Lung Cancer in Mayak Workers

University of Utah, Salt Lake City, Utah, United States
Radiation Research (Impact Factor: 2.91). 12/2004; 162(5):505-16. DOI: 10.1667/RR3259
Source: PubMed


The cohort of nuclear workers at the Mayak Production Association, located in the Russian Federation, is a unique resource for providing information on the health effects of exposure to plutonium as well as the effects of protracted external dose. Lung cancer mortality risks were evaluated in 21,790 Mayak workers, a much larger group than included in previous evaluations of lung cancer risks in this cohort. These analyses, which included 655 lung cancer deaths occurring in the period 1955-2000, were the first to evaluate both excess relative risk (ERR) and excess absolute risk (EAR) models and to give detailed attention to the modifying effects of gender, attained age and age at hire. Lung cancer risks were found to be significantly related to both internal dose to the lung from plutonium and external dose, and risks were described adequately by linear functions. For internal dose, the ERR per gray for females was about four times higher than that for males, whereas the EAR for females was less than half that for males; the ERR showed a strong decline with attained age, whereas the EAR increased with attained age until about age 65 and then decreased. Parallel analyses of lung cancer mortality risks in Mayak workers and Japanese A-bomb survivors were also conducted. Efforts currently under way to improve both internal and external dose estimates, and to develop data on smoking, should result in more accurate risk estimates in the future.

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Available from: Mikhail E Sokolnikov, Apr 18, 2014
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    • "It is also the first cancer study to make use of the recently updated dosimetry system MWDS-2008. Neoplasms of the lung, liver, and bone are highly lethal, and therefore, the quantitative differences between the results of this study and those obtained from the earlier studies (Gilbert et al. 2004; Sokolnikov et al. 2008) are likely due mainly to the use of the revised dosimetry system (MWDS-2008 in place of earlier systems; e.g., Doses-2005), although the additional follow-up may also contribute. The results of Sokolnikov et al. (2008) can be compared most easily to this study. "
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    ABSTRACT: This paper presents the results of analyses of the incidence of malignant neoplasms in lung, liver, and bone and associated connective tissues among Mayak nuclear workers exposed to both internally incorporated plutonium and to external gamma radiation. The study cohort included 22,373 individuals employed at the reactors and radiochemical and plutonium production facilities of the Mayak nuclear complex during 1948-1982 and followed up to the end of 2004. All analyses were carried out by Poisson regression, and the doses used were derived using a recently available update of organ doses, Mayak doses-2008. There was clear evidence for the linear association between internal plutonium dose and the risk of lung cancer. For males, there was evidence of a significant internal plutonium dose response for all histological types of lung cancer evaluated (adenocarcinoma, squamous-cell, and other epithelial); the estimated excess relative risk (ERR)/Gy for adenocarcinoma was the largest (ERR/Gy = 32.5; 95% CI: 16.3; 71.9), about 11-fold higher than that for squamous-cell lung cancer (ERR/Gy = 3.1; 95% CI: 0.3; 9.1). The relationship between liver cancer risk and plutonium exposure was best described by a linear-quadratic (LQ) function, but the LQ effect was diminished after restricting internal doses <2 Gy. Hepatocellular cancer was the most frequently observed type of liver cancer associated with internal plutonium exposure, and hemangiosarcomas were exclusively observed only at high internal plutonium doses (>4 Gy). For malignant neoplasms of bone and associated connective tissues, the trend was not statistically significant in relation to internal plutonium dose, but a statistically significantly higher risk (RR=13.7; 95% CI= 3.0; 58.5) was found among unmonitored female plutonium workers who were employed in the most hazardous plutonium production facility commissioned prior to 1950.
    Full-text · Article · Aug 2013 · Health physics
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    • "Insufficient data was given in many published papers for others to evaluate lung cancer risk at low doses. Low-dose and smoking data used to determine the excess relative risk (ERR) for lung cancer in Mayak workers was not provided (Kreisheimer et al. 2000; Shilnikova et al. 2003; Gilbert et al. 2004). Lung cancer mortality estimates for the Semipalatinsk cohort, downwind from the Kazakhstan weapons test site, did not adequately control for smoking; no data was given for the 20–70 mSv cohort and data for the 70–249 mSv cohort was combined from several dose groups (Bauer et al. 2005). "
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    ABSTRACT: Confounding factors in radiation pulmonary carcinogenesis are passive and active cigarette smoke exposures and radiation hormesis. Significantly increased lung cancer risk from ionizing radiation at lung doses < 1 Gy is not observed in never smokers exposed to ionizing radiations. Residential radon is not a cause of lung cancer in never smokers and may protect against lung cancer in smokers. The risk of lung cancer found in many epidemiological studies was less than the expected risk (hormetic effect) for nuclear weapons and power plant workers, shipyard workers, fluoroscopy patients, and inhabitants of high-dose background radiation. The protective effect was noted for low- and mixed high- and low-linear energy transfer (LET) radiations in both genders. Many studies showed a protection factor (PROFAC) > 0.40 (40% avoided) against the occurrence of lung cancer. The ubiquitous nature of the radiation hormesis response in cellular, animal, and epidemio-logical studies negates the healthy worker effect as an explanation for radiation hormesis. Low-dose radiation may stimulate DNA repair/apoptosis and immunity to suppress and eliminate cigarette-smoke-induced transformed cells in the lung, reducing lung cancer occurrence in smokers.
    Full-text · Article · Jan 2008 · Dose-Response
    • "The study showed that the additive model was a poor fit to the data, compared to the multiplicative model. The estimated ERR adjusted for smoking (ERR per unit internal 5 yr lagged lung dose from incorporated plutonium for male was 4.5, GSE 1.4) expresses good agreement with estimations of extended cohort study (Gilbert et al., 2004). "
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    ABSTRACT: Assessment of relative biological effectiveness (RBE) for a radiation in the cases of inhalation of radon progeny and incorporation of plutonium in lung is based on simulation of lung cancer radiation risk for alpha and external reference types of radiation. Specific radiation risk models developed on the results of direct epidemiological studies are used for simulation. These include published risk models for nuclear workers of the Mayak facilities in the former Soviet Union exposed to incorporated plutonium (Kreisheimer et al., 2003; Gilbert et al., 2004) and underground miners exposed to radon progenies (BEIR VI, 1999). Additionally, a lung cancer risk model is developed for a case of population indoor radon exposure. Lung cancer risk related to external exposure is estimated using the risk model developed for the analyses of Japanese atomic bomb survivors (Preston et al., 2003). Uncertainties of risk models parameters are considered and the uncertainties of RBE are estimated using the results of lifetime lung cancer risk simulation, which is done implementing a Monte Carlo approach. Estimated median value of RBE in case of indoor radon exposure is 1.5 with 90% range 0.4-7. In the case of the two models developed by BEIR VI for lung cancer risk due to radon exposure in underground miners, the median values of RBE are 2.1 and 4.4 with 90% ranges 0.3-17 and 0.7-45, respectively. The two different models for lung cancer risk related to plutonium exposure resulted in close estimates of RBE: median value of 12 and 13 with 90% range 4-104 and 4-136, respectively.
    No preview · Article · May 2006 · Journal of Toxicology and Environmental Health Part A
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