ULTRAVIOLET ENHANCED REACTIVATION OF HERPES SIMPLEX VIRUS INACTIVATED BY DIFFERENT WAVELENGTHS OF UV RADIATION

The degree of ultraviolet enhanced reactivation (UVR) exhibited by mammalian cells when infected with Herpes simplex virus inactivated by different wavelengths of far ultraviolet (UV) radiation was measured. A wavelength dependence for this effect is presented over the wavelength region 238–297 nm. Within the limits of the deviations obtained, the degree of UVR exhibited is similar at each wavelength. This suggests that virus irradiated with different wavelengths of UV radiation received the same type of damage or that cells repaired the different types of viral damage with the same efficiency.     

Exposure to ultraviolet radiation enhances mortality and pathology associated with influenza virus infection in mice

Ultraviolet radiation (UVR) causes systemic immune suppression, decreasing the delayed type and contact hypersensitivity responses in animals and humans and enhancing certain mycobacterial, parasitic and viral infections in mice. This study tests the hypothesis that prior exposure to UVR enhances influenza infections in mice. BALB/c female mice were exposed to 0-8.2 kJ/m2 of UVR. Exposed and unexposed mice were infected intranasally three days later with 150-300 plaque-forming units/mouse (lethal dose (LD)20-LD40) of mouse-adapted Hong Kong Influenza A/68 (H3N2) virus or sham infected with 50 microL Hanks' balanced salt solution/mouse. Mortality from viral infection ranged from 25-50%. UVR exposure increased virus-associated mortality in a dose-dependent manner (up to a two-fold increase at 8.2 kJ/m2). The increased mortality was not associated with bacterial pneumonia. The highest dose of UVR also accelerated the body weight loss and increased the severity and incidence of thymic atrophy associated with influenza infection. However, UVR treatment had little effect on the increase in lung wet weight seen with viral infection, and, to our surprise, did not cause an increase in virus titers in the lung or dissemination of virus. The mice died 5-6 days after infection, too early for adaptive immune responses to have much impact. Also, UVR did not interfere with the development of protective immunity to influenza, as measured by reinfection with a lethal challenge of virus. Also, cells adoptively transferred from UVR or untreated mice were equally protective of recipient mice challenged with a lethal dose of virus. The mice resemble mice succumbing to endotoxin, and influenza infection increased the levels of tumor necrosis factor alpha (TNF-alpha) in bronchoalveolar lavage fluid and serum cortisol levels; however, UVR preexposure did not increase either of these responses to the virus. The results show that UVR increased the morbidity, mortality and pathogenesis of influenza virus in mice without affecting protective immunity to the virus, as measured by resistance to reinfection. The mechanism of enhanced mortality is uncertain, but the data raises concerns that UVR may exacerbate early responses that contribute to the pathogenesis of a primary viral infection.     

HOST CELL REACTIVATION AND UV-ENHANCED REACTIVATION IN SYNCHRONIZED MAMMALIAN CELLS

Abstract— Does host cell reactivation (HCR) or UV-enhanced reactivation (UVER) of UV-irradiated Herpes simplex virus (UV-HSV) vary during the host mammalian cell cycle? The answer could be useful for interpreting UVER and/or the two-component nature of the UV-HSV survival curve. Procedures were developed for infection of mitotically-synchronized CV-1 monkey kidney cells. All virus survival curves determined at different cell cycle stages had two components with similar D₀'s and intercepts of the second components. Thus, no single stage of the host cell cycle was responsible for the second component of the virus survival curve. When the cells were UV-irradiated immediately prior to infection, enhanced survival of UV-HSV occurred for cell irradiation and virus infection initiated during late G₁/early S phase or late S/early G₂ phase but not during early G₁ phase. For infection delayed by 24 h after cell irradiation, UVER was found at all investigated times. These results indicate that: (1) HCR is similar at all stages of the host cell cycle; and (2) the “induction” of UVER is not as rapid for cell-irradiation in early G₁ phase. This latter observation may be one reason why normal, contact-inhibited cells do not express UVER as rapidly as faster growing, less contact-inhibited cells.     

