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PubMed1983

Associations among cataract prevalence, sunlight hours, and altitude in the Himalayas.

The relationship between cataract prevalence, altitude, and sunlight hours was investigated in a large national probability sample survey of 105 sites in the Himalayan kingdom of Nepal, December 1980 through April 1981. Cataract of senile or unknown etiology was diagnosed by ophthalmologists in 873 of 30,565 full-time life-long residents of survey sites. Simultaneously, the altitude of sites was measured using a standard mountain altimeter. Seasonally adjusted average daily duration of sunlight exposure for each site was calculated by a method which took into account latitude and obstructions along the skyline. Age- and sex-standardized cataract prevalence was 2.7 times higher in sites at an altitude of 185 meters or less than in sites over 1000 meters. Cataract prevalence was negatively correlated with altitude (r = -0.533, p less than 0.0001). However, a positive correlation between cataract prevalence and sunlight was observed (r = 0.563, p less than 0.0001). Sites with an average of 12 hours of sunlight exposure had 3.8 times as much cataract as sites with an average of only seven hours of exposure. Sunlight was blocked from reaching certain high altitude sites by tall neighboring mountains.

Adolescent↗
PubMed1996

Sunlight, cholesterol and coronary heart disease.

We investigated the relationship between geography and incidence of coronary heart disease, looking at deficiency of sunlight and thus of vitamin D as a factor that might influence susceptibility and thus disease incidence. Sunlight deficiency could increase blood cholesterol by allowing squalene metabolism to progress to cholesterol synthesis rather than to vitamin D synthesis as would occur with greater amounts of sunlight exposure, and the increased concentration of blood cholesterol during the winter months, confirmed in this study, may well be due to reduced sunlight exposure. We show evidence that outdoor activity (gardening) is associated with a lower concentration of blood cholesterol in the summer but not in the winter. We suggest that the geographical variation of coronary heart disease is not specific, but is seen in other diseases and sunlight influences susceptibility to a number of chronic diseases, of which coronary heart disease is one.

Cholesterol↗
PubMed2002

Sunlight-induced DNA damage in human mononuclear cells.

In this study of 301 blood samples from 21 subjects, we found markedly higher levels of DNA damage (nonpyrimidine dimer types) in the summer than in the winter detected by single-cell gel electrophoresis. The level of DNA damage was influenced by the average daily influx of sunlight < 50 days prior to blood sampling. The 3 and 6 day periods before sampling influenced DNA damage the most. The importance of sunlight was further emphasized by a positive association of the DNA damage level to the amount of time the subjects had spent in the sun over a 3 day period prior to the sampling. The effect of sunlight was comparable to the interindividual variation, indicating that sunlight exposure and the individual's background were the two most important determinants for the basal level of DNA damage. Influence of other lifestyle factors such as exercise, intake of foods, infections, and age could not be detected. Our results suggest that sunlight penetrates the outer layer of the human epidermis and damages the DNA in mononuclear cells circulating in the vessels of the skin.

Adult↗
PubMed1993

Sunlight, keratotic skin lesions and skin cancer in renal transplant recipients.

In a retrospective follow-up study, 36 renal transplant recipients with, and 101 without, skin cancer, who had received their first transplant before January 1981 and who were still alive with a functioning graft on 1 August 1989, were assessed to determine the risk of non-melanoma skin cancer in relation to exposure to sunlight during childhood and adolescence. The contribution of the number of keratotic skin lesions to the skin cancer risk was also assessed. The estimated relative risks (odds ratios) of skin cancer in relation to exposure to sunlight and the presence of keratotic skin lesions were calculated by maximum likelihood estimation in a logistic model. The majority of skin cancers and keratotic skin lesions were confined to sun-exposed skin. After adjustment for possible confounding variables, the odds ratios of skin cancer for moderate and high cumulative life-time exposure to sunlight, respectively, compared with low exposure, were 2.4 (95% confidence interval [CI] 0.64-9.3) and 47.6 (95% CI 5.4-418). Exposure to sunlight before the age of 30 contributed more to the risk of developing skin cancer later in life than exposure after the age of 30. No association was found between cumulative life-time exposure to sunlight and the number of keratotic skin lesions. Nevertheless, these lesions behaved as a strong independent risk factor in the development of skin cancer. The adjusted odds ratio of skin cancer for 50-99 lesions compared with < 50 lesions was 4.5 (95% CI 1.1-18.2); the adjusted odds ratio for > or = 100 lesions compared with < 50 lesions was 20.8 (95% CI 5.3-81.7).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2004

History of psoriasis response to sunlight does not predict outcome of UVB phototherapy.

