Environmental plastics in the context of UV radiation, climate change, and the Montreal Protocol.

There are close links between solar UV radiation, climate change, and plastic pollution. UV-driven weathering is a key process leading to the degradation of plastics in the environment but also the formation of potentially harmful plastic fragments such as micro- and nanoplastic particles. Estimates of the environmental persistence of plastic pollution, and the formation of fragments, will need to take in account plastic dispersal around the globe, as well as projected UV radiation levels and climate change factors.

Plastics in the environment in the context of UV radiation, climate change and the Montreal Protocol: UNEP Environmental Effects Assessment Panel, Update 2023.

This Assessment Update by the Environmental Effects Assessment Panel (EEAP) of the United Nations Environment Programme (UNEP) considers the interactive effects of solar UV radiation, global warming, and other weathering factors on plastics. The Assessment illustrates the significance of solar UV radiation in decreasing the durability of plastic materials, degradation of plastic debris, formation of micro- and nanoplastic particles and accompanying leaching of potential toxic compounds. Micro- and nanoplastics have been found in all ecosystems, the atmosphere, and in humans. While the potential biological risks are not yet well-established, the widespread and increasing occurrence of plastic pollution is reason for continuing research and monitoring. Plastic debris persists after its intended life in soils, water bodies and the atmosphere as well as in living organisms. To counteract accumulation of plastics in the environment, the lifetime of novel plastics or plastic alternatives should better match the functional life of products, with eventual breakdown releasing harmless substances to the environment.

The adverse consequences of not using sunscreens.

The adverse effects of solar ultraviolet radiation (UVR) on normal skin are well established, especially in those with poorly melanized skin. Clinically, these effects may be classified as acute, such as erythema or chronic such as keratinocyte and melanocyte skin cancers. Apart from skin type genetics, clinical responses to solar UVR are dependent on geophysical (e.g., solar intensity) and behavioural factors. The latter are especially important because they may result in 'solar overload' with unwanted clinical consequences and ever greater burdens to healthcare systems. Correctly used, sunscreens can mitigate the acute and chronic effects of solar UVR exposure. Laboratory studies also show that sunscreens can inhibit the initial molecular and cellular events that are responsible for clinical outcomes. Despite public health campaigns, global trends continue to show increasing incidence of all types of skin cancer. Large-scale epidemiological studies have shown the benefits of sunscreen use in preventing skin cancer, though it is likely that sunscreen use has not been optimal in such studies. It is evident that without substantial changes in sun-seeking behaviour, sunscreen use is a very important part of the defence against the acute and chronic effects of solar exposure. Ideally, sunscreens should be able to provide the level of protection that reduces the risk of skin cancer in susceptible skin types to that observed in heavily melanized skin.

Les effets indésirables des rayons ultraviolets (UVR) du soleil sur une peau saine sont bien établis, en particulier chez les personnes dont la peau est faiblement concentrée en mélanine. Sur le plan clinique, ces effets peuvent être classés comme aigus, comme un érythème, ou chroniques, comme des cancers de la peau kératinocytaires et mélanocytaires. Outre la génétique du type de peau, les réponses cliniques aux UVR du soleil dépendent de facteurs géophysiques (par exemple, intensité du soleil) et comportementaux. Ces réponses sont particulièrement importantes, car elles peuvent entraîner un « trop-plein de soleil ¼ avec des conséquences cliniques indésirables et des charges de plus en plus importantes pour les systèmes de santé. Utilisés correctement, les protections solaires peuvent atténuer les effets aigus et chroniques de l'exposition aux UV du soleil. Des études en laboratoire montrent également que les protections solaires peuvent inhiber les événements moléculaires et cellulaires initiaux, qui sont responsables des effets cliniques. Malgré les campagnes de santé publique, les tendances mondiales continuent de montrer une incidence croissante de tous les types de cancer de la peau. Des études épidémiologiques à grande échelle ont montré les bénéfices de l'utilisation d'une protection solaire dans la prévention du cancer de la peau, même s'il est probable que l'utilisation d'une protection solaire n'a pas été optimale dans ces études. Il est évident que, sans changements substantiels du comportement d'exposition au soleil, l'utilisation d'une protection solaire est un aspect très important de la défense contre les effets aigus et chroniques de l'exposition au soleil. Idéalement, les protections solaires devraient pouvoir offrir aux types de peau sensibles le niveau de protection qui réduit le risque de cancer de la peau observé pour les peaux fortement concentrées en mélanine.

