alliant energy corporation interstate power company · 2.3 selection of chemicals of potential...

Alliant Energy CorporationInterstate Power Company

Engineering Evaluation/Cost AnalysisPart II - Baseline Risk AssessmentClinton Manufactured Gas Plant SiteClinton, Iowa

Part II

August 2001

40221549

•VI W M SUPERFUND RECORDSMONTGOMERY WATSON HARZA

ENGINEERING EVALUATION/COST ANALYSISPART II - BASELINE RISK ASSESSMENT

FOR THE

FORMER MANUFACTURED GAS PLANT SITECLINTON, IOWA

Prepared for

ALLIANT ENERGY CORPORATIONMADISON, WISCONSIN

Project No. 1911539.061602

August 2001

Prepared by

Montgomery Watson Harza11153 Aurora Avenue

Des Moines, Iowa 50322515-253-0830


TABLE OF CONTENTS

PAGE

EXECUTIVE SUMMARY ES-1

SECTION! INTRODUCTION 1-11.1 Baseline Risk Assessment Scope and Approach 1-11.2 Organization of the Baseline Risk Assessment 1-21.3 Data Used for Risk Assessment 1-2

SECTION 2 IDENTIFICATION AND SELECTION OF CHEMICALS OF POTENTIALCONCERN 2-1

2.1 Selection of Chemicals of Potential Concern in Soil 2-12.1.1 Surface Soils 2-22.1.2 Subsurface Soils 2-2

2.2 Selection of Chemicals of Potential Concern in Groundwater 2-32.3 Selection of Chemicals of Potential Concern in River Sediment 2-42.4 Selection of Chemicals of Potential Concern in River Surface Water 2-42.5 Summary of Chemicals of Potential Concern 2-5

SECTION 3 TOXICITY ASSESSMENT 3-13.1 Toxicological Effects and Properties 3-1

3.1.1 Noncarcinogenic Effects 3-23.1.2 Carcinogenic Effects 3-3

3.2 Health Effects Criteria for the Chemicals of Potential Concern 3-4

SECTION 4 HUMAN EXPOSURE ASSESSMENT 4-14.1 Site Characterization and Receptor Selection 4-1

4.1.1 Alliant Energy/IPC Property 4-14.1.2 Former Allied Steel Property 4-24.1.3 Off-Site Mississippi River Corridor 4-3

4.2 Potential Exposure Pathways 4-44.2.1 Potential Exposure Pathways Under Present Land

Use Conditions 4-44.2.1.1 Alliant Energy/IPC Property 4-54.2.1.2 Former Allied Steel Property 4-6

4.2.2 Potential Exposure Pathways Under Future Land Use 4-74.2.2.1 Alliant Energy/IPC Property 4-74.2.2.2 Former Allied Steel Property 4-7


TABLE OF CONTENTS (CONTINUED)

PAGE

SECTION 4 HUMAN EXPOSURE ASSESSMENT (CONTINUED)4.2.3 Summary of Potentially Complete Exposure Pathways 4-8

4.2.3.1 Alliant Energy/IPC Property - Present LandUse Conditions 4-8

4.2.3.2 Alliant Energy/IPC Property - Potential FutureConditions 4-8

4.2.3.3 Former Allied Steel Property - Present LandUse Conditions 4-9

4.2.3.4 Former Allied Steel Property - Potential FutureLand Use 4-9

4.2.3.5 Off-Site Mississippi River Corridor - Present andFuture Conditions 4-10

4.3 Quantification of Exposure Point Concentrations 4-104.3.1 Concentrations in Soil 4-114.3.2 Concentrations in Mississippi River Sediment 4-114.3.3 Concentrations in Groundwater 4-11

4.4 Quantification of Exposure 4-124.4.1 Average Chronic Daily Doses Under Present Land

Use Conditions 4-134.4.2 Inhalation, Dermal Contact, and Incidental Ingestion of Soil 4-134.4.3 General Exposure Factors for Soil Contact 4-134.4.4 Incidental Ingestion Factors for Soil Contact 4-144.4.5 Dermal Absorption Factors for Soil Contact 4-154.4.6 Inhalation Exposure Factors for Soil 4-154.4.7 General Exposure Factors for Groundwater Use 4-174.4.8 Summary of Exposure Assessment 4-17

4.4.8.1 Present/Future Conditions 4-174.4.8.2 Potential Future Conditions 4-18

SECTION 5 RISK CHARACTERIZATION 5-15.1 General Methodology 5-1

5.1.1 Noncarcinogenic Risks 5-15.1.2 Carcinogenic Risks 5-25.1.3 Lead 5-3

5.2 Risk Associated with Present Site and Future LandUse Conditions 5-45.2.1 Construction Workers - Present and Future Conditions 5-4

5.2.1.1 Alliant Energy/IPC Property Construction Workers 5-45.2.1.2 Former Allied Steel Property Construction Workers 5-5



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SECTION 5 RISK CHARACTERIZATION (CONTINUED)5.2.2 On-Site Workers and Site Visitors/Trespassers - Present and

Future Conditions 5-65.2.2.1 Alliant Energy/IPC Property On-Site Worker 5-75.2.2.2 Alliant Energy/IPC Property Site Visitors/Trespassers 5-75.2.2.3 Former Allied Steel Property Industrial Worker 5-75.2.2.4 Former Allied Steel Property Site Visitors/Trespassers 5-85.2.2.5 Former Allied Steel Property Future Child

Recreational Visitor 5-85.2.2.6 Former Allied Steel Property Future Residents 5-8

5.3 Summary of Human Health Risk Evaluation 5-95.3.1 Exposure Assessment 5-9

5.3.1.1 Present Conditions 5-95.3.1.2 Future Conditions 5-10

5.3.2 Summary of the Health Risk Estimates 5-10

SECTION 6 SCREENING LEVEL ECOLOGICAL RISK ASSESSMENT 6-16.1 Approach and Scope of Assessment 6-16.2 Problem Formulation 6-2

6.2.1 Habitat Assessment/Identification of Receptors 6-36.2.1.1 On-Site and Adjacent Properties 6-36.2.1.2 Mississippi River and Backwater Areas 6-4

6.2.2 Threatened and Endangered Species 6-46.2.3 Identification of Chemicals of Potential Ecological Concern 6-56.2.4 Identification of Exposure Pathways/Conceptual Site Model 6-6

6.3 Screening Analysis 6-76.4 Risk Characterization 6-8

6.4.1 Sediment Associated Biota 6-96.4.2 Soil Associated Biota 6-96.4.3 Summary of Health Risks 6-9

SECTION 7 DISCUSSION OF UNCERTAINTIES 7-1

SECTION 8 SUMMARY AND CONCLUSIONS 8-18.1 Summary and Conclusions of Human Health Evaluation 8-18.2 Summary and Conclusion of Screening Level Ecological Assessment 8-2

REFERENCES R-l



APPENDIX A

APPENDIX B

APPENDIX C

APPENDIX D

APPENDIX E

APPENDIX F

LIST OF APPENDICES

- TOXICOLOGY PROFILES

- QUANTITATION OF UPPER CONFIDENCE LIMITS

- EQUATIONS USED FOR QUANTIFICATION OF EXPOSUREESTIMATES

- CALCULATION OF CHEMICAL SPECIFIC SOIL TO AIRVOLATILIZATION FACTORS

- SUPPORTING DATA FOR DEVELOPMENT OF EXPOSURE

POINT CONCENTRATIONS

- EXPOSURE AND RISK ESTIMATES

A-l

B-l

C-l

D-l

E-l

F-l

LIST OF TABLES

TABLENO.

2-1 Selection of Chemical of Potential Concern (COPCs) for Surface Soil (0-1 Foot)

2-2 Selection of Chemical of Potential Concern (COPCs) for Subsurface Soil(1-10 Feet)

2-3 Selection of Chemical of Potential Concern (COPCs) for Subsurface Soil(10-20 Feet)

2-4 Selection of Chemical of Potential Concern (COPCs) for Groundwater

2-5 Selection of Chemical of Potential Concern (COPCs) for Sediment

2-6 Selection of Chemical of Potential Concern (COPCs) for Surface Water

3-1 Chemical Toxicity Values and Absorption Estimates

3-2 Health Effect Endpoints for Chronic and Subchronic Exposures to Site Soils

4-1 Selection of Exposure Pathways

4-2 Summary of Statistical Information for Surface Soil (0-1 foot) COPCs

4-3 Summary of Statistical Information for Subsurface Soil (1 -10 feet) COPCs

4-4 Summary of Statistical Information for Subsurface Soil (10-20 feet) COPCs

4-5 Summary of Statistical Information for Sediment COPCs

4-6 Summary of Statistical Information for Groundwater COPCs

IV



LIST OF TABLES (CONTINUED)

TABLENO.

5-1 Summary of Health Risk Estimates Under Present and Future Land UseConditions - Reasonable Maximum Exposure

6-1 Comparison of Sediment Sample Concentrations in the Mississippi River Valleyto Benchmark Values

LIST OF FIGURES

FIGURENO.

2-1 On-Site Surface Soil Sample Locations2-2 Off-Site Surface Soil Sample Locations2-3 Subsurface Sampling Locations2-4 Monitoring Well and Piezometer Locations2-5 Mississippi River Sampling Locations

EXECUTIVE SUMMARY

A baseline risk assessment (B1RA) was conducted to characterize potential risks to human healthand the environment resulting from exposures to chemicals detected at and in the area of theAlliant Energy Corporation/Interstate Power Company (Alliant Energy/IPC) formermanufactured gas plant (FMGP) site. Results of this B1RA, and the nature and extent ofimpacted media as discussed in the June 2000 Engineering Evaluation/Cost Analysis Part I - SiteCharacterization, provide a basis for determining the need for remedial activities to manage therisks at the site.

Standard U.S. Environmental Protection Agency (EPA) methodologies were used to estimatepotential levels of exposure and health risks. Conservative exposure scenarios were evaluatedfor present and future land use conditions. The exposure potential was evaluated separately forthe Alliant Energy/IPC property and the contiguous former Allied Steel property. Human healthrisks were calculated for noncarcinogenic and carcinogenic health effects for potential exposuresto chemicals in soils. For chemicals exhibiting carcinogenic effects, the upper bound lifetimeexcess cancer risks presented in this report are appropriately compared to EPA's risk range forhealth protectiveness at Superfund sites of 10"4 to 10'6 (EPA, 1990).

For noncarcinogenic effects, the contaminant intake was estimated using exposure assumptionsfor site conditions. This dose was compared to a risk reference dose (estimated daily intake ofthe chemical that is likely to be without appreciable risk of health effects) developed by the EPA.The resulting ratio is called a health index (HI). His that are less than one (1) are unlikely to beassociated with significant health risks, even for sensitive populations.

Current site conditions will reduce ingestion, dermal contact, and inhalation of contaminated soilas compared to bare soil conditions because the impacted soils are located below buildings,pavement, gravel, or lawn. In addition, chemically-impacted groundwater is not used as adrinking water source because the site and surrounding area are supplied by a municipal watersystem. However, a quantitative risk assessment that incorporates potential drinking waterexposure is required by EPA protocol to make risk management decisions at Superfund sites.Therefore, this baseline risk assessment includes estimates of risk for exposures to hypotheticalfuture residents (adult and child) from potential potable use of groundwater.

Present conditions are not considered to present a potential public health concern to site workers,construction works, visitors, and trespassers involved in nonintrusive soil activities. However, ifconstruction workers or site workers were to excavate into the subsurface soils and becomeexposed to impacted soils through incidental ingestion or dermal contact there is the potential forelevated noncarcinogenic (HI >1) and carcinogenic (cancer risk >lxlO"4) risks. The primarychemicals of concern are volatile organic compounds (VOCs), polynuclear aromatichydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and arsenic. These risk estimatesassume the workers do not use protective clothing (e.g., gloves) to prevent soil exposure, andperform manual labor that would bring them in direct contact with soil at the highestconcentrations during their entire exposure period.

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Under potential future conditions, it was assumed impacted subsurface soils are brought to thesurface through development or otherwise become accessible and remain accessible at thehighest concentrations for many years (i.e., 10 to 25 years). Under these conditions, exposure tosoil (either surface or subsurface), could then potentially pose an elevated risk (i.e., HI >1 andcancer risk >lxlO"4). This could only occur if site workers, visitors, or trespassers would comein direct contact with the soil. That is, current buildings, pavement, gravel, or lawn would bereplaced with bare soil, and the concentrations would remain the same throughout time.

Also under future conditions, use of impacted groundwater at the site would pose a concern forcarcinogenic and noncarcinogenic health risks for hypothetical residents. The groundwater onand around the site is currently not used.

The cancer risk estimates for the reasonable maximum soil exposure scenarios evaluated at thissite range from 5xlO"6 to 2xlO"3. The greatest risk estimates are associated with exposure tosubsurface soil (1-10 feet) by on-site workers. His for the reasonable maximum soil exposurescenarios range from 0.6 to 18; the greatest value is associated with a construction workerscenario. However, these risk estimates are based on several conservative assumptions per EPAprotocols; e.g., no worker protection methods are applied and all of the exposed skin of aconstruction worker is exposed to each of the soil contaminants at the exposure pointconcentration (often the maximum concentration) for 8 hours per day for 190 days per year.Likewise, it is assumed that the on-site worker would be performing intrusive soil activities for8 hours per day, 190 days per year for 25 years.

Similarly, impacted soil and groundwater beyond the site boundaries are not reasonablyaccessible under current land uses and, therefore, do not constitute an exposure pathway. Surfacewater in the Mississippi River was determined not to be impacted from the site, and it wasconcluded humans would not be exposed to the impacted sediment.

A screening level ecological risk assessment (ERA) was performed as part of the baseline riskassessment. Within the ERA, a habitat assessment was conducted to define groups of ecologicalreceptors that may be exposed to chemicals of potential ecological concern. Only one set ofpotential ecological receptors was identified: sediment-associated biota. Based on a comparisonof site investigation data to published toxicity benchmark values, it was concluded that the levelsof analytes detected in the Mississippi River sediment would not be expected to pose a threat toecological receptors. We conclude that no further ERA is necessary.

An evaluation of the indoor air pathway for the Alliant Energy/TPC district office building will besubmitted as an addendum under separate cover.

ES-2

SECTION 1 - INTRODUCTION

Alliant Energy Corporation/Interstate Power Company (Alliant Energy/IPC) and the UnitedStates Environmental Protection Agency, Region VII (EPA) have entered into an AdministrativeOrder on Consent for Engineering Evaluation/Cost Analysis (Consent Order), DocketNo. VO-97-F-0020, for the former manufactured gas plant (FMGP) site in Clinton, Iowa.Pursuant to the Consent Order, Alliant Energy/IPC is conducting an engineering evaluation/costanalysis (EE/CA) at the Clinton FMGP site.

Major components of the EE/CA are being submitted as separate documents which, together,comprise the overall EE/CA for the site. The documents are: Engineering Evaluation/CostAnalysis Part I - Site Characterization, Engineering Evaluation/Cost Analysis Part n - BaselineRisk Assessment, and Engineering Evaluation/Cost Analysis Part EQ - Remedial AlternativesEvaluation.

This portion (Part IT) presents the methodology, assumptions, and results of a Baseline RiskAssessment (B1RA) completed for the site as part of the EE/CA activities. The objective of theB1RA is to characterize potential risks to human health and the environment, and provide a basisfor determining the need for remedial activities or institutional controls to reduce or eliminate therisks.

This B1RA explores human health and ecological risks resulting from potential exposures tochemicals detected during the Site Screening Inspection (SSI) and EE/CA site characterizationinvestigations. The B1RA was conducted in accordance with Subpart E, Section 300.430(d) ofthe revised National Oil and Hazardous Substances Pollution Contingency Plan (NCP), aspromulgated on March 8, 1990 (EPA, 1990). Paragraph (d)(4) of this section of the NCP directsa B1RA be conducted to characterize the actual and potential threats to public health and theenvironment that may be posed by chemicals migrating to groundwater or surface water, releasedto air, leaching through soil, remaining in the soil, and bioaccumulating in the food chain. Therisk assessment is consistent with relevant guidance and standards developed by the EPA(EPA, 1986; 1989; 199la; 1999). Results of the B1RA are intended to assist in making riskmanagement decisions concerning the necessity for remediation, the nature and extent ofremediation, and selection of remedial alternatives.

1.1 - BASELINE RISK ASSESSMENT SCOPE AND APPROACH

The scope of this B1RA addresses chemicals of potential concern (COPCs) detected in the mediaat the site that may pose risks to human health and the environment. These media include soils(both surface and subsurface), groundwater, and surface water and sediment in the MississippiRiver.

Since current and future site uses will vary between the Alliant Energy/IPC side of the site andthe contiguous former Allied Steel property (currently owned by Riverview Partners who areproperty developers), risks associated with these portions of the site have been evaluated

1-1

independently under different exposure scenarios. In addition, the risks associated withMississippi River sediments and surface water have been addressed.

The calculated risks are based on the concentrations of chemicals detected and; therefore,represent the total risk, not just those that may be related to the FMGP operations. Areas off siteand beyond the extent of impacted soil and groundwater have not been evaluated.

1.2 - ORGANIZATION OF THE BASELINE RISK ASSESSMENT

The B1RA is composed of an evaluation of human health and ecological risk, as well as theuncertainty associated with the risk estimates. The B1RA is organized as follows:

Identification of Chemicals of Potential Concern. The chemicals detected inapplicable media investigated during the site investigations are identified anddiscussed. Based on an evaluation of the data, COPCs are selected for furtherevaluation.

Toxicity Assessment. The methodology used to describe the potential toxicity ofchemicals to humans and the range of toxic effects for each COPC are presented.Chemical-specific toxicity criteria to be used in the quantitative risk assessmentare presented.

Human Exposure Assessment. The potential pathways by which humanpopulations may be exposed to COPCs are discussed and exposure pathways areselected for further evaluation. For each pathway selected for quantitativeevaluation, the chemical concentrations at the point of potential exposure areestimated. The magnitude, frequency, and duration of exposure are estimated foreach pathway, and exposures are quantified. /

Risk Characterization. The general principles of the risk assessment process aredescribed. For each exposure pathway selected for evaluation, quantitative riskestimates are developed by combining the estimated exposure values forpotentially exposed populations with toxicity criteria.

Screening Level Ecological Risk Assessment. This portion of the B1RA providesa screening level ecological assessment for the reach of the Mississippi River thatis adjacent to the site area, and which contains ecological habitat.

• Discussion of Uncertainties. This discussion focuses on the major sources ofuncertainty affecting the risk assessment.

• Summary and Conclusions. This section summarizes results of the B1RA.

1.3 - DATA USED FOR RISK ASSESSMENT

This B1RA relied on the findings of the SSI and EE/CA site investigations to determine risksassociated with soil, groundwater, and Mississippi River surface water and sediment on or nearthe site. These site investigations have adequately determined the nature and extent of impacted

1-2

media, and the necessary physiographic and demographic information for completing the B1RA,and was gathered and summarized in the June 2000 Engineering Evaluation/Cost AnalysisPart I - Site Characterization (EE/CA Part I).

Data summarization and grouping was performed using procedures in accordance with EPAguidance (EPA, 1989). These summary procedures are described below:

Only data collected, analyzed, and validated according to the procedures presentedin the Quality Assurance Project Plan (QAPP) of the EE/CA Work Plan were usedas the basis of the B1RA, and in the selection of COPCs for this assessment.

The data was divided into groups based on the environmental conditions, siteuses, and potential routes of exposure relevant to the B1RA. Grouping of the dataallows for the characterization of different locations within an investigated area.Grouping data also helps in determining exposure point concentrations for targetpopulations.

1-3

SECTION 2 - IDENTIFICATION AND SELECTION OFCHEMICALS OF POTENTIAL CONCERN

This section of the B1RA discusses the identification and selection of COPCs for detailedevaluation. The purpose of selecting COPCs for the risk assessment is to identify thosechemicals associated with the site which are most likely to be of concern to human health and theenvironment.

The selection of COPCs for the site also followed procedures based on EPA guidance(EPA, 1989). The purpose of selecting COPCs is to eliminate from the risk assessment: 1) thosechemicals that are associated with sampling or laboratory artifacts, 2) those chemicals existing ator below naturally occurring levels at the site, and 3) those chemicals that are essential humannutrients and unlikely to pose risks to human health.

It is important to recognize the selection of a COPC does not necessarily indicate it poses apotential risk. The selection of a chemical only indicates there is a need to evaluate that chemicalin the B1RA to determine if its concentrations detected represent potential health risks. Thefollowing methodology was used in selecting COPCs from the summarized data:

Site data was compared to available blank (laboratory and trip) data asrecommended in EPA guidance (EPA, 1989). If the maximum detectedconcentration of a common laboratory contaminant in a site sample grouping wasless than ten times the maximum concentration in the blanks, the chemical wasnot selected in that grouping for evaluation in the risk assessment. This isdiscussed in Section 5 of EE/CA Part I. For those organic or inorganic chemicalsthat are not considered by EPA to be common laboratory contaminants, thechemical was not selected in that grouping for evaluation in the risk assessment, ifthe maximum detected concentration was less than five times the maximumdetected concentration in the blanks.

Based on EPA guidance (EPA, 1989), chemicals that are essential humannutrients, and toxic only at very high doses, were not considered for evaluation.Of the analytical parameters of the site investigations, only iron was included inthis category.

Prior to selecting COPCs, the data was segregated by medium, and area. The segregation tookplace so that those areas that meet the de minimis risk criteria (i.e., hazard quotient <1 or lifetimeexcess cancer risk <lxlO"6) could be eliminated as No Further Action (NFA) areas.

All compounds detected in at least one sample in subsurface soil (0-1 foot) subsurface soil(1-10 feet), and subsurface soil (10-20 feet) were retained as COPCs. Tables 2-1, 2-2, and 2-3present summaries of the COPC selection for these media. Similarly, all compounds detected inat least one groundwater sample were retained as COPCs for groundwater exposure. Table 2-4presents the groundwater COPC selection. Tables 2-5 and 2-6 present a summary of theselection of COPCs for sediment and surface water, and the rational for their selection.

2-1

2.1 - SELECTION OF CHEMICALS OF POTENTIAL CONCERN IN SOIL

The soil data was segregated into surface and subsurface soil data for the selection of COPCs.This segregation was performed because of the different potential for exposure to surficial soilscompared to subsurface soil. All compounds detected in at least one sample in surface andsubsurface soil were retained as COPCs for surface and subsurface soils.

In addition, the soils were segregated by their general area on the site (i.e., the AlliantEnergy/TPC side versus the former Allied Steel side). The following is a description of theCOPCs for surface and subsurface soils.

2.1.1 - Surface Soils

A summary of results of the surface soil analytical results (0-1 foot below ground surface [bgs])is provided in Section 6.3.2 of EE/CA Part I. Surface soil sample locations are shown inFigures 2-1 and 2-2. Within the surface soil samples volatile organic compounds (VOCs)(i.e., benzene, ethylbenzene, toluene, and xylenes [BETX]), polynuclear aromatic hydrocarbons(PAHs), pentachlorophenol, some metals, and polychlorinated biphenyls (PCBs) were detected.The most widespread analytes detected were the PAHs and metals. Other compounds, such asVOCs and PCBs were detected infrequently in surface soils. All chemicals detected wereretained as COPCs. Table 2-7 summarizes the COPCs by area on the site.

2.1.2 - Subsurface Soils

Subsurface soil impacts were evaluated in four primary vertical intervals during the sitecharacterization: 1) 1 to 10 feet bgs, 2) 10 to 20 feet bgs, 3) 20 to 50 feet bgs, and 4) greater than50 feet bgs. Within the risk assessment, only the first two depth intervals (1 to 10 feet bgs and10 to 20 feet bgs) were considered applicable, because it is not anticipated people would beexposed to soils below 20 feet bgs.

The 1- to 10-foot depth interval generally coincides with the unsaturated zone at the site. Thisdepth range is also reasonably accessible by excavation for buildings or buried utilities. The10-to 20-foot depth interval represents the uppermost portion of the water table aquifer.Although less accessible than the overlying soil and continuously saturated, these depths may bereached during maintenance or reconstruction of on-sile sewer lines which lay at depths up toapproximately 20 feet bgs. The selection of COPCs is segregated by the two different depthintervals and general areas on site (i.e., Alliant Energy/IPC or Allied Steel sides of the site). Allchemicals detected were retained as COPCs.

The nature and extent of subsurface soil contamination is discussed in detail withinSection 6.3.3.4 of EE/CA Part I. Subsurface sampling locations are shown in Figure 2-3. Withinsubsurface soils the primary COPCs detected were VOCs (primarily BETX), PAHs, and metals.

The primary VOCs detected within the depth intervals were BETX. However, chloromethaneand methylene chloride were detected occasionally at low concentrations in some subsurfacesoils samples.

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PAH concentrations are most prevalent at the locations of the former gas plant, gas holders, andcore of the former sluice pond. The distribution of PAHs in the 10- to 20-foot depth interval ismore uniform over the FMGP operation areas and the former sluice pond than observed in the1- to 10-foot interval. In both the 1- to 10-foot depth interval and 10- to 20-foot depth intervals,acid extractable compounds were detected on the Allied Steel side of the property (i.e., one ormore of the following: 2,4-dimethylphenol, 2-nitrophenol, 3&4-nitrophenol, or phenol) weredetected only at one location (SB-31). No acid extractable compounds were detected in soilsamples from the Alliant Energy/IPC side of the property. Within subsurface soils, metals weredetected in each area of the site. For subsurface soils, metals were not screened againstsite-specific background concentrations, because of elevated metals concentrations in thebackground (off-site) samples. For this reason, all metals were retained as COPCs by default insubsurface soil. However, metals occur naturally in soil; therefore, the estimated risk reflects alevel of risk related to background, as well as potentially to the site.

2.2 - SELECTION OF CHEMICALS OF POTENTIAL CONCERN IN GROUNDWATER

Groundwater samples were taken from three distinct zones in the alluvial aquifer. The watertable aquifer wells were screened to intersect the water table to provide data at the groundwatersurface. The intermediate depth wells were intended to identify a lower boundary in lightlyimpacted areas, and quantify a transition zone for areas with greater vertical impact. The wellsscreened at the bedrock surface were used to determine if the COPCs have the potential to impactthe bedrock aquifer. The selection of COPCs was based on data collected from the water tableaquifer and intermediate depth wells only because groundwater at the bedrock surface is notimpacted and is not considered a part of the plume. For the water table aquifer and intermediatedepth groundwater wells, all compounds, detected in at least one sample were retained asCOPCs. Only data from the water table aquifer and intermediate depth wells were used to.calculate EPCs. It should be noted, metals concentrations in groundwater were not screenedagainst upgradient well data, because what is considered upgradient varies, depending upon thestage of the Mississippi River.

Analytical results for the groundwater samples are summarized in Section 6.3.4 of EE/CA Part I.Locations of the monitoring wells and piezometers are shown in Figure 2-4. The VOCs detectedin groundwater included benzene, bromomethane, chloromethane, 1,2-dichloroethane,ethylbenzene, toluene, and xylenes. BETX were the most consistently detected VOCs and theirconcentration decreased with depth interval. Each of the PAHs was detected in unfilteredgroundwater samples. PAHs were detected in 83 of the 107 groundwater samples analyzed.Concentration of PAHs also decreased with the depth interval of the wells. Acid extractablecompounds were detected only in a subset of the water table wells, and included only2,4-dimethylphenol, and phenol. Each of the inorganic analytes was detected in one or more ofthe samples. The metals samples were collected and analyzed on an unfiltered or total metalsbasis. The concentrations of metals decreased with depth interval, and many of the metalsdetected within the water table or intermediate zone wells were below detection limits in thebedrock surface wells.

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2.3 - SELECTION OF CHEMICALS OF POTENTIAL CONCERN IN RIVERSEDIMENT

Sediment samples were collected upstream and downstream of the former sluice pond seweroutfall. A detailed discussion of the sediment analytical results is provided in Section 6.3.5.2 ofEE/CA Part I. As shown in Figure 2-5, sediment samples were collected from 11 of the14 locations attempted in the Mississippi River channel. In 3 of the 14 locations, zebra musselpopulations were so numerous that sediment could not be recovered.

Analytical results from the sampled locations indicate VOCs were detected only at two locations(i.e., MR-05 and MR-06 as shown in Figure 2-5). Low concentrations of toluene and methylenechloride were the only VOCs detected.

PAH compounds were detected at 6 of the 11 locations where samples were recovered, includingthe upstream location (MR-01). Three sediment sample locations (MR-04, MR-05, and MR-06)had total PAH concentrations greater than the upstream location. These are the sample locationsclosest to the existing and former city sewer outfalls and the former sluice pond outfall.Downstream of these locations, PAH compounds were detected only at MR-13. Based on theseries of samples with no detectable concentrations (MR-10 through MR-12 and MR-14), and thepotential background concentrations defined at MR-01, the magnitude and extent of PAHimpacts potentially related to current or historic sewer discharges to the river have been defined,and are limited to the immediate vicinity of the sewer discharge points (i.e., MR-05 and MR-06).

None of the acid extractable compounds were detected in the sediment samples.

With the exception of cyanide, which was not detected in sediments, the inorganic compounds ofconcern were detected in one or more of the river sediment samples. Sediment samples MR-01and MR-03 through MR-06 generally had a more diverse representation of the inorganiccompounds and at higher overall concentrations than did samples collected from MR-09 throughMR-14. Samples MR-09 through MR-14 were collected from slightly further into the riverchannel, where faster currents maintain a higher percentage of sand than the locations closer tothe riverbank, which contain more silt and clay, and would naturally have a higher concentrationof metals. As with the VOCs and PAHs, the highest concentrations of the inorganic compoundswere generally detected at MR-05 and MR-06. Each of the metals detected in sediments were athigher concentrations downstream of the former sluice pond outfall compared to upstreamconcentrations and, therefore, were retained as COPCs. Table 2-5 presents a summary of theriver sediment data and the rationale for the selection of chemicals as COPCs. Any compounddetected in Mississippi River sediment was retained as a COPC, with the exception of chemicalswhich are not site related.

2.4 - SELECTION OF CHEMICALS OF POTENTIAL CONCERN IN RIVER SURFACEWATER

Based on results for the surface water samples collected from the eight locations in theMississippi River (MR-01 through MR-08 as shown in Figure 2-5), the samples exhibited

2-4.

virtually the same analytical results from the upstream to downstream sampling locations. NoVOCs, PAHs, or acid-extractable compounds were detected in any of the surface water samplescollected from the Mississippi River. With respect to the inorganic compounds, only iron, lead,and sulfate were detected. Based on the samples collected, water quality in the Mississippi Riveris not impacted by the site. For this reason, no analytes were selected as COPCs in MississippiRiver surface water. Table 2-6 provides the rational for exclusion of chemicals in surface waterfrom further risk analysis.

2.5 - SUMMARY OF CHEMICALS OF POTENTIAL CONCERN

Table 2-7 summarizes the COPCs by medium, area (Alliant Energy/IPC or former Allied Steel),and zones (soil depth) where applicable. Within each medium, except Mississippi River surfacewater, COPCs were selected and retained for further consideration.

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SECTION 3 - TOXICITY ASSESSMENT

This section provides the analytical framework for the characterization of human health risks.The information presented in this section provides a basis for the dose-response assessmentcarried out in the quantitative risk assessment.

3.1 - TOXICOLOGICAL EFFECTS AND PROPERTIES

Evaluation of the toxic potential of a chemical involves the examination of available data thatrelate observed toxic effects to doses. Generally, there are two categories of information that areconsidered in this part of a quantitative risk assessment:

Information on the potential acute or chronic noncancer effects (noncarcinogeniceffects) of chemicals.

Information on the potential for chemicals to initiate or promote cancers(carcinogenic effects).

Two general criteria are used to describe carcinogenic and noncarcinogenic effects: excesslifetime cancer risk (for chemicals which are thought to be potential human carcinogens) and thehazard quotient (HQ) for chemicals that cause noncarcinogenic effects. For potentialcarcinogens, the current regulatory guidelines (EPA, 1989) use a conservative approach in whichit is assumed any level of exposure to a carcinogen could cause cancer. This is contrary to thetraditional toxicological approach to toxic chemicals, in which finite thresholds are identified,below which toxic effects are not expected to occur. This traditional approach still is applied tononcarcinogenic chemicals.

At the present time, most cancer potency values represent plausible upper bounds on risk. Whensuch a value is used to estimate numbers of cancer cases, it is important to understand that theresult is also an upper bound. It is also important to note that the EPA's current methodologiesfor developing reference doses (RfDs) and reference concentrations (RfCs) are designed toprotect sensitive populations. If data on sensitive human populations are available (and there isconfidence in the quality of the data), then the RfD is set at the dose level at which no adverseeffects are observed in the sensitive population (e.g., RfDs for fluoride and nitrate). If no suchdata are available (for example, if the RfD is developed using data from humans of average orunknown sensitivity) then an additional 10-fold factor is used to account for variability betweenthe average human response and the response of more sensitive individuals (EPA, 1995).

The toxicity information, i.e., subchronic and chronic RfDs, and cancer slope factor values usedin this risk assessment were obtained from the following EPA sources in this hierarchy:

1. Integrated Risk Information System (IRIS) (EPA, 2000).

2. Health Effects Assessment Summary Tables (HEAST) (EPA, 1997).

3. EPA's Office of Research and Development's (ORD) National Center forEnvironmental Assessment (NCEA) Superfund Technical Support (as providedby M. Beringer, EPA Region 7 toxicologist, March 2001).

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The information derived from these sources is shown in Table 3-1. The upper end of the oralslope factor range is used in cases where EPA provides a range of cancer slope factors. Thisapproach is very cautious. It ensures a greater risk that adds to the other cautious assumptionsinherent in the EPA model.

3.1.1 - Noncarcinogenic Effects

In general, noncarcinogenic (acute or chronic systemic) effects are considered to have thresholdvalues, while carcinogenic effects are considered to not have thresholds. Toxicity studies for theformer focus on identifying where this threshold occurs. The threshold can be related to a RfD.Acceptable doses that are sanctioned by the EPA are called verified RfDs. A chronic RfD is anestimate of a daily exposure level for which people, including sensitive individuals, do not havean appreciable risk of suffering significant adverse health effects. Exposure doses above an RfDcould possibly cause health effects. Chronic RfDs are applicable for 7 years to lifetime exposure,and subchronic RfDs are applicable to exposure durations from two weeks to 7 years (EPA,1989).

The assessment of noncarcinogenic effects is complex. There is a broad interaction of timescales (acute, subchronic, and chronic) with varying kinds of effects. In addition, there arevarious levels of "severity" of effect.

For many noncarcinogenic effects, protective mechanisms must be overcome before the effect ismanifested. Therefore, a finite dose (threshold), below which adverse effects will not occur, isbelieved to exist for noncarcinogens. Noncarcinogenic health effects include birth defects, organdamage, behavioral effects, and many other health impacts. A single chemical might elicitseveral adverse effects depending on the dose, the exposure route, and the duration of exposure.For a given chemical, the dose that elicits no effect when evaluating the most sensitive response(the adverse effect which occurs at the lowest dose) in the most sensitive species is used toestablish an acceptable dose (toxicity value) for noncarcinogenic effects.

The RfD value is used as a measure of potential chronic health risks. These values serve asbenchmarks for assessing the potential for noncarcinogenic health effects. They represent"threshold" health effect values below which no effects are expected. So that these benchmarksare set low enough, uncertainty in the supporting database is taken into account through theapplication of uncertainty or safety factors.

The IRIS defines the reference dose as an estimate (uncertainty spanning perhaps an order ofmagnitude) of a daily exposure to the human population (including sensitive subgroups) that islikely to be without an appreciable risk of deleterious effects during a lifetime. A critical effectrefers to the health endpoint upon which the reference dose is based. The uncertainty factorcontributes as a divisor to the dose associated with the critical effect, which is usually ano-adverse-effect-level (NOAEL) or a lowest-adverse-effect level (LOAEL). Most uncertaintyfactors are standardized and include:

Ten-fold factor for extrapolation from animals to humans.

Ten-fold factor for variability in the human population.

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Ten-fold factor for use of a less-than-chronic study.

One- to ten-fold factor for extrapolation from an LOAEL.

The use of ten-fold uncertainty factors is traditional. However, there may be situations wheredata support the application of smaller uncertainty factors. There is ongoing research directed atthe use of physiologically-based pharmacokinetic modeling for interspecies extrapolation.However, at this time, no specific guidance is provided on the use of this method for developingbetter extrapolation (from animal to human, and administered versus absorbed) values forapplication.

Modifying factors also contribute as divisors to the NOAEL or LOAEL, and are usually one.However, in certain instances professional judgment can be applied to use the modifying factorto adjust the RfD (e.g., epidemiological evidence). Confidence in the RfD refers to a qualitativejudgment with regard to the quality of the critical study, the supporting database, and the dosedeveloped.

3.1.2 - Carcinogenic Effects

Studies of carcinogenicity tend to focus on identifying the slope of the linear portion of a curve ofdose versus response. A plausible upper-bound value of the slope is called the cancer slopefactor (CSF) or cancer potency factor (CPF). The product of the CSF and the exposure dose is anestimate of the risk of developing cancer. In accordance with current scientific policy concerningcarcinogens, it is assumed any dose, no matter how small, has some associated response. This iscalled a nonthreshold effect. In this assessment, the nonthreshold effect was applied to allprobable carcinogens.

Identification of chemicals as known, probable, or possible human carcinogens is based on anEPA weight-of-evidence classification scheme in which chemicals are systematically evaluatedfor their ability to cause cancer in mammalian species and conclusions are reached about thepotential to cause cancer in humans. The EPA classification scheme (EPA, 1989) contains sixclasses based on the weight of available evidence, as follows:

A Known human carcinogen.

Bl Probable human carcinogen — limited evidence in humans.

B2 Probable human carcinogen — sufficient evidence in animals and inadequate datain humans.

C Possible human carcinogen — limited evidence in animals.

D Inadequate evidence to classify.

E Evidence of noncarcinogenicity.

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Some chemicals in Class D may have the potential to cause cancer, but adequate data are notcurrently available to change the classification. In this risk assessment, evaluations of thelikelihood of a carcinogenic effect include chemicals in Classes A, Bl, B2, and C.

3.2 - HEALTH EFFECTS CRITERIA FOR THE CHEMICALS OF POTENTIALCONCERN

Table 3-1 presents chronic oral, inhalation, and dermal toxicity values (slope factors/RfDs) forthe COPCs selected to be quantitatively evaluated in this assessment. For each COPC, currentlexicological data was used to characterize the chemical's noncarcinogenic and/or carcinogenicpotential. Toxicological properties of the COPCs are presented in Appendix A.

The oral and inhalation toxicity values were obtained from one of the following threeEPA-approved sources unless otherwise noted in Table 3-1.

Primary Source - Integrated Risk Information System (IRIS)Secondary Source - Health Effects Summary Tables (HEAST)Tertiary Source - National Chemical Exposure Assessment (NCEA)

IRIS is an on-line database of toxicity values along with supporting lexicological data used todevelop the value. The toxicily values in IRIS are more crilically developed Ihen the values fromthe other iwo sources (HEAST and NCEA). An extensive search of ihe IRIS dalabase wasconducled in December 1999 for those chemicals delecled al Ihe sile.

HEAST was lasl revised in 1997, and provides an easy look-up lable for toxicity values. Inaddition to chronic toxicity values, HEAST also provides subchronic toxicity values fornoncarcinogenic effects, which are not found in IRIS. Values found in IRIS are not duplicated inHEAST, but rather a reference to IRIS is provided.

The NCEA group within EPA provides, when possible, provisional toxicity values forcompounds where there is not sufficient data to develop a toxicity value to put in HEAST orIRIS. For purposes of this assessment, the provisional values from NCEA were used, asnecessary, in this assessment in the absence of IRIS or HEAST toxicity values.

Although the EPA has developed toxicity values for the oral and inhalation routes of exposure,they have not developed toxicity values for the dermal route of exposure. For this reason, adermal toxicity value was estimated for each COPC by adjusting the oral toxicity values becauseno toxicity data are presently available for directly evaluating dermal exposures to contaminants.EPA has developed a method to extrapolate oral toxicity values for use in dermal riskassessments (EPA, March 2001). The extrapolation method applies a gastrointestinal absorptionfactor (ABSci) to the available oral toxicity values to account for the absorption efficiency of anadministered dose across the gastrointestinal tract and into the bloodstream.

The oral toxicity values are generally based on the level of chemical "administered" to a testanimal, rather than the amount of the dose that is "absorbed" into the animal's blood stream.

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However, the oral toxicity values based on an administered dose can be adjusted to account forthis absorption factor by incorporating an estimate of the level of oral absorption which is likelyto occur. In the present risk assessment, for each analyte, it was necessary to adjust the oraltoxicity values based on "administered" doses to estimate an "absorbed" dose basis, becausecontaminant dose estimates for the dermal exposure route are absorbed doses. The adjustedvalues are referred to as dermal toxicity values. The following equations were used to arrive atthe dermal toxicity values (EPA, 1998):

Oral Reference Dose (administered) x Oral Absorption Estimate = Dermal ReferenceDose (absorbed)

Oral Slope Factor (administered)/Oral Absorption Estimate = Dermal Slope Factor(absorbed)

The current convention is to use an oral absorption estimate equal to 100 percent for thosechemicals that, based on literature studies, have an oral absorption efficiency of 50 percent orgreater. This is due to the fact that the inherent variability in such data is great enough thatunless the oral absorption efficiency is less than 50 percent, it is not considered significantenough to make an adjustment to the oral toxicity value. The 100 percent value is also used forcompounds where data on oral absorption is not available. For those compounds where the oralabsorption efficiency is below 50 percent, then the actual value on absorption efficiency is usedin the above equations to estimate the dermal toxicity values. The values used to adjust the oraltoxicity values to dermal values are presented in Table 3-1. Target endpoints for chronic andsubchronic exposures to the COPCs are summarized in Table 3-2.

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SECTION 4 - HUMAN EXPOSURE ASSESSMENT

The purpose of this section is to describe how, and to what extent, human populations maybecome exposed to COPCs identified in site media (e.g., soil, air groundwater, surface water, andsediment). As part of this evaluation, information on the exposure setting and the potentiallyexposed populations was compiled, followed by an assessment of exposure pathways throughwhich populations could be exposed to the chemicals detected. For each potentially completeexposure pathway selected for quantitative evaluation, the chemical concentrations at the pointsof exposure and the potential chemical intakes were estimated.

4.1 - SITE CHARACTERIZATION AND RECEPTOR SELECTION

EPA guidance requires an approach that defines reasonable maximum exposure (RME) based onthe nature of the activities of the exposed group. By assessing the potential level of exposure to,and risk from the site to these RME receptor groups, the many other receptor groups with lesserlevels of exposure should be covered. The following is a discussion of the selection of the RMEreceptor groups for each area on the site. A range of RME populations is selected to provide arange of potential levels of chemical exposure. Table 4-1 provides a matrix of potentiallyexposed populations, which is elaborated upon in later sections of this Exposure Assessment.

As discussed in earlier sections, the site is divided into two distinct properties under separateownership: the Alliant Energy/IPC side of the site, and the former Allied Steel property. Therailroad dividing the two sides of the site is operated by the I&M Rail Link Railroad. This railline is very active and will likely remain active in the future. The railroad corridor is defined bythe site fences. Potential RME populations are discussed below for each area on the site (AlliantEnergy/IPC side and former Allied Steel property), as well as the off-site Mississippi Rivercorridor under present land use conditions.

4.1.1 - Alliant Energy/IPC Property

The Alliant Energy/IPC side of the site is utilized by Alliant Energy/IPC as a service center anddistrict office. Affected areas of this portion of the site are primarily accessible only to AlliantEnergy/IPC personnel. A chain-link fence that is topped with three strands of barbed wiresurrounds the service center area. Areas accessible by the general public are mostly paved orcovered by the district office building. Only the area between the district office building andNorth 2nd Street is not hard-surfaced. However, this area is covered by grass, which ismaintained for appearance.

The following potential receptor groups were selected as representative RME populations for thisportion of the site under present land use conditions:

Alliant Energy/IPC employees.

Alliant Energy/IPC property construction workers.

Alliant Energy/IPC customers and vendors (site visitors).

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The Alliant Energy/IPC side of the property is expected to continue its current operations for theforeseeable future. For this reason, other potential RME receptors, such as on-site residenceswere not considered likely and, per EPA guidance (EPA, 1989), were not evaluatedquantitatively in this B1RA. Groundwater is not used as a drinking water source because the siteand surrounding area are supplied by a municipal water system. However, a quantitative riskassessment that incorporates potential drinking water exposure is generally necessary to makerisk management decisions at Superfund sites. Therefore, this B1RA includes a quantification ofrisk for exposures to hypothetical future residents (adult and child) from potential use ofgroundwater. Also, potential exposures to receptors involved in soil intrusive activities(e.g., construction or utility workers) may come into contact with groundwater. This potentialexposure is discussed qualitatively in this B1RA.

4.1.2 - Former Allied Steel Property

The former Allied Steel property is presently vacant. Hard surfacing on this portion of the siteconsists of the floors of the former Allied Steel buildings. The remainder of the site is coveredby grass or gravel. Although surrounded by a chain-link fence and posted with no trespassingsigns, the fence is in poor condition and evidence of trespassers is commonly observed.

The following potential receptor groups were selected as representative RME populations for thisportion of the site under present land use conditions:

Riverview Partners employees.

Former Allied Steel property construction workers.

Trespassers.

In the future, this portion of the site may be developed into a recreational center, or redevelopedas an industrial property. The following potential receptor groups were selected as representativeRME populations for this portion of the site under future land use conditions:

Child recreational visitor.

Industrial worker.

Under an exposure scenario that soils are exposed during future development, the potential levelof exposure under this scenario was assessed for a young child (ages 1-6 years) for an RMErecreational visitor scenario. The City of Clinton Master Plan for the Riverview Park area, whichincludes the former Allied Steel property, includes a baseball stadium, an interpretive sculpture(including a wading pool), a band shell, greenspace, access roads, bicycle and pedestrian paths,and parking. The most likely reuse for the Allied Steel portion is as a park. Therefore, the RMEpopulation selected for future land use conditions is represented by a child recreational visitor tothe park. As the future land use of this site is not definitive, an industrial/commercial workerscenario has also been selected to characterize future risk at this site.

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It is unlikely that groundwater at the site will be used for potable purposes, given the proximityof municipal water supply lines to the area. However, a quantitative risk assessment thatincorporates potential drinking water exposure is generally necessary to make risk managementdecisions at Superfund sites. Therefore, this B1RA includes estimates of risk for exposures tohypothetical future residents from potential use of groundwater. Potential risk to receptorsinvolved in soil intrusive activities at this site will be discussed qualitatively.

4.1.3 - Off-Site Mississippi River Corridor

Beyond the site boundaries are Riverview Park, commercial/retail districts, and limitedresidential development. Most of Riverview Park is an open expanse of grass with isolatedlandscaping and trees. The park is heavily used for general recreation, art and craft fairs, and alarge annual 4lh of July festival. Near the site the park also includes a swimming pool andminiature golf course that are heavily used during the summer months. These areas are fenced tolimit access to specific hours when the park staff is present. Riverview Park, the swimming pool,and golf course are owned and maintained by the City of Clinton Park Commission. East ofRiverview Park is the Mississippi River and flood control levee. Along the top of the levee are aconcrete road and a multi-use trail. A riverboat casino and community theater are the majorattractions along the riverfront near the site. The results of the site investigation indicate thatPAHs were detected in soil at several off-site locations, including the Mississippi River corridor.However, Alliant Energy/IPC has concluded that off-site soil contamination is not due toactivities at the FMGP.

Recreational uses of the Mississippi River adjacent to the site include fishing, boating, and waterskiing. There are no beaches or swimming areas on the riverfront near the site. For thesereasons, there are no potential receptors for the Mississippi River environment. Commercialfishing may be conducted in the area; however, this activity is not believed to be occurring nearthe site at this time.

Direct exposure to sediments is unlikely because the face of the flood control levee is coveredwith large stone riprap. The riprap extends well below the water surface and into the channelwhere swift currents are encountered. Based on the inaccessibility of this area, it was concludedhumans would not be exposed to sediments in the Mississippi River. As mentioned previously inthe selection of COPCs, Mississippi River surface water was not found to be contaminatedadjacent to the former discharge area. In addition, fish consumption would not likely result inchemical exposure because of the small area of impacted sediment relative to the overall size ofthe aquatic environment, and the low potential for the chemicals detected in the sediments tobioconcentrate in fish. For these reasons, there are no potential human receptors for theMississippi River environment. Rather, the levels of chemicals detected in sediment areevaluated later within the screening level ecological assessment (Section 6).

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4.2 - POTENTIAL EXPOSURE PATHWAYS

Based on Superfund Risk Assessment Guidance, an exposure pathway describes the course achemical takes from its location to the exposed individual (EPA, 1989, 1998). It is defined byfour elements:

A source and mechanism of chemical release to the environment.

An environmental transport medium (e.g., groundwater, surface water) for thereleased constituent.

A point of potential contact with the contaminated medium (referred to as theexposure point).

An exposure route (e.g., ingestion, and inhalation) at the exposure point.

When all four of these elements are present, an exposure pathway is considered "complete." In arisk assessment, only complete exposure pathways are evaluated. In this section, potentiallycomplete human exposure pathways at the site are identified based on present land use conditionsand potential future land use conditions.

4.2.1 - Potential Exposure Pathways Under Present Land Use Conditions

For each RME human population selected above under present land use conditions, an exposurepathway analysis was conducted for each portion of the site. The analysis consisted ofdetermining which exposure pathways were complete for each RME population. An exposurepathway was considered complete if all four conditions discussed above were satisfied(i.e., source, transport mechanism, exposure point, and exposure route). As discussed above,exposure pathways are in essence the ways in which people are exposed to impacted media.

Results of the exposure assessments for each portion of the site and potentially exposedpopulations are summarized in the following subsections. These summaries indicate theexposure medium, source and/or release mechanism, exposure point, potential receptor, androute of exposure. These summaries also indicate whether each pathway is potentially completeand also identifies those pathways that are quantitatively evaluated in the B1RA. Results of theexposure pathway analysis are summarized in Table 4-1. Current land use exposure scenarioswere evaluated for both present conditions and future conditions.

An exposure pathway analysis indicates potentially completed pathways for soil and groundwaterat this site. Each of the RME subpopulations have potential exposure to soil and fugitiveemissions derived from soil. The construction worker has additional potential contact withgroundwater for soil intrusive activities.

The potential for the future construction worker to have exposure to contaminated groundwater

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during soil intrusive activities such as excavation, utility repair, maintenance, or constructionactivities is considered insignificant for the following reasons:

1. Construction workers do not stand in, or expose their skin to, contaminatedgroundwater for extended periods of time.

2. Construction workers wear protective clothing to minimize direct skin contactwith groundwater.

3. Construction workers move about the site and are not exposed to groundwatercontaminants at a particular location via an inhalation pathway for an extendedperiod of time.

This exposure is not quantified further in the B1RA because it is considered insignificant.

The site is supplied with municipal water, and no water supply wells are located in the alluvialaquifer in close proximity to the site. In addition, no buildings with basements, sumps, or pitsexist on site that may intersect groundwater. On-site groundwater monitoring wells are cappedand locked to prevent unauthorized or accidental access. For this reason, it is unlikely that RMEpopulations (except the construction worker) would be exposed to contaminated groundwater onsite. However, groundwater exposures for a hypothetical future resident has been quantified forcomparison purposes per EPA RAGS Part B guidance. The following is a qualitative discussionof the potential level of exposure each RME subpopulation may have to soil.

4.2.1.1 - Alliant Energv/IPC Property.

Alliant Energy/IPC Employees. Under present site conditions, surface soils are coveredwith buildings, pavement, or lawn. These coverings will decrease the potential for exposureto soil and fugitive dust/vapor emissions. For this reason it is considered unlikely that AlliantEnergy/IPC employees would be significantly exposed to soils. For example, on the AlliantEnergy/IPC property, many of the service center staff are on site only at the beginning andend of the workday. While on site, their activities are typically limited to indoors, or onpaved or graveled surfaces while outdoors. District office staff is almost exclusively indoorsduring business hours. The only accessible surface soils are vegetated and employees areunlikely to frequent these areas. More specifically, greater than 90 percent of the site area iscovered by buildings, pavement, compacted gravel, or vegetative cover; therefore, the areaavailable for exposure to surface soils or fugitive dust is quite limited. For these reasons,surface soil exposure is assessed only under a future scenario for employees, assumingsurface soils become exposed as a result of a dramatic change in property use consistent withcommercial industrial land use. For the reasons stated above, this current pathway isconsidered complete but insignificant. Site characteristics decrease potential soil andvapor/particulate exposure for current Alliant Energy/IPC employees.

Alliant Energy/IPC Property Construction Workers. Construction workers performingintrusive activities on site, such as excavation in areas of chemically-impacted soils areanticipated to have the greatest potential for chemical exposure under present land use

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conditions. While digging in the surface and subsurface soil, construction workers may beexposed to chemicals by direct contact with soil, incidental ingestion of soil, and inhalationof dust and/or vapor emissions created during the excavation activities. For purposes of therisk assessment, it was assumed construction workers have the greatest potential to beexposed to soil concentrations detected at any depth above the water table (approximately10 feet bgs). However, sewer systems in this part of Clinton are as much as 20 feet deep andoccasional replacement or repair may be conducted.

Unlike facility employees, the construction workers performing activities on the site may alsobe exposed to impacted groundwater. As noted above, the depth to water table on thisportion of the site is approximately 10 feet bgs. Although this depth is greater than a typicalutility trench or building excavation, the major deep sewer lines may be below the watertable. However, it was considered unlikely that workers would contact groundwater in thetrench, with the exception of their work boots, since the trench would have to be dewateredfor workers to be able to work in the trench. For this reason, exposure of constructionworkers to groundwater is handled qualitatively in the risk characterization section of thereport.

Alliant Energy/IPC Customers and Vendors (Site Visitors/Trespassers). Customers andvendors visiting the site for business purposes would not be involved in any type of intrusiveactivities nor would they spend time on areas of exposed soil. For this reason, this receptorgroup would not be exposed to contaminated media. Therefore, they were eliminated as areceptor of potential concern except under a future scenario where the soils become exposedand present site use changes.

4.2.1.2 - Former Allied Steel Property.

Riverview Partners Employees. Under the present land use conditions, employees,including contractors, would be involved only in minor site maintenance such as mowing,site inspection, or fence repair. Present maintenance activities would not include anyintrusive activities that would create the potential for exposure to impacted subsurface soil orgroundwater. Employees and contractors visit the site only for short periods of time and atirregular intervals. For these reasons under present site conditions, significant soil exposureis considered unlikely except under a future scenario where surface soils or subsurface soilsare exposed. As was discussed for the Alliant Energy/IPC side of the site, potentialemployees' exposure is assessed under this scenario for both surface and subsurface soils.Therefore, under an exposure scenario that soils are exposed during future development, thepotential level of exposure under this scenario was assessed for a young child (ages 1-6 years)for a RME recreational visitor scenario. The City of Clinton Master Plan for the RiverviewPark area, which includes the former Allied Steel property, includes a baseball stadium, aninterpretive sculpture (including a wading pool), a band shell, greenspace, access roads,bicycle and pedestrian paths, and parking.

Former Allied Steel Property Construction Workers. As with the Alliant Energy/IPC sideof the site, construction workers performing intrusive activities in areas of impacted soils are

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anticipated to have the greatest potential for chemical exposure. During intrusive work,construction workers may be exposed to chemicals by direct contact with soil, incidentalingestion of soil, and inhalation of dust and/or vapor emissions created during the excavationactivities. The greatest potential for exposure to impacted surface and subsurface soil is atdepths less than 10 feet bgs. However, exposures to impacted soils at depths ranging from10 to 20 feet bgs are also possible because construction workers may be involved in sewermaintenance or construction.

Construction workers performing activities on the former Allied Steel side of the site mayalso be exposed to impacted groundwater through sewer maintenance or construction. Asdiscussed previously, exposure to groundwater while performing construction maintenanceactivities is expected to be minimal and will be assessed qualitatively.

Trespassers. Similar to the on-site employees, adult or child trespassers may be exposed tosoil under present and future conditions. Therefore, potential exposure to soil under thisscenario was assessed for trespassers.

4.2.2 - Potential Exposure Pathways Under Future Land Use

The purpose of assessing exposures under potential future land use is to determine if reasonableland use changes would lead to an increased human exposure to contaminated media. If suchchanges appear possible, exposure estimates are also determined based on the potential futureland use conditions.

4.2.2.1 - Alliant Energy/IPC Property. The exposure scenarios for Alliant Energy/IPCdescribed above consider land uses consistent with the current industrial/commercial zoning.Alliant Energy/IPC has a district office and repair shop on their portion of the property. Theexpectation for this operation to continue into the foreseeable future is reasonable. Thecontinued use of the Alliant Energy/IPC site in its current state is, therefore, the same as futureland use. For management purposes, a resident is quantified to represent RME exposure togroundwater beneath this site.

4.2.2.2 - Former Allied Steel Property. Riverview Partners intends to redevelop the formerAllied Steel site in the future. The decisions for redevelopment are not final but current plansindicate the most likely reuse of this site is a park. As the plans are not final, and the area iscurrently zoned industrial commercial, other nonresidential other nonresidential land reuse is alsopossible. Until site land reuse occurs, the current characterization of the site visitor/trespasseralso applies to a future trespasser risk scenario.

Recreational Child Visitor. A young recreational child visitor is considered representativeof the RME for possible park reuse because a small child could go to the park and couldcome in contact with impacted soil while playing in the park. The frequency of visits to thepark are expected to be moderated by weather and climate conditions, and it is expected theduration (i.e., hours) that the recreational child visitor spends in the park is less than in his orher own home. Therefore, under an exposure scenario in which soils are exposed during

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future development, the potential level of exposure under this scenario was assessed for ayoung child (ages 1-6 years) for a RME recreational visitor scenario.

Industrial/Commercial Worker. The industrial/commercial worker is a surrogate RMEpopulation for commercial/industrial land uses. It will be assumed the industrial/commercialworker is exposed per USEPA default guidance parameters.

4.2.3 - Summary of Potentially Complete Exposure Pathways

The following are the exposure pathways that are considered to be complete under present landuse conditions (i.e., present and/or future conditions). Under present land use, exposurescenarios were evaluated for both present conditions and future conditions. As previously noted,additional exposure scenarios were not selected for evaluation under future land use, because theproperty will likely continue to be used for commercial/industrial property in the future.

4.2.3.1 - Alliant Energy/IPC Property - Present Land Use Conditions.

Alliant Energy/IPC Employees

Incidental ingestion and dermal contact with surface soils by on-site workers isgreatly reduced or limited, but not zero. Thus, this pathway is considered to becomplete, but exposure to contaminated soil is significantly diminished becausecontaminated soils are under pavement, buildings, and grassy areas.

Inhalation of fugitive dust (exposure route by this route is diminished because muchof the site is vegetated or paved).

Alliant Energy/IPC Property Construction Workers

- Incidental ingestion and dermal contact with surface and subsurface soils byconstruction workers performing intrusive activities in impacted soils.

- Inhalation of fugitive dusts and volatile vapors generated during intrusive activities.

- Incidental ingestion and dermal contact with groundwater by construction workersperforming intrusive activities in saturated soils (qualitative assessment).

Alliant Energy/IPC Customers and Vendors

- None anticipated.

4.2.3.2 - Alliant Energy/IPC Property - Potential Future Conditions.


- Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil by employees working in areas of newly exposed soils.

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Incidental ingestion and dermal contact with surface and subsurface soils byconstruction workers performing intrusive activities in impacted soils.

Inhalation of fugitive dusts and volatile vapors generated during intrusive activities.


Alliant Energy/IPC customers and vendors (Site Visitors/Trespassers)

- Incidental- ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil in areas of newly exposed soils.

Hypothetical Resident (adult and child)

- Ingestion and dermal contact with groundwater, and inhalation of volatiles whileshowering.

4.2.3.3 - Former Allied Steel Property - Present Land Use Conditions.

Riverview Partners Employees

None anticipated.

Former Allied Steel Property Construction Workers



Incidental ingestion and dermal contact with groundwater by construction workersperforming intrusive activities in saturated soils (qualitative assessment).

Trespassers/Site Visitors

- Incidental ingestion and dermal contact with soil, and inhalation of fugitivedust from surface soil in areas of exposed soils.

4.2.3.4 - Former Allied Steel Property - Potential Future Land Use.


- Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil by employees working in areas of newly exposed soils.

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Trespassers/Site Visitors

Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil in areas of newly exposed soils.

Child Recreational Visitor (redevelopment as a park)

Incidental ingestion and dermal contact with soils and inhalation of volatiles fromnewly exposed surface soils.

Industrial Worker

Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil.


Ingestion and dermal contact with groundwater, and inhalation of volatiles whileshowering.

4.2.3.5 - Off-Site Mississippi River Corridor - Present and Future Conditions.

Local Recreational Users, Visitors, and Tourists

- None anticipated.

4.3 - QUANTIFICATION OF EXPOSURE POINT CONCENTRATIONS

In order to calculate the magnitude of exposures and the associated risks that may be experiencedby an individual, the concentration of the COPCs in the exposure medium must be known orestimated. This concentration is referred to as an exposure point concentration. In order toestimate exposures, this concentration is combined with assumptions regarding the rate andmagnitude of contact with the constituent. Exposure point concentrations for soil, and sediment(for ecological assessment) were determined using the complete investigation data set. Thefollowing text summarizes the basis for the exposure point concentrations for each completepathway to be quantitatively evaluated.

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4.3.1 - Concentrations in Soil

The exposure point concentration for soil was generally represented by the 95 percent upperconfidence limit (UCL) on the arithmetic mean. In other words, the 95 percent UCL represents avalue where there is 95 percent confidence that the mean concentration of the data set is nogreater than that value. This approach is based on a conservative assumption that the data fitlognormal distributions. This assumption is conservative because 95 percent UCLs from alognormal distribution produce EPCs that are greater than 95 percent UCLs from a normaldistribution. Thus, the risk estimates generated by this approach are greater than the riskestimates based on EPCs from normal distributions. If the 95 percent UCL exceeded themaximum concentration detected on site, the maximum concentration was used for the exposurepoint concentration. However, due to the small number of surface soil samples, the maximumconcentration detected was applied as the exposure point concentration for these chemicals.Within Appendix B are the process and equations used for calculating the 95 percent UCL for thesoil data.

Prior to calculating the 95 percent UCL, soils data for the site were segregated into three depthcategories.

1. Surface soil samples that employees, trespasser, and construction workers mayhave exposure to either under present or future conditions. Surface soil sampleswere defined as a depth of 1 foot or less bgs.

2. Subsurface soils generally available for contact as a result of development weredefined as those from 1 to 10 feet bgs. These subsurface soils were assumed to bepotentially available for contact by construction workers, and as potential surfacesoils by on-site workers or site visitors/trespassers if soils are unearthed in thefuture.

3. Subsurface soils from 10 to 20 feet bgs were generally considered unavailable forcontact as a result of development, but potentially available for contact if sewerlines were in need of repair. These subsurface soils were assumed to bepotentially available only to a select group of construction workers.

Summary statistics and EPCs for surface soil (0-1 foot), subsurface soil (1-10 feet), andsubsurface soil (10-20 feet) are presented in Tables 4-2 through 4-4. Appendices C, D, and Eprovide additional information.

4.3.2 - Concentrations in Mississippi River Sediment

Because no completed pathway existed for human exposure, the detected concentrations wereutilized only for ecological risk evaluation. The exposure point concentrations for the sedimentare listed in Table 4-5.

4.3.3 - Concentrations in Groundwater

For risk management purposes, a hypothetical future resident (adult and child) was evaluated forpotable use of groundwater. Prior to calculating a 95 percent UCL, concentrations for each well

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were averaged (excluding the bedrock aquifer zone), and these averaged concentrations wereused to develop groundwater EPCs following the same procedures as described in Section 4.3.1(concentrations in soil). More specifically, the exposure point concentration for groundwater wasgenerally represented by the 95 percent upper confidence limit (UCL) on the arithmetic meanvalue. This approach is based on a conservative assumption that the data fit lognormaldistributions. If the 95 percent UCL exceeded the maximum concentration detected on site, themaximum concentration was used for the exposure point concentration. Within Appendix B arethe process and equations used for calculating the 95 percent UCL for the groundwater data.

Groundwater monitoring data at this site are organized by aquifers, i.e., Water Table Aquifer,Intermediate Zone, and Bedrock Surface. Water in the Bedrock Surface zone is not impacted.Therefore, only site groundwater data in the Water Table Aquifer and Intermediate Zone, wereused. Exposure point concentrations were determined in the following manner. An averageconcentration for each contaminant in each well in the plume was determined. A 95 percentUCL was then calculated using these averages. For nondetect data, one-half of the analyticaldetection limits were used as "proxy" concentrations.

Summary statistics and EPCs for groundwater are presented in Table 4-6. Appendix E alsoprovides a summary of groundwater chemical concentration data, maximum contaminant levels,and maximum contaminant level goals. It should be noted that the maximum detectedconcentration of benzene in any sampling event is 12,300 ug/L, but the well-averaged maximumconcentration for benzene is 11,850 ug/L. Thus, per the procedures described in Appendix B theEPC for benzene is 11,850 ug/L.

4.4 - QUANTIFICATION OF EXPOSURE

Exposures are estimated by combining predicted environmental concentrations at the selectedexposure points with information describing the extent, frequency, and duration of exposure foreach receptor of concern. This section presents an overview of the approaches used to quantifyexposures, followed by specific details for each selected exposure pathway. The approaches usedin this section to quantify exposures are consistent with guidance produced by the EPA(EPA, 1989, 199 Ib).

Exposure estimates were made for the ingestion, inhalation, and dermal absorption routes bycalculating an average chronic daily intake (referred to as a GDI) or dose expressed in units ofmilligram (mg) of constituent/kilogram (kg) body weight-day (mg/kg-day). Dose can be definedas an exposure rate to a chemical determined over an exposure period per unit body weight, andit is calculated similarly for both ingestion, inhalation, and dermal routes. There are, however,significant differences in the meaning and terms used to describe doses for the ingestion andinhalation, and dermal routes. For the oral and inhalation routes of exposure, the dosescalculated in this assessment are referred to as "administered doses." The administered dose isthe amount of chemical ingested or inhaled, and is analogous to the administered dose in adose-response toxicity experiment. For the dermal absorption pathways, the estimated dose isreferred to as an "absorbed dose." The absorbed dose reflects the amount of chemical that hasbeen absorbed into the body and is available for interaction with biologically important tissues.

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Average GDIs are estimated differently for chemicals exhibiting noncarcinogenic effects andthose exhibiting carcinogenic effects. Average GDIs for noncarcinogens are averaged over theduration of exposure. For carcinogens, average daily doses are averaged over a lifetime.

The GDIs are estimated using exposure point concentrations of chemicals together with otherexposure parameters that specifically describe the exposure pathway. Based on EPA riskassessment guidance (EPA, 1989, 1991b), exposures were quantified by estimating the RMEassociated with the pathway of potential concern. The term RME is defined as the maximumexposure that is reasonably expected to occur at a site (EPA, 1989). In terms of EPA exposureassessment guidance (EPA, 1992), the RME risk estimates can be termed as high-end riskdescriptors, using the highest exposure that is reasonably expected to occur. The RME isintended to place a conservative upper bound on the potential risks, meaning that the riskestimate is unlikely to be underestimated, but it may very well be overestimated. The likelihoodthat this RME scenario may actually occur is small, due to the combination of conservativeassumptions incorporated into the scenario. The RME for a given pathway is derived bycombining the selected exposure point concentration of each chemical with reasonable maximumvalues describing the extent, frequency, and duration of exposure (EPA, 1989). Many of theexposure parameter values used in this assessment have been defined by EPA (EPA, 1989,199 Ib) for the RME case.

4.4.1 - Average Chronic Daily Doses Under Present Land Use Conditions

Under present land use conditions, exposures associated with ingestion, inhalation, and dermalcontact with a medium were assessed when applicable. The exposure point concentrations arepresented in Tables 4-2 through 4-6, while the equations and values used in quantifying chemicalexposures are presented in Appendices C, D, and E, and the exposure factors are presented inTable 4-7. Some exposure factors (e.g., exposure duration) are also summarized in more detailbelow.

4.4.2 - Inhalation, Dermal Contact, and Incidental Ingestion of Soil

Potential exposures through incidental ingestion of soil, dermal contact with soil, and inhalationof particulates and vapors were estimated for the current and/or potential future receptorspreviously described: on-site workers, site visitor/trespasser, construction workers, childrecreational visitors, and industrial worker. The following sections describe the parameters usedfor these receptors which are summarized in Table 4-7.

Although the EPA has developed toxicity values for the oral and inhalation routes of exposure,they have not developed toxicity values for the dermal route of exposure. For this reason, adermal toxicity value was estimated for each COPC by adjusting the oral toxicity values.

4.4.3 - General Exposure Factors for Soil Contact

The frequency of exposure estimates for soil contact for all receptors were obtained from EPAguidance, except where the parameter is sufficiently supported by local weather data with theexception of the on-site worker and construction worker. For the on-site worker and construction

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worker, the 190 days per year exposure duration was based on the assumption that workers work250 days per year (5 days per week for 50 weeks) but for 60 of these days they are not exposed tosoil due to snow cover. These values are supported by local historical weather data fromDubuque, Iowa and Moline, Illinois for the average number of days with 1 inch or more ofsnowcover. For 50 percent of the years recorded, the data from the two cities yielded an averageof 58 days with 1 or more inches of snowcover (State of Iowa's Climatologist's Office facsimilecommunication to Montgomery Watson, April 19, 2000, and National Oceanic and AtmosphericAdministration climatic data, July 2001). The exposure duration for a site visitor was developedassuming that a person in this population would be on site 3 days per week for the 9 warmermonths of the year. These values represent the highest exposure reasonably expected to occur atthis site (RAGS, Part A, p. 6-5). The exposure duration for the child recreational visitor wasdeveloped assuming 2 days per week for the warmest months (April 15 through October 15).The industrial worker scenario assumes the EPA default worker exposure of 250 days per year,but for 60 of these days they are not exposed to soil due to snow cover.

The exposure duration for employees and industrial workers was assumed to be 25 years, whichis the EPA's default value for this parameter. For the site visitor/trespasser the exposure durationwas set based on professional judgment at 10 years as a conservative number of years a personmay frequent a site. Young children and adolescent visitors/trespassers were from ages 7 to16 years old were selected as the most sensitive age group that would likely frequent the siteareas. This value is slightly greater than the average number of years (9) a person is expected tolive at a given residence (EPA, 1997a) and, therefore, is considered to provide a conservativeestimate for the number of years a site visitor/trespasser may frequent the site. The RMEexposure duration for a construction worker was set at 1 year, based on professional judgmentthat the typical construction project at the site would be completed within 1 year. The childrecreational visitor scenario assumes exposure duration of 6 years as the child may frequent thesite from birth to age 6.

The RME estimate of body weight for employees, and construction workers is 70 kg, which isthe EPA-recommended default value for this parameter. The EPA recommends the average bodyweight be used for the RME exposure scenario (EPA, 1989). The rationale is that body weightcorrelates with other variables (e.g., skin surface area and inhalation rate), and that keeping bodyweight constant minimizes error from this dependence. Using an RME value for intake, incombination with an average body weight, is believed to result in an overall RME exposureestimate.

For site visitors/trespassers, data compiled by EPA for males and females between the ages of7 and 16 were averaged to yield an average body weight of 43 kg (EPA, 1997a). The childrecreational visitor scenario is also the EPA default of 15 kg for a child 0 to 6 years.

4.4.4 - Incidental Ingestion Factors for Soil Contact

The recommended average soil ingestion rate for an adult is 50 mg/day, and this value was usedfor the on-site worker and industrial worker (EPA, 1997a). For site visitors/trespasser who wereconservatively estimated to be children and adolescents, the RME soil ingestion rate was

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assumed to be 50 mg/day. This value corresponds to a conservative mean soil ingestion rate forchildren (EPA, 1997a). For construction workers, 480 mg/day was used for the RME, which isconsidered a conjectural value for outdoor activities that was published by Hawley (1985), butdid not have supporting documentation (EPA, 1997b). A 200 mg/day soil ingestion rate wasused for the child recreational visitor (EPA, 1997).

The fraction ingested (FI) value represents the proportion of the soil that is ingested fromaffected areas on the site. An FI of 1 assumes all soil is ingested from the contaminated area onsite. An FI of 1 was used for on-site employees, industrial and construction workers, sitevisitors/trespassers, and child recreational visitors.

4.4.5 - Dermal Absorption Factors for Soil Contact

Additional parameters needed to assess the dermal exposure scenario include the area of exposedskin, the amount of soil adhering to the skin, and the amount of chemical absorbed through theskin from soil. For on-site workers, industrial workers, and construction workers the EPAdermal guidance recommends a skin surface area of 3,300 square centimeters (cm2) whichaccounts for exposed skin on the hands, forearms, and head (EPA, March 2001). For adolescentsunder the site visitors/trespassers scenario, the RME skin surface area was assumed to equal5,700 cm2, which is the default value for adults in the guidance. The EPA default value of2,900 cm2 was used for the child recreational visitor.

The soil-to-skin adherence factor is the amount of soil that adheres to a square centimeter of skin.These values have been measured for different activities. Adherence values for the receptorsselected have been estimated by comparing the activity that a receptor engages into the mostsimilar activity for which measurements have been conducted. The most appropriate soil-to-skinadherence factors were selected from EPA guidance (EPA, 2001).

