PUBLIC HEALTH ASSESSMENT
SHERWOOD MEDICAL COMPANY
NORFOLK, MADISON COUNTY, NEBRASKA
This section of the public health assessment describes environmental sampling previously conductedat the site and identifies contaminants of concern found in specific environmental media. Thecontaminants of concern are evaluated later in the health assessment to determine if exposure to them will affect the public's health.
ATSDR selects and discusses contaminants of concern using the following information:
- concentrations of contaminants on and off the site;
- quality of field and laboratory data, and sample design;
- comparison of on- and off-site contaminant concentrations with comparison values for noncancer and cancer endpoints; and
- community health concerns.
As discussed previously, the listing of a contaminant in the following tables does not mean that itwill cause adverse health effects if people are exposed at the reported concentrations. Rather, thelisting of a contaminant indicates that the contaminant will be evaluated further in this public healthassessment. When a contaminant is selected as a contaminant of concern in one medium, itspresence or absence in all media sampled will be discussed. In addition, when a contaminant isidentified as a contaminant of concern on site, its potential to migrate off site will also be discussed.
The data tables include the following acronyms and abbreviations:
|=||Cancer Risk Evaluation Guide|
|=||Environmental Media Evaluation Guide|
|=||Reference Dose Media Evaluation Guide|
|=||Lifetime Health Advisory|
|=||Maximum Contaminant Level Goal|
|=||Maximum Contaminant Level|
|=||Proposed Maximum Contaminant Level Goal|
|=||not available or not analyzed|
|=||parts per billion|
|=||parts per million|
|=||milligrams per liter|
|=||micrograms per liter|
|=||compound was found in associated blank as well as in the sample, ornumerical value is above instrument detection limit (DL) and belowcontract-required detection limit (CRDL)|
|=||compound identified in an analysis at a secondary dilution factor|
|=||estimated numerical value; or concentration exceeds the calibrationrange of the instrument for the specific analysis|
|=||estimated numerical value, or value is above CRDL and is estimatedbecause of a quality control (QC) protocol|
|=||numerical value is less than limit of quantitation or less than contract-required quantitation limits, or duplicate injection precision was notmet; therefore, numerical value may be semi-quantitative|
Comparison values are contaminant concentrations in specific media used to select contaminants forfurther evaluation. These values include Environmental Media Evaluation Guides (EMEGs),Reference Dose Media Evaluation Guides (RMEGs), Cancer Risk Evaluation Guides (CREGs), andother relevant guidelines.
EMEGs are media-specific values developed by ATSDR for use in selecting environmentalcontaminants of potential health concern. EMEGs are calculated using noncancer health endpointsand do not consider potential carcinogenic effects. RMEGs are media-specific values developed byATSDR from EPA Reference Doses (RfDs). RfDs are EPA's estimate of the daily exposure to acontaminant that is unlikely to cause adverse health effects. CREGs are estimated contaminantconcentrations expected to cause no more than one excess cancer in a million persons exposed overa lifetime (70 years). Maximum Contaminant Level Goals (MCLGs) are EPA-developed drinkingwater health goals. EPA believes that MCLGs represent levels at which no known or anticipatedadverse effect on the health of persons should occur that allow an adequate margin of safety. Proposed Maximum Contaminant Level Goals (PMCLGs) are MCLGs that are being proposed. Maximum Contaminant Levels (MCLs) represent contaminant concentrations that EPA deems to beprotective of public health (considering the availability and economics of water treatmenttechnology) over a lifetime (70 years) at an exposure rate of 2 liters water per day. EPA's LifetimeHealth Advisories (LTHAs) represent the level of a contaminant in drinking water (with a margin ofsafety) at which adverse noncancer health effects would not be anticipated during a lifetime (70years) of exposure. MCLs are regulatory concentrations; PMCLGs, MCLGs, and LTHAs are not.
A considerable amount of sampling data has been collected from environmental media on and offthe Sherwood Medical site since October 1987. The data were obtained mainly by the NebraskaDepartment of Environmental Control, the Nebraska Department of Health, and the U.S. EPA(through contractors.) Relevant contaminant data from the past sampling efforts, which weredescribed in the Site Description and History section, are discussed and evaluated in the On-SiteContamination and Off-Site Contamination subsections following. For the purpose of this healthassessment, "on-site" refers to sampling locations on the Sherwood Medical plant property, while"off-site" indicates sampling locations outside the plant property line (e.g., at the Park Mobile HomeCourt.)
As previously discussed, in September 1989 an EPA contractor inactivated a 2,000-gallon UST andconcrete settling basin at the Sherwood Medical plant. During the inactivation, the contractorremoved waste liquids and sludge solids from the UST and settling basin and sampled the liquids forVOCs and the solids for VOCs and EP toxic metals. At that time, liquids and solids in an on-sitefacility septic tank also were sampled for VOCs and EP toxic metals (solids only). In December1990, sludge solids from the facility septic tank, which had been taken out of service during theprevious month, were sampled for VOCs and metals. The location of the UST and settling basin is shown in Figure 3.
As indicated in Table 1a, several VOCs were detected in liquid wastes from the UST/settling basin and septic tank.
The waste sludge solids contained several VOCs and metals (Table 1b). Sludge metals generallywere found at levels similar to background soil levels for the western United States (12), exceptantimony and mercury, which were found at slightly elevated levels.
|Chloroform||500M - 1,000M||9/89||13, 14|
|1,1-dichloroethane||1,900 - 2,600||9/89||13, 14|
|Methylene chloride||78,000*||9/89||13, 14|
|1,1,1-trichloroethane||21,000 - 22,400||9/89||13, 14|
|Chloroform||0.775M - 65M||9/89, 12/90||13, 15|
|1,1-dichloroethane||0.775M - 980||9/89, 12/90||13, 15|
|Methylene chloride||ND - 1,200M||9/89, 12/90||13, 15|
|1,1,1-trichloroethane||4.8 - 64,000||9/89, 12/90||13, 15|
|Tetrachloroethylene||1.7 - 9,680||9/89, 12/90||13, 15|
During the July 1988 expanded site investigation, samples from four of the plant's wastewaterdischarges to Sherwood Lake were collected and analyzed for VOCs. The April and May 1991RI/FS activities also included collection of wastewater samples, which were analyzed for VOCs andmetals. Figure 4 shows the locations of the wastewater effluent samples. As shown in Table 1c.,the 1988 wastewater samples contained low levels of several VOCs. These samples were collectedwhile the plant was using untreated VOC-contaminated well water (from Sherwood well #5) forcooling water purposes and, after use, discharging the cooling water to Sherwood Lake. InSeptember 1989, the plant discontinued the use of Sherwood well #5 as a cooling water source, asevidenced by the 1991 wastewater samples, which showed only trace levels of one VOC--1,1,1-TCA (Table 1c). The 1991 samples also contained low levels of several metals; only arsenic wasfound at levels exceeding ATSDR's comparison values. Table 1c. Contaminant Concentrations in On-site Waste Materials (WastewaterDischarges to Sherwood Lake)
Table 1c. Contaminant Concentrations in On-site Waste Materials (WastewaterDischarges to Sherwood Lake)
|Contaminant||Concentration Range (µg/L)||Reference||Comparison|
|1,1-dichloroethane||ND - 13.0||ND||2, 16||None|
|1,1-dichloroethene||ND - 6.0||ND||2, 16||90||EMEG|
|Tetrachloroethylene||ND - 6.0||ND||2, 16||100||RMEG|
|1,1,1-trichloroethane||ND - 61.0||ND - 1J||2, 16||200||LTHA|
|Arsenic||NA||ND - 9.6B||2, 16||3||EMEG|
|Barium||NA||122B - 404||2, 16||700||RMEG|
|Lead||ND||ND - 4.7J||2, 16||15||AL|
On-site soil samples were collected from monitoring well borings during Stage I and Stage IB RI/FSdrilling activities in April and May 1991 and August 1991, respectively. Each sample represented a2-foot soil segment taken between 0 and 14 feet below ground surface; therefore, data for surfacesoil (less than or equal to 3 inches deep) could not be separated out. The samples were analyzed forEPA Contract Laboratory Program (CLP) VOCs and Target Analyte List (TAL) inorganic analytes. Figure 4 shows the soil sampling locations.
As indicated in Table 2a, several VOCs and metals were detected in the soil samples. The levels ofmetals found, however, were similar to background soil concentrations for the western United States(12). It should be noted that the concentrations of VOCs detected in on-site soil samples generallyincreased with depth from 0 to 14 feet below ground surface. Soil samples collected at depths abovethe normal influence of groundwater did not contain detectable levels of VOCs. However, soilsamples from below the normal water table surface did contain low concentrations of VOCs. Thosefindings indicate that VOC contamination of site soils is generally due to contact with VOCs in site groundwater.
In June 1992, approximately 15 soil samples were collected from Stage II soil borings at four areasidentified from previous sampling results as potential groundwater contamination sources. The fourareas identified were the CS/CN Area, the UST Area, the Cullet Silo Area, and the Grassy KnollArea (see Figure 3). Each sample represented a 2-foot soil segment collected at a depth rangingfrom 0 feet to a maximum of 12 feet below ground surface.
