scholarly journals Potential for Adult-Based Epidemiological Studies to Characterize Overall Cancer Risks Associated with a Lifetime of CT Scans

2014 ◽  
Vol 181 (6) ◽  
pp. 584-591 ◽  
Author(s):  
Igor Shuryak ◽  
Jay H. Lubin ◽  
David J. Brenner
2021 ◽  
Vol 94 (1126) ◽  
pp. 20210471 ◽  
Author(s):  
Amy Berrington de Gonzalez ◽  
Elisa Pasqual ◽  
Lene Veiga

20 years ago, 3 manuscripts describing doses and potential cancer risks from CT scans in children raised awareness of a growing public health problem. We reviewed the epidemiological studies that were initiated in response to these concerns that assessed cancer risks from CT scans using medical record linkage. We evaluated the study methodology and findings and provide recommendations for optimal study design for new efforts. We identified 17 eligible studies; 13 with published risk estimates, and 4 in progress. There was wide variability in the study methodology, however, which made comparison of findings challenging. Key differences included whether the study focused on childhood or adulthood exposure, radiosensitive outcomes (e.g. leukemia, brain tumors) or all cancers, the exposure metrics (e.g. organ doses, effective dose or number of CTs) and control for biases (e.g. latency and exclusion periods and confounding by indication). We were able to compare results for the subset of studies that evaluated leukemia or brain tumors. There were eight studies of leukemia risk in relation to red bone marrow (RBM) dose, effective dose or number of CTs; seven reported a positive dose–response, which was statistically significant (p < 0.05) in four studies. Six of the seven studies of brain tumors also found a positive dose–response and in five, this was statistically significant. Mean RBM dose ranged from 6 to 12 mGy and mean brain dose from 18 to 43 mGy. In a meta-analysis of the studies of childhood exposure the summary ERR/100 mGy was 1.78 (95%CI: 0.01–3.53) for leukemia/myelodisplastic syndrome (n = 5 studies) and 0.80 (95%CI: 0.48–1.12) for brain tumors (n = 4 studies) (p-heterogeneity >0.4). Confounding by cancer pre-disposing conditions was unlikely in these five studies of leukemia. The summary risk estimate for brain tumors could be over estimated, however, due to reverse causation. In conclusion, there is growing evidence from epidemiological data that CT scans can cause cancer. The absolute risks to individual patients are, however, likely to be small. Ongoing large multicenter cohorts and future pooling efforts will provide more precise risk quantification.


1998 ◽  
Vol 28 (4) ◽  
pp. 715-724 ◽  
Author(s):  
Lennart Hardell ◽  
Mikael Eriksson ◽  
Olav Axelson

Since the late 1970s several epidemiological studies have appeared linking exposure to phenoxy herbicides or chlorophenols to some malignant tumors. Most of these compounds are contaminated with dioxins and dibenzofurans; for example, 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) is a contaminant of 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), a component of Agent Orange which was sprayed in Vietnam during the war. The results of some of the epidemiological studies on cancer risks associated with exposure to these compounds have been manipulated and misinterpreted, particularly by the Australian Royal Commission on the Use and Effects of Chemical Agents on Australian Personnel in Vietnam. Furthermore, a book on Australian war history entitled Medicine at War, commissioned by the Federal Government, reiterates several of these misinterpretations, despite available contrary evaluations from Australian and U.S. authorities. These remarkable and confusing circumstances in the scientific process are considered also in the light of the recent classification of TCDD as carcinogenic to humans, Group 1, by a Working Group at the International Agency for Research on Cancer in Lyon, France.


2020 ◽  
Vol 70 (7) ◽  
pp. 476-484 ◽  
Author(s):  
H Chartier ◽  
P Fassier ◽  
K Leuraud ◽  
S Jacob ◽  
C Baudin ◽  
...  

Abstract Background Medical workers are the largest group of workers occupationally exposed to low doses of ionizing radiation (IR) worldwide. Aims This review presents all the cohorts of medical workers exposed in the world and summarizes cancer risks associated with radiation exposure in this population. Methods Epidemiological studies on health professionals exposed to IR published from 1975 to 2019 were reviewed. Strength of evidence was assessed according to the modified Royal College of General Practitioners three-star system. Results Among the 16 epidemiological studies focusing on cancers from 11 cohorts among medical staff exposed to radiation, higher risks of cancer were observed for pre-1950 exposure and for medical workers who performed fluoroscopically guided interventional procedures or radionuclides procedures compared to those who did not. However, strength of evidence supporting the associations remains moderate as several methodological limits including the lack of dosimetry data, lifestyle factors and recent updates may obscure the link between medical occupational exposure and cancer occurrence. Conclusions Excess risk of cancer is suspected for high and former exposures. The more highly exposed professions, i.e. interventional physicians and nuclear medicine workers, should be monitored carefully. Collaborative projects aiming to increase the quantity and quality of information of the studied populations would be a key point


2019 ◽  
Vol 64 (5) ◽  
pp. 81-88
Author(s):  
В. Уйба ◽  
V. Uyba ◽  
А. Аклеев ◽  
A. Akleev ◽  
Т. Азизова ◽  
...  

