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Effects of artificial light at night on human health: A literature review of observational and experimental studies applied to exposure assessment


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It has frequently been reported that exposure to artificial light at night (ALAN) may cause negative health effects, such as breast cancer, circadian phase disruption and sleep disorders. Here, we reviewed the literature assessing the effects of human exposure to ALAN in order to list the health effects of various aspects of ALAN. Several electronic databases were searched for articles, published through August 2014, related to assessing the effects of exposure to ALAN on human health; these also included the details of experiments on such exposure. A total of 85 articles were included in the review. Several observational studies showed that outdoor ALAN levels are a risk factor for breast cancer and reported that indoor light intensity and individual lighting habits were relevant to this risk. Exposure to artificial bright light during the nighttime suppresses melatonin secretion, increases sleep onset latency (SOL) and increases alertness. Circadian misalignment caused by chronic ALAN exposure may have negative effects on the psychological, cardiovascular and/or metabolic functions. ALAN also causes circadian phase disruption, which increases with longer duration of exposure and with exposure later in the evening. It has also been reported that shorter wavelengths of light preferentially disturb melatonin secretion and cause circadian phase shifts, even if the light is not bright. This literature review may be helpful to understand the health effects of ALAN exposure and suggests that it is necessary to consider various characteristics of artificial light, beyond mere intensity.
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Chronobiology International
The Journal of Biological and Medical Rhythm Research
ISSN: 0742-0528 (Print) 1525-6073 (Online) Journal homepage:
Effects of artificial light at night on human
health: A literature review of observational
and experimental studies applied to exposure
YongMin Cho, Seung-Hun Ryu, Byeo Ri Lee, Kyung Hee Kim, Eunil Lee &
Jaewook Choi
To cite this article: YongMin Cho, Seung-Hun Ryu, Byeo Ri Lee, Kyung Hee Kim, Eunil Lee &
Jaewook Choi (2015): Effects of artificial light at night on human health: A literature review
of observational and experimental studies applied to exposure assessment, Chronobiology
International, DOI: 10.3109/07420528.2015.1073158
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ISSN: 0742-0528 print / 1525-6073 online
DOI: 10.3109/07420528.2015.1073158
Effects of artificial light at night on human health: A literature review
of observational and experimental studies applied to exposure
YongMin Cho
, Seung-Hun Ryu
, Byeo Ri Lee
, Kyung Hee Kim
, Eunil Lee
, and Jaewook Choi
Institute for Occupational & Environmental Health, Korea University, Seoul, Republic of Korea and
Department of
Preventive Medicine, College of Medicine, Korea University, Seoul, Republic of Korea
It has frequently been reported that exposure to artificial light at night (ALAN) may cause negative health effects, such
as breast cancer, circadian phase disruption and sleep disorders. Here, we reviewed the literature assessing the effects
of human exposure to ALAN in order to list the health effects of various aspects of ALAN. Several electronic databases
were searched for articles, published through August 2014, related to assessing the effects of exposure to ALAN on
human health; these also included the details of experiments on such exposure. A total of 85 articles were included in
the review. Several observational studies showed that outdoor ALAN levels are a risk factor for breast cancer and
reported that indoor light intensity and individual lighting habits were relevant to this risk. Exposure to artificial bright
light during the nighttime suppresses melatonin secretion, increases sleep onset latency (SOL) and increases alertness.
Circadian misalignment caused by chronic ALAN exposure may have negative effects on the psychological,
cardiovascular and/or metabolic functions. ALAN also causes circadian phase disruption, which increases with longer
duration of exposure and with exposure later in the evening. It has also been reported that shorter wavelengths of
light preferentially disturb melatonin secretion and cause circadian phase shifts, even if the light is not bright. This
literature review may be helpful to understand the health effects of ALAN exposure and suggests that it is necessary
to consider various characteristics of artificial light, beyond mere intensity.
Keywords: Artificial light at night, breast cancer, circadian rhythm, light exposure, light pollution
Light is a necessity for a comfortable life, productivity
and safety of human beings. More than ever, modern
humans rely on artificial light for a substantial part of
the day. While artificial light increases convenience,
excessive exposure to artificial light may have negative
impacts on ecosystems and on human health (Gaston
et al., 2015; Haim & Zubidat, 2015). Moreover, because
of this increased use of artificial light, humans spend
less time in the dark at night.
The most common health effects of artificial light at
night (ALAN) are disruption of the biological clock and
suppression of the nocturnal production of melatonin
(Reiter et al., 2007). This ALAN-induced circadian
disruption and suppression of melatonin secretion are
associated with an increased cancer risk (Blask, 2009;
Davis & Mirick, 2006; Kantermann & Roenneberg, 2009;
Stevens et al., 2007, 2014). More specifically, several
ecological and observational studies have shown that
greater levels of exposure to ALAN may increase the risk
of breast (Bauer et al., 2013; Chepesiuk, 2009; Kloog
et al., 2008, 2010; Yang et al., 2014) and prostate cancers
(Kloog et al., 2009) in the population.
Aside from cancer, sleep disturbance due to ALAN
exposure may also have an impact on aging and
metabolic processes (Hood et al., 2004; Stevens et al.,
2007), as well as on heart disease, diabetes, mood
disorders and obesity, which have become pandemic
(Gangwisch, 2014; Stevens, 2009). Therefore, ALAN
exposure increases public health concerns in modern
societies (Dickerman & Liu, 2012).
However, which characteristics of ALAN affect
human health requires further investigation. Given
that ALAN is a single potential environmental risk
factor (Dickerman & Liu, 2012), it does not affect the
human body in the form of direct toxicity or physical
energy, as other environmental risk factors, i.e. chemical
Correspondence: Jaewook Choi, Department of Preventive Medicine, Institute for Occupational & Environmental Health, College
of Medicine, Korea University, 73, Inchon-ro, Seongbuk-gu, Seoul 136-705, Republic of Korea. Tel: +82 2 920 6407. Fax: +82 2 927
7220. E-mail:
Submitted March 27, 2015, Returned for revision July 2, 2015, Accepted July 13, 2015
Downloaded by [Korea University] at 19:13 17 September 2015
toxicants or radiation, do. Consequently, unlike other
risk factors, it is difficult to explain the doseresponse
relationship of ALAN per se.
To understand how ALAN affects the human body
and to prevent its effects on public health, it may be
necessary to establish which aspects of ALAN exposure
are associated with these health effects. Therefore, we
conducted a literature review of the observational and
experimental studies assessing the effects of ALAN
exposure. In such studies, the estimated individual (or
grouped) ALAN exposure level, controlled bright light
exposure or similar control of other characteristics of
light exposure, such as wavelength and exposure dur-
ation, were viewed as exposure factors. The reported
impact of ALAN on humans is listed according to the
characteristics of ALAN exposure.
Articles published through August 2014 were collected
from several electronic databases (PubMed, ScienceDir-
ect and ScholarOne). Only peer-reviewed articles were
collected for this review and conference reports and
proceedings were excluded. The articles collected were
those that assessed the effects of exposure to ALAN on
human health. The terms used in the search (in full text)
were as follows: (light at night OR dim light OR artificial
light) AND (sleep) AND (exposure) AND (health OR
melatonin OR circadian OR breast cancer), (light at
night) AND (light pollution OR light exposure OR health)
AND (artificial light OR light at night OR health)
AND (exposure assessment OR light pollution). Further
relevant publications were obtained by scanning the
reference lists of the collected articles.
The criteria for inclusion in the literature review were
original research articles that specified the methods
used for assessment of exposure of ALAN or LAN (light
at night) exposure assessment in human subjects.
Exposure assessment studies refer to studies that
identified the relationship between ALAN exposure
and health outcomes that also include the actual
measurements of ALAN levels, the lighting habits of
individuals by means of questionnaires and experimen-
tal trials in which subjects were exposed to lighting in a
controlled way. Ecological studies were included in the
analysis on ALAN level and the incidence of disease.
Studies that did not investigate the impact of artificial
light were excluded. For example, studies on health
effects from polar night at high latitudes, studies mainly
focused on daytime exposure (or ultraviolet exposure
from sun light), rather than on nighttime exposure to
light, studies assessing the treatment effects of daytime
or morning light exposure (particularly for depression
and dementia), studies examining non-day shift workers
that did not use ALAN as an evaluation factor and
studies measuring light pollution that only evaluated
light emission, but not the impact on humans, were all
excluded. Review papers and brief letters that were not
original articles were also excluded from the analysis, as
were animal, in vivo/vitro, and cell studies.
The data in each article were individually reviewed by
two researchers and recorded in a standardized form.
This form included the following categories: study
design, exposure conditions and factors, reason for
exclusion (when excluded), study subjects, health out-
come, methods applied to assess outcome, units for
exposure assessment, exposure factor considered and
main results. The advantages, particulars and limits of
the research were also recorded. When there were
differences between the information recorded by each
reviewer, the paper was reviewed again.
Among the 412 articles collected, 261 papers were
excluded from the analysis after reviewing the abstracts
(one of which was duplicated). After the full text review,
66 additional papers were excluded. Ultimately, 85
papers were included in the literature review (Figure 1).
The ALAN exposure conditions applied in each study
were divided into light intensity, exposure characteris-
tics and light characteristics. These are the characteris-
tics considered as ALAN exposure factors by the
researchers. The health effects that were demonstrated
in response to each exposure factor were described.
Light intensity
Outdoor ALAN level
Among the studies that applied outdoor ALAN level as a
surrogate marker, individual or group residential areas
were found to be a key factor. Data from the United
States Department of Defense’s Defense Meteorological
Satellite Program (DMSP) were generally used to deter-
mine the outdoor ALAN level. Kloog and colleagues used
the DMSP data in their ecological studies to show that
the ALAN level increased the risk of breast cancer in
women and of prostate cancer in men; these results
were independent of other cancers, including lung
cancer (Kloog et al., 2008, 2009, 2010). In a case-referent
study that compared the ALAN exposure level of breast
cancer cases and lung cancer referents among registered
cancer patients in Georgia, USA, the DMSP data were
also used to show that breast cancer incidence was
associated with increased ALAN exposure (Bauer et al.,
2013). Similarly, DMSP data were used for a cohort
study targeting female teachers in California, USA,
which showed an association between outdoor ALAN
levels and breast cancer (Hurley et al., 2014). When
examining other health effects of outdoor ALAN expos-
ure, it was found that adolescents living in city areas
with a high ALAN level had a stronger evening-type
inclination than adolescents living in relatively dark
rural areas (Vollmer et al., 2012). However, Hurley et al.
reported no relevant correlations between the outdoor
ALAN level and urinary 6-sulftoxymelatonin concentra-
tion, a proxy for circulating melatonin levels, in a
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cross-sectional study based on DMSP data (Hurley et al.,
Individual lighting habits
Davis et al. evaluated individual ALAN exposure levels in
a survey on sleep habits and bedroom lighting charac-
teristics (Davis et al., 2001). This study reported that
lighting habits while sleeping did not increase the risk of
breast cancer, but night shift work did so. In further
studies, these and similar survey items were used as
factors to evaluate the individual ALAN level while
sleeping. These did not involve measurements of actual
light intensity, but rather was an attempt to classify the
estimated ALAN level exposure in bed.
Kloog et al. divided the nighttime bedroom light level
into a four-point scale, ranging from ‘‘completely dark’’
to ‘‘very strong light – all lights switched on’’, and
reported that the odds ratio (OR) of breast cancer
incidence was significantly predicted by light intensity
(Kloog et al., 2011). In a population-based case-control
study by O’Leary et al. in the USA, it was reported that
the groups that turned on the light in bed more
frequently had an increased risk of breast cancer
(O’Leary et al., 2006). However, research by Li et al.
did not find any significant correlation between expos-
ure to indoor lighting factors, such as bedroom lighting,
or television viewing habits, and the risk of breast cancer
(Li et al., 2010).