The results of the VOC analyses of the Stage II soil samples (Table 2b) are discussed in the following paragraphs.
At the UST and Grassy Knoll areas, the only contaminants detected were PCE and toluene,respectively.
At the Cullet Silo Area, PCE was detected in one sample at a depth of 0 to 2 feet, while benzene,toluene, ethylbenzene, and xylene (BTEX compounds) were found in samples at depths of 8 to 12feet. The presence of these BTEX contaminants is likely due to gasoline leakage from a 550-gallonUST in use from 1977 to 1991. The gasoline storage tank, which was removed in November 1991,was directly upgradient of the area where BTEX soil contaminants were found.
At the CS/CN Area, PCE, TCA, and toluene were detected in samples from two soil borings. Thehighest levels of these compounds were found at a depth of 6-8 feet below ground surface. Inaddition, the level of PCE increased with depth from 2 to 8 feet. Because the normal depth to thegroundwater surface in this area ranges from about 7 to 11 feet, significant soil contamination in thevadose (unsaturated) zone is indicated in the CS/CN area.
In summary, the soil sampling results indicate significant VOC soil contaminant above the watertable in the CS/CN areas but not in any of the other three suspected source areas. However, VOCsoil contamination below the groundwater surface is possible at the CS/CN area and the UST area.
It is noted that no on-site surface soil (0 inches - 3 inches deep) samples were collected during theRI. However, analytical data from soil samples taken at a depth of 0 to 2 feet below ground surfaceshow that significant VOC soil contamination is not present above a depth of 2 feet. Instead, soilcontamination at the site is generally limited to a depth of 7 to 11 feet except at the CS/CN areawhere contamination is present at a depth of 6-8 feet. These findings are reasonable because VOCsoil contamination at the site resulted from subsurface sources, such as solvents from the UST/septicsystem, and from contact with contaminants in the groundwater table. Because contamination ofsurface soils is not believed to be a problem at the site, the lack of surface soil sampling data is not important.
|1,1-dichloroethane||ND - 0.026||(1)||2||None|
|Tetrachloroethylene||ND - 2.4||(1)||2||10||CREG|
|1,1,1-trichloroethane||ND - 0.10||(1)||2||None|
|Arsenic||ND - 3.5||(1)||2||0.4||CREG|
|Barium||21.2B - 383||(1)||2||100||RMEG|
|Beryllium||ND - 0.61B||(1)||2||0.2||CREG|
|Lead||1.5 - 11.9||(1)||2||None|
|Mercury||ND - 0.19||(1)||2||None|
|Vanadium||2.6B - 20.6||(1)||2||6||EMEG|
|Tetrachloroethylene||ND - 3,400||6/92||7||10||CREG|
|1,1,1-trichloroethane||ND - 580||6/92||7||None|
|Benzene||ND - 0.22||6/92||7||20||CREG|
|Ethylbenzene||ND - 0.26||6/92||7||200||RMEG|
|Toluene||ND - 14||400||7||400||RMEG|
|m & p-Xylene||ND - 0.78J||6/92||7||4,000||RMEG|
|o-Xylene||ND - 0.54J||6/92||7||4,000||RMEG|
Groundwater - Monitoring Wells
As previously discussed, groundwater monitoring wells were installed at the Sherwood Medical siteduring Stage I RI/FS field activities in April and May 1991 and during Stage IB in August andSeptember 1991. A total of 45 monitoring wells--30 on site and 13 off site--were drilled. Forty-two of the wells were screened in the alluvial aquifer; the remainder were screened in bedrock. Thelocation of the monitoring wells is shown in Figures 3 and 4. Round 1 groundwater samples werecollected in June 1991 from the 35 Stage I monitoring wells and analyzed for VOCs, metals, semi-volatile organic compounds, and pesticides. Round 2 and Round 3 groundwater samples werecollected in September 1991 and December 1991, respectively, from Stage 1 and 1B monitoringwells. The Round 2 samples were analyzed for VOCs; the Round 3 samples were tested for VOCsand metals. Note: Filtered and unfiltered samples were collected for metals analysis in Rounds 1and 3. However, only data from the unfiltered samples will be presented and evaluated in thispublic health assessment because using data from filtered samples could underestimate actualgroundwater contaminant loads and potential human exposure levels. The use of data fromunfiltered samples for risk assessment purposes is also consistent with EPA Superfund guidance(17).
Groundwater monitoring results indicated the presence of VOCs at several locations. The primarycontaminants of concern detected were 1,1-dichloroethene (1,1-DCE), 1,1-DCA, 1,1,1-TCA, PCE,and TCE. However, as shown in Table 3, other VOCs also were present at levels of concern. Inaddition, various metals were found in unfiltered groundwater samples from the on-site monitoringwells; the concentrations, however, were generally similar to levels found in the off-site backgroundmonitoring well (MW 1).
Metals found in the unfiltered groundwater samples were believed to be associated with sampleturbidity, and not the result of site contamination, because 1) the levels of metals in unfilteredgroundwater samples were higher than metal levels in filtered samples, and 2) the levels of metals inupgradient well samples were equal to or greater than the levels in downgradient well samples. Inaddition, metals found in on-site soils were at levels similar to natural background soil levels.
To demonstrate that levels of metals found in the groundwater samples were not representative ofgroundwater conditions at the site, a Metals Verification Test (MVT) was conducted in April andMay 1992. As part of the MVT, non-turbid, non-filtered groundwater samples (referred to as Round4 samples) were collected from selected background and on-site monitoring wells to determine thelevel of mobile metals (i.e., metals that move with the groundwater) in site groundwater. Forcomparison purposes, filtered and unfiltered samples were also collected using the same samplingprocedures that were used for Rounds 1, 2, and 3.
|Benzene||ND - 230E||(1)||2, 6||1||CREG|
|Carbon tetrachloride||ND - 1,000E||(1)||2, 6||0.3||CREG|
|Chloroethane||ND - 7||(1)||2, 6||None|
|1,2-dibromoethane||ND - 19||(1)||2, 6||0.0004||CREG|
|1,1-dichloroethane||ND - 1,700D||(1)||2, 6||None|
|1,2-dichloroethane||ND - 51E||(1)||2, 6||0.4||CREG|
|1,1-dichloroethene||ND - 26,000E||(1)||2, 6||0.06||CREG|
|Methylene chloride||ND - 1,300DJ||(1)||2, 6||5||CREG|
|Tetrachloroethylene||ND - 14,000D||(1)||2, 6||0.7||CREG|
|1,1,1-trichloroethane||ND - 43,000E||(1)||2, 6||200||LTHA|
|1,1,2-trichloroethane||ND - 130E||(1)||2, 6||0.6||CREG|
|Trichloroethylene||ND - 100||(1)||2, 6||3||CREG|
|Vinyl chloride||ND - 4||(1)||2, 6||0.7||EMEG|
|Antimony||ND - 25.5B||(2)||2, 6||3||LTHA|
|Arsenic||ND - 218J||(2)||2, 6||0.02||CREG|
|Barium||195B - 1,470J||(2)||2, 6||2000||LTHA|
|Beryllium||ND - 7.4J||(2)||2, 6||0.008||CREG|
|Cadmium||ND - 8.7||(2)||2, 6||20||EMEG|
|Chromium||ND - 56.3J||(2)||2, 6||100||LTHA|
|Lead||ND - 80||(2)||2, 6||15||AL|
|Manganese||32.5 - 4,650J||(2)||2, 6||200||RMEG|
|Vanadium||ND - 194J||(2)||2, 6||100||EMEG|
Analytical results from the Round 4 MVT samples (non-turbid, unfiltered) are presented in Table3b. These data showed that the concentrations of metals in the non-turbid Round 4 samples weremuch lower than the levels in the turbid samples from Rounds 1, 2, and 3. Moreover, only twometals--arsenic and manganese--were detected at levels exceeding ATSDR's comparison values. The results of the MVT confirmed that 1) the presence of metals in the Round 1, 2, and 3groundwater samples was due to fine-grained, filterable particles (i.e., turbidity) from the aquiferformation, and 2) site groundwater has not been contaminated by metals from site activities (7,18).
|Antimony||ND||4/92, 5/92||7, 18||3||LTHA|
|Arsenic||ND - 16.3||4/92, 5/92||7, 18||0.02||CREG|
|Barium||160 - 431||4/92, 5/92||7, 18||2000||LTHA|
|Beryllium||ND||4/92, 5/92||7, 18||0.008||CREG|
|Cadmium||ND||4/92, 5/92||7, 18||20||EMEG|
|Chromium||ND||4/92, 5/92||7, 18||100||LTHA|
|Lead||ND||4/92, 5/92||7, 18||15||AL|
|Manganese||ND - 826J||4/92, 5/92||7, 18||200||RMEG|
|Vanadium||ND||4/92, 5/92||7, 18||100||EMEG|
The RI monitoring well data indicate that two groundwater VOC plumes are present at the site. Figure 5 shows the approximate location and extent of the two plumes.
The larger VOC plume originated from the UST/settling basin area (where solvents such as 1,1,1-TCA were disposed of) on the southwestern side of the plant. That plume descends from the sourcearea in a northeasterly direction to the mid and deep portions of the alluvial aquifer, as indicated bydata from monitoring wells 5, 6, and 7. The western edge of the plume is east of the MW 12location (2).
