High prevalence of breast cancer in light polluted areas in urban and rural regions of South Korea: An ecologic study on the treatment prevalence of female cancers based on National Health Insurance data

<div><p>It has been reported that excessive artificial light at night (ALAN) could harm human health since it disturbs the natural bio-rhythm and sleep. Such conditions can lead to various diseases, including cancer. In this study, we have evaluated the association between ALAN and prevalence rates of cancer in females on a regional basis, after adjusting for other risk factors, including obesity, smoking, alcohol consumption rates and PM₁₀ levels. The prevalence rates for breast cancer were found to be significantly associated with ALAN in urban and rural areas. Furthermore, no association was found with ALAN in female lung, liver, cervical, gastric and colon cancer. Despite the limitations of performing ecological studies, this report suggests that ALAN might be a risk factor for breast cancer, even in rural areas.</p></div

Outdoor artificial light at night, obesity, and sleep health: Cross-sectional analysis in the KoGES study

<p>Obesity is a common disorder with many complications. Although chronodisruption plays a role in obesity, few epidemiological studies have investigated the association between artificial light at night (ALAN) and obesity. Since sleep health is related to both obesity and ALAN, we investigated the association between outdoor ALAN and obesity after adjusting for sleep health. We also investigated the association between outdoor ALAN and sleep health. This cross-sectional survey included 8526 adults, 39–70 years of age, who participated in the Korean Genome and Epidemiology Study. Outdoor ALAN data were obtained from satellite images provided by the US Defense Meteorological Satellite Program. We obtained individual data regarding outdoor ALAN; body mass index; depression; and sleep health including sleep duration, mid-sleep time, and insomnia; and other demographic data including age, sex, educational level, type of residential building, monthly household income, alcohol consumption, smoking status and consumption of caffeine or alcohol before sleep. A logistic regression model was used to investigate the association between outdoor ALAN and obesity. The prevalence of obesity differed significantly according to sex (women 47% versus men 39%, <i>p</i> < 0.001) and outdoor ALAN (high 55% versus low 40%, <i>p</i> < 0.001). Univariate logistic regression analysis revealed a significant association between high outdoor ALAN and obesity (odds ratio [OR] 1.24, 95% confidence interval [CI] 1.14–1.35, <i>p</i> < 0.001). Furthermore, multivariate logistic regression analyses showed that high outdoor ALAN was significantly associated with obesity after adjusting for age and sex (OR 1.25, 95% CI 1.14–1.37, <i>p</i> < 0.001) and even after controlling for various other confounding factors including age, sex, educational level, type of residential building, monthly household income, alcohol consumption, smoking, consumption of caffeine or alcohol before sleep, delayed sleep pattern, short sleep duration and habitual snoring (OR 1.20, 95% CI 1.06–1.36, <i>p</i> = 0.003). The findings of our study provide epidemiological evidence that outdoor ALAN is significantly related to obesity.</p

Relative Risk of Myocardial Infarction per 1°C Change in Temperature above Threshold temperature by Subgroup.

<p>Model adjusted for precipitation, humidity, sea level pressure, and air pollutants (PM10, NO₂) using a spline function.</p><p>RR = Relative risk.</p><p>STEMI: ST elevation myocardial infarction.</p><p>Non-STEMI: Non-ST elevation myocardial infarction.</p><p>Spring: March–May, Summer: June–August, Autumn: September–November, Winter: December–February.</p><p>*<b><i>P</i></b><0.05;</p><p>** <b><i>P</i></b><0.001.</p>a<p>For heat exposure, temperature increase of 1°C above threshold.</p>b<p>For cold exposure, temperature decrease of 1°C below threshold.</p>c<p>Maximum temperature.</p>d<p>Mean temperature.</p>e<p>Minimum temperature.</p>f<p>Threshold temperature.</p>g<p>No threshold effect was identified.</p

Summary Statistics for Temperature and other Meteorological Variables with the Level of Air pollutants in Study Areas.

<p>SD: Standard deviation.</p><p>IQR: Interquartile range.</p

Relative Risk of Myocardial Infarction per 1°C Change in Diurnal Temperature Range (DTR) above the Threshold Temperature in All Regions by Season.

<p>Model adjusted for precipitation, humidity, sea level pressure, and air pollutants (PM10, NO₂) using a spline function.</p><p>RR = Relative risk.</p><p>STEMI: ST elevation myocardial infarction.</p><p>Non-STEMI: Non-ST elevation myocardial infarction.</p><p>Spring: March–May, Summer: June–August, Autumn: September–November, Winter: December–February.</p><p>*<b><i>P</i></b><0.05;</p><p>** <b><i>P</i></b><0.001.</p>a<p>Threshold temperature.</p>b<p>No threshold effect was identified.</p

Relative Risk of Myocardial Infarction per 1°C Change in Successive Daily Temperature Changes by Subgroup.

<p>Model adjusted for precipitation, humidity, sea level pressure, and air pollutants (PM10, NO₂) using a spline function.</p><p>RR = Relative risk.</p><p>STEMI: ST elevation myocardial infarction.</p><p>Non-STEMI: Non-ST elevation myocardial infarction.</p><p>Spring: March–May, Summer: June–August, Autumn: September–November, Winter: December–February.</p><p>*<b><i>P</i></b><0.05;</p><p>** <b><i>P</i></b><0.001.</p>a<p>Temperature rise between consecutive days.</p>b<p>Temperature fall between consecutive days.</p>c<p>No threshold effect was identified.</p

Daily adjusted emergency visit (DAEV) rate for MI according to maximum temperature by regions: A. Combined regions, B. Central region, C. Southern region.

