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8
Conclusions
In this chapter, the committee further evaluates the peer-reviewed published literature to draw conclusions about the long-term human health outcomes associated with exposure to natural uranium (as occurred in uranium-processing mills and other facilities and in residences) or depleted uranium (as occurred in the Gulf War). The discussion is organized according to cancer (or malignant) and noncancer (or nonmalignant) health outcome. Tables included at the end of this chapter contain results from the studies on which the committee bases its conclusions.
The traditional 5% level of statistical significance is used in describing the committee’s conclusions regarding associations. Associations that did not reach the 5% level of statistical significance are described below as nonsignificant.
CANCER OUTCOMES
This section presents the strength of associations between exposure to natural or depleted uranium and particular cancer outcomes. It draws on the information from the many studies that were described in Chapter 7 and on Gulf War and Health, Volume 1: Depleted Uranium, Pyridostigmine Bromide, Sarin, Vaccines (IOM, 2000; hereafter referred to as Volume 1). The committee focused on the following sites: leukemias, lymphomas, and cancers of the lung, bone, kidney, bladder, stomach, central nervous system, prostate, and testis.
Most of the studies examined cancer mortality, but several studies of UK Gulf War veterans, Balkans veterans, and the Finnish drinking-water cohort also investigated cancer incidence. Because several cancers of interest are associated
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with a generally good chance of survival, cancer incidence (ascertainable from cancer-registration programs) is a better indicator of cancer risk than cancer-related mortality.
Results of cancer studies conducted in animal models are inconsistent (see Chapter 3). Several studies reported positive findings with respect to the development of a variety of cancers (including lung and renal cancers, leukemia, and sarcoma) in animals exposed by inhalation of uranium-ore dust or uranium dioxide, intratracheal injection of 235U (as tetravalent or hexavalent uranium), or implantation of depleted-uranium pellets (Leach et al., 1973; Filippova et al., 1978; Mitchel et al., 1999; Hahn et al., 2002; Miller et al., 2005). However, other studies reported no increase in tumor development in animals exposed by inhalation of uranium-ore dust or ingestion of uranium (Maynard and Hodge, 1949; Cross et al., 1981; ATSDR, 1999).
Lung Cancer
Twenty-three studies of uranium-processing workers examined the association between exposure to uranium and lung cancer, as did three studies of military populations and three studies of residents (see Table 8-1). Four of the uranium-processing studies reported statistically significantly increased standardized mortality ratios (SMR) (that is, above 100). All four of those studies involved the same cohort of Oak Ridge, Tennessee, and all included employees of the Y-12 plant (see Table 8-2). The specific study populations overlapped, but each study took a different approach and examined a different timeframe. The most recent study of the cohort, by Richardson and Wing (2006), did not demonstrate a statistically significant increase in lung-cancer mortality in any dose stratum. However, when assessing the dose-response relationship with a 5-year lag assumption, they found a dose-response trend between external exposure and lung-cancer mortality (due largely to a small number of excess deaths among those who accumulated an external dose of 50 mSv or more) but did not find a similar trend for internal exposure. Analyses of the joint effects of external and internal exposures found that compared to the referent group (defined as less than 10 mSv external and internal dose), the rate ratio estimates were increased for each group defined by higher cumulative concentrations of internal and/or external dose; however, the results were not statistically significant and a dose-response trend was not observed. One major limitation of the uranium-processing worker studies is the lack of control for smoking, a major risk factor for lung cancer.
Contrary to the Y-12 cohort finding, a UK study of processors found significant reductions in both mortality from lung cancer (SMR, 85; p < 0.05) and incidence of lung cancer (standardized incidence ratio [SIR], 75; p < 0.001) but is limited by having only external-exposure data (McGeoghegan and Binks, 2000b). Beral et al. (1988) also reported a significant deficit in lung-cancer mortality (SMR, 64; p < 0.01) in employees of UK atomic-weapons research establish-
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ments with radiation records but found a significant positive association between cumulative exposure and lung-cancer mortality in a test for trend. One study of residents living near former nuclear-material processing plants found a significant reduction in risk of lung-cancer death (relative risk [RR], 0.95; 95% confidence interval [CI], 0.93-0.98) (Boice et al., 2003b); this study is limited by imprecise and incomplete data on exposure and information on risk factors.
