SEARCH · PubMed Health

Results for “Sunlight”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1989

Sunlight, skin sensitivity, and senile cataract.

This study explores the association between sunlight exposure and senile cataract, taking into account such individual differences as skin sensitivity to sunlight and the use of sun-shielding devices, i.e., sunglasses and hats. A case-control study was conducted among 160 matched pairs of subjects between October 1, 1984 and June 1, 1985 at the University of Iowa Hospitals and Clinics in Iowa City, Iowa. Cases were selected from among all patients admitted for inpatient or outpatient cataract surgery who were at least 40 years old. Controls were selected from among those waiting for a friend or relative who was attending one of the ophthalmology clinics. Controls were matched to the cases on a 1:1 basis on sex and age (+/- one year). No association was observed between history of sunlight exposure and senile cataract. However, independent of sunlight exposure, the cases with nuclear cataracts reported a more severe acute skin response upon exposure to sunlight for the first time in the summer (a severe burn with blistering) than did their age- and sex-matched controls (McNemar odds ratio (OR) = 1.73, 95% confidence interval (CI): 1.03-2.91). In addition, independent of sunlight exposure, the male controls reported a greater average lifetime use of head coverings in summer which shaded their eyes from the sun than did their age- and sex-matched cases (McNemar OR = 0.48, 95% CI: 0.25-0.94).

Adult↗

PubMed1991

Sunlight and the survival of enteric bacteria in natural waters.

Escherichia coli and some salmonellas were exposed in seawater and freshwater to natural sunlight, visible light of comparable intensity, and light containing a similar proportion of u.v. as natural sunlight but of a much lower intensity. Direct viable bacterial counts and culturable counts on selective and non-selective media were made at intervals. The rate of decrease in numbers of culturable bacteria was significantly faster in seawater than in freshwater when exposed to natural sunlight. No significant difference was found between the rates of decrease in numbers of culturable bacteria in seawater and those in freshwater when bacteria were exposed to light with a small u.v. component of similar intensity. The effect of salinity no loss of culturability is, therefore, more significant in the presence of u.v. radiation. Direct counts by the acridine orange direct viable count method decreased much more slowly than the culturable counts in seawater but comparably with culturable counts in freshwater in natural sunlight. Direct viable counts and culturable counts decreased at a similar rate in seawater and in freshwater in visible light. This may signify the evolution of enteric bacteria towards a viable but non-culturable form in seawater when exposed to natural sunlight. The presence of humic acids significantly reduced loss of culturability but only in low salinity conditions. Salinity appears to be an important factor influencing culturability in bacteria exposed to sunlight.

Escherichia coli↗

PubMed1992

Cumulative sunlight exposure and the risk of developing skin cancer in Florida.

Epidemiologic evidence suggests that the risk of developing skin cancer is higher in certain geographic regions where sunlight is excessive. Even in such high risk regions, two distinct populations of long-term residents exist: people with, and people without skin cancer. We have compared the quantitative lifetime sunlight exposure between 11 nonmelanoma skin cancer patients who have lived in South Florida for 23.7 +/- 5.1 years and 9 age-matched normal, healthy individuals who have lived in South Florida for 23.4 +/- 4.1 years. An estimation of personal cumulative sunlight exposure was determined for each subject from data collected through detailed interviews. We found that there was no detectable, significant quantitative difference in cumulative sunlight exposure during life between these two groups. Because these individuals had previously been phenotyped for the effects of ultraviolet-B (UVB) radiation on induction of contact hypersensitivity, our results suggest that UVB-susceptibility may be a better indicator of skin cancer risk than cumulative lifetime sunlight exposure. Thus, although there is little doubt that sunlight exposure is an important factor in the development of skin cancer, our results emphasize the importance of host genetic factors in the pathogenesis of this disease.

Aged↗

PubMed1986

Rise in lens temperature on exposure to sunlight or high ambient temperature.

The effect of increase ambient temperature and sunlight on the temperatures of the rabbit lens and posterior chamber (PC) aqueous humour was measured by needle thermistor probes while the rectal temperature was monitored. Exposure of rabbits to sunlight (35 degrees-42 degrees C), in New Haven, Connecticut, USA, resulted in significant temperature increases in PC (4.3 degrees C), lens (3.2 degrees C), and rectum (2.3 degrees C). Returning animals to the shade resulted in a progressive decrease in the temperatures of the PC or lens in the tested eye, but repeating exposure to sunlight resulted in significant increases of the baseline (PC) temperature (increase 2.68 degrees C) of the second eye. Exposure of rabbits to sunlight at 49 degrees C in Chandigarh, India, resulted in increased PC temperature of 4.48 degrees C after 9 minutes. Increased PC and lens temperatures after exposure to sunlight are due both to an ambient temperature effect through the cornea and to increased body temperature. In dry and hot tropical areas of the world temperature increases in the lens after exposure to sunlight may initiate or accelerate the formation of senile cataracts.

