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8.3 Radiological sciences

8.3 Radiological sciences
Oxford Textbook of Public Health

8.3
Radiological sciences

Arthur C. Upton

Introduction
Ionizing radiation

Nature, sources, and environmental levels

Nature and mechanisms of injury

Clinical manifestations of acute injury

Carcinogenic effects

Heritable effects

Effects of prenatal irradiation

Prevention
Non-ionizing radiation

Ultraviolet radiation

Visible light

Infrared radiation

Prevention

Microwave radiation

Extremely low-frequency electromagnetic fields

Ultrasound
Summary and conclusions
Chapter References

Introduction
This chapter reviews the health effects of electromagnetic waves, including ionizing and non-ionizing radiations, accelerated atomic particles, high-intensity ultrasound, and electromagnetic fields. These various forms of energy differ from one another in their biological effects so that each is considered separately in the remarks that follow, beginning with a discussion of the effects of ionizing radiation.
Ionizing radiation
Nature, sources, and environmental levels
Ionizing radiations are those forms of radiation which can deposit enough localized energy in living cells to dislodge electrons from atoms. Such radiations include electromagnetic waves of extremely short wavelength (Fig. 1) and accelerated atomic particles (for example, electrons, protons, neutrons, a particles). Doses of ionizing radiation are measured in terms of energy deposition (Table 1).

Fig. 1 The electromagnetic spectrum. (Source: Mettler and Upton 1994.)

Table 1 Quantities and dose units of ionizing radiation

Natural sources of ionizing radiation include cosmic rays, radium and other radio-active elements in the Earth’s crust, internally deposited 40K, 14C, and other radionuclides present normally in living cells, and inhaled radon and its daughter elements (Table 2). The dose received from cosmic rays can differ appreciably from the value tabulated, depending on one’s elevation; that is, it can be twice as high at a mountainous site (for example, Denver) as at sea level, and it is up to two orders of magnitude higher at jet aircraft altitudes (NCRP 1987). Likewise, the dose received from radium may be increased by a factor of 2 or more in regions where the underlying earth is rich in this element (NCRP 1987). In any case, however, the largest dose is usually that received by the bronchial epithelium from inhaled 222Rn, a colourless odourless a-emitting gas formed by the radio-active decay of 226Ra (Table 2); furthermore, depending on the concentration of radon in indoor air, the dose from radon and its decay daughters may vary by an order of magnitude or more (NCRP 1984). In cigarette smokers, moreover, even larger doses (up to 0.2 Sv (20 rem) per year) are received by the bronchial epithelium from the polonium (another a-emitting decay product of radium) that is normally present in tobacco smoke (NCRP 1984).

Table 2 Average amounts of ionizing radiation received annually from different sources by a member of the United States population

In addition to ionizing radiation from natural sources, people are exposed to radiation from artificial sources as well, the largest being the use of X-rays in medical diagnosis (Table 2). Lesser sources of exposure to manmade radiation include radio-active minerals (for example, 238U, 232Th, 40K, 226Ra) in building materials, phosphate fertilizers, and crushed rock; radiation-emitting components of TV sets, smoke detectors, and other consumer products; radio-active fallout from atomic weapons (for example, 137Cs, 90Sr, 89Sr, 14C, 3H, 95Zr); and nuclear power (for example, 3H, 14C, 85Kr, 129I, 137Cs) (Table 2).
In various occupations, some workers receive additional doses of ionizing radiation, depending on their job assignments and working conditions. The average annual effective dose received occupationally by monitored radiation workers in the United States is less than that received from natural background, and in any given year less than 1 per cent of such workers receive a dose approaching the maximum permissible yearly limit (50 mSv (5 rem)) (NCRP 1989). Substantially larger occupational doses, however, are received by workers in less-developed countries, where adequate facilities, equipment, and safety measures are often lacking (UNSCEAR 1988).
Nature and mechanisms of injury
As ionizing radiation penetrates living cells, it collides randomly with atoms and molecules in its path, giving rise to ions and free radicals, which break chemical bonds and cause other molecular alterations that may injure the cells. The spatial distribution of such events along the path of an impinging radiation depends on the energy, mass, and charge of the radiation; X-rays and g-rays are sparsely ionizing in comparison with charged particles, which typically are densely ionizing.
Although any molecule in the cell may be altered by radiation, DNA is the most critical biological target because of the limited redundancy of the genetic information it contains. A dose of radiation large enough to kill the average dividing cell (2 Sv (200 rem)) causes hundreds of lesions in the cell’s DNA molecules (Ward 1988). Most such lesions are reparable, but the complex lesions produced by a densely ionizing radiation (such as a proton or an a particle) are generally less reparable than those produced by a sparsely ionizing radiation (such as an X-ray or a g-ray) (Goodhead 1988; Ward 1988). For this reason, the relative biological effectiveness of densely ionizing radiations is higher than that of sparsely ionizing radiations for most forms of injury (ICRP 1991).
Any damage to DNA that remains unrepaired or is misrepaired may be expressed in the form of mutations, the frequency of which approximates 10–5 to 10–6 per locus per sievert (NAS 1990). Because the mutation rate appears to increase as a linear non-threshold function of the dose, it is inferred that traversal of the DNA by a single ionizing particle may, in principle, suffice to cause a mutation (NAS 1990).
Also resulting from radiation damage to the genetic apparatus are changes in chromosome number and structure, the frequency of which increase with the dose in radiation workers and others exposed to ionizing radiation. So well characterized is the dose–response relationship that the frequency of chromosome aberrations in blood lymphocytes can serve as a useful biological dosimeter in radiation accident victims (IAEA 1986).
Radiation damage to genes, chromosomes, and other vital organelles may be lethal to affected cells, especially dividing cells, which are highly radiosensitive as a class (ICRP 1984). Measured in terms of proliferative capacity, the survival of dividing cells tends to decrease exponentially with increasing dose; 1 to 2 Sv (100 to 200 rem) generally suffices to reduce the surviving population by about 50 per cent (Fig. 2).

