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Table of Contents
ROP description
Eugenics against oxygen
Slandering oxygen
Oxygen study frauds  
Alleged study results
Later deaths
Futility and harm

Fluorescent ROP lamps >>

Damaging irradiance
Preemie vulnerabilities
Studies of light and ROP
Frauds in LIGHT-ROP
Coverup stonewalling

 

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Bioethics LIGHT-ROP

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Bioethics own violations

Bioethics Consent

Bioethics 1955 Oxygen

Unethical Bioethics 1

Unethical Bioethics 2

Unethical Bioethics 3

Unethical Bioethics 4

Hypocritical Nature

False Medical Denials

Pre-Nuremberg Bioethics

Protect Humans in Research

Avaaz Petition to WHO

 


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Footnotes :

 

 

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

 

[2]  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.

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

[11]  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).

 

[12]  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.

 

[13]  SILVERMAN WA. Retrolental Fibroplasia: a modem parable. Monographs in Neonatology. New York: Grune & Stratton, 1980: page 17.

 

[14]  Sylvania Engineering Bulletin 0-283: "Spectral Energy Distribution Curves of Sylvania F40T12 Fluorescent Lamps", Code 753. undated, received in 1985.

 

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

 

[16]  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).

 

[17] 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.

 

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

 

[19]  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).

 

[20]  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).

 

[21]  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.

 

[22]  SLINEY DH, WOLBORSHT ML. Safety standards and measurement techniques for high intensity light sources. Vision Res 1980: 20: 1133-41 (see page 1137).

 

[23]  Edward A. Boetnner and J. Reimer Wolter: “Transmission of the ocular media”, Investigative Ophthalmology, Volume 1, December 1962, 776-783, see pages 779 to 781 for transmittance curves and data

 

[24]  S. Lerman: “An Experimental and Clinical Evaluation of Lens Transparency and Aging”, Journal of Gerontology, 1983, Volume 38, Nr. 3, pages 293-301, see page 295.

 

[25]  American Conference of Governmental Industrial Hygienists:  “1997 Threshold Limit Values for Chemical Substances and Physical Agents Biological Exposure Indices”,  Cincinnati, 1997, see pages 118 and 119.

 

[26]  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.

 

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

 

[28]  American Academy of Pediatrics and American College of Obstetricians and Gynecologists: Guidelines for Perinatal Care, 2nd edn. 1988: page 90 (top).

 

 


 


 

  

 

  

 Baby-harming medical research

 

about baby-blinding retinopathy of prematurity

by H. Peter Aleff, 2005 to 2009

 
 

 

Chapter 3: Evidence against fluorescent nursery lighting

Besides killing thousands upon thousands of babies and inflicting irreversible brain damage on many others, the failure of the medical community to acknowledge and thus end its doctrine-enshrined hidden euthanasia program of oxygen withholding also prevents nursery doctors from addressing or even admitting the real reasons for the eye damage that the misguided oxygen rationing is supposed to prevent. 

 

3.1. Parallel beginnings of fluorescent lamps and ROP

Already Dr. 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]

Similarly, he wrote again a couple of 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"[4].

And by 1946, he was ailing but had his comments 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"[5].

The new factor which Terry had postulated was indeed a new kind of light that had been commercially introduced at the New York World Fair of 1938 and 1939, a couple of years before his first ROP patients were born.  

From then on, ROP quickly became an epidemic in hospitals across America where these lamps quickly became popular because their light made the rooms look cleaner and was also believed to kill germs. During the soon following world war and its immediate aftermath, ROP remained confined to the U.S.. But over the next few years, it appeared just as suddenly in other industrialized countries, again in parallel with the introduction there of these lamps.

England was the first of these new ROP countries. 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 United Kingdom. 

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].

Sylvania cool white deluxe spectrum

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. 

As Murphy’s Law appears to have dictated it, the wavelength region where the retina is most vulnerable to damage from light is precisely the region from 435 to 440 nm. These wavelengths in the blue-violet region have caused much concern among specialists in Occupational Safety for adult industrial workers.  

Already the 1974 Symposium on Illumination, sponsored by the U.S. National Institute of Occupational Safety and Health, NIOSH, warned that high lighting levels in this 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” [21].

These blue-light hazard values are for normal adult eyes that have already begun their gradual age-related yellowing and therefore block at least in part some of the worst blue and violet wavelengths. 

