Table Info

Table 2.

List of reviewed studies, organized chronologically by publication year¹

REF²	Year	Study type³	Cohort size and study design	Main results	Limitations
ALAN
ALAN and sleep
[111]	2002	Field	154 postmenopausal women, with a mean age of 66.7 years, underwent one-week continuous recordings of light exposure and sleep using wrist actigraphy. Mood was evaluated using a questionnaire.	Pre-bedtime illumination (median 24 lux) had no significant impact on sleep. However, total 24-hour light exposure correlated with shorter sleep latency (P < 0.01), wakefulness within sleep (P < 0.05), and depressed mood (P < 0.01)	A homogeneous cohort in age and gender may influence light preferences and health. Actigraphy sensors may not fully capture light exposure, and ambient light recordings are limited. Spectral composition was also not considered
[10]	2013	Lab	10 healthy volunteers were exposed to two conditions over two nights: no light and 40 lux luminance, while PSG monitored sleep parameters.	Nights with lights-on were associated with increased N1 sleep, decreased SWS, and increased arousal. Moreover, brain activity was observed to decrease during NREM sleep under lights-on conditions.	Small cohort sizes and controlled conditions may not fully reflect real-world scenarios. The study did not account for spectral composition and relied solely on a single light intensity.
[114]	2013	Lab	30 individuals were exposed to light sources with temperatures of 6,500 K, 2,500 K, and 3,000 K at intensities ranging from 27 to 29.2 lux. The study protocol included dark conditions followed by 2 h of exposure sleep metrics were monitored using a PSG device.	All-night NREM EEG power density showed lower frontal power with 6,500 K light compared to 2,500 K (0.8%) and 3,000 K (0.2%). Additionally, SWS activity decreased by 0.4% and 0.3%, and total sleep time was shorter by 4 min and 12.7 min with 6,500 K light compared to 2,500 K and 3,000 K, respectively.	A small cohort size and controlled conditions may not accurately reflect real-world scenarios. Additionally, the study did not account for changes in light intensity.
[110]	2017	Field	20 healthy volunteers were monitored for three weeks using PSG and actigraphy to collect sleep metrics. Their light exposure was monitored using wrist actigraphy.	Later circadian phases were linked to lower light intensity (P < 0.01), delayed light exposure (P < 0.001), and later sleep timing (P < 0.001). Light exposure above 10 lux increased awakenings (P < 0.05), while delayed exposure reduced REM latency (P < 0.05). Lower light levels were associated with more REM sleep (P < 0.001), and higher light intensity with early exposure led to greater SWS accumulation (P < 0.05).	Limitations include a small cohort, potential obstruction of actigraphy light sensors, and reliance on ambient light measurements that may not accurately reflect perceived light. Additionally, the study did not account for the light’s spectral composition.
[115]	2017	Lab	19 volunteers (mean age 24.3 years) were exposed to light from computer screens with varying intensities (80 lux and 350 lux) and wavelengths (460 nm and 650 nm). Sleep metrics were collected with PSG, MLT levels from urine, and body temperature were recorded at set times. Behavioral evaluation was performed using questionnaires.	SWL exposure was linked to shorter sleep duration (8.6 min to 16.4 min), increased WASO by 2.1% to 3.1% (P < 0.01), decreased SE by 2.1% to 3.1% (P < 0.01), and reduced SWS by 6.5% to 7.7% (P < 0.05). On SWL exposure nights, body temperature was higher, MLT levels were lower (P < 0.05), and subjective sleep quality, mood, and attention were worse, with attention impairment significant (P < 0.05).	The 22-inch LED screens used may not represent other technologies or sizes. Measurements were limited to one night per light condition, restricting long-term effects. Daytime exposure, which influences MEL levels and circadian function, was not recorded. The small cohort and controlled setting may not reflect real-world scenarios.
[112]	2023	Field	59 volunteers wore wrist actigraphy to measure light exposure and collect sleep metrics over seven days, from February to July 2022. Personal attributes were collected using questionnaires and sleep diaries	Earlier bedtimes were linked to afternoon light exposure (13:00–17:00). Longer bedtimes corresponded to extended sleep on high light exposure (> 1 lux) days, while more natural light was associated with earlier sleep onset. ALAN exposure above 10 lux before sleep was tied to earlier sleep onset, peaking in the last 30 min before bedtime. Each 1 log lux increase in light exposure extended sleep onset by 0.5 h (P < 0.05).	The five-month data collection period may introduce seasonal bias. Questionnaires are prone to omission and recall biases. Actigraphy light sensors could be obstructed, recording ambient rather than perceived light. Additionally, the spectral composition was not considered
ALAN and MLT
[119]	1980	Lab	6 volunteers underwent a two-night protocol: 500 lux on the first night and 2,500 lux on the second. Two volunteers continued for two additional nights, with 1,500 lux on the third night and darkness on the fourth. Light intensities were measured at eye level, and MLT synthesis was assessed via blood samples.	MLT levels decreased (P < 0.05) within 10 min to 20 min of exposure to 2,500 lux incandescent light, nearing daytime levels within 1 h (P < 0.01). MLT levels quickly rebounded to pre-exposure levels within 40 min after returning to darkness. Exposure to 500 lux did not affect MLT levels significantly. Subjects exposed to 1,500 lux light showed intermediate MLT levels, with recovery similar to that after exposure to 2,500 lux.	The small cohort size and controlled conditions may not accurately reflect real-world scenarios. Additionally, the study did not account for the spectral composition or personal confounders of the volunteers.
[124]	1995	Lab	11 blind patients with no conscious perception of light and 6 healthy men aged 20 years to 25 years were exposed to 10 lux to 15 lux during baseline and 6,000 lux to 13,700 lux during stimulus exposures. Body temperature and blood samples for plasma MLT evaluation were collected at fixed intervals	All healthy individuals showed MLT suppression in response to bright light, with levels averaging 66% lower during the last 60 min of exposure compared to 24 h earlier. Blind patients who did not experience sleep difficulties, also showed MLT suppression, with a 69% decrease following bright light exposure. These blind patients maintained stable entrainment to a 24-hour day in repeated measurements	A small cohort size and controlled conditions, which may not fully represent real-world scenarios.
[120]	2001	Lab	15 volunteers (mean age 31.8 years) were exposed to light spectra (470 nm to 660 nm) aimed at the pupil. Over a 6-week protocol, they experienced various spectral conditions. Saliva MLT was sampled at fixed intervals.	The shorter wavelengths (470 nm, 497 nm, and 525 nm) caused significant MLT suppression, ranging from 65% to 81% (P < 0.0001). They also resulted in the greatest delay in simulated light MLT onset on the second night, ranging from 27 min to 36 min.	A small cohort size and controlled conditions may not accurately represent real-world scenarios.
[12]	2005	Lab	48 individuals, with a mean age of 23 years, were exposed to light intensities ranging from < 0.03 lux to 9,500 lux over three consecutive days. During the study, body core temperature and blood plasma MLT levels were monitored at regular intervals.	Significant shifts in MLT peak midpoint were seen at all light intensities compared to < 0.03 lux (P < 0.05). Suppression was minimal below 15 lux but complete above 200 lux. The circadian system responds logarithmically, with half-maximal effects at 50–160 lux and saturation at 1,400 lux. MLT suppression reached half-max effects at 10–200 lux and saturation at 1,100 lux.	Background light could significantly influence the responsiveness of the circadian timing system. Additionally, the study did not account for spectral composition. Lastly, the study was conducted under controlled conditions, which may not accurately reflect real-world scenarios.
[125]	2007	Lab	2 blind subjects participated in parallel experiments: a 56-year-old male and an 87-year-old female, both without light perception. In Experiment #1, the male underwent a 14-day inpatient study with random exposure to 555 nm and 460 nm light for 6.5 h, with plasma MLT measured via blood samples and sleep assessed by EEG. In Experiment #2, the female’s pupil constriction response to various monochromatic light wavelengths and irradiances was tested for 10 s.	In Experiment #1, 555 nm light had no effect on plasma MLT, while 460 nm light reduced it by 57% and caused a 1.2-hour phase delay in the circadian MLT rhythm, compared to a 0.4-hour delay with 555 nm light. Blue light increased alpha EEG activity and reduced subjective sleepiness, consistent with its effects in sighted individuals. In Experiment #2, irradiance-response curves matched vitamin A opsin-pigment nomograms (P < 0.01) for all three cones, indicating pupil constriction was driven by a photopigment with a peak at 476 nm. This suggests that ipRGCs mediate both pupillary and circadian responses to light, even in the absence of rods and cones.	A small cohort size and controlled conditions may not fully represent real-world scenarios. Additionally, the male subject received a pupil dilator before each experimental light exposure. While this approach is acceptable in experimental settings, it may not fully replicate real-world conditions of light exposure.
[129]	2011	Retro	116 healthy volunteers aged 18 to 30 participated in two inpatient studies. In Study #1, 104 volunteers followed a 9–10 day protocol involving enforced wakefulness for 30–50 h. In Study #2, 12 volunteers were exposed to 200 lux daily for 14 days, followed by a 40-hour constant routine under the same light intensity. Blood samples were collected at intervals to monitor plasma MLT concentrations.	In Study #1, MLT onset occurred 23 min before sleep under room light conditions (< 200 lux) but 1 h and 57 min before bedtime under dim light (P < 0.05), marking a 94-minute earlier onset. Room light reduced MLT secretion duration by 1 h and 32 min compared to dim light (P < 0.05). Additionally, 78.6% of volunteers had earlier MLT onset by over an hour, and MLT concentrations were reduced by 71.4% on average under room light. In Study #2, four of five individuals showed significant MLT suppression with room light exposure, while seven of eight experienced greater suppression with higher light intensities (~200 lux).	Study conditions, specifically dim and bright light exposures, were not balanced, which could affect the accuracy of comparisons. Additionally, the study did not account for spectral composition. Lastly, the studies were conducted under controlled conditions that may not fully reflect real-life scenarios.
[122]	2013	Lab	9 volunteers (mean age 26.3 years) were exposed to six light conditions, varying in intensity from < 10 lux to 500 lux and temperature from 2,000 K to 6,000 K, over six days. MLT concentration was measured from saliva, and alertness was assessed via questionnaires.	Comparisons showed significant decreases in MLT levels with three of the four lamps containing blue components (P < 0.03). The 500 lux, 6,000 K condition did not significantly affect MLT levels (P = 0.07), and the 130 lux, 2,000 K condition had no effect. Subjective alertness significantly increased after exposure to the 130 lux, 6,000 K; 500 lux, 6,000 K; and 500 lux, 5,000 K conditions (P < 0.05).	The study’s small cohort size and controlled conditions may not fully represent real-world scenarios. Additionally, as suggested by the authors, it lacks outcome variables such as sleep parameters and objective measures of behavioral variables.
[126]	2018	Lab	18 healthy blind subjects were exposed to 6,807 lux from a 4,100 K source. The study included 5–6 days of inpatient observation followed by a 38-day protocol where 10 volunteers adjusted to a 28-hour “day” which included light stimuli. Saliva and blood samples were collected to measure MLT concentration, and body core temperature was recorded at set intervals.	During 6.5 h of light exposure, MLT concentrations decreased by an average of 71.6% in five blind participants, with each showing reductions over 33%. Four had a normally phased 24-hour rhythm in urinary MLT before the study, while the fifth, with an irregular rhythm and opaque scleral shells, showed a positive response after removing the shells. Among those without MLT suppression, only one had a 24-hour urinary rhythm prior to the study, likely due to non-photic cue entrainment.	A small cohort size and controlled conditions, which may not fully represent real-world scenarios.
[121]	2019	Retro	To model the relationship between alpha-opic illuminances and MLT suppression, early study results were reanalyzed and validated.	The study found the highest R² value (0.87) with melanopic lux and melanopsin-weighted irradiances, indicating that MLT suppression is strongly predicted by melanopsin-weighted illuminance. MLT suppression was found to be most sensitive at 480 nm SWS light and is enhanced by blue-enriched light stimuli. Moreover, the model demonstrated good predictive performance.	The model is based on a single dataset capturing a narrow circadian phase, limiting its applicability to other phases and conditions. Moreover, its reliance on controlled settings may not reflect real-world scenarios.
[123]	2022	Lab	100 healthy volunteers (aged 18 to 30) completed a nine-day protocol involving 30- and 50-hour constant routines and exposure to various light spectra and intensities. Saliva and blood samples were collected to assess MLT secretion.	MLT suppression and circadian phase resetting were best modeled with peak sensitivities at 481 nm and 483 nm, respectively. Initially, MLT suppression peaked at 441 nm and 550 nm, indicating significant early contributions from S and L+M cones. Over time, the peak shifted to 485 nm, reflecting a predominant influence of melanopsin. Similarly, circadian phase resetting showed peak sensitivities from 445 nm to 487 nm, with a shift from S-cones to melanopsin as exposure continued.	The study was conducted under controlled conditions, and participants used a pupil dilator, which may not reflect real-life scenarios. Additionally, it was not documented whether maximum pupil dilation was maintained throughout the 6.5-hour light exposure, potentially affecting the results.
[127]	2022	Field	580 participants (mean age 71) monitored short-wavelength ALAN exposure and sleep metrics over two days using a headband for light, actigraphy for sleep data, and a PSQI questionnaire for subjective evaluation. Daily urine samples assessed MLT levels. The study was conducted from November 2012 to March 2014.	Increased short-wavelength ALAN was significantly linked to higher global PSQI scores and sleep disturbances (P = 0.004 and P = 0.006). Multivariable analysis showed a higher OR for disturbances in the highest tertile compared to the lowest (P = 0.006). MLT levels were significantly lower in the highest tertile (P = 0.039). Objective sleep measures revealed longer sleep onset latency (P < 0.001), increased WASO (P < 0.05), and decreased SE (P < 0.001) in the highest tertile.	The study’s extended duration raises concerns about seasonal effects. Despite a large cohort, each volunteer was observed for only two days, limiting individual data. Inconsistent MLT and sleep measurements, a cross-sectional design, and reliance on a homogeneous elderly population limit generalizability and introduce potential bias.
Health effects of ALAN exposure and MLT suppression
[132]	2007	Lab	10 volunteers (mean age 21.9) were asked to wear wrist actigraphy for one week to measure light exposure and to sleep in the lab during a night session with 2 h of exposure to 1,000 lux bright light. Saliva samples were collected for MLT measurement, and subjective sleep data were obtained via questionnaires. The study, conducted in winter and summer, to assess seasonal effects	Awakening occurred about 30 min earlier in winter (P < 0.05), with higher MLT amplitude. MLT concentration decreased with light exposure, but the suppression percentage was significantly greater in winter (66.6%) compared to summer (37.2%) (P < 0.01). Winter ambient light levels were about half those of summer (P < 0.01). There was considerable variability in MLT levels, light exposure, and suppression among individuals. Other sleep and MLT metrics showed no significant seasonal differences.	The small cohort size and controlled conditions may not accurately reflect real-world scenarios. Additionally, using a wrist-worn device to measure light could be inaccurate if the light sensor becomes obstructed. Moreover, the study did not account for variations in light spectra, which could differ between ALAN sources and sunlight across different seasons.
[157]	2019	Lab	11 healthy volunteers (mean age 23 for the control group, 27 for the exposure group) underwent a 4-day simulated night shift protocol. After a 24-hour baseline, participants followed a 10-hour delayed sleep schedule. The control group was exposed to dim light (< 10 lux), while the exposure group received 6,500 lux of bright light. Blood samples were for MLT measurement and microarray analysis.	In a study of 492 probe sets with a 24-hour rhythm, 67% showed altered circadian expression under bright light during a simulated night shift, with gene rhythms delayed by 7.8 h on average. The bright light group had a significantly greater delay in the midpoint of MLT secretion (7.6 h) compared to controls (0.4 h, P = 0.014). Gene analysis indicated bright light's strong phase-shifting effect, affecting genes related to immune processes, lipid metabolism, and circadian rhythm regulation.	The study is limited by a small cohort size, a narrow age range (18–30 years), and a skewed sex distribution (10 males vs. 1 female). Furthermore, the controlled conditions employed may not fully replicate real-world scenarios.
Noise
Noise sleep and CORT
[193]	1983	Field	26 healthy individuals, who had lived near a busy street slept under various conditions, including changes in bedroom location, earplugs, and double-glazed windows, to simulate both quiet and typical nighttime environments. Their sleep behaviors were monitored using EEG signals, while sound was recorded with microphones and tape recorders.	Noise peaks of 50.3 dB(A) can cause awakenings, while changes in sleep state occur at 48.5 dB(A), and transient reactions at 47.6 dB(A). The study suggests that limiting noise peaks to below 40 dB(A) can prevent 80% of sleep disturbances and 87% of awakenings while keeping noise below 45 dB(A) can avoid two-thirds of sleep impairments. Additionally, peak noises during quiet conditions caused shifts in sleep at lower intensities [42–44 dB(A)] compared to noisier conditions [50–53 dB(A)].	Changes in sleep settings affected room temperature and other environmental factors, which may have influenced sleep. This complicates the observed relationship between noise and sleep, as other interactions could have played a role. Additionally, the study’s small sample size limits the generalizability of its findings.
[194]	1987	Lab	The study included a pilot with one participant exposed to noise levels from 40 dB(A) to 70 dB(A) in 5 dB(A) increments, and a main study with 9 individuals exposed to: (a) a single truck pass, (b) continuous all-night traffic noise, and (c) a combination of both. Sleep metrics were recorded using PSG, and mood was assessed via questionnaires.	Awakening reactions in response to car passages were observed at 55 dB(A) (P < 0.05). An increase in noise level from 45 dB(A) to 55 dB(A) significantly affected sleep stages (P < 0.01). Additionally, noise peaks relative to background levels were better predictors of arousal and changes in sleep stages than absolute noise peak levels. Subjective mood and sleep quality questionnaires supported these findings.	The study’s small cohort size and controlled conditions may not fully reflect real-world scenarios.
[195]	1990	Lab	18 individuals (mean age 20.8) were divided into three groups. The first and second groups were exposed to infrasound and low-frequency sounds (10–63 Hz) at 50–105 dB(A). The third group was subjected to simulated traffic noise (25–1,600 Hz) at 40 dB(A), 50 dB(A), and 60 dB(A) for 30 s every 20 min during sleep. Sleep patterns were monitored using EEG.	The reaction rate during N1 was significantly higher than in other sleep stages, with REM and N2 being more affected than N3 (P < 0.01), indicating that lighter sleep stages are more sensitive to infrasound and low-frequency sounds. However, in groups one and two, the relationship between infrasound, low-frequency sounds, and sleep metrics was insignificant compared to control nights. In group three, exposure to 40 dB(A), 50 dB(A), and 60 dB(A) led to awakening rates of 33%, 50%, and 100%, respectively, with 40 dB(A) also causing changes in sleep stages in 51% of cases.	The study’s small cohort and controlled conditions may not reflect real-world scenarios. It also did not account for indoor noise from appliances, which could impact results. Additionally, variability in noise perception among the three groups may introduce bias and affect the findings.