Fig. 2 Typical dose–survival curves for mammalian cells exposed to X-rays and fast neutrons. (From Hall 1988.)

Although a dose below 0.5 Sv (50 rem) kills too few cells to cause clinically detectable injury in most organs other than those of the embryo, a larger dose may kill enough of the dividing progenitor cells in a tissue to interfere with the orderly replacement of its senescent cells, thereby causing the tissue to undergo atrophy (Fig. 3). The rapidity with which the atrophy ensues will depend in part on the cell population dynamics within the affected tissue; that is, in organs characterized by slow cell turnover, such as the liver and vascular endothelium, the process is typically much slower than in organs characterized by rapid cell turnover, such as the bone marrow, epidermis, and intestinal mucosa (ICRP 1984). In so far as the injury is dependent on the extent to which cell renewal in the exposed tissue is impaired, its severity tends to be reduced by the compensatory proliferation of surviving cells when only a small volume of tissue is irradiated or when the dose is accumulated gradually over an extended period of time.

Fig. 3 Characteristic sequence of events in the pathogenesis of non-stochastic effects of ionizing radiation.

Clinical manifestations of acute injury
After its discovery by Roentgen, in 1895, the X-ray was introduced into medical practice so rapidly that radiation injuries began to be encountered almost immediately. The first such injuries were predominantly acute skin reactions on the hands of those working with the early equipment, but within less than a decade many other types of injury also were observed, including the first cancers attributed to radiation (Upton 1986).
The acute effects of radiation encompass a wide variety of reactions (Mettler and Upton 1995), which vary markedly in dose–response relationships, clinical manifestations, timing, and prognosis (Table 3). Such reactions generally result from the severe depletion of progenitor cells in the affected tissues (Fig. 3) and are, consequently, elicited only by doses large enough to kill many such cells. Organs in which cells normally turn over rapidly tend to be the most radiosensitive and the first to exhibit injury. Such a reaction is not elicited unless the dose of radiation exceeds the substantial threshold needed to kill many cells and therefore such reactions are viewed as being non-stochastic (or deterministic) in nature (ICRP 1984); this is different to mutagenic and carcinogenic effects of radiation, which are viewed as stochastic phenomena resulting from random molecular alterations in individual cells that increase in frequency as linear non-threshold functions of the dose (NAS 1990; ICRP 1991).

Table 3 Approximate threshold doses of conventionally fractionated therapeutic X-radiation for clinically detrimental non-stochastic effects in various tissues

Radiation injury of normal tissue within or adjoining the treatment field occurs to some degree in most radiotherapy patients, but few persons treated with today’s methods experience severe or disabling radiation injuries. By the same token, modern safety practices have all but eliminated injuries from excessive occupational exposure such as were prevalent among early radiation workers. In spite of marked improvements in radiation protection, however, some 285 nuclear reactor accidents (excluding the Chernobyl accident) were reported in various countries between 1945 and 1987, causing more than 1350 persons to be irradiated, 33 of whom were injured fatally (Lushbaugh et al. 1987).
Although such accidents have become less frequent, they continue to be reported from time to time, the latest occurring in a processing plant near Tokyo on 30 September 1999, when a critical mass of enriched uranium was produced accidentally, releasing large amounts of radiation. Three workers were injured seriously as a result, and more than 60 others, including seven golfers on a neighbouring course, were exposed to high levels of radiation (Normile 1999). In most such accidents, however, unlike the Chernobyl accident (discussed below), the public was not affected directly.
The Chernobyl accident—the most serious reactor accident to date—released enough radio-activity to require tens of thousands of inhabitants to be evacuated from the surrounding area. This accident, occurring during a reactor test in April 1986, resulted from the improper withdrawal of control rods and inactivation of important safety systems (in violation of the operating rules) which caused the reactor to overheat, explode, and catch fire (UNSCEAR 1988).
The damage to the reactor core and control building allowed large quantities of radiation and radio-active materials to be released during the ensuing 10 days, resulting in radiation sickness and burns in more than 200 emergency personnel and firefighters, 31 of whom were injured fatally. Although the heaviest contamination occurred in the vicinity of the reactor itself and, to a lesser extent, in neighbouring countries of Eastern Europe, the population of the northern hemisphere as a whole is estimated to have received a collective dose commitment of 600 000 person-Sv (60 million person-rem), 70 per cent of which is attributed to 137Cs, 20 per cent to 134Cs, 6 per cent to 131I, and the remainder to various shorter-lived radionuclides (UNSCEAR 1988). Those living in the vicinity of the reactor were given potassium iodide preparations to inhibit the thyroidal uptake of radio-iodine, but infants in a number of areas elsewhere in Eastern Europe are estimated to have received an average of more than 20 mSv (2 rem) to the thyroid gland, largely through ingestion of radio-iodine via cow’s milk, and the prevalence of thyroid cancer in such persons has since risen dramatically in Belarus (Astakhova et al. 1998) and in the Ukraine (Tronko et al. 1999). Organs other than the thyroid typically received only a small fraction of the dose normally accumulated each year from natural background radiation. In areas outside of Belarus, Russia, and the Ukraine, the highest average effective dose during the first year, received in Bulgaria, is estimated to have approximated 760 µSv, or slightly less than one-third of the average annual effective dose from natural sources (UNSCEAR 1988). Although the dose decreased rapidly with increasing distance from Chernobyl, the accident is estimated to have resulted in a collective dose commitment to the population of the northern hemisphere which is of the order of approximately 600 000 person-Sv (UNSCEAR 1988). Because of the small magnitude of the average dose to a given individual, however, the long-term health effects of the radiation cannot be predicted with certainty. Nevertheless, non-threshold risk models for carcinogenic effects (discussed below) imply that it may cause up to 30 000 additional cancer deaths during the next 70 years, although, with few exceptions, the number of additional cancers in any given country is likely to be too small to be detectable epidemiologically (USDOE 1987).
While less catastrophic than reactor accidents, accidents involving medical and industrial g-ray sources have been far more numerous, and some have also caused severe injury and loss of life. For example, the improper disposal of a 137Cs source in Goiania, Brazil, in 1987, resulted in the irradiation of dozens of unsuspecting victims, four of whom were injured fatally as a consequence (UNSCEAR 1993).
Although a comprehensive discussion of radiation injuries is beyond the scope of this review, prominent reactions of some of the more radiosensitive tissues are described briefly in the following.
Skin
Owing to the radiosensitivity of cells in the germinal layer of the epidermis, rapid exposure of the skin to a dose of 6 Sv or more produces erythema in the exposed area, which typically appears within a day after exposure, lasts a few hours, and is followed 2 to 4 weeks later by one or more waves of deeper and more prolonged erythema, as well as epilation. If the dose exceeds 10 to 20 Sv, blistering, necrosis, and ulceration may ensue within 2 to 4 weeks, followed by fibrosis of the underlying dermis and vasculature, which may lead to atrophy and a second wave of ulceration months or years later (ICRP 1984).
Bone marrow and lymphoid tissue
Lymphocytes are sufficiently radiosensitive that a dose of 2 to 3 Sv delivered rapidly to the whole body results in a marked depression of the lymphocyte count and immune response within hours (UNSCEAR 1988). Haemopoietic cells in the bone marrow are, likewise, killed in sufficient numbers by a comparable dose that causes profound leucopenia and thrombocytopenia, which develop within 3 to 5 weeks; after a larger dose, such changes may be severe enough to result in fatal infection and/or haemorrhage (Table 4).

