Radiation: There IS NO "SAFE" Level!!

[Satyagraha]

February 11, 2009

Study: No Radiation Level Safe
Read more: http://www.cbsnews.com/stories/2005/06/29/health/main705127.shtml#ixzz1Ihk4cTU6

(AP)  The preponderance of scientific evidence shows that even very low doses of radiation pose a risk of cancer or other health problems and there is no threshold below which exposure can be viewed as harmless, a panel of prominent scientists concluded Wednesday.

The finding by the National Academy of Sciences panel is viewed as critical because it is likely to significantly influence what radiation levels government agencies will allow at abandoned nuclear power plants, nuclear weapons production facilities and elsewhere.

The nuclear industry, as well as some independent scientists, have argued that there is a threshold of very low level radiation where exposure is not harmful, or possibly even beneficial. They said current risk modeling may exaggerate the health impact.

The panel, after five years of study, rejected that claim.

"The scientific research base shows
that there is no threshold of exposure below which
low levels of ionized radiation
can be demonstrated to be harmless or beneficial,"
said Richard R. Monson, the panel chairman and a professor of epidemiology at Harvard's School of Public Health.

The committee gave support to the so-called "linear, no threshold" model that is currently the generally acceptable approach to radiation risk assessment. This approach assumes that the health risks from radiation exposure declines as the dose levels decline, but that each unit of radiation — no matter how small — still is assumed to cause cancer.

The panel, formally known as the Committee on Biological Effects of Ionizing Radiaton, or BEIR, generally supported previous cancer risk estimates — the last one by an earlier BEIR group in 1990.

Contrary to assertions that risks from exposure
from low-level radiation may have been overstated,
the panel said "the availability of new and more extensive data
have strengthened confidence in these (earlier) estimates."

The committee examined doses of radiation of up to 100 millisievert, a measurement of accumulated radiation to an individual over a year. By comparison, a single chest X-ray accounts for 0.1 millisievert and average background radiation 3 millisievert.

The committee estimated that 1 out of 100 people would likely develop solid cancer or leukemia from an exposure of 100 millisievert of radiation over a lifetime.

[agentbluescreen]

'No safe levels' of radiation in Japan
Experts warn that any detectable level of radiation is "too much".

http://english.aljazeera.net/indepth/features/2011/04/20114219250664111.html

Eating and X-Ray machine (unlike merely passing by one that flashes you for a second) that never turns off is totally destructive and deadly to you.

The sorts of permanent elemental chemical and particulate nuclear-isotopic "irradiators" we are talking of here (like depleted uranium dust that the criminal US fascist "defense establishment" is spreading about the earth on innocent brown people for their Likudnik masters) are like bullets in a Russian Roulette gun - you buy it, it terminally poisons or kills you.

The un-"natural" current criminal "background levels" they lie about are unnatural and overwhelmingly already the horrific result of the criminal fascist's phony left-right-socialist Cold War childishly petulant nuke-test pissing match "debate" that the peaceful ex-Soviets clearly morally won, hands-down. (by recognizing the prices and debts were creating and selflessly altering their behavior for the better)

Americans are just too stupid to realize that they lost (the most due to and in) the Cold War, and blundered on blindly continuing their folly under the falsely myopic misapprehension that they had proved their own equally invalid hatefully mass-destructive corruptions valid - their continued purposeless and self-destructive, bankrupting, criminal fascist behaviors now are proof of it

And now all those Cold War crimes are coming home to roost...

Leuren Moret - Scientists declare northern 1/3 of Japan uninhabitable and should be evacuated

VIDEO REPORT: http://vimeo.com/22003275

She also explains how they have used a manmade unnatural HAARP High Pressure convection zone to pollute southern US and Mexico most with this mess

[shipgeek]

More bad news here.

Japan Expects Yet Another Nuclear Plant Explosion


TOKYO - Troubles continue at Japan’s crippled nuclear plant, where technicians believe they have solved one big problem but are confronting another.

Officials said Wednesday they have finally stopped a leak of radioactive water from the Fukushima power station that was raising radiation in the nearby ocean to millions of times the legal limit.

But now they are worried about a build-up of hydrogen inside the containment vessel at another of the plant’s six reactors, creating the risk of an explosion that could release large amounts of radiation into the atmosphere. Plant officials said they may pump nitrogen into the reactor in an attempt to halt the chemical reaction.

Also Wednesday, Chief Cabinet Secretary Yukio Edano apologized to neighboring countries for Japan’s failure to notify them before it began pumping thousands of tons of low-level radioactive water into the sea near the plant.

Edano said the action, which could continue until Friday, is necessary to make room in a storage area for water that is 200 thousand times more dangerous. But he said steps have been taken to ensure better communication with nearby countries before such steps are taken in future.

Edano said the water leak, which had sent radiation levels in the nearby ocean to 7.5 million times the allowable limit on Saturday, had been stopped by 5:38 a.m. Wednesday. But he said it is too early to say with confidence that the problem has been solved, and that officials are still trying to determine whether radioactive water is leaking from any other locations.

Officials at the Tokyo Electric Power Company, which operates the Fukushima plant, said the latest threat of a hydrogen build-up is taking place at its number-one reactor. Japan’s NHK television quoted officials saying the build-up is occurring inside the containment vessel that keeps radiation from escaping into the atmosphere, and is an indication that the reactor’s core has been damaged.

Hydrogen explosions destroyed the outer buildings housing the number-one and three reactors earlier in the crisis, which began when a massive earthquake and tsunami destroyed the power plant’s cooling systems on March 11. Those blasts may also have damaged the containment vessels.

The high radiation levels in the nearby ocean were caused by water leaking from a storage pit next to the number two reactor. After days of failed efforts, technicians managed to stop the leak by injecting a hardening agent called liquid glass into the soil and gravel around the pit. TEPCO is still exploring ways to make sure the seal is permanent.

Highly radioactive water has accumulated in the basements of several of the plant’s reactors after weeks in which workers have pumped massive amounts of water over the reactors to prevent their fuel rods from overheating. The water needs to be removed before workers can complete repairs to the permanent cooling systems.

Technicians began Tuesday to pump 11,500 tons of lightly radioactive water into the ocean to make room in a storage area for the most dangerous water, most of it in the basement and utility tunnels at the number-two reactor. But South Korea has protested the action, suggesting it may violate international law.

National police said Wednesday the confirmed death toll in the March 11 disasters now stands at 12,468, with more than 15,000 people still unaccounted for.

Source:  VOA News

http://www.eagleworldnews.com/2011/04/06/japan-expects-yet-another-nuclear-plant-explosion/

 

[Satyagraha]

A study conducted by The National Research Council of the National Academies found that there is no level of radiation that could be considered "safe". As we watch government agencies 'raising' the acceptable level of radiation that humans can be exposed to, understand that they do this while blatantly lying about the health risks. There is NO SAFE level of radiation: radiation will do damage to your cells. Period.

The study that follows concludes with this:

CONCLUSION
http://www.nap.edu/openbook.php?record_id=11340&page=323

The committee concludes that the current scientific evidence is consistent with the hypothesis that
there is a linear, no-threshold dose-response relationship
between exposure to ionizing radiation and the development of cancer in humans.

Here are Excepts from the original study, available at this link:
http://www.nap.edu/openbook.php?record_id=11340&page=R1

==================================

HEALTH RISKS FROM
EXPOSURE TO LOW LEVELS OF IONIZING RADIATION
BEIR VII PHASE 2

Committee to Assess Health Risks from Exposure to Low Levels of Ionizing Radiation
Board on Radiation Effects Research
Division on Earth and Life Studies
NATIONAL RESEARCH COUNCIL OF THE NATIONAL ACADEMIES

THE NATIONAL ACADEMIES PRESS
Washington, D.C.
www.nap.edu

==================================

Background Information
http://www.nap.edu/openbook.php?record_id=11340&page=19

This report focuses on the health effects of low-dose, low-LET (low linear energy transfer) radiation. In this chapter the committee provides background information relating to the physical and chemical aspects of radiation and the interaction of radiation with the target molecule DNA. The committee discusses contributions of normal oxidative DNA damage relative to radiation-induced DNA damage and describes the DNA repair mechanisms that mammalian cells have developed to cope with such damage. Finally, this chapter introduces a special subject, the physical characteristics that determine the relative biological effectiveness (RBE) of neutrons, estimates of which are required in the derivation of low-LET radiation risk estimates from atomic bomb survivors.

PHYSICAL ASPECTS OF RADIATION

The central question that must be resolved when considering the physical and biological effects of low-dose ionizing radiation is whether the effects of ionizing radiation and the effects of the free radicals and oxidative reaction products generated in normal cellular metabolism are the same or different. Is ionizing radiation a unique insult to cells, or are its effects lost in the ocean of naturally occurring metabolic reaction products? Can cells detect and respond to low doses of ionizing radiation because of detectable qualitative and quantitative differences from endogenous reaction products?


