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

HEALTH OUTCOME DATA

In general terms, health outcome data are morbidity and mortality data for the Fernald community. ATSDR evaluates these data to determine the overall health status of the community and to identify specific adverse health effects that may be occurring in the community as a result of exposure to chemicals and radioactive materials from the Fernald facility.

ATSDR evaluated the following sources of health outcome data for this public health assessment: (1) CDC's Fernald Risk Assessment Project (FRAP) (CDC 1998, 1999); (2) preliminary results of cancer analyses among participants in the Fernald Medical Monitoring Program (FMMP) (Pinney 1999b); and (3) a Master of Science thesis on b-2-microglobulin levels in urine of potentially exposed persons living near the Fernald site (Kammer 1998).

The CDC's National Institute for Occupational Safety and Health (NIOSH) has conducted and initiated several investigations involving Fernald workers. A brief description of these projects is provided (below). These studies are not reviewed as part of this public health assessment, because they pertain to Fernald workers and not the community as a whole..

Lastly, the community group Fernald Residents for Environmental Safety and Health, Inc. (FRESH) has conducted an extensive survey of adverse health effects reported by residents of the Fernald community. The survey indicates that Fernald residents are concerned about various types of cancer and a variety of other non-cancer effects. A compilation of the survey findings is provided in the ACommunity Concerns@ section of this report.

Fernald Risk Assessment Project

The CDC's National Center for Environmental Health (NCEH) conducted the FRAP to provide a comprehensive summary of the potential health effects of the Fernald site on the surrounding community (CDC 1998, 1999). The risk assessments used information in the Fernald Dosimetry Reconstruction Project (FDRP) (Voilleque et al. 1995; Shleien et al. 1995; Killough et al. 1998a, 1998b), and demographic information about the population around the Fernald site, to produce community-level estimates of cancer risk. (The Fernald Dosimetry Reconstruction Project is discussed in Appendix D of this report.) Cancer risk was estimated for people exposed to radioactive materials released from the Fernald site during its years of operation - specifically, for persons who resided within the assessment domain (i.e., within 10 kilometers of the Fernald facility boundary) for any length of time between 1951 and 1988. There have been two phases of the FRAP to date.

Phase I

Because the results of the FDRP indicated that lung cancer was the most likely adverse health outcome associated with exposure to radionuclides produced while Fernald was operating, Phase I focused on potential lung cancer risk in the community (CDC 1998). Phase I's goal was to produce a realistic (not worst-case) estimate of the number of lung cancer deaths associated with Fernald-related radiation exposure in the assessment population. The assessment used realistic (not maximum) assumptions about factors affecting exposure.

To estimate risk for the entire community living in the assessment domain, NCEH researchers divided the assessment domain into 160 cells and obtained information about the number, age, and gender of people living in those cells during the years of plant operations. The researchers used software produced by FDRP to generate estimates of radiation exposure and accompanying risk of lung cancer for different subgroups within this population. Life-table methodology, which models mortality in a population over time, was used in conjunction with lung cancer risk estimates to estimate possible lung cancer deaths over time. Estimates were projected through 2088, the year in which someone first exposed in 1988 (the last year of plant operations) would turn 100. The number of Abackground@ lung cancer deaths that would normally be expected to occur in this population was also estimated.

The Phase I report estimated that between 40,000 and 53,000 people lived in the assessment domain for some period of time between 1951 and 1988. Lung cancer deaths in this population were predicted to be between 1% and 12% greater than the number expected if that population had not been exposed to radiation from Fernald. (This range was the 90% credibility interval; the median estimate was 3%.) This translates to a range of 25 to 309 lung cancer deaths, with a median of 85 deaths. The majority of these deaths were estimated to occur among smokers (65 deaths) rather than among people who have never smoked (20 deaths). Fernald-related lung cancer mortality was highest closest to and east of the site, with declining rates farther from and west of the site. Because the installation of containment measures in the K-65 silos in 1979 greatly reduced radon emissions, mortality in people first exposed between 1951 and 1979 was compared to mortality in people first exposed in 1980 and later. It was found that almost all of the estimated increase in lung cancer deaths occurred among those first exposed before 1980.

Phase II

Phase I of the FRAP focused on lung cancer mortality, primarily resulting from exposure to radon and radon decay products, because radon and radon decay products were estimated by the FDRP to comprise the majority of the radiation exposure dose, and radon and its decay products primarily affect the lung (CDC 1998). However, the FDRP also found that uranium and other radionuclides accounted for part of the radiation exposure dose. These radionuclides primarily affect body organs other than the lung. Therefore, Phase II focused on potential health effects resulting from exposure to radionuclides other than radon. The health outcomes addressed were kidney cancer, female breast cancer, bone cancer, and leukemia (CDC 1999). These cancers were selected based on scientific information and community concerns.

Unlike the Phase I evaluation, which was intended to provide a realistic estimate of increased lung-cancer mortality, the Phase II evaluation was intended to provide a screening-level estimate of the increased incidence of selected cancers. The Phase II report used estimates of the maximum Fernald-related radiation dose that members of the assessment population may have received to provide an Aupper-bound,@ or worst-case, estimate of the number of resulting cancers. It was assumed that all members of this population were breathing contaminated air, receiving external radiation exposure, and using contaminated irrigation water. In addition, it was assumed that all of the milk, eggs, fish, meat, and vegetables eaten by this population were contaminated by radiation. As in the Phase I report, the researchers used the software produced by the FDRP to generate estimates of radiation exposure based on these assumptions.

The Phase II report analyzed the same assessment population (people living within the assessment domain for any period of time between 1951 and 1988) as the Phase I report. This domain was divided into 12 geographical areas, for which risk estimates were produced; in addition, a risk assessment was produced for a hypothetical individual who received the maximum exposure previously described and drank contaminated well water. The FDRP report indicated that at least three off-site wells south of Fernald were likely contaminated with radionuclides by the mid-1960s. Of these, a well designated as Well 15 was found to have the highest concentrations of radionuclides. Thus, the contamination levels estimated over time for this well by the FDRP were used to derive estimates of maximum dose for an individual using contaminated well water for drinking and irrigation. The number of persons who were exposed to contaminated well water is likely very small. However, this exposure pathway is of particular interest, because the radiation dose to the organs considered in the Phase II report may be substantially greater among persons who drank, and irrigated their gardens with, water from contaminated wells.

To translate the estimated doses into cancer risks, the report used risk values recommended by the International Council on Radiation Protection (ICRP), the National Council on Radiation Protection (NCRP), and the U.S. Environmental Protection Agency (EPA). These values are based on the cancer experience of human populations exposed to ionizing radiation, primarily atomic-bomb survivors and people exposed to radiation for medical reasons. Based on these risk values, researchers produced upper-bound estimates of the number of cases of certain types of cancer that might occur in the assessment population as a result of exposure to radiation released from Fernald during its years of operation. This estimate was produced first for the hypothetical population that did not use contaminated well water. A new estimate was then produced using the assumption that all persons residing in the two areas 1 to 4 kilometers southeast and southwest of the site used contaminated well water. (This is a conservative assumption that likely greatly overestimates the number of people who used contaminated well water). Estimates for Fernald-related incidences of kidney cancer, breast cancer, and bone cancer in the assessment population as a whole did not change when it was assumed that contaminated well water was used. The leukemia incidence estimate did increase from a range of 1 to 18 additional cases to a range of 3 to 23.

Including the assumption that a segment of the population used contaminated well water, the report estimated that exposure to Fernald-related radiation in the entire assessment population resulted in 23 or fewer additional cases of leukemia, 4 or fewer additional cases of kidney cancer, 4 or fewer additional cases of bone cancer, and 3 or fewer additional cases of female breast cancer over what would be expected in the assessment population in the absence of exposure to radiation from Fernald.

Individual risks to the small segment of the population that used contaminated well water were also estimated using a hypothetical individual exposure scenario. The median estimates of the percentage increase in the lifetime risk of cancer for this hypothetical individual were as follows: 0.7% for kidney cancer, 0.03% for breast cancer, 6% for bone cancer, and 6% for leukemia. Judging from the results of the Phase II report, CDC did not recommend a more detailed analysis of the potential risk for kidney, female breast, or bone cancer resulting from radiation released from the site.

Further Work

As a follow-up to the Phase I and Phase II studies, NCEH conducted a Feasibility Assessment for a Community-Based Epidemiologic Study of Lung Cancer and Radiation Exposures near the Former Feed Materials Production Center (Garbe 1999). Based on their assessment, they concluded that an in-depth epidemiological study of Fernald-related radiation exposures and lung cancer is not feasible at this time. Such a study would not address community concerns about cancer related to the site, primarily because the availability and quality of local records does not appear to be adequate for systematic, unbiased, and complete identification of past residents (Garbe 1999).

The Fernald Medical Monitoring Program (FMMP) and the Fernald Workers Medical Monitoring Program (FWMMP)

In January 1985, Fernald area residents filed a class action lawsuit against National Lead of Ohio (the Fernald site manager from 1954 to 1985) and the DOE. These legal actions resulted in the establishment of a Settlement Fund and two programs: the Fernald Medical Monitoring Program (FMMP) and the Fernald Workers Medical Monitoring Program (FWMMP).

The objectives of the FMMP are to (1) provide a complete medical evaluation of the current health status of eligible persons, (2) provide a comprehensive evaluation of risk factors for illnesses or diseases of participants, (3) provide education to participants on how to modify risk factors for illness or disease, and (4) establish a good baseline database which may be useful for subsequent epidemiological research (Pinney 1999a).

Persons who lived or worked within 5 miles of the former Feed Materials Production Center for any 2-year continuous period, between January 1, 1952, and December 18, 1984, are eligible to participate in the residents' program (FMMP). Persons who worked at the production center as employees of National Lead of Ohio or National Lead Industries are excluded from participating. Participation is on a volunteer basis. Participants initially complete questionnaires on health risk, health status, lifestyle, and possible exposure. A physician administers a history, a physical exam, and medical tests. The first set of formal examinations was initiated in December 1990. From 1990 to November 1998, medical examinations was offered every 3 years. As of December 1998, medical examinations are offered every 2 years. The FMMP is slated to operate for 25 years in total. Confidentiality of medical records is maintained, and data on participants are stored in a computerized database. Participants receive medical advice based on the results of their examinations and tests. In addition, each woman over 40 years old receives an annual mammogram.

As of June 1999, a total of 8,520 adult participants (persons 18 years or older at the time of their first examinations) have enrolled in the FMMP and had their first medical examinations. As of December 1, 1998, the age range of participants is 19 to 95, and slightly more than half (55%) of the participants are women, almost all (99%) are Caucasian, most (73%) are married, and most (84%) have education beyond high school (Pinney 1999b).

Medical examinations, questionnaires, follow-up documentation, and death certificates are sources of disease information collected for the FMMP. Information collected by questionnaire include new medical problems, hospitalizations, surgeries, smoking and alcohol consumption, and medications used. When needed, follow-up documentation (e.g., outside medical records such as death certificates, pathology reports, medical test reports, and operative and discharge summaries) of diseases are obtained for the participants (Pinney 1999b).

Two research questions are being addressed by the FMMP. The first question addresses whether the number of newly diagnosed cancer cases among participants of the FMMP, for the first 4 years in the program (first medical examination plus 48 months of follow-up), is greater than what would be expected among a similar population. The analysis includes FMMP participants (7,937 persons in FMMP) who had their first medical examinations before December 1, 1993, and who were diagnosed at the first medical exam plus 48 months (i.e., each participant contributes about 1 to 4 person-years). This analysis has been funded by FMMP which arose out of a class action lawsuit and settlement.

Analyses were performed for 16 cancer systems and for all cancer sites combined. Four different comparison populations are used in the analysis: (1) the National Cancer Institute's Surveillance, Epidemiology, End Result (SEER) data for all of the United States; (2) the SEER data for Ohio; (3) the Ohio Cancer Surveillance (for three counties, Butler, Warren, and Clermont); and (4) the Ohio Cancer Surveillance (for Ohio as a whole ). The a priori best comparisons are the SEER data for Ohio and the tri-county Ohio Cancer Surveillance data.

The findings indicate that in the FMMP population, the number of new cancer cases for three types of cancer (urinary system and kidney/renal pelvis, melanoma of the skin, and prostate) was greater than expected. The incidence of urinary system cancer in the FMMP population was statistically significant with all four comparisons. Within the urinary system, the incidence for kidney/renal pelvis cancer was significant compared only to the tri-county Ohio area (2.50, 1.14 - 4.75). The incidence of melanomas of the skin and prostate cancer were significant compared only to the SEER Ohio data; e.g., melanomas (2.22, 1.11 - 3.97) and prostate cancer (1.53, 1.12 - 2.70). The researchers acknowledge that the greater than expected incidence of prostate cancer was possible due to the introduction of a new diagnostic test (i.e., PSA) that improved the identification of existing cases, rather than an actual increase in the number of new cases. Although not statistically significant, the expected number of new lung cancer cases among FMMP participants increased from 1% to 12% over the expected number of cases. This is consistent with the predictions made in the CDC's Community-Based Lung Cancer Risk Assessment (Pinney 1999b).