Ritz (1999) found a weak dose-response relationship with a 15-year lag per 100 mSv of external dose in workers in a uranium-processing plant. Cragle et al. (1988) reported a nonsignificant increase in lung cancer mortality (8 deaths) for salaried and hourly nuclear-fuels production-plant workers (SMR 152) but lower SMRs (also nonsignificant) for only hourly or only salaried workers. The study lacks exposure data. Pinkerton et al. (2004) reported a statistically nonsignificant increase in lung cancer mortality among uranium millers (SMR, 113; 95% CI, 89-141, compared to US referent rates) that was not found in earlier studies of this cohort. When compared to regional referent rates, the increase reached statistical significance (SMR, 151; 95% CI, 119-189). This study is limited by lack of assessment of individual exposure to uranium and other substances in the milling environment.
In summary, there is no consistent evidence of an effect of exposure to natural or depleted uranium on lung-cancer incidence in the studies reviewed. The finding is unchanged when one considers evidence from the studies with the strongest designs, for example, with measurement of cumulative exposure at the individual level, internal controls, a large study population, long followup, and controlling for confounders. The pattern among studies is varied: some studies show increases in risk of lung cancer, and others show decreases. A major short-coming of the studies is the lack of individual data on smoking, a primary risk factor for lung cancer.
The committee concludes that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and lung cancer exists.
This conclusion on lung cancer differs from the one in Volume 1. The previous committee concluded that there is limited/suggestive evidence of no association between exposure to uranium and lung cancer at cumulative internal doses lower than 200 mSv and that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and lung cancer exists at higher cumulative exposure (> 200 mSv). The present committee did not place quantitative limits on the dose for the following reasons:
There is substantial uncertainty in the measurement of uranium exposure in the studies reviewed.
The types of quantitative measure vary widely from study to study, from individual biomonitoring data to external or internal exposure measurements
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(often lacking data on many study subjects) to group estimates based on job title to a general category of years of employment. Furthermore, different dose-reconstruction methods were used to estimate dosage, and different cut-points were often used to categorize the dose in the data analysis, so it was difficult to draw a conclusion.
Some studies of lung cancer that reported dose had small samples and often did not adjust for risk factors, such as smoking.
Because inhaled uranium dust remains in lung tissues and hilar lymph-node tissues for several years, they are potential targets for uranium radiation. Furthermore, lung cancer is a common malignancy and the leading cause of cancer death; even a modest effect could result in a meaningful increase in the number of cases of lung cancer (that is, an increase in an exposed group compared to an unexposed group might be detectable given the frequency of lung cancer occurrence). Therefore, the committee assigns high priority to continuing to monitor a possible association between exposure to depleted uranium and lung cancer.
Leukemias
The results of only one of the 23 studies reviewed by the committee achieved statistical significance: a residential study by Boice et al. (2003b) (see Table 8-3). The authors reported a reduction in mortality from leukemia (RR [computed by comparing SMRs from the study counties with control counties], 0.91; 95% CI, 0.86-0.97). However, that study is limited by a lack of exposure data and information on other risk factors. The remaining 22 studies showed both increases and decreases in risk associated with exposure to uranium, all of which were nonsignificant. There was no consistent evidence of effect, and the pattern among studies was highly varied. The same pattern was observed after restriction of consideration to the “larger studies” (those with a sample population of about 10,000 or more or with more than 10 cases).
The committee concludes that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and leukemias exists.
Leukemia is a relatively uncommon malignancy, so large study populations are generally needed to demonstrate any significant moderate effects. The studies reviewed by the committee generally did not have adequate sample size. Earlier studies were complicated by the broad grouping of and changes in classification for leukemia. On the basis of the evidence to date, the committee would assign a low priority to additional study of an association between exposure to depleted uranium and leukemias.
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Lymphomas
This section includes discussion of two types of lymphoma: Hodgkin lymphoma (also known as Hodgkin’s disease) and non-Hodgkin lymphoma (NHL). The risk of lymphatic malignancy is of particular interest because uranium is known to accumulate in lymph-nodel tissues. Study results are summarized in Tables 8-4 and 8-5.