Urokinase activity in corneal fibroblasts may be modulated by DNA damage and secreted proteins

Proteases like urokinase-type plasminogen activator (uPA) play an important role in tumor invasion. Cells derived from ultraviolet radiation (UVR)-induced corneal sarcomas of Monodelphis domestica produce relatively high levels of uPA compared to the untransformed keratocytes suggesting a mechanism for their invasiveness. Because UVR is known to stimulate uPA production in many cell types, UVR exposure may further increase uPA expression in corneal tumor cells, thus enhancing their ability to infiltrate. We investigated control of basal uPA levels and the induction of uPA by UVR in transformed and untransformed corneal keratocytes from Monodelphis. These studies took advantage of the fact that Monodelphis possesses an active photolyase that can be stimulated to remove UVR-induced pyrimidine dimers by exposure to long-wavelength visible photoreactivating light (PRL). Our studies showed that significant induction of uPA occurred in response to 200 J/m2 UVR. This induction was partially blocked by treatment with PRL, indicating that DNA damage, the pyrimidine dimer in particular, played a role in uPA induction. In untransformed cultured corneal fibroblasts, the heparin-binding protein inhibitor, suramin, reduced basal uPA levels, UVR-induced uPA production and cell proliferation. Basic fibroblast growth factor, a heparin-binding growth factor known to be UVR-inducible in mesenchymal cells, stimulated uPA production and cell proliferation; however, anti-bFGF antibodies did not significantly decrease proliferation or basal uPA production. These findings suggested that basal levels of uPA secretion were modulated in response to heparin-binding growth factors and that these growth factors may also have mediated the effect of UVR on uPA levels.     

In vivo EXPOSURE TO ULTRAVIOLET RADIATION ENHANCES PATHOGENIC EFFECTS OF MURINE LEUKEMIA VIRUS, LP-BMS, IN MURINE ACQUIRED IMMUNODEFICIENCY SYNDROME

LP-BM5 murine leukemia virus (MuLV) induces an immunodeficiency syndrome (MAIDS) in C57BL/6 mice which resembles immunological abnormalities observed in early stages of human AIDS. In our study, MAIDS virus-infected mice were exposed to low doses of ultraviolet radiation (UVR) before and after virus inoculation and compared with MAIDS-infected but not UVR-exposed mice. In all tested parameters (blood IgM levels; mitogenic responses to PHA, ConA, LPS and anti-mu; MLR; antigenic response to SRBC; enlargement and histopathologic changes of the spleen) we observed the same trend: changes due to MAIDS infection were more pronounced in the UVR-exposed group than in the unexposed group. Statistically significant differences between these two groups were seen for mitogenic responses at two different time points after virus inoculation. These results demonstrate that in vivo UVR exposure enhances the immunosuppressive effects of a retroviral infection. UVR exposure may affect the progression of AIDS in a similar manner.     

Impact of solar ultraviolet radiation on marine phytoplankton of Patagonia, Argentina

Patagonia area is located in close proximity to the Antarctic ozone "hole" and thus receives enhanced ultraviolet B (UV-B) radiation (280-315 nm) in addition to the normal levels of ultraviolet A (UV-A; 315-400 nm) and photosynthetically available radiation (PAR; 400-700 nm). In marine ecosystems of Patagonia, normal ultraviolet radiation (UVR) levels affect phytoplankton assemblages during the three phases of the annual succession: (1) prebloom season (late summer-fall), (2) bloom season (winter-early spring) and (3) postbloom season (late spring-summer). Small-size cells characterize the pre- and postbloom communities, which have a relatively high photosynthetic inhibition because of high UVR levels during those seasons. During the bloom, characterized by microplankton diatoms, photosynthetic inhibition is low because of the low UVR levels reaching the earth's surface during winter; this community, however, is more sensitive to UV-B when inhibition is normalized by irradiance (i.e. biological weighting functions). In situ studies have shown that UVR significantly affects not only photosynthesis but also the DNA molecule, but these negative effects are rapidly reduced in the water column because of the differential attenuation of solar radiation. UVR also affects photosynthesis versus irradiance (P vs E) parameters of some natural phytoplankton assemblages (i.e. during the pre- but not during the postbloom season). However, there is a significant temporal variability of P vs E parameters, which are influenced by the nutrient status of cells and taxonomic composition; taxonomic composition is in turn associated with the stratification conditions (e.g. wind speed and duration). In Patagonia, wind speed is one of the most important variables that conditions the development of the winter bloom by regulating the depth of the upper mixed layer (UML) and hence the mean irradiance received by cells. Studies on the interactive effects of UVR and mixing show that responses of phytoplankton vary according to the taxonomic composition and cell structure of assemblages; therefore cells use UVR if >90% of the euphotic zone is being mixed. In fact, cell size plays a very important role when estimating the impact of UVR on phytoplankton, with large cells being more sensitive when determining photosynthesis inhibition, whereas small cells are more sensitive to DNA damage. Finally, in long-term experiments, it was determined that UVR can shape the diatom community structure in some assemblages of coastal waters, but it is virtually unknown how these changes affect the trophodynamics of marine systems. Future studies should consider the combined effects of UVR on both phytoplankton and grazers to establish potential changes in biodiversity of the area.     

