Tuesday, 15 March 2011 14:58

Ultraviolet Radiation

Written by
Rate this item
(1 Vote)

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

Sunlight

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

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.

Photosensitization

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

ELF020T1

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).

Measurement

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.

Conclusions

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.

 

Back

Read 5065 times Last modified on Wednesday, 17 August 2011 17:53

" DISCLAIMER: The ILO does not take responsibility for content presented on this web portal that is presented in any language other than English, which is the language used for the initial production and peer-review of original content. Certain statistics have not been updated since the production of the 4th edition of the Encyclopaedia (1998)."

Contents

Preface
Part I. The Body
Part II. Health Care
Part III. Management & Policy
Part IV. Tools and Approaches
Part V. Psychosocial and Organizational Factors
Part VI. General Hazards
Barometric Pressure Increased
Barometric Pressure Reduced
Biological Hazards
Disasters, Natural and Technological
Electricity
Fire
Heat and Cold
Hours of Work
Indoor Air Quality
Indoor Environmental Control
Lighting
Noise
Radiation: Ionizing
Radiation: Non-Ionizing
Vibration
Violence
Visual Display Units
Part VII. The Environment
Part VIII. Accidents and Safety Management
Part IX. Chemicals
Part X. Industries Based on Biological Resources
Part XI. Industries Based on Natural Resources
Part XII. Chemical Industries
Part XIII. Manufacturing Industries
Part XIV. Textile and Apparel Industries
Part XV. Transport Industries
Part XVI. Construction
Part XVII. Services and Trade
Part XVIII. Guides

Radiation: Non-Ionizng References

Allen, SG. 1991. Radiofrequency field measurements and hazard assessment. J Radiol Protect 11:49-62.

American Conference of Governmental Industrial Hygienists (ACGIH). 1992. Documentation for the Threshold Limit Values. Cincinnati, Ohio: ACGIH.

—. 1993. Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati, Ohio: ACGIH.

—. 1994a. Annual Report of ACGIH Physical Agents Threshold Limit Values Committee. Cincinnati, Ohio: ACGIH.

—. 1994b. TLV’s, Threshold Limit Values and Biological Exposure Indices for 1994-1995. Cincinnati, Ohio: ACGIH.

—. 1995. 1995-1996 Threshhold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati, Ohio: ACGIH.

—. 1996. TLVs© and BEIs©. Threshold Limit Values for Chemical Substances and Physical Agents; Biological Exposure Indices. Cincinnati, Ohio: ACGIH.

American National Standards Institute (ANSI). 1993. Safe Use of Lasers. Standard No. Z-136.1. New York: ANSI.

Aniolczyk, R. 1981. Measurements of hygienic evaluation of electromagnetic fields in the environment of diathermy, welders, and induction heaters. Medycina Pracy 32:119-128.

Bassett, CAL, SN Mitchell, and SR Gaston. 1982. Pulsing electromagnetic field treatment in ununited fractures and failed artrodeses. J Am Med Assoc 247:623-628.

Bassett, CAL, RJ Pawluk, and AA Pilla. 1974. Augmentation of bone repair by inductively coupled electromagnetic fields. Science 184:575-577.

Berger, D, F Urbach, and RE Davies. 1968. The action spectrum of erythema induced by ultraviolet radiation. In Preliminary Report XIII. Congressus Internationalis Dermatologiae, Munchen, edited by W Jadassohn and CG Schirren. New York: Springer-Verlag.

Bernhardt, JH. 1988a. The establishment of frequency dependent limits for electric and magnetic fields and evaluation of indirect effects. Rad Envir Biophys 27:1.

Bernhardt, JH and R Matthes. 1992. ELF and RF electromagnetic sources. In Non-Ionizing Radiation Protection, edited by MW Greene. Vancouver: UBC Press.

Bini, M, A Checcucci, A Ignesti, L Millanta, R Olmi, N Rubino, and R Vanni. 1986. Exposure of workers to intense RF electric fields that leak from plastic sealers. J Microwave Power 21:33-40.

