Melissa Kaplan's
Herp Care Collection
Last updated January 1, 2014

Abstracts on the Adverse Effects of Ultraviolet Radiation (UVR) Exposure on Health

Compiled by Melissa Kaplan


Retinal injury induced by near-ultraviolet radiation in aphakic and pseudophakic monkey eyes. A preliminary report.
Li ZL, Tso MO, Jampol LM, Miller SA, Waxler M. Georgiana Theobald Ophthalmic Pathology Laboratory, Department of Ophthalmology, University of Illinois, Chicago College of Medicine. Retina 1990;10(4):301-14

The effect of repeated exposures to low-intensity, near-ultraviolet (UV) radiation on the retinas of phakic, aphakic, and pseudophakic monkey eyes was studied. Ten eyes (4 aphakic eyes, 3 pseudophakic eyes, and 3 normal phakic eyes) of five rhesus monkeys were used. The near-UV radiation was generated by a high-pressure mercury vapor lamp with a total radiance of 14.43 µW/cm2/sr. Exposure regimens were 5 minutes a day for 10 days, 15 minutes a day for 5 days, or 60 minutes a day for 5 days. The retinas of aphakic and pseudophakic eyes were exposed to a daily dose of more than 0.97 J/cm2, or a total dose of more than 4.9 J/cm2 in 5 days at a retinal irradiance of more than 1.0 µW/cm2. Three of four aphakic eyes and one of three pseudophakic eyes showed clinical and pathologic retinal lesions after radiation. None of the three phakic eyes was damaged. The retinal lesions showed mild opalescent thickening ophthalmoscopically and retinal pigment epithelial staining by fluorescein angiography. Histopathologically, the retinal pigment epithelium was the site of primary injury by near-UV radiation.

Coolwhite fluorescent light mutagenesis is due to avoidable leakage of ultraviolet light
Hartman, P.E; Biggley, W.H. Henrikson, E.Jan 31 1994. Environmental and Molecular Mutagenesis.

Coolwhite fluorescent lamps are mutagenic and lethal to Salmonella. Measurements with an Eppley calibrated linear thermopile and an ultraviolet (UV) intensity meter with Radiometer UVX sensors demonstrate that about 6% of total illuminance of Sylvania and General Electric F15T8 and F15T12 lamps is UV light (below 400 nm). In contrast, corresponding values for F15T8 Philips lamps are 3% UV of which only about 2% is UVB, showing that it is possible to engineer lamps with a low output below 320 nm. The former two brands exhibit much greater mutagenicity and lethal effects than do Philips lamps. Allele-specific colony hybridization coupled with PCR and DNA sequencing demonstrate a striking homology between the spectra of reversions in strain TA2410 (hisG46 uvrB pKM101) and TA2678 (hisG428 uvrB pKM101) induced by coolwhite and by germicidal (UVC) lamps. In hisG46, transitions far outnumber transversions. In his G428, no AT{r_arrowGC transitions are induced; AT{r_arrow}TA transversions and GC{r_arrow}AT transitions are common. Tandem double mutations (TTC, ATC, and CAT) from CCC of hisG46 and GTGT, AAAA and ACAA from GTAA of his G428 are frequent with both light sources, but GTGT predominates only with coolwhite light. We conclude that mutagenic and cell-lethal UV radiations are emitted by some, but not all, prevalent brands of coolwhite fluorescent lamps as often used unshielded in homes today.


The Role of the Cellular Antioxidant Defense in Oxidant Carcinogenesis
Peter Cerutti, Rita Ghosh, Yukiko Oya, and Paul Amstad. Department of Carcinogenesis, Swiss Institute for Experimental Cancer Research, Epalinges/Lausanne, Switzerland. Environ Health Perspect 102(Suppl 10):123-130 (1994)

