NEA Comments on Specific Paragraphs (Submission 3 of 5) (88) Although dose records are for individuals the dose coefficients on which they are based are derived for reference individuals. If doses approach or exceed the dose constraints, then investigations may need to be undertaken to address workplace and individual specific characteristics in the dose assessment. The committed effective dose coefficients from the intake of a radionuclide are also used for prospective dose estimates of individual members of the public. In these cases a commitment period of 50 years is used for the adult and the effective dose to age 70 years for infants and children. (Comment: This paragraph is not particularly clear. Does the second sentence imply that detailed re-assessment with personalised dose coefficients is needed for any person exceeding a dose constraint? It is not stated what committment periods should be used for worker prospective dose estimates. The second part of the paragraph seems to suggest the use of reference-individual dose coefficients for specific, individual members of the public, where this was not recommended for retrospective studies. The message, what dose coefficients to use for retrospective, compliance and prospective dose assessments should be clarified.) 3.5.2 (Deleted: Control of) Control of Tissue Reactions (Comment: This section discusses tissue reactions more than control, so the title should be altered) (94) Tissue reactions are the result of the loss of function of a significant number of cells in a tissue. The dosimetric situation causing this loss of function is complex. If the dose is approximately uniform over the tissue, the mean absorbed dose is an appropriate starting point. If the dose is far from uniform, the localised damage may not reduce the performance of the tissue, but the localised damage may be severe. The biological consequences of these situations depend heavily on the spatial and temporal distributions of absorbed dose. The only approach is to make qualitative judgements based on the distribution of absorbed dose in location and time. For this last purpose, estimates of the distribution of absorbed dose, possibly weighted by selected values of relative biological effectiveness (RBE), will be needed. The unit of the RBE-weighted absorbed dose is J kg-1 and the special name, proposed in Publication 92 (ICRP, 2003c), is the gray-equivalent (Gy-Eq).(Comment: This new unit will clarify the situation, and this is a good change) (96) The adverse health effects of radiation exposure may be grouped in two general categories: tissue reactions (Comment: Keep Deterministic Effects instead of tissue reactions,) and cancer development in exposed individuals and heritable disease in their offspring due to mutation of somatic and reproductive (germ) cells respectively. In Publication 60 (ICRP, 1991a), the Commission classified tissue reactions as deterministic effects and used the term stochastic effects for cancer and heritable disease. Since 1990 ICRP has reviewed many aspects of the biological effects of radiation. The views developed are summarised in this Chapter and in Annex A. A more detailed document is to be published as ICRP (2005), a Task Group report of ICRP Committee 1. 4.2 The induction of cancer, (Deleted: and) hereditary effects (insert: and other effects ) (Comments: The title should be modified because this section talks about effects on the embryo and fetus (4.2.4) and non-cancer (4.2.6)) 4.2.1 Risk of cancer (Comment: Many of the details in this section should be considered for an annex to better balance the document.) (100) The accumulation of cellular and animal data relevant to radiation tumorigenesis have, since 1990, greatly strengthened the view that DNA damage response processes in cells are of critical importance to the post-irradiation development of cancer. These mechanistic data on cellular response and animal tumorigenesis together with rapid advances in knowledge of the cancer process in general, give increased confidence that detailed information on DNA damage response/repair and the induction of gene/chromosomal mutations can contribute significantly to judgements on cancer risk at doses between a few mSv and a few tens of mSv; (Comment Is this an absolute dose or dose above background?? The explination of the use of this range, in which cancer risks are valid, is extremely important to specify.) also to associated judgements on RBE/radiation weighting and dose rate effects. Of particular importance are the advances in understanding of the induction by radiation of complex forms of DNA double strand breaks, the problems experienced by cells in correctly repairing these complex forms of DNA damage and the consequent appearance of cancer-related gene/chromosomal mutations. Advances in the microdosimetric aspects of radiation-induced DNA damage have also contributed significantly to this understanding. (105) In principle, epidemiological data on protracted exposures may be informative on judgements on the dose and dose-rate effectiveness factor (DDREF) to be used in radiological protection. However, the statistical precision afforded by many of these studies is limited and for this reason the Commission reached a judgement on a suitable value for DDREF that is based on a combination of experimental data from quantitative cellular/animal studies and dose-response features of the LSS. From these data the Commission finds no good reasons to change its 1990 recommendations of a DDREF of 2. (Comment: The explanation of this should be in an annex or another document. The USE of this number (for what dose rates or doses, etc.) needs clear explanation.) This risk reduction factor of 2 is to be applied to acute dose data in order to take account of the biologically expected decrease in cancer risk at low doses and low dose rates. (106) There are some post-1990 human and animal data on the quantitative aspects of radiation-induced germ cell mutation that impact on the Commission’s judgement on the risk of induction of genetic disease expressing in future generations. There have also been substantial advances in the fundamental understanding of human genetic diseases and the process of germ line mutagenesis including that occurring