B. Ultraviolet Effects on the Skin:
The ultraviolet spectrum is divided into three specific regions
which are related to the different biological responses of these
regions. In the skin, UV-A (315 - 400 nm) can cause erythema and
hyperpigmentation.
In addition to thermal injury caused by ultraviolet energy, there
is the possibility of radiation carcinogenesis from UV-B (280
- 315 nm) either directly on DNA or from effects on potential
carcinogenic intra-cellular viruses.
There is limited data available describing the reaction of skin
exposed to ultraviolet radiation in the range from 200 nm to 280
nm from highly monochromatic laser sources. Chronic exposure to
narrow-band, non-laser ultraviolet wavelengths in this range can
result in carcinogenic effects on the skin as well as producing
a severe erythematous response.
On the basis of these studies with non-coherent ultraviolet radiation,
exposure in the UV-B range is most injurious to skin. Exposure
in the shorter UV-C (200 - 280 nm) and the longer UV-A ranges
seems less harmful to human skin. The shorter wavelengths are
absorbed in the outer dead layers of the epidermis (stratum corneum)
and the longer wavelengths have an initial pigment-darkening effect
followed by erythema if there is exposure to excessive levels.
It should be kept in mind that phototoxic and photosensitizing
chemicals in the skin may potentiate the effects of laser operating
in the visible and ultraviolet regions. Studies on the stimulating
effect of very low level exposures of the ruby laser on hair growth,
phagocytosis index and wound healing are of interest in any consideration
of chronic effects.
Recent studies with Excimer ultraviolet lasers have, however,
demonstrated a specific, nearly non-thermal, tissue reaction that
causes a molecular bond breaking at wavelengths below 340 µm.
This may offer a unique tool in the future for some surgical applications.
Biological effects of laser radiation have not been observed
on internal organs of man except for very severe conditions where
the outer tissues were either surgically removed or massive laser
exposures were delivered to the tissue surface to cause surface
ablation. In this condition sufficient energy may be transmitted
to the underlying organs and produce tissue damage.
The results of studies on the exposure levels required to produce
minimal reactions in the human skin for six common laser types
emitting in the visible and IR are summarized in Table III-3.
The data presents the minimal reactive dose (measured at the 50%
probability level) for the different wavelengths and lasers. The
variations, or spread, in the data were found to be directly related
to the degree of absorption in the tissues.
The thermal reaction of absorbed radiant energy in tissues is
strongly dependent upon both duration and area of the exposure.
The early work of Henriques and Moritz investigated the time-temperature
response for tissue exposures of thermal insults of to 70 deg.
C. Their data indicates that skin can withstand brief temperature
rises for very short exposure times. The response appears to be
logarithmic as the exposure times become shorter.
For example, a 21 deg. C rise above body temperature (37 deg.
C) to 58 deg. C will produce cell destruction for exposures longer
than 10 seconds. Tissues, however, can withstand temperatures
up to 70 deg. C if the duration of the exposure is maintained
less than 1 sec. The basic mechanisms of thermally induced tissue
destruction result from denaturation of cell protein, interference
with basic cell metabolism and secondary effects such as interference
with vascular blood supply.
Healing of laser induced skin lesions is similar to any localized
thermal wound and should be medically treated in a similar fashion.
Laser induced lesions on the retina tissues of the eye will usually
cause irreversible vision function loss and is difficult to medically
treat.
C. Ocular Effects of Laser Radiation:
The principal hazard associated with laser radiation is exposure
to the eye. This is particularly important in the visible and
near-infrared spectral regions (400 - 1400 nm). There are, however,
other serious potential hazards in other spectral regions as outlined
in the following sections.
The eye may be conceptually considered as a slightly flattened
globe which is transparent to the light passing through an aperture
pupil) and which has an efficient light absorber on the inside
(retinal surface), opposite the aperture. The transparent region
of the eye includes several structures which operate to control
the exposure to the retina.
The cornea, the transparent window, is the primary refracting
structure of the eye. Because of the differences in refractive
indices of air and the cornea, more than 80 percent of the refraction
of light takes place as the light enters the eye. Between the
cornea and the lens is one of the two chambers of the eye. The
aqueous chamber contains the aqueous fluid.
