BASELINE RISK ASSESSMENT SUSSEX COUNTY LANDFILL #5 · 2020. 7. 5. · quantitative risk assessment...

BASELINE RISK ASSESSMENT

SUSSEX COUNTY LANDFILL #5

Prepared By US-EPA, Region III

Reginald Harris, Toxicologist

Superfund Technical Support Section

July 30, 1993

BASELINE RISK ASSESSMENT

SUSSEX COUNTY LANDFILL NUMBER 5

INTRODUCTION

The Baseline Risk Assessment for the Sussex County LandfillNumber 5 describes the potential for adverse health effects dueto exposure to contaminated media at the Sussex County LandfillNumber 5 Site. In the risk assessment process, informationregarding the concentrations of constituents of concern and thetoxicological data relating to those constituents are utilized toderive a numerical estimate of the potential health effects dueto exposure to the constituents in question. This assessmentconstitutes an evaluation of the no-action alternative requiredunder section 300.68 (f) (v) of the National Contingency Plan(NCP).

The Baseline Risk Assessment follows EPA guidance for riskassessment in general and for Superfund sites in particular (EPA1989a, 1989b, and 1989c). This document includes thirteenSections (I to XIII) describing the chemical data from the site,the toxicity information and the risk calculations.

SUMMARY OF CONCLUSIONS

For adults, an increased carcinogenic risk of 9.25E-05 wascalculated for the ingestion of groundwater. An increasedcarcinogenic risk of 3.80E-05 was calculated for the inhalationof volatiles during showering and bathing, and a total combinedrisk of 1.30E-04 was calculated for the combination of bothresidential well exposure pathways. The total combined risk forthe use of this groundwater exceeds the Agency's carcinogenicrisk range.

The noncarcinogenic risk calculated for adult and childhoodexposure to contaminants in the residential wells was due to theinhalation of volatile contaminants during showering and bathing.The Hazard Index values calculated were 4.39E+00 and 4.68E+00,respectively for adults and children. These calculationsindicate that adverse health effects may be expected forresidential use of this water. Beryllium, which is naturallyoccurring, does not make any significant contribution to thenoncarcinogenic risk. Benzene is the major contributor to thenoncarcinogenic risk in this situation.

I. SCOPE OF THE RISK ASSESSMENT

The risk assessment is a formal procedure with protocolsestablished by the U.S. Environmental Protection Agency (EPA)(EPA 1989a, 1989b, 1989c). The risk assessment evaluates theconstituents found in the various media at the site anddetermines which are site related contaminants of concern tohuman health. The risk assessment also evaluates the likelihoodof contact with these contaminants by humans. The concentrationsof the constituents at the point of exposure are then used toestimate the potential for adverse effects on human health.

All chemical substances may produce some health effects ifthe concentration is sufficiently high. The amount of thesubstance entering the body (dose) determines the impact of thatconstituent on the receptor. Significantly high doses mayproduce deleterious health effects in the receptor. The riskassessment is designed to estimate if the concentrations of thecontaminants of concern are sufficiently high to cause concernfor human health.

The Baseline Risk Assessment is conducted using generallyconservative assumptions according to general guidelines outlinedby USEPA. The purpose of using conservative assumptions is toexplore the potential for adverse health effects using conditionsthat tend to overestimate risk so that final estimates willaccount for uncertainties and highly sensitive individuals in thepopulation will be protected. This Baseline Risk Assessment isnot intended to be an absolute estimate of risk to humanreceptors, but rather is a conservative analysis intended toindicate the potential for adverse impacts to occur.

This risk assessment evaluates a Reasonable Maximum Exposure(RME) scenario, which is based on the upper 95th percentconfidence interval of the arithmetic mean or the maximumobserved constituent concentration values as applicable.

II. ORGANIZATION OF THE RISK ASSESSMENT

The risk assessment process is composed of four steps:Identification of the Chemicals of Concern, the ExposureAssessment, the Toxicity Assessment, and Risk Characterization.Each step as outlined below corresponds to a specific subsectionof the Baseline Risk Assessment.

Selection Of The Chemicals Of Concern

Chemical selection is based on toxicity, concentration,mobility, persistence, frequency of detection, likelihood ofassociation with activities at the site, laboratorycontamination, and background concentrations.

Exposure Assessment

Potential pathways by which populations may be exposed undercurrent or potential future land use conditions were evaluated.Concentrations of chemicals in environmental media at potentialexposure points are identified. Concentration estimates arederived using available analytical data.

Toxicity Assessment

The methodology used to describe the potential toxicity ofchemicals to humans and the range of toxic effects is presented.Chemical specific health effects criteria to be used in thequantitative risk assessment are identified.

Risk Characterization

Concentrations of site-related contaminants at exposurepoints are compared with Applicable or Relevant and AppropriateRequirements (ARARs). Since ARARs are not available for allcontaminants in all media, quantitative risk estimates are alsodeveloped by assessing the estimated intakes of potentiallyexposed populations according to health effects criteria. Theseestimates are derived using conservative assumptions regardingcontact rate, exposure duration, frequency, and the absorption ofcontaminants. The potential carcinogenic and noncarcinogenichealth effects, and the associated uncertainties related to thisassessment, are also presented.

III. SELECTION OF THE CHEMICALS OF CONCERN

Results of sampling performed during the RI are summarizedin this section to identify contaminants associated with siteoperations, and to determine contaminants to be evaluated in thisrisk assessment. Sampling results are discussed below byenvironmental medium. Data are summarized by presentingfrequencies of detection, arithmetic means, ranges ofconcentrations, and maximum detected values of each chemical ofpotential concern in an individual medium. The followingguidelines are used in evaluating data:

1. Where more than one set of valid RI data for a Iparticular sampling point is available, each set is Iused to calculate the overall mean.

2. The highest value measured was used to representthe maximum concentration.

3. To calculate the mean values for media in which acontaminant was positively detected in one or more

AR30HU9

sample, non-detects were included in the mean by usingone-half of the detection limit.

4. If the contaminant was not positively identified inany sample, the non-detects were assigned a value ofzero.

Preliminary screening procedures to establish the ChemicalData set for the Risk Assessment are as follows. Thecontaminants of potential concern must be:

1. Positively detected in at least one sample in agiven medium.

2. Detected at levels significantly elevated abovethose in associated blanks.

3. Detected at levels significantly above confirmedbackground levels.

4. Detected as a TIC and associated with the site orconfirmed by SAS.

5. Identified as a transformation product of a site-associated contaminant.

The purpose of identifying the chemicals of potentialconcern is to ensure that only those contaminants that areattributable to the site and are likely to contribute to risk arecarried through the assessment. Several criteria were applied tothe constituents measured in each medium on a study area widebasis in order to eliminate those chemicals which may not be ofpotential concern to human health. Chemical constituents wereeliminated from further consideration based on the followingcriteria:

1. The chemical constituent was measured at similarlevels in laboratory blanks.

2. The chemical constituent both has low toxicity andis present at low concentrations.

3. The chemical constituent was detected infrequentlyand at concentrations below risk based levels.

4. The chemical constituent is not related toactivities that occurred at the facility.

5. The chemical constituent is not present at levelssignificantly above background.

AR30H50

IV. CONTAMINANTS OF CONCERN

The contaminants of concern in groundwater at this site wereselected on the basis of Agency criteria cited above and Regionalscreening guidance provided by "Selecting Exposure Routes andContaminants of Concern by Risk-Based Screening" (EPA/903/R-93-001:January 1993).

Using this selection process, the following chemicalconstituents were selected as chemicals of concern at the SussexCounty Landfill Number 5:

Residential Wells

BenzeneVinyl Chloride1,2-Dichloropropane1,4-Dichlorobenzene

Table 1 presents the screening criteria used for the selection ofthe Contaminants of Concern in the Residential Wells.

Monitoring Wells

BenzeneVinyl Chloride1,2-Dichloropropane1,4-DichlorobenzeneTrichloroethylene

Table 2 presents the screening criteria used for the selection ofthe Contaminants of Concern in the Monitoring Wells.

V. FATE AND TRANSPORT

Consideration must be given to the fate and transportmechanisms of site-related chemicals. Upon release into theenvironment chemicals may be acted upon by any number ofprocesses that may lead to their transport to other locations ormedia, or that may lead to changes in physical or chemical state.Listed below are a number of the fate and transport mechanismsthat may effect site-related chemicals.

1. Contaminants may be transported downstream in wateror on suspended sediments, or through the atmosphere.

2. The constituents may be physically transformedthrough volatilization, precipitation, or other similarprocesses.

3. The chemical substances under evaluation may bechemically transformed through photolysis, hydrolysis,oxidation, reduction, etc..

4. Substances of concern may be biologicallytransformed through biodegradation.

5. Site-related contaminants may be accumulated in oneor more media.

VI. FATE AND TRANSPORT OF CONTAMINANTS OF CONCERN

BENZENE - Volatilization is the major transport process forbenzene from surface waters to ambient air, and atmospherictransport of benzene occurs readily. With volatilization beingthe main transport process accounting for the removal of benzenefrom water, the atmospheric destruction of benzene is probablythe most likely fate process. Adsorption onto organic materialmay be significant under conditions of constant exposure.Sorption processes are likely removal mechanisms in both surfacewater and groundwater. The presence of other hydrocarbons mayenhance the rate of biodegradation of benzene.

1,4-DICHLOROBENZENE - Dichlorobenzenes are expected to volatilizeat a relatively rapid rate, and atmospheric transport can occur.Dichlorobenzenes are reported to be reactive with hydroxylradicals in air with a half-life of about 3 days, but indirectevidence indicates that they do not hydrolyze at a significantrate under normal environmental conditions. Their high logoctanol/water partition coefficients indicate that adsorption toorganic matter in aquatic systems and soils is probably animportant environmental fate process. Bioaccumulation is thoughtto be a significant fate process, and they appear to be resistantto biodegradation. Sorption, bioaccumulation, and volatilizationwith subsequent atmospheric oxidation are likely to be competingprocesses, with the dominant fate being determined byenvironmental conditions.

1,2-DICHLOROPROPANE - Volatilization and subsequentphotooxidation are probably important environmental fateprocesses for 1,2-dichloropropane. In surface water and soils,hydrolysis may also be a significant fate process, especially incases where clays are present. Soil microbes can biodegrade 1,2-dichloropropane, but this generally occurs more slowly thanvolatilization. This compound is considered to be moderatelypersistent in the environment.

TRICHLOROETHYLENE - Trichloroethylene rapidly volatilizes intothe atmosphere where it reacts with hydroxyl radicals to producehydrochloric acid, carbon monoxide, carbon dioxide, andcarboxylic acid. This is the most important fate and transport

AR30H52

process for trichloroethylene in surface water and in the upperlayer of soil. It adsorbs to organic matter and can bebioaccumulated to some degree. There is some evidence that itmay be metabolized by some higher organisms. Trichloroethyleneleaches to groundwater fairly readily.

VINYL CHLORIDE - Volatilization from aquatic systems is the mostimportant transport process for distribution of vinyl chloride inthe environment. Photooxidation in the atmosphere is thedominant environmental fate of vinyl chloride. It reacts rapidlywith hydroxyl radicals, forming hydrogen chloride or formylchloride. Formyl chloride, if formed, decomposes rapidly toyield carbon monoxide and hydrogen chloride. In the atmosphere,vinyl chloride will be destroyed within one or two days of itsrelease. The hydrogen chloride formed is removed from thetroposphere during precipitation. Hydrolysis, sorption,bioaccumulation, and biodegradation do not appear to be importantfate and transport processes.

Beryllium is not a Contaminant of Concern at the SussexCounty Landfill Number 5 because it does not appear to be siterelated. However, it is a source of risk for site residents.Therefore fate and transport information for beryllium isincluded in this document.

BERYLLIUM - Most common beryllium compounds are soluble inwater. However, in water, soluble beryllium salts are hydrolyzedto form beryllium hydroxide. Beryllium hydroxide is not verysoluble within the pH range of most natural waters. It istherefore likely that most beryllium is present in particulaterather than in the dissolved form in most natural aquaticenvironments. • Beryllium is expected to adsorb onto clay mineralsurfaces at low pH and to complex into insoluble compounds athigh pH. It may be accumulated to a slight extent by aquaticorganisms, but there is no evidence that it biomagnifies.Airborne transport of particulates may occur.

VII. EXPOSURE POINT CONCENTRATIONS

Exposure point concentrations are evaluated as theReasonable Maximum Exposure (RME), as indicated by Agencyguidance. The 95th percent upper confidence limit value of thearithmetic mean is used as the exposure point concentration valuefor all appropriate risk calculations. In cases where the RMEvalue exceeds the maximum reported concentration for a givencontaminant, or in cases where the data set is not sufficient forthe calculation of an RME value, the maximum reported value isused for exposure point calculations. If a contaminant has beendetermined to be present in samples for a given medium, but isreported as a non-detect for a given sample, one half of thedetection limit is used in RME calculations for that contaminant.

AR3GH53

Tables presenting the 95th percent upper confidence limit values,and maximum detected contaminant values are presented in theAppendix.

Residential Wells

Two rounds of groundwater samples were collected from 13residential wells during the investigation. Significant levelsof contaminants were detected in one residential well, GW-2.Contaminants identified in this residential well include benzene,1,4-dichlorobenzene, 1,2-dichloropropane, and vinyl chloride (acomplete listing of the contaminants detected in this well isfound in the Exposure Characterization). Those residential wellresults were then used for risk assessment purposes. The maximumconcentrations of the selected contaminants of concern were usedas exposure point concentrations since only two rounds ofsampling data were available for the well, and all 95th percentupper confidence limit values exceeded the maximum contaminantconcentrations. Non-detects were represented as being one halfthe detection limits in all RME calculations. (See Appendix)

Residential well GW-33 was selected as being representativeof the beryllium contamination present in the residential wellsat the site. It should be noted that beryllium was detected inboth upgradient and downgradient wells and appears to benaturally occurring. Residential well GW-33 represented themaximum beryllium concentration seen in a residential well and istherefore being used to represent the risk to residents due tothis contaminant. Due to the limited data available the maximumconcentration of beryllium reported for this well will be usedfor risk assessment purposes. (From RI Data)

Other than beryllium, inorganic contaminants were notregarded as being of toxicological significance at this site.

Monitoring Wells

One round of groundwater samples was collected for the RIfrom the monitoring wells. Monitoring wells LD-1, LS-7R, and LS-16 are felt to be representative of the center of the on-siteorganic contaminant plume and lie outside of the landfillboundary, thus they were selected for risk assessment purposes.Contaminants identified in these monitoring wells includebenzene, 1,4-dichlorobenzene, 1,2-dichloropropane, TCE, and vinylchloride (a complete listing of the contaminants detected isfound in the Exposure Characterization). The concentrations ofeach of the selected contaminants of concern were used forcalculation of the 95th percent upper confidence limit values forthe monitoring well grouping. The 95th percent upper confidencelimit values computed for each of the contaminants exceeded themaximum contaminant concentration, therefore the maximumcontaminant values were used as exposure point concentrations for

8

each of the contaminants of concern. The exposure pointconcentrations were used for RME calculation and arerepresentative of the exposure of receptors, if the monitoringwells were to be used for drinking purposes.

In cases where the non-detect values for selectedcontaminants identified in Monitoring Well LD-1 were the maximumcontaminant concentrations detected for contaminants found in theLD-1, LS7R, LS-16 monitoring well cluster, one-half of those non-detect values were determined to be the maximum contaminantconcentration value to be used for risk assessment purposes.This determination was made only in instances where thecontaminant was positively detected in either monitoring well LS-7R or LS-16, was positively detected in residential well GW-2,and the detection limit for monitoring well LD-1 exceeded thedetected value for the contaminant in either of the other twomonitoring wells. The detection limits for monitoring well LD-1are considerably higher than those of the other two monitoringwells being evaluated in the cluster (more than an order ofmagnitude in some cases). If the contaminants are detected inother monitoring wells in the cluster at levels much lower thanthe detection limits reported for monitoring well LD-1, and theyare positively identified in the residential well directlydowngradient, then these contaminants are considered to bepresent in monitoring well LD-1. The contaminants are not beingdetected due to the elevated detection limits of Monitoring WellLD-1. All risk assessment calculations will use one-half thedetection limit value as the maximum detected values for thecontaminants in monitoring well LD-1 that meet the criteriaoutlined above. (See Appendix)

Inorganic contaminants were not seen as being oftoxicological significance for the monitoring wells. However, aspreviously mentioned, beryllium was present at significant levelsin groundwater samples around the site. This naturally occurringconstituent was evaluated to determine the potential risk it maypose to site residents. Monitoring Well LS-09 which showed thehighest concentration of beryllium in any of the filteredmonitoring well samples was used as an exposure point.

Site Conceptual Model

Exposure to contaminants at the Sussex County LandfillNumber 5 may potentially occur through several pathways withinthe selected route of exposure. Preliminary screening andevaluation of the site media data indicated that the only routeof exposure of toxicological significance at the Sussex CountyLandfill Number 5 Superfund Site is the groundwater route.

Contaminants from the landfill are thought to have migratedto groundwater. The residents are then exposed to thecontaminated groundwater through the consumption of drinking

water and household use of the contaminated groundwater forshowering, bathing, and numerous other household activities.These means of exposure are expected to occur in both current andfuture use scenarios.

VIII. EXPOSURE ASSESSMENT

A. Groundwater

The Agency's default exposure parameters are being used forthe exposure assessment.