Oxidant carcinogens interact with multiple cellular targets including membranes, proteins, and nucleic acids. They cause structural damage to DNA and have the potential to mutate cancer-related genes. At the same time, oxidants activate signal transduction pathways and alter the expression of growth- and differentiation-related genes. Indeed, the carcinogenic action of oxidants results from the superposition of these genetic and epigenetic effects. All cells possess elaborate antioxidant defense systems that consist of interacting low and high molecular weight components. Among them, superoxide dismutases (SOD), glutathione peroxidases (GPx), and catalase (CAT) play a central role. Our studies with mouse epidermal cells demonstrate that the balance between several antioxidant enzymes rather than the activity of a single component determines the degree of protection. Unexpectedly, increased levels of Cu,Zn-SOD alone in stable transfectants resulted in sensitization to oxidative chromosomal aberrations and DNA strand breaks. However, a concomitant increase in CAT or GPx in double transfectants corrected or overcorrected the hypersensitivity of the SOD clones depending on the ratios of activities CAT/SOD or GPx/SOD. The cellular antioxidant capacity also affected oxidant induction of the growth-related immediate early protooncogene c-fos. Increases in CAT or SOD reduced the accumulation of c-fos message, albeit for different reasons. The cellular antioxidant defense also affects the action of UVB light (290-320 nm) that represents the most potent carcinogenic wavelength range of the solar spectrum. UVB light is known to exert its action in part through oxidative mechanisms. Increases in CAT and GPx protected mouse epidermal cells from UVB-induced DNA breakage. An increase in GPx enhanced the induction of c-fos by UVB probably because it diminished DNA breaks. DNA breaks appear to exert a long-range effect on chromatin confirmation, which is incompatible with efficient transcription.


Breakthrough of ultraviolet light from various brands of fluorescent lamps: Lethal effects on DNA repair-defective bacteria.
Hartman, P.E; Biggley, W.H. Jan 31 1996, Environmental and Molecular Mutagenesis

In a comparative study of 17 pairs of 15 W fluorescent lamps intended for use in homes and purchased in local stores, we detect over 10-fold differences in UVB + UVC emissions between various lamps. This breakthrough of ultraviolet (UV) light is in part correlated with ability of lamps to kill DNA repair-defective recA{sup {minus}}uvrB{sup {minus}} Salmonella. Relative proficiency of lamps in eliciting photoreactivation of UV-induced DNA lesions also plays a prominent role in the relative rates of bacterial inactivation by emissions from different lamps. Lamps made in Chile, such as Phillips brand lamps and one type of General Electric lamp, produce far less UVB + UVC and fail to kill recA{sup {minus}} uvrB{sup {minus}} bacteria. In contrast, all tested lamps manufactured in the USA, Hungary, and Japan exhibit readily observed deleterious biological effects. When an E. coli recA{sup {minus}} uvrB{sup {minus}} phr{sup {minus}} (photolyase-negative) triple mutant is used for assay, lethal radiations are detected from all lamps, and single-hit exponential inactivation rates rather closely correlate to amount of directly measured UVB + UVC output of each pair of lamps. Although all lamps tested may meet international and Unite States standards for radiation safely, optimal practices in lamp manufacture are clearly capable of decreasing human exposure to indoor UV light. 38 refs., 3 figs., 1 tab.

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Note that the above fluorescent lamps are regular household/office fluorescents, not the ones made for reptiles which are designed to transmit HIGHER levels of UVB that these household/office lamps are.


Ultraviolet irradiation, systemic immunosuppression and skin cancer: role of urocanic acid.
Finlay-Jones JJ, Hart PH. Department of Microbiology and Infectious Diseases, School of Medicine, and Flinders Cancer Centre, Flinders University of South Australia, Adelaide, Australia. Australas J Dermatol 1997 Jun;38 Suppl 1:S7-12

Ultraviolet (UV) radiation, particularly in the UVB region (280-320 nm), is immunosuppressive. This modulation of the immune response to antigens following UV irradiation allows the outgrowth of UV-induced skin cancers. Because UV irradiation penetrates only a few millimetres into the skin, yet can induce not only a local but also a systemic immunosuppression, the transducing mechanisms must be superficially located. Three mechanisms have been put forward, one which identifies epidermal urocanic acid as the photoreceptor, one that identifies DNA, and one that identifies cell membrane lipid peroxidation as initiating immunomodulation. While a number of mechanisms may operate (or cooperate), and do so differentially for local vs systemic suppression, considerable evidence supports urocanic acid as a key photoreceptor for immunosuppression. This review examines the immunomodulatory effects of urocanic acid, as well as its role in facilitating the outgrowth of UV-induced skin cancer.


Risk Assessment for the Harmful Effects of UVB Radiation on the Immunological Resistance to Infectious Diseases
Wim Goettsch, Johan Garssen, Wout Slob, Frank R. de Gruijl, and Henk Van Loveren. Environ Health Perspect 106: 71-77 (February 1998).