A study on interactions between occupational expos-
ure to low-frequency magnetic fields and ALAN reported
that melatonin secretion was significantly decreased
after exposure to both magnetic fields and ALAN
(Juutilainen & Kumlin, 2006). In addition, women who
slept later were reported to show a trend toward having
high serum estradiol and testosterone levels and a low
urinary 6-sulfatoxymelatonin level (Nagata et al., 2008;
Wada et al., 2012). However, Wada et al. failed to find a
significant difference in the concentration of melatonin
among preschool children in Japan exposed to different
levels of ambient bedroom light (Wada et al., 2013a).
Another study has reported that a group with lower
bedroom brightness showed reduced obesity rates
(McFadden et al., 2014), while another study showed
no correlation with myopia in children (Czepita et al.,
Indoor illumination level
In some observational studies, individual light exposure
or indoor illumination intensity during subjects’ daily
lives were directly measured, using devices, such as a
photometer, ActiWatch, StowAway light intensity data
logger or a HOBO pendant.
Melatonin levels were found to be significantly lower
in nurses who work night shifts than in those who work
day shifts, and the former were also exposed to signifi-
cantly more intense light levels (lumen/m
) during sleep
(Grundy et al., 2009). In addition, rotating shift workers
with erratic levels of light exposure also showed abnor-
mal melatonin levels (Borugian et al., 2005).
Furthermore, when subjects whose chronotypes were
the morning- or evening-type were exposed to light at
different times of day, no difference was identified when
FIGURE 1. PRISMA diagram of the screen-
ing process (Adapted from Moher et al.,
Records idenfied through database
(n = 412)
Addional records idenfied through
other sources
(n = 0)
Records aer duplicates removed
(n = 411)
Records screened
(n = 411)
Records excluded
(n = 260)
Full-text arcles assessed for
(n = 151)
Full-text arcles excluded,
with reasons
(n = 66)
Studies included in literature
(n = 85)
Human health effects of artificial light at night 3
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light exposure was adjusted for their circadian phase
(Goulet et al., 2007). Similarly, the total amount of light
exposure did not differ between night nurses whose
melatonin release timing had adapted to night shift
work by circadian phase advance, circadian phase delay
or by no change in circadian phase; however, the 24-h
profile of light exposure was different among groups
(Dumont et al., 2001).
In a study conducted by Obayashi et al., a signifi-
cantly higher OR for subjective insomnia was identified
within the group exposed to more intense ALAN
(Obayashi et al., 2014c). In another study, evening-type
subjects with higher light exposure levels had poor sleep
quality and fatigue (Martin et al., 2012). It was also
reported that adolescents with delayed sleep phase
disorder (DSPD) were exposed to significantly brighter
ALAN than the control group (Auger et al., 2011). In
addition, an increase in evening and nighttime light
exposure significantly raised sleep onset latency (SOL)
(Obayashi et al., 2014b). According to a study by
Wallace-Guy et al., light exposure over 4 h prior to
bedtime was not significantly related to SOL, sleep
amount or depressed mood; while the total amount of
illumination over 24 h period was correlated with a
shorter SOL, reduced waking during sleep and a less
depressed mood (Wallace-Guy et al., 2002). In a study
on elderly depression, the depressed group had signifi-
cantly higher ALAN exposure than the non-depressed
group (Obayashi et al., 2013a).
In studies which measured ALAN exposure during the
nighttime by installing a 1-min interval light meter at
the bedside, it was reported that ALAN exposure was
associated with a higher OR for obesity (BMI) and
dyslipidemia (Obayashi et al., 2013b), and significantly
increased nighttime blood pressure (Obayashi et al.,
2014a). In addition, circadian changes were weaker in a
group with a lower daynight light contrast (Martinez-
Nicolas et al., 2014).
Bright light exposure at night
In studies of nocturnal sleep or sleep deprivation,
differences in the physiological reactions between a
bright light (BL) exposure group and a dim light (DL)
exposure group were frequently assessed using within-
or between-subject designs.
In one study, BL exposure at 25002800 Lux sup-
pressed melatonin secretion relative to DL exposure at
5100120 Lux (Bunnell et al., 1992; Yokoi et al., 2006).
Compared to exposure to DL at510 Lux, a BL group had
lower melatonin concentrations when exposed to 100
Lux and showed greatly lowered levels after exposure to
5000 Lux (Ru
¨ger et al., 2005). Exposure to BL during
nighttime can reduce nocturnal melatonin concentra-
tions in adolescents (Harada, 2004), and melatonin
concentration declines when the eyes are exposed to BL
¨nen et al., 1999; Ru
¨ger et al., 2003). In one study,
melatonin secretion was suppressed when exposed to
white BL (3000 Lux) relative to red DL (515 Lux), while
no difference in cortisol secretion was observed (Lavoie
et al., 2003). In addition, BL-induced melatonin sup-
pression was much higher in subjects diagnosed with
premenstrual dysphoric disorder (PMDD) (Parry et al.,
In a group exposed to BL at approximately 3000 Lux,
a significantly higher DL melatonin onset (DLMO) was
observed compared to a group exposed to DL at 1.9 Lux
(Burke et al., 2013). Likewise, while a high level of night
light exposure induced a DLMO delay (Benloucif et al.,
2006; Figueiro & Rea, 2012), a phase response curve
(PRC) was created when exposed to bright white light at
8000 Lux for an hour, this was not observed when
exposed to DL at 53 Lux (St Hilaire et al., 2012).
Compared to DL (53 Lux), exposure to moderate light
(5200 Lux) before bedtime (ca. 24:00) suppressed mela-
tonin, resulting in a later melatonin onset (Gooley et al.,
2011). A significant circadian phase shift was found
when exposed to a very bright light at 9500 Lux
(Shanahan et al., 1999). Iris color did not affect DLMO
phase delay significantly (Canton et al., 2009).
Zeitzer et al. (2005) reported that melatonin phase
shift and melatonin suppression increased with Lux,
showing a nonlinear increase that rose rapidly at 100
Lux. However, according to research conducted by Foret
et al. (1996), nighttime BL (1000 Lux) exposure sup-
pressed levels of the melatonin metabolite aMT6s, while
exposure to 100 Lux did not. On the other hand, it was
also reported that an increase in the intensity of
illumination (2000–8000 Lux) did not change DLMO
(Dewan et al., 2011) and that extraocular light exposure
had no impact on phase delay or melatonin secretion
(Lushington et al., 2002).
Furthermore, when individuals were exposed to 40
Lux ALAN with the source at 1 m away from the eyes
during sleep, they slept less deeply, demonstrated
periodic arousal and had altered brain activity (Cho
et al., 2013). When exposed to BL, sleep latency was high
(Bunnell et al., 1992; Komada et al., 2000; Lavoie et al.,
2003; Tzischinsky & Lavie, 1997), and exposure to BL
during nighttime delayed sleep initiation and reduced
overall sleep quality (Kubota et al., 1998; Tzischinsky &
Lavie, 1997). Exposure to BL during the night inhibits
alertness and task performance (Chang et al., 2013;
Daurat et al., 2000), maintains high skin and rectal
temperature (Bunnell et al., 1992; Kubota et al., 1998;
Lavoie et al., 2003; Ru
¨ger et al., 2006; Yokoi et al., 2003,
2006) and increases the heart rate and systolic blood
pressure (Kohsaka et al., 2001; Ru
¨ger et al., 2006; Yokoi
et al., 2006). In an experiment by Ru
¨ger et al., sleepiness
on the Karolinska Sleepiness Scale was not reduced by
nighttime exposure to 100 Lux, but was significantly
reduced by exposure to 5000 Lux (Ru
¨ger et al., 2003,
2005) and also significantly dropped after exposure to
BL at 42500 Lux relative to DL (5150 Lux) (Yokoi et al.,
Additionally, there were no differences in the amount
of breath hydrogen induced by exposure to BL relative
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to DL (Hirota et al., 2010). Exposure to BL during the
night decreased leg discomfort in patients with restless
legs syndrome (Whittom et al., 2010).
Exposure characteristics
Exposure duration/time
Chang et al. reported that light exposure during sleep
could suppress melatonin acutely and induce subjective
sleepiness in a manner dependent on the duration of the
light exposure (Chang et al., 2012). In another experi-
ment, conducted by Dewan et al., an increase in the
duration, but not the intensity of light exposure, altered
the circadian melatonin rhythm (Dewan et al., 2011). In
addition, exposure to BL for 4 h, but not 2 h, increased
sleep latency but improved task performance (Thessing
et al., 1994). All night BL exposure induced greater
increases in alertness and performance than observed
after short exposure (Daurat et al., 2000), and the change
in the circadian phase shift becomes clearer as the
exposure continued (Deacon & Arendt, 1994). In add-
ition, the effects of light exposure on the circadian
melatonin rhythm and alertness are affected by the
history of prior light exposure (Chang et al., 2011, 2013).
Carrier and Dumont exposed subjects to BL at
different times of day, and found that evening exposure
induced a greater shift in the circadian temperature
rhythm than exposure in the morning or afternoon
(Carrier & Dumont, 1995). Comparison between evening
and early morning BL exposure showed that evening BL
exposure affected the circadian phases (rectal body
temperature, melatonin, phase delay) (Foret et al., 1998;
Gordijn et al., 1999).
Light:dark cycle
Both transient sleep displacement and habitual changes
in sleep time bring about delays in DLMO (Gordijn et al.,
1999; Wright et al., 2005). In addition, short nights
associated with evening light exposure can reduce
circadian phase advances (Burgess, 2013). Both clock
gene expression and the circadian melatonin rhythm
were also altered by a 40-h period of continuous sleep
deprivation and light exposure (Cajochen et al., 2003;
Kavcic et al., 2011).
Light characteristics
Several studies have reported the biological impacts of
light characteristics beyond merely light intensity.
Subjects exposed to 460-nm ALAN experienced
decreased subjective drowsiness and increased alertness
compared to those exposed to 550-nm ALAN (Lockley
et al., 2006; Rahman et al., 2014). Exclusion of shorter
wavelength light (5480 nm) prevented both the sup-
pression of melatonin secretion and alterations in
circadian temperature rhythm, increased cortisol secre-
tion, disrupted peripheral clock gene expression
(Rahman et al., 2011; van de Werken et al., 2013) and
had reduced effects on circadian temperature fluctu-
ation. Blue light exposure decreased both melatonin
concentration and sleepiness while raising alertness
(Phipps-Nelson et al., 2009; Santhi et al., 2012;
Wahnschaffe et al., 2013). Even at a low intensity,
blue-enriched light can influence EEG (electroencepha-
lographic) activity during sleep (Chellappa et al., 2013).
In contrast, another study found that nighttime per-
formance and sleepiness ratings were not strongly
affected by blue-enriched light, but melatonin levels
were (Figueiro et al., 2009).
Light with a higher color temperature (6500 K) more
strongly suppressed circadian temperature and mela-
tonin rhythms than did a cooler (3000 K) light (Morita &
Tokura, 1996). Similarly, another study found that
melatonin is suppressed by exposure to artificial light
with a high color temperature, but not by light with a
low color temperature (Wada et al., 2013b).
Artificial light exposure at night causes a suppression of
melatonin, deterioration in sleep quality and disturb-
ance in biorhythms. Such effects increase with the
brightness of the light and the length of the exposure
period. Even light that is not particularly bright can have
a stronger influence if the light is blue, with a shorter
wavelength, or if the exposure occurs in the evening
before going to bed. Habitual lighting of the bedroom
may also have an impact on circadian rhythms and
increase cancer risk, and bright outdoor settings can act
as a risk factor for cancer.
