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Author Cho, Y.M.; Ryu, S.-H.; Lee, B.R.; Kim, K.H.; Lee, E.; Choi, J.
Title Effects of artificial light at night on human health: A literature review of observational and experimental studies applied to exposure assessment Type Journal Article
Year 2015 Publication Chronobiology International Abbreviated Journal Chronobiol. Int.
Volume 32 Issue 9 Pages 1294-1310
Keywords Artificial light at night; breast cancer; circadian rhythm; light exposure; light pollution
Abstract It has frequently been reported that exposure to artificial light at night (ALAN) may cause negative health effects, such as breast cancer, circadian phase disruption and sleep disorders. Here, we reviewed the literature assessing the effects of human exposure to ALAN in order to list the health effects of various aspects of ALAN. Several electronic databases were searched for articles, published through August 2014, related to assessing the effects of exposure to ALAN on human health; these also included the details of experiments on such exposure. A total of 85 articles were included in the review. Several observational studies showed that outdoor ALAN levels are a risk factor for breast cancer and reported that indoor light intensity and individual lighting habits were relevant to this risk. Exposure to artificial bright light during the nighttime suppresses melatonin secretion, increases sleep onset latency (SOL) and increases alertness. Circadian misalignment caused by chronic ALAN exposure may have negative effects on the psychological, cardiovascular and/or metabolic functions. ALAN also causes circadian phase disruption, which increases with longer duration of exposure and with exposure later in the evening. It has also been reported that shorter wavelengths of light preferentially disturb melatonin secretion and cause circadian phase shifts, even if the light is not bright. This literature review may be helpful to understand the health effects of ALAN exposure and suggests that it is necessary to consider various characteristics of artificial light, beyond mere intensity.
Address b Department of Preventive Medicine , College of Medicine, Korea University , Seoul , Republic of Korea
Corporate Author Thesis
Publisher Taylor & Francis Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0742-0528 ISBN Medium
Area Expedition Conference
Notes PMID:26375320 Approved no
Call Number IDA @ john @ Serial 1269
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Author Dauchy, R.T.; Xiang, S.; Mao, L.; Brimer, S.; Wren, M.A.; Yuan, L.; Anbalagan, M.; Hauch, A.; Frasch, T.; Rowan, B.G.; Blask, D.E.; Hill, S.M.
Title Circadian and melatonin disruption by exposure to light at night drives intrinsic resistance to tamoxifen therapy in breast cancer Type Journal Article
Year 2014 Publication Cancer Research Abbreviated Journal Cancer Res
Volume 74 Issue 15 Pages 4099-4110
Keywords *Cancer; breast cancer; melatonin; endocrinology; tamoxifen; *Circadian Rhythm; circadian disruption; human health; epidemiology
Abstract Resistance to endocrine therapy is a major impediment to successful treatment of breast cancer. Preclinical and clinical evidence links resistance to antiestrogen drugs in breast cancer cells with the overexpression and/or activation of various pro-oncogenic tyrosine kinases. Disruption of circadian rhythms by night shift work or disturbed sleep-wake cycles may lead to an increased risk of breast cancer and other diseases. Moreover, light exposure at night (LEN) suppresses the nocturnal production of melatonin that inhibits breast cancer growth. In this study, we used a rat model of estrogen receptor (ERalpha(+)) MCF-7 tumor xenografts to demonstrate how altering light/dark cycles with dim LEN (dLEN) speed the development of breast tumors, increasing their metabolism and growth and conferring an intrinsic resistance to tamoxifen therapy. These characteristics were not observed in animals in which the circadian melatonin rhythm was not disrupted, or in animals subjected to dLEN if they received nocturnal melatonin replacement. Strikingly, our results also showed that melatonin acted both as a tumor metabolic inhibitor and a circadian-regulated kinase inhibitor to reestablish the sensitivity of breast tumors to tamoxifen and tumor regression. Together, our findings show how dLEN-mediated disturbances in nocturnal melatonin production can render tumors insensitive to tamoxifen. Cancer Res; 74(15); 4099-110. (c)2014 AACR.
Address Departments of Structural and Cellular Biology and Tulane Cancer Center and Louisiana Cancer Research Consortium; Tulane Circadian Cancer Biology Group; and
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0008-5472 ISBN Medium
Area Expedition Conference
Notes PMID:25062775; PMCID:PMC4119539 Approved no
Call Number IDA @ john @ Serial 355
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Author Davis, S.; Mirick, D.K.; Stevens, R.G.
Title Night Shift Work, Light at Night, and Risk of Breast Cancer Type Journal Article
Year 2001 Publication JNCI Journal of the National Cancer Institute Abbreviated Journal JNCI Journal of the National Cancer Institute
Volume 93 Issue 20 Pages 1557-1562
Keywords light at night; oncogenesis; melatonin; shiftwork; breast cancer; *Cancer
Abstract Exposure to light at night may increase the risk of breast cancer by suppressing the normal nocturnal production of melatonin by the pineal gland, which, in turn, could increase the release of estrogen by the ovaries. This study investigated whether such exposure is associated with an increased risk of breast cancer in women. Methods: Case patients (n = 813), aged 20–74 years, were diagnosed from November 1992 through March 1995; control subjects (n = 793) were identified by random-digit dialing and were frequency matched according to 5-year age groups. An in-person interview was used to gather information on sleep habits and bedroom lighting environment in the 10 years before diagnosis and lifetime occupational history. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by use of conditional logistic regression, with adjustment for other potential risk factors. Results: Breast cancer risk was increased among subjects who frequently did not sleep during the period of the night when melatonin levels are typically at their highest (OR = 1.14 for each night per week; 95% CI = 1.01 to 1.28). Risk did not increase with interrupted sleep accompanied by turning on a light. There was an indication of increased risk among subjects with the brightest bedrooms. Graveyard shiftwork was associated with increased breast cancer risk (OR = 1.6; 95% CI = 1.0 to 2.5), with a trend of increased risk with increasing years and with more hours per week of graveyard shiftwork (P = .02, Wald chi-squared test). Conclusion: The results of this study provide evidence that indicators of exposure to light at night may be associated with the risk of developing breast cancer.
