimal protection, most likely due to the light scattering/refraction effect of a polymeric component of the formulation.

    Antioxidants can complement sunscreens in providing photoprotection to human skin.

  11. S. Seité1, S. Grether-Beck2, T. Jaenicke2, K. Reinhold2, C.Oresajo3 And J. Krutmann2
    1 La Roche Posay Pharmaceutical Laboratories, Asnières, France
    2 Institut für Umweltmedizinische Forschung gGmbH, Düsseldorf, Germany
    3 Research & Innovation, USA

    Daily exposure to ultraviolet radiation (UVR) is able to induce a number of detrimental effects in human skin including premature aging (photoaging). Studies on the mechanisms by which UVA causes skin aging have revealed that an increased expression of matrix metalloproteinase 1 (MMP-1) is of importance and that this induction is mediated through the generation of reactive oxygen species (ROS). As a consequence, prevention of photoaging should be directed at prevention of UVA radiation-induced upregulation of genes related to oxidative stress and MMP-1.

    Fourty four (44) healthy volunteers were recruited for this study. The volunteers were split in 2 groups. No product was applied to the first group of 14 volunteers. Exposure of 20, 60 or 80 J/cm2 intensity of UVA was performed on 4cm x 4cm marked areas on the buttock skin. The biopsy samples were collected 24h or 72h after exposure. The lamp that was used (UVASUN 5000) was equipped with Schott WG335/3mm filter and two UG5/3mm filters in order to obtain a spectrum between 320 and 400 nm. In the second group of 30 volunteers, prior to irradiation at 80 J/cm² using the same UVA Lamp as in the first group, 2mg/cm2 of broad spectrum moisturizing cream was applied to 4cm x 4cm marked areas on the buttock skin. The second test site was left untreated but was irradiated at 80 J/cm² as well. 24 hours later, 4mm punch biopsies were obtained from treated irradiated site, untreated irradiated site and from an adjacent area that received neither UVA nor treatment (naïve site). Total RNA was isolated from these biopsies and SOD (superoxide dismutase), CAT (catalase), GPX (glutathione peroxidase), MMP-1 and 18S rRNA expression was assessed by real-time RT-PCR. A significant induction of the analyzed genes was observed 24h post-exposure. However the application of broad-spectrum daily moisturizing cream (SPF15, UVA-PF 15) prior to 80J/cm² UVA exposure significantly reduced the UVA induced increase in MMP-1 and antioxidant defence mRNA expression.

    This study demonstrates the effective protection offered by a broad-spectrum daily moisturizing cream (SPF15, UVA-PF 15) in the prevention from UVA radiation-induced photoaging, directed at prevention of UVA-induced upregulation of genes related to oxidative stress and MMP-1.

  12. Ryoichi Kamide
    Department of Dermatology, Daisan Hospital, The Jikei University School of Medicine, Tokyo, Japan

    The Japanese Society of Photodermatology was established on March 25, 2012, when we held the first meeting of the society in Tokyo. This society represents an expansion from the UV-ABClub, which was a closed society for photodermatology in Japan existing since 1975. Now the society is open for everyone who is interested in photodermatology with the express purpose of enhancing photodermatological research and clinical practice in Japan. All the directors of the UV-ABClub have agreed with this expansion. We are also considering international collaboration in the near future. We will hold the second meeting on Feb.17, 2013 in Nagoya under the presiding of Prof. Akimichi Morita in Nagoya City University. In the presentation, a statistics of photosensitivity dermatoses and recent research work on xeroderma pigmentosum, erythropoietic protoporphyria and drug-induced photosensitivity in Japan will be reviewed.

  13. Marko Siegesmund, Jorge Frank, Sandra Hanneken, and Norbert J. Neumann
    Department of Dermatology and Porphyria Specialist Center, Heinrich Heine University, Duesseldorf, Germany.

    Hereditary coproporphyria (HCP) is one of the acute hepatic porphyrias and results from an autosomal dominantly inherited partial deficiency of coproporphyrinogen oxidase (CPOX), the sixth enzyme in heme biosynthesis. Clinically, the disease is characterized by acute neurovisceral attacks and, rarely, by blistering photosensitivity on the sun-exposed body sites. Usually, the disease does not manifest before puberty. A 3-year-old girl presented with severe photosensitivity, blistering and erosions on the hands and face since early childhood. Biochemical analysis revealed highly increased urinary levels of uroporphyrin and coproporphyrin and a markedly elevated fecal coproporphyrin III/coproporphyrin I ratio. Under the diagnosis of homozygous HCP or variegate porphyria we initiated molecular genetic studies. Automated sequencing analysis of the CPOX gene showed compound heterozygosity for two missense mutations, designated R328C and G333D, respectively, indicative of homozygous HCP. The causality of these mutations in disease pathogenesis was subsequently confirmed by prokaryotic expression of the mutant alleles. In infants and children with early-onset blistering photosensitivity the rare occurrence of a homozygous hepatic porphyria, as in this patient, should be considered.
  14. Sunil Kalia, Yue Kay Kali Kwong, Marius Laurentiu Haiducu, Harvey Lui
    Department of Dermatology and Skin Science, University of British Columbia & Photomedicine Institute, Vancouver Costal Health; Vancouver, BC, Canada.

    The incidence of skin cancer in North America continues to increase each year. Identification of populations at highest skin cancer risk is imperative in designing public education campaigns. This study aimed to compare sun protective behaviours in urban versus rural health regions across a timespan of five years.

    National cross-sectional data from the 2005 and 2010 Canadian Community Health Surveys were analysed. A total of 28, 417 respondents answered the Sun Safety Behaviours module over the two years, with roughly equal number of respondents in each survey. The primary outcome variable of interest was the presence of sunburn over the last 12 months. Other outcome variables included mid-day sun exposure levels and frequencies of seeking shade, wearing a hat, or wearing sunscreen. The primary explanatory variable was urban versus rural health regions. Age, sex, marital status, education, and ethnicity were also included as covariates. Stepwise logistic regression analysis was performed, with the final multiple logistic regression model including only variables significant at p<0.01 (Wald chi-square test).

    Rural health regions remained a high-risk group for skin cancer risk between 2005 and 2010, with patterns of sun protection behaviours similar in both years. Compared to urban regions, rural regions had higher incidence of sunburn in 2005 (OR: 1.18; 95% CI: 1.09-1.28) and 2010 (OR: 1.14; 95% CI: 1.04-1.24). Rural regions were also more likely to have higher sun exposure and less likely to use sunscreen. Interestingly, there is a higher rate of hat wearing in rural regions.

    These results highlight rural regions as a high-risk group for skin cancer risk. Persistent trends of the low rate of sun protection behaviours suggest that aggressive educational and screening campaigns may be required to target this group.






Upcoming

The Photodermatology is planning a virtual annual meeting which will be held March 18, 2021. If you are a Society member or have paid for registration only, you will be sent a link to join the Zoom meeting.

A program draft can be found under the Meetings tab.