The researchers state that the FMMP volunteer population is representative of the general population, although they acknowledge possible sources of bias due to a Ahealthy volunteer screening effect@ and because a volunteer study population, rather than a representative sample of the entire Fernald community, was used. These results are considered to be screening-level, because the analysis only addressed whether there is an excess of a specific type of cancer in Fernald residents. No data analyses were performed to determine if this excess is related to historical radiation or chemical exposures from the Fernald site (Pinney 1999b).

The second research question being addressed is whether the rate of certain chronic medical conditions, reported by participants in the FMMP at the time of their first medical examination, is greater than the rate reported from national health databases - the National Health and Nutrition Examination Survey (NHANES) and National Health Interview Survey (NHIS). The chronic conditions being analyzed were selected by a review of the scientific literature, interviews with the medical community, and input from Fernald residents (Pinney 1999b). This phase of analysis of FMMP data is being funded by the ATSDR's Division of Health Studies. The findings are currently being reviewed by ATSDR prior to release to the public.

The FWMMP (for former workers) is similar to the FMMP (for residents) in many ways, although there are some important differences. It involves Fernald workers, and information collected from participants focuses on occupational histories. Participants are re-examined annually. The FWMMP has about 3,000 participants. Because the focus of this public health assessment is on community residents, rather than workers, this report does not discuss the FWMMP in depth.

Effects of Uranium-Contaminated Drinking Water on Urinary b-2-Microglobulin Concentration

A retrospective study, conducted by a Master of Science student from the University of Cincinnati College of Medicine, evaluated renal (kidney) effects from drinking water contaminated with uranium by residents living near the Fernald site (Kammer 1998). Contaminated wells were identified using water concentration measurements with results equal to or greater than 20 mg uranium per liter of water. These measurements were made by contractors for DOE, ODH, and OEPA. The exposure group (25 people) was defined as participants in the FMMP who drank water from contaminated wells within the area of the South Plume, as characterized in 1991. The control group (569 people) consisted of Fernald area residents who resided within 4 to 5 miles of the Fernald site and who drank water from wells. The age and gender distribution of South Plume residents and control residents are similar (Kammer 1998).

The biological marker b-2-microglobulin was used to measure the effect of uranium on kidney function. This marker is not specific for uranium-induced renal toxicity, because there are numerous other diseases and chemicals (e.g., chronic active and viral hepatitis, preclampsia, rheumatoid arthritis) that cause alterations in urinary b-2-microglobulin concentrations (Kammer 1998). Concentration measurements for urinary b-2-microglobulin were not available for all South Plume residents or for the entire control group. (They were available for 24 South Plume residents and for 499 people in the control group.) Likewise, concentrations of urinary b-2-microglobulin, standardized for creatinine, were only available for 22 South Plume residents and 496 control residents. Mean urine b-2-microglobulin concentrations in the South Plume and control groups were not statistically different, and mean urine b-2-microglobulin concentrations, standardized for creatinine, were also not statistically different.

Although the findings indicate that South Plume residents did not have increased urine b-2-microglobulin concentrations compared to the control group of residents, several issues must be considered when interpreting these results (Kammer 1998). The most important of these is the relatively imprecise estimation of uranium exposure and the use of urinary b-2-microglobulin as a biological marker of effect.

For exposure to uranium, water measurements were used to define the boundaries of the South Plume in 1991. Actual measurements of uranium concentrations at residences within the plume (and outside the plume) would provide more precise estimates of exposure concentrations, and changes in concentrations, over the period of exposure. This is important because uranium concentrations varied over time, and maximum concentrations were presumably present in the 1960s, not the 1990s. In addition, such data would help minimize misclassification bias (based on exposure).

The use of urinary b-2-microglobulin concentrations as a marker of effect, and the length of time between exposure and measurement of b-2-microglobulin concentration, may have hampered the ability of this study to detect positive associations if they were present. As mentioned previously, concentrations of uranium in the South Plume varied over time. The maximum period of exposure was presumably the 1960s; concentrations decreased substantially from the 1960s to the 1990s. Many residents were provided bottled water to drink in 1984. Measurements of urinary b-2-microglobulin concentrations were made in the late 1990s, thirty years or more after maximum exposure occurred. The kidneys of South Plume residents may have recovered from any toxicity by the time urinary b-2-microglobulin concentrations were measured. Few studies have examined the chronic effects of uranium on the kidney and its ability to repair itself once exposure to uranium has ended (Kammer 1998). While urinary b-2-microglobulin is a valid marker for acute toxicity, it may not be appropriate for use in chronic exposure conditions.

NIOSH Activities

NIOSH has conducted various investigations involving past and current workers at the Fernald site. At present, they are conducting an exposure assessment of hazardous waste, decontamination and decommissioning, and clean-up workers and a retrospective exposure assessment for workers at the Fernald plant. These and other NIOSH activities are not discussed in detail in this report, which addresses health issues related to the surrounding community. Further information about NIOSH's activities at the Fernald site can be obtained by calling or writing the NIOSH contact person listed in the AFor Additional Information@ section of this report.

COMMUNITY CONCERNS

Background

ATSDR representatives first met with members of the Fernald community in May 1992, during the initial visit to the Fernald area. Many times since then, ATSDR representatives have traveled to the Fernald area and met with various members of the community, both in public and private meetings. The purpose of the visits was to learn more about the Fernald site and to hear from community members about their health concerns. The most concerted efforts to compile community concerns in the Fernald community were public availability sessions (or open-house meetings) sponsored by ATSDR on December 6, 7, and 8, 1993. Four open-house meetings were held, two each in Crosby and Ross, at which concerned citizens met individually, in pairs, or in small groups with ATSDR representatives. The public availability sessions were advertised widely in local and area newspapers. The advertisements stated that the purpose of the availability sessions was to hear the community's health concerns related to the Fernald Environmental Management Project and the former Feed Materials Production Center. ATSDR representatives met with approximately 110 people and recorded their concerns, questions, and comments. Personnel from Boston University's School of Public Health, the U.S. Environmental Protection Agency's National Air and Radiation Environmental Laboratory (NAREL), and the National Center for Environmental Health (NCEH) assisted ATSDR staff at the public availability sessions.

The public availability sessions attracted a reasonable cross-section of the community, including residents affiliated with local government, representatives of local community organizations, and former workers at the site. Many of the people who attended the public availability sessions gave their names, but some spoke anonymously. ATSDR made every effort to maintain confidentiality for the residents who came to the sessions; representatives of the news media were not allowed to sit in on conversations or record them.

In addition to the public availability sessions, ATSDR representatives have attended meetings sponsored by DOE, Fernald Residents for Environmental Safety and Health, Inc. (FRESH), NCEH, and the National Institute for Occupational Safety and Health. ATSDR representatives have attended meetings of the Fernald Citizens Advisory Board, formerly the Fernald Citizens Task Force, since March 1994. Upon receiving an invitation from the board (or task force), an ATSDR representative has occupied an ex-officio chair at the meetings since December 1995. Representatives also have attended meetings of the Fernald Health Effects Subcommittee (FHES) since its inception and have reviewed and compiled public comments sent to the FHES by mail (see below). ATSDR scientists have also reviewed information collected by the community group, FRESH, concerning health problems reported by local residents. Many Fernald residents have spoken with ATSDR personnel on the telephone, anonymously. ATSDR staff have also visited with community members in their homes or their automobiles.

With the assistance of personnel from NAREL, ATSDR conducted an environmental sampling program in the Fernald area. Our visits to the area to collect environmental samples, including setting up radon detection canisters in residents' homes, gave us ample opportunity to talk with many residents of the area, particularly those who live close to the facility.

Fernald Community Concerns

Throughout all of the meetings and activities sponsored and attended by ATSDR representatives, an ongoing list of community concerns related to the Fernald site has been kept. In many cases, ATSDR representatives do not know where some of the respondents live or lived, because this information was not always provided.

We have grouped the community concerns under the following headings:

HEALTH CONCERNS
     Cancers
     Non-Cancer Effects
ENVIRONMENTAL EXPOSURES
      Air
      Soil
      Surface Water
      Groundwater
       Biota
SPECIFIC POPULATIONS
PROCEDURAL CONCERNS
      Remediation
      Lack of Trust
      Emergency Response
      Monitoring or Sampling
      General
      Recommendations by the Public

Of the concerns that the representatives heard, ATSDR did not record any that were addressed during the public availability sessions or other meetings, or any that had already been reported and recorded. A summary of the concerns, and ATSDR's responses, is presented in Appendix C of this report. Also included in Appendix C is a summary of concerns submitted to the FHES and compiled by FRESH.

CONCLUSIONS

ATSDR scientists evaluated chemicals and radioactive materials in completed and potential exposure pathways for the Fernald site. ATSDR scientists reached the following conclusions:

  • One exposure pathway evaluated by ATSDR, ingestion of uranium in water from privately owned off-site wells in the South Plume, poses a public health hazard under past conditions at the site. The pathway poses a health hazard because available information indicates that people were exposed to contaminants at levels that could result in adverse health effects. Also, one pathway evaluated by CDC, inhalation of radon and radon decay products, poses a public health hazard under past conditions at the site. This pathway poses a public health hazard because available information and the estimation of exposures from modeling this pathway indicate that people were potentially exposed to contaminants at levels that could result in adverse health effects. Although human exposure to chemicals and radionuclides may have occurred via other exposure pathways, the levels and conditions of exposure (e.g., duration, frequency, route of exposure) were not sufficient to cause adverse health effects, even for the most sensitive individuals. Other exposure pathways contribute minimally to the total exposure to chemicals and radioactive materials by Fernald area residents under past conditions at the site.

  • According to the information reviewed by ATSDR, there are no exposure pathways that pose a public health hazard to the surrounding community under current conditions at the site. However, ATSDR has only limited information about one current exposure pathway, ingestion of chemicals and radioactive materials in water from off-site privately owned wells. Therefore, ATSDR concludes that this pathway poses an indeterminate public health hazard under current conditions at the site. Additional information about exposure (e.g., concentrations of chemicals and radioactive materials in these wells, number and location of wells with contamination) is needed to assess the level of health hazard for this pathway.

  • Future exposures to chemicals and radioactive materials from the Fernald site pose no apparent public health hazard to surrounding communities under normal operating conditions.

RECOMMENDATIONS

Based on the information reviewed, ATSDR recommends the following:

Environmental Issues

  • An in-depth assessment of past exposure to chemical and radioactive contaminants in privately owned residential wells near the Fernald facility should be conducted using available environmental sampling data and appropriate modeling techniques (e.g., spatial analysis, transport and fate modeling).

  • DOE should continue monitoring groundwater in the South Plume. This monitoring should include analyses for contaminants that may be drawn into the South Plume (from sources other than the Fernald facility) due to groundwater remediation activities.

  • An in-depth assessment should be conducted of current usage of, and potential exposure to chemical and radioactive contaminants from, privately owned residential wells that are most likely to be impacted by contaminants from the site. This assessment should use existing and new environmental sampling data. Analysis of samples should include a full spectrum of chemicals and radionuclides, from the Fernald site and other sources near it, that are being introduced into the South Plume by remediation activities at the Fernald site. If contamination of these wells is found at levels that pose a health hazard, additional activities should be considered to determine the source of contamination and the need for further public health actions.

  • More frequent analyses should be conducted for uranium/thorium decay products, especially radium 226 and radium 228, in all biota samples collected off site of the Fernald facility. There should be routine quality control reviews of these analyses.

  • Monitoring for radon and radon daughters should be continued in the Fernald area during remediation activities at the site, particularly those involving the K-65 silos. Consideration should be given to using alpha-track detectors in addition to continuous monitors in case of power supply failures, interference from drastic temperature changes, etc. Additional sampling locations should be added (especially on the west fenceline) during remediation of the silos.

Additional Considerations

  • Further evaluation of possible risk factors for adverse health effects among participants in the Fernald Medical Monitoring Program should be considered.
  • Additional health education activities, including workshops for health care providers in the Cincinnati area, should be considered.

PUBLIC ACTION HEALTH PLAN

The Public Health Action Plan (PHAP) for the Fernald Environmental Management Project (formerly the Feed Material Production Center) contains a description of the public health actions taken and those planned to be taken by ATSDR, DOE, and/or responsible state agencies at, and in the vicinity of the site based on the recommendations of this public health assessment. The purpose of the PHAP is to ensure that this public health assessment not only identifies public health hazards but also provides a plan of action designed to mitigate and prevent adverse human health effects resulting from exposure to hazardous substances in the environment. The public health actions that are completed, being implemented, or planned are as follows:

Public Health Actions Taken:

  • DOE is monitoring and plans to continue monitoring for radon and radon decay products during remediation activities at the site.

  • ATSDR's Division of Health Education and Promotion (DHEP) has co-sponsored, with the University of Cincinnati College of Medicine and Mercy Hope Partners, two educational programs for health care professionals in the Cincinnati area.

