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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 (

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.

In the 1950s, the Mayak nuclear weapons facility in Russia discharged liquid radioactive wastes into the Techa River causing exposure of riverside residents to protracted low-to-moderate doses of radiation. Almost 10,000 women received estimated doses to the stomach of up to 0.47 Gray (Gy) (mean dose=0.04 Gy) from external gamma-exposure and (137)Cs incorporation. We have been following this population for cancer incidence and mortality and as in the general Russian population, we found a significant temporal trend of breast cancer incidence. A significant linear radiation dose-response relationship was observed (P=0.01) with an estimated excess relative risk per Gray (ERR/Gy) of 5.00 (95% confidence interval (CI), 0.80, 12.76). We estimated that approximately 12% of the 109 observed cases could be attributed to radiation.

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.