1. Residential Wells

Adult receptors may contact groundwater through theingestion of contaminated water, and the inhalation of volatilecompounds during showering and bathing. While adults may alsocome into dermal contact with these contaminants during showeringand bathing, screening indicates that the risk associated throughthis pathway is insignificant for adults. Children may come intocontact with the groundwater through the ingestion ofcontaminated groundwater, the inhalation of volatile compoundsduring showering and bathing, and due to dermal contact with thecontaminants during bathing. These exposures are determined tobe applicable to both current and future use scenarios for theresidents7 use of groundwater from residential wells. Theseexposure scenarios assume that the condition of the sitegroundwater and of all other exposure related conditions willremain as they are now in the future. The exposure pointconcentrations computed for exposure to groundwater from theappropriate residential well will be used to characterize currentuse by off-site residents, and will be used for future useevaluation at that same locality since this represents the actualexposure of a receptor. All calculations assume that noremediation will occur at this site.

Residential well GW-2 is being used as the point ofresidential exposure since it represents the center of theresidential well contaminant plume. Through screening it wasnoted that the maximum risk to residential receptors at this timeis occurring at this location.

Organic contaminants identified at residential well GW-2 towhich receptors are exposed include benzene, tert-butylbenzene,chlorobenzene, DOT, 1,2-dichlorobenzene, 1,4-dichlorobenzene,dichlorodifluoromethane, 1,-dichloroethane, cis-1,2-dichloroethene, trans-l,2-dichloroethene, 1,2-dichloropropane,ethylbenzene, isopropylbenzene, 4-isopropyltoluene, naphthalene,N-propylbenzene, tetrachloroethylene, toluene, trichloroethylene,1,2,4-trimethylbenzene, 1,3,5-trimethylbenzene, vinyl chloride,and total xylenes.

10

AR3Ql*t*56

Through risk-based screening it was determined that benzene,1,4-dichlorobenzene, 1,2-dichloropropane, and vinyl chloriderepresent contaminants that were present at concentrations thatexceed risk based levels of concern, and therefore are to beconsidered contaminants of concern.

Benzene and vinyl chloride were each detected in ResidentialWell GW-2 at 4 ppb in both rounds of groundwater sampling. 1,2-Dichloropropane was detected at 1 and 2 ppb respectively in thetwo rounds of residential well sampling. 1,4-Dichlorobenzene wasdetected at 1 ppb in both rounds of residential well sampling.The 95th percent upper confidence limit values were calculatedfor each chemical using the concentrations reported above. Inall four cases the 95th percent upper confidence limits valueswere either equal to or greater than the maximum contaminantconcentrations, therefore the maximum contaminant values wereused as the exposure point concentrations in the risk assessment.The exposure point concentrations for the organic contaminants

identified in Residential Well GW-2 are 4 ppb for benzene, 4 ppbfor vinyl chloride, 2 ppb for 1,2-dichloropropane, and 1 ppb for1,4-dichlorobenzene. (See Appendix)

Beryllium was reported at risk-based concentrations ofconcern, but was not considered to be a site related contaminant.Risk due to beryllium will be assessed since it does contribute

to the total risks of receptors at the site. Other inorganicconstituents were not determined to be of toxicologicalsignificance, and were therefore not determined to becontaminants of concern.

Beryllium was detected in a number of upgradient anddowngradient residential wells at the site. It appears that thiscontaminant is naturally occurring or at least is not thought tobe site related. It should be noted that receptors are not ableto distinguish contamination that is site related from that whichis not, so according to Agency guidance, the exposure ofreceptors to this contaminant will be assessed.

The highest concentration of beryllium reported in aresidential well at the site was 2.9 ppb, reported at ResidentialWell GW-33. This concentration of beryllium will be used torepresent the risk posed by beryllium to site residents.

2. Monitoring Wells

Monitoring well exposure point concentrations are being usedto assess the exposure of on-site receptors to groundwater in acurrent use scenario, and in a future use scenario for off-sitereceptors. It is assumed that the contaminants may migrate tovarious areas on and off-site where they may impact thereceptors. Site residents may come into contact with thecontaminants in groundwater through any number of groundwater use

11

activities. In order to be most protective of human health, theconcentrations of groundwater contaminants represented by thecentral portion of the organic contaminant plume will be used toassess exposure and risk due to the contamination detected in themonitoring wells. At the present time the organic contaminantplume for the monitoring wells may be used to represent theexposure of on-site residents, if the monitoring wells were to beused for residential use. It should be noted that presently,this water is not used by residents. The concentrations reportedfor the monitoring wells will also be used to represent theexposure of off-site residents in a future use scenario due toplume migration.

Adult receptors may come into contact with thesecontaminants through ingestion of contaminated groundwater andthrough inhalation of and dermal contact with volatile organicconstituents of contaminated groundwater during showering andbathing. Only ingestion and inhalation will be assessed foradults, since dermal contact during showering and bathing appearsto be of no major significance after screening. Children maycome into contact with these contaminants through ingestion ofcontaminated groundwater, the inhalation of volatile organicconstituents of contaminated groundwater during showering andbathing, and through dermal contact with constituents duringbathing. Conservative assumptions are made that assume that theconcentrations of these contaminants in the central portion ofthe plume will remain at their present levels for both thecurrent and future use scenarios.

Monitoring wells LD-1, LS-7R, and LS-16 represent the centerof the organic contaminant plume that is considered to be thesource of exposure to receptors if the monitoring wells were tobe used for residential purposes, or if this plume were tomigrate to some other location over the course of time that maypotentially expose receptors to the concentrations of thecontaminants represented by the exposure point concentration.The contaminants identified in this monitoring well cluster arebenzene, chlorobenzene, chloroethane, ODD, DDE, 1,4-dichlorobenzene, dichlorodifluoromethane, 1,1-dichloroethane,cis-l,2-dichloroethene, 1,2-dichloropropane, diethylphthalate,2,4-dimethylphenol, endrin, endrin aldehyde, endosulfan II,ethylbenzene, isopropylbenzene, 4-isopropyltoluene, 2-methylnaphthalene, N-propylbenzene, tetrachloroethylene, toluene,trichloroethylene, 1,2,4-trimethylbenzene, 1,3,5-trimethylbenzene, vinyl chloride, and total xylenes.

Benzene, 1,4-dichlorobenzene, 1,2-dichloropropane,trichloroethylene, and vinyl chloride have been identified as thecontaminants providing the most significant exposure to receptorsif the groundwater from Monitoring Wells LD-1, LS-7R, and LS-16were to be used by human receptors.

12

AR30«*l*58

Benzene was reported at concentrations of 3, 3, and 9 ppb inthe monitoring wells LS-7R, LS-16, and LD-1 respectively. The95th percent upper confidence limit value calculated for thisdata set exceeded the maximum benzene concentration of 9 ppb,therefore 9 ppb was used at the exposure point concentration forbenzene.

1,2-Dichloropropane was detected at 0.5 ppb in LS-7R and at0.7 ppb in LS-16. This contaminant was reported as a non-detectin Monitoring Well LD-1. Since 1,2-dichloropropane was detectedin both monitoring wells LS-7R and LS-16, was detected at 2 ppbin Residential Well GW-2 which is downgradient from LD-1, thedetection limits for LD-1 are higher than for the othermonitoring wells, and the non-detect value for 1,2-dichloropropane in LD-1 exceeds the detected values in both LS-7Rand LS-16; it was determined that this contaminant is present inMonitoring Well LD-1. One-half the detection limit for 1,2-dichloropropane at Monitoring Well LD-1 (1 ppb) will therefore beused as the concentration of that contaminant at that particularsample location. The 95th percent upper confidence limit valuefor 1,2-dichloropropane exceeds the maximum contaminantconcentration of 1 ppb, therefore the maximum value will be usedas the exposure point concentration for 1,2-dichloropropane.

1,4-Dichlorobenzene was reported at 0.4 ppb in LS-7R, at 0.8ppb in LS-16, and at 4 ppb in LD-1. The 95th percent upperconfidence limit value calculated for 1,4-dichlorobenzeneexceeded the maximum reported concentration, therefore themaximum concentration was used as the exposure pointconcentration.

Trichloroethylene was reported at 1 ppb in LS-7R and at 0.5ppb in LS-16. This contaminant was reported as a non-detect inLD-1 at 4 ppb. TCE was detected in monitoring wells LS-7R andLS-16, was detected at 1 ppb in Residential Well GW-2 which isdowngradient from LD-1, the detection limits for LD-1 are higherthan for the other monitoring wells, and the non-detect value forTCE in LD-1 exceeds its detected values in both LS-7R and LS-16;therefore TCE is considered to be present in Monitoring Well LD-1. One-half the detection limit for TCE at Monitoring Well LD-1(2 ppb) will therefore be used as the concentration of TCE atthat sample location. The 95th percent upper confidence limitvalue for TCE exceeds the maximum contaminant concentration of 2ppb, therefore the maximum value will be used as the exposurepoint concentration.

Vinyl chloride was reported in Monitoring Well LS-7R at 0.6ppb. It was not detected in Monitoring Well LS-16 or LD-l. Thedetection limits for wells LD-1 and LS-16 were 4 and 0.3 ppbrespectively. Since vinyl chloride was detected in LS-7R, wasdetected at 4 ppb in Residential Well GW-2 which is downgradientfrom LD-l, the detection limits for LD-1 are higher than for the

13

other two monitoring wells, and the detection limit for vinylchloride at LD-1 (4 ppb) is higher than the detected value at LS-7R; vinyl chloride is considered to be present in Monitoring WellLD-1. one-half the detection limit for vinyl chloride in LD-1(2 ppb) will therefore be used as the concentration of vinylchloride at that sample location. Since the 95th percent upperconfidence limit value for the vinyl chloride data set exceedsthe maximum value of 2 ppb, the maximum value will be used as theexposure point concentration for vinyl chloride.

(See Appendix and Table 2 concerning Monitoring Well data)

Inorganic constituents were not identified as contaminantsof concern in the monitoring wells. Beryllium was identified innumerous monitoring well samples. As previously indicated,beryllium is not considered to be site related, but may be asource of exposure for receptors at the site. The highestreported detection of beryllium in a dissolved monitoring wellsample was 5.8 ppb at Monitoring Well LS-09. This value will beused as an exposure point concentration for beryllium for themonitoring wells. It should be noted that this value is flagged"L", meaning that the reported value is biased low, making theactual value probably higher.

B. Soils

It has been determined through preliminary screening thatsoils would not be a significant contributor to site risk. Theexposure of receptors to on-site soils is limited due to thevegetation cover of the landfill, limited site access due tofencing and farms located on either side of the landfill thatdiscourage trespassing across their property to the landfill, andthe prohibition on building on the landfill in the future. Onthis basis it was determined that soils did not represent aviable pathway for evaluation at the site.

C. Surface Water

For the purposes of Human Health Risk Assessment the wateron the landfill is not surface water in the true sense of theword. It appears to be small areas of ponded rain water thatevaporates or drains into the surface after a short time period.Therefore, surface water was not considered to be an appropriatepathway for evaluation.

D. Sediments

Sediments are not thought to be of toxicologicalsignificance at the site.

14

IX. EXPOSURE ASSUMPTIONS USED IN RISK CHARACTERIZATION

A. Residential Exposure: Ingestion of Chemicals in Drinking Water

Equation: Intake (mg/kg-day) = CW x IR x EF x EDBW x AT

CW - Chemical Concentration in Water (mg/liter)

IR = Ingestion Rate (liters/day)

EF = Exposure Frequency (days/year)

ED = Exposure Duration (years)

BW - Body Weight (kg)

AT = Averaging Time (period over which exposure is averaged-days)

Variable Values

CW = Site specific measured or modelled value

IR =• 2 liters per day (90th percentile; EPA 1989d)

EF = 350 days per year

ED — 30 years lifetime residence6 years (child)

BW - 70 kg (Adult)15 kg (children)

AT = (ED x 365 days/year for noncarcinogens)(70 years x 365 days/year for carcinogens)

15

AR301U6I

B. Residential Exposure: Inhalation of Airborne (Vapor Phase)Chemicals

Equation: Intake (mg/kg-day) = CA x IR x ET x EF x EDBW x AT

CA = Contaminant Concentration in air (mg/m3)

IR = Inhalation rate (m3/hr)

ET = Exposure Time (Hours/Day)


BW = Body Weight (kg)

AT = Averaging Time (period of exposure - days)

Variable Values:

IR = 30 m3/day (adults)20 m3/day (child)

ET = 20 minutes

ED = 30 years lifetime (adult)6 years Children


BW = 70 kg (adult)15 kg (child)

AT = (ED x 365 days/year)(70 years x 365 days/year for carcinogens)

Foster and Chrostowski Model used for Inhalation During Showeringand Bathing.

16

AR30H62

C. Residential Exposure: Dermal Contact With Chemicals WhileShowering or Bathing

Equation:Absorbed Dose (mg/kg-day) = CW x SA x PC x ET x EF x ED x CF

BW x AT

CW = Chemical Concentration in Water (mg/liter)

SA = Skin Surface Area Available for Contact (cm2)

PC = Chemical-specific Dermal Permeability Constant (cm/hr)

ET - Exposure Time (hours/day)

EF = Exposure Frequency (days/year)


CF = Volumetric Conversion Factor for Water (1 liter/1000cm3)

BW = Body weight (kg)

AT = Averaging Time (period over which exposure is averaged-days)

Variable values:

SA = 10470 cm2 Child

PC = 8.00E-04

ET = 20 minutes


ED = 6 years (child)

BW - 15 Kg (Child)

AT - (ED x 365 days/year for noncarcinogens)(70 years x 365 days/year for carcinogens)

Complete sets of all data for each assessment is included inAppendix A. Each set of data includes the name of eachcontaminant, toxicity values, the RME concentration used forassessment, the calculated doses for adults and children, and thecomputed Hazard Index or carcinogenic risk.

17

AR3QH63

, X. TOXICITY ASSESSMENT:-HEALTH EFFECTS AND TOXICITYOF CONTAMINANTS OF CONCERN

A. Benzene

Benzene is an important solvent and chemical intermediatemade from coal and oil. It is used to make other chemicalsincluding some types of plastics, detergents, and pesticides. Itis also an important component of gasoline.

Qualitative Description of Health Effects

Benzene is rapidly absorbed by the lungs. Nomiyama et al.(1974a,b) observed exposure of men and women to benzene at 52 to64 ppm for four hours. Lung absorption was measured at 47% withno sexual specificity. The rate of absorption was the greatestduring the first five minutes and reached a constant levelbetween 15 minutes (Srobova et al., 1950) and three hours(Nomiyama et al. 1974a, b) of continuous exposure. Althoughdefinitive data are not available for humans, oral absorption inexperimental animals has been demonstrated to be between 90%(Park and Williams, 1953) and 97% (Sabourin et al., 1987).Dermal'absorption of benzene is approximately 0.2% (Franz, 1984).

Benzene preferentially distributes to organs with high lipidcontent including fatty tissue, bone marrow, and the brain, alsoto well perfused organs including the liver and kidneys.

The rate of exposure does not appear to have a substantialeffect on the metabolism of benzene. Benz'ene is metabolizedthrough the cytochrome P-450 mixed-function oxidase system.These enzymes are ubiquitous, but the hepatic cytochrome P-450system has been more closely studied in benzene metabolism thanhave the cytochrome P-450 systems from other organs (Klaassen CDand Amdur MO et al., 1986). Metabolites of benzene includephenol, catechol, hydroquinone, and 1,2,4-trihydroxy benzene.Several pathways are probably responsible for thebiotransformation of benzene.

Acute exposure to high concentrations of benzene hasresulted in death as a result of central nervous systemdepression or fatal cardiac arrhythmias. Chronic exposure to lowlevels of benzene, as seen in the work place, result inhematopoietic toxicity. Toxic effects associated with benzeneexposure include pancytopenia, aplastic anemia, and leukemia(Snyder and Kocsis 1975). Data suggests that toxic effects ofchronic benzene exposure are a function of the metabolites ofbenzene (Henderson, et al., 1989).

Benzene is classified by the EPA in Group A - human

18

carcinogen. This classification is based on severalepidemiological studies which demonstrate an increased incidenceof non-lymphocytic leukemia from occupation exposure. In onestudy, Turkish workers employed in the shoe industry had anincidence of 13/100,000 leukemias or pre-leukemias after anaverage employment length of 9.7 years (Aksoy et al., 1974),greater than twice the incidence of the general population. Thepeak exposure was reported to be 210-650 ppm.

Benzene also alters both cellular and humoral immunology(ATSDR, 1991h). There is no evidence that benzene is teratogenicbut it may impair fertility in females (ATSDR, 199Ih). Sisterchromitid exchanges occur in tissue cultures exposed to benzenein the presence of microsomal enzymes (cytochrome P-450 mixedoxidase function system), necessary for benzenebiotransformation.

Quantitative Description of Health Effects

A study by Ren.sky et al. (1981) that was updated in 1987examined the standard mortality ratio (SMR) from leukemia ofworkers exposed to benzene for at least 24 years. The generalpopulation SMR was 560. For workers with more than five yearsexposure, the SMR was 2100. Exposure ranged from 10 to 100 ppm 8hour TWA. In the update, the SMR was calculated to be 109 atcumulative benzene exposure under 50 ppm years and increased to6637 at 400 ppm years or more.

Ott et al.. (1978) observed three deaths among 594 workersfollowed for 23 years. Exposures ranged from less than 2 ppm togreater than 25 ppm 8 hour TWA. The increase was notstatistically significant.