Public Health Actions Planned:

  • ATSDR's Division of Health Education and Promotion (DHEP) will continue to develop health care provider training programs for health care professionals in the Fernald community. Primary care providers will be given information about studies and assessments being conducted by ATSDR, NCEH, and NIOSH and important findings from the Fernald Medical Monitoring Program. In addition, they will be provided information needed to diagnose, treat, and counsel persons concerned about the potential health impact of the Fernald site.

  • ATSDR's DHEP will also work with members of the Fernald Health Effects Subcommittee to develop and implement community health education programs as requested by the community.

ATSDR is discussing the implementation of the additional recommendations contained in this public health assessment with DOE and the responsible state agencies. The resulting actions planned or agreed to by these agencies will be reported in the final release of this public health assessment.

FOR ADDITIONAL INFORMATION

ATSDR's Division of Health Assessment and Consultation (Public Health Assessment)
Carol Connell
Health Physicist, Energy Section
Federal Facilities Assessment Branch
Division of Health Assessment and Consultation
Agency for Toxic Substances and Disease Registry
1600 Clifton Road, NE, Mailstop E-56
Atlanta, GA 30333
(404) 639-6060

ATSDR's Division of Health Education and Promotion (Health Care Providers Workshops)
Joe Maloney
Division of Health Education and Promotion
Agency for Toxic Substances and Disease Registry
1600 Clifton Road, NE, Mailstop E-42
Atlanta, GA 30333
(404) 639-6350

CDC's National Center for Environmental Health (NCEH)
(Fernald Dosimetry Reconstruction Project, Fernald Risk Assessment Project, and Fernald Health Effects Subcommittee)
Mike Donnelly
Deputy Chief, Radiation Studies Branch
National Center for Environmental Health
Centers for Disease Control and Prevention
1600 Clifton Road, NE, Mailstop E-39
Atlanta, GA 30333
(404) 639-2550

CDC's National Institute for Occupational Safety and Health (NIOSH)
Dave Pedersen, Ph.D.
CDC-NIOSH
Mailstop P03/R19
Cincinnati, OH
(513) 841-4223

Ohio Environmental Protection Agency
Tom Ontko
Ohio Environmental Protection Agency
Southwest District Office
401 East Fifth Street
Dayton, OH 45402-2911
(937) 285-6073

Ohio Department of Public Health
Jim Colleli
Ohio Department of Health
Bureau of Radiation Protection
246 North High Street
Columbus, OH 43226
(614) 644-2727

Environmental Protection Agency, Region V
Gene Jablonowski
U.S. Environmental Protection Agency
Region V, SRF-5J
Chicago, IL 60604-3590
(312) 886-4591
Fax: (312) 353-8426

U.S. Department of Energy
Johnny W. Reising
Fernald Remedial Action Project Manager
DOE Fernald Area Office
P. O. Box 538705
Cincinnati, OH 45253-8705
(513) 648-3155

Fernald Citizens Advisory Board (FCAB)
James C. Bierer, Chair
Fernald Citizens Advisory Board
Mailstop 76, P. O. Box 538704
Cincinnati, OH 45253-8704
(513) 648-6478

Fernald Medical Monitoring Program and Fernald Workers Medical Monitoring Program
Susan Pinney, Ph.D.
Associate Professor
Department of Environmental Health
College of Medicine
University of Cincinnati
Holmes Hospital, 1st Fl, Rm. 1001
Eden and Bethesda Avenues
Cincinnati, OH 45268-0684
(513) 558-0684

Fernald Residents for Environmental Safety and Health, Inc. (FRESH)
Edwa Yocum
9860 Hamilton Cleves Pike
Harrison, OH 45030
(513) 738-1659

PREPARERS OF REPORT

Brenda K. Weis, M.S., Ph.D.
Health Scientist
Federal Facilities Assessment Branch
Division of Health Assessment and Consultation

Carol Connell
Health Physicist
Federal Facilities Assessment Branch
Division of Health Assessment and Consultation

Contributors

ATSDR acknowledges the contribution to this public health assessment made by Ms. Jerri Anderson and Mr. Kevin Liske, GIS Analysts, Electronic Data Systems, Inc.

ATSDR acknowledges the contribution to this public health assessment made by Dr. Scott Teloffski from U.S. EPA's National Air and Radiation Environmental Laboratory, Montgomery, AL.

ATSDR acknowledges the contribution to this public health assessment made by Ms. Julie Watts, M.S., from the Boston University School of Public Health.

ATSDR acknowledges the contribution to this public health assessment made by Ms. Rebekah Lacey and Mr. Matthew Mitchell, Eastern Research Group, Lexington, MA.

Reviewers of Report

Burt J. Cooper, M.S.
Chief, Energy Section
Federal Facilities Assessment Branch
Division of Health Assessment and Consultation
ATSDR

Sandy Isaacs
Chief, Federal Facilities Assessment Branch
Division of Health Assessment and Consultation

REFERENCES

ATSDR, 1992. Toxicological profile for boron. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). July, 1992.

ATSDR, 1993. Public health assessment guidance manual. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR).

ATSDR, 1995a. Health consultation for milk produced near the Fernald Environmental Management Project. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). June, 1995.

ATSDR,1995b. Health consultation for the K-65 silos. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). May, 1995.

ATSDR, 1996a. Health consultation for nonpotable use of uranium contaminated groundwater near the Fernald Environmental Management Project. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). February, 1996.

ATSDR, 1996b. Health consultation for consumption of produce grown near the Fernald Environmental Management Project. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). January, 1996.

ATSDR, 1997a. Toxicological profile for lead. Draft for public comment. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). August, 1997.

ATSDR, 1997b. Toxicological profile for manganese. Draft for public comment (update). U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). September, 1997.

ATSDR, 1998a. Toxicological profile for chromium. Draft for public comment (update). U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). August, 1998.

ATSDR, 1998b. Toxicological profile for arsenic. Draft for public comment. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). August, 1998.

ATSDR, 1998c. Toxicological profile for sulphur dioxide. Final. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). December, 1998.

ATSDR, 1999a. Demographic analysis for populations residing within one mile, 5 kilometers, and 10 kilometers of the Fernald site. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR), Spatial Analysis Activity.

ATSDR, 1999b. Toxicological profile for uranium. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). September, 1999.

Brown, D.P., and Bloom, T., 1987. Mortality among uranium enrichment workers. Report to National Institute for Occupational Safety and Health, Cincinnati, Ohio. NTIS PB87-188991.

Calabrese, E., and Stanek, E., 1998. Soil ingestion estimation in children and adults: A dominant influence in site-specific risk assessment. ELR News and Analysis 28: 10,660 - 10,671.

CDC, 1998. Estimation of the impact of the Former Feed Materials Production Center (FMPC) on lung cancer mortality in the surrounding community. Atlanta, GA: Centers for Disease Control and Prevention (CDC). December, 1998.

CDC, 1999. Screening level estimates of the lifetime risk of developing kidney cancer, female breast cancer, bone cancer, and leukemia resulting from the maximum estimated exposure to radioactive materials released from the Former Feed Materials Production Center (FMPC). Draft. Centers for Disease Control and Prevention (CDC). Atlanta, GA: 1999.

Diamond, G.L., 1989. Biological consequences of exposure to soluble forms of natural uranium. Radiation Protection Dosimetry 26: 23 - 33.

Domingo, J.L., Llobert, J.M., Tomas, J.M., et al., 1987. Acute toxicity of uranium in rats and mice. Bull Environ Contam Toxicol 39:168 - 174.

DOE, 1972 - 1999. Environmental monitoring annual reports for 1972 - 1995, and integrated site environmental reports for 1997 - 1999. U.S. Department of Energy, Fernald Environmental Management Project (and Feed Materials Production Center).

DOE, 1994. Remedial investigation report for operable unit 5, Appendix A - baseline risk assessment, Fernald Environmental Management Project, U.S. Department of Energy. October, 1994.

DOE, 2000. Fernald Report. U.S. Department of Energy, Fernald Environmental Management Project. Cincinnati, OH: January, 2000.

EPA, 1999. Exposure factors handbook. EPA/600/C-99/001. U.S. Environmental Protection Agency, Office of Research and Development. (CD-ROM).

EPA, 2000. SCREEN3 model and executable source code and SCREEN3 user's guide. (http://www.epa.gov/ttn/scram)

Garbe, P., 1999. Feasibility assessment for a community-based epidemiologic study of lung cancer and radiation exposures near the Former Feed Materials Production Center. Presentation to the Fernald Health Effects Subcommittee. September 22, 1999.

Gilman, A.P., Villeneuve, D.C., Secours, V.E., et al., 1998. Uranyl nitrate: 91-day toxicity studies in the New Zealand white rabbit. Toxicol Sci 41: 129 - 137.

Hodge, H.C., 1953. Resume of chapters 18 to 28. In: Voegtlin, C., and Hodge, H.C., eds. Pharmacology and toxicology of uranium compounds. National Nuclear Energy Series, Division VI, Vol. 1, Part IV. New York: McGraw-Hill.

ICRP, 1979. Limits for intake of radionuclides by workers. International Commission on Radiological Protection. ICRP Publication 30, Part 1. Oxford: Pergamon Press.

ICRP, 1991. 1990 Recommendations of the International Commission on Radiological Protection. International Commission on Radiological Protection. ICRP Publication 60. Oxford: Pergamon Press.

ICRP, 1994. Human respiratory tract model for radiological protection. International Commission on Radiological Protection. ICRP Publication 66. Annals of the ICRP 24(1-3). Oxford: Elsevier Science Ltd.

ICRP, 1995a. Age-dependent doses to members of the public from intake of radionuclides: Part 3, ingestion dose coefficients. International Commission on Radiological Protection. ICRP Publication 69. Oxford: Pergamon Press.

ICRP, 1995b. Age-dependent doses to members of the public from intake of radionuclides: Part 4, inhalation dose coefficients. International Commission on Radiological Protection. ICRP Publication 71. Oxford: Pergamon Press.

IT, 1986. Final interim report - air, soil, water, and health risk assessment in the vicinity of the FMPC. Fernald, OH: November, 1986.

James, A.C., 1994. Dosimetry of inhaled radon and thoron progeny. International Radiation Dosimetry, Health Physics Society 1994 Summer School. Madison, WI: Medical Physics Publishing, 161 - 180.

Kammer, J.W., 1998. Effects of uranium contaminated drinking water on urinary b-2-microglobulin concentration. A thesis submitted to the Division of Research and Advanced Studies of the University of Cincinnati in partial fulfillment of the requirements for the Master of Science. 1998.

Killough, G.G., Case, M.J., Meyer, K.R., et al., 1998a. The Fernald Dosimetry Reconstruction Project, Task 4 - environmental pathways - models and validation. Radiological Assessment Corporation (RAC) Report No. CDC-3. Neeses, SC: 1998.

Killough, G.G., Case, M.J., Meyer, K.R., et al., 1998b. The Fernald Dosimetry Reconstruction Project, Task 6 - radiation doses and risk to residents from FMPC Operations from 1951 - 1988. Volumes I and II (final report). Radiologic Assessment Corporation (RAC) Report No. CDC-1. Neeses, SC: September, 1998.

Klaassen, C.D., et al., eds. 1996. Casarett and Doull's toxicology: The basic science of poisons. New York: McGraw-Hill, Health Professions Division, 1996.

Leggett, R.W., 1989. The behavior and chemical toxicity of U in the kidney: A reassessment. Health Physics 57(3): 365 - 383.

Leggett, R.W., 1994. Basis for ICRP's age-specific biokinetic model for uranium. Health Physics 67: 589 - 601.

Maynard, E.A., and Hodge, H.C., 1949. Studies of the toxicity of various uranium compounds when fed to experimental animals. In: Voegtlin, I.C., and Hodge, H.C., eds. Pharmacology and toxicology of uranium compounds. National Nuclear Energy Series (VI). New York: McGraw-Hill, 309 - 376.

McDonald-Taylor, C.K., Singh, A., and Gilman, A., 1997. Uranyl nitrate-induced tubule alterations in rabbits: A quantitative analysis. Toxicol Pathol 25(4): 381 - 389.

Morris, S.C., and Meinhold, A.F., 1995. Probabilistic risk assessment of nephrotoxic effect of uranium in drinking water. Health Physics 69: 897 - 908.

NCRP, 1984. Evaluation of occupational and environmental exposures to radon and radon daughters in the United States, National Council on Radiation Protection and Measurements Report No. 78. Bethesda, MD: May 1984.

NEA/OECD, 1988. Committee on radiation protection and public health. Report on the expert group on gut transfer factors. NEA/OECD Report, Paris.

NIOSH, 1998. Endocrine disruptors. Presentation to the Fernald Health Effects Subcommittee by Steven Schrader, National Institute of Occupational Safety and Health. March 18, 1998.

ODH, 1988. Ohio Department of Health study of radioactivity in drinking water and other environmental media in the vicinity of the U.S. Department of Energy's Feed Materials Production Center and Portsmouth Gaseous Diffusion Plant. December, 1988.