Molecular and Cellular Responses to Ionizing Radiation
http://www.nap.edu/openbook.php?record_id=11340&page=43

Since the early years of radiobiology the cellular effects of ionizing radiation have been studied in the context of induced chromosomal aberrations, and early models of radiation action were largely based upon such studies (Savage 1996). In the 1970s, somatic cell genetic techniques were developed to allow the quantification and characterization of specific gene mutations arising in irradiated cultures of somatic cells. In more recent years, findings of persistent postirradiation genomic instability, bystander effects, and other types of cellular response have posed additional questions regarding the mechanisms underlying the cytogenetic and mutagenic effects of radiation and their potential to contribute to radiation tumorigenesis.

This chapter considers the general aspects of dose-response relationships for radiobiological effects and subsequently reviews the largely cellular data on a range of radiobiological end points. The main focus of the review is the issue of cellular effects at low doses of low-LET (linear energy transfer) radiation. Many of the conclusions reached from this review, when aggregated with those of Chapters 1 and 3, contribute to the judgments made in this report about human cancer risk at low doses and low dose rates.

Heritable Genetic Effects of Radiation in Human Populations
http://www.nap.edu/openbook.php?record_id=11340&page=91

INTRODUCTION AND BRIEF HISTORY

Naturally occurring mutations in somatic and germ cells contribute respectively to cancers and heritable genetic diseases (i.e., hereditary diseases). The discoveries by Muller (1927) of the mutagenic effects of X-rays in fruit flies (Drosophila) and by Stadler (1928a, 1928b) of similar effects in barley and maize, and the subsequent extension of these findings to other types of ionizing radiation (and also to ultraviolet) and other organisms, conclusively established the genetic damage-inducing effects of radiation. However, widespread and serious concern over the possible adverse genetic effects of exposure of large numbers of people to low levels of radiation first arose in the aftermath of the detonation of atomic bombs over Hiroshima and Nagasaki in World War II, some 20 years after the discoveries of the mutagenic effects of X-rays. In June 1947, at the meeting of the Conference on Genetics convened by the Committee on Atomic Casualties of the U.S. National Research Council to assess the program of research on the heritable effects of radiation to be undertaken in Japan, the leading geneticists voted unanimously to record the following expression of their attitude toward the program: “Although there is every reason to infer that genetic effects can be produced and have been produced in man by atomic radiation, nevertheless the conference wishes to make it clear that it cannot guarantee significant results from this or any other study on the Japanese material. In contrast to laboratory data, this material is too much influenced by extraneous variables and too little adapted to disclosing genetic effects. In spite of these facts, the conference feels that this unique possibility for demonstrating genetic effects caused by atomic radiation should not be lost …” (NRC 1947). Thus came into existence the genetics program in Hiroshima and Nagasaki under the auspices of the Atomic Bomb Casualty Commission (ABCC), the newly formed joint agency of the Japanese Ministry of Health and Welfare and the U.S. National Academy of Sciences. The ABCC was renamed the Radiation Effects Research Foundation in 1976. In the late 1940s, the mouse was chosen as the primary surrogate for assessing the genetic radiosensitivity of humans, and extensive studies were initiated in different research centers in the United States, England, and Japan.

In the mid-1950s, one major international and several national scientific bodies came into existence, including the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR), the Committee on the Biological Effects of Atomic Radiation (the BEAR committee; renamed the Committee on the Biological Effects of Ionizing Radiation [BEIR] in 1972) set up by the U.S. National Academy of Sciences, and the Committee of the British Medical Research Council. The UNSCEAR and the BEIR committees have continued their work up to the present, periodically reviewing the levels of radiation to which human populations are exposed and improving assessment of the somatic and genetic risks of radiation exposure (NRC 1972, 1980, 1988, 1990, 1999; UNSCEAR 1993, 2000b, 2001).

From the beginning of these efforts, it was obvious that in the absence of direct human data on radiation-induced germ cell mutations, quantitative estimates of genetic risk could be derived only through a knowledge of the prevalence of naturally occurring hereditary ill health in the population, the role of spontaneous mutations in supporting this burden, and plausible assumptions on the rates of induced germ cell mutations in humans. The methods developed and used by the above committees for risk estimation, therefore, were necessarily indirect. All were geared toward using human data on genetic diseases as a frame of reference, together with mouse data on radiation-induced mutations, to predict the radiation risk of genetic disease in humans. Both the UNSCEAR and the BEIR committees are cognizant of the need to make assumptions given the consequent uncertainties in extrapolating from mouse data on induced mutation rates to the risk of genetic disease in humans.

Details of the genetics program that evolved in Japan and the vast body of data that emerged from these studies have been published in a series of articles. The most relevant ones have now been compiled in a single volume (Neel and Schull 1991). The most important finding of these studies is that there are no statistically demonstrable adverse genetic effects attributable to radiation exposures sustained by the survivors. Although cited and discussed in the UNSCEAR and BEIR reports over the years, these results did not constitute part of the “mainstream thinking” of genetic risk estimators and therefore were not used in risk estimation.
During the past few years, estimates of the baseline frequencies of Mendelian diseases have been revised and mathematical methods have been developed to estimate the impact of an increase in mutation rate (as a result of radiation exposures) on the frequencies of different classes of genetic diseases in the population. Additionally, there have been several advances in our understanding of the molecular basis and mechanisms of origin of human genetic diseases and of radiation-induced mutations in experimental systems. As a result of these developments, it now is possible to reexamine the conceptual basis of risk estimation, reformulate some of the critical questions in the field, and address some of the problems that could not be addressed earlier.
This chapter summarizes the general framework and the methods and assumptions used in risk estimation until the publication of BEIR V (NRC 1990). This is followed by a discussion of the advances in knowledge since that time, their impact on the concepts used in risk estimation, and how they can be employed to revise the risk estimates. Throughout this chapter, the terms “genetic diseases,” “genetic effects,” and “genetic risks” are used exclusively to mean “heritable genetic diseases,” “heritable genetic effects,” and “heritable genetic risks,” respectively.

GENERAL FRAMEWORK

Goal of Genetic Risk Estimation

The goal of genetic risk estimation, at least as envisioned and pursued by UNSCEAR and the BEIR committees, remains prediction of the additional risk of genetic diseases in human populations exposed to ionizing radiation, over and above that which occurs naturally as a result of spontaneous mutations. The concept of “radiation-inducible genetic diseases,” which emerged early on in the field, is based on two established facts and an inference. The facts are that (1) hereditary diseases result from mutations that occur in germ cells and (2) ionizing radiation is capable of inducing similar changes in all experimental systems adequately investigated. The inference, therefore, has been that radiation exposure of human germ cells can result in an increase in the frequency of genetic diseases in the population. Worth noting is the fact that although there is a vast amount of evidence for radiation-induced mutations in diverse biological systems, there is no evidence for radiation-induced germ cell mutations that cause genetic disease in humans.
Germ Cell Stages and Radiation Conditions of Relevance

From the standpoint of genetic risks, the effects of radiation on two germ cell stages are particularly important. In the male, these are the stem cell spermatogonia, which constitute a permanent germ cell population in the testes and continue to multiply throughout the reproductive life span of the individual. In the female, the corresponding cell stages are the oocytes, primarily the immature ones. The latter constitute the predominant germ cell population in the female. Female mammals are born with a finite number of oocytes formed during fetal development. These primordial oocytes, as they are called, grow, and a sequence of nuclear changes comprising meiosis takes place in them. The latter however are arrested at a particular stage until just before ovulation. Because oocytes are not replenished by mitosis during adult life and immature oocytes are the predominant germ cell population in the female, these are clearly the cell stages whose irradiation has great significance for genetic risks.

The radiation exposures sustained by germ cells in human populations are generally in the form of low-LET (linear energy transfer) irradiation (e.g., X-rays and γ-rays) delivered as small doses at high dose rates (e.g., in diagnostic radiology) or are greatly protracted (e.g., continuous exposures from natural and man-made sources). In estimating genetic risks to the population therefore, the relevant radiation conditions are low or chronic doses of low-LET irradiation. As discussed later, most mouse data used for estimating the rates of induced mutations have been collected at high doses and high dose rates. Consequently, assumptions have to be made to convert the rates of induced mutations at high doses and dose rates into mutation rates for radiation conditions applicable for risk estimation in humans.


GENETIC DISEASES
http://www.nap.edu/openbook.php?record_id=11340&page=91

Since the aim of genetic risk estimation is to predict the additional risk of genetic diseases relative to the baseline frequency of such diseases in the population, the concept of genetic diseases and their classification and attributes are considered in this section. The term genetic diseases refers to those that arise as a result of spontaneous mutations in germ cells and are transmitted to the progeny.

