RESEARCH REPORT

g DETERMINATION of '

' ’ OCULAR THRESHOLD
LEVELS for INFRARED
RADIATION
CATARACTOGENESIS

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SEPT 91980 n

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EETERMINATION 0F ifiéfifllh’

OCULAR THRESHOLD LEVELS FOR 55/)
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INFRARED RADIATION CATARACTOGENESIS fl/‘v
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Donald G. Pitts, O.D., Ph.D.
Anthony P. Cullen, O.D., M.Sc.
Pierrette Dayhaw—Barker, Ph.D.

University of Houston
College of Optometry
Houston, Texas 77004

NIOSH # 77—0042—7701

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES, ”*1‘? ~"
Public Health Service
Center for Disease Control
\% National Institute for Occupational Safety and HealthJ
Division of Biomedical and Behavioral Science
Cincinnati, Ohio 45226

JUNE 1980

 

For Ille by the Superintendent of Documentl. U.S. Government
Printing Office, Walhlngton. D.C. 20402

   

       
      

 

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DISCLAIMER

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The contents of this report are reproduced herein

as received from the contractor. The opinions, findings,
and conclusions expressed herein are not necessarily
those of the National Institute for Occupational Safety
and Health, nor does mention of company names or products
constitute endorsement by the National Institute for
Occupational Safety and Health.

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NIOSH Project Officer: C. Eugene Moss
Principal Investigators: Donald G. Pitts, 0.D., Ph.D.
Anthony P. Cullen, 0.D., Ph.D.

ACKNOWLEDGMENTS

The authors wish to express appreciation to Karsten Neilsen, 0.D., for
assistance in all of the primate research and the latter stages of the

rabbit studies.

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Author/Title:

Donald G; Pitts et al.
Determination of ocular threshold
levels for infrared radiation
cataractogenesis.

 

 

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£5 KEV
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ABSTRACT )tZZflZ§//

A 5000 watt Xenon high pressure lamp was used to expose 100 pigmented
rabbit eyes and 10 monkey eyes to both infrared radiation and the full
optical spectrum of the source. The primary ocular lesion was an '
anterior epithelial sub—capsular opacity which initially was seen as
small whitish dots that developed into white patches in that area of

the anterior capsule just beneath and in contact with the iris. No
lenticular opacities were induced by direct exposure to the lens.

Ocular damage from infrared exposure was related to the rate of delivery
of the radiation. Infrared irradiances up to 3.9 W'cm"2 resulted in
thresholds for the rabbit eye of 5000 Jocm‘2 for the cornea, 3500 J-cm‘2
for the iris, and 3750 J-cm‘2 forthe lens while irradiances above

4.0 W-cm‘2 gave rabbit ocular thresholds of 1250 J-cm'2 for the cornea,
1250 J-cm"2 for the iris, and 2250 J~cm‘2 for the lens. Exposures with
the full optical spectrum of the source showed that the visible and the
ultraviolet radiation were additive for damage to the lens. The monkey
ocular thresholds were a factor of 6 above the respective rabbit threshold.
The methodology for ocular protection, the criteria for ocular damage,
and the levels of allowable infrared exposure are discussed.

iii

205574

 

CONTENTS

Abstract
Acknowledgments
Introduction
Purpose of the Research
Review of the Literature
Eyelids
Cornea
Iris
Crystalline Lens
Retina and Choroid
Instrumentation and Procedures
Infrared Source
Infrared Source Measurement
Experimental Animals
Exposure Procedures
Evaluation Procedures
Results
Discussion
Summary
References

 

INTRODUCTION

Purpose of the Research

 

The purpose of the research was to establish the ocular threshold exposure
values for infrared radiation (IR) in the 700 to 1400 nanometers (nm)
wavelength range necessary to produce cataracts in the crystalline lenses
of experimental animals relevant to man, to identify and report effects
observed in other ocular structures, and to recommend valid criteria for
safety standards against ocular exposure to IR.

Review of the Literature

 

An extensive review of the literature was not necessary because of the
papers of Turner (1), and Duke-Elder (2) and the exhaustive review by

Moss et al. (3). Therefore, this section covers selected research, which
produced experimental data, in an attempt to acquaint the reader with the
irradiance levels in the IR spectrum necessary to produce ocular damage or
to confirm that such data do not exist.

An understanding of the absorptive or transmittance properties of the eye

in the wavelength region of concern will assist in explaining some of the
observed biological effects. Weisinger et al. (4), Geeraets et al. (5),
Boettner and Wolter (6), Prince (7), and Geeraets and Berry (8) have pub-
lished transmittance data for the rabbit, primate and human in the wavelength
range from 300 nm to 2000 nm (Figures 1—3). These reports indicate that the
mammalian ocular media are transparent to the near IR (radiation in the 750 nm
to 1400 nm wavelength range) and essentially opaque to the far IR (radiation
greater than 1400 nm). The corneal transmittance exceeds 90% between 500 and
1300 nm. Beyond 1300 nm, absorption bands at about 1430 nm and 1950 nm are found
for the cornea but its transmittance remains high between these bands. Beyond
2000 nm, the IR absorption of the cornea appears to be almost complete. The
aqueous humor transmits to about 2400 nm and has absorption bands centered at
980, 1200, 1430 and 1950 nm. The crystalline lens shows high transmittance

to about 1400 nm with absorption bands centered at 980, 1200, and 1430 nm.

The transmittance of the vitreous humor exceeds 90% and demonstrates absorption
bands at 980 nm and 1200 nm with essentially no transmittance of IR beyond

1400 nm.

Thus, IR above 2000 nm is absorbed almost entirely by the cornea and aqueous
humor. Almost all of the near IR impinging on the iris is absorbed by the

iris pigment epithelium layer which lies next to the lens. The near IR which
passes through the pupil shows strong absorption bands above 900 nm while almost
none of the IR above 1400 nm reaches the retina. The IR which is transmitted
through the ocular media to the retina is absorbed by the pigment epithelium

of the retina .

The ocular effects of IR on the different anatomical structures beginning
with the eyelid and proceeding posteriorly to the retina will be reviewed.

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Eyelids

The effects of IR on the eyelids range from erythema to third degree burns

and necrosis of the skin (2). To obtain these effects, the eyelid must be
exposed to very high levels of IR delivered over a short period of time or
exposed to low to moderate levels of IR over a long period of time. IR eyelid
damage is not ordinarily experienced in the industrial environment.

Cornea

IR effects on the cornea consist essentially of protein coagulation of the
epithelium and the stroma; however, the drying of the cornea and reflex

closure of the lids occur prior to any coagulation (5). Verhoeff and Bell (9)
emphasize that the posterior layers of the cornea may demonstrate more

damage than the anterior layers because the lacrimal fluid and the air cooling of
the anterior layers of the cornea are more effective than the aqueous cooling of
the posterior layers of the cornea by convection. The coagulation of corneal
tissues results in immediate pain, reflex closure of the eyelids, and

protective movements of the head and eye.

Dawson (10) used a Sylvania DFA tungsten filament lamp with a parabolic

reflector to expose the left corneas of 26 cats. The spectral output of

the lamp was not measured,but Dawson reported its wavelength range as

400 nm to 2600 nm with a total radiant emittance at 150 W of 7.04 g-cal-sec‘l-cm‘2
(29.5 J-cm‘z). Exposure durations were from 15 s to 365 s. The exposed

eyes were examined by slit—lamp with changes in the cornea ranging from

mild to ulcerating lesions while cataract formation was seen in the lenses.

Dawson summarized the results as follows:

Total Dose Ocular Effect
100 g-cal-cm‘2 No immediate effect
(418.5)* J-cm'2 24 hours — mild leukoma
72 hours — complete recovery
100 g-cal-cm‘2 t0 Corneal opacities
300 g-cal-cm‘2 Corneal vascularization
(418.5 to 1255.5)* J-cm’2 Penetrating ulcers
300 g-cal-cm-2 Deep penetrating corneal ulcers

(1255.5)* J-cm'2

2 was used for conversion

*4.185 J-cm"2 per gecal-cm'
It should be remembered that certain tungsten lamps produce a spectrum in the
ultraviolet (UV) beginning at about 250 nm and some of the effects described
above parallel closely the description of those produced by UV exposures.

Iris

Duke—Elder (2) has summarized the effects of IR on the iris. He stated that
even moderate doses of IR result in an aqueous flare, hyperemia, and miosis.
Severe exposures may result in a paralytic mydriasis, congestion with
hemorrhages, thrombosis, and stromal inflammation. These effects result

in necrosis of the iris with bleached, atrophic areas forming within a

few days. In addition, there is a loss of pigment at the edge of the iris
within two to four days after exposure. Unfortunately, the radiant exposure
levels were not quantified.

Crystalline Lens

The first mention of the effects of IR on the crystalline lens was in 1739 (1).
Many authors pointed out the relationship between certain types of cataracts
and occupations which required prolonged exposure to heat. Meyenhofer (11)

was the first to study glassworkers and to provide data on the number of
workers who developed cataracts. He described the posterior cortical opacity
which has become accepted as the early stages of the IR—induced cataract.

In 1907, Legge (12, 13) was instrumental in establishing the glassblowers
cataract as a legal occupational disease. Robinson (14) argued that the IR
was the cause of the "heat cataract."

Vogt (15, 16) used a carbon arc lamp (4000 K) filtered through water and
iodine sulphate to expose rabbit eyes. The principal effects reported were
to the cornea, iris, and lens. Vogt maintained that the cataract was due
to direct absorption of the IR by the lens. The results reported by Vogt
could have been the result of UV exposure since the carbon arc source was
rich in UV and filtered by water.

Verhoeff and Bell (9) are noted for their research on the effects of UV;
however, their research extended to the IR spectrum, using a low pressure
quartz lamp, the magnetite arc, and the sun. The lower limit of the spectrum
was controlled by crown and flint ophthalmic glass filters. When the lower
spectrum was limited to 305 nm, the lens was damaged, but if the spectrum
was limited at 295 nm, the endothelium, iris, and lens were damaged. They
filtered sunlight with a 2 mm thickness of UVlOl glass and used a large
mirror to focus the transmitted energy to the iris and the pupil of the
pigmented rabbit eye. Exposure durations were 15 seconds and 30 seconds
with the animal's eye placed at 1.0 meter from the mirror. The anterior
lens epithelium of the pupil was unaffected but the lens epithelium beneath
the pupil and in contact with the iris pigment epithelium demonstrated a
"mitosis similar to observations produced in other experiments by abiotic
(UV) radiations." In other words, that portion of the lens covered by,

and in contact with, the iris showed lenticular opacities but no response
was found in that portion of the lens seen through the pupil. They argued
that the cataract was due to interference with normal ciliary body function
*and the subsequent interference with lens metabolism.