Animals↗

PubMed1989

Sunlight regulates the cutaneous production of vitamin D3 by causing its photodegradation.

Exposure to sunlight initiates the formation of vitamin D3 in skin as the UV B radiation in the solar spectrum causes the photoconversion of 7-dehydrocholesterol to previtamin D3. A heat-induced isomerization then converts previtamin D3 to vitamin D3 over a period of days. A number of irradiation products of vitamin D3 are known to form upon irradiation with high intensity UV radiation, but the effect of subsequent exposures to sunlight on the vitamin D3 formed in skin is not known. To investigate this phenomenon, human skin containing vitamin D3 was exposed to sunlight in Boston. A model system of [3H]vitamin D3 in methanol was also used to study the effects of sunlight on vitamin D3 throughout the year. Vitamin D3 proved to be exquisitely sensitive to sunlight, and once formed in the skin, exposure to sunlight resulted in its rapid photodegradation to a variety of photoproducts, including 5,6-transvitamin D3, suprasterol I, and suprasterol II.

Boston↗

PubMed1990

An approach towards understanding the genesis of sunlight-induced skin cancer.

The molecular basis of the sunlight-induced skin carcinogenesis has been elucidated. Of the two ultraviolet components of sunlight that reach the earth's surface the UV-B is known to be carcinogenic but the mode of action of UV-A, the predominant component of sunlight, is ill understood. Using the liposomes as a model system, it has been shown here that UV-A causes dose-dependent lipid peroxidation as estimated by measurements of conjugated dienes, lipid hydroperoxides, malondialdehydes and the fluorescent adducts (Schiff bases) produced by the reaction of MDA with glycine. Direct exposure to sunlight has also been shown to cause dose-dependent lipid peroxidation. The UV-A induced lipid peroxidation has also been shown to be dependent on dose rate. While the sodium formate, dimethyl sulphoxide, superoxide dismutase and EDTA do not have any significant effect, sodium azide, histidine, beta-carotene and dimethylfuran were shown to inhibit significantly the UV-A induced lipid peroxidation, thereby providing significant evidence of the involvement of singlet oxygen (1O2) as the initiating agent. The use of D2O in place of H2O as the liposome dispersing medium enhanced to great extent the UV-A induced lipid peroxidation, thereby lending additional support to the finding that singlet oxygen was the initiating agent. The possible mode of formation of 1O2 on exposure to UV-A was discussed. This study also highlighted the role of environmental factors on the sunlight-induced cutaneous damage. Finally, the relation between lipid peroxidation, DNA damage and carcinogenesis has been discussed in a way to suggest the possible link between sunlight exposure and causation of skin cancer.

Humans↗

PubMed1992

Spectrum of mutations in single-stranded DNA phage M13mp2 exposed to sunlight: predominance of G-to-C transversion.

Sunlight is regarded to be a cause of skin cancer, though the mechanisms underlying the causation are still unclear. The genotoxic effects of sunlight are believed to be induced by pyrimidine photoproducts produced by the action of the UV portion of sunlight. However, it is not clear whether these pyrimidine modifications are the sole sources for the mutations. In the present study, we have analyzed the mutagenic potential of sunlight on the lacZ alpha region of single-stranded DNA phage M13mp2 using an SOS-deficient recA- strain and an SOS-induced rec+ strain of Escherichia coli as hosts. Exposure to sunlight caused mutations; approximately 10-fold increases in the mutation frequency were observed with the use of both hosts. When SOS functions were induced in the host CSH50, the mutation frequencies increased another 10-fold over those obtained with the host lacking the SOS functions. DNA sequences of the mutants were analyzed by automated DNA sequencers. Sequence changes were identified in 53 mutants from the mutant DNAs obtained using NR9099 as host and in 78 mutant samples obtained using UV-treated CSH50. Most of the mutations were transversions of guanine, either G to C or G to T. Furthermore, 59% of the identified sequence changes in the SOS- host and 40% of those in the SOS-induced host were G-to-C transversions. These transversions may be caused by unidentified guanine damages or by the effects of damage at pyrimidines distal from guanines to be mutated.

Bacteriophages↗

PubMed1990

Sunlight and breast cancer incidence in the USSR.

