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An environmental pathways analysis is conducted in order to determine the implications ofcontamination at and around the site. Such an assessment consists of determining the nature andextent of contamination, evaluating whether complete environmental pathways exist, andassessing the implications of those pathways. A complete environmental pathway consists offive elements: (1) a source of contamination, (2) an intra or intermedia migration route, (3) apoint at which a human can become exposed, (4) routes of exposure, and (5) a receptorpopulation. The public health implications of contamination existing at a point where apopulation may become exposed is dependent on the existence of an exposure route (amechanism by which individuals become exposed to contaminants e.g., ingestion, inhalation,and dermal contact) and the magnitude and frequency of the exposures which may occur.

The first step in performing this analysis is to identify contaminants of concern that will befurther evaluated in subsequent sections of this public health assessment to determine the publichealth significance of exposure to them. Inclusion of a contaminant in tables and discussion heredoes not imply that exposure would result in adverse health effects. When selected as acontaminant of concern in one medium, that contaminant is recorded in all media tables.

ATSDR selects contaminants of concern based upon one or more of the following factors:

  1. Concentrations of contaminants on and off site.
  2. Field data quality, laboratory data quality, and sampling plan design.
  3. Relationship of contaminant concentrations to medium-specific comparison values.
  4. Community health concerns.

Data tables include the following abbreviations:

  • MDNR
  • CREG
  • EMEG
  • EPA
  • RMEG
  • LTHA
  • ppb
  • ppm
  • BDL
  • ND
  • MCL
  • = Michigan Department of Natural Resources
    = Cancer Risk Evaluation Guide
    = Environmental Media Evaluation Guide
    = Environmental Protection Agency
    = Michigan Toxic Substance Control Commission
    = Reference Dose Media Evaluation Guide
    = Lifetime Health Advisory for drinking water (EPA)
    = parts per billion
    = parts per million
    = Below Detection Limit
    = Not Detected
    = Maximum Contaminant Level

    ATSDR uses several types of medium-specific comparison values to assist in selecting thecontaminants that will be evaluated later for public health significance. For this assessment thespecific comparison values include Environmental Media Evaluation Guides (EMEGs), CancerRisk Evaluation Guides (CREGs), and Reference Dose Media Evaluation Guides (RMEGs). EMEGs are estimated comparison concentrations that are based on the Minimal Risk Levels(MRLs) presented in the ATSDR Toxicological Profiles for specific chemicals. At this time,MRLs consider only non-carcinogenic toxic effects of a chemical substance. CREGs areestimated contaminant concentrations that are based on one excess cancer for a million personsexposed over a lifetime and are calculated from EPA's cancer slope factors. RMEGs arecalculated from EPA's Reference Doses and are based on their estimates of the daily exposure toa contaminant that is unlikely to cause adverse health effects.


    Most of the environmental data used in this report to assess the nature and extent ofcontamination is taken from the EPA Remedial Investigation Report (RI) dated August 23, 1990. Previous investigations at the site were conducted by the MDNR, MDPH, MTSCC, and theconsulting firm of Neyer, Tiseo, and Hindo, LTD. Data collected during some of theseinvestigations is included in the RI along with data gathered during EPA's remedialinvestigation.

    During the various environmental investigations groundwater samples were collected from bothon-site and off-site locations. Air, soil gas, surface soil, subsurface soil, and leachate sampleswere collected on the site. In addition, sediment and surface water samples were collected fromMcBride Drain, which lies adjacent to the site.

    Analyses of the samples during the EPA Remedial Investigation were performed at laboratoriesparticipating in the EPA's Contract Laboratory Program (CLP). CLP analyses conducted onsubsurface soil, surface soil, sediment, surface water, and groundwater samples include tests forTarget Compound List (TCL) volatiles, TCL semi-volatiles, pesticides & PCBs, oil & grease,unfiltered metals, and cyanide. In addition, filtered metals analysis was performed ongroundwater and surface water (1). Air samples were analyzed for the presence of eight organiccompounds. Soil gas samples were analyzed for total organic vapors.

    Environmental investigations at this site have indicated that leachate and groundwater haveconsistently contained elevated levels of organic and inorganic contaminants. Contaminantsdetected at elevated levels include: ammonia, antimony, arsenic, barium, benzene, cadmium,chromium, 1,2 dichloroethane, lead, manganese, methylene chloride, methyl ethyl ketone,nickel, nitrates, selenium, tetrachloroethylene (PCE), trichloroethylene (TCE), vanadium, vinylchloride, and zinc. Between 1984-1987 several organic contaminants were detected inresidences during indoor air sampling. These contaminants may be related to building materialsand household products. The available data did not indicate significant surface soil, surfacewater, subsurface soil, or sediment contamination.


    The following chemicals were detected in on-site leachate samples at elevated concentrationsbetween the years 1982-1988: methylene chloride, benzene, PCE, TCE, vinyl chloride,cadmium, lead, nickel, zinc, arsenic, chromium, selenium, and manganese. Refer to Table 1 for maximum concentrations.

    Leachate samples collected in 1988 were drawn directly from the sumps of the leachatecollection system. One sample was collected at the northeastern corner of Site 9 and the otherwas collected from the central portion of the southern property line of Site 9a. EPA officialsconsider these locations representative of both sites. Potential chemicals of concern detected inthese samples are: methylene chloride, nickel, zinc, and manganese. Maximum concentrationsfor chemicals detected were found in the samples from Site 9a.

    Table 1

    Leachate: Samples collected between 1983-1988

    ContaminantMaximum Concentration
    Source, YearComparison Value
    methylene chloride13,000MDNR 19835.0 CREG
    lead680MDNR 1983NONE
    benzene40MTSCC 19831.0 CREG
    PCE110MTSCC 19830.7 CREG
    TCE130MTSCC 19833.0 CREG
    vinyl chloride30MTSCC 19830.2 EMEG
    zinc87,000MTSCC 19833000 RMEG
    arsenic120,000MTSCC 19830.02 CREG
    chromium260,000MTSCC 198350 RMEG
    cadmium146,000local resident7.0 EMEG
    selenium6,988,000local resident30 EMEG
    nickel940,000EPA 1988200 RMEG
    manganese33,300EPA 198850 RMEG

    Leachate samples from earlier investigations in 1982 and 1983 contained high levels of benzene,methylene chloride, TCE, vinyl chloride, PCE, nickel, chromium, arsenic, and selenium. Someof the leachate samples were collected from the leachate collection system at Site 9a as part of asurvey conducted by the MDNR in September 1983. Other samples were collected from amanhole near the southern border of Site 9a by the MTSCC in July 1983, and from anunidentified location by a nearby resident in 1982. Limited off-site leachate data was availablefor review by ATSDR; thus a thorough assessment of the implications of historical offsiteleachate contamination of residential yards and basements cannot be conducted. In 1991,MDPH provided ATSDR with results from water sampled in the sump pit of a residentialbasement and sediment and standing water in a residential yard. These results will be discussedin the residential sampling section.