A value of 0.2 mg/cm2 was selected as the RME for an on-site worker and industrial worker(EPA, 2001). This value is for a gardener, and reflects an average value for an activity thatresults in more soil adherence than is typical for general activities. An RME of 0.2 mg/cm2 wasestimated for children based on both average measurements of children playing in wet soil(which is an activity that results in a relatively high amount of soil adherence) and a95lh percentile estimate of soil adherence for children playing in a day care center. Forconstruction workers, the RME adherence factor was estimated to equal 0.2 mg/cm2, based onmeasurements of utility workers (EPA, 2001).

The amount of chemical that is absorbed through the skin into the body from soil is needed toestimate the dose resulting from dermal exposures to soil. This parameter is termed the fractionof dermal absorption, and is chemical-specific. Values have been established by EPA guidance,and are summarized in Table 3-1. Where recommended values were not available, conservativeestimates of the fraction of dermal absorption were assumed.

4.4.6 - Inhalation Exposure Factors for Soil

As described in Section 4.2, the receptors have the potential to inhale dusts and vapors. Toevaluate this exposure, it is necessary to estimate the amount of air inhaled by the receptors.

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Inhalation rates can be provided in terms of the amount of air inhaled per hour in combinationwith the number of hours of exposure, or the amount of air inhaled per day. The nature of theavailable information determined which form was most appropriate for a given receptor. Therationale for each of the inhalation rates can be found in the footnotes (i.e., i series) contained inTable 4-7.

This is an active commercial/industrial site. The "on-site workers" are individuals who areemployed to carry out the business activities at this location. Site visitors are individuals whovisit this location to conduct business (e.g., bill payers and vendors). Construction workers areindividuals who may become involved in intrusive soil activities in the 1- to 20-foot soil profile.Utility workers are people who perform work on sewer lines in the 10- to 20-foot soil profile.

On-site workers and industrial workers were assumed to engage in moderate activity, whichcorresponds to an inhalation rate of 1.5 cubic meter per hour (m3/hr) (EPA, 1997b). Sitevisitors/trespassers, and child recreational visitors were assumed to engage in light activity,which corresponds to an inhalation rate of 1.0 cubic meter per hour (m3/hr) (EPA, 1997b). Theexposure time for on-site workers was assumed to be 8 hours per day by convention. Sitevisitors/trespassers and child recreational visitors were assumed to be on site 2 hours per day, asa conservative upper limit, based on professional judgment.

For construction workers, the inhalation rates employed in the RME scenario, was 2.5 m3/hr.These values correspond to the average value for outdoor workers engaged in heavy andmoderate activity, respectively (EPA, 1997b). The exposure time for construction workers wasassumed to be 8 hours per day.

The final parameters in the estimate of inhalation exposure are the amount of dust or vapor in theair. For dust, EPA recommends the calculation of a ratio between the concentration of theconstituent in soil, and the concentration of the dust in air. This ratio is called the paniculateemission factor (PEF). The value of 1.32xl09 cubic meter per kilogram (m3/kg) used for most ofthe receptors is the EPA default value for this parameter (EPA, 1996a).

The default PEF value was not used for construction workers because the default value onlyaccounts for wind-generated dust, whereas mechanical equipment creates additional dust at aconstruction site. The PEF for construction workers was assumed to be IxlO6 m3/kg (the lowerthe PEF, the more dust generated). This value equates to a dust concentration of 1 milligram percubic meter (mg/m3), which is an estimate of the minimum level at which dust is visible in air.This value represents a reasonably high average dust concentration in air for construction-relatedactivities, based on professional judgment.

For vapors, EPA recommends calculation of a ratio between the concentration of the constituentin soil and its concentration in air (EPA, 1996a). This ratio is called the volatilization factor(VF). Values of VF have been calculated as shown in Appendix D, and are chemical specific.VFs are only developed for the more volatile compounds (i.e., VOCs). For surface soils, thevolatilization of chemicals was incorporated in risk and hazard estimates for on-site workers.

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4.4.7 - General Exposure Factors for Groundwater Use

The exposure factors for the adult and child resident potable use of groundwater are the standardEPA default parameters. The potable uses quantified in this assessment are ingestion, dermalcontact, and inhalation of volatiles during showering. For the adult resident, it was assumed thathe would ingest 2 liters per day, 350 days per year, for 24 years of exposure. Body weight isassumed to be 70 kg. A 15 kg child is assumed to ingest 1 liter of water per day, 350 days peryear for 6 years of exposure. These exposure factors for the ingestion exposure route, as well asthe exposure factors for dermal absorption and inhalation of volatiles during showering, arepresented in Table 4-7.

4.4.8 - Summary of Exposure Assessment

The exposure assessment was performed to identify human populations potentially exposed tochemicals detected in media on the site. The present and future land uses at this site arecommercial/industrial. Therefore, the human populations included on-site workers, constructionworker, site visitor/trespasser population, child recreational visitor, industrial worker, andresident. In addition, levels of potential exposure were quantified for each potentially completeexposure pathway.

The estimates of chemical exposure are used with estimates of toxicity to predict health risks inthe next section of this report. The following are the exposure pathways that are considered to becomplete under present land use conditions (i.e., present and/or future conditions). Under presentland use, exposure scenarios were evaluated for both present conditions and future conditions.As previously noted, the Alliant Energy/IPC property will likely continue to be used in its presentoperations in the future. However, the future redevelopment of the former Allied Steel propertyis not definitive. Possible future land reuse may include a park or another industrial/commercialestablishment. Although groundwater is not currently used at the site, for management purposes,a residential (adult and child) exposure to groundwater is quantified.

4.4.8.1 - Present/Future Conditions.




Incidental ingestion and dermal contact with groundwater by construction workersperforming intrusive activities in saturated soils (qualitative assessment).



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4.4.8.2 - Potential Future Conditions.

AHiant Energy/IPC Employees

Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom with surface soil by employees working in areas of exposed soils.

Alliant Energy/IPC Customers and Vendors (Site Visitors/Trespassers)

- Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil in areas of exposed soils.


Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil in areas of exposed soils.

Trespassers/Site Visitors on Former Allied Steel Property

Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil by site visitors/trespassers in areas of exposed soils.

Child Recreational Visitor on Former Allied Steel Property


Industrial Worker on Former Allied Steel Property



Ingestion and dermal contact with groundwater, and inhalation of volatiles duringshowering.

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SECTION 5 - RISK CHARACTERIZATION

In this section, the human health risks associated with the human exposure pathways previouslyidentified are discussed. This section discusses how calculated exposure doses are converted intopotential health risks. The health risks are presented by potentially exposed population andmedium.

5.1 - GENERAL METHODOLOGY

Risk characterization involves the integration of health effects information developed as part ofthe dose-response assessment with exposure estimates developed as part of the exposureassessment. The result is a quantitative estimate of chronic noncarcinogenic risks based on thepresumption that a threshold dose is required to elicit a response, as well as a quantitativeestimate of carcinogenic risks presumed to exist regardless of the dose. These estimates areusually presented in either probabilistic terms (e.g., one-in-one-million), or with reference tospecific benchmark or threshold levels. Because risk estimates are based on a combination ofmeasurements and assumptions, it is important to provide information on sources of uncertaintyin risk characterization. The key elements of risk characterization included in this section are anestimation of risk, a presentation of risk, and an uncertainty analysis.

5.1.1 - Noncarcinogenic Risks

The HQ is the ratio of the estimated exposure dose to the RfD. This ratio is used to evaluatenoncarcinogenic health effects due to exposure to a chemical. An HQ greater than 1.0 indicatesthe estimated exposure dose for that chemical exceeds acceptable levels for protection againstnoncarcinogenic effects. Although an HQ of less than 1.0 suggests noncarcinogenic healtheffects should not occur, an HQ of slightly greater than 1.0 is not necessarily an indication thatadverse effects will occur.

The EPA has developed a set of health-based benchmark numbers, called RfDs, as guideposts ina risk assessment. RfDs are an adaptation of the earlier toxicological measure of "acceptabledaily dose" (ADI). The unit of a reference dose is mg/kg-day. The RfDs provide an estimate ofthe daily exposure level for human populations, including sensitive subpopulations, which arelikely to be without appreciable risk of deleterious effects during a lifetime. The potential foradverse effects on human health (other than cancer) is evaluated by comparing an intake over aspecific time period (subchronic or chronic) with an RfD derived for a similar exposure period.In this B1RA, only chronic RfDs were used because EPA has not developed subchronic RfDs formany of the COPCs for this site.

The HQ is the ratio (unitless) of the estimated exposure dose of a compound to an RfD judged tobe without adverse effects given long-term exposure. Thus, the quotient is used as a measure ofpotential noncarcinogenic health risks. Due to the margin of safety built into the RfD value,exceedance of the number has no immediate meaning with regard to specific health effects, thefrequency of effects, or the magnitude of effects. However, exceedance of the number should

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serve as an indicator that the potential for unacceptable exposure does exist and furtherevaluation needs to be considered. The effects of noncarcinogens in the body vary greatly withregard to potential target organs, threshold dose, and "severity" of effect. Therefore, theindividual toxicity for each compound needs to be assessed with the following equation:

Hazard Quotient (HQ) = Chronic Daily Intake (CDI)/Reference Dose (RfD)

If the HQ is less than 1.0, then no chronic health effects are expected to occur. If the HQ isgreater than 1.0, then adverse health risks are possible. In the case of noncarcinogenic effects,chronic exposure below a threshold dose results in a nonresponse or a diminished response.

The sum of the HQs is termed the hazard index (HI). Current regulatorymethodology assumes His can be summed across exposure routes for all media atthe site to derive a "Total Site Risk." The EPA has stated sites with anoncarcinogenic HI less than 1.0 generally do not warrant remedial action(Clay, 1991).

5.1.2 - Carcinogenic Risks

Public health risks are evaluated separately for carcinogenic and noncarcinogenic effects. Theexcess lifetime cancer risk is an estimate of the increased risk of cancer that results from lifetimeexposure, at specified average daily dosages, to chemicals detected in media at a site. Excesslifetime cancer risk, equal to the product of the exposure dose and the SF, is estimated for eachknown, probable, or possible carcinogenic chemical in each medium. The risk values providedin this report are an indication of the increased risk, above that applying to the generalpopulation, which may result from the exposure scenarios described in the Exposure Assessmentin Section 4. The risk estimate is considered to be an upper bound estimate; therefore, it is likelythat the true risk is less than the predicted value. Current regulatory methodology assumesexcess lifetime cancer risks can be summed across routes of exposure and chemicals to derive a"Total Site Risk" (EPA, 1989). The EPA (Clay, 1991) has stated sites with a total site riskexcess less than 10"4 (1 in 10,000) generally do not warrant remedial action.

The incremental risk is calculated for each exposure scenario based on the following basicequation:

Cancer Risk = Exposure Dose x Slope Factor (SF)

where the CSF is in units of (mg/kg/day)"1 based on a compound-specific cancerbioassay dose response curve.

The exposure dose is adjusted over a 70-year lifetime. The summation of dose is in keeping withthe concept that for some compounds there is no threshold dose and implies that total, lifetimeexposure is of greater importance than the actual dose during the exposure event(s). Ingestionand inhalation risks are calculated separately since compounds often have different CSFs for

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differing routes of exposure. The different CSFs relate to the pharmacokinetics inherent in eachchemical/organ and the specific routes of uptake.

SFs are derived by EPA in an intentionally conservative way, that is, the actual risk is notexpected to exceed the predicted risk, and could be considerably lower. Cancer risks calculatedusing these conservative SFs and reasonable maximum exposure estimates are upper boundestimates of excess cancer risk potentially arising from exposure to the chemicals in question. Anumber of assumptions have been made in the derivation of these values, many of which arelikely to overestimate exposure and toxicity. The actual incidence of excess cancers is likely tobe lower than these estimates and may be zero.

Lifetime daily intakes, using an averaging time of up to 70 years, effectively prorate the totalcumulative dose over a lifetime. This approach is based on the assumption for carcinogens that ahigh dose received over a short period of time at any age is equivalent to a corresponding lowdose received over a lifetime (EPA, 1989). This assumption is unlikely to be true for allcarcinogens, and introduces uncertainty into the assessment of potential risk. This assumptionmay also lead to an overestimate or underestimate of potential risk, depending upon the actualtiming of exposure and the mechanism of action of individual carcinogens.

5.1.3 - Lead

The risk associated with lead exposure is assessed using special EPA models, which take intoaccount lead exposure from multiple routes and sources. According to the EPA TechnicalWorkgroup for Lead (TRW) guidance document (EPA, 1999), a reasonable screening level forsoil lead at industrial/commercial sites is 750 mg/kg. Depending upon the exposure conditions,much higher soil lead concentrations may also be considered to pose no public health concerns.For residential exposures, EPA considers an average lead concentration of 400 mg/kg to be areasonable screening level (EPA, 1998).

The detected lead concentrations on the Alliant Energy/IPC property range from 69 mg/kg to551 mg/kg in six of nine samples. The average soil lead concentration for this property is177.5 mg/kg. The current and foreseeable future land use of this property isindustrial/commercial purposes. All of the detected concentrations are below the reasonableindustrial/commercial soil lead screening level of 750 mg/kg. The average soil leadconcentration (177.5 mg/kg) is below both the industrial/commercial and residential screeninglevels of 750 mg/kg and 400 mg/kg, respectively.

The detected lead concentrations on the Allied Steel portion of the property range from 32 mg/kgto 1470 mg/kg in thirteen of thirteen samples. Twelve of the thirteen samples collected hadconcentrations less than 688 mg/kg. The average soil lead concentration for this property is393.6 mg/kg. Currently the property is unused and foreseeable future land uses may includeindustrial/commercial purposes or re-use as a recreational park. The average soil leadconcentration (393.6 mg/kg) is below both the industrial/commercial and residential screeninglevels of 750 mg/kg and 400 mg/kg, respectively.

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Average soil-lead concentrations for the Alliant Energy/IPC property and for the Allied Steelportion of the site are below the EPA industrial/commercial and residential screening levels forsoil lead. For these reasons, current and possible future exposures to lead in soils are notexpected to pose a public health concern for any identified site receptors, including childrenplaying in the park.

5.2 - RISK ASSOCIATED WITH PRESENT AND FUTURE LAND USE CONDITIONS

The following is a discussion of the health risk associated with each site-specific exposurescenario by complete exposure pathway under present land use conditions. It should be notedthat the construction worker scenario is potentially applicable under present site conditions.However, the health risk estimates for on-site workers and site visitors/trespassers are potentiallyapplicable under future site conditions only if site conditions would change to expose surfacesoils or if subsurface soils were brought to the surface. The distinction is summarized below andin Table 5-1 where the potential health risks are summarized by potentially exposed population.

5.2.1 - Construction Workers - Present and Future Conditions

The following is a discussion of potential health risks for construction workers on the AlliantEnergy/IPC property and the former Allied Steel properties, respectively. The constructionworkers were considered to be potentially exposed to surface and subsurface soils. Forsubsurface soils, the risks associated with soils (1 to 10 feet in depth) and (10 to 20 feet in depth)were evaluated separately. Construction workers would unlikely be exposed to soils below10 feet during construction activities, but the potential does exist if they were to excavate soil torepair or replace existing sewer lines that are as deep as 20 feet in the vicinity of the site. Thefollowing were the exposure pathways assessed for construction worker on both sides of theproperty.

Incidental ingestion and dermal contact with surface and subsurface soils byconstruction workers working in impacted soils.


• Incidental ingestion and dermal contact with groundwater by construction workersworking in saturated soils (qualitative assessment).

5.2.1.1 - Alliant Energy/IPC Property Construction Workers. Refer to Tables F-l throughF-6 in Appendix F for the chemical-specific risks for Alliant Energy/IPC property constructionworkers. The overall risk estimates are provided in Table 5-1.

Based on the exposure assumptions used, it was estimated noncarcinogenic health effects wouldpotentially occur in construction workers exposed to the surface soils (HI = 18). The majorchemicals contributing to the total noncarcinogenic risks for this scenario include exposure toPCBs (86 percent) arsenic (12 percent). Noncarcinogenic health effects would also be expectedfor construction workers exposed to subsurface soil as the His were equal to 10 and 2 for shallow

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and deep subsurface soils, respectively. Noncarcinogenic health effects for these depth intervalswere based primarily on naphthalene and benzene. Noncarcinogenic health effects are notexpected for construction workers who may have incidental contact with contaminatedgroundwater.

The cumulative cancer risk for surface soil (4xlO"5), and deep subsurface soil (4xlO"5) do exceedIxlO"4. However, the risk to shallow subsurface soil (4x10~4) is greater than IxlO"4. The majorchemical contributing to the total carcinogenic risks from the shallow subsurface soil wasbenzo(a)pyrene (92 percent). This was also the case for the deeper subsurface soil(i.e., 75 percent). The cancer risk associated with surface soils was primarily associated with thePCBs (25 percent), arsenic (52 percent), and benzo(a)pyrene (15 percent). Carcinogenic healtheffects are not expected for construction workers who may have incidental contact withcontaminated groundwater.

The risk associated with contact with groundwater was considered potentially complete belowthe water table, which is approximately 10 feet. However, for construction workers that work inthe trench or excavation, it is considered reasonable to assume the excavation would bedewatered; therefore, little if any exposure with groundwater would occur. For this reason, thispotential exposure pathway was not quantitatively assessed, because it was consideredinsignificant from an exposure standpoint compared to other exposure pathways (i.e., soilingestion).

5.2.1.2 - Former Allied Steel Property Construction Workers. Refer to Tables F-7 throughF-12 in Appendix F for the chemical-specific risks for former Allied Steel property constructionworkers. The overall risk estimates are provided in Table 5-1.

Based on the exposure assumptions used, it was estimated noncarcinogenic health effects couldpotentially occur in construction workers exposed to the surface soils (HI = 4.4). The majorchemicals contributing to the total noncarcinogenic risks for this scenario are exposure tochromium VI (38 percent), iron (32 percent), and arsenic (24 percent). Noncarcinogenic healtheffects, based on chronic RfDs, would be expected for construction workers exposed tosubsurface soil, as the HI was above 1 for both shallow and deep subsurface soils (HI = 6.9 and6.6, respectively). Benzene is the major contributor to these His (38%).

The cumulative cancer risk for surface soil (2xlO"5) and shallow subsurface soil (IxlO"4), arebelow or equal to IxlO"4. The risks to deep subsurface soil (5 xlO"4) are greater than IxlO"4. Themajor chemical contributing to the total carcinogenic risks from the deep subsurface soil wasbenzo(a)pyrene (78 percent). This was also the case for the shallow subsurface soil(i.e., 69 percent). The cancer risk associated with surface soils was primarily associated withchromium (43 percent) and arsenic (41 percent).

The risk associated with groundwater contact was considered potentially complete below thewater table, which is approximately 10 feet. However, for construction workers that work in thetrench or excavation, it is considered reasonable to assume the excavation would be dewatered;therefore, little if any exposure with groundwater would occur. For this reason, this potential

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exposure pathway was not quantitatively assessed, because it was considered insignificant froman exposure standpoint compared to other exposure pathways (i.e., soil ingestion).

5.2.2 - On-Site Workers and Site Visitors/Trespassers - Present and Future Conditions

The following is a discussion of potential health risks for on-site workers and sitevisitors/trespassers on the Alliant Energy/TPC property and the former Allied Steel properties,respectively. Under present land use conditions, only soil exposure for on-site workers wasquantified. Soil exposure for the visitor/trespasser is anticipated to be insignificant, because thesoils are covered with buildings, pavement, gravel, or lawn, and the duration and frequency ofvisits are limited. Risks associated with soil exposure were estimated for future conditions(i.e., commercial/industrial) for various scenarios to provide an indication of the risk associatedwith the soils on site. The risks associated with soils (1 to 10 feet in depth) were evaluated underthe scenario that during future redevelopment of the property, the subsurface soils were broughtto the surface. On-site workers and site visitors/trespassers were not expected to be exposed tosoils below 10 feet, a limit typically considered reasonable for redevelopment of a property. Thefollowing were the exposure pathways that were assessed for each receptor group on both sidesof the property.


Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil by employees working in areas of exposed soils.


- Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil in areas of exposed soils.

Former Allied Steel Property Industrial Workers

Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil by employees working in areas of exposed soils.

Former Allied Steel Property Trespassers/Site Visitors

Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil by trespassers/site visitors in areas of exposed soils.

Former Allied Steel Property Child Recreational Visitor

- Incidental ingestion and dermal contact with soil, and inhalation of fugitive dustfrom surface soil by child recreational users in a park land re-use setting.

Hypothetical Future Site Resident

- Ingestion and dermal contact with groundwater, and inhalation of volatile vapors byhypothetical future on-site residents.

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5.2.2.1 - Alliant Energy/IPC Property On-Site Worker. Refer to Tables F-13 through F-16 inAppendix F for the chemical-specific risks for Alliant Energy/IPC property on-site workers. Theoverall risk estimates are provided in Table 5-1.

Based on the exposure assumptions used, it was estimated noncarcinogenic health effects, basedon chronic RfDs, would potentially occur if on-site workers were exposed to the surface soils(HI = 4.3), or shallow subsurface soils (HI = 2.2). The major chemical contributing to the totalnoncarcinogenic risks in surface soils is PCBs (Arochlor 1260 at 90 percent). The majorchemicals contributing to the total noncarcinogenic risks in shallow subsurface soils are benzene(36 percent) and naphthalene (43 percent).

The cumulative cancer risk for surface soil (IxlO"4) and shallow subsurface soil (2xlO~3), areequal to or above IxlO"4. The cancer risk associated with surface soils was primarily associatedwith arsenic (33 percent), PCBs (38 percent), and benzo(a)pyrene (22 percent). The majorchemical contributing to the total carcinogenic risks from the shallow subsurface soil wasbenzo(a)pyrene (92 percent).

5.2.2.2 - Alliant Energy/IPC Property Site Visitors/Trespassers. Refer to Tables F-17through F-20 in Appendix F for the chemical-specific risks for Alliant Energy/IPC property sitevisitor/trespasser. The overall risk estimates are provided in Table 5-1.

Based on the exposure assumptions used and chronic RfDs, it was estimated noncarcinogenichealth effects would potentially occur if on-site workers/trespassers were exposed to the surfacesoils (HI = 5.4 ), or shallow subsurface soils (HI = 1.9). The major chemicals contributing to thetotal noncarcinogenic risks in surface soils are PCBs (92 percent) and arsenic (6 percent) insurface soils. The major chemicals contributing to the total noncarcinogenic risks in shallowsubsurface soils are naphthalene (65 percent) and fluorene (11 percent).

The cumulative cancer risk for surface soil (7x10~5) was below IxlO"4. The cumulative cancerrisk for shallow subsurface soil (IxlO"3) is above IxlO"4. The cancer risk associated with surfacesoils was primarily associated with the PCBs (40 percent) and arsenic (29 percent). The majorchemical contributing to the total carcinogenic risks from the shallow subsurface soil wasbenzo(a)pyrene (92 percent).

5.2.2.3 - Former Allied Steel Property Industrial Worker. Refer to Tables F-21 through F-24in Appendix F for the chemical-specific future risks for former Allied Steel property industrialworker. The overall risk estimates are provided in Table 5-1.

Based on the exposure assumptions used and chronic RfDs, it was estimated noncarcinogenichealth effects would not occur in future industrial workers exposed to the surface soils (HI = 0.6),but may potentially occur if exposed to shallow subsurface soils (HI = 2.2). The major chemicalscontributing to the total noncarcinogenic risks in surface soils are iron (45 percent) and arsenic(26 percent). The major chemical contributing to the total noncarcinogenic risks in shallowsubsurface soils is benzene (68 percent).

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The cumulative cancer risk for surface soil (5x10) is below 1x10" , but shallow subsurface soil(6x10" ) is above this benchmark. The cancer risk associated with surface soils was primarilyassociated with the arsenic (52 percent), and benzo(a)pyrene (32 percent). The major chemicalcontributing to the total carcinogenic risks from the shallow subsurface soil was benzo(a)pyrene(76 percent).

5.2.2.4 - Former Allied Steel Property Site Visitors/Trespassers. Refer to Tables F-25through F-28 in Appendix F for the chemical-specific risks for former Allied Steel propertyvisitors and trespassers. The overall risk estimates are provided in Table 5-1.

Based on the exposure assumptions used and chronic RfDs, it was estimated noncarcinogenichealth effects would not occur if site visitors/trespassers were exposed to the surface soils(HI = 0.7), but may potentially occur if exposed to shallow subsurface soils (HI = 1.1). Themajor chemicals contributing to the total noncarcinogenic risks in shallow subsurface soils arebenzene (23 percent) and naphthalene (18 percent).

The cumulative cancer risk for surface soil (2xlO"5) is below IxlO"4, but for shallow subsurfacesoil (3xlO"4), is above the benchmark. The cancer risk associated with surface soils wasprimarily associated with arsenic (48 percent) and benzo(a)pyrene (35 percent). The majorchemical contributing to the total carcinogenic risks from the shallow subsurface soil wasbenzo(a)pyrene (77 percent).

5.2.2.5 - Former Allied Steel Property Future Child Recreational Visitor. Refer toTables F-29 and F-30 in Appendix F for the chemical-specific risks for former Allied Steelproperty future child recreational visitor. The overall risk estimates are provided in Table 5-1.

In surface soils, the estimated noncarcinogenic health effects for the child recreational visitors(HI = 1.0) is equal to the benchmark when using chronic RfDs for this estimate. The majorchemicals contributing to the total noncarcinogenic risks in surface soils are arsenic (40 percent)and Arochlor 1242 (31 percent). The cumulative cancer risk for surface soil is 5xlO"6. Thecancer risk associated with surface soils was primarily associated with the arsenic (74 percent).

5.2.2.6 • Former Allied Steel Property Future Residents. Refer to Tables F-31 through F-34in Appendix F for the chemical-specific risks for former Allied Steel property future hypotheticalresident (adult and child). The overall risk estimates are provided in Table 5-1.

A quantitative risk assessment for a future resident scenario that incorporates potential drinkingwater exposure is necessary to make risk management decisions at this site. Therefore, thisB1RA includes estimates of hypothetical exposures to child and adults using EPA reasonablemaximum exposure assumptions for potential exposure to contaminated groundwater. Theprimary contributor to cancer and noncarcinogenic risk associated with groundwater is benzenecontamination associated with monitoring wells MW-5 and MW-12.

The cumulative cancer risk estimates for groundwater exposures to adults and children are 8xlO"3

and 6xlO"3, respectively. The cancer risk estimates for adults and children associated with

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groundwater are primarily associated with benzene (85 and 70 percent of total risk, respectively).Noncarcinogenic health effects, based on chronic RfDs, for hypothetical future residents exposedto groundwater are greater than one for both the child (HI= 420) and the adults (HI = 180). Theprimary contributors to carcinogenic noncarcinogenic health effects for child and adult isbenzene.

5.3 - SUMMARY OF HUMAN HEALTH RISK EVALUATION

This human health evaluation evaluated the potential exposures of human receptors to chemicalsdetected in media on or near the site. Standard EPA methodologies were used to estimate levelsof exposure and health risk by potentially exposed populations. The following is a summary ofresults of the human health component of the B1RA.

5.3.1 - Exposure Assessment

Under present land use, exposure scenarios were evaluated for both present conditions and futureconditions. As previously noted, additional exposure scenarios for the Alliant Energy/IPCproperty were not selected for evaluation under future land use, because the property will likelycontinue to be used for commercial/industrial property in the future. The following is a summaryof the exposure pathways considered to be complete under present and future conditions. Theexposure potential was evaluated separately for the Alliant Energy/IPC property and formerAllied Steel property.

5.3.1.1 - Present Conditions.


- Incidental ingestion and dermal contact with surface and subsurface soils byconstruction workers working in impacted soils.


Incidental ingestion and dermal contact with groundwater by construction workersworking in saturated soils (qualitative assessment).


Incidental ingestion and dermal contact with surface and subsurface soils byconstruction workers working in impacted soils.


- Incidental ingestion and dermal contact with groundwater by construction workersworking in saturated soils (qualitative assessment).

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5.3.1.2 - Future Conditions.


Incidental ingestion and dermal contact with soil, and inhalation of fugitiveemissions with surface soil by employees working in areas of exposed soils.


Incidental ingestion and dermal contact with soil, and inhalation of fugitiveemissions with surface soil in areas of exposed soils.


- Incidental ingestion and dermal contact with soil, and inhalation of fugitiveemissions with surface soil in areas of exposed soils.

Trespassers/Site Visitors and Child Recreational Visitor on Former Allied SteelProperty

Incidental ingestion and dermal contact with soil, and inhalation of fugitiveemissions with surface soil by site visitors /trespassers and child recreational visitorin areas of exposed soils.

Hypothetical Future Residents (adult and child)

Ingestion and dermal contact with groundwater and inhalation of volatiles duringshowering.

5.3.2 - Summary of the Health Risk Estimates

Under present conditions, health risk estimates for exposure to surface and subsurface soilindicate a potential risk to on-site industrial and construction workers. However, chemicalsdetected in the soils on site are located below buildings, pavement, or lawns and vegetativecover. These conditions will reduce ingestion, dermal contact, and inhalation of contaminatedsoil as compared to the assumed bare soil conditions for the surface soil exposures. In addition,chemically-impacted groundwater is not used as a drinking water source, because the site andsurrounding area are supplied by a municipal water system. Indoor air measurements in the on-site district office building were generally below EPA reference concentrations; this informationwill be provided under separate cover at a later date. For these reasons, present conditions arenot considered to present a potential public health concern to site workers, visitors or trespassers.

Under present conditions, if construction workers or on-site industrial workers would dig into thesurface and subsurface soils and become exposed to the soils through incidental ingestion ordermal contact there is the potential for elevated noncarcinogenic (HI >1) and carcinogenic(cancer risk >lxlO"4) risks. The primary chemicals of concern are PAHs, PCBs, and arsenic.

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These risk estimates assume the workers do not use protective clothing (e.g., gloves) to preventsoil exposure, and perform manual labor that would bring them in direct contact with the soil.

Under future conditions, if the surface and or subsurface soils become accessible and remainaccessible for many years (i.e., 10 to 25 years), site worker's, visitor's or trespasser's exposure tosoil (either surface or subsurface), could potentially pose a health concern (i.e., HI >1 and cancerrisk >lxlO~4). This could only occur if site workers, visitors, or trespassers would come in directcontact with the soil. Residential use of groundwater under hypothetical future conditions wouldalso pose a concern for carcinogenic and noncarcinogenic health effects.

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SECTION 6 - SCREENING LEVEL ECOLOGICAL RISK ASSESSMENT

This section discusses the potential impacts to nonhuman receptors associated with exposures tothe COPCs at the site. The format of this ecological risk assessment (ERA) is consistent with thefollowing guidelines:

Guidelines for Ecological Risk Assessment, EPA, April 1998

Ecological Risk Assessment Guidance for Superfund: Process for Designing andConducting Ecological Risk Assessments, EPA, June 1997 (This document servesas the primary guidance for the development of the Ecological Risk Assessment.)

Representative Sampling Guidance Document, Volume 3: Ecological, EPA,May 1997

• ECO Update, Intermittent Bulletins, EPA, 1991 to 1996

6.1 - APPROACH AND SCOPE OF ASSESSMENT

The ERA follows the approach suggested in the more recent ERA guidelines, (EPA, 1997 and1998 and Efroymson, et al., 1997). Ecological assessments are conducted using a tieredapproach where the complexity of the assessment increases with each successive tier. Each tierconsists of a problem formulation step, an analysis step (consisting of an exposure assessmentand stressor assessment), and risk characterization.

This ecological assessment is a screening level assessment. The screening level ERA, or Tier 1ERA, is a conservative preliminary assessment. The assessment is designed so exposurepathways that have the potential to pose ecological risks are not screened from further evaluation.Because of the conservative nature of the screening level ERA, the results are not sufficient tosupport remediation by themselves. The purpose of the screening level ERA is to determinewhether there is a need for further assessment, or support the decision that there are no completedpathways that pose significant risk to receptors. This screening level ERA was composed of thefollowing three steps:

1. Preliminary Problem Formulation

2. Screening Analyses

3. Risk Characterization

This assessment started with a problem formulation stage to determine the assessment endpointsand measurement endpoints. Once the assessment and measurement endpoints were determined,then the analysis was performed. The analysis consisted of comparing the level of ecologicalreceptor exposure (through the use of sediment and soil data), and screening levels of ecologicalreceptor exposure (toxicity benchmarks). Finally the data from the analysis steps were combinedto characterize the risk (i.e., risk characterization).

A conservative approach was taken throughout this screening assessment so that an obviousindication could be made whether the site poses little or no ecological risk. If the conclusion of

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this screening assessment clearly demonstrates no risk exists, then no additional assessment iswarranted. However, if there is not a clear conclusion of any risk, additional tiers of datacollection and analysis may need to be performed to refine the preliminary screening ecologicalassessment, and determine if ecological risks are likely. Additional assessment tiers may includeconducting more complex fate and transport modeling, bioassays, or field studies to determine ifecological effects are likely.

6.2 - PROBLEM FORMULATION

The ecological assessment started with a problem formulation stage. Within the problemformulation an identification of chemicals of ecological concern is made, and an initial exposureassessment, which includes identification of potential receptor species, and identification ofpotential exposure pathways is conducted. Information from this step was used during theScreening Analysis step of the ERA, which describe site-specific exposures and toxic ecologicaleffects. The main focus of the problem formulation stage for this screening level ERA was todetermine the assessment endpoints and measurement endpoints. The following is a generalbasis for the selection of assessment and measurement endpoints.

Assessment endpoints are "explicit expressions of environmental values to be protected" at thesite (EPA, 1999). The purpose of identifying assessment endpoints is to focus the ERA anddefine the scope of the assessment. Because assessment endpoints are environmental values,they are often location sensitive. For purposes of this screening level ecological assessment, theMississippi River aquatic environmental adjacent to the site was the valued environmentalresource that was considered to require protection. The terrestrial environment on site is used ascommercial property and adjacent to the site as a community park area that is regularly mowed,but does not contain sensitive ecological habitat requiring protection. Considering theMississippi River chemical data collected during the investigation, for this screening level ERA,the assessment endpoint selected for the site was the protection of the health of benthicinvertebrates living in the sediments of the Mississippi River. This was considered a reasonableassessment endpoint, because the sediment was the medium that was found to be potentiallycontaminated due to site activities. Mississippi River surface water samples did not revealchemical site impacts to the Mississippi River.

Assessment endpoints cannot usually be measured directly, so measurement endpoints areselected which are indirect measures of whether the assessment endpoint is being achieved. Forthe assessment endpoint provided above, the measurement endpoint selected for protecting thehealth of benthic invertebrates is a direct comparison of the sediment analyte concentrations totoxicity benchmark values. This is elaborated upon in more detail latter.

The following is a more detailed discussion of the three main components of the ProblemFormulation that included:

1. Habitat Assessment/Identification of Receptors

2. Identification of Chemicals of Potential Ecological Concern (COPECs)

3. Identification of Exposure Pathways

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6.2.1 - Habitat Assessment/Identification of Receptors

Dr. Michael Kierski, a Montgomery Watson Environmental Toxicologist performed a walkoversurvey of the site and surrounding area to identify significant habitats and potential ecologicalreceptors. Field observations focused on identifying suitable habitat for federal or state-listedthreatened and endangered species as well as more common terrestrial and aquatic species.

The flood control levee along the Mississippi River divides the developed areas of Clinton fromthe river and undeveloped floodplain to the east. Areas on and around the site provide lowquality habitat potential for the following reasons:

There are no forest or prairie lands; all grassed areas are regularly mowed andtrees tend to be isolated and intended for landscaping or shade.

• There are no surface water or wetland areas.

There are no trees on the levee or riverbank for roosting or perching.

East of the levee, the Mississippi River, backwater areas, and flood plain provide the greatestpotential for suitable habitat with relatively undisturbed wetlands and woodlands.

6.2.1.1 - On-Site and Adjacent Properties. Most of the Alliant Energy/IPC portion of the siteis continuously occupied and has little if any potential habitat. On the former Allied Steelproperty, the land is presently unoccupied, but offers little habitat potential. Along the westernfenceline is a narrow strip of unmanaged woody growth and underbrush. This area is not mowedand is littered with trash. This area has also been utilized on occasion by vagrants, as evidencedby abandoned clothing and bedding, and empty food containers.

The remainder of the former Allied Steel property consists of mowed grassy areas and concreteor asphalt paving. Climbing fauna, shrubs, and small trees are found at various locations alongthe chain-link fencing on the northern and eastern sides of this portion of the site.

The Riverview Park area is largely devoid of trees or other potential habitat. Decorative trees areplanted along both sides of Park Drive and larger native species are found in the miniature golfcourse area and the southern section of the park. Trees in these areas tend to be individualizedwith little or no canopy interconnection and no understory growth to support potential habitat.

Typical mammals to be found in these areas may include mice, raccoon, opossum, groundhog,and squirrel. Groundhogs and several underground groundhog dens were seen on the eastern sideof the former Allied Steel property during the site investigation. Avifauna may include owls,hawks, eagles, scavengers (such as crows), and songbirds. Berries growing along portions of thefence on the former Allied Steel property may be eaten by birds, while the unmanaged growthalong the western fence of the former Allied Steel property may provide food and shelter forreptiles and small mammals.

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6.2.1.2 - Mississippi River and Backwater Areas. The Mississippi River and backwater areasinclude the river channel, backwater channels, shallow wetland sloughs, and floodplain forest.Flow and clastic bedload transport in the main river channel likely prevents the establishment ofaquatic macrophytes in the main channel. However, the coarse riprap along the levee doesprovide a foundation for mussel colonies such as the zebra mussels found at several of theproposed sediment sampling locations.

Shallow backwater areas may contain phytoplankton as well as emergent, submergent, andfloating macrophytes. The backwater ecosystem may also provide diverse habitat for aquaticfauna such as zooplankton, fish, and benthic invertebrates in addition to water-dependent birds,mammals, amphibians, and reptiles. Terrestrial species from adjacent uplands forage these areasfor food and water. Water-tolerant trees and shrubs provide nesting cover for songbirds andcolony nesting birds. Dead tree limbs provide riverside hunting perches. Tree snags createimportant habitat for hollow tree nesters including wood ducks, owls, and woodpeckers.

Habitat cover in the backwater areas likely includes submerged tree stumps, limbs, and root wadsof fallen trees. The still backwater areas provide important reproductive habitat for several fishspecies and breeding grounds for amphibians. Vegetative cover in the marsh sloughs providesprotected feeding areas for turtles, frogs, and waterbirds. The muddy sediments offer goodburrowing habitat for worms and mussels.

The floodplain forest provides high-quality habitat for terrestrial and wetland-dependent species.Seasonal flooding of low depressions within the floodplain also provides temporary wetlandhabitat for resident floodplain species and visitors from adjacent uplands. The moist broadleafforest with large, mast-producing trees is attractive to a variety of wildlife including birds,mammals, reptiles, and amphibians. The trees provide leafy canopies for nesting, crops of seedsand nuts, and trunks riddled with nesting cavities and bark insects.

Despite its disturbed nature, the eastern edge of the Mississippi River floodplain likely providessome wildlife habitat. The edge where the open agricultural, industrial, or residential areas meetthe floodplain forest typically supports birds and mammals that depend on both forest and openareas to meet habitat requirements for food and shelter. Herbivorous mammals such as rabbitsand white-tail deer may graze or rest in the vegetation near the woods. The grasses and floweringplants attract insects, birds, and rodents such as voles and mice that eat plant seeds.

6.2.2 - Threatened and Endangered Species

The U.S. Department of the Interior (DOT) listed four federally-listed endangered and threatenedspecies for Clinton County. The Higgin's eye pearly mussel and Iowa Pleistocene snail wereidentified as endangered species by the DOI, while the bald eagle and Northern monkshood werelisted as threatened. In the vicinity of the site, the DOI indicated two of the species may bepresent: bald eagle and Higgin's eye pearly mussel. The bald eagle has since been downgradedto a protected classification, but bald eagles were observed flying over the Mississippi Riverduring the site investigations. No nesting or hunting perches have been observed on the site.

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With respect to the Higgin's eye pearly mussel, the DOI noted some mussel beds "downstream ofthe site starting at river mile 519.5." The site is actually located close to river mile 518.5;approximately 1 mile downstream of the stated mussel bed location. One factor in perpetuatingtheir endangered status is that they tend to get overrun with zebra mussels and no longer haveaccess to food. Extensive zebra mussel beds were encountered along the levee rip rap in the riveralong the site, and repeated attempts to penetrate the mussel colonies to collect sediment sampleswere unsuccessful.

6.2.3 - Identification of Chemicals of Potential Ecological Concern

The surface water and sediment samples collected from the Mississippi River were intended todetermine if the site has a direct impact on the river system and to characterize the extent of anyimpacts potentially related to the site.

The surface water samples collected from the eight locations in the Mississippi River allexhibited virtually the same analytical results from the upstream to downstream samplinglocations. No VOCs, PAHs, or acid-extractable compounds were detected in any of the surfacewater samples. With respect to the inorganic compounds, only iron, lead, and sulfate weredetected. Based on the samples collected, no changes in water quality were detected in theMississippi River along the site (See EE/CA Part I, Section 6.3.5.1.) Therefore, based on theconclusion presented in EE/CA Part I that the site has not impacted the surface waters of theMississippi River, surface water in the river was not considered further in this screening levelERA.

Based on the screening-level problem formulation approach there are no sensitive habitats forterrestrial receptors. With respect to aquatic life, the data for sediments in the Mississippi Riverwere compared to ecotox thresholds. For this screening level ecological risk assessment,chemical contaminants at this site that could pose concern for sensitive habitats or ecologicalreceptors were evaluated.

The chemical analyses performed for the sediments (VOCs, PAHs, and metals) were used toevaluate the COPECs. The COPECs were selected by screening against ecological riskassessment endpoints per EPA guidance. (Luftig, 1999; EPA, 19965). More specifically, theecological risk assessment end points were screening benchmark values (i.e., survival) for biotaexposure to sediments based on EPA and ORNL published values.

Sediment samples were collected from 11 of the 14 locations attempted in the Mississippi Riverchannel, as shown in Figure 2-5. Analytical results from these samples indicate VOCs weredetected only at MR-05 and MR-06. At both locations, toluene was detected at concentrationsless than 0.07 mg/kg. In addition to toluene, methylene chloride was reported at MR-06 at aconcentration of 0.009 mg/kg. None of the other VOCs were detected at any of the sedimentsampling locations.

PAH compounds were detected at 6 of the 11 locations where samples were recovered, includingthe upstream location (MR-01). Locations with total PAHs greater than the upstream location

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were MR-04, MR-05, and MR-06. These are the locations closest to the existing and former Cityof Clinton sewer outfalls and the former sluice pond outfall. Downstream of these locations,PAH compounds were detected only at MR-13. Based on the series of samples with nodetectable concentrations (MR-10 through MR-12 and MR-14), and the potential backgroundconcentrations defined at MR-01, the magnitude and extent of PAH impacts potentially related tocurrent or historic sewer discharges to the river have been defined.

None of the acid extractable compounds were detected in any of the sediment samples.

With the exception of cyanide, all of the inorganic compounds of concern were detected in one ormore of the river sediment samples. Sediment samples MR-01 and MR-03 through MR-06generally had a more diverse representation of the inorganic compounds and at higher overallconcentrations than did samples collected from MR-09 through MR-14. Samples MR-09through MR-14 were collected from slightly further into the river channel, where faster currentsmaintain a higher percentage of sand than the locations closer to the riverbank. As with theVOCs and PAHs, the highest concentrations of the inorganic compounds were generally detectedat MR-05 and MR-06.

Because the sewer system is combined storm and sanitary service, the amount of water cominginto the pump station during large storm or runoff events can exceed the capacity of the system.In these instances, the excess water is pumped over the levee and discharged directly into theMississippi River. Therefore, identifying a specific source of the compounds of concern detectedin the sediments cannot be done with certainty. The VOCs, PAHs, and inorganic compoundsdetected may have been derived from any number of potential sources, including parkinglot/street runoff, business and residential discharges, and/or groundwater infiltration from thesite. However, it is suspected that the methylene chloride reported at MR-06 is due to residuallaboratory contamination of the sample.

The analytical data for sediments were evaluated against published EPA ecotox thresholds.(EPA, 1996b). With the exception of two PAH compounds, none of the Mississippi Riversediment contaminants exceed EPA published ecotox thresholds, i.e., maximum detectedconcentrations exceeded sediment quality benchmarks or "Effects Range-Low" (ERL)(Longetal. 1995 and EPA, 1996b). The PAH compounds that exceeded the ERL werebenzo(a)pyrene and phenanthrene, and these exceedances occurred only in a single samplecollected at MR-06. This location is near a sewer outfall.

6.2.4 - Identification of Exposure Pathways/Conceptual Site Model

This section uses the information gathered concerning ecological habitats and the chemicalcharacteristics within each habitat to define potential exposure pathways for ecological receptors.For purposes of this screening level ecological assessment, the receptors of primary concern werethose that would have direct contact with the impacted media within areas that representecological habitat. It should be noted, based on site characteristics, only the Mississippi Riveraquatic environment was considered to reasonably represent valued ecological habitat. Theupland property that has been developed does not afford valued ecological habitat. For these

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reasons, the remainder of the screening level ecological assessment focuses on the potential risksassociated with sediment chemical concentrations in the Mississippi River. While a variety ofaquatic receptors could be selected (as described in the habitat assessment), for purposes of thescreening level ERA, only general classes of receptors were selected because the analysisperformed in a screening level ERA is not typically species-specific.

Based on observations of the Mississippi River at relatively high, moderate and low stages,groundwater is not considered to be a media of concern for aquatic life in the Mississippi River.Vertical gradients between the water table and intermediate depths are generally in a downwarddirection on the Alliant Energy/IPC portion of the site and generally in an upward direction onthe Allied Steel portion of the site (EE/CA Part I, Table 6-2). However, the magnitude (and to alesser degree, direction) of the gradient varies with river stage. At lower river stages the upwardvertical gradient on the Allied Steel portion of the site becomes slighter, or becomes a downwardvertical gradient. On the Alliant Energy/IPC portion of the site, the downward vertical gradientbecomes greater at lower river stages. This genera] distribution of vertical flow componentsindicates the Alliant Energy/IPC portion of the site is an area of groundwater recharge in thelocal flow system. As explained in EE/CA Part I, at high and moderate river stages theMississippi River recharges groundwater and during low river stages the Mississippi River likelyreceives groundwater discharge.

The Mississippi River is the dominant factor controlling water levels and flow directions in thealluvial aquifer at the site. At higher river stages, the Mississippi River recharges groundwater.At lower river stages, the groundwater discharges to the Mississippi River. However, otherfactors (areas of surface water infiltration and leakage into the municipal sewer system) havesignificant impact on the groundwater flow direction at the water table, masking the effects of theriver stage. The effects of river stage on groundwater flow are apparent in the intermediate depthand bedrock surface potentiometric surfaces. Therefore, groundwater is not evaluated as apotential pathway for ecological receptors because groundwater does not come in direct contactwith ecological receptors.

For the river habitat, sediment associated biota were selected as the receptors of primary concern.These would include such organisms as amphibians, invertebrates, and wetland plants.

The potential for bioaccumulation to higher trophic levels is considered unlikely based on thenature of the contaminants (i.e., the metals and PAHs do not readily bioconcentrate in fish forexample), and/or distribution of the contaminants (i.e., concentrations above background occur inan isolated spot). Considering these circumstances and the large home range of most animalsthat are higher on the food chain, bioconcentration is not considered a significant concern.

6.3 - SCREENING ANALYSIS

While the Problem Formulation step is mainly qualitative in nature, the Screening Analysisinvolves quantifying those factors that determine whether a COPEC poses an ecological concern.According to current EPA guidance, the Screening Analysis step of an ERA consists of anassessment of the magnitude of potential exposure to COPECs, and an assessment of the toxicity

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of these stressors and other nonchemical stressors. The Screening Analysis uses informationfrom the Problem Formulation (e.g., conceptual site model) to determine an appropriatequantitative approach to define levels of COPEC exposure and toxicity. For purposes of thisscreening level ecological assessment, the maximum concentration of each COPEC detectedwithin sediment was used to define quantitatively the potential level of chemical exposure thatecological receptors may have. To estimate the toxicity of each chemical to sediment associatedbiota, toxicity benchmarks were obtained from the following source:

U.S. Department of Energy, 1997c. Toxicological Benchmarks for Contaminantsof Potential Concern for Effects on Sediment-Associated Biota

• Guidelines for Ecological Risk Assessment, USEPA, April 1998

Ecological Risk Assessment Guidance for Superfund: Process for Designing andConducting Ecological Risk Assessments, USEPA, June 1997, RepresentativeSample Guidance Document, Volume 3: Ecological, USEPA, May 1997

. ECO Update, Intermittent Bulletins, USEPA, 1991 to 1996

Sediment COPECs and their respective toxicity benchmarks are summarized in Table 6-1. Thetoxicity benchmarks available for sediment are generally developed to protect aquatic life usingwhat data is available on plant, invertebrate, and fish species toxicology. However, it should benoted the methods used are generally conservative, and aim to protect even the most sensitiveaquatic receptors.

6.4 - RISK CHARACTERIZATION

Risk characterization is the integration of the exposure into a quantitative characterization of riskposed by the COPECs to the ecological receptors of concern (i.e., sediment or soil associatedbiota). The site-specific chemical data was used to estimate the potential exposure pointconcentration of each COPEC.

Chemical exposure can lead to either noncarcinogenic health effects and/or carcinogenic healtheffects. For purposes of this ERA, only noncarcinogenic health effects were assessed. Cancer isgenerally an endpoint that occurs only after a chronic period of chemical exposure, and anextended latency period. For this reason, in the environment with the normal predator-preyrelationships, most animal species do not live long enough for cancer to manifest itself. Inaddition, the incidence of chemically induced cancer cases in a species population would likelybe insignificant, and not impact the overall population dynamics of the species.

Potential risks associated with noncarcinogenic effects of chemicals were calculated by means ofthe hazard index technique where HQs and His are used to assess the potential for concerns.Similar to the human health risk evaluation, ecological risks are evaluated in a manner consistentwith Menzie et al. (1992), as follows:

HQ or HI less than 1: no adverse effects on ecological receptors are anticipated.

6-8

HQ or HI between 1 and 10: there is limited potential for adverse effects onecological receptors.

HQ or HI between 10 and 100: there is potential for adverse effects on ecologicalreceptors.

HQ or HI exceeds 100: there is significant potential for adverse effects onecological receptors.

The ecological risk associated with each medium is presented below.

6.4.1 - Sediment Associated Biota

For the screening level risk calculations, the hazard quotient has been used. The ecologicalhazard quotient, HQ, is the estimated environmental concentration for a chemical divided by achemical-specific, NOAEL (expressed as an environmental concentration).

Four samples in the vicinity of sample MR-06 were collected. The distances from MR-06 tothese samples range from approximately 140 feet to 225 feet. The concentrations of several PAHchemicals are elevated, and compared with the downstream data, the data for this sample may beconsidered to be outliers. With regard to the sediment, an isolated impact to the MississippiRiver was noted at MR-06 (i.e., total PAH concentration of 11.8 mg/kg). However, upstreamand downstream of this location, levels of analytes seemed comparable, indicating MR-06appears to be an isolated hotspot. The data for MR-06 appear to be influenced by the seweroutfall. Based on the maximum concentrations of chemicals detected at MR-06, a comparison totoxicity benchmark values was made in Table 6-1. The resultant HI was 44, which indicatesthere is the potential for adverse effects on ecological receptors in the localized hotspot.

The primary risk is associated with PAHs within the area (i.e., fluoranthene, naphthalene, andanthracene). PAHs have the potential to bioaccumulate in organisms (Lee et al., 1978).However, the hotspot is isolated, and outside of this isolated area there would be no adverseeffects on ecological receptors anticipated. Because of the small spatial scale of the hotspot,there would not be expected to be an ecological concern associated with this area.

6.4.2 - Soil Associated Biota

Based on the lack of viable terrestrial habitat, risks for soil associated biota were not calculated.

6.4.3 - Summary of Health Risks

Based on results of the screening level ecological assessment, levels of analytes detected in theMississippi River sediment environment would not be expected to pose a health concern toecological receptors. For this reason, additional ERA was not considered necessary for purposesofthisBlRA.

6-9

SECTION 7 - DISCUSSION OF UNCERTAINTIES

The health risk estimates are calculated using the best scientific information available, but eachfactor used to generate the risk estimates has some level of uncertainty. In addition, for certainrisk assessment factors there is no readily available information and, therefore, professionaljudgment and site information must be used to estimate these values. The level of uncertaintyassociated with values based on professional judgment is less well known. For these reasons, aconservative approach is used so as not to underestimate human health risks. Therefore, thehealth risk estimates should be conservatively high compared to the "true" level of health risklikely associated with the site.

The following is a summary of some of the assumptions and uncertainty factors applied in therisk assessment, as well as indications of their resulting biases.

It was assumed interim measures would be taken to limit the potential forexposure to soil or groundwater in the future, thus reducing associated healthrisks. These include:

- Fences would be repaired and adequately maintained.

Intrusive construction activities would not be conducted without usingproperly trained personnel that have been briefed on the site conditions.

Monitoring wells will be locked and properly maintained to preventunauthorized or accidental access.

• It was assumed that the potential for construction workers to come in contact will belimited because trenches will be dewatered before entry by construction workers;however, risks associated with such contact are vary with the specific type constructionactivities (e.g., electrical wiring, roofing, trenching, etc.)

Site characteristics (i.e., more than 90 percent of the area is covered by buildings,pavement, or vegetative cover) decrease the potential soil and vapor/particulateexposure for current Alliant Energy/IPC employees. However, these exposureroutes have not been totally eliminated. So, this pathway is considered complete,but insignificant. The other scenarios quantified in this risk assessment(e.g., construction worker) will result in greater exposure, thereby providingsufficient risk information.

It was assumed the site has been well characterized with regard to the nature andextent of contamination. However, the focus of the SSI and EE/CA investigationson source areas may overestimate site-wide concentrations and related risks.

It was assumed that all data fit a lognormal distribution; however, this assumptionmay overestimate RME in cases where the data set does not fit this distribution.

7-1

It was assumed the identified chemicals with toxicity factors (including ecologicaltoxicity benchmarks) are associated with the majority of site health risks. Thepresence of highly toxic compounds not analyzed for, or compounds for whichlittle toxicity information exists, may result in an underestimation of site risks.For each compound detected on the site, there was one or more EPA identifiedtoxicity factors to address human health risks. With regard to the screening levelecological assessment, some of the analytes did not have toxicity benchmarkvalues to assess their ecotoxicology. This is a common shortcoming of mostecological assessments, and is due to the limited data available on ecological risksfor many analytes. However, most analytes detected on the site not havingtoxicity benchmarks were generally associated with classes of chemicals that arenot normally thought to present an ecological concern, because they are low intoxicity and/or readily metabolized and not biomagnified. Therefore,uncertainties associated with not addressing the toxicity of each compound havebeen minimized within both the human health and ecological assessment.

The human toxicity values may overestimate risk. RfDs incorporate maximumlevels of conservative uncertainty factors, and CSFs estimate upper bound95th percentile values.

Risks within an exposure route are assumed to be additive. This may result in anover- or underestimation of risk, because using this approach does not take intoaccount potentiation, antagonistic, or synergistic interactions. At this time, dataare not available to determine whether the COPCs would cause potentiation,antagonistic, or synergistic effects on one another.

Critical toxicity values derived primarily from animal studies may over- orunderestimate human health risk. There is a fundamental uncertainty inextrapolating animal toxicity data to humans. Several factors may introduce theuncertainty, including differences in species' chemical absorption characteristics,pharmacokinetics, target organ sensitivity, etc. However, a conservative approachhas been used by the EPA to develop the toxicity values so that the human toxicityof a chemical is not underestimated.

Human behavioral patterns cannot be predicted with certainty. However,reasonable maximum levels of exposure were assumed; therefore, the actuallevels of exposure and health risk has probably been overestimated.

Species sensitivity to chemicals varies greatly and, therefore, the risks can beminimized if the proper ecological receptors are not selected. In the case of thescreening level ecological assessment, conservative toxicity benchmarks havebeen selected that should protect even sensitive species, because of how thebenchmarks were developed. For this reason, this limitation has been minimizedusing this approach.

7-2

It was assumed the media concentrations would remain constant over time. Thisassumption results in a probable overestimation of health risks, since passive oractive remediation is considered and organic contaminants will degrade naturallyover time.

The risk characterization methods developed by EPA estimate the upper boundsof potential risk. An advantage of this upper-bound estimate is that the actual riskof harm is unlikely to any greater than the estimate. By overstating the actual risk,upper-bound estimates reflect a conservative approach to risk assessment in aneffort to protect public health. The estimates produced using EPA methodologiescontain many conceptual and statistical uncertainties. Consequently, theestimated risks are unlikely to become real risks.

7-3

SECTION 8 - SUMMARY AND CONCLUSIONS

This B1RA explored the potential human health and ecological risks resulting from exposures tochemicals detected at and in the area of the site. Potential human health risks were assessed forthose populations that may have the potential for exposure to the site, and potential ecologicalrisks were assessed for select ecological receptor groups. For each potentially exposedpopulation, the pathways that they may be exposed to impacted media were assessed and theassociated risks quantified.

8.1 - SUMMARY AND CONCLUSIONS OF HUMAN HEALTH EVALUATION

Based on results of the site investigations and conditions, a set of COPCs was selected and thepotential for exposure to the COPCs assessed. Exposure pathways that were evaluated underpresent and potential future land use conditions are summarized below.

Health risks were calculated based on noncarcinogenic and or carcinogenic health effects of thechemicals. For chemicals exhibiting carcinogenic effects, the individual upper bound excesslifetime cancer risks were calculated. A risk level of IxlO"6, for example, represents an upperbound probability of one-in-one-million that an individual could contract cancer as a result ofexposure to the potential carcinogen over a 70-year lifetime under the specified exposureconditions assessed in the B1RA. Potential risks associated with noncarcinogenic effects ofchemicals were calculated by means of an HI technique as recommended by EPA.

The health risks calculated for the site (i.e., His and cancer risks) under current site conditionsare summarized in Table 5-1. The health risk estimates are compared against two benchmarks.The upper bound lifetime excess cancer risks presented in this report can be compared to EPA'srisk range for health protectiveness at Superfund sites of 10~4 to 10"6 (EPA, 1990). This range isrepresentative of risks which are acceptable for the selection of remedial alternatives. Fornoncarcinogenic effects, His which are less than one (1) are not likely to be associated withsignificant health risks. Standard EPA methodologies and conservative exposure scenarios wereused to estimate potential levels of exposure and health risks for present and potential future landuse conditions. The exposure potential was evaluated separately for the Alliant Energy/IPCproperty and the former Allied Steel property. Human health risks were calculated fornoncarcinogenic and carcinogenic health effects for potential exposures to chemicals in soils.The cancer risk estimates for the RME soil exposure scenarios evaluated at this site range from5x10~6 to 2xlO"3. The greatest carcinogenic risk estimates are associated with exposure tosubsurface soil (1-10 feet) by on-site workers.

For noncarcinogenic effects, the contaminant intake was estimated using exposure assumptionsfor site conditions. This dose was the compared to a RfD (estimated daily intake of the chemicalthat is likely to be without appreciable risk of health effects) developed by the EPA. For this site,His for the RME soil exposure scenarios range from 0.6 to 18; the greatest value is associatedwith a construction worker scenario. However, the estimates are based on several conservativeassumptions per EPA protocols, e.g., all of the exposed skin of a construction worker is exposed

8-1

to each of the soil contaminants at the exposure point concentration (often the maximumconcentration) for 8 hours per day for 190 days per year. Similar assumptions were made for anon-site worker (e.g., office employee) for an assumed duration of employment based on EPAdefault exposure factors. Thus, the estimates are conservative.

Current site conditions will reduce ingestion, dermal contact, and inhalation of contaminated soilas compared to bare soil conditions because the impacted soils are located below buildings,pavement, or lawns and vegetative cover. In addition, chemically-effected groundwater is notused as a drinking water source, because the site and surrounding area are supplied by amunicipal water system. Indoor air measurements in the on-site district office building weregenerally below EPA reference concentrations; this information will be provided under separatecover at a later date. For these reasons, present conditions are not considered to present apotential public health concern to site workers, construction workers, visitors, or trespassersinvolved in nonintrusive activities

Under present conditions, if construction workers would dig into the surface and subsurface soilsand become exposed to the soils through incidental ingestion or dermal contact there is thepotential for elevated noncarcinogenic (HI >1) and carcinogenic (cancer risk >lxlO"4) risks. Theprimary chemicals of concern are PAHs, PCBs, and arsenic. These risk estimates assume theworkers do not use protective clothing (e.g., gloves) to prevent soil exposure, and performmanual labor that would bring them in direct contact with the soil.

Under potential future conditions, if the surface and or subsurface soils become accessible andremain accessible for many years (i.e., 10 to 25 years), site worker's, visitor's or trespasser'sexposure to soil (either surface or subsurface), could potentially pose a health concern (i.e., HI >1and cancer risk >lxlO"4). This could only occur though if site workers, visitors, or trespasserswould come in direct contact with the soil.

8.2 - SUMMARY AND CONCLUSIONS OF SCREENING LEVEL ECOLOGICALASSESSMENT

Based on results of the site investigations, a set of COPCs was selected. Within the ERA, ahabitat assessment was conducted to define groups of ecological receptors that have the potentialto be exposed to the COPCs. One set of ecological receptors was selected: sediment-associatedbiota.

To assess the potential level of exposure for each of these receptors groups, the site investigationdata was used directly for comparison to toxicity benchmark values. Based on results of thescreening level ecological assessment, levels of analytes detected in the Mississippi Riversediment environment would not be expected to pose a health concern to ecological receptors.For this reason, additional ERA was not considered necessary for purposes of this BIRA.

8-2

REFERENCES

Clay, Don R. 1991. "Role of Baseline Risk Assessment in Superfund Remedy SelectionDecisions." U.S. EPA, Office of Solid Waste and Emergency Response, Washington, D.C.April 21. OSWER Directive 9355.0-30.

Code of Federal Regulations, 29 CFR 1910.1000.

Efroymson, R.A., Suter, G.W. n, B.E. Sample, and D.S. Jones, 1997. Preliminary RemediationGoals for Ecological Endpoints. Prepared for the U.S. Department of Energy.ES/ER/TM-162/R2.

Hawley, J.K., 1985. "Assessment of Health Risk from Exposure to Contaminated Soil." RiskAnalysis 5(4):289-302.

HEAST (Health Effects Assessment Summary Tables), 1997. U.S. Environmental ProtectionAgency, Environmental Criteria and Assessment Office, Office of Health andEnvironmental Assessment, Cincinnati, Ohio.

IRIS (Integrated Risk Information System), 2000. U.S. Environmental Protection Agency, Officeof Health and Environmental Assessment.

Jones, D.S., G.W. Suter n, and R.N. Hull. 1997. Toxicological Benchmarks for ScreeningContaminants of Potential Concern for Effects on Sediment-Associated Biola: 1997Revision. Oak Ridge National Laboratory. U.S. Department of Energy. 1997.ES/ER/TM-95/R4.

Lee, R.F. et al., 1978. "Fate of Polycyclcilic Aromatic Hydrocarbons in Controlled EcosystemEnclosures," Environmental Science & Technology 12(7), 832-838, July.

Long, E.R., D.D. MacDonald, S.L. Smith, and F.D. Calder. 1995. Incidence of AdverseBiological Effects Within Ranges of Chemical Concentrations in Marine and EstuarineSediments. Environmental Management 19(l):81-97.

Luftig, Stephen D. 1999. "Issuance of Final Guidance: Ecological Risk Assessment and RiskManagement Principles for Superfund Sites," U.S. Environmental Protection Agency,Office of Emergency and Remedial Response, Washington, D.C. October 7. OSWERDirective 9285.7-28P).

National Oceanic and Atmospheric Administration (NOAA) CIRES Climate Diagnostic Center,Listing of snowfall for cities in Iowa and Illinois, July 2001.www. cdc.noaa.gov/USclimate/index. html.

R-l

State of Iowa Climatologist Office, fax communication to Montgomery Watson, April 19, 2000.Listing of snow cover statistics for Iowa cities.

U.S. Army Environmental Center (USAEC), 1995. Toxicity Values From theU.S. Environmental Protection Agency Integrated Risk Information System and HealthEffects Assessment Summary Table. October 1995.

U.S. Environmental Protection Agency (EPA), 1986. Guidelines for Carcinogenic RiskAssessment, 51 FR 33992, September 24, 1986.

U.S. Environmental Protection Agency (EPA), 1989. Risk Assessment Guidance for Superfund:Volume I—Human Health Evaluation Manual (Part A, Baseline Risk Assessment). InterimFinal. EPA/540/1-89/002.

U.S. Environmental Protection Agency (EPA), 1990. National Contingency Plan. FederalRegister. March 8. 55,8666.

U.S. Environmental Protection Agency (EPA), 199la. Human Health Evaluation Manual,Supplemental Guidance: Standard Default Exposure Factors. OSWER Directive9285.6-03. March 1991.

U.S. Environmental Protection Agency (EPA), 1991b. Risk Assessment Guidance forSuperfund: Volume I—Human Health Evaluation Manual (Part B, Development ofRisk-Based Preliminary Remediation Goals). Interim. Publication 9285.7-01B.December 1991.

U.S. Environmental Protection Agency (EPA), 1992. EPA Guidelines on Exposure Assessment.Federal Register, 57, 22890. May 29.

U.S. Environmental Protection Agency (EPA), 1995. Health Effects Assessment SummaryTables, FY-1995. Office of Solid Waste and Emergency Response. EPA/540/R-95/036.

U.S. Environmental Protection Agency (EPA), 1996a. "Air/Superfund Guide to PollutantToxicity." Office of Air Quality Planning and Standards Research. Research Triangle, NC.March. EPA-451/R-96-006

U.S. Environmental Protection Agency (EPA), 1996b. "ECO Update." Office of Solid Wasteand Emergency Response. Washington, D.C. January. EPA 540/F-95/038.

U.S. Environmental Protection Agency (EPA), 1997a. Exposure Factors Handbook: VolumeI—General Factors. Update to Exposure Factors Handbook (EPA/600/8-89/043-May 1989). EPA/600/P-95/002Fa. August 1997.

R-2

U.S. Environmental Protection Agency (EPA), 1997b. Exposure Factors Handbook:Volume m—Activity Factors. Update to Exposure Factors Handbook (EPA/600/8-89/043-May 1989). EPA/600/P-95/002Fc. August 1997.

U.S. Environmental Protection Agency (EPA), 1997b. Exposure Factors Handbook:Volume m—Activity Factors. Update to Exposure Factors Handbook (EPA/600/8-89/043-May 1989). EPA/600/P-95/002Fc. August 1997.

U.S. Environmental Protection Agency (EPA), 1997c. Health Effects Assessment SummaryTables. FY 1997 Update. EPA-540-R-97-036. July 1997.

U.S. Environmental Protection Agency (EPA), 1998. Clarification to the 1994 Revised InterimSoil Lead Guidance for CERCLA Sites and RCRA Corrective Action Facilities. OSWERDirective 92.4-27p. 1998. Provides a reasonable screening level for soil lead at residentialsites.

U.S. Environmental Protection Agency (EPA), 1999. Technical Work Group for Lead (TRW),Frequently Asked Questions on the Adult Lead Model Guidance Document, April 1999.Provides reasonable screening levels for soil lead at commercial/industrial sites.

U.S. Environmental Protection Agency (EPA), 2001. Supplemental Guidance for DevelopingSoil Screening Levels for Superfund Sites, Peer Review Draft. Office of Solid Waste andEmergency Response. OSWER 0355.4-24. March 2001.