The second, smaller VOC plume originated from contaminated soil at the MW 8--CS/CN area onthe northern part of the plant property. The groundwater contamination from that area has beenlimited primarily to the shallow well at MW 8. The clayey soil layer found at the MW 8 location,between the depths of 8 and 16 feet, has likely inhibited vertical downward migration of thecontaminants from the MW 8--CS/CN point source area. The MW 8--CS/CN source area has likelycontributed to the Park Mobile Home Court main well contamination and may be responsible forcontamination detected in the shallow well at MW 10. The MW 10 location, however, is notdirectly downgradient of the MW 8--CS/CN area (2).
The eastern edge of the UST/settling basin plume and the western edge of the MW 8-- CS/CNplume are believed to merge downgradient of the MW 8--CS/CN source area. The combined plumeextends northeasterly to approximately the MW 11 and MW 14 areas. The eastern edge of thecontamination likely runs along a line between MW 2, MW 9, and MW 11, primarily within theupper and intermediate portions of the alluvial aquifer (2).
Groundwater - On-Site Supply Wells
Sherwood Medical industrial supply wells 3, 4, 5, and 6 have been sampled for VOCS at varioustimes since December 1987. The four wells were tested for VOCs during the expanded siteinvestigation (ESI) follow-up activities in January 1989, and during the RI/FS field activities(Round 3) in December 1991. In addition, Sherwood supply well 3 has been tested regularly(approximately once a month) for VOCs since installation of the mobile home park water treatmentsystem in September 1989. Also, as part of the first two RI/FS sampling rounds, Sherwood well 5 was tested in July 1991 for VOCs and metals, and Sherwood well 4 was sampled for VOCs inSeptember 1991. Figure 3 shows the locations of the plant supply wells.
The results of the groundwater analyses showed high levels of VOCs, including 1,1-DCA, 1,1-DCE,PCE, and 1,1,1-TCA, in the plant's industrial supply wells. Several metals also were detected inconcentrations similar to those found in the background monitoring well (Table 4). However, noneof the metals, except arsenic, were at levels exceeding the applicable comparison value.
|Carbon tetrachloride||ND - 10.8||(1)||(3)||0.3||CREG|
|Chloroethane||ND - 2.6||(1)||(3)||None|
|Chloromethane||ND - 2.5||(1)||(3)||3||LTHA|
|1,1-dichloroethane||ND - 280||(1)||(3)||None|
|1,2-dichloroethane||ND - 2||(1)||(3)||0.4||CREG|
|1,1-dichloroethene||ND - 5,400||(1)||(3)||0.06||CREG|
|Methylene chloride||ND - 88J||(1)||(3)||5||CREG|
|Tetrachloroethylene||ND - 18,100||(1)||(3)||0.7||CREG|
|1,1,2,2-tetrachloroethane||ND - 6||(1)||(3)||0.2||CREG|
|1,1,1-trichloroethane||ND - 10,000||(1)||(3)||200||LTHA|
|1,1,2-trichloroethane||ND - 8||(1)||(3)||0.6||CREG|
|Trichloroethylene||ND - 34||(1)||(3)||3||CREG|
|Arsenic||ND - 6.8B||(2)||(4)||0.02||CREG|
|Barium||280 - 301||(2)||(4)||2,000||LTHA|
|Lead||ND - 5.4||(2)||(4)||15||AL|
|Manganese||ND - 8.4B||(2)||(4)||200||RMEG|
|Vanadium||ND - 5B||(2)||(4)||100||EMEG|
Surface water samples from Sherwood Lake were taken in July 1988 (VOCs only) during the ESIand in May 1991 (VOCs and metals) during the RI/FS field activities. The RI/FS surface watersampling locations are shown in Figure 4. Low levels of two VOCs--1,1-DCA and 1,1,1-TCA--were found in the 1988 surface water samples (Table 5). These samples were collected whilethe plant was discharging VOC-contaminated cooling water to Sherwood Lake. In September 1989,the plant discontinued the use of VOC-contaminated well water for cooling water. Therefore, the1991 Sherwood Lake water samples contained no VOCs (Table 5). Several metals were detected inthe 1991 samples, but only arsenic was at levels in excess of the ATSDR comparison value.
|Contaminant||Concentration Range (µg/L)||Reference||Comparison Value||July 1988|
|1,1-dichloroethane||ND - 8.0||ND||2, 16||None|
|1,1,1-trichloroethane||ND - 31.0||ND||2, 16||200||LTHA|
|Arsenic||NA||ND - 5B||2||3||EMEG|
|Chromium||NA||ND - 5.3B||2||50||RMEG|
|Lead||NA||ND - 6.2J||2||15||AL|
|Manganese||NA||7.3B - 8.1B||2||50||RMEG|
Sediment samples from Sherwood Lake were taken in July 1988 (VOCs only) during the ESI and inMay 1991 (VOCs and metals) during the RI/FS field activities (see Figure 4). No VOCs weredetected in sediments at levels of concern. As shown in Table 6, several metals were found atlevels exceeding ATSDR's comparison values. However, the levels were generally similar tobackground soil levels for the western U.S. (12).
|Antimony||ND - 11.2J||5/91||2||0.8||RMEG|
|Arsenic||0.87J - 5.6J||5/91||2||0.4||CREG|
|Barium||54.3 - 194||5/91||2||100||RMEG|
|Chromium||3.5 - 21.4||5/91||2||10||RMEG|
|Lead||3.9J - 29.7J||5/91||2||None|
|Vanadium||5.5B - 17.6||5/91||2||6||EMEG|
No on-site ambient air data were available to ATSDR during the development of this public healthassessment. However, based on the levels of VOCs in site groundwater, soil, and soil gas, it isunlikely that ambient air is contaminated at the site.
Soil gas samples on the Sherwood Medical property were collected and analyzed for PCE and 1,1,1-TCA during the ESI in July 1988 and during the ESI follow-up in January 1989. Also, during theApril and August 1991 RI/FS field activities, diffusional organic vapor monitors were installed onthe Sherwood property to monitor VOCs in ambient soil gas. The monitors remained in place for 31days and then were submitted to a laboratory and analyzed for 1,1-DCE, 1,1-DCA, 1,1,1-TCA, andPCE.
Results of the soil gas sampling events are shown in Table 7 and Figure 6. The data indicated fourareas on the Sherwood Medical site where organic vapors were found at measurable levels. Thefour areas identified, as shown in Figures 3 and 6, were 1) the former UST/settling basin area on thewestern side of the plant building (near the entrance); 2) the monitoring well 8 (MW-08)--CS/CNarea; 3) the cullet silos area on the eastern side of the plant; and 4) the Grassy Knoll on thenortheastern portion of the site (2).
|1,1-dichloroethane||ND - 247||(1)||2, 16, 22||None|
|1,1-dichloroethene||ND - 5||(1)||2, 16, 22||0.005||CREG|
|1,1,1-trichloroethane||ND - 9,010||(1)||2, 16, 22||700||EMEG|
|Tetrachloroethylene||ND - 9,428||(1)||2, 16, 22||0.3||CREG|
The results of the soil gas survey at the former UST/settling basin area and the MW-08--CS/CNarea indicated two discrete areas of high soil gas concentrations, surrounded by an area with rapidlydecreasing levels. Groundwater contamination in these two areas was confirmed by shallowmonitoring well samples that contained VOCs at the parts per million (ppm) level. In addition,analysis of Stage II soil boring samples revealed significant VOC soil contamination in the CS/CN area.
VOCs found in soil gas near the cullet silos on the eastern side of the plant likely volatilized fromshallow contaminated groundwater (2). However, the VOCs may also have volatilized fromgasoline-contaminated soils near a former gasoline UST in that area.
Finally, soil gas sampling in the Grassy Knoll area (northeast of MW-09) indicated the presence of1,1,1-TCA during both the ESI and RI/FS. The source of VOC contamination in the Grassy Knollarea, however, has not been clearly identified (2).
Soil gas survey results for the north leachfield area (north of the UST) indicated low concentrationsof VOCs. However, the absence of detectable VOCs in MW-12, which is 250 feet northeast(downgradient) of the north leachfield, indicates that the north leachfield is not a source ofgroundwater contamination. The presence of VOCs in soil gas samples from the north leachfieldarea could be attributed to the plant's concrete parking lot, which would tend to prevent residualVOCs in underlying soils from escaping into the ambient air.
Off-site soil samples were collected in May 1991 during the installation of MW 10. The samples,which were obtained from borings 6 to 8 feet below ground surface, were analyzed for EPAContract Laboratory Program (CLP) VOCs and Target Analyte List (TAL) inorganic analytes. Figure 4 shows the soil sampling locations. As shown in Table 8, no VOCs were detected in the soilsamples; however, several metals were detected at levels similar to those found in background soil concentrations for the western United States (12).
