Kruithof Revisited

A Human-Centric Perspective

Ian Ashdown, P. Eng., FIES

Chief Scientist, Lighting Analysts Inc.

[ Please send comments to allthingslighting@gmail.com ]

Related Posts

The Kruithof Curve

A previous blog article – The Kruithof Curve: A Pleasing Solution – examined the history of the Kruithof curve (Kruithof 1941]) shown in FIG. 1:

Kruithof Revisited - FIG 1

FIG. 1 – Kruithof curve, modern version (source: Wikipedia).

To summarize the article, “The Kruithof curve itself was thoroughly debunked a quarter-century ago with three exhaustive studies involving up to 400 participants (as opposed to two people in Kruithof’s study, including himself).” These studies were Bodman (1967), Boyce and Cuttle (1990), and Davis et al. (1990).

In other words, the weight of scientific evidence is firmly against use of the Kruithof curve as a guide to modern lighting design practices. Case closed, yes?

No.

The problem with the above studies – and indeed any studies to date that have addressed our preferences regarding correlated color temperature (CCT) versus illuminance – is that they were based on constant CCT light sources.

This is completely understandable in that while we have had dynamic color-changing luminaires for over a decade (e.g., Ashdown 2006), color-changing luminaires for general illumination purposes have only become available in the past year or so. However, it begs the question: is there a relationship between CCT preferences and circadian rhythms?

Circadian Rhythms

Another blog article – Entraining Circadian Rhythms: Intensity versus Color – examined the question of whether the change in yellow-blue color ratio during twilight is more efficient in entraining circadian rhythms than changes in daylight intensity.

As noted in this article, the research (Walmsley et al. 2015) considered the behavior of wild mice rather than humans. The problem, of course, is that humans and mice see the world very differently in terms of perceived color. Whereas our retinal cones are responsive to the visible spectrum ranging from approximately 400 nm (violet) to 700 nm (deep red), those of wild mice are responsive to a spectrum ranging from below 330 nm (ultraviolet UVB) to 625 nm (medium red). Being dichromatic, mice are also likely to have poor color-distinguishing capabilities compared to humans.

Kruithof Revisited - FIG. 2

Figure 2 – Wild mouse spectral responsivity. Source: Walmsley et al. (2015).

Regardless, Walmsley et al. make a compelling argument that the ratio of yellow-to-blue light remains reasonably constant throughout the day, whereas the intensity of daylight may vary randomly and markedly due to cloud cover. From an evolutionary perspective, it therefore makes sense that human circadian rhythms are primarily entrained by changes in daylight color at dawn and dusk rather than changes in illuminance.

We must also remember, however, that illuminance and color are not the only factors influencing our circadian rhythms. Yetish et al. (2015) studied the sleep patterns of three pre-industrial societies: the Hadza in Tanzania, the Kalahari San in Namibia, and the Tsimane in Bolivia. What they found was that all three groups exhibited similar sleep patterns. With no cross-cultural influences, it is reasonable to assume that these represent core human sleep patterns for pre-industrial Homo sapiens.

Kruithof Revisited - FIG. 4

FIG. 3 – Light versus activity plots (Yetish et al., 2015)

The patterns are interesting. The hunter-gatherer/horticulturalists sleep on average 6.4 hours a day, with one more hour in winter than in summer. Most surprising, they fall asleep about 3.3 hours after sunset, during the nightly period of falling temperature. Further, they usually awaken before sunrise, when the daily temperature is lowest.

From a lighting perspective, it is equally interesting that light exposure was maximal in the morning and greatly decreased at noon, with all three groups seeking shade (FIG. 2). This is likely attributable to all three groups living in the tropics, but it has the effect of providing maximal light activation of the suprachiasmatic nucleus (SCN) and its influence on circadian rhythms in the morning.

From this, the authors surmise that the daily cycle of temperature change, “largely removed from modern sleep environments,” may be more important than daily changes in illumination in regulating sleep patterns. With near-constant temperatures in our offices and residences (and presumably sleep laboratories), temperature changes become yet another variable in establishing a baseline for circadian rhythm disruption studies.

Illuminance, color, ambient temperature … could it get any more complicated? Yes, of course! A paper published just today in Cell Metabolism (Breton et al. 2015) has shown that our appetites for food are controlled not only by our brains, but by intestinal bacteria telling us via proteins they produce that they are sated, and that we should stop eating on their behalf. Designing experiments to elucidate circadian rhythm behavior therefore involves much more than simply dimming the lights. When and what the test subjects eat or drink is a critical factor in designing repeatable and relevant circadian rhythm experiments.

Kruithof Revisited - FIG. 4

FIG. 4 – Intestinal bacteria signaling pathway (Source: Breton et al., 2015)

So what does this say about the Kruithof curve?

Circadian Kruithof

The problem with ascertaining preferences of any kind is that experiments need to be designed to control all the factors that may be involved. In doing so, the resultant laboratory conditions are often far removed from the real world.

This is precisely the problem with the Kruithof curve studies such as Bodman (1967), Boyce and Cuttle (1990), Davis et al. (1990), and others – they all (necessarily at the time) relied on constant CCT light sources, and ignored the test subjects’ circadian rhythm states.

Surprisingly, a review of the academic literature on this topic reveals … almost nothing. The closest relevant discussion is Poldma (2009), in which the author merely proposes “integrating [static] color and light theories with new contexts of dynamic, integrated human experiences of color and light in interior spaces.” Ellis et al. (2013a, 2013b) considers luminaire color temperature, but only in the context of matching daylight CCT for elderly patients with dementia.

The evidence of Walmsley et al. (2015) suggests that our preferences for CCT versus illuminance may be intimately associated with the state of our circadian rhythms. The popularity of products such as the Philips Wake-Up Lights with their simulated sunrise colors would certainly indicate that this is the case.

Kruithof Revisited - FIG. 5

FIG. 5 – Philips HF3510/60 Wake-up Light

There are of course many other examples, including “romantic mood” lighting in restaurants and CCT preferences for outdoor street and area lighting in residential areas. Our CCT preferences may vary throughout the day based on the state of our circadian rhythms and our activities.

At the end of the day, the modern interpretation of the Kruithof curve as shown in FIG. 1 remains “thoroughly debunked.” (The original curve presented by Kruithof in 1941 addressed a different issue.) However, it provides a framework for further research focused on human-centric lighting and circadian rhythms.

The problem, of course, lies in how to design an experiment that quantifies these preferences. It may be that the problem is intractable, at least in a laboratory setting. Perhaps the best answers will come from crowdsourced experiments – give millions of people the ability to change the luminaire CCTs in their environments and see what they prefer.

Today, this is mostly a theoretical approach. However, with the expected deployment of pervasive Internet-of-Things device in every luminaire over the coming few years, the necessary data will become available. Such an experiment may then be as simple as writing an appropriate search string for Google Analytics to process.

References

Ashdown, I. 2006. “Changing White Light,” LD+A 36(12):45-48 (December).

Bodman, H. W. 1967. “Quality of Interior Lighting Based on Luminance,” Transactions of the Illuminating Engineering Society of Great Britain 32(1):22.

Boyce, P. R., and C. Cuttle. 1990. “Effect of Correlated Colour Temperature on the Perception of Interiors and Colour Discrimination,” Lighting Research and Technology 22(1):19-36. (DOI: http://dx.doi.org/10.1177/096032719002200102)

Breton, J., et al. 2015. “Gut Commensal E. coli Proteins Activate Host Satiety Pathways following Nutrient-Induced Bacterial Growth,” Cell Metabolism (in press). (DOI: http://dx.doi.org/10.1016/j.cmet.2015.10.017)

Davis, R. G., and D. N. Ginthner. 1990. “Correlated Color Temperature, Illuminance Level, and the Kruithof Curve,” Journal of the Illuminating Engineering Society 19(1):27-38. (DOI: http://dx.doi.org/10.1080/00994480.1990.10747937)

Ellis, E. V., et al. 2013a. “Auto-tuning Daylight with LEDs: Sustainable Lighting for Health and Well-being,” Proc. ARCC 2013, pp. 465-473.