R-3

TABLE 2-1

SELECTION OF CHEMICALS OF POTENTIAL CONCERN (COPCs) FOR SURFACE SOIL (0-1 FOOT)

Area

Allied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAlliecfSteeT"Allied SteelIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC Side

Chemical

1,1,1-Trichloroethane1 , 1 ,2,2-Tetrachlorethane1 , 1 ,2-Trichlorore thane1,1-Dichloroethane1,1-Dichloroethene1,2-Dichloroe thane1,2-DichJoropropaneBenzeneBromodichloromethaneBromoformBromomethaneCarbon TetrachlorideChlorobenzeneChloroe thaneChloroformChloromethanecis- 1 ,3-DichloropropeneDibromochloromethaneEthylbenzeneMethylene ChlorideTetrachloroetheneToluenetrans- 1 ,2-Dichloroethenetrans- 1 ,3-DichloropropeneTrichloroetheneVinyl ChlorideXylenes, TotalArochlor 1016Arochlor 1221Arochlor 1232Arochlor 1242Arochlor 1248Arochlor 1254Arochlor 1260AcenaphtheneAcenaphthyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k)fluorantheneChryseneDibenzo(a,h)anthraceneFluorantheneFluoreneIndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanthrenePyreneArsenicChromiumCopperCyanideIronLeadNickelZinc2,4,5-Trichlorophenol2,4,6-Trichlorophenol2,4-Dichlorophenol2,4-Dimethylphenol2,4-Dinitrophenol2-Chlorophenol2-Methyl-4,6-Dinitrophenol2-Nitrophenol4-Chloro-3-Methylphenol4-NitrophenolPentachlorophenolPhenol1,1,1 -Trichloroethane, 1 ,2,2-Tetrachlorethane, 1 ,2-Trichlororethane,1-Dichloroethane,1-Dichloroethene,2-Dichloroethane,2-Dichloropropane

BenzeneBromodichloromethaneBromoformBromomethaneCarbon TetrachlorideChlorobenzeneChloroe thaneChloroformChloromethanecis-l,3-DichloropropeneDibromochloromethaneEthylbenzene

Number ofSamples

666666666666666666666666666999999966666666666666661313136131313136666666666669999999999999999999