Ortega, A., Domingo, J.L., Llobert, J.M., et al., 1989. Evaluation of the oral toxicity of uranium in a 4-week drinking water study in rats. Bull Environ Contam Tox 42: 935 - 941.

Pavlakis, N., Pollock, N.A., McLean, G., et al., 1996. Deliberate overdose of uranium: Toxicity and treatment. Nephron 72(2): 313 - 317.

Pinney, S., 1999a. Fernald medical monitoring program update. Presentation at the Fernald Health Effects Subcommittee meeting. March 3, 1999.

Pinney, S., 1999b. Cancer incidence in participants of the Fernald medical monitoring program. Presentation at the Fernald Health Effects Subcommittee meeting, June 23, 1999.

Pinney, S., 2000. Personal communication with Brenda K. Weis, Agency for Toxic Substances and Disease Registry (ATSDR). February, 2000.

Rothstein, A., 1949. Uranium dioxide. In: Voegtlin, C., and Hodge, H.C., eds. Pharmacology and toxicology of uranium compounds. National Nuclear Energy Series: Manhattan Project Technical Section, Division VI, Vol. 1. New York: McGraw-Hill.

SED, 1998. Site-wide environmental database. U.S. Department of Energy, Fernald Environmental Management Project. Electronic transfer to the Agency for Toxic Substances and Disease Registry (ATSDR).

Shleien, B., Rope, S.K., Case, M.J., et al., 1995. The Fernald Dosimetry Reconstruction Project, Task 5 - review of historic data and assessments for the FMPC. Radiological Assessment Corporation (RAC) Report No. CDC-4. Neeses, SC: 1995.

Spoor, N.L., and Hursh, J.B., 1973. Protection criteria. In: Hodge, H.C., Stannard, J.N., Hursh, J.B., eds. Handbook of experimental pharmacology. Berlin: Springer-Verlag, 241 - 270.

Stokinger, H.E., Baxter, R.C., Dygent, H.P., et al., 1953. In: Voegtlin, C., and Hodge, H.C., eds. Toxicity following inhalation for 1 and 2 years. National Nuclear Energy Series: Manhattan Project Technical Section, Division VI, Vol. 1. New York, NY: McGraw-Hill.

Tannenbaum, A., and Silverstone, H., 1951. Studies on acquired tolerance to uranium. In: Tannenbaum, A., ed. Toxicology of uranium. National Nuclear Energy Series, Division IV, Vol. 23, New York: McGraw-Hill.

Voilleque, P.G., Meyer, K.R., Schmidt, D.W., et al., 1995. The Fernald Dosimetry Reconstruction Project, Tasks 2 and 3 - radiologic source terms and uncertainties. Radiological Assessment Corporation (RAC) Report No. CDC-5. Neeses, SC: 1995.

Voilleque, P., 1999. Personal communication with Brenda K. Weis, Agency for Toxic Substances and Disease Registry (ATSDR), at the Fernald Health Effects Subcommittee meeting, June, 1999.

Weis, B.K., and Susten, A.S., 1999. Groundwater contamination by PCE and TCE: ATSDR's approach to evaluate public health hazard. Presented at the Annual Meeting of the American Society for Civil Engineers. Washington, DC: July, 1999.

Zhao, L.-S., and Zhao, S.F., 1990. Nephrotoxic limit and annual limit on intake for natural U. Health Physics 58: 619 - 623.

APPENDIX A - SELECTION OF CONTAMINANTS

ATSDR scientists used several criteria for selecting the chemical and radioactive contaminants for the exposure pathways identified at the Fernald site. These criteria include (1) environmental levels exceeding the media-specific comparison value, (2) noted community health concerns, and (3) the quality and extent of sampling data with which to evaluate potential exposure and human health hazard. For inorganic compounds (metals) and radionuclides, background values may also be considered, since some of these substances occur naturally.

For chemicals, the highest environmental concentration detected in off-site samples is compared with the media-specific comparison values to determine if it is high enough to warrant further evaluation. Generally, if the contaminant concentration exceeds one or more media-specific comparison values, then the contaminant is evaluated further in the AExposure Pathways Analyses@ and APublic Health Implications@ sections of the public health assessment.

Media-specific comparison values are chemical contaminant concentrations in specific environmental media (e.g., soil, water, air) that are considered to be Asafe@ under default assumptions about exposure. Comparison values are not thresholds of toxicity. While concentrations at or below comparison values may be considered safe, it does not automatically follow that any environmental concentration that exceeds a comparison value would produce adverse health effects. To reiterate, if a chemical concentration exceeds a comparison value, this does not mean that a public health concern exists; rather, it indicates the need to consider the contaminant further in the AExposure Pathways Analyses@ and APublic Health Implications@ sections of the report.

The media-specific chemical comparison values used in this public health assessment include ATSDR's environmental media evaluation guides (EMEGs), cancer risk evaluation guides (CREGs), and reference dose media evaluation guides (RMEGs) (ATSDR 1992). Similar values developed by the U.S. Environmental Protection Agency (EPA) and used in this health assessment are maximum contaminant levels (MCLs) and Region III Risk-Based Concentrations (EPA 1989).

EMEGs are media-specific chemical comparison values that are developed for soil, water, and air. EMEGs are derived from ATSDR's minimal risk levels (MRLs), which are presented in ATSDR's Toxicological Profiles. An MRL is a health-based comparison value representing an estimate of daily human exposure to a chemical that is not likely to pose appreciable risk of adverse non-cancer effects over a specified duration of exposure. MRLs are developed for acute (less than 14 days), intermediate (15 to 364 days), and chronic (365 days or more) exposure durations.

RMEGs are media-specific chemical comparison values derived from EPA's reference doses (RfDs). RfDs are health-based guidelines for non-cancer effects. An RMEG is used when an EMEG is not available for a chemical. An RfD is an estimate of daily exposure to a contaminant below which adverse non-cancer effects are not likely to occur over a lifetime (EPA 1989).

CREGs are estimated chemical contaminant concentrations in a specific medium that are anticipated to result in one excess cancer in one million persons exposed over a lifetime. CREGs are calculated from EPA's cancer slope factors (CSFs), also known as cancer potency factors (CPFs). CPFs are cancer potency estimates for chemicals shown to be carcinogenic in either animals or humans (EPA 1989).

MCLs are contaminant concentrations in water derived by EPA to be protective of public health (considering the availability and economics of water treatment technology) over a lifetime at an ingestion rate of 2 liters of water per day. MCLs are enforceable regulatory values.

APPENDIX A - SELECTION OF CONTAMINANTS
(for Completed Exposure Pathways)

Groundwater Pathway (Privately owned Wells)

ATSDR scientists used sampling data collected from 1981 to the present to select contaminants for groundwater pathways. A summary of sampling programs and activities that include privately owned off-site wells is in Table A-1. A brief description of these programs and activities follows.

Uranium in Privately Owned Wells

In 1981, the Department of Energy (DOE) first detected uranium at concentrations above background levels in privately owned drinking water wells south of the facility. Because of the elevated uranium concentrations, DOE began routine monitoring of the private wells near the Fernald site in 1982. In 1984, the monitoring program was formally established as the Radiological Environmental Monitoring Program. Sampling results were reported in the annual Site Environmental Reports (DOE 1972 - 1999). In addition, property owners could request sampling of residential well water for uranium, in which case the one-time results would be reported to the owners. If any of the samples showed above-background concentrations of uranium, the owners had the option to participate in the routine monitoring program (DOE 1972 - 1999).

Of the wells routinely sampled by the facility, only four wells (numbers 12, 13, 15, and 17) located south of the Fernald site showed uranium concentrations above the proposed drinking water standard of 20 mg/L (Voilleque et al. 1995; DOE 1972 - 1999). Because maximum uranium concentrations in these wells exceeded both proposed drinking water standards and ATSDR's media-specific comparison value for ingestion of chemical uranium, we selected total uranium as a chemical contaminant of concern for groundwater pathways. Uranium concentrations were not measured in private wells before 1981, but were estimated using existing sources of environmental data and information (Voilleque et al. 1995). Table A-2 presents maximum yearly concentrations of uranium in private wells 12, 13, 15, and 17, during the period from 1982 to 1997.

From 1986 to 1988, groundwater monitoring was also being conducted at the Fernald facility under the Resource Conservation Recovery Act (RCRA). The RCRA Groundwater Monitoring Program included four private wells off site of the facility. In 1989, DOE began consolidating groundwater monitoring efforts at the Fernald site to avoid duplication of sampling efforts under the various site programs (e.g., Remedial Investigation/Feasibility Study, Routine Monitoring Program, RCRA). In 1990, DOE contractors managed all long-term, environmental monitoring efforts at the site under the Comprehensive Groundwater Monitoring Program. In 1996, this program became part of the Integrated Environmental Monitoring Program (DOE 1997).

Table A-1. Summary of sampling programs and activities that include privately owned wells off site of the Fernald facility

 Date of Sampling

Program or Activity

Parameters Analyzed in Well Water

Wells Sampled and Comments

1981 to 1996

Routine Monitoring:

Radiological Environmental Monitoring Program and Comprehensive Groundwater Monitoring Program; special sampling (owner=s request); and State Route 128 (SR 128) study, in 1990

(DOE 1972B1999)

Monthly, quarterly, or annual analyses for total uranium and 16 metals and elements (Primary and Secondary Drinking Water Standards); monthly analyses for nitrate-nitrogen (from 1983 to 1985)

The Fernald facility conducted routine monitoring of up to 37 off-site private wells; special sampling was conducted on a one-time basis at the owner=s request; and the SR 128 study sampled 18 wells and some cisterns along a 2-mile stretch of SR 128, south of the Fernald site, and analyzed water for total uranium. The facility conducted monthly analyses for nitrate-nitrogen (1983 to 1985) for up to 26 off-site private wells.

1978 to 1982

Sampling by International Technology, Inc. (IT 1986)

Sampling of off-site groundwater and analyses for total uranium

Seventeen off-site groundwater samples, five of which had uranium concentrations above background (0.8 mg/L). Maximum concentration was 268 mg/L. No information about whether any wells were private.

1985 to 1988

Sampling conducted by the Ohio Department of Health (ODH 1988)

Sampling of off-site private wells and cisterns, mostly from 1985 to 1986

Ohio Department of Health (ODH) sampled more than 200 private wells, selected on a voluntary basis at the owner=s request. Three wells had uranium concentrations above background and the proposed water standard of 20 mg/L. Two of these wells were used by local industries; only one of them was used for drinking water (maximum uranium concentration in this well was 370 + 10 mg/L). DOE reported a 30% higher uranium concentration than ODH in split samples from this well.

1986 to 1988

RCRA Program monitoring

(DOE 1972B1999)

Quarterly analyses for metals, elements, total phenol, and nitrates

Fernald facility sampled water from off-site private wells 8, 12, 15, 17, and 26 only

1996 to present

Integrated Environmental Monitoring Program (DOE 1972B1999)

Quarterly analyses for total uranium

Fernald facility sampled water from off-site private wells 12, 13, and 14 only


Table A-2. Maximum yearly concentrations of uranium (in mg/L or ppb) in private wells 12, 13, 15, and 17 off site of the Fernald facility from 1982 to 1995

Year

Well 12

Well 13

Well 15

Well 17

Comments

1960s

918 to 4,144*

NA

918 to 4,144*

918 to 4,144*

Concentration range represents the highest estimated yearly median concentration (lower bound) to the highest estimated yearly 95th percentile (upper bound) concentration based on uranium measurements in the storm sewer outfall ditch (SSOD) and Paddy=s Run and known releases to the SSOD (Voilleque et al. 1995).

1982

310

NA

554

99

Fernald facility began sampling private wells.

1983

306

NA

578

68

 

1984

270

NA

365

68

 

1985

243

NA

360

55

 

1986

332

1

378

61

 

1987

410

1

330

170

Wells 12, 15, and 17 used for monitoring purposes only

1988

300

2

310

73

Wells 12, 15, and 17 used for monitoring purposes only

1989

350

1

320

54

Wells 12, 15, and 17 used for monitoring purposes only

1990

210

2

330

56

Wells 12, 15, and 17 used for monitoring purposes only

1991

190

14

310

54

Wells 12, 13, 15, and 17 used for monitoring purposes only

1992

307

30

260

50

Wells 12, 13, 15, and 17 used for monitoring purposes only

1993

176

78

264

NS

Wells 12, 13, and 15 used for monitoring purposes only; well 17 not sampled after September 1992

1994

162

99

219

NS

Wells 12, 13, and 15 used for monitoring purposes only; well 17 not sampled after September 1992

1995

177

93

177

NS

Wells 12, 13, and 15 used for monitoring purposes only; well 17 not sampled after September 1992

1996

41

120*

NS

NS

Maximum uranium concentrations were detected in well 13 in 1996; concentrations in well 12 were reported in SED, and concentrations in well 13 were estimated from trend analysis (IEMP 1998).

1997

145*

60*

NS

NS

Concentrations in wells 12 and 13 were estimated from trend analysis (IEMP 1998). Wells 15 and 17 were not included in routine groundwater sampling in 1997.