[191]	2001	Retro	This study is based on the results of road traffic noise and urine catecholamine levels during sleep. Overnight urine samples were analyzed for adrenaline and NA. Noise exposure was assessed through traffic counts, and indoor exposure was evaluated through questionnaires.	A significant increase in renal adrenaline was associated with a higher number of cars per day (P < 0.05). Additionally, subjective perceptions of indoor noise by volunteers were strongly correlated with urinary NA secretion (P < 0.001). Renal adrenaline levels were 26% higher in women experiencing high levels of disturbance compared to those with low disturbance (P < 0.05).	The study lacked data on daytime noise exposure, making it difficult to assess cumulative effects on adrenaline and NA secretion. Additionally, noise exposure was estimated from traffic counts rather than direct measurements, potentially misrepresenting actual noise conditions.
[192]	2002	Field	16 volunteers were exposed to airport noise for 40 nights, peaking at 65 dB(A). The noise occurred from 23:00 to 06:00, with an average continuous level of 42 dB(A). Urine samples were collected nightly to measure CORT, adrenaline, and NA, and subjective data were gathered via a questionnaire.	Nocturnal noise exposure significantly increased CORT levels in men but not in women, suggesting greater men sensitivity to noise (P = 0.038). Variability in adaptation types was observed, with changes in CORT excretion patterns and significant associations between adaptation differences and CORT variations (P = 0.004).	The study is limited by its small sample size and its exclusive focus on airplane noise, which restricts the generalizability of the findings to other common noise sources, such as road traffic and indoor appliances.
[206]	2003	Lab	10 volunteers (mean age 24.7) were exposed to 8 h of 75 dB(A) mill noise. Sleep was monitored with PSG and questionnaires, and blood samples were collected to measure CORT levels.	On the exposure night, both REM sleep and total sleep durations were significantly reduced compared to quiet conditions (P < 0.001 and P < 0.05, respectively). REM sleep onset was delayed (P < 0.01), and there were more frequent stage shifts (P < 0.001). SE fell below 80%, and CORT levels were elevated during the exposure night.	The controlled conditions and small sample size limit the study’s applicability and generalizability to real-world settings. Additionally, the brief exposure duration restricts the assessment of continuous effects.
[209]	2006	Field	360 individuals, equally divided between children (mean age 10.9 years) and parents (mean age 42 years), provided sleep habit information through questionnaires and interviews. Noise exposure was categorized by road traffic levels [< 55 dB(A), 55–59 dB(A), 60–64 dB(A), and > 64 dB(A)].	For parents, road traffic noise significantly (P < 0.05) affected sleep quality, awakenings, and perceived interference. Children also showed a notable link between noise and sleep quality, as well as daytime sleepiness. Despite reporting better sleep quality and fewer awakenings, children’s wrist-actigraphy showed that parents had better objective sleep (P < 0.001). Both groups experienced acute sleep disturbances at 60 dB(A) to 64 dB(A) noise levels.	Actigraphy, which tracks body movements, may misclassify children’s sleep due to their higher sleep activity compared to adults. The study’s noise assessment, categorized by road traffic noise, might not accurately reflect direct exposure. Additionally, sleep questionnaires are prone to recall and response biases.
[72]	2011	Lab	12 volunteers with a mean age of 27 years underwent a 3-day lab exposure protocol, with the first night serving as an adaptation period. On the second and third nights, noise stimuli were presented every 30 s during sleep, starting at 40 dB(A) and increasing in 5 dB(A) increments until arousal, a change in sleep stage, or a maximum of 70 dB(A). PSG was used to collect sleep metrics.	Increased sound levels significantly disturbed sleep, with effects varying by sound type. Arousal probabilities differed among sleep stages: N2 was different from N3 and REM (P < 0.001), while N3 and REM were similar. Arousal rates were lower during N3 compared to N2, and REM had a more consistent arousal response to different sounds. Sound-induced arousals significantly increased HR, with the highest responses during REM, followed by N3 and N2. Additionally, HR response times from arousal onset to peak were shorter during REM sleep.	The small cohort, narrow age range, and controlled conditions limit the study’s generalizability. Real-world noise exposure is more variable and interactive, which may amplify physiological and psychological effects differently than the fixed noise administration used in the study.
[196]	2011	Field	40 healthy volunteers, with a mean age of 48.5 years, participated in the study. Half of the cohort was exposed to road traffic noise, while the other half was exposed to rail noise. Data were collected over two consecutive nights, including sound recordings and PSG to measure sleep metrics.	Road traffic noise did not affect sleep, but rail noise exposure was significantly linked to increased WASO and reduced REM sleep (P < 0.01). A significant difference was found in arousals and REM sleep between rail noise levels below and above 50 dB(A) (P = 0.02). Specifically, exposure to rail noise above 50 dB(A) resulted in shorter REM sleep, while exposure below 50 dB(A) led to more arousal.	The study did not control for non-traffic noises, and unattended data recording prevented sensitivity adjustments. Personal confounders and individual noise sensitivity were not analyzed. The small sample size and brief duration may not fully capture noise effects or variability, limiting generalizability and may introduce bias.
[198]	2012	Retro	Data from 7,019 participants (mean age 50.5) in the Finnish Public Sector Study Cohort (2004–2009) were analyzed for sleep duration and insomnia. Nighttime traffic noise levels were calculated, and personal confounders and socioeconomic attributes were assessed via questionnaires	Participants exposed to noise levels > 55 dB(A) had significantly higher OR for insomnia symptoms and nonrestorative sleep compared to those exposed to ≤ 45 dB(A). Frequent nighttime awakenings were notably linked to higher anxiety scores at > 55 dB(A). The impact of noise exposure > 55 dB(A) on insomnia was more pronounced among women and obese individuals compared to men and those who were not obese.	The study’s generalizability is limited by its homogeneous population and incomplete traffic data. Key limitations include exposure misclassification, missing nighttime traffic intensity data, and potential bias from variations in noise levels and survey timing.
[201]	2014	Lab	103 patients, with a mean age of 60 years, across 29 ward rooms, completed the PSQI and the Leeds Sleep Evaluation Questionnaire to evaluate their sleep performance. Noise exposure during one night of sleep was measured using type-1 noise level dosimeters.	The study found significant declines in sleep quality among patients. Overall, 86% reported disturbed sleep, linked to daily average noise levels of 63.5 dB(A) (P < 0.05). Female patients had higher PSQI scores (P = 0.06), and those with severe disease had poorer sleep (P = 0.04). Patients not on sleep-interfering medications fared better (P = 0.08). Noise levels above 49.3 dB(A) during the day and 34.2 dB(A) at night were associated with increased disturbances, with common sources being caregivers, visitors, other patients, toilet flushing, and medical devices.	The small cohort limits statistical power and generalizability. Sleep assessments via questionnaires may suffer from omissions and recall bias. Dosimeters did not capture detailed noise characteristics, and psychological factors like stress and depression, which are common among patients, were not considered.
[210]	2015	Retro	The study, based on a 2007 environmental and health survey in Sweden, included 2,612 participants (median age 46 years) living near rail and noisy roads. Noise exposure was categorized into six levels: < 40 dB(A), 40–44 dB(A), 45–49 dB(A), 50–54 dB(A), 55–59 dB(A), and ≥ 60 dB(A). The survey assessed participants’ annoyance, sleep quality, bedroom window orientation, and subjective noise perception.	Access to a quiet or green space decreased with higher noise levels. A bedroom window facing green space significantly reduced noise annoyance (P < 0.05) and concentration problems. Higher noise exposure was linked to poorer sleep quality. Men reported fewer sleep issues compared to women, while those under financial strain experienced more sleep problems.	Limitations include reliance on potentially biased self-reported data, unconsidered factors like OSA, and unvalidated scales. With a 54% response rate, there may be selection bias, especially in high-noise areas. Noise assessments lacked details on building characteristics and other sources, and combining noise types could skew results. Assigning noise exposure by building rather than individual units may also introduce errors.
[203]	2018	Lab	64 patients, averaging 63.9 years, completed RCSQ. Noise exposure was recorded for one night using a microphone and laptop.	A daily average sound pressure of 54 dB(A) was associated with poorer sleep (P < 0.05). Additionally, women reported better sleep quality than men (P < 0.01).	Small cohort limits generalizability. Sleep questionnaires may introduce recall and response biases, especially in critically ill patients. A single night’s measurement does not capture long-term effects.
[207]	2018	Lab	48 day-shift workers (mean age 45.1) were split into two groups: one experienced high noise followed by low noise, and the other the reverse. CORT levels were measured from blood samples, and sleep was recorded using PSG.	Sleeping after exposure to 76.8 dB(A) was linked to longer sleep durations but decreased SWS and SE (P < 0.05). Additionally, blood pressure, sympathetic activity, and CORT levels significantly increased following noise exposure (P < 0.05).	Controlled conditions and a small sample size limit generalizability and may increase Type II errors. Protocol deviations, unmonitored lab noise, and non-representative noise composition may also impact results.
[208]	2019	Field	From May to November 2016, 105 volunteers from 94 households (mean age 52.1 years) wore wrist actimeters for seven consecutive days to monitor sleep. Environmental and room acoustics were assessed through outdoor and sound measurements.	Average noise exposure was not a significant predictor of sleep quality. However, noise during the first 4 h of bedtime reduced sleep latency by 5.6 min per 10 dB(A) increment. Conversely, noise exposure during the final 3 h before waking decreased SE by 2% to 3% per 10 dB(A) increment.	Indoor noise was estimated from outdoor measurements, potentially misrepresenting conditions. Censoring noise levels below 20 dB(A) and missing nightly data on window positions contributed to exposure misclassification, reducing statistical power.
[220]	2020	Lab	50 volunteers (mean age 51.2 years), including 24 living near a wind turbine, participated in a 3-night study: habituation, wind turbine noise exposure, and quiet control. Sleep was assessed with PSG, CORT levels were measured from saliva samples, and subjective experiences were evaluated with morning questionnaires.	During exposure nights, REM duration increased by 16.8 min, while the amount of REM sleep decreased by 11.1 min (−2.2%). Other objective sleep measures did not differ significantly between nights. Self-reported sleep quality was consistently worse on exposure nights, and individuals living near wind turbines reported poorer overall sleep compared to the reference group.	The study faced potential self-selection bias, as the exposed group included individuals who had complained about wind turbines. The small sample size, deviations from requirements, and laboratory setting may not reflect real-life conditions, introducing bias. Awareness of experimental conditions could also influence self-reported outcomes.
[211]	2021	Survey	A total of 495 participants completed a questionnaire covering sleep performance, occupational strain, and demographic and lifestyle factors. Nocturnal noise exposure was modeled using road traffic data based on the Nordic prediction method.	Nocturnal traffic noise was negatively associated with self-reported poor sleep, while poor sleep was more common in medium- and high-traffic areas. A quiet bedroom façade reduced the incidence of poor sleep, especially at 45–50 dB(A). No difference in poor sleep prevalence was found between windows facing no street and those facing a low-traffic street.	The study relied on self-reported sleep data, which may be biased by misclassification and recall issues. It did not directly link disturbances to road noise, affecting accuracy. A restrictive sleep cut-off and lack of OSA screening could have influenced results. Incomplete data on bedroom orientation and noise exposure, with traffic noise as a proxy, may have biased estimates, and missing details on building specifics and other noise sources could have affected findings.
[197]	2022	Field	40 participants, mean age of 29.1 years, were monitored with PSG over five consecutive nights. Indoor sound levels were recorded using a type-1 sound level meter, while road traffic counts were obtained via a radar detector and analyzed into sound levels using custom-developed acoustic software.	Traffic noise events were positively associated with REM sleep (P < 0.001) and increased probability of awakening due to maximum noise pressure (P = 0.03) and age (P < 0.005). Conversely, a negative association was observed with SWS (P = 0.017) and the interaction between REM and age (P = 0.017).	The small sample size limits generalizability. Study locations with high noise levels may not represent other urban areas. Noise exposure was assessed from traffic counts rather than direct measurements, and the study did not consider confounders such as occupation, income, or temperature.
[204]	2022	Lab	148 patients in intensive care units, scheduled for surgery, with a mean age of 63 years, completed the RCSQ on their first night of admission. Noise levels were monitored over six weeks using a type-2 sound meter.	The study found no overall correlation between nighttime sound levels and sleep quality. However, patients with a Visual Analog Scale (VAS) score > 3 or those on hypnotic drugs had lower RCSQ scores (P < 0.05 and P < 0.01, respectively). Excluding these patients showed that each 1 dB(A) increase in nighttime noise was associated with a 3.92-point drop in RCSQ scores (P < 0.05).	The study did not account for pre-existing sleep disorders, age, obesity, or disease severity. The sound meter mostly captured staff noise rather than patient-specific sources. Assessments were based on the first night of admission, missing long-term effects, daytime sleep, and circadian disruptions, and lacked patient feedback on perceived sleep disruption causes.
The combined effect of ALAN and noise
[83]	1999	Field	In a 4-year study of 184 residents (mean age 83.9 years) from eight nursing homes, participants were divided into an intervention group and a control group. The intervention aimed to reduce noise and ALAN exposure. Light and noise levels were recorded with a light meter and microphone, while sleep metrics were collected via actigraphy.	While their behavioral intervention resulted in significant reductions in ALAN and noise exposure compared to the control group (P < 0.01), no significant changes were found in sleep patterns.	Noise intensity remained high post-intervention, with peaks over 50 dB(A), possibly impacting sleep and reducing effectiveness. The study also overlooked daytime napping, personal factors like medical conditions, and recorded ambient rather than direct exposure, potentially introducing bias.
[223]	2016	Eco	19,136 individuals aged 18 to 99 years completed questionnaires, including self-assessed noise levels. ALAN data were obtained from the Defense Meteorological Satellite Program using NASA’s VIIRS instruments.	Increased exposure to outdoor ALAN correlated with delayed bedtimes, later wake-up times, shorter sleep durations, and increased daytime sleepiness (P < 0.01). Intriguingly, noise levels showed no statistically significant correlation with sleep metrics.	Self-reported data may suffer from recall and misclassification biases. Relying on self-reported noise and average ALAN measurements could introduce exposure bias. The study also did not analyze the combined impact of ALAN and noise.
[70]	2021	Eco	7,230 individuals with a mean age of 34.5 years completed a national survey focusing on health and well-being, including sleep patterns. Outdoor ALAN exposure was assessed using NASA’s VIIRS data, while noise exposure was interpolated from road density maps.	Increased road density and ALAN intensity were associated with reductions in sleep duration (4.5% and 3%, respectively) and increases in sleep difficulty (3.5% and 11%, respectively) (P < 0.01). An interaction effect showed that higher ALAN in noisy areas led to longer sleep but greater sleep difficulty (P < 0.01), possibly due to ALAN penetrating sleeping areas where residents close shades due to heat and humidity.	This ecological study combines individual data with environmental estimates, risking misspecification and uncontrolled confounding, which prevents the establishment of causality. Additionally, relying on outdoor ALAN and noise estimates rather than direct indoor measurements may introduce exposure bias.
[229]	2021	Lab	103 patients in the intensive care unit, with a mean age of 53.6 years, completed the RCSQ. Their exposure to noise and ALAN was monitored hourly over one night using a Type 1 noise meter and a light meter.	The study revealed a mean noise level of 63.9 dB(A), with peak noise reaching 102 dB(A). The measured ALAN intensity averaged 104.1 lux, peaking at 271 lux. Both stressors were identified as significant predictors of poor sleep (P < 0.001).	As a cross-sectional study, causality is unclear. Self-reported data and ambient exposure measurements may introduce bias. Medication, psychological conditions, and the hospital setting might also affect sleep, limiting real-life applicability.
[153]	2022	Eco	Data from 51,562 individuals (mean age 66.8 years) in the California Teacher Study cohort were analyzed to evaluate sleep performance. ALAN exposure was assessed using the New World Atlas , and noise levels were derived from the US National Park Service Sound Map. Environmental factors, such as green spaces and air pollution, along with demographic and socioeconomic attributes, were also considered.	ALAN and air pollution were linked to shorter sleep durations (< 7 h), while noise was associated with longer sleep onset latency (> 15 min) per 10 dB(A) (P < 0.05). Conversely, green space was associated with increased sleep duration and decreased latency.	Self-reported data may be affected by recall and misclassification biases. The study lacks information on the timing of outdoor light exposure and did not consider pre-bedtime device use. Additionally, the US Parks noise model may be less accurate for smaller roadways, and data on ALAN and noise exposure during the night is missing, which could contribute to exposure bias.
[228]	2022	Survey	552 volunteers, with a mean age of 36.7 years, completed questionnaires detailing demographic attributes and reported exposure to ALAN and noise. They also filled out the PSQI, Munich Chronotype Questionnaire, Cognitive Failures Questionnaire, and General Health Questionnaire.	The perception of ALAN was significantly associated with poorer sleep quality (P < 0.002), while individuals reporting noise in their bedroom had higher PSQI scores (P = 0.018), suggesting poorer sleep. However, noise within the bedroom showed no significant correlation with sleep duration.	As a cross-sectional study, it cannot determine causality. Additionally, self-reported data may introduce recall bias and misclassification. Perceptions of ALAN and noise were not measured directly, which may lead to exposure bias. Moreover, ALAN measurements did not include pre-bedtime exposure.
[71]	2023	Field	72 volunteers, with a mean age of 44 years, from 44 localities in Israel, wore smartwatches to record their sleep metrics and used a smartphone to log exposure to ALAN and noise for 30 consecutive nights. Diaries recorded subjective data, and questionnaires were used to gather demographic, behavioral, habitual, and health information.	Exposure to ALAN and noise before bedtime significantly reduced sleep duration by 9.7% to 9.9% and SE by 2.4% to 2.8% (P < 0.01). While ALAN exposure during sleep had no significant impact, noise was notably disruptive, reducing sleep duration by 13.5% and SE by 4.4%. The combined effect of ALAN and noise led to a substantial decrease in sleep metrics, with reductions of 15.3% in duration and 8% in SE before sleep, and 14% and 9%, respectively, during sleep. The results suggest that ALAN and noise may amplify each other’s effects, potentially worsening health outcomes.	The study’s limitations include its short duration (one month) and single-country scope, which may limit generalizability. Most participants were under 60, potentially overlooking age-related impairments. Variability in personal smartphones and smartwatches, as well as the lack of seasonal and spectral considerations for light and noise, may also affect results.