No surface soil (less than or equal to 3 inches deep) data were available for off-site areas. However,contaminants from the site are unlikely to have affected off-site surface soils.
|Barium||25.2B - 36B||5/91||2||100||RMEG|
|Lead||2.7J - 3J||5/91||2||None|
|Vanadium||3B - 3.4B||5/91||2||6||EMEG|
Groundwater - Monitoring Wells
Off-site groundwater monitoring wells (MW 10, 11, and 14) were sampled during the 1991 RI/FSfield activities. The locations of the wells are shown in Figures 3 and 4. Round 1 groundwatersamples were collected in June 1991 from monitoring wells 10 and 11 and analyzed for VOCs,metals, semi-volatile organic compounds, and pesticides. Round 2 and 3 groundwater samples werecollected in September 1991 and December 1991, respectively, from monitoring wells 10, 11, and14. Round 2 samples were analyzed for VOCs; Round 3 samples were tested for VOCs and metals.
The groundwater sampling results (Table 9) indicated the presence of various VOCs in the off-sitemonitoring wells. The primary contaminants of concern were the same as those found in the on-sitemonitoring wells. However, the off-site concentrations were generally about two orders ofmagnitude lower than the on-site levels. Several metals were detected in groundwater samples atlevels similar to those measured in the background monitoring well (MW-1). Metals found at levelsexceeding their respective comparison values are shown in Table 9.
|Carbon tetrachloride||ND||(1)||2, 6||0.3||CREG|
|Chloroethane||ND - 1||(1)||2, 6||None|
|1,1-dichloroethane||ND - 48E||(1)||2, 6||None|
|1,2-dichloroethane||ND - 1||(1)||2, 6||0.4||CREG|
|1,1-dichloroethene||ND - 160D||(1)||2, 6||0.06||CREG|
|Methylene chloride||ND - 4J||(1)||2, 6||5||CREG|
|Tetrachloroethylene||ND - 26||(1)||2, 6||0.7||CREG|
|1,1,1-trichloroethane||ND - 860D||(1)||2, 6||200||LTHA|
|Trichloroethylene||ND - 10||(1)||2, 6||3||CREG|
|Vinyl chloride||ND - 2||(2)||2, 6||0.2||EMEG|
|Arsenic||6.2J - 25.6||(2)||2, 6||0.02||CREG|
|Barium||280 - 1,270||(2)||2, 6||700||RMEG|
|Beryllium||ND - 4.5B||(2)||2, 6||0.008||CREG|
|Cadmium||ND - 31.7||(2)||2, 6||7||EMEG|
|Chromium||ND - 103||(2)||2, 6||50||RMEG|
|Lead||3.4 - 51||(2)||2, 6||15||AL|
|Manganese||91.1 - 1,870J||(2)||2, 6||50||RMEG|
|Vanadium||ND - 129||(2)||2, 6||30||EMEG|
Groundwater - Private Wells
The principal off-site private wells near the Sherwood Medical plant include the two Park MobileHome Court wells (main and back-up) and several residential and commercial wells. Forconvenience, the two private well categories are discussed in separate subsections of this publichealth assessment. Private wells in the site area are identified in Figures 2 and 3.
Park Mobile Home Court Wells
VOCs were initially found in the two Park Mobile Home Court wells in 1987. Since thattime, the wells have been resampled several times, most recently during the 1991 RI/FS fieldactivities.
Sampling data for the mobile home park wells are presented in Table 10a. This tablecontains only data from samples collected while the mobile home park wells were being usedas a water supply source for the mobile home park residents. Therefore, data from wellsamples collected after September 1989, when the mobile home park was hooked up to theSherwood Medical plant's new central water treatment system and use of the mobile homepark wells was discontinued, are excluded. Table 10a also includes data from samplescollected between February 1988 and September 1989 when water from the mobile homepark wells was being treated by a temporary carbon treatment system. Because the watersamples were obtained after the water had passed through the treatment system, they shouldbe representative of the quality of the mobile home park's drinking water during that time.
As shown in Table 10a, low-to-moderate levels of various VOCs were found in the mobilehome park wells. The principal contaminants of concern were generally the same as thosefound in other on- and off-site groundwater samples. Chloroform andchlorodibromomethane, which were not found in other well samples, were identified ascontaminants of concern in the mobile home park wells. These two contaminants may havebeen associated with the mobile home park's chlorination system rather than the site'sgroundwater VOC contamination. No sampling data for metals in the mobile home parkwells were found during the development of this public health assessment.
|Carbon tetrachloride||ND - 25||(1)||(2)||0.3||CREG|
|Chloroethane||ND - 9||(1)||(2)||None|
|Chloroform||ND - 260||(1)||(2)||6||CREG|
|Chloromethane||ND - 13||(1)||(2)||3||LTHA|
|Chlorodibromomethane||ND - 2||(1)||(2)||0.4||CREG|
|1,1-dichloroethane||ND - 89||(1)||(2)||None|
|1,2-dichloroethane||ND - 6.6||(1)||(2)||0.4||CREG|
|1,1-dichloroethene||ND - 24||(1)||(2)||0.06||CREG|
|Tetrachloroethylene||ND - 100||(1)||(2)||0.7||CREG|
|1,1,1-trichloroethane||ND - 180||(1)||(2)||200||LTHA|
|1,1,2-trichloroethane||ND - 1||(1)||(2)||0.6||CREG|
|Trichloroethylene||ND - 12||(1)||(2)||3||CREG|
|Vinyl chloride||ND - 2||(1)||(2)||0.2||EMEG|
*sample collected after passing through PMHC carbon filter
Other Private Wells
Private residential and commercial wells in the vicinity of the Sherwood Medical plant havebeen tested for VOCs several times since December 1987. (The wells have not been sampledfor metals.) Sampling was most comprehensive during the ESI follow-up activities inJanuary 1989 and during the RI/FS field activities in June, September, and December 1991;additional limited sampling was conducted in December 1994. No VOCs were detected inany of the upgradient residential wells along Sherwood Road. However, as seen in Table10b, low levels of several VOCs, primarily 1,1-DCA, 1,1,1-TCA, TCE, and PCE, werefound in five commercial or industrial wells downgradient of the Sherwood Medicalproperty. Two of the wells are at private businesses northeast of the Sherwood Medicalproperty; the other three are at the Madison County Maintenance Building, the MadisonCounty Weed Control Shop, and the Civil Defense/Emergency Management Building northof the plant property. Note: Sherwood Medical Co. has provided potable drinking water tothe two private businesses since 1992 or 1993 and to the three county operations since early1995; therefore, these five affected wells are no longer used for drinking water purposes.
|Benzene||ND - 1J||(1)||(2)||1||CREG|
|Chloromethane||ND - 0.56J||(1)||(2)||3||LTHA|
|1,1-dichloroethane||ND - 10||(1)||(2)||None|
|1,1-dichloroethene||ND - 2||(1)||(2)||0.06||CREG|
|Methylene chloride||ND - 7J||(1)||(2)||5||CREG|
|Tetrachloroethylene||ND - 8.5J||(1)||(2)||0.7||CREG|
|1,1,1-trichloroethane||ND - 21||(1)||(2)||200||LTHA|
|Trichloroethylene||ND - 2.9J||(1)||(2)||3||CREG|
Groundwater - Public Supplies
No sampling data for public water supply wells were found during the development of this publichealth assessment. The nearest public wells (city of Norfolk) are more than 2.5 miles from the ParkMobile Home Court and the furthest edge of the site groundwater plume. Therefore, no public wellsare likely to be affected by site-related groundwater contamination.
Surface water samples for VOCs were collected from Medelmans Lake, which is just north of thePMHC, in July 1988 during the ESI. No VOCs were detected in the surface water samples.
Sediment samples from Medelmans Lake were taken in July 1988 during the ESI. No VOCs werefound at detectable levels in the sediment samples.
No ambient air data for the site area were found during the development of this health assessment. However, as previously discussed, ambient air is not likely to be significantly affected bycontaminants from the site.
Off-site soil gas samples were collected for 1,1,1-TCA and PCE as part of the ESI in July 1988 andas part of the ESI follow-up in January 1989. The off-site soil gas data are shown in Table 11.
Low concentrations of 1,1,1-TCA and PCE were detected in the soil gas samples at the Park MobileHome Court. Higher levels of PCE and 1,1,1-TCA were found at two locations east of theSherwood Medical property--near the western edge of the former Ron Kinning facility and near thenorthern end of the Theisen Brothers property. Soil gas contamination in those two areas isprobably from unrelated, isolated sources, especially since buried drums and debris were discoveredthere and nearby dumping was reported.
|1,1,1-trichloroethane||ND - 50||(1)||16, 22||700||EMEG|
|Tetrachloroethylene||ND - 23||(1)||16, 22||0.3||CREG|
ATSDR conducted a search of the EPA Toxics Release Inventory (TRI) records for facilities in theNorfolk, Nebraska, area. The search showed that some area facilities, including Sherwood MedicalCompany, have released VOCs, such as 1,1,1-TCA, into the air. The TRI contained no record ofVOC disposal via land, surface water, or groundwater during the 1987 through 1989 reportingperiod. The database does not provide sufficient information to estimate any airborne contaminantconcentrations. Also, airborne VOC releases are not likely to contribute to groundwatercontamination at the site. Therefore, the reported airborne releases are not considered further in thispublic health assessment.