Mendelian Diseases

Diseases caused by mutations in single genes are known as Mendelian diseases and are further divided into autosomal dominant, autosomal recessive, and X-linked, depending on the chromosomal location (autosomes or the X chromosome) and transmission patterns of the mutant genes. In an autosomal dominant disease, a single mutant gene (i.e., in the heterozygous state) is sufficient to cause disease. Examples include achondroplasia, neurofibromatosis, Marfan syndrome, and myotonic dystrophy. Autosomal recessive diseases require homozygosity (i.e., two mutant genes at the same locus, one from each parent) for disease manifestation. Examples include cystic fibrosis, phenylketonuria, hemochromatosis, Bloom’s syndrome, and ataxia-telangietasia.
The X-linked recessive diseases are due to mutations in genes located on the X chromosome and include Duchenne’s muscular dystrophy, Fabry’s disease, steroid sulfatase deficiency, and ocular albinism. Some X-linked dominant diseases are known, but for most of them, no data on incidence estimates are currently available. Therefore, these diseases are not considered further in this report. The general point with respect to Mendelian diseases is that the relationship between mutation and disease is simple and predictable.

Multifactorial Diseases

The major burden of naturally occurring genetic diseases in human populations, however, is not constituted by Mendelian diseases, which are rare, but by those that have a complex etiology. The term “multifactorial” is used to designate these diseases to emphasize the fact that there are multiple genetic and environmental determinants in their etiology. Their transmission patterns do not fit Mendelian expectations. Examples of multifactorial diseases include the common congenital abnormalities such as neural tube defects, cleft lip with or without cleft palate, and congenital heart defects that are present at birth, and chronic diseases of adults (i.e., with onset in middle and later years of life) such as coronary heart disease, essential hypertension, and diabetes mellitus.

Evidence for a genetic component in their etiology comes from family and twin studies. For example, first-degree relatives of patients affected with coronary heart disease have a two- to sixfold higher risk of the disease than those of matched controls, and the concordance rates of disease for monozygotic twins are higher (but never 100%) than those for dizygotic twins (Motulsky and Brunzell 1992; Sankaranarayanan and others 1999).

As mentioned earlier, multifactorial diseases are presumed to originate from the joint action of multiple genetic and environmental factors; consequently, the presence of a mutant allele is not equivalent to having the disease. For these diseases, the interrelated concepts of genetic susceptibility and risk factors are more appropriate. The genetic basis of a common multifactorial disease is the presence of a genetically susceptible individual, who may or may not develop the disease depending on the interaction with other genetic and environmental factors. These concepts are discussed further in Annex 4A. The important general point is that unlike the situation with Mendelian diseases, the relationships between mutations and disease are complex in the case of multifactorial diseases. For most of them, knowledge of the genes involved, the types of mutational alterations, and the nature of environmental factors remains limited. Among the models used to explain the inheritance patterns of multifactorial diseases and to estimate the recurrence risks in relatives is the multifactorial threshold model (MTM) of disease liability. The MTM, its properties, and its predictions are discussed in Annex 4A.

Chromosomal Diseases

Historically, both UNSCEAR and the BEIR committees have always had an additional class of genetic diseases—“chromosomal diseases”—in their lists that included those that had long been known to arise as a result of gross (i.e., microscopically detectable), numerical (e.g., Down’s syndrome, which is due to trisomy of chromosome 21), or structural abnormalities of chromosomes (e.g., cri du chat syndrome, due to deletion of part or the whole short arm of chromosome 5 [5p-]). As discussed later, this is really not an etiological category, and deletions (microscopically detectable or not) are now known to contribute to a number of constitutional genetic diseases grouped under autosomal dominant, autosomal recessive, and X-linked diseases.

Atomic Bomb Survivor Studies
http://www.nap.edu/openbook.php?record_id=11340&page=141

INTRODUCTION

The Life Span Study (LSS) cohort consists of about 120,000 survivors of the atomic bombings in Hiroshima and Nagasaki, Japan, in 1945 who have been studied by the Radiation Effects Research Foundation (RERF) and its predecessor, the Atomic Bomb Casualty Commission. The cohort includes both a large proportion of survivors who were within 2.5 km of the hypocenters at the time of the bombings and a similar-sized sample of survivors who were between 3 and 10 km from the hypocenters and whose radiation doses were negligible. The LSS cohort has several features that make it uniquely important as a source of data for developing quantitative estimates of risk from exposure to ionizing radiation. The population is large, not selected because of disease or occupation, has a long follow-up period (1950–2000), and includes both sexes and all ages at exposure, allowing a direct comparison of risks by these factors.

Doses are reasonably well characterized and cover a useful range. Doses are lower than those usually involved in medical therapeutic exposures, but many survivors were exposed at doses that are sufficiently large to estimate risks with reasonable statistical precision. In addition, the cohort includes a large number of survivors exposed at low doses, allowing some direct assessment of effects at these levels. The exposure is a whole-body exposure, which makes it possible to assess risks for specific cancer sites and to compare risks among sites. Because of the use of the Japanese family registration system, mortality data are virtually complete for survivors who remained in Japan. High-quality tumor registries in both Hiroshima and Nagasaki allow the study of site-specific cancer incidence with reasonably reliable diagnostic data. In addition, the LSS cohort is probably less subject to potential bias from confounding than many other exposed cohorts because a primary determinant of dose is distance from the hypocenter, with a steep gradient of dose as a function of distance. Finally, special studies involving subgroups of the LSS have provided clinical data, biological measurements, and information on potential confounders or effect modifiers.

The LSS also has limitations, which are important to consider in using and interpreting results based on this cohort. The subjects were Japanese and exposed under wartime conditions and, in this sense, differ from various populations for which risk estimates are desired. To be included in the study, subjects had to survive the initial effects of the bombings, including the acute effects of radiation exposure, and it is possible that this might have biased the findings. Dose estimates are subject to uncertainty, especially that due to survivor location and shielding. The cohort provides no information on dose-rate effects since all exposure is at high dose rates. Estimates of linear risk coefficients tend to be driven by doses that exceed 0.5 Gy; although estimates based only on survivors with lower doses can be made, their statistical uncertainty is considerably greater than those that include survivors with higher doses. Even at higher doses, data are often inadequate for evaluating risks of cancers at specific sites, especially those that are not common (although, for many site-specific cancers, the LSS provides more information than any other study).

Because of its many advantages, the LSS cohort of A-bomb survivors serves as the single most important source of data for evaluating risks of low-linear energy transfer radiation at low and moderate doses. This chapter describes the LSS cohort and presents findings for leukemia and for solid cancers as a group. The most recent major publications on cancer mortality (Preston and others 2003) and incidence (Preston and others 1994; Thompson and others 1994) are emphasized, but papers addressing special issues such as the shape of the dose-response function are also considered. Results for cancers of specific sites, including results from the three publications just noted, are discussed along with material from various special studies. Risks from in utero exposure are discussed separately. Although cancer is the main late effect that has been demonstrated in the

A-bomb survivor studies, several studies have addressed the effects of radiation exposure on other health outcomes including benign tumors and mortality from causes of death other than cancer. These are discussed at the end of the chapter. In general, the committee has summarized papers on cancer incidence, cancer mortality, and noncancer mortality in the LSS cohort that have been published since BEIR V (NRC 1990).
This chapter is based on published material and does not include results of analyses conducted by the committee, which are described in Chapter 12. At the time of this writing, detailed analyses of mortality data covering the period 1950–1997 and of incidence data covering the period 1958–1987 had been published. The committee’s analyses were based on the most recent DS02 dosimetry system, whereas most of the published analyses described in this chapter were based on the earlier DS86 dosimetry system (see discussion of dosimetry below for further comment). Preston and colleagues (2004) recently evaluated the impact of changes in dosimetry on cancer mortality risk estimates using mortality data through 2000; these results are summarized in the discussion of dosimetry.

DESCRIPTION OF THE COHORT

The full LSS cohort consists of approximately 120,000 persons who were identified at the time of the 1950 census. It includes 93,000 persons who were in Hiroshima or Nagasaki at the time of the bombings and 27,000 subjects who were in the cities at the time of the census but not at the time of the bombings. This latter group has been excluded from most analyses since the early 1970s because of inconsistencies between their mortality rates and those for the remainder of the cohort.

Health End Point Data

Data on health end points are obtained from several sources. Vital status is updated in 3-year cycles through the legally mandated Japanese family registration system in which deaths, births, marriages, and divorces are routinely recorded. This ensures virtually complete ascertainment of death regardless of where individual subjects reside in Japan. Death certificates provide data on the cause of death. The Leukemia Registry has served as a resource for leukemia and related hematological disease (Brill and others 1962; Ichimaru and others 1978). In the 1990s, it became possible to link data from both the Hiroshima and the Nagasaki tumor registries to the LSS cohort, which allows the evaluation of cancer incidence (Mabuchi and others 1994). An advantage of the registry data, in addition to the inclusion of nonfatal cancers, is that diagnostic information is of higher quality than that based on death certificates. Both tumor registries employ active approaches for case ascertainment and provide high-quality data from 1958 onward. Published analyses based on these data cover the period 1958–1987 (Thompson and others 1994). Limitations of the incidence data are that they are not available before 1958 and do not include subjects who have migrated from Hiroshima or Nagasaki.1
The Adult Health Study (AHS) is a resource for data on health end points that require clinical data. The AHS cohort is a 20% subsample of the LSS, oversampled to provide greater representation of subjects in high-dose categories. Since 1958, AHS subjects have been invited to participate in biennial comprehensive health examinations at RERF. The level of participation has been between 70 and 85% for those living in the Hiroshima and Nagasaki areas (Ron and others 1995a).