 

Goldmann (17—24) exposed rabbit eyes to a specially designed furnace
source. He measured ocular transmittance of IR and experimentally induced
cataracts in the crystalline lens in that portion of the lens under the
iris. Goldmann was not able to produce cataracts by direct exposure of the
lens through the pupil. Goldmann claimed that IR or heat cataracts were
not due to direct absorption of the IR by the lens but due to the raising
of the temperature indirectly through heat absorbed by the iris.

From the 19305 to date there were many reviews of the literature, very few
epidemiological studies, and a few experimental studies which provided data
on which some conclusions could be reached. Kutscher (25) reviewed the
literature on "glassblower's cataract" and concluded that it was in the third
decadeof life that puddlers, tin platers, and steel rollers appeared to
develop cataracts. He also reviewed the Vogt-Goldmann controversy for the
cause of cataracts without arriving at a conclusion. Salit (26) discussed
the rise in incidence in cataracts one year after a very dry, hot summer in
Iowa together with data reports from the weather bureau. He concluded that
more attention should be paid toward environmental conditions as causative
agents for cataracts. Dunn (27) reviewed the causes of industrial cataracts
in workers at the Corning Glass Works. He concluded that the cataracts were
not caused by IR but by other etiological factors. He calculated the
irradiance at eye level from glass manufacturers to be 2.0 g-cal-cm'z-min'l
or 0.139 W'cm'z. Keatinge et al. (28) surveyed the incidence of lenticular
changes in an iron rolling mill. Of 44 workers examined only 3 (6.8%) of
the workers, all over 65 years of age, showed the "classical posterior
cortical lenticular changes" described as typical of heat or IR cataracts.
They calculated the radiation at the rolling mill to be from 0.08 W-s‘l-cm'
to 0.42 W-s'l-cm‘z, The control group showed 16 posterior capsular opacities
(15%), of which 7 were in workers under 50 years of age. The authors state
that cataracts OCCur in the general population at equal or greater levels

of incidence than in iron rolling mill workers, but that certain individuals
maylxamore susceptible to radiation cataracts than others. Hence, the
workers and control individuals who developed cataracts may simply have been
susceptible individuals.

Wallace et al. (29) examined 1000 steel workers, 100 of whom were not at risk
and 900 of whom were exposed to low, intermediate, and high levels of IR.
The workers were scored on the infrared exposure levels as 3 for a high
exposure, 2 for intermediate, 1 for low, and 0 for no exposure. They
classified cataracts according to type: Type I were small lenticular
disturbances which did not interfere with vision; Type II were posterior
subcapsular saucer—shaped opacities causing minimal interference with Vision;
and Type III were dense posterior subcapsular opacities which produced

gross disturbances in vision. An exposure index was calculated by multi—
plying the number of years on the job by the exposure risk. The exposure
index was compared to the type cataract which was found. No Type III
cataracts were found. The percentage of Type I cataracts increased with age
from about 50% at the age of 40 to about 62% at the age of 65. They found
only two exposed workers with cataracts which were attributed to their
occupation; however, a slightly higher incidence of the common cataract due
to aging was found in the groups exposed to IR.

Langley et a1. (30) repeated the experiments of Goldmann and hypothesized
that both visible light and IR must be absorbed by the iris for cataracts
to be produced. Six groups of 5 rabbits were each exposed to a 100 W
zirconium arc lamp with a focused image of 6.75 mmz, an irradiance of
0.154 W-cm‘z, for 30 s which gave a radiant exposure of 4.62 J'cm‘z.

The exposure beam was directed to the iris. The animals were sacrificed
at 30, 60, 90, 120, and 150 days after irradiation. The clinical sequence
was a burn-like thickening and clouding of the cornea, an anterior uveitis,
and a disruption of the iris followed by iris pits or holes if the radiant
exposure was high. Within 2 to 3 weeks, the lens developed a whitish area
which changed to a grayish opacity below the anterior capsule. By 6 weeks,
the lenticular opacity extended toward the equator and joined with a cup-
shaped posterior sub-capsular opacity to form a U—shaped cataract. The
opacity remained unchanged at this stage or progressed to encompass the
whole crystalline lens. Langley et a1. stated that if the iris were exposed
midway between the pupillary margin and the root of the iris, a cataract
could be produced in almost every eye. They argued that it was not the
total heat applied to the eye, but the increase in the temperature at a
local area which produces the cataract.

Most of the experimental evidence appears to support the theory of

Goldmann; however, there are speculations which still question this view.
For example, the excessive number of "solar cataracts" found in India

could be due to UV and/or nutrition. Not all workers in the metal industry
develop cataracts;and,many studies attempting to support Goldmann's theory
used sources which contained UV which was apparently not filtered out.
Nevertheless, most of the opinion is strongly in favor of the Goldmann
hypothesis. It is also interesting to note that most researchers found
posterior lenticular cataracts induced by IR only after a long latency of
30 to 90 days. In contrast the IR cataracts described in some research
were described as anterior subcapsular opacities with the posterior sub—
capsular and equatorial involvement being found only after long latencies.
Pitts and Cullen (31) have recently reported that 100% of the pigmented rab—
bits used in experiments demonstrated a posterior subcapsular lenticular
opacity which radiated laterally along the horizontal posterior suture line,
in some rabbits almost to the equator, and occasionally projected anteriorly
from the posterior suture line at the posterior pole of the lens into the
cortex and into the nucleus of the lens. The density and proliferation of
these opacities increases normally with age. The findings suggest that

long term effects which have been reported in the literature may be nothing
more than the normal aging process of the rabbit.

Retina and Choroid

The primary effect of IR on the retina and the choroid is increased
temperature. It is beyond the scope of this study to review all of the
data in the literature relative to retinal lesions from photic stimulation.
This is especially so Since most research in retinal burn lesions employed

 

broad band spectral sources which usually included some UV, the visible,
and the IR spectra. Hence, it is difficult to separate from each other

the effects of different regions of the spectrum. Therefore, a few reports
have been selected from which IR damage data may be evaluated.

The experimental variables in producing retinal lesions include pupil size,
spectral transmittance of the ocular media, spectral absorbance of the retina
and choroid, the optical quality of the retinal image, exposure duration,
size of the source, location on the retina, size of the retinal image, the
type of source, spectral distribution of the source, rate of delivery of the
energy, and the criteria used to evaluate the exposures. Exposure duration
is an important parameter even if all other parameters are held constant.

As the exposure duration increases, the radiant power entering the eye
necessary to produce a retinal lesion decreases until duration becomes
ineffective and a lesion appears to be determined by the irradiance reaching
the retina. ’

Bredemeyer et a1. (32) used an air-cooled mercury lamp for the UV and short
visible radiation, a high—pressure Xenon lamp for a continuous wavelength
spectrum from 250 to 1300 nm, and a carbon arc system which provided a

250 nm to 5000 nm continuous spectrum to study the effects of narrow spectral
wavelength exposures on the eye. They exposed adult pigmented rabbits to

six wavebands while maintaining constant retinal image size and exposure
durations. Their data showed that the longer wavelength radiation required
higher irradiances at the cornea to produce a retinal burn.

Jacobson et a1. (33) exposed adult chinchilla rabbits to the visible and near
IR region of the spectrum. They used a Zeiss photocoagulator with a 1600 W
Xenon lamp source and varied the rate of delivery, the retinal image size,
the exposure duration, and the spectral characteristics of the source. Their
data for LD—50 and spectral characteristics are summarized as follows:

 

 

Ocular Wavelength Corneal Dose Corneal Dose
Structure in nm in cal-cm‘2 in J-cm‘
Cornea: 370—480 0.70 2.93

480-590 0.75 3.14
620—1100 1.20 5.02
870-1120 1.90 7.95
1200—1670 0.70 2.93

Iris: 0.3 to 0.5 cal-cm‘2 (1.25 J-cm"2 to 2.09 J'Cm'z) produced a minimal
irreversible lesion. Iris exposures given below are measured at plane
of the cornea.

Wavelength Corneal Dose Corneal Dose Corrected Corneal Corrected Corneal

 

 

in mm in J-cm"2 in cal-cm"2 Dose in J-cm'”2 Dose in cal-cm—2
370-480' 3.97 0.95 1.63 0.39
480—590 3.26 0.78 1.72 0.41
620—830 3.35 0.80 2.13 0.51
880-1120 11.29 2.70 4.89 1.17

Lens: 9.21 to 10.05 cal-cm'2 (38.53 to 42.05 J-cm‘z) measured at the
plane of the cornea resulted in no visible lesion to the lens.
There was no filter used during this exposure phase.

370—900 nm - radiant exposure of 2.4 to 4.59 cal-cm"2 (10.0 to 19.21 J'Cm_2)
resulted in no visible lesion to the lens.

880-1120 nm - radiant exposure of 1.77 to 1.88 cal-cm"2 (7.41 to
7.87 J-cm‘z) resulted in no visible lesion to the lens.

The data of Jacobson et a1. indicate that ocular damage can occur to the iris
with radiant corneal exposures as low as 0.39 J°cm‘2 and to the lens with
more than 42.05 J-cm‘z.

Ham et a1. (34) recently reported that to produce retinal lesions of 159 pm in
size in the rhesus monkey radiant exposures on the retina from two spectral
wavebands, 400 to 800 nm and 700 to 1400 nm,were required with exposure
durations of l, 10, 100, and 1000 seconds. They found reciprocity was
maintained for exposures to the 400 to 800 nm waveband for exposure durations
10 s or longer with the radiant exposure being 400 J-cm'z. A radiant expo—
sure of 6.91 x 104 J-cm‘2 was required for the 1000 sexposure using the

near IR of 700 to 1400 nm wavelength range. They were unable to produce a
retinal burn with exposure durations less than 1000 3.

Levels of Exposure to Workers

 

Barthelmess and Borneff (35) measured the total daily radiation received by
glassblowers working near the melting furnaces and found the total radiation
to be 2000 to 3000 J-cm‘z. Approximately 10% of that total was IR below

1400 nm. Sliney and Freasier (36) stated that the IR corneal dose rate

from daylight is about 10‘ W-cm'z. They report that glass and steel workers
exposed to IR irradiances on the order of 0.04—0.08 w-cm'2 daily for 10-15
years develop lenticular cataracts. IR corneal irradiances of 0.1 w-cm'2 are
often used as a guideline for protection against far IR lasers. Sliney and
Freasier suggest that the chronic exposure criterion for IR in the 780 to
1400 nm wavelength range should be on the order of 0.01 W-cm‘z. Moss et a1. (3)
provide an excellent tabular summary of industrial IR sources which may
provide a hazard to the eye.

