The basis for almost all laser-induced eye injuries is the concentration of the radiation in the visible and near infra red range on the retina. The effect of this concentration is that the energy required to produce a visible retinal lesion is minuscule, about 50 microjoule for a Q- switched 532 nm laser. Even at lower energies the radiation can cause dazzle and flash blindness. At higher energies it can produce lesions which are ophthalmoscopically invisible, and at even higher energies, lesions that are visible and permanent. Higher energies still produce vitreous hemorrhage. The functional results of visible lesions depend not only on the energy impinging on the retina but mostly on the location of the injury. Foveal lesions will cause permanent reduction in visual functions, extrafoveal injuries will cause temporary visual incapacitation, and lesions further away from the macula may cause unnoticeable damage. Temporary incapacitation by intraocular hemorrhage can be engendered by a lesion anywhere in the eye. The latter is usually absorbed spontaneously or can be surgically removed by vitrectomy. An over-threshold injury anywhere on the posterior pole of the eye will lead to severance of the retinal nerve fiber layer, and thus to blind spots in parts of the retina unaffected by the original lesion. A common late, visually devastating, effect of laser lesions is retinal scarring which may lead to retinal holes, retinal detachment and delayed blindness.

The time course of the ophthalmoscopic and functional consequences of eight human laser accident cases from military laser systems is described. All patients reported subjective vision loss with ophthalmoscopic evidence of retinal alteration ranging from vitreous hemorrhage to retinal burn. Five of the cases involved single or multiple exposures to Q-switched neodymium radiation at close range whereas the other three incidents occur over large ranges. Most exposures were within 5 degrees of the foveola, yet none directly in the foveola. High contrast visual activity improved with time except in the cases with progressive retinal fibrosis between lesion sites or retinal hole formation encroaching the fovea. In one patient the visual acuity recovered from 20/60 at one week to 20/25 in four months with minimal central visual field loss. Most cases showed suppression of high and low spatial frequency contrast sensitivity. Visual field measurements were enlarged relative to ophthalmoscopic lesion size observations. Deep retinal scar formation and retinal traction were evident in two of the three cases with vitreous hemorrhage. In one patient, nerve fiber layer damage to the papillo-macular bundle was clearly evident. Visual performance measured with a pursuit tracking task revealed significant performance loss relative to normal tracking observers even in cases where acuity returned to near normal levels. These functional and performance deficits may reflect secondary effects of parafoveal laser injury.

Legal entanglements prevent publication of details on most laboratory and industrial laser accidents in the USA. Many macular injuries involving the fovea show no signs of recovery after several years. Both single eye (usually the dominant one) and binocular exposures are found usually resulting in large deficits in visual performance. The primary lesion is rarely, if ever, centered in the fovea, but is eccentric, superior and nasal and in the parafoveal zone. Accidental laser exposures below the damage threshold are sometimes falsely implicated causally in pre-existing retinal pathology, the grandmother syndrome. Another source of confusion is malingering, either hysterical or purposeful. One test for macular function has been designed to detect malingering, the flash Amsler grid. Functional loss has not been seen without retinal pathology that is easily visible with an ophthalmoscope. The circumstances of almost all accidents resulting in permanent damage are similar and involve Q-switched Nd:YAG lasers at 1,064 nm with the exposure individual staring directly at something in the beam path on purpose. The injurious exposure to the beam occurs by reflection or through an improperly used attenuator. Almost all were foreseeable by well established hazard analysis techniques and preventable by standard laser safety programs or conventional engineering controls.

Ocular injuries resulting from exposure to laser beams are relatively uncommon since there is normally a low probability of a relatively small-diameter laser beam entering the pupil of an eye. This has been the accident experience to date with lasers used in the research laboratory and in industry. A review of the accident data suggests that at least one type of laser is responsible for the majority of accidental injuries that result in a visual loss in the exposed eye. This is the q-switched neodymium:YAG laser. Although a continuous-wave laser causes a thermal coagulation of tissue, a q-switched laser having a pulse of only nanoseconds duration disrupts tissue. A visible or near-infrared laser can be focused on the retina, resulting in a vitreous hemorrhage. Examples of laser ocular injuries will be presented. Despite macular injuries and an initially serious visual loss, the vision of many patients recovers surprisingly well. Others may have severe vision loss. Corneal injuries resulting from exposure to reflected laser energy in the far-infrared account for surprisingly few reported laser accidents. The explanation for this accident statistic is not really clear. However, with the increasing use of lasers operating at many new wavelengths in the ultraviolet, visible and infrared, the ophthalmologist may see more accidental injuries from lasers.

