UV doses of American children and adolescents.

The ultraviolet (UV) doses of American young adults were never measured, but are needed for assessing UV-related health risks. These doses were calculated using a novel approach. The National Human Activity Pattern Survey recorded the daily minute-by-minute activities of about 2000 young adults (0-19 years) over the course of 2 years to assess their exposure to environmental pollutants. From that survey, only the outdoor daylight data of northern and southern girls and boys were extracted and stratified by season and age to find the time American children (0-5 and 6-12 years) and adolescents (13-19 years) spend outside. They spend about 10% of the day outdoors, but only get about 30% of the available terrestrial UV radiation (on a horizontal plane). American children have about the same percent personal ambients as adults (3.1%), 2.8% for girls and 3.4% for boys. Adolescents have the lowest personal ambients (2.6%), 2.1% for girls and 3.1% for boys. To get their UV doses, their percent ambients are multiplied by the total available terrestrial UV. Excluding vacation, the erythemally weighted UV doses for American children are 25 kJ/m2/year, 23 for girls and 28 for boys. Adolescents get the lowest UV exposure of any group, 21 kJ/m2/year, 18 for girls and 24 for boys. Young adult northern girls get 18 kJ/m2/year and boys get 21 kJ/m2/year, whereas southern girls get 24 kJ/m2/year and boys get 31 kJ/m2/year. The youngest children (0-5 years) get slightly higher summer doses. Thus, we can now assess the UV-related health risks for American children and adolescents.     

Study of UV radiation dose received by the Spanish population

Excess exposure to UV radiation can affect our health by causing sunburn, skin cancer, etc. It is therefore useful to determine the UV dosage received by people as a way of protecting them from the possible negative effects that this kind of radiation can cause. In this work, the personal outdoor percentage, which shows the time spent in outdoor activities, as well as personal UV doses, has been calculated by means of global UV radiation on a horizontal plane. A database of average daily UVB radiation on the horizontal plane given by the National Institute of Meteorology has been used. In this work we evaluate the standard erythema dose of the Spanish population throughout the year.     

UV doses of Americans.

The UV doses of Americans were never measured, but are needed for assessing the risks of UV-related health effects. We calculated these doses using a novel approach. The Environmental Protection Agency's (EPA) National Human Activity Pattern Survey (NHAPS) recorded the activity profiles of 9386 Americans over 24 months to assess their exposure to environmental pollutants, one of which is UV radiation. NHAPS used randomized telephone interviews to get their previous day's minute-by-minute activities. From NHAPS we extracted only the outdoor-daylight data of the northern and southern indoor workers (95%), stratifying by season, sex and age (0-21, 22-40, 41-59 and 60+ years) to find the average time Americans spend outdoors. Knowing the total daylight time and that while outdoors Americans are exposed to about 30% of the available solar UV (on a horizontal plane), we calculated their percent ambients. The average American's percent ambients are 2.6 and 2.5% for northern and southern females, respectively, and 3.5 and 3.6% for northern and southern males, respectively. Men over 40 years of age have the highest ambients (4%). From their ambients we calculated their annual doses using seasonal averages of UV measurements taken daily for over 2 years by EPA Brewer spectrophotometers located in four quadrants of the United States: Atlanta, GA; Boston, MA; Bozeman, MT and Riverside, CA. The average erythemal UV doses of Americans are about 25,000 J/m2/year, 22,000 for females and 28,000 for males, or 33,000 J/m2/year including a conservative continental U.S. vacation (7800 J/m2). Thus, we can now assess the risks of UV-related health effects for Americans.     

Action spectrum conversion factors that change erythemally weighted to previtamin D3-weighted UV doses

