The data on mouse skin thickness reported here was prompted by the need to know the true position of basal cells of the epidermis and hair follicles as these are important "cells at risk" for a variety of skin reactions including carcinogenesis following exposure to radiation. There is little reliable data in the literature and most previous reports have ignored the shrinkage of skin that occurs because of its natural elasticity. The values determined for mouse flank skin in telogen--the resting phase of the hair cycle for the different skin layers--are epidermis 10 micron, corium 250 micron, adipose layer 150 micron, and hair follicle depth 150 micron. Three days after chemical depilation which triggers the hair follicles into active cycle (anagen) the epidermis doubles in thickness, remains at this value for 7 days, and then gradually returns to telogen values by day 18. The corium and adipose layers also increase significantly to reach approximately 390 micron and approximately 260 micron, respectively, by day 10 and then return to control values from day 15 onward. The change in hair follicles depths are more dramatic with active follicle basal cells reaching approximately 450-550 micron into the adipose layer between days 7 and 15. One important finding is that chemical depilation does not affect the telogen thickness of skin-the teleogen values for the epidermis and dermis immediately prior to and immediately after depilation were similar to those 23 days later at the beginning of the next telogen phase.

An attempt has been made to clarify the two most important issues relevant to personal eye dosimetry. This involves the identification of the cells which are most at risk from radiation and the specification of their position in the eye. A survey of the radiobiological literature concerning animals and humans shows that the epithelial cells in the equatorial region of the lens are those which are involved in radiation cataract induction. The depth of these cells has been evaluated in the human eye by means of geometrical construction. The relevant dimensions have been determined from a survey of published anatomical data and supplemented by new data obtained by slit-image photography. In a normal adult population (20-65 years) the minimum depth of the incriminated cells is 2.3 plus or minus 0.4 mm; the upper and lower values are associated with young and old subjects respectively. Approximate calculations for isotropic 90Sr/90Y and 106Rh beta-radiation fields indicate that a planar dosemeter, which integrates the tissue dose between depths of 2.5-3.5 mm, should give a reasonable measure of the mean equatorial dose for the variety of eye and irradiation geometries likely to be met during a life-time exposure. The long established, but tentative, value of 3 mm for the effective depth of the lens is thus confirmed.

Since its inception in 1955 the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) has periodically undertaken a broad review of the sources and the effects of ionising radiation. This latest report is in two concurrently published separate volumes. Volumes I and II provide updated reviews of sources and effects of ionising radiation respectively. A considerable amount of new material supports the review of sources. The review of biological effects takes on board various contemporary issues raised by the `linear-no-threshold' controversy. Particular emphasis has been given to the evaluation of exposures and health consequences of the Chernobyl accident. As usual the report has an extended summary (17 pages) backed up by a number of technical annexes (A-J). The annexes have a wealth of basic data, extensive tables and voluminous reference lists. The two volumes are available separately from the United Nations and cost £60 per volume. They are also available from the Stationery Office, but only as a two volume set. If you are interested only in `sources' then you should be aware that the source-related aspects of the Chernobyl accident are largely covered in volume II on effects. Annex A of volume I provides a description of the methodologies used for the assessment of doses from natural, man-made environmental, medical and occupational radiation exposures, which are presented in subsequent annexes B, C, D and E respectively. The components of natural radiation (cosmic rays, terrestrial gamma rays, inhalation and ingestion) have been evaluated and added to provide an estimate of the global average exposure. Since there are wide distributions of exposures from each source, the consequent effective doses combine in various ways at each location, depending on the specific concentration of radionuclides in the environment and in the body, the latitude and altitude of the location, and many other factors. The total annual global per caput effective dose due to natural radiation sources is 2.4 mSv. A typical range of individual doses is considered to be 1-10 mSv. In any large population about 65% would be expected to have annual effective doses between 1 and 3 mSv, about 25% of the population would have annual effective doses less than 1 mSv and 10% would have annual effective doses greater than 3 mSv. The main man-made contribution to the environmental exposure of the world's population has come from the testing of nuclear weapons in the atmosphere that occurred mainly between 1945-1980. Since the previous UNSCEAR review of this topic in 1982 new information, previously classified, has become available on the numbers and yields of nuclear tests. An updated listing of atmospheric nuclear tests conducted at each of the test sites is included in this report. Although the total explosive yields of each test have been divulged, the fission and fusion yields are still mostly suppressed. Some general assumptions have been made to allow the evaluation of fission and fusion yields of each test in or...

