The bill referred to is the Australian Radiation Protection and Nuclear Safety Bill, 1998
At present the object of the bill is to protect from the ‘harmful’ effects of radiation. ‘Harmful’ is not defined in the bill. However it would not be unreasonable to suggest that what is meant by ‘harmful’ is the most deleterious effect of radiation - early cancers and in excessive numbers. As with the terms "as low as reasonably achievable", or "acceptable dose limits", the word harmful, in this context, may create too many problems.
There is no ‘safe dose of radiation – that is a dose below which harm will not occur. However, such ‘harm’ may not be obviously manifest. The effects of radiation are: fatal or non-fatal cancers, genetic(hereditary) defects and non-genetic defects. This latter category may be subtle cell damage which can cause problems, for example, to a person’s immune system. However, such damage is almost impossible to diagnose in the ordinary sense (it takes very specialist knowledge and equipment, if it is even considered) – and may certainly never be part of a statistical survey. This sort of damage, which is acknowledged will happen in any population exposed to radiation, may not be recognised and/or measured. Thus this may not be covered by the definition of "harmful." It is understood that those involved in wording this bill have said that there is a threshold of radiation below which there is only "negligible harm.". This flies in the face of accepted science on radiation protection. See the following
- a brief section from a UNEP report which gives the view of ‘no safe dose’. This brief summary also gives an idea of the intergenerational impact of radiation exposure – a key point in the debate in measuring how "harmful" the effects are. If the majority of damage from a given exposure does not manifest itself in this generation will it be said that the exposures are nor ‘harmful’?
- secondly, a copy of the press release from the UK National Radiological Protection Board which describes one of the most recent important studies on low dose radiation and health. This states there is no safe dose of radiation – and that one ‘hit’ of radiation may cause cell damage that leads to a cancer.
- A report from the New Scientist on the work of the Medical Research Council in the UK on cell damage from low-dose radiation. This reinforces the potential impact on future generations from radiation exposure today.
All three papers note damage to the cell – which in important in both cancer initiation and hereditary damage. The MRC work is particularly important in this context as cells damage, how it might become manifest and how it might be measured is vital to diagnosis and statistical studies. Such damage is, at present, is not possible to determine using ordinary techniques. However, as the article notes, significant impacts may result from such cell damage and this may go undetected and therefore unchecked. The initial cell damage would, presumably, come under the heading of ‘negligible harm’ - a concept introduced in order to push through the APRANSA bill.
It would be interesting to know how ARPANSA will monitor for the longer term, significant damage of the supposedly ‘negligible harm’ to people’s cells be monitored?
Further, do the regulations contain a mechanism by which a medical/molecular/cellular study of a population might be instigated, and by whom would such a study be undertaken? The ARPANSA people under the Department of Health, should regulators also be independent arbiters of the impact of damage they might have allowed to occur?
The wording of the object of the ARPANSA bill and associated regulations, because of the lax approach, are something of a mess and in many respects throw up more problems than they solve.
- The fourth paper in on the estimated radiation exposures from the proposed Jabiluka/Ranger operation – exposures may exceed the 1mS/yr level recommended internationally.
It is believed that the regulations attached to the ARPANSA bill will allow for a dose limit of 1mSv per annum for a member of the public. The current UK limit is 0.3 from any single installation and the US limit is 0.25mSv from all sources combined. However, it is worth noting the following from a report commissioned by Sutherland Shire Council from MHB, which notes:
"another standard, that was adopted by the United States Environmental Protection Agency (USEPA) is also noteworthy for it is based also on a concept of maximum individual risk (mir), a social judgement as to the lifetime risk of fatal cancer to which a member of the public should be subjected by a licensed enterprise involving radioactive material. Interestingly, the mir was set at 1 chance in 10,000 and based upon the radiation risk estimates at that time that effective dose limit was correspondingly set at 0.1 mSv/yr (a factor of three tighter than the ANSTO standard)." (Ref: An evaluation of public exposure to routine radioactive releases from the Lucas Heights science and technology centre at ANSTO, MHB Technical Associates, for Sutherland Shire Council, 11/25/97).
Note: the ANSTO ‘standard’ referred to is a self-imposed limit which ANSTO set after the 1993 Research Reactor Review when it was pointed out that major nuclear installations overseas worked to lower limits.