However, preemie eyes are still entirely transparent to these, and also to many of the even more energetic ultraviolet wavelengths. Their lenses as well as the aqueous and vitreous humors that fill their eyeballs let in all radiation down to about 300 nm[23].  Even the lenses of children aged up to ten years transmit over 75% of the 300 to 400 nm UV radiation[24]

Baby eyes are therefore more comparable to “aphake” eyes, that is, eyes without the protection of a lens, like those that have undergone cataract surgery. Because people with such totally unprotected eyes are even more vulnerable to short wavelength light, the American Conference of Governmental Industrial Hygienists in Cincinnati began in 1991 to include in its annually updated “Biological Exposure Indices” also the Aphakic Hazard Function for such people.  

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.

 


Table 1.: Damage weighted irradiance from the "Deluxe Cool White" fluorescent lamp
which the American Academy of Pediatrics specifies for intensive care nurseries.

Wave-length in nano-meters Irradiance in Watts per 10 nm, scaled from graph Blue-light hazard function for normal eye Blue-light damage-weighted irradiance Aphakic eye photic hazard function Aphakic eye damage- weighted irradiance

 

 

 

 

 

 

315

0.122

--

--

6.00

0.7320

355

0.122

--

--

5.22

0.6368

365

0.955

--

--

4.29

4.0970

375

0.321

--

--

3.56

1.1428

385

0.416

--

--

2.31

0.9610

395

0.581

invisible ultraviolet 

1.58

0.9180

400

--

0.10

--

1.43

 

405

2.432

0.20

0.4864

1.30

3.1616

410

--

0.40

--

1.25

 

415

0.959

0.80

0.7672

1.20

1.1508

420

--

0.90

--

1.15

 

425

1.137

0.95

1.0802

1.11

1.2621

430

--

0.98

--

1.07

 

435

6.120

1.00

6.1200

1.03

6.3036

440

--

1.00

--

1.00

 

445

1.338

0.97

1.2979

0.97

1.2979

450

--

0.94

--

0.94

 

455

1.440

0.90

1.2960

0.90

1.2960

460

--

0.80

--

0.80

 

465

1.527

0.70

1.0689

0.70

1.0689

470

--

0.62

--

0.62

 

475

1.650

0.55

0.9075

0.55

0.9075

480

--

0.45

--

0.45

 

485

1.727

0.40

0.6908

0.40

0.6908

490

--

0.22

--

0.22

 

495

1.839

0.16

0.2942

0.16

0.2942

500

--

0.10

--

0.10

 

505

1.935

--

0.2419

 

0.2419

515

1.990

--

0.0995

 

0.0995

525

2.118

--

0.0678

 

0.0678

535

2.233

--

0.0447

 

0.0447

545

4.307

--

0.0560

 

0.0560

555

2.476

--

0.0198

 

0.0198

565

2.598

--

0.0130

 

0.0130

575

3.179

--

0.0095

 

0.0095

585

2.905

--

0.0058

 

0.0058

595

2.991

--

0.0030

 

0.0030

600

--

0.01

--

0.01

 

605

3.073

--

0.0031

 

0.0031

615

3.029

--

0.0030

 

0.0030

625

2.952

--

0.0030

 

0.0030

635

2.808

--

0.0028

 

0.0028

645

2.664

--

0.0027

 

0.0027

655

2.355

--

0.0024

 

0.0024

665

2.074

--

0.0021

 

0.0021

675

1.548

--

0.0015

 

0.0015

685

1.021

--

0.0010

 

0.0010

695

0.188

--

0.0002

 

0.0002

700

--

0.001

--

0.001

 

 

 

 

 

 

 

Total

71.130 Watt

 

14.6 Watt

 

26.5 Watt

% of output

100%

 

20.51%

 

37.26%

 

 

 

 

 

 

 

Column 1 in this Table lists the wavelengths in nanometers (nm) in which the “Cool White Deluxe” lamp emits its radiation.

Column 2 shows the energy of that emission in Watts for each wavelength interval of ten nm. Please note the emission spike at 435 nm.

The third column gives the U.S. Occupational Safety Guidelines' action spectrum for the "blue-light hazard function" which the National Institute for Occupational Safety and Health (NIOSH) first published in 1980. It shows the maximum vulnerability range from 435 to 440 nm where the emission from the lamp is strongest[22] .

The fourth column multiplies the irradiance from the lamp in column 2 with the value of that “blue-light hazard function” in column 3 to obtain the "damage-weighted irradiance" from that wavelength band that reaches the retina in a normal adult eye. The lens of that eye is usually yellowed and so filters out much of the most damaging blue and violet radiation.

Column 5 lists the corresponding photic hazard function for aphakic eyes, that is, eyes like those of preemies whose lens is not yet yellowed and therefore lets through the even more damaging radiation at shorter and therefore more energetic wavelengths.

The last column lists the damage-weighted irradiance from those fluorescent nursery lamps on the retinae of unprotected aphake eyes like those of preemies.

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