Although visual function following retinal laser injuries has traditionally been assessed by measuring visual acuity, this measure only indicates the highest spatial frequency resolvable under high-contrast viewing conditions. Another visual psychophysical parameter is contrast sensitivity (CS), which measures the minimum contrast required for detection of targets over a range of spatial frequencies, and may evaluate visual mechanisms that do not directly subserve acuity. We used the visual evoked potential (VEP) to measure CS in a population of normal subjects and in patients with ophthalmic conditions affecting retinal function, including one patient with a laser injury in the macula. In this patient, the acuity had recovered from <EQ 20/100 initially after the exposure, to 20/16 at the time of this investigation (5 months post exposure). Visual stimuli consisted of counterphasing, sinusoidally-modulated luminance gratings presented at various spatial frequencies. VEPs were recorded with a gold cup electrode on the occipital scalp, and were demodulated in real time by a lock-in amplifier referenced to the stimulus counterphase frequency. As each grating was presented, its contrast was swept logarithmically from 0% to 50% over a 12-sec epoch. The CS was scored as the reciprocal of the lowest contrast within the sweep which elicited a response synchronized to the counterphase frequency. We found a CS deficit that appeared for a 3 degree(s) test field but not for larger test fields. These data indicated that contrast sensitivity measurements may reveal alterations in visual neural processing mechanisms not detected with standard clinical tests of acuity.

Damage criteria from laser irradiation have relied on fundoscopic and/or histological evidence. These methodologies have provided limited information regarding the functional impact of any observed damage and more importantly, do not lend themselves to assessments of the transition zone between temporary and permanent effects. Using a behavioral techniques, we have explored this transition zone with CW and Q-switched lasers. Our results demonstrate that daily exposure within the power levels of the transition zone become additive resulting in longer recovery times for successive exposures at the same power levels. Below this zone the impact of daily exposures appears non-additive; i.e., baseline acuity recovers to pre-exposure levels and both the magnitudes and durations of the recoveries appear unaffected by previous exposures. The additivity of successive exposures at the transition zone was most easily observed when relatively large-diameter (> 100 (mu) ), prolonged CW (100 msec) retinal exposures were made. When relatively small diameter (< 50 (mu) ), Q-switched (15 nsec) exposures were presented, significant decrements in acuity were not easily detected even with relatively intense exposures presented as single or multiple pulses within or across test sessions. These findings may reflect the contributions of different damage mechanisms evident in the transition zone.

Retinal damage thresholds (ED₅₀s) were determined in Rhesus monkey eyes for 100 ms exposures to collimated radiation from a tunable Ti:Sapphire laser at several wavelengths from 700 nm to 900 nm. Prior research using 15 ns duration laser pulses showed a strong variability of ED₅₀ with wavelength for retinal exposure in Rhesus monkeys to laser radiation in the near infrared spectrum. Current studies with the Ti:Sapphire laser show similar variability of ED₅₀ with wavelength for 100 ms retinal exposures. Previously measured light transmission and absorption properties of ocular tissues do not provide a complete or obvious explanation for the significant variations of threshold with small changes in wavelength. Similar wavelength dependencies of ED₅₀ for the two exposure durations in the wavelength range of 750 nm to 830 nm suggest that linear absorption is a cause of the variability. However, differences in the ED₅₀ curves at other wavelengths show that nonlinear mechanisms also contribute.

Energy absorption, heat transfer, thermodenaturation under the action of laser radiation pulse on pigmented spherical granules in heterogeneous laminated biotissues are investigated on the base of mathematical simulation. The possibility of selective interaction between short radiation pulses and pigmented retina biotissues is noted which results in the formation of thermodenaturation microregions inside and near the melanosomes. These denaturation microregions can originate in the eye biotissue under laser radiation intensities less than about 2 - 4 times the threshold ones determined ophthalmoscopically. These microdamages can appear without being detected by the standard ophthalmoscopical methods.