The lens is the dynamic refractive medium in the eye, and is
responsible for the range of focus of the eye. The retina is the
light absorbing structure of the eye containing the neural receptors
which initiate the vision process. A blind spot in the retinal
surface is located at the point where the optic nerve enters into
the eye. The fovea is the portion of the retina which is most
sensitive to detail and which discriminates color. This structure
fills an angle of approximately two degrees in the central portion
of the retina. The fovea is located in a small dip in the center
of the area called the macula lutea. The macula fills an area
of about 1 mm diameter.
The various structures of the eye transmit, reflect, and absorb
optical energy. The effects of laser exposure on the retina are
influenced by the transmission losses of the ocular media. The
transmittance of the ocular media are such that retinal effects
can be anticipated only for laser wavelengths between 400 nm and
1400 nm. Outside that range, structures other than the retina
are affected.
The retinal effects of visible optical radiation are also influenced
to some degree by the size of the retinal image and the time duration
of the laser exposure.
Early in the history of lasers, it was recognized that lasers
and great potential for causing retinal injury. The reason was
that a laser could produce retinal intensities orders of magnitude
greater than conventional light sources, and, in fact brighter
than the sun.
The optical system of the eye, like any optical system, will
have a limitation (called the diffraction limit) on the smallest
size of image it may resolve and focus. To determine the effect
of a source imaged on the retina it is necessary to know the retinal
image size. A large amount of the research on retinal burns indicates
that the size of the source is an important variable. For a first
approximation, one can show that a laser with a 1 milliradian
beam spread can produce a retinal spot of approximate size of
17 µm if sharply focussed.
If an unaccommodated eye (an eye focused at infinity) views a
collimated source such as a distant star in the night sky or a
laser, a "point" image should be produced on the retina.
In practice, however, a true point image of that light source
is not produced. The optical system of the eye, or any optical
instrument, has certain limitations caused by diffraction which
will cause the light rays passing through an aperture to bend.
The aperture of an optical system is the edge which produces the
diffraction. The aperture in the eye is the iris. If a laser beam
is larger than the pupil, diffraction of the beam occurs at the
edge of the iris.
If the beam is smaller than the pupil, spherical aberrations
and forward scattering cause the "point" image to spread.
The actual distribution of light from a point source will be spread
out somewhat rather than be focused to a diffraction limited spot.
In general, the larger the pupil, the smaller the point spread
and the greater the magnification factor (concentration) of light
at the retina as compared with the irradiance at the cornea. Estimations
of the magnification factor, based on diffraction effects only,
range from 10(5) to 10(7) for pupil diameters between 2 and 7
mm.
In any event, the optical gain for a 7 mm diameter pupil is at
least 1 x 10(5) and may be greater, depending on the magnitude
of the experimental error in determining the data used in the
estimates.
The location of the exposure in the eye determines the degree
of incapacitation from a retinal injury. The fovea (the central
two degrees of the visual field) is the region of the retina which
is most sensitive to visual detail. The remainder of the retina,
the parafovea to the peripheral retina, is increasingly less sensitive
to light.
However, the parafovea and peripheral retina are not as sensitive
and do not contribute significantly to fine detail in the vision
process. Therefore, and injury to the fovea will severely reduce
visual functions of visual detail and resolution. An injury to
the parafovea or peripheral retina is less incapacitating and
may be undetectable from a functional point- of-view.
D. Extended Source Viewing:
When viewing an extended source, such as the reflection of a laser
from a highly reflective diffuse surface, the geometry of the
situation results in a retinal image which is of constant brightness
(constant retinal irradiance) until the observer moves away so
far that the eye can no longer resolve the spot of the laser light.
At this point a critical image size is reached. When this occurs,
the brightness will stay constant or decrease in value. Retinal
spot size effects are related to the differential effects of conduction
of heat away from the image which are a function of both exposure
time and image size. For long exposures, the large and small image
size damage thresholds are different because of thermal conduction.
By thermal conduction in this context is meant the cooling of
laser heated tissue by contact with surrounding tissue and by
circulation of the blood.
