r

REMEDIAL INVESTIGATIONREPORT

FOR THE

SINCLAIR REFINERY SITEWellsville, New York

VOLUME IVOFIVAPPENDIX K

PREPARED FOR

ARCOBY

EE&SGOAn ENSERCH* Engineering and Construction Company

REMEDIAL INVESTIGATIONREPORT

FOR THE

SINCLAIR REFINERY SITEWellsville, New York

VOLUME IV OF IVAPPENDIX K

PREPARED FOR

ARCOBY

ER\SCOAn ENSERCH* Engineering and Construction Company

MARCH 1991

COMz

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Appendix KEPAfs Endangerment Assessment

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ARCS169.122/95SAPPENDIX B/TYPE PIECES

3/91

MAR 0119911 EXPRESS MAIL

John A. A. ZannosProject ManagerAtlantic Richfield Company (ARCO)515 South Flower StreetLos Angeles, CA 90071

Re; Sinclair Refinery Site. Wellsville. New YorkRemedial Investigation/Endanaerment Assessment

Dear Mr. Zannos:

The purpose of this letter is to transmit to ARCO the revised FinalEndangerment Assessment (EA) for the above referenced site and torespond to ARCO's letter of November 9, 1990 regarding finalizationof the Sinclair Refinery Remedial Investigation (RI).

Enclosed please find the revised Final EA for the Sinclair Refinerysite in Wellsville, New York. The revised document incorporatesthe following changes:

• Page 2-11 indicates that the metal concentrations in soils maybe attributable to local background levels.

Page 2-20 deletes benzo(a)pyrene from the selected indicatorchemicals at the offsite tank farm.

The chemical concentration in air (CA) and the LifetimeAverage Daily Exposure (LADE) in table 3-6 were corrected dueto a math error (the CA and LADE were an order of magnitudetoo high and E-06 became E-07).

Because of these three changes, the following pages and tables alsorequired adjustment: Page 3-23, Page 3-29, Table 3-6, Page 3-35,Page 3-38, Table 3-11, Table 4-2, Table 4-5, Table 4-6, Table 4-8, Table 4-9, Table 4-12, Page 4-17, Table 4-13, Table 4-14, Table4-17, Table 4-18, Page 5-2, and Page 5-3.

Please also note that after these changes were made, the highest Mnon-carcinogenic risk from the site remains the inhalation of Mbarium and lead dust particles by adults that work and attend z

vocation school on the refinery site. The chronic hazard index for othe inhalation route is 9.45E-02. The previous version of the oreport cited a value of 9.45E-01 for this route. Since the non- M

carcinogenic hazard index for this exposure point does not exceed ^unity (nor did it in the original calculation), adverse non- CDcarcinogenic effects are not expected. ^

Referencing ARCO's letter to the U.S. Environmental ProtectionAgency (EPA) dated November 9, 1990, three points of conflict wereraised by ARCO regarding the site EA. The inclusion ofbenzo(a)pyrene as an indicator compound at the Off-Site Tank Farmand the fact that mean inorganic compound levels and associatedrisks were determined without regard to local background levelshave been addressed as explained above. The remaining point ofconflict involved Versar's selection of parameters for the flow andcontaminant transport calculations. EPA and Versar chose topresent a conservative scenario for contaminant flow by using thehighest gradient on site and one of the highest hydraulicconductivity values. Although this combination of aquifercharacteristics does not truly represent site hydrogeologicalconditions, their use constitutes a "worst-case" scenario forgroundwater flow. The spatial extent of contaminants was addressedby averaging contaminant flow from several river-fronting segmentscentered around monitoring wells MW-7, -9, -10, -11, -27, -32, and-55, all of which occur close to the site boundary along theGenesee River. Ultimately, however, no site risk was associatedwith the ingestion of contaminants via surface water at the site,even using the worst-case scenario. Therefore, even if ARCOconsiders Versar's approach geologically unrealistic, the issuebecome s i rre1evant.

The final point raised in ARCO's November 9 letter regarded thepresentation of the EA and ARCO's own Risk Assessment (RA) in theRI. As previously stated by EPA and expressed in a letter from EPAto ARCO dated October 9, 1990, EPA Region II policy is and has beenfor EPA to develop risk assessments in RI/FSs conducted byPotentially Responsible Parties (PRPs). Therefore, ARCO willsubmit the site RI with the EPA EA, presented either as a sectionof the RI document itself or under separate cover as a clearlyidentified addendum to the RI. ARCO then has the option ofsubmitting their own RA separately to EPA, whereby it will beincluded in the administrative record but not the RI/FS. The RIwill, then, make no reference to the RA performed by ARCO. Anynecessary changes to the RI to comply with this policy should bedone accordingly.

Upon receipt of this letter and in accordance with paragraph 29 ofthe Administrative Order on Consent between ARCO and EPA, which wassigned by EPA on July 28,1988, ARCO will have twenty (20) businessdays to submit the revised RI report to EPA.

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r If you have any questions on this matter, please contact MichaelNegrelli, Sinclair Refinery project manager, at (212) 264-1375.

Sincerely yours,

Carole Petersen, ChiefNew York/Caribbean Superfund Branch II

Enclosure

cc (letter only):

R.W. Simmons - ARCOM.D. Smith - ARCOJ. White - NYSDECM. Marshall - USDOJ

cc (with enclosure):

T. Granger - Ebasco

C. Bems - USEPAK. Lynch - DSEPAS. Schofield - CDM-FPCS. Odland - CDM-FPC

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WORK ASSIGNMENT NO. C02064EPA CONTRACT NO. 68-W9-0002

DOC. NO. OlOOy

REVISED FINAL ENDANGERMENT ASSESSMENTSINCLAIR REFINERY SITEWELLSVILLE, NEW YORK

SUBMITTED TO:

CDM FEDERAL PROGRAMS CORPORATIONSUITE 200

13135 LEE JACKSON MEMORIAL HIGHWAYFAIRFAX. VIRGINIA 22033

SUBMITTED BY:

VERSAR. INC.6850 VERSAR CENTER

SPRINGFIELD, VIRGINIA 22151 wMZ

JUNE 25. 1990

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TABLE OF CONTENTSPage No.

1.0 INTRODUCTION ............................................. 1-11.1 Objective and Scope ................................ 1-11.2 Site Description and History ...................... 1-11.3 Report Organization ................................ 1-5

2.0 SITE CHARACTERIZATION .................................... 2-12.1 Data Summary ....................................... 2-12.2 Contaminant Distribution ........................... 2-112.3 Selection of Chemicals of Potential Concern ........ 2-19

3.0 EXPOSURE/TOXICITY ASSESSMENT ............................. 3-13.1 Fate and Transport/Toxicity Summary ................ 3-13.2 Characterization of Exposure Setting ............... 3-83.3 Identification of Potential Exposure Pathways ...... 3-133.4 Potentially significant Exposure Pathways .......... 3-183.5 Evaluation of Exposure and Chemical Intakes ........ 3-19

4.0 RISK EVALUATION .......................................... 4-14.1 Human Health ....................................... 4-14.2 Evaluation of Potential Impacts on Environmental

Receptors .......................................... 4-174.3 Assessment of Method Uncertainties ................. 4-25

5.0 SUMMARY/CONCLUSIONS ...................................... 5-1

REFERENCES

FIGURES

1-1 Sinclair Refinery Vicinity Map ........................... 1-21-2 Sinclair Refinery Site Map ............................... 1-32-1 Ground Water Monitoring Well Locations ................... 2-52-2 Surface Soil Composite Sampling Areas .................... 2-62-3 Soil Auger Boring Sampling Locations ..................... 2-72-4 Surface Water Sampling Locations ......................... 2-82-5 Offsite Tank Farm Sampling Locations ..................... 2-92-6 Oil Water Separator Sampling Locations ................... 2-102-7 Contaminant Distribution with Depth ...................... 2-142-8 VOC Concentrations in Surface Soils ...................... 2-152-9 SNA Concentrations in Surface Soils ...................... 2-162-10 Metal Concentrations in Surface Soils .................... 2-17

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TABLE OF CONTENTS(Continued)

Page No.

TABLES

2-1 List of Chemicals Analyzed for at Sinclair RefinerySite ................................................... 2-2

2-2 Summary Statistics of Compounds Detected at SinclairRefinery ............................................... 2-4

2-3 Comparison of Total Metal Concentrations in Soil atSinclair Refinery Site ................................. 2-12

2-4 Indicator Chemical Selection Calculations ................ 2-213-1 Applicable or Relevant and Approporiate Requirements ..... 3-23-2 Potential Migration Pathway and Exposure Route Evaluation 3-153-3 Mean Chemical Concentrations in Surface Soil and Dust

Emissions Rates ........................................ 3-233-4 Plume Heights Used in Near Field Box Model ............... 3-273-5 Ambient Concentrations for Fugitive Dust at 10 Meters .... 3-293-6 Fugitive Dust Inhalation Exposure ........................ 3-303-7 Subsurface Soil Volatiles Inhalation Exposure ............ 3-333-8 Surface. Water Ingestion Exposure Based on Modeling Results 3-363-9 Surface Water Ingestion Exposure Based on Modeling Data . . 3-373-10 Surface Soil Ingesting Via Direct Contact at Main Refinery

Site for Children ...................................... 3-393-11 Intakes from Surface Soil Ingestion Via Direct Contact

at Offsite Tank Farm for Children ...................... 3-403-12 Sursurface Soil Ingestion Via Direct Contact for

Excavation Workers ..................................... 3-414-1 Critical Toxicity Values ................................. 4-24-2 Summary of Chronic Human Intakes for Adults .............. 4-44-3 Summary of Chronic Human Intakes for Children ............ 4-54-4 Summary of Subchronic Human Intakes for Excavation Workers 4-64-5 Summary of Chronic Human Intakes from Offsite Tank Farm

for Children ........................................... 4-74-6 Summary of Lifetime Average Daily Exposures for Adults . . . 4-84-7 Summary of Lifetime Average Daily Exposures for Children . 4-94-8 Summary of Lifetime Average Daily Exposures from Offsite

Tank Farm for Children ................................. 4-104-9 Calculation of Chronic Hazard Index for Adults ........... 4-124-10 Calculation of Chronic Hazard Index for Children ......... 4-134-11 Calculation of Subchronic Hazard Index for Excavation

Workers ................................................ 4-144-12 Calculation of Chronic Hazard Index from Offsite Tank

Farm for Children ...................................... 4-15

OU)

TABLE OF CONTENTS(Concluded)

Page No.

A-13 Risk Estimates for Carcinogens Using Modeled Data forAdults ................................................. 4-18

4-14 Risk Estimates for Carcinogens Using Monitored Data forAdults ................................................. 4-19

4-15 Risk Estimates for Carcinogens Using Modeled Data forChildren ............................................... 4-20

4-16 Risk Estimates for Carcinogens Using Monitored Data forChildren ............................................... 4-21

4-17 Risk Estimates for Carcinogens Using Modeled Data fromOffsite Farm for Children .............................. 4-22

4-18 Risk Estimates for Carcinogens Using Monitoring Data fromOffsite Tank Farm for Children ......................... 4-23

4-19 Comparison of Surface Water Concentrations with WaterQuality Criteria for the Protection of AquaticFreshwater Life ........................................ 4-24

APPENDICES

A. Compounds and Elements Detected at the Sinclair Refinery SiteB. Fate/Transport and Toxicity ProfilesC. Supporting Calculations

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1.0 INTRODUCTION

COM Federal Programs Corporation (FPC) received a work assignment(Contract No. 68-W9-0002, WA No. C0206A) to provide technical support tothe U.S. Environmental Protection Agency (EPA) as part of the second phaseof the remedial investigation/feasibility study (RI/FS) being conductedfor the Sinclair Refinery located in Vellsville. New York, by thepotentially responsible party. Through a subcontract with COM FPC, Versarwill provide the technical support which included the completion of thisEndangerment Assessment.

1.1 Oblective and Scope

The objective of this Endangerment Assessment is to provide the U.S.EPA with an evaluation of the risks the Sinclair Refinery site poses toboth human health and the environment under baseline conditions. CurrentEPA guidance manuals were used during the preparation of the report whichinclude: Risk Assessment Guidance for Superfund-Human Health EvaluationManual, 1989, Superfund Public Health Evaluation Manual, 1986, ExposureFactors Handbook, 1989, and Superfund Exposure Assessment Manual, 1988.The methods described within this Federal guidance materials are intendedto provide a conservative evaluation of site risks.

The site consists of a landfill and the refinery. A Record ofDecision (ROD) was signed in 1985 for the landfill on the SinclairRefinery site. Therefore, this report is intended to support EPA's futureROD for only the refinery portion of the site. This report evaluatesbaseline conditions; therefore, it does not determine the risks associatedwith specific remedial actions, currently under consideration by the U.S.EPA, that may be incorporated into the pending Remedial Response Plan.

1.2 Site Description and Historyw

The Sinclair Refinery site, adjacent to the Town of Uellsville in ^Allegheny County, New York, occupies approximately 102.5 acres (Figure 1-1). 0

The site consists of a 12.5-acre landfill in the southeast sector, which 2was used as a disposal area by the refinery, and a 90-acre portion where the ^refinery processing, storage and administration operations were conducted o

<ji(Figure 1-2). In addition, there is a small 6.6-acre offsite tank farm,approximately 2,000 feet west of the main refinery site.

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Figure 1.1 Sinclair RefineryVicinity Map (Ebasco, 1989)

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Figure 1-2 Sinclair RefinerT.Site Map (Ebasco, 1989)

ADAPTED MOM MC MARTIN PHASE I lift MA

Oil refining operations have taken place at the site since the late1800s. The Sinclair Refinery Company purchased the refinery in 1924 andoperated it until 1958 when a fire halted operations. Sinclair RefiningCompany sold parcels of the site to several entities, including the Townof Wellsville. The Town of Wellsville subsequently conveyed some of theparcels to various interests, most of whom currently occupy the refineryportion of the site. These buyers include a branch campus of the StateUniversity of New York (SUNY), which maintains a trade and vocationsschool at the site. In 1969, the Sinclair Refinery Company merged withthe Atlantic Richfield Company (ARCO).

In the mid-1970s, debris from the landfill was reported to havewashed onto the banks of the Genesee River downstream from the SinclairLandfill. Reports from the community and site inspections, conducted bythe New York State Department of Environmental Conservation (DEC) in thefall of 1981, indicated that site conditions warranted proposing the sitefor the National Priorities List (NFL). In January 1983, drums and otherwaste materials were removed from the floodplain downstream from thelandfill. In March 1983, a dike was constructed to separate the GeneseeRiver from the eroding face of the landfill. The Sinclair Refinery sitewas listed on the NFL on September 8, 1983. A Cooperative Agreement,signed by the New York DEC and the EPA Region II that year, identifiedDEC as the lead agency responsible for the oversight of the remedialcleanup activities for the Sinclair Refinery Superfund site.

In 1984, DEC initiated a RI/FS for the landfill portion of the site.SMC Martin completed a Phase I Remedial Investigation and submitted areport in 1985. A Record of Decision (ROD) was signed in 1985 for thelandfill on the Sinclair Refinery site. Also in 1985, EPA authorized therelocation of the surface water intake for the village of Wellsvillepublic water supply to a location upstream from the refinery site. The w

[_

relocation of the surface intake was completed in the Spring of 1988. 3Ebasco, under contract for ARCO, completed an additional Remedial 0

oInvestigation and submitted the draft report in 1989. M

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The 1989 Draft RI Report, prepared by Ebasco, used mostly SMC Martindata which was not fully validated according to the Region II standardoperating procedures which are based on National Contract LaboratoryProgram (CLP) Functional Guidelines for CLP Data Review. The RI datapackage received from Ebasco had 1,067 classes (i.e., volatile organics,semivolatile organics, and inorganics) of analytical results, 751 or 70percent originated from the SMC Martin remedial investigation. Inaccordance with the EPA's decision, this endangennent assessment reportwill be based on the data used in Ebasco's 1989 Draft RI Report.

1.3 Report Organization

Section 2 of this report presents the site characterization. Thissection includes the results of the comprehensive review of the datapackage which leads to the selection of chemicals of potential concern.This section will also discuss and illustrate the spacial distribution ofsoil contaminants in order to identify the contaminant migration pathwaysthat could adversely affect either human or ecological receptors on or

near the site.

Section 3 presents the exposure and toxicity assessments. Theexposure assessment characterizes the exposure setting and potentialpathways attributed to the refinery portion of the site. The fate andtransport mechanism of the chemicals of potential concern will besummarized. The exposure assessment will provide an estimation ofexposure point concentrations for the potentially significant contaminantmigration pathways. Monitoring data was used whenever possible in orderto provide reasonable estimates of contaminant levels at potentialreceptor points. If receptor point monitoring data was not available,conservative dispersion and transport models were used to determinedowngradient contaminant levels. Finally, the exposure assessment Co*-fconcludes with an estimation of chemical intakes using standard EPA ^exposure scenario calculations. ^

1-5OlOOy

The toxicity assessment portion of Section 3 summarizes thecarcinogenic and noncarcinogenic toxicity values for the chemicals ofpotential concern along with their identified state and Federal Standards.This section will also include toxicity profiles for each of thechemicals of interest.

Section 4 quantitatively presents the risk evaluation for carcinogenicand noncarcinogenic chemicals to both human health and the environment.The carcinogenic and non-carcinogenic risk analysis will evaluatenumerically the adverse impacts that may result from exposure to thechemicals onsite representative of baseline conditions. This section willalso provide a qualitative evaluation of the potential risks to humanreceptors followed by a discussion of the uncertainties and assumptionsused.

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2.0 SITE CHARACTERIZATION

2.1 Data

The U.S. EPA Region II provided Versar with two sets of analyticaldata. One set of data was collected by SMC Martin, who initiated the RI,but only completed Phase I of the investigation. Ebasco, Inc. completedPhase II of the RI in August 1988 by collecting additional samples.

Tallies for samples collected by each principal investigator for eachmedia are presented below:

SMC EBASCO

Ground Water Volatile organics 73 39Semivolatile organics 73 24Inorganics 73 47

Soil Volatile organics 129 34Semivolatile organics 129 33Inorganics 129 118

Surface Water Volatile organics 51 9Semivolatile organics 27 0Inorganics 51 12

TOTAL 751 316

The objective of the Phase II study was to gather data to determinethe nature and extent of additional remedial actions: thus, locationswhich were most likely to indicate the presence of contaminants weretargeted for sampling. Samples were analyzed for the Hazardous SubstanceList (HSL) [i.e., volatile organics, Semivolatile organics(base/neutral/acid extractable organics). metals, and cyanide], theTarget Compound List (i.e., volatile organics, and Semivolatileorganics), and the Target Analyte List (i.e., metals and cyanide). Alisting of the compounds and elements resolved by the analytical methodsused is presented in Table 2-1.

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TABLE 2-1 LIST OF CHEMICALS ANALYZED FOR AT SINCLAIR REFINERY SITE *

VOLATILE ORGANIC COMPOUNDS

ChtoroMthane•roatonethaneVinyl ChlorideChloroethwwNethylene ChlorideAcetoneCerbon Dlsuiflde1.1-Olchloroethene1.1-OlchloroethaneTrent-1,2-DlchloroetheneChloroforie1.2-Olchloroethene2-futenone1,1.1-TrIchloroetheneCerbon letrechlorldeVinyl AcetateIroModlchloronethene1,1.2,2-Tetrachloroethane1,2-Olchloropropene

•j» Tram-1.3-Dlchloropropenes, Trlchloroethene

DlbroMochloroiaethane1,1.2-Trlchtoroethane•enienecla-1,3-Dlchloropropene2-Chloroethylvlnyl Ether•roMoforai2-HeKanone4-Hethyl-2-PentanoneletrechloroetheneTolueneChtorobenteneEthylbenzeneStyreneTotal Xylenee

TENTATIVELY IDENTIFIED VOCe

CyclohexaneeTotel Alkyl Cyclohenanes

SENIVOLATILE ORGANIC CONPOUNDS

Phenolble (2-Chloroethyl) Ether2-Chlorophenol1.3-Dlchlorobenzene1.4-Dlchlorobenzeneleniyl Alcohol1,2-Dlchlorobenzene2-Nethytphenolbit (2-Chloroleopropyl) Ether4-MethylphenolN-Nl troio-Dl -n-PropyleeilneNexachloroethaneNitrobenzeneIsophorone2-Nltrophenot2.4-DiMthylphenol•entolc Acidbla C2-chloroethoKy) Nethene2,4-Olchlorophenol1,2.4-TrlchlorobemeneNaphthalene4-ChloroenlllneNeiiechlorobutedlene4-Chloro-S-Nethylphenol2-HethytnephtheleneNexechlorocyclopentadlene2,4,6-TrIchlorophenol2.4,5-Trlchlorophenol2-CnloroneptitheleiM2-NitroenltlneDlMthyl PhtheleteAcenephthylene3-NltroanlllneAcenephthene2,4-Dlnltrophenol4-NltrophenolDlbenzofuren2,4-Dlnltrotoluene2,6-DlnltrotolueneOiethyl Phthelete

SENIVOLATILES (CONTINUED)

4-Chlorophenyl Phenyt EtherFluorene4-Nltroenltlne4,«-Dlnltro-2-NethylphenolN-Nltrosodlphenyle«lne4-lroMophenyl Phenyl EtherNeiiech I or obenzenePentechlorophenolPhenenthreneAnthraceneDI-N-lutyl PhtheleteFluorenthenePyrene•utyt •enzyl Phthelete3.3'-Olchlorobenzldine•ento(A)Anthreceneble C2-Ethylhenyl) PhtheleteChryeeneDI-N-Octyl Phthelete•enzo(b)Fluorenthene•enzoCklFluorenthene•enzo(e)PyreneIndeno (1,2,3-cd) PyreneDlbenzo(e(h)Anthracene•enio(g,h,I)Perylene

INORGANIC METALS AND CYANIDE

AlUMlnueAntliaonyAreenlc•arlun•erylllunCadmlueCelcltMthrow! uaCobaltCopperIronleadNagneelueNangeneeeNercuryNickelPoteeelunSetenluaSilverSodlueThelllumVenadlueline

Cyanide

MISCELLANEOUS INORGANIC COMPOUNDS

Phenol a (ug/L In eojueoue eaaplet)Totel Dlieolved SolIdaTotel Organic Carbon

• Froai SHC Martin and Ebatco Inc. K.I. data sets.

2T6T TOO NIS

The data was compiled and evaluated to determine the classes ofcontaminants identified on site. Appendix A represents a summary ofconcentrations for all compounds and elements detected at the SinclairRefinery site. Versar eliminated the results from ground-water samplesthat were filtered prior to laboratory submit tal to provide moreconservative concentrations of compounds in the ground water. When acompound was not detected, half the detection limit was used to calculatethe mean. Rejected data was omitted from the calculations of means.Table 2-2 presents summary statistics for the compounds by media [i.e.,ground water (GW) , surface water (SW), and soil locations (SL)]. Summarystatistics include frequency, maximum concentrations and the geometricmean, as well as acceptable intakes for subchronic and chronic exposure(AIS and AIC) , carcinogenic potency factors (CPF) , severity of effectrating values (RVe), and carginogenic weight of evidence scores. TheRVes are unitless ingeters ranging from 1 to 10 (i.e., death or pronouncedlife sortening), corresponding to the levels of severity of effects. Theweight of evidence ratings qualify the level of evidence that supportsdesignating a chemical as a human carcinogen from E (i.e., no evidence)to A (i.e., sufficient evidence).

Approximate sample locations for ground water, soil (i.e., compositesurface soil, auger soil borings, off site tank farm, and oil waterseparator), and surface water are presented in Figures 2-1, 2-2, 2-3,2-4, 2-5 and 2-6. Soil samples were collected from three depth intervalsin auger borings: shallow (0-0.5 feet), middle (2-4 feet), and deep(8-10 feet).

Of the volatile organics, methyl chloride, acetone, benzene,ethylbenzene, and xylenes (ortho- , meta- and para- isomers) were the mostprevalent compounds observed in over 50 percent of the samples collected.The geometric means for vinyl chloride and benzene in ground water exceed *•*

Sithe maximum contaminant levels (MCLs) promulgated under the Safe DrinkingWater Act. o

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TABLE 2-2SU4MARY StAIISTICS Of COMPOUNDS DETECTED AT SINCLAIR REriHEUT

•ITS/TOTAL ANALYSES MEAN <PP8)

VOAtVINYL CRIOII INETMVL CHLORIDEACETONETRANS-1.2-DICHLOROETNENE2-MITAMONETRICNLOROETHENE•EHZENE4-NETNVL-2-PEHTANONE1,1.2,2-TEIRACm.OROEIHANETOIUENEETMVLKHZENETOTAL XTLENES

•NAiPHENOL1.4-DICNLOROBENZENENITROIENZENE2-MCTHYLHAPNTNALENEOIKNZOriMAN

^ N-NITROSODIPNENVLANINE*• PHENANTHIIENE

DI-n-HIIVlPNTHALATEPYRENERUTVLKNZVLPHTHALATEKNZO(«|ANTNRACENE

01 SU

2/77 0/264/77 a/2618/77 is/260/77 11/260/61 8/101/77 6/2624/77 13/261/77 2/261/77 0/2617/77 9/2618/77 7/2623/77 8/26

0/62 2/2S0/62 4/291/62 7/298/62 3/250/62 0/290/62 9/293/62 3/290/62 7/291/62 2/290/62 7/290/62 0/29

•ISI2-ETNVLHEXVLIPNTNALATE 0/62 12/25•ENZOf k| FLOMANTNEKC•ENZOUIPVRENE

INORGANICSALSIAS•AIEcuFEPIMNNGHIVNZN

0/62 6/290/62 1/29

14/78 7/260/78 0/2614/78 7/2615/78 10/268/78 1/2614/78 4/2615/78 7/2315/78 13/2615/78 10/260/73 9/2614/76 14/2614/78 0/2615/78 16/21

SL W SU

0/136 5V*64/136 4.25 7.5369/136 26.63 10.673/13612/1191/136 2.5041/136 28.248/136 5.239/136 2.6111/136 3.7112/136 7.4922/136 39.19

8/1620/1622/162 8.4828/162 17.686/1624/16229/162 7.2849/16224/162 9.4811/16215/16238/16215/16218/162

.97

.53

.35

.45

.01

.66

.29

.71

.01

.98

.02

.81

.70

.72

.04

.76

.93

.23

.68

.04

94/229 10864.0 97.419/229188/224 114.2 6.494/229 929.8 103.7100/229 2.9 2.9219/226 109.4 12.399/229 92534.9 89.2224/230 57.2 5.196/229 59.5 21.671/198 • 0.1201/215 84.4 33.093/228 24.1212/219 3797.1 19.2

SL

12.9631.13.64.79.64.65.62.17.69.67

4.63

159.66

164.54229.03163.56167.48141.09345.99151.43167.56167.84364.07198.88183.88

254836.06152.77738.241488.7548.8

17695.5240242.430006.418078.2

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97006000330068005000330020000

5438002700

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43603797.1

556

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2030015589702.21622

330

SL

4964780002970360005940145051002100

1666.5360026000

1100

24037000670580

220006800300001900170001350002200019000

22700000182300372000313000051000

11830004360000011900003660000

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Figure 2-6 Oil Water SeparatorSampling Locations (Ebasco, 1989)

OZ6I 100 NIS

LSemi volatile organics were predominantly found in soil. Over 30

percent of the semivolatile organic hits were phthalate esters.However, phthalate compounds are common laboratory contaminants, andmay not be indicative of site contamination. Additionally, none ofthe SMC Martin data, comprising over 70 percent of the data, has beenvalidated, so laboratory contamination cannot be discounted. Onlyfour semivolatile organics were present in ground-water samples:nitrobenzene, 2-methylnaphthalene, phenanthrene, and pyrene. Surfacewater semivolatile organics were detected at a greater frequency thanin ground water, suggesting some contribution from the surface soilsin the vicinity.