Ellis, E. V., et al. 2013b. “Chronobioengineering Indoor Lighting to Enhance Facilities for Ageing and Alzheimer’s Disorder,” Intelligent Buildings International Vol. 5 Supplement 1. (DOI: http://www.dx.doi.org/10.1080/17508975.2013.807764)

Kruithof, A. A. 1941. “Tubular Luminescence Lamps for General Illumination,” Philips Technical Review Vol. VI, No. 3, pp. 65-73.

Poldma, T. 2009. “Learning the Dynamic Processes of Color and Light in Interior Design,” Journal of Interior Design 34(2):19-33. (DOI: http://dx.doi.org/10.1111/j.1939-1668.2008.01017.x)

Walmsley, L., L. Hanna, J. Mouland, F. Martial, A. West, A. R. Smedley, D. A. Bechtold, A. R. Webb, R. L. Lucas, and T. M. Brown. 2015. “Colour as a Signal for Entraining the Mammalian Circadian Clock,” PLOS Biology, April 17. (DOI: http://dx.doi.org/10.1371/journal.pbio.1002127)

Yetish, G., et al. 2015. “Natural Sleep and Its Seasonal Variations in Three Pre-industrial Societies,” Current Biology 25:1-7. (DOI: http://dx.doi.org/10.1016/j.cub.2015.09.046)

Seeing Ultraviolet

Keeping Time with Neuropsin

Ian Ashdown, P. Eng., FIES

Chief Scientist, Lighting Analysts Inc.

[ Please send comments to allthingslighting@gmail.com ]

UPDATE 15/11/08 – The following text briefly notes that some people can see near-ultraviolet radiation following cataract surgery due to the UV transmittance of their artificial intraocular lens. An example of this is reported in considerable detail here.

What does it mean to “see?” The word is ubiquitous in the English language, with dozens of different meanings. However, according to the Oxford English Dictionary, the most common definition is to “perceive with the eyes.” It is so common, in fact, that it ranks as one of the thousand most frequently used words in English.

“I see,” said the blind man, “what you mean.”

What we see are photons with varying wavelengths. Our eyes are most sensitive to photons with a wavelength of 555 nm, which we perceive as yellow-green. This sensitivity decreases towards ends of the visible spectrum, as shown by the CIE 1931 luminous efficiency function (FIG. 1). For all practical purposes, we cannot see photons with wavelengths shorter than 400 nm (deep violet) or longer than 700 nm (deep red). We are in particular blind to ultraviolet radiation (photons with wavelengths ranging from 100 nm to 400 nm) … or are we?

Seeing Ultraviolet - FIG. 1

FIG. 1 – CIE 1931 luminous efficiency function V(λ).

Ultraviolet Radiation

The CIE Lighting Vocabulary classifies ultraviolet radiation as follows:

Name Wavelength Range
UV-A 315 nm to 400 nm
UV-B 280 nm to 315 nm
UV-C 100 nm to 280 nm

Ultraviolet radiation offers both benefits and dangers to human health. UV-B radiation, for example, induces the production of vitamin D in exposed skin. This essential vitamin helps regulate bone health, and debatably provides other health benefits. Both UV-B and UV-A radiation promote the formation of melanin in the skin, which in addition to causing the skin to visibly tan, protects the skin cells from UV-B radiation damage.

The dangers of ultraviolet radiation include skin damage (sunburn and possible skin cancer through both direct and indirect DNA damage), and eye damage. Short-term exposure to UV-C (present in welders’ electric arcs) and UV-B (present in direct sunlight) can cause photokeratitis (“snow blindness” – basically sunburnt cornea), while long-term cumulative exposure can lead to the formation of cataracts in the lens of the eye and other eye diseases.

Given these dangers, it should come as no surprise that we cannot see ultraviolet radiation. The lens of the human eye is opaque to UV-A radiation, while the cornea blocks UV-B and UV-C radiation (FIG. 2). (Cataract removal operations involve the replacement of the lens with an artificial intraocular lens. These lenses were originally made from molded PMMA plastic, which were transparent to UV-A radiation. As a result, some patients could subsequently perceive ultraviolet radiation.)

Seeing Ultraviolet - FIG. 2FIG. 2 – Human eye. Source: Wikipedia.

We may not be able to see ultraviolet radiation, but other animals certainly can. Wild mice, for example, can see both UV-A and UV-B radiation (Kojima 2011). Other animals include birds, reptiles, fish, insects, and crustaceans, which use their ultraviolet vision for identifying food, sex recognition, and celestial navigation. Many nocturnal insects, for example, navigate by the ultraviolet emissions of celestial objects, and so are disoriented by and attracted to ultraviolet “bug zapper” traps.

Humans, on the other hand, are diurnal animals. Being active in the daytime under the tropical sun, it makes sense that our eyes evolved to protect the retina from ultraviolet radiation damage, notwithstanding the potential advantages of being able to see ultraviolet identification patterns on food sources. Ergo, we cannot see ultraviolet radiation … or can we?

Opsins

We know that our eyes perceive more than just visual images projected onto the rods and cones of the retina. In addition to an estimated 4.5 million cone cells and 90 million rod cells (Curcio et al. 1990), there are also some 3,000 intrinsically photosensitive retinal ganglion cells (ipRGCs) in the retina (Dacey et al. 2005). The high density of cones and rods is necessary to form visual images; the ipRGCs need only detect light.

Lighting designers familiar with circadian-based lighting (e.g., Roos 2015) will recognize ipRGCs. These cells contain melanopsin, which is most sensitive to cyan light with a peak at 490 nm. Upon activation, the cells send electrical signals to the suprachiasmatic nucleus (SCN), a tiny region of some 20,000 cells located in the hypothalamus of the brain. The SCN is the master clock which controls our circadian rhythms.

Melanopsin (OPN4) is but one of a thousand or so known opsins, a group of light-sensitive proteins that occur in prokaryotes (single-celled organisms), some algae, and all animals (Terakita 2005, Shichida et al. 2009). Of particular interest are the “vertebrate visual opsins” that occur in human retinas:

Name Peak sensitivity Photo-receptor
Rh1 (rhodopsin) 510 nm Rod
OPN1SW (“blue opsin”) 440 nm Cone
OPN1MW (“green opsin”) 545 nm Cone
OPN1LW (“red opsin”) 570 nm Cone
OPN4 (melanopsin) 490 nm ipRGC

Rhodopsin provides us with scotopic vision, while the three “cone opsins” provide us with photopic color vision.

There are also other opsins in the human body, including OPN3 (encephalopsin), which is found mostly in the brain (Blackshaw et al. 1999), and OPN5 (neuropsin), which is found in the neural tissues of both humans and mice (Tarttelin et al. 2003, Kojima et al. 2011). Being photosensitive, their functions have been hypothesized to be related to the entrainment of our circadian and/or seasonal clocks in some manner, but the mechanisms are unknown.

Seeing Ultraviolet - FIG. 3FIG. 3 – Photosensitive opsins in the human retina. Source: Kojima et al. 2011.

Neuropsin is mostly sensitive to UV-A radiation, with peak sensitivity at 380 nm. When it absorbs ultraviolet photons, it converts into a blue-absorbing photoproduct with maximum absorption at 470 nm, which is stable in the dark. Orange illumination then converts it back into its ultraviolet-absorbing state (Kojima et al. 2011). It is present (“expressed”) in the retinal neurons of mice, which makes sense – they can see ultraviolet radiation (FIG. 4). However, it has also been found to be present in the cornea of the mouse eye, and presumably is also present in the cornea of the human eye (Buhr et al. 2015). What is it doing there?