ALAN: artificial light at night; CORT: cortisol; Eco: ecological; EEG: electroencephalographic; WASO: wakes after sleep onset; HR: heart rate; ipRGCs: intrinsic photosensitive retinal ganglion cells; S: shor wavelengths of light; L: long wavelengths of light; M: medium wavelengths of light; Lab: laboratory; MLT: melatonin; NREM: non-rapid-eye-movements; N1–N3: NREM 1 to 3 sleep stages; OR: odd ratio; OSA: obstructive sleep apnea; PSG: polysomnography; SWL: short wavelength light; PSQI: Pittsburgh sleep quality index; RCSQ: Richards-Campbell sleep questionnaire; REM: rapid eye movements; Retro: retrospective; SE: sleep efficiency; LED: light emitted diode; SWS: slow-wave sleep; NA: noradrenaline; VIIRS: Visible Infrared Imaging Radiometer Suit; ¹ Arranged from oldest to newest and excludes reviews, letters, or books, focusing primarily on studies investigating the relationship with circadian cycles, sleep, and MLT; ² Ref numbers are organized in the order they appear in the text; ³ The category “laboratory” covers research conducted in medical institutions, research facilities, and controlled clinical settings, whereas the “ecological” category includes both individual-based and population-based epidemiological studies

Declarations

Acknowledgments

The author wishes to express sincere gratitude to Boris A. Portnov from the University of Haifa for his invaluable insights, which have significantly enhanced this review. Special thanks are also extended to Noa Weiss and Noga Becker for their valuable assistance with language editing.