Risk assessment comprises four steps: hazard identification, dose-response assessment, exposure assessment, and risk characterization. In this study, the effects of increased ultraviolet B (UVB, 280-315 nm) radiation on immune functions and the immunological resistance to infectious diseases in rats were analyzed according to this strategy. In a parallelogram approach, nonthreshold mathematical methods were used to estimate the risk for the human population after increased exposure to UVB radiation. These data demonstrate, using a worst-case strategy (sensitive individuals, no adaptation), that exposure for approximately 90 min (local noon) at 40°N in July might lead to 50% suppression of specific T-cell mediated responses to Listeria monocytogenes in humans who were not preexposed to UVB (i.e., not adapted). Additionally, a 5% decrease in the thickness of the ozone layer might shorten this exposure time by approximately 2.5%. These data demonstrate that UVB radiation, at doses relevant to outdoor exposure, may affect the specific cellular immune response to Listeria bacteria in humans. Whether this will also lead to a lowered resistance (i.e., increased pathogenic load) in humans is not known, although it was demonstrated that UVB-induced immunosuppression in rats was sufficient to increase the pathogenic load. Epidemiology studies are needed to validate and improve estimates for the potential effects of increased UVB exposure on infectious diseases in humans. Key words : immunosuppression, immune system, Listeria, risk assessment, UVB radiation.


UV-induced changes in the immune response to microbial infections in human subjects and animal models.Norval M, Garssen J, Van Loveren H, el-Ghorr AA. Department of Medical Microbiology, University of Edinburgh Medical School, UK. J Epidemiol 1999 Dec;9(6 Suppl):S84-92

Exposure to UV is a recognised risk factor for skin cancer and it also induces immunosuppression to a variety of antigens encountered following the irradiation. The latter property has been demonstrated in rodent models of infections with the microbial agents including viruses, bacteria, protozoa and helminths. In the majority of cases the severity of the symptoms and the microbial load in the host are increased as a result of the immunomodulation. UV can also affect the pathogenesis of some natural microbial infections of human subjects, such as causing recrudescence of herpes simplex virus and contributing to the oncogenic potential of papillomaviruses. Sufficient data have been generated from the animal models to construct a risk assessment in humans for suppression of microbial immune responses induced by sunlight exposure. This estimation requires verification from epidemiological studies and from further work to assay modulation in human immunity to particular pathogens experienced before and after the UV radiation.


Possible effects of sunlight on human lymphocytes.
Green MH, Petit-Frere C, Clingen PH, Bentham G, Cole J, Arlett CF. MRC Cell Mutation Unit, University of Sussex, Brighton, United Kingdom. J Epidemiol 1999 Dec;9(6 Suppl):S48-57

The human population is exposed to both the ultraviolet A (UVA) and B (UVB) regions of the solar spectrum. UVB induces mainly dipyrimidine photoproducts in DNA by a direct photochemical mechanism, whereas UVA is absorbed by other cellular constituents and induces mainly oxidative damage indirectly. The proportions of the different dipyrimidine photoproducts, and the ratio of dipyrimidine to oxidative damage depend on the exact spectral output of a UV source. Irradiation of human epidermal keratinocytes induces release of cytokines, with cyclobutane pyrimidine dimers playing a significant role in the process. These cytokines may then modulate the activity of cells of the immune system. Freshly isolated human lymphocytes are exquisitely sensitive to UVB irradiation, because of their low deoxyribonucleotide pools. They also have a separate defect in removal of cyclobutane pyrimidine dimers from their DNA. We have observed that frequencies of mutations at the hprt locus in human T-lymphocytes and translocations involving the bcl2 locus in B-lymphocytes appear to be associated with sunlight levels over the period before the blood sample was taken. This may be an indirect cytokine-mediated effect, and may be relevant to the possible link between non-Hodgkin's lymphoma and sunlight. On the other hand, sunlight can have beneficial effects, and may protect against autoimmune diseases including type I diabetes and multiple sclerosis.