    The EPA collected groundwater samples during three sampling events: January 1989, July 1989,and November 1989. The MDNR, the MDPH, the MTSCC, and the consulting firm of Neyer,Tiseo, and Hindo, Ltd, collected groundwater samples during varying times between 1983 and1991. The groundwater sample results will be separated into two major categories: on- and off-site monitoring results and residential well results. The former category is subdivided byspecific aquifer. The residential well information cannot be discussed by specific aquiferbecause available well construction information is not sufficient to allow classification of themby aquifer (1).


    The local aquifer system is composed of three interdependent aquifers: the shallow, theintermediate, and the deep. Discontinuous clay layers allow flow paths from the three aquifers to merge.

    Chemicals detected above comparison values are as follows: benzene, vinyl chloride, methylenechloride, zinc, lead, cadmium, nickel, arsenic, chromium, antimony, barium, manganese, andvanadium. In on-site monitoring wells, the maximum contaminant levels were detected in eitherthe shallow or the intermediate aquifer. Chemicals having maximum concentrations within theshallow aquifer include: benzene, methylene chloride, lead, cadmium, antimony, andmanganese. Vinyl chloride, zinc, nickel, arsenic, chromium, barium, and vanadium hadmaximum concentrations within the intermediate aquifer. Refer to Table 2 for concentration levels.

    The following chemicals were detected in off-site monitoring wells at levels exceedingcomparison values: zinc, lead, cadmium, nickel, arsenic, chromium, antimony, barium, andmanganese. Six out of ten maximum concentrations were detected within the intermediateaquifer. The remaining maximums were detected within the deep aquifer. It is important tonote that Michigan has some extensive geographic areas with elevated levels of arsenic ingroundwater known to be naturally occurring. Refer to Table 3 for concentration levels.

    Table 2

    On-site Monitoring Wells: Data collected between 1983-89, Maximum Concentration in ppb

    ContaminantShallow AquiferIntermediate
    Deep AquiferComparisonValueSource
    benzene36 6-22 ND1.0CREG
    methylene chloride170019195.0CREG
    vinyl chloride2533 *ND0.2EMEG
    arsenic78 †1-2192-360.02CREG
    lead2-12607-445850 *NONE
    manganese77-13000 31-12300 42-12800 50RMEG

    ND: not detected
    NC: not detected at a level of concern
    * : MDNR investigation, 1983
    † : NTH investigation, 1987
    Unless otherwise noted data results are from the 1989 EPA investigation.

    Table 3

    Off-site Monitoring Wells: Data collected between 1983-89, Maximum Concentration in ppb

    ContaminantShallowAquiferIntermediateAquiferDeep AquiferComparisonValueSource
    antimonyND 66-231 ND 4.0RMEG
    arsenicNC7-66NC0.02 CREG
    lead31-396-481920 †NONE

    ND: not detected
    NC: not detected at a level of concern
    * : MDNR investigation, 1983
    † : NTH investigation, 1987
    Unless otherwise noted data results are from the 1989 EPA investigation.


    Though the presence of contaminants at levels of potential concern in residential wells were notnoted by the latter EPA investigation, earlier investigations (1983 and 1984) conducted by stateand local agencies initially concluded that residential wells were contaminated with VOCs. TheMDPH has established a policy for replacement of private water supplies where syntheticorganic chemicals are found at detectable levels. This policy has been partially based upon theinability for private wells to be regularly monitored to detect the encroachment of highercontaminant levels at a later date. Thus, once impacted wells were identified near the SMDAsite, residents were instructed not to use their water. Most residential wells are no longer in use. Refer to Table 4 for contaminant concentration levels in residential wells.

    Table 4

    Residential Wells: Data collected by MDNR/MDPH between 1983-90, Concentration Range or Maximum in ppb

    ContaminantConcentrationRangeComparisonValue Source
    arsenicND-40* 0.02CREG
    1,2 dichloroethaneND-90.4CREG
    leadND-225 None
    methylene chlorideND-545.0CREG
    methyl ethyl ketoneND-1827200LTHA

    * Reference 5a

    Data collected during MDPH residential well sampling rounds indicate sporadic low levels oforganic contaminants such as styrene, trichloroethylene, and chloroform. Contaminants such asbenzene, methyl ethyl ketone, methylene chloride and ammonia were detected more frequentlyand at higher levels. There were no consistently elevated levels of heavy metals. In many wellselevated concentrations were detected only once. One example of this is a well where lead wasdetected at 225 ppb in 1988. In addition, the presence of ether and freon type compounds wasobserved frequently. ATSDR, however, does not have any concentration data for thesecompounds. It should also be noted that methane was detected in the water of two residentialwells in 1986 using a gas water separation technique. The majority of affected wells werelocated at residences along 24 Mile Road between the years 1983 and 1988.


    Benzene was detected in McBride Drain at a concentration of 39 ppb during the MDNR surveyconducted in 1983. This concentration is nearly eight times greater than EPA's maximumcontaminant level for benzene in drinking water. The laboratory that analyzed the surface watersample, however, indicated the possibility that contamination of the sample within the laboratoryduring analysis may have affected the accuracy of the analytical results. The sample location isreportedly downstream of McBride Drain just below the SMDA site, parallel to the southernedge of the landfill. Several leachate outbreaks have occurred along this stretch of the Drain,which is also thought to be a surface discharge point of the intermediate aquifer.


    Groundwater, soil gas, indoor air, standing water, sediment, and sump water samples werecollected at several residences near the SMDA site from 1983 to 1991. Residential wellsampling results are discussed in the Groundwater Section. Residential soil gas sampling resultsare discussed in the Soil Gas Section. The analytical results of samples from the remainingmedia will be discussed in this section.

    In 1982, following a complaint by a resident that red "ooze" from the landfill had seeped into abasement, analysis on sump water and a sludge like material was conducted. Although traces ofsome volatile organic compounds (VOCs) (toluene, 1,2-dichloroethene, and 1,1-dichloroethane -- under 10 ppb) were detected in sump water in the residential basement, an evaluation by aresearcher at Wayne State University attributed the red slime to the high iron content of theshallow groundwater and iron-loving bacterial growths (e.g. Gallionella ferrugina). The samekind of reddish growths were found in McBride Drain upstream from the landfill (3).

    Between 1984 and 1987 MDPH conducted indoor air sampling at three residences near theSMDA site. Toluene, fluorotrichloromethane, 1,1 dichloroethane, 1,2 dichloroethane, xylene,and 1,2-dichloropropane were detected in one or more of the residences. These chemicals maynot be related to the landfill. Methane levels were not tested. The production of methane gasfrom the breakdown of wastes is often associated with landfills.

    In May of 1991, officials of the MDPH and MDNR conducted sediment and standing watersampling on residential property adjacent to the site. The bulk of the chemicals detected weremetals. Iron, manganese and lead in the water samples were above background and within therange of on-site ground water concentrations. Lead was the only chemical detected abovebackground levels in the sediment samples (7).