The laboratory reports and data sheets reviewed for this public health assessment indicate that, ingeneral, appropriate quality assurance/quality control (QA/QC) procedures were followed duringdata collection and analysis. RI/FS documents, for example, report that RI/FS field activitiesadhered to the QA/QC procedures and methods specified in the Field Sampling Plan and QualityAssurance Project Plan (QAPP). In addition, each analytical report was validated by an EPAcontractor. Data qualifiers resulting from the validation have been included, where appropriate, inthe preceding contaminant tables.
No significant chemical or physical hazards were observed during the January 1992 site visit. However, at the time of the site visit, access to the plant property was not restricted. Therefore, itwas thought that children living near the plant were at some risk of drowning in Sherwood Lake orat risk of injury from broken glass noted near the solid waste disposal bin near the east side of theplant. Since the site visit, the plant property has been posted with "no trespassing" signs. Furthermore, according to the company, no children have ever been observed trespassing on theplant property. For these reasons, it now seems unlikely that children will come into contact withany potential physical hazards at the site.
To determine whether nearby populations are exposed to contaminants from the Sherwood MedicalCompany site, ATSDR has evaluated the environmental and human components leading to humanexposure. This pathway analysis considers five elements: 1) a source of contamination; 2) anenvironmental medium (e.g., air, water, soil) in which contaminants may be present or throughwhich contaminants may be transported; 3) a point of exposure, 4) a route of human exposure, and5) an exposed population.
ATSDR classifies exposure pathways as completed or potential. For a completed pathway to exist,all five elements must exist and indicate that exposure to a contaminant has occurred in the past, iscurrently occurring, or will occur in the future. A potential pathway exists when at least one of thefive elements is missing, but could exist (e.g., exposure to a contaminant could have occurred in thepast, could be currently occurring, or could occur in the future.) A pathway is eliminated when atleast one of the five elements is missing and will never exist.
Pathway analyses conducted for the Sherwood Medical Company site indicate that there are twocompleted pathways associated with groundwater. The completed pathway elements aresummarized in Table 12 of this section. The analyses also show several potential pathwaysinvolving groundwater, surface water, and soil. The potential pathway elements are summarized in Table 13 of this section.
Estimates of the number of exposed persons for completed exposure pathways and the number ofpotentially exposed persons for potential exposure pathways are shown in Tables 14 and 15, respectively, of this section.
The discussion that follows the four tables pertains only to pathways considered important or relevant to the site. Exposure pathways that have been eliminated are also discussed.
|EXPOSURE PATHWAY ELEMENTS||TIME||SOURCE||MEDIUM|| POINT OF|
|EXPOSURE PATHWAY ELEMENTS||TIME||SOURCE||MEDIUM||POINT OF|
| ROUTE OF|
|Sourcechemicals; waste materialsand soil||In-plant areaswhere solventswere used andhandled;|
|Worker-DrinkingWater||On-site wastes||Groundwater||In-plant drinkingwater||Ingestion||Plant employees||Past|
|Other PrivateWells||On-site wastes||Groundwater||Nearby businessesand/or residenceswith private wellsnot currentlyimpacted by sitecontamination||Ingestion|
employees andresidents whouse such wells
|ESTIMATED EXPOSED POPULATIONS THAT ARE AFFECTED BY A COMPLETED EXPOSURE PATHWAY*|
|EXPOSED POPULATIONS||COMPLETED EXPOSURE PATHWAY FOR:|
|PMHC residentspreviously supplied bythe two contaminatedPMHC wells|
|300||PMHC Wells||PMHC Wells||PMHC Wells||PMHC Wells||PMHC Wells|
|Owners and employeesof downgradientcommercial & industrialoperations withcontaminated wells|
|* Refer to Table 12 for summary of completed exposure pathways.|
|ESTIMATED POTENTIALLY EXPOSED POPULATIONS THAT ARE AFFECTED BY A POTENTIAL EXPOSURE PATHWAY*|
| POTENTIALLY |
|POTENTIAL EXPOSURE PATHWAY FOR:|
|1,1-DCA||1,1,1-TCA||TCE||PCE||Other VOCs (e.g., 1,1-DCE)|
|Nearby businessowners and employeesand residents withprivate wells notcurrently affected bysite contamination|
|NotKnown||Other PrivateWells||Other PrivateWells||Other PrivateWells||Other PrivateWells||Other PrivateWells|
|* Refer to Table 13 for summary of potential exposure pathways.|
Park Mobile Home Court (PMHC) Wells Pathway
Previous studies and environmental sampling indicate that waste sources at the Sherwood Medicalsite, such as the facility UST and septic tank and an undetermined source in the CS/CN area, havecontaminated the underlying soils and groundwater with various VOCs. In general, VOCs such asthose found at the site are fairly mobile in soil and groundwater, especially in soils of low organiccarbon that have low adsorption capacities. Those compounds, therefore, are likely to migrate fromon-site source areas into groundwater. Migration of the site contaminants has, in fact, beenconfirmed by several sampling events that have detected VOCs in both on- and off-site wells,including the two Park Mobile Home Court wells.
Residents of the Park Mobile Home Court were exposed to VOCs in water drawn from the twowater supply wells (before being shut down in September 1989) for drinking and other domesticpurposes (e.g., bathing, showering). Exposure to VOCs would have occurred primarily viaingestion of contaminated drinking water and via inhalation of contaminants that have volatilizedinto the air during showering and bathing. Limited exposure to VOCs via dermal contact withcontaminated water during showering and bathing was also possible because these compounds canbe absorbed through the skin.
Sampling data for metals in the Park Mobile Home Court wells are not available. Unfilteredgroundwater samples from site monitoring wells and supply wells contained low levels of metals. However, further groundwater sampling revealed that metals present in the earlier samples were theresult of turbidity from the aquifer formation that was introduced into samples when they werecollected. More importantly, the later sampling results indicate that site groundwater is notcontaminated by metals. Therefore, it is unlikely that the Park Mobile Home Court residents wereexposed to significant levels of metals in their drinking water.
It is estimated that up to 300 persons in the Park Mobile Home Court were exposed to groundwaterVOCs before use of the mobile home park wells was discontinued. This figure was calculated usingthe highest reported mobile home park occupancy (117 units, in 1987), and the average residentialoccupancy rate for Madison County (2.6 persons per residence). As previously indicated, the Sherwood Medical plant has been operating since 1961 and has usedchlorinated solvents (primarily 1,1,1-TCA) since 1963. Because the mobile home park was firstoccupied in late 1966 (5), and water from the mobile home park's wells was not carbon treated untilFebruary 1988 (when the EPA temporary treatment system was installed), the maximum period ofexposure to site-related contaminants would have been about 21 years. This estimated exposureperiod is reasonable even when contaminant transport time is considered. For example, using theestimated flow velocity of 800 feet per year for groundwater in the site area (7) and the estimatedsite-specific retardation factor for PCE of 1.5 (7) results in a contaminant transport velocity of 533feet per year. At that rate, contaminants released from the Sherwood UST/septic tank area wouldreach the main mobile home park well--about 1450 feet away--in approximately 3 years. Therefore,contaminants released on site as early as 1963 could have migrated to the mobile home park wellsby 1966. This means that residents of the mobile home park could have been exposed to site-relatedVOCs from late 1966 to early 1989, or for a maximum period of about 21 years. It should be noted,however, that only those residents who lived in the mobile home park continuously from 1966through 1989 would have been exposed to site-related contaminants for the estimated maximum 21-year period.
Industrial/Commercial Wells Pathway
Two private wells at commercial operations northeast (approximately 2300 to 2600 feet) of theSherwood Medical plant and east of the Park Mobile Home Court are used primarily to wash downindustrial equipment. These wells were also believed to have been used in the past as a source ofdrinking water. The two wells are downgradient of the plant and, based on previous soil gasinvestigations, are believed to be within the plume of groundwater contamination. Moreover, pastgroundwater sampling indicates that the two wells are contaminated with low levels of VOCs. Thecompounds detected include 1,1-DCA, 1,1-DCE, 1,1,1-TCA, PCE, and TCE. Owners and workersat the commercial operations who drank water from these wells were subject to exposure in the pastto those contaminants. It is likely that exposure to contaminants via dermal contact and inhalationwas minimal when compared with exposure via ingestion.
Sampling data for metals are not available for these two wells. However, as previously discussed,sampling data from groundwater monitoring wells indicate that site groundwater is not contaminatedwith metals. Therefore, persons who drank water from these two wells were not likely to besignificantly exposed to metals.
The number of persons exposed to VOCs in groundwater used at the two commercial operations isnot known. However, because the operations are believed to be family owned and operated, thenumber is likely to be relatively small.
It is not known when the two businesses began operating at their current locations; therefore, theperiod of exposure cannot be calculated. By assuming that the operations have been in existencesince the mobile home park was established, and by using the contaminant transport rate anddistance discussed previously, it can be estimated that exposure to contaminants could have begun asearly as 1968. Exposures to VOCs from the commercial wells likely ceased in 1992 or 1993 whenSherwood Medical began supplying these businesses with potable drinking water. Therefore, themaximum exposure period would not have exceeded 24 or 25 years. The results of pastgroundwater sampling suggest that the actual exposure period may have been much shorter.
As previously discussed, although exposure to low levels of VOCs in the two industrial wells hasprobably occurred in the past, exposure is no longer believed to be occurring because SherwoodMedical Company supplies the two businesses with bottled drinking water (4,9,11).