Table 4 Major forms and features of the acute radiation syndrome

Intestine
Stem cells in the epithelium lining the small bowel are also highly radiosensitive; an acute dose of 10 Sv can deplete their numbers sufficiently to cause the overlying intestinal villi to become denuded within days (ICRP 1984; UNSCEAR 1988). If a large enough area of the mucosa is affected, a fulminating and rapidly fatal dysentery-like syndrome results (Table 4).
Gonads
Although mature spermatozoa can survive large doses (> 100 Sv), spermatogonia are so radiosensitive that a dose as low as 0.15 Sv delivered rapidly to both testes will cause oligospermia, and a dose of 2 to 4 Sv will result in permanent sterility. Oocytes, likewise, are radiosensitive: a dose of 1.5 to 2.0 Sv delivered rapidly to both ovaries is sufficient to cause temporary sterility, and a larger dose will result in permanent sterility, depending on the age of the woman at the time of exposure (ICRP 1984).
Respiratory tract
The lung is not a highly radiosensitive organ, but alveolar cells and pulmonary vasculature can be injured sufficiently by rapid exposure to a dose of 6 to 10 Sv to cause acute pneumonitis to develop within the following 1 to 3 months. If a large volume of the lung is affected, the process may terminate in respiratory failure within the ensuing weeks, or in pulmonary fibrosis and cor pulmonale months or years later (ICRP 1984; UNSCEAR 1988).
Lens of the eye
Cells of the anterior epithelium of the lens continue to divide throughout life and are relatively radiosensitive. As a result, acute exposure of the lens to more than 1 Sv may be followed within months by the formation of a microscopic posterior polar opacity, and 2 to 3 Sv received in a single brief exposure (or 5.5 to 14 Sv accumulated over a period of months) may cause a vision-impairing cataract (ICRP 1984).
Other tissues
The tissues mentioned above are generally of higher radiosensitivity than others (Table 3). It is noteworthy, however, that the vulnerability of all tissues is increased when they are in a rapidly growing state (ICRP 1984).
Whole-body radiation injury
If a major part of the body is exposed rapidly to more than 1 Sv, the acute radiation syndrome may result. This syndrome is characterized by an initial prodromal stage involving malaise, anorexia, nausea, and vomiting, an ensuing asymptomatic latent period, a second (main) phase of illness, and finally either recovery or death (Table 4). The main phase of the illness typically takes one of the following four forms, depending on the predominant locus of radiation injury: haematological, gastrointestinal, cerebral, or pulmonary. Another syndrome, termed ‘chronic radiation sickness’, has been reported in chronically exposed workers of the Mayak nuclear facility and in persons residing down river from the facility who were exposed to radio-active effluents from the plant. The clinical findings in such persons, yet to be reported in other irradiated populations, include varying and persistent leucopenia, thrombocytopenia, arthralgia, asthenia, and various other ill-defined neurological complaints (Kossenko et al. 1994).
Localized radiation injury
In contrast to the clinical manifestations of acute whole-body radiation injury, which are often dramatic and prompt, the reaction to sharply localized irradiation, whether from an external radiation source or from an internally deposited radionuclide, tends to evolve slowly and to produce few symptoms unless the volume of tissue irradiated and/or the dose are relatively large (see Table 3).
In this connection, it is noteworthy that although some radionuclides (such as tritium, 14C, and 137Cs) tend to be distributed systemically and to irradiate the whole body to varying degrees, others are characteristically taken up and concentrated in specific organs, producing injuries that are localized accordingly. Radium and 90Sr, for example, are deposited predominantly in bone and injure skeletal tissues primarily, whereas radio-active iodine concentrates in the thyroid gland, which is the chief site of any resulting injury (Stannard 1988).
Carcinogenic effects
The carcinogenicity of ionizing radiation was first manifested early in the twentieth century by the occurrence of skin cancer and leukaemia in certain radiation workers. It has since been documented extensively by dose-dependent excesses of osteosarcomas and cranial sinus carcinomas in radium dial painters, carcinomas of the respiratory tract in underground hardrock miners, and cancers of many types in atomic bomb survivors, radiotherapy patients, and experimentally irradiated laboratory animals (Upton 1986).
The growths induced by irradiation characteristically take years or decades to appear and exhibit no known features distinguishing them from those induced by other causes. With few exceptions, moreover, their induction has been detectable only after relatively large doses (> 0.5 Sv (50 rem)) and has varied with the type of neoplasm as well as the age and sex of those exposed. In laboratory animals and cultured cells, the carcinogenic effects of radiation have been observed to include initiating effects, promoting effects, and effects on the progression of neoplasia, depending on the experimental conditions in question (NAS 1990). While the molecular mechanisms of these effects remain to be elucidated, the activation of oncogenes and/or the inactivation or loss of tumour suppressor genes appear to be implicated in many, if not all, instances (NAS 1990). The carcinogenic effects of radiation also resemble those of chemical carcinogens in being generally modifiable in similar ways by hormones, nutritional variables, and other modifying factors. In combination with chemical carcinogens the effects of radiation may be additive, synergistic, or mutually antagonistic, depending on the specific chemicals and exposure conditions in question (UNSCEAR 1982, 1986).
Because the existing data do not suffice to describe the dose–incidence relationship unambiguously for any type of neoplasm or to define how long after irradiation the risk of the growth may remain elevated in an exposed population, any risks attributable to low-level irradiation can be estimated only by extrapolation, based on models incorporating assumptions about the relevant parameters (NAS 1990; NCRP 1997).
Various dose–effect models have been used to estimate the risks of low-level irradiation, most of which involve the assumption that the overall risk of cancer increases in proportion with the dose at low dose levels; however, as the carcinogenic potency of X-rays and g-rays in laboratory animals has been found to be reduced by as much as an order of magnitude when the exposure is prolonged, the risk to humans is generally estimated to increase less steeply with the dose at low doses and dose rates than at high doses and dose rates. Furthermore, as has been emphasized elsewhere (NAS 1990; NCRP 1997), the available data do not exclude the possibility that there may be a threshold in the millisievert dose range, below which the carcinogenicity of radiation is absent altogether. For this reason, the existing estimates cannot be used without caution to predict the risks of cancer that may be attributable to small doses or doses accumulated over weeks, months, or years. The aforementioned uncertainties notwithstanding, models applied to epidemiological data from the atomic bomb survivors and other irradiated populations have nevertheless yielded estimates of the lifetime risks of different forms of cancer that may be attributable to ionizing irradiation (Table 5). In interpreting the estimates, however, it should not be forgotten that they are based on population averages and hence cannot be assumed to apply equally to all individuals. Susceptibility to certain types of cancer (notably cancers of the thyroid and breast) is substantially higher in children than in adults, and susceptibility is also increased in association with certain hereditary disorders, such as retinoblastoma and the naevoid basal cell carcinoma syndrome (Sankaranarayanan and Chakraborty 1995). Although quantitative estimates are, therefore, limited by the aforementioned sources of uncertainty, they are nevertheless judged in some quarters to provide the only rational basis for assessing the extent to which a cancer that arises in a previously irradiated person is attributable to the dose of radiation in question (NIH 1985).

Table 5 Estimated lifetime risks of cancer attributable to 0.1 Sv rapid irradiation