Potential of Solar UV Radiation for Inactivation of Coronaviridae Family Estimated from Satellite Data

The pandemic COVID‐19 disease affects people dramatically overall the globe by illness and death. Several strategies are applied to restrict the spread of this disease such as lockdown, adequate social distance in different activities, hand disinfection and the use of masks. Potential hazard outdoors comes from released viruses, which may remain in the air for a while and settle down afterward and contaminating surfaces. Solar ultraviolet radiation (UVR) is known to act as a natural environmental virucide. The virucidal effectivity of UVR depends on a first order on the sensitivity of the virus against UVR as well as on the amount of incoming UVR. Here, we present estimates of the potential of solar UVR in inactivating SARS‐CoV‐2 in the environment. This is done by combining DNA‐damaging surface solar UVR retrieved by satellites and the available information on fluence for inactivation of Coronaviridae. Our results show that solar UVR has a high potential to inactivate these viruses, but the degree depends strongly on location and season. In the subtropics (Sao Paulo, 23.5°S), the daily survival fraction is lower than 10^?4 during the whole year, while close at norther latitudes (Reykjavik, 64°N), such a reduction can be found in June and July only.     

ULTRAVIOLET RADIATION INDUCES A CHANGE IN CELL MEMBRANE POTENTIAL in vitro: A POSSIBLE SIGNAL FOR ULTRAVIOLET RADIATION INDUCED ALTERATION IN CELL ACTIVITY

The regulation of a transmembrane ionic gradient, reflected by the cellular membrane potential, has been shown in several cell systems to be involved in the regulation of cell function. This investigation presents evidence that biologically relevant doses of ultraviolet radiation (UVR) will alter the membrane potential of keratinocytes in vitro. Estimation of the relative change in the steady-state membrane potential of the murine keratinocyte cell line PAM 212, the murine myelomonocytic cell line P388D1, and normal human keratinocytes in culture, were made through the use of the lipophilic cationic membrane potential sensitive probe; triphenylmethylphosphonium. Our observations indicate that UVR composed primarily of UVB (280-320 nm) radiation at doses as low as 100 J/m2 can induce a depolarization in the murine cell lines and a hyperpolarization in human keratinocytes. Evidence suggests that this difference in the direction of the membrane potential response reflects a difference in Na+/K+ ATPase activity following UVR. These results suggest a possible mechanism for modulation of keratinocyte activity induced by UVR.     

Dunaliella tertiolecta (Chlorophyta) Avoids Cell Death Under Ultraviolet Radiation By Triggering Alternative Photoprotective Mechanisms

The effect of different ultraviolet radiation (UVR) treatments combining PAR (P), UVA (A) and UVB (B) on the molecular physiology of Dunaliella tertiolecta was studied during 6 days to assess the response to chronic UVR exposure. UVR reduced cell growth but did not cause cell death, as shown by the absence of SYTOX Green labeling and cellular morphology. However, caspase‐like enzymatic activities (CLs), (regarded as cell death proteases), were active even though the cells were not dying. Maximal quantum yield of fluorescence (F_v/F_m) and photosynthetic electron transport rate (ETR) dropped. Decreased nonphotochemical quenching (NPQ) paralleled a drop in xanthophyll cycle de‐epoxidation under UVB. Reactive oxygen species (ROS) and D1 protein accumulation were inversely correlated. PAB exhibited elevated ROS production at earlier times. Once ROS decayed, D1 protein recovered two‐fold compared with P and PA at later stages. Therefore, PsbA gene was still transcribed, suggesting ROS involvement in D1 recovery by its direct effect on mRNA‐translation. We add evidence of an UVB‐induced positive effect on the cells when P is present, providing photoprotection and resilience, by means of D1 repair. This allowed cells to survive. The photoprotective mechanisms described here (which are counterintuitive in principle) conform to an important ecophysiological response regarding light stress acclimation.     

