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

Abstract

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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Effects of artificial light at night on human
health: A literature review of observational
and experimental studies applied to exposure
assessment
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
To link to this article: http://dx.doi.org/10.3109/07420528.2015.1073158
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Chronobiology International, Early Online: 1–17, (2015)
!Taylor & Francis.
ISSN: 0742-0528 print / 1525-6073 online
DOI: 10.3109/07420528.2015.1073158
REVIEW ARTICLE
Effects of artificial light at night on human health: A literature review
of observational and experimental studies applied to exposure
assessment
YongMin Cho
1
, Seung-Hun Ryu
1
, Byeo Ri Lee
1
, Kyung Hee Kim
1
, Eunil Lee
2
, and Jaewook Choi
1,2
1
Institute for Occupational & Environmental Health, Korea University, Seoul, Republic of Korea and
2
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
INTRODUCTION
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: shine@korea.ac.kr
Submitted March 27, 2015, Returned for revision July 2, 2015, Accepted July 13, 2015
1
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toxicants or radiation, do. Consequently, unlike other
risk factors, it is difficult to explain the doseresponse
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.
METHODS
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.
RESULTS
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.,
2013).
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.,
2012).
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
2
) 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.,
2009).
Records idenfied through database
searching
(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
eligibility
(n = 151)
Full-text arcles excluded,
with reasons
(n = 66)
Studies included in literature
review
(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 daynight 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 25002800 Lux sup-
pressed melatonin secretion relative to DL exposure at
5100120 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
(Ha
¨to
¨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.,
2010).
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.,
2003).
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).
DISCUSSION
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
b
/
main statistics applied References
Outdoor ALAN level/
satellite data
Ecological – Race, per capita income,
population, birth rate,
electricity consump-
tion, fertility rate, lung
cancer
a
Incidence of BC (ASR) B¼0.121 and 0.277/OLS
regression
Kloog et al. (2008, 2010)
Ecological – GDP, urban population,
electricity consump-
tion, region, lung
cancer
a
Incidence of prostate
cancer (ASR)
B¼0.1500.160/OLS
regression
Kloog et al. (2009)
Case-referent 34 053 BC cases and
14 458 lung cancer
referents
Race, tumor grade and
stage, smoking, statis-
tical status, etc.
Incidence of BC OR for LAN ¼1.12 (95%
CI ¼1.041.20)/
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
regression
Hurley et al. (2014)
Cross-sectional 1507 adolescents Time use of electronic
screen media, intake of
stimulants, type of
school, age, puberty
status, etc.
Chronotype
(eveningness-type)
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
concentration
n.s
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
controls
Education, ethnicity,
fertility, alcohol con-
sumption, TV on while
sleeping
Incidence of BC OR for bedroom light
¼1.220 (95%
CI ¼1.1181.311)/
logistic regression
Kloog et al. (2011)
Case-control 576 with BC and 585
controls
Menopausal status,
history of oophorec-
tomy or hysterectomy,
smoking, hormone
therapy
Incidence of BC OR for lighting habit
during sleep hrs ¼1.65
(95% CI ¼1.022.69)/
logistic regression
O’Leary et al. (2006)
Cross-sectional 60 women Daytime occupational
electromagnetic expos-
ure,
c
age, smoking
Excretion of 6-OHMS The lowest mean in the
group of both MF and
LAN/ANOVA
Juutilainen & Kumlin (2006)
Longitudinal 206 postmenopausal
women
Age, BMI, smoking and
drinking habits, phys-
ical activity, medical
and reproductive his-
tory, day length of the
day previous to urine
collection
Concentration of serum
estradiol and urinary
6-sulfatoxymelatonin
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
gestation
Maternal and umbilical
serum testosterone
level
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
circumference
Significant ORs of indica-
tors of obesity for
middle or darkness
level compared with
the lightest level ¼0.94
0.76/logistic
regression
McFadden et al. (2014)
Case-control 813 BC patients and 793
controls
Parity, family history of
BC, oral contraceptive
use, hormone replace-
ment therapy
BC prevalence
n.s
OR for ambient light
levels ¼1.01.4 (not
significant)/logistic
regression
Davis et al. (2001)
Case-control 363 BC cases and 356
controls
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
n.s
OR for keeping lights on
while sleeping ¼1.4
(95% CI ¼0.72.7)/
logistic regression
Li et al. (2010)
Cross-sectional 438 children Age, BMI, sex, sex steroid
hormones
Melatonin levels
n.s
No significant difference
between factors of
bedroom ambient light
level/ANOVA
Wada et al. (2013a)
Cross-sectional 3905 schoolchildren Family history of myopia
and eye health status
Myopia incidence
n.s
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
nurses
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
2
test
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 ¼1.052.45)/
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
b
/
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
controls
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 ¼0.0200.247) for
evening light exposure/
linear regression
Obayashi et al. (2014b)
Cross-sectional 154 women Age, season Depressed mood, sleep
latency
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,
etc.
