Bill Sacks

Subjecting Radiological Imaging to the Linear No-Threshold Hypothesis: A Non Sequitur of Non-Trivial Proportion

Radiologic imaging is claimed to carry an iatrogenic risk of cancer, based on an uninformed commitment to the 70-y-old linear no-threshold hypothesis (LNTH). Credible evidence of imaging-related low-dose (<100 mGy) carcinogenic risk is nonexistent; it is a hypothetical risk derived from the demonstrably false LNTH. On the contrary, low-dose radiation does not cause, but more likely helps prevent, cancer. The LNTH and its offspring, ALARA (as low as reasonably achievable), are fatally flawed, focusing only on molecular damage while ignoring protective, organismal biologic responses. Although some grant the absence of low-dose harm, they nevertheless advocate the “prudence” of dose optimization (i.e., using ALARA doses); but this is a radiophobia-centered, not scientific, approach. Medical imaging studies achieve a diagnostic purpose and should be governed by the highest science-based principles and policies. The LNTH is an invalidated hypothesis, and its use, in the form of ALARA dosing, is responsible for misguided concerns promoting radiophobia, leading to actual risks far greater than the hypothetical carcinogenic risk purportedly avoided. Further, the myriad benefits of imaging are ignored. The present work calls for ending the radiophobia caused by those asserting the need for dose optimization in imaging: the low-dose radiation of medical imaging has no documented pathway to harm, whereas the LNTH and ALARA most assuredly do.

Epidemiology Without Biology: False Paradigms, Unfounded Assumptions, and Specious Statistics in Radiation Science (with Commentaries by Inge Schmitz-Feuerhake and Christopher Busby and a Reply by the Authors)

Radiation science is dominated by a paradigm based on an assumption without empirical foundation. Known as the linear no-threshold (LNT) hypothesis, it holds that all ionizing radiation is harmful no matter how low the dose or dose rate. Epidemiological studies that claim to confirm LNT either neglect experimental and/or observational discoveries at the cellular, tissue, and organismal levels, or mention them only to distort or dismiss them. The appearance of validity in these studies rests on circular reasoning, cherry picking, faulty experimental design, and/or misleading inferences from weak statistical evidence. In contrast, studies based on biological discoveries demonstrate the reality of hormesis: the stimulation of biological responses that defend the organism against damage from environmental agents. Normal metabolic processes are far more damaging than all but the most extreme exposures to radiation. However, evolution has provided all extant plants and animals with defenses that repair such damage or remove the damaged cells, conferring on the organism even greater ability to defend against subsequent damage. Editors of medical journals now admit that perhaps half of the scientific literature may be untrue. Radiation science falls into that category. Belief in LNT informs the practice of radiology, radiation regulatory policies, and popular culture through the media. The result is mass radiophobia and harmful outcomes, including forced relocations of populations near nuclear power plant accidents, reluctance to avail oneself of needed medical imaging studies, and aversion to nuclear energy—all unwarranted and all harmful to millions of people.

The Birth of the Illegitimate Linear No-Threshold Model: An Invalid Paradigm for Estimating Risk Following Low-dose Radiation Exposure.

This paper examines the birthing process of the linear no-threshold model with respect to genetic effects and carcinogenesis. This model was conceived >70 years ago but still remains a foundational element within much of the scientific thought regarding exposure to low-dose ionizing radiation. This model is used today to provide risk estimates for cancer resulting from any exposure to ionizing radiation down to zero dose, risk estimates that are only theoretical and, as yet, have never been conclusively demonstrated by empirical evidence. We are literally bathed every second of every day in low-dose radiation exposure due to natural background radiation, exposures that vary annually from a few mGy to 260 mGy, depending upon where one lives on the planet. Irrespective of the level of background exposure to a given population, no associated health effects have been documented to date anywhere in the world. In fact, people in the United States are living longer today than ever before, likely due to always improving levels of medical care, including even more radiation exposure from diagnostic medical radiation (eg, x-ray and computed tomography imaging examinations) which are well within the background dose range across the globe. Yet, the persistent use of the linear no-threshold model for risk assessment by regulators and advisory bodies continues to drive an unfounded fear of any low-dose radiation exposure, as well as excessive expenditures on putative but unneeded and wasteful safety measures.

Dose Optimization to Minimize Radiation Risk for Children Undergoing CT and Nuclear Medicine Imaging is Misguided and Detrimental

A debate exists within the medical community on whether the linear no-threshold model of ionizing radiation exposure accurately predicts the subsequent incidence of radiogenic cancer. In this article, we evaluate evidence refuting the linear no-threshold model and corollary efforts to reduce radiation exposure from CT and nuclear medicine imaging in accord with the as-low-as-reasonably-achievable principle, particularly for children. Further, we review studies demonstrating that children are not, in fact, more radiosensitive than adults in the radiologic imaging dose range, rendering dose reduction for children unjustifiable and counterproductive. Efforts to minimize nonexistent risks are futile and a major source of persistent radiophobia. Radiophobia is detrimental to patients and parents, induces stress, and leads to suboptimal image quality and avoidance of imaging, thus increasing misdiagnoses and consequent harm while offering no compensating benefits.