Number ofDetections

000000010000000000140200011000105130456

~~~65560436164121213613131313000000.0000000000000100000000001

Frequency ofDetection, %

0.000.000.000.000.000.000.0016.670.000.000.000.000.000.000.000.000.000.0016.6766.670.0033.330.000.000.0016.6716.670.000.000.0011.110.00

55.5611.1150.000.0066.6783.33100.00100.0083.3383.33100.000.00

66.6750.00100.0016.67100.0066.6792.3192.31100.00100.00100.00100.00100.00100.000.000.000.000.000.000.000.000.000.000.000.00 "0.000.000.000.000.000.000.000.0011.110.000.000.000.000.000.000.000.000.000.0011.11

MinimumDetected

Cone.

NDNDNDNDNDNDND

0.112NDNDNDNDNDNDNDNDNDND

0.0340.005ND

0.006NDNDNDND

0.045NDNDND0.35ND

0.066

0.090.39ND0.020.130.01

~ (H&0.030.030.02ND0.080.030.020.050.040.143.38.412.1

. 9.49722

329.149NDNDNDNDNDNDNDNDNDNDNDNDNDNDNDNDNDNDND


0.028

MaximumDetected

Cone.

NDNDNDNDNDNDND


0.0340.005ND

0.044NDNDNDND

0.045NDNDND0.35ND

0.1900.0996.4ND4.214.35.66.8" '4.33.912.8ND2.88.13.3

0.0535.94.384.511367915.1

203000147044.92860NDNDNDNDNDNDNDNDNDND -N D ~NDNDNDNDNDNDNDND


0.028

COPC?

NNNNNNNYNNNNNNNNNN '

YYNYNNNNYNNNYNYYYYNYYYYYYNYYYYYYYYYYYYYYNNNNNNNNNN

" NNNNNNNNNYNNNNNNNNNNY

Rationale for Selection asCOPC

Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical detected.Chemical detected.Chemical not detected.Chemical detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical detected.Chemical not detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical not detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical not detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.

~Chemical nordetected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical detected.

TABLE 2-1

SELECTION OF CHEMICALS OF POTENTIAL CONCERN (COPCs) FOR SURFACE SOIL (0-1 FOOT)

Area

Allied SteelIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC Side

Chemical

1,1,1 -TrichloroethaneMethylene ChlorideTetrachloroetheneToluenetrans- 1 ,2-Dichloroethenetrans- 1 ,3-DichloropropeneTrichloroetheneVinyl ChlorideXylenes, TotalArochlor 1016Arochlor 1221Arochlor 1232Arochlor 1242Arochlor 1248Arochlor 1254Arochlor 1260AcenaphtheneAcenaphthyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k)fluorantheneChryseneDibenzo(a,h)anthraceneFluorantheneFluoreneIndeno(l,2,3-cd)pyreneNaphthalenePhenanthrenePyreneArsenicChromiumCopperCyanideIronLeadNickel

"'Zinc ~~ "2,4,5-Trichlorophenol2,4,6-Trichloropheno!2,4-Dichlorophenol2,4-Dimethylphenol2,4-Dinitrophenol2-Chlorophenol2-Methyl-4,6-Dinitrophenol2-Nitrophenol4-Chloro-3-Methylphenol4-NitrophenolPentachlorophenolPhenol

Number ofSamples

699999999999999999999999999999999999999

•9 - -999999999999

Number ofDetections

000100001000000620799997909491988984968

-9 - -

000000000020


0.000.000.0011.110.000.000.000.0011.110.000.000.000.000.000.0066.6722.220.0077.78100.00100.00100.00100.0077.78100.000.00

100.0044.44100.0011.11100.0088.8988.89100.0088.8944.44100.0066.6788.89100.00-0.000.000.000.000.000.000.000.000.000.0022.220.00

MinimumDetected

Cone.

NDNDND

0.042NDNDNDND

0.037NDNDNDNDNDND

0.1300.010ND

0.0100.0300.0600.0400.0300.0300.040ND0.11

0.0200.0300.0100.0300.200

2.23.47.22.0

5760696.6

-^ 14.9- -NDNDNDNDNDNDNDNDNDND3.84ND

MaximumDetected

Cone.

NDNDND

0.042NDNDNDND

0.037NDNDNDNDNDND73.22.60ND1.2015.212.19.47.13.512.6ND39.32.505.702.606.4032.7170147817.9

4660055119.4

- -^ 1-310 "-NDNDNDNDNDNDNDNDNDND26.3ND

COPC?

NNNYNNNNYNNNNNNYYNYYYYYYYNYYY .YYYYYYYYYYYNNNNNNNNNNYN

Rationale for Selection asCOPC

Chemical not detected.Chemical not detected.Chemical not detected.Chemical detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical detected.Chemical detected.Chemical not detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical not detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected. • ~Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical detected.Chemical not detected.

TABLE 2-2

SELECTION OF CHEMICALS OF POTENTIAL CONCERN (COPCs) FOR SUBSURFACE SOIL (MO FEET)

Depth

1-10 Ft.1-10 Ft.

1-10 Ft.1-10 Ft.

1-10 Ft.1-IOFL

1-lOFl

1-IOFL1-IOFL1-10 Ft.

l-IOFl.1-10 Ft.

1-10 Ft.1-10 Ft.

1-10 Fl

1-10 Ft.1-10 Ft.

1-10 Ft.

1-10 Ft.

1-IOFt .1-10 FL1-10 Fl.1-10 Ft.1-10 Ft.

1-10 Ft.1-10 Ft.

1-IOFt .1-10 Ft.1-10 Ft.1-10 Ft.

1-10 Ft.

1-10 Ft.

1-IOFt .

1-10 Ft1-10 Ft.

I-10FL1-lOFl.

1-10 Ft.

1-10 Ft.1-10 FL1-IOFL

1-10 FL

1-10 FL

1-10 Ft.1-10 FL

1-10 FL

1-IOFL1-10 FL1-10 Ft.1-lOFt.

1-10 FL1-10 Ft.1-10 Ft.

1-IOFt.1- IOFL

1-IOFt.1-IOFt.1-10 Ft.

1-IOFL1-10 Ft.

1 - I O F t .1-IOFt.1-10 Ft.

1-10 Ft.

1-IOFL

1-10 Ft.

1-10 FL

1-10 Ft.

1-10 Ft.1-10 FL

1-IOFL1-10 Ft.

1-10 Ft.1-10 Ft.

1-10 Ft.

1-10 FL1-IOFt.

1-10 Ft.

1-IOFt.

1-10 FL1-10 Ft.1-10 Ft.1-10 Ft.1-10 Ft.1-10 Ft.

1-10 Ft.

1-10 Ft.1-lOFl.

1 - I O F L1-10 Ft.1-lOFl.

1- IOFt .1-IOFt .

1 - I O F L

1-IOFt.

1-10 Ft.1-IOFL

1-10 Ft.

1-10 Ft.1-IOFt.1-10 FL

1-10 FL1-IOFL1-IOFt.1-10 Ft.1-10 Ft.

Area

Allied SteelAllied Steel

Allied Steel

Allied SteelAllied SteelAllied Steel

Allied Steel



Allied Steel

Allied Steel


Allied Steel

Allied Steel

Allied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied Steel

Allied SteelAllied SteelAllied SteelAllied SteelAllied Steel

Allied Steel

Allied Steel

Allied Steel



Allied SteelAllied SteelAllied SteelAllied Steel

Allied Steel

Allied Steel


Allied Steel


Allied Steel

Allied SteelAllied SteelAllied SteelAllied Steel




Allied Steel

IPC Side

IPC SideIPC Side

IPC Side

IPC Side

IPC SideIPC Side

IPC Side

IPC SideIPC Side

IPC Side

IPC Side

IPC SideIPC Side

IPC Side

IPC Side

IPC SideIPC SideIPC SideIPCSideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC Side

IPC SideIPC Side

IPC Side

IPC SideIPC SideIPC Side

IPC Side


IPC Side

IPC SideIPC SideIPC SideIPC Side

Croup

VOCsVOCs

VOCsVOCs

VOCsVOCs

VOCs

VOCsVOCsVOCs

VOCsVOCsVOCsVOCs

VOCs

VOCs

VOCs

VOC»VOCs

VOCsVOCsVOCs

VOCsVOCsVOCs

VOCs

VOCsPAHsPAHsPAHs

PAHs

PAHs

PAHsPAHs

PAHsPAHs

PAHsPAHs

PAHsPAHsPAHs

PAHs

PAHs

MetalsMetals

MetalsMetals

MetalsMetalsMetals

Metals

AEOsAEOsAEOsAEOs

AEOsAEOsAEOs

AEOsAEOs

AEOsAEOs

AEOs

VOCsVOCs

VOCs

VOCs

VOCs

VOCsVOCs

VOCsVOCs

VOCs

VOCs

VOCs

VOCsVOCs

VOCs

VOCs

VOCsVOCsVOCsVOCs —VOCsVOCsVOCs

VOCsVOCsVOCsVOCs

PAHsPAHsPAHs

PAHs

PAHs

PAHsPAHs

PAHs

PAHsPAHsPAHs

PAHsPAHsPAHsPAHs

PAHs

Chemical

1,1.1-Trichloroe thane

1 , 1 ,2,2-Telrachloroethane, 1 ,2-Trichlororethane

, I -Dichloroethane,1-Dichloroethene

,2-Dichloroethane

,2-Dichloropropane

BenzeneBromodichloromelhaneBromoform

Jromomethanelaibon TetrachlorideChlorobenze-ne

Chloroethane

Chloroform

Chloromethanccis- 1 ,3-Dichloropropene

Dibromochloromethane

EthylbenzeneMelhylene ChlorideTetrachloroethene

Toluenetrans- 1 ,2-Dichloroethenetrans- 1 ,3-DichloropropeneTrichloroethene

Vinyl ChlorideXylcnes, TotalAcenaphtheneAccnaphthyleneAnthracene

9enzo(a)anthracene3enzo(a)pyrene

3enzo(b)fluorantheneBenzo(g,h,i)perylene

Benzo(k)fluoranthene

ChryseneDibenzo(a,h)anthracene

Fluoranthene

FluoreneIndeno( 1 ,2,3-cd)pyrene

NaphthalenePhenanlhrene

Pyrene

Arsenic

ChromiumCopper

Cyanide

Iron _LeadNickelZinc

2.4,5-Trichlorophenol2,4,6-Trichlorophenol2,4-Dichlorophenol

2.4-Dimethylphenol

2,4-Dinitrophenol2-Chorophenol

2-Methyl-4,6-Dinitrophenol2-Nitropheno!4-Chloro-3-Methylphenol

4-NitrophenolPentachlorophenol

Phenol1,1,1-Trichloroethane

, 1 ,2,2-Tetrachlorethane

, 1 ,2-Trichlororethane

,1-Dichloroethane

, 1 -Dichloroethene

,2-Dichloroethanc1,2-Dichloropropane

BenzeneBromodichloromethane

Bromoform

BromomethaneCarbon Tetrachloride

ChlorobenzeneChloroethane

Chloroform

Chloromethane

cis- 1 ,3-Dichloropropene

DibromochloromethaneEthylbenzeneMetKylene UhlbfideTetrachloroetheneToluene

trans- 1 ,2-Dichloroethene

trans- 1 ,3-DichloropropeneTrichloroetheneVinyl ChlorideXylenes, Total

AcenaphtheneAcenaphlhyleneAnthracene

Benzo(a)anthracene

Benzo(a)pyrene9enzo(b)fluoranlheneBenzo(g,h.i)perylene


ChryseneDibenzo(a,h)anthraceneFluoranthene

Fluorene

[ndeno(l,2,3-cd)pyreneNaphthalenePhenanthrcne

Pyrene

Units

mg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kgmg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kgmg/kg

mg/kgmg/kgmg/kgmg/kg


mg/kgmg/kgmg/kg

mg/kg

nig/kgmg/kgmg/kgmg/kg

mg/kg

mg/kgmg/kgmg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg


mg/kg

mg/kgmg/kgmg/kg


mg/kgmg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kgmg/kgmg/kg

mg/kgmg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kgmg/kg"mg/kgmg/kg

mg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kg

mg/kg

mg/kgmg/kgmg/kg

mg/kg

mg/kg

mg/kgmg/kgmg/kg


mg/kg

Number ofSamples

19191919191919151515151515151515151515151515151515151515151515151515151515151515151515151515151515̂1515151515151515151515151515151515151515151915151515151515191515191915191515

•15151919191919191919191918191919191819

Number ofDetections

00000004

0000000000520400005535999648087478710151510151515150000000I1000000000090000000200102080000101081112131286132913813138


0.00

0.000.00

0.000.00

0.00

0.0026.670.00

0.00

0.000.000.00

0.00

0.00

0.000.00

0.00

52.63

10.530.00

42.11

0.000.00

0.00

0.0052.6333.3320.0033.3342.11

57.89

63.1668.4263.1642.11

0.00

68.4211.1147.3768.42

53.33

68.42

66.67

100.00100.0057.89

100.00100.00100.00

100.000.000.000.00

0.000.000.000.00

6.670.00

6.670.00

0.00

0.000.00

0.00

0.000.000.000.00

47.37

0.00

0.000.00

0.000.00

0.00

0.00

10.53

0.00

0.0052.6310.530.00

42.11

0.000.000.00

0.0052.63

52.6342.11

57.8942.11

57.89

63.1668.42

63.1642.11

31.5868.42

11.1147.3768.42

72.22

68.42

MinimumSQL

0.007

0.0070.007

0.0070.007

0.007

0.007

0.0070.007

0.007

0.020.0070.007

0.01

0.007

0.010.007

0.0070.007

0.0140.007

0.0070.0070.0070.007

0.010.0070.330.010.01

0.33

0.330.33

0.010.01

0.010.0 1

0.010.330.010.33

0.33

0.33

0.9500

0.15

0~b00

1.670.33

0.33

0.330.330.331.671.67

0.331.671.67

0.33

0.0010.001

0.001

0.0010.001

0.0010.001

0.0010.001

0.0010.002

0.001

0.0010.001

0.001

0.001

0.001

0.0010.0010:0050.001

0.0010.001

0.0010.0010.0010.001

0.330.01

0.0 1

0.33

0.330.33

0.01

0.010.010.010.01

0.330.010.330.33

0.33

Maximum SQL

5.05.05.05.05.05.05.00.75.05.010.05.05.05.05.05.05.05.00.11.25.00.75.05.05.05.00.110.0

10.04.31.81.81.810.04.31.8

20.0

1.84.34.34.34.3

100.0

200100008585

85.0

85.085.085.085.0

85.085.085.0

85.0

85.0

22.023.0

22.0

22.022.0

22.022.0

1.022.0

22.0

90.022.022.0

68.0

22.0

45.0

22.0

22.01.0

56.022.0

1.022.022.022.0

68.01.0

10.0

10.0

4.31.81.81.8

10.0

4.31.8

20.01.84.34.34.34.3

100.0

Minimum DetectedConcentration

NDNDNDNDNDNDND


0.1180.037ND

0.165NDNDNDND

0.262 .0.65.3311.91.70.20.2

0.030.40.06ND0.02

0.051.93

0.995

0.07

0.01

4.57.29.8

0.179

9370"9 ~ .8.728.5NDNDNDNDNDNDND67.9ND20.5

NDNDNDNDNDNDNDNDND

0.186

NDNDNDNDNDNDND

0.117

NDND

0.1180.037ND

0.165NDNDNDND

0.2621.61.70.21.70.20.2

0.030.4

0.062.4

0.02

0.051.93

0.9951.2

0.01

Maximum DetectedConcentration

NDNDNDNDNDNDND97.1NDNDNDNDNDNDNDNDNDND24025ND169NDNDNDND30913401050

30324816812885.653.6532ND184354969.62930

1370

141559.2

83177175

83100" "597" "

621780NDNDNDNDNDNDND67.9ND20.5NDNDNDNDNDNDNDNDND53NDNDNDNDNDNDND1.42

NDND122

"0.101ND230NDNDNDND560 .

7560

191002354

25081141.5

20821229412.7

51.9

6166229

19200

757130.7

COPC?

NoNoNoNoNoNoNoYesNoNoNoNoNoNoNoNoNoNoYesYesNoYesNoNoNoNoYesYesYesYesYesYesYesYesYesYesNoYesYesYesYesYesYesYesYesYesYesYes

" Yes

YesYesNoNoNoNoNoNoNoYesNoYesNoNoNoNoNoNoNoNoNoYesNoNoNoNoNoNoNoYesNoNoYes

~Yes" "NoYesNoNoNoNoYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYes

Rationale for Selection orRejection as COPC

Chemical not detected.

Chemical not detected.Chemical not delected.Chemical not detected.



Chemical not delected.Chemical detected.



Chemical not detected.Chemical not detected.






Chemical detected.

Chemical detected.

Chemical not delected.Chemical detected.Chemical not detected.Chemical not detected.

Chemical not detected.Chemical not detected.Chemical detected.

Chemical detected.Chemical detected.Chemical detected.

Chemical detected.

Chemical detected.Chemical detected.


Chemical detected.Chemical not detected.

Chemical detected.Chemical detected.Chemical detected.Chemical detected.

Chemical detected.


Chemical detected.

Chemical detected.

Chemical delected.Chemical detected.Chemical detected.Chemical detected.

Chemical delected.Chemical not detected.Chemical not detected.


Chemical nol delected.Chemical not detected.Chemical not delected.

Chemical not detected.Chemical detected.Chemical not detected.

Chemical detected.


Chemical nol detected.


Chemical not delected.Chemical not detected.Chemical not delected.


Chemical not detected.Chemical detected.







Chemical detected.

whemical not detected.

Chemical not detected.Chemical detected.Chemical detected.Chemical not detected.

Chemical detected.Chemical not detecled.Chemical nol detecled.Chemical not detected.Chemical not detecled.

Chemical delected.Chemical detected.

Chemical delected.


Chemical detected.

Chemical detected.

Chemical detected.


Chemical detected.

Chemical detected.Chemical detected.Chemical detected.Chemical delected.


TABLE 2-2

SELECTION OF CHEMICALS OF POTENTIAL CONCERN (COPCs) FOR SUBSURFACE SOIL (1-10 FEET)

Depth

1-10 Ft.

1-10 Ft.

1-10 Ft.1-10 Ft.1-10 Ft.

1-10 Ft.

1-10 Ft.

I - IOFL1-10 Ft.

I-IOFt.

1-10 Ft.1-IOFt.1-10 Ft.1-10 Ft.

1-IOFL

1-IOFt.1-10 Ft.

1-10 Ft.1-lOFu1-10 Ft.

Area

IPC Side

IPC Side


IPC Side

IPC SideIPC Side

IPC Side


IPC Side

IPC Side

IPC SideIPC SideIPC SideIPC SideIPC Side

Group

Metals

Metals

MetalsMetals

MetalsMetals

Metals

MetalsAEOs

AEOs

AEOs

AEOsAEOs

AEOs

AEOs

AEOsAEOsAEOs

AEOsAEOs

Chemical

Arsenic

ChromiumCopper

CyanideIron

Lead

Nickel

Zinc2,4,5-Trichlorophenol

2,4,6-Trichlorophenol

2,4-Dichlorophenol

2,4-Dimethylphenol2,4-Dinitrophenol

2-Chorophenol2-Methyl-4.6-Dinitrophenol

2-Nitrophenol4-Chloro-3-Methylphenol

4-NitrophenolPentachlorophenolPhenol

Units

mg/kgmg/kg

mg/kg

mg/kgmg/Vg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kgmg/kgmg/kg

mg/kgmg/kg

mg/kgmg/kgmg/kg

mg/kgmg/kg

Number ofSamples

1919191918191919191919191919191919191919

Number ofDetections

1219191118191919000000000000


63.16

100.00100.00

57.89100.00

100.00

100.00

100.000.00

0.00

0.000.000.00

0.000.006.67

0.006.670.00

0.00

MinimumSQL

0.9500

0.150000

1.65

0.330.330.331.65

0.33

1.650.33

0.330.660.660.33

Maximum SQL

0.95

0010000

206.3

41.341.341.3206.3

41.3

206.3

41.341.2582.582.5

41.25


2.06

7.29.8

0.1799370

98.7

28.5NDNDNDNDNDNDND67.9ND20.5NDND

Maximum DetectedConcentration

8.821.4

5145.9

30800

34035.5374NDNDNDNDNDNDND67.9ND20.5NDND

COPC?

YesYesYesYesYesYesYesYesNoNoNoNoNoNoNoNoNoNoNoNo

Rationale for Selection orRejection as COPC

Chemical detected.

Chemical detected.Chemical detected.Chemical detected.

Chemical detected.

Chemical detected.

Chemical detected.Chemical detected.Chemical not detected.






Chemical not detected.Chemical not delected.Chemical not delected.

TABLE 2-3

SELECTION OF CHEMICALS OF POTENTIAL CONCERN (COPCs) IN SUBSURFACE SOIL (10-20 FEET)

Depth

10-20 Fl.IO-20FI.

10-20 FL

10-20 FL10-20 FLIO-20FI.10-20 Fl.

10-20FI.

10-20 Fl.10-20FI.

10-20 Fl.10-20 Fl.10-20 FL10-20 FL10-20 Fl.10-20 FL10-20 Ft.10-20 FL10-20 Ft.10-20FL10-20 FL10-20 Ft.10-20 FL10-20 FL10-20 FL10-20 FL10-20FL10-20 FL10-20 FL10-20 FL10-20 FL10-20 Ft.10-20 Ft.

10-20 Fl.

10-20FL

10-20 Ft.10-20 Ft.10-20 Fl.10-20 Fl.

10-20 Fl.10-20 Fl.

10-20 Fu

10-20 Ft.10-20 Ft.10-20 Fl.IO-20FI.

10-20 Ft.10-20 FL10-20 Fl.

10-20 FL

10-20FL10-20 Fl.10-20 Ft.10-20FL

IO-20FL

10-20 FL10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Fl.10-20 Fl.10-20 Fl.10-20FI.10-20 FL10-20 Fl.10-20 FL10-20 Ft.10-20 Fl.IO-20FI.10-20 Fl.

10-20 Fl.

10-20 Fl.10-20 Fl.10-20 FL10-20 Fl.

10-20 FLIO-20FI.10-20F1.

IO-20FI.

10-20FI.10-20 Fl.10-20FL

10-20 FL

10-20 FL10-20 Fl.10-20 FL10-20FL10:20 Fl.10-20 Fl.10-20 FL

10-20 FL10-20 Fl.

10-20 Fl.

10-20 FL

10-20 Fl.10-20 Fl.

10-20 Fl.10-20 Fl.

10-20 Fl.

10-20 Fl.

10-20 Fl.IO-20FI.

IO-20FL

10-20 Fl.10-20 FLIO-20FL10-20 R.10-20 Fl.10-20 FL10-20 Fl.

Area

Allied SieelAllied SieelAllied SteelAllied SteelAllied SteelAllied SteelAllied Sice]Allied SteelAllied SieelAllied SteelAllied SteelAllied SteelAllied SteelAllied SicelAllied SieelAllied SteelAllied SteelAllied SteelAllied SieelAllied SieelAllied SieelAllied SieelAllied SieelAllied SieelAllied SteelAllied SieelAllied SteelAllied SteelAllied SieelAllied SteelAllied SieelAllied SieelAllied SteelAllied SieelAllied SieelAllied SieelAllied SieelAllied SieelAllied SieelAllied SieelAllied SteelAllied SieelAllied SieelAllied SieelAllied SieelAllied SteelAllied SteelAllied SieelAllied SieelAllied SteelAllied SteelAllied Sieel

'Allied SieelAllied SteelAllied SieelAllied SteelAllied SteelAllied SieelAllied SteelAllied SteelAllied SieelAllied Steel

1PC Side1PC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC Side

Group

AEOsAEOs

AEOs

AEOs

AEOsAEOsAEOs

AEOs

AEOs

AEOs

AEOs

MetaJsMetalsMetal:MetalsMetal]MetalsMetalsMetalsPAHsPAHs

PAHs

PAHs

PAHs

PAHsPAHsPAHs

PAHs

PAHsPAHs

PAHs

PAHsPAHs

PAHs

PAHs

VOCs

VOCs

VOCs

VOCs

VOCsVOCs

VOCs

VOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVCCsVOCsVOCsVOCsVOCsVOCsVCCsVOCs

VOCsVOCsVOCsVOCjAEOsAEOs

AEOsAEOs

AEOs

AEOs

AEOs

AEOsAEOs

AEOs

AEOs

MetalsMetalsMetalsMetalsMetalsMetalsMetalsMetalsPAHsPAHs

PAHs

PAHs

PAHs

PAHsPAHs

_PAHs.PAHsPAHs

PAHsPAHs

PAHs

PAHs

PAHs

PAHs

VOCsVOCs

VOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCs

VOCsVOCsVOCs

Chemical

2,4,5-Trichlorophenol2,4,6-Trichlorophenol2,4-Dichlorophenol2,4-Dimeihylphenol2,4-Dinilrophenol2-Melhyl-4.6-Dinitrophenol2-Nilrophenol4-Chloro-3-Meihylphenol4-NiirophenolPeniachlorophenolPhenolArsenicZhromiumCopperCyanideIronLead .NickelZincAcenaphiheneAcenaphthyleneAnthraceneBenzo(a)anihracene9enzo(a)pyreneBenzo(b)nuorantheneBenzotg.h.Uperylene3enzo(k)fluorantheneChrysene[)ibenzo(a.h)anihraceneFluoranlheneFluoreneIndeno(1.2.3-cd)pyreneSaphihalenePhenanlhrenePyrene1 , 1 , 1 -Trichloroethane1 , 1 ,2,2-Tetrachlorelhane1.1.2-Trichlororeihanel.l-Dichloroethane1.1-Dichloroelhene1.2-Dichloroeihane1.2-DichloropropaneBenzeneBromodichloromeUianeBromoformBromomethaneCarbon TetrachlorideChlorobenzeneChloroethaneChloroformChloromelhanecis-l,3-DichloropropeneDibroraochloromelhane"EthylbenzeneMethylene ChlorideTetrachloroetheneToluenetrans- 1 ,2-Dichioroethenetrans- 1.3-DichloropropeneTrichloroetheneVinyl ChlorideXylenes. Toial2.4,5-Trichlorophenol2.4.6-Trichlorophenol2,4-Dichlorophenol2,4-Dimethylphenol2.4-Dinitrophenol2-Methyl-4,6-Diniirophenol2-Nitroptienol4-Chloro-3-Mclhylphenol4-Nitrophenol

Peniachlorophenol

Phenol

ArsenicChromiumCopper

CyanideIronLead

Nickel

Zinc

AcenaphtheneAcenaphthyleneAnthracene

Benzo(a)anihraceneBenzo(a)pyrene

Benzo(b)fluoranlheneBenzo(g,h.i)peryleneBenzoQOfluorantheneChrysene

Dibenzo(aji)anlhraceneFluoranihene

Fluorene

lndeno( 1 ,2.3-cd)pyreneNaphthalene

Phenanthrene

Pyrene

l.l.l-Trichlorcethane1 . 1 ,2.2-Teirachlorethane

1.1,2-Trichloroethane

l.l-Dichloroethane

1.1-Dichloroethene1,2-Dichloroethane

1,2-DichloropropaneBenzene

Bromodichloromethane

BroraoformBromomelhane

Carbon Telrachloride

ChlorobenzeneThlorofonn

Units

mg/kg

rag/kg

mg/kg

mg/kg

mg/kgmg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

rag/kgmg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kgmg/kg

mg/kg

mg/kg

mg/kg

rag/kgrag/kg

mg/kg

mg/kgmg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kgmg/kg

mg/kg

mg/kg

mg/kgrag/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kg

me/kgmg/kgmg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kg

mg/kg

mg/kgmg/kg

Number ofSamples

3737

37

37

373737

37

3737

37

3737

37

37

37

37

373737373737373737

37

37

373737

3737

37

3737

37

3737373737373737

37

373737373737

' 37 " '37

3737373737

37

3737

20

20

2020

202020202020

20

2020

2020202020202020

20

202020202020

2020

202020

20

202020

202020202020

20

2020

20

20

20

Number ofDetections

000100

00i01

1936321137303237322331303132232930215

33

28293580000000150000000000 "~223180000230000000000012192052016

20

201711

13

13

12

16

1211

120515

12

14

15

3

00000008000000

Number ofNondetecU

3737

37

363737

37

373637361815260750514

6

7

6514

87

35224

98

2

29

3737

3737373737

22373737373737373737

' • 37 -

153436293737373714

20

20

2020

20

20

2020

20

20

208101504

00397784

89 .820155865

17

2020

20

20

20

20

20

12

2020

20

20

20

20


0.00.0

0.02.70.00.00.0o.o2.7

0.0

2.751.4

97.386.5

29.7

100.0

81.186.5100.086.562.283.881. 183.886.562.278.481.15.4

40.589.275.778.4

94.6

21.60.00.00.00.00.00.00.0

40.50.00.00.00.00.00.00.00.00.0

"0.059.58.12.7

21.60.00.00.00.0

62.20.00.00.00.00.00.00.00.0

0.0

0.00.060.0

95.0100.025.0100.080.0

100.0100.085.055.0

65.065.060.080.0 .

60.055.0

60.00.0

25.075.060.070.075.0

15.00.00.0

0.0

0.0

0.00.0

0.040.00.00.00.0

0.00.00.0

MinimumSQL

I.6J

0.330.330.331.651.650.330.330.660.66

0.332.0

3.03.0

1.0

unknown55

unknown0.010.010.010.010.010.010.010.010.010.010.010.010.010.010.010.01

0.005

0.0050.0050.0050.0050.0050.0050.0010.0010,0010.0020.001o.ooi0.0010.0010.001O.OOI

' 0:00 r0.0010.005o.ooio.ooi0.001O.OOI0.0010.0010.0011.650.330.330.331.651.650.330.330.66

0.660.332.03.03.01.0

unknown55

unknown0.010.010.010.010.010.010.010.010.010.0 10.0 10.010.010.010.010.01o.ooiO.OOI

o.ooi0.0010.0010.001O.OOI0.001O.OOI0.0010.002

o.ooi0.0010.001

MaximumSQL

8.25

1.651.651.658.258.251.651.653.33.31.652.03.03.01.0

unknown505.0

unknown1.005.000.1050

0.100.105.000.10501002000.022.00.100.022502222222555105555

5535255555555

82.516.51.651.658.2582.51.651.653333

16.52.03.03.01.0

unknown5

5.0unknown

0.01.02.00.20.00.01.0 .1.00.2

20.050.020.01.00.02.0

200.00.50.5

0.50.50.50.50.50.10.50.51.00.50.50.5

MinimumDetected Cone.

ND

NDND94ND

NDNDND1.66ND25.12.23.24.6

12680

5.27

80.07

0.590.010.010.020.030.080.020.015.9

0.030.020.030.050.030.04ND

ND

ND

NDND

NDND

0.008NDNDNDNDNDNDNDND

ND

-' ND

0.0030.0220.0220.28NDNDNDND

0.002NDNDNDNDNDNDNDNDND

ND

ND

2.1

4.54.4

1

31506

5.810.50.070.1

0.020.010.010.010.050.02

0.01ND

0.060.020.010.030.026.9ND

ND

ND

ND

NDND

ND

0.02NDNDND

ND

ND

ND

MaximumDetected Cone.

ND

NDND94

ND

ND

NDND

1.66

ND25.1266122050

51300199050

1090269026901240122682259042825711348.9

8750

2520331

48305000729NDNDNDNDNDNDND94.9ND

ND

NDNDNDNDNDNDNDND'

49.5

2.930.02281.1

NDND

ND

ND

102

NDNDNDNDNDNDNDNDND

ND

ND12.2

48

41

172$400

964225812121173120

87.974.558.637.820

90.4ND

98225135:8316053971.8NDND

ND

ND

NDNDND

11.3

ND

ND

ND

ND

NDND

COPC?

No

NoNoYesNo

NoNoNoYesNo

YesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesNoNoNoNoNoNoNoYesNoNoNoNoNoNoNoNoNoNoYesYesYesYesNoNoNoNoYesNo

NoNo

No

No

No

NoNo

No

No

No

YesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesNo

YesYesYesYesYesYesNoNoNo

NoNoNoNoYesNoNoNo

NoNoNo

Rationale for Selection or Rejectionas COPC

Chemical not delected.Chemical not detected.Chemical not delected.Chemical delected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not delected.Chemical detected.Chemical not delected.Chemical detected.Chemical detected.Chemical delected.Chemical delected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical delected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical delected.Chemical detected.Chemical delected.Chemical delected.Chemical detected.Chemical delected.Chemical delected.Chemical deiecied.Chemical deiecied.Chemical detected.Chemical delected.Chemical not detected.Chemical not detected.Chemical not delected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical delected.Chemical noi delected.Chemical not delected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical noi delected.Chemical not detected.Chemical not detected.Chemical not delected.Chemical not detected.Chemical detected.Chemical delected.Chemical detected.Chemical deiecied.Chemical noi delected.Chemical not detected.Chemical not deiecied.Chemical not delected.Chemical detected.Chemical not detected.Chemical not detected.Chemical not detected.Chemical noi detected.Chemical not detected.Chemical not delected.Chemical not delected.Chemical not detected.Chemical not detected.Chemical not delected.Chemical noi delected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical detecied.Chemical delected.Chemical detecied.Chemical detected.Chemical detected.Chemical detected.Chemical detected.Chemical delected.Chemical delected.Chemical not delected.Chemical delected.Chemical detected.Chemical detected.Chemical delected.Chemical detecied.Chemical detecied.Chemical not detecied.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not detecied.Chemical not detected.Chemical not detected.Chemical detected.Chemical not detecied.Chemical not detecied.Chemical not detected.Chemical not detected.Chemical not detected.Chemical not delected.

TABLE 2-3

SELECTION OF CHEMICALS OF POTENTIAL CONCERN (COPCs) IN SUBSURFACE SOIL (10-20 FEET)

Depth

10-20 Fl.IO-20FI.10-20 FL

10-20 Ft.

10-20 Fl.10-20 Ft.

IO-20FL

10-20 FL

10-20 Ft.IO-20FI.10-20 Fl.

10-20 FL

10-20 Fl.

Ana

IPC SideIPC Side

IPC Side

IPC Side

IPC SideIPC Side

IPC Side

IPC Side


IPC Side

IPC Side

Group

VOCsVOCs

VOCs

VOCs

VOCsVOCs

VOCs

VOCs

VOCsVOCsVOCs

VOCsVOCs

Chemical

ChloromeUi&necis- 1 ,3-Dichloropropene

Dibromochloro methane

Eihytbenzene

Melhylene ChlorideTetrachloroelhene

Toluene

trans- 1 ,2-Dichtoroeihene

trans- 1 ,3-DichloropropcneTrichloroetheneVinyl Chloride

Xylenes. TotalChloroethane

Units

mg/kgrag/kg

rag/kg

mg/kg

rag/kgmg/kg

mg/kg

mg/kg

mg/kgmg/kgmg/kg

mg/kgmg/kg

Number ofSamples

20202020202020

202020202020

Number ofDetections

200

12

606000

0120

Number ofNondttecu

18202081420

14

202020

20

8

20


10.00.0

0.060.030.00.0

30.0

o.o0.00.0

0.060.00.0

MinimumSQL

0.0010.001

0.00 1

0.0010.0050.001

0.001

o.ooi0.0010.001

0.001

0.0010.001

MaximumSQL

0.10.50.5

0.0052.50.50.10.50.50.5

0.3

0.0050.5

MinimumDetected Cone

0.271ND

ND

0.0050.012ND

0.359

NDNDND

ND0.019ND

MaximumDetected Cone

3.44

ND

ND

16.40.121

ND

11.1

NDNDND

ND

53.5ND

COPC?

YesNoNoYesYesNo

YesNoNoNo

No

YesNo

Rationale for Selection or Rejectionas COPC

Chemical delected.Chemical not delected.

Chemical nol detected.Chemical delected.Chemical detected.


Chemical detected.Chemical nol detected.Chemical not delected.Chemical nol delected.

Chemical not detected.Chemical delected.Chemical not detected.

TABLE 2-4

SELECTION OF CHEMICALS OF POTENTIAL CONCERN (COPCs) FOR GROUNDWATER

Group

VOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsVOCsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsMetalsMetals " 'MetalsMetalsMetalsMetalsMetalsInorganics

Inorganics

AEOsAEOsAEOsAEOsAEOsAEOsAEOsAEOsAEOs

Chemical

1,1,1-Trichloroethane1 , 1 ,2,2-Tetrachlorethane1 , 1 ,2-Trichlororethane1,1-Dichloroethane1,2-Dichloroethane1,2-DichloropropaneBenzeneBromodichloromethaneBromoform

BromomethaneCarbon TetrachlorideChloro benzeneChloroethaneChloroformChloromethanecis- 1 ,3-DichloropropeneDibromochloromethaneEthylbenzeneMethylene ChlorideTetrachloroetheneToluenetrans- 1 ,2-Dichloroethenetrans- 1 ,3-DichloropropeneTrichloroetheneVinyl ChlorideXylenes, TotalAcenaphtheneAcenaphthyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k)fluorantheneChryseneDibenzo(a,h)anthraceneFluorantheneFluoreneIndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanthrenePyreneArsenicChromiumCopperIronLeadNickelZincCyanide

Sulfate

2,4,6-Trichlorophenol2,4-Dichlorophenol2,4-Dimethylphenol2,4-Dinitrophenol2-Methyl-4,6-Dinitrophenol2-Nitrophenol4-NitrophenolPentachlorophenolPhenol

Units

Mg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LHg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/Lmg/Lmg/Umg/Lmg/Lmg/Lmg/Lmg/Lmg/L

mg/L

Mg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/L

MinimumPQL

1111

0.411111

0.3111111151111111

0.50.50.050.020.030.050.050.020.050.020.050.1

0.050.5

0.050.050.005

~ 0.03"-0.03

unknown0.0050.050.030.007

Unknown

101010101010201010

MaximumPQL

5050

. 505020501

505050155050505050501

250501

50505050

10.525

0.050.020.030.050.050.020.050.020.050.1

0.050.5

0.050.050.0050.030.03

unknown0.0050.050.030.078

Unknown

101010101010201010

Sample Count

72727272727272727272727272727272727272727272727272727272727272727272727272727272727272-72727272727272

72

727272727272727272

Number ofNondetects

7272727271723972727171727272717272437272467272727238254131454751545348715332562327456

— 28240819127

0

727264727272727234

Number ofDetections

000010

330011000100290026000034473141272521181924

119401649452766

• 44-- - -

487264

536065

72

0080000038

DetectionFrequency, %

0.000.000.000.001.390.00

45.830.000.001.391.390.000.000.001.390.000.0040.280.000.0036.110.000.000.000.00

47.2265.2843.0656.9437.5034.7229.1725.0026.3933.331.39

26.3955.5622.2268.0662.5037.5091.67

- - 61.11"66.67100.0088.8973.6183.3390.28

100.00

0.00

0.0011.110.000.000.000.000.00

52.78

MinimumDetected

Cone.

...

...

—...9...1.1...._

42.2............1.2...1.10.5......1

—...._...2.90.51.40.10.10.10.10.10.10.2

0.080.31.3

0.070.50.50.3

0.01-0.0380.0360.1480.0060.0610.0320.007

1

—...84.9...............27

MaximumDetected

Cone.

...

...

...

—9

—12300......

42.2....„......14...

37202490......

5390

—.......„

3390717310046219720017116679.61920.08494111031

43301490769

0.136- 1.11 -

0.5183782.360.7853.311.72

1790

—...3670......

——...

697

COPC?

NoNoNoNoYesNoYesNoNoYesNoNoNoNoYesNoNoYesNoNoYesNoNoNoNoYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYesYes

No

NoNoYesNoNoNoNoNoYes

Basis for Selection or Rejectionas COPC

Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound detected.Compound not detected.Compound detected.Compound not detected.Compound not detected.Compound detected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound detected.Compound not detected.Compound not detected.Compound detected.Compound not detected.Compound not detected.Compound detected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound-detected:Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound detected.Compound not detected abovehealth-based criterion.Compound not detected.Compound not detected.Compound detected.Compound not detected.Compound not detected.Compound not delected.Compound not detected.Compound not detected.Compound detected.

TABLE 2-5

SELECTION OF CHEMCIALS OF POTENTIAL CONCERN (COPCs) FOR SEDIMENT

Analytical Parameters

VOCsBenzeneBromodichloromethaneBromoform

BromomethaneCarbon TelrachlorideChlorobenzeneCloroelhaneChloroformChloromethaneDibromochloromethane1,1-Dichloroethane1,2-Dichloroethane1,1-Dichloroethenetrans- 1 ,2-Dichloroethene1 ,2-Dichloropropanecis- 1 ,3-Dichloropropenetrans- 1 ,3-DichloropropeneEthylbenzeneMethylene Chloride1,1,2,2-TetrachlorethaneTetrachloroetheneToluene1,1,1-Trichloroe thane1,1,2-TrichlororethaneTrichloroelheneVinyl ChlorideXylenes, Total

AEOs. PAHs. and SVOCs

Acenaphthene

Acenaphthylene

Anthracene

Benzo(a)anthracene

Benzo(a)pyrene

Benzo(b)fluoramhene ~

Benzo(g,h,i)perylene


Chrysene

Dibenzo(a,h)amhracene

Fluoranlhene

Fluorene

lndeno( 1 ,2,3-cd)pyrene

Naphthalene

Phenanthrene

Pyrene

4-Chloro-3-Methylphenol2-Chorophenol2,4-Dichlorophenol2,4-Dimethylphenol2,4-Dinilrophenol2-Methyl-4,6-Dinitrophenol2-NifropherT6r "" ~~~4-NitrophenolPentachlorophenolPhenol2,4,5-Trichlorophenol2.4,6-Trichlorophenol

Units

mg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

Tig/kg"

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kgmg/kgmg/kgmg/kgmg/kgmg/kg

~mg/kgmg/kgmg/kgmg/kgmg/kgmg/kg

MinimumSQL

0.0010.0010.001

0.0010.0010.0010.0010.0010.0010.0010.0010.0010.001

0.0010.0010.0010.0010.0010.0010.001

0.0010.0010.0010.0010.0010.0010.001

0.01

0.01

0.01

0.01

0.01

~070T

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.330.330.330.331.651.65

" ~ 0^330.660.010.331.65

0.33

MaximumSQL

0.0010.0010.002

0.0010.0010.0010.0010.0010.0010.001

0.0010.00!

0.0010.0010.0010.0010.0010.0010.0010.0010.0010.0010.0010.0010.0010.0010.001

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.01

0.330.330.330.331.651.65

0.33' "0.660.660.331.650.33

Number ofSamples

999999999999999999999999999

9

9

9

9

9

9

9

9

9

9

9

9

9

9

9

9

999999

" " 9 "99999

Number ofDetections

000000000000000000200200000

2

0

2

3

3

4

1

2

3

1

4

0

1

1

2

2

000000

~ XT ~-

00000

MiniumumDetected

Cone.

...

...

...

...

...

...

...

...

...

...

...

...

...

...

...

...

...

...9......35...............

0.3

...

0.03

0.02

0.03

01)7

0.4

0.02

0.01

0.02

0.04

...

0.4

0.6

0.02

0.03

...

...

...

...

...

...

..'. ^~~

...

...

...

...

...

MaximumDetected

Cone.

...

...

...

...

...

...

...

...

...

...

...

...

...

...

...

...

...

...9......67...............

4.4

...

0.4

0.9

1.3

0.2

0.4

0.4

0.9

0.02

0.7

...

0.4

0.6

0.1

0.5

...

...

...

...

...

...• : . : - -............

—

SedimentCOPC?

NoNoNoNoNoNoNoNoNoNoNoNoNoNoNoNoNoNoYesNoNoYesNoNoNoNoNo

Yes

No

Yes

Yes

Yes

Yes

Yes

Yes

Yes

Yes

Yes

No

Yes

Yes

Yes

Yes

NoNoNoNoNoNo

•^--Ntf- 'NoNoNoNoNo

Rationale for Selection or Rejection

Compound not detected.Compound not delected.Compound not detected.Compound not delected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound not delected.Compound not detected.Compound not detected.Compound not delected.Compound delected.Compound not detected.Compound not delected.Compound detected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.Compound not detected.

Detected downstream concentraiion greaterthan upstream concentration.

Compound not detected.

Delected downstream concentration greaterthan upstream concentration.

Delected downstream concentration greaterthan upstream concentration.

Detected downstream concemralion greaterthan upstream concentration.

Detecied downstream concentration greaterthan upstream concentration.

Detected downstream concentration greaterthan upstream concentration.

Detected downsiream concentraiion greaterthan upstream concentraiion.

Delected downsiream concentration grealerthan upstream concentration.

Delected downstream concentration greaterthan upstream concentraiion.

Detected downsiream concentration grealerthan upsiream concenlration.


Detected downstream concenlration greaterthan upsiream concentration.

Detecied downsiream concentration greaterthan upstream concenlration.

Detected downstream concentration greaierthan upstream concemralion.

Detected downstream concentraiion greaterthan upstream concenlration.

Compound nol detected.Compound nol detected.Compound not detected.Compound not detected.Compound nol delecled.Compound not detected.Compound n"6Taetected.~ " ""- - ~Compound not detected.Compound not delected.Compound not detected.Compound not detected.Compound not detecled.

TABLE 2-5

SELECTION OF CHEMCIALS OF POTENTIAL CONCERN (COPCs) FOR SEDIMENT


Metals

Arsenic

Chromium

Copper

Iron

Lead

Nickel

Zinc

Cyanide

Units

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

mg/kg

MinimumSQL

1

3

3

5

5

5

b

1

MaximumSQL

2

3

3

5

5

5

b

1

Number ofSamples

9

9

9

9

9

9

9

9

Number ofDetections

3

8

4

9

4

6

9

0

MiniumumDetected

Cone.

2.4

3.3

8.8

3530

8.8

5.2

8.1

...

MaximumDetected

Cone.

2.4

19.3

19.4

27100

22

15.6

82

...

SedimentCOPC?

Yes

Yes

Yes

Yes

Yes

Yes

Yes

No

Rationale for Selection or Rejection

Detected concentration downstream greaterthan upstream at former sluice pond outfal l .



Delected concentration downstream greaterthan upstream at former sluice pond outfal l .

Detected concentration downstream greaterthan upstream at former sluice pond outfall.




Notes:Detections of ammonia (as total nitrogen) and sulfate were observed in sediment samples collected near a sewer outfall in 1998. These chemicals were not observed in sediment sample:collected in 1999. The detections are not believed to be associated with the site.

a. Chemical groups:AEOs = Acid extracable organics.

Inorganics = Metals and non-organic anions/cations.

SVOCs = Semivolatile organic compounds.

VOCs = Volatile organic compounds.

b. Unknown

TABLE 2-6

SUMMARY OF RATIONALE FOR SELECTION OR REJECTION OFCHEMICALS OF POTENTIAL CONCERN (COPCS) FOR SURFACE WATER

Analytical ParametersChemical

GroupSurface Water

COPC?Basis for Selection orRejection as COPC

VOCs

Benzene

Bromodichloromethane

Bromoform

Bromomethane

Carbon Tetrachloride

Chlorobenzene

Chloroethane

Chloroform

Chloromethane

Dibromochloromethane

1,1-Dichloroethane

1,2-Dichloroethane

1,1-Dichloroethene

trans-1,2-Dichloroethene

1,2-Dichloropropane

cis-1,3-DichIoropropene

trans- 1,3-DichIoropropene

Ethylbenzene

Methylene Chloride

1,1,2,2-Tetrachlorethane

Tetrachloroethene

Toluene

1,1,1 -Trichloroethane

1,1,2-Trichlororethane

Trichloroethene

Vinyl Chloride

Xylenes, Total

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

No

No

No

No

No

No

No

No

No

No

No

No

No

. No

No

No

No

No

No

No

No

No

No

No

No

No

No




























TABLE 2-6 (CONTINUED)


Analytical ParametersChemical Surface Water

Group COPC?Basis for Selection orRejection as COPC

AEOs. PAHs. and SVOCs

Acenaphthene

Acenaphthylene

Anthracene

Benzo(a)anthracene a

Benzo(a)pyrene a

Benzo(b)fluoranthene a


Benzo(k)fluoranthene a

Chrysene a

Dibenzo(a,h)anthracene "

Fluoranthene

Fluorene

Indeno(l,2,3-cd)pyrenea

Naphthalene

Phenanthrene

Pyrene

4-Chloro-3-Methylphenol

2-Chorophenol

2,4-Dichlorophenol

2,4-Dimethylphenol

2,4-Dinitrophenol

2-Methyl-4,6-Dinitrophenol

2-Nitrophenol

4-Nitrophenol

Pentachlorophenol

Phenol


2,4,6-TrichlorophenoI

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

SVOCs

AEOs

AEOs

AEOs

AEOs

AEOs

AEOs

AEOs

AEOs

AEOs

AEOs

AEOs

AEOs

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No

No




















Compound not detected.Compound not detected.











Notes:

Chemical Surface WaterGroup COPC?

Basis for Selection orRejection as COPC

Metals

Arsenic

'Chromium

Copper

Iron

Lead

Nickel

Zinc

Cyanide

Nitrogen, Ammonia

Sulfate

Inorganics

Inorganics

Inorganics

Inorganics

Inorganics

Inorganics

Inorganics

Inorganics

Inorganics

Inorganics

No

No

No

No

No

No

No

No

No

No




Compound detected, but is notassociated with site activities.

Compound detected, but is notassociated with site activities.'





Compound detected, but is notassociated with site activities.

a Suspected carcinogenic polynuclear aromatic hydrocarbon (PAH) compound.

Chemical Groups:AEOs = Acid extracable organics.Inorganics = Metals and nonorganic anions/cations.VOCs = Volatile organic compounds.SVOCs = Semivolatile organic compounds.

TABLE 2-7

SUMMARY OF CHEMICALS OF POTENTIAL CONCERN PARAMETERS


VOCsBenzeneBromodichloromethaneBromoformBromomethaneCarbon TetrachlorideChlorobenzeneChloroethaneChloroformChloromethaneDibromochloromethane1,1-Dichloroethane1,2-Dichloroethane1,1-Dichloroethenetrans- 1 ,2-Dichloroethene1 ,2-Dichloropropanecis- 1 ,3-Dichloropropenetrans- 1 ,3-DichloropropeneEthylbenzeneMethylene Chloride1 , 1 ,2,2-TetrachlorethaneTetrachloroetheneToluene1,1,1 -Trichloroethane1 , 1 ,2-TrichlororethaneTrichloroetheneVinyl ChlorideXylenes, Total

SoilsSurface Soil

IPC

0-1 ft

X

X

X

X

Allied

0-1 ft

X

XX

X

X

Subsurface Soil

IPC

1-10 ft

X

X

XX

X

X

10-20 ft

X

X

XX

X

X

Allied

1-10 ft

X

XX

X

X

10-20 ft

X

XX

XX

X

Groundwater Monitoring Wells

WaterTable

Aquifer

X

X

X

X

X

X

IntermediateZone

X

X

X

X

X

Mississippi River

Sediment

X

X

SurfaceWater




PAHsAcenaphtheneAcenaphthyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k)fluorantheneChryseneDibenzo(a,h)anthraceneFluorantheneFluoreneIndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanthrenePyrene

Acid Extractable4-Chloro-3-Methylphenol2-Chorophenol2,4-Dichlorophenol2,4-Dimethylphenol2,4-Dinitrophenol2-Methyl-4,6-Dinitrophenol2-Nitrophenol4-NitrophenolPentachlorophenolPhenol2,4,5-Trichlorophenol2,4,6-Trichlorophenol

SoilsSurface Soil

IPC

0-1 ft

X

XXXXXXX

XXXXXX

X

Allied

0-1 ft

X

XXXXXXX

XXXXXX

,

Subsurface Soil

IPC

1-10 ft

XXXXXXXXXXXXXXXX

10-20 ft

XXXXXXXXX

XXXXXX

Allied

1-10 ft

XXXXXXXXX

XXXXXX

XX

10-20 ft

XXXXXXXXXXXXXXXX

X

X

X


WaterTable

Aquifer

XXXXXXXXXXXXXXXX

X

X

IntermediateZone

XXXXXXXXX

XXXXXX

Mississippi River

Sediment

X

XXXXXXXXX

XXXX

SurfaceWater




VletalsArsenicChromiumCopperIronLeadNickelZincCyanide

PCBsArochlor 1016Arochlor 1221Arochlor 1232Arochlor 1242Arochlor 1248Arochlor 1254Arochlor 1260

SoilsSurface Soil

IPC

0-1 ft

XXXXXXXX

X

Allied

0-1 ft

XXXXXXXX

X

XX

Subsurface Soil

IPC

1-10 ft

XXXXXXXX

10-20 ft

XXXXXXXX

Allied

1-10 ft

XXXXXXXX

10-20 ft

XXXXXXXX


WaterTable

Aquifer

XXXXXXXX

IntermediateZone

XXXXXXXX

Mississippi River

Sediment

XXXXXXX

SurfaceWater

XX

TABLE 3-1

CHEMICAL TOXICITY VALUES AND ABSORPTION ESTIMATES

VOLATILES

BenzeneBromodichloromethane

Bromoform

Bromomethane

Carbon TetrachlorideChlorobenzene

Chloroethane

ChloroformChloromethane

Dibromochloromethane1,1-Dichloroethane

1,2-Dichloroethane

1,1-Dichloroethene

trans- 1 ,2-DichIoroethene

1 ,2-Dichloropropane

cis- 1 ,3-Dichloropropene

trans- 1 ,3-Dichloropropene

Ethylbenzene

Methylene Chloride

1 , 1 ,2,2-Tetrachloroe thane

TetrachloroetheneToluene

1,1,1 -Trichloroethane

1 , 1 ,2-TrichloroethaneTrichloroethene

Vinyl Chloride

Total XylenesPAHs

Acenaphthene

Anthracene

Benzo(a)anthracene

Benzo(a)pyrene

Benzo(b)fluoranihene


Reference Dose (mg/kg-day)

OralSubchronic

NI

2.00E-02 H2.00E-01 H

5.00E-03

7.00E-03

NI

NI

l.OOE-02 H

NI

2.00E-01 H

l.OOE+00 H

NI

9.00E-03

2.00E-01NI

3.00E-03 H

3.00E-03 H

NI

6.00E-02 H

NI

l.OOE-OI H

2.00E+00 H

NI

4.00E-02 H

NI

3.00E-03 C

NI^

6.00E-01 H

3.00E+00 H

NI

NI

NI

NI

Chronic

3.00E-03 K

2.00E-02 I

2.00E-02 I

1.40E-03 I7.00E-04 I

2.00E-02 I

NI

l.OOE-02 I

NI

2.00E-02 I

l.OOE-01 H

3.00E-02 K

9.00E-03

2.00E-02

NI

3.00E-04 I

3.00E-04 I

l.OOE-01 I

6.00E-02 I

6.00E-02 K

l.OOE-02 I

2.00E-01 I

2.00E-02 K

4.00E-03 I

6.00E-03 K

3.00E-03 12

2.00E+00 I

6.00E-02 I

3.00E-01 I

NI

NI

NI

NI

Dermal3

Subchronic

NI

2.00E-02

2.00E-01

5.00E-03

7.00E-03

NI

NI

l.OOE-02

NI

2.00E-01

l.OOE+00

NI

9.00E-03

2.00E-01

NI

3.00E-03

3.00E-03

NI

6.00E-02

NI

l.OOE-01

2.00E+00

NI

4.00E-02

NI

3.00E-03

NI

6.00E-OI

3.00E+00NI

NI

NI

NI

Chronic

3.00E-03

2.00E-02

2.00E-02

1.40E-037.00E-04

2.00E-02

NI

l.OOE-02

NI

2.00E-02

l.OOE-013.00E-02

9.00E-03

2.00E-02

NI

3.00E-04

3.00E-04

l.OOE-016.00E-02

6.00E-02

l.OOE-02

2.00E-OI

2.00E-02

4.00E-03

6.00E-03

3.00E-03

2.00E+00

6.00E-02

3.00E-01

NI

NI

NI

NI

Inhalation1*Subchronic

NI

NI

NI

3.71E-02

5.71E-03

NI

2.86E+00 H

NI

NI

NI

1.43E+00 A

NI

NI

NI

3.71E-03 H

5.71E-03 H5.71E-03 H

NI

8.57E-01 H

NI

NI

NI

NI

NI

NI

2.86E-03 C

NI

NI

NI

NI

NI

NI

NI

Chronic

1.70E-03 K

NI

NI

I.43E-03 K5.71E-04 K

I.70E-02 K

2.86E+00 I

8.60E-05 K

8.60E-02 K

NIj

1.43E-01 H

1140E-03

NI

NI

(.14E-03 I

5.7IE-03 I

5.71E-03 I

2.86E-01 I

8.57E-01 HNI

1.40E-OI1.14E-OI I

2.86E-01 KNI

NI

2.86E-03 J

NI

NI

NI

NI

NI

NI

NI

Slope Factors (kg-day/mg)Oral

5.50E-02 I

6.20E-02 I

7.93E-03 I

NC

1.30E-01 I

NC

NC

6.10E-03 I

1.30E-02 H

8.40E-02 INI

9.10E-02 I

6.00E-01 I

NC

6.80E-02 H

1.80E-OI HI.80E-01 H

NC

7.50E-03 I

2.00E-01 I5.20E-02 K

NC

NC

5.70E-02 I

1.10E-02 K

1.4E+00 12

NC

NC

NC

7.30E-01 K

7.30E+00 K7.30E-01 K

NC

Dermal0

5.50E-02

6.20E-02

7.93E-03

NC

1.30E-01

NC

NC

6.10E-03

1.30E-02

8.40E-02

NI

9.10E-02

1.75E+00

NC

6.80E-02

1.80E-01

1.80E-01

NC

7.50E-03

2.00E-01

5.20E-02

NC

NC

5.70E-02

1.10E-02

I.40E+00

NC

NC

NC

7.30E-01

7.30E+00

7.30E-01NC

Inhalation

2.90E-02 I

NI

3.90E-03 I

NC

5.30E-02 I

NC

NC

8.10E-02 I

6.30E-03 E

NI

NI

9.10E-02 I

1.75E-01 I

NC

NI

1.30E-01 H1.30E-01 H

NC

1.65E-03 I

2.00E-01 I

2.00E-03 KNC

NC

5.70E-02 I

6.00E-03 K

3.0 E-02 12

NC

NC

NC

3.10E-01 L

3.10E+00 K

3.10E-01 L

NC

AbsorptionEfficiency

(for Dermal)"1

! 1.00 D*

1.00 D*

1.00 D*

1.00 D*

1.00 D*

1.00 D*

1.00 D*

1.00 D*

1.00 D*

: 1.00 D*

1.00 D*

1.00 D*

1.00 D*

1.00 D*

1.00 D*

1.00 D*1 1.00 D*

1.00 D*

1 1.00 D*

1.00 D*

1.00 D*

1.00 D*

1.00 D*

' 1.00 D*

1.00 D*

1.00 D*

' 1.00 D*x

•• 0.89 D

0.89 D

0.89 D

0.89 D

0.89 D

0.89 D

DermalAbsorption

FactorsABS

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.13 D

0.13 D

0.13 D

0.13 D

0.13 D

0.13 D

Weightof

Evidence"

A

B2

B2

D

B2

D

NA

B2

C

C

C

B2

C

NA

B2

B2

B2

D

B2

C

C-B2

D

D

C

C-B2

A

D

NA

D

B2

B2

B2

D



PAHs (Continued)


Chrysene

Dibenz(a,h)anthracene

Fluoranthene

Fluorene

Indeno( 1 ,2,3-cd)pyrene

Naphthalene

Phenanthrene

Pyrene

Acid Extractable

4-Chloro-3-Methylpheno!

2-ChlorophenoI

2,4-Dichlorophenol

2,4-DimethyIphenol

2,4-Di nitrophenol

2-Methyl-4,6-Dinitrophenol

2-Nitrophenol

4-Nitrophenol

Pentachlorophenol

Phenol


2,4,6-TrichlorophenolMetals

Arsenic

Chromium VI

Copper

Iron

Lead

Nickel

Zinc

Cyanide

Reference Dose (mg/kg-day) (

OralSubchronic

NI' NI

NI

4.00E-01 H

4.00E-01 H

NININI

3.00E-01 H

2.00E+00 H

5.00E-02 H

3.00E-03 H

2.00E-01 H

2.00E-03 H

NININI

3.00E-02 H

6.00E-OI H

l.OOE+00 H

NI

3.00E-04 H

2.00E-02 H

3.70E-02 H

NI

NI

2.00E-02 H

3.00E-01 H

2.00E-02 H

Chronic

NINI

NI

4.00E-02 I

4.00E-02 I

NI2.00E-02 I

NI3.00E-02 I

NI5.00E-03 I

3.00E-03 I

2.00E-02 I

2.00E-03 1

NININI

3.00E-02 I

6.00E-01 I

l.OOE-01 I

NI

3.00E-04 I

3.00E-03 I

3.70E-02 H

3.00E-01 K

NI

2.00E-02 I

3.00E-01 I

2.00E-02 I

Dermal0

Subchronic

NINI

NI

4.00E-01

4.00E-01

NININI

3.00E-01

2.00E+00

5.00E-02

3.00E-03

2.00E-01

2.00E-03

NININI

3.00E-02

6.00E-01

l.OOE+00NI

3.00E-04

5.00E-04

1.11E-02

NI

NI

8.00E-04

3.00E-01

2.00E-02

Chronic

NI

NINI

4.00E-02

4.00E-02

NI2.00E-02

NI3.00E-02

NI5.00E-03

3.00E-03

2.00E-02

2.00E-03

NININI

3.00E-02

6.00E-01

l.OOE-01NI

3.00E-04

6.00E-05

1.11E-02

4.50E-02

NI

8.00E-04

3.00E-012.00E-02

Inhalation"Subchronic

NINI

NI

NINININININI

NINININININININININININT

NI

NININI

NI

NININI

1 Chronic

ij NI

NI1 NI

i NI

NI

!. N1

8.57E-04 I

NINI

NINI

! NINTNINI

1 NI

NININININI

!' NI

2 86E-05 I

NINT

NT: NT

NI


7.30E-02 K

7.30E-03 K

7.30E+00 K

NCNC

7.30E-01 K

NCNCNC

NCNCNCNCNCNCNCNC

1.20E-01 I

NCNC

1.10E-02 I

1.50E+00 I

NINCNC

NI

NINCNC

Dermal0

7.30E-02

7.30E-03

7.30E+00

NCNC

7.30E-01

NCNCNC

NCNCNCNCNCNCNCNC

1.20E-01

NCNC

1.10E-02

1 .50E+00

NTNCNC

NI

NINCNC

Inhalation

3.10E-02 L

3.10E-03 L

3.10E+00 L

NCNC

3.10E-01 L

NCNCNC

NCNCNCNCNCNCNCNCNINCNC

l.OOE-02 I

1.50E+01 I

4.10E+01 H

NCNC

NT

NINCNC

1


(for Dermal)*1

0.89 D

0.89 D

0.89 D

0.89 D

0.89 D

i 0.89 D

0.89 D

0.89 D

0.89 D'

1.00 D*

1.00 D*

1. 00 D*

1. 00 D*

1.00 D*

1.00 D*

1.00 D*

1.00 D*

, 0.76 D

1.00 D*

1.00 D*

1.00 D*

0.95 D

0.025 D

0.30 A

, 0.15 A

0.15 A

! 0.04 Dn

1.00 D

1.00 D*

DermalAbsorption

FactorsABS

0.13 D

0.13 D

0.13 D

0.13 D

0.13 D

0.13 D

0.13 D

0.13 D

0.13 D

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.10 Ds

0.25 D

0.10 Ds

0.10 Ds

0.10 Ds

0.03 D

0.01 Ds

0.01 Ds

0.01 Ds

0.01 Ds

0.01 Ds

0.01 Ds

0.01 Ds

Weightof

Evidence*

B2B2

B2

DDB2DDD

NANANANANANANANAB2D

NAB2

A

AD

NA

B2

Under Review

DD



PCBs

Arochlor 1016(1)Arochlor 1221 (1)Arochlor 1232(1)Arochlor 1242(1)Arochlor 1248(1)Arochlor 1254(1)Arochlor 1260(1)

Reference Dose (mg/kg-day)

OralSubchronic

5.00E-05 H5.00E-05 (1)5.00E-05 (1)5.00E-05 (1)5.00E-05 (1)5.00E-05 H5.00E-05 (1)

Chronic

7.00E-05 I2.00E-05 (1)2.00E-05 (1)2.00E-05 (1)2.00E-05 (1)2.00E-05 I2.00E-05 (1)

Dermal8

Subchronic

5.00E-055.00E-055.00E-055.00E-055.00E-055.00E-055.00E-05

Chronic

7.00E-052.00E-052.00E-052.00E-052.00E-052.00E-052.00E-05

Inhalation1*Subchronic

NININININININI

Chronic

NININI

: NINl

1 NI•: NIi


7.00E-02 I2.00E+00 I2.00E+00 I2.00E+00 I2.00E+00 I2.00E+00 I2.00E+00 I

Dermal0

7.00E-022.00E+002.00E+002.00E+002.00E+002.00E+002.00E+00

Inhalation

7.00E-02 I2.00E+00 I2.00E+00 I2.00E+00 I2.00E+00 I2.00E+00 I2.00E+00 I


(for Dermal)d

)

) 0.80 D! 0.80 D! 0.80 D) 0.80 D; 0.80 D

0.80 D0.80 D

1

DermalAbsorption

FactorsABS

0.14 D0.14 D0.14 D0.14 D0.14 D0.14 D0.14 D

Weightof

Evidence"

NANANANANANANA

Notes:

Dermal RfD = Oral RfD if the Absorption efficiency for oral is greater than 50% x Oral Absorption.Dermal RfD - Oral RfD * Absorption Efficiency (Dermal) if the absorption efficiency is less than 50%.Refer to Risk Assessment Guidance for Superfund: Volume J, Human Health Evaluation Manual (Part D), Interim, January 1998.Value converted from unit risk provided in the reference (mg/m3 for reference doses, or ug/m3 for slope factors) to dose (mg/kg-day), by using a human body weight of 70 kg and an inhalation rate of 20 m3/day

c Dermal Slope Factor (SF) = Oral SF/Oral AbsorptionThe absorption factor (Dermal) is equivalent to absorption factor for oral.Weight of Evidence classifies chemicals as a carcinogen or a noncarcinogen. Chemicals classified as A,Bl,B2,or C are considered carcinogenic.

(1) = Arochlor 1254 used as a surrogate for all other Arochlors.

A Value for GI absorption of metals obtained from U.S. Army Environmental Center, 1995, where values were not recommended by USEPA as a conservative measure. Toxicity Values from the U.S. Environmental Protection Agency Integrated Risk Information Systemand Health Effects Assessment Summary Table. October 1995.

C Chronic RfD adopted as Subchronic RfD in the absence of other information.

D Value obtained from U.S. EPA, "Supplemental Guidance for Developing Soil Screening Levels for Superfund Sites," Peer Review Draft, March 2001. OSWER 9355.4-24.

D* Ibid. It should be noted that for GI absorption 100 % was used as a convention, since absorption for other organic compounds are generally greater than 50 % ( cut off above which adjustment to the toxicity values are not required).

Ds Screening default based on best professional judgement.

H U.S. EPA, 1997. Health Effects Assessment Summary Tables: FY1997 Update. July 1997. EPA 540/R-97-036.

1 Toxicity values obtained from the U.S. EPA Integrated Risk Information System, July 2001.12 Toxicity values obtained from the U.S. EPA Integrated Risk Information System, July 2001 for lifetime exposure.

J U.S. Environmental Protection Agency, NCEA. Toxicology Review of Vinyl Chloride - External Review Draft. May 20, 1999.

K Provisional toxicity values from U.S. Environmental Protection Agency, NCEA.L The inhalation slope factors for PAHs were calculated by using the inhalation slope factor for Benzo(a)pyrene relative potency factor. U.S. Environmental Protection Agency, July 1993. Provisional Guidance for Quantitative Risk Assessment of Poly cyclic Aromatic

Hydrocarbons, Office of Research and Development, EPA/600/R-93/089.

NA Not available.

NC Not classified as a carcinogen by U.S. EPA.

NI No information available.

TABLE 3-2

HEALTH EFFECT ENDPOINTS FOR CHRONIC AND SUBCHRON1C EXPOSURES TO SITE SOILS

CASRN

83-32-9208-96-8120-12-711096-82-511097-69-11 1 104-28-211141-16-512672-29-612674-11-253469-21-97440-38-271-43-256-55-350-32-8205-99-2191-24-2207-08-975-27-475-25-274-83-956-23-559-50-7108-90-775-00-367-66-374-87-395-57-818540-29-9218-01-97440-50-857-12-553-70-3124-48-175-34-3107-06-275-35-4156-60-5120-83-278-87-5I006I-OI-5542-75-610061-02-6105-67-9

51-28-5100-41-4206-44-086-73-7193-39-57439-89-67439-92-175-09-291-20-37440-02-0

88-75-5100-02-787-86-585-01-8108-95-2129-00-079-34-5127-18-4108-88-371-55-679-00-579-01-688-06-295-95-475-01-41330-20-7

7440-66-6

Chemical

AcenaphtheneAcenaphthyleneAnthraceneArochlor 1260Arochlor 1254Arochlor 1221Arochlor 1232Arochlor 1248Arochlor 1016Arochlor 1242ArsenicBenzeneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluoranlheneBenzo(g,hj)peryleneBenzo(k)fluoranlheneBromodichloro methaneBromoformBromomethaneCarbon Tetrachloride4-Ch!oro-3- MethylphenolChlorobenzeneChloroethaneChloroformChloromethane2-ChlorophenolChromium VIChryseneCopperCyanideDibenz(a,h)anlhraceneDibromochloromethanf1,1-Dichloroeihane1,2-DichIoroelhane1 , 1 -Dichloroethenetrans- 1 ,2-Dichloroethenc2,4-Dichlorophenol1 ,2-Dichloropropanecis- 1 ,3-Dichloropropene1 ,3-Dichloropropenetrans- 1 ,3-Dichloropropene2,4-Dimethylphenol

2,4-DinilrophenolElhylbenzeneFluoranthcneFluorenelndeno( 1 ,2,3-cd)pyreneIronLeadMelhylene chlorideNaphthaleneNickel

2-Niirophenol4-NitrophenolPentachlorophenolPhenanthrenePhenolPyrene1 , 1 ,2,2-TetrachloroelhaneTetrachloroeiheneToluene1,1,1 -Trichloroethane1 . 1 ,2-TrichloroethaneTrichloroethene2,4,6-Trichlorophenol2,4,5-TrichlorophenolVinyl ChlorideXylenes, Total

Zinc

Subchronic Oral RfD Effect

Hepalotoxicity

None Observed

Immune System Toxicit)

Skin and Vascular Effects

Kidney Cylomegal)Liver Effects

Decreased Weight Gain

Liver Lesions

Reproductive EffectsNone Observed

Gastrointestinal IrritationMyelin Degeneration

Liver LesionsNone Observed

Liver LesionsAlkaline Phosphatase IncreaseAltered Immune Functior

Increased Organ WeightNervous System Effects

Cataract

Kidney, Liver, Blood EffectDecreased Red Blood Cells

Liver Toxicily

Decreased Body Weight, DecreasedOrgan Weight

Fetotoxicity

Decreased Fetal WeighiKidney Effects

HepatotoxicilyAltered Liver and Kidney

Clinical Chemistry Alteration.*

Liver and Kidney Effect*Liver Cell Polymorphisn

Increased Blood Enzyme

Subchronic Oral RID Source

HEAST (07/97)HEAST (07/97)HEAST (07/97)NAHEAST (07/97)NANANANANAHEAST (07/97)NANANANANANAHEAST (07/97)HEAST (07/97)Contact TSCContact TSCHEAST (07/97)NANAHEAST (07/97)NAHEAST (07/97)HEAST (07/97)NAHEAST (07/97)HEAST (07/97)NAHEAST (07/97)HEAST (07/97)NAHEAST (07/97)HEAST (07/97)HEAST (07/97)NA

HEAST (07/97)HEAST (07/97)

HEAST (07/97)Contact TSCHEAST (07/97)HEAST (07/97)NANANAHEAST (07/97)NAHEAST (05/95)

NADIFQRAHEAST (07/97)NAHEAST (07/97)HEAST (07/97)NAHEAST (07/97)HEAST (07/97)NAHEAST (07/97)NANAHEAST (07/97)IRIS (8/2000)

HEAST (07/97)

Chronic Oral RfD Effect

Hepatotoxiciry

None Observed

Ocular. Immuno Effect.'

Reduced Birth Weights

Skin and Vascular Effects

Kidney Cylomegal>Liver LesionsForestomach HyperplasiaLiver Lesions

Liver

Fatty Cyst Formation

Reproductive EffectsNone Observed

Gastrointestinal IrritationMyelin Degeneration

Liver LesionsNone Observed

Liver LesionsAlkaline Phosphatase IncreaseDelayed Hypersensitivity

Increased Organ Weightincreased Organ WeighiNeurotoxicity, Clinical Signs (lethargy, prostration, andalaxia), and Hemotological ChangesCataract FormationUverand Kidney ToxicitjKidney, Liver. Blood EffectDecreased Red Blood Cells

Liver ToxicityDecreased Mean Terminal Body WeightDecreased Body Weight, Decreased Organ Weighi

Liver and Kidney Paihologj

Decreased Fetal Body WeighiKidney Effects

Liver EffectsLiver and Kidney Weighi

Clinical Chemistry Alteration;

Liver and Kidney PathologyCellular Necrosis. Liver Cell Polymorphisn

CNS Effects. Decreased Body Weight. Increased Mortality(males)Decreased Superoxide

Chronic Oral RfD Source

IRIS (04/01/94).HEAST (07/97)IRIS (1994)NA[R IS (10/0 1/94)NANAIRIS (04/01/94)IRJS (01/01/93)NAIRIS (1994)(10/07/99)NANANANANAIRIS (1994)IRIS (1994)IRIS (1994)IRIS (1994)NAIRLS0994)NCEAIRIS (1994)NAIRIS (07/01/93IRIS (09/03/98)HEAST (07/97)HEAST (07/97)IRIS (1994)NAJRIS (1994)HEAST (07/97)(10/07/99)IRIS (1994)IRIS (1994)IRIS (1994)NA

IRIS (1994)IRIS (1994)IRIS (11/01/90)

IRIS (07/01/91)IRIS (1994)IRIS (1994)IRIS (1994)NA'(10/07/99)NAIRIS (1994)IRIS (09/1 7/98)IRIS (1994)

NAHEAST (07/97)IRIS (02/01/93)HEAST (07/97)IRIS (02/01/90)IRIS (07/01/93)(10/07/99)IRJS (03/01/88)IRIS (04TO1/94)1(10/07/99)IRIS (1994)RBA (10/07/99)NAIRIS (03/01/88)IRIS (8/2000)IRIS (09/30/87)

IRIS (10/01/92)

Subchronic Inhalation RfC Effect

•

Fetotoxicity

Kidney Damage

Nasal Mucosa Hyperplasia

Nasal EpithelialNasal Mucosa Hypertrophy

Liver Toxicit)

Subchronic Inhalation RfC Source

NA •;HEAST (07/97)NA 'NANANA ;NANANANANAContact TSCNA !NANANA iNANANA 'iContact TSCContact TSCNAContact TSC ''HEAST (07/97)Contact TSCContact TSCNAContact TSCDIFQRA ,NANANANAHEAST (07/97)Contact TSCNANA 'NA 'HEAST (07/97)

IRIS (01/01/91) !HEAST (07/97)

t\

NA 'NAContact TSC ,NANANADIFQRANAHEAST (07/97)NANA

NADIFQRANADIFQRA iNA (NANANAContact TSCContact TSCNANANANAIRIS (8/2000) •:NA '

i

NA

Chronic Inhalation RfC Effect

Olfactory Epilheliurr

Delayed Fetal Ossification

Bronchioalveolar Lavage Fluit

Kidney Damage

Nasal Mucosa Hyperplasia

Nasal Epithelial HypertrophyNasal Epithelial Hypertrophy

Developmental To.iicit)

Liver ToxicityNasal Hyperplasia and Metaplasia

CNS Effects (human)

Chronic Inhalation RfC Source

NAHEAST (07/97)HEAST (08/04/94)NANANANANANANANANAHEAST (08/04/94)NANANANANAIRIS (12/01/93)IRIS (10/01/92)

NA

IRIS (04/01/91)

NAIRIS (09/03/98)HEAST (07/93)NANANANAHEAST (07/97)NANANANAIRIS (12/01/91)

IRIS (1/1/97)IRIS (01/01/91)NA

HEAST (06/13/91)IRIS (03/01/91)HEAST (08/04/94)NANAHEAST (07/93)NAHEAST (07/97)IRIS (09/17/98)NA

NAHEAST (07/93)NAHEAST (07/94)HEAST (02/22/90)HEAST (08/04/94)NA

IRIS (08/01/92)HEAST (03/93)NANAHEAST (04/21/91)HEAST (04/21/91)IRIS (8/2000)NA

NA

HEAST = EPA Health Effects Assessment Summary Tables IRIS = EPA Integrated Risk Information System NA = "Not Available" NCEA = EPA National Center for Environmental Assessment

TABLE 4-1

SELECTION OF EXPOSURE PATHWAYS

Scenario

Timeframe

Current

Future

Current and Future

Current and Future

Medium

Soil

Soil

Soil

Soil

Exposure

Medium

Surface Soil

Surface Soil and SubsurfaceSoil (as potential surface soil)

Surface Soil

All Soil (i.e., surface andsubsurface

[1-10 ft and 10-20 ft])

Exposure

Point

Site Grounds (IPCside or Allied side)


Businesses Adjacentto the Site


Receptor

Population

On-site Worker

On-site Worker

Off-site Worker

On-site ConstructionWorker

Receptor

Age

Adults

Adults

i

1

Adults'

Adults

Exposure

Route

Ingestion

Derma] Contact

Inhalation

Ingestion

Dermal Contact

Inhalation

Ingestion

Dermal Contact

Inhalation

. Ingestion

Dermal Contact

Inhalation

Route

Complete ?

X

X

X

X

X

X

0

0

0

X

X

X

I

, Rationale for Selection or Exclusion

of Exposure Pathway

Pathway considered complete, but incidental exposures areinsignificant because contaminated soils are under pavement,buildings or grassy area. Inhalation of fugitive dust is consideredunlikely, because much of the site is vegetated or paved.

ii

Pathway complete in the future if the site land use changes wherethe surface soils are exposed. Under this scenario workers mayincidentally ingest and contact soil while on-site. Inhalation offugitive dust.is considered a potential scenario if the site hadsubstantial areas of bare soil.

i

'ii

Pathway considered incomplete as soil contamination does notextend to off-site businesses, and significant fugitive dustemissions arc not anticipated to occur.

|

/,

Pathway complete as construction workers may incidentally ingestand contact soil while on-site performing excavation activities. Thepotential for exposure to subsurface soils down to 20 ft belowground surface was considered, because the sewer line that runsthrough the site is as deep as 20 ft. Inhalation of fugitive dust andvapors is corsidered a potential exposure route too, since duringdigging operations fugitive vapors and dusts may be created.



ScenarioTimeframe

Current

Future

Current and Future

Future

Medium

Soil

Soil

Water

Water

ExposureMedium

Surface Soil

Surface Soil and SubsurfaceSoil (as potential surface soil)

Croundwater (most current 2rounds of data)

Groundwater (most current 2rounds of data)

ExposurePoint



None

On-site Well

ReceptorPopulation

Site Visitors/Trespassers


On-site Worker, Visitors,or Trespassers

On-site Residents

ReceptorAge

Children/Adult

Children/ Adult

fi

1\

i

Adults/Children

Child/Adult

ExposureRoute

Ingestion

Dermal Contact

Inhalation

Ingestion

Dermal Contact

Inhalation

Ingestion

Dermal Contact

Inhalation

Ingestion

Dermal Contact

Inhalation

RouteComplete ?

X

X

X

X

X

X

0

0

0

0

0

0

iiRationale for Selection or Exclusion

of Exposure Pathway1

i]

Pathway considered complete, but incidental exposures areinsignificant because contaminated soils are under pavement,buildings or grassy area. Inhalation of fugitive dust is consideredunlikely, because much of the site is vegetated or paved.

i

Pathway complete in the future if the site land use changes wherethe surface soils are exposed. Under this scenario, visitors ortrespassers onjlhe property may incidentally ingest and contactsoil while on-site. Inhalation of fugitive dust is considered apotential exposure route too, if potions of the site have barepatches of soil.

11(I!j\

Pathway incomplete as groundwater at site is not used as a sourceof drinking water. Rather the site area is supplied a municipalwater company in Clinton, Iowa.

1i;

!i

Pathway incomplete as groundwaler at site is not used as a sourceof drinking water. Rather the site area is supplied a municipalwater company in Clinton, Iowa.

1•ii



Scenario

Timeframe

Future

Future

Current and Future

Current and Future

Current and Future

Medium

Soil

Soil

Sediment

Surface Water

Fish

Exposure

Medium

All Soil (i.e., surface andsubsurface)

All Soil (i.e., surface andsubsurface)

Sediment

Surface Water

Fish

Exposure

Point

On-site residence(IPC side or Allied

side)

On-site residence(IPC side or Allied

side)

Mississippi River

Mississippi River

Home CookedMeals

Receptor

Population

On-site Residents

On-site Resident

Recreational User

Recreational User

Recreational User

ReceptorAge

Child/Adult

Child/Adult

IChildren/Adult

!•

1

Children/Adult1

Children/Adult

Exposure

Route

Ingestion

Dermal Contact

Inhalation

Ingestion (i.e., of garden produce)

Ingestion

Dermal Contact

Inhalation

Ingestion

Dermal Contact

Inhalation

Ingestion

Dermal Contact

Inhalation

Route

Complete ?

0

0

0

0

0

0

0

0

0

0

0

0

0

1Rationale for Selection or Exclusioni' of Exposure Pathway

iPathway considered incomplete in the future, since property iscurrently zonelcommercial/industrial and would not be expected tobe used as residential property. A qualitative assessment of thisscenario is retained for informational purposes only.

ii

1Pathway considered incomplete in the future, since property iscurrently zone commercial/industrial and would not be expected tobe used as residential property. A qualitative assessment of thisscenario is retained for informational purposes only.

1

\'i

Pathway considered incomplete as this reach of the MississippiRiver has swift currents and large riprap line the shoreline. Forthese reasonsjit is unlikely recreational users would swim in thisreach

Pathway incomplete as surface water in Mississippi was not foundto be affected near the site.

1

(

Pathway considered incomplete as surface water in Mississippiwas not found to be affected near the site, and sediments areaffected in a very limited area with analytes that would not beexpected to bioconcentrate in fish.

Legend: O = Exposure Pathway Considered IncompleteX = Exposure Pathway Considered Potentially Complete

TABLE 4-2

SUMMARY OF STATISTICAL INFORMATION FOR SURFACE SOIL (0-1 FOOT) COPCs

Depth

0-1 Ft.0-1 Ft.0-1 Ft.

0-1 Ft.0-1 Ft.

0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.

0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.

0-1 Ft.0-1 Ft.

0-1 Ft.

0-1 Ft.

0-1 Ft.0-1 Ft.0-1 Ft.

0-1 Ft.0-1 Ft.0-1 Ft.

_,0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.

0-1 Ft.

0-1 Ft.0-1 Ft.0-1 Ft.0-1 Ft.

Area

Allied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied Steel

Allied Steel


IPC SideIPC SideIPC SideIPC.Side,IPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC Side

IPC Side


Group

VOCsVOCsVOCsVOCsVOCsPCBsPCBsPCBsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsMetalsMetalsMetalsMetals

Metals

MetalsMetalsMetals

VOCsVOCsVOCsVOCs .PCBsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsMetalsMetalsMetalsMetals

Metals

MetalsMetalsMetalsAEOs

Chemical

BenzeneEthylbenzeneMethylene ChlorideTolueneXylenes, TotalArochlor 1242Arochlor 1254Arochlor 1260AcenaphtheneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k)fluorantheneChryseneFluorantheneFluoreneIndeno( 1 ,2,3-cd)py reneNaphthalenePhenanthrenePyreneArsenicChromiumCopperCyanide

Iron

LeadNickelZinc

BenzeneEthylbenzeneTolueneXylenes, TotalArochlor 1260AcenaphtheneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k)fluorantheneChryseneFluorantheneFluoreneIndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanthrenePyreneArsenicChromiumCopperCyanide

Iron

LeadNickelZincPentachlorophenol

Number ofSamples

66666999666666666666661313136

13

131313

999999999999999999999999

9999

Number ofDetections

11421151345665564361641212136

13

131313

111162799997994919889849

6892


16.6716.67

66.6733.3316.67

11.1155.5611.11

50.0066.6783.33100.00100.0083.3383.33100.0066.6750.00100.0016.67100.0066.6792.3192.31100.00100.00

100.00

100.00100.00100.00

11.1111.1111.1111.11 -66.6722.2277.78100.00100.00100.00100.0077.78100.00100.0044.44100.0011.11100.0088.8988.89100.0088.8944.44

100.00

66.6788.89100.0022.22

MiniumumDetected

Cone.

0.1120.0340.0050.0060.0450.35

0.0660.09

0.390.020.130.010.020.030.030.020.080.030.020.050.04

0.143.38.412.19.4

9722

329.149

0.0340.0280.0420.0370.1300.0100.0100.0300.0600.0400.0300.0300.0400.11

0.0200.0300.0100.0300.2002.23.47.22.0

5760

696.614.93.84

MaximumDetected

Cone.

0.1120.0340.0050.0440.0450.350.1900.0996.4

4.214.35.66.84.33.912.82.88.13.3

0.0535.9

4.384.511367915.1

203000

147044.92860

0.0340.0280.042

_ 0.03773.22.601.2015.212.19.47.13.512.639.32.505.702.606.4032.71701478

17.9

46600

55119.41310

26.3

Mean

0.0190.00610.00420.00870.00791.550

44.0911.027

16.2830.7452.7261.6351.7050.9630.7932.3779.0881.4680.9780.0956.1509.29020.44642.592160.5314.417

53540.2

393.622.808834.8

0.0040.0040.005

. 0.0058.4140.6220.2623.5402.6932.2541.8400.9073.03010.3030.3871.2660.2951.6365.68723.0788.73326.5113.200

14988.9

177.511.611

236.3223.606

StandardDeviation

0.0460.014

0.00130.0170.0182.098

72.9391.379

39.2511.6935.7022.4422.7311.6471.5455.11720.0683.2601.3880.19914.57520.00723.24330.104182.2066.330

51909.7

387.910.602907.6

0.0110.0090.0140.01224.2980.9930.4345.7774.3753.2342.4651.2704.84316.0590.810

1.8760.8642.38210.30955.2153.62423.3245.640

12395.1

185.05.092

410.1098.589

95% UCL

NANANANANANANANANANANANANANANANANANANANANANANANANANA

1.09E+05

NANANA

NANANANA-NANANANANANANANANANANANANANANANANANANA

2.53E+04

NANANANA

EPC

0.1120.0340.0050.0440.0450.350.1900.0996.44.214.35.66.84.33.912.82.88.13.30.0535.94.384.511367915.1

108,565°

393.6b

44.92860

0.0340.0280.0420.03773.22.61.2

15.212.19.47.13.512.639.32.55.72.66.4

32.71701478

17.9

25,317°

177.5 b

19.41310

26.3

EPCs for iron are "the 95% UCL concentrations. The 95% UCL was calculated "to provide a more representative concentration" for iron which'was detectedln'a wide range~'ofconcentrations across the site.

EPCs for lead are mean concentrations. See Section 5.1.3

TABLE 4-3

SUMMARY OF STATISTICAL INFORMATION FOR SUBSURFACE SOIL (1-10 FEET) COPCs

Depth

1-10 Ft.1-10 Ft.1-10 Ft1-IOFt1-10 FL1-lOFi.1-10 Ft.1-10 Ft.1-10 Ft.1-10 FL1-10 FL1-10 Ft.1-IOFt.1-10 Ft.1-10 FL1-10 Ft.1-10 Fi.1-10 Ft.1-IOFt.1-10 Ft.1-10 Ft.I-10Ft.1-10 FL1-10 Ft.1-10 Fi.I - I O F L1- lOFl .1- IOFt .1-10 Ft.1-10 Ft.I - I O F L1-10 FLI - I O F L1-10 Ft.1-10 Ft.\-10FLI-IOFL1-10 Ft.1-10 Ft.1-10 FL1-10 Ft.1-10 Ft.1-10 Ft.I - lOFt .1-10 Ft.1-10 Ft.I - I O F L1-10 FL1-IOFt .1-10 Fi.1-IOFt.1-IOFt.1-10 Ft.1-IOFl .1- IOFt .1-10 Ft.1-10 Ft.1- IOFl .1-10 Ft.1-10 Ft.

Area

Allied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied Steel

IPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC Side -IPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC Side

Group

VOCsVOCsVOCsVOCsVOCsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsMetalsMetalsMetalsMetalsMetalsMetalsMetalsMetalsAEOsAEOsVOCsVOCsVOCsVOCsVOCsVOCsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHs

--PAHsPAHsPAHsPAHsMetalsMetalsMetalsMetalsMetalsMetalsMetalsMetals

Chemical

BenzeneEthylbenzeneMelhylene ChlorideTolueneXylenes, TotalAcenaphthyleneAcenaphtheneAnthraceneBenzo(a)anlhraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g.h,i)peryleneBenzo(k)fluorantheneChryseneFluorantheneFluoreneIndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanthrenePyreneArsenicChromiumCopperCyanideIronLeadNickelZinc2-Nitrophenol4-NitrophenolBenzeneChloromethaneEthylbenzeneMethylene ChlorideTolueneXylenes, TolalAcenaphthyleneAcenaphtheneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g.h,i)peryleneBenzo(k)f1uorantheneChryseneDibenzo(a,h)anthraceneFluorantheneFluoreneIndeno(l.2l3-cd)pyrene~NaphthalenePhenanihrenePyreneArsenicChromiumCopperCyanideIronLeadNickelZinc

Units

mg/kgmg/kgmg/kgmg/kgmg/kgmg/lcgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kg"nig/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kg

Number ofSamples

151515151515151515151515151515151515151515151515151515151515191919191919191919191919191919181919

-|9 •19IS191919191918191919

Number ofDetections

4524535599964

8874787101515101515151510921028108101112131286132913S^1^131381219191118191919


26.6733.3313.3326.6733.3320.0033.3333.3360.0060.0060.0040.0026.6753.3353.3346.6726.6746.6753.3346.6766.67100.00100.0066.67100.00100.00100.00100.006.670.00

47.3710.5352.6310.5342.1152.6342.1152.6357.8963.1668.4263.1642.1131.5868.4211.1147.3768.42

-^ T7T1T68.4272.2242.1163.16100.00100.0057.89100.00100.00100.00100.00

MinimumSQL

0.0070.0070.0140.0070.0070.010.330.010.330.330.330.010.010.010.010.330.010.330.330.330.95

00

0.150000

1.671.67

0.0010.0010.0010.0050.0010.0010.010.330,010.330.330.330.010.010.010.010.010.33

~O.OI~0.330.330.330.95

00

0.150000

Maximum SQL

0.70.11.20.70.110.010.04.31.81.81.8

10.04.31.81.84.34.34.34.3

100.020010000

85.085.01.0

45.01.0

56.01.01.0

10.010.04.31.81.81.810.04.31.8

20.01.84.34.34.34.3

100.00.95

0010000


0.8560.1180.0370.1650.2625.330.611.91.70.20.2

0.030.40.060.020.051.93

0.9950.070.014.57.29.8

0.1799370

98.7

28.567.920.5

0.1860.1170.1180.0370.1650.262

1.61.60.21.70.20.2

0.030.4

0.062.4

0.020.051.93

0.9951.2

0.012.067.29.8

0.1799370

98.7

28.5

MaximumDetected

Concentration

97.12402516930910501340303248168128

85.653.6532184354969.629301370

. 141559.283177175

8310059762

178067.920.553

1.42122

0.101230560