Leukemia

This section reviews analyses of mortality data for the period 1950–1990 (Pierce and others 1996) and of incidence data for the period 1958–1987 (Preston and others 1994). Leukemia mortality data for the period 1950–2000 were analyzed by Preston and colleagues (2004) and used to develop the committee’s models for estimating leukemia risks; these analyses are described in Chapter 12.

Leukemia was the first cancer to be linked with radiation exposure in A-bomb survivors (Folley and others 1952) and has the highest relative risk of any cancer. Pierce and colleagues estimated that 78 of 176 (44%) leukemia deaths among survivors with doses exceeding 0.005 Sv were due to radiation exposure. Leukemia risks increased with dose up to about 3 Sv, with evidence of upward curvature; that is, a linear-quadratic function fitted the data significantly better than a linear function. With this linear-quadratic function, the excess risk per unit of dose at 1 Sv was about three times that at 0.1 Sv.

For those exposed under about age 30, nearly all of the excess deaths occurred before 1975, but for those exposed at older ages, the excess risk appeared to persist throughout the follow-up period. The temporal trends also differed by sex, with evidence of a steeper decline in risk for males than for females. Both the nonlinear dose-response and the complex patterns by age and time since exposure mean that simple models cannot adequately summarize leukemia risks.

Preston and colleagues (1994) analyzed data from the leukemia registry. An important recent development in studies of leukemia is the reclassification of leukemia cases by new systems and criteria (Matsuo and others 1988; Tomonaga and others 1991), which allows meaningful analyses of specific types of leukemia. Preston and colleagues evaluated patterns of risk by sex, age at exposure, and time since exposure for four major subtypes of leukemia: acute lymphocytic leukemia (32 cases), acute myelogenous leukemia (103 cases), chronic myelogenous leukemia (57 cases), and adult T-cell leukemia (39 cases). Dose-response relationships were seen for the first three but not for adult T-cell leukemia. The estimated numbers of cases in excess of background were 17.1 for acute lymphocytic leukemia, 29.9 for acute myelogenous leukemia, and 25.9 for chronic myelogenous leukemia. The other major type of leukemia, chronic lymphocytic leukemia, showed no excess, but it is infrequent in Japan.

Results of analyses of all types of leukemia showed dependencies on sex, age at exposure, and time since exposure similar to those for the mortality data and led to a model similar to that based on mortality data. Preston and colleagues note that allowing overall modification by sex and age at exposure in an EAR model did not significantly improve the fit once time since exposure was included in the model, but that these factors significantly modified the time since exposure effects. Specifically, risks for those exposed early in life decreased more rapidly than for those exposed later, and the decrease was less rapid for women than for men. Analyses of specific leukemia types indicated that there were significant differences in the effects of age at exposure and sex and in the temporal pattern of risks. The shape of the dose-response did not show statistically significant differences among the subtypes.

ALL SOLID CANCERS

Analyses of cancers in this category, which excludes leukemia and other hematopoietic cancers, are useful for providing summary information and models based on larger numbers than are available for cancers of specific sites (discussed below). The discussion in this section is based on both mortality (Preston and others 2003) and incidence data (Thompson and others 1994). Mortality analyses were based on 9335 solid cancer deaths that occurred during 1950–1997, whereas incidence analyses included 8613 incidence cases occurring during 1958–1987.⁶ The incidence data do not include cases of subjects who migrated and were diagnosed with cancer outside of Hiroshima and Nagasaki; as noted above, analyses were adjusted for migration.

Preston and collegues estimate that 8% of the 5502 solid cancer deaths among those with doses exceeding 0.005 Sv were due to radiation, much lower than the corresponding percentage of 44% for leukemia. This percentage was slightly higher for the incidence data, where 11% of 4327 cancers in the exposed were estimated to result from radiation exposure (Thompson and others 1994).

=======================

6  These numbers contrast with 10,127 solid cancer deaths occurring in 1950–2000 and 12,778 incident cases of solid cancer excluding thyroid and nonmelanoma skin cancer occurring in 1958–1998, the periods covered by analyses conducted by the committee and described in Chapter 12.

=======================

Estimating Cancer Risk
http://www.nap.edu/openbook.php?record_id=11340&page=267

INTRODUCTION

This chapter presents models that allow one to estimate the lifetime risk of cancer resulting from any specified dose of ionizing radiation and applies these models to example exposure scenarios for the U.S. population. Models are developed for estimating lifetime risks of cancer incidence and mortality and take account of sex, age at exposure, dose rate, and other factors. Estimates are given for all solid cancers, leukemia, and cancers of several specific sites. Like previous BEIR reports addressing low-LET (linear energy transfer) radiation, risk models are based primarily from data on Japanese atomic bomb survivors. However, the vast literature on both medically exposed persons and nuclear workers exposed at relatively low doses has been reviewed to evaluate whether findings from these studies are compatible with A-bomb survivor-based models. In many cases, results of fitting models similar to those in this chapter have been published.

Risk estimates are subject to several sources of uncertainty due to inherent limitations in epidemiologic data and in our understanding of exactly how radiation exposure increases the risk of cancer. In addition to statistical uncertainty, the populations and exposures for which risk estimates are needed nearly always differ from those for whom epidemiologic data are available. This means that assumptions are required, many of which involve considerable uncertainty. Risk may depend on the type of cancer, the magnitude of the dose, the quality of the radiation, the dose-rate, the age and sex of the person exposed, exposure to other carcinogens such as tobacco, and other characteristics of the exposed individual. Despite the abundance of epidemiologic and experimental data on the health effects of exposure to radiation, data are not adequate to quantify these dependencies precisely. Uncertainties in the BEIR VII risk models are discussed, and a quantitative assessment of selected sources of uncertainty is made.

In recent years, several national and international organizations have developed models for estimating cancer risk from exposure to low levels of low-LET ionizing radiation. These include the work of the BEIR V committee (NRC 1990), the International Commission on Radiological Protection (ICRP 1991), the National Council on Radiation Protection and Measurements (NCRP 1993), the Environmental Protection Agency (EPA 1994, 1999), the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR 2000b), and the National Institutes of Health (NIH 2003). The approaches used in these past assessments are described in Annex 12A.

DATA EVALUATED FOR BEIR VII MODELS

As in earlier BEIR reports addressing health effects from exposure to low-LET radiation, the committee’s models for risk estimation are based primarily on the Life Span Study (LSS) cohort of survivors of the atomic bombings in Hiroshima and Nagasaki. As discussed in Chapter 6, the LSS cohort offers several advantages for developing quantitative estimates of risk from exposure to ionizing radiation. These include its large size, the inclusion of both sexes and all ages, a wide range of doses that have been estimated for individual subjects, and high-quality mortality and cancer incidence data. In addition, because the exposure was to the whole body, the LSS cohort offers the opportunity to assess risks for cancers of a large number of specific sites and to evaluate the comparability of site-specific risks.

Another consideration in the choice of data was that it was considered essential that the data used by the committee eventually be available to other investigators. The Radiation Effects Research Foundation (RERF) has developed a policy of making summarized data available to those who request it, thus enabling other investigators to analyze data used by the BEIR VII committee. This is not the case for data sets on most other radiation-exposed cohorts.

Although the committee’s models have been developed from A-bomb survivor data, attention has been given to their compatibility with data from other cohorts. Fortunately, for most cohorts with suitable data for developing quantitative risk models, analyses based on models similar to those used by the committee have been conducted and published. This facilitated the committee’s evaluation of data from other studies. Pooled analyses of thyroid cancer risks (Ron and others 1995a) and of breast cancer risks (Preston and others 2002a) were especially helpful in this regard, as were several meta-analyses by Little and colleagues. In addition, the many published analyses based on A-bomb survivor data have guided and facilitated the committee’s efforts in its choice of models. The committee notes particularly the main publications on mortality (Preston and others 2003) and incidence data (Thompson and others 1994) and the models developed by UNSCEAR (2000b) and NIH (2003).