The small eye of the snake was used in combination with confocal scanning laser ophthalmoscopy to evaluate acute laser retinal damage effects at the in vivo cellular level. Because the snake eye has optical powers that allow high magnification and good ocular transmission the photoreceptors of this retina can be imaged in vivo. With a confocal scanning laser ophthalmoscope, we simultaneously imaged acute laser exposure at either the photoreceptor or epiretinal vascular layer of the snake. Equal energy 50 microjoule Argon laser exposures at 10 msecs produced larger lesion diameters and more photoreceptor loss than equal energy exposures at 80 msecs. Angiography measures demonstrated a deeper lesion depth extending for short pulse vs long pulse exposure. Q-switched 532 nm Neodymium laser exposure produced lesions more than three times the diameter of those induced with higher energy Argon laser energies. Histopathology showed selective damage to the macro and micro-oil droplet structures of this retina, suggesting an alteration in the photoreceptor optical transmission system. Pathophysiological slowing and stoppage of blood cell flow was induced following acute laser exposure.

We have evaluated the acute effects of Argon laser injury to the retinal nerve fiber layer (NFL) in the non-human primate. Single Argon laser exposures of 150 millijoules were employed to induce retinal NFL injury. Retinal NFL injury is not acute; unlike its parallel in retinal disease it has two components that emanate from the acute retinal injury site. The ascending component is more visible, primarily because it is ascending toward the disk, representing ganglion cell axons cut off from their nutrient base, the ganglion cell body; the descending component may require up to 3 weeks to develop. Its characterization depends on the distribution of retinal NFL and the slower degeneration of the ganglion cell bodies. Fluorescein angiography suggest a retinal capillary loss that occurs in the capillary bed of the retinal NFL defect. It may reflect a reduced capillary vascular requirement of the NFL as well as a possible reduction of activity in the axonal transport mechanisms in the ascending NFL defect.

Argon laser photocoagulation is a standard and effective clinical technique for a variety of disease conditions. However there is evidence that coagulation produces more widespread alterations in the retina than the local scarring at the injury site. For example, in diabetic retinopathy multiple photocoagulations in the retinal periphery can control blood vessel growth in the central retina. Therefore we have studied the changes in retinal glial cells following photocoagulation using immunocytochemical techniques with an emphasis on the spread of cellular reactions by using whole, flatmounted retinal preparations. Muller glial cells do not normally express the cytoskeletal protein GFAP (glial fibrillary acidic protein) but do so after a variety of injuries. We found that there is a very widespread expression of GFAP by Muller cells even after very focal coagulations and that this persists for 1 - 1.5 months after coagulation. The microglial cells are primed to react to injury and can release very powerful effector molecules and we therefore also examined the microglial reaction to see whether it correlated with the Muller cell reaction. However, we found that the microglial response, in terms of anatomical changes, was very focally confined to regions of direct cellular injury. We also examined MHC II expression to see whether microglia expressed this activity related protein without anatomical changes but we found no evidence of wide spread changes. In summary we find that inflammatory reactions are very localized after coagulation but the macroglial changes are more widespread and therefore the distant effects of photocoagulation may be more related to macroglial reactions.

Eight Cynomolgus fasciculata who had graded laser lesions placed in one eye 6 years previously were evaluated by a stimulation and electrophysiologic recording technique to produce maps of retinal function. All animal testing was performed under IACUC approved protocols. The single q-switched pulses from a neodymium-YAG laser produced lesions of 4 types: no visible change, minimal visible lesions, `white dot' lesions (localized circumscribed retinal blanching) and `red dot' lesions (contained retinal hemorrhage) in the eye at the time of placement. Single exposures had been made in four locations: 5 degrees superior, inferior and temporal to the fovea, and one foveally. The multifocal (perimetric) electroretinogram was recorded from specialized contact lenses through hospital grade amplifiers. Initial analyses gave field maps that demonstrated apparent relative loss of function in some lesion sites. However, these losses were variable and occasionally patchy (i.e. disconnected areas of low signal). Repeated examinations of the same retinal areas showed high variability, even with 15 minute acquisition times and no apparent gaze drift. Apparent losses did not appear to correlate with visible retinal changes at the lesion site. Further research is needed to determine the biological substrate for this variability in response topography.