Exposure to ultraviolet radiation causes dendritic cells/macrophages to secrete immune-suppressive IL-12p40 homodimers.
Schmitt DA, Ullrich SE. Department of Immunology, University of Texas, M. D. Anderson Cancer Center, and Graduate School of Biomedical Sciences, Houston, TX 77030, USA.. J Immunol 2000 Sep 15;165(6):3162-7

UV-induced immune suppression is a risk factor for sunlight-induced skin cancer. Exposure to UV radiation has been shown to suppress the rejection of highly antigenic UV-induced skin cancers, suppresses delayed and contact hypersensitivity, and depress the ability of dendritic cells to present Ag to T cells. One consequence of UV exposure is altered activation of T cell subsets. APCs from UV-irradiated mice fail to present Ag to Th1 T cells; however, Ag presentation to Th2 T cells is normal. While this has been known for some time, the mechanism behind the preferential suppression of Th1 cell activation has yet to be explained. We tested the hypothesis that this selective impairment of APC function results from altered cytokine production. We found that dendritic cells/macrophages (DC/Mphi) from UV-irradiated mice failed to secrete biologically active IL-12 following in vitro stimulation with LPS. Instead, DC/Mphi isolated from the lymphoid organs of UV-irradiated mice secreted IL-12p40 homodimer, a natural antagonist of biologically active IL-12. Furthermore, when culture supernatants from UV-derived DC/Mphi were added to IL-12-activated T cells, IFN-gamma secretion was totally suppressed, indicating that the IL-12p40 homodimer found in the supernatant fluid was biologically active. We suggest that by suppressing DC/Mphi IL-12p70 secretion while promoting IL-12p40 homodimer secretion, UV exposure preferentially suppress the activation of Th1 cells, thereby suppressing Th-1 cell-driven inflammatory immune reactions.


Broad-spectrum sunscreens offer protection against urocanic acid photoisomerization by artificial ultraviolet radiation in human skin.
van der Molen RG, Out-Luiting C, Driller H, Claas FH, Koerten HK, Mommaas AM. Center for Electron Microscopy, Departments of Dermatology and Immunohaematology and Bloodbank, Leiden University Medical Center, Leiden, The Netherlands. J Invest Dermatol 2000 Sep;115(3):421-6

Cis-urocanic acid (UCA) has been indicated as an important mediator of ultraviolet (UV)-induced immunosuppression. In this study we describe a rapid, noninvasive method for the determination of the protective capacity of various sunscreens against the UV-induced isomerization of trans-UCA into its cis form. For this purpose we applied sunscreens prior to in vivo exposure of human volunteers with single or repeated broadband UVB irradiations of 100 µJ per cm2. We found significant but different levels of protection against UCA photoisomerization by all sunscreens that correlated with the sun protection factor. A comparison of various sunscreens with a sun protection factor of 10, showed that the best protection was offered by the sunscreens (containing organic UV filters or TiO2) with broad absorption spectra. The ability to inhibit cis-UCA formation was not influenced by the penetration characteristics of sunscreens, as determined by application of the sunscreen on quartz glass that was placed on the skin, preventing penetration of sunscreen in the skin. In addition ex vivo UV exposure of human skin was employed to permit other tests of immunomodulation, in this case the mixed epidermal cell lymphocyte reaction. The advantage of this ex vivo method is that there is no need to take biopsies from volunteers. Ex vivo irradiation of human skin with a single dose of 200 µJ per cm2 resulted in similar protection by the sunscreens against cis-UCA formation as in the in vivo system. Furthermore, the mixed epidermal cell lymphocyte reaction data correlated with the cis-UCA findings. We conclude that UCA isomerization is an excellent method to determine sunscreen efficacy and that broad-spectrum sunscreens offer good immunoprotection.


Communications: high dermal mast cell prevalence is a predisposing factor for basal cell carcinoma in humans.
Grimbaldeston MA, Skov L, Baadsgaard O, Skov BG, Marshman G, Finlay-Jones JJ, Hart PH. Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University, Adelaide, Australia. J Invest Dermatol 2000 Aug;115(2):317-20

Ultraviolet B radiation (280-320 nm) can initiate skin cancer as well as suppress the immune system, thereby preventing the rejection of ultraviolet-B-induced tumors. Recently we reported that there was not only a correlation but also a functional link between dermal mast cell prevalence and susceptibility to ultraviolet-B-induced systemic immunosuppression in multiple strains of mice. In this study, we investigated whether increased dermal mast cell prevalence is a significant predisposing factor for basal cell carcinoma development in humans. In 21 Danes with a history of basal cell carcinoma and 20 control subjects of similar age, sex, skin phototype, and recreational sun exposure over the past 12 mo, dermal mast cell prevalence was quantified on non-sun-exposed buttock skin. We investigated this skin site in order to avoid any changes in mast cell prevalence caused by sun exposure and assumed that the prevalence of mast cells in buttock skin correlated with that at sun-exposed sites at critical times in the development of basal cell carcinomas. Patients with a history of basal cell carcinoma had a significantly higher median dermal mast cell prevalence than control subjects (p = 0.01, Mann-Whitney U ). No correlation was observed between dermal mast cell prevalence and age of basal cell carcinoma patients and control subjects. These results suggest that increased dermal mast cell prevalence is a predisposing factor for basal cell carcinoma development in humans. We hypothesize that mast cells function in humans, as in mice, by initiating immunosuppression and thereby allowing a permissive environment for basal cell carcinoma development.