Key
* - estimated concentrations
NA = data not available
NS = not sampled
SED = Site-Wide Environmental Database
mg/L = micrograms of uranium per liter of water
ppb = parts per billion

Sources: DOE 1972B1999; Voilleque et al. 1995


Other Contaminants in Privately Owned Wells

As part of routine environmental monitoring at the Fernald facility, private well water samples were analyzed for metals from 1986 to 1993 (DOE 1972 - 1999). The maximum concentrations of metals detected in the samples are presented in Table A-3. Iron and manganese were frequently detected in private well water at concentrations above secondary federal drinking water standards, although high concentrations of iron and manganese are typical for groundwater in this area (DOE 1972 - 1999). Manganese and manganese compounds were not routinely used in operations at Fernald. Manganese was a minor impurity (< 1%) in uranium ores and ore concentrates (DOE 1994). Potential sources of manganese at the Fernald site are the local soils, the waste pit area, flyash piles, South field area, solid waste landfill, Plant 1 area, Plant 2/3 area, Plant 8 area, and laboratory area.

Maximum concentrations of iron and manganese in all the wells were below ATSDR's media-specific comparison values. Therefore, they were not selected as contaminants of concern for groundwater. Several other metals (e.g., arsenic, cadmium, chromium, lead, selenium, and zinc) were found at concentrations above federal drinking water standards in a very few private well water samples collected from 1986 to 1995. Because these contaminants were detected so infrequently, we could not identify any patterns of contamination in the wells, nor could we identify any individual wells that were consistently found to be contaminated. Therefore, we did not select any of these metals as contaminants of concern for groundwater pathways.

 

Table A-3. Maximum concentrations of metals found in samples from private wells off site of the Fernald facility from 1986 to 1993

Year

 

Iron Concentration (in mg/L or ppm)
and
(number of wells above standard of 0.3 ppm/
number of wells sampled)

Manganese Concentration
(in mg/L or ppm)
and
(number of wells above standard of 0.05 ppm/
number of wells sampled)

Other Metals Detected and Comments

1986

4.43 (13/24)

0.393 (13/24)

No other metal concentrations exceeded standards.

1987

2.95 (11/25)

0.45 (17/25)

No other metal concentrations exceeded standards.

1988

6.09 (15/26)

0.399 (14/26)

No other metal concentrations exceeded standards.

1989

3.6 (14/25)

0.56 (15/25)

Concentrations of arsenic and selenium in one well (well 19) exceeded standards, and concentrations of selenium in 12 other wells exceeded standard. Maximum concentrations of arsenic and selenium found in all wells were 0.071 and 0.034 ppm, respectively.

1990

17 (16/32)

1.8 (15/32)

No other metal concentrations exceeded standards.

1991

16 (15/34)

0.49 (17/34)

Concentrations of cadmium and zinc exceeded standards in one well each (wells 11 and 15), with concentrations of 0.02 ppm and 32 ppm, respectively.

1992

12 (18/37)

0.39 (17/37)

No other metal concentrations exceeded standards.

1993

4.0 (16/36)

0.36 (18/36)

Concentrations of lead exceeded standards in five wells (wells 11, 12, 19, 22, and 29), with a maximum concentration of 0.043 ppm. The drinking water standard changed from 0.0.5 ppm to 0.15 ppm in 1992.

1994

3.57 (12/31)

0.298 (13/31)

Concentrations of arsenic exceeded standards in one well (well 19), with a concentration of 0.063 ppm.

1995

31.37 (13/32)

0.43 (18/32)

Concentrations of arsenic, cadmium, chromium, and lead exceeded standards, each in one of four wells, with maximum concentrations of 13.1 ppm (well 3), 0.012 ppm (well 12), 0.0231 ppm (well 34), and 0.0196 ppm (well 12), respectively.

Key
mg/L = milligram per liter
ppm = parts per million

Sources: DOE 1972B1999; Voilleque et al. 1995


APPENDIX A - SELECTION OF CONTAMINANTS
(for Potential Exposure Pathways)

Soil Pathway

ATSDR scientists used soil sampling data collected from 1971 to the present to select contaminants for soil pathways. These data are summarized in Table A-4 (below). Uranium was detected in off-site samples at concentrations that exceed media-specific comparison values. Maximum uranium concentrations were found in samples collected along the northeastern and eastern facility boundary and along the outfall line to the Great Miami River. Uranium was selected as both a chemical and radioactive contaminant of concern for soil pathways.

Off-site soil samples were analyzed for organic compounds and metals on a few occasions from 1991 to 1993. Samples were collected at five to six different locations east and northeast of the facility boundary. A greater number of samples were collected and analyzed for metal contaminants. These samples were considered representative of background concentrations because they were collected upwind of air pathways and upstream of surface water and groundwater pathways from the Fernald site. Overall, there is a limited amount of information on levels of organic compounds and metals in off-site soils. Analyses for these contaminants were not routinely conducted because these chemicals were not generated or used in significant quantities during routine operations at the facility.

One organic compound, benzo(a)pyrene, was positively detected and quantified in one (sample SS-58) of six off-site soil samples. Although the level of benzo(a)pyrene in this sample was slightly above ATSDR's media-specific comparison value, benzo(a)pyrene was not selected as a contaminant for soil pathways because this location represents the only potential point of human exposure, and any exposure to this concentration is expected to occur with a limited frequency and duration.

Several metals (e.g., arsenic, barium, beryllium, boron, cadmium, chromium, lead, manganese, and thallium) were found at levels above media-specific comparison values in soils off site of the Fernald facility. However, none of these metals was present at concentrations that exceeded background concentrations. Of the metals in surface soil, beryllium, cadmium, and thallium were not selected as contaminants for the following reasons: (1) they were detected infrequently in surface soil samples, (2) maximum concentrations in surface soil samples were just above the lower limit of analytical detection, and (3) maximum concentrations were similar to (or lower than) background soil concentrations.

Table A-4. Summary of analytical data used for selecting chemical contaminants in soil pathways

 Contaminant*

Sample with Maximum Concentration

Maximum Concentration
(mg/kg or ppm)

Mean ConcentrationH
(mg/kg or ppm)

Sample Year

Range of Contamination

Freq. of Detection

Media-Specific Comparison Value (mg/kg or ppm)

UraniumC Current Exposure

Past ExposureI

C-2 (just off site, east, excavated)
2393 (off site, south)

BS-3 (eastern facility boundary)

87

18

137

NA

NA

NA

1991

1990

1973

ND(11)B87

 

2.9B136.5

NA

NA

NA

6 (ATSDR EMEG)

PAHC Benzo(a)pyrene

SS-58 (just off site, NE)

0.110

NA

1993

NDB0.110

1/6

0.088 (benzo(a)pyrene)
(EPA III)

Arsenic

SS-58 (just off site, NE)
1873 (NW of site)

5.3
9.2

5 (n=31)

1993
1992

1.9B5.3
ND(2.9)B9.2

5/5
22/26

0.37
(EPA III)

Barium

SS-56 (just off site, east)
1873 (NW of site)

237
331

77 (n=35)

1993
1992

14.3B237
31B331

5/5
30/30

100
(ATSDR EMEG)

Beryllium

SS-55 (just east of site)
1873 (NW of site)

1.3
0.6

NA
1

1993
1992

ND(0.11)B1.3
ND(0.47)B0.6

1/5
1/30

   

Boron

No samples immediately off site
1831 (NW of site)

NA
1,140

NA
97 (n=14)

NA
1992

NA
ND(12.2)B1,140

NA
14/30

200
(ATSDR EMEG)

Cadmium

No positive detections off site
1762 (NW of site)

NA
0.95

NA
0.7 (n=30)

NA
1992

NA
ND(0.47)B0.95

0/5
7/35

    

 

Chromium

SS-56 (just off site, east)
1758 (NW of site)

12.1
18.1

11 (n=35)

1993
1992

5.6B12.1
6.7B18.1

5/5
30/30

10 (hexavalent)
(ATSDR EMEG)

Lead

SS-58 (just off site, NE)
1875 (NW of site)

28.5
40.3

18 (n=32)

1993
1992

8.3B28.5
ND(15.6)B40.3

5/5

27/29

NA

Magnesium

C-7 (off site, east; excavated)
SS-58 (just off site, NE
1758 (NW of site)

24,800'
[3,060]
3,590

2,421 (n=35)

1991
[1993]
1992

1,540B24,800
1,020B3,590

5/5
30/30

300
(ATSDR EMEG)

Manganese

SS-56 (just off site, east)
1873 (NW of site)

3,420
4,850

921 (n=35)

1993
1992

400B3,420
189B4,850

5/5
30/30

300
(ATSDR EMEG)

Thallium

SS-58 (just off site, NE)
1827 (NW of site)

0.42
0.58

0.4 (n=35)

1993
1992

ND(0.24)B0.42
ND(0.48)B0.58

2/5
1/30

 

     

Key
mg/kg = milligrams of substance per kilogram of soil
ppm = parts per million
PAH = polyaromatic hydrocarbon
NW = northwest
NE = northeast
Range of Contamination = analytical range of contaminant concentration
ND = not detected
NA = not available or not analyzed
Freq. of Detection = frequency of analytical detection, i.e., number of positive detections/total number of samples
Comparison Value = media-specific comparison value, as described in introduction to Appendix ACSelection of Contaminants

* Contaminants were selected using all surface soil samples collected from 1971 to the present, and reported in the following sources: DOE 1972B1999; Killough et al. 1998; and SED 1998. Only contaminants listed in bold were selected as contaminants in soil pathways.
H Mean concentrations were calculated from all off-site samples with reported concentrations above analytical detection levels.
I Past exposure was evaluated for only one contaminant of concern, uranium, because analytical data are not available for any other contaminants.
' Soil concentration of magnesium of 24,800 mg/kg is considered a statistical outlier and not representative of actual levels.


References

ATSDR, 1992. Public health assessment guidance manual. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR).

DOE, 1972 - 1999. Environmental monitoring annual report for 1972 - 1995, and the integrated environmental monitoring program for 1997 - 1999. U.S. Department of Energy, Fernald Environmental Management Project (and Feed Materials Production Center).

DOE, 1994. Remedial investigation report for operable unit 5, Fernald Environmental Management Project. U.S. Department of Energy, Fernald Field Office. June, 1994.

DOE, 1997. DOE's integrated environmental monitoring plan. U.S. Department of Energy No. 2505-WP-0022. Cincinnati, OH: March, 1997.

EPA, 1989. Risk assessment guidance for Superfund, Vol. 1, human health evaluation manual (part A). EPA/540/1-89/002. Washington, DC: U.S. Environmental Protection Agency.

IT, 1986. Final interim report - air, soil, water, and health risk assessment in the vicinity of the FMPC. Fernald, OH: November, 1986.

Killough, G.G., Case, M.J., Meyer, K.R., et al., 1998. The Fernald Dosimetry Reconstruction Project, Task 6 - radiation doses and risk to residents from FMPC operations from 1951 - 1988. Volume II appendices. RAC Report No. CDC-1, Radiological Assessment Corporation. Neeses, SC.

ODH, 1988. Ohio Department of Health study of radioactivity in drinking water and other environmental media in the vicinity of the U.S. Department of Energy's Feed Materials Production Center and Portsmouth Gaseous Diffusion Plant. December, 1988.

SED, 1998. Site-wide environmental database. U.S. Department of Energy, Fernald Environmental Management Project. Electronic transfer to the Agency for Toxic Substances and Disease Registry (ATSDR).

Voilleque, P.G., Meyer, K.R., Schmidt, D.W., et al. 1995. The Fernald Dosimetry Reconstruction Project, Tasks 2 and 3 - radiologic source terms and uncertainties. RAC Report No. CDC-5, Radiological Assessment Corporation. Neeses, SC.

APPENDIX B - EXPOSURE DOSES AND HEALTH-BASED GUIDELINES

Chemicals

The following general equation is used to estimate human exposure dose for chemical contaminants:

 

Estimated Exposure Dose
(mg/kg/day)

=

C x IR x EF x ED
BW x AT

 
 Where:   
 

Estimated Exposure Dose

= Exposure dose calculated as milligrams of contaminant per kilogram of body weight per day (mg/kg/day) 
 C =Contaminant concentration, in milligrams per kilogram (mg/kg) or milligrams per liter (mg/L) 
 IR=Intake rate for ingestion or inhalation, in milligrams or kilograms per day (mg/day or kg/day) or cubic meters per day (m3/day) 
 EF= Exposure frequency, or number of exposure events per unit of time (e.g., year) of exposure 
 ED = Exposure duration, or the duration over which exposure occurs (e.g., years) 
 BW=Body weight, in kilograms (kg) 
 AT=Averaging time, or the time period over which cumulative exposures are averaged (e.g., total years of exposure x 365 days per year)
 

For exposure to chemical uranium, the following equation is used to estimate dose to the kidney:

 

Dose to the Kidney
(µg/g)

=

Estimated Exposure Dose x ABS x DC x BW x CF
Kidney WT

 
 
Where:

   
 

Dose to the Kidney

= Dose calculated as micrograms of uranium per gram of kidney (mg/g) 
 
Estimated Exposure Dose

=Calculated using the equation provided above (in mg/kg/day) 
 ABS =Absorption factor, or fraction of uranium in soil that is absorbed from the gastrointestinal tract into the blood (unitless) = Distribution factor, or fraction of the absorbed dose that is distributed to the kidney (unitless) 
 
DC

= Distribution factor, or fraction of the absorbed dose that is distributed to the kidney (unitless)  
 
BW

=Body weight, in kilograms (kg)  
 
CF

=Conversion factor, or 103 micrograms per gram  
 
Kidney WT

=Average weight of two kidneys, in grams (e.g., 120 g per kidney for a child, and 310 g per kidney for an adult)
 

The assumptions ATSDR used to calculate exposure doses for chemicals in completed or potential exposure pathways are provided in the discussion section for each pathway (i.e., groundwater, soil, air, surface water, biota). ATSDR used the estimated exposure doses in the AExposure Pathways Analyses@ section of this report as screening-level analyses of public health hazard. ATSDR then compared the estimated exposure doses with health-based guidelines for the chemical, route of exposure, and exposure duration (i.e., acute, intermediate, or chronic). When an estimated exposure dose for a chemical exceeded its corresponding health-based guideline, ATSDR then evaluated the chemical further (see the APublic Health Implications@ section of the report), using a more in-depth, weight-of-evidence approach.