A model of human visual detection performance has been developed, based on available anatomical and physiological data for the primate visual system. The inhomogeneous retino- cortical (IRC) model computes detection thresholds by comparing simulated neural responses to target patterns with responses to a uniform background of the same luminance. The model incorporates human ganglion cell sampling distributions; macaque monkey ganglion cell receptive field properties; macaque cortical cell contrast nonlinearities; and a optical decision rule based on ideal observer theory. Spatial receptive field properties of cortical neurons were not included. Two parameters were allowed to vary while minimizing the squared error between predicted and observed thresholds. One parameter was decision efficiency, the other was the relative strength of the ganglion-cell center and surround. The latter was only allowed to vary within a small range consistent with known physiology. Contrast sensitivity was measured for sinewave gratings as a function of spatial frequency, target size and eccentricity. Contrast sensitivity was also measured for an airplane target as a function of target size, with and without artificial scotomas. The results of these experiments, as well as contrast sensitivity data from the literature were compared to predictions of the IRC model. Predictions were reasonably good for grating and airplane targets.

Laser-induced central retinal damage not only may diminish visual function, but also may diminish afferent input that provides the ocular motor system with the feedback necessary to move the target to the fovea. Local visual field stabilizations have been used to demonstrate that central artificial occlusions in the normal retina suppress visual function. The purpose of this paper is to evaluate the effect of local field stabilizations on the ocular motor system in a contrast sensitivity task. Five subjects who tested normal in a standard clinical eye exam viewed landolt rings at varying visual angles under three artificial scotoma conditions and a no scotoma condition. The scotoma conditions were a 2 degree(s) and 5 degree(s) stabilized central scotoma and a 2 degree(s) stabilized scotoma positioned 1 degree(s) nasal to the fovea. A Dual Purkinje Eye-Tracker (SRI, version 5) was used to provide eye-position data and to stabilize the artificial scotoma on the retina. The data showed a consistent preference for placing the target in the superior retina under the 2 degree(s) and 5 degree(s) conditions with a strong positive correlation between visual angle and deflection of the eye position into the superior retina. These data suggest that loss of visual function from laser-induced foveal damage may be due in part to a disruption in the ocular motor system. Thus, even if some function remains in the damage site ophthalmoscopically, the ocular motor system may organize around a nonfoveal retinal location, behaviorally suppressing foveal input.

The effects of human laser eye damage may be modeled by stabilizing a small portion of the visual field on the retina. We compared the effects of such artificial scotomas with accidental human laser induced retinal damage on contrast and recognition sensitivity. Horizontal and vertical output voltages from a purkinje eye-tracker controlled video generated scotomas. Contrast sensitivity functions were obtained with focal acuity targets ranging in spatial frequency from 0.5 to 20 cycles/degree. Target vehicular recognition functions were obtained for larger targets and restricted size range. Artificial scotoma effects demonstrated uniform loss in contrast sensitivity in the presence of central scotomas; paracentral scotomas had minimal effects beyond 10 cycles/degree but were effective from 0.5 to 10 cycles/degree. Similar results were obtained for vehicular recognition sensitivity functions. On the other hand, patient macular injuries resulted in greater suppression of the contrast sensitivity function regardless of whether injury was foveal or parafoveal. Secondary laser induced damage such as scar formation, traction or retinal nerve fiber layer injury may mediate high spatial frequency as well as low spatial frequency loss. The uniform suppression of contrast sensitivity may involve selection of a superior retinal site with an ocular motor component to fine tune the search for remaining `islands' of high photoreceptor density. Such high density photoreceptor patches may serve as a pseudo fovea, if laser induced secondary damage effects are minimal.

The purpose of this study was to identify cytokines produced by the retina after laser injury. With the aid of a scanning laser ophthalmoscope (SLO), right eyes of mice received lesions from a continuous wave argon laser. Left eyes served as unirradiated controls. At 2, 4, 6, 12, 24, and 48 hr after laser irradiation groups of 3 mice were euthanized and retinas fixed for histology or isolated for RNA. Messenger RNA (mRNA) was reverse-transcribed into complementary DNA (cDNA) and subjected to polymerase chain reaction for the following cytokines: tumor necrosis factor-(alpha) (TNF-(alpha) ), interleukin-1(alpha) /(Beta) (IL- 1(alpha) /(Beta) ), interleukin-6 (IL-6), transforming growth factor-(Beta) 1 (TGF- (Beta) 1), macrophage colony stimulating factor (M-CSF), inducible nitric oxide synthase (iNOS), and glyceraldehyde 3-phosphate dehydrogenase (G3PDH). Histologically, lesions were confined to the photoreceptors, retinal pigment epithelium, and choroid. In laser-injured retinas, mRNA levels were elevated for IL-1(alpha) , TGF-(Beta) 1, iNOS, and G3PDH, but not TNF-(alpha) , IL-1(Beta) , or IL-6. It appears that the retina, in response to laser injury, upregulates a select number of cytokines in a time-course dependent fashion.

