Chapter 13
VISIBLE LIGHT and INFRARED RADIATION

James A. Hathaway and David H. Sliney

Visible light is generally defined as that portion of the electromagnetic spectrum between approximately 380–400 nm and approximately 760 nm.1 Some reference sources list the upper limit of the visible light band as 780 or 800 nm.2,3 Within the visible light spectrum, blue light (400–500 nm) is of particular importance. Infrared radiation is divided into the following three bands: IR-A is between 760 and 1400 nm, IR-B is between 1.4 µm (1400 nm) and 3 µm, and IR-C is between 3 and 1000 µm (1 mm). This ABC notation is sometimes referred to as near, middle, and far IR.

OCCUPATIONAL SETTING

Visible light, along with the adjacent portions of the ultraviolet and infrared bands of radiation, makes up much of the solar radiation reaching the surface of the Earth. Outdoor occupations naturally have greater exposure to visible light and IR radiation. Visible light reflecting off sand and snow can create hazardous conditions that require eye protection. Ambient IR radiation can contribute to heat load, particularly in persons who work outdoors while wearing impervious clothing. Issues related to heat stress are covered in Chapter 6. Man-made sources of broad-spectrum intense visible light include arc welding or cutting, arc lamps, spotlights, gas and vapor discharge tubes, flash lamps, open flames, and explosions.4 Even though ultraviolet radiation is the main concern with many of these exposures, the potential for visible light-induced damage cannot be ignored. More recent concerns have been raised regarding potential blue light hazards from crystal glassblowing, use of LED dental illumination applications, and newer types of theater projectors.5–7

Infrared radiation is emitted by many sources besides the sun. Man-made sources include heated metals, molten glass, home electrical appliances, incandescent bulbs, radiant heaters, furnaces, welding arcs, and plasma torches. Glassblowing and working in glass and steel plants are considered potentially hazardous due to excessive IR radiation.8,9

MEASUREMENT ISSUES

Among the adaptive responses to intense visible light are constriction of the pupil, light adaptation of the retina, squinting, and blinking. Intense light causes a natural aversion response, including shutting the eyes and turning away from the source of exposure. Measurement of continuous visible light emissions is usually not necessary to determine if the level of exposure is excessive or not, because the human eye itself provides adequate warning. Pulsed sources of visible light and sources that are turned on suddenly may present problems if the intensity of light is high enough to cause damage before an aversion response can take place. Usually such sources will be labeled with appropriate warnings; specific measurement of output levels will not be necessary.

Unfortunately, there are virtually no instruments designed as optical safety meters; so when measurements are necessary, a scientist experienced in radiometry may have to be consulted. A variety of instruments that use photodiodes or thermal detectors may be required for the measurement of visible light levels. These devices detect optical energy and convert the optical radiation to a measurable electrical signal. Similar instruments are also available to measure infrared radiation. IR radiation is most frequently measured using thermal detectors such as thermopiles or disk calorimeters.10,11 These detectors measure heat from absorbed energy; they are suitable for the entire range of IR radiation, although the response time is slow. Lamp safety standards require the lamp manufacturer to perform detailed radiometric measurements of the optical radiation hazards and to group the lamp in one of four risk groups.

EXPOSURE GUIDELINES

Visible light and the near portion of the IR spectrum have threshold limit values (TLVs®) developed by the American Conference of Governmental Industrial Hygienists (ACGIH).12 These TLVs® are for visible and near-infrared radiation between 400 and 3000 nm. The TLVs® apply to 8 hours exposures and require knowledge of the spectral radiance and total irradiance of the source as measured at the eyes of the worker. Moderately complex formulas and reference tables are required to calculate the TLV® for each exposure situation; these calculations are beyond the scope of this book. TLVs® can be calculated for three types of injury—retinal thermal injury from exposure to 400–3000-nm radiation, retinal photochemical injury from chronic blue light (400–500-nm) exposure, and possible delayed effects leading to cataract formation from exposure to 770–1400-nm radiation. There are additional calculations for persons who have had a lens removed (cataract surgery) and not had a UV-absorbing intraocular lens surgically inserted. Such persons (although now rare) are at increased risk for photochemical retinal injury. The International Commission on Non-Ionizing Radiation Protection (ICNIRP) has published guidelines for human exposure and these are available at no cost from the ICNIRP web site (http://www.icnirp.org).13,14

NORMAL PHYSIOLOGY

Life on Earth would not be possible without visible light and infrared radiation. Infrared radiation provides warmth, allowing a climate where life is possible; visible light provides the energy upon which life is based. Plant life uses chlorophyll to acquire energy from visible light. Using this energy, it converts carbon dioxide and water to carbohydrates in a process called photosynthesis. Plant-eating animals ingest stored carbohydrates in plants, and meat-eating animals acquire photosynthetically produced energy directly by feeding on plant-eating animals. The energy in all food consumed by humans is ultimately derived from visible light reaching the Earth’s surface. Most animal species have a sense of vision that is responsive in the near-UV, visible, or near-IR portion of the electromagnetic spectrum. For humans, visual response defines the relatively narrow band of radiation called visible light (400–760 nm). Photons of light enter the eye and are focused by the cornea and lens onto the retina. In the retina, there are two types of photoreceptors: the cones, which are responsible for color vision and detailed visual acuity, and the rods, which allow peripheral vision and are responsive to lower light levels. The macula is an area on the retina that is densely packed with cones; it is the site of maximum visual acuity.