Metal contaminants were prevalent in all media. When compared toground-water geometric means, MCLs were exceeded for arsenic (50 ppb)and lead (50 ppb). In addition, the secondary drinking water standardfor iron (300 ppb) was exceeded. Metal contamination in soils isoften difficult to assess since most metals are naturally occurringconstituents served from the underlying bedrock. In order todetermine if levels of metals found in soil samples at the SinclairRefinery site represent an increased health risk, comparisons weremade to regional ranges and averages. As shown in Table 2-3, the meanconcentrations for lead and copper, which typify the region geologicalformation, were slightly exceeded; however, these levels may bepartially attributable to local background levels.

2.2 Contaminant Distribution

This section will focus on both the horizontal and verticalextent of contamination as it relates to soil contamination. It isreasonable to assume that the contamination in the refinery areaoriginally resulted from surface sources (e.g., oil-water separators, ^

Moperational spills, storage units). Therefore, an evaluation of a:contaminant distribution trends in the soil will provide useful input ooin the selection of applicable and significant exposure pathways for Mexposure assessment. »->

«>NJf-i2-11

TABLE 2-3TOTAL COMPARISON OF METAL CONCENTRATIONS IN SOIL

AT SINCLAIR REFINERY SITE

METALS(PP-)

ALUMINUMANTIMONYARSENICBARIUMBERYLLIUMCADMIUMCALCIUMCHROMIUMCOBALTCOPPERIRONLEADMAGNESIUMMANGANESEMERCURYNICKELPOTASSIUMSELENIUMSILVERTHALLIUMVANADIUMZINC

ObservedConcentration Ranges

20 -0.68 -0.1 -20 -

0.115 -O.S -500 -

1 -2.7 -1.1 -10 -

O.S -486.5 -

1.5 -0.02 -0.9 -

14 -0.125 -

0.0235 -0.23 -4.4 -

2 -

22700182.3

5723130

5121.6

688009625

118343600

11901200036609.4357

25007.9

40.711.6

302037

6eoMtr1c Mean(All Saeplei)

254.8366.1537.738

41.4890.5490.618

828.5909.0595.993

17.695240.24230.006

951.62218.0780.045

16.639587.232

0.5171.0851.0996.945

62.039

Typical BackgroundConcentrations

In Tioga Scries. N.T. Soils (a)

Notes: (a) USOA. Soil Conservation Service Study (IMS)

18.8

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Figure 2-7 depicts the relative contaminant levels by class for theshallow, medium, and deep soil strata. As illustrated, the volatileorganic compound (VOC) and base/neutral/acid (SNA) concentrations areapproximately equivalent in each soil strata. However, metal concentra-tions in the subsurface soils are significantly higher. This contaminantdistribution suggests that subsurface soil contamination, although lessavailable for direct exposure (e.g., soil ingestion, dermal contact), willlikely contribute to ongoing ground water contamination as the solublemetals continue to leach.

Because past operations at the refinery site were likely to producesoil contamination at the surface, and because ground-water and surfacewater contamination often stems from the diffusion of contaminants fromthe soil, detailed evaluation of the areal distribution of contaminantsin surface soils is warranted. Figures 2-8, 2-9, and 2-10 depict theresults of analyses of surface soil samples for VOCs, BNAs, and metals asthree-dimensional surface reflecting contaminant plots using SURFER*.a computer graphics program (Golden Software, 1989). The plots depictingthe areal extent of surface soil contamination are oriented such that thelower left corner of the three-dimensional figures corresponds to thelower left corner of map views of the site presented in this endangermentassessment and the RI report. With this orientation, the view is towardsthe Genesee River (east) with the northern site features on the left andthe southern features on the right. The vertical axis reflects theactual concentration of contaminants, with units of parts per billion.

Salient features at the site are identified and located relative tothe concentration surface. In general, contaminant distribution portrayedon these plots indicates higher VOC concentrations in the southern portionof the site, and evenly distributed BNA concentrations towards the eastern

COportion of the site. The following discussion highlights the anomalous £areas of contamination and provides details on the position of those "hotspots" relative to past and present site features. 3

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FIGURE 2-7

CONTAMINANT DISTRIBUTION WITH DEPTH(BNAs & METALS IN PPT, VOCS IN PPB/10)

BWiOH

I/GUM

\\\\\\\\\\\icr/ts

ENAs

VDCs

TOO NIS CONCENF TTON

2-8 '

VOC CONCENTRATIONS IN SURFACE SOILS

83-12/232.5 ppb

Southern OH Separator

Southern Drum Storage Area

Northern Drum Storage AreaSS-7/126.5 ppb

Northern ON Separator

VOC CONCENTRATION IN SURFACE SOILS

BNA CONGELATIONS IN SURFACE SOILS83-25/38,039 ppb

88-11/38.185 ppb

Southern Drum Storage Area

Southern CM Separator

Lead Sludge Pit Northern ON Separator

BNA CONCENTRATION IN SURFACE SOILS

___ J _

••I

N*•!-•vl

FIGURE 2-10

METAL CONCENTRATIONS IN SURFACE SOILS

AB 53/76.010 ppb

Z.36I TOO NIS

Northern Drum Storage Area

Southern Drum Storage Area

LaadShKfaeni

O - I

Nor them OH Separator

OR Separator

METAL CONCENTRATIONS IN SURFACE SOILS

An anomalous high peak was generated in the diagram of volatile ^_^organic compound concentrations (Figure 2-8). As noted in the figure,this peak (hot spot) has a concentration of 232.5 ppb. This area ofmaximum contamination is defined by the concentration from analysis ofsurface soil sample SS-12 which resulted primarily from elevated levelsof methyl chloride. This sample was taken at the location of a previouslyused coal pit, just west of the southern drum storage area and thesouthern oil separator used at the refinery. Relatively high levels of ;VOCs are found in the remainder of the southern portion of the site. The :

anomalous high VOC concentration is approximately 300 feet south of the ,Mapes Industries facility, 300 feet west of the Otis Eastern storage yard, )and 500 feet southeast of the Butler-Larkin facilities. A small peak t(126.5 ppb) from sample SS-07 stands out in the otherwise low northern iportion of the site. The minor peak is at the same location as thenorthern drum storage area. >

iTwo very high peaks stand out on the diagram of total concentrations

for the base/neutral/acid extractable compounds (Figure 2-9). One highpoint with a value of 38,185 ppb (from sample SS-11), which resulted from _^elevated concentrations of a number of compounds such as anthracene,benzo(a)anthracene and benzo(a)pyrene, was identified at the southern drumstorage area. This peak in SNA levels is located between the Mapes ,Industries and Otis Eastern facilities, approximately 200 feet from each. IThe area around the former coal pit and the southern oil separator containsrelatively low levels of contamination. A secondary peak (38,039 ppb fromsample SS-25) was identified in the north east portion of the siteattributed by elevated levels of phenol and di-n-butylphthalate, andappears to reflect a trend towards increasing concentrations nearer theGenesee River. This secondary peak is located just northeast of the leadsludge pits, the northern oil separator, and the northern drum storagearea used at the Sinclair Refinery. The high contaminant levels at this £Jpeak are from a drainage swale sample approximately 700 feet north of theNational Fuel Company building. 2

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The plot of metal concentrations for the Sinclair Refinery site(Figure 2-10) does not demonstrate significant hot spots or anomalies aswere shown in the plots for BNAs and VOCs. Instead, there appears to bea trend of increased concentrations on the eastern portion of the sitetowards the Genesee River with an area of high values along a line justeast of center for the site. The high values range from 40,000 ppb to75,000 ppb along this area, 25,000 to 40,000 ppb to the east of thisarea, and 2,500 ppb to 10,000 ppb in the mid-western portions of thesite. The northern drum storage area is just west of the highest peak inthe diagram (26,010 ppb from sample AB-53).

This evaluation of lateral contaminant distribution is intended tohelp in the identification process for exposure pathways at the SinclairRefinery site. By graphically presenting the relationships betweencontaminant distribution in surface soils, and past and present sitefeatures, current and future risk to human health can be more accuratelyassessed.

2.3 Selection of Chemicals of Potential Concern

This endangerment assessment focuses oh site contaminants that havebeen identified through a screening process as posing potentially the mostsignificant adverse effect on human health or the environment. These"indicator" chemicals are selected based on consideration of thecontaminants (1) intrinsic toxicological properties, (2) quantity andprevalence at the site, and (3) physical and chemical propertiesaffecting the mobility through various media.

The indicator chemical selection process was based on the approachoutlined in the Superfund Public Health Evaluation Manual (SPHEM October1986). The geometric mean of the monitoring data concentrations for

03detected site contaminants was used as- the representative concentration £?value. In cases where a compound was not detected, the geometric mean

V was calculated using a concentration of 1/2 the detection limit to approx- 2imate the compound's concentration. The highest detected concentration

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2-19OlOly

ranked and compared for each media separately. The selection processalso involved a comparison of the relative prevalence in each impactedmedia. The final phase of the selection process involved aqualitative evaluation of other pertinent contaminant properties(e.g., vapor pressure, environmental persistence, and solubility) thatcould influence the extent or rate of release. Table 2-4 shows thecalculations used to establish a ranking of the contaminants by mediaand toxicological effect.

The selection process for the Sinclair Refinery site identifiedeleven contaminants, including four volatile organic compounds, twosemivolatile organic compounds, and five metals. One semivolatilecompound, benzo(a)pyrene was not detected in any samples collectedfrom the offsite tank farm. Benzo(a)pyrene will not be evaluated forthe offsite tank farm.The selected chemicals upon which thisendangerment assessment will be based are listed below.

Chemicals of Potential Concern

Volatile Organic Compounds

methyl chloride (chloromethane)trichloroethene

benzenexylene

S«mivolatil« Organic Compounds

nitrobenzenebenzo(a)pyrene (excluded for

the offsite tank farm)

Inorganic Matals

arsenicbariumleadnickelzinc

The following section will evaluate the migration routes andrelated exposure pathways for each of these contaminants of concern.The receptors and resulting chemical intakes will then be estimatedbased upon either monitoring data or conservative dispersion modelingapproaches that use data from identified waste sources.

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3.0 EXPOSURE/TOXICITY ASSESSMENT

This section will begin with a discussion of the physical andchemical characteristics of the contaminants of potential concern at thesite. The exposure setting will then be characterized with respect tothe spacial distribution of contamination. Next, the potentialcontaminant migration pathways will be defined for each impacted media.Finally, chemical exposures will be estimated for the significantpathways.

3.1 Fate and Transport/Toxicitv Summary

This section includes a summary of the fate and transport mechanismfor each chemical of concern along with a condensed toxicity profileincluding Federal/State health based standards. A more comprehensiveanalysis of these topics for each chemical is appended to this report.Intermedia transfer of contaminants from soil to either the air or groundwater are considered potential migration pathways for the SinclairRefinery Site. Table 3-1 summarizes the standards for the contaminants.

3.1.1 Methyl Chloride

Methyl chloride (chloromethane) (CH-C1) is a gas at normaltemperatures; it has a boiling point of -23.7°C. The low organiccarbon partition coefficient (Koc), which is a measure of the tendency fororganics to be adsorbed by soil or sediment, of methyl chloride (35 mg/g)and high water solubility (6,450-7250 mg/1) indicate loose bonding withsoil particles and therefore the chemical is most likely to be found inwater and air. The high vapor pressure of methyl chloride (4,310 moHg)suggest that the major transport and fate mechanism is volatilization fromsoil and surface water.

Reference doses and carcinogenic potency factors are not availablefor methyl chloride. The Occupational Safety and Health Act (OSHA)Permissible Exposure Limit - Time Weighted Average (PEL-TWA) is 210milligrams per cubic meter (mg/m ). MCLs and New York ambient waterquality standards are not established for methyl chloride. The New York

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TABU 3-1STANDARDS

111I OSHAIPEL-TWA1

Ks»|s.3>1

Metbyl Chloride

Tricbloroatben*Bensene

Xylene

Nitrobentene

Banco (>) Pyrene

ArsenicBuiw

LeadNickelZinc

|I 10}1I 2701 3011 051I NO

1

1 NO

11 0.21 0.5|<»ol.

1 e°»P>| 0 OS

1 i.o

1 11 | HA HOC1 m Aobient (For Protection

EPA | Ground WatarjOf Aquatic Lif*MCt2 | Crit»ri«3 (Freshwater Acut*

(u»|l) | (u«|l) | Toxicity2

1 1 u«/l1 1

HD |SO (suidencel HD| value) |

5 | 10 | 45,000*5 ("Not D«t*e- | 5,300*

1 tad" |10,000 |SO (cuidancel KD

| valua) |MD |30 ((uidancaj 27.000

| valua) |ID |"Hot Datac- | HD

1 tad- |SO | 23 | K>

3.000 | 1.000 | K>

1 11 1

30 | 25 | 80*«30 | HD | l.*00««

1 S(«inc| 5.000 | 3.000 | 1301 o«ide)|(SNa.) | |I I I 1I I I 1

1EPA HOC |

For Protactlon | AHQC ForOf Aquatic Llfa | Protactlon Of

Fraibwatat Chronic | Buaan BaaitbToxicity2 (a«|l>

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ND

m>NO

KD

HD

HD

HDHD

3.2*«60"

110

SO ui/123.* «•/!•

3 (orcaao-laptlc)

MD - Hot datanined, no data available• - Lowest value known to be toxic•* - Haxdneu dependent criteria (100 •«/! uaed)1ACCIfl. ThresboU Unit Value and Biolo»ical Expoaura Indices for 1986-892CZXCLA CU-plianea With Other Laws Hanual. Au«ust 8. 1988HYSDEC Aotoient Water Quality Standards and Guidance Values

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3-20102T

ambient ground -water quality guidance is 50 ug/1. The EPA ambient waterquality criteria for the protection of human health estimates acarcinogenic risk of 10* with a lifetime exposure of 0.19 microgramsper liter (ug/1). Criteria for the protection of aquatic life have notbeen determined.

3.1.2 Trichloroethene

Trichloroethene (C-HCl-) has a Koc value of 126 mg/g indicatingthat it forms loose bonds with soil particles. This factor in additionto a high water solubility of 1.000 mg/1 , gives trichloroethene asignificant leaching potential.

It does, however, possess some ability to adsorb to organic materialsand will bioaccumulate to a certain extent. The significant transport andfate mechanism for trichloroethene is volatization from soil and surfacewater (vapor pressure - 60 mmHg) .

Trichloroethene is a probable human carcinogen (EPA Group B2) with a-2 -1carcinogenic potency factor of 1.3 x 10 (mg/kg/day) for the

-2 -1inhalation route and 1.1 x 10 (mg/kg/day) for the oral route.Reference doses have not been established for trichloroethene. The OSHAPEL-TWA for trichloroethene is 540 mg/m . The EPA has set the MCL at astringent 5 ug/1 and the Nev York ambient groundwater (source of potablewater supply) quality standard was set at 10 ug/1. The EPA has reportedthe lowest value known to be toxic (acute) in aquatic organisms forfreshwater to be 45 mg/1. The EPA has estimated a human carcinogenicrisk of 10 associated with a lifetime exposure to a concentration of2.7 ug/1.

3.1.3 Benzene

Benzene's (C,H,) relatively low Koc value (83 mg/g) and relativelyhigh water solubility (1.780 mg/1) indicate that it has a tendency to leachfrom the soil. Its major transport process is volatization from soil and

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3-301027

' surface water (vapor pressure - 75 mmHg) . Data have shown that benzene maybe photo -oxidized rapidly in the atmosphere and thus atmospheric destruc-

| tion of benzene is the significant fate process (Clement, 1985).

Benzene is an identified human carcinogen (EPA Croup A) with a-2 -1carcinogen potency factor of 2.9 x 10 [ (mg/kg/day) ] for both the

oral and inhalation routes. Reference dose have not been established forbenzene. The OSHA PEL-TWA is 10 mg/1. The EPA has set the MCL forbenzene at a stringent 5 ug/1. The New York ground-water quality standardwas set at "not detectable". The EPA has reported the lowest value knownto be toxic (acute) in aquatic organism for freshwater to be 5,300 ug/1.The EPA has estimated a human carcinogenic risk of 10 associated witha lifetime exposure of 0.66 ug/1.

i 3.1.4 Xylene

Xylene [C,H, (CH,)-] has a relatively high Koc value of240 mg/g and a comparatively low solubility of 160 mg/1. It has atendency to bind with sediment in water and with organics in soil.

; Xylene therefore has a small potential for leaching into ground water.The significant transport and fate of xylene are volatilization (vapor

T pressure - 10 mmHg) and ultimately photo -oxidation (Clement, 1985).!1 Reference dose and carcinogenicity have not been determined for• xylene. The OSHA PEL-TWA is 435 mg/m3. The U.S. EPA has not; promulgated an MCL for xylene (the proposed maximum contaminant level is

440 ug/1). New York has not promulgated an ambient water qualityI standard (the ambient ground-water quality guidance value is 50 ug/1).

_ 3.1.5 Nitrobenzene

Nitrobenzene has a relatively high solubility (1,900 mg/1) and lowKoc value (35 mg/g). These factors indicate that leaching and surfacewater runoff are the major transport processes from nitrobenzene. Theaquatic fate of nitrobenzene includes both photochemical and biological Codegradation.

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Reference doses for nitrobenzene are 6 x 10 mg/kg/day (subchronic)-4 -3and 6 x 10 mg/kg/day (chronic) for the inhalation route, and 5 x 10

-4mg/kg/day (subchronic) and 5 x 10 mg/kg/day (chronic) for the oralroute. The EPA and the NYSDEC have not determined ambient water qualitycriteria for nitrobenzene. The New York ambient ground-water (source ofpotable water supply) quality guidance value is 30 ug/1.

3.1.6 Benzo(a)Pyrene

Benzo (a) pyrene is virtually insoluble in water (solubility -1.2 ug/1) and has an extremely high Koc value (5,500,000 mg/g). As aresult, benzo (a) pyrene will adsorb onto suspended particulates andorganic matter and be transported by runoff. The fate of benzo(a)pyreneis believed to be biodegration and biotransformation.

Benzo (a) pyrene is a probable human carcinogen (EPA Group B2) witha carcinogenic potency factor of 1.15 x 10 (mg/kg/day)" for theinhalation route and 6.1 (mg/kg/day)* for the oral route.

Reference doses have not been determined for benzo(a)pyrene and EPAhas not promulgated any water quality criteria. The New York ground-water (source of potable water supply) quality standard is a stringent"not detectable".

3.1.7 Arsenic

Arsenic (As) is a metal that can be found in both organic andinorganic compounds and can exist in any of four valence states. Arsenicis generally insoluble in water; although some salts are soluble.Mobility of arsenic differs with the .state of the chemical, but arsenicis generally highly mobile. Important transport processes for arsenicare sorption by sediment and volatization during high biological activity(arsenic is metabolized by some organisms) (Clement, 1985).

Arsenic is a human carcinogen (EPA Group A). It has a carcinogenic-1 ~°potency factor of 50 (mg/kg/day) for the inhalation route and "

.115 (mg/kg/day) for the oral route. Reference doses for arsenic have

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not been determined. The OSHA PEL-TWA for arsenic is a stringent500 ug/m . The EFA has set the MCL at 50 ug/1 and the New York ambientground-water (source of potable water supply) quality standard is an evenlower 25 ug/1. The ambient water quality criterion (USEPA) for theprotection of aquatic life (freshwater acute toxicity) is 440 ug/1. Thefreshwater chronic toxicity criterion has not been determined. The EPAhas estimated a human carcinogenic risk of 10* associated with alifetime exposure concentration of 0.01 to 1.8 mg/1 (U.S.EPA 1989c).

3.1.8 Barium

Barium (Ba) is an insoluble metal that decomposes in water and willform insoluble carbonate or sulfate salts. Barium is generally found insurface and ground waters only in extremely small amounts. Insolublecompounds of barium are not highly toxic, however, barium may becomesoluble and toxic when combined with chlorides or other ions (Clement,1985). The major transport and fate process for barium is sedimentrunoff.

Reference doses for the inhalation route are 1 x 10* mg/k§/d*y-4subchronic and 1 x 10 mg/kg/day chronic, and for the oral route is

_25 x 10 mg/kg/day for both subchronic and chronic. There are noindications that barium is carcinogenic. The OSHA PEL-TWA is 0.5 mg/m(for soluble compounds). The EPA has set the MCL at 1,000 ug/1 and theNew York ambient ground water (source of potable water supply) qualitystandard was set at a low 1.0 mg/1.

3.1.9 Lead

Lead (Pb) is a metal that can be found in three oxidation states.Lead is generally insoluble, although some organic compounds aresoluble. Most compounds of lead are not highly mobile in surface andground water. Major transport and fate processes are atmosphericparticulate movements with eventual photolysis and adsorption toinorganic solids and organic materials in aquatic environments.

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Lead is a probable human carcinogen (EPA Group B2). Reference dosesand a carcinogenic potency factor have not been determined. The OSHAPEL-TWA for lead is 50 ug/m . The EPA has set the HCL at 50 ug/1 andthe New York ambient water quality standard for ground-water (source ofpotable water supply) was set at a lower 25 ug/1. The EPA ambient waterquality criteria for the protection of aquatic life for active lead is.(1.34 [In (hardness)] - 2.014) ug/1 (freshwacer acute toxlcity) and.(1.34 [In (hardness)] - 5.245) ug/1 ^.^ proteccion of hunan

health, the criterion is 50 ug/1.

3.1.10 Nickel

Elemental nickel (Ni) is insoluble although many nickel compoundsare highly soluble. The high solubility of nickel compounds makes nickela highly mobile metal. In the aquatic environment, sorption andcoprecipitation with hydrous iron and manganese oxides make leaching andsurface runoff important transport processes for nickel whileincorporation into bed sediments is an important fate, although much ofthe nickel will be deposited to the oceans (Clements, 1985).

Nickel, in the form of refinery dust and nickel subsulfide, is ahuman carcinogen with carcinogenic potency factors of 0.084(mgAg/day) (refinery dust) and 1.7 (mg/kg/day) (nickelsubsulfide). The reference doses for the oral route are 2.0 x

-210 mg/kg/day for both subchronic and chronic. Reference doses forthe inhalation route have not been determined. The OSHA PEL-TWA is1 mg/m . The EPA has not promulgated an HCL for nickel. The New Yorkambient surface water quality standard and the EPA ambient water qualitycriteria for the protection of aquatic life (freshwater chronic toxicity)for nickel are e<°-76 <ln 'hardness to PP«>] + 1.06) A York

standard for ground water has not been determined. For the protection ofhuman health, the criterion is 13.4 ug/1.

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3.1.11 Zinc

Zinc (Zn) is a relatively mobile metal that may be found in bothsuspended and dissolved forms. Leaching from soil or sediment runoffappear to be major transport processes for zinc while sorption of thedivalent cation by hydrous iron and manganese oxides, clay mineral, andorganic material is an important fate.

.2The reference doses for the oral route are 2 x 10 mg/kg/day f°r

both subchronic and chronic. Reference doses for the inhalation routehave not been determined. The OSHA PEL-TWA is 5 mg/m for zinc oxide.The EPA has not promulgated an MCL for zinc (the secondary maximumcontaminant level (SMCL) is 5,000 ug/1). The New York ambientground-water (source of potable water supply) quality standard is also5,000 ug/1. The EPA ambient water quality criteria for the protection ofaquatic life is e(0'83 (ln <h«dne,s)] + 1-95) ug/1 (freshwater acute

toxicity) and 47 ug/1 (freshwater chronic toxicity). For the protectionof human life the organoleptic criterion is 5 mg/1.

3.2 Characterization of Exposure Setting

The physical setting for the Sinclair Refinery site, and the offsitetank farm, plays an important role in evaluation of potential exposuresand risks. The following sections summarize the salient features ofphysical setting as they apply to the assessment of risk. A moredetailed discussion of the physical characteristics of the site is foundin the Rl report prepared by Ebasco (1989).

3.2.1 Geology/Hydrogeology

The Sinclair Refinery site is located in Western New York in theAllegheny Plateau region of the Appalachian Uplands Physiographicprovince. This geologic region is characterized by Devonian and UpperMississippian sandstone, shale, and conglomerate overlain byunconsolidated pleistocene and holocene glacial and fluvial deposits.Oil and gas wells are present in the vicinity of the site and several £large oil fields are located to the north and south (Ebasco 1989). o

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3-80102T

The site itself is immediately underlain by fill material composedof sand, silt, clay, gravel, slag, concrete, and construction debris.This fill, which ranges from 0.5 to 8 feet thick, was dominantly used inthe central portion of the site for grading purposes. Discontinuousfifteen to thirty foot thick fluvial sand, silt, clay, and graveldeposits comprise the uppermost natural soils at the site (Ebasco 1989).

