BASELINE HUMAN HEALTH RISK ASSESSMENT OF THE FORMER WESTINGHOUSE TRANSFORMER PLANT, SHARON, PENNSYLVANIA '\J-
APRIL 7,1998
prepared by:
ChemRlsk* A Service of McLaren/Hart Environmental Engineering Corporation Stroudwater Crossing 1685 Congress Street Portland, Maine 04102 (207)774-0012
A Division of McLaren/Hart n ,} - - o n Environmental Engineering ' l\ \\\1\) J / 0 J fihemRisk A Division of McLaren/Hart v Environmental Engineering 'i R i 0 3 7 9 f) "V BASELINE HUMAN HEALTH RISK ASSESSMENT OF THE FORMER WESTINGHOUSE TRANSFORMER PLANT, SHARON, PENNSYLVANIA
ChemRisk Project No, 12.0802130.018.001
April 7,1998
Prepared for: Westinghouse Electric Corporation 11 Stanwix Street ' Pittsburgh, PA 15222-1384 Prepared by: ChemRisk* - A Service of McLaren/Hart Environmental Engineering Corporation 1685 Congress Street Portland, ME 04102
Russell E. Keenan, Ph.D. Mark C. Maritato Chief Health Scientist ..*'•' . Senior Health Scientist Vice President v ..
•AR30379 I TABLE OF CONTENTS . "^
1.0 INTRODUCTION AND PURPOSE ...... 1-1 1.1 Site Background...... 1-2 1.2 Regulatory History ...... ,'.;'..; 1-3 1.3 Urban Renewal Land Use Plan ...... ,...... ,....;.. ^..... 1-3 1.4 Risk Assessment Conceptual Site Model;,...... ,...... '... 1-4 2.0 DATA EVALUATION ...... 1...... ;.,...... M 2.1 General Data Discussion ...... 2-1 2.2 DataGrouping ...... 2-3 2.2.1 River Sector ...... ;...... 2-4 2.2.2 North Sector ...... 2-6 2.2.3 MiddleSector ...... ,.2-7 2.2.4 South Sector ...... ;...... , 2-8 2.2.5 Mjjat Sector ...... 2-8 2.2.6 Railroad Right-of Way (ROW) ...... 2-8 2.2.7 Groundwater Data Grouping...... ^...... _...... 2-9 2.2.7.1 Alluvial Central Plume ...... :...... 2-9 2.2.7.2 Alluvial Southern Plume ...... 2-9 2.2.7.3 Bedrock Aquifer ...... 2-10 2.3 Qualitative Data Summary ...... v ...... 2-10 2.3.1 North Sector...... 2-10 2.3.2 Middle Sector ...... 2-11 2.3.3 South Sector...... v...... 2-11 2.3.4 EPA Residential Soil Sampling Program ...... 2-12 2.4 Selection of Chemicals of Potential Concern ...... 2-13 2.4.1 Surface Soils ...... 2-15 2.4.2 Subsurface Soils ...... :...... 2-15 2.4.3 Sediments ...... 2-15 2.4.4 Storm Water Runoff ...... '...... *. 2-15 2.4.5 Groundwater...... 2-16 2.4.6 Air ...... ;... 2-16
3.0 HYPOTHETICAL RECEPTOR ANALYSIS ...:...... 3-1 3.1 Identification of Potential Exposures...... 3-1 3.2 Exposure Point Concentrations ...... ,.....,...... *... 3-5 1 3.3 Quantification of Exposures ...... 3-7 3.3.1 RiverSector ...;...... 3-13 3.3.1.1 .- ChildWader.../..../...,...... 3-13 3.3.2 North, Middle and South Sectors :...... 3-18
CHEMRISK^-A DIVISION OF MCLAREN/HART
ARJU3792 TABLE OF CONTENTS (CONT'D) 3.3.2.1 Indoor Employee ...... 3-18 3.3.2.2 Indoor Construction Worker ...;...... 3-19 3.3.2.3 Outdoor Construction Worker ...... 3-29 3.3.3 Moat Sector ...... ;....,...... 3-37 3.3.3.1 Maintenance Worker ., .'...... 3-37 3.3.3.2 Child Trespasser ...... ;.,...... 3-37 3.3.3.3 Construction Utility Worker...... 3-38 3.3.4 Railroad Sector ...... ,...... :...... 3-40 3.3.4,1; Maintenance Worker ...... 3-40 3.3.4.2 Child Trespasser .....:...... ;...;... 3-40 3.3.5 Hypothetical Future Use of Groundwater ...... 3-41 3.3.5.1 Hypothetical Resldehtial Groundwater Use ...... 3-42 3.3.5.2 Hypothetical Industrial/Commercial Groundwater Use ...... J...... 3-46" . % ' • • ' •' . i 4.0 TOXICITY ASSESSMENT ...... 4-1 4.1 Carcinogenic Response ...... 4-2 4.2 Noncarcinogenic Response ...... (...... 4-5 4.3 Relative Absorption Factors ,...... ,..•••••••••-•••••• 4-6 5.0 HUMAN HEALTH RISK CHARACTERIZATION ...... M 5.1 Carcinogenic Risk...... :...... 5-2 5.2 Noncarcinogenic Hazard ...... 5-4 5.3 EPA Calcubted Risk Estimates /...... 5-6 5.4 Identification of Uncertainties ..*...*...... 5-6 5.5 Risk Perspective ...... 5-13 5.5.1 Acceptable Risk Defined Under Existing Regulatory Initiatives ..... 5-14
6.0 SUMMARY AND CONCLUSIONS ...... ;...... 6-1 7.0 REFERENCES ...... !...... 7-1
cw3JEwmwEJnNafti««viDC.wK> U CHEMRJSK«-A DIVISION OF MCLAREN/HAftT
: LIST OF FIGURES Figure 1-1 Sectors of Interest Figure 2-1 Schematic Diagram of COPC Selection Process LIST OF TABLES Table 2-1 , Westinghouse Electric Corporation Former Sharon Transformer Plant Representative Sampling Locations by Sector • . " ' v Table 2-2 PADEP Detected Surface Water Constituents Compared to Standards and Guidelines Table 3-1 Hypothetical Receptor Summary table 3-2 Shenango River Sediment EPC Calculation Table 3-3 Middle Sector Subsurface Soil EPC Calculation Table 3-4 Moat Sector Surface Soil EPC Calculation , Table 3-5 Moat Sector Subsurface Soil EPC Calculation Table 3-6 Railroad ROW Sector Surface Soil EPC Calculation Table 3-7 Railroad Sector Surface Water Runoff EPC Calculation , i y ' • .1 Table 3-8 Alluvial Southern Plume Monitoring Well EPC Calculation Table 3-9 Alluvial Central Plume Monitoring Well COPC Screen Table 3-10 Bedrock Monitoring Well EPC Calculation Table 3-11 Middle Building Indoor Air COPC Screen Table 3-12 Hypothetical Child Wader Exposure Parameters Table 3-13 Hypothetical Employee Exposure Parameters D iii CHEMRISK*-A DIVISION OF MCLAREN/HART '______TABLE OF CONTENTS (CONT?D) i . . . ^-"^ •______LIST OF TABLES (CONT'D) Table 3-14 Hypothetical Indoor Construction Worker Exposure Parameters v . / ' • - - ' , Table 3-15 Hypothetical Respirable Particle Emissions from Outdoor Construction Table3-16 Hypothetical Outdoor Construction Worker Exposure Parameters Table 3-17 Hypothetical Moat Maintenance Worker Exposure Parameters - Table 3-18 Hypothetical Child Moat Trespasser Exposure Parameters Table 3-19 Hypothetical Respirable Particle Emissions from Moat Maintenance/Utility Worker Trench Excavation Table 3-20 Joint Frequency Distribution of Wind Speed and Direction for Youngstown, OH for the Years 1988-1992 Table 3-21 Hypothetical Moat Maintenance Utility Worker Exposure Parameters i . i Table 3-22 Hypothetical Railroad ROW Maintenance Worker Exposure Parameters i - _ ' , _. • - ', ; . , . • ' . Table 3-23 Hypothetical Railroad ROW Child Trespasser Exposure Parameters Table 3-24 Hypothetical Residential Groundwater Use Exposure Parameters Table 3-25 " Hypothetical Industrial Groundwater Use Exposure Parameters Table 3-26 Calculation of Chemical-specific Transfer Efficiency ' j x Table 4-1 USEPA Weight-of-Evidence Classification System for Carcinogenicity Table 4-2 Oral Toxicit- y Values for Potentia. . I l Carcinogeni'. c Effect.: s , ' ' Table 4-3 Inhalation Toxicity Values for Potential Carcinogenic Effects .Table 4-4 PCDD/F Toxic Equivalency Factors [TEFs] . • '. ' • - ' - !. ' ' Table 4-5 Oral Toxicity Values for Potential Noncarcinogenic Effects '-•••••>,• iv- CHEMRISK».A DIVISION OF MCLAREN/HART , " AR3U3795 TABLE OF CONTENTS (CONT'D) LIST OF TABLES (CONT'D) . Table 4-6 Inhalation Toxicity Values for Potential Noncarcinogenic Effects Table 4-7 Route-Specific Absorption Efficiencies for COPCs , Table 4-8 Relative Absorption Factors for COPC Table 4-9 Dermal Permeability Coefficients for COPC Table 5-1 Summary of Hypothetical Carcinogenic and Noncarcinogenic Risks APPENDICES Appendix A PADEP Shenango River Surface Water and Sediment Sample Data Appendix B Hydrogeologic and Chemical Transport Summary Appendix C Screening for Chemicals of Potential Concern (COPC) Appendix D Calculations of Exposure Point Concentrations (EPCs) ' • . . Appendix E Modeling Approach for Estimating Indoor and Outdoor Air Concentrations of Volatile and Semivolatile Organic Compounds Originating from LNAPL or Groundwater ._/ Appendix F Modeling Approach for Estimating Indoor and Outdoor Air Concentrations of Chemical Originating from Soils , " . Appendix G lexicological Profiles Appendix H Carcinogenic and Noncarcinogenic Risk Calculations ' Appendix I EPA Comments on the Baseline Risk Assessment CHEMRisK*-A DIVISION OF MCLAREN/HART >1R;*()3796 1.0 INTRODUCTION AND PURPOSE On behalf of Westinghouse Electric Corporation (Westinghouse), ChemRisk*. the human health and ecological risk assessment division of McLaren/Hart Environmental Engineering Corporation was retained to prepare the following baseline human health risk assessment (HHRA) in support of the completed remedial investigation activities at Westinghouse's former Sharon,' Pennsylvania transformer plant. This report is a deliverable under the Consent Order and Agreement dated September 21, 1988, between Westinghouse and the Pennsylvania Department of Environmental Resources (PADER) (now the Pennsylvania Department of ^Environmental Protection (PADEP)) for the performance of a Remedial Investigation/Feasibility Study (RI/FS). The final RI site report, prepared by Cummings/Riter Consultants, Inc. (CRC), was approved by PADEP (after consultation with the U.S. Environmental Protection Agency (EPA)) in its May 24, 1996'transmittal to Westinghouse. This HHRA relies extensively upon site information contained in the RI report, earlier site^ investigation reports, and pertinent information provided by PADEP and EPA in various investigation activities conducted by the Agencies, as well as comments articulated during the review period of the RI report. Because of the interrelationship between this assessment and information contained in the RI Report, and its supporting Appendices, the reader is encouraged to consult both documents to obtain a, broader understanding of site conditions. Moreover, the approach utilized in this report has been reviewed and approved by PADEP in comments issued on the Data Evaluation Report (submitted April 5, 1996) and the Risk Assessment Conceptual Site Model (submitted June 27, 1996). EPA and PADEP have extensively reviewed the Baseline Human Health Risk Assessment. In response to PADEP and EPA comments, Westinghouse has revised this Baseline Human Health Risk Assessment accordingly. On September 30, 1996, Westinghouse received a first set of comments and responded with a revised risk assessment (November 26, 1 997 submittal). EPA and i j o\aiEOTs\wEsTwoH\]99i\«sEciwpD • 1-1 CHEMRISK* - A SERVICE OF MCLAREN/HART PADEP submitted a second set of comments to Westinghouse on February 10, 1998. Additional comments on the air modeling component of the risk assessment were also submitted on March 11, 1998. All EPA and PADEf comments as well as Westinghouse's response to those comments are attached to this report as Appendix I (please note that since the preparation of this report, Westinghouse has become CBS Corporation (CBS) and is referred to as such in most documentation dated after January 1, 1998). When reviewing this document, therefore, the reader is strongly encouraged to read Appendix 1. ' In most cases, the comments contained in the Agencies February 10 letter to Westinghouse have been incorporated into this report. Where comments have not been specifically incorporated, the appropriate discussion points are included in Appendix I. Westinghouse did not make some changes • / • - • to the risk assessment because they were determined not t•o j significantly change the overall risk results. In fact, in most cases, PADEP, EPA, and Westinghouse are in complete agreement about the results of this Human Health Risk Assessment The only exception is unrestricted worker access to the Moat. Because Westinghouse did not consider unrestricted access a baseline condition (due to institutional controls already in place), this exposure scenario was not evaluated in this risk assessment. Nevertheless, the revised Table 5-1 clearly identifies the risks to this receptor, as estimated by EPA. Westinghouse has also agreed to address hypothetical unrestricted.worker access to the Moat in the FS. ' ' 1.1 SITE BACKGROUND The RI report presented a detailed summary of historical and current site background information. In brief, the nearly 58 acre plant site has had a long history of industrial use, including iron foundry manufacturing and flour milling dating back to the mid-1800s when a branch of the Erie Canal passed through what is today referred to, on-site, as the moat. Westinghouse acquired the property from the Savage Arms Corporation in 1922, and operated it over a period of 62 years until it ceased operation in 1984. The Sharon plant produced distribution transformers, power transformers, and related electrical apparatus. During World War II, two-thirds of the facility was used and controlled by the United States government for manufacturing activities in support of the war effort. Specific activities included development and production of underwater ordinance and radio and radar transformers and transformer cores (CRC; 1996). G*LIENTS\WESTINC*l In November 1980, the facility qualified for Interim Status under Subtitle C of RCRA when Westinghouse filed a Notification or Hazardous Waste Activity and Part A of a RCRA Permit Application to treat, store or dispose of hazardous waste. Westinghouse withdrew the Part A Permit Application in July 1983 and converted to generator-only status. < . Westinghouse Originally submitted an NPDES permit application in 1972, Section 1.5.1 oftheRI contains a detailed discussion of the NPDES permitted outfalls since 1981. ' In July 1983,,EPA conducted an inspection of the facility pursuant to the Toxic Substance Control Act (TSCA). In April 1985, PADER issued Westinghouse an Administrative Order to undertake a subsurface investigation to determine the horizontal and vertical extent of impacted groundwater and soil (final report submitted by Westinghouse in September 1986), and for Westinghouse to submit a Proposed Plan and Schedule for the cleanup of contaminant impacted soils and groundwater (submitted by Westinghouse in October 1986). . The site was proposed for inclusion on the National Priorities List (NPL) in June 1 988 and was listed on... th. e NPL in Augus. t 1990. . . '• In September 1988, Westinghouse entered into a Consent Order and Agreement with PADER to conduct an RI/FS to determine the nature and extent of contamination at the site. In May 1990, Westinghouse requested permission to extract and dispose of light non-aqueous phase liquids (LNAPL) from the site. In follow up to this request, hi February 1994, the EPA issued a Unilateral Administrative Order for the development and implementation of a Response Action Plan for the removal of LNAPL from groundwater underneath the tank farm in the Middle Sector in order to reduce the threat of off-site migration of the LNAPL. A Pilot Study report and addendum letter was approved by the EPA in August 1995., 1.3 URJBAN RENEWAL LAND USE PLAN The Westinghouse site is part of an industrial re-development and expansion program under the direction of the Shenango Valley Industrial Development Corporation and Perm Northwest Development Corporation (CRC, 1996). Since the facility's closure in 1984, Westinghouse has I ; OACLIENTS\WESTINGH\l»IVWSEClWPD l'3 CHEMRISK* - A SERVICE OF MCLAREN/HART worked in partnership with state and local public and private interests to identify alternative beneficial uses of the buildings and property. Several buildings formerly owned by Westinghouse are now used by other firms to manufacture and store inventory, including: Armco Steel, which owns and occupies the large building north of Clark Street along Sharpsville Avenue (Refer to Figure I -1); Winner International which owns and occupies the former Westinghouse building south of the Middle Sector Buildings on Sharpsville, Avenue; and, the Shenango Valley Industrial Development Corporation, which owns and occupies the building south of the Middle Sector Buildings near the moat. The Middle Sector Buildings are also being considered for industrial re- development. V 1.4 RISK ASSESSMENT CONCEPTUAL SITE MODEL On May 22,1995, ChemRisk submitted a conceptual site model (CSM) outline to the Agencies for » . the prospective human health and ecological site risk assessments. The purpose of this submission was to provide PADEP and EPA with a preliminary evaluation of key site exposure assessment issues and to establish a dialogue on other pertinent risk assessment matters. During a group (PADEP, EPA, Westinghouse, CRC, and ChemRisk) meeting on June 11, 1996, ChemRisk presented a refined CSM for the HHRA and stand alone ecological risk assessment (ERA), taking into consideration issues raised by the Agencies during comments received by Westinghouse on the draft RI Report and on the site Risk Assessment Data Evaluation Report, which ChemRisk submitted on April 5,1996. Final revisions to the CSM were submitted to the Agencies on June 28,1996, and subsequently approved by PADEP on August 15,1996. The CSM identified six sectors as illustrated in Figure 1-1 where possible exposure could occur to site-related compounds: (1) River Sector, (2) North Sector, (3) Middle Buildings Sector, (4) South Sector, (5) Moat Sector, and (6) Railroad Right-of-Way. Accordingly, with the exception of the groundwater exposure evaluation, the sampling data discussion in Section 2.0 to follow has been organized to reflect these sector groupings. 1 -4 CHEMRISK* • A SERVICE OF MCLAREN/HART tfU03800 2.0 DATA EVALUATION As noted above, on April 5,1996, ChemRisk submitted a Risk Assessment Data Evaluation report to PADEP and EPA. This report was prepared in response to PADEP's request for the data assessment section of the HHRA, prior to submission of the complete HHRA report. Upon review of the Data Evaluation report, PADEP and EPA prepared comments and submitted them to Westinghottse in a May 24, 1996 response letter. ChemRisk revised the data evaluation in this HHRA based on the procedures agreed to during the group meeting on June 11,1996 at PADEP's Meadville, PA, office, and in writing on August 15,1996. ..'•"• i ... The data evaluation discussion presented below is organized into the following four primary sections: • General Data Discussion • Data Grouping for Quantitative Baseline Risk Assessment • Qualitative VDat, a Summary . ; . • • Selection of Chemicals of Potential Concern (COPC) '••.n.. . The general data discussion section briefly describes the various stages of data collection for the Westinghouse site and the useability of the data for the baseline HHRA. The data grouping section presents the organization of quantitatively useable data by exposure sector and/or by exposure media. Data that were determined to be unacceptable for use in the quantitative evaluation are summarized in the qualitative data summary section. Finally, ChemRisk discusses the procedures used to select the COPCs for each media. 2.1 GENERAL DATA DISCUSSION ' i •. • . . - . N This section siurtmarizes the analytical data collected during the different stages of site investigation at the Westinghouse site and the procedures used to assess the useability of those data (Le., validation 2-1 CHEMRISK* - A SERVICE OF MCLAREN/HART R i 0 38 0 procedures). Based on the data useability evaluation, ChemRisk identified data to be used for the quantitative portion of the HHRA as well as those to be used solely for qualitative discussion purposes. Section 4.0 of the RI Report (CRC, 1996) presented an extensive discussion of the various sampling programs and analytical results which collectively comprised the site remedial investigation. Additional indoor air sampling was also conducted subsequent to the RI. Indoor air sampling locations and procedures are provided in the Air Monitoring Plan Middle Sector Buildings Former Transformer Facility, Sharon Pennsylvania (CRC, 1997). The reader is encouraged to consult these reports for specific sampling details. Environmental sampling and analyses efforts were conducted during the RI in order to characterize the overall physical setting and characteristics of soils, sediments, surface water and groundwater. The RI was performed in three phases; Phase IA, IB and II. The Phase IA/IB sampling program included a determination of site migration pathways and analyses of groundwater, light and dense non-aqueous phase liquids (LNAPL and DNAPL), surface and subsurface soils, water and sediment in area storm sewers and Shenango River sediment. Phase II included additional sampling and analysis of sofls, groundwater, LNAPL and DNAPL, surface water and sediments, in addition to an ecological characterization and an industrial/residential well survey. Samples were analyzed for select target compound list (TCL) organics, volatile organic compounds (VOCs), semi-volatile organic compounds (SVOCs), pesticides/polychlorinated biphenyls (PCBs), dioxins and furans, and target analyte list (TAL) inorganics (metals and cyanide). Phase IA, IB, and H were conducted in accordance with their respective Agency-approved Field Sampling Plans (Rizzo Associates, 1989a; 1992) and the Field Sampling Plan Addendum (Revision 4.0) (CRC, 1994), also approved by the EPA and PADEP. Details relating to specific sampling and analytical methods employed were presented in the Quality Assurance Project Plan (QAPP) (Rizzo Associates, July 1989b). Data obtained from the Phase IA, IB, and II sampling efforts were reviewed for use in this HHRA. As discussed with and agreed to by the Agencies during the June 11, 1996 Westinghouse project meeting, because the Phase IA data were not collected with the specific purpose of supporting a risk assessment (the primary purpose of Phase IA sampling was to define media-specific chemicals of interest for the subsequent RI/FS), it was concluded that these data should not be used quantitatively in the HHRA. Nevertheless, these data do provide important information that are considered on a qualitative level throughout this report. • Phase IB analytical data were validated by Rizzo Associates in 1992 in accordance with USEPA National Functional Guidelines for Organic Data Review (Revised June 1991) and Laboratory Data 2-2 CHEMRISK* - A SERVICE OF MCL.AREN/HART HJ3802 Validation Functional Guidelines for Evaluating Inorganics Analyses (July 1988). The Phase IB data were revalidated in 1995 by QSEA and CRC with respect to blank evaluation procedures found in the USEPA Region in Modifications to the Functional Guidelines for organics (September 1994) and inorganics (April 1993). Phase II analytical data were validated by STAT in 1994 in accordance with the Region HI Modifications to the Functional Guidelines for organics (June 1992) and inorganics (April 1993). STAT reevaluated the Phase II data in 1995 with respect to blank evaluation procedures in the September 1994 (organics) and April 1993 (inorganics) Region III Modifications to the Functional Guidelines. Because the datasets and CSM were approved by PADEP on August 15, 1996, both Phase IB and II data are used quantitatively in this HHRA. The indoor sampling was conducted on October 2, 199? to assess the current indoor air quality of the Middle Sector buildings. Samples were collected and analyzed for volatile organic chemicals and PCBs. These data have been validated in accordance with the Region HI Modifications to the : Functional Guidelines for organics and are used quantitatively in the HHRA. i 2.2 DATA GROUPING This section addresses the organization of sampling data by exposure sector (as noted on Figure 1-1) or, in the case of groundwater, by different groundwater zones (i.e. , Alluvial Central plume, Alluvial Southern plume, and bedrock aquifer). The sampling data used in the data groupings are limited to those identified as useable for quantitative assessment as described above. The dataset used quantitatively in this HHRA consists of data from Phase IB and Phase II of the RI and the 1997 indoor air sampling data, as these data were intended to document the nature and extent of chemical constituents in consideration of potential exposure pathways, and were subject to validation measures consistent with the most recent relevant Region III modifications to the National Functional Guidelines. Moreover, as agreed upon with PADEP and EPA, PADEP split sample surface water and sediment data, which contain a longer list of analytes compared to the RI media sampling results. were used to augment the RI data. Although a substantial amount of additional pertinent site data are available, including earlier site investigation data, PADEP fish data, and EPA residential soil sampling data, it is qualitatively addressed in this report due to its incompatibility with the most recently validated Phase IB and Phase II RI data. iwwttAp^^ 2-3 CHEMRISK* - A SERVICE OF MCLAREN/HART V • ' '. •: '.- 1RUJ3803 In preparation for the HHRA, at PADEP and EPA's request, a final conceptual site model (CSM) and validated dataset for use in the HHRA was submitted on June 28, 1996, and subsequently approved by PADEP on August 15, 1996. The final CSM laid out all of the receptors to be characterized in the HHRA, the exposure factors to be used in the exposure equations, and the various data groupings either by sector or groundwater zone. As a result of PADEP agreement and approval of the data groupings, the remainder of this section summarizes the specific data points (tabulated in Table 2-1) used in the various data groupings. 2.2.1 River Sector Although not included in the Phase II Sampling Plan, Westinghouse agreed that the Shenango River sediment and surface water split samples collected by PADEP, and analyzed for a wider array of constituents,- could be used to augment the RI data (Westinghouse data) in the HHRA. For sediments, PADEP collected a total of eleven samples, and one duplicate, corresponding to RI Phase n sediment sampling stations 11 through 17. Sediments were analyzed for TCL/TAL parameters plus dioxins and furans. The analytical results were previously summarized in Table 3 of Appendix I in the RI Report (CRC, 1996), and are reproduced in Appendix A of this document. The RI reported the surface water analytical results for only those chemicals that were identified in the FSP and approved by the agencies (the surface water target analyte list). Subsequent to the RI J approval EPA invalidated the surface water data, and, in some cases, reported analytical results that differed from those reported in the RI. In addition, EPA reviewed the results of chemicals that were not included in the surface water target analyte list. For this assessment, only the chemicals included in the surface water target analyte fist identified in the FSP and reported in the RI are used. However, EPA has evaluated the result of non-target analyte list chemicals by comparing these results to the Region HI RBCs for tap water. EPA reports that lead, chloroform, heptachlor, and dieldrin exceed the Region HI Tap water RBC in at least one surface water sample collected upstream of the Westinghouse facility, and that trichloroethene, chloroform, heptachlor, heptachlor epoxide, and aldrin exceed the Region in Tap water RBC tn at least one surface water sample collected downstream of the Westinghouse facility. This HHRA assesses risk only from potential exposure to shallow sediments (0 to 6 inches deep), as exposure to deeper sediment (6 to 50 inches) for prolonged durations is highly unlikely. Thus, three PADEP sediment data points were eliminated from this assessment: Sed()4B (6 to 30 inches deep). 2-4 CHEMRISK* - A SERVICE OF MCLAREN/HART SedOSB (6 to 50 inches deep), and Sed07B (6 to 50 inches deep). All remaining PADEP sediment data points are used in the HHRA and are summarized in Table 2-1 • ' .... • • ' ' Three surfece water samples were also collected by PADEP from the Shenango River. The PADEP samples were collocated with the RI surface water sampling locations SW-12, SW-14, and SW-17 (PADEP, 1996a). Their locations are denoted on Figure 2-2 of the RI report and detected - concentrations summarized in Table 2-2 of this report. In an effort to determine whether the surface water exposure pathway could pose a potential health . \ . risk for the hypothetical consumption of river water (conservatively assuming no water treatment); ChemRisk compared PADEP up river (W04), cross river (WTP03), and down river (W02) sampling locations to chemical-specific drinking water ingestion values (Le., MCLs, SMCLs, MCLGs, and Region in risk-based tap water criteria). It should be recognized that both MCLs and Region HI RBCs are based on conservative residential exposure factors, which assume that an individual is consuming up to 2 liters/day over a 30-year period. Because the likelihood is exceedingly low that an individual would actually be consuming untreated river water for this duration, this screening comparison is highly conservative. . As shown in Table 2-2, all three sampling stations exceed secondary maximum contaminant levels i j (SMCLs) for aluminum, iron, and manganese; however, these criteria have been developed primarily to address aesthetic characteristics (e.g., taste, odor, and color) (EPA, 199 la). Indeed, none of these compounds exceeds its respective Region III Tap Water RBC at any of the three stations, indicating that the measured concentrations do not pose a potential health risk. Arsenic was the only compound *•* that exceeded the Region III Tap Water RBC. All three sample stations were reported to have similar concentrations (4.2 to 4.4 Mg/L), all of which were well below the MCL for arsenic of 50 Mg/L. In addition. EPA has noted that several additional chemicals not on the surface water target analyte list exceeded their RBC for tap water. Similarly, the RI Report indicated that in 1988, PADER (currently known as PADEP) conducted PCB surface water sampling at the Shenango Valley Water Company intake/located approximately 1,600 feet downstream from the Clark Street Bridge. Analytical results indicated that PCB concentrations were below the method detection limits in raw river water, treated water, filter backwash water, and filter backwash sludge (CRC, 1996). Other more recent surface water analyses ' (1990; 1991; 1994) conducted by the Shenango Valley Water Company on raw intake water, substantiates the lack, of site-related effects on Shenango River water. 2-5 CHEMRISK* - A SERVICE OF MCtAREN/HART /IRMJ3805 Based on these comparisons, it can be concluded that river surface water is not impacted by site- related chemicals. Because PCBs are more likely to settle and accumulate in sediments rather than be retained in the water column, river surface water as a potential exposure medium was eliminated from further consideration in this HHRA. While consumption offish in the Shenango River proximate to the site was not raised as an exposure pathway of concern by PADEP or EPA during negotiations and finolization of the approved site Field Sampling Plans, Westinghouse is aware that PADEP has collected and compited fish data over several years (1979. 1982, 1988, and 1992) (PADEP, 1988; 1995). Moreover, the Pennsylvania Fish and Boat Commission (PFBC) has produced a report entitled, Analysis of Fish Tissue Contaminants Near the Westinghouse-Sharon Superfund Site (PFBC, 1995) using PADEP's fish data. However, these data do not appear to have been validated according to CERCLA and EPA Region III data validation protocols. Moreover, the data are not sufficiently site-specific to be directly correlated to Westinghouse site conditions; the data are more appropriate to assess conditions in general along a substantial length of the Shenango River system with multiple potential sources of PCBs and other constituents. Section 3.3.1.2 of this document presents a more detailed discussion of the PFBC (1995) study findings and conclusions. 2.2.2 North Sector As noted in the RI, the North Sector building (currently occupied by Armco) was used principally for the final packaging and shipment operations at the Westinghouse facility. Soils within the North sector are covered with asphalt, concrete, and a building. Each of these physical attributes help to ensure that direct human contact with soil is very limited. Although several surface and subsurface soil samples have been collected in the North Sector, the data from these samples were obtained outside the scope of the RI and approved dataset and are not appropriate for use in the quantitative assessment in the HHRA. These data are, however, used in a qualitative manner to ascertain the likely conditions that would be experienced in the North and South Sectors. 2-6 CHEMRISK* - A SERVICE OF MCLAREN/HART 11)3806 2.2.3 Middle Sector Substantial subsurface soil and groundwater sampling investigations have been conducted in the Middle Sector, either prior to, or during the site RI. Because groundwater contamination in this location extends beyond Westinghouse's property boundary, it was agreed that the HHRA would assess potential risk via groundwater plume delineation in lieu of sector groupings. Accordingly, groundwater plume data point groupings are discussed separately in Section 2.2.7. As agreed upon by PADEP and EPA in their approval of the Field Sampling Plan, limited subsurface soil sampling data were collected from within the Middle Sector during the RI. However, a substantial number of subsurface soil borings were advanced through the A/B Slab area, which is located immediately adjacent to the Middle Sector. Thus, these data are used in the HHRA to evaluate potential risks to contaminants in Middle Sector subsurface soils. Table 2-1 shows the combined subsurface soil sample locations from within the AB Slab area and Middle Sector .used in theHHRA. To evaluate potential inhalation risks related to chemical vapor migration from groundwater into the Middle Sector Buildings, Westinghouse estimated potential inhalation exposures for two scenarios; the future employee and the indoor construction worker. For the future employee, Westinghouse i , relied on the indoor air sampling data collected on October 2, 1997. For the indoor construction worker, Westinghouse relied on the vapor transport modeling alone to estimate potential inhalation • exposures. As agreed upon by PADEP and EPA during the June 11,1996 project meeting, vapor phase transport modeling used to evaluate indoor air exposures conservatively assumes that the elevated contaminant concentrations present in LNAPL in groundwater beneath the Middle Sector • extends Over an area equal to the entire floor area within the Middle Sector. Consequently, all indoor Middle Building vapors from non-soil contaminant sources is assumed to originate only from LNAPL. , Corresponding air sampling data used to evaluate future employee risks, and data used to model groundwater/LNAPL related vapor flux into the Middle Sector ore shown in Table 2-1. In 1995, USEPA Region III completed a risk assessment of the interior of the Middle Building Sector. As noted in the report, the building is currently inactive and is fenced and guarded to ensure that unauthorized individuals do not gain access. EPA concluded that lead and PCBs in dust, and PCBs on certain surfaces were elevated, and that these levels could pose a health risk to future occupants. In the event that the building were to be used and occupied prior to cleaning and refurbishing, Westinghouse would view the safety and health Issues relating to its use and occupancy 2-7 CHEMRISK*-A SERVICE OF MCLAREN/HART as felling under the purview of OSHA, and not CERCLA. Westinghouse intends to address interior building issues in parallel with implementation of the site Feasibility Study (prior to use and occupancy of the building). 2.2.4 South Sector As noted in Section 2.2.3. the subsurface soils database for the South Sector consists of a considerable number of shallow borings advanced in the AB Slab area. These data were used in the HHRA as a conservative indication of potential risks associated with subsurface soil constituents throughout South Sector soils. The individual soil boring locations are summarized in Table 2-1, and ore depicted in Figure 2-1 of the RI Report. 2.2.5 Moat Sector As described in Section 6.1.1 of the RI Report, impacted Moat Sector soils have been partially remediated. However, constituents remain in surface and subsurface soils. Relevant sampling data for inclusion in the Moat Sector exposure assessments are shown in Table 2-1. 2.2.6 Railroad Right-of Way (ROW) The data grouping summary for the Railroad ROW Sector is shown in Table 2-1 (sampling locations are shown in Rgure 2-1 of the RI Report). All surface soil sampling data collected along the railroad right-of-way were retained in the risk assessment database. V In addition, EPA raised the possible concern that children walking along the railroad ROW might be exposed to site-related chemicals from storm water runoff during and after storm events. Accordingly, Westinghouse agreed that the HHRA should quantify hypothetical risks for this receptor and exposure pathway. As a worst-case measure of possible risk from contacting storm water runoff, sampling data results from within three storm water sewers where storm water leaves the Westinghouse site were considered (SW-5, Clark Street Sewer; SW-7, Franklin Street Sewer; and SW-9, Wishart Court Sewer). These data points are shown on Table 2-1. 2-8 CHEMRISK* - A SERVICE OF MCLAREN/HART tiR3()3808 2.2.7 Groundwater Data Grouping As agreed upon with PADEP. hypothetical groundwater baseline risks were evaluated from three separate and distinct groundwater groupings. The groupings were designed to reflect contamination patterns at the site. The first is primarily a PCB/chlorobenzene plume, which is within the alluvial aquifer and is located along the western border of the Westinghouse site. The second plume, primarily containing solvents, is also in the alluvial aquifer but it is located in the southern portion of the site. Finally, the third groundwater grouping represents the bedrock aquifer. Groundwater in the alluvium occurs under unconfined conditions across the site. Depth to groundwater ranges from two to 20 feet below grade, and averages approximately ten feet below grade. Groundwater in the alluvium generally flows west-southwest toward the Shenango River. Flow in the confined, bedrock aquifer is controlled primarily by fractures which direct the bedrock groundwater flow to the west-southwest (CRC, 1996). Although both hydrogeologic units are characterized as flowing west-southwesterly, no apparent impact to the Shenango River has occurred via this pathway. Further detail regarding local groundwater flow and contaminant transport is provided in Appendix B. .2.2.7.1 Alluvial Central Plume - * ^^ Groundwater sampling data for the central plume were aggregated as shown in Table 2-1. The groupings were approved by PADEP in an August 15, 1996 letter. The datapoints which comprise the central plume grouping represent sampling locations not impacted by light nonaqueous phase liquid (LNAPL). Because LNAPL in groundwater in this plume is the subject of a CERCLA removal action, and because the aesthetic characteristics of LNAPL would render its consumption improbable, the central plume grouping only includes data points that are not within the lateral extent of the presently defined LNAPL layer. • 2.2.7.2 Alluvial Southern Plume Datopoint groupings representative of the southern plume are shown in Table 2- 1 . As with the central plume datapoint grouping, the southern plume sample locations were previously accepted by PADEP in a letter dated August 15, 1996. Generally, the alluvial southern plume contains chemicals that differ from those found to predominate in the central alluvial plume. For example, 1 ,2-dichloroethene, 1 ,2- \ ' ' ' 2-9 CHEMRISK" - A SERVICE OF MCLAREN/HART rtR.iu3809 dichbroethane, 1,1,1-trichloroethane, and methylene chloride were undetected in the wells identified as southern alluvial aquifer wells. In addition, PCBs, which are predominant in the alluvial central plume, are detected in only one well associated with the alluvial southern plume. Because of the difierences in chemical constituents and the fact that each plume may need to be addressed differently in the feasibility study, the decision was made to differentiate between the two plumes in the HHRA. This decision was supported by PADEP and EPA during the June 11 meeting, and subsequent approval of the revised CSM on August 15. 