Abstract Many solar UV measurements, either terrestrial or personal, weight the raw data by the erythemal action spectrum. However, a problem arises when one tries to estimate the benefit of vitamin D(3) production based on erythemally weighted outdoor doses, like those measured by calibrated R-B meters or polysulphone badges, because the differences between action spectra give dissimilar values. While both action spectra peak in the UVB region, the erythemal action spectrum continues throughout the UVA region while the previtamin D(3) action spectrum stops near that boundary. When one uses the previtamin D(3) action spectrum to weight the solar spectra (D(eff)), one gets a different contribution in W m(-2) than what the erythemally weighted data predicts (E(eff)). Thus, to do proper benefit assessments, one must incorporate action spectrum conversion factors (ASCF) into the calculations to change erythemally weighted to previtamin D(3)-weighted doses. To date, all benefit assessments for vitamin D(3) production in human skin from outdoor exposures are overestimates because they did not account for the different contributions of each action spectrum with changing solar zenith angle and ozone and they did not account for body geometry. Here we describe how to normalize the ratios of the effective irradiances (D(eff)/E(eff)) to get ASCF that change erythemally weighted to previtamin D(3)-weighted doses. We also give the ASCF for each season of the year in the northern hemisphere every 5 degrees from 30 degrees N to 60 degrees N, based on ozone values. These ASCF, along with geometry conversion factors and other information, can give better vitamin D(3) estimates from erythemally weighted outdoor doses.     

Assessment of cutaneous photosensitivity of TOOKAD (WST09) in preclinical animal models and in patients

TOOKAD (WST09) is a new, long-wavelength palladium bacteriopheophorbide photosensitizer that targets tissue vasculature. The cutaneous phototoxicity of TOOKAD was assessed in normal rat and pig animal models and in patients in a Phase-I trial of TOOKAD-mediated photodynamic therapy (PDT) for recurrent prostate cancer. Controlled skin exposures were administered using solar-simulated light at various times after drug administration. Two different spectral ranges were used. In the first, the UV portion of the spectrum was removed (UV(-)) because UV irradiation in nondrugged control animals produced an erythema response at incident energy densities (J/cm(2)) lower than those required to induce a PDT response. In the second, the full solar spectrum (UV(+)) was used, and the potentiation by the photosensitizer of the UV-mediated minimum erythema dose was assessed. Results showed that the PDT skin response was negligible at clinical drug doses of 2 mg/kg for any period after administration at light doses of 128 J/cm(2) in the animal models. In patients, there was no observed UV(-) skin response at doses of up to 2 mg/kg, drug-light intervals of 1-3 h or greater and light exposures up to 128 J/cm(2). At higher drug doses in the rat and pig models, the duration of skin phototoxicity was found to be approximately 3 h and less than 1 h, respectively. Using the full spectrum of solar-simulated light, the presence of TOOKAD did not measurably enhance the UV(+)-induced erythema in the rats, pigs or patients.     

Sun Exposure, Sunscreen and Their Effects on Epidermal Langerhans Cells

This study examined the effects of chronic and current sun exposure on the number of Langerhans cells in epidermal sheets of UV-exposed and unexposed skin of the arms and assessed the effect of sunscreens. Participants were enrolled in a skin cancer prevention trial and had been using sunscreen daily for the previous 3 years. There were significantly fewer Langerhans cells on the exposed (463 cells/mm2) than on the unexposed forearm (528 cells/mm2) (P = 0.0001). High sun exposure in the previous 2 weeks and a history of predominantly outdoor occupations were both associated with a reduced number of Langerhans cells, although age and other biological indicators of chronic exposure were not associated. Sunscreen use was protective against the effects of current but not chronic sun exposure, with a suggestion of a greater effect at higher levels of exposure. Unexpectedly, people with a past history of nonmelanoma skin cancer had more Langerhans cells in both the exposed and the unexposed skin. These results emphasize the need for continued public health education to protect the immune system from the damaging effects of UV radiation .     

UV exposure of elementary school children in five Japanese cities

A 1 week UV‐exposure measurement and outdoor‐activity pattern survey was conducted for elementary school children for four seasons at five sites in Japan, i.e. Sapporo (43°05′N, altitude 40 m), Tsukuba (36°05′N, 20 m), Tokyo (35°40′N, 45 m), Miyazaki (31°60′N, 40 m) and Naha (26°10′N, 5 m), and UV exposure was measured directly and estimated using outdoor‐activity records. The study site with largest UV exposure was Miyazaki, a southern rural area. Comparing the results for boys and girls, UV exposure was larger in boys. UV exposure was large in spring and summer and small in winter. The total amount of UV exposure in spring and summer contributed 57.7–73.4% of total exposure for the year. As a whole, 8.1% and 1.8% of the schoolchildren were exposed to more than 1 minimum erythemal dose (MED) and 2 MED of solar UV in a day, respectively. The estimated yearly UV exposure ranged from 49 207 J/m² in Miyazaki to 31 520 J/m² in Tsukuba. The actual UV exposure correlated to potential UV exposure, estimated using outdoor‐activity records and ambient UV irradiance, but the ratio differed by season and site. The yearly average of percent UV exposure to ambient UV on a horizontal plane ranged from 9.9% in Tokyo to 4.0% in Naha. In the questionnaire survey on outdoor‐activity pattern, a short question “How long did you spend time outdoors between 0900 and 1500 h?” gives the best estimates of UV exposure.     