Buhr, E, E Sutter, and Dutch Health Council. 1989. Dynamic filters for protective devices. In Dosimetry of Laser Radiation in Medicine and Biology, edited by GJ Mueller and DH Sliney. Bellingham, Wash: SPIE.

Bureau of Radiological Health. 1981. An Evaluation of Radiation Emission from Video Display Terminals. Rockville, MD: Bureau of Radiological Health.

Cleuet, A and A Mayer. 1980. Risques liés à l’utilisation industrielle des lasers. In Institut National de Recherche et de Sécurité, Cahiers de Notes Documentaires, No. 99 Paris: Institut National de Recherche et de Sécurité.

Coblentz, WR, R Stair, and JM Hogue. 1931. The spectral erythemic relation of the skin to ultraviolet radiation. In Proceedings of the National Academy of Sciences of the United States of America Washington, DC: National Academy of Sciences.

Cole, CA, DF Forbes, and PD Davies. 1986. An action spectrum for UV photocarcinogenesis. Photochem Photobiol 43(3):275-284.

Commission Internationale de L’Eclairage (CIE). 1987. International Lighting Vocabulary. Vienna: CIE.

Cullen, AP, BR Chou, MG Hall, and SE Jany. 1984. Ultraviolet-B damages corneal endothelium. Am J Optom Phys Opt 61(7):473-478.

Duchene, A, J Lakey, and M Repacholi. 1991. IRPA Guidelines On Protection Against Non-Ionizing Radiation. New York: Pergamon.

Elder, JA, PA Czerki, K Stuchly, K Hansson Mild, and AR Sheppard. 1989. Radiofrequency radiation. In Nonionizing Radiation Protection, edited by MJ Suess and DA Benwell-Morison. Geneva: WHO.

Eriksen, P. 1985. Time resolved optical spectra from MIG welding arc ignition. Am Ind Hyg Assoc J 46:101-104.

Everett, MA, RL Olsen, and RM Sayer. 1965. Ultraviolet erythema. Arch Dermatol 92:713-719.

Fitzpatrick, TB, MA Pathak, LC Harber, M Seiji, and A Kukita. 1974. Sunlight and Man, Normal and Abnormal Photobiologic Responses. Tokyo: Univ. of Tokyo Press.

Forbes, PD and PD Davies. 1982. Factors that influence photocarcinogenesis. Chap. 7 in Photoimmunology, edited by JAM Parrish, L Kripke, and WL Morison. New York: Plenum.

Freeman, RS, DW Owens, JM Knox, and HT Hudson. 1966. Relative energy requirements for an erythemal response of skin to monochromatic wavelengths of ultraviolet present in the solar spectrum. J Invest Dermatol 47:586-592.

Grandolfo, M and K Hansson Mild. 1989. Worldwide public and occupational radiofrequency and microwave protection. In Electromagnetic Biointeraction. Mechanisms, Safety Standards, Protection Guides, edited by G Franceschetti, OP Gandhi, and M Grandolfo. New York: Plenum.

Greene, MW. 1992. Non Ionizing Radiation. 2nd International Non Ionizing Radiation Workshop, 10-14 May, Vancouver.

Ham, WTJ. 1989. The photopathology and nature of the blue-light and near-UV retinal lesion produced by lasers and other optic sources. In Laser Applications in Medicine and Biology, edited by ML Wolbarsht. New York: Plenum.

Ham, WT, HA Mueller, JJ Ruffolo, D Guerry III, and RK Guerry. 1982. Action spectrum for retinal injury from near ultraviolet radiation in the aphakic monkey. Am J Ophthalmol 93(3):299-306.

Hansson Mild, K. 1980. Occupational exposure to radio-frequency electromagnetic fields. Proc IEEE 68:12-17.

Hausser, KW. 1928. Influence of wavelength in radiation biology. Strahlentherapie 28:25-44.

Institute of Electrical and Electronic Engineers (IEEE). 1990a. IEEE COMAR Position of RF and Microwaves. New York: IEEE.