Innovative digital solution supporting sun protection and vitamin D synthesis by using satellite-based monitoring of solar radiation.

Public health campaigns advise minimising UV radiation (UVR) exposure to prevent skin cancer and precancer, e.g. actinic keratosis (AK). A 3-day clinical field study, in Brazil, was performed to evaluate the mobile app Sun4Health® by siHealth Ltd. The app performs real-time monitoring of both erythemal and vitamin D-effective solar radiation doses using satellite data, enabling personalised recommendations on optimal sun exposure time and sunscreen use. When coupled to a wearable device, the app also provides body-site specific recommendations ("3D" version). 59 healthy volunteers were randomised into 3 groups, each given a different app providing: (1) ultraviolet index only (control app), (2) personalised recommendations and sun overexposure alerts (Sun4Health® app), (3) as (2) but connected via Bluetooth to a wearable device to monitor sun exposure in 3D (Sun4Health®-3D app). Participants were offered sunscreens (SPF 30 and 50) to use at their discretion. Erythema, quantified by reflectance spectroscopy, was assessed daily in the mornings and evenings on six body sites. Serum vitamin D (25(OH)D3) was measured before and after the study. Mean increase of erythema (Mexameter® units ± SD) of all exposed body sites combined over 3 days showed 55.76 ± 47.47 for group 1, 40.27 ± 37.91 for group 2 and 37.12 ± 30.69 for group 3 (p < 0.05 for all groups). Mean increase of serum 25(OH)D3 (nmol/l ± SD) showed 1.32 ± 36.49 for group 1, 6.38 ± 21.19 for group 2 and 18.68 ± 35.45 for group 3 (p > 0.05 for all groups). The results show that the Sun4Health® app is safe to use and can modify behaviour to reduce skin erythema (sunburn) yet not decreasing vitamin D status.

Perspectives on Cyclobutane Pyrimidine Dimers-Rise of the Dark Dimers.

Some early reports demonstrate that levels of cyclobutane pyrimidine dimers (CPD) may increase after UVR exposure had ended, although these observations were treated as artifacts. More recently, it has been shown unequivocally that CPD formation does occur post-irradiation, with maximal levels occurring after about 2-3 h. These lesions have been termed "dark CPD" (dCPD). Subsequent studies have confirmed their presence in vitro, in mouse models and in human skin in vivo. Melanin carbonyls have a role in the formation of dCPD, but they have also been observed in amelanotic systems, indicating other, unknown process(es) exist. In both cases, the formation of dCPD can be prevented by the presence of certain antioxidants. We lack data on the spectral dependence of dCPD, but it is unlikely to be the same as for incident CPD (iCPD), which are formed only during irradiation. There is evidence that iCPD and dCPD may have different repair kinetics, although this remains to be elucidated. It is also unknown whether iCPD and dCPD have different biological properties. The formation of dCPD in human skin in vivo has implications for post solar exposure photoprotection, and skin carcinogenesis, with a need for this to be investigated further.

A new visible light absorbing organic filter offers superior protection against pigmentation by wavelengths at the UVR-visible boundary region.

Skin pigmentation by solar ultraviolet radiation (UVR; ~295-400 nm) is well established. More recently, visible light (VL; 400-740 nm) has been shown to induce rapid pigmentation. Such pigmentation is thought to be caused by oxidative stress, which has associations with skin cancer and photoageing. However, the UVR-VL boundary region has been less well studied. The lower back of healthy Fitzpatrick skin type II-IV individuals was irradiated with increasing doses of narrow-band 385 nm and 405 nm radiation. Pigmentation change was measured immediately, 6 h and 24 h post-irradiation using two reflectance spectroscopy devices and visual grading. Pigmentation was dose-dependently increased in all skin types and time points for both spectra. Two sunscreens, both labelled SPF 15 and UVA protective in the EU and USA (but with different Boots star rating in the UK, 2* vs 5*) were compared. Their formulations were the same apart from the addition of a new organic filter bis-(diethylaminohydroxybenzoyl benzoyl) piperazine (BDBP) that absorbs between 350 and 425 nm. The product that lacked BDBP provided minimal protection against pigmentation, but its addition provided almost complete protection. This demonstrates the needs to improve photoprotection at the UVR-visible border and for sunscreens to act as neutral density filters.

A revised action spectrum for vitamin D synthesis by suberythemal UV radiation exposure in humans in vivo.