191007560235425081141.520821229412.751.96166229

19200757130.78.8

21.451

45.93080034035.5374

Mean

5.44182.989128.21750.4463.162

125.465152.50038.241333.40814.989

1073.723440.63220.4420.7830.7830.7830.7830.7830.7835.6900.7830.7832.8480.7830.7832.0640.7831.5040.7830.7836.963

31040.000363.91338.24122.7441.773

1035.271417.240128.21783.1978.800

344.774155.831137.9280.3950.3950.3950.3950.395 "0.3950.39511.8550.3950.3950.8970.3950.3950.5010.3950.450

StandardDeviation

10.67078.888539.047184.7136.289

330.480371.40083.480

1412.49152.009

4391.3831780.03456.5962.5392.5392.5392.5392.5392.53915.0672.5392.53910.2742.5392.5397.7582.5395.1242.5392.53911.004

18673.618473.52783.48045.9952.629

4375.1551730.000539.047186.73018.217

861.664359.946366.5750.8610.8610.8610.8610.8610.8610.86130.7360.8610.8611.7180.8610.8610.8700.8610.860

95%UCL

10115.121041305134.2182132996.4124997612422.0675271.7811355.1831156.393381.6566281.022169.133776.07422993.18326497.451528.799111.900812136.599554.7699490.053130.538724.515198.90951351.344246596.79346.980939.398261712.16572.1167570.964154.8564328.7652628.7652628.7652628.7652628.76526322776734775.511623.2941568.861561.47

245.5813387.4439688.621930.550842.73227490.27094310.281373.7533136230512625.35387.59088.32948328.7652628.7652628.7652628.7652628.7652628.7652628.76526

EPC

97.1240251693091050134030324816812885.653.6532184354969.629301370141559.283177175

8310059762

178067.920.553

1.42122

0.101230560

191007560235425081141.520821229412.751.96166'22919200757130.78.8

21.451

45.93080034035.5374

TABLE 4-4

SUMMARY OF STATISTICAL INFORMATION FOR SUBSURFACE SOIL (10-20 FEET) COPCs

Depth

1 0-20 Ft.10-20 Fl.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10- 20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Fl.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20FI.10-20 Ft.10-20 Ft.10- 20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Fl.10-20 Ft.10-20FI.10-20 Fl.10-20 Ft.10-20 Fl.10-20 Ft.10-20 Fl.10-20 Ft.10-20 Ft.10-20 Ft.10- 20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20 Ft.10-20FI.10-20 Ft.10-20 Ft.10-20 Ft.

Area

Allied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelAllied SteelIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC Side- ~IPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC SideIPC Side

Group

VOCsVOCsVOCsVOCsVOCsVOCsPAHsPAHsPAHsPAHsPAHsPAHsPAHaPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsMetalsMetalsMetalsMetalsMetalsMetalsMetalsMetalsAEOsAEOsAEOsVOCsVOCsVOCsVOCsVOCsVOCsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHs-PAHsPAHsPAHsPAHsPAHsPAHsMetalsMetalsMetalsMetalsMetalsMetalsMetalsMetals

Chemical

BenzeneEthylbenzeneMethylene ChlorideTetrachloroetheneTolueneXylenes, TotalAcenaphtheneAcenaphthyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenza(k)fluorantheneChryseneDibenzo(a,h)anthraceneFluoramheneFluoreneIndeno( 1 ,2,3-cd)pyreneNaphthalenePhenamhrcnePyreneArsenicChromiumCopperCyanideIronLeadNickelZinc2,4-Dimethylphenol4-NitrophenolPhenolBenzeneChlorome thaneEthylbenzeneMethylene ChlorideTolueneXylenes, TotalAcenaphtheneAcenaphthyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k)fluorantheneChrysene -FluorantheneFluoreneIndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanthrenePyreneArsenicChromiumCopperCyanideIronLeadNickelZinc

Units

mg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kg

Number ofSamples

3737373737373737373737373737373737373737373737373737373737373737372020202020202020202020202020

- 202020202020202020202020202020

Number ofDetections

1322318

233223313031322329302153328293581936321137303237111821266121711131312

- 1612

,' • 11- -~ia-^=

5151214153121920520162020

MinimumDetected Cone.

0.0080.0030.0220.0220.28

0.0020.070.590.010.010.020.030.080.020.015.9

0.030.020.030.050.030.042.23.24.6

126805.278

941.6625.10.02

0.2710.0050.0120.3590.0190.070.1

0.020.010.0 10.010.050.02

- -' 0.01-—0.060.020.010.030.026.92.14.54.4

13150

65.810.5

MaximumDetected Cone.

94.949.52.93

0.02281.1102

269026901240122682259042825711348.9

87502520331

483050007292661

22050

51300199050

109094

1.6625.111.33.4416.4

0.12111.153.512121173120

87.974.558.637.820

90:4- -

98225135.8316053971.812.2484117

284009642258


40.559.58.12.7

21.662.286.562.283.881.183.886.562.278.481.15.4

40.589.275.778.494.621.651.497.386.529.7100.081.186.5100.02.72.72.7

40.010.060.030.030.060.085.055.065.065.060.080.060.055.060.0 •25.075.060.070.075.015.060.095.0100.025.0100.080.0100.0100.0

Mean

4.0016.2531.7750.3404.06811.034198.54153.0977.32959.91243.98529.96219.55714.36958.9923.441

357.30140.5116.553341.79303.2754.1153.18912.90019.1162.69114509116.1513.838102.205.0656.1973.2021.0740.2041.9540.1761.6346.202100.12114.148.6856.9216.0424.4563.2351.694

• 7.140 = -57.69227.5932.735

244.1537.43611.1253.05015.08515.5951.6951530413.64016.11532.000

StandardDeviation

15.66511.4783.1290.62613.85421.371473.61449.32208.34201.07134.94696.86670.14942.569185.668.525

1457.76418.4754.293844.39831.07134.324.4029.70236.2628.23710437

400.439.792192.4715.3438.5894.8262.6440.7643.8510.2783.52512.939284.43295.4426.90619.84816.79113.1058.6784.540

- 20.314219.0075.0828.016

736.67120.40426.6952.82810.8638.5433.7627153

20.7299.19953.038

MaximumDetected

Concentration

94.949.5

2.93E+002.20E-028.11E+011.02E+022.69E+032.69E+031.24E+031.23E+038.22E+025.90E+024.28E+022.57E+021.13E+038.90E+008.75E+032.52E+033.31E+024.83E+035.00E+037.29E+022.60E+016.10E+012.20E+02

505.13E+04I.99E+035.00E+01

109094

1.66E+0025.1

1.13E+013.44

I.64E+011.21E-01

11. 153.5

1.21E+031.17E+031.20E+028.79E+017.45E+015.86E+013.78E+012.00E+01

- 9.04E+019.82E+022.51E+023.58E+013.16E+035.39E+027.18E+011.22E+014.80E+014.10E+011.70E+01

284009642

2.58E+02

95% UCL

312812128721.6310.00547

8319587967375735

2598591046729010091643937430468705092

12688658.8

1469894585482

3513970596972305408182519

3.9916.227.82.61

18613124.118.513815.6

0.57711.924807.896

2589300.11140941

15455808206230

42783073102931116213526745750

194.9- 16470

45247856003427

12445126996453152474.6222.919.72.15

1990720.720.672

EPC

9.49E+014.95E+012.93E+005.47E-038.11E+011.02E+022.69E+032.69E+031.24E+031.23E+038.22E+025.90E+024.28E+022.57E+021.13E+038.90E+008.75E+032.52E+033.31E+024.83E+035.00E+037.29E+023.99E+001.62E+012.78E+012.61E+001.86E+041.24E+021.85E+011.38E+021.56E+015.77E-OI1.19E+01U3E+013.44E+001.64E+011.11E-011.11E+015.35E+011.21E+031.17E+031.20E+028.79E+017.45E+015.86E+013.78E+012.00E+019.04E+01 -9.82E+022.51E+023.58E+013.16E+03539E+027.18E+OI4.62E+002.29E+01I.97E+012.15E+00I.99E+042.07E+012.06E+017.16E+OI

Page 1

TABLE 4-5

SUMMARY OF STATISTICAL INFORMATION FOR SEDIMENT COPCs


VOCsMeihylene ChlorideToluene

AEOs. PAHs. and SVOCsAcenaphlheneAnthraceneBenzo(a)anlhraceneBenzo(a)pyreneBenzo(b)fl uorantheneBenzo(g,h,i)peryleneBenzo(k)fluorantheneChryseneDibenzo(a,h)anthraceneRuorantheneIndeno( 1 ,2.3-cd)pyreneNaphthalenePhenanthrenePyrene

MetalsArsenicChromiumCopperIronLeadNickelZinc

Units

mg/kgmg/kg

mg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kg


Number ofSamples

99

99999999999999

9999999

Number ofDetections

22

2233412314

1122

3849469


22.222.2

22.222.233.333.344.411. 122.233.311. 144.4I I . 111. 122.222.2

33.388.944.4100.044.466.7100.0

MiniumumDetected

Concentration

0.0090.035

0.30.030.020.030.070.4

0.020.010.020.040.40.6

0.020.03

2.43.38.8

35308.85.28.1

MaximumDetected

Concentration

0.0090.067

4.40.40.91.30.20.40.40.9

0.020.70.40.60.10.5

2.419.319.4

2710022

15.6

82

Mean Concentration(•>

3.20E-03I.I7E-03

4.19E-025.00E-035.00E-03I.29E-024.83E-025.00E-035.00E-035.83E-036.88E-033.79E-025.00E-037.1IE-027.50E-03I.38E-02

1 .78E+008.29E+007.13E+00I.09E+047.96E+00I.76E+023.27E+OI

StandardDeviation

2.I7E-032.37E-03

1.04E-01O.OOE+00O.OOE+002.08E-027.87E-026.22E-11O.OOE+002.04E-035.30E-037.27E-026.22E-II1.98E-016.I2E-031.71E-02

1.35E+005.92E+007.44E+008.89E+037.30E+005.10E+022.93E+01

95% UCL< h )

NCNC

NCNCNCNCNCNCNCNCNCNCNCNCNCNC

NCNCNCNCNCNCNC

EPC(C|

0.0090.067

4.40.40.91.3

10.40.40.9

0.020.70.40.61.50.5

4.919.319.4

2710022

15.682

Notes:

a. Mean concentration calculated using detected concentrations and one-half SQL as "proxy" concentration for nondetects.

TABLE 4-6

SUMMARY OF STATISTICAL INFORMATION FOR GROUNDWATER COPCs

Group

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

VOCs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

PAHs

Metals

Metals

Metals

Metals

Metals

Metals

Metals

Inorganics

AEOs

AEOs

Chemical

Benzene

Bromomethane

Carbon tecrachloride

Chloromethane

1.2-Dichloroethane

Ethylbenzene

Toluene

Xylenes, Total

Acenaphthene

Acenaphthylene

Anthracene

Benzo(a)anthracene

Benzo(a)pyrene

Benzo(b)fluoranlhene

Benzo(g,h.i)perylene

Benzo(k)nuoranthene

Chrysene

Dibenzo(a,h)anlhracene

Fluoranthene

Fluorene


Naphthalene

Phenanthrene

Pyrene

Arsenic

Chromium

Copper

Iron

Lead

Nickel

Zinc

Cyanide

2,4-Dimethylphenol

Phenol

Units

Mg/L

Mg/L

Mg/L

Mg/L

Mg/L

"g/L

Mg/L

Mg/L

Mg/L

Mg/L

Mg/L

Mg/L

Mg/LM&/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/LMg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/L

Mg/LMg/L

SampleCount

72727272727272727272727272727272727272727272727272727272727272727272

DetectionFrequency, %

45.831.391.391.391.39

40.2836.1147.2265.2843.0656.9437.5034.7229.1725.0026.3933.331.39

26.3955.5622.2268.0662.5037.5091.6761.1166.67100.0088.8973.6183.3390.28100.0052.78

MinimumDetection

1.142.27.51.29

0.51

2.90.51.40.10.10.20.10.10.10.2

0.080.51.3

0.070.50.50.3

0.010.0380.0360.1480.0060.0610.0320.00784.927

MaximumDetection

1230042.27.5149

249055953235647

2930462197

135.6110.416650.9129.40.0849476031

87901490769

0.1361.11

0.5183602.36

0.7853.311.723670697

Mean *

1554.15.3391.1754.0171.967405.1601.7824.8218.0582.224.9858.8566.3105.1407.2202.4805.9300.06113.950113.31.783

1628.694.3534.4490.03270.1240.130103.660.1020.1530.3370.265132.1437.29

StandardDeviation

3416.49.7353.16010.5603.188791.71370.21212.3297.5987.379.60634.39926.70022.40029.01910.20025.200.18266.58221.05.7782756.7265.99132.700.03010.1910.143123.410.3410.1560.5210.536548.47115.50

95% UCL »•

1.19E+043.12E4004.90E-013.35E+009.26E-015.82E-f047.36E+041.47E+051.88E+042.28E+056.47E+016.82E-017.27E-044.51E-013.12E-011.31E-019.72E-014.90E-038.20E+007.41E+033.01E-011.76E-f069.76E+022.32E+014.12E-031.98E-022.14E-022.18E+034.54E-034.33E-028.64E-028.44E-021.73E+026.92E+01

EPC

1.19E+043.12E+004.90E-013.35E+009.26E-012.49E+035.60E+033.24E+036.47E-M322.93E+036.47E+016.82E-017.27E-014.51E-013.12E-011.31E-019.72E-014.90E-038.20E+007.60E+023.01E-OI8.79E+039.76E+022.32E+014.12E+001.98E+012.14E+013.60E+024.54E-034.33E-028.64E-028.44E-021.73E+026.92E+01

* Based on all monitoring wells.** Determined by EPA Region vn methodology.

TABLE 4-7

EXPOSURE FACTORS USED FOR THE CALCULATION OF EXPOSURE ESTIMATES - REASONABLE MAXIMUM EXPOSURE SCENARIOS

Parameter

General Parameters (g)Exposure FrequencyBody WeightExposure DurationAveraging Time, Non-Carcinogenic EffectsAveraging Time, Carcinogenic Effects

Soil Ingestion Parameters (s)Soil Ingestion RateSoil Fraction IngestedUnits Conversion Factor

Soil Dermal Exposure Parameters (d)Skin Surface Area

Soil Adherence Factor

Dermal AbsorbanceUnits Conversion Factor

Inhalation Parameters (i)Inhalation Rate

Exposure Time

Units

days/year

kgyearsdaysdays

mg/dayunitlesskg/mg

cm2

mg/cm2-day

unitlesskg/mg

m3/day orm3/hr

hrs/day

On-SiteWorker

1907025

912525550

501

0.000001

3300

0.2

Chem..Spec.0.000001

1.5m3/hr

8

(gl)(g4)(g6)(g9)

(glO)

(si)(s4)

(dl)

(d2)

(d3)

OD

04)

IndustrialWorker

1907025

912525550

501

0.000001

3300

0.2

Chem. Spec.0.000001

1 .5 m3/hr

8

(gl)(g4)(g6)(g9)

(glO)

(si)(s4)

(dl)

(d2)

(d3)

(il)

(i4)

Site Visitor/Trespasser

1084310

365025550

501

0.000001

5700

0.2

Chem. Spec.0.000001

l.OnvVhr

2

(g2)(g5)(g7)(g9)

(glO)

(s2)(s4)

(dl)

(d2)

(d3)

(12)

(15)

ChildRecreational

Visitor

48156

219025550

2001

l.OOE-06

2900

0.2

Chem. Spec.0.000001

l.OmVhr

2

(g3)(g5)

(g2a)(g9)

(glO)

(s2)(s4)

(dl)

(d2)

(d3)

(12)

(15)

ConstructionWorker

190701

36525550

4801

0.000001

3300

0.2

Chem. Spec.0.000001

2.5 m3/hr

8

(g3)(g4)(g8)(g9)

(glO)

(s3)(s4)

(dl)

(d2)

(d3)

(13)

(16)Paniculate Emission Factor

Volatilization Factor

m3/kg

m3/kg

1.32E+09 (17) 1.32E+09 (17) 1.32E+09 (17) 1.32E+09 (17) l.OOE+06 (18)

Chem. Spec. (19) Chem. Spec. (19) Chem. Spec. (19) Chem. Spec. (19) Chem. Spec. (19)


EXPOSURE FACTORS USED FOR THE CALCULATION OF EXPOSURE ESTIMATES - REASONABLE MAXIMUM EXPOSURE SCENARIOS*

Parameter

General Parameters (g)Exposure FrequencyBody WeightExposure DurationAveraging Time, Non-Carcinogenic EffectsAveraging Time, Carcinogenic Effects

Drinking Water Ingestion Parameters (s)Water Ingestion RateWater Fraction IngestedUnits Conversion Factor

Water Dermal Exposure Parameters (d)Skin Surface AreaExposure timeUnits Conversion FactorPermeability constant

Inhalation Parameters (0Inhalation RateVolatilization Factor

Units

days/year

kgyearsdaysdays

L/dayunitlesskg/mg

cm2hr/dayL/cm3cm/hr

m3/day or m3/hrunitless

ChildResident

350156

210025550

11

l.OOE-06

29000.25

0.000001Chemical-specific

10 m3/d0.0005 x 1000 L/m3

(gla)(g5)(g3)(g9)(glO)

(wl)(s4)

(dl)(d4)(d5)(d6)

(12)09)

AdultResident

3507030

1095025550

21

0.000001

33000.25

0.000001Chemical-specific

20 m3/d0.0005 x 1000 IVm3

(gla)(g4)(g8)(g9)

(glO)

(wl)(s4)

(dl)(d4)(d5)(d6)

(13)09)

: Hypothetical benchmark scenarios



Footnotes:

General (g)

gl. Best professional judgement based on site-specific climate data from Iowa state (2000) and NOAA (2001) climatology resources. Assumes 250 days per year minus60 days for snow cover.

gla. Recommended value provided in EPA guidance (i.e., "Standard Default Exposure Factors," U.S. EPA, 1991). Assumes a resident spends 350 days per year at home.

g2. Best professional judgement based on site-specific climate data from Iowa state (2000) and NOAA (2001) climatology resources. Assumes 3 days per week for the9 warmer months of the year.

g3. Best professional judgement based on site-specific climate data from Iowa state (2000) and NOAA (2001) climatology resources. Assumes 2 days per week for6 months (i.e., April 15 to October 15).

g4. Within the Exposure Factors Handbook (U.S. EPA, 1997) a 71.8 kg body weight is recommended; however, since many of the toxicity values were developed usingthe assumption of a 70 kg body weight, the 70 kg body weight was used by convention.

g5. Average body weight of younger children and adolescent children ages 7 to 16 years old derived from data presented in USEPA 1997 (Table 7-3).

g6. This value is the average of the life long tenure at an occupation recommended for men (30.1) and women (18.8) over the age of 70 (see Section 15.4.2Recommendations: Occupational Mobility in the Exposure Factors Handbook (U.S. EPA, 1997)).

g7. Assumes conservatively that a site visitor or trespasser visits the site over a ten year period (e.g., from years 7 to 16).

g8. It was assumed, based on professional judgment, that a construction worker may be working on a particular construction project at this site for one year.

g9. By convention the noncarcinogenic averaging time is equal to the exposure duration in units of days.

glO. By convention the averaging time for carcinogenic effects is set at a 70 year lifetime in units of days.

Soil Ingestion (s)

si. The soil ingestion rate is the recommended average value for adults presented in Table 4-23 of the Exposure Factors Handbook (U.S. EPA, 1997).

s2. The soil ingestion rate is the recommended conservative mean value for children presented in Table 4-23 of the Exposure Factors Handbook (U.S.EPA, 1997).

s3. The soil ingestion rate is considered a conjectural value (not a recommended value) in the 1997 Exposure Factors Handbook for outdoor activities. The value wasbased on research by Hawley (1985) for outdoor activities, but did not have supporting documentation. It is used as an RME estimate for construction workeractivities.

s4. Fraction ingested value is the recommended value provided by U.S. EPA risk assessment guidance (see U.S. EPA, "Supplemental Guidance for Developing SoilScreening Levels for Superfund Sites," Peer Review Draft, Office of Solid Waste and Emergency Response, Washington, D.C. March 2001. OSWER 9355.4-24).



Footnotes:

Soil and Water Dermal (d)

dl. The skin surface area estimates are defaults for adult residents, child residents, and workers provided by U.S. EPA in a early release of the final dermal riskassessment guidance (see U.S. EPA, "Supplemental Guidance for Developing Soil Screening Levels for Superfund Sites," Peer Review Draft, Office of Solid Wasteand Emergency Response, Washington, D.C. March 2001. OSWER 9355.4-24).The surface area estimate for adults was used as an estimate for an adolescent's skinsurface area for the trespasser/site visitor scenario.

d2. The soil adherence values (AFs) are defaults provided by U.S. EPA (see U.S. EPA, March 2001).

d3. Chemical-specific. Values represent defaults provided by U.S. EPA where available.

d4. Showering 15 minutes per day. Draft Dermal Exposure Assessment. EPA, 1992.

d5. Necessary to convert to appropriate units (m/lOOcm x 1000 L/m3).

d6. Chemical specific. Values represent defaults provided by U.S. EPA where available. Draft Dermal Exposure Assessment. EPA, 1992.

Soil Inhalation (i)

11. Assume workers perform moderate activities the majority of the time. The inhalation rate is the recommended value for adults for moderate activities.(U.S. EPA,1997; Table 5-23).

12. Assume children perform light activities the majority of the time on the site. The inhalation rate is the recommended value for children for light activities (U.S. EPA,1997; Table 5-23).

13. Represents the recommended mean inhalation rate for outdoor workers performing heavy activities (see Table 5-23 within U.S. EPA, 1997).

14. Assumed by convention that workers would work on site eight hours per day.

15. Assumed that a site visitor or trespasser would frequent the site approximately 2 hours per day.

16. An eight hour work day is assumed by convention for construction workers.

17. The paniculate emission factor (PEF) corresponds to the default value recommended by U.S. EPA in the Soil Screening Guidance Technical Document (U.S. EPA,1996).

18. Represents a PEF which equates to a dust concentration of 1 mg/m3, which is an estimate of the minimum level at which dust is visible in air. The value represents areasonably high average dust concentration in air for construction-related activities based on professional judgement.

19. The volatilization factors (VFs) are chemical specific; refer to exposure tables in Appendices D for these values. The VFs were derived using procedures in theU.S. EPA Soil Screening Guidance Technical Document (U.S. EPA, 1996). The specific parameters used to calculate each chemical specific VF can be found inTable D-l.

Legend:

NA = Not applicable

TABLE 5-1

SUMMARY OF HEALTH RISK ESTIMATES UNDER CURRENT AND FUTURE LAND USE CONDITIONS - REASONABLE MAXIMUM EXPOSURE

Table Index

Current/Future Site

Exposed Population:

Table F-l (C)Table F-2 (NC)

Table F-3 (C)Table F-4 (NC)



Table F-9 (C)Table F-IO(NC)

Table F- 11 (C)Table F-l 2 (NC)

Table F-l 3 (C)Table F-l 4 (NC)




Receptor

Conditions'

On-Site Construction Workers

On-Site Conslruction Workers-IPC

On-Site Construction Workers-IPC

On-Site Construction Workers-IPC

On-Site Construction Workers-Allied



On-Sile Workers-IPC

On-Site Workers-IPC

Site Visitor/Trespasser-lPC

Site Visitor/Trespasser-Allied

iHazard Index by Route Cancer Risks By Route

Medium Exposure Point Ingestion Dermal Inhalation Total Ingestion Dermal Inhalation Total

Soil Surface Soil I.5E+OJ 2.6E+00 7.4E-02 2.E+01 2.6E-05 3.0E-06 7.0E-06 4.E-05

fSoil Subsurface Soil (1-10 ft.) 4.6E+00 ', 7.9E-01 4.9E+00 l.E+01 3.3E-04 5.8E-05 7.9E-06 4.E-04

i

Soil Subsurface Soil (10-20 ft.) 9.3E-01 , 1.5E-01 9.6E-01 2.E+00 3.5E-05 ' 6.2E-06 2.8E-06 4.E-05

1

Soil Surface Soil 2.7E+00 ' 1.1E+00 5.9E-01 4.E+00 9.5E-06 f 8.2E-07 I.3E-05 2.E-05i

Soil Subsurface Soil (1-10 ft.) 3.0E+00 i 4.3E-01 3.5E+00 7.E+00 8.4E-05 ^ 1.4E-05 1.1E-05 l.E-04

1Soil Subsurface Soil (10-20 ft.) 2.5E+00 \ 7.1E-01 3.3E+00 7.E+00 3.9E-04 ' 7.0E-05 8.5E-06 5.E-04

\

Soil Surface Soil 1.6E+00 2.7E+00 5.6E-04 4.E+00 6.8E-05 j 7.6E-05 8.0E-08 l.E-04i

Soil Subsurface Soil (1-10 ft.) 5.3E-01 8.7E-OI 8.5E-OI 2.E+00 8.5E-04 1.5E-03 2.9E-07 2.E-03

1

Soil Surface Soil I.5E+00 3.9E+00 7.9E-05 5.E+00 2.5E-05 4.5E-05 4.6E-09 7.E-05

Soil Surface Soil 2.6E-OI ; 4.2E-01 2.8E-04 7.E-01 9.2E-06 ) 1.2E-05 8.2E-09 2.E-05i

i i,1

i l1 I


SUMMARY OF HEALTH RISK ESTIMATES UNDER CURRENT AND FUTURE LAND USE CONDITIONS - REASONABLE MAXIMUM EXPOSURE

Table Index

Potential Future Site

Exposed Population:

TableF-19(C)Table F-20 (NC)





Hypothetical Future

Exposed Population:

Hazard Index by Route

Receptor Medium Exposure Point Ingestion Dermal Inhalation Total

Conditions


Site Visitor/Trespasser-IPCa Soil Subsurface Soil (1-10 ft.) 4.5E-01 I.3E+00 I.2E-01 2.E+00

Industrial Workers-Allied" Soil Surface Soil 2.8E-OI 2.8E-01 2.0E-03 6.E-01

Industrial Workers-Allied" Soil Subsurface Soil (1-10 ft.) 3.1E-01 3.9E-01 1.5E+00 2.E+00

Site Visitor/Trespasser-Allied3 Soil Subsurface Soil (1-10 ft.) 2.7E-01 5.7E-01 2.2E-OI l.E+00

Child Recreational Visitor-Allied11 Soil Surface Soil 9.9E-01 3.2E-02 2.8E-05 l.E+00

i

Groundwater Exposure Scenarios

Hypothetical Residents

Table F-31 (C) On-Site Adult Resident Groundwater Upper Aquifer Zones 1.6E+02 l.OE+OI 7.9E+00 2.E+02Table F-32 (NC)

Table F-33 (C) On-Site Child Resident Groundwater Upper Aquifer Zones 3.7E+02 2.0E+01 3.7E+01 4.E+02Table F-34 (NC)

Cancer Risks By Route

Ingestion Dermal Inhalation Total

2.9E-04 8.7E-04 1.6E-08 l.E-03

2.5E-05 2.0E-05 1.4E-07 5.E-05

2.2E-04 3.6E-04 5.4E-07 6.E-04

I1

7.5E-05 ! 2.1E-04 3.1E-08 3.E-04

4.1E-06 7.6E-07 5.2E-12 5.E-06

ii

7.1E-03 ' 2.1E-04 3.0E-05 7.E-03

4.IE-03 ! 2.8E-04 1.8E-03 6.E-03

Footnotes:I

This table summarizes the health risks by exposed population and medium. Refer to the risk tables indexed to review the chemical-specific risk estimates.

Current/Future Site Conditions represent exposure scenarios that are current and expected to remain similar in the foreseeable future.

Potential Future Site Conditions represent possible future exposures due to: 'a impacted soils brought to the surface through development or otherwise become accessible and remain accessible for many years,

possible land reuse for industrial or municipal park settings. ji

(C) - Carcinogenic(NC) - Noncarcinogenic /

BLE 6-1

COMPARISON OF SEDIMENT SAMPLE CONCENTRATIONS IN THE MISSISSIPPI RIVER TO BENCHMARK VALUES

Type

vocvoc

svocsvocsvocsvocsvocsvocsvocsvocsvocsvocsvocsvocsvocsvoc

MTLMTLMTLMTLMTLMTLMTL

COPECs

Methylene chlorideToluene

AcenaphtheneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k)fluoramheneChryseneDibenz(a,h)anthraceneFluorantheneIndeno(l ,2,3-cd)pyreneNaphthalenePhenanthrenePyrene

ArsenicChromiumCopperIronLeadNickelZinc

Unite

Mg/kg

Mg/kg

Mg/kgug/kgMg/kgug/kgMg/kgMg/kgMg/kgMg/kgMg/kgMg/kgMg/kgMg/kgMg/kgMg/kg


No. SamplesDetected

12

22335124241142

3g49469

No.Sampled

99

99999999999999

9999999

MinimumDetected

Concentration

935

3030203030400201010404006002030

2.43.38.8

35308.85.28.1

MaximumDetected

Concentration

967

440040090013001000400400900207004006001500500

4.919.319.4

2710022

15.682

ToxicityBenchmarkSediment

NI6.7E+02

NI620260430NI17024034028.2290480

32.75560660

8.28134

200004721150

ToxicityBenchmark

Source

MlEPA SQB

EPA SQCARCS/TECEPA ERL

NIO MOE/LowO MOE/LowO MOE/LowARCS/PECEPA SQCEPA SQB

ARCSfTECO MOE/Low

EPA ERL

EPA ERLEPA ERLEPA ERL

O MOE/LowEPA ERLEPA ERLEPA ERL

HQSediment

NIl.OE-01

NI6.5E-013.5E+003.0E+00

NI2.4E+001.7E+002.6E+007.1E-012.4E+008.3E-011.8E+012.7E+007.6E-01

6.0E-012.4E-015.7E-011.4E+004.7E-017.4E-015.5E-01

Number ofSamples Exceeding

Benchmark

_

0

—011-111010110

0001000

Location(s) ofSamples Exceeding

Benchmark

MR-06MR-06

MR-06MR-06MR-06

MR-06

MR-06MR-06

MR-06

Hazard Index = 4.4E+01

Notes:

1. The list of analytes presented in this table represents those (hat were detected above their respective detection limit within sediment samples collected at theClinton FMGP Site.

2. Toxicity benchmark concentrations for plant toxicity were obtained from Table 4 of Toxicological Benchmarks for Screening Contaminants of Potential Concernfor Effects on Sediment-Associated Biota: 1997 Revision. (ORNL 1997; ES/ER/TM-95/R4).

3. The hazard index (HI) represents the sum of individual hazard quotients.

NI = No toxicity benchmark value available for the analyte.HQ = Hazard quotient, which in the case of the screening level ecological assessment represents the maximum analyte concentration divided by the appropriatetoxicity benchmark (i.e., soil invertebrate or plant). Hazard quotients over a value of one have been bolded.ARCS/TEC = Assessment and Remediation of Contaminated Sediments Program/Threshold Effect ConcentrationARCS/PEC = ARCS/Probable Effect ConcentrationEPA ERL = Effects range - low (Long et al., 1995)EPA SQB = Sediment quality criteria (EPA, 1996)EPA SQC = Sediment quality criteria (EPA, 1996)0 MOE/Low = Ontario Ministrv of the Environment/lowest effect level and is the 5th nercentile of the screenine level concentration.

SITE BOUNDARY-

ASPHALT PARKING

WAREHOUSE-GARAGE-

CONC.-

BAND SHELL-

ASPHALT-

RIVERVIEW PARK

-RETAINING WALL-PUMP STATION

,BY-PASSPUMP

\STATION- -KIDDYPOOL

GRASS

POOL

[BATHliHOUSE 1

SS-16Q

o

-OFFICE

-CONC. PAD

-SCALE

\•

•VOLLEYBALL .COURT /

\ MINIATURE i\GOLF I

FORMER ALLIED STEEL BUILDINGiSS-12

iSS-13

\\\

^SS-10SS-11

/SS-;

GRAVEL

ss-

* 1STORAGE-

ss-iSS-2

MONTGOMERY WATSON

©SS-7

CONC.

/ h

SJ

CONC.

AEDC

:Z]A~

J.LIANTNERGY(STRICT)FFICE

QSS-1

GRASS

SS-8 J

GRAVEL

SUBSTATION

GRASS 1

I

-SITE BOUNDARY

• GARAGE

-CONC.CONTAINMENT

DOQO O

!_> J^-CONTROL HOUSE

i

CQNC.

\RAGE

(ft

A/. 2nd STREET

O 120

SCALE IN FEET

LEGEND:

O SURFACE SOILSAMPLING LOCATION

ALLIANT ENERGY/INTERSTATE POWER COMPANY

CLINTON FMGP SITE - CLINTON, IOWA

ON-SITESURFACE SOIL SAMPLE

LOCATIONSFIGURE 2-1

ISUBJTATKJN H-d=JY.-UIC] I

MONTGOMERY WATSONAPPROXIMATELY 1000 FEETWEST OF N. 2nd STREET

LEGEND:

SURFACE SOILSAMPLE LOCATION



OFF-SITESURFACE SOIL SAMPLE

LOCATIONSFIGURE 2-2

MONTGOMERY WATSON

O 150

SCALE IN FEET

• WATER TABLE MONITORING WELL

© INTERMEDIATE MONITORING WELL

® BEDROCK SURFACE MONITORING WELL

+ PIEZOMETER

« SOIL BORING

® SITE SCREENING INSPECTION SOIL BORING(APPROXIMATE LOCATION)



SUBSURFACE SAMPLINGLOCATIONS

FIGURE 2-3

O 150

SCALE IN FEET

O 0 Pz-2LEGENDj

WATER TABLE MONITORING WELL

INTERMEDIATE MONITORING WELL

® BEDROCK SURFACE MONITORING WELL

4- PIEZOMETER

(S)MW-23• MW-22©MW-40

oo Ooowuccrrc

y •MW-S


CLINTON FMGP SITE - CLINTON, IOWA\ —nMONITORING WELLAND PIEZOMETER

LOCATIONSMONTGOMERYFIGURE 2-4

MR-02+ (ZEBRA MUSSELS-- NO SAMPLE RECOVERED)

APPROXIMATE EXTENT OF RIPRAP

CURRENT RIVER BANK

FORMER RIVER BANK (1951)

(ZEBRA MUSSELS-NO SAMPLE RECOVERED) I

X

LIGHTHOUSE-*(ZEBRA MUSSELSNO SAMPLE RECOVERED)

CITY SEWEROUTFALL

FORMERCITY SEWER

FORMER IPCSTORNA SEWERS

RETAINING WALL

PUMP STATIONBAND SHELL

ASPHALTBY-PASPUMPSTATIONRIVERVIEW PARK

GRASSDIVING .POOL /


CLINTON FMGP SITE - CLINTON, IOWA-f APPROXIMATE MISSISSIPPI RIVER

SAMPLING LOCATION MISSISSIPPI RIVERSAMPLING LOCATIONSMONTGOMERY WATSON

APPENDIX A

TOXICITY PROFILES

ARSENIC

(CAS RN 7440-38-2)

Arsenic is a naturally occurring element in the earth's crust usually found combined with one or more otherelements, especially copper or lead. When combined with oxygen, chlorine, or sulfur it is referred to as inorganicarsenic, and when combined with carbon and hydrogen it is referred'to as organic arsenic. Both forms are releasedto the environment by human activities such as fossil fuel consumption, pesticide use and copper smelting, and vianatural processes such as volcanic emissions, weathering of arsenic-containing minerals and ores, and forest fires(ATSDR, 1998).

Absorption/Distribution/Metabolism/Excretion

Water soluble inorganic arsenic compounds are substantially absorbed (more tha"n 90 percent) from the GI tract ofhumans and laboratory animals. Estimates of absorption following oral exposure of humans to water soluble,inorganic arsenic compounds range from 54 to 95 percent (Bettley and O'Shea, 1975 cited in ATSDR, 1998). Lesswater soluble forms are absorbed to a smaller degree. For example, only 30 to 40 percent of an oral dose of arsenictrioxide, is absorbed by laboratory animals (Marafante and Vahter, 1987 cited in ATSDR, 1998). Water soluble,inorganic arsenic compounds are also rapidly and substantially absorbed via inhalation in both animals and humans.Studies have indicated that 75 to 85 percent of deposited arsenic is absorbed from the lungs within 4 days (Hollandet al., 1959 cited in ATSDR, 1998). Less soluble arsenic compounds (e.g., lead arsenate, gallium arsenide) are lesscompletely absorbed (about 55 percent of an administered dose absorbed in 3 days) (Marafante and Vahter, 1987cited in ATSDR, 1998). Once absorbed, arsenic is rapidly cleared from the blood in humans and animals (except inrats where it is bound to red blood cells) and distributed to the liver, kidney, lung, spleen, aorta, skin, hair and upperGI tract (Rhodes and Sanders, 1985; Liebscher and Smith, 1968 cited in ATSDR, 1998). These tissues are thencleared rapidly except for skin and hair, where arsenic tends to accumulate. Most absorbed arsenic is metabolized inthe liver to methylated products and excreted in the urine (ATSDR, 1998).

Acute Toxicity

Oral doses of about 50 to 300 mg inorganic arsenic may be fatal to adults, and subchronic oral exposure to about 3mg/day can be fatal to infants exposed via contaminated milk. On the basis of these observations, the minimumacute and subacute oral lethal dose in humans is estimated to be about 1 to 3 mg/kg/day (ATSDR, 1998). Inhalationor dermal exposure has not been associated with acute lethality in humans. Animals are less sensitive to the toxiceffects of arsenic. Reported lethal doses in animals (10 to 300 mg/kg) are significantly higher than lethal dosesreported in humans (0.6 to 2 mg/kg).

Target Organ Toxicitv

The EPA has published a chronic oral RfD of 3.0E-04 mg/kg-day for arsenic (IRIS, 1999). This value is based onobservations of keratosis, hyperpigmentation, and possible vascular complications in humans exposed to arsenic intheir drinking water.

Developmental Toxicitv

There is only suggestive evidence that exposure to arsenic results in developmental toxicity in humans (ATSDR,1998). Studies in animals, however, do support the view that arsenic is a developmental toxicant, causing reducedbirth weight, a variety of fetal malformations (both skeletal and soft tissue), and increased fetal mortality (ATSDR,1998). However, the doses required to cause effects were high and often resulted in significant maternal toxicity oreven lethality.

Genoloxicity

The results of tests for genotoxicity of arsenic are mixed, but in general the inorganic arsenicals appear to be eitherinactive or weak mutagens (Jacobson-Kram and Montalbano, 1985 cited in ATSDR, 1998).

BENZENE(CAS RN 71-43-2)

Benzene is a colorless nonpolar liquid which is slightly soluble in water. As summarized in USAF (1989), benzenewas a widely used solvent in the past, and prior to WW II the major use for benzene was as an octane-raisingadditive in gasoline. As its adverse health effects have become known, usage has declined to the point where it isnow minimal. Currently, most benzene is consumed in the chemical industry where it is used as a starting materialfor the synthesis of other organic compounds. Benzene is now an important contaminant of gasoline, making up to2.0 percent.

Absorption/DistributionyMetabolism/Excretion

Benzene is absorbed via both the respiratory and GI tracts. It is also absorbed dermally. For example, recent studiessuggest that approximately 17 percent of a total dose of benzene in ambient air may be absorbed dermally (Blank,I.H. and D.J. McAuIiffe, 1985 cited in USAF, 1989). Retention of inhaled benzene varies around 30 to 50 percent ofthe inspired dose, but has been reported at 79.8 to 84.8 percent by the human system when inhaled at concentrationsof 10 to 16 mg/L (Von Oettingen, 1940 cited in Sandmeyer, 1981). A considerable amount of what is absorbed iseliminated in the expired air, and most of the rest is metabolized and excreted in the urine.

Absorption of orally administered benzene in the range between 340 to 500 mg/kg has been studied in rats. Forty-three percent of the administered dose is eliminated in expired air, 34.5 percent is eliminated as various conjugatedand unconjugated metabolites in the urine, and the remaining 5 to 10 percent is retained in the body in adipose tissueand bone marrow (Parke and Williams, 1973 cited in NRC, 1980).

Metabolism of benzene is now recognized as an important determinant in the toxic effects attributed to benzeneexposure. It is metabolized in the liver by the mixed function oxidases to a highly reactive intermediate arene oxide,benzene oxide, which can spontaneously rearrange to phenol, undergo enzymatic hydration followed bydehydrogenation to catechol, react enzymatically to form a glutathione conjugate, or bind covalently with cellularmacromolecules. Benzene oxide, catechol, and another benzene metabolite, hydroquinone, are considered to belikely candidates responsible for the toxicity of benzene. Covalent binding of benzene metabolites to DNA offers apotential mechanism for inhibition of cell replication or for the initiation of leukemia.

Acute Toxicity

Short exposures to relatively high levels of benzene cause CNS depression, narcosis, and death in various species ofanimals. LC5Q values range from 10,000 to 40,000 ppm and LD50 values range from 3,800 to 4,700 mg/kg inlaboratory rodents (USAF, 1989).

In humans, benzene is a CNS depressant at high concentrations and may cause acute narcotic reactions. Dependingupon the concentration and duration of exposure, these effects may range from mild manifestations such as headacheand lightheadedness to more severe effects such as convulsions, respiratory paralysis, and death (Finkel, A.J., ed.,1983 cited in USAF, 1989). Concentrations of 50 to 250 ppm may cause headache; concentrations of 3,000 to 7,500ppm may result in toxic signs within one hour; and concentrations around 20,000 ppm have resulted in death(Clayton, G.D. and F.E. Clayton, eds., 1981 cited in USAF, 1989). Ingestion of 2 mL of benzene may produce toxicsymptoms, while ingestion of 10 mL may cause death in humans (Thienes, C.H. and T.J. Haley, 1972 cited in USAF,1989).

Subtle CNS effects induced in animals by short term exposure to benzene include impaired learning ability in ratsgiven 550 mg/kg for three days (Geist, C.R. et al., 1983 cited in USAF, 1989) and behavioral disturbance in miceexposed to 100 to 300 ppm for one or five days (Dempster, A.M. et al., 1984 cited in USAF, 1989). Other effectsreported after short term exposures to benzene include: depressions in peripheral blood lymphocytes and erythrocytesin mice exposed to 20 and 100 ppm benzene 6 hrs/day for 6 days (Rozen, M.G. et al., 1984 cited in USAF, 1989);

Reproductive Toxicity

Evidence of an effect of benzene exposure on human reproduction is not sufficient to demonstrate a causalassociation (ATSDR, 1992).

Genotoxicitv

Benzene is not mutagenic in bacterial systems (USAF, 1989). However, benzene and/or its metabolites seem to begenotoxic causing primarily chromosomal aberrations. Chromosomal abnormalities in bone marrow cells resultingfrom subcutaneous or intraperitoneal administration of benzene have been reported in various species of animalsincluding rats, rabbits, and mice (EPA, 1980 cited in USAF, 1989). Most of the induced abnormalities werechromatid breaks or deletions. Rats exposed to benzene vapor at concentrations of 100 to 1,000 ppm for 6 hoursshowed a significant increase in chromosomal abnormalities in their bone marrow cells (Styles J.A. and C.R.Richardson, 1984 cited in USAF, 1989). Sister chromatid exchanges have been observed in bone marrow cells ofmice exposed to benzene via inhalation (Tice et al., 1982 cited in USAF, 1989). Benzene has also proved to be aneffective inducer of micronuclei in the mouse in both bone marrow-derived and peripheral erythrocytes (Choy et al.,1985; Mohtashamipur E. et al., 1987 cited in USAF, 1989).

Chromosomal aberrations have also been reported in the lymphocytes of humans occupationally exposed to lowconcentrations (0.2 to 12.4 ppm) of benzene and in the workers of a rotogravure plant (Sarto et al., 1984; Forni, A. etal., 1971 cited in USAF, 1989).

Carcinogenicity

There is sufficient evidence that benzene is carcinogenic in animals and man. EPA has classified benzene as an A-human carcinogen on the basis of several studies of nonlymphocytic leukemia from occupational exposure andincreased incidence of neoplasia in rats and mice exposed by inhalation and gavage (IRIS, 2000). The NTP hascategorized these data as providing clear evidence of carcinogenic activity.

Aksoy et al. (1974 cited in IRIS, 2000) reported 26 cases of leukemia and a total of 34 leukemias or preleukemiasamong 28,500 Turkish workers employed in the shoe industry where peak benzene exposures ranged up to 650 ppmand mean exposure duration was 9.7 years. This corresponds to an incidence of 13/100,000 (by comparison to6/100,000 for the general population). A follow-up paper (Askoy, 1980 cited in IRIS, 2000) reported eight additionalcases of leukemia as well as evidence suggestive of increases in other malignancies.

Infante et al. (1977a, b cited in IRIS, 2000) examined leukemogenic effects of benzene exposure in 748 white malesexposed while employed in the manufacturing of rubber products. A statistically significant increase of leukemiaswas found by comparison to the general U.S. population. In a subsequent study of this same population, Rinsky et al.(1981 cited in IRIS, 2000) observed seven deaths from leukemia among 748 workers exposed to benzene. Thisincreased incidence was statistically significant. Exposures to these individuals were estimated to have ranged from10 to 100 ppm for at least 24 years. Elevated leukemia deaths among this population has been confirmed in a recentstudy (Rinsky et al., 1987 cited in IRIS, 2000).

Wong et al. (1983 cited in IRIS, 2000) reported on the mortality of male chemical workers who were exposed tobenzene for at least 6 months during the years 1946 to 1975. The study population of 4,062 persons was drawn fromseven chemical plants, and jobs were categorized as to peak exposure. Those with at least 3 days/week exposure(3,036 subjects) were further categorized on the basis of an 8-hour time-weighted average (TWA). The controlsubjects held jobs at the same plants for at least 6 months but were never subject to benzene exposure. Dose-dependent increases were seen in leukemia and lymphatic and hematopoietic cancer. The incidence of leukemia wasresponsible for the majority of the increase. It was noted that the significance of the increase is due largely to a lessthan expected incidence of neoplasia in the unexposed subjects.

BROMOMETHANE

(CASRN 74-83-9)

Bromomethane, also known as methyl bromide, is a colorless liquid or gas (boiling point 4.6° C.). Bromomethaneis soluble in water (900 mg/L at 20° C.). The principal use of bromomethane is as a soil or space fumigant.

The oral Reference Dose (RfD) is based on the assumption that thresholds exist for certain toxic effects such ascellular necrosis. It is expressed in units of mg/kg-day. In general, the RfD is an estimate (with uncertainty spanningperhaps an order of magnitude) of a daily exposure to the human population (including sensitive subgroups) that islikely to be without an appreciable risk of deleterious effects during a lifetime. The oral chronic RfD for methylbromide is 1.4 E-3 mg/kg/day; the critical effect is epithelial hyperplasia of the forestomach. The literature alsoreports that chronic exposures to methyl bromide at concentrations above the RfD can cause central nervous systemdepression or kidney injury.

The inhalation Reference Concentration (RfC) is analogous to the oral RfD and is likewise based on the assumptionthat thresholds exist for certain toxic effects such as cellular necrosis. The inhalation RfC considers toxic effects forboth the respiratory system (portal-of-entry) and for effects peripheral to the respiratory system (extrarespiratoryeffects). It is expressed in units of mg/cu.m. In general, the RfC is an estimate (with uncertainty spanning perhaps anorder of magnitude) of a daily inhalation exposure of the human population (including sensitive subgroups) that islikely to be without an appreciable risk of deleterious effects during a lifetime. The RfC is 5 E-3 mg/m3; the criticaleffect is degenerative and proliferative lesions of the olfactory epithelium of the nasal cavity. The RfC is basedprincipally on chronic (29-month) inhalation toxicity and carcinogenicity studies of methyl bromide in Wistar rats(Reuzeletal, 1987 and 1991).

The Environmental Protection Agency (EPA) has determined that bromomelhane is not classifiable as to its humancarcinogenicity. There are no studies available to indicate that bromomethane is carcinogenic to people. Animalstudies do not provide conclusive evidence. Therefore, the EPA weight o-of-evidence classification for thiscompound is D; not classifiable as to human carcinogenicity and inadequate human and animal data.

CHLOROMETHANE(CAS RN 74-87-3)

Chloromethane, or methyl chloride, is a volatile, clear liquid used in the manufacture of silicones, production of butylrubber, and as a fuel additive.


Like many of the halogenated methanes and ethanes, chloromethane is toxic to the hepatic and renal system. At highdoses, it induces headache, dizziness, drowsiness, nausea, vomiting, diarrhea, blurred vision, cyanosis, and comaleading to death. Occupational exposure of levels in the range of from 200 to 400 ppm results in blurred vision,slurred speech, staggering gait, and irritability. The symptom disappear rapidly following cessation of exposure.

Prolonged low-level exposure to chloromethane to rodents results in fatty liver development and chronic renaldysfunction. Exposure to levels of 100 ppm continuously or 400 ppm intermittently results in degeneration andatrophy of the cerebellum. Higher levels of exposure results in muscle impairment, splenic atrophy, and renal andhematopoietic effects.

Reproductive Toxicitv

Administration of up to 1500 ppm chloromethane to male rats results in testicular degeneration and loss of spermviability. Administration of chloromethane to pregnant mice results in congenital heart malformations in offspring.

Carcinogenicity

Administration of chloromelhane in two-year, chronic rodent bioassays results in the development of hepatocellulartumors in the B6C3F1 mouse (NTP, 1987). In addition, renal tumors developed in the same study. Chloromethaneis considered a C category carcinogen with a slope factor of 1.3 E-02 mg/kg/day via ingeslion and 6.3E-03 viainhalation (HEAST, 1997).

REFERENCES

Health Effects Assessment Summary Tables (HEAST). 1997. U.S. Environmental Protection Agency (EPA), FourthQuarter FY-1990. PB90-921104.

National Toxicology Program (NTP), 1986. Toxicology and carcinogenesis studies of dichloromethane (methylenechloride) in F344/N rats and B6C3F1 mice (inhalation studies). Research Triangle Park, North Carolina,NTP-82-061.

COPPER(CAS RN 7440-50-8)

Copper is a reddish metal that occurs naturally in rock, soil, water, sediment, and air. Its average concentration in theearthfs crust is about 50 parts per million. It is insoluble in hot and cold water but soluble in nitric acid or hotsulfuric acid (Weast, 1983, as cited in HSDB, 2000). Copper also occurs naturally in plants and animals. It is anessential element for all known living organisms including humans and other animals (ATSDR, 1990). Copper canbe easily molded or shaped. Its reddish color is most commonly seen in the United States penny, electrical wiring,and some water pipes (ATSDR, 1990). Copper is used as a metal for electrical and electronic products (e.g., wire),building construction (e.g., plumbing pipes), industrial machinery, and equipment. In the transportation industry it isused in automobiles (HSDB, 2000). Copper has a boiling point of 2595°C, and a melting point of 1083°C (TheMerck Index, 1983, as cited in HSDB, 2000).


Copper oxide was observed in alveolar capillaries three hours after rats were exposed to a welding dust aerosolgenerated from pure copper wires (Batsura, 1969, as cited in ATSDR, 1990). Copper is absorbed in the stomach andsmall intestine. The site of maximal copper absorption is not known for humans, but it is assumed to be the stomachand upper intestine because of the rapid appearance of MCu in the plasma after oral administration (Beam andKunkel, 1955, as cited in ATSDR, 1990).

Copper is absorbed from the GI tract as ionic copper, or is bound to amino acids (Crampton et al., 1965 as cited inATSDR, 1990). Numerous factors may affect copper absorption. These factors include: (1) competition with othermetals, including zinc and cadmium (Davies and Campbell, 1977, as cited in ATSDR, 1990); (2) the amount ofcopper in the stomach (Fairer and Mistilis, 1967, as cited in ATSDR, 1990); (3) certain dietary components; and (4)form of copper. The absorption of copper appears to be inversely related to the amount of copper in the GI tract(Strickland et al., 1972, as cited in ATSDR, 1990).

Absorbed copper loosely binds to plasma albumin and amino acids in the portal blood, and is taken to the liver(Marceau et al., 1970, as cited in ATSDR, 1990). In the liver, copper is incorporated into ceruloplasmin and releasedinto the plasma. Radioactive copper does not accumulate in extrahepatic organs unt i l after the emergence ofceruloplasmin-MCu, suggesting that ceruloplasmin is a copper donor for the tissues (Owen, 1965, as cited in ATSDR,1990).

The metabolism of copper consists mainly of its transfer to and from various organic ligands, most notablysulfhydryls and imidazole groups on amino acids and proteins. Several specific binding proteins for copper havebeen identified that are important in the uptake, storage, and release of copper from tissues. In the liver and othertissues, copper is stored bound to metallothionein and amino acids and in association with copper-dependentenzymes. Several studies have shown that copper exposure induces metallothionein synthesis (Mercer et al., 1981,as cited in ATSDR, 1990).

Bile is the major pathway for the excretion of copper. After the oral administration of radioactive copper as copperacetate in healthy humans, 72% was excreted in the feces (Bush et al., 1955, as cited in ATSDR, 1990). Normally,0.5 - 3.0 percent of daily copper intake is excreted into the urine (Cartwrighl and Wintrobe, 1964, as cited inATSDR, 1990). Biliary excretion of copper does not increase proportionally with dosage, suggesting that thehepatobiliary transport of copper is salurable (Gregus and Klaassen, 1986, as cited in ATSDR, 1990). Thus, at highcopper intakes, urinary copper excretion increases (Gitlan et al., 1960, as cited in ATSDR, 1990).

Acute Toxicity

The only significant example of copper toxicity in humans is Wilsonfs disease (Hepatolenticular degeneration), anautosomal recessive disorder that affects normal copper homeostasis. The disease is characterized by excessive

rat hepatocytes; however strand breaks did occur at high concentrations (0.04 mM Cu as copper sulfate) (Sina et al.,1983, as cited in ATSDR, 1990). Although there are no data on the mutagenicity of copper in humans, in vivostudies and mammalian syslem in vitro studies suggest that copper is a potential human mutagen.

Carcinogenicitv

An elevated incidence of cancer has not been observed in humans or animals exposed to copper via inhalation, oral,or dermal routes of exposure. The US EPA classifies copper as a Class D carcinogen (not classified) based on thefact that there are no human data, inadequate animal data from assays of copper compounds, and equivocalmutagenicity data (IRIS, 2000).

REFERENCES

Agency for Toxicological Substances and Disease Registry (ATSDR). Draft Toxicological Profile for Copper,February 16, 1990.

Health Effects Assessment Summary Tables (HEAST). 1997. U.S. Environmental Protection Agency (EPA).

Integrated Risk Information System (IRIS). 2000. Copper. U.S. Environmental Protection Agency (EPA), updatedannually.

U.S. Environmental Protection Agency (US EPA). Hazardous Substances Database (HSDB). 2000.

CHROMIUM(CAS RN [Cr3] 16065-83-1; [Cr6] 18540-29-9)

Chromium III, or +3, is a naturally occurring element found in soil, volcanic dust, and gases. It is considered to bean essential nutrient involved in the maintenance of normal glucose metabolism, cholesterol, and fat in humans. Aminimum human daily ingestion of 50 to 100 |ig/day (0.0007 to 0.003 mg/kg/day) has been estimated to be safe andadequate. The only toxic effect associated with chromium III reported to occur in humans is sensitization (anallergic reaction) following occupational dermal exposure.

Most known toxic effects of chromium have been attributed to chromium VI, or +6, which is not naturally occurring.It is produced and released to the environment primarily as a result of industrial processes involving the use ofchromium containing pigments, in metal finishing and in wood treatment. Chromium 0, or metallic chromium, isless prevalent in the environment than either III or VI and is not well characterized in terms of levels of exposure orpotential health effects.

Chromium has been known to enter the environment as a result of chromium hide processing. In this process, largeamounts of chromium oxide (Cr O ) and chromium sulfate (Cr2(S04))3 are used, discharged into the wastewater, andsubsequently enter any existing surface impoundments.


Absorption of chromium from the GI tract is relatively low and depends on its valence state. Less than 1 and 11percent of oral doses of chromium III and VI, respectively, are absorbed by humans. GI absorption in animalsappears to be slightly higher. Values of up to 3 percent for chromium III and up to 25 percent for chromium VI havebeen reported. Occupational studies demonstrating chromium in urine, serum, and blood cells indicate that bothchromium III and VI are absorbed through the lungs in humans, although the percentage absorbed is unknown.Animal studies indicate that 5 to 30 percent of administered chromium III is absorbed through the lungs, while 53 to85 percent of administered chromium VI is. Chromium VI and III are only minimally absorbed through eitheranimal or human skin.

Following absorption, chromium is distributed primarily to lungs and kidneys with additional distribution to the liver,bladder, spleen, bone and heart. Chromium III is excreted in the urine. Chromium VI appears to be readily reducedto Chromium III in the liver and lung and then excreted in the urine. There is no indication that significant oxidationof chromium III to chromium VI occurs in vivo.

Acute Toxicity

Chromium VI is irritating, and short-term high level exposure can result in adverse effects at the site of contact suchas: ulcers of the skin following dermal contact, irritation of the nasal mucosa and perforation of the nasal septumfollowing inhalation of 0.01 to 0.024 mg/m3 chromium VI; and, irritation of the GI tract following ingestion. Acuteoral exposure to about 2 g chromate (chromium VI) has been reported to result in tubular necrosis (cell death) of thekidney, diffuse necrosis in the liver and subsequent death. Acute oral exposure to 5 g or more of chromatecompounds results in GI bleeding, and massive fluid loss prior to death as a result of cardiovascular shock.

Acute dermal exposure to high levels of chromium VI through the application of antiscabies ointment has also beenreported to result in renal tubular necrosis with subsequent uremia (presence of urinary constituents in blood resultingfrom decreased urination). At lower concentrations, chromium VI compounds are sensitizers and commonly causeallergic dermatitis in printers, cement workers, metal factory workers, painters and leather tanners.

The most commonly observed adverse effects associated with intermediate or chronic exposure to chromium VI inhumans occur via inhalation. Ulcerated or perforated nasal mucosa occurs in workers exposed to chromium VI atconcentrations ranging from 0.06 to 0.72 mg/m . Slight, transient decreases in lung function have also been

The EPA considers that confidence in this RfD is low because the critical study used only 21 exposed rats andexamined only a small number of parameters. Moreover, no dose demonstrating certain toxicity was observed in thisstudy or in any other studies. It is possible that other toxic effects could have occurred but remained unobserved; or,that even higher doses could have been administered without resulting in adverse effects. Other studies reviewed bythe EPA indicating a dose-response relationship are also of low quality. Finally, possible teratogenic or reproductiveeffects of oral exposure to chromium VI have not been evaluated.

The highest No Observed Adverse Effect Level (NOAEL) following oral exposure to chromium III is 1,468mg/kg/day. Groups of 60 male and female rats exposed to this dose for 2 years exhibited no effects on survival, bodyweight, blood, and urine clinical chemistry values, or on gross and microscopic appearance of organs and tissues(Ivankovic and Preussmann, 1975). This dose is the basis for the chronic oral RfD for chromium III as calculated byEPA (IRIS, 2000). When this value is adjusted to account for the possibilities that: 1) humans may be more sensitivethan rats to the toxic effects of chromium; 2) some members of'the human population may be especially susceptibleto the toxic effects of chromium; and, 3) the critical study failed to identify adverse effects that were actually present,it becomes I.5E+00 mg/kg/day, which is the oral RfD for chromium III. The UF of 100 associated with this value isbased on a factor of 10 each for interhuman and interspecies variability.

The EPA considers that confidence in this RfD is low because explicit detail on study protocol and results in thecritical study were not provided; and, because no dose demonstrating toxicity was observed in this or in any otherstudies. The true NOAEL could therefore be considerably higher than that observed in the critical study.

Developmental and Reproductive Toxicitv

Increased fetal death and an increase in external abnormalities were observed in hamsters treated by intravenousinjection with CrO3 (chromium VI) on a single day of gestation. Fetal weight depression and an increase in externalabnormalities has been reported in mice treated intraperitoneally with 15 24 mg/kg CrO3 chromium III on gestationday8.

Adverse reproductive effects have been reported in mice given a single intraperitoneal injection of 20 mg/kgpotassium dichromate (chromium VI) or 21 injections of 2 mg/kg potassium dichromate. Testicular effects havebeen reported in rabbits injected intraperitoneally with 2 mg/kg/day chromium III nitrate or potassium dichromale VIfor 3 to 6 weeks.

Genotoxicity

Chromosomal aberrations have been demonstrated in blood lymphocytes of some workers exposed to chromium VIbut not in others. Tests of chromium VI for gene mutation, chromosome aberrations, and cell transformation in invitro nonhuman assays have been consistently positive. Results are consistently negative for chromium III except atvery high concentrations or in cells with phagocytic activity. Chromium VI is therefore considered to be a moreactive genotoxin than chromium III.

Carcinogenicitv

Epidemiologic studies of chromate production facilities in the United States (Machle and Gregorius, 1948; Brinton etal., 1952; Mancuso and Hueper, 1951; Mancuso, 1975; Baetjer, 1950; Taylor, 1966; Enterline, 1974; Hayes et a!.,1979; Hill and Ferguson, 1979), Great Britain (Bidstrup, 1951; Bidstrup and Case, 1956; Alderson et al., 1981),Japan (Watanabe and Fukuchi, 1975; Ohsaki et al., 1978; Sano and Mitohara, 1978; Satoh et al., 1981), and WestGermany (Korallus et al., 1982; Bittersohl, 1971) have established an association between chromium exposure andlung cancer. Studies of workers in the chrome pigment industry have also found an association between occupationalchromium exposure (predominantly chromium VI) and lung cancer (Langard and Norseth, 1975; Davies 1978, 1979;Frentzel-Beyme, 1983).

MacKenzie R.D.; R.U. Byerrum; C.F. Decker; C.A. Hoppert; and F.L. Langham. 1958. Chronic toxicity studies. II.Hexavalent and trivalent chromium administered in drinking water to rats. AMA. Arch. Ind. Health. 18:232-234.

Mancuso T.F. 1975. Consideration of chromium as an industrial carcinogen. In: Hulchinson T.C., ed. Proceedingsof the International Conference on Heavy Metals in the Environment. Toronto: Toronto Institute forEnvironmental Studies, pp. 343-356.

Mancuso T.F.; and W.C. Heuper. 1951. Occupational cancer and other health hazards in a chromate plant. Amedical appraisal. I. Lung cancers in chromate workers. Ind. Med. Surg. 20: 358-363.

Nettesheim P.; M.G. Hanna Jr; D.G. Doherty; R.F. Newell; and A. Hellman. 1971. Effect of calcium chromate dust,influenza virus, and 100 R whole-body X-radiation on lung tumor incidence in mice. J. Nat. Cancer Inst.47: 1129-1144.

Ohsaki Y.; S. Abe; K. Kimura; Y. Tsunita; H. Mikami; and M. Murao. 1978. Lung cancer in Japanese chromateworkers. Thorax. 33: 372-364.

Taylor F.H. 1966. The relationship and duration of employment as reflected by a cohort of chromate workers. Am.J. Public Health. 56: 218-229.

Integrated Risk Information System (IRIS). 2000. Chromium VI; Chromium III. U.S. Environmental ProtectionAgency (EPA), updated annually.

CYANIDE, free

(CASRN 57-12-5)

Cyanide is usually found joined with other chemicals to form compounds. Examples of simple cyanide compoundsare hydrogen cyanide, sodium cyanide and potassium cyanide. Cyanide can be produced by certain bacteria, fungi,and algae, and it is found in a number of foods and plants. In the body, cyanide combines with a chemical to formVitamin Bi2. The term "free cyanide" refers to the cyanide anion.

Chronic exposure to cyanide in humans via inhalation results in effects on the CNS, such as headaches, numbness,tremor, and loss of visual acuity. Other effects in humans include cardiovascular and respiratory effects, an enlargedthyroid gland, and irritation to the eyes and skin.

The oral Reference Dose (RfD) is based on the assumption that thresholds exist for certain toxic effects such ascellular necrosis. It is expressed in units of mg/kg-day. In general, the RfD is an estimate (with uncertaintyspanning perhaps an order of magnitude) of a daily exposure to the human population (including sensitivesubgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. The EPA RfD forchronic oral exposures to free cyanide is 2 E-2 mg/kg/day based on weight loss, thyroid effects, and myelindegeneration in rats (IRIS, 2000). A chronic inhalation RfC is not available at this time.

The Environmental Protection Agency (EPA) has determined that free cyanide is not classifiable as to its humancarcinogenicity. There are no studies available to indicate that free cyanide is carcinogenic to people. Animalstudies do not provide conclusive evidence. Therefore, the EPA weight-of-evidence classification for thiscompound is D; not classifiable as to human carcinogenicity and inadequate human and animal data.

1,2-DICHLOROETHANE(CAS RN 107-06-2)

1,2-Dichloroethane is a clear, man-made liquid. 1,2-Dichloroethane is used mostly to make vinyl chloride andseveral solvents that remove grease, glue, and dirt. In the past it was also found in trace amounts in solvents thatindustry used to clean cloth, remove grease from metal, and to break down oils, fats, waxes, resins, and rubber.1,2-Dichloroethane is also added to lead gasoline to remove lead.

Small amounts of 1,2-Dichloroethane released into water or onto soil first evaporate into the air. 1,2-Dichloroethanedoes not stay in the air for very long because it is readily broken down by the sun. 1,2-Dichloroethane remaining onsoil from a spill or improper disposal can travel through the ground into water; the chemicaJ may remain in water orsoil for more than 40 days.

The primary route of human exposure to 1,2-dichloroethane is expected to be inhalation of vapors in ambient air,either in the workplace or in areas surrounding hazardous waste sites. Both human and animal data indicated that1,2-dichloroethane is readily absorbed through the lungs.


Based on its high vapor pressure and high serum/air partition coefficient, 1,2-dichloroethane is readily absorbedthrough the lungs following inhalation exposure in both humans and experimental animals (Erickson et al., 1980).Because of its high lipid-water partition coefficient, 1,2-dichloroethane is rapidly absorbed through the lungs byhumans and is accumulated in breast milk of nursing women.

From case studies that described toxic effects subsequent to the accidental or intentional ingestion of 1,2-dichloroethane by humans, it can be inferred that 1,2-dichloroelhane is rapidly absorbed into the systemic circulationfollowing exposure by the oral route (Hueper and Smith, 1935; Lochhead and Close, 1951; Yodaiken and Babcock,1973). Studies in experimental animals indicate that the oral absorption of 1,2-dichloroelhane is rapid, complete, andessentially linear (Reitz et al., 1980, 1982; Spreafico et al., 1980). 1,2-Dichloroethane is absorbed by passivetransport across the GI tract.

Percutaneous absorption via contact with contaminated water or the chemical itself may be a significant route ofexposure to 1,2-dichloroethane in humans (Urusova, 1953). However, results from animal studies indicated thatdermal absorption of 1,2-dichloroelhane is low in comparison to absorption for other compounds (Tsurata, 1975;Jakobsen, 1982).

No studies were located regarding distribution in humans following inhalation, oral, or dermal exposure to 1,2-dichloroelhane. However, detection of 1,2-dichloroethane in breast milk and in the breath of workers one hour afterleaving the workplace (0.063 ppm 1,2-dichloroethane in air) suggests 1,2-dichloroethane is rapidly distributedfollowing inhalation (Urusova, 1953).

Studies in rats found that 1,2-dichloroethane was found in blood, liver, lung, and fat (Spreafico et al., 1980). Thehighest concentrations were found in fat. In pregnant rats following inhalation exposures, 1,2-dichloroethane wasfound in placenta! tissue, amniotic fluid, and fetal tissue (Vozovaya, 1977) following inhalation exposures. Oraladministration reveals similar results as those seen in inhalation studies (Spreafico et al., 1980). Hence there is littledifference between oral and inhalation exposure with regard to tissue distribution in animals, and specific targetorgan toxicity cannot be explained by differential distribution of 1,2-dichloroethane.

No studies were located regarding metabolism in humans following inhalation, oral, or dermal exposure to 1,2-dichloroethane. The biotransformation of 1,2-dichloroethane has been studied extensively in rats and mice both invivo and in vitro. The results of the in vivo studies indicate that 1) 1,2-dichloroethane was readily metabolized in thebody, 2) the primary route of biotransformation involved conjugation with glutathione to yield non-volatile urinary

transaminase (SGPT) and ammonia, were observed in the case study of the exposed individual reported by Nouchi etal.(1984).

An induction of liver enzyme levels was reported in animals (rats, guinea pigs, and monkeys) (Brondeau et a!.,1983). However, it is not clear whether this induction was associated with liver damage.

Renal Effects. Acute renal damage resulting from ingestion of 1,2-dichloroethane has been observed in humans. Inone case study, renal damage that resulted from acute oral poisoning of a 25-year-old man was not considered severeor permanent and the patient fully recovered (Przezdziak and Bakula, 1975). The amount of 1,2-dichloroethaneingested was not reported. Severe kidney damage, documented as diffuse renal necrosis, was reported in individualsthat died following ingestion of 15 to 30 mL 1,2-dichloroethane (Hueper and Smith, 1935; Lochhead and Close,1951; Yodaiken and Babcock, 1973).

No adverse renal effects were noted in mice following acute oral administration of up to 49 mg 1,2-dichloroethane/kg/day by gavage for 90 days or at doses of up to 189 mg 1,2-dichIoroethane/kg/day in drinking waterfor 90 days (Munson et al., 1982). In rats, chronic administration of 25 mg 1,2-dichloroethane/kg body weight infood for 2 years had no effect on kidney function as measured by changes in serum levels of urea and uric acid, butthe kidneys were neither examined grossly nor microscopically (Alumotet al., 1976). 1,2-DichIoroethane is acutelynephrotoxic in humans following inhalation exposure. In the Nouchi et al. (1984) case study it was reported that highserum ammonia and eventually kidney failure preceded general organ failure and death. Microscopic examinationrevealed acute tubular necrosis (Nouchi et al., 1984).

Immunological Effects. No studies were located regarding immunological effects in humans following oralexposure to 1,2-dichloroethane.

However, adverse immunological effects were shown to occur in animals following oral exposure to 1,2-dichloroethane. Reduced IgM response and a reduction in cell-mediated immune response to sheep erythrocyteswere observed in mice following a 14-day exposure by gavage to 4.9 and 49 mg l,2-dichloroethane/kg/day (Munsonet al., 1982). However, mice given drinking water containing 189 mg 1,2-dichloroethane/kg/day for 90 daysdisplayed no treatment-related effects on either the antibody-forming cell response or the delayed-typehypersensitivity response after immunization with sheep erythrocyte antigens (Munson et al., 1982). The differencein effect observed in mice treated by gavage and those exposed to 1,2-dichloroethane in drinking water may reflectdifferences in compound administration and exposure duration as discussed earlier.

Neurological Effects. 1,2-Dichloroethane is an anesthetic narcotic in humans; it is as noxious as gasoline, benzene,carbon tetrachloride, and chloroform when inhaled for periods of an hour or more, and less noxious for shorterexposure periods (Garrison and Leadingham, 1954). Neurological effects, such as CNS depression, have beenreported in humans following acute oral intoxication with 1,2-dichloroethane (Lochhead and Close, 1951; Yodaikenand Babcock, 1973). Morphological alterations in the nervous system were observed in patients who died of acuteoral poisoning by 1,2-dichloroethane. These alterations included vascular disorders, diffuse changes in cerebellarcells, parenchymous changes in brain and spinal cord, myelin degeneration, hyperemia and hemorrhage of the brain(Hueper and Smith, 1935; Lochhead and Close, 1951). The morphological changes observed in the cerebellum mayaffect the coordination of muscular movements. The Nouchi et al. (1984) case study reported the neurologicalsymptoms such as irritability and periodic vomiting followed acute exposure to 1,2-dichloroethane. These symptomswere followed by drowsiness, delirium, tremor and ultimately coma. An autopsy revealed that the Purkinje cell layerof the cerebellum demonstrated a shrunken appearance with pyknotic nuclei.

No studies were located regarding neurological effects in animals following oral exposure to 1,2-dichloroethane.

Dermal/Ocular Toxicity. Clinical observations reveal that 1,2-dichloroethane caused eye irritation in a man;clouding of the cornea has been reported in humans after inhalation of 1,2-dichloroethane (PCOC, 1966; Garrisonand Leadingham, 1954).

produced mortality in 80 to 100 percent of treated mice within 24 hours (Storer et al., 1984). No conclusions can bemade from this study because the DNA damage occurred at very high (lethal) doses.

REFERENCES

ATSDR, 1989. Toxicological Profile for 1,2-Dichloroethane.

Cal EPA. 1992. California Cancer Potency Factors. California Environmental Protection Agency, Office ofEnvironmental Health Hazard Assessment, Standards and Criteria Workgroup. June.

U.S. Environmental Protection Agency (EPA), 1980. Ambient water quality criteria for chlorinated ethanes.EPA/440/5-80-029.

Integrated Risk Information System (IRIS), 2000. U.S. Environmental Protection Agency (EPA), updated annually.

All other references as cited in ATSDR documents.

2,4-DIMETHYLPHENOL(CAS RN 87-86-5)

There is relatively little lexicological information available for 2,4-dimethylphenol. Following is a discussion of thegeneral toxicology of phenolic compounds including 2,4-dimethylphenol, 2-methylphenol, 4-methyIphenoI, andphenol. The individual compounds of the family vary from liquid to solid at room temperature and are used for anumber of different purposes. The compounds listed above will be discussed briefly with regard to their individualtoxicity and biological characteristics. Phenol is presented in more depth due to the consideration that it is the mostrepresentative individual compound of the group.

Phenol is a white crystalline solid which is used widely in the production and manufacture of a variety of products.It has an acrid, aromatic odor. It has been estimated that as many as 10,000 workers are occupationally exposed tophenol during the production of paints, paint removers, asbestos goods, wood preservatives, rubber, fertilizer, cokearid i l luminating gas among others. It is also used as a disinfectant in other industry processes, such as themanufacture of soap, toys, leather and paper as well as in agriculture. Phenol is also known as carbolic acid, phenicacid, phenyl hydrate and hydroxybenzene among other synonyms (Sittig, 1985).

Acute Effects

Phenol is a primary skin irritant producing corrosion of tissue upon contact. It causes a whitening of skin but doesnot cause pain, whereas it causes damage to the point of blindness in eyes. If the phenol is not removed quicklyabsorption can occur potentially leading to systemic toxicity (Sittig, 1985).

An acute lethality study done in conjunction with another study exposed rats to 10,000 ppm (780 mg/kg/day) indrinking water for 90 days. All animals survived the specified exposure period (NCI, 1980).

Systemic Effects