Depressive symptoms aOR for light intensity (5
Lux) ¼1.89 (95%
CI ¼1.103.25), aOR
for exposure duration
(30 min) ¼1.71 (95%
CI ¼1.012.89)/logistic
regression
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 ¼1.183.04), aOR
for abdominal ¼1.62
(95% CI ¼1.022.57),
aOR for dyslipidemia
¼1.72 (95%
CI ¼1.112.68)/logistic
regression
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 ¼3.9225.395; 
for DBP ¼2.7732.825/
linear regression
Obayashi et al. (2014a)
Cross-sectional 131 young adults Interaction between
variables
Circadian rhythm Comparisons of wrist
temperature due to
day–night light con-
trast/ANOVA
Martinez-Nicolas et al. (2014)
Cross-sectional 12 M-type and 12 E-type
subjects
Shift work, travelling to
another time zone in
the past 3 months,
smoking, drug or
medication, hormonal
contraceptive
Circadian phase
n.s
Comparison circadian
phase angle between
M-types and E-types/
ANOVA
Goulet et al. (2007)
Cross-sectional 30 nurses Smoking, medication,
pregnancy, lactating,
sleep disorders
Phase advance and
delay
n.s
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-
ent/ANOVA
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.
a
In these studies, lung cancer was a comparison target, used for emphasis, rather than acting as a confounder.
b
Data in this table show results that were statistically significant.
c
In this study, authors analyzed the synergistic effect of electromagnetic field and LAN exposure to melatonin production.
n.s
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
(04:30)
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
latency
Bunnell et al. (1992)
36 young adults
(21.9)
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,
sleepiness
Ru
¨ger et al. (2005)
14 adults (22–35) Bright white light about
3000
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
¨to
¨nen et al. (1999)
12 males (21.8) 5000 510 24:0004:00 ANOVA, Paired t-test CBT, sleepiness, suppres-
sion of melatonin
Ru
¨ger et al. (2003)
10 adolescents (14–
15)
2000 60 19:25–22:30 Wilcoxon test Melatonin concentration Harada (2004)
36 young adults
(22)
2984 1.9 3 h of bright light expos-
ure, starting 1 h prior to
habitual wake time
t-test DLMO, circadian phase
shifts
Burke et al. (2013)
6 (48.6) for ex. 1
7 (23) for ex. 2
100 (green light) 51 (red light) 23:3000:30 in 1st session
and 60 min in 2nd and
3rd session for ex. 1
60 min for ex. 2
ANOVA Melatonin suppression,
DLMO
Figueiro & Rea (2012)
16 young (29.3) and
14 older (67.1)
adults
3500 10 4 h at night ANOVA DLMO, DLMOff Benloucif et al. (2006)
34 young adults
(21.8)
58000 53 1 h at night Non-linear least-square
analysis
(LevenbergMarquardt
algorithm)
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 (700013 000) 1015 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
analysis)
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
temperature
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–
25)
2000 550 20:00–08:00 ANOVA Alertness, performance,
suppression of mela-
tonin metabolite
aMT6s
Daurat et al. (2000)
24 males (23.1) 55000 510 Daytime experiment:
12:00–16:00
Nighttime experiment:
00:00–4:00
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
n.s
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
exposure
n.s
Lushington et al. (2002)
10 females (20.5) 2000 50 15:00–24:00 Paired t-test Amount of breath
hydrogen
n.s
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.
n.s
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,
sleepiness
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
exposure)
Thessing et al. (1994)
8 young adults
(19–25)
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
effects
Chang et al. (2011, 2013)
23 adults (22.8) 6000–13 000 Exposure time Morning exposure
(08:30–13:30)/after-
noon exposure
(13:30–18:30)/evening
exposure (18:30–23:30)
ANOVA Phase shift delay and
sleep latency in the
evening exposure
group
Carrier & Dumont (1995)
8 males (19–23) 700–1000 Lux Exposure time Evening exposure
(20:00–24:00)/morning
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
(18:00–21:00)/morning
exposure
(06:00–09:00)/sleep
displacement
Wilcoxon
signed-rank
test
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
calculated
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
n.s
Cajochen et al. (2003)
ALAN, artificial light at night; LD cycle, light:dark cycle; DLMO, dim light melatonin onset.
n.s
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.
(2006)
12 adults (25.8) Wavelength Filtered 5460nm and
5480 nm light
Unfiltered light Melatonin and cortisol
secretion, clock gene
expression, alertness,
performance
Rahman et al. (2011)
22 adults (23.1) Polychromatic evening
light condition
Near-darkness/blue-depleted/blue-intermediated/blue-
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.
(2013)
8 adults (32.1) Wavelength 460 nm 640 nm Alertness Phipps-Nelson et al.
(2009)
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.
(2013)
5 males (20.0) Color temperature Daylight (6500 K; 1000 Lux)/warm white (3000 K; 1000 Lux)/
control (50 Lux)
Circadian phase Morita & Tokura
(1996)
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) (KruskalWallis 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
levels.
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 14. 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
influence.
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
determined.
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,
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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.
DECLARATION OF INTEREST
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).
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