This report presents the analysis of 50 years of mortality (1950–1999) and 31 years of cancer incidence (1969–1999) in a cohort of 2645 male Port Hope, Ontario, radium and uranium processing workers first employed sometime in 1932–1980. This is one of the largest cohort studies comprised of workers exposed to a unique combination of radium, uranium and γ-ray doses as a result of the refining and processing of radium and uranium. Overall, workers had similar rates of all causes of death and had lower rates of all cancers compared to the age-adjusted and calendar year-adjusted rates for the general male Canadian population, a likely healthy worker effect.22
A small but not significant association between workers’ occupational RDP exposure and lung cancer mortality was observed. It was somewhat smaller compared to the risks estimated in studies of Canadian uranium miners (ERR/100 WLM=0.21 (95% CI <−0.45 to 1.59), compared to 0.96 (0.56 to 1.56), 0.37 (0.23 to 0.59) and 0.47 (0.28 to 0.65) for Beaverlodge, Port Radium and Fluorspar miners, respectively).12
This was probably due to lower mean lifetime cumulative occupational RDP exposures (13.3, compared to 84.80, 180.08 and 377.70 WLM, respectively) and associated lower statistical power. The formal test of heterogeneity in risks with Beaverlodge and Port Radium miners was significant (p<0.001), indicating that RDP-associated risks of lung cancer were significantly different among Port Hope workers. While RDP risk estimates were generally similar for lung cancer mortality, risks of incident lung cancer were fourfold higher among uranium workers compared to radium workers, but CIs overlapped. No statistically significant increases in risks were estimated for any other cancer site or cause of death from RDP or γ-ray doses or a combination of both.
One of the strongest advantages of this study is its long-term follow-up with essentially complete ascertainment of cancer incidence and mortality. Another advantage is the comparatively high rates of follow-up, which were achieved by substantial improvements to the completeness of the nominal roll and work history files, multiple internal linkages to eliminate duplicate records, linkages to the Historic Tax Summary File, CMDB and CCDB, and the manual resolution of potential computer links. The large size of the cohort with detailed annual exposure information (n=2645), percentage of workers deceased (41.5%) and the length of follow-up for mortality (50 years) and cancer incidence (31 years) were substantially greater compared to other studies.3–7
Incidence and mortality data provided a complementary view of the effects of RDP exposures and γ-ray doses on the risk of cancer. Finally, we were able to identify workers primarily exposed to radium and those primarily exposed to uranium. This identification and analysis of radium workers are of particular interest since their risks would be expected to be different from those of uranium workers not exposed to radium. Although there is evidence of internal exposures to radium and uranium, the data are insufficient for meaningful dose calculations.
The most important limitation of this study is its limited statistical power due to the cohort size and low RDP exposures. This could be addressed through further follow-up and pooling of this study cohort with others from similar radium and uranium processing operations. There was no information on behavioural risk factors. For smoking to confound the RDP-related risk for lung cancer, it should be correlated with both RDP exposure and lung cancer. Smoking was banned at the Port Hope facility in the 1940s and 1950s, and was allowed on a very limited basis thereafter; however, people still smoked outside the workplace. There is no evidence it is associated with RDP exposure in Port Hope workers. We observed that mortality and incidence of tobacco-related cancers were similar to the general population of Canada, suggesting that smoking was not substantially elevated relative to the general population.
No assessment of RDP or γ-ray dose measurement errors on the risk estimates was conducted. RDP concentration estimates were based on plant inventories of radium-bearing materials, published or otherwise known values of radon emanation rates from various materials, building volumes and estimated air exchange rates. The material inventories very likely varied from day to day, but over the year it would have been exact and, therefore, not a significant contributor to error in annual average concentrations. Random errors in the radon emanation rates and building volumes would have been small and a small contributor to error. The equilibrium factor relating RDP to radon concentrations is a function of the air exchange rate and could be a significant contributor to errors in RDP exposures.
There was no individual γ-ray external dosimetry at the time of start-up, so all early exposures were estimated. For some early years, there were missing data on inventories in specific steps of the operation, but a statistical analysis of film badge readings through these years showed that the variance was small and this was not a significant contributor to error. Of greater importance was the variation in individual work habits and the question of whether an individual was actually present in the assumed location in the specific time period. But since the γ-ray dose estimates were estimated based on annual averages, the likely errors would be small. The measurement errors in exposure estimation almost certainly decreased with calendar time; thus, recent workers had lower mean errors than earlier workers.