2-methylphenoI (o-cresol) has an oral reference dose (RfD) reported by both IRIS (2000) and HEAST (1997) to beestimated at 5E-2 mg/kg/day. The estimate is based on the evidence of neurotoxicity and decreased body weight at alowest-observed-adverse-effects level (LOAEL) of 150 mg/kg/day in rats (EPA, 1986, 1987). A previous oral RfDestablished for 4-methylphenol (p-cresol) has been withdrawn, pending further evaluation by EPA (IRIS, 2000). Anoral RfD of 2E-2 mg/kg/day has been estimated for 2,4-dimethylphenol based on clinical signs and hematologicalchanges in mice at a LOAEL of 250 mg/kg/day (IRIS, 2000).

Carcinogenic Effects

The cresols are classified by the EPA as a possible human carcinogen (C) (IRIS, 2000; HEAST, 1997). The humandata is considered inadequate and the animal data is considered limited but does provide some evidence ofcarcinogenic potential following dermal exposure. The lowest concentrations found to produce skin papillomas wasfound to be 25 jjl of 0.3 percent dimelhylbenzanthracene in mice (Boutwell and Bosch, 1959).

2-Methylphenol (o-cresol) and 4-methylphenol (p-cresol) are generally used as a mixture of isomers along with n-cresol rather than separately. The compounds are used as disinfectants, an ore flotation agent as well as anintermediate in the manufacture of other products such as plastics, dye, chemicals, and antioxidants. The isomericcompounds are found as a colorless or slightly yellowish or pinkish liquid. Cresols are potentially combustible andare soluble in alcohol and glycol.

The available data are considered insufficient at this time to completely assess the carcinogenic potential of phenol.The EPA has evaluated the compound and is currently reviewing its findings (IRIS, 2000).

Integrated Risk Information System (IRIS). 2000. 2,4-Dimethylphenol. U.S. Environmental Protection Agency(EPA), updated annually.

IRIS. 2000. O-cresol. U.S. Environmental Protection Agency (EPA), updated annually.

IRIS. 2000. P-cresol. U.S. Environmental Protection Agency (EPA), updated annually.

IRIS. 2000. Phenol. U.S. Environmental Protection Agency (EPA), updated annually.

U.S. Environmental Protection Agency. 1986. O, M, P-Cresol. 90-day oral subchronic toxicity studies in rats.Office of Solid Waste, Washington, DC.

U.S. Environmental Protection Agency. 1987. O, M, P-Cresol. 90-day oral subchronic neurotoxicity study in rats.Office of Solid Waste, Washington, DC.

ETHYLBENZENE(CAS RN 100-41-4)

Ethylbenzene is widely distributed in the environment. It is found naturally in coal tar and petroleum and as acomponent of many man-made products, gasoline contains 2 percent ethylbenzene by weight. Ethylbenzeneevaporates easily, moving into the air from water and soil; consequently, it is commonly found as a vapor in air.Sunlight acts to breakdown ethylbenzene in the air in about 3 days. In surface water, ethylbenzene reacts with othercompounds. While ethylbenzene in the soil is primarily broken down by soil bacteria, it does not bind to soil andmoves quickly into groundwater.


Mean retention rates of 49 to 64 percent were reported in human volunteers inhaling 23 to 85 ppm ethylbenzene(Bardodej and Bardodejova, 1970; Gromiec and Piotrowski, 1984 cited in ATSDR, 1990). The retention rate in ratswas reported to be 44 percent (Chin et al., 1980 cited in ATSDR, 1990). Recovery of ethylbenzene metabolites inthe urine of rabbits or rats was 72 to 92 percent of an oral dose, indicating ethylbenzene is well absorbed followingoral administration (El Masry et al., 1956; Climie et al., 1983 cited in ATSDR, 1990). Dermal absorption ofethylbenzene vapors is minimal while absorption via direct contact with the liquid is extensive and rapid (ATSDR,1990).

In humans, retention of ethylbenzene in adipose tissue was estimated to be 2 percent of total uptake (Engstrom andBjurstrom, 1978 cited in ATSDR, 1990). In rats, inhaled ethylbenzene was distributed throughout the body (Chin etal., 1980 cited in ATSDR, 1990). The order of distribution was: carcass, liver, GI tract, and adipose tissue.

Ethylbenzene is rapidly and extensively metabolized, primarily by the mixed function oxidases of the liver (Kieseand Lenk, 1974; Sullivan et al., 1976 cited in ATSDR, 1990). The adrenal cortex may also participate inethylbenzene metabolism. Metabolism does not appear to depend on the route of administration but does varyaccording to species, sex, and nutritional status (ATSDR, 1990).

Ethylbenzene is rapidly eliminated from the body, primarily in the urine, in both humans and animals (ATSDR,1990). Ethylbenzene does not appear to be eliminated in expired air. The urinary route of elimination ispredominate regardless of route of exposure.

Acute Toxicity

Deaths have occurred in animals, but not humans, following exposure to ethylbenzene. Deaths in animals haveoccurred following oral exposure to 4,728 mg/kg/day, inhalation exposure to 1,200 to 13,367 ppm, and dermalexposure to 15,415 mg/kg body weight. Short-term exposure of animals to higher concentrations of ethylbenzenealso resulted in CNS depression, ataxia, changes in motor behavior, and narcotic effects (Yant et al., 1930; Molnar etal., 1986 cited in ATSDR, 1990). It is unlikely that chronic exposure to low levels of ethylbenzene will be fatal.Ocular irritation occurred in both humans and animals following acute exposure to ethylbenzene vapors (Thienes andHaley, 1972; Yant et al., 1930 cited in ATSDR, 1990). Vertigo and dizziness have also been reported in humansexposed to air concentrations of impure ethylbenzene (Yant et al., 1930 cited in ATSDR, 1990).

Target Organ Toxicity

Systemic effects of ethylbenzene reported in human case reports have been pulmonary and ocular irritation andpossible hematologic alterations; however, the exposure conditions were not quantified and may have involvedconcurrent exposure to other toxic substances (ATSDR, 1990).

The EPA has calculated a RfD for oral exposure to ethylbenzene of l.OE-01 mg/kg/day based on liver and kidneytoxicity observed in a 182-day gavage study in female rats (Wolf et al., 1956 cited in IRIS, 2000). The effects

poor analysis, and small number of animals. The above observations may represent adaptive enzyme inductionrather than a hepatotoxic effect.

Renal toxicity. Species specific renal susceptibility to ethylbenzene has been observed in animal studies (ATSDR,1990). Histopathological and enzymatic changes and increases in kidney/body weight have been observed inanimals, with rats and mice being the more susceptible species (Biodynamics, 1986; Elovaara et al., 1985; Toftgardand Nilsen, 1982; Wolf et al., 1956 cited in ATSDR, 1990). These studies, which reported similar effects in theliver, were limited by poor descriptions, poor analysis, and small number of animals.

Neurotoxicity. Non-specific neurological effects have been reported in humans and animals following short-termexposure to high concentrations (ATSDR, 1990). No behavioral changes or histopathological alterations have beenreported in mice, rats or rabbits following repeated exposure to elhylbenzene (Cragg et al., 1989 cited in ATSDR,1990). Changes in neurotransmitiers have been reported in mice, rats, and rabbits following a 3 to 7 day exposure toethylbenzene (Andersson et al., 1981 cited in ATSDR, 1990).

Developmental Toxicity

There was no information available on the possible effects of ethylbenzene on development in humans(ATSDR, 1990).

The incidence of fetuses with extra ribs was increased in rats exposed to maternally toxic concentrations ofethylbenzene during gestation or prior to mating and during gestation (Andrew et al., 1981 cited in ATSDR, 1990).An increased incidence of anomalies of the uropoietic apparatus was observed in the fetuses of mice exposed to 115ppm during gestation, and decreased female fetal weights were observed in rabbits under the same exposureconditions (Andrew et al., 1981 cited in ATSDR, 1990).

Reproductive Toxicity

There were no studies on the reproductive effects of ethylbenzene in humans (ATSDR, 1990).

The reproductive effects of ethylbenzene in animals have not been adequately studied. The data are limited toancillary histopathology data of reproductive organs in chronic exposure studies (ATSDR, 1990). There are nogenerational studies examining traditional reproductive parameters such as number of implantations, resorplions, livebirths, etc.

Genotoxicity

Ethylbenzene was negative in a number of in vitro mutation assays using prokaryotic organisms, Chinese hamsterovary cells, rat liver epithelial cells, and in vivo using mouse bone marrow cells (ATSDR, 1990). A positivemutagenic effect was observed in mouse lymphoma cells, and a marginal increase in sister chromatid exchange wasobserved in human lymphocytes. Although ethylbenzene was nonmutagenic in the majority of studies, the twopositive results suggest the potential for genotoxicity.

Carcinogenicity

Occupational exposure to ethylbenzene has not been associated with increased risk of cancer (ATSDR, 1990). Aninhalation carcinogenicity bioassay is currently being conducted by the NTP. The carcinogenicity of orallyadministered ethylbenzene was investigated in rats (Maltoni et al., 1985 cited in ATSDR, 1990). An increase in totalmalignant tumors was reported in females and in males and females combined administered 500 mgethylbenzene/kg/day. However, no data on specific tumor type were reported. In addition, the study was limited bythe use of only 1 dose and the lack of information on survival rates. The EPA has classified ethylbenzene D; notclassifiable as to human carcinogenicity due to lack of animal bioassays and human studies (IRIS, 2000).

IRON

(CASRN 7439-89-6)

Iron is a constituent of hemoglobin, myoglobin, and several enzymes, but toxicological considerations are importantin terms of accidental acute exposures and chronic iron overload due to idiopathic hemochromatosis or as aconsequence of excess dietary iron or frequent blood transfusions. Daily iron intake in the U.S. averages 10.7mg/day, with most of the iron coming from food, including iron added to food as a form of enrichment (Murphy andGalloway, 1986). The RDA is 10 mg/day for children (NRC, 1989).

The toxicity of iron is governed by absorption. The more you lake in the more you are at risk. The iron is absorbedin the ferrous state by cells of the intestinal mucous. Gastric and intestinal secretions can reduce ferric ions (theunusable form of the iron) to the ferrous (absorbable) state. Ferrous iron reacts with hydrogen peroxide (H202) toform OH, in the reaction: Fe(II) + H2O2--> OH. + OH- + Fe(III) Under normal conditions, the free radicals formedare controlled and removed by antioxidants, but if you have an over abundance of iron in your body, the freeradicals will not be removed fast enough and there will be a build up. Factors that influence iron toxicity are:

• Copper Level• Phosphorus Level• Vitamin E level

Factors that enhance iron absorption are:• Valine and Histidine• Ascorbic Acids, with or without Vitamin E• Succinate• Pyruvic Acid• Citric Acid

Ferritin is a unique iron storage protein containing 24 storage proteins. When excess dietary iron is absorbed, thebody produces more ferritin. Ferritin is greatly abundant in the heart and liver, therefore there is a large amount inthese organs, and iron rushes to these organs for storage. The body can only produce so much of these proteins,however, so excess iron builds up in these organs and causes tissue destruction. Iron Overload is characterized byincreased levels of ferrilin (the iron storage protein), haemosiderin (another storage protein), and iron catalyzed lipidperoxidation.

EPA does not provide chronic oral RfD estimates for iron in its IRIS or HEAST databases. However, EPA RegionHI provides an oral RfD for iron as 3 E-l mg/kg/day.

The Environmental Protection Agency (EPA) has not classified the iron as its potential carcinogenicity.

LEAD(CAS RN 7439-92-1)

Lead is a naturally occurring bluish-grey metal found in small amounts in the earth's crust. It is found in plants andanimals, air, drinking water, rivers, lakes, oceans, dust, and soil. Lead remains in soil for many years. Mixed ores orrecycled scrap are the source of lead to industry. Its main use is in the manufacture of storage batteries followed byproduction of chemicals including paints, gasoline additives, various metal products, and ammunition.

The largest source of lead in air is from vehicle exhaust. Other sources include emissions from iron and steelproduction, smelting operations, municipal waste incinerators, and lead-acid-battery manufacturers. Lead is alsopresent in tobacco smoke. The main sources of lead released to water are lead plumbing and solder in buildings;lead-containing dust and soil carried into water by rain and wind; and wastewater from industries using lead.

Exposure to lead may occur via breathing air, drinking water, and eating soil or foods that contain lead. Anothersource, for children, is from swallowing non-food items such as chips of lead-containing paint (i.e., pica).


The rate and degree of lead absorption are largely related to its solubility in body tissues and fluids, among otherfactors. Upon inhalation, some fraction of inhaled airborne and orally ingested lead is deposited in the respiratorytract. The rale of deposition in adult humans is approximately 30 percent to 50 percent. Upon deposition in thelower respiratory tract, all chemical forms of lead are almost completely absorbed. Approximately 20 percent ofinhaled lead was absorbed within 1 hour, and 70 percent was absorbed within 10 hours in humans breathing lead-containing engine exhausts or lead oxide and lead nitrate aerosols at 2 to 10t(Jg/m lead (Chamberlain et al., 1978cited in ATSDR, 1986). Inhaled lead is absorbed extensively and rapidly in animals as well. Morgan and Holmes(1978 cited in ATSDR, 1986) estimated absorption rates of 50 percent within 1 hour and 98 percent within 7 days inadult rats breathing the equivalent of 6 mg/m lead.

The primary site of lead absorption in children is the GI tract (approximately 50 percent) upon oral exposure,compared to 8 percent in adults (Hammond, 1982 cited in ATSDR, 1986) or 15 percent (Chamberlain et al., 1978cited in ATSDR, 1986). Absorption may be as high as 45fpercent in fasting adults (Chamberlain et al., 1978 cited inATSDR, 1986). GI absorption in children (from nonfood sources) is estimated to be approximately 30 percent fromdirt/dust and 17 percent from paint chips (Drill et al., 1979 cited in ATSDR, 1986). Absorption values are similar inanimals (i.e., I percent to 15 percent in adults). The extent of GI absorption is age dependent (i.e., younger animalsabsorb 40 to 50 times more lead via the diet than do adults). GI absorption is enhanced by milk products, lowcalcium and vitamin D levels, fasting, or iron deficiencies. Dermal absorption is much less significant due to agreatly reduced dermal absorption rate. In humans, approximately 0 percent to 0.3 percent absorption has beenmeasured (ATSDR, 1986).

Once in the body, lead is dispersed primarily to the bone, blood, and soft tissue pools regardless of the route ofabsorption. The half-life of lead in blood is approximately 36 days, in soft-tissue is 40 days and in bone is 10 days.Greater than 99 percent of blood lead is associated with the red blood cells. Over 50 percent of this blood pool isbound to hemoglobin, with lesser amounts bound to other proteins. Fetal hemoglobin has a greater affinity for leadthan does adult hemoglobin. The biological half-life of lead in the blood of 2 year-old children is approximately 10months.

In human adults approximately 95 percent of the total lead body burden is present in the bones. In children, thisvalue is 73 percent. Bone lead levels increase with age. In most soft tissue, lead does not appear to accumulate as afunction of age in humans over 20 years old.

Any dietary lead not absorbed by the GI tract is eliminated in the feces of both humans and animals. Rosen (1985cited in ATSDR, 1986) demonstrated that 50 percent to 60 percent of the absorbed fraction of lead was excreted on a

physiological processes including reduced hemoglobin synthesis, reduction of hemoproteins, renal endocrine effects,and hepatic effects.

Studies in animals have shown delays in reflex development in rats during early postnatal life at greater than 59ug/dL (Kishi et al., 1983 cited in ATSDR, 1986). Decreased visual acuity in young rats have been observed inseveral studies at mean blood lead levels of 65 ug/dL. Blood lead levels as low as 15 to 20 ug/dL were associatedwith slower learning and higher rates of inappropriate responses (Cory - Slechta et aJ., 1985; Schlipkoter andWinneke, 1980 cited in ATSDR, 1986).

Exposure of male rats had an effect on cardiovascular function at levels of 50 ppm lead. Lead acetate was given indrinking water for 160 days with results of markedly increased blood pressure (182/138) as compared to 129/98 incontrols (lannaccone et al., 1981 cited in ATSDR, 1986). The mean blood lead level in the treated group was 38.4ug/dL.

Animal studies provide evidence of nephropathy similar to that in humans, particularly after acute exposures. Leadappears to affect vitamin D metabolism in renal tubule cells such that circulating levels of the vitamin D hormone,1,25 - dihydroxyvilamin D, are reduced (Smith et al., 1981 cited in ATSDR, 1986). High calcium diets protectedagainst this effect. In vitro studies with rat pituitary cells showed that lead inhibited the thyrolropin-releasinghormone (TRH) and stimulated release of thyrotropin-stimulating hormone (TSH) in a dose-related manner(Huseman et al., 1987 cited in ATSDR, 1986). This supports the conclusions drawn from human data.

Developmental and Reproductive Toxicitv

The EPA has concluded, based on a review of several studies, that a definitive association between prenatal leadexposure in humans and the occurrence of congenital anomalies has not been demonstrated. Various studies havereported decreased birth weights, sti l l births, and placenta! weight. However, as noted by EPA, the majority of thesestudies did not account for possible confounding variables (i.e., socioeconomic status and concurrent exposures).Therefore, the above conclusion has been made. It has been noted, however, that gestational age may be reduced asprenatal lead exposure increases, even at blood lead levels below 15 ug/dL. Several studies have indicated negativecorrelations between maternal or cord blood lead levels and gestational age.

In one prospective study of the effects of pre- and postnatal lead exposure on child development McMichael et al.(1986 cited in ATSDR, 1986) studied 831 pregnant women and followed 774 pregnancies to completion in a leadsmelter town. Blood lead levels were significantly higher in women who lived in the town compared to thoseresiding outside the town (11.2 ug/dL versus 7.5 ug/dL). No association between lead exposure and congenitalanomalies was noted when factors such as smoking and alcohol consumption were reviewed. Also observed was agreater incidence of low-birth weight (less than 2,500 g at gestational age greater than or equal to 37 weeks) in thetown. More miscarriages and stillbirths occurred in the Port Pirie mothers compared to others. Neurobehavioraldevelopment, therefore, appears to be deleteriously affected by prenatal lead exposures. Transplacental transfer oflead in humans has been demonstrated in a number of studies. Fetal uptake of lead occurs by the 12th week ofdevelopment and increases throughout development (Barltrop, 1969; Horiuchi et al., 1959 cited in ATSDR, 1986).Highest lead levels were measured in fetal bone, kidney, and liver tissue and lesser amounts in the brain and heart.

Teratogenicity studies in rats and mice provide no evidence that lead compounds (acetate or nitrate) are teratogenicwhen exposure occurs by natural routes. Intravenous or inlraperitoneal injection of lead compounds into pregnantrats, mice or hamsters, however, has produced malformations in several studies. There are indications, as well, thatlead accumulates in the placenta in times of fetal stress.

Severe occupational exposure (primarily via inhalation) to lead has been shown to be associated with a highlikelihood of spontaneous abortions. The EPA has concluded that reproduction effects on the sperm or testes of menchronically exposed at blood lead levels of 40 to 50 ug/dL may occur. Lancranjan et al. (1975 cited in ATSDR,1986) studied 150 men with long-term lead exposure, categorized as follows: lead-poisoned (mean blood lead level

METHYLENE CHLORIDE(CAS RN - 75-09-2)

Methylene chloride is a colorless liquid that has a mild sweet odor, evaporates quickly, and will not easily burn. Itdoes not appear to occur naturally in the environment. It is made from methane gas and wood alcohol. Methylenechloride is used for the following: a solvent in paint strippers and removers; a propellant in aerosols; a processsolvent in the manufacture of drugs, pharmaceutical, and film coatings; a metal cleaning and finishing solvent;electronics manufacturing; and urethane foam blowing (NTP, 1989). Methylene chloride is also used as anextraction solvent for spice oleoresins, hops, and for the removal of caffeine from coffee, although the latter use is inthe decline. Last of all, methylene chloride is approved for use (by the Food and Drug Administration) as post-harvest fumigant for grains and strawberries and as a degreasing agent for citrus fruit (Hearne et al., 1990;Mannsville Chemical Products, 1988; Meister, 1989; NTP, 1989).


The principal route of human exposure to methylene chloride is inhalation. During absorption through the lungs, theconcentration of methylene chloride in alveolar air, in equilibrium with pulmonary venous blood content, approachesthe concentration in inspired air until a steady state is achieved. After tissue and total body steady state is reachedthrough the lungs and other routes, uptake is balanced by metabolism and elimination. Steady state blood methylenechloride concentrations appear to be reached after 2-4 hours of exposure (DiVincenzo and Kaplan, 1981; McKennaetal., 1980).

Evaluation of pulmonary uptake in humans indicated that 70-75% of inhaled methylene chloride vapor was absorbed(DiVencenzo and Kaplan, 1981). Initial absorption of methylene chloride was rapid, as indicated by an uptake ofmethylene chloride into the blood of approximately 0.6 mg/L in the first hour of exposure to levels of 100-200 ppm.At a dose of 50 ppm, the increase in blood methylene chloride concentrations was 0.2 mg/L for the first hour(DiVincenzo and Kaplan, 1981). There was direct correlation between the steady state blood methylene chloridevalues and the exposure concentration, with a proportionality constant of approximately 0.008 ppm in blood per ppmin air (DiVincenzo and Kaplan, 1981). The blood concentrations reached steady state values during the 4th through8lh hour of continuous exposure to the vapor. Once exposure ceased, methylene chloride was rapidly cleared fromthe blood. Only traces of methylene chloride were present 6 hours after the end of exposure in the highest dosegroup. All other dose groups had returned to baseline concentrations.

Methylene chloride absorbed by the lungs is expected to dissolve in the lipoprotein components of the blood andenter the systemic circulation after passage through the heart. It is distributed from the systemic circulation to thebody organs. However, no quantitative data were located that showed the distribution of methylene chloridefollowing human inhalation exposure. Some data are available which relate to the uptake of methylene chloride byhuman adipose tissues. These data indicate that the methylene chloride concentrations in the adipose deposits of leansubjects are greater than those in obese subjects. However, the total methylene chloride adipose tissue load is greaterfor the obese subjects due to their greater adipose mass (Engstrom and Bjurstrom, 1977).

Available data suggest that there are two pathways by which methylene chloride is metabolized. One pathwayutilizes the mixed function oxidase (MFO) enzymes and produces CO. the other pathway involves the glutathionetransferase (GST) and produces C02. It has been postulated that C02 can also be produced by the MFO pathway ifthe reactive intermediate in this pathway (postulated to be formyl chloride) reacts with a nucleophile prior toelimination of the chloride ion and formation of CO (Gargas et al., 1986).

The MFO pathway seems to be the preferred pathway for methylene chloride metabolism following inhalationexposures. Human subjects exposed by inhalation to 500 ppm or greater for 1 or 2 hours experienced elevated CO-Hb concentrations, indicating that methylene chloride was metabolized to CO by the MFO pathway (Stewart et al.,1972). The CO-Hb concentrations rose to an average of 10.1 % saturation 1 hour after the exposure of three subjectsto 986 ppm methylene chloride for 2 hours. The mean CO-Hb concentration at 17 hours post exposure remained

exposed to vapors of methylene chloride at concentrations of 500 ppm or greater, and signs of increased proteinbreakdown in the cerebrum at 1,000 ppm (Savolainen et al., 1981). DNA concentration decreased in thehippocampus and cerebrum in gerbils exposed to 210 ppm or greater methylene chloride, indicating decreased celldensity in these brain regions, probably due to cell loss (Karlsson et al., 1987; Rosengren et al., 1986). Levels ofaminobutyric acid increased in the posterior cerebellar vermis of gerbils exposed to 210 ppm melhylene chloride;however, the significance of this finding is uncertain (Brivig et al., 1986). The mechanism by which methylenechloride exerts its effects on the CNS is not clear. Based on behavioral responses that were reported in humansfollowing acute inhalation exposure at levels of 300 ppm or greater, it seems likely that methylene chloride producesnonspecific anesthetic effects to those produced by other halogenated hydrocarbons.

Hepatic Toxicity. A slight exposure-related increase in serum bilirubin (but not at levels of clinical significance)was observed in workers with exposure up to an average of 475 ppm of methylene chloride, but serum levels ofhepatic enzymes (e.g., aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and alkalinephosphatase) were not elevated (Ott et al., 1983a). Based on these data, the liver does not appear to be a major targetorgan in humans.

Cardiotoxicity. Studies in humans exposed to 75-475 ppm did not reveal an association between occupationalexposure to methylene chloride and cardiac abnormalities (Cherry et al., 1981) or mortality due to ischemic heartdisease (Hearne et al., 1990; Ott et al., 1983b). Further, a cross-sectional study of workers showed no excess ofelectrocardiographic abnormalities among those exposed to methylene chloride (Ott et al., 1983c). The absence ofelectrocardiograph abnormalities or increased death due to ischemic heart disease in humans occupationally exposedto levels up to 475 ppm suggest that the heart is not a target following exposure to methylene chloride.

Dermal/Ocular Toxicity. No studies were located on dermal/ocular effects in humans by any route of exposure. Inanimals, small increases in corneal thickness and intraocular tension were reported after exposure to vapors of 490ppm methylene chloride or greater, but effects were reversible within 2 days after exposure ceased (Ballantyne et al.,1976). Inflammation of the conjunctivae and eyelids as well as increases in corneal thickness and intraocular tensionwere observed following direct contact of methylene chloride (0.1 ml) with the eyes of rabbits. Effects werereversible within 3-9 days (Ballantyne et al., 1976).

Immunotoxicity. No studies were located regarding immunological effects in humans after inhalation, oral, ordermal exposure.

Reproductive Toxicity. Data on reproductive toxicity in humans are limited to one case series study reporting lowsperm counts in workers who inhaled vapors of methylene chloride and who had direct contact with the liquid (Kelly,1988). It is uncertain if effects were due to methylene chloride, since workers may have had multiple compoundexposures and the study group was small. Based on these data, methylene chloride does not appear to pose a hazardto human reproduction.


Animal studies demonstrated that inhalation of methylene chloride vapors at concentrations of 1,250 ppm producedminor skeletal variants (delayed ossification of sternebrae in rats and extra center of ossification in the sternum ofmice and rats) (Schwetz et al., 1975). Fetal weight was reduced and behavioral changes occurred in rat pupsfollowing exposure of dams to 4,500 ppm methylene chloride (Bornsheim et al., 1980; Hardin and Manson, 1980).The significance of these observations is uncertain since each of the three studies used only one dose level and theobserved effects occurred at maternally toxic doses. Although fetal body weights were decreased, the absence ofother fetoxic effects, embryolethality, and major malformations suggest that methylene chloride is not likely to causedevelopmental effects and behavioral changes at low concentrations.

NICKEL(CAS RN 7440-02-0)

Nickel is a naturally occurring silvery metal that is found in the earth's crust in the form of various nickel minerals.Nickel is primarily used in the manufacture of various steels and alloys and in electroplating.

Exposure of the general population may occur via breathing air, ingesting drinking water and food that contain nickelcompounds, and skin contact with a variety of products. The single largest source of nickel to the atmosphere isfrom fuel oil combustion. Sources of nickel in water and soil include storm water runoff, soil amended withmunicipal sewage sludge, wastewater from municipal sewage treatment plants, and ground water near landfill sites.


Very little nickel may be absorbed from the respiratory tract of humans as indicated by Kalliomaki et al. (1981). Theresults of this study indicated that urinary nickel increased very litt le even as the nickel content of inhaled fumesreached up to 30 |ig/m in steel welders. It is noted that greater absorption occurs in soluble nickel compounds. Thehalf-life of nickel clearance from the nasal mucosa is estimated at 3.5 years. Absorption of nickel compounds inanimals following inhalation is dependent on the deposition of particles in the lungs. Wehner and Craig (1972) foundthat 45 days after exposure of rats to nickel oxide (particle size of 1.0 to 2.5 urn), approximately half was still presentin the lungs.

Human studies reviewed by EPA (1986) indicate that 1 to 10 percent of dietary (orally administered) nickel isgaslrointestinally absorbed. Studies in rats, dogs, and mice reveal the same percentages of absorption following oralexposure to nickel, nickel sulfate hexahydrate, or nickel chloride.

Several studies indicate that nickel can penetrate human skin. Norgaard (1955) used aqueous solutions of nickelsulfate to find that 55 to 77 percent of the nickel applied to occluded skin was absorbed; most absorbed during thefirst 24 hours following application. It is also evidenced that nickel ions from a chloride solution pass through theskin about 50 times faster than ions from sulfate solutions. Lloyd (1980) demonstrated that approximately 1 hourfollowing nickel (II) application to shaved guinea pigs skin, nickel had accumulated in keratinaceous areas and inhair sacs. Nickel metal does not readily penetrate the skin.

Once inside the body following inhalation exposure, nickel is distributed primarily to the lungs. Studies in laboratoryanimals also indicate concentrations in the spleen, bone, and kidneys. In human and rabbit blood, nickel is found inserum as ultrafilterable nickel, albumin-bound nickel, and in a metalloprotein. Nickel levels in serum were noted toincrease in volunteers at 5.6 ing nickel as nickel sulfate (Christensen and Lagesson, 1981). The half-life of nickel inthe serum was 11 hours. Following oral exposure to mice, nickel localized in the kidneys, lungs, and CNS(Oskarsson and Tjalve, 1979). Whanger (1973) found that as the amount of nickel in rat diets increased, the nickelcontent of the kidney, liver, heart, and testis also increased. Whanger observed the highest levels in the rat kidneys.

Once absorbed, nickel binds to albumin, L-histidine, and 2-macroglobulin in human serum. Binding in animals issimilar. Increased levels of serum nickel have been reported in cases of acute myocardial infraction. Serum nickellevels are also elevated in acute stroke and extensive burn injury patients.

Regardless of the route of exposure, absorbed nickel is excreted in the urine in both animals and humans.Unabsorbed nickel is excreted in the feccs. Nickel is also excreted in the hair and sweat following oral exposure.

Acute Toxicity

Human Toxicity. The lung is the primary target for nickel in humans following inhalation exposure. Humaninhalation exposure to nickel refinery dust that contains nickel subsulfide is associated with lung cancer. Asthma, anallergic response, has been observed in nickel-plating workers exposed to nickel sulfate, welders exposed to nickel

anaplastic, and pleomorphic carcinomas. The results of the following studies have been used by the EPA indeveloping a unit risk slope for nickel.

o

Disease risks of workers were studied by Enterline and Marsh (1982). Exposures varied from 5 mg/m nickel forrefinery workers to 0.01 to 0.75 mg/m nickel for other workers. An excess risk of nasal sinus cancer was noted inthe refinery workers. An overall excess of lung cancer was not noted.

A 1977 mortality study of 937 nickel refinery workers by Doll et al. identified 145 lung and 56 nasal cancer cases.Nearly all nasal sinus cancers were found in workers who began work prior to the use of respiratory protection.

Chovil et al. (1981) studied a cohort of 495 sinter workers. The expected cases and deaths of lung cancer werereported as 6.38 and 4.25, respectively. Numbers observed by this study were 54 cases and 37 deaths.

Magnus et al. (1980) studied a cohort of 2,247 refinery workers who had been employed in the industry for at least 3years. Risks of nasal cancer were increased in all job categories examined, with the highest observed inroasting/smelting workers. An excess risk of laryngeal cancer was also observed (highest risk seen in electrolysisworkers). An assessment of the combined effects of smoking and nickel exposure to the risk of lung cancer led theauthors to state that the effects are likely to be additive.

A long-term inhalation study of nickel subsulfide in rats, conducted by Ottolenghi et al. 1974, reportedly is the mostrelevant animal study to human exposure. The study showed an increase in hyperplastic and neoplastic changes inthe lungs for both males and female rats.

From available data in humans, the EPA has estimated that lifetime exposure to 1 microgram of nickel refinery dustper cubic meter of air would result in 2,400 additional cases of cancer in a population of 10,000,000 people.Lifetime exposure to 1 microgram of nickel subsulfide per cubic meter of air would result in 4,800 additional cancercases in a population of 10,000,000 people. (The major sources of both of these nickel compounds are nickelrefineries; there are no operating refineries in the United States.)

Based on human epidemiological data, the EPA has classified nickel refinery dust from pyrometallurgical sulfidenickel matte refineries as a Group A carcinogen (a known human carcinogen). An inhalation uni t risk of 2.4E-04 (u.g/m3)'1 has been established (IRIS, 2000). An inhalation slope factor of 8.4E-OI (mg/kg/day)"1 has also beenestablished (HEAST, 1997). It is noted that the above uni t risk should not be used if air concentrations exceed 40 u.g/m , since above this value the slope factor may differ from that stated.

The data from the 1974 Ottolenghi et al. study and in vitro studies, along with the fact that nickel subsulfide is amajor component of nickel refinery dust, are sufficient for the EPA to classify nickel subsulfide as a Group Acarcinogen as well. An inhalation unit risk of 4.8E-04 (u.g/m ) has been established (IRIS, 2000). An inhalationslope factor of 1.7E+00 (mg/kg/day) has also been established (HEAST, 1997). It should be noted, however, thatthe cited unit risk should not be used if the air concentration exceeds 20 Hg/m , since above this concentration theslope factor may differ from that stated.

REFERENCES

Ambrose, A.M.; P.S. Larson; J.R. Borzelleca; and G.R. Hennigar, Jr. 1976. Long term toxicologic assessment ofnickel in rats and dogs. J. Food. Sci. Technol. 13: 181-187.

Benson, J.N.; D.G. Burl; R.L. Carpenter; et al. 1988. Comparative inhalation toxicity of nickel sulfate to F344/Nrats and B6C3FI mice exposed for twelve days. Fund. Appl. Toxicol. 10(1): 164-178.

Bingham, E.; W. Barkley; M. Zerwas; K. Stemmer; and P. Taylor. 1972. Responses of alveolar macrophages tometals. I. Inhalation of lead and nickel. Arch. Environ. Health. 25: 406-414.

Wehner, A.P.; and O.K. Craig. 1972. Toxicology of inhaled NiO and CoO in Syrian golden hamsters. Am. Ind.Hyg. Assoc.J. 33: 147-155.

Whanger, P.D. 1973. Effects of dietary nickel on enzyme activities and mineral content in rats. Toxicol. Appl.Pharmacol. 25:323-331.

NITROPHENOLS

2-NITROPHENOL

(CASRN 88-75-5)

4-NITROPHENOL

(CASRN 100-02-7)

Nitrophenols include two chemicals, 2-nitrophenol and 4-nitrophenol, which are very similar to each other. Theyare manufactured chemicals that do not occur naturally in tfie environment. The manufacture of one almost alwaysproduces a little of the other, so they are grouped together when discussing their properties and harmful effects.

These compounds are solids at ambient temperatures; they are very soluble in water. 2-Nitrophenol, also referred toas ortho-nitrophenol, is a light yellow solid with a peculiar sweet smell. 4-Nitrophenol, also referred to as para-nitrophenol, is a colorless to light yellow solid with very little odor. 2-Nitrophenol is used mainly to make dyes,paint coloring, rubber chemicals, and substances that kill molds. 4-Nitrophenol is used mainly to make drugs,fungicides, dyes, and to darken leather.

There are no studies that have looked at the effects of the nitrophenols in humans. Some studies in animals haveshown that 4-nitrophenol is more harmful than 2-nitrophenol when given in high amounts over a short time, but wehave very little other information on the effects from longer time exposures at lower levels. Rats that breathedmoderate levels of 4-nitrophenol for two weeks developed a blood disorder that reduced the ability of the blood tocarry oxygen to tissues and organs. However, these abnormalities disappeared a few days after exposure stopped.No other harmful effects to other systems or organs were seen. Skin irritation has been noted in animals that hadlarge amounts of 4-nitrophenol applied to their skin, and eye irritation when it was applied to the eye. These effectsare most likely due to the large amount used and not to a specific harmful effect of nitrophenols. No birth defectswere seen in the offspring of animals that ingested large quantities of 4-nitrophenol. There is no information fromanimal studies on the effects of ingesting low levels of nitrophenols. The amounts given to animals that produce theharmful effects are several hundred to several thousand times higher than those people are generally exposed to.

EPA does not provide chronic oral RfD estimates for the o-or p- isomers of nitrophenol in its IRIS or HEASTdatabases. However, EPA Region III provides an oral RfD for 4-nitrophenol (i.e., p-nitrophenol) as 8 E-3mg/kg/day. The health effects data for 4-nitrophenol were reviewed by the U.S. EPA RfD/RfC Work Group anddetermined to be inadequate for the derivation of an inhalation RfC.

The Environmental Protection Agency (EPA) has not classified the nitrophenols as to their human carcinogenicity.

PENTACHLOROPHENOL(CAS RN 87-86-5)

Pentachlorophenol (PCP) is a chlorinated hydrocarbon which is used as a wood preservative and a fungicide,herbicide, and algicide. PCP is a solid, either colorless or light grey to light brown. When heated above its meltingpoint it can emit highly toxic chloride fumes. Other decomposition products include hydrogen chloride, chlorinatedphenols, and carbon monoxide (IRIS, 2000; Sittig, 1985).

Acute Toxicity

PCP is an acute toxin with a lethal human ingestion dose estimated at 50-500 mg/kg for a 70 kg person. Ingestioncauses an increase in blood pressure, respiration, bowel action, and urinary output followed by a decrease in thoseactions into collapse with convulsions and possibly death. Ingestion of PCP can also affect the liver and kidneys(IRIS, 2000; Sittig, 1985).

Inhalation of PCP can cause general central nervous system depression indicated by dizziness, headache, nausea, andweakness. Inhalation of large concentrations can also cause heart failure and possibly death. PCP is an eye andupper respiratory irritant upon inhalation contact. Contact either to vapor phase in the air or other dermal contact cancause contact dermatitis (IRIS, 2000; Sitting, 1985).


An oral reference dose (RfD) for PCP is reported in both IRIS (2000) and HEAST (1997). The RfD.estimate is 3E-2mg/kg/day as based on the study by Schwetz et al (1978) described below. No inhalation reference concentration(RfC) is given at this time (IRIS, 2000; HEAST, 1997).

The principal and supporting study used as a basis for the estimation of the PCP RfD is a study conducted bySchwetz et al., 1978. The study exposed 25 rats of each sex. The exposure concentration of 3 mg/kg/day wasidentified as the no-observed-adverse-effects level (NOAEL). The group which received 10 mg/kg/day showedincreased liver and kidney pigmentation among other histological changes. Ten mg/kg/day was identified as thelowest-observed-adverse-effects level (LOAEL).

Developmental And Reproductive Toxicity

Several studies have investigated the potential of teratogenic effects following oral exposure to PCP. In general, thestudies found no real teratogenic effects, but rather what was thought to be secondary effects to maternal toxicity.The no-observed-adverse-effects level (NOAEL) is the same as identified for the chronic studies used for theextrapolation of the RfD, 3 mg/kg/day (IRIS, 2000).

The embryonal and fetal effects of pentachlorophenol in rats were assessed in a series of studies by Schwetz et al(1974). Statistically significant, dose-related decreases in maternal weight gain were noted.

Daily oral administration of 1.25 to 20 mg/kg PCP to Syrian golden hamsters on days 5 to 10 of pregnancy resultedin fetal deaths and/or resorptions in three of six test groups (Hinkle, 1973). No other data were provided.

In a single generation reproduction study, Sprague-Dawley rats were fed 0, 3 or 30 mg/kg/day of purified PCP for 62days prior to mating, throughout gestation and up to 21 days postpartum. The 30 mg/kg dose resulted in a significantdecrease in the number of pups born alive and significantly decreased survival to days 7, 14 and 21 of lactation, buthad no effect on fertility. A significantly increased number of litters showed skeletal anomalies at this dose, theaverage litter size was decreased and mean neonatal body weight was significantly less than controls. No adverseeffects were noted at doses of 3 mg/kg/day (Schwetz, 1978).

PHENOL(108-95-2)

Phenol is white crystalline solid which is used widely in the production and manufacture of a variety of products. Ithas an acrid,aromatic odor. It has been estimated that as many as 10,000 workers are occupationally exposed tophenol during the production of paints, paint removers, asbestos goods, wood preservatives, rubber, fertilizer, cokeand illuminating gas among others. It is also used as a disinfectant in other industry processes, such as themanufacture of soap, toys, leather and paper as well as in agriculture. Phenol is also known as carbolic acid, phenicacid, phenyl hydrate and hydroxybenzene among other synonyms (Sittig,1985).

Acute Effects

Phenol is a primary skin irritant producing corrosion of tissue upon contact. It causes a whitening of skin but doesnot cause pain, whereas it causes damage to the point of blindness in eyes. If the phenol is not removed quicklyabsorption can occur potentially leading to systemic toxicity (Sitlig, 1985).

An acute lethality study done in conjunction with another study exposed rats to 10,000 ppm (780 mg/kg/day) indrinking water for 90 days. All animals survived the specified exposure period (NCI, 1980).


Other studies report symptoms of the systemic toxicity of phenol as limited to reduced bodyweight or unspecifiedkidney inflammation in animals. A study by NCI (1980) exposured rats to 0 to 344 mg/kg/day and mice to 0 to 500mg/kg/day for 103 weeks. Findings included both a dose-related reduction in body weight of male and female ratsand mice and an increase in chronic inflammation of the kidney in all dosage groups of female rats and the highestdosage group of male rats. Comparable results were reported by a study conducted by the Armed Forces Institute ofPathology (1980). A lowest observed adverse effects level (LOAEL) of 313 mg/kg/day in mice and 344 mg/kg/dayis reported in rats based on depression of body weight.

Another study by Dow (1945) reported lower NOAELs and LOAELs than the NCI (1980) study possibly due todifferences in the mode of administration.


The oral reference dose (RFD) as reported by USEPA's Integrated Risk Information System (IRIS) is based on astudy by NTP (1983) regarding the developmental effects of phenol is 6E-01 mg/kg/day (IRIS, 2000). The studyincluded oral exposure of pregnant rats to 0, 30, 60 and 120 mg/kg/day on days 6 to 15 of gestation. Rats weresacrificed and examined on day 20 of gestation. Researchers observed no maternal or clinical signs of toxicity asrelated to dose received. Reported observations of significance included a reduction in fetal body weights in the 120mg/kg/day dose group. A no observed adverse effect level (NOAEL) of 60 mg/kg/day was reported and is used asthe basis for the derived RfD cited above.

Carcinogenicity

The available data are considered insufficient at this time to completely assess the carcinogenic potential of phenol.The USEPA has evaluated the compound and is currently reviewing its findings (IRIS, 2000).

POLYCHLORINATED BIPHENYLS

(CAS RN 1336-36-3)

Polychlorinated biphenyls (PCBs) are man-made chemicals synthesized by chlorination of biphenyl (2 benzene ringsconnected by a single bond). The products of chlorination are 209 different compounds with different physical andlexicological properties. PCBs may be oily liquids or solids, ranging from colorless to light yellow; they are withouttaste or smell. PCBs are not naturally found in the environment. When PCBs do enter the environment they aregenerally found as a mixture. PCBs have not been manufactured in the United States since 1977 due to evidencethat they build up in the environment and may cause harmful effects. Because of the complexity of PCB chemistry,evaluation of toxicological effects has focused on the commercially available PCB mixtures, called Aroclors(ATSDR, 1998).


Workers are exposed to PCBs largely via inhalation or dermal exposure. Dermal absorption has been estimated tobe 100 percent in humans (Wolff, 1985 cited in ATSDR, 1998). Proof of absorption is based on detection ofindividual PCBs in the tissues and body fluids of exposed workers (Wolff, 1985 cited in ATSDR, 1998). Similarly,detection of PCBs in the liver of rats following inhalation exposure provides indirect evidence of absorption acrossthe lungs in animals. Dermal absorption efficiency has been estimated to be 15 to 60 percent of an applied dose inanimals (ATSDR, 1998). Absorption of PCBs from the GI tract of animals is well documented but not wellquantified. Oral absorption is rapid (peak at 2 hours) and complete (85 to 90 percent of an administered dose isretained) (ATSDR, 1998).

In humans, PCBs are preferentially distributed to fatty tissues. Additionally, PCBs have been measured in adiposetissue, blood plasma, sperm fluid, follicular fluid and human milk (ATSDR, 1998). PCB metabolism is complicatedby the large number of individual compounds. Little is known concerning metabolism in humans. Although itappears that preferentially accumulated (retained) PCBs are metabolism-resistant. These compounds are generallymore highly chlorinated and lack unsubstituted meta-para-vicinal positions (ATSDR, 1998).

In humans and animals, PCBs are excreted in the urine and feces, with fecal elimination predominating followingoral administration. In lactaling women, excretion of PCBs in the milk is the major excretory route (ATSDR, 1998).

Acute Toxicity

No deaths have been reported in humans exposed to PCBs. Deaths have occurred in animals following ingestion ofa single high dose or repeated lower doses of PCBs (ATSDR, 1998). The cause of death was unclear but principlesigns of toxicity were GI hemorrhage and ulceration, diarrhea, respiratory depression, dehydration. Death was alsoreported in hairless mice following dermal administration.


The EPA has established a chronic oral RfD of 7.00E-05 mg/kg-day (IRIS, 1999).


Shorter mean gestational ages, resulting in lower mean birth weights, were reported for 51 infants born to motherswith direct occupational exposure to Aroclors 1254, 1242, and/or 1016 for at least 1 year prior to birth compared tomothers with indirect occupational exposure (ATSDR, 1998). A positive correlation was reported between levels oftotal PCBs in cord serum from babies born to mothers who had consumed moderate to large quantities of PCB-contaminated Lake Michigan fish.

The effects of oral administration of PCBs during gestation and lactation have been extensively studied in rodents(ATSDR, 1998). In general, repeated administration of Arocolors to rats or mice during gestation was not

POLYCYCLIC AROMATIC HYDROCARBONS

Polycyclic aromatic hydrocarbons (PAHs) are formed during (he incomplete combustion of organic substances (e.g.,coal, oil, gas, garbage). There are over 100 PAHs; among the most common are: acenaphthene, acenaphlhylene,anthracene, benzo(a)anthracene, benzo(a)pyrene, benzo(b)fluoranthene, benzo(g,h,i)perylene, benzo(k)fluoranthene,fluoranthene, fluorene, indeno(l,2,3-cd)pyrene, naphthalene, phenanthrene, and pyrene. The toxicity informationavailable on PAHs is limited. Therefore, the potential health effects of "unknown" PAHs are inferred from thoselisted above. PAHs are generally found in the environment as mixtures of 2 or more compounds. Most PAHs arenot readily soluble in water. Some easily volatilize into air; generally, PAHs will persist in the environment formonths to years. PAHs are found throughout the environment. Background levels are 0.02 to 1.2 mg/m3 (rural) to0.15 to 19.3 mg/m3 (urban) and 4 to 24 ng/L, for air and water respectively.

PAHs can be classified according to the electron density associated with the molecule as alternate or non-alternate.This distinction is lexicologically significant because the two classes appear to behave differently, particularly withrespect to how the molecule is metabolized.


PAHs appear to be readily bioavailable following inhalation exposure. Absorption of PAHs following inhalationhas been inferred from the presence of urinary metabolites of PAHs in humans following exposure (Becher andBjorseth, 1983 Cited in ATSDR, 1990). However, the dose-uptake relationship was not linear over the exposureconcentration range, probably due to incomplete availability of the PAHs adsorbed to airborne particulate matter.Studies in animals suggest that clearance of PAHs from the lung is the product of direct absorption into the bloodstream and clearance by mucociliary action and subsequent ingestion. The size of the particles to which the PAHsare adsorbed will influence the relative degree of absorption into the blood stream from the lungs (Sun et al., 1982;Cresia et al., 1976 cited in ATSDR, 1990). Benzo(a)pyrene was not bioavailable following direct nasal instillationin hamsters, monkeys, or dogs; local mucosal absorption and metabolism were predominant (Dahl et al., 1985 andPetridou-Fischer et al., 1988 cited in ATSDR, 1990).

The oral bioavailability of PAHs is variable. Benzo(a)pyrene could not be detected in human feces followingingestion of broiled meat containing benzo(a)pyrene; blood levels did not appear to have been measured (Hecht etal., 1979 cited in ATSDR, 1990). Many of the animal studies only evaluated recovery of the administered dose inthe feces and failed to measure blood or urine levels; therefore, a direct indication of bioavailability was notdetermined. In two studies, benzo(a)pyrene and benzo(a)anthracene were detected in the liver, lung, kidney, blood,and brain; however, no quantitative data were given (Yamazaki et al., 1987; Modica et al., 1982 cited in ATSDR,1990).

PAHs are absorbed through the skin of both humans and animals. PAHs could be detected in the blood followingapplication of crude coal tar to the skin of humans (Storer et al., 1984 cited in ATSDR, 1990). Three percent of anapplied dose of MC-benzo(a)pyrene permeated human skin in vitro (Kao et al., 1985 cited in ATSDR, 1990). Inmice, 93 percent of a dermally applied dose of HC-benzo(a)pyrene was recovered in the feces after 7 days, indicatingthat only about 7 percent was absorbed (Sanders et al., 1986 cited in ATSDR, 1990). Fifty-three percent of adermally applied dose of MC-anthracene was recovered in the urine, feces, and tissues of rats over a 6 day period(Yang et al., 1986 cited in ATSDR, 1990). A number of other PAHs were absorbed following dermal exposure, butthe amount absorbed is not linear with dose, suggesting saturation of an uptake process (Sanders et al., 1986 cited inATSDR, 1990).

The distribution of PAHs in humans is unknown. In animals, benzo(a)pyrene has been predominant PAH studied.PAHs were more widely distributed following oral exposure than inhalation exposure; and, distribution was limitedfollowing dermal exposure. Typically, the highest distribution was to the lung, liver, kidney, and GI tract (Weyandand Bevan 1986, 1987, 19888; Schnizlein et al., 1987; Sun et al., 1982; Bartosek et al., 1984; Daniel et al., 1967cited in ATSDR, 1990). Concentrations of PAHs were delected in the fetus following oral administration to thedam. However, the differences in fetal concentration appeared to reflect differences in GI uptake in the dam and notability to permeate the placenla (Shendrikova and Aleksandrov, 1974 cited in ATSDR, 1990). The majority ofradioactivity was recovered in the lipid fraction of the tissues (Yamazaki et al., 1987 cited in ATSDR, 1990).PAH metabolism has been studied extensively in vivo (animals) and in vitro (human and animal cells) (ATSDR,1990). In general, metabolism transforms lipophilic PAHs into more water-soluble, excretable compounds.

Hematological Toxicity. Bone marrow depression (aplastic anemia and pancytopenia) leading to death wasobserved in mice whose AHH enzyme was not inducible following oral administration of 120 mgbenzo(a)pyrene/kg/day for 180 days (Robinison et al., 1975 cited in ATSDR, 1990).

Hepatic Toxicity. A number of hepatic effects (enzyme and foci induction, liver regeneration, and increasedweights) have been observed in animals administered PAHs. These effects are not life-threatening but may precedethe onset of more serious effects. A single intragastric administration of 200 mg/kg of benzo(a)pyrene,benzo(a)anthracene, or dibenz(a,h)anthracene induced the formation of preneoplastic hepatocytes in apromotion/initiation bioassay in partially hepatectomized rats fed 2-acetylaminofIuorene (Tsuda and Farber, 1980cited in ATSDR, 1990). PAHs stimulate liver regeneration in partially hepatectomized rats following administrationin the diet for 10 days. Non-carcinogenic PAHs required higher doses (Gershbein, 1975 cited in ATSDR, 1990).

Dermal Toxicity. Dermal exposure to benzo(a)pyrene in humans was associated with epidermal changes indicativeof neoplastic proliferation, chronic dermatitis and hyperkeratosis, or exacerbation of pre-existing skin lesions(Cottini and Mazzone, 1939; EPA, 1988 cited in ATSDR, 1990). Topical application of PAHs have been associatedwith adverse effects in animals including skin cancer, effects on sebaceous glands, increased number of skinmelanocytes, dermal inflammation, allergic contact hypersensitivily, and photosensitization (Bock and Mund, 1958;Iwata et al., 1981 Klemme et al., 1987; Old et al., 1963 and Forbes et al., 1976 cited in ATSDR, 1990).

Immunotoxicity. Immunotoxic effects have been observed following dermal and parenteral administration inanimals. PAHs that are carcinogenic are also immunosuppressive with the same rank order of potency (ATSDR,1990). Effects observed have included inhibition of T-cell dependent and independent antibody production andinhibition of lymphocyte mediated immunity (Blanton et al., 1986; Lyte and Bick, 1985; Whit and Holsapple, 1984;Wojdani et al., 1984 cited in ATSDR, 1990).


There is no information on the developmental effects of exposure to PAHs in humans (ATSDR, 1990).

In animals, in ulero exposure to benzo(a)pyrene (10, 40, or 160 mg/kg/day orally during gestation) was associatedwith reduced mean postnatal pup weight and increased incidence of sterility associated with alterations in gonadalmorphology and germ-cell development in male mice (Mackenzie and Angevine, 1981 cited in ATSDR, 1990). Anobserved increased incidence of stillborns, resorptions, and malformations following dietary administration of 120mg benzo(a)pyrene/kg/day to the dam was associated with the metabolic responsiveness of the offspring and thedams (Legraverend et al., 1984 cited in ATSDR, 1990). Parental administration of a number of PAHs has beenassociated with a number of developmental effects: stillbirths, increased fetal resorptions, malformations, adversegonadal histology, and decreased fetal survival. The implications of the results obtained following parenteraladministration, which by-passes first-pass metabolism of the liver, to human exposure are that adverse effects on thefetus are possible.


There is no information on the effect of PAH on reproduction in humans (ATSDR, 1990).

Benzo(a)pyrene decreased the percentage of pregnant females at parturition in pregnant CD-I mice (Mackenzie andAngevine, 1981 cited in ATSDR, 1990) and reduced the incidence of pregnancy in rats (Rigdon and Rennels, 1964cited in ATSDR), but it had no effect on fertili ty of Swiss mice (Rigdon and Neal, 1965 cited in ATSDR, 1990).Increased resorptions and decreased number of corpora lutea, uterine weights, and fetal survival were observedfollowing parenteral administration of benzo(a)pyrene (Swarlz and Mattison, 1985; Bui et al., 1986 cited in ATSDR,1990). The implications of the results obtained following parenteral administration, which by-passes first-passmetabolism of the liver, to human exposure are that adverse effects on reproduction are possible.

hamsters, and rats (EPA, 1991 cited in IRIS, 2/93). Inhalation exposure of hamsters to benzo(a)pyrene at 9.5mg/cubic m/day for 10 weeks was associated with development of tumors of the nasal cavity, larynx, trachea, andpharynx. At the next highest dose, 45 mg/mVday, neoplasms were also observed in the upper digestive tract. Thelowest dosed (2.2 mg/mVday) animals did not develop tumors (Thyssen et al., 1981 cited in IRIS, 2/93).Intraperitoneal and subcutaneous injection of benzo(a)pyrene is associated with injection site tumors (EPA, 1991cited in IRIS, 2/93). Based on no human data and sufficient animal data benzo(a)pyrene is classified, B2; probablehuman carcinogen. EPA has calculated an oral slope factor of 7.3E+00 (mg/kg/day)-1. Cal EPA has established anoral and inhalation slope factor of 1.2E+OI (mg/kg/day)-1 (Cal EPA, 1992).

Benzo(k)fluoranthene (CASN 207-08-9). In a lifetime study in female rats, lung implants of 0.65, 3.4, or17 mg/kg benzo(k)fluoranthene exhibited a dose-related increase in the incidence of epidermoid carcinomas in thelung and thorax. Equivocal incidences of lung adenomas and hepatic adenomas and hepatomas were reported inmice administered intraperitoneal injections of 120 ug benzo(k)fluoranthene/mouse on days 1, 8, and 15 of age(LaVoie et al., 1987 cited in IRIS, 2/93). Benzo(k)fluoranthene was positive in mouse skin-painting assays (VanDuuren et al., 1966; LaVoie et al., 1982; Amin et al., 1985 cited in IRIS, 2/93). Based on these data, EPA hasclassified benzo(k)fluoranthene as B2 "probable" human carcinogen. Using a potency equivalency factor (PEF) of0.1 and the benzo(a)pyrene slope factor of 1.2E+01 (mg/kg/day)-l, Cal EPA has established oral and inhalationslope factors of 1.2E+00 (mg/kg/day)-1 for benzo(k)fluoranthene (Cal EPA, 1992).

Indeno(l,2,3-cd)pyrene (CASN 193-39-5). EPA has classified indeno(I,2,3-cd)pyrene as a B2 probable humancarcinogen (IRIS, 1995). Using a PEF of 0.1 and the benzo(a)pyrene slope factor of 1.2E+01 (mg/kg/day)-1, CalEPA has established oral and inhalation slope factors of 1.2E+00 (mg/kg/day)-l for indeno(l,2,3-cd)pyrene (CalEPA, 1992).

Benzo(b)fluoranthene (CASN 205-99-2). In a lifetime study in female rats, lung implants of 0.4, 1.2, or 4.1 mg/kgbenzo(b)fluoranthene exhibited a dose-related increase in the incidence of epidermoid carcinomas and pleomorphicsarcoma in the lung and thorax. Equivocal incidences of lung adenomas and hepatic adenomas and hepatomas werereported in mice administered intraperitoneal injections of 126 jag benzo(b)fluoranthene/mouse on days I, 8, and 15of age (LaVoie et al., 1987 cited in IRIS, 2/93). Injection site sarcomas were observed in mice administeredsubcutaneous injections of benzo(b)fluoranthene (2.6 mg total dose) over 2 months (Lacassagne et al., 1963 cited inATSDR, 1990). Benzo(b)fluoranthene was positive for complete carcinogenesis and initiation in mouse skin-painting assays (Wynder and Hoffmann, 1959; LaVoie et al., 1982; Amin et al., 1985 cited in IRIS, 2/93). Based onthese data, EPA has classified benzo(k)fluoranlhene as B2 "probable" human carcinogen. Using a PEF of 0.1 andthe benzo(a)pyrene slope factor of 1.2E+01 (mg/kg/day)-1, Cal EPA has established oral and inhalation slopefactors of 1.2E+00 (mg/kg/day)-1 for benzo(b)fluoranthene (Cal EPA, 1992).

Dibenz(a,h)anthracene (CASN 53-70-3). U.S. EPA has calculated an oral slope factor of 7.3E+00 (mg/kg/day)-1for dibenz(a,h)anthracene, based on its relative toxicity to benzo(a)pyrene. Dibenz(a,h)anthracene has beenclassified as a B2 probable human carcinogen. Cal EPA has established an oral and inhalation slope factor of 4.1(mg/kg/day)-1 (Cal EPA, 1992).

Acenaphthylene (CASN 208-96-8). Dermal application of acenaphlhylene (0.25 percent) did not cause tumordevelopment in a lifetime study in mice (Cook, 1932). While no control was used in this study, other PAHs testeddid result in skin tumor formation. EPA has classified acenaphthylene as a class D carcinogen; not classifiable as tohuman carcinogenicily (IRIS, 2/93).

Anthracene (CASN 120-12-7). EPA has listed anthracene as a class D carcinogen; not classifiable as to humancarcinogenicity due to lack of human data and inadequate animal bioassay data (IRIS, 1995).

Phenanthrene (CASN 85-01-8). Two skin painting assays were negative for complete carcinogenic activity; 1 outof 5 mouse skin painting assays was positive for initiation (IRIS, 2/93). Tumorigenic activity was not detectedfollowing intraperitoneal injection of phenanthrene (0.25 mg total dose) on days 1, 8, and 15 after birth (Buening etal.. 1979 cited in IRIS, 2/93). A single subcutaneous injection of 40 |jg phenanthrene in albino mice was not overtlytumorigenic (Grant and Roe, 1963 cited in IRIS, 2/93). No tumors were reported in mice receiving a singlesubcutaneous injection of 5 mg phenanthrene (Steiner, 1955 cited in IRIS, 2/93). EPA has classified phenanthreneas a class D carcinogen; not classifiable as to human carcinogenicity.

TETRACHLOROETHENE(CAS RN 127-18-4)

Tetrachloroethene (PCE) is a man-made substance widely used for dry cleaning fabrics and textiles and for metal-degreasing operations. It is also used as a starting material for making other chemicals and is used in some consumerproducts. PCE enters the environment mostly by evaporating into the air during use, but it can also enter theenvironment by migrating from disposed sewage sludge or factory waste, and by leaching or evaporating fromstorage and waste sites.


PCE is rapidly and completely absorbed following inhalation or ingestion by both humans and animals. In humanspulmonary uptake of PCE is proportional to ventilation rate, duration of exposure, and (at lower atmosphericconcentrations of PCE) to the concentrations of PCE in the inspired air (Hake and Stewart, 1977 cited in ATSDR,1990).

By contrast, dermal absorption of vapors of PCE in both humans and animals is insignificant. In human subjectsfitted with a full facepiece respirator to prevent inhalation, only 1.0 percent of a dose that would have been expectedto be inhaled was absorbed through the skin (Riihimake and Pfaffli, 1978 cited in ATSDR, 1990). An in vivo dermal

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absorption rate of 0.24 mg/cm /h in mice and an in vitro dermal absorption rate of 0.0055 mg/cm /h in rats has beenreported (Tsuruta, 1975 cited in ATSDR, 1990). Regardless of the route of exposure, most of the absorbed PCE isexcreted unchanged in exhaled air.

Once absorbed, physiologically based pharmacokinetic models indicate that PCE is largely distributed to fat tissue(Guberan and Fernandez, 1974 cited in ATSDR, 1990). This has been confirmed by experimental observation inanimals. Following exposure of rats to 200 ppm PCE vapor for 5 days, PCE was distributed primarily to adiposetissue, especially the perirenal fat (Savolainen et al., 1977 cited in ATSDR, 1990); and, following gavageadministration of PCE to pigs, PCE was concentrated mainly in subcutaneous fat (Vemmer et al., 1984 cited inATSDR, 1990). There is also evidence that once absorbed, PCE is able to cross the placenta and distribute to thefetus and amniotic fluid (Ghantous et al., 1986 cited in ATSDR, 1990).

As noted by Travis et al. (1989), the metabolic pathways of PCE are still speculative, but there is convincingevidence that the principal site of metabolism is the hepatic microsomal cytochrome P-450 system. The first productof this system is thought to be a highly reactive, epoxide intermediate, 1,1,2,2-tetrachloroethene oxide, which thenrearranges to form PCE's most prominent metabolite, trichloroacetic acid (TCA). There is evidence that the epoxideintermediate binds to cellular macromolecules. Both the epoxide and the ultimate metabolite, TCA, have beenindicated as putative carcinogenic moieties (Travis et al., 1989). This metabolic pathway has been shown to besaturable. This means that the rate of production of these toxic metabolites is limited by the activity of themetabolizing enzymes.

In addition to this primary TCA pathway, PCE is believed to be metabolized also by secondary pathways thatproduce other principal metabolites, oxalic acid and C02 (Travis et al., 1989). These pathways are not believed tobe saturable.

Acute Toxicity

Acute inhalation exposure to levels of PCE above 100 to 200 ppm in humans results in eye and upper respiratoryirritation, headache, dizziness, and drowsiness (ATSDR, 1990). An inhalation LC5Q value of 5,200 ppm PCE formice and oral LD^ values of 3,835 and 3,005 mg/kg for male and female rats, respectively, have been reported(Friberg et al., 1953; Hazen et al., 1986 cited in ATSDR, 1990). Longer exposures to oral doses above 1,000 mg/kg5 days/week result in death in rats (NCI, 1977 cited in ATSDR, 1990). Decreased longevity in mice and rats results

induce protein droplet nephropathy bind to gamma-2u globulin, yielding a complex that is more resistant to theproteolytic enzymes in the lysosomes, leading to the accumulation of the complex in the tubule cells and subsequentnephropalhy. Gamma-2u globulin has not been found in immature male rats, female rats, or humans (Alden, 1986cited in ATSDR, 1990). If PCE induces nephropathy by the suggested mechanism, the absence of gamma-2uglobulin in humans raises the question of the relevance to humans of the PCE-induced kidney lesions in male rats.

Cardiotoxicity. There are few reported cases of PCE-associated cardiotoxicity. A case study describing a 24-yearold male who experienced skipped heart beats within one month after starting work in a dry-cleaning operationsuggests an association of PCE with effects on the heart, but the man described may have been an unusually sensitiveindividual (Abeden et al., 1980 cited in ATSDR, 1990). It was hypothesized that exposure to PCE may havesensitized the myocardium to endogenous epinephrine. In an experiment in dogs, however, inhalation exposure tohigh levels of PCE failed to sensitize the heart to epinephrine (Reinhardt et al., 1973 cited in ATSDR, 1990). Incontrast, intravenous administration of PCE enhanced myocardial sensitivity to an exogenous epinephrine challenge(Kobayashi et al., 1982 cited in ATSDR, 1990).

Immunotoxicity. Exposure of mice to 50 ppm PCE for 3 hours increased their susceptibility to bacterial respiratoryinfection (Aranyi et al., 1986 cited in ATSDR, 1990), suggesting that PCE may have an immunotoxic effect. Thereare no data on the potential immunotoxicity of PCE in humans.


Developmental studies have been conducted in rats and mice (one study) exposed to PCE by inhalation. The resultsof these studies indicate that PCE is fetotoxic, but not teratogenic, at concentrations that are also maternally toxic(ATSDR, 1990). This means that developmental toxicity resulting from direct effects of PCE is not easilydiscernible from developmental toxicity resulting from changes occurring in nature. Felotoxicity was usuallyexpressed by decreased fetal weight and delayed skeletal ossification. These effects have been associated withexposures greater than or equal to 300 ppm. Gestational exposure of rats to higher concentrations of PCE (900 ppm)were associated with minor behavioral and neurochemical alterations in some offspring, but this may also be areflection of maternal nutritional deprivation rather than a direct effect of PCE (Nelson et al., 1980 cited in ATSDR,1990).