Epidemiological and laboratory evidence suggest that vitamin D may play a role in reducing risk of breast cancer. Lack of exposure to ultraviolet sunlight can increase the prevalence of vitamin D deficiency, and may place some populations at higher risk of breast cancer. The association between total average annual sunlight energy striking the ground and age-adjusted breast cancer incidence rates in the USSR was evaluated. Breast cancer had a threefold range of incidence. Sunlight levels varied from 210 to 400 calories per cm2 per day. A statistically significant negative association was found between breast cancer incidence rates and total sunlight levels (R = -0.75, p = 0.001). The slope of the regression line corresponded to two additional cases per 100,000 per year for each reduction of 35 calories per cm2 of sunlight. The pattern of increased breast cancer incidence in regions of low solar radiation in the USSR is consistent with the geographical pattern seen for breast cancer mortality in the US and worldwide. A positive relationship between socioeconomic status and breast cancer incidence was also present in the Soviet Union, based on an approximate socioeconomic measure, the number of doctors per 1000 population (R = +0.89, p = 0.0001). The possibility that correlates of socioeconomic status, such as dietary, ethnic, or behavioural factors, could account for the association is discussed.

Breast Neoplasms↗

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↗

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↗

PubMed1979

Relative effectiveness of the 300--320 NM spectral region on sunlight for the production of primary lethal damage in E. coli cells.

Cell inactivation by sunlight exposure has been studied in E. coli CSR 603 (uvrA recA phr), a K12 derivative which is deficient in all known repair systems. Under suitable conditions, unfiltered sunlight inactivates these cells to 10(-3) survival within 30 sec. The effects of unfiltered sunlight have been compared with those of sunlight filtered through 1-cm layers of aqueous caffeine solutions ranging in concentration from 1 to 20 mg/ml. In the wavelength region of solar emission below 320 nm, which is most critical for DNA damage, the transmission of these liquid filters changes from 10 to 90% within 8-nm intervals. Thus our results permit minimum estimates for the fraction of lethal lesions produced by the solar spectrum below certain wavelenghts. In an experiment analyzed in this manner more than 80% of primary lethal lesions are caused by wavelengths less than 321 nm, and more than 50% by wavelengths less than 306 nm, while the contribution of wavelengths greater than 380 nm to primary lethal damage is below 1%.

DNA Repair↗

PubMed1990

Natural summer and winter sunlight exposure patterns in seasonal affective disorder.

Twelve subjects with winter depression who lived in the Chicago area recorded their times of going outside during daylight hours for one week during the winter and one week during the summer. These records produced estimates of the duration of daily sunlight exposure and of perceived dawn, dusk and skeleton photoperiod. There was more than twice as much sunlight exposure in summer compared to winter (3.0 vs. 1.2 h/day). The perceived skeleton photoperiod was 4-5 h longer in summer than winter, with a later perceived dusk contributing more to the lengthening than an earlier perceived dawn. The duration of sunlight exposure and perceived skeleton photoperiod in both seasons was much less than what was possible given the available daylight. These results are discussed with reference to the modern urban life style, bright light treatment of winter seasonal affective disorder, and factors which affect the perceived intensity of sunlight.

Adult↗

PubMedDate not supplied

Occupational sunlight exposure and melanoma in the U.S. Navy.

Melanoma is the second most common cancer, after testicular cancer, in males in the U.S. Navy. A wide range of occupations with varying exposures to sunlight and other possible etiologic agents are present in the Navy. Person-years at risk and cases of malignant melanoma were ascertained using computerized service history and inpatient hospitalization files maintained at the Naval Health Research Center. A total of 176 confirmed cases of melanoma were identified in active-duty white male enlisted Navy personnel during 1974-1984. Risk of melanoma was determined for individual occupations and for occupations grouped by review of job descriptions into three categories of sunlight exposure: (1) indoor, (2) outdoor, or (3) indoor and outdoor. Compared with the U.S. civilian population, personnel in indoor occupations had a higher age-adjusted incidence rate of melanoma, i.e., 10.6 per 100,000 (p = .06). Persons who worked in occupations that required spending time both indoors and outdoors had the lowest rate, i.e., 7.0 per 100,000 (p = .06). Incidence rates of melanoma were higher on the trunk than on the more commonly sunlight-exposed head and arms. Two single occupations were found to have elevated rates of melanoma: (1) aircrew survival equipmentman, SIR = 6.8 (p less than .05); and (2) engineman, SIR = 2.8 (p less than .05). However, there were no cases of melanoma or no excess risk in occupations with similar job descriptions. Findings on the anatomical site of melanoma from this study suggest a protective role for brief, regular exposure to sunlight and fit with recent laboratory studies that have shown vitamin D to suppress growth of malignant melanoma cells in tissue culture. A mechanism is proposed in which vitamin D inhibits previously initiated melanomas from becoming clinically apparent.

Adolescent↗

PubMed1990

Biologically effective doses of sunlight for immune suppression at various latitudes and their relationship to changes in stratospheric ozone.