Glacial deposits, which directly underlie these surface soils, aredominated by up to 100 feet of glaciolacustrine clay. Monitoring wellsthat penetrated the clay deposit encountered gravel, sand, and silt below.In most areas of the site, the clay layer was encountered at between ISand 30 feet below the surface. In the northwestern portion of the site,the clay was found to be more variable in depth and thickness. In one ofthe auger borings, the clay was never encountered in the 50 foot deephole. Two nearby wells encountered thin clay beds at depths of 64 and 75feet, while a third nearby well encountered 10 feet of clay at a depth of *15 feet. This irregularity is attributed to ancient river channels thathave dissected the glaciolacustrine clay deposits (Ebasco 1989).

No wells or borings on the site were drilled to bedrock. However, atthe off site tank farm, auger borings encountered bedrock at depthsbetween 9 and 27 feet. An earlier seismic profile indicates that thebedrock under the site dips steeply from approximately 70 feet below SouthBrooklyn Avenue to more than 250 feet below the Genesee River (Ebasco1989).

Information obtained from the RI suggests that there are at leastthree hydrologic units beneath the site: an upper aquifer of recentfluvial deposits, an aquitard of glaciolacustrine clay, and one morelower aquifer of glacial sands. Sandy, silty, and gravelly soilscomprise the 10 to 20 foot thick upper (water table) aquifer, whichincludes the saturated fluvial deposits overlying the glaciolacustrineclay. Lenses as much as 1,000 feet long and 15 feet thick of less

3-9oiozy

permeable clay and silty clay have been encountered in the upperaquifer. A laterally extensive glaciolacustrine clay and silty claydeposit underlies the surface aquifer. Variable thickness within thisaquitard, or confining layer, is due to the presence of ancient riverchannels. The lower (confined) aquifer, which is composed of glacialsands, silts, and clays, is 70 to 250 feet thick and extends down tobedrock beneath the site (Ebasco 1989) .

Hydrologic properties of the water table aquifer were determinedthrough well observation and well tests. The potentiometric surface wasevaluated to generate hydraulic gradients for the site. The highesthydraulic gradients (1.6 feet per 100 feet) were identified in thenorthern and southern portions of the site, with minimum values (0.6 feetper 100 feet) in the central area. Ground-water flow is generally intothe Genesee River from the west and southwest. Two pump tests and 20slug tests performed on the water table aquifer yielded hydraulicconductivities from 5 to 245 feet per day (Ebasco 1989). Pump test datafor well MW-56 indicate an apparent boundary condition in the aquifer,which was interpreted as an aquifer inhomogeneity with an area of lowtransmissivity farther away from the well. Pump tests from well MW-57produced anomalous data, where a portion of the data was masked by latervalues. Pump tests used to determine aquifer properties may haveprovided inconsistent conclusions but the differences in hydraulicproperties between the northern and central portions of the site wereapparent in the pump test results. Slug test results provided supportfor the pump test data but are considered less accurate than the pumptest method (Ebasco 1989). Infiltration at the site was determined usingdouble-ring infiltrometer tests. Results indicate the highestinfiltration rates were in the central portion of the site where thecover material is dominant ly well sorted sand. Low infiltration ratesfrom the northern portion of the site are attributable to the poorlysorted and clayey surface soils (Ebasco 1989).

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3.2.2 Demographics/Current Sice Use

The Wellsville refinery site is located in Allegheny County, astridethe border between the Town and Village of Wellsville. Population datafrom the U.S. Bureau of Census (Ebasco, 1989) indicate sparse populationsin the area. Allegheny County has 50,500 residents, the Town ofWellsville, 7,940, and the Village of Wellsville, 5,070. Three publicschools and a university dormitory are located within one mile of therefinery. Four residences are located immediately south of the refinery.At least twenty additional residences are located adjacent to theabandoned offsite tank farm.

Nine private and government groups own parcels of land at the site,many of which are vacant at present. Businesses operating at the siteinclude: Butler-Larkin, Inc.; Current Controls, Inc.; Mapes Industries,Inc.; National Fuel Company, Inc.; Otis Eastern Service, Inc.; andRelease Coatings, Inc. Butler-Larkin manufactures oil, gas, and waterwell drilling equipment, and completion equipment at the site. NapesIndustries manufactures finished wood products on site and CurrentControls manufactures electrical components. Release Coatings produces achemical to facilitate the release of molded products from molds. OtisEastern maintains storage facilities for construction equipment at thesite. National Fuel maintains a vehicle storage lot and customer serviceoffice on the site. The SUNY at Alfred campus is an agricultural andtechnical college with auto repair shops.

Many of the businesses on site generate heavy vehicular traffic.Both National Fuel and Otis Eastern use the site for storage andmaintenance of large fleets of trucks and heavy construction equipment.Great numbers of passenger vehicles use the roads on site related toemployment at the site and the vocational college.

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Hazardous materials are generated on site and have been noted inKYSDEC documents (Ebasco 1989). In the mid-1980s, NYSDEC found evidenceof illegal disposal of hazardous waste inside and outside theButler-Larkin and Mapes Industries buildings. These wastes, whichallegedly included solvents, paint solid residue, cutting oil, and wastefrom a phosphatizing process, reportedly were discharged, either directlyor indirectly, into the main drainage swale and the Genesee River (Ebasco1989). Ebasco observed the application of an asphaltic coating topipelines, and surface soils, in the Butler-Larkin facility. Steamcleaning of engines, with no facility to trap waste oil, was observed atthe SUNY auto shop (Ebasco 1989).

3.2.3 Climatology

Vellsville, and the rest of New York, is in the moist continentalclimatic regime, with warm, humid summers, dominantly sub-freezingwinters, and abundant rainfall throughout the year. The hilly terrain inthe vicinity of Wellsville is in the Western Plateau climatic division ofNew York state. Specific weather information for this division isprovided by the U.S. Department of Commerce (Ebasco 1989). Based on datacollected from 1941-1970. the average daily temperature varies from a highin July of 68.1'F, to a low in January of 23.'F. Precipitationfor the same period ranges from 2.18 inches in February to 43.79 inchesin Hay. Annual precipitation for the entire climatic division averages37.3 inches (Ebasco, 1989).

More detailed weather information for the area of Vellsville is notavailable due to the scarcity of weather stations in that part of thestate. The nearest weather station to the site is 69 kilometers away, inBradford, Pennsylvania (Gem 1989). Data gathered at the Bradford stationfrom 1951 to 1980 yields average daily temperatures ranging from19.9'F in January to 76.5'F in July, with an annual average daily w

t«jtemperature of 43.5*F. Precipitation at the Bradford weather station zranges from 2.88 inches in February to 4.26 in June, with an annual total o

of 42.71 inches (NOAA 1982). 3

3-12OlOZy

3.2.4 Topography

The Sinclair Refinery Site lies in the floodplain of the GeneseeRiver among the rolling hills and mountains of south-central Pennsylvania.The surrounding topography is dominated by gently rolling hills withmaximum elevations of 2,000 to 2,200 feet above mean sea level (msl) andmoderate to steep slopes leading to valleys as low as 1,500 feet abovemsl. The area in the immediate vicinity of the site is generally flatterrain sloping gently to the Genesee River on the eastern border of thesite. This flat land is the floodplain for the Genesee River, which liesat about 1,500 feet above msl. The edges of the floodplain are marked byan abrupt change in topography. Surface water drainage from the site isnortheastward, towards the river. A network of surface culverts andstorm sewers carries most of the runoff directly into the Genesee Riveradjacent to the site. A large drainage swale runs along the northeasternmargin of the site, preventing most of the surface runoff from enteringthe Genesee River (Ebasco 1989).

The off site tank farm (OSTF) is located to the west of the refinerysite on a sloping area on a hill adjacent to the site. The OSTF issituated at approximately 1,650 feet above msl. A small stream, whichdrains towards the refinery site, bisects the OSTF area. This streamterminates at the drainage swale along the north end of the refinery.Previous tank locations are identified by 15 -foot high berms, which haveproduced pools or wet areas at the OSTF (Ebasco 1989).

3.3 Identification of Potential Exposure Pathways

This section incorporates the information from the previous analysesto develop a list of potential contaminant exposure pathways associatedwith the site. The remaining sections of this chapter will identify andevaluate the potentially significant migration pathways, and concludewith an estimation of exposure point concentrations and related chemicalintakes.

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Several chemical migration pathways -are possible for contaminantreleases at the Sinclair Refinery including surface water, ground water,soil, and air. Table 3-2 summarizes the potential migration pathways andhuman receptors. The following is a discussion of the migration pathwaysidentified for each impacted media at the Sinclair Refinery site.

3.3.1 Air Pathways

There are two pathways for contaminant release into the air, bothamendable to chemical constituents at the site. The first, isvolatization which occurs when chemicals evaporate directly from soil toair. Since air sampling was not performed at this site, actual volatileorganic compound (VOC) concentrations in the ambient atmosphere areundetermined. As discussed in Section 3.2, the VOCs are distributedequally in the surface and subsurface soils. In addition, only 3 of the14 surface soil auger borings samples found VOCs above their respectivedetection limit. Based on this evaluation of VOC distribution, exposureto VOCs would be expected to be a concern only under limitedcircumstances. For example, excavation workers could be exposed to VOCsespecially since excavation activities would disturb the soil and releasecontaminants trapped in soil pore spaces. The contaminants which may bereleased through this pathway include methyl chloride, trichloroethene,benzene, and xylene. Since all of these contaminants have relativelyhigh vapor pressures, they can be expected to readily volatilize into theatmosphere if exposed to the air. The volatilization pathway isconsidered to be of less concern than the other air pathway, fugitivedust inhalation.

The release of fugitive dust particles is expected to dominateexposures via air at this site. This pathway was identified aspotentially significant since the roadways and parking areas on this siteare covered with a thin surface of gravel which facilitates thegeneration of dust due to vehicular traffic. Facility members of the

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TABLE 3-2POTENTIAL MIGRATION PATHWAY AND EXPOSURE ROUTE EVALUATION

PotentialMigrationPathway

Air

Soil

SurfaceWater

GroundWater

PotentialExposure OnsiteRoute Occupants

VOC Inhalation XDust Inhalation X

IngestionDermal Contact

IngestionFish IngestionDermal Contact

IngestionDermal Contact

Possible Human ReceptorsLocal Onsite

Resident Temp. Workers

X XX

XX

XXX

X*X*

OnsiteTrespassers

XX

XX

*Ground water impacts surface water media • ground water not used as drinkingwater source.

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I- SUNY campus indicated chat during dry conditions, the property has a dustproblem caused by automobile and truck traffic. The contaminants that

~~] are of particular concern include the metals and semi-volatile organiccompounds which are generally sorbed onto soil particles. Intake resultswhen the soil particles are inhaled, and the chemicals are desorbed inthe lungs.

3.3.2 Soil Pathways

Contaminants present in soil will contribute to air contaminationthrough volatilization and dust emissions and ground-water contaminationthrough infiltration. However, the only direct routes of exposure

I identified are through either inadvertent soil ingestion or dermalabsorption. Inadvertent soil ingestion is typically evaluated in the

| context of the normal mouthing behavior of children between 1 and 6 yearsof age. An evaluation of soil ingestion exposure is viable because an

*

elementary school is located approximately 1-mile from the site.Although a portion of the site is currently occupied by the SUNY Campusand various commercial interests, a larger portion is not secured and

• easily accessible. The contaminants of concern that have the highestingestion toxicity values include arsenic, nitrobenzene, benzo(a)pyrene,

I and lead, all of which were detected in the surface soils.

Dermal absorption of contaminants through the skin boundary isanother potential route of exposure of soil, however, the significance ofthis pathway is likely to be negligible in comparison with the soil

I ingestion scenario. In addition, dermal absorption is known to be moresignificant in aquatic media where a greater skin surface area is

— contacted with dissolved contaminants.

3.3.3 Surface Water Pathways

Contaminant loading to the surface water adjacent to the site likelyoccurs through migration of contaminants with ground water as it flows

I from the site to the river, and through deposition of suspended enf*^

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contaminants in surface water run-off. The potential exposure routesinvolving surface water include: (1) residential ingestion during periodswhen the public drinking water intake, located downgradient of the site,from surface water is used, (2) ingestion of fish caught near the site,and (3) dermal contact with the surface water during recreation.

As previously discussed, a new drinking water intake for the Town ofWellsville was installed upstream of the site in 1985. Since that time,the old water intake and treatment plant have been used as a backupsystem. According to the Public Works Department of Wellsville, the downstream intake is used in emergencies when the upstream intake andtreatment system are not working. The downstream intake has been used,on the average one day per month during the initial start-up period, butthe Public Works Department expects the frequency to decline over time(HacFarquar, D. 1989). Therefore, the risks associated with theingestion of surface water will reflect only current conditions. Thisexposure is expected to be substantially reduced once the new treatmentplant becomes the sole drinking water intake system.

According to a local resident, local children have been observedfishing in the Genesee River at the Village of Wellsville, however, hestates that it is relatively uncommon (MacFarquar, D. 1989). Accordingto the New York State Fish Commission, most of the downstream sportfishing begins approximately 2 miles from the site near the golf course.This portion of the river is stocked and heavily fished. According tothe Fish Commission, the section of the river through Wellsville is notstocked.

Dermal contact with surface water is a potential exposure pathway,however there is minimal support for this exposure scenario as beingeither particularly significant or critical. There are no designatedbeach areas in the Town of Wellsville, and except for an annual raftingrace, the river seems to be used very infrequently for recreational ig

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purposes adjacent to and directly downstream of the site. Dermal contactwith surface water is expected to be less of a health threat than eitherthe surface water ingestion or fish ingestion exposure scenarios.

3.3.4 Ground- Water Pathways

The results of a water well inventory of the facilities andresidences immediately surrounding the Sinclair Refinery site, presentedin the RI Report (Ebasco, 1989), indicate that only two wells arecurrently operational outside the southern portion of the site. One wellis located at the Uellsville School District bus garage and the other isjointly owned by four residents north of the Weidrick Road near thesouthern boundary of the site. The RI Report indicates that these wellshave been completed in the deep aquifers. Analytical results from all ofthe five deep aquifer monitoring wells installed at the site provides noconvincing evidence that the deep aquifers have been adversely impacted.In addition, hydraulic gradient data, obtained during the remedialinvestigation, indicate that the ground-water flow at the site isgenerally north to northeast towards the Genesee River away from thesepotential receptors. Due to both limited data on the water quality ofthe deep aquifer system and the location of the two drinking water wellsupgradient of the site, a drinking water exposure scenario for residentalground water was not considered in this assessment. The focus of thisassessment was on the contaminants identified in the shallow aquiferunder the site. The RI Report did not identify any uses of the waterfrom the shallow aquifer, however, hydraulic gradient data supports theconclusion that the aquifer flows towards the Genesee River.

3.4 Potentially Significant Exposure Pathways

3.4.1 Human Exposure Pathways

All possible exposure routes illustrated in Table 3-2 were evaluatedin order to determine the most significant exposure pathways at theSinclair Refinery site. Four exposure scenarios that could adversely

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impact human health will be quantitatively evaluated. The four exposurescenarios are as follows:

• Inhalation of volatile organic compounds by excavation workersexposed to subsurface soils,

• Inhalation of fugitive dust emissions of metals and semi-volatile organic contaminants by onsite occupants,

• Inadvertent ingestion of soil contaminants by both excavationworkers and trespassing children, and

• Ingestion of dissolved contaminants in surface water by localresidents.

3.4.2 Environmental Exposure Pathways

The evaluation of the potential environmental impacts will focus onthe Genesee River. The New York State Department of EnvironmentalConservation, Division of Regulatory Affairs, provided a regional mapindicating the locations of sensitive environmental populations andsurface water catagories. From this information, it was determined thatthe closest wetlands is less than 1 mile southeast and hydraulicallyupgradient of the site (Taft, K. 1989). The closest downgradient wetlandsarea is more than 3 miles from the site. Information from the New YorkState Fish Commission indicates that the section of the Genesee River inUellsville, has a concrete bottom and minimal aquatic vegetation (Evans,J. 1989). The only potential environmental receptors identified are theindigenous fish in the river next to the site. The risks associated withthis environmental exposure will be evaluated in the following section.The portion of the Genesee River, where game fish are released andcaught, is roughly 2 miles downstream from the site (MacFarquar, D. 1989).The modeling and monitoring surface water contaminant levels aresufficiently low to safely assume that contaminants attributed to thesite will not adversely impact the local game fish population.

3.5 Evaluation of Exposure and Chemical IntakesM

This chapter includes detailed description and related calculations 3

that lead to estimation of exposure point concentrations for each impacted omedia through the identified potentially significant exposure pathways. *""

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[I. The chemical intakes for receptors were calculated using formulas

recommended by the U.S. EPA (1989). For each different exposure route,specific information was combined to calculate the number of milligramsof chemical consumed per kilogram of body weight each day (mg/kg/day).

The general equation for this calculation is:

C x CR x EF x EDBW x AT

where:I - intake (mg/kg.day),C - chemical concentration at exposure point (e.g., mg/liter),CR - contact rate (e.g., liters/day),EF - exposure frequency (days/yr).ED - exposure duration (years)BW - body weight of exposed individual (kg), andAT - averaging times (days; period over which exposure is averaged).

For each exposure scenario, the units of concentration, C, and contactrate, CR, may change, but the intake, I, has the same units regardless ofexposure route. Also, additional route-specific terms may be introducedto account for other important factors such as percent of the chemicalactually absorbed by the body.

The values of most of the factors in the intake equation must beassumed. Host of the assumptions are standardized and recommended valuespublished by the EPA in various documents (U.S. EPA 1989a-b). However,some factors are unique to each exposure scenario, and situation-specificassumptions must be made. In these cases, realistically conservativeassumptions were used.

Three types of time-dependent intakes can be calculated using theintake equations. Subchronic daily intake (SDI) can be calculated forexposure scenarios in which exposure is limited to a time frame rangingapproximately from 90 days to seven years. For the SDI, the overall w

T

length of exposure is used for both the ED (years) and AT (days) terms in **the intake equation. For exposures lasting longer, the chronic daily oointake (GDI) can also be calculated. For the GDI too, the ED and AT *-*

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3-2001027

represent the same length of exposure (in different units). The SDI andthe GDI are used to calculate risks of non-carcinogenic effects. Thethird type of time-dependent exposure that can be calculated is theLifetime Average Daily Exposure (LADE). The LADE is used to calculaterisks of carcinogenic effects based on exposures averaged over a 'lifetime. Correspondingly so, the AT for the LADE calculation is always27,400 days (75 years, U.S. EPA 1989b). However, the ED can vary ;depending on the length of exposure.

For the purpose of a baseline risk assessment. GDI and LADE exposure :

scenarios are generally calculated. Subchronic daily intakes are moreapplicable to those exposures resulting from relatively brief contact withsite contaminants. As expected, most of the exposures for CERC1A sitesare associated with exposures over extended periods of time. For this iEndangerment Assessment Report, the only legitimate subchronic exposure 'identified relates to contracted workers that would be on the site for a .finite period of time and potentially exposed to site contaminants in thesubsurface through excavation type activities.

The following sections will address contaminant exposures and intakesfor each identified significant migration pathway by media.

!3.5.1 Air Pathway I

Two transport processes may be present at the Sinclair Refinery site jwhich have the potential for air contamination: fugitive dust exposure 'and volatile organic exposure. Fugitive dust can be generated by I

ivehicular traffic on unpaved roadways and parking lots on the site. ;

These unpaved roads are covered in dirt or gravel and allow contaminatedsoil to be carried into the air. In addition, volatile organics in aircan be generated by volatilization of organics in subsurface soil exposedthrough excavation. A probable scenario would involve the excavation of ia trench to access utility transmission conduits.

vFueitive dust exposure. Wind transported dust may be an inhalation co 1

^"^ 1hazard at the Sinclair Refinery site. Based on laboratory analysis of assamples collected from the ground surface at the site, surface soils on o I

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01027

site are contaminated by BNAs and metals. The exposure pathway expectedfor these compounds is as windblown, or fugitive dust. Fugitive dust maybe released into the air through vehicular traffic. The site is presentlyin use and more than a thousand vehicles per day may drive on and off thesite.

In order to assess the contaminant concentrations present onsite dueto fugitive dust emissions, details about site usage were acquired. Mapand site observations and interviews with site personnel provided most ofthe information necessary to estimate the rate of dust generation. Thefugitive dust emission calculations require information about the massfraction of a contaminant in particulate emissions, vehicle-kilometersper hour travelled onsite, percent of silt in the road surfaces, vehiclespeed, weight and number of wheels, and the number of days per year withat least 0.245 nun (0.01 inches) of precipitation.

The emission rate calculation for vehicle induced dust emissions atthe Sinclair Refinery site is as follows (GRI, 1988):

• la 0

Where:

QIQ - emission rate of particles 10 microns and smaller (mg/hr),a - mass fraction of contaminant in particulate emissions (mg/kg),EIQ - an emission factor (kg), andVk - vehicle-kilometers travelled onsite in one hour, totaled

across all vehicles (1/hr).

The mass fraction of contaminant in particulate emissions, a,was approximated using the mean contaminant concentrations in surfacesoils acquired from the site investigation. These values are found inTable 3-3 of this report.

According to site personnel, daily vehicular traffic onsite involvesapproximately 893 vehicles. The vehicle-kilometers travelled onsite, Vk,was estimated using 0.305 km as the average distance travelled onsite per gday. Given an average of 8-hour* per day of site usage, the average ovehicle-kilometers travelled onsite in one hour was determined to be 34.0 &I/hour (i.e., 893 vehicles x 0.305 km/vehicle + 8 hours). »-«

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3-220102y

TABLE 3-3MEAN CHEMICAL CONCENTFATIONS IN SURFACESOILS AND DUST EMISSION RATES AT THE

SINCLAIR REFINERY SITE

CONTAMINANT GEOMETRIC MEAN(mg/kg)

EMISSION RATE

Arsenic

Bariua

Benzo(a)pyrene

Lead

Nickel

Nitrobenzene

Zinc

8.80E+00

5.65E+01

1.89E-01

7.03E+01

1.83E+01

1.65E-01

8.28E+01

2.07E-05

1.33E-04

4.43E-07

1.65E-04

4.29E-05

3.87E-07

1.94E-04

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The emission factor, EIQ, used herein differs slightly from the oneused in the SEAM (U.S. EPA, 1988), which is based on data from heavierequipment (up to 142 metric tons as opposed to a maximum of 26 tons). Inaddition, because particle size analysis to determine percent silt lessthan 10p was performed on surface sediment, the silt term wasmodified to reflect observed site conditions. The emission factor wascalculated as follows:

E1Q -0.85 (s) (S/24)0-8 (U/7)°-3 (w/6)1'2 ( (365-p)/365) (GRI. 1988)

Where :

EIQ - emission factor for an unpaved road per vehicle-kilometer oftravel (kg),

s - percent silt of particles less than 10^ in road surface(0 < s < 100) (percent),

S - mean vehicle speed (km/hr) ,V - mean vehicle weight (metric tons, kkg) ,w - mean number of wheels (unitless), andp - number of days per year with at least 0.254p

(0.01 inches) of precipitation (unitless).Silt content on site was determined through a particle size analysis.

Boring AB-56, located on a well-travelled gravel roadway, was taken as arepresentative location. The percentage of silt (< 10mm) at that locationwas 7.5 percent (EBASCO, 1984).

Vehicles using the site vary in weight and number of wheels.Telephone interviews were conducted with a variety of facilities andbusinesses on site. Based on this investigation, 848 cars, 20 ten wheeltrucks, and 25 eighteen wheel trucks travel on the site every dayproviding a total of 893 vehicles for the site. The mean number ofwheels was estimated to 4.5.

The average weight for cars was estimated at 4,000 pounds, 38,500pounds for trucks. The average weight for trucks was calculated assumingthe trucks enter (exit) full and exit (enter) empty. This method providesan average of the full and empty weights of each type of truck. The10 -wheeled trucks commonly weigh 22,000 pounds empty and 55,000 pounds

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full, yielding an average of 38,500 pounds. Eighteen wheel trucks weigh30,000 pounds empty and 80,000 pounds full, providing and average of55,000 pounds. Using these average weights, the numbers of vehicles, theaverage vehicle weight for all vehicles using the site was estimated as6,200 pounds (2.8 metric tons).

Because site specific information was unavailable, the number ofdays with at least 0.245 mm (0.01 inches) of precipitation was determinedfrom Figure 2-3 of the Superfund Exposure Assessment Manual (U.S. EPA,1988). The site is between the 150 and 170 day contours so 160 waschosen as a reasonable estimate.

In summary, the values used to calculate the emission factor, E,Qare:

s - 7.5 percent,S - 33 km/hr,W - 2.8 metric tons,w - 4.5, andp - 160 days.

The emission factor, EIQ was calculated to be 0.248 kg. Fugitive dustemission rates from vehicular traffic at the Sinclair Refinery site arepresented in Table 3-3.

The airborne pollutants at the Sinclair Refinery site are expectedto have the most impact on individuals working on site. In order toevaluate the contaminant concentrations on site, a model designed forshort distances should be used. An alternative was used based on simpleconservation of mass in the dispersion of contaminated particles. A nearfield box model, which is accurate at short downwind distances (i.e.,less than 100 meters), was selected because it is applicable to scenarioswhere the receptor is onsite or very nearby (Pasquill, 1975 and Horst,1979 as cited in GRI, 1988).

The equations for the near field box model are presented below.OT

C - Q/(H W u) (GRI, 1988) g

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I Where:

,_, _. C - concentration of contaminant in ambient air onsite (g/m ),I Q - emission rate of contaminant (g/s),

H - downwind height of box (m),U - width of box (m), andu - average wind speed through the box (m/s).The downwind height of the box, H, is estimated using a specific

relationship between the length and height of the box. As seen inTable 3-4 (Pasquill. 1975 and Horst, 1979 as cited in GRI, 1988), a box

I _ height of 1.4 m, which roughly corresponds to the human breathing zone,I provides a distance from source to receptor of 10 m. This value allows

evaluation of the onsite risks associated with chemical contaminants in| the breathing zone. To provide a concentration comparable with that

variability, a distance from receptor to source of 50 meters was chosen.The box height that corresponds to that distance is 3.8 from Table 3-4.Box width of 1.000 m was estimated from the crosswind width of site based

' on previously used direction of west to southwest.