Address
Corporate Author Thesis
Publisher Place of Publication Editor
Language Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0027-8874 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number IDA @ john @ Serial 164
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Author Haim, A.; Zubidat, A.E.
Title Artificial light at night: melatonin as a mediator between the environment and epigenome Type Journal Article
Year 2015 Publication Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences Abbreviated Journal Philos Trans R Soc Lond B Biol Sci
Volume 370 Issue Pages 20140121
Keywords Human Health; melatonin; epigenetic modifications; epigenetics; epigenome; light pollution; breast cancer; oncogenesis; tumorigenesis; biomarkers
Abstract The adverse effects of excessive use of artificial light at night (ALAN) are becoming increasingly evident and associated with several health problems including cancer. Results of epidemiological studies revealed that the increase in breast cancer incidents co-distribute with ALAN worldwide. There is compiling evidence that suggests that melatonin suppression is linked to ALAN-induced cancer risks, but the specific genetic mechanism linking environmental exposure and the development of disease is not well known. Here we propose a possible genetic link between environmental exposure and tumorigenesis processes. We discuss evidence related to the relationship between epigenetic remodelling and oncogene expression. In breast cancer, enhanced global hypomethylation is expected in oncogenes, whereas in tumour suppressor genes local hypermethylation is recognized in the promoter CpG chains. A putative mechanism of action involving epigenetic modifications mediated by pineal melatonin is discussed in relation to cancer prevalence. Taking into account that ALAN-induced epigenetic modifications are reversible, early detection of cancer development is of great significance in the treatment of the disease. Therefore, new biomarkers for circadian disruption need to be developed to prevent ALAN damage.
Address The Israeli Center for Interdisciplinary Research in Chronobiology, Department of Evolutionary and Environmental Biology, University of Haifa, Mount Carmel, Haifa 31905, Israel; ahaim@research.haifa.ac.il
Corporate Author Thesis
Publisher Royal Society Place of Publication Editor
Language English Summary Language English Original Title
Series Editor Series Title The biological impacts of artificial light at night: from molecules to communities Abbreviated Series Title
Series Volume Series Issue Edition
ISSN ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number IDA @ john @ Serial 1119
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Author He, C.; Anand, S.T.; Ebell, M.H.; Vena, J.E.; Robb, S.W.
Title Circadian disrupting exposures and breast cancer risk: a meta-analysis Type Journal Article
Year 2014 Publication International Archives of Occupational and Environmental Health Abbreviated Journal Int Arch Occup Environ Health
Volume 88 Issue 5 Pages 533-547
Keywords Human Health; Circadian disruption; Breast cancer; Meta-analysis; Oncogenesis; BrCA; shift work; meta-analysis
Abstract PURPOSE: Shift work, short sleep duration, employment as a flight attendant, and exposure to light at night, all potential causes of circadian disruption, have been inconsistently associated with breast cancer (BrCA) risk. The aim of this meta-analysis is to quantitatively evaluate the combined and independent effects of exposure to different sources of circadian disruption on BrCA risk in women. METHODS: Relevant studies published through January 2014 were identified by searching the PubMed database. The pooled relative risks (RRs) and corresponding 95 % confidence intervals (CIs) were estimated using fixed- or random effects models as indicated by heterogeneity tests. Generalized least squares trend test was used to assess dose-response relationships. RESULTS: A total of 28 studies, 15 on shift work, 7 on short sleep duration, 3 on flight attendants, and 6 on light at night were included in the analysis. The combined analysis suggested a significantly positive association between circadian disruption and BrCA risk (RR = 1.14; 95 % CI 1.08-1.21). Separate analyses showed that the RR for BrCA was 1.19 (95 % CI 1.08-1.32) for shift work, 1.120 (95 % CI 1.119-1.121) for exposure to light at night, 1.56 (95 % CI 1.10-2.21) for employment as a flight attendant, and 0.96 (95 % CI 0.86-1.06) for short sleep duration. A dose-response analysis showed that each 10-year increment of shift work was associated with 16 % higher risk of BrCA (95 % CI 1.06-1.27) based on selected case-control studies. No significant dose-response effects of exposure to light at night and sleep deficiency were found on BrCA risk. CONCLUSIONS: Our meta-analysis demonstrates that circadian disruption is associated with an increased BrCA risk in women. This association varied by specific sources of circadian disrupting exposures, and a dose-response relationship remains uncertain. Therefore, future rigorous prospective studies are needed to confirm these relationships.
Address Department of Epidemiology and Biostatistics, College of Public Health, University of Georgia, 101 Buck Road, Health Sciences Campus, B.S. Miller Hall, Athens, GA, 30602, USA, willahe@uga.edu
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0340-0131 ISBN Medium
Area Expedition Conference
Notes PMID:25261318 Approved no
Call Number IDA @ john @ Serial 1064
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