Ocular light exposure has important influences on human health and well-being through modulation of circadian rhythms and sleep, as well as neuroendocrine and cognitive functions. Prevailing patterns of light exposure do not optimally engage these actions for many individuals, but advances in our understanding of the underpinning mechanisms and emerging lighting technologies now present opportunities to adjust lighting to promote optimal physical and mental health and performance. A newly developed, international standard provides a SI-compliant way of quantifying the influence of light on the intrinsically photosensitive, melanopsin-expressing, retinal neurons that mediate these effects. The present report provides recommendations for lighting, based on an expert scientific consensus and expressed in an easily measured quantity (melanopic equivalent daylight illuminance (melaponic EDI)) defined within this standard. The recommendations are supported by detailed analysis of the sensitivity of human circadian, neuroendocrine, and alerting responses to ocular light and provide a straightforward framework to inform lighting design and practice.

International standard CIE S 026:2018 provides lighting professionals and field researchers in chronobiology with a method to characterize light exposures with respect to non-visual photoreception and responses. This standard defines five spectral sensitivity functions that describe optical radiation for its ability to stimulate each of the five α-opic retinal photoreceptor classes that contribute to the non-visual effects of light in humans via intrinsically-photosensitive retinal ganglion cells (ipRGCs). The CIE also recently published an open-access α-opic toolbox that calculates all the quantities and ratios of the α-opic metrology in the photometric, radiometric and photon systems, based on either a measured (user-defined) spectrum or selected illuminants (A, D65, E, FL11, LED-B3) built into the toolbox. For a wide variety of ecologically-valid conditions, the melanopsin-based photoreception of ipRGCs has been shown to account for the spectral sensitivity of non-visual responses, from shifting the timing of nocturnal sleep and melatonin secretion to regulating steady-state pupil diameter. Recent findings continue to confirm that the photopigment melanopsin also plays a role in visual responses, and that melanopsin-based photoreception may have a significant influence on brightness perception and aspects of spatial vision. Although knowledge concerning the extent to which rods and cones interact with ipRGCs in driving non-visual effects is still growing, a CIE position statement recently used melanopic equivalent daylight (D65) illuminance in preliminary guidance on applying “proper light at the proper time” to manipulate non-visual responses. Further guidance on this approach is awaited from the participants of the 2nd International Workshop on Circadian and Neurophysiological Photometry (in Manchester, August 2019). The new α-opic metrology of CIE S 026 enables traceable measurements and a formal, quantitative specification of personal light exposures, photic interventions and lighting designs. Here, we apply this metrology to everyday light sources including a natural daylight time series, a range of LED lighting products and, using the toobox, to a smartphone display screen. This collection of examples suggests ways in which variations in the melanopic content of light over the day can be adopted in strategies that use light to support human health and well-being.

The widespread use of electric light and electronic devices has resulted in an excessive exposure to light during the late-evening and at night. This late light exposure acutely suppresses melatonin and sleepiness and delays the circadian clock. Here we investigate whether the acute effects of late-evening light exposure on our physiology and sleepiness are reduced when this light exposure is preceded by early evening bright light. Twelve healthy young females were included in a randomised crossover study. All participants underwent three evening (18:30-00:30) sessions during which melatonin, subjective sleepiness, body temperature and skin blood flow were measured under different light conditions: (A) dim light, (B) dim light with a late-evening (22:30-23:30) light exposure of 750 lx, 4000 K, and (C) the same late-evening light exposure, but now preceded by early-evening bright light exposure (18.30-21.00; 1200 lx, 4000 K). Late-evening light exposure reduced melatonin levels and subjective sleepiness and resulted in larger skin temperature gradients as compared to dim. Interestingly, these effects were reduced when the late-evening light was preceded by an early evening 2.5-hour bright light exposure. Thus daytime and early-evening exposure to bright light can mitigate some of the sleep-disruptive consequences of light exposure in the later evening.

Light‐induced melatonin suppression data from 29 peer‐reviewed publications was analysed by means of a machine‐learning approach to establish which light exposure characteristics (ie photopic illuminance, five α‐opic equivalent daylight illuminances [EDIs], duration and timing of the light exposure, and the dichotomous variables pharmacological pupil dilation and narrowband light source) are the main determinants of melatonin suppression. Melatonin suppression in the data set was dominated by four light exposure characteristics: (1) melanopic EDI, (2) light exposure duration, (3) pupil dilation and (4) S‐cone‐opic EDI. A logistic model was used to evaluate the influence of each of these parameters on the melatonin suppression response. The final logistic model was only based on the first three parameters, since melanopic EDI was the best single (photoreceptor) predictor that was only outperformed by S‐cone‐opic EDI for (photopic) illuminances below 21 lux. This confirms and extends findings on the importance of the metric melanopic EDI for predicting biological effects of light in integrative (human‐centric) lighting applications. The model provides initial and general guidance to lighting practitioners on how to combine spectrum, duration and amount of light exposure when controlling non‐visual responses to light, especially melatonin suppression. The model is a starting tool for developing hypotheses on photoreceptors’ contributions to light's non‐visual responses and helps identifying areas where more data are needed, like on the S‐cone contribution at low illuminances.