10

 

INSTRUMENTATION AND PROCEDURES

Infrared Source

The source for the infrared energy was a 5 kW Xenon high pressure lamp,

powered by a 10 kW, DC power supply regulated to 0.5% and capable of delivering
from 1 to 80 amperes at 25 to 65 volts to the lamp electrodes (Figure 4).

The lamp housing was cooled by two air blowers and continuous flow water
through copper tubing. The air in the laboratory was conditioned and humidity
controlled to with i 10%. The 5 kW Xenon source provided a continuous
spectrum from 200 nm to 5000 nm with approximately 45% in the IR region.

The radiation from the source was focused at the entrance slit of a
McPherson Model 2501, single grating monochromator. The monochromator
grating had a wavelength range of 185 nm to 10.4 p, was blazed at 1200 nm,
had 150 lines/mm with a linear dispersion of 6.6 mm per mm of exit slit,
and allowed a total band pass of 66 nm while providing an accuracy of 0.05 nm.
The monochromator optical system was aligned and the wavelength counter
calibrated with a HeNe laser. Stray light was greater than 20% in the IR
region of the spectrum; therefore, a Schott RG—715 filter blocking filter
was placed in the optical system just beyond the exit slit of the mono—
chromator (Figure 4). The Schott RG—715 filter reduced stray light to an
unmeasurable level. The transmittance characteristics of the Schott RG-715
filter were measured with a Beckman Mark VI spectrophotometer and are given
in Figure 5.

In addition to using the monochromator as a wavelength device, the grating
was positioned at zero wavelength counter reading to allow the central

image to pass through the system without undergoing diffraction. The central
image contained the full spectrum of the source but could be controlled for
exposure durations and filtered to produce the desired wavebands for exposure.
When filtered with the Schott RG-715 filter, the spectrum reaching the lens
had a wavelength range of 715 nm to 1400 nm because the longer IR was absorbed
by the cornea and the aqueous (Figures 3 and 5).

Exposure durations were controlled with an Hewlett Packard Model 53303 preset
counter which operated a Gerbands electronic shutter. The shutter system
allowed exposure durationsof any desired length with millisecond accuracy.

The size of the optical beam at the plane of the cornea could be reduced in
size by placing the two lenses in the optical system just beyond the filter.
When the lenses were omitted from the optical system, the beam exiting the
monochromator was essentially collimated and measured 1.5 cm x 2.5 cm at the
plane of the exposure. An exposure made under these conditions was called
an "unfocused beam" and covered essentially the entire cornea. With the
lenses in the optical system, the beam measured 0.8 cm x 1.5 cm at the plane
of the exposure and was called a "focused beam." The focused beam provided

11

ZI

AIR ‘-

    
  

PRE' SET TIMER

 

MONOCHROMATOR

FILTER
WATER SHUTTER THEMOP'LE
IN WATER
9 OUT
<- AIR

L J IN

Figure 4. Schematic of the exposure instrumentation. See
text for details of description of the system,
source measurement, and exposure procedures.

SOOOW Xe ARC

PLANE OF EXPOSED EYE

MICROVOLT
AMMETER

SI

('lo)

TRANSMITTANCE

IOO'

 

 

 

 

IO}
0

760 ' "60' I560 ' 1960 '23'00 ' 27bo ‘ 3:60 '

WAVELENGTH (nm)

Figure 5. _ Spectral transmittance of the Schott RG-715 filter.

two advantages. First, the radiant energy was concentrated into a smaller
area increasing the irradiance and, second, the vertical rectangular beam
could be directed to expose only the lens (with a dilated pupil), only the
iris, or both the lens and the iris simultaneously. The flexibility allowed
by the focused beam proved helpful during the course of the research, but eye
movements with the focused beam resulted in greater variability in the thres-
hold exposure data than that when the unfocused beam was used. The beam
profile was essentially flat throughout its extent.

A special device was constructed and incorporated into the optical system

to insure the proper alignment of the animal's eye with the optical beam
(Figure 6). The device consisted of two "L" shaped tungsten source filaments
which were aligned precisely with the central optical axis of the monochromator
optics and were optically focused at the correct distance for exposure. When
the animal was placed at the proper distance and aligned with the optical

axis for exposure, the "L" filaments formed a cross or "+." A slight lateral
or longitudinal misplacement resulted in the loss of the cross of "+" image

as illustrated in Figure 6 for longitudinal displacement. The alignment device
was used for the initial alignment of the animal's eye for exposure and
periodically throughout the experiment to check on alignment.

Infrared Source Measurement

 

The IR source was measured with an Eppley l6—junction thermopile traceable

to an NBS standard source. The thermopile was located in the same position
that the animal's cornea would occupy during exposures. The readout amplifier
was a Keitheley 150 B microvoltmeter. The irradiance incident on the thermo-
pile was determined by the following formula:

E = K'VT (1)

where E is the irradiance in W'cm‘z, K the thermopile calibration constant
in W-cm‘z'mV'l, and VT the thermopile voltage in mV. Equation (1) is valid
for the measurement of the irradiance of sources with a diameter equal to or
larger than the aperture of the radiometer. To use the thermopile to measure
source sizes smaller than the area of the thermopile detector surface, the
irradiance formula must be corrected as shown below for the area effects:

E = K'VT- £9 (2)
AB
In equation (2) AD is the area of the thermopile detector surface and AB is
the beam area of radiation striking the detector.
The radiant exposure (H) in J-Cm'2 was calculated by use of the equation:
H = E't (3)

where H is the radiant exposure in J'c:m'2 and t is the exposure duration
in seconds.

14

 

 

   
  

/ PROJECTOR I a

PROJECTOR 2 [a

Figure 6. Schematic of the optical alignment system. Projector 1
located vertically above the monochromator produced an
"L" and project 2 below produced an inverted "L.” The
projectors were aligned to produce a "+" on the corneal
apex when the eye was aligned laterally, vertically, and
longitudinally from the monochromator.

    
   

FROM
MONOCHROMA‘I’OR

 

 
    

EXPOSED E YE

 

T 00
CLOSE

IN
FOCUS

TOO
FAR

Thus, the source can be measured in irradiance or radiant power units and
the exposure duration t varied to obtain different values for the radiant
exposure H. The exposure duration t, irradiance E, and radiant exposure

H were determined for each exposure using the above procedures. It was
estimated that the measurement accuracy of the source was approximately

‘: 15%. Figure 7 presents an example of the relative spectral irradiance
of the 5 kW Xenon source measured at 50 nm wavelength intervals up to

2100 nm through the RG—715 filter. The spectral irradiance of the source
was less than 1.5 x 10'4 W-cm'2 for 50 nm waveband intervals up to 3500 nm.

Experimental Animals*

 

Healthy adult cynomolgous monkesy (Macaca fasciculais), 6.6 to 8.0 kg in
weight,and pigmented rabbits, 2 to 3 kg in weight, were the animals used
during experimentation without regard to sex.

Since research on UV, visible, and IR effects on ocular structures has been
primarily with the rabbit, continuation of the IR research with the rabbit
would allow better comparison of the different radiation damage research.
The anatomy of the rabbit eye is well known and the differences from the
human eye are well established. The rabbit is small, easily handled, and
can be examined readily with the biomicroscope and ophthalmoscope.

The cyanomolgous monkey was used because its eye, although smaller than the
human eye, more closely approximates the human eye. Therefore, the monkey
exposures allow better validation of any proposed protection criteria document.

Exposure Procedures

The experimental protocol was initially intended to determine the action
spectrum for IR in 50 nm bandwidths over the 700 to 1400 nm wavelength range.
Preliminary exposures using 50 nm waveband at 1050 nm with 1.48 mW irradi-
ance showed that exposure durations up to 13,480 3 or 20 J-cm"2 did not
result in ocular damage. Care was taken to perform all exposures under as
normal a physiological condition as possible; however, the preliminary expo—
sures indicated that anesthesia was necessary to prevent discomfort to the
animal since the pupil constricted and the nictitating membrane began to
move over the cornea within 40 minutes after the exposure began. A second
part of the experimental protocol was to test the hypotheses of Goldmann

and of Vogt on the development of cataracts from exposure to IR.

In these experiments, the IR spectrum was the output of the source that was
transmitted through the RG-715 filter. The full Spectrum output included the
UV, visible, and IR spectra. The exposure durations were given within a

15 minute to 8 hour time range. These durations were defined in an attempt

to limit the laboratory exposures to durations equivalent to the use of sources
in industrial processes and to simulate the normal working day for humans.

* The care of the experimental animals used or intended for use in the
performance of this research complies with "The Guide for the Care and
Use of Laboratory Animals," Institute of Laboratory Resources, National
Academy of Sciences — National Research Council (HEW Publication (NIH) 73-23)
and "The Principles for Use of Laboratory Animals," Department of Health,
Education and Welfare.

16

 

SPECTRAL IRRADIANCE ( w~cm'2 'peISO nm bandwidth I

 

Figure 7.

 

o IRRADIANCE OF THE SOURCE
O INCIDENT ON THE AQUEOUS
0 INCIDENT ON THE LENS

D INCIDENT ON THE VITREOUS
A INCIDENT ON THE RETINA

2000'
WAVELENGTH (nm)

The spectral irradiance of the 5 kW Xenon source measured
with an Eppley thermopile in 50 nm wavebands at the plane
of exposure after transmittance through the Schott RG-715
filter. The irradiance incident on the aqueous, lens,
vitreous, and retina was calculated from the rabbit trans-
mittance data of Barker.

17

To accomplish the goals of the experimental protocol, the following exposure
conditions were used:

1.

The

Infrared spectrum, unfocused beam, and normal pupil — The exposure beam
was essentially collimated,and it covered the entire cornea, the iris,
and the pupil since the beam was 2.5 cm x 1.5 cm in size at the plane

of the cornea.

Infrared spectrum, focused beam, and miotic pupil — The focused exposure

 

beam was 0.8 cm x 1.5 cm at the plane of the cornea. The miotic pupil
allowed the beam to simultaneously expose the iris and the anterior lens
surface through the pupil. The data were intended to study cornea, lens,
and iris effects.

Infrared spectrum, focused beam, and normal pupil -— The exposure condi—

 

tions were intended to study only corneal threshold effects.

Infrared spectrum, focused beam, dilated (normal) pupil - The focused

 

beam could be directed through the dilated or normal pupil to the
retina. These exposures were intended to study the effects of IR
exposure to the retina.

Full spectrun,focused beam, and miotic pupil — The focused beam allowed

 

maximum exposure to the cornea, iris, and anterior surface of the lens.
The exposures were intended to establish the full spectrum (UV, visible,
and IR) effects on the cornea and the lens to study the additive or
synergistic effects of the UV and visible spectrum to the IR spectrum.