Studies to ascertain whether the rates of cancer and other diseases do, in fact, vary detectably with natural background radiation levels have been inconclusive thus far. A few studies have even suggested an inverse relationship, which has been interpreted by some observers as evidence for the existence of beneficial (or hormetic) effects of low-level irradiation (Luckey 1991); however, such a relationship has not usually persisted after controlling for the effects of confounding variables (NAS 1990; UNSCEAR 1994). That populations residing in areas of elevated natural background radiation have not exhibited significant increases in cancer rates (NAS 1990; UNSCEAR 1994) is not unexpected, given the low levels of exposure in question; that is, the estimates tabulated above (Table 5) imply that no more than 3 per cent of all cancers in the general population are attributable to natural background radiation. On the other hand, although epidemiological studies of the effects of indoor radon have been inconclusive thus far, owing in part to uncertainties in dosimetry and difficulties in controlling for the influence of smoking and other confounding variables, the data imply that up to 10 per cent of lung cancers in the United States population may conceivably result from residential exposure to radon (NAS 1998). In view of the sizeable magnitude of the presumed risks, guidelines for limiting residential radon concentrations have been recommended in the United States and elsewhere (USEPA 1992).
In occupationally exposed workers, carcinogenic effects of irradiation are no longer readily demonstrable, thanks to modern radiation protection practices, although some cohorts of underground hardrock miners continue to exhibit excessive mortality from lung cancer (NAS 1998). In nuclear workers, likewise, analysis of the pooled data from several large cohorts suggests a dose-dependent excess of leukaemia in this population (Cardis et al. 1995) comparable in magnitude with the estimate tabulated above (Table 5). Multiple myeloma and other forms of cancer also have been reported to be increased in frequency in some cohorts of occupationally exposed workers, but such excesses have been observed only inconsistently and are of equivocal significance (Mettler and Upton 1995; NCRP 1997).
Among populations exposed to radio-active fallout, carcinogenic effects on the thyroid gland have been well documented in Marshall Islanders who received large doses to the thyroid in childhood and infancy (possibly up to 20 Gy (2000 rad)) from radio-active iodine, tellurium, and external g-ray emitters in fallout released by a thermonuclear weapons test at Bikini Atoll in 1954 (Robbins and Adams 1989). The incidence of thyroid cancer has also been observed to be increased in United States children who resided downwind from the Nevada nuclear weapons test site (Kerber et al. 1993) and in children living in areas of Belarus and the Ukraine that were contaminated by radionuclides released in the Chernobyl accident (Astakhova et al. 1998; Heidenreich et al. 1999).
The occurrence of clusters of leukaemia in children residing in the vicinity of nuclear plants in the United Kingdom has suggested the possibility that such cancers may have resulted from radio-activity released by the plants; however, the releases are estimated to have increased the total radiation dose to such populations by less than 2 per cent, so that other explanations are considered more likely (Doll et al 1994). The possibility that the leukaemias in question may have resulted from heritable oncogenic effects caused by occupational irradiation of the fathers of the affected children has also been suggested (Gardner et al. 1990); however, this hypothesis is generally discounted for reasons that are discussed below.
Heritable effects
Heritable effects of irradiation, although well documented in other organisms, have yet to be observed in humans. Thus, intensive study of the more than 76 000 children of Japanese atomic bomb survivors, carried out over four decades, has failed to disclose any heritable effects of radiation in this population, as measured by untoward pregnancy outcomes, neonatal deaths, malignancies, balanced chromosomal rearrangements, sex chromosome aneuploids, alterations of serum or erythrocyte protein phenotypes, changes in sex ratio, or disturbances in growth and development (NAS 1990). Estimates of the risks of heritable effects of radiation to future generations must, therefore, rely heavily on extrapolation from findings in laboratory animals.
From the available data, it is inferred that human germ cells are no more radiosensitive than those of the mouse and that the dose required to double the rate of heritable mutations in the human species must be at least 1.0 Sv (NAS 1990). Hence, on the basis of the existing evidence, it is estimated that fewer than 1 per cent of all genetically determined diseases in the human population are attributable to natural background irradiation (Table 6).