Average wind speed through the box, u, is estimated with thefollowing equation:

^ u - 0.22 (v) ln(2.5 H) (GRI, 1988)t

Where:

. v - the average annual wind velocity at the site (m/s). This value: was determined from the National Weather Service station in' Binghamton, New York. The average wind speed was 10.3 miles per

hour (4.6 m/s) (Ebasco 1989).!I The wind speed, u, which corresponds to the human breathing zone (i.e, H_ equals 1.4 m) is 1.27 m/s. The wind speed, u, which corresponds to what

j a worker might be exposed to during 30 years (i.e., H equals 3.8 m) it2.28 m/s.

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TABLE 3-4PLUME HEIGHTS USED IN NEAR FIELD BOX MODEL

Length of Side of Box, x Box Height, H(m) (a)

102030405060708090100

1.42.12.73.33.84.34.85.35.86.2

Reference: CRI, 1988. derived from work by Pasquill, 1975 and Horst. 1979.

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3-270102T

The resulting concentrations of contaminants in the air from vehicleinduced fugitive dust are presented in Table 3-5.

Fugitive dust intake. The equation for calculation of intakes fromfugitive dust inhalation is as follows:

C A x I R x E T x E F x E DBW x AT

where:CA - chemical concentration in air (mg/nr),IR - inhalation rate (m3/hr) ,ET - exposure time (hrs/day) , andI, EF, ED, BW, and AT are as defined for the general equation (seepage 3-20).

This scenario was developed to address possible exposures resultingfrom inhalation of airborne dust at the site. This scenario assumesadults are at the site for 8 hours per day (ET), and 5 days per week for50 weeks per year (EF - 250 days per year) for 20 years. Chronic intakes(GDI) and LADE are calculated. The values for the variables used in thisscenario are:

CA - air concentration as predicted by modeling in Table 3-5 (mg/m3) ,IR - 1.25 nr/hr (adult, suggested upper bound value, U.S. EPA 1989)ET - 8 hours/day, (assumption),EF - 250 days/yr, (assumption),ED - 20 years, (assumption),BU - 70 kg (adult. U.S. EPA, 1989), andAT - 7,300 days (ED x 365 days/yr) chronic for non-carcinogenic effects

• 27,400 days (75 years x 365 days/yr) for LADE, carcinogeniceffects.

The concentrations of contaminants in the air, CA, were predictedusing a near- field box model (GRI 1988). This model incorporates intothe predictions the amount of dust-preventing precipitation in the area.Therefore, the number of no-dust days versus dusty days has already been

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accounted for in the calculations. The calculation of intakes via dustinhalation are shown in Table 3-6. oo

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TABLE 3-6

FUGITIVE OUST INHALATIONEXPOSURE POINT: SINCLAIR REFINERY SITE (ADULTS)

CHEMICAL

Arsenic

Barlua

Beniena

Benzolalpyrene

Lead

Methyl Chloride

w Nickelio Nitrobenzene

Trlchloroethene

Xylene

Zinc

CA IR ET EF EO BU(10 •)

(e«/M3) (att/hr) (hr/day) (days/yr) (yrs) (kg)

1.17E-05

7.49E-05

0

2.50E-07

9.30E-OS

0

2.42E-05

2.20E-07

0

0

1.09E-04

1.25

1.25

1.25

1.25

1.25

1.25

1.25

1.25

1.25

1.25

1.25

8.00

8.00

8.00

8.00

8.00

8.00

8.00

8.00

8.00

8.00

8.00

250

250

250

250

250

250

250

250

250

250

250

20

20

20

20

20

20

20

20

20

20

20

70

70

70

70

70

70

70

70

70

70

70

AT Chronic LADEIntake (Carcinogens)

(days) dag/kg.day) deg/kg.dey)

7.30E+03

7.30E»03

7.30E+03

7.30E*03

7.30E+03

7.306*03

7.30E»03

7.30E+03

7.30E+03

7.30E+03

7.30E+03

1.UE-06

7.33E-06

0

2.45E-08

9.10E-U

0

2.37E-06

2.15E-08

0

0

1.07E-05

3.05E-07

0

0

A.52E-09

0

0

6.31E-07

0

0

0

0

Not MI Zero* are shown for volatile compounds (not found In dust).LADE It calculated only for chemicals potentially carcinogenic via thisexposure route.

TOO

Volatile organic compounds exposure. The second transport processthat may affect air quality at the Sinclair Refinery site is volatizationof organic contaminants from soil. A potential exposure route for thesubsurface soils is the excavation of a trench for the installation,inspection, replacement, or repair of underground utility transmissionconduits (e.g.. pipes, cables, and drains). Based on the site size,layout, ground-water depth, and an estimate of utility requirements, a1-meter wide 2-meter deep trench, 300 meters long was chosen. A trenchof this size would be capable of providing access for utility workers toinstall or repair a wide range of existing utility transmission conduits.

Volatilization is dependent on physical and chemical propertiesrelated to the particular chemical in question, and on the site'senvironmental characteristics. Chemical specific factors which affect itsdistribution between soil, soil water, soil air, and the atmosphereinclude: vapor pressure, solubility in water, molecular weight andstructure, and type and number of functional groups.

Environmental factors include the contaminants concentration in thesoil; soil water content; wind, humidity, and temperature; and sorptiveand diffusion characteristics of the soil (e.g., organic matter content,porosity, density, and clay content). Wans, moist, windy conditions willfavor volatilization as opposed to cool, dry, calm conditions. Soilsthat have a high sorptive capacity tend to decrease volatilization ratesby binding contaminants, though volatilization will still occur. Therelatively high vapor pressures of benzene (95.2 ma Hg), methyl chloride(4,310 ma Hg), and trichloroethene (57.9 ma Hg) compared to water (vaporpressure, 18 ma Hg) will act as a driving force for the migration of VOCsinto the gaseous phase, and ultimately into the atmosphere throughdiffusion. Although xylene has a lower vapor pressure (10 ma Hg), it isappreciable enough to follow a similar pattern as the other VOCs.Generally, compounds having vapor pressures below 0.1 mm Hg (20*C)begin to demonstrate measurably less volatilization potential. M

3

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voa\ro3-31

oiozy

The calculations used to estimate emission rates and exposure pointconcentrations are provided in Appendix C.I.

Volatile organic compound intake. The equation for intakes ofchemicals by inhalation of airborne (vapor phase) chemicals is:

CA x IR x ET x EF x ED6V x AT

where :CA - chemical concentration in air (mg/nr ) ,IR - inhalation rate (nr/hr) ,ET - exposure time (hrs/day) , andI, EF. ED, BW, and AT are as defined for the general equation (seepage 3-20).

This exposure scenario is an extension of the worker/excavationscenario and was created to address the possibility of workers inhalingvolatile contaminants in the air as they work in the excavation area.This scenario was developed to address the possibility of constructionworkers encountering subsurface soil during excavation activities. The

t scenario is for adult workers weighing 70 kg, being exposed for 15 daysof one year. The short duration of this scenario prevents calculation of

"7 the GDI, so only SDI is calculated. Values used for the variables in theequation are:

CA - air concentration as predicted by modeling in Table C-2 (mg/m ) ,j IR - 1.25 m3/hr (adult, suggested upper bound value, U.S. EPA 1989)

ET - 8 hours/day, (assumption),EF - 15 days/yr, (assumption),

1 ED - 1 year, (assumption).I BV - 70 kg (adult. U.S. EPA, 1989), and

AT - 15 days (EF only for subchronic exposure) for non- carcinogenic( — effects

The concentrations of contaminants in the atmosphere in the vicinityof an excavation area were predicted using a near field box model (CRI1988). Details of the modeling are provided in Appendix C.I. Table 3-7shows the calculation of intakes for inhalation of volatile organiccompounds by excavation workers.

oo

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3-320102y

gJj5

If

• *"i

IS

8

Mt

MI

MI

MI

in

Mt

Mt

Mt

MI

MI

MI

s s s s88888888

«••»•••«

a a a a a a

1

3S251

J I

;i! s! 8

OloovO

3-33

3.5.2 Surface Water Pathway

The equation for intakes of chemicals by ingesting drinking wateris:

CW x 1R x EF x EDI -BV x AT

where:CW - chemical concentration in surface water (mg/liter),IR - ingestion rate (liters/day), andI, EF, ED, BW, and AT are as defined for the general equation (seepage 3-20).This exposure scenario was created to address the possibility of

contaminated water from the Genesee River being used as a supply for theWellsville public drinking water supply. The scenario assumes that theriver water will be used only 15 days out of the year, and that residentswill live within the supplied area for 30 years. Standard assumptions ofbody weight (70 kg) and water ingestion rate (2 liters/day) are used.Chronic and LADE exposures for the drinking of surface water wereconsidered. Values for the variables in the equations are:

CW - monitoring data or predicitions based on ground water modeling,IR - 2 liters/day, (adult. 90th percentile, U.S. EPA, 1989),EF - 15 days/yr, (assumption)ED - 30 years (national upper-bound time (90th percentile) at one

residence. U.S. EPA, 1989)BW - 70 kg (adult, U.S. EPS, 1989). andAT - 10,950 days (ED x 365 days/yr) for chronic non-carcinogenic

effects• 27,400 days (75 yrs x 365 days/yr) for LADE, carcinogeniceffects.

For the water concentrations, CW, downgradient surface watermonitoring data were used. The average of data from several monitoringlocations was used to create an expected average concentration for eachcontaminant of concern. However, since the monitoring data representsonly the contaminant concentrations at a given time--a "snap shot" of ^

arconditions in the river, a means of predicting long-term concentrationsin the river was used. The Modified Universal Soil Loss Equation (MUSLE) o

vo

3-340102y

and the Soil Contamination evaluation Methodology (SOCEM) were used tomodel migration of contaminants to the river from the site in groundwater and in surface runoff, respectively. Details of the MUSLE andSOCEM modeling are provided in Appendix C.2 and C.3, respectively.Table 3-8 shows the calculation of chemical intakes from surface wateringestion using modeled concentrations, while Table 3-9 shows thecalculations using monitoring data.

3.5.3 Soil Pathway

The soil pathways include children playing on the site and at theoffsite tank farm, and construction workers encountering subsurfacesoil during excavation activities. The equation for intake ofchemicals by ingestion of surface and subsurface soil is:

I ™ CS x IR x CF x DF x EF x EDBW x AT

where:CS - chemical concentration in soil (mg/kg),IR - ingestion rate (mg/day),CF - a conversion factor (10"' kg/mg),DF - desorption factor (from 0 to 1), andI, EF, ED, BW, and AT are as defined for the general equation.

The exposure scenario to address the possibility of children whounintentionally ingest contaminated soil playing on the site and atthe offsite tank farm assumes that the children weigh 16 kg, play onthe site for 100 days out of the year, and accidentally ingest 200 mgof contaminated soil on each of those days. This activity is assumedto continue for 6 years, so GDI and LADE are calculated. Benzo(a)-pyrene was not detected in any samples collected from the offsite tankfarm; therefore, benzo(a)pyrene will not be evaluated as an indicatorchemical for the offsite tank farm. Without chemical specificdesorption information, the desorption factors for all chemicals are wMset at their maximum value of 1. Values used for the variables in the 3equation are: o

o

vo<y\

3-35

TAItE 3-8SURFACE UATEI INGESTION

IASEO ON GMUNDUATEI NOOCLINO IE SUITSEXPOSURE MINT: UELLSVILLE ICSIDENCES

Ul

CHEMICAL

Araenlc

larlua

•eniena

lento la) pyrena

Lead

Methyl Chloride

Nickel

Nitrobenzene

Trlchloroethena

Xylena

Zinc

CV II It ED Ml(Adult)

(av/l) (I/day) (days/year) (yeara) (kg)

1.56E-03

1.81E-03

2.SSE-04

8.26E-M

7.72E-OS

8.26E-M

2.04E-04

1.37E-03

4.96E-06

1.92E-04

1.10E-02

2

2

2

2

2

2

2

2

2

2

2

IS

IS

IS

IS

IS

IS

IS

IS

IS

IS

IS

30

30

30

30

30

30

30

30

30

30

30

70

70

70

70

70

70

70

70

70

70

70

AT COI LADE(Carcinogens)

(day*) (ag/kg.day) (a*/kg.day)

10950

10950

10950

10950

10950

10950

10950

10950

10950

10950

10950

1.83E-06

2.13E-06

2.99E-07

9.70E-09

9.06E-08

9.70E-09

2.40E-07

1.84E-06

S.82E-09

2.2SE-07

1.29E-OS

7.32E-07

0

1.20E-07

3.88E-09

0

0

0

0

2.33E-09

0

0

Notea: LADE la calculated only for cheaHcala potentially carcinogenic via thleaxpoaura route.

£961 TOO

TABLE 3-9SURFACE WATER DIGESTION

•ASED ON SURFACE WATER MONITORING DATAEXPOSURE MINT! UEUSVILIE RESIDENCES

CHEMICAL

Arsenic

•arlua

•entene

•entofalpyrcntLead

Methyl ChlorideNickel

Nitrobenzene

Trlchloroethene

Xylene

line

01 III EF ED BU(Adult)

(•W/l) (I/day) (days/year) (years) (kg)

7.01E-03

9.59E-02

4.92E-03

5.00E-03

4. HE-OS

S.OOE-03

4.09E-02

S.ME-03

S.OOE-03

S.OOE-03

1.UE-02

22

2

222

22

2

2

2

15

15

15

15

15

15

IS

15

15

15

15

30

30

30

30

30

30

30

30

30

30

30

70

70

70

70

70

70

70

70

70

70

70

AT Chronic LADEDally Intake (Carcinogens)

(days) (ng/kg.day) (atg/kg.dsy)

10950

10950

10950

10950

10950

10950

10950

10950

10950

10950

10950

8.23E-06

1.13E-04

5.78E-06

5.87E-06

4.82E-06

5.67E-06

4.80E-05

6.62E-06

S.B7E-06

5.87E-06

1 .696-05

3.29E-06

0

2.31E-06

2.35E-06

0

0

0

0

2.3SE-06

0

0

Notca: LADE la calculated only for chenlcais potentially carcinogenic via thlaexposure route.

8961 TOO

CS - monitoring data for surface soils; geometric mean values,IR - 200 mg/day, (young children, suggested average,

U.S. EPA 1989)EF - 100 days/yr, (assumption),ED - 6 years, (assumption),BW - 16 kg (child, U.S. EPA, 1989), andAT - 2,190 days (ED x 365 day/yr) for chronic non-carcinogenic

effects- 27,400 days (75 yrs x 365 days/yr) for LADE carcinogenic

effects

Table 3-10 shows the calculation of intakes for surface soilingestions at the refinery site. Table 3-11 shows the correspondingintakes of surface soils for children at the offsite tank farm.

The scenario to address the possibility of construction workersencounters subsurface soil during excavation activities assumes thatadult workers weigh 70 kg, and are exposed for 15 days of one year.The short duration of this scenario prevents calculation of the GDI,so only SDI is calculated. Values used for the variables in theequation are:

CS - monitoring data subsurface soils; geometric mean values,IR - 200 mg/day, (assumption),ET - 8 hours/day, (assumption),EF - 15 days/yr, (assumption),ED - 1 year, (assumption),BW - 70 kg (adult, U.S. EPA, 1989), andAT - 15 days (EF only for subchronic exposure) for

non-carcinogenic effects

Table 3-12 shows the calculations of intakes for subsurface soil\ ingestion.

3.4.4 Exposed Population

Limited populations are potentially exposed via the fourpotentially significant exposure scenarios. For the excavation workerscenario, it is expected that less than 30 workers will be exposed,

COdepending on the size and extent of the excavation. M2J

oo

voo\3-38 »

TABLE 3-10

SURFACE SOIL INGESTION VIA DIRECT CONTACTEXPOSURE POINT! SINCLAIR REFINERY (CHILDREN)

UU»

CHEMICAL

ArsenicBarlua

temene•enzolalpyrene

LeadMethyl Chloride

Nickel

Nltrobentene

Trlchloroethene

Xylene

Zinc

CS III

(•g/kg) (Kg/day)

8.80E+00

5.65E+01

2.50E-03

1.89E-01

?.01E«01

9.47E-03

1.83E«01

1.6SE-01

2.506-OJ

2.50E-03

8.286*01

200.0

200.0

200.0

200.0

200.0

200.0

200.0

200.0

200.0

200.0

200.0

CF

<kfl/«9)

1.00E-06

I.OOE-06

1.00E-06

I.OOE-06

I.OOE-06

1.00E-06

I.OOE-06

I.OOE-06

I.OOE-06

I.OOE-06

I.OOE-06

OF EF ED BU(child)

(diys/yr) (years) (Kg)

1

1

1

1

1

1

1

1

1

1

1

100

100

100

100

100

100

100

100

100

100

100

6

6

6

6

6

6

6

6

6

6

6

16

16

16

16

16

16

16

16

16

16

16

AT Chronic LADEDally Intake (Carcinogens)

(days) (ng/kg.day) (av/kg.day)

2190

2190

2190

2190

2190

2190

2190

2190

2190

2190

2190

3.01E-OS

1.93E-04

8.56E-09

6.47E-07

2.40E-M

3.24E-08

6.27E-05

S.6SE-07

8.S6E-09

8.S6E-09

2.84E-04

2.41E-06

0

6.84E-10

5.17E-08

0

0

0

0

6.84E-10

0

0

Notes: LADE It calculated only for chemicals potentially carcinogenic via thisexposure rout*.

OL6t too HIS

TABLE 3-11

INTAKES FROM SURFACE SOU INCESTION VIA DIRECT CONTACTEXPOSURE POINT: OFF SITE TANK FARM (CHILDREN)

U)

*>o

CHEMICAL

Arsenic

BarluaBenzeneLead

Methyl Chloride

Nickel

Nltrobentatw

TrlchloroathenaXylene

Zinc

CS IR

(•B/kg) <a«/day)

1.ME+013.37E+01

1.00E-03

1.12E+02

1.12E-02

8.18E+00

1.6SE-01

2.50E-03

2.50E-036.86E+01

200.0

200.0

200.0

200.0200.0

200.0200.0

200.0200.0200.0

CF DF EF ED IW(child)

(kg/*B) (days/yr) (years) (Kg)

1.00E-061.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1

1

1

1

1

1

1

1

1

1

100

100

100

100

100

100

100

100

100100

66

6

6

6

6

6

6

6

6

16

16

16

16

16

16

16

16

16

16

AT Chronic LADEDally Intake (Carcinogens)

(days) (av/kg.dey) (•B/kg.dey)

2190

2190

21902190

2190

2190

2190

2190

2190

2190

6.16C-05

1.15E-04

3.42E-09

3.83E-04

3.83E-08

2.BOE-05

5.65E-07

8.56E-09

8.56E-09

2.35E-04

4.93E-06

0

2. WE- 10

0

0

0

0

6.84E-10

0

0

Notes: LADE If calculated only for chealcals potentially carcinogenic via thisexposure route.

TOO MIS

TABLE 3-12

SUBSURFACE SOIL INGESTION VIA DIRECT CONTACTEXPOSURE POINT: SINCLAIR REFINERY SITE (EXCAVATION WORKERS)

CHEMICAL

Arsenic

••Hun

•enstnt

Bentofalpyrene

Lead

Methyl ChlorideNickel

Nitrobenzene

Trlchloroethene

Xylene

Zinc

CS IR

(•g/kg) dug/day)

7.40E«00

«.«OE«01

4.12E-03

1.87E-01

1.67E+01

1.22E-02

1.74E*01

1.64E-01

2.50E-03

6.ME-03

4.ME+01

200.0

200.0

200.0

200.0

200.0

200.0

200.0

200.0

200.0

200.0

200.0

CF

(kg/ng)

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

1.00E-06

DF EF EO BU AT Sufcchronlc(adult) Daily Intake

(dayt/yr) (year*) (Kg) (days) (mg/kg.day)

1

1

1

1

1

1

1

1

1

1

1

IS

15

IS

15

15

15

15

15

15

15

15

1

1

1

1

1

1

1

1

1

1

1

70

70

70

70

70

70

70

70

70

70

70

15

15

15

15

15

15

IS

15

15

15

15

2.11E-OS

1.266 -M

1.16E-OB

5.35E-07

4. 786-05

3.47E-08

4.971-05

4.69E-07

7.UE-09

1.90E-08

1.42E-04

ZL6T TOO

Numbers of site occupants for the adult exposure scenario aretabulated below:

Entity

Butler Larkin, Inc.Current Controls, Inc,Hapes Industries, Inc,National Fuel Company,Otis Eastern Service,Release Coatings, Inc.SUNY

TOTAL

Number ofPeople Reference

Inc.Inc.

4050*9

5214Unknown6B5 (Students & faculty)

850+

(Tilley, 1989)(Joyce. 1989)(Ellenson, 1989)(Cox, 1989)(Joyce. 1989)

* - EstimateThe total of 850 is regarded as a minimum since no information was

obtained regarding Release Coatings, Inc. A reasonable estimate of thetotal number of adults potentially exposed onsite is 900.

Demographics for the residential area surrounding the site indicatethat the community is stable, characterized by low mobility families. Acommunity representative in Uellsville City Hall indicated that the 1980census data are representative of current population figures. Aqualitative assessment of the available information indicates that thenumber of children who frequent the site and offsite tank farm is likelyto be small.

COHasoo

\ 10JCO

3-420102y

4.0 RISK EVALUATION4.1 Ht Health

The objective of this risk evaluation is to quantify information inthe exposure and toxicity assessment (Section 3.0) in order to evaluatepotential human health risks associated with the Sinclair Refinery site.Risk refers to the probability of injury, disease, or death resultingfrom exposure to the chemicals identified in this study.

Noncarcinogenie impacts of chemicals on human health are evaluatedby comparing projected or estimated intakes to reference levels for thechemicals of concern. A reference level represents an acceptableexposure level at which there will be no observable adverse effect or thelowest observable adverse effect on human health. Reference doses (RfD)are intake levels with no expected adverse health effects. The RfD isused for chronic exposures, while the subchronic reference doses (RfDs)is used for subchronic exposures. A list of these reference dosesappears in Table 4-1. Carcinogenic risk values are generally expressedin scientific notation; an individual lifetime risk of one in 10,000 is

-4represented as 1 x 10 or IE-04. The impact of carcinogenic chemicalsis assessed by comparing calculated risks and target risks for known orsuspected carcinogens. The extremes of the acceptable range forcarcinogenic risk are IE-04 to IE-07 with a target level of IE-06.

For the Sinclair Refinery site, potential exposures were identifiedvia six general pathways. These include (1) inhalation of fugitive dust,(2) inhalation of volatile emissions from subsurface soil, (3) ingestionof surface water (predicted two different ways), (4) ingestion of surfacesoil, (5) ingestion of tank farm surface soil, and (6) ingestion ofsubsurface soil. These exposure routes were developed from four possibleexposure scenarios. Risks quantified for each of these scenarios are:(1) adults on site and in Wellsville, (2) children onsite, (3) excavationworkers onsite, and (4) children on the offsite Tank Farm and in ^Wellsville. *

oo(-1

\-tvo

4-1 *"0103?

TAILB 4-1

ClltTICAL TOXICITT VALUES

INHALATION ORAL

RID'.CHEMICAL

(a«/kg. day) (

Arienlc

Bartue

•enteno

•en(o(a|pyreno

Lead

Methyl Chloride

Nickel

Nltrobenaeno

Trlchloroethene

Xylene

fine

0

I. 001-01 (b)

0

•4.10B-01 (d)

0

0

•.001-01 (b)

S. 001-01 (d)

T.OOE-OI (b)

0

RfD CarcinogenicPotency Factor

aw/kg. day) l/(o«/kg.d*y)

0

l.OOE-04 (b)

0

0

4.101-04 (a)

0

0

•.001-04 (b)

2.00E-02 (g)

4.00R-01 (b)

0

3.00E+OI (a)

0

2.09E-02 (a)

0. IDE +00 (e)

0

0

l.rOE+00 (e)

0

1.10E-02 (b)

0

0

RfD' a RfD CarcinogenicPotency Factor

(••/kg. day) (at/kg. day) l/(e«/kg.day)

l.OOE-02 (d)

S.OOE-02 (b)

0

0

1.40E-02 (d)

0

2.00E-02 (a)

S.OOE-01 (b)

l.OOE-01 (d)

4.00E*00 (b)

2.00E-01 (b)

l.OOE-01 (c)

S.OOE-02 (a)

0

0

1.40B-01 (e)

0

2.00E-02 (a)

S.OOE-04 (b)

l.OOE-02 (a)

2.00E*00 (a)

2.00E-01 (b)

l.OOEtOO (f)

0

2.09E-02 (a)

l.DEtOl (e)

0

0

0

0

1.10E-02 (b)

0

0

Notoat leroe represent unavailable or inapplicable data•ourceit (•) IRIS

(b) HEA Suenary Tablet(c) EitlMted bated on HCt(d) CitliMC*d fro* chronle RfD(•) HCA »ourc« (SPHEH)(I) EittMted from unit rltk In Rlik Ai«e*nient Forte* Report(l) fated on eonverelon of oral RID

MIS

The first scenario includes dust inhalation and surface waterconsumption. The intakes from these two exposure routes are combined tocalculate the risks for the adults onsite and in Vellsville scenario.Because two different methods for determining intakes were used for thesurface water exposure route, two risk quantifications were prepared,each using a different surface water intake calculation. Similarcombining of intakes was performed for the remaining three scenarios.The children onsite scenario includes residential surface water and soilingestion with the assumption they will consume the local public waterfor a lifetime. The excavation workers scenario includes subsurface soilingestion and subsurface soil volatile inhalation, and the children onthe offsite Tank Farm and in Wellsville scenario includes tank farmsurface soil and surface water ingestion. Tables 4-2 through 4-5 presentthe summaries of intake combining for GDIs (SDIs for Table 4-4), andTables 4-6 through 4-8 present the summaries for LADEs. Intakes inTable 4-2 through 4-8 each are divided into oral and inhalation pathways.