2.2.7.3 Bedrock Aquifer Beneath the alluvium lies a relatively impermeable strata of glacial till material, and beneath that lies the shale and sandstone bedrock (CRC, 1996). Because the glacial till acts as an aquatard , preventing substantial vertical migration of overburden groundwater, the bedrock aquiier is considered separately in this assessment. Table 2-1 contains the datapoint groupings representative of the bedrock aquifer; these locations were also approved by PADEP in a letter dated August 15, 1996. 2.3 QUALITATIVE DATA SUMMARY As discussed in Section 2.1, all data collected at the Westinghouse facility prior to the Phase IB RI was not validated to the extent deemed necessary for use in the quantitative assessment of this HHRA. This results in some nonvalidated data that cannot be used to quantify human health risks. This data con, however, be used to identify a general trend for a particular area or medium, and can also be used to provide additional support to the results of the quantitative portion of the HHRA. Therefore, a summary of the pre-Phase IB data is provided for those sectors where data are available. 2.3.1 North Sector As described on pages 1-33 and 1-34 of the RI (CRC, 1996), an earlier environmental assessment of the North Sector was completed by Clement Associates, Inc., in December 1985, prior to the transfer of the North Sector building and real estate. PCBs were the principal constituent of interest of that investigation. Four shallow (1.0 to 1.5 foot deep) soil borings were hand augured along the railroad tracks, with PCB (Aroclor 1260) concentrations ranging from 32 to 180 mg/kg. Twenty-eight surface soil samples were collected from the some general area and from a parking lot adjacent to the railroad tracks. PCB Aroclor 1260 concentrations ranged from < 1.0 mg/kg to 95 mg/kg, while Aroclor 1242 concentrations ranged from < 1.0 mg/kg to 330 mg/kg. Scrape samples from an area identified as a 2-10 CHEMRISK* • A SERVICE OF MCLAREN/HART zone of probable PCB contamination were reported to contain Arbclor 1260 in concentrations ranging from 1.4 to 470 mg/kg, Aroclor 1248 at 5.4 nig/kg, and Aroclor 1242 at 5.7 mg/kg fo 120 mg/kg (Clement Associates, Inc., 1985). As a result of this investigation, all exposed surficial soil areas were paved. In 1986, Rizzo Associates performed a site-wide subsurface investigation. In the North Sector, seven borings were advanced in preparation for .the installation of groundwater monitoring wells, located adjacent to potential source areas. Analyses of subsurface soil from those borings indicated that PCBs, trichlorobenzene, trichloroethylene, and total xylenes were not detected in soil (Rizzo Associates, 1986). Methyl ethyl ketone was detected at low levels in soil (< 1 ppm) from a single boring (N-6), along with toluene (up to 54 ppb) and oil and grease (up to 160 ppm) (Rizzo Associates, 1986). 2.3.2 Middle Sector During the 1986 Rizzo Associates subsurface investigation, PCBs greater than 50 mg/kg (up to 2,200 mg/kg) were detected in seven borings advanced in preparation for the installation of groundwater monitoring wells, located adjacent to potential source areas. Four out of seven borings were reported to contain less than or equal to 50 mg/kg PCBs (Rizzo Associates, 1986). Trichlorobenzene was detected in 12 of 105 soil samples from the Middle Sector, with only a single elevated sample (1,700 L j mg/kg); the remainder of the samples had low-level (ppm) trichlorobenzene concentrations (Rizzo Associates, 1986). Trichloroethylene was detected in eight of 105 samples from four borings, with reported concentrations all less than 1 mg/kg (Rizzo Associates, 1986). Trace concentrations of xylenes were also found in three borings. Finally, oil and grease was detected in 21 soil samples from 11 Middle Sector borings, with reported concentrations up to 22,000 mg/kg (Rizzo Associates, 1986). 2.3.3 South Sector The 1986 Rizzo Associates subsurface soil investigation also included some limited soil analyses from four monitoring well borings located in the South Sector. The borings were advanced in preparation for the installation of groundwater monitoring wells, and were located adjacent to potential source areas. Approximately 93 percent of the samples were nondetect for PCBs. For samples containing PCBs, concentrations up to 8 mg/kg were detected (Rizzo Associates, 1986). Trichlorobenzene and toluene were detected in a single sample (6.1 and 0.07 mg/kg, respectively); methyl ethyl ketone was not detected in South Sector soils. 2-11 CHEMRISK"-A SERVICE OF MCLAREN/HART ifUQ38l I 2.3.4 EPA Residential Soil Sampling Program As described in Section 1 of the RIf in 1994, EPA conducted on off-site surface soil sampling program to assess whether site-related chemicals from Westinghouse had migrated off-site to nearby residential, commercial and industrial properties. In all, 31 soil samples were collected and analyzed for PCBs, pesticides, metals, cyanide, volatile organics, semi-volatile organics; dioxins and dibenzo furans were analyzed at a select subset of sampling locations (R. F. Weston, 1994). On March 1,1995, a lexicologist within EPA's Technical Support Section summarized this group's interpretation of the analytical results in a memorandum to the EPA Remedial Project Manager. That memorandum concluded that lead was elevated in two sampling locations, while PAHs were elevated in three locations; the remaining surface soil sampling data did not indicate the presence of chemicals in concentrations that would constitute a potential "emergency situation". Most recently, EPA (1997) commented that "most residential yards ore associated with Hazard Indices and cancer risks at or below the target risks specified in the NCR" Moreover, EPA stated that "the pattern of contamination found at the Westinghouse site was not observed in residential soils, particularly the high levels of PCBs." Through various transmittols and meetings with PADEP and EPA, Westinghouse agreed to include a qualitative discussion of EPA's study results and significant conclusions in the HHRA. Accordingly, the discussion which follows fulfills this commitment. Lead Results EPA commented that two sampling locations had total lead concentrations exceeding 1,000 mg/kg, and that these results raised a potential health concern for children and pregnant women. However, as EPA is aware, a primary source of lead in urban environments is lead-based paint that has been removed or weathered from older structures and left in surface soil surrounding the buildings. Surface transport of this deposited lead is possible via surface water runoff and wind erosion. Other potential sources of lead in surface soil include runoff from roadways once contaminated by tetra ethyl lead (a former gasoline anti-knock additive) in vehicular exhaust particles deposited on roadways. Thus, while EPA's elevated surface soil lead concentrations may affirm the presence of lead in this urban setting, the results do not provide definitive conclusions regarding the source of the lead. In addition, the lead results do not provide an indication of overall or average lead levels that might occur in soils, further increasing the uncertainty surrounding these results. 2-12 CHEMRISK" - A SERVICE OF MCLAREN/HART PAHs It was noted by EPA in the March 1995 memorandum that PAHs were detected in most of the surface soil samples, and were elevated in three locations distant from one another. EPA stated that t4these chemicals, which are formed from the combustion of organic material, occur in the environment both as naturally occurring chemicals and as ubiquitous anthropogenic chemicals. ,They are common environmental contaminants, especially in urban areas." Westinghouse agrees with EPA's observation concerning the apparently universal nature of PAH contamination in urban environments. Indeed, with PAHs present in asphalt road and roofing material, in various petroleum products, and in most burned materials (including combusted wood, coal, garbage and other organic matter (ATSDR, 1995)), it is not surprising that they have been identified in surface soil in the general environment surrounding the Westinghouse site. As a result, little can be said about the overall or average concentration of PAHs in soils. The random nature of the locations of the three elevated surtace soil samples suggests that there are likely multiple potential sources of these chemicals. There is no association that can be established between these elevated sampling stations and their location with respect to the Westinghouse facility. Other Contaminants Finally, aluminum, antimony, arsenic, beryllium, chromium, manganese, zinc, and pesticides were reported by EPA to exceed their conservative residential (Region III) risk-based screening criteria for chronic exposure, but not their respective threshold concentrations used to identity imminent hazard conditions. With the exception of zinc, the four surface soil samples (S 28 through S 31) that EPA's contractor (Weston) identified as background samples were reported to contain similar concentrations of these same compounds (note: ChemRisk was unable to ascertain pesticide qualitative trends in the four background samples, as these data were missing from the September 28, 1994 Region III Data QA Review). In summary, there is no evidence that elevated surtace soil concentrations reported for the off-site soil sampling program ore related to the Sharon site. 2.4 SELECTION OF CHEMICALS OF POTENTIAL CONCERN An early step in a baseline human health risk assessment is the identification of chemicals of potential concern (COPC). The purpose of identifying(COPC is to properly focus the assessment on those chemicals which comprise a significant fraction of the theoretical risk. Guidance on the selection of COPC is presented in the EPA's Risk Assessment Guidance for Superfund Volume I, Human Health Evaluation Manual (Part A) - Interim Final (RAGS) (EPA, 1989a). Additional guidance is provided 2-13 CHEMRISK*-A SERVICE OF MCLAREN/HART AR3U38I3 in EPA Region Hi's Technical Guidance Manual "Selecting Exposure Routes and Contaminants of Concern by Risk Based Screening" (EPA, 1993a). EPA Region III suggests modifications to the COPC selection methodology discussed in RAGS by stipulating that, at the earliest stages of the baseline risk assessment, compounds that do not contribute significantly to the overall risk posed by exposure to contaminated media should be identified and excluded from further consideration. According to Region HI, this process should follow a tiered COPC selection system that first excludes compounds not detected in any environmental media, and retain only those compounds present at levels that may be associated with potential risks. This analysis relied upon EPA's tiered methodology to derive site- and sector-specific COPC. As diagramed in Figure 2-1, the first step in the data reduction process involved identification and selection of compounds detected at least once in each of the media evaluated. Thus, all nondetected compounds were eliminated from further consideration. Similarly, consistent with EPA (1989a), sample concentrations that were identified as potentially resulting from laboratory contamination were not considered positive results, and were therefore assumed to be non-detect in the selection of COPCs. The next step in the process involved identification and exclusion of human nutrients from the list of remaining compounds as recommended by EPA (1989a) which states that "compounds that are both essential human nutrients, and also present at low concentrations (e.g., only slightly elevated above naturally occurring levels) may be excluded from further consideration in the quantitative human health risk assessment". Nutrients contained in the dataset that were found to meet these criteria include calcium/'magnesium, potassium, and sodium. Although iron is an essential nutrient, high doses may be associated with adverse human health effects. As a result, iron was retained for quantitative analysis. Consistent with EPA guidance (EPA, 1989a; 1993a), further reduction of the chemicals of concern was accomplished by screening against EPA Region III Risk Based Concentrations (RBCs). The RBCs are published by EPA Region HI on a biannual basis, and provide conservative screening-level risk-based contaminant levels for a variety of exposure pathways and media. ChemRisk used the June 4, 1996 RBC tables provided by Region III (EPA, 1996a). As agreed during the group meeting on June 11, 1996, ChemRisk modified (adjusted) the RBC values based on noncarcinogenic effects for a Target Hazard Quotient (THQ) of 0.1 rather than the default THQ of 1.0. RBCs based on carcinogenic effects were not modified prior to comparison to the maximum detected chemical concentrations. 2-14 CM EM RISK" - A SERVICE OF MCLAREN/HART 2.4.1 Surface Soils Surface soils were screened for COPC in the Moat, and Railroad Sectors. Compounds in each of these sectors were conservatively screened against residential THQ adjusted RBC (even though the actual possible exposure might occur only through trespassing activities). COPC selection for these sections are summarized in Tables C-2 and C-3 in Appendix C. 2.4.2 Subsurface Soils Subsurface soils were screened for COPC in the South (AB Slab) and Middle Sectors, as well as the Moat. Compounds detected in subsurface soils were compared with Region HI industrial RBCs (with THQ adjustment, where appropriate). COPC selection for these sectors are summarized in Tables C-4 and C-5 in Appendix C. For indirect exposures to vapors and soil particles originating from subsurface Middle Sector soils, ChemRisk used the COPCs identified using the Region III industrial soil ihgestion RBCs (with THQ adjustment, where appropriate). The industrial RBCs were used because 1) no industrial-based soil to air inhalation RBCs exist; and 2) the daily dose of a chemical resulting from ingestion of soil is likely to be greater than that from volatilization or particle entrainment with subsequent inhalation. Thus, it was assumed that the COPC screen using the industrial soil ingestion RBCs was an appropriate alternative. 2.4.3 Sediments Region III has not developed RBCs based upon ingestion of sediments; therefore, Shenango River sediments were screened against THQ adjusted residential soil RBCs. COPC screening for Shenango River sediments is summarized in Table C-6 in Appendix C. 2.4.4 Storm Water Runoff Region III does not have risk based screening values based on dermal contact with storm water However, PADEP (1996b) maintains a table of Water Quality Criteria for Toxic Substances where surface water criteria for the protection of human health are defined for a specific effect (carcinogenicity, taste and odor, general human health). ChemRLsk used, the PADEP Water Quality HApwuEcrawEnwo»i99«DiLUTius\icrexT«ec3\sEciwpo 2- 15 CHEMRISK* - A SERVICE OF MCLAREN/HART 4R.HJ38I5 Criteria as screening values for this exposure pathway. The use of the PADEP Water Quality Criteria is appropriate because, for most chemicals, the criteria were derived to he protective of human health. Of the chemicals sampled for in the storm water runoff, only ehlorobenzene and xylenes had Water s—^ Quality Criteria derived based on a criterion other than human health (i.e., taste and odor criterion). Generally, it would be inappropriate to screen chemicals using a taste and odor criterion; however, both chlorobenzene and xylenes were not detected in the storm water runoff. The COPC screening for the storm water data is summarized in Table C-7 in Appendix C. 2.4.5 Groundwater . COPC selection for hypothetical groundwater exposures in each of the groundwater units (Alluvial Central, Alluvial Southern, and Bedrock) are summarized in Tables C-8 through C-10 in Appendix C. Unfiltered groundwater samples were used in the calculation of risks because these data are expected to more accurately represent potential exposure. Most individuals with private wells do not have extensive filtering systems and therefore, they might be exposed to the unfiltered concentration. Using the unfiltered samples is generally more conservative than using data from filtered samples. Groundwater COPCs for each groundwater unit were selected by comparing maximum detected concentrations of chemicals in groundwater within a unit to their respective THQ adjusted RBCs. If the maximum concentration of a chemical did not exceed its THQ adjusted RBC, it was excluded from ^_^> the risk .assessment. Compounds lacking RBC values were retained for further consideration in the risk assessment database. 2.4.6 Air For this HHRA, there are three air exposure pathways evaluated, the future employee, indoor construction worker, and the outdoor construction worker. For the future employee, air quality sampling data were evaluated against their respective THQ adjusted air RBCs. If the maximum concentration of a chemical did not exceed its THQ adjusted RBC, it was excluded from the risk assessment. Chemicals lacking RBCs were retained for quantitative assessment. Table C-ll of Appendix C summarizes the COPC screening for measured air levels. COPC selection for indirect exposures (i.e., inhalation of vapors) to chemicals in groundwater is conducted for two hypothetical situations, 1) vapors entering the Middle Building, and 2) vapors emitting from the ground surface outside of any buildings. As agreed in the June 11 group meeting, 2-16 CHEMRISK* - A SERVICE OF MCLAREN/HART ^^•^^ ,|R.(U38I6 the potential for vapors to enter the Middle Building is evaluated using the components of LNAPL found beneath portions of the Middle Building. Principal components of the LNAPI, are mineral oil and PCBs (Aroclors 1248, 1254, and 1260) (CRC, 1996). ChemRisk included all ot'.the detected Aroclor mixtures as COPCs for the indirect exposure assessment of LNAPL vapor. For indirect exposures to chemical vapors while outdoors, ChemRisk assumed that the vapors could originate from either the Alluvial Southern or Central groundwater plumes. COPCs for outdoor indirect vapor exposures were selected by combining the COP, C lists for the Alluvial Southern and the Alluvial Central groundwater plumes (Tables C-8 and C-9 in Appendix C); the list of COPCs was expanded to include all chemicals detected in either the Alluvial Southern or Alluvial Central groundwater plume. For indirect exposures to vapors originating from the groundwater, ChemRisk used the COPCs identified using the Region III tap water RBCs (with THQ adjustment, where appropriate). The Region HI tap water RBCs were used because I) no groundwater to air inhalation RBCs exist; and 2) the daily dose of a chemical resulting from ingestion of groundwater,is likely to be greater than that from volatilization with subsequent inhalation. Thus, it was assumed that the COPC screen using the Region III tap water RBCs was an appropriate alternative. i o.vuEyi3\wEsnNc»i««9KiEcn.wpD 2-17 CHEMRISK*-A SERVICE OF MCLAREN/HART ttR-303617 3.0 HYPOTHETICAL RECEPTOR ANALYSIS 3.1 IDENTIFICATION OF POTENTIAL EXPOSURES As noted in Section 1.3, six sectors (River, North, Middle Buildings, South, Moat, and Railroad Right-of-Way), and three groundwater zones, comprise the range of locations where humans may contact site-related COPCs at the Westinghouse site. EPA approved of these exposure locations in the August 15, 1996 approval letter. In summary, the following is a brief description of the geographical extent of each sector as denoted on Figure 1-1: River Sector encompasses the Shenango River from the Clark St. Bridge to the Wishart Court Sewer Outfall; North Sector: represents the northern portion of the site, north of Clark Street, including the Armco building (formerly Westinghouse) and the land westward to the railroad right-of- way (ROW); Middle Buildings Sector includes Westinghouse's Middle Buildings (parallel to Sharpsville Avenue) and the paved areas west of the building to the railroad ROW; South Sector includes the concrete foundation of the former Westinghouse A and B Buildings (AB Slab) immediately south of the Middle Buildings, and two former Westinghouse buildings now owned/operated by Winner International and the Shenango Valley Industrial Development Corp., respectively; Moat Sector: represents the moat from the fence under the Conrail railroad bridge at the southwestern corner of the Westinghouse Middle Buildings Sector to Wishart Court at the moat's southernmost end adjacent to Winner International; and, 3~ 1 CHEMRISK* - A SERVICE OF MCLAREN/HART Railroad ROW: includes the entire Conrail railroad ROW adjacent to the North and Middle \ Buildings Sector. The discussion which follows describes the potential human receptors who may be exposed currently or in the foreseeable future to COPC in the respective sectors and groundwater units. Table 3-i presents a summary of each of the receptors and the potential routes of exposure evaluated in the baseline risk assessment. .River Sector The Shenango River may potentially attract children to wade or swim in shallow portions of the river, or to play along the river bank and/or large storm sewer outfalls that discharge to the river in close proximity to the Westinghouse site. Accordingly, dermal contact and incidental ingestion of sediment and surface water-may be possible. Surface water contact or incidental ingestion exposures, white possible, are unlikely to be significant relative to direct contact sediment exposures. This is due to the fact that river surface water sampling results in the vicinity of the site (see Section 2.2.1) have generally demonstrated background levels (Le., no significant increase in site-related COPC surface water concentrations) of target analytes. Therefore hypothetical risks for the sediment pathway are •-.quantifie• ••••••d and• the rive• r surtac• • e wate•r exposur.••e— route s wil' l-.- not• b'••e addresse• - ••d: furthe.r in this •assessment • . A second potential hypothetical receptor relevant to this sector is a recreational angler who catches and consumes fish from the Shenango River in the general vicinity of the site. As agreed upon with PADEP and EPA, the fish ingestion scenario is evaluated qualitatively, as the sampling data compiled by PADEP is not sufficiently site specific, nor has it been validated to the degree required to permit a quantitative risk analysis. North. South, and Middle Buildings Sectors Potential exposures to COPC in the North, South, and Middle Building Sectors are expected to be similar, due either to their current industrial uses or, in the case of the Middle Buildings, their likely future industrial use. In the process of facility expansion/modification in any of these sectors, construction workers may inadvertently be exposed to COPC in subsurface soils via direct dermal contact, incidental ingestion, and inhalation of fugitive dust and vapors. As a conservative estimate of possible worker risks to COPC in all three sectors, the HHRA utilizes subsurface soil sampling 3-2 CHEMRISK* -A SERVICE 'OF MCLAREN/HART AR3038I9 , < data results from South Sector borings advanced through the concrete foundation of the former A and B buildings (AB Slab), directly south of the Middle Sector Buildings, and from one boring 1 I advanced in the former tank farm area west of the Middle Building. This dataset was selected (and approved by PADEP) as a screening surrogate because it represents an area where significant storage and handling of COPC is documented to have occurred, and thus constitutes a likely worst case possibility Of environmental release to subsurface soils. Exposure pathways to be evaluated under the hypothetical construction worker scenario include dermal contact, incidental ingestion, and inhalation of dust and vapor. These hypothetical exposure pathways are quantified for both an interior and exterior construction worker exposure scenario. A second receptor of concern applicable to each of these three sectors is an employee working in an industrial enterprise, subject to potential inhalation exposures from impacted soil and groundwater beneath buildings in the three sectors. Accordingly, risks for this hypothetical receptor are quantified. «««^_^v^^^_«Moat Sector* ' , , ' • * . , As described in the RI Report, under the current administrative order from PADEP, the moat is completely enclosed by a chain link fence and under Westinghouse control Access into the moat occurs via a locked chain link fence gate. Regarding potential future exposures,'periodic brush i j control maintenance is likely to be required in the moat during growing season months (April to ^"^ October) and would be earned out by workers responsible for landscape care. Possible exposure to residual COPC in moat surficial (0 - 6") soils could occur by dermal contact, incidental ingestion, and inhalation of dust. w _ , - 1" i - ' A stormwater sewer line runs beneath the Moat Sector, and it is conceivable that occasional maintenance of this line would be necessary. Therefore, ChemRisk evaluated the potential contact of a storm sewer maintenance worker with COPCs in both surface and subsurface soil in the Moat Sector. Potential exposure pathways to COPC in soil that are evaluated include dermal contact, incidental ingestion and inhalation of dust particles. While not likely to occur on a regular or prolonged basis, a child trespass scenario is also included in this HHRA to characterize the complete range of plausible receptor populations potentially contacting COPC in the Moat Sector. , . 3-3 .CHEMRISK*. A SERVICE OF MCLAREN/HART nR. Additionally, it is possible for trespassers traversing through the area to be exposed to site'-related COPC. Children were selected to represent a sensitive receptor group. Exposure to COPC in right* of-way surface soils was modeled for the dermal contact and incidental ingestion exposure pathways. Because the railroad ROW surface consists primarily of ballast stone and compacted, encrusted soils, the potential for wind entrained dust is minimal, and it is unlikely that the dust inhalation pathway for the railroad ROW trespasser would be significant. Indeed, even if the surface were considered a "limited reservoir*' as defined in Cowherd et aL (1985), historic wind gusts at the site would have substantially depleted that source. Therefore, the particle inhalation pathway will not be evaluated quantitatively for the railroad trespass scenario. Particle inhalation is quantitatively evaluated for the railroad ROW maintenance'worker because of the potential for the workers to break through the encrusted soi. l -o r beneat•h ballas:t' t.o expos. e a new "limite, d reservoir'*' '•• . : -..'••",- •. . As noted in the RI, a majority of the Westinghouse property is covered either with buildings or concrete and asphalt Therefore, infiltration of (ainfall onto the property is limited, and the surface water drainage in the areas adjacent to the site and the site itself is controlled by storm sewers (CRC, 1996). Figure 2-2 in the RI illustrates the locations of the catch basins which collect surface water runoff from the site. The three catch basins that collect surface water runoff include the Wishart Court, Franklin Street, and Clark Street storm sewer catch basins. All three catch basins ore in the vicinity of the railroad ROW. ChemRisk evaluated a hypothetical scenario whereby a puddle of storm water runoff was assumed to form in the railroad ROW, and a child trespasser subsequently wades and plays in the puddle. ChemRisk used data presented in the RI for each of the three storm water sewer catch basins. All data used for this scenario were collected during a storm event, so the data are representative of water which would flow off the site. The child trespasser is evaluated for dermal exposure to the pooled surface water runoff. , • 3-4 CHEMRISK* - A SERVICE OF MCLAREN/HART rtRJU'3821 Groundwater . ! There are no current users of groundwater for any purpose at; or in the vicinity, of the site as confirmed by the well survey conducted in support of the RI (CRC, 1996). The well survey included all properties between the site and the Shenango River, as described in Section 2.6.6 of the RI. Moreover, considering the heavUyirdustri^ Of the Shenango River, and the availability of municipal water, foreseeable future uses of groundwater for any purpose (especially consumption) are also unlikely. Nevertheless, at PADEP and EPA's request, Westinghouse agreed to quantify risks in conjunction with the hypothetical use of two separate and distinct contaminant plumes in the alluvial aquifer, and for the hydrogeologically separate bedrock aquifer. These groundwater units are quantified for both a hypothetical resident and an industrial/commercial employee. Exposure pathways of potential concern for both hypothetical receptors include ingestion, dermal contact, and inhalation of vapors during showering. Section 3.2 to follow presents a discussion on the derivation of exposure point concentrations for each receptor group in all exposure sectors and groundwater plumes. 3.2 EXPOSURE POINT CONCENTRATIONS The exposure point concentration (EPC) As detailed in Appendix D, the lower value of either the 95th UCL of the arithmetic mean of the distribution of sampling results or the maximum concentration from the same distribution was selected as the EPC for each COPC in each medium. The lower of these two values was selected because the 95th UCL ofte\n exceed-'-'•'s the maximu.m concentration detected for small datasets and isJ therefore not a realistic estimator of the concentration of the contaminant. The 95th UCL for datasets with less than three data points (n<3) cannot be accurately calculated, so for cases where less than three data points were available, ChemRisk used the maximum detected concentration as the EPC. 3-5 CHEMRISK" -A SERVICE OF MCLAREN/HART ARJU3822 Data qualified with a B were treated as non-detected analytes with the reported value considered to be the detection limit for that analyte, so that one-half the value was used in determining the EPC. Data qualified with an R were rejected values and were removed from the data set when determining the EPC. , ' -. - / ' _ .' ' - •'•". • ^ ' • As EPA (1992a) points out, in most cases it is reasonable to assume that Superfund sampling data are lognormally distributed. EPA's evaluation of the lognormality of the data is discussed in greater detail in comment #10 of Appendix I. ChemRisk agrees with this statement, so the datasets were assumed to follow a lognormol distribution. Therefore, ChemRisk calculated the 95 percent UCL of the arithmetic mean for a tognormolly distributed datoset following the guidance provided in EPA U992a). , , . • . The sampling data were log-transformed prior to deriving the 95th UCL consistent with EPA guidance (EPA, 1992a). The 95th UCL was based upon the arithmetic average for each distribution, both because the arithmetic average is most representative of the concentration to which a receptor may be exposed over time, and also because carcinogenic and chronic non-carcinogenic toxicity criteria are based oh lifetime average exposures. The equation used to derive the 95th UCL of the arithmetic mean of the distribution of sampling data for each COPC is presented below; UCL = . • , « • *• ' where: UCL = upper confidence limit , e = constant (base of the natural log, equal to 2.718) 5 = mean of the transformed data s = standard deviation of the transformed data H = H-statistic (e.g., from table published in Gilbert 1987) n " » number of samples For non-detected data points, ChemRisk used one-half the sample quantitation limit as a surrogate value for that data point when calculating the EPC. , . o«ajnfrawEinNCHU99i«isEcn;w» 3-6 CHEMRISK*-A SERVICE OF MCLAREN/HART 3.3 QUANTIFICATIONi OF EXPOSURES . . Exposure assessment is me process of measuring or estimating the intensity, frequency, and duration of human or animal exposures to chemicals already present or released into the environment (EPA, 1992b; Paustenbach, 1989a; Paustenbach. 1990a). In its most complete form, an exposure assessment should describe the magnitude, duration, schedule, and route of exposure; the size, nature and classes of the human or wildlife populations exposed; and the uncertainties inherent in all estimates (NAS. 1983). v The potential for the occurrence of an adverse health effect associated with exposure to a chemical depends on the degree of systemic uptake (amount absorbed into the blood and tissues). For any route of exposure, the uptake (U) is the product of exposure (E) and the absorption efficiency (A): EPCs used in exposure assessment ore-detailed in Appendix D for each exposure pathway in fables D-2throughD-ll, SummarystatisticsforeachEPCareprovidedinTables3-2through3-ll. ^ j Although a number of different factors are used to quantify exposure, the mathematical relationship shown above holds true for all exposure routes. When calculating potential carcinogenic risk, the chronic intake is modeled as the lifetime average daily intake,.(LADI), whereas potential noncarcinogenic risk is modeled as the average daily intake (ADI). Both the LADI and ADI are expressed in units of milligrams of chemical per kilogram body weight per day (mg/kg-day). The equations for estimating either the LADI or ADI for each specific exposure pathway follow. Definitions for variables that remain constant across pathways ore provided for the first pathway only. Parameters that are unique to a pathway are defined for that specific pathway. Air , . - ',.••'•'••' • \ • ; . - \ ' - Inhalation of measured vapor levels or airborne vapors due to showering Intake = C.xIhRxRIAxEFxEDx I/ATx 1/BW 3-7 CHEMRISK" - A SERVICE OF MCLAREN/HART .VR.W382 where C.» concentration in air (mg/m3) . DiR s quantity of air inhaled per day (mVd) RIA s relative inhalation absorption (unitless) • EF = exposure frequency (d/yr) ' , : ' ED m exposure duration (yrs) AT»averaging time (days) ^ BW a body weight (kg) Inhalation of vapor modeled from both soil and groundwater Intake «(Cvs + Cvg) xlhRx RIAxEFx ED x I/AT xl/BW •I - • . where . • ; i , \ . - Cvs = concentration of chemical vapor from soil (mg/m3) ; Cvg = concentration of chemical vapor from ground water (mg/m3) Inhalation of dust and vapors Intake «t(Cvs +Cvg) + (Cs x Cp x CF x LDF)] x IhR x RIA x EF x ED x I/AT x 1/BW where' , . Cs = concentration of chemical in soil (mg chemical/kg soil) Cp = concentration of airborne particles (mg soil/m3) CF = conversion factor (IE-6 kg/mg) LDF »lung deposition fraction (unitless) 3-8 CHEMRISK* * A SERVICE OF MCLAREN/HART ARJU3825. Water • ' , ,K Dermal contact Intake = CWxSAxt>CxETxEFxEDxCFxl/ATxl/BW where , , , '••-.- CW = concentration in surface water (mg/L) SA = skin surface area (cm2) PC = Chemical-specific dermal permeability coefficient (cm/hr) , ET = Exposure time (hours/day) CF * conversion factor (1 liter/1000 cm3) Ingestion . ' '...