Table 6 Estimated frequencies of heritable disorders attributable to natural background ionizing irradiation

The possibility that an excess of leukaemia and non-Hodgkin’s lymphoma in young people residing in the village of Seascale, in northern England, was caused by the occupational irradiation of their fathers who worked at the Sellafield nuclear installation, has been suggested by a case–control study (Gardner et al. 1990), as noted above. Conflicting with this interpretation, however, are (a) the lack of any comparable excess in larger numbers of children born outside Seascale to fathers who had received similar, or even larger, occupational doses at the same nuclear plant (Wakeford et al. 1994a), (b) the lack of similar excesses in French (Hill and LaPlanche 1990), Canadian (McLaughlin et al. 1993), or Scottish (Kinlen et al. 1993) children born to fathers with comparable occupational exposures, (c) the lack of excesses in the children of atomic bomb survivors (Yoshomoto et al. 1990), (d) the lack of excesses in United States counties containing nuclear plants (Jablon et al. 1991), (e) the fact that the frequency of radiation-induced mutations implied by the interpretation is far higher than established rates (Wakeford et al. 1994b), and (f) evidence that the mutations causing childhood leukaemia are of a severity likely to interfere with the viability of affected germ cells (Evans 1990). On balance, therefore, the available data fail to support the paternal gonadal irradiation hypothesis (Doll et al. 1994). Although interpretation of the observed clusters is complicated by various sources of uncertainty (Ross et al. 1999), the possibility of an infectious aetiology for them has been suggested by the occurrence of comparable excesses of childhood leukaemia at other places in the United Kingdom that have experienced similar large influxes of population (Kinlen 1988). By the same token, there is insufficient evidence to conclude that radiation from the Chernobyl accident or other sources is responsible for creating the clusters of childhood leukaemia that have been observed (Alexander and Greaves 1999).
Effects of prenatal irradiation
Throughout prenatal life, radiosensitivity is relatively high, but the effects of a given dose vary markedly depending on the developmental stage of the embryo or fetus at the time of exposure. During the pre-implantation period, the embryo is maximally susceptible to killing by irradiation. Subsequently, during critical stages in organogenesis, it is susceptible to the induction of malformations and other disturbances of development (UNSCEAR 1986), as exemplified by the dose-dependent increase in frequency of mental retardation and the dose-dependent decrease in IQ test scores occurring in atomic bomb survivors who were irradiated between the 8th and 15th weeks (and, to a lesser extent, between the 16th and 25th weeks) after conception (UNSCEAR 1986; NAS 1990).
Susceptibility to the carcinogenic effects of radiation also appears to be relatively high throughout the prenatal period, judging from the association between childhood cancer (including leukaemia) and prenatal exposure to diagnostic X-irradiation (NAS 1990; Doll and Wakeford 1997). This association, although yet to be established as causal in nature, has been observed consistently in many case–control studies and is equally strong in twins (NAS 1990; Doll and Wakeford 1997).
While no excess of childhood cancer has been recorded in prenatally irradiated A-bomb survivors, their numbers were relatively small (Yoshimoto et al. 1990). Hence the results of the various case–control studies are interpreted to imply that prenatal irradiation causes a 40 per cent per sievert increase in the risk of leukaemia and other cancers during childhood (UNSCEAR 1988; NAS 1990; Doll and Wakeford 1997).
Prevention
In order to minimize the risks of injury from ionizing radiation, the following principles are recommended as guidelines to be observed in any activities involving exposure to this agent (ICRP 1991): (a) no such activity should be considered justifiable unless it produces a sufficient benefit to those who are exposed, or to society at large, to offset any harm it may cause; (b) in any such activity, the dose and/or likelihood of exposure should be kept as low as is reasonably achievable, all relevant economic and social factors being taken into account; (c) the radiation exposure of individuals resulting from any combination of such activities should be subject to dose limits (Table 7) that are far enough below the thresholds for non-stochastic effects to prevent such effects altogether, and that are also low enough to keep the risks of any resulting stochastic effects (which may have no thresholds) from exceeding socially acceptable levels.