Photochemical reactions take place in both the cones and the rods. This stimulus results in a neurosensory transmission to the brain where visual images are perceived. The retina and its photoreceptors are able to adapt to a wide range of light intensities. Adaptation to brighter levels of light typically occurs rapidly in a period of a few seconds. Adaptation to darkness requires many minutes, and in some cases more than an hour, to achieve maximum adaptation. In most circumstances, visible light is not hazardous. In addition to light adaptation, other normal protective mechanisms such as pupillary constriction, squinting, and blinking occur rapidly when bright light is encountered. When exposed suddenly to a highly intense visible light source, most people exhibit an aversion response that includes blinking and turning the head. This response typically occurs within 0.25 second; this time period is used to calculate exposure limits for radiation in the visible spectrum. The eyes are also naturally shaded from ambient sunlight by the eyebrows and the periorbital socket ridge.

Under some circumstances, visible light can be harmful—for example, when it is presented suddenly, as in a flash or explosion, or when equipment is first turned on. If the intensity is high enough to cause damage in <0.25 second, the natural protective mechanisms will be insufficient. It is also possible to create a hazardous situation by suppressing the aversion response and staring directly at a high-intensity light source such as the sun (solar maculopathy or eclipse photoretinitis) or a welding arc (welding-arc photoretinitis).

PATHOPHYSIOLOGY OF INJURY

Potential adverse health effects from overexposure to visible light or infrared radiation occur primarily in either the eye or the skin. Systemic effects of infrared radiation from general body heating are considered in Chapter 6. Adverse effects can result from acute and chronic exposure. In the case of the eye, injury can result in different structures depending on the wavelength of radiation.

Acute chorioretinal injury

Visible light and near-infrared radiation from 400 to 1400 nm can be focused on the retina.

Sudden exposures to high-intensity sources of such radiation can cause adverse effects ranging from temporary flash blindness and afterimages to chorioretinal burns that produce scotomas (i.e., blind spots) in the field of vision. Retinal burns from gazing at the sun or observing a solar eclipse have been described throughout history. Man-made sources of luminance comparable to the sun have been developed in more recent decades. Even so, there have been fewer incidents of chorioretinal burns from man-made sources such as electric arcs, explosions, and nuclear fireballs than from directly viewing the sun.4 Measurement of the spectral radiance of the sun has shown that the exposure limits for blue light can easily be exceeded when viewing the sun. The exposures increase with solar elevation. Viewing the sun directly can be very hazardous and should be avoided.15

Several factors are important in determining the exposure to the retina. These include (i) pupil size, (ii) spectral transmission through the ocular media, (iii) spectral absorption by the retina and choroid, and (iv) the size and quality of the image. A dark-adapted pupil may be as large as 7 mm, as compared to a normal pupil size of 2–3 mm in outdoor sunlight. The area of a 7-mm pupil is about 12 times greater than a 2-mm pupil; thus, it allows that much more radiation to enter the eye. Although some radiation from 400 to 1400 nm can reach the retina, absorption in the ocular media (cornea, aqueous humor, lens, and vitreous humor) varies by wavelength. Optical transmission is greater from 500 to 900 nm, dropping about 50% to 1000 nm, rising again to 1100 nm, and dropping to low levels by 1200–1400 nm. Absorption of energy by the choroid and retina peaks around 500–700 nm, dropping gradually as the wavelength increases to 1000 nm, with a small rise peaking at about 1100 nm and with very little absorption past 1200 nm. The more energy that reaches and is absorbed by the retina and choroid, the greater the potential damage. For large, uniform images, the total absorbed dose per area on the retina is a good predictor of damage. Small images or images with “hot spots” blur as they are focused on the retina due to diffraction and therefore produce reduced peak retinal irradiance. Involuntary eye movements also spread the radiant energy over larger retinal areas.16

The mechanism of injury from accidental exposure to arc lamps or the sun was once thought to be primarily thermal, resulting in protein denaturation and enzyme inactivation. Today we know that most retinal injuries from staring at the sun or at a welding arc actually result from photochemical reactions that dominate particularly with exposure to wavelengths of visible light between 400 and 500 nm.17 However, thermal effects are still important. The threshold for thermal injury is dependent on light absorption, heat flow, and duration of exposure. Thermal injury is a rate-dependent process, so there is no single critical temperature that results in damage. In general, shorter exposures require higher temperatures to produce the same degree of damage.4

