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Tuesday, 15 March 2011 14:58

Ultraviolet Radiation

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Like light, which is visible, ultraviolet radiation (UVR) is a form of optical radiation with shorter wavelengths and more energetic photons (particles of radiation) than its visible counterpart. Most light sources emit some UVR as well. UVR is present in sunlight and is also emitted from a large number of ultraviolet sources used in industry, science and medicine. Workers may encounter UVR in a wide variety of occupational settings. In some instances, at low ambient light levels, very intense near-ultraviolet (“black light”) sources can be seen, but normally UVR is invisible and must be detected by the glow of materials that fluoresce when illuminated by UVR.

Just as light can be divided into colours which can be seen in a rainbow, UVR is subdivided and its components are commonly denoted as UVA, UVB and UVC. Wavelengths of light and UVR are generally expressed in nanometres (nm); 1 nm is one-billionth (10–9) of a metre. UVC (very short-wavelength UVR) in sunlight is absorbed by the atmosphere and does not reach the Earth’s surface. UVC is available only from artificial sources, such as germicidal lamps, which emit most of their energy at a single wavelength (254 nm) that is very effective in killing bacteria and viruses on a surface or in the air.

UVB is the most biologically damaging UVR to the skin and eye, and although most of this energy (which is a component of sunlight) is absorbed by the atmosphere, it still produces sunburn and other biological effects. Long-wavelength UVR, UVA, is normally found in most lamp sources, and is also the most intense UVR reaching the Earth. Although UVA can penetrate deeply into tissue, it is not as biologically damaging as UVB because the energies of individual photons are less than for UVB or UVC.

Sources of Ultraviolet Radiation


The greatest occupational exposure to UVR is experienced by outdoor workers under sunlight. The energy of solar radiation is greatly attenuated by the earth’s ozone layer, limiting terrestrial UVR to wavelengths greater than 290-295 nm. The energy of the more dangerous short-wavelength (UVB) rays in sunlight is a strong function of the atmospheric slant path, and varies with the season and the time of day (Sliney 1986 and 1987; WHO 1994).

Artificial sources

The most significant artificial sources of human exposure include the following:

Industrial arc welding. The most significant source of potential UVR exposure is the radiant energy of arc-welding equipment. The levels of UVR around arc-welding equipment are very high, and acute injury to the eye and the skin can occur within three to ten minutes of exposure at close viewing distances of a few metres. Eye and skin protection is mandatory.

Industrial/workplace UVR lamps. Many industrial and commercial processes, such as photochemical curing of inks, paints and plastics, involve the use of lamps which strongly emit in the UV range. While the likelihood of harmful exposure is low due to shielding, in some cases accidental exposure can occur.

“Black lights”. Black lights are specialized lamps that emit predominantly in the UV range, and are generally used for non-destructive testing with fluorescent powders, for the authentication of banknotes and documents, and for special effects in advertising and discotheques. These lamps do not pose any significant exposure hazard to humans (except in certain cases to photosensitized skin).

Medical treatment. UVR lamps are used in medicine for a variety of diagnostic and therapeutic purposes. UVA sources are normally used in diagnostic applications. Exposures to the patient vary considerably according to the type of treatment, and UV lamps used in dermatology require careful use by staff members.

Germicidal UVR lamps. UVR with wavelengths in the range 250–265 nm is the most effective for sterilization and disinfection since it corresponds to a maximum in the DNA absorption spectrum. Low-pressure mercury discharge tubes are often used as the UV source, as more than 90% of the radiated energy lies at the 254 nm line. These lamps are often referred to as “germicidal lamps,” “bactericidal lamps” or simply “UVC lamps”. Germicidal lamps are used in hospitals to combat tuberculosis infection, and are also used inside microbiological safety cabinets to inactivate airborne and surface microorganisms. Proper installation of the lamps and the use of eye protection is essential.

Cosmetic tanning. Sunbeds are found in enterprises where clients may obtain a tan by special sun-tanning lamps, which emit primarily in the UVA range but also some UVB. Regular use of a sunbed may contribute significantly to a person’s annual UV skin exposure; furthermore, the staff working in tanning salons may also be exposed to low levels. The use of eye protection such as goggles or sunglasses should be mandatory for the client, and depending upon the arrangement, even staff members may require eye protectors.