UVAI-induced edema and pyrimidine dimers in murine skin

The induction of edema and pyrimidine dimers in epidermal DNA was determined in the skin of SKH:HR1 mice exposed to graded doses of ultraviolet radiation AI (UVAI; 340-400 nm). Exposure to UVAI induced 1.6 +/- 0.08 x 10(-6) (mean +/- standard error of mean) pyrimidine dimers per 10(8) Da of DNA per J/m2. Edema in irradiated animals was determined as an increase in skinfold thickness. A dose of 1.8 x 10(6) J/m2 of UVAI that resulted in a 50% increase in skinfold thickness (SFT50%) would have induced 1.0 x 10(5) dimers per basal cell genome. A similar increase in SFT induced by full spectrum solar ultraviolet radiation (290-400 nm) would accompany the induction of 11.0 x 10(5) pyrimidine dimers per basal cell genome. These results support a hypothesis that UVAI-induced pathological changes of the skin are mediated through the formation of nondimer photoproducts.     

Inflammatory doses of UV may not be necessary for skin carcinogenesis

The UV wavelengths in sunlight are the main cause of skin cancer in humans. Sunlight causes gene mutations, immunosuppression and, at higher doses, inflammation. While it is clear that immunosuppression and gene mutations are essential biologic events via which UV causes skin cancer, the requirement for UV-induced inflammation is less certain. Both the UVB (290-320 nm) and UVA (320-400 nm) wavebands within sunlight can cause skin cancer, gene mutations and immunosuppression. However, UVB, but not UVA, at realistic doses can cause inflammation, and UVB induces skin cancer, immunosuppression and gene mutations at doses much lower than those required to cause inflammation. Inflammation enhances skin carcinogenesis, but may not be UV induced, and inflammatory mediators at doses too low to cause inflammation may be required. UV-induced mutations can cause epidermal cells to make proinflammatory factors or to induce them in the surrounding stroma, creating an oxidizing environment in which additional oncogenic mutations are likely to take place, even in the absence of UV. Our hypothesis is therefore that subinflammatory doses of both UVA and UVB cause benign skin tumors. One of the effects of sunlight-induced mutations may be the production of inflammatory mediators that enhance carcinogenesis.     

Solar UVR exposure, concurrent activities and sun-protective practices among primary schoolchildren

Comprehensive measures of ultraviolet radiation (UVR) exposure, concurrent activities and sun-protective practices are needed to develop and evaluate skin cancer prevention and sun protection interventions. The UVR exposures of 345 primary schoolchildren at 23 schools around New Zealand were measured using electronic UVR monitors for 1-week periods over 12 weeks in 2004 and 2005. In addition, ambient UVR levels on a horizontal surface were measured on-site at each school. Children completed activity diaries during the period UVR measurements were made and provided information on their indoor and outdoor status and clothing and sun protection worn. Mean total daily UVR exposure (7:00-20:00 h NZST + 1) at the body location where the UVR monitors were worn was 0.9 SED (standard erythemal dose, 1 SED = 100 J m(-2)). This was 4.9% of the ambient UVR on a horizontal surface. Mean time spent outdoors was 2.3 h day(-1). Differences in children's UVR exposure could be explained in part by activity, where outdoor passive pursuits were associated with higher UVR exposure rates than outdoor active and outdoor travel pursuits. Compared with older children, the activities of younger children, although labeled the same, resulted in different UVR exposures, either as a result of reporting differences or a real difference in UVR exposure patterns. UVR exposure rates were generally higher on weekdays compared with the weekend, confirming the important role of school sun protection and skin cancer prevention programs. High UVR exposure activities included physical education, athletics and lunch break.     