Full spectrum, focused beam, and dilated pupil -— These exposures were

 

intended to study corneal, lenticular, and retinal damage for additive
or synergistic effects of the ultraviolet or visible spectra to the
IR spectrum.

following procedures were used for each experiment:

Ketamine HCl, 20 mg/Kg body weight, was administered intramuscularly (IM)
to the rabbit for anesthesia. For the monkey, 15 mg/Kg body weight of
Ketamine HCl was administered IM. Repeat doses of 5 mg of Ketamine were
given as indicated by the arousal of the animal or by excess movements
of the eyes.

For pupillary constriction (miosis) two drops of l% pilocarpine ophthalmic
solution were instilled into the eye to be exposed at 5 minute intervals
for a total of 4 drops. This procedure was accomplished approximately

20 minutes prior to the exposure of the eye to IR.

Pupillary dilation in the rabbit was achieved by administering two drops

of 5% Homatropine followed in 5 minutes by two drops of 1% Tropicamide.
Primates were given one drop of 1% Tropicamide in each eye.

18

 

4. Prior to exposure, each eye was examined thoroughly with the biomicro—
scope and the indirect ophthalmoscope in accordance with the Evaluation
Procedures. Animals with anomalies of the anterior ocular structures
(cornea, anterior chamber, iris, and lens) or the retina were rejected.

5. Rabbits were placed in a specially designed holder for exposure sessions
and biomicroscopic examination. Primates were placed in a stereotaxic
instrument for exposure and examination (Figure 8).

Primates were permitted to blink without restrainingthe eyelids; however,
occasionally a reflex or protective ptosis of the upper lid had to be
prevented by manually elevating the eyelid. Extreme care was taken to
minimize corneal dehydration during this procedure. An advantage in using
ketamine hydrochloride was that sensory reflexes are present and one can
observe sensory responses of the animal.

Evaluation Procedures

 

Ocular damage criteria are given in Table 1. Two observers independently
examined the eye immediately after exposure to determine the criteria status
and the classification for each structure of the eye as given in Table I.

The criteria for the severity of the exposure for each structure was indi—
cated as negative (—), possibly positive (i), positive (+), moderately
positive (++), extremely positive (+++), and severely positive (++++) on

the laboratory record sheet. If more than 50% of the criteria for any
structure were positive (+), that structure was classified as above threshold
(+); if 50% of the criteria for any structure were positive (+), the criteria
resulted in a possibly positive (i) or threshold classification (H); less than
50% positive criteria resulted in a below threshold classification (—). The
exposed eyes were examined, criteria established, and classifications made
immediately after exposure, 24 hours after exposure, and at regular intervals
as dictated by the severity of the damage for as long as 3 months.

After the experimental exposure and follow-up of an eye were completed, a
review of the record of ocular damage was made,with all investigators present
and participating, to arrive at a final classification. The final classifi—
cation was based on the ocular structures damaged and the severity of the
damage.

Any definite corneal, lenticular, iris, vitreous, or retinal damage was
classified as positive (+). Minimal damage to the cornea, iris, lens,
vitreous and retina that reversed to normal within 24 hours after exposure
was classified as threshold (H). If no ocular structures were damaged,
the final classification was negative (—). When a rated exposure was
classified as negative and the next higher radiant exposure was classified
positive but their difference was less or equal to the error of source
measurement, the threshold radiant exposure (H) was calculated as the mean
of these two exposures.

19

 

Figure 8.

Cynomolgous monkey restrained in a modified stereotaxic
system in the correct position for irradiation. Ketamine
hydrochloride was used for anesthesia.

 

Figure 9.

A dry swollen nictitating membrane was frequently observed
following high levels of radiant exposure.

20

 

Table I.

Ocular Structure

Cornea

a. Epithelium
b. Stroma
c. Endothelium

Anterior Chamber

Lens

Iris

Vitreous Humor

Retina

Instrument

Biomicroscope

Biomicroscope

Biomicroscope

Biomicroscope

Biomicroscope
Indirect
Ophthalmoscope

Biomicroscope
with ruby lens

Indirect
Ophthalmoscope

21

Ocular Structures Examined Pre- and Post-Exposure
for Damage Criteria

Expected Damage

Corneal opacification, debris,
haze, exfoliation

Thickening

Haze

Opacities

Endothelial damage or
disturbance

Aqueous flare
Aqueous cells
Iritic pigment in aqueous

Increased prominence in
anterior and/or posterior
suture line

Anterior capsular Opacities

Pos ter ior capsular opac it ies

Increased opacification of
cortex and/or nucleus

Exfoliation of the Capsule

Sluggish pupillary reaction
Synechia formation, posterior
Stromal haze

Vascular engorgement

Necrosis

Exfoliation of iris stroma
Pigmentary dispersion

Haze
Opacification
Syneresis

Vascular disturbance
Loss of pigment
Retinal edema
Retinal lesion (burn)

RESULTS

IR exposures were made on 100 pigmented rabbit eyes and 10 primate eyes
(cynomolgous monkeys) during the experiments. The data are presented in
Tables II through VI for the rabbits and in Table VII for the primates.

A summary of the radiant exposures classified as threshold for the cornea,
iris and crystalline lens is given in Table VIII. The exposure conditions
are included in the legends for each table. The column headings for each
Table provide the animal identification number, the source irradiance in
w-cm‘z, the exposure duration in seconds, the radiant exposure in J-cm'z,
and a classification of the results of the exposure for the cornea—C,

the iris—I where applicable, the crystalline lens—L, and the retina-R.

The animal identification number is composed of three letters and arabic
numerals; for example, IRllR or L and IP4L. The capital letter I identified
the waveband of exposure as including IR, the capital R identified the
animal as the pigmented rabbit and the capital P as the primate, the arabic
numeral contained the number of the animal, and the R and L indicated which
eye was exposed. Finally, H was used to indicate that the threshold radiant
exposure had been achieved with the subscript indicating the part of the eye.
The exposure durations in the results may differ slightly from that given
due to rounding procedures.

It can be seen from Table II that neither corneal, iris, lenticular nor
retinal threshold exposures were achieved for the IR (715 nm — 1400 nm)
with an unfocused beam in spite of exposure levels exceeding the damage
exposure data which are published in the literature and referenced in this
report. In addition, three exposures were made using a 50 nm waveband
unfocused source centered at 1050 nm. Radiant exposures to about 14,000 J-cm‘2
were made without apparent effects to the cornea, iris, or lens. These
results caused changes in the research protocol to include the focused beam
in order to increase the irradiance at the cornea, dilated pupil to allow
exposure of the lens only, miotic pupil to allow the iris and the lens to
be exposed simultaneously or independently, and the use of the full source
spectrum in order to compare IR exposures with exposures which contained

UV and visible radiation.

The data in Table III were obtained using the 0.8 x 1.5 cm focused beam and

a miotic pupil. The iris and the lens were exposed simultaneously. It can
be seen that the threshold exposure for the cornea, iris and lens varies

with the rate of delivery of the energy. For example, the corneal threshold
exposure is close to 5000 J-cm"2 at irradiances below 40 w-cm‘2 and is about
1000 J-cm“2 for irradiance levels above 4 W-cm‘z. The lenticular threshold
exposure decreases as the rate of delivery of the energy increases (Figure 10).
At low levels of irradiance the threshold for the lens is less than that of
the cornea. This means that the lens could be damaged in low levels of
irradiance or very high short duration exposures, without the cornea becoming
involved; however, at high levels of exposure the cornea would become damaged

22

 

 

Table II. Rabbit Infrared Spectrum Exposure Data
Wavelength Range, UnfOCUSEd Beam, and
Normal Pupils

Radiant
Animal Irradiance Exposure Exposure Classification
Number W-cm‘2 x 10'3 Duration-s J-cm‘2 C L R
IR4R 32.3 167 5 — — —
IR3R 32.3 335 11 — — —
IR5L 32.3 837 27 - — -
IR8L 31.4 1,590 50 — - -
IR6R 31.4 3,180 100 — — —
IRlOR 34.5 5,797 200 — — —
IR9L 43.4 6,912 300 - — —
IR2R 41.2 14,570 600 - - -
IR2L 47.9 20,895 1,000 - — —
IR9R 45.6 29,000 1,323 - — -
IRllR 48.2 29,000/day 4,196 - - -
For 3 days
IR12R 48.3 29,000/day 7,004 — — —
For 5 days
IR13L 66.8 29,000/day 9,686 — — —
For 5 days

23

Table III. Rabbit Infrared Exposure Data
Wavelength Range, Focused Beam; and
Miotic Pupil

 

Radiant
Animal Irradiance Exposure Exposure Classification
Number w-cm“2 Duration-s J-cm"2 C I L
IR37R 2.93 1365 4000 — HI HL
5500** +HC
IR24L 2.75 2636 7250 + + -
IR25L 2.75 2636 7250 + + .1
IR28R 2.75 2727 7500 i i —
IR28L 2.75 2818 7750 + + —
IR27R 2.33 3437 8010 - + —
IR27L 2.33 3652 8510 — +to++ —
IR36R 3.39 960 3250 — + -
IR36L 3.39 1034 3500 - + —
IR35R 3.39 1108 3760 — HI .i
IR35L 3.39 1181 4000 — + HL
IR34R 3.39 1255 4250 - + +
IR34L 3.39 1329 4500 - + +
IR33L 3.49 1362 4750 HC + +
IR18L* 3.39 1475 5000 + - —
IR33R 3.49 1434 5000 + + +
IR32L 3.59 1460 5240 + + +
IR32R 3.59 1600 5740 + + +
IR16L 3.49 1912 6670 + + +
IR23L* 3.59 1877 6740 + + —
IR22L 3.59 1946 6990 + + +
IR19L* 3.49 2000 6980 + + -
IR21L 3.39 2212 7500 ++ + +
IR50L 4.14 637 2640 - — —
IR49L 4.14 690 2860 - - -
IR49R 4.14 734 3040 - - -
IR48L 4.14 796 3300 — - —
IR52R 4.02 870 3500 — HI .i
IR53R 4.02 870 3500 - + HL
IR48R 4.14 849 3510 - + HL
IR51L 3.80 986 3750 - + ito+
IR53L 4.02 933 3750 - + HL
IR51R* 3.80 1053 4000 - + :
IR52L 4.02 995 4000 — + —
5000** HC

* Animal moved excessively during exposure.
**Mean extrapolated exposure.