We prospectively asked 146 consecutive patients starting narrow-band UVB (NB-UVB) for psoriasis about the effects of sunlight on their psoriasis. Eighty-eight (60%) patients reported improvement with sunlight, six (4%) reported worsening, and 52 (36%) had not noted any change in their psoriasis with sunlight exposure. Overall, 101 (69%) were recorded to reach clearance or minimal residual activity (MRA), 24 (16.5%) to achieve moderate improvement, and 21 (14.5%) had other recorded outcomes (mainly 'did not attend'), with UVB phototherapy. Forty-two (72%) of the 58 who did not report improvement with sunlight went on to clearance/MRA with UVB compared to 59/88 (67%) of those who did report improvement (95% confidence interval for difference in percentage improving, -10% to 20%, P = 0.49). Patients' replies to questions about how their psoriasis responds to sunlight do not appear to predict response to UVB phototherapy in our patient population.

Adolescent↗
PubMed2002

Sunlight inactivation of fecal indicator bacteria and bacteriophages from waste stabilization pond effluent in fresh and saline waters.

Sunlight inactivation in fresh (river) water of fecal coliforms, enterococci, Escherichia coli, somatic coliphages, and F-RNA phages from waste stabilization pond (WSP) effluent was compared. Ten experiments were conducted outdoors in 300-liter chambers, held at 14C (mean river water temperature). Sunlight inactivation (k(S)) rates, as a function of cumulative global solar radiation (insolation), were all more than 10 times higher than the corresponding dark inactivation (k(D)) rates in enclosed (control) chambers. The overall k(S) ranking (from greatest to least inactivation) was as follows: enterococci > fecal coliforms greater-than-or-equal E. coli > somatic coliphages > F-RNA phages. In winter, fecal coliform and enterococci inactivation rates were similar but, in summer, enterococci were inactivated far more rapidly. In four experiments that included freshwater-raw sewage mixtures, enterococci survived longer than fecal coliforms (a pattern opposite to that observed with the WSP effluent), but there was little difference in phage inactivation between effluents. In two experiments which included simulated estuarine water and seawater, sunlight inactivation of all of the indicators increased with increasing salinity. Inactivation rates in freshwater, as seen under different optical filters, decreased with the increase in the spectral cutoff (50% light transmission) wavelength. The enterococci and F-RNA phages were inactivated by a wide range of wavelengths, suggesting photooxidative damage. Inactivation of fecal coliforms and somatic coliphages was mainly by shorter (UV-B) wavelengths, a result consistent with photobiological damage. Fecal coliform repair mechanisms appear to be activated in WSPs, and the surviving cells exhibit greater sunlight resistance in natural waters than those from raw sewage. In contrast, enterococci appear to suffer photooxidative damage in WSPs, rendering them susceptible to further photooxidative damage after discharge. This suggests that they are unsuitable as indicators of WSP effluent discharges to natural waters. Although somatic coliphages are more sunlight resistant than the other indicators in seawater, F-RNA phages are the most resistant in freshwater, where they may thus better represent enteric virus survival.

Bacteriophages↗
PubMed2000

Sunlight-induced propagation of the lysogenic phage encoding cholera toxin.

