Already Terry, the discoverer of the eye damage from ROP, suspected that it was most likely caused by light.  He first observed the new condition in two children born in July and November 1940 in Boston[1].  Already in his initial paper about this discovery, published in 1942, he postulated that "some new factor has arisen in extreme prematurity to produce such a condition"[2], and from 1943 on, he argued consistently that this new factor was most likely excess light:

"Premature exposure to light has impressed many of the physicians with whom this problem has been discussed. (...) Myelination of the optic nerve is proportional to the period of postnatal life in the premature as well as in the full-term infant, so that premature exposure to light, even through the thin eyelids, does influence ocular development"[3]

"the precocious exposure to light may be the most important factor. Animals whose eyes are extremely undeveloped at birth have their eyes sealed for a varying period after birth, and often light is further excluded by hair, usually dark, on the lids"^[4].

"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"^[5].

Two of these reports described the first cases of ROP in two babies, one born in 1946 in Birmingham and the other in 1948 in Oxford.  Both noted that from then on, the incidence of the disease in those centers had increased rapidly[6]^,[7].  

The other two papers discussed experiments with fluorescent lighting in hospitals.  One of their authors expressed his appreciation to the General Electric Company for their help in making the special fittings required for these lamps "so soon after the war"[8]^,[9].   

After this jump overseas, ROP appeared soon also in other countries.  In 1952, Dr. Leona Zacharias from the Harvard Medical School published a literature survey, with 219 references, of just about all that was then known about ROP.  Her compilation included the times of its first reported occurrence in other countries:  Israel in 1947; Australia, Canada, and Sweden in 1948; Switzerland in 1949, then Cuba, France, Holland, Italy, South Africa, and Spain all in 1950[10].

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 claimed to have found a few isolated and uncertain cases, beginning in 1937[11]^,[12], 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[13].

This new light was different from any other that anyone had seen before because fluorescent lamps do not emit a smoothly continuous spectrum like that of any natural or incandescent radiation source.  Instead, they concentrate a major portion of their energy in a few high-energy spikes, and the most energetic of these spikes radiates precisely in that wavelength region in which the unprotected mammalian retina is the most vulnerable to damage from light.  

3.2. Fluorescent light and retinal damage

Fluorescent tubes contain an almost vacuum-like thin mixture of mercury vapor and some noble gases in which electromagnetic fields between the ends of the tube accelerate ions to high speeds and energy levels.  When such a fast ion hits a mercury atom, that atom emits a high-energy photon, mostly in two wavelengths in the ultraviolet region.  To transform this invisible stream of photons into visible light, the inside of the fluorescent lamp tube is coated with a layer of phosphors (Greek for "light bringer").  

These phosphors absorb most of the UV radiation and then re-emit it in longer wavelengths that usually cover the entire visible range but concentrate much of their energy output in a few narrow spikes.  These occur in all fluorescent lamps with the same relative intensities at the same wavelengths: 365.0 nanometer; 404.7 nm; 435.8 nm; 546.1 nm; and 578 nm, with the one at 435.8 nm being by far the most energetic[14].  The differences between the various types of fluorescent lamps, such as “Cool White Deluxe” or “Warm White”, are mostly in the broadband spectrum between those narrow spikes which the type-specific phosphor formulations reradiate differently.

Fluorescent lamps emit their light waves independently of each other, unlike lasers which emit them in-phase as coherent light.  The dangers from laser light have received much more regulatory concern than those from fluorescent light, but both types of light are equally damaging to the unprotected retina.  The light receptors in the retina absorb the energy from these waves one photon at a time, whether that photon arrives in step with others or as part of an unorganized group[15].  

Indeed, retinal damage from coherent and non-coherent light sources is indistinguishable, and the experimentally derived threshold values for retinal damage from any specific wavelength are in fairly close agreement whether the light comes from non-coherent xenon lamps and carbon arcs or from coherent helium-neon, ruby, or argon lasers[16].  