In response to the higher ANSTO level, one of the MHB recommendations was that the government "consider revision of ANSTO standard for the releases at LHSTC to limit the effective dose to 0.1mSv/yr, of which no more than 0.03 mSv/yet is from radioiodines".
STAKEHOLDERS: Apparently the Mayor of Sutherland Shire Council has said written that the Council agrees with the ARPANSA Bill, without having seen the regulations and without having guaranteed how they might be amended so as not to contradict their own commissioned reports (and without having checked on the definition of ‘harmful’ re. health effects of radiation). However, the Council has called for health studies in the area in the past. As you can see from the papers I have sent, such damage as might arise may not be detectable through the usual methods. The best course of action would surely have been to have taken more time over this bill and the associated regulations to prevent damage.
Equally relevant is the fact that the lowest dose estimate for Jabiluka is 2.5 times higher than the dose MHB is recommending Sutherland Shire Council press for from Lucas Heights. What if the 0.1mSv/yr level was put into the regulations as a limit from given installations? How might this impact on current and proposed uranium mines – and their profitability? Who will win in this debate, the residents of Sutherland Shire or the mining companies? Worse still, might there be separate levels, with lower doses for Sutherland Shire and higher doses permitted for communities near uranium mines – a form of radiation apartheid.
To date the Bill has not been formally discussed with the appropriate stakeholder groups – including traditional owners living near uranium mines, as well as the people of Sutherland Shire. The regulations which form such an integral part of this bill are still being held in confidence. What guarantee will there be that enough time will be allowed to consider the regulations if and when they are released?
These questions certainly need answering before the ARPANSA bill goes through, as there is no guarantee there will be effective screening and amendments of the regulations afterwards.
Jean McSorley, mcsorley@compassnet.com.au
Mobile 0417 662 720
Home 02-9568 3265ATTACHMENT 1
Extract from United Nations Environment Programme publication
‘RADIATION – Doses, Effects, Risks.’
December 1985 (p.49).
"Radiation, by its very nature, is harmful to life. At low doses, it can start off only partially understood chains of events which lead to cancer or genetic damage. At high doses, it can kill cells, damage organs and cause rapid death.
The damage done by high doses normally becomes evident within hours or days. Cancers, however, take many year – usually decades – to emerge. And, by definition, the hereditary malformations and diseases caused by genetic damage take generations to show; it is the children, grandchildren, or remoter descendants of the people originally irradiated who will be affected.
Whereas it is usually quite easy to identify the early, acute effects at high doses, it is almost always extremely hard to pin down these "late" effects from low ones. This is partly because you have to wait much longer for them to become evident. Even then, it is hard to apportion blame because both cancer and genetic damage are not specific to radiation but have many other causes.
Radiation doses have to reach a certain level to produce acute injury – but not to cause cancer of genetic damage. In theory, at least, just the smallest dose can be sufficient. So, no level of exposure to radiation can be described as safe."(emphasis added)
ATTACHMENT 2
National Radiological Protection Board, Chilton, Didcot, Oxon. Tel 012351 831600
PRESS RELEASE
Not for publication or broadcast before 00.01 hours on Monday, 16th October 1995.
NO THRESHOLD, DOSE-RESPONSE RELATIONSHIP REAFFIRMED
We have reaffirmed that we should base radiation protection on the following assumptions: low radiation doses – even extremely low doses – do have an associated risk which increases with increase in dose.
Dr John Stather, NRPB’s senior assistant direction and one of the authors of a major review of the biological effects of radiation, made this statement to summarise the conclusion of the review when it was published.
He and his colleagues had carried out a thorough study of the data available for assessing the risk of radiation-induced cancer. They were particularly concerned with assessing risks at low doses and low dose rates. They brought together the results of epidemiological investigations and fundamental studies of molecular and cellular mechanisms involved in radiation damage.
Additionally, they supplemented this information with experimental studies which provided further guidance on the form of the dose-response relationship for cancer-induction.
The NRPB study was performed under contract to the Institute Protection et de Surete Nucleaire (IPSN) a French public organisation carrying out research and expert evaluations in various matters relevant to the control of radiation risks, safety technology, protection of man and of the environment, management of accident conditions, and security of transport. The conclusions of the report represent the position of the NRPB and not necessarily the views of the IPSN.
Epidemiological studies provide a substantial amount of direct, quantitative information on the risks of cancer in man following radiation exposure. The main source of data is the Life Span Study of the survivors of the atomic bombings of Hiroshima and Nagasaki in 1945. The population shows a pattern of increasing risk with increasing dose for leukaemia and most types of cancer. In addition, a number of other studies provide information on the risk of childhood cancer following exposure of a mother’s abdomen during pregnancy.