24

 

 

Table III. continued

 

Radiant

Animal Irradiance Exposure Exposure Classification
Number W-cm"2 Duration-s J-cm‘ C I L
IR3OR 3.81 1640 6250 + + +
IR3OL* 3.81 1772 6750 + + ito+
IR29R* 3.81 1903 7250 + ++ ito+
IR29L 3.81 2034 7750 + ++ +
IR59R 4.55 275 1250 HC HI —
IR59L 4.55 330 1500 + + —
IR58R 4.55 384 1750 + + -
IR58L 4.55 439 2000 + E —
IR57L 4.44 507 2250 + + HL
IR57R 4.44 563 2500 + + .i
IR55L 4.66 590 2750 + + +
IR56L 4.44 676 3000 + + +
IR55R* 4.66 644 3000 + + —
IR56R 4.44 732 3250 + + .i
IR54L 4 .66 695 3240 + + _-c_-
IR54R 4.66 751 3500 + + +

* Animal moved excessively during exposure.

25

Figure 10.

THRESHOLD RADIANT EXPOSURE(chm’2)

  
  

 

 

61
HC 0---o\ ‘
\
5- 9
\
\
\
4- ”L I
\
\
INFRARED > 7l5 nm “
3' MIOTIC RABBIT EYE
I
\
2' I
I
I
o
'—

IRRADIANCE (Wcm'z)

The threshold radiant exposure versus irradiance for the
rabbit. These data show that the threshold varies with

the rate of delivery of the source when the irradiance
exceeds 3.5 w-cm‘z.

 

earlier than the lens. These data also demonstrate greater variability
due to movements of the animal during exposure. None of the exposures
caused damage to the retina.

Table IV presents the data for the IR spectrmn,focused beam, and with a
normal pupil. These dataverr:intended as a check on the corneal threshold
for an almost constant level of irradiance. The corneal threshold expo—
sure was 5500 J-cm“2 for an irradiance of 3.6 W'Cm_2. These data compare
quite favorably with exposure values obtained using a fOCused beam and
miotic pupil (Tables III and IV) when the i 15% measurement error for the
source is considered. An exposure at 6000 J-cm'2 with an irradiance of
2.9 W-Cm"2 resulted in a slight stippling and loss of the orange peel
appearance at the anterior capsule of the lens.

The effects of retinal exposure are presented in Table V. It is not
possible using these data to make valid conclusions regarding the level
of IR necessary to produce retinal damage. The optics of the source
were not constructed for retinal effects study and extensive modification
would have been necessary. When an animal was aligned to the optical beam,
the beam was directed toward the band of medullated nerve fibers on the
retina. Re—orientation of the animal would result in compensatory eye
movements. One must be able to move the optical beam while keeping the
animal stationary to study retinal effects. Despite these limitations,

a retinal burn was found in animals IRlSR and IRl7L and retinal damage
was caused in animals IR47R and IR39L from the IR spectrum. In addition,
retinal damage was found in animals exposed to the full source spectrum
with a focused beam and a dilated pupil. In each instance the exposure
was greater than 6000 J-Cm' at the cornea but these data do not reflect
true retinal damage exposure value for IR.

A corneal lesion as observed by the biomicroscope, progressed with
increased exposure levels from an initial epithelial haze, to a stromal
haze, and then to erosion of the epithelium. A qualitative description
of the effects of the exposure of the rabbit eye follows:

Adnexa:

No damage to the eyelids in the rabbit was produced. A drying and swelling
of the nictitating membrane (Figure 9) was a common observation at the
higher radiant exposures for both IR and full Spectrum radiation.

Cornea:

The corneal changes were apparent immediately after exposure. This

confirmed the thermal nature of the lesion in contrast to the longer
latencies found in the abiotic UV lesions. The damage to the cornea

varied from epithelial haze to corneal erosion (Figure ll). All corneal
damage healed rapidly, usually within 24 hours, with no scarring and the
return of the cornea to a clinically normal transparency. No endothelial
damage was found for the levels of radiant exposure used in these experiments.

27

Table IV. Rabbit Infrared Exposure Data,
Focused Beam, Normal Pupil for
Corneal Threshold Study

Radiant
Animal Irradiance Exposure Exposure Classification
Number W-Cm'2 Duration-s J-cm’2 C L R
IR41R 3.39 886 3000 - - —
IR41L 3.39 1033 3500 - — —
IR37L 2.90 1380 4000 — — -
IR40R 3.39 1181 4000 - — -
IR40L 3.39 1477 5000 +to- - —
IR42R 3 .60 1390 5000 Eto— - -
IR43R 3.60 1460 5260 jfio- — —
IR44R 3.60 1529 5500 Hc — —
IR42L 3.60 1599 5760 + — -
IR39L 3.39 1772 6010 +to++ — —
IR38R 2.90 2068 6000 + — -
IR38L 2.90 2068 6000 ito+ — -
IR39R 3.39 2067 7010 + - -

28

Table V. Rabbit Infrared Exposure Data, Focused
Beam, Dilated Pupil for Retina Effects Study

Radiant
Animal Irradiance Exposure Exposure Classification
Number w-cm‘2 Duration—s Jocm‘2 C L R
IRl7L 3.49 1891 6600 ++ - +
IR45R 3.39 2067 7010 + — -
IR45L 3.39 2362 8010 I — -
IR46L 3.81 2100 8000 + - —
IR47R 3.81 2100 8000 + - :
IR46R 3.81 2625 10,000 ++ - -
IR47L 3.81 2625 10,000 ++ - —

29

 

Infrared corneal burns showing epithelial haze, stromal haze
and epithelial exfoliation.

Top: Immediately after exposure.

Bottom: One hour after exposure.

Figure ll.

30

Iris:

Miosis due to irritation was observed approximately 5 minutes after an
exposure began for those rabbits which had not been administered topical
miotics or mydriatics. There was a stromal haze and swelling in the region
of irradiation. Aqueous flare was only slight with cells noted occasionally
in the anterior chamber when they could be detected. At exposure levels
which produced lenticular damage, the iris involvement became more severe
with the final stage being the production of fibrinous inflammatory by—
products.

Lens:

Lens damage could not be produced by direct exposure of the lens to the
irradiance and radiant exposure levels used in the experiments. Lens

damage was easily produced when the iris overlying the lens was irradiated
(Figures 12 and 13). At suprathreshold levels of radiant exposure, the
anterior capsule and anterior stroma became slightly hazy and a few minute
subcapsular opacities were found. The characteristic progression of the
lesions for higher levels of radiant exposure is shown in Figure 13. The
involvement of the overlying iris was considerable with exfoliation of

the posterior pigment onto the anterior capsule of the lens together with
fibrinous inflammatory material. There was an immediate involvement of

the anterior lens and the anterior capsule (Figure 14A). They appeared

hazy and white in the area underneath the irradiated iris. Within 1% hours
after exposure, the lenticular lesion began to change into a white opacity
surrounded by an area of haze (Figure 14B). This lenticular area corres—
ponded to the overlying area of the irradiated iris which was in contact
with the lens capsule (Figure 14C). The formation of the lenticular opacity
was complete within one month, but occasionally residue pigment from the
posterior of the iris remained on the anterior lens capsule (Figures 15 and 16).

Retina:

No retinal damage was observed following irradiation when the pupil had
been miotic during the period of exposure. Retinal burns were produced
(Figures 17 and 18) with IR alone and the full spectrum when the pupils
were dilated. Threshold data could not be obtained because the exposure
system was not designed to localize an exposure on a chosen area of the
retina.

Table VI provides data for rabbit full spectrum, fOCused beam with miotic

and dilated pupils. The purpose of these experiments was to determine if

UV and visible radiation were additi e or synergistic with IR. The threshold
radiant exposure was about 750 J'cm_ for the cornea and 2250 J-cm‘2 for the
lens. These threshold values may be compared with a corneal radiant expo—
sure of less than 1200 J-cm'2 and a lenticular radiant exposure of 2250 J-cm‘2
using only IR and equivalent exposure conditions in Table VIII.

Low levels of IR exposure produced no obvious subjective signs in the rabbit.
As the exposure levels increased, a reflex blepharospasm of the lids and

31

 

Figure 12. Extreme swelling of the iris stroma with ectrOpion of
the uveae. The radiant exposure was 12,500 J-cm‘2
delivered in 2567 s (IPSR) with an irradiance at 4.87 W.cm‘2.

 

Figure 13. Narrow strip of iris pigment is seen adherent to the anterior
capsule of the lens. Radiant exposure was 12,500 J'cm'2
delivered in 2567 s with an irradiance of 4.87 w-cm"2 (IPSR).
One month after exposure.

32

C

Figure 14.

 

D

Characterisitc progression of lenticular opacities in the

rabbit.

A. Epithelial haze, stromal haze of the iris, opacification
of the lens in the irradiated area underlying the iris.

B. Discrete lenticular lesion surrounded by haze, upper
border corresponds to the lower border of the pupil.
Pigment spots and fibrinous inflammatory material seen
just above pupillary margin.

C. Lenticular lesion has become well organized.

D. Lesion characteristic of IR or full spectrum exposure.

Iris involvement is greatly reduced with only a small
marginal tuft apparent. IR31R, 2250 J-cm‘z, 484 3, full
spectrum, miotic pupil at an irradiance of 4.66 W-cm‘z.

33

 

Figure 15. Retroillumination of the lenticular opacity shown in Figure 14D
reveals the granular nature of the perimeter of the lesion. The
translucency of the center of the lesion suggests that the
disturbance is intrafibrillular rather than structural damage
or protein coagulation of the lens fibers (IR31R).

 

Figure 16. Lenticular lesions of the rabbit from exposure of the overlying
iris with 8030 J-cm—2 in 1800 s to the full spectrum beam with
a miotic pupil. Lesions such as these were consistently 2
reversible within 4 weeks (IRlSR). The irradiance was 4.46 w-cm' .

34

Figure 17.

Figure 18.

 

Rabbit chorioretinal lesion produced through a dilated pupil.
The central burn is surrounded by severe retinal edema.

Radiant exposure was 6600 J-cm‘2 of infrared radiation measured
at the cornea and delivered in 1891 s (IRl7L) with an irradiance

of 3.49 w-cm‘z.

 

Severe chorioretinal burn of the rabbit retina produced through
a dilated pupil. The radiant exposure was 6000 J'cm— full
spectrum measured at the cornea and delivered in 1288 s (IR17R)
with an irradiance of 4.66 w-cm“2.