E. Eye Effects at Different Wavelengths:
1. Exposure to Ultraviolet Wavelengths:
Excessive ultraviolet exposure of the eye can produce photophobia
accompanied by redness, tearing, discharge from the mucous membrane
that lines the inner surface of the eyelid (conjunctiva), corneal-surface
cell-layer splitting (exfoliation) and stromal haze. This is the
syndrome of photokeratitis which is radiant energy induced damage
to the outer epidermal cell layer of the cornea. In the ultraviolet
"C" and "B" regions (UVC and UVB), photokeratitis
is the primary result of excessive acute (short-term) exposures.
In the ultraviolet "A" region (UVA), cataracts may result
from chronic high-level exposures. The actions of ultraviolet
"A" and "B" radiation are believe to be photochemical.
However, some recent evidence suggests that the damage mechanism
of UVA is thermal in nature particularly at wavelengths above
340 nm.
In the skin of the eyelid, UVA can cause skin redness (erythema,
lenticular fluorescence), and can cause increased pigmentation
("tanning"). Exposure to UVB is, perhaps, of most potential
hazard to the skin. Exposures in this range are known to cause
cancer and severe erythemal reactions.
Exposures to the short-wavelength UVC while potentially hazardous,
may not be as dangerous since this wavelength can be easily absorbed
by protective clothing or in the outer dead layers of the epidermis
(stratum corneum).
It is important to note that phototoxic and photosensitizing
drugs or chemicals taken internally or applied on the skin may
intensify the effects of lasers operating in the ultraviolet and/or
visible wavelength regions.
2. Exposure to Visible and Near Infrared Wavelengths:
The ocular hazards which represent a potential for injury to the
different structures of the eye generally depend upon which structure
absorbs the most radiant energy per unit volume of tissue. Retinal
effects are possible when the laser wavelength is in the visible
and near-infrared spectral regions. Laser radiation directly from
the laser or from a specular reflection entering the eye at these
wavelengths can be focused to an extremely small spot-image on
the retina causing an excessive irradiance (W/cm(2)) or radiant
exposure (J/cm(2)) incident on the retinal tissues even for modest
corneal exposure levels.
In the visible portion of the spectrum (beginning near 380 nm
and extending to nearly 760 nm), the cornea, lens, and ocular
media are largely transparent. Only about 5% of the incident radiation
is actually used for vision; the remainder is absorbed in the
pigment granules in the pigment epithelium layer of the retina
and the choroid layer which lies under the rods and cones (photoreceptors).
The absorbed energy is converted into heat and, if the incident
laser energy is too great, can cause an irreversible retinal burn.
a. Intrabeam Viewing:
A retinal injury occurring in the macula is a very serious trauma
since the vision functions are most highly developed in that area.
Destruction of this area (less than one-millimeter in diameter)
degrades one's visual acuity to the point where the "large
E" on the Snellen chart is no longer discernible; vision
function is reduced to 10/200 or worse. In this case, the individual
is legally blind.
Of major concern is the fact that blindness can be the result
of a laser exposure that lasts only an infinitesimal fraction
of a second. On the other hand, similar damage in the periphery
of the retina will often have minimal, if any functional significance
since a large "blind spot" in the periphery has only
a small effect on vision function. A macular burn would be the
most probable result if the individual is viewing the beam directly
or via a specular reflection under conditions where the eye is
resolving the laser source directly onto the macula. A peripheral
burn might occur through an accidental exposure when the eye is
not directly viewing the beam and the eye is not "relaxed"
but viewing something other than the laser point source.
b. Extended-Source Viewing:
Viewing extended source lasers or diffuse reflections of a laser
beam can sometimes produce a much larger retinal image spot size
than direct intra-beam viewing.