General lighting. Fluorescent lamps are common in the workplace and have been used in the home for a long time now. These lamps emit small amounts of UVR and contribute only a few percent to a person’s annual UV exposure. Tungsten-halogen lamps are increasingly used in the home and in the workplace for a variety of lighting and display purposes. Unshielded halogen lamps can emit UVR levels sufficient to cause acute injury at short distances. The fitting of glass filters over these lamps should eliminate this hazard.

Biological Effects

The skin


Erythema, or “sunburn”, is a reddening of the skin that normally appears in four to eight hours after exposure to UVR and gradually fades after a few days. Severe sunburn can involve blistering and peeling of the skin. UVB and UVC are both about 1,000 times more effective in causing erythema than UVA (Parrish, Jaenicke and Anderson 1982), but erythema produced by the longer UVB wavelengths (295 to 315 nm) is more severe and persists longer (Hausser 1928). The increased severity and time-course of the erythema results from deeper penetration of these wavelengths into the epidermis. Maximum sensitivity of the skin apparently occurs at approximately 295 nm (Luckiesh, Holladay and Taylor 1930; Coblentz, Stair and Hogue 1931) with much less (approximately 0.07) sensitivity occurring at 315 nm and longer wavelengths (McKinlay and Diffey 1987).

The minimal erythemal dose (MED) for 295 nm that has been reported in more recent studies for untanned, lightly pigmented skin ranges from 6 to 30 mJ/cm2 (Everett, Olsen and Sayer 1965; Freeman, et al. 1966; Berger, Urbach and Davies 1968). The MED at 254 nm varies greatly depending upon the elapsed time after exposure and whether the skin has been exposed much to outdoor sunlight, but is generally of the order of 20 mJ/cm2, or as high as 0.1 J/cm2. Skin pigmentation and tanning, and, most importantly, thickening of the stratum corneum, can increase this MED by at least one order of magnitude.


Occupational health specialists frequently encounter adverse effects from occupational exposure to UVR in photosensitized workers. The use of certain medicines may produce a photosensitizing effect on exposure to UVA, as may the topical application of certain products, including some perfumes, body lotions and so on. Reactions to photosensitizing agents involve both photoallergy (allergic reaction of the skin) and phototoxicity (irritation of the skin) after UVR exposure from sunlight or industrial UVR sources. (Photosensitivity reactions during the use of tanning equipment are also common.) This photosensitization of the skin may be caused by creams or ointments applied to the skin, by medications taken orally or by injection, or by the use of prescription inhalers (see figure 1 ). The physician prescribing a potentially photosensitizing medication should always warn the patient to take appropriate measures to ensure against adverse effects, but the patient frequently is told only to avoid sunlight and not UVR sources (since these are uncommon for the general population).

Figure 1. Some phonosensitizing substances


Delayed effects

Chronic exposure to sunlight—especially the UVB component—accelerates the ageing of the skin and increases the risk of developing skin cancer (Fitzpatrick et al. 1974; Forbes and Davies 1982; Urbach 1969; Passchier and Bosnjakovic 1987). Several epidemiological studies have shown that the incidence of skin cancer is strongly correlated with latitude, altitude and sky cover, which correlate with UVR exposure (Scotto, Fears and Gori 1980; WHO 1993).

Exact quantitative dose-response relationships for human skin carcinogenesis have not yet been established, although fair-skinned individuals, particularly those of Celtic origin, are much more prone to develop skin cancer. Nevertheless, it must be noted that the UVR exposures necessary to elicit skin tumours in animal models may be delivered sufficiently slowly that erythema is not produced, and the relative effectiveness (relative to the peak at 302 nm) reported in those studies varies in the same way as sunburn (Cole, Forbes and Davies 1986; Sterenborg and van der Leun 1987).

The eye

Photokeratitis and photoconjunctivitis

These are acute inflammatory reactions resulting from exposure to UVB and UVC radiation which appear within a few hours of excessive exposure and normally resolved after one to two days.

Retinal injury from bright light

Although thermal injury to the retina from light sources is unlikely, photochemical damage can occur from exposure to sources rich in blue light. This can result in temporary or permanent reduction in vision. However the normal aversion response to bright light should prevent this occurrence unless a conscious effort is made to stare at bright light sources. The contribution of UVR to retinal injury is generally very small because absorption by the lens limits retinal exposure.

Chronic effects

Long-term occupational exposure to UVR over several decades may contribute to cataract and such non-eye-related degenerative effects as skin ageing and skin cancer associated with sun exposure. Chronic exposure to infrared radiation also can increase the risk of cataract, but this is very unlikely, given access to eye protection.