Using information on solar irradiance at different latitudes derived from a radiative transfer model and a detailed in vivo action spectrum for immune suppression in a murine system, we report here calculations of the "biologically effective" irradiance of sunlight for immune suppression. From 40 degrees N to 40 degrees S in summer, under normal stratospheric ozone concentrations this value ranged from 0.27 W/m2 (40 degrees N or S) to a peak of 0.33 W/m2 (20 degrees N or S) predicting that 50% immune suppression in the Balb/c mouse would occur after 21-26 min of sunlight exposure within this latitude range. We also found that the most effective wavelengths for immune suppression shift from a peak of 270 nm in the laboratory to near 315 nm in sunlight. Furthermore, using ozone depletion scenarios of 5 to 20%, at latitudes 20 degrees S and 40 degrees N, a 0.6% increase in biologically effective irradiance levels of solar UVB for immune suppression was predicted for each 1% decrease of ozone. This value rose to a nearly 1% increase for each 1% decrease in ozone at 60 degrees N latitude in wintertime. These data indicate that activation of immune suppression, in a murine model, requires relatively low levels of sunlight and that these levels are easily obtainable over most of the populated regions of the world. Since a UVB-activated photoreceptor, urocanic acid, regulates immune suppression in mice and since this same compound exists on other mammalian skin, including human skin, suppression of the mammalian immune system is predicted to increase if substantial stratospheric ozone depletion takes place.

Animals↗

PubMedDate not supplied

Monocular eye closure in sunlight.

Monocular eye closure in sunlight is often noted in patients with intermittent exotropia. Neither the reason for eye closure nor its frequency of occurrence in other populations is known. We questioned 147 consecutive nonoperated patients (and/or their parents) ages 1-45 years, 93 with strabismus with onset prior to 7 years of age and 54 without strabismus, for a history of closing one eye in sunlight. Monocular eye closure in sunlight was reported most frequently by patients with intermittent exotropia but was also reported by those with other forms of strabismus as well as by nonstrabismic normals. Cooperative subjects were studied further to determine the cause for eye closure. Each subject was exposed to a source of intense illumination while fixating a target. All who closed one eye under these conditions reported photalgia associated with the high light intensity, most noting less discomfort after closing one eye. None reported diplopia prior to eye closure. Monocular and binocular photophobia thresholds were then measured for each subject. The mean monocular photophobia threshold was significantly higher than the binocular threshold. In addition, binocular photophobia thresholds were significantly lower in those reporting eye closure compared with those who did not. Monocular eye closure in sunlight is a mechanism used to reduce photophobia and is not related to avoidance of diplopia.

Adolescent↗

PubMed1989

The effects of bergapten and sunlight on cutaneous pigmentation.

The effects of bergapten-containing preparations in sunlight-induced skin pigmentation were evaluated. Oil and lotion vehicles with bergapten/UV-B sunscreen or sunscreen alone were applied to the backs of subjects twice weekly for 4 weeks and the subjects were exposed to gradually increasing doses of midday sunlight. The degree of skin darkening was assessed by clinical examination, reflectometry, and light microscopy of skin biopsy specimens. At 5 weeks, 1 week after the last sunlight exposure, the sites treated with either the bergapten/UV-B sunscreen lotion or the lotion vehicle were significantly darker than the sites treated with the sunscreen lotions without bergapten. Oil preparations produced less clearcut results, possibly because of a less potent sunscreen or because the bergapten did not leave the vehicle and absorb into the epidermis. In type I skin, the bergapten/sunscreen and the oil vehicle alone produced the same amount of tanning; both yielded more tanning than the sunscreen in oil by clinical examination. The findings were not confirmed by reflectometry or by light microscopy. Thus, we conclude that bergapten added to a UV-B sunscreen lotion preparation can increase skin pigmentation over the sunscreen alone when one is exposed to sunlight. The bergapten/UV-B sunscreen combination is a potentially useful product since one can develop a psoralen and UV-A-induced tan while being protected from UV-B-induced sunburn by the UV-B sunscreen incorporated into the formulation.

5-Methoxypsoralen↗

PubMed1986

Effects of sunlight exposure on Langerhans cells and melanocytes in human epidermis.

The effects of 12 daily, half-hour exposures to sunlight on epidermal Langerhans cells (LC), and melanocytes were studied in 31 healthy volunteers. Nineteen were of Celtic and 12 of mixed European descent. Sunlight appeared to have both a direct, transient, detrimental effect and an indirect stimulating effect on the LC, and a direct and an indirect stimulating effect on the melanocytes. The mixed Europeans had a somewhat greater increase in the melanocyte population density following exposure to sunlight than the Celts. However, the number of LC fell following sunlight exposure regardless of the melanocyte response. Thus the melanocytes did not appear to provide the LC with immediate protection from ultraviolet light.

Adult↗