—. 1990b. IEEE COMAR Position Statement On Health Aspects of Exposure to Electric and Magnetic Fields from RF Sealers and Dielectric Heaters. New York: IEEE.

—. 1991. IEEE Standard for Safety Levels With Respect to Human Exposure to Radiofrequency Electromagnetic Fields 3 KHz to 300 GHz. New York: IEEE.

International Commission on Non-Ionizing Radiation Protection (ICNIRP). 1994. Guidelines on Limits of Exposure to Static Magnetic Fields. Health Phys 66:100-106.

—. 1995. Guidelines for Human Exposure Limits for Laser Radiation.

ICNIRP statement. 1996. Health issues related to the use of hand-held radiotelephones and base transmitters. Health Physics, 70:587-593.

International Electrotechnical Commission (IEC). 1993. IEC Standard No. 825-1. Geneva: IEC.

International Labour Office (ILO). 1993a. Protection from Power Frequency Electric and Magnetic Fields. Occupational Safety and Health Series, No. 69. Geneva: ILO.

International Radiation Protection Association (IRPA). 1985. Guidelines for limits of human exposure to laser radiation. Health Phys 48(2):341-359.

—. 1988a. Change: Recommendations for minor updates to the IRPA 1985 guidelines on limits of exposure to laser radiation. Health Phys 54(5):573-573.

—. 1988b. Guidelines on limits of exposure to radiofrequency electromagnetic fields in the frequency range from 100 kHz to 300 GHz. Health Phys 54:115-123.

—. 1989. Proposed change to the IRPA 1985 guidelines limits of exposure to ultraviolet radiation. Health Phys 56(6):971-972.

International Radiation Protection Association (IRPA) and International Non-Ionizing Radiation Committee. 1990. Interim guidelines on limits of exposure to 50/60 Hz electric and magnetic fields. Health Phys 58(1):113-122.

Kolmodin-Hedman, B, K Hansson Mild, E Jönsson, MC Anderson, and A Eriksson. 1988. Health problems among operations of plastic welding machines and exposure to radiofrequency electromagnetic fields. Int Arch Occup Environ Health 60:243-247.

Krause, N. 1986. Exposure of people to static and time variable magnetic fields in technology, medicine, research and public life: Dosimetric aspects. In Biological Effects of Static and ELF-Magnetic Fields, edited by JH Bernhardt. Munchen: MMV Medizin Verlag.

Lövsund, P and KH Mild. 1978. Low Frequency Electromagnetic Field Near Some Induction Heaters. Stockholm: Stockholm Board of Occupational Health and Safety.

Lövsund, P, PA Oberg, and SEG Nilsson. 1982. ELF magnetic fields in electrosteel and welding industries. Radio Sci 17(5S):355-385.

Luckiesh, ML, L Holladay, and AH Taylor. 1930. Reaction of untanned human skin to ultraviolet radiation. J Optic Soc Am 20:423-432.

McKinlay, AF and B Diffey. 1987. A reference action spectrum for ultraviolet induced erythema in human skin. In Human Exposure to Ultraviolet Radiation: Risks and Regulations, edited by WF Passchier and BFM Bosnjakovic. New York: Excerpta medica Division, Elsevier Science Publishers.

McKinlay, A, JB Andersen, JH Bernhardt, M Grandolfo, K-A Hossmann, FE van Leeuwen, K Hansson Mild, AJ Swerdlow, L Verschaeve and B Veyret. Proposal for a research programme by a European Commission Expert Group. Possible health effects related to the use of radiotelephones. Unpublished report.

Mitbriet, IM and VD Manyachin. 1984. Influence of magnetic fields on the repair of bone. Moscow, Nauka, 292-296.

National Council on Radiation Protection and Measurements (NCRP). 1981. Radiofrequency Electromagnetic Fields. Properties, Quantities and Units, Biophysical Interaction, and Measurements. Bethesda, MD: NCRP.

—. 1986. Biological Effects and Exposure Criteria for Radiofrequency Electromagnetic Fields. Report No. 86. Bethesda, MD: NCRP.