Direct information on the effects of low dose chronic radiation exposure is also becoming available from studies of radiation workers in the UK and elsewhere. Some provide indications of excess cancer risk, notably for leukaemia. The findings are generally consistent with the risk estimates developed by the International Commission on Radiological Protection in its Publication No. 60 and with the assumption of a cancer risk even at low doses and low dose rates.
Studies at the molecular, cellular, tissue and whole animal level have demonstrated that radiation damage increases with dose and that at least for low-LET radiation, at high doses it is often greater per unit of exposure than at low dose rates. A reduction factor is normally applied to estimates of risk calculated from populations exposed at high doses and dose rates to provide risk estimates for protection purposes.
Taken together the available human and experimental data suggest that it is appropriate to apply a low value of this reduction factor, a value of 2, as presently recommended by the ICRP in Publication 60, and a value of less than 3, as recommended by the United Nations Scientific Committee on the Effects of Atomic Radiation, seems justified.
Increasingly interpretation of epidemiological and experimental studies at low doses is being influenced by accumulating information on the fundamental nature of the tumorigenic process. Neoplasm in tissue is now seen as a complex, multistage process that can be subdivided into four phases: neoplastic initiation, promotion, conversion and progression with gene specific mutations acting principally to drive the process. (emphasis added).
Although radiation-induced mutation may in principle influence all stages of the neoplastic process, it is argued in the report that neoplastic initiation is the key stage that is primarily targeted by low doses of radiation. It is also argued that, with very few exceptions, tumours arise from single cells and by implication, develop from a gene-specific mutation in a single cell in the originating tissue. On this basis, a single mutational events in a critical gene in a single larger cell in vivo can create the potential for neoplastic development. Thus, a single track traversing the nucleus of an appropriate target cell has a finite probability, albeit it very low, of generating specific damage to DNA that can result in the development of a tumour.
As a consequence, at the level of DNA damage, there is no basis to assume that there is likely to be a dose threshold below which the risk of tumour induction would be zero. For radiation protection purposes, it is appropriate therefore to assume a progressive increase in risk wit increasing dose with no threshold. (emphasis added)
There is some evidence that low dose radiation may induce or activate cellular DNA repair functions, the so-called adaptive response. The majority of such effects seen to date have been short term, and the current consensus is that knowledge of their relevance to neoplastic processes is insufficiently developed and understood to influence current judgements on tumorigenic responses at low doses and low dose rates.
Further information: NRPB Press Office. 01235 822744
Background note:
The new publication supplements information published by NPRB in September 1993 in the following: Estimates of late radiation risks to the UK population, Documents of the NRPB Vol 4 No. 4 (1993)
Risk factors are expressed in terms of risk per unit dose of radiation and in that publication NRPB published the following values: 6 in 100,000 per millisievert for the whole population and 5 in 100,000 per millisievert for workers. These remain unchanged by the new publication.
ATTACHMENT 3
New Scientist Planet Science: RADIATION ROULETTE
"http://www.newscientist.com/home.html">
NEW SCIENTIST
Archive: 15 November1997
RADIATION ROULETTE
The discovery that radiation damages DNA in a new and unexpected way has raised fears that it may cause a far wider range of diseases than previously.
Rob Edwards reports
EAT enough arsenic and you'll die. Death is swift and sure. Radiation, on the other hand, is far less predictable. Expose yourself to even a low dose of radiation and it might or might not kill you some time in the future. This hit-and-miss effect on the body, along with the fact that it's invisible, and so mysterious, is why most people have a profound mistrust of radiation.
Epidemiological studies of survivors from Hiroshima and Nagasaki show that people started dying of leukaemia five years after the bombs were dropped. It took another 15 years for cancers to develop in the lung, breast and urinary tract. Scientists have used these and other studies to reduce emissions from nuclear plants to levels that they predict will keep the likely number of deaths from radiation-induced disease to a vanishingly small figure. At present, it's internationally accepted that a member of the public should not receive more than 1 millisievert a year. Yet, despite these safeguards, mistrust of radiation and the nuclear industry persists.