Hodgkin Lymphoma
The studies considered (see Table 8-4), split virtually evenly between showing an increase in risk of Hodgkin lymphoma associated with exposure to natural or depleted uranium and showing no change or a decrease in risk of Hodgkin lymphoma associated with uranium exposure. The same pattern was observed after restriction of consideration to the “larger studies” (those with a sample population of about 10,000 or more or with more than 10 cases). Only the study by Nuccetelli et al. (2005) achieved a statistically significant finding, showing a significant increase in the risk of Hodgkin lymphoma. Most of the smaller studies show nonsignificantly decreased risk of incidence or death.
Non-Hodgkin Lymphoma and Other Lymphatic Cancers
Table 8-5 presents the results of 24 published studies of a possible relationship between exposure to natural or depleted uranium and NHL. Most of them showed that exposed subjects experienced a risk of NHL equal to or lower than that in unexposed subjects. The same is true if one considers only the larger studies. One study indicated a significant increase in risk: the study by Archer et al. (1973), which had a sample size of only 662, including four cases of lymphatic cancer.
The committee concludes that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and lymphomas exists. This conclusion applies to both Hodgkin lymphoma and non-Hodgkin lymphoma.
On the basis of the available evidence, the committee concludes that there is a lack of strong and consistent evidence of an association between uranium exposure and lymphatic cancers. The finding is unchanged when one considers evidence from the studies with larger samples and stronger designs: there is no consistent evidence of effect. The pattern among studies is highly varied, as one would expect if there truly were no effect in the population. Although the available evidence does not justify further consideration of a possible association
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between depleted uranium and lymphatic cancers, the committee concludes that further study of this type of cancer may be warranted on biologic grounds, given that uranium is known to accumulate in the lymph nodes.
Bone Cancer
Twelve studies of uranium-processing workers, one study of a deployed population, and two residential studies assessed bone-cancer outcomes. In most of the studies, the risk of bone cancer was the same or decreased after exposure to natural or depleted uranium (see Table 8-6). Only one study had a significant finding: a statistically significant increase in bone-cancer incidence—four cases—in a Danish military population deployed to the Balkans (SIR, 600; 95% CI, 160-1,530) (Storm et al., 2006). However, because three of the four cases occurred within the first year after deployment, it is unlikely that deployment-related exposure was a factor, given the latency of cancer. After lagging 1 year after deployment, bone-cancer incidence dropped to one case, with a nonsignificant SIR of 170 (95% CI, 0-1,010).
The committee concludes that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and bone cancer exists.
Overall, the available studies do not provide clear and consistent evidence of an association between natural or depleted uranium and bone cancer. The estimated effects vary greatly from study to study, showing decreased risk, the same risk, or higher risk after exposure. Given that bone cancer is a relatively uncommon malignancy, relatively large study populations are generally needed to demonstrate any significant moderate effects. The studies reviewed by the committee generally did not have adequate sample size. On the basis of the available evidence, the committee would assign a low priority to additional study of an association between exposure to depleted uranium and bone cancer.
Renal Cancer
The committee considered 20 studies of an association between natural or depleted uranium and renal cancer. None of the published results demonstrated a significant increase in risk after uranium exposure (see Table 8-7). The reported SMRs, SIRs, and RRs varied above and below unity except for one residential study (Boice et al., 2003c), which indicated a statistically significant decrease in renal-cancer mortality associated with uranium exposure (RR, 0.58; p < 0.05). That study did not include exposure assessment or information on other risk factors. In a more detailed analysis, Dupree-Ellis and colleagues (2000) examined a possible dose-response relationship and found an increasing trend, driven primar-
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ily by four renal-cancer deaths in the highest-dose group (excess risk, 10.5/mSV; 90% CI, 0.6-57.4). That result was not statistically significant.
The committee concludes that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and renal cancer exists.
None of the 20 studies considered by the committee demonstrated a significant increase in risk of renal cancer after exposure to uranium. When attention was restricted to the studies with the largest samples, there was no positive evidence of an effect at the low exposures observed in the studies. On the basis of the available evidence, the committee would assign a low priority to further study of an association between exposure to depleted uranium and renal cancer.
