Formative research for developing targeted skin cancer prevention programs for children in multiethnic Hawaii. (1/289)

Skin cancer is a significant and increasing public health problem. Improvement in sun protection practices among children holds great promise for prevention, and parents and caregivers play important roles. Health promotion programs are most likely to succeed when based on a systematic planning process including an understanding of current practices, beliefs, social norms and environments. This article describes formative research used to help develop the SunSmart skin cancer prevention program in Hawaii. Group discussions and interviews were conducted with 216 children in grades 1, 2 and 3, 15 parents, and 27 recreation staff. Children's discussion groups took place in intact classrooms. A combination of quantitative and qualitative methods was used. Multiple raters and an iterative process were used to analyze data from survey forms, observer impressions and audio tapes, and to draw the main conclusions. Sun protection practices in all groups were inconsistent, though general awareness about prevention was widespread. Children reported a reluctance to cover up with long pants and sleeves, and wide-brim hats, and did not understand what skin cancer was. Parents and recreation staff were supportive of education and policy supports, to improve both their own and the children's prevention habits. They were enthusiastic about interactive and creative activities. We conclude that targeted skin cancer prevention messages and strategies for Hawaii's children should promote gradual changes, provide environmental supports, and involve parents and recreation staff. Both the findings and procedures have implications for prevention elsewhere.  (+info)

The use of observational methods for monitoring sun-protection activities in schools. (2/289)

Evaluation of health promotion interventions aimed at behavioural or environmental change involves assessing change that occurs as a result of the program. Direct observational methods can be used for this purpose and this paper describes three such methods that we pilot tested for use in a 5-year intervention study aimed at reducing sun exposure in primary school children. (1) Monitoring 'No hat, no play' policies. This method involved video taping children in selected school play areas during lunch time and analysing the content of the videos to assess the proportion of children wearing various types of hats. (2) Assessing shade provision in the playground. This method involved taking aerial photographs of each school and using them to estimate the proportion of shade in play areas available to children at lunchtime. (3) Shade use. This involved children wearing polysulphone film badges to measure the amount of UV-B exposure they received during one lunch period, relative to the total possible dose registered on index badges. Each method was implemented successfully, and we demonstrated that the video and aerial photography methods produced highly reproducible results and that all three methods were feasible. These three methods will be used in our intervention study to assess longitudinal change in schools' sun-protection policy and practice.  (+info)

Evaluation of an intervention to reduce sun exposure in children: design and baseline results. (3/289)

The Kidskin Study is a 5-year intervention study (1995-1999) involving 1,776 5- and 6-year-old children attending 33 primary schools in Perth, Western Australia. The aim of the study is to design, implement, and evaluate an intervention to reduce sun exposure in young children. There are three study groups: a control group, a "moderate intervention" group, and a "high intervention" group. The control schools receive the standard Western Australian health education curriculum, while the moderate and high intervention schools receive a specially designed curricular intervention. In addition, children in the high intervention group receive program materials over the summer holidays, when exposure is likely to be highest, and are offered sun-protective swimwear at low cost. The main outcome measure is the number of nevi on the back. Other outcomes include nevi on the chest (boys only), face, and arms, levels of suntanning, degree of freckling, and sun-related behaviors. At baseline, the three groups were similar with respect to nevi and freckling after adjustment for observer and month of observation. Sun exposure was slightly higher in the high intervention group. The groups were also similar with respect to most potential confounders, although they differed with respect to Southern European ethnicity and parental education.  (+info)

Galectin-7 overexpression is associated with the apoptotic process in UVB-induced sunburn keratinocytes. (4/289)