National Radiological Protection Board (NRPB). 1992. Electromagnetic Fields and the Risk of Cancer. Vol. 3(1). Chilton, UK: NRPB.

—. 1993. Restrictions On Human Exposure to Static and Time-Varying Electromagnetic Fields and Radiations. Didcot, UK: NRPB.

National Research Council (NRC). 1996. Possible health effects of exposure to residential electric and magnetic fields. Washington: NAS Press. 314.

Olsen, EG and A Ringvold. 1982. Human corneal endothelium and ultraviolet radiation. Acta Ophthalmol 60:54-56.

Parrish, JA, KF Jaenicke, and RR Anderson. 1982. Erythema and melanogenesis: Action spectra of normal human skin. Photochem Photobiol 36(2):187-191.

Passchier, WF and BFM Bosnjakovic. 1987. Human Exposure to Ultraviolet Radiation: Risks and Regulations. New York: Excerpta Medica Division, Elsevier Science Publishers.

Pitts, DG. 1974. The human ultraviolet action spectrum. Am J Optom Phys Opt 51(12):946-960.

Pitts, DG and TJ Tredici. 1971. The effects of ultraviolet on the eye. Am Ind Hyg Assoc J 32(4):235-246.

Pitts, DG, AP Cullen, and PD Hacker. 1977a. Ocular effects of ultraviolet radiation from 295 to 365nm. Invest Ophthalmol Vis Sci 16(10):932-939.

—. 1977b. Ultraviolet Effects from 295 to 400nm in the Rabbit Eye. Cincinnati, Ohio: National Institute for Occupational Safety and Health (NIOSH).

Polk, C and E Postow. 1986. CRC Handbook of Biological Effects of Electromagnetic Fields. Boca Raton: CRC Press.

Repacholi, MH. 1985. Video display terminals -should operators be concerned? Austalas Phys Eng Sci Med 8(2):51-61.

—. 1990. Cancer from exposure to 50760 Hz electric and magnetic fields: A major scientific debate. Austalas Phys Eng Sci Med 13(1):4-17.

Repacholi, M, A Basten, V Gebski, D Noonan, J Finnic and AW Harris. 1997. Lymphomas in E-Pim1 transgenic mice exposed to pulsed 900 MHz electromagnetic fields. Radiation research, 147:631-640.

Riley, MV, S Susan, MI Peters, and CA Schwartz. 1987. The effects of UVB irradiation on the corneal endothelium. Curr Eye Res 6(8):1021-1033.

Ringvold, A. 1980a. Cornea and ultraviolet radiation. Acta Ophthalmol 58:63-68.

—. 1980b. Aqueous humour and ultraviolet radiation. Acta Ophthalmol 58:69-82.

—. 1983. Damage of the corneal epithelium caused by ultraviolet radiation. Acta Ophthalmol 61:898-907.

Ringvold, A and M Davanger. 1985. Changes in the rabbit corneal stroma caused by UV radiation. Acta Ophthalmol 63:601-606.

Ringvold, A, M Davanger, and EG Olsen. 1982. Changes of the corneal endothelium after ultraviolet radiation. Acta Ophthalmol 60:41-53.

Roberts, NJ and SM Michaelson. 1985. Epidemiological studies of human exposure to radiofrequency radiation: A critical review. Int Arch Occup Environ Health 56:169-178.

Roy, CR, KH Joyner, HP Gies, and MJ Bangay. 1984. Measurement of electromagnetic radiation emitted from visual display terminals (VDTs). Rad Prot Austral 2(1):26-30.

Scotto, J, TR Fears, and GB Gori. 1980. Measurements of Ultraviolet Radiations in the United States and Comparisons With Skin Cancer Data. Washington, DC: US Government Printing Office.

Sienkiewicz, ZJ, RD Saunder, and CI Kowalczuk. 1991. Biological Effects of Exposure to Non-Ionizing Electromagnetic Fields and Radiation. 11 Extremely Low Frequency Electric and Magnetic Fields. Didcot, UK: National Radiation Protection Board.