Bladder Cancer
The committee evaluated 20 published studies of a potential association between exposure to natural or depleted uranium and bladder cancer: 14 uranium-processing studies, two studies of military populations, and four residential studies (see Table 8-8). Most of the studies reported the same or reduced bladder-cancer mortality or incidence in exposed subjects. Only one finding achieved statistical significance: a UK processing study found a significant reduction in bladder-cancer incidence (SIR, 76; p < 0.05) but roughly equal mortality (SMR, 92; nonsignificant) (McGeoghegan and Binks, 2000b). That study is limited by a lack of data on internal radiation exposure and other risk factors. Two studies of veterans deployed to the Balkans reported increased but nonsignificant SIRs for bladder cancer, but both studies were based on very small numbers of observed cases (Gustavsson et al., 2004; Storm et al., 2006).
The committee concludes that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and bladder cancer exists.
Overall, the committee finds little evidence that exposure to natural or depleted uranium increases the risk of bladder cancer. Most of the studies, whether small or large, show the same or reduced risk of bladder cancer in people exposed to uranium. Although the two studies of deployed populations showed nonsignificant increases in risk, the estimates were based on small numbers of cases—two and seven. A small number of cases renders findings less robust in that changes in exposure or outcome status in only one or two people could have altered the findings substantially, so confidence in the findings is reduced. The committee would assign a low priority to further study of an association between exposure to depleted uranium and bladder cancer.
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Brain and Other Central Nervous System Cancers
Findings of 20 published studies of an association between uranium exposure and brain and other central nervous system cancers are described in Table 8-9. Almost all failed to demonstrate statistically significant associations between uranium exposure and brain and other central nervous system cancers, but they are roughly evenly split between those showing increases in and those showing the same or decreases in mortality or incidence. That overall pattern is unchanged if one restricts attention to the larger or better designed studies. Only two studies had significant results: significant decreases in risk after uranium exposure. The study by Cragle et al. (1988) reported a statistically significant decrease in mortality after exposure in hourly workers at a nuclear-fuels production facility (SMR, 23; p < 0.05). However, the SMRs for salaried workers and for combined hourly and salaried workers were not statistically significant. In addition to a possible healthy-worker effect, the study may be limited by a lack of detailed exposure assessment and the use of “hourly” vs “salaried” as a proxy for socioeconomic status. Beral et al. (1988) also reported a significant deficit in mortality from brain and other nervous system cancers in processing workers (SMR, 32; p < 0.05).
The committee concludes that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and cancers of the central nervous system, including brain cancer, exists.
The published studies show inconsistent results that do not lead to a conclusion of an association between natural or depleted uranium and cancers of the central nervous system. Studies of some other cancers (for example, bladder cancer) showed an equal or reduced risk after exposure, but the distribution of studies of brain and other central nervous system cancers is more balanced: results are roughly equally divided between studies that show increased risk and studies that show the same or decreased risk. Because of that pattern, the committee believes that further study of an association between depleted uranium and central nervous system cancers may be warranted but should not be assigned a high priority.
Stomach Cancer
The committee considered 21 published studies of a possible association between natural or depleted uranium and stomach cancer, including 16 processing studies, one study of military populations, and four residential studies (see Table 8-10). All but three had statistically nonsignificant results, and most demonstrated the same or decreased mortality or incidence. The pattern is unchanged if one restricts consideration to the larger or better designed studies. The three studies that had statistically significant results all showed a decrease in mortality or incidence (Beral et al., 1988; Dupree-Ellis et al., 2000; McGeoghegan and
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Binks, 2000b). McGeoghegan and colleagues found a significantly decreased risk of stomach cancer (SIR, 76; p < 0.05) but an approximately equal risk of stomach-cancer death (SMR, 92; nonsignificant) in workers at the Springfields uranium-production facility (McGeoghegan and Binks, 2000b); however, the study is limited by inadequate data on exposure, particularly internal exposure.
The committee concludes that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and stomach cancer exists.