    Very few organic chemicals were detected in the samples. Those detected in sediments were atconcentrations greater than background levels and within the range of concentrations detected inon-site soil samples collected by EPA. The concentrations of organics found in the watersamples were inconsistent with EPA groundwater sample results. Several concentrations ofcontaminants detected at the residence either were below background or below concentrationsdetected on-site. In addition, some of the contaminants had not been detected on-site. Toluene,1,4-dichlorobenzene, and 1,2,4-trichlorobenzene were detected at concentrations within therange of those detected on-site by EPA (7).

    MDNR concluded that most of the chemicals detected in the samples were related to the SMDAsite and identified the contamination as a result of a leachate outbreak. Although most of thechemicals detected were at background levels, MDNR recommended that the soils and waterfrom this area not be used (7).

    In August of 1991, MDPH conducted sampling of sump water from the basement of a residence. Several organics were tentatively identified during analysis. However, due to prematuretermination of the analytical test a more conclusive identification of the contaminants was notpossible (6).


    A total of 105 soil gas samples were collected during two surveys. The samples were collectedat points surrounding the perimeters of the landfill areas (Sites 9 and 9a, excluding the westernside), from within the cap material, from residential and adjacent properties north of 24 MileRoad, and at background surface soil sample points. Sample values were presented as totalvolatile organics. Soil gas samples collected during the surveys were analyzed by two differentmethods: organic vapor analyses and photoionization detection. Organic vapor analyses showedpositive deflections which indicated probable concentrations of methane gas (1).


    Crop foliage was tested in 1982 for polychlorinated biphenyls, TCE, and various pesticides. None of these contaminants were detected. Green peppers and green tomatoes were tested bythe Michigan Department of Agriculture in 1983. Traces of inorganics (not specified) werefound. The same year the Michigan State Cooperative Extension Service reported that observedtomato stunting and leaf silvering may be due to high soluble salt and nitrate levels in the soil. Residential soil sampling in 1991 did detect contaminants thought to be related to the SMDAsite. It is not clear whether biota in the area was affected by the contamination.


    Quality assurance and quality control (QA/QC) methods were utilized on data obtained for theRI. EPA reports that during the laboratory analyses, some parameters were determined to beoutside the quality control limits. These deviations are clearly indicated in the remedialinvestigation report and do not significantly impact use of data (9). QA/QC documentation wasonly partially available for data from previous investigations and information submitted toATSDR by state and local agencies. The ATSDR recognizes that many limitations on the qualityof that data may exist. Because of the history of this site, we deemed it desirable to examinedata collected prior to EPA involvement.


    The composition of waste materials deposited in landfills may allow for the production ofmethane, a highly explosive gas. Both on- and off-site monitoring have indicated the possiblepresence of methane. During winter periods when topsoil is frozen, lateral movement ofmethane gas can result in potentially explosive conditions in the basement of homes and otherconfined spaces under circumstances where venting is not provided. Although the EPAinvestigation reported no trends between sample points and no "significant" concentrationsabove background, additional information is needed before an assessment can be made of thepotential for explosion due to the existence of methane and other landfill gases around this site.


    Both groundwater and surface water contamination have been documented by past investigationsconducted on and around the site. The environmental pathway of greatest concern at this site isgroundwater. The associated human exposure routes include ingestion and dermal contact withcontaminated groundwater and inhalation of volatiles emanating from contaminatedgroundwater. Exposure is believed to have occurred in the past, may presently be occurring, andmay occur in the future.

    Although the surface water pathway is complete, it is not presently of concern. The potential forMcBride Drain to become contaminated does exist, however, as of the most recent investigationthe drain was not found to be contaminated. The drain is not normally used for recreationalpurposes but it does flows through a golf course and golfers undoubtedly retrieve their strayballs from the surface water body. Thus, if McBride Drain were to become contaminated due toa leachate outbreak a small risk of exposure due to direct contact with the water in the Drainwould be possible.

    Other potential environmental pathways at this site include the surface soil, and biota pathways. These pathways would be due to contamination of surface soil and surface water resulting fromleachate outbreaks. Although there has been one confirmed leachate outbreak in recent years therisk of exposure through this pathway is small. In addition, exposure via inhalation of entrainedsoil particles and ingestion of crops which have bioaccumulated contaminants is highly unlikely.


    Movement of Contaminants from Soil/Waste Layers to Groundwater

    Similar contaminants were detected both in onsite monitoring wells and residential wells usedfor drinking water. Because individuals were at risk for exposure in the past and may currentlybe at risk for exposure, the groundwater pathway is complete.

    An important migration mechanism at this site is infiltration. Infiltration is the process by whichprecipitation moves through soil layers to replenish moisture, recharge aquifers, and supportstreamflows. The rate at which contaminants in soils and buried wastes migrate along withinfiltrating water is dependent upon several factors. Three major factors are the climate, thephysical characteristics of the soil, and the physical and chemical characteristics of the contaminants.

    Macomb County has an average yearly precipitation of 28.07 inches (9). The soil at the site isbest described as a mixture of sandy loams, fine sands, and clay loam. EPA determined that thepermeability of the cap material at Site 9 was higher than that at Site 9a (9). This indicates thatinfiltration through the cap layer would occur at a faster rate on Site 9 as compared to Site 9a.

    Chemicals released from landfill materials during infiltration episodes are transported in a plumeof leachate which percolates through soil and waste layers and into groundwater. The plumedisperses both downward and laterally. As discussed in the on-site contamination section, thepresence of discontinuous clay layers allows for contaminant movement between the threeaquifers. Contaminants may enter the shallow aquifer, move downward into the intermediateand deep aquifers, and then move laterally off the site.

    Organic contaminants with high organic carbon partition coefficients (Koc) tend to adsorb toorganic matter in waste and soils; while organic chemicals having low Koc's (<100) such asbenzene (Koc:83) and methylene chloride (Koc:8.8) tend to migrate more freely intogroundwater. Both of these chemicals were detected in the leachate and in the groundwater atthe site. The extent to which inorganic contaminants will be mobile in leachate is morecomplicated and is dependent on several factors including pH, oxidation-reduction potential, andthe presence of other anions or cations. The leachate at this site contained several inorganiccontaminants which were also detected in the groundwater samples. It is important to note thatthis area of Michigan is known to have naturally occurring high inorganic metal content in soil. Two elements in particular that are found in high concentrations are iron and arsenic.

    The distribution of organic and inorganic contaminants within the three aquifers is both spatiallyand temporally erratic. This pattern is consistent for landfills. Due to the nature of a landfillingoperation, source areas are often not discrete but may exist at random locations throughout thesite. Contaminant migration from these sources is also not expected to occur at a continuousrate. It is more realistic to expect slugs of contamination to move away from sources at varioustimes and at varying rates. These rates depend on the characteristics of the chemicals containedwithin those areas and the environmental conditions which may influence or inhibit migration. The range of contaminant concentrations detected during the many sampling events is evidence of this.