Table 7 Recommended effective dose limits of ionizing radiation for occupationally exposed workers and members of the public

Implicit in these guidelines are the requirements that any facility dealing with ionizing radiation is properly designed, carefully plans and oversees its operating procedures, has in place a well-conceived radiation protection programme, ensures that its workers are adequately trained and supervised, and maintains a well-developed and well-rehearsed emergency preparedness plan, in order to be able to respond promptly and effectively in the event of a malfunction, spill, or other type of radiation accident (Shapiro 1990).
As medical radiographic examinations and indoor radon constitute the most important controllable sources of exposure to ionizing radiation for members of the general public (Table 1), prudent measures to limit irradiation from these sources also are warranted (Upton et al. 1990). Other potential risks to human health and the environment calling for increased attention are the millions of cubic feet of radio-active and mixed wastes (mine and mill tailings, spent nuclear fuel, waste from the decommissioning of nuclear power plants, dismantled industrial and medical radiation sources, radio-active pharmaceuticals and reagents, heavy metals, polyaromatic hydrocarbons, and other contaminants) which are present in ever-growing quantities and severely tax existing storage capacities at numerous sites (USDOE 1993). Also, as noted above, there is a widespread and urgent need in less-developed countries for more adequate safeguards to protect occupationally exposed workers and members of the public against excessive exposure to radiation (UNSCEAR 1988).
Non-ionizing radiation
Ultraviolet radiation
Nature, sources, and environmental levels
Ultraviolet radiations (UVR) comprise a spectrum (Fig. 1) of electromagnetic waves, subdivided for convenience into three bands: (a) UVA, 400 to 320 nm (‘black light’); (b) UVB, 320 to 280 nm; (c) UVC, 280 to 100 nm (which is germicidal). The chief source of UVR for members of the public is sunlight, which varies in intensity with latitude, elevation, and season (AMA 1989). Important manmade sources of high-intensity exposure include sun/tanning lamps, welding arcs, plasma torches, germicidal and black-light lamps, electric arc furnaces, hot-metal operations, mercury vapour lamps, and lasers. Common low-intensity sources include fluorescent lamps and certain laboratory equipment (NIOSH 1972).
Nature and mechanisms of injury
As UVR does not penetrate deeply into human tissues, the injuries it causes are confined chiefly to the skin and eyes. Reactions of the skin to UVR, which are common among fair-skinned people, include sunburn, skin cancers (basal cell and squamous cell carcinomas, and to a lesser extent melanomas), ageing of the skin, solar elastoses, and solar keratoses (English et al. 1997). Injuries of the eye include photokeratitis, which may result from brief exposure to a high-intensity UVR source (‘welder’s flash’) or from more prolonged exposure to intense sunlight (‘snow blindness’), cortical cataract, and pterygium (Lerman 1988).
The effects of UVR result chiefly from its absorption in DNA with the production of pyrimidine dimers, causing mutational changes in exposed cells. Sensitivity to UVR may be increased by DNA repair defects (for example, xeroderma pigmentosum), by agents (such as caffeine) that inhibit the repair enzymes, and by photosensitizing agents (such as psoralens, sulphonamides, tetracyclines, nalidixic acid, sulphonylureas, thiazides, phenothiazines, furocumarins, and coal tar) which produce UVR-absorbing DNA photoproducts (Harper and Bickers 1989). The carcinogenic action of UVR is mediated primarily through direct effects on the exposed cells, but may involve depression of local immunity as well (Kripke 1988). UVB, although far less intense than UVA in sunlight, plays a more important part in sunburn and skin carcinogenesis (English et al. 1997); UVA also, however, contributes to the latter, as well as to tanning, some photosensitivity reactions, ageing of the skin, photokeratitis, and cortical lens opacities (AMA 1989).
Prevention
Excessive exposure to sunlight or other sources of UVR should be avoided, especially by fair-skinned individuals. In addition, protective clothing, UVR screening lotions or creams, and UVR blocking sunglasses should be used for the purpose when necessary. To protect occupationally exposed workers, it is recommended that exposure be limited to 1.0 mW/cm2 for periods longer than 1000 s and 1000 mW/cm2 (1.0 J/cm2) for periods of 1000 s or less (NIOSH 1972; ACGIH 1997).
From an environmental perspective, it is noteworthy that the protective layer of ozone in the stratosphere is being depleted by chlorofluorocarbons and other air pollutants (Rex et al. 1997), and that every 1 per cent decrease in ozone is expected to increase the UVR reaching the earth by 1 to 2 per cent, thereby increasing the rates of non-melanotic skin cancer by 2 to 6 per cent (Henriksen et al. 1990). The increase in cancer rates is, of course, only one of the adverse effects to be expected; the most serious, perhaps, is the far-reaching impact of increased UVR on vegetation and crop production (Worrest and Grant 1989).
Visible light
Nature, sources, and environmental levels