MINIMUM DOSES OF ULTRAVIOLET RADIATION REQUIRED TO INDUCE MURINE SKIN EDEMA and IMMUNOSUPPRESSION ARE DIFFERENT and DEPEND ON THE ULTRAVIOLET EMISSION SPECTRUM OF THE SOURCE*

Many photoimmunological studies have used UV radiation sources that emit nonsolar UV spectral energy and UV doses based on nonimmunological endpoints, e.g. erythema and skin edema. Interpretation of these data has led to misunderstanding when extrapolated to hypothetical effects in humans exposed to solar UV. The purpose of this study was to: (1) establish UV dose response relationships for murine skin edema and immunosuppression, and (2) determine how different UV spectra affect these relationships. Back skin and ear minimum edema doses (MEdD) for Kodacel-filtered FS20 sunlamp UV (290–400nm) were greater than two-fold higher than those for unfiltered FS20 sunlamp UV (250–400nm). Xenon arc solar simulator UV (295–400nm) MEdD were > 10-fold higher than those for unfiltered sunlamp UV. Back skin and ear MEdD differed two- to five-fold between C3H/ HeN, SWR/J and HRA/Skh-1 mice. The minimum immunosuppression doses (MISD) in C3H mice showed similar UV source spectrum dependence. The solar simulator UV MISD was 5.4- and 1.5-fold higher than for unfiltered and Kodacel-filtered sunlamp UV MISD, respectively. Furthermore, MISD were from 3- to 50-fold higher than the MEdD for the three UV sources. The UV bioeffectiveness spectra indicated that UVC energy (250–290nm) contributed 12% and 18%, respectively, of the total skin edema and immunosuppression UV energy. These data demonstrate the variability in UV sensitivity among mouse strains, the significant differences between murine MEdD and MISD and how these differences are influenced by nonsolar regions (below 295 nm) of the UV spectrum.     

Solar UV Exposure of Seafarers along Subtropical and Tropical Shipping Routes

Seafarers working on decks of vessels at low latitudes are exposed to extremely high solar UV radiation. Their risk of developing skin cancer may be enhanced. Solar erythemal UV irradiance and exposure were measured for the first time on merchant vessels going along typical international routes at low latitudes. The measurements taken at horizontal incidence on the observation deck, and on different parts of the seaman (head, shoulder, chest and back) doing typical outdoor work show the highest portion (40–80% of horizontal exposure) incident on the head. 2 years of measurements of solar UV and VIS/NIR irradiance taken on the mast top of the Research Vessel METEOR were added to the data base. Radiative transfer model calculations were performed along all the routes with satellite‐based input data of ozone and aerosol for clear sky health‐effective radiation including vitamin D3 (VD3). Measured data show extremely high noontime UV index values up to 19 with clear sky, and up to 22 due to cloud scattering. Eight hours erythemal exposure values are more than double of typical midlatitude summer values. Based on the results, an algorithm is presented to derive a seafarer's personal erythemal exposure according to his/her personal record of sea service.     

An overview of the ultraviolet index and the skin cancer cases in Brazil

This study relates regional and seasonal UV index (UVI) variations, number of skin cancer cases and population skin-color distribution in Brazil. UVI calculations were performed using the UV Global Atmospheric Model (UVGAME), whose characteristics and validations are provided in thiis article. Health and racial data sets are based on the health and census data collected by Brazilian governmental agencies in the past. The discussion covers cultural customs and details of health and educational campaigns in Brazil. Despite lower UV levels in the South and Southeast regions, the results show a number of nonmelanoma skin cancer (NMSC) cases regions, where the white population is predominant. In general, in the southern regions about 50 new NMSC cases per 100000 inhabitants have been diagnosed each year. These rates decrease almost 40% in the Central-North regions and more than 80% in Northeast region, where miscegenation is common. In addition, the UVI evaluation is extended to other South American sites with singular characteristics, e.g. populous cities located in high altitudes or those affected by the Antarctic ozone hole in the extreme south of the continent.     

