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FEED MATERIALS PRODUCTION CENTER (US DOE)
[a.k.a. FERNALD ENVIRONMENTAL MANAGEMENT PROJECT]
HAMILTON AND BUTLER COUNTIES, OHIO

PUBLIC HEALTH IMPLICATIONS

Introduction

The exposure pathways analyses for groundwater, soil, air, surface water, and biota indicate that chemicals and radioactive materials have been released from the Fernald site to the environment. These contaminants have migrated to off-site areas, where human exposure has occurred or may be occurring. As the AExposure Pathways Analyses@ section describes, ATSDR scientists used available information to estimate human exposure doses at off-site locations where human exposure is likely to occur. We estimated exposure doses for hypothetical scenarios of exposure that we developed for each of the exposure pathways (i.e., groundwater, soil, air, surface water, and biota). Table 2A presents a summary of the completed exposure pathways for the Fernald site. Table 2B presents a summary of the potential exposure pathways for the site.

In this section, we evaluate these exposures in depth, using a weight-of-evidence approach (Weis and Susten 1999). The weight-of-evidence approach considers the results of the exposure pathways analyses, together with information in the ACommunity Concerns@ and AHealth Outcome Data@ sections, to determine the site=s potential health impact on the surrounding community.

Not all environmental exposures result in adverse health effects. Therefore, as part of the weight-of-evidence approach, ATSDR scientists consider several factors that influence whether an exposure to a chemical or radionuclide can cause harm. These factors are exposure concentration, duration and frequency of exposure, route of exposure, toxicity or radioactivity of the substance, and how the body handles the substance following exposure. We also consider factors related to a person=s overall health and nutritional status, lifestyle (e.g., smoking and alcohol consumption, diet, level of physical activity), and genetic makeup, because these factors can affect whether exposure to a chemical or radionuclide results in adverse health effects. The weight-of-evidence evaluation typically includes a re-examination of exposure pathways and estimated exposure doses under less conservative, more realistic conditions of exposure than those described in the APathways Analyses@ section.

In this section, ATSDR makes a qualitative statement about the likelihood that exposure to chemicals and radioactive materials, through exposure pathways identified for the site, will cause adverse human health effects. We also consider the overall (combined) health impact on Fernald residents of simultaneous exposure to chemical uranium and radioactive materials in all exposure pathways for the site.

Uranium is the only chemical contaminant evaluated in this section, because the exposure pathways analyses indicate that estimated exposure doses for other chemicals present in off-site environmental media do not exceed their respective health-based guidelines.

Uranium and other radioactive contaminants also are evaluated in this section.

In the AConclusions@ and ARecommendations@ sections of this report, ATSDR determines the level of public health hazard posed by the site and makes recommendations for follow-up health activities at the site.

Uranium

Pathways of Exposure

Uranium is a chemical contaminant evaluated in all exposure pathways for the Fernald site. Table 25 summarizes ATSDR=s estimated past exposure doses (body doses and doses to the kidney) for exposure to chemical uranium in completed and potential exposure pathways; Table 26 summarizes ATSDR=s estimated current exposure doses of the same kind. Uranium as a radioactive contaminant is included in Table 28 with radiation exposure doses from all radioactive contaminants. Table 29 summarizes total chemical (uranium) and radiation estimated exposure doses for all exposure pathways at the site. For the summary doses, ATSDR scientists assumed that a child or adult was exposed to uranium in all exposure pathways simultaneously; for an adult, however, no soil pathway dose was included in the summary dose, because the hypothetical scenario for that pathway involved only children. Of the exposure pathways evaluated for chemical contaminants from the Fernald site, only one pathway poses a human health hazard: ingestion of uranium in groundwater from privately owned wells in the South Plume, a hazard under past conditions at the site. Other exposure pathways contribute minimally to total uranium doses to Fernald residents.

Contractors for CDC estimated past uranium exposure concentrations in the most highly contaminated private wells in the South Plume (Voilleque et al. 1995). ATSDR scientists used these predicted concentrations, as well as actual uranium measurements for these wells, to estimate exposure doses under past conditions at the site. Table 25 contains our estimated doses for a child and an adult.

ATSDR has determined that residents who drank water from privately owned wells in the South Plume, at the maximum uranium concentrations estimated in the past (e.g., in well 15), were likely to have experienced adverse health effects. These effects were likely to have been mild and transient (short-lived). They may have involved biochemical or histological (structural) changes to the kidney. ATSDR provides a detailed discussion of uranium toxicity, and the health-based guidelines for uranium, below.