35

Table VI. Rabbit Full Spectrum Exposure Data

 

Radiant
Animal Irradiance Exposure Exposure Classification
Number w~cm“2 Duration—s J-cm'2 C I L
A. Focused Beam, Miotic Pupil
1R26R 3.81 52 200 — - —
IR26L 3.81 131 500 - — —

750* HO

IR25R 3.81 262 1000 + HL —
IR31L 4.65 258 1200 + + +
IR24R 3 .81 525 2000 + + i
IR19R 4.66 429 2000 + + HL
IR23R 4.66 483 2250 + + +
IR31R 4 .66 484 2250 + + +
IR22R 4.66 536 2500 + + +
IR21R 4.46 673 3000 + + +
IR18R 4.66 858 4000 ++ + +
IRISR 4 .46 1800 8030 ++ -H- +
B. Focused Beam, Dilated Pupil
IR17R 4.66 1288 6000 + — —
IR20R 4.66 1800 8390 + — —
C. Unfocused Beam, Miotic Pupil
IR15L 0.11 7200 790 + — —
IR14L 0.16 7200 1150 + + —

* Mean extrapolated exposure

36

miosis of the pupil in normal animals were found. The total spectrum expo-
sures were accomplished only at relatively high levels of irradiance and
produced extreme photophobia, reflex blepharospasm, and pupillary constriction.
There was a tendency for the rabbit cornea to become "dry" and corneal

damage from exposure was evident at lower radiant exposure levels when the
"drying" occurred. The results of "drying" were a loss of corneal trans—
parency, lowered corneal radiant exposure thresholds, and an effective
protection of the iris and lens resulting in the raising of their radiant
exposure thresholds.

The rabbit data generally showed greater variability because it took time

to devise an adequate restraint for the eyelids. In early exposures some
rabbits had no restraint of the lids and responded with a protective ptosis,
a partial closure of the nictitating membrane, or a complete closure of their
eyes. Restraint of eyelid movements was attempted by using an ocular
speculum, by using surgical tape to hold the lids open, and by using fixation
sutures in the anterior part of the ocular globe. The ocular speculum was
abandoned quickly because the interruption of the tear flow across the
cornea resulted in corneal drying affecting the exposure levels. Taping

the lids open was the method adopted because it allowed better control of

the tear flow and reduced the subsequent drying of the cornea.

The primate exposure data are given in Table VII. The radiant exposure

levels required to achieve a threshold response were 8000 J-cm"2 for the
cornea and iris and 12,500 J-cm"2 for the lens. These values are considerably
higher than those found for the rabbit. All primate exposures included the
iris and part of the pupil with the focused beam. A qualitative description
of each of the ocular components should assist in understanding the result:

Adnexa:

No damage occurred in the eyelids of the monkey.

Iris:

The iris involvement was essentially the same as that for the rabbit.
Cornea:

At irradiance levels above 4.0 W-cm‘z, the blink rate of the monkey increased
and probably afforded some protection to the cornea. It was felt that the
increased blink rate was caused by reflex activity induced by increased heating
of the cornea. Other effects observed were increased epithelium debris and
haze. No significant corneal disturbance was produced until the radiant
exposure attained 8000 J-cm‘z; however, these signs may have resulted from
forcibly opening the eye (with normal lid position) because of the excessive
blinking. Nevertheless, higher levels of radiant exposure resulted in more
severe damage which included granules, stippling, epithelial haze, and stromal
haze.

37

Table VII. Primate Infrared Exposure Data,
Focused Beam, and Miotic Pupil

 

Radiant

Animal Irradiance Exposure Exposure Classification
Number W'cm_2 Duration-s J-cm'2 C I L
IPlL 4.55 440 2000 - i_ —
IP2L 4.55 494 2250 - i. —
IP2R 4.55 549 2500 — .i -
IPlR 4.55 604 2750 - :_ —
IP3R 4.87 718 3500 - i_ -
IPSL 4.87 1437 7000 — + +
IP4R 4 .23 1891 8000 BC HI Eto+
IP4L 4.23 2364 10,000 110+ + HL
IPSR 4.87 2567 12,500 + + +
IPSL 4.87 3080 15,000 + + +

38

Iris:

No damage to the iris was found until a radiant exposure of 8000 J'cm'2
was reached. At this radiant exposure a localized stromal haze of the
iris was seen. The stromal haze increased and swelling was seen at the
10,000 J-cm‘2 radiant exposure. At 12,500 J-cm‘z, flare was seen in the
anterior chamber and there was an extreme swelling of the iris stroma
with ectropion of the uvea (Figure 16). One month later, a narrow strip
of pigment was seen adherent to the anterior lens capsule (Figure 17).
This pigment probably represented remnants of the posterior pigment
epithelium of the iris and indicated an old inflammation of the iris.

Lens:

No lenticular damage was produced by direct irradiation of the lens through
the pupil at exposure levels up to 15,000 J'cm‘z. With radiant exposures

of 8000 J-cm‘2 and 10,000 J-cm"2 through the iris, only very subtle lens
changes were detected. These included a few minute subcapsular opacities

at 10,000 J-cm‘2 which were visible only with high magnification and
specular reflection. Subcapsular haze and discrete opacities of the primate
lens were found with radiant exposures of 12,500 J°c1n‘2 (Figure 16). No
permanent cataracts were produced.

Retina:
No retinal damage occurred to the primates during exposure.

Table VIII summarizes the threshold exposure data for the cornea, iris, and
the lens using the IR spectrum and the full spectra, and with miotic or
dilated pupils for both the rabbit and the primate. These data demonstrate
that the radiant exposure depends on the level of irradiance for the IR
spectrum. The radiant exposure to attain a threshold response for the
primate requires an increase of a factor of about 8.0 when compared to

the rabbit. These data also show that with equal levels of irradiance, the
rabbit radiant exposure threshold compares favorably for both the IR and
full Spectra exposures.

39

Table VIII. Summary of All Threshold Radiant Exposure (J-Cm_2) Data
for the Cornea, Iris, and Lens

Irradiance (W-cm‘z) Cornea Iris Lens

A. Rabbit Infrared Spectrum, Focused Beam, Miotic Pupil (Table III)

2.3 — 2.9 5500 4000 4000
3.4 — 3.6 4750 3760 4000
3£-—4J SWO 3W0 3WD
4.4 - 4.7 1250 1250 2250

B. Rabbit Full Spectrum, Focused Beam, Miotic Pupil (Table VI)

3.8 750 1000 2000

C. Primate Infrared Spectrum, Focused Beam, Miotic Pupil (Table VII)

4.2 - 4.9 8000 8000 10,000

40

DISCUSSION

The mechanism of the formation of IR cataracts has centered around three
hypotheses. Vogt (15, 16) interpreted his data to indicate that the

IR induced cataracts were the result of the direct absorption of the radiant
energy by the crystalline lens. There is some experimental evidence to
support Vogt since ocular transmittance measurements demonstrate absorption
bands of IR in the 800 nm to 1200 nm bandwidth. However, Vogt's own
description of the source used to expose the animals could negate these
interpretations. Vogt described the source as a carbon arc (Bogen lamp)
"whose light was filtered through water, iodine and carbon disulfate"

(deren Lict durch Wasser und Jod schwefelkohlenstoff filtriert wurde) (16).
It is known that water absorbs IR in bands much like the aqueous and the
vitreous, thus reducing the IR available for absorption by the anterior
segment of the eye. Furthermore, iodine readily transmits the UV radiation
produced by the carbon arc lamp. Vogt's descriptions of conjunctivitis and
lenticular opacities are the same as those found for UV exposure (37). Thus,
it is suspected that the direct absorption by Vogt's animals was UV radiation
rather than IR.

Verhoeff and Bell (9) suggested that the Vogt hypothesis was not sufficient.
They argued that the outer surface of the cornea was air cooled and that

the anterior capsule of the lens was cooled by circulation of the aqueous;
thus, the cataract formed on the posterior surface of the lens. They further
postulated that the heat interfered with the function of the ciliary body
which subsequently interfered with the metabolism of the crystalline lens.
Nearly every researcher, including Verhoeff and Bell, has reported anterior
lenticular opacities and corneal involvement. Therefore, the air and
aqueous are not sufficient to prevent anterior lens and corneal involvement.
If the ciliary body was damaged some evidence should be seen in the aqueous
and very little or no aqueous involvement has been observed. Thus, it
appears that the model of Verhoeff and Bell, also, does not account for the
experimental evidence. On the other hand, in many experiments the cornea
could be dry during the exposure.

The actual mechanism of the formation of IR cataracts was probably proposed
by Goldmann (17—24). He interpreted his research to indicate that the
subsequent cataract was due to the IR being absorbed by the iris and the
indirect transmittance of the heat to the lens. Goldmann believed that the
effects of the direct absorption of the IR were minimal. The experimental
evidence accumulated has been substantially in favor of the hypothesis of
Goldmann (30). Some research (38, 39) suggests that both direct absorption
by the lens and indirect heating of the lens through the absorption of the
iris account for IR induced cataracts. Our research supports the hypothesis
of Goldmann because we were not able to produce a lenticular opacity by
directly exposing the lens but obtained lenticular opacities only when the
iris was exposed and then the opacity was directly beneath the area of the
exposed iris. The contribution of direct exposure to the lens appears to
be minimal.

41

What does an IR induced cataract or lenticular opacity look like? Where

is the lenticular opacity located within the crystalline lens? Meyenhofer (11)
described the chronic exposure "glassworker's cataract" as a posterior
cortical opacity which took the shape of "stars.” Edbrooke and Edwards (40)
contended that heat-induced cataracts started with an initial cobweb—like
appearance and developed into a well—defined opacity in the outer layers of
the posterior cortex of the crystalline lens. Vogt (15, 16) described grayish
dots in the anterior lens epithelium from acute exposure which progressed to
a posterior subcapsular opacity. Verhoeff and Bell (9) reported that the
initial response was a mitosis of the lens epithelium in the area beneath
and in contact with the iris pigment epithelium. They also described the
posterior subcapsular opacity as a later phase of development. Goldmann's
description (19) was almost identical to that given by Vogt. Langley,
Mortimer and McCullough (30) described the clinical appearance as beginning
in the region of exposure under the iris as diffuse, fine gray anterior
subcapsular dots with iris pigment which may be adherent to the anterior
lens capsule. The next stages involved clouding of the equator, migration
into the anterior cortex of the anterior grayish dots, the appearance of a
saucer—shaped posterior opacity, and the joining of the anterior cortex—
equator-posterior complex into a "U" shaped opacity. Their conclusion was
that the posterior lenticular opacity had a latent period of 60 to 90 days.

The latent period for the cataract to develop may assist in establishing
whether or not the lenticular opacity was caused by IR. If the lesion

was induced by IR through the action(3fheat or temperature, the lesion

should occur immediately after the exposure achieved or exceeded threshold.
Vogt's description of the anterior lens epithelium dots indicated that they
were the initial mitotic response and most certainly occurred within the

first 24 hours. Goldmann also described the anterior subcapsular changes

as an immediate or an initial response. Langley, Mortimer and McCulloch
stated that their fine gray anterior subcapsular dots occurred within 24 hours.
In our present study, the latency for the threshold response was as short as
1% hours and never as long as 24 hours but almost consistently close to

6 hours after exposure. It appears that most of the research has demonstrated
anterior lens epithelium dots or granules occurring almost immediately after
exposure and not more than 24 hours after exposure.