The EPA has derived an oral and inhalation slope factorbased on pooled data from the Rinsky et al. (1981; 1987) and Ottet al. (1978) studies. The results were adjusted for the resultsof a study by Wong et al. (1973) who reported on the mortalityrate of chemical workers during the years 1946-75. Confidence inthis risk estimate is high. The pooled cohorts were large andwere followed for an adequate period of time. Effects of benzeneexposure were dose-related.

No oral RfD for benzene has been developed. The riskassessment for chronic inhalation exposure is under review by anEPA work group.

19

SUMMARY OF BENZENE CRITERIA

EPA Carcinogenic ClassificationMaximum Contaminant Level (MCL)

Maximum Contaminant Level Goal(MCLG)Inhalation RfD

Oral SF

Inhalation SF

Group A5 Mg/L

0 M9/L

5.71E-05mg/kg/day2.9E-02(mg/kg-day) "1(2.91E-02)mg/kg/day"1

SOURCE

EPA,1992a

EPA,1992a

EPA,1992a

RBCT, 1993 *

EPA, 1992a

IRIS

EPA Drinking Water Health Advisories (HA)Lifetime HA

Longer-term HAChildAdult

Shorter-term HATen-day HA (Child)One-day HA (Child)

NotAvailable

NotAvailableNotAvailable

0.2 mg/L0.2 mg/L

EPA, 1991b

EPA, 1991bEPA, 1991b

DWSHA, 5/93DWSHA, 5/93

* Risk Based Concentration Table, First Quarter 1993.

20

AR30H66

B. 1.4-Dichlorobenzene

Chemical waste dump leachates and direct manufacturing effluentsare reported to be the major source of pollution of thechlorobenzenes (including the dichlorobenzenes) to Lake Ontario.The major source of 1,4-dichlorobenzene emission to the atmosphere isvolatilization from use in toilet bowl deodorants, garbage deodorantsand moth flakes. (HSDB, 1/20/93)


Occupational exposure to 1,4-dichlorobenzene by inhalation anddermal routes probably occurs during its manufacture and its uses asa space deodorant, moth control agent and chemical intermediate.General population exposure may occur through oral consumption ofcontaminated drinking water and food (particularly fish), especiallyin areas near effluent discharges for example, certain areas in LakeOntario and the Great Lakes. General population exposure may alsooccur through inhalation of contaminated ambient air since 1,4-dichlorobenzene has wide spread monitoring detection in may areas ofthe USA. Inhalation exposure will occur in the near vicinity oftoilet bowl and garbage deodorants and moth flakes containing 1,4-dichlorobenzene. (HSDB, 2/11/93)

The dichlorobenzenes may be absorbed through the lung,gastrointestinal tract, and intact skin. Relatively low watersolubility and high lipid solubility favor their penetration of mostmembranes by diffusion, including pulmonary and GI epithelia, thebrain, hepatic parenchyma, renal tubules, and the placenta. (HSDB,2/11/93)

Solid particles, vapor, or fumes of 1,4-dichlorobenzene are verypainful to the eyes and nose. Vapor is painful to most people inconcentration between 50 and 80 ppm and the discomfort becomes quitesevere at 160 ppm. Vapors may cause irritation to skin, throat, andeyes. Prolonged exposure to high concentrations may cause weakness,dizziness, loss of weight, liver injury may develop. In addition,exposure to 1,4-dichlorobenzene may cause headache, swelling aroundthe eyes, and a runny nose. (HSDB, 2/11/93)

Solid 1,4-dichlorobenzene has very little effect on the skin.It does produce a burning sensation when held in close contact forexcessive periods of time. (HSDB, 2/11/93)

Ingestion of 1,4-dichlorobenzene can cause burning pain instomach, nausea, vomiting, and diarrhea. Hemoglobin may change tomethemoglobin with resulting dusty color of skin, and the liver andkidney may be damaged. (HSDB, 2/11/93)


No quantitative information was available in IRIS or HSDB.

21

AR30M67

SUMMARY OP 1,4-DICHLOROBENZENE CRITERIA

EPA Carcinogenic ClassificationOral Slope Factor

Inhalation Unit RiskOral RfDInhalation RfDMaximum Contaminant Level (MCL)

Maximum Contaminant Level Goal(MCLG)

Group c2.4E-02(mg/kg/day)"1

No Data0.1 mg/kg/day2.3E-01(mg/kg/d)

0.075 (mg/L)

0.075 (mg/L)

SOURCE

HEAST

HEAST

IRIS 2/8/93

DWSHA

HEAST

EPA 5/93

EPA 5/93

EPA Drinking Water Health Advisories (HA)Lifetime HALonger-term HA

AdultChild

Shorter-term HAOne-day HATen day HA

0.075 (mg/L)

40 (mg/L)10 (mg/L)

10 (mg/L)10 (mg/L)

EPA 5/93

EPA 5/93EPA 5/93

EPA 5/93EPA 5/93

* Risk Based Concentration Table, First Quarter 1993

22

AR30H68

C. 1,2-Dichloropropane

1,2-Dichloropropane may be released into the atmosphere orwastewater during its production 6r from its former use as a soilfumigant for nematodes. It is used as: a chemical intermediate inthe production of carbon tetrachloride and perchloroethylene; a leadscavenger for antiknock fluids; a solvent; an ion exchange in resinmanufacture; a paper coating; a scouring, spotting, and metaldegreasing agent; and an insecticide for stored grain. It may alsobe present in municipal landfill leachates (HSDB, 1993).


Human exposure is primarily due to inhalation, although it canalso occur through ingestion, eye, and skin contact. The generalpublic is exposed to 1,2-dichloropropane from ambient air viainhalation and from contaminated drinking water. Workers may beexposed via inhalation and dermally during its application as a soilfumigant and by being near fields within several days aftertreatment. Occupational exposure will also occur via inhalation anddermally during its production and use (HSDB, 1993).

Symptoms of 1,2-dichloropropane poisoning include headache,vertigo, lacrimation, and irritation of the mucous membrane.Changes in the blood are similar to those of marked anemia. 1,2-dichloropropane may cause dermatitis by defatting of the skin. Moresevere irritation may occur if it is confined against the skin byclothing. Undiluted, it is moderately irritating to the eyes, butdoes not cause permanent injury (HSDB, 1993).

Intoxication by 1,2-dichloropropane, either by ingestion orinhalation, can cause acute renal and hepatic injury, hemolyticanemia, and disseminated intravascular coagulation (HSDB, 1993).Pharmacokinetic studies indicate that dichloropropane is rapidlyabsorbed, metabolized and excreted after oral gavage or inhalationexposure (IRIS, 1993).


A 13-week inhalation toxicity study with rats identified anLOAEL of 69.3 mg/cu m. An NOAEL was not identified (IRIS, 1993).

23

AR30l*l*69

SUMMARY OF 1,2-DICHLOROPROPANE CRITERIA

EPA Carcinogenic Classification

Oral Slope Factor

Inhalation Unit Risk

Oral RfD

Inhalation RFD

Maximum Contaminant LevelMaximum Contaminant Level Goal

Group B2

6.8E-02(mg/kg/day) "1No Data

No Data

1.14E-03mg/kg/day0.005 (mg/L)

Zero

SOURCE

HEAST

HEAST

IRIS2/5/93

IRIS2/5/93

IRIS,1993*

EPA 5/93

EPA 5/93

EPA Drinking Water Health Advisories (HA)Lifetime HA

Long-term HAAdultChild

Short-term HAOne-day HATen day HA

No Data

No DataNo Data

No Data0.09 (mg/L)

EPA 5/93

EPA 5/93EPA 5/93

EPA 5/93EPA 5/93


24

D. Trichloroethene

Trichloroethene (TCE) is a manmade chlorinated hydrocarbon thatis an excellent degreaser for fabricated metal parts. It is alsoused as a degreaser in the textile industry and as a chemicalintermediate in the production of polyvinyl chloride and otherpolychlorinated compounds.


Absorption after inhalation and oral exposure to TCE is rapidand thought to be complete. Studies of dermal absorption of TCE inhumans and animals have been complicated by the use of neat TCEwhich, as a potential degreaser, disrupts the stratum corneum therebyenhancing its own uptake. During normal industrial use, uptake ofTCE through the skin appears slow (ATSDR 1992a).

Tissue distribution of TCE suggests that TCE is preferentiallydeposited in fat tissues although at least at low concentrations, theparent compound is metabolized first pass through the liver.Metabolism of TCE is thought to occur through the cytochrome P450system. At least in experimental animals, 25% of total metabolism isextra hepatic. The lung, which is high in cytochrome P450 accountsfor much of the extra hepatic metabolism (ATSDR 1992a).

Following inhalation exposure, some of the parent compound TCEis exhaled unmetabolised and a minor amount of trichloroethanol isexhaled. Metabolites of TCE are primarily eliminated in the urine.The primary metabolites are trichloroethanol, trichloroethanolglucuronide and trichloro acetic acid (ATSDR 1992a).

Several deaths have been reported from breathing highconcentrations of TCE fumes. Concentration of the TCE could not beestablished for these reports. A few of these deaths were cause bycardiac arrhythmias. The LC50 for mice and rats have been reportedat 8,450 ppm and 12,500 ppm respectively. Cardiac arrhythmias havenot been reproduced in animals but TCE does increase cardiacsensitization to epinephrine in both dogs and rabbits (ATSDR 1992a).

In humans, the primary effects of acute and chronic exposure arecentral nervous system disturbances. Acute exposure to highconcentrations of TCE has been reported to produce dizziness,headache, nausea, confusion, numbness, and blurred vision (EPA 1985).Subjects exposed to 27, 81, and 201 ppm TCE in air for four hoursexhibited drowsiness at 27 ppm, headaches at 81 ppm, and developeddizziness and anorexia at 201 ppm (Nomiyama and Nomiyama 1977).Workers exposed to 85 pm TCE in air for 3.75 years reported vertigo,fatigue, and headache more frequently than workers exposed to 13 or34 ppm doses (Grandjean et al. 1955). Other epidemiological studieshave infrequently reported liver and kidney dysfunction in humansexposed to TCE.

In animal studies, inhalation of TCE has caused behavioral

25

changes, hepatotoxic effects and kidney effects. In studies withrats, oral exposure to TCE has produced kidney dysfunction,histological renal tubular alterations, and nephropathy. Oralexposure to TCE in mice has produced hematological effects such asdecreased erythrocyte counts, increased fibrinogen, and a shortenedprothrombin time (ATSDR, 1992a).

Epidemiological studies of occupationally-exposed workers havebeen conducted, but are considered inconclusive by EPA (1985h). Twoof these studies reported increased tumor incidence (Barret et al.1985; Blair et al. 1979), but in both cases exposure was to complexmixtures that contained other potential carcinogens besides TCE. EPA(1985h) concluded that all of the reviewed studies have limitationsthat restrict the conclusions that can be drawn from the data. Sincethe time of the EPA review, slight increases in the incidence ofbladder cancer and lymphomas in exposed workers have been reported.

In rats, inhalation exposure to TCE has resulted in increasedincidence of testicular Leydig cell tumors and slight increases inleukemia and renal adenocarcinomas. Oral exposure has resulted in anincreased incidence of leukemia (Maltoni et al. 1986). Two studiesin mice, one using technical-grade TCE and the second usingepichlorohydrin-free TCE, revealed significant increases in theincidence of liver tumors when orally exposed. Another study withmice reported an increased incidence of pulmonary adenocarcinomas inmice after inhalation exposure (Fukuda et al. 1983). In a morerecent study an increased incidence of both pulmonary and livertumors were reported in mice after inhalation exposure (Maltoni etal., 1986).

Both positive and negative results have been reported from invivo and in vitro genotoxicity assays. Positive results reported inhuman systems include tests for unscheduled DNA synthesis in humanlymphocytes in vitro and sister chromatid exchanges in circulatinglymphocytes in workers. However, the dose levels to which workerswere exposed were not specified (Gu et al. 1981). Positive resultshave also been reported in vitro assays with yeast, mammalian cell,and bacterial assays (ATSDR, 1992a). In vivo studies with livers ofrats and mice have found TCE to induce DNA damage (Nelson and Bull1986; Walles 1986). ATSDR concluded that the evidence from thesepositive tests combined with negative results from other assayssuggests that TCE is genotoxic. EPA (1985h) has also concluded thatit may be a weakly active mutagen.

Teratogenic effects have not been observed in the offspring ofrats or mice exposed to 500 ppm TCE in air (Hardin et al. 1981).External hydrocephalus was observed in the offspring of rabbitssimilarly exposed. The authors concluded that this result could notbe discounted due to the rarity of the anomaly; however, EPA (1985h)regarded the result as inconclusive. Fetotoxic effects includingincreased numbers of resorptions, reduced fetal body weight anddelays in skeletal ossification have been observed in Wistar ratsexposed to 100 ppm TCE in air during gestation (Healy et al. 1982).Similar effects were not seen in Sprague-Dawley rats or Swiss-Webster

26

AR3QH72

28

mice exposed to 300 ppm,in air (Schwetz et al. 1975) or in Long-Evansrats exposed to 1,800 ppm (Dorfmueller et al. 1979).

aberrations in humans have yielded inconsistent results (EPA, 1985a).

Inhalation exposure of rats, rabbits, and mice to vinyl chloridedid not induce teratogenic effects (EPA, 1985a). Potential effectson reproductive capacity have not been studied.


The oral SF for vinyl chloride is based on a study by Feron etal. (1981). Exposure was for 4 hours a day, 5 days/week for 2 years.Statistically significant increases in hepatic angiosarcoma of theliver were observed in the 2-year study at 5.6 mg/kg/day in males and17 mg/kg/day in females. Statistically significant increases inneoplastic nodules of the liver were also observed at concentrationsas low as 1.8 mg/kg/day in females and 5.6 mg/kg/day in males. TheEPA (1992b) has derived an oral SF from this study of 1.9E+00 (mg/kg-day)"1. This SF is cited in HEAST and is currently under review byEPA.

The inhalation SF for vinyl chloride is based on a study byMaltoni et al. (1981). In this study, Sprauge-Dawley rats wereexposed to vinyl chloride 5 days/week for 52 weeks at concentrationsranging from 1 to 30,000 ppm. Statistically significant increases inliver angiosarcomas were observed at concentrations as low as 50 ppra.The EPA (1992b) derived an inhalation SF of 3.0E-01 (mg/kg-day)"1based on this study. This inhalation SF is cited in HEAST and iscurrently under review by EPA.

SUMMARY OF VINYL CHLORIDE CRITERIA

EPA Carcinogenic Classification

Maximum Contaminant Level (MCL)

Maximum Contaminant Level Goal(MCLG)Maximum Contaminant Level(California)Oral SF

Inhalation SF

Group A

2 jug/L

0 Mg/L

0.5 M9/L

1.9E+00| mg/kg-day )"

3.0E-01^mg/kg-day) "

EPA,1992bATSDR19926

ATSDR1992e

ATSDR1992e

HEAST

HEAST

Toxicity information is included for beryllium since it has beendetected at risk based levels of concern. Beryllium is notconsidered to be a Contaminant of Concern.

29

F. Beryllium

Beryllium (Be) is a hard, grayish element that is moderatelyrare in its natural form. The element does occur as a chemicalcomponent in certain rocks, soils, and volcanic dust. Pure berylliummetal has applications in nuclear weapons and reactors, aircraft andspace vehicle structures and instruments, X-ray machines, andmirrors. Beryllium oxide is made from beryllium ores and is used tomake specialty ceramics for electrical and high technologyapplications. Beryllium is also converted into alloys used inproduction of electronic parts, construction materials for machineryand molds for plastics (ATSDR, 1992d). Beryllium oxide is used as asubstrate for production of transistor and silicon chips.


Absorption of beryllium occurs after inhalation exposure andoral exposure. The inhalation route is of greatest concern forsystemic effects, because beryllium and its compounds are poorlyabsorbed after oral (< 1%) and dermal exposure. However, skin contactcan cause an allergic reaction particularly in sensitizedindividuals. No studies were located regarding distribution inhumans of beryllium or its compounds after oral exposure.

In individuals exposed to beryllium via inhalation, inhaledberyllium is deposited in the lungs where it remains for extendedperiods. From animal studies, it has been shown that berylliumslowly mobilizes from the lungs to blood and then is rapidlydistributed to various tissues and stored in kidney, liver, blood,pulmonary lymph nodes, and bone (ATSDR, 1992d).

Occupational exposure to beryllium can cause chemicalpneumonitis. Symptoms include cough, substernal burning, shortnessof breath, anorexia, and increasing fatigue. Exposure to lowerconcentrations can cause chronic beryllium disease (berylliosis)resulting in pulmonary granulomas, pulmonary fibrosis and emphysema.The disease is characterized by reduction in vital lung capacity,total lung capacity, forced expiratory volume, and diffusioncapacity. In addition, exposure to beryllium in the workplace hasresulted occasionally in right atrial and ventricular hypertrophy andhyperemia of the kidney and adrenal gland.

Data regarding occupational exposure to beryllium and itscompounds indicate an increased evidence of lung cancer. However,the integrity of these studies has been severely criticized. Animalstudies indicate increases in lung cancer caused by inhalationexposure to beryllium or its compounds. Beryllium is considered ananimal carcinogen and a probable human carcinogen.


