Polonium-210 is a naturally occurring radioactive
element that decays by emitting an alpha particle. It is in the air we breathe and also a component of tobacco
smoke.
Polonium-210 is used as an anti-static device in printing presses and gained widespread notoriety in 2006 after the
poisoning and subsequent death of a Russian citizen in London. More is known about the lethal effects of
polonium-210 at high doses than about late effects from low doses.
Cancer mortality was examined among 7,270 workers at the Mound nuclear facility near Dayton,
OH where
polonium-210 was used (1944-1972) in combination with
beryllium as a source of neutrons for triggering nuclear weapons. Other exposures included external gamma radiation and to a lesser extent
plutonium-238,
tritium and neutrons. Vital status and cause of death was determined through 2009. Standardized mortality ratios (SMRs) were computed for comparisons with the general population. Lifetime occupational doses from all places of employment were sought and incorporated into the analysis. Over 200,000 urine samples were analyzed to estimate radiation doses to body organs from
polonium and other internally deposited
radionuclides. Cox proportional hazards models were used to evaluate dose-response relationships for specific organs and tissues. Vital status was determined for 98.7% of the workers of which 3,681 had died compared with 4,073.9 expected (SMR 0.90; 95% CI 0.88-0.93). The mean dose from external radiation was 26.1 mSv (maximum 939.1 mSv) and the mean lung dose from external and internal radiation combined was 100.1 mSv (maximum 17.5 Sv). Among the 4,977 radiation workers, all
cancers taken together (SMR 0.86; 95% CI 0.79-0.93),
lung cancer (SMR 0.85; 95% CI 0.74-0.98), and other types of
cancer were not significantly elevated. Cox regression analysis revealed a significant positive dose-response trend for
esophageal cancer [relative risk (RR) and 95% confidence interval at 100 mSv of 1.54 (1.15-2.07)] and a negative dose-response trend for
liver cancer [RR (95% CI) at 100 mSv of 0.55 (0.23-1.32)]. For
lung cancer the RR at 100 mSv was 1.00 (95% CI 0.97-1.04) and for all
leukemias other than
chronic lymphocytic leukemia (CLL) it was 1.04 (95% CI 0.63-1.71). There was no evidence that
heart disease was associated with exposures [RR at 100 mSv of 1.06 (0.95-1.18)]. Assuming a relative biological effectiveness factor of either 10 or 20 for
polonium and
plutonium alpha particle emissions had little effect on the dose-response analyses.
Polonium was the largest contributor to lung dose, and a relative risk of 1.04 for
lung cancer at 100 mSv could be excluded with 95% confidence. A dose related increase in
cancer of the esophagus was consistent with a radiation etiology but based on small numbers. A dose-related decrease in
liver cancer suggests the presence of other modifying factors of risk and adds caution to interpretations. The absence of a detectable increase in total
cancer deaths and
lung cancer in particular associated with occupational exposures to
polonium (mean lung dose 159.8 mSv), and to
plutonium to a lesser extent (mean lung dose 13.7 mSv), is noteworthy but based on small numbers. Larger combined studies of U.S. workers are needed to clarify radiation risks following prolonged exposures and
radionuclide intakes.