Author contributions

NMG: Conceptualization, Investigation, Methodology, Writing—review & editing, Writing—original draft.

Conflicts of interest

The author declares that he has no conflicts of interest.

Ethical approval

Not applicable.

Consent to participate

Not applicable.

Consent to publication

Not applicable.

Availability of data and materials

Not applicable.

Funding

Not applicable.

Copyright

References

Falchi F, Cinzano P, Elvidge CD, Keith DM, Haim A. Limiting the impact of light pollution on human health, environment and stellar visibility. J Environ Manage. 2011;92:2714–22. [DOI] [PubMed]

Longcore T, Rich C. Ecological light pollution. Front Ecol Environ. 2004;2:191–8. [DOI]

Goines L, Hagler L. Noise pollution: a modern plague. South Med J. 2007;100:287–94. [DOI] [PubMed]

Slabbekoorn H. Noise pollution. Curr Biol. 2019;29:R957–60. [DOI] [PubMed]

Coates PA. The Strange Stillness of the Past: Toward an Environmental History of Sound and Noise. Environ Hist Durh N C. 2005;10:636–65. [DOI]

Smolensky MH, Sackett-Lundeen LL, Portaluppi F. Nocturnal light pollution and underexposure to daytime sunlight: Complementary mechanisms of circadian disruption and related diseases. Chronobiol Int. 2015;32:1029–48. [DOI] [PubMed]

Ekirch RA. At Day’s Close: a History of Nighttime. London: Weidenfeld & Nicolson; 2005.

Jr KPW, McHill AW, Birks BR, Griffin BR, Rusterholz T, Chinoy ED. Entrainment of the human circadian clock to the natural light-dark cycle. Curr Biol. 2013;23:1554–8. [DOI] [PubMed] [PMC]

Haim A, Portnov BA. Light pollution as a new risk factor for human breast and prostate cancers. Light Pollution as a New Risk Factor for Human Breast and Prostate Cancers. Haifa (IL): Dordrecht Springer; 2013. pp. 1–168.

10.

Cho JR, Joo EY, Koo DL, Hong SB. Let there be no light: the effect of bedside light on sleep quality and background electroencephalographic rhythms. Sleep Med. 2013;14:1422–5. [DOI] [PubMed]

11.

Zeitzer JM, Dijk DJ, Kronauer R, Brown E, Czeisler C, Dijk DJ, et al. Sensitivity of the human circadian pacemaker to nocturnal light: melatonin phase resetting and suppression. J Physiol. 2000;526 Pt 3:695–702. [DOI] [PubMed] [PMC]

12.

Zeitzer JM, Khalsa SBS, Boivin DB, Duffy JF, Shanahan TL, Kronauer RE, et al. Temporal dynamics of late-night photic stimulation of the human circadian timing system. Am J Physiol Regul Integr Comp Physiol. 2005;289:R839–44. [DOI] [PubMed]

13.

Harari YN. Sapiens: A Brief History of Humankind. New York: Harper Perennial; 2018.

14.

Ross DL, Murphy RL. STRESS, PERCEPTUAL DISTORTIONS, AND HUMAN PERFORMANCE. In: Guidelines for Investigating Officer-Involved Shootings, Arrest-Related Deaths, and Deaths in Custody. London: Routledge; 2017. pp. 68–95.

15.

Stearns PN. The Industrial Revolution in World History. New York: Routledge; 2020. [DOI]

16.

Cowan RS. The “Industrial Revolution” in the Home: Household Technology and Social Change in the 20th Century. Technol Cult. 1976;17:1–23. [PubMed]

17.

Blitz A, Kazi K. Mapping technology roadblocks and opportunities in the transportation revolution. Strategy & Leadership. 2019;47:43–6. [DOI]

18.

Wokekoro E. Public Awareness of the Impacts of Noise Pollution on Human Health. WJRR. 2020;10:27–32.

19.

Falchi F, Furgoni R, Gallaway TA, Rybnikova NA, Portnov BA, Baugh K, et al. Light pollution in USA and Europe: The good, the bad and the ugly. J Environ Manage. 2019;248:109227. [DOI] [PubMed]

20.

Bara S, Bouroussis C, Jechow A, Longcore A, Motta J, Sanhueza M, et al. Bio-Environment Working Group Report. In: On-line Workshop Dark and Quiet Skies for Science and Society Report and Recommendations. United Nations; 2020. pp. 92–117.

21.

Basner M, McGuire S. WHO Environmental Noise Guidelines for the European Region: A Systematic Review on Environmental Noise and Effects on Sleep. Int J Environ Res Public Health. 2018;15:519. [DOI] [PubMed] [PMC]

22.

Czeisler CA, Gooley JJ. Sleep and circadian rhythms in humans. Cold Spring Harb Symp Quant Biol. 2007;72:579–97. [DOI] [PubMed]

23.

Czeisler CA, Duffy JF, Shanahan TL, Brown EN, Mitchell JF, Rimmer DW, et al. Stability, precision, and near-24-hour period of the human circadian pacemaker. Science. 1999;284:2177–81. [DOI] [PubMed]

24.

Mirjam M, Brøndsted AE, Brown SA, Gjedde A, Kantermann T, Martiny K, et al. The Effect of Light on Humans. In: Changing perspectives on daylight: Science, technology, and culture. Science/AAAS; 2017. pp. 16–23.

25.

Roenneberg T, Kantermann T, Juda M, Vetter C, Allebrandt KV. Light and the human circadian clock. Handb Exp Pharmacol. 2013;217:311–31. [DOI] [PubMed]

26.

Patton AP, Hastings MH. The Mammalian Circadian Time-Keeping System. J Huntingtons Dis. 2023;12:91–104. [DOI] [PubMed] [PMC]

27.

Balsalobre A, Damiola F, Schibler U. A serum shock induces circadian gene expression in mammalian tissue culture cells. Cell. 1998;93:929–37. [DOI] [PubMed]

28.

Hirota T, Fukada Y. Resetting mechanism of central and peripheral circadian clocks in mammals. Zoolog Sci. 2004;21:359–68. [DOI] [PubMed]

29.

Yamazaki S, Numano R, Abe M, Hida A, Takahashi R, Ueda M, et al. Resetting central and peripheral circadian oscillators in transgenic rats. Science. 2000;288:682–5. [DOI] [PubMed]

30.

Schibler U, Ripperger J, Brown SA. Peripheral Circadian Oscillators in Mammals: Time and Food. J Biol Rhythms. 2003;18:250–60. [DOI] [PubMed]

31.

Brown SA, Azzi A. Peripheral circadian oscillators in mammals. Handb Exp Pharmacol. 2013;217:45–66. [DOI] [PubMed]

32.

Laposky AD, Bass J, Kohsaka A, Turek FW. Sleep and circadian rhythms: key components in the regulation of energy metabolism. FEBS Lett. 2008;582:142–51. [DOI] [PubMed]

33.

Blume C, Garbazza C, Spitschan M. Effects of light on human circadian rhythms, sleep and mood. Somnologie (Berl). 2019;23:147–56. [DOI] [PubMed] [PMC]

34.

Collop NA, Salas RE, Delayo M, Gamaldo C. Normal sleep and circadian processes. Crit Care Clin. 2008;24:449–60. [DOI] [PubMed]

35.

Thau L, Gandhi J, Sharma S. Physiology, Cortisol. Treasure Island (FL): StatPearls Publishing; 2023. [PubMed]

36.

Halberg F. Chronobiology. Annu Rev Physiol. 1969;31:675–725. [DOI] [PubMed]

37.

Richardson GS. The human circadian system in normal and disordered sleep. J Clin Psychiatry. 2005;66:quiz 42–3. [PubMed]

38.

Kryger MH, Carskadon MA, Dement WC, editors. Principles and Practice of Sleep Medicine. 5th en. Elsevier; 2011. pp. 6–26. [DOI]

39.

Harvey R Colten, Bruce M Altevogt, editors. Sleep Disorders and Sleep Deprivation: An Unmet Public Health Problem. Washington (DC): National Academies Press (US); 2006. [DOI] [PubMed]

40.

Boostani R, Karimzadeh F, Nami M. A comparative review on sleep stage classification methods in patients and healthy individuals. Comput Methods Programs Biomed. 2017;140:77–91. [DOI] [PubMed]

41.

Herman-Bonert VS, Melmed S. Growth Hormone. In: Melmed S, editor. The Pituitary. 2022; pp. 91–129. [DOI]

42.

Adrien J. Neurobiological bases for the relation between sleep and depression. Sleep Med Rev. 2002;6:341–51. [PubMed]

43.

Garcia AN, Salloum IM. Polysomnographic sleep disturbances in nicotine, caffeine, alcohol, cocaine, opioid, and cannabis use: A focused review. Am J Addict. 2015;24:590–8. [DOI] [PubMed]

44.

Drake C, Roehrs T, Shambroom J, Roth T. Caffeine effects on sleep taken 0, 3, or 6 hours before going to bed. J Clin Sleep Med. 2013;9:1195–200. [DOI] [PubMed] [PMC]

45.

Sabanayagam C, Shankar A. The association between active smoking, smokeless tobacco, second-hand smoke exposure and insufficient sleep. Sleep Med. 2011;12:7–11. [DOI] [PubMed] [PMC]

46.

Sandman N, Valli K, Kronholm E, Revonsuo A, Laatikainen T, Paunio T. Nightmares: risk factors among the Finnish general adult population. Sleep. 2015;38:507–14. [DOI] [PubMed] [PMC]

47.

Martire VL, Caruso D, Palagini L, Zoccoli G, Bastianini S. Stress & sleep: A relationship lasting a lifetime. Neurosci Biobehav Rev. 2020;117:65–77. [DOI] [PubMed]

48.

Steiger A, Pawlowski M. Depression and Sleep. Int J Mol Sci. 2019;20:607. [DOI] [PubMed] [PMC]

49.

Cox RC, Olatunji BO. A systematic review of sleep disturbance in anxiety and related disorders. J Anxiety Disord. 2016;37:104–29. [DOI] [PubMed]

50.

Thorpy MJ. Classification of sleep disorders. Neurotherapeutics. 2012;9:687–701. [DOI] [PubMed] [PMC]

51.

Salahuddin N, Barroso J, Leserman J, Harmon JL, Pence BW. Daytime sleepiness, nighttime sleep quality, stressful life events, and HIV-related fatigue. J Assoc Nurses AIDS Care. 2009;20:6–13. [DOI] [PubMed] [PMC]

52.

McNicholas WT, Hansson D, Schiza S, Grote L. Sleep in chronic respiratory disease: COPD and hypoventilation disorders. Eur Respir Rev. 2019;28:190064. [DOI] [PubMed] [PMC]

53.

Silvani A. Sleep disorders, nocturnal blood pressure, and cardiovascular risk: A translational perspective. Auton Neurosci. 2019;218:31–42. [DOI] [PubMed]

54.

Floras JS. Sleep Apnea and Cardiovascular Disease: An Enigmatic Risk Factor. Circ Res. 2018;122:1741–64. [DOI] [PubMed]

55.

D'Elia C, Gozal D, Bruni O, Goudouris E, Cruz MME. Allergic rhinitis and sleep disorders in children - coexistence and reciprocal interactions. J Pediatr (Rio J). 2022;98:444–54. [DOI] [PubMed] [PMC]

56.

Tedjasukmana R, Budikayanti A, Islamiyah WR, Witjaksono AMAL, Hakim M. Sleep disturbance in post COVID-19 conditions: Prevalence and quality of life. Front Neurol. 2023;13:1095606. [DOI] [PubMed] [PMC]

57.

Reiter J, Gileles-Hillel A, Cohen-Cymberknoh M, Rosen D, Kerem E, Gozal D, et al. Sleep disorders in cystic fibrosis: A systematic review and meta-analysis. Sleep Med Rev. 2020;51:101279. [DOI] [PubMed] [PMC]

58.

Irwin MR, Vitiello MV. Implications of sleep disturbance and inflammation for Alzheimer's disease dementia. Lancet Neurol. 2019;18:296–306. [DOI] [PubMed]

59.