Residents have expressed concerns about possible adverse health effects from past exposure to uranium in water from privately owned wells near the facility. Preliminary analyses of data from residents participating in the Fernald Medical Monitoring Program (FMMP) suggest a higher than expected occurrence of kidney cancer. Because the FMMP participants may not be representative of the Fernald community as a whole, these findings should be interpreted with caution. It is not known whether any of the observed increases in health effects are related to chemicals and radioactive releases from the Fernald site, because there has been no in-depth assessment of past exposures to site-related contaminants in individual wells near the site and because there are contaminant sources other than the Fernald facility near the site.

According to our estimated total uranium doses for all exposure pathways under past conditions at the site (shown in Table 29), the health hazard posed by the groundwater pathway may have been compounded by exposure to uranium via other potential pathways (i.e., soil, air, surface water, and biota). However, compared to groundwater, these other pathways contribute minimally to total uranium exposure to Fernald residents.

Ingestion of surface water in Paddy=s Run Creek by a young child (2 to 4 years old) contributed more than other pathways to the total chemical uranium dose for a child residing near the Fernald site under past conditions. Our estimated exposure dose (body dose) for past exposure under this scenario slightly exceeds the health-based guideline, although our estimated dose to the kidney is lower than the lower-bound threshold for kidney toxicity by a factor of almost 100.

ATSDR used very conservative assumptions to estimate exposure doses (body doses) and kidney doses for surface water pathways. First, we assumed that a child ingests one-quarter of a liter of surface water every day, 6 months a year, for 4 consecutive years, and that this water is contaminated at the maximum concentrations of uranium ever detected in the creek. This is probably unrealistic, because Paddy=s Run Creek is an intermittent stream and flows only a few months a year; there is probably not enough water in the creek during many of the days of these months for a child to ingest any water. Second, a child of this age (2 to 4 years) would most likely be accompanied by an adult or older caregiver and would not have been allowed to play in the creek and ingest surface water this frequently. Last, the child would probably not frequent the most contaminated area of the creek every day while playing or wading in the creek. It is more likely that the child would frequent various areas of the creek on different days, and be exposed to a range of uranium concentrations. If we had used more realistic assumptions, the estimated doses would have been considerably lower, not exceeding any health-based guidelines. Therefore, exposure to uranium via surface water pathways at the site contributes minimally to the total uranium dose to Fernald residents under past conditions.

Considering available data evaluated by ATSDR, we determined that there are no exposure pathways that pose a public health hazard under current conditions at the site. Likewise, total uranium exposure to Fernald residents for all pathways combined is not likely to result in adverse human health effects.

However, ATSDR has only limited information for one exposure pathway, ingestion of uranium in privately owned wells in the South Plume, under current conditions at the site. Judging from available information, we do not expect adverse human health effects to result from current exposure to uranium in private wells; however, additional information is needed to make a more definitive assessment of the level of public health hazard. Therefore, we determined that this pathway poses an indeterminate public health hazard under current conditions at the site.

Table 25. Summary of estimated chemical uranium exposure doses for completed and potential past exposure pathways for the Fernald site

Past Exposure - Completed Exposure Pathways

Groundwater PathwayCExposure to Water (South Plume) in Privately Owned Drinking Water Wells

Estimated Body Dose (mg/kg/day)

Estimated Kidney Dose (mg/g)

Number of Potentially Exposed Persons*

Scenario #1: child

0.04B0.3

0.003B0.1

UnknownC110 maximum

Scenario #2: adult

0.02B0.1

0.01B0.08

UnknownC812 maximum

Past Exposure - Potential Exposure Pathways

Soil Pathway

 

 

 

Child

0.0002

0.00007

UnknownC110 maximum

Air Pathway

 

 

 

Scenario #1: child

0.0006

0.002

UnknownC110 maximum

Scenario #2: adult farmer

0.001

0.004

UnknownC812 maximum

Surface Water Pathway

 

 

 

Scenario #1: young child

0.005

0.002

UnknownC110 maximum

Scenario #2: older child

0.0001

0.00005

UnknownC110 maximum

Biota Pathway

 

 

 

Scenario #1: child

0.002

0.001

UnknownC110 maximum

Scenario #2: adult

0.0007

0.0004

UnknownC812 maximum

Key
mg/kg/day = milligrams of uranium per kilogram of body weight per day
mg/g = micrograms of uranium per gram of kidney

* The number of potentially exposed individuals is estimated using 1990 Census data for persons residing within 1 mile of the Fernald property boundary. The number of older children (> 6 years old) and adults in this population is not known; an upper-bound estimate was made by subtracting the number of children under 6 from the total population.