Health guidelines include ATSDR's minimal risk levels (MRLs) and EPA's reference doses (RfDs) for non-cancer effects, and cancer risk ranges (1 in 10,000 to 1 in 1,000,000 excess cancer risk) for cancer effects. MRLs and RfDs are conservative values because they are based on levels of exposure reported in the scientific literature, which represent no-observed-adverse-effect-levels (NOAELs) and lowest-observed-adverse-effect-levels (LOAELs) for the most sensitive outcome for a given route of exposure (e.g., ingestion or inhalation). In addition, uncertainty factors are applied to NOAELs and LOAELs to account for variation in the human population and uncertainty in extrapolating from animals to humans, and for added protection of the most sensitive individuals. Therefore, MRLs and RfDs may have uncertainties spanning an order of magnitude or more.

When evaluating the potential for cancer to occur, ATSDR scientists often use cancer risk ranges based on EPA's cancer potency factors (CPFs). CPFs define the relationship between exposure doses and the likelihood of increased risk of developing cancer over a lifetime. CPFs are developed using data from animal or human health studies and often require extrapolation from high exposure doses administered in animal studies to the lower exposure levels typical of exposure to environmental contaminants. CPFs represent the upper-bound estimates of the probability of developing cancer at a defined level of exposure; therefore, they tend to be conservative and may even overestimate the actual risk, in order to account for uncertainties in the data used in the extrapolation.

ATSDR scientists may also use cancer effect levels (CELs) reported in the scientific literature to determine possible cancer effects from exposure at the exposure doses estimated for the contaminant of concern and pathway. The CELs are similar to LOAELs for non-cancer effects, but they represent minimal levels of effect for cancer effects. The CELs are derived from animal and human health studies and represent the lowest dose of a chemical in a study, or group of studies, that produces a significant increase in the occurrence of tumors in the exposed population as compared to an unexposed group.

Radiation

The following general equation is used to estimate human exposure dose (committed effective or equivalent doses) for radioactive contaminants:

 
Committed Effective or Equivilent Dose
(lifetime dose in sieverts from specified intake)

=      C x IR x EF x ED x IDC

 
 
Where:

   
 

Committed Equivalent Dose

= Equivalent dose rate received in a particular tissue or organ over a person's lifetime following the intake of radioactive materials into the body 
 
Committed Effective Dose

=Sum of the committed tissue or organ equivalent doses and the appropriate organ or tissue weighting factor integrated over the person's lifetime 
 C=

Contaminant concentration, in becquerels per gram (Bq/g), or becquerels per liter (Bq/L)

 
 
IR

=

Intake rate for ingestion or inhalation

 
 
EF

=Exposure frequency, or number of exposures per unit of time of exposure 
 
ED

=Exposure duration, or the duration over which exposure occurs 
 
IDC

=Age-dependent ingestion or inhalation dose coefficients, in sieverts per becquerels (Sv/Bq) 


The committed effective and equivalent doses for radioactive contaminants in completed or potential exposure pathways are presented in the discussion section for each pathway (i.e., groundwater, soil, air, surface water, biota). At the screening-level analysis phase in the exposure pathways analyses, ATSDR used the maximum concentrations to estimate committed effective or equivalent doses (to the target organ). In assessing public health implications, we determined the likelihood of developing a fatal cancer (or organ-specific cancer) over a person's lifetime based on the committed effective or equivalent doses.

APPENDIX B - EXPOSURE DOSES AND HEALTH-BASED GUIDELINES
(for Potential Exposure Pathways)

(Soil Pathway)

ATSDR's estimated ingestion doses and health-based guidelines for metals in soil pathways are presented in Table B-1. We estimated these doses assuming the same hypothetical exposure scenarios described in the AExposure Pathways Analyses@ section of this report under ASoil Pathway.@ Under this scenario, we assumed exposure to a child, 1 to 6 years old and weighing 13 kilograms, who plays in off-site areas and exhibits Apica-like@ behavior. We assumed this child ingests 200 milligrams (mg) of maximally contaminated soil per day, on 35 days a year, for 4 consecutive years. Additional assumptions that we used to estimate exposure doses for metals selected as contaminants for soil pathways (i.e., arsenic, barium, boron, chromium, lead, and manganese) are presented below. We have also provided information about health-based guidelines for these contaminants. As Table B-1 shows, none of ATSDR's estimated exposure doses for metals in off-site soils exceed the health-based guidelines.

Arsenic

The maximum concentration of arsenic detected in off-site surface soil is 9.2 milligrams per kilogram of soil (mg/kg) in a sample (sample 1873) collected northwest of the site. Because this area is upwind of any airborne transport and upstream of any water transport pathways from the Fernald site, it is considered representative of background conditions, as it is unlikely to have been affected by site contaminants.

The maximum concentration of arsenic detected in surface samples near the site is 5.3 mg/kg in a sample (sample SS-58) collected just outside the eastern facility boundary in 1993. This area has been affected by contaminants released from the site, as other chemicals and radionuclides that have also been detected on site have been identified in soil there.

Arsenic concentrations are lower in areas that may have been affected by the Fernald site. Nonetheless, to estimate exposure doses, ATSDR scientists used the maximum concentration of arsenic in all off-site samples (9.2 mg/kg), as they did not know whether human exposure to this level is possible.

Table B-1. Estimated exposure doses and health-based guidelines for chemical (metal) contaminants in soil pathways

Contaminant

Estimated Ingestion Dose for a Child (mg/kg/day)*

Health-Based GuidelinesH

Uranium

 

 

Estimated doses are presented in the AExposure Pathways Analyses,@ ASoil Pathway@ section.

2 x 10-3 mg/kg/day (ATSDR int/chr oral MRL)
0.1 to 1 mg/g (dose to the kidney) (Morris and Meinhold 1995)

Arsenic

8 x 10-6

3 x 10-3 mg/kg/day (ATSDR chr oral MRL)
1.5 (mg/kg/day)-1 (EPA oral CSF)
0.0043 (per mg/m3) (EPA inhal unit cancer risk)

Barium

5 x 10-4

0.07 mg/kg/day (EPA oral RfD)

Boron

2 x 10-3

0.01 mg/kg/day (ATSDR int oral MRL)
0.09 mg/kg/day (EPA oral RfD)

Chromium (VI)

3 x 10-5

5 x 10-3 mg/kg/day (EPA oral RfD)
0.2 mg/day (ATSDR interim oral intake)

Lead

5.9 mg/dLI

10 mg/dL (CDC/ATSDR blood screening level, children)

Manganese

7 x 10-3

0.07 mg/kg/day (ATSDR interim oral guideline)

Key
MRL = Minimal Risk Level
int = intermediate
chr = chronic
int/chr = intermediate/chronic
RfD = Reference Dose
CSF = EPA=s Cancer Slope Factor
CDC = Centers for Disease Control and Prevention
EPA = U.S. Environmental Protection Agency
mg/dL = micrograms of lead per deciliter of blood
mg/g = milligrams of lead per gram of kidney
mg/kg/day = milligrams of substance per kilogram of body weight per day
mg/day = milligrams of chromium per day
* Equations used to calculate exposure doses are described in the introduction to this appendix.H Health-Based Guidelines are discussed in the introduction to this appendix.
I Dose presented as micrograms of lead per deciliter of blood (see text for discussion).

Arsenic is present in the environment in both inorganic and organic forms. (Note: the term Aorganic@ refers to compounds containing carbon and hydrogen.) Inorganic forms of arsenic predominate in soils and are more toxic than the organic forms (NEPI 1998). When humans and other animals are exposed to inorganic arsenic, they metabolize it to the much less toxic, methylated organic form, which is readily excreted from the body in urine. This methylation is effective as long as the inorganic arsenic intake remains below a level of 0.2 to 1 mg of arsenic per day (ATSDR 1998a), indicating that people can tolerate a certain level of arsenic exposure without experiencing adverse effects. At higher exposure levels, the body's capacity to detoxify arsenic may be exceeded or saturated, leading to increased blood levels of arsenic and possible adverse effects.

Saturation of the body's detoxification mechanism may explain why both non-cancer and cancer effects of arsenic appear to have a threshold, or minimum effective dose. Adverse health effects may result when exposure levels exceed the threshold. In addition, a growing body of scientific evidence suggests that arsenic carcinogenicity may result from mechanisms other than direct attack on genetic material, which supports the belief that there is a threshold for arsenic (ATSDR 1998a).

The amount of arsenic taken into the body following exposure depends to a large extent on the solubility of the arsenic compound. Soluble arsenic compounds are almost completely absorbed into the blood from the gastrointestinal tract (stomach and small intestine) while less soluble compounds have a lower absorption rate. Inorganic compounds vary widely, from 10% to 95%, in their solubility (NEPI 1998). ATSDR scientists do not have specific information about the types (and solubilities) of arsenic compounds present in surface soils; therefore, they made very conservative assumptions that all arsenic was present as inorganic compounds that are completely soluble (i.e., 100% absorbed from the gastrointestinal tract into the blood).

ATSDR's estimated exposure dose for ingestion of arsenic-contaminated soil is presented in Table B-1. This dose is equivalent to 0.0001 mg arsenic per day, which is many times lower than the levels required to saturate they body's arsenic detoxification mechanisms.

The lowest levels at which toxicity, including skin and gastrointestinal effects, has been reported in humans are 0.014 to 0.05 mg/kg/day. These findings are based on a study of Taiwanese persons who drank arsenic-contaminated water for 45 years (Tseng et al. 1968; Tseng 1977). EPA derived a health guideline of 3 x 10-4 mg/kg/day for adverse effects on the skin (e.g., hyperpigmentation, keratosis) and a cancer slope factor of 1.5 (mg/kg/day)-1 for skin cancer, based on the Taiwanese study (IRIS 1998). Although ATSDR's estimated doses are lower than levels shown to cause adverse effects in the Taiwanese people, the study has important limitations that must be considered when public health hazard is evaluated.

First, the study reported an association between arsenic in drinking water and skin cancer but failed to account for a number of potential confounding factors, including exposure to other nonwater sources of arsenic, genetic susceptibility to arsenic, and poor nutritional status of the exposed population. Therefore, arsenic exposure may have been underestimated in the study, possibly leading to an overestimation of cancer effects associated with exposure levels. Second, the cancer slope factor for arsenic is based on the conservative assumption that no threshold exists for cancer. As discussed previously, arsenic carcinogenicity appears to have a threshold. Lastly, the adverse effects observed in the Taiwanese people were due to absorbed arsenic. ATSDR scientists assumed that all arsenic off site of the Fernald facility was present as completely soluble, inorganic arsenic compounds. These assumptions resulted in a dose estimate that was not realistic and most likely overestimated the actual absorbed dose.

Considering these limitations, ATSDR scientists conclude that adverse effects are not likely from ingestion of arsenic-contaminated soil. This is supported by the fact that ATSDR's estimated doses were many times lower than levels required to saturate arsenic detoxification mechanisms in the body. It is important to note that the maximum arsenic concentrations that were used to estimate dose were similar to background levels, indicating regional soil conditions.

Barium

The maximum concentration of barium detected in off-site surface soil is 331 mg/kg in a sample (number 1873) collected northwest of the site. This area is considered representative of background conditions because it is unlikely that site contaminants would have affected the area. The highest level of barium detected in surface samples near the site, and likely to have been affected by contaminants released from the site, is 237 mg/kg in a sample (SS-56) collected just outside the eastern facility boundary in 1993. ATSDR scientists used the maximum concentration of barium detected in off-site surface soil to estimate exposure doses. For purposes of estimating exposure dose, we assumed that 100% of the ingested barium was absorbed from the gastrointestinal tract into the blood.

