Table 4.1 summarizes laser biological effects. The primary laser danger is to the eye.
This is the most common type of laser injury besides electrocution and these injuries
may be permanent. The location and type of injury will depend on the type of laser
(visible, infrared, ultraviolet) and the amount of energy (both total and deposition
rate, J/sec) deposited in or on the eye. Figure 4.1 shows the interaction of various
electromagnetic radiation frequencies/energies with the eye.
Figure 4.1: Electromagnetic Radiation and the Eye
Most higher energy x- and gamma rays pass completely through the eye with relatively little absorption. Absorption of short-ultraviolet (UV-B and UV-C) and far-infrared (IR-B and IR-C) radiation occurs principally at the cornea. Near ultraviolet (UV-A) radiation is primarily absorbed in the lens. Light is refracted at the cornea and lens and absorbed at the retina; near infrared (IR-A) radiation is also refracted and absorbed in the ocular media and at the retina.
The eye transmits more than merely visible light (400−700 nm), certain infrared
frequencies (e.g., IR-A) are also transmitted and may cause retinal injury. For aperson to receive an eye injury: (1) they must be looking with unprotected eye or optical sight, (2) the laser must be oriented so it passes through the sight or into the eye, and (3) central vision is affected only if the person is looking directly at or near the laser source. Even though it is possible to be injured by light entering through the “corner of the eye,” it is unlikely that a single pulse will result in injury; however, if thousands of pulses are directed into an area, one or more persons might be injured.
Table 4.1: Potential Biological Laser Effects
||Erythema (sunburn), skin cancer
||Accelerated skin aging, pigmentation
||Pigmentation darkening, photsensitive reaction, skin burn
||Photochemical and thermal retinal injury
|| Photosensitive reaction, skin burn
||Cataract, retinal burn
||Corneal burn, aqueous flare, possibly cataract
Light (400 − 760 nm) and near-infrared (IR-A: 760 − 1400 nm) is sharply focused onto the retina. When an object is viewed directly, the light forms an image in the fovea at the center of the macula. This central area, approximately 0.25 mm in diameter for humans, has the highest density of cone photoreceptors. The typical result of a retinal injury is a blind spot within the irradiated area. A blind spot due to a lesion in the peripheral retina may go unnoticed. However, if the blind spot is located in the fovea, which accounts for central vision, severe visual defects will result. Such a central blind spot would occur if an individual were looking directly at the laser source during the exposure. The size of the blind spot depends upon whether the injury was near-to or far-above the threshold irradiance, the angular extent of the source of radiation, and the extent of accommodation.
The blind spot may be temporary or permanent.
• A hemorrhagic lesion is a severe eye injury characterized by severe retinal burnswith bleeding, immediate pain and immediate loss of vision. Such an injury requires a high intensity laser. The spreading hemorrhage will produce long lasting (months) vision degradation/loss and ultimately produces a permanent blind spot (blind spot in visual field) at the point of hemorrhage.
• A thermal lesion requires less laser energy/intensity than is needed to produce a hemorrhagic lesion. However, it still produces a permanent blind spot.
• Flash blindness is a temporary degradation of visual activity resulting from a brief but intense exposure to visible radiation. It is similar to the effects of a flashbulb. In flash blindness, the blind spot is temporary and its size depends upon the length of exposure and location of focus on the retina. Scatter of the laser beam through the atmosphere or an off-axis exposure may increase the blind spot size and result in an increased obscurence of the field of vision. There is a threshold of laser energy to produce flash blindness, but the energy is less than that which causes a thermal lesion. Flash blindness is differentiated from glare by the fact that the afterimage (blind spot) moves with eye movement and the afterimage lasts for a short period of time (minutes) after the laser exposure and recovery times range from a few seconds to a few minutes.
• Glare/Dazzle is an effect similar to flash blindness. Vision degradation occurs only during laser exposure and the glare stays in the same point in the visual field so one can move the eye to eliminate the effect.
In summary, retinal effects are due to visible and near IR laser exposure. Retinal lesions can occur even if there is no prolonged loss of vision (i.e., at periphery of vision field), however a retinal lesion is not always produced even when visual function disturbance has occurred (flash blindness, glare). If a retinal lesion is temporary, total visual recovery is seen within approximately three minutes.