Galectin-7 is a beta-galactoside binding protein specifically expressed in stratified epithelia and notably in epidermis, but barely detectable in epidermal tumors and absent from squamous carcinoma cell lines. Galectin-7 gene is an early transcriptional target of the tumor suppressor protein P53 [Polyak, K., Xia, Y., Zweier, J., Kinzler, K. & Vogelstein, B. (1997) Nature (London) 389, 300-305]. Because p53 transcriptional activity is increased by genotoxic stresses we have examined the possible effects of ultraviolet radiations (UVB) on galectin-7 expression in epidermal keratinocytes. The amounts of galectin-7 mRNA and protein are increased rapidly after UVB irradiation of epidermal keratinocytes. The increase of galectin-7 is parallel to P53 stabilization. UVB irradiation of skin reconstructed in vitro and of human skin ex vivo demonstrates that galectin-7 overexpression is associated with sunburn/apoptotic keratinocytes. Transfection of a galectin-7 expression vector results in a significant increase in terminal deoxynucleotidyltransferase-mediated UTP end labeling-positive keratinocytes. The present findings demonstrate a keratinocyte-specific protein involved in the UV-induced apoptosis, an essential process in the maintenance of epidermal homeostasis.  (+info)

Oral contraceptive use and risk of melanoma in premenopausal women. (5/289)

Melanoma has been increasing in white populations. Incidence rates rise steeply in women until about age 50, suggesting oestrogen as a possible risk factor. Oestrogens can increase melanocyte count and melanin content and cause hyperpigmentation of the skin. We examined prospectively the association between oral contraceptive (OC) use and diagnoses of superficial spreading and nodular melanoma among 183,693 premenopausal white women in the Nurses' Health Study (NHS) and the Nurses' Health Study II (NHS II) cohorts. One hundred and forty six cases were confirmed in NHS during follow-up from 1976 to 1994, and 106 cases were confirmed in NHS II from 1989 to 1995. Skin reaction to sun exposure, sunburn history, mole counts, hair colour, family history of melanoma, parity, height and body mass index were also assessed and included in logistic regression models. A significant twofold increase in risk of melanoma (relative risk (RR) = 2.0, 95% confidence interval (CI) 1.2-3.4) was observed among current OC users compared to never users. Risk was further increased among current users with 10 or more years of use (RR = 3.4, 95% CI 1.7-7.0). Risk did not appear elevated among past OC users, even among those with longer durations of use, and risk did not decline linearly with time since last use. In conclusion, risk of premenopausal melanoma may be increased among women who are current OC users, particularly among those with longer durations of use. Further research is needed to determine whether low-dose oestrogen pills in particular are associated with an increase in risk and to describe possible interactions between OC use and sun exposure or other risk factors for melanoma.  (+info)

Evaluation of apoptotic cells induced by ultraviolet light B radiation in epidermal sheets stained by the TUNEL technique. (6/289)

Two major components of epidermal cells, keratinocytes and Langerhans cells, are injured by ultraviolet light B radiation, resulting in sunburn cell (apoptotic cell) formation, impaired function, and a reduced number of Langerhans cells. Quantitative analysis of Langerhans cell damage is usually performed using epidermal sheets, whereas that of keratinocytes has been performed by counting the number of sunburn cells in vertical tissue sections. In this study we assessed the influences of ultraviolet light B radiation on epidermal cells by apoptotic cell formation, using murine epidermal sheets stained by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling technique. Ten to 75 mJ per cm2 of ultraviolet light B radiation induced apoptotic cells in abdominal skin of C3H mice. The cells were induced in 6 h after 50 mJ per cm2 of ultraviolet light B irradiation with the peak in number in 24 h, 18.8 +/- 5.0 per mm2 and 97.7 +/- 7.4 per mm2, respectively. One week later, the apoptotic cells were not visualized. As C3H/He, BALB/C, and C57BL/6 mice showed almost the same frequency of apoptosis in epidermal sheets from 50 mJ per cm2 ultraviolet light B-irradiated skin, the induction of the cells by ultraviolet light B radiation did not depend on the genetic trait of the mouse. Xeroderma pigmentosum type A gene-deficient mice, however, showed a greater induction of apoptotic cells (216.9 +/- 25.2 per mm2) by ultraviolet light B radiation than xeroderma pigmentosum type A wild-type mice (89.5 +/- 13.6 per mm2) and conventional mice. Pretreatment with a SPF 60 sunscreen agent was quite effective in reducing the induction of apoptotic cells. Using confocal laser scanning microscopy and double staining, 1.5 +/- 2.7% of apoptotic cells were Ia-positive cells in 24 h after 50 mJ per cm2 of ultraviolet light B radiation. Apoptotic Ia-positive cells were not observed 48 h after the radiation. On the other hand, no apoptotic dendritic epidermal T cells were observed in up to 75 mJ per cm2 of ultraviolet light B radiated skin. Thus, nearly all apoptotic cells were keratinocytes, and Langerhans cells and dendritic epidermal T cells appeared resistant to ultraviolet light B-induced apoptosis. Compared with the assessment in vertical tissue sections, the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling technique with epidermal sheets appeared to be a more physiologically relevant method for quantitative evaluation of apoptotic epidermal cells induced by ultraviolet light B radiation.  (+info)