Overall, the committee finds little evidence to suggest that exposure to natural or depleted uranium increases the risk of stomach cancer. Most of the studies showed similar or reduced risk of stomach-cancer death and incidence in people exposed to uranium. Although four uranium-processing studies showed nonsignificant increase in SMRs, the findings were based on 15 or fewer cases. Similarly, the study of Danish deployed populations that showed a nonsignificant increase in risk was based on two cases. Therefore, confidence in the findings is low. In the view of the committee, further study of an association between depleted uranium and stomach cancer would have a low priority.
Male Genital Cancers
Prostatic cancer is the most frequently diagnosed cancer in men in the United States, and any increase in risk could result in a large increase in the number of cases or deaths. Testicular cancer, the most common cancer among young men, is of special interest to Gulf War veterans, and some studies of veterans suggested a higher but nonsignificantly increased risk (IOM, 2006).
Prostatic Cancer
The committee evaluated 19 published studies of a potential association between exposure to natural or depleted uranium and prostatic cancer, including 14 processing studies, two studies of deployed populations, and three residential studies (see Table 8-11). Only one reported a statistically significant finding: McGeoghegan and Binks (2000b) found a significant reduction in prostatic-cancer incidence (SIR, 77; p < 0.05) but not mortality (SMR, 89; nonsignificant) in workers at the Springfields uranium-processing plant. The study is limited by the lack of data on internal radiation exposure. Three other studies of processing workers reported increased prostatic-cancer mortality, but none of the SMRs was statistically different from the null value indicating no effect (Beral et al., 1988; Loomis and Wolf, 1996; Ritz, 1999).
The larger studies (those with samples of about 10,000 or more or with more than 10 affected cases) had more findings of decreased risk than of increased
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risk in those exposed to uranium. No study showed a statistically significant increase in risk. The only statistically significant finding was a decrease in cancer incidence (SIR, 77; p < 0.05). Overall, there is little evidence of an association between uranium exposure and prostatic cancer.
The committee concludes that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and prostatic cancer exists.
Of the 19 studies considered, none demonstrated a significantly increased risk of prostatic cancer after exposure to uranium, and one showed a significant decrease in cancer incidence but not mortality. If only the studies with the largest samples are considered, the committee finds that there is no affirmative evidence of effect. On the basis of the available evidence, the committee would assign a low priority to further study of an association between exposure to depleted uranium and prostatic cancer.
Testicular Cancer
Table 8-12 summarizes the findings of 15 published studies considered by the committee for a possible relationship between exposure to natural or depleted uranium and testicular cancer, including 11 studies of uranium-processing workers, three studies of military populations, and one study of residents living near a nuclear facility in Pennsylvania. None of the results achieved statistical significance. All studies of processing workers showed reduced testicular-cancer mortality in people exposed to uranium but did not reach the 5% level of statistical significance. All three studies of deployed veterans found increased incidence rate ratios or SIRs, but they also did not reach statistical significance (Macfarlane et al., 2003; Gustavsson et al., 2004; Storm et al., 2006).
The committee concludes that there is inadequate/insufficient evidence to determine whether an association between exposure to uranium and testicular cancer exists.
The committee finds no consistent evidence that uranium exposure increases the risk of testicular cancer. All occupational cohorts had lower mortality. Testicular cancer, although very rare in the general population, is common in young adults and therefore prevalent in deployed veterans. The nonsignificant excess in incidence observed in the studies of military populations could be due in part to routine medical surveillance of the deployed veterans. Despite the inconsistent evidence, testicular cancer is of special interest to Gulf War veterans. The committee believes that further study of an association between depleted uranium and testicular cancer may be warranted but should not be assigned a high priority.
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Other Cancers
A study of health outcomes in 53,462 Gulf War veterans reported only all-cancer incidence, not site-specific incidence (Macfarlane et al., 2005). It did not find a statistically significant increase in cancer incidence (mortality rate ratio, 1.01; 95% CI, 0.79-1.30). However, the 13-year followup period may be too short for most cancers to have developed.
Early studies by Archer et al. (1973), Wagoner et al. (1964), and Waxweiler et al. (1983) combined hematopoietic and lymphopoietic cancers, but only one (that by Archer et al.) found a significant increase (SMR, 392; p < 0.05). Beral et al. (1988) also found a significantly lower RR of all lymphopoietic and hematopoietic cancers (RR, 0.46; 95% CI, 0.23-0.94) in workers with radiation-exposure records than in those without exposure records.