This provides, at first consideration, some degree of protection
since the retinal irradiance will be significantly lower due to
the larger spot size. Some lasers are, however, of sufficient
power (Class IV) as to be extended source (diffuse reflection)
hazards. In this case, the degree of retinal damage would be significant
due to the larger retinal spot-sizes associated with a typical
extended source viewing condition. Also, larger image sizes (typically
100 µm or greater) of longer exposure times (greater than
10 seconds) do not dissipate the heat build up as rapidly as smaller
image sizes. Consequently, the retinal irradiance which produces
a minimal burn on the retina will be about 10-100 times lower
for larger image sizes than for the smaller (20 µm) point
source image sizes. Hence, different exposure criteria are needed
for the two exposure conditions (point source and the larger extended
source criteria).
3. Exposure to Far Infrared Wavelengths:
A transition zone between retinal effects and effects on the front
segments of the eye (cornea, lens, aqueous media) begins at the
far-end of the visible spectrum and extends into the infrared
"A" region (0.700 -1.4 µm).
In the infrared "B" region (1.4 - 3.0 µm) damage
is observed to both the lens and cornea. The ocular media becomes
opaque to radiation in the infrared "C" region (3.0
µm - 1 mm) as the absorption by water (a major portion of
all body cells) is high in this region. In the infrared "C"
region, as in the UVA and UVB regions, the threshold for damage
to the cornea is comparable to that of the skin. Damage to the
cornea, however, is much more disabling and of much greater concern.
F. Biological Damage Mechanisms:
Until the late 1970's, it was assumed that all permanent retinal
injury from intense visible light sources was thermal in nature
when exposures durations exceeded more than 10 microseconds. It
had been recognized that there would be a temporary loss of visual
function (flashblindness) from sudden exposure to bright light,
but it was not known that photochemical retinal injury mechanisms
existed in addition to thermal injury.
The laser safety thresholds and exposure limits for exposure
durations from 10 microseconds up to 10 seconds seem to follow
a constant power function which is dependent upon exposure duration
which implies only a thermal damage process. In this time domain,
the retinal tissue is raised in temperature to a point where protein
(or enzyme) damage takes place.
1. Thermal Injury:
The thermal injury threshold levels were initially established
in the period 1965-1975 through the biological research investigations
conducted at various university and military laboratories in the
U.S. and by numerous research groups in Europe. The threshold
studies of all these groups generally lend strong support to the
present levels for allowable exposure limits for exposure durations
of less than 10 seconds provided that only a single long duration
exposure is considered.
Repetitive short exposures (less than 20 µs) show a curious
reduction in the threshold, which cannot be completely explained
purely on the basis of thermal injury. The effects from pulses
separated by several milliseconds appear to add, which would not
be predicted on the basis of heat flow. For example, the effects
from two or three exposures of 10 µs pulses spread over
several milliseconds are almost linearly additive.
It is important to note that the Federal Laser Product Performance
Standard does not include any corrections whatsoever for multiple
pulse exposures. Such pulse additivity may be related to some
interference with the normal repair mechanisms of the retinal
tissue.
The safety limits in all standards are typically a factor of
ten or more lower than the actual damage "thresholds"
commonly encountered in the biological literature. This factor
of ten is sometimes erroneously referred to as a "safety
factor." In fact the values often termed thresholds in the
biological literature are often termed ED (50) doses, that is,
doses where 50% of the exposures resulted in injury and 50% of
the exposures did not result in changes which were visible by
an ophthalmoscope. Obviously safety limits must be concerned with
whether there may be permanent or delayed visual loss and tissue
damage and not whether the damage is (or is not) simply visible
ophthalmoscopically.
Many studies have been performed to determine at what levels
below the ED(50) dose some loss of visual function (or morphological
change in the retinal tissue) will be encountered. These studies
generally suggest that for exposure durations of 10 µseconds
to 10 seconds, changes are still observed (by histological evaluation)
at power/energy levels reduced from the ED(50) value by a factor
in the range of from 2 to 5. Hence, the apparent safety factor
of 10 based on ophthalmoscopic (visible burn) criteria is, in
reality, only a value of 2 above the level of actual morphological
or histological change.
The present exposure limits for single pulses in the time domain
from 10 µseconds to 10 seconds are probably realistic and
unlikely to be changed unless there is substantive new biological
data generated which obviates the vast quantities of data currently
available. When the amount of time (and money) already spent in
determining these thresholds is considered, it seems unlikely
that future research will reveal any unexpected injury at levels
near to the present safety limit for these exposure times.
