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The deadline for comment to the US NRC on the 100 mSv per year exposure proposal, also known as cancer for everyone, is tonight November 19th at 11.59 pm. http://www.regulations.gov/#!docketDetail;D=NRC-2015-0057 As outlined at the bottom of today’s blog post, these high levels will also increase risk of cardiovascular disease, cataracts, and other degenerative conditions, according to the ICRP. Thus, complaint to government officials and education needs to continue after this date. In particular, the NRC should be put under investigation for even considering this petition, which is both deadly and a waste of taxpayer money.
death grim reaper

According to the US taxpayer funded National Academy of Sciences BEIR VII, Phase 2 (2006) report, for each 100 mSv of radiation exposure there will be an estimated 1,000 out of a population of 100,000, i.e. 1 in 100, who will get cancer, above and beyond cancers which already occur. This would be the expected excess cancer risk PER YEAR of the proposed 100 mSv (0.1 Sv), according to BEIR. Over the course of a lifetime of 100 mSv per year, the excess cancer risk would be roughly 80%. On average, around half of those will die of life-shortening cancers (14 to 15 years), according to BEIR. (p. 279) That means no life after retirement. The current proposal being examined by the NRC is 100 mSv per year.

However, based on a recently published three country study of nuclear workers by Richardson, et. al. (Oct. 2015) the risk may be 15 times (or more) greater, i.e. 15 extra cancers per 100 people for each 100 mSv. This means that less than 10 years exposure would result in an extra cancer for everyone! The doses in the study were very low. The workers were exposed on average to 4.1 mSv (median average of half above-half below) over their entire career (the arithmetic average was 20.9 mSv – still very low). This was NOT 4 mSv per year, but rather 4 mSv total! This was NOT 21 mSv per year but rather total! See: https://miningawareness.wordpress.com/2015/12/19/another-look-at-the-recent-low-dose-radiation-exposure-study-inworks/

There is nothing “low” about 100 mSv. Rather, it is the beginning of medium dose, according to BEIR.

Furthermore, as BEIR VII (2006) explains:
The risk depends on both sex and age at exposure, with higher risks for females and for those exposed at younger ages. On average, assuming a sex and age distribution similar to that of the entire U.S. population, the BEIR VII lifetime risk model predicts that approximately 1 person in 100 would be expected to develop cancer (solid cancer or leukemia) from a dose of 0.1 Sv above background,…“( p.8) 0.1 Sv is 100 mSv. This is 1% per 100 mSv. Over the course of a lifetime, 100 mSv would lead to an average 80% excess (extra) cancer rate, and 100% for women, according to BEIR estimates (See Table 12-6, p. 281 ) and the risk may even be several times higher. This 80 % ignores both accumulation in the environment and other causes of cancer besides nuclear power (e.g. Medical radiation exposure, fallout from historic weapons testing, etc.)


The BEIR VII committee concludes that current scientific evidence is consistent with the hypothesis that there is a linear dose-response relationship between exposure to ionizing radiation and the development of radiation-induced solid cancers in humans. The committee further judges it unlikely that a threshold exists for the induction of cancers but notes that the occurrence of radiation-induced cancers at low doses will be small. The committee maintains that other health effects (such as heart disease and stroke) occur at high radiation doses, but additional data must be gathered before an assessment can be made of any possible connection between low doses of radiation and noncancer health effects. Additionally, the committee concludes that although adverse health effects in children of exposed parents (attributable to radiation-induced mutations) have not been found, there are extensive data on radiation-induced transmissible mutations in mice and other organisms. Thus, there is no reason to believe that humans would be immune to this sort of harm.” (p. 10)

One reason that genetic risks are low is that only those genetic changes compatible with embryonic develop-ment and viability will be recovered in live births.” (p.9)

In the case of in utero exposure (exposure of the fetus during pregnancy), excess cancers can be detected at doses as low as 10 mSv“. (p.6)

100 mSv per year means that, on average, the unborn may be exposed 75 mSv, i.e. to over 7 times the levels known to lead to excess cancers!