Comparative quantification of IL-1beta, IL-10, IL-10r, TNFalpha and IL-7 mRNA levels in UV-irradiated human skin in vivo.
Brink N, Szamel M, Young AR, Wittern KP, Bergemann J. Beiersdorf AG, Paul Gerson Unna Skin Research Center, Hamburg, Germany. Inflamm Res 2000 Jun;49(6):290-6

OBJECTIVE AND DESIGN: Ultraviolet (UV) exposure induces local immunosuppression and inflammation in human skin. Cytokines are, in part, responsible for these responses. To investigate the effects of UV-induced gene expression at the molecular level we established a sensitive in vivo/ex vivo method for a comparative quantification of cytokines and receptors involved in the local skin immune reactions.

MATERIAL AND METHODS: Specific mRNA levels of human UV-irradiated skin were determined by real time quantification (TaqMan RT-PCR). Highly efficient PCR-reaction conditions were obtained by designing very short PCR-templates (72-87 bp). The most sensitive PCR-conditions were obtained by optimisation of primer and Mn(OAc)2-concentrations, which led to significant PCR signals (C(T)-value) of less than 36 cycles. A strong correlation between PCR efficiency of the internal control (GAPDH) compared to targets (IL-1beta, IL-10, IL-10r, TNFalpha, IL-7) allowed the use of deltadelta C(T)-method to quantify comparable mRNA levels.

RESULTS: Interleukin-1beta (IL-1beta), Interleukin-10 (IL-10), and tumour necrosis factor alpha (TNFalpha) mRNA levels were increased in a time- and dose-dependent manner. Interleukin-1beta induction reached a maximum (approx. 44-fold) 6 h after a UV-dose equivalent to 3 times the minimal erythemal doses just perceptible (MEDjp). Maximal TNFalpha mRNA expression (approx. 14-fold) was also detected 6 h after UV exposure. Interleukin-10 mRNA induction reached a maximum of approximately 14-fold 24 h after UV-irradiation of 3 MEDjp. Time- and dose-dependent changes in Interleukin-7 and Interleukin-10 receptor mRNA levels did not occur after UV-irradiation.

CONCLUSIONS: Time-distinct gene induction of IL-1beta, TNFalpha and IL-1beta is involved in UV-induced immune reactions, but no considerable changes were found for IL-10r or IL-7.


UV-induced immune suppression and sunscreen.
Gil EM, Kim TH. Gyeongsang Institute for Neuroscience, Gyeongsang National University, Chinju, Korea. Photodermatol Photoimmunol Photomed 2000 Jun;16(3):101-10

Sun protection factor (SPF) that measures sunscreen protection against erythema and edema may not be enough to measure a sunscreen's activity against many other biologic reactions induced by ultraviolet radiation (UV). It may be better to evaluate sunscreen efficacy using various tools including immune protection factor (IPF), mutation protection factor (MPF) and protection against photocarcinogenesis. In terms of immune protection, sunscreens protected against UV-induced immune suppression significantly. But protection in some cases was partial and often the IPF of sunscreens were less than the SPF. IPF may differ with various immunological endpoints, and it may be better to use a couple of different assays to measure sunscreen protection more objectively. Sunscreen use protects against most UV-induced non-melanoma skin cancers and actinic keratoses but its activity against melanoma is not clear. More studies with broad-spectrum stable sunscreens and better models for the investigation of malignant melanoma are required.


The neuro-immuno-cutaneous system and ultraviolet radiation.
Misery L. Department of Dermatology, University Hospital, Saint-Etienne, France. Photodermatol Photoimmunol Photomed 2000 Apr;16(2):78-81

Numerous cells are closely associated with cutaneous nerve fibers, which through the action of neuropeptides are able to modulate cellular function. Anatomical and physiological links between immune cells and nerves and other cells in skin are so close that we propose the concept of a neuro-immuno-cutaneous system (NICS). Under the impact of ultraviolet radiation (UVR) virtually all properties of the NICS are modified. UVR induces melanin synthesis and immunosuppression, events in which neuropeptides, especially melanocyte stimulating hormone (MSH) and the calcitonin gene-related peptide CGRP, play a role.