With regard to exposure to light, the intensity,
duration and biological time of exposure all have critical
effects on the circadian rhythm (Ku
¨ller, 2002; Reiter
et al., 2007; Wright et al., 2005). In addition, suppression
of melatonin caused by light exposure is dependent on
the intensity and wavelength (Blask, 2009; Skene et al.,
1999). Therefore, the health effects of ALAN are related
to the exposure conditions and characteristics of the
light, and not only to the amount of light.
Exposure conditions of light that may cause negative
health effects
Most environmental pollutants cause negative health
effects when humans are exposed to an ‘‘amount’’ in
excess of a threshold. In the case of light, the ‘‘amount’’
may mean not only the intensity, but also the duration
and cycle of exposure. Excessive noise causes a hearing
loss, but noise is defined as unwanted sound, rather
than excessive (absolutely too loud) sound, and brings
about many types of health effects besides hearing
defects. As in the case of noise, unwanted light at night
means not only excessive light in terms of brightness.
Some experimental studies reviewed here reported
that brighter light induced greater health effects, i.e.
melatonin concentration reduction. However, the
threshold of light intensity that triggers a response in
terms of human health effects is unknown. One study
used a DL condition of 100 Lux and found no melatonin
Human health effects of artificial light at night 5
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TABLE 1. Observational studies of exposure to artificial light at night (ALAN) and health outcomes.
Factor of LAN considered/
data source of exposure Study design Subjects
Main confounders
considered Significant associations
Outcome assessment
main statistics applied References
Outdoor ALAN level/
satellite data
Ecological Race, per capita income,
population, birth rate,
electricity consump-
tion, fertility rate, lung
Incidence of BC (ASR) B¼0.121 and 0.277/OLS
Kloog et al. (2008, 2010)
Ecological GDP, urban population,
electricity consump-
tion, region, lung
Incidence of prostate
cancer (ASR)
Kloog et al. (2009)
Case-referent 34 053 BC cases and
14 458 lung cancer
Race, tumor grade and
stage, smoking, statis-
tical status, etc.
Incidence of BC OR for LAN ¼1.12 (95%
CI ¼1.041.20)/
Logistic regression
Bauer et al. (2013)
Cohort 106 731 women Age, race, birthplace,
family history of BC,
menses, pregnancy,
breastfeeding, etc.
Incidence of BC HR ¼1.12 and 1.34 (95%
CI ¼1.00–1.26; 1.07–
1.69, respectively)
Cox proportional hazards
Hurley et al. (2014)
Cross-sectional 1507 adolescents Time use of electronic
screen media, intake of
stimulants, type of
school, age, puberty
status, etc.
B¼0.105 (between LAN
and chronotype)/
regression analysis
Vollmer et al. (2012)
Cross-sectional 303 adults Age, parity, pregnancy,
smoking, alcohol,
contraceptive, hor-
mone therapy, meno-
pausal status, etc.
Urinary aMT6s
B¼0.0028 and 0.0062
(p¼0.73 and 0.62)/
regression analysis
(stepwise approach)
Hurley et al. (2013)
Lighting habit/question-
naire for nighttime
bedroom lighting or
sleep time
Case-control 794 with BC and 885
Education, ethnicity,
fertility, alcohol con-
sumption, TV on while
Incidence of BC OR for bedroom light
¼1.220 (95%
CI ¼1.1181.311)/
logistic regression
Kloog et al. (2011)
Case-control 576 with BC and 585
Menopausal status,
history of oophorec-
tomy or hysterectomy,
smoking, hormone
Incidence of BC OR for lighting habit
during sleep hrs ¼1.65
(95% CI ¼1.022.69)/
logistic regression
O’Leary et al. (2006)
Cross-sectional 60 women Daytime occupational
electromagnetic expos-
age, smoking
Excretion of 6-OHMS The lowest mean in the
group of both MF and
Juutilainen & Kumlin (2006)
Longitudinal 206 postmenopausal
Age, BMI, smoking and
drinking habits, phys-
ical activity, medical
and reproductive his-
tory, day length of the
day previous to urine
Concentration of serum
estradiol and urinary
The lower geometric
means in women who
were not asleep at or
after 1:00 a.m./ANOVA
Nagata et al. (2008)
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Longitudinal 236 women Age, sex of offspring,
parity, smoking, pre-
pregnant height and
weight, weeks of
Maternal and umbilical
serum testosterone
Higher among those who
were awake at or after
01:00 a.m./Student’s t-
test and correlation test
Wada et al. (2012)
Cross-sectional 113 343 women Alcohol consumption,
smoking, hours of
sleep, physical activity,
shift work, childbirth
history, age, socioeco-
nomic status
BMI, waist:hip ratio,
waist:height ratio, waist
Significant ORs of indica-
tors of obesity for
middle or darkness
level compared with
the lightest level ¼0.94
McFadden et al. (2014)
Case-control 813 BC patients and 793
Parity, family history of
BC, oral contraceptive
use, hormone replace-
ment therapy
BC prevalence
OR for ambient light
levels ¼1.01.4 (not
Davis et al. (2001)
Case-control 363 BC cases and 356
Age, race and ethnicity,
BMI, age at first men-
strual period, meno-
pausal status, lactation,
family history of BC,
alcohol consumption,
smoking, age at first
full-term birth
BC incidence
OR for keeping lights on
while sleeping ¼1.4
(95% CI ¼0.72.7)/
logistic regression
Li et al. (2010)
Cross-sectional 438 children Age, BMI, sex, sex steroid
Melatonin levels
No significant difference
between factors of
bedroom ambient light
Wada et al. (2013a)
Cross-sectional 3905 schoolchildren Family history of myopia
and eye health status
Myopia incidence
during school years
Not associated with light-
ing conditions until the
age of two years/Chi-
square test
Czepita et al. (2012)
Indoor illumination level/
light intensity data
logger (real measure-
ment in living)
Cross-sectional 61 female rotating shift
Health history, medica-
tion use, smoking,
alcohol and caffeine
consumption, sleep
duration, physical
activity, parity
Melatonin concentration Parameter esti-
mate ¼0.40 (log ng/
mL); p¼0.002/multiple
linear regression
Grundy et al. (2009)
Cross-sectional 22 shift workers Medication, education,
marital status, meno-
pausal status
Melatonin concentration p¼0.002 between mela-
tonin categories and
shift types/likelihood-
ratio X
Borugian et al. (2005)
Cross-sectional 857 elderly individuals Age, gender, BMI, daytime
physical activity, UME,
bedtime, rising time,
day length
Insomnia, Sleep quality Final adjusted OR ¼1.61
(95% CI ¼1.052.45)/
linear regression model
for trends
Obayashi et al. (2014c)
Cross-sectional 88 student workers Sleep quality, fatigue Martin et al. (2012)
(continued )
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TABLE 1. Continued
Factor of LAN considered/
data source of exposure Study design Subjects
Main confounders
considered Significant associations
Outcome assessment
main statistics applied References
Commuting time, living
environment, number
of days off
Sleep on and offset time
of E-type were different
from M-type/ANOVA
Cohort 16 adolescents with DSPD
and 22 unaffected
Mood and depression,
medication use,
tobacco and caffeine
DSPD Higher light exposure in
the evening time in the
DSPD group/repeated
measures linear model
Auger et al. (2011)
Longitudinal 192 elderly individuals Alcohol consumption,
BMI, smoking, income,
education, sleep medi-
cation use, eGFR, day-
time physical activity
Sleep onset latency B¼0.133 (95%
CI ¼0.0200.247) for
evening light exposure/
linear regression
Obayashi et al. (2014b)
Cross-sectional 154 women Age, season Depressed mood, sleep
R¼0.29 (p50.001) for
sleep latency and
R¼0.21 (p50.01) for
depressed mood with a
24-h illumination/mul-
tiple regression
Wallace-Guy et al. (2002)
Cross-sectional 516 elderly individuals BMI, smoking, alcohol
consumption, SES,
sleep duration, habit-
ual bedtime, eGFR,
diabetes, medical his-
tory, daytime exposure,
Depressive symptoms aOR for light intensity (5
Lux) ¼1.89 (95%
CI ¼1.103.25), aOR
for exposure duration
(30 min) ¼1.71 (95%
CI ¼1.012.89)/logistic
Obayashi et al. (2013a)
Cross-sectional 528 elderly individuals Smoking, drinking,
income, education,
medications, habitual
sleep duration and
bedtime, day length,
physical activities
Obesity, dyslipidemia aOR for BMI (of LAN 3
Lux) ¼1.89 (95%
CI ¼1.183.04), aOR
for abdominal ¼1.62
(95% CI ¼1.022.57),
aOR for dyslipidemia
¼1.72 (95%
CI ¼1.112.68)/logistic
Obayashi et al. (2013b)
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Cross-sectional 528 elderlies BMI, smoking, alcohol
consumption, drug use,
diabetes mellitus,
eGFR, time to bed,
duration in bed and
nocturia frequency, day
length, UME
Nighttime blood pressure Significant for
SBP ¼3.9225.395;
for DBP ¼2.7732.825/
linear regression
Obayashi et al. (2014a)
Cross-sectional 131 young adults Interaction between
Circadian rhythm Comparisons of wrist
temperature due to
day–night light con-
Martinez-Nicolas et al. (2014)
Cross-sectional 12 M-type and 12 E-type
Shift work, travelling to
another time zone in
the past 3 months,
smoking, drug or
medication, hormonal
Circadian phase
Comparison circadian
phase angle between
M-types and E-types/
Goulet et al. (2007)
Cross-sectional 30 nurses Smoking, medication,
pregnancy, lactating,
sleep disorders
Phase advance and
24-h profile of light
exposure of three
groups (phase delayed,
phase advanced, non-
shift) was significantly
different. but the total
amount of light was not
(phase delayed, phase
advanced, non-shift
group) was not differ-
Dumont et al. (2001)
In these observational studies, outdoor ALAN levels, individual lighting habits during sleep, and measurement values of indoor illumination level were applied as indicators of ALAN exposure.
ALAN, artificial light at night; ASR, age-standardizes rate; Bor , regression coefficient; BC, breast cancer; BMI, body mass index; DSPD, delayed sleep phase disorder; DLMO, dim light
melatonin onset; CBT, core body temperature; OLS, ordinary least squares; OR, odds ration; aOR, adjusted odds-ratio; CI, confidence interval; HR, hazard ratio; 6-OHMS, 6-hydroxy melatonin
sulfate; UME, urinary 6-sulfatoxymelatonin excretion; E-type, subjects of evening-type in the chronotype test; M-type, subjects of morning type in the chronotype test; eGFR, estimated
glomerular filtration rate; SES, socioeconomic status; SBP, systolic blood pressure; DBP, diastolic blood pressure; MF, magnetic field.
In these studies, lung cancer was a comparison target, used for emphasis, rather than acting as a confounder.
Data in this table show results that were statistically significant.
In this study, authors analyzed the synergistic effect of electromagnetic field and LAN exposure to melatonin production.
Not significant variable.
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TABLE 2. Experimental studies of exposure of human subjects to controlled bright light in the laboratory.
