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and a documentation of  baby-blinding light levels in hospital nurseries

 

 
Footnotes:

 

26. Encyclopedia Britannica, 1965 edition. "Lighting" (page 104 bottom right).

 

27. Luxor Lighting Products, Inc., Lyndhurst, New Jersey, undated company flyer: Cavalcade of Progress, form 1103: "1938 - Even before fluorescent light was introduced at the 1939 N.Y. World's Fair, our company had built a medium-base, screw-in fluorescent lamp."

 

28. TERRY TL. Extreme prematurity and fibroplastic overgowth of persistent vascular sheath behind each crystal-line lens. I. Preliminary report. Am J Ophthalmol 1942: 25: 203-4.

 

29. ZACHARIAS L. Retrolental Cibroplasia: A survey. Am J Ophthalmol 1952: 35: 1426-54 (see pp. 1435 and 1436).

 

30. HOULTON ACL. A study of cases of retrolental Fibroplasia seen in Oxford. Trans Ophthalmol Soc U.K. 1952: 71: 583-90.

 

31. CROSSE VM. The problem of retrolental fibroplasia in the City of Birmingham. Trans Ophthalmol Soc U.K. 1952: 71: 609-12.

 

32. LANG R. An experiment in ward lighting. Trans Ophthalmol Soc U.K. 1952: 71: 563-71 (quote on page 570).

 

33. LAW FW. Ward lighting. Trans Ophthalmol Soc U.K. 1952: 71: 573-81.

 

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.

 

37. TERRY TL. Fibroblastic overgrowth of persistent tunica vasculosa lentis in premature infants. Arch Ophthalmol 1943: 29: 54-68 (quote on page 59).

 

38. TERRY TL. Ocular maldevelopment in extremely premature infants. JAMA 1945: 582-5 (quote on page 583).

 

39. TERRY TL. Retrolental fibroplasia. J Pediatr 1946: 29: 770-3 (quote on page 772).

 

40. ALPERN M. The Eyes and Vision. Chapter 12. In: DRISCOLL WG. VAUGHAN WV. eds. Handbook of Optics. New York: McGraw Hill. 1978: 12-27.

 

41. CALKINS JL, HOCKHEIMER BF. Retinal light exposure from operation microscopes. Arch Ophthalmol 1979: 97: 2363-7 (see page 2365 bottom right and page 2366 top right).

 

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.

 

44. Committee on Fetus and Newborn of the American Academy of Pediatrics: "Standards and Recommendations for Hospital Care of Newborn Infants". 1977, page 27.

 

45. 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 (see page 382 middle right).

 

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).

 


 


 

  

 

  

  Preemies get more retinal irradiance

 

than safety guidelines allow for adults

 
 

Davidpreem02.jpg (21412 bytes)

Baby-blinding retinopathy of prematurity and intensive care nursery lighting    by H. Peter Aleff
 

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ROP and
the introduction of fluorescent light

Fluorescent lamps were first introduced commercially at the World Fairs of 1938/39 in San Francisco and 1939/40 in New York (26, 27) and proliferated in factories, hospitals, and other large buildings across the U.S. After the war, fluorescent lamps were welcomed in most other industrialized countries with equal enthusiasm. Once the Second World War was over and normal trade as well as factory building resumed, this new and money-saving, technology spread in all directions. Everywhere, hospitals were among the first to install the new lamps, since their bright light was considered helpful against dirt and germs.

The first 2 babies reported to have suffered ROP were born in July and November 1940 in Boston (28). The mysterious condition soon appeared in most intensive care nurseries across the U.S., and after 1948 in intensive care nurseries in many other industrialized countries.

In 1952, Dr. Leona Zacharias from the Harvard Medical School published a 219-reference literature survey of just about all that was then known about ROP. She documented the time of first occurrence in other countries: Israel -- 1947; Australia, Canada, and Sweden -- 1948; Switzerland 1949, Cuba, France, Holland. Italy South Africa, and Spain -- 1950 (29).

The U.K. was the earliest. Both fluorescent lamps and ROP made their debut there right after the war, according to four reports presented at the 1951 session of the Ophthalmological Society of the U.K. Two of these reports described the First cases of ROP in 2 babies, one born in 1946 in Birmingham and the other in 1948 in Oxford. Both reports noted that the incidence of the disease increased rapidly (30, 31). The other two papers discussed experiments with fluorescent lighting in hospitals; one of the 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" (32, 33).

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).

When Dr. Theodore L. Terry first described the new disease in 1942, he postulated that "some new factor has arisen in extreme prematurity to produce such a condition" (28). In 1943, he argued that this new factor was 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" (37).

He expressed the same argument again several years later:

"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" (38).

A year later, Dr. Terry's comments were read to the American Academy of Pediatrics:

"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" (39).

Retinal vulnerability to fluorescent light

Fluorescent tubes contain a thin mixture of mercury vapor and some noble gases. Electromagnetic fields in the lamp accelerate ions to high speeds and energy levels. When these fast ions hit the mercury atoms, these emit high-energy streams of photons, mostly in two wavelengths in the ultraviolet region. To transform these into the longer wavelengths of visible light, the inside of the fluorescent lamp tube is coated with a layer of phosphor (Greek for "light bringer").

Phosphor absorbs light and then reemits that radiation spontaneously for hours and in a different color, as in a luminous watch dial. The photon bombardment from the excited mercury atoms inside the tube greatly multiplies and accelerates this reradiating glow. The photons emitted from the mercury enter the phosphor atoms and exit at a longer wavelength, using, the phosphor atoms like so many launch-pads up into visibility.

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 that those from fluorescent light, although both types of light are equally damage to the 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 (40). Indeed, retinal damage from coherent and noncoherent light sources is similar. The experimentally derived threshold values 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 (41).

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.

The fluorescent lamps in intensive care nurseries are the "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 (44).
 

CoolwhiteDeluxegraph.jpg (24622 bytes)

Figure 1: Spectrum of typical "Deluxe Cool White" fluorescent lamp.
Graph from Sylvania.

Transcriber's Note: Graph shows the energy for each wavelength; it is a smooth hill except for four spikes, with one much taller than the other three.

The distribution of the energy from this type of lamp over the different wavelengths of the spectrum is shown in Figure 1 and is copied from Sylvania, a maker of these lamps. The corresponding curves for "Deluxe Cool White" lamps from other manufacturers look similar and feature the same narrow-line photon emission spikes.

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).

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