Now, radiation biologists are concluding that the public may well have been right all along. They have found a previously unknown pathway by which radiation can subvert living cells. Radiation, they say, may cause a much wider range of diseases than epidemiological studies predict. Even levels of exposure below 1 millisievert a year could be harmful, and thousands of people could face early death as a result. Worst of all, the small doses of radiation that millions habitually receive could be poisoning the human gene pool, wreaking damage on future generations. "It is a horrifying concept," says Eric Wright from the Medical Research Council at Harwell in Oxfordshire. "But we now have early indications that it may be happening."
Conventional wisdom says that when ionising radiation hits a living cell there are three possible outcomes. Either the cell is unharmed, or it is killed, or it survives with its DNA damaged. If the DNA is not mended by the cell's repair enzymes and the cell divides, the damage will be passed on to its daughter cells. Depending on the type of cell and which genes, if any, are damaged, the result could be uncontrolled growth and eventually cancer. (emphasis added)
But Wright, who is head of experimental haematology at the MRC's Radiation and Genome Stability Unit, has found a fourth possibility. Radiation can also, he says, inflict damage on cells that at the moment can only be detected after they have divided several times. He calls this radiation-induced genomic instability. (emphasis added)
The eventual effects of the instability include broken or misshapen chromosomes and mutated genes, and early cell death. Research from around the world has shown that it can be produced by neutrons, X-rays, gamma rays and alpha radiation. In the laboratory, a dozen cell divisions over a couple of weeks are enough to generate chromosomal defects in up to 30 per cent of an irradiated cell's progeny. "I regard the phenomenon as established," says Wright. "There is no doubt that genomic instability is a real consequence of radiation exposure."
Vulnerable cells
Inside the body, this process could have big implications. In an average lifetime, a human being will experience 1016 cell divisions, mostly in the first few years of life and during puberty. But stem cells in the bone marrow, which keep the blood replenished with red and white cells, as well as cells in the gut and skin, continue to divide throughout adult life. Likewise, sperm are constantly produced by cell division in adult males. In these cases, the potential for radiation-induced instability to do its worst appears to be highest.
Wright, Munira Kadhim, and colleagues announced the discovery of genomic instability in 1992. They exposed stem cells from the bone marrow of mice to plutonium-238, giving them a dose of about 0.5 grays of alpha radiation. This is the equivalent of a single alpha particle passing through a cell, the lowest dose the cell could receive.
The cells were kept in Petri dishes for 11 days until they had divided between 10 and 13 times, each producing between 10 000 and 100 000 daughter cells. Wright found that the progeny of the irradiated cells contained three and a half times as many chromosome aberrations as the descendants of cells that were not irradiated. In a letter to Nature, he concluded that the "relative biological effectiveness"--a measure of how damaging low-level radiation can be in the body--for isotopes that emit alpha particles is "effectively infinite".
In 1994, Wright repeated the experiment with stem cells taken from four people. After between 10 and 15 divisions, up to 25 per cent of the progeny of cells from two of the individuals were riddled with broken and distorted chromosomes. The fact that cells from the other two subjects showed no signs of induced instability may mean that some people carry genes that protect them from this type of damage, Wright argues.
Mounting evidence
At least six other laboratories around the world have now found similar results. Bo Lambert from the Karolinska Institute in Stockholm, for example, showed that X-rays damage the chromosomes of the descendants of irradiated human lymphocytes. Robert Ullrich from the University of Texas in Galveston discovered chromosome aberrations in the offspring of human breast cells caused by neutron and gamma irradiation. Last year, researchers from NASA and the University of Naples in Italy reported that the offspring of skin cells developed chromosome aberrations after exposure to X-rays and alpha particles. They concluded that genomic instability "could determine late genetic effects and should therefore be carefully considered in the evaluation of risk for space missions".
These studies all use cells grown in laboratories, and so are open to the criticism that something different might happen in living animals. At least two experiments, however, suggest that radiation also causes genomic instability in vivo. In a previously unnoticed study in 1989, Christian Streffer from the University of Essen in Germany exposed fertilised eggs of mice to X-rays. When skin cells were taken from the growing fetuses, they contained more chromosome aberrations than cells taken from unirradiated fetuses.
In addition, last year, Wright and his colleagues at the MRC irradiated stem cells from the bone marrow of male mice and transplanted them into female mice. (The transplants and their progeny contained a Y chromosome so could be easily distinguished from the females' cells.) The researchers detected "persisting chromosomal instability" in the male cell line up to a year later.