Whatever molecular mechanism is envisaged for radiation, at very low doses (e.g., 0– 5 mGy low LET), increases in dose simply increase the probability that a given single cell in the tissue will be intersected by an electron track which will have a nonzero probability of inducing a biological effect. Therefore, at these very low doses, a linearity of response is almost certain (Chapter 3). Second, given the intimate relationship established between DNA damage response, gene or chromosomal mutations, and cancer development, the form of the dose-response for mutation induction in single cells should be broadly informative for cancer initiation.” (BEIR VII, 2006, p.245) [As we’ve discussed elsewhere, in the context of external low-LET radiation, mGy is essentially mSv. See BEIR p. 8. For high LET alpha and neutrons the weighting factor is 20 (i.e. 1 mGy is 20 mSv). Sv describes the biological impact of radiation on living cells. Thus, it seems that reporting should always be in mSv to be safe, but is not.]


It is important to note that those petitioning the US NRC to raise the radiation exposure level make money from it and “It is difficult to get a man to understand something, when his salary depends upon his not understanding it!” (Upton Sinclair). That being said, the fact that the petitioners are at or well past retirement, is patently strange. They have reached an age which they want to forbid others from reaching. Some psychologists claim that if people repeat the same lie often enough that they come to actually believe it. Is this the case or are we looking at pure evil?

Carol S. Marcus, Ph.D., M.D., was and maybe still is, Director of the Nuclear Medicine Outpatient clinic, UCLA Medical Center, and Professor at UCLA. Even though she is long past retirement age, the dangers of radiation were well-known before she even entered university.

In 1950, William Russell of Oak Ridge National Labs stated: “There is no threshold dose. In other words, genetic changes may be expected at any dose, no matter how small…

Petitioner Mohan Doss is a physicist from India, who gives support for Nuclear Medicine, PET, CT, Radiographic & Fluoroscopic Systems at a cancer center (Fox Chase). He’s also worked for the Lawrence Berkley (Nuclear) Lab in the US, and at the U. of Saskatchewan – Cameco uranium mining country. Petitioner Mark Miller is associated with the Sandia (nuclear) lab. Based on one of his presentations, Miller’s objective appears to be to do away with evacuation zones after nuclear accidents. See: https://miningawareness.wordpress.com/2015/08/18/sandia-us-nuclear-lab-found-quick-easy-solution-for-radiation-at-fukushima-chernobyl-other-contaminated-zones/

Medical Overexposure Liability

If 100 mSv per year becomes acceptable for nuclear power, fuel processing and nuclear waste emissions, it would also theoretically reduce concerns about over-exposure from medical uses of radionuclides. Carol Marcus was behind the fact that patients treated with radio-iodine 131 can expose anyone they meet to 5 mSv, without notice, which is 20 times greater than the US EPA limit of 0.25 mSv for the body from nuclear facilities, and 6 times the EPA’s thyroid dose from nuclear facilities. And, guess what happened after this was pushed through:
Use of radioactive iodine for treatment of thyroid cancer on the rise” Date: August 17, 2011
Source: JAMA and Archives Journals
Summary: Despite uncertainty about the appropriate use of radioactive iodine after surgery for different stages of thyroid cancer, between 1990 and 2008 its use has increased among patients with all tumor sizes, and there was wide variation in use of this treatment among hospitals, according to a new study.
This is probably due to two reasons. A probable increase in thyroid cancer from the long-term impacts of I 129 (half-life 15 million years) from weapons testing and nuclear reactors, which would take several decades to be seen, as well as the 5 mSv outpatient rule (from the early 90s), which makes it cheaper and easier to do.

From the current proposal by Carol Marcus:
The petitioner recommends the following changes to 10 CFR part 20:
(1) Worker doses should remain at present levels, with allowance of up to 100 mSv (10 rem) effective dose per year if the doses are chronic.
(2) ALARA should be removed entirely from the regulations. The petitioner argues that “it makes no sense to decrease radiation doses that are not only harmless but may be hormetic.”
(3) Public doses should be raised to worker doses. The petitioner notes that “these low doses may be hormetic. The petitioner goes on to ask, “why deprive the public of the benefits of low dose radiation?”
(4) End differential doses to pregnant women, embryos and fetuses, and children under 18 years of age.

From BEIR VII, 2006: “…, studies of cancer in children following exposure in utero or in early life indicate that radiation-induced cancers can occur at low doses. For example, the Oxford Survey of Childhood Cancer found a 40 percent increase in the cancer rate among children up to [age] 15. This increase was detected at radiation doses in the range of 10 to 20 mSv. There is also compelling support for the linearity view of how cancers form. Studies in radiation biology show that “a single radiation track (resulting in the lowest exposure possible) traversing the nucleus of an appropriate target cell has a low but finite probability of damaging the cell’s DNA.