The eye is continually subjected to ambient radiation. The benign function of this light is to direct vision and circadian rhythm. However, under intense light from artificial sources such as lasers and operating room microscopes the natural protection of eye against light damage may be undermined. The damage can be a result of a photochemical, thermal or mechanical injury which can all disrupt ocular tissues. The mechanism for the above damage involves the production free radical and reactive oxygen intermediates either as a primary effect of the absorbance of the light or as a secondary effect due to an inflammatory response to heat or mechanical injury. This can induce a cytokine cascade as well as induce the increased production of nitric oxide. Glutathione mimics can block light induced free radical and oxygen radical intermediates in the eye. For instance, singlet oxygen is scavenged at a rate of 10⁶ M^-1 s^-1; hydroxyl radical is scavenged at a rate of 10⁹ M^-1 s^-1 and superoxide is scavenged at a rate of 10³ M^-1 s^-1. In addition thiols block nitric oxide and other intermediates involved in an inflammatory response. Glutathione mimics which have offered in vivo protection against light damage to the lens and retina, have the potential to protect against laser-induced damage to the human eye.

An active duty marine corps service member had bilateral full thickness macular holes induced following accidental Q-switched laser exposure from a hand held Neodymium range finder (ANGVS-5). The right eye had a large hole nasal to the fovea, while the left eye had a much smaller hole closer to the fovea centralis. Over the 18 months following the injury, the left eye demonstrated mild progressive degradation in visual function, but retained 20/20 final visual acuity. In contrast, the hole in the right eye increased in size, developed a localized retinal detachment with cystic changes in the fovea, and had atrophy of the retinal pigment epithelium. Within 6 months after injury, acuity declined to 20/100. Macular hole surgery was performed with a goal of sealing the edges of the hole in order to allow resolution of the localized detachment and cystic changes in the fovea. In spite of surgical techniques that are generally successful in the treatment of macular holes associated with other etiologies, the fundus findings remained unchanged and visual acuity declined to 20/400. To the best of our knowledge, this is the first case report of macular hole surgery for this condition.

Many retinal injuries result in an irreversible neuronal loss, which can not yet be reduced by pharmacological methods. To determine whether glutamate-receptor blockers can serve as neuroprotective agents in the retina, as they do in the central nervous system, we examined the effects of MK-801, an NMDA-receptor antagonist, on laser-induced retinal injury in a rat model. Immediately and 8 h after argon laser retinal photocoagulation, rats were treated with intraperitoneal injections of MK-801 (3 mg/kg) or saline. After 3, 20 or 60 days the animals were sacrificed and their retinal lesions were evaluated histologically and morphometrically. Photoreceptor cell loss, both immediately and up to 2 months after laser irradiation, was significantly smaller in MK-801-treated rats than controls. MK-801 exhibits neuroprotective property in the retina. This points to the involvement of glutamate in the laser-induced retinal neuronal damage. Glutamate-receptor blockers should be further investigated for therapy of retinal diseases characterized by neuronal cell destruction.

Up to 10% of all combat casualties involve eye injuries which are becoming more severe, bilateral and likely to lead to a retained intraocular foreign body. The modern battlefield is permeated with laser radiation from range finders, target designators and perhaps laser weapons aimed at producing visual incapacitation. In future wars, therefore, the likelihood of eye injuries is very high. We sought to devise means to protect the eye from military relevant injurious agents. Almost all ballistic injuries can be prevented by using polycarbonate goggles. They must not, however, interfere with the soldier's functions such as the use of binoculars or limit his visual fields. These problems are not insurmountable and we shall demonstrate new goggles design which we believe will be acceptable to the troops. The solution to laser protection is more difficult. For that purpose the goggles include outserts filters for various groups of laser wavelengths. The soldier will use the appropriate filter according to a reading from a laser detector which will indicate which filter is protective against the wavelength detected.

Laser technology has significantly impacted our everyday life. Lasers are now used to correct your vision, clear your arteries, and are used in the manufacturing of such diverse products as automobiles, cigarettes, and computers. Lasers are no longer a research tool looking for an application. They are now an integral part of manufacturing. In the case of Class IV lasers, this explosion in laser applications has exposed thousands of individuals to potential safety hazards including eye damage. Specific protective eyewear designed to attenuate the energy of the laser beam below the maximum permissible exposure is required for Class 3B and Class IV lasers according to laser safety standards.