NONCANCER OUTCOMES
The following subsections present the strength of the evidence of associations between exposure to natural or depleted uranium and specific nonmalignant health outcomes. They draw on the information from the many studies that were described in Chapter 7 and Volume 1. The committee has highlighted the relevant findings on nonmalignant outcomes from the literature, with a focus on outcomes related to the organs and organ systems likely to be affected by natural or depleted uranium, such as the kidneys and the respiratory, central nervous, and reproductive systems. The findings show both positive and negative associations between uranium and nonmalignant health outcomes.
Nonmalignant Renal Disease
Mortality
Fourteen studies assessed the association between occupational exposure and renal-disease mortality. Four reported an excess in mortality that was not statistically significant (see Table 8-13). Two of those followed the mortality experience of uranium millers in the Colorado Plateau region. In 1983, Waxweiler and colleagues reported an excess in deaths from chronic nephritis (SMR, 167; 95% CI, 60-353). However, all deaths in the group occurred in short-term workers, and this lessened the likelihood that the deaths were related to uranium exposure (IOM, 2000). In a followup study of the Colorado group, Pinkerton and colleagues also observed an increase in mortality due to chronic renal disease (SMR, 135; 95% CI, 58-267) (Pinkerton et al., 2004) that was not statistically significant. Similarly, Dupree-Ellis and colleagues (2000) found an excess in mortality from chronic nephritis (SMR, 188; 95% CI, 75-381) in workers at the Mallinckrodt Chemical works plant that was not statistically significant. The authors noted that
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TABLE 8-15 Mortality from Nonmalignant Respiratory Disease
Study
Cohort/Study Site
Population
No. Observed Deaths
No. Expected Deaths
SMR (95% CI)
Disease Classification
Waxweiler et al., 1983
Uranium mills, Colorado Plateau
2,002
55
33.7
163 (123-212)
ICD-7 470-527
Pinkerton et al., 2004
Uranium mills, Colorado Plateau
1,484
100
70.16
143 (116-173)
ICD-9 460-519
State rates
94
79.32
1.9 (0.96-1.45)
Ritz, 1999
Uranium-processing plant, OH
4,014
53
79.78
66 (50-87)
ICDA-8 460-519
Checkoway et al., 1988
Y-12 uranium-materials fabrication plant, Oak Ridge, TN
6,781
37
48.9
76 (53-104)
ICD-8 460-519
Frome et al., 1990
Y-12, K-25 uranium-enrichment facilities, research laboratory, Oak Ridge, TN
28,008
792
634.11
125 (117-133)a
ICDA-8 460-519
Polednak and Frome, 1981
Y-12 uranium-processing plant, Oak Ridge, TN
18,869
340
310.11
122 (110-136)b
Diseases of respiratory system
Frome et al., 1997
Four uranium-processing plants, Oak Ridge, TN
27,982
1,568
1,400c
112 (NS)
ICDA-8 460-519
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Ritz et al., 2000
Rocketdyne/Atomics International
2,297
30
40.26
75 (50-106)
ICD-8 460-519
Boice et al., 2006
Rocketdyne/Atomics International
5,801
68
NR
67 (52-84)
ICD-9 460-479, 488-519
Dupree-Ellis et al., 2000
Mallinckrodt Chemical works plant, St. Louis, MO
2,514
64
80
80 (62-101)
ICD-8 460-519
McGeoghegan and Binks, 2001
British Nuclear Fuels plant, Chapelcross site
2,628
22
45.43
48 (p < 0.01)d
Diseases of respiratory system
McGeoghegan and Binks, 2000b
British Nuclear Fuels plant, Springfields site
19,454
379
481.09
79 (p = 0.02)
Diseases of respiratory system
McGeoghegan and Binks, 2000a
British Nuclear Fuels plant, Capenhurst
12,543
53
75.62
70 (p = 0.008)
Diseases of respiratory system
Cragle et al., 1988
Nuclear-fuels production facility, Savannah River Plant, SC
9,860
17
41.02
41 (24-66)e
ICDA-8 460-519
NOTE: CI = confidence interval, ICD = International Classification of Diseases, ICDA = International Classification of Diseases, Adapted, NR = not reported, NS = not significant, SMR = standardized mortality ratio.
aConfidence interval calculated by Committee on Health Effects Associated with Exposure During the Gulf War; not stated in study (IOM, 2000).
bCorrected for incomplete ascertainment of deaths and for deaths of unknown cause.
cNumber of expected deaths calculated by committee; not stated in study.
dSMR based on population rates for England and Wales.
eListed SMR for hourly workers only.