Action spectra are important biological weighting functions for risk/benefit analyses of ultraviolet (UV) radiation (UVR) exposure. One important human benefit of exposure to terrestrial solar UVB radiation (∼295 to 315 nm) is the cutaneous synthesis of vitamin D3 that is initiated by the photoconversion of 7-dehydrocholesterol to previtamin D3 An action spectrum for this process that is followed by other nonphotochemical steps to achieve biologically active vitamin D3 has been established from ex vivo data and is widely used, although its validity has been questioned. We tested this action spectrum in vivo by full- or partial-body suberythemal irradiation of 75 healthy young volunteers with five different polychromatic UVR spectra on five serial occasions. Serum 25-hydroxyvitamin D3 [25(OH)D3] levels, as the most accurate measure of vitamin D3 status, were assessed before, during, and after the exposures. These were then used to generate linear dose-response curves that were different for each UVR spectrum. It was established that the previtamin D3 action spectrum was not valid when related to the serum 25(OH)D3 levels, as weighting the UVR doses with this action spectrum did not result in a common regression line unless it was adjusted by a blue shift, with 5 nm giving the best fit. Such a blue shift is in accord with the published in vitro action spectra for vitamin D3 synthesis. Thus, calculations regarding the risk (typically erythema) versus the benefit of exposure to solar UVR based on the ex vivo previtamin D3 action spectrum require revision.

Physical Determinants of Vitamin D Photosynthesis: A Review.

Vitamin D synthesis by exposure of skin to solar ultraviolet radiation (UVR) provides the majority of this hormone that is essential for bone development and maintenance but may be important for many other health outcomes. This process, which is the only well-established benefit of solar UVR exposure, depends on many factors including genetics, age, health, and behavior. However, the most important factor is the quantity and quality of UVR reaching the skin. Vitamin D synthesis specifically requires ultraviolet B (UVB) radiation that is the minority component (<5%) of solar UVR. This waveband is also the most important for the adverse effects of solar exposure. The most obvious of which is sunburn (erythema), but UVB is also the main cause of DNA damage to the skin that is a prerequisite for most skin cancers. UVB at the Earth's surface depends on many physical and temporal factors such as latitude, altitude, season, and weather. Personal, cultural, and behavioral factors are also important. These include skin melanin, clothing, body surface area exposed, holiday habits, and sunscreen use. There is considerable disagreement in the literature about the role of some of these factors, possibly because some studies have been done by researchers with little understanding of photobiology. It can be argued that vitamin D supplementation obviates the need for solar exposure, but many studies have shown little benefit from this approach for a wide range of health outcomes. There is also increasing evidence that such exposure offers health benefits independently of vitamin D: the most important of which is blood-pressure reduction. In any case, public health advice must optimize risk versus benefit for solar exposure. It is fortunate that the individual UVB doses necessary for maintaining optimal vitamin D status are lower than those for sunburn, irrespective of skin melanin. © 2020 The Authors. JBMR Plus published by Wiley Periodicals LLC. on behalf of American Society for Bone and Mineral Research.

Dark cyclobutane pyrimidine dimers are formed in the epidermis of Fitzpatrick skin types I/II and VI in vivo after exposure to solar-simulated radiation.

INTRODUCTION: Unlike "light" cylobutane pyrimidine dimers (CPD) formed during ultraviolet radiation (UVR) exposure, dark CPD (dCPD) are formed afterwards. Studies have attributed this to delayed melanin sensitization. There are no data on the role of melanin in dCPD formation in human skin. METHODS AND RESULTS: Volunteers of Fitzpatrick skin types (FST I/II vs. VI) were exposed to erythemally equivalent doses of solar simulated radiation. CPD were assessed by semi-quantitative immunostaining in whole epidermis and in three epidermal zones, and quantitative HPLC-MS/MS (whole epidermis) at different times post-exposure up to 24 hr. A CPD peak that appeared at 1-2 hr post-exposure in whole epidermis measurements, in all skin types, demonstrated dCPD. However, both dCPD and light CPD were absent in the basal layer of FST VI with the greatest melanin concentration. Modelling the whole epidermis data showed no differences between the repair kinetics of FST I/II and VI. DISCUSSION: Melanin may be a sensitizer or "sunscreen" for dCPD depending on its location and concentration. Previous CPD repair studies in human skin have assumed peak CPD immediately after UVR exposure and so have overestimated total repair.

Nanomaterials fusing with the skin: Alpha-tocopherol phosphate delivery into the viable epidermis to protect against ultraviolet radiation damage.