Subjects (mean age
or age range) BL control (Lux) DL control (Lux) Exposure time
Main statistical method
applied Significant association References
8 males (22.0) 2800 120 From midnight (21:00) to
early in the morning
ANOVA Melatonin concentration,
rectal temperature, SBP
Yokoi et al. (2006)
5 males (20–28) 2500 5100 2h at night Wilcoxon matched-pairs
signed ranks test,
Paired t-test
Salivary melatonin, rectal
temperature, sleep
Bunnell et al. (1992)
36 young adults
100 for ex.1
5000 for ex. 2, 3
510 24:00 to 04:00 for ex.1, 2
12:00 to 4:00 for ex 3
Paired t-test Melatonin concentration,
¨ger et al. (2005)
14 adults (22–35) Bright white light about
Dim red light 515 00:30–04:30 ANOVA Melatonin suppression,
CBT, sleep latency
Lavoie et al. (2003)
8 adults (20–53) 2000 510 24:00–02:00 ANOVA Melatonin concentration Ha
¨nen et al. (1999)
12 males (21.8) 5000 510 24:0004:00 ANOVA, Paired t-test CBT, sleepiness, suppres-
sion of melatonin
¨ger et al. (2003)
10 adolescents (14–
2000 60 19:25–22:30 Wilcoxon test Melatonin concentration Harada (2004)
36 young adults
2984 1.9 3 h of bright light expos-
ure, starting 1 h prior to
habitual wake time
t-test DLMO, circadian phase
Burke et al. (2013)
6 (48.6) for ex. 1
7 (23) for ex. 2
100 (green light) 51 (red light) 23:3000:30 in 1st session
and 60 min in 2nd and
3rd session for ex. 1
60 min for ex. 2
ANOVA Melatonin suppression,
Figueiro & Rea (2012)
16 young (29.3) and
14 older (67.1)
3500 10 4 h at night ANOVA DLMO, DLMOff Benloucif et al. (2006)
34 young adults
58000 53 1 h at night Non-linear least-square
PRC St Hilaire et al. (2012)
116 youth and
adults (18–30)
200 5
3 Nighttime before bedtime
(ca. 24:00)
ANOVA Melatonin suppression Gooley et al. (2011)
23 males (22.1) 9500 (700013 000) 1015 24:00–05:00 ANOVA CBT, plasma melatonin Shanahan et al. (1999)
48 males (23) 9500/1260/600/180/12/50.03 5 h early biological night Logistic model (non-
linear least square
Melatonin suppression Zeitzer et al. (2005)
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8 adults 1000 100 18:00–08:00 ANOVA Suppression of melatonin
metabolite aMT6s
Foret et al. (1996)
10 adults (27) 40 (Light on) Light off 23:00 to before waking Wilcoxon signed-rank test Sleep depth and stability Cho et al. (2013)
7 adults (22.7) 2500 10 During 40 min before
sleep onset
Wilcoxon test Sleep latency (EEG stage) Komada et al. (2000)
12 males (23.5) 2500 200 Evening (2 h for DL; 0.5 h
for BL) after sunset
Paired t-test, ANOVA Sleep latency, oral
Tzischinsky & Lavie (1997)
6 males (21–35) 3000 150 19:00–21:30 t-test Rectal temperature nadir,
sleep initiation and
overall sleep quality
Kubota et al. (1998)
14 adults (23.5) 90 1 During nighttime sleep
(6.5 h)
ANOVA Alertness, performance Chang et al. (2013)
8 young adults (19–
2000 550 20:00–08:00 ANOVA Alertness, performance,
suppression of mela-
tonin metabolite
Daurat et al. (2000)
24 males (23.1) 55000 510 Daytime experiment:
Nighttime experiment:
Post-hoc ANOVA Heart rate, CBT Ru
¨ger et al. (2006)
8 males (22.0) 2800 120 21:00–04:30 ANOVA Skin/rectal temperature,
sleepiness, Theta/alpha
wave activity
Yokoi et al. (2003)
9 females (21.0) 5000 200 18:00–20:00 Wilcoxon signed-rank test Heart rate variability Kohsaka et al. (2001)
56 adults (29) Increasing of light intensity (2000–8000) During sleep (1, 2 or 3 h) ANOVA DLMO
Dewan et al. (2011)
13 adults (22.1) Extraocular light (behind
the right knee) 11 000
01:00–04:00 ANOVA Phase delay, melatonin
excretion, and CBT in
extraocular BL
Lushington et al. (2002)
10 females (20.5) 2000 50 15:00–24:00 Paired t-test Amount of breath
Hirota et al. (2010)
ex., experiment; BL, bright light; DL, dim light; SBP, systolic blood pressure; CBT, core body temperature; PMDD, premenstrual dysphoric disorder; DLMO, dim light melatonin onset; DLMOff,
dim light melatonin offset; PRC, phase response curve; EEG, electroencephalographic; MBP, mean blood pressure.
Not significant variable.
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TABLE 3. Experimental studies of ALAN exposure characteristics on human health effects.
Subjects (mean age
or age range) Light intensity Considered factor Exposure control
Main statistical
method applied Significant association Reference no.
39 young adults (22.2) 510 000 Lux Exposure duration 0.2/1.0/2.5/4.0/6.5 h
during sleep
ANCOVA Circadian timing system,
melatonin suppression,
Chang et al. (2012)
56 adults (20–40) 2000/4000/8000 Lux Exposure duration 1–3 h during sleep ANOVA Magnitude of light-
induced delays
Dewan et al. (2011)
30 adults (21) 48000 Lux Exposure duration 2/4 h at night ANOVA Sleep latency, perform-
ance (only with 4-h
Thessing et al. (1994)
8 young adults
2000 Lux Exposure duration Short exposure
(20:00–00:00 and
04:00–08:00) All night
exposure (20:00–08:00)
ANOVA Alertness, performance,
melatonin level
Daurat et al. (2000)
6 adults (24.3) 1200 Lux Exposure duration Days 1–3 ANOVA Circadian phase shift Deacon & Arendt (1994)
17 adults (23.8)/14
adults (23.5)
90 Lux Photic history 6.5 h at night ANOVA Melatonin suppression,
phase shift, alerting
Chang et al. (2011, 2013)
23 adults (22.8) 6000–13 000 Exposure time Morning exposure
noon exposure
exposure (18:30–23:30)
ANOVA Phase shift delay and
sleep latency in the
evening exposure
Carrier & Dumont (1995)
8 males (19–23) 700–1000 Lux Exposure time Evening exposure
exposure (04:00–08:00)
ANOVA Difference in rectal tem-
perature in the evening
exposure group
Foret et al. (1998)
12 adults (39.3) 2500 Lux Exposure time/LD cycle Evening exposure
Melatonin concentration,
body temperature
Gordijn et al. (1999)
34 adults (30.5) 450/150 Lux LD cycle and wakeful-
ness-sleep schedules,
Prior light history
Habitual sleep time of
individuals was
t-test DLMO Wright et al. (2005)
12 adults (28.5) 15–18 Lux LD cycle 9/6 h sleep with DL ANOVA Decreasing of circadian
phase advance (with
evening light exposure
and daytime nap)
Burgess (2013)
6 males (26) 500 Lux LD cycle Sleep deprivation under
light condition
ANOVA Clock gene expression,
melatonin concentra-
tion, cortisol level
Kavcic et al. (2011)
12 adults (22.1) 5–13 Lux LD cycle L:D ¼16:8 and 40:8
(sleep deprived)
ANOVA Melatonin profile
Cajochen et al. (2003)
ALAN, artificial light at night; LD cycle, light:dark cycle; DLMO, dim light melatonin onset.
Not significant variable.
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TABLE 4. Experimental studies of light characteristics and human health effects.
Subjects (mean age or
age range, years) Light characteristic Light conditions Controls Significant association References
16 adults (23.8)/
16 adults (23.3)
Wavelength 460 nm 555 nm Sleepiness, performance Rahman et al. (2014)
and Lockley et al.
12 adults (25.8) Wavelength Filtered 5460nm and
5480 nm light
Unfiltered light Melatonin and cortisol
secretion, clock gene
expression, alertness,
Rahman et al. (2011)
22 adults (23.1) Polychromatic evening
light condition
enhanced/bright blue-enhanced
Circadian phase Santhi et al. (2012)
9 adults (26.3) Light temperature DL(510 Lux)/Bathroom yellow (130 Lux, 2000 K)/office day-
light white (500 Lux, 6000K)/bathroom daylight white
(130 Lux, 6000 K)/planon warm white (500 Lux, 2800 K)/
hall daylight white (500 Lux, 5000 K)
Circadian rhythm Wahnschaffe et al.
8 adults (32.1) Wavelength 460 nm 640 nm Alertness Phipps-Nelson et al.
30 adults (25.2) Light temperature Blue-enriched (6500 K)/classic (3000K)/warm (2500 K) Sleep Chellappa et al. (2013)
14 adults (21–46) Wavelength Red (630 nm) 10 and 40 Lux/blue (470 nm) 10 and 40 Lux Circadian phase Figueiro et al. (2009)
33 males (22.6) Wavelength DL(55 Lux)/short wavelength (5530 nm; 193 Lux)/full
spectrum light (256 Lux)
Circadian phase van de Werken et al.
5 males (20.0) Color temperature Daylight (6500 K; 1000 Lux)/warm white (3000 K; 1000 Lux)/
control (50 Lux)
Circadian phase Morita & Tokura
94 males (20.3) Color temperature Low color light at night No exposure at night Improving melatonin
secretion and sleep
quality under low color
light exposure
Wada et al. (2013b)
All studies except Wada et al. (2013a, b) (KruskalWallis and correlation test) were applied with ANOVA for statistical method.
DL, dim light.
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suppression in study subjects, in contrast to the BL
condition of 1000 Lux (Foret et al., 1996), while another
study reported melatonin suppression under 100-Lux
conditions (Zeitzer et al., 2005). Furthermore, there are
no absolute definitions for BL and DL conditions. We
can assume that exposure to strong light carries more
risk than exposure to low levels of light, and low levels of
light than dimmer light, and dimmer light than com-
plete darkness, especially when sleeping at night.
Furthermore, even at the same level of brightness,
short wavelength blue or blue-enriched light has more
significant effects on the circadian rhythm. Blue light,
mostly emitted from electronic devices, enhances alert-
ness even while sleeping at night, and suppresses
melatonin secretion and circadian activities.
In addition to light intensity and wavelength, the
duration, cycle and time of exposure are also important
in the health effects of ALAN. Some studies reported that
the duration of exposure to light at night caused
significant health effects, such as circadian disruption.
In addition, evening light exposure before bedtime
affected circadian phase more than did afternoon
exposure. Thus, excessive exposure to artificial light
does not involve only too bright light, but also too long
or irregular exposure.
While the experimental studies reviewed in this
article show acute health outcomes following light
exposure, observational studies show chronic effects
due to common nighttime lighting habits and exposure
levels. ALAN exposure over a long period is related to an
individual’s lifestyle and/or dwelling characteristics.
Unintended nighttime light exposure flows from light
trespass in dwellings, which constitutes a form of light
pollution. In areas with a high outdoor ALAN levels, light
trespass is more likely to occur. If unintended ALAN
exposure from the environment occurs and results in
health effects, such as cancer, it is of critical significance
in terms of public health. Intended ALAN exposure
related to human behavioral patterns is also of signifi-
cance. Particularly, many of the studies reviewed here
showed that exposing children and adolescents to bright
light while sleeping results in negative health effects.
Many members of this age group frequently use TVs,
PCs or tablet computers, mobile phones and other light-
emitting (especially blue-enriched) electronic devices at
night, which increases their exposure to blue light and
alters biorhythms and metabolic activities, and causes
sleep disorders.
Whenever intended or unintended, a bright indoor
environment at night can increase the risk of cancer and
circadian disruption. Furthermore, outdoor light levels,
which represent nighttime activities, also represent light
exposure at night and are related to cancer and circa-
dian disruption. Outdoor illumination levels from satel-
lite data are an index for measuring light exposure levels
of regional population groups, while indoor lighting
habits are an index for measuring individual exposure
Health outcomes caused by ALAN
Health outcomes induced by ALAN are related to the
entrainment of the biological clock. In humans and
mammals, the pacemaker of the biological clock is
located in the suprachiasmatic nucleus, and this is
affected by the photoperiod. Therefore, many studies
that investigated health effects of ALAN have reported
effects on the circadian rhythm, i.e. melatonin suppres-
sion, phase shift, sleep latency and body temperature.