Visible light consists of electromagnetic waves varying in wavelength from 380 nm (violet) to 760 nm (red) (Fig. 1). Sources of visible light in the environment vary widely in the intensity of their emissions; common high-intensity sources other than the Sun include lasers, electric welding or carbon arcs, and tungsten filament lamps.
Nature and mechanisms of injury
Too bright a light can injure the eye through photochemical reactions in the retina; that is, sustained exposure to intensities exceeding 0.1 mW/cm2, such as can result from fixating a bright source of light, may produce photochemical blue-light injury, and brief exposure of the retina to intensities exceeding 10 W/cm2, depending on image size, may cause a retinal burn (Sliney and Wolbarsht 1980). The lens, iris, cornea, and skin also are vulnerable to injury from the thermal effects of laser radiation (Sliney and Wolbarsht 1980). Conversely, too little illumination can also be harmful, causing eyestrain (Huer 1983) and/or seasonal affective disorder (Rosenthal et al. 1988).
Prevention
As bright continuously visible light normally elicits an aversion response, which acts to protect the eye against injury, few sources of light are large and bright enough to cause a retinal burn under normal viewing conditions. One must never look directly at a solar eclipse, and in situations involving potential exposure to such high-intensity sources as carbon arcs or lasers, appropriate training, proper design of equipment, and protective eye shields are indicated (Sliney and Wolbarsht 1980; ANSI 1986; ACGIH 1997).
Infrared radiation
Nature, sources, and environmental levels
Infrared radiation (IR) consists of electromagnetic waves ranging in wavelength from 7 × 10–5 m to 3 × 10–2 m (Fig. 1). Some such radiation is emitted by all objects with temperatures above absolute zero, but potentially hazardous sources of IR include furnaces, ovens, welding arcs, molten glass, molten metal, and heating lamps.
Nature and mechanisms of injury
The injuries caused by IR are limited chiefly to burns of the skin and cataracts of the lens of the eye. The warning sensation of heat usually prompts aversion in time to prevent the skin from being burned by IR; however, the lens of the eye is vulnerable in lacking both heat-sensing and heat-dissipating ability. As a result, glass blowers, blacksmiths, oven operators, and those working around heating and drying lamps are at risk of IR-induced cataracts (Lydahl 1984).
Prevention
Control of IR hazards requires appropriate shielding of sources, proper training and supervision of potentially exposed persons, and use of protective clothing and goggles. It is also recommended that exposures to IR not exceed 10 mW/cm2 (ACGIH 1997).
Microwave radiation
Nature, sources, and environmental levels
Microwave and radiofrequency radiation (MW/RFR) consists of electromagnetic waves ranging in frequency from about 3 kHz to 300 GHz (Fig. 1). Sources of MW/RFR occur widely in radar, television, radio, cellular phones, and other telecommunications systems, and are also used in various industrial operations (for example, heating, welding, and melting of metals, processing of wood and plastic, high-temperature plasma), household appliances (such as microwave ovens), and medical applications (for example, diathermy and hyperthermy) (ILO 1986).
Nature and mechanisms of injury
The biological effects of MW/RFR have traditionally been regarded as primarily thermal in nature. MW/RFR-induced burns of the skin and other tissues have occasionally resulted from faulty or improperly used household microwave ovens and from the overexposure of patients in whom cutaneous pain and temperature senses that usually warn of impending injury are impaired. Because of the deep penetration of MW/RFR, the cutaneous burns it causes tend to involve dermal and subcutaneous tissues, which heal slowly. Cataracts of the lens of the eye also have been reported to result from high-intensity exposures (> 1.5 kW/m2) (McRee 1972; Lipman et al. 1988), and death from hyperthermia has been encountered in the industrial use of MW/RFR sources (McLaughlin 1957; Roberts and Michaelson 1985). Also well documented is the ability of MW/RFR to interfere with cardiac pacemakers and other medical devices (NCRP 1986).
Although the biological effects of MW/RFR have been attributed primarily to thermal mechanisms in the past, there is growing evidence suggesting the possibility that MW/RFR may elicit some types of effects through non-thermal mechanisms as well. Such effects, which are yet to be documented conclusively, include damage to DNA, impairment of fertility, developmental disturbances, neurobehavioural abnormalities, depression of immunity, stimulation of cell proliferation, and carcinogenic effects in model systems and in humans (NCRP 1986; Tenforde 1998; Elwood 1999; Moulder et al. 1999).
Prevention
Proper design and shielding of MW/RFR sources, along with appropriate training and supervision of potentially exposed persons (especially those wearing cardiac pacemakers or other sensitive devices), are indicated. Exposure to MW/RFR power densities exceeding the threshold limit values tabulated (Table 8) may cause detectable heating of tissue and should be avoided (NCRP 1986; ILO 1986; ANSI 1992; ACGIH 1997; ICNIRP 1998).

