Abstract: Living for extended periods in Antarctica exposes base personnel to extremes of daylength (photoperiod) and temperature. At the British Antarctic Survey base of Halley, 75 degrees S, the sun does not rise for 110 d in the winter and does not set for 100 d in summer. Photoperiod is the major time cue governing the timing of seasonal events such as reproduction in many species. The neuroendocrine signal providing photoperiodic information to body physiology is the duration of melatonin secretion which reflects the length of the night: longer in the short days of winter and shorter in summer. Light of sufficient intensity and spectral composition serves to suppress production of melatonin and to set the circadian timing and the duration of the rhythm. In humans early observations suggested that bright (>2000 lux) white light was needed to suppress melatonin completely. Shortly thereafter winter depression (Seasonal Affective Disorder or SAD) was described, and its successful treatment by an artificial summer photoperiod of bright white light, sufficient to shorten melatonin production. At Halley dim artificial light intensity during winter was measured, until 2003, at a maximum of approximately 500 lux in winter. Thus a strong seasonal and circadian time cue was absent. It seemed likely that winter depression would be common in the extended period of winter darkness and could be treated with an artificial summer photoperiod. These observations, and predictions, inspired a long series of studies regarding human seasonal and circadian status, and the effects of light treatment, in a small overwintering, isolated community, living in the same conditions for many months at Halley. We found little evidence of SAD, or change in duration of melatonin production with season. However the timing of the melatonin rhythm itself, and/or that of its metabolite 6-sulphatoxymelatonin (aMT6s), was used as a primary marker of seasonal, circadian and treatment changes. A substantial phase delay of melatonin in winter was advanced to summer phase by a two pulse 'skeleton' bright white light treatment. Subsequently a single morning pulse of bright white light was effective with regard to circadian phase and improved daytime performance. The circadian delay evidenced by melatonin was accompanied by delayed sleep (logs and actigraphy): poor sleep is a common complaint in Polar regions. Appropriate extra artificial light, both standard white, and blue enriched, present throughout the day, effectively countered delay in sleep timing and the aMT6s rhythm. The most important factor appeared to be the maximum light experienced. Another manifestation of the winter was a decline in self-rated libido (men only on base at this time). Women on the base showed lower aspects of physical and mental health compared to men. Free-running rhythms were seen in some subjects following night shift, but were rarely found at other times, probably because this base has strongly scheduled activity and leisure time. Complete circadian adaptation during a week of night shift, also seen in a similar situation on North Sea oil rigs, led to problems readapting back to day shift in winter, compared to summer. Here again timed light treatment was used to address the problem. Sleep, alertness and waking performance are critically dependent on optimum circadian phase. Circadian desynchrony is associated with increased risk of major disease in shift workers. These studies provide some groundwork for countering/avoiding circadian desynchrony in rather extreme conditions.

Abstract: BACKGROUND: Literature has identified detrimental health effects from the indiscriminate use of artificial nighttime light. We examined the co-distribution of light at night (LAN) and breast cancer (BC) incidence in Georgia, with the goal to contribute to the accumulating evidence that exposure to LAN increases risk of BC. METHODS: Using Georgia Comprehensive Cancer Registry data (2000-2007), we conducted a case-referent study among 34,053 BC cases and 14,458 lung cancer referents. Individuals with lung cancer were used as referents to control for other cancer risk factors that may be associated with elevated LAN, such as air pollution, and since this cancer type was not previously associated with LAN or circadian rhythm disruption. DMSP-OLS Nighttime Light Time Series satellite images (1992-2007) were used to estimate LAN levels; low (0-20 watts per sterradian cm(2)), medium (21-41 watts per sterradian cm(2)), high (>41 watts per sterradian cm(2)). LAN levels were extracted for each year of exposure prior to case/referent diagnosis in ArcGIS. RESULTS: Odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression models controlling for individual-level year of diagnosis, race, age at diagnosis, tumor grade, stage; and population-level determinants including metropolitan statistical area (MSA) status, births per 1,000 women aged 15-50, percentage of female smokers, MSA population mobility, and percentage of population over 16 in the labor force. We found that overall BC incidence was associated with high LAN exposure (OR = 1.12, 95% CI [1.04, 1.20]). When stratified by race, LAN exposure was associated with increased BC risk among whites (OR = 1.13, 95% CI [1.05, 1.22]), but not among blacks (OR = 1.02, 95% CI [0.82, 1.28]). CONCLUSIONS: Our results suggest positive associations between LAN and BC incidence, especially among whites. The consistency of our findings with previous studies suggests that there could be fundamental biological links between exposure to artificial LAN and increased BC incidence, although additional research using exposure metrics at the individual level is required to confirm or refute these findings.