Table 26. Summary of estimated chemical uranium exposure doses for completed and potential current exposure pathways for the Fernald site

Current Exposure - Completed Exposure Pathways

Groundwater PathwayCExposure to Water (South Plume) in Privately Owned Drinking Water Wells

Estimated Body Dose (mg/kg/day)

Estimated Kidney Dose (mg/g)

Number of Potentially Exposed Persons*

Scenario #1: child

0.006B0.008

0.003B0.005

UnknownC110 maximum

Scenario #2: adult

0.003B0.02

0.002B0.007

UnknownC812 maximum

Current Exposure - Potential Exposure Pathways

Soil Pathway

 

 

 

Child

0.00003B0.0001

0.000009B0.00004

UnknownC110 maximum

Air Pathway

 

 

 

Scenario #1: child

0

0

UnknownC110 maximum

Scenario #2: adult farmer

0

0.000002

UnknownC812 maximum

Surface Water Pathway

 

 

 

Scenario #1: young child

0.0005

0.0002

UnknownC110 maximum

Scenario #2: older child

0.00003

0.00002

UnknownC812 maximum

Biota Pathway

 

 

 

Scenario #1: child

0.009

0.003

UnknownC110 maximum

Scenario #2: adult

0.002

0.001

UnknownC812 maximum

Key
mg/kg/day = milligrams of uranium per kilogram of body weight per day
mg/g = micrograms of uranium per gram of kidney

* The number of potentially exposed individuals is estimated using 1990 Census data for persons residing within 1 mile of the Fernald property boundary. The number of older children (> 6 years old) and adults in this population is not known; an upper-bound estimate was made by subtracting the number of children under 6 from the total population.

The groundwater pathway contributes most to the total uranium dose to Fernald residents under current conditions at the site. ATSDR has no information about the number and location of privately owned wells near the Fernald site that are currently being used for drinking purposes. In addition, we do not have current measurements of chemical and radioactive uranium concentrations in these wells, and some of these wells have never been sampled.

Because we do not have current measurements of contaminant concentrations in privately owned wells, we estimated exposure doses using the range of uranium concentrations detected in monitoring wells in the South Plume. We assumed that residents near the site, who are currently using privately owned wells for drinking purposes, are being exposed to the maximum uranium concentrations currently found in the monitoring wells. Uranium concentrations in the South Plume have been declining since the facility stopped operating. In 1989, 1990, and 1993, the maximum uranium concentration detected in a former privately owned well (well 15) was 283 micrograms per liter of water (mg/L). We used 283 mg/L as an upper-bound exposure concentration to estimate exposure doses under current conditions. In 1999, maximum concentrations in this well were not detected above 100 mg/L. We used 100 mg/L as a lower-bound exposure concentration to estimate exposure doses under current conditions.

Our estimated upper-bound exposure doses for ingestion of water from privately owned wells under current conditions exceed the health-based guideline for ingested uranium by a factor of 10, while our estimated lower-bound doses exceed the guideline by a factor of 3. All of our estimated kidney doses are at least 14 times lower than the proposed lower-bound threshold for kidney toxicity (Morris and Meinhold 1995). Therefore, we do not expect adverse human health effects to result from current exposure to uranium in private wells; however, additional information is needed to make a more definitive assessment of the level of public health hazard for this pathway.

Our estimated exposure doses for one additional current exposure pathway, ingestion by a child of biota grown and raised near the Fernald site, exceed the health-based guideline for ingested uranium. Uranium can be taken up into plants or fish. Root vegetables (like potatoes and radishes) that are grown in uranium-contaminated soils sometimes contain more uranium than other types of vegetables. Uranium can get into livestock through contaminated food, water, and soil; however, uranium does not stay in the body long and is eliminated quickly in urine and feces (ATSDR 1999b). Our estimated exposure doses for the total body slightly exceed the health-based guideline for ingestion of uranium, but our estimated kidney dose is almost 100 times lower than the proposed lower threshold limit for kidney toxicity (Morris and Meinhold 1995). Given the conservative assumptions we used to estimate exposure dose, we conclude that current exposure via this pathway is not likely to result in adverse health effects.

Properties Affecting the Chemical Toxicity of Uranium

Uranium is a radioactive metal. Small amounts of uranium are present in rocks, soil, surface water and groundwater, air, plants, and animals; this contributes to natural background radiation. The amount of background radiation that has been measured in drinking water in different parts of the United States is generally less than 1 picocurie (pCi) per liter of water (or approximately 1.5 mg/L) (ATSDR 1999b).