Subsets of this damage, such as ionization “spurs” that can cause multiple damage in a short length of DNA, may be difficult for the cell to repair or may be repaired incorrectly. The committee has concluded that there is no compelling evidence to indicate a dose threshold below which the risk of tumor induction is zero.” (p. 10)

At the low-dose exposures that are the focus of this report, so-called late effects, such as cancer, are produced many years after the initial exposure. In this report, the committee has defined low doses as those in the range of near 0 up to about 100 milligray (mGy) of low-LET radiation [i.e. 0 to 100 mSv], with emphasis on the lowest doses for which meaningful effects have been found. Additionally, effects that may occur as a result of chronic exposures over months to a lifetime at dose rates below 0.1 mGy/min, irrespective of total dose, are thought to be most relevant. Medium doses are defined as doses in excess of 100 mGy up to 1 Gy, and high doses encompass doses of 1 Gy or more, including the very high total doses used in radiotherapy (of the order of 20 to 60 Gy). Well-demonstrated late effects of radiation exposure include the induction of cancer and some degenerative diseases (e.g., cataracts). Also, the induction of mutations in the DNA of germ cells that, when transmitted, have the potential to cause adverse health effects in offspring has been demon-strated in animal studies.” (p. 11)

Hormesis has been defined as ‘the stimulating effect of small doses of substances which in larger doses are inhibitory.’… the meaning has been modified in recent times to refer not only to a stimulatory effect but also to a beneficial effect. In other words, hormesis now connotes a value judgment whereby a low dose of a noxious substance is considered beneficial to an organism. The committee has reviewed evidence for ‘hormetic effects’ after radiation exposure, with emphasis on material published since the previous BEIR study on the health effects of exposure to low levels of ionizing radiation.” [BEIR then lists some sources.] “Much of the historical material on radiation hormesis relates to plants, fungi, algae, protozoans, insects, and nonmammalian vertebrates (Calabrese and Baldwin 2000). For the purposes of this report on human health effects, the committee focused on recent information from mammalian cell and animal biology and from human epidemiology” [Note that Ed Calabrese, apparent “Godfather” of hormesis, was allowed to present before the BEIR committee. They clearly did not find his arguments convincing!]

Theoretical Considerations

Pollycove and Feinendegen have made a theoretical argument that the hazards of radiation exposure are negligible in comparison to DNA damage that results from oxidative processes during normal metabolism… Oxidative damage is much more complex than they appreciate…” [BEIR fails to mention that ionizing radiation actually increases oxidative damage because radiolysis creates ROS (reactive oxidative species) as Mousseau and Møller point out (See for instance: https://miningawareness.wordpress.com/2015/11/19/hormesis-is-silly-and-makes-no-sense-from-a-fundamental-genetics-point-of-view-says-geneticist/

Direct measurements of SSBs in unirradiated cells indicate levels several orders of magnitude less than that estimated by Pollycove and Feinendegen… They also hypothesize that low-dose radiation induces a specific repair mechanism that then acts to reduce both spontaneous and radiation-induced damage to below spontaneous levels, thus causing a hormetic effect. The evidence for such a repair mechanism is weak and indirect and is contradicted by direct measures of DSB repair foci at low doses (Rothkamm and Lobrich 2003)” (p. 332)

Evidence from Cell Biology

Possible stimulatory effects have been reported for radiation exposure, such as mobilization of intracellular calcium (Liu 1994), gene activation (Boothman and others 1993), activation of signal transduction pathways (Liu 1994; Ishii and others 1997), increase in antioxidants such as reduced glutathione (GSH; Kojima and others 1997), increase in lipoperoxide levels (Petcu and others 1997), and increase in circulating lymphocytes (Luckey 1991). The general thesis presented is that stress responses activated by low doses of radiation, particularly those that would increase immunological responses, are more beneficial than any deleterious effects that might result from the low doses of ionizing radiation. Although evidence for stimulatory effects from low doses has been presented, little if any evidence is offered concerning the ultimate deleterious effects that may occur. In the section of this report on observed dose-response relationships at low doses, bystander effects and hyper radiation sensitivity for low-dose deleterious effects in mammalian cells have been observed for doses in the 10–100 mGy range. End points for these deleterious effects include mutations, chromosomal aberrations, oncogenic transformation, genomic instability, and cell lethality. These deleterious effects have been observed for cells irradiated in vivo as well as in vitro.