Stefani A, Högl B. Sleep in Parkinson’s disease. Neuropsychopharmacology. 2019;45:121–8. [DOI] [PubMed] [PMC]

60.

Wickwire EM, Geiger-Brown J, Scharf SM, Drake CL. Shift Work and Shift Work Sleep Disorder: Clinical and Organizational Perspectives. Chest. 2017;151:1156–72. [DOI] [PubMed] [PMC]

61.

Liew SC, Aung T. Sleep deprivation and its association with diseases- a review. Sleep Med. 2021;77:192–204. [DOI] [PubMed]

62.

Phillips AJK, Clerx WM, O'Brien CS, Sano A, Barger LK, Picard RW, et al. Irregular sleep/wake patterns are associated with poorer academic performance and delayed circadian and sleep/wake timing. Sci Rep. 2017;7:3216. [DOI] [PubMed] [PMC]

63.

Cingi C, Emre IE, Muluk NB. Jetlag related sleep problems and their management: A review. Travel Med Infect Dis. 2018;24:59–64. [DOI] [PubMed]

64.

Krishnan V, Collop NA. Gender differences in sleep disorders. Curr Opin Pulm Med. 2006;12:383–9. [DOI] [PubMed]

65.

Ohayon MM, Carskadon MA, Guilleminault C, Vitiello MV. Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: developing normative sleep values across the human lifespan. Sleep. 2004;27:1255–73. [DOI] [PubMed]

66.

Saini EK, Keiley MK, Fuller-Rowell TE, Duke AM, El-Sheikh M. Socioeconomic Status and Sleep among Couples. Behav Sleep Med. 2021;19:159–77. [DOI] [PubMed] [PMC]

67.

Cao B, Chen Y, McIntyre RS. Comprehensive review of the current literature on impact of ambient air pollution and sleep quality. Sleep Med. 2021;79:211–19. [DOI] [PubMed]

68.

Schroer S, Hölker F. Light Pollution Reduction. In: Handbook of Advanced Lighting Technology. Cham: Springer; 2014. p.1–17.

69.

Chepesiuk R. Missing the dark: health effects of light pollution. Environ Health Perspect. 2009;117:A20–7. [DOI] [PubMed] [PMC]

70.

Gabinet NM, Portnov BA. Assessing the impacts of ALAN and noise proxies on sleep duration and quality: evidence from a nation-wide survey in Israel. Chronobiol Int. 2021;38:638–58. [DOI] [PubMed]

71.

Gabinet NM, Portnov BA. Investigating the combined effect of ALAN and noise on sleep by simultaneous real-time monitoring using low-cost smartphone devices. Environ Res. 2022;214:113941. [DOI] [PubMed]

72.

Buxton OM, Ellenbogen JM, Wang W, Carballeira A, O’Connor S, Cooper D, et al. Sleep disruption due to hospital noises. Proceedings of the Institute of Acoustics. 2011;33:618–26.

73.

Muzet A. Environmental noise, sleep and health. Sleep Med Rev. 2007;11:135–42. [DOI] [PubMed]

74.

Arendt J, Aulinas A. Physiology of the Pineal Gland and Melatonin. In: Feingold KR, Anawalt B, Blackman MR, Boyce A, Chrousos G, Corpas E, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2022. [PubMed]

75.

Xie Z, Chen F, Li WA, Geng X, Li C, Meng X, et al. A review of sleep disorders and melatonin. Neurol Res. 2017;39:559–65. [DOI] [PubMed]

76.

Yaghoubi K, Alimohammadi I, Abolghasemi J, Shandiz MS, Aboutaleb N, Ebrahimi H. The relationship between noise annoyance and salivary cortisol. Applied Acoustics. 2020;160:107131. [DOI]

77.

Roenneberg T, Foster RG. Twilight times: light and the circadian system. Photochem Photobiol. 1997;66:549–61. [DOI] [PubMed]

78.

Rea MS, Figueiro MG, Bullough JD, Bierman A. A model of phototransduction by the human circadian system. Brain Res Brain Res Rev. 2005;50:213–28. [DOI] [PubMed]

79.

Daiber A, Frenis K, Kuntic M, Li H, Wolf E, Kilgallen AB, et al. Redox Regulatory Changes of Circadian Rhythm by the Environmental Risk Factors Traffic Noise and Air Pollution. Antioxid Redox Signal. 2022;37:679–703. [DOI] [PubMed] [PMC]

80.

Lick JR, Unger TE. The External Validity of Behavioral Fear Assessment: The Problem of Generalizing from the Laboratory to the Natural Environment. Annu Rev Clin Psychol. 1997;1:283–306. [DOI]

81.

Shiffman S, Stone AA, Hufford MR. Ecological momentary assessment. Annu Rev Clin Psychol. 2008;4:1–32. [DOI] [PubMed]

82.

Lechat B, Scott H, Decup F, Hansen KL, Micic G, Dunbar C, et al. Environmental noise-induced cardiovascular responses during sleep. Sleep. 2022;45:zsab302. [DOI] [PubMed]

83.

Schnelle JF, Alessi CA, Al-Samarrai NR, Jr RDF, Ouslander JG. The nursing home at night: effects of an intervention on noise, light, and sleep. J Am Geriatr Soc. 1999;47:430–8. [DOI] [PubMed]

84.

Einstein A. On a Heuristic Point of View about the Creation and Conversion of Light. In: Haar DE, editor. The Old Quantum Theory; 1967. pp. 91–107. [DOI]

85.

Houser KW, Boyce PR, Zeitzer JM, Herf M. Human-centric lighting: Myth, magic or metaphor? Lighting Research & Technology. 2021;53:97–118. [DOI]

86.

Kruisselbrink T, Dangol R, Rosemann A. Photometric measurements of lighting quality: An overview. Build Environ. 2018;138:42–52. [DOI]

87.

Chellappa SL, Gordijn MCM, Cajochen C. Can light make us bright? Effects of light on cognition and sleep. Prog Brain Res. 2011;190:119–33. [DOI] [PubMed]

88.

Berson DM, Dunn FA, Takao M. Phototransduction by retinal ganglion cells that set the circadian clock. Science. 2002;295:1070–3. [DOI] [PubMed]

89.

Willoughby CE, Ponzin D, Ferrari S, Lobo A, Landau K, Omidi Y. Anatomy and physiology of the human eye: effects of mucopolysaccharidoses disease on structure and function – a review. Clin Exp Ophthalmol. 2010;38:2–11. [DOI]

90.

Cao D. Color Vision and Night Vision. In: Ryan’s Retina. 2013. pp. 285–99. [DOI]

91.

Vilotijević A, Mathôt S. Functional benefits of cognitively driven pupil-size changes. Wiley Interdiscip Rev Cogn Sci. 2024;15:e1672. [DOI] [PubMed]

92.

Grzybowski A, Kupidura-Majewski K. What is color and how it is perceived? Clin Dermatol. 2019;37:392–401. [DOI] [PubMed]

93.

De Moraes CG. Anatomy of the visual pathways. J Glaucoma. 2013;22:S2–7. [DOI] [PubMed]

94.

Duda M, Domagalik A, Orlowska-Feuer P, Krzysztynska-Kuleta O, Beldzik E, Smyk MK, et al. Melanopsin: From a small molecule to brain functions. Neurosci Biobehav Rev. 2020;113:190–203. [DOI] [PubMed]

95.

Mure LS. Intrinsically Photosensitive Retinal Ganglion Cells of the Human Retina. Front Neurol. 2021;12:636330. [DOI] [PubMed] [PMC]

96.

Spitschan M, Bock AS, Ryan J, Frazzetta G, Brainard DH, Aguirre GK. The human visual cortex response to melanopsin-directed stimulation is accompanied by a distinct perceptual experience. Proc Natl Acad Sci U S A. 2017;114:12291–6. [DOI] [PubMed] [PMC]

97.

Brown TM, Tsujimura S, Allen AE, Wynne J, Bedford R, Vickery G, et al. Melanopsin-based brightness discrimination in mice and humans. Curr Biol. 2012;22:1134–41. [DOI] [PubMed] [PMC]

98.

Holland N, Robbins TW, Rowe JB. The role of noradrenaline in cognition and cognitive disorders. Brain. 2021;144:2243–56. [DOI] [PubMed] [PMC]

99.

Pizza F, Barateau L, Dauvilliers Y, Plazzi G. The orexin story, sleep and sleep disturbances. J Sleep Res. 2022;31:e13665. [DOI] [PubMed]

100.

Zhao H, Zhang B, Yang S, Rusak B. The role of lateral habenula-dorsal raphe nucleus circuits in higher brain functions and psychiatric illness. Behav Brain Res. 2015;277:89–98. [DOI] [PubMed]

101.

Carthy E, Ellender T. Histamine, Neuroinflammation and Neurodevelopment: A Review. Front Neurosci. 2021;15:680214. [DOI] [PubMed] [PMC]

102.

Kanczkowski W, Sue M, Bornstein SR. Adrenal Gland Microenvironment and Its Involvement in the Regulation of Stress-Induced Hormone Secretion during Sepsis. Front Endocrinol (Lausanne). 2016;7:156. [DOI] [PubMed] [PMC]

103.

Chowdhury I, Sengupta A, Maitra SK. Melatonin: fifty years of scientific journey from the discovery in bovine pineal gland to delineation of functions in human. Indian J Biochem Biophys. 2008;45:289–304. [PubMed]

104.

Arendt J. Melatonin and human rhythms. Chronobiol Int. 2006;23:21–37. [DOI] [PubMed]

105.

Grubisic M, Haim A, Bhusal P, Dominoni DM, Gabriel KMA, Jechow A, et al. Light Pollution, Circadian Photoreception, and Melatonin in Vertebrates. Sustainability. 2019;11:6400. [DOI]

106.

Flyktman A, Mänttäri S, Nissilä J, Timonen M, Saarela S. Transcranial light affects plasma monoamine levels and expression of brain encephalopsin in the mouse. J Exp Biol. 2015;218:1521–6. [DOI] [PubMed]

107.

Sun L, Peräkylä J, Kovalainen A, Ogawa KH, Karhunen PJ, Hartikainen KM. Human Brain Reacts to Transcranial Extraocular Light. PLoS One. 2016;11:e0149525. [DOI] [PubMed] [PMC]

108.

Tedford CE, DeLapp S, Jacques S, Anders J. Quantitative analysis of transcranial and intraparenchymal light penetration in human cadaver brain tissue. Lasers Surg Med. 2015;47:312–22. Erratum in: Lasers Surg Med. 2015;47:466. [DOI] [PubMed]

109.

Salehpour F, Sadigh-Eteghad S, Mahmoudi J, Kamari F, Cassano P, Hamblin MR. Light Penetration into Brain. Synthesis Lectures on Biomedical Engineering. 2023;Part F1286:33–48.

110.

Wams EJ, Woelders T, Marring I, Rosmalen Lv, Beersma DGM, Gordijn MCM, et al. Linking Light Exposure and Subsequent Sleep: A Field Polysomnography Study in Humans. Sleep. 2017;40:zsx165. [DOI] [PubMed] [PMC]

111.

Wallace-Guy GM, Kripke DF, Jean-Louis G, Langer RD, Elliott JA, Tuunainen A. Evening light exposure: implications for sleep and depression. J Am Geriatr Soc. 2002;50:738–9. [DOI] [PubMed]

112.

Didikoglu A, Mohammadian N, Johnson S, Tongeren Mv, Wright P, Casson AJ, et al. Associations between light exposure and sleep timing and sleepiness while awake in a sample of UK adults in everyday life. Proc Natl Acad Sci U S A. 2023;120:e2301608120. [DOI] [PubMed] [PMC]

113.

Beersma DG, Daan S, Hut RA. Accuracy of circadian entrainment under fluctuating light conditions: contributions of phase and period responses. J Biol Rhythms. 1999;14:320–9. [DOI] [PubMed]

114.

Chellappa SL, Steiner R, Oelhafen P, Lang D, Götz T, Krebs J, et al. Acute exposure to evening blue-enriched light impacts on human sleep. J Sleep Res. 2013;22:573–80. [DOI] [PubMed]

115.

Green A, Cohen-Zion M, Haim A, Dagan Y. Evening light exposure to computer screens disrupts human sleep, biological rhythms, and attention abilities. Chronobiol Int. 2017;34:855–65. [DOI] [PubMed]

116.

Lerner AB, Case JD, Takahashi Y, Lee TH, Mori W. ISOLATION OF MELATONIN, THE PINEAL GLAND FACTOR THAT LIGHTENS MELANOCYTES1. J Am Chem Soc. 1958;80:2587. [DOI]

117.

Classen DC, Evans RS, Pestotnik SL, Horn SD, Menlove RL, Burke JP. The timing of prophylactic administration of antibiotics and the risk of surgical-wound infection. N Engl J Med. 1992;326:281–6. [DOI] [PubMed]

118.