In toxigenic Vibrio cholerae, the cholera enterotoxin (CT) is encoded by CTXPhi, a lysogenic bacteriophage. The propagation of this filamentous phage can result in the origination of new toxigenic strains. To understand the nature of possible environmental factors associated with the propagation of CTXPhi, we examined the effects of temperature, pH, salinity, and exposure to direct sunlight on the induction of the CTX prophage and studied the transmission of the phage to potential recipient strains. Exposure of cultures of CTXPhi lysogens to direct sunlight resulted in approximately 10,000-fold increases in phage titers. Variation in temperature, pH, or salinity of the culture did not have a substantial effect on the induction of the prophage, but these factors influenced the stability of CTXPhi particles. Exposure of mixed cultures of CTXPhi lysogens and potential recipient strains to sunlight significantly increased both the in vitro and in vivo (in rabbit ileal loops) transduction of the recipient strains by CTXPhi. Included in these transduction experiments were two environmental nontoxigenic (CTXPhi(-)) strains of V. cholerae O139. These two O139 strains were transduced at high efficiency by CTXPhi, and the phage genome integrated into the O139 host chromosome. The resulting CTXPhi lysogens produced biologically active CT both in vitro and in rabbit ileal loops. This finding suggests a possible mechanism explaining the origination of toxigenic V. cholerae O139 strains from nontoxigenic progenitors. This study indicates that sunlight is a significant inducer of the CTX prophage and suggests that sunlight-induced transmission of CTXPhi may constitute part of a natural mechanism for the origination of new toxigenic strains of V. cholerae.

Animals↗
PubMed1988

Influence of season and latitude on the cutaneous synthesis of vitamin D3: exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin.

Sunlight has long been recognized as a major provider of vitamin D for humans; radiation in the UVB (290-315 nm) portion of the solar spectrum photolyzes 7-dehydrocholesterol in the skin to previtamin D3, which, in turn, is converted by a thermal process to vitamin D3. Latitude and season affect both the quantity and quality of solar radiation reaching the earth's surface, especially in the UVB region of the spectrum, but little is known about how these influence the ability of sunlight to synthesize vitamin D3 in skin. A model has been developed to evaluate the effect of seasonal and latitudinal changes on the potential of sunlight to initiate cutaneous production of vitamin D3. Human skin or [3 alpha-3H]7-dehydrocholesterol exposed to sunlight on cloudless days in Boston (42.2 degrees N) from November through February produced no previtamin D3. In Edmonton (52 degrees N) this ineffective winter period extended from October through March. Further south (34 degrees N and 18 degrees N), sunlight effectively photoconverted 7-dehydrocholesterol to previtamin D3 in the middle of winter. These results quantify the dramatic influence of changes in solar UVB radiation on cutaneous vitamin D3 synthesis and indicate the latitudinal increase in the length of the "vitamin D winter" during which dietary supplementation of the vitamin may be advisable.

Alberta↗
PubMed1999

Relationship between pterygium/pinguecula and sunlight exposure among postmen in central Taiwan.

BACKGROUND: The purpose of this study was to investigate outdoor hazards and their relationship to conjunctival disorders experienced by postmen. METHODS: Three hundred and ninety-four employees (248 postmen and 146 officers) working in 11 post offices in central Taiwan were recruited and participated in the 1994 annual labor health examination. Pinguecula and pterygium were diagnosed by an ophthalmologist. Meanwhile, detailed personal and occupational information was obtained using a structured questionnaire. The cumulative occupational sunlight exposure was calculated for each postman by considering the duration of their employment as postmen, the average working hours per day and their spectacle use (sunglasses and eyeglasses). A logistic regression was used to analyze the relationship between cumulative occupational sunlight exposure and pinguecula. RESULTS: Among the postmen, the prevalences of pinguecula and pterygium were 62.9% and 7.3%, respectively. The outdoor nature of postal work was significantly associated with the occurrence of pinguecula as well as pterygium (p < 0.05). When the cumulative occupational sunlight exposure increased by one unit (one year x hour/day), the risks of developing pinguecula and pterygium were raised by 2.1% and 0.8%, respectively. CONCLUSIONS: The results indicate that conjunctival disorders were associated with the cumulative occupational sunlight exposure of postmen working outdoors. This study reinforces the importance of ocular protection from sunlight.

Adolescent↗
PubMed1989

Biological amplification factor for sunlight-induced nonmelanoma skin cancer at high latitudes.