Vitamin E (alpha tocopherol, α-T) is an important skin antioxidant, but its penetration into the viable epidermis, where it acts, is very limited. This study investigated if phosphorylating α-tocopherol (α-TP) to form a provitamin, improved its interactions with skin, its passage into the tissue, and thus its ability to protect the skin from ultraviolet radiation (UVR) damage. At pH 7.4, when the α-TPO4-1 microspecies predominated in solution, dynamic light scattering measurements showed that α-TP formed nanoaggregates with a median hydrodynamic diameter of 9 nm (Critical aggregation constant, CAC, - 4.2 mM). At 9.0 when the α-TPO4-2 microspecies predominated there was no aggregation. The passage of α-TP nanoaggregates through regenerated cellulose membranes was significantly slower than the α-TP monomers (at pH 9) suggesting that aggregation slowed diffusion. However, a lotion formulation containing the nanoaggregates delivered more α-TP into the skin compared to the formulation containing the monomers. In addition, the nanosized α-TP aggregates delivered 8-fold more active into the stratum corneum (SC) (252.2 µg/cm2 vs 29.5 µg/cm2) and 4 fold more active into the epidermis (85.1 µg/cm2 vs 19 µg/cm2, respectively, p < 0.05) compared to α-T. Langmuir subphase injection studies at pH 7.4 (surface pressure 10 mN m-1) showed that the α-TP nanoaggregates more readily fused with the SC compared to the monomers and the membrane compression studies demonstrated that α-TP fluidised the SC lipids. Together the fusion with the SC and its fluidisation were proposed as the causes of the better α-TP penetration into the skin, which enhanced potential of α-TP to protect from UVR-induced skin damage compared to α-T.

Insufficient Sun Exposure Has Become a Real Public Health Problem.

This article aims to alert the medical community and public health authorities to accumulating evidence on health benefits from sun exposure, which suggests that insufficient sun exposure is a significant public health problem. Studies in the past decade indicate that insufficient sun exposure may be responsible for 340,000 deaths in the United States and 480,000 deaths in Europe per year, and an increased incidence of breast cancer, colorectal cancer, hypertension, cardiovascular disease, metabolic syndrome, multiple sclerosis, Alzheimer's disease, autism, asthma, type 1 diabetes and myopia. Vitamin D has long been considered the principal mediator of beneficial effects of sun exposure. However, oral vitamin D supplementation has not been convincingly shown to prevent the above conditions; thus, serum 25(OH)D as an indicator of vitamin D status may be a proxy for and not a mediator of beneficial effects of sun exposure. New candidate mechanisms include the release of nitric oxide from the skin and direct effects of ultraviolet radiation (UVR) on peripheral blood cells. Collectively, this evidence indicates it would be wise for people living outside the tropics to ensure they expose their skin sufficiently to the sun. To minimize the harms of excessive sun exposure, great care must be taken to avoid sunburn, and sun exposure during high ambient UVR seasons should be obtained incrementally at not more than 5-30 min a day (depending on skin type and UV index), in season-appropriate clothing and with eyes closed or protected by sunglasses that filter UVR.

The UV/Visible Radiation Boundary Region (385-405 nm) Damages Skin Cells and Induces "dark" Cyclobutane Pyrimidine Dimers in Human Skin in vivo.

The adverse effects of terrestrial solar ultraviolet radiation (UVR) (~295-400 nm) on the skin are well documented, especially in the UVB region (~295-320 nm). The effects of very long-wave UVA (>380 nm) and visible radiation (≥400 nm) are much less known. Sunscreens have been beneficial in inhibiting a wide range of photodamage, however most formulations provide very little protection in the long wave UVA region (380-400 nm) and almost none from shortwave visible wavelengths (400-420 nm). We demonstrate photodamage in this region for a number of different endpoints including cell viability, DNA damage (delayed cyclobutane pyrimidine dimers), differential gene expression (for genes associated with inflammation, oxidative stress and photoageing) and induction of oxidizing species in vitro in HaCaT keratinocytes and in vivo in human volunteers. This work has implications for phototherapy and photoprotection.

Sub-optimal Application of a High SPF Sunscreen Prevents Epidermal DNA Damage in Vivo.

