PUBLIC HEALTH ASSESSMENT
OGDEN DEFENSE DEPOT
OGDEN, WEBER COUNTY, UTAH
Question #1. In the Summary (paragraph #1) it is stated that non-ordnance items were present, but later there are descriptions of chemical warfare agents (ordnance) stored and disposed on DDOU. The "non" should be removed as a prefix for ordnance.
Response #1. The sentence was changed to:
"DDOU has stored, maintained, and issued ordnance and non-ordnance items to military installations since 1941."
Question #2. The last complete paragraph on page 1 should perhaps contain some qualifying language to point out that this assessment is based on current toxicologic and risk assessment knowledge, in the likely event that future risk may change with the improved biomedical knowledge and techniques.
Response #2. ATSDR uses various health criteria to make decisions on whether or not a given situation is likely to pose a threat to public health. Those criteria are subject to change as on-going research efforts generate new data and as public health policies change. When new information becomes available that changes the determinations made in the public health assessment, the assessments are updated. The public health action plan (PHAP) is part of the public health assessment. The PHAP is to ensure that this public health assessment not only identifies public health hazards, but provides a plan of action designed to mitigate and prevent adverse human health effects resulting form exposure to hazardous substances in the environment. Included is a commitment on the part of ATSDR to follow up on this plan to ensure that it is implemented.
Question #3. The Summary states that DDOU is within the city limits, while this (Background) section states DDOU is northwest of the city limits; this disparity should be corrected.
Response #3. The sentence was changed to:
"Defense Depot Ogden (DDOU) is a 1,139 acre installation at 1200 South Tomlinson Road, northwest of the city of Ogden, Weber County, Utah."
Question #4. The first complete paragraph on page four lists burial site 3-C as part of OU1. Burial site 3-C is now being remediated as a part of OU3. This correction should also be made on page five under the description of OU3. In addition, Table 1 should be revised to reflect these recent changes.
Response #4. Burial site 3-C was moved to OU3 and Table 1 was amended.
Question #5. Under the descriptions of operable units 1,2, and 4, the groundwater contaminants should be listed and described since it (shallow groundwater) is considered a part of the OUs.
Response #5. This sentence was added:
"Shallow groundwater is considered part of OUs 1,2, and 4."
The contaminants are discussed in the Environmental Contamination and Other Hazards Section of the document.
Question #6. Table 1. lists phosgene while omitting lewisite for OU3 soil analyses, which conflicts with the report on page 5. Lewisite (an arsenical compound) should be added to Table 1, and the presence of phosgene (a potent toxicant -COCL2) should be fully described with its associated health risks.
Response #6. Lewisite was added to Table 1. A public health assessment only discusses chemicals in detail when there is evidence of exposure. The public health assessment does not quantitate risk.
Question #7. Surface water should also be listed as a media in which contaminants have been detected (under On-Site Contamination Part A.)
Response #7. Surface water was added to the sentence:
"Contaminants have been detected in soil, surface water, sediment, groundwater, and indoor air samples."
Question #8. Soil gas levels for OU4 as listed appear to be low and not moderate; therefore "moderate" should be removed from paragraph #3, page 15.
Response #8. The soil gas levels at OU4 were less than 1.6 ppb for TCE and would be considered low. Moderate has been removed from the sentence.
Question #9. A major technical problem exists with the questionable assertation in the last paragraph on page 15, where it is stated that the PCB levels are not a contaminant of concern. The EPA calculates that an excess population (1 in one million) risk for cancer would occur at 0.22 mg/kg (ppm) of PCB in residential soils and at 0.37 mg/kg (ppm) of PCB in occupational soils; thus, the levels of 0.17 - 2.13 (ppm) found here would not be considered to be free from health risks. A better reference and solid scientific/medical rational is needed to support this assertation about PCBs.
Under "Actions Undertaken" on page 41, the premise that PCBs are not a contaminant of concern should be removed or else better justified, especially in light of the exposure at a playground site where levels exceed those that can pose a risk of cancer greater than one excess in one million people.
Response #9. ATSDR uses various health criteria to make decisions on whether or not a given situation is likely to pose a threat to public health. When existing research or exposure data are available that are adequate to clearly determine what health effects might be associated with exposures to specific chemicals, those data are used. ATSDR used PCB exposure information from a variety of sources. One source, ATSDR's Toxicological Profile for Polychlorinated Biphenyls, compiled data from 19 studies of populations without occupational exposures to PCBs. Beginning in 1982, pilot studies involving 766 subjects exposed to PCBs from 12 toxic waste sites in the United States were conducted. Although PCB contamination levels as high as 2.5 ppb in well water and 330 ppm (330,000 ppb) in soil samples were measured, serum PCB levels in exposed people from 10 of the 12 sites were not higher than serum PCB levels in the nonoccupationally exposed populations. The higher serum PCB levels found in exposed people at two sites may be attributed to the historic prevalence of occupationally related exposures. Therefore, it does not appear that PCB levels in soils are absorbed to an extent that would influence the serum levels. The soils in several of those studies were in residential neighborhoods where children would be expected to have come in contact with them on a daily basis. In the playground at Ogden, it is not expected that children will have daily contact with contaminated soil or that contact would occur over many years (>5); therefore, it is not anticipated that the intermittent exposures of the children to PCB contaminated soil would be of public health concern.
