The harmful effects of light at night on humans are now well recognized by the general public. As previously reported, people exposed to light at night can have increased incidence of a wide range of illnesses, including sleep and psychiatric disorders, obesity, diabetes, and several kinds of cancers. In modern society, people are routinely exposed to electrical lighting during evening hours, after the onset of melatonin production, to partake in work, recreational, and social activities. Gooley et al. [1] reported that this indoor room light profoundly alters the timing, duration, and amount of melatonin synthesis, the health consequences of which are unknown. Blue light, which is particularly beneficial during the daytime, seems to be more disruptive at night, and induces the strongest melatonin inhibition [2]. Sensitivity of human nocturnal melatonin suppression [3,4] peaks in the blue portion of the light spectrum around 460 nm, most effective in the range between 446 and 477 nm [5]. Because photoresponse such as adaptation of the circadian clock is mediated by retinal ganglion cells expressing the photopigment melanopsin which is most sensitive to blue light, blue wavelengths can potentially exert more powerful effects on human circadian rhythm than green and yellow wavelengths [5,6].

Nocturnal blue light exposure is currently increasing, due to the proliferation of energy-efficient lighting [light-emitting-diodes (LEDs)] and electronic devices. Thus, the development of lighting systems that preserve the melatonin rhythm could reduce the health risks induced by chronodisruption [2]. Organic light-emitting diodes (OLEDs), which emit less blue light than traditional LEDs, are an energy-efficient and physiologically friendly form of lighting [7,8]. OLED light exposure (LE) could decrease the adverse health outcomes of artificial light at night, but no studies have investigated its effects on sleep quality and the circadian system. Our team previously conducted the first direct comparative study of how OLED and LED affect melatonin profile, sleep, and vigilance. We reported that early-night OLED LE exerts weaker effects on the melatonin phase delay than LED LE at a color temperature of 4,000 K [9].

This is a follow-up to that study. We here investigate the effects of OLED LE and LED LE on melatonin profile, sleep, and vigilance at a different color temperature (3,000 K) that is more commercialized for indoor lighting. Currently, there are two types of OLEDs that are commercially available in the market with color temperatures of 4,000 K and 3,000 K. The 4,000 K color temperautre is used in the office, shopping mall or daily residential outdoor lighting because it provides a normal bright light, while the 3,000 K color temperautre creates a warm atmosphere that makes us feel relaxed, so it is often used for home decoration lighting. Since we have already found that 4,000 K OLED LE affects melatonin secretion, we aimed to see if similar results were obtained with a 3,000 K OLED, which is more commonly used as indoor lighting. In this study, we also hypothesized that evening OLED LE would result in less melatonin suppression, smaller circadian phase delays, and better sleep quality and daytime vigilance compared to LED LE.

This study is a follow-up to our team’s previous study [9], and we applied the same laboratory settings and study protocol.

In this study, we compared the effects of exposure to OLED and LED used as room lights on melatonin profile, sleep quality, and vigilance in young adults. We found that the mean melatonin level at 24:00 under LED LE was significantly lower than that under DL, but there was no significant difference between OLED LE and DL. The percentage of N3 sleep under LED LE was lower than that under OLED LE.

Blue light is known to suppress secretion of melatonin, which can disrupt the circadian rhythm and sleeping behavior [18,19]. Brainard et al. [3] reported approximately 60% suppression of melatonin after 2 h of light at 460 nm and 12.1 μW/cm2. In another recent report, exposure to 3,000 K LED ceiling light induced statistically significant melatonin suppression compared with melatonin concentrations under a dim condition. Lightinduced melatonin AUC %change relative to the AUC under the dim condition was 30.4% in adults (41.7±4.4 years old) and 58.1% in children (8.9±2.2 years old) [20].