UV Exposition During Typical Lifestyle Behavior in an Urban Environment

In this study the personal exposure to solar UV radiation in an urban environment was measured. Lifestyle in an urban environment is characterized by staying indoors during most of the day. Furthermore, the ambient UV radiation is mitigated by shadowing by buildings. The aim of the study was to find out activities which may contribute to UV-induced health risk in a low exposure environment. Exposure was measured during typical outdoor activities: shopping, walking, sitting in a sidewalk café, cycling, sightseeing and at an open-air pool (solar elevation: 10°–70°). Measurements were taken with an optoelectronic device which was fixed on the chest. Besides the UV Index we used the sun burn time (SBT) for risk assessments. Generalization of our results was made by calculating ratios of personal exposure to the ambient UV radiation. UV exposure was by far the highest when our study subject stayed at the swimming pool. The SBT was around 30 min for melano-compromised skin type. For all other activities, except shopping, the SBT range up to 1 h. With respect to photodamage we found that at high solar elevation (>45°) photoprotective measures should be applied for certain activities even within a city.     

Common fluorescent sunlamps are an inappropriate substitute for sunlight

Fluorescent sunlamps are commonly employed as convenient sources in photobiology experiments. The ability of Kodacel to filter photobiologically irrelevant UVC wavelengths has been described. Yet there still remains a major unaddressed issue--the over representation of UVB in the output. The shortest terrestrial solar wavelengths reaching the surface are approximately 295 nm with the 295-320 nm range comprising approximately 4% of the solar UV irradiance. In Kodacel-filtered sunlamps, 47% of the UV output falls in this range. Consequently, in studies designed to understand skin photobiology after solar exposure, the use of these unfiltered sunlamps may result in misleading, or even incorrect conclusions. To demonstrate the importance of using an accurate representation of the UV portion of sunlight, the ability of different ultraviolet radiation (UVR) sources to induce the expression of a reporter gene was assayed. Unfiltered fluorescent sunlamps (FS lamps) induce optimal chloramphenicol acetyltransferase (CAT) activity at apparently low doses (10-20 J/cm2). Filtering the FS lamps with Kodacel raised the delivered dose for optimal CAT activity to 50-60 mJ/cm2. With the more solar-like UVA-340 lamps somewhat lower levels of CAT activities were induced even though the apparent delivered doses were significantly greater than for either the FS or Kodacel-filtered sunlamp (KFS lamps). When DNA from parallel-treated cells was analyzed for photoproduct formation by a radioimmuneassay, it was shown that the induction of CAT activity correlated with the level of induced photoproduct formation regardless of the source employed.     

EVALUATION OF SKIN CANCER RISK RESULTING FROM LONG TERM OCCUPATIONAL EXPOSURE TO RADIATION FROM ULTRAVIOLET LASERS IN THE RANGE FROM 190 TO 400 nm

The relative risk of occupational exposure to radiation from UV lasers was estimated using a mathematical model based on both epidemiological data and animal experiments. Calculations were performed for the 193 nm ArF excimer laser cornea shaping, the 308 nm XeCl excimer laser for coronary angioplasty, and other UV lasers in a laboratory environment. The model included the effects of direct exposure and exposure to scattered radiation. The results show that for the two medical applications the increase in the relative risk is comparable to that of one additional day of sunbathing per year. For subjects exposed to UV lasers in a laboratory setting, the relative risk may increase to a value comparable to that of people with an outdoor profession.     

UV doses of young adults

Since 1986, people have been informed that they get about 80% of their lifetime ultraviolet (UV) dose by the age of 18. This belief originated from the mathematical conclusion that diligent use of sunscreens (sun protection factor 15 or higher) during the first 18 years of life would reduce the lifetime incidence of nonmelanoma skin cancers by 78%. These data were misconstrued to mean that individuals also got about 80% of their lifetime dose of UV by the age of 18 (linear relationship). However, these calculations were based on the incidence of nonmelanoma skin cancers being related to the square of the UV dose. Careful analysis of UV exposure data shows that Americans actually get less than 25% of their lifetime UV dose by the age of 18. This finding also appears to be true worldwide because Australia, UK and The Netherlands report a similar UV exposure pattern. UV-initiated damage early in life can be promoted by subsequent exposures to progress into tumors later in life. For example, the nonmelanoma skin cancer, squamous cell carcinoma, is dependent on the cumulative UV dose. Thus, a better educational approach for reducing skin cancers would be to instruct fair-skinned individuals to protect themselves throughout their lives from being exposed to too much UV radiation.     