The role of cytokines in UV-induced systemic immune suppression.
Ullrich SE, Schmitt DA. Department of Immunology, The University of Texas, M.D. Anderson Cancer Center, Houston, TX 77030, USA. J Dermatol Sci 2000 Mar;23 Suppl 1:S10-2

Exposure to ultraviolet radiation induces skin cancer. In addition, UV exposure suppresses the immune response. The mechanism by which skin exposure to UV induces systemic immune suppression is not entirely clear, but a role for cytokines secreted by irradiated epidermal cells has been described. Ultimately, these immune regulatory cytokines affect antigen presenting cell function at distant sites. We describe here preliminary findings suggesting that one consequence of UV exposure is an alteration of IL-12 production by lymph node dendritic cells that result in impaired immune function.


Improved protection against solar-simulated radiation-induced immunosuppression by a sunscreen with enhanced ultraviolet A protection.
Fourtanier A, Gueniche A, Compan D, Walker SL, Young AR. Galderma Research & Development, Sophia Antipolis, France. J Invest Dermatol 2000 Apr;114(4):620-7

Ultraviolet radiation-induced immunosuppression is thought to play a part in skin cancer. Several studies have indicated that sunscreens that are designed to protect against erythema failed to give comparable protection against ultraviolet radiation-induced immunosuppression. One possible reason for this discrepancy is inadequate ultraviolet A protection. This study evaluated the level of immunoprotection in mice afforded by two broad-spectrum sunscreens with the same sun protection factor, but with different ultraviolet A protection factors. Both sunscreens contained the same ultraviolet B and ultraviolet A filters, in the same vehicle, but at different concentrations. Solar simulated radiation dose-response curves for erythema, edema, and systemic suppression of contact hypersensitivity were generated and used to derive protection factors for each end-point. The results of three different techniques for determining immune protection factor were compared. A comparison of the two sunscreens showed that the protection factor for erythema in mice was similar to that determined in humans (sun protection factor) but the protection factor for edema in mice was lower. Both sunscreens protected against suppression of contact hypersensitivity but the product with the higher ultraviolet A-protection factor showed significantly greater protection. The three techniques for determining immunoprotection gave very similar results for a given sunscreen, but immune protection factor was always lower than sun protection factor. These data suggest that sun protection factor may not predict the ability of sunscreens to protect the immune system and that a measure of ultraviolet A protection may also be necessary.


Sunscreens, skin photobiology, and skin cancer: the need for UVA protection and evaluation of efficacy.
Gasparro FP. Photobiology Laboratory, Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. Environ Health Perspect 2000 Mar;108 Suppl 1:71-8

Sunscreens are ultraviolet radiation (UVR)-absorbing chemicals that attenuate the amount and nature of UVR reaching viable cells in the skin. They are selected and tested for their ability to prevent erythema. No sunscreen prevents photodamage, as it has been demonstrated that suberythemal doses of UVR cause a variety of molecular changes (including DNA damage) in these cells. Furthermore, the spectrum of UVR reaching viable cells is altered by topically applied sunscreen. In this review, the basic aspects of sunscreens and skin photobiology are reviewed briefly. Although there can be no question concerning the efficacy of sunscreens for the prevention of erythema, questions remain because of the possible cumulative effects of chronic suberythemal doses and the increased exposure of skin cells to longer UVR wavelengths. The current major issue surrounding sunscreens involves their ability to protect skin cells against the effects of UVA radiation. These UVA effects may be direct damage (base oxidations) or effects on the skin immune system, yet there is no uniformly accepted method for the evaluation of UVA protection. This review is focused primarily on the latter topic covering action spectra that implicate the need for UVA protection. In addition, in vivo and in vitro methods proposed for the evaluation of candidate sunscreen formulations of UVA protective ability are reviewed. Finally, revisions in the terminology used to describe the protection afforded by sunscreens are suggested. It is proposed that SPF ("sun" protection factor) be renamed "sunburn" protection factor and that "critical wavelength" be designated "long wave index."