EPA has established an inhalation unit risk of 2.4 E-3 per(jug/cu.m) based on data available on occupational exposure toberyllium oxide. EPA has also established AWQC for consumption of

30

AR30M76

water and fish of 0.0068 Mg/L and 0.117 Mg/L for protection of humanhealth from fish consumption alone.

The oral RfD for beryllium is based primarily on the study bySchroeder and Mitchner (1975). Fifty-two weanling Long-Ears rats ofeach sex received 5 ppm (0.54 mg/kg day) of beryllium sulfate forlife. At death, the rats were dissected. Gross, microscopic changeswere noted in the heart, kidney, liver and spleen. Similar studieswere carried out on Swiss (CO strain) mice in groups of 54/sex atdoses of approximately 0.95 mg/kg/day without adverse effect.Differences between treated and control groups were deemed non-significant. A NOAEL was assigned to the rat dosage of 0.54 (mg/kg-day). An uncertainty factor of 100, applied for interspeciesconversion and for the protection of sensitive human subpopulations,resulted in an oral Rfd of 0.005 mg/kg/day.

31

SR3QH77

SUMMARY OF BERYLLIUM CRITERIA

EPA Carcinogen ClassificationMaximum Contaminant Level (MCL)

Maximum Contaminant Level Goal(MCLG)Oral SF

Oral RfD

Inhalation Risk

B20-. 001 mg/L

0 mg/L

4.3 (mg/kg-day)'15.0E-3 (mg/kg-day)8.4E+0(mg/kg-day) "12.4E-3 Mg/cu-m

SOURCE

EPA, 1992a

EPA, 1992a

EPA, 1992a

EPA, 1992a

EPA, 1992a

RBCT,1993*

EPA, 1992a

Ambient Water Quality CriteriaHuman (water and fishconsumption)Human (fish consumption only)

6.8E-3 Mg/L1.17E-1 Mg/L

EPA, 1992aEPA, 1992a

Freshwater Aquatic OrganismsAcute LEGChronic LEG

1.3E+2 Mg/L5.3 Mg/L

EPA, 1992aEPA, 1992a


32

XI. RISK CHARACTERIZATION:RISK ASSOCIATED WITH THE EXPOSURE TO CONTAMINANTS

IDENTIFIED IN GROUND WATER WELLS

A. Residential Well Results

Data for the residential wells in the vicinity of the site wasreviewed. Only Residential Well GW-2 showed any significantorganic contamination. Due to the limited amount of data collectedfor the risk assessment, maximum contaminant values were used forrisk calculation as in the case of the monitoring wells.Contaminants of concern in Residential Well GW-2 are vinyl chloride,benzene, 1,2-dichloropropane, and 1,4-dichlorobenzene.

Risk calculations developed from the data for Residential WellGW-2 represents current off-site risk in a residential use scenarioas well as future off-site risk in that same locality in aresidential use scenario as well.

Based upon the data from Residential Well GW-2, the combinedincreased cancer risks calculated for adult residential exposurethrough ingestion of groundwater was calculated as 9.25E-05. Theincreased cancer risk calculated for the inhalation of volatileorganic compounds during showering and bathing for adults wascalculated as 3.80E-05. The total combined increased carcinogenicrisk for adult residential exposure is 1.30E-04. This combinedincreased cancer risk for current adult residential use in an off-site location exceeds the Agency's acceptable risk range of l.OE-06to l.OE-04. Neither of the individual pathways, ingestion ofgroundwater or inhalation of volatile contaminants during showeringand bathing produced risks exceeding the Agency's risk range. Vinylchloride contributes 95.4% of the total carcinogenic risk for adultsin this scenario.

The combined increased cancer risk calculated for theresidential exposure of children to the contaminants in groundwateris calculated as 8.63E-05 for the ingestion of groundwater, 8.34E-06for the inhalation of volatile contaminants during showering andbathing, and 2.44E-07 for dermal contact during bathing. The totalcombined increased carcinogenic risk for children has been calculatedas 9.49E-05. Vinyl chloride contributes 96.1% of the total increasedcarcinogenic risk for children. The total combined increased cancerrisk calculated for children falls just inside the Agency's riskrange.

Noncarcinogenic risk is evaluated as a function of Hazard Index.If a Hazard Index value exceeds l.OE+00, adverse health effects maybe expected to occur. In the adult residential exposure scenario aHazard Index value of 4.39E+00 was derived for inhalation duringshowering and bathing. Based upon this risk estimate, adverse healtheffects are expected for an adult exposed to this groundwater in aresidential setting. No Hazard Index could be calculated for theingestion of groundwater because no RfDs are available for any of thecontaminants selected as contaminants of concern for the residential

33

wells.

The total combined noncarcinogenic Hazard Index calculated forthis scenario is 4.39E+00, which indicates that adverse healtheffects may be expected to occur .if this groundwater were to be usedby adult receptors. Benzene is responsible for more than 99% of thetotal noncarcinogenic risk in the adult residential use exposurescenario. Inhalation of volatile organics during showering andbathing contributes nearly 100% of the total combined noncarcinogenicrisk.

In the residential use scenario for children a Hazard Indexvalue of 4.68E+00 was derived for inhalation of volatile contaminantsduring showering and bathing. Since no oral RfD values are availablefor the contaminants found in the residential well, no Hazard Indexvalues could be calculated for ingestion of groundwater or for dermalcontact during showering and bathing. The total combinednoncarcinogenic Hazard Index calculated for this scenario is4.68E+00, which indicates that adverse health effects may be expectedto occur if this groundwater were to be used by children. Based uponthe Hazard Index value of 4.68E-fOO calculated for the inhalation ofvolatile compounds during showering and bathing by children, thatroute of exposure would be expected to elicit adverse noncarcinogenichealth effects upon exposure of receptors. Benzene is responsiblefor more than 99% of the total noncarcinogenic risk for children.Inhalation of volatile organics during showering and bathingcontributes nearly 100% of the total combined noncarcinogenic risk.

Concern usually arises when contaminants may not be evaluateddue to a lack of appropriate toxicity criteria. Due to the lack oftoxicity evaluative criteria, the risk to receptors associated withthe ingestion and dermal contact pathways could not be evaluated fromthe standpoint of noncarcinogenic potential. The risk to receptorsthrough ingestion and dermal contact was adequately addressed becausethe carcinogenic potential of the contaminants was evaluated forthose pathways, and the carcinogenic potential of the contaminantsidentified in the residential well outweighs any noncarcinogeniceffects in the ingestion and dermal contact pathways.

Beryllium was identified in numerous wells around the site atrisk based levels of concern. Beryllium was detected in bothupgradient and downgradient wells and was determined not to be a siterelated contaminant. It was reported at a concentration of 2.9 ppbin Residential Well GW-33, which was the highest reported detectionof beryllium in any of the residential wells. This concentration ofberyllium is used to represent a worst case scenario for residents atthe site that may be exposed to beryllium in home wells.

The carcinogenic risk attributable to the ingestion of berylliumin residential well water containing beryllium as reported at 2.9 ppbis 1.46E-04 for adults. This value exceeds'the Agency's l.OE-06 tol.OE-04 carcinogenic risk range.

For children the increased carcinogenic risk calculated for the

34

AR3QH80

ingestion of drinking water containing 2.9 ppb of beryllium is 1.37E-04. This calculated increased carcinogenic risk also exceeds theAgency's l.OE-06 to l.OE-04 risk range.

The noncarcinogenic effects due to the ingestion of thisgroundwater containing beryllium at the reported level would elicitHazard Index values of 1.59E-02 for adults and 7.42E-02 for children,respectively. No adverse non-carcinogenic health effects would beexpected from this exposure based upon the risk calculations.

B. Monitoring Well Results

The combined increased cancer risks calculated for adultresidential exposure through ingestion of groundwater and inhalationof volatile organic compounds during showering and bathing are 4.99E-05 and 2.46E-05 respectively. The total combined increasedcarcinogenic risk for adult residential exposure is 7.45E-05 if thiswater were to be consumed by on-site residents. Vinyl chloridecontributes 83.3% of the total carcinogenic risk in this scenario.Ingestion of groundwater accounts for 66.98% of the total risk. Thetotal combined increased carcinogenic risk of 7.45E-05 for adultresidential exposure falls within the Agency's carcinogenic riskrange of l.OE-06 to l.OE-04.

The increased cancer risks calculated for residential exposureof children to the contaminants in this groundwater, if it were to beused for drinking, are calculated as 4.65E-05 for the ingestion ofgroundwater, 5.37E-06 for the inhalation of volatile contaminantsduring showering and bathing, and 2.04E-07 for dermal contact duringbathing. Ingestion of groundwater accounts for 89.4% of the risk tochildren. The total combined increased carcinogenic risk forchildren has been calculated as 5.20E-05. With vinyl chloridecontributing 87.7% of the total risk. The total combined increasedcancer risk calculated for children fall within the Agency's riskrange of l.OE-06 to l.OE-04.

Noncarcinogenic risk is evaluated as a function of Hazard Index.If a Hazard Index value exceeds l.OE+00, adverse health effects maybe expected to occur. In the adult residential exposure scenario aHazard Index value of 9.13E-03 was calculated for the ingestion ofgroundwater, and a Hazard Index of 9.73E+00 was derived forinhalation during showering and bathing. No adverse non-carcinogenichealth effects are expected due to the ingestion of this groundwater.The total combined noncarcinogenic Hazard Index calculated for thisscenario is 9.74E+00, which indicates that adverse health effects maybe expected to occur if this groundwater were to be used by adultreceptors. It should be noted that inhalation of volatilecontaminants during showering and bathing is the pathway thataccounts for the adverse health effects in this scenario based uponthe Hazard Index value of 9.73E+00 calculated for that route ofexposure. Benzene is responsible for 99.2% of the totalnoncarcinogenic risk in the adult residential exposure scenario.Inhalation of volatile organics during showering and bathing

35

AR30H8I

contributes 99.9% of the total combined noncarcinogenic risk.

In the residential exposure scenario for children a Hazard Indexvalue of 4.26E-02 was calculated for the ingestion of groundwater.No adverse health effects are expected for this pathway based uponthese results. A Hazard Index of 1.04E+01 was derived for inhalationduring showering and bathing. Adverse health effects are to beexpected due to the use of this groundwater for showering and bathingby children. A Hazard Index value of 2.04E-04 was calculated fordermal contact during bathing, which indicates that no adverse healtheffects are expected to occur by this pathway of exposure. The totalcombined noncarcinogenic Hazard Index calculated for this scenario is1.04E+01, which indicates that adverse health effects may be expectedto occur if this groundwater were to be used by children for normalresidential use. The Hazard Index value of 1.04E+01 calculated forthe inhalation of volatile compounds during showering and bathing bychildren indicates that this particular pathway in the route ofexposure would be expected to elicit adverse noncarcinogenic healtheffects while non would be expected via the other pathways. Benzeneis responsible for 99% of the total noncarcinogenic risk forchildren. Inhalation of volatile organics during showering andbathing contributes nearly 100% of the total combined noncarcinogenicrisk.

Beryllium contamination at the site is not considered to be siterelated. In order to assess the totality of risks to which receptorsare exposed, beryllium is being assessed for its carcinogenic andnoncarcinogenic potentials. Based upon the concentration ofberyllium detected in Monitoring Well LS-09 (5.8 ppb) an increasedcarcinogenic risk of 2.93E-04 is calculated for the exposure ofadults through ingestion of drinking water in a residential usescenario. The increased carcinogenic risk calculated for children inthis scenario is 2.73E-04. Both of these increased cancer risksexceed the Agency's l.OE-06 to l.OE-04 risk range.

The noncarcinogenic risks calculated for the ingestion of thisdrinking water by adults and children are 3.18E-02 and 1.48E-01,respectively. No adverse noncarcinogenic health effects are expectedto occur based upon these risk calculations for the ingestion of thisdrinking water by either adults or children.

It is significant to note that the beryllium concentration inMonitoring Well LS-09 was flagged "L", indicating that the actualvalue is probably higher than reported. The increased carcinogenicrisk reported for receptors in that portion of the site couldpossible be higher than has been reported. Of course it must benoted that this water is not currently being used by receptors fordrinking or other uses.

36

XII. SUMMARY OF RISKS

A. Groundwater

1. Residential Wells

For adults an increased carcinogenic risk of 9.25E-05 wascalculated for the ingestion of groundwater. An increasedcarcinogenic risk of 3.80E-05 was calculated for the inhalation ofvolatiles during showering and bathing, and a total combined risk of1.30E-04 was calculated for the combination of both residential wellexposure pathways. The total combined risk for the use of thisgroundwater exceeds the Agency's carcinogenic risk range.

Beryllium was determined not to be a site related contaminant,but would impact any receptors exposed to drinking water. Adultsconsuming groundwater with the maximum concentration of berylliumreported in the residential wells at the site may be exposed to anincreased cancer risk of 1.46E-04.

The total carcinogenic risk to adults in residence at the sitemay be as high as 2.76E-04, with 52.9% of that total risk beingcontributed by beryllium which is not site related.

For children the increased carcinogenic risks calculated were8.63E-05 for the ingestion of groundwater, 8.34E-06 for theinhalation of volatiles during showering and bathing, and 2.44E-07for dermal contact during showering and bathing. The total combinedincreased cancer risk attributable to exposure to this groundwater bychildren is 9.49E-05, which lies within the Agency's risk range.

When the total combined increased cancer risk for children iscombined with the risk due to beryllium, increased carcinogenic risksas high as 2.32E-04 are calculated. Beryllium contributes 59.1% ofthat total risk.

The noncarcinogenic risk calculated for adult and childhoodexposure to contaminants in the residential wells was due to theinhalation of volatile contaminants during showering and bathing.The Hazard Index values calculated were 4.39E+00 and 4.68E+00,respectively for adults and children. These calculations indicatethat adverse health effects may be expected for residential use ofthis water. Beryllium, which is naturally occurring, does not makeany significant contribution to the noncarcinogenic risk. Benzene isthe major contributor to the noncarcinogenic risk in this situation.

All risks are assumed to be applicable to off-site residents ina current use scenario and for residents in that vicinity in a futureuse scenario.

2. Monitoring Wells

If the monitoring wells were to be used for residential purposesat the site, on-site adults and children would be exposed to

37

increased cancer risks of 4.99E-05 and 4.65E-05, respectively foringestion of this groundwater. The increased cancer risks associatedwith inhalation exposures would be 2.46E-05 and 5.37E-06 for adultsand children, respectively. Children would additionally have anincreased dermal risk exposure of 1.39E-07. The total combinedincreased cancer risks for adults and children if this groundwaterwere to be used for residential purposes would be 7.45E-05 and 5.20E-05, respectively. These risks fall within the Agency's risk range.If receptors were to consume groundwater containing the concentrationof beryllium reported at Monitoring Well LS-09 along with the organiccontaminants reported, total increased carcinogenic risks of 3.68E-04and 3.25E-04 are derived for adults and children respectively.

Noncarcinogenic impacts for adults and children as evaluated byHazard Index would be 9.13E-03 and 4.26E-02, respectively if thiswater were to be used for drinking purposes. The Hazard Index valuescalculated for adults and children for inhalation exposure werecalculated as 9.73E+00 and 1.04E+01, respectively. The children'sHazard Index value for dermal contact would be 2.04E-04. Totalcombined Hazard Index values are 9.74E+00 for adults and 1.04E+01 forchildren. Adverse noncarcinogenic effect would be expected for bothadults and children using this water. Adults and children alsoexposed to beryllium at the level detected in Monitoring Well LS-09in addition to the contaminants mentioned above would have nosignificant increase in noncarcinogenic risks, since beryllium is nota significant contributor to the Hazard Index.

XIII. UNCERTAINTY

Exposure Characterization

Uncertainty associated with the assessment of risk at the SussexCounty Landfill Number 5 may be characterized as being associatedwith exposure estimation, toxicity assessment, and in riskcharacterization. The policy of this Agency is to be protective ofhuman health and the environment. In accordance with this policy,exposure estimates and the parameters used in the characterization ofthe exposures at the Sussex County Landfill Number 5 are of aconservative nature. These conservative parameters are design toinsure that all estimates are protective and that all sensitivesubpopulations are considered. Some of these exposure parameters maybe overestimates of the actual exposures experienced by the receptorsat the site.

Monitoring well exposures are probably overestimated by virtueof the fact that the characterization of risk is conducted withexposure being estimated for the central portion of the plume. Eventhough this concentration accurately characterizes the highestexposure point concentration, it probably represents concentrationsof contaminants greater than the receptors actually encounters. Itshould also be noted that this water from the monitoring wells is notcurrently being consumed by receptors and estimates of exposure andrisk represent the exposures and risks to be assumed if this water

38

were to be used for drinking.

It is also assumed that the concentrations of contaminants willremain the same over time. Since the contaminant concentrations maydecrease over time, the exposures of receptors may be overestimatesor future exposure.

Toxicity Characterization

Uncertainty associated with toxicity characterization may be dueto factors including extrapolation from subchronic to chronic data,intraspecies extrapolation, interspecies variability, lack of certaintypes of data, data limitations, and other relevant modifyingfactors. All of these factors are taken into account when evaluatingthe toxicity of the contaminants in question. In the case ofsubstances of carcinogenic concern; it must be noted that uncertaintymay also be associated with the extrapolation of data obtained fromanimal studies in which short term exposure to very highconcentrations of contaminant produced some carcinogenic effects topossible human effects produced by low dose long term exposures.