Adaptive Response

The radiation-adaptive response in mammalian cells was demonstrated initially in human lymphocyte experiments (Olivieri and others 1984) and has been associated in recent years with the older concept of radiation hormesis… Radiation adaptation, as it was initially observed in human lymphocytes, is a transient phenomenon that occurs in some (but not all) individuals when a conditioning radiation dose lowers the biological effect of a subsequent (usually higher) radiation exposure. In lymphocyte experiments, this reduction occurs under defined temporal conditions and at specific radiation dose levels and dose rates (Shadley and others 1987; Shadley and Wiencke 1989). However, priming doses less than 5 mGy or greater than ~200 mGy generally result in very little if any adaptation, and adaptation has not been reported for challenge doses of less than about 1000 mGy…. results suggest that occupational exposure may have induced chromosomal damage in the worker population while protecting lymphocytes from a subsequent experimental radiation exposure administered years after initiation of the chronic exposure. It is unclear whether such competing events would result in a net gain, net loss, or no change in health status…. When radioresistance is observed after doses that cause some cell lethality— for example, after chronic doses that continually eliminate cells from the population—the radioresistance that emerges may be caused either (1) by some inductive phenomenon or (2) by selecting for cells that are intrinsically radioresistant. Either process 1 or process 2 could occur as the radiosensitive cells are selectively killed and thus eliminated from the population as the chronic irradiation is delivered. In the end, an adaptive or hormetic response in the population may appear to have occurred, but this would be at the expense of eliminating the sensitive or weak components in the population. In chronic low-dose experiments with dogs (75 mGy/d for the duration of life), vital hematopoietic progenitors showed increased radioresistance along with renewed proliferative capacity (Seed and Kaspar 1992). Under the same conditions, a subset of animals showed an increased repair capacity as judged by the unscheduled DNA synthesis assay (Seed and Meyers 1993). Although one might interpret these observations as an adaptive effect at the cellular level, the exposed animal population experienced a high incidence of myeloid leukemia and related myeloproliferative disorders. The authors concluded that ‘the acquisition of radioresistance and associated repair functions under the strong selective and mutagenic pressure of chronic radiation is tied temporally and causally to leukemogenic transformation by the radiation exposure” (Seed and Kaspar 1992).” (p.333)



The term hormesis is not commonly used in the epidemiologic literature. Rather, epidemiologists discuss associations between exposure and disease. A positive association is one in which the rate of disease is higher among a group exposed to some substance or condition than among those not exposed, and a negative (or inverse) association is one in which the rate of disease is lower among the exposed group. If an association is judged to be causal, a positive association may be termed a causal effect and a negative association could be termed a protective effect. One type of epidemiologic study that has been used to evaluate the association between exposure to radiation and disease is the “ecologic” study in which data on populations, rather than data on individuals, are compared. These data have been used to argue for the existence of radiation hormesis…. BEIR V discussed the effect of confounders and the ecological fallacy [2] in the evaluation of high-background-radiation areas and concluded that “these two problems alone are enough to make such studies essentially meaningless” (NRC 1990). Another important consideration is the expected magnitude of the increase in health effect induced by excess back-ground radiation. If one assumes a linear no-threshold response, a calculation can be made for expected cancers induced by excess radiation in a high-background-radiation area. As an example, consider the elevated levels of gamma radiation in Guodong Province, Peoples’ Republic of China (PRC). In this study, a population receiving 3–4 mGy per year was compared to an adjacent control population receiving 1 mGy per year. No difference in cancers was noted between the high-background area and the control area (NRC 1990). One can estimate the expected excess percentage of cancers resulting from the 2–3 mGy difference in exposure per year using a linear nonthreshold model and the lifetime risk estimates developed in this report. A calculation by this committee indicated that the expected percentage of cancers induced by the excess background radiation would be 1–2% above the cancers occurring from all other causes in a life-time. Even if all confounding factors were accounted for, it is questionable whether one could detect an excess cancer rate of 1–2%. Excess cancers may indeed be induced by elevated radiation exposure in high-background areas, but the excess may not be detectable given the high lifetime occurrence of cancer from all causes… A second type of epidemiologic study that has been used to evaluate the association between exposure to radiation and disease is the retrospective cohort study. Persons who have had past exposure to radiation are followed forward in time, and the rate of disease is compared between exposed and nonexposed subjects or between exposed subjects and the general population. Especially valuable are occupational studies that include both unexposed and exposed subjects, so that a dose-response evaluation can be made of the relation between radiation exposure and health outcome. Typically, study populations in retrospective cohort studies include persons who have worked with radiation in medical facilities or in the nuclear industry or patients with cancer or other disease who have been treated with radiation