Noncarcinoeenic Effects

Reference doses (RfDs) have been developed by EPA for indicating thepotential for adverse health effects from exposure to chemicals exhibitingnoncarcinogenic effects. RfDs, which are expressed in units of mg/kg-day,are intake levels with no adverse health effects, including sensitiveindividuals. Estimated intakes of chemicals from environmental media(e.g.. the amount of a chemical ingested from contaminated drinkingwater) can be compared to the RfD. RfDs are derived from human epidemic-logical studies or animal studies to which uncertainty factors have beenapplied (e.g., to account for the use of animal data to predict effectson humans). These uncertainty factors help ensure that the RfDs will notunderestimate the potential for adverse noncarcinogenic effects to occur.The Acceptable Intake or Subchronic Exposure (AIS) is the highest humanintake of a chemical that is not expected to cause adverse effects whenexposure is short term (i.e., for an interval that does not constitute asignificant portion of the life span). The Acceptable Intake for ChronicExposure (AIC) is the highest human intake of a chemical that is notexpected to cause adverse effects when exposure is long term (i.e., for alifetime).

4-30103T

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S-k 31W1

TAILE 4-4

SUMMtT: SUBCHRONIC HUMAN INTAKESEXPOSURE POINT: REFINERY (EXCAVATION UORKERS)

JCNENICAL t<

Antnlc

•arlua

•era en*

tonzofalpyrtna

Lead

Ntthyl Chloride

Nickel

Nitrobenzene

TrlcMoroethene

Xylene

Zinc

tubturfece>ll IngMt.

SOI

2.11E-05

1.26E-M

1. IK-08

3.35E-07

4.78E-05

3.47E-00

4.97E-05

4.69E-07

7.UE-09

1.90E-M

1.42E-04

TotalOrat

SOI

2.11E-OS

T.26E-M

1.18E-08

5.35E-07

4.78E-OS

3.47E-00

4.97E-05

4.69E-07

7.14E-09

1.90E-08

1.42E-04

VOAInhalation

SOI

0

0

2.67E-03

0

0

4.B4E-03

0

0

0.71E-04

6.73E-03

0

TotalAirSOI

0

0

2.67E-03

0

0

4.84E-03

0

0

6.71E-04

6.73E-03

0

roo Nig

TABLE 4-5SUMMART:CHMMIC HUMAN INTAKES

EXPOSURE POINT! Off SITE TANK FARM (CHILDREN)

CHEMICAL

Arsenic••Hun

•enzene

Lead

Methyl ChlorideNickel

*> Nitrobenzenei""* Trlchloroethene

XyleneZinc

Surface Surface Sol 1Water A Water • Ingest I onCOI 0)1 CDI

1.83E-06 8.23E-06 6.16E-05

2.13E-06 1.13E-04 1.15E-04

2.99E-07 S.78E-06 3.42E-09

9.06C-08 4.B2E-06 3.83E-04

9.706-09 S.B7E-06 3.83E-08

2.40E-07 4.80E-05 2.00C-OS

1.84E-06 6.62E-06 S.65E-075.B2E-09 5.87E-06 8.S6E-09

2.2SE-07 5.B7E-06 8.S6E-09

1.29E-05 1.69E-05 2.3SE-M

Totsl TotslOral A Oral t

COI COI

6.35E-05

1. IK-04

3.03E-07

3.83E-04

4. ME -08

2.83E-052.41E-06

1.44E-08

2.34E-07

2.4BE-04

6.99E-OS

2.28E-04

S.78E-06

3.87E-04

S.91E-06

7.60E-OS

7.19E-06

S.88E-06

5.88E-06

2.52E-04

Notest 'A' refers to Intskes using Modeled dsts'•' refers to Intskes using Monitored dstsAtl values In MB/kg/day.Zeros represent unavailable or unappl (cable data

0861 TOO MIS

TABLE 4-6

SUMMARY: LADE'S (CARCINOGENS ONLY)EXPOSURE POINT: ADULTS

Ioo

CHEMICAL

Arsenic

Barlua)Benzene

•enzotalpyranaLead

Methyl ChlorideNickel

NitrobenzeneTrlchloroathana

XyleneZinc

SurfacaWatar A

7.32E-07

0

1.20E-07

3.ME-09

0

0

00

2.33E-090

0

SurfacaWatar I

3.29E-06

02.31E-06

2.35E-06

0

0

0

0

2.35E-06

0

0

TotalOral A

7.32E-07

0

1.20E-07

3.88E-09

0

0

0

0

2.33E-09

0

0

TotalOral • 1

3.29E-060

2.31E-06

2.3SE-06

0

0

0

0

2.35E-06

0

0

DostInhalation 1

3.05E-07

0

0

6.S2E-09

0

0

6.31E-07

0

0

0

0

TotalInhalation

3.05E-07

0

0

6.S2E-09

0

0

6.31E-07

0

0

0

0

Notaa: 'A' rafara to Intakea ualng Modeled data'•' rafara to Intakaa ualng annltorad dataAll valuaa In atf/kg/day.Zaroa represent unavailable or inapplicable data

1861 TOO NIS

1siw •*. IBi

O ••

5 «f

i" 18

-.

2|

o "5^}

fifSurfacaWatar •

I

1*ai3i

8 °

in8

«

a

8 •

iiiM8 °

fe •

i•« .

f |

* *

8IUIVg^e\8MK.

^^I*

s

e °IVg

oo

1in

aMg

oo

Ml

SIVgo

o1•4•

15

o

|^

6

If

0

0

g

0

0

a<v

o

o

»

o

o•1•

o

o

g

o

o1a

o

e

g

o

e•

i ^

• 5

= ! 1 * -

i-I *• * —5'

&11 !*5

• i

nilin!e e

e *

• ••!.'".'"i?-e*

W0oI— 1

03NJ

\

4-9

TABLE 4-8

SUMMARY: LADE'S (CARCINOGENS ONLY)EXPOSURE POINT: OFF SITE TAMC FARM (CHILDREN)

It-»o

CHEMICAL

Arsenic

gerlus

genzeneLesd

Methyl Chloride

NickelNitrobenzene

TrlchloroetheneXylene

Zinc

SurfeceWater A

7.32E-070

1.20E-07

0

00

02.33E-09

0

0

SurfeceWater •

3.29E-060

2.31E-06

0

0

0

0

2.35E-06

0

0

Surfecesoil

Ingestlon

4.93E-06

0

2.74E-10

0

0

0

0

6.84E-10

0

0

TotelOrel A

5.666-06

0

1.20E-07

0

0

0

0

3.01E-09

0

0

TotslOrel g

8.22E-06

0

2.31E-06

0

0

0

0

2.3SE-06

0

0

Notes: 'A' refers to Intake* using Modeled dets'•' refers to Intekes using Monitored detsZeros sre shown for non-cerclnogenlc

cheeriest*

£861 TOO NIS

Potential concern for noncarcinogenic effects of a single contaminantin a single medium is expressed as the hazard quotient (HQ) (or the ratioof the estimated intake derived from the contaminant concentration in agiven medium to the contaminant's reference dose). By adding the HQs forall contaminants within a medium or across all media to which a givenpopulation may reasonably be exposed, the Hazard Index (HI) can begenerated. The HI provides a useful reference point for gauging thepotential significance of multiple contaminant exposures within a singlemedium or across media.

Any potential health effects are identified by computing hazardindices derived from subchronic and chronic intake levels. The hazardindex is a simple means of comparing intake levels (SDIs and GDIs) toacceptable intake levels: acceptable intake for subchronic exposure(RfDs) and acceptable intake for chronic exposure (RfD). The hazardindex is computed as follows:

DI. DI. DIHazard Index - ___ + __ + . .. + _"

AI, AI, AIJL t. n

Where DI - subchronic or chronic daily intake (mg/kg/day)Where AI - subchronic or chronic acceptable intake level

(mg/kg/day)The assumption that the combined effects of the chemicals will be

additive may not be accurate. Actual effects may be multiplicative ormay not be related at all. However, it is generally agreed that if thehazard index is less than one, deleterious health effects are unlikely.If the hazard index is greater than one, then the individual effects ofeach chemical should be considered to determine the liklihood of illeffects.

Versar evaluated the noncarcinogenic effects of exposure to the coindicator chemicals via both the oral and the inhalation route. Hazard a

indices for total oral and total inhalation exposures for each of the oexposure scenarios at the Sinclair Refinery site are presented in M

Tables 4-9 through A-12. All hazard indices are less than one. vooo*»

4-110103y

TABLE 4-9

CALCULATION OF CHRONIC HAZARD INDEXEXPOSURE MINT: SINCLAIR REFINERY (ADULTS)

*>I-1K)

CHEMICAL

Arsenic

••Hunlenient

•enzolalpyrene

Lead

Methyl ChlorideNickel

Nitrobenzene

TrlchloroetheneXylene

Zinc

CDI

1.UE-06

7.33E-06

02.45E-06

9. 10E-M

02.37E-06

2.1SE-08

0

01.071-05

Hazard

InhalationRfO

01.00E-04

0

0

4.30E-04

0

0

6.00E-04

2.60E-02

4.00E-01

0

Index:

COI:RfD

0

7.33E-020

0

2.12E-0200

3.59E-05

0

0

0

9.45E-02

CDI

1.83E-06

2.13E-06

2.99E-07

9.70E-09

9.06E-08

9.70E-09

2.406-07

1.846-06

S.82E-09

2.25E-07

1.29E-05

Hazard

ORAL A

RfD

1.006-03

5.006-02

0

0

1. 406-03

0

2. 006-02

5.006-04

1.00E-02

2.006+00

2.00E-01

Index:

CDI:RfO

1

4

6

1

3

51

6

5

.836-03

.256-05

0

0

.47E-05

0

.206-05

.696-03

.826-07

.136-07

.466-05

.TOE -03

CDI

8.236 06

1.13E-04

5.78E-06

S.87E-06

4.826-06

5.876-06

4.806-05

6.626-06

S.87E-06

5.87E-06

1.69E-05

Hazard

ORAL I

RfD

1.006-03

5.006-02

0

0

1.40E-03

0

2.006-02

5.006-04

1.006-02

2.006*00

2. 006-01

Index:

COI:RfD

8.236-03

2.256-03

0

0

3.44E-03

0

2.406-03

1.32E-02

5.876-04

2.94E-06

8.446-05

3.02E-02

Notes: 'A' refers to exposure calculations using Modeled data'•' refers to exposure calculations using Monitored dataZeros represent unavailable or inapplicable data

S86T TOO NIS

TAIL* 4-10

CALCULATION Of CHROMIC HAZARD INDEXexrosuu roim SINCLAIR uriNnr (CNILDRIN>

CHEMICAL

Arcenlo

•arlua

•ensena

•enie|a|*>yrene

*• Lead1U Methyl Chl>rl4e

NlekeL

Nltrobenaena

Tr Ichloreethene

XflefM

line

GDI

3

1

3

•

1

4

•

2

1

2

z

.JOE-OS

.MI-04

.001-01

.371-07

.401-04

.211-00

.2*1-03

.411-0*

.441-00

.341-07

.*M-04

ORAL A

RfD

1.001-03

3. 001-02

0

0

1.401-01

0

2.001-02

3.001-04

1.001-02

2.00E400

2.00E-01

Retard Indent

COIiRfD

1.201-01

l.flE-01

0

0

1.7ZI-01

0

3.131-01

4.021-01

1.44E-0*

1.17E-07

1.40E-01

2.171-01

3.

3.

3.

«.

2.

3.

1.

7.

3.

3.

3.

COI

04E-03

OtE-04

7*E-0*

IlE-Ot

431-04

Ml-0«

HE-04

1*E-0«

ROE-0*

*OE-0<

OOE-04

ORAL •

RfD

l.OOE-01

3.00R-OZ

0

0

1.40E-01

0

2.00E-02

3. OOE-04

l.OOE-02

2.00E400

2.00C-01

R*i«r4 Indent

GDI i RfD

) I4E-02

(.12E-01

0

0

1.73E-01

0

3.31E-01

1.44E-02

S.OSE-04

2.«*E-0«

1.30E-01

2.41E-01

Not«*i 'A' r*f«n to ••poiur* calculation* u»ln» aodclcd dat*'•' refer* to •••*•«»• o«lcul«tlen* u«ln§ Bonltorcd dataZero* r«pr***nt unavailable or unappllcahle data

9861 TOO MIS

TABLE 4-11

CALCULATION OF SMCHRONIC HAZARD INDEXEXPOSURE POINT: EXCAVATION UORKERS

Inhalation ORALCHEMICAL

SDI RfO'S SOI:RfD's SOI RfD's SDI:RfO's

Arsenic 0 0 0 2.11E-05 1.00E-02 2.11E-03

•arlin 0 1.00E-03 0 1.26E-04 S.OOE-02 2.51E-03

•enxena 2.67E-03 0 0 1.18E-OB 0 0

•entotalpyrene 0 0 0 5.35E-07 0 0

lead 0 4.30E-OS 0 4.78E-05 1.40E-02 3.41E-03

Nethyl Chloride 4.84E-03 0 0 3.47E-M 0 0Nickel 0 0 0 4.97E-05 2.00E-02 2.49E-03

Nltrobeniene 0 6.00E-03 0 4.69E-07 5.00E-03 9.38E-05Trlchloroethene 6.71E-04 2.60E-01 2.58E-03 7.UE-09 1.00E-01 7.UE-08

Xylene 6.73E-03 7.00E-01 9.61E-03 1.90E-06 4.00E+00 4.74E-09

Zinc 0 0 0 1.42E-04 2.00€-01 7.08E-04

Natard Indem 1.22E-02 Haisrd Index: 1.13E-02

Notest 'A' refers to Intakes us 1m sndeted data'•' refers to Intakes uslnfl annltored dataZeros represent unavailable or inapplicable data

NIS

TABLE 4-12

CALCULATION OF CHRONIC HAZARD INDEXEXPOSURE POINT: OFF SITE TANK FARM (CHILDREN)

in

CHEMICAL

Arsenic 6.Barium 1.Benzene 3.Lead 3.

Methyl Chloride*.Nickel 2.

Nitrobenzene 2.

ORAL A

COI RfD

35E-05

18E-04

03E-07

83E-04

80E-0883E-05

41E-06

Trichloroethene1.44E-OBXylene 2.Zinc 2.

34E-0748E-04

Hazard

1.006-035.00E-02

1

2

5122

0.40E-03

0.OOE-02

.OOE-04

.OOE-02

.OOE+00

.OOE-01

CDI:RfD

6

2

2

14

.3SE-02

.35E-03

0

.73E-01

0

.41E-03

.82E-03

1.44E-06

1

1

Index;

.17E-07

.24E-03

0.35

6

2

53

577

55

2

COI

.99E-05

.Z8E-04

.78E-06

.87E-04

.91E-06

.60E-05

.19E-06

.88E-06

.88E-06

.52E-04

Hazard

ORAL BRfO

15

1

2

512

2

.OOE-03

.OOE-02

0

.40E-03

0

.OOE-02

.OOE-04

.OOE-02

.OOE+00

.OOE-01

CDI:RfD

6

4

2

3

1

S2

1

Index:

.99E-02

.56E-030

•77E-01

0

.80E-03

.44E-02

.88E-04

.94E-06

.26E-03

0.37

Note*: 'A' refer* to intakes using Modeled data'•' refer* to Intakes using Monitored dataAll value* In «g/kg/dav.Zero* represent unavailable or inapplicable data

8861 TOO HIS

Carcinogenic Effects

Cancer potency factors (CPFs) have been developed by EPA's Carcino-genic Assessment Croup for estimating excess lifetime cancer risksassociated with exposure to potentially carcinogenic chemicals. For

potential carcinogens, risks are estimated by the probability of increasedcancer incidence. A carcinogenic potency factor represents the upper95 percent confidence limit of the probability of response per unitintake of the contaminant over a lifetime, and converts estimated intakesdirectly to incremental risk (U.S. EPA, 1986). CPFs, which are expressedin units of (mg/kg-day) , are multiplied by the estimated intake of a

potential lifetime cancer risk associated with exposure at that intakelevel. The term "upper bound" reflects the conservative estimate of therisks calculated from the CPF. Use of this approach makes underestimationof the actual cancer risk highly unlikely. Because all inputs into theexposure assessments are conservatively based, the resulting risks

identified for the Sinclair Refinery Site represent upper-bound riskestimates, and may overestimate the actual risk from exposures to theindicator chemicals studied. Cancer potency factors are derived from theresults of human epidemiological studies of chronic animal bioassays towhich animal-to-human extrapolation and uncertainty factors have beenapplied. Additional data would be required to derive a statisticallyvalid estimate of error in the exposure and risk calculations.

Excess lifetime cancer risks are determined by multiplying the intakelevel with the cancer potency factor. These risks are probabilities thatare generally expressed in scientific notation (e.g., 1 x 10' or IE-6).As excess lifetime cancer risk of 1x10* indicates that, as a plausibleupper bound, an individual has a one in one million chance of developingcancer as a result of site-related exposure to a carcinogen over a 75-yearlifetime under the specific exposure conditions at a site. EPA's risk M

range for carcinogens is 10" to 10" . The carcinogenic risks for a:each of the exposure scenarios involving chronic exposure were calculated o

oas: M

(-•vooo10

4-16

Risk - LADE x CPF

Where LADE - Lifetime Average Daily Exposure (mg/kg/day)CPF - Carcinogenic Potency Factor (mg/kg/day)

Of the eleven indicator chemicals for the Sinclair Refinery site,arsenic, benzene, benzo(a)pyrene, and trichloroethene are recognizedas potential carcinogens via both the inhalation and oral pathways,and nickel is recognized as a carcinogen via the inhalation pathwayonly.

Tables 4-13 through 4-18 show the calculation of the total upper-bound carcinogenic risk for exposure to the indicator chemicals foradults and children. Adult risks range from a high of 4.93E-05 forthe adult exposure route using monitored data to a low of 1.02E-05from the offsite tank farm.

4.2 Evaluation of Potential Impacts on Environmental Receptors

As discussed in Section 3.3 of this report, the only potentialenvironmental receptors identified are related to the organisms in theGenesee River, especially the fish population. In order tocharacterize the potential impact on these environmental receptors,the average and maximum surface water concentrations for each of theindicator chemicals were compared to the available Water Quality CoCriteria for Freshwater Aquatic Life (Table 4-19). The criteria for ^the protection of aquatic life specify pollutant concentrations which,if not exceeded, should protect most, but not necessarily all, aquatic 2life and its uses (Federal Register, Vol. 45, No. 231. Nov. 28, 1980).As illustrated, none of the maximum surface water concentrations £

oexceeds the Aquatic Freshwater Levels for acute toxicity. Only themaximum surface water concentration of zinc exceeds the acute andchronic toxicity level while the mean concentration is below theFreshwater Chronic Toxicity Criteria.

The New York State Department of Environmental Conservation, Divisionof Regulatory Affairs, indicated that the closest wetlands area is lessthan 1 mile southeast of the site. This wetlands area, however, isupstream of the site along the Genesee River (Taft, K. 1989). Based on

4-17

A

TABLE 4-13

RISK ESTIMATES FOR CARCINOGENS USING MODELED DATAEXPOSURE POINT: SINCLAIR REFINERY (ADULTS)

CHEMICAL

Arsenic••Hunlent en*

lento (alpyrene

Lead

Methyl ChlorideNickel

Nitrobenzene

TrlchloroetheneXylene

Zinc

LADE CarcinogenicExposure Potency FactorRoute (Mg/kg.day) 1/dsg/kg.day)

Oral AInhalationOral AInhalationOral AInhalationOral AInhalationOrel AInhalationOral AInhalationOral AInhalationOral AInhalationOrel AInhalationOral AInhalationOral AInhalation

7.32E-073.0SE-07

00

1.20E-070

3.ME-096.52E-09

00000

6.31E-0700

2.33E-0900000

t.80£+ooS.OOE+01

00

2.09E-022.09E-021.15E+016.10E+00

00000

1.70E+0000

1.10E-OZ1.30E-02

0000

Total Upper

Route- TotalSpecific Chemical-specific

Risk Risk

1.32E-061.53E-05

00

2.SOE-090

4.46E-M3.98E-08

00000

1.07E-0600

2.56C-1100000

•ound Risk •

1.66E-05

0

2.SOE-09

8.43E-08

0

0

1.07E-06

0

2.S6E-11

0

0

1.77E-05

Notes: 'A' refers to Intakes using Modeled dataZeros represent unavailable or inapplicable data. I.e. zero* are shownfor non-carcinogenic cheailcals.

TOO

TABLE 4-U

RISK ESTIMATES FOR CARCINOGiHS USING MONITORED DATAEXPOSURE POINT: SINCLAIR REFINERY (ADULTS)

CHEMICAL ExposureRout*

LADE

(•g/kg.day)CarcinogenicPotency Factor1/(«g/kg.day)

Route-SpecificRUk

TotalChealcsl-speclflc

Ritk

Arsenic

•arlui

Benzene

Benzotalpyreno

LtadMethyl Chloride

NickelNitrobenzeneTrlchloroethene

Xylene

Zinc

Oral • 3.29E-06 1.80£»00 S.92E-06Inhalation 3.05E-0/ 5.00E»01 1.53E-05Oral • 0 0 0Inhalation 0 0 0Oral • 2.31E-06 2.096-02 4.636-08Inhalation 0 2.09E-02 0Oral • 2.3SE-06 1.156*01 2.70E-OSInhalation 6.52E-09 6.106*00 3.9BE-08Oral 1 0 0 0Inhalation 0 0 0Oral B O O 0Inhalation 0 0 0Oral B O O 0Inhalation 6.31E-07 1.706*00 1.07E-06Oral B O O 0Inhalation 0 0 0Oral B 2.3SE-06 1.106-02 2.S8E-08Inhalation 0 1.30E-02 0Oral B O O 0Inhalation 0 0 0Oral B O O 0Inhalation 0 0 0

Total Upper Bound Rltk •

2.12E-050

4.B3E-OB2. TOE-05

00

1.07E-060

2.SOE-OB

00

4.93E-05

Notes: 'B' refers to Intakes using Monitored date.Zeros represent unavailable or unapplicable data, i.e. zeros are shoimfor non-carcinogenic chesilcals.

2661 100 HIS

TMLE *-tS

RISK ESTIMATES FOR CARCINOGENS USINO NODELEO DATAEXPOSURE POINT! SINCUIR REFINERT fCNUOREN)

CNENICAL

Arsenic

•arlus

•entene•eniolalpyrene

Lead

Methyl Chloride

Nickel

Nltrobeniene

Trlchloroethene

Kylene

Zinc

ExposureRoute

Oral AInhalationOral AInhalationOral AInhalationOral AInhalationOral AInhalationOral AInhalationOral AInhalationOral AInhalationOral AInhalationOral AInhalationOral AInhalation

LADE CarcinogenicPotency Factor

(•g/kg.dey) 1/(«g/kg.day)

3.UE-06000

1.20E-070

3.56E-08000000000

3.011-0900000

1.80E+005.001*01

00

2.09E-022.09E-021.15E«016.10E»00

00000

1.70E«0000

1.10E-021. JOE-02

0000

Total Upper

Route- TotalSpecific Cttaailcal-epeelflc

Risk Risk

5.65E-M000

2.S2E-090

6.40E-07000000000

3.31E-1100000

•ound Risk •

S.6SE-06

0

2.S2E-09

6.40E-07

0

0

0

0

3.31E-11

0

0

6.30E-06

Not MI 'A' refer* to Intakes mint Modeled dataZeros represent unavailable or inapplicable data. I.e. tero* are shownfor non-carcinogenic cheailcals.

too

TARIE 4-16

RISK ESTIMATES FOR CARCINOGENS USING MONITORED DATAEXPOSURE POINT! SINCUIR REPINERT (CNIIOREN)

CHEMICAL ExposureRout*

LADE

Og/kg.day)CarcinogenicPotency factor1/(av/kg.day)

Route-SpecificRUk

TotalChenlcal-speclflc

RUk

Arsenic

•arlua

Rentene

Reniofalpyrem

Lead

Methyl Chloride

Nickel

Nitrobenzene

TrlchloroethcneXylene

Zinc

Oral • 5.TOE-04 1.80E+00 1.03E-05inhalation 3.00E+01 0Oral I 0 0 0inhalation 0 0Oral I 2.31E-06 2.09E-02 4.83E-OBInhalation 2.09E-02 0Oral • 2.40E-06 1.15E*Ot 2.76E-OSInhalation 6.10E+00 0Oral R 0 0 0Inhalation 0 0Oral • 0 0 0Inhalation 0 0Oral 1 0 0 0Inhalation 1.70E+00 0Oral R O D 0Inhalation 0 0Oral I 2.35E-06 1.10E-02 2.58E-08Inhalation 1.30E-02 0Oral R 0 0 0Inhalation 0 0Oral R 0 0 0Inhalation 0 0

Total Upper Round Risk -

1.03E-OS

0

4.B3E-08

2.76E-OS

0

0

0

0

2.S8E-08

0

0

3.79E-05

Notes: '•' refers to Intakes using mnltored deta.Zeros represent unavailable or unappl(cable data. I.e. teros are shounfor non-carcinogenic chemicals.

TOO NIS

TABLE 4-17

RISK ESTIMATES FOR CAKCINOGENS USING MODELED DATAEXPOSURE POINT: OFF SITE TANK FARM (CHILDREN)

ito

CHEMICAL

Araenlc•arlua

•eniene

Lead

ExposureRoute

Oral AOral AOral AOral A

Methyl CMorldeOral A

NickelNitrobenzene

Oral AOral A

TrlchloroetheneOrat AXylene

Zinc

Oral AOral A

LADE CarcinogenicPotency Factor

(•g/kg.day) 1/(*v/kg.dey>

5.66E-060

1.20E-07

0

0

00

3.01E-090

0

1. 806+00

0

2.09E-02

0

0

0

0

1.10E-02

0

0

Total Upper

Route- TotalSpecific Che«lcal-*pectflcRUk RUk

1.02E-OS

0

2.516-09

0

0

0

0

3.31E-11

0

0

Sound RUk •

I.02E-050

2.51E-09

00

00

3.316-11

0

0

1.02E-OS

Not MS 'A' refert to Intake* utlng Modeled dataZero* represent unavailable or unappl(cable data, I.e. teroa•how for non-careInooenlc chemical*.