The assumption of radon-induced cancer risk

We read with interest the article by Axelsson et al. [1] about the potential risk of lung cancer due to inhalation of radioactive radon gas. Indeed, this has been the subject of many scientific papers around the world for years without clarification of whether there is risk or there is no risk when the radon concentration is low. The paper by Axelsson et al. [1] states that ‘‘residential exposure to radon is considered to be the second cause of lung cancer after smoking.’’ The authors cite the publications of many well-known radon experts, especially the analysis of 13 European case–control studies by Darby et al. [2]. They underscore their basic argument that in Sweden, there is a 16 % increase in the risk of radoninduced lung cancer per 100 Bq/m. However, there appear to be logical mistakes in their reasoning, which are presented below. The first mistake concerns their chosen dose–response model. They determine the 16 % increase in risk per 100 Bq/m by using the linear no-threshold (LNT) hypothesis. According to this hypothesis, the excess risk increases linearly versus Bq/m (or vs. mSv effective dose) from zero to the maximum. There are no data that support the validity of this hypothesis over the whole range of doses. All existing studies are subject to a number of limitations. Moreover, there is a huge scatter in the results, so it is impossible to reach a coherent conclusion [3]. In fact, the LNT hypothesis has been criticized fundamentally in many independent studies [4]. The second fallacy—the ‘‘zero radon environment’’—is related to the previous one. The authors [1] widely invoke the value ‘‘0 Bq/m,’’ which makes no sense from both the All signers of this letter are members or associate members of SARI (Scientists for Accurate Radiation Information, http://radiationeffects. org/). The above letter represents the professional opinions of the signers and does not necessarily represent the views of their affiliated institutions.

Preserving the Anti-Scientific Linear No-Threshold Myth: Authority, Agnosticism, Transparency, and the Standard of Care

The linear no-threshold (LNT) assumption is over 70 years old and holds that all ionizing radiation exposure leaves cumulative effects, all of which are harmful regardless of how low the dose or dose rate is. The claimed harm centers on the risk of future radiogenic cancer. This has been shown countless times to be fallacious, and hundreds of scientific studies—both experimental and observational/epidemiological—demonstrate that at low enough doses and dose rates, ionizing radiation stimulates an evolved adaptive response and therefore is beneficial to health, lowering rather than raising the risk of cancer. Yet the myth of uncorrected lifetime cumulative risk still pervades the field of radiation science and underlies the policies of virtually all regulatory agencies around the world. This article explores some of the motivations behind, and methods used to assure, the extreme durability of the LNT myth in the face of the preponderance of contrary evidence and the manifest harms of radiophobia. These include subservience to the voice of authority, tactics such as claiming agnosticism on behalf of the entire field, transparent references to contrary evidence while dismissing the findings without refutation, and seeking shelter behind the legally protective medical standard of care.

The BEIR VII Estimates of Low-Dose Radiation Health Risks Are Based on Faulty Assumptions and Data Analyses: A Call for Reassessment

The 2006 National Academy of Sciences Biologic Effects of Ionizing Radiation (BEIR) VII report is a well-recognized and frequently cited source on the legitimacy of the linear no-threshold (LNT) model—a model entailing a linear and causal relationship between ionizing radiation and human cancer risk. Linearity means that all radiation causes cancer and explicitly excludes a threshold below which radiogenic cancer risk disappears. However, the BEIR VII committee has erred in the interpretation of its selected literature; specifically, the in vitro data quoted fail to support LNT. Moreover, in vitro data cannot be considered as definitive proof of cancer development in intact organisms. This review is presented to stimulate a critical reevaluation by a BEIR VIII committee to reassess the validity, and use, of LNT and its derived policies.

Comment on "Background Ionizing Radiation and the Risk of Childhood Cancer: A Census-Based Nationwide Cohort Study".