Seeing Ultraviolet - FIG. 4FIG. 4 – Photosensitive opsins in the mouse retina. Source: Kojima et al. 2011.

(It should be noted that mouse and human opsins are not chemically identical, but rather are orthologs that evolved from common ancestors (Terakita 2005). Human blue opsin and mouse UV opsin, for example, evolved from a common ancestor but have different spectral responses. For neuropsin, however, it is assumed that they are biologically equivalent.)

Cellular Clocks

When we refer to the “circadian clock” in our bodies, we must remember that it is not a single mechanism located somewhere in our brain, but a holistic component of our entire body (Albrecht 2012). We have literally trillions of cells in our bodies, each of which (with a few rare exceptions) has a cellular clock to determine when to use energy, when to rest, when to repair or replicate DNA, and so on. This all happens on the molecular level of proteins and gene expression, with the SCN serving as the master timekeeper for the body, in part by instructing the pineal gland to secrete the hormone melatonin while we are sleeping.

The retina of the human eye has its own local circadian clock that is not synchronized with signals from the SCN (Storch et al. 2007). One of the more curious functions of this clock is to control the electrical coupling between the rods and cones (Ribelayga et al. 2008). Our rods are sensitive to dim light, while our cones are sensitive to bright light, giving us scotopic and photopic vision respectively. During the day, the electrical coupling between adjacent rods and cones is weak, which means that they operate independently in forming visual images. At night, however, the electrical coupling becomes remarkably robust. As a result, the cone circuitry is able to receive signals from the rods under low light-level conditions; this presumably facilitates the detection of large dim objects at night.

How the retinal circadian clock was entrained by the day-night cycle remained unknown until recently, when it was shown that entrainment was due to the presence of neuropsin in the mammalian retina and cornea (Buhr et al. 2015). Surprisingly, none of the other retinal opsins appear to be involved.

Kojima et al. (2011) noted that even if neuropsin is present in the human retina, there does not appear to be sufficient retinal irradiance to activate it. Our lenses are basically opaque to ultraviolet radiation, and even our sensitivity to violet light drops significantly as we age and our lenses turn progressively yellow (Fig. 5).

Seeing Ultraviolet - FIG. 5Figure 5 – Human eye lens spectral transmittance. Source: Turner et al. 2008.

(As noted by Turner et al. (2008), ipRGCs play a vital role in human physiology and health. As the lens transmittance in the blue and violet region of the visible spectrum decreases with age, we become increasingly susceptible to insomnia, depression, cognitive decline, and numerous systemic disorders due to the lack of circadian rhythm entrainment.)

These results notwithstanding, Buhr et al. (2015) reported that a breed of laboratory mice lacking rods, cones, and ipRGCs were still able to synchronize their retinal circadian rhythms to light/dark cycles, presumably by means of neuropsin in their retinas. Conducting their experiments ex vivo with fresh and cultured tissues, they conclusively demonstrated that OPN1SW (blue opsin) and OPN3 (encephalopsin) were not involved.

What they did not discuss is that Kojima et al. (2011) identified the epidermal and muscle cells of the outer ears as major sites of neuropsin expression in mice. Given that mouse ears typically have few hairs on their surfaces, it was hypothesized that the outer ears may perceive UV-A radiation (but it noted that further studies are required). Thus, while Buhr et al. (2015) demonstrated the role of ocular neuropsin in retinal circadian entrainment, it is not yet clear whether it is solely responsible for entrainment in vivo.

Contradicting Kojima et al. (2011), Buhr et al. (2015) surmised that even in humans with essentially UV-opaque lenses, there may be enough retinal irradiance in blue light to activate the retinal neuropsin when the eyes are exposed to full sunlight. This is possible but unlikely – it implies a presumably important biological function that relies on marginal signaling conditions. (Turner et al. 2008 note that the threshold for circadian rhythm entrainment via melanopsin appears to require daylight illuminance levels, especially for the elderly. The human lens and cornea, however, are mostly transparent to cyan light.)

The presence of neuropsin in the cornea is equally puzzling. Buhr et al. (2015) again surmised that it may involve an ocular (i.e., not just retinal) photoentrainment that is separate from SCN entrainment. However, the corneal cells which host this opsin are not as yet known, nor are the biochemical details of how it functions in vivo.

So what is neuropsin doing in the cornea? It is photosensitive, but then it is also found in the brain, where it has an unknown role. On the other hand, by being present in the human cornea, it is fully exposed to UV-A radiation. This suggests that it is involved in ocular photoentrainment.

Regardless of these unknowns, it is evident that the retinal circadian clock is dependent on neuropsin, and that it involves UV-A radiation rather than visible light. Ergo, we most likely perceive ultraviolet radiation.

Ultraviolet Radiation Requirements

From a human-centric lighting perspective then, this raises an interesting question: do we need exposure to ultraviolet radiation in order to maintain the health and nighttime performance of our eyes? Fluorescent lamps emit a small but significant amount of ultraviolet radiation, with eight hours of exposure at interior illumination levels roughly equivalent to one minute of direct sunlight exposure (NEMA 1999). However, LED lamps and modules emit no ultraviolet whatsoever. Whether this will affect, for example, long-term care patients who do not have daily access to sunlight or other near-ultraviolet radiation sources is an open question.

Yet another hypothesis – more research is required.

References

  1. Albrecht, U. 2012. “Timing to Perfection: The Biology of Central and Peripheral Circadian Clocks,” Neuron Review 74(2):246-260. (http://dx.doi.org/1016/j.neuron.2012.04.006)
  2. Blackshaw, S., et al. 1999. “Encephalopsin: A Novel Mammalian Extraretinal Opsin Discretely Localized in the Brain,” Journal of Neuroscience 19()10:3681-3690.
  3. Buhr, E. D., et al. 2015. “Neuropsin (OPN5)-mediated Photoentrainment of Local Circadian Oscillators in Mammalian Retina and Cornea,” Proceedings of the National Academy of Sciences (PNAS) Early Edition September 21. (http://dx.doi.org/10.1073/pnas.1516259112)
  4. Curcio, C. A., et al. 1990. “Human Photoreceptor Topography,” Journal of Comparative Neurology 292(4):497-523. (http://dx.doi.org/10.1002/cne.902920402)
  5. Dacey, D.M., et al. 2005. “Melanopsin-expressing Ganglion Cells in Primate Retina Signal Colour and Irradiance and Project to the LGN,” Nature 433:749–54. (http://dx.doi.org/10.1038/nature03387)
  6. Kojima, D., et al. 2011. “UV-Sensitive Photoreceptor Protein OPN5 in Humans and Mice,” PLoS ONE 6(10):e26388. (http://dx.doi.org/10.1371/journal.pone.0026388)
  7. 1999. Ultraviolet Radiation from Fluorescent Lamps, LSD 7-1999. Rosslyn, VA: National Electrical Manufacturers Association.
  8. Ribelayga, C., et al. 2008. “The Circadian Clock in the Retina Controls Rod-Cone Coupling,” Neuron 59:790-801. (http://dx.doi.org/10.1016/j.neuron.2008.07.017)
  9. Roos, S. 2015. “The Case for Circadian Correct Lighting,” LD+A 45(1):32-36.
  10. Shichida, Y., et al. 2009. “Evolution of Opsins and Phototransduction,” Philosophical Transactions of the Royal Society B 364:2881-2895. (http://dx.doi.org/10.1098/rstb.2009.0051)
  11. Storch, K.-F., et al. “Intrinsic Circadian Clock of the Mammalian Retina: Importance for Retinal Processing of Visual Information,” Cell 130:730-741. (http://dx.doi.org/10.1016/j.cell.2007.06.045)
  12. Tarttelin, E. E., et al. 2003. “Neuropsin (Opn5): A Novel Opsin Identified in Mammalian Neural Tissue,” FEBS Letters 554:410-416. (http://dx.doi.org/1016/S0014-5793(03)01212-2)
  13. Terakita, A. 2005. “The Opsins,” Genome Biology 6:213. (http://dx.doi.org/10.1186/gb-2005-6-3-213)
  14. Turner, P. L., and M. A. Mainster. 2008. “Circadian Photoreception: Ageing and the Eye’s Important Role in Systemic Health,” British Journal of Ophthalmology 92:1439-1444. (http://dx.doi.org/10.1136/bjo.2008.141747)

 

Entraining Circadian Rhythms

Intensity versus Color

Ian Ashdown, FIES

Chief Scientist, Lighting Analysts Inc.