The use of data on persons exposed at low doses and low dose rates merits special mention. Of these studies, the most promising for quantitative risk assessment are the studies of nuclear workers who have been monitored for radiation exposure through the use of personal dosimeters. These studies, which are reviewed in Chapter 8, were not used as the primary source of data for risk modeling principally because of the imprecision of the risk estimates obtained. For example, in a large combined study of nuclear workers in three countries, the estimated relative risk per gray (ERR/Gy) for all cancers other than leukemia was negative, and the confidence interval included negative values and values larger than estimates based on A-bomb survivors (Cardis and others 1995).

Since the publication of BEIR V, data on cancer incidence in the LSS cohort from the Hiroshima Tumor Registry have become available, whereas previously only data from the Nagasaki Tumor Registry were available. Thus, the committee could use both incidence and mortality data to develop its models. The incidence data offer the advantages of including nonfatal cancers and of better diagnostic accuracy. However, the mortality data offer the advantages of covering a longer period (1950–2000) than the incidence data (1958–1998) and of including deaths of LSS members who migrated from Hiroshima and Nagasaki to other parts of Japan.


Summary and Research Needs
http://www.nap.edu/openbook.php?record_id=11340&page=313

The research needs stated here relate to the committee’s primary task: “To develop the best possible risk estimate for exposure to low-dose, low-LET [linear energy transfer] radiation in human subjects.”

EVIDENCE FROM BIOLOGY

Molecular and Cellular Responses to Ionizing Radiation

This chapter discusses the biological effects of the ranges of radiation dose that are most relevant for the committee’s deliberations on the shapes of dose-response relationships. Considering the levels of background radiation, the maximal permissible levels of exposure of radiation workers now in effect, and the fact that much of the epidemiology of low-dose exposures includes people who in the past have received up to 500 mGy, the committee has focused on evaluating radiation effects in the low-dose range of <100 mGy, with emphasis on the lowest doses when relevant data are available. Effects that may occur as the radiation is delivered chronically over several months to a lifetime are thought to be most relevant.

At low doses, damage is caused by the passage of single particles that can produce multiple, locally damaged sites leading to DNA double-strand breaks (DSBs). DNA DSBs in the low-dose range can be quantified by a number of novel techniques, including immunofluorescence, comet assay, chromosome aberrations, translocation, premature chromosome condensation, and others. Some of these indicators of DSBs show linearity down to doses of 5 to 10 mGy.

In vitro data on the introduction of gene mutations
by low-LET ionizing radiation are consistent with knowledge
of DNA damage response mechanisms and imply
a nonthreshold low-dose response for mutations
involved in cancer development.

Experiments that quantified DNA breakage, chromosomal aberrations, or gene mutations induced by low total doses or low doses per fraction suggest that the dose-response over the range of 20 to 100 mGy is linear. Limited data indicate that the dose-response for DNA breakage is linear down to 1 mGy, and biophysical arguments suggest that the response should be linear between zero and 5 mGy.

In vitro studies of gene mutation induction provide evidence for a dose and dose rate effectiveness factor (DDREF) in the range of 2–4. The DDREF has been used in past estimates of risk to adjust data obtained from acute exposures at Hiroshima and Nagasaki to the expected lower risk posed by chronic low-dose exposures that the general population might experience.

Research Need 1. Determination of the level of various molecular markers of DNA damage as a function of low-dose ionizing radiation

Currently identified molecular markers of DNA damage and other biomarkers that can be identified in the future should be used to quantify low levels of DNA damage and to identify the chemical nature and repair characteristics of the damage to the DNA molecule. These biomarkers have to be evaluated fully to understand their biological significance for radiation damage and repair and for radiation carcinogenesis.
Most studies suggest that the repair of ionizing radiation damage occurs through nonhomologous end joining and related pathways that are constitutive in nature, occur in excess, and are not induced to higher levels by low radiation doses.

Data from animal models of radiation tumorigenesis were evaluated with respect to the cellular mechanisms involved. For animal models of radiation carcinogenesis that are dependent on cell killing, there tend to be threshold-like dose-responses and high values of DDREF; therefore, less weight was placed on these data. Once cell-killing dependence is excluded, animal data are not inconsistent with a linear nonthreshold (LNT) dose response, and DDREF values are in the range 2–3 for solid cancers and somewhat higher for acute myeloid leukemia.

Research Need 2. Determination of DNA repair fidelity, especially as regards double- and multiple-strand breaks at low doses, and determination of whether repair capacity is independent of dose

Repair capacity at low levels of damage must be investigated, especially in light of conflicting evidence for stimulation of repair at low doses.

In such studies the accuracy of DNA sequences rejoined by these pathways has to be determined, and the mechanisms of error-prone repair of radiation lesions must be elucidated. Identification of critical genetic alterations that can be characteristic of radiation exposure would be important.

Consideration of Phenomena That Might Affect
Risk Estimates for Carcinogenesis at Very Low Doses

A number of biological phenomena that could conceivably affect risk estimates at very low radiation doses have been reported. These phenomena include the existence of radiation-sensitive human subpopulations, hormetic or adaptive effects, bystander effects, low-dose hyperradiosensitivity, and genomic instability.

Radiation-Sensitive Subpopulations

Epidemiologic, clinical, and experimental data provide clear evidence that genetic factors can influence radiation cancer risk. Strongly expressing human mutations of this type are rare and are not expected to influence significantly the development of estimates of population-based, low-dose risks. They are, however, potentially important in the context of high-dose medical exposures. Evidence for the complex interaction of weakly expressing genetic factors in cancer risk is growing, but current understanding is insufficient for a detailed consideration of the potential impact on population risk.

Adaptive Response

Adaptive responses have been well documented in bacteria, where exposures to radiation or chemicals induce subsequent resistance to these agents by inducing expression of DNA damage repair genes. This induced expression of repair genes does not occur to a significant extent in human cells, although changes in signal transduction do take place. A type of apparent adaptive response, however, has been documented for the induction of chromosomal aberrations in human lymphocytes stimulated to divide.

In most studies, a priming or adaptive dose of about 10 mGy significantly reduces the frequency of chromosomal aberrations and mutations induced a few hours later by 1000–3000 mGy. Similar effects are sometimes seen with other end points. However, priming doses less than 5 mGy or greater than ~200 mGy generally give very little, if any, adaptation, and adaptation has not been reported for challenge doses of less than about 1000 mGy. To have relevance for risk assessment, the adaptive response has to be demonstrated for both priming and challenging doses of 1–50 mGy.

Furthermore, the induction and magnitude of the adaptive response in human lymphocytes are highly variable, with much heterogeneity demonstrated among different individuals. The adaptive response could not be induced when noncycling lymphocytes were given the priming dose. Although inhibitor and electrophoretic studies suggest that alterations in messenger RNA transcription and protein synthesis are involved in the adaptive response in lymphocytes, no specific signal transduction or repair pathways have been identified. At this time, the assumption that any stimulating effects from low doses of ionizing radiation will have a significant effect in reducing long-term deleterious effects of radiation on humans is unwarranted.

Bystander Effects

The bystander effect that results from irradiated cells’ reacting with nearby nonirradiated cells could influence dose-response relationships. Such an effect might come into play at low-LET doses below 1–5 mGy, where some cells of the body would not be irradiated. Current limitations of low-LET bystander studies include the lack of demonstrated bystander effects below 50 mGy and uncertainties about whether the effect occurs in vivo. Another complication is that both beneficial and detrimental effects have been postulated for bystander effects by different investigators. Until molecular mechanisms are elucidated, especially as they relate to an intact organism, and until reproducible bystander effects are observed for low-dose low-LET radiation in the dose range of 1–5 mGy, where an average of less than 1 electron tracks traverse the nucleus, the assumption should be made that bystander effects will not influence the shape of the low-dose, low-LET dose-response relationship.

Hyperradiosensitivity for Low Doses

In some cell lines, hyperradiosensitivity (HRS) has been reported for cell lethality induced by low-LET radiation at doses less than 100–200 mGy. In this dose range, survival decreases to 85–90%, which is significantly lower that projected from data obtained above 1–2 Gy. It is not known whether HRS for cell lethality would cause an increase in deleterious effects in surviving cells or would actually decrease deleterious effects by increased killing of damaged cells. Until molecular mechanisms responsible for HRS that may or may not play a role in carcinogenesis are understood, the extrapolation of data for HRS for cell lethality to the dose-response for carcinogenesis in the 0–100 mGy range is not warranted.

Genomic Instability

During the last decade, evidence has accumulated that under certain experimental conditions, the progeny of cells surviving radiation appear to express new chromosomal aberrations and gene mutations over many postirradiation cell generations. This feature is termed radiation-induced persistent genomic instability. Some inconsistencies were identified in the data that describe the diverse manifestation of induced genomic instability, and clear evidence of its general involvement in radiation-induced cancer is lacking. Although developing data on the various phenomena classified as genomic instability may eventually provide useful insights into the mechanisms of carcinogenesis, it is not possible to predict whether induced genomic instability will influence low-dose, low-LET response relationships.