It is common in cohort studies of occupational populations to observe that the overall mortality rate is lower than that of the general population, commonly about 15%. This is not interpreted to mean that work per se reduces the risk of mortality, but rather that healthy persons start to work more often than unhealthy persons (Monson 1990).” The “healthy worker effect” (HWE) is “observed in most occupational studies, including those of radiation workers, and should not be interpreted to mean that low doses of radiation prevent death from cancer or other causes.”

A third type of epidemiologic study that has been used to evaluate the association between exposure to radiation and disease is the case-control study… While no phenomenon similar to the HWE is observed in case-control studies, the play of chance is always operative,.. it is inappropriate to select only those that are consistent with an excess or deficit of disease. Rather, the entire distribution must be examined to assess the likely relationship between exposure and disease. The studies discussed here illustrate the variability that is inherent in all epidemiologic studies and the need to evaluate the entire body of relevant literature in order to assess possible associations between radiation and disease, be they positive or negative. In its evaluation of the literature and in its discussions, the committee has found no consistent evidence in the epidemiologic literature that low doses of ionizing radiation lower the risk of disease or deaththe weight of the evidence does not lead to the interpretation that low doses of radiation exert what in biological terms is called hormesis.


The committee concludes that 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 the radiation exposure is unwarranted at this time.” (p.334)

[Footnote p. 334] “2Ecological fallacy: two populations differ in many factors other than those being evaluated, and one or more of these may be the underlying reason for any difference noted in their morbidity or mortality experience (Lilienfeld and Stolley 1994)“.

Recent evidence indicates that exposure to radiation from Chernobyl is associated with an increased risk of thyroid cancer and that the relationship is dose dependent. These findings are based on individual estimates of thyroid radiation dose and reveal strong and statistically significant dose-related increased risks that are consistent across studies.” ( p. 238)

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 pre-ponderance of available experimental information does not support the contention that low levels of ionizing radiation have a beneficial effect. The mechanism of any such pos-sible 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.” (p. 315)

Although this BEIR VII report is about low-LET radiation, the committee has considered some information derived from complex exposures that include radiation from high-LET and low-LET sources. High-LET or mixed radiations (radiation from high-LET and low-LET sources) are often described in units known as sievert. The units for low-LET radiation can be sievert or gray. For simplicity, all dose units in the Public Summary are reported in sieverts (Sv). ” “Public Summary & Executive Summary.” Health Risks from Exposure to Low Levels of Radiation: BEIR VII Phase 2. Washington, DC: The National Academies Press, 2006“, p.2

In Appendix E, p. 336, the 2005 “Fifteen-Country Workers Study” was discussed. It was submitted after the BEIR VII draft was written so was not considered. It gives risk estimates which are not only higher than BEIR VII, but even higher than the recent three country study by Richardson et. al. Thus, the high risk rate found by Richardson et. al. appears conservative, middle of the road.

The overall average cumulative recorded dose was 19.4 mSv…. The excess relative risk estimate for all cancers excluding leukemia was reported as 0.97 Gy–1 (95% CI 0.14, 1.97) and for all solid cancers 0.87 Gy–1 (95% CI 0.03, 1.88). These estimates are somewhat higher than, but statistically compatible with, the estimates on which current radiation protection recommendations are based. Analyses of smoking-and non-smoking-related causes of death indicate that although confounding by smoking may be present, it is un-likely to explain all of this increased risk. The excess relative risk estimate for leukemia excluding chronic lymphocytic leukemia was reported as 1.93 Gy–1 (95% CI <0, 8.47). This estimate, although not statistically significantly elevated, is close to that observed in previous nuclear workers studies.” (BEIR VII p. 336)

Compare and contrast of the “Fifteen Country Workers Study”, BEIR and the new Richardson et. al. study found here: https://miningawareness.wordpress.com/2015/10/21/new-study-of-us-uk-french-nuclear-workers-supports-linear-no-threshold-model-radiation-is-bad-for-you-increased-dose-is-increased-risk-hormesis-debunked-funding-from-pro-nuclear-govts-nuclea/
Richardson et. al. study found in its entirety at the first link.