Actinic ultraviolet radiation (UVB and UVC) is strongly absorbed by the cornea and conjunctiva. Overexposure of these tissues causes keratoconjunctivitis, commonly referred to as “welder’s flash”, “arc-eye” or “snow-blindness”. Pitts has reported the action spectrum and time course of photokeratitis in the human, rabbit and monkey cornea (Pitts 1974). The latent period varies inversely with the severity of exposure, ranging from 1.5 to 24 hours, but usually occurs within 6 to 12 hours; discomfort usually disappears within 48 hours. Conjunctivitis follows and may be accompanied by erythema of the facial skin surrounding the eyelids. Of course, UVR exposure rarely results in permanent ocular injury. Pitts and Tredici (1971) reported threshold data for photokeratitis in humans for wavebands 10 nm in width from 220 to 310 nm. The maximum sensitivity of the cornea was found to occur at 270 nm—differing markedly from the maximum for the skin. Presumably, 270 nm radiation is biologically more active because of the lack of a stratum corneum to attenuate the dose to the corneal epithelium tissue at shorter UVR wavelengths. The wavelength response, or action spectrum, did not vary as greatly as did the erythema action spectra, with thresholds varying from 4 to 14 mJ/cm2 at 270 nm. The threshold reported at 308 nm was approximately 100 mJ/cm2.

Repeated exposure of the eye to potentially hazardous levels of UVR does not increase the protective capability of the affected tissue (the cornea) as does skin exposure, which leads to tanning and to thickening of the stratum corneum. Ringvold and associates studied the UVR absorption properties of the cornea (Ringvold 1980a) and aqueous humour (Ringvold 1980b), as well as the effects of UVB radiation upon the corneal epithelium (Ringvold 1983), the corneal stroma (Ringvold and Davanger 1985) and the corneal endothelium (Ringvold, Davanger and Olsen 1982; Olsen and Ringvold 1982). Their electron microscopic studies showed that corneal tissue possessed remarkable repair and recovery properties. Although one could readily detect significant damage to all of these layers apparently appearing initially in cell membranes, morphological recovery was complete after a week. Destruction of keratocytes in the stromal layer was apparent, and endothelial recovery was pronounced despite the normal lack of rapid cell turnover in the endothelium. Cullen et al. (1984) studied endothelial damage that was persistent if the UVR exposure was persistent. Riley et al. (1987) also studied the corneal endothelium following UVB exposure and concluded that severe, single insults were not likely to have delayed effects; however, they also concluded that chronic exposure could accelerate changes in the endothelium related to ageing of the cornea.

Wavelengths above 295 nm can be transmitted through the cornea and are almost totally absorbed by the lens. Pitts, Cullen and Hacker (1977b) showed that cataracts can be produced in rabbits by wavelengths in the 295–320 nm band. Thresholds for transient opacities ranged from 0.15 to 12.6 J/cm2, depending on wavelength, with a minimum threshold at 300 nm. Permanent opacities required greater radiant exposures. No lenticular effects were noted in the wavelength range of 325 to 395 nm even with much higher radiant exposures of 28 to 162 J/cm2 (Pitts, Cullen and Hacker 1977a; Zuclich and Connolly 1976). These studies clearly illustrate the particular hazard of the 300-315 nm spectral band, as would be expected because photons of these wavelengths penetrate efficiently and have sufficient energy to produce photochemical damage.

Taylor et al. (1988) provided epidemiological evidence that UVB in sunlight was an aetiological factor in senile cataract, but showed no correlation of cataract with UVA exposure. Although once a popular belief because of the strong absorption of UVA by the lens, the hypothesis that UVA can cause cataract has not been supported by either experimental laboratory studies or by epidemiological studies. From the laboratory experimental data which showed that thresholds for photokeratitis were lower than for cataractogenesis, one must conclude that levels lower than those required to produce photokeratitis on a daily basis should be considered hazardous to lens tissue. Even if one were to assume that the cornea is exposed to a level nearly equivalent to the threshold for photokeratitis, one would estimate that the daily UVR dose to the lens at 308 nm would be less than 120 mJ/cm2 for 12 hours out of doors (Sliney 1987). Indeed, a more realistic average daily exposure would be less than half that value.

