Cancer risk following alpha-emitter exposure

2018 ◽  
Vol 47 (3-4) ◽  
pp. 115-125
Author(s):  
M. Tirmarche
Keyword(s):  
Lung Cancer ◽  
General Population ◽  
Cancer Risk ◽  
Epidemiological Studies ◽  
Task Group ◽  
Radiological Protection ◽  
Alpha Emitters ◽  
Decay Products ◽  
Alpha Emitter ◽  
Organ Specific

The International Commission on Radiological Protection (ICRP) mandated a task group (Task Group 64) to review recently published epidemiological studies related to cancer risk and incorporated alpha emitters, and to evaluate whether the results might consolidate or challenge assumptions underlying the current radiation protection system. Three major alpha emitters were considered: radon and its decay products, plutonium, and uranium. Results came mainly from cohorts of workers, while for radon, major studies of the general population contributed to a better understanding of the risk of lung cancer at low and chronic exposure. Selection criteria for the review were: assessment of individual exposure of the target organ, long duration of the health survey, availability of attained age at end of follow-up, and adjustment for major co-factors. Task Group 64 is composed of members from ICRP Committees 1 and 2 (because epidemiological and dosimetric expertise were needed) and external experts. A first report (ICRP Publication 115) considered the risk of lung cancer related to inhalation of radon and its decay products. As the estimated excess risk per unit of exposure was higher by a factor of 2 compared with a previous ICRP estimate in 1993, Task Group 64 suggested a reconsideration of the reference levels for the workplace and for the general population. A second report, using the same standardised methodology (lung cancer baselines, population, life expectancy), will include estimation of the cancer risk of nuclear workers exposed to plutonium, focusing on the risk of lung cancer. A comparison of these risks with those of populations exposed to external gamma radiation alone will be made in the near future. For uranium, the results related to the organ-specific dose were too sparse to draw reliable conclusions, despite a recent publication. More research is needed on this topic.

scholarly journals Characteristics of Thoron (220Rn) and Its Progeny in the Indoor Environment

2020 ◽  
Vol 17 (23) ◽  
pp. 8769
Author(s):  
Shinji Tokonami
Keyword(s):  
Lung Cancer ◽  
Cancer Risk ◽  
Half Life ◽  
Indoor Environment ◽  
Lung Cancer Risk ◽  
Epidemiological Studies ◽  
Radiological Protection ◽  
Activity Levels ◽  
Radon Exposure ◽  
Thoron Progeny

The present paper outlines characteristics of thoron and its progeny in the indoor environment. Since the half-life of thoron (220Rn) is very short (55.6 s), its behavior is quite different from the isotope radon (222Rn, half-life 3.8 days) in the environment. Analyses of radon and lung cancer risk have revealed a clearly positive relationship in epidemiological studies among miners and residents. However, there is no epidemiological evidence for thoron exposure causing lung cancer risk. In contrast to this, a dosimetric approach has been approved in the International Commission on Radiological Protection (ICRP) Publication 137, from which new dose conversion factors for radon and thoron progenies can be obtained. They are given as 16.8 and 107 nSv (Bq m−3 h)−1, respectively. It implies that even a small quantity of thoron progeny will induce higher radiation exposure compared to radon. Thus, an interest in thoron exposure is increasing among the relevant scientific communities. As measurement technologies for thoron and its progeny have been developed, they are now readily available. This paper reviews measurement technologies, activity levels, dosimetry and resulting doses. Although thoron has been underestimated in the past, recent findings have revealed that reassessment of risks due to radon exposure may need to take the presence of thoron and its progeny into account.

scholarly journals Second Cancers After Squamous Cell Carcinoma and Adenocarcinoma of the Cervix

2009 ◽  
Vol 27 (6) ◽  
pp. 967-973 ◽  
Author(s):  
Anil K. Chaturvedi ◽  
Ruth A. Kleinerman ◽  
Allan Hildesheim ◽  
Ethel S. Gilbert ◽  
Hans Storm ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Squamous Cell Carcinoma ◽  
General Population ◽  
Cancer Risk ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Lung Cancer Risk ◽  
Second Cancer ◽  
Second Cancers ◽  
Second Cancer Risk

Purpose Although cervical squamous cell carcinoma (SCC) and adenocarcinoma (AC) are both caused by human papillomavirus (HPV) infection, they differ in cofactors such as cigarette smoking. We assessed whether these cofactor differences translate into differences in second cancer risk. Patients and Methods We assessed second cancer risk among 85,109 cervical SCC and 10,280 AC survivors reported to population-based cancer registries in Denmark, Finland, Norway, Sweden, and the United States. Risks compared to the general population were assessed using standardized incidence ratios (SIR). Results Overall cancer risk was significantly increased among both cervical SCC survivors (n = 10,559 second cancers; SIR, 1.31; 95% CI, 1.29 to 1.34) and AC survivors (n = 920 second cancers; SIR, 1.29; 95% CI, 1.22 to 1.38). Risks of HPV-related and radiation-related cancers were increased to a similar extent among cervical SCC and AC survivors. Although significantly increased in both groups when compared with the general population, risk of smoking-related cancers was significantly higher among cervical SCC than AC survivors (P = .015; SIR for cervical SCC = 2.07 v AC = 1.78). This difference was limited to lung cancer (SIR for cervical SCC = 2.69 v AC = 2.18; P = .026). The increased lung cancer risk among cervical AC survivors was observed for both lung SCC and lung AC. SIRs for second cancers of the colon, soft tissue, melanoma, and non-Hodgkin's lymphoma were significantly higher among cervical AC than SCC survivors. Conclusion The second cancer profiles among cervical SCC and AC survivors mirror the similarities and differences in cofactors for these two histologies. Because smoking is not a cofactor for cervical AC, the increased lung cancer risk suggests a role for additional factors.