There are essentially three kinds of mixtures of uranium: natural uranium, enriched uranium, and depleted uranium. The mixtures are composed of uranium isotopes that are chemically similar, but have different numbers of neutrons. Natural uranium is primarily a mixture of three isotopes, uranium 234 (U-234), uranium 235 (U-235), and uranium 238 (U-238). All three isotopes are radioactive, but they have different amounts of radioactivity per gram of material. U-238 has the lowest specific activity (radioactivity per gram of material). U-234 has the highest specific activity. By weight, more than 99% of natural uranium is U-238, 0.72% is U-235, and 0.005% is U-234.

Uranium can harm people in two ways, as a chemical toxin and as a radioactive substance. Because natural uranium produces very little radioactivity, the chemical effects of uranium are generally more harmful than the radioactive effects. However, exposure to more radioactive mixtures, such as enriched uranium, can produce greater injury to the kidney than natural uranium due to the combined effects of chemical and radioactive properties. There is evidence from studies of dogs and rodents that exposure to 90% enriched uranium produces greater kidney toxicity than chemical and radioactive effects would separately, because the chemical and radiological effects appear to be additive (Filippova et al. 1978). However, the uranium used in these studies was 90% enriched U-235, which has a much higher specific activity than the enriched uranium used and produced at the Fernald site. The Fernald site used and produced 1.25% enriched uranium (Voilleque et al. 1995). No studies were found in which 1.25% enriched uranium produced additive effects on the kidney; additive effects are not likely at this level of enrichment because the specific activity is low.

The kidney is the target organ for the toxic effects of ingested and inhaled uranium. This means that renal toxicity is the first adverse effect that occurs as exposure dose increases from low to high levels. The extent of toxicity is determined primarily by the route of exposure, type of uranium compound, and solubility of that compound in water. Ingested uranium compounds are generally less toxic than inhaled uranium compounds, partly because uranium is poorly absorbed (e.g., less than 5%) from the gastrointestinal tract following ingestion. Highly soluble uranium compounds are generally more toxic to the kidneys than less-soluble compounds when exposure occurs by ingestion, because more-soluble compounds are more readily absorbed from the gastrointestinal tract into the blood (Tannenbaum and Silverstone 1951). Table 27 (below) categorizes the relative water solubility and kidney toxicity of several uranium compounds.

Table 27. Relative water solubility and kidney toxicity of various uranium compounds

 Relative Water Solubility

Relative Toxicity to Kidney

Uranium Compound

Most water soluble

Most toxic

Uranyl nitrate hexahydrate
Uranyl fluoride (uranium hexafluoride)
Uranium tetrachloride
Uranium pentachloride

Low water solubility

Low to moderate toxicity

Uranium trioxide
Sodium diuranate
Ammonium diuranate

Relatively insoluble

Least toxic

Uranium tetrafluoride
Uranium dioxide
Uranium peroxide Triuranium octaoxide

The uranium compounds used and produced by the Fernald facility (e.g., uranium dioxide, uranium trioxide, uranium tetrafluoride, and uranium hexafluoride) ranged from insoluble to most water soluble. Acids were used in many of the production processes at the facility; if they were released to the environment along with the uranium, these acids may have enhanced the uranium=s water solubility.

Evidence for Uranium Toxicity and Health-Based Guidelines

There are very few epidemiological or occupational studies indicating that ingestion of uranium results in adverse effects on the kidney. There is one case study of an individual who developed kidney damage within 16 hours of ingesting 15 grams of uranyl acetate in a suicide attempt (Pavlakis et al. 1996). The kidney damage persisted for 6 months before the kidneys began to recover. However, normal kidney function did not fully return. Assuming that this individual weighed 70 kilograms, the estimated exposure dose (body dose) to this individual was 210 milligrams per kilograms (mg/kg). In contrast, our maximum estimated exposure dose for Fernald residents exposed to uranium in water from privately owned wells in the South Plume is 0.3 mg/kg (Table 25) - many times lower than the dose ingested during this suicide attempt.

Studies using laboratory animals provide the majority of evidence for kidney toxicity from ingestion of uranium. Several studies have been conducted in which animals were exposed to uranium in drinking water and the diet for acute (less than 14 days), intermediate (15 days to less than 365 days), and chronic (more than 365 days) durations. The animals developed kidney toxicity when uranium was present at sufficient doses (Maynard and Hodge 1949; Tannenbaum and Silverstone 1951; Domingo et al. 1987; Ortega 1989; Gilman et al. 1998; ATSDR 1999b).