Three additional wells, at the Madison County Maintenance Building, the Madison County WeedControl Shop, and the Civil Defense/Emergency Management Building, have also been shown tocontain low levels of VOCs. Contaminants detected in those wells included 1,1-DCA, PCE, andTCE. The wells are adjacent to the Park Mobile Home Court, approximately 1,500 to 1,700 feetnorth-northeast of the Sherwood Medical UST/septic tank area. The wells are believed to be usedprimarily for equipment washing and maintenance. These wells were also believed to have beenused in the past for drinking water supply. Therefore, exposure to well contaminants would bemainly via ingestion (i.e., through drinking water.) Exposure via inhalation and dermal contact isassumed to be minimal. Although sampling data for metals are not available, significant exposure tometals in groundwater from these two wells is unlikely.
The number of persons exposed to contaminants in the three wells is not known, but would includeany county workers or other personnel who used the wells for drinking water. The length of theexposure period is also unknown but would not have exceeded 27 or 28 years because groundwatercontaminants could not have reached the wells before 1966 and the wells have not been used fordrinking water since early 1995. Past groundwater sampling data suggest that the actual exposureperiod may have been much shorter. Human exposure to contaminants from the wells is no longeroccurring because occupants of the three buildings are supplied with bottled drinking water.
Worker-Waste Material Pathway
Sherwood Medical Company employees who used or handled chlorinated solvents, primarily 1,1,1-TCA, on the job may have been exposed in the past to VOCs through skin contact, inhalation, andpossibly incidental ingestion. However, the extent of potential exposure and contaminant uptakecannot be estimated using available information. The potential for Sherwood Medical employees tobe exposed to VOCs on the job was eliminated in 1992 when the use of all chlorinated solvents bythe plant was discontinued.
Contractor workers who participated in the September 1989 and November 1990 activities involvingremoval of waste materials from the plant's septic tank and UST could have been exposed to VOCsvia skin contact, inhalation, and possibly incidental ingestion of waste materials and contaminatedsoils. Available information indicates that appropriate personal protective equipment was usedduring the removal activities. Therefore, any exposure to contaminants in the waste material wasprobably insignificant.
Worker-Drinking Water Pathway
Significant levels of several VOCs, including 1,1-DCA, 1,1-DCE, PCE, 1,1,1-TCA, have beenfound in the Sherwood Medical plant's water supply wells #4 and #5. Before September 1989, thesewells were used to supply the plant's water needs including potable drinking water. Therefore,employees who worked at the Sherwood Medical plant in the past could have been exposed to VOCsin the plant's drinking water. Exposure to VOCs from the drinking water supply via inhalation and skin contact is assumed to be insignificant compared with exposure via ingestion.
Although the levels of VOCs actually ingested by plant employees are unknown, the levels wereprobably much lower than the contaminant levels found in the water supply wells. According tocompany officials, the plant's drinking water supply was carbon treated, either at the wellhead(before 1979), or at the point of use (i.e., drinking fountains) (from 1979 to September 1989) evenbefore the plant's current carbon treatment units were installed in September 1989. Therefore, thecompany believes that VOCs were never present at significant levels in the plant's drinking water. To support its position, the company submitted the analytical results of a sample collected from theplant's water distribution system in December 1987 showing virtually no detectable levels of VOCs. ATSDR believes that one sample over a period of more than 25 years is insufficient to adequatelycharacterize the plant's drinking water quality; therefore, it is possible that plant employees wereexposed to VOCs to some extent from the plant's drinking water before September 1989.
The number of persons potentially exposed in the past to contaminants via ingestion of plantdrinking water cannot be accurately determined; however, a maximum estimate based on pastemployment levels at the plant would be 450 (5). The exact period of potential exposure is also notknown, but probably would not have exceeded 25 years. That figure was estimated using thefollowing assumptions:
- contamination of groundwater in the septic tank area began no earlier than 1963;
- contaminants reached the nearest of the supply wells approximately one year later (using a maximum migration rate of 533 feet per year and a distance of 675 feet to the nearest supply well);
- exposures stopped in September 1989 when the plant's new water treatment system wasinstalled.
Since September 1989, all water pumped from the plant's supply wells has been treated by a large,centralized carbon treatment system to remove VOCs before distribution within the plant; therefore,plant employees are not likely to be exposed to VOCs from the plant's drinking water supply now orin the future.
Other Private Wells Pathway
A number of private wells (residential and commercial) are near the Sherwood Medical plant. These wells include the private residential wells along Sherwood Road just south of the plant, thetwo Park Mobile Home Court wells north/northeast of the plant, and several commercial wellsnorth, northeast, and east of the plant. Among these, only the PMHC wells and 5 commercial wellsnorth and northeast of the site have been shown to be contaminated with VOCs (see previousdiscussion under Completed Exposure Pathways--Industrial/Commercial Wells heading). However,it is possible that some of the remaining private wells close to the site, especially those downgradient(i.e., northeast) of the Sherwood Medical plant, could become contaminated by groundwater VOCsmigrating from the site. Users of such wells could be exposed, via ingestion, inhalation, skincontact or all three, in the future to VOCs in their well water. Future levels of groundwatercontaminants and the number of persons who might be exposed are unknown. It should be notedthat future groundwater remediation actions could minimize or eliminate such potential exposures.
Surface Water Pathway
Trespassers, especially children from the Park Mobile Home Court and from homes along SherwoodRoad, who wade or swim in Sherwood Lake could theoretically be exposed to contaminants in thelake. Exposures could occur through skin contact and, to a lesser extent, through incidentalingestion. However, the most recent sampling data (from the 1991 RI/FS) showed no VOCs in thelake surface water or sediment and only one low-level VOC in the plant's wastewater discharges tothe lake. Furthermore, company officials report that the plant property has been posted and notrespassers have ever been found in or around Sherwood Lake. Because 1) VOCs are not likely tobe present in the lake at levels of concern, 2) any VOCs discharged to the lake will rapidly volatilizeto the atmosphere, and 3) children are not likely to come in contact with the lake, exposures toVOCs in Sherwood Lake are not expected. Therefore, this potential exposure pathway is beingeliminated from further discussion in this public health assessment.
Soil Gas Pathway
Groundwater at the Sherwood Medical plant and Park Mobile Home Court has been shown to becontaminated with various volatile compounds. In the areas where groundwater is contaminated,volatile compounds are likely to be released from the water table into the overlying soil. In fact,previous site investigations have confirmed the presence of volatile compounds in soil gas samplescollected above contaminated groundwater areas, such as the UST area and the CS/CN area. Thevolatile soil gas contaminants can migrate upward to ground level and enter buildings overlying thesoil through crawl spaces, plumbing holes, other floor holes, and foundation cracks. Volatilecontaminants entering the buildings can accumulate in confined spaces, such as basements, therebysubjecting the building occupants to inhalation exposures.
At the Sherwood Medical site, human exposure to VOCs in indoor air is not expected for thefollowing reasons. First, previous investigations did not indicate that significant levels of VOCswere migrating in soil gas other than in the suspected source areas. Second, only one home with abasement is close to or downgradient of the site. This residence, which is north of the site, is notunderlain by contaminated groundwater and is several hundred feet from the nearest location wheresoil gas contaminants were detected. Third, mobile homes in the Park Mobile Home Court locatedover areas of contaminated groundwater do not have foundations and do not sit directly on theground surface. Therefore, soil gas VOCs migrating to the ground surface are not likely toaccumulate in any of the mobile homes. For these reasons, significant exposures to VOCs from sitesoil gas are unlikely and will not be discussed further in this public health assessment.
Food Chain Pathways
Agricultural land uses have not been identified in the immediate vicinity of the Sherwood Medicalsite. Therefore, exposures involving site-related contaminants in commercially grown food cropsare unlikely.
Exposure to site-related contaminants from eating home-grown vegetables is not a concern becausethe types of contaminants found in site soils and groundwater (volatile organic compounds) are notsignificantly taken up by plants. Furthermore, residents most likely to have vegetable gardens areupgradient of the Sherwood Medical plant (along Sherwood Road) and are not affected bygroundwater contamination.
Exposure to site-related contaminants from eating domestic livestock or wild game that may haveconsumed VOC-contaminated water or plants in contact with VOC-contaminated water is unlikelybecause animals do not accumulate VOCs to significant levels.
Finally, the potential for exposure to VOCs via consumption of fish is remote because 1) VOCswere found only at low levels in Sherwood Lake, VOCs do not accumulate significantly in fish, andconsumption of significant quantities of fish from the lake is unlikely.
For these reasons, potential exposures via food chain pathways will not be considered further in thispublic health assessment.
In this section, we will evaluate the potential health effects in persons exposed to the contaminantsof concern for which completed and potential pathways exist, discuss health outcome data, andaddress the specific community health concerns.