We had limited data on incorporation and internal exposures to radium and uranium from urinalyses tests conducted since the mid-1960s, which could not be used for internal dose calculations. A recent study of workers employed at the AREVA NC uranium processing plant in France indicated that uranium carcinogenicity may depend both on its radiological and chemical qualities.25
The study reported a higher carcinogenic effect of slowly soluble reprocessed uranium on lung cancer and haematological cancers. Port Hope workers were exposed to a variety of uranium compounds of various levels of solubility (U3
) at higher concentrations and of greater solubility than was found in the ore. We did not have quantitative information on workers’ exposures to processing chemicals or uranium compounds, but observed that uranium workers had a fourfold higher association between RDP exposures and lung cancer incidence compared to radium workers, although the difference was not statistically significant. We also did not have information on quartz or fine silica dust exposures, which have been shown to independently increase the risk of lung cancer.26
However, a small fraction of Port Hope employees before 1955 would have had some dust exposure and the quartz content of that dust would have been much less than that from some of the other uranium properties operating at the time.
Cancers of the respiratory system (trachea, bronchus and lung; laryngeal and pleural cancer), lymphatic and haematopoietic tissue (leukaemia and non-Hodgkin's disease), digestive system (oesophageal, stomach, colorectal and pancreatic cancer), urinary system (kidney and bladder cancer) and other sites (bone, brain and CNS) and prostate were non-significantly elevated in several cohorts of nuclear workers with potential internal exposures to uranium.28
Studies of uranium processing workers reported increased risks of lymphatic,3
and non-malignant respiratory3
and renal diseases.3
In our analysis, the observed rates of sites potentially related to radium and uranium were significantly lower or similar to the general population and none of these cancer sites were found to be significantly related to workers’ RDP (internal) exposures or γ-ray doses. A similar absence of any significant increase in the risks of cancers potentially related to milling operations were recently reported for 904 non-miners employed at the Grants uranium mill in the USA.4
We observed higher rates of CVD mortality compared to the general population, especially a significantly increased mortality from hypertensive diseases. We retrieved and examined all death certificates for the hypertensive deaths (no autopsies). One case was miscoded, while in several other deaths, hypertension was mentioned among as many as five underlying causes of death, including diabetes and stroke, suggesting that hypertension could have been one of the many symptoms arising from the underlying cause of death. The net effect of this examination was to reduce the number of deaths from hypertensive disease by as much as half, eliminating the statistical significance of the elevated SMR.
Our analyses also indicated increased radiation-related risks of CVD mortality (ERR/100 WLM=0.10, 95% CI −0.05 to 0.32 and ERR/Sv=0.19, 95% CI −0.07 to 0.55), mostly driven by increased risks of ischaemic heart disease, although not statistically significant (ERR/100 WLM=0.16, 95% CI −0.05 to 0.50 and ERR/Sv=0.31, 95% CI −0.05 to 0.88). In models with two terms for RDP exposures and γ-ray doses, risks were due to γ-ray doses only, and the fit of the model did not improve with addition of the RDP exposures term (p=0.70). While some studies of uranium miners reported no association between RDP exposures and CVD mortality,16
a recent study suggested that increased risks might be due to slowly soluble uranium.31
Significant positive associations between γ-ray doses and increased risks of CVD mortality were reported in relation to low-dose (ERR/Sv=0.10, 95% CI 0.04 to 0.15)17
and moderate-dose radiation exposures (ERR/Sv=0.14, 95% CI 0.06 to 0.23).32
No association in relation to γ-ray doses was reported in the cohort of Wismut uranium miners,23
but the cumulative mean γ-ray dose for exposed miners was threefold lower compared to our cohort (47 vs 138 mSv). In the Wismut study,23
and in the Techa River Cohort exposed to internal and external exposures from various uranium fission products,33
CVD radiation-related risks increased with increasing lag time. In our analysis, risk estimates remained unchanged with 10-year and 15-year lags.
In conclusion, in this analysis of a cohort of workers exposed to radium and uranium refining and processing with detailed annual exposure information, over 90% of workers were followed up for at least 20 years, allowing sufficient time for occupationally induced cancers to develop. Port Hope workers were healthy compared to the general Canadian male population. We observed a small but not statistically significant increase in risk of lung cancer due to RDP exposures. Lung cancer risks of those exposed to uranium did not differ from those exposed to radium. All other causes of death or cancer incidence were not associated with occupational RDP exposures and γ-ray doses. Continued follow-up of the cohort and pooling with other cohorts of workers exposed to by-products of radium and uranium processing could provide valuable insight into risks from occupational uranium exposures and γ-ray doses and into suspected differences in risk with uranium miners.