The evaluation of the uncertainty associated with toxicity alsoincludes an assessment of the certainty with respect to RfD valuesand the safety factors built into the toxicity values used for theevaluation of contaminants. It should be noted that in applying theAgency's RfD methodology, strong arguments may be made for variousRfD values within a factor of 2 or 3 of the current RfD value.Additionally, the RfD computation methodology derives a number withinherent uncertainty that may span an order of magnitude.

The IRIS database includes information related to theuncertainty factors and the confidence in the RfD values for a givencontaminant.

Beryllium (Found to be Naturally Occurring) has an uncertaintyfactor associated with its RfD of 100 and the confidence is the RfDis listed as low.

Toxicity values for benzene, TCE, and vinyl chloride are underreview at this time. If changes are made in toxicity values,uncertainty may increase or decrease accordingly.

Risk Characterization

Uncertainty associated with the characterization of risk isrelated to the uncertainty of the exposure and toxicitycharacterizations. It is noted that risk is a function of the intakeof a contaminant as based on the exposure scenario and the toxicityof the contaminant to which the receptor has been exposed. It isacknowledged that the uncertainty associated with the use of thedefault exposure parameters are conservative and thereforeoverestimate the actual exposure. The uncertainty associated withRfDs and other toxicity data values is based upon the methodologyused to derive the data values, the quality of the data derived from

39

AR3QH85

the various studies used to assess the toxicity of the contaminant,and the'margins of safety built into these values.

Residential And Monitoring Wells

In the case of the risk values generated for both theresidential and monitoring wells there is need to note theuncertainty issues discussed above. The size of the data sets forboth the monitoring wells and the residential wells were limited.There was one round of samples for three monitoring wells and tworounds of samples from one residential well. In accordance with theRAGS guidance document, the maximum concentrations of eachcontaminant were used for risk assessment purposes since the 95th%upper confidence limit values all exceeded the maximumconcentrations.

Risks due to the exposure of residents to contaminantsidentified as being present in the selected on-site monitoring wellsat the site were used to assess future risk to site residents. Theexposure point concentrations derived for this risk assessment werebased upon the maximum contaminant concentrations of each of theselected contaminants of concern based upon the analytical resultsreported for monitoring wells LD-01, LS-07R, and LS-16.

The residential well at the Joseph property was used to estimatecurrent risks at the site and as a future risk projection at thatlocation. Maximum contaminant concentrations were used in thisassessment since only this single residential well showed evidence ofcontamination.

Risk estimates provided in this risk assessment evaluateresidential use scenarios. Uncertainty is effected by the type ofland use at the site. If the site were to change from residential tooccupational, risk estimates would then be an overestimation of risk.On the other hand, if additional residential development were tooccur at the site, risk to site residents may be underestimated.

Uncertainty associated with the naturally occurring levels ofberyllium is due to the use of maximum concentrations due to thelimited amount of data available. This may lead to either anunderestimation or an overestimation of risk, since theconcentrations utilized in this risk assessment may not berepresentative of actual risk. In addition the use of an "L" flaggedconcentration as a representative concentration of beryllium for themonitoring wells may lead to an underestimation of risk, since theactual risk is probably higher than that which has been reported.

40

AR30H86

APPENDIX

Contents

Table 1: Organic Data (Residential Well GW-2)

Table 2: Organic Data (Monitoring Wells)

UCL Calculations

Risk Calculations For Groundwater

References

AR30H.87

TABLE 1ORGANIC DATA EVALUATION FOR GW-2 (Joseph Residence)

SUSSEX COUNTY LANDFILL

PARAMETER

Benzene

Chlorobenzene

Cis-l,2-Dichloroethene

4,4'-DDT

1,2— Dichlorobenzene

1,4- Dichlorobenzene

Dichlorodifluoromethane

1,1— Dichloroethane

1,2- Dichloropropane

Trans- 1,2-dichloroethene

Ethyl benzene

Isopropyl benzene

4— Isopropyl toluene

Naphthalene

N-propyi benzene

Tert-butyl benzene

Tetrachloroethene

Toluene

Trichloroethene

1,2,4-Trimethyl benzene

1,3,5— Trimethyl benzene

Vinyl Chloride

Total Xylenes

CONCENTRATION l(ug/1)

4

1

5J

0.01J

0.3J

1

8

2

2J

0.07J

U

1

0.7

2J

0.2J

0.6J

0.6

0.1J

1

0.5

0.1J

4

5

BACKGROUNDCONCENTRATION 2

(ug/1)

ND(O.l)

ND(O.l)

ND(O.l)

ND (0.05)

ND(O.l)

ND(0.15)

ND (0.25)

ND (0.05)

ND(O.l)

ND(0.15)

ND(O.l)

ND(O.l)

ND(O.l)

ND(O.l)

ND(O.l)

ND(O.l)

ND(O.l)

ND(O.l)

ND(0.15)

ND(0.15)

ND(O.l)

ND(0.15)

ND (0.15-0.2)

MCL(ug/1)

5

NA

70

NA

600

75

NA

NA

5

100

700

NA

NA

NA

NA

NA

5

1000

5

NA

NA

2

10000

10-<YHQ0.1RISK

CONCENTRATION 3(ug/1)

0.35

3.9

6.1

0.23

37

0.55

39

81

0.2

12

130

150

NA

150

NA

NA

1.3

75

1.9

NA

NA

0.023

1200

cocf|

YES

YES

YES

<

YES

NOTES:1 Maximum detected concentration above the sample quantitation limit (SQL). Values are based onJune and December 1992 Weston sampling results.

2 Background groundwater is LS-15.3 Values taken from "Selecting Exposure Routes and Contaminants of Concern by Risk-Based Screening"; EPA/903/R-93-001;

January 1993.ND = Not detected. The number or range is 1/2 the SQL.NA =s Not applicable.

AR30H88

oT-4

<uoo

NO1—I

ICfl

S I n<5, I • I £>I - — | | -

<&r-I

I-

Sond

" 8

Io)Iao*•*z

O

<*. , , - c * ^

•l:

1<f H5g|~-r^isO Q '"'

'" §

i4 £"iti!§§•ops ?iis3g<**

3. • o*, • . .2J,^

c*

vUsrr\Q

-{§

: 1?rS " ^•, • ^C .*5"' ;'

••.:. "*"' •*•*•'; y;'

• '•••; :pE. >jv ..

: ' 's:''

P5•': ' R

cu

S 1 - I

V O O N ^ ' — ' f H * < ^ ; V ^ O N » - 4 C ^ O C ' ' . ^ H«*5 c<S f~ NO n J "O - °o ci S " -!O 000 * '

« « < ; < g < < p < < ^ « < ^2 Z Z Z Z Z Z

S " i ? v T ' ^ ( n > v ? ( / : r v ? > v ? s s v : r ' i ^ ( n io ' d ' ^ C 3 ' : 5 c 5 ' ~ ! r N i c ? d ' ~ ' ' - ' < : ^• — » s ^ - O ~ ~ ' O O O O O < — ' Q Q Oi i Q g Q Q Q Q Q i 2 Z Q- & x : ' Z ' C Z Z Z Z Z ' 1 ' Z

f. <<". CO <O «<1 fl C<~, C<~. C<~, <<~i CO CO CO

(O CO ^ CN i-l i-l CO i-l CO CN CO •-! 1-1

< * * 3 * a g * ^ ^ - o 5 gs °

w S 5 w g g 2 S 5 S a 3 §d c5 d

u uc eo> eg£ G - C —

s.l 1 1 1 1 1 i1 l ° Q U - i § l - l ' i ' l

s J i | A Q Q . l l l S § . §S 2 S ^ . Q Q Q O Q Q ^ Q . Sa l l 1 . 1 . 1 ' 1 i i « i -o§ 2 2 .sa '^ ^ ^ .a - ^ .a ^ e« U U U T ) - T r — i Q — i - n Q c ^ W

^

CN

V?Od• ^Q

C«1

T— 1

8d

§d

1 Endrin Aldehyde

•8D.MD

t .'« ^w "3° S

• S a* In °

.f 1 15^ 3T3 3 ^U O O

P 1„ 2 3&S co 5S IA O5 « -a£.§ 1Ou -fi« 3 w•a .a— • tia t-i§a |Si i1 S j JS l - e* o.g. §•§ gU '| w.1 J S e^ ry 0 oJg w"g.«•5 j> cs •«Jjs o g

g«2 S"I'i-S§I'B -llsg^ § ||

T3 § *T3

8 5 T3 *•a * « 13§ S i ™SI-81"° s h «g § J= t>3 o ob 8J jg 2 "3.

1? fo.. I S'3 St« .5 -2 - -SE.s§g|gSZ 2Z,2 M (S f)

MO " ' '

I

i

IaCMO

CN

•8CM

Q

05

a

orto

1

10~6/HQ 0.1

RISK

CONCENTRATION

(ug/I)S

df

BACKGROUND4

CONCENTRATION

("g/0

ir*

Q

i1BW

O O Q O , _. O ^ COi-j co in <; <J v, <J _;

8 V ,_ <J «£ <! •< «£Z ^ Z Z Z Z Z

v^ TH i— t *-i »n *— i i— < T-<g d _ o ^ d x g ' o ^ o ^ o ^XQ'Q'Q'Z Q'Q'Q'g Z Z Z Z Z Z

CO CO CO CO CO CO CO CO

w i i - ( i - i i - i « n , H i - i i - tOd

CO

1 3 » | - S | 3

<U 4>

a "3 -g, 1 -i S l t s g j j gI j i l f l l lS S ^ 4 c N Z 2 ^

S §

2 2 0-

o ^ ^ or-t 2 IZJ O

t-H

2 ^ -5 5 s o*»-• c3 o '-' o 'n ^* n '^ 2S LJ O *2 Q2 Z 2 2 2 S

Q

o", e*; en en en en

cs oi <n en «— • oi

<N * 00 t*~. ** ~<CN CNbt- CD

._ .. ^ <N '-J TJ-\O • C*J »G • ^JO O ^j O

<D 4>

4) a?

| I" -I" Jj M

8 i f ^ 9 141 *a 1 1 ^— „-5 1 S P 1* |§_ f5 ,4 - > H

sr

§§£§O * * " »Hj OOOO

(A

I „ §§§§

+• (MIMCMOJtM

omor-o

•5 1 ^S * •*«*»••- 3 c Kin KI torno

§§§§ ? X §§§§§-J Z C

< a TI* S M OMOOO

§§§§ « s§ss§

S 7 §§§§ I I §§§§§J*» ^ • •£3 - - - _

S

II *&atu et uj -" ui

2 S S It ^S"* as * *-So o Zz ae "2 -tujoS •- 5 _iSS5z>• N i i uzziM<4-«


RESIDENTIAL WSLL_ US*-SCENARIO - CURRENT AND FUTURE USE

ADULT INGESTION OF GROUNDWATER

CARCINOGENIC RISK

CONTAMINANT CONC. ADI RISK(ug/L) (mg/kg/day) (mg/kg/day)-l

VINYL CHLORIDE 4.00E+00 4.70E-05 8.92E-05BENZENE 4.00E+00 4.70E-05 1.36E-061,2-DICHLOROPROPANE l.OOE+00 2.35E-05 1.60E-061,4-DICHLOROBENZENE l.OOE+00 1.17E-05 2.82E-07

TOTAL INGESTION RISK 9.25E-05

ADULT INHALATION OF VOLATILES DURING SHOWERING AND BATHING

CARCINOGENIC RISK

CONTAMINANT CONC. ADI RISK(ug/m3) (mg/kg/day) (mg/kg/day)-l

VINYL CHLORIDE 7.14E+01 1.16E-04 3.49E-05BENZENE 6.45E+01 1.05E-04 3.06E-061,2-DICHLOROPROPANE 2.69E+01 4.38E-05 N/A1,4-DICHLOROBENZENE 1.23E+01 2.01E-05 N/A

TOTAL INHALATION RISK 3.801-05

TOTAL ADULT RISKS BY CONTAMINANT

CARCINOGENIC RISK

CONTAMINANT RISK(mg/kg/day)-!

VINYL CHLORIDE 1.24E-04BENZENE 4.42E-061,2-DICHLOROPROPANE 1.60E-061,4-DICHLOROBENZENE 2.82E-07

COMBINED TOTAL CARCINOGENIC RISKS FOR ADULTS 1.301-04

AR30H92


iSIDENTIAL WELL USB SCENARIO - CURRENT AND FUTURE USE

ULT INGESTION OF GROUNDWATER

NONCARCINOGENIC RISK

CONTAMINANT CONC. ADI HI(ug/L) (mg/kg/day)

VINYL CHLORIDE 4.00E+00 1.10E-04 N/ABENZENE 4.00E+00 1.10E-04 N/A1,2-DICHLOROPROPANE l.OOE+00 5.48E-05 N/A1,4-DICHLOROBENZENE l.OOE+00 2.74E-05 N/A

TOTAL INGESTION HAZARD INDEX N/A

ADULT INHALATION OP VOLATILES DURING SHOWERING AND BATHING


CONTAMINANT CONC. ADI HI(ug/m3) (mg/kg/day)

VINYL CHLORIDE ' 7.14E+01 2.72E-04 N\AZENE 6.45E+01 2.45E-04 4.30E+00-DICHLOROPROPANE 2.69E+01 1.02E-04 8.97E-02-DICHLOROBENZENE 1.23E+01 4.69E-05 2.05E-04

V ^V9 •

«'.

. :TOTAL INHALATION HAZARD INDEX 4.39E+00

TOTAL ADULT HAZARD INDEX VALUES BY CONTAMINANT


CONTAMINANT HI

VINYL CHLORIDE N/ABENZENE 4.30E+001,2-DICHLOROPROPANE 8.9 7E-021,4-DICHLOROBENZENE 2.05E-04

COMBINED TOTAL HAZARD INDEX FOR ADULTS 4.39E+00

flR30H93


RESIDENTIAL WELL USB SCENARIO - CURRENT AND FUTURE USE

INGESTION OF GROUNDWATER BY CHILDREN

CARCINOGENIC RISK


VINYL CHLORIDE 4.00E+00 4.38E-05 8.33E-05BENZENE 4.00E+00 4.38E-05 1.27E-061,2-DICHLOROPROPANE l.OOE+00 2.19E-05 1.49E-061,4-DICHLOROBENZENE l.OOE+00 1.10E-05 2.63E-07


INHALATION OF VOLATILES DURING SHOWERING AND BATHING BY CHILDREN

CARCINOGENIC RISK


VINYL CHLORIDE 2.24E+01 2.56E-05 7.68E-06BENZENE 1.97E+01 2.25E-05 6.54E-071,2-DICHLOROPROPANE 7.88E+00 8.99E-06 N/A1,4-DICHLOROBENZENE 3.55E+00 4.05E-06 N/A

TOTAL INHALATION RISK 8.34E-06

DERMAL CONTACT WITH VOLATILES DURING SHOWERING AND BATHING BY CHIL

CARCINOGENIC RISK


VINYL CHLORIDE 4.00E+00 1.22E-07 2.3IE-07BENZENE 4.00E+00 1.87E-07 5.42E-091,2-DICHLOROPROPANE l.OOE+00 8.8IE-08 5.99E-091,4-DICHLOROBENZENE l.OOE+00 7.93E-08 1.90E-09

TOTAL DERMAL RISK 2.44E-07

TOTAL CARCINOGENIC RISKS BY CONTAMINANT

CARCINOGENIC RISK

CONTAMINANT RISK(mg/kg/day)-l

VINYL CHLORIDE 9.12E-05INZENE 1.93E-0612-DICHLOROPROPANE 1.50E-06

", 4-DICHLOROBENZENE 2.65E-07

COMBINED TOTAL CARCINOGENIC RISKS FOR CHILDREN 9.49E-05

AR30H95


RESIDENTIAL WELL USB SCENARIO - CURRENT AND FUTURE USE




VINYL CHLORIDE 4.00E+00 5.11E-04 N/ABENZENE 4.00E+00 5.11E-04 N/A1,2-DICHLOROPROPANE l.OOE+00 2.56E-04 N/A1,4-DICHLOROBENZENE l.OOE+00 1.28E-04 N/A

TOTAL INGESTION HAZARD INDEX N/A




VINYL CHLORIDE 2.24E+01 2.99E-04 N\ABENZENE 1.97E+01 2.62E-04 4.59E+001,2-DICHLOROPROPANE 7.88E+00 1.05E-04 9.20E-021,4-DICHLOROBENZENE 3.55E+00 4.73E-05 2.07E-04

TOTAL INHALATION HAZARD INDEX 4.68E+00




VINYL CHLORIDE 4.00B+00 1.42E-06 N/ABENZENE 4.00E+00 2.18E-06 N/A1,2-DICHLOROPROPANB l.OOE+00 1.03E-06 N/A1,4-DICHLOROBENZENE l.OOE+00 9.25E-07 N/A

TOTAL INHALATION HAZARD INDEX N/A

TOTAL CHILD HAZARD INDEX VALUES BY CONTAMINANT


CONTAMINANT HI

JIR30M96

CHLORIDE N/AINZENE 4.59E+00J2-DICHLOROPROPANE 9.20E-021,4-DICHLOROBENZENE 2..07E-04

COMBINED TOTAL HAZARD INDEX FOR CHILDREN 4.68E+00

HR30H97

PollutantAdult TemplateChild Template

DOSE-RESPONSE INFORMATION:

Oral RfO: Inhaled RfD:(mo/kg/d) (mg/kg/d)

OralPotencyFactor:(1/<mg/kg/d»