-.' Intake = CW x IR x EF x ED x I/AT x 1/BW where CW = concentration in drinking water (mg/L) ( \ IR = average daily consumption of drinking water (L/day) • ' • '.'''"' Soil and Sediment .. ,:•'••• Ingestio' n ' ' ' ' ' ' '•''', ' Intake = Cs x IgR x IgRF x ROA x EF x ED x CF x I/AT x 1/BW where Cs = concentration in soil or sediment (mg/kg) IgR = soil or sediment ingestion rate (mg/day) IgRF= fraction of soil/sediment ingested that is attributable to the site (unitless) ROA = relative oral absorption (unitless) ' CF* conversion factor (I E-6kg/mg) 3-9 CHEMRISK* - A SERVICE OF MCLAREN/HART R.iu3'826 1 . f Dermal contact CsxSAxDAFxFSAxRDAxEFxEDxCFxl/ATxl/BW '•-_'• \ , SA = total body surface area (cm2) . DAF = dermal adherence factor'(mg/cm2-day) FS A = fraction of body surface area exposed (unittess) RDA - relative dermal absorption factor (unittess) CF= conversion factor (IE-6 kg/mg) Sections 3.3.1 through 3.3.5 present receptor- and pathway-specific assumptions used in this HHRA to estimate exposures to site-related COPC, and constitutes PADEP-approved methodologies for evaluating risks at this site. A summary discussion of the more significant exposure factors follows. Common Exposure Parameters In this risk assessment, the parameters that are common to certain exposure'scenarios include soil/sediment ingestion rate, dermal adherence factor, total body surface area, inhalation rate, body weight, averaging time, fraction of surface area exposed, exposure frequency and exposure duration. /•'-."' • ' ' •'/'.' Soil/Sediment Ingestion Rate, In this risk assessment, default soil ingestion rates of 100 mg/day for adults and 200 mg/day for children recommended by EPA (1989a; 1996a) are used. It is Important to note, however, that the default value for children is based on the findings of tracer element studies conducted by Binder et at (1986) and Clausing et aL (1987). These studies had limited sample sizes and did not account for dietary contributions of the tracer elements. Calabrese et aL (1989) evaluated soil ingestion by children 1 to 4 years of age using a mass-balance methodology. The median values of the most reliable tracers ranged from approximately 9 mg/day to 40 mg/day. these findings are consistent with those of Binder et al (1986) and Clausing et aL (1987) when these studies are corrected for ingestion of tracers in food and medicine (Calabrese et aL, 1989). Thus, the default soil ingestion rates recommended by EPA (1989a) likely overestimate soil ingestion by children (and, by analogy, adults) by at least 4-fold. The conservative default soil ingestion rates were used to provide a screening-level estimate of risks from this pathway. For the construction worker soil ingestion scenarios, ChemRisk used a soil ingestion rate of 100 mg/day. This ingestion rate represents a blended (weighted average) intake rate, between the average ,/ : ' • ' : 3-10 CHEMRISK* - A SERVICE OF MCLAREN/HART uR303827 ,50 mg/day rate, and the upper-end 480 mg/day rate (which should only be used for short-term exposure events for highly intrusive earth moving activities). The risk assessment assumes that ten percent of the total time spent on construction activities will befor intrusive earth moving activities, while the remainder of time (ninety percent) is spent on typical construction activities. Mathematically, the weighting expression is as'follows: ((0.1 x 480 rag/day)i + (0.9 x 50 mg/day)) = 93 mg/day, which we rounded up to 100 mg/day.. It should be recognized that the 480 mg/day soil ingestion rate very likely overstates the true potential for soil ingestion by workers. Indeed, this value is based on a study by Hawley (1985) who assumed .' that the soil covering one half of the inside of the fingers and thumbs of both hands was ingested twice daily. In short, there is little scientific basis to support this "enhanced" soil ingestion rate. > . . • '• ' . - In addition to the 100 mg/day base soil ingestion rate, ChemRisk added the mass of inhaled soil particles that are subsequently ingested (62.5 % of the inhaled particles). There is a difference in concentration of airborne dust modeled for each of the different construction scenarios (2 mg/m3 for the outdoor construction and 5 mg/m3 for the indoor construction). Therefore, there is a difference between the indoor and outdoor construction worker ingestion rates. For the indoor construction worker approximately 63 mg/day due to inhalation and swallowing are added to the base 100 mg/day i j (100 mg/day + (0.625 x 5 mg/m3 x 20 mVday) = 163 mg/day). For the outdoor construction worker only 25 mg/day are added to the base 100 mg/day (100 mg/day + (0.625 x 2 mg/m3 x 20 mVday) - 125 mg/day). . ( , Sediment ingestion by children has not been quantified in the scientific literature. In the absence of these data, sediment ingestion is conservatively assumed to occur at the same rate as soil ingestion. Dermal Adherence Factor. In accordance with the recommendation of EPA (1996e), a dermal adherence factor of 0.2 mg/cm2 was used in this assessment. The scientific literature provides a range of adherence factors from several studies (Kissel et aL, 1996, Lepow et aL, 1975; Roels et aL, 1980; QueHee et aL, 1985; Driver et aL, 1989, Sedmon, 1989, and Yang et aL, 1989). In evaluating these studies, the EPA indicated that each study has some degree of associated uncertainty (EPA, 1996e). Kissel et aL (1995) identified a range of soil adherence factors related to the type of activity. EPA (1996c) recommends that when selecting a soil adherence rate for exposure assessment, the risk assessor select the activity that best approximates the exposure scenario of concern and then use the 3- 1 1 CHEMRISK* * A SERVICE OF MCLAREN/HART R.H)3828 soil adherence factors that correspond to the activity of interest for the exposed skin surfaces. The study by Kissel et aL indicates that soil adherence varies from a low of 0.0008 for groundskeepers to a high of 58 for kids in mud. As related to the Westinghouse site, soil adherence on the hands (0.2) for an irrigation installer was selected as that scenario that most closely resembles outdoor construction. Dermal Absorption Factor. Following the recommendations of EPA Region Hi's Technical Guidance Manual for Assessing Dermal Exposure from Soil (EPA; 1995a), absorption of chemicals from soil was estimated using absorption factors from EPA (1992c), Wester et aL (1993), and Ryan et aL (1987). Wester et aL (1993) report an arsenic absorption factor of 3.2% which EPA Region III recommends using as a default factor. EPA (1992c) reports ranges of absorption factors for PCBs, PCDD/Fs, and cadmium. EPA Region III recommends using the upper limit of the range of absorption factors for each chemical or chemical group. Likewise, Ryan et aL (1987) suggests default ranges of absorption factors for chemical groups including metals,; volatile organic compounds, semivolatile organic compounds, and pesticides. Guidance from EPA Region III supports the use of the upper limit of these ranges for chemicals without specific values. The specific absorption factors used in the risk assessment are identified in Table 4^8. \ i ; • • , ' Total Skin Surface Area. Total skin surface area varies with age. Data from the EPA Exposure Factors Handbook (EPA, 1989b) were used to estimate age-weighted median total surface areas for males and females combined, for ages 7 through 12 years, 13 through 18 years, and for ah adult (>18 years). Resulting total skin surface areas ore 10,500 cm2U5,700 cm2, and 18,000 cm2, for the three age groups, respectively. Body Weight, For the age groups evaluated in this analysis, average body weights were calculated using the 50th percentile values for moles and females as provided by the EPA (1989b) Exposure Factors Handbook. The average body weight for the 7 to 12 year age group was calculated to be 33 kg. For the 13 to 18 year age group, on average body weight of 56 kg was calculated. Lastly, for all adults (age greater than 18 years), the EPA (1989b) recommends 70 kg as an appropriate estimate of body weight This value was derived from mean adult male and female body weights (EPA,1989b). 3-12 CHEMRISK* - A SERVICE OF McLAREN/HARf i\ R ;i 03829 Averaging Time. For carcinogens, intakes were calculated by averaging the dose over a lifetime of 70 years or 25,550 days (EPA, 1989a). For the evaluation of noncarcinogenic effects, an averaging time equal to the exposure duration expressed in years was used (EPA, 1989a). 3.3.1 River Sector 3.3.1.1 ChOdWader As discussed in Section 3.1, children may wade along shallow portions of the Shenango River or play along the river bank and/or storm sewer outfalls in the vicinity of the Westinghouse site. Potential exposures may include ingestion o£ and dermal contact with, sediments containing site COPCs. For the purpose of this assessment, it is assumed that children in the age range of 7 to 12 years are most likely to be wading and thus exposed to sediments. Younger children would not have the freedom to roam the area unaccompanied by adults, and adolescents do not characteristically spend much time wading. Adolescent use of the Shenango River near the site is more likely to be limited to swimming, an activity that may not incur significant sediment exposures. ; Exposure Frequency. This analysis assumes that a'child may wade in the Shenango River near the site five days per week during the summer months when there is no school (June through August), one day per week during the months of April, May, September, and October, and not at all during cold weather months (November through March), for a total exposure frequency Of 82 days per year. Exposure Duration. The exposure duration is assumed to encompass the entire age range of 6 years (age? to 12). Table 3-12 shows all exposure parameter values and their source references/justification for the child wader. Tables H-l through H-4 in Appendix H present the results of the exposure assessment and dose-rate calculations for the hypothetical child wader. . Fish Consumption ; . Consumption of fish from the Shenango River by recreational anglers is a potential route of exposure to COPC present in environmental media. While consumption of fish in the Shenango River proximate to the site was not raised as an exposure pathway of concern by PADEP or EPA during negotiations and finalization of the approved site Field-Sampling Plans, PADEP has requested that 3-13 CHEMRISK"- A SERVICE OF MCLAREN/HART PADEP has collected and compiled fish data from the Shenango River over several years (PADEP, 1988; 1995). In addition, the Pennsylvania Fish and Boat Commission (PFBC) has produced a report entitled. Analysis of Fish Tissue Contaminants' Near the Wextinghouse-Sharon Superfund Site (PFBC, 1995) using PADEP's data. As discussed below, concerns pertaining to protocols, documentation, and methods associated with these data limit their potential utility for purposes of estimating risk within the context of the RI/FS for the Westinghouse site. As agreed to during the group project meeting on June 11, 1996, and in subsequent transmittals with the Agencies, one objective of this section is to provide a qualitative evaluation of the information provided in the PFBC (1995) report. The adequacy of the data is evaluated and implications concerning potential risks associated with* consumption of fish from the Shenango River are discussed. A second objective is to qualitatively discuss the fish ingestion pathway for stretches of urban rivers similar to the Shenango near the Westinghouse site. ^ Pennsylvania fish and Boat Commission Report There are numerous concerns regarding the quality of the data utilized by the PFBC (1995) in their assessment offish tissue analyses for the Shenango River. First, the PFBC (1995) report states that fish tissue data were collected by PADEP between 1979 and 1994 and analyzed by the DEP Bureau . of Laboratories. PFBC obtained these data from the EPA's Storage and Retrieval (STORET) system in My 1995. However, a complete summary of the data obtained is not presented in the report which hinders a complete interpretation of the analysis. More complete documentation, including the printout obtained from STORET, as well as any available laboratory data sheets, should be included as an appendix or addendum to the report to allow for a thorough evaluation of all available data. In addition to not presenting all available data, information regarding the sampling or analytical methodologies was also not provided. EPA guidance (1989a) recommends consideration of several different aspects of data quality prior to evaluating potential health risk/The current dataset does not (WOJEOTawEsnNC»i9»9«Ecn.wH) ' . 3-14 CHEMRISK* -A SERVICE OF MCLAREN/HART AR.i0383! provide adequate detafl to allow an evaluation consistent with agency guidance (EPA, 1989c). As presented by PFBC (1995), it is unclear whether analyses were based on individual fish or composite , samples. In addition, preservation methods, holding times, and sample preparation methods are neither discussed nor evaluated. The specific analytical technique should also be reported for the purpose of evaluating confidence in the data because different analytical techniques can result in varying accuracy of reported concentrations. The PFBC (1995) report implies that the analytical methods used were screening-level; however, EPA (1989b) specifies that screening-level analytical results are not generally appropriate for quantitative risk assessment. In addition, when combining datasets, it is very important to ensure that the analytical methodologies used are comparable. It is also important to note that the fish data utilized by the PFBC (1995) do not appear to have been validated according to Comprehensive Environmental Recovery and Liability Act (CERCLA) and . EPA Region HI data validation protocols. In addition, information regarding Quality Assurance/ Quality Control (QA/QC) samples (e.g., field, trip, method blanks, duplicates, matrix spikes) is not provided, and it is unclear whether any such samples were collected. Without this information, confidence in the accuracy and precision of the data is low. , The question of confidence in the data quality notwithstanding, the sample size, particularly in the vicinity of the facility, is too small to determine if the observed differences between upstream and I j ' downstream samples are statistically significant. Less than twenty samples were evaluated, only four of which were conducted on fish collected in the vicinity of the site. The majority of the data evaluated were collected from areas downstream of the facility. For example, the mean PCB concentration reported upstream of the facility (0.62 mg/kg) is based on three samples, while the mean reported for downstream of the facility (1.62 mg/kg) is based on fifteen samples. These 1 differences in upstream versus downstream sample sizes and the variant time periods represented by the data do not allow for the credible differentiation among downstream data points and the Westinghouse site. f' Although it is true that combining data from multiple species may not be appropriate, caution should be taken in making assumptions regarding risk based on concentrations of PCBs in a single species, such as carp. As bottom feeding fish, carp tend to accumulate higher concentrations of sediment- associated chemicals (Le.v PCBs) relative to pelagic feeding fish, such as bass or trout. In addition, carp are not widely targeted for consumption by recreational anglers. Therefore, evaluation of this L species is likely to overestimate possible exposures to consumers of fish. aftajEKravwESiiNC»i9W*iNiJusnTEXT««s3.wpd / 3-15 CHEMRISK*-A SERVICE OF McLAREN/HART ' Finally it is important to note that the data utilized may not reflect current conditions. The majority of PADEP samples from the Shenahgo River were collected between 1988 and 1992, which may not be indicative of present-day fish tissue concentrations. •• '"N • '• . / The PFBC report (1995) draws a number of conclusions based on data of very limited utility, as discussed above. While such conclusions are questionable solely due to the data on which they are based, the conclusions themselves are unsubstantiated and appear to be based on a limited understanding of regression analysis and risk assessment methods. The following discussion evaluates the validity and rationale of the conclusions presented by PFBC. The PFBC (1995) report strives to define a "zone of influence" based on the slope of a graph plot of tissue concentration against distance downstream (Figure 2 of the PFBC report). Even if the fish tissue data were reliable, the approach used by PFBC would be incomplete and misleading in several ways. First, it is stated that the slope in Figure 2 cannot be said to differ from zero; however, the numerical value of the sbpe is not provided, nor is its derivation, statistical significance, or R2 value. Without this information, it cannot be determined whether or not the slope truly differs from zero. Second, the weak correlation observed between lipid content and PCB concentration (Figure 3 of the PFBC report) appears to be due to the model tested, rather than the data values themselves as inferred by PFBC. White the simple model of y .* mx + b may show only a weak relationship, a relatively strong nonlinear relationship may exist. As is standard practice in regression analysis, various transformations (e.g., logarithm, natural logarithm, square, square root) of the Upid content and/or PCB concentration data should be explored to evaluate whether a relationship does, in fact, exist between these two variables. Furthermore, when the PCB concentration data are lipid- normalized, a rapid decline in concentration is observed five miles (eight kilometers) downstream of the facility. The decrease in lipid-normalized concentration with distance appears to provide a good fit to a nonlinear model Third, the PFBC (1995) report's statement that the zone of influence extends 45 kilometers downstream strongly depends upon the results of a single sample that was collected in 1988 from river mile 0.9, which exceeded the PDA PCB tolerance limit of 2.0 mg/kg. That sample, which was collected from Site 13. had a PCB concentration of 2.60 mg/kg. No other fish tissue samples collected as much as 26 miles (42 kilometers) upstream of Site i 3 exceeded the PDA limit or differed substantially from upstream (Le., background) concentrations. Given the unknown quality of all the 3-16 CHEMRISK*- A SERVICE OF MCLAREN/HART ;iR:i(J383'3 fish tissue data, it is misleading to base the size of the zone of influence on the results of a single sample. , , The PFBC's (1995) statement that "fish tissue samples indicate that both human health and environmental risks to fish are not only possible, but are actually present" is unsupported. A risk is a probability that an event will occur (generally an adverse health effect to humans or ecological populations), based oh consideration of potential exposures (dose rates) to chemicals of concern and expected toxicity of those chemicals. As probabilities (Le., risks) were not calculated by PFBC (1995), it is misleading to state that risks are present. Furthermore, Such probabilities cannot be1 properly estimated using the existing dataset. Fish Ingestion and Urban Rivers Potential health risks associated with fish consumption are highly variable. An individual's potential intake of chemicals from consuming Shenango River fish is primarily a function of the rate at which fish are consumed, the chemical concentrations in fish, and fish cooking practices. Assumed fish consumption rates should be specific to the species, location, arid time under consideration. Secondary factors that contribute to chemical intake rate for recreational anglers include species preference, fishing location preference, seasonably of angling behavior, seasonal species availability, fish size, parts of the fish consumed, angling technique and skill, and number of years angling is practiced. . The fish consumption rate (and, hence, the chemical intake) for the Shenango River is expected to be relatively tow for several reasons, First, the current fish consumption advisory that is in place for the Shenango River from the Shenango Lake Dam to the mouth is intended to reduce public exposures (PADEP, 1988). Second, the fish consumption rate within the area of Interest is likely tow due to the industrial nature of the reach. Third, any consumption rate applied in the estimation of potential risks should be limited to the rate of consumption offish taken from only this water body. Many annual fish consumption rates reported in the literature combine the rates of consumption of fish taken from an water bodies recreationally fished and/or fish purchased at markets and restaurants. Such.sources of fish ingestion rates are clearly not applicable to an industrial waterbody like the Shenango River proximate to the Westinghouse site. • In summary, for the reasons articulated above, the existing PADEP fish data are not useful to assess the relationship, if any, between the Westinghouse site and the reported occurrence of PCBs in carp. 3-17 CHEMRISK*. A SERVICE OF MCLAREN/HART ilR;*U383.l» Moreover, even if the data were suitable for quantitative analysis, it is not possible to evaluate the potential magnitude of other industrial and nonpoint source contaminant impacts to the Shenango and to its resident fish populations. Given that an advisory against carp consumption already exists for the Shenango River (and many other river systems in Pennsylvania), the fish ingestion scenario is not evaluated farther in this HHRA. 3.3.2 North, Middle and South Sectors As described earlier, there are three plausible exposure scenarios that exist for the North, Middle, and South Sectors; 1) indoor employee, 2) future indoor construction worker, and 3) future outdoor construction worker. This section defines each of these scenarios and describes the potential exposure pathways that could pose a potential threat to the workers specific to each scenario. In addition, algorithms used to quantify the potential heath risk associated with each exposure pathway are quantified. . 3.3.2.1 Indoor Employee - The indoor employee is defined as an individual performing light industrial/commercial duties primarily within the confines of an existing or possibly a newly constructed building. For all three sectors, the existence of extensive pavement and concrete in the areas surrounding the buildings will likely eliminate the potential for direct contact with surface soils. Hypothetical exposure to indoor chemical vapors is ah exposure pathway quantified in this HHRA. However, it should be noted that the sampling data used to evaluate this exposure pathway was collected prior to any interior building cleanup. . ; - "; . • , ' ' ' / . - • "' • Inhalation Rate. The inhalation rate for the indoor worker is assumed to be consistent with that of an adult working at a light to moderate activity as defined in EPA (1989b). ChemRisk applied an inhalation rate of 10.8 raVday to this activity level which represents the average inhalation rate of both males and female adults for an eight-hour working period. Exposure Frequency. Consistent with EPA (199Ib), this assessment assumes that the indoor worker is at the place of employment for 250 days per year, which is equal to 5 days/week for 50 weeks per year (allows for two weeks of vacation away from the office per year). 3~18 CHEMRISK*- A SERVICE OF MCLAREN/HART , /tfUU3835 Exposure Duration. ChemRisk assumed the worker remains employed at the same facility for 25 , years, consistent with the upper-end duration expressed in EPA ('199lb). Table 3-13 siirranarizes an exposure parameters and their source references or justifications pertaining to the hypothetical Employee. Table H-5 and H-6 in Appendix H summarizes the results of the hypothetical indoor Employee Direct exposure to groundwater is addressed separately in Section ' ' 3.3.5.; ' . . .. , , . i r 3.3.2.2 Indoor Construction Worker . The hypothetical indoor construction worker evaluated for the HHRA could potentially be involved in intrusive activities that, at times, bring the worker into contact with the subsurface soil This contact may result in incidental ingestion and dermal contact with soil In addition, the potential exists for the hypothetical construction worker to inhale chemical vapors and soil particles originating from the subsurface spil during construction activities that penetrate the building's foundation and disturb the upper soil layers (Le., installation of utilities). Furthermore, an additional source of chemical vapors, LNAPL, may contribute to the overall indoor air concentration of vapor phase chemicals to which the worker may be exposed. LNAPL To Indoor Air Transport Modeling As specified in the CSM and subsequently agreed on in the June 11, 1996 agency meeting and subsequent transmittals, the interior vapor risk assessment is based on the subsurface soil data collected from beneath the AB Slab. Vapor contribution from LNAPL is evaluated in lieu of that from dissolved phase chemicals as this is a more conservative and simplified analysis. Thus, the use of pure phase chemical (LNAPL) conservatively estimates vapor phase contribution to the indoor air from chemicals residing below the vadose zone. The technical approach used to model LNAPL and soil vapor flux into the Middle Sector building air follows. To predict indoor air concentrations of COPCs volatilizing from LNAPL, a vapor transport model was first applied to estimate the rate Of migration of chemical vapors from groundwater through the saturated and unsaturated soil overlying the groundwater in the vicinity of the Middle Sector . 3-19 CHEMRISK* - A SERVICE OF MCLAREN/HART • . ' . . ,} • • - - ' . ;iR.U)3836 Buildings, The vapor transport model yields a flux rate describing the potential rate of chemical migration per unit area of open floor space. The flux rate was then applied to an indoor air mixing i J model to estimate the concentration of chemicals in indoor air. ^"^ Model Descriptions , - . Vapor flux was evaluated using the Farmer model (Farmer et aL, 1978,1980) with a correction to account for transport resistance in the capillary fringe. A simple mass balance model was used to simulate indoor air mixing. These two models are briefly discussed below. Detailed mathematical explanations of the Fanner and indoor air mixing models are provided in Appendix E. Farmer Model Generally, the Fanner model combines Pick's First Law of steady state diffusion with Millington and Quirk's (1961) tortuosity model to estimate the flux of a chemical through the ground surface given a source of chemicals in groundwater or LNAPL (EPA, 1992d). The Farmer model assumes that complete equilibrium is established between the chemicals in groundwater or LNAPL, soil pore water, and soil pore vapor. For low concentrations of chemicals in groundwater, the vapor phase concentrations of the chemicals are estimated assuming that chemical equilibrium follows Henry's Law and is not affected by other components in the system. If LNAPL is evaluated, vapor phase concentrations of LNAPL are determined based on the partial pressures of the LNAPL components s .•..-. • . . • .. . The version of the Farmer model used for this analysis recognizes that there is no clear distinction between the saturated soil below groundwater or LNAPL and the air-filled pore spaces above. Indeed, the model accounts for the presence of a capillary fringe layer above the water table, where the soil pore spaces are fiBed with water, but not necessarily at the same concentration as in the bulk groundwater. For water tables that are not tidolly influenced, the pore water in the capillary fringe does not move laterally with groundwater and, therefore, is not at the same concentration as the bulk groundwater (EPA, 1992d). The chemicals in the bulk groundwater move under liquid phase diffusion through the pore water and into the overlying unsaturated pore spaces. Liquid phase diffusion rates of chemicals through water are typically four orders of magnitude smaller than their respective vapor phase diffusion rates (EPA, I992d). As such, the concentration at the top of the capillary fringe is less than that in bulk groundwater. Additionally, the concentration of chemicals 3-20 CHEMRISK*-A SERVICE op MCLAREN/HART R According to the EPA (1992d), with these corrections for the capillary fringe and water-filled pore spaces, the Farmer model yields a reasonable yet overestimated flux rate through floors. This conservatism results because the model does not account for many attenuating factors. Rather, the model conservatively assumes that: . * Source(s) of chemicals do not decrease over time (groundwater concentration is time I J independent); . . * •: ' • • • Chemicals are not lost to degradation during transport; : '. ' '• ' , ' ' i • • No irreversible adsorption occurs; and ~ • Concentrations at the concrete floor surface remain zero, resulting in maximum diffusion. ChemRisk estimated the average flux rates of each COPC detected in LNAPL that may impact the middle Sector buildings or the ambient air (in the cose of the exterior construction worker). As discussed in the followin"„•'*g section. , the resultant" flux rates will be' sconverted to average indoor air < concentrations using an indoor air mixing model. 3-2 1 * CHEMRISK* - A SERVICE OF MCLAREN/HART UJ3838 Indoor Air Mixing Model ..'•" .' ' ' ' • • ~ > A mass balance indoor air mixing model was used to estimate the chemical concentration in indoor air resulting from the flux of a chemical through the floor of the building and into the indoor air. The mixing model assumes that the air-filled portion of the building is in a continuous and instantaneous state of mixing, such that the concentration of a given chemical is the same everywhere within the building. As chemicals enter the building through the floor, they are mixed with indoor air which constantly mixes with clean outdoor air at a known exchange rate. As detailed in Appendix E, ChemRisk integrated the flux rate of chemicals through the floor, the size of the mixing compartment, and the outdoor air exchange rate to yield predicted indoor air concentrations. The indoor air mixing model does not account for losses due to chemical reaction, degradation, or adsorption to surface materials within the structure. It also assumes that the only source of COPCs to indoor air is the groundwater, as simulated in the Farmer model ' ''".'• i ' ' • . ' Model Input Requirements . , Additional information required to conduct the vapor transport modeling includes: 'Chemical specific data; physical characteristics of the groundwater and the overlying soil; and physical characteristics of the buildings. The following sections describe the sources,and values of these parameters. Characteristics of Chemicals in LNAPL or Groundwater The relationships used to describe vapor phase transport of chemicals depend on the chemicals' physical and chemical interactions with the different components of soil The chemical specific parameters that describe these interactions include: *•• • - . • Henry's Law constant, ( • Molecular weight, . • Air phase diffusion coefficient, . ' • Liquid phase diffusion coefficient, and • Vapor pressure. o«lJE^f^\WB^wcMl9mPINlJUSlo^Exnfcco.«p« 3-22 CHEMRLSK" - A SERVICE OF McLAREN/HART JU3839 ChemRisk applied scientific literature values for the Henry's Law constant, vapor pressure and the molecular weight. The chemical specific diffusion coefficients Were obtained from the scientific literature where available, or they were be calculated using standard estimation methods described byLymanetaL(1990). ; Physical Characteristics of LNAPL or Groundwater The depth to groundwater relative to the building floor represents the vertical distance that vapor phase chemicals must migrate to enter the building. Depth to groundwater is the only physical characteristic of groundwater required by the model Based on the RI, the average depth to groundwater within the Middle Sector is approximately 10 feet. Physical Characteristics of Overlying Soil * The Fanner model requires data on the physical characteristics of the Overlying soil including: soil type, total soil porosity, volumetric air content, and volumetric water content. Soil type is also used to define the height of the capillary fringe above the water table. Because retardation of vapor transport due to adsorption is not addressed by this model, the organic carbon content of the soil is no„ t neede. • d to^ calculat. ' e flux"'. . .-•-- .:•: ;" . ;:;. :. '/' . •' - Based on the RI (CRC, 1996), the geology comprising the vodose zone at the site is composed of two layers, fin and the alluvial till The fill material is present at varying amounts throughout the site. The fill is made up of loose to dense cinders, an• d slagi with some• woo. d and brick fragments• , an• d trace amounts of sand and silt. The alluvial till consists of sand, gravel, silt, and clay. Because of the heterogeneous nature of the material comprising the vadose zone, ChemRisk assumed that soils are primarily sandy. Based on this, ChemRisk used the properties of sandy soil (Le., total porosity, volumetric air content, and volumetric water content) as model input. Specific input values are summarized in Appendix E. ' ' • ' ' The effects of sofl type on capillary fringe height have been reported by Heath (1982), Harr (1962), and Todd (1980). ChemRisk used a capillary fringe height of 8 cm which is representative of the ;fringe height associated with a sandy soil. , . . 3-23 CHEMRISK*-A SERVICE OF MCLAREN/HART Physical Characteristics of The Building^ ^ The physical characteristics of the buildings that were used as input in the model include: height of the structure ceiling, and air exchange rate for thebuilding. These parameters, their values, and their sources are summarized in Appendix E. • • i i / . • . Subsurface Soil to Indoor Air Vapor Transport Model The Behavior Assessment Model (BAM) (Jury et aL, 1983,1984a,b,c, 1990) was used to estimate the rate of migration of chemical vapors from subsurface soils to the indoor air of the Middle Building. TTie output of BAM is the rate of vapor phase chemical migration from soil to air. The flux rate calculated by BAM was used as input for an indoor air mixing model to estimate the indoor air concentration of vapor phase chemicals in indoor air. The vapor transport and indoor air mixing models are described briefly below. A complete description of the BAM model is provided in Appendix F. Behavior Assessment Model (BAM) . . , \ ' BAM(JuryetaL, 1983; 1984a,b,c, 1990)^wos originally developed as an environmental screening test for classifying pesticides with respect to persistence, mobility, and volatilization. More recently, EPA (1996c) has adopted BAM as the preferred soil-vapor transport model when assessing potential volatilization pathways. BAM is a one-dimensional equilibrium model that incorporates net first- order degradation kinetics and simulates chemical movement to the atmosphere via a stagnant air boundary layer at the soil surface (Jury etal, 1983). BAM estimates a time-dependent volatilization flux of a chemical, which can then be averaged over a given time period, Le., time averaged. BAM mathematically describes the interactions that take place between chemicals in three distinct components of soil, including the air filled pore spaces, the water filled pore spaces, and the organic carbon fraction. The model accounts for the effect of soil moisture on tortuosity and also includes the effect of liquid-phase diffusivity (EPA, 1996c), While the EPA (1996*c) has proposed a modified version of BAM, that modification does not readily allow tor the calculation Of time, neglects the effects of a stagnant air boundary layer, and does not take into account convective mobility processes such as evaporation or leaching. Because the EPA's (1996c) assumption regarding the stagnant air boundary layer is not representative of actual site conditions, ChemRisk did not use this modified form of the model 3-24 CHEMRISK*-A SERVICE OF MCLAREN/HART Jury et al (1983) simplified the description of chemical transport based on several assumptions- •- "'• . '. :'-•." ••:' .-••• . ' ."•. • ••' ..". • Soil properties, including water content, chemical content, bulk density, porosity, , liquid water flux, and organic carbon fraction, are assumed to be uniform throughout all soils; • Adsorption is described through a linear equilibrium isotherm; • Uquid-vapor partitioning is based on linear equilibrium; and, • Loss of the chemical and water to the atmosphere is limited by gaseous diffusion through a stagnant air boundary layer, above which the contaminant has zerp concentration (the air is at 50 percent relative humidity). The average flux of subsurface chemicals from soil representative of that beneath the AB Slab was estimated. The flux rates were converted to average indoor air concentrations using the indoor air mixing model described below. . • * ' . • • I j Indoor Air Mixing Model The same indoor air mixing model was used as that described for the groundwater to air vapor transport to estimate indoor air concentrations of PCBs. The reader is referred to the above section describing the indoor air mixing model and to Appendix F for further information regarding the indoor air mixing model / Soil Data to be Used in Modeling V • ' " " _ . h - • ..'••', The analytical data from soil samples collected beneath the AB Slab was used as discussed in Section 3.2. The EPC for each chemical was used as the starting point for the soil vapor transport modeling. According to EPA (I991b). inhalation of chemical vapors is only relevant for chemicals with Henry's law constants of IE-5 atm-mVmol or greater and a molecular weight of less than 200 g/mole. Three chemicals detected in the subsurface soil, endosulfan II, endosulfan sulfate, and endrin ketone, have Henry's law constants greater than IE-5 atm-mVmol and molecular weights greater than 200 g/mole. 3-25 CHEMRISK' - A SERVICE OF MCLAREN/HART R.HI38U2 Therefore, these chemicals, although detected in the subsurface soils, were not evaluated for vapor phase transport. - •"' "- ' • " "•- ' . • : Other Model Input Requirements In addition to the representative soil concentrations (discussed above), BAM requires several other types of input data, including: a) chemical and physical characteristics of the chemicals of interest; b) physical and chemical characteristics of the soil; c) physical characteristics of the buildings; and d) duration of emission flux. While emission flux may continue as long as a source of vapors is available, the duration is most relevant in terms of the potential for human exposure. Hence, BAM was programmed to simulate volatilization of chemical vapors over the time span of one year (for the construction worker scenarios). The following sections describe the sources of information and assumptions relating to chemical and physical characteristics of the COPCS, soil, and the physical characteristic of the Middle Building. Chemical Characteristics of COPCs in Soil The chemical-specific input data required for the BAM model include the effective solute pore velocity (VJ, effective solute diffusion coefficient (DJ, stagnant air coefficient (HJ, and the effective solute decay rate (u). The value for the effective solute pore velocity, V,, is a function of annual precipitation. Values for D, and H, are calculated for each chemical based on the chemical-specific organic partition coefficient (KJ, Henry's Law constant (H), diffusivity in air (DJ, and diffusivity in water (Dw), as well as the physical parameters related to soil and depth of contamination. The values for KK and H were obtained from the scientific literature (Mackay et aL, 1992) and the diffussivities were either obtained directly from scientific literature or calculated using standard estimation techniques (Lyman et aL, 1990). It was conservatively assumed that no biodegradation of the chemicals occurs in soil so the value for the decay rate, u, was set equal to zero. Chemical- specific values used to derive D. and H, are defined in Appendix F as well as other input parameter values and the physical parameters used to derive them. 3-26 . CHEMRISK*-A SERVICE OF MCLAREN/HART RJU38U3 ' Physical Characteristics of Subsurface Soil ,• i ' . \^S As previously discussed, the geology underlying the site is composed of two layers, fill and alluvial till The fin material is present at varying amounts throughout the site. The fill is made up of loose to dense cinders, and slag with some wood and brick fragments, and trace amounts of sand and silt. The alluvial tin consists of sand, gravel, silt, and clay (CRC, 1996). Because of the heterogeneous t ' nature of the material comprising the vadose zone, it was assumed that the soils are primarily sandy. Based on this, the properties of sandy soil (Le., total porosity, volumetric air content, and volumetric water content) were used as model input, as presented in Appendix F. Modeling the flux of chemicals from subsurface soil to indoor air also requires some understanding of the distribution and occurrence of constituents in soils. Based on data collected for the RI, it is clear that the constituents tio not occur equally in the soil throughout the site. Therefore, it was conservatively assumed that the constituents were present in the soil uniformly to a depth equivalent to the average depth to the water table, 10 feet 'This assumption is conservative because it is unlikely that the constituents are present in the soil uniformly to this great a depth; essentially, this assumption likely artificially adds to the mass of chemical actually in the soil \ ' . t m • t - Physical Characteristics of Building . " '• . : -,. • . '- •••-• - -..