The cyclobutane pyrimidine dimer (CPD) is a potentially mutagenic DNA photolesion that is the basis of most skin cancers. There are no data on DNA protection by sunscreens under typical conditions of use. The study aim was to determine such protection, in phototypes I/II, with representative sunscreen-user application. A very high SPF formulation was applied at 0.75, 1.3 and 2.0 mg/cm2. Unprotected control skin was exposed to 4 standard erythema doses (SED) of solar simulated UVR, and sunscreen-treated sites to 30 SED. Holiday behaviour was also simulated by UVR exposure for 5 consecutive days. Control skin received 1 SED daily, and sunscreen-treated sites received 15 (all 3 application thicknesses) or 30 (2.0 mg/cm2) SED daily. CPD were assessed by quantitative HPLC-tandem mass spectrometry (HPLC-MS/MS) and semi-quantitative immunostaining. In comparison with unprotected control sites, sunscreen significantly (p ≤ 0.001-0.05) reduced DNA damage at 1.3 and 2.0 mg/cm2 in all cases. However, reduction with typical sunscreen use (0.75 mg/cm2) was non-significant, with the exception of HPLC-MS/MS data for the 5-day study (p <0.001). Overall, these results support sunscreen use as a strategy to reduce skin cancer, and demonstrate that public health messages must stress better sunscreen application to get maximal benefit.

Diffuse Reflectance Spectroscopy as a Reliable Means of Comparing Ultraviolet Radiation-induced Erythema in Extreme Skin Colors.

Erythema is widely considered an indicator of skin cancer susceptibility, but assessments are challenging in black skin because melanin can mask erythema under traditional visual and advanced objective Commission Internationale de l'Eclairage (CIE) L*a*b* assessments. Using spectral measurements (400-700 nm) from a spectrophotometer, an algorithm was developed to measure erythema in white Caucasians (n = 9) and black West Africans (n = 11) 19-24 h postsolar simulated radiation (SSR) exposures to the volar forearm. The derived spectrum achieved showed a strong maximum peak for hemoglobin at 580 nm and a linear slope between 650 and 700 nm for melanin absorption, as reported by other authors. Absorption by hemoglobin at 580 nm was used as a proxy for erythema, and melanin was quantified between 650 and 700 nm. Our algorithm corrected the erythema measurements for stray specular (mirror-like) reflection and the melanin-masking effect. A linear relationship between SSR exposure and erythema was evident (p < 0.0001 for white and black skin), and white skin is 8.4 times more responsive to SSR compared to black skin. The prediction of ultraviolet radiation sensitivity is vital in both clinical and investigative dermatology especially in the determination of starting phototherapy doses. Our methodology allows for the accurate assessment of erythema independent of constitutive pigmentation.

Melanin distribution in human epidermis affords localized protection against DNA photodamage and concurs with skin cancer incidence difference in extreme phototypes.

Epidermal DNA damage, especially to the basal layer, is an established cause of keratinocyte cancers (KCs). Large differences in KC incidence (20- to 60-fold) between white and black populations are largely attributable to epidermal melanin photoprotection in the latter. The cyclobutane pyrimidine dimer (CPD) is the most mutagenic DNA photolesion; however, most studies suggest that melanin photoprotection against CPD is modest and cannot explain the considerable skin color-based differences in KC incidence. Along with melanin quantity, solar-simulated radiation-induced CPD assessed immediately postexposure in the overall epidermis and within 3 epidermal zones was compared in black West Africans and fair Europeans. Melanin in black skin protected against CPD by 8.0-fold in the overall epidermis and by 59.0-, 16.5-, and 5.0-fold in the basal, middle, and upper epidermis, respectively. Protection was related to the distribution of melanin, which was most concentrated in the basal layer of black skin. These results may explain, at least in part, the considerable skin color differences in KC incidence. These data suggest that a DNA protection factor of at least 60 is necessary in sunscreens to reduce white skin KC incidence to a level that is comparable with that of black skin.-Fajuyigbe, D., Lwin, S. M., Diffey, B. L., Baker, R., Tobin, D. J., Sarkany, R. P. E., Young, A. R. Melanin distribution in human epidermis affords localized protection against DNA photodamage and concurs with skin cancer incidence difference in extreme phototypes.

Vitamin E inhibits the UVAI induction of "light" and "dark" cyclobutane pyrimidine dimers, and oxidatively generated DNA damage, in keratinocytes.