Studies of delayed systemic effects of ultraviolet B radiation (UVR) on the induction of contact hypersensitivity, 2. Evidence that interleukin-10 from UVR-treated epidermis is the critical mediator.
Kurimoto I, Kitazawa T, Streilein JW. Schepens Eye Research Institute and Department of Dermatology, Harvard Medical School, Boston, MA 02114, USA. Immunology 2000 Jan;99(1):134-40

Acute, low-dose ultraviolet B radiation (UVR) alters cutaneous immunity at the local site as well as systemically. Within 2-3 days of UVR exposure, recipient mice lose their capacity to develop contact hypersensitivity (CH) when hapten is painted on unexposed skin. This loss correlates temporally with a functional deficit among dendritic antigen-presenting cells within non-draining lymph nodes and spleen. In the experiments described, the delayed systemic immune deficiency following acute, low-dose UVR exposure was found to be eliminated with neutralizing anti-interleukin-10 (IL-10) antibody. Intracutaneous injection of IL-10 generated a deficiency of systemic immunity as well as a functional deficit among lymph node dendritic cells that was similar to that induced by UVR. The skin itself was found to be the source of the IL-10 responsible for these defects, and epidermis (presumably keratinocytes) rather than mast cells was found to be the source of IL-10 within UVR-exposed skin. The potential relationships are discussed between the delayed systemic immune deficit created by acute, low-dose UVR, and the systemic immune deficits caused by chronic, high-dose UVR and by a single, high-dose UVR exposure.


Mechanisms involved in ultraviolet light-induced immunosuppression.
Beissert S, Schwarz T. Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, Department of Dermatology, University of Munster, Germany. J Investig Dermatol Symp Proc 1999 Sep;4(1):61-4

Ultraviolet light (UV) represents one of the most relevant environmental factors influencing humans, especially with regard to its hazardous health effects, which include premature skin aging, skin cancer, and exacerbation of infectious diseases. Several of these effects are mediated by the immunosuppressive properties of UV. UV can compromise the immune system in several ways, e.g., by affecting the function of antigen-presenting cells, inducing the release of cytokines, and modulating the expression of surface molecules. Recently a link between UV-induced immunosuppression and apoptosis was recognized. In the following, the basic mechanisms underlying UV-induced immunosuppression will be discussed.


Effect of ultraviolet light on the release of neuropeptides and neuroendocrine hormones in the skin: mediators of photodermatitis and cutaneous inflammation.
Scholzen TE, Brzoska T, Kalden DH, O'Reilly F, Armstrong CA, Luger TA, Ansel JC. Department of Dermatology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.. J Investig Dermatol Symp Proc 1999 Sep;4(1):55-60

Ultraviolet (UV) irradiation of the skin causes both inflammation and alterations in the skin immune system. There is increasing experimental evidence that UV-induced skin inflammation is influenced by the sensory nervous system and the neuroendocrine system in the skin. The resulting complex network of cytokines, chemokines, neuropeptides, neuropeptide-degrading enzymes, neurohormones, and other inflammatory mediators mediate photodermatitis and cutaneous inflammation. Neuropeptides such as substance P (SP) and calcitonin gene-related peptide (CGRP) are released from sensory nerves innervating the skin upon UV exposure. In addition, a variety of cells in the skin produce increased neuroendocrine hormones such as proopiomelanocortin (POMC) peptides and their receptors as well as neurotrophins after UV exposure. Neuropeptides and neurohormones are capable of directly or indirectly mediating UV-induced cutaneous neurogenic inflammation by the induction of vasodilatation, plasma extravasation, and augmentation of UV-induced cytokine, chemokine, or cellular adhesion molecule expression required for activation and trafficking of inflammatory cells into the inflamed tissue. Neuropeptides and neurotrophins may also play a role in the repair of cutaneous UV injury. In addition to proinflammatory effects, UV-induced neuropeptides and neurohormones such as CGRP and alpha-melanocyte-stimulating hormone may have immunosuppressive effects in the skin. This review will focus on the role that SP, CGRP, POMC peptides, and their receptors may play in modulating UV-induced inflammation in the skin.