- • ••:' . / •• - The physical characteristics of the building that were used as input parameters in the model include: area of exposed floor, height of the ceiling, and air exchange rate. The values used for these parameters and their sources are presented in Appendix F. • j ' - . •' . •> • . • •' . ' . The indoor air concentrations of chemicals from LNAPL and subsurface soil are added together to yield an overall indoor air concentration to which the indoor construction worker could theoretically ' 'be exposed. - ' J The construction worker is assumed to be in the areas of the middle building where the ceiling height is approximately 18 meters (60 feet). For a detailed description of the models used to estimate the indoor air concentration of vapor phase chemicals, see Appendix E. . 3-27 CHEMRISK* - A SERVICE op MCLAREN/HART ' Subsurface Soil To Indoor Air Vapor Transport Model .. ' • '' • ' •• ' '- ' ' ' ' < \J The subsurface sofl to indoor air vapor modeling was performed using the same BAM model as ^"^ described above for the outdoor worker. Indeed, the indoor air mixing model is also that which was described above., However, the height of the ceiling was increased to a height representative of the open areas of the Middle Building interior. A summary of the BAM model and the indoor air mixing models are provided above, and complete mathematical descriptions are found in Appendices E« andR : "••••'. •.'-/, •. ' • Airborne Particle Emissions It was assumed that the concentration of airborne respirable soil particles is equivalent to the OSHA Subpart Z regulation for respirable fraction nuisance dust, or 5 mg/m3 (58 FR 40191, July 27, 1993). Other exposure parameters used to estimate the daily intake of chemicals for the indoor construction worker are provided above in the common exposure parameter section or are detailed below. A complete summary is provided in Table 3-14. Estimates of chemical intake are detailed in Tables H-7 through H-12 in Appendix H. • i ' / • ' . . Fraction of Soil Ingestio•n Attributabl• e to the Site. It- was assumed' that all of the* soil ingested' by the indoor construction worker was attributable to the site. Exposure Frequency. For the indoor construction worker, it was assumed that the worker could be present 5 day/week for 3 months out of the year. This reduces to an exposure .frequency of 65 days/year. Exposure Duration. It was assume: d tha' t a constructio" n• worker migh. t conduc- t indoor repair\ ' s activities twice in a working life time. Hence, the total combined exposure duration is two years. Inhalation Rate. For the indoor construction worker, workers were assumed to be performing activities that would be characterized as a moderate activity level as suggested in EPA (1989b) guidance. Activities falling into this category include heavy indoor cleanup, performing major indoor repairs and alterations, and climbing stairs. The inhalation rate over the working day (Le., the period of time that exposure would occur) is 20 mVday. 3-28 CHEMRISK" - A SERVICE OF MCLAREN/HART Lung Deposition Fraction. Following inhalation of airborne respirable particles, a portion of the particles will be exhaled and a fraction will be retained in the lungs. Of the fraction inspired, approximately ?5 percent of the particles are exhaled, 25% are deposited in the lower respiratory tract (of which half, 12.5 percent, are eliminated from the lungs and swallowed), and 50 percent are deposited in the upper respiratory tract and swallowed (ICRP. 1975; EPA, .1984; Paustenbach et aL, 1992). These values result in a lung deposition fraction of 0.125 (12.5%), and an ingestion fraction .of 0.625 (62.5%). Fraction of Exposed Surface Area. Indoor construction workers were assumed to have their hands, forearms, and lower legs uncovered and available for panicle deposition or direct contact with the soil Based on that, ah exposed skin surface area fraction of 0.22 (Le., 22%) was calculated using data provided in EPA (1989b). 3.3.2.3 Outdoor Construction Worker , Future outdoor construction and excavation activities in the Middle Sector could result in worker exposure to impacted soil, vapors, and entrained soil particles. Routes of exposure to site chemicals may include inhalation of chemical vapors and airborne particle bound compounds, ingestion of impacted sofl, and dermal contact with impacted material Because there are no outdoor construction projects presently planned for the site, a hypothetical excavation/hauling scenario is used as the basis for the exposure calculations. The outdoor future construction worker exposure analysis assumes that heavy construction activities occur whereby impacted subsurface soils from beneath the concrete AB Slab are excavated and subsequently transported over the slab to an off-site location. The excavated material is assumed to be loaded directly from the excavator into haulers for transport, such that no soil piles remain on-site or if left on site, are covered to prevent erosion and soil loss. Excavation activities may uncover impacted soil which might be directly contacted by construction workers. Also, the physical agitation of the sofl during excavation may cause the release of airborne respirable panicles and volatile organic vapors. Similarly, transport of the soil in haulers over the slab could result in physical entrainment of panicles residing on the slab surfacV e which could be subsequentl> y inhaled .by the worker. It is f ' • - conservatively assumed that all of the dust on the concrete slab surface that the haulers drive over is contaminated at the same concentrations as the subsurface soil.. No dust controls, such as water Particle Bound Emissions Model For the outdoor construction worker, there are two major sources of respirable airborne particles, those generated by excavation'activities and those entrained by trucking traffic. Both of these activities have the potential to entrain PM-10 (respirable paniculate matter with an aerodynamic diameter of 10 microns or less) into the surrounding air. The generation of PM-10 is a function of the physical properties of the material being disturbed and the mechanical energy responsible for the generation of particles. The relationship between the physical characteristics of the soil and the mechanics used to dig and haul the sofl is used to estimate the potential emission of particulates from a hypothetical excavation project. The models described below incorporate the physical properties of the material and the mechanical energy components using the empirical expression of the general form.. : " . i ' ' • • • c = Kpamb where , , e = emission factor p = physical properties m = mechanical properties . ' K, a, and b » adjustment coefficients that reflect the relationship determined from actual open dust source testing (RTI, 1987). ^ The empirical relationships that have been developed to estimate particulate matter emissions from various construction activities are found in the EPA's Air/Supcrfund National Technical Guidance Study Series - Models for Estimating Air Emissions from Superfitnd Remedial Actions (EPA, 1993b). The remedial action scenarios evaluated in this document are identical to the hypothetical . ' . 3-30 CHEMRISK*- A SERVICE OF MCLAREN/HART R. The PM-10 emissions from soil excavation can be estimated with the following equation: (0.35) (0.0016) (M) (—)'J .. ',- -,.... . • •, E,—————————_il_ -. • • : where ..••£• - PM-10 emissions, g 0.35 = particle size multiplier for PM-10, unitless 0.0016 = empirical constant, g/Kg. . M * mass of soil handled, Kg ,] -. ^ u = mean wind speed, m/s 2.2 ; = empirical constant, m/s ' , , • , • , XMO '"» percent moisture, percent (EPA, 1993b). It is assumed that the construction activity being performed outdoors consists of removal of the entire AB slab and excavation of the subsurface soil to a depth of approximately 0.76 m (2.5 feet) over this entire area. The surficial dimensions of the AB slab ore approximately 243 m by 76 m. Based on this scenario, the approximate in-place volume of soil to be handled over the course of the hypothetical construction project is 11,325 m3, which, assuming an average bulk density of 1.5 g/cm3, equates to 3-31 CHEMRISK"-A SERVICE OF MCLAREN/HART R.iU38U8 a mass of approximately 1.7 X 107 Kg of soil excavated. Averaged over the 195 day construction period, the average daily excavation rate is 87,115 Kg soil/day. Using the default estimate of 10 percent moisture, the mass of PM-10 emitted per day from the excavation process is calculated to be approximatery 5 grams, which Js equivalent to a continuous emission rate of 1.57 x lO^g/s for an 8-hour work day. Transforming the PM-10 emission rate from the excavation into a worst case air concentration that the worker may be exposed to is calculated using the following moss balance box model: where - }• . . Cto '.».• concentration of PM-10 in the worker breathing . space adjacent to the excavation, ug/m3 - Q]0 ss emission rate of PM-10 from the excavation, g/s • . 10* = conversion factor, ug/g. : ii a mean wind speed, m/s' ( - . Hw = height of the worker, m ; * L* = lateral distance traversed by the worker, m. Assuming that the construction laborer is working adjacent to and directly downwind from the excavation, is approximately 2 meters tall, traverses 3 meters perpendicular to the prevailing wind while working, and that the mean wind speed is 2 m/s, the average concentration of PM-10 in the workers breathing zone is 13 Mg/m3. This concentration is likely to be biased high because the mass balance model used in this scenario does not allow for dispersion or settling of PM-10, nor does it account for wind shifts. Estimating the contribution^of PM-10 from the hauler truck traffic is performed using the following equation: ^10 =220 x - i 0.3 3-32 ' CHEMRISK*-A SERVICE OF MCLAREN/HART R HJ38U9 where ' •V_> En = total mass of PM-10 entrained per vehicular kilometer traveled, g/VKT 220 = empirical constant, g/VKT sL « .silt surface loading, g/m2 22 = empirical constant, g/m2 (EPA, 1993b). , / "•'•-'• Because the surface silt loading of the concrete slab is unknown, a default value of 8 g/m2 was used (EPA, 1993b). Using the above equation the approximate mass of PM-10 emitted per kilometer traveled is 195 g. Assuming that the trucks travel a distance of 0.3 kilometers (roughly one-half of the perimeter of the.slab), the mass of PM-10 emitted by the truck traffic is 58.g per one way trip. \ • ' ' • 1 The average airborne concentration of the PM"-10 entrained from each one way trip is calculated using the following equation: <1Q3> where C/o = airborne concentration of PM-10 behind trucks, jig/mj En • total mass of PM-10 entrained per vehicular kilometer traveled, g/VKT. Wt = Width of the truck, m ^ H, s Height of truck, m Dt = Distance traveled for one way haul, km 103 s conversion factor (^g* km/g • m). V ' ' • • Assuming that a 9.2 m3 (12 cy) hauler will be used and its dimensions are approximately 3 meters in height and 2 meters wide, the average airborne concentration of PM-10 just behind the truck will be 32.467 ^ig/m5. Emissions from the hauler traffic will occur only intermittently throughout the day, when the hauler is full and has driven away from the excavation activities, and again when it returns. The entrapment \3-33 CHEMRISK". A SERVICE OF MCLAREN/HART R- The total time that the hypothetical construction worker is exposed to the dust per day is a function of the number of truck passes made throughout the day. As discussed above, the total in-place volume of soil excavated for the life of the project is 11,325 m3. Assuming that the construction takes place over a 195 day time period, the daily in-pbce soil volume excavated is 58 m3. With a bulking factor of 30%, the actual excavated soil volume is 75 mVday. Given a 9.2 m3 hauler, the number of trips at capacity is approximately 8 per day. Accounting for the return trip, a total of 16 passes may be made per day. If the hypothetical worker is standing in the dust cloud for 2 minutes per pass, then the total time the worker stands in the PM-10 dust cloud generated by the truck traffic is 32 minutes per day. . The time-weighted average PM-10 concentration the worker is exposed to is a function of the length of time that he/she remaini s in an area wit* h a give, n PM-10 concentration•, . The worke. r is assume' d to be at the site for 8-hours/day or 480 minutes/day. Of that time, 32 minutes are assumed to be spent in the hauler truck PM-lOcloud at 32,200 ug/m3 PM-10, and the remaining 480 minutes are spent directly down wind of the excavation. Therefore, the time-weighted average daily PM-10 concentration, Cp, the worker is exposed to is; Cp.32,467 ' or Cp * 2,177 , 2.177 m" TO 3~34 CKEMRisK" - A SERVICE OF MCLAREN/HART R. Groundwater to Outdoor Air Vapor Transport Modeling ( 1 ' ' ' • ' ChemRisk used the Farmer model (Fanner et ol, 1978, 1980) to estimate the vapor transport of dissolved phase chemicals in groundwater to the ambient air for the outdoor construction worker scenario. The Farmer model used is identical to the model described above in Section 3.3.2.1, except that for this scenario no reduction in flux is accounted for due to a vapor barrier (ie., a concrete floor). The result of the Farmer modeling is a ground level flux rate for each chemical in the vapor phase. The chemicals modeled include those detected in the groundwater associated with the southern alluvial plume and the central alluvial plume. If a chemical is considered a COPC for both plumes, ChemRisk used the maximum of the two EPCs as the most conservative representative groundwater concentration. , Ambient Air Mixing Model fBox Mndeft . ' i ChemRisk used an ambient air or box mixing model to estimate the airborne vapor concentration of chemicals that the outdoor construction worker may encounter from the contaminated groundwater. For outdoor exposures, vapor concentrations were calculated using the following box model equation: • \. '': ' , ^ ' ' , ' Cv = (Js x Aemit)/(Vwind x Awind) where, Cv = Outdoor vapor concentration (mg/m3) Js s . Flux rate of COPC computed by BAM (mg/m2-s) Aemit * Emitting area (unpaved area) Vwind •* Windspeed (m/s) Awind = Area of wind (box height x wind width) (m2) For the outdoor construction worker scenario, the emitting area, Aemit, was estimated to be 17,400 m2 from site blueprints provided by GRC (1996). A typical value of 2 m/s was selected for Vwind, while Awind was calculated assuming a box height of 2 m and a site cross-sectional area (wind width) of 741 m, again based on site blueprints. A detailed description of the Farmer model and a summary of the model input and results are provided in Appendix E. 3-35 CHEMRISK* - A SERVICE op MCLAREN/HART ' ; The subsurface soil to outdoor air vapor modeling for the outdoor construction scenario was performed using the same BAM model as described above for the employee and indoor construction worker in Section 3.3.2. 1 but the calculated flux was applied as input to an ambient air box mixing model As detailed above, the results of the BAM model is a time averaged ground level flux of chemicals to the overlying air space. A summary of the BAM model is provided above, and a complete mathematical description is found in Appendix F. The ambient air mixing model is described below/•••. ' . > ' .' •• ' i . ... ' _ Ambient Air Mixing Model flBox ModeH ' ' • • • . ••••''.' ChemRisk used an ambient air or box mixing model to estimate the airborne vapor concentration of chemicals that the outdoor construction worker may encounter from the impacted soil The air mixing model is identical to that discussed above for the groundwater to air vapor transport model A detailed description of the air mixing model and a summary of the results are provided in Appendix • F. ' ' - • - • • ' ''•''. Other exposure parameters used to estimate the doily intake of chemicals for the outdoor construction ( J worker are provided above in the cofnmon exposure parameter section or are detailed below. Fraction of Soil Ingestion Attributable to the Site. All soil ingested by the outdoor construction worker was assumed to be attributable to the site. Therefore a value of 1.0 is assigned to this variable. ' • Exposure Frequency. 'For the outdoor constructio*• n worker, the' worker was assumed to be presen* t• - 5 day/week for 9 months out of the year. This reduces to an exposure frequency of 195 days/year. i . ' ' ' • ~ ' Exposure Duration. The duration of the outdoor subsurface construction work is assumed to be one 'year. .' " • ' • '. • ..•'-.•-. Inhalation Rate. Like the indoor construction worker, the outdoor construction worker is assumed to be performing activities that would be characterized as moderate in EPA ( 1989h). Activities falling into the moderate activity level according to EPA ( 1989b) include heavy indoor cleanup, performing Oi^aJEm»WES^NCWl99WNLRmoTC3Cl^Swl3.wp 33.3 Moat Sector 3.3.3.1 Maintenance Worker , , - ' . .,,-•• "*"•>.' The moat maintenance worker exposure analysis assumes that scrubby growth within the Moat Sector wfll require occasional pruning with equipment that may result in limited disturbance of surface soils and the generation of entrained dust. The consequent relevant exposure pathways modeled in this HHRA include dermal contact with disturbed surface soil, incidental ingestion related to the handling of dust-contaminated equipment, and inhalation of contaminated entrained dust. Tables H-19 through H-24 in Appendix H present the results of the exposure^ assessment and dose-rate calculations for the hyppthetkal landscape maintenance worker. The analysis Conservatively assumes that a full-day moat maintenance activity occurs seven times (days) per year, and that the same worker or workers would consistently be responsible for this maintenance activity over a 25-year period. Table 3-17 shows all exposure values, including their source references/justification. 3.3.3.2 Child Trespasser White the moat is completely fenced and periodically inspected to ensure its integrity, children and adolescents may breech the security fence for unauthorized recreational activities. Thus, the potential 3-37 CHEMRISK" * A SERVICE OF MCLAREN/HART 38-5l» exists for exposure to site-related COPC on an infrequent basis. Two age groups were selected to represent the complete range of plausible receptor groups: 7 to 12 year olds (children) and 13 to 18 year olds (adolescents). Table 3-18 depicts a summary of afl exposure parameter values used to estimate dose rates calculated for this exposure pathway. The quantitative exposure assessment for the child trespasser is provided in Tables H-25 through H-32 in Appendix H. 3.3.3 J Construction Utility Worker Because a storm sewer exists within the Moat Sector, it is possible that servicing of the sewer may be required by a construction utility worker. The construction utility worker may be exposed to chemicals in surface and subsurface soils leading to chemical intake via incidental ingestion, dermal contact, and inhalation of contaminated dust particles. . ' For the inhalation scenario, airborne particles were assumed to be the result of two activities, excavation and wind erosion of continuously active soil storage piles. The respirable fraction of dust entrained in the air during soil excavation was calculated using the same emission model as described in Section 3.3.2.3 for outdoor construction worker. For the sewer maintenance worker, excavation related emissions were based on the assumption that the hypothetical worker excavates a trench that is two meters wide, three meters deep, and 20 meters in length. Moreover, it was assumed that the trench excavation would occur for three hours during each day. Model input values used for excavation modeling and the results of the modeling are shown in Table 3-19. i • . It was further assumed that the trench excavation would result in a temporary soil storage pile along the length of the trench. Soil particle erosion with subsequent emrainment into the surrounding air was modeled using a model for wind erosion from a continuously active soil storage pile in EPA (1993) guidance. The following equation was used to estimate the PM-10 emission rate from this soil pile. • EF » 0.5 x 1 a-«^OTS\WEsnNGiftiwnpiNiJusicvrexi*«awpd 3-38 CHEMRISK* - A SERVICE OF MCLAREN/HAR' ' T R.HJ385.5 where " - t_ . • ' • • / • ' ' ' i J EF = PM-10 emission factor (g/m2-day), - ...'••• ^^ 0.5 * fraction of wind entrained dust as PM-10 (unitless), 1.9, * empirical constant (g/m2-day), S =• percent silt of aggregate (percent), 365 = days per year (days), . p « , number of days per year with precipitation >0.01 inches (days), 235 . * empirical constant (days), , , f a, fraction of time wind speed >5.4 m/sec at mean pile height (unitless), and 15 = empirical constant (unitless). . ' • - ^ ''-,••N' ' '• ', ' The percent silt content of the soil in the moat was not known, consequently the EPA(1993b) default value of 8 percent was used. EPA(1993b) provides a figure of the Unites States with isopleths of mean annual number of days with at least 0.01 inches of precipitation. The value used for the Westinghouse site is 150 days. To determine the fraction of the time the wind speed exceeds 5.4 m/s, ChemRisk obtained five, years of meteorological data from the National Weather Service Station in nearby Youngstown, Ohio. The joint frequency distribution of wind speed and .direction were determined for all five years of data. The percent of time the wind exceeds 5.4 m/s is approximately 23 percent Table 3-20 displays the joint frequency distribution of wind speed and direction for the Youngstown area. \ . The soil storage pile was assumed to be three meters wide at the base and run the entire length of the trench (20 meters). The volume of the pile was calculated as the in place soil volume (2 m x 3m x 20m =120 m3) times a bulking factor of 1.3, or 156 m3. Knowing the length, base width, and volume of the pile, the surface area exposed to the wind was calculated to be 216 m2. The emission factor (EF) was then multiplied by trmcalcubtedpaesurfx-e area to yield a PM-10 emission rate. This emission rate was subsequently applied to a simple box model and a estimated air concentration was calculated. Table 3-19 summarizes the equations and input values used to calculate the airborne concentration of PM-10 resulting from the excavation of the underground sewer line. i '"''•', , ' Sewer maintenance was assumed to take 2 days to complete, and that the sewer required maintenance every 5 years (GRI* 1988). It was further assumed that the same worker would be called to service the sewer over a twenty five year period, thereby resulting in a twenty five year exposure duration. 3-39 CHEMRISK" - A SERVICE OF MCLAREN/HART 38 56 A complete summary of exposure parameters for the moat storm water sewer maintenance worker is provided in Table 3-21. The results of the exposure assessment for the moat maintenance worker are summarized in Tables H-26 through H-38 in Appendix H. 3.3.4 RailroaV d Sector / ' • ' • . .-,'',• 3.3.4.1 Maintenance Worker . While likely an overestimate of the potential for human exposure to site-related COPC along the Conrail right-of-way, ChemRisk calculated dose rates for a hypothetical rail employee assuming that the tracks and HOW would require annual maintenance resulting in contact with contaminants in '; ' . ' surface soil 5 work days per year over a period of 25 years. The exposure parameters used to assess the hypothetical maintenance worker exposure are shown on Table 3-22. The exposure spreadsheets for the hypothetical railroad maintenance worker scenario are located in Tables H-39 through H-44 in Appendix H. -Using the 95% UCL of the surface soil concentrations for COPCs identified along the railroad ROW (Section 2.2.6), dose .rates were estimated for chronic exposure to carcinogenic and noncarcinogenic site-related compounds via the dermal contact, incidental ingestion, and dust inhalation exposure pathways. ' ' i j 3.3.4.2 Child Trespasser Children traversing along the railroad ROW may be exposed to site-related COPC in surface soil and potentially pooled storm water runoff. For soils, hypothetical child and adolescent exposures were modeled in this baseline assessment for the dermal contact and incidental ingestion exposures routes. The exposure parameter values for this receptor group are identical to those described in Section 3.3.3.2. It was conservatively assumed that a child would spend the equivalent of 78 days per year in contact with railroad ROW surface soils, and that this exposure would occur over a period of 12 years (age 7 through age 18). Regarding potential storm water runoff exposures, because site specific data were not available, potential health risks were evaluated via dermal contact with storm water runoff from the upgradient (in-pipe) Clark Street, Wishart Court Interceptor, and Franklin Street water sampling data. Because few storm water runoff data points are available, statistical analysis of the data was not possible. 3-40 CHEMRISK*-A SERVICE OF MCLAREN/HART Therefore, it was assumed that the child trespasser would come into contact with pooled storm water runoff containing the maximum detected concentration of chemicals from all data points. - • ' • ' ' .•-''• '' Fraction of Skin Surface Area Exposed For the child ages 7 to 12 and 13 to 18, ChemRisk assumed that the hands, forearms, and lower legs ore exposed to the pooled surface water runoff. This equates to a fraction of skin surface area of 0.22 and 0.23, respectively (EPA, 1989b). > Exposure Frequency, the child trespasser was assumed to come into contact \wit h the poolee d surface water four days per year. A complete summary of exposure parameters used to evaluate this exposure pathway is provided in Table 3-23. Estimated daily intakes are summarized in tables H-45 through H-56 Appendix H. 3.3.5 Hypothetical Future Use of Groundwater As discussed in Section 2.2.5, three distinct groundwater groupings have been identified for this site; the central alluvial plume grouping, southern alluvial plume grouping, and the bedrock aquifer grouping. Groundwater within these groupings is known to be impacted with chlorinated and non- chlorinated volatile organic compounds (VOCs), chlorinated semivolatile organic chemicals (SVOCs), polychlorinated biphenyls (PCBs), and inorganic chemicals. The degree and extent of groundwater impacted varies throughout the site for each group'of chemicals. VOCs, SVOCs, and PCBs have reportedly been detected in groundwater in dissolved phase at some locations whereas at other locations, these chemicals make up a LNAPL or DNAPL. Local residences and businesses are connected to a public water supply system for potable water purposes. There is no current human consumption or documented industrial use of the local groundwater. Nevertheless, the Agencies have required evaluation of two future groundwater use exposure scenarios. The two scenarios that will be assessed are the hypothetical future residential use of groundwater and an industrial/commercial use scenario. , Both the residential and the industrial/commercial use scenarios calculate exposures from the following pathways: , , .. 3-41 CHEMRISK*-A SERVICE OF McLAREN/HARf :iR,Hi3858 • Ingestion of groundwateI - r 1 . • Inhalation of chemicals during showering . • Dermal contact with water during showering. • . • ' • , Fof each scenario (residential and industrial/commercial) all three groundwater groupings were evaluated independently using identical exposure parameters, with only the COPCs and EPC changing for each groundwater grouping. The independent groundwater grouping was done in anticipation of the Feasibility Study, and the potential need to evaluate each of the groundwater groupings for remediation using differing technologies and remedial endpoints. The following sections describes the exposure assessment ChemRisk used to evaluate the risks posed by hypothetical groundwater use. tables H-57 through H-88 in Appendix H summarizes the results of the groundwater exposure assessment. 3.3.5.1 Hypothetical Residential Groundwater Use ' ' • ' ' ' \ i 1 Potential exposure to chemicals in groundwater resulting from a residential use scenario can occur via ingestion of groundwater, dermal contact with groundwater, and inhaling chemicals that have ' • volatilized from groundwater during showering. ChemRisk estimated the residential exposure to chemicals from each groundwater grouping based oh these exposure pathways. Section 3.3 L j summarizes the algorithms used to quantify the exposure to chemicals in groundwater. Exposure parameters used in these algorithms are discussed below and are summarizes in Table 3-24. In this assessment, the adult age group is considered to include any individual within the age range of 18 to 70 yrs. To account for age-specific differences in certain exposure parameters used to assess adult exposures, average values were derived tor the following parameters: * body weight, • .water ingestion rates, , ' \t • exposed dermal surface area, and ' • . .. . inhalation rates. The common exposure parameters that are used to determine the exposure to the hypothetical residential users of groundwater are: 3-42 CHEMRISK*- A SERVICE OF MCLAREN/HART RiU3859 • Exposure duration 30yrs • Exposure frequency 350days/yr , , • Lifetime ' 70 yrs Body weight 70kg Exposure Duration, the 30 year exposure duration is consistent with the 90th percentile value for the number of years an individual resides in the some house (EPA, 1989b). ChemRisk assumed that the resident spends two weeks or 15 days away from their residence during the year resulting in a 350 day per year exposure frequency. The 15 days away from the home are reasonably assumed to be due to vacations, holidays, and recreational activities outside the home (EPA, 1991b). , Averaging Time. For carcinogenic exposures, the resident's lifetime was estimated to be 70 years, a value that has been historically used in risk assessments when population-specific data are unavailable. Because the estimated doily intake during the 30 year exposure duration for each pathway is averaged over the resident's entire lifetime for evaluating carcinogenic risk, the application of a larger value for lifetime results in a lower lifetime 'average dally intake. Although EPA (1996) suggests using an averaging time of 75 years, a 70-year lifetime was used in this assessment as a . conservative measure. For the non-carcinogenic evaluation, the averaging time is equal to the exposure duration, or 30 years \*S expressed in days (EPA, 1989a). Body Weight. The adult body weight value of 70 kg is derived by rounding the average Of the body weights for men and women between the ages of 18 to 70 (EPA, 1989b). Groundwater Ingestion Ingestion Rate. The groundwater ingestion rate for the hypothetical adult resident is 2.0 liters per day (EPA, 1989b, 1995b). This value represents the upper 90th percentile of fluid intake based on a study by Cantor et at (1987) which was in close agreement to the 90th percentile value of 1.9 liters per day calculated by Gillies and Paulin (1983). 3-43 CHEMRISK'* - A SERVICE OF MCLAREN/HART While showering with groundwater contaminated with chlorinated VOCs. two exposure pathways will likely contribute to the potential chronic daily intake of COPC: inhalation of volatilized chemicals and dermal absorption of chemicals. This section describes the equations and parameters that are used to estimate the intake of chemicals via inhalation that a hypothetical resident may be subjected to while showering with contaminated groundwater. The exposure algorithm ChemRisk used to calculate the average doily intake of chemicals via inhalation during showering is given in Section 3.3. The following discusses the, model used to derive chemical specific air concentrations and the exposure parameters applied to the residential exposure scenario. ..:..•••-•• Chemical Concentration in Shower Air. Air concentrations of groundwater contaminants resulting from volatilization during showering and bathing are calculated based on a model proposed by McKone (1987), and McKone and Bogen (1991). The principal components of the volatilization model are based on the transfer efficiencies ofgroundwate r contaminants from the shower water into the shower stall air, the volume of the shower compartment, the ventilation rate of the shower expressed as a volumetric flow rate, the flow rate of the shower, and the length of time the shower is in operation. The equation used to estimate the shower or bath air concentrations is as follows: ' where, 1 Ca = Chemical concentration in air (mg/m3), Cw = . Chemical concentration in groundwater (mg/l), TC = Transfer efficiency coefficient (unitless), - Flow rate of shower (1/min), = Time shower is running (min), . = Volume of shower area (m3), and AXR -= Air exchange rote' (mVhr). 3-44 CHEMRISK* - A SERVICE OF MCLAREN/HART <(i386l Transfer efficiency coefficients, TC, for each compound were calculated based on the equation presented in McKone (1987). The transfer coefficients were estimated based on measured transfer coefficients of radon in showers and assuming that the transfer efficiencies of other chemicals are proportional to the overall mass-transfer coefficient at the liquid/gas boundary/Temperature differences were not found to play a significant role in the transfer efficiencies of the chemicals: The transfer efficiencies were calculated using the following equation. "l* t_*rv ' 2 2 Kn n where ~ ' $1 = transfer efficiency for chemical j (unitless), 4*1** a transfer efficiency of radon (unitless), > . \ p| = liquid phase diffusion coefficient (mVs), R =5 • • universal gas constant (0.0624 Torr-mVmol-K), T =« temperature (K), ' ,' . - D» = gas phase diffusion coefficient (mVsec), and H = Henry's law constant (Torr-mVmol). ' i • ' ' * • : ' > ' ' ' Shower Flow Rate. The shower flow rate, Qshower, is estimated to be 15.4 liters per minute which is the arithmetic mean of measured flow rates for non-conserving shower heads reported by EPA ( 1996*0 in the Er/wwwrtf Factors Handbook - Review Draft. ; - . ' . • Showering Time, The time spent in the shower, ishower, was assumed to be equal to 12 minutes per day, which is conservative with respect to the mean shower duration reported in EPA (1996f). Shower Stall Volume and Air Exchange Rate. The volume of the shower stall, Vshower, is assumed to be 2 ra' (McKone and Bogen, 1991). The shower is confined to an enclosed shower stall The air exchange rates for the shower is 12 mVhr, respectively (McKone and Bogen, 1991). 3-45 CHEMRISK* -A SERVICE OF MCLAREN/HART 'iR.iu3862 Inhalation Rate. The inhalation rate, IhR, for the adult is assumed to be equivalent to the average adult (both men and women) ventilation rate at a light activity or 6.01 mVmin or 0.6 mVrain. (EPA, 1989b). Dermal Contact . : ' - - • • . • • ' The steady state dermal absorption model was employed as described in EPA (1989a). This model assumes that the calculated exposure is actually an absorbed dose, and not simply the mass of chemical that contacts the skin on a time weighted basis. The equation describing the absorbed dose calculation is shown in Section 3.3 and the pertinent exposure parameters are discussed below. Note that the groundwater/shower water concentration has been corrected to account for the fraction of chemical lost due to volatilization. Permeability Coefficient. The permeability coefficient is a value equal to the flux, normalized to concentration, that represents the rate which a chemical penetrates the skin. .The permeability coefficients that are used in this assessment are chemical specific values derived from EPA's guidance document; Dermal Exposure Assessment: Principles and Applications (EPA, 1992c). Further discussion regarding permeability coefficients is presented in Section 4. ( ; Surface Area. The value used to represent the dermal surface area for adults is represented by the arithmetic average (50th percentile) of the total dermal surface area of adult women and men (EPA, 1989b). / ; \ , Fraction of Exposed Skin. The fraction of exposed skin used for the adult is assumed to be equal to one. That is, the entire surface area of the exposed individual is assumed to come into contact with impacted water, ' . ' 3.3.5.2 Hypothetical industrial/Commercial Groundwater Use . Similar to the residential groundwater use, ChemRisk calculated the potential exposures from the ingestion, dermal, and inhalation pathways. The same algorithms and models as those described above, were used to estimate the doily intake of chemicals for the industrial/commercial groundwater use scenario. Because the industrial/commercial user does not follow the same general water use patterns as the residential user, the exposure parameters for the industrial/commercial worker differ. ofta^NT»wEsiiNG»i»T«NiAisKvre)ri\SKt3.wp«i 3-46 CHEMRISK* -' A SERVICE OF MCLAREN/HART R,Hi3863 The following summarizes common exposure parameters for all pathways (ingestion, dermal contact, _ and inhalation). A list of all exposure parameters is provided in Table 3-25. ) .--*.,.' • '• ~ ^*** . • Exposure frequency 250days/yr • Exposure duration 25 yrs > Lifetime 70 yrs • Body weight 70 kg Exposure frequency. Because exposure to the hypothetical worker will only occur while at work, the exposure frequency is equal to the time that the worker spends at work on an annual basis. For this assessment, it is assumed that the individual is at work for five days per week. It is further assumed that two weeks out of the year ore taken as vacation away from the workplace. This results in an exposure frequency of 250 days per year (EPA, 1991 b). •'.,-'. / . Exposure duration. The duration of exposure is equal to the number years that a worker is likely to be employed at a facility. EPA recommends that a 25-year exposure duration be used when evaluating worst case potential health risks to workers. The 25-year exposure duration was derived by the US Bureau of Labor Statistics and represents the 95th percentile value for the length of time on employee remains at the same work location (EPA, 1991b). ; • • • •' .'• "' . •• , . • • ' ' ' , - ; Body weight The body weight of worker is assumed to be equalto70kg(EPA, 1991b). The adult body weight value of 70 kg is derived by rounding the average of the body weights for men and women between the ages of 18 to 70 (EPA, 1989b). Averaging Time. For carcinogenic exposures, the worker's lifetime was estimated to be 70 years, a value that has been historically used in risk assessments when population-specific data are unavailable (EPA, 1991b). More recently, the EPA (1989b) suggests that 75 years may be a more appropriate average lifetime value for males and females combined. Because the estimated daily intake during the 25 year exposure duration for each pathway is averaged over the,worker's entire lifetime for evaluating carcinogenic risk, the application of a larger value for lifetime results in a lower , chronic daily intake. Thus, the application of a 70-year lifetime in this assessment is likely overly conservative. 