Research Need 3. Evaluation of the relevance of adaptation, low-dose hypersensitivity, bystander effects, and genomic instability for radiation carcinogenesis

Mechanistic data are needed to establish the relevance of these processes to low-dose radiation exposure (i.e., <100 mGy). Relevant end points should include not only chromosomal aberrations and mutations but also genomic instability and induction of cancer. In vitro and in vivo data are needed for delivery of low doses over several weeks or months at very low dose rates or with fractionated exposures. The cumulative effect of multiple low doses of less than 10 mGy delivered over extended periods has to be explored further. The development of in vitro transformation assays utilizing nontransformed human diploid cells is judged to be of special importance.

Hormesis

The possibility that low doses of radiation may have beneficial effects (a phenomenon often referred to as “hormesis”) has been the subject of considerable debate. Evidence for hormetic effects was reviewed, with emphasis on material published since the 1990 BEIR V study on the health effects of exposure to low levels of ionizing radiation. Although examples of apparent stimulatory or protective effects can be found in cellular and animal biology, the preponderance of available experimental information does not support the contention that low levels of ionizing radiation have a beneficial effect. The mechanism of any such possible effect remains obscure. At this time, the assumption that any stimulatory hormetic effects from low doses of ionizing radiation will have a significant health benefit to humans that exceeds potential detrimental effects from radiation exposure at the same dose is unwarranted.

Research Need 4. Identification of molecular mechanisms for postulated hormetic effects at low doses

Definitive experiments that identify molecular mechanisms are necessary to establish whether hormetic effects exist for radiation-induced carcinogenesis.

Radiation-Induced Cancer:
Mechanism, Quantitative Experimental Studies,
and the Role of Molecular Genetics

A critical conclusion on mechanisms of radiation tumorigenesis is that the data reviewed greatly strengthen the view that there are intimate links between the dose-dependent induction of DNA damage in cells, the appearance of gene or chromosomal mutations through DNA damage misrepair, and the development of cancer. Although less well established, the data available point toward a single-cell (monoclonal) origin for induced tumors and suggest that
low-dose radiation acts predominantly as a tumor-initiating agent.
These data also provide some evidence on candidate, radiation-associated mutations in tumors. These mutations are predominantly loss-of-function DNA deletions, some of which are represented as segmental loss of chromosomal material (i.e., multigene deletions).

This form of tumorigenic mechanism is broadly consistent with the more firmly established in vitro processes of DNA damage response and mutagenesis considered in Chapters 1 and 2. Thus, if as judged in Chapters 1 and 2, error-prone repair of chemically complex DNA double-strand damage is the predominant mechanism for radiation-induced gene or chromosomal mutation, there can be no expectation of a low-dose threshold for the mutagenic component of radiation cancer risk.

One mechanistic caveat explored was that novel forms of cellular damage response, collectively termed induced genomic instability, might contribute significantly to radiation cancer risk. The cellular data reviewed in Chapter 2 identified uncertainties and some inconsistencies in the expression of this multifaceted phenomenon.

However, telomere-associated mechanisms did provide a coherent explanation for some in vitro manifestations of induced genomic instability. The data considered did not reveal consistent evidence for the involvement of induced genomic instability in radiation tumorigenesis, although telomere-associated processes may account for some tumorigenic phenotypes. A further conclusion was that there is little evidence of specific tumorigenic signatures of radiation causation, but rather that radiation-induced tumors develop in a tumor-specific multistage manner that parallels that of tumors arising spontaneously.

Quantitative animal data on dose-response relationships provide a complex picture for low-LET radiation, with some tumor types showing linear or linear-quadratic relationships while other studies are suggestive of a low-dose threshold, particularly for thymic lymphoma and ovarian cancer. Since, however, the induction or development of these two cancer types is believed to proceed via atypical mechanisms involving cell killing, it was judged that the threshold-like responses observed should not be generalized.

Radiation-induced life shortening in mice is largely a reflection of cancer mortality, and the data reviewed generally support the concept of a linear dose-response at low doses and low dose rates. Other dose-response data for animal tumorigenesis, together with cellular data, contributed to the judgments developed and the choice of a DDREF for use in the interpretation of epidemiologic information on cancer risk.

Adaptive responses for radiation tumorigenesis have been investigated in quantitative animal studies, and recent information is suggestive of adaptive processes that increase tumor latency but not lifetime risk. However, these data are difficult to interpret, and the implications for radiological protection remain most uncertain.

Research Need 5. Tumorigenic mechanisms

Further cytogenetic and molecular genetic studies are needed to reduce current uncertainties about the specific role of radiation in multistage radiation tumorigenesis; such investigations would include studies with radiation-associated tumors of humans and experimental animals.

The review of cellular, animal, and epidemiologic or clinical studies on the role of genetic factors in radiation tumorigenesis suggests that many of the known strongly expressing cancer-prone human genetic disorders are likely to show an elevated risk of radiation-induced cancer, probably with a high degree of organ specificity. Cellular and animal studies suggest that the molecular mechanisms underlying these genetically determined radiation effects largely mirror those that apply to spontaneous tumorigenesis and are consistent with knowledge of somatic mechanisms of tumorigenesis. In particular, evidence was obtained that major deficiencies in DNA damage response and tumor-suppressor-type genes can serve to elevate radiation cancer risk.

Limited epidemiologic data from follow-up of second cancers in gene carriers receiving radiotherapy were supportive of the above conclusions, but quantitative judgments about the degree of increased cancer risk remain uncertain. However, since major germline deficiencies in the genes of interest are known to be rare, it has been possible to conclude from published analyses that they are most unlikely to create a significant distortion of population-based estimates of cancer risk. The major practical issue associated with these strongly expressing cancer genes is judged to be the risk of radiotherapy-related cancer.

A major theme developing in cancer genetics is the interaction and potential impact of more weakly expressing variant cancer genes that may be relatively common in human populations. The animal genetic data provide proof-of-principle evidence of how such variant genes with functional polymorphisms can influence cancer risk, including limited data on radiation tumorigenesis. Attention was also given to human molecular epidemiology data on associations between functional polymorphisms and cancer risk, particularly with respect to DNA damage response genes.

Given that functional gene polymorphisms associated with cancer risk may be relatively common, the potential for significant distortion of population-based risk was explored with emphasis on the organ specificity of the genes of interest. An interim conclusion was that common polymorphisms of DNA damage response genes associated with organ-wide radiation cancer risk would be the most likely source of major interindividual differences in radiation response.

Research Need 6. Genetic factors in radiation cancer risk

Further work is needed in humans and mice on gene mutations and functional polymorphisms that influence the risk of radiation-induced cancers. Where possible, human molecular genetic studies should be coupled with epidemiologic investigations.

GENETIC EFFECTS OF RADIATION ON HUMAN POPULATIONS

As noted in BEIR V, heritable effects of radiation are estimated using what is referred to as the “doubling dose method” and expressed in terms of increases in the frequencies of genetic diseases in the population over and above those that occur as a result of spontaneous mutations. The doubling dose (DD) is the amount of radiation required to produce as many mutations as those that occur spontaneously in a generation and is calculated as a ratio of the average rates of spontaneous and induced mutations in defined genes. If the DD is small, the relative mutation risk per unit dose (i.e., 1/DD) is high, and if DD is large, the relative mutation risk is low. The DD, therefore, provides a convenient yardstick to express risks and a perspective of whether the predicted increases are trivial, small, or substantial relative to the baseline.

===================================

CONCLUSION
http://www.nap.edu/openbook.php?record_id=11340&page=323

The committee concludes that the current scientific evidence is consistent with the hypothesis that
there is a linear, no-threshold dose-response relationship
between exposure to ionizing radiation and the development of cancer in humans.

===================================
References: http://www.nap.edu/openbook.php?record_id=11340&page=337
===================================

[Satyagraha]

Ann Coulter went to great pains to explain that radiation can actually be good for you.
She is full of shit. We knew that already, but in the study I posted above, the issue of 'radiation is good for you' is addressed.

First, let's hear Ann Coulter's bullshit:


http://www.youtube.com/watch?v=w7Pge9F5SpE

============================

Now for some facts:

Hormesis
http://www.nap.edu/openbook.php?record_id=11340&page=315

The possibility that low doses of radiation may have beneficial effects (a phenomenon often referred to as “hormesis”) has been the subject of considerable debate.

Evidence for hormetic effects was reviewed, with emphasis on material published since the 1990 BEIR V study on the health effects of exposure to low levels of ionizing radiation. Although examples of apparent stimulatory or protective effects can be found in cellular and animal biology,

"...the preponderance of available experimental information
does not support the contention that low levels of ionizing radiation
have a beneficial effect."