More recently, in order to test his suspicion that some people carry genes that predispose them to genomic instability, Wright has shown that some strains of mice are more vulnerable to genomic instability than others. In one experiment, he exposed bone marrow cells from three strains to radiation. Daughter cells from two of these strains went on to develop more chromosome aberrations than cells from the other.
Wright and other radiobiologists are now searching for the mechanisms behind genomic instability. In one experiment, Wright found abnormal levels of highly reactive free radicals in cells derived from irradiated cells. There is good evidence that raised levels of free radicals can induce chromosomal damage, and Wright believes that a buildup of these chemicals over several generations could be the root cause of genomic instability.
Keith Baverstock, a senior radiation scientist with the WHO, has a different theory. He believes radiation could damage a gene for one of the DNA repair enzymes. DNA is not a static molecule but changes all the time, and repair enzymes constantly cut out damaged sections and patch them up. If radiation stops one of these enzymes doing its job, a subsequent error may not be properly repaired. When the cell divides, its progeny will inherit this imperfection along with the disabled enzyme, which will carry out further imperfect repairs, and so on, piling up flaws down the generations. "Finally it gets so bad that the whole thing just breaks up and you get instability," argues Baverstock.
At this point, the question becomes the same as that asked for all forms of DNA damage caused by radiation--how does the damage cause disease? Most work on this question has focused on cancer and scientists believe that certain genes may hold the key. If a gene that promotes cell division is damaged, for example, that cell can divide over and over again. Other possible contenders are genes, such as p53, that normally suppress the development of cancer. If a person's two copies of p53 are damaged, a tumour is likely to grow.
All these suggestions could be different parts of the same complex puzzle. Baverstock compares the difficulties of identifying the biological mechanisms to a long car journey. "You may know that a car started in Glasgow and finished in Cambridge," he says. "But the number of different routes it could have taken in between is immense."
Despite the holes in our understanding of induced genomic instability, Wright feels that we already know enough to start worrying. He believes that in addition to cancers such as leukaemia, it may cause small increases in a wide range of other diseases. These could include developmental defects in fetuses, such as deformed limbs and cleft palates, and brain disorders such as Alzheimer's, Parkinson's and motor neuron diseases. But he stresses that these suspicions are not yet backed up by experimental evidence.
The amount of radioactivity needed to induce instability could be tiny. Wright's director at the MRC unit, Dudley Goodhead, argues that a single alpha particle is enough to injure a cell and increase the risk of disease. Those who swallow just one atom of plutonium are hence marginally more likely to die early. "It's like Russian roulette," says Goodhead.
Wright and Goodhead are not the only ones to be concerned. Two years ago this month, more than 30 radiobiologists and health specialists from around the world gathered in Helsinki for a workshop on the public health aspects of radiation-induced genomic instability. They cite 26 studies which, they say, suggest that the accepted rules about how to calculate the biological impact of radiation should be rewritten. "Genomic instability changes our way of thinking about how radiation damages cells and produces mutations," says Jack Little, professor of radiobiology at the Harvard School of Public Health in Boston, who attended the workshop.
Last year, participants in the workshop produced a report for the WHO and, although it was not published, New Scientist has obtained a copy. It suggests that instability is an early, key event in the process that leads to cancer. It points out that people with the inherited disorder Fanconi anaemia develop the same sort of chromosome aberrations seen in radiation-induced instability and about 15 per cent of these contract leukaemia.
Instability is also a "plausible mechanism" for explaining illnesses other than cancer, the report says. "It would seem likely that if genomic instability led to health effects these would not be specific but may include developmental deficiencies in the fetus, cancer, hereditary disease, accelerated aging and such non-specific effects as loss of immune competence." Epidemiology would be "powerless" to detect any relationship between the incidence of such diseases and exposure to radiation, the report says, because the number of people who would suffer any single disease would be too low.
Baverstock, who was the main organiser of the Helsinki workshop, and Wright, believe that the world should be more wary of low-level radiation. If genomic instability is causing unpredicted disease, and if some people are genetically predisposed to it, the regulatory system starts to look inadequate. Existing measures meant to protect people, argue Wright and Baverstock, are less than reassuring.
To check that people do not receive more than 1 millisievert a year, the British Ministry of Agriculture, Fisheries and Food monitors "critical groups" of people who, because of their lifestyle, are likely to receive the highest doses of radioactivity from nuclear plants. The Sellafield complex in Cumbria has been the largest emitter of radiation in Britain, discharging radioactive gas into the air and liquid into the Irish Sea. The critical groups here have included fishermen working the Irish Sea, people who eat seaweed and occupants of houseboats moored on contaminated Cumbrian estuaries.