To evaluate health effects, we have estimated human exposure doses of the groundwatercontaminants and compared these with health effects information in the ATSDR toxicologicalprofiles. This discussion is limited to potential health effects that can occur at exposure levelssimilar to those found at this site or a discussion of effects at the lowest doses that can produce aneffect. ATSDR has developed Minimal Risk Levels (MRLs) to evaluate non-cancer health effects. An MRL is an estimate of daily human exposure, in milligrams per kilogram of body weight per day(mg/kg/day), to a contaminant below which non-cancer, adverse health effects are unlikely to occur. MRLs are developed for the oral and inhalation routes of exposure, and for the length of exposure,such as acute (14 days or less), intermediate (15 to 365 days), and chronic (greater than 365 days). An EPA Reference Dose (RfD) is an estimate of a daily exposure (mg/kg/day) of the general publicto a contaminant that is likely to be without an appreciable risk of deleterious effects during alifetime. Cancer effects are evaluated by estimating the risk of developing cancer over a lifetime. The EPA has estimated cancer slope factors (CSF) for certain chemicals. These CSFs are estimatesof the potency of a chemical to cause cancer and are used in conjunction with the exposure dose toestimate the cancer risk.
The toxicological evaluation of exposure to the contaminants discussed in this section assumes thatresidents used the groundwater for drinking and cooking (ingestion) and other household uses(bathing and showering, which would involve inhalation and dermal contact) daily for 21 years. The exposure dose assessment assumes that adults drink 2 liters of tap water per day and childrendrink 1 liter of tap water per day. For noncarcinogens, ingestion assumptions for children wereevaluated because children receive a larger dose as a result of their larger ingestion-to-body weightratio than adults. When evaluating the carcinogenic potential, it is assumed that an adult drank themaximum contaminant level detected for 21 years. Inhalation of volatilized VOCs duringshowering and other activities is assumed to be equivalent to ingestion exposure.
Only the residents of PMHC were known to be exposed to carbon tetrachloride ingroundwater. Levels as high as 25 ppb have been detected. Levels such as this exceed EPA'schronic oral RfD (0.0007 mg/kg/day) when children's exposure is estimated. Estimatedexposures of adults would not exceed the RfD. Animal studies and reports of humanpoisoning have shown that the liver is the primary target organ; the kidneys also showsensitivity to carbon tetrachloride. No adverse noncancer health effects have been reported atlevels as low as those seen in the groundwater at this site. The lowest-observed-adverse-effect-levels (LOAEL) in animal studies (10 mg/kg/day) resulted in liver serum enzyme andtissue changes (23).
Both the International Agency for Research on Cancer (IARC) and EPA have concludedthere is sufficient evidence that carbon tetrachloride is carcinogenic in experimental animals. Animal studies have shown it to cause liver tumors. Drinking water contaminated with 25ppb carbon tetrachloride for 21 years would result in no apparent increased risk of cancer.
Assuming an equivalent exposure via inhalation of volatilized carbon tetrachloride, thecombined ingestion and inhalation dose would exceed the RfD for an adult. However, thisdose would not be expected to result in any adverse noncancer health effects. Insufficienttoxicokinetic information precludes a dose estimation from dermal exposure.
Chloroform was detected in the PMHC wells at levels up to 260 ppb but not in other off-sitewells or the plant supply wells. Chloroform is a byproduct of water chlorination. Themaximum level of 260 ppb exceeds ATSDR's chronic oral MRL (0.01 mg/kg/day) whenchildren's exposure is estimated . Estimated adult exposure doses would not exceed theMRL. The liver is the primary target of chloroform. The lowest oral dose administered toanimals in chronic studies was 15 mg/kg/day, which increased liver enzymes. Biochemicaltests indicate that liver function in humans was affected by use of mouthwash for 5 yearsproviding 2.46 mg/kg/day chloroform. The kidney is also a target of chloroform, althoughless sensitive (24). The levels of chloroform found in the PMHC wells are well below thelevels that would result in adverse noncancer health effects.
Chloroform is classified by EPA as a probable human carcinogen and by IARC as a possiblehuman carcinogen. Chloroform has not been identified as the sole or primary cause ofincreased cancer risks associated with chlorinated water, but it is one of several volatileorganic contaminants found in drinking water that are considered to have carcinogenicpotential. Chloroform has been shown to cause kidney and liver tumors in animal studies. Drinking water contaminated with 260 ppb of chloroform for 21 years would result in noapparent increased risk of cancer.
Assuming an equivalent exposure via inhalation of volatilized chloroform, the combinedingestion and inhalation dose would be approximately equal to the chronic MRL for an adult. Insufficient toxicokinetic information precludes a dose estimation from dermal exposure.
DCE was detected in the PMHC wells at levels up to 24 ppb. This maximum level does notexceed ATSDR's chronic oral MRL (0.009 mg/kg/day) for either children or adults. Theliver is the primary target organ of this chemical. The MRL is based on the lowest observedadverse effect level of 9 mg/kg/day, corresponding to a concentration of 50,000 ppb in water. The effect was a minimal amount of liver cellular swelling and an increase in cellular fat. Athigher doses, an increase in serum enzymes, indicating liver dysfunction, may be seen. There is some evidence in animals that poor nutritional status increases DCE liver toxicity(25). Exposure to DCE at levels found in the PMHC wells would not be expected to result in adverse noncancer health effects.
DCE is classified by EPA as a possible human carcinogen. This classification applies tochemicals for which there is limited evidence of carcinogenicity in animals. Drinking watercontaminated with 24 ppb of DCE for 21 years could result in a low increased risk of cancer.
DCE volatilizes into the air during normal household use of the well water. An MRL of 0.02ppm has been developed for intermediate-duration inhalation exposure (15-365 days) toDCE. This MRL is based on a no-observed-adverse-effect-level of 5 ppm for hepatic effectsin guinea pigs continuously exposed to DCE. The limited information on human exposure toDCE indicates that inhalation of volatilized DCE is probably toxic to the human liver andkidney, although effective exposure doses are unknown.
EPA has derived a cancer potency factor for inhalation of DCE based on an animal studyreporting an increase in total mammary tumors. The lowest dose producing tumors (cancereffect level) was 10 ppm. The study had a number of limitations; therefore, the evidence forcarcinogenicity from inhalation exposure is considered to be inconclusive (25). Because airsampling was not conducted, health effects from inhalation of DCE cannot be evaluated.
Assuming an equivalent exposure via inhalation of volatilized DCE, the combined ingestionand inhalation dose would not change the results. Insufficient toxicokinetic informationprecludes a dose estimation from dermal exposure.
PCE was detected in the PMHC wells at levels up to 100 ppb. Levels such as this areapproximately equal to the chronic oral RfD (0.01 mg/kg/day) when children's exposure isestimated. Adult exposure would not exceed the RfD. In experimental animals, the liver isthe primary target organ of PCE via ingestion. The lowest observed adverse effect level of100 mg/kg/day has resulted in increased liver weight in mice. Higher levels will begin tocause liver necrosis and an increase in certain serum enzymes. The kidney is a target organfor PCE but is less sensitive than the liver (26). No adverse noncancer health effects would be expected from drinking water containing 100 ppb of PCE.
IARC has classified PCE as reasonably anticipated to be a carcinogen. The EPA isconsidering classifying PCE as either a probable human carcinogen or possible humancarcinogen. Drinking water contaminated with 100 ppb of PCE for 21 years would result inno apparent increased cancer risk. The National Cancer Institute conducted a carcinogenicitybioassay of rats and mice (26). No increases in tumor incidence were observed for thetreated rats. Statistically significant increases in liver tumors occurred in the mice; however,the study had a number of limitations. These limitations included a small control group,numerous dose adjustments during the study, early mortality, and pneumonia.
Assuming an equivalent exposure via inhalation of volatilized PCE, the combined ingestionand inhalation dose would exceed the oral RfD for a child's exposure but not for an adult'sexposure. Neither the adult's nor the child's combined exposure dose would expected toresult in adverse noncancer health effects. Dermal uptake cannot be estimated from theavailable information.
TCE was detected in the PMHC wells at levels up to 12 ppb. This maximum level does notexceed ATSDR's intermediate (15-365 days) oral MRL of 0.002 mg/kg/day for estimatedexposures of children or adults. For this site, an intermediate MRL is not as appropriate as achronic MRL; however, ATSDR has not developed one. In addition, no other long-termhealth guidelines are available. As a regulatory standard, EPA has established a MCL of 5ppb and a MCLG of 0; however, these values are not applicable for the evaluation of healtheffects from TCE exposure at this site.
The intermediate oral MRL is based on a study in which heart abnormalities were noted inthe developing fetuses of pregnant rats exposed to TCE in drinking water before and duringpregnancy. These findings were supported by a similar study with chicken embryos thatfound an association between TCE exposure and heart abnormalities, and by a humanepidemiological study that found increased incidence of congenital heart defects in childrenborn to mothers who were exposed to TCE in drinking water.
TCE exposure may also affect the nervous system, liver, and kidney based on effectsreported in humans or animals or both (27). No adverse noncancer health effects would beexpected from drinking water contaminated with TCE at the levels found in the PMHC wells.
The link between oral exposure to TCE and the incidence of cancer in humans iscontroversial. Support for an association comes from a report of increased childhoodleukemia among a population in Woburn, Massachusetts. That population drank TCE-contaminated wellwater. This association was supported by a second study of New Jersey communities wherean increase in the standardized mortality ratio for leukemia was found in women exposed toTCE-contaminated drinking water. However, these studies had serous shortcomings. Anumber of researchers have questioned the associations drawn from these studies between theincidence of leukemia and other cancers and oral exposure to TCE.