Human health effects from ALAN exposure are based on
‘‘not dark night’’. Insomnia, sleep disorders and dis-
turbances of deep sleep are induced by ALAN exposure.
These outcomes may result in other, more chronic,
health effects.
Circadian misalignment caused by chronic ALAN
exposure may have negative effects on the psycho-
logical, cardiovascular and/or metabolic functions, as
listed in Tables 14. ALAN exposure is regarded as an
environmental stressor that can affect the immune
system (Haim & Portnov, 2013). High levels of bright-
ness and/or changes in the light environment act as a
stressor to humans, especially when unintended. In
addition, changes in pineal melatonin levels can affect
the metabolic rate. Disruption of the circadian rhythm
may lead to metabolic alterations, which may lead to
obesity and/or diabetes (Haim & Portnov, 2013;
McFadden et al., 2014), which has become a pandemic.
In terms of cancer effects, breast and prostate cancer
may also be considered to result from chronic ALAN
exposure related to lifestyle. Acute signs of circadian
misalignment may develop as disease. In fact, ALAN is
considered as a ‘‘modernized’’ phenomenon, and it may
cause many ‘‘modernized’’ health problems. Many
factors other than ALAN exposure lead to the develop-
ment or exacerbation of these diseases, e.g. smoking,
diet and air pollution. Nevertheless, ALAN may be
considered an important risk factor given its known
Limitations and conclusion
This research reviewed studies of exposure to ALAN and
its assessment on health effects, as categorized by the
light exposure conditions. Since this was not a meta-
analysis, this review is not capable of proving the causal
relationship between particular factors. Instead, this
review detailed the known health effects of each risk
factor. This review suggests that further meta-analysis of
factor-by-outcome studies is needed to identify associ-
ations between various factors of ALAN exposure, and
more diverse health outcomes are not yet clearly
Although, previous papers have reviewed ALAN
exposure and health outcomes, this review categorized
various aspects of ALAN exposure and identified the
health outcomes reported for the types of exposure.
Moreover, this review assessed the effects by classifica-
tion exposure as intended/unintended and acute/
chronic. Light intensity, exposure duration or timing,
14 Y. M. Cho et al.
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wavelength, individual light habits, outdoor ALAN level
data obtained by satellite are also factors related to
ALAN exposure conditions. However, other exposure
conditions may also affect human health. For instance,
flickering light at night may cause symptoms or dis-
eases, and thus other characteristics of ALAN exposure
should be determined, which will require a longitudinal
study, as some diseases do not become evident over a
short period.
The authors declare no conflicts of interests. The
authors alone are responsible for the content and
writing of this article.
This work was supported by a future environmental
R&D grant funded by the Korean Environmental
Industry and Technology Institute (RE201206020).
Auger RR, Burgess HJ, Dierkhising RA, et al. (2011). Light exposure
among adolescents with delayed sleep phase disorder: A
prospective cohort study. Chronobiol Int. 28:911–20.
Bauer SE, Wagner SE, Burch J, et al. (2013). A case-referent study:
Light at night and breast cancer risk in Georgia. Int J Health
Geogr. 12:23.
Benloucif S, Green K, L’Hermite-Bale
´riaux M, et al. (2006).
Responsiveness of the aging circadian clock to light.
Neurobiol Aging. 27:1870–9.
Blask DE. (2009). Melatonin, sleep disturbance and cancer risk.
Sleep Med Rev. 13:257–64.
Borugian MJ, Gallagher RP, Friesen MC, et al. (2005). Twenty-four-
hour light exposure and melatonin levels among shift workers. J
Occup Environ Med. 47:1268–75.
Bunnell DE, Treiber SP, Phillips NH, et al. (1992). Effects of evening
bright light exposure on melatonin, body temperature and
sleep. J Sleep Res. 1:17–23.
Burgess HJ. (2013). Evening ambient light exposure can reduce
circadian phase advances to morning light independent of
sleep deprivation. J Sleep Res. 22:83–8.
Burke TM, Markwald RR, Chinoy ED, et al. (2013). Combination of
light and melatonin time cues for phase advancing the human
circadian clock. Sleep. 36:1617–24.
Cajochen C, Jewett ME, Dijk DJ. (2003). Human circadian mela-
tonin rhythm phase delay during a fixed sleep–wake schedule
interspersed with nights of sleep deprivation. J Pineal Res. 35:
Canton JL, Smith MR, Choi HS, et al. (2009). Phase delaying the
human circadian clock with a single light pulse and moderate
delay of the sleep/dark episode: No influence of iris color.
J Circadian Rhythms. 7:8.
Carrier J, Dumont M. (1995). Sleep propensity and sleep architec-
ture after bright light exposure at three different times of day.
J Sleep Res. 4:202–11.
Chang AM, Santhi N, St Hilaire M, et al. (2012). Human
responses to bright light of different durations. J Physiol. 590:
Chang AM, Scheer FA, Czeisler CA, et al. (2013). Direct effects of
light on alertness, vigilance, and the waking electroencephalo-
gram in humans depend on prior light history. Sleep. 36:
Chang AM, Scheer FA, Czeisler CA. (2011). The human circa-
dian system adapts to prior photic history. J Physiol. 589:
Chellappa SL, Steiner R, Oelhafen P, et al. (2013). Acute exposure to
evening blue-enriched light impacts on human sleep. J Sleep
Res. 22:573–80.
Chepesiuk R. (2009). Missing the dark: Health effects of light
pollution. Environ Health Perspect. 117:A20–7.
Cho JR, Joo EY, Koo DL, et al. (2013). Let there be no light: The
effect of bedside light on sleep quality and background
electroencephalographic rhythms. Sleep Med. 14:1422–5.
Czepita D, Mojsa A, Czepita M, et al. (2012). Myopia and night
lighting. Investigations on children with negative family history.
Klin Oczna. 114:22–5.
Daurat A, Foret J, Benoit O, et al. (2000). Bright light during
nighttime: Effects on the circadian regulation of alertness and
performance. Biol Signals Recept. 9:309–18.
Davis S, Mirick DK, Stevens RG. (2001). Night shift work, light
at night, and risk of breast cancer. J Natl Cancer Inst. 93:
Davis S, Mirick DK. (2006). Circadian disruption, shift work and the
risk of cancer: A summary of the evidence and studies in
Seattle. Cancer Causes Control. 17:539–45.
Deacon SJ, Arendt J. (1994). Phase-shifts in melatonin,
6-sulphatoxymelatonin and alertness rhythms after treatment
with moderately bright light at night. Clin Endocrinol (Oxf). 40:
Dewan K, Benloucif S, Reid K, et al. (2011). Light-induced changes
of the circadian clock of humans: Increasing duration is more
effective than increasing light intensity. Sleep. 34:593–9.
Dickerman B, Liu J. (2012). Does current scientific evidence
support a link between light at night and breast cancer
among female night-shift nurses? Review of evidence and
implications for occupational and environmental health nurses.
Workplace Health Saf. 60:273–81.
Dumont M, Benhaberou-Brun D, Paquet J. (2001). Profile of 24-h
light exposure and circadian phase of melatonin secretion in
night workers. J Biol Rhythms. 16:502–11.
Figueiro MG, Bierman A, Plitnick B, et al. (2009). Preliminary
evidence that both blue and red light can induce alertness at
night. BMC Neurosci. 10:105.
Figueiro MG, Rea MS. (2012). Preliminary evidence that light
through the eyelids can suppress melatonin and phase shift
dim light melatonin onset. BMC Res Notes. 5:221.
Foret J, Daurat A, Tirilly G. (1998). Effect of bright light at night on
core temperature, subjective alertness and performance as a
function of exposure time. Scand J Work Environ Health. 24:
Foret J, Daurat A, Touitou Y, et al. (1996). The effect on
body temperature and melatonin of a 39-h constant routine
with two different light levels at nighttime. Chronobiol Int. 13:
Gangwisch JE. (2014). Invited commentary: Nighttime light expos-
ure as a risk factor for obesity through disruption of circadian
and circannual rhythms. Am J Epidemiol. 180:251–3.
Gaston KJ, Visser ME, Ho
¨lker F. (2015). The biological impacts of
artificial light at night: The research challenge. Philos Trans R
Soc Lond B Biol Sci. 370:20140133.
Gooley JJ, Chamberlain K, Smith KA, et al. (2011). Exposure to
room light before bedtime suppresses melatonin onset and
shortens melatonin duration in humans. J Clin Endocrinol
Metab. 96:E463–72.
Gordijn MC, Beersma DG, Korte HJ, et al. (1999). Effects of light
exposure and sleep displacement on dim light melatonin onset.
J Sleep Res. 8:163–74.
Goulet G, Mongrain V, Desrosiers C, et al. (2007). Daily light
exposure in morning-type and evening-type individuals. J Biol
Rhythms. 22:151–8.
Grundy A, Sanchez M, Richardson H, et al. (2009). Light intensity
exposure, sleep duration, physical activity, and biomarkers of
melatonin among rotating shift nurses. Chronobiol Int. 26:
Human health effects of artificial light at night 15
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Haim A, Portnov BA. (2013). Light pollution as a new risk factor for
human breast and prostate cancers. Dordrecht, Heidelberg,
New York, London: Springer.
Haim A, Zubidat AE. (2015). Artificial light at night: melatonin as a
mediator between the environment and epigenome. Philos
Trans R Soc Lond B Biol Sci. 370:20140121.
Harada T. (2004). Effects of evening light conditions on salivary
melatonin of Japanese junior high school students. J Circadian
Rhythms. 2:4.
¨nen T, Alila-Johansson A, Mustanoja S, et al. (1999).
Suppression of melatonin by 2000-Lux light in humans with
closed eyelids. Biol Psychiatry. 46:827–31.
Hirota N, Sone Y, Tokura H. (2010). Effect of evening exposure to
bright or dim light after daytime bright light on absorption of
dietary carbohydrates the following morning. J Physiol
Anthropol. 29:79–83.
Hood B, Bruck D, Kennedy G. (2004). Determinants of sleep quality
in the healthy aged: The role of physical, psychological,
circadian and naturalistic light variables. Age Ageing. 33:159–65.
Hurley S, Goldberg D, Nelson D, et al. (2014). Light at night and
breast cancer risk among California teachers. Epidemiology. 25:
Hurley S, Nelson DO, Garcia E, et al. (2013). A cross-sectional
analysis of light at night, neighborhood sociodemographics and
urinary 6-sulfatoxymelatonin concentrations: Implications for
the conduct of health studies. Int J Health Geogr. 12:39.
Juutilainen J, Kumlin T. (2006). Occupational magnetic field
exposure and melatonin: Interaction with light-at-night.
Bioelectromagnetics. 27:423–6.
Kantermann T, Roenneberg T. (2009). Is light-at-night a health risk
factor or a health risk predictor? Chronobiol Int. 26:1069–74.
Kavcic P, Rojc B, Dolenc-Groselj L, et al. (2011). The impact of
sleep deprivation and nighttime light exposure on clock gene
expression in humans. Croat Med J. 52:594–603.
Kloog I, Haim A, Stevens RG, et al. (2008). Light at night co-
distributes with incident breast but not lung cancer in the
female population of Israel. Chronobiol Int. 25:65–81.
Kloog I, Haim A, Stevens RG, et al. (2009). Global co-distribution of
light at night (LAN) and cancers of prostate, colon, and lung in
men. Chronobiol Int. 26:108–25.