Reiter RJ, Calvo JR, Karbownik M, Qi W, Tan DX. Melatonin and its relation to the immune system and inflammation. Ann N Y Acad Sci. 2000;917:376–86. [DOI] [PubMed]

119.

Lewy AJ, Wehr TA, Goodwin FK, Newsome DA, Markey SP. Light suppresses melatonin secretion in humans. Science. 1980;210:1267–9. [DOI] [PubMed]

120.

Wright HR, Lack LC. Effect of light wavelength on suppression and phase delay of the melatonin rhythm. Chronobiol Int. 2001;18:801–8. [DOI] [PubMed]

121.

Prayag AS, Najjar RP, Gronfier C. Melatonin suppression is exquisitely sensitive to light and primarily driven by melanopsin in humans. J Pineal Res. 2019;66:e12562. [DOI] [PubMed]

122.

Wahnschaffe A, Haedel S, Rodenbeck A, Stoll C, Rudolph H, Kozakov R, et al. Out of the lab and into the bathroom: evening short-term exposure to conventional light suppresses melatonin and increases alertness perception. Int J Mol Sci. 2013;14:2573–89. [DOI] [PubMed] [PMC]

123.

Hilaire MAS, Ámundadóttir ML, Rahman SA, Rajaratnam SMW, Rüger M, Brainard GC, et al. The spectral sensitivity of human circadian phase resetting and melatonin suppression to light changes dynamically with light duration. Proc Natl Acad Sci U S A. 2022;119:e2205301119. [DOI] [PubMed] [PMC]

124.

Czeisler CA, Shanahan TL, Klerman EB, Martens H, Brotman DJ, Emens JS, et al. Suppression of melatonin secretion in some blind patients by exposure to bright light. N Engl J Med. 1995;332:6–11. [DOI] [PubMed]

125.

Zaidi FH, Hull JT, Peirson SN, Wulff K, Aeschbach D, Gooley JJ, et al. Short-wavelength light sensitivity of circadian, pupillary, and visual awareness in humans lacking an outer retina. Curr Biol. 2007;17:2122–8. [DOI] [PubMed] [PMC]

126.

Hull JT, Czeisler CA, Lockley SW. Suppression of Melatonin Secretion in Totally Visually Blind People by Ocular Exposure to White Light: Clinical Characteristics. Ophthalmology. 2018;125:1160–71. [DOI] [PubMed]

127.

Mitsui K, Saeki K, Tone N, Suzuki S, Takamiya S, Tai Y, et al. Short-wavelength light exposure at night and sleep disturbances accompanied by decreased melatonin secretion in real-life settings: a cross-sectional study of the HEIJO-KYO cohort. Sleep Med. 2022;90:192–8. [DOI] [PubMed]

128.

Ostrin LA. Ocular and systemic melatonin and the influence of light exposure. Clin Exp Optom. 2019;102:99–108. [DOI] [PubMed]

129.

Gooley JJ, Chamberlain K, Smith KA, Khalsa SBS, Rajaratnam SMW, Reen EV, et al. Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans. J Clin Endocrinol Metab. 2011;96:E463–72. [DOI] [PubMed] [PMC]

130.

Touitou Y, Reinberg A, Touitou D. Association between light at night, melatonin secretion, sleep deprivation, and the internal clock: Health impacts and mechanisms of circadian disruption. Life Sci. 2017;173:94–106. [DOI] [PubMed]

131.

Swope CB, Rong S, Campanella C, Vaicekonyte R, Phillips AJ, Cain SW, et al. Factors associated with variability in the melatonin suppression response to light: A narrative review. Chronobiol Int. 2023;40:542–56. [DOI] [PubMed]

132.

Higuchi S, Motohashi Y, Ishibashi K, Maeda T. Less exposure to daily ambient light in winter increases sensitivity of melatonin to light suppression. Chronobiol Int. 2007;24:31–43. [DOI] [PubMed]

133.

Stevenson TJ, Visser ME, Arnold W, Barrett P, Biello S, Dawson A, et al. Disrupted seasonal biology impacts health, food security and ecosystems. Proc Biol Sci. 2015;282:20151453. [DOI] [PubMed] [PMC]

134.

Muñoz-Jurado A, Escribano BM, Caballero-Villarraso J, Galván A, Agüera E, Santamaría A, et al. Melatonin and multiple sclerosis: antioxidant, anti-inflammatory and immunomodulator mechanism of action. Inflammopharmacology. 2022;30:1569–96. [DOI] [PubMed] [PMC]

135.

Maldonado M, Romero-Aibar J, Calvo J. The melatonin contained in beer can provide health benefits, due to its antioxidant, anti-inflammatory and immunomodulatory properties. J Sci Food Agric. 2023;103:3738–47. [DOI] [PubMed]

136.

Moradkhani F, Moloudizargari M, Fallah M, Asghari N, Khoei HH, Asghari MH. Immunoregulatory role of melatonin in cancer. J Cell Physiol. 2020;235:745–57. [DOI] [PubMed]

137.

Majidinia M, Reiter RJ, Shakouri SK, Mohebbi I, Rastegar M, Kaviani M, et al. The multiple functions of melatonin in regenerative medicine. Ageing Res Rev. 2018;45:33–52. [DOI] [PubMed]

138.

Shuai Y, Liao L, Su X, Yu Y, Shao B, Jing H, et al. Melatonin Treatment Improves Mesenchymal Stem Cells Therapy by Preserving Stemness during Long-term In Vitro Expansion. Theranostics. 2016;6:1899–917. [DOI] [PubMed] [PMC]

139.

Nicolae AC, Drăgoi CM. Melatonin - Molecular Biology, Clinical and Pharmaceutical Approaches. Croatia: IntechOpen; 2018.

140.

Targhazeh N, Hutt KJ, Winship AL, Reiter R, Yousefi B. Melatonin as an oncostatic agent: Review of the modulation of tumor microenvironment and overcoming multidrug resistance. Biochimie. 2022;202:71–84. [DOI] [PubMed]

141.

Zubidat AE, Haim A. Artificial light-at-night - a novel lifestyle risk factor for metabolic disorder and cancer morbidity. J Basic Clin Physiol Pharmacol. 2017;28:295–313. [DOI] [PubMed]

142.

Blask DE, Brainard GC, Dauchy RT, Hanifin JP, Davidson LK, Krause JA, et al. Melatonin-depleted blood from premenopausal women exposed to light at night stimulates growth of human breast cancer xenografts in nude rats. Cancer Res. 2005;65:11174–84. [DOI] [PubMed]

143.

Stevens RG, Brainard GC, Blask DE, Lockley SW, Motta ME. Breast cancer and circadian disruption from electric lighting in the modern world. CA Cancer J Clin. 2014;64:207–18. [DOI] [PubMed] [PMC]

144.

Kloog I, Portnov BA, Rennert HS, Haim A. Does the modern urbanized sleeping habitat pose a breast cancer risk? Chronobiol Int. 2011;28:76–80. [DOI] [PubMed]

145.

Hurley S, Goldberg D, Nelson D, Hertz A, Horn-Ross PL, Bernstein L, et al. Light at night and breast cancer risk among California teachers. Epidemiology. 2014;25:697–706. [DOI] [PubMed] [PMC]

146.

Rybnikova NA, Haim A, Portnov BA. Is prostate cancer incidence worldwide linked to artificial light at night exposures? Review of earlier findings and analysis of current trends. Arch Environ Occup Health. 2017;72:111–22. [DOI] [PubMed]

147.

Garcia-Saenz A, Miguel ASd, Espinosa A, Valentin A, Aragonés N, Llorca J, et al. Evaluating the Association between Artificial Light-at-Night Exposure and Breast and Prostate Cancer Risk in Spain (MCC-Spain Study). Environ Health Perspect. 2018;126:047011. [DOI] [PubMed] [PMC]

148.

Menéndez-Menéndez J, Martínez-Campa C. Melatonin: An Anti-Tumor Agent in Hormone-Dependent Cancers. Int J Endocrinol. 2018;2018:3271948. [DOI] [PubMed] [PMC]

149.

Sirhan-Atalla M, Gabinet NM, Portnov BA. Disaggregating the effects of daytime and nighttime light exposures on obesity, overweight, prostate and breast cancer morbidity worldwide. Chronobiol Int. 2023;40:483–514. [DOI] [PubMed]

150.

Rybnikova NA, Haim A, Portnov BA. Does artificial light-at-night exposure contribute to the worldwide obesity pandemic? Int J Obes (Lond). 2016;40:815–23. [DOI] [PubMed]

151.

Park YM, White AJ, Jackson CL, Weinberg CR, Sandler DP. Association of Exposure to Artificial Light at Night While Sleeping With Risk of Obesity in Women. JAMA Intern Med. 2019;179:1061–71. [DOI] [PubMed] [PMC]

152.

Lee E, Kim M. Light and Life at Night as Circadian Rhythm Disruptors. Chronobiology in Medicine. 2019;1:95–102. [DOI]

153.

Zhong C, Longcore T, Benbow J, Chung NT, Chau K, Wang SS, et al. Environmental Influences on Sleep in the California Teachers Study Cohort. Am J Epidemiol. 2022;191:1532–9. [DOI] [PubMed] [PMC]

154.

Cipolla-Neto J, Amaral FG, Afeche SC, Tan DX, Reiter RJ. Melatonin, energy metabolism, and obesity: a review. J Pineal Res. 2014;56:371–81. [DOI] [PubMed]

155.

Wyse CA, Biello SM, Gill JMR. The bright-nights and dim-days of the urban photoperiod: implications for circadian rhythmicity, metabolism and obesity. Ann Med. 2014;46:253–63. [DOI] [PubMed]

156.

Campos-Rodriguez F, Martinez-Garcia MA, Martinez M, Duran-Cantolla J, Peña Mdl, Masdeu MJ, et al. Association between obstructive sleep apnea and cancer incidence in a large multicenter Spanish cohort. Am J Respir Crit Care Med. 2013;187:99–105. [DOI] [PubMed]

157.

Kervezee L, Cuesta M, Cermakian N, Boivin DB. The Phase-Shifting Effect of Bright Light Exposure on Circadian Rhythmicity in the Human Transcriptome. J Biol Rhythms. 2019;34:84–97. [DOI] [PubMed]

158.

Molcan L, Babarikova K, Cvikova D, Kincelova N, Kubincova L, Sutovska HM. Artificial light at night suppresses the day-night cardiovascular variability: evidence from humans and rats. Pflugers Arch. 2024;476:295–306. [DOI] [PubMed] [PMC]

159.

Martin JS, Hébert M, Ledoux E, Gaudreault M, Laberge L. Relationship of chronotype to sleep, light exposure, and work-related fatigue in student workers. Chronobiol Int. 2012;29:295–304. [DOI] [PubMed]

160.

Yao Y, Zhu L, He L, Duan Y, Liang W, Nie Z, et al. A meta-analysis of the relationship between vitamin D deficiency and obesity. Int J Clin Exp Med. 2015;8:14977–84. [PubMed] [PMC]

161.

Hussain Gilani SY, Bibi S, Siddiqui A, Ali Shah SR, Akram F, Rehman MU. Obesity And Diabetes As Determinants Of Vitamin D Deficiency. J Ayub Med Coll Abbottabad. 2019;31:432–5. [PubMed]

162.

Der T, Bailey BA, Youssef D, Manning T, Grant WB, Peiris AN. Vitamin D and prostate cancer survival in veterans. Mil Med. 2014;179:81–4. [DOI] [PubMed]

163.

Park S, Lee DH, Jeon JY, Ryu J, Kim S, Kim JY, et al. Serum 25-hydroxyvitamin D deficiency and increased risk of breast cancer among Korean women: a case–control study. Breast Cancer Res Treat. 2015;152:147–54. [DOI] [PubMed]

164.

Tosini G, Ferguson I, Tsubota K. Effects of blue light on the circadian system and eye physiology. Mol Vis. 2016;22:61–72. [PubMed] [PMC]

165.

Esenwah, Azuamah, Okorie, Ikoro. The Aging Eye and Vision: A Review. Int J Health Sci Res. 2014;4:218–26.

166.

Ayaki M, Muramatsu M, Negishi K, Tsubota K. Improvements in sleep quality and gait speed after cataract surgery. Rejuvenation Res. 2013;16:35–42. [DOI] [PubMed] [PMC]

167.

Sariyeva Ismayilov A, Sariyeva Aydamirov A, Göktaş E, Sariyeva Ismayilov A, Sariyeva Aydamirov A, Göktaş E. The effect of cataract surgery on quality of life and sleep in geriatric patient group. Arch Ophthalmol Res. 2024;1:5–9. [DOI] [PubMed]

168.

Shishegar N, Boubekri M, Stine-Morrow EAL, Rogers WA. Tuning environmental lighting improves objective and subjective sleep quality in older adults. Build Environ. 2021;204:108096. [DOI]

169.