The degree of impairment caused by an acute chorioretinal injury depends on the size of the lesion in the retina and its location. If the source of exposure was directly viewed, as in gazing at a solar eclipse or looking at an explosion, the macula of the eye will be involved. Since fine visual acuity is dependent on intact macular function, damage in this area typically causes significant impairment of visual acuity. Injury to peripheral regions of the retina produces scotomas in the visual fields, but in many cases, peripheral lesions have minimal effect on overall visual function. Obviously, larger lesions cause more impairment than small lesions in the same location.

Chronic blue light-induced retinal injury

Whereas thermal effects of visible and near-infrared radiation on the retina are acute phenomena, the photochemical effects of blue light photoretinitis are additive over time periods of seconds to hours and are probably partially additive even over many years. Exposure to light capable of causing thermal injury that does not cause actual injury is virtually not additive with subsequent exposures. In contrast, blue light, especially 400–500 nm radiation, can cause subclinical changes, which with repeated exposures can result in observable retinal damage. Subacute retinal injury due to photochemical mechanisms can occur at thresholds well below those of thermal injury. This threshold is only slightly higher than normal exposures to sunlight in outdoor work environments.18 A number of mechanisms have been proposed to explain these effects, including photooxidative membrane damage, toxic chemical production in the outer retina, and metabolic disruption from extended overbleaching of retinal pigments. Ophthalmic examinations of experimental animals show both edema and pigmentary changes.

Some researchers believe that even typical or “normal” outdoor exposure to sunlight can result in damage to the retina over a period of many years. They believe that macular degeneration, which is an important cause of blindness in older persons, is the result of lifelong exposure to the blue light portion or possibly the entire visible spectrum of ambient sunlight. Many of these researchers regularly wear amber or red-tinted glasses to reduce blue light exposure. Even though the link between macular degeneration and chronic blue light or visible exposure must still be considered hypothetical, the results of subacute experiments provide support for the theory.19

Near-infrared exposure and cataracts

Near-infrared radiation is capable of producing cataracts; such damage has been noted historically in glassblowers and furnace men. Radiation between 800 and 1200 nm is most likely responsible for temperature increases in the lens itself because of its spectral-absorption characteristics. Visible wavelengths may also contribute to the problem, since the heat absorbed by the iris could result in heat transfer to the lens.20 Other structures of the eye, such as the cornea, absorb at longer wavelengths beyond 1200 nm and may also conduct thermal energy to the lens. Both mechanisms probably play a role in the relative importance of each being dependent on the wavelength characteristics of the exposure.21

Clinically, glassblowers’ cataract has been described as a well-defined opacity in the outer layers of the axial posterior cortex of the lens, appearing as an irregular latticework with a cobweb appearance.22 If exposure to IR between 700 and 800 nm or between 1200 and 1400 nm is a more significant factor, the cataracts are more likely to occur in the periphery of the lens.23

Acute skin, cornea, and iris injury

Both the skin and the cornea of the eye are opaque to wavelengths >1400 nm. IR radiation in this region produces injury through thermal mechanisms, with absorbed radiation being converted to heat. Injury to the cornea is described as a gray appearance detectable by slit lamp that is caused by energy just above the threshold for injury.24 Larger amounts of energy can produce extensive opacification of the cornea or even more severe injury. Focused sources of energy can create localized burns to the skin that resemble those caused by other sources of heat. There is some transmission of energy into the skin for radiation between 750 and 1300 nm, with maximum transmission at 1100 nm. At this wavelength, 20% of the energy will reach a depth of 5 mm. The nature of the injury will still be thermal. IR radiation below 3000 nm will penetrate into different depths of the cornea to varying degrees, depending on the specific wavelength. The iris of the eye can absorb energy and play a role only at wavelengths below approximately 1300 nm.

Solar urticaria and drug-induced photosensitivity

Although photosensitivity per se is primarily due to ultraviolet radiation, solar urticaria is often the result of visible light radiation, while drug-induced photosensitivity may be caused by visible light in the blue region, depending on the action spectrum of the specific drug. Solar urticaria is manifested by urticaria lesions on sun- or light-exposed areas of the body. Typically, the reaction begins as reddened skin; mild to moderate itching develops rapidly into urticaria lesions with edema.25 The lesions resolve over several hours. Different parts of the body have variable degrees of susceptibility. Typically, chronically sun-exposed areas such as the face and arms are more tolerant to light exposure.