after radiation. The Commission has re-appraised the methodology used in Publication 60 (ICRP, 1991a) for the estimation of hereditary risks including risks of multifactorial diseases (Publication 83; ICRP, 1999b). The Commission has now adopted a new framework for the estimation of hereditary risks that employs data from human and mouse studies (see UNSCEAR, 2001). Also, for the first time, a scientifically justified method for the estimation of risk of multifactorial disease has been included (Publication 83). (Comment: In this paragraph, it should be noted that no hereditary effects have thus far been seen in humans) (108) The new estimate for genetic risks up to the second generation is around 0.2% per Gy (1 case in 500 live births per Gy). (Comment: Why this was estimated only up to the 2nd generation should be explained and/or referenced.) As a result, these new estimates of genetic risk by the Commission will tend to reduce the value of the tissue weighting factor for the gonads (see Annex A). This value relates to continuous low dose-rate exposures over these two generations i.e. doses to the grandparental and parental generations. 4.2.3 Nominal probability coefficients for stochastic effects (Comment: This section is using incident rates instead of cancer survival, in effect discounting the detriment of contracting cancer simply because some cancers may today be cured.) (Comment: These risk figures are for application in a statistical fashion, and represent average characteristics, not those of specific individuals. This should be more clear from the text in this section.) (112) In respect of Table 6 it is important to note that the detriment weighted nominal probability coefficient for cancer estimated here has been computed in a different manner from that of Publication 60. The present estimate is based upon lethality/life impairment weighted data on cancer incidence (Annex A) whereas in Publication 60, detriment was based upon fatal cancer risk weighted for non-fatal cancer, relative life lost for fatal cancers, and life impairment for non-fatal cancer. In this respect it is also notable that the nominal probability coefficient for fatal cancer in the whole population that may be projected from the cancer incidence data of Table A1.a of Annex A is 4.4% per Sv (Comment: This number gives the impression of precision, which does not exist) as compared with the Publication 60 value of 5% per Sv. Table 6: Nominal probability coefficients for stochastic effects (10-2 Sv-1)1 (Comment: The numbers in this table imply more precision than is supported scientifically. The end result of a risk assessment should be rounded to one significant figure. However, retaining two or three significant figures during intermediate stages of a risk assessment can reduce overall rounding errors, which can be significant. For example, if three parameters of the values 1.5, 2.5, and 3.5 were rounded to 2, 3, and 4 before being multiplied, the result would be almost twice as large as the result of rounding afterwards. This is clearly a question of presentation, but perhaps deserves some further thought, and perhaps text, by the Commission.) Exposed population Lethality adjusted cancer risk Lethality adjusted heritable effects Detriment Detriment Pub.60 Whole population 6.2 0.2 6.5 7.3 Adult workers 4.8 0.1 4.9 5.6 1 Values from Tables A1.a and A1.b in Annex A.(Comment: Need two footnotes: coefficients should not be used in the range where determiistic effects start. Also, these risk figures are very uncertain at low doses, e.g. a few mSv) 4.2.4 Radiation effects in the embryo and fetus (Comment: This section, in general, needs clarification and should be simplified and rewritten.) (118) Publication 90 also reviewed data concerning cancer risk following in utero irradiation. The largest studies of in utero medical irradiation provided evidence of increased childhood cancer. The Commission recognises that there are uncertainties on the risk of in-utero-induced solid cancers. However, the Commission suggests that it is reasonable to assume that life-time cancer risk following in utero exposure will be similar to that following irradiation in early childhood. From the studies reviewed in Publication 90 it is concluded that it is not possible to develop a system of tissue weighting factors for the embryo/fetus for use in the estimation of in utero risks from internal radiations. Finally, for the reasons given in Publication 82 (ICRP; 1999a), the Commission suggests that in utero exposure should not be a specific protection case in common prolonged exposure situations where the prolonged dose is well below about 100 mSv. (Comment This is much to high a number to put here. Effects on the embryo and fetus are known at much lower doses, such that further precision on this number is possible, and should be supplied by the ICRP's recommendations.) (119) The issue of inter-individual genetic differences in susceptibility to radiation-induced cancer was noted in Publication 60 and reviewed in Publication 79 (ICRP, 1998a). Since 1990, there has been a remarkable expansion in knowledge of the various single gene human genetic disorders, where excess spontaneous cancer is expressed in a high proportion of carriers of certain genes – the so called high penetrance (Comment: Here, penetrance most likely refers to traits, not to genes.) genes which are strongly expressed as excess cancer. Studies with cultured human cells and genetically altered laboratory rodents have also contributed much to knowledge and, with more limited epidemiological/clinical data, suggest that a high proportion of single gene, cancer prone disorders will show increased sensitivity to the tumorigenic effects of radiation. (123) Since 1990 evidence has accumulated that the frequency of non-cancer diseases is increased in irradiated populations. The strongest evidence for the induction of these non-cancer effects at doses in the order of 1 Sv derives from the A-bomb LSS, and the most recent mortality analysis (Preston et al., 2003) has strengthened the statistical evidence for an association with dose – particularly for heart disease, stroke, digestive disorders, and respiratory disease. However, the Commission notes current uncertainties on the shape of the dose-response at low doses and that the LSS data are consistent both with there being no dose threshold for risks of disease mortality and with a threshold of around 0.5 Sv. (Comment: Taking into account the precautionary principle, this sentence does not seem to be sufficient to justify the Commission's decision. For example, the shape of the dose-response curve is also uncertain for cancer effects.) It is unclear what forms of cellular/tissue mechanisms might underlie such a diverse set of non-cancer disorders, reported among the LSS data, although some association with sub-clinical inflammation (e.g. Hayashi et al., 2003) is possible. 