3-47 CHEMRISK*. A SERVICE OF MCLAREN/HART . > 4R.4U3861* ., For non-carcinogen exposure, the averaging time is equal to the exposure duration or, in the case of th' e hypothetica;, -.-l -.-worker' , 2'5 year•'s (EPAv , 1991b)<" . '-. • -•'• :• .' ..- •' •. Exposure parameters that are specific to an exposure pathway are presented below. Ingestinn 4 Ingestion Rate. The groundwater ingestbn rate for the hypothetical industrial/commercial adult worker used for estimating the doily intake is 1.0 liters per day (EPA, 199 Ib). This value represents half of the typical daily consumption rate that EPA uses to evaluate residential exposures. It is conservatively assumed that all water that the worker ingests is impacted groundwater. ( .'"''.'• ' ' ' - ' Inhalation of Chemicals While Showering n Showering Time. The time the industriaVcommercial worker spends in the shower was assumes to be approximately equal to the median shower length or about eight minutes (EPA, 1989B). All other exposure parameters pertaining to showering are equal to those defined above for the residential receptor. * Derma! Contact , . * ( j To estimate the dairy chemical intake from dermal contact, the exposure parameters identified for the residential groundwater were used. The only differences are the exposure frequency and exposure duration which are specified above for the industrial/commercial worker. 3-48 CHEMRISK* - A SERVICE OF MCLAREN/HART 4.0 TOXICITY ASSESSMENT Toxicity assessment is defined by the EPA (1989a) as an evaluation of the inherent toxicologic potential associated with exposure to a chemical Toxicity assessment is a two-step process that includes hazard identification and dose-response assessment. Whereas hazard identification is a qualitative description of the potential health effects associate\. d with exposure to a .given chemical, dose-response assessment is a quantitative1 analysis of the relationship between the magnitude of the dose received and the observed toxicologic responses within an exposed population (EPA, 1989a). In an ideal situation, actual human data would be used quantitatively to characterize the potential occurrence of adverse effects. In most instances, however, such data are not available. Therefore, the scfentific understanding of the dose-response relationship is largely based on data collected from animal studies (usually rodent bioassays) and hypotheses about what might occur in humans. Mathematical models are used to estimate the possible responses in humans at levels far below those tested in animals. These models contain several limitations which should be considered when risk estimates are evaluateV d (EPA, 1989a).''•', as discusse' d in the uncertainty evaluatio" n (Sectio' ' n 5.3). In an effort to determine whether exposure to a chemical can cause an increase in the incidence of cancer in animals or in humans, the EPA characterizes the nature and strength of causation according to the **weight-of-evidence" carcinogen classification system (EPA, 1989a). This classification system is summarized in Table 4-1. The EPA weight-of-evidence carcinogen classification for each COPC is given in Tables 4-2 and 4-3. ' Toxicity values for each COPC were obtained from one of the following sources: the EPA Integrated Risk Information System (IRIS), the Health Effects Assessment Summary Tables (HEAST) (EPA, 1995c), or EPA criteria documents. The IRIS database contains descriptive and quantitative toxicity i information and is considered to be the most authoritative source of verified EPA toxicity values, including cancer slope factors (CSFs) and reference doses (RfDs) for human risk assessments (EPA, 1989a). Although IRIS values ore recommended by the Agency to ensure consistency in risk 1 • • ' r . CAOJEKTTWEnTNCWIWTINLJUSICVTEXT-«4-JJd ' ! 3H ' CHEMRISK* - A SERVICE OF MCLAREN/HART :iR.U)3866 assessments, it is important to note that alternative toxicity values may also be used in Superfund risk assessments if they are based upon more recent, credible, or relevant toxicological data (EPA, 1993b). For the purpose of this human health risk assessment, however, EPA-derived toxicity values were used for all chemicals. HEAST is prepared annually by EPA's Environmental Criteria and Assessment Office (ECAO) and provides information on chemicals commonly found at both Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) and Resource Conservation and Recovery Act (RCRA) sites. In addition to verified toxicity values. HEAST lists interim CSFs and RfDs. For this assessment, information contained in IRIS superseded all other sources of information and other sources were consulted only when information was not available in IRIS. Consistent with EPA (1989a) guidance, EPA criteria documents (i.e., EPA, 199 Ib) were also consulted as sources of toxicity information for chemicals without published values in IRIS. Additionally, EPA Region in documents (EPAt 1996a) were consulted to obtain toxicity information when toxicity values were not available from IRIS, HEAST, or other EPA sources. When no toxicity values were available for specific COPCs, values for similar chemicals were employed. The surrogate chemicals are chosen based upon structural similarities to the COPC for which no data exist. For instance, a general value for the carcinogenic effects of PCBs was utilized t i for Aroclors 1242,1248, 1254, and 1260 in the a"bsence of toxicity data specific to each Aroclor. Summary toxicity profiles for the COPCs identified in Section 2.2 are presented in Appendix G. In cases where a group of chemicals share similar physical chemical, and/or toxicologic properties, such as dioxins, PAHs, or PCBs, a single toxicity profile was prepared for all the chemicals belonging to that group. Toxicity information for all COPCs is also summarized in Tables 4-2 and 4-3. • ' •' - '. ' ' ' ' • " ' 4.1 CARCINOGENIC RESPONSE Both human epidemiological studies and animal bioassays are used to assess the carcinogenic potential of chemicals. Frequently, epidemiological studies have been conducted for occupational populations because they are typically exposed to. higher concentrations of chemicals than the general population. Animal carcinogenicity bioassays involve measuring the tumor incidence in rats or mice following administration of various doses of the chemical for the estimated lifetime of the animal. 4-Z CHEMRISK* -A SERVICE OF MCLAREN/HAR' T AR.JU3867 For regulatory purposes, it is assumed that any dose of a carcinogen, no matter how small, presents some level of risk. To estimate the theoretically potential response at these tow doses, various mathematical models have been developed. The accuracy of the projected risk at the dose of interest is a function of the accuracy of the mathematical model in predicting the true (but not measurable) relationship between dose and risk at low dose .levels. EPA generally uses the linearized multistage (LMS) model for low dose extrapolation from animal studies (Munro and Krewski, 1981). This model assumes that the slope of a dose-response curve con be extrapolated to zero in a linear manner. The numerical expression for the carcinogenic potency of a chemical calculated by the LMS model is known as the %*, or cancer slope factor. The %* represents the 95 percent upper confidence limit on the sbpe of a dose-response curve derived from either animal or human studies, The slope of the dose-response curve is a quantitative estimate of a chemical's carcinogenic potency and is calculated as the change in tumor incidence (y-axis) over the change in dose (x-axis). Thus, the units of q,* are the probability of tumor incidence divided by the dose level given m milligrams (mg) of chemical per kilogram (kg) of body weight per day ([mg/kg-day]*1). . Cancer slope factors are considered to be theoretical upper bound estimates of risk at a 95 percent upper confidence level (Le., there is a 95 percent probability that the true risks do not exceed these levels and are likely to be much lower). The« EPA'' s Huma' n .Healt h Assessmen- t Group (HHAG),' formerly called the Carcinogen Assessment Group, stated that the use of the LMS model and upper-bound risk estimates is appropriate, but that the lower limit of risk may be as tow as zero (EPA, 1986a). The HHAG stated that an "established procedure does not yet exist for making 'most likely* or 'best' estimates of risk within the range of uncertainty defined by the upper and tower limit estimates" (EPA, 1986a). "..'•" ' . ' . ~, > ' '-. Regulatory Agencies in the United States continue to base CSFs on the nonthreshold LMS model (EPA, 1989a). For the purposes of this human health risk assessment, the CSFs established by EPA were used to assess the potential carcinogenic risks to hypothetically exposed populations. These CSFs are presented in Tables 4-2 and 4-3. i - • • In its weight-of-evidence determination of carcinogenicity, EPA has classified PCBs in Group B2 (probable human carcinogen) based on sufficient evidence of carcinogenicity in rodents (EPA, 1988). In September 1996, EPA published a reassessment of the carcinogenic potential of PCBs (EPA, 1996b). That reassessment specified a new set of CSFs for PCBs, including both upper-bound cancer potency estimates and central-tendency estimates. On October 1, 1996, those revised CSFs were £3 ' CHEMRISK* - A SERVICE OF MCLAREN/HART , ;iR.|u3868 listed on EPA's IRIS. The revised estimates were based largely on a comprehensive study of PCBs in rats completed by Battelle Laboratories under GE sponsorship. The reassessment also took into account all the prior carcinogenicity data, a revaluation of the histopathology in the prior data by Moore et aL (1994), and a revised cross-species scaling factor. The reassessment specifies a range of CSFs,'depending on the exposure pathway and the degree of chlorination of the PCBs. For PCB mixtures other than those containing minimal amounts of the more highly chlorinated congeners, the central-tendency CSFs range from 0.3 to 1 (mg/kg-day)'1 and the upper-bound CSFs range from 0.4 to 2 (mg/kg-day)'1 (EPA, 1996b). The tower end of these ranges is to be used for vapor inhalation, dermal exposures (if no dermal absorption factor is applied), and water ingestion, and the upper end is to be used for soil or sediment ingestion, dermal exposures (if an absorption factor is applied), dust inhalation, and food chain exposures. Lower CSFs — 0.04 and. 0.07 (mg/kg-day)'1 for central- tendency and upper-bound estimates, respectively -- are prescribed for PCB mixtures in which congeners with more than four chlorines comprise less than 0.5 percent of the total PCBs. The upper-bound CSFs specified for more highly chlorinated PCB mixtures in EPA's reassessment document will be used to assess the carcinogenic potential of PCBs in the risk assessment. Specifically, a CSF of 0.4 (mg/kg-day)'1 will be used for ambient air inhalation, while a CSF of 2 (mg/kg-day)'1 will be used for soil and sediment ingestion, dust inhalation, and dermal exposures. ChemRisk believes that, for dermal exposures, it is more appropriate to apply a dermal absorption facto• r tha- •n to ignor•• e tha,.;:.t. factor and use a lower, CSF. .' -' , .' For certain classes of carcinogenic compounds that are structurally similar, and for which data are insufficient to calculate individual CSFs, regulatory Agencies have adopted the use of toxicity equivalence factor (TEF) schemes as an interim procedure (EPA, 1989d, 1993c, 1994). Such schemes are used to predict the carcinogenic potency for those compounds for which chronic carcinogenicity bioassays have not been conducted. The TEF methodology estimates the toxicity of each compound within a defined chemical class relative to a reference compound for which adequate dose response data are available. In theory, the application of TEFs allows the concentration of each individual compound or congener to be converted into ari equivalent concentration of the reference compound for use in assessing risks. In general, TEFs are estimated from the results of short-term in vivo and in vitro toxicity bioassays (EPA, 1989d, I993c, 1994). 4-4 CHEMRISK" -A SERVICE OF MCLAREN/HART ,'IR HI3669 TEF schemes have been used by the EPA for evaluation of compounds such as PCDD/Fs, carcinogenic PAHs, and coplanar PCBs (EPA, 1989d, 1993c, 1995b). Consistent with EPA practice, TEFs have been used in this assessment to evaluate the carcinogenic potential of PCDD/Fs and carcinogenic PAHs. For PCDD/Fs, EPA currently employs the International Toxic Equivalency Factor or I-TEF scheme, and assigns a TEF to each congener based on its assumed toxicity relative to that of 2,3,7,8-TCDD (Table 4-4) (EPA, 1989d). However, as described in further detail in the uncertainty analysis (Section 5.3) recent evidence demonstrates that the biological activity of PCDD/F congeners in environmental media may be far less than additive. Specifically, the predicted biological activity of the PCDD/F mixture (when the TEF approach is applied as above) may be much greater than measured in an in vitro or m vivo assay system (EPA, 1989d). Hence, because additivity was assumed in this assessment, the PCDD/F-related risks described in this human health risk assessment are likely over-estimated. However, this over-estimation may be balanced by the fact that dioxii^-like PCB congeners were not evaluated as part of this assessment. For carcinogenic PAHs, interim oral potencies are based on the estimated carcinogenic potency relative to benzo(a)pyrene (Table 4-2) (EPA,1993c). - • 1 ••''-,. 4.2 NONCARCINOGENIC RESPONSE It is widely accepted in the scientific community that noncancer effects related to exposure to chemical substances occur only after a threshold dose has been achieved (Klaassen et aL, 1986). A threshold dose is a level of intake below which adverse effects ore not expected to occur. For the purposes of establishing toxicological benchmarks for noncarcinogenic chemicals, the threshold dose is usually estimated from the no-observed-adverse-effect-level (NOAEL) or the lowest-observed- adverse-effect-level (LOAEL). The NOAEL is defined as the highest dose at, which no adverse effects occur, while the LOAEL Is defined as the lowest dose at which adverse effects are observed. NOAELs and LOAELs derived from both animal and human studies are used by EPA to establish chronic reference doses (RfDs) for humans. EPA (1989a) defines a chronic RfD as "an estimate (with uncertainty spanning an order of. ,magnitud V e or greater. ) of a' daily exposure level fo\ r. the• human population, including sensitive subpopulations, that is likely to be without an appreciable risk of deleterious effects during a lifetime.** Uncertainty factors are incorporated into RfDs in an attempt to account for limitations in the quality or quantity of available data. Many RfDs include a 100-fold • . • i safety factor to account for uncertainties in extrapolating animal data to human health effects (a factor often) and differences in sensitivity within the human population (another factor pf ten). However, if the available databases are incomplete, an additional uncertainty factor, known as a modifying 4-5 CHEMRISK* - A SERVICE OF MCLAREN/HART /)Ri(J3870 factor, may be applied. For example, if available data do not establish a NQAEL and/or there are data gaps for some types of health effects, a safety factor of 1,000, representing an uncertainty factor of \^ J " 100 and a modifying factor of 10, could be used to establish the RfD. ^"^*^^ ~ ' m ' • ' Tables 4-5 and 4-6 presents the health criteria used to evaluate noncarcinogenic effects resulting from oral exposures. For the purposes of this human health risk assessment, oral reference doses and/or inhalation reference concentrations established by EPA were used as the basis for assessing the potential noncarcinogenic chronic health hazards for the hypothetically exposed populations. As noted later in Section 5, manganese accounts for the largest fraction of noncancer risk. Accordingly, it is of value to review the basis of the inhalation reference concentration (RfC). The EPA has derived an inhalation RfC of 5.0E-05 mg/m3 for manganese based on the findings of Roels et aL (1987, 1992). Results of these studies indicate neurobehavioral dysfunction in manganese- exposed workers at a LOAEL of 0.34 mg/m3 for total dust of mixed forms and measured respirable dust fraction of MnO2 (IRIS, 1996). The RfC value is determined using an uncertainty factor of 1,000, which allows for a factor of 10 for sensitive individuals, 10 for the use of a LOAEL, and 10 for database limitations due to less-than-chronic exposures and unquantified differences in the toxicity of the forms of manganese. Furthermore, the EPA has assigned medium confidence in the principal studies and medium confidence in the database (IRIS, 1996), suggesting that there is a recognized I ) level of uncertainty in the underlying toxicblogicol studies. - '' • •"' , '•",'. .-' 4.3 RELATIVE ABSORPTION FACTORS - Relative absorption factors (RAFs) are factors used in risk calculations to account for differences in the absorption potentials of COPCs under the experimental conditions upon which the applicable toxicity criteria are based relative to the site-specific absorption potentials (EPA, 1989a). A unique chemical-specific RAF is derived for each route of exposure (e.g., inhalation, soil ingestion) using the following two factors: 1) the absorption efficiency for the particular exposure route and medium (e.g., air, water, soil, sediment) being evaluated at the site; and 2) the absorption efficiency for the ; route and medium (gavage, diet, water) evaluated in the toxicity study. The RAF is the product of the site-specific absorption efficiency and the inverse of the absorption efficiency specific to the toxicity study (EPA, 1989a). RAFs are calculated as follows: AbsorptionEfficiency^ ———, „ Absorption EfficiencySTUDY „„„„,„„„„, ,„ twure 4-6 CHEMRISK"- A SERVICE OF MCLAREN/HAR'T ;lR:tU387l Absolute absorption efficiencies were estimated based upon data available in the scientific literature. Secondary sources consulted for absorption information included the EPA's Dermal Exposure Assessment: Principles and Applications, and lexicological profiles prepared by the Agency for Toxic Substances and Disease Registry (ATSDR). Available primary literature sources were also consulted. In the absence of chemical-specific data, default absorption assumptions were made. Absorption efficiencies estimated from scientific data were rounded to one significant digit to reflect the uncertainty in the values. Due to the complexity of inhalation exposures and the paucity of data on absorption efficiencies, all .COPC were assumed to be 100% absorbed through the respiratory tract. Table 4-7 shows absolute absorption efficiencies for the site COPC. Tables 4-8 and 4-9 show calculated relative absorption efficiencies and dermal permeability coefficients, respectively. 4-? CHEMRISK0 - A SERVICE OF MCLAREN/HART . 5.0 HUMAN HEALTH RISK CHARACTERIZATION Risk characterization integrates all aspects of the health risk assessment process and provides a scientific interpretation of the overall assessment (EPA, 1989a, 1992b). In the risk characterization, all data, results, conclusions, and uncertainties from the hazard identification, dose-response assessment, and exposure assessment are evaluated in order to draw scientifically supportable conclusions. Not only are the potential noncarcinogenic and carcinogenic health risks quantified (NAS, 1983), but also, the risk characterization presents and discusses the critical uncertainties of the analysis (EPA, I992b). the EPA (1992b) Exposure Assessment guidelines specify that four critical tasks be accomplished by the risk characterization. According to EPA, **the risk characterization: .• . ' \ • • ( j 1. Integrates the individual characterizations from the hazard identification,' dose- response, and exposure assessments; : 2. Provides an evaluation of the overall quality of the assessment and the degree of confidence the authors have in the estimates of risk and conclusions drawn; 3. Describes risks to individuals and population in terms of extent and severity of . probable harm; and , - ,4; Communicates results of the risk assessment to the risk manager" (EPA, 1992b). > In this risk characterization, chemical-specific, hypothetical risk estimates calculated by Westinghouse are presented. In addition to these risk estimates, in the February 10,1998 comments to Westinghouse (see Appendix I). EPA recalculated risks for all the exposure scenarios. In most •' cases, EPA's risk estimates do not substantially differfrom Westinghouse's calculations. However for the Moat, EPA estimated risks that exceeded the target benchmark compared to Westinghouse's i J , 0;\aiENTS\WESTINGH\i99l\»SECTSWPD ; 5'1 CHEMRlSK^A SERVICE OF MCLAREN/HART ARHU3873 calculations. For one exposure scenario specifically, EPA estimated risks for unrestricted worker access to the Moat while Westinghouse did not consider this a baseline exposure scenario. Both sets of risk estimates are provided in Table 5-1, although the text only reters to Westinghouse's estimates. . Consistent with EPA guidance (1989a), the potential exposures have been combined across relevant exposure pathways and across the various COPC in order to present upper-bound, cumulative carcinogenic and noncarcinogenic risk estimates. Cumulative risks and hazard indices are compared to acceptable benchmark levels supported by PADEP and EPA Region III In keeping with the EPA (1992b) guidance, professional judgment was used to select the most significant uncertainties (those ' that define and explain the risk estimates) for discussion in this risk characterization, V ' • ' - • ' ,. _•"'•. 5.1 CARCINOGENIC RISK Upper-bound incremental lifetime cancer risks were estimated for a variety of hypothetical sector-- and groundwater grouping-specific human exposures to COPC in surface and subsurface soil, _ sediment, air, groundwater, and surface runoff. Risks were calculated by multiplying estimated doses) , expresse.d as LADIs calculated in Sectiov , n 3.3, by the. appropriat• e toxicity- values- , as reported in Section 4.0. For most cases, the equation for estimating cancer risk is as follows; , - -• . •'' '- . , • -: '-••••.,.,. ' " - Risk = LADIxCSF where: • Risk = Lifetime incremental cancer risk (unitless; expressed as a - probability); LADI =» Lifetime average daily intake (mg/kg-day); and CSF m Cancer slope factor (mg/kg-day)"1. For cases where hypothetical risks were calculated to be greater than 1 x 10"2, ChemRisk used the one-hit equation described in EPA (1989a). The one-hit equation is as follpws: Risk - l-exp(-LADIxCSF) / "•,'.' '•'".. These equations yield an approximation of incremental cancer risk above the background cancer rate. In the United States, the background cancer rates for men and women are 1 in 3 (33%) for women and 1 in 2 (50%) for men (ACS, 1996). G«.IENTS\WESTINGHM9M\9KECt5WPD 5-2 CHEMRlSK^A SERVICE OF MCL-AREN/HART Cumulative risks were calculated by summing acros• s all chemicals /to determine the total incremental v ' • ' ••'•'•, '-, . - lifetime cancer risk for hypothetically exposed individuals in each sector. The chemical-specific \*~s carcinogenic risk estimates for each hypothetical receptor are presented in Appendix H, and summarized in Table 5-1. As evident for the River Sector, the total incremental lifetime cancer risk estimate for the Child Wader is 8 x 10"6. In comparison, the target range of incremental cancer risk for CERCLA sites as stipulated by the National Contingency Pbn (NCP) is 1 x 10*6 to 1 x 10"4 (one in a million to one in ten thousand) (EPA, 1990b). Thusi the hypothetical Child Wader risk estimate lies within the NCP target cancer risk management benchmark. Although risks from consumption offish were not quantified, this pathway is of potential concern given the elevated sediment levels at certain locations in the Shenango River. ' The hypothetical indoor and outdoor construction worker scenarios resulted in total incremental carcinogenic risk estimates of 2 x 10*6 and 7 x 10'6, respectively, and therefore within the NCP target risk range. For the Moat, the carcinogenic risk estimates were as follows: hypothetical maintenance worker: 9 x 10**; hypothetical child and adolescent trespasser: 3 x 10"*; hypothetical adolescent trespasser: 1 x 10"*; and hypothetical utility worker: 1 x 10"*. Consequently* all of the Moat carcinogenic risk estimates lie within the NCP target range. , • • • . ' - ' ^ . For the hypothetical Railroad Right-of-Way (ROW) exposure scenarios, the maintenance worker was estimated to have an incremental carcinogenic risk of 1 x 10"5, while the child and adolescent trespasser contacting soil were estimated to have an incremental carcinogenic risks of 1 x 10"4 and 5 x 10*5, respectively, and risks of 3 x 10"6 and 2 x 10"6, respectively, associated with contacting pooled surface water runoff. Direct soil contact exposure for the hypothetical child .trespasser along the Railroad Right-of-Way therefore equals the high end (1 x 10*4) of the NCP carcinogenic risk management benchmark. As discussed previously in Section 3 and shown in Table 3-6, this is largely the result of a few data points (n=6) nearest the former bulk chemical storage area proximate to the Middle Building whose surface soil concentrations in relation to the remainder of samples from the Railroad ROW are substantially higher. Because of the relatively small sample size of the ROW sample database, this HHRA had to rely upon the maximum concentration to characterize risk for the hypothetical child and adolescent trespasser. Accordingly, risk estimates for this receptor very likely exaggerate (overstate) upper-bound carcinogenic risks for this receptor. .*'.-'.' . -,,.!' - i ' . Future employee risk estimates were derived for exposure to the Middle Sector building indoor air. The carcinogenic risk estimate for this pathway is 2 x 10*4, exceeding the NCP carcinogenic risk i management benchmark. \ [ <»aEnawEsiii«3»i99«wsECTs.wpD . ,5-3 CHEMRis K* ASERVIC E OF MCLAREN/HART ' - .'-',' • • '.'•'.. ' . - . \ . .iR 11)3875 ' There are several factors which should be considered when evaluating the estimated risk to the indoor employee. First, the computed risk to the future employee is driven by the result of a single data point for 1,2-dichloroethane among a limited number of air samples (n=5). In fact, only one other air sample contained detectable concentrations of 1,2-dichloroethane. Second, this assessment is based on only one round of air sampling. Because of the relatively high mobility of air ^is an exposure medium, the likelihood for varying concentrations with time is greater than for media such as soil or groundwater. Thirdly, 1,2-dichloroethane is not known to be a significant soil and/or groundwater contaminant at this site. In fact, 1,2-dichloroethane has riot been detected in any soil samples collected from any sector. Similarly, 1,2-dichloroethane has been detected only once in all the groundwater samples evaluated for this HHRA (Central and Southern plumes as well as bedrock). The single 1,2-dichloroethane detection was 6 ug/L which was an approximate concentration, below the detection limit of 20 ug/L. In addition, many other volatile chemicals detected in the site groundwater and soils were not detected in any air samples; - • ~ / • ' ' . • ; • ' i Finally, it must benioted that the air quality samples used to evaluate risks to thcTfuture employee were collected prior to the planned interior building cleanup or facility buildout, both of which have to occur prior to its regular occupancy by the future employee. The interior cleanup will remove or otherwise limit exposure to residual materials from building surfaces. Therefore, if the source of the l,2=dichloroethane is an interior residue, its presence should be mitigated by the interior cleanup. These factors taken together strongly suggest that: 1) the data point used to evaluate risk to 1,2- dichloroethane is highly uncertain due to likely temporal variation; 2) the source of the 1,2- dichloroethane is not likely to be the soil or groundwater underlying the building; and 3) interior building cleanup and buildout renovations will further reduce concentrations of chemicals in indoor air. • • Finally, carcinogenic risk estimates for the hypothetical Resident and Worker consuming and using local groundwater from the Southern Alluvial plume, Central Alluvial plume, and Bedrock aquifer all exceed the high end of the NCP risk management benchmark] Individual numerical risk estimates are provided in Table 5-1. - 5.2 NONCARCINOGENIC HAZARD Noncarcirlogenic hazard indices were estimated for each sector and groundwater plume grouping. Hazard indices were calculated by dividing exposures, expressed as the ADIs calculated in Section o\cti£NTs\wESTiNG»i9«\«sEcrswpo " * 5-4 CHEMRIS^A SERVICE OF MCLAREN/HART , j ^" mf ' ' ' . .1R.1U3876 ' 3.3, by the appropriate reference doses, as reported in Section 4.2. The equation for estimating the noncarcinogenic hazard quotient is as follows: . , • <'' Hazard Quotient = ADl/RfD where: ..'/•' Hazard Quotient = Ratio of estimated doses to toxicity criteria; ADI (= Average daily intake (mg/kg-day); and ( RfD • " . . • Reference Dose (rrig/kg-day). Composite hazard indices were calculated by summing across all chemicals, without regard to target organ, to determine the total hazard index for hypothetical individuals within each sector and/or groundwater grouping. The chemical-specific noncarcinogenic hazard quotients for each hypothetical receptor are presented in Appendix Hv Total 1hazard indices are summarized by receptor in the right hand column of Table 5-1. A total receptor hazard index greater than I is typically considered by EPA to represent a potential concern for noncarcinogenic health effects (EPA, 1989a, ' 1996a). . ; ; • ' In summary, the River Sector (child wader) noncancer risk estimates do not exceed the benchmark criterion of 1. The hypothetical indoor and outdoor construction worker receptor noncancer risk x_x estimates, on the other hand, indicate hazard indices substantially higher than the target threshold. ^ For the indoor construction worker, particle-bound manganese accounts for roughly one-half of the hazard index, and for the outdoor construction worker it accounts for essentially all of the hazard index. The exposure point concentration for manganese is elevated principally due to samples from TB-8andTB-10. Samples from the remaining eleven borings had manganese Concentrations which . . we.re closer to those measured in the EPA residential sampling program. Because the EPC for manganese is driven by the two soil borings, the hazard, indices for the indoor and outdoor construction workers are likely to be overstated (conservatively high). All noncancer risk estimates for the Moat (which include the hypothetical maintenance worker, child/adolescent trespasser, and utility worker) were below the noncancer risk management threshdld of 1. For the Railroad ROW, the hypothetical maintenance worker noncancer risk estimate was below the regulatory threshold, while the hypothetical child and adolescent trespasser hazard index exceeded unity. Noncancer risk estimates associated with dermal contact with pooled stormwater runoff for the child and adolescent trespasser were well below the noncancer criterion. : -.'-'. ' . v ' _ . 0\CLIEOTS\WESTINGH\I99I\9ISECTSWPD 5'5 CHEMRlSK^A SERVICE OF MCLAREN/HART Noncancer risks estimates for the future employee exposed to indoor air exceeded the noncancer benchmark hazard index of I . As with the carcinogenic risks, a majority of the noncancer risk was due to single elevated 1,2-dichloroethane detection. The discussion regarding trie presence of 1.2- dichloroethane and how it effects the estimate of risks for the future employee presented in Section 5.1 is also applicable to noncancer risks. Finally, noncancer risk estimates associated with the hypothetical industrial. consumption (i.e., ingestion and showering) use of groundwater show exceedances of the benchmark hazard Index of 53 EPA CALCULATED RISK ESTIMATES EPA has calculated risks for the exposure scenarios evaluated by Westinghouse as well as unrestricted industrial and construction worker access to the Moat and ingestion of groundwater by achtlcl The results of these risk calculations are reported in Appendix I. As calculated by EPA, potential cancer risk to.an industrial worker with unrestricted Moat access is estimated to be 2 x 104. Potential noncarcinogenic hazard is estimated by EPA to be 3'.5. For the construction worker, potential risks have been calculated by EPA as 2 x 10'* and 0.5 for cancer and noncancer, respectively. Finally, EPA's cancer risk calculations for dermal contact and ingestion of groundwater by a child are 9x 10°, approximately equal to 1.0, and 2 x 10"3 for southern, central, and bedrock groundwater, respectively. Noncancer hazards for a child from dermal contact and ingestion of southern, central, and bedrock groundwater as reported by EPA are 1700, 5.0 x 106, and 350, respectively. 5.4 IDENTIFICATION OF UNCERTAINTIES An important facet of the method and use of human health risk assessment concerns the recognition of uncertainties and limitations inherent in the process which arise in connection with dose-response models, animal to human extrapolation, chemical fate and transport, models of potential exposure, and site-specific characteristics. From a regulatory perspective, these uncertainties and limitations may be addressed by developing and employing assumptions which typically overestimate the magnitude of many variables. In this fashion, Agencies charged with the protection of public health have often assumed that their mandate would best be met by overestimating potential risks from exposure to environmental contarninants (Paiistenbach^ 1990b). However, aspuT awareness of these uncertainties improves, along with our understanding of how to best characterize them, the result - 5-6 CHEMRiSK^A SERVICE OF MCLAREN/HART i J ' i^""^^ AfUu3878 will almost certainly be risk assessments that are more credible and thus more useful to risk managers (Paustenbach, l^90b; Keenan et al., 1994). To that end, contemporary EPA risk assessment guidance (EPA, 1992b) incorporates refinements in the treatment of uncertainty. Following are discussions of the major sources of uncertainty associated with this assessment. Residential Groundwater Scenario Evaluation of hypothetical future residential or industrial uses which would result in ingestion of or direct contact with local groundwater are not believed to represent realistic exposure scenarios. The 1 • • , • s • • site and the vast majority of surrounding facilities that are hydrogeologically cross- or down-gradient of the site have been used for the purpose of heavy industrial manufacturing for long periods - spme exceeding 100 years. Because of this mature industrial land base, a well developed public water supply system (operated by the Shenango Valley Water Authority) is in place. In addition, the City of Sharon supports efforts to redevelop the site for industrial use. The Agencies required that risks to hypothetical residential receptors be quantified in this HHRA. Accordingly, the risk estimates discussed above in Sections 5.1 and 5.2 for this exposure pathway are highly unrealistic (i.e., overstate the true potential) compared to the estimated risks typically associated with industrial use of a property (i.e., excluding future groundwater uses resulting in ingestion or direct contact). Moreover, for purposes of identifying remedial alternatives for the Westinghouse site, the quantitative results for this pathway do not provide practical or cost-effective information for developing sound risk management practices regarding future use of this property. In considering future land use for the site, it is important that realistic assumptions be employed as the basis of the risk assessment. Remedial alternatives and cleanup requirements selected for the site should be reasonably anticipated current and future uses of the property. Due consideration must also be given to the no-action alternative, i.e., unrestricted use in the absence of remediation. Although several metals, including lead, exceeded risk-based targets (i.e., a hazard quotient of one, MCLs), the majority of risks from groundwater are driven by PCBs and other chlorinated organics. In light of this information, ia detailed comparison of metal concentrations to background was not completed. As a result, the hypothetical risks from metals in groundwater may not be site related. G\CLIENTS\WESTINGH\19W«SECT5WPD , '. 5-7 CHEMRlSK** SERVICE OF MCLAREN/HART '- Health Risks Associated with Lead In Soils < Lead is a COPC in soil for the Shenango River sediments. Moat Sector subsurface soils, and the • '.•' -, . RRROW surface soils. Because there are no "no-effects" threshold levels established for lead. EPA does not recommend the use of toxicity values for lead (RfD or CSF). Therefore/the risks associated with lead in these soils were not numerically derived. However, it is possible to put these concentrations into perspective using existing EPA guidance. The EPCs for lead in the Shenango River sediments, the RRROW surface soil, and the Moat Sector subsurface soils are 786 mg/kg, 624 mg/kg, and 451 mg/kg respectively. EPA (1994) recommends, using a screening level of 400 mg/kg to evaluate soils in a residential setting. Residential soils with lead concentrations below 4QO mg/kg are not likely to pose a significant risk to children. Although the lead EPCs for the Shenango River sediments, RRROW surface soil, and the Moat Sector subsurface soils slightly exceed 400 mg/kg. exposure to these soils are not likely to be as frequent or for the same duration as would be expected for a residential exposure scenario. Steady-State Dermal Model The steady-state dermal absorption model is based on Kick's first law of diffusion where a chemical moves though a membrane due to a concentration gradient. However,,steady-state conditions may not be realized during the relatively short periods of time that exposure is expected to occur for the scenarios defined in Section 3. Therefore, the use of the steady-state dermal model, although recommended in EPA (1989a), may be a less conservative model for dermal absorption than a non- steady-state model. , Cancer Slope Factor and Risk Estimates In establishing slope factors, regulatory Agencies implement methods that introduce multiple sources of uncertainty that ultimately increase the overall conservatism inherent to the cancer risk estimates. Major uncertainties exist in the extrapolation from animals to humans and from high doses to low doses (51 FR 185:33992-34003, September 24* 1986). For example, species differ substantially in their uptake, metabolism, organ distribution, and target-site susceptibility of carcinogens. While laboratory animals are exposed to controlled concentrations at extremely high doses, humans are typically exposed to lower environmental levels (Crump et ah, 1989). In addition, the potency of a chemical is influenced by the size and lifespan of the species experimentally exposed. This has important implications due to the long latency period of many carcinogenic responses. An individual's susceptibility to a carcinogenic compound is also influenced by the variability that exists within human populations. Variables include genetic constitution, diet, occupational and home 5-8 CHEMRjsit»-A SERVICE OF MCLAREN/HART j 4U3880 . environments, activity patterns, and other cultural factors (51 CFR 185:3399204003, September 24, 1986).