January 21, 2015

[ Please send comments to allthingslighting@gmail.com ]

There is a fascinating research paper called “Colour as a Signal for Entraining the Mammalian Circadian Clock” that has just been published in the open access journal PLOS Biology (Walmsley et al. 2015). While it is an exceedingly technical paper, the basic premise is this: the change in yellow-blue color ratio during twilight may be more effective in entraining circadian rhythms (at least in mice) than changes in daylight intensity.

Why is this important to professional lighting designers? Well, the answer involves the current interest in circadian-based (or biologically-effective) lighting. Quoting a recent LD+A article called “The Case for Circadian Correct Lighting” (Roos 2015), lighting designers are advised to:

Expose normal populations to high-levels of blue-rich light near 460 nm in the morning through early afternoon, and eliminate these shorter wavelengths and reduce light levels in the late-afternoon. After 10 p.m., total darkness is ideal – or if this is not practical – very low levels of warmer red-rich light. Even an incandescent lamp can disrupt the circadian cycle if it is too bright.

The goal, of course, is to provide electric lighting that mimics the temporal changes in natural daylight that we as a mammalian species experienced on a daily and seasonal basis prior to the introduction of electric lighting. Roos’s advice – which is reasonably good – is based on numerous medical studies over the past decade or so concerning our circadian rhythms and their relation to light exposure.

The latest paper, however, demonstrates in no uncertain terms that our knowledge of circadian rhythms is incomplete. While it does not necessarily negate the above advice, it does bring to mind new questions and possible opportunities for lighting design.

Circadian Rhythms

To better understand this topic, we begin with circadian rhythms, which Wikipedia defines as “any biological process that displays an endogenous [i.e., self-sustained], entrainable oscillation of about 24 hours.” In humans, these daily rhythms include those shown in Figure 1.

Entraining Circadian Rhythms - Fig. 1

Figure 1 – Human circadian rhythms. Source: Wikipedia.

These rhythms are entrained (i.e., synchronized) by external cues called zeitgebers (“time-givers”), the most important being – as you might expect – changes in daylight. We become acutely aware of these rhythms when we suffer from jet lag. Specifically, the change in daylight schedule disrupts our circadian clock, leaving us physically exhausted and having difficulties sleeping.

From a clinical perspective, there are several ways of measuring circadian rhythms in human subjects. One way is to measure the core body temperature, but this involves placing a temperature sensor somewhat uncomfortably “where the sun don’t shine” in the subject’s body. Another more reliable method is to measure the concentration of the hormone melatonin in the subject’s blood or saliva (e.g., Benloucif et al. 2005). The disadvantage, of course, is that the subject is sleeping when melatonin is present in measurable quantities. In short, reliably measuring circadian rhythms in humans is not an easy task.

There are numerous studies that correlate the secretion of melatonin in the body with circadian rhythms (e.g., Revell et al. 2005). What is more interesting to lighting designers, however, is the relation between melatonin secretion and the human eye.

Retinal Ganglion Cells

In addition to the cones and rods that provide us with color and night-time vision respectively, the mammalian retina has intrinsically photosensitive retinal ganglion cells (ipRGCs) that play a major role in entraining our circadian rhythms (e.g., Zaidi et al. 2007). The relationship between ipRGCs and melatonin secretion has been extensively studied (e.g., Lucas et al. 2013). These cells are connected to a region deep in the brain called the suprachiasmatic nucleus (SCN). When the ipRGCs do not receive light for an hour or more, the SCN triggers the pineal gland within the brain to begin secreting melatonin, which in turn promotes sleep in humans.

Of particular interest to lighting designers is the spectral responsivity of the ipRGCs. Whereas our cones and rods have spectral responsivities defined by the V(l) and V’(l) functions for photopic and scotopic vision, ipRGCs have a different spectral responsivity, referred to as melanopic (FIG. 2).

Entraining Circadian Rhythms - Fig. 2

Figure 2 – Human spectral responsivity.

This has become the basis for today’s evolving recommended practices in circadian-based (aka “biologically-effective” in Europe) lighting. For example, DIN SPEC 67600, Biologically Effective Illumination – Design Guidelines (DIN 2013) bases its recommendations solely on melanopic illumination. Similarly, luminaire manufacturers are currently looking at ways of optimizing the spectral power distributions of their products to produce biologically-effective white light; that is, white light with an abundance of blue light centered on the melanopic peak wavelength (e.g., Roos 2015).

… but science is all about endlessly attempting to prove that everything we think we know is either wrong or incomplete.

Experimental Design and Bias

Designing biological experiments is intrinsically difficult. You begin by hypothesizing that some action x will result in some event y. You then design an experiment in an effort to determine the correlation between the action and the event. For example, you may want to administer a vaccine and see whether it protects human subjects from contracting some viral disease.

The difficulty comes in designing the experiment. You do not, for example, want to administer an Ebola vaccine to a group of subjects living in North America – the likelihood of their being exposed to the Ebola virus is essentially zero. The experimental design in this case would be clearly biased towards an extremely positive (but essentially meaningless) correlation.

Taking circadian rhythms as another example, one problem is that the variability of retinal illuminance due to daylight exposure is typically both high and unpredictable due to cloud cover. The solution to this problem is appealingly simple: ensure that the subjects are exposed to electric lighting whose intensity and spectral power distribution (or at least its correlated color temperature) can be tightly controlled. By eliminating uncontrolled variables such as daylight, the experiment becomes more predictable and, most important, repeatable.

This solution however introduces significant experimental bias. In particular, the researcher typically assumes that:

  1. ipRGCs are sensitive primarily to blue light;
  2. ipRGCs are solely responsible for melatonin suppression; and
  3. Melatonin secretion is an indicator of the circadian rhythm associated with sleep.

These assumptions are of course based on many previous experimental results. They are still however assumptions – what if they prove to be wrong or incomplete?

Intensity versus Color

In their paper “Colour as a Signal for Entraining the Mammalian Circadian Clock,” Walmsley et al. (2015) began with a markedly different hypothesis. Noting that the mammalian circadian clock must have evolved over hundreds of millions of years, they reasoned that it makes sense to begin with natural daylight as the zeitgeber. They therefore began by measuring the spectral power distribution of daylight from 280 to 700 nm over a period of 41 days (September through October) from a location in Manchester, UK. The data were then carefully averaged to obtain a typical day in terms of absolute spectral irradiance.

The results were surprising. As shown in Figure 3, the variation in twilight color (horizontal axis) over 41 days is much less than the variation in irradiance (vertical axis), a result the authors attribute to ozone absorption in the upper atmosphere when the sun is below the horizon (Hulbert 1953).

Entraining Circadian Rhythms - Fig. 3

Figure 3 – Daylight color versus irradiance variability. Source: Walmsley et al. (2015).