Ham et al. (1982) determined the action spectrum for photoretinitis produced by UVR in the 320–400 nm band. They showed that thresholds in the visible spectral band, which were 20 to 30 J/cm2 at 440 nm, were reduced to approximately 5 J/cm2 for a 10 nm band centred at 325 nm. The action spectrum was increasing monotonically with decreasing wavelength. We should therefore conclude that levels well below 5 J/cm2 at 308 nm should produce retinal lesions, although these lesions would not become apparent for 24 to 48 hours after the exposure. There are no published data for retinal injury thresholds below 325 nm, and one can only expect that the pattern for the action spectrum for photochemical injury to the cornea and lens tissues would apply to the retina as well, leading to an injury threshold of the order of 0.1 J/cm2.

Although UVB radiation has been clearly shown to be mutagenic and carcinogenic to the skin, the extreme rarity of carcinogenesis in the cornea and conjunctiva is quite remarkable. There appears to be no scientific evidence to link UVR exposure with any cancers of the cornea or conjunctiva in humans, although the same is not true of cattle. This would suggest a very effective immune system operating in the human eye, since there are certainly outdoor workers who receive a UVR exposure comparable to that which cattle receive. This conclusion is further supported by the fact that individuals suffering from a defective immune response, as in xeroderma pigmentosum, frequently develop neoplasias of the cornea and conjunctiva (Stenson 1982).

Safety Standards

Occupational exposure limits (EL) for UVR have been developed and include an action spectrum curve which envelops the threshold data for acute effects obtained from studies of minimal erythema and keratoconjunctivitis (Sliney 1972; IRPA 1989). This curve does not differ significantly from the collective threshold data, considering measurement errors and variations in individual response, and is well below the UVB cataractogenic thresholds.

The EL for UVR is lowest at 270 nm (0.003 J/cm2 at 270 nm), and, for example, at 308 nm is 0.12 J/cm2 (ACGIH 1995, IRPA 1988). Regardless of whether the exposure occurs from a few pulsed exposures during the day, a single very brief exposure, or from an 8-hour exposure at a few microwatts per square centimetre, the biological hazard is the same, and the above limits apply to the full workday.

Occupational Protection

Occupational exposure to UVR should be minimized where practical. For artificial sources, wherever possible, priority should be given to engineering measures such as filtration, shielding and enclosure. Administrative controls, such as limitation of access, can reduce the requirements for personal protection.

Outdoor workers such as agricultural workers, labourers, construction workers, fishermen and so on can minimize their risk from solar UV exposure by wearing appropriate tightly woven clothing, and most important, a brimmed hat to reduce face and neck exposure. Sunscreens can be applied to exposed skin to reduce further exposure. Outdoor workers should have access to shade and be provided with all the necessary protective measures mentioned above.

In industry, there are many sources capable of causing acute eye injury within a short exposure time. A variety of eye protection is available with various degrees of protection appropriate to the intended use. Those intended for industrial use include welding helmets (additionally providing protection both from intense visible and infrared radiation as well as face protection), face shields, goggles and UV-absorbing spectacles. In general, protective eyewear provided for industrial use should fit snugly on the face, thus ensuring that there are no gaps through which UVR can directly reach the eye, and they should be well-constructed to prevent physical injury.

The appropriateness and selection of protective eyewear is dependent on the following points:

  • the intensity and spectral emission characteristics of the UVR source
  • the behavioural patterns of people near UVR sources (distance and exposure time are important)
  • the transmission properties of the protective eyewear material
  • the design of the frame of the eyewear to prevent peripheral exposure of the eye from direct unabsorbed UVR.


In industrial exposure situations, the degree of ocular hazard can be assessed by measurement and comparison with recommended limits for exposure (Duchene, Lakey and Repacholi 1991).


Because of the strong dependence of biological effects on wavelength, the principal measurement of any UVR source is its spectral power or spectral irradiance distribution. This must be measured with a spectroradiometer which consists of suitable input optics, a monochromator and a UVR detector and readout. Such an instrument is not normally used in occupational hygiene.

In many practical situations, a broad-band UVR meter is used to determine safe exposure durations. For safety purposes, the spectral response can be tailored to follow the spectral function used for the exposure guidelines of the ACGIH and the IRPA. If appropriate instruments are not used, serious errors of hazard assessment will result. Personal UVR dosimeters are also available (e.g., polysulphone film), but their application has been largely confined to occupational safety research rather than in hazard evaluation surveys.


Molecular damage of key cellular components arising from UVR exposure occurs constantly, and repair mechanisms exist to deal with the exposure of skin and ocular tissues to ultraviolet radiation. Only when these repair mechanisms are overwhelmed does acute biological injury become apparent (Smith 1988). For these reasons, minimizing occupational UVR exposure continues to remain an important object of concern among occupational health and safety workers.



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