Chellappa SL. Individual differences in light sensitivity affect sleep and circadian rhythms. Sleep. 2021;44:zsaa214. [DOI] [PubMed] [PMC]

170.

Xiao Q, Gee G, Jones RR, Jia P, James P, Hale L. Cross-sectional association between outdoor artificial light at night and sleep duration in middle-to-older aged adults: The NIH-AARP Diet and Health Study. Environ Res. 2020;180:108823. [DOI] [PubMed] [PMC]

171.

Thewissen JGM. Sensory Evolution on the Threshold : Adaptations in Secondarily Aquatic Vertebrates. Berkeley: University of California Press; 2008.

172.

Krasil’nikov VA, Overbeck CJ. Sound and Ultrasound Waves. Am J Phys. 1965;33:1093. [DOI]

173.

Blake EC, Cross I. The acoustic and auditory contexts of human behavior. Curr Anthropol. 2015;56:81–103. [DOI]

174.

Maroonroge S, Emanuel DC, Letowski TR. BASIC ANATOMY OF THE HEARING SYSTEM. In: Helmet-Mounted Displays: Sensory, Perceptual, and Cognitive Issues. USAARL; 2009. pp. 279–306.

175.

Alvord LS, Farmer BL. Anatomy and orientation of the human external ear. J Am Acad Audiol. 1997;8:383–90. [PubMed]

176.

Hayes SH, Ding D, Salvi RJ, Allman BL. Anatomy and physiology of the external, middle and inner ear. HCN. 2013;10:3–23.

177.

Krenz-Niedbała M, Łukasik S, Macudziński J, Chowański S. Morphometry of auditory ossicles in medieval human remains from Central Europe. Anat Rec (Hoboken). 2022;305:1947–61. [DOI] [PubMed]

178.

Winer JA, Lee CC. The distributed auditory cortex. Hear Res. 2007;229:3–13. [DOI] [PubMed] [PMC]

179.

Newsom RJ, Osterlund C, Masini CV, Day HE, Spencer RL, Campeau S. Cannabinoid receptor type 1 antagonism significantly modulates basal and loud noise induced neural and hypothalamic-pituitary-adrenal axis responses in male Sprague–Dawley rats. Neuroscience. 2012;204:64–73. [DOI] [PubMed] [PMC]

180.

Spreng M. Central nervous system activation by noise. Noise Health. 2000;2:49–58. [PubMed]

181.

Cheng H, Sun G, Li M, Yin M, Chen H. Neuron loss and dysfunctionality in hippocampus explain aircraft noise induced working memory impairment: a resting-state fMRI study on military pilots. Biosci Trends. 2019;13:430–40. [DOI] [PubMed]

182.

Arjunan A, Rajan R. Noise and brain. Physiol Behav. 2020;227:113136. [DOI] [PubMed]

183.

Kraus KS, Canlon B. Neuronal connectivity and interactions between the auditory and limbic systems. Effects of noise and tinnitus. Hear Res. 2012;288:34–46. [DOI] [PubMed]

184.

Šimić G, Tkalčić M, Vukić V, Mulc D, Španić E, Šagud M, et al. Understanding Emotions: Origins and Roles of the Amygdala. Biomolecules. 2021;11:823. [DOI] [PubMed] [PMC]

185.

Chai Y, Gehrman P, Yu M, Mao T, Deng Y, Rao J, et al. Enhanced amygdala–cingulate connectivity associates with better mood in both healthy and depressive individuals after sleep deprivation. Proc Natl Acad Sci U S A. 2023;120:e2214505120. [DOI] [PubMed] [PMC]

186.

Knierim JJ. The hippocampus. Curr Biol. 2015;25:R1116–21. [DOI] [PubMed]

187.

Marshall L, Born J. The contribution of sleep to hippocampus-dependent memory consolidation. Trends Cogn Sci. 2007;11:442–50. [DOI] [PubMed]

188.

Saper CB, Lowell BB. The hypothalamus. Curr Biol. 2014;24:R1111–6. [DOI] [PubMed]

189.

Environmental noise guidelines for the European Region [Internet]. Copenhagen: World Health Organization; c2024 [cited 2024 May 28]. Available from: https://iris.who.int/handle/10665/279952

190.

Ising H, Braun C. Acute and chronic endocrine effects of noise: Review of the research conducted at the Institute for water, soil and air hygiene. Noise Health. 2000;2:7–24. [PubMed]

191.

Babisch W, Fromme H, Beyer A, Ising H. Increased catecholamine levels in urine in subjects exposed to road traffic noise: the role of stress hormones in noise research. Environ Int. 2001;26:475–81. [DOI] [PubMed]

192.

Maschke C, Harder J, Ising H, Hecht K, Thierfelder W. Stress hormone changes in persons exposed to simulated night noise. Noise Health. 2002;5:35–45. [PubMed]

193.

Vallet M, Gagneux JM, Blanchet V, Favre B, Labiale G. Long term sleep disturbance due to traffic noise. J Sound Vib. 1983;90:173–91. [DOI]

194.

Eberhardt JL, Stråle LO, Berlin MH. The influence of continuous and intermittent traffic noise on sleep. J Sound Vib. 1987;116:445–64. [DOI]

195.

Okada A, Inaba R. Comparative study of the effects of infrasound and low-frequency sound with those of audible sound on sleep. Environ Int. 1990;16:483–90. [DOI]

196.

Aasvang GM, Øverland B, Ursin R, Moum T. A field study of effects of road traffic and railway noise on polysomnographic sleep parameters. J Acoust Soc Am. 2011;129:3716–26. [DOI] [PubMed]

197.

Sanok S, Berger M, Müller U, Schmid M, Weidenfeld S, Elmenhorst E, et al. Road traffic noise impacts sleep continuity in suburban residents: Exposure-response quantification of noise-induced awakenings from vehicle pass-bys at night. Sci Total Environ. 2022;817:152594. [DOI] [PubMed]

198.

Halonen JI, Vahtera J, Stansfeld S, Yli-Tuomi T, Salo P, Pentti J, et al. Associations between nighttime traffic noise and sleep: the Finnish public sector study. Environ Health Perspect. 2012;120:1391–6. [DOI] [PubMed] [PMC]

199.

Andrade EdL, Silva DCdCE, Lima EAd, Oliveira RAd, Zannin PHT, Martins ACG. Environmental noise in hospitals: a systematic review. Environ Sci Pollut Res Int. 2021;28:19629–42. [DOI] [PubMed] [PMC]

200.

Konkani A, Oakley B, Penprase B. Reducing hospital ICU noise: a behavior-based approach. J Healthc Eng. 2014;5:229–46. [DOI] [PubMed]

201.

Park MJ, Yoo JH, Cho BW, Kim KT, Jeong W, Ha M. Noise in hospital rooms and sleep disturbance in hospitalized medical patients. Environ Health Toxicol. 2014;29:e2014006. [DOI] [PubMed] [PMC]

202.

Buysse DJ, 3rd CFR, Monk TH, Berman SR, Kupfer DJ. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research. Psychiatry Res. 1989;28:193–213. [DOI] [PubMed]

203.

Simons KS, Verweij E, Lemmens PMC, Jelfs S, Park M, Spronk PE, et al. Noise in the intensive care unit and its influence on sleep quality: a multicenter observational study in Dutch intensive care units. Crit Care. 2018;22:250. [DOI] [PubMed] [PMC]

204.

Guisasola-Rabes M, Solà-Enriquez B, Vélez-Pereira AM, Nadal Md. Noise Levels and Sleep in a Surgical ICU. J Clin Med. 2022;11:2328. [DOI] [PubMed] [PMC]

205.

Richards KC, O’Sullivan PS, Phillips RL. Measurement of sleep in critically ill patients. J Nurs Meas. 2000;8:131–44. [PubMed]

206.

Gitanjali B, Ananth R. Effect of acute exposure to loud occupational noise during daytime on the nocturnal sleep architecture, heart rate, and cortisol secretion in healthy volunteers. J Occup Health. 2003;45:146–52. [DOI] [PubMed]

207.

Lin C, Tsai P, Lin K, Chen C, Chung L, Wu J, et al. Will daytime occupational noise exposures induce nighttime sleep disturbance? Sleep Med. 2018;50:87–96. [DOI] [PubMed]

208.

Röösli M, Brink M, Rudzik F, Cajochen C, Ragettli MS, Flückiger B, et al. Associations of Various Nighttime Noise Exposure Indicators with Objective Sleep Efficiency and Self-Reported Sleep Quality: A Field Study. Int J Environ Res Public Health. 2019;16:3790. [DOI] [PubMed] [PMC]

209.

Öhrström E, Hadzibajramovic E, Holmes M, Svensson H. Effects of road traffic noise on sleep: Studies on children and adults. J Environ Psychol. 2006;26:116–26. [DOI]

210.

Bodin T, Björk J, Ardö J, Albin M. Annoyance, sleep and concentration problems due to combined traffic noise and the benefit of quiet side. Int J Environ Res Public Health. 2015;12:1612–28. [DOI] [PubMed] [PMC]

211.

Bartels S, Ögren M, Kim J, Fredriksson S, Waye KP. The impact of nocturnal road traffic noise, bedroom window orientation, and work-related stress on subjective sleep quality: results of a cross-sectional study among working women. Int Arch Occup Environ Health. 2021;94:1523–36. [DOI] [PubMed] [PMC]

212.

Broner N. The effects of low frequency noise on people—A review. J Sound Vib. 1978;58:483–500. [DOI]

213.

Almeida J, Marques L, Figueiredo JP, Ferreira A. Exposure to Infrasound and Low Frequency Noise—A Case Study of Guarda City Population (Portugal). In: Galvão JRdCS, Brito P, Neves FdS, Almeida HdA, Mourato SdJM, Nobre C, editors. Proceedings of the 3rd International Conference on Water Energy Food and Sustainability (ICoWEFS 2023). Cham: Springer; 2024. pp. 513–23. [DOI]

214.

Hébert S, Lupien SJ. Salivary cortisol levels, subjective stress, and tinnitus intensity in tinnitus sufferers during noise exposure in the laboratory. Int J Hyg Environ Health. 2009;212:37–44. [DOI] [PubMed]

215.

Waye KP, Bengtsson J, Rylander R, Hucklebridge F, Evans P, Clow A. Low frequency noise enhances cortisol among noise sensitive subjects during work performance. Life Sci. 2002;70:745–58. [DOI] [PubMed]

216.

Bolin K, Bluhm G, Eriksson G, Nilsson ME. Infrasound and low frequency noise from wind turbines: Exposure and health effects. Environ Res Lett. 2011;6:035103. [DOI]

217.

Van Kamp I, Van den Berg F. Health Effects Related to Wind Turbine Sound, Including Low-Frequency Sound and Infrasound. Acoust Aust. 2018;46:31–57. [DOI]

218.

Van Kamp I, Breugelmans O, Van Poll R, Baliatsas C, Van Kempen E. Determinants of annoyance from humming sound as indicator of low frequency noise. In: Acoustics 2017 Proceedings paper. Annual conference of the Australian Acoustical Society; 2017 Nov 1–22; Perth, Australia. AAS; 2017. pp. 1–7.

219.

Baliatsas C, Kamp Iv, Poll Rv, Yzermans J. Health effects from low-frequency noise and infrasound in the general population: Is it time to listen? A systematic review of observational studies. Sci Total Environ. 2016;557–558:163–9. [DOI] [PubMed]

220.

Smith MG, Ögren M, Thorsson P, Hussain-Alkhateeb L, Pedersen E, Forssén J, et al. A laboratory study on the effects of wind turbine noise on sleep: results of the polysomnographic WiTNES study. Sleep. 2020;43:zsaa046. [DOI] [PubMed] [PMC]

221.

Liebich T, Lack L, Hansen K, Zajamšek B, Lovato N, Catcheside P, et al. A systematic review and meta-analysis of wind turbine noise effects on sleep using validated objective and subjective sleep assessments. J Sleep Res. 2021;30:e13228. [DOI] [PubMed]

222.

Lafon B, Henin S, Huang Y, Friedman D, Melloni L, Thesen T, et al. Low frequency transcranial electrical stimulation does not entrain sleep rhythms measured by human intracranial recordings. Nat Commun. 2017;8:1199. [DOI] [PubMed] [PMC]

223.

Ohayon MM, Milesi C. Artificial Outdoor Nighttime Lights Associate with Altered Sleep Behavior in the American General Population. Sleep. 2016;39:1311–20. [DOI] [PubMed] [PMC]

224.

Version 1 VIIRS Day/Night Band Nighttime Lights [Internet]. NOAA; c2019 [cited 2020 Feb 25]. Available from: https://www.ngdc.noaa.gov/eog/viirs/download_dnb_composites.html

225.