Controversy exists regarding the biological effectiveness of low energy x-rays used for mammography breast screening. Recent radiobiology studies have provided compelling evidence that these low energy x-rays may be 4.42 +/- 2.02 times more effective in causing mutational damage than higher energy x-rays. These data include a study involving in vitro irradiation of a human cell line using a mammography x-ray source and a high energy source which matches the spectrum of radiation observed in survivors from the Hiroshima atomic bomb. Current radiation risk estimates rely heavily on data from the atomic bomb survivors, and a direct comparison between the diagnostic energies used in the UK breast screening programme and those used for risk estimates can now be made. Evidence highlighting the increase in relative biological effectiveness (RBE) of mammography x-rays to a range of x-ray energies implies that the risks of radiation-induced breast cancers for mammography x-rays are potentially underestimated by a factor of four. A pooled analysis of three measurements gives a maximal RBE (for malignant transformation of human cells in vitro) of 4.02 +/- 0.72 for 29 kVp (peak accelerating voltage) x-rays compared to high energy electrons and higher energy x-rays. For the majority of women in the UK NHS breast screening programme, it is shown that the benefit safely exceeds the risk of possible cancer induction even when this higher biological effectiveness factor is applied. The risk/benefit analysis, however, implies the need for caution for women screened under the age of 50, and particularly for those with a family history (and therefore a likely genetic susceptibility) of breast cancer. In vitro radiobiological data are generally acquired at high doses, and there are different extrapolation mechanisms to the low doses seen clinically. Recent low dose in vitro data have indicated a potential suppressive effect at very low dose rates and doses. Whilst mammography is a low dose exposure, it is not a low dose rate examination, and protraction of dose should not be confused with fractionation. Although there is potential for a suppressive effect at low doses, recent epidemiological data, and several international radiation risk assessments, continue to promote the linear no-threshold (LNT) model. Finally, recent studies have shown that magnetic resonance imaging (MRI) is more sensitive than mammography in detecting invasive breast cancer in women with a genetic sensitivity. Since an increase in the risk associated with mammographic screening would blur the justification of exposure for this high risk subgroup, the use of other (non-ionising) screening modalities is preferable.

Recent radiobiological studies have provided compelling evidence that the low energy X-rays as used in mammography are approximately four times--but possibly as much as six times--more effective in causing mutational damage than higher energy X-rays. Since current radiation risk estimates are based on the effects of high energy gamma radiation, this implies that the risks of radiation-induced breast cancers for mammography X-rays are underestimated by the same factor. The balance of risk and benefit for breast screening have been re-analysed for relative biological effectiveness (RBE) values between 1 and 6 for mammography X-rays. Also considered in the analysis is a change in the dose and dose-rate effectiveness factor (DDREF) from 2 to 1, women with larger than average breasts and implications for women with a family history of breast cancer. A potential increase in RBE to 6 and the adoption of a DDREF of unity does not have any impact on the breast screening programme for women aged 50-70 years screened on a 3 yearly basis. Situations for which breast screening is not justified due to the potential cancers induced relative to those detected (the detection-to-induction ratio (DIR)) are given for a range of RBE and DDREF values. It is concluded that great caution is needed if a programme of early regular screening with X-rays is to be used for women with a family history of breast cancer since DIR values are below 10 (the lowest value considered acceptable for women below 40 years) even for modest increases in the RBE for mammography X-rays.