Systemic autoimmunity due to mercury vapor exposure in genetically susceptible mice: dose-response studies.
Warfvinge K, Hansson H & Hultman P. Toxicol Appl Pharmacol 132(2):299-309 (1995)

Six groups of genetically mercury-suspectible female SJL/N (H-2(5)) mice were exposed to mercury vapor at a concentration of 0.3-1.0 mg Hg/m3 air for 0.5-19 hr/day 5 days a week for 10 weeks. The absorbed doses calculated to be between 75 and 2365 ug Hg/week/kg body wt (ug Hg/week/kg). The correlation between the dose and the concentration of Hg in Kidney, spleen, and thymus was significant (p <0.0001; Spearman's rank correlation test). The lowest observed adverse effect level (LOAEL) for serum IgG antinuclear antibodies (ANoA) was 170 ug Hg/week/kg, corresponding to a renal mercury concentration of 4.0+/-0.76 ug Hg/g wet wt. The correlation between the absorbed dose and the ANoA titer was highly significant (p <0,0001; Spearmen's rank correlation test), and all mice were ANoA-positive at a dose of 480 ug Hg/week/kg. High-titer ANoA targeted the nucleolar 34-kDa protein fibrillarin. The LOAEL for B-cell stimulation, measured as an increase in serum IgG2a and IgG1 concentrations, was 360 ug Hg/week/kg, but the increase was fivefold higher and also included IgE at a dose of 690 to 2365 ug Hg/week/kg. The serum Ig concentrations peaked after 2-4 weeks and then slowly declined but, except for IgE, remained significantly increased during the entire exposure time. Glomerular, mesangial IgG immune complex (IC) deposits, accompanied by systemic vessel wall IC deposits, were first detected at a dose of 480 ug Hg/week/kg, The mesangium also showed increased titers of IgM IC deposits and complement factor C3c. The correlation between the absorbed dose, and the individual titer of IgG, IgM, and C3c, was highly significant (p <0.0001; Spearmen's rank correlation test). In conclusion, mercury vapor efficiently induced an autoimmune syndrome in genetically suceptible mice, and the LOAEL for adverse effects varied in the order ANoA < B-cell stimulation < IC deposits. Comparing the body burden of mercury in mice at the LOAEL for autoantibodies with the body burden in populations of occupationally exposed humans suggests that the safety margin may be narrow for genetically suspectible individuals.


Retinal injury induced by near-ultraviolet radiation in aphakic and pseudophakic monkey eyes. A preliminary report.
Li ZL, Tso MO, Jampol LM, Miller SA, Waxler M. Georgiana Theobald Ophthalmic Pathology Laboratory, Department of Ophthalmology, University of Illinois, Chicago College of Medicine. Retina 1990;10(4):301-14

The effect of repeated exposures to low-intensity, near-ultraviolet (UV) radiation on the retinas of phakic, aphakic, and pseudophakic monkey eyes was studied. Ten eyes (4 aphakic eyes, 3 pseudophakic eyes, and 3 normal phakic eyes) of five rhesus monkeys were used. The near-UV radiation was generated by a high-pressure mercury vapor lamp with a total radiance of 14.43 µW/cm2/sr. Exposure regimens were 5 minutes a day for 10 days, 15 minutes a day for 5 days, or 60 minutes a day for 5 days. The retinas of aphakic and pseudophakic eyes were exposed to a daily dose of more than 0.97 J/cm2, or a total dose of more than 4.9 J/cm2 in 5 days at a retinal irradiance of more than 1.0 µW/cm2. Three of four aphakic eyes and one of three pseudophakic eyes showed clinical and pathologic retinal lesions after radiation. None of the three phakic eyes was damaged. The retinal lesions showed mild opalescent thickening ophthalmoscopically and retinal pigment epithelial staining by fluorescein angiography. Histopathologically, the retinal pigment epithelium was the site of primary injury by near-UV radiation.

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Ultraviolet Light: A Hazard to Children, American Academy of Pediatrics, 1999: Broken glass covers of mercury vapor lamps pose a health threat due to the release of mercury vapors; eye and other damage in relation to UVR is also discussed.

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Occupational Health & Safety Hazardous Substance No. 34: Ozone, CAW - TCA, Canada: mercury vapor lamps as source of indoor ozone air pollution, which has many health consequences after short- and long-term exposures.

Mercury Vapor Lamps (Abstracts)

UV radiation induces vitamin A deficiency in skin, From the University of Michigan.

The Two Faces of Immunity: Th1 and Th2, Dennis Blakeslee PhD, JAMA 1998

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National Toxicology Program's Center for Phototoxicology

Dangerous UV Light Snakes Its Way Into the Shade

Cataract Development: It's Cumulative

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