IARC lists TCE as not classifiable for cancer. EPA assigned a classification of B2 (probablehuman carcinogen) to TCE in 1987 and derived a cancer potency estimate for TCE based onincidence data for lung tumors in female Swiss mice and tumor incidence data from otherstudies. In 1988, the Scientific Advisory Board for EPA indicated that TCE would be moreaccurately classified between C and B2 (possible-probable human carcinogen). At present,the weight-of-evidence classification for TCE is "under review" by EPA. For the SherwoodMedical site, ATSDR evaluated the cancer risk associated with ingestion of TCE-contaminated water by using the 1987 EPA cancer potency factor. This evaluation indicatesthat drinking water containing 12 ppb TCE for 21 years from the PMHC wells would pose noincreased cancer risk.
Assuming an equivalent exposure via inhalation of volatilized TCE, the combined ingestionand inhalation dose would not change the results. Dermal uptake cannot be estimated fromthe available information.
Vinyl chloride was detected in the PMHC wells at levels up to 2 ppb. This maximum levelexceeds ATSDR's chronic oral MRL (0.00002 mg/kg/day) for children and adults. The liveris the primary target organ of this chemical. The MRL is based on the lowest-observed-adverse-effect-level of 0.018 mg/kg/day, which caused an increase in certain types of cellularnuclei in the liver. At slightly higher doses, animals have been shown to experienceincreased blood coagulation and an increase in skin collagen (28).
Vinyl chloride is classified as a human carcinogen by EPA and IARC. Long-term cancerstudies have shown vinyl chloride to cause liver tumors in experimental rats and mice. Drinking water containing vinyl chloride at 2 ppb would cause no apparent increased cancerrisk.
Given an equivalent exposure dose via inhalation of volatilized vinyl chloride, the combinedingestion and inhalation dose would be doubled. Similar to ingestion, the liver is the primarytarget organ for inhalation of volatilized vinyl chloride. The adverse effect first noted frominhalation exposure is increased liver weight. A combined ingestion and inhalation dose fora child would be almost 50 times less than the lowest dose which produced an observedadverse effect in rats, and, for adults, more than 150 times less than the lowest observedadverse effects level. Therefore, a combined ingestion and inhalation exposure to watercontaminated with 2 ppb of vinyl chloride would not be expected to result in adversenoncancer health effects. Dermal uptake cannot be estimated from the available information.
Toxicological information on 1,1,1-trichloroethane is limited but it is clear from the existingstudies that high levels are required to produce adverse health effects. Slight to moderatereversible skin irritation has been seen in animal studies (29). The levels in groundwater atthe PMHC (180 ppb) appear to be far below the levels producing any adverse health effects.
Chloroethane was detected in the PMHC wells at levels up to 9 ppb. Toxicologicalinformation on chloroethane is very limited and the existing information is concernedprincipally with inhalation and, secondarily, dermal exposure. Existing information indicatesthat high levels are required to produce adverse health effects. Formerly, chloroethane wasused as a medical anesthetic (30). The levels detected in the groundwater at the PMHC arefar below those that could cause adverse health effects.
Chloromethane was detected in the PMHC wells at levels up to 13 ppb. No information isavailable on the health effects from oral exposure to chloromethane. Animal studies of long-term inhalation exposure to chloromethane have shown effects to the liver, kidney, nervoussystem, and reproductive system (31). Residential exposure to volatilized chloromethanewould not be at levels of health concern.
Toxicological information on 1,1-dichloroethane is very limited. Knowledge of healtheffects via ingestion is limited to animal studies at high exposures. The available cancerstudies with experimental animals have been inconclusive because of study limitations anderrors. A 1977 NCI study suggested that 1,1-dichloroethane can cause tumors in bloodvessels, mammary glands, and the uterus of rats and mice. Information on health effects viainhalation is available only for very high levels of exposure (32). The maximum level of1,1-dichloroethane detected in the PMHC wells was 89 ppb. Exposure at this level wouldnot be expected to result in adverse health effects.
1,2-dichloroethane was detected in the PMHC wells at levels up to 6.6 ppb. Most of theavailable toxicological information on this chemical describes effects of acute, high-doseexposures. Chronic, low-dose animal studies have involved principally liver and kidneyeffects. Liver tumors have developed in rats after ingestion of low levels of 1,2-dichloroethane (33). Combining inhalation and ingestion doses would result in an exposurefar less than the ATSDR intermediate oral MRL of 0.2 mg/kg/day; therefore, no adversenoncancer health effects would be expected.
EPA has classified 1,2-dichloroethane as a probable human carcinogen for both oral andinhalation routes of exposure. A combined inhalation and ingestion exposure to watercontaminated with 6.6 ppb of 1,2-dichloroethane for 21 years would pose no apparentincreased cancer risk.
Insufficient toxicological information is available to evaluate the health effects fromexposure to this site's mixture of groundwater contaminants. The effect of two or morechemicals given simultaneously could produce a response that may be simply additive of theindividual responses or a response that may be greater or less than that expected by additionof the individual responses. Residents of PMHC were exposed to a mixture of the chemicalspreviously discussed; however, that exposure was not likely to have been at maximum levelsat any one time. The contaminants were chlorinated solvents with similar target organs forchronic, low-level exposure. The liver and kidneys are the susceptible to most of thesechemicals. Although the health effects of exposure to a mixture of these chemicals areunknown, the contaminants are similar and do affect the same organs. Therefore, it ispossible that the adverse effects from the combined exposure would be greater than effectsfrom the individual constituents.
In summary, long-term (i.e., 21-year) exposure to VOCs in the PMHC wells may have represented apublic health hazard for noncancer health effects and may have posed a low increased risk of cancer for PMHC residents.
As stated earlier, metals were not analyzed in the PMHC wells. Metals were detected in the off-site monitoring wells and in the on-site supply wells at levels generally similar to the off-sitebackground monitoring well. The levels of these metals in groundwater would not be expected to be of public health concern.
Other Private Wells
The data evaluated from the five downgradient commercial wells contained several chlorinatedsolvents that were not at levels of public health concern. Sampling for metals was not conducted,but if the metal levels are similar to the levels in on-site and off-site monitoring wells, health effectsare unlikely.
- On-Site Supply Wells
Although VOCs, including DCE and PCE, were detected in the plant's water supply wellswere at levels of public health concern, the contaminant levels actually ingested by plantemployees from the plant's drinking water system are not known. Because the plant'sdrinking water was historically carbon treated to some extent, the VOC levels in the drinkingwater were probably much lower than the levels in the supply wells themselves. Therefore, itis unlikely that plant employees would suffered any health effects from ingesting VOCs inthe plant's drinking water.
Some plant employees were exposed to chlorinated solvents, primarily 1,1,1-trichloroethane(TCA), as part of their on-the-job activities. The exposures were principally via inhalationand dermal contact. Although actual exposure data are not available, an employee's report ofdrunken-like reactions after inhalation of solvent vapors is consistent with the knownneurological effects of TCA. These effects include dizziness, lightheadedness, and loss ofcoordination from inhalation exposure at moderate to high TCA levels (>500 ppm). Atsomewhat lower levels of exposure (>175 ppm), impaired performance ofpsychophysiological function tests has been observed. The effects tend to subside rapidlyafter exposure has ceased. In addition to neurological effects, acute exposure to TCA hasalso been associated with hypotension, cardiac arrhythmia, diarrhea and vomiting, mildhepatic effects, and dermal and ocular irritation.
Studies involving chronic (long-term) human exposure to TCA are limited and do notprovide definitive conclusions about the health effects of chronic TCA exposure. A recentreport suggests that impaired memory and deficits in balance were persistent effects in agroup of workers after chronic exposure to moderate to high levels of TCA. However, thevalidity of these new findings has not yet been determined.
Health outcome data refer to information on the health status of a population. This information mayinclude pre-existing health conditions and morbidity (disease) and mortality (death) rates. Healthoutcome data were not evaluated in this assessment for the following reasons. The health outcomedatabases are not appropriate for the study of a population the size of the PMHC. The smallestpopulation unit for which health outcome data have been summarized is Madison County, which istoo large an area in comparison to the PMHC. For example, cancer rates are not elevated inMadison County but this may not be reflective of PMHC (34). The rates in PMHC may be dilutedwhen combined with the rest of the county. In addition, only a small number of residents haveresided at the PMHC for 21 years. This number of residents would not be statistically large enoughto show effects from exposures at these contamination levels. Finally, many of the exposedresidents have likely moved away and may not be included in the Madison County health data.
The community health concerns gathered as part of this public health assessment involve workerexposure to chemicals used on the job. As is often the case, workers are exposed to higher levels ofchemicals in the normal course of their work than are surrounding residents. Known health effectsassociated with worker exposure to site chemicals are discussed in the Occupational Exposure,Toxicologic Evaluation subsection of the Public Health Implications section of this public health assessment.
The Occupational Safety and Health Administration (OSHA) and its state counterparts are thegovernment agencies responsible for safeguarding workers' health and safety. ATSDR recognizesthe valid concerns of workers at the Sherwood Medical plant and has referred them to theappropriate agencies.