It appears that the anterior subcapsular opacity is common to almost all
types of radiation induced cataracts. Cogan, Donaldson and Reese (41)
described the characteristics of the x—ray, the atomic bomb, and the cyclotron
exposure induced cataracts. The initial or least advanced lesion consisted
of spottiness and attenuation of the anterior subcapsular epithelium. There
was a piling up of the equatorial cells with the failure of these cells to
"drop off" into the cortex. The advanced stage in humans as seen with the
ophthalmoscope was a doughnut-shaped configuration with sharply demarcated
anterior boundary and a bivalve configuration. This description is very
similar to the IR cataract progression given by Langley et al. (30). Duke—
Elder (42) stated that the most interesting type of cataract was that caused
by ionizing radiation, including x—rays, B-rays, y—rays, and neutrons.

42

Histologically, the anterior subcapsular epithelium was primarily involved
along with secondary involvement of the cells of the equatorial area of

the lens. The UV induced lenticular opacity was described as small, circum—
scribed white spots located in the anterior epithelium just posterior to the
anterior capsule (37). The experimentally induced IR opacity appeared
similar to the UV induced opacity (9, 37) and was located in the anterior
lens epithelium (9, 30, 37). The preponderance of experimental evidence
describes the radiation induced cataract of both ionizing and non-ionizing
radiation as an anterior epithelial opacity.

The experimental evidence in the literature indicates that the acute IR
induced lenticular opacities are not the "classically described posterior
subcapsular opacities'that develop with a latency of 60 to 90 days. Past
research and our present study indicate that the acute IR induced opacities
lie in the anterior subcapsular or anterior epithelium of the lens. The
acute opacities appear as discrete "whitish dots” or granules. If a suffi-
cient exposure has been given, the granules or whitish dots form into a
diffuse whitish opacity. We have followed exposed eyes for up to 45 days
and did not observe the migration of the anterior opacities either equatorily
or posterior subcapsularly into the anterior cortex but, instead, the anterior
opacities faded and disappeared within 6 weeks after exposure. Pitts and
Cullen (37) have described a posterior subcapsular lenticular opacity in

the normal rabbit. The posterior opacity followed the posterior suture
horizontally as far as the equator and could be described as saucer—shaped
in appearance. Often, the posterior opacity projected a white filament
anteriorly from the posterior pole to the lens nucleus and, occasionally,
the lens nucleus took on a diffuse, whitish appearance. The posterior
subcapsular cataract, found in 1002 of our laboratory rabbits, took on a
denser appearance as the animal aged, much like the classical description

of the IR cataract. We must emphasize that none of the lenticular opacities
induced by either full spectrum or the IR spectrum exposures were posterior
subcapsular opacities. For the above reasons, we conclude that the IR
induced cataract is an anterior subcapsular opacity while the posterior
subcapsular opacity is due mainly to the normal aging process which may or
may not be accelerated by the exposure to IR.

If it were accepted that the experimental evidence of the present study
proves that the anterior epithelial opacities are caused by IR, an
explanation of the origin or development of the "classical posterior
subcapsular cataract" is needed. The epidemiological literature left no
doubt that the number of workers in the iron, steel, glass and rail
industries who have developed the "IR or heat induced posterior subcapsular
cataracts" exceeded the number of workers in other industries. This is
particularly evident in the epidemiological literature of the late 18903
and early 19005 (12, 25). Beginning in the 19203, epidemiological

studies (27, 33) seem to indicate that workers in the "heat industries"
show equal or fewer cataracts than control populations. What was the cause
of this change? First, statistical procedures in handling epidemiological
data had improved by the 19203. One example is the study of Eiller et al. (43)

on the incidence of cataracts caused by sunlight. Their excellent study
warns that definitive conclusions cannot be made because only inadequate
records of cataract incidence and surgery were available. It is to be noted
that if sunlight were the causative agent, UV radiation would necessarily

be implicated because the atmosphere transmits radiation down to 295 nm and
the 295 nm - 320 nm wavelength range comprises the ultraviolet action
spectrum for cataracts. Finally, the decrease in incidence of IR cataracts
from the worker's environment may be due to improved environmental conditions
including protective devices for the eyes, automation of the manufacturing
processes, and probably better dietary habits of the worker.

Most experiments that report posterior subcapsular cataracts used massive
radiant exposure levels. Duke—Elder (2) reported Meesman as stating that
his radiant exposures were "3 cal-cmz-seE equal to 30 or more hours of
radiation over 4 months." This calculates to a radiant exposure of 1.4 x
106 J-cm‘2 which is an extremely high exposure and approximately a factor

of 100 above any exposure given during this study. Other researchers do

not give measurements of their source but the description of the damage
which resulted from their exposures indicates massive exposures. One should
not forget that there are two phases to coagulation. The first phase is
denaturation, a chemical change that involves hydrolysis. The second phase
involves the flocculation of the denatured molecules in which coagulation
occurs, perhaps by a physical process. These two processes may be separated
by an indefinite period of time. Thus, the IR could be absorbed by the
anterior epithelium of the lens and denaturation would occur. The white
dots or grayish anterior haze would represent the denaturation process.

The coagulation process is completed when the posterior lens material
becomes opaque. The degree of opaqueness is related to the health of the
individual and the level of radiation absorbed. The posterior subcapsular
cataract would represent the agglutination portion of the coagulation process.
Under this scheme, damage to the anterior lenticular epithelium by the
absorption of the IR results in an increase in the posterior subcapsular
cataract. Thus, the size and density of the posterior opacity might depend
on the initial damage to the anterior epithelium. Since our radiant expo-
sures were intended to determine threshold exposures, subsequent posterior
cataracts were not found in our experiments. This analysis would account
for the extensive delay in the development of the posterior subcapsular
cataract which has been reported in the literature in spite of the fact

that faint opacities occur naturally in the rabbit.

The irradiances used for the exposures during this study varied from

0.002 to 4.7 W-cm" and the majority of the exposures compare favorably
with the 0.02 to 0.4 W'cm"2 irradiance levels experienced by glassworkers,
steel workers, brass workers, arc welders, and locomotive firemen. Despite
these comparisons, the present data must be considered as reflecting acute
rather than chronic exposure since most animals were exposed once and
observed for only about 10 days. The total radiant exposure received by an
annual during a single experiment might not equal the constant exposure
received by a worker over years on the job. However, it appears that if
protection were provided for the worker based on acute exposures, the chronic
factors might be alleviated.

hb

It is difficult to compare data from various researchers for many reasons.
Most researchers have failed to define their source and, therefore, one
cannot be certain of the limits of the spectrum. Many researchers did not
even measure the irradiance of their sources and provided only the durations
of their exposures and the ocular damage which resulted. Many used sources
which were thought to be only IR in output but have subsequently been shown
to include more visible and UV radiation than the IR which was being studied.
Even when the irradiance, exposure duration, radiant exposure, and wavelength
range of the source are given, it becomes impossible to compare data. For
example, Jacobson et al. used a 1600 W Xenon lamp to establish the corneal
threshold at 5.8 J-cm‘2 for2 the wavelength range of 800 nm to 1670 nm with
an irradiance of 34.2 W- cm 2for duration of 150 ms. The corneal radiant
exposure threshold in this study was 5500 J- -cm 2 using a source with an
irradiance of 3. 6 W cm 2 delivered over a duration of 1529 s using a source
size of 0.8 cm x 1.5 cm (1.2 cm 2) at the plane of the cornea (Table IV).
Which data are correct? Both sets of data are correct because of the source
differences. The source of Jacobson et al. had an irradiance which was a
factor of 9.5 greater than the irradiance of our source. Jacobson's et a1.
exposure was delivered in 150 ms, a factor of 10,000 less than the duration
of the exposure in our experiments. Finally, the size of the images at the
plane of the cornea differed greatly. Hence, one may contrast but not
compare the effects of the two different exposures.

The rabbit data in Figure 10 may assist in a further understanding of the
differences between certain studies. It appears that as long as the IR
source irradiance is 3.5 W-cm'2 or less and the source area remains constant,
there is little difference in minimal lesion exposures. As the irradiance
exceeds 4 W-cm‘z, the radiant exposure decreases by a factor of 4.0 for the
cornea and by a factor of about 2.0 for the lens with all other experimental
variables held constant. Furthermore, the differences between the full
spectrum data and the IR spectrum data for higher irradiances are minimal.
This indicates that the visible and UV spectra combined with the IR spectrum
are not synergistic but additive because almost identical threshold exposures
are found for both conditions. Thus, these data would indicate that the
damage was due to heat from the absorbed radiant energy and as long as the
irradiance or rate of delivery exceeds a certain level, the damage should
occur over a given exposure duration regardless of the spectral distribution
of the source. These data indicate that the visible and UV radiation must
be considered when establsihing protective criteria and formulating safety
standards, especially for the IR region.

Figure 19 shows the radiant exposure in J-cm‘2 versus the exposure duration

in seconds required to reach threshold damage. The plot can be represented

by a straight line whose formula y = 2.83 x + 619.5 indicates that the
threshold radiant exposure HL may be calculated by multiplying the

irradiance by 2.83 and adding the constant 619.5. The straight line
characteristics of these data are taken to indicate that a single process

was in operation during exposure which produced the minimal observable

lesion. All evidence from these experiments indicate that heat is probably
the causative agent. The data also demonstrate that in spite of the different

45

9V

THRESHOLD RADIANT EXPOSURE (Jcm'z)

80001

7000-

6000-

5000‘

4000-

3000-

2000-

l000‘

 

 

 

Figure 19.

560 IO'OO ns'OO 2000
EXPOSURE DURATION (Seconds)

Radiant exposure required to produce a minimal lesion in
the rabbit eye for different exposure durations. HL in
J-cm' is plotted on the ordinate and exposure duration in
seconds along the abscissa. The symbol (0) represents data
for the IR spectrum, focused beam, and miotic pupil while

the (A) is the data for full spectrum, focused beam, and
miotic pupil.

irradiance levels and exposure durations used during experimentation
the evaluation criteria and procedures arrived at a fairly uniform and
consistent threshold value.

Based on the above it can be stated that the threshold radiant exposure

for the IR spectrum, above 700 nm with a 1.2 cm2 source image at the plane
of the cornea and a source irradiance below 3.9 W-cm"'2 was 5000 J-cm"2 for
the cornea, about 3500 J-cm‘2 for the iris, and 4000 J-cm‘2 for the lens.