In general, the nonoccupationally exposed population has a serum PCB level in the range of 1-20 ppb. Most people have exposures to PCBs through food. In 1975, approximately 50% of the U.S. fish population had PCBs levels above 0.22 ppm (or 220 ppb) (the EPA cancer risk concentration). That estimate involved an examination of market fish and did not consider the exposures to fish from sport or subsistence fishing. Another nonoccupational exposure route is through the air in areas where there are landfills and PCB incinerators. Indoor air levels of PCBs have been measured as being higher than outdoor levels. Studies have not yet investigated the effects on blood levels from those air exposures as compared to exposures through food. Studies have also not been done to investigate trends in the levels of PCBs in blood or fat tissue. As a part of the Third National Health and Nutrition Evaluation Survey (NHANES III), the levels of PCBs in human blood samples will be evaluated. That study will add more information on background levels in the general population.
There are few studies that examine the bioavailability of PCBs from soil, air, or water. Those studies would help in the evaluation of the exposure estimates that are used.
The references used for the evaluation of potential health effects of the low levels of PCBs detected in the playground area included the following:
ATSDR. Toxicological Profile for Selected PCBs (Aroclor -1260, -1254, -1248, -1242, -1232, -1221, and -1016). June 1992.
Sittig M. Handbook of Toxic and Hazardous Chemicals and Carcinogens. 2nd edition. Park Ridge, NJ: Noyes Publications, 1985.
Shalat SL, True LD, Fleming LE, and PE Pace. "Kidney Cancer in Utility Workers Exposed to Polychlorinated Biphenyls (PCBs)." British Journal of Industrial Medicine 1989; 46:823-824.
Lawton RW, Ross MR, Feingold J, and JF Brown. "Effects of PCB Exposure on Biochemical and Hematological Findings in Capacitor Workers." Environmental Health Perspectives 1985; 60:165-184.
Fischbein A. "Liver Function Tests in Workers with Occupational Exposure to Polychlorinated Biphenyls (PCBs): Comparison with Yusho and Yu-Cheng." Environmental Health Perspectives 1985; 60:145-150.
Fischbein A, Wolff MS, Lilis R, Thorton J, and IJ Selikoff.
"Clinical Findings among PCB-Exposed Capacitor Manufacturing Workers." Annals of the New York Academy of Sciences 1979; 320:703-715.
Reggiani G and R Bruppacher. "Symptoms, Signs, and Findings in Humans Exposed to PCBs and Their Derivatives." Environmental Health Perspectives 1985; 60:225-232.
Kimbrough RD. "Human Health Effects of Polychlorinated Biphenyls (PCBs) and Polybrominated Biphenyls (PBBs)." Annual Review of Pharmacology and Toxicology 1987; 27:87-111.
Emmett EA, Maroni M, Schmith JM, Levin BK, and J Jeffreys.
"Studies of Transformer Repair Workers Exposed to PCBs: I. Study Design, PCB Concentrations, Questionnaire, and Clinical Examination Results." American Journal of Industrial Medicine 1988; 13:415-427.
Fischbein A, Wolff MS, Berstein J, Selikoff IJ, and J Thornton.
"Dermatological Findings in Capacitor Manufacturing Workers Exposed to Dielectric Fluids Containing Polychlorinated Biphenyls (PCBs)." Archives of Environmental Health 1982; 37(2):69-74.
Fischbein A, Rizzo JN, Soloman SJ, and MS Wolff.
"Oculodermatological Findings in Workers with Occupational Exposure to Polychlorinated Biphenyls (PCBs)." British Journal of Industrial Medicine 1985; 42:426-430.
Taylor JS. "Environmental Chloracne: Update and Overview." Annals of the New Academy of Sciences 1979; 320:295-307.
Taylor PR, Stelma JM, and CE Lawrence. "The Relation of Polychlorinated Biphenyls to Birth Weight and Gestational Age in the Offspring of Occupationally Exposed Mothers." American Journal of Epidemiology 1989; 129(2):395-406.
