Previously I had suspected typically 200 hz CCFL dimming PWM flicker as source of eye strain but that has been ruled out as a cause since.

"Medical scientists have discovered that blue light is strongly absorbed in the retina tissues. This absorption, if at high energy levels like that found in welding, has the capability to ultimately cause ocular problems such as macular degeneration and retina damage."

"There is growing evidence implicating welding as a possible risk factor for uveal melanoma. The major culprit is high-energy blue light exposure" High energy blue light filtration: An evidence-based assessment www.eyeworld.org/ewsupplementarticle.php?id=295

 

I recently found information which seems to support a hypothesis of eye strain induced by poorly filtered spikes at very specific frequencies of blue light - this would also explain why computer safety glasses that are orange tinted are said to help with computer display induced eye strain - they reduce or filter this blue out a great deal.

http://www.recoveredscience.com/Babyblindinglights01.htm

ROP = retinopathy of prematurity

"Each year, thousands of premature babies in intensive care nurseries lose their sight to ROP. This blinding began with the introduction of fluorescent lamps. Industrial safety researchers have determined the wavelengths where the retina is most vulnerable to blue-light damage. The most intense energy spike in the spectrum of the fluorescent lamp shines precisely into that vulnerability window. Typical nursery lighting exposes the preemie in 15 minutes or less to the US industrial safety regulations' danger-limit dose of retinal irradiation for adults. Preemies have none of the adults' protections against damaging light.
Light hitting a preemie's still migrating retinal cells can garble the cells' migrating instructions and make them stick to other cells. Under the electron microscope, retinae damaged by light and by ROP show the same abnormal adhesions between cells."

"The first babies to develop ROP were born in 1940. ROP had never been observed before and could not be traced in retrospective studies of older blind people. Its sudden appearance coincided with the appearance of fluorescent lamps which had been introduced commercially at the New York World Fair in 1938/39."
"Like the lamps, ROP long remained unknown anywhere else until 1948/49, when fluorescent lamps became available in post-war Europe and other industrial countries; then, ROP suddenly affected preemies in these countries, too."

"Because the disease had appeared so suddenly, some physicians wondered if it had been there all along but had simply not been recognized before. They organized several large-scale retrospective studies on ROP among older blind people. Some of these studies found a few isolated and uncertain cases beginning, in 1937 (34, 35), but they all concluded that if ROP had existed before 1940 in the U.S.A., or before 1946 in the U.K., it must have been exceedingly rare (36)."

34. HEPNER WR, KRAUSE AC, NARDIN HE. Retrolental fibroplasia (11. Encephala-ophthalmic dysplasia). Study of 66 cases. Pediatrics 1950: 5: 771-82. (These authors mentioned one isolated case each in 1937, 1938, and 1939 in Chicago).
35. ZACHARIAS L. Retrolental fibroplasia: A survey. Am J Ophthalmol 1952: 35: 1426-54. See page 1434. This survey listed four cases in 1938 and one in 1939 in Boston.
36. SILVERMAN WA. Retrolental Fibroplasia: a modem parable. Monographs in Neonatology. New York: Grune & Stratton, 1980: page 17.

"Wombs have no fluorescent lamps, and preemies meant to have stayed in their protected darkness are much more vulnerable to harsh light than adult workers."

"It appears that a common exciting factor is related to premature birth and incubator life. It seems logical that, of the etiologies limited to the eyes alone, precocious exposure to light is still the leading factor in the cause of ocular developmental abnormalities"

"The lowest threshold value for light damage to animal retinae is reported for non-coherent blue light (42) like that from the most intense of the energy spikes in the fluorescent lamp spectrum. When the photons emerge from the phosphor atoms in the fluorescent lamp, they shoot out in specific wavelengths and form intense spikes of concentrated energy radiation. These spikes occur in all fluorescent lamps at the same wavelengths 365.0 nm; 404.7 nm; 435.8 nm; 546.1 nm; and 578 nm -- and approximately with the same relative intensities (43). The differences between the different types of fluorescent lamps are mostly in the broadband spectrum reradiated by the different phosphor formulations. "

42. SPERLING G. Functional Changes and Cellular Damage Associated with Two Regimens of Moderately Intense Blue Light Exposure in Rhesus Monkey Retinae. Association for Research in Vision and Ophthalmoloy, Spring 1978 meeting, ARVO Abstracts page 267.
43. Sylvania Engineering Bulletin 0-283: "Spectral Energy Distribution Curves of Sylvania F40T12 Fluorescent Lamps", Code 753. undated, received in 1985.

http://www.recoveredscience.com/CoolwhiteDeluxegraph.jpg

"Figure 1 does not show the full height of these spikes, since it averages the energies over bandwidths of 10 nm. The spike at 435.8 nm, for instance, is only 0.1 nm wide (45) and would appear almost 100 times higher on the graph if it was not averaged with the neighboring wavelengths. This spike packs 8.5% of a typical nursery lamp's total energy output (see Table 1).