2. Photochemical Retinal Injury:
Non-thermal, presumably photochemical damage mechanism for long
term laser exposure to short wavelengths in the visible and UVA
regions were first shown in 1975 by Dr. William T. Ham, Jr. and
colleagues at the Medical College of Virginia. This injury is
unlike thermal damage in which a threshold variation over perhaps
an order of magnitude might be expected in shifting from 0.400
to 1.10 µm SOLELY on the basis of changes in retinal absorption.
In reality, a range of greater than 1000-fold in retinal sensitivity
to damage was discovered between the most hazardous wavelength
of 0.442 µm and the less hazardous wavelength, 0.633 µm
for an exposure duration of 1000 seconds.
All of these studies reported ophthalmoscopically visible and
also histologically damaged tissue as a result of long term exposure
to visible light. In some experiments, very large areas of the
retina were exposed with different wavelengths of the argon laser
for four hours. The data points corroborated the limits for thresholds
reported earlier by Dr. Ham. The tests used a spot size smaller
than the 500 µm spot used in Ham's earlier studies and also
showed far more emphatically a difference between the delayed
appearance of the photochemical lesion and the nearly immediate
appearance of thermal injury.
The fact that a photochemical lesion takes up to 24 or even 48
hours to appear perhaps explains why earlier studies looking for
thermal injury could form no consistent picture of the photochemical
effect.
Along those lines, retinal exposure to the near infrared output
of high repetition rate gallium-arsenide diode laser pulses for
30 seconds have also shown similar delayed effects. The mechanism
for this type of damage is not well understood, but it may be
related to the repetitive pulsing at several kilohertz pulse repetition
rates characteristic of these laser types.
Wavelength dependent functional effects were also demonstrated
as early as 1971. The studies showed permanent loss of blue color
vision as a result of blue light exposure. These levels were the
basis for the long term intrabeam "safe" laser exposure
criteria (approximately 1 uW/cm(2)).
3. Long-term Exposure to Diffused Laser Light:
Certain adverse effects of a vision function nature have been
demonstrated in behavior studies with trained monkeys to evaluate
visual acuity changes in an effort to determine if a distinction
exists between visible lesions and functional loss. The data suggests
both adverse and long term irreversible changes of retinal function,
particularly to color vision and small angle acuity, resulting
from large field DIFFUSE REFLECTION EXPOSURES to visible argon
laser light. These effects occur at retinal irradiance levels
in the magnitude of 10(-7) W/cm(2), well below the present safety
limits.
The data also suggests that the effects are dependent on the
speckle pattern which is characteristic of diffused laser light.
When the speckle was removed by vibrating diffusers in the laser
beam projection optics, the effect was not noticed in associated
experiments.
It is important to note that all of the functional changes have
been found only for very large fields of view. Indeed, almost
by definition, they could not really be tested for point source
exposure conditions. Only diffused laser sources will produce
significant speckle pattern.
4. Eye Movement:
The safety limits for long term exposures to a point source are
difficult to compare with calculations for the dwell time on the
retina of a scanning presentation. The studies on so-called saccadic
or micronystagmic eye movements have shown that a point source
will never remain for extended periods in one spot of the retina
unless the eye has been anesthetized. Exposures to welding arcs
by individuals purposely staring at such point sources give a
clue as to the size of the retinal area that might be exposed
over a period of a few minutes. Some studies had found that a
welding arc produced a geometrical retinal image size of perhaps
20 µm, which corresponds to the spot size commonly encountered
for intrabeam viewing of a laser. However, the lesion size resulting
from several minutes fixation exceeded 100 µm. From the
present studies of photochemical damage mechanisms it is clear
that the expanded lesion resulted from eye movement. In other
words, due to eye movements, the point source was scanned over
an area larger than the point source image. Hence for an accumulated
dose concept for photochemical damage, it is unrealistic to assume
that the point source threshold achieved in an animal experiment,
where the eye movements are stabilized by anesthetic or mechanical
limitation, is directly applicable to the human exposure conditions.