    During the EPA investigation the maximum contaminants in leachate were found in samplestaken from Site 9a, despite the greater permeability noted earlier in the surface soils coveringSite 9. This seems to suggest that either 1) wastes buried in Site 9a may collectively act as agreater potential source of contamination that can potentially migrate to the shallow aquifer andbeyond, or that 2) wastes disposed of at Site 9a may be more contaminated than those at Site 9 (9).

    The EPA has identified two contaminant plumes; one in the intermediate aquifer and the other inthe shallow aquifer. Neither of the plumes are well defined but, of the two, the shallow is theleast defined due to the low number of samples collected during the remedial investigation (9). A plume has not been identified in the lower aquifer. The sampling data in Table 2 show lesscontamination in this aquifer than in the upper aquifers.

    Groundwater beneath the site exhibits multi-directional flow patterns as a result of moundingeffects. The primary flow pattern or route of off-site migration for groundwater has beenidentified as being through the intermediate aquifer. The leachate plume first enters the shallowaquifer. Flow to the north is restricted by the slurry wall and flow towards the east, west, andsouth is expected to quickly enter the intermediate aquifer. Once in the intermediate aquifer,contaminants have greater potential to move laterally off the site toward residential wells.

    ATSDR has been informed that one of the leachate collection systems does not capture the entireleachate plume (8). Some of the leachate not collected by the system at Site 9 is believed to becaptured by the system at 9A. If leachate not collected by either system migrates through theshallow aquifer in the southeasterly direction, area crock wells may be affected.

    Exposure to contaminated groundwater from use of residential wells is believed to have occurredin the past. There is a small risk that it may currently be occurring and that it may occur in thefuture. The exposure routes of concern associated with this medium are ingestion, inhalation,and dermal exposure. Several remedial actions have taken place since the contamination ofresidential wells was first detected. Most residences near the site are now connected tomunicipal water, approximately nine are not connected. Although monitoring through February1995 has not indicated the presence of contamination, the potential for future exposure tocontaminated groundwater does exist, but is highly unlikely (8a).


    Movement of Contaminants from Groundwater to Surface Water

    At Site 9a, leachate entering the shallow aquifer is primarily captured by the leachate collectionsystem. It may be possible that a small amount of leachate is not captured by this system. Leachate not captured by the leachate collection system can possibly migrate into theintermediate aquifer. Because McBride Drain is thought to be the surface discharge point for theintermediate aquifer, contaminants may reach McBride Drain. The current sampling resultsindicate that McBride Drain is not contaminated. Although contamination was documented inthe past, this pathway is currently incomplete because: 1) contamination of the McBride Draindoes not currently exist and 2) is not likely to occur in the future due to proposed remediation of the site.

    If this pathway becomes complete due to migration via leachate seeps or discharge of thegroundwater plume to McBride Drain, there may be a small risk for human exposure via directcontact. Additional pathways which could be indirectly affected are air and biota. The airpathway may be affected because as contaminated groundwater surfaces at McBride Drain,VOCs will volatilize into the atmosphere. The biota pathway may be affected because waterfrom the creek is used downstream for irrigation of crops and at the golf course for irrigation ofthe greens. Uptake of contaminants by terrestrial biota may occur. There are reportedly no sportfish in McBride Drain, so aquatic biota that might be consumed by humans is not likely to be aconcern. Exposure resulting from these pathways would likely be minimal due to the infrequentnature of contamination of the Drain and dilution effects of the contamination which may enter the drain area.


    Overflow of Leachate onto Adjacent Properties during Flooding

    Local residents have raised complaints regarding leachate flooded fields. During periods ofextreme stress on the leachate collection system (periods of increased infiltration beyond thestorage capacity of the system), it may be possible for leachate to overflow. However, this ishighly unlikely since the leachate is removed from the collection systems at regular intervals.

    The MDNR and EPA have responded to citizens complaints of leachate outbreaks and floodingon several occasions. Testing of the liquid samples taken during those times rarely substantiateleachate outbreaks. There was, however, a confirmed off-site leachate outbreak in 1991 due tobubbling up of the leachate plume. This pathway is complete, but the risk of future occurrenceis considered small due to the infrequent nature of confirmed incidents and the duration whichan individual may be exposed to contaminants.

    Leachate outbreaks may occur easier in areas of the landfill affected by erosion, the southernperimeter and barren areas. Because these areas do not support vegetation well, they are athigher risk for natural and leachate induced erosion. Two consequences of leachate inducederosion are: 1) contamination of McBride Drain directly by leachate and/or migration ofcontaminated soil particles contaminated by leachate and 2) entrainment of contaminated soilparticles into the air. The pathways associated with surface water contamination have alreadybeen discussed. Risk of inhalation of contaminated entrained particles is considered minor dueto the infrequent nature of confirmed leachate outbreaks.

    The overall risk of exposure to contaminants through the surface soil pathway due to leachatecontamination is very small due to the infrequent nature of confirmed outbreaks. In addition,there reportedly is an on-site engineer who is responsible for maintaining the cap surface inorder to prevent leachate outbreak occurrences. If conditions change, this pathway should befurther evaluated since recreational and residential areas surround the site.


    Leachate Overflow and Uptake from Soil

    Residents have raised concerns about the impact of leachate outbreaks both indirectly anddirectly affecting their crops. Testing of foliage and vegetables in 1982 and 1983 by theMichigan Department of Agriculture and the Michigan State Cooperative Extension Servicecould not substantiate these claims. Soil sampling on private property in 1991 did confirm theoccurrence of a leachate outbreak. The area in which contamination was found was adjacentused for growing crops. The residents were told not to use soils and water from the affectedarea. If residents do not use this area there is no risk of exposure.


    MDNR has received reports that leachate is released to area manholes instead of being taken to atreatment center three times a week. If leachate is being disposed of in this manner, workerscould be exposed dermally, as well as via inhalation and incidental ingestion (due to splashes)while pumping the leachate into the manholes. In addition, workers who may need to entermanholes may be exposed via inhalation of vapors (confined space) and dermal contact.



    The contaminants of concern disposed (released) into the environment at SMDA have thepotential to cause adverse health effects. However, for adverse health effects to occur thepathway for exposure must be completed. A release does not always result in exposure. Aperson can only be exposed to a chemical if they come in contact with the chemical. Exposuremay occur by breathing, eating, or drinking a substance containing the contaminant or by skin(dermal) contact with a substance containing the contaminant.

    Several factors determine the type and severity of health effects that occur from an exposure to acontaminant. Such factors include the exposure concentration (how much), the frequency and/orduration of exposure (how long), the route or pathway of exposure (breathing, eating, drinking,or skin contact), and the multiplicity of exposure (combination of contaminants). Once exposureoccurs, characteristics such as age, sex, nutritional status, genetics, life style, and health status ofthe exposed individual influence how the individual absorbs, distributes, metabolizes, andexcretes the contaminant. Together those factors and characteristics determine the health effectsthat may occur as a result of exposure to a contaminant.