5661 100

TAKE 4-18

RISK ESTIMATES FOR CARCINOGENS USING MONITORING DATAEXPOSURE POINT: OFF SITE TANK FARM (CHILDREN)

itoLJ

CHEMICAL ExposureRoute

Arsenic Oral I

Rarlue Oral •

•enzene Oral •

Lead Orel I

Methyl CMorldeOral 1

Nickel Orel •

Nitrobenzene Orel •

TrlcMoroetheneOral •

Xylene Oral I

Zinc Orel •

LADE iPI

(ng/kg.day) 1

6.22E-06

0

2.31E-06

0

0

0

0

2.3SE-06

0

0

Carcinogenicotency Factor/(•g/kg.day)

i.eoe»oo0

2.09E-02

0

0

0

0

1.10E-02

0

0

Totel Upper

Route-Specific

Rlik

l.tSE-OS

0

4.UE-06

0

0

0

0

2.58E-OB

0

0

Round Rlik «

TotalCh«alcal-

Rlsk

1.4BE-OS

0

4.B3E-08

0

0

0

0

2.58E-08

0

0

I.49E-05

Notes: 'R' refers to Intakes using mnltored dataZeros represent unavailable or inapplicable data. I.e.Shown for non-carcinogenic dimicals.

inn NTS

TABLE 4-19

COMPARISON OF SURFACE WATER CONCENTRATIONSWITH WATER QUALITY CRITERIA FOR THE

PROTECTION OF AQUATIC FRESHWATER LIFE

Contaminant

AverageSurf ace Water

Concentration (ug/l)

MaximumSurface Water

Concentration (ug/l)

FreshwaterAquatic Life

Acute ToxfcHy (1)(UQ/I)

FreshwaterAquatic Life

Chronic ToxlcHy(l)

Trichloroethene

Benzene

Arsenic

Zinc

3.35

3.45

6.39

19.17

5940

1450

89

330

45000

5300

NA

130

NA

NA

NA

110

(1) CERCLA. 1988NA - Not AvalaMe

the potentiometic surface map of the water table found in the RemedialInvestigation Report prepared by Ebasco, the ground- water flow in theupper aquifer is towards the river in a north to northeast direction.Therefore, the wetlands area southeast of the site is not expected to beadversely impacted by either contaminated surface water runoff or groundwater. Another wetlands area, indicated by the NYDEC is approximately3 miles northwest and downstream of the site. Based on a comparison ofUater Quality Criteria for the protection of aquatic life in freshwatersystems, discussed above, the relatively low contaminant levels currentlyfound in the surface water are likely to be even further reduced oncethey reach the downstream wetlands area.

The Genesee River, in the Town of Uellsville, was provided with aconcrete bottom and spill -way system as part of the regional floodcontrol program. This type of bottom surface precludes the growth ofaquatic vascular plants along the site. As a result, the number ofspecies at the top of the aquatic food chain, indigenous to the rivernear the site, would be expected to be small. In addition, the fishingpatterns of the area, as. referenced in Section 3.3, is likely to be muchsmaller in comparison in other areas of the river.

The New York State Department of Environmental Conservation did notidentify, from currently available information, any potential impacts onendangered, threatened, or special concern wildlife species (Evans, J.1989). In conclusion, the environmental impacts resulting from chemicalreleases from the Sinclair Refinery Site are expected to be negligible.

4.3 Assessment of Method Uncertainties

There are a number of uncertainties associated with the carcinogenicrisk estimate discussed above. These uncertainties are introduced becauseof (1) the need to extrapolate below the dose range of experimental testsusing animals, (2) the variability of the receptor population, (3) assumedequivalency of dose* response relationship between animals and humans, and

cc

4-250103y

differences in exposure routes in test animals versus routes expectedonsite. In addition to contaminant concentration, route, and duration ofexposure, there are many other factors that may influence the likelihoodof developing cancer. These include differences between individualnutritional and health status, age and sex, and inherited characteristicsthat may affect susceptability (USDHHS, 1985). Risk calculation alsoassumes that intake levels will be small, without synergistic orantagonistic chemical effects, and that individuals will be exposed toeach of the indicator chemicals and elicit a carcinogenic response.

v.»-2

4-260103T

5.0 SUMMARY/CONCLUSIONContaminant screening was performed on analytical results from the

soil, surface water, and ground-water samples collected by SHC Martin andEbasco and compiled in Ebasco's 1989 Draft Remedial Investigation Report.The contaminant screening process identified eleven chemicals of potentialconcern: 4 volatile organic compounds, 2 semivolatile organic compounds,and 5 metals. The indicator chemicals used in this EndangermentAssessment were: methyl chloride, trichloroethene, benzene, xylene,nitrobenzene, benzo(a)pyrene, arsenic, barium, lead, nickel, and zinc.These compounds or elements were selected based on their toxicologicalproperties, potentially critical exposure routes, and higherconcentrations present in comparison to other contaminants.

Environmental fate and transport mechanisms were evaluated for eachof the indicator chemicals based on an assessment of the site'senvironmental setting and chemical and physical properties of eachcontaminant. Predominant transport mechanisms identified included:(1) leachate percolation through soils to ground water and subsequentmigration to the Genesee River, (2) runoff of surface soils to the riverduring storm events, and (3) dispersion of fugitive dust particles byvehicular traffic on the site.

Potentially exposed populations include: temporary site excavationworkers, children trespassing onto the refinery site and off site tankfarm, local residents, students and faculty members of the onsite SUNYcampus, and employees of current onsite businesses.

Four exposure scenarios were evaluated: (1) inhalation of volatileorganic compounds (VOCs) by excavation workers exposed to subsurfacesoils, (2) inhalation of fugitive dust emissions of metals andsemivolatile contaminants by onsite occupants, (3) inadvertent ingestionof soil contaminants by both excavation works and trespassing children,and (4) ingestion of dissolved contaminants in surface water by localresidents.

cc

ecc

5-1

Total body burden rates were computed based on all exposureroutes using an average body mass of 70 kilograms (adults) or 16kilograms (child) and an average 75-year lifetime (for chronic andcarcinogenic exposures) . The evaluation of excavation workersubchronic exposure through VOC inhalation and inadvertent ingestionof subsurface soils assumed individuals could be exposed for 15 daysin 1 year. For the fugitive dust exposure evaluation, it was assumedthat site occupants would be exposed for 8 hours per day, 5 days perweek, and 50 weeks per year for 20 years. It was assumed thattrespassing children would be exposed to the surface soils for 100days per year for 6 years and to surface water for 15 days per yearfor 30 years. The evaluation of residential ingesting of surfacewater, through the secondary water intake system downstream of thesite, assumed exposure for 15 days per year for 30 years.

The calculations presented in Tables 4-9 thru 4-12, indicate thatthe greatest noncarcinogenic risk from the site is associated with theinhalation of barium and lead dust particles by adults that work andattend vocational school on the refinery site. The chronic hazardindex for the inhalation route is 9.45E-02. The total exposure pointchronic hazard index for adults onsite, based on inhalation offugitive dust particles and ingest-on of water, was determined to be1.25E-01. The next highest noncarcinogenic risk is for childrentrespassing on the offsite tank farm. The chronic hazard index forthis route was determined to be 3.7E-01, primarily as a result ofingesting of inorganic metals in the surface soil. The chronic hazardindex for children trespassing on the refinery portion of the site wascalculated to be 2.41E-01. The total exposure point subchronic hazardindex for excavation workers is 1.17E-01.

A summary of the carcinogenic risks associated with the site aredisplayed on Tables 4-13 thru 4-18. The greatest carcinogenic riskidentified is associated with the inhalation of arsenic by adults that

oo

OO

5-2

work and attend the vocational school on the refinery site. Thecarcinogenic risk for the inhalation route was calculated to be1.53E-05. The total upper bound risk for these adults, based oninhalation of fugitive dust particles and ingestion of water is4.93E-05. The next highest carcinogenic risk is 3.79E-05 for childrenthat trespass on the refinery area. Again, the risk to children ismainly associated with the ingestion arsenic and benzo(a)pyrene.Children that trespass on the offsite tank farm have a total upperbound risk of 1.49E-05.

Since the noncarcinogenic hazard index for each exposure pointdoes not exceed unity, adverse noncarcinogenic effects are notexpected. The highest total upper bound carcinogenic risk is4.93E-05. It is not in the scope of this report to determine suitablebackground levels for the Sinclair Refinery site, or establishremediation cleanup levels.

oo

rooo

5-3

REFERENCES

ATSDR. 1987. lexicological Profile for Benzo(a)pyrene. Agency for ToxicSubstances and Disease Registry. U.S. Public Healch Service. October1987.

Baes, C.F., R.O. Sharp. 1983. A Proposal for Estimation of Soil LeachingConstants for Use in Assessment Models, Journal of EnvironmentalQuality, Vol. 12. No. 1, 1983.

CERCLA Compliance Vith Other Lavs Manual, Draft Guidance, OSWER Directive9234.1-01, August 8, 1988.

Clement Associates. 1985. Chemical. Physical and Biological Properties ofCompounds present at hazardous waste sites. September, 1985.

Cox, G.E. 1989. Personal communications with Rob Lackey, Versar, Inc.,(May 15. 1989), National Fuel Company, Inc.

Domenico, P.A. and V. V. Palciquskas, 1982. Alternative Boundaries inSolid Waste Management, Ground Water, Vol. 20, No. 3, pp. 303-311.

Ebasco, 1989. Draft Remedial Investigation Report, May 1989.

Ellenson, 1989. Personal communications with Rob Lackey, Versar, Inc.,(May 15, 1989), Mapes Industries. Inc.

Evans, J. 1989. Personal communications with Mike Bond, Versar, Inc.,(May 1989) regarding fishing patterns in Wellsville area.

Federal Register. 1980 Water Quality Criteria Documents; Availability.Vol. 45, No. 231, p. 79322.

Federal Register. 1985. Proposed Rules, Vol. 50, No. 219, p. 46969.November 13, 1985.

GRI. 1988. Management of Manufactured Gas Plant Sites; Volume III; RiskAssessment, prepared for the Gas Research Institute by Atlantic Environ-mental Services.

Haith, D.A., Mills, W.B. 1982. A Mathematical Model for Estimated Pesti-cide Losses in Runoff, Journal of Environmental Quality, 9(3); 428-433.

IARC, 1986. Evaluation of the Carcinogenic Risk of Chemicals to Humans, wVolume 41, February, 1986. 25

IRIS, Integrated Risk Information System (Data base). 1989. U.S. EPA. gWashington, D.C. (accessed May 1989). M

toooU)

R-l0101?

REFERENCES(Continued)

Joyce, C. 1989. Personal communications with Rob Lackey, Versar, Inc.,(May 15. 1989). Otis Eastern Service. Inc.

Lyman, W.J., W.F. Reehl, and D.H. Rosenblatt, eds. 1982. Handbook ofChemical Property Estimation Methods, Environmental Behavior or OrganicCompounds. McCraw-Hill, New York.

McFarquar, D. 1989. Personal communications with Tom Willard, Versar,Inc., (June 6, 1989) regarding recreational uses of the river in theVillage of Wellsville, and utilization of current drinking water intakesystems.

Meverrett, D. 1989. Personal communcations with Rob Lackey, Versar, Inc.,(May 15. 1989). Branch Campus of the Collect of Technology at Alfred, NY

Mills, W.B., J.D. Dean, D.B. Porcella, et al. 1982. Water QualityAssessment: A Screening Procedure for Toxic and Conventional Pollutants;Part 1. U.S. EPA, Environmental Research Laboratory, Office of Researchand Development.

Taft, K. 1989. Letter to Tom Willard, Versar, Inc., regarding potentialimpacts on endangered, threatened, or special concern wildlife speciesor other significant habitat areas. New York Department of Environmen-tal Conservation Service, Division of Regulatory Affairs (June 16, 1989)

Tilley, G. 1989. Personal communications with Rob Lackey, Versar. Inc.,(May 15, 1989), Butler Larkin Co., Inc., or Valley Steel Products Co.

U.S. EPA. 1979. Water-Related Environmental Fate of 129 PriorityPollutants, Volume II, Office of Water, Planning and Standards.December 1979.

U.S. EPA. 1984. Health Effects Assessment for Benzo(a)pyrene Final Draft,Environmental Criteria and Assessment Office Cincinnati. Ohio.September 1984.

U.S. EPA. 1986. Superfund Public Health Evaluation Manual. Office ofEmergency and Remedial Assessment. May 1989. EPA 600/8-S9/-43.September 1984.

MU.S. EPA. 1988. Superfund Exposure Assessment Manual. Office of ZEmergency and Remedial Response. OSWER Directive 9285.5-1. March 22,1988. ' §

tooo

R-20105y

REFERENCES(Concluded)

U.S. EPA. 1989a. Exposure Factors Handbook. Office of Health andEnvironmental Assessment. May 1989. EPA 600/8-89/-A3.

U.S. EPA. 1989b. Human Health Evaluation Manual. Office of EmergencyResponse, Washington, D.C. July 1989. EPA 9285.701A.

U.S. EPA. 1989c. Health Effects Assessment Summary Tables. ThirdQuarter. FY 1989.

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R-3OlOSy

APPENDIX ACOMPOUNDS AND ELEMENTS DETECTEDAT THE SINCLAIR REFINERY SITE

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1 Benzene

Fate and TransportT"

Volatilization appears to be the major transport process of benzene

from surface waters to the ambient air. and atmospheric transport ofbenzene occurs readily (USEPA, 1979), although direct oxidation ofbenzene in environmental waters is unlikely, cloud chamber data indicatethat it may be photo-oxidized rapidly in the atmosphere. Inasmuch asvolatilization is likely to be the main transport process accounting forthe removal of benzene from water, the atmospheric destruction of benzeneis probably the most likely fate process. Values for benzene's logoctanol/water partition coefficient indicate that adsorption onto organic

imaterial may be significant under conditions of constant exposure.Sorption processes are likely removal mechanisms in both surface waterand ground water. Although the bioaccumulation potential for benzene

i appears to be low, gradual biodegradation by a variety of microorganismsI probably occurs. The rate of benzene biodegradation may be enhanced by

the presence of other hydrocarbons (Clements, 1985).i

Pharmacokineti.es

Benzene is a recognized human carcinogen [IARC, (1982) cited in' Clements, 1985]. Several epidemiological studies provide sufficient< evidence of a causal relationship between benzene exposure and leukemiai in humans, with a latent period of up to 10 years. It produces

leukopenia and thrombocytopenia, which may progress to pancytopenia.Similar adverse effects on the blood-cell-producing system occur inanimals exposed to benzene. In both humans and animals, benzene exposureis associated with chromosomal damage, although it is not mutagenic inmicro-organisms. Benzene was fetotoxic and caused embryolethality inexperimental animals (Clements, 1985).

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Human Health

Exposure to very high concentrations of benzene [about 20,000 ppm(66,000 mg/m3) in air] can be fatal within minutes (IARC, (1982) citedin Clements, 1985]. The prominent signs are central nervous systemdepression and convulsions, with death usually following as a consequenceof cardiovascular collapse. Milder exposures can produce vertigo,drowsiness, headache, nausea, and eventually unconsciousness if exposurecontinues. Deaths from cardiac sensitization and cardiac arrhythmiashave also been reported after exposure to unknown concentrations.Although most benzene hazards are associated with inhalation exposure,dermal absorption of liquid benzene may occur, and prolonged or repeatedskin contact may produce blistering, erythema, and a dry scaly dermatitis(Clements, 1985).

Environmental Toxicitv

The EC5D values for benzene in a variety of invertebrate andvertebrate freshwater aquatic species range from 5,300 g/liter to386,000 g/liter [USEPA, (1980) cited in Clements, 1985]. However,only values for the rainbow trout (5,300 pg/litter) were obtainedfrom a flow based on remeasured concentrations. Results based onunmeasured concentrations in static tests are likely to underestimatetoxicity for relatively volatile compounds like benzene. A chronic testwith Daohnia mayna was incomplete, with no adverse effects observed attest concentrations as high as 98,000 pg/liter (Clements, 1985).

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i.1 Methvl Chloride

Fate and Transport

Methyl chloride (Chloromethane) is known to be ubiquitous in the( environment. It enters the environment from natural as well as

anthropogenic sources, and has been detected in finished drinking water,in seawater, and in the troposphere (USEPA, 1979).

Volatilization is the major transport process for removal of methyl, chloride from aquatic systems. Once in the troposphere, methyl chloridei is attacked by hydroxyl radicals with the subsequent formation of fornyl

chloride as the principal initial product. Any unreacted methyl chloride\

reaching the stratosphere will undergo photodissociation.

Based on the information currently reviewed, it appears thatI oxidation, hydroysis, and biodegradation are not important fate processes

of methyl chloride in the aquatic environment. No information was found| indicating that adsorption and bioaccumulation are important environmental

transport processes for methyl chloride (USEPA, 1979).

Table A-l summarizes the aquatic fate data for methyl chloride(USEPA, 1979).

i Sorption of methyl chloride to soil or sediment has not beenstudied; however, its relatively low log octanol/water partition

[ coefficient (0.91) suggest that partition occurs primarily into air orwater (Clement, 1985).

i Pharmacokinetic

/ _~ According to the International Agency for Research on Cancer (IARC),I methyl chloride is excreted in human blood and expired air. Increased

excretion of urinary S-methylcysteine was reported in persons exposed tomethyl chloride. (IARC, 1986). Exposure to high concentrations adverselyaffect the central nervous system, kidney, and liver in humans. Co(Clements, 1985). z

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TABLE A-lSUMMRY OF AQUATIC FATE OF METHYL CHLORIDE

EnvironmentalProcess

SStati Rate

Ball-Life Confidence(tl/2) of Data

Photolysis

Oxidation6

Hydrolysis

Probably not significant inaquatic systems

The predominant fata of this 8.5x10 cm seecompound is attack by hydroxylradicals in the troposphere.

Is probably not a significant 1.9x10 sec£at«.

*17 days

Medium

0.37 years* High

High

Volatilization Primary transport process fromthe aquatic environment.

27 minutes Mediu

Sorption

BioaeeuBulation

Probably not significant.

Probably does not signifi-cantly bioaccunulate inorganisms.

Mediu

Mediu

Biotransformation/ Probably not important. (tedium

a. Reported as a lifetime (time for reduction to 1/e of original concentration) of 0.37 years.b. Half-lives are on the order of several minutes to a few hours, depending on the degree of agitation.

The value reported was determined in a stirred container.c. The predominant environmental process which is thought to determine the fate of the compound.

(USEPA. 1079)

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Hunan Health

Methyl chloride was found to be carcinogenic in male mice exposed toT the compound via inhalation for a 2-year period. A significantly

increased incidence of benign and malignant kidney tumors was found inanimals exposed to 2,100 mg/m . An increased incidence ofhepatocellular carcinomas that was marginally significant was also found

, using an acturial analysis of the data. Negative results forcarcinoginicity for female mice and male and female rats were obtained in

I the same study. Methyl chloride has been found to be mutagenic using the' Ames assay, with and without a metabolic activivating system. Methyl

chloride has also been shown to be teratogenic in nice, causing heartdefects in fetuses exposed to utero at a airborne concentration of 1,050mg/m on gestation days 6 to 17 (Clements, 1985).

i Methyl chloride is not considered to be highly toxic. Repeated or

f prolonged human exposure to sufficient concentrations (greater than 100) mg/m ) can result in central nervous system (CNS) effects including

blurred vision, headache, nausea, loss of coordination, and personalityI changes. Renal and heptic toxicity have also been reported in humans.

^___ Animal studies shown CNS effects and binding sulfhydryl-containing' cellular macromolecules. This latter effect interferes with metabolism

and is probably responsible for the observed tissue toxicity (Clements,f 1985).I

Environmental Toxicitv1I The only information available on the effects of methyl chloride in

wildlife is an acute study on the bluegill that reported an LC^Q valuei of 500 mg/liter for this species. Data on the other chlorinated methanes

indicate that aquatic toxicity declines with decreased chlorination.Thus methyl chloride should be less toxic than chloroform or carbontetreachloride, neither of which had any effect on Daohnia magna or the

f fathead minnow, respectively, during chronic exposure to 3,400 CoMg/liter. No information on the toxicity of methyl chloride to ^terrestrial wildlife or domestic animals was found in the literature ooreviewed (Clements, 1985). ^

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Dose Response

Estimates of the carcinogenic risks associated with lifetime exposureto various concentrations of halome thanes in water are:

Risk ConcentrationlO'l 1.910'° 0.1910'6 0.019

OSHA established a TWA for methyl chloride as 210 mg/m , with a ceilinglevel of 420 mg/m3 (Clements, 1985).

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Nitrobenzene

Fate and Transport

The aquatic fate of metrobenzene might involve both photoreductionof the mitro group and biodegradation. It is not possible with theavailable data, to determine which of these two fates predominates. Itshould be noted that both photochemical and biological degration can leadpotentially to a large variety of organic metrogen compounds (USEPA,1979).

Photoreduction of the nitro group and/or hydrooxylation of the ringwhile adsorbed on humans could be an important abiotic fate. Biodegrationto the same type of reduction products could also be an important fateprocess. (USEPA, 1979).

Pharmaeokinetics

Nitrobenzene acts through an unknown intermediate to change

hemoglobin to methemoglobin. The intense methemoglobinemia produced byall these chemicals may lead to asphyxia, sever enough to injure thecells of the central nervous system. Pathologic findings in acutefatalities from nitrobenzene derivitives, include chocolate color of theblood, injury to the kidney, liver, and spleen, and hemolysis. Bladderwall ulceration and necrosis may also occur [Dreisbach, (1977) cited inClements, 1985].

Hunan Health

Nitrobenzene causes cyanosis at methemoglobin levels above 15percent, headache, shallow respiration and dizziness at methemoglobinlevels of 40-50 percent, confusion, drop in blood pressure, lethargy andstupor at 60 percent, and convulsions, coma, blood pressure fall, andpossibly death at methemoglobin levels of 70 percent or higher. Jaundice,

pain, or urination and amenia may appear later [Dreisbach, (1977) citedin Clements, 1985] .

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Environmental Toxicitv

Nitrobenzene is considered a reproductive coxin to mammals. Noenvironmental toxicity information is available for nitrobenzene.

Dose-Response

The fatal dose (LD5Q) in animals for nitrobenzene is 700 mg/kg.Ingestion of 1 gram of nitrobenzene may cause death. The TLV fornitrobenzene is 1 ppm (Oreisbach, (1977) cited in Clements, 1985].

The oral acceptable intake for nitrobenzene is 5.0 E-03 (rag/kg/clay)subchronic and 5.0 E-04 (rag/kg/day) chronic. The inhalation intake fornitrobenzene is 6.0 E-03 (mg/kg/day) subchronic and 6.0 E-04 (mg/kg/day)chronic (SPHEM, 1988).

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Trichloroechvlenfe

~~r ~ Fate and Transport

Trichloroethylene (TCE) rapidly volatilizes into the atmosphere whereic reacts with hydroxyl radicals to produce hydrochloric acid, carbonmonoxide, carbon dioxide, and carboxylic acid. This is probably the noseimportant transport and fate process for trichloroethylene in surface

water and in the upper layer of soil. TCE absorbs to organic materialsand can be bioaccunulated to some degree. However, it is unclear whethertrichloroethylene bound to organic material can be degraded by micro-

organisms or must be desorbed to be destroyed. There is some evidencethat higher organisms can metabolize TCE. Trichloroethylene leaches into

the ground water fairly readily, and it is a common contaminant of ground

I water around hazardous waste sites.-•

Pharmacokineci.es

' Trichloroethylene is carcinogenic to mice after oral administration,

: producing hepatocellular carcinomas [NCI. (1976), NTP, (1982) cited inClements, 1985]. It was found to be mutagenic using several microbial

^— assay systems. Trichloroethylene does not appear to cause reproductive\ toxicity or teratogenicity.

Human HealthiI TCE has been shown to cause renal toxicity, hepatotoxicity, neurotox-

icity, and demeratological reactions in animals following chronic exposure\ to levels greater than 2,000 mg/m for 6 months. Trichloroethylene has

low acute toxicity; the acute oral LDcn value in several species rangedI from 6,000 to 7,000 mg/kg.

Environmental Toxicitv

There was only limited data on the toxicity of trichloroethylene toaquatic organisms. The acute toxicity to freshwater species was similarin the three species tested, with LCc/j values of about 50 mg/liter. No

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B-9OlOiy

LC-Q values were available for saltwater species. However, a dose of2 mg/liter caused erratic swimming and loss of equilibrium in the grassshrimp. No chronic toxicicy tests were reported.

No information on the toxicicy of trichloroethylene to domesticanimals or terrestrial wildlife was available in the literature reviewed.

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Xvlene

'"~1 Fate and Transport

Volatilization and subsequent photo-oxidation by reaction withhydroxyl radicals in atmosphere are probably important transport and fateprocesses for xylene in the upper layer of soil and in aquaticenvironments. Products of the hydroxylation reaction include carbondioxide, peroxyacetylnitrate (PAN), and cresol. Xylene binds to sediment

! in water and to organics in soils and undergoes microbial degradation.' Biodegradation is probably the most important fate process in both soilsI and the aquatic environment. Xylene have been shown to persist for up toI 6 months in soil. Because of their low water solubility and rapid

biodegration, xylenes are unlikely to leach into ground water in high[ concentrations.

• Pharmacokinecics

The National Toxicology Program (NTP) is testing xylene forI carcinogenicity by administering it orally to rates and mice. Although

the results have not been finalized, it does not appear to be'—- carcinogenic in rates. Results have not been reported for mice. Xylene| was not found to be mutagenic in a batter of short-term assays. Xylene

is not teratogenic but has caused fetotoxicity in rates and mice(Clements. 1985).

Hunan Health

1 Acute exposure to rather high levels of xylene affects the centralnervous system and irritates the mucous membranes. There is limited

| evidence of effects on other organ systems, but, it was not possible toattribute these effects solely to xylene as other solvents were present.The oral LDe/j value of xylene in rates is 5,000 rag/kg.