Kloog I, Portnov BA, Rennert HS, et al. (2011). Does the modern
urbanized sleeping habitat pose a breast cancer risk?
Chronobiol Int. 28:76–80.
Kloog I, Stevens RG, Haim A, et al. (2010). Nighttime light level co-
distributes with breast cancer incidence worldwide. Cancer
Causes Control. 21:2059–68.
Kohsaka M, Kohsaka S, Fukuda N, et al. (2001). Effects of bright
light exposure on heart rate variability during sleep in young
women. Psychiatry Clin Neurosci. 55:283–4.
Komada Y, Tanaka H, Yamamoto Y, et al. (2000). Effects of bright
light pre-exposure on sleep onset process. Psychiatry Clin
Neurosci. 54:365–6.
Kubota T, Uchiyama M, Hirokawa G, et al. (1998). Effects of
evening light on body temperature. Psychiatry Clin Neurosci.
¨ller R. (2002). The influence of light on circarhythms in humans.
J Physiol Anthropol Appl Human Sci. 21:87–91.
Lavoie S, Paquet J, Selmaoui B, et al. (2003). Vigilance levels during
and after bright light exposure in the first half of the night.
Chronobiol Int. 20:1019–38.
Li Q, Zheng T, Holford TR, et al. (2010). Light at night and
breast cancer risk: Results from a population-based case-
control study in Connecticut, USA. Cancer Causes Control. 21:
Lockley SW, Evans EE, Scheer FA, et al. (2006). Short-wavelength
sensitivity for the direct effects of light on alertness, vigilance,
and the waking electroencephalogram in humans. Sleep. 29:
Lushington K, Galka R, Sassi LN, et al. (2002). Extraocular light
exposure does not phase shift saliva melatonin rhythms in
sleeping subjects. J Biol Rhythms. 17:377–86.
Martin JS, He
´bert M, Ledoux E, et al. (2012). Relationship of
chronotype to sleep, light exposure, and work-related fatigue in
student workers. Chronobiol Int. 29:295–304.
Martinez-Nicolas A, Madrid JA, Rol MA. (2014). Day–night contrast
as source of health for the human circadian system. Chronobiol
Int. 31:382–93.
McFadden E, Jones ME, Schoemaker MJ, et al. (2014). The
relationship between obesity and exposure to light at night:
Cross-sectional analyses of over 100 000 women in the
Breakthrough Generations Study. Am J Epidemiol. 180:245–50.
Moher D, Liberati A, Tetzlaff J, Altman DG, The PRISMA Group.
(2009). Preferred reporting items for systematic reviews and
meta-analyses: The PRISMA Statement. PLoS Med. 6:e1000097.
Morita T, Tokura H. (1996). Effects of lights of different color
temperature on the nocturnal changes in core temperature and
melatonin in humans. Appl Human Sci. 15:243–6.
Nagata C, Nagao Y, Yamamoto S, et al. (2008). Light exposure at
night, urinary 6-sulfatoxymelatonin, and serum estrogens and
androgens in postmenopausal Japanese women. Cancer
Epidemiol Biomarkers Prev. 17:1418–23.
Obayashi K, Saeki K, Iwamoto J, et al. (2013a). Exposure to light at
night and risk of depression in the elderly. J Affect Disord. 151:
Obayashi K, Saeki K, Iwamoto J, et al. (2013b). Exposure to light at
night, nocturnal urinary melatonin excretion, and obesity/
dyslipidemia in the elderly: A cross-sectional analysis of the
HEIJO-KYO study. J Clin Endocrinol Metab. 98:337–44.
Obayashi K, Saeki K, Iwamoto J, et al. (2014a). Association between
light exposure at night and nighttime blood pressure in the
elderly independent of nocturnal urinary melatonin excretion.
Chronobiol Int. 31:779–86.
Obayashi K, Saeki K, Iwamoto J, et al. (2014b). Effect of exposure to
evening light on sleep initiation in the elderly: A longitudinal
analysis for repeated measurements in home settings.
Chronobiol Int. 31:461–7.
Obayashi K, Saeki K, Kurumatani N. (2014c). Association between
light exposure at night and insomnia in the general elderly
population: The HEIJO-KYO cohort. Chronobiol Int. 31:976–82.
O’Leary ES, Schoenfeld ER, Stevens RG, et al. (2006). Shift work,
light at night, and breast cancer on Long Island, New York. Am J
Epidemiol. 164:358–66.
Parry BL, Meliska CJ, Sorenson DL, et al. (2010). Increased
sensitivity to light-induced melatonin suppression in premen-
strual dysphoric disorder. Chronobiol Int. 27:1438–53.
Phipps-Nelson J, Redman JR, Schlangen LJ, et al. (2009). Blue light
exposure reduces objective measures of sleepiness during
prolonged nighttime performance testing. Chronobiol Int. 26:
Rahman SA, Flynn-Evans EE, Aeschbach D, et al. (2014). Diurnal
spectral sensitivity of the acute alerting effects of light. Sleep.
Rahman SA, Marcu S, Shapiro CM, et al. (2011). Spectral modu-
lation attenuates molecular, endocrine, and neurobehavioral
disruption induced by nocturnal light exposure. Am J Physiol
Endocrinol Metab. 300:E518–27.
Reiter RJ, Tan DX, Korkmaz A, et al. (2007). Light at night,
chronodisruption, melatonin suppression, and cancer risk: A
review. Crit Rev Oncog. 13:303–28.
¨ger M, Gordijn MC, Beersma DG, et al. (2003). Acute and phase-
shifting effects of ocular and extraocular light in human
circadian physiology. J Biol Rhythms. 18:409–19.
¨ger M, Gordijn MC, Beersma DG, et al. (2005). Weak relation-
ships between suppression of melatonin and suppression of
sleepiness/fatigue in response to light exposure. J Sleep Res. 14:
16 Y. M. Cho et al.
Chronobiology International
Downloaded by [Korea University] at 19:13 17 September 2015
¨ger M, Gordijn MC, Beersma DG, et al. (2006). Time-of-day-
dependent effects of bright light exposure on human psycho-
physiology: Comparison of daytime and nighttime exposure.
Am J Physiol Regul Integr Comp Physiol. 290:R1413–20.
Santhi N, Thorne HC, van der Veen DR, et al. (2012). The spectral
composition of evening light and individual differences in the
suppression of melatonin and delay of sleep in humans. J Pineal
Res. 53:47–59.
Shanahan TL, Kronauer RE, Duffy JF, et al. (1999). Melatonin
rhythm observed throughout a three-cycle bright-light stimulus
designed to reset the human circadian pacemaker. J Biol
Rhythms. 14:237–53.
Skene DJ, Lockley SW, Thapan K, et al. (1999). Effects of light on
human circadian rhythms. Reprod Nutr Dev. 39:295–304.
St Hilaire MA, Gooley JJ, Khalsa SB, et al. (2012). Human phase
response curve to a 1 h pulse of bright white light. J Physiol. 590:
Stevens RG, Blask DE, Brainard GC, et al. (2007). Meeting report:
The role of environmental lighting and circadian disruption in
cancer and other diseases. Environ Health Perspect. 115:
Stevens RG, Brainard GC, Blask DE, et al. (2014). Breast cancer and
circadian disruption from electric lighting in the modern world.
CA Cancer J Clin. 64:207–18.
Stevens RG. (2009). Light-at-night, circadian disruption and breast
cancer: Assessment of existing evidence. Int J Epidemiol. 38:
Thessing VC, Anch AM, Muehlbach MJ, et al. (1994). Two- and 4-
hour bright-light exposures differentially effect sleepiness and
performance the subsequent night. Sleep. 17:140–5.
Tzischinsky O, Lavie P. (1997). The effects of evening bright light on
next-day sleep propensity. J Biol Rhythms. 12:259–65.
van de Werken M, Gime
´nez MC, de Vries B, et al. (2013). Short-
wavelength attenuated polychromatic white light during work
at night: Limited melatonin suppression without substantial
decline of alertness. Chronobiol Int. 30:843–54.
Vollmer C, Michel U, Randler C. (2012). Outdoor light at night
(LAN) is correlated with eveningness in adolescents.
Chronobiol Int. 29:502–8.
Wada K, Nagata C, Nakamura K, et al. (2012). Light exposure at
night, sleep duration and sex hormone levels in pregnant
Japanese women. Endocr J. 59:393–8.
Wada K, Nakamura K, Tamai Y, et al. (2013a). Associations of
urinary 6-sulfatoxymelatonin with demographics, body mass,
sex steroids, and lifestyle factors in preschool Japanese chil-
dren. Ann Epidemiol. 23:60–5.
Wada K, Yata S, Akimitsu O, et al. (2013b). A tryptophan-rich
breakfast and exposure to light with low color temperature at
night improve sleep and salivary melatonin level in Japanese
students. J Circadian Rhythms. 11:4.
Wahnschaffe A, Haedel S, Rodenbeck A, et al. (2013). Out of the lab
and into the bathroom: Evening short-term exposure to con-
ventional light suppresses melatonin and increases alertness
perception. Int J Mol Sci. 14:2573–89.
Wallace-Guy GM, Kripke DF, Jean-Louis G, et al. (2002). Evening
light exposure: Implications for sleep and depression. J Am
Geriatr Soc. 50:738–9.
Whittom S, Dumont M, Petit D, et al. (2010). Effects of melatonin
and bright light administration on motor and sensory symp-
toms of RLS. Sleep Med. 11:351–5.
Wright Jr KP, Gronfier C, Duffy JF, et al. (2005). Intrinsic
period and light intensity determine the phase relationship
between melatonin and sleep in humans. J Biol Rhythms. 20:
Yang WS, Deng Q, Fan WY, et al. (2014). Light exposure at night,
sleep duration, melatonin, and breast cancer: A dose–response
analysis of observational studies. Eur J Cancer Prev. 23:269–76.
Yokoi M, Aoki K, Shimomura Y, et al. (2003). Effect of bright light
on EEG activities and subjective sleepiness to mental task
during nocturnal sleep deprivation. J Physiol Anthropol Appl
Human Sci. 22:257–63.
Yokoi M, Aoki K, Shimomura Y, et al. (2006). Exposure to bright
light modifies HRV responses to mental tasks during nocturnal
sleep deprivation. J Physiol Anthropol. 25:153–61.
Zeitzer JM, Khalsa SB, Boivin DB, et al. (2005). Temporal dynamics
of late-night photic stimulation of the human circadian
timing system. Am J Physiol Regul Integr Comp Physiol. 289:
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... These central neuronal clocks interact with peripheral clocks, which are found in a multitude of tissues throughout the human body [16]. However, ALAN exposure imposes a direct challenge to circadian rhythms as it has been found to disrupt SCN activity and various ensuing mechanisms, particularly by suppressing and dysregulating melatonin release from the pineal gland [17][18][19][20]. As most of our physiological functions are regulated by the cross-talk between the central and peripheral pacemakers, ALAN exposure can consequently alter organ function at different levels by disrupting the synchrony between these pacemakers [21]. ...
... In addition to exposure in the home or at workplaces (particularly due to shift work), streetlights and light-emitting diodes (LEDs), particularly on the screens of televisions, computers, and mobile phones, are increasingly pervasive sources of ALAN in society. In the past two decades, several epidemiological studies have demonstrated that ALAN exposure has detrimental impacts on sleep and sleeping behaviour [18,20,[22][23][24]. While the majority of existing ALAN studies were primarily focused on sleep, some recent studies have demonstrated that ALAN is also associated with other physiological and behavioural functions. ...