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TABLE 8-16 Nonmalignant Respiratory Disease—Morbidity Risk
Study
Population
Exposure
Outcomes
Results
Adjustments
Comments
Boiano et al., 1989
146 (70%) of 208 eligible long-term employees at FFMPC after releases of uranium oxide from dust collectors in November-December 1984
Self-reported exposure incidents, job history, assessed urinary-uranium data
Lung function, symptoms
Ratio of FEV1 to FVC associated with job-history–derived uranium-exposure index; other spirometry results not associated; shortness of breath significantly associated with self-reported uranium-exposure incidents
Smoking
Limitations in exposure partly based on recall; crude, imprecise exposure categories (low, medium, high)
Cross-sectional
Pinney et al., 2003
8,464 people in FMMP; comparison rates NHIS (and NHANES, not listed)
Residential proximity (less than 2 miles) to FFMPC in direction of groundwater runoff or possible well or cistern contamination in January 1952-December 1984
Self-reported symptoms of chronic bronchitis, asthma, emphysema
Asthma: SPR, 85 (99% CI, 73-98)
Chronic bronchitis: SPR, 19 (99% CI, 14-24)
Emphysema: SPR, 61 (99% CI, 41-86)
Age, sex
Study questionnaires not directly comparable; FMMP self-selected volunteer group
Cohort
NOTE: CI = confidence interval, FEV1 = forced expiratory volume in 1 second, FFMPC = Fernald Feed Materials Production Center, FMMP = Fernald Medical Monitoring Program, FVC = forced vital capacity, NHANES = National Health and Nutrition Examination Survey, NHIS = National Health Interview Study, SPR = standardized prevalence ratio.
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TABLE 8-17 Mortality from Neurologic Disease
Study
Cohort/Study Site
Population
No. Observed Deaths
No. Expected Deaths
SMR (95% CI)
Disease Classification
Frome et al., 1990
Y-12, K-25 uranium-enrichment facilities, research laboratory, Oak Ridge, TN
28,008
76
81.76
93 (71-115)a
ICDA-8 320-389
Polednak and Frome, 1981
Y-12 uranium-processing plant, Oak Ridge, TN
18,869
38
49.3
77 (49-105)a
Diseases of nervous system
Dupree-Ellis et al., 2000
Mallinckrodt Chemical works plant, St. Louis, MO
2,514
11
13.41
82 (43-141)
ICD-8 320-389
Frome et al., 1997
Four uranium-processing plants, Oak Ridge, TN
27,982
148
211.43b
70 (NS)
ICDA-8 320-329
Boice et al., 2006
Rocketdyne/Atomics International
5,801
30
NR
96 (65-137)
ICD-9 320-389
McGeoghegan and Binks, 2000b
British Nuclear Fuels plant, Springfields site
19,454
40
58.25
69 (p < 0.05)
Diseases of nervous, sense organs
McGeoghegan and Binks, 2000a
British Nuclear Fuels plant, Capenhurst
12,543
10
10.25
98 (NS)
Diseases of nervous, sense organs
McGeoghegan and Binks, 2001
British Nuclear Fuels plant, Chapelcross site
2,628
5
7.06
71 (NS)
Diseases of nervous, sense organs
Cragle et al., 1988
Nuclear-fuels production facility, Savannah River plant, SC
9,860
8
9.92
81 (NS)c
ICDA-8 320-389
NOTE: CI = confidence interval, ICD = International Classification of Diseases, ICDA = International Classification of Diseases, Adapted, NR = not reported, NS = not significant, SMR = standardized mortality ratio.
aConfidence interval calculated by Committee on Health Effects Associated with Exposure During the Gulf War; not stated in study (IOM, 2000).
bNumber of expected deaths calculated by committee; not stated in study.
cListed SMR for hourly workers only.