The mechanism of any such possible effect remains obscure. At this time, the assumption that any stimulatory hormetic effects from low doses of ionizing radiation will have a significant health benefit to humans that exceeds potential detrimental effects from radiation exposure at the same dose is unwarranted

=========================

Whoever gave Ann Coulter her bullshit talking points didn't do their research.
This study quoted above was produced by The National Research Council of the National Academies, and published by the National Academies Press in Washington, D.C.
She's a tool for the globalists who want us to believe that there is such a thing as an 'acceptable' level of radiation. It's not true, and it's certainly not good for you, as Coulter suggests.

Perhaps she's had too much exposure to radiation; it might explain her cognitive dysfunction.

[Catalina]

This story sums up how bad radiation is. Near Fukushima plant, hundreds of corpses uncollected because of contamination fears

http://www.msnbc.msn.com/id/42441638/ns/world_news-disaster_in_japan/

a 1,000-page protocol issued by the National Council on Radiation Safety in the United States and similar guidelines from the Centers for Disease Control — urge against cremation, calling instead for deep burial in a sealed container marked by radiation warning symbols.

[chris jones]

Little Ann Coulter,gosh golly, gee whiz its good for you, wow, realy.
       Thats cute Anny, you and Hillary make a good pair. 

[Monkeypox]

Little Ann Coulter,gosh golly, gee whiz its good for you, wow, realy.
       Thats cute Anny, you and Hillary make a good pair.  

(M)Ann Coulter and Hitlary Klinton are a pair of Left and Right bookends.

If radiation is so good for us, why aren't we sprinkling uranium dust on our cornflakes every morning?

[mkultra1canuck]

Well I live in Vancouver, BC. And it has been completely downplayed only reporting initial fallout and then keeping shut.

[grapecrusher1]

Well I live in Vancouver, BC. And it has been completely downplayed only reporting initial fallout and then keeping shut.

I was driving through Kits on Monday and it was POURING rain and there were dozens of vancouverites out playing soccer and jogging etc.

getting healthy.

[chris jones]

  Silent death, no form, no smell, zip, nothing. The victim hasn't a clue he has been recieved a lethal dose.
  Nowhere to run, nowehere to hide, GOTCHA ,,,death.

 The USA has 140 nuclear power plants in operation, dotted across the nation.
Many moons ago Walt Disney played up nuclear power, as did our dear regimes, MSM, scientific community etc.
  Depite the fact they never accomplished the promises given to the public, depsite the fact these monuments of death were a drain on taxes, despite the fact one accident could reult in a national tragedy, despite the fact the waste alone is invisible death, no cheap power was ever provided or will be, in short their a complete FN dud.
  Why did their construction continue, their usage and expanision. I may be a hangover from the cold war, the effects of that period of time.     I just never trusted this H.S. and never will.

[Brocke]

Fukushima nuclear workers urged to store stem cells

Posted 16 minutes ago

A group of Japanese doctors have urged workers at the Fukushima nuclear plant to have their blood stem cells stored as a safeguard should they be exposed to life-threatening levels of radiation.

The technique entails storing autologous peripheral blood stem cells (PBSCs), which are immature cells that differentiate into blood cells.

PBSC transplants are often used in cancer treatment to boost depleted blood cell counts among patients who have had radiotherapy to destroy a tumour.

In a letter to the British medical weekly, The Lancet, cancer specialists at four Japanese hospitals argued that it made sense to store blood from the hundreds of workers battling to save the Fukushima nuclear plant from catastrophe.

They doctors say teams are working in extremely hazardous conditions at the plant.

"The process to completely shut down the reactors is expected to take years. The risk of accidental radiation exposure will thus accumulate for the nuclear workers and banking of their PBSCs will become increasingly important," the letter said.

"The most important mission is to save the nuclear workers' lives and to protect the local communities.

"Such an approach would be the industry's best defence: if a fatal accident happened to the nuclear workers, the nuclear power industry of Japan would collapse."

The doctors complained Japan's nuclear industry resisted storing the workers' PBSCs because it was fearful doing so would harm its reputation.

read more:http://www.abc.net.au/news/stories/2011/04/15/3192354.htm?section=justin

[egypt]

I heard on a Bob Chapman appearance that Europe is telling people to not drink or eat milk products for six months...

Didn't Janet Napolitano tell her friends at a dinner party to store up on foods for 6 months?  I find this quite condemning from all angles that the Japan Event was known in advance about.

Love, e

[agentbluescreen]

I heard on a Bob Chapman appearance that Europe is telling people to not drink or eat milk products for six months...

Didn't Janet Napolitano tell her friends at a dinner party to store up on foods for 6 months?  I find this quite condemning from all angles that the Japan Event was known in advance about.

Love, e

A Half-life is the period of time during which only-likely half of the numbers of a radiating isotope's atoms are most likely to decay into whatever they  are destined to become which is usually the stable and non-decaying atomic form of the element in question. The other half of them remain radioactive (alpha-beta) for yet another 'half life' period, not to mention what becomes of the decaying element's thus-released most dangerous gamma neutrons that are so released by the final stage of those decays and what that does to more distant surrounding tissues. In actuality there is no guarantee any atom will decay within any specific period, and the larger the numbers involved the multiples of 100% local radiation-dose exposures/times can be many months or years for any given dose of ¹³¹Iodine or any other inhaled particulate or gas isotope that remains in the body regardless of any statistical "half life" rating.

Half life is to decay as doubling time is to population - it is in no way indicative of how long any individual will "radiate"(live). This average-of-probabilities "estimation of odds" is like Russian Roulette, consider this decay chart that illustrates how the law of large numbers effects a given set of circumstances:

The animation illustrates how 1 out of 4 times even after 4 "half lives" half still remains! In fact any given isotope atom can survive any length of time it feels like, emitting as much radiation as it will inside of you. Exposures just depend on which one(s) you happen to eat. The law of large numbers makes the above statement still true regardless of quantities, though the multiple of more serious prolonged radiation exposures only increases.

http://en.wikipedia.org/wiki/Half-life
 
Longer or shorter lived isotopes (of the same element) do not emit equal total-amounts of radiation. It depends how excited (how much/many subatomic energies) they have absorbed and the unwinding vagaries of how they are released. Unstable isotopes can be unstable in a myriad (6 X 6 or more) of other differently interactive ways, aside from the added neutron(s). There are whole different little circuses of quarks and leptons playing around in/with them. Their individual instabilities are all highly varied and circumstantial.


From this you can see that even after a month even the "least troublesome" 8 day half life of ¹³¹Iodine is still a matter of chance that can remain active in you a month! Any level of any radioactive ingestion is Russian Roulette but much more than just Iodine is in these clouds:

4/14/2011 -- RADIATION FALLOUT UPDATE -- Asia, USA, Canada receiving HIGH-mid levels http://youtu.be/xaup0qywTto



Updated links now available!

http://transport.nilu.no/products/fukushima?searchterm=fuk

http://www.eurad.uni-koeln.de/


********************

all old links below still functioning...

Full mid levels of Cesium , Xenon, and Iodine.. particulate matter, in the cloud vapor from surface level to 5000m (15,000 feet) ..

These levels are now a full level higher than all the previous forecasts.

It is up to you to decide how you want to approach this data.

Personally, I believe it to be IN THE PRECIPITATION for sure.. which means you do not want to get the rain or snow on you, and do not want to injest the fluid.. (i.e. drink the water) until levels deminish.

here are all the links: make sure to refresh each one so you get the most current data:

the revealed US site:

http://www.atmos.umd.edu/~tcanty/hysplit/

http://www.woweather.com/weather/news/fukushima?LANG=us&VAR=niluhemis131&...

http://www.woweather.com/weather/news/fukushima?LANG=us&VAR=niluhemis133&...

http://www.woweather.com/weather/news/fukushima?LANG=us&VAR=niluhemis137&...

http://www.woweather.com/weather/news/fukushima?LANG=us&VAR=eurad5000&...

Here is a list of the radioactive particles in the air.
Taken from the 3-16-11 on ZAMG site.

XE-133
CS-134
BA-136M
CS-136
CS 137
I-131
I-132
I-133
TE-132

[egypt]

I do not believe it was an accident that the radiation fallout from Japan comes right over America, at this time, like this.  I believe those nuclear power plant reactors were specifically-placed there in Japan, and elsewhere as bombs.

What.  Was the atomic bombing of Nagasaki and Hiroshima a beta test to make sure for exact placement?  I do understand from reading what half-life is.  Strontium 90 radioactive isotope is bad. 90 Sr according to Wikipedia has a half-life of 28.8 years.

There are fine particles landing on my skin that need scrubbing off daily and can kinda be picked off.  These particles burn, too.  I feel like grit is all over.  I'm taking KIO3, but cannot do *that* forever, right?  Cancer risk can be reduced many ways and come what may!

If it is estimated that men will be sterile by 2025, goodbye Humanity!

All I know is -- I want my DNA Repair Pill.  But, I don't want a DNA Repair Pill that the government has anything to do with!

