Abstract: Artificial light at night can be harmful to the environment, and interferes with fauna and flora, star visibility, and human health. To estimate the relative impact of a lighting device, its radiant power, angular photometry and detailed spectral power distribution have to be considered. In this paper we focus on the spectral power distribution. While specific spectral characteristics can be considered harmful during the night, they can be considered advantageous during the day. As an example, while blue-rich Metal Halide lamps can be problematic for human health, star visibility and vegetation photosynthesis during the night, they can be highly appropriate during the day for plant growth and light therapy. In this paper we propose three new indices to characterize lamp spectra. These indices have been designed to allow a quick estimation of the potential impact of a lamp spectrum on melatonin suppression, photosynthesis, and star visibility. We used these new indices to compare various lighting technologies objectively. We also considered the transformation of such indices according to the propagation of light into the atmosphere as a function of distance to the observer. Among other results, we found that low pressure sodium, phosphor-converted amber light emitting diodes (LED) and LED 2700 K lamps filtered with the new Ledtech's Equilib filter showed a lower or equivalent potential impact on melatonin suppression and star visibility in comparison to high pressure sodium lamps. Low pressure sodium, LED 5000 K-filtered and LED 2700 K-filtered lamps had a lower impact on photosynthesis than did high pressure sodium lamps. Finally, we propose these indices as new standards for the lighting industry to be used in characterizing their lighting technologies. We hope that their use will favor the design of new environmentally and health-friendly lighting technologies.

Abstract: The endogenous circadian oscillator in mammals, situated in the suprachiasmatic nuclei, receives environmental photic input from specialized subsets of photoreceptive retinal ganglion cells. The human circadian pacemaker is exquisitely sensitive to ocular light exposure, even in some people who are otherwise totally blind. The magnitude of the resetting response to white light depends on the timing, intensity, duration, number and pattern of exposures. We report here that the circadian resetting response in humans, as measured by the pineal melatonin rhythm, is also wavelength dependent. Exposure to 6.5 h of monochromatic light at 460 nm induces a two-fold greater circadian phase delay than 6.5 h of 555 nm monochromatic light of equal photon density. Similarly, 460 nm monochromatic light causes twice the amount of melatonin suppression compared to 555 nm monochromatic light, and is dependent on the duration of exposure in addition to wavelength. These studies demonstrate that the peak of sensitivity of the human circadian pacemaker to light is blue-shifted relative to the three-cone visual photopic system, the sensitivity of which peaks at approximately 555 nm. Thus photopic lux, the standard unit of illuminance, is inappropriate when quantifying the photic drive required to reset the human circadian pacemaker.

Abstract: The effect of light on circadian rhythms and sleep is mediated by a multi-component photoreceptive system of rods, cones and melanopsin-expressing intrinsically photosensitive retinal ganglion cells. The intensity and spectral sensitivity characteristics of this system are to be fully determined. Whether the intensity and spectral composition of light exposure at home in the evening is such that it delays circadian rhythms and sleep also remains to be established. We monitored light exposure at home during 6-8wk and assessed light effects on sleep and circadian rhythms in the laboratory. Twenty-two women and men (23.1+/-4.7yr) participated in a six-way, cross-over design using polychromatic light conditions relevant to the light exposure at home, but with reduced, intermediate or enhanced efficacy with respect to the photopic and melanopsin systems. The evening rise of melatonin, sleepiness and EEG-assessed sleep onset varied significantly (P<0.01) across the light conditions, and these effects appeared to be largely mediated by the melanopsin, rather than the photopic system. Moreover, there were individual differences in the sensitivity to the disruptive effect of light on melatonin, which were robust against experimental manipulations (intra-class correlation=0.44). The data show that light at home in the evening affects circadian physiology and imply that the spectral composition of artificial light can be modified to minimize this disruptive effect on sleep and circadian rhythms. These findings have implications for our understanding of the contribution of artificial light exposure to sleep and circadian rhythm disorders such as delayed sleep phase disorder.