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TABLE 8-18 Reproductive and Developmental Effects
Study
Population
Exposure
Outcomes or Outcome Measures
Results
Adjustments
McDiarmid et al., 2000
29 exposed Gulf War veterans exposed to DU during friendly-fire incidents in February 1991, 38 unexposed veterans, examined in March-June 1997
Exposure to DU by friendly fire, may have inhaled, ingested airborne DU particles, experienced wound contamination by DU; assessed urinary and seminal uranium concentration
Neuroendocrine measures: FSH, LH, prolactin, testosterone; semen characteristics
Prolactin, 2.1-17.7 µg/g of creatinine; low urinary uranium, 1.66; high urinary uranium, 12.47; p = 0.04
Stratification at median into low-, high-result groups
Case series
McDiarmid et al., 2001
50 exposed Gulf War veterans divided into low-uranium and high-uranium groups, examined in March-July 1999
Exposure to DU by friendly fire, may have inhaled, ingested airborne DU particles, experienced wound contamination by DU; assessed urinary uranium concentration
Neuroendocrine measures: FSH, LH, TSH, free thyroxine, prolactin, testosterone; semen characteristics
No statistically significant differences in FSH, LH, prolactin, testosterone, thyroid measures between low- and high-urinary-uranium groups
Prescription psychotropic-, antidepressant-drug use
Case series
Semen characteristics: Total sperm count [≥40 million] Low urinary uranium, 286.6 ± 44.8 million; high urinary uranium, 583.5 ± 106.1 million; p = 0.02
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Total progressive sperm (WHO Class A and B) [≥20 million]
Low urinary uranium, 108.2 ± 19.2 million; high urinary uranium, 220.9 ± 44.0 million; p = 0.03
Total rapid progressive sperm (WHO Class A) [≥10 million]
Low urinary uranium, 81.3 ± 15.4 million; high urinary uranium, 155.5 ± 31.1 million; p = 0.04
McDiarmid et al., 2004
39 Gulf War veterans exposed to DU during friendly-fire incidents in February 1991, examined in April-July 2001, followup 1994-2001
Same exposure as in McDiarmid et al., 2001
Neuroendocrine measures: FSH, LH, prolactin, TSH, free thyroxine, testosterone; semen characteristics
No statistically significant differences in reproductive-health measures
Case series
McDiarmid et al., 2006
32 Gulf War veterans exposed to DU during friendly-fire incidents, examined in April-July 2003
Same exposure as in McDiarmid et al., 2001
Neuroendocrine measures: FSH, LH, prolactin, TSH, free thyroxine, testosterone; semen characteristics
No statistically significant differences in reproductive-health measures
Case series
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Study
Population
Exposure
Outcomes or Outcome Measures
Results
Adjustments
McDiarmid et al., 2007
34 Gulf War veterans exposed to DU during friendly-fire incidents, examined in April-June 2005
Exposure to DU by friendly fire, may have inhaled, ingested airborne DU particles, experienced wound contamination by DU; assessed urinary uranium concentration; both current and cumulative exposure measures reported
Neuroendocrine measures, semen characteristics
No statistically significant differences in reproductive-health measures
Case series
Sumanovic-Glamuzina et al., 2003
All liveborn, stillborn neonates in Maternity Ward of Mostar University Hospital of western Herzegovina, part of Bosnia and Herzegovina immediately (1995) and 5 years after (2000) 1991-1995 military activities
Living in western Herzegovina after military activities
Major congenital malformations
1995 cohort: Major malformations in 40 of 1,853 neonates (2.16%; 95% CI, 1.49-2.82%)
Pre-post comparison
2000 cohort: Major malformations in 33 of 1,463 neonates (2.26%; 95% CI, 1.50-3.01%)
NOTE: BDI = Beck Depression Inventory, CI = confidence interval, DU = depleted uranium, FSH = follicle-stimulating hormone, LH = luteinizing hormone, TSH = thyroid-stimulating hormone, WHO = World Health Organization.
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