Radon progeny can plate out on skin and give rise to exposure of the superficial epidermis from alpha emitters Po-218 (7.7 MeV, range approximately 66 microm) and Po-214 (6 MeV, range approximately 44 microm). Dose rates from beta/gamma emitters Pb-214 and Bi-214 are low and only predominate at depths in excess of the alpha range. This paper reviews the evidence for a causal link between exposure from radon and its progeny, and deterministic and stochastic biological effects in human skin. Radiation induced skin effects such as ulceration and dermal atrophy, which require irradiation of the dermis, are ruled out for alpha irradiation from radon progeny because the target cells are considerably deeper than the range of alpha particles. They have not been observed in man or animals. Effects such as erythema and acute epidermal necrosis have been observed in a few cases of very high dose alpha particle exposures in man and after acute high dose exposure in animals from low energy beta radiations with similar depth doses to radon progeny. The required skin surface absorbed doses are in excess of 100 Gy. Such effects would require extremely high levels of radon progeny. They would involve quite exceptional circumstances, way outside the normal range of radon exposures in man. There is no definitive identification of the target cells for skin cancer induction in animals or man. The stem cells in the basal layer which maintain the epidermis are the most plausible contenders for target cells. The majority of these cells are near the end of the range of radon progeny alpha particles, even on the thinnest body sites. The nominal depth of these cells, as recommended by the International Commission on Radiological Protection (ICRP), is 70 microm. There is evidence however that some irradiation of the hair follicles and/or the deeper dermis, as well as the inter-follicular epidermis, is also necessary for skin cancer induction. Alpha irradiation of rodent skin that is restricted to the epidermis does not produce skin cancer. Accelerator generated high energy helium and heavy ions can produce skin cancer in rodents at high doses, but only if they penetrate deep into the dermis. The risk figures for radiation induced skin cancer in man recommended by the ICRP in 1990 are based largely on x and beta irradiated cohorts, but few data exist below absorbed doses of about 1 Gy. The only plausible finding of alpha-radiation induced skin cancer in man is restricted to one study in Czech uranium miners. There is no evidence in other uranium miners and the Czech study has a number of shortcomings. This review concludes that the overall balance of evidence is against causality of radon progeny exposure and skin cancer induction. Of particular relevance is the finding in animal studies that radiation exposure of cells which are deeper than the inter-follicular epidermis is necessary to elicit skin cancer. In spite of this conclusion, a follow-on paper evaluates the attributable risk of radon to skin cancer in the UK on the basis that targe...

This paper describes the evaluation of an inexpensive, commercially available 35 mm transparency slide scanner as a potential alternative scanning device for GafChromic HD-810 radiochromic dye film. Besides its low cost, the principal advantages of this type of scanner are high spatial resolution and high speed (a typical scan taking less than 1 min). With broad-band illumination the useful dose range using grey-scale imaging of GafChromic HD-810 is limited to about 50-800 Gy. By using the colour-scale imaging capability of the scanner we have been able to achieve a significant extension covering a similar range (15-2000 Gy) to that attainable using monochromatic illumination. The short-term reproducibility of the system is good, with a coefficient of variation of doses estimated from repeat scanning of uniformly exposed calibration films of less than 2%. Long-term stability is ensured by the scanning of a manufacturer-supplied test slide. The slide scanner system has been used in the determination of depth dose distributions from a model 'hot particle' source containing 106Ru/Rh. GafChromic dye film stacks irradiated by the source were read out on both the slide scanner and a conventional Joyce Loebl MDM6 scanning stage microdensitometer. The overall agreement between the dose estimates provided by the two systems was within 10%.

It has been suggested that spatially non-uniform radiation exposures, such as those from small radioactive particles ('hot particles'), may be very much more carcinogenic than when the same amount of energy is deposited uniformly throughout a tissue volume. This review provides a brief summary of in vivo and in vitro experimental findings, and human epidemiology data, which can be used to evaluate the veracity of this suggestion. Overall, this supports the contrary view and indicates that average dose, as advocated by the ICRP, is likely to provide a reasonable estimate of carcinogenic risk (within a factor of approximately +/- 3). There are few human data with which to address this issue. The limited data on lung cancer mortality following occupational inhalation of plutonium aerosols, and the incidence of liver cancer and leukaemia due to thorotrast administration for clinical diagnosis, do not appear to support a significant enhancement factor. Very few animal studies, including mainly lung and skin exposures, provide any indication of a hot-particle enhancement for carcinogenicity. Some recent in vitro malignant transformation experiments provide evidence foran enhanced cell transformation for hot-particle exposures but, properly interpreted, the effect is modest. Few studies extend below absorbed doses of approximately 0.1 Gy.