The health guideline for ingestion of barium was derived by EPA and takes into account recent findings from both human (epidemiologic) studies of adult males and from various chronic animal (rodent) studies of barium in drinking water (IRIS 1998). The guideline is derived from a no-observed-adverse-effect-level (NOAEL) of 0.07 mg/kg/day, which is the dose that does not increase blood pressure when barium is ingested over a chronic duration. Our estimated dose for ingestion of barium-contaminated soil is many times lower than this NOAEL. Therefore, adverse human health effects are not likely to result from exposure to barium at the maximum concentrations found in soil off site of the Fernald facility.

Boron

No boron measurements have been made within close proximity to the Fernald facility boundary. Several samples have been collected northwest of the Fernald facility in an area that is considered representative of background conditions because it is unlikely to have been affected by contaminants released from the site.

The maximum concentration of boron in off-site surface soil is 1,140 mg/kg. This value is considered a statistical outlier, and not likely to represent actual environmental concentrations, because it is almost 100 times higher than other boron measurements made in the same area. Of a total of 30 samples collected in off-site surface soil, 14 have positive detections for boron. Of these 14 samples, the next highest boron concentration is 27.6 mg/kg, detected in sample 1758 from the same area. The average boron concentration in the 14 samples is 97 mg/kg when the value of 1,140 mg/kg is included in the averaging, but the average is only 16.8 mg/kg when this extreme value is excluded. Although it is unlikely that contaminants from the Fernald site have affected this area northwest of the site, ATSDR scientists estimated exposure dose using the maximum concentration of 1,140 mg/kg, because they do not know whether it represents an actual environmental concentration, and whether human exposure at this level is possible.

No human studies were identified in the literature for ingestion of boron or boron compounds. Health guidelines for boron ingestion are based on reproductive (testicular) effects in dogs exposed to borax and boric acid in their diet for intervals ranging from 90 days to 2 years (Weir and Fisher 1972; ATSDR 1992a; IRIS 1998). A no-observed-adverse-effect-level (NOAEL) of 8.8 mg/kg/day was reported for the 2-year study. An additional study of rats fed borax and boric acid in their diet for 2 years reported a lowest-observed-adverse-effect-level (LOAEL) of 58.5 mg/kg/day based on adverse effects on the testes (Weir and Fisher 1972). Of these animal species, the dog is considered more sensitive than the rat to boron toxicity (IRIS 1998). ATSDR's estimated dose for the Fernald site is many times lower than the NOAEL and LOAEL reported in these studies.

Chromium

The maximum concentration of chromium in off-site surface soil is 18.1 mg/kg in a sample (number 1758) collected northwest of the site. This area is considered representative of background conditions, because it is unlikely that site contaminants would have affected it. The maximum concentration of chromium in surface samples near the site is 12.1 mg/kg in a sample (SS-56) collected just outside the eastern facility boundary in 1993. ATSDR scientists used the maximum concentration of chromium detected in all off-site samples, or 18.1 mg/kg, to estimate exposure doses.

Chromium occurs in the environment in several forms, depending on its valence state, e.g., trivalent (III) chromium or hexavalent (VI) chromium. Chromium in the environment (e.g., soil, water) and in the body is more commonly found as chromium VI than as chromium III (ATSDR 1998b). Chromium VI is considerably more toxic to humans than the chromium III. ATSDR scientists do not have specific information about the form of chromium present in surface soils off site of the Fernald facility. Therefore, we made a conservative assumption that all chromium found in off-site soil is in the more toxic, hexavalent form.

ATSDR has not established a health guideline for ingestion of chromium because the available data are insufficient or too contradictory to establish minimum levels of effect (e.g., LOAELs). Because chromium is an essential nutrient in the body, the National Research Council has established a range of Aestimated safe and adequate daily dietary intakes@ (ESADDIs) for chromium; the upper end of the range is 0.2 mg/day (NRC 1989). This value has been adopted by ATSDR as an interim guideline for oral exposure to chromium VI and chromium III compounds (ATSDR 1998b).

ATSDR's interim guideline is similar to the health guideline established by EPA for chronic ingestion of chromium VI. EPA's guideline is 0.005 mg/kg/day and is based on studies in animals (IRIS 1998). EPA's guideline is equivalent to an adult exposure of 0.35 mg/day and a child exposure of 0.065 mg/day. The estimated exposure dose for this pathway is many times lower than the upper bound ESADDI for chromium. Therefore, adverse effects from ingestion of chromium-contaminated soil off site of the Fernald facility are not likely.

Lead

The maximum concentration of lead in off-site surface soil is 40.3 mg/kg in a sample (number 1875) collected northwest of the site. This area is considered representative of background soil conditions. The highest level of lead detected in surface samples near the site is 28.5 mg/kg in a sample (SS-58) collected northeast of the site in 1993. ATSDR scientists used the maximum concentration of lead in all off-site samples, or 40.3 mg/kg, to estimate exposure doses, because they do not know whether human exposure at this level is possible.

Health guidelines for lead are based on blood lead concentrations rather than exposure doses. A strong positive correlation exists between exposure to lead-contaminated soils and human blood lead levels. Generally, blood lead levels rise 3 to 7 micrograms per deciliter (mg/dL) of blood for every 1,000 mg/kg increase in soil or dust lead levels (ATSDR 1992b). The relationship between lead in environmental media and lead in blood has been described mathematically by the following equation (where ln is the natural logarithm):

ln (blood lead conc) = 0.879 + 0.241 ln (environmental lead conc.)

The increase in blood lead concentration as a function of soil lead concentration is not linear. At high lead concentrations in soil (many times higher than maximum concentrations in soil off site of Fernald) the rate of increase in blood lead tapers off. The equation is considered appropriate when exposure to lead occurs at relatively low levels (i.e., levels similar to maximum concentrations found in off-site surface soil). The equation is used to calculate blood lead concentrations assuming exposure to lead in soil via multiple routes of exposure (e.g., ingestion, inhalation).

The Centers for Disease Control and Prevention (CDC) and ATSDR consider a blood lead level of 10 mg/dL for children a health-based screening level (ATSDR 1992b; CDC 1991). When estimated or measured blood lead levels are 10 mg/dL or higher, then further evaluation of potential health hazard is warranted. Blood lead levels above 10 mg/dL in children may be associated with neurological and behavioral problems, such as impaired learning ability and reduced intelligence quotient (ATSDR 1992b, 1997a; CDC 1991).

Bioavailability of lead refers to the ability of humans and animals to absorb lead into their bodies following exposure by ingestion or inhalation. Bioavailability of lead can vary considerably depending on various factors, such as the size and chemical composition of the ingested or inhaled particles. In the absence of information about the bioavailability of the lead from soil off site of Fernald, ATSDR scientists made the conservative assumption that all lead present off site was completely (100%) bioavailable for uptake by humans.

Using the above equation, which correlates dietary intake of lead to blood lead level, ATSDR's estimated blood lead level for poeple exposed to contaminated soil off site of the Fernald facility is 5.9 mg/dL. This level is considerably lower than the screening level of 10 mg/dL. This difference is not surprising, however, because the maximum environmental lead concentrations off site are lower than levels shown to be correlated with elevated blood lead levels.

Manganese

The maximum concentration of manganese detected in off-site surface soil is 4,850 mg/kg in a sample (number 1873) collected northwest of the site. This area is considered representative of background conditions because it is unlikely that site contaminants would have affected the area. The maximum concentration of manganese in surface samples near the site is 3,420 mg/kg in a sample (SS-56) collected just outside the eastern facility boundary in 1993. ATSDR used the maximum concentration of manganese in all soil samples, or 4,850 mg/kg, to estimate exposure doses.

Manganese is a naturally occurring element that is essential for normal functioning of the human body. Toxicity in humans has been associated with both deficiencies and excess intake of manganese. Manganese deficiencies have not been observed in the general population, because manganese is found in a variety of foods, including whole grains, nuts, leafy vegetables, and tea. Suboptimal manganese intake may be more of a concern than excess intake: several diseases, including multiple sclerosis, cataracts, osteoporosis, and epilepsy, may be associated with low levels of manganese in the body (ATSDR 1997b). Two cases of manganese deficiency have been reported for persons consuming from 0.11 to 0.34 mg of manganese per day (Doisy 1973; Friedman et al. 1987).

It is difficult to define safe and adequate daily intakes of manganese because several factors, both environmental and biological, greatly influence an individual's response to manganese (ATSDR 1997b). Because manganese is essential in the human diet, the National Research Council has established a range of Aestimated safe and adequate daily dietary intakes@ (ESADDIs) for manganese. The ESADDIs are 0.3 to 2.0 mg/day for children under age 6 and 2 to 5 mg/day for persons over age 11 (NRC 1989). The World Health Organization estimates that the average consumption of manganese in the adult diet ranges from 2 to 9 mg/day, and that an intake of 8 to 9 mg/day is Aperfectly safe.@ ATSDR has established an interim health guideline for manganese ingestion of 0.07 mg/kg per day (ATSDR 1997b). This guideline is equivalent to a daily intake of 4.9 mg for a 70-kg adult and 0.91 mg for a 13-kg child.

ATSDR's estimated ingestion dose for manganese (Table B-1) is equivalent to a daily intake of 0.49 mg for adults (assuming a body weight of 70 kilograms) and 0.091 mg for children (assuming a body weight of 13 kilograms). Therefore, ATSDR's estimated ingestion doses are lower than the ATSDR interim health guideline for ingestion of manganese and lower than Asafe and adequate@ daily intakes established by the National Research Council and World Health Organization. Manganese deficiency is not likely for Fernald area residents, however, because additional sources of manganese are contributed by the diet and possibly the environment (manganese is naturally high in groundwater in the Fernald area). Considering these additional sources of manganese exposure, estimated daily intakes for Fernald area residents are likely to be within Asafe and adequate@ ranges and are not likely to result in adverse health effects.

EXPOSURE DOSES AND HEALTH BASED GUIDELINES
(for Potential Exposure Pathways)

Air Pathway

ATSDR's estimated inhalation doses and health-based guidelines for metals in air pathways are presented in Table B-2. We estimated these doses assuming the same two hypothetical exposure scenarios described in the AExposure Pathways Analyses@ section of this report, under AAir Pathway.@

Under scenario #1, we assume exposure to a child, 1 to 6 years old and weighing 13 kilograms, who inhales airborne contaminants while playing near the site. The airborne contaminants are from resuspended soil. We assumed this child inhales 5 cubic meters of maximally contaminated air per day, on 351 days a year, for 6 consecutive years. Under scenario #2, we assume exposure to an adult farmer who weighs 70 kilograms and inhales airborne contaminants while performing heavy work near the site. We assumed this farmer inhales 51 cubic meters of maximally contaminated air per day, on 351 days a year, for 10 consecutive years (or the period from 1989 to 1998) (EPA 1999; ATSDR 1993; Killough et al. 1998).

For both scenarios, we assume that soil contaminated with metals becomes resuspended in air and is a source of potential exposure to off-site residents via air pathways. Because there are no measurements of metal concentrations in air at the site, we estimated the airborne concentrations using measured concentrations of metals in surface soil and measured concentrations of total suspended particulates in air off site of the facility.

For both scenarios, we also assume that 100% of the airborne concentration of metal is deposited into the respiratory tract and is completely available for absorption into the blood. These are conservative assumptions considering that the chemical form of each metal in off-site surface soil is not known for the Fernald site, the bioavailability of metals varies considerably by compound, and resuspended soils are likely to be large (10 microns in diameter or more) and, therefore, deposited in the upper regions of the respiratory tract where absorption is minimal (NEPI 1998). Additional information about maximum concentrations of metals in off-site surface soil is provided in the AExposure Pathways Analyses@ section of this report, under ASoil Pathway.@ Additional information about the methods ATSDR used to estimate airborne concentrations of metals in air is provided in the AExposure Pathways Analyses@ section of this report under AAir Pathway.@

In the following section, we have provided additional information about health-based guidelines for the metal contaminants in air pathways. As Table B-2 shows, none of ATSDR's estimated exposure doses for metals in off-site air exceed health-based guidelines.

Table B-2. Estimated exposure doses (for a child and an adult farmer) and health-based guidelines for chemical (metal) contaminants in air pathways

8 x 10-3 mg/m3 (ATSDR int inhal MRLCinsoluble uranium) 3.4 x 10-4 mg/m3 (ATSDR chr inhal MRL-soluble uranium)

Contaminant Estimated Airborne Concentration (mg/m3) Estimated Inhalation Doses (mg/kg/day) for a Child and an Adult Farmer* Health-Based Guidelines*

 

 

Child

Adult

 

Uranium

Estimated airborne concentrations and exposure doses are presented in the AExposure Pathways Analyses,@ AAir Pathway@ section of this report.