Due to the higher photochemical energy of shorter wavelengths, this spike in the short-wave end of the visible spectrum accounts for an even higher percentage of the total photochemical activity produced by the lamp: in vitro experiments of bilirubin conversion by fluorescent lamps have shown that the single energy spike at 435.8 nm is responsible for more than 50% of the conversion reaction (46)."

46. AGATI G, FUSI F, PRATESI R. Configurational photoisomerization of bilirubin in vitro - II. A comparative study of phototherapy fluorescent lamps and lasers. Photochem Photobiol 1985: 41: 381-92 (Ref. 45, page 382 top left).

"The 1974 Symposium on Illumination, sponsored by the U.S. National Institute of Occupational Safety and Health, NIOSH, warned that high lighting levels in that region of the spectrum could cause much damage to the eye, particularly retinal and macular degeneration (the macula is the most light-sensitive part of the retina).

Included in the Public Health Service's "Guide to the Recognition of Occupational Diseases" is this statement in the section on laser light:

'even a diffuse reflection from a high power laser can present an ocular hazard. An action spectrum has been recently developed to account for the variation in retinal sensitivity with wavelength for exposure times greater than ten seconds. The minimum threshold dose for retinal lesions occurs at 440 nm and is thought to be due to a photochemical process rather than to a thermal mechanism as in wavelengths greater than 500 nm' (47). "

47. KEY MM, HENSCHEL AF, BUTLER J, LIGO RN, TABERSHAW IR, EDE L. Occupational Diseases - A Guide to their Recognition. National Institute for Occupational Safety and Health, U.S. Government Printing Office, June 1977, page 496 top.

http://www.recoveredscience.com/Bluelightbarrier.jpg
(from http://www.recoveredscience.com/Babyblindinglights03.htm )

"The NIOSH data for this table and graph derive mostly from experiments which destroyed the retinae of monkeys, pigs, rats, and a variety of other mammals. The retinal structure of all mammals is virtually the same (49). Clinical experience with victims of welding accidents and accidental exposures to excess laser light confirms that humans are just as vulnerable in the same wavelength region as test animals. There is, thus, no basis for assuming that the developing preemie retina during its period of greatest vulnerability is immune to irradiation in a wavelength which quickly burns the retinae of other mammals. Much of the nursery lamps' energy is concentrated in precisely the wavelength that is known to cause the most damage to the retina."

49. Y CAJAL SR. (first published in 1892 in "La Cellule", Paris), translated by THORPE SA, GLICKSTERN M. The Structure of the Retina. Springfield: Charles C. Thomas Publishers. 1972: pp. 93 and 153.

"60 ftc intensive care nursery lightning will expose a preemie's retinae in 15 min or less to the dose of retinal irradiance which NIOSH has established as the occupational danger limit for healthy adult industrial workers."

"Direct sunshine can be hazardous to unprotected eyes also. In more primitive times, societies punished some of their worst criminals by making them stare into the sun until their eyes were destroyed. Nowadays some nursery staffs appear unaware of the dangers from sunlight.

A report from a nursery in Washington, D.C., describes how a group of babies near the nursery windows had "on occasion" been left lying with the sun in their faces, exposed to light intensities in excess of 400 ftc. Most of them went blind. The authors of the report computed the chances as 199 in 200 that it was this exposure to sunlight which had blinded the babies (69).

69. GLASS P, AVERY GB, SLUBRAMIANIAN KNS, KEYS MP, SOSTEK AM, FRIENDLY DS. Effects of bright light in the hospital nursery on the incidence of retinopathy of prematurity. New Engl J Med 1985: 313: 401-4 (see page 402 bottom right and 403 middle left).

Such carelessness about sunlight is not an isolated case. The above-mentioned nursery in Seattle, for instance, that had the high light levels and a tripling of babies with ROP in the early 1980s, reported measurements of nursery luminance with direct sunlight entering the room. The mean of these measurements taken right next to the isolettes works out to 226 ftc, and the maximum measured was given as 1124 ftc (66)."

66. HAMIER RD, DOMN V, MAYER MJ. Absolute thresholds in human infants exposed to continuous illumination. Invest Ophthalmol Vis Sci 1984: 25: 381-8 (see page 383 top right).

"Preemies also cannot blink to give their retinae brief periods of rest; infants do not acquire this reflex until they are about 6 months old (75). Preemies stare a lot. When their eyes are open, they fix their graze for long times at whatever attracts their attention, more so even than term newborns who also have a tendency to stare (76). Bright light is likely to fascinate them. "

75. HASSETT J. A Primer of Psychophysiology. San Francisco: W. H. Freeman & Co., 1978: page 82 (bottom).
76. SPRUNGEN LB. KURTZBERG D. VAUGHAN HG. Patterns of looking behavior in full-term and low birth weight infants at 40 weeks post-conceptional age. Dev Behav Ped 1985: 6: 287-94.