Jacobson JL, Jacobson SW, and HEB Humphrey. "Effects of In Utero Exposure to Polychlorinated Biphenyls and Related Contaminants on Cognitive Functioning in Young Children." Journal of Pediatrics 1990; 116:38-45.
Gladen BC, Rogan WJ, Hardy P, Thullen J, Tingelstad J, and M Tully.
"Development after Exposure to Polychlorinated Biphenyls and Dichlorodiphenyl Dichloroethene Transplacentally and Through Human Milk." Journal of Pediatrics 1988; 113:991-995.
Fait A, Grossman E, Self S, Jeffries J, Pellizzari ED, and EA Emmett. "Polychlorinated Biphenyl Congeners in Adipose Tissue Lipid and Serum of Past and Present Transformer Repair Workers and a Comparison Group." Fundamental and Applied Toxicology 1989; 12:42-55.
Emmett EA, Maroni M, Jeffreys J, Schmith J, Levin BK, and A Alvares. "Studies of Transformer Repair Workers Exposed to PCBs: II. Results of Clinical Laboratory Investigations." American Journal of Industrial Medicine 1988; 14:47-62.
Kreiss K. "Studies on Populations Exposed to Polychlorinated Biphenyls." Environmental Health Perspectives 1985; 60:193-199.
Kreiss K, Roberts C, and HEB Humphrey. "Serial PBB Levels, PCB Levels, and Clinical Chemistries in Michigan's PBB Cohort." Archives of Environmental Health 1982; 37(3):141-147.
Jacobson JL, Humphrey HEB, Jacobson SW, Schantz SL, Mullin MD, and R Welch. "Determinants of Polychlorinated Biphenyls (PCBs), Polybrominated Biphenyls (PBBs), and Dichlorodiphenyl Trichloroethane (DDT) Levels in the Sera of Young Children." American Journal of Public Health 1989; 79(10):1401-1404.
Jensen AA. "Background Levels in Humans." In: Kimbrough RD and AA Jensen, eds. Halogenated biphenyls, terphenyls, naphthalenes, dibenzodioxins, and related products. New York: Elsevier, 1989:345-380.
Stehr-Green PA, Burse VW, and E Welty. "Human Exposure to Polychlorinated Biphenyls at Toxic Waste Sites: Investigations in the United States." Archives of Environmental Health 1988; 43(6):420-424.
Question #10. The second to last paragraph on page 16 does not describe what chemical(s) the bore sample analyses tested as low (<1ppm); it is assumed to be VOCs. Please clarify.
Response #10. The following clarification was added:
"Borehole sample analyses were low (<1 ppm). The samples were analyzed for BNAEs, VOCs, pesticides/PCBs and metals."
Question #11. The last paragraph on page 16 describes results for OU3 subsurface soils on adamsite (a previously undescribed arsenical), but not for lewisite which had been identified earlier; this analytical disparity should be clarified.
Response #11. ATSDR reviewed the analytical data for the subsurface soils for OU3. It is reported here. Lewisite was not detected in subsurface soils.
Question #12. The relatively high (9,580 ppm) levels of lead in the subsurface soils at the Plain City Canal (which is now a part of OU1 and not OU4) were not adequately addressed; i.e., was this a single sample or mean, what was the source, and what might be the risk from exposure?
Response #12. The text has been changed to reflect that the Plain City Canal is now part of OU1.
The text states that the lead sample was taken from a test pit (TP-2) and had elevated levels of lead (9,580 ppm). The average test pit was eight feet deep, 15 feet long, and three feet wide and that test pits were excavated in suspected burial areas at all of the OUs. Contaminated soils may expose people who live or work near a site to contaminants at levels of health concern. Ingestion of contaminated soil, particularly by children, is a primary concern. ATSDR has defined surface soil as the top three inches of soil. At DDOU, personnel can only be exposed to subsurface soil during excavation or construction. If remediation of the Plain City Canal involves excavation, current health and safety regulations require personnel protection to prevent exposure.
Question #13. The public health assessment should document that DDOU is currently planning to further investigate the surface water and sediment pathway.
Response #13. Pages 17 and 18 contain the following information on the proposed
"DDOU will conduct further stream analysis."
"DDOU will conduct further sediment analysis."
Question #14. A discrepancy exist between the stated high TCE levels of 17 ppb in paragraph 4 on page 18 and the much higher levels shown in Figure 13 on page 61 where TCE levels in groundwater are up to 100 ppb, greatly exceeding the MCL of 1 ppb. Please clarify.
Response #14. The groundwater contamination plume displayed in Figure 13 is for vinyl chloride. The figure will be correctly titled. The current MCL for TCE is 5 ppb.