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Artificial light at night (ALAN) exposure is associated with the disruption of human circadian processes. Through numerous pathophysiological mechanisms such as melatonin dysregulation, it is hypothesised that ALAN exposure is involved in asthma and allergy, mental illness, and cancer outcomes. There are numerous existing studies considering these relationships; however, a critical appraisal of available evidence on health outcomes has not been completed. Due to the prevalence of ALAN exposure and these outcomes in society it is critical that current evidence of their association is understood. Therefore, this systematic scoping review will aim to assess the association between ALAN exposure and asthma and allergy, mental health, and cancer outcomes. This systematic scoping review will be conducted in accordance with the Preferred Reporting Items for Systematic reviews and Meta-Analyses statement. We will search bibliographic databases, registries, and references. We will include studies that have described potential sources of ALAN exposure (such as shift work or indoor and outdoor exposure to artificial light); have demonstrated associations with either allergic conditions (including asthma), mental health, or cancer-related outcomes; and are published in English in peer-reviewed journals. We will conduct a comprehensive literature search, title and abstract screening, full-text review, and data collection and analysis for each outcome separately.
... Since academics are a professional group who work in front of a computer, tablet, etc., screen for a long time due to their profession, they are more likely to be exposed to artificial light. According to studies, exposure to artificial light later in the day causes a shift in the circadian phase, suggesting that academics are (Cho et al. 2015). Considering that academics are a group that works without the concept of overtime and have a high work intensity, it is evident that studies should be conducted to raise awareness about the protection of mental and physical health of academics, and that information studies about chronotypes and their impact on health should be a focus in nutritional counseling. ...
Academics are an occupational group that works at an intense pace. The number of studies on chronotype and night eating behavior in academics is limited, and there is insufficient data on whether fear of COVID-19 is also a risk for developing eating disorders. This study aimed to investigate the relationship between chronotype and night eating syndrome (NES) and examine the influence of fear of COVID-19 on night eating behavior in academics. The study data were collected using the personal information form, “Morningness-Eveningness Questionnaire, The Night Eating Questionnaire (NEQ), and the Fear of COVID-19 Scale.” According to the chronotypes of the academicians, it was determined that the score compatible with NES and the scores of the Fear of COVID-19 Scale differed statistically significantly, and the score compatible with NES and Fear of COVID-19 Scale scores were also higher in the evening type at a rate of 29.2% compared to other chronotypes (p < .05). The Fear of COVID-19 scale and Morningness-Eveningness Questionnaire scores were significantly correlated with the Night Eating Questionnaire (R = .391 R2 = .153 p < .05). The variables of the Fear of COVID-19 Scale and the Morningness-Eveningness Questionnaire explained 15% of the total variance of the Night Eating Questionnaire scores. Considering that academics are a group that works without the concept of overtime and whose work intensity is high, it is clear that studies should be conducted to raise awareness to protect the physical health of academics and prevent the development of eating disorders. There is a need for studies that question the relationship between chronotype, diet, and health.
... Specifically, exposure to artificial light before bedtime hours suppresses the release of melatonin, a sleep-promoting hormone that typically increases hours before bedtime. Acute and extreme exposure to artificial light before bedtime may delay the circadian phase of the melatonin rhythm [10,11], thus delaying the onset of sleep [12]. Melatonin suppression by a light stimulus of 580 lux (typical indoor light levels) in children has been reported to be almost twice that of adults [13]. ...
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Our study examines the acceptability and feasibility of Moshi, an audio-based mobile application, among children 3–8 years old using a parent–child dyadic approach. Our 10-day within-subject pre–post study design consisted of five nights of a normal bedtime routine and a subsequent five nights exposed to one story on the Moshi application during the intervention. Each five-night period spanned three weeknights and two weekend nights. The Short-Form Children’s Sleep Habits Questionnaire (SF-CSHQ) was used to measure children’s sleep at baseline and post-intervention. The PROMIS, Epworth Sleepiness Scale and Pittsburgh Sleep Quality Index were used to assess parents’ sleep. Among the 25 child–parent dyads, the mean child age was 4 (SD = 1.23) and 63% were male (n = 15). Mean parent age was 35 (SD = 5.83), 84% were female (n = 21), and 48.0% were Black (n = 12). For child-only comparisons, mean post-SF-CSHQ measures were lower compared to baseline. A trend in parent sleep is reported. This study shows the potential of an audio-based mobile sleep aid to improve sleep health in a racially diverse parent and child dyad sample.
... The results indicate that the main biomarker is eating jet lag and its components since, respectively, the most important factor in each case is pmd, jlatm and pmtm. Thus, night shift work previously related to various pathologies [35] is, according to our model, the main factor to take into account for pregnancy disturbances, being also an important factor for the time until reaching the first pregnancy, although in this case behind other indicator factors of chronodisruption such as sleep timing and quality. ...
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Chronodisruption alters circadian rhythms, which has negative consequences on different pathologies and mental disorders. This work studies whether factors related to chronodisruption of circadian rhythms motivated by shift works influence on reproductive health or not. In particular, this influence is studied on four particular aspects related to reproductive health: reproductive health disease, first pregnancy attempt, problems during pregnancy and gestation period. Some explainable machine learning models based on trees have been employed. These methods provided information about the importance of each predictor. The most important variables provided by each method were aggregated using a ranking aggregation function in order to reach a consensus ranking of variables that made possible to understand whether the chronodisruption factors had an effect on each of the aspects studied. The data have been obtained from 697 health professionals. Information about classical biomarkers, sleep quality indices and also other new variables related to eating jet lag, sleep hygiene and how the sleep is affected by shift works were considered as input data. Experiments have shown how some of these novel biomarkers are ranked in the top positions of the issues studied in relation to reproductive health. In particular, the light level and the use of electronic devices, which are features related to chronodisruption, are highlighted as biomarkers.
... These effects have been documented across diurnal, crepuscular, nocturnal and cathemeral organisms, across microbes, fungi, plants, and invertebrate and vertebrate animals, and across terrestrial, freshwater and marine ecosystems (Rich and Longcore, 2006;Bennie et al., 2016;Gaston et al., 2021;Sanders et al., 2021). Consequences for human health have also been highlighted, although discriminating between those that arise from outdoor and from indoor lighting environments (and the indoor incursion of outdoor lighting) remains problematic (Cho et al., 2015;Hatori et al., 2017;Lunn et al., 2017;Pacheco-Tucuch et al., 2012;Tasciotti, 2017;Walker et al., 2020). Additional negative effects of light pollution occur for both the scientific study and wider human experience of celestial bodies and phenomena (Dill, 2021;Dunnett, 2015), with these experiences having potential consequences for people's sense of place in the universe (Major, 2015;Stone, 2021). ...
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Key to understanding the negative impacts of artificial light at night (ALAN) on human health and the natural environment is its relationship with human density. ALAN has often primarily been considered an urban issue, however although over half of the population is urbanized, the 46 % that are not inhabit a dispersed array of smaller settlements. Here, we determine the global relationships between two dimensions of ALAN, namely direct emissions (radiance) and skyglow, and human density, and how these relationships vary across continents. We correct the Visible Infrared Imaging Radiometer Suite Day/Night Band (VIIRS DNB) product for albedo, skyglow, airglow, the aurora and permanent snow and ice to represent upward radiance overland at 1.61 ∗ 2.12 km resolution from artificial sources only. For skyglow we use the World Atlas of Artificial Sky Brightness. Globally (between 59°N and 55°S), direct emissions were detected over 26.5 % and skyglow over 46.9 % of land area. Over half of all cumulative direct emissions (54.9 %) were emitted at low levels by the non-urban population, whilst these populations experienced the negative impacts of over two-thirds of all cumulative skyglow (69.8 %). This emphasises the extent of ALAN outside of urban areas, and its similarity in this regard to a number of other forms of pollution. Although powerful sources of rural direct emissions (e.g., industry, recreation) are important contributors of light pollution, cumulatively they only contributed 10 % to total direct emissions. The relationship between each dimension of ALAN and population density varied across continents, driven by powerful rural emissions, non-urban populations and urban design. These relationships reflect the unique socio-economic and geographical make-up of each region and inform on where best to target light pollution mitigation strategies, not only in urban areas but also in rural ones.
We present a hypothesis for low vitamin D as a sign of untimely relocation of the human being during its history. This improper displacement prone our species to infectious and non-infectious diseases during our life journey, low vitamin D is a sign that needs to be addressed as a marker of the unsafe journey in our lifetime not the cause for diseases that are associated with it and replacement of vitamin D is the least that we have done.
Purpose This study aims to elucidate the underlying relationship between the expression profiles of circular RNAs (circRNAs) and the ovarian dysfunction induced by continuous light. Methods High-throughput sequencing was used to profile the transcriptome of differentially expressed circRNAs (DEcircRNAs) in rat ovary under continuous light exposure (12 h:12 h light/light cycle, L/L group) and a control cycle (12 h:12 h light/dark cycle, L/D group). Gene ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and circRNAs-microRNAs-messenger RNAs networks were performed to predict the role of DEcircRNAs in biological processes and pathways. A quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) assay was conducted to verify the high-throughput sequencing results and the expression level of circadian rhythm genes. Results In total, 305 circRNAs were differentially expressed between the L/L and L/D groups. Among these, 211 circRNAs were up regulated, while 94 were down regulated. Eight candidate circRNAs from 305 DEcircRNAs were verified by qRT‐PCR. Further bioinformatics analysis revealed that interactions between DEcircRNAs and a set of microRNAs involved in ovarian dysfunction-related pathways, such as regulation of androgen receptors, gonadotrophin releasing hormone signaling pathway, endocrine resistance, etc. Subsequently, we identified rno_circ:chr2:86868285-86964272 and rno_circ:chr1:62330221-62360073 may participate in the pathophysiology of ovarian dysfunction by constructing circRNAs-microRNAs-messenger RNAs networks. Meanwhile, constant light reduced the expression of circadian rhythm genes CLOCK, BAML1, PER1, and PER2 compared with that of controls. Caspase3 and Bax were up regulated in the L/L group compared with the L/D group, while Bcl-2 was down regulated. Conclusions In summary, the results reveal that the expression profiles and potential functions of DEcircRNAs in rat ovaries may play important roles in continuous light-induced ovarian dysfunction. These findings provide novel clues and molecular targets for studying the mechanisms and clinical therapy of ovarian dysfunction.