基于杂交链式反应辅助多重信号放大的端粒酶灵敏检测

端粒酶是真核细胞维持端粒长度的关键逆转录酶,其生物活性的高低可以为多种癌症的临床诊断和预后治疗提供有价值的信息.本研究以人宫颈癌细胞(HeLa细胞)裂解液中的端粒酶为研究对象,通过借助杂交链式反应辅助多重信号放大策略,提出了一种新颖、灵敏的检测端粒酶电化学方法.首先将端粒酶的延伸引物自组装在金电极表面,当端粒酶存在时,端粒酶能够催化引物的延伸,产生与发卡环探针H1部分互补的序列,进而引发杂交链式反应,形成由两个发卡环探针(H1和H2)交替杂交而形成的DNA长链.由于H1和H2末端均修饰有生物素,加入链霉亲和素修饰辣根过氧化物酶后,辣根过氧化物酶被被连接到电极表面,催化邻苯二胺氧化生成2,3-二氨基吩嗪,产生显著的电化学信号.实验结果表明,本研究建立的端粒酶电化学检测方法高效、可行,线性范围宽,灵敏度高,可以检测每毫升10个HeLa细胞裂解液中的端粒酶.本方法具有较好的选择性,能有效区分端粒酶和对照蛋白.     

EFFECT OF ULTRAVIOLET RADIATION ON THE ENERGY METABOLISM OF THE CORNEAL EPITHELIUM OF THE RABBIT

The present research was directed at quantifying possible alterations in corneal epithelial metabolic activity secondary to in vivo exposure to ultraviolet radiation (UVR). Microfluorometric energy metabolite assays on microgram (microgram) sized, freeze-dried tissue samples were used as an in vitro means of assessing overall metabolic activity in the epithelium of control rabbit corneas and in the epithelium of UVR-exposed rabbit corneas 2 min after discontinuation of exposure. The specific assays were for glucose, glycogen, adenosine triphosphate (ATP), and phosphocreatine (PCr). The radiant exposures were kept constant at 0.05 J cm-2 for all UVR wavelengths utilized (290, 300, 310 and 360 nm). Experimental UVR exposure conditions served to increase epithelial glucose and glycogen concentrations. Although the epithelial ATP concentrations were unchanged, the epithelial PCr concentrations (a high energy phosphate bond reservoir) decreased as a result of UVR exposure. Overall, the data demonstrate a decrease in corneal epithelial metabolic activity, which may be wavelength-dependent, as a result of UVR exposure. It is suggested that immediate metabolic stress can be responsible for the pattern of epithelial cell loss seen in photokeratitis.     

Opsin Expression in Human Epidermal Skin

Human skin is constantly exposed to solar light containing visible and ultraviolet radiation (UVR), a powerful skin carcinogen. UVR elicits cellular responses in epidermal cells via several mechanisms: direct absorption of short‐wavelength UVR photons by DNA, oxidative damage caused by long‐wavelength UVR, and, as we recently demonstrated, via a retinal‐dependent G protein‐coupled signaling pathway. Because the human epidermis is exposed to a wide range of light wavelengths, we investigated whether opsins, light‐activated receptors that mediate photoreception in the eye, are expressed in epidermal skin to potentially serve as photosensors. Here we show that four opsins—OPN1‐SW, OPN2, OPN3 and OPN5—are expressed in the two major human epidermal cell types, melanocytes and keratinocytes, and the mRNA expression profile of these opsins does not change in response to physiological UVR doses. We detected two OPN3 splice variants present in similar amounts in both cell types and three OPN5 splice isoforms, two of which encode truncated proteins. Notably, OPN2 and OPN3 mRNA were significantly more abundant than other opsins and encoded full‐length proteins. Our results demonstrate that opsins are expressed in epidermal skin cells and suggest that they might initiate light–induced signaling pathways, possibly contributing to UVR phototransduction.     

Response of Growth and Photosynthesis of Emiliania huxleyi to Visible and UV Irradiances under Different Light Regimes

Microalgae are capable of acclimating to changes in light and ultraviolet radiation (UVR, 280–400 nm). However, little is known about how the ecologically important coccolithophore Emiliania huxleyi responds to UVR when acclimated to different light regimes. Here, we grew E. huxleyi under indoor constant light or fluctuating sunlight with or without UVR, and investigated its growth, photosynthetic performance and pigmentation. Under the indoor constant light regime, the specific growth rate (μ) was highest, while fluctuating outdoor solar radiation significantly decreased the growth rate. Addition of UVR further decreased the growth rate. The repair rate of photosystem II (PSII), as reflected in changes in PSII quantum yield, showed an inverse correlation with growth rate. Cells grown under the indoor constant light regime exhibited the lowest repair rate, while cells from the outdoor fluctuating light regimes significantly increased their repair rate. Addition of UVR increased both the repair rate and intracellular UV‐absorbing compounds. This increased repair capability, at the cost of decreased growth rate, persisted after the cells were transferred back to the indoor again, suggesting an enhanced allocation of energy and resources for repair of photosynthetic machinery damage by solar UVR which persisted for a period after transfer from solar UVR.     