The key here was not to assume, for example, that ipRGCs influence melatonin production and so eliminate as many experimental variables as possible, but to recreate as natural a luminous environment as possible for the test subjects (which in their experiments were laboratory mice).

(As an aside, it should be noted that there is evidence that circadian rhythms are influenced by input from not only ipRGCs, but also the retinal rods and cones. The authors cite half a dozen papers that address this topic.)

Using this information, the authors designed a LED-based lighting system for their laboratory mice. Unlike humans with their red-, green-, and blue-sensitive cones (technically long-, medium-, and short-wavelength sensitivity, designated SWS, MWS, and LMS respectively), the retinal cones of wild mice are primarily sensitive to ultraviolet (UVS) and green (MWS) wavelengths (FIG. 4), as determined by the various photosensitive opsins found in these specialized cells.

Entraining Circadian Rhythms - Fig. 4

Figure 4 – Wild mouse spectral responsivity. Source: Walmsley et al. (2015).

Unfortunately, the green-sensitive (MWS opsin) cones overlap in sensitivity with the rod (scotopic) and ipRGC (melanopic) sensitivities, which complicate the issue of measuring circadian clock entrainment. The authors therefore used a transgenic breed of mice called OpnlmwR, in which the MWS opsin cones are replaced by human long-wavelength sensitive (LMS) cones. These mice basically see ultraviolet (365 nm peak) and amber-red light (564 nm peak) only, regions of the spectrum to which the rods and ipRGCs have little to no sensitivity (Walmsley 2015, Lucas 2014).

The authors therefore used 400 nm ultraviolet and 590 nm amber high-flux LEDs for one of their lighting systems. The advantage of course is that these wavelengths minimally excite the rods and ipRGCs that presumably contribute to circadian rhythm entrainment. They further used Cnga3-/- mice, which lack cones but have retinal rods and ipRGCs, to confirm that rods and ipRGCs were not being significantly influenced by the bicolor illumination. (They also used a separate system with 365 nm, 460 nm, and 600 nm LEDs for experiments with normal “wild” mice.)

Rather than measuring melatonin levels, the authors surgically implanted tiny temperature loggers in the mice to measure core body temperature as a biological marker for circadian rhythms. The mice were then exposed to temporal lighting conditions that recreated a summer’s day in Stockholm, Sweden, including twilight, over a period of two weeks. The northern latitude was chosen specifically to achieve a protracted period of twilight and so maximize its influence on circadian rhythm entrainment.

The rest of the experiment involved some rather gruesome details involving decapitation and sliced brains in order to measure responses of the SCN to amber and ultraviolet light. What the authors found was that the ratio of amber-to-ultraviolet light (which correspond to the yellow-blue light ratio in humans[1]) had a considerably greater effect on circadian rhythm entrainment than did the variation in absolute intensity of amber-plus-ultraviolet light with constant color ratio.

What is significant about this is that the ratio of yellow-to-blue light remains reasonably constant throughout the day, but changes drastically and consistently before sunrise and after sunset (FIG. 5) over a period of about 30 minutes (that is, twilight). Conversely, the intensity of daylight may vary randomly and markedly throughout the day due to cloud cover. From an evolutionary perspective, it therefore makes more sense for the mammalian circadian clock to have evolved to respond to color rather than intensity changes in daylight as its zeitgeber.

Entraining Circadian Rhythms - Fig. 5

Figure 5 – Yellow-blue daylight ratio. Source: Walmsley et al. (2015).

From an electrical engineering perspective, it also makes sense that the color change (which happens rapidly and predictably) would become an important zeitgeber. In terms of phase-locked loop design, a sudden but consistent periodic pulse is better for entrainment than a variable and noisy signal such as daylight intensity.

This is not to say of course that ipRGCs and rods do not also play a role in circadian rhythm entrainment – they do (e.g., Güler et al. 2008). Further studies will (as always) be required to tease out the relationship between cones, rods, and ipRGCs in this process.

Lighting Design Perspective

From a lighting designer’s perspective … well, the world of circadian-based lighting has become considerably more interesting. Until now, it has been assumed that circadian rhythms are driven by input from the ipRGCs alone, and that these in turn are excited by blue-green light centered on 490 nm. (Melanopsin has a peak sensitivity at 480 nm [e.g., Lucas et al. 2014], but the ipRGC response is skewed towards 490 nm by the spectral transmittance of the adult human cornea, which preferentially absorbs blue light.)

This paper shows that the science may be much more complicated. Its value as an academic study is that it demonstrates that under “natural” conditions involving daylight, blue-yellow color discrimination complements, and may even dominate intensity changes via ipRGCs in circadian rhythm entrainment.

At the same time, however, these natural conditions do not reflect the decidedly artificial conditions we subject ourselves to with electric lighting, particularly at night or at the end of a night shift. It has, for example, been established that several hours of exposure to high-CCT illumination from tablet computers can significantly disrupt our circadian rhythms (van der Lely et al. 2015).

It is also important to recognize that it is the change in yellow-blue color ratio that influences circadian rhythm entrainment in natural lighting conditions, not the color ratio itself. Studies using lighting with constant color temperature (e.g., Bellia et al. 2014), which found that different color temperatures have little effect on circadian stimulus, may be eliminating precisely those experimental variables that are of the most interest.

Without predicting the results of future studies, suppose that the dominant geitzeber for circadian rhythm entrainment is the change in yellow-blue color ratio of daylight rather than constant or even changing melanopic illuminance. If this proves to be true, then the current recommendations for circadian-based / biologically effective lighting may be in serious need of revision.

If this does prove to be true, however, it may simplify the lighting design requirements. It would, for example, be much easier to use color-tunable luminaires with programmable color temperatures that change to signal the beginning and end of the day, than it would be to ensure absolute levels of melanopic illuminance.

There are conflicting opinions about whether we know enough about the circadian system in humans to design biologically-effective lighting systems. The current paper will do nothing to resolve this debate, as it shows how little we really do know.

On the other hand, I prefer to take a positive approach. It is difficult to imagine a situation where any reasonable lighting system design can physically harm people. Given this, I have no problem with taking the “best available science” and designing lighting systems accordingly. Whatever recommendations we have will most likely involve programming of color-tunable luminaires with varying spectral power distributions and intensity on a daily cycle. The beauty of this is that as the science improves, the lighting systems will only require a software or driver firmware update.

In the meantime, more research is (as always) required.

References

Bellia, L., A. Pedace, and G. Narbato. 2014. “Indoor Artificial Lighting: Prediction of the Circadian Effects of Different Spectral Power Distributions,” Lighting Research and Technology 46(4):650-660.

Benloucif, S., M. J. Guico, K. J. Reid, L. F. Wolfe, M. L’hermite-Balériaux, and P. C. Zee. 2005. “Stability of Melatonin and Temperature as Circadian Phase Markers and their Relation to Sleep Times in Humans,” Journal of Biological Rhythms 20(2):178-188.

DIN. 2013. Biologically Effective Illumination – Design Guidelines, DIN SPEC 67600 (2013-04). Deutsches Berlin, Germany: Institut für Normung e.V.

Güler, A. D., J. L. Ecker, G. S. Lall, S. Haq, C. M. Altimus, H. W. Liao, A. R. Barnard, H. Cahill, T. C. Badea, H. Zhao, M. W. Hankins, D. M. Berson, R. J. Lucas, K. W. Yau, and S. Hattar. 2008. “Melanopsin Cells are the Principal Conduits for Rod-cone Input to Non-image-forming Vision,” Nature 453(7191):102-105.

Hulbert, E. O. 1953. “Explanation of the Brightness and Color of the Sky, Particularly the Twilight Sky,” Journal of the Optical Society of America 43(2):113–118.