Sun Exposure at School

There is strong evidence that sun exposure during childhood and adolescence plays an important role in the etiology of skin cancer, in particular cutaneous melanoma. Between the age of 6 and 18, most children and adolescents will spend around 200 days per year at school and may receive a substantial fraction of their daily total solar ultraviolet radiation (UVR) exposure while at school. This study estimated the average daily erythemally effective dose of 70 grade 8 students from a high school in Townsville during 5 school days in July 1998. Through UV measurements of shade locations at the school and a combination of frequency counts and a questionnaire of grade 8 students, it was possible to determine the fraction of solar UVR reaching under the shade structures during lunch breaks and routine outdoor activities. Also, a routinely operating UV-Biometer provided the annual variation of the daily dose that was used to calculate exposure levels for the 70 students. Our results suggest that up to 47% of the daily total dose fell within the time periods where students were outdoors during school hours. For students not seeking shade structures during the breaks (which usually was the case when involved in sport activities such as basketball or soccer), the average daily dose could have been as high as 14 SED (standard erythemal dose). Using results from the questionnaire of 70 grade 8 students, their average annual dose while at school was 414 SED or 2 SED per school day. However, the distribution of average daily erythemal effective dose per grade 8 student over the whole year showed that on 31% of all school days in 1998, this dose was exceeded. Because most previous attempts to change arguably poor sun-protective behavior of young Australian children and adolescents at school showed little success, one way of decreasing the amount of harmful UVR reaching unprotected skin is the more careful design of shade structures at schools.     

The Injury and Cumulative Effects on Human Skin by UV Exposure from Artificial Fluorescence Emission

The injury and cumulative effects of UV emission from fluorescence lamp were studied. UV intensity from fluorescence lamp was measured, and human skin samples (hips, 10 volunteers) were exposed to low‐dose UV irradiation (three times per week for 13 consecutive weeks). Three groups were examined: control group without UV radiation; low‐dose group with a cumulative dose of 50 J cm^?2 which was equivalent to irradiation of the face during indoor work for 1.5 years; and high‐dose group with 1000 J cm^?2 cumulative dose equivalent to irradiation of the face during outdoor activities for 1 year. Specific indicators were measured before and after UVA irradiation. The findings showed that extending the low‐dose UVA exposure decreased the skin moisture content and increased the transepidermal water loss as well as induced skin color changes (decreased L* value, increased M index). Furthermore, irradiated skin showed an increased thickness of cuticle and epidermis, skin edema, light color and unclear staining collagen fibers in the dermis, and elastic fiber fragmentation. In addition, MMP‐1, p53 and SIRT1 expression was also increased. Long‐term exposure of low‐dose UVA radiation enhanced skin photoaging. The safety of the fluorescent lamp needs our attention.     

INHIBITION OF 12-O-TETRADECANOYLPHORBOL-13-ACETATE-INDUCED TUMOR PROMOTION IN MURINE SKIN BY SYSTEMIC EFFECTS OF ULTRAVIOLET IRRADIATION

Systemic effects of UVB irradiation (280-320 nm) have been shown to prevent subsequent chemical tumorigenesis induced by an initiation-promotion protocol. The present investigation was designed to determine whether initiation or promotion is prevented by UV irradiation. Groups of 25 B6D2F1/J mice received 12 weeks of intermittent dorsal UVB radiation treatments administered before, or 3 weeks after, initiation with a single application of 7,12-dimethylbenz[a]anthracene on the ventral skin. All mice were promoted ventrally with 5 micrograms 12-O-tetradecanoylphorbol-13-acetate (TPA) applied three times weekly throughout the experiment. UV irradiation consisted of five 30-min exposures per week to a bank of 6 Westinghouse FS40 sunlamps. UV irradiation applied before or after initiation resulted in a decrease of 18-16 tumors per group of 25 mice, for a reduction of 61 and 50%, respectively, at 24 weeks after the first TPA treatment. Thus, prevention of tumor development was similar whether the UV influence was present or not during initiation. This finding suggests that the UV prevention of promotion could account for UV inhibition of skin tumors induced by an initiation-promotion regimen. Consistent with this concept, pretreatment of mice with dorsal UVB radiation was found to reduce DNA synthesis after exposure to TPA by 46%, although it did not decrease tritiated benzo[a]pyrene binding to DNA, in ventral epidermis. Thus, UVB irradiation systemically reduced TPA-induced tumor promotion in murine skin.