THE EFFECTS OF HOST-CELL REACTIVATION ON ASSAY OF U.V.-IRRADIATED HAEMOPHILUS INFLUENZAE TRANSFORMING DNA

Abstract— The host cell reactivation (HCR) mechanism in Haemophilus influenzae cells is inhibited by sub-microgram concentrations of acriflavine (as is already known to be true for Escherichia coli ). Exposure of these cells to similar concentrations of the drug during bacterial transformation increases the apparent ultraviolet light (u.v.) sensitivity of previously irradiated transforming DNA, indicating a repair of this DNA after uptake by the cells under normal conditions. Repair is inhibited by applying acriflavine at any time up to one hour after competent cells contact the irradiated transforming DNA. The fraction of the u.v. damage repaired by HCR is very different for different genetic markers. Those markers which are most u.v. sensitive when assayed in the absence of acriflavine are most poorly repaired, suggesting that this is the reason for their higher sensitivity. For all markers the fraction of the damage repairable by in vitro photoreactivation is approximately constant, and strongly overlaps the damage repairable by HCR. The degree of HCR achieved can be altered by experimental treatment of the H. influenzae DNA prior to transformation. Thus treatment of irradiated DNA with an enzyme from Micrococcus lysodeikticus –known to attack u.v. damaged, but not undamaged DNA–prevents subsequent intracellular repair of the same u.v. lesions whose repair is inhibited by acriflavine. Similarly, partial replacement of the thymine in transforming DNA by 5-bromouracil (BU) strongly inhibits repair of subsequent u.v. damage. As in bacteriophage, the BU effect is relieved if the u.v. exposure occurs in the presence of cysteamine. It is clear that intracellular repair must be considered in interpreting experiments with u.v.-irradiated transforming DNA.     

A microfluidic device based on gravity and electric force driving for flow cytometry and fluorescence activated cell sorting

A novel method based on gravity and electric force driving of cells was developed for flow cytometry and fluorescence activated cell sorting in a microfluidic chip system. In the experiments cells flowed spontaneously under their own gravity in a upright microchip, passed through the detection region and then entered into the sorting electric field one by one at an average velocity of 0.55 mm s(-1) and were fluorescence activated cell sorted (FACS) by a switch-off activation program. In order to study the dynamical and kinematic characteristics of single cells in gravity and electric field of microchannels a physical and numerical module based on Newton's Law of motion was established and optimized. Hydroxylpropylmethyl cellulose (HPMC) was used to minimize cell assembling, sedimentation and adsorption to microchannels. This system was applied to estimate the necrotic and apoptotic effects of ultraviolet (UV) light on HeLa cells by exposing them to UV radiation for 10, 20 or 40 min and the results showed that UV radiation induced membrane damage contributed to the apoptosis and necrosis of HeLa cells.     

IDENTIFICATION OF A TRANSFORMING ras ONCOGENE IN AN ULTRAVIOLET RADIATION-INDUCED CORNEAL TUMOR OF Monodelphis domestica

Chronic exposure of the gray, short-tailed oppossum, Monodelphis domestica to ultraviolet radiation (UVR) induces mesenchymal tumors of the cornea. High molecular weight DNA samples from 6 UVR-induced corneal tumors were assayed for their ability to transform NIH 3T3 cells to tumorigenicity. NIH 3T3 cells transfected with DNA from 5 of the corneal tumors produced 14 tumors in nude mice. Cell lines were established from these tumors. DNA from 13 of 14 tumor cell lines contained repetitive opossum DNA sequences. Southern blot analysis revealed that DNA from 3 of 4 cell lines derived from tumorigenic NIH 3T3 cells transfected with DNA from a single oppossum tumor contained opossum Ki-ras oncogene sequences in addition to the murine Ki-ras gene. Northern blot analysis of mRNA from a mouse tumor cell line containing opossum Ki-ras gene sequences showed mRNA species identical in size to opossum Ki-ras mRNA, as well as murine Ki-ras mRNA species. These results suggest that an activated Ki-ras oncogene was present in one of the original opossum corneal tumors tested. Thus, activation of Ki-ras may play a role in the development of UVR-induced corneal tumors in Monodelphis domestica. Further characterization of ras oncogenes in these opossum tumors may provide information on the molecular mechanisms by which UVR induces corneal tumors in this species.     