Environmental Toxicitv £2( Z' Xylene adversely affected adult trout at concentrations as low as

o3.6 mg/liter in a continuous flow system and trout fry avoided xylene at °concentrations greater than 0.1 mg/liter. The LC50 value in adult trout

B-llOlOSy

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was determined to be 13.5 mg/licer. LC5Q values for other freshwaterfish were around 30 mg/licer in a static system, which probablyunderestimated toxicicy. Only a few studies have been done on thetoxicity of xylene to saltwater species. These indicated that the m- ando-xylene isoners probably have similar coxicities and are probably lesstoxic than p-xylene, and that saltwater species are generally moresusceptible than freshwater species to the determental effects on xylene(LC-Q - 10 mg/liter for m- and o-xylene and LC^Q - 2 rag/liter forp-xylene). However, it should be stressed that these generalizationsare based on limited data (Clements, 1985).

No information on the toxicity of xylenes to terrestrial wildlifeand domestic animals was available in the literature reviewed. However,because of the low acute coxicicy of xylenes. it is unlikely that theywould be coxic to wild or domestic birds or mammals.

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Benzo (a 1 pvrene

Fate and Transport

Benzo(a)pyrene is relatively insoluble in water and has a high logoctanal/water partition coefficient. As a result, benzo(a)pyrene will

adsorb onto suspended parciculates and biota and its transport will belargely determined by the hydrogeologic conditions of the aquaticsystem. The ultimate fate of benzo(a)pyrene is believed to bebiodegradation and bio -transformation by benthic organisms, although theprocess may be slow. (USEPA. 1979).

Lu, et al using a laboratory model ecosystem, studied theenvironmental fate and transport of radiolabed benzo(a)pyrene. Their

14studies failed to detect any volatile radioactivity or CO. in traps

from their aquatic microsy, thus supporting the premise thatbenzo(a)pyrene is not significantly transported by volatilization (USEPA.1979).

Pharmacokinetics

Benzo(a)pyrene is readily absorbed by inhalation, oral, and dermalroutes of administration. Metabolism is important in absorption ofbenzo(a)pyrene via the lungs and the skin; intestinal absorption appearsto be less dependent on metabolic factors.

Absorbed benzo(a)pyrene is rapidly distributed to several tissues.Benzo(a)pyrene metabolites are subject to enteroheptic circulation asevidenced by time 'dependent increases in the intestinal tissueconcentrations of these intermediates (ATSDR. 1987).

Human Health

No quantitative information on the absorption of benzo(a)pyrene viathe respiratory tract was found for human subjects. Absorption of to

f

benzo(a)pyrene via this route is inferred from the isolation of urinary z

metabolites of benzo(a)pyrene in subjects exposed to polycyclic aromatic o

B-13oiosr

hydrocarbons in an industrial environment (ATSDR, L987). Dermal absorp-tion of benzo(a)pyrene through human skin was determined under ultroconditions. The extent of permeation after 24 hours was established as

14 23 percent of an applied dose of ( C) benzo(a) pyrene (10 ug/cm ).

(ATSDR, 1987).

Benzo(a) pyrene is a moderately potent experimental carcinogen in

many species by many routes of exposure. There are no reports directlycorrelating human benzo(a)pyrene exposure and tumor development, althoughhumans are likely to be exposed by all routes. There are a number of

reports associating human cancer and exposure to mixtures of PAHs thatinclude benzo(a)pyrene . In view of these observations and its well

established carcinogenic activity in laboratory animals, it is reasonable

to conclude that benzo(a)pyrene would be expected to be carcinogenic inhumans by all routes of exposure (ATSDR, 1987).

Environmental Toxic itv

There is very little information on the environmental toxicity of

PAHs. They probably are not very toxic to aquatic organisms (Clements,1985).

Dose Response

Exposure criteria and TLVs have been developed for benzo( a) pyrene.The Occupational Safety and Health Administration has set an 8-hour TVAconcentration limit of 02. mg/m for the benzene -soluble fraction ofcoal tar pitch volatiles (anthracene, benxo ( a ) pyrene , phenanthrene ,acridine, chrysene, pyrene) NIOSH (1977) recommends a concentration limitfor coal tar, coal tar pitch, creosote and mixtures of these substancesat 0.1 mg/m of the cyclohexane-extractable fraction of the sample,

determined as a 10-hour TVA. NIOSH (1977) concluded that these specificcoal tar products, as well as coke oven emissions, are carcinogenic andcan increase the risk of lung and skin cancer in workers. NIOSH (1977)also recommends a ceiling limit for exposure to asphalt fumes for 5 mgairborne particulates/m of air (USEPA, 1984).

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Environmental quality criteria for PAH have been recommended forambient water, which specify concentration limits intended to protecthumans against adverse health effects. The [U.S. EPA (1980b) cited inClements, 1985] has recommended a concentration limit of 28 ng/1 for thesum of all carcinogenic PAHs in ambient water. This value is based on amathematical extrapolation of the results from studies with micetreated orally with benzo(a)pyrene, and acknowledges the conservativeassumption that all carcinogenic PAHs are equal in potency tobenzo(a)pyrene. Daily consumption of water containing 28 ng/1 ofcarcinogenic PAH over an entire lifetime is estimated on the basis ofthe animal bioassay to keep the lifetime risk of cancer development below1 change in 100,000 (USEPA, 1984). The U.S. EPA computed a q^ of 1.53(mg/kg/day) for oral exposure and q,* of 6.11 (mg/kg/day) forinhalation exposure (USEPA, 1984).

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Arsenic

Fate and Transport

In the natural environment, arsenic has four different oxidationstates and chemical speciation is important in determining arsenic'sdistribution and mobility. Interconversions of the +3 and +5 states aswell as organic complextion, are the most important. Arsenic isgenerally quite mobile in the environment. In the aquatic environment,volatilization is important when toxicological activity or highlyreducing conditions produce arsine methylarsenics. Sorption by thesediment is an important fate for the chemical. Arsenic is metabolizedto organic arsenics by a number of organisms: this increases arsenic'smobility in environment. Because of its general mobility, arsenic tendsto cycle through the environment. Its ultimate fate is probably the deepocean, but it may pass through numerous stages before finally reachingthe sea (Clements, 1985).

Pharmaeokinetics

Arsenic has been implicated in the production of skin cancer inhumans. There is also extensive evidence that inhalation of arseniccompounds causes lung cancer in workers. Arsenic compounds causechromosome damage in animals, and humans exposed to arsenic compoundshave been reported to have an elevated incident of chromosomeaberrations. Arsenic compounds have been reported to be teratogenic,fetotoxic, and embryotoxic in several animal species, and an increasedincidence of multiple malformations among children born to womenoccupationally exposed to arsenic has been report (Clements, 1985).

Human Health

Arsenic compounds also cause moncancerous, possibly precancerous,skin changes in exposed individuals. Several cases of progressivepolyneuropathy involving motor and memory nerves and particularly gjaffecting the extremities. Also methylinated long-axon neurons have beenreported in individuals occupationally exposed to inorganic arsenic. M

Polyneupathies have also been reported after the ingestion of woarsenic-contaminated foods (Clements, 1985). <jico

B-16oiOSy

Environmental Toxicirv

>—1 Various inorganic forms of arsenic appear to have similar levels oftoxicity. They all seem to be much more coxic than organic forms. Acute

[ toxicity to adult freshwater animals occurs at levels of arsenic trioxideas low as 812 pg/liter and at levels as low as 40 Mg/liter inearly life stages of aquatic organisms. Acute toxicity co saltwater fish

I

' occurs at levels around--mg/liter, while some invertebrates are unaffectedat much lower levels (508 g/liter). Arsenic toxicity does not appearto increase greatly with chronic exposure, and it does not seem thatarsenic is bioconcentrated to a great degree (Clements, 1985).

Arsenic poisoning is a rare but uncommon toxic syndrome amongdomestic animals. Arsenic causes hyperemia and edema of thegastrointestinal tract, hemorrhage of the cardiac serosal surfaces andperitoneum, and pulmonary congestion and edema; to terrestrial wildlifewas not reported in the literature reviewed (Clements, 1985).

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Barium

Fate and Transport

Barium is extremely reactive, decomposes in water, and readily formsinsoluble carbonate and sulfate salts. Barium is generally present in

solution in surface or ground water only in trace amounts. Large amountswill not dissolve because natural waters usually contain sulfate, and thesolubility of barium sulfate is generallly low. Barium is not soluble atmore than a few parts per million in water that contains sulfate at morethan a fee parts per million. However, barium sulfate may become

considerably more soluble in the presence of chloride andother anions.Monitoring programs whow that ic is rare to find barium in drinking waterat concentrations greater than 1 mg/liter. Atmospheric transport ofbarium, in the form of parcicultes, can occur. Bioaccumulation is not animportant process for barium (Clements, 1985).

Pharmacokinetics

There are no reports of carcinogenicity, tnutagenicity, or teratogeni-cicy associated with exposure to barium to its compounds. Effects ongametogenesis and on the reproductive organs are reported in male andfemale rates after inhalation of barium carbonate; intratesticularinjection of barium chloride affects the male reproductive organs(Clements, 1985).

Human Health

Insoluble forms of barium, particularly barium sulface, are not toxicby ingestion or inhalation because only minimal amount are absorbed. How-ever, soluble barium compounds are highly toxic, in humans afcer exposureby either route. The most important effect of acute barium poisoning isa strong, prolonged stimulant action on muscle. Smooth, cardiac, andskeletal muschels are all affected, and a transient increase in blood

COpressure due to vasoconstriction can occur. Effects on the hematopoietic gsystem and cerebral cortex have also been reported in humans. Accidental

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I ingestion of soluble barium salts has resulted in gastroenteritis,, - muscular paralysis, and ventricular fibrillation and extra systoles.< Potassium deficiency can occur in cases of acute poisoning. Does of

barium carbonate anf barium chloride of 57 mg/kg and 11.4 mg/kg,I respectively, have been reported to be fatal in humans. Digitalis-like^ toxicity, muscle stimulation, and effects on the hematopoietic and

i central nervous systems have been confirmed in experimental animals.There are no adequate animal data available for determine the chronic

1 ~ effects of low level exposure to barium by ingestion (Clements, 1985).

Baritosis, a benign pneumoconiosis, is an occupational disease: arising from the inhalation of barium sulfate dust, bariim oxide dust,

and barium carbonate. The radiologic changes produced in the lungs are| reversible with cessation of exposure. Other reports of industrial

exposure to barium compounds describe pulmonary nodulation with or withouta decrease in lung function. Dusts of barium oxide are consideredpotential agents of dermal and nasal irritation. The biological half-life

: for barium is less than 24 hours (Clements. 1985).

Environmental Toxicitv

Adequate data for characterization of toxicity to wildlife anddomestic animals are not available.

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Lead

Fate and Transport

Some industrially produced lead compounds are readily soluble inwater (USEPA, 1979). However, metallic lead and the common lead mineralsare insoluble in water. Natural compounds of lead are not usually mobilein normal surface or ground water because the lead leached from ores isadsorbed by ferric hydroxide or combines with carbonate or sulfate ionsto form insoluble compounds.

Movement of lead and its inorganic and organolead compounds asparticulates in the atmosphere is a major environmental transportprocess. Lead carried in the atmosphere can be removed by either wet ordry deposition. Although little evidence is available concerning thephotolysis of lead compounds in natural waters, photolysis in theatmosphere occurs readily. These atmospheric processes are important indetermining the form of lead entering aquatic and terrestrial systems(Clements, 1985).

The transport of lead in the aquatic environment is influenced bythe speciation of the ion. Lead exists mainly as the divalent cation inmost unpolluted waters and becomes adsorbed into particulate phases.However, in polluted waters, organic complexation is mot important.Volatilization of lead compounds probably is not important in mostaquatic environments (Clements, 1985).

Sorption processes appear to exert a dominant effect on thedistribution of lead in the environment. Adsorption to inorganic solids,organic materials, and hydrous iron and manganese oxides usually controlsthe mobility of lead and results in a strong partitioning of lead to thebed sediments in aquatic systems. The sorption mechanism most importantin a particular system varies with geological setting, pH, Eh.availability of ligands, dissolved and particulate ion concentrations,salinity, and chemical composition. The equilibriem solubility of leadwith carbonate, sulfate, and sulfide is low. Over most of the normal pH

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range, lead carbonate, and lead sulface control solubility of lead inaerobic conditions, and lead sulfide and the metal control solubility in

' anaerobic conditions. Lead is stomgly complexed to organic materialspresent in aquatic systems and soil. Lead in soil is not easily taken up

' by plants, and therefore, its availability co terrestrial organisms issomewhat limited (Clements, 1985).

Bioaccumulacion of lead has been demonstrated for a variety of

organisms, and bioconcentration factors are within the range of 100-1,000.I Microcosm studies indicate that lead is not biomagnified through the food

chain. Bioraethylation of lead by micor-organisms can remobilize lead to

the environment. The ultimate sink of lead is probably the deep oceans(Clements, 1985).

I Pharmacokinecics

~ There is evidence that several lead salts are carcinogenic in mice or. rates, causing tumors of the kidneys after either oral or parenteral

administration. Data concerning the care inogeni city of lead in humans areinconclusive. The available data are not sufficient to evaluate thecarcinogenicity of organic lead compounds or metallic lead. There isequivocal evidence that exposure to lead causes genotoxicity in humans

iand animals. The available evidence indicates that lead presents a hazardto reproduction and exerts a toxic effect on conception, pregnancy, and

> the fetus in humans and experimental animals [USEPA, (1977, 1980) cited, in Clements, 1985]

' Human Health

I Many lead compounds are sufficiently soluble in body fluids to betoxic [USEPA, (1977 and 1980) cited in Clements, 1985]. Exposure ofhumans or experimental animals to lead can result in toxic effects in thebrain and central nervous system, the peripheral nervous system, the

f kidneys, and the hematopoietic system. Chronic exposure to inorganiclead by ingestion or inhalation can cause lead encephalopathy, and severecases can result in permanent brain damage. Lead poisoning may causeperipheral neuropathy in adults

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and children, and permanent learning disabilities chat are clinicallyundeteccable in children may be caused by exposure Co relatively lowlevels. Short-term exposure to lead can cause reversible kidney damage,but prolonged exposure at high concentrations may result in progressivekidney damage and possibley kidney failure. Anemia, due to inhibition ofhemoglobin synthesis and a reduction in the life span of circulating redblood cells, is an early tnanif iestation of lead poisoning. Severalstudies with experimental animals suggest that lead may interfere withvarious aspects of the immune response.

Environmental Toxic itv

Freshwater vertebrates and invertebrates are more sensitive to leadin soft water than in hard water [USEPA, (1980, 1983) cited in Clements,1985}. At a hardness of about 50 mg/liter CaCO-, the median effectconcentrations for nine families range from 140 /ig/ liter to 236,600Mg/liter. Chronic values for Daohnia maena and the rainbow trout ofabout 50 mg/liter. Acute -chronic ratios calculated for three freshwaterspecies ranged from 18 to 62. fiioconcentration factors, ranging from 42for young brook trout to 1,700 for a snail, were reported. Freshwateralgae show an inhibition of growth at concentrations above 500Mg/liter (Clements, 1985).

Acute values for twelve saltwater species range from 476 pg/literfor the common mussel to 27,000 Mg/liter for the softshell clam.Chronic exposureto lead causes adverse effects in mysid shrimp at 37Mg/liter, but not at 17 Mg/liter. The acute-chronic ratio forthis species is 118. Reported bioconcentration factors range from 17.5for Quahog clam to 2,570 for the blue mussel. Saltwater algae areadversely affected at approximate lead concentrations as low as 15.8Mg/liter (Clements. 1985).

COAlthough lead is known to occur in the tissue of many free- living a;

wild animals, including birds, mammals, fishes, and invertebrates, oO

reports of poisoning usually involve waterfowl. There is evidence that M

B-22OXOSy

lead, at concentrations occasionally found near roadsides and smelters,can eliminate or reduce populations of bacteria and fungi on leafsurfaces and in soil. Many of these micro-organisms play key roles inthe decomposer food chain (Clements, 1985).

Cases of lead poisoning have been reported for a variety of domesticanimals, including cattle horses, dogs, and cats. Several types ofanthropogenic sources are cited as the source of lead in these reports.Because of their curiosity and their indiscriminate eating habits, cattleexperience the greatest incidence of lead toxicity among domestic animals

(Clements, 1985).

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Nickel

Fate and Transport

Nickel is a highly mobile metal in aquatic systems because manynickel compounds are highly soluble in water. However, the insolublesulfide is formed under reducing conditions and in the presence ofsulfur. Above pH 9, precipitation of the hydroxide or carbonate exhibitssome control on nickel mobiliity. In aerobic environments below pH 9,soluble compounds are formed with hydroxide, carbonate, sulfate, andorganic ligands (Clements, 1985).

In natural, unpolluted waters, sorption and coprecipitation processesinvolving hydrouls iron and manganeise oxides are probably at leastmoderately effective in limiting the mobility of nickel. In more organic -rich, polluted waters, it appears that little sorption of nickel islikely. The lack of other controls on nickel mobility probably makesincorporation into bed sediments an important fate of nickel in surfacewaters. However, much of the nickel entering the aquatic environment willbe transported to the oceans (Clements, 1985).

In general, nickel is not accumulated in significant amounts byaquatic organisms. Bioconcentration factors are usually on the order of100 to 1,000. Uptake of nickel from the soil by plants can also occur.Photolysis, volatilization, and biotransformaton are not importantenvironmental fate processes for nickel. However, atmospheric transportof nickel and nickel compounds on particulate matter can occur (Clements,1985).

Pharmacokinetics

There is extensive epidemiological evidence indicating excess cancerof the lung and nasal cavity for workers at nickel refineries andsmelters, and weaker evidence for excess risk in workers at nickel

03electroplating and polishing operations. Respiratory tract cancers have £occurred in excess at industrial facilities that are methllurgicallydiverse in their operations. The nickel compounds that have been 2

o01

B-24OlOSy

implicated at having carcinogenic potential are insoluble dusts of nickelsubsulfide and nickel oxides, the vapor of nickel carbonyl, and soluble

I studies with experimental animals suggest that nickel subsulfide andnickel carbonyl are carcinogenic in racs. Evidence for thecarcinogenicity of nickel metal and other compounds is relatively thatnickel compounds can also produce various types of malilgnant tumors in

/I experimental animals after administration by other routes, including

sugcutaneious, intramuscular, implantation, intravenous, intrarenal, andI - intrapleural. Carcinogenic potential is not strongly dependent on route

or site of administration but appears to be inversely related to the1 solubility of compounds in aqueous media. Insoluble compounds, such

nickel carbonyl, and nickelocene are carcinogenic, whereas soluble nickelsalts such as nickel chloride, nickel sulfate, and nickel ammonium

sulfate, are not (Clements, 1985).

Mammalian cell transformation data indicate that several nickelcompounds are mutagenic and can cause chromosomal alteratins. Theavailable information is inadequate for assessing teratogenic andreproductive effects of nickel in humans and experimental animals

^ (Clements, 1985).

H"Tian Health

Dermatitis and other dermatological effects are the most frequenteffects of exposure to nickel and nickel-containing compounds. Thedermatitis is a sensitization reaction. Host information regarding acutetoxicity of nickel involves inhalation exposure to nickel carbonyl.Clinical manifestations of acute poisoning include both immediate anddelayed symptoms. Acute chemical pneumonitis is produced, and death mayoccur at exposures of 30 ppm (107 mg/m ) for 30 minutes. Rhinitis,nasal sinusitis, and nasal mucosal injury are among the effects reportedamong workers chronically exposed to various nickel compounds. Studies

• with experimental animals suggest that nickel and nickel compounds haveo

relatively low acute and chronic oral toxicity (Clements, 1985). o

tooOl-J

B-25oiosr

Environmental Toxicitv

In freshwater, toxicicy depends on hardness; nickel tends to be moretoxic in softer water. Acute values for exposure to a variety of nickelsalts, expressed as nickel, range from 510 ng/liter for Daohnia maenato 46,200 g/liter for banded killifish at comparable hardness levels.Chronic values range from 14.8 jig/liter for Daohnia mama in softwater to 530 /jg/liter for the fathead minnow in hard wacer.Acute-chronic ratios for Daohnia mama range from 14 in hard water to 83in soft water, and are approximately 50 in both hard and soft water forthe fathead minnow. Residue data for the fathead minnow indicate abioconcentracion factor of 61. Freshwater algae experience reduced growthat nickel concentrations as low as 100 ^g/liter (Clements, 1985).

Acute values for saltwater species range from 152 g/licer formysid shrimp to 350,000 g/liter for the mummichog. A chronic valueof 92.7 Mg/liter is reported for the mysid shrimp, which gives anacute-chronic ratio of 5.5 for the species. Reduced growth is seen insaltwater algae at concentratons as low as 1,000 ig/liter.Bioconcentration factors ranging from 299 to 416 have been reported forthe oyster and mussel (Clements, 1985).

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B-26oiosr

1 Zinc

^-i Fate and Transport

Zinc can occur in both suspended and dissolved forms. Dissolved zincmay occur as the free (hydraced) zinc ion or as dissolved complexes andcompounds with varying degrees of stability and toxicity. Suspended

| (undissolved) zinc may be dissolved following minor changes in waterchemistry or may be sorbed to suspended matters. The predominant fate of

I zinc in aerobic aquatic systems is sorption of the divalent cation byhydrous iron and manganese oxides, clay minerals, and organic material.The efficiency of these materials in removing zinc from solution variesaccording to their compositions and concentrations; the pH and salinityof the water; the concentrations of complexing ligands; and theconcentration of zinc. Concentrations of zinc in suspended and bedsediments always exceed concentrations in ambient water. In reducing

: environments, precipitation of zinc sulfide limits the mobility of zinc.However, under aerobic conditions, precipitation of zinc compounds isprobably important only where zinc is present in high concentrations.Zinc tends to be more readily sorbed at higher pH than lower pH and tends

< to be desorbed from sediments as salinity increases. Compounds of zinci with the common ligands of surface waters are soluble in most neutral and

acidic solutions, so that zinc is readily transported in most unpolluted,relatively organic- free waters (Clements, 1985) .

The relative mobility of zinc in soil is determined by the sanefactors affecting its transport in aquatic systmes. Atmospherictransport of zinc is also possible. However, except near sources such assmelters, zinc concentrations in air are relatively low and fairlyconstant (Clements, 1985).

i Since it is an essential nutrient, zinc is strongly bio -accumulatedeven in the absence of abnormally high ambient concentrations. Zinc doesnot appear to be biomagnified. Although zinc is actively bioaccumulated

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B-27OlOSy

in aquatic systems, the biota appear to represent a relatively minor sinkcompared to the sediments. Zinc is one of the most important mecals inbiological systems. Since it is actively bioaccumulated, the environ-mental concentrations of zinc probably exhibit seasonal fluctuations(Clements, 1985).

Pharmacokinetics

Testicular tumors have been produced in racs and chickens when zincsalts are injected intratesticularly, but not when other routes of admin-istration are used. Zinc may be indirectly important with regard tocancer since its presence seems to be necessary for the growth oftumors. Laboratory studies suggest that although zinc-deficient animalsmay be more susceptible to chemical induction of cancer, tumor growth isslower in these animals. There is not evidence that zinc deficiency hasany etiological role in human cancer. There are no data available tosuggest that zinc is mutagenic or teratogenic in animals or humans(Clements, 1985).

Studies with animals and humans indicate that metabolic changes mayoccur due to the interaction of zinc and other changes may occur due tothe inteeaction of zinc and other metals in the diet. Exposure tocadmium can cause changes in the distribution of zinc, with increases inthe liver and kidneys, organs where cadmium also accumulates. Excessiveintake of zinc may cause copper deficiencies and result in anemia.Interaction of zinc with iron or lead may also lead to changes that areproduced when the metals are ingested individually (Clements, 1985).

Human Health

Zinc is an essential trace element that is involved in enzymefunctions, protein synthesis, and carbohydrate metabolism. Ingestion ofexcessive amounts of zinc may cause fever, vomiting, stomach cramps, anddiarrhea. Fumes of freshly formed zinc oxide can penetrate deep into the en

Malveoli and cause metal fume fever. Zinc oxide dust does not produce z

this disorder. Contact with zinc chloride can cause skin and eye ooirritation. Inhalation of mists or fumes may irritate the respiratory M

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B-28OlOSy

and gastrointestinal tracts. Zinc in excess of 0.25 percent in diet ofrates causes growth retardation, hypochromic anemia, and defectivemineralization of bone. No zinc toxicity is observed at dietary levelsbelow 0.25 percent (Clements, 1985).

Environmental Toxicitv

Zinc produces acute toxicity in freshwater organisms over a range ofconcentrations from 90 to 58,100 Mg/liter and appears to be less toxicin harder water. Acute toxicity is similar for freshwater fish andinvertebrates. Chronic toxicity values range from 47 to 852 Mg/literand appear to be relatively unaffected by hardness. A final acute-chronicratio for freshwater species of 3.0 has been reported. Although most

freshwater plants appear to be insensitive to zinc, one species, the algaSeleanstrum capricornuturo. exhibited toxic effects at concentrations from30 to 700 Mg/lil«r. Reported acute toxicity values range from 2,730to 83,000 Mg/liter for saltwater fish and from 166 to 55,000Mg/liter for invertebrate saltwater species. Zince produces chronictoxicity in the mysid shrimp at 166 Mg/licer . The final acute -chronicratio for saltwater species is 3.0. Toxic effects are observed insaltwater plant species in zinc concentrations of 50 to 25,000Mg/liter. Bioconcentration factors of edible portions of aquaticorganisms range from 43 for the soft-shell clam to 16,700 for the oyster(Clements, 1985).