<p>Lower figures showed change of R² values in each temperature by piecewise analysis and maximum R² value was chosen as the inflection point. The maximum R² value of the central region was 30.5°C; however, it did not show a threshold effect.</p

Widespread Anthropogenic Nitrogen in Northwestern Pacific Ocean Sediment

Sediment samples from the East China and Yellow seas collected adjacent to continental China were found to have lower δ¹⁵N values (expressed as δ¹⁵N = [¹⁵N:¹⁴N_sample/¹⁵N:¹⁴N_air – 1] × 1000‰; the sediment ¹⁵N:¹⁴N ratio relative to the air nitrogen ¹⁵N:¹⁴N ratio). In contrast, the Arctic sediments from the Chukchi Sea, the sampling region furthest from China, showed higher δ¹⁵N values (2–3‰ higher than those representing the East China and the Yellow sea sediments). Across the sites sampled, the levels of sediment δ¹⁵N increased with increasing distance from China, which is broadly consistent with the decreasing influence of anthropogenic nitrogen (N^ANTH) resulting from fossil fuel combustion and fertilizer use. We concluded that, of several processes, the input of N^ANTH appears to be emerging as a new driver of change in the sediment δ¹⁵N value in marginal seas adjacent to China. The present results indicate that the effect of N^ANTH has extended beyond the ocean water column into the deep sedimentary environment, presumably via biological assimilation of N^ANTH followed by deposition. Further, the findings indicate that N^ANTH is taking over from the conventional paradigm of nitrate flux from nitrate-rich deep water as the primary driver of biological export production in this region of the Pacific Ocean

The effect of dim light at night on cerebral hemodynamic oscillations during sleep: A near-infrared spectroscopy study

<p>Recent studies have reported that dim light at night (dLAN) is associated with risks of cardiovascular complications, such as hypertension and carotid atherosclerosis; however, little is known about the underlying mechanism. Here, we evaluated the effect of dLAN on the cerebrovascular system by analyzing cerebral hemodynamic oscillations using near-infrared spectroscopy (NIRS). Fourteen healthy male subjects underwent polysomnography coupled with cerebral NIRS. The data collected during sleep with dim light (10 lux) were compared with those collected during sleep under the control dark conditions for the sleep structure, cerebral hemodynamic oscillations, heart rate variability (HRV), and their electroencephalographic (EEG) power spectrum. Power spectral analysis was applied to oxy-hemoglobin concentrations calculated from the NIRS signal. Spectral densities over endothelial very-low-frequency oscillations (VLFOs) (0.003–0.02 Hz), neurogenic VLFOs (0.02–0.04 Hz), myogenic low-frequency oscillations (LFOs) (0.04–0.15 Hz), and total LFOs (0.003–0.15 Hz) were obtained for each sleep stage. The polysomnographic data revealed an increase in the N2 stage under the dLAN conditions. The spectral analysis of cerebral hemodynamics showed that the total LFOs increased significantly during slow-wave sleep (SWS) and decreased during rapid eye movement (REM) sleep. Specifically, endothelial (median of normalized value, 0.46 vs. 0.72, <i>p</i> = 0.019) and neurogenic (median, 0.58 vs. 0.84, <i>p</i> = 0.019) VLFOs were enhanced during SWS, whereas endothelial VLFOs (median, 1.93 vs. 1.47, <i>p</i> = 0.030) were attenuated during REM sleep. HRV analysis exhibited altered spectral densities during SWS induced by dLAN, including an increase in very-low-frequency and decreases in low-frequency and high-frequency ranges. In the EEG power spectral analysis, no significant difference was detected between the control and dLAN conditions. In conclusion, dLAN can disturb cerebral hemodynamics via the endothelial and autonomic systems without cortical involvement, predominantly during SWS, which might represent an underlying mechanism of the increased cerebrovascular risk associated with light exposure during sleep.</p

Bright light exposure before bedtime impairs response inhibition the following morning: a non-randomized crossover study

<p><b>Introduction</b>: Bright light exposure in the late evening can affect cognitive function the following morning either by changing the biological clock and/or disturbing sleep, but the evidence for this effect is scarce, and the underlying mechanism remains unknown. In this study, we first aimed to evaluate the effect of bright light exposure before bedtime on frontal lobe activity the following morning using near-infrared spectroscopy (NIRS) during a Go/NoGo task. Second, we aimed to evaluate the effects of bright light exposure before bedtime on polysomnographic measures and on a frontal lobe function test the following morning.</p> <p><b>Methods</b>: Twenty healthy, young males (mean age, 25.5 years) were recruited between September 2013 and August 2014. They were first exposed to control light (150 lux) before bedtime (from 20:00 h to 24:00 h) for 2 days and then to bright light (1,000 lux) before bedtime for an additional 5 days. We performed polysomnography (PSG) on the final night of each light exposure period (on nights 2 and night 7) and performed NIRS, which measures the concentrations of oxygenated and deoxygenated hemoglobin (OxyHb and DeoxyHb, respectively), coupled with a Go/NoGo task the following morning (between 09:30 h and 11:30 h). The participants also completed frontal lobe function tests the following morning.</p> <p><b>Results</b>: NIRS showed decreased hemodynamic activity (lower OxyHb and a tendency toward higher DeoxyHb concentration) in the right frontal lobe during the NoGo block after 1000-lux light exposure compared with that during the NoGo block after 150-lux light exposure. The commission error rate (ER) during the Go/NoGo task was higher after 1000-lux light exposure than that during the Go/NoGo task after 150-lux light exposure (1.24 ± 1.09 vs. 0.6 ± 0.69, <i>P </i>= 0.002), suggesting a reduced inhibitory response.</p> <p><b>Conclusion</b>: This study shows that exposure to bright light before bedtime for 5 days impairs right frontal lobe activation and response inhibition the following morning.</p