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Fisher, N. A. (2006). Reclaiming the „Dark Sky“. Electrical Contracting Products, 9(6), 30–31.
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Anisimov, V. N. (2006). Light pollution, reproductive function and cancer risk. Neuroendocrinology Letters, 27(1-2), 35–52.
Abstract: At present, light pollution (exposure to light-at-night) both in the form of occupational exposure during night work and as a personal choice and life style, is experienced by numerous night-active members of our society. Disruption of the circadian rhythms induced by light pollution has been associated with cancer in humans. There are epidemiological evidences of increased breast and colon cancer risk in shift workers. An inhibition of the pineal gland function with exposure to the constant light (LL) regimen promoted carcinogenesis whereas the light deprivation inhibits the carcinogenesis. Treatment with pineal indole hormone melatonin inhibits carcinogenesis in pinealectomized rats or animals kept at the standard light/dark regimen (LD) or at the LL regimen. These observations might lead to use melatonin for cancer prevention in groups of humans at risk of light pollution.
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Curtis, A. M., & FitzGerald, G. A. (2006). Central and peripheral clocks in cardiovascular and metabolic function. Ann Med, 38(8), 552–559.
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Figueiro, M. G., Rea, M. S., & Bullough, J. D. (2006). Does architectural lighting contribute to breast cancer? J Carcinog, 5, 20.
Abstract: OBJECTIVES: There is a growing interest in the role that light plays on nocturnal melatonin production and, perhaps thereby, the incidence of breast cancer in modern societies. The direct causal relationships in this logical chain have not, however, been fully established and the weakest link is an inability to quantitatively specify architectural lighting as a stimulus for the circadian system. The purpose of the present paper is to draw attention to this weakness. DATA SOURCES AND EXTRACTION: We reviewed the literature on the relationship between melatonin, light at night, and cancer risk in humans and tumor growth in animals. More specifically, we focused on the impact of light on nocturnal melatonin suppression in humans and on the applicability of these data to women in real-life situations. Photometric measurement data from the lighted environment of women at work and at home is also reported. DATA SYNTHESIS: The literature review and measurement data demonstrate that more quantitative knowledge is needed about circadian light exposures actually experienced by women and girls in modern societies. CONCLUSION: Without such quantitative knowledge, limited insights can be gained about the causal relationship between melatonin and the etiology of breast cancer from epidemiological studies and from parametric studies using animal models.
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Haus, E., & Smolensky, M. (2006). Biological clocks and shift work: circadian dysregulation and potential long-term effects. Cancer Causes Control, 17(4), 489–500.
Abstract: Long-term epidemiologic studies on large numbers of night and rotating shift workers have suggested an increase in the incidence of breast and colon cancer in these populations. These studies suffer from poor definition and quantification of the work schedules of the exposed subjects. Against this background, the pathophysiology of phase shift and phase adaptation is reviewed. A phase shift as experienced in night and rotating shift work involves desynchronization at the molecular level in the circadian oscillators in the central nervous tissue and in most peripheral tissues of the body. There is a change in the coordination between oscillators with transient loss of control by the master-oscillator (the Suprachiasmatic Nucleus, SCN) in the hypothalamus. The implications of the pathophysiology of phase shift are discussed for long-term health effects and for the design of ergonomic work schedules minimizing the adverse health effects upon the worker.
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