ATSDR=s health-based guidelines for intermediate and chronic exposure to uranium via ingestion is based on kidney toxicity in rabbits exposed to uranyl nitrate hexahydrate, a soluble uranium compound, in drinking water for 90 days. A dose-dependent change in kidney structure, considered indicative of kidney toxicity, was noted at a lowest-observed-adverse-effect-level (LOAEL) of 0.06 mg/kg/day (Gilman et al. 1998). Dogs and rabbits appear to be the most sensitive species to uranium toxicity (ATSDR 1999b). The LOAEL was divided by 30 to account for uncertainty in extrapolating data from animal studies to humans and to be protective of individuals who may be more sensitive than the general population to uranium toxicity. The health-based guideline is 0.002 mg/kg/day. At this body dose, the estimated dose to the kidney is 0.002 micrograms per gram of body weight (mg/g) for an adult (70 kilograms in weight) and 0.001 mg/g for a child (13 kilograms in weight). Adverse effects on the kidney have not been observed in animals or humans at doses lower than this LOAEL for uranium ingestion. None of ATSDR=s estimated doses for past or current exposure to uranium in any exposure pathway, or all pathways combined, exceed this LOAEL for uranium toxicity.

ATSDR has established health guidelines for inhalation of both soluble and insoluble uranium compounds. The guideline for insoluble uranium is 8 x 10-3 mg/m3, based on structural changes (lesions) in kidneys of dogs exposed to uranium dioxide dust 6 hours a day, 6 days a week, for 5 weeks (Rothstein 1949). At this exposure level, the estimated dose to the kidney is 0.4 mg/g for adults and 0.02 mg/g for a child 1 to 6 years old. The Rothstein study provided no information about the size of uranium particles used. Therefore, the guideline was based on the conservative assumption that uranium particles were 2 microns or less in diameter. Available environmental sampling data and historical process information indicate that most uranium particulates released from the Fernald facility were larger than 2 microns in diameter and were composed primarily of insoluble uranium compounds. Because the respiratory tract can absorb smaller particles more readily than larger particles, the guideline serves as a conservative basis for screening the possibility of causing health hazards for individuals near this site. None of ATSDR=s estimated past and current airborne concentrations of uranium (presented in the AExposure Pathways Analyses@ section of this report, under AAir Pathways@) exceed the health-based guideline for inhalation.

The health guideline for inhalation of soluble uranium is 3 x 10-4 mg/m3, based on kidney lesions in dogs exposed to uranium chloride in air 6 hours a day, 6 days a week, for 1 year (Stokinger et al. 1953). At this exposure level, the estimated dose to the kidney is 0.001 mg/g for adults and 0.0007 mg/g for a child 1 to 6 years old. Because the Stokinger study provided no information about uranium particle size, ATSDR scientists assumed that particles were 2 microns or less in diameter. ATSDR=s estimated airborne uranium concentrations, under only past conditions at the site, slightly exceed this health-based guideline (by a factor less than 10). In that estimation, however, we used conservative assumptions, and a considerable amount of public health protection is built into the guideline. As stated previously, most uranium particulates released from the Fernald facility were larger than 2 microns in diameter and were composed primarily of insoluble uranium compounds. Therefore, ATSDR does not consider this health-based guideline to be as relevant to the Fernald site as the guideline for insoluble uranium compounds (discussed above).

Other federal agencies have set limits for uranium in the environment and workplace. In 1991, the U.S. EPA established a Maximum Contaminant Level (MCL) for uranium in drinking water of 20 mg/L (or 20 parts per billion). EPA is considering increasing the standard to 80 mg/L based on recent information about dietary intake and uptake into the body.

Mechanisms of Uranium Toxicity

Several mechanisms for uranium-induced kidney toxicity have been proposed. In one of these, uranium accumulates in specialized (epithelial) cells that enclose the renal tubule and reacts chemically with ion groups on the inner surface of the tubule. This interferes with ion and chemical transport across the tubular cells, causing cell damage or cell death. Cell division and regeneration occur in response to cell damage and death, resulting in enlargement and decreased kidney function. Heavy metal ions, such as uranyl ions, may also delay or block the cell division process, thereby magnifying the effects of cell damage (Leggett 1989, 1994; ATSDR 1999b).