Data for the incidence of basal cell carcinomas (BCCs) and squamous cell carcinomas (SCCs) of the skin, registered for six regions of Norway during 10 years (1976-1985), were used to evaluate the biological amplification factor Ab for induction of these cancers by sunlight. Ab is the ratio of the increment in skin cancer production to the increment in causative sunlight exposure. Two different approximations were used for the action spectrum for carcinogenesis: an erythema action spectrum; and an action spectrum for mutagenesis of cells in the basal layer of the skin. These two fundamentally different approaches yielded Ab values that were similar to within about 10%: 2.1-2.3 for BCCs; and 1.6-1.8 for SCCs. Using a radiation amplification factor for ozone depletion of 0.8-1.1, we find that the total amplification factor for BCCs is within the range 1.6-2.1 and that that for SCCs is within the range 1.3-1.7 at northern latitudes of 60-70 degrees. Thus, an ozone depletion of 1% will result in an increase in the incidence of BCCs by 1.6-2.1% and of SCCs by 1.3-1.7%. There were no significant differences between the values for men and women. Neither was there any significant difference between Ab values found for skin commonly exposed to sunlight (face) and for skin sites normally covered by clothes and therefore receiving much lower exposures, in spite of the fact that the tumor density per unit skin area was a factor of 20 or more larger at the former sites. This observation, as well as the curves relating cancer incidence with annual exposure to carcinogenic sunlight, supports a power law relationship between cancer incidence and annual sun exposure. Sunlight appears to be the main cause of BCCs and SCCs even at the high latitudes of Northern Norway. All over, BCCs were found to be about 6 times more frequent than SCCs. The ratio of the incidence of BCCs to that of SCCs seemed to be independent of the latitude. Finally, BCCs were found to be equally frequent among men and women, while SCCs were found to be about twice as frequent among men as among women.

Basal Cell Carcinoma↗
PubMed1985

Effect of sunlight and its component wavebands on contact hypersensitivity in mice and guinea pigs.

Exposure of mice to UVB (280-320 nm) radiation is known to suppress the development of contact hypersensitivity (CHS) to chemicals that are applied subsequently to unirradiated skin, and this suppression is associated with the generation of suppressor lymphocytes. In this study, the systemic effect of other wavebands of nonionizing radiation on the development of CHS has been tested. Large doses of visible (greater than 400 nm) radiation produced a small but consistent systemic suppression of CHS in mice. In contrast, a large dose of UVA (320-400 nm) radiation did not suppress CHS but, rather, enhanced this immune response. Exposure of both mice and guinea pigs to sunlight produced systemic suppression of CHS. The suppression could be transferred to normal syngeneic animals by injection of splenic lymphoid cells obtained from animals that exhibited suppression, indicating that suppressor cells are associated with sunlight-induced systemic suppression of CHS. The immunomodulatory effect of sunlight was partially abrogated by a Mylar filter or prior application of a sunscreen containing para-aminobenzoic acid to the exposed skin. Thus, wavelengths mainly in the UVB portion of sunlight (295-320 nm) are responsible for sunlight-induced suppression of CHS, although wavelengths in the visible region may also play a role.

Animals↗
PubMed1995

Induction of cyclobutane pyrimidine dimers, pyrimidine(6-4)pyrimidone photoproducts, and Dewar valence isomers by natural sunlight in normal human mononuclear cells.

Immunocytochemistry was used for the direct measurement of cyclobutane pyrimidine dimers, (6-4) photoproducts, and Dewar isomers in normal human mononuclear cells following irradiation by natural sunlight or by a FS20 broad spectrum UVB sunlamp. The induction of each type of photoproduct was detected following 30-60 min sunlight exposure or with FS20 fluences as low as 50-100 Jm-2. With increasing FS20 fluences, there was a dose-dependent increase in the binding of pyrimidine dimer, (6-4) photoproduct, and Dewar isomer-specific monoclonal antibodies. The relative ratio of Dewar isomer to (6-4) photoproduct antibody binding sites was much higher following exposure to natural sunlight than to broad spectrum UVB. With the (6-4) monoclonal antibody, a small increase in binding sites was evident after a 1-h exposure to natural sunlight. This remained relatively constant with further exposure. These results are consistent with the hypothesis that, following irradiation with natural sunlight, the majority of (6-4) photoproducts are converted into Dewar valence isomers.