Silverman, C. 1990. Epidemiological studies of cancer and electromagnetic fields. In Chap. 17 in Biological Effects and Medical Applications of Electromagnetic Energy, edited by OP Gandhi. Engelwood Cliffs, NJ: Prentice Hall.

Sliney, DH. 1972. The merits of an envelope action spectrum for ultraviolet radiation exposure criteria. Am Ind Hyg Assoc J 33:644-653.

—. 1986. Physical factors in cataractogenesis: Ambient ultraviolet radiation and temperature. Invest Ophthalmol Vis Sci 27(5):781-790.

—. 1987. Estimating the solar ultraviolet radiation exposure to an intraocular lens implant. J Cataract Refract Surg 13(5):296-301.

—. 1992. A safety manager’s guide to the new welding filters. Welding J 71(9):45-47.
Sliney, DH and ML Wolbarsht. 1980. Safety With Lasers and Other Optical Sources. New York: Plenum.

Stenson, S. 1982. Ocular findings in xeroderma pigmentosum: Report of two cases. Ann Ophthalmol 14(6):580-585.

Sterenborg, HJCM and JC van der Leun. 1987. Action spectra for tumourigenesis by ultraviolet radiation. In Human Exposure to Ultraviolet Radiation: Risks and Regulations, edited by WF Passchier and BFM Bosnjakovic. New York: Excerpta Medica Division, Elsevier Science Publishers.

Stuchly, MA. 1986. Human exposure to static and time-varying magnetic fields. Health Phys 51(2):215-225.

Stuchly, MA and DW Lecuyer. 1985. Induction heating and operator exposure to electromagnetic fields. Health Phys 49:693-700.

—. 1989. Exposure to electromagnetic fields in arc welding. Health Phys 56:297-302.

Szmigielski, S, M Bielec, S Lipski, and G Sokolska. 1988. Immunologic and cancer related aspects of exposure to low-level microwave and radiofrequency fields. In Modern Bioelectricity, edited by AA Mario. New York: Marcel Dekker.

Taylor, HR, SK West, FS Rosenthal, B Munoz, HS Newland, H Abbey, and EA Emmett. 1988. Effect of ultraviolet radiation on cataract formation. New Engl J Med 319:1429-1433.

Tell, RA. 1983. Instrumentation for measurement of electromagnetic fields: Equipment, calibrations, and selected applications. In Biological Effects and Dosimetry of Nonionizing Radiation, Radiofrequency and Microwave Energies, edited by M Grandolfo, SM Michaelson, and A Rindi. New York: Plenum.

Urbach, F. 1969. The Biologic Effects of Ultraviolet Radiation. New York: Pergamon.

World Health Organization (WHO). 1981. Radiofrequency and microwaves. Environmental Health Criteria, No.16. Geneva: WHO.

—. 1982. Lasers and Optical Radiation. Environmental Health Criteria, No. 23. Geneva: WHO.

—. 1987. Magnetic Fields. Environmental Health Criteria, No.69. Geneva: WHO.

—. 1989. Non-Ionization Radiation Protection. Copenhagen: WHO Regional Office for Europe.

—. 1993. Electromagnetic Fields 300 Hz to 300 GHz. Environmental Health Criteria, No. 137. Geneva: WHO.

—. 1994. Ultraviolet Radiation. Environmental Health Criteria, No. 160. Geneva: WHO.

World Health Organization (WHO), United Nations Environmental Programme (UNEP), and International Radiation Protection Association (IRPA). 1984. Extremely Low Frequency (ELF). Environmental Health Criteria, No. 35. Geneva: WHO.

Zaffanella, LE and DW DeNo. 1978. Electrostatic and Electromagnetic Effects of Ultra-High-Voltage Transmission Lines. Palo Alto, Calif: Electric Power Research Institute.

Zuclich, JA and JS Connolly. 1976. Ocular damage induced by near-ultraviolet laser radiation. Invest Ophthalmol Vis Sci 15(9):760-764.