-•.-. • .--. ;••^, .-..••.•:- .•••; -.-• •-. - ,.-.'.... - . To compensate for these various sources of uncertainty in the dose response assessment, conservatism is incorporated into the derivation of the slope factor. The slope factor represents the upper 95th percent confidence limit on the probability of a carcinogenic response per unit intake of a chemical over a lifetime (EPA, 1989a). In other words, there is only a five percent chance that the probability of a response would be greater than the estimated value. Therefore, slope factors/by definition, overestimate the actual potency of a carcinogen. \ The accuracy of risk estimates, associated with low doses, predicted by the LMS model is unknown, but may in fact be zero (EPA, 1986). 1(1 For PCBs, ChemRisk has provided risk estimates using the new CSFs described in detail in Section 4 of this document. . Reference Doses and Hazard Quotient Estimates . - ' Significant uncertainty is associated with the evaluation of noncafcinogenic effects of chemicals in the environment. Primary sources of uncertainty include the derivation and use of chemical-specific toxicity values and the limitations inherent in the hazard index methodology, such as the assumption of additivity for multiple chemical exposure and the inability of the,Hazard Quotient (HQ) to predict the likelihood of adverse effects occurring at doses above the RfD. Toxicity values based on human epidemiological studies are not available for most chemicals, and in general human studies suffer from a lack of exposure data and any number of potential confounding factors, including concomitant exposure to multiple chemicals, recall bias, and lifestyle effects. Therefore, for many chemicals, data from studies of lato>ratory animals provide the basis for toxicity values. The practice of extrapolating effects observed in experimental animals to predict human toxic response to chemicals is a major source of uncertainty in risk assessment (EPA, 1989a). A hazard quotient (HQ) is the ratio of the estimated chronic intake level of a chemical to the reference ddse (RfD) for that chemical (EPA, 1989a). Since the RfD is established at a dose level at and below which adverse effects would not be expected, an HQ at or below 1 is considered to be a level that would not result in an increased health risk (EPA, 1989a). 5-9 CHEMRISK* A SERVICE OF MCLAREN/HART 4R.m388 Therefore, an HI is typically defined as the sum of HQs for the. individual chemicals of concern at the site. This approach assumes that exposures to multiple chemicals may result in adverse effects even if no single chemical exposure exceeds its RfD. As with single contaminant exposures, an HI at or below 1.0 is regarded as unlikely to result in an increased health risk even for sensitive . populations (EPA, 1989a). EPA ( 1 989a) guidance, specifying that individual HQs and total site His should not exceed a value of 1, represents conservative and health protective regulatory toxicological criteria. That is. an HI value greater than 1 does not necessarily indicate that adverse health effects are likely, because the RfD contains a measure of conservatism to ensure health protection. .. First, the development of RfDs is a highly conservative process. RfDs are generally developed by dividing NOAELs from animal studies by "safety factors", to adjust for uncertainties in the physiological differences between humans and laboratory animals, variation in sensitivity among individuals of human subpopulations, and differences between subchronic and chronic exposures. These ten-fold safety factors are typically applied in multiples of 10 to NOAELs. thus, when all three factors are combined, the resultant safety factor is equal to 1,000 (10 x 10 x 10) (Barnes and ' Dpurson, 1988). However, analysis of toxicological data indicate that a value less than ten for an individual safety i J factor may be adequate, depending on the relative magnitude of uncertainty associated with the critical study. For example, Lewis, et aL (1990) reviewed the data from eighteen laboratory animal studies and found that the average difference between NpAELs based on subchronic exposures and NOAELs based on chronic exposures was a factor of 3.5 or less, not the default value of 10 that is typically applied. Similarly, a factor of 1 for extrapolation from laboratory animals to humans is . appropriate if there are adequate data which indicate a likelihood that the test species is significantly more sensitive to the chemical-specific effect than humans. In cases when the RfD is based on a study which reports a LOAEL but does not report a NOAEL, an additional safety factor is generally applied to the LOAEL to derive an estimated NOAEL. This - safety factor may range from 1 to 10, depending upon the study and the severity of the effects observed. When Dourson and Starra (1983) compared LOAELs and NOAELs from a variety of studiesthat reported both, they found that 96 percent of those studies had LOAEL:NOAEL ratios of 5:1 or less. Based on their evaluation, Dourson and Starra (1983) concluded that a safety factor in the range of 1 to 10 is supportable for extrapolating from a LOAEL to a NOAEL. In addition, 5-10 CHEMRiSK*A SERVICE OF MCLAREN/HART " -1R.UJ3882 Dourson and Starra (1983) suggested that the severity of the effect is a critical determinant in . establishing a LOAEL to NO AEL safety factor. For example, for liver necrosis, a relatively severe effect, a relatively high value (i.e., 10) was suggested. However, for a less severe effect, such as fatty infiltration of the liver, which results in increased liver weight, a factor of 3 was suggested (Dourson andStarra, 1983). . • Thereis regulatory precedent for use of safety factors totaling less than 1.000. In calculating an RfD • for 2,4-dichlorophenol, EPA applied an uncertainty (or safety) factor of100 to the value reported as a NOAEL to account for extrapolation from animal data to humans and for protection of sensitive populations. In deriving the RfD for Aroclor 1254, the EPA applied a safety factor of 300 to the LOAEL observed in the criticaTstudy. EPA justified the safety factor of 300 by reasoning that: a 10- fold factor for interspecies was unnecessary due to similarities between humans and monkeys; only a "partial factor" was needed to account for use of a LOAEL because the effect (hail bed changes) was not considered serious; and a "reduced" factor for extrapolation from subchronic to chronic exposure was adequate because the critical effects did not appear to be dependent upon the duration of the study. Thus, the uncertainty factor of 300 applied by EPA in this case was significantly lower than the safety factor of 10,000 which would have resulted if four individual uncertainty factors of 10 had been combined. ( • in conclusion, many conservative assumptions are used to account for various sources of uncertainly associated with the evaluation of noncarcinogenic effects. One example of this conservatism and the health-protective nature of His calculated in this assessment is the use of multiple safety factors in the derivation of the RfD. Typically, a safety factor of l,00ais applied to the NOAEL in deriving an RfD; however, the EPA has applied combined safety factors as low as 100. Therefore, use of a -safety factor of 1,000 may be overly conservative for some chemicals by a factor of ten or more (Lewis, et al., 1990), , ,. Use of Relative Toxicity Values . • As described by EPA (1989a), there is significant uncertainty associated with the use of relative toxicity values, such as TEFs; these uncertainties are the focus of a number of current research programs, m me absence of chemical-specific toxicity formation and COM 1993c, 1994b) interim guidance and practice, relative toxicity schemes were employed for evaluating risks associated with exposure to PCDD/PCDFs (EPA, 1989d). < / 0 \tLENTS\WESTINGWI9WMSECTJWPD 5-11 CHEMR|SK*-A SERVICE OF MCLAREN/HART aR MJ3883 Additivitv of Risk and Hazard - A high level of uncertainty is also associated with exposures to multiple chemicals. For evaluation of cumulative effects from exposure to multiple chemicals. EPA (1989a) recommends that risks be summed across chemicals for each exposure - pathway. This assumption does not account for dissimilarities in mechanisms of action or synergistic or antagonistic effects, but is considered appropriate for screening level analyses (EPA; 1 992b). Therefore, in this assessment it was assumed that risks and hazards are additive. , Selection of Exposure Pathways There is considerable uncertainty regarding the extent and likelihood of exposure to chemicals across the exposure sectors and groundwater plumes identified in this assessment. For example, it is believed that exposures associated with direct contact with groundwater are entirely hypothetical and, in all probability, are unrealistic. Similarly, the direct contact soil exposure scenarios have been modeled using exposure frequencies which are also believed to overestimate possible health risks, For example, the outdoor construction worker scenario assumes that a single individual is exposed to the 95th UCL concentration in soil five days/week , for nine months. Given that any outdoor •- --...'.' construction at the site that results in disturbance of the soil is likely to last only a short period of time, relative to the entire construction project, the estimate of 195 days/year of exposure is expected to be an overestimat' •e actua' -."•.•l exposure: -. . . ..- • • - ' •-."." • Exposure Point Concentrations ( For all exposure pathways there are chemicals whose concentrations are highly variable. In fact, the range of variability is so great that the maximum concentrations of COPC were used to calculate risk estimates for those chemicals where the 95 UCL exceeded the maximum value. While statistically this is appropriate, it is highly improbable that individuals will contact the maximum measured media concentrations on a prolonged basis. Thus, using the maximum concentration detected may overestimate the true potential for risk. Another important uncertainty associated with the exposure point concentrations is the assumption that chemical concentrations in various impacted media will remain constant over the entire exposure periodl In reality, many compounds, especially organic compounds, tend to naturally break down over time. With containment or removal of a primary source of chemicals, a breakdown of a -' compound often leads to a decrease in concentration, which in turn would result in successively lower corresponding health risks. On the other hand, chemicals detected in site soils may eventually migrate to the underlying groundwater, thus becoming a source of future groundwater contamination. • 5-12 CHEMRiSK** SERVICE OF MCLAREN/HART j It is important to note that in some cases, risks may be underestimated where detection limits exceed the ,RBC. .• • . Chemical• s that were not detecte' d •i n media on-site. • ! bui still exceede' d th'e RBC were not evaluated further in the risk assessment. Finally, some of the data used to calculate EPCs for the Shenango River sediment and the-southerh and central alluvial groundwater were not validated using USEPA Region til Modifications to the Functional Guidelines. Volatile organic data from samples collected from wells S-10.M-14,M-1, S-12R, M-9, M-I IB, S-IB, S-2B, S-8B, N-2B, NOB, N-6B, and N-7B could not be fully validated • because laboratory quality control data were not available for review. In addition, for M-15. results and detection limits for all inorganic chemicals, except manganese and cyanide could not be verified because of difficulty obtaining supporting data. ^ Averaging Time / - \ v Consistent with EPA (1989a) guidance, this assessment assumes a carcinogenic averaging time of 70 years. However, there is evidence to indicate that 75 years may be a more accurate estimate of lifetime (EPA, 1989a). Thus, carcinogenic exposures and risks estimated in this analysis may be overestimated in this analysis. * ''.•."..'' Due to the relatively high degree of turbulence and mixing of air, both indoor and outside, the concentrations of components in air are likely to vary considerably. Such variations may not have been elucidated with the sampling conducted in the Middle Sector building. Further uncertainty results from the fact that the data used to represent the indoor worker exposure were derived from a single sampling event. Therefore, it is possible that the levels of chemicals measured are not representative of long-term average conditions. 5.5 RISK PERSPECTIVE In the risk assessment and risk management fields, health risks are defined as an estimate of the probability that a given exposure to an agent in a particular environmental setting will result in an adverse health effect (NAS, 1983; Paustenbach, 1989b), Adverse health effects may include death (mortality), illness (morbidity), or injury to individuals or a population as a whple. Historically, regulatory policy has been directed toward identifying and managing risks posed by carcinogens (EPA, 1986). A key justification for concerns over carcinogens likely stems from the fact that approximately one of every three individuals in the United States will be diagnosed with some form of cancer during their lives (i.e., a cancer incidence rate of 33%) (ACS, 1993). While noncancer 5-13 ,. CHEMRisK^A SERVICE OF MCLAREN/HART fUi)3885 effects (e.g., reproductive, unmunologicaL etc.) are rapidly being thrust into a new category of heightened regulatory concern, carcinogens remain the highest priority. An individual cancer risk value is an estimate of the probability that art individual member of a population will develop cancer as a result of a lifetime of exposure to a cancer-causing agent. The cumulative incidence of cancer in the U.S. population ranges between 33% for females and 50% for males, or 330,000 to 500,000 cases of cancer in 1,000,000 people (ACS. 1996). Using the lower end of that range (33%), an individual exposed to a chemical over the course of his or her lifetime resulting in an estimated incremental cancer risk level of 1, in 1.000,000 is equivalent to stating that the lifetime total cancer risk for this person is not greater than 330.001 chances in 1.000.000 (33.0001%) rather than 330,000 in 1,000,000. Population risk, on the other hand, is a measure of the upper-limit estimate of the number of additional incidences of cancer in the exposed population (Travis et al., 1987; EPA, 1992b). It is expressed as the product of the individual risk estimate and the size of the population that is potentially exposed. Because risk management decisions involve a balancing of individual risks, population risks, and site-specific considerations (Travis et al., 1987), such decisions and remedies under the Superfund or RCRA programs of EPA are not based on a simple "bright-line** test at an individual risk level of 1 x 10"*. In fact, these EPA programs allow for cancer risks associated with certain hazardous waste sites as high as 1 x 10*4 (EPA, 1990a). As described below, other regulatory initiatives have dealt with the "range-of-risk" approach. 5.5.1 Acceptable Risk Defined Under Existing Regulatory Initiatives The foundation for risk management decisions is the selection of a cancer risk criterion which is considered to be either acceptable or de minimis with respect to the protection of public health and the environment The term de minimis risk is used by risk assessors and regulators to define insignificant risks, or those risks that are not of regulatory concern (Travis et al., 1987). In actuality, a'de minimis risk should be characterized as one that is judged by society to be of negligible public health concern and too small to justify the expenditure of limited risk management resources (Whipple, 1989). Often times the terms acceptable risk or de minimis risk are used-interchangeably. o \aiEKrs\wEsriNQH\i9M\9isECT3WPD 5-14 CHEMRlSK*-A SERVICE OF MCLAREN/HART iR:nj3886 A common misconception within the field of .risk assessment is that all occupational and environmental regulations adopt a theoretical maximum cancer risk of 10** as the de minimis or. acceptable level of risk. When this criterion is exceeded, the public and the media often view the situation as a serious public threat to public health. In 1987, Dt. Frank Young, then commissioner of the U.S. Food and Drug Administration (PDA), addressed this misconception as it related to setting tolerances for methylene chloride residues in decaffeinated coftee (Young; 1987): \ • ' , The risk level of one in one million is often misunderstood by the public and the media. It is not an actual risk;-i.e., we do not expect one out of every million people , to get cancer if they drink decaffeinated coffee. Rather, it is a mathematical risk based on scientific assumptions used in risk assessment. PDA uses a conservative estimate to ensure that the risk is not understated: We interpret animal test results conservatively and we are extremely careful when we extrapolate risks to humans. , When PDA uses the risk level of one in one million, it is confident that the risk to ' humans is virtually nonexistent. 1 * ' • ,; • * * « * • ' i • ' ' ; Implicit within the PDA's use of the 10"* risk level for establishing a "safe level" of methylene' chloride in decaffeinated coffee is the intent to protect the very large potentially exposed population of coffee drinkers. In the case of very small populations, such as pesticide applicators, de minimis risk levels as low as 10"3 for some pesticides have been deemed acceptable (Rodricks et al., 1987). In recent years, mbst Jregulator y decisions 'relate * d to environmental exposur. e have bee; n based on- 'd 'e minimis risk levels ranging from 10"1 to 10*. On the other hand, the theoretical risks associated with occupational exposure limits are usually in the range of 10"2 to 104 (Paustenbach, 1990a). Acceptable Risk Under CERCLA ". Final revisions to the National Contingency Plan (NCP) (EPA, 1990a) under CERCLA establish a range of 1 x IfrVto.l x 10*6 for generally acceptable risks at Superfund sites [40 CFR 300.430(e)(2XI)(A)(2)]. In establishing this rjsk range, the EPA rejected the argument that a risk range, rather than a single risk criterion, does not adequately protect health and the environment [55 FR 8716-17, March 8, 1990]. The EPA noted that "CERCLA does not require the complete elimination of risk"; rather, remedies comply with CERCLA **when the amount of exposure is reduced so that the risk posed by contaminants is very small, i.e., at an acceptable level. EPA's risk range of 10"4 to 10* represents EPA's opinion on what are generally acceptable levels'* [55 FR 8716]. The EPA stated that, after starting at an incremental cancer risk of 10"*, selection of appropriate risks o;\cLiENTs\wESTO4o»i99iwisECTswro _, 5-15 CHEMRjsK*-A SERVICE OF MCLAREN/HART within the range should be based on "consideration of a variety of site-specific or remedy-specific factors" [55 Fed. Reg. 8717]. According to the EPA [55 FR 8717], the appropriate factors include,' but are not limited to, exposure factors, uncertainty factors, and technical factors: Included under exposure factors are: the cumulative effect of multiple contaminants, the potential for human exposure from other pathways at the site, population sensitivities, potential impacts on environmental receptors, and cross-media impacts of alternatives. Factors related to uncertainty may include: the reliability of alternatives, the weight of scientific evidence concerning exposures arid individual and cumulative health effects, and the reliability of exposure data, Technical factors may include: detection/quantification limits for contaminants, technical limitations to remediation, the ability to monitor and control movement of contaminants, and background levels of contaminants. , . * L '.''_•.- Overview of Regulatory In a retrospective review of the use of cancer risk estimates in 132 federal decisions, Travis et al. (1987) examined the cancer risks that triggered regulatory action. The authors considered three risk issues: individual risk, the size of the population exposed, and the population risk. The results of the review showed that for exposures resulting hi a small-population risk, regulatory action was never taken for individual risks below 1 x 10"*, whereas regulatory Agencies almost always took action when the cancer risk exceeded approximately 4 x 10°. For large-population risks (e.g., the entire U.S. population), Agencies typically acted on risks of about 3 x 10"4, and de minimis risk was typically defined as 1 x 10"*, These decisions demonstrate that the size of a potentially impacted population does have bearing, as it should, on the selection of acceptable risk, criteria within regulatory Agencies. Based on the findings of Travis et al. ( 1 987), and upon further examination of the database, Graham (1990) has suggested using a range of 1 xlO^to Ix 10"6 for acceptable lifetime cancer risk for the average exposed individual and a less stringent risk range for smaller, more highly exposed sub-populations of the general population. As indicated in the above discussion, cancer risk levels deemed acceptable have been a function of a number of factors, including the size and characteristics of the potentially affected population, and other factors such as technical feasibility. Therefore, single cancer risk values do not provide flexibility for making risk management decisions on a case-by-case basis. An acceptable risk range is more appropriate for determining site-specific remedies. [ a \cuENTs\wE$TiNG»i»t\«sECTswpD • 5-16 CHEMRKK^A SERVICE 6F MCLAREN/HART ' '• i«R. 103888 In comparison to background incidences of cancer in the U.S. population, incremental risks of 10~* to TO"6 are negligible. As previously mentioned, the background incidence of all cancers tn the U.S. V J population is between 33% arid 55%, or I in 3 to 1 in 2 (ACS, 1996). Using the lower end of that ^***"^^ • ' . ' . w - ' ' ' • range (33%), an incremental risk level of 1 x 10"4 would indicate that a given lifetime exposure would increase the potential lifetime cancer risk from approximately 33% to 33.01%. OACLiENTRWESTiNGifti9«\«SECT3.wPD - 5-17 CHEMRlSK*A SERVICE OF MCLAREN/HART AR 1U3889 6.0 SUMMARY AND CONCLUSIONS This HHRA has evaluated hypothetical upper-bound carcinogenic and noncarcinogenic risks to various potential receptors of COPC in impacted media at the Westinghouse site. As noted, through meetings and correspondence, PADEP and EPA have had a substantial opportunity to review and comment on specific risk assessment issues including RI sampling data values, human receptor populations, exposure algorithms, and individual exposure parameter values (See Appendix I). PADEP concurrence with the risk assessment conceptual site model was issued in an August 15, 1996 approval letter. Because this assessment has relied upon conservative assumptions and input parameter values throughout, it is believed that the risk estimates presented herein conservatively estimate the reasonable" maximum exposures. Thus, the numeric values summarized in Chapter 5 and Table 5*1 should be considered highly conservative upper bound estimates of risk. The EPA's own guidance languag' e states tha• t actual carcinogenic risk" s will likely -b e less, and may even" be zero (EPA, 1986). ., Regarding carcinogenic risk estimates, the principal area of concern would be related to potential child trespassers exposed to surficial soils within the railroad right-of-way. As noted in the text discussion, this excess risk is largely the result of a few elevated PCB concentrations proximate to the Middle Building. Future employee exposure to indoor air also resulted in excess risk. However, as discussed in Section 5.1, this risk may not realistically represent chronic exposure to the indoor air and will be addressed prior to the use of the building by a future employee., While calculated groundwater risks are significantly elevated for all three groundwater units, consumption and/or direct contact of groundwater on a prolonged basis, as assumed in the quantitative assessment discussed in Section 5.0, is extremely unlikely. On this basis, risks related to future groundwater use are viewe4 d as entirely hypothetical. - . In additio• n to these potentia• l carcinogenic •risks , EPAV. calculations of unrestricted worker access to the Moat resulted in risk estimates beyond the NCP O:\CLIENTS\WESTINGWl9WMSECr6WPD 6M CHEMRlSK^A SERVICE OF MCLAREN/HART target range. The results of EPA's assessment have been included in Table 5-1 and will be explicitly addressed by the FS, , • - , Excess noncarcinogenic risks emerged for the child trespasser within the railroad right-of-way, the future employee, the indoor and outdoor construction worker, and the unrestricted worker in the ' Moat. As noted earlier, PCBs play a significant role; in contributing to total noncancer risks for the railroad right-of-way child trespasser. Manganese plays a significant role in contributing to total noncancer risk to both construction worker scenarios, and is elevated even among background residential properties sampled by EPA. This may indicate that manganese is elevated in soils on a regional basis and may not be an artifact of the Westinghouse site operations. 1,2-Dichloroethane is the predominant chemical impacting estimates of noncancer risks to the future employee. Finally. EPA calculations for unrestricted worker access to the Moat resulted in an a noncancer hazard greater than one. - • , Finally, because risk is a function of exposure to an environmental toxicant, it follows that restricting or eliminating exposure is often the most prudent risk reduction measure at a given site. In the Westinghouse site Feasibility Study, which constitutes the next phase of site activity, further analysis , will be undertaken to evaluate the level of risk reduction achieved by various remedial alternatives. Included in this analysis will be a characterization of possible control measures than can be used to \J eliminate uncontrolled exposures to impacted media. - U G:\CLIEVTS\WESTINCHM9W9BECT6WPD 6'2 CHEMRlSK*-A SERVICE OF MCLAREN/HART 7.0 REFERENCES ACS. 1996. Cancer Facts & Figures-1996. American Cancer Society, Atlanta. GA. ATSDR. 199la. Toxicological Chemical Profiles. Agency for Toxic Substances and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public Health Service. (Cited in EPA, 1997c). ' ' - . ' ATSDR. 1991b. Toxicological Profile for Lead. Agenci y for Toxic Substances and Disease. Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public Health Service. (Cited in EPA, 1997c). ATSDR, 199 Ic. Toxicological Profile for Manganese. Agency for Toxic Substances and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public Health Service. (Cited in EPA, 1997c). ATSDR. 199Z Toxicological Chemical Profiles. Agency for Toxic Substances and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public Health Service. (Cited in EPA, 1997c). . ATSDR. 1993. Toxicological Profile for Chromium. Agency for Toxic Substances and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public Health Service. (Cited in EPA, 1997c). ATSDR. 1995. Toxicological Profile for Polycyclic Aromatic Hydrocarbons. Agency for Toxic Substances and Disease Registry, Atlanta, G A and U.S. Department of Health and Human Services, Public Health Service. 7-1 ' CHEMRISK"-•'.'•.':.•'•A SERVIC'E OF MCLAREN/HAR,..'' T• , 'O AR iU3892 Barnes, D.G. and M. Dourson. 1988. Reference dose (RfD): Description and use in health risk - assessments••••.; Reg. Toxicol" .•;-. Pharmacol• . 8:471-486•••.-. • ,- • '•-.. •'•-. ..'• :'•• , , Binder, S.,D.Sokai and D.Maughan. 1986. Estimating soil ingestion: The use of tracer elements in estimating the amount of soil ingested by young children. Arch. Environ. Health 41(6):341-345. Calabrese. EJ.. R. Barnes, E.J. Stanek, H. Pastides, C.E. GUbert, P. Veneman^ X. \v"ang, A/Lasztity, and P.T. Kostecki. 1989. How much soil do young children ingest: An epidemiologic study. Reg. Toxicol Pharmacol 10:123-137, :.;.'. Cantor, K.P., R. Hoover, P. Hartge, T;J. Mason, D.T. Silverman, R. Altaian. D.F. Austin, M.A. Child, C.R. Key, L.D. Marrett, M.H. Myers, AS. Narayana, L.I. Levin, J.W..Sullivan, G.M. Swanson, D.B. Thomas, and D.W. West. 1987. Bladder cancer, drinking water source, and tap water consumption: A case-control study. / NatL Cancer Inst. 79(6):1269-1279. Clausing, P., B. BrUnekreef and J.H. van Wijnen. 1987. A method for estimating soil ingestion by children. Int. Arch. Occup. Environ. Health 59:73-82. Clement Associates, Inc. 1985. A Risk Evaluation of PCB Exposure at the Westinghouse I j Transformer Facility in Sharon, Pennsylvania. Prepared for Cyclops Corporation, Sawhill Tubular Division. December 11. .' Cowherd, C., G.E. Mukski, P.J. Englehart, and D: A. Gillette. 1985. Rapid assessment of exposure to paniculate emissions from surface contamination sites. The 78th Annual Meeting of the Air ' '- Pollution Control Association, Detroit, MI. CRC. 1994. 'Field Sampling Plan Addendum (Revision 4.0); Phase II Remedial Investigation, Sharon Transformer Facility, Sharon, Pennsylvania. Prepared by Cummings Ritter Consultants, Inc., Monroeville, PA. May 20. , ( r • . , : ' ' CRC. 1996. Remedial Investigation Report: Westinghouse Electric (Sharon Plant), Sharon, Pennsylvania; Volume I of IV. Cummings Ritter Consultants, Inc., Monroeville, PA. Project No. 93111.20/13. March20. 7-2 CHEMRISK*- A SERVICE OF MCLAREN/HART t»R.I03893 CRC 1997. Air Monitoring Plan Middle Sector Buildings Former Transformer Facility, Sharon, Pennsylvania. Prepared by Cummings Ritter Consultants, Inc., Monroeville, PA for Westinghouse Electric Corporation, Pittsburgh, PA. IProject No. 93111.30/01. September 22. Crump, K., B. AQen, and A. Shipp. 1989. Choice of dose measure for extrapolating carcinogeneic risk from animals to humans: An empirical investigation of 23 chemicals. Health Phys. 57:387-393. Dourson, M.L. and J.F. Stara. 1983. Regulatory history and experimental support of uncertainty (safety) factors. ReguL ToxicoL Pharmacol, 3:224-238. < Driver, J.H., JJ. Konz and GJC Whitmyre. 1989. Soil adherence to human skin. Bull. Environ. Contam. ToxicoL 43:814-820. This is filed in the topical files under dermal absorption. fePA. 1984. Risk Analysis of TCDD Contaminated Soil. U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Office of Research and Development, Washington, DC EPA-600/8-84-031. November. EPA. 1986. Guidelines for Carcinogen Risk Assessment. U.S. Environmental Protection Agency, Washington, D.C 51 Federal Register 185:33992-34003. September^ EPA. 1988. Drinking Water Criteria Document for Polychlorinaied Biphenyls (PCBs). Final Report. U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH. ECAO-CIN-414. ApriL EPA. 1989a.. Risk Assessment Guidance for Superfund; Volume I; Human Health Evaluation Manual (Part A)-Interim Final. U.S. Environmental Protection Agency, Office of Emergency and Remedial Response, Washington, D.C. EPA/540/1-89-002. July. EPA. 1989b. Expdsure Factors Handbook. U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Washington, D.C EPA/6W8-89/043. July. 7-3 CHEMRisK*-A SERVICE OF MCLAREN/HART \R:fi)389U EPA. 1989c. Assessing Human ffealth Risks from Chemically Contaminated Fish and Shellfish: A Guidance Manual. U.S. Environmental Protection Agency, Office of Marine and Estuarine Protection, Washington, DC. EPA-503/8-89-002. September. EPA. 1989d. Interim Procedures for Estimating Risks Associated with Exposures to Mixtures of Chlorinated Dibenzp-p'Dioxins and Dibenzofurans (CDDs and CDFs) and 2989 Update. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, D.C EPA/625/3-89/016. . March. . EPA. 1990a. Environmental Protection Agency -National Oil and Hazardous Substances Pollution Contigency Plan Under the Comprehensive Environmental Response Compensation, and Liability Act of 2980. U.S. Environmental Protection Agency, Office qf Solid Waste and Emergency Response, Washington, DC. . • EPA. 1990b. Drinking Water Criteria Document for Heptachlor, Heptachlor Epoxide and Chlordane. U.S. Environmental Protection Agency, Office of Drinking Water, Washington, DC. ECAO-CIN-406. "'••', i • ' <• ' EPA. 1991a. Fact Sheet: National Secondary drinking Water Standards. U.S. Environmental (j Protection Agency, Office of Water, Washington, DC, EPA 57Q/9-91-019FS. September. ^•^ , - ' • '• • r • ' ' •.'••' •',•''". • ' EPA. 199 lb. Risk Assessment Guidance for Superfund: Volume I ~ Human Health Evaluation Manual Supplemental Guidance ?Standard Default Exposure Factors®. U.S. Environmental Protection Agency, Office of Emergency and .Remedial Response, Toxics Integration Branch, Washington, D.C EPA-54Q/1-89/002/ March 25. . EPA. 1992a. Supplemental Guidance to RAGS."Calculating the Concentration Term. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, D.C PB92-963373. May. ' V EPA. 1992K Final Guidelines for Exposure Assessment; Notice. U.S. Environmental Protection . ' .. ' Agency, Washington, D.C, 57 Federal Register 104:22888-22938. May 29. 7-4 CHEMRlSK*-A SERVICE OF MCLAREN/HART (U3895 EPA. 1992c. Dermal Exposure Assessment: Principles and Applications; Interim Report. U.S. Environmental Protection Agency, Office of Research and Development, Washington, D.C. EPA/600/8-91/Q11B. January. EPA. 1992A Airfiuperfund National Technical Guidance Study Series: Assessing Potential Indoor Air Impacts for Superfund Sites. U.S. Environmental Protection Agency, Office of Air Quality, Planning and Standards, Research Triangle Park, NC. EPA-451/R-92-002. September. EPA. 1993a. Selecting Exposure Routes and Contaminants of'Concer n by Risk-Based Screening. U.S. Environmental Protection Agency, Region III, Hazardous Waste Management Division, Office of Superfund Programs, Philadelphia, PA. EPA/903/R-93-001. January. EPA. 1993b. Air/Superjund National Technical Guidance Study Series: Models for Estimating Air Emission Rates from Superfund Remedial Actions. U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-45 l/R-93-001. March. * EPA. 1993c. Memorandum to the Directors of Waste Management Division, Emergency and Remedial Response Division, Hazardous Waste Management Division, and Hazardous Waste Division from W.H. Farland and H.L Longest, U.S. Environmental Protection Agency, Washington, D.C. RE: Use of IRIS Values in Superfund Risk Assessments. OSWER Directive #9285.7-16. December 21. EPA. 1993d. Provisional Guidance for Quantitative Risk Assessment of Polycyclic Aromatic Hydrocarbons. U.S. Environmental Protection Agency, Office of Research and Development, Washington, D.C ECAO-CN-842. March. EPA. 1994a. Memorandum to the Regional Adminstrators I-X, U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, D.C. from Elliot P. I-aws, , * Assistant Administrator, U.S. Environmental Protection Agency, Washington, D.C. Re: Revised Interim Soil Lead Guidance for CERCLA Sites and RCRA Corrective Action Facilities. OSWER Directive #9355.4-12. July 14. 7-5 CHEMRisK*-A SERVICE OF MCLAREN/HART 3896 EPA. 1994b. Estimating Exposure to Dioxin-Uke Compounds, Volume 2: Properties, Sources, Occurrence and Background Exposures. U.S. Environmental Protection1 Agency, Office of Research ' and Development, Washington. D.C. EPA/600/6-88/005Cb. June. EPA. 1995a. Region III Technical Guidance Manual; Risk Assessment: Assessing Dermal Exposure from Soil. U.S. Environmental Protection Agency, Region HI, Hazardous Waste Management Division, Office of Superfund Programs, Philadelphia, PA. EPA/903-K-95-003. December. , . > EPA. 1995b. Exposure Factors Handbook - Review Draft. U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC. EPA/600/P-95/002A. June. EPA. 1995c. Health Effects Assessment Summary Tables FY-1995 Annual. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, D.C. EPA/540/R- 95/036. May. EPA. 1995d Reassessment of IRIS Cancer Potency Factor for Polychlorinated Biphenyls (PCBs) and Setting State Water Quality Standards for PCBs. Memorandum from William H. Farlahd, 'December, 6, 1995. U.S. Environmental Protection Agency, National Center for Environmental ( ,' Assessment Washington, DC. ^^••^ ; .' ' i • _ , • . ' 1 • • • - ' ' , • * ,; • • ' ' . ' ' EPA. 1995e. Land Use in the CERCLA Remedy Selection Process. U.S. Environmental Protection Agency, OflSce of Solid Waste and Emergency Response, Washington, DC. OSWER Directive No. 9355.7-04. May23. " 1 . • ' ' '. ' EPA. 1996a. Risk-Based Concentration Table, January-June 2996. Dr. Roy L. Smith, U.S. Environmental Protection Agency, Region III, Office of RCRA, Technical and Program Support Branch, Philadelphia,PA. April30. . EPA. 1996b. PCBs: Cancer Dose-Response Assessment and Application to Environmental Mixtures -DRAFT. U.S. Environmental Protection Agency, Office of Research and Development, National Center for Environmental Assessment, Washington, D.C. January. 7-6 CHEMRLSK"-A SERVICE OF MCLAREN/HART EPA. 1996c. Soil Screening Guidance: Technical Background Document. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, DC. EPA/540/R- 95/128. May. EPA. 1996d. Draft Proposed Guidelines for Carcinogenic Risk Assessment. U.S. Environmental Protection Agency, Office of Research and Development, National Center for Environmental Assessment, Washington, D.C. . , EPA. 1996e. Exposure Factors Handbook; Volume I of III: General Factors - Review Draft. U.S. Environmental Protection Agency, National Center for Environmental Assessment, Office of Research and Development, Washington, D.C. EPA/600/P-95/002Ba. August. EPA. 19961 Exposure Factors Handbook: Volume IIIofIII: Activity[Factors-Review Draft U.S. Environmental Protection Agency, National Center for Environmental Assessment, Office of Research and Development, Washington, D.C. EPA/600/P-95/002Bc. August EPA. 1997a. Updated Risk-Based Concentration Tables. Dr. Roy L. Smith, U.S. Environmental Protection Agency, Region in, Office of RCRA, Technical and Program Support Branch, Philadelphia, PA. March 17. ( ..'