Lucas, R. J., S. N. Peirson, D. N. Berson, T. M. Brown, H. M. Cooper, C. A. Czeisler, M. G. Figueior, P. D. Gamlin, S. W. Lockley, J. B. O’Hagan, L. L. A. Price, I. Provencio, D. J. Skene, and G. C. Brainard. 2013. “Measuring and Using Light in the Melanopsin Age,” Trends in Neuroscience 37(1):1-9.

Revell, V. L. H. J. Burgess, C. J. Gazda, M. R. Smith, L. F. Fogg, and C. I. Eastman. 2005. “Advancing Human Circadian Rhythms with Afternoon Melatonin and Morning Intermittent Bright Light,” Journal of Clinical Endocrinology & Metabolism 91(1):54-59.

Roos, S. 2015. “The Case for Circadian Correct Lighting,” LD+A 45(1):32-36.

van der Lely, S., S. Frey, C. Garbazza. A. Wirz-Justice, O. G. Genni, R. Steiner, S. Wolf, C. Cajochen, V. Bromundt, and C. Schmidt. 2015. “Blue Blocker Glasses as a Countermeasure for Alerting Effects of Evening Light-Emitting Diode Screen Exposure in Male Teenagers,” Journal of Adolescent Health 56(1):113-119.

Walmsley, L., L. Hanna, J. Mouland, F. Martial, A. West, A. R. Smedley, D. A. Bechtold, A. R. Webb, R. L. Lucas, and T. M. Brown. 2015. “Colour as a Signal for Entraining the Mammalian Circadian Clock,” PLOS Biology, April 17.

Zaidi, F. H., J. T. Hull, S. N. Peirson, K. Wulff, D. Aeschbach, J. J. Gooley, G. C. Brainard, K. Gregory-Evans, J. F. Rizzo, C. A. Czeisler, R. G. Foster, M. J. Moseley, and S. W. Lockley. 2007. “Short-wavelength Light Sensitivity of Circadian, Pupillary, and Visual Awareness in Humans Lacking an Outer Retina,” Current Biology 17(24): 2122-2128.

[1] In humans, our neural circuitry combines the signals received from the short-wavelength sensitive (SMS) cones with the combined signals from the medium-wavelength sensitive (MWS) and long-wavelength sensitive (LWS) cones to generate blue-yellow discrimination. This opponent color theory posits that our color vision consists of blue-versus-yellow, red-versus-green, and black-versus-white channels that our brains further process. Given evolution’s penchant for recycling good ideas, it may be that the blue-versus-yellow signal also contributes to circadian rhythm entrainment. The authors speculate that this may even have been the original evolutionary purpose of color vision.

Blue Light Hazard … or Not?

Argumentum ab Auctoritate

Ian Ashdown, P. Eng., FIES

Chief Scientist, Lighting Analysts Inc.

[ Please send comments to allthingslighting@gmail.com. ]

As a professional lighting designer, you will likely have read about the “blue light hazard” associated with white light-emitting diodes. You will have seen warnings like this (Willmorth 2014a):

“… long term exposure to blue light at 441nm caused lesions on the retinas of rhesus monkeys.”

and recommendations like this from the same author:

“Use the lowest CCT LED color with the highest CRI available to suit the lighting application – including avoidance of high CCT (> 5000K), low CRI (<80) sources altogether, and eliminate use of blue-light rich products, such as those generating >5500K at <65CRI.”

and even this (Kitchel 2000):

“…all persons with vision problems should be removed from a light environment where the predominant light waves are a temperature above 3500K or a wavelength less than approximately 500 nm.”

It is a confusing situation for lighting designers, as there are well-documented vision and health benefits to the use of high-CCT lighting. These benefits include circadian rhythm entrainment (e.g., Holzman 2010) and improved visibility (e.g., Berman et al. 2006). Taken together, the recommendations are at best contradictory.

As always, “… there is a need for more focused research leading to practical recommendations on this subject” (Willmorth 2014a). In the meantime however, lighting designers need to make informed decisions on behalf of their clients. What to do?

There is no short answer. As this article demonstrates, the issue of blue light causing retinal lesions is based on a misunderstanding of vision research work done in the 1970s. It is still an open question as to whether long-term chronic exposure to blue light may cause vision problems, but the evidence to date (known to this author at least) is not persuasive. [Update 14/11/08 – see concluding paragraphs and SCENIHR (2012).]

[UPDATE 14/12/11 – See revised concluding paragraphs and GLA 2012.]

The recommendation above – “Use the lowest CCT LED color with the highest CRI available to suit the lighting application” – also highlights the danger to journalists when combining reviews of the academic literature with design recommendations. While it could be construed from the article that this recommendation is based on concerns about vision problems, it is instead advice that the author would communicate to any client (Willmorth 2014b), regardless of the academic literature.

To be perfectly clear, this article is in no way meant as a criticism of Willmorth (2014a). It is instead an exploration of how scientific research can be misinterpreted and then promulgated in good faith as scientific fact. It is a problem that all science journalists face, myself included.

More to the point however, this article attempts to clarify some of the issues concerning the “blue light hazard.” As lighting designers, it is important to realize that direct viewing of extremely high-brightness LEDs may cause eye damage. At the same time, it is important to understand that these concerns are distinct from everyday interior lighting design practices.

Background

Lighting Research Center researcher John Bullough published “The Blue-Light Hazard: A Review” in the Journal of the Illuminating Engineering Society (Bullough 2000), in which he summarized the research on the role of short-wavelength (i.e. deep blue) light and ultraviolet radiation in retinal damage. Quoting from this paper:

“For practical purposes with ‘white’ light sources, any condition resulting in direct exposure to luminances under 10,000 cd/m2 is unlikely to present a risk of photochemical injury to the retina. For such sources, calculation of the blue light hazard is not necessary.”

Putting this into context:

“… might lead one to believe [that] fluorescent lamps present greater risk than incandescent lamps, because they produce a greater portion of their light in the short-range portion of the visible spectrum. However, because fluorescent lamps also have low luminances (T12 lamps: 8,000 cd/m2; T8 lamps: 11,000 cd/m2; T5 lamps: 20,000 cd/m2), their potential risk for photochemical injury is negligible …”

Bullough examined potential risks in the context of medical equipment, industrial equipment, and high-flux theatrical lighting. In terms of extremely high-brightness LEDs, there is clearly a risk in viewing them directly. People with aphakia (absence of the lens of the eye, often due to surgical removal) may also be at risk. In general however, there is no blue light hazard for interior lighting applications.

Trust in Authority

So where did the current “blue light hazard” meme originate? Willmorth (2014a) notwithstanding, why are lighting designers now being advised to avoid high-CCT lighting wherever and whenever possible?

The underlying problem is that lighting designers cannot be expected to follow the medical literature on which these recommendations may be based. How many people for example outside of the medical profession read such journals as Epidemiology and Biostatistics or Investigative Ophthamology & Visual Science? (How many people can even spell “ophthalmology” correctly, for that matter?)

The solution is beguilingly simple: trust in those who are experts in such matters. Lighting designers read trade journals such as Lighting Design & Application and Architectural SSL because of these publications’ reputation for accurate and useful information. Their technical articles are after all either written by qualified experts, or by staff writers who consult them.

Who we trust however is subject to the logical fallacy of argumentum ab auctoritate, or “argument from authority” (including trust in those who, like me, quote Latin phrases). In more colloquial terms, “Just because you say it’s so don’t make it so!”

To illustrate this argument, consider the quotation above (Willmorth 2014a):

“… long term exposure to blue light at 441nm caused lesions on the retinas of rhesus monkeys.”

The article in question is titled, “The Dark Side of BLUE LIGHT,” which was written by Kevin Willmorth, Consulting Editor for Architectural SSL. Educated at the University of Phoenix, he has over 33 years of experience in lighting design and product development. Given this, there is no reason to question his authority per se. However, we need to ask where this worrisome statement came from.