Limited information is available regarding the reproductive effects of inhaled PCE in animals (ATSDR, 1990).Abnormal sperm were observed in mice exposed to 500 ppm; however, definitive evidence that PCE or itsmetabolites or impurities reached the germinal tissue and actually damaged DNA is not available (Beliles et al.,1980, cited in ATSDR, 1990). Although the results of a dominant-lethal assay with rats were negative (Beliles et al.,1980, cited in ATSDR, 1990), it should be recognized that this is a relatively insensitive assay that is generallythought to measure gross chromosome damage (EPA, 1985a cited in ATSDR, 1990).

Genotoxicitv

Tetrachloroethene itself has not been clearly shown to be a mutagen (ATSDR, 1990). Certain commercial andtechnical preparations have induced positive responses in the Ames bacterial test, a yeast recombogenic assay, ahost-mediated assay, and DNA repair assays, but the responses were weak and required high concentrations of thechemica,! and no clear dose-response relationships could be established (ATSDR, 1990). The ATSDR considers thatthere is inadequate information to classify PCE as either nonmutagenic or mutagenic (ATSDR, 1990).

TOLUENE(CAS RN 108-88-3)

Toluene is a colorless liquid used as a solvent, raw material, or thinner in chemical, rubber, paint, and drugindustries. It is naturally occurring in crude oil and the tolu tree. Toluene is insoluble, but moderately volatile, inwater. Toluene is sufficiently volatile that the majority of the toluene in the environment exists in air (ATSDR,1989).


Toluene is rapidly absorbed following inhalation and less rapidly following ingestion. Absorption of toluene throughthe skin is less rapid and more limited. Up to 96 percent of an inhaled dose may be retained, of that 20 percent willbe excreted unchanged, and 85 percent will be metabolized by the liver.

Because of toluene's lipophilic properties, the highest concentrations of toluene are achieved in the fatty tissues.Immediately after inhalation toluene was found in body fat, bone marrow, spinal nerves, spinal cord, and whitematter of the brain; lesser amounts were found in the blood, kidney, and liver (Bergman, 1979 cited in ATSDR,1989). Very high concentrations of nonvolatile radioactivity, suggesting a toluene conjugate, were found in thekidney and liver.

Toluene is converted to benzyl alcohol by cytochrome P-450 enzymes, rapidly oxidized to benzoic acid by the mixedfunction oxidases of the liver, and finally conjugated with glycine or hippuric acid prior to excretion by the kidney.

Sixty to 75 percent of an absorbed dose of toluene is excreted by the kidney as hippuric acid conjugate (Ogata et al.,1970 cited in ATSDR, 1989). The majority of a dose is eliminated 12 hours after exposure. The half-life for toluenein the adipose tissue of humans has been estimated at 0.5 to 2.7 days (Carlsson and Ljungquist, 1982 cited inATSDR, 1989).

Acute Toxicitv

The majority of loxicity information on toluene is derived from inhalation exposure studies; there are few or nostudies on the effects of oral or dermal exposure to toluene in humans or animals. CNS effects, irritation of therespiratory tract, disturbance of vision, nausea, cardiac effect, and possibly death have been observed in humans andanimals following acute inhalation exposures to toluene. The severity of the symptoms increased with the level ofexposure (ATSDR, 1989). In monkeys, cognitive function and motor abilities were impaired following acuteinhalation exposure to concentrations below that at which ataxia and tremors were observed (Hartman et al., 1984cited in ATSDR, 1989). Acute oral toxicity of toluene has been studied in rats; very high doses were necessary toachieve death (Kimura et al., 1971 cited in ATSDR, 1989).


Information on the toxicity of toluene in humans is derived from epidemiologic studies of solvent abusers oroccupationally-exposed workers. Chronic exposure is associated with CNS effects and impaired neuromuscularfunction; permanent damage has been reported in long-time abusers of toluene (ATSDR, 1989). Toluene has beenextensively studied in animals, usually by the inhalation route of exposure. As with humans, the predominate toxiceffects of toluene in animals are on the CNS. Oral administration of toluene for 13 weeks or 6 months wasassociated with minimal toxicity (NTP, 1989; Wolf et al., 1956). Toluene was associated with abnormal skinconditions in humans and was irritating to animal skin following dermal application (EPA, 1983; Wold et al., 1956;Hazleton Laboratories, 1962).

dysfunction is severe enough to result in death. Chronic exposure to high levels have been reported to result inpermanent CNS effects, such as ataxia, tremors, atrophy, impaired speech, hearing, and vision, and alterations inEEC activity (Devathasan et al., 1984; King et al., 1981; Suzuki et al., 1983 cited in ATSDR, 1989).

In mice and rats, the extent of CNS damage was correlated with depressed function (Bruckner and Peterson, 1981cited in ATSDR, 1989). In addition, nystagmus and disturbances in the vestibular and opto-oculomotor systemswere reported in rats exposed to toluene (Tham et al., 1982; Larsby et al., 1986 cited in ATSDR, 1989). These datasuggest the cerebellum is a target site of toluene. Hippocampal theta wave activity was also disrupted, suggesting aneffect on the area of the brain responsible for the integration of information from sensory tissues and organs withresponses from visceral and motor control areas (Naaisuno, 1986 cited in ATSDR, 1989). Changes in the levels ofbrain neurotransmitters have been reported in animals exposed to toluene (Honma et al., 1982; Ikeda et al., 1986;Arito et al., 1985 cited in ATSDR, 1989). Finally, brain weight and total phospholipid content were decreasedfollowing inhalation toluene exposure in rats (Kyrklund et al., 1987 cited in ATSDR, 1989), while increased relativebrain weight and brain necrosis were observed following oral toluene exposure in mice and rats (NTP, 1989 cited inATSDR, 1989). Toluene may also exert a toxic effect on the auditory system in animals (Pryor et al., 1984; Johnsonet al., 1988; Wood et al., 1983 cited in ATSDR, 1989). The CNS is considered a target organ of toluene toxicity.


Adverse developmental effects have been reported to occur in humans following in utero exposure. An increasedincidence of neural tube defects was observed in children exposed to mixed solvents (including toluene) in utero(Holmberg, 1979). An increase in defects of the urinary tract was associated with children whose mothers wereexposed to aromatic solvents, the majority of which were identified as toluene (McDonald et al., 1987 cited in IRIS,2000). Other developmental effects were reported in 7 children whose mothers were chronic solvent abusers(Goodwin et al., 1988; Hersh et al., 1985; cited in ATSDR, 1989).

In animals, toluene is clearly a developmental toxicant. Skeletal anomalies, retarded skeletal development, low fetalweights, and maternal toxicity were observed following acute exposure to toluene in mice, rabbits, and rats(Courtney, et al., 1986; Ungvary and Tatrai, 1985; Ungvary, 1985; cited in ATSDR, 1989). Toluene was associatedwith adverse developmental effects when rats were exposed to toluene for 24 but not 6 hours on days 6 through 15 ofgestation (API, 1978 cited in ATSDR, 1989). Fetal weight and skeletal retardation were observed in mice thatinhaled 1,000 mg/m toluene on days 6 to 15 of gestation (Ungvary and Tatrai, 1985 cited in IRIS, 2000).Embryolethality was reported in mice exposed to 780, 1,300, or 2,600 mg/kg/day on days 6 through 15 of gestation(Nawrot and Staples, 1979 cited in IRIS, 2000). Fetotoxicity, fetal malformations, and maternal toxicity werereported in pregnant rats exposed to 1,000 or 1,500 mg/ m 24 hours/day on days 9 through 14 or 1 through 8 or 1through 21 of gestation (Hudak and Ungvary, 1978 cited in IRIS, 2000). In a two-generation exposure study, growthof the offspring from both generations was inhibited following exposure to 2,000 ppm toluene. Decreased open fieldactivity was observed in mice receiving oral doses of toluene pre- and postnatally; however, this decrease wasinversely related to dose administered (Kostas and Hotchin, 1981 cited in ATSDR, 1989). In a study specificallydesigned to evaluated neurobehavioral effects, no toluene-related adverse findings were observed in the offspring ofhamsters or rats following inhalation of 800 mg/m 6 hours/day on gestational days 14 through 20 (rats) or 6 through11 (hamsters) (DaSilva et al., 1990 cited in IRIS, 2000). No developmental effects were observed when pregnantmice were administered oral doses up to 2,350 mg/kg/day (Seidenberg et al., 1986; Smith, 1983 cited in ATSDR,1989).


No reliable data on the reproductive effects of toluene in humans were available.

In animal studies, toluene was without effect on dominant lethal mutations in sperm cells, pre- or post-implantationloss of embryos, or histopalhology of the ovaries or testes (API, 1981; CUT, 1980 cited in ATSDR, 1989). Inaddition, in a two-generation exposure study, toluene had no effect on survival or reproductive parameters (API,

XYLENE(CAS RN 1330-20-7)

Xylene, as a man-made chemical, is produced from petroleum and coal in which it is also naturally occurring.Xylene is also produced during forest fires. There are three isomeric forms of xylene: meta-, ortho-. and para-.These forms occur together in a mixture; "total xylenes" is used to refer to the three forms of xylene. Mixed xylenerefers to mixtures containing the 3 isomers and smaller amounts of other chemicals, particularly ethylbenzene.Xylene is a solvent with wide industrial applications; its wide environmental distribution is primarily from industrialsources and automobile exhaust. Xylene evaporates into air where it persists for several days prior to decompositionby sunlight. Although xylene does not mix well with water, it can leak into soil, surface water, or ground waterwhere it may remain for 6 months or longer.


Detection of xylene metabolites in the urine following inhalation or ingestion by humans indicates xylene isabsorbed. The level of metabolites in the urine increases in proportion to exposure and ventilatory rates (Ogata et al.,1970; Riihimaki and Pfaffli, 1978; Riihimaki et al, 1979; Sedivec and Flek, 1976; Senczuk and Orlowski, 1978;Wallen et al, 1985; Astrand, 1982; Astrand et al, 1978; Engstrom and Bjurstrom, 1978; Riihimaki and Savolainen,1980 cited in ATSDR, 1990). Absorption following inhalation is biphasic: an initial fast phase, followed byestablishment of an equilibrium between inhaled xylene and blood. Dermal absorption studies indicate that xylenedoes penetrate the skin. Dermal absorption is estimated to be O.I to 0.2 percent that of inhalation exposure(Riihimaki and Pfaffli, 1978 cited in ATSDR, 1990). In animal studies, absorption following inhalation is presumedbased on the observed effects on microsomal enzymes (ATSDR, 1990). Eighty-seven to 92 percent of an oral doseof xylene is absorbed by animals (Bray et al, 1949 cited in ATSDR, 1990).

Xylenes are highly soluble in blood (Astrand, 1982 cited in ATSDR, 1990) and are primarily distributed to theadipose tissues. In humans, approximately 5 to 10 percent of an absorbed dose is accumulated in the adipose tissues;this amount may increase following exercise or chronic occupational exposure (Astrand, 1982; Engstrom andBjurstrom, 1978; Riihimaki et al, 1979 cited in ATSDR, 1990). In animals, xylene is distributed to lipid-rich tissues,e.g., brain, blood, fat, and well-perfused organs, e.g., liver and kidney (Ghantous and Danielsson, 1986; Carlsson,1981 cited in ATSDR, 1990). Xylene has been demonstrated to cross the placenta in the mouse, and accumulationappeared to be related to the animals metabolic rate (Ghantous and Danielsson, 1986; Savolainen et al, 1979 cited inATSDR, 1990).

Metabolism of xylene in humans and animals is similar. Biotransformation proceeds through oxidation by themicrosomal mixed function oxidases, followed by conjugation with glycine. This metabolic pathway is the sameregardless of isomeric form, route of administration, administered dose, or duration of exposure. Althoughglucuronic acid conjugates, in addition to glycine conjugates (ATSDR, 1990), were detected in animals. This shiftmay owe to the much larger doses that animals received compared to human exposures.

The major route of elimination of xylene in humans is via the kidney; approximately 95 percent of an inhaled dose isexcreted as urinary metabolites. Elimination in humans is biphasic: a rapid distribution of xylene into the tissuecompartments followed by slower elimination from muscles and adipose tissue. Renal excretion, which is presumedto involve active tubular secretion, is not rate-limiting (ATSDR, 1990).

Acute Toxicitv

Short-term xylene exposure results in a variety of nervous system effects in humans and animals. Temporarysymptoms of nausea, vomiting, and gastric discomfort have been reported in workers exposed to xylene vapors(Goldie, I960; Klaucke et al, 1982; Nersessian et al, 1985 cited in ATSDR, 1990). In animals, the respiratorysystem may also be affected. High levels of exposure produce unconsciousness and death in both animals andhumans. One of three men died following inhalation of paint fumes containing 10,000 ppm xylene (Morley et al.

was also observed following oral administration of 750 to 1,500 mg/kg/day; histopathology of these kidneysindicated early chronic nephropathy (NTP, 1986; Hazelton Labs, 1988; Condie et al., 1988 cited in ATSDR, 1990).These data, and the fact that the kidney is exposed to high concentrations of xylene and xylene metabolites, suggestthe kidney might be a target of xylene loxicity.

Neurotoxicity. Acute inhalation exposure of xylenes in humans has been associated with impaired short-termmemory, impaired reaction time, performance decrements in numerical ability, and alterations in equilibrium andbody balance (ATSDR, 1990). Exposure to 64 to 150 ppm g-xylene did not cause neurological effects in humans(Hake et al., 1981; Olson et al., 1985 cited in ATSDR, 1990). Accidental ingestion of an unknown quantity of xyleneproduced coma in 1 human (Recchia et al., 1985 cited in ATSDR, 1990). Epidemiologic studies are difficult toevaluate due to concurrent exposure to other solvents; however, these occupational studies and case reports suggestthat chronic inhalation exposure to xylene or solvent mixtures containing xylene may be associated with headache,nausea, dizziness, fatigue, agitation, confusion, tremors, labored breathing, incoordination, and sensitivity to noise(Arthur and Curnock, 1982; Goldie, 1960; Hipolito, 1980; Klaucke et al., 1982; Morley et al., 1970; Nersesian et al.,1985; Roberts et al., 1988 cited in ATSDR 1990). This conclusion is strengthened by the observation ofneurotoxicity findings in animal studies. Rats, mice, and gerbils exhibited narcosis, prostration, incoordination,tremors, muscular spasms, labored breathing, behavioral changes, hyperreactivity to stimuli, elevated auditorythresholds, hearing loss, changes in brain enzyme activity, and biochemical changes in the brain following inhalationof mixed xylene or xylene isomers (ATSDR, 1990). These effects were observed following a single exposure lastinga few hours, or after repeated daily exposures for several weeks. While these data suggest the CNS is a possibletarget organ of toxicity, the neurologic effects of life-time inhalation exposure to low levels of xylenes has not beenstudied. Following oral administration of xylene neurologic symptoms were limited to hyperactivity, convulsions,salivation, and epistaxis; no adverse histopathological effects were observed (NTP, 1986; Hazleton Labs, 1988 citedin ATSDR, 1990).


There are no reliable human studies for assessing the relationship of xylene exposure and developmental effects. Allof the available studies have involved concurrent exposure to other solvents (ATSDR, 1990).

The developmental effects of inhaled xylenes have been extensively studied in animals. The concentration at whicheffects were observed depended on the composition and concentration of the mixed xylene in addition to the animalstrain and species. Developmental effects consisting of increased incidences of skeletal variations, delayedossification, fetal resorptions, hemorrhages in fetal organs, and decreased fetal body weights were observedfollowing maternal concentrations as low as 12 ppm; frequently these doses were also associated with maternaltoxicity. The incidences of cleft palate were increased and fetal body weights were decreased in the offspring fromrats administered 2,060 mg/kg/day during gestation; this dose was also associated with maternal toxicity, includingdeath (Marks et al., 1982 cited in ATSDR, 1990). Oral administration of 2,000 mg/kg/day m-xylene was withouteffect (Seidenberg, 1986 cited in ATSDR, 1990). Decreased brain enzyme activity was reported following dermaladministration of xylene to rats (Mirkova et al., 1979 cited in ATSDR, 1990). The fetotoxic effects observed mayhave been secondary to maternal toxicity.


There are no human studies on the reproductive effects of xylene.

No effect on reproduction parameters was observed in rats exposed to 500 ppm or less mixed xylene duringpremaling, mating, pregnancy, and lactation (Bio/dynamics, 1983 cited in ATSDR, 1990). There were no effects onreproductive organs following oral administration of mixed xylene or xylene isomers (NTP, 1986; Hazelton, 1988cited in ATSDR, 1990).

ZINC(CAS RN 7440-66-6)

Metallic zinc and various zinc salts are used extensively in the metal plating industry. Zinc is used in galvanizing,electroplating, dry cells, alloying, soldering fluxes, smoke generators, and zinc oxide is used as a pigment for paintsand cosmetics. The toxicity of zinc depends on the particular form and salt of zinc and on the route ofadministration. Zinc is an essential nutrient and is found in a number of metalloenzymes including carbonicanhydrase, carboxypeptidase, alcohol dehydrodgenase, lactic dehydrogenase and alkaline phosphatase (Klaassen etal., 1986).

Zinc salts are used therapeutically as topical astringents, antiseptics, and emetics. Zinc undecylenate is commonlyused in athlete's foot preparations and zinc pyridinethione is a common ingredient in antidandruff shampoos. Zinc isoften used as a carrier salt for insulin preparations and bactericides.

Acute Toxicity

Acute exposure to zinc salts via ingestion results in nausea and gastrointestinal irritation. The most common form ofacute zinc intoxication is in the inhalation of metal fumes. Zinc fume intoxication results in ocular, mucousmembrane, and dermal irritation, malaise, fatigue, headache, blurred vision, and muscle cramping with pulmonaryedema at very high concentrations. Upper respiratory tract irritation and sore throat are common symptoms of fumeexposures. Acute, lethal exposure results in severe pulmonary edema followed by cyanosis, coma and death(Proctor, 1989).


The EPA has calculated a RfD for oral exposure to zinc of 3.0E-01 mg/kg/day based on decreases in erythrocylesuperoxide dismutase (ESOD) levels observed in adult females (IRIS, 2000).

Chronic Toxicity

In brass foundry workers, zinc oxide was found to produce zinc fume fevers due to inhalation of fumes duringmanufacturing processes. Clinical recovery is usually complete in 24 to 48 hours. Chronic exposure to fumes has notshown adverse effects (NIOSH, 1986). Chronic exposure often results in bronchial pneumonia.

A fine salt of strong mineral acids can be corrosive to the skin and irritating to the gastrointestinal tract. However, theuse of zinc oxide in many topical dermatologic preparations has demonstrated a low potential for skin irritation. Anoccupational dermatitis "Oxidepox" was reported in alloy workers exposed to zinc oxide particulates (ATSDR,1989). It was concluded that zinc oxide particulates and lack of personal hygiene contributed to the minor eruptions.These were reversible with the institution of good hygiene practices (Clayton, 1981).

Gastrointestinal disturbances with peptic-ulcer-like symptoms have been supported in workers employed for years inbrass foundries (Clayton, 1981). Clinically latent liver dysfunction has been reported in workers exposed to highlevels of zinc oxide. Evidence of peptic ulcers was felt to be indicative of gastrointestinal tract damage (NIOSH,1986).

Zinc is a nutritionally essential metal and deficiency results in several health consequences. Excessive exposure tozinc is relatively uncommon and requires very heavy exposure.

APPENDIX B

QUANTITATION OF UPPER CONFIDENCE LIMITS

For each compound detected within a medium, the 95% UCL of the arithmetic mean was calculated assuming thedata are distributed lognormally. The 95% UCL values have been used to represent exposure point concentrationsfor chemicals selected as chemicals of potential concern, unless the 95% UCL exceeds the maximum concentrationdetected on-site. In this case, according to EPA guidance (1992), the maximum is used as the estimate of theexposure point concentration (EPC). The exception to this was for the screening level ecological assessment andsurface soils samples (except in the case of iron analyses in surface soil samples) where the maximum concentrationwas used.

CALCULATIONS

For each chemical detected within a medium, the following methods were used:

1. Data Set Preparation

1.1 Determine the maximum detected concentration of each compound of potential concern in the sourcearea for each media.

1.2 For non-detect results, calculate '/z the SQL (sample quantitation limit)

'/z SQL = SQL X 0.5

where:

SQL = Sample quantitation limits, as presented in the analytical data in the RI Report.

1.3 Compare the '/2 SQL value to the maximum detected concentration. Eliminate Vi SQL values thatexceed the maximum detected concentration.

1.4 Prepare a data set table of the positive detects and Vi SQLs as evaluated above for each media ofinterest.

2. Calculation of 95% Upper Confidence Limits. To calculate the lognormal 95% UCL requires the data set tobe transformed (using the natural log) before the 95% UCL can be calculated. For each compound:

2.1 Transformed data set. Calculate the natural log of each value in the data set.

2.2 Calculate the arithmetic average of the transformed data set.

2.3 Calculate the standard deviation of the transformed data set.

2.4 Calculate the variance for the transformed data set.

2.5 Determine the number of data points or sample size (n) included in the data set (i.e., the positivedetects and Vi SQLs). The sample size (n) for each chemical will vary depending upon the number ofsamples collected for the particular medium.

APPENDIX B (CONTINUED)

QUANTITATION OF UPPER CONFIDENCE LIMITS

2.6 Determine the H value statistic. This value is taken from statistical tables for a one-sided upper 95%confidence limit on a log-normal mean (geometric mean; the geometric mean was used to estimate the"true" mean) as presented in Gilbert (1987). The standard deviation and the number of data points (n)are required to determine this value.

2.7 Calculate the lognormal 95% UCL:

EXP[AVE + (0.5 VAR) + ((STD*Hv) / SQRT (n-1))]

where:

EXP - Inverse base e logarithm.AVE = Arithmetic average of the transformed data set.STD = Standard deviation of the transformed data set.VAR = Variance (STD*STD)H value = As determined in 2.6 above.SQRT = Square root.n = Sample size

2.8 Determine the value to be used for the exposure point concentration. Compare the 95% UCL value tothe maximum detection concentration. The 95% UCL value is used unless it exceeds the maximumdetected concentration.

APPENDIX C

EQUATIONS USED FOR QUANTITATION OF EXPOSURE ESTIMATES

Incidental Ingestion of Contaminants in Soil

Intake (mg/kg-day) = CS x IngR x CF x EF x EDBWxAT

CS = Contaminant concentration in soil (mg/kg)IngR = Ingestion rate (mg soil/day)

CF = Conversion factor (10"* kg/mg)EF = Exposure frequency (days/year)ED = Exposure duration (years)BW = Body weight (kg)AT = Averaging Time (period over which exposure is averaged - days)

Dermal Contact with Contaminants in Soil

Absorbed Dose (mg/kg-day) = CS x CF x SA x AF x ABS x EF x EDBWxAT

CS = Contaminant concentration in soil (mg/kg)

CF = Conversion factor (10"6 kg/mg)

SA = Skin surface area available for contact (cm2/event)

AF = Adherence factor of soil (mg/cm2-day)ABS = Skin absorption factor (unilless)EF = Exposure frequency (days/year)ED = Exposure duration (years)BW = Body weight (kg)AT = Averaging Time (period over which exposure is averaged - days)

Inhalation of Fugitive Soil Emissions

Intake (mg/kg-day) = CS x InhR x EF x ED x (1/PEF + 1/VF)B W x A T

CS = Contaminant concentration in soil (mg/kg)

InhR = Inhalation rate (m3/day)EF= Exposure frequency (days/year)ED = Exposure duration (years)

PEF = Particulate emission factor (m3/kg)

VF = Volatilization factor (nVVkg)BW = Body weight (kg)AT = Averaging Time (period over which exposure is averaged - days)

APPENDIX C (CONTINUED)

EQUATIONS USED FOR QUANTITATION OF EXPOSURE ESTIMATES

Ingestion of Contaminants in Groundwater

Intake (mg/kg-day) = CS x IngR x EF x EDBWxAT

CS = Contaminant concentration in groundwater (mg/L)IngR = Ingestion rate (L/day)EF = Exposure frequency (days/year)ED = Exposure duration (years)BW = Body weight (kg)AT = Averaging Time (period over which exposure is averaged - days)

Dermal Contact with Contaminants in Groundwater

Absorbed Dose (mg/kg-day) = CS x CF x PC x ET x SA x EF x EDB W x A T

CS = Contaminant concentration in groundwater (mg/L)CF = Conversion factor (m/100 cm x IOOOL/m3)PC = Permeability constant (cm/hr)ET = Exposure time (hours/day)SA = Skin surface area available for contact (cm2/event)AF = Adherence factor of soil (mg/cm2-day)ABS = Skin absorption factor (unitless)EF = Exposure frequency (days/year)ED = Exposure duration (years)BW = Body weight (kg)AT = Averaging Time (period over which exposure is averaged - days)

Inhalation of VOCs from Groundwater During Household Use

Intake (mg/kg-day) = CS x InhR x K x EF x EDB W x A T

CS = Contaminant concentration in groundwater (mg/L)InhR = Inhalation rale (m3/day)K = Volatization factor (L/m3)EF = Exposure frequency (days/year)ED = Exposure duration (years)BW = Body weight (kg)AT = Averaging Time (period over which exposure is averaged - days)

JE^mXAPPENBIX D

SUPPORTING DATA FOR DETERMINING EXPOSURE POINT CONCENTRATIONS

Volatilization Factor (VF) :

Calculation of Chemical Specific Soil to Air Volatilization Factors

VF (m3/kg) =

Where: Q/C =DA =T =pb =

DA (cm2/s) =

Q_C x (3 .14xD A xD l / 2 x 10"4 (m2/cm2)

(2 x pb x DA)

Inverse of the mean concentration at center of square source (g/m2-s per kg/m3)Apparent Diffusity (cm2/s) (See equation below for calculating DA).Exposure Interval (s)Dry bulk soil density (g/cm3)

[(Theta_a'0/3 x Dt x H') + (Theta_wI0/3 x Dw)]/n2

ParameterTheta_aTheta_w

D,H'Dw

npbps

Kd

Koc

foe

[(pb x Kd) + Theta_w + (Theta_a x H')]

Parameter Description (units')Air filled soil porosity (Lair/Lsoil)Water filled soil porosity (Lwater/Lsoil)Diffusivity in air (cm2/s)Dimensionless Henry's Law ConstantDiffusivity in water (cm2/s)Total soil porosity (Lpore/Lsoil)Dry soil bulk density (g/cm3)Soil particle density (g/cm3)Soil-water partition coefficient (cm3/g)

Soil organic carbon-water partition coefficient (cm3/g)

Organic carbon content of soil (g/g)

Parameter ValueCalculated

Chemical-specificChemical-specificChemical-specificChemical-specific

0.381.652.65

Calculated

Chemical-specific

0.006

Sourcea

bba

a

NoteTheta_a = n-Theta_w

n = 1 - (Pb/ps)

Kd = K,,,. x foc

Sources(a) All formulas and default values obtained from U.S. EPA, 1996,

Soil Screening Guidance Technical Document, 2nd Edition, EPA/540/R95/128.

(b) Site-specific estimate based on soil types.

APPENDIX D

SUPPORTING DATA FOR DETERMINING EXPOSURE POINT CONCENTRATIONS


Volatilization Factor (VF):

VF (m7kg) =

Where: Q/C =

DA =T =pb =

DA (cmVs) =

ParameterTheta_aTheta_w

DIH'Dw

npbps

Kd

Q_C x (3.14 x DA xT)"2 x 10"4 (m:

(2 x pb x DA)

Inverse of the mean concentration at center of square source (g/m2-s perkg/m3)Apparent Diffusity (cm2/s) (See equation below for calculating DA).Exposure Interval (s)Dry bulk soil density (g/cm3)

'0/3[ ( T h e t a _ a x D i x H ' ) (Theta.w 10/3 x DJ]/n2

[(pb x K<,) + Theta_w + (Theta_a x H')]

Parameter Description (units)Air filled soil porosity (Lair/Lsoil)Water filled soil porosity (Lwater/Lsoil)Diffusivity in air (cm2/s)Dimensionless Henry's Law ConstantDiffusivity in water (cm2/s)Total soil porosity (Lpore/Lsoil)Dry soil bulk density (g/cm3)Soil particle density (g/cm3)Soil-water partition coefficient (cm3/g)

Soil organic carbon-water partition coefficient (cm3/g)Organic carbon content of soil (g/g)

Parameter ValueCalculated

Chemical-specificChemical-specificChemical-specificChemical-specific

0.381.652.65

Calculated

Chemical-specific0.006

Source Notea Theta_a =

b n =ba

Kd =

a

_a = n-Theta_w

1 - (Pb/Ps)

(a) All formulas and default values obtained from U.S. EPA, 1996,Soil Screening Guidance Technical Document, 2nd Edition, EPA/540/R95/128.

(b) Site-specific estimate based on soil types.

Table D-l


Clinton FMGP SiteClinton, Iowa

Chemical

VOLATILESBenzeneBromodichloromethaneBromoformBromomethaneCarbon tetrachlorideChlorobenzeneChloroformChloromethaneDibromochloromethane1,1-Dichloroethane

1,2-Dichloroethane1,1-Dichloroethenetrans- 1 ,2-Dichloroethene1 ,2-Dichloropropanecis- 1 ,3-DichIoropropenetrans- 1 ,3-DichloropropeneEthylbenzeneMethylene chloride1 , 1 ,2,2-TetrachloroethaneTetrachloroetheneToluene1,1,1 -Trichloroethane1 , 1 ,2-Trichloroethane

Koc

(I/kg)

62 A55 A126 A9 A

152 A224 A53 A5.5 E63.1 A53 A

38 A65 A38 A47 A27 A27 b

204 A

10 A79 A

265 A140 A135 A75 A

Kd

(I/kg)

3.7E-013.3E-017.6E-015.4E-029.1E-011.3E+003.2E-013.3E-023.8E-013.2E-01

2.3E-013.9E-012.3E-OI2.8E-011.6E-01I.6E-011.2E+006.0E-024.7E-011.6E+008.4E-018.1E-014.5E-01

HLC

(atm

9.9E-03

H'

(unitless)

2.28E-013.21E-022.19E-022.56E-011.25E+001.52E-011.50E-01

3.21E-022.30E-011.67E-011.07E+003.85E-011.15E-017.26E-017.26E-013.23E-018.98E-021.41E-027.54E-012.72E-017.05E-013.74E-02

H'

(unitless)

2.3E-01 A3.21E-02 A2.19E-02 A2.6E-01 A1.3E+00 A1.5E-01 A1.5E-01 A4.1E-01 E3.2E-02 A

2.30E-01 A

1.7E-01 d1.07E+00 A3.9E-01 A1.15E-01 A7.26E-01 A7.26E-01 b3.2E-01 A8.98E-02 A1.4E-02 A7.5E-01 A2.7E-01 A7.1E-01 A3.7E-02 A

Di

(cm2/sec)

8.80E-02 A2.98E-02 A1.49E-02 A7.28E-02 A7.80E-02 A7.30E-02 A1.04E-01 A1.06E-01 f1.96E-02 A7.42E-02 A7.36E-02 d9.00E-02 A7.07E-02 A7.82E-02 A6.26E-02 A6.26E-02 b7.50E-02 A

1.01E-01 A7.10E-02 A7.20E-02 A8.70E-02 A7.80E-02 A7.80E-02 A

Dw

(cm2/sec)

9.80E-06 A1.06E-05 A1.03E-05 A1.21E-05 A8.80E-06 A8.70E-06 AI.OOE-05 A1 .23E-06 f1 .05E-05 A1.05E-05 A

1.13E-05 d1.04E-05 A1.19E-05 A8.73E-06 Al.OOE-05 Al.OOE-05 b7.80E-06 A1.17E-05 A7.90E-06 A8.20E-06 A8.60E-06 A8.80E-06 A8.80E-06 A

DA

(cm2/sec)

5.39E-042.97E-055.39E-061.28E-031.16E-031.04E-044.76E-043.01E-031.78E-055.11E-044.66E-042.13E-039.68E-043.01E-041.74E-031.74E-032.44E-046.61E-042.36E-054.21E-043.32E-047.58E-047.08E-05

Table D-l



Chemical

TrichloroetheneVinyl chlorideTotal Xylenes

Koc

d/kg)

94 A18.6 A249 A

Kd

d/kg)

5.6E-011.1E-011.5E+00

HLC(atm

H'(unitless)

4.22E-011.11E+002.76E-01

H'(unitless)

4.2E-01 A1.1E+00 A2.8E-01 A

Di(cm2/sec)

7.90E-02 A1.06E-01 A7.80E-02 A

Dw

(cm2/sec)

9.10E-06 A1.23E-06 A8.74E-06 A

DA(cm2/sec)

6.34E-044.62E-031.82E-04

Notes:All Equations and parameters used in the calculations for DA and VF are listed under VF Parameters.Values for total xylenes are an average of o-xylene, m-xylene, and p-xylene.

A U.S. EPA, 1996, "Soil Screening Guidance Technical Document", 2nd Edition, EPA/540/R95/128.E Information obtained from Electronic Handbook of Risk Assessment Values (EHRAV), 1999.

b - 1,3-Dichloropropene used as a surrogate because no data was available for analyte.c - ethylbenzene value used as a surrogate because no data was available for analyted - 1,2-Dichloroethene cis value used as a surrogate because no data was available for analytef - vinyl chloride value used as a surrogate because no data was available for analyte

AAG/

[Madl_serverl/jobs/l217/431/newdata/rnasterclinton/VF Parameters (Tbl 7- Sheet l).xls]

J """.

• le E-l

Summary of Soils Exposure Point Concentrations and Maximum Detections

AnalyticalParameters

VOCsBenzeneBromodichloromethaneBromoformBromomethaneCarbon TetrachlorideChlorobenzeneChloroethaneChloroformChloromethaneDibromochloromethane1,1-Dichloroethane1,2-Dichloroethane1,1-Dichloroethenetrans- 1 ,2-Dichloroethene1 ,2-Dichloropropanecis- 1 ,3-Dichloropropenetrans- 1 ,3-DichloropropeneEthylbenzeneMethylene Chloride1 ,1 ,2,2-TetrachlorethaneTetrachloroetheneToluene1,1,1 -Trichloroethane1 , 1 ,2-TrichlororethaneTrichloroetheneVinyl ChlorideXylenes, Total

PAHsAcenaphtheneAcenaphthyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k)fluorntheneChrysene3ibenzo(a,h)anthraceneFluorantheneFluorene[ndeno(l ,2,3-cd)pyreneNaphthalenePhenanthrenePyrene

Acid Extractable4-Chloro-3-Methylphenol2-Chorophenol2,4-Dichlorophenol2,4-Dimethylphenol2,4-Dinitrophenol2-Methyl-4,6-Dinitrophenol2-Nitrophenol4-NitrophenolPentachlorophenolPhenol2,4,5-Trichlorophenol

MetalsArsenicChromiumCopperIronLeadNickelZincCyanide

PCBsArochlor 1016Arochlor 1221Arochlor 1232Arochlor 1242Arochlor 1248Arochlor 1254Arochlor 1260

Soils (mg/kg)Surface Soil

IPC

EPC, 0-1 ft

3.40E-02

2.80E-02

4.20E-02

3.70E-02

2.60E+00

1.20E+001.52E+011.21E+019.40E+007.10E+003.50E+001.26E+01

3.93E+012.50E+005.70E+002.60E+006.40E+003.27E+01

2.63E+01

1.70E+021.40E+017.80E+012.53E+041.78E+021.94E+011.31E+031.79E+01

7.32E+01

MaximumDetection

3.40E-02

2.80E-02

4.20E-02

3.70E-02

2.60E+00

1.20E+001.52E+011.21E+019.40E+007.10E+003.50E+001.26E+01

3.93E+012.50E+005.70E+002.60E+006.40E+003.27E+01

2.63E+01

1.70E+021.40E+017.80E+014.66E+045.51E+021.94E+011.31E+031.79E+01

7.32E+01

Allied

EPC, 0-1 ft

1.12E-01

3.40E-025.00E-03

4.40E-02

4.50E-02

9.64E+01

4.20E+001.43E+015.60E+00

-6r80E+004.30E+003.90E+001.28E+01

2.80E+008.10E+003.30E+005.00E-023.59E+OI4.30E+00

8.45E+011.13E+026.79E+021.09E+053.94E+024.49E+012.86E+031.51E+01

3.50E-01

1.90E-019.00E-02

MaximumDetection

1.12E-01

3.40E-025.00E-03

4.40E-02

4.50E-02

9.64E+01

4.20E+001.43E+015.60E+006.80E+00-4.30E+003.90E+001.28E+01

2.80E+008.10E+003.30E+005.00E-023.59E+014.30E+00

8.45E+011.13E+026.79E+022.03E+051.47E+034.49E+012.86E+031.51E+01

3.50E-01

1.90E-019.00E-02

Subsurface SoilIPC

l-10ft

5.30E+01

1.42E+00

1 .22E+021.01E-01

2.30E+02

5.60E+02

7.56E+031.91E+042.35E+032.50E+028.1IE+024rl-5E+012.08E+022.12E+022.94E+021.27E+015.19E+016.17E+032.29E+021.92E+047.57E+033.07E+01

8.80E+002.14E+015.10E+013.08E+043.40E+023.55E+013.74E+024.59E+01

10-20 ft

1.13E+01

3.44E+00

1.64E+011.11E-01

1.11E+01

5.35E+01

1.21E+031.I7E+031.20E+028.79E+017.45E+01

-5.86E+013.78E+012.00E+019.04E+01

9.82E+022.51E+023.58E+013.16E+035.39E+027.18E+01

4.62E+002.29E+011.97E+011.99E+042.07E+012.06E+017.16E+012.15E+00

Allied

1-10 ft

9.71E+01

2.40E+022.50E+01

1.69E+02

3.09E+02

1.34E+031.05E+033.03E+022.48E+021.68E+021.28E+028.56E+015.36E+015.32E+02

1 .84E+035.49E+026.96E+012.93E+031.37E+031.42E+03

6.79E+012.05E+01

5.92E+018.30E+011.77E+028.31E+045.97E+026.20E+011.78E+031.75E+02

10-20 ft

9.49E+01

4.95E+012.93E+00

5.00E-038.11E+01

1.02E+02

2.69E+032.69E+031.24E+031.23E+038.22E+025.90E+024.28E+022.57E+021.13E+038.90E+008.75E+032.52E+033.31E+024.83E+035.00E+037.29E+02

1.56E+01

5.77E-01

1.19E+01

3.99E+001.62E+012.78E+011.86E+041.24E+021.85E+011.38E+022.61E+00

Table E-2

Summary of Groundwater Exposure Point Concentrations and Federal MCLs/MCLGs

Chemical Group

VOCsVOCsVOCsVOCsVOCsVOCsVOCs

SVOCsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHs

Acid Extractable OrganicsAcid Extractable Organics

MetalsMetalsMetalsMetalsMetalsMetalsMetals

Inorganics

CASRN

71-43-274-83-956-23-574-87-3100-41-4108-88-31330-20-7108-95-283-32-9

208-96-8120-12-756-55-350-32-8

205-99-1191 -24-2207-08-9218-01-953-70-3

206-44-086-73-7193-39-591-20-385-01-8129-00-0105-67-9108-95-2

7440-38-21 8540-29-97440-50-87439-89-67439-92-17440-02-07440-66-6

57-12-5

Chemical

BenzeneBromomethaneCarbon tetrachlorideChloromethaneEthylbenzeneTolueneXylenes, totalPhenolAcenaphtheneAcenaphthyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluoraniheneBenzo(g,h,i)peryleneBenzo(k)fluorantheneChryseneDibenzo(a,h)anthraceneFluoranlheneFluoreneIndeno( 1 ,2,3-cd)py reneNaphthalenePhenanthrenePyrene2,4-DimethylphenolPhenolArsenicChromium (total)CopperIron^eadNickelZincCyanide

Units

mg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/Lmg/L

Water Table Aquifer andIntermediate Zone

1.19E+OI3.12E-034.90E-043.35E-032.49E+005.60E+003.24E+006.92E-026.47E-012.93E+006.47E-026.82E-047.27E-044.51E-043.12E-041.31E-049.72E-044.90E-068.20E-037.60E-013.01 E-048.79E+009.76E-012.32E-021.73E-016.92E-024.12E-031 .98E-022.14E-023.60E+024.54E-034.33E-028.64E-028.44E-02

MCL

0.005

0.005

0.71

10

0.0002

0.050.11.3*

0.015*

0.2

MCLG

0

0

0.71

10

0

none0.11.3

0

0.2

* Value indicates action level. Copper and lead are regulated by a Treatment Technique that requires systems tocontrol the corrosiveness of their water. If more than 10% of tap water samples exceed the action level, watersystems must take additional steps.

Table E-3

Summary of Mississippi River Sediment Concentrations

ChemicalGroup

METALSMETALSMETALSMETALSMETALSMETALSMETALSMETALSMETALS

PAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsPAHsVOCsVOCs

Chemical

ArsenicChromium

CopperIronLead

NickelNitrogen, Ammonia

SulfateZinc

AcenaphtheneBenzo(a)anthracene

Benzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k) fl uoranthene

ChryseneFluoranthene

Indeno( 1 ,2,3-cd)pyrenePhenanthrene

Methylene chlorideToluene

All Samples

Units

mg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kgmg/kg

Number ofSamples

615053550867687678689

MinimumDetected

Concentration

NDNDNDNDNDNDNDNDND0.3ND0.060.07NDND0.010.04ND0.020.0090.035

MaximumDetected

Concentration

NDNDNDNDNDNDNDNDND0.3ND0.060.2NDND0.010.2ND0.020.0090.067

DetectionFrequency,

%

0.00.00.00.00.00.00.00.00.012.50.014.333.3i0.00.0

1

l'6.728.60.016.712.522.2

Upstream || Downstream |

Mean

2.10E+007.20E+004.95E+007.44E+037.50E+006.70E+002.50E+011.11E+032.50E+014.50E-025.50E-02l.OOE-02l.OOE-02l.OOE-02l.OOE-02l.OOE-023.00E-02l.OOE-02l.OOE-025.00E-03l.OOE-03

StandardDeviation || Mean

1.41E-013.39E+002.76E+006.17E+033.54E+002.40E+007.07E+001.56E+022.12E+014.95E-026.36E-02O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+002.83E-02O.OOE+00O.OOE+00O.OOE+00O.OOE+00

2.67 !

10.7 :10.4

1420011.59.5346.2179.344

0.1070.010.0270.0930.010.010.010.0830.010.0130.0050.012 '

StandardDeviation

1.13E+005.82E+007.10E+009.28E+036.62E+004.04E+002.83E+019.11E+023.03E+011.67E-011.65E-102.89E-029.71E-021.65E-101.65E-101.65E-101.02E-011.65E-105.77E-031.33E-032.35E-02

MR-06

2.40E+001.31E+011.81E+011.55E+041.54E+011.10E+014.70E+013.36E+036.60E+014.40E+009.00E-011.30E+00l.OOE+004.00E-014.00E-019.00E-012.00E-024.00E-011.50E+009.00E-036.70E-02

APPENDIX F

CARCINOGENIC AND NONCARCINOGENIC EXPOSURE AND HEALTHRISK ESTIMATE TABLES

Key to abbreviations used in the tables:

EPC - Exposure Point ConcentrationVF - Volatilization FactorNC - Not Classified as a CarcinogenNT - No Information

Medium: IPC Side Surface SoilLandUse: Current/Future

l e F - 1

Carcinogenic Exposure and Health Risk Estimates

Clinton FMGP Site

Clinton, Iowa

Receptor: On-sile Construction WorkerExposure Pathway: Incidental Ingestion, Dermal Contact, and

Inhalation of Fugitive Dust/Vapors

CHEMICAL OFPOTENTIAL CONCERN

VOCsBenzene

EihylbenzeneTolueneTotal Xylenes

PAHsAcenaptwtene

Anthracene

Bcnzo(a)amhraccnc

Benzo(a)pyrcnc

Benzo(b)fluoranthcm:

Bcnzo(g.h.i)pcrylcneBen/o(k)fluoranihcne

ChryscncFluoranthcncFluoroncIndeno( 1 ,2,3-cd)pyrene

NaphthalenePhenanthicne

l*yrcnc

Acid ExtractablePentachlorophenol

MetalsArsenicChromium VICopper

Iron

LeadNickelZincCyanide

PCBsAroclor 1260

EPC(nig/kg)

3.40E-02

2.80E-024.20E-023.70E-02

2.60E+001.20E+00

1.52E+01

1.21E+OI

9.40E+00

7.10E+003.50E+00

1.26E+013.93E+012.50E+005.70E+00

2.60E+006.40E+003.27E+01

2.63E+01

1.70E+02I.40E+017.80E+012.53E-f04

5.5IE+021.94E+011.31E+03

1.79E+01

7.32E+01

VF(Calculated)

3.48E+03

5.17E+034.43E+035.99E+03

Chronic Dailv Intake Value

mg/kg-dayOral Dermal Inhalation

1.73E-09 2.38E-IO 2.08E-08

1.43E-09 I.96E-10 1.16E-082.14E-09 2.94E-10 2.02E-081.89E-09 2.59E-10 I.32E-08

1.33E-07 2.37E-08 5.52E-096.12E-08 1.09E-08 2.55E-09

7.75E-07 1.39E-07 3.23E-08

6.17E-07 1.10E-07 2.57E-08

4.79E-07 8.57E-08 2.00E-08

3.62E-07 6.47E-08 1.51E-081.78E-07 3.19E-08 7.44E-09

6.43E-07 1.15E-07 2.68E-082.00E-06 3.58E-07 8.35E-08I.27E-07 2.28E-08 5.31E-092.91E-07 5.20E-08 1.21E-08

I.33E-07 2.37E-08 5.52E-093.26E-07 5.83E-08 I.36E-081.67E-06 2.98E-07 6 95E-08

1.34E-06 4.6IE-07 5.59E-08

8.67E-06 3.58E-07 3.61E-077.14E-07 9.82E-09 2.97E-083.98E-06 5.47E-08 I.66E-071.29E-03 1.78E-05 5.38E-052.81E-05 3.86E-07 1.17E-069.89E-07 1 36E-08 4.12E-086.68E-05 9.19E-07 2.78E-06

9.13E-07 1.26E-Q8 3.80E-08

3.73E-06 7.19E-07 1.56E-07

Slope Factors

kg-duy/mgOral Dermal Inhalation

5.50E-02 5.50E-02 2.90E-02

NC NC NCNC NC NCNC NC NC

NC NC NCNC NC NC

7.30E-OI 7.30E-01 3.10E-01

7.30E+00 7.30E+00 3.IOE+00

7.30E-01 7.30E-01 3.10E-01

NC NC NC7.30E-02 7.30E-02 3.10E-02

7.30E-03 7.30E-03 3.IOE-03NC NC NCNC NC NC

7.30E-01 7.30E-01 3.IOE-OI


I.20E-OI 1.20E-01 Nl

1.50E+00 I.50E+00 1.50E+01NI NI 4.10E+01NC NC NCNC NC NCNI NI NINI NI NINC NC NCNC NC NC

2.00E+00 2.00E+00 2.00E+00

Cancer Risks

Oral Dermal Inhalation

9.54E-11 I.31E-11 6.04E-10NI NI NINI NI NINI NI NI

NI NI NINI NI NI

5.66E-07 l.OIE-07 l.OOE-08

4.50E-06 8.05E-07 7.97E-08

3.50E-07 6.25E-08 6.19E-09

NI NI NI1.30E-08 2.33E-09 2.3 IE- 10

4.69E-09 8.38E-10 8.30E-11Nl NI NINI NI NI

2.12E-07 3.79E-08 3.75E-09

NI NI NINI NI NINI NI NI

1.61E-07 5.53E-08 NI

1.30E-05 5.36E-07 5.42E-06Nl NI 1.22E-06NI NI NINI NI NINI NI NINl NI NINI Nl NINI NI NI

7.47E-06 1.44E-06 3.11E-07

Total Risks

%ofTotal Total

7.12E-10 0

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

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

6.77E-07 2

5.39E-06 15

4.19E-07 1

O.OOE+00 0I.56E-08 0

5.61 E-09 0O.OOE+OO 0O.OOE+00 02.54E-07 1


2.16E-07 1

1.90E-05 521.22E-06 3

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

9.21E-06 25

Total Risk by Route 2.63E-05 3.04E-OS

Total Risk

7.05E-06

3.6E-OS

AAG/

tMadl_serverl/jobs/1217/431/anaIyticaldatabaseynewdata/clintonmaster/IPCSurfCancCW(TblW-9).xls]Page 1 of 2

^^^ab

Medium: 1PC Side Surface SoilLandUse: Current/Future

Table F-2

Noncarcinogenic Exposure and Health Risk Estimates


Receptor: On-site Construction WorkerExposure Pathway: Incidental Ingestion, Dermal Contact, and



VOCsBenzene

EthylbenzeneTolueneTotal Xylenes

PAHsAcenaphiheneAnthraceneBenzo(a)amhraccneBenzo(a)pyrene

Benzo(b)(luoranihcne3enzo(g,h.i)perylcneBenzofWfluoramheneChryseneRuoranihencFluorcne

[ndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanihrcncPyrene

Acid Extractable

Pentachlorophenol

MetalsArsenicChromium VICopperIron


PCBsAroclor 1260

EPC(mR/kg)

3.40E-02

2.80E-024.20E-023.70E-02

2.60E+001.20E+001.52E+011.21E+OI

9.40E+007.IOE+003.50E+001.26E+013.93E+012.50E+005.70E+00

2.60E+00

6.40E+003.27E+OI

2.63E+01

1.70E+02I.40E+OI7.80E+012.53E+04

5.51E+021.94E+011.31E+03

1.79E+OI

7.32E+01

VF(Calculated)

3.48E+03

5.17E+034.43E+035.99E+03

Chronic Daily Intake Value


1.21E-07 1.67E-08 I.46E-06

9.99E-08 I.37E-08 8.09E-071.50E-07 2.06E-08 1.42E-061.32E-07 1.82E-08 9.24E-07

9.28E-06 1.66E-06 3.87E-074.28E-06 7.66E-07 1.78E-075.43E-05 9.70E-06 2.26E-064.32E-05 7.72E-06 1.80E-06

3.36E-05 6.00E-06 1.40E-062.53E-05 4.53E-06 1.06E-061.25E-05 2.23E-06 5.21E-07

4.50E-05 8.04E-06 1.87E-06I.40E-04 2.5IE-05 5.85E-068.92E-06 1.60E-06 3.72E-072.03E-05 3.64E-06 8.48E-07

9.28E-06 1.66E-06 3.87E-072.28E-05 4.08E-06 9.52E-071.I7E-04 2.09E-05 4.86E-06

9.39E-05 3.23E-05 3.91E-06

6.07E-04 2.50E-05 2.53E-055.00E-05 6.87E-07 2.08E-062.78E-04 3.83E-06 I.16E-05

9.04E-02 I.24E-03 3.77E-031.97E-03 2.70E-05 8.I9E-056.92E-05 9.52E-07 2.89E-064.68E-03 6.43E-05 1.95E-04

6.39E-05 8.79E-07 2.66E-06

2.61E-04 5.03E-05 1.09E-05

Reference Doses


3.00E-03 3.00E-03 I.70E-03I.OOE-01 I.OOE-01 2.86E-01

2.00E+00 2.00E+00 1.14E-012.00E+00 2.00E+00 NI

6.00E-OI 6.00E-OI Nl3.00E+00 3.00E+00 NI

NI NI NINI Nl NINI NI NINI NI NINI NI NINI NI NI

4.00E-01 4.00E-01 NI4.00E-01 4.00E-OI NI

NI NI NI

2.00E-02 2.00E-02 8.57E-04NI NI NI

3.00E-01 3.00E-01 NI

3.00E-02 3.00E-02 NI

3.00E-04 3.00E-04 NI3.00E-03 6.00E-05 2.86E-053.70E-02 1.11E-02 NI

3.00E-01 4.50E-02 NINl NI NI

2.00E-02 8.00E-04 NI3.00E-01 3.00E-01 NI

2.00E-02 2.00E-02 NI

2.00E-05 2.00E-05 NI

Hazard Quotient


4.05E-05 5.56E-06 8.57E-04

9.99E-07 1.37E-07 2.83E-067.50E-08 1.03E-08 1.24E-056.60E-08 9.08E-09 NI

1.55E-05 2.76E-06 NI1.43E-06 2.55E-07 NI

NI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

3.5IE-04 6.27E-05 NI2.23E-05 3.99E-06 NI

NI NI Nl4.64E-04 8.29E-05 4.51E-04

NI NI NI3.89E-04 6.9$E-05 NI

3.13E-03 1.08E-03 NI

2.02E+00 8.34E-02 NI1.67E-02 1.15E-02 7.29E-027.52E-03 3.45E-04 NI

3.01E-01 2.76E-02 NINI NI NI

3.46E-03 1.19E-03 NI1.56E-02 2.14E-04 NI

3.19E-03 4.39E-05 NI

1.31E+OI 2.5IE+00 NI

Total Hazard Ouotienl

%ofTotal Total

9.03E-04 0

3.97E-06 01.25E-05 07.51E-08 0

1.82E-05 01.68E-06 0



O.OOE+00 04.I3E-04 02.63E-05 0O.OOE+00 0

9.98E-04 0O.OOE+00 04.59E-04 0

4.20E-03 0

2.11E+00 121.01E-01 1

7.87E-03 03.29E-01 2O.OOE+00 04.65E-03 01.58E-02 0

3.24E-03 0

1.56E+01 86

Total Hazard Index by Route 1.S4E+01

Total Hazard Index

2.64E+00 7.42E-02

1.8E+01

AAG/

[Mad;_serverWjobsn2n/431/analyucaldaiabase/newdata/clintonmaster/IPCSur(NCCW(TblW-10).xls5 Page 1 of 1

Medium: IPC Side Subsurface Soil (1-10 ft.)LandUsc: Current/Future

Table F-3


Clinton FMGPSite

Clinton, Iowa




VOCsBenzene

ChloromethaneElhylbenzeneMeihylene ChlorideTolueneToial Xylcnes

PAHsAccnaphtheneAcenaphthylencAnthracene

Bcnzo(a)amhracencBenzo(a)pyreneBcnzo(b)fluoramheneBcnzo(g,h,i)pcrylencBenzodOfluoranihcncChrysene

Dibenz(a,h)amhraccneFluoranlheneFluorenc

lndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanlhrcncI"yrene

MetalsArsenic

Chromium VICopperIronLeadNickel

ZincCyanide

EPC(mg/kg)

5.30E+011.42E-fOO1.22E+02I.01E-01

2.30E+02

5.60E+02

7.56E+03I.9IE+04

2.35E+032.50E+02

8.11E+024.15E+012.08E+022.12E+02

2.94E+02

1.27E+015.19E+OI6.17E+03

2.29E+021.92E+047.57E+033.07E+01

8.80E+002.14E+01S.10E+013.08E+043.40E4023.55E+013.74E+024.59E+01

VF(Calculated)

3.48E+031.47E+035.17E+033.14E+034.43E+03

5.99E+03



2.70E-06 3.72E-07 3.25E-057.24E-08 9.96E-09 2.05E-066.22E-06 8.55E-07 5.04E-055.I5E-09 7.08E-10 6.85E-081.17E-05 1.61E-06 1.11E-042.86E-05 3.93E-06 2.00E-04

3.86E-04 6.89E-05 1.61E-059.74E-04 1.74E-04 4.06E-051.20E-04 2.I5E-05 5.00E-06

1.27E-05 2.28E-06 5.31E-07

4.14E-05 7.39E-06 1.72E-062.12E-06 3.78E-07 8.82E-081.06E-05 1.90E-06 4.42E-071.08E-05 I.93E-06 4.50E-07

1.50E-05 2.68E-06 6.25E-07

6.48E-07 1.16E-07 2.70E-082.65E-06 4.73E-07 1.10E-073.I4E-04 5.62E-05 1.31E-05

1.17E-05 2.09E-06 4.87E-079.79E-04 1.75E-04 4.08E-053.86E-04 6.90E-05 1.61E-05

1.57E-06 2.80E-07 6.52E-08

4.49E-07 I.85E-08 1.87E-08

1.09E-06 1.50E-08 4.55E-082.60E-06 3.58E-08 1.08E-071.57E-03 2.16E-05 6.54E-051.73E-05 2.38E-07 7.22E-07

1.81E-06 2.49E-08 7.54E-081.91E-05 2.62E-07 7.95E-07

2.34E-06 3.22E-08 9.75E-08

Slope Factors

kg-day/mgOral Dermal Inhalation

5.50E-02 5.50E-02 2.90E-021.30E-02 1.30E-02 6.30E-03

NC NC NC7.50E-03 7.50E-03 1.65E-03

NC NC NCNC NC NC


7.30E-01 7.30E-01 3.10E-01

7.30E+00 7.30E+00 3.10E+007.30E-01 7.30E-01 3.IOE-OI

NC NC NC7.30E-02 7.30E-02 3.10E-02

7.30E-03 7.30E-03 3.IOE-037.30E+00 7.30E+00 3.10E+00

NC NC NCNC NC NC

7.30E-OI 7.30E-01 3.10E-01NC NC NCNC NC NCNC NC NC

1.50E+00 I.50E+00 I.50E+01

Nl NI 4.10E+01NC NC NCNC NC NCNI NI NlNI NI NlNC NC NCNC NC NC

Cancer Risks


1.49E-07 2.04E-08 9.41 E-079.41E-10 1.29E-10 1.29E-08

Nl NI NI3.86E-11 5.31E-12 1.13E-10

NI NI NINI NI NI


9.31E-06 1.66E-06 1.65E-07

3.02E-04 5.40E-05 5.34E-061.54E-06 2.76E-07 2.73E-08

NI Nl NI7.89E-07 1.41 E-07 I.40E-08

I.09E-07 1.96E-08 1.94E-094.73E-06 8.45E-07 8.36E-08

Nl NI NINI NI NI

8.52E-06 1.52E-06 1.51 E-07NI NI NINI NI NINI NI . NI

6.73E-07 2.78E-08 2.80E-07

NI NI I.86E-06NI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

Total Risks

%ofTotal Total

1.11E-06 01.40E-08 0

O.OOE+00 0I.57E-10 0

O.OOE+00 0

O.OOE+00 0


1.11E-05 33.61E-04 921 .85E-06 0

O.OOE+00 09.44E-07 0

1.31 E-07 05.66E-06 1O.OOE+00 0O.OOE+00 0

1.02E-05 3O.OOE+00 0O.OOE+00 0

O.OOE+00 0

9.8 1 E-07 01.86E-06 0


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

Total Risk by Route 3.28E-04 5.85E-05

Total Risk

7.94E-06

3.9E-04

AAG/

(Mad 1 .server 1 /jobs/1217/431 /analytical database/newdata7clinlonmaster/IPCSsubCancCW(0-10)(Tbl W-11 J.xls]

Page 1 of 2

Medium: IPC Side Subsurface Soil (1-10 ft.)Landllse: Current/Future

Table F-4



Receptor: Construction WorkerExposure Pathway: Incidental Ingestion, Dermal Contact, and



VOCs

BenzeneChloro methane

EthylbenzeneMelhylene ChlorideTolueneToial Xylencs

PAHsAcenaphiheneAcenapluhylencAnthraceneBenzo(a)anihraceneBenzo(a)pyreneBenzo(b)fluoraniheneBenzo(g.h.i)perylencBenzo(k)fluoran{hcncChryseneDibenz(a.h)amhraccne^luoranlhcncFluoreneIndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanlhrenePyrene

MetalsArsenicChromium VICopperIronLeadNickelZincCyanide

EPC(mg/kg)

5.30E+OI1.42E+00

1.22E+02

1.01E-012.30E+025.60E+02

7.56E+031.91E+042.35E+032.SOE+028.11E+024.15E+012.08E+022.12E+022.94E+021.27E4015.19E+016.17E+032.29E+021 .92E+047.57E+033.07E+01

8.80E+002.14E+OI5.IOE+013.08E+043.40E+023.55E+OI3.74E+024.59E+01

VF(Calculated)

3.48E+031.47E+03

5.17E+03

3.14E+034.43E+035.99E+03



1.89E-04 2.60E-05 2.27E-035.07E-06 6.97E-07 I.44E-04

4.35E-04 5.99E-05 3.53E-03

3.61E-07 4.96E-08 4.80E-068.21 E-04 I.13E-04 7.75E-032.00E-03 2.75E-04 1.40E-02

2.70E-02 4.82E-03 1 . 1 2E-036.82E-02 1.22E-02 2.84E-038.40E-03 1.50E-03 3.50E-048.92E-04 1.60E-04 3.72E-052.89E-03 5.17E-04 1.21E-041.48E-04 2.65E-05 6.17E-067.42E-04 I.33E-04 3.09E-057.57E-04 1.35E-04 3.15E-05I.05E-03 1.88E-04 4.37E-054.53E-05 8.10E-06 1.89E-061.85E-04 3.3IE-05 7.72E-062.20E-02 3.93E-03 9.17E-048.I7E-04 1.46E-04 3.4IE-056.85E-02 1.23E-02 2.86E-032.70E-02 4.83E-03 1.I3E-031.10E-04 1.96E-05 4.57E-06

3.14E-05 1.30E-06 1.31E-067.64E-05 1.05E-06 3.18E-06

.82E-04 2.50E-06 7.59E-06

.10E-01 1.51E-03 4.58E-03

.21E-03 1.67E-05 5.06E-05

.27E-04 1.74E-06 5.28E-06

.33E-03 1.84E-05 5.56E-05

.64E-04 2.25E-06 6.83E-06

Reference Doses


3.00E-03 3.00E-03 1.70E-03NI NI 8.60E-02

l.OOE-01 l.OOE-OI 2.86E-01

6.00E-02 6.00E-02 8.57E-012.00E+00 2.00E+00 1.14E-012.00E+00 2.00E+00 NI

6.00E-01 6.00E-01 NINI NI NI

3.00E+00 3.00E+00 NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

4.00E-02 4.00E-02 NI4.00E-02 4.00E-02 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI NI3.00E-02 3.00E-02 NI

3.00E-04 3.00E-04 NI3.00E-03 6.00E-05 2.86E-053.70E-02 I.1IE-02 NI3.00E-01 4.50E-02 NI

NI NI NI2.00E-02 8.00E-04 NI3.00E-OI 3.00E-01 NI2.00E-02 2.00E-02 NI

Hazard Ouotient


6.31E-02 8.67E-03 1.34E+00NI NI 1.67E-03

4.35E-03 5.99E-04 1.23E-02

6.01 E-06 8.26E-07 5.59E-064.10E-04 5.64E-05 6.78E-029.99E-04 1.37E-04 NI

4.50E-02 8.04E-03 NINI NI NI

2.80E-03 5.01 E-04 NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

4.63E-03 8.28E-04 NI5.50E-01 9.84E-02 NI

NI NI NI3.43E+00 6.13E-01 3.33E+00

NI NI NI3.65E-03 6.53E-04 NI

1.05E-01 4.32E-03 NI2.55E-02 1.75E-02 1.11E-0!4.92E-03 2.26E-04 NI3.66E-01 • 3.36E-02 NI

NI NI NI6.34E-03 2.18E-03 NI4.45E-03 6.12E-05 NI8.19E-03 I.I3E-04 NI


%ofTotal Total

1.41E-tOO 141.67E-03 0

1.73E-02 0

1.24E-05 06.83E-02 11.14E-03 0

5.30E-02 1O.OOE+00 03.30E-03 0O.OOE+00 0O.OOE+00 0O.OOE+OO 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 05.46E-03 06.49E-OI 6O.OOE+00 07.37E+00 72O.OOE+00 04.3IE-03 0

I.09E-01 11.54E-01 25.15E-03 04.00E-OI 4O.OOE+00 08.51E-03 04.51E-03 08.30E-03 0

Total Hazard Index by Route 4.62E+00

Total Hazard Index

7.88E-01 4.86E+00

l.OE+01

AAG/

[Madl_serverl/jobs/1217/43I/analyticaldatabase/newdata/clintonmaster/IPCSsubNCCW(0-10)(TblW-12).xls]

Page 1 of 1

Medium: IPC Side Subsurface Soil (10-20 fl.)LandUse: Current/Future

Table F-S






VOCsBenzeneChloromethane

ElhylbenzeneMeihylene ChlorideToluene.Toial Xylcnes

PAHsAcenaphlheneAcenaptuhylene

Anthracene

Benzo(a)antnraccncBcnzo(a)pyreneBenzo(b)riuoranlhcne

Benzo(g,h,i)perylcneBenzo(k)fluoramhcneChryscneFluoranlhene^luorene

[ndeno( 1 ,2,3-cd)pyreneNaphthalene^henanlhrene^yrene

MetalsArsenicChromium VI

CoppertonLead

NickelZincCyanide

EPC(mg/kg)

1.13E+013.44E+00

1.64E+011.11E-011.11E+015.35E+OI

I.2IE+031.17E+031.20E+02

8.79E+01

7.45E+015.86E+013.78E+012.00E+01

9.04E+019.82E+022.51E+023.58E+01

3.16E+035.39E+027.18E+01

4.62E+002.29E+01

1.97E+011.99E+04

2.07E+012.06E+01

7.16E+012.15E+00

VF(Calculated)

3.48E+031.47E+03

5.I7E+033.14E+034.43E+035.99E+03



5.76E-07 7.92E-08 6.92E-061.75E-07 2.41E-08 4.97E-06

8.36E-07 1.I5E-07 6.77E-06

5.65E-09 7.77E-10 7.52E-085.66E-07 7.78E-08 5.34E-062.73E-06 3.75E-07 I.91E-05

6.18E-05 1.IOE-05 2.58E-065.98E-05 1.07E-05 2.49E-066.I2E-06 1.09E-06 2.55E-07

4.48E-06 8.01 E-07 1.87E-073.80E-06 6.79E-07 I.58E-072.99E-06 5.34E-07 1.25E-071.93E-06 3.45E-07 8.03E-081.02E-06 I.82E-07 4.25E-08

4.61 E-06 8.24E-07 1.92E-075.01E-05 8.95E-06 2.09E-061.28E-05 2.29E-06 5.33E-071.83E-06 3.26E-07 7.61E-081.61E-04 2.88E-05 6.71 E-062.75E-05 4.91 E-06 1.15E-063.66E-06 6.54E-07 I.53E-07

2.36E-07 9.72E-09 9.82E-09

.I7E-06 .60E-08 4.86E-08

.01 E-06 .38E-08 4.19E-08

.02E-03 .40E-05 4.23E-05

.05E-06 .45E-08 4.39E-08

.05E-06 .45E-08 4.39E-083.6JE-06 5.02E-08 1.52E-071.10E-07 1.5IE-09 4.57E-09

Slope Factors


5.50E-02 5.50E-02 2.90E-021.30E-02 1.30E-02 6.30E-03

NC NC NC7.50E-03 7.50E-03 1.65E-03

NC NC NCNC NC NC


7.30E-01 7.30E-01 3.10E-017.30E+00 7.30E+00 3.10E+007.30E-01 7.30E-01 3.10E-01

NC NC NC7.30E-02 7.30E-02 3.10E-02

7.30E-03 7.30E-03 3.10E-03NC NC NCNC NC NC

7.30E-01 7.30E-01 3.IOE-OI


I.50E+00 1.50E+00 1.50E+01

NI NI 4.10E+01NC NC NCNC NC NCNI NI NINI NI NINC NC NCNC NC NC

Cancer Risks


3.17E-08 4.36E-09 2.01E-072.28E-09 3.14E-10 3.13E-08

NI NI NI4.24E-11 5.83E-12 1.24E-10

NI NI NINI NI NI


3.27E-06 5.85E-07 5.79E-08

2.77E-05 4.96E-06 4.91 E-072.18E-06 3.90E-07 3.86E-08

NI NI NI7.44E-08 1.33E-08 1.32E-09

3.37E-08 6.02E-09 5.95E-10NI NI NINI NI NI

1.33E-06 2.38E-07 2.36E-08NI NI NINI NI NINI NI NI

3.53E-07 1.46E-08 1.47E-07NI NI 1.99E-06


Total Risks

%ofTotal Total

2.37E-07 I3.39E-08 0

O.OOE+00 01.72E-10 0



3.91E-06 9

3.32E-05 752.61 E-06 6O.OOE+00 08.91E-08 0

4.03E-08 0O.OOE+00 0O.OOE+00 01.59E-06 4


5.15E-07 11.99E-06 5



Total Risk by Route 3.50E-OS 6.20E-06

Total Risk

2.78E-06

4.4E-05

AAG/

[Madl_serverl/jobs/12l7/431/analylicalda[abase/newdaia/clintonmaster/IPCSsubCancCW(10-20)(TblW-13).xls]

Page 1 of 1

Medium: IPC Side Subsurface Soil (10-20 ft.)LandUse: Current/Future

Table F-6






VOCsBenzeneChloromethaneEthylbenzeneMethylene ChlorideTolueneFoul Xylencs

PAHsAcenaphiheneAcenaphlhyleneAnthraceneBenzo(a)anlhraceneBenzo(a)pyreneBcnzo(b)lluoraniheneBenw>(fi,h,i)perylencBenzo(k)fluoranlheneChryscncFluoranlhene^uorcncIndeno( 1 ,2.3-cd)pyreneNaphthalenePhcnanihrenePyicne


EPC(mg/kg)

1.13E+013.44E+001.64E+011.IIE-01I.HE-fOI5.35E+01

1.21E+03I.17E+03I.20E+028.79E+017.45E+015.86E+013.78E+OI2.00E+019.04E+019.82E+022.51E-f023.58E+013.16E+035.39E+027.18E+01

4.62E+002.29E+011.97E+011.99E+042.07E+012.06E+017.16E+012.15E+00

VF(Calculated)

3.48E+03I.47E+035.17E+033.14E+034.43E+035.99E+03

Chronic Dailv Intake Valuemg/kg-day


4.03E-05 5.55E-06 4.84E-04I.23E-05 1.69E-06 3.48E-045.85E-05 8.05E-06 4.74E-043.96E-07 5.44E-08 5.26E-063.96E-05 5.45E-06 3.74E-04I.9IE-04 2.63E-05 1.34E-03

4.33E-03 7.73E-04 .80E-044.19E-03 7.48E-04 .74E-044.28E-04 7.66E-05 .78E-053.14E-04 5.61E-05 .31E-052.66E-04 4.75E-05 .11E-052.09E-04 3.74E-05 8.72E-061.35E-04 2.41E-05 5.62E-067.I4E-05 1.28E-05 2.97E-063.23E-04 5.77E-05 1.34E-053.5IE-03 6.27E-04 I.46E-048.96E-04 1.60E-04 3.73E-05I.28E-04 2.28E-05 5.32E-06I.13E-02 2.02E-03 4.70E-041.92E-03 3.44E-04 8.02E-052.56E-04 4.58E-05 1.07E-05

1.65E-03 6.80E-07 6.87E-078.I6E-05 1.12E-06 3.40E-067.04E-05 9.69E-07 2.93E-067.11E-02 9.77E-04 2.96E-037.38E-05 1.01E-06 3.08E-067.37E-05 1.01E-06 3.07E-062.55E-04 3.51E-06 1.06E-057.68E-06 1.06E-07 3.20E-07

Reference Dosesmg/kg-day


3.00E-03 3.00E-03 1.70E-03NI NI NI

l.OOE-01 l.OOE-01 2.86E-OI6.00E-02 6.00E-02 8.57E-012.00E+00 2.00E+00 1.I4E-012.00E+00 2.00E+00 NI

6.00E-01 6.00E-01 NINI NI MI

3.00E+00 3.00E+00 NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

4.00E-01 4.00E-OI NI4.00E-01 4.00E-01 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI Nl3.00E-02 3.00E-02 NI

3.00E-04 3.00E-04 NI3.00E-03 6.00E-05 2.86E-053.70E-02 1.I1E-02 NI3.00E-01 4.50E-02 Nl


Hazard Ouotienl


1.34E-02 1.85E-03 2.85E-01NI NI Nl

5.85E-04 8.05E-05 I.66E-036.59E-06 9.07E-07 6.14E-06I.98E-05 2.72E-06 3.27E-039.55E-05 1.31E-05 NI

7.21E-03 1.29E-03 NINI NI Nl

1.43E-04 2.55E-05 NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

8.76E-03 1.57E-03 NI2.24E-03 4.00E-04 NI

NI NI NI5.64E-01 1.01E-01 5.48E-01

NI NI NI8.54E-03 1.53E-03 NI

5.50E-02 2.27E-03 NI•2.72E-02 I.87E-02 1.I9E-01

I.90E-03 8.73E-05 Nl2.37E-01 2.17E-02 NI

Nl NI NI3.68E-03 1.27E-03 NI8.52E-04 1.17E-05 NI3.84E-04 528E-06 NI

Total Hazard Ouotienl%of

Total Total

3.00E-01 IJO.OOE+00 02.32E-03 0I.36E-05 03.30E-03 01.09E-04 0

8.50E-03 0O.OOE+00 0I.68E-04 0

O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 01.03E-02 12.64E-03 0O.OOE+00 01.21E+00 59O.OOE+00 01.01E-02 0

5.72E-02 31.65E-01 81.99E-03 02.59E-01 13O.OOE+00 04.95E-03 08.63E-04 03.89E-04 0

Total Hazard Index by Route 931E-01

Total Hazard Index

1.52E-01 9.57E-01

2.0E+00

AAG/

[Madl_serverl/jobs/I2l7/43l/analyucaldatabase/newdata/clintonmaster/IPCsubNCCW(10-20)(TblW-14).xls]

Page 1 of 1

^âble

Medium: Allied Side Surface SoilLandUse: Current/Future

Table F-7


Clinton FMGP Site

Clinton, Iowa


Inhalation of Fugitive DustA'apors


VOCsBenzeneEthylbenzeneMethylene ChlorideTolueneTotal Xylenes

PAHsAcenaphthcncAnthracene3enzo(a)anthracene3enzo(a}pyrene3cnzo(b)fluoranlhenc


3enzo(k)nuoranlheneChrysenePluoranlhenc

Fluorene

Indeno(l,2.3-cd)pyreneNaphthalenePhenanihrene'yrene

Metals

ArsenicChromium VICopperônêad

NickelZincCyanide

PCBsAroclor 1242

Aroclor 1254

Aroclor 1260

EPC(mg/kg)

1.12E-013.40E-025.00E-034.40E-024.50E-02

9.64E+01

4.20E+001.43E+015.60E+006.80E+004.30E+00

3.90E+001.28E+012.80E+00

8.10E+00

3.30E+005.00E-023.59E+014.30E+00

8.45E+011.I3E+026.79E+021 .09E+051.47E+03

4.49E+012.86E+031.51E+01

3.50E-01

1.90E-01

9.00E-02

VF(Calculated)

3.48E+035.I7E+033.I4E+034.43E+035.99E403



5.71E-09 7.85E-10 6.86E-08

1.73E-09 2.38E-10 1.40E-082.55E-10 3.51E-11 3.39E-092.24E-09 3.09E-10 2.12E-082.29E-09 3.16E-10 1.61E-08

4.92E-06 8.79E-07 2.05E-07

2.14E-07 3.83E-08 8.92E-097.29E-07 1.30E-07 3.04E-082.86E-07 5.10E-08 1.I9E-083.47E-07 6.20E-08 1.44E-082.19E-07 3.92E-08 9.14E-09

1.99E-07 3.55E-08 8.29E-096.53E-07 1.17E-07 2.72E-081.43E-07 2.55E-08 5.95E-094.13E-07 7.38E-08 I.72E-08

I.68E-07 3.01E-08 7.0IE-092.53E-09 4.56E-10 I.06E-101.83E-06 3.27E-07 7.63E-082.19E-07 3.92E-08 9.14E-09

4.3IE-06 1.78E-07 1.80E-07

5.76E-06 7.92E-08 2.40E-073.46E-05 4.76E-07 1.44E-065.54E-03 7.61E-05 2.31E-047.50E-05 1.03E-06 3.12E-06

2.29E-06 3.15E-08 9.54E-081.46E-04 2.01 E-06 6.08E-067.70E-07 1.06E-08 3.21E-08

1.78E-08 3.44E-09 7.44E-IO

9.69E-09 1.87E-09 4.04E-104.59E-09 8.83E-10 1.9 IE- 10

Slope Factors


5.50E-02 5.50E-02 2.90E-02

NC NC NC7.50E-03 7.50E-03 1.65E-03

NC NC NCNC NC NC

NC NC NCNC NC NC

7.30E-01 7.30E-01 3.10E-017.30E+00 7.30E+00 3.10E+007.30E-01 7.30E-01 3.10E-01

NC NC NC7.30E-02 7.30E-02 3.10E-027.30E-03 7.30E-03 3.10E-03

NC NC NCNC NC NC

7.30E-01 7.30E-01 3.10E-01NC NC NCNC NC NCNC NC NC

1.50E+00 I.50E+00 1.50E+01NI NI 4.IOE+01NC NC NCNC NC NCNI NI NINI NI MlNC NC NCNC NC NC

2.00E+00 2.00E+00 2.00E+00

2.00E+00 2.00E+00 2.00E+00

2.00E+00 2.00E+00 2.00E+00

Cancer Risks


3.14E-10 4.32E-11 1.99E-09NI NI NI

I.91E-12 2.63E-I3 5.58E-12NI NI NINI NI NI

NI NI NINI NI NI

5.32E-07 9.52E-08 9.42E-092.08E-06 3.73E-07 3.69E-08

2.53E-07 4.52E-08 4.48E-09NI NI NI

1.45E-08 2.60E-09 2.57E-104.76E-09 8.52E-10 8.43E-11

NI NI NINI NI NI

I.23E-07 2.20E-08 2.17E-09NI NI NINI NI NINI NI NI

6.46E-06 2.67E-07 2.69E-06NI NI 9.84E-06NI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

3.57E-08 6.87E-09 1.49E-091.94E-08 3.73E-09 8.07E-109.18E-09 1.77E-09 3.82E-10

Total Risks

%ofTotal Total

2.35E-09 0O.OOE+00 07.75E-12 0O.OOE+00 0O.OOE+00 0

O.OOE+00 0O.OOE+00 06.37E-07 3

2.49E-06 1 13.03E-07 1O.OOE+00 0

I.74E-08 05.70E-09 0O.OOE+00 0O.OOE+00 0

1.47E-07 1O.OOE+00 0O.OOE+00 0

O.OOE+00 0

9.42E-06 419.84E-06 43O.OOE+00 0O.OOE+00 0O.OOE+00 0


4.41E-08 02.39E-08 0

1.13E-08 0


Total Risk 2JE-05

USE-OS

AAG/

[Madl_serverl/|obs/1217/431/analyucaldatabase/newdata/clintonmaster/AlliedSurfCancCW)(TblW-15).xls] Page 1 of 1

Medium: Allied Side Surface SoilLondUse: Current/Future

Table F-8






VOCsBenzeneEthylbenzeneMethylene ChlorideTolueneTotal Xylencs

PAHs

Acenaptuhene

Anthracene

Benzo(a)anthracene

9enzo(a)pyrene

Benzo(b)fluorarithene

Benzo(g,h.i)perylcne

BcnzoQOfluoramhenc

Chrysene

Fluoranthene

^luorenc

indeno(l ,2,3-cd)pyreneNaphthalenePhenanlhrene

?yrene

MetalsArsenicChromium IVCopperron-eadNickelZincCyanide

PCBsAroclor 1242

Aroclor 1254

Aroclor 1260

EPC(mg/kg)

1.12E-013.40E-025.00E-034.40E-024.50E-02

9.64E+014.20E+001.43E+015.60E+006.80E+004.30E+003.90E+001.28E+012.80E+008.10E+003.30E+005.00E-023.59E+014.30E+00

8.45E+011.13E+026.79E+021.09E+05I.47E+034.49E+012.86E+031.51E+01

3.50E-OI1.90E-019.00E-02

VF(Calculated)

3.48E+035.17E+033.14E+034.43E+035.99E+03



4.00E-07 5.50E-08 4.80E-061.21E-07 1.67E-08 9.83E-071.78E-08 2.45E-09 2.37E-071.57E-07 2.I6E-08 I.48E-061.6IE-07 2.21E-08 1.12E-06

3.44E-04 6.15E-05 1.43E-05I.50E-05 2.68E-06 6.25E-075.10E-05 9.12E-06 2.13E-062.00E-05 3.57E-06 8.33E-072.43E-05 4.34E-06 I.01E-061.53E-05 2.74E-06 6.40E-071.39E-05 2.49E-06 5.80E-074.57E-05 8.17E-06 1.90E-069.99E-06 1.79E-06 4.16E-072.89E-05 5.17E-06 1.20E-061.18E-05 2.11E-06 4.91E-071.78E-07 3.19E-08 7.44E-09I.28E-04 2.29E-05 5.34E-061.53E-05 2.74E-06 6.40E-07

3.02E-04 1.24E-05 I.26E-054.03E-04 5.35E-05 I.68E-052.42E-03 3.33E-05 1.01E-043.88E-01 5.33E-03 1.61E-025.25E-03 7.21E-05 2.19E-04I.60E-04 2.20E-06 6.68E-061.02E-02 1.40E-04 4.25E-045.39E-05 7.41 E-07 2.25E-06

1.25E-06 2.40E-07 5.21E-086.78E-07 I.31E-07 2.83E-083.21E-07 6.18E-08 1.34E-08



3.00E-03 3.00E-03 NIl.OOE-01 l.OOE-01 NI6.00E-02 6.00E-02 8.57E-012.00E+00 2.00E+00 1.14E-012.00E+00 2.00E+00 NI

6.00E-OI 6.00E-01 NI3.00E+00 3.00E+00 NI

NI NI NINI NI NTNI NI NINI NI NINI NI NINI NI NI

4.00E-02 4.00E-02 NI4.00E-02 4.00E-02 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI NI3.00E-02 3.00E-02 NI

3.00E-04 3.00E-04 NI3.00E-03 6.00E-05 2.86E-053.70E-02 1.11E-02 NI3.00E-01 4.50E-02 NI

NI NI NI2.00E-02 8.00E-04 NI3.00E-01 3.00E-01 NI2.00E-02 2.00E-02 NI

2.00E-05 2.00E-05 NI2.00E-05 2.00E-05 NI2.00E-05 2.00E-05 NI

Hazard Quotient


1.33E-04 I.83E-05 NI1.21E-06 1.67E-07 NI2.97E-07 4.09E-08 2.77E-077.85E-08 1.08E-08 I.30E-05S.03E-08 I.10E-08 NI

5.73E-04 1.03E-04 NI5.00E-06 8.93E-07 NI


2.50E-04 4.47E-05 NI7.23E-04 1.29E-04 NI

NI NI NI8.92E-06 I.60E-06 8.68E-06

NI NI NI5.12E-04 9.I5E-05 NI

I.01E+00 4.15E-02 NI1.34E-01 9.24E-01 5.88E-016.55E-02 3.00E-03 NI1.29E+00 1.18E-01 NI

NI NI NI. 8.01 E-03 2.75E-03 NI

3.40E-02 4.68E-04 NI2.69E-03 3.71E-05 NI

6.25E-02 1.20E-02 NI3.39E-02 6.53E-03 NI1.6IE-02 3.09E-03 NI

Total Hazard Quotient%of

Total Total

1.52E-04 01.38E-06 06.15E-07 01.3IE-05 09.14E-08 0

6.76E-04 05.89E-06 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 02.95E-04 08.52E-04 0O.OOE+00 01.92E-05 0

O.OOE+00 06.03E-04 0

1.05E+00 241.65E+00 386.85E-02 21.41E+00 32O.OOE+00 01.08E-02 03.45E-02 12.73E-03 0

7.45E-02 24.04E-02 11.92E-02 0


Total Hazard Index

1.11E+00 5.88E-01

4.4E+00

AAG/

[Madl_serverI/jobs/1217/431/analyticaldatabase/newdata/clintonmaster/AlliedSurfNCCVO(TblW-16).xls]

Page 1 of 1

Medium: Allied Side Subsurface Soil (1-10 ft.)LandUse: Current/Future

le F-9


Clinton FMGP Site

Clinton, Iowa



CHEMICAL OFPOTENTIAL CONCERNVOCsBenzeneEthylbenzeneMethylene ChlorideTolueneToial Xylenes

PAHsAcenaphiheneAcenaphlhyleneAnihraceneBenzo(a)anihraceneBenzo(a)pyreneBenzo(b)fluoranthencBenzo(g.h.i)perylencBenzo(k)fluoranthcnc

Chryscne

Fluoramhcne

Fluorenc

Indeno( 1 ,2.3-cd)pyreneNaphthalenePhenanihrencPyrene

Acid Extractable2-Nitrophenol4-Nitrophenol

MetalsArsenicChromium VICopper[ronLeadNickelZincCyanide

EPC(mg/kg)

9.71E+012.40E+022.30E+011.69E+023.09E+02

1.34E+031.05E+033.03E+022.48E+02I.68E+021.28E+028.56E+015.36E4015.32E+021.84E+035.49E+026.96E+012.93E+031.37E+031.42E+03

6.79E4012.05E+OI

5.92E+018.30E+011.77E+028.31E+045.97E+026.20E+011.78E+031.75E+02

VF(Calculated)

3.48E+035.17E+033.I4E+034.43E+035.99E+03



4.95E-06 6.81E-07 5.95E-051.22E-05 1.68E-06 9.91E-051.27E-06 1.75E-07 I.70E-058.62E-06 1.18E-06 8.13E-05I.58E-05 2.17E-06 1.10E-04

6.83E-05 1.22E-05 2.85E-065.35E-05 9.57E-06 2.23E-061.55E-05 2.76E-06 6.44E-071.26E-05 2.26E-06 5.27E-078.57E-06 1.53E-06 3.57E-076.53E-06 1.I7E-06 2.72E-074.36E-06 7.80E-07 .82E-072.73E-06 4.89E-07 .14E-072.71E-05 4.85E-06 .13E-069.40E-05 1.68E-05 .92E-062.80E-05 5.00E-06 .17E-063.55E-06 6.34E-07 .48E-07I.49E-04 2.67E-05 6.23E-066.99E-05 1.25E-05 2.91E-067.22E-05 1.29E-05 3.01 E-06

3.46E-06 4.76E-07 1.44E-07I.05E-06 1.44E-07 4.36E-08

3.02E-06 I.25E-07 .26E-074.23E-06 5.82E-08 .76E-079.03E-06 1.24E-07 3.76E-074.24E-03 5.83E-03 .77E-043.04E-05 4.19E-07 .27E-063.16E-06 4.35E-08 .32E-079.08E-05 1.25E-06 3.78E-068.92E-06 1.23E-07 3.72E-07

Slope Factors


5.50E-02 5.50E-02 2.90E-02NC NC NC



7.30E-01 7.30E-01 3.10E-017.30E+00 7.30E+00 3.10E+007.30E-01 7.30E-01 3.10E-01

NC NC NC7.30E-02 7.30E-02 3.10E-027.30E-03 7.30E-03 3.10E-03

NC NC NCNC NC NC

7.30E-01 7.30E-0! 3.10E-01NC NC NCNC NC NCNC NC NC

NC NC NCNC NC NC

1.50E+00 1.50E+00 1.50E+OINI NI 4.10E+01NC NC NCNC NC NCNI NI NINI NI NINC NC NCNC NC NC

Cancer Risks


2.72E-07 3.74E-08 1.72E-06NI NI NI

9.56E-09 1.3IE-09 2.79E-08NI NI NINI NI NI


9.23E-06 1.65E-06 1.63E-076.25E-05 I.12E-05 1.11 E-064.76E-06 8.52E-07 8.43E-08

NI NI NI2.00E-07 3.57E-08 3.53E-091.98E-07 3.54E-08 3.50E-09

NI NI NINI Ml NI


NI NI NINI NI NI

4.53E-06 I.87E-07 1.89E-06NI NI 7.23E-06NI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

Total Risks

%ofTotal Total

2.03E-06 2O.OOE+00 03.88E-08 0O.OOE-fOO 0O.OOE-fOO 0

O.OOE-fOO 0O.OOE+00 0O.OOE+00 01.10E-05 107.48E-05 695.70E-06 5O.OOE+00 02.39E-07 02.37E-07 0O.OOE+00 0O.OOE+00 03.IOE-06 3O.OOE+00 0O.OOE+00 0O.OOE+00 0


6.60E-06 67.23E-06 7O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0

Total Cancer Risk by Route 8.41E-05

Total Cancer Risk 1.1E-04

1.44E-05 1.06E-05

AAG/[Mad 1 .server I /jobs/1217/43 I/analytical database/newdata/clintonmaster/AlliedSubCancCW)(0-10)(Tbl W-17).xls]

Page 1 of I

^^^^^^iblc p 10



Clinton FMGPSiteClinton, Iowa




VOCsBenzeneElhylbenzeneMethylene ChlorideTolueneTotal Xylcnes

PAHsAccnaphthencAcenaptuhyleni:AnthraceneDcnzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluoramneni;Bcnzo(g.h.i)pcryleneBenzodOnuoranihcneChryseneRuoranthencRuorencIndenof 1 ,2,3-cd)pyreneNaphthalenePhenanlhrenePyrene



EPC(mg/kg)

9.71E+012.40E+022.50E+011.69E+023.09E+02

1.34E+031.05E+033.03E+022.48E+021.68E+02I.28E+028.56E+015.36E+015.32E+02I.84E+035.49E+026.96E+012.93E+031.37E+031.42E+03

6.79E+012.05E+01

5.92E+018.30E+011.77E+028.31E+045.97E+026.20E+011.78E+031.75E+02

VF(Calculated)

3.48E+035.I7E+033.14E+034.43E+035.99E+03


NoncarcinogenicOral Dermal Inhalation

3.47E-04 4.77E-05 4.16E-038.57E-04 1.18E-04 6.94E-038.92E-05 1.23E-05 1.19E-036.03E-04 8.29E-05 5.69E-031.10E-03 1.52E-04 7.72E-03

4.78E-03 8.55E-04 1.99E-043.75E-03 6.70E-04 1.56E-041.08E-03 1.93E-04 4.51E-058.85E-04 1.58E-04 3.69E-056.00E-04 1.07E-04 2.50E-054.57E-04 8.17E-05 I.90E-053.06E-04 5.46E-05 1.27E-051.91E-04 3.42E-05 7 97E-061.90E-03 339E-04 7.91E-056.58E-03 1.18E-03 2.74E-04I.96E-03 3.50E-04 8.17E-052.48E-04 4.44E-05 1.04E-05I.05E-02 1.87E-03 4.36E-044.89E-03 8.74E-04 2.04E-045.05E-03 9.03E-04 2.10E-04

2.42E-04 3.33E-05 1.01E-057.32E-05 I.OIE-05 3.05E-06

2.11E-04 8.72E-06 8.80E-062.96E-04 4.07E-06 1.23E-056.32E-04 8.69E-06 2.63E-052.97E-01 4.08E-03 I.24E-022.13E-03 2.93E-05 8.88E-052.21 E-04 3.04E-06 9.22E-066.35E-03 8.74E-05 2.65E-046.25E-04 8.59E-06 2.60E-05

Reference Doses


3.00E-03 3.00E-03 I.70E-03l.OOE-01 l.OOE-OI 2.86E-OI6.00E-02 6.00E-02 8.57E-OI2.00E+00 2.00E+00 1.I4E-012.00E+00 2.00E+00 NI

6.00E-02 6.00E-02 NINI NI NT

3.00E-01 3.00E-01 NINI NI NINI NI NlNI NI NINI NI NINI NI NINI NI NI

4.00E-02 4.00E-02 Nl4.00E-02 4.00E-02 NI

NI Nl Nl2.00E-02 2.00E-02 8.57E-04

NI NI NI3.00E-02 3.00E-02 NI

NI NI NINI NI NI

3.00E-04 3.00E-04 NI3.00E-03 6.00E-05 2.86E-053.70E-02 1.11E-02 NI3.00E-OI 4.50E-02 Nl

Nl NI NI2.00E-02 8.00E-04 NI3.00E-01 3.00E-01 NI2.00E-02 2.00E-02 Nl

Hazard Quotient


I.16E-01 1.70E-03 2.45E+008.57E-03 2.86E-01 2.43E-021.49E-03 2.05E-04 1.38E-033.02E-04 4.15E-05 4.98E-025.51 E-04 7.58E-05 ' NI

7.97E-02 1.42E-02 NINI NI NI

3.61 E-03 6.44E-04 NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

1.64E-01 NI NI4.90E-02 NI NI

NI Nl NI5.23E-01 8.57E-04 5.08E-OI

NI NI NI1.68E-01 NI NI

Nl NI NINI NI NI


NI NI NII.11E-02 3.80E-03 NI2.12E-02 2.91 E-04 NI3.I2E-02 4.29E-04 Nl

Total Hazard Quotient

%ofTotal Total

2.57E+00 373.19E-01 53.08E-03 05.02E-02 16.27E-04 0

9.40E-02 1O.OOE+00 04.25E-03 0O.OOE+00 0O.OOE+00 0O.OOE-fOO 0O.OOE+00 0O.OOE+00 0O.OOE+00 01.64E-OI 24.90E-02 1O.OOE+00 01.03E+00 15O.OOE+00 01.68E-01 2


7.33E-01 1 15.31E-OI 81.79E-02 01.08E+00 16O.OOE+00 01.49E-02 02.15E-02 03.17E-02 0


Total Hazard Index

4.29E-01 3.46E+00

6.9E+00

AAG/

[Mad 1 .server 1 /jobs/1217/431 /analytical database/newdala/clintonmaster/AlliedSubNCC W)(0-10)(TblW-18).xls]Page 1 of 1


ReF-ll


Clinton FMGP Site

Clinton, Iowa




VOCsBenzeneEthylbenzeneMeihylene ChlorideTeirachloroeiheneTolueneRilal Xylenes

PAHsAcenaphlhcncAccnaphlhyleneAnthraceneBenzo(a)anlhraccne3enzo(a)pyrcneBen/.n(b)fluoranlheneBeiuo(g.h.i)perylencRcnzofkjfluorantheneChryseneDibenz{a.h)anthracenttFluoramheneRuoreneIndenot 1 ,2.3-cd)pyrene

NaphthalenePhcnanthrcnePyrene

Acid Extractable2,4-Dimelhylphenol4-Nilrophcnol

Phenol


EPC(lUE/kg)

9.49E+OI4.95E+012.93E+005.47E-038.I1E+OII.02E+02

2.69E+032.69E+031.24E+031.23E+038.22E+025.90E+024.28E+022.57E+02I.I3E+038.90E+008.75E+032.52E+033.31E+02

4.83E+035.00E+037.29E+02

1.56E+015.77E-01

1.19E+01

3.99E+001.62E+012.78E+011.86E+04

1.24E+021.85E+011 .38E+022.6IE+00

VF(Calculated)

3.48E+035.17E+033.14E+033.94E+034.43E+O35.99E+03


mg/kg-dayOral Derma) Inhalation