•-.. • • . ' - ' •: • > . ; • . - ' . - ' • . EPA. 1997K Health Effects Assessment Summary Tables: FY1997 Update. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, DC. EPA-54Q-R* 97-036. July. EPA. 1997c. Memorandum to V. Janosik, RPM, Western PA Remedial Section from J. Hubbard, Toxicotogist, U.S. Environmental Protection Agency, Region HI, Philadelphia, PA Re: Review of Westinghouse Sharon Draft Risk Assessment. July 16. Farmer, W.J., M.S. Yang, J. Letey, W.F. Spencer, and M.H. Roulier. 1978. Land disposal of hexachlorobenzene wastes: Controlling vapor movement in soil In: Land Disposal of Hazardous Wastes. Proceedings of the Fourth Annual Research Symposium, U.S. Environmental Protection Agency, Municipal Environmental Research Laboratory, San Antonio, TX, March 6-8. 7-7 CHE MRISK"- A SERVICE OF MCLAREN/HART R.HJ389B Farmer, W.J., M.S. Yang, J. Letey, W.F, Spencer, and M.H. Roulier. 1980. Land Disposal of Hexachlorobenzene Wastes: Controlling Vapor Movement in Soil. U.S. Environmental Protection Agency, Office of Research and Development, Municipal Research Laboratory. Cincinnati, OH. Gillies, M.E. and H.V. Paulin. 1983. Variability of mineral intakes from drinking water: A possible explanation for the controversy over the relationship of water quality to cardiovascular disease. Int. J. EpidemioL 12(1):45-50. Graham* J- 1990. New Clean Air Act. Congressional Research Service, Washington, D.C ' GRI. 1988. Management of Manufactured Gas Plant Sites - Volume III: Risk Assessment. Prepared for Gas Research Institute, Chicago,! IL. GRI-87/0260.3. May. Harr, M.E. 1962, Groundwater Seepage. New York, NY: McGraw-Hill. Heath, R.C. 1982. Basic Ground-Water Hydrology. USGS Water-Supply Paper 2220. ' ICRP. 1975. Anatomical values for reference man. In: Report of the Task Group on Reference Man. First edition. New York, NY: Pergamon press. / ••••" '••:• -'•'• '- •. •'-," • • --:; •-'•"'. .--. •'•'• •' '. IEHR. 1991, Reassessment of Liver Findings in Five PCB Studies in Rats. Institute for Evaluating Health Risks, Washington, D.C IRIS. 1987. Chemical Search for Heptachlor. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH and National Research Library of Medicine, Bethesda, MD. IRIS. 1995. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati OH and National Research Library of Medicine, Bethesda, MD. , 7-8 CHEMRISK'-A SERVICE OF MCLAREN/HART AR:iU38.99 IRIS. 1996. Chemical Search for Manganese. Integrated Risk Information System, U.S. Environmental Protection Agency; Office of Health and Environmental Assessment, Cincinnati, OH and National Research Library of Medicine, Bethesda, MD. IRIS. 1997. Chemiaal Search for Cadmium. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH and National Research Library of Medicine, Bethesda, MD. Jury, W.A., W.F. Spencer, and W.J. Farmer. 1983. Behavior assessment model for trace organics in soil: I. Model description. J. Environ. Quality 12(4):558-564. Jury, W.A., WJ. Farmer, and W.F. Spencer. 1984a. Behavior assessment model for trace organics in soil: II. Chemical classification and parameter sensitivity. /. Environ. Quality 13(4):567-571. Jury, W.A., W.F. Spencer, and W.L. Farmer. 1984b. Behavior assessment model for trace organics in soil: HI. Application of screening model /. Environ. Quality l3(4):573-579. Jury, W.A., W.F. Spencer, and W.L. Farmer. 1984c. Behavior assessment model for trace organics in soil: IV. Review•' o• f experimenta• - l evidence"• •-. J. Environ• . Quality 13(4):580-586. • .-.-•' • - Jury, W.A., D. Russo, G. Streite, and H.E. Abd. 1990. Evaluation of volatilization by organic chemicals residing below the soil surface. Water Resources Res. 26(1):13-20. J ' - : : • ' • . Kimbrough, R.D. 1995; Polychlorinated biphenyls (PCBs) and human health: An update. Crifc Rev. 'Toxicol. 25(2):133-163. Kissel, J., K. Richter, and R. Fenske. 1996. Field measurements of dermal soil loading attributable to various activities: Implications for exposure assessment. Risk Anal. 16(1):116-125. Klaassen, C.D., M.O. Amdur, and J. DouU. 1986. Casarett and Doull=s Toxicology: The Basic Science of Poisons. New York, NY: MacMUlan Publishing. :-. 7-9 CHEMRKK*-A SERVICE OF McLAREN/HART .1U3900 Lepow, M.L., L. Bruckman, M. Gillette, S. Markowitz, R. Robino, and. J. Kapish. 1975. Investigations into sources of lead in the environment of urban children. Environ. Res. 10:415-426 ,'.; •>•->'.:•• v • • .-, --:':: .••• . , ' Lewis,-S.C., J.R. Lynch, and A.I. Nikiforov. 1990. A new approach to deriving community exposure guidelines from "No-observed-adverse-effect levels." ReguL Toxicol. Pharmacol. li:3l4-33Q. ' ' • ' • ' ' i Lyman, W.J., W.F. Reehl, and D.H. RosenblatL 1990. Handbook of Chemical Property Estimation Methods: Environmental Behavior of Organic Compounds. Washington, DC: American Chemical Society. , . - • '*•'•',".• ' \ ' • ' ' Mackay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated Handbook of Physical-Chemical Properties and Environmental Fate for Organic Chemicals; Volume I: Monoaromatic Hydrocarbons, Chlorobenzenes, and PCBs. Chelsea, MI: Lewis Publishers. McKone, T.E. 1987. Human exposure to volatile organic compounds in household tap water: The indoor inhalation pathway. Enviroq. ScLTechnol. 21(12):1194-1201. McKone, T.E. and K.T. Bogea 1991. Predicting the uncertainties in risk assessment. Environ. Sci. TechnoL25(lQ):\614-mi. - , . '• ' . . ".-- • ' •"•-.•'"•••' • ••'.. ' ••' " '' Means and Company, Inc. 1993. Means Site Work and Landscape Data. 12* Annual edition. Mfflington, R.J. and J.Mr Quirk. 1961. Permeability of poroussolids.' Trans. ParadaySoc. 37:1200- '1207. -• '. - ;..." ;; •.''.-•.'-.'•-• * . Moore, J.A, J.F. Hardisty, D.A. Banas, and M.A. Smith. 1994. A comparison of liver tumor diagnoses from seven PCB studies in rats. Reg. Toxicol. Pharmacol. 20:362-370. Mucro, 1C and D.R. Krewskl 1981. Risk assessment and regulatory decision making. Fd. Cosmet Toxicol. 19:549-560. NAS. 1983. Risk Assessment in the Federal Government: Managing the Process. Academy Press: Washington, D.C. , 7-10 CHEMRJSK*- A SERVICE OF MCLAREN/HART R.JIK3901 NCEA. 1993. Chemical Data. National Center for Environmental Assessment, Washington, D.C. (Cited in EPA, 1997c). -'. ' ^ •' ' .'- '" . . ' - •'"• NCEA. 1994. Chemical Data. National Center for Environmental Assessment, Washington, D.C. (Cited in EPA, 1997c). ^ NCI. 1978. Bioassay of Aroclor 1254 for Possible Carcinogenicity. NCI-GC-TR-38. National Cancer Institute, Bethesda, MD. ••''•' > ' " ' • . . ' PADEP. 1988. Letter to P.P. Jack, Westinghouse Electric Corporation from M.E. German, Bureau. of Waste Management; Re: A copy of PCB/pesticide analytical results from fish tissue samples collected by PADER, Commonwealth of Pennsylvania Department of Environmental Resources, Harrisburg, PA. October 18. •• PADEP. 1995. Letter to P. Ot=Hara, Cummings-Riter Consultants, Inc. from CL. Tordella,. Hazardous Site Cleanup; Re: Westinghouse Sharon Site - PADER 1992 Fish Tissue Sampling Data, Commonwealth of Pennsylvania Department of Environmental Resources, Harrisburg, PA. June 2. PADEP. 1996a_ Letter to G. Taylor, Senior Project Manager, Westinghouse Electric Corporation, from C. Tordella, Project Manager, Pennsylvania Department of Environmental Protection, Hazardous Sites Cleanup, Meadville, PA; Re: Westinghouse Electric (Sharon Plant) Site PADEP Phase n Shenango River Split Samples. July 16. 1 " - -• PADEP.' 1996b. Applicable or Relevant and Appropriafe Requirements (ARARs) for Cleanup Response and Remedial Actions in Pennsylvania - Final Report. Pennsylvania Department of Environmenta15. . l Protection. : •, Burea_ u "o f •;•.;Land- Recyclin, ' g an.-'.d -Wast '•e Management. •" , Harrisburg- , PA. May• PADEP. 1997. Letter to G. Taylor, Senior Project Manager, Westinghouse Electric Corporation, from C. Tordella, Project Manager, Pennsylvania Department of Environmental Protection, Hazardous Sites Cleanup, Meadville, PA; Re: Westinghouse Electric (Sharon Plant) Site, September 30,1996; Baseline Human Health Risk Assessment. August 6. 7- 1 1 OtEMRis K*- A SERVICE OF MCLAREN/HART HJ3902 PADER. 1988. Untitled Press Release. Pennsylvania Department of Environmental Resource*, ' • Harrisburg•- -. , PA• . :Augus •• t 9"••. • •••': -;.;•' • -' •" ' -.-..•• "-.-' PADER. 1995. Letter to G. Taylor, Senior Project Manager, Westinghouse Electric Corporation, from C. Tordella, Project Manager, Pennsylvania Department of Environmental Resources, Hazardous Sites Cleanup, Meadvule, PA; Re: Phase IIRI/FS Split Samples. Februarys. Paustenbach, p. J. 1989a. The Risk Assessment of Environmental and Human Health Hazards: A Textbook of Case Studies. New York, NY: John Wiley & Sons. .)'•:*, • . • •- 'j • • " Paustenbach, D.J. 1989b. Important recent advances in the practice of health risk assessment: Implications for the 1990's. Reg. Toxicol. Pharmacol. 10:204-243. . •" . i - . ' ' ' Paustenbach, D. J. 1990a. Occupational exposure limits: Their critical role in preventive medicine and risk management. Am. Ind. Hyg. Assoc. J. 51:A-332-A-336. Paustenbach, D. 19905. Health risk assessment and the practice of industrial hygiene. J. Am. Ind. Hyg. Assoc. 7.51:339-351. .- \ • ' ...... -( , t . . ( j Paustenbach, D.J., J.D. Jemigan, R. Bass, R. Kalmes, and P. Scott. 1992. A proposed approach to regulating contaminated soil: Identify safe concentrations .for seven of the most frequently encountered exposure scenarios. Reg. Toxicol. Pharmacol. 16:21-56. PFBC. 1995. Analysis of Fish Tissue Contaminants Near the Westinghouse-Sharon Superfund Site. Pennsylvania Fish and Boat Commission, Division of Environmental Services. December 15. Que flee.. S.S., B. Peace, C.S. Clark, J.R. Boyle, R.L. Bornschein and P.B. Hammond. 1985. Evolution 6f efficient methods to sample lead sources, such as house dust and hand dust, in the homes of children. Environ. Res. 38:77-95. This is fded in the chemical files under lead. ,'.'''.. ' ',•;"• ' • ' ' ' • \ '. '- ' ' Rizzo Associates. 1986. Comprehensive Subsurface Study. Sharon Transformer Plant, Westinghouse Electric Corporation, Sharon, PA. Paul C. Rizzo Associates, Monroeville, PA. August. ' , , 7- 12 CHEMRisK*-A SERVICE OF MCLAREN/HART .iR. Rizzo Associates. 1992. Field Sampling Plan: Remedial Investigation/Feasibility Study. Sharon Transformer Plant Site, Sharon, PA. Paul C. Rizzo Associates, Monroeville, PA. August. Rodricks, J.V., S.M. Brett, and G.C. Wrenn. 1987. Significant risk decisions in federal regulatory agencies. ReguLToxicoL Pharmacol, 7:307-320. j . Roels, H.A., J.P. Buchet, R.R. Lauwerys, P. Bruaux, F. Claeys-Thoreau, A. Lafontaine and G. Verduyn. 1980. Exposure to lead by the oral and the pulmonary routes of children living in the vicinity of a primary lead smelter. Environ. Res. 22:81-94. This is filed in the chemical files under lead. \ • . Roels, R, R. Lauwerys, J.-P. Buchet et aL 1987. Epidemiological survey among workers exposed to manganese: Effects on lung, central nervous system, and some biological indices. Am. 3. Med. 11:307-327. (Cited in IRIS, 1996) - Roels, H, P. Ghyselen, J.-P. Buchet, E. Ceulemans, and R.R. Lauwerys. 1992, Assessment of the permissible exposure level to manganese in workers exposed to manganese dioxide dust. Br. /. Ind. Med. 49:25-34. (Cited in IRIS, 1996) ' f RTL 1987. A Method for Estimating Fugitive Particulate Emissions from Hazardous Waste Sites, i Prepared by the Research Triangle Institute for U.S, Environmental Protection Agency, Washington, DC. August '• " , _ '' Ryan, E.A., ET. Hawkins, B. Magee, and S.L. Santos. 1987. Assessing risk from dermal exposure at hazardous waste sites. In: Superfund >87: Proceedings of the Eighth National Conference, Washington, DC, November 16-18. p. 166-168'. • GsojErns\wEsnNc»i997\FiHLRis»Tixp««7.wpi 7-13 CHEMRlSK*-A SERVICE OF MCLAREN/HART R.U)390l4 , Sedman,R.M. 1989. The development of applied action levels for soil contact: A scenario for the exposure of humans to soil in a residential setting. Environ. Health Persp. 79:291-313. ^^"•^ j • • , . • • " ''•'.'' Todd,DX 1980. Groundwater Hydrology. New York, NY: John Wiley & Sons. ] Travis, C.C., S.A. Richter, E.A.C. Crouch, R. Wilson, and E.D. Klema. 1987. Cancer risk management: 'A review of J32 federal regulatory decisions. Environ. Sci. Technol. 21:415-420. Vater, S.T., S.F. Velazquez, and V.J. Coghano. 1995. A case study of cancer data set combinations for PCBs. Reg. Toxicol. Pharmacol. 22:2-10. ,.-.•• ' ' '.'!•• Wester, R.C., H.I. Maibach, L. Sedik, J. Melendres, and M. Wade. 1993. Percutaneous absorption of PCBs from soil: In vivo rhesus monkey in vitro human skin, and binding to powered human stratum cprneum. /. Toxicol. Environ. Health 39:375-382. R.F.Weston. 1994. Memorandum to D. Turner, Remedial Project Manager, EPA, Philadelphia, PA from J.J. Mueck, Jr., Technical Assistance Team, Region IH, Wheeling, WV Re: Trip Report - y Westinghouse Sharon NPL Site, Sharon Mercer County, Pennsylvania, TDD# 9410-160 PCS31160. ••''.Novembers• . '••"': • ' -' • : •• • '•• : •.'• -. ' Yang, J. J., T.A. Roy, A.J. Krueger, W. Neil, and C.R. Mackerer. 1989. In vitro and in vivo percutaneous absorption of benzo(a)pyrene from petroleum crude-fortified soil in the rat Bull. Environ.. Contain. ToxicoL 43:207-214. '. '' ' ' • :. • ' . j ..,- ._ , ' | . . ^ Young, F. E. 1987. Risk assessment: The convergence of science and the law/ Regul. Toxicol PharmacoLl-.m-m. 7-14 CHEMRISK*-A SERVICE OF MCLAREN/HART --:-''-'. • - ': .-•.': . "'""^ .' • :• ••' ''' 1R.1U3906- H/IC/CO IOMOOCI V_X FlguwM. Schematic Diagram of COPC Selection Process ^ NO Detected in Any Sample? YES 1 r YES Essential Human 4 . . ——— =- Nutrient? NO i • < ——— s. . Maximum Concentration > RBC YES Y .1 r • ' Eliminate , COPC for AsCOPC Risk Assessment s a s* III j I *t ™. rf i * *s ' . I^II : i 1 3 4 cf;j£2 S ^« 1a *§- IS i ' j j Ii ^i .• fil. j jl s nfi — gg iI 1 IS 9 • | • - -.a a* *i1« *^ J a I J a-- 'rI• ;«»l P"s sis 8 Ii 3 : Hi if si-^2 ^ P " v? = £ S I 311 2V i iS* . • i B J i i J s ij mi i n i\\ I i!'i JM!? I HiiiiJ 5 « J BE \ Mi ! • a \ t* hill! » l i- '£!•] '' it l!l!lli Mi:Sd iJilij! i l1i ^ ..R.HJ3908 Table 2-2. PADEP Detected Surface Water Constitutents (ug/L) Compared to Standards and Guidelines Maximum W02 WTPOS WfU Compound (PlneSL) (Water Plant) /ii .!_-_ v Contamlnaot Region m tap Water B: Reported value Is less than CRDL but frealer than IDL If; Parameter Dot detected at f tvea quutiution Umic W: Port-digwtk>o ipike out of control limits a: Secooduyniaxiniiinooiiianiiituit level (SMCL) b: Maximum coDcentnaioa level gotl (MC1XJ) c: Drioking water effect level (DWEL) NC: No criteria available d: Lifetime health advisory (HA) Table 3-1. Hypothetical Receptor Summary Hypothetical Exposure Area Hypothetical Receptor___Potential Exposure Routes River Sector Child Wader Sediment ingestion Dennal contact with sediment North, Middle, South Sectors Employee .. Inhalation Indoor Construction Worker Soil ingestion Dennal contact with soil Inhalation of particulates (dust) Inhalation of vapors Outdoor Construction Soil Ingestion Worker Dennal contact with soil Inhalation of particulates (dust) . Inhalation of vapors Moat - Maintenance Worker Soil Ingestion ^ Dennal contact with soil Inhalation of particulates (dust) . Child Trespasser Soil ingestion . Dermal contact with soil Utility Worker Soil ingestion . Dennal contact with soil Inhalation of particulates (dust) RailRoad Right-of-Way . Maintenance Worker Soil ingestion Dermal contact with soil Inhalation of particulates (dust) Child Trespasser Soil ingestion Dennal contact with soil Dennal contact with pooled stonnwater Southern Solvent, Central Resident Ingestion, dermal contact and PCB/Chlorobenzene; Bedrock inhalation of vapors via residential Aquifer ' groundwater uses Industrial Worker , Ingestion, dermal contact and inhalation of vapors via industrial '______'______groundwater uses______ 4R3U39I-0 i S ".•"•••«! 15 IU UJ Ul UI U CZ1 • 5*5o 3o S<* > ?«•1 sc*o , a 21 , » S S S S fi SS S m ri 3! Q «n o'.y.i'* ""**'** «««•« is r*.r*- f i..--.;-, -i e ! 1 I < CQ CQ ca oa E ft, <^ AR. C j' U] U] t£ j 3 j oi 1g s3 «i £ S I 1j3 15 < I i ••' . ' V ' ' - - /' SB ,1039.12 • 0S0 « «"N "S «' oo "a° •a S3 00 «Ti •s 1 s gIIg IIi m p r* 5 s. o-5o obin" ,w5 *• "* ^ sm *"' P- I** l s. « <3 •3 I & I.SI => e> o e o S 8;s „, 2S « «9 a «8i ~ S n or S3.^ R^cJ ^.^.Q .8 x O I ~<*' ^*\ _& _n • ^^ g- ' s I g s S 2 ?*5 15*" 2 S a^f 2 2 2 * 2 K S SI- -S £ fl | |f i SII 55 I ^ « *• -* r- o r- r- rj(sr4ts«N S f | B &' & I ZL U Cj *n •* *5^ < i -,. AR:1U39I3 .1, ov K V r* rf ^ * « Iff I *** *"* ^* ^T* " ^1 •si a q oq S ?J 2 o q r] - ?.» — K -c5 ' mmMw-t>ooo oo vtcn~* I d- f.. s. ^ .3 I wS , 8 •« 2 m 2 ^ I SO vo >O -O 1 i * . a . -• • ' ' S S^* v JT . N* , 3 a t> U „ H i 9 ta ' <• l A R303911* Table 3-6. Railroad ROW Sector Surface Sot! EPC Calculation 95% UCL of Frequency Arithmetic Mean of Range of Detected onLognormal Exposure Point Chemical N Detection Values Distribution Concentration Min Max Semivolatile Organic Chemicals (ug/kg) . Acenaphthylene 4 50% 51 59 1.06E+20 59 Benzo(a)anthracene 4 100% 580 5.050 2.15E+05 5,050 Benzo(a)pyrene •- '' . < 100% : 440 4,800 3.54E405 4^00 Benzo(b)fluoranthene ' , 4i ' 100% 1,200 8,000 1.45E405 8,000 Benzo(g,h,i)perylene 4 100% 270 2,950 5J6E+05 2,950 Dibenz(ath)anthracene ••• '4 25% 160 160 5.98E+12 160 !hdeno(l,23-cd)pyrene 4 . 100% 360 3,300 1.77E+05 3,300 Phenanthrene " . 4 ' • 100% 870 4,500 3^2E+04 4^00 F«tfc ides/PCB s (ug/kg) Aroclor-1248 6 33% 37 ' 210.000 4.09E+16 210.000 ArocIor-1254 6 100% 790 27Q.006 3.40E+10 270,000 Arodor-1260 6 100% 1,400 170,000 1.67E+08 170,000 . Dieldrin 6 33% 3.7 440 U2E+08 440 Endrin aldehyde 6 67% 100 3,200 1.18E+05 3.200 , Heptachlor epoxide 6 50% 4.0 215 1^9E406 215 Inorganic Chemicals (mg/kg) Aluminum ,:•'•" 4 , 100% 1,860 11.000 2.75E+05 11,000 Antimony 4 100% 9.6 30 7.16E401 30 .Arsenic 4 100% 16 48 9.77E+01 48 Beryllium 4 100%, 0.62 1.6 3.47E400 1.6 ". Cadmium 4 100% 8.4 26 I^4E-fC2 26 Chromium 4 100% 15 81 U6E+Q3 81 Copper 4 100% 54 972 1.78E+06 972 . Iron 4 100% . 39,700 '59.800 6.25E404 59.800 Lead 6 100% 95 624 1.10E+03 624 Manganese 4 100% 255 1,215 1^7E+04 1,215 Mercury 4 100% 0.39 0.95 1 J1E+00 0.95 Thallium -'4 -'; 100% 1.5 3.6 634E400 3.6 Zinc • '4 l.- 100% 1,140 15,600 1.87E-f07 15,600 Dioxins (ug/kg) Total Equivalent 2,3,7.8-TCDD 4 100% 0.013 1.6 ' • NA 1.6 NA - 95 % UCL's for these chemicals could not be calculated given the size of the data set Riiu'3'9-15 s o •s * Z Z Z oo • I n oo «» Q op oo I , I Z m m i I "a a M 4 J5 -" I 4R3IJ39I6 Table 3-8. Alluvium Southern Plume Monitoring Well EPC Calculation u--... ••-••• ,.;•:•-.-. 95% UCL of i' Frequency Arithmetic Mean ' 1 of Range of Detected on Lognonnal Exposure Point : Chemical N Detection Values Distribution Concentration Min Max Volatile Organic Chemicals (ugfl) Vinyl Chloride 5 20% 15 15 5.80E401 .-.- 15 1,2-Dichloroethene (total) 5 . '. 80% 15 3,300 4.63E409 . 3300 1,1-Dichloroethene 5 60% 2.0 2.0 U2E402 2.0 Trichlorocthene : 5 60% 56 170 1.05E+04 170 Chlorobenzenc 5 80% , 6.0 230 6.16E+04 230 Semlvolatile Organic Chemicals (ug/l) * • 1 ,3-Dichlorobenzcne 5 60% 180 560 U5E408 560 1,4-Dichlorobenzene ! '5' 60% 27 450 5.83E+05 450 , 1,2-DichIorobenzene 5 60% 31 152 1.11E+04 152 1.2,4-Trichlorobenzene 5 80% 4.0 110 2.52E+04 110 2,4-Dichloropnenol 5 40% 4.0 12 1.08E+01 11 PesticMes/PCBs(ug/Q: • Aroclor-1254 5 20% 14 14 , , 5.76E+02 14 Inorganic Chemicals (mg/l) 1 '"'• - • Aluminum . 5 100% 28 98 , 1.35E+02 • 98 Arsenic 4 , 100% 0.035 0.39 5.15E401 0.39 Barium . * 5 100% 0.26 0.90 LOlE-fOO 0.90 U Beryllium 5 40% 0.00 0.01 5.92E-02' . 0.007 Cadmium 5 20% 0.0018 0.0052 4.58E-03 0.0046 Chromium . 5 100% 0.04 0.48 U2E+00 0.48 Copper 5 ' 100% 0.07 0.39 6^3E-01 0.39 Iron 5 100% 121 308 3.25E+02 308 - Lead 4 100% 0.064 0.25 l.OSE-KX) 0.25 Manganese 5 100% 2.4 7.5 8.59E400 7^ Mercury 5 • 40% 0.0002 0.0015 3.92E-02 0.0015 Nickel 5 100% 0.03 0.72 5.37E-KX) 0.72 Vanadium 5 . 100% 0.051 0.18 2^5E-01 0.18 ( '' ' . Zinc . - - ' •' V 3 100% : 0.22 1.8 3.78E400 1.8 Dioxins (ng/l) Total 2378-TCDD Equivalent 2 100% 0.0047 0.014 3.03E+52 0.0142 NA - 95% UCL's for these chemicals could not be calculated given the size of the data set Table 3-9. Alluvium Central Plume Monitoring W«II COPC Screen 95% UCL of Arithmetic Mean Exposure Frequency Range of Detected on Lognormal Point Chemical N of Detection Values Distribution Concentration Min Max Volatile Organic Chemicals (ug/l): - " 1,1-DichIoroethene 13 8% 5 5 . 2.79E+01 5.0 1,2-Dichloroethene (total) 13 8% 9.0 9.0 2.83E+01 9.0 . 1,2-DichIoroe thane 13 8% 6.0 6.0 2.38E+01 6.0 1,1,1-Tricnloroethane 13 8% 98 y» 6.59E+01 66 Trichloroethene 13 15% 240 5,400 3.92E+03 3920 Benzene 13 15% 16 290 3.57E402 290 Tetrachloroethene 13 8% . 25 25 . 3.59E+OI 25 Chlorobenzene 13 54% 45 310 2.56E+03 l 310 Semivofatile Organic Chemicals (ug/l): 1,3-Dichlorobenzene 13 31% 72 510 , 4.32E+04 510 1,4-Dichlorobenzene 13 31% 24 360 2.16E+04 360 1,2-Dichlorobenzene 13 38% 4.9 910 3.10E+04 910 1,2,4-Trichlorobenzene 13 62% 2a 48,000 2.99E+08 48000 PCB$(ugn): Aroclor-1242 . 13 , 8% 5.7 5.7 2.90E+10 5.7 Aroclor-1248 13 8% 30,000 30,000 3.00E+11 30,000 Aroclor-1254 13 46% 0.75 47,000 7.34E+10 47.000 Arodor-1260 13 8% 5.6 5.6 1.07E+10 5.6 inorganic Chemlcals(mg/l) * . Aluminum 11 100% 14 162.00 1.40E+02 140 Arsenic 6 100% 0.003 0.0349 8.22E-02 0.035 Barium 11 100% 0.156 1.42 9.80E-01 0.98 Beryllium 11 73% 0.0023 0.012 2.99E-02 0.012, Cadmium 11 36% 0.0054 0.07 4.34E-02 0,067 Chromium . 11 91% , 0.029 0.25 2.41E-01 0.25 Copper, 11 91% 0.0366 0.95 7.79E-01 0.78 Iron . . 11 100% 40.6 477.00 4.77E+02 477 Lead 7 86% P.0507 0.28 5.05E400 0.69 Manganese 11 100% 4.56 124.00 V 5.05E+01 . 50 Mercury 6 . 67% 0.00024 124 4.34E-03 0.00096 Nickel 11 100% 0.0262 0.29 . 3.48E-01 0.29 Silver 11 9% 0.061 0.06 1.40E-02 0.014 Vanadium 11 91% 0.062 '•- 0.28 2.65E-01 0.27 Zinc 11 100% 0.13 39 1.82E401 18 Cyanide (ug/l) 12 8% 205 205 3.63E+01 36 Dioxins (ng/t) • Total 2378-TCDD Equivalent (ng/l) 0 ' 100% 0.0083 0.0083 NA 0.008 NA - 95 % UCL's could not be calculated given the size of the data set. AR.I039I8 W ,ii ': • ' •-'. • ." '-"• •'-. £ SB 'SSP 3'S- plsilsr 1 a 1 , o °' 1 & ° o' tS O . ' ,' • • ' .' d "M 8SS. g| .p-§-§2j §.§•'§.. - |' u ui u u3tu ujwuujwtiuJuS s l ' Si Ii H (*• S rn oo p^ ^O * "^ O oo oo ^ ««r-^v ffs — .- /: ;""'-.:::/ •''• :.^--. .'»R.*u39l9 TabI*3-U. Middle Building Indoor Air COPC Screen 95% UCL of ,-.-.. Frequency Arithmetic Mean ^ of Range of Detected onLognormal Exposure Point Chemical N Detection Values Distribution Concentration 1 . Min Max Volatile Organic* (ug/m* ) ,• " , 1,1-Dicnloroetbene ;. 5 20% 3.9 3.9 13 3.9 Freonll3 5 80% 16 21 56 21 1,2-Dicbloroctbanc 5 • - 40% 7 40 377 40 Benzene 5 60% 3.5 4 6.5 4;0 Trichloroethene 5 20% 73 7.5 6.8 6.8 Tetrachloroetbene 5 20% 8 8 7.1 7.1 Pesttcides/PCBt (ug/at3) 'L Aroclor-1242 5 100% 0.067 0.199 0.26 0.20 Table 3-12. Hypothetical Child Wader Exposure Parameters Parameter Value Source Soil Ingestion Rate (mg/d) 200 EPA,1996e Fraction Attributable to Source 03 Assumed Dennal Adherence Factor (mg/cm2) 0.2 EPA.1992C , Total Body Surface Area (cm2) 103QO EPA, 1989a Fraction of Surface Area Exposed 0.3 EPA,1989a - (Hands, forearms, tower legs) v' Exposure Frequency (d/yr) 82 5 d/wk, 3 mo/yr; 1 d/wk, 4 mo/yr Exposure Duration (yr) 6 EPA,1989b Body Weight (kg) 33 . EPA,1989a • \ ' . ' • - • v Averaging Time, Carcinogen (d) 25350 EPA, 1989b Averaging Time, Noncarcinogen (d) 2,190 EPA,1989b .IRJU392I Table 3-13. Hypothetical Employee Exposure Parameters Parameter Value Source Inhalation Rate (m3/d) 10.8 EPA, 1989a (Light- moderate activity, 8 hr/d) Exposure Frequency (d/yr) 250 EPA, 1991b Exposure Duration (yr) 25 EPA, 1991b Body Weight (kg) 70 EPA,1989b Averaging Time, Carcinogen (d) 25350 EPA,1989b Averaging Time, Noncarcinogen (d) 9,125 EPA, 1989b M*OJBCT3\WESTINO»l9«tfWALRISIOTAlSFICaTW3-l»* W 3 (2) IR 3U.39 2 2 Table 3-14. Hypothetical Indoor Construction Worker Exposure Parameters Parameter . . Value Source Soil Ingestion Rate (mg/d) 100 (see text explanation) Fraction Attributable to Source 1.0 Assumed ' Dennal Adherence Factor (mg/cm3) 0.2 EPA.1992C Total Body Surface Area (cm3) 18,000 EPA,1989a Fraction of Surface Area Exposed 0.22 EPA,1989a (Hands, forearms, lower legs) Inhalation Rate (mVd) 20 EPA,1989b Respirable Particle Concentration (mg/m3) "5 (58 FR 40191, July 27/1993) Exposure Frequency (d/yr) 65 5 d/wk, 3 mo/yr Exposure Duration (yr) 2 • ', . Assumed, Body Weight (kg) 70 EPA,1989b Averaging Time, Carcinogen (d) 25350 EPA,I989b { Averaging Time, Noncarcinogcn (d) 730 EPA.1989b R.HJ3923 "2 -I I 9t i o |r* w * -v -. • * a 2 fai tuf &, P" II R « u » " a * 2 2 uT 2 « UI 3 U . * , * 4 m (^ m ?? ^ ^ St N ' 2 i I1o 3<^ •3 '* ""a i5 «^ B ' • -3 ' JJ •" « "a _h«§g88.Ms i I tila B a a a « 1 .9 .Sg .5 1 Ia i=r « - I'1 « ? Ot W a s ° s ta s » ft.a 3 uj Cx U m 53 u S S ' 1 I l t I | .fO | t i! t-5 2* . Ji '13 Ml 11I 5 f.s 1*i 3s 1 H H AR HJ39214 Table 3-16. Hypothetical Outdoor Construction Worker Exposure Parameters Parameter , ' Value Source Soil Ingestion Rate (mg/d) 100 (see text explanation) Fraction Attributable to Source 1.0 Assumed Dermal Adherence Factor (mg/cm2) ...a2' EPA, 1992b Total Body Surface Area (cm2) 18,000 EPA, 1989a Fraction of Surface Area Exposed 0.22 EPA,1989a . ' J ..--'' (Hands, forearms, lower tegs) Inhalation Rate (mVd) 20 EPA, 1989b Respirable Dust Concentration (mg/m3) Site-Specific (refer to Table 3-14) Exposure Frequency (d/yr) ' 195 > 5 d/wk, 3 mo/yr Exposure Duration (yr) 1 Assumed Body Weight (kg) 70 EPA,1989b Averaging Time, Carcinogen (d) 25,550. EPA,1989b Averaging Time, Noncarcinogen (d) 365 EPA,1989b AfUU3925 Tabto 3-17. Hypothetical Moat Maintenance Worker Exposure Parameter* Parameter Value Source Soil Ingestion Rate (mg/d) 100 EPA,1996e Fraction Attributable to Source 1.0 ' Assumed Dennal Adherence Factor (mg/cm2) 0.2 EPA,1992c Total Body Surface Area (cm2) 18,000 EPA, 1989a Fraction of Surface Area Exposed 0.14 EPA.1989* (Hands, forearms, face) Inhalation Rate (ms/d) ' 20 EPA, 1989a (for moderate activity, males only, 8 hr/d) - Paniculate Emission Factor (m'/kg) . 1.30E+9 EPA,1996c ' Exposure Frequency (d/yr) . 7 lAno, 7 months (April to October) Exposure Duration (yr) • ' 25 ; / EPA, 1991b Body Weight (kg) 70 EPA.1989b • - i; Averaging Tune, Carcinogen (d) 25,550 EPA,1989b Averaging Time, Noncarcinogen (d) . 9,125 EPA, 1989b \J Table 3-18. Hypothetical Child Moat Trespasser Exposure Parameters Parameter Value for Age Range • Source 7 to 12 years 13 to 18 Tears i , - • Soil Ingestion Rate (mg/d) : 200 100 EPA, 1996e Fraction Attributable to Source 04 0.5 Assumed Dennal Adherence Factor (mg/cm2) 0.2 0.2 EPA,1992c . Total Body Surface Area (cm2) 10,500 16,000 EPA.1989a Fraction of Skin Surface Area Exposed 0.22 0.23 EPA, 1989a (Hands, forearms, lower legs) Exposure Frequency (d/yr) 4 .* Assumed Exposure Duration (yr) 6 6 EPA. 1989b Body Weight (kg) 33 56 EPA, 1989a Averaging Time, Carcinogen (d) 25,550 25,550 EPA,1989b Averaging Time, Noncarcinogen (d) 2,190 2,190 EPA,1989b ARHQ3927 b I> 8 1 £ * r. « -> m i m « O2\^ ^SfrK •1 OH2 ^ u ^ ^nSf ro ^u3. OTN) H^ & *Q^* 2^?* 8^w!i .^ S1^ 1I -gd 5 5 5 I 3 115 s" 5 "---"-- Ha a o 3 u (3 «_ a- a a -g a - III * M « •« R 51. ^2^3? ?3 9 o ______aj!2 >< V* \R.5U3928 Table 3-20. Joint Frequency Distribution of Wind Speed and Direction for '' Youngstown, OH for the Years 1983-1992. U- .' • Direction from I. . - ' ' which the wind blows Wind Speed (m/s) Total 0.51 to 1. 2.1 to 3.1 3.6 to 5.1 5.7 to 8.2 8.5 to 10. >10.8- N 0.002129 0.015891 '0.020732 0.011468 0.000532 0.000139 0.050892 * NNE 0.001394 0.012812 0.014142 0.005297 0.000317 0.000089 0.034051 NE' 0.002002 0.01546 0.0129 0.003181 0.00000 0.000013 0.033556 ENE •• : 0.002344 0.016626 0.00972 0.002066 0.000089 0.00000 0.030844 E 0.002611 0.019528 0.012394 0.003079 0.000177 0.000013 0.037802 ESE 0.003105 0.022443 0.01731 0.007477 0.0009 0.000114 0.051348 SE 0.003371 0.023596 0.025193 0.012558 .0.000938 0.000063 0.065719 SSE 0.003472 0.018666 0.022113 0.007667 0.000165 0.00000 0.052083 . . V S 0.004068 0.02755 0.035102 0.011228 0.000342 0.000013 0.078302 ssw 0.004042 ,0.027866 0.031744 0.014092 0.000798 0.000076 0.078619 sw , 0.004752 0.031415 0.041464 0.029653 0.003041 0.000621 0.110946 wsw 0.003269 0.018388 0.029298 0.028665 0.005462 0.001318 0.0864 W 0.002775 0.017653 0.024255 0.024445 0.004676 0.000862 0.074665 WNW . 0.002332 0.014979 vO.021328 0.014776 0.001749 0.000253 0.055416 NW . .' . 0.002915 0.02058 0.024458 0.017653 0.001457 0.000127 0.067189 NNW 0.00218 0.016297 0.020212 0.014332 0.001204 0.000089 0.054314 Total 0.046761 0>319749 0.362366 0.207636 0.021847 0.003789 0.962146 Frequncy of Calm winds "0.037 Percent of tune wind exceeds 5.1 m/s - 0.23327 I»:VllOJECTS\WESTINCH\l99l\PtNALIUSlC\TABSFICS\™J-M*U\tBU.»(l) AR.3G3929 .. Table 3-21. Hypothetical Moat Maintenance Utility Worker Exposure Parameters Parameter Value Source Soil Ingestion Rate (mg/d) 100 EPA. 1996c Fraction Attributable to Source 1.0 Assumed Dennal Adherence Factor (mg/cm2) 0.2 EPA, 1992c ' ' i . Total Body Surface Area (cm3) 18,000 EPA* 1989a , Fraction of Surface Area Exposed : 0.14 EPA,1989a .(Hands, forearms, face) Inhalation Rate (m3/d) 20 EPA* 1989a (for moderate activity, mates only, 8 hr/d) Respirable Particle Concentration (mg/m3) Site Specific (Refer to Table 3-18) Exposure Frequency (d/yr) 0.4 GRI.1988 Exposure Duration (yr) 25 EPA, 1991b Body Weight (kg) 70 EPA,1989b Averaging Time. Carcinogen (d) 25^50 EPA,1989b Averaging Time, Noncarcinogen (d) 9.125 EPA. 1989b KMiwwitt^^ , . . AR:JU39'30 . . . ,. . Table 3-22. Hypothetical Railroad ROW Maintenance Worker Exposure Parameters Parameter Value Source Soil Ingestion Rate (mg/d) . 100 C,rf\FPA , IQOAI / .suce Fraction Attributable to Source . 1.0 Assumed i Dennal Adherence Factor (mg/cm2) ••0.2 EPA.iy92c Total Body Surface Area (cm2) ' 18,000 EPA, I08(/a . Fraction of Surface Area Exposed a 14 EPA,1989a (Hunds, forearms, face) Inhalation Rate (mVd) 20 EPA, J989a (for moderate activity, males only. 8 hr/d). Respirable Particle Concentration (mg/m3) 'l.3E+9 EPA, 1996 Exposure Frequency (d/yr) 5 5 days/year for 25 years Exposure Duration (yr) .; . 25 , EPA,1991b Body Weight (kg) 70 EPA,1989b Averaging Time, Carcinogen (d) 25,550 EPA, 1989b ' Averaging Tune, Noncarcinogen (d) 9.125 : EPA,1989b ,iR.iU393l v Table 3-23. Hypothetical Ralh-oad ROW Child Trespasser Exposure Parameter! Parameter Value for Age Range . Source ______' ______TtoUyean utolgyean ______Soil Ingestion Rate (mg/d) 200 100 EPA. 1996e Fraction Attributable to Source 0.5 0.5 Assumed Dermal Adherence Factor (mg/cm2) 0-2 0.2 EPA, 1992c Tbtal Body Surface Area (cm2) W-500 16.000 EPA, 1989a Fraction of Skin Surface Area Exposed 0.22 0.23 EPA, 1989a (Hands, forearms, and lower legs) Exposure Frequency (d/yr) 78 78 (2 times per week. 9 months) Pooled Water Dermal Permeability Coefficient (cm/hr) chemical specific EPA. 1992c Pooled Water Exposure Frequency (d/yr) 4 4 Assumed Fraction of Skin Area Exposed (pooled water) 0.22 0.23 EPA, 1989a Exposure Duration (yr) 6 6 EPA. 1989b Body Weight (kg) 33 56 EPA. 1989a Averaging Time, Carcinogen (d) 25^50 25,550 EPA, 1989b , Averaging Time, Noncarcinogen (d) 2,190 2.190 EPA, 1989b \^,/ •5 i i*•' ,11 a S to £ v w3W3ooi •S -8 1 1 *fi i a ff j JJ M i I M e Itfftte> e« ^ M K 6 i Q JB - •« I*> "5 .tt > < iiR.Hi3933 a § -S I 999 & A * « .0 o « at CQ CQ "^ p^ S w ^* W O^ 922 9^ v* •5 ^5 CT2*^ A9 O°No 4^44 u u a o a 3 a pu u3 >u tu pu 1 ^ «) ' M f f I * l Jl I intlli "a-I'll 1 a "a a AO «Q pxi ' \A aw ;£ •o"-I^a*Mf4ri~®~aoa a s ~. s -16 ^ fl- « a »^ M w* -3 . .9 P* > .3 • $ D 1131 1 .3 ime , C -SI .-a- * 1 a 'o«'e.^ala'S«^'g a"?! 1 "g f filSil I88 i8 8 1.1 Sits 3 posu r fit Hi a < •< CQ O CU U Ing e Pe r Sur f l AR.1U393U e e o.o 00600000 •>.. Vc . • • . 000000000600 i — — ^r^^M^ririmao*, I3- I 5i f ^ as s-a «•% r* • i! B I l^i 1 * X ' 11 " •f * Table 4-1. USEPA Welght^-Evldenee Classification System for Carcinogenicity Group Description A . Human carcinogen Blor Probable human carcinogen , B2 B 1 indiates that limited human data are available B2 indicates sufficient evidence in animals and inadequate or no evidence in humans C Possible human carcinogen D Not classifiable as to human carcinogenicity E Evidence of noncarcinosenicity for humans Source: USEPA, 1989a \J JR.103936 a $ a! fisSfiS'fi-: *t; s I £ *" «* ^ .x * «Sr «Sc Srj t S£faf*,* 8 .t S "1 *f-. -f iS .I> S i¥- I• -*. r8 -g S8 - gj g eg gj g e.fisp. & g. § " . Q .e 1C O Q.EO.§@S Z OQU^-I S ^i ^-,H*-H--^,s-:s>l A ft.'1039 3 7 !£'^FiiciTi«riviewit*virt jB vi m - - |^S33- - tu *•* e -' &^ ^*> -**s ^s ^s — 8-! ,,,1,1 i i8 •8 a II 1 la *.i sJJ 1 .1 -e c ci M -• aC i'» 91 iiiill 1 Ii y Is 8 ' J 3 I J1J1IIJ Z •II ARJU3938 'o ' j «" • B a is" "' S" u § • -• U .1.4.1. v SB £2" S2 « en I "8 IH : if 31 HI *B B f «u S°< SSSaSSoo Saa 2 = -=» : o o o J. I'Mu=ii!i in M tit iiiiJ i 18 I i S: .H 3* -S (r IiI g 3 s3 J3=:* I III I I III s"3 i 5 I -I4 3 ; AR303939 Ovs *9 J9S &* 9* v9s CT. &. ic a* oifliHeaoiMMx; 9 j §£££§ i i,-BIB2 53 «B 5 « l|« Ji w !! . tl II O Q n 1 •i JB I J! 5 i 3 fi '- . a !? I c*« r* ^ j *** — eigh t o f knc c CQ CQ CQU •% 03 aa H B,«p.^ A n H 4tn < ' *.• J t 1 w .5 Slop e F (rngftf-df t .i I ii I .i i £.1 ' ils**2 s If! • 91* J Ji Z 1 AR.J039UO Table 4-4. PCDD/F Toxic Equivalency Factors [TEFs] Toxic Equivalency Factor Convener (USEPA. 1989d) ' PolychlorinaiedDibenzo-p-dioxins .UJ.S-Tctrachlorodibenro-fKlioxin 1 1,23.7,8-Pentachlorodibenzo-pHiioxin 0.5 l,23.4,7,&-HexachJorodlbenzop-dioxin 0.1 I,23,73.9-Hexachlorodibenzo-p-dioxin 0.1 1.23.6.7,8-Hexachlonxilbenzo-p-dioxin 0.1 1,23,4,6,7,8-Heptachlorodibenzo-p-dioxin 0.01 Octachlorodibenzo-p-dloxin 0.001 Polycblorinated Dibenzofurans 23,7,S-Tetrachlorodibenzo-p-furan 0.1 2JA7,8-Pentachlorodibenzofuran 0.5 1.2,3.7.8-Pentachlorodibenzofuran 0.05 1,23.4.7,8-Hexachlorodibenzofuran ,0.1 1,2^,6,7,8-HexachIorodibenzofuran 0.1 1,23,7,8,9-Hexachlorodlbenzofuran 0.1 23i4,6,7,&-Hexachlonxllbenzofiiran 0.1 1,23,4,6,7,8-Heptachlorodibenzofuran 0.01 1.23,4,7«8.9-Keptachlorodibenzofuran 0.01 Octachlorodlbenzcifuran 0.001 ARJ039U iiiiiiiiliiii i iii 1a sHa -iS <*"*"* ^ I .... J j >* c Z IIII I . I I § i i 3.8 51 !01 >. I ! l I 1 1 » II .••... I * ^ tg 0WWW 4? 5! S 5 SiSiiBJii3tBi3i2 U [j] El. Ol ? i i}2i- ARJ039U2 •t •' :• ' ..-'/I ; fl'y( 1S6 *> SsSSBS-iSBfv> m' m vt <• ff\" vt ,x £ l£ i-fsf £&$•& £g ' $%l 4<3 rgg]XT .£B .K ".Eji Sj •tf^S _ 6&r3 • f6& 3 *^ '-•f6^t • ••* 'BgS* yij _ff* jiT Eff: m *"§2§ 8 "2iml§ s! f 5 i I i H I I o .? ¥J(89 ll > Jiliii ^ 1 i .i§ 4 ' 4 4 I ts •! i s.3 I $•* wi1! i«"oi i s aa U.UUIIIU pBj22ZMF>illjilj NI fitHfll- * |j| ! ||| pi ||g||| i I| a s8i a ' & as ^ 3 Hi i t J I • j !His•Rs ss* * i a. 2 I S i n*9" ^...'""""*" p*""1? •» V K -fi, M M .«•*•» -f .*f • |'j jgj o&o Cigtj iet s eS sa ga£ *5£ 5Se e 3 g -f j -9ggP* ]^ a 3* & ill S. & ,,... \W "E Tt M c ah m f o i ••••, . -'•i . •••••* ! a E- | " OpBp35SZcftH'p* HR3039U5 Motet EPA has calculated alternative values for the dermal ABS factor and the oral-to-dermal adjustment factor. See Appendix I. Table 4-7 . Route-SpecUk Absorption Emciendes* for COPCs Chemical ______Dermal Soil Source Or.il Soil/Diet Source Inhalation/Air Source Inorganic Chemicals Aluminum 0.27 b 1.0 i 1.0 j AnUmony O.I . c- 1.0 i 1.0 , j Arsenic . / 0.032 d 1.0 i 1.0 j Barium 1.0 d 1.0 i 1.0 j Beryllium 0.01 c .1.0 i 1.0 j Cadmium, 0.025 e. '1.0 j 1.0 , j Chromium 0.01 f 1.0 j 1.0 j Copper I'.O d 1.0 j 1.0 j Iron . 1.0 d 1.0 j 1.0 j Lead NA 1.0 k 1.0 J Manganese 1.0 d 1:0 1 1.0 J Mercury 0.15 g - 1.0 J 1.0 J Nickel 0.1 h ^ 1.0 J 1.0 j Silver 1.0 d 1.0 j 1.0 j Thallium' 1.0 d 1.0 J 1.0 - J Vanadium . 0.02 , . b 1.0 j IX) * j Zinc . 0.25 h 1.0 j 1.0 j Volatile Organk Chemicals ' Benzene 0.0005 d 1.0 j 1.0 J Chtorobenzene 0.03 d LO , j 1.0 j 1,2-dichloroethane 0.0005 d 1.0 j 1.0 j U-flchloroethene 0.03 d 1.0 J 1.0 J 1,2-dichloroetnene ,0.03 d 1.0 j 1.0 j Freonin, NA NA 1.0 J Tetrachloroethcne 0.03 d . 1.0 j 1.0 J Trichtoroethene 0.03 d 1.0 - j 1.0 / j Vinyl Chloride ' , 0.0005 . d 1.0 j 1.0" j KVKOI BCT»WBsnNOHU9»II.*»-Tj.rt.» 4-7 (Q Note: EPA has calculated alternative values for the dermal A US factor and the onl-to-dermal adjustment factor; See Appendix I. , • _ , : ' Table 4-7 Route - Specific Absorption Efficiencies* for COPCs Chemical Dermal Soil Source Oral Soil/Diet Source Inhalation/Air Source • • SemlvolatUe Organic Chemicals . ' . Acenaphthylene 0.1 V ; d, 1.0 j 1.0 J Benzo(a)anthracene 0.1 tl 1.0 J . 1.0 j Benzo(a)pyrene 0.1 d 1.0 . j 1.0 J Benzo(b)fluoranlhene 0.1 d 1.0 j ,1.0 j Benzo(g.h,i)perykne 0.1 d . 1.0 j 1.0 j Bis(2-ethy Ibex yOphthal ate 0.1 d 1,0 j 1.0 J 1,2-dichlorobenzene 0.1 d i.O ., j 1.0 J 1,3-dichlorobenzene 0.1 d , 1.0 j 1.0 J 1.4-dichlorobenzene 0.1 d 1.0 j 1.0 j 1,2-dichloroethane 0.03 1:0 a 1.0 j 1.1-dichloroethene 0.0005 1.0 j 1.0 j; 1,2-dicnloroethene 0.0005 1-0 j 1,0 j Indeno( l,23-cd)pyrene 0.1 'd 1.0 ••;. • J 1.0 . j Pbenanthrene 0.1 d i.O ' - j 1.0 j 1,2,4-Trichlorobenzcnc 0.1 d 1.0 J 1.0 j PesticIdes/PCBs • • / . ." Aroclor -1242 ' 0.06 d 1.0 j 1.0 j Aroclor -1248 0.06 d 1.0 j 1.0 j Aroclor - 1254 0.06 d 1.0 J 1.0 j Aroclor- .260 0.06 d 1.0 J 1.0 j Dieldrin 0.1 d 1.0 j 1.0 j Endrin aldehyde 0.1 d I.O j ' 1.0 , j Heptachlor expoxide 0.1 d > 1.0 : j 1.0 r Dioxlns/Furans ' Total 23.7,8-TCDD Equivalents 0.03 d 0.5 j, 1.0 j a. Efficiencies expressed as fraction absorbed b. ATSDR. 1992 C. NCEA, 1994 d. EPA. 1996a - e. IRIS, 1997 f. ATSDR. 1993 g. NCEA. 1993 h. NCEA. 1992 i. ATSDR, 199.U : j. Complete (100%) absorption is assumed as a default k. ATSDR, *991b 1. ATSDR, 1991c Notts: EPA has calculated alternative values for the dermal A US factor and the oral- to-dermal adjustment factor; See Appendix L Table4-8 Relative Absorption Factors for COPC Chemical______Dermal Soil Oral Soil/Diet Inhalation/Air Inorganic Chemicals .Aluminum 0.01 1.0 1.0 Antimony 0.01 1.0 1.0 Arsenic 0.032 1.0 1.0 Barium ' 0.01 1.0 ' 1.0 Beryllium 0.25 1.0 l.a Cadmium 0.01 LQ . v 1.0 Chromium 0.01 1.0 1.0 Copper ' 0.01 1.0 1.0 Iron 0.01 1.0 1.0 Lead 0.02 1.0 1.0 Manganese 0.2 1.0 1.0 Mercury 0.01 1.0 1.0 Nickel 0.01 .1.0 1.0 Silver 0.01 1.0 1.0 TTiallium 0.01 1.0 1.0 Vanadium 0.01 1.0 1.0 , Zinc 0.01 1.0 1.0 Volatile Organic Chemicals Benzene 0.0005 - 1.0 1.0 Chlorobenzene 0.03 1.0 1.0 U-dichloroetbane 0.0005 1.0 1.0 1,1-dichlorocthenc '0.03 1.0 1.0 U-tfcMoroethene 0.03 1.0 1.0 Freonll3 NA NA 1.0 Tetrachtorocthene 0.03 1.0 1.0 Trichloroethcne 0.03 1-0 I.O Vinyl Chloride 0.03 1.0 1.0 • Note: EPA has calculated alternative values for the dermal ABS factor and the oral- to-dermal adjustment factor; See Appendix I. Table 4-8 Relative Absorption Factors for COPC Chemical______Dermal Soil Oral Soil/Diet In ha lut Ion/Air Semlvolatlle Organic Chemicals Acenapthylene • O.lO % 1.0 1.0 Benzo(a)amhracene 0.10 I.O 1.0 Benzo(a)pyrene 0.10* I.O 1.0 Benzo(b)nuorantbene 0.10 1.0 1.0 Benzo(gXi)peryIenc , 0.10 1.0 1.0 Bis(2-ethylbexyl)phthalate 0.10 1.0 1.0 1.2-dichlorobenzene 0.10 1.0 1.0 i,3-dichloTObenzene • 0.10 1.0 1.0 1,4-dichlorobenzene 0.10 1.0 . 