Question #15. A major difficulty with this report regards the contention made in paragraph 4 on page 19 that the elevated levels of metals in groundwater did not come from DDOU at OU3. The rational presented actually supports the opposite conclusion, since the authors expected arsenic and chromium to be elevated at OUs 1 and 4 as well, but they were not. The presented argument is not scientifically strong enough to soundly support the report's conclusion; that high metal levels are simply coming from leachates of soils with naturally high metal levels. This conclusion and its consequences for health risk should be strengthened and clarified, or else removed and more quality data obtained to confirm this scientifically weak hypothesis. Furthermore, the public health assessment should state that DDOU modified its methods for obtaining groundwater samples since the Draft (For Public Comment) health assessment was written. New methods do not filter the water prior to analysis.
Again, the third paragraph on page 38 makes a highly questionable assumption that metal contamination does not emanate from DDOU.
Response #15. The information reviewed by ATSDR did not conclusively define the source of the metals contamination in groundwater. However, EPA and the state agreed with DDOU that the source of metals contamination in groundwater cannot be attributed to DDOU (11)(12). From a public health perspective, people may be exposed to contaminated groundwater through the use of their private wells. Groundwater may be used for potable purposes west of the DDOU boundary. Seven private wells west of the depot boundary will be sampled and their use determined by DDOU if requested by the residents. ATSDR recommends that the analyses include unfiltered metals samples because the source of metals in groundwater is yet undetermined. ATSDR does not consider the filtered samples adequate for comparison to EPA drinking water standards (MCLs), which are based on unfiltered samples. The paragraph has been amended for clarity.
ATSDR reviewed the current workplan for groundwater sampling and analysis in April 1992. That plan included field-filtering the groundwater samples prior to analysis for metals.
Question #16. The reason for the high detection limits cited in the last paragraph on page 20 needs additional clarification, since it implies all (not just other halogenated hydrocarbons) contaminants had detection limits raised because of the very high DCE levels. This depends greatly on the chemical method, sample preparation, and the analyte; thus, such a "blanket" statement cannot be made validly from the information in their report.
Response #16. The sentence was clarified to read:
"The high detection limits may mask the presence of other halogenated hydrocarbons in the samples."
Question #17. The background levels presented in Table 2 seem low, and are suspect as perhaps not being representative, since the entire group of metals is consistently lower than the regional values.
Response #17. The background metals in Table 2 are compiled from a list that DDOU compiled from 60 soil samples they thought represented background concentrations.
Question #18. What about the contaminants of concern for OU3? The information reported (in Table 3) is not taken from the most recent DDOU documents.
Response #18. ATSDR has requested the most recent information from DDOU. DDOU did not comment on Table 3 or the contaminants of concern at OU3.
Question #19. The top line on page 36 should be qualified by reading as "Currently, no significant exposures...".
Response #19. The word "significant" and similar words are not descriptive for characterizing exposures and therefore ATSDR avoids using them in public health assessments. Instead, ATSDR will state whether or not any exposures have occurred in the past, present, or may occur in the future.
Question #20 The last sentence of the last paragraph on page 36 should be revised to reflect DDOU's current plan to reevaluate and investigate the surface water at DDOU. DDOU is currently in the process of developing a work plan for this investigation.
Response #20. The text has been changed to:
"DDOU will conduct further surface water and sediment sampling. ATSDR will review the information as it becomes available."
Question #21. The second sentence on page 38 appears to contradict the first and the overall conclusion; since it says that the data do not indicate that people are not being exposed, implying that people may in reality be exposed.
Response #21. The sentence contained a typo. It has been corrected to:
"The available data do not indicate that people are being exposed to contamination."
Question #22. The second paragraph on page 38 should qualify that "only low levels" of BNAEs, pesticides, and metals were found in comparison to the VOCs.
Response #22. ATSDR is interested in the contaminants that exceed comparison values, not a comparison of contaminant concentrations. While VOCs may be the most concentrated and wide-spread contaminant, some contaminants exceeding comparison values are not listed for inclusion in future analyses. ATSDR would like to see all contaminants exceeding their comparison values included in the list of analytes so we can determine if exposure to the contaminants at the detected levels may be of public health concern.
Question #23. Number 1 on page 40 should expound the need for surveillance by suggesting that all analytes from Table 4 on page 23 be included for testing prior to completion of remediation.
Response #23. The text has been changed to:
"1. All contaminants exceeding their comparison values should be included in the list of future analytes (Table 4)."
Question #24. The Summary on page 2 indicated that no follow-up activities are planned; however, number six on page 42 indicated that there will be follow-up activities annually. Please clarify.
Response #23. The follow-up health activities referred to in the summary are conducted by
ATSDR. All public health actions (conducted by ATSDR and others) will be followed up
on by ATSDR. The text has been changed to reflect this difference.