Animal and human studies conducted in 1940s and 1950s provide evidence that humans can tolerate certain levels of uranium, only suffering minor effects on the kidney (Leggett 1989). Most of these studies involved inhalation exposures to uranium; however, the kidney is also the target organ for inhaled uranium. On the basis of this tolerance, the International Council on Radiologic Protection (ICRP) adopted a maximal permissible concentration of 3 mg/g for occupational exposure in 1959 (Spoor and Hursh 1973). This level has often been interpreted as a threshold for chemical toxicity.

More recent papers have been published on effects of uranium at levels below 3 mg/g, and have discussed possible mechanisms of uranium toxicity (Diamond 1989; Leggett 1989, 1994; Zhao and Zhao 1990; Morris and Meinhold 1995). It is thought that the kidney may develop an acquired tolerance to uranium after repeated doses; however, this tolerance involves detectable histological (structural) and biochemical changes in the kidney that may result in chronic damage. Cells of the inner surface of the tubule that are regenerated in response to uranium damage are flattened, with fewer energy-producing organelles (mitochondria). Transport of ions and chemicals across the tubule is also altered in the tubule cells (Leggett 1989, 1994; McDonald-Taylor et al. 1997). These effects may account for the decreased rate of filtration through the kidney and loss of concentrating capacity by the kidney following uranium exposure. Biochemical changes include diminished activity of important enzymes (such as alkaline phosphatase), which can persist for several months after exposure has ended. Therefore, acquired tolerance to uranium may not prevent chronic damage, because the kidney that has developed tolerance is not normal (Leggett 1989). Based on this recent information for uranium, researchers have suggested that exposure limits be reduced to protect for these chronic effects on the kidney.

Renal damage appears to be definite at concentrations above 3 mg/g for a number of different animal species, but mild kidney injury can occur at uranium concentrations as low as 0.1 to 0.4 mg/g in dogs, rabbits, guinea pigs, and rats after they inhale uranium hexafluoride or uranium tetrachloride over several months (Maynard and Hodge 1949; Hodge 1953; Stokinger et al. 1953; Diamond 1989). Zhao and Zhao proposed a limit of uranium to the kidney of 0.26 mg/g based on renal effects in a man who was exposed to high concentrations of uranyl tetrafluoride dust for 5 minutes in a closed room (Zhao and Zhao 1990). The man showed signs of kidney toxicity, including increased protein content of the urine (proteinuria) and non-protein nitrogen. These persisted for 4.6 years, gradually returning to normal values. The kidney content 1 day after the accident was estimated to be 2.6 mg/g.

A review of studies of uranium effects on the kidney (Morris and Meinhold 1995) suggests a probability distribution of threshold values for kidney toxicity ranging from 0.1 to 1 mg/g, with a peak at about 0.7 mg/g (Figure 7).

Figure 7 - Probability distribution of toxic thresholds for uranium in the kidney.
Adapted from Morris and Meinhold (1995)

The researchers proposed that severity of effects increases with increasing dose to the kidney. There are probably no effects below 0.1 to 0.2 mg/g, possibly mild effects on the kidney at 0.5 mg/g, and more severe effects beginning at 1 mg/g and more definitely at 3 mg/g and above (Morris and Meinhold 1995; Killough et al. 1998b).

ATSDR=s health-based guidelines for ingested (and inhaled) uranium are lower than the lower limit threshold for kidney toxicity proposed by Morris and Meinhold (1995). This is probably because ATSDR=s guidelines are derived using levels of toxicity observed in animal studies, and incorporate safety factors to account for uncertainty in extrapolating from animals to humans and to protect the most sensitive human individuals (ATSDR 1993).

Mild effects on the kidney can be detected by sensitive tests of kidney function. Some tests provide insight into the nature of the damage, while others are fairly non-specific for uranium toxicity. Increased urinary excretion of proteins (proteinuria), amino acids (aminoaciduria), or glucose (glucosuria) may indicate kidney damage or cell death. Increased urinary excretion of enzymes that are important to kidney function, such as catalase, alkaline phosphatase, N-acetyl-b-glucosaminidase (NAG), and hydrolase, may also indicate kidney damage. Catalasuria, or increased urinary excretion of catalase, may be one of the most important indicators of uranium toxicity to the kidney (Leggett 1989; ATSDR 1999b). Other urinary biochemicals, such as b-2-microglobulin and non-protein nitrogen, are commonly used indicators of kidney damage.