We read with interest the article by Spycher et al. The authors claim their results suggest an increased risk of cancer among children exposed to external dose rates of background ionizing radiation of ≥ 200 nSv/h, compared with those exposed to < 100 nSv/h. However, all that the data show is a positive correlation rather than a causal result, which the word “risk” implies. Besides, these dose rates correspond to annual exposure levels of approximately 1.8 and 0.9 mSv, respectively. Considering that the average natural background exposure rate in the world is on the order of 2 mSv annually, with regions that range up to as much as 260 mSv (Ghiassi-Nejad et al. 2002), these are very low doses. Importantly, the background exposure rates were based not on actual measurements at children’s homes but on a geographic model. The authors noted they could not “exclude biases due to inaccurate exposure measurement.” It comes as no surprise, therefore, that the various hazard ratios are for the most part extremely low, and most of the 95% confidence intervals include the value of unity. Essentially, for children putatively exposed to a background dose rate exceeding 200 nSv/h, only the confidence intervals for all cancers, leukemias, and acute lymphoblastic leukemias exclude unity. This, taken seriously, would suggest a markedly increased cancer risk for these children, based on those exposure rates, but only if one begins by assuming that these levels of radiation contribute to producing cancers. There are numerous studies that show that such levels, in fact, elicit protective biological responses that lower the risk of cancer (Doss and Little 2014; Luckey 2008). Furthermore, given the very low attributed exposure rates and the imprecision in the actual exposure estimates, it is more likely than not that this increased childhood cancer occurrence is due to causes other than the background radiation exposure. For example, it is of interest that those children experiencing the highest estimated background dose rates are those who live in rural areas and in neighborhoods of lowest socioeconomic status. The authors state that adjustments were made for these two confounding factors, but since not much detail was provided regarding the adjustments made, the adequacy of the removal of these factors as causative contributions cannot be independently verified. Nevertheless, it is far more likely that these two factors are more important causes of childhood disease than the extremely low background exposures involved. Moreover, if it were true that exposure rates above 200 nSv/h, low though they be, were to somehow result in such a markedly increased cancer risk for children, the only reasonable governmental policy action would be to evacuate those children living in rural areas and poor neighborhoods, and relocate them to areas with lower radiation exposure in order to save lives. Failure to act in this manner would leave the government liable for allowing its younger citizens to die at an alarming rate. Studies like this cannot be taken seriously without such public health policy implications being likewise taken seriously.

Radiation Dose Does Indeed Matter: Proof That Invalidates The Linear No-Threshold Model

number of spontaneous, endogenous double-strand breaks (DSBs) (EDSBs), and further studies of the close fidelity of DSB repairs between EDSBs and radiation-induced DSBs (RIDSBs) for low doses/dose rates (as with CT scans) demonstrate that there can be no identifiable, increased CT-induced cancer risk compared with the background risk from spontaneous EDSBs in the whole body. This results from the body’s adaptive responses to LDR. Many CT scans produce doses less than 10 mSv, most are less than 20 mSv, and all are low in the LDR range. For a typical, lowdose CT scan covering 10% of the body, current literature shows that such low doses affect only DNA in a small fraction of cells in the target mass/volume. The RIDSBs from those are only about 3 in 1 million of the spontaneous EDSBs occurring in the body over the same time. Unor misrepaired RIDSBs from higher doses are about 0.001% of the unor misrepaired EDSBs in the body over the same time. For an essentially equal repair fidelity of RIDSBs and EDSBs, as discussed previously (6), unor misrepaired RIDSBs are only about 0.0003% of unor misrepaired EDSBs in the body over the same time. Further, all unor misrepaired DSBs still require other low-probability events (which are also addressed by adaptive response) to arrive at some cancerous prelude. Finally, the U.S. government has recently reported that cancer incidence declined by about 1%/y, and cancer mortality declined by about 1.6%/y over recent years, whereas CT usage has expanded, in support of increasing early detection and decreasing cancer mortality. Duncan et al. (1) repeat the words that ‘‘a threshold requires processes that leave no cells harboring DNA mutations’’ (3). Contradictorily, Duncan et al. (1) then cite how DNA errors of EDSB repair can lead to inactivating tumor suppression genes through premalignant lesions. These are obviously background, spontaneous DNA events, and with large contributions of EDSBs harboring DNA mutations, the fallacy of the quotation (3) is apparent: large, spontaneous, EDSB backgrounds exist in the body due to its metabolism, environments, and other factors; thresholds exist because LDR stimulates adaptive responses to remove IRDSBs and EDSB backgrounds, an enhanced dose response that reduces the body’s inventory of potential cancer precursors.

Nuclear Medicine Procedures Do Not Pose Cancer Risks in Women—Unappreciated or Otherwise

1Nuclear Physics Enterprises, Marlton, New Jersey; 2North Augusta, South Carolina; 3Departments of Radiology and Medicine (Emeritus), University of Cincinnati Medical Center, Cincinnati, Ohio; 4U.S. FDA (Retired, Diagnostic Radiologist), Green Valley, Arizona; 5Departments of Radiation Oncology, of Molecular and, Medical Pharmacology (Nuclear Medicine), and of Radiological Sciences (Retired), David Geffen School of Medicine at UCLA, Los Angeles, California; and 6Chair, Radiation Dose Assessment Resource (RADAR), Nashville, Tennessee