Guinea Pig Skin,a Model for Epidermal Cellular and Molecular Changes Induced by UVR in vivo and in vitro: Effects on Mycobacterium bovis Bacillus Calmette–Guérin Vaccination

Previously, we reported that ultraviolet B‐radiation (UVR) suppressed Bacillus Calmette–Guérin (BCG) vaccine‐induced resistance to Mycobacterium tuberculosis in guinea pigs (GP). Herein, we investigated the cellular and molecular changes within the irradiated GP epidermis and the in vivo effect of supernatants from UV‐irradiated (200 J m^?2) epidermal cells (UV‐sup) on M. bovis BCG vaccination. UVR increased the number of nucleated keratinocytes in the skin, but caused a decrease in the proportions of CD25⁺T cells. In the spleen, UVR resulted in a decrease in the proportions of T‐cell subsets including CD25⁺T cells, and major histocompatibility complex (MHC) class II⁺ and CD14⁺ cells. Similarly, significant up‐regulation of several cytokine mRNAs including IL‐10 was also observed. Furthermore, UV‐sup significantly reduced the MHC class II expression in peritoneal cells and reduced T‐cell proliferation to ConA. The proliferation to purified protein derivative (PPD) was restored to normal levels by anti‐IL‐10 antibody. The UV‐sup when injected into BCG‐vaccinated GP significantly diminished the skin test response and T‐cell proliferation to PPD and up‐regulated the expression of IL‐10, IL‐4, IL‐1β and Foxp3 mRNAs in the lymph node or spleen. Thus, whole body UVR induces profound cellular and molecular changes and injection of UV‐sup from epidermal cells mimics the effect of whole body UVR in BCG‐vaccinated GP.     

The effect of the eye's surface topography on the total irradiance of ultraviolet radiation on the inner canthus

Basal cell carcinoma is the most commonly occurring skin cancer in sub tropical climates. The link between ultraviolet radiation (UVR) and basal cell carcinomas (BCC) is strong. Numerous studies have investigated the spatial distribution of BCCs over the head and neck region and the relative UVR dose, with little or no correlation found between the UVR dose and occurrence rates. This is particularly noted in the inner canthus region. The inner canthus' field of view is restricted by the eye brow ridge, eye orbit and the cheek bone. Yet, the occurrence rate here of BCC's when compared to other regions that are more directly exposed to the environment is significantly higher. A possible causal effect for the increase in occurrence rate in this region is the focussed reflection of UVR from the tear film surface associated with the eye not previously considered in earlier studies. This paper investigates the potential for the surface topography of the eye to reflect focussed radiation towards the inner canthus using a ray tracing programme where the analysis is conducted at a cellular level. Defined hot spots, or striations, of increased irradiation were evidenced across the surface of the inner canthus. This increase in irradiation was not observed with macroscopic detectors which also possibly explain why this increased dose has not previously been detected during environmental measurements with large detectors on manikins or humans.     

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.     

Sex as a Risk Factor for Solar Ultraviolet Radiation Exposure?–Dosimetry in Danish Outdoor Workers

Solar ultraviolet radiation (UVR) exposure is a known risk factor for the development of skin cancer. Heterogeneity in solar UVR exposure may explain the diversity in skin cancer incidence between men and women. This, however, has not previously been investigated in Danish outdoor workers using UVR dosimetry. The aim of this study was to evaluate sex differences in solar UVR dosimetry in Danish outdoor workers on working and leisure days. A cross-sectional design was used to collect dosimetry data during the Danish summer season (May to September). Analysis was based on an electronic questionnaire and dosimetry data from 450 outdoor workers (88 women, 362 men). Dosimetry data were reported as standard erythema dose (SED). The daily median SED (Interquartile range) on working days was 1.6 (2.5) in men and 1.5 (2.1) in women while on leisure days it was 0.5 (1.4) in men and 0.6 (1.3) in women. Analysis by multiple linear regression did not show any association between daily median SED and sex on either working or leisure days. In conclusion, solar UVR exposure in Danish outdoor workers did not vary according to sex.