InhaledPotencyFactor:<1/<mg/k3/d»

VINYL CHLORIDE 1.90E+00 3.00E-011.90E+00 3.00E-01

BENZENE 5.71E-05 2.90E-02 Z.91E-025.71E-05 2.90E-02 2.91E-02

1,2-DICHLOROPROPANE 1.14E-03 6.80E-021.14E-03 6.80E-02

1,4-DICHLOROBENZENE 2.29E-01 2.40E-022.29E-01 2.40E-02

(Foster I Chrostouski, continued)(Cancer) (Non-cancer)Lifetime Chronic Upper BoundIntake Intake Lifetime Hazard Index

mg/kg/d mg/kg/d Cancer Risk (Intake/RfO)O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00 O.OOE+00 O.OOE+00 O.OOE+00

1.16E-04 2.72E-04 3.49E-05 O.OOE+002.56E-05 2.99E-04 7.68E-06 O.OOE+00

1.05E-04 2.45E-04 3.06E-06 4.30E+002.25E-05 2.62E-04 6.54E-07 4.59E+004.38E-05 1.02E-04 O.OOE+00 8.97E-028.99E-06 1.05E-04 O.OOE+00 9.20E-022.01E-05 4.69E-05 O.OOE+00 2.05E-044.05E-06 4.73E-05 O.OOE+00 2.07E-04

ADULT RISK ADULT HI3.80E-05 4.39E+00

CHILD RISK CHILD HI8.34E-06 4.68E+00

AR30H99

INHALATION DURING SHOWERING AND BATHING (Foster & Chrostowski, 1986)

Molecular Henry's [Overall ra[Concentra[ConcentraWeight Constant Kl Kg KL KLts Cd Ca(g/mole) (atm-m3/mole) (cm/h) (cm/h) (cm/h) (cnt/h) (ug/l) ug/m3)9.21E+016.70E-031.38E+011.33E+031.33E+011.78E+01O.OOE+00 O.OOE+009.21E+01 6.70E-03 1.38E+01 1.33E+03 1.33E+01 1.78E+01 O.OOE+00 O.OOE+00

6.30E+016.30E+01

7.80E+017.80E+01

1.13E+021.13E+02

1.47E+021.47E+02

8.19E-028.19E-02

5.59E-035.59E-032.31E-032.31E-03

2.89E-032.89E-03

1 .67E+011.67E+01

1.50E+011.50E+011.25E+011.25E+01

1.09E+011.09E+01

1.60E+031.60E+03

1.44E+031.44E+03

1.20E+031.20E+03

1.05E+031.05E+03

1.67E+011.67E+01

1 .44E+011.44E+011.13E+011.13E+01

1.01E+011.01E+01

2.23E+012.23E+01

1.93E+011 .93E+01

1.51E+011.51E+01

1 .35E+011 .35E+01

2.10E+006.60E-01

1.89E+005.78E-01

7.90E-012.32E-01

3.62E-011.04E-01

7.14E+012.24E+01

6.45E+011.97E+01

2.69E+017.88E+00

1.23E+013.55E+00

DRINKING WATER(Cancer) (Non-cancer)

Ambient Lifetime Chronic Upper BoundCone. Intake Intake Lifetime Hazard Index(ug/l) mg/kg/d mg/kg/d Cancer Risk (Intake/RfD)

O . O O E + 0 0 O . O O E + 0 0 O . O O E + 0 0 O . O O E + 0 0O.OOE+00 O.OOE+00 O.OOE+00 O.OOE+00

4.00E+00 4.70E-05 1.10E-04 8.92E-05 O.OOE+004.00E+00 4.38E-05 5.11E-04 8.33E-05 O.OOE+00

4.00E+00 4.70E-05 1.10E-04 1.36E-06 O.OOE+004.00E+00 4.38E-05 5.11E-04 1.27E-06 O.OOE+002.00E+00 2.35E-05 5.48E-05 1.60E-06 O.OOE+002.00E+00 2.19E-05 2.56E-04 1.49E-06 O.OOE+00


ADULT RISK ADULT HI9.25E-05 O.OOE+00

CHILD RISK CHILD HI8.63E-05 O.OOE+00

DERMAL INTAKE DURING BATHING (Foster & Chrostowski, 1986)Average Octanol: (Cancer) (Non-cancer)Bathwater Water Lifetime Chronic Upper Bound

Concentration Part. Coeff. Intake Intake Lifetime Hazard Index(ug/l) (Kou) mg/kg/d mg/kg/d Cancer Risk (Intake/RfD)

O.OOE+00 6.90E+02 O.OOE+00 O.OOE+00 O.OOE+00 O.OOE+00

4.00E+004.00E+00 1.38E+00 1.22E-07 1.42E-06 2.31E-07 O.OOE+00

4.00E+004.00E+00 2.12E+00 1.87E-07 2.18E-06 5.42E-09 O.OOE+00

2.00E+002.00E+00 2.00E+00 8.81E-08 1.03E-06 5.99E-09 O.OOE+00

1.00E+00l.OOE+00 3.60E+00 7.93E-08 9.25E-07 1.90E-09 O.OOE+00

CHILD RISK CHILD HI2.44E-07 O.OOE+00

RISKS COMBINED ACROSSCHEMICALS AND EXPOSURE ROUTES

TotalUpper Bound TotalLifetime Hazard IndexCancer Risk (Intake/RfD)

O.OOE+00O.OOE+00O.OOE+00 O.OOE+00

T.24E-04 O.OOE+009.12E-05 O.OOE+004.42E-06 4.30E+001.93E-06 4.59E+001.60E-06 8.97E-021.50E-06 9.20E-02

2.82E-07 2.05E-042.65E-07 2.07E-04



AR30l»50"3


MONITORING WELLS - LD-1, LS-7R, LS-16

RESIDENTIAL USE SCENARIO - CURRENT AND FUTURE USE


CARCINOGENIC RISK


VINYL CHLORIDE 2.00E+00 2.35E-05 4.46E-05BENZENE 9.00E+00 1.06E-04 3.06E-061,2-DICHLOROPROPANE l.OOE+00 1.17E-05 7.98E-071,4-DICHLOROBENZENE 4.00E+00 4.70E-05 1.13E-06TRICHLOROETHYLENE 2.00E+00 2.35E-05 2.58E-07



CARCINOGENIC RISK


VINYL CHLORIDE 3.57E+01 5.82E-05 1.75E-05BENZENE 1.45E+02 2.36E-04 6.88E-061,2-DICHLOROPROPANE 1.34E+01 2.19E-05 N/A1,4-DICHLOROBENZENE 4.93E+01 8.03E-05 N/ATRICHLOROETHYLENE 2.69E+01 4.39E-05 2.63E-07

TQTAi INHALATION RISK 2,461-91

TOTAL ADULT RISKS BY CONTAMINANT

CARCINOGENIC RISK


VINYL CHLORIDE 6.2IE-05BENZENE 9.95E-061,2-DICHLOROPROPANE 7.98E-071,4-DICHLOROBENZENE 1.13E-06TRICHLOROETHYLENE 5.22E-07

COMBINED TOTAL CARCINOGENIC RISKS FOR ADULTS 7.45E-05


iNITORING WELLS - LD-1, LS-7R, LS-16

RESIDENTIAL USE SCENARIO - CURRENT AND FUTURE USE




VINYL CHLORIDE 2.00E+00 5.48E-05 N/ABENZENE 9.00E+00 2.47E-04 N/A1,2-DICHLOROPROPANE l.OOE+00 2.74E-05 N/A1,4-DICHLOROBENZENE 4.00E+00 1.10E-04 N/ATRICHLOROETHYLENE 2.00E+00 5.48E-05 9.13E-03

TOTAL INGESTION HAZARD INDEX 9.13E-03




INYL CHLORIDE 3.57E+01 1.36E-04 N\ABENZENE 1.45E+02 5.52E-04 9.66E+001,2-DICHLOROPROPANE 1.34E+01 5.11E-05 4.49E-021,4-DICHLOROBENZENE 4.93E+01 1.87E-04 8.19E-04TRICHLOROETHYLENE 2.69E+01 1.02E-04 1.71E-02

TQTJft INHALATION BIND IHB1X 9:731*99TOTAL ADULT HAZARD INDEX VALUES BY CONTAMINANT


CONTAMINANT HI

VINYL CHLORIDE N/ABENZENE 9.66E+001,2-DICHLOROPROPANE . 4.49E-021,4-DICHLOROBENZENE 8.19E-04TRICHLOROETHYLENE 2.62E-02

COMBINED TOTAL HAZARD INDEX FOR ADULTS 9.74E+00


MONITORING WELLS - LD-1, LS-7R, LS-16

RESIDENTIAL USB SCENARIO - CURRENT AND FUTURE USE


CARCINOGENIC RISK


VINYL CHLORIDE 2.00E+00 2.19E-05 4.16E-05BENZENE 9.00E+00 9.86E-05 2.86E-061,2-DICHLOROPROPANE l.OOE+00 1.10E-05 7.45E-071,4-DICHLOROBENZENE 4.00E+00 4.3SE-05 1.05E-06TRICHLOROETHYLENE 2.00E+00 2.19E-05 2.41E-07



CARCINOGENIC RISK


VINYL CHLORIDE 1.12E+01 1.28E-05 3.84E-06BENZENE 4.43E+01 5.05E-05 1.47E-061,2-DICHLOROPROPANE 3.94E+00 4.50E-06 N/A1,4-DICHLOROBENZENE 1.42E+01 1.62E-05 N/ATRICHLOROETHYLENE 7.89E+00 9.01E-06 5.40E-08TOTAL INHALATION RISK 5.37E-06


CARCINOGENIC RISK


VINYL CHLORIDE 2.00E+00 6.08E-08 1.16E-07BENZENE 9.00E+00 4.20E-07 1.22E-081,2-DICHLOROPROPANE l.OOE+00 4.41E-08 3.00E-091,4-DICHLOROBENZENE 4.00E+00 3.17E-07 7.61E-09TRICHLOROETHYLENE 2.00E+00 1.05E-07 1.15E-09

TOTAL DIRMAL RIIK 1,391-07TOTAL CARCINOGENIC RISKS BY CONTAMINANT

CARCINOGENIC RISK


VINYL CHLORIDE 4.56E-05BENZENE 4.34E-061,2-DICHLOROPROPANE 7.48E-071,4-DICHLOROBENZENE 1.06E-06TRICHLOROETHYLENB 2.96E-07COMBINED TOTAL CARCINOGENIC RISKS FOR CHILDREN 5.208-05

AR3014506

SUSSEX COUNTY LANDFILLMONITORING WELLS - LD-1, LS-7R, LS-16

SIDENTIAL USE SCENARIO - CURRENT AND FUTURE USE

ESTION OF GROUNDWATER BY CHILDREN

NONCARCINOGENIC RISKCONTAMINANT CONC. ADI HI

(ug/L) (mg/kg/day)VINYL CHLORIDE 2.00E+00 2.56E-04 N/ABENZENE 9.00E+00 1.15E-03 N/A1,2-DICHLOROPROPANE l.OOE+00 1.28E-04 N/A1,4-DICHLOROBENZENE 4.00E+00 5.1IE-04 N/ATRICHLOROETHYLENE 2.00E+00 2.56E-04 4.26E-02

TOTAL INGESTION HAZARD INDEX 4.26E-02




VINYL CHLORIDE 1.12E+01 1.49E-04 N\ABENZENE 4.43E+01 5.90E-04 1.03E+011,2-DICHLOROPROPANE 3.94E+00 5.25E-05 4.60E-021,4-DICHLOROBENZENE 1.42E+01 1.89E-04 8.26E-04TRICHLOROETHYLENE 7.89E+00 1.05E-04 1.75E-02TOTAL INHALATION HAZARD INDEX 1.04E+01

DERMAL CONTACT WITH VOLATILES DURING SHOWERING AND BATHING BY CHILNONCARCINOGENIC RISK

TAMINANT CONC. ADI HI(ug/L) (mg/kg/day)

TNYL CHLORIDE 2.00E+00 7.09E-07 N/ABENZENE 9.00E+00 4.90E-06 N/A1,2-DICHLOROPROPANE l.OOE+00 5.14E-07 N/A1,4-DICHLOROBENZENE 4.00E+00 3.70E-06 N/ATRICHLOROETHYLENE 2.00E+00 1.22E-06 2.04E-04

TOTAL INHALATION HAZARD INDEX 2.04I»04

TOTAL CHILD HAZARD INDEX VALUES BY CONTAMINANT

NONCARCINOGENIC RISKCONTAMINANT HI

VINYL CHLORIDE N/ABENZENE 1.03E+011,2-DICHLOROPROPANE 4.60E-021,4-DICHLOROBENZENE 8.26E-04TRICHLOROETHYLENE ' 6.03E-02COMBINED TOTAL HAZARD INDEX FOR CHILDREN 1.04E+01

PollutantAdult TemplateChild Template


Oral RfD: Inhaled RfD:(mg/kg/d) (mg/kg/d)

Oral InhaledPotency PotencyFactor: Factor:(1/(mg/kg/d)) (1/(mg/kg/d))

SUSSEXCOUNTY LANDFILLLD-I, LS-7R, LS16VINYL CHLORIDE 1.90E+00 3.00E-01

1.90E+00 3.00E-01

BENZENE 5.71E-05 2.90E-02 2.91E-025.71E-05 2.90E-02 2.91E-02

1,2-DICHLOROPROPANE 1.14E-03 6.80E-021.14E-03 6.80E-02

1,4-DICHLOROBENZENE 2.29E-01 2.40E-022.29E-01 2.40E-02

TRICHLOROETHYLENE 6.00E-03 1.10E-02 6.00E-036.00E-03 1.10E-02 6.00E-03


Ambient Lifetime Chronic Upper BoundCone. Intake Intakt Lifetime Hazard Index(ug/l) mg/kg/d mg/kg/d Cancer Risk (intake/RfD)

O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00 O.OOE+00 O.OOE+00 O.OOE+00


9.00E+00 1.06E-04 2.47E-04 3.06E-06 O.OOE+009.00E+00 9.86E-05 1.15E-03 2.86E-06 O.OOE+001.00E+00 1.17E-05 2.74E-05 7.98E-07 O.OOE+001.00E+00 1.10E-05 1.28E-04 7.45E-07 O.OOE+00


2.00E+00 2.35E-05 5.48E-05 2.58E-07 9.13E-032.00E+00 2.19E-05 2.56E-04 2.41E-07 4.26E-02

ADULT RISK ADULT HI4.996-05 9.13E-03

CHILD RISK CHILD HI4.65E-OS 4.26E-02

INHALATION DURING SHOWERING AND BATHING (Foster & Chrostowski, 1986)

Molecular Henry's [Overall mCConcentraCConcentraWeight Constant Kl Kg KL KLts Cd Ca(g/mole) (atm-mS/mole) (cm/h) (cm/h) (cm/h) (cm/h) (ug/l) ug/m3)9.21E+016.70E-031.38E+011.33E+031.33E+011.78E+01O.OOE+00 O.OOE+009.21E+01 6.70E-03 1.38E+01 1.33E+03 1.33E+01 1.78E+01 O.OOE+00 O.OOE+00

6.30E+016.30E+01

7.80E+017.80E+01

1.13E+021.13E+02

1.47E+021.47E+02

1.31E+021.31E+02

8.19E-028.19E-02

5.59E-035.59E-03

2.31E-032.31E-03

2.89E-032.89E-03

9.10E-039.10E-03

1.67E+011.67E+01

1.50E+011 .50E+01

1.25E+011.25E+01

1.09E+011.09E+01

1.16E+011.16E+01

1.60E+031 .60E+03

1.44E+031.44E+03

1.20E+031.20E+03

1.05E+031.05E+03

1.11E+031.11E+03

1.67E+011.67E+01

1.44E+011 .44E+01

1.13E+011.13E+01

1.01E+011.01E+01

1.13E+011.13E+01

2.23E+012.23E+01

1.93E+011 .93E+01

1.51E+011.51E+01

1 .35E+011 .35E+01

1.51E+011.51E+01

1.0SE+003.30E-01

4.26E+001 .30E+00

3.95E-011.16E-01

1 .45E+004.18E-01

7.91E-012.32E-01

3.57E+011.12E+01

1 .45E+024.43E+01

1.34E+013.94E+00

4.93E+011 .42E+01

2.69E+017.89E+00

(Foster t Chrostowski, continued)(Cancer) (Non-cancer)Lifetime Chronic Upper BoundIntake Intake Lifetime Hazard Index

mg/kg/d mg/kg/d Cancer Risk (Intake/RfD)O . O O E + 0 0 O . O O E + 0 0 O . O O E + 0 0 O . O O E + 0 0O.OOE+00 O.OOE+00 O.OOE+00 O.OOE+00

5.82E-05 1.36E-04 1.75E-05 O.OOE+001.28E-05 1.49E-04 3.84E-06 O.OOE+00

2.36E-04 5.52E-04 6.88E-06 9.66E+005.05E-05 5.90E-04 1.47E-06 1.03E+012.19E-05 5.11E-05 O.OOE+00 4.49E-024.50E-06 S.2SE-05 O.OOE+00 4.60E-02

8.03E-05 1.87E-04 O.OOE+00 8.19E-041.62E-05 1.89E-04 O.OOE+00 8.26E-04

4.39E-05 1.02E-04 2.63E-07 1.71E-029.01E-06 1.05E-04 5.40E-08 1.75E-02



DERMAL INTAKE DURING BATHING (Foster I Chrostouski, 1986)Average Octanol: (Cancer) (Non-cancer)Bathwater Water Lifetime Chronic Upper Bound