Zinc poisoning has occurred in cattle. In one outbreak, poisoningwas caused by food accidentally contaminated with zinc at a concentrationof 20 g/kg. An estimated intake of 140 gram of zinc per cow per day forabout 2 days was reported. The exposed cows exhibited severe enteritis,and some died or had to be slaughtered. Postmortem findings showed severepulmonary emphysema with changes in the myocardium, kidneys, and liver.Zinc concentrations in the liver were extremely high. Based on relativelylimited data, some researchers have speculated that exposure to excessiveamounts of zinc may constitute a hazard to horses. Laboratory studies

B-2901097

and findings in foals living near lead-zinc smelters suggest thatexcessive exposure co zinc may produce bone changes, joint afflictions,and lameness. In pigs given dietary zinc at concencrations greater than1,000 rag/kg, decreased food intake and weight gain were observed. Atdietary levels greater than 2,000 rag/kg, deaths occurred as soon as2 weeks after exposure. Severe gastrointestinal changes and braindamage, both of which were accompanied by hemorrhages, were observed, aswell as changes in the joints. High concentrations of zinc were found inthe liver (Clements, 1985).

03Har

8-30oiosy

EPA's Comments regarding:Draft Sinclair Refinery Endangerment Assessment Report

Page Par Comment

1-1 2 Identify EPA guidance manuals used duringthe preparation of the report

1-5 1 Typo - operating3 Typo - downgradient

2-1 2 Replace "evaluate the need for" with "gather data todetermine the nature and extent"

2-2 Add footnote noting chemicals analyzed by SMCMartin and EBASCO

2-3 1 Typo - carcinogen2-3 3 Clarify last sentence

2-4 Provide frequency as fraction in "hits" column

2-5 Add footnote noting groundwater wells depictedare both shallow and deep

2-11 2 Delete "national and"Reword last sentence removing comparison tonational averages

2-12 Remove "National Range" column andmodify footnotes

2-18 1 Typo - location

2-19 1 Change "ridge" to "area" andTypo - northern

3-1 2 Change "ARAR" to "standard" andadd sentence noting likely contaminant migrationpathway is from soil to groundwater

Oo

too3-2 Reword Title to Table 3-1 removing reference

to ARARs

3-9 4 Typos - "an" and "aquifer"

3-14 2 Typo - pore

3-18 2 Change "five" to "four" andadd sentence clarifying known uses of upperaquifer

3-21 2 Typos - "exposures" and "legitimate"3 Typo - volatile

3-31 3 Typo - matter

3-34 2 Add phrase to clarify that downgradient surfacewater samples were used for this exposurescenario

4-1 2 Modify explanation of RfD by inserting"intake levels with no expected adverse healtheffect" andTypo - "doses" and "RfDs"

4-3 2 Modify explanation of RfD as above, andReplace "does not" with " is not expected to", andReplace "which does not" with "that is not expectedto"

4-16 2 Typo - million, andReplace "acceptable target risk" with "EPAs riskrange, andReplace "generally range from" with "is"

5-3 2 Delete "is within.....risk limits."

COM55

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APPENDIX CSUPPORTING CALCULATIONS

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too-J01

The emission rate from the exposed soil area was estimated for aten-hour period, simulating 10 hours of continuous exposure. The depthof dry zone, d, was estimated at approximately 1 centimeter. This is areasonable estimate based on the face that when the trench is excavated,

the soils will be exposed at the surface for the first time. This term

represents the depletion of the contaminant at the soil surface with timedue to the volatilization of organics in successive unimolecular layersfrom soil particles (Versar. 1988).

Volatilized contaminants are expected to remain in the trench. Allcompounds have, vapor densities greater than 1, which is the vapor density

of air and are, therefore, heavier than air. Emission rates forvolatiles released from the trench are presented in Table C-l.

Deposition of volatilized contaminants through precipitationscavenging is expected to impact off site soils, surface waters andpotentially edible biota only to a limited extent due to the extremely

low emission rates. These intermedia transfers are difficult to quantifyand therefore deposition will not be modeled in this assessment.

Ambient air concentration in the trench for each chemical wasdetermined using the same box model used in evaluating dust concentrationson site. Concentrations were estimated at distances of 10m and 50m toevaluate risk to workers and those adjacent to the trench. Box heightsof 1.4m and 3.8m, which correspond to 10m and 50m distances, were alsoemployed. Because the orientation of a future trench is not known, thewidch of the trench relative to the dominant wind direction cannot bedetermined exactly. The most conservative width (1m) would be from windparallel to the trench, while the lease conservative width (300m) wouldbe perpendicular to the trench. A crossvind width of 50m was chosen tosimulate the dominant ly oblique angle that the wind would take much ofthe time. An annual average windspeed of 4.6 m/s was acquired from theBinghamton, New York weather station (Ebasco, 1989). Ambient w

Mconcentrations of volatile organic compounds emitted from the trench are z

presented in Table G-2. o

C-2

TABLE C-lEMISSION RATES FOR VOLATILES ESCAPING SOILS IN TRENCH

SIDED^ CQ Cb AREA LEHSTH DEPTH

(cm2/sec> <g/cm2> (g/em2) (ca2) <m) (em)

Benxene 7.81E-03 2.32E-08 2.03E-06 1.50E+07 38.73 l.OOE+00Methyl Chloride 7.19E-C2 *.25E-09 6.95E-06 l.SOE+07 33.73 l.OOE+00Triehloroethene 1.18E-02 2.50E-09 8.32E-06 1.50E+07 38.73 l.OOE+00Xylene 8.09E-03 3.92E-08 3.64E-05 1.50E+07 38.73 l.OOE+00

TIME EMISSION RATES<»> ((/*) (mg/s)

3.60E+04 1.66E-03 1.66E+003.60E+0* 3.0 IE-03 3.01E+003.60E+0* *.17E-04 4.17E-013.60E+04 4.18E-03 A . 18E+00

EMISSION RATE CALCULATION

E •i

20 C AAB n

i- d

E -£ «DABCoC«

<2DabCuA>/[d+SORTC(C2D«bCut>/Cbtxl 2)1Emission rat* of contaminant ov«r• Phase transfer coefficient,

(g/s)

« Liquid phase concentration of contaminant in soil, approximated bymean ground-water concentration in monitoring wells on site, (g/s)• Max contaminant concentration in soil (ug/kg). assuming a soilbuilt density of !.<• g/ca>3, EX: (10 ug/fcg) (i.* g/cmJ) " 1.4E-02

A • Contaminated surface «re*. surface area.of 30.000cm long trench.200cm deep and 100cm wid« * 1.5E+07 cmj

d • Depth of "Dry Zone", assume contamination and soil moisture arevirtually at the surface in freshly dug trench

t - Time, ten hour day of exposure. 36,000s

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C-3

TABU C-2AMBIENT COHCEMTRATIOIIS FOR VOLATILES ESCAPING FROM TRENCH (10 •)

Mean Emission

COMPOUND

BenxeneMethylene ChlorideTrichloroetheneXylen*

Max.(Cm**)(»/•)(A)

1.66E-033.01E-034 17E-044 13E-03

BoxWidth(W)(a)(B)

SOSOSOso

Wind SpeedOn Site(ulO)(m/s)(C)

4.6

4 6

46

k.6

BoxHeitht(B)(m)(0)

1.4

1.4

1.4

1.4

Wind Speed Mean AmbientIn Box Concentration(ua> (Coax)(m/s) (»/a3)CE) (F)

1.27 1.87E-OS1.27 3.39E-031 27 4 70E-061.27 4.71E-OS

(Caax)

(BW/aJ)(F)

1.87E-023 391-024. 70E-034.71E-02

AMBIEHT CONCENTRATIONS FOR VOLATILES ESCAPING FROM TRENCH (SO m)

Mean Eouktiou

COMPOUND

BenieneMethylene ChlorideTrichloroetheneXylene

Max.(Qaax)(t/s)(A)

1.66E-033.011 034.17E-044 1SE-03

Box Wind Speed BoxWidth(W)(m)(B)

SOSOsoso

On Site Heixht(ulO) (B)(a/s) (a)(C) (D)

4.6 3.64.6 3.64.6 3.846 3.8

Wind SpeedIn Box<IB»)

(m/s)(E)

2.282.282.:s2 28

Mean AabientConcentration

(Caax)(§/a3)(F)

3.63E-066.93E-069.63E-079.66E-06

(Caax)(a»/a3>(F)

3.S3E-036.9SE-039.63E-049 . 66E-03

Notes:

A - Froei Table 2-S. _B • Asauaunc an oblique attach an*le for Mind for most of the year.C • Froa Bradford. PA weather station data (Geaa. 1989).D • Frcei Table J-S for a 10 • and 10 m receptor.E • Frost supporting (.alculationa in text.

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C-4

C.2 SURFACE RUNOFF CONTAMINATION ANALYSIS

Releases by overland flow of contaminants from source areas atSinclair Refinery are estimated using the Modified Universal Soil LossEquation (MUSLE) and sorption partition coefficients derived from eachcompound's octanol-water partition coefficient K (Haith, 1980; Mills,et al., 1982). The MUSLE allows estimation of the amount of surface soileroded in a storm event of given intensity, while sorption coefficientsallow the projection of the amounts of contaminant carried along with thesoil and the amount carried in dissolved form.

Soil loss calculation: The modified universal soil loss equation is(Mills et al., 1982):

Y(S)£ - a (V )0'56 KLSCP

Where: Y(S)E - sediment yield (metric tons)a - conversion constant (11.8 metric)Vr - volume of runoff (nr)qp - peak flow rate (nr/sec)K - soil credibility factor (tons/acre/runoff)L - slope-length factor (dimensionless)S - slope-steepness factor (dimensionless)C - cover factor (dimensionless, 1.0 for bare soil)P - erosion control practice factor (dimensionless,

1.0 for uncontrolled waste site)

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C-5

Volume of runoff (Vr)

V -

Where: a - conversion constant (1UO metric)A - contaminated area, (ha)

- 24.28 ha (digitized from site map)Qr - depth of runoff, (cm)

- (Rc - 0.2Sw)2/(Rt + 0.8SW)

w

- total storm rainfall, (cm)- 2.54 cm (1-inch storm)- water retention factor (cm)- (1000/CN-10)aCN - curve number (dimensionless)

- 82 (Versar, 1988, Table 3-4)a - conversion constant (2.54 metric)

(1000/CN-10)2.54- 5.56 cm

Qr - [2 .54 cm - 0 . 2 ( 5 . 5 6 c m ) ] V [ 2 . 5 4 cm- 0.29 cm

0 . 8 ( 5 . 5 6 cm)]

Vr - 100 (24 .28 ha) (0.29 cm)- 704.2 m3

Peak Flow Rate

- 0.2Sw)

Where Tr - peak storm duration (hours), assume 1 houra - conversion factor, 0.028 metric

( 0. 028 U 24. 28haH 2. 54cm) (0 .29cm)qp " (1 hr)[2.54cm - 0.2(5. 56cm)]

- 0.351 m3/s*c

env«25

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C-6

Soil Erodibilitv Factor

K - 0.64 (Estimated)

Slope Length and Slope Steepness Factors

LS - 0.1 (USEPA, 1988, Figure 2-6)

Cover Factor

C - 0.042 (USEPA, 1988. Table 2-4)

Erosion Control Practice Factor

P - 1.0 (USEPA. 1988)

Soil Loss Calculation

Y(S)E - (11.8)((704.2m3)(0.351m3/sec)]°-56 (0.64)(0.01)(0.042)(1)

- 0.694 metric tons/event

The following equations were used to predict the degree of soil/waterpartitioning for given compounds once storm event soil loss has beencalculated.

Dissolved/sorbed contaminant loading calculation: (USEPA, 1988, p. 2-41)

S ri y /1 _i_ A /i/ o \ i /* As ~ l*/vi * Wg/Kgp;j t-so£^ A

Ds - [1/(1 + (Kd/3)/Sc)] Csoil A

Where: Ss - sorbed substance quantity, (kg)DS — dissolved substance quantity, (kg)6C - available water capacity of the top cm of soil,

(dimensionless)Kg - sorption partition coefficient, (cnr/g)0 - soil bulk density, (g/cor)Csoii - soil substance concentration, (kg/ha-cm)A - contaminated area (ha-cm) 0}

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C-7

Available Water Capacity

9C - 0.139 cm available water/cm soil (dimensionless) (Baes, et al,1983)

Sorotlon Partition Coefficient

Chemical Kd (

Arsenic 6 . 70Barium 33.7Benzene 8 , 300Benzo(a)pyrene 5.5E+08Lead 99Methyl Chloride 3,500Nickel 54.6Nitrobenzene 3,600TCG 12 , 600Xylene 24 , 000Zinc 16

Kd for As, and Zn from Baes et al., 1983.Kg for Bezene, Benzo(a)pyrene, Methyl Chloride, Nitrobenzene, TCE, and

Xylenes from Koc as published in SPHEM (U.S. EPA, 1986) and using Kd -Koc/Organic Carbon Content (O.C.) O.C. estimated at IX (0.01)

Kd for Barium estimated using Koc method; Koc estimated from solubility,S, for BaSo4 in water of 1.6 mg/L and using Koc-3.64-0.551og(S) , (Lyman,1982)

Kd for Ni estimated by comparison with other metals and consideringcontroling factors such as atomic radius and valence number

Soil Bulk Density

B - 1.49 g/cnr (Based on site information).

03t-iar

OCONJ

C-8 1

Soil Substance Concentration

Average Concentration found in Surface Soils (me/ke)

Arsenic 8.43Barium 49.1Benzene 0.0028B«nzo(a)pyrene 0.188Lead 57.1Methyl Chloride 0.0098Nickel 17Nitrobenzene 0.165TCG 0.0025Xylene 0.0025Zinc 74.3

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C-9

Conversion of concentrations form mg/kg to kg/ha:

kg mg chem. .,^_ ™ « _ _ ^ _ * Pha kg soil

^£ - C . ft . (0.01)ha

g soil 1 kg soil 1 kg chem.

1000 g soil 1x10 mg chem

1x1

cm

2CD

ha

1cm•

lCD

The soil contaminant concentrations are as follows:

Arsenic 8.43 mgAg x 1.49 g/cnr x 0.1Barium 49.1 mg/kg x 1.49 g/cm3 x 0.1Benzene O.J028 mg/kg x 1.49 g/cm3 x 0.1Benzo(a)pyrene 0.188 mg/kg x 1.49 g/cm3 x 0.1Lead 57.1 mg/kg x 1.49 g/cm3 x 0.1Methyl Chloride 0.0098 mg/kg x 1.49 g/cm3 x 0.1Nickel 17 mg/kg x 1.49 g/cm3 x 0.1Nitrobenzene 0.165 mg/kg x 1.49 g/cm3 x 0.1TCG 0.0025 mg/kg x 1.49 g/cm3 x 0.1Xylene 0.0025 mg/kg x 1.49 g/cm3 x 0.1Zinc 74.3 mg/kg x 1.49 g/cm3 x 0.1

Calculation of Sorbed/Dissolved Substance Quantity

1.267.324.17E-042.80E-028.51I.46E-032.532.46E-023.73E-043.73E-04II.1

Ss -

Ds -

0.139/Kd x 1.49)] Csoil A

(Kd x 1.49)/0. 0139)1 Csoll A

(cm /g) (kg/ha) A (ha) y (kg) DS (kg)

ArsenicBariumBenzeneBenzo(a)pyreneLeadMethyl ChlorideNickelNitrobenzeneTCGXyleneZinc

6.7033.70

8 , 300 . 005 . 50E+08

99.00e 3.500.00

54.603,600.0012.60024 , 000

16

1.267.324.17E-042.80E-028.511.46E-032.532.46E-023.73E-043.73E-0411.1

0.190.190.190.190.190.190.190.190.190.190.19

2.35E-011.397.93E-055.32E-031.612.77E-044.80E-014.67E-037.08E-057.08E-052.09

3.28E-033.84E-038.91E-109.03E-131.52E-037.39E-098.21E-041.21E-075.24E-102.75E-101.22E-02

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C-10

Loading Co Estuary from Surface Water

Total Loading - PXi + PQiPXi - [Y(S)E/aA0)SsPQi - [Qr/Rtl Ds

Where: PX^ - sorbed substance loss per event, (kg)PQi - dissolved substance loss per event, (kg)a - constant (100, metric)

and as calculated before:

Y(S)E -A

Qr -Rt -

Chemical

ArsenicBariumBenzeneBenzo ( a ) py r eneLeadMethyl ChlorideNickelNitrobenzeneTCCXyleneZinc

0.649 metric tons24.28 ha1.49 g/cm30.29 cm2.54 cm

s

(kg)

2.35E-011.397.93E-055.32E-031.612.77E-044.80E-014.67E-037.08E-057.08E-052.09

D

(kg)

3.28E-033.84E-038.91E-109.03E-131.52E-037.39E-098.21E-041.21E-075.24E-102.75E-101.22E-02

PXi(kg)

7.81E-064.60E-052.63E-091.77E-075.36E-059.20E-091.59E-051.55E-072.35E-092.35E-096.94E-05

PQi(kg)

3.74E-044.38E-041.02E-101.03E-131.74E-048.44E-109.37E-051.38E-085.98E-113.14E-111.39E-03

Total(kg)

3.82E-044.84E-042.73E-091.77E-072.27E-04l.OOE-081.10E-041.69E-072.41E-092.38E-091.46E-03

CO1-1ss

OCD(Jl

C-ll

C.3 GROUND-WATER MODELING

The Soil Contamination Evaluation Methodology (SOCEM)(CH2M Hill,

1985) was used to characterize the impact that contaminated ground waterbelow the Sinclair Refinery site may have on the Genesee River. Versarhas used actual ground-water monitoring results to estimate contaminantconcentrations reaching Genesee River. The model assumes the following:

• steady state conditions,• continuous source of contaminants.• constant source concentration,• no retardation of contaminants,• no losses or decay mechanisms (degradation, volatilization),• no longitudinal dispersion.• no diffusion, and• no precipitation recharge.

These assumptions will produce a conservative estimate of potentialoffsite contaminant concentrations. The numbers can be viewedessentially as a "worst-case" situation since they do not allow forimportant loss mechanisms. Exposure levels computed from these numberswill therefore be biased high. This conservative approach is taken toensure that the potential human or environmental health risks will beidentified, and that selected remedial alternatives will be protective.

The codified version of SOCEM used in this endangermenc assessmentwas based on the EPA Vertical and Horizontal Spread (VHS) model (50 PR7882) , adapted from an equation presented by Domenico and Palciauskas(1982). The SOCEM version of their equation is given by:

COM55oo

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C-L2

cgw - co * erf[Z/(2(d*X)°-5)] * erf [Y/(4(d*X)°-5> ]

Where: Cgw - Contaminant concentration at the ground-waterreceptor, in this case. Genesee River;

C0 - Initial ground-water contaminant concentration atthe source , in this case , concentrations inmonitoring wells;

d - Aquifer transverse dispersivity;X - Distance to receptor in the direction of

ground-water flow;Y - Width of contaminated zone at the site boundary

(measured perpendicular to the direction ofground-water flow) ;

Z - Thickness of the contaminated zone at the siteboundary (measured downward from the ground-watertable); and

erf(f) - The error function of any function (f).

The developers of SOCEM (CH2M Hill. 1985) intended that the methodbe used to evaluate the effect that alternate remedial options may haveon reducing contaminant concentrations at the receptor. They suggestthat it be used as a straight forward, simplified procedure tocharacterize the threat that contaminated soil may pose to ground waterat Super fund sites, even though they do not suggest a way of estimatingone of the most critical input values to the SOCEM model, the initialsource concentration in ground water from contaminated soil. To reduceuncertainty associated with generated ground-water concentration valuesfrom soil concentration values, the ground-water exposure assessmentrelies on the ground-water monitoring data and not soils concentrationdata. In such an approach, each monitoring well with constituentconcentration, C , acts as a source of contaminated ground water thatwill be transported to Genesee River.

If each location where samples were taken is treated as a source ofcontamination, the contribution of contamination introduced to GeneseeRiver can be calculated using the VHS model or SOCEM. SOCEM was used tocalculate concentrations of contaminated water released to Genesee River

Cofor each indicator chemical identified at each sampling location, and H-- »totaled for all Indicator chemicals from each sampling location. oo

COVI

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In order to determine the values for che parameters used in the SOCEMequation, seven monitoring wells were chosen co represent sourcecontamination at che site. These wells, KW-/, -9, -10, -11. -27. -32.

and -55 were chosen based on their proximity co the river, and the depthat which each well was screened.

Pertinent well-specific information used in the modeling is shown inthe following tables, while the sources of che information is explained

here. Chemical concentration data were obtained from the Ebasco RIReport, 1989 and appear as the second column in the tables. The distancefrom source (monitoring well) co receptor (Oenesee River) was measuredfor each of the seven wells from a scale map in che RI report.Contamination zone width, Y, was determined by measuring the length ofthe sice boundary (che river) represented by che seven wells, and chendividing by seven co obtain the approximate length represented by eachwell. Transverse dispersivity, d. for each well was determined byexaming well log information in the RI report and assigning a value of0.3 or 3 depending on soil characteristics as reported in the logs.Contamination zone chickness was also determined from well logs bysubstracting the dept to water from either rhe depth to the bottom of chewell screening or the depth to the aquitard clay layer, whichever wasshallower.

The SOCEM tables also show the results of the modeling as an averageconcentration entering che river of all of che modeled wells. The amountof contaminant entering the river was determined by combining the concen-tration information with ground-water flow rate information. Ground-waterflow rate was determined by examining pump test and slug test data forwells near the seven modeled wells to obtain a maximum value forhydraulic conductivity, k, of 140 ft/day (42.67 ra/day), (140 is greaterthan 14/15 of all pump test results). The hydraulic gradient, i. was w

Mreported to be 0.016 ft/ft (or m/m) in the northern portion of the site, Zso this value was used to determine q, the ground-water flow rate as: o

oq - k x

10oCO00

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The resulting ground-water flow race was used in the equation:

Q - q(JL) * A (m2) * 1000 i_ * L day

W" 3day m 86400 secco determine Q, che ground-wacer volumetric flow rate, where A is thecross-sectional area into which the ground water is flowing. The cross-sectional area was determined by representing the are at the Genesee Riverinto which che ground water flows as a rectangle ac length 1, and and adepth equal to the average thickness at the aquifer as determined by theseven SOCEM modeled wells. The value used for 1 and depth are:

1 - 1096m (3,598 fc)and d - 3.51m (11.52 ft)so, therefore:

A - 3849 m2

and Q - 30.42 L

SecThe concentrations of contaminants in che Genesee River are che

result of contributions of suspended and dissolved contaminants fromsurface runoff and contributions of contaminants from ground-watermigration. The following equation provides a rough estimate of theconcentration of a substance downstream from a point source release into aflowing water body, after dilution by the receiving water body (Versar,1988, p 3-31).

C Qe xeQt

Where Cr - concentration of substance in stream,Ce - concentration of substance in effluent, (pg/L)Qe - effluent flow rate, (L/sec)Qt - combined effluent and stream flow rate, (L/sec)

The three contaminant contributions include (1) surface runoff, suspended ^contaminants (srs), (2) surface runoff, dissolved contaminants (srd) , and *(3) ground-water interception (gw) . Therefore, the contaminant oconcentration in che stream is as follows: o

o00VO

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(C • Q ) + (C ,• Q ) + (C • Q )srs sr srd sr gw xgwc

Where Cx - concentration, (jig/D . of contributor x, andQx - is flow rate, (I/sec) of contributor x.

Since the surface runoff and ground water infiltration flow rates aremuch smaller than the river flow rate. Q has been replaceed by Q ,the river flow rate. This Q is not the sane as the runoff depth usedin the MUSLE equation which uses the same notation. Flow rates in

Genesee River were reported to be 10.052 I/sec on the average, with aminimum rate of 679 I/sec.

Contaminant Concentration in Surface Runoff. Suspended

C - sorbed substance loss per eventsrs runoff depth x area

- RC.QrA

Where A - 24.289 ha x (1 x 106 dm2/ha) - 2.42 x 107 dm2PX.

Csrs "(0 .29cm)(0 .1 d«/cm)(2.42 x 10? d m ^ ) ( l l/dm3)

IL (1Q9M8

701,800

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Chemical PX (Kg) C (Mg/D______ i srs_____

Arsenic 7.81E-06 1.11E-12Barium 4.60E-05 6.53E-12Benzene 2.63E-09 3.73E-16Benzo(a)pyrene 1.77E-07 2.51E-14Lead 5.36E-05 7.61E-12Methyl Chloride 9.20E-09 1.31E-15Nickel 1.59E-05 2.26E-12Nitrobenzene 1.55E-07 2.20E-14TCG 2.35E-09 3.33E-16Xylene 2.35E-09 3.33E-16Zinc 6.94E-05 9.85E-12

Contaminant Concentration in Surface Runoff Dissolved

C « dissolved substance loss per eventsrd runoff depth x area

701,800

Chemical s PC^ (Kg) C . (Mg/D

Arsenic 3.74E-04 5.31E-11Barium 4.38E-04 6.22E-11Benzene L.02E-LO 1.44E-17Benzo(a)pyrene 1.03E-13 1.46E-20Lead 1.74E-04 2.47E-11Methyl Chloride 8.44E-10 1.20E-16Nickel 9.37E-U5 1.33E-11Nitrobenzene 1.38E-08 1.96E-15TCG 5.98E-11 8.50E-18Xylene 3.14E-11 4.46E-18Zinc 1.39E-03 1.98E-10

0}Surface Runoff Flow Rate H————tB*UbbK__UU———US——— ^,

Qsr" - 4e §AC ^Where At - total storm duration, assume 1 hour \>o

L *»1__

Q. - 0.29em(0.10dm/cni)(2.41 x 105dm2'> dm3sr Ihr (3600 sec/hr)

- 194.9 L/secC-17

Contaminant Concentration in Ground Water

Ground-water contaminant concencracions were obtained fora the VHSmodeling (SOCEM).

Chemical

ArsenicBariuaBenzeneBenzo(a)pyreneLeadMethyl ChlorideNickelNitrobenzeneTCCXyleneZinc

515599.00

84.32.7325.52.7367.4520

1.6463.33647

The resulting surface wacer concencracions are as follows:

Chemical

ArsenicBariuaBenzeneBenzo(a)pyreneLeadMechyl ChlorideNickelNitrobenzeneTCCXyleneZinc

56E+0081E+0055E-0126E-0372E-0226E-0304E-0157E-0096E-0392E-01

1.10E+01

CO

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