Bernstein L, Allen M, Anton-Culver H, Deapen D, Horn-Ross PL, Peel D, et al. High breast cancer incidence rates among California teachers: results from the California Teachers Study (United States). Cancer Causes Control. 2002;13:625–35. [DOI] [PubMed]

226.

Falchi F, Cinzano P, Duriscoe D, Kyba CCM, Elvidge CD, Baugh K, et al. The new world atlas of artificial night sky brightness. Sci Adv. 2016;2:e1600377. [DOI] [PubMed] [PMC]

227.

Miller NP. US National Parks and management of park soundscapes: A review. Applied Acoustics. 2008;69:77–92. [DOI]

228.

Cleary-Gaffney M, Espey B, Coogan AN. Association of perceptions of artificial light-at-night, light-emitting device usage and environmental noise appraisal with psychological distress, sleep quality and chronotype: A cross sectional study. Heliyon. 2022;8:e11284. [DOI] [PubMed] [PMC]

229.

Younis MB, Hayajneh F, Alshraideh JA. Effect of noise and light levels on sleep of intensive care unit patients. Nurs Crit Care. 2021;26:73–8. [DOI] [PubMed]

230.

Zhang N, Cao B, Zhu Y. Indoor environment and sleep quality: A research based on online survey and field study. Build Environ. 2018;137:198–207. [DOI]

231.

Foo CT, O'Driscoll DM, Ogeil RP, Lubman D, Young AC. Barriers to sleep in acute hospital settings. Sleep Breath. 2022;26:855–63. [DOI] [PubMed]

232.

Ramar K, Malhotra RK, Carden KA, Martin JL, Abbasi-Feinberg F, Aurora RN, et al. Sleep is essential to health: an American Academy of Sleep Medicine position statement. J Clin Sleep Med. 2021;17:2115–9. [DOI] [PubMed] [PMC]

233.

Baranwal N, Yu PK, Siegel NS. Sleep physiology, pathophysiology, and sleep hygiene. Prog Cardiovasc Dis. 2023;77:59–69. [DOI] [PubMed]

234.

Rybnikova N, Haim A, Portnov BA. Artificial Light at Night (ALAN) and breast cancer incidence worldwide: A revisit of earlier findings with analysis of current trends. Chronobiol Int. 2015;32:757–73. [DOI] [PubMed]

235.

Kjellberg A, Landström U, Tesarz M, Söderberg L, Åkerlund E. The effects of nonphysical noise characteristics, ongoing task and noise sensitivity on annoyance and distraction due to noise at work. J Environ Psychol. 1996;16:123–36. [DOI]

236.

Pyko A, Eriksson C, Oftedal B, Hilding A, Östenson C, Krog NH, et al. Exposure to traffic noise and markers of obesity. Occup Environ Med. 2015;72:594–601. [DOI] [PubMed]

237.

Lyzwinski LN. Public health perspectives on noise and cardiovascular disease. World J Cardiovasc Dis. 2014;04:23–34. [DOI]

238.

Wysocki LE, Dittami JP, Ladich F. Ship noise and cortisol secretion in European freshwater fishes. Biol Conserv. 2006;128:501–8. [DOI]

239.

Lim H, Kang W, Park W, Jang K, Ann J, Moon J. Insomnia and hearing impairment among occupational noise exposed male workers. Ann Occup Environ Med. 2017;29:36. [DOI] [PubMed] [PMC]

240.

Wright B, Peters E, Ettinger U, Kuipers E, Kumari V. Understanding noise stress-induced cognitive impairment in healthy adults and its implications for schizophrenia. Noise Health. 2014;16:166–76. [DOI] [PubMed]

241.

Perron S, Plante C, Ragettli MS, Kaiser DJ, Goudreau S, Smargiassi A. Sleep Disturbance from Road Traffic, Railways, Airplanes and from Total Environmental Noise Levels in Montreal. Int J Environ Res Public Health. 2016;13:809. [DOI] [PubMed] [PMC]

242.

Azuma K, Uchiyama I. Association between environmental noise and subjective symptoms related to cardiovascular diseases among elderly individuals in Japan. PLoS One. 2017;12:e0188236. [DOI] [PubMed] [PMC]

243.

McMahon TA, Rohr JR, Bernal XE. Light and noise pollution interact to disrupt interspecific interactions. Ecology. 2017;98:1290–9. [DOI] [PubMed] [PMC]

244.

Vitaterna MH, Takahashi JS, Turek FW. Overview of circadian rhythms. Alcohol Res Health. 2001;25:85–93. [PubMed] [PMC]

245.

Gentry NW, Ashbrook LH, Fu Y, Ptáček LJ. Human circadian variations. J Clin Invest. 2021;131:e148282. [DOI] [PubMed] [PMC]

246.

Dijk D, Archer SN. Light, sleep, and circadian rhythms: together again. PLoS Biol. 2009;7:e1000145. [DOI] [PubMed] [PMC]

247.

Figueiro MG. Disruption of Circadian Rhythms by Light During Day and Night. Curr Sleep Med Rep. 2017;3:76–84. [DOI] [PubMed] [PMC]

248.

Basner M, Babisch W, Davis A, Brink M, Clark C, Janssen S, et al. Auditory and non-auditory effects of noise on health. Lancet. 2014;383:1325–32. [DOI] [PubMed] [PMC]

249.

Basner M, Müller U, Elmenhorst E. Single and combined effects of air, road, and rail traffic noise on sleep and recuperation. Sleep. 2011;34:11–23. [DOI] [PubMed] [PMC]

250.

Fletcher MD, Jones SL, White PR, Dolder CN, Leighton TG, Lineton B. Effects of very high-frequency sound and ultrasound on humans. Part I: Adverse symptoms after exposure to audible very-high frequency sound. J Acoust Soc Am. 2018;144:2511. [DOI] [PubMed]

251.

Beutel ME, Brähler E, Ernst M, Klein E, Reiner I, Wiltink J, et al. Noise annoyance predicts symptoms of depression, anxiety and sleep disturbance 5 years later. Findings from the Gutenberg Health Study. Eur J Public Health. 2020;30:516–21. [DOI] [PubMed]

252.

Kempen Ev, Kamp Iv, Fischer P, Davies H, Houthuijs D, Stellato R, et al. Noise exposure and children’s blood pressure and heart rate: the RANCH project. Occup Environ Med. 2006;63:632–9. [DOI] [PubMed] [PMC]

253.

Rybnikova NA, Portnov BA. Outdoor light and breast cancer incidence: a comparative analysis of DMSP and VIIRS-DNB satellite data. Int J Remote Sens. 2016;38:5952–61. [DOI]

254.

Kloog I, Stevens RG, Haim A, Portnov BA. Nighttime light level co-distributes with breast cancer incidence worldwide. Cancer Causes Control. 2010;21:2059–68. [DOI] [PubMed]

255.

Kloog I, Haim A, Stevens RG, Barchana M, Portnov BA. Light at night co-distributes with incident breast but not lung cancer in the female population of Israel. Chronobiol Int. 2008;25:65–81. [DOI] [PubMed]

256.

Wakefield J. Ecologic studies revisited. Annu Rev Public Health. 2008;29:75–90. [DOI] [PubMed]

257.

Vohland K, Land-Zandstra A, Ceccaroni L, Lemmens R, Perelló J, Ponti M, et al., editors. , editors. The Science of Citizen Science. In: The Science of Citizen Science. Cham: Springer; 2021. p. 529.

258.

Guerrini CJ, Majumder MA, Lewellyn MJ, McGuire AL. Citizen science, public policy. Science. 2018;361:134–6. [DOI] [PubMed] [PMC]

259.

Irwin A. Constructing the scientific citizen: Science and democracy in the biosciences. Public Understand Sci. 2001;10:1–18.

260.

Fan X, Shao H, Sakamoto M, Kuga K, Lan L, Wyon DP, et al. The effects of ventilation and temperature on sleep quality and next-day work performance: pilot measurements in a climate chamber. Build Environ. 2022;209:108666. [DOI]

261.

Cao T, Lian Z, Ma S, Bao J. Thermal comfort and sleep quality under temperature, relative humidity and illuminance in sleep environment. J Build Eng. 2021;43:102575. [DOI]

262.

Schwartz RS, Olds J. The psychiatry of light. Harv Rev Psychiatry. 2015;23:188–94. [DOI] [PubMed]

263.

Campbell SS, Terman M, Lewy AJ, Dijk DJ, Eastman CI, Boulos Z. Light treatment for sleep disorders: consensus report. V. Age-related disturbances. J Biol Rhythms. 1995;10:151–4. [DOI] [PubMed]

264.

Terman M, Terman JS. Light therapy for seasonal and nonseasonal depression: efficacy, protocol, safety, and side effects. CNS Spectr. 2005;10:647–63:quiz672. [DOI] [PubMed]

265.

Daansen PJ, Haffmans J. Reducing symptoms in women with chronic anorexia nervosa. A pilot study on the effects of bright light therapy. Neuro Endocrinol Lett. 2010;31:290–6. [PubMed]

266.

Cuesto G, Everaerts C, León LG, Acebes A. Molecular bases of anorexia nervosa, bulimia nervosa and binge eating disorder: shedding light on the darkness. J Neurogenet. 2017;31:266–87. [DOI] [PubMed]

267.

Krysta K, Krzystanek M, Janas-Kozik M, Krupka-Matuszczyk I. Bright light therapy in the treatment of childhood and adolescence depression, antepartum depression, and eating disorders. J Neural Transm (Vienna). 2012;119:1167–72. [DOI] [PubMed]

268.

Sloane PD, Williams CS, Mitchell CM, Preisser JS, Wood W, Barrick AL, et al. High-intensity environmental light in dementia: effect on sleep and activity. J Am Geriatr Soc. 2007;55:1524–33. [DOI] [PubMed]

269.

Kolberg E, Hjetland GJ, Thun E, Pallesen S, Nordhus IH, Husebo BS, et al. The effects of bright light treatment on affective symptoms in people with dementia: a 24-week cluster randomized controlled trial. BMC Psychiatry. 2021;21:377. [DOI] [PubMed] [PMC]

270.

Videnovic A, Klerman EB, Wang W, Marconi A, Kuhta T, Zee PC. Timed Light Therapy for Sleep and Daytime Sleepiness Associated With Parkinson Disease: A Randomized Clinical Trial. JAMA Neurol. 2017;74:411–8. [DOI] [PubMed] [PMC]

271.

McDonnell MD, Ward LM. The benefits of noise in neural systems: bridging theory and experiment. Nat Rev Neurosci. 2011;12:415–26. [DOI] [PubMed]

272.

Halley JM. Ecology, evolution and 1 f -noise. Trends Ecol Evol. 1996;11:33–7. [DOI] [PubMed]

273.

Warjri E, Dsilva F, Sanal TS, Kumar A. Impact of a white noise app on sleep quality among critically ill patients. Nurs Crit Care. 2022;27:815–23. [DOI] [PubMed]

274.

Ebben MR, Yan P, Krieger AC. The effects of white noise on sleep and duration in individuals living in a high noise environment in New York City. Sleep Med. 2021;83:256–9. [DOI] [PubMed]

275.

Golrou A, Sheikhani A, Motie Nasrabadi A, Saebipour MR. Enhancement of Sleep Quality and Stability Using Acoustic Stimulation During Slow Wave Sleep. Int Clin Neurosci J. 2018;5:126–34. [DOI]

276.

Schade MM, Mathew GM, Roberts DM, Gartenberg D, Buxton OM. Enhancing Slow Oscillations and Increasing N3 Sleep Proportion with Supervised, Non-Phase-Locked Pink Noise and Other Non-Standard Auditory Stimulation During NREM Sleep. Nat Sci Sleep. 2020;12:411–29. [DOI] [PubMed] [PMC]

277.

Schnelle JF, Cruise PA, Alessi CA, Ludlow K, al-Samarrai NR, Ouslander JG. Sleep hygiene in physically dependent nursing home residents: behavioral and environmental intervention implications. Sleep. 1998;21:515–23. [PubMed]

278.

Head, WB. Wicked problems in public policy. Cham: Palgrave Macmillan; 2022. [DOI]

279.

Ersoy EO, Demir AU, Topeli A. Yoğun bakımda uyku: Var mı, yok mu? J Med Surg Intensive Care Med. 2016;7:28–33. Turkish.

280.

Morillas JMB, Gozalo GR, González DM, Moraga PA, Vílchez-Gómez R. Noise Pollution and Urban Planning. Curr Pollut Rep. 2018;4:208–19. [DOI]

281.

Saad R, Portnov BA, Trop T. Saving energy while maintaining the feeling of safety associated with urban street lighting. Clean Technol Environ Policy. 2021;23:251–69. [DOI]

282.

Aussat Y, Rosmanis A, Keshav S. A power-efficient self-calibrating smart lighting system. Energy Build. 2022;259:111874. [DOI]