"The medical literature on accidental retinal burns reports many cases where patients just kept staring at the sun or at a welding arc in light-induced absentmindedness."

"eyelids do not offer much protection. Measurements of light propagation through slices of pig and cow tissue 0.55 mm and 0.94 mm thin (and therefore about comparable to the thickness of preemie eyelids) showed that only about 7.5 to 10% of the light was absorbed in the tissue; the rest was scattered, mostly forward (77). "

"The blue-light hazard function on which the light exposure safety standards are based shows less danger to the retina for wavelengths below 415 nm, because those short wavelengths mostly do not reach the adult retina. But a preemie's eyes are more transparent to more wavelengths and let through about 90% of the visible light above 400 nm plus 80 to 85% of the ultraviolet light down to about 320 nm. "

"Electron microscope pictures of light-damaged retina segments from albino rats (100) show that after exposure to light the cell membranes of the photoreceptors and of the pigment epithelium cells form massive microvilli, little hairlike tendrils, which grip each other like the hooks and loops on a patch of Velcro. This causes the cell membranes to stick together permanently. "

100. KURABARA T, GORN RA. Retinal damage by visible light. Arch Ophthalmol 1968: 79: 69-70.

"Neonatologists who say that the nursery lights do preemies no harm base this assertion on a small scale trial published in 1952 which claimed to have ruled out a connection between exposure to light and ROP. The authors reported that just as many preemies had developed the disease when their eyes were patched with gauze as when they were not. However, in that study the babies' eyes were patched, not immediately, but within up to 24 h after birth (103). That is more than enough time for the fluorescent light to overdose their fragile retinae with damaging blue radiation.

103. LOCKE JC, REESE AB. Retrolental fibroplasia - the negative role of light, mydriatics, and the ophthalmoscopic examination in its etiology. Arch Ophthalmol 1952: 48: 44 47 (see page 46 top).

A year after this misleading study, another flawed but very influential study asserted that oxygen was the major cause of ROP. In that study, 18 nurseries withheld oxygen from some of the preemies and found fewer cases of ROP among the survivors of that group (104). This result was acclaimed as a victory over ROP and led to severe oxygen rationing for most preemies that has endured to this day. However, the unacknowledged reason for the apparent reduction in the incidence of ROP was that fewer preemies, with immature lungs and eyes, survived long enough to display the symptoms of ROP. In fact, the lack of sufficient oxygen killed most of the babies whom ROP would have blinded, plus many more whom ROP would have spared (105).

105. SILVERMAN WA. Retrolental fibroplasia: a modem parable. Monographs in Neonatology. New York: Grune & Stratton, 1980. Chapter 9: "The Determinative Era of Oxygen Treatment", see particularly pp. 62 ff.

A British researcher estimated two decades later that each case of ROP avoided by withholding oxygen "may have cost some 16 deaths" (106)."

106. SILVERMAN WA. Retrolental fibroplasia: a modem parable. Monographs in Neonatology. New York: Grune & Stratton. 1980. Chapter 8: "The Consequences of Oxygen Restriction", see particularly pages 54-57 and 63, 65.

"By the mid and late 1960s, researchers studying the safety of laser light for industrial applications discovered that light could damage eyes not just by burning, the retina with heat as in welding accidents or Sun-staring -- but also through a slower, non-thermal process which they found to be photochemical (108-110). "

108. NOELL WK, WALKER VS, KANG BS, BEPMAN S. Retinal damage by light in rats. Invest Ophthalmol Vis Sci 1966: 5: 450-73.
109. GORN RA, KUWABARA T. Retinal damage by visible light: a physiologic study. Arch Ophthalmol 1967: 77: 115 ff.
110. KUWABARA T, GORN RA. Retinal damage by visible light: an electron microscope study. Arch Ophthalmol 1968: 79: 69 ff.

"In August 1970, a team of physicians from Boston and Philadelphia described in their paper "Retinal Changes produced by Phototherapy" (67) how they had placed newborn piglets under phototherapy lamps with a total irradiance of 300 ftc "to determine if retinal damage does in fact occur during phototherapy of the newborn infant".

67. SISSON TRC, GLAUSER SC, GLAUSER EM, TASMAN W, KUWABARA T. Retinal changes produced by phototherapy. J Pediatr 1970: 77: 221-7 (see page 225 middle left).

"They had picked piglets because "the newborn piglet eye is developmentally of close approximation to the human of comparable age, and since the piglet is a diurnal animal whose eyes are similarly pigmented".

One of the piglets lost the patch over its control eye which had not been dilated, and which remained relatively protected by its heavy eyelids, covered with hair, and thick eyelashes. Although that eye was exposed to the lights for less than 12 h, the next day that piglet had become totally blind. When its retinae were examined 3 weeks later under an electron microscope, both showed virtually the same "marked damage" as the other exposed piglets' retinae."