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Previous studies suggest that both acute and protracted radiation exposures are associated with an increased risk of leukaemia (Curtis et al, 1994; Preston et al, 1994; Gilbert, 2009; Daniels and Schubauer-Berigan, 2011). An estimate of the proportion of leukaemia cases associated with natural background exposures has been made using published risk models (Kendall et al, 2011) and variation in the risk of childhood leukaemia associated with variation in natural background radiation levels observed (Kendall et al, 2013). The challenge remains to quantify and describe the dose–response relationship from low dose (

For almost 50 y, the Life Span Study cohort of atomic bomb survivor studies has been the primary source of the quantitative estimates of cancer and non-cancer risks that form the basis of international radiation protection standards. However, the long-term follow-up and extensive individual dose reconstruction for the Russian Mayak worker cohort (MWC) and Techa River cohort (TRC) are providing quantitative information about radiation effects on cancer risks that complement the atomic bomb survivor-based risk estimates. The MWC, which includes ~26 000 men and women who began working at Mayak between 1948 and 1982, is the primary source for estimates of the effects of plutonium on cancer risks and also provides information on the effects of low-dose rate external gamma exposures. The TRC consists of ~30 000 men and women of all ages who received low-dose-rate, low-dose exposures as a consequence of Mayak's release of radioactive material into the Techa River. The TRC data are of interest because the exposures are broadly similar to those experienced by populations exposed as a consequence of nuclear accidents such as Chernobyl. In this presentation, it is described the strengths and limitations of these three cohorts, outline and compare recent solid cancer and leukemia risk estimates and discussed why information from the Mayak and Techa River studies might play a role in the development and refinement of the radiation risk estimates that form the basis for radiation protection standards.

Background Previous studies have shown that acute external in utero exposure to ionizing radiation can increase cancer risk. It is not known whether chronic exposure at low dose rates, including due to radionuclide intake, influences the lifetime risk of solid cancers in the offspring. The objective of this study was to investigate solid cancer risk after in utero irradiation. Methods Cancer incidence and mortality over a 60-year period (from January 1950 to December 2009) were analyzed in the Urals Prenatally Exposed Cohort (UPEC). The cohort comprised in utero exposed offspring of Mayak Production Association female workers and of female residents of Techa River villages. Some of the offspring also received postnatal exposure, either due to becoming radiation workers themselves or due to continuing to live in the contaminated areas of the Techa River. The mortality analyses comprised 16,821 subjects (601,372 person-years), and the incidence analyses comprised 15,813 subjects (554,411 person-years). Poisson regression was used to quantify the relative risk as a function of the in utero soft tissue dose (with cumulative doses up to 944.9 mGy, mean dose of 14.1 mGy in the pooled cohort) and the postnatal stomach dose for solid cancer incidence and mortality. Results When a log-linear model was used, relative risk of cancer per 10 mGy of in utero dose was 0.99 (95% confidence interval (CI) = 0.96 to 1.01) based on incidence data and 0.98 (CI = 0.94 to 1.01) based on mortality data. Postnatal exposure to ionizing radiation was positively associated with the solid cancer risk in members of the UPEC, with a relative risk of 1.02 per 10mGy CI = 1.00 to 1.04). Conclusions No strong evidence was found that chronic low-dose-rate exposure of the embryo and fetus increased the risk of solid cancers in childhood or in adulthood. For both incidence and mortality, a tendency towards a decreased relative risk was noted with increasing doses to soft tissues of the fetus. Further follow-up will provide more precise radiation risk estimates of solid cancer as cohort members are approaching their 60s and cancer becomes more common.

Beginning in 1950, people living on the banks of the Techa River received chronic low-dose-rate internal and external radiation exposures as a result of releases from the Mayak nuclear weapons plutonium production facility in the Southern Urals region of the Russian Federation. The Techa River cohort includes about 30,000 people who resided in riverside villages sometime between 1950 and 1960. Cumulative red bone marrow doses range up to 2 Gy with a mean of 0.3 Gy and a median of 0.2 Gy. Between 1953 and 2005, 93 first primary cases of leukemia, including 23 cases of chronic lymphatic leukemia (CLL), were ascertained among the cohort members. A significant linear dose-response relationship was seen for leukemias other than CLL (P < 0.001), but not for CLL. The estimated excess relative risk per Gy is 4.9 (95% confidence interval (CI): 1.6; 14.3) for leukemias other than CLL and less than 0 (95% upper bound 1.4) for CLL.

Our understanding of cancer risk from ionizing radiation is largely based on studies of populations exposed at high dose and high dose rates. Less certain is the magnitude of cancer risk from protracted, low-dose and low-dose-rate radiation exposure. We estimated the dose-response relationship for solid cancer mortality in a cohort of 29,730 individuals who lived along the Techa River between 1950 and 1960. This population was exposed to both external γ radiation and internal (90)Sr, (137)Cs and other radionuclides after the release of radioactive waste into the river by the Mayak Radiochemical Plant. The analysis utilized the latest individualized doses from the Techa River Dosimetry System (TRDS) 2009. We estimated excess relative risks (ERRs) per Gy for solid cancer mortality using Poisson regression methods with 95% confidence intervals (CIs) and P values based on likelihood ratio tests. Between 1950 and 2007, there were 2,303 solid cancer deaths. The linear ERR/Gy = 0.61 (95%; CI 0.04-1.27), P = 0.03. It is estimated that approximately 2% (49.7) of solid cancers deaths were associated with the radiation exposure. Our results, based on 2,303 solid cancer deaths and more than 50 years of follow-up, support an increased risk of solid cancer mortality following protracted radiation exposure from the Techa River contamination. The wide confidence interval of our estimate reflects the challenges of quantifying and describing the shape of the dose-response relationship in the low dose range. Nevertheless, the risk estimates provide important information concerning health risks from whole-body radiation exposure that can occur from accidents that result in wide-scale environmental contamination.

In the present paper, analysis of solid cancer mortality and incidence risk after radiation exposure in the Techa River Cohort in the Southern Urals region of Russia is described. Residents along the Techa River received protracted exposure to ionizing radiation in the 1950s due to the releases of radioactive materials from the Mayak Production Association. The current follow-up through December 2003 includes individuals exposed on the Techa riverside within the Chelyabinsk and Kurgan oblasts using mortality data, and within the Chelyabinsk oblast using incidence data. The analysis was performed by means of the biologically based two-stage clonal expansion (TSCE) model and conventional excess relative risk models. For the mortality and incidence cohorts, central estimates of the excess relative risk per dose of 0.85 Gy(-1) (95% CI 0.36; 1.38) and 0.91 Gy(-1) (95% CI 0.35; 1.52) were found, respectively. For both the mortality and incidence cohorts, the best description of the radiation risk was achieved with the same TSCE model including a lifelong radiation effect on the promotion rate of initiated cells. An increase in the excess risk with attained age was observed, whereas no significant change of risk with age at exposure was seen. Direct comparison of the mortality and incidence cohorts showed that the excess relative risk estimates agreed very well in both cohorts, as did the excess absolute risk and the hazard after correction for the different background rates.