Antibodies, Monoclonal↗
PubMedDate not supplied

[Physiological effects of sunlight on Bacillus subtilis strains with varying capacity to repair photoproducts].

Nonlethal doses of sunlight were established to cause a growth delay in Bacillus subtilis strain 1201 possessing an unimpaired repair system. This effect was not observed with the 1201-10 uvr1 mutant deficient in DNA excision repair; however, addition of an extract of uvr1+ cells restorated the phenomenon of growth delay by sunlight in this mutant. Experiments with glass light filters showed that a weakened growth delay in strain 1201 could also be produced by rays of sunlight with wavelengths greater than 380 nm. Maximum growth delay was observed after irradiation with the complete spectrum of sunlight. Experiments with the protein synthesis inhibitor chloramphenicol indicated that sunlight promotes synthesis of proteins preventing the dying of cells. The presence of Casamino acids is favorable for the synthesis of protective proteins.

Bacillus subtilis↗
PubMed1996

Sunlight and sunburn in human skin cancer: p53, apoptosis, and tumor promotion.

Sunlight is a carcinogen to which everyone is exposed. Epidemiology indicates that most carcinogenic sunlight exposure takes place several decades before the tumor arises. Some of the early events have been identified by searching for genes having ultraviolet (UV)-specific mutations. Over 90% of squamous cell carcinomas and more than 50% of basal cell carcinomas from New England patients contain UV-like mutations in the p53 tumor suppressor gene. From the mutation pattern, it can be concluded that the carcinogenic DNA lesions were pyrimidine-cytosine photoproducts caused by the UVB portion of sunlight. Particular codons of the p53 gene are most susceptible, apparently because of slower DNA repair at specific sites. Sunlight is sufficiently mutagenic often to mutate both p53 alleles. These mutations are also found in the precancer for squamous cell carcinoma, actinic keratosis, implying an early role. The function of p53 in normal skin is indicated by the observation that inactivating p53 in mouse skin reduces the appearance of sunburn cells, apoptotic keratinocytes generated by UV overexposure. Skin thus appears to possess a p53-dependent "cellular proofreading" response to DNA damage in which precancerous cells self-destruct. If this response is reduced in a single cell by a prior p53 mutation, sunburn can thereafter select for clonal expansion of the p53-mutated cell into an actinic keratosis. Sunlight appears to act twice: as tumor initiator and as tumor promoter.

Animals↗
PubMedDate not supplied

[Effect of substances, absorbing ultraviolet irradiation on Bacillus subtilis resistance to inactivation and mutagenic action of natural sunlight].

Substances, absorbing UV-irradiation from sunlight (triptophan, cistein, catalase) decrease Bacillus subtilis resistance to sunlight-induced lethal and mutagenic damages. Possible, they act as exogenous photosensitizers. Tryptophan was found to be the most active photosensitizer. Cistein and catalase are not so active. Casaminoacids being present in the bacterial suspensions during illumination protect bacteria from mutagenic action sunlight. In this studies we can demonstrate, that sunlight damage B. subtilis membranes and allows substances to penetration into cells. Following, that polishing of the environmental by chemical agents can strength genetic risk for organisms permanently exposure to sunlight.

Bacillus subtilis↗
PubMed2001

Determination of S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]glutathione, a novel metabolite of L-histidine, in tissue extracts from sunlight-irradiated rat by capillary electrophoresis.