We examined whether ambient lighting conditions during extended wakefulness modulate the homeostatic response to sleep loss as indexed by. slow wave sleep (SWS) and electroencephalographic (EEG) slow-wave activity (SWA) in healthy young and older volunteers. Thirty-eight young and older participants underwent 40 hours of extended wakefulness [i.e., sleep deprivation (SD)] once under dim light (DL: 8 lux, 2800 K), and once under either white light (WL: 250 lux, 2800 K) or blue-enriched white light (BL: 250 lux, 9000 K) exposure. Subjective sleepiness was assessed hourly and polysomnography was quantified during the baseline night prior to the 40-h SD and during the subsequent recovery night. Both the young and older participants responded with a higher homeostatic sleep response to 40-h SD after WL and BL than after DL. This was indexed by a significantly faster intra-night accumulation of SWS and a significantly higher response in relative EEG SWA during the recovery night after WL and BL than after DL for both age groups. No significant differences were observed between the WL and BL condition for these two particular SWS and SWA measures. Subjective sleepiness ratings during the 40-h SD were significantly reduced under both WL and BL compared to DL, but were not significantly associated with markers of sleep homeostasis in both age groups. Our data indicate that not only the duration of prior wakefulness, but also the experienced illuminance during wakefulness affects homeostatic sleep regulation in humans. Thus, working extended hours under low illuminance may negatively impact subsequent sleep intensity in humans.

Aims/hypothesis: In our modern society, artificial light is available around the clock and most people expose themselves to electrical light and light-emissive screens during the dark period of the natural light/dark cycle. Such suboptimal lighting conditions have been associated with adverse metabolic effects, and redesigning indoor lighting conditions to mimic the natural light/dark cycle more closely holds promise to improve metabolic health. Our objective was to compare metabolic responses to lighting conditions that resemble the natural light/dark cycle in contrast to suboptimal lighting in individuals at risk of developing metabolic diseases. Methods: Therefore, we here performed a non-blinded, randomised, controlled, crossover trial in which overweight insulin-resistant volunteers (n = 14) were exposed to two 40 h laboratory sessions with different 24 h lighting protocols while staying in a metabolic chamber under real-life conditions. In the Bright day–Dim evening condition, volunteers were exposed to electric bright light (~1250 lx) during the daytime (08:00–18:00 h) and to dim light (~5 lx) during the evening (18:00–23:00 h). Vice versa, in the Dim day–Bright evening condition, volunteers were exposed to dim light during the daytime and bright light during the evening. Randomisation and allocation to light conditions were carried out by sequential numbering. During both lighting protocols, we performed 24 h indirect calorimetry, and continuous core body and skin temperature measurements, and took frequent blood samples. The primary outcome was plasma glucose focusing on the pre- and postprandial periods of the intervention. Results: Spending the day in bright light resulted in a greater increase in postprandial triacylglycerol levels following breakfast, but lower glucose levels preceding the dinner meal at 18:00 h, compared with dim light (5.0 ± 0.2 vs 5.2 ± 0.2 mmol/l, n = 13, p=0.02). Dim day–Bright evening reduced the increase in postprandial glucose after dinner compared with Bright day–Dim evening (incremental AUC: 307 ± 55 vs 394 ± 66 mmol/l × min, n = 13, p=0.009). After the Bright day–Dim evening condition the sleeping metabolic rate was identical compared with the baseline night, whereas it dropped after Dim day–Bright evening. Melatonin secretion in the evening was strongly suppressed for Dim day–Bright evening but not for Bright day–Dim evening. Distal skin temperature for Bright day–Dim evening was lower at 18:00 h (28.8 ± 0.3°C vs 29.9 ± 0.4°C, n = 13, p=0.039) and higher at 23:00 h compared with Dim day–Bright evening (30.1 ± 0.3°C vs 28.8 ± 0.3°C, n = 13, p=0.006). Fasting and postprandial plasma insulin levels and the respiratory exchange ratio were not different between the two lighting protocols at any time. Conclusions/interpretation: Together, these findings suggest that the indoor light environment modulates postprandial substrate handling, energy expenditure and thermoregulation of insulin-resistant volunteers in a time-of-day-dependent manner. Trial registration: ClinicalTrials.gov NCT03829982. Funding: We acknowledge the financial support from the Netherlands Cardiovascular Research Initiative: an initiative with support from the Dutch Heart Foundation (CVON2014–02 ENERGISE). Graphical