Concentration Part. Coeff. Intake Intake Lifetime Hazard Index(ug/l) (KOM) mg/kg/d mg/kg/d Cancer Risk (Intake/RfD)

O.OOE+00 6.90E+02 O.OOE+00 O.OOE+00 O.OOE+00 O.OOE+00

2.00E+002.00E+00 1.38E+00 6.08E-08 7.09E-07 1.16E-07 O.OOE+00

9.00E+009.00E+00 2.12E+00 4.20E-07 4.90E-06 1.22E-08 O.OOE+00

1.00E+001.00E+00 2.00E+00 4.41E-08 S.14E-07 3.00E-09 O.OOE+00

4.00E+004.00E+00 3.60E+00 3.17E-07 3.70E-06 7.61E-09 O.OOE+002.00E+002.00E+00 2.38E+00 1.0SE-07 1.22E-06 1.15E-09 2.04E-04

CHILD RISK CHILD HI1.39E-07 2.04E-04




6.21E-05 O.OOE+004.S6E-05 O.OOE+00

9.95E-06 9.66E+004.34E-06 1.03E+01

7.98E-07 4.49E-027.48E-07 4.60E-02

1.13E-06 8.19E-041.06E-06 8.26E-04

5.22E-07 2.62E-022.96E-07 6.03E-02


CHILD RISK CHILD HI5.20E-OS 1.04E+01

Pollutant

Adult TemplateChild Template




SUSSEX COUNTY LANDFILL GW-33

BERYLLIUM 5.00E-035.00E-03

4.30E+00 8.40E+004.30E+00 8.40E+00



O . O O E + 0 0 O . O O E + 0 0 0 . O O E + 0 0 O . O O E + 0 0O.OOE+00 O.OOE+00 O.OOE+00 O.OOE+00

2.90E+00 3.41E-05 7.95E-OS 1.46E-04 1.59E-022.90E+00 3.18E-05 3.71E-04 1.37E-04 7.42E-02



O . O O E + 0 0 O . O O E + 0 0 O . O O E + 0 0 O . O O E + 0 0O.OOE+00 O.OOE+00 O.OOE+00 O.OOE+00

2.90E+00 3.41E-05 7.95E-05 1.46E-04 1.59E-022.90E+00 3.18E-05 3.71E-04 1.37E-04 7.42E-02

AR3Qi*5l6




1.46E-04 1.59E-021.37E-04 7.42E-02

Pollutant

Adult TemplateChild Template




SUSSEX COUNTY LANDFILL LS-09

BERYLLIUM 5.00E-035.00E-03

4.30E+00 8.40E+004.30E+00 8.40E+00



——————————o.oOE+00 O.OOE+00 O.OOE+00 O.OOE+00O.OOE+00 O.OOE+00 O.OOE+00 O.OOE+00

5.80E+00 6.81E-05 1.59E-04 2.93E-04 3.18E-025.80E+00 6.36E-05 7.42E-04 2.73E-04 1.48E-01

AR3Q145I9




2.93E-04 3.18E-022.73E-04 1.48E-01

REFERENCES

Benzene

Agency for Toxic Substances and Disease Registry (ATSDR) 1989.Toxicological Profile for Benzene, Oak Ridge National Laboratoryunder DOE Interagency Agreement No. 1857-B026-A1.

Agency for Toxic Substances and Disease Registry (ATSDR) 1990.Toxicological Profile for Chlorobenzene. TP-90-06.

Agency for Toxic Substances and Disease Registry (ATSDR) 1989.Toxicological Profile for Toluene.

Agency for Toxic Substances and Disease Registry (ATSDR)Draft Toxicological Profile for Benzene. United States Departmentof Health and Human Services. ATSDR. Atlanta: ATSDR.

Aksoy, M. 1985. Malignancies due to occupational exposure tobenzene. Am. J. Ind. Med. 7:395-402.

American Conference of Governmental Industrial Hygienists(AC6IH). 1986. Documentation of the Threshold Limit Values andBiological Exposure Indices. 5th ed. Cincinnati, Ohio.

American Conference of Governmental Industrial Hygienists(ACGIH). 1990. Documentation of Threshold Limit Values andBiological Exposure Indices. 5th ed. Cincinnati, Ohio.

Andrew, F.D., R.L. Buschbom, R.A. Cannon, L.F. Miller, D.W.Montgomery, Phelps, et al. 1981. Teratologic assessment ofethylbenzene- and 2-ethyoxyethanol. Battelle Pacific NorthwestLaboratory, Richland, Washington. PB-83208074.

Bowers, S.E., M.S. Cannon, and D.H. Jones 1982 Ultrastructuralchanges in livers of young and aging rats exposed to methylatedbenzenes Am. J. Vet. Res 43:679-683.

Carpenter, C.P., E.R. Kinkead, D.J. Gerary, Jr., L.J. Sullivan,and J.M. King. 1975. Petroleum hydrocarbon toxicity studies.v. Animal and human response to vapors of mixed xylanes.Toxicol. Appl. Pharmacol. 33:543-558.

Chemical Industry Institute of Toxicology (CUT). 1980. Atwenty-four month inhalation toxicology study in Fischer-344 ratsexposed to atmospheric toluene. Executive Summary and DataTables. October 15, 1980.

Chin, B.H., J.A. McKelvey, T.R. Tyler, L.J. Calisti, S.J.Kozbelt, and L.J. Sullivan. 1980. Absorption, distribution andexcretion of ethlbenzene, ethyleyclohexane and methylethylbenzene isomers in rats. Bull. Environ. Contam. Toxicol.24:477-483 (As cited in EPA 1985a).

Cronkite, E.P., R.T. Drew, T. Inone, and J.E. Bullis 1985Benzene hematotoxicity and leukemogenesis Am. J. Ind. Med.7:447-456.

Florin, I., L. Ruthberg, M. curvall, and C.R. Enzell. 1980.Screening of Tobacco Smoke Constituents for Mutagenicity Usingthe Ames Test. Toxicity. 18:219-232 (As cited in USEAP 1985a).

Hardin, B.D., G.P. Bond, M.R. sikov, F.D. Andrew, R.P. Beliles,and R.W. Niemeier. 1981. Testing of Selected Workplace chemicalsfor Teratogenic Potential. Scand. J. Work Environ. Health7:66-75 (As cited in USEPA 1985a).

Hudak, A. and G. Ungvary, 1978 Embryotoxic Effects of Benzeneand its Methyl Derivatives: Toluene in the Mouse, Abstract,Teratology 19:41A.

International Agency for Research on Cancer (IARC). 1982. IARCMonographs on the Evaluation of the Carcinogenic Risk ofChemicals to Humans. Volume 27: Some Aromatic Amines,Anthraquinonea and Nitroso Compounds, and Inorganic FluoridesUsed in Drinking-Water and Dental Preparations. World HealthOrganization, Lyon, France.

Jenkins, L.J., Jr., R.A. Jones, and J. Siegal 1970 Long-terminhalation screening studies on benzene, toluene, o-xylene, andcumene on experimental animals Toxicol Appl. Pharmacol.16:818-823.

Knapp, W.K., W.M. Busey, W. Kudzins. 1972. Subacute OralToxicity of Monochlorobenzene in Dogs and Rats. Toxicol• Appl.Pharmacol. 19:393.

Litton Bionetics. 1978. Teratology studies in rats: Xylene.Final report to American Petroleum Institute, Washington, D.C.LSI Project No. 20698-5 (As cited in USEPA 1984).

National Academy of Science (NAS). 1987. Health Effects ofBenzene: A Review Committee on Toxicology, Assembly of lifeSciences. National Research council, Washington, D.C.National Toxicology Program (NTP) 1985 Toxicology andCarcinogenesis studies of Benzene (CAS No. 71-43-2) in F344/NRats and B6C3F1 Mice (Gavage Studies) Technical Report Series No289 NIH Publication No. 86-2545.

National Toxicology Program (NTP). 1986. NTP Technical Reporton the Toxicology and Carcinogenesis of Xylenes (MXED) in F344/NRats and B6C3F1 Mice. NTPTR 327. NIH Publ. No. 86-2583.

Nawrot, P.S., and R.E. Staples. 1979. Embryo-fetal toxicity an

AR30U522

teratogenicity of benzene and toluene in the mouse. Teratology19:41A (Abstract).

Ott, M.G., J.C. Townsend, W.A. Fishbeck, and R.A. Langner 1978Mortality Among individuals occupationally exposed to benzeneArch. Environ. Health 33:3-10.

Rinsky, R.A., A.B Smith, R. Hornung, T.G. Filloon, R.J. Young,A.H. Okun, and P.J. Long 1987. Benzene and Leukemia: AnEpidemiologic Risk Assessment. N. Eng. j.Med. 316:1044-1050.

Rinsky, R.A., R.J. Young, and A.B. Smith. 1981. Leukemia inbenzene workers. Am. J. Ind. Med. 3:217-255.

Snyder, C.A., B.D Goldstein, A.R. Sellakumar, I. Bromberg, S.Laskin, and R.E. Albert. 1980. The inhalation toxicology ofbenzene: Incidence of hematopoietic neoplasms and hematotoxicityin AKR/J and C57BL/6J mice. Toxicol. Appl. Pharmacol.54:323-331.

U. S. Environmental Protection Agency (EPA) 1980. Ambient WaterQuality Criteria for Benzene. Environmental Criteria andAssessment Office, Cincinnati, Ohio. EPA 40/5-80-0018. NTIS PB81-117293.

U. S. Environmental Protection Agency (EPA) 1980. Ambient WaterQuality Criteria for Ethylbenzene. Office of Water Regulationsand Standards, Washington, D.C. October 1980. EPA 440/5-80-048.

U. S. Environmental Protection Agency (EPA) 1987.Chlorobenzene. Health Adviiory office of Drinking Water•Washington, D.C.

U. S. Environmental Protection Agency (EPA) 1985. Draft HealthAdvisory for Benzene. Office of Drinking Water, Washington, D.C.September 30.

U. S. Environmental Protection Agency (EPA) 1935. Draft HealthAdvisory of Ethylbenzene. Office of Drinking Water, Washington,D.C. September.

U. s. Environmental Protection Agency (EPA) 1985. DrinkingWater Criteria Document for Benzene (Final Draft). Office ofDrinking Water, Washington, D.C. April 1985.U. S. Environmental Protection Agency (EPA) 1985. DrinkingWater Criteria Document for Hexachlorobenzene. EnvironmentalCriteria and Assessment Office, Cincinnati, Ohio. ECAO-CIN-424.(Final Draft).

U. S. Environmental Protection Agency (EPA) 1985. Drinking

Water Criteria Document for Toluene. Office of Drinking Water,Washington, D.C. March.

U. S. Environmental Protection Agency (EPA) 1984. DrinkingWater Criteria Document for Xylene. Environmental Criteria andAssessment Office, Cincinnati, Ohio. September 1984. EPA540/1-86-066.

U. S. Environmental Protection Agency (EPA) 1985. DrinkingWater Criteria Document of Xylenes (Final Draft). EnvironmentalCriteria and Assessment Office, Cincinnati, Ohio. March 1985.ECAO-CIN-416. EPA 600

U. S. Environmental Protection Agency (EPA) 1991. DrinkingWater Regulations and Health Advisories by Office of WaterWashington, D.C. November 1991.

U. S. Environmental Protection Agency (EPA) 1986. Evaluation ofthe Potential Carcinogenicity of Benzene (71-43-2). Prepared byCarcinogen Assessment Group for the Office of Response.Washington, D.C. OHEA-C-073-29.

U. S. Environmental Protection Agency (EPA) 1986. Guidelinesfor carcinogenic risk assessment. Red. Reg. 51:33992-34003.(September 24).

U. S. Environmental Protection Agency (EPA)1993. HazardousSubstances Database (HSDB).

U. S. Environmental Protection Agency (EPA) 1987. HealthAdvisories for 25 Organics. Office of Drinking Water.Washington, D.C. PB87-235578.U. S. Environmental Protection Agency (EPA) 1985. HealthAssessment Document for Chlorinated Benzenes: Final Report. EPA600/8-84/015F.

U. S. Environmental Protection Agency (EPA) 1984. HealthEffects Assessment for Benzene. Environmental Criteria andAssessment Office. Cincinnati, Ohio. September 1984. EPA 540

U. S. Environmental Protection Agency (EPA) 1984. HealthEffects Assessment for Chlorobenzene. EPA 540/1-86/040.

U. S. Environmental Protection Agency (EPA) 1984. HealthEffects Assessment for Ethylbenzene. Environmental Criteria andAssessment Office, Cincinnati, Ohio. September 1984. EPA540-1-86-008.

U. S. Environmental Protection Agency (EPA) 1984. HealthEffects Assessment for Toluene. Final Draft. EnvironmentalCriteria and Assessment Office, Cincinnati, Ohio. September

1984. EPA 540

U. S. Environmental Protection Agency (EPA) 1989. HealthEffects Assessment Summary Tables. Fourth Quarter EnvironmentalCriteria and Assessment Office, Cincinnati, Ohio.

U. S. Environmental Protection Agency (EPA) 1992. IntegratedRisk Information System. Cincinnati, Ohio.U. S. Environmental Protection Agency (EPA) 1992. IntegratedRisk Information System. Benzene. June 1992.

U. S. Environmental Protection Agency (EPA) 1992. IntegratedRisk Information System. Ethylbenzene. June 1992.

U. S. Environmental Protection Agency (EPA) 1985. Nationalprimary drinking water regulations, volatile synthetic organicchemicals, proposed rulemaking. Fed. Reg. 50:46901-46933(November 13).

U. S. Environmental Protection Agency (EPA) 1987. NationalPrimary Drinking Water Regulations: Synthetic Organic Chemicals;Monitoring for Unregulated Contaminants. Final Rule. FederalRegister 52:25690-25717.

U. S. Environmental Protection Agency (EPA) 1985. Nationalprimary drinking water regulations; synthetic organic chemicals,inorganic chemicals and microorganisms, proposed rule. Fed. Reg.50:46936-47022. (November 13).

U. S. Environmental Protection Agency (EPA) 1985. Nationalprimary drinking water regulations; synthetic organic chemicals,inorganic chemicals and microorganisms, proposed rule. Fed. Reg.50:46936-47025. (November 13).

U. S. Environmental Protection Agency (EPA) 1985. Nationalprimary drinking water regulations; volatile synthetic organicchemicals, final rule. Fed. Reg. 50:46880-46901 (November 13).

U. S. Environmental Protection Agency (EPA) 1986. VerifiedReference Doses (RfDs) of the USEPA (Including Addendum of May14, 1986) ADI Work Group of the Risk Assessment Forum,Washington, D.C. January 1986. ECAO-CIN-475.

U. S. Environmental Protection Agency (EPA) 1980 Ambient WaterQuality Criteria for Benzene Environmental Criteria andAssessment Office, Cincinnati, Ohio EPA 40/5-80-0018 NTIS PB81-117293.

U. S. Environmental Protection Agency (EPA) 1980. Ambient WaterQuality Criteria for Benzene. Environmental Criteria and

AR30W25

Assessment Office, Cincinnati, Ohio. EPA 40/5-80-0018. NTIS PB81-117293.

U. S. Environmental Protection Agency (EPA) 1985 Draft HealthAdvisory for Benzene Office of Drinking Water, Washington, D.CSeptember 30.

U. S. Environmental Protection Agency (EPA) 1985. Draft HealthAdvisory for Benzene. Office of Drinking Water, Washington, D.C.September 30.

U. S. Environmental Protection Agency (EPA) 1985 Drinking WaterCriteria Document for Benzene (Final Draft) Office of DrinkingWater, Washington, D.C April 1985.

U. S. Environmental Protection Agency (EPA) 1985. DrinkingWater Criteria Document for Benzene (Final Draft). Office ofDrinking Water, Washington, D.C. April 1985.

U. S. Environmental Protection Agency (EPA) 1986 Evaluation ofthe Potential Carcinogenicity of Benzene (71-43-2) Prepared byCarcinogen Assessment Group for the Office of ResponseWashington, D.C OHEA-C-073-29.

U. S. Environmental Protection Agency (EPA) 1986. Evaluation ofthe Potential Carcinogenicity of Benzene (71-43-2). Prepared byCarcinogen Assessment Group for the Office of Response.Washington, D.C. OHEA-C-073-29 .

U. S. Environmental Protection Agency (EPA) 1986 Evaluation ofthe Potential Carcinogenicity of Benzene. Review Draft.Carcinogen Aiissi&ent Group, Office of Health and EnvironmentalAssessment. OHEA-C-073-29.

U. S. Environmental Protection Agency (EPA) 1984 Health EffectsAssessment for Benzene Environmental Criteria and AssessmentOffice Cincinnati, Ohio

09/01/84 EPA 540/1-86-037.

U. S. Environmental Protection Agency (EPA) 1984. HealthEffects Assessment for Benzene. Environmental Criteria andAssessment Office. Cincinnati, Ohio. September 1984. EPA540/1-86-037.

Wolf, M., V. Rowe, D. McCollister, R. Hollingsworth, and F.Oyen, 1956 Toxicoloigcal Studies of Certain Alkylated Benzenesand Benzene, Archives of Industrial Health 14:387-398.

Wong, O. 1982. An Industry-wide Mortality Study of ChemicalWorkers Occupationally Exposed to Benzene. Prepared for theChemical Manufacturers Association by Environmental HealthAssociates, Oakland, California.