Solar ultraviolet radiation (UVR)-induced DNA damage has acute, and long-term adverse effects in the skin. This damage arises directly by absorption of UVR, and indirectly via photosensitization reactions. The aim of the present study was to assess the effects of vitamin E on UVAI-induced DNA damage in keratinocytes in vitro. Incubation with vitamin E before UVAI exposure decreased the formation of oxidized purines (with a decrease in intracellular oxidizing species), and cyclobutane pyrimidine dimers (CPD). A possible sunscreening effect was excluded when similar results were obtained following vitamin E addition after UVAI exposure. Our data showed that DNA damage by UVA-induced photosensitization reactions can be inhibited by the introduction of vitamin E either pre- or post-irradiation, for both oxidized purines and CPD (including so-called "dark" CPDs). These data validate the evidence that some CPD are induced by UVAI initially via photosensitization, and some via chemoexcitation, and support the evidence that vitamin E can intervene in this pathway to prevent CPD formation in keratinocytes. We propose the inclusion of similar agents into topical sunscreens and aftersun preparations which, for the latter in particular, represents a means to mitigate on-going DNA damage formation, even after sun exposure has ended.

Mycosporine-Like Amino Acids for Skin Photoprotection.

BACKGROUND: Excessive human exposure to solar ultraviolet radiation (UVR) continues to be a major public health concern, with skin cancer rates increasing year on year. The major protective measure is the use of synthetic UVR filters formulated into sunscreens, but there is a growing concern that some of these chemicals cause damage to delicate marine ecosystems. One alternative is the use of biocompatible mycosporine-like amino acids (MAA), which occur naturally in a wide range of marine species. Their role within nature is mainly thought to be photoprotective. However, their potential for human photoprotection is largely understudied. OBJECTIVE: To review the role of MAA in nature and assess their potential as natural sunscreens for human skin photoprotection. METHOD: A literature review of all relevant papers was conducted. CONCLUSION: MAA are natural photostable compounds that are thought to offer photoprotection to marine species. Initially thought of as protective based on their absorption properties in the solar UVR spectrum, it is clear that MAA are multifunctional photoprotective compounds acting as chemical and biological anti-oxidants. This suggests that MAA may offer a novel eco-friendly approach to human skin photoprotection. Most studies have been carried out in vitro and current data strongly suggest that MAA have potential for development as natural biocompatible sunscreens that protect against a diverse range of solar UVR induced adverse effects on human health.

The acute effects of ultraviolet radiation on the blood transcriptome are independent of plasma 25OHD3.

The molecular basis of many health outcomes attributed to solar ultraviolet radiation (UVR) is unknown. We tested the hypothesis that they may originate from transcriptional changes in blood cells. This was determined by assessing the effect of fluorescent solar simulated radiation (FSSR) on the transcriptional profile of peripheral blood pre- and 6h, 24h and 48h post-exposure in nine healthy volunteers. Expression of 20 genes was down-regulated and one was up-regulated at 6h after FSSR. All recovered to baseline expression at 24h or 48h. These genes have been associated with immune regulation, cancer and blood pressure; health effects attributed to vitamin D via solar UVR exposure. Plasma 25-hydroxyvitamin D3 [25OHD3] levels increased over time after FSSR and were maximal at 48h. The increase was more pronounced in participants with low basal 25OHD3 levels. Mediation analyses suggested that changes in gene expression due to FSSR were independent of 25OHD3 and blood cell subpopulations.

ASTHMA - comparing the impact of vitamin D versus UVR on clinical and immune parameters.

The incidence of asthma has increased markedly since the 1960s and is currently estimated to affect more than 300 million individuals worldwide. A number of environmental factors are implicated in asthma pathogenesis, one of which is vitamin D. Vitamin D deficiency is a global health concern and has increased in parallel with asthma incidence. Epidemiological studies report associations between low vitamin D status, assessed as circulating levels of 25-hydroxyvitamin D, with asthma incidence, severity, exacerbations and responses to treatment. This has led to clinical studies to test whether increasing the levels of vitamin D improves asthma management. Despite being highly variable in dosing regimens, design and outcomes, meta-analyses suggest overall positive outcomes with respect to reduced asthma exacerbations and steroid requirements. The primary mechanism for increasing vitamin D levels in the body is through exposure of the skin to the ultraviolet B (UVB) component of ultraviolet radiation (UVR), most commonly from sun exposure. However, only a limited number of studies investigating the impact of UVR on the asthmatic response have been performed; these generally report on the impact of latitude as a surrogate of sun exposure, or address this in animal models. To the best of our knowledge no comprehensive trials to assess the impact of UVB radiation on asthma outcomes have been performed. Within this review we discuss observational and clinical studies in this field, and innate and adaptive immune mechanisms through which UVR and vitamin D may impact respiratory health, and asthma. We highlight the heterogeneity of asthmatic disease, which is likely to impact upon the efficacy of interventional studies, and briefly overview more recent findings relating to the impact of vitamin D/UVR on the development of asthma.