    ATSDR considers the above physical and biological characteristics when developing healthassessment guidelines. Toxicological profiles prepared by ATSDR summarize chemical specifictoxicological and adverse health effects information. Health assessment guidelines such asATSDR's MRL and EPA's Reference Dose (RfD) and Cancer Slope Factor (CSF) are includedin the toxicological profiles. Those health assessment guidelines are used by ATSDR healthprofessionals in determining the potential for developing adverse noncarcinogenic health effectsand/or cancer from exposure to a hazardous substance.

    A Minimal Risk Level (MRL) provides a basis for comparison with concentrations ofcontaminants in different environmental medium (soil, air, water, and food) to which peoplemight be exposed. If daily exposure occurs at an amount below the MRL, harmful noncanceroushealth effects are not expected to occur. The method for deriving MRLs does not includeinformation about cancer, therefore, an MRL does not imply anything about the presence,absence, or level of cancer risk.

    An EPA Reference Dose is an estimate of the daily exposure for the human population,including sensitive subpopulations, that is likely to be without appreciable risk of adversenoncarcinogenic health effects during a lifetime (70 years). The RfD is a health guideline forthe oral route of exposure. For carcinogenic substances, EPA has established the Cancer SlopeFactor (CSF) as a health guideline. The CSF is used to determine the number of excess cancersexpected from exposure to a contaminant.

    To link the site's human exposure potential with health effects that may occur under site-specificconditions, ATSDR estimates human exposure to the site contaminant from ingestion and/orinhalation of different environmental media. The following relationship is used to determine theestimated exposure to the site contaminant:

          ED = (C x IR x EF) / BW
        ED = exposure dose (mg/kg/day)
        C = contaminant concentration (mg/kg)
        IR = intake rate (kg/day)
        EF = exposure factor (unitless)
        BW = body weight (kg)

    ATSDR uses standard intake rates for ingestion of water. The intake rate for drinking water is 2L/day for adults and 1 L/day for children. Standard body weights for adults and children are 70kg and 10 kg, respectively. The maximum contaminant concentration detected at a site for aspecific medium is used to determine the estimated exposure. Use of the maximumconcentration detected in a specific medium will result in the most protective evaluation forhuman health. In addition, some exposures occur on an intermittent or irregular basis. For thoseexposures, an exposure factor (EF) is calculated that averages the dose over the exposure period. Since the exposure period is not known at SMDA, 70 years was used for a conservative estimate.

    The contaminants of concern at this site are benzene, methylene chloride, arsenic, ammonia, 1,2-dichloroethane, lead, methyl ethyl ketone, nitrates, and cadmium. These contaminants weredetected in residential wells during the years 1983-1990 at levels which exceed ATSDRcomparison values. Exposure to contaminated groundwater is believed to have occurred throughthe ingestion, dermal contact, and inhalation routes due to past use of contaminated privatewells. An MDPH/MCHD survey has indicated that nine residential wells near the site may stillbe in use. Monitoring through 1991 has indicated that these wells are not contaminated. Thepotential for future exposure exists but can be eliminated once residences connect to municipalwater and completely refrain from using water for non-potable purposes.

    The above chemicals may potentially impact on public health because chronic exposure to levelsassociated with adverse health effects may have occurred and future exposure may occur unlessall private wells are abandoned. Toxicological implications resulting from exposure to the abovechemicals are discussed below. However, more detailed information regarding exposurefrequency and duration is necessary to make a more accurate site specific assessment.

    For additional information on each chemical, please see Appendix B.


    Benzene was detected in five residential wells at concentrations up to 17 ppb. At the time ofdetection residents were already being provided alternate drinking and bathing water.

    Exposure to benzene may have occurred in the past via ingestion, inhalation, or dermal contactwith benzene contaminated water. The lowest concentrations of benzene that may causechronic, non-cancerous adverse effects via ingestion are largely unknown, and health guidelinesidentifying a safe level have not been established (11). Thus, ATSDR cannot predict what non-cancerous adverse health effects, if any, may result from exposures at levels detected in wellsnear SMDA.

    Based on calculations for a lifetime of oral exposure to the benzene detected, there is noapparent increased risk of developing cancer.

    The most common exposure to benzene comes from breathing air containing it because benzeneevaporates very quickly (11). Levels of benzene in the air at which noncancerous adverse healtheffects have been observed are one hundred-fold higher than those expected from private wellsin the SMDA area. Thus, noncancerous adverse health effects are not expected to result frominhalation exposure to benzene contaminated water.

    There has not been any air monitoring done at the SMDA site. Based on the groundwaterconcentrations, inhalation of benzene would result in an increased risk of cancer. Benzene isconsidered to be a human carcinogen via inhalation by the EPA, the Occupational Safety andhealth Administration, the World Health Organization, and the International Agency forResearch on Cancer (11). A review of several studies by Aksoy (1985) showed sufficient datademonstrating benzene as a potent carcinogen causing leukemia, malignant lymphoma, multiplemyeloma, and lung cancer (11). Leukemia has occurred in some workers chronically exposed tobenzene (levels of exposure were not reported). Benzene-induced leukemia has a latency periodof 5 to 15 years and, in some instances, is proceeded by aplastic anemia (11). Aplastic anemia isa condition caused by bone marrow failure. However, the idea that exposure to low levels ofbenzene may be carcinogenic is not universally accepted (11).

    Benzene can enter your body through the skin. However, studies regarding human dermalexposure to benzene were not reported (11). Adverse dermal effects have been observed inlaboratory animals following skin contact with undiluted benzene. Dermal contact with benzenesimilar to the concentrations detected in private wells should not be of public health concern.

    Several factors may predispose an individual's sensitivity to the adverse health effects of benzeneexposure. Young people are vulnerable with nutrition, genetics, and immunoresponse playing arole. Pregnant women and their fetuses are at risk since benzene can cross the placenta. Also,drug and alcohol consumption contribute to an individual's sensitivity to benzene.


    Methylene chloride was detected in one residential well at 54 ppb. The estimated oral exposuredose is ten-fold below the RfD. Also, there is no increased cancer risk from methylene chlorideexposure at the concentrations detected. Thus, cancerous and non-cancerous adverse healtheffects are not expected to result from oral exposure to methylene chloride in private wells.

    Human and animal studies demonstrate that the liver and kidneys are primary targets ofmethylene chloride toxicity following inhalation (14). Animal studies suggest that chronic orrecurring exposures to methylene chloride may cause cell changes in the liver and kidney. However, based on these animal studies and those of workers occupationally exposed to high butunknown levels of methylene chloride, it seems unlikely that serious liver or kidney damage inhumans will occur unless exposure levels are extremely high (14). Therefore, the methylenechloride levels detected at this site are unlikely to cause adverse liver or kidney damage via inhalation.

    Several populations may be especially sensitive to the adverse health effects of methylenechloride. Methylene chloride is often metabolized to carbon monoxide in the liver, thus raisingthe carbon monoxide level in the blood. Persons with cardiovascular disease and respiratorydysfunction may experience adverse effects at lower levels than others (14). Smokers alreadyhave increased carbon monoxide levels in their blood, thus they are sensitive to methylene chloride.