Protecting the eye from coherent light sources is of critical concern to both military and civilian laser users. Laser protective eyewear degrades visual performance. Common and emerging applications use lasers emitting at numerous wavelengths or single lasers emitting at multiple wavelengths. Protection against multiple wavelengths increases the difficulty in selecting or building protective eyewear and concomitantly usually increases the performance penalty. Pursuit tracking performance decrements were measured as a function of bandwidth and peak wavelength transmission for 12 bandpass filters. Eight volunteers tracked a target subtending 34 milliradians (mrad) at a constant velocity of 5 mrad/sec for 15 sec. The target traversed an arc located 5 m from the tracker. Each volunteer received two training days and two test days. Twelve bandpass filters, with bandwidths of 10, 25, 40, and 70 nm, and peak wavelengths of 450, 550, and 650 nm were randomly inserted into the optics of the tracker. No volunteer received all 4 bandwidths of one peak wavelength on either test day, thereby reducing any adaptational effect. Luminance was equated across filters using Neutral Density (ND) filters. An ND filter of equal Optical Density served as the control. The total luminance at the eye was 0.8 cd/m². Trials were collected at a rate of 4 per filter. The 10 nm blue filter elicited the poorest performance, followed by the 25, 40, and 70 nm blue filters. The red filters enhanced performance across all but the narrowest bandwidth. It can be assumed that the blue end of the visible spectrum with it's `forward of the retina' focusing properties and the low number of blue photoreceptors are responsible for the large decrements. Current philosophy in laser eye protection is to allow as much of the blue end of the spectrum through a filter to preserve scotopic transmission. The shortwave transmission may inadvertently increase error rates for visual tasks.

An earlier report documented exposure parameters for inducing corneal, lens, and retinal damage with a laser emitting in the `eye-safe' wavelength range (Nd:YAG laser radiation at 1.318 micrometers and 1.356 micrometers ). Ocular damage thresholds are much higher for these wavelengths than for visible wavelength lasers. However, it was also noted that an exposure in the `eye-safe' wavelength range may result in multiple damage sites throughout the ocular medium and retina/choroid; that seemingly unaffected exposure sites, when monitored over time, may reveal slowly developing (days or longer) tissue degeneration; and, that the tissue degradation may ultimately involve regions greater in area than those directly irradiated by the laser. In order to elucidate the nature of tissue degeneration following IR laser exposure, the comparative pathology of retinal tissues exposed to argon and IR laser radiation is reported. Further, periodic post-exposure exams were conducted using scanning laser ophthalmoscopy to monitor the in vivo progress of the ocular tissue response following IR exposures. These observations are also contrasted to the results of corresponding examinations following visible wavelength laser exposures.

Laser eye protection (fixed wavelength) can be grouped into three broad categories: adsorptive (dyes, phosphate glass), interference (dielectric, holographic and rugate), or hybrid (i.e., absorptive and interference, interference and interference, etc.). The approaches differ markedly in design complexity, cost, and their impact on visual performance. The challenge is to achieve a balance between complexity and cost while minimizing the impact on visual performance. The data to be discussed are resolution thresholds set by five observers with a corrected or uncorrected acuity of 20/20. The observer modulates the spatial frequency of a sinusoidal grating while grating contrast is fixed at 5, 10, 20, 40 and 80%. The first study quantifies visual performance from low photopic (10 ftL) down through low scotopic light levels (5E-5 ftL). The data show a sharp drop in acuity as ambient light level drops from 1 to .001 ftL (roughly equivalent to a quarter moon). The second study measures visual acuity over the same range of light levels while the observer wears: (1) multi line absorptive laser eye protection, (2) hybrid laser eye protection, and (3) neutral density equivalents. The results demonstrate that once the data is normalized for spectral compatibility and scotopic transmittance there are no significant differences between the filters. A third study assesses the loss in visual performance as scotopic transmittance is reduced from 40 to 30 to 20%. The implications for filter requirements and design will be discussed.

A compact device for the characterization of laser incoming radiation based on a novel concept is presented. The device has the ability of performing simultaneously the following tasks: (1) To identify positively the incoming radiation as laser light; (2) To determine the wavelength of the radiation; and (3) To determine the direction of the radiation. Being based on low-cost components, these devices are expected to find applications in laser safety as well as in laser games and entertainment systems. A prototype of the device was built and tested.