G. Exposure Limits:
1. Long Term CW Exposures (ANSI Correction Factor CB):
The Federal Laser Product Performance (CDRH) Standard assumes
only a simple linearly additive biological effect for exposure
durations to visible light between 10 and 10(4) seconds (2.8 hours).
The cumulative radiant energy level that the CDRH standard accepts
as the level that will not cause a biological effect is 3.85 mJ.
Hence for a 10 second total accumulated exposure, this corresponds
to a power, entering a 7 mm aperture of 385 µW (0.385 mW),
and for a total accumulated exposure of 10(4) seconds to 3 x 10(4)
seconds, this corresponds to 0.385 µW.
The ANSI-Z136 and CDRH allowable exposure limits for CW lasers
(Class I limits) are essentially identical for wavelengths between
400 and 550 nm. The ANSI limits are, however, more relaxed for
wavelengths between 0.550 and 1.4 µm. ANSI recognizes a
decreased biological hazard in the red and infrared end of the
spectrum that is not recognized by the CDRH.
The ANSI-Z136 Maximum Permissible Exposure (MPE) level for a
very long term exposure by a helium-neon laser is, in fact, seventeen
times greater than the CDRH standard. In the 1976 revision, ANSI-Z136
introduced the correction factor CB, such that:
C(B) = 10(15) (LAMBDA -0.550) where: C(B) = 1.0 in the range
0.400-0.550 µm (blue light) LAMBDA = Laser wavelength (µm).
This correction factor has a value of 17.5 at the 633 nm HeNe
laser wavelength, and, thus, permitted a radiant exposure of 185
mJ/cm(2) accumulated exposure. This applies for periods of T(1)
= 453 to 10(4) seconds, and 17.5 W/cm(2) (7 µW in a 7 mm
limiting aperture) for continuous operation of very long exposure
durations exceeding 10(4) seconds. The comparable exposure for
an argon laser at 0.488 to 0.514 µm would be 1.0 µW/cm(2)
(0.4 µW in a 7 mm limiting aperture).
2. Repetitively Pulsed Exposures:
Current laser safety standards (ANSI Z-136) require a decrease
in the maximum permissible exposure (MPE) for scanned or repetitive
pulse radiation as compared to continuous wave radiation for pulse
repetition frequencies (PRF) in the general range of 1-15 KHz.
For reasons that are not yet well understood, scanned or repetitively
pulsed radiation with repetition rates less than 15 KHz have lower
retinal damage threshold levels than CW radiation of comparable
power.
As has been mentioned previously, one important distinction between
ANSI-Z136 and CDRH laser limits is that although both assume a
7 mm aperture, the ANSI standard has further restrictions regarding
the exposures which occur with a repetitively pulsed or a scanning
laser beam.
Typical scanning laser beams have a dwell time across the pupil
of the eye of the order of a few microseconds. CDRH assumes that
if a single scan exposure does not exceed the limits established
for a microsecond duration single pulse laser, and that if the
multiple scans in linear addition do not exceed the Class I limit,
then the device presents no ocular hazard (i.e., it is Class I
for one emission duration). However, the ANSI Z-136 Standard,
has a reduction factor of the threshold for each of the single
pulses based on biological data that is yet well explained by
any theory. The CDRH standard does not recognize this repetitively
pulsed correction factor. However, some experts envision the possibility
of a repetitively pulsed laser which is Class I by the CDRH standard
and perhaps Class II or even Class IIIB by the ANSI-Z-136 standard.
If this is true, injury may result after an exposure of only a
few seconds.
The ANSI standard requires that multiple pulse (scanning) lasers
operating from 1 to 15,000 Hz have a correction to the single
pulse MPE. The correction factor is determined by taking the fourth
root of the total number of pulses in a pulse train. Then, the
correction factor is calculated such that the MPE radiant exposure
or integrated radiance of an individual pulse within the train
is reduced by a factor N(-1/4) as follows: MPE(multiple pulse)
= [N(-1/4)] x MPE(single pulse) Where: N = number of pulses in
the train MPE(single pulse) = MPE applicable to a single pulse
of the pulse length.
The choice of "on-time" to determine the total number
of pulses is one of the variables that often leads to some confusion.