    Carbon monoxide may have adverse consequences on fetal development. Animal studies showthat methylene chloride readily crosses the placenta and can enter breast milk. Therefore,pregnant women should take extra precaution to avoid methylene chloride exposure. Inaddition, methylene chloride may be mildly irritating to skin on repeated contact and has beenreported to cause dermatitis in some cases, therefore children playing around leachate areas maybe at risk (14).


    The maximum arsenic concentration detected is 40 ppb. The estimated exposure dose is 1.14µg/kg/day. Non-cancerous adverse health effects have not been observed after exposure atsimilar doses. Human studies indicate that oral doses in the range of 20-60 µg/kg/day mayproduce signs of arsenic toxicity. These signs include digestive tract irritation, anemia,abnormal heart function, and liver and/or kidney injury (15). The severity of these symptomstend to increase as exposure time increases (15).

    An increased cancer risk may result from oral exposure to arsenic at the concentrations detected. Arsenic is classified by the EPA as a human carcinogen via oral exposure. Arsenic ingestionmay increase the risk of liver, bladder, kidney, and lung cancer (15). There is substantialevidence that chronic oral exposure to elevated levels of arsenic increases the risk of skin cancer. The largest study of this relationship was conducted by Tseng, et al., in 1968. Over 40,000people with well water arsenic levels ranging from 1-1820 ppb were examined. The incidenceof skin cancer was correlated with arsenic levels in the water, and a strong relationship betweenskin cancer and other symptoms of arsenic toxicity was noted. Therefore, arsenic levelsassociated with SMDA Sites 9 and 9A could, upon ingestion, increase the probable risk ofcancer of the skin, liver, bladder, kidney, and lungs.

    Some people may be at an increased risk to the toxic effects of arsenic. Individuals withprotein-poor diets or choline deficiency, deficiency in a B-complex vitamin essential to liverfunction, may be especially sensitive to arsenic exposure. Also, individual genetic variabilityinvolving the liver's ability to detoxify arsenic may predispose one to the adverse effects of arsenic.


    Ammonia was detected in residential wells at a maximum concentration of 82,000 ppb duringthe years 1983-1990. The estimated exposure dose exceeds the MRL of 0.3 mg/kg/day. Pastexposure to ammonia likely occurred through inhalation and ingestion of and dermal contactwith groundwater contaminated with ammonia. Exposure may still be occurring through the useof private wells.

    Ammonia is a colorless gas with a very sharp odor. The odor is familiar to most people, becauseammonia is used in household cleaners, window cleaning products, and smelling salts. You cansmell ammonia when it is in the air at a level higher than 50,000 ppb. Adverse health effectshave not been reported at levels below 50,000 ppb. Therefore, you will probably smell ammoniabefore you are exposed to a concentration in air that may harm you (18).

    The health effects resulting from short- or long-term human exposure to water containingspecific concentrations of ammonia via ingestion are not known. Information available forpeople exposed to ammonia through ingestion usually involve case reports of people whoswallowed household ammonia. Thus, the information is from acute exposure to high, butunknown, concentrations. Because of this, it cannot be determined if any non-cancerous adversehealth effects would result, or resulted in the past, from ingestion of ammonia associated with SMDA.

    Dermal exposure to ammonia has produced adverse respiratory, cardiovascular, gastrointestinal,renal, and dermal/ocular effects in humans (18). However, these effects resulted after exposureto massive amounts of ammonia vapor or highly concentrated ammonia, the exact concentrationis unknown. Thus, the concentrations of ammonia that may result in certain adverse healtheffects are largely unknown.

    Carcinogenic potential of ammonia has not been established in humans exposed by theinhalation, ingestion, or dermal routes of exposure.

    There were not any populations identified that might be especially sensitive to the effects ofammonia exposure. However, farmers can be exposed to ammonia when applying fertilizer ordecaying manure.


    A maximum concentration of 9 ppb of 1,2-DCA was detected in residential wells. Theestimated exposures from ingestion are below the levels that would be anticipated to cause acute(short-term) effects. However, little is known about the effects on health of long-term, low-levelexposure [27]. In addition, exposures through inhalation and dermal absorption have not beenconsidered in that estimate and reports in the literature suggest that exposure through inhalationduring bathing is at least equal to exposure from ingestion. Because the levels at which 1,2-DCA could cause particular adverse health effects in humans are largely unknown, ATSDRcannot determine if chronic (70 years) exposure to 1,2-DCA in groundwater at SMDA could result in adverse, noncancerous effects.

    Estimated exposure to 1,2-DCA through ingestion and inhalation of the groundwater would notresult in an increased risk of cancer. Therefore, exposure to 1,2-DCA is not a public healthconcern regarding cancer.

    There were not any populations identified that might be especially sensitive to the effects of 1,2-DCA exposure.


    Lead was detected at a maximum concentration of 225 ppb in residential wells. Ingestion is theprimary route of exposure to lead. Dermal and inhalation exposure are not very significantbecause little lead passes through the skin and it does not volatilize from water. The biologiceffects are the same regardless of how lead enters the body (20). At the present time, no studieshave established what concentrations of lead present in various environmental media may resultin blood lead levels associated with adverse health affects. Because of this, ATSDR cannotdetermine if exposures to lead associated with SMDA would result in blood lead levelsassociated with adverse health effects. Small exposures to lead can result in chronic toxicitybecause the body accumulates it over a lifetime and releases it slowly (20). The bones and teethcontain more than 95% of total lead in the body.

    Lead primarily affects the peripheral and central nervous systems, reproduction, development,blood cells, and the metabolism of vitamin D (20). Exposure to lead resulting in high blood leadlevels (blood lead concentrations exceeding 80 ug/dL) can severely damage the brain andkidneys of adults and children and may affect the male reproductive system after short- andlong-term exposure. Long-term exposure resulting in blood lead levels between 15-30 ug/dLhas been reported to cause decreased growth and Intelligence Quotient (IQ) in young childrenand increased blood pressure in middle-aged males. Both short- and long-term exposureresulting in blood lead levels between 10-15 ug/dL in pregnant women can result in pre-termbirth, decreased birth weight, and reduced mental ability of their offspring (20).

    The nervous system is the most sensitive target of lead toxicity. Lead is a serious threat to thecentral nervous system (CNS) of infants and children. One study showed that CNS damage intwo-year-olds caused by lead exposure resulted in continued deficits in neurologicaldevelopment. Cognitive deficits and lower IQ scores were observed in these children at age five(20). Children with increased teeth lead levels have exhibited decreased attention spans andclassroom performance, concentration problems, deficits in speech and language processing, andnegative social behavior (20). In addition, hearing acuity has been shown to decrease withincreasing blood lead levels (20). Hearing loss may contribute to the poor concentration andlearning disabilities experienced by children with increased lead levels. Neurological symptomsincluding impaired concentration, subtle behavioral changes, and fatigue have been seen inadults with blood lead levels as low as 40 ug/dL (20).