8 x 10-3 mg/m3 (ATSDR int inhal MRL-insoluble uranium) 3.4 x 10-4 mg/m3 (ATSDR chr inhal MRL-soluble uranium)

Arsenic

2 x 10-6

8 x 10-7

1 x 10-6

0.0043 (per mg/m3) (EPA inhal unit cancer risk)

Boron

5 x 10-4

2 x 10-4

3 x 10-4

10 mg/m3 (OSHA PEL)
0.01 mg/kg/day (ATSDR int oral MRL)
0.09 mg/kg/day (EPA oral RfD)

Chromium (VI)

7 x 10-6

3 x 10-6

5 x 10-6

5 x 10-4 mg/m3 (ATSDR int inhal MRL)
0.012 (per mg/m3) (EPA inhal unit cancer risk)
3 x 10-3 mg/kg/day (EPA oral RfD)
0.2 mg/day (ATSDR interim oral intake)

Manganese

2 x 10-6

7 x 10-4

1 x 10-4

0.04 mg/m3 (ATSDR chr inhal MRL)
0.07 mg/kg/day (ATSDR interim oral guideline)

Key
MRL = Minimum Risk Level
inhal = inhalation
int = intermediate
chr = chronic
int/chr = intermediate/chronic
EPA = U.S. Environmental Protection Agency
OSHA = Occupational Safety and Health Administration
PEL = permissible exposure limit

* Equations used to estimate exposure doses and the Health-Based Guidelines are discussed in the introduction to Appendix BCEstimation of Exposure Doses and Health-Based Guidelines.


Arsenic

When humans and other animals are exposed to inorganic arsenic, that metabolize it to the much less toxic, methylated organic form, which is readily excreted from the body in urine. This methylation is effective as long as the inorganic arsenic intake remains below a level of 0.2 to 1 mg of arsenic per day (ATSDR 1998a), indicating that people can tolerate a certain level of arsenic exposure without experiencing adverse effects. At higher exposure levels, the body's capacity to detoxify arsenic may be exceeded or saturated, leading to increased blood levels of arsenic increase and possible adverse effects.

ATSDR's estimated dose for incidental inhalation is presented in Table B-2 of this appendix. The dose is equivalent to 5 x 10-8 (or 0.00000005) mg/day, which is many times lower than levels required to saturate the body's arsenic detoxification mechanisms. The dose is based on an estimated arsenic particulate concentration of 2 x 10-4 mg/m3 that we calculated using the methods described previously in this appendix.

EPA has derived a unit cancer risk for inhalation of inorganic arsenic of 0.0043 per mg/m3 arsenic in air, based on the incidence of lung cancer among male smelter workers (IRIS 1998). The unit risk can be interpreted to mean that there are 0.0043 additional lung cancer cases expected for every mg/m3 increase in arsenic concentration. Based on this unit cancer risk and our estimated airborne arsenic concentration, there is no expected increased risk of cancer from inhalation of arsenic-contaminated soil off site of the Fernald facility. Again, this is supported by the fact that our estimated exposure dose for arsenic is many times lower than levels required to saturate detoxification mechanisms for arsenic in the body.

Boron

A study of workers in the borax industry who were employed an average of 11 years reported that average exposures of 4.1 mg/m3 are associated with dryness of the mouth, nose, and throat; sore throat; and productive cough (Garabrant et al. 1984). Borates are considered mild irritants at concentrations exceeding the Occupational Safety and Health Association's (OSHA) Permissible Exposure Level (PEL) of 10 mg/m3 in the workplace (ATSDR 1992a). Our estimated boron airborne concentration is many times lower than the OSHA PEL for boron, indicating that adverse health effects from incidental inhalation of boron-contaminated soil are not likely.

Chromium

ATSDR's health guideline for intermediate (less than 1 year) inhalation of particulate chromium VI compounds is 5 x 10-4 mg/m3. This guideline is based on respiratory effects, such as slightly decreased lung function among workers exposed to chromium for an average of 2 2 years (Lindberg and Hedenstiema 1983; ATSDR 1998b). The no-observed-adverse-effect-level (NOAEL) reported for these effects is 0.001 mg/m3 (or 1 mg/m3).

ATSDR's estimated exposure dose for incidental inhalation is 1 x 10-8 (or 0.00000001) mg/kg/day. This dose is based on a chromium air particulate concentration of 6 x 10-7 mg/m3 that we estimated using methods described previously in this appendix. Our estimated chromium airborne concentration is many times lower than the health-based guideline. The actual particulate concentration of chromium VI from airborne soils off site of the Fernald facility is probably even lower than estimated (above) because ATSDR scientists assumed that all chromium was present as chromium VI, and it is more likely that the soils contained both chromium VI and less toxic chromium III compounds.

EPA has established a unit cancer risk of 0.012 per mg/m3 chromium in air, based on a lung cancer mortality rate in chromate-exposed male workers compared to the U.S. white, male population (Mancuso 1975; IRIS 1998). The unit risk can be interpreted to mean that there are 0.012 additional lung cancer deaths expected for every mg/m3 increase in chromium exposure concentration. The worker studies involved exposure to both chromium III and chromium VI, although it was assumed that only chromium VI contributed to lung cancer deaths, and that no less than one-seventh of total chromium exposure involved chromium VI. Other scientists have argued that the assumption that the ratio of chromium III to chromium VI is 6 to 1 may lead to a seven-fold underestimation of cancer risk. Because the smoking habits of chromate workers were assumed to be similar to those of the general U.S. white male population, it has also been argued that this assumption may lead to an overestimation of cancer risk, because it is generally accepted that the proportion of smokers is higher for industrial workers than for the general population (IRIS 1998).

Based on this unit cancer risk and our estimated airborne concentrations, there is no expected increased risk of cancer from inhalation of chromium-contaminated soil off site of the Fernald facility. However, when considered together with the possible contribution from radionuclide exposure to lung cancer occurrence in Fernald area residents (CDC 1998), any addition to lung cancer risk may be important.

Manganese

ATSDR's health guideline for chronic (more than 1 year) inhalation of manganese is 4 x 10-5 mg/m3 (ATSDR 1997b). The guideline is based on neurological effects in foundry workers exposed to manganese dust, at concentrations ranging from 0.2 to 1.4 mg/m3 (median = 0.14 mg/m3) for 1 to 35 years (Iregren 1990). Exposed workers had below-average scores on neurobehavioral tests such as reaction time and finger tapping. A lowest-observed-adverse-effect-level (LOAEL) of 0.14 mg/m3 was reported for this study. The health-based guideline is considerably lower than the reported LOAEL, because of uncertainty in extrapolating from occupational to chronic (continuous) exposure to account for effects from continuous exposure and because of differences in the toxicity of different forms of manganese exposure in the available studies (ATSDR 1997b). The findings of this study are supported by other studies involving occupational exposure to manganese among battery and alloy factory workers (Roels et al. 1987, 1992; Mergler et al. 1994). Workers in these later studies had decreased performance in neurobehavioral tests and other neurological deficits from chronic exposure to various manganese compounds in dusts.

Our estimated airborne concentration of manganese is 0.002 mg/m3 for air pathways at the Fernald site. Although our estimated airborne concentration is higher than the health-based guideline, there is considerable margin of uncertainty in the derivation of the guideline from the reported LOAEL (ATSDR 1997b). Our estimated air concentration is several times lower than the reported LOAEL for neurotoxic effects in workers (ATSDR 1997b).

Because manganese is essential in the human diet, the National Research Council has established a range of Aestimated safe and adequate daily dietary intakes@ (ESADDIs) for manganese. The ESADDIs are 0.3 to 2.0 mg/day for children less than under age 6 and 2 to 5 mg/day for persons over age 11(NRC 1989). The World Health Organization estimates that the average daily consumption of manganese in the adult diet ranges from 2 to 9 mg/day, and that an intake of 8 to 9 mg/day is Aperfectly safe.@ ATSDR has established an interim health guideline for manganese ingestion of 0.07 milligrams (mg) manganese per kilogram (kg) body weight per day (ATSDR 1997b). This guideline is equivalent to a daily intake of 4.9 mg for a 70-kg adult and 0.91 mg for a 13-kg child.

ATSDR's estimated manganese inhalation doses for air pathways (Table B-2) are equivalent to a daily intake of 0.02 mg/day for adults (assuming a body weight of 70 kilograms) and 0.009 mg/day for a child (assuming a body weight of 13 kilograms). Therefore, our estimated exposure doses are lower than ATSDR's interim health guideline for ingestion of manganese and lower than Asafe and adequate@ daily intakes established by the National Research Council and World Health Organization. Manganese deficiency is not likely for Fernald area residents, however, because additional sources of manganese are contributed by the diet and possibly the environment (manganese is naturally high in groundwater in the Fernald area). Considering these additional sources of manganese exposure, estimated daily intakes for Fernald area residents are likely to be within Asafe and adequate@ ranges and are not likely to result in adverse health effects.

References

ATSDR. 1992a. Toxicological profile for boron. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). July, 1992.

ATSDR, 1992b. Analysis paper: Impact of lead-contaminated soil on public health. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). May, 1992.

ATSDR, 1993. Public health assessment guidance manual. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR).

ATSDR, 1997a. Toxicological profile for lead. Draft for public comment. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). August, 1997.

ATSDR, 1997b. Toxicological profile for manganese. Draft for public comment (update). U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). September, 1997.

ATSDR, 1998a. Toxicological profile for arsenic. Draft for public comment. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). August, 1998.

ATSDR, 1998b. Toxicological profile for chromium. Draft for public comment (update). U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). August, 1998.

ATSDR, 1999. Toxicological profile for uranium. U.S. Public Health Service, Agency for Toxic Substances and Disease Registry (ATSDR). September, 1999.

CDC, 1991. Preventing lead poisoning in young children. U.S. Public Health Service, Centers for Disease Control and Prevention (CDC). October, 1991.

CDC, 1998. Estimation of the impact of the former Feed Materials Production Center (FMPC) on lung cancer mortality in the surrounding community. National Centers for Environmental Health, Division of Environmental Hazards and Health Effects, Radiation Studies Branch. December, 1998.

DOE, 1972 - 1999. Environmental monitoring annual report for 1972 - 1995, and the integrated environmental monitoring program for 1997 - 1999. U.S. Department of Energy, Fernald Environmental Management Project (and Feed Materials Production Center).

Doisy, E.A., 1973. Effects of deficiency in manganese upon plasma levels of clotting proteins and cholesterol in man. Trace element metabolism. In: Animals-2, 2nd ed. Hoekstra, W.G., Suttie, J.W., Ganther, A.E., and Mertz, W., eds. Baltimore, MD: University Park Press, 668 - 670.

EPA, 1989. Risk assessment guidance for Superfund, Vol. 1, human health evaluation manual (part A). EPA/540/1-89/002. Washington, DC: U.S. Environmental Protection Agency.

EPA, 1999. Exposure factors handbook. EPA/600/C-99/001. U.S. Environmental Protection Agency, Office of Research and Development. (CD-ROM).

Friedman, B.J., Freeland-Graves, J.H., Bales, C.W., et al., 1987. Manganese balance and clinical observations in young men fed a manganese-deficient diet. J Nutr 117: 133 - 143.

Garagrant, D.H., Bernstein, L., Peters, J.M., et al., 1984. Respiratory and eye irritation from boron oxide and boric acid dusts. J Occup Med 26: 584 - 586.

IRIS, 1998. Integrated risk information system. U.S. Environmental Protection Agency. Online.

IT, 1986. Final interim report - air, soil, water, and health risk assessment in the vicinity of the FMPC, Fernald, Ohio. November, 1986.

Killough, G.G., Case, M.J., Meyer, K.R., et al., 1998. The Fernald Dosimetry Reconstruction Project, Task 6 - radiation doses and risk to residents from FMPC operations from 1951 - 1988. Volume II appendices. Radiological Assessment Corporation (RAC) Report No. CDC-1. Neeses, SC: September, 1998.

Lindberg, E., and Hedenstierna, G., 1983. Chrome plating: Symptoms, findings in the upper airways, and effects on lung function. Arch Environ Health 38: 367 - 374.

Mancuso, T.F., 1975. Consideration of chromium as an industrial carcinogen. International Conference on Heavy Metals in the Environment, Toronto, Ontario, Canada: October 27 - 31, 343 - 356.

Mergler, D., Huel, G., Bowler, R., et al., 1994. Nervous system dysfunction among workers with long-term exposure to manganese. Environ Res 64(2): 151 - 180.

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ODH, 1988. Ohio Department of Health study of radioactivity in drinking water and other environmental media in the vicinity of the U.S. Department of Energy's Feed Materials Production Center and Portsmouth Gaseous Diffusion Plant. December, 1988.

Roels, H.A., Lauwerys, R., Buchet, J.P., et al., 1987. Epidemiological survey among workers exposed to manganese: Effects on lung, central nervous system, and some biological indices. Am J Ind Med 11: 307 - 327.

Roels, H.A., Ghyselen, P., Buchet, J.P., et al., 1992. Assessment of the permissible exposure level to manganese in workers exposed to manganese oxide dust. Br J Ind Med 49(1): 25 - 34.

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Tseng, W.P., 1977. Effects and dose-response relationship of skin cancer and blackfoot disease with arsenic. Environ Health Perspect 19: 109 - 119.

Weir, R.J., and Fisher, R.S., 1972. Toxicologic studies on borax and boric acid. Toxicol Appl Pharmacol 23: 351 - 364.

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