Urinalysis has limitations as a test for kidney toxicity. First, the presence of substances in urine may indicate that kidney damage has occurred, but cannot be used to determine whether the damage was caused by uranium. Second, most uranium leaves the body within a few days of exposure, so urine tests can only be used to determine whether exposure has occurred in the past week or two. Last, the tests may be used to detect mild effects on the kidney, but such effects are generally transient in nature and may not result in permanent damage.

More severe effects involve greater damage to the kidney that is likely to be clinically manifest and longer lasting. The kidney has incredible reserve capacity and can recover even after showing pronounced clinical symptoms of damage; however, biochemical and functional changes can persist in a kidney that appears to have recovered structurally (Leggett 1989, 1994; CDC 1998).

Radioactive Materials and Radiation Exposures

Pathways of Exposure

For each current pathway evaluated, the period of time covered by the sampling programs varied, as did the types of analysis. For groundwater and soil, the radiation exposure evaluation was based on uranium detected in private wells and in off-site soil. For the air pathway, radon, radon decay products and external exposures were evaluated separately; the other radionuclides evaluated include total uranium; strontium 90; technetium 99; cesium 137; radium 226 and 228; thorium 228, 230, and 232; neptunium 237; and plutonium 238 and 239. For surface water, the radiation exposure evaluation was based on strontium 90, radium 226 and 228, and total uranium. For the biota pathway, there were four major groups analyzed for different radioactive contaminants. These groups include the following:

  • Vegetables, analyzed for total uranium;
  • Meat, analyzed for uranium 234, 235/236, and 238; thorium 228, 230, and 232; radium 226; strontium 90; cesium 137; and plutonium 238 and 239;
  • Milk, analyzed for total uranium; uranium 234, 235/236, and 238; thorium 228, 230, and 232; radium 226 and 228; protactinium 234; strontium 90; and cesium 137; and
  • Fish, analyzed for total uranium.

Although it would be expected that the radioactive material with the highest concentration in media would be uranium, this is not always the case. In surface water, for example, the radioactive contaminant with the highest concentration downstream in the Great Miami River is radium 228. Furthermore, the radioactive contaminant with the highest concentration is not always the main contributor to the exposure dose estimate - for example, the largest contributor to the bone surface dose, especially in children, is radium 228. Not all media were analyzed for radium 228 and 226, but it might be advisable to do so.

Table 28 summarizes ATSDR=s estimated current exposure doses (to the whole body, bone surface, and lungs) from radioactive contaminants in completed and potential exposure pathways. Table 29 summarizes total radiation doses for all exposure pathways.

Of the exposure pathways evaluated for radioactive contaminants from the Fernald site, none pose a human health hazard under current conditions. Likewise, total radiation exposure to Fernald residents for all pathways combined is not likely to result in adverse human health effects.

CDC determined that inhalation and direct radiation effects of radon and radon decay products in air posed a human health hazard under past conditions at the site.

According to CDC=s reported doses from past exposure to radon, radon decay products, and other radioactive contaminants in air, there was a moderate to high increased likelihood that Fernald residents would develop lung cancer. CDC=s Fernald Dosimetry Reconstruction Project and Fernald Risk Assessment Project indicate that while the facility was operating, Fernald residents were exposed to radioactive materials from the site at levels that were greater than expected from background sources, and that these exposures resulted in an increased number of lung cancer deaths: 1% to 12% greater than expected in a community without exposures from the Fernald facility (CDC 1998).

Since the plant discontinued operations in 1988, most of the airborne contaminants (primarily radon and radon decay products) have come from Silos 1 and 2. We determined that these contaminants would not pose a public health hazard (including lung cancer) to persons off site under current conditions.

Radiological Effects of Radioactive Materials and Radiation Exposure

When radioactive materials undergo spontaneous transformation (decay), they transform into other elements, emitting radiation energy in the form of particles (such as alpha or beta particles) or waves (such as gamma rays or x-rays). Each radioactive material has a unique decay pattern, and each transformation (decay) gives off a unique energy level. Alpha particles are relatively large and do not travel far, depositing all of their energy near where they were emitted. Gamma rays and x-rays are energy waves, not particles, and can travel long distances, releasing their energy gradually. Each emission interacts with tissue differently and has a different effect on tissues and organs of the body. Also, a person=s age affects how much of a contaminant he or she ingests/inhales and how sensitive his or her tissues/organs are to radiation interactions. Therefore, for each radioactive contaminant and age, there are unique conversion factors used to convert from concentrations in media to the potential dose received by a person.