Love, e

[Brocke]

Japan to stick with nuclear power - ruling

    * From: AAP
    * April 22, 2011 9:28PM

JAPAN will review its energy policy in light of the Fukushima atomic plant disaster but will stick with nuclear power, the secretary general of the centre-left ruling party said today.

The March 11 earthquake-triggered tsunami that devastated Japan's northeast coast slammed into the plant, causing reactors to overheat in a crisis that its operator has said will not be stabilised until at least year's end.

Katsuya Okada, secretary general of the ruling Democratic Party of Japan (DPJ), said the government would have to check all nuclear installations and that, "based upon that, we will have to review our energy policy".

"We cannot do without nuclear energy, but we have to think about the way nuclear plants are built and the speed of their construction," Okada, the party's number two after Prime Minister Naoto Kan, told foreign journalists.

Read more: http://www.news.com.au/breaking-news/japan-to-stick-with-nuclear-power-ruling/story-e6frfku0-1226043511866#ixzz1KIGnbTwu

[Okinawa]

Kan nuclear adviser fed up, quits
Tokyo professor calls response impromptu, says short-term thinking resulted in delays
http://search.japantimes.co.jp/cgi-bin/nn20110430x2.html

Kyodo, AP

Prime Minister Naoto Kan defended his government's handling of the nuclear crisis at the Fukushima No. 1 plant on Saturday, a day after one of his advisers on the emergency vowed to resign in protest at what he called the state's lax response.

Kan told the Lower House Budget Committee the departure of Toshiso Kosako, a professor on antiradiation safety measures at the University of Tokyo's graduate school who assumed the advisory post March 16, is extremely unfortunate.

"We are dealing with the crisis based on the advice that comes as a result of discussions by the Nuclear Safety Commission of Japan. Our handling of the crisis has never been impromptu," Kan said.

Kosako told the government Friday he will resign as Kan's adviser.

"The government has belittled laws and taken measures only for the present moment, resulting in delays in bringing the situation under control," Kosako said.

It is extremely rare for an intellectual adviser appointed by the prime minister to resign in protest at measures the government has taken.

Kosako told reporters at the Diet on Friday it is problematic for the government to have delayed the release of forecasts on the spread of radiation from the Fukushima plant, done by the Nuclear Safety Technology Center's computer system, called the System for Prediction of Environmental Emergency Dose Information (SPEEDI).

He also blasted the government for hiking the upper limit for emergency workers seeking to bring the crippled plant under control to 250 millisieverts from 100 millisieverts after the crisis broke out.

"The prime minister's office and administrative organizations have made impromptu policy decisions, like playing a whack-a-mole game, ignoring proper procedures," the radiation expert said.

He also urged the government to stiffen guidelines on upper limits on radiation levels the education ministry recently announced as allowable levels for elementary school grounds in Fukushima Prefecture, where the radiation-leaking plant is located.

The guidelines announced by the Education, Culture, Sports, Science and Technology Ministry "are inconsistent with internationally commonsensical figures and they were determined by the administration to serve its interests," he said.

As the only country to experience an atomic bombing, Japan has long had a powerful antinuclear movement, and such protests have become louder.

Yoshiko Nakamura, 50, a part-time worker, was among 450 who gathered Saturday in Tokyo's Yoyogi Park. The demonstrators beat drums, shouted "No more nukes" and held banners that read "Electricity in Tokyo, sacrifice in Fukushima."

"We knew all along nuclear power was dangerous. I just didn't know how to express myself," said Nakamura, taking part in her second demonstration in two weeks. "This is a great opportunity to send a message and voice my fears."

Such demonstrations have become more frequent, including during the Golden Week holidays, which continue through the weekend and this week. "What I had feared might happen has become reality," said Kenji Kitamura, a 48-year-old office worker. "It is outrageous children are being exposed to such high levels of radiation."

The Japan Times: Saturday, April 30, 2011
(C) All rights reserved

[Okinawa]

Apr 30, 5:05 AM EDT
Criticism up on Japan PM's handling of nuke crisis
http://ap.stripes.com/dynamic/stories/A/AS_JAPAN_EARTHQUAKE?SITE=DCSAS&SECTION=HOME&TEMPLATE=DEFAULT#3846d32a-e63f-49f9-ad70-e1215bbbd299
By YURI KAGEYAMA
Associated Press

TOKYO (AP) -- Criticism of the Japanese government's handling of the crisis at a radiation-spewing nuclear power plant increased Saturday, with a new poll indicating three-quarters of the people disapprove and a key adviser quitting in protest.

A Kyodo News service poll released Saturday showed that Prime Minister Naoto Kan's support ratings were plunging.

The poll reported that 76 percent of the respondents think Kan is not exercising sufficient leadership in handling the country's earthquake, tsunami and nuclear triple crisis, up from 63.7 percent in the previous survey in late March.

It also showed 23.6 percent of respondents think Kan should resign immediately, up from 13.8 percent in the previous survey.

The nationwide telephone survey of 1,010 people eligible to vote was conducted Friday and Saturday. No margin of error was provided.

Toshiso Kosako, a professor at the University of Tokyo's graduate school and an expert on radiation exposure, announced late Friday that he was stepping down as a government adviser over what he lambasted as unsafe, slipshod measures.

Kan appointed Kosako after the magnitude-9.0 earthquake and tsunami struck northeastern Japan on March 11. The disaster left 26,000 people dead or missing and damaged several reactors at the Fukushima Dai-ichi nuclear power plant, setting off the world's worst nuclear crisis since Chernobyl in 1986.

In a tearful news conference, Kosako said he could not stay and allow the government to set what he called improper radiation limits of 20 millisieverts a year for elementary schools in areas near the plant.

"I cannot allow this as a scholar," he said. "I feel the government response has been merely to bide time."

Kosako also criticized the government as lacking in transparency in disclosing radiation levels around the plant, and as improperly raising the limit for radiation exposure for workers at Fukushima Dai-ichi, Kyodo reported.

The prime minister defended the government's response as proper.

"We welcome different views among our advisers," Kan told parliament Saturday in response to an opposition legislator's questions.

A government advisory position is highly respected in Japan, and it is extremely rare for an academic to resign to protest government policy.

The science and education ministry has repeatedly defended the 20-millisievert limit for radiation exposure as safe, saying that efforts are under way to bring the limit down to 1 millisievert. Some people have expressed concerns, noting that children are more vulnerable to radiation than adults.

Workers in the U.S. nuclear industry are allowed an upper limit of 50 millisieverts per year. A typical individual might absorb 6 millisieverts a year from natural and man-made sources such as X-rays.

Radiation specialists say cumulative doses of 500 millisieverts raise cancer risks. Evidence is less clear on smaller amounts, but in theory, any increased radiation exposure raises the risk of cancer.

Japan, which has 54 nuclear reactors, has long been a major proponent of atomic power, constantly billing its technology as top-rate and super-safe. Japan's government has also been trying to make deals to build nuclear power plants in other countries, although such attempts are likely to fall flat after the Fukushima Dai-ichi accident.

As the only country in the world to suffer atomic bombings, as it did at Hiroshima and Nagasaki during World War II, Japan has long had a powerful anti-nuclear movement, and such protests have become louder recently.

About 1,000 protesters gathered Saturday in Tokyo's Yoyogi Park, beating drums, shouting "No more nukes" and holding banners that read "Electricity in Tokyo, sacrifice in Fukushima."

"We knew all along nuclear power was dangerous. I just didn't know how to express myself," said one of the protesters, 50-year-old Yoshiko Nakamura, who was taking part in her second demonstration in two weeks. "This is a great opportunity to send a message and voice my fears."

Tokyo Electric Power Co., the utility that runs Fukushima Dai-ichi, said Saturday that the radiation exposures for two workers, upon more careful recalculation, was found to have reached near the crisis-time limit of 250 millisieverts.

Usually, TEPCO plant workers are limited to 100 millisieverts of radiation exposure over five years, with no year exceeding 50 millisieverts. That was raised to 250 millisieverts, with government approval, because of the crisis.

One worker was measured at 240.8 millisieverts, while another at 226.6 millisieverts. Both workers were temporarily hospitalized last month after being exposed to highly radioactive water that had leaked into the reactor turbine room.

Last week, TEPCO said one female worker at Fukushima Dai-ichi was exposed to radiation three times the legal limit, at 17.55 millisieverts. Exposure for women is limited to 5 millisieverts over 3 months because of pregnancy concerns.

TEPCO spokesman Junichi Matsumoto said the company had been preoccupied with monitoring radiation for male workers, and forgot that women's limits were far lower.

"We are extremely sorry," he told reporters last week.

Also on Saturday, parliament's lower house approved a special 4 trillion yen ($50 billion) budget to help finance post-tsunami rebuilding efforts, in what officials say will likely be the first installment of reconstruction funding.

The budget now goes to the less powerful upper house, where opposition is unlikely, and the budget is expected to win passage early next week.

(This version CORRECTS to year instead of hour in paragraph

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