The current paper is devoted to the outcomes of the 66-th UNSCEAR Session which took place in Vienna during 10–14 June 2018. Within the framework of the meetings of the Working Group and subgroups the documents on the following projects were discussed: R.733. Evaluation of selected health effects and inference of risk due to radiation exposure. R.734. Evaluation of medical exposures to ionizing radiation. R.735. Evaluation of occupational exposures to ionizing radiation. R.736. Lung cancer from exposure to radon. R.737. Biological mechanisms relevant for the inference of cancer risks from low-dose radiation. R.738. Levels and effects of radiation exposure due to the accident at the Fukushima Daiichi nuclear power station: implications of information published since the 2013 UNSCEAR report. R.739. Second primary cancer after radiotherapy. R.740. Epidemiological studies of radiation and cancer. The Committee also discussed: the future research program; report to the UN General Assembly; implementation of a strategy plan to improve collection, analysis and dissemination of data on radiation exposure; public outreach activity including the strategy for the period 2020–2024.


2020 ◽  
Vol 2020 (56) ◽  
pp. 188-200 ◽  
Author(s):  
Michael Hauptmann ◽  
Robert D Daniels ◽  
Elisabeth Cardis ◽  
Harry M Cullings ◽  
Gerald Kendall ◽  
...  

Abstract Background Ionizing radiation is an established carcinogen, but risks from low-dose exposures are controversial. Since the Biological Effects of Ionizing Radiation VII review of the epidemiological data in 2006, many subsequent publications have reported excess cancer risks from low-dose exposures. Our aim was to systematically review these studies to assess the magnitude of the risk and whether the positive findings could be explained by biases. Methods Eligible studies had mean cumulative doses of less than 100 mGy, individualized dose estimates, risk estimates, and confidence intervals (CI) for the dose-response and were published in 2006–2017. We summarized the evidence for bias (dose error, confounding, outcome ascertainment) and its likely direction for each study. We tested whether the median excess relative risk (ERR) per unit dose equals zero and assessed the impact of excluding positive studies with potential bias away from the null. We performed a meta-analysis to quantify the ERR and assess consistency across studies for all solid cancers and leukemia. Results Of the 26 eligible studies, 8 concerned environmental, 4 medical, and 14 occupational exposure. For solid cancers, 16 of 22 studies reported positive ERRs per unit dose, and we rejected the hypothesis that the median ERR equals zero (P = .03). After exclusion of 4 positive studies with potential positive bias, 12 of 18 studies reported positive ERRs per unit dose (P  = .12). For leukemia, 17 of 20 studies were positive, and we rejected the hypothesis that the median ERR per unit dose equals zero (P  = .001), also after exclusion of 5 positive studies with potential positive bias (P  = .02). For adulthood exposure, the meta-ERR at 100 mGy was 0.029 (95% CI = 0.011 to 0.047) for solid cancers and 0.16 (95% CI = 0.07 to 0.25) for leukemia. For childhood exposure, the meta-ERR at 100 mGy for leukemia was 2.84 (95% CI = 0.37 to 5.32); there were only two eligible studies of all solid cancers. Conclusions Our systematic assessments in this monograph showed that these new epidemiological studies are characterized by several limitations, but only a few positive studies were potentially biased away from the null. After exclusion of these studies, the majority of studies still reported positive risk estimates. We therefore conclude that these new epidemiological studies directly support excess cancer risks from low-dose ionizing radiation. Furthermore, the magnitude of the cancer risks from these low-dose radiation exposures was statistically compatible with the radiation dose-related cancer risks of the atomic bomb survivors.


2015 ◽  
Vol 370 (1667) ◽  
pp. 20140121 ◽  
Author(s):  
Abraham Haim ◽  
Abed E. Zubidat

The adverse effects of excessive use of artificial light at night (ALAN) are becoming increasingly evident and associated with several health problems including cancer. Results of epidemiological studies revealed that the increase in breast cancer incidents co-distribute with ALAN worldwide. There is compiling evidence that suggests that melatonin suppression is linked to ALAN-induced cancer risks, but the specific genetic mechanism linking environmental exposure and the development of disease is not well known. Here we propose a possible genetic link between environmental exposure and tumorigenesis processes. We discuss evidence related to the relationship between epigenetic remodelling and oncogene expression. In breast cancer, enhanced global hypomethylation is expected in oncogenes, whereas in tumour suppressor genes local hypermethylation is recognized in the promoter CpG chains. A putative mechanism of action involving epigenetic modifications mediated by pineal melatonin is discussed in relation to cancer prevalence. Taking into account that ALAN-induced epigenetic modifications are reversible, early detection of cancer development is of great significance in the treatment of the disease. Therefore, new biomarkers for circadian disruption need to be developed to prevent ALAN damage.


Author(s):  
Vincent Bessonneau ◽  
Ruthann A. Rudel

Breast cancer is an important cause of morbidity and mortality for women, yet a significant proportion of variation in individual risk is unexplained. It is reasonable to infer that unexplained breast cancer risks are caused by a myriad of exposures and their interactions with genetic factors. Most epidemiological studies investigating environmental contribution to breast cancer risk have focused on a limited set of exposures and outcomes based on a priori knowledge. We hypothesize that by measuring a rich set of molecular information with omics (e.g., metabolomics and adductomics) and comparing these profiles using a case-control design we can pinpoint novel environmental risk factors. Specifically, exposome-wide association study approaches can be used to compare molecular profiles between controls and either breast cancer cases or participants with phenotypic measures associated with breast cancer (e.g., high breast density, chronic inflammation). Current challenges in annotating compound peaks from biological samples can be addressed by creating libraries of environmental chemicals that are breast cancer relevant using publicly available high throughput exposure and toxicity data, and by mass spectra fragmentation. This line of discovery and innovation will extend understanding of how environmental exposures interact with genetics to affect health, and provide evidence to support new breast cancer prevention strategies.


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