In our health implication analysis, the potential effects from each radioactive material in each route of exposure for different age groups were reviewed for each year of potential exposure from 1989 through 1998. Also, the potential health effects of total radiation exposure from all routes were considered for both whole body doses and organ doses for children and adults, using the year of exposure with the highest potential dose. The maximum total whole body dose (potentially received by an adult) is less than 100 millirem (1 millisievert), which should not result in any adverse effects. The International Commission on Radiological Protection (ICRP) currently recommends that the general public be exposed to no more than 100 millirems above background per year of exposure (ICRP 1991). ICRP=s recommendations are for chronic exposure over a 70-year life span. It is a level at which no adverse health effects have been seen. ICRP=s recommended cancer risk numbers were also used to determine the likelihood of developing any fatal cancer or bone cancer. Risk factors for radon, radon decay products, and other alpha-emitting radionuclides discussed by Anthony C. James at the Health Physics Society 1994 Summer School were also used in determining the likelihood of developing lung cancer (James 1994). The results showed no apparent increased likelihood of developing any fatal cancer, bone cancer, or lung cancer from radiation exposures since 1988.

Table 28. Summary of estimated radiation exposure doses for completed and potential current exposure pathways for the Fernald site

Current ExposureCCompleted Exposure Pathway

Groundwater PathwayCExposure to Water (South Plume) in Privately Owned Drinking Water Wells

Committed Effective Dose (whole body) in mrem (mSv) for 1-Year Intake

Committed Equivalent Dose (bone surface or lung) in mrem (mSv) for 1-Year Intake

Number of Potentially Exposed Persons

Scenario #1: child

22 (0.22)

321 (3.21)Cbone surface

UnknownC110 max.

Scenario #2: adult

24 (0.24)

380 (3.80)Cbone surface

UnknownC812 max.

Current ExposureCPotential Exposure Pathways

Soil Pathway

 

 

 

Child

0.12 (0.001)

1.8 (0.018)Cbone surface

UnknownC110 max.

Air Pathway

 

 

 

Scenario #1: child

0.42 (0.004)

90 (0.9)Cbone surface93 mrad (0.93 mGy)Clung

UnknownC110 max.

Scenario #2: adult

1.2 (0.012)

250 (2.5)Cbone surface
69 to 309 mrad (0.69 to 3.09 mGy)Clung

UnknownC812 max.

External Exposure

 

 

 

Scenario #1: adult to NE of site

12B13 (0.12B0.13)

 

UnknownC812 max

Scenario #2: adult to W of silos

17B59 (0.17B0.59)

 

UnknownCapprox 20

Surface Water Pathway

 

 

 

Scenario #1: child

5.23 (0.052)

177 (1.77)Cbone surface

UnknownC110 max.

Scenario #2: adult

3.7 (0.037)

162 (1.62)Cbone surface

UnknownC812 max.

Biota Pathway

 

 

 

Scenario #1: child

28.8 (0.288)

752 (7.52)Cbone surface

UnknownC110 max.

Scenario #2: adult

12.1 (0.121)

277 (2.77)Cbone surface

UnknownC812 max.

Key

mrem = millirems
mSv = millisieverts
max. = maximum
mrad = millirads
mGy = milligrays
approx.=approximate
NE = northeast
W = west

Table 29. Total chemical uranium and radiation estimated exposure doses for all exposure pathways at the Fernald site

Time of Exposure and Hypothetically Exposed Persons

Total Chemical Uranium Body Dose (mg/kg/day)

Total Chemical Uranium Kidney Dose (mg/g)

Total Committed Effective Dose (whole body) from Intake of Radioactive Contaminants in 1 Year in rem (Sv)

Total Committed Equivalent Dose (Bone Surface or Lung) from Intake of Radioactive Contaminants in 1 Year in rem (Sv) for Bone Surface, in rad (Gy) for Lung

Current Exposure

     

Bone Surface

Lung

Child

0.02

0.006B0.008

~0.07 (~7E-04)

1.34
(0.013)

0.03B0.15
(3E-04B1.5E-03)

Adult

0.005B0.02

0.003B0.008

0.053B0.100
(5.3E-04B1E-03)

1.07 (0.011)

0.06B0.30
(6E-04B3E-03)

Past Exposure

 

 

 

 

 

Child

0.05B0.3

0.008B0.1

NA

NA

NA

Adult

0.02B0.1

0.01B0.08

NA

NA

NA

Key
mg/kg/day = milligrams of uranium per kilogram of body weight per day
mg/g = micrograms of uranium per gram of kidney
NA = not analyzed

 

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