As the source irradiance exceeded 4.0 W-cm‘2 the threshold radiant exposure
was 1250 J-cm‘2 for the cornea, 1250 J-Cm'2 for the iris, and 2250 J-Cm'2
for the lens. The radiant threshold exposure for the full spectrum from the
source was 750 J-c:m‘2 for the cornea, 2250 J-cm‘2 for the iris, and

2250 J-cm‘2 for the lens.

The monkey IR exposure data are approximately a factor of 6 above the

rabbit data (Tables VII and VIII). It is difficult to account for such

a large increase in threshold exposure but several factors may combine

to account for at least part of the increase. The stroma of the iris of

the monkey is much more vascular than that of the rabbit and, consequently,
as the primate iris heats up, the vessels dilate, allowing more blood to
pass and adding the the cooling capacity of the iris. The stroma of the
monkey iris is thicker, denser, and more pigmented than that of the rabbit
and these factors, along with increased blood flow, would dissipate heat
prior to its reaching the iris pigment epithelium. Although the above
factors should serve to increase the monkey threshold it is difficult to
conceive of such a large increase in threshold. The increased transmittance
by the primate cornea may offset at least some of the effects noted. Hence,
the reasons for the increase in the primate threshold remain largely unsolved.

Retinal lesions were produced with a corneal irradiance of 3.5 Them"2

for a duration of 1288 s with a corneal radiant exposure of 6000 J-Cm‘2
(Figure 17, IRl7R) and for an exposure duration of 1891 s with a corneal
radiant exposure of 6600 J'cm‘2 (Figure 16, IR17L). The area of the source
at the cornea was calculated to be 0.035 cm2 with the retinal irradiance

of 29.7 w-cm'2 if a 0.7 cm pupil and 0.70 integrated transmittance was
assumed. The retinal lesion was discrete and seen 24 hours after exposure.

Ham et al. (44) exposed the rhesus monkey to the same wavelength range of

IR and produced a threshold retinal lesion with a retinal irradiance of

23.4 W-cm‘2 from a retinal image diameter of 1000 um (0.008 cm2 area) in

180 seconds (retina radiant exposure of 4212_J-cm‘2). A retinal image of

158 um required 97.4 w-cm“2 for 180 seconds duration to produce a retinal
lesion (retinal radiant exposure of 17,532 J-cm‘z). Thus, as the size of

the retinal image decreased, the retinal radiant exposure required to produce
a retinal lesion increased. The 158 um lesion required 4 times the retinal
radiant exposure to produce a threshold lesion as the 1000 um retinal image
exposure.

47

The experimental research variables on retinal lesions include pupil

size, spectral transmittance of the ocular media, spectral absorption

of the retina and choroid, the criteria used to evaluate the exposures,
exposure duration wavelength or waveband of the source and the size of

the retinal area exposed. As the exposure duration increases, the

radiant power entering the eye to produce a retinal lesion decreases until
exposure duration becomes ineffective and the lesion depends on the power
density entering the eye. The retinal lesion data of this study cannot

be validly compared to the data of Ham et al. because the experimental
apparatus was not designed for retinal lesion research, the exposure
durations differed by a factor of at least 7, the animal species differed,
and the exposures were suprathreshold. Ham has also showed a threshold
radiant exposure of 6. 91 x 104 J cm‘ 2for a 1000 5 exposure to the primate
from IR in the 700 nm to 1400 nm wavelength range. The data of Ham et a1.
should be considered whenever safety criteria are formulated for retinal
protection against IR.

In the early days, ocular protection was an empirical exercise in using
protective devices of different types until it was demonstrated that the
worker had been protected. The initial problem in any industrial environ—
ment is determining the spectral distribution of the undesirable source

of the Optical radiation. This may be a very difficult task but it allows
subsequent protection philosophy to be based on valid concepts rather than
becoming a hit—and—miss exercise. The government and industry now realize
the importance of establishing the spectral distribution of the source and
publications providing measurements of various industrial sources are
beginning to appear in the literature.

Ocular protection has commonly taken the form of goggles, shields, or
helmets using absorptive orreflective filters to control the undesirable
optical radiation. Filters that absorb IR are manufactured by incorporating
oxides of iron into the glass meld. For example, Crookes glass absorbs
about 95% of the IR and 100% of the UV radiation. Absorptive filters

absorb the undesirable radiation and transmit the visible spectrum necessary
for vision. The use of absorptive filters to control IR may be a questionable
concept because the absorbed radiation raises the temperature of the filter
and the filter then becomes a secondary source for the re—radiation of heat
directly into the eye. Protective transmittance filters have been
standardized into shade numbers with specific shade numbers recommended for
specific industrial tasks (45, 46).

Reflective filters are usually metallic coatings applied to the front

surface of the filters and provide protection by reflecting the undesirable
optical spectrum while transmitting the visible spectrum to allow one to

see the task. Reflective filters are the most desirable method for ocular
protection against IR because there is not heat build-up of the filter.
Reflective filters can be very effective when properly chosen; for example,

a gold coating reflects 96% of the IR and transmits maximally the part

of the visible spectrum that is most efficient in providing vision. Platinum,

48

aluminum, and inconel (a mixture of iron, nickel and chromium) are other
metals which provide excellent IR reflectance. The major difficulty in

using reflective metallic coatings is their susceptibility to scratching,
abrasions, and other ”breakdowns" of the coating. This problem has been
overcome by depositing hard protective coatings over the metallic film or

by sandwiching the reflective coating between two layers of optical material.
The second layer, that is the layer next to the eye, could then be made
absorptive to control other unwanted optical radiations such as UV radiation.
An example of an excellent combination protective filter was the Pfund's
glass developed by American Optical Company. It consisted of a thin gold
layer placed between a layer of Crookes A glass and clear crown ophthalmic
glass. The clear ophthalmic crown glass provided protection for the metallic
coating. The gold layer reflects 96% of the IR while it allows 75% of the
visible radiation peaked at 550 nm to be transmitted. The Crookes A glass
absorbs 100% of the UV radiation. The major advantage of metallic reflective
coatings, in addition to their control of IR is that the lens is cooler and
more acceptable to the wearer.

It may appear that the recommendation to use metallic coatings to control
IR reaching the eye is "over—protection” since the data in this study
clearly shows that a substantial IR exposure is needed to produce acute
ocular injury. Metallic coatings provide a measure of protection against
the low level chronic IR exposures typically encountered in glass and
steel injuries, and serve to reduce the total heat load reaching the eye.
In addition, the long term effects of acute exposure, such as those given
during this study, are not known and maximum protection should be provided
until the effects are more fully documented.

The American Conference of Governmental Industrial Hygienists (ACGIH) has
recently published notice of intent to establish threshold limit values for
the near IR in the 770 nm to 1400 nm wavelength range £47). The recommended
IR exposure for wavelengths above 770 nm was 10 mW-cm‘ . The data in this
study indicate that the 10 mW-cm‘2 figure is conservative and could be
increased. We recognized that ACGIH recommendations are intended for
delayed effects of chronic exposure while the data of this study concern
from acute exposures; however, we are certain that our exposures were only
to IR while recent measurements of rolling mills, glass furnaces, etc.,
indicate that a much higher proportion of UV may be contained in these
relatively low temperature sources than previously suspected (42, 43).

It has been shown that UV radiation in the 295 nm — 320 nm range is most
efficient in producing lenticular opacities (39). In fact, the 295 nm
waveband with a threshold radiant exposure of 0.15 J-cm2 is 8.3 x 10

more effective in producing lenticular opacities than the 1250 J-cm“2
threshold for IR. Permanent lenticular opacities could not be produced
with the IR exposures but were easily achieved with UV radiation. For
these reasons, it is felt that the 10 mW-cm‘2 recommended exposure limit
for IR should be re—evaluated and increased to the more appropriate value
of 25 mw-cm-Z.

49

SUMMARY AND CONCLUSIONS

A 5000 watt Xenon high—pressure lamp was used to expose 100 pigmented

rabbit eyes and 10 primate eyes to IR in the 700 nm to 1400 nm wavelength
range and to the full spectrum output of the source. The ocular expo-

sures were evaluated independently with the biomicroscope by two researchers
and classified. The following findings and conclusions were drawn:

1.

The primary ocular lesions resulting from exposure to IR were

corneal, iris, and lenticular. Corneal damage varied from epithelial
haze to erosion and usually healed within 24 hours. No endothelial
damage was found. The iris showed stromal haze and swelling in the
region of exposure with severe damage resulting in fibrinous inflammatory
byproducts. Lenticular opacities appeared as small white dots that
occurred at the level of the anterior epithelium just beneath the
anterior capsule. No lenticular opacities could be induced by direct
exposure to the lens nor was it possible to produce permanent lenti—
cular damage. All lens damage depended on iris involvement.

Ocular damage from IR was related to the rate of delivery of the IR
(Figure 10). The data indicate that as the irradiance level increases,
the radiant exposure threshold decreases. Irradiance at and below

3.9 W-Cm"2 resulted in threshold radiant exposures of 5500 J'Cm'2

for the cornea, 3500 J-cm‘2 forthe iris, and 4000 J-cm'2 for the lens.
If the irradiance exceeded 4.0 W-cm‘z, the threshold radiant exposure
was 1250 J-cm"2 for the cornea, 1250 J-cm'2 for the iris, and 2250 J-Cm‘
for the lens.

A plot of the threshold radiant exposure versus the duration of expo—
sure indicates that the IR ocular damage was a single process and all
evidence (Figure 18) points toward heat as that process.

Exposures for the full optical spectrum, which included the visible
and the UV spectra in the optical beam, were found to be additive

for irradiance levels at 4 W-cm“2 and above. The threshold radiant
exposures of 750 J-cm"2 for the cornea, 1000 J'cm‘2 for the iris, and
2000 J-cm‘2 for the lens were essentially identical to the IR exposure
thresholds for the same irradiance levels.

The prflmate threshold radiant exposure was a factor of 6 above the

respective rabbit thresholds. With irradiance levels above 4 W-cm‘z,
the radiant exposure thresholds for the primate were 8000 J-cm‘2 for
the cornea, 8000 J-cm"2 for the iris, and 10,000 J'cm“2 for the lens.

The recommended method for ocular protection against IR exposure was

reflective metallic coatings to control the IR and absorptive filters
to controlother undesirableoptical radiations. The metallic coating

50

should be the initial surface to intercept the optical beam and
prevent heating of the protective lens.

Research on the ocular effects of IR from acute exposure is needed
to produce more detailed information on the dependence of the rate
of delivery of cataractogenesis. In addition, daily long—term low
level exposure should be performed.

51

10.

11.

12.

13.

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