    Lead has produced profound adverse effects on human reproduction when exposure levels werehigh. A study by Wildt et al. (1983) found that men who had blood lead levels greater than 50ug/dL resulting from occupational exposure exhibited adverse testicular effects. Effects seenincluded decreased prostate/seminal vesicle function, lowered semen volumes, and lowerfunctional maturity of sperm (20). In pregnant women, occupational exposure to lead has beenassociated with an increased likelihood of miscarriage. In addition, Nordstrom et al. (1978)discovered an increased frequency of miscarriages in women living near a lead smelter.

    Lead absorbed by pregnant women can transfer to the fetus via the placenta. Developmentalconsequences of pre-natal exposure to lead include premature birth, decreased birth weight, andneurobehavioral deficits (21). Lead can also be transferred through maternal milk to the nursinginfant. Evidence of an association between prenatal lead exposure and congenital malformationshas not been found.

    Exposure to lead may result in adverse effects on blood cells. Lead inhibits the body's ability tomanufacture hemoglobin, the oxygen carrying component of red blood cells. Exposure to leadmay result in anemia. Anemia is evident only when the blood lead level is significantly elevated(>75 ug/dL) (20). However, in children, lead poisoning rarely results in anemia (20).

    Occupational, clinical, and general population studies imply that lead exposure may result inadverse cardiovascular effects. Two large-scale studies provide evidence of a small butstatistically significant link between blood lead levels and blood pressure in men (21). In thesestudies, men with blood lead levels higher than 37 ug/dL had a higher proportion ofhypertension than other men. This effect appears to occur more in middle-aged men.

    Lead appears to affect vitamin D metabolism in the kidney. Lead causes a reduction in thecirculation of the vitamin D hormone and a disturbance in calcium metabolism. These effectscan lead to impaired bone and tooth development (21).

    Case reports have implicated lead as a potential renal carcinogen in humans. However, the EPAhas concluded that human data is inadequate to determine the potential carcinogenicity of leadexposure. Exposure to lead salts has caused kidney tumors in laboratory animals. Therefore, theEPA classifies lead as a probable human carcinogen based on animal studies.

    Several populations may be sensitive to the adverse health effects caused by lead. Pregnantwomen, fetuses, and children are particularly affected by lead exposure. Children with glucose6-phosphate dehydrogenase deficiency have greater blood lead levels than non-deficient childrenwith similar exposure. Persons with sickle-cell anemia may be especially sensitive to theneurological effects of lead exposure. Middle-aged men are at a risk for increased bloodpressure resulting from lead exposure. In addition, those with dietary deficiencies in calcium,iron, and zinc may be susceptible to the adverse effects of lead.


    MEK was detected in private wells at a maximum concentration of 1827 ppb. The estimatedoral exposure dose is ten-fold below the RfD. Thus, non-cancerous adverse health effects arenot expected to result from oral exposure to MEK in private wells.

    MEK is readily absorbed by all routes of exposure. Volunteers exposed to 25,000 ppb MEK inair for five minutes were not affected. They experienced mild irritation of the nose and throatupon exposure to 100,000 ppb (22). Workers chronically exposed to 300,000-500,00 ppb MEKin air experienced headache, irritation, and nausea. Because air concentrations associated withSMDA are expected to be far below those experimental levels, no adverse health effectsresulting from inhalation of MEK is expected.

    No information regarding dermal exposure to diluted or low concentrations of MEK was foundin the literature.

    The data on possible carcinogenicity of MEK is inadequate to determine if it is a human carcinogen.


    Cadmium was detected in residential wells at a maximum concentration of 13.6 ppb. For adults,the estimated exposure dose does not exceed the RfD, however, the estimated dose for childrendoes exceed the RfD. Exposure to cadmium via ingestion and/or inhalation can cause adverseeffects on the kidneys, skeletal system, and the lungs. However, cadmium volatilization is lowfrom water, therefore exposure from inhalation at this site is expected to be negligible. Littlecadmium is absorbed through the skin, thus dermal exposure is not of great concern.

    The kidney is the most sensitive tissue to long-term cadmium exposure. Kidney damage may becaused by cadmium via oral exposure or inhalation. However, the lowest dose thought toproduce kidney damage (0.01 mg/kg/day) is well above the dose expected to result fromingestion of 13 ppb cadmium (3.89 X 10-4 mg/kg/day).

    It is not known if cadmium exposure causes cancer in humans. There is not any human oranimal evidence demonstrating that oral or dermal exposure to cadmium causes cancer. However, cadmium exposure via inhalation has been linked to cancer. Some epidemiologicalstudies of workers exposed to cadmium suggest a possible connection between cadmiuminhalation and lung and prostate cancer (23). Evidence from animal studies show that chronicinhalation of cadmium chloride produces an increased frequency of lung tumors in animals. Based on animals studies, the EPA has classified cadmium as a probable human carcinogenwhen inhaled. However, inhalation exposure of cadmium at this site is expected to be negligible.

    Several populations may be sensitive to cadmium exposure. Those with dietary deficiencies incalcium and protein, renal disease, and those who smoke are at an increased risk to the adverseeffects of cadmium. Children and fetuses may also be at an increased risk due to a highercadmium absorption rate than adults.


    ATSDR uses health outcome data to help characterize the overall health of a potentially exposedcommunity and to delineate possible relationships between environmental exposures and adversehealth outcomes. Health outcome data include medical records and tests, health studies, cancerincidence and mortality data, and demographic data. Several sources of health outcome datawere available for SMDA. Community specific health data that were evaluated by an ATSDRphysician include one resident's physical examination report, an area "Death Survey" conductedby two area residents, and a consultant's statement regarding the autopsy report of an arearesident. General data on a county, state, and national level that were reviewed include vitalstatistics information, Cancer Incidence and Mortality reports, the Riggins Tape, and 1990Census data.

    A report of one citizen's physical examination was also evaluated by an ATSDR physician. Theinformation provided is limited and does not allow for a full evaluation. In addition, thepatient's age and family medical history is not given. The patient had a minimally elevated lacticdehydrogenase (LDH) level and a persistent rash mainly to his arms, legs, and to other bodyparts. The physical examination report concluded that the patient had hepatitis and possiblychloracne. However, the physical examination report did not mention anything regarding liversize, tenderness, jaundice, or gastrointestinal complaints, which are all associated with hepatitis. Also, there is no mention of the two classic lesions of chloracne, the chloracne cyst and the comedo.

    The "Death Survey" conducted by two area residents was reviewed by an ATSDR physician. Additional information is needed to sufficiently address the issue of whether the deaths are inexcess of expected numbers. The information needed includes lifestyle and risk factors forcardiovascular disease and cancer, the types of cancer, and the geographic boundaries of the survey.