5.2 The principles of protection (Comment: Justification should be discussed here as one of the principles of RP) (143) The Commission has noted the conventional definition of occupational exposure to any hazardous agent as including all exposures at work, regardless of their source. However, because of the ubiquity of radiation, the direct application of this definition to radiation would mean that all workers should be subject to a regime of radiological protection. The Commission therefore limits its use of the phrase ‘occupational exposure (to radiation)’ to exposures incurred at work as a result of situations that can reasonably be regarded as being the responsibility of the operating management. (Comment: The further clarification of occupational exposure provided in paragraph 169 is welcome.) (145) Public exposure is incurred as a result of a range of controllable sources. Dose limits for public exposure can be used only as a basis for national policy. Dose limits cannot in principle be applied to operational control, because neither the operator nor the regulator has the information about the totality of sources contributing to the dose to be limited in normal situations. The only feasible approach is to select a single source, or a small group of sources, and to estimate the exposure to the most exposed individual or the most highly exposed group of individuals (the critical group). For normal situations, it is unlikely that the total exposure from the defined controlled sources can be judged against the dose limit. (Comment In practice, this is not true. Regulators can very well assess all significant doses to individuals exposed to multiple sources.) This is because the selected sources are only a part of the whole group of likely sources. Therefore, an individual dose from single source during normal situations has to be judged against the constraint. (160) Doses above the natural background will entail an increasing need for action. Individual doses of several tens of millisieverts, whether they are received either singly or repeatedly, require that action be considered. Exposures that are within the natural background range are legitimate matters for concern, sometimes calling for significant action. (161) The need for action should decrease for doses additional to those due to the background of natural sources, if they are well below the annual background dose. Provided that the additional sources come from practices that have not been judged to be frivolous, the need for action should be low for doses less than about one hundredth of background dose.(Comment: Paragraph 160 refers to above the natural background, and Paragraph 161 it refers to In addition to natural background. This should be consistently presented.) (169) Workers in ‘controlled areas’(Comment: This term is not defined in the report. Note that the BSS also uses Supervised Areas) of workplaces are not strictly volunteers, but they are well informed and are specially trained, thereby forming a separate group of informed individuals. Other workers, such as administrative and support staff, might be included in the group of general individuals, and treated as members of the public.(Comment: Does this mean that public dose limits should be applied to these workers? The Commission should specify its recommendation here, taking into account the definition of occupational exposure used by the ILO.) (Comment Could maybe get around the problem of areas by referring to a worker’s training and knowledge instead of where the person is located. Could also refer to the graded approach to regulation of workers) (insert: For workers whose doses are controlled by personal dosimetry monitoring, the application of dose limits may be more practical then the application of dose constraints.) (175) In Publication 60 (ICRP, 1991a), the Commission concluded that there was no reason to distinguish between the two sexes in the control of occupational exposure. However, if a woman has declared that she is pregnant, additional controls have to be considered to protect the unborn child. It is the Commission’s policy that the methods of protection at work for women who may be pregnant should provide a level of protection for any conceptus broadly comparable to that provided for members of the general public. This is reasonable since while the mother may have chosen to be a radiation worker, the unborn child has not made such a decision. The Commission considers that this policy will be adequately applied if the mother exposed (insert: is protected against occupational exposures,) (Deleted: exposed) (Comment: To be more in line with the notion of protection) prior to her declaration of pregnancy, under the system of protection recommended by the Commission. Once pregnancy has been declared, and the employer notified, additional protection of the fetus should be considered. The working conditions of a pregnant worker, after declaration of pregnancy, should be such as to make it unlikely that the additional radiation weighted dose to the fetus will exceed about 1 mSv during the remainder of the pregnancy. (177) The exposure of patients who may be pregnant is dealt with in Chapter 9. For members of the public the (insert:constraint) (deleted: limit) (Comment: It is not clear whether the Commission meant limit or constraint, but this points out the confusion of terms) on effective dose means that the embryo/fetus is adequately protected and no further restrictions are recommended. These conclusions are also found in the report of a Task Group of ICRP Committee 1 (Publication 90; ICRP, 2003a).