Scaremongering
The underlying assumption is that everybody is equally vulnerable to radiation, and that possible health effects depend purely on levels of exposure. But if the critical groups do not contain people who are genetically predisposed to genomic instability, then this system will overestimate the level of radiation deemed "safe". These people could then be exposed to levels of radiation that could harm them. So the number of people to have died or suffered from radiation released from Sellafield, nuclear weapons tests, the Chernobyl accident and from medical X-rays and radon in buildings, could be much greater than anyone has dared to admit.
This is regarded as unscientific scaremongering by Britain's National Radiological Protection Board at Harwell. Roger Cox, head of the radiation effects department at the NRPB, does not dispute that his colleagues across the road at the MRC have found unstable changes in cells descended from irradiated cells. But he disagrees that they are likely to have any impact on health.
"The basic science is not the problem here, it is their interpretation of it," Cox argues. There is no proof that genomic instability leads to cancer or other diseases, no studies that have shown an association between illness and instability and there is no hard evidence of any causal mechanisms. Even if instability causes an increased rate of illness, it would already be taken into account by existing safety limits. "We're quite some way from having serious doubts about the risk estimates we make," he says.
In particular, Cox dismisses the suggestion that genomic instability can cause small increases in a wide range of diseases as "totally speculative". Although he admits that such an effect cannot be ruled out, he argues that if it exists it must be very minor, contained within the statistical noise of epidemiological studies. "There is rigorous medical surveillance of Hiroshima and Nagasaki victims," he says. "It would be a surprise if there was any major effect on any aspect of health that had not been picked up."
Wright concedes that there is no proof that instability causes cancer, but he argues that it is "highly unlikely" to be irrelevant to the process. Cox fails to appreciate, he says, that the scattergun effect of instability--small increases in a wide range of diseases--would by its very nature escape the notice of epidemiologists. Wright also questions the relevance of studies of atom bomb survivors to the understanding of genomic instability. Extrapolating from a group of people exposed to a large, acute dose of radiation to a group receiving small, chronic doses may not be valid. Two different mechanisms may be involved, and it's important to learn if this is the case. Instead, says Wright, the NRPB gets defensive and criticises "anything and everything that does not fit their corner of the world".
His biggest concern is that instability could blight future generations. He has collaborated with Brian Lord from the Patterson Institute for Cancer Research at the Christie Hospital in Manchester in a study that is due to be published soon. It gives the first clear experimental evidence that instability can be passed from a mole to his offspring in sperm.
Lord found that the pups of male mice exposed to alpha radiation suffered chromosome aberrations in their bone marrow likely to be associated with genomic instability. The finding lends support to the controversial theory advanced in 1990 by the late Martin Gardner from Southampton University that the children of fathers exposed to radiation at Sella-field run a higher than normal risk of contracting leukaemia.
But Wright and Baverstock fear that the consequences could extend far beyond the leukaemia cases. Millions of people worldwide are exposed to low level radiation. The damage inflicted on their DNA could be passed to their children, and to their children's children. The human gene pool could be permanently polluted.
Furthermore, argue Wright and Baverstock, there is no logical reason why such damage should be confined to ionising radiation. Carmel Mothersill from the Dublin Institute of Technology told meetings in Toulouse and Oxford last month that the offspring of cells exposed to low levels of cadmium and nickel also suffer high rates of cell death--a tell-tale sign of genomic instability. Chemicals in tobacco smoke, air pollution or pesticides might also destabilise the genome.
These ideas are already irritating scientists working in radiation protection, who believe that existing safeguards are adequate. Wright and Baverstock themselves accept that institutional change will be slow and that there is much still to be learnt about the biology of genomic instability. In the meantime, they are minimising their own exposure to radiation. Baverstock refused dental X-rays which were not medically necessary. Wright too avoids medical X-rays unless his dentist or doctor can convince him they are essential. And he does not eat fish from the Irish Sea, for fear of contamination by plutonium from Sellafield.