Table 8 Threshold limit values for radiofrequency/microwave radiation

Extremely low-frequency electromagnetic fields
Nature, sources, and environmental levels
Extremely low-frequency electromagnetic fields (EMFs)—that is, time-varying magnetic fields with frequencies below 300 Hz—are present throughout the environment. The largest such fields arise intermittently from solar activity and thunderstorms, during which they may reach intensities on the order of 0.5 T. Far stronger than such naturally occurring EMFs are the localized 50- to 60-Hz fields that are generated by electric power lines, transformers, motors, household appliances, video display tubes (VDTs), and various medical devices, notably magnetic resonance imaging (MRI) systems (OTA 1989; Tenforde 1992).
For example, the flux density on the ground beneath a 765-kV, 60-Hz power line carrying 1 kA per phase is of the order of 15 T, and close to common household appliances the flux density may range up to 2.5 mT (Tenforde 1992). As the strength of such fields decreases rapidly with distance, however, the average ambient value in the home environment is less than 0.3 T (3 mG). By the same token, while flux densities at video display terminals typically range up to 5 T, those at the location of the operator are generally less than 1 T (Tenforde 1992).
Nature and mechanisms of injury
Extremely low-frequency EMFs induce electrical currents that can alter the properties of cell membranes and exert effects on electrically active tissues (nerves, neuromusculature, retina, heart) and on cardiac pacemakers. Induced current densities under 1 to 10 mA/m2 produce few, if any, irreversible effects, which is not surprising as similar current densities exist endogenously in many tissues. Induced current densities above 10 mA/m2, on the other hand, although not genotoxic, reportedly produce various changes in the biochemistry and physiology of cells and tissues (for example, alterations in metabolism, growth rate, melatonin secretion, endocrine activity, and immune response), and current densities above 1 A can cause neural excitation and irreversible effects, such as cardiac fibrillation (Tenforde 1992, 1998).
In addition to the effects produced by strong EMFs, epidemiological data have suggested the possibility of severe effects from long-continued exposure to weaker EMFs; that is, that the risks of leukaemia may be increased by residential exposure to household EMFs in children, that the risks of brain cancer and leukaemia may be increased by occupational exposure to EMFs in utility workers, and that the risks of reproductive disorders may be increased by chronic exposure to EMFs through the operation of VDTs in pregnant women (Bates 1991; Tenforde 1992, 1996; NAS 1996). As yet, however, such epidemiological data are inconclusive, and their interpretation is complicated by uncertainties in exposure assessment and by the lack of established biological mechanisms for the effects in question (NAS 1996; Tenforde 1998). Nevertheless, the fact that such fields have been reported to influence ion transport, melatonin secretion, and tumour promotion in some model systems (Tenforde 1992, 1998) has reinforced public health concern (OTA 1989; NAS 1996).
Prevention
Areas containing EMFs stronger than 0.5 mT, such as exist around transformers, accelerators, MRI systems, and other electric devices, should be posted with warning signs and should be avoided by persons wearing pacemakers. In addition, it is recommended that the strength of any 60-Hz time-varying magnetic field, such as typically exists around an MRI system, should be limited to 1 mT for occupational exposures and to 0.1 mT for those wearing cardiac pacemakers or for continuous exposures involving members of the general public (ACGIH 1997). To minimize the risks, if any, that may be associated with the use of electric blankets, wiring design changes have been introduced by some manufacturers to cancel the surface 60-Hz EMFs that such blankets would otherwise generate (Tenforde 1992, 1996).
Ultrasound
Nature, sources, and environmental levels
Although often classified for public health purposes with non-ionizing radiation, ultrasound is not a component of the electromagnetic spectrum but actually consists of mechanical vibrations at frequencies above the audible range (that is, above 16 kHz) (NCRP 1983). Sources of high-power low-frequency ultrasound are used widely in science and industry for cleaning, degreasing, plastic welding, liquid extracting, atomizing, homogenizing, and emulsifying operations, as well as in medicine for lithotripsy and other applications. Low-power high-frequency ultrasound is used widely in analytical work and in medical diagnosis (such as ultrasonography).
Nature and mechanisms of injury
The biological effects of ultrasound are similar in mechanism to those of mechanical vibration. High-power low-frequency ultrasound, transmitted through the air or through bodily contact with the generating source, has been observed to cause a variety of effects in occupationally exposed workers, including headache, earache, tinnitus, vertigo, malaise, photophobia, hypercusia, peripheral neuritis, and autonomic polyneuritis. The possibility that it may cause adverse effects on the embryo also has been suggested (NCRP 1983).
Although excessive exposure to high-frequency ultrasound through bodily contact with the source may be expected, in principle, to cause complaints similar to those above, no adverse effects have been observed to result from exposure to high-frequency ultrasound at the low power levels used in medical ultrasonography (NCRP 1983).
Prevention
Protection against injury by ultrasound requires appropriate isolation and insulation of generating sources, as well as proper training and ear protective devices for those working around such sources. Yearly audiometric and neurological examinations of occupationally exposed workers also are recommended (WHO 1982).
Summary and conclusions
The adverse effects on human health caused by different forms of radiant energy are diverse, ranging from rapidly fatal injuries to cancers, birth defects, and hereditary disorders appearing months, years, or decades after exposure. The nature, frequency, and severity of effects depend on the type of radiant energy in question and the particular conditions of exposure. Most such effects are produced only by appreciable levels of exposure and can, therefore, be prevented by keeping any exposure from exceeding relevant thresholds. The genotoxic and carcinogenic effects of ionizing and UVR, in contrast, are presumed to increase in frequency as linear non-threshold functions of the dose and therefore not to be entirely preventable without eliminating all exposures to these forms of radiation. As it is not feasible to eliminate exposure to these two forms of radiation completely, protection against their mutagenic and carcinogenic effects requires that exposures to these agents be limited sufficiently to keep any associated risks from exceeding acceptable levels.
To achieve the desired level of protection against each of the different forms of radiation requires knowledge of the relevant exposure–risk relationships, appropriate design and operation of all radiation sources, proper training and supervision of operating personnel, and education of the public in prudent measures for safeguarding health.
These requirements can be met satisfactorily in most situations involving radiation hazards, given the necessary commitment of effort and resources. Unresolved public health problems calling for particular attention at this time, however, include (a) assessment of the risks associated with residential exposure to indoor radon, and of the pertinent remediation strategies, (b) development and implementation of measures for dealing with the hazards posed by the large and growing quantities of radio-active and mixed wastes, (c) assessment of the risks that may be associated with exposure to 60 Hz electromagnetic fields, and (d) further evaluation of atmospheric ozone depletion and its implications for UVR-induced impacts on human health.
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