Thus, OLED can be a good substitute for LED because the spectrum of an OLED contains a smaller proportion of blue light, which has the greatest influence on the melanopsin in intrinsically photosensitive retinal ganglion cells. Furthermore, OLED has several benefits as a future lighting source with high efficiency and low power consumption [21,22]. In addition, OLED light panels emit diffuse light from their surfaces, which helps to reduce fatigue in the human eye. It is presumed that OLED is a human-friendly type of lighting that will disturb the circadian rhythm less than other light sources and facilitate sleep [23].

However, only a few studies have directly compared the effects of LED LE and OLED LE. Our team previously reported that early-night OLED LE exerts weaker effects on the melatonin phase delay than LED LE at a color temperature of 4,000 K [9]. There was no difference in melatonin onset between OLED and LED LE (p=0.078), however melatonin onset under LED LE was significantly delayed under DL (p=0.007), whereas under OLED LE, there was no significant delay compared to DL (p=0.287) [9]. In this study, we investigated the effects of OLED LE and LED LE on melatonin profiles at a different color temperature (3,000 K), which is widely commercialized for indoor lighting.

Our present data show that melatonin onset time did not differ significantly between OLED and LED LE. Although melatonin suppression also did not differ between OLED and LED LE, we attribute that to our inability to measure salivary melatonin level during sleep. Typically, melatonin level begins to rise significantly around 21:00 and peaks in the middle of the night, around 03:00. We measured the amount of melatonin when patients were awake from 18:00 to 24:00 and found that the amount of melatonin from 18:00 to 23:00 did not differ between the two LED groups, but there was a significant difference at 24:00. The mean melatonin level at 24:00 under LED LE was significantly lower than that under DL, but there was no significant difference between OLED LE and DL.

Our data also show that the percentage of N3 sleep was significantly lower under LED LE than under OLED LE. Stage N3 is considered as deep sleep and generally cycles frequently in the first third of the night and begins to decrease toward the second half of the night [24]. Therefore, we hypothesize that LED LE affects deep sleep early in the night. Considering that these results are linked to the lower melatonin level at 24:00 under LED LE, we propose that LED LE suppresses melatonin secretion at bedtime and prevents people from falling into deep sleep in the initial period of sleep.

When we put together the results of our previous study conducted at a 4,000 K color temperature and those of the present study at 3,000 K, we found that OLED LE caused smaller delay in melatonin onset time and less disturbed melatonin secretion than did LED LE. However, those differences between OLED and LED LE were not as distinct as we expected, possibly due to the limitations of our studies. First, we did not control subjects’ light exposure during the daytime. The participants were allowed to perform their daytime activities as usual before entering the unit. Although we monitored the amount of LE by actigraphy data from the day before the visit, a more definite difference would have been made if the daytime LE was more strictly controlled. Second, another limitation in our study is the absence of a control night, when no light pulses were conducted. Thus, the extent to which light affects sleep structure remains unclear. Although it was confirmed that the baseline circadian profile was similar using wrist actigraphy, control night data was required for accurate evaluation. Third, the amount of light actually delivered to the eyes would have been less than we had expected. We used the ceiling-mounted light panels, but participants spent most of their time reading books in the head-down position. Thus a sufficient amount of light may not have delivered to the eyes for 6.5 hours of LE. Firth, evening LE under a specific condition was performed for only one night during each session in this study. That short-term exposure might have been insufficient to detect alterations in the circadian rhythm and sleep. Finally, an illuminance of 150 lux seems not to be bright enough to interfere with circadian rhythms and sleep in young, healthy participants, even during the evening.

Although those limitations did affect our study, the present experimental setting might better reflect real lighting environments during the evening and nighttime. Despite those limitations, we did find that OLED LE had less effect on melatonin phase and sleep quality than did LED LE. Further research in a strictly controlled experimental setting with a larger number of subjects is needed to identify the significant effects of evening light sources on sleep and vigilance.

In conclusion, we suggest that evening and early-night OLED LE may induces less melatonin suppression and less disturbs deep sleep compared to LED LE. It needs further follow-up test to confirm that OLED is a suitable evening light source to minimize the harmful effects of artificial light on melatonin and sleep quality.