AR30!*526

REFERENCES

Beryllium

Agency for Toxic Substances and Disease Registry (ATSDR).Toxicological Profile for Beryllium. United States Department ofHealth and Human Services, Public Health Service. Atlanta: ATSDR.ATSDR/TP-88/07.

Agency for Toxic Substances and Disease Registry (ATSDR).Toxicological Profile for Beryllium. Prepared by SyracuseResearch Corporation under Contract 68-C8-0004. U.S. PublicHealth Service. ATSDR/TP-88/09.

Bayliss, D.L. and J.K. Wagoner. Bronchogenic cancer andcardio-respiratory disease mortality among white males employedin a beryllium production facility. OSHA Beryllium hearing, 1977,Exhibit 13.F. (Cited in U.S. EPA, 1987a).

Bayliss, D.L. and W.S. Lainhart. Mortality patterns inberyllium production workers. Presented at the Am. Ind. HygieneAssoc. Conf. OSHA Exhibit No. 66, Docket No. H005. (Cited inU.S. EPA, 1987a).

Bayliss, D.L., W.S. Lainhart, L.J. Crally, R. Ligo, H. Ayer andF. Hunter. Mortality patterns in a group of former berylliumworkers. In: Tran. 334rd Ann. Meeting ACGIH, Toronto, Canada.p. 94-107. (Cited in U.S. EPA, 1987a).

Constantinidis, K. Acute and chronic beryllium disease. Br. J.Clin. Praot. 32i 127- 136. (Cited in U.S. SPA, 1987a).Crowley, J.F., J.6. Hamilton and K.J. Scott. The metabolism ofcarrier-free radioberyllium in the rat. J. Biol. Chem. 177:975-984.

Freiman, D.G. and H.L. Hardy. Beryllium disease: the relationof pulmonary pathology to clinical course and prognosis based ona study of 130 cases from the U.S. Beryllium Case Registry. Hum.Pathol. 1: 25-44. (Cited in Kriebel et al., 1988b).

Hall, T.C., C.H. Wood, J.D. Stoeckle and L.B. Tepper. Case datafrom the Beryllium Registry. Am. Med. Assoc. Arch. Ind. Health19: 100-103.

Kriebel, D., J.D. Brain, N.L. Sprince and H. Kazemi. Thepulmonary toxicity of beryllium. Am. Rev. Respir Dis. 137:464-473.

Kriebel, D., N.L. Sprince, E.A. Eisen, I.A. Greaves, H.A.Feldman and R.E. Greene. Beryllium exposure and pulmonary

function: A cross sectional study of beryllium workers. Br. J.Ind. Med. 45: 167-173.

Mancuso, R.F. Mortality study of beryllium industry workers'occupational lung cancer. Environ. Res. 21: 48-55.

Mancuso, T.F. Occupational lung cancer among beryllium workersin dusts and disease. In: R. Lemen and J. Dement, Eds. Proc.Conf. Occup. Exp. to Fibrous and Particulate Dust and TheirExtension into the Environment. Pathrotox Publishers, Inc.(Cited in USEPA, 1987).

Mancuso, T.F. Relation of duration of employment and priorillness to respiratory cancer among beryllium workers. Environ.Res. 3: 251-275.

Meehan, W.R. and L.E. Smyth. Occurrence of beryllium as a traceelement in environmental materials. Environ. Sci. Technol. 1:839-844.

Nishimura, M. Clinical and experimental studies on acuteberyllium disease. Nagoya J. Med. Sci. 18: 17-44. (Cited in U.S.EPA, 1987a).

Reeves, A.L. The absorption of beryllium from thegastrointestinal tract. Arch. Environ. Health 11: 209-214.

Reeves, A.L. and A.J. Vorwald. Beryllium Carcinogenesis. II.Pulmonary deposition and clearance of inhaled beryllium sulfatein the rat. Cancer Res. 27: 446-451.

Reeves, A.L. and D. Deitch. Influence of age on thecarcinogenic response to beryllium inhalation. In: S. Harishima,Ed. Proc. 16th Internat. Cong. Occup. Health, Tokyo, Japan.Japan Industrial Safety Association, Tokyo, Japan, p. 651-652.

Schepers, G.W.H., T.M. Durkan, A.B. Delahant and F.T. Creedon.The biological action of inhaled beryllium sulfate: Apreliminary chronic toxicity study on rats. Am. Med. Assoc Arch.Ind. Health 15: 32-38.Schroeder, H.A. and M. Mitchener Life-term studies in rats;Effects of aluminum, barium, beryllium and tungsten J. Nutr. 105:421-427.

Stiefel, T., K. Schulze, H. Zorn and G. Tolg. Toxicokinetic andtoxicodynamic studies of beryllium. Arch. Toxicol. 45: 81-92.

Tepper, L.B., H.L. Hardy and R.J. Chamberlin. Toxicity ofBeryllium Compounds. Elsevier, New York, pp. 146-168. (Cited in

ATSDR, 1988).

U. S. Environmental Protection Agency (EPA). Drinking Watercriteria Document for Beryllium. Prepared by the Office of Healthand Environmental Assessment, Environmental Criteria andAssessment Office, Cincinnati, OH for the office of DrinkingWater.

U. S. Environmental Protection Agency (EPA). Health AssessmentDocument for Beryllium. Prepared by the Office of Health andEnvironmental Assessment, Environmental Criteria and AssessmentOffice, Research Triangle Park, NC. External Review.

U. S. Environmental Protection Agency (EPA). Health AssessmentDocument for Beryllium. Office of Health and EnvironmentalAssessment, U.S. EPA. (EPA/600/8-84/026F).

U. S. Environmental Protection Agency (EPA). Health EffectsAssessment for Beryllium and Compounds. Prepared for Office ofSolid Waste and Emergency Response by Environmental Criteria andAssessment Office, Office of Health and Environmental Assessment,Environmental Criteria and Assessment Office, Cinncinati, OHECAO-CINN-H108.

Vorwald A.J., P.C. Pratt and E.J. Urban. The production ofpulmonary cancer in albino rats exposed by inhalants to anaerosol of beryllium sulfate. Acta. Unio. Int. Cancrum. 11: 735.(Cited in U.S. EPA, 1987a).

Vorwald, A.J. Adenocarcinoma in the lung of albino rats exposedto compounds of beryllium. In: Cancer of the Lung - AnEvaluation of the Problem. Proc. of the Scientific Session,Annual Meeting, November. Am. cancer Soc., New York. p. 103-109. (Cited in U.S. EPA, 1987a).Vorwald, A.J., A.L. Reeves and E.J. Urban. Experimentalberyllium toxicology. In: H.E. Stokinger, Ed. Beryllium - Itsindustrial Hygiene Aspects. Academic Press, New York. pp.201-234.

Wagoner, J.K., P.P. Infante and D.L. Bayliss. Beryllium: Anetiologic agent in the induction of lung cancer, nonneoplasticrespiratory disease and heart disease among industrially exposedworkers. Environ. Res. 21: 15-34.

General

Clement Associates, Inc. for the United States EnvironmentalProtection Agency. 1985. Chemical, Physical, and BiologicalProperties of Compounds at Hazardous Waste Sites. Final Report.

Sittig, M. 1985. Handbook of Toxic and Hazardous Chemicals andCarcinogens. Second Edition. Noyes Publications, Park Ridge,New Jersey.

United States Environmental Protection Agency. 1986. SuperfundPublic Health Evaluation Manual. Office of Emergency andRemedial Response, Washington, D.C.

United States Environmental Protection Agency. 1989. ExposureFactors Handbook. EPA/600/8-89/043. Exposure Assessment Group,Office of Health and Environmental Assessment, Washington, D.C.May.United States Environmental Protection Agency. 1989. RiskAssessment Guidance for Superfund. Volume I: Human HealthEvaluation Manual (Part A). Interim Final. Office of Emergencyand Remedial Response, Washington, D.C. December 1989.

United States Environmental Protection Agency. 1991. HumanHealth Evaluation Manual, Supplemental Guidance: Standard DefaultExposure Factors. OSWER Directive 9285.6-03. Office of SolidWaste and Emergency Response, Washington, D.C. March 25.

Agency for Toxic Substances and Disease Registry (ATSDR) 1988. Draft ToxicologicalProfile for Trichloroethylene. U.S. Public Health Service. January 1988.

Agency for Toxic Substances and Disease Registry (ATSDR) 1992. Draft ToxicologicalProfile for Trichloroethylene. U.S. Public Health Service 1992.

Agency for Toxic Substances and Disease Registry (ATSDR) Toxicological Profile forTrichloroethylene. Prepared by Syracuse Research Corporation, under Contract No.68-C8-0004 for ATSDR, U.S. Public Health Service. ATSDR/TP-88/24.

Axelson O. 1986. Epidemiological studies of workers exposed to tri- and tetrachloro-ethylenes. In: Chambers, P.L., Gehring, P., and Sasaki, F., eds. New Concepts andDevelopments in Toxicology. Proceedings of the 4th International Congress ofToxicology. Amsterdam, the Netherlands.

Barret L, Faure J,'and Danel V. 1985. Epidemiological study of cancer in a communityof workers occupationally exposed to trichloroethylene and cutting oil. J Toxicol ClinToxicol; 23:4-6. (As cited in ATSDR 1988).

Beliles, R.P., DJ. Bursisk and FJ. Meclec. 1980. Teratogenic, mutagenic risk ofworkplace contaminants; trichloroethylene, perchloroethylene and carbon disulfide.Unpublished studies U.S. Dept of Health, Education and Welfare. Contract 210-77-0047, Litton Bionetics Inc., Kensington, MD. (Cited in EPA, 1988).

Bell, Z.G., K.H. Olson and TJ. Benja. Final Report of Audit Findings of theManufacturing Chemists Association: Administered Trichloroethylene Chronic InhalationStudy at Industrial Biotest Laboratories, Inc., Decatur, IL. Unpublished. (Cited in U.S.EPA, 1987).

Buben JA, and O' Flaherty EJ. 1985 Delineation of the role of metabolism in thehepatotoxicity of trichloroethylene and perchloroethylene: A dose-effect. Toxicol ApplPharmacol; 78:105-122.

Cerna M, and Kypenova H. 1977. Mutagenic activity of chloroethylenes analyzed byscreening system tests. Mutat Res; 46:214-215.

Defalque, J.R. Pharmacology and toxicology of trichloroethylene. A critical review ofthe world literature. Clin. Pharmacol. Ther. 2: 665-688. (Cited in IARC, 1979).

Dorfmueller MA, Henne SP, York RG, Bornschein RL, Manson JM. 1979. Evaluationof teratogenicity; and behavioral toxicity with inhalation exposure of maternal rats totrichloroethylene. Toxicology; 14:153-166. (As cited in ATSDR 1988).

Fukuda K, Takemoto K, Tsurauta H. 1983. Inhalation Carcinogenicity oftrichlorethylene in mice and rats. Ind Health; 21:243-254. (As cited in ATSDR 1988).

Grandjean E, Muchinger R, Turrian V, Haas PA, Knownpfel HK, Rosenmund 1955Investigations into the effect of exposure to trichloroethylene in mechanical engineering.BrJIndMed; 12:131-142.

Gu, ZW, Sele B, Jalbert P, et al. 1981. Induction d'echanges entre les chromatidessours (SCE) par le trichloroethylene at ses metabolites. Toxicolo Eur Res; 3:63-67. (Ascited in ATSDR 1988).

Healy TE, Poole TR, and Hooper A. 1982. Rat fetal development and maternalexposure to tri-chloroethylene at 100 ppm. Br J Anaesth; 54:337-341 (-as cited inATSDR 1988).

Henschler, D. and R. Hoos. Metabolic activation and deactivation mechanisms of di,tri, and tetrachloroethylenes. In Snyder, R., et al., Eds. Biological Reactive

5R3QU532

Intermediates-II: Chemical Mechanisms and Biological Effects. Plenum Press, NewYork. p. 659-666.

Kjellstrand, P., B. Holmquist, P. Aim, et al. Trichlorothylene: Further studies of theeffects on body and organ weights and plasma butyryl cholinesterase activity in mice.Acta Pharmacol. Toxicol. 53: 375-384.

Kjellstrand, P., M. Kanje, L. Manson, et al. Trichloroethylene: Effects on body andorgan weights in mice, rats, and gerbils. Toxicology 21: 105-115.

Landrigan, P.J., G.F. Stein, J.R. Kominski, et al. Common-source community andindustrial exposure to trichloroethylene. Arch. Environ. Health 42: 327-332.

Maltoni C, Lefemine G, Cotti G. 1986. Experimental research on trichloroethylenecarcino- genesis. In: Maltoni C, and Mehlman MA, eds. Archiv. Res. IndustrialCarcinogenesis Series, Vol V. Princeton, NJ: Princeton Scientific Publishing Co., Inc. p.393. (As cited in ATSDR 1988).

Maltoni, C., G. Lefemine, G. Gotti, et al. Long-term Carcinogenicity bioassays ontrichloroethylene administered by inhalation to Sprague-Dawley rats and Swiss andB6C3F1 mice. Ann. N.Y. Acad. Sci. 534: 316-342.

Mazza, V. and A. Brancaccio. Characteristics of the formed elements of the blood andbone marrow in experimental trichloroethylene intoxication. Folia Med. 50: 318- 324.(Cited in U.S. EPA, 1985)

Milby, T.H. Chronic trichloroethylene intoxication. J. Occup. Med. 10: 252-254.

Monster, A. Difference in uptake, elimination, and metabolism in exposure totrichloroethylene, 1,1,1-trichloroethane and tetrachloroethylene. Int. Arch. OccupEnviron. Health 42: 311-317.

National Toxicology Program (NTP). Carcinogenesis Bioassay of Trichloroethylene inF344 Rats and B6C3F1 Mice. CAS No. 79-01-6. U.S. Department of Health.and HumanServices, National Institutes of Health, Bethesda, MD. NTP 81-84, NIH Publ. 82-1799.

Nelson JL, and Bull RJ. 1986. Induction of DNA strand breaks in rat liver withtrichloroethylene (TCE). Pharmacologist; 28:182. (As cited in ATSDR 1988).

Nomiyama K, and Nomiyama H. 1974. Reevaluation of subchronic toxicity oftrichloroethylene. Toxicol Lett; 31(Suppl):225 (abstract). (As cited in ATSDR 1988).

Sanders, V.M., A.N. Tucker, K.L. White, Jr., et al. Humoral and cell-mediated immunestatus in mice exposed to trichloroethylene in drinking water. Toxicol. Appl. Phannacol.62: 358-368.

Sato A, and Nakajima T. 1978. Differences following skin or inhalation exposure in theabsorption and excretion kinetics of trichloroethylene and toluene. Br J Ind Med; 35:43-49. (As cited in ATSDR 1988).

Savolainen, H., P. Paffli, M. Tengen, et al. Trichloroethylene and 1,1,1- trichloroethane:Effects on brain and liver after five days intermittent inhalation. Arch. Toxicol. 38:229-237.

Schwetz BA, Leong KJ, and Gehring PJ. 1975. The effect of maternally inhaledtrichloroethylene, perchloroethylene, methylchloroform, and methylene chloride onembryonal and fetal development in mice and rats. Toxicol Appl Pharmacol; 32:84-96.(As cited in ATSDR 1988).

Stott, W.T., J.F. Quast and P.O. Watanabe. Pharmacokinetics and macromolecularinteractions of trichloroethylene in mice and rats. Toxicol. Appl. Pharmacol. 62: 137-151.

Tucker, A.N., V.M. Sanders, D.W. Barnes, et al. Toxicology of trichloroethylene in themouse. Toxicol. Appl. Pharmacol. 62: 351-357.

U. S. Environmental Protection Agency (EPA) Addendum to the Health AssessmentDocument for Trichloroethylene. Updated Carcinogenicity Assessment forTrichloroethylene. External Review Draft. Office of Health and EnvironmentalAssessment, Office of Research and Development.

U. S. Environmental Protection Agency (EPA) 1992. Hazardous Substances Database.

U. S. Environmental Protection Agency (EPA) Health Assessment Document forTrichloroethylene. Final Report. Office of Health and Environmental Assessment,Environmental Criteria and Assessment Office, Research Triangle Park, NC.EPA/600/8-82/006F.

U. S. Environmental Protection Agency (EPA) 1985. Health Assessment Document forTrichloroethylene. Office of Health and Environmental Assessment. Research TrianglePark, NC.

U. S. Environmental Protection Agency (EPA) 1985. Health Assessment Document forTrichloroethylene. Office of Health and Environmental Assessment. Research TrianglePark,NC.

United States Air Force (USAF) Trichloroethylene. In: The Installation RestorationProgram Toxicology Guide. Vol. 1. pp. 16-1 to 16-36. Wright-Patterson Air Force Base,Ohio: Harry G. Armstrong Aerospace Medical Research Laboratory.

U.S. Environmental Protection Agency (EPA). 1993. Hazardous Substance Database(HSDB).

U.S. Environmental Protection Agency (EPA). 1993. Integrated Risk InformationSystem (IRIS) Database.

BASELINE RISK ASSESSMENT SUSSEX COUNTY LANDFILL #5 · 2020. 7. 5. · quantitative risk assessment...

Documents

Transcript of BASELINE RISK ASSESSMENT SUSSEX COUNTY LANDFILL #5 · 2020. 7. 5. · quantitative risk assessment...