Like most trade journals, Architectural SSL has an aversion to publishing full references in its technical articles. There are two likely reasons for this: 1) very few readers will be interested in reading the referenced papers; and 2) full references consume valuable advertising space. Regardless of the reasons, the author can do no more than identify the name of the researcher and possibly the paper’s title in the text of the article.

In other words, trust in authority.

Full References

Thankfully, Willmorth was fairly specific in referencing (in the same sentence) “The Effects of Blue Light on Ocular Health (Kitchel, E. American Printing House for the Blind.” (The more common alternative is to simply say, “According to …”) A simple Web search leads directly to http://www.cclvi.org/contributions/effects1.htm. It is an online article, but it was originally published in the Journal of Visual Impairment and Blindness (Kitchel 2000).

Elaine Kitchel is Low Vision Project Leader at the American Printing House for the Blind, with a Masters of Education from the University of Arizona. In her review article, she writes:

“In an early study conducted by Ham, Ruffolo, Mueller and Guerry, (1980) rhesus monkeys were exposed to high‑intensity blue light at 441nm for a duration of 1000 seconds. Two days later lesions were formed in the retinal pigmented epithelium (RPE.) These lesions consisted of an ‘inflammatory reaction accompanied with clumping of melanosomes and some macrophage invasion with engulfment of melanosomes which produce hypopigmentation of the RPE’ (Ham et al., 1980, p.1110).”

We now have a reference for the original quote, including a page number … or do we? Once again, the article does not include references, rather unhelpfully stating, “A bibliography is available separately.” Fourteen years after publication, it is unlikely that this unnamed document will still be available.

Trust in authority.

Monkey Business

Fortunately, it is possible with some effort to ascertain the proper reference. It is:

Ham, W. T., Jr., H. A. Mueller, J. J. Ruffolo Jr., and D. Guerry. 1980. “The Nature of Retinal Radiation Damage: Dependence on Wavelength, Power Level, and Exposure Time,” Vision Research 20(12):1105-1111.

William T. Ham and his fellow researchers were at the time associated with the Department of Biophysics, Virginia Commonwealth University (Richmond, VA). Vision Research being a highly respected peer-reviewed journal, their paper of course included copious references.

Trust in authority? Not quite … if you obtain and read the review paper, you will find no mention of “blue light at 441 nm” on page 1110. Here is what the authors wrote:

“Histological data, Ham et al., (1978), on the retina of the rhesus monkey demonstrate that short wavelength light plays a role in the clumping and phagocytosis of melanin. The appearance of a mild lesion in the RPE of the rhesus monkey at 90 days postexposure suggests a striking similarity to senile macular degeneration. In the opinion of the authors, long-term, chronic exposure to short wavelength light is a strong contributing factor to senile macular degeneration.”

This is an interesting observation that is apparently still valid – see for example Berman and Clear (2014) – but it is not what we are after.

In reading the full paper, there is an interesting figure caption on page 1107:Blue Light Hazard - FIG. 3Fig. 3 – Retinal response in the same eye as Fig. 2 at 2 days after a 1000 sec exposure to 441 nm light (10 nm bandpass). The image diameter at the retina was 1 mm, and the radiant exposure was 33 J/cm2. (Source: Ham et. al. 1980.)

This microphotograph of a rhesus monkey’s retina is from research reported by Ham et al. (1978), which was based on an earlier paper (Ham et al. 1976), both listed in the references. The arrows in the image indicate the observed lesions.

It helps to have some appreciation of the nature of this research. Ten rhesus monkeys were anesthetized and laser beams shone into their eyes in order to determine the damage threshold for various beam intensities and wavelengths. The primates were then later “sacrificed” and their eyes dissected to obtain the microphotographs showing possible radiation damage. This is clearly not the sort of research that can be conducted on human subjects.

In their paper, the authors reported the following radiation damage thresholds for a 441.6 nm helium-cadmium laser:

1 second 16 seconds 100 seconds 1000 seconds
0.91 watts / cm2 0.41 watts / cm2 0.20 watts / cm2 0.03 watts / cm2

(A joule is one watt-second, so 0.03 watts per square centimeter for 1,000 seconds is 30 joules/cm2, as indicated in Figure 3 above.)

In their 1978 paper, the authors replaced the laser beam with a 2,500-watt xenon lamp and a 6 nm bandwidth interference filter at 441 nm with associated optics to focus the beam onto a 1-mm diameter region of the monkey’s retina for up to 1,000 seconds. (Kids, don’t try this science experiment at home …)

Grim and disturbing details aside, we have finally answered the question – where did the information quoted by Kitchel and through her by Willmorth come from?

What we have not answered however is the question of whether this research is relevant to the “blue light hazard” issue.

Inadmissible Evidence

It is true that Ham et al. (1976, 1978) established that exposure to blue light can cause retinal lesions, however microscopic. However, maximum exposure times of 1,000 seconds (16 minutes) are hardly “long-term exposure” as described by Willmorth (2014). Simply put, the research of Ham et al. did not address the issue of long-term exposure to blue light.

Equally interesting is this quote: (Ham et al. 1976):

“… the solar retinal irradiance at 440 nm for a 20-nm spectral band is approximately 0.20 W/cm2 at midday for an eye gazing directly at the Sun at sea level for a 2-mm diameter pupil. In comparison, the threshold irradiance for a 100-sec exposure to the 441-nm laser line of He-Cd is 0.20 W/cm2. Thus, sungazing at bright midnoon for 100 sec can produce a threshold lesion … those subject to exposure to bright sunlight over long periods should take precautions to shield their eyes from the short wavelengths of solar radiation.”

In other words, what Ham et al. discovered through careful experiment was the glaringly obvious: do not stare at the noonday sun without blinking for longer than fifteen minutes. This is not mockery of their research – Ham et al. were investigating the distinction between thermal and photochemical effects of high-intensity light on the retina. Their comparison with sungazing, while instructive, was merely by way of analogy to put the beam intensity levels into context for the reader.

This is not to say that long-term chronic exposure to blue-rich light does not result in adverse health effects, including cataracts and age-related macular degeneration. Ham et al. did their work nearly forty years ago. There may well be more recent research that is relevant to the “blue light hazard,” such as for example Shang et al. (2014). (Whether this fundamentally flawed paper is applicable to human vision is a separate issue.)

Regardless, the research of Ham et al. is “inadmissible evidence” (to use the legal expression) with respect to the long-term effects of blue light exposure. It is not a question as to whether it is right or wrong, but simply that it does not apply.

The problem – the real problem – is that journalists are expected to interpret academic research for the general public. Like Willmorth and Kitchel, they may have considerable knowledge in their fields of expertise. Unfortunately, the “blue light hazard” issue intersects research fields in both lighting and medicine. As such, journalists need to take particular care in interpreting published papers on the topic. For whatever reason, there was some miscommunication in this case.

Conclusion

To summarize, there may possibly be persuasive evidence that long-term chronic exposure to blue-rich (i.e., high CCT) lighting may adversely affect our vision and health. Articles such as “The Dark Side of BLUE LIGHT” (Willmorth 2014a) and “The Effects of Blue Light on Ocular Health” (Kitchel 2000) have referred to the academic research literature (Ham et al. 1980) as evidence of danger. Unfortunately, all that this research proved in the context of the “blue light hazard” was the obvious: do not stare at the noonday sun without blinking for longer than fifteen minutes.

As Kevin Willmorth said, “… there is a need for more focused research leading to practical recommendations on this subject.” In the meantime however, this author at least is still looking for persuasive evidence that there is any significant blue light hazard associated with high-CCT LED lighting.

At the same time, I agree with Kevin when he says (Willmorth 2014b), “I cannot recommend [that] anyone apply poor-quality, low color performance light sources of any type when alternative are available” … but this is just our opinion. In the absence of evidence to the contrary, there does not appear to be any scientific reason to be concerned about blue-rich lighting in typical interior environments.