From New Scientist, 11 October1997
Attachment 4
RADIATION EXPOSURES TO THE PUBLIC FROM THE PROPOSED JABILUKA/RANGER OPERATION
IN BRIEF
Radiation exposure to the public from the proposed Jabiluka/Ranger uranium mine development is estimated to exceed radiation exposures arising from major nuclear facilities in the UK. Lowest dose estimates for Jabiluka/Ranger show exposures may equal the maximum recommended levels in the US. Highest dose estimates show that traditional owners living near the proposed Jabiluka/Ranger operation may exceed 1 milliSievert (mSv) per annum, the maximum exposure limit recommended by the International Commission on Radiological Protection (ICRP) (1).
EXPLANATION
In its response to the Environmental Impact Statement from Energy Resources of Australia, Environment Australia (2) noted that radiation exposure from the combined operation of Jabiluka/Ranger to "occupants of Mudginberri is predicted to be approximately 0.25mSv, or 25% of the applicable dose limit". (Mudginberri is an Aboriginal Community area placed immediately adjacent to the Jabiluka lease and down stream & down wind from Ranger). The exposure limit in the US is 0.25mSv from all sources. However, the US Environment Protection Agency has also recommended an annual exposure limit of 0.1mSv, based on the notion of ‘maximum individual risk’ (mir)(3).
Environment Australia also raise the possibility that the dose limit of 0.25 mSv per annum from the Jabiluka/Ranger mine may be underestimated, and that doses of 0.49mSv may arise and that in some instances members of the public may even be exposed over the 1mSv limit. The ICRP limit of 1mSv is the total dose which should arise from all man-made sources of radiation exposure (excluding medical procedures). It is understood that Australia, as a signatory to the statute of the International Atomic Energy Agency, should not allow radiation exposures in excess of ICRP limits.
The estimate of radiation exposure from Jabiluka/Ranger is close to the 0.3 mSv per annum limit set by Australian Nuclear Science and Technology Organisation (ANSTO) for exposure from the radioactive discharges from the Lucas Heights reactor and radioisotope production facility. In its 1995-1996 report, ANSTO estimates the maximum dose received as a result of its discharges was 0.013mSv (4) almost 20 times less than the lowest dose estimated from the Jabiluka/Ranger proposal.
A further comparison between the expected dose from the Jabiluka/Ranger operation can be made with the radiation exposure arising from the discharges of the spent nuclear reprocessing plant at Sellafield in England (Sellafield is the largest routine discharger of radioactive waste in the world). In its 1995, report the UK Ministry of Agriculture Fisheries and Food (MAFF) estimated that radiation doses arising from Sellafield (from consumption of fish and shellfish contaminated by the marine discharges) were between 0.04-0.14 mSv (5), both lower than the estimates given for the Jabiluka/Ranger operation. In the UK the constraint limit set by the National Radiological Protection Board from any single operating installation is 0.3mSv (6).
The estimated radiation exposures from Jabiluka /Ranger may, therefore, be:
greater than the MIR limit set by the US EPA of 0.1mSv
equal to the dose limit used in the US (0.25mSv)
in excess of the single site 0.3mSv dose limit used in the UK
in excess even of the ICRP’s own limit of 1mSv.
It is also important to note that the calculations may not include all pathways – that is some key aspects of potential exposure may not have been included (e.g. uptake from radioactive dust on leafy vegetables). If there are additional pathways, or underestimates of exposure in key pathways over time, then actual radiation exposure resulting from Jabiluka/Ranger might prove to be higher than EA’s estimates.
Prepared for the Gundjehmi Corporation by Jean McSorley MPS,
mcsorley@compassnet.com.auTel (h) + 61 2 9568 3265 or 041766 2720
19th June 1998
- ICRP. 1990 Recommendations of the International Commission on Radiological Protection, Publication 60. Annals of the ICRP, 21, Nos 1-3 (1991)
- Environment Australia Environmental Assessment Report on the Proposal to Extract, Process and export Uranium from Jabiluka Orebody No 2. The Jabiluka Proposal. Environmental Assessment Branch, August 1997. P. 95
- Title 40, United States Code of Federal Regulation, Part 61,.102 (Originally published in Federal Register 12/15/89. P.51697)
- Australian Nuclear Science and Technology Organisation, Annual Report 1995-1996 p.83
- Ministry of Agriculture, Fisheries and Food, Aquatic Environment Monitoring Report Number 45. Radioactivity in Surface and Coastal Waters of the British Isles, 1994. Lowestoft: UK
- National Radiological Protection Board, Press Release, 27th April 1993.
Many thanks to Jean McSorley for supplying this article to SEA-US Inc.
Page last updated October 31, 1998.
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