Some patients react only to ultraviolet radiation in the 320–400 nm region, whereas others have an action spectrum of 400–500 nm. Still other patients have a broad-action spectrum of 280–600 nm. The mechanism of action is believed to be immunologic; in some cases, sensitivity can be transferred by a patient’s serum. An antigen may be formed in the skin of susceptible individuals following exposure to light, leading to an antigen–antibody reaction that produces the urticaria.26 In some individuals, a nonimmunologic mechanism may be present where light causes the production of a substance that causes the urticaria directly.

Drug-induced photosensitivity may be caused by exposure to ultraviolet radiation or visible light in the blue region, depending on the action spectrum of the particular substance. For example, the action spectrum for coal tar pitch is 340–430 nm and for dimethylchlorotetracycline, it is 350–450 nm. Both of these are examples where visible blue light as well as near UV can cause reactions. The clinical presentation may vary greatly. Lesions are usually on the light-exposed areas of the body, such as the face, the “V” of the neck, the back of the hands, and the extensor surfaces of the arms. Various degrees of redness, edema, and vesicle formation may occur. In chronic cases, scaling and lichenification may occur.

Either phototoxicity (most common) or photoallergy may cause drug-induced photosensitivity. The former can be photodynamic, requiring oxygen, or it can be oxygen independent. Phototoxicity is usually targeted at nuclear DNA or cell membranes. Photodynamic sensitizers interact with oxygen to form phototoxic compounds in the presence of UV or blue light. Oxygen-independent photosensitizers form toxic photoproducts even in the absence of oxygen. Photoallergy is the result of an immunologic response. The drug or chemical absorbs a photon of UV or blue light and is converted to a photoproduct that binds to a soluble or membrane protein to form an antigen.27

Porphyrias

While a number of conditions—such as systemic lupus erythematosus, atopic dermatitis, acne vulgaris, and herpes simplex—can be aggravated by exposure to UV radiation, the porphyrias are the result of blue light interaction with porphyrins produced by aberrations in the enzymatic control of heme synthesis. The action spectrum is most predominant between 400 and 410 nm. Photons in this narrow wavelength band cause porphyrins to go to an “excited” state. Reactions with oxygen lead to peroxide formation, which in turn damages vital components of cell membranes, leading to cell death. The porphyrias may be due to either hereditary or acquired abnormalities in heme synthesis. They are classified into hepatic or erythropoietic categories, depending on the site of excess porphyrin. Most of the porphyrias are due to autosomal dominant defects in the enzymes responsible for heme synthesis. Porphyria cutanea tarda is the most common form and photosensitivity is the major finding. The disease, which usually manifests itself in middle age, may be triggered by exposure to certain medications such as barbiturates, phenytoin, and tolbutamide.

TREATMENT

Thermal burns to the skin from visible or infrared radiation are treated like any thermally caused burn. If minor in nature, burns to the cornea are evaluated using fluorescein stain and slit lamp. Treatment focuses on the prevention of infection during healing. Typically it includes the use of cycloplegic agents and antibiotics in addition to patching of the eyes. Injuries to the deeper structures of the eye do not lend themselves well to specific treatment; they often result in permanent damage. Visual impairment depends on the extent and location of the injury.

Photosensitivity reactions can be treated with nonsteroidal anti-inflammatory agents to control fever and pain. Corticosteroids may be needed for severe reactions and can be used both topically and systemically.

MEDICAL SURVEILLANCE

Medical surveillance has not been generally recommended for individuals exposed to intense levels of visible or infrared radiation. Surveillance would not be appropriate for the acute effects of visible or IR radiation. Nor have specific subclinical effects been identified that would be useful for the surveillance of individuals with chronic exposures. Also, the magnitude of most occupational exposure is dwarfed by the contribution from ambient sunlight. Examination of the lens of the eye by slit lamp has shown a far greater prevalence of opacities of the lens in IR-exposed individuals than in controls.26 However, it was not possible to demonstrate a dose–response in these studies, and the changes noted were indistinguishable from naturally occurring cataracts. Although this type of examination has been worthwhile in epidemiological study, it is doubtful that it would be useful for individual medical surveillance.

PREVENTION

Exposure to man-made sources of visible and infrared radiation can be prevented through engineering controls and protective equipment. Typical controls include barriers and reflectors or opaque shields to eliminate exposure to individuals. Viewing windows or ports can be equipped with glass or plastic with appropriate tinting materials to block the radiation. For visible light, neutral density filters are commonly used. When eye exposure is the major concern, tinted glasses, goggles, or face shields can be used.28 Reflective suits can help reduce thermal loading from exposures to the entire body and prevent burns.

To prevent photosensitivity reactions, exposure to sources of bright light including sunlight should be minimized. Simple measures include wearing long-sleeved shirts and broad-brimmed hats and using canopies or awnings. Sunscreen agents also offer some protection from blue light photosensitivity reactions. Beta-carotene in doses of 60–80 mg/day can help to prevent photosensitivity reactions in persons with porphyria.

References

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