UPDATE – November 8, 2014

In 2010, the French Agency for Food, Environmental and Occupational Health & Safety (ANSES) published a 310-page report (in French) titled, “Health Effects of Lighting Systems Using Light-Emitting Diodes (LEDs)” (ANSES 2010), with an English-language opinion and summary (ANSES 2010b). Page 3 of the summary reads:

“Some scientific studies [Dawson et al., 2001, Ueda et al., 2009], based on laboratory experiments with blue LEDs conducted on monkeys, give reason to suspect a danger for the retina related to exposure to light-emitting diodes.”

Déjà vu, non?

The remainder of the summary offers recommendations that are reasonable in view of the photobiological risks of high-brightness LEDs. However, the risk of having the “reason to suspect” statement taken out of context in support of the “blue light hazard” meme remains.

Reading the referenced papers of course provides more information. Dawson et al. (2001) sacrificed five rhesus monkeys after exposing them to between 5 and 54 joules/cm2 of blue light from a 458 nm argon laser. Again, this is roughly equivalent to staring at the noonday sun without blinking for 3 to 25 minutes.

Ueda et al. (2009) sacrificed eight monkeys (two rhesus and six long-tailed macaque) after exposing them to between 20 and 60 joules/cm2 from Nichia NSPB550S blue LEDs with a dominant wavelength of 465 nm. Similar to the earlier studies of Hall et al. (1976), they reported retinal lesions after exposure to 35 joules/cm2, but no detectable results after exposure to 20 joules/cm2.

Blue Light Hazard - Macaque

Long-tailed macaque (photo credit: Lea Maimone)

There must be something apparently irresistible about such studies, as van Norren et al. (2011) provide a critical review of no fewer than 56 papers on the topic. What is interesting is that the results of eight such experiments (including Ham et al. 1976) yielded essentially the same results for rabbits and monkeys:

Blue Light Hazard - Norren

Dose for retinal damage versus wavelength. Source: Fig. 1(b), van Norren et al. (2011)

while the results for rodents (including both albino and pigmented rats) were equally similar. To summarize these results, do not stare at the noonday sun without blinking for longer than fifteen minutes. Once again, the evidence that long-term chronic exposure to blue-rich (i.e., high CCT) lighting may adversely affect our vision and health is not persuasive.

A much more interesting publication was recently published by the International Energy Agency (IEA 2014). Providing a wealth of information on the photobiological hazards of solid-state lighting, it concludes in Section 5.6.3, Potential Effects of Long-term Exposures, that:

“The ICNIRP exposure limit values do not take into account the possibility of an exposure over an entire lifetime. Very little is known about the effects of lifelong cumulated exposures to blue light emitted by LEDs. According to the Scientific Committee on Emerging and Newly Identified Health risks (SCENIHR) of the European Commission [SCENIHR 2012], no evidence was found indicating that blue light from artificial lighting belonging to Risk Group 0 would have any impact on the retina graver than that of sunlight. The SCENIHR states that IEC 62471 gives limits that are protective against acute effects, while longterm effects are only marginally considered and estimated to be of negligible or small risk.”

Following the paper trail to its end, we have (SCENIHR 2012):

“Evidence from in vitro experiments suggest that blue light at 10 W/m2 induces photochemical retinal damages (Class II) up on acute (hours) exposure, and animal experiments and in vitro studies suggest that cumulative blue light exposure below the levels causing acute effects also can induce photochemical retinal damage.

“There is no consistent evidence from epidemiological studies regarding the effect of long-term exposure to sunlight (specifically the blue component of sunlight) and photochemical damage to the retina (particularly to the retinal pigment epithelium), which may contribute to age-related macular degeneration (AMD) later in life. Whether exposure from artificial light could have effects related to AMD is uncertain.

“There is no evidence that artificial light from lamps belonging to RG0 or RG1 would cause any acute damage to the human eye. Studies dedicated to investigating whether retinal lesions can be induced by artificial light during normal lighting conditions are not available. Lamp types belonging to RG2 and higher are usually meant to be used by professionals in locations where they do not pose a risk. Chronic exposure to blue light from improperly used lamps could, in theory, induce photochemical retinal damage in certain circumstances. There is however no evidence that this constitutes a risk in practice. It is unlikely that chronic exposures to artificial light during normal lighting conditions could induce damage to the cornea, conjunctiva or lens.”

and finally from the abstract (ibid):

There is no evidence that blue light from artificial lighting belonging to Risk Group 0 (“exempt from risk”) would have any impact on the retina graver than that of sunlight. Blue light from improperly used lamps belonging to Risk Groups 1, 2, or 3 could, in theory, induce photochemical retinal. There is no evidence that this constitutes a risk in practice. Other damages to the eye from chronic artificial light exposure during normal lighting conditions are unlikely. Exposure to light at night (independent of lighting technology) while awake (e.g. shift work) may be associated with an increased risk of breast cancer and also cause sleep, gastrointestinal, mood and cardiovascular disorders.

In the end, we have no option but to appeal to authority (argumentum ab auctoritate). SCENIHR (2012) represents the opinions of a dozen medical professionals who are presumed experts in the field. The difference however is that they are specifically addressing the issue of “blue light hazard” with full knowledge (circa 2012) of existing lighting technologies. Their 118-page report includes a staggering 341 references to the academic literature.

[UPDATE 14/12/11: The Global Lighting Association, representing ten regional lighting industry associations from around the world, released a white paper in March 2012 with the abbreviated title “Optical Safety of LEDs.” There are two versions, one being a 22-page document with a detailed and in-depth analysis of the photobiological risks of common “white light” lamp types, and the other being a 4-page abridged document. Their well-documented position statement is simple: “… based on accepted and widely adopted safety standards for lamps, is that all general lighting sources, including LED and CFL sources (either lamps or systems) and luminaires, can be safely used by the consumer when used as intended.”]

There may be medical studies yet to be conducted that will demonstrate a blue light hazard for solid-state lighting in typical interior lighting applications. However, the absence of such evidence to date is highly persuasive: there is no scientific reason to be concerned about blue-rich lighting in typical interior environments.

References

ANSES. 2010a. Effets sanitaires des systèmes d’éclairage utilisant des diodes électroluminescentes (LED). Maisons-Alfort, France: French Agency for Food, Environmental and Occupational Health & Safety.

ANSES. 2010b. Opinion of the French Agency for Food, Environmental and Occupational Health & Safety in response to the internally-solicited request entitled “Health Effects of Lighting Systems Using Light-Emitting Diodes (LEDs).” Maisons-Alfort, France: French Agency for Food, Environmental and Occupational Health & Safety.

Berman, S., M. Navvab, M. J. Martin, and J. Sheedy. 2006. “A Comparison of Traditional and High Color Temperature Lighting on the Near Acuity of Elementary School Children,” Lighting Research & Technology 38(1):41-52.

Berman, S., and R. Clear. 2013. “Another Blue Light Hazard?,” Lighting Design & Application 43(3):65-68.

Bullough, J. D. 2000. “The Blue-Light Hazard: A Review,” Journal of the Illuminating Engineering Society 29(2):6-14.

Dawson, W., T. Nakanishi-Ueda, D. Armstrong, D. Reitze, D. Samuelson, M. Hope, S. Fukuda, M. Matsuishi, T. Ozawa, T. Ueda and R. Koide. 2001. “Local Fundus Response to Blue (LED and Laser) and Infrared (LED and Laser) Sources,” Experimental. Eye Research 73:137-147.

GLA. 2012. Optical and Photobiological Safety of LED, CFLs, and Other High Efficiency General Lighting Sources. Global Lighting Association.

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