The anterior structures of the eye are the cornea, conjunctiva, aqueous humor, iris and lens. The cornea is exposed directly to the environment except for the thin tear film layer. The corneal epithelium (i.e., the outermost living layer of the cornea), over which the tear layer flows, is completely renewed in a 48-hour period. The cornea, aqueous humor and lens are part of the optical pathway and, as such, are transparent to light. One of the more serious effects of corneal injury is a loss of transparency. At very short wavelengths in the ultraviolet and long wavelengths in the infrared, essentially all of the incident optical radiation is absorbed in the cornea. Because of rapid regrowth, injury to this tissue by short ultraviolet radiation seldom lasts more than one or two days unless deeper tissues of the cornea are also affected. Thus, surface epithelium injuries are rarely permanent.
• Photokeratitis can be produced by high doses of UV (UV-B and UV-C: 180
- 400 nm) radiation to the cornea and conjunctiva that cause keratoconjunctivitis.
This is a painful effect also known as snow blindness or welder’s flash.
It occurs because the UV energy causes damage to or destruction of the epithelial cells. Injury to the epithelium is extremely painful as there are many
nerve fibers located among the cells in the epithelial layer; however, it is usually
temporary because the corneal epithelial layer is completely replaced in
a day or two. The reddening of the conjunctiva (conjunctivitis) is accompanied
by lacrimation (heavy tear flow), photophobia (discomfort to light),
blepharospasm (painful uncontrolled excessive blinking), and a sensation of
”sand” in the eye. Corneal pain can be severe but recovery usually only takes
one to two days.
• Corneal opacities can occur when near-ultraviolet (UV-A: 315 − 400 nm) and far-infrared (IR-B and IR-C: 1.4 − 1000 μm) radiation damage the stroma causing an invasion of the entire cornea by blood vessels which turns the cornea milky. Because exposure is normally followed by a latent period lasting between 6 and 12 hours (varies with the exposure and wavelength), cause and effect may be difficult to pinpoint. Ordinary clear glass or plastic lenses or visors will protect the eye from far-infrared laser radiation such as that emitted from the CO2 laser.
• Cataract formation is also possible for UV-C, UV-B, UV-A, visible, IR-A, and IR-B wavelengths. Nearultraviolet and near-infrared radiation (UV-A, IR-A, and possibly IR-B) are absorbed heavily in the lens of the eye. Damage to this structure is serious because the lens has a very long memory. An exposure from one day may result in effects which will not become evident for many years (e.g., glassblower’s or steel puddler’s cataract). New tissue is continually added around the outside of the lens, but the interior tissues remain in the lens for the lifetime of the individual. The lens has much the same sensitivity to ultraviolet as the cornea, however:
1. The cornea is such an efficient filter for UV-C that little if any reaches the lens
except at levels where the cornea is also injured.
2. In the UV-A band, the cornea has substantial transmission while the lens
has high absorption (due to a pigment which accumulates throughout life and
which could become dense enough to turn the lens almost black).
3. UV-B appears to be effective in causing lenticular opacities, however, if the
exposure is low, the opacity may last only for a few days and then disappear.
4. For infrared wavelengths greater than 1.4 μm (IR-B and IR-C) the cornea and
aqueous humor absorb essentially all of the incident radiation, and beyond 1.9
μm the cornea is considered the sole absorber, however, absorption of energy
may cause heating of the interior structures which could contribute to opacities
in the crystalline lens (at least for short exposure times).
5. For IR-A irradiation, damage appears to be due to the breakdown of crystalline
cells contributing to opacities.
Because of the skin’s great surface area, the probability of laser skin exposure is
greater than the probability of laser eye exposure. However, despite the facts that
injury thresholds to the skin and eye are comparable except in the retinal hazard
region, laser injury to the skin is considered secondary to eye injury. For far-infrared
and UV (regions where optical radiation is not focused on the retina) skin injury
thresholds are approximately the same as corneal injury thresholds. Threshold
injuries resulting from short exposure to the skin from far-infrared and UV radiation
are very superficial and may only involve changes to the outer, dead layer (i.e., the
“horny layer”) of skin cells. Skin injury requires high powered laser exposure in
the spectrum from 180 nm to 1 mm depending upon the wavelength, dose rate,
and total energy absorbed. Such a temporary injury to the skin may be painful if
sufficiently severe, but eventually it will heal, often without any sign of the injury
because it lacks deep tissue involvement. Although unlikely to occur, injury to large
areas of skin are more serious as they may lead to serious loss of fluids, toxemia,
and systemic infection.
previous page | index | next page