DOSIMETRIC AND EPIDEMIOLOGICAL APPROACHES TO RADON LUNG CANCER RISK ASSESSMENT

2019 ◽  
Vol 184 (3-4) ◽  
pp. 285-289
Author(s):  
J P Mc Laughlin
Keyword(s):  
Lung Cancer ◽  
Risk Assessment ◽  
Cancer Risk ◽  
Lung Cancer Risk ◽  
Epidemiological Studies ◽  
Cancer Risk Assessment ◽  
Radon Exposure ◽  
Conversion Factors

Abstract The two principal approaches used to assess the risk of lung cancer due to radon exposure are those based on dosimetric modelling and on epidemiology. Outline accounts are given of the main features of dosimetric models that have evolved over past decades. The main results of some occupational and residential epidemiological studies are also discussed. The doubling of the ICRP radon dose conversion factors estimated using the epidemiological based dose conversion convention in the period 1993–2010 are discussed. Also discussed is the more recent ICRP approach in which it is recommended that in future the doses should be estimated on the basis of dosimetric and biokinetic models thereby treating radon and its progeny as other radionuclides within its system of protection.

scholarly journals Impact of occupational carcinogens on lung cancer risk in a general population

2012 ◽  
Vol 41 (3) ◽  
pp. 711-721 ◽  
Author(s):  
Sara De Matteis ◽  
Dario Consonni ◽  
Jay H Lubin ◽  
Margaret Tucker ◽  
Susan Peters ◽  
...  
Keyword(s):  
Lung Cancer ◽  
General Population ◽  
Cancer Risk ◽  
Lung Cancer Risk

scholarly journals Existing General Population Models Inaccurately Predict Lung Cancer Risk in Patients Referred for Surgical Evaluation

2011 ◽  
Vol 91 (1) ◽  
pp. 227-233 ◽  
Author(s):  
James M. Isbell ◽  
Stephen Deppen ◽  
Joe B. Putnam ◽  
Jonathan C. Nesbitt ◽  
Eric S. Lambright ◽  
...  
Keyword(s):  
Lung Cancer ◽  
General Population ◽  
Cancer Risk ◽  
Lung Cancer Risk ◽  
Population Models ◽  
Surgical Evaluation

scholarly journals Occupational exposure to organic dust increases lung cancer risk in the general population

Thorax ◽  
2011 ◽  
Vol 67 (2) ◽  
pp. 111-116 ◽  
Author(s):  
Susan Peters ◽  
Hans Kromhout ◽  
Ann C Olsson ◽  
Heinz-Erich Wichmann ◽  
Irene Brüske ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Occupational Exposure ◽  
General Population ◽  
Cancer Risk ◽  
Lung Cancer Risk ◽  
Organic Dust

Passive Smoking and Lung Cancer Association: A Result of Bias?

1987 ◽  
Vol 6 (6) ◽  
pp. 517-524 ◽  
Author(s):  
P.N. Lee
Keyword(s):  
Lung Cancer ◽  
Cancer Risk ◽  
Passive Smoking ◽  
Lung Cancer Risk ◽  
Smoking Habit ◽  
Epidemiological Studies ◽  
The Other ◽  
Smoking Habits ◽  
Self Reports ◽  
Never Smokers

1 Epidemiological studies have reported that non-smokers married to smokers have a lung cancer risk 20-50% higher than that of non-smokers married to non-smokers. 2 In contrast, extrapolation based on relative smoke exposure of passive and active smokers would predict a much smaller effect. 3 This paper examines the possibility that bias due to misclassification of smoking habits, coupled with between spouse smoking habit concordance, could account for this discrepancy. 4 One thousand seven hundred and seventy-five subjects were asked about their smoking habits and use of other nicotine products in a non-health context likely to minimize underreporting of smoking. One thousand five hundred and thirty-seven provided saliva for cotinine analysis. Of 808 who claimed not to be users of such products, 2.5% had cotinine values above 30 ng/ml, suggesting their self reports were false. In another study 540 subjects were interviewed in 1980 and in 1985. Ten per cent claiming on one occasion never to have smoked, made inconsistent statements on the other occasion. A third study showed a strong tendency for smokers to marry smokers. 5 Estimates of bias based on these data indicate that misclassification can explain the unexpectedly high lung cancer risk associated with spouse smoking in epidemiological studies of self-reported never smokers.

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