This "on time" is chosen to be some appropriate time
factor, typically ranging from 10 to 1000 seconds. The ANSI standard
does indicate, however, that 10 seconds is a valid time for invisible
(NIR) radiation.
The allowable exposures given in all of the present safety standards
attempt to follow as closely as possible, the actual biological
data obtained with the different lasers. The ANSI-Z-136 standard
probably gives the best fit with the real biological hazards.
In this regard, it should be again noted that the upper limit
for Class I Helium Neon lasers in the Federal Laser Standard is
seventeen times less than the present ANSI-Z-136 (1980) standard.
In 1973, the two standards were almost identical, but by 1976
the ANSI limits for lasers operating in the red and near-infrared
regions of the optical spectrum were relaxed considerably because
of new biological data that was unavailable in 1973.
H. Maximum Permissible Exposure Limits:
A summary of Maximum Permissible Exposure (MPE) limits for direct
ocular exposures for some of the more common lasers is given in
Table III-3. For further information on MPE values, refer to the
Z-136.1 "Safe Use of Lasers" Standard of the American
National Standards Institute.
For further information on MPE values, refer to the ANSI Z-136.1
"Safe Use of Lasers" Standard.
I. Associated (Non-Beam) Laser Hazards:
In some laser operations, particularly in the research laboratory,
other aspects may require consideration.
1. Industrial Hygene Considerations:
Potential hazards associated with compressed gases, cryogenic
materials, toxic and carcinogenic materials and noise should be
considered. Adequate ventilation shall be installed to reduce
noxious or potentially hazardous fumes and vapors, produced by
laser welding, cutting and other target interactions, to levels
below the appropriate threshold limit values, e.g., American Conference
of Governmental Industrial Hygienists (ACGIH) threshold limit
values (TLV's). [Additional references can be found in Appendix
F: "Special Considerations" of ANSI Z136.1 (1986)].
2. Explosion Hazards:
High pressure arc lamps and filament lamps or laser welding equipment
shall be enclosed in housings which can withstand the maximum
pressures resulting from lamp explosion or disintegration. The
laser target and elements of the optical train which may shatter
during laser operation shall also be enclosed.
3. Other Non-Beam Optical Radiation Hazards:
This relates to optical beam hazards other than laser beam hazards.
Ultraviolet radiation emitted from laser discharge tubes, pumping
lamps and laser welding plasmas shall be suitably shielded to
reduce exposure to levels below the ANSI Z-136.1 (extended source)
and/or ACGIH - TLV's.
4. Collateral Radiation:
Radiation, other than laser radiation, associated with the operation
of a laser or laser system, e.g., radiofrequency (RF) energy associated
with some plasma tubes, x-ray emission associated with the high
voltage power supplies used with excimer lasers, shall be maintained
below the applicable protection guides. The appropriate protection
guide for RF and microwave energy is that given in the American
National Standard "Safety levels with respect to human exposure
to radio frequency electromagnetic fields, 300 kHz to 100 GHz,"
ANSI C95.1; the appropriate protection guides for exposure to
X-ray emission is found in the Department of Labor Occupational
Safety and Health Standards, 29 CFR Part 1910.96 and the applicable
State Codes. Lasers and laser systems which, by design, would
be expected to generate appreciable levels of collateral radiation,
should be monitored.
5. Electrical Hazards:
The intended application of the laser equipment determines the
method of electrical installation and connection to the power
supply circuit (for example, conduit versus flexible cord). All
equipment shall be installed in accordance with the National Electrical
Code and the Occupational Safety and Health Act. [Additional specific
recommendations can be found in Section 7.4 of ANSI Z136.1 (1986)].
6. Flammability of Laser Beam Enclosures:
Enclosure of Class IV laser beams and terminations of some focussed
Class IIIB lasers, can result in potential fire hazards if the
enclosure materials are exposed to irradiances exceeding (Equation,
see printed copy). Plastic materials are not precluded as an enclosed
material but their use and potential for flammability and toxic
fume release following direct exposure should be considered. Flame
resistant materials and commercially available products specifically
designed for laser enclosures should also be considered.
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