    The autopsy findings of a resident who lived adjacent to the landfill were questioned by arearesidents. The autopsy report stated that the death was caused by alcoholic cirrhosis and massivebilateral pneumonia. Family members claim that the deceased never consumed alcohol and thussought other opinions on the cause of death. The autopsy report and medical records of thedeceased were not available to ATSDR, however, the statements made by a consultant to theconcerned citizens were provided to and reviewed by an ATSDR physician.

    The consultant states that the cirrhosis could not have resulted from alcohol because acutepancreatitis or inflammation of the pancreas was not observed. However, pancreatitis is not acommon occurrence in alcoholic cirrhosis. Thus, pancreatitis is not a prerequisite for thediagnosis of alcoholic cirrhosis. Also, the consultant totally disregards the role of massivebilateral pneumonia in the death of the resident. Pneumonia is a common complication inalcoholics. The consultant also rules out alcohol as the primary cause of death because massivedestruction of the convoluted tubules of the kidney was noted in the autopsy report. He statesthat alcohol is not known to be toxic to the kidney. This is true, however, it certainly does notrule out alcohol as a contributing factor to the death. Moreover, several drugs used to treatpneumonia are toxic to the kidney and could have caused the observed damage.

    The consultant's statement notes that cadmium was found in the deceased's liver in the parts permillion range. The average expected concentrations for cadmium in the liver are 1.0-1.3 ppm. The levels of cadmium found in the deceased are needed to determine if they actually exceed thenormal concentrations. The target organ for cadmium is the kidney and cadmium accumulatesin the liver and lungs as well as the kidney. Smokers are more sensitive to cadmium's effects, sotheir levels are higher than non-smokers in general. The deceased's smoking history is notnoted. Cadmium levels were not mentioned for organs other than the liver.

    All the factors that determined the autopsy results are not possible to discern without the medicalreport. In addition, the evidence provided by the consultant does not accurately dispute any ofthe autopsy findings. There is also not any known plausible evidence of exposure from thelandfill.

    Census data from 1980 and cancer incidence and mortality data for Macomb County wereexamined to try to determine the expected cancer rates for the population of concern. Thecensus data was analyzed to obtain the population estimated for the area of concern. A one mileradius around the site encompasses approximately 20% of Census tract number 2053. Thepopulation was 1,855 for this tract in 1980 while the population was 694,600 for MacombCounty. Since the area of concern is one-fifth of the tract and the cancer data is available onlyon a county level, the cancer information is for a population 1000 fold greater than thepopulation of concern. Therefore, information regarding expected cancer rates in the populationof concern cannot be determined.

    The evaluation of health outcome data by an ATSDR physician did not provide any clearconnections between reported adverse health effects in the local community and possibleexposure to landfill contamination. However, the health outcome data sources available did notprovide enough specific and complete information to adequately assess health outcomes thatmay be related to this site.


    ATSDR staff met with citizens during the August 1990 site visit and the May 1991 EPA publicmeeting and discussed their health concerns. Those concerns are summarized in the"Community Health Concerns" section and are addressed as follows:

    1. Citizens are concerned about cases of apparent increased liver enzyme levels and the healthof area children.

      Several area citizens have had their liver enzymes tested for possible enzyme elevation. The laboratory test results for three children were evaluated by an ATSDR physician. According to the children's test results, the specific enzymes that directly test liver function,Serum Glutamic Oxaloacetic Transaminase (SGOT) and Serum Glutamic PyruvicTransaminase (SGPT), are not elevated above the ranges normally found in children. Thechildren's LDH and alkaline phosphatase levels are in the high normal range. However,measurement of total LDH is not a good indicator of adverse liver effects because it ispresent in all organs and liver disease may not produce a marked increase in LDH levels. Alkaline phosphatase is produced by several tissues, especially bone, intestine, liver, andplacenta. Also, alkaline phosphatase levels are elevated during periods of increased calciumdeposition into the bone such as childhood, adolescence, and advanced pregnancy. Theslightly elevated levels of alkaline phosphatase in the three children are likely due to bone growth.

      The incidence of elevated liver enzymes among the general public is not that uncommondue primarily to a large number of causative agents. The most common causes of elevatedliver enzymes tend to be alcohol, viral hepatitis, and certain therapeutic drugs. Smokingand exposure to solvents may also contribute to elevated liver enzyme levels. As mentionedabove, periods of bone growth can produce elevated levels of some liver enzymes.

    2. Citizens are concerned about cancer deaths in the area.

      Information regarding expected cancer rates in the population of concern cannot bedetermined. Cancer information is discussed in the "Health Outcome Data Evaluation"section.

    3. Residents are concerned about several general health problems.

      Area citizens have documented a variety of health concerns that they believe may be causedby exposure to the landfill. These include persistent colds, skin rashes, headaches, earinfections, and eye irritations. To adequately address these concerns, more complete andspecific information is needed.

      Trichloroethylene, methylene chloride, and arsenic have all been detected at SMDA and allmay cause skin rashes. However, the concentrations of these chemicals associated with skinirritation are higher than those present at SMDA. Methylene chloride, benzene, and toluenehave been known to produce headaches after extended periods of exposure to high orunknown concentrations. However, with the limited information available, ATSDR isunable to relate the health problems experienced by the community to the chemicals present at SMDA.

    4. Area citizens believe that past illnesses and deaths of animals, including fish, living near thesite were caused by exposure to landfill contamination.

      A survey of area veterinarians was conducted in 1987 by the MTSCC to try to determine ifany animal problems could be linked to exposure to the SMDA landfill. Any relationshipof animal illness or death to the landfill could not be established (24). Also, one residenthad the liver and kidney tissues from a dead cow that had grazed near the landfill analyzedfor various heavy metals. The examination of sections of liver and kidney tissue by theKrause Veterinary Clinic revealed no abnormal histopathology (25). With the limitedinformation available, ATSDR is unable to establish any relationship between animal healthproblems and exposure to the SMDA site.

    5. Local farmers are worried about possible contamination of crops grown near the landfill.

      A resident who grew crops adjacent to the landfill had three green tomatoes and four greenpeppers tested for various pesticides and heavy metals in 1982. The analysis detected zincat 2 ppm in both crops and cadmium at 0.03 ppm in the green peppers (26). The normallevels of zinc range from 10-100 ppm in most crops and pastures (27). Typical cadmiumlevels in vegetables and grains range from 0.005 to 0.450 ppm (28). The levels of zinc andcadmium detected are not above normal concentrations and do not appear to be high enoughto be of public health concern.

    6. Several citizens suspect that landfill contamination was responsible for one resident's death.

      This cannot be determined without full evaluation of the medical report. Also, there is notany known plausible evidence of exposure from the landfill. This is discussed in the"Health Outcome Data Evaluation" section. In addition, the contaminant concentrationsdetected are not as high as those associated with death.

    7. One citizen is concerned about the stress of living near the landfill and the constant worryabout clean well water.

      ATSDR cannot evaluate the effects of psychological stress combined with exposure toenvironmental contamination, because little information is available. Municipal water isnow available to those residences affected by the groundwater contamination related to the site.

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