Background: Burnout is a hidden productivity killer in organizations. Finding a solution to efficiently measure and proactively prevent or rehabilitate employees with burnout is a challenge. To meet this unabated demand, companies and caregivers can focus on proactive measures to prevent "Burnout as an Occupational Phenomenon." Objective: We aimed to address effectiveness, reliability, and validity of the empowerment for participation (EFP) batch of assessments to measure burnout risk in relation to the efficacy of web-based interventions using cognitive behavioral therapy (CBT) and floating to improve mental health and well-being. We introduced three risk assessments: risk for burnout, risk of anxiety, and risk for depression. Methods: We used an interventional, empirical, and parallel design using raw EFP psychometric data to measure the effectiveness of web-based therapy to reduce the risk of burnout between a control group and web-based therapy group. A total of 50 participants were selected. The rehabilitation and control groups consisted of 25 normally distributed employees each. The rehabilitation group received therapy, whereas the control group had not yet received any form of therapy. IBM SPSS was used to analyze the data collected, and a repeated measures ANOVA, an analysis of covariance, a discriminant analysis, and a construct validity analysis were used to test for reliability and validity. The group was selected from a list of employees within the My-E-Health ecosystem who showed a moderate or high risk for burnout. All assessments and mixed-method CBT were web-based, and floating was conducted at designated locations. The complete EFP assessment was integrated into a digital ecosystem designed for this purpose and therapy, offering a secure and encrypted ecosystem. Results: There was a statistically significant difference between pre- and postassessment scores for burnout. The reliability of the burnout measure was good (Cronbach α=.858; mean 1.826, SD 3.008; Cohen d=0.607; P<.001) with a high validity of 0.9420. A paired samples 2-tailed test showed a good t score of 4.292 and P<.001, with a good effect size, Cohen d=0.607. Web-based therapy reduced the risk for burnout in participants compared with the control group. Tests of between-subject effects show F=16.964, a significant difference between the control group and the web-based therapy group: P<.001, with movement between the group variables of 0.261 or 26.1% for the dependent variable. Conclusions: This study suggests good reliability and validity of using web-based interventional mixed methods CBT to reduce the risk of burnout. The EFP batch of web-based assessments could reliably identify morbidity risk levels and successfully measure clinical interventions and rehabilitation with consistently reliable results to serve as both a diagnostic and therapeutic tool worthy of major research in the future. Trial registration: NCT05343208;
Introduction: light intensity and duration are physical factors that affect hormone secretion and circadian rhythms. This study aimed to determine the effects of various light intensities on serum melatonin and cortisol levels. Materials and methods: This experimental study was carried out on 32 male rats: Group 1 as the control group, received a brightness of 150 lux, and groups 2, 3, and 4 as the exposure groups received light intensities of 300, 5000, and 8000 lux for 14 days, respectively. To evaluate hormone levels, blood samples were taken on before and after 7 and 14 days of exposure. Then cortisol and melatonin levels were determined by ELISA. Data were analyzed using SPSS. Results: The results showed that cortisol levels after seven days of exposure in the groups exposed to the light intensity of 300, 5000, and 8000 lux increased significantly compared to the control group, and after 14 days, the level of cortisol in the groups. Exposure to a light intensity of 5000 and 8000 lux increased significantly compared to the control. Also, melatonin levels in the group of rats exposed to the light intensity of 5000 lux and 8000 lux after 7 and 14 days of exposure compared to the control significantly decreased. Conclusion: Increased light intensity is associated with increased melatonin suppression and cortisol levels. It is suggested that more studies be done to prove the effect of different light intensities on changes in the levels of these hormones at varying hours of the day.
Facility design and animal care practices impact the quality of life of sheltered dogs, and there is a growing body of data and anecdotal information showing that appropriate housing and husbandry can mitigate the negative impact of many detrimental features commonly attributed to shelters. Using the facility and caring for animals in a way that balances behavioral, medical, and operational considerations while ensuring opportunities for assessment, enrichment, training, and rehabilitation is essential to operating a humane animal shelter. A well‐designed and maintained physical facility can facilitate the development and delivery of an efficient and effective behavioral program in a shelter, with the quality of housing substantially impacting animal health and well‐being.
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Systematic reviews and meta-analyses have become increasingly important in health care. Clinicians read them to keep up to date with their field [1],[2], and they are often used as a starting point for developing clinical practice guidelines. Granting agencies may require a systematic review to ensure there is justification for further research [3], and some health care journals are moving in this direction [4]. As with all research, the value of a systematic review depends on what was done, what was found, and the clarity of reporting. As with other publications, the reporting quality of systematic reviews varies, limiting readers' ability to assess the strengths and weaknesses of those reviews. Several early studies evaluated the quality of review reports. In 1987, Mulrow examined 50 review articles published in four leading medical journals in 1985 and 1986 and found that none met all eight explicit scientific criteria, such as a quality assessment of included studies [5]. In 1987, Sacks and colleagues [6] evaluated the adequacy of reporting of 83 meta-analyses on 23 characteristics in six domains. Reporting was generally poor; between one and 14 characteristics were adequately reported (mean = 7.7; standard deviation = 2.7). A 1996 update of this study found little improvement [7]. In 1996, to address the suboptimal reporting of meta-analyses, an international group developed a guidance called the QUOROM Statement (QUality Of Reporting Of Meta-analyses), which focused on the reporting of meta-analyses of randomized controlled trials [8]. In this article, we summarize a revision of these guidelines, renamed PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses), which have been updated to address several conceptual and practical advances in the science of systematic reviews (Box 1). Box 1: Conceptual Issues in the Evolution from QUOROM to PRISMA Completing a Systematic Review Is an Iterative Process The conduct of a systematic review depends heavily on the scope and quality of included studies: thus systematic reviewers may need to modify their original review protocol during its conduct. Any systematic review reporting guideline should recommend that such changes can be reported and explained without suggesting that they are inappropriate. The PRISMA Statement (Items 5, 11, 16, and 23) acknowledges this iterative process. Aside from Cochrane reviews, all of which should have a protocol, only about 10% of systematic reviewers report working from a protocol [22]. Without a protocol that is publicly accessible, it is difficult to judge between appropriate and inappropriate modifications.
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Daily, lunar and seasonal cycles of natural light have been key forms of environmental variation across the Earth’s surface since the first emergence of life. They have driven the development of biological phenomena from the molecule to the ecosystem, including metabolic and physiological pathways, the behaviour of individuals, geographical patterns of adaptation and species richness, and ecosystem cycles (e.g. [1–4]). Indeed, biological systems are arguably organized foremost by light [5–7]. The natural patterns of light have over the last 100 years come to be greatly disrupted through the introduction of artificial light into the night-time environment: artificial light at night (ALAN). This derives from a diversity of sources, including street lighting, advertising lighting, architectural lighting, security lighting, domestic lighting and vehicle lighting. ALAN disrupts natural patterns of light both via direct effects of illumination from these sources as well as via skyglow (the scattering by atmospheric molecules or aerosols in the atmosphere of ALAN that is emitted or reflected upwards; [8–10]).
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The adverse effects of excessive use of artificial light at night (ALAN) are becoming increasingly evident and associated with several health problems including cancer. Results of epidemiological studies revealed that the increase in breast cancer incidents co-distribute with ALAN worldwide. There is compiling evidence that suggests that melatonin suppression is linked to ALAN-induced cancer risks, but the specific genetic mechanism linking environmental exposure and the development of disease is not well known. Here we propose a possible genetic link between environmental exposure and tumorigenesis processes. We discuss evidence related to the relationship between epigenetic remodelling and oncogene expression. In breast cancer, enhanced global hypomethylation is expected in oncogenes, whereas in tumour suppressor genes local hypermethylation is recognized in the promoter CpG chains. A putative mechanism of action involving epigenetic modifications mediated by pineal melatonin is discussed in relation to cancer prevalence. Taking into account that ALAN-induced epigenetic modifications are reversible, early detection of cancer development is of great significance in the treatment of the disease. Therefore, new biomarkers for circadian disruption need to be developed to prevent ALAN damage. © 2015 The Author(s) Published by the Royal Society. All rights reserved.
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Purpose: The aim of our study was to investigate if ambient lighting at night before the age of 2 years is associated with the occurrence of myopia in a large population of Polish children. To eliminate the influence of genetic factors, only children with a negative family history of myopia were included. Material and methods: A total of 3905 students, all of whom had a negative family history of myopia were examined (1800 boys and 2105 girls, aged 6−18 years, mean age 12.2, S.D. 3.3 years). The examination included retinoscopy under cycloplegia with 1% tropicamide. Myopia in the subjects was defined as a spherical equivalent of at least -0.50 dioptres. The parents of all students examined completed a questionnaire on the child’s family history of myopia as well as the child’s exposure to light emitted by incandescent or fluorescent lamps before the age of two years. Data analysis was performed using chi-squared Pearson test; p-values of <0.05 were considered statistically significant. Results: Sleeping until the age of two with a room light is not associated with the presence of myopia during school years (p>0.05). No differences in the use of light emitted by incandescent or fluorescent lamps on the prevalence of myopia was found (p>0.05). Conclusions: Myopia is not associated with night light use before age of 2 years in a population of Polish children with a negative family history of myopia. Because both, the restricted population and results differ from our previous positive associations, perhaps early light exposure and family history/genetics interact in influcencing the occurance of myopia.
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Background: There is convincing evidence that circadian disruption mediated by exposure to light at night promotes mammary carcinogenesis in rodents. The role that light at night plays in human breast cancer etiology remains unknown. We evaluated the relationship between estimates of indoor and outdoor light at night and the risk of breast cancer among members of the California Teachers Study. Methods: Indoor light-at-night estimates were based on questionnaire data regarding sleep habits and use of nighttime lighting while sleeping. Estimates of outdoor light at night were derived from imagery data obtained from the US Defense Meteorological Satellite Program assigned to geocoded addresses of study participants. Analyses were conducted among 106,731 California Teachers Study members who lived in California, had no prior history of breast cancer, and provided information on lighting while sleeping. Five thousand ninety-five cases of invasive breast cancer diagnosed 1995-2010 were identified via linkage to the California Cancer Registry. We used age-stratified Cox proportional hazard models to calculate hazard ratios (HRs) with 95% confidence intervals (CIs), adjusting for breast cancer risk factors and neighborhood urbanization and socioeconomic class. Results: An increased risk was found for women living in areas with the highest quintile of outdoor light-at-night exposure estimates (HR = 1.12 [95% CI = 1.00-1.26]; test for trend, P = 0.06). Although more pronounced among premenopausal women (HR = 1.34 [95% CI = 1.07-1.69]; test for trend, P = 0.04), the associations did not differ statistically by menopausal status (test for interaction, P = 0.34). Conclusions: Women living in areas with high levels of ambient light at night may be at an increased risk of breast cancer. Future studies that integrate quantitative measurements of indoor and outdoor light at night are warranted.
Humans are diurnal organisms whose biological clock and temporal organization depend on natural light/dark cycles. Changes in the photoperiod are a signal for seasonal acclimatization of physiological and immune systems as well as behavioral patterns. The invention of electrical light bulbs created more opportunities for work and leisure. However, exposure to artificial light at night (LAN) affects our biological clock, and suppresses pineal melatonin (MLT) production. Among its other properties, MLT is an antioncogenic agent, and therefore its suppression increases the risks of developing breast and prostate cancers (BC&PC). To the best of our knowledge, this book is the first to address the linkage between light pollution and BC&PC in humans. It explains several state-of-the-art theories, linking light pollution with BC&PC. It also illustrates research hypotheses about health effects of light pollution using the results of animal models and population-based studies. © Springer Science+Business Media Dordrecht 2013. All rights are reserved.
Introduction Artificial lighting has benefited society by extending the length of a productive day, but it can be ”light pollution” when it becomes excessive. Unnecessary exposure to artificial light at night can cause myopia, obesity, metabolic disorders and even some type of cancers. Materials and methods We recruited 10 subjects (4 females, mean age 27) who are good sleepers and have no history of any major health problems. They underwent two fullnight polysomnographic (PSG) and electroencephalographic (EEG) recordings with one month interval, once with bedside light off and again with light on. Sleep staging was performed and PSG variables were obtained for two conditions. Spectral analysis was performed on EEG recordings and spectral power of functional frequency bands was calculated. Analysis and comparison was also performed on slow waves and sleep spindles. Results Eight participants reported subjective discomfort when they woke up after light on condition. Comparison between PSG variables showed that sleep with light on was associated with increased stage N1, decreased slow wave sleep, and increased arousal index (p < 0.05). Spectral analysis revealed that slow oscillation and delta power during NREM and theta during REM were significantly decreased (p < 0.05) in light on condition. Spindle activity was also increased during NREM period, but did not survive multiple comparisons test. Slow wave analysis showed that the number and amplitude of slow waves were decreased during sleep with light on. Conclusion Our study reports that sleeping with light on not only causes change in sleep quality during sleeping, but also has persistent effect on brain oscillations. Change in slow wave and spindle activities during NREM sleep, both hallmarks of deep sleep, and theta in REM sleep provides electrophysiological evidence that bedside light can disturb the quality of sleep. Current study provides additional hazardous effect of light at night on health and sleep quality.