4.84E-06 6.65E-07 5.81E-052.52E-06 3.47E-07 2.04E-051.49E-07 2.05E-08 1.99E-062.79E-10 3.83E-1I 2.96E-094.14E-06 5.69E-07 3.90E-055.20E-06 7.I5E-07 3.64E-05

1.37E-04 2.45E-05 5.72E-06I.37E-04 2.45E-05 5.72E-066.32E-05 I.13E-05 2.63E-066.25E-05 1.12E-05 2.60E-064.19E-05 7.49E-06 1.75E-063.01 E-05 5.38E-06 1.25E-062.18E-05 3.90E-06 9.09E-071.3IE-05 2.34E-06 5.46E-07

5.78E-05 1.03E-05 2.4IE-064.54E-07 8.11E-08 1.89E-084.46E-04 7.98E-05 I.86E-051.29E-04 2.30E-05 5.35E-061.69E-05 3.02E-06 7.03E-07

2.46E-04 4.40E-05 1.03E-052.55E-04 4.56E-05 I.06E-053.72E-05 6.ME-06 1.55E-06

7.97E-07 1.10E-07 3.32E-082.94E-08 4.05E-09 1.23E-09

6.07E-07 8.35E-08 2.53E-08

2.03E-07 8.39E-09 8.48E-098.27E-07 1.14E-08 3.44E-08I.42E-06 1.95E-08 5.90E-089.49E-04 I.31E-05 3.95E-056.33E-06 8.70E-08 2.64E-07

9.42E-07 1.30E-08 3.92E-087.03E-06 9.67E-08 2.93E-07I.33E-07 I.83E-09 5.54E-09

Slope Factors


5.50E-02 5.50E-02 2.90E-02NC NC NC

7.50E-03 7.50E-03 I.65E-035.20E-02 5.20E-02 2.00E-03

NC NC NCNC NC NC


7.30E-01 7.30E-01 3.IOE-017.30E+00 7.30E+00 3.10E+007.30E-OI 7.30E-01 3.10E-OI

NC NC NC7.30E-02 7.30E-02 3.10E-02

7.30E-03 7.30E-03 3.10E-037.30E+00 7.30E+00 3.10E+OO

NC NC NCNC NC NC

7.30E-01 7.30E-01 3.10E-01



l.SOE+00 1.50E+00 1.50E+01Nl NI 4.10E40INC NC NCNC NC NCNl NI NINl NI NINC NC NCNC NC NC

Cancer Risks


2.66E-07 3.66E-08 1.69E-06NI NI NI

1.12E-09 1.54E-10 3.27E-091.45E-11 I.99E-I2 5.92E-12

Nl NI NlNl Nl NI

Nl NI NlNI NI NlNI NI NI

4.56E-05 8.16E-06 8.08E-073.06E-04 5.47E-05 5.41E-062.20E-05 3.93E-06 3.89E-07

NI NI NI9.57E-07 1.71E-07 1.69E-084.22E-07 7.55E-08 7.47E-093.31E-06 5.92E-07 5.86E-08

NI NI NINI NI NI

1.23E-05 2.20E-06 2.I8E-07NI NI NINI NI NINI NI Nl

NI NI NINI NI NINl NI NI

3.05E-07 I.26E-08 1.27E-07NI NI I.4IE-06NI NI NINI NI NINI NI NINI NI NINI NI NlNI NI NI

Total Risks%of

Total Total

1 .99E-06 0O.OOE+00 04.54E-09 02.24E-1I 0O.OOE+OO 0O.OOE+00 0

O.OOE+00 0O.OOE+00 0O.OOE+00 05.46E-05 123.66E-04 782.63E-05 6O.OOE+00 01.14E-06 05.05E-07 03.96E-06 1O.OOE+00 0O.OOE+00 0

I.47E-05 3O.OOE+00 0O.OOE+00 0O.OOE+00 0


4.45E-07 0

1.41E-06 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0

Total Risk by Route 3.91E-O4 6.98E-05

Total Risk

8.45E-06

4.7E-04

AAG/

[MadLsei-vcrl/jobs/1217/431/analyticaldauibase/newdata/clintonmasicr/AlliedSubCancCW)(10-20)(TblW-l9).xls]

Page 1 of 1

^^^at

Medium: Allied Side Subsurface Soil (10-20 ft.)LnndUse: Current/Future

,bleF-12


Clinton FMCP SiteClinton, Iowa




VOCsBenzeneElhylbenzeneMethylene ChlorideTeti'achloroeiheneTolueneTotal Xylenes

PAHsAcenaphlheneAccnaphthyleneAnthracene3enzo(a)anthraceneBenzo(a)pyrene-lenzo(b)fluoranthcneDenzolg.h.'DperyleneBenzodOfluoranthenc

ChryseneDibcnz(a.h)anthracene-luoranlhcneFluorcnelndeno( 1 ,2.3-cd)pyrene

NaphthalenePhenanlhrenePyrene

Acid Extractable2,4-Dimethylphcnol4-NitrophenolPhenol

MetalsArsenicChromium VICopperjonLeadNickelZincCvanide

EPC(mg/kg)

9.49E+OI4.95E+012.93E+005.47E-038.I1E+011.02E+02

2.69E+032.69E+03I.24E+031 .23E+038.22E+025.90E+024.28E+022.57E+02

1.13E+038.90E+008.75E+032.52E+03

3.31E+024.83E+035.00E+037.29E+02

I.56E+OI5.77E-011.19E+01

3.99E+00I.62E+012.78E+011.86E+041.14E+021.8SE+011 .38E+022.61E+00

VF(Calculated)

3.48E+035.17E+033.14E+033.94E+034.43E+035.99E+03



3.39E-04 4.66E-05 4.07E-031.77E-04 2.43E-05 I.43E-031.05E-05 1.44E-06 1.39E-041.95E-08 2.68E-09 2.07E-072.89E-04 3.98E-05 2.73E-033.64E-04 5.01E-05 2.55E-03

9.60E-03 1.72E-03 4.00E-049.60E-03 1 .72E-03 4.00E-044.43E-03 7.9IE-04 1.84E-044.38E-03 7.82E-04 I.82E-042.93E-03 5.24E-04 1.22E-042.I1E-03 3.76E-04 8.77E-051.53E-03 2.73E-04 6.37E-059.17E-04 1.64E-04 3.82E-05

4.05E-03 7.24E-04 I.69E-043.18E-05 5.68E-06 1.32E-063.12E-02 5.58E-03 1.30E-039.00E-03 1.61E-03 3.75E-04

1.18E-03 2.11E-04 4.92E-051.72E-02 3.08E-03 7.18E-041.78E-02 3.19E-03 7.44E-042.60E-03 4.65E-04 1 .08E-04

5.58E-05 7.67E-06 2.33E-062.06E-06 2.83E-07 8.58E-084.25E-05 5.85E-06 1.71E-06

I.42E-05 5.87E-07 5.93E-075.79E-05 7.96E-07 2.41E-069.9IE-05 1.36E-06 4.I3E-066.64E-02 9.14E-04 2.77E-034.43E-04 6.09E-06 1.85E-056.59E-05 9.07E-07 2.75E-064.92E-04 6.77E-06 2.05E-059.31E-06 1.28E-07 3.88E-07

Reference Doses


3.00E-03 3.00E-03 I.70E-03I.OOE-OI I.OOE-OI 2.86E-016.00E-02 6.00E-02 8.57E-01l.OOE-02 l.OOE-02 1.40E-OI2.00E-01 2.00E-01 1.14E-OI2.00E+00 2.00E+00 NI

6.00E-02 6.00E-02 NINI NI NI

3.00E-OI 3.00E-OI NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI MlNI NI NI

4.00E-02 4.00E-02 NI4.00E-02 4.00E-02 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI NI3.00E-02 3.00E-02 NI

2.00E-02 2.00E-02 NINI NI NI

6.00E-01 6.00E-01 NI

3.00E-04 3.00E-04 NI3.00E-03 6.00E-05 2.86E-053.70E-02 I.I1E-02 NI3.00E-01 4.50E-02 NI

-NI NI NI2.00E-02 8.00E-04 NI3.00E-OI 3.00E-01 NI2.00E-02 2.00E-02 NI

Hazard Quotient


1.13E-01 1.70E-03 2.39E+001.77E-03 2.86E-01 5.01 E-03I.74E-04 2.40E-05 1.62E-041.95E-06 2.68E-07 I.48E-061.45E-03 1.99E-04 2.39E-021.82E-04 2.50E-05 NI

1.60E-OI 286E-02 NINI NI NI

1.48E-02 2.64E-03 NINI NI NINI NI NINI NI NINI NI NI


7.81E-01 I.40E-01 NI

2.25E-01 4.02E-02 NINI NI NI

8.62E-01 1.54E-01 8.38E-01NI NI NI

8.67E-02 1.55E-02 NI

2.79E-03 3.84E-04 NINI NI NI

7.09E-05 9.74E-06 NI

4.75E-02 1.96E-03 NI1.93E-02 1.33E-02 8.44E-022.68E-03 1.23E-04 NI2.2IE-01 2.03E-02 NI

NI NI NI3.30E-03 I.13E-03 NI1.64E-03 2.26E-05 NI4.65E-04 6.40E-06 NI


%ofTotal Total

2.5IE+00 382.92E-01 43.61E-04 03.70E-06 02.56E-02 02.07E-04 0

1.89E-OI 3O.OOE+00 01.74E-02 0


O.OOE+00 0O.OOE+00 0O.OOE+00 09.20E-01 14

2.65E-01 4O.OOE+00 0I.85E+00 28O.OOE+00 01.02E-01 2

3.17E-03 0O.OOE+00 08.06E-05 0

4.94E-02 11.17E-01 22.80E-03 02.42E-OI 4O.OOE+00 04.43E-03 0I.66E-03 04.72E-04 0

Total Hazard Index by Route

Total Hazard Index

7.0SE-01 3.34E+00

6.6E+00

AAG/

[Madl_serverl/iobs/1217/431/analyticaldatabase/newdata/c!intonmaster/AlliedSubNCCW)(10-20)(Tb!W-20).)ils]

Medium: IPC Side Surface SoilLandUse: Future

[Table F-13


Clinton FMGP Site

Clinton, Iowa

Receptor: On-site WorkerExposure Pathway: Incidental Ingestion, Dermal Contact, and



VOCsBenzeneEthyibenzene

TolueneToial Xylcnes

PAHsAccnaphihcncAnthracene3enzo(a)amhracenc3enzo(a)pyrenc3cnzo(b)tluoramhcno3enzo(g.h.i)pcrylcneBenzo(k)tluoramheneChryseneFluoranlhencFluorenelndeno(l ,2,3-cd)pyreneNaphthalenePhenanilirenePyrenc


MetalsArsenicChromium VICopperronLeadNickelZincCyanide

PCBsAroclor 1260

EPC(mg/kg)

3.40E-022.80E-02

4.20E-023.70E-02

2.60E4001.20E+001.52E+01I.2IE+019.40E+007.10E+003.50E+001.26E+OI3.93E+012.50E+005.70E+002.60E+006.40E+003.27E+01

2.63E+01

1.70E+02I.40E+017.80E+014.66E+045.51E+021.94E+011.3IE+031.79E+01

7.32E+01

VF(Calculated)

3.48E+035.17E+03

4.43E+035.99E+03

Chronic Daily Intake Valuemg/kg-day


4.51E-09 5.96E-09 3.11E-073.72E-09 4.91 E-09 1.73E-07

5.58E-09 7.36E-09 3.02E-074.91 E-09 6.49E-09 1.97E-07

3.45E-07 5.92E-07 6.28E-111.59E-07 273E-07 2.90E-112.02E-06 3.46E-06 3.67E-101.61E-06 2.76E-06 2.92E-101.25E-06 2.14E-06 2.27E-IO9.43E-07 1.62E-06 1.7 IE- 104.65E-07 7.98E-07 8.45E-I11.67E-06 2.87E-06 3.04E-IO5.22E-06 8.96E-06 9.49E-103.32E-07 5.70E-07 6.04E-1 17.57E-07 I.30E-06 1.38E-103.45E-07 5.92E-07 6.28E-I18.50E-07 1.46E-06 1.55E-IO4.34E-06 7.45E-06 7.90E-IO

3.49E-06 1.15E-05 6.35E-10

2.26E-05 8.94E-06 4.10E-09I.86E-06 2.45E-07 3.38E-10I.04E-05 1.37E-06 1.88E-096.19E-03 8.17E-04 1 13E-067.32E-05 9.66E-06 1 .33E-082.58E-06 3.40E-07 4.68E-101.74E-04 2.30E-05 3.16E-082.38E-06 3.14E-07 4.32E-10

9.72E-06 1.80E-05 1.77E-09

Slope Factorskg-day/mg


5.50E-02 5.50E-02 2.90E-02NC NC NC

NC NC NCNC NC NC

NC NC NCNC NC NC

7.30E-01 7.30E-OI 3.IOE-017.30E+00 7.30E+00 3.10E+007.30E-01 7.30E-01 3.10E-01

NC NC NC7.30E-02 7.30E-02 3.10E-027.30E-03 7.30E-03 3.10E-03

NC NC NCNC NC NC


1.20E-01 I.20E-01 NI

I.50E+00 1.50E+00 1.50E+OINI NI 4.10E+01NC NC NCNC NC NCNI NI NINI NI NINC NC NCNC NC NC

2.00E+00 2.00E+00 2.00E+00

Cancer Risks


2.48E-10 3.28E-10 9.03E-09NI NI NI

NI NI NINI NI NI

NI NI NINI NI NI

1.47E-06 2.53E-06 1.14E-101.17E-05 2.01E-05 9.06E-109.11E-07 I.56E-06 7.04E-11

NI NI NI3.39E-08 5.82E-08 2.62E-121.22E-08 2.10E-08 9.43E-I3

NI NI NINI NI NI


4.19E-07 1.38E-06 NI


1.94E-05 3.59E-05 3.53E-09

Total Risks%of

Total Total

9.60E-09 0O.OOE+00 0


O.OOE+00 0O.OOE+00 04.00E-06 33.19E-05 222.47E-06 2O.OOE+00 09.22E-08 03.32E-08 0O.OOE+00 0O.OOE+00 01.50E-06 1O.OOE+00 0O.OOE+00 0O.OOE+00 0

1.80E-06 1

4.73E-05 331.39E-08 0


5.54E-05 38


Total Risk

8.01E-08

1.4E-04

Page 1 of 1

Medium: IPC Side Surface SoilLandllse: Future

Table F-14






VOCsBenzeneEthylbenzeneTolueneToial Xylencs

PAHsAccnaphthcneAnthraceneBcnzoMamhraccne3enzo(a)pyrencUcnzo(b)fluoranlhcncRtnzo(g.h.i)pcrylcncBenzo(k)lluoramheneChryscnoFluoranlhent:Ruorcnc

lndeno(l,2,3-cd)pyreneNaphthalenePhenanlhrcnc

Pyrcnc

Acid ExtraclablePentachlorophenol

MetalsArsenicChromium VICopper

ronLeadNickelZincCyanide

PCBsAroclor 1260

EPC(mg/kg)

3.40E-022.80E-024.20E-023.70E-02

2.60E+001.206*001.52E+011.21E+019.40E+007.10E+003.50E+001.26E+013.93E+01

2.50E+005.70E+002.60E+006.40E+003.27E+OI

2.63E+01

1.70E+021.40E+017.80E+014.66E+045.5IE+021.94E+011.31E+031.79E+01

7.32E+01

VF(Calculated)

3.48E+035.17E+034.43E+035.99E+03



1.26E-08 1.67E-08 8.72E-071.04E-08 1.37E-08 4.83E-071.56E-08 2.06E-08 8.45E-07I.38E-08 1.82E-08 5.51E-07

9.67E-07 1.66E-06 1.76E-104.46E-07 7.66E-07 8.11E-115.65E-06 9.70E-06 1.03E-094.50E-06 7.72E-06 8.18E-103.50E-06 6.00E-06 6.35E-102.64E-06 4.53E-06 4.80E-101.30E-06 2.23E-06 2.37E-104.68E-06 8.04E-06 8.52E-101.46E-05 2.51E-05 2.66E-099.30E-07 160E-06 I.69E-102.12E-06 3.64E-06 3.85E-IO9.67E-07 I.66E-06 1.76E-102.38E-06 4.08E-06 4.33E-101.22E-05 2.09E-05 2.21E-09

9.78E-06 3.23E-05 I.78E-09

6.32E-05 2.50E-05 1.15E-085.21E-06 6.87E-07 9.46E-102.90E-05 3.83E-06 5.27E-091.73E-02 2.29E-03 3.15E-062.05E-04 2.70E-05 3.72E-087.2IE-06 9.52E-07 1.3IE-094.87E-04 6.43E-05 8.86E-086.66E-06 8.79E-07 I.21E-09

2.72E-05 5.03E-05 4.95E-09

Reference Doses


3.00E-03 3.00E-03 I.70E-03I.OOE-01 l.OOE-01 2.86E-012.00E-01 2.00E-01 1.I4E-012.00E+00 2.00E+00 NI

6.00E-02 6.00E-02 NI3.00E-01 3.00E-01 NI


4.00E-02 4.00E-02 NI4.00E-02 4.00E-02 NI

NI Nl NI2.00E-02 2.00E-02 8.57E-04

Nl NI NI3.00E-02 3.00E-02 NI

3.00E-02 3.00E-02 Nl

3.00E-04 3.00E-04 NI

3.00E-03 6.00E-05 2.86E-053.70E-02 1.11E-02 NI3.00E-01 4.50E-02 NI

Nl NI NI2.00E-02 8.00E-04 NI3.00E-01 3.00E-01 NI2.00E-02 2.00E-02 NI

2.00E-05 2.00E-05 Nl

Hazard Quotient


4.21E-06 5.56E-06 5.13E-04I.04E-07 1.37E-07 I.69E-067.81E-08 1.03E-07 7.40E-066.88E-09 9.08E-09 NI

1.6IE-05 2.76E-05 NI1.49E-06 2.55E-06 NI

Nl NI NINI NI NINI Nl NINI NI NINI NI NINI NI NI

3.65E-04 6.27E-04 NI2.32E-05 3.99E-05 Nl

NI Nl Nl4.83E-05 8.29E-05 2.05E-07

NI Nl Nl4.05E-04 6.95E-04 NI

3.26E-04 I.08E-03 NI

2.11E-01 8.34E-02 NI2.86E-05 3.31E-05

7.84E-04 3.45E-04 NI

5.78E-02 5.08E-02 NINI NI NI

3.61E-04 1.19E-03 Nl1.62E-03 2.14E-04 NI3.33E-04 4.39E-05 NI

1.36E+00 2.51E+00 Nl


%ofTotal Total

5.22E-04 01.93E-06 07.58E-Q6 01 .60E-08 0

4.38E-05 04.04E-06 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0

O.OOE+00 0O.OOE+00 09.92E-04 06.31E-05 0O.OOE+00 01.3IE-04 0

O.OOE+00 01.10E-03 0

I.40E-03 0

2.94E-01 76.17E-05 01.I3E-03 01.09E-0! 3

O.OOE+00 01.55E-03 01.84E-03 03.77E-04 0

3.88E+00 90

Total Hazard Index

Total Hazard Index by Route 1.63E+00 2.65E+00 S.SSE-04

4.3E+00

AAC/

[Mad 1 .server I /jobs/1217/43 I/analytical database/newdata/climonmaster/IPCSurfNCOn-Sitework(Tbl W-2J.xls]

Page i ol 1

•Table F

Medium: IPC Side Subsurface Soil (1-10 ft.)LandUse: Future

-15


Clinton FMGP Site

Clinton, Iowa




VOCs

BenzeneChloromeihaneEthylbenzeneMethylene ChlorideTolueneTotal Xylenes

PAHsAcenaphihene

AcenaphlhylcneAnthraceneBcnzo(a)anlhracencBenzo(a)pyreneBenzo(b)fluoraniheneBcnzo(g,h,i)perylcneBenzo(k)fluorantheneChrysene

Dibcnz(a.h)anthraceneRuoranthcncFluorene

Indeno(l,2,3-cd)pyrene

MaphthalenePhenanlhrcne

Pyrene

MetalsArsenicChromium VICopperIronLead

NickelZincCyanide

EPC(mg/kg)

5.30E+011 .42E+001.22E+021.01E-012.30E+025.60E+02

7.56E+03I.91E+04

2.35E+032.50E+028.11E+024.15E+012.08E+022.I2E+02

2.94E+02

1.27E+015.J9E+OI6.I7E+032.29E+021.92E+047.57E+033.07E+01

8.80E+002.14E+015.10E+013.08E+04

3.40E+023.55E+013.74E+024.59E+01

VF(Calculated)

3.48E+031.47E+035.17E+033.14E+03

4.43E+035.99E+03



7.04E-06 9.29E-06 4.85E-041.89E-07 2.49E-07 3.07E-05

I.62E-05 2.14E-05 7.52E-041.34E-08 1.77E-08 I.02E-063.05E-05 4.03E-05 1.65E-037.44E-05 9.82E-05 2.98E-03

l.OOE-03 1.72E-03 1.83E-07

2.54E-03 4.35E-03 4.61E-073.13E-04 5.36E-04 5.68E-083.32E-05 5.70E-05 6.04E-091.08E-04 I.85E-04 I.96E-085.5IE-06 946E-06 l.OOE-092.76E-05 4.74E-05 5.02E-092.82E-05 4.83E-05 5.I2E-09

3.90E-05 6.70E-05 7.10E-09

1.69E-06 2.89E-06 3.07E-106.89E-06 1.18E-05 I.25E-098.19E-04 1.41E-03 I.49E-07

3.04E-05 5.22E-05 5.53E-09

2.55E-03 4.38E-03 4.64E-07I.01E-03 1.73E-03 1.83E-074.08E-06 700E-06 7.41E-10

1.17E-06 4.63E-07 2.I2E-10

2.84E-06 3.75E-07 5.17E-IO6.77E-06 8.94E-07 I.23E-094.09E-03 5.40E-04 7.44E-074.51E-05 5.96E-06 8.21E-094.71E-06 6.22E-07 8.57E-10

4.97E-05 6.56E-06 9.03E-096.10E-06 8.05E-07 l . I IE-09

Slope Factors


5.50E-02 5.50E-02 2.90E-021.30E-02 I.30E-02 6.30E-03

NC NC NC7.50E-03 7.50E-03 I.65E-03

NC NC NCNC NC NC


7.30E-01 7.30E-OI 3.10E-017.30E+00 7.30E+00 3.10E+007.30E-OI 7.30E-01 3.10E-01

NC NC NC7.30E-02 7.30E-02 3.10E-02

7.30E-03 7.30E-03 3.10E-03

7.30E+00 7.30E+00 3.10E400NC NC NCNC NC NC

7.30E-01 7.30E-01 3.10E-01


I.50E+00 1.50E+00 I.50E+01NI NI 4.10E+01NC NC NCNC NC NCNI NI NINI NI NINC NC NCNC NC NC

Cancer Risks


3.87E-07 5.11E-07 1.41E-052.45E-09 3.24E-09 1.94E-07

NI NI NI1.0 IE- 10 1.33E-10 1.69E-09

NI NI NINI NI NI


2.42E-05 4.16E-05 I.87E-097.86E-04 1.35E-03 6.07E-084.02E-06 6.90E-06 3.11E-10

NI NI NI2.06E-06 3.53E-06 1.59E-10

2.85E-07 4.89E-07 2.20E-I1

1.23E-05 2.11E-05 9.5 IE- 10NI NI NINI NI NI

2.22E-05 3.81E-05 1.71E-09


1.75E-06 6.94E-07 3.19E-09

NI NI 2.12E-08NI NI NINI NI NINI NI NINI NI NTNI NI NINI NI NI

Total Risks

%ofTotal Total

1.50E-05 11.99E-07 0

O.OOE+00 01.92E-09 0


O.OOE+00 0

O.OOE+00 0O.OOE+00 06.58E-05 32.14E-03 921 .09E-05 0

O.OOE+00 05.58E-06 0

7.74E-07 0

3.34E-05 IO.OOE+00 0O.OOE+00 06.03E-05 3


2.45E-06 0

2.12E-08 0O.OOE+00 0O.OOE+00 0O.OOE+00 0



Total Risk 2.3E-03

2.85E-07

AAG/

[Madl_serverl/jobs/1217/431/analyticaldatabasc/newdata/clintonmaster/IPCSubCanOn-Sitework(0-IO)(Tbl\V-3).xls]

Page 1 of 1

Medium: 1PC Side Subsurface Soil (MO ft.)LandUse: Future

Table F-16



Receptor: On-Site WorkerExposure Pathway: Incidental Ingestion, Dermal Contact, and



VOCsBenzeneChloromethaneEihylbenzeneMethylene ChlorideTolueneTotal Xylencs

PAHsAcenaphlhcncAcenaphihyleneAnthraceneBenzo(a)anihraceneBenzo(a)pyreneBenzo(b)fluoranihencBenzo(g.h.i)pcrylcncBenzodOlluoranlhcneChryseneDibenz(a,h)anihracencRuoranlhcncFluorene

Indeno(1.2,3-cd)pyrene

NaphthalenePhenanthrenePyrcne

MetalsArsenicChromium VICopperIronLeadNickelZincCvanide

EPC(mg/kg)

5.30E+011.42E+00I.22E+021.01E-01

2.30E+025.60E+02

7.56E+031.91E+042.35E+032.50E+028.1IE+024.15E+012.08E+022.I2E+022.94E+021.27E+015.19E+016.I7E+032.29E+02I.92E+047.57E+033.07E+01

8.80E+002.14E+015.10E+013.08E+043.40E+023.55E+013.74E+024.59E+OI

VF(Calculated)

3.48E+031.47E+035.17E+033.14E+034.43E+035.99E+03



1.97E-05 2.60E-05 1.36E-035.28E-07 6.97E-07 8.61 E-054.54E-05 5.99E-05 2.IOE-033.76E-08 4.96E-08 2.87E-068.55E-05 1.13E-04 4.63E-032.08E-04 2.75E-04 8.34E-03

2.81E-03 4.82E-03 5.11E-077.10E-03 1.22E-02 1.29E-068.75E-04 1.50E-03 1.59E-079.30E-05 1.60E-04 1.69E-083.02E-04 5-17E-04 5.48E-081.54E-05 2.65E-05 2.81E-097.73E-05 1.33E-04 1.41E-087.88E-05 1.35E-04 1.43E-081.09E-04 1.88E-04 1.99E-084.72E-06 8.10E-06 8.59E-10I.93E-05 3.31 E-05 3.51E-092.29E-03 3.93E-03 4.17E-078.51 E-05 1.46E-04 1.55E-087.14E-03 1.23E-02 1.30E-062.82E-03 4.83E-03 5.12E-071.14E-05 1.96E-05 203E-09

3.27E-06 .30E-06 5.95E-107.96E-06 .05E-06 1.45E-091.90E-05 2.50E-06 3.45E-09.15E-02 .51E-03 2.08E-06.26E-04 .67E-05 2.30E-08.32E-05 .74E-06 2.40E-09.39E-04 .84E-05 2.53E-08.71 E-05 2.25E-06 3 IOE-09

Reference Doses


3.00E-03 3.00E-03 1.70E-03NI NI 8.60E-02

l.OOE-0! l.OOE-01 2.86E-OI6.00E-02 6.00E-02 8.57E-012.00E-01 2.00E-01 1.14E-012.00E+00 2.00E4OO NI

6.00E-02 6.00E-02 NINI NI NI

3.00E-01 3.00E-01 NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

4.00E-02 4.00E-02 NI4.00E-02 4.00E-02 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI NI3.00E-02 3.00E-02 NI



Hazard Ouotienl


6.57E-03 8.67E-03 7.99E-01NI NI l.OOE-03

4.54E-04 5.99E-04 7.37E-036.26E-07 8.26E-07 3.35E-064.28E-04 5.64E-04 4.05E-021.04E-04 1.37E-04 NI

4.68E-02 8.04E-02 NINI NI NI

2.92E-03 5.01E-03 NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

4.82E-04 8.2SE-04 NI5.73E-02 9.84E-02 NI

NI NI NI3.57E-01 6.13E-01 1.51E-03

NI NI NI3.80E-04 6.53E-04 NI

I.09E-02 4.32E-03 NI2.65E-03 1.75E-02 5.06E-055.I3E-04 2.26E-04 NI3.82E-02 3.36E-02 NI


Total Hazard Ooutient

%ofTotal Total

8.14E-01 36l.OOE-03 08.42E-03 04.80E-06 04.15E-02 22.42E-04 0

I.27E-01 6O.OOE+00 07.92E-03 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0I.31E-03 01.56E-01 7

O.OOE+00 09.71E-OI 43O.OOE+00 01.03E-03 0

I.52E-02 12.02E-02 17.38E-04 07.18E-02 3O.OOE+00 02.84E-03 05.25E-04 09.66E-04 0

Total Hazard Index by Route 5.27E-01

Total Hazard Index

8.66E-01 8.50E-01

2.2E+00

AAG/[Madl_serverl/jobs/l2l7/43I/analytical database/newdata/dintonmaster/IPCSubNCOn-Sitework(0-IO)(TblW-4).xls]

Page 1 of 1


Table F-17


Clinton FMGPSite

Clinton, Iowa

Receptor: Site Visitors/TrespassersExposure Pathway: Incidental Ingestion, Dermal Contact, and



VOCsBenzeneEthylbenzeneTolueneTola] Xylenes

PAHsAwnaphlheneAnthraceneBenzo(a)amhraccncBenzo(a)pyrilncBenzo(b)fluoramhcneBcnzo(g,h.i)peryleneBcnzo(tOfluoranihcneChryseneFluoraruheneRuorencIndeno(l.2.3-cd)pyreneNaphthalene

PhenanihrencPyrcnc

Acid ExtractablePemachlorophenol

MetalsArsenicChromium VICopperronLeadNickelZincCyanide

PCBsAroclor 1260

EPC(ing/kg)

3.40E-022.80E-024.20E-023.70E-02

2.60E+001.20E+001.52E+01I.21E+OI9.40E+007.10E+003.50E+001.26E+013.93E+OI2.50E+005.70E+002.60E+006.40E+003.27E+01

2.63E+01

1.70E+021.40E+017.80E+012.53E+04551E+02I.94E+011.3IE+031.79E+01

7.32E+01

VF(Calculated)

3.48E+035.17E+034.43E+035.99E+03



I.67E-09 3.53E-09 I.7SE-081.38E-09 2.9IE-09 9.86E-092.06E-09 4.36E-09 I.73E-081.82E-09 3.84E-09 I.13E-08

1.28E-07 3.5IE-07 3.59E-125.90E-08 1.62E-07 1.65E-127.47E-07 2.05E-06 2.10E-1!5.95E-07 1.63E-06 I .67E-I14.62E-07 I.27E-06 1.30E-113.49E-07 9.58E-07 9.79E-121.72E-07 4.72E-07 4.83E-126.19E-07 1.70E-06 1.74E-111.93E-06 5.30E-06 5.42E-1II.23E-07 3.37E-07 3.45E-122.80E-07 7.69E-07 7.86E-I2

1.28E-07 3.5IE-07 3.59E-I23.I5E-07 8.63E-07 8.83E-I21.61E-06 4.41E-06 4.5IE-1I

I.29E-06 6.82E-06 3.63E-II

8.36E-06 5.29E-06 2.34E-106.88E-07 I.45E-07 1.93E-113.83E-06 8.09E-07 1.08E-101.24E-03 2.63E-04 3.49E-082.7IE-05 5.72E-06 7.60E-109.54E-07 2.01E-07 2.68E-116.44E-05 1.36E-05 1.8IE-098.80E-07 1.86E-07 2.47E-II

3.60E-06 1.06E-05 1.01E-10

Slope Factors



NC NC NCNC NC NC

7.30E-01 7.30E-01 3.10E-017.30E+00 7.30E+00 3.10E+007.30E-01 7.30E-01 3.10E-01

NC NC NC730E-02 7.30E-02 3.10E-027.30E-03 7.30E-03 3.10E-03

NC NC NCNC NC NC

7.30E-OI 7.30E-OI 3.10E-OINC NC NCNC NC NCNC NC NC

I.20E-OI I.20E-OI Nl

I.50E+00 I.50E+00 I.50E+OINl NI 4.IOE+OINC NC NCNC NC NCNl NI NlNI NI NINC NC NCNC NC NC

2.00E+00 2.00E+00 2.00E+00

Cancer Risks


9.19E-11 1.94E-10 5.I6E-IONI NI NINI NI NlNl NI Nl

Nl NI NlNI NI NI

5.45E-07 1.50E-06 6.50E-124.34E-06 1.I9E-05 5.17E-113.37E-07 9.26E-07 4.02E-12

NI NI NII.26E-08 3.45E-08 1.50E-134.52E-09 I.24E-08 5.39E-14

Nl NI NINI NI NI

2.05E-07 5.61 E-07 2.44E-12Nl NI NINl NI NINI Nl NI

1.55E-07 8.19E-07 • Nl

1.25E-05 7.94E-06 3.52E-09NI NI 7.92E-10NI Nl NlNI Nl NINI - NI NlNl NI NINI NI NINl NI NI

7.20E-06 2.13E-05 2.02E-10

Total Risks% of

Total Total

8.02E-10 0O.OOE+00 0O.OOE+00 0O.OOE+00 0

O.OOE+00 0O.OOE+00 02.04E-06 31.63E-05 231.26E-06 2

O.OOE+00 04.70E-08 01.69E-08 0

O.OOE+00 0O.OOE+00 07.66E-07 1O.OOE+00 0O.OOE+00 0O.OOE+00 0

9.74E-07 1


2.85E-05 40

Total Risk by Route 2.S3E-OS 4.50E-05

Total Risk 7.0E-05

4.S8E-09

AAG/

[Madl_serverl/jobs/1217/431/analyucaldatabase/newdata/clintonmaster/IPCSurfCancVisitor_Tres(TblW2l).xls]

Page I of 1


Table F-18






VOCsBenzeneEUiylbenzeneTolueneTola! Xylenes

PAHs

Acenaphihenc

Anthracene

Benzo(a)amhracene

Bcnzo(a)pyrenc

Uenzo(b)fluoramhenc

Bcnzofg.h.Dperylcne

Benzo(lc)lluoran(hene

Chryscnc

Fluoranlhcnc

Fluorenc

]ndeno(l,2,3-cd)pyrene

Naphthalene

Phenanlhrcnc

Pyrcne



PCBsAroclor 12ISO

EPC(mg/kg)

3.40E-022.80E-024.20E-023.70E-02

2.60E+001.20E+001.52E+011.21E+OI9.40E+007.10E+003.50E+001.26E+013.93E+012.50E+005.70E+002.60E+006.40E+003.27E+01

2.63E+01

I.70E+021.40E+OI7.80E+012.53E+045.5IE+02J.94E+011.31E+03I.79E+01

7.32E+01

VF(Calculated)

3.48E+035.17E+034.43E+035.99E+03



I.I7E-08 2.47E-08 1.25E-079.63E-09 2.03E-08 6.90E-081.45E-08 3.05E-08 1.21E-071.27E-08 2.69E-08 7.88E-08

8.95E-07 2.46E-06 2.5 IE- 114.13E-07 1.13E-06 I.16E-115.23E-06 1.44E-05 I.47E-104 16E-06 1.14E-05 1.17E-103.23E-06 8.88E-06 9.07E-112.44E-06 6.70E-06 6.85E-1 11.20E-06 3.30E-06 3.38E-114.34E-06 1.I9E-05 1.22E-101.35E-05 3.7IE-05 3.79E-108.60E-07 2.36E-06 2.41E-11I.96E-06 5.38E-06 5.50E-1I8.95E-07 2.46E-06 2 .51E-1I2.20E-06 6.04E-06 6.18E-I1I.13E-05 3.09E-05 3.16E-10

9.05E-06 4.78E-05 2.54E-10

5.85E-05 3.70E-05 I.64E-094.82E-06 1.02E-06 1.35E-102.68E-05 5.67E-06 7.53E-IO8.71E-03 I.84E-03 2.44E-071.90E-04 4.00E-05 5.32E-096.67E-06 1.4IE-06 1.87E-104.51E-04 9.52E-05 I.26E-086.16E-06 1.30E-06 1.73E-IO

2.52E-05 7.44E-05 7.07E-IO



3.00E-03 3.00E-03 1.70E-03l.OOE-OI I.OOE-OI 2.86E-012.00E-OI 2.00E-OI 1.14E-012.00E+00 2.00E+00 Nl

6.00E-02 6.00E-02 NI3.00E-01 3.00E-OI NI

NI NI NINI NI NlNI NI NlNI NI NINI Nl NlNI NI NI

4.00E-02 4.00E-02 Nl4.00E-02 4.00E-02 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI NI3.00E-02 3.00E-02 Nl

3.00E-02 3.00E-02 NI

3.00E-04 3.00E-04 NI3.00E-03 6.00E-05 2.86E-053.70E-02 1.11E-02 Nl3.00E-01 4.50E-02 NI

NI NI NI2.00E-02 8.00E-04 NI3.00E-01 3.00E-01 Nl2.00E-02 2.00E-02 NI

2.00E-05 2.00E-05 NI

Hazard Quotient


3.90E-06 8.23E-06 7.32E-059.63E-08 2.03E-07 2.42E-077.23E-08 1.53E-07 1.06E-066.37E-09 U4E-08 NI

1.49E-05 4.09E-05 NI1.38E-06 3.78E-06 NI

NI Nl NINI NI NINl NI NINl NI NINI Nl NINl NI NI

3.38E-04 9.28E-04 NI2.15E-05 5.90E-05 NI

Nl Nl NI4.47E-05 1.23E-04 2.93E-08

Nl NI NI3.75E-04 1.03E-03 NI

3.02E-04 1.59E-03 NI

1.95E-01 1.23E-01 Nl1.61E-03 1.69E-02 4.73E-067.25E-04 5.IOE-04 Nl2.90E-02 4.09E-02 NI

Nl NI NI3.34E-04 1.76E-03 NlI.50E-03 3.17E-04 NI3.08E-04 6.50E-05 NI

1.26E+00 3.72E+00 NI

Total Hazard Quotient%of

Total Tolal

8.54E-05 05.41 E-07 01.28E-06 01.98E-08 0

5.58E-05 05.15E-06 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 01.27E-03 08.05E-05 0O.OOE+00 01.68E-04 0

O.OOE+00 01.40E-03 0

I.89E-03 0

3.18E-01 61.86E-02 01.24E-03 06.99E-02 1O.OOE+00 02.10E-03 01.82E-03 03.73E-04 0

4.98E+00 92

Total Hazard Index

Total Hazard Index by Route 1.49E+00 3.91 E+00 7.93E-OS

S.4E+00

AAG/

[Mad l_serverl/jobs/1217/43 I/analytical database/newdaia/clintonmaster/IPCSurfNCVisitor_Tres(TblW22).xls]

Page I of I

^^abl

Medium: IPC Side Subsurface Soil (1-10 ft)LandUse: Future

Table F-19


Clinton FMGP Site

Clinton, Iowa



CHEMICAL OFPOTENTIAL CONCERNVOCsBenzeneChloromethaneEthylbenzeneMethylene ChlorideTolueneTotal Xylcncs

PAHsAcenaphthencAcenapnihyleneAnthracene3enzo(a)anthraccneBenzo(a)pyreneBenzo(b)fluoranlheneBenzols. h.ijperylcneBenzo(k)fluoraniheneChryseneDibenz(a.h)anihraccneFluorantheneFluoreneIndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanthrenePyrenc


EPC(mg/kg)

5.30E+011.42E+001.22E-K)21.01E-012.30E+025.60E+02

7.56E+031.91E+042.35E+032.50E+028.11E+024.I5E+012.08E+022.12E+022.94E+021.27E+015.I9E+016.I7E+032.29E+021.92E+047.57E+033.07E+01

8.80E+002.14E+015.10E+013.08E+043.40E+023.55E+013.74E+024.59E+01

VF(Calculated)

3.48E+031.47E+035.I7E+033.14E+034.43E+035.99E+03



2.41E-06 5.50E-06 2.77E-056.46E-08 I.47E-07 1.76E-065.55E-06 1.27E-05 4.30E-054.60E-09 1.05E-08 5.85E-081 .05E-05 2.39E-05 9.45E-052.55E-05 5.81E-05 1.70E-04

3.44E-04 1.02E-03 1.04E-088.69E-04 2.58E-03 2.63E-08I.07E-04 3.I8E-04 3.25E-091.14E-03 3.37E-05 3.45E-103.69E-05 1.09E-04 1.12E-091.89E-06 5.60E-06 5.72E-119.47E-06 2.81E-05 2.87E-109.65E-06 2.86E-05 2.92E-101.34E-05 3.97E-05 4.05E-105.78E-07 1.71E-06 1.75E-1I2.36E-06 7.00E-06 7 . I6E-I12.81E-04 8.32E-04 8.50E-091.04E-05 3.09E-05 3.16E-108.74E-04 2.59E-03 2.65E-083.45E-04 1.02E-03 I.04E-081.40E-06 4.I4E-06 4.23E-11

4.00E-07 2.74E-07 1.2 IE- 119.74E-07 2.22E-07 2.95E-112.32E-06 5.29E-07 7.03E-I11.40E-03 3.20E-04 4.25E-081.55E-05 3.53E-06 4.69E-10I.62E-06 3.68E-07 4.90E-111.70E-05 3.88E-06 5.16E-102.09E-06 4.76E-07 6.33E-I1

SloDe Factors


5.50E-02 5.50E-02 2.90E-021.30E-02 1.30E-02 6.30E-03

NC NC NC7.50E-03 7.50E-03 1.65E-03

NC NC NCNC NC NC


7.30E-01 7.30E-OI 3.10E-017.30E+00 7.30E+00 3.IOE+007.30E-OI 7.30E-OI 3.10E-01

NC NC NC7.30E-02 7.30E-02 3.10E-027.30E-03 730E-03 3.IOE-037.30E+00 7.30E+00 3.IOE+00

NC NC NCNC NC NC


I.SOE+00 I.50E+00 1.50E+OINI NI 4.10E+01NC NC NCNC NC NCNI NI NINI NI NINC NC NCNC NC NC

Cancer Risks


I.33E-07 3.02E-07 8.04E-078.40E-10 1.92E-09 1.11E-08

NI NI NI3.45E-11 7.86E-11 9.63E-11

NI NI NINI NI NI

NI NI NINI ' NI NINI NI NI

8.31E-06 2.46E-05 1.07E-102.69E-04 7.99E-04 3.47E-091.38E-06 4.09E-06 1.77E-11

NI NI NI7.04E-07 2.09E-06 9.06E-129.77E-08 2.90E-07 I.26E-124.22E-06 1.25E-05 5.43E-1I

NI NI NINI NI NI

7.61E-06 2.26E-05 9.79E-I1NI NI NINI NI NINI NI NI

6.01E-07 4.1IE-07 1.82E-10NI NI 1.2IE-09NI NI NINI NI NlNI NI NINI NI NINl NI NINI Nl NI

Total Risks

%a(Total Total

1.24E-06 0I.38E-08 0

O.OOE+00 02.09E-10 0O.OOE+00 0O.OOE+00 0

O.OOE+00 0O.OOE+00 0O.OOE+00 03.29E-05 31 .07E-03 925.47E-06 0O.OOE+00 02.79E-06 03.87E-07 01 .67E-05 1


1.01E-06 01.21E-09 0



Total Risk

1.63E-08

1.2E-03

AAG/[Mad l_serverl/jobs/1217/43 I/analytical database/newdata/clintonmaster/IPCSubCancVis_Tres(0-10)(TW23).xls]

,ge 1 of 1

Medium: IPC Side Subsurface Soil (1-10 ft)LandUse: Future

Table F-20






VOCsBenzeneChloro methaneEthylbenzeneMethylene ChlorideTolueneTotal Xylenes

PAHsAcenaphtheneAcenaphthylcneAnthraceneBenzo(a)amhraceneBenzo(a)pyreneBenzo(b)lluoraniheneBenzo(g.h.i)peryleneBenzo(k)nuoranihcncChryseneDibcnz(a.h)anthraceneFluoranihcncFluoreneIndenot 1 ,2,3-cd)pyreneNaphthalenePhenanthrenePyrene


EPC(mg/kg)

5.30E+011.42E+001.22E+021.01E-012.30E+025.60E+02

7.56E+031.91E+042.35E+032.50E+028.1IE+024.I5E+012.08E+022.12E+022.94E+021.27E+01

5.19E+016.17E+032.29E+021.92E+04

7.57E+033.07E+01

8.80E+002.14E+OI5.10E+013.08E+043.40E+023.55E+013.74E+024.59E+OI

VF(Calculated)

3.48E+031.47E+035.17E+033.I4E+034.43E+035.99E403



I.69E-05 3.85E-05 1.94E-044.52E-07 1.03E-06 1.23E-053.89E-05 8.86E-05 3.01 E-043.22E-08 7.34E-08 4.IOE-077.33E-05 1.67E-04 6.61 E-041.78E-04 4.07E-04 1.19E-03

2.41E-03 7.14E-03 7.30E-086.08E-03 1.80E-02 1.84E-077.50E-04 2.22E-03 2.27E-087.96E-05 2.36E-04 2.41E-092.58E-04 7.66E-04 7.83E-091.32E-05 3.92E-05 4.01E-106.63E-05 1.96E-04 2.0IE-096.7JE-05 2.00E-04 2.05E-099.37E-05 2.78E-04 2.84E-094.05E-06 1.20E-05 1.23E-10I.65E-05 4.90E-05 5.01E-101.96E-03 5.82E-03 5.95E-087.30E-05 2.I6E-04 2.21E-096.12E-03 1.81E-02 1.85E-072.41E-03 7.15E-03 7.3IE-089.78E-06 2.90E-05 2.96E-10

2.80E-06 1.92E-06 8.50E-I16.82E-06 1.55E-06 2.07E-101.62E-05 3.70E-06 4.92E-109.81E-03 2.24E-03 2.97E-071.08E-04 2.47E-05 3.28E-09USE-OS 2.58E-06 3.43E-101.19E-04 2.72E-05 3.61E-091.46E-05 3.33E-06 4.43E-10

Reference Doses


3.00E-03 3.00E-03 1.70E-03Nl Nl 8.60E-02

l.OOE-01 l.OOE-01 2.86E-016.00E-02 6.00E-02 8.57E-012.00E-01 2.00E-01 1.14E-012.00E+00 2.00E+00 Nl

6.00E-02 6.00E-02 NlNl Nl Nl

3.00E-01 3.00E-01 NlNl Nl NlNl Nl NlNl Nl NlNl Nl NlNl Nl NlNl Nl NlNl Nl Nl

4.00E-02 4.00E-02 Nl4.00E-02 4.00E-02 Nl

Nl Nl Nl2.00E-02 2.00E-02 8.57E-04

Nl Nl Nl3.00E-02 3.00E-02 Nl

3.00E-04 3.00E-04 Nl3.00E-03 6.00E-05 2.86E-053.70E-02 1.11E-02 Nl3.00E-01 4.50E-02 Nl

Nl Nl Nl2.00E-02 8.00E-04 Nl3.00E-01 3.00E-01 Nl2.00E-02 2.00E-02 Nl

Hazard Ouotient


5.63E-03 1.28E-02 I.14E-01Nl Nl 1.43E-04

3.89E-04 8.86E-04 1 .05E-035.36E-07 1.22E-06 4.78E-073.66E-04 8.35E-04 5.79E-038.92E-05 2.03E-04 Nl

4.01E-02 1.19E-OI NlNl Nl Nl

2.50E-03 7.41E-03 NlNl Nl NlNl Nl NlNl Nl NlNl Nl NlNl Nl NlNl Nl NlNl Nl Nl

4.13E-04 1.23E-03 Nl4.91E-02 1.46E-01 Nl

Nl Nl Nl3.06E-01 9.06E-01 2.16E-04

Nl Nl Nl3.26E-04 9.66E-04 Nl

9.34E-03 6.39E-03 Nl2.27E-03 2.59E-02 7.23E-064.39E-04 3.34E-04 Nl3.27E-02 4.97E-02 Nl

Nl Nl Nl5.65E-04 3.22E-03 Nl3.97E-04 9.06E-05 Nl7.31 E-04 I.67E-04 Nl

Total Hazard Ouotient

%ofTotal Total

1.33E-01 71.43E-04 02.33E-03 02.24E-06 06.99E-03 02.93E-04 0

1.39E-OI 9O.OOE-fOO 09.91E-03 1O.OOE-fOO 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0

O.OOE+00 0O.OOE+00 01.64E-03 01.95E-01 11

O.OOE+00 01.21E+00 65O.OOE+00 01.29E-03 0

O.OOE+00 0

1.57E-02 12.82E-02 27.73E-04 08.24E-02 4O.OOE+00 03.79E-03 04.88E-04 08.98E-04 0


Total Hazard Index

1.28E+00 1.21E-01

1.9E+00

AAG/

[Mad 1 .server 1/jobs/l 217/43 I/analytical database/newdata/climonmasler/IPCSubNCVis_Tres(0-10)(TW24).xls]

Paje I of I

Medium: Allied Site Surface SoilLandUsc: Future

Table F-21


Clinton FMGP Site

Clinton, Iowa

Receptor: Industrial WorkerExposure Pathway: Inhalation of Fugitive Dust/Vapors


CHEMICAL OFPOTENTIAL CONCERNVOCsBenzeneEthylbenzeneMethylene ChlorideTolueneToial Xylracs

PAHs

Acenaphlhcne

Anthracene

BcnzoMamhraccnc

9enzo(a)pyrcne

Benzo(b)fluoramhene

Benzo(g.h.i)pcrylene

Benzo(k)nuoramhene

Chrysenc

PluoranthcncFluorenc

Indenod ,2,3-cd)pyreneNaphthalenePhenanthrene

Pyrcne

Metals

ArsenicChromium VICopperIronLeadNickelZincCyanide

PCBsAroclor 1242

Aroclor 12.MAroclor 1260

EPC(nig/kg)

I.12E-013.40E-025.00E-034.40E-024.50E-02

9.64E+014.20E+001.43E+015.60E+006.80E+004.30E+003.90E+00I.28E+012.80E+008.10E+003.30E+005.00E-023.59E+014.30E+00

8.45E+01I.13E+026.79E+021.09E+051.47E+034.49E+OI2.86E+031.51E+01

3.50E-OII.90E-019.00E-02

VF(Calculated)

3.48E+035.17E+033.I4E+034.43E+035.99E+03



1.49E-08 1.96E-08 1.03E-064.5IE-09 5.96E-09 2.10E-076.64E-10 8.76E-10 5.07E-085.84E-09 7.7IE-09 3.16E-075.98E-09 7.89E-09 2.39E-07

1.28E-05 2.20E-05 2.33E-095.58E-07 9.57E-07 l .OIE-10I.90E-06 3.26E-06 3.45E-107.44E-07 1.28E-06 1.35E-109.03E-07 I.55E-06 1.64E-105.71E-07 9.80E-07 1.04E-105.18E-07 8.89E-07 9.42E-111.70E-06 2.92E-06 3.09E-103.72E-07 6.38E-07 6.76E-I11.08E-06 1.85E-06 1.96E-IO4.38E-07 7.52E-07 7.97E-116.64E-09 1.14E-08 1.21E-I24.77E-06 8.18E-06 8.67E-105.71E-07 9.80E-07 1.04E-10

1.12E-05 4.44E-06 2.04E-091.50E-05 1.98E-06 2.73E-099.02E-05 1.19E-05 1.64E-081.44E-02 1.90E-03 2.62E-061.95E-04 2.58E-05 3.55E-085.96E-06 7.87E-07 1.08E-093.80E-04 5.01 E-05 6.9 IE-OS2.01E-06 2.65E-07 3.65E-10

4.65E-08 8.59E-08 8.45E-122.52E-08 4.66E-08 4.59E-121.20E-08 2.21E-08 2.17E-12

Slorte Factorskg-day/mg


5.50E-02 5.50E-02 2.90E-02NC NC NC


NC NC NCNC NC NC

7.30E-01 7.30E-01 3.10E-017.30E+00 7.30E+00 3.10E+007.30E-OI 7.30E-OI 3.10E-OI

NC NC NC7.30E-02 7.30E-02 3.10E-027.30E-03 7.30E-03 3.10E-03

NC NC NCNC NC NC

7.30E-01 7.30E-OI 3.10E-01NC NC NCNC NC NCNC NC NC

I.50E+00 I.30E+00 1.50E+OINI NI 4.10E+01NC NC NCNC NC NCNI NI NINI NI NINC NC NCNC NC NC

2.00E+00 2.00E+00 2.00E+002.00E+00 2.00E+00 2.00E+002.00E+00 2.00E+00 2.00E+00

Cancer Risks


8.18E-10 I.08E-09 2.97E-08NI NI NI


NI NI NINI NI NI

I.39E-06 2.38E-06 1.07E-105.43E-06 9.32E-06 4.19E-106.59E-07 1.13E-06 5.09E-11

NI NI NI3.78E-08 6.49E-08 2.92E-121.24E-08 2.13E-08 9.58E-13

NI NI NINI NI NI

3.20E-07 5.49E-07 2.47E-1INI NI NINI NI NINI NI NI


9.30E-08 I.72E-07 I.69E-I15.05E-08 9.33E-08 9.17E-122.39E-08 4.42E-08 4.35E-12

Total Risks%of

Total Total

3.16E-08 0O.OOE+00 09.50E-11 0O.OOE+00 0O.OOE+00 0

O.OOE+00 0O.OOE+00 03.77E-06 81.47E-05 321.79E-06 4

O.OOE+00 01.03E-07 03.37E-08 0O.OOE+00 0O.OOE+00 08.69E-07 2O.OOE+00 0O.OOE+00 0O.OOE+00 0

2.35E-05 521.12E-07 0


2.65E-07 11.44E-07 0681E-08 0


Total Risk 4.5E-OS

1.43E-07

AAG/

[Madl_serverI/jobs/1217/43 I/analytical database/newdaia/dintonmastcr/AlliedSurfCancOn-Siiework(TblW-5).xls]

Page I of I

Medium: Allied Side Surface SoilLandUse: Future

VableF-22


Clinton FMGPSiteClinton, Iowa

Receptor: Industrial WorkerExposure Pathway: Incidental Ingestion, Dermal Contact, and



VOCs

BenzeneEthylbenzeneMethylene ChlorideToluene

Total Xylenes

PAHsAcenaphlhcne

Anthracene9enzo(a)amhraccne

Benzo(a)pyrencBenzo(b)(luoranihcne

Benzo(g.h.i)perylene3cnzo(k)fluoranthenc

ChrysencFluoranihenefHuorent;

lndeno(l ,2,3-cd)pyreneNaphthalene

PhcnanihrencPyrene

MetalsArsenicChromjum VICopperIron_eadNickelZincCyanide

PCBsAroclor 1242Aroclor 1254

Aroclor 1260

EPC(mg/kg)

1.I2E-OI

3.40E-025.00E-034.40E-024.50E-02

9.64E+OI

4.20E+001.43E+01

5.60E+006.80E+00

4.30E+003.90E+001.28E+012.80E+008.10E+003.30E+005.00E-023.59E+014.30E+00

8.45E+01I.I3E+026.79E+02I.09E+05

1.47E+034.49E+01

2.86E+031.5IE+01

3.50E-011.90E-01

9.00E-02

VF(Calculated)

3.48E+035.17E+033.14E+034.43E+035.99E+03



4.16E-08 5.50E-08 2.87E-061.26E-08 1.67E-08 5.87E-071.86E-09 2.45E-09 1.42E-071.64E-08 2.16E-08 8.86E-071.67E-08 2.2IE-08 6.70E-07

3.58E-05 6.15E-05 6.52E-091.56E-06 2.68E-06 2.84E-105.32E-06 9.12E-06 9.67E-10

2.08E-06 3.57E-06 3.79E-IO2.53E-06 4.34E-06 4.60E-101.60E-06 2.74E-06 2.9 IE- 101.45E-06 2.49E-06 2.64E-104.76E-06 8.17E-06 8.65E-101.04E-06 1.79E-06 1.89E-103.0IE-06 5.17E-06 5.48E-IO1.23E-06 2.HE-06 2.23E-10

1.86E-08 3.19E-08 3.38E-121.33E-05 2.29E-05 2.43E-091.60E-06 2.74E-06 2.91E-10

3.14E-05 I.24E-05 5.7IE-094.20E-05 5.55E-06 7.64E-092.52E-04 3.33E-05 4.59E-084.04E-02 5.33E-03 7.35E-065.47E-04 7.21 E-05 9.94E-081.67E-05 2.20E-06 3.04E-091.06E-03 1.40E-04 1.93E-075.61E-06 7.41E-07 1.02E-09

1.30E-07 2.40E-07 2.37E-117.06E-08 1.31E-07 1.28E-11

3.35E-08 6.18E-08 6.08E-12

Reference Doses


3.00E-03 3.00E-03 I.70E-03l.OOE-OI l.OOE-01 2.86E-01

6.00E-02 - 6.00E-02 8.57E-012.00E-01 2.00E-01 1.14E-012.00E+00 2.00E+00 NI

6.00E-02 6.00E-02 NI


4.00E-02 4.00E-02 NI4.00E-02 4.00E-02 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI NI3.00E-02 3.00E-02 NI

3.00E-04 3.00E-04 NI

3.00E-03 6.00E-05 2.86E-053.70E-02 1.I1E-02 NI3.00E-OI 4.50E-02 NI


2.00E-05 2.00E-05 Ml2.00E-05 2.00E-05 NI

2.00E-05 2.00E-05 NI

Hazard Quotient


1.39E-05 1.83E-05 1.69E-031.26E-07 1.67E-07 2.05E-06

3.10E-08 4.09E-08 1.66E-078.18E-08 1.08E-07 7.75E-068.37E-09 I.10E-08 NI

5.97E-04 1.03E-03 NI


2.60E-05 4.47E-05 NI7.53E-05 1.29E-04 NI

NI NI NI9.30E-07 1.60E-06 3.94E-09

NI NI NI5.33E-05 9.15E-05 NI

1.05E-01 4.15E-02 NI1.40E-02 9.24E-02 2.67E-04

6.82E-03 3.00E-03 NII.35E-01 _ 1.19E-01 NI

NI ' NI NI8.35E-04 2.75E-03 NI3.54E-03 4.68E-04 NI2.81E-04 3.71E-05 NI

6.51E-03 1.20E-02 NI3.53E-03 6.53E-03 NII.67E-03 3.09E-03 NI


%ofTotal Total

1.72E-03 02.35E-06 02.38E-07 07.94E-06 01.94E-08 0

1.62E-03 01.41 E-05 0


O.OOE+00 0O.OOE+00 0O.OOE+00 07.07E-05 0

2.04E-04 0O.OOE+00 02.53E-06 0O.OOE+00 01.45E-04 0

1.46E-01 261.07E-01 199.83E-03 22.53E-01 45O.OOE+00 03.59E-03 14.01E-03 13.18E-04 0

1.85E-02 31.01E-02 24.77E-03 1


Total Hazard Index

2.82E-01 1.97E-03

5.6E-01

AAG/

[Mad 1 .server I /jobs/1217/431 /analytical daiabase/newdata/climonmaster/AlliedSurfNCOn-Sitework(Tbl W-6).xls]Page 1 of 1

Medium: Allied Side Subsurface Soil (1-10 ft.)Land Use: Future

Table F-23


Clinton FMGP Site

Clinton, Iowa

Receptor: Industrial WorkerExposure Pathway: Incidental Ingestion, Dermal Contact, and



VOCsBenzeneEthylbenzeneMeihylene ChlorideToluenefotal Xylcncs

PAHsAcenaphtheneAcenaphlhylcneAnthraceneBenzo(a)anthraceneBcnzo(a)pyreneBcnzo(b)fluoranthcneBenzo(g,h,i)peryleneBenzo(k)fluoramncneChryseneFluoranlhencFluoreneIndeno(l,2.3-cd)pyreneNaphthalene^henanlhrcnt:Pyrene

Acid Extractable2-Nitrophenol4-Nitropheno!

MetalsArsenicChromium VICopperIron_eadNickelZincCyanide

EPC(mg/kg)

9.71E+012.40E+022.50E+OII.69E+023.09E+02

I.34E+031.05E+033.03E+022.48E+02I.68E+021.28E+028.56E+015.36E+015.32E+O21.84E+035.49E+026.96E+012.93E+03I.37E+031.42E+03

6.79E+012.05E+01

5.92E+OI8.30E+011.77E+028.31E+045.97E+026.20E+011.78E+031 .75E+02

VF(Calculated)

3.48E+035.17E+033.I4E+034.43E+035.99E+03



I.29E-05 1.70E-05 8.89E-043.19E-05 4.21E-05 1.48E-033.32E-06 4.38E-06 2.54E-042.24E-05 2.96E-05 1.21E-034.10E-05 5.42E-05 1.64E-03

1.78E-04 3.05E-04 3.24E-081.39E-04 2.39E-04 2.54E-084.02E-05 6.90E-05 7.32E-093.29E-05 5.65E-05 5.99E-092.23E-05 3.83E-05 4.06E-091.70E-05 2.92E-05 3.09E-091.14E-05 .95E-03 2.07E-097.12E-06 .22E-05 1.29E-097.06E-05 .21E-04 I.28E-082.45E-04 4.20E-04 4.45E-087.29E-05 .25E-04 1.33E-089.24E-06 .59E-05 1.68E-093.89E-04 6.68E-04 7.07E-081.82E-04 3.12E-04 3.31E-081.88E-04 3.22E-04 3.42E-08

9.02E-06 1.19E-05 1.64E-092.72E-06 3.59E-06 4.95E-10

7.86E-06 3.11E-06 1.43E-091.10E-05 1.45E-06 2.00E-092.35E-05 3.10E-06 4.27E-091.10E-02 1.46E-03 2.01E-067.93E-05 1.05E-05 1.44E-088.23E-06 1.09E-06 1.50E-092.36E-04 3.12E-05 4.30E-082.32E-05 3.07E-06 4.23E-09

Slone Factors


5.50E-02 5.50E-02 2.90E-02NC NC NC

7.50E-03 7.50E-03 I.65E-03NC NC NCNC NC NC


7.30E-01 7.30E-01 3.10E-017.30E+00 7.30E+00 3.10E+007.30E-01 7.30E-01 3.10E-01

NC NC NC7.30E-02 7.30E-02 3.10E-027.30E-03 7.30E-03 3.10E-03

NC NC NCNC NC NC


NC NC NCNC NC NC

1.50E+00 I.50E+00 1.50E+OINI NI 4.10E+01NC NC NCNC NC NCNI NI NINI NI NINC NC NCNC NC NC

Cancer Risks


7.09E-07 9.36E-07 2.58E-05NI NI NI



2.40E-05 4.13E-05 1.86E-09I.63E-04 2.79E-04 1.26E-081.24E-05 2.13E-05 9.58E-IO

NI NI NI5.20E-07 8.92E-07 4.01E-115.I6E-07 8.85E-07 3.98E-I1

NI NI NINI NI NI


NI NI NINI NI NI

1.I8E-05 4.67E-06 2.14E-08NI NI 8.22E-08NI NI NINI NI NINI ' NI NINI NI NINI NI NINI NI NI

Total Risks

%ofTotal Total

2.74E-05 5O.OOE+00 04.75E-07 0O.OOE+00 0O.OOE+00 0

O.OOE+00 0O.OOE+00 0O.OOE+00 06.53E-05 1 14.42E-04 763.37E-05 6O.OOE+00 01.4IE-06 01.40E-06 0

O.OOE+00 0O.OOE+00 01.83E-05 3




Total Risk by Route 2.I9E-04 3.60E-04

Total Risk

5J7E-07

5.8E-04

AAG/

[Madl_ser\'erl/jobs/l217/43I/analytical daiabase/newdata/clintonmaster/AlliedSubCancOn-Sitework(0-10)(TblW-?^3]on

Medium: Allied Side Subsurface Soil (1-10 ft.)LandUse: Future

Table F-24






VOCs

BenzeneEthylbenzeneMeihylene ChlorideTolueneToial Xylencs

PAHsAcenaphlhcne

AcenaphihyleneAnthraceneBenzo(a)an(hraceneBenzo(a)pyrene

Benzo(b)fluoranlheneBenzo(g,h.i)peryleneBenzo(k)fluoranlhene

ChryseneFluorantheneFluorene


NaphthalenePhenamhrene

Pyrene

Acid Extractable2-Niirophenol4-Niirophenol

MetalsArsenicChromium VICopperIronLeadNickel

Zinc2yanide

EPC(mg/kg)

9.71E+012.40E+022.30E+011.69E+023.09E+02

1.34E+031.05E+033.03E+022.48E+021.68E+02

1.28E+028.56E+01

5.36E+OI5.32E+021.84E+035.49E+02

6.96E+01

2.93E+031.37E+031.42E+03

6.79E+01

2.05E+01

S.92E+018.30E+01

1.77E+028.31E+045.97E+026.20E+01

1.78E+031.75E+02

VF(Calculated)

3.48E+035.I7E+033.14E+034.43E+035.99E+03



3.6IE-05 4.77E-05 2.49E-038.92E-05 1.18E-04 4.14E-039.30E-06 1.23E-05 7.10E-046.28E-05 8.29E-05 3.40E-031.15E-04 1.52E-04 4.60E-03

4.98E-04 8.55E-04 9.06E-083.90E-04 6.70E-04 7.10E-081.13E-04 I.93E-04 2.05E-089.22E-05 1.58E-04 1.68E-086.25E-05 1.07E-04 1.14E-084.76E-05 8.17E-05 8.65E-093.18E-05 5.46E-05 5.79E-091.99E-05 3.42E-05 3.62E-091.98E-04 3.39E-04 3.60E-086.85E-04 1.18E-03 1.25E-072.04E-04 3.50E-04 3.71E-08

2.59E-05 4.44E-05 4.71E-09I.09E-03 1.87E-03 1.98E-075.09E-04 8.74E-04 9.26E-085.26E-04 9.03E-04 9.57E-08

2.52E-05 3.33E-05 4.59E-09

7.62E-06 1.01E-05 1.39E-09

2.20E-05 8.72E-06 4.00E-09

3.09E-05 4.07E-06 5.61 E-096.58E-05 8.69E-06 1.20E-083.09E-02 4.08E-03 5.62E-062.22E-04 2.93E-05 4.04E-082.31E-05 3.04E-06 4.I9E-09

6.62E-04 8.74E-05 1.20E-07

6.51E-05 8.59E-06 1 18E-08

Reference Doses


3.00E-03 3.00E-03 1.70E-03l.OOE-01 I.OOE-01 2.86E-016.00E-02 6.00E-02 8.57E-012.00E-01 2.00E-01 1.I4E-01

2.00E+00 2.00E+00 NI

6.00E-02 6.00E-02 NINI NI NI


4.00E-02 4.00E-02 NI

4.00E-02 4.00E-02 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI NI3.00E-02 3.00E-02 Ml

NI NI NINI NI NI

3.00E-04 3.00E-04 NI

3.00E-03 6.00E-05 2.86E-053.70E-02 1.11E-02 NI3.00E-01 4.50E-02 NI

NI NI NI2.00E-02 8.00E-04 NI

3.00E-01 3.00E-01 NI2.00E-02 2.00E-02 NI

Hazard Ouotient


1.20E-02 1.59E-02 1.46E+008.92E-04 1.18E-03 1.45E-021.55E-04 2.05E-04 8.28E-043.14E-04 4.15E-04 2.98 E-02

5.74E-05 7.58E-05 NI

8.30E-03 1.42E-02 NINI NI NI

3.76E-04 6.44E-04 NI


1.71 E-02 2.94E-02 NI

5.10E-03 8.76E-03 NINI NI NI

5.45E-02 9.35E-02 2.31E-04NI NI NI

1.75E-02 3.01 E-02 NI

NI NI NINI NI NI

7.34E-02 2.91 E-02 NI1.03E-02 6.79E-02 1.96E-041.78E-03 7.83E-04 NI1.03E-01 9.06E-02 NI

NI NI NI1.15E-03 3.80E-03 NI

2.2IE-03 2.91E-04 NI3.25E-03 4.29E-04 NI


%ofTotal Total

1.49E+00 681.66E-02 11.19E-03 03.05E-02 I1.33E-04 0

2.26E-02 1O.OOE+00 01.02E-03 0


O.OOE+00 0O.OOE+00 0O.OOE+00 04.65E-02 2

1.39E-02 1O.OOE+00 01.48E-01 7

O.OOE+00 0

4.76E-02 2

O.OOE+00 0

O.OOE+00 0

1.02E-01 57.84E-02 42.56E-03 01.94E-01 9

O.OOE+00 04.96E-03 0

2.50E-03 03.68E-03 0


Total Hazard Index

3.87E-01 1.51 E+00

2.2E+00

AAG/

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Pags 1 of 1

^^HfolF-25



Clinton FMCP Site

Clinton, Iowa

Receptor: Site VisitorsfTrespassersExposure Pathway: Incidental Ingestion, Dermal Contact, and

Inhalation or Fugitive Dust/Vapors


VOCsBenzeneEUiylbenzeneMeihylene ChlorideTolueneTola! Xylcnes

PAHs

Acenaphihcnc

Anthracene

9enzo(a)amhracene

Bcnzo(a)pyrene

Benzo(b)(luoramhene

Rcnzo(g.h,i)pcrylcne

Benzo(k)fluoranlhcne

Chrysene

Fluoranthcnc

Fluorcne


NaphthalenePhenanlhrene

Pyrene


PCBsAroclor 1242

Aruclor 1254

Aroclor 1260

EPC

(rng/kg)

1.I2E-013.40E-025.00E-034.40E-024.50E-02

9.64E+014.20E+001.43E+015.60E+006.80E+004.30E+003.90E+001.28E+012.80E+008.10E+003.30E+005.00 E-023.59E+OI4.30E+00

8.45E+011.13E+026.79E+021.09E+05I.47E+034.49E+012.86E+03I.51E+01

3.50E-011.90E-019.00E-02

VF(Calculated)

3.48E+035.17E+033.14E+034.43E+035.99E+03



5.50E-09 1.16E-08 5.86E-081.67E-09 3.53E-09 1.20E-082.46E-IO 5.19E-10 2.90E-092.16E-09 4.57E-09 I.8IE-082.21E-09 4.67E-09 I.37E-08

4.74E-06 1.30E-05 1.33E-IO2.06E-07 5.67E-07 5.79E-127.03E-07 1.93E-06 I.97E-1I2.75E-07 7.55E-07 7.72E-I23.34E-07 9.17E-07 9.38E-I22.11E-07 5.80E-07 5.93E-I21.92E-07 5.26E-07 5.38E-I26.29E-07 1.73E-06 1.77E-11I.38E-07 3.78E-07 3.86E-123.98E-07 1.09E-06 I . 1 2 E - 1 I1.62E-07 4.45E-07 4.55E-I22.46E-09 6.74E-09 6.90E-I41.76E-06 4.84E-06 4.95E-112.11E-07 5.80E-07 5.93E-12

4.15E-06 2.63E-06 1.17E-105.55E-06 "1.17E-06 1.56E-103.34E-05 7.05E-06 9.36E-105.34E-03 1.13E-03 I.50E-077.23E-05 I.53E-05 2.03E-092.21E-06 4.66E-07 6.I9E-111.41E-04 2.97E-05 3.94E-097.42E-07 1.57E-07 2.08E-11

1.72E-08 5.08E-08 4.83E-I39.34E-09 2.76E-08 2.62E-134.42E-09 I.31E-08 I.24E-13

Slooe Factorskg-day/mg


5.50E-02 5.50E-02 2.90E-02NC NC NC


NC NC NCNC NC NC

7.30E-01 7.30E-01 3.IOE-017.30E+00 7.30E+00 3.10E+007.30E-OI 7.30E-01 3.10E-01

NC NC NC7.30E-02 7.30E-02 3.IOE-027.30E-03 7.30E-03 3.10E-03

NC NC NCNC NC NC


I.50E+00 1.50E+00 1.50E+01NI NI 4.IOE+01NC NC NCNC NC NCNI NI NTNI N! NINC NC NCNC NC NC

2.00E+00 2.00E+00 2.00E+002.00E+00 2.00E+00 2.00E+002.00E+00 2.00E+00 2.00E+00

Cancer Risks


3.03E-IO 6.39E-10 1.70E-09NI NI NI

I.84E-12 3.89E-12 4.77E-I2NI NI NINI NI NI

NI NI NINI NI NI

5.13E-07 1.41E-06 6.11E-122.01E-06 5.51E-06 2.39E-I12.44E-07 6.70E-07 2.91E-I2

NI NI NI1.40E-08 3.84E-08 1.67E-134.59E-09 I.26E-08 5.47E-14

NI NI NINI NI NI

I.18E-07 3.25E-07 1.41E-12NI NI NINI NI NINI NI NI


3.44E-08 1.02E-07 9.65E-131.87E-08 5.52E-08 5.24E-138.85E-09 2.61 E-08 2.48E-I3

Total Risks%of

Total Total

2.64E-09 0O.OOE+00 01.05E-11 0


O.OOE+00 0O.OOE+00 01.92E-06 97.52E-06 359.14E-07 4O.OOE+00 05.24E-08 01.72E-08 0



1.36E-07 17.39E-08 03.50E-08 0


Total Risk 2.1E-05

8.18E-09

AAG/

[Mad 1 .server I/jobs/1217/43 I/analytical daiabase/newdata/climonmasier/A]liedSurfCancVist_Trcs(TblW25).xls]

: I of 1

^^Tabl


Table F-26






VOCsBenzeneEihylbenzeneMethylene ChlorideTolueneToial Xylencs

PAHsAcenaphiheneAnthraceneBenzo(a)amhraceneBenzo(a)pyreneBenzo(b)fluoramheneBenzo(g.h,r)pcrylcneBenzo(k)nuoraniheneChryseneFluoranihencFluorcnc

Indeno( 1 ,2.3-cd)pyreneNaphthalenePhcnanthrencPyrene


PCBsAroclor 1242Aroclor 1254Aroclor 1260

EPC(mg/kg)

1.I2E-OI3.40E-025.00E-034.40E-024.50E-02

9.64E+014.20E+001.43E+015.60E+006.80E+004.30E+003.90E+001.28E+012.80E+008.10E+003.30E+005.00E-023.59E+014.30E+00

8.45E+011.13E+026.79E+021.09E+051.47E+034.49E+012.86E+031.51E+01

3.50E-011.90E-019.00E-02

VF(Calculated)

3.48E+035.17E+033.14E+034.43E+035.99E+03



3.85E-08 8.14E-08 4.10E-071.17E-08 2.47E-08 8.38E-081.72E-09 3.63E-09 2.03E-081.51E-08 3.20E-08 1.27E-071.55E-08 3.27E-08 9.58E-08

3.32E-05 9.10E-05 9.3 IE- 101.45E-06 3.97E-06 4.05E-114.92E-06 I.35E-05 1.38E-101.93E-06 5.29E-06 5.41E-112.34E-06 6.42E-06 6.56E-111.48E-06 4.06E-06 4.I5E-111.34E-06 3.68E-06 3.76E-1I4.40E-06 1.21E-05 1.24E-109.63E-07 2.64E-06 2.70E-I12.79E-06 7.65E-06 7.82E-I1I.14E-06 3.12E-06 3.19E-I11.72E-08 4.72E-08 4.83E-I3I.24E-05 3.39E-05 3.47E-10I.48E-06 4.06E-06 4.15E-I1

2.91E-05 1.84E-05 8.I6E-103.89E-05 8.21E-06 1.09E-092.34E-04 4.93E-05 6.55E-093.74E-02 7.89E-03 1.05E-065.06E-04 1.07E-04 1.42E-081.54E-05 3.26E-06 4.33E-109.84E-04 2.08E-04 2.76E-085.20E-06 1.IOE-06 I.46E-IO

1.20E-07 3.56E-07 3.38E-126.54E-08 1.93E-07 1.83E-123.10E-08 9.15E-08 8.69E-13



3.00E-03 3.00E-03 1.70E-03l.OOE-01 l.OOE-01 2.86E-016.00E-02 6.00E-02 8.57E-012.00E-01 2.00E-01 1.14E-012.00E+00 2.00E+00 NI

6.00E-02 6.00E-02 NI3.00E-OI 3.00E-01 NI

NI NI NINT NI NINI NI NINI NI NINI NI NINI NI NI

4.00E-02 4.00E-02 NI4.00E-02 4.00E-02 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI NI3.00E-02 3.00E-02 NI



2.00E-05 2.00E-05 Ml2.00E-05 2.00E-05 NI2.00E-05 2.00E-05 NI

Hazard Ouotienl


1.28E-05 2.71E-05 2.41E-04I.17E-07 2.47E-07 2.93E-072.87E-08 6.05E-08 2.37E-087.57E-08 1.60E-07 1.11E-067.74E-09 1.63E-08 NI

5.33E-04 1.52E-03 NI4.82E-06 1.32E-05 NI

Ml NI NINI NI NINI NI NINI NI NINI NI NINI NI NI

2.4IE-05 6.61E-05 NI6.97E-05 1.91E-04 NI

NI NI NI8.60E-07 2.36E-06 5.63E-10

NI NI NI4.93E-05 1.35E-04 NI

9.69E-02 6.I4E-02 NI1.30E-02 1.37E-01 3.82E-056.31E-03 4.44E-03 NI1.25E-01 1.75E-OI NI


6.02E-03 I.78E-02 NI3.27E-03 9.66E-03 NI1.55E-03 4.58E-03 NI

Total Hazard Ouotienl%of

Total Total

2.8IE-04 06.57E-07 01.I3E-07 01.34E-06 02.4 IE-OS 0

2.07E-03 01.80E-05 0

O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 09.02E-05 02.61E-04 0O.OOE+00 03.22E-06 0O.OOE+00 01.85E-04 0

1.58E-01 231.50E-OI 221.08E-02 23.00E-01 45O.OOE+00 04.85E-03 13.97E-03 13.I5E-04 0

2.38E-02 41.29E-02 26.12E-03 1


Total Hazard Index

4.17E-01 2.81E-04

6.7E-01

Page 1 of 1


Table F-27


Clinton FMGP Site

Clinton, Iowa



CHEMICAL OFPOTENTIAL CONCERNVOCsBenzeneEthylbenzeneMethylene ChlorideTolueneTotal Xylcnes

PAHsAcenaphthencAcenaphthylencAnthraceneBenzo(a)anthraceneBcnzo(a)pyrcnuBenzo(b)flunramhencBcnzo(g.h.i)perylcneBcnzo(k)nucirnnlhcne

ChryseneFluoranihcneFluoreneIndenof 1 ,2,3-cd)pyreneNaphthalene?henanihrcncPyrene



EPC(mg/kg)

9.71E+012.40E+022.50E+011.69E+023.09E+02

1.34E+031.05E-t033.03E+022.48E+021.68E+02I.28E+028.56E+015.36E+OI5.32E+021.84E+035.49E+026.96E+OI2.93E+031.37E+031.42E+03

6.79E+012.05E+01

5.92E+018.30E+011.77E+028.31E+045.97E+026.20E+011.78E+031 .75E+02

VF(Calculated)

3.48E+035.I7E+033.14E+034.43E+035.99E+03



4.42E-06 1.01E-05 5.08E-051.09E-05 2.49E-05 8.45E-051.14E-06 2.59E-06 1.45E-057.69E-06 1.75E-05 6.94E-05I.41E-05 3.21E-05 9.40E-05

6.10E-OS 1.81E-04 1.85E-094.78E-05 1.42E-04 I.45E-091.38E-05 4.09E-05 4.18E-101.I3E-05 3.35E-05 3.42E-107.65E-06 2.27E-05 2.32E-105.83E-06 1.73E-05 1.77E-103.90E-06 1.15E-05 1.18E-102.44E-06 7.23E-06 7.39E-112.42E-05 7.I8E-05 7.34E-108.39E-05 2.49E-04 2.54E-092.50E-05 7.41E-05 7.57E-103.17E-06 9.39E-06 9.60E-I1I.33E-04 3.95E-04 4.04E-096.23E-05 1.85E-04 1.89E-096.44E-05 1.91E-04 1.95E-09

3.09E-06 7.05E-06 9.36E-119.33E-07 2.13E-06 2.83E-11

2.69E-06 1.84E-06 8.16E-113.78E-06 8.61E-07 1.I4E-108.06E-06 1.84E-06 2.44E-103.78E-03 8.62E-04 1.15E-072.72E-05 6.19E-06 8.23E-102.82E-06 6.43E-07 8.55E-118.10E-05 1.85E-05 2.45E-097.96E-06 1.82E-06 2.4 IE- 10

Slone Factors


5.50E-02 5.50E-02 2.90E-02NC NC NC



7.30E-OI 7.30E-01 3.10E-OI7.30E+00 7.30E+00 3.10E+007.30E-01 7.30E-01 3.10E-OI

NC NC NC7.30E-02 7.30E-02 3.10E-027.30E-03 7.30E-03 3.10E-03

NC NC NCNC NC NC


NC NC NCNC NC NC

1.50E+00 1.50E+00 1.50E+01Nl NI 4.10E+01NC NC NCNC NC NCNI NI NlNI NI NINC NC NCNC NC NC

Cancer Risks


2.43E-07 5.54E-07 1.47E-06NI NI NI



8.24E-06 2.44E-05 1.06E-105.58E-05 I.65E-04 7.18E-104.25E-06 1.26E-05 5.47E-11

NI NI NI1.78E-07 5.28E-07 2.29E-12I.77E-07 5.24E-07 2.27E-12

Nl NI NINI NI NI


Nl NI NlNl NI NI

4.04E-06 2.76E-06 1.22E-09NI NI 4.69E-09Nl NI NINI NI NINl NI NINI NI NINI NI NINI NI Nl

Total Risks

%ofTotal Total

2.27E-06 1O.OOE+00 05.18E-08 0O.OOE+00 0O.OOE+00 0

O.OOE+00 0O.OOE+00 0O.OOE+00 03.27E-05 1 12.21E-04 771.69E-05 6

O.OOE+00 07.06E-07 07.0IE-07 0O.OOE+00 0O.OOE+00 09.17E-06 3O.OOE+00 0O.OOE+00 0O.OOE+00 0

O.OOE+OO 0O.OOE+00 0



Total Risk 2.9E-04

3.07E-08

AAG/

[Mad 1 .server 1 /jobs/1217/43 I/analytical database/newdala/climonmasier/AlliedSubCanc VisTres(0-10)(TW27).xls]Page I of I


Table F-28






VOCsBenzeneEthylbenzeneMethylene ChlorideTolueneTola! Xylencs

PAHsAcenaphlhencAcenaphihylencAnthraceneBenzo(a)anihraceneBcnzo(a)pyrencBcnzo(b)nuoranihcneBenzo(g,h.i)pery!eneBenzo(k)fluoraniheneChryscncRuoranlheneRuoreneIndeno( 1 ,2.3-cd)pyreneNaphthalenePhenanihrenePyrenc

Acid Ex-tractable2-Nitrophenol4-Nitrophenol


EPC(mg/kg)

9.71E+012.40E+022.50E+011.69E+023.09E+02

1.34E+03I.05E+033.03E+022.48E+021.68E+02I.28E+028.56E+015.36E+015.32E+021 .84E+035.49E+026.96E+012.93E+031.37E+031.42E-f03

6.79E+012.05E+01

5.92E+OI8.30E+011.77E+028.31E+045.97E+026.20E+01I.78E+031.75E+02

VF(Calculated)

3.48E+035.17E+033.14E+034.43E+035.99E+03



3.09E-05 7.05E-05 3.56E-047.65E-05 I.74E-04 5.92E-047.96E-06 1.82E-05 1.01E-045.38E-05 1.23E-04 4.86E-049.84E-05 2.24E-04 6.58E-04

4.27E-04 1.27E-03 1.29E-083.35E-04 9.91E-04 1.01E-089.65E-05 2.86E-04 2.93E-097.90E-05 2.34E-04 2.39E-095.35E-05 1.59E-04 1.62E-094.08E-05 1.21E-04 I.24E-092.73E-05 8.08E-05 8.26E-101.71E-05 5.06E-05 5.17E-101.69E-04 5.02E-04 5.14E-095.87E-04 1.74E-03 1.78E-081.75E-04 5.18E-04 5.30E-092.22E-05 6.57E-05 6.72E-109.33E-04 2.77E-03 2.83E-084.36E-04 1.29E-03 1.32E-084.51E-04 1.34E-03 1.37E-08

2.16E-05 4.93E-05 6.55E-106.53E-06 1.49E-05 1.98E-10

1.89E-05 1.29E-05 5.72E-102.64E-05 6.03E-06 8.01E-105.64E-05 1.29E-05 1.71E-092.65E-02 6.04E-03 8.02E-071.90E-04 4.34E-05 5.76E-091.98E-05 4.50E-06 5.99E-105.67E-04 1.29E-04 1.72E-085.58E-05 1.27E-05 1.69E-09

Reference Doses


3.00E-03 3.00E-03 I.70E-03I.OOE-OI l.OOE-OI 2.86E-016.00E-02 6.00E-02 8.57E-012.00E-01 2.00E-01 1.14E-012.00E+00 2.00E+00 NI

6.00E-02 6.00E-02 NINI NI NI


4.00E-02 4.00E-02 NI4.00E-02 4.00E-02 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI NI3.00E-02 3.00E-02 NI

NI NI NINI NI NI

3.00E-04 3.00E-04 NI

3.00E-03 6.00E-05 2.86E-053.70E-02 1.11E-02 NI3.00E-01 4.50E-02 NI


Hazard Quotient


1.03E-02 2.35E-02 2.09E-017.65E-04 I.74E-03 2.07E-031.33E-04 3.03E-04 1.18E-042.69E-04 6.14E-04 4.25E-034.92E-05 1.12E-04 NI

7.11E-03 2.11E-02 NINI NI NI


1.47E-02 4.35E-02 NI4.37E-03 1.30E-02 NI

NI NI NI4.67E-02 1.38E-OI 3.30E-05

NI NI NI1.50E-02 4.45E-02 NI

NI NI NINI NI NI

6.29E-02 4.30E-02 NI8.8IE-03 l.OOE-01 2.80E-051.52E-03 1.16E-03 NI8.82E-02 1.34E-01 NI



%ofTotal Total

2.43E-01 234.58E-03 03.54E-04 05.I3E-03 0I.61E-04 0

2.82E-02 3O.OOE+00 01.28E-03 0

O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 05.82E-02 61.73E-02 2

O.OOE+00 0I.85E-01 18

O.OOE+00 05.96E-02 6


1.06E-01 101.09E-01 102.68E-03 02.22E-OI 21O.OOE+00 06.62E-03 12.32E-03 03.42E-03 0

AAG/


Total Hazard Index

5.73E-01 2.I6E-01

1.1E+00

[Madl_serverl/jobs/l217/431/analytical database/newdata/clintonmaster/AlliedSubNCVisTres(0-10)(TW28).xls p"8e 1 of 1


Table F-29



Receptor: Child Recreational Site VisitorsExposure Pathway: Incidental Ingestion, Dermal Contact, and


CHEMICAL OF

POTENTIAL CONCERN

VOCs

Benzene

Elhylbenzenc

Melhylenc Chloride

Toluene

Toial Xylcnes

PAUsAcenaphthcne

Anthracene

Bcnzo(a)amhracene

Benzo(a)pyrene

BenzotrOfluoramhene

Bcnzots.h.Operylene

Oenzo(k)fluoranihene

CtiryseneFluoranihene

-luorene

lndeno(l.2.i-cd)pyrene

Naphthalene

Phcnamhrene

Pyrene

Arlil Evtraclable

Metals

Arsenic

Chromium VI

Copper

ron

xad

Nickel

Zinc

Cyanide

PCBs

Aroclor 1242

Aroclor 1254

Aroclor 1260

EPC

(mg/kg)

I.12E-01

3.40E-02

5.00E-03

4.40E-02

4.50E-02

9.64E+OI

4.20E+00

I.43E+OI

5.60E+00

6.80E-fOO

4.30E+00

3.90E+00I.28E+01

2.80E+00

8.10E+00

3.30E+00

5.00E-02

3.59E+OI

4.30E+00

8.45E+01

1.I3E+02

6.79E+02

I.09E+05

1.47E+03

4.49E+01

2.86E+03

1.51E+OI

3.50E-01

1.90E-01

9.00E-02

VF

(Calculated)

3.48E+03

5.17E+03

3.I4E+03

4.43E+03

5.99E+03


mc/kc-dayOral

1.40E-09

4.26E-10

7.51E-IO

5.51E-10

5.64E-IO

I.21E-06

5.26E-08

1.79E-07

7.0IE-08

8.52E-08

5.39E-08

4.88E-081.60E-07

3.5IE-08

1.01E-07

4.13E-08

6.26E-10

4.50E-07

5.39E-08

I.06E-06

I.42E-06

8.50E-06

1.36E-03

I.84E-05

5.62E-07

3.58E-05

1.89E-07

5.26E-08

2.86E-08

1.13E-Q9

Dermal

4.07E-IO

1.23E-10

2.18E-10

I.60E-IO

1.63E-10

4.55E-07

1.98E-08

6.75E-08

2.54E-08

3.21E-08

2.03E-08

1.84E-08

6.04E-08

1.32E-08

3.82E-08

1.56E-08

2.36E-10

I.70E-07

2.03E-08

2.78E-07

4.IOE-08

2.47E-07

3.95E-05

5.34E-07

I.63I--08

1.04E-06

5.48E-09

2.14E-08

I.16E-08

4.S8E-10

Inhalation

4.03E-09

8.24E-10

2.39E-09

1.24E-09

9.4 IE- 10

3.99E-I3

2.16E-I3

Slone Factors

kc-dav/mcOral

5.50E-02

NC

7.50E-03

NC

NC

NC

NC

7.30E-OI

7.30E+00

7.30E-01

NC7.30E-02

7.30E-03

NC

NC7.30E-OI

NC

NC

NC

l.50E*On

NI

NC

NC

NI

NT

NC

NC

2.00E+00

2.00E+00

2.QQE+00

Dermal

5.50E-02

NC

7.50E-03

NC

NC

NC

NC

7.30E-OI

7.30E*00

7.30E-01

NC7.30E-02

7.30E-03

NC

NC

7.30E-01

NC

NC

NC

1.50E+00

NI

NC

NC

NI

NI

NC

NC

2.00E+00

2.00E+00

2.00E-MJO

Inhalation

2.90E-02

NC

I.65E-03

NC

NC

NC

NC

3 10E-01

3.IOE+00

3.10E-OI

NC3.10E-02

3.10E-03

NC

NC

3.10E-OI

NC

NC

NC

I.50E+01

4.IOE401

NC

NC

NI

NI

NC

NC

2.00E+00

2.00E+00

2.00E-MX)

Cancer Risks


7.72E-11 2.24E-11 1.I7E-10

NI NI NI

5.54E-I2 1.63E-12 3.94E-I2

NI NI NI

NI NI NI

NI NI NI

NI NI NI

1.31E-07 4.93E-08 O.OOE+00

5.12E-07 1.93E-07 O.OOE+00

6.22E-08 2.34E-08 O.OOE+00

NI NI NI

3.57E-09 1.34E-09 O.OOE+00

1.17E-09 4.41E-10 O.OOE+00

NI NI NI

NI NI NI

3.02E-08 1.I4E-08 O.OOE+00

NI NI NI

NI NI NI

NI NI NI

3.19E-06 4.17E-07 O.OOE+00

NI NI O.OOE+00

NI NI NI

NI NI NI

NI NI NI

NI NI NI

NI NI NI

NI NI NI

I.05E-07 4.27E-08 7.97E-13

5.7IE-08 2.32E-08 4.33E-13

2.25E-09 9.15E-10 O.OOE+00

Total Risks

%of

Total Total

2.16E-IO 0

O.OOE+00 0

I.12E-11 0

O.OOE+00 0

O.OOE+00 0

O.OOE+00 0

O.OOE+00 0

1.80E-07 4

7.05E-07 15

8.56E-08 2

O.OOE+00 04.91E-09 0

1.61E-09 0

O.OOE+00 0

O.OOE+00 0

4.15E-08 1

O.OOE+00 0

O.OOE+00 0

O.OOE+00 0

3.61E-06 74

O.OOE+00 0

O.OOE+00 0

O.OOE+00 0

O.OOE+00 0

O.OOE+00 0

O.OOE+00 0

O.OOE+00 0

1.48E-07 3

8.03E-08 2

3.17E-09 0

Page 1 of I Total Risk by Route 4.10E-06 7.63E-07

Total Risk 4.9E-06

3.I7E-12

^Tablf


'able F-30





CHEMICAL OF

POTENTIAL CONCERN

VOCsBenzeneEthylbenzene

Methylene ChlorideTolueneTotal Xylerws

PAHsAccnaphihcncAnihracem:Benzo(a)amhiaceneBcnzo(a)pyrcnc

Bcnzo(b)fluoranihcneBenzo(g,li.i)peryleneBenzo(kjnuoranihene

ChryscneFluoranthencFluorcneIndenof 1 ,2,3-cd)pyrene

NaphthalenePhenanthrencPyrcne

Acid Extractable

Metals

ArsenicChromium VICopperIron


PCBsAroclor 1242Aroclor 1254

Aroclor 1261)

EPC(mg/kg)

1.12E-013.40E-025.00E-034.40E-024.50E-02

9.64E+014.20E4001.43E+OI5.60E+00

6.80E+004.30E+00

3.90E+00I.28E+012.80E+008.IOE+003.30E-fOO

5.00E-023.59E+OI4.30E+00

8.45E+OI1.13E4026.79E+021.09E+051.47E+034.49E+012.86E+031.51E+01

3.50E-OI

1.90E-019.00E-02

VF(Calculated)

3.48E+035.17E+033.I4E+034.43E+035.99E+03



1.64E-07 4.75E-09 4.70E-084.97E-08 1.44E-09 9.61E-098.77E-08 2.54E-09 2.79E-086.43E-08 1.86E-09 1.45E-086.58E-08 1.9IE-09 I.10E-08

I.4IE-04 5.31E-066.14E-06 2.31E-072.09E-05 7.88E-078.18E-06 3.08E-07

9.94E-06 3.75E-076.28E-06 2.37E-07

5.70E-06 2.I5E-071.87E-05 7.05E-074.09E-06 1.34E-071.18E-05 4.46E-074.82E-06 1.82E-077.3 IE-OS 2.75E-095.25E-05 I.98E-066.28E-06 2.37E-07

1.23E-04 1.07E-061.65E-04 4.79E-079.92E-04 2.88E-061.59E-01 4.60E-04

2.15E-03 6.23E-066.J6E-05 1.90E-074.I8E-03 1.21E-05

2.21 E-05 6.40E-08

6.14E-06 2.49E-07 4.65E-12

3.33E-06 I.35E-07 2.52E-121.32E-07 5.34E-09

Reference Doses


3.00E-03 3.00E-03 1.70E-03I.OOE-01 l.OOE-01 2.86E-016.00E-02 6.00E-02 8.57E-012.00E+00 2.00E+00 I.14E-012.00E+00 2.00E+00 Nl

6.00E-02 6.00E-02 NI3.00E-01 3.00E-01 NI

NI NI NINI NI NINI NI NlNI NI NINI NI NINI NI NI

4.00E-02 4.00E-02 NI4.00E-02 ' 4.00E-02 NI

NI NI NI2.00E-02 2.00E-02 8.57E-04

NI NI Nl3.00E-02 3.00E-02 NI

3.00E-04 3.00E-04 NI3.00E-03 6.00E-05 2.86E-OS3.70E-02 1.11E-02 Nl

NI NI NlNI Nl NI

2.00E-02 8.00E-04 Nl3.00E-01 3.00E-01 Nl2.00E-02 2.00E-02 NI

2.00E-05 2.00E-05 NI

2.00E-05 2.00E-05 NI2.00E-05 2.00E-05 Nl

Hazard Quotient


5.46E-05 1.58E-06 2.77E-054.97E-07 I.44E-08 3.36E-081.46E-06 4.24E-08 3.26E-083.21E-08 9.32E-10 1.27E-073.29E-08 9.53E-10 NI

2.35E-03 8.85E-05 NI2.05E-05 7.71E-07 NI

NI NI NINl NI NINI NI NINI NI NINI NI NINI NI NI

I.02E-04 3.86E-06 NI2.96E-04 1.12E-05 NI

Nl NI NI3.65E-06 1.38E-07 O.OOE+00

NI NI NI2.09E-04 7.90E-06 NI

4.12E-01 3.58E-03 NI5.50E-02 7.98E-03 NC2.68E-02 2.59E-04 NI

NI Nl NINl NI Nl

3.28E-03 2.38E-04 NI1.39E-02 4.04E-05 NII.10E-03 3.20E-06 NI

3.07E-01 1.25E-02 NI

1.67E-01 6.76E-03 NI6.58E-03 2.67E-04 NI


%ofTotal Total

8.38E-05 05.45E-07 01.54E-06 01 .60E-07 03.38E-08 0

2.44E-03 02.12E-05 0O.OOE+00 0O.OOE+00 0

O.OOE+00 0O.OOE+00 0O.OOE+00 0O.OOE+00 01.06E-04 03.07E-04 0

O.OOE+00 03.79E-06 0O.OOE+00 02.17E-04 0

4.15E-01 406.30E-02 62.71E-02 3O.OOE+00 0O.OOE+00 03.52E-03 0I.40E-02 11.11E-03 0

3.19E-01 311.73E-01 17

6.84E-03 1

Page 1 of 1 Total Hazard Index by Route 9.95E-01

Total Hazard Index

3.17E-02 2.79E-OS

l.OE+00

Medium:LandUse:

GroundwaterFuture Residential

Table F-31

Carcinogenic Exposure and Health Risk Estimates (Reasonable Maximum Exposure)

Receptor: On-site Residents (Adult)Exposure Pathway: Incidental Ingesu'on and

Inhalation of Vapors in Shower

CHEMICAL OFCHEMICAL OF

POTENTIAL CONCERNVOCsBenzeneBrontomeihaneCarbon TetrachlorideChloromethane1.2-DichloroethaneElhylbenzeneTolueneloial Xylenes

PAHsAccnaphlheneAcenaphthyleneAnthraceneBenzo(a)anlhraceneBenzo(a)pyreneBenzo(b)f1uoranlheneBenzotg.h.OperyleneBenzo(k)fluorontheneChryseneDibenz(a,h)anthracencFluorantheneRuorene[ndeno{ 1 ,2,3-cd)pyreneNaphthalenePhenanthrenePyrcne

Acid Extractable2,4-DUnethylphenolPhenol


EPC

(mg/L)

1.19E+013.12E-034.90E-043.35E-039.26E-012.49E+005.60E+003.24E+00

6.47E-012.93E+006.47E-026.82E-047.27E-044.5IE-043.12E-041.3IE-049.72E-044.90E-068.20E-037.60E-OI3.01E-048.79E+009.76E-012.32E-02

1.73E-016.92E-02

4.I2E-03I.98E-022.14E-023.60E+024.54E-034.33E-028.64E-028.44E-02

PC(mg/cm1)

2.10E-023.00E-032.20E-024.20E-035.30E-037.40E-024.50E-028.00E-02

0.0790.0790.079

8.10E-011.20E+00I.20E+00

0.0790.079

8.10E-010.079

3.60E-010.079

1.90E+006.90E-02

0.0790.079

0.0791.37E-04

l.OOE-03l.OOE-03l.OOE-03l.OOE-034.00E-06l.OOE-036.00E-04l.OOE-03

Chronic Dailv Intake Valuemg/kg-dav

Oral

1.I2E-012.93E-054.61E-063.15E-058.70E-032.34E-025.26E-023.04E-02

6.08E-032.75E-026.08 E-046.41E-066.83E-064.24E-062.93E-06I.23E-069.13E-064.60E-087.70E-057.14E-032.83E-068.26E-029.17E-032.18E-04

1.62E-036.50E-04

3.87E-051.86E-042.01E-043.38E+004.26E-054.07E-048.12E-047.93E-04

Dermal

6.75E-032.53E-072.91E-073.80E-071.33E-044.98E-036.80E-036.99E-03

I.38E-036.25E-031.38E-041.49E-052.36E-05I.46E-056.66E-072.79E-072.13E-051.05E-087.97E-051.62E-031.54E-051.64E-022.08E-034.95E-05

3.68E-042.56E-07

1.11E-075.35E-073.78E-079.72E-034.90E-101.I7E-06I.40E-062.28E-06

Inhalation

4.19E-03I.10E-061.73E-071.18E-063.26E-048.77E-041.97E-031.14E-03

Slope Factorskg-dav/mg

Oral

5.50E-02NC

1.30E-01I.OOE+009.IOE-02

NCNCNC

NCNCNC

7.30E-017.30E+007.30E-01

NC7.30E-027.30E-037.30E+00

NCNC

7.30E-01NCNCNC

NCNC

1.50E+00NINCNCNlMlNCNC

Dermal

5.50E-02NC

1.30E-01l.OOE+009.10E-02

NCNCNC

NCNCNC

7.30E-017.30E+007.30E-01

NC7.30E-027.30E-03

NINCNCNINCNCNC

NCNC

1.50E+00NlNCNCNININCNC

Inhalation

2.90E-02NC

5.30E-026.30E-039.10E-02

NCNCNC

NCNCNC

3.10E-013.10E+003.10E-01

NC3.10E-023.10E-033.10E+00

NCNC

3.IOE-01NCNCNC

NCNC

1.50E+01630E+00

NCNCNININCNC

Cancer Risks

Oral

6.15E-03NI

5.99E-073.15E-057.92E-04

NININI

NININl

4.68 E-064.99E-053.09E-06

NI8.98E-086.67E-083.36E-07

NINI

2.06E-06NININl

NINl

5.81E-05NINlNININININl

Dermal

3.71E-04NI

3.79E-083.80E-071.21E-05

NININI

NININl

1 .09E-05I.72E-041.07E-05

NI2.04E-081.55E-07

NININININlNINI

NINI

1.67E-07NINININlNININI

Inhalation

1.22E-04Nl

9.I6E-097.43E-092.97E-05

NININI

NININININININlNINININININlNININl

NINI

NINININININININI

Total Risks

Total

6.64E-03O.OOE+006.46E-073.19E-058.33E-04O.OOE+00O.OOE+00O.OOE+00

O.OOE+00O.OOE+00O.OOE+001.56E-052.22E-041.38E-05

O.OOE+001.IOE-072.22E-073.36E-07O.OOE+00O.OOE+002.06E-06O.OOE+00O.OOE+00O.OOE+00

O.OOE+00O.OOE+00

5.82E-05O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00

%of

Total

84.900011000

000030000000000

0

00

10000000


Total Risk

2.97E-05

7.8E-03

Medium: GroundwalerLandUse: Future Residential

Table F-32

Noncarcinogenic Exposure and Health Risk Estimates (Reasonable Maximum Exposure)

Receptor: On-site Residents (Adult)Exposure Pathway: Incidental Ingestion and


CHEMICAL OF

POTENTIAL CONCERN

VOCsBenzeneBromomethaneCarbon TetrachlorideChloromethane1.2-DichloroethaneEthylbenzeneTolueneTotal Xylenes

PAHsAcenaphtheneAcenaphihyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluoraniheneBenzo(g,h,i)peryleneBenzo(k)fluorantheneChryseneDibenz(a.h)anthraceneFluoranthencFluorenc[ndeno( 1 ,2,3-cd)pyreneNaphthalenePhenanihrenePyrene

2,4-DimethylphenolPhenol


EPC

(mg/L)

1.I9E+013.12E-034.90E-043.35E-039.26E-OI2.49E+005.60E+003.24E+00

6.47E-012.93E+006.47E-026.82E-047.27E-044.51E-043.12E-04I.31E-049.72E-044.90E-068.20E-037.60E-013.01E-048.79E+009.76E-012.32E-02

1.73E-016.92E-02

4.12E-031.98E-022.14E-023.60E+024.54E-034.33E-028.64E-028.44E-02

PC

(mg/cmj)

2.10E-023.00E-032.20E-Q24.20E-035.30E-037.40E-024.50E-028.00E-02

0.0790.0790.079

8.10E-011.20E+001.20E+00

0.0790.079

8.10E-010.079

3.60E-010.079

I.90E+006.90E-02

0.0790.079

0.079I.37E-04

l.OOE-03I.OOE-03l.OOE-03l.OOE-034.00E-06l.OOE-036.00E-04l.OOE-03


mg/kg-dav

Oral

3.26E-018.55E-051.34E-059.18E-052.54E-026.82E-021.53E-018.86E-02

1.77E-028.03E-021.77E-031.87E-051.99E-051.24E-058.55E-063.59E-062.66E-051.34E-072.25E-042.08E-028.25E-062.41E-012.67E-026.36E-04

4.73E-031.90E-03

1.13E-045.42E-045.86E-049.86E+001.24E-041.19E-032.37E-032.31E-03

Dermal

1.97E-027.37E-078.50E-071.11E-063.87E-041.45E-021.98E-022.04E-02


1.07E-037.47E-07

3.25E-071.56E-061.69E-062.84E-021.43E-093.41E-064.08E-066.65E-06

Inhalation

1.22E-023.21E-065.04E-073.44E-069.51E-042.56E-035.75E-033.32E-03


Oral

3.00E-031.40E-037.00E-W

NI3.00E-02l.OOE-012.00E-012.00E+00

6.00E-02NI

3.00E-01NINININI

NI

NI

NI4.00E-024.00E-02

NI2.00E-02

NI3.00E-02

2.0QE-026.00E-01

3.00E-04l.OOE-033.70E-023.00E-01

NI2.00E-023.00E-012.00E-02

Dermal

3.00E-031 .40E-037.00E-04

NI3.00E-02l.OOE-012.00E-012.00E+00

6.00E-02NI

3.00E-01NININININININI

4.00E-024.00E-02

NI2.00E-02

NI3.00E-02

2.00E-026.00E-01

3.00E-04l.OOE-031.I1E-024.50E-02

NI8.00E-043.00E-019.40E-03

Inhalation

1.70E-031 .43E-035.71E-048.60E-021.40E-032.86E-01I.14E-01

NI

NININININININININININININI

8.57E-04NINI

NINI

NI5.70E-05

NINININININI

Hazard Quotient

Oral

1.09E+026.11E-021.92E-02

NI8.46E-016.82E-017.66E-014.43E-02

2.95E-01NI

5.91E-03NINININI

NI

NINI

5.62E-035.21E-01

NI1.20E+01

NI2.I2E-02

2.36E-013.16E-03

3.76E-OI5.42E-011.58E-02

3.29E+01NI

5.93E-027.89E-031.I6E-01

Dermal

6.56E+005.27E-041.21E-03

NI1.29E-02I.45E-019.92E-021.02E-02

6.71E-02NI


5.81E-031.I8E-01

NI2.39E+00

NI4.81E-03

5.37E-021.24E-06

1.08E-031.56E-031.52E-046.30E-01

NI4.26E-031.36E-057.07E-04

Inhalation

7.19E+002.24E-038.82E-044.00E-056.80E-018.95E-035.03E-02

NI

NININININININININININININI

O.OOE+00NINI

NINI

NI

NINININININI


Total

1.22E+026.38E-022.13E-024.00E-051.54E+008.36E-019.16E-OI5.45E-02

3.63E-01O.OOE+007.25E-03O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00

1.I4E-026.39E-01O.OOE+001.44E+01O.OOE+002.60E-02

2.90E-013.16E-03

3.77E-015.44E-011.60E-023.35E+01O.OOE+006.36E-027.90E-031.16E-01

foot

Total

690001010

0000000000

000800

00

000190000

Total Hazard Index by Route 1.S8E+02

Total Hazard Index 1.8E+02

1.01E+01 7.93E+00

Medium: GroundwaterLandUse: Future Residential

^Table F-33

Carcinogenic Exposure and Health Risk Estimates (Reasonable Maximum Exposure)

Receptor: On-site Residents (Child)Exposure Pathway: Incidental Ingestion and


CHEMICAL OF

POTENTIAL CONCERNVOCsBenzeneBromome thaneCarbon TetrachlorideChloromethane1.2-DichloroethaneEthylbenzeneTolueneTotal Xylenes

PAHsAcenaphiheneAcenaphthyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h.i)peryleneBenzo(k)fluorantheneChryseneDibenz(a,h)anthraceneRuorantheneFluorenelndeno(l ,2,3-cd)pyreneNaphthalenePhenanthrenePyrene

Acid Extractable2,4-DimethylphenolPhenol

MetalsArsenicChromiumCopper'ionLeadNickelZincCyanide

EPC

(mg/L)

1.19E+013.12E-034.90E-043.35E-039.26E-012.49E+005.60E+003.24E+OO

6.47E-012.93E+006.47E-026.82E-047.27E-044.51E-043.12E-041.31E-049.72E-044.90E-068.20E-037.60E-013.01 E-048.79E+009.76E-012.32E-02

1.73E-016.92E-02

4.12E-031.98E-022.14E-023.60E+024.54E-034.33E-028.64E-028.44E-02

PC

(mg/cm2)

2.10E-023.00E-032.20E-024.20E-035.30E-037.40E-024.50E-028.00E-02

0.0790.0790.079

8.IOE-011.20E+001.20E+00

0.0790.079

8.10E-010.079

3.60E-010.079

1.90E+006.90E-02

0.0790.079

0.0791.37E-04

l.OOE-03l.OOE-03l.OOE-03l.OOE-034.00E-06l.OOE-036.00E-04l.OOE-03


Oral

6.52E-021.71E-052.69E-061.84E-055.07E-031.36E-023.07E-021.77E-02

-

3.55E-031.61E-023.55E-043.74E-063.98E-062.47E-061.71E-067. 1 8E-075.33E-062.68E-084.49E-054.16E-031.63E-064.82E-025.35E-031.27E-04

9.46E-043.79E-04

2.26E-051.08E-041.17E-041.97E+002.49E-052.37E-044.73E-044.62E-04

Dermal

3.26E-031.22E-071.41E-071.83E-076.40E-052.40E-033.28E-033.38E-03


1.78E-041.24E-07

5.37E-082.58E-072.79E-07469E-032.37E-105.65E-076.76E-07I.10E-06

Inhalation

4.89E-021.28E-052.02E-061.38E-053.81E-031.02E-022.30E-021.33E-02

Slope Factors

Oral

5.50E-02NC

1.30E-011.30E-029.10E-02

NCNCNC

NCNCNC

7.30E-017.30E+007.30E-01

NC7.30E-027.30E-037.30E+00

NCNC

7.30E-01NCNCNC

NCNC

1.50E+00NINCNCNININCNC

Dermal

5.50E-02NC

I.30E-011.30E-029.10E-02

NCNCNC

NCNCNC

7.30E-017.30E+007.30E-01

NC7.30E-027.30E-037.30E+00

NCNC

7.30E-01NCNCNC

NCNC

1.50E+00NINCNCNININCNC

Inhalation

2.90E-02NC

5.30E-026.30E-039.10E-02

NCNCNC

Cancer Risks

Oral

3.59E-03NI

3.49E-072.39E-074.62E-04

NININI

NININI

2.73E-062.91E-051.80E-06

NI5.24E-083.89E-081.96E-07

NINI

1.20E-06NININI

NINI


Dermal

1.79E-04NI

1.83E-082.39E-095.82E-06

NININI

NININI

5.26E-068.31E-055.15E-06

NI9.85E-097.50E-083.69E-08

NINI

5.44E-06NININI

NINI


Inhalation

1 .42E-03NI

I.07E-078.67E-083.46E-04

NININI

NINININININININININININININININI

NINI

NINININININININI

Total Risks

Total

5.18E-03O.OOE+004.74E-073.28E-078.14E-04O.OOE+00O.OOE+00O.OOE+00

O.OOE+00O.OOE+00O.OOE+OO7.99E-061.12E-046.96E-06O.OOE+006.23E-081.14E-072.33E-07O.OOE+00O.OOE+006.65E-06O.OOE+00O.OOE+00O.OOE+00

O.OOE+00O.OOE+00

3.39E-05O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00

Total

8400013000

0000200000000000

00

10000000


Total Risk

1.76E-03

6.2E-03

Medium: GroundwalerLandUse: Future Residential

Table F-34

Noncarcinogenic Exposure and HeaJth Risk Estimates (Reasonable Maximum Exposure)

Receptor: On-site Residents (Child)Exposure Pathway: Incidental Ingestion and

Inhalation of Vapors in Showei


VOCsBenzeneBromomethaneCarbon TetrachlorideChloromethane1 ,2-DichlorocthaneEthylbenzencTolueneFotal Xylencs

PAHsAcenaphtheneAcenaphthyleneAnthraceneBenzo(a)anthraceneBenzo(a)pyreneBenzo(b)fluorantheneBenzo(g,h,i)peryleneBenzo(k)nuorantheneChryscneDibenz(a,h)anthniceneFluoraniheneFluorene[ndeno( 1 ,2.3-cd)pyreneNaphthalenePhenanthrenePyrene

Acid Extractable2,4-DimethylphenolPhenol


EPC

(mg/L)

I.I9E+013.12E-034.90E-043.35E-039.26E-OI2.49E+OO5.60E+003.24E+00

6.47E-012.93E+006.47E-026.82E-047.27E-044.51E-043.12E-041.31E-049.72E-044.90E-068.20E-037.60E-013.0IE-048.79E+009.76E-OI2.32E-02

I.73E-OI6.92E-02

4.12E-031.98E-022.14E-023.60E+024.54E-034.33E-028.64E-028.44E-02

PC(mg/cnT)

2.IOE-023.00E-033.00E-034.20E-035.30E-037.40E-024.50E-028.00E-02

7.90E-027.90E-027.90E-028.IOE-011.20E+001.20E+007.90E-027.90E-028.10E-OI7.90E-023.60E-017.90E-021.90E+006.90E-027.90E-027.90E-02

7.90E-021.37E-04

l.OOE-03I.OOE-03I.OOE-03I.OOE-034.00E-06l.OOE-036.00E-041 .OOE-03

Chronic Dailv Intake Valuemg/kg-dav

Oral

7.58E-011.99E-043.14E-052.14E-045.92E-021.59E-013.58E-OI2.07E-01

4.I4E-021 .87E-014.14E-034.36E-054.65E-052.88E-051.99E-058.37E-066.21E-053.13E-075.24E-044.86E-021.92E-055.62E-016.24E-021.48E-03

1.10E-024.42E-03

2.63E-041.27E-031.37E-032.30E+012.90E-042.77E-035.52E-035.40E-03

Dermal

3.79E-021.42E-062.24E-072.14E-067.47E-042.80E-023.83E-023.94E-02

7.78E-033.52E-027.78E-048.40E-051.33E-048.23E-053.75E-06I.57E-061.20E-045.89E-084.49E-049.I3E-038.70E-059.23E-021.I7E-022.79E-04

2.07E-031.44E-06

6.27E-073.01 E-063.26E-065.48E-022.76E-096.59E-067.89E-06I.28E-05

Inhalation

5.68E-02I.50E-052.35E-061.61E-054.44E-03I.I9E-022.68E-021.53E-02


6ral

3. OOE-031.40E-037.00E-04

Nl3.00E-02I.OOE-012.00E-012.00E+00

6.00E-02NI

3.00E-01NlNINININININI

4.00E-024.00E-02

NI2.00E-02

NI3.00E-02

2.00E-026.00E-01

3.00E-04l.OOE-033.70E-023.00E-01

NI2.00E-023.00E-OI2.00E-02

Dermal Inhalation

3. OOE-031 .40E-037.00E-04

NI3.00E-02l.OOE-012.00E-012.00E+00

6.00E-02Nl

3.00E-01NINlNlNINlNINI

4.00E-024.00E-02

NI2.00E-02

NI3.00E-02

2.00E-026.00E-01

3.00E-04I.OOE-031.1IE-024.50E-02

NI8.00E-043.00E-OI9.40E-03

1.70E-031.43E-035.71E-048.60E-021.40E-032.86E-01I.I4E-OI

Nl

NININININININININININININl

8.57E-04NINI

NINI

NI5.70E-05

NlNININlNINl

Hazard Quotient

Oral

2.53E+02I.42E-014.48E-02

Nl1.97E+001.59E+001.79E+001.03E-01

6.89E-01Nl

I.38E-02NININININlNINl

1.3IE-021.21E+00

Nl2.81E+01

NI4.94 E-02

5.52E-017J7E-03

8.78E-011.27E+003.70E-027.67E+OI

NlI.38E-011.84E-022.70E-OI

Dermal

1.26E+OI1.02E-033.20E-04

NI2.49E-022.80E-011.92E-011.97E-02

1.30E-01Nl


I.12E-022.28E-OI

Nl4.61E+00

Nl9.30E-03

1.04E-012.40E-06

2.09E-033.01E-032.93E-041.22E+00

NI8.23E-032.63E-051.37E-03

Inhalation

3.34E+011.05E-024.12E-031.87E-043.17E+004.18E-022.35E-01

NI

NINlNININlNINlNlNINININlNINININI

NINI

NINININININlNINI


Total

2.99E+021.54E-014.92E-021.87E-045.17E+001.91E+002.21E+00I.23E-01

8.I9E-OIO.OOE+001.64E-02

O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+002.43E-02I.44E+00O.OOE+003.27E+OIO.OOE+005.87E-02

6.55E-017.38E-03

8.80E-011.27E+003.73E-027.79E+01O.OOE+OOI.47E-011.84E-022.71E-01

footTotal

70.30001010

000000000000080

0

00

000180000

Total Hazard Index by Route 3.68E+02Total Hazard Index

1.95E+01 3.69E+01

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