Exposure of the skin to sunlight results in an increase in the content of epidermal urocanic acid, a key metabolite of L-histidine, and some portions of the metabolite penetrate into the body fluid. S-[2-Carboxy-1-(1H-imidazol-4-yl)ethyl]glutathione (GS(CIE)), an adduct of glutathione and urocanic acid, was proposed to be an origin of a urinary compound, S-[2-carboxy-1-(1 H-imidazol-4-yl)ethyl]-L-cysteine (Cys(CIE)). Various catabolites of Cys(CIE) were also isolated from human urine previously. However, no direct evidence to show the existence of GS(CIE) as a biological material had been found. By using capillary electrophoresis, the glutathione adduct has now been found in the extracts of rat tissues from the kidney, liver, skin and blood when the rat was kept under conditions of sunlight irradiation after the fur on the dorsal skin had been clipped. On the other hand, no or a trace of GS(CIE) was determined in rat tissue extracts when the animal was kept indoor in usual manner. The glutathione adduct was isolated from the kidney extract of the sunlight-irradiated rat using ion-exchangers and high-voltage paper electrophoresis, and determined by fast-atom-bombardment mass spectrometry. These results indicate that GS(CIE) formation actually occurs in the body and that the formation is accelerated by exposing the rat to sunlight irradiation. From these findings, we propose an alternative pathway of histidine metabolism which is initiated by the adduction of urocanic acid to glutathione to form GS(CIE) and terminates with the formation of the urinary compounds via Cys(CIE).

Animals↗
PubMed1999

Involvement of 5-methylcytosine in sunlight-induced mutagenesis.

In human skin cancers, more than 30 % of all mutations in the p53 gene are transitions at dipyrimidines within the sequence context CpG, i.e. 5'-TCG and 5'-CCG, found at several mutational hotspots. Since CpGs are methylated along the p53 gene, these mutations may be derived from solar UV-induced pyrimidine dimers forming at sequences that contain 5-methylcytosine. In Xorder to define the contribution of 5-methylcytosine to sunlight-induced mutations, we have used mouse fibroblasts containing the CpG-methylated lacI transgene as a mutational target. We sequenced 182 UVC (254 nm UV)-induced mutations and 170 mutations induced by a solar UV simulator, along with 75 mutations in untreated cells. Only a few of the mutations in untreated cells were transitions at dipyrimidines, but more than 95% of the UVC and solar irradiation-induced mutations were targeted to dipyrimidine sites, the majority being transitions. After UVC irradiation, 6% of the base substitutions were at dipyrimidines containing 5-methylcytosine and only 2.2% of all mutations were transitions within this sequence context. However, 24% of the solar light-induced mutations were at dipyrimidines that contain 5-methylcytosine and most of them were transitions. Two sunlight-induced mutational hotspots at methylated CpGs correlated with sequences that form the highest levels of cyclobutane pyrimidine dimers after irradiation with sunlight but not with UVC. The data indicate that dipyrimidines that contain 5-methylcytosine are preferential targets for sunlight-induced mutagenesis in cultured mammalian cells, thus explaining the large proportion of p53 mutations at such sites in skin tumors in vivo.

5-Methylcytosine↗
PubMedDate not supplied

The untenability of the sunlight hypothesis of cataractogenesis.

The excess prevalence of cataract in third world countries led early this century to the hypothesis that sunlight causes cataract. The hypothesis, which ignored differences in diet, culture, poverty and prevalence of other diseases such as diarrhoea, received little support until about thirty years ago when biochemical studies were set up to explore the browning of lens proteins, which is a common feature of cataract on the Indian subcontinent. Initially these studies were encouraging in that exposure to sunlight caused some changes seen in cataractous lenses, but eventually the hypothesis was rejected because the first change in the laboratory was the destruction of tryptophan, but this was not found in brown cataract lenses. A brown nuclear cataract could not be produced artificially in the laboratory using sunlight or UV exposure. Exposure of laboratory animals has produced lens opacities, but in most experiments the doses required have also caused keratitis, conjunctivitis, iritis and inflammation. The cornea seems more sensitive than the lens, which is not surprising, as it gets the first chance to absorb damaging UV. The biochemical rejection of the hypothesis coincided with the re-start of the epidemiological studies. Most of these are simply latitude studies and are no more than a repeat of what was available sixty years ago. They do not help to find a cause. Two studies showed that cataract was less common at higher altitude in the Himalayas, but unfortunately led to opposing conclusions. On the basis of common knowledge that UV exposure was greater at higher altitude, the first altitude study led to the rejection of the sunlight hypothesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Cataract↗