Temporal events in skin injury and the early adaptive responses in ultraviolet-irradiated mouse skin. (7/289)

We examined the effects of ultraviolet (UV) radiation on the time course for induction of sunburn (apoptotic) cells and expression of proteins known to be associated with growth arrest and apoptosis in SKH-hr1 mouse skin. Mice were irradiated with a single dose (2.5 kJ/m(2)) of UV from Kodacel-filtered (290-400 nm) FS40 sunlamps and the skin tissues were analyzed at various times after irradiation for the presence of apoptotic cells and expression of p53, p21(Waf-1/Cip1), bcl-2, bax, and proliferating cell nuclear antigen. The results indicated that p53 expression was induced early in the epidermis, reaching maximum levels 12 hours after irradiaton, and p21(Waf-1/Cip1) expression in the epidermis peaked at 24 hours after irradiation. In contrast, UV radiation induced high levels of bax at 24 to 72 hours after irradiation with a concomitant decrease in bcl-2 expression. Coinciding with these changes, apoptotic cells began to appear 6 hours after irradiation and reached a maximum at 24 hours after irradiation. Interestingly, proliferating cell nuclear antigen expression, which was initially confined to the basal layer, became dispersed throughout the basal and suprabasal layers of the skin at 48 hours and paralleled marked hyperplasia. These results suggest that UV irradiation of mouse skin induces apoptosis mediated by the p53/p21/bax/bcl-2 pathway and that the dead cells are replaced by hyperproliferative cells, leading to epidermal hyperplasia. This implies that UV-induced apoptosis and hyperplasia are closely linked and tightly regulated and that dysregulation of these two events may lead to skin cancer development.  (+info)

Sensitivity to sunburn is associated with susceptibility to ultraviolet radiation-induced suppression of cutaneous cell-mediated immunity. (8/289)

Skin cancer incidence is highest in white-skinned people. Within this group, skin types I/II (sun sensitive/tan poorly) are at greater risk than skin types III/IV (sun tolerant/tan well). Studies in mice demonstrate that ultraviolet radiation (UVR)-induced suppression of cell-mediated immune function plays an important role in the development of skin cancer and induces a susceptibility to infectious disease. A similar role is suspected in humans, but we lack quantitative human data to make risk assessments of ambient solar exposure on human health. This study demonstrates that ambient levels of solar UVR, typically experienced within 1 h of exposure to noonday summer sunlight, can suppress contact hypersensitivity (CHS) responses in healthy white-skinned humans in vivo (n = 93). There was a linear relationship between increase in erythema and suppression of CHS (P < 0.001), and a moderate sunburn (two minimal erythema doses [2 MED]) was sufficient to suppress CHS in all volunteers by 93%. However, a single suberythemal exposure of either 0.25 or 0.5 MED suppressed CHS responses by 50 and 80%, respectively, in skin types I/II, whereas 1 MED only suppressed CHS by 40% in skin types III/IV. The two- to threefold greater sensitivity of skin types I/II for a given level of sunburn may play a role in their greater sensitivity to skin cancer.  (+info)