Actually, the lowest threshold value for light damage to animal retinae in the large sampling of studies consulted happened to have been reported for non-coherent blue light at 440 nm[17], very close to the radiation from the most intense of the energy spikes at 435.8 nm in the fluorescent lamp spectrum.

The lamps in intensive care nurseries are the fluorescent "Deluxe Cool White" type, as specified by the Committee on Fetus and Newborn of the American Academy of Pediatrics in its 1977 Standards and Recommendations for Hospital Care of Newborn Infants[18].  The distribution of the energy emitted by this type of lamp over the different wavelengths of its spectrum, shown in Figure 2 below, is copied from Sylvania, a maker of these lamps.  The corresponding curves for "Deluxe Cool White" lamps from other manufacturers look very similar and feature the same narrow-line photon emission spikes in the same locations.

Like these other spectrum graphs, this one does not show the full height of the emission 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[19].  It would appear almost 100 times higher on the graph if it was not averaged with the neighboring wavelengths.  

This one spike alone packs about 8.6% of a typical nursery lamp's total energy output (see Table 1 at the bottom of this page).  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, at least in one experiment, that the single energy spike at 435.8 nm is responsible for more than 50% of the conversion reaction from the entire spectrum of the lamp[20].

Figure 2.: Spectrum of typical "Deluxe Cool White" fluorescent lamp. This graph from Sylvania shows the energy in Watts for each wavelength band of 10 nanometer; it is a smooth hill except for four spikes, with the one centered on 435 nm much taller than the other three. 

“... 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” [21].

This function, as copied from the 1997 edition of these Indices[25], and the damage-weighted retinal irradiance computed with it for each wavelength group, appear in the last two columns of Table 1 below.

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.  However, the retinal structure of all mammals is virtually the same[26], and clinical experience with victims of welding accidents and inadvertent exposures to excess laser light confirms that humans are just as vulnerable to the same wavelengths as any of the test animals.  

Nursery doctors have therefore no basis whatsoever for assuming that the developing preemie retina during its period of greatest vulnerability could be somehow immune to intense irradiation in a wavelength which quickly burns the retinae of all other mammals.  Yet, much of the standard nursery lamps' energy is concentrated in precisely the wavelength region that is known to cause the most damage to all mammalian retinae.

Figure 3: Irradiance from “Cool White Deluxe” fluorescent lamp, retinal blue-light hazard protection barrier for normal adult eyes, and blue-light damage-weighted irradiance behind the “vulnerability window” in that barrier.  All use wavelength as the horizontal axis.

The graph illustrates how the most intense emission spike from the fluorescent lamp passes right through the broad breach in the retinal protection barrier -- the "retinal vulnerability window".  If the “Aphakic Hazard Function” applies to the babies’ more transparent eyes, then the left part of the protection barrier is eliminated, and the damage-weighted irradiance curve behind it continues down to 300 nm deep into the ultraviolet radiation.  In either case, the high blue-violet spike of the fluorescent lamps at 435.8 nm penetrates the retinal protection barrier virtually unhindered as damage-weighted retinal irradiance.

The American Academy of Pediatrics prescribes for unprotected preemies weeks and months of continuous irradiation with lamps of extra high output in that most damaging wavelength, and at an intensity reaching their retinae that is far in excess of adult tolerance levels.  Its Committee on Fetus and Newborn specified in its 1977 Standards and Recommendations for Hospital Care of Newborn Infants that all infant care areas should have 100 foot-candles (ftc) of illumination from "Deluxe Cool White" fluorescent tubes[27].  

In October 1988 the Academy reduced this intensity to 60 ftc[28].  However, as you can see in the next section, 60 ftc of intensive care nursery lighting still expose a preemie's retinae in 15 min or less to the dose of damage-weighted retinal irradiance which NIOSH has established as the occupational danger limit for healthy adult industrial workers.  This danger limit is not to be exceeded cumulatively over an eight-hour shift but the preemies reach it in their first quarter hour.

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