Read the entire BEIR VII, Phase 2 report here. Although it was apparently finished in 2005, the copyright is listed as 2006: http://www.researchgate.net/publictopics.PublicPostFileLoader.html?id=55269d36cf57d7cd308b45f3&key=2e28f191-dbed-4d88-a780-77772105d712
It is also available for free at the National Academy of Science web site.

The ICRP says: “… a ‘threshold dose’ of 0.5 Gy is proposed here for both cardiovascular disease and cerebrovascular disease on the basis that this dose might lead to approximately 1% of exposed individuals developing each disease in question. Nevertheless, there are notable uncertainties in determining risks of these diseases at this level of dose.” (ICRP, p.292)

This then means that over 5 years of 100 mSv there would be a 1% increase in cardiovascular and cerebrovascular disease. This ignores the non-radiological impacts of Cesium and Strontium which mimic potassium and calcium, thus negatively impacting heart and nerve function.

An approximate threshold dose of around 0.5 Gy has been proposed for acute and fractionated/protracted exposures, on the basis that this might lead to circulatory disease in only one to a few percent of exposed individuals, although the estimation of risk at this level of dose is particularly uncertain.” (p. 304, ICRP 118).

IRCP 118, Summary:
ICRP Statement on Tissue Reactions / Early and Late Effects of Radiation in Normal Tissues and Organs – Threshold Doses for Tissue Reactions in a Radiation Protection Context ICRP Publication 118 Ann. ICRP 41(1/2), 2012, by F.A. Stewart, A.V. Akleyev, M. Hauer-Jensen, J.H. Hendry, N.J. Kleiman, T.J. MacVittie, B.M. Aleman, A.B. Edgar, K. Mabuchi, C.R. Muirhead, R.E. Shore, W.H. Wallace
Abstract – This report provides a review of early and late effects of radiation in normal tissues and organs with respect to radiation protection. It was instigated following a recommendation in Publication 103, and it provides updated estimates of ‘practical’ threshold doses for tissue injury defined at the level of 1% incidence. Estimates are given for morbidity and mortality endpoints in all organ systems following acute, fractionated, or chronic exposure. The organ systems comprise the haematopoietic, immune, reproductive, circulatory, respiratory, musculoskeletal, endocrine, and nervous systems; the digestive and urinary tracts; the skin; and the eye.
” See:

According to the US National Cancer Institute-National Institute of Health:
Radiation cataractogenesis, particularly occurrence of posterior subcapsular opacities has been considered to be another classic example of a deterministic late effect. Formerly, the threshold was reported to be 2 Gy for acute radiation exposure, 4 Gy for fractionated doses and even higher levels for long-term exposure, but recent human and mechanistic studies suggest a lower (eg, around 0.5 Gy) or no threshold.” Linet, Martha S. et al. “Cancer Risks Associated with External Radiation From Diagnostic Imaging Procedures.” CA: a cancer journal for clinicians 62.2 (2012): 75–100. PMC. Web. 22 June 2015.(Emphasis added) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548988/ Once again, this 0.5 Gy is equivalent to 500 mSv (500 mGy).

According to the US FDA re Cataracts:
More recent studies suggest that the lowest cataractogenic dose in people is much less than these values, is statistically compatible with no threshold at all, and that increasing dose is associated with an increasing prevalence of cataracts.9,10,11,12
9 E. Nakashima, K. Neriishi, and A.Minamoto, “A reanalysis of atomic-bomb cataract data, 2000–2002: a threshold analysis,” Health Phys. Vol. 90, pp. 154–160, 2006.
10 Kazuo Neriishi et al., “Postoperative Cataract Cases among Atomic Bomb Survivors: Radiation Dose Response and Threshold,” Radiat. Res. Vol. 168, pp. 404-408, 2007.
11 Gabriel Chodick, “Risk of Cataract after Exposure to Low Doses of Ionizing Radiation: A 20-Year Prospective Cohort Study among US Radiologic Technologists,” American Journal of Epidemiology Vol. 168, No. 6, pp. 620-631, 2008.
12 E. A. Ainsbury et al., “Radiation Cataractogenesis: A Review of Recent Studies,” Radiation Research Vol. 172, pp. 1-9, 2009.

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