A. General Overview:
Laser radiation of sufficient intensity and exposure time can cause irreversible damage to the skin and eye of man. The most common cause of laser induced tissue damage are thermal in nature. The process is one where the tissue proteins are denatured due to the temperature rise following absorption of laser energy. The thermal damage process is generally associated with lasers operating at exposure times greater than 10 microseconds and in the wavelength region from the near ultraviolet to the far infrared (0.315 – 103 µm).
For example, photochemical reactions are the principal cause of tissue damage following exposures to either actinic ultraviolet radiation (200 – 315 nm) for any exposure time or “short- wave” visible radiation (400 – 550 nm) when exposures are greater than 10 seconds. Tissue damage may also be caused by thermally induced acoustic-shock waves following exposures to very short-time laser exposures (submicrosecond).
The principle tissue damage mechanism for repetitively pulsed or scanned laser exposures is still in question. Current evidence would indicate that the major mechanism is a thermal process wherein the effects of the individual pulses are additive. There appears to be a different damage process for repetitively pulsed laser exposures when the individual pulses are shorter than 10 microseconds than when the pulses are longer. Both acute and chronic exposures to all forms of optical radiation can produce skin damage of varying degrees.
Numerous types of lasers have been explored rather extensively for the treatment of skin disorders. Certainly, skin injury is of lesser importance than eye damage; however, with the expanding use of higher-power laser systems, the unprotected skin of personnel using lasers may be exposed more frequently to hazardous levels.
For the common laser sources in the 0.3 to 1.0 µm range, almost 99% of the radiation penetrating the skin will be absorbed in at least the outer 4 mm of tissue.
In most all cases, the absorption will occur in tissue thicknesses less than 4mm.
For wavelengths greater than 400 nm, the reaction of the skin to absorbed optical radiation is essentially that of a thermal coagulation necrosis. This type of injury can be produced by any optical radiation source of similar parameters and is, therefore, not a reaction specific to laser radiation. It is similar in causality and clinical appearance to the tissues reaction of the deep electrical burn.
For pulsed laser irradiation, including exposures of the picosecond domain, there may be other secondary reactions in the tissue. Studies have shown that the volume of vaporized tissues produced by high-level irradiation with laser pulses in the millisecond domain can backscatter a significant portion of the incident energy. This effectively reduces the amount of absorbed radiation in the tissues.
The principal thermal effects of laser exposure depend upon the following factors:
Absorption and scattering coefficients of the tissues at the laser wavelength
Irradiance or radiant exposure of the laser beam
Duration of the exposure and pulse repetition characteristics, where applicable
Extent of the local vascular flow
Size of the area irradiated.
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) =
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.
Guidelines for Laser Safety and Hazard Assessment
Source: Occupational Safety & Health Administration, Guidelines for Laser Safety and Hazard Assessment PUB 8-1.7 (tablular data and equation illustrations have been omitted)