1.0 Indeno(l,2,3-cd)pyrene < 0.10 1.0 1.0 2-methylnaphthalene 0.10 1.0 1.0 Phenanthrene 0.10 . . 1*0 1.0 lA4-frichlorobenzene 0.10 1.0 1.0 ' ' : • Pestlcides/PCBs Aroclor-1242 0.06 1.0 1-° Aroclor-1248 0.06 1.0 1.0 Aroclor-1254 0.06 1.0 1.0 Aroclor-1260 ^ > 0.06 1.0 1.0 Dieldrin 0.10 1.0 1.0 Endrin aldehyde 0.10 1.0 1.0 Heptachlor epoxide 0.10 1.0 1.0 " Dioxlns/Furans Total 2.3,7,8-TCDD Equivalents > 0.03 0.6 1.0 Table 4-9 Dermal Permeability Coefficients for COPC Dermal Water (Kp Chemical ______cm/hr)______Source Inorganic Chemicals . Aluminum l.OOE-03 , a , Antimony l.OOE-03 a Arsenic , l.OOE-03 a Barium l.OOE-03 a Beryllium l.OOE-03 a Cadmium " l.OOE-03 a Chromium l.OOE-03 a Copper.,, 1.00t>03 a Cyanide l.OOE-03 a Iron l.OOE-03 a Lead 4.00E-06 a Manganese l.OOE-03 a Mercury l.OOE-03 a Nickel 9.00E-06 a Silver \ 6.00E-04 'a Thallium l.OOE-03 a Vanadium l.OOE-03 a 22nc 6.00E-04 a Volatile Organic Chemicals Benzene 2.00E-02 a Chlorobenzene 4.10E-02 a W-d-cWoroetbane * . . , 5.30E-03 a Ll-dichloroethene 1.60E-02 a 1^-dichloroethene l.OOE-02 a Tetrachloroetl.ene ! 4.80E-02 a ltU-Trichtoroethane 1.70E-02 a Trichloroethene 1.60E-02 a Vinyl Chloride , 7.30E-03 a Semtvolatlk Organic Chemicals . r Acenapthylene ; 4.70E-01 a. calculated Bcnzo(a)antDracene 8.10E-OI a Benzo(a)pyrene l!20E+00 a BenzoO>)nuoranthene 1.20E+00 a Benzo(g4.,i)perytene 1.20E+00 a flfl: a.EPA,1992c AR;u)395l 1! ss s s1 si 99 T* 99*'* '999 ^9999999999 9 9 ?'?'•*' * u U •s S s s s s s . s u fi*ilf l* ac 5 % ^_ . , _ ' ' . SS h 9*S 1?99? 1 99??999?9?99l9??9l?"? * ^s 2£ stScsS >--"t^tsS u2 tv-._u tu & atS ua-saa^ u u) ^) ui LU Uja w WM(4 u 3 t^3^3a LIJ [5 til ji ^-! S S s 9 |s^ 9 i|2^' $&$ ss^ s??^ ? t^U' Uc « tULUU— ae -*l » CLlUlCUUlUCUUCUUlUlR i*>ri-»Oi riv^p^iov*-U ^ UJtUCUUMr^>e^pUJ s s d z Q ? — " G pti ta tU tu tO Ctj UJ U UJ U (UtHCu LUCUu [UptipUW "3 t"" ^.N -. ^ —. -, r-ri'»o,>rIwi)N'Ovi^ — « w •». ^> I "3 ^ "3 ' "5 "3 "5 "3 ^4 S I I I I ; ^.5 . «• 5 J .q M 4 M -S e '*» "S •fl ll "3" ll'S llUi I 1*3 .2! ll |f3 ^ ^ < 1 ^ h - 3 ,«? e S 5 ,^ e 9 f^ i r^ I \l i 13^ J^i* 11J 1 -j B ra - I J 2 illl ill! M C i •i -i i s •= I I i 1 .„; ' i i •r • I le lB ^3 al .I5 —1i aI I .a I * i i. *" i v> ;iR.iN395Z * : ' ' , ssssss ssss s ssss sssssssss sii-if II? 1I?' $ % 1^3? ? • 1$S? MM ?-MM V 8 Ii aIF .* *• ssssss ssss ssss ssss ssss ? •*""^ 51 lsl^^^.^ttt'Tf§ ^s^ MS f ,9£ 9ft?*g^^ ^ss^ 1a ttts^.f l -1 .... "*"*""* "" * -a sss s sss ssss s ssss [£} GU CM CtJ W Ifi til W Eiti ....1 t.... 11 sss sss ssss ssss '!• * J| _-,— — ._ v * « e 2 e 1 ti^-^ A.g J 22^K HS2 p^ 2.4% "•*' •X-T ^ ^ -^ ' •** ^ ^ ^^ ^ •^ •* ^* ^^ "^ ^™ ^^ *^ * •• i*i w -.; I • : . I l ' i t I I I t ' 3 &£ && &$ SS S&M SSS £&£ pfSl if g I * ,- • .. . •• ,,.••• • I AR3U3953 u sss ssss * a - ED .* =3 ?35 3 53; .5 3 g t ,3-*f-.«-ir-«^K s ***. !i * 3 ' : "j i -; ;: s s 1 f s ss s s s I 3*3 *.rt ^s ^^ Qa 5a w<» a tw U) ci] td Cd b at M rt ^ fp| r^ M •• (» El L - I — p. ,— -1SSS S S * 3 ' «» IIi 1 •o«EPA ' •• 8s 1 J ' SB.. .* ^1 81 s .£* 3 •t 8 If < I dl 1 -ft ' ._-._- I .Ii I £J .9 .a ? * S e j * « ™ •« « * 'J 1 I! Hila S1Sl1 1 i ARHIJ395I4 I Appendix A PADEP Shenango River Surface Water and Sediment Sample Data AR303955 Table A-l. PADEP Surface Water Sampling Data, „ W02 WTP03 WM (PlneSt) (Water Plant) (Upstream) V2J94 8^94 8/2A4 vol^tl}* Of sanies tniill ^mJH 11&S3&) y^ZLfe^ff1 J'-i'Wff^fBmn&iwimsttiilffiiffi**** Chloromcibane 10 U 10 U 10 U 3nxnomethane 10 U 10 U 10 U Vinyl Chloride 10 U 10 U 10 U Chloroethane 10 U 10 U 10 U Methylene Chloride SU SU SU Acetone 10 U 10 U 10 U Carbon Dis ulf.de SU SU SU 1,1-Dichloroethene SU SU SU 1,1-Dichkroe thane SU SU SU 1 J-Dichloroetbene (total]) SU SU SU Chloroform ' SU SU SU [,2-Dichloroethane . SU SU SU !-Butanooe . , 10 U 10 U 10 U 1,1.1-Trichloroethane SU, SU SU Carboo Tetrachloride SU ;SU SU Vinyl Acetate 10 U 10 U* 10 U. \ mnwf L^h Inrnifielhaipfl 5U SU SU ,2-Dichioropropane SU SU 5U nf-13-DicbJoropropene SU SU SU TicbJoroetbene SU SU SU }ibnnKxhlgrcinethane SU SU 5U 1,1,2-Trichloroethane SU SU SU. lenzene SU SU SU ran*- 1 3-Dicbloropropene SU SU SU Ironoforn. SU SU SU 4-Methyl-2-PenUnoae 10 U 10 U 10 U •Hexaoooe . v 10 U 10 U 10 U 'etrachloroethene SU SU SU 1,1.12-Tetrachloroc thane SU SU SU blueoe 5U SU SU Chloiobenzene SU SU SU Ithytbenzene SU SU SU ityreae SU SU SU Xylenee (total) SU SU SU ^daUH2KBnlnfBrm ^^^^^^^^^^^^^^^9 10 U 10 U 10 U t>ii(2-Caloroethyl) ether 10 U 10 U 10 U Z^ChlorophenoI wu 10 U 10 U l^-Dichlorobeazeoe 10 U 10 U ' 10 U 1,4-Oichlorobenzeiie , 10 U 10 U 10 U Baayi Alcohol 10 U 10 U 10 U U-Dich.oiobea.voe 10 U 10 U 10 U Z-Methylpbenol 10 U 10 U 10 U bii<2-CbJoTOUopropyl)Ether 10 U 10 U 10 U i-Methylphcnol 10 U 10 U 10 Ui N-Nitroto-dj-o-piopylamine tou 10 U 10 U foachloioethane 10 U 10 U 10 U Nitrobenzene ; 10 U 10 U 10 U Jaopborone , 10 U 10 U 10 U PlfB 1 (kf4 ' iiR.:*U3956 Table A-l. PADEP Surface Water Sampling Data. W02 WTP03 W04 (Pine St) (Water plant) (Upstream) 8^94 8/2/94 8/2/94 5eirifto!attle OrsanIcsYup/I']| iiMTiiffi fr^ V1T* 2-Nitrophenol .. 10 U IOU IOU 2,4-Dimethylphenol 10 U IOU IOU Jenznic Acid sou sou sou bit(2-Chloroetboxy) methane 10 U ,10 U IOU 2,4-Dichlorophenol 10 U IOU IOU U.4-Trichlorobcnzcne 10 U 10 U IOU Naphthalene 10 U , IOU 10 U 4-Chloroiniline 10 U IOU 10 y Hexachlorobutadicne 10 U IOU IOU 4-Chloro-3-methylphcnol 10 U IOU IOU 2-Methylnapbthalenc 10 U IOU IOU Hexachlorocyclopentadiene 10 U IOU IOU 2,4,6-TricbJorophcDol 10 U IOU IOU 2,4PS-TrichloropheDol sou sou sou 2-ChloroMphthaIene 10 U IOU IOU 2-Nitroaniline sou sou sou Dimetbylphthalate 10 U 10 U IOU Acenaphthylcne 10 U IOU IOU 2,6-Dinitrotolucoe • , - 10 U 10 U IOU "Nitroaniline sou so u sou Acenaphthene 10 U IOU 10 U 2,4-Dinitrophenol ; sou sou sou -Nitrophenol sou sou sou Dibenzofuran . 10 U IOU IOU 2,4-Dinitrotolucne 10 U 10 U IOU Diethylpbthalate 10 U IOU IOU -Chlorophenyl-phenylether 10 U IOU IOU luorene 10 U IOU IOU -Nitro«niDnc sou sou sou ,6-Dlnitro-2-methylphenol sou sou sou N-Nltrosodiphenylamine 10 U IOU 10 U -Bromopbenyl-pfaenylether 10 U IOU IOU Eexachlorobenzene 10 U IOU IOU 'entachlorophcnol 50 U sou sou tienanthrene 10 U IOU 10 U Anthracene 10 U 10 U IOU D.-n-butylphthalate 10 U IOU IOU Fluonnthene 10 U IOU IOU Pyrenc 10 U IOU IOU utylbenzylphthalate IOU IOU 10 U 3.3'-Dkhlorobcn2idine 20 U 20 U 20 U cozo(a)anthracene IOU . IOU IOU Chryiene ; IOU IOU IOU bii(2-Ethylbexyl) phtbalate IOU IOU IOU Di-n-octylphtbalate IOU IOU IOU enzo(b)fluoranthene IOU IOU IOU BetUDGOfluonnthefle IOU 10 U 10 U Bcnzo HR3U3957 Table A-l. PADEP Surface Water Sampling Data. W02 WTP03 W04 (PlneSt) (Water Plant) (Upstream) 8^/94 8^/94 8/2/94 pSa^td3?pCB.*7iE/ii7S^t ^^-^>^M(BgJ^.^ail|iTlte»J!litJfeliiti Dibenz(a,h)anthraceae IOU IOU IOU Benao(|4.4)perylene IOU IOU IOU 4.4-DDD 0.1 U 0.1 U 0.1 U 4,4'-DDE 0.1 U 0.1 U 0.1 U 4.4-DDT 0.1 U 0.1 U 0.1 U Aldrin O.OS U 6.05 U 0.05 U ilpba-BHC 0.05 U 0.05 U O.OS U ftlpha-Chlordane 0.5 U~ 0.5 U OJU Aroclcr-1016 OJU OJU OJU Anxlor-1221 OJU OJU OJU Aioclor-1232 05 U OJU OJU ArocIor-1242 03 U OJU OJU Aroclcr-1248 0.5 U OJU OJU Arocloc-1254 1U 1U - IU Arodor-1260 1U IU IU beta-BHd 0.05 U 0.05 U 0.05 U delta-BHC 0.05 U 0.05 U 0.05 U Jieldrin 0.1 U 0.1 U 0.1 U •ndoiulfanl O.OSU 0.05 U 0.05 U Endosulfan n 0.1 U 0.1 U 0.1 U .ndosulfaa sulfate ^ 0.1 U 0.1 U 0.1 U indrin 0.1 U 0.1 U 0.1. U .ndria ketooe 0.1 U 0.1 U 0.1 U gamma-BHC O.OSU - 0.05 U 0.05 U E^tnntf^hkf^^nf OJU OJU OJU leptachlor 0.05 U 0.05 U 0.05 U leptachlor epoxide 0.05 U O.OSU 0.05 U ifethoxychlor OJU OJU OJU 'oxapbene 1U IU IU n^reanics iu*/ii^U&isk*i^ Llununont 205 274 194 B Antimoay 13.0 U 13.0 U 13.0 U Arsenic 43 B 4.4 B 43 B tarium 26.2 B 24.7 B 26.5 B leryUiun. 1.0 U 1.0 U 1.0 U '•Antiink 3.0 U 3.0 U 3.0 U Calcam 30.500 28,400 28,100 Juxxniiiai 2.0 U 2.0 U 2.0 U Cobak 3.0 U 3.0 U- 3.0 U topper 2.0 U 2.9 B 2.0 U ion 688 749 539 jud 1.0 UW 1.2 B IX) B fagncsium - 6.310 6,000 6.010 rfanganese 297 307 265 Mercury 0.2 U 01 U 01 U Nickel 6.0 U 6.0 U 6.0 U •otasiium 2,680 B , 2,460 B 2^30 B Sekninra \ '• 2.0 U 2.0 UW 2.0 U Silver 2.0 U 2.0 U 2.0 U Page) of 4 ;/lR:i03958 Table A-l. PADEP Surface Water Sampling Data. . W02 WTP03 W04 (PlneSt) (Water Plant) (Upstream} 8/2/94 8/2/94 8^94 rnorg.tnfCTfugmM.maeimaao ijfpmmim Sodium , ' 9,970 8J80 8,610 Inallium 2.0 U 2.0 U 10 U Vanadium' 2.1 B 2.0 U 2.0 U Zinc 33.1 114 6.0 B Cyanide 5.0 U 5.0 U 5.0 U page 4 of4 . . AIU03959 IP p p a a p p a a a a a aaapaaaaaaaaa.-»aaaaaaaa U |a a a a a a -. a a a a a a p p a a a a a a a a ^ a a a ^. a -. a a x "••^•^-^•^W-*<3 \ PPPPPPPPPP paaaaa^aaaaaa aaaaaaaa p aaaaaaaaaa DPPPPP-.PDPPPP aaaapaaa pppaaaaaapppppppaapppppppppppppppp 1 paaaaaaaaaa-ppappaappppppppppppppp \J paaaaaaapaaaaaaaaaapppppaaaaaaaaaa i r*P*Kr*r*r*t^t^^^2Vr*i^i^^i^r*e^^K^r^t^i^Kr»Krir*r*VVr* . /' . ' • -,'-'. Ip PPPPPPPPPP PPPPPPPPPPPPP-PPPPPPPP U= H lr-^iJr*KKr*.^KVVV^t*^r*2'r*t*KVri»Sr'Kc*.^. 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L. _. _.|H d^C7i co a a 1 S 5; R w» o d •8 i **• map ^ tb H i I 3? nap ll 4si tm an . , A a a S" **? X d *^ VfM *"! x •":'": E3(a-:.r'«^ »T ^i**^ — -^ o -^^^^a^-^^sldS-^^^^-1- r ' i §9l'BigSg __„„„--,_-_, AR:ru396U Appendix B Hydrogeologic and Chemical Transport Summary JIR31J3965 MEMO . TO: Mr.MarkMaritato Project No. 93 111.20/12 ChemRisk - . FROM: Mr. William A. Baughman r «(*Y September 25, 1996 Cummings/Riter Consultants, Inc. RE: EVALUATION-IMPACT OF GROUNDWATER AT THE FORMER SHARON TRANSFORMER FACILITY ON SHENANGO RIVER WATER QUALITY The objective of this memorandum is to document our current understanding of the impact of groundwater associated with the Westinghouse Electric Corporation (Westinghouse) former Transformer Facility on Shenango River water quality. The groundwater monitoring well network utilized to evaluate the effect of groundwater associated with the former Transformer Facility and the Shenango River consists of 61 on-site monitoring wells located within portions of the North, Middle and South Sectors of the former Transformer Facility, 21 off-site monitoring wells installed during the remedial investigation (RI), and additional monitoring wells installed by \ ) representatives of Armco Steel and Roemcr Industries at their respective facilities. Each : of these facilities is located between the former Transformer Facility and the Shenango River. This evaluation was conducted by comparing on-site groundwater quality with downgradient (off-site) groundwater quality and the results for surface water sampling and analysis for the Shenango River. •Groundwater is associated with the^consolidated deposits consisting of glacial outwash or alluvium, and the underlying bedrock. Information provided in the RI Report (Cummings/Riter, 1996) indicates that groundwater generally flows west-southwest towards the Shenango River, the most probable discharge point for both the alluvial aquifer and the bedrock aquifer. Groundwater in the alluvium occurs under unconfined conditions,. whereas the groundwater associated with the uppermost bedrock unit is confined. These groundwater-bearing units are separated by glacial till, which acts as an aquitard. mra""" -1- ,'iR;MJ3966 As described hi the RI Report, groundwater in bedrock does not appear to be significantly impacted bv~the site. The only reported possible evidence of site related detections was PCBs in two bedrock wells, M-4B at 7 ng/1 and S-1B at 2.6 ug/l (Tables 4-4B, 4-4C, 4*4D, 4-4E and Figure 4-17 of the RI Report). These wells are located approximately 1,700 feet from the Shenango River. Bedrock Monitoring Well M-l IB, located in an area where LNAPL and DNAPL exist in the overlying alluvial aquifer (Figures 3-19 and 3-20 of the RI Report), does not contain reportable concentrations of PCBs or other substances analyzed above the method detection limit. The RI Report concluded that these reported detections require confirmation. Therefore, groundwater associated with bedrock at the former Transformer Facility is not discernibly impacting the Shenango River. Based on available information, groundwater associated with alluvium does not appear to be impacting the Shenango River. Groundwater samples collected for alluvial monitoring wells located immediately downgradient of the former Transformer Facility (OS-1 A, OS-IB, OS-2A, OS-2B,OS-3A, OS-3B, OS-4A, OS-4B, OS-5A, OS-5B, MW-17AR, S-l A, and S-2A) were below the method detection limit for PCBs (Tables 4-4A, 4-4B, 4-4C, 4-4E, 4-4F and Figure 4-14 of the RI Report). The nearest alluvial monitoring wells (MW-14A and MW-14B) to the Shenango River with a reported occurrence of PCBs in groundwater above method detection limits are located approximately 1,000 feet from the Shenango River. The occurrence of PCBs in groundwater samples collected from Wells MW-14A and MW-14B is bounded in the downgradient location by Wells MW-17AR, OS-4A and OS-4B which monitor the alluvial aquifer (Figure 4-14 of the RI Report). The occurrence of chlorinated aliphatic hydrocarbons is limited to two locations. The highest oh-site concentration of chlorinated aliphatic hydrocarbons in groundwater associated with the alluvium (Well S-10) is bounded by downgradient Monitoring Well S-8A (Figure 4-12 of the RI Report). Concentrations of TCE and 1,2-DCE in groundwater sampled from Wells OS-2A and OS-2B, located south of Roemer Industries, are similar to concentrations in the Roemer Industries monitoring wells. A PADEP approved soil vapor extraction system was installed by representatives of Roemer Industries in response to the groundwater study conducted at the Roemer Industries facility. This facility is located approximately 1,800 feet from the Shenango River. ,iR.ili3967 The highest concentration of chlorinated aliphatic hydrocarbons in groundwater reported during the^RI isat Well MW-3B, located on the ARMCO property, west (downgradient) of the Conrail railroad tracks and the Westinghouse Middle Sector Building (Figure 4-12 of the RI Report). This occurrence is bounded in the downgradient direction by Well MW-7, which had no detections of chlorinated aliphatics. ; Chlorinated benzenes were detected in groundwater associated with alluvium along the western (downgradient) portions of the Middle and South Sector areas of the former Transformer Facility (Figure 4-13 of the RI Report). The extent of chlorinated benzenes has been delineated, with the exception of the area west (downgradient) of Monitoring Wells OS-2A/OS-2B and OS-3A/OS-3B. The highest downgradient concentration of chlorinated benzenes in groundwater from this area is 4,400 ug/l (Well OS-3B), located over 1,900 feet from the Shenango River. Additional monitoring well(s) are anticipated to be installed in this area of the site during remedial design. It is also anticipated that additional monitoring of specific parameters in groundwater will be conducted to evaluate the natural attenuation rate of substances identified in on-site groundwater, which is expected to further limit the future potential for impact to the Shenango River from groundwater associated with the former Transformer Facility. Finally, none of the samples of Shenango River water obtained during the RI had detectable levels of PCBs, chlorinated aliphatics, or chlorinated benzenes. There is no evidence of adverse impacts from groundwater associated with the former Transformer Facility on water quality in the Shenango River. WAB/jmc QUMMINGS '3~ ;JR:1U3968 Appendix C Screening for Chemicals of Potential Concern (COPC) AR.1U3969 Table C-l. Date Qualifier DcfinitioM Qualifier Explanation i Correlation coefficient for the MSA is less than 0.995 * Duplicate analysis not within control limits — . No sediment was available at this location during this round of sampling B Parameter was detected in associated blank. Reported concentration is less than 5 or 10 times the highest concentration in any associated blank, (organics) May Include contributions from other TCDF isoraers, second column C confirmation not performed. E Reported value exceeds calibration range (organics) E Reported value is estimated because of the presence of interference (metals) J Analyte was detected below quantitation limits • value is estimated K Reported value may be biased high L Reported value may be biased low N Spiked sample recovery not within control limits NA Sample not analyzed for this parameter ND Parameter not detected above unspecified quantitation limit P Reported value may be of poor precision R Reported value should be rejected in making critical decisions (organics) S ( Inorganics) Reported value determined by Method of Standard Additions S (Dioxins/Furans) Signal-to-noise requirement not met for M-[COC1]+ Ion U Analyte was not detected. Value shown Is the sample detection limit Post-digestion spike out of control limits, while sample absorbance is less than W 50% of spike absorbance Peak indicating presence of Polychlorinated Dipnenyl Ether also detected at same X retention time z Detected peak failed mulitple identification criteria - No regulatory standard or guidance value for this parameter Dioxin sampling data was converted to total 23.7,8-TCDD equivalents using the I MB TEF .(1989) scheme. Therefore individual congeners were not evaluated Independently in the COPC screen. 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Data Qualifier Definitions Qualifier Explanation • Correlation coefficient for the MSA is less than 0.995 * Duplicate analysis not within control limits — No sediment was available at this location during this round of sampling B Parameter was detected in associated blank. Reported concentration Is less than 5 or 10 times the highest concentration in any associated blank, forpanics)_____ May include contributions from other TCDF isomers, second column C confirmation not performed. E Reported value exceeds calibration range (organics) E Reported value is estimated because of the presence of interference (metals) j Analyte was detected below quantitation limits - value is estimated K Reported value may be biased high L Reported value may be biased low N Spiked sample recovery not within control limits NA Sample not analyzed for this parameter ND Parameter not detected above unspecified quantitation limit P Reported value may be of poor precision R Reported value should be rejected in making critical decisions (organics) S ( Inorganics) Reported value determined by Method of Standard Additions S (Dioxins/Furans) Signal-to-noise requirement not met for M-{COC1]+ ion U Analyte was not detected. 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I D DD §ff«O- gM1 - a S DDD oB A r-" D D-D 3 D af EX. w% •<* so S j D 1 £ S ni " M lo r cb l ui n D i —~, t?C "—i C5Q sH 5H E S u Appendix E Modeling Approach for Estimating Indoor and Outdoo',' r: ' Air' Concentration! s of Volatile and Semivolatile Organic Compounds Originating from Groundwater AR3UUO.U9 Appendix E Modeling Approach for Estimating Indoor and Outdoor Air Concentrations of Volatile and Semivolatile Organic Compounds Originating from ENAPL or Groundwater This appendix describes the screening modeling that was used to estimate the migration of vapors from LNAPL or groundwater to the surface and the resulting indoor and outdoor air concentrations for the Middle Buildings Sector of the Westinghouse facility. The scenarios evaluated included the Indoor Construction Worker and the Outdoor Construction Worker. Vapor Transport Model Assumptions This screening-level model uses the most conservative assumptions, as follows: • Steady-state conditions • Migration is by diffusion only • No adsorption or adsorption sites already saturated • No degradation of chemicals •. i J • Constant source term (Le., transport to the groundwater surface is not rate limiting) • Surface concentration is zero, yielding the highest driving force Transport Equations i ' ' i ' ' * The concentration, C, in a porous media at a distance, x, from a source and over time, t, is described by the following partial differential equation: dx E-1 CHEMRlSK*-A DIVISION OF MCLAREN/HART 1 Where, r C = vapor concentration, mg/ms (=ug/L) I J- ,' ' t « time,sec ^ x = distance from source, m D » difiusion cpefificient, mVsec At steady-state, the concentration is independent of time and the left side of the equation becomes zero, yielding an ordinary second order equation: , TaxTt " (2) Two boundary conditions are required to solve the equation: C * Q, at % a= 0, where 0 is the location of the source; and, C = C,, at x = L,, where L, is the distance from the source term to the surface. The steady-state solution for the concentration with distance, x, from the source is thus: (3) At steady-state, the flux, F, is defined by Pick's Law as: n d£ - s "D—d x (4) Where F = flux, mg/m2-sec. Differentiating Equation 3 with respect to x and substituting into Equation 4 yields: (5) ^ Assuming that the surface concentration, Cf, is zero results in the maximum flux rate: E-2 CHEMRJSK*-A DIVISION OF MCLAREN/HART ' .' Equation 6 was used to calculate the maximum flux. Source Terms There are two possible sources of vapor flux from the soil/groundwater interface: volatilization of soluble chemicals and free product. The volatilization of soluble chemicals was evaluated in;this analysis for the Outdoor Construction Worker. Because the light nonaqueous phase liquid (LNAPL) is present beneath much of the Middle Building, the volatilization of chemicals from beneath the building is assumed to come principally from the LNAPL and not the dissolved phase constituents. Therefore, volatflzation from LNAPL was evaluated for the Indoor Construction Worker Scenario. . -. . ' . * For volatile compounds in groundwater, the vapor concentration at the boundary, x = 0, is assumed to be in equilibrium with the soluble fraction as defined by Henry's Law: -•.'.' "~~"> C^HCW (7) ^ Where, H = dimensionless Henry's Law constant Cw = concentration in water, mg/m3 (=ug/L) For free product, the vapor concentration at the boundary is assumed to be a function of its partial pressure in the presence of other compounds, as defined by Raoult's Law and the universal gas law: ' XpvMW c-—5T- (8) o«iJEOT»wBTOo»i«mraiJusicn»i*H«i««»m)E»».^Ni E-3 CHEMRlSK*-A DIVISION OF McLAREN/HART ' Where, ' . X = mole fraction of component in free product, M/M pv= vapor pressure of pure component, atm R = universal gas constant, 8.21xlO'5 m3-atm/M-°K MW = molecular weight, mg/M T • absolute temperature, °K At 20 °C, the vapor concentration above free product becomes: C0 Again, because tree product is beneath a substantial portion of the Middle BuUding, the Construction ' •' Worker scenario is evaluated based on volatilization from the free product and not dissolved phase chemical Effective Diffusion Coefficients •' : - - . • ' i • • Diffusion through the soil column from the groundwater/soil interface occurs both through the gas ( ; and liquid in the pore spaces. Hence, for a given soil layer, the effective diffusion is taken as a function of the effective gas and liquid diffusions: Where, '•- . ,: •. , , . V Dg = effective gas diffusion coefficient, mVsec D| . • effective liquid diffusion coefficient, mVsec The effective gas and liquid diffusion coefficients are related to the pure molecular diffusivities in air and water respectively by the Millington-Quirk tortuosity model: E-4 CHEMRJSK*- A DIVISION OF MCLAREN/HART AR;i(Jlt053 (6,)' (0 )1(V3 * ' *" »** *•* Where, ' D, = air diffusion coefficient, mVsec Dw = water diffusion coefficient, mVsec 6t » . total porosity, cmVcm3 ' 0t = air porosity, cmVcm3 6W = water porosity, cmVcm3 • In general, the vadose zone is comprised of several soil layers, with different moisture contents and porosities. For those systems, the overall diffusion coefficient between the source, x = 0, and the surface, x a I* is: .,"."..' /: />» For soil systems composed of n distinct layers, Equation 13 reduces to: -i • •* m m mr * * Ll The overall effective diffusion coefficient can be calculated from the soil layer data and used in Equation 6 to calculate the flux rate in the soil column. Vapor fluxes were estimated using conservative assumptions within the modeling framework described above. The parameters and the corresponding values used to derive flux rates from LNAPL beneath the Middle Buildings and from groundwater near the AB slab are presented in Table E-l and E-2. Values from the scientific literature or professional judgement were chosen fpr those parameters for which site-specific information was not available\' . ' - ' • - avuEKnwenwGHUMOTNu..^^ E-5 CHEMRISK*-A DIVISION OF MCLAREN/HART Indoor and Outdoor Air Concentration Box While the screening model described above was used to predict vapor emission rates via groundwater and LNAPL, on-site concentrations of vapors were developed using mass balance equations that incorporate a theoretically enclosed space or box over the area of interest, known as a box model This model assumes that the chemical concentration within the box is a function of both input (emission rate from groundwater) and output (air exchange or dispersion by wind). It further assumes that the flux is instantly and uniformly mixed with air flowing across a specified area. This is mathematically expressed as the mass rate entering the box divided by the volumetric rate of air that flows through the box. For indoor exposures, vapor concentrations were calculated using the following box model equation: (15) i ' : • ' where, , Cv = Indoor vapor concentration (mg/m3) f a Fraction of basement floor area through which vapors enter T- = Air exchange rate (s) F = Flux rate of COPC (mg/m2-s) t / " h « Box height (m) . For outdoor exposures, vapor concentrations were calculated using the following box model equation: • , . Cv*(FxAemit)/(Vwindx Awind) (16) where, '. Cv a= Outdoor vapor concentration (mg/mj) , F = Flux rate of COPC (mg/m2-s) .. Aemit = Emitting area (unpaved area) Vwind » Windspeed (m/s) Awind = Area of wind (box height x wind width) (m2) , The indoor scenario evaluated for the Middle Buildings Sector included the Construction Worker. For this scenario, the fraction of basement floor through which vapors enter was set equal to 0.01. E-6 CHEMRISK*- A DIVISION OF MCLAREN/HART (1R30U055 An air exchange rate of 8,500 seconds per exchange was applied to the model, based on 0.42 air exchanges per hour, as recommended by American Society of Heating, Refrigerating, and Air- Conditioning Engineers (ASHRAE) (1990). For the Construction Worker scenario, the approximate height of the building, 60 feet (18.3 m), was used as the height of the box. For the Outdoor Construction Worker scenario, the emitting area, Aemit, was estimated to be 17,400 m2. This area is representative of the AB-Slab as shown on site drawings provided in the RI (Cummings/Riter, 1996). A typical value of 2 m/s was selected for Vwind, while Awind was calculated assuming a box height of 2 m and a site cross-sectional area (wind width) of 241 m, again based on site drawings. Table E-3 summarizes the results of the indoor air modeling for the Indoor Construction Worker. The Indoor Construction Worker receptors is impacted by LNAPL beneath the Middle Building. Table E-4 summarizes the results of the outdoor air box modeled which is used to assess the daily intake of chemicals to the Outdoor Construction Worker. The Outdoor Construction Worker is assumed to be exposed to vapors from chemicals dissolved in groundwater. E-7 CHEMRISK*-A DIVISION OF MCLAREN/HART Table E-la. Calculation of Chcmlc.* Vapor Flux torn LNAPL. Middle BaUdinf Sector of We-tinjhauc Facility. $baron, PA Scenario: fadoor Construction Wariccr i • • EcruBtSoiw ' Ir>dex dwmlcal H Dw (an*/p«c> Da (OD'/MC) Co (nfegfa* Cv m(j*F*ryk 1 Aroclor-1248 102E-02 5.11634E-06 0.050034543 17.84 Fm(D/Lt)*Co 2 Aroclor-1254 0.0202 5.03243E-06 Q.048954391 102 Dl • Dw*(( Sw) IVif( 0t) *) 3 Aroclor.1260 0.0137 4.80613E-06 0.046101005 1.03 D* *Dg+Dl/H ' [Parameter Symbol Value Unto Comment Indoor Air Coocwtratic-t CV Calculated (we Table E- mjAn1 Baaed on mearand RIdata(O-nuninss/Riter{199t Flux Rate F Calculated , • mg-onta1-* . Total Poroaity l ' 6l 0.4 ( ... DJmensionleu Jury, 1983. Def-wlt for aafldy Mil Water Volume faction 0w tbrVadowZone DkaeaiionleM Jury. 1983. Default tor tandywU Ak Volume faction 6a Hi- 9w i . , Tortuoui Liquid Difluiion Coefficient Dl Calculated . cm'feec See equation above TortuouB Oa» Diffluion Coefficient Dg Calculated . em'/tec See equation above Effective DifAuion Coefficient Dt Calculated cn'/wc See equation above Henry* i Uw Comtant H Chemical-jpecific OtmeuioQleu Mackay et al., 1992 , i Water DifRuion Coefficient Dw Chemical^pecific , cm'/wc Calculated based on Lyraan, 1992. ' ' Air Dttturion Coefficieat Da ' Chemical^peciric cm'/cec Calculated bated on Lynuo. 1992- Fraction of door apace open f , 0.01 - vnitleu Selectioo baaed on expected perateatkn fbifbt of Building k ' 305 . cm Correjpoo4iloifjpn»imalcly 10ftccUln{bef(bt Air Enhance Rale • T 8500 i . ASHRAE, 1989 Initial Vapor Concentration Co Cnonical-ipecific ngfa? Catcnlatcd, aee Table E-lb. , ,. ' Repre.eat5 froundwat-r table at 1 ft below (roud wrf.ce. 8 cm la comprbed of tbe capillary fr-H0* ^ ' ' , .nd22Jcm beompriMdofptoo-utunreduod. Depth to Oroundw-ter , Lt 30.3 cm ChcmlaJ Arodor.1248 Anclnr.1254 Araclnr.l2«0 Chemical Index < . 1 23 Layer 1: Capillary Fringe ' .. w ' ' 8 ^' ' .•'.',.§ • ' ' • ; 9t 0.4 0.4 0.4 - 9w 0.4 0.4 0.4 9a ', ' 00 0 Dt 1.5079E-06 1.48317&06 1.41445E-fXS ft . ^00 0 Dt 7.46486E-05 7.34243E-05 0.000103392 De/tt 9.33108E-06 9.17804E-06 1.2924E-05 U/Dt 107168.7878 , 108953.6853 77375.17293 1 Layer 2; VadaicZoiu ' ., • • U : 22.3 22.5 22.5 et 0.4 0.4 0.4 . 0w 0 0 0 9a 0.4 0.4 0.4 Dt 0 0 0 ft " 0.014752201 0.01442802 0.013587WM °** . 6.014732201 0.01442802 0.0135870U4 Dt/Lt 0.000655653 (t.000641245 0.(XX)603867 Lt/Dt 1325.196087 1559,4655 1655.994163. . KUDe) 108693.9839 Il05l5.15(* 79031.16711 D/Umlf(_(li/Dt)) 9.200I4E-06 9.04853E-H6 .1.26332E-03 f 0.01 (>.(» 0.01 F '- : 1.64B-04 1.82E-05 1.30&05 R HJU057 Table E-lb. Initial Vapor Phase Concentration or LNAPL Constituent*. c, '' Pi x, Pv ^•Ceh Concentration MW MoUir Mol. Vapor, Vapor inLNALP Percent Mol. Wt. Density* Fraction' Pressure Cone. Aroclor (mg/1) of LNAPL (g/mol> (moI/L) (unitless) . (atm> (mg/m3) Aroclor- 1248 79,170a 8% 264,840 0.2989352 0.0983858 1.65E-05 17.836377 Aroclor- 1254 57.330a 6% 297.48b 0.1927188 0.0634278 2.57E-06 2.0158368 Aroclor- 1260 55,5 lOa 6% 325.95b 0.1703022 0.05605 1.35E-06 1.0252959 Mineral oil 807,990a 81% 34()c 2.3764412 0.7821364 NAf NA Footnotes: * 1 a. LNAPL constituent concentration were estimated using the reported mass-based concentrations in the RI Report (Cummings/Riter, 1996). The term, Ci, was cnculated using the following equation. Ci (mg/1) - CLNAK. (mg/kg) x 0.91(g/ml) x kg/lOOOg x lOOOml/1 where: CUJAPL- Mass-based concentration of PCB in LNAPL. 0,9 1 mg/I « approximate density of mineral oil. . Mineral oil concentration was assumed to be equal to 1x10* PPM less the sum of the aroclor concentrations. b. Calculated average molecular weights using data from PCBs in the United States • Industrial Use and Environmental Distribution (EPA. 1976). c. Because mineral oil is a mixture, the value shown is an estimate based on data for a generic mineral oil. e. Molar density, pi- Cixl/MWXlg/lOOOmg , • . \ J f. Mole Fraction, Xi « pi x l/£pi. ._• ' . N-^ g. NA - not applicable . h. Co-XjxPvxMWxl/RT. . ,lfUUl*058 * * JJ-J1 JJ « .« 33*8 h «5 3 *l * i I 22£5!* iJ 1 Ua i!jiiii J1I1 illMl ! I Jl 4!J AR30U059 55? 51155 ii Ij Ij O I4 1 1.-j , .".•• . - -^ Table E-3. Estimated Indoor Construction Worker Air Exposure Concentrations via Flux From LNAPL Sector/Scenario: Middle Buildings/Indoor Construction Worker Cv«(fxTxFVh . where, Cv « Concentration of vapor-phase chemical in indoor air (mg/m3) . ; f« Fraction Of basement floor area through which vaporsienter (0.01) T« Air exchang rate (8500s) ' . F » Flux rate of COPC (mg/m2-sec), from Table E-la h»Box height (60 ft or 18.3 m) . .. , LNAPL Chemical Concentration '. p F Cv (m»/L) (me-cm/m -sec) (mj?/m2-sec) (mg/m3) Aroclor-1248 79,170 1.64E-04 1.64E-06 • 7.62E-06 Aroclor-1254 57,330 , 1.82E-05 1.82E-07 8.47E-07 Aroclor-1260 55,510 1.30E^)5 1.30E-07 6.03E-07 Table E-4. Estimated Outdoor Air Exposure Concentrations via Flux From Ground wutcr' Sector/Scenario: Middle Buildings/Outdoor Construction Worker Cv M (F x Aemity( Vwind x Awind) where, Cv m Ambient concentration of vapor-phase chemical in air (nig/m1) F • Flux rate of chemical of interest (mg/m2-.ec), from Table E-2b. Aemit • Emitting area (unpaved area) (17,400 m2) Vwind • Windspccd (2 m/sec) , Awind m Area of wind (box height x wind width) (482m3) •'_••- , Groundwater Chemical -. Concentration ;• F'1", F Cv Cv' (UK/L) (us-cm/l-s) (ms/ma-K) (mj!/mO (mR/m1) Vinyl Chloride 15 5.74E-06 5.74E-08 ' 1.04E-06 4.76E-07 1,1-Dicbloroethene 5 6.74E-07 6.74E-09 1.22E-07 5.58E-08 1 ,2-Dichloroetbene (total) 3300 , 3.06E-06 3.06E-08 5 J3E-07 , 2^3E-07 1,2-Dkhloroclhane 6 2.01E-06 2.01E-08 3.63E-07 1.66E-07 1,1.1-Trichloroelhane 66 2.12E-05 2.12E-07 3.83E-06 , 1.75E-06 Trichloroethene ' 4029 1.16E-03 l.lfiE-05 , 2.09E-04 ' 9.56E-05 Benzene 290 1X)3E-04 1.03E-Ofi 1.86E-05 8 JOE-06 Tetracbloroetbene 25 7J3E-06 7.53E-08 1.36E-06 6.22E-07 Cblorobcnzcne 310 9.67E-05 , 9.67E-07 1.75E-05 8.00E-06 1 ,3-Dichlorobcnzene 560 . , 1.32E-04 1.32E-(W 2.39E^)5 1.10E-05 1,4-Dicblorobcnzcne 450 9.10E-05 9.10E-07 1.64E-05 7JOE-0 6 12-bichlarobenzcae 910 2.32E-04 2.32E-06 4.[9E45^ 1.92E-Q5 1,2,4-Trichlorobenzene 48000 8.53E-03 8.53E-05 1 .54E-03 ' 7.04E-04 Aroclor-1242 5.65 8.65E-07 8.65 E-09 1.56E-07 7.13E-08 Aroclor-1248 30000 4.76E-03 4.76E-05 8.59E-04 .' 3.93E-04 Aroclor-1254 f; 47000 7.33E-03 7.33E-05 1.32E-03 ; 6.04E-04 Aroclor-1260 5.6 7.73E-07 7.73E-09 1.40E-07 6.40E-08 Total 2378-TCDD Equivalent 2.238-02 6.14E-13 6.14E-15 1.11E-13 1.92E-14 notes: . - ,- - • - •. '.-;'..•.-..• a - The values shown in this column are those computed by EPA Region 111. The methods used to derive these values' are provided in Appendix I. The risk/hazards resulting from the use of these estimates are provided in Tables H-17 and H-l8a. aVUENmWE3TWIftlMfU.twii.tjM..* Mc-to (.) Appendix F Modeling Approach for Estimating Indoor and Outdoor Air Concentrations of Chemical Originating from Soils R.iUt»063 Appendix F Modeling Approach for Estimating Indoor and Outdoor Air • ' Concentrations of Chemical Originating from Soils / ' ;. » ' Indoor and outdoor air concentrations of COPCs via subsurface soil were derived from flux rates computed using the Behavior Assessment ivlodel (BAM) developed by Jury et al (1983; 1984a,b,c; 1990). EPA (1996) recommends BAM for modeling volatilization of chemicals from soft to air. On- ^ site air concentrations associated with each Middle Building Sector scenario (Indoor Construction Worker and Outdoor Construction Worker) were then derived through the use of box models. The applications of BAM and the box models are described in this appendix. •, i , . ' • • BAMTheory B AM is a one-dimensional equilibrium mc<-el whkh mcorporates net first-order degradation and simulates chemical movement to the atmosphere via a stagnant air boundary layer at the soil i , surface (Jury et aL, 1983). As an equilibrium model it assumes that vapor, aqueous, and sorted or solid phases of a chemical are in equilibrium, as prescribed by the organic carbon-water partition ' coefficient (Koc), dissociation constant (Kd), and Henry's Law constant (H) for organic carbon- liquid, solid-liquid, and liquid-vapor equilibrium partitioning, respectively. Other assumptions used by Jury etal (1983) include: ' • Soil properties, including water content, bulk density, porosity, liquid water flux, and organic . carbon fraction, are assumed to be uniform throughout the site; • Initial concentration of the chemical of interest is assumed to be uniform between the surface (zl) and maximum depth of contamination (z2); and. i F-l CHEMRISK* -A DIVISION OF MCLAREN/HART '•'.'» R..JUU 06U • • Loss of the chemical to the atmosphere is limited by gaseous diffusion through a stagnant air boundary layer, above which the contaminant has zero concentration arid the air is at 50 percent relative humidity. • Adsorption is described through a linear equilibrium isotherm; • Solute Transport occurs only along the vertical axis and not solute loss or gain occurs • * • i . - laterally. i - • • i In summary, BAM predicts flux rates based on partitioning between the three phases and mass conservation of a single chemical undergoing first-order decay in a one-dimensional homogeneous porous medium. The model's theory is comprehensively described by the authors (Jury et aL, 1983; 1984a,b,c; 1990). The basic equation for mass conservation of a single chemical undergoing first-order decay in a one* V J dimensional, homogenous porous medium is equivalent to (Jury, 1983): s.-*a» where, / , : P •" , Cto = mass of solute per soil volume (mg/cm3) F = Solute mass flow per area per time (flux) (mg/cm2-s) f, • •, m degradation rate constant (sec*1) T = time (sec) z s Depth contaminated soil (cm) F-2 CHEMRISK» - A DIVISION OF MCLAREN/HART ;.R.fuU065' Equation 1 describes the change in the total soil concentration over time as a function of the flux rate and the degradation of the solute in soil The mass flux of the solute (F) or contaminant mobility is afanction of gaseous diffusion, liquid oUl^ion, ami convection by mass flow of soil in solution (Jury etaL, 1983): ; where, Da = soil-gas diffusion coefficient (cm2(gas)/s) Dl = soil-liquid diffusion coefficient (cm2(liquid)/s) , Fw = net water flux (cm(liquidys^) ^ CI = solution concentration (mg/cm3 soil solution) Cg = vapor phase concentration (mg/cm3 soil air) ,.; ' " • , . • . • I " , . ' CI and Cg in Equation 2 are related to the total solute concentration (Cto) by Equation 3. The concentration in each phase of the soil and soil pores [te., solid (Cs), liquid (CI), and gaseous ^ ' ' ' ~ , • '',''.' (Cg)l contributes to the total concentration (Jury et aL, 1983): > Cto = pCi * 6wC/ + QaCg , (3) .'•.where,', . ' , '. - -'.'''..•-'.- • " • ' ',_•! p = soil dry bulk density (mg/cm3) • ~ / Cs as adsorbed concentration (mg/kg soil) ' • . . ' ' . •-. " v ' 6 w = soil volumetric water content (cmVcm3) / 8 a -* soil volumetric air content (cmVcm3) As described in Equation 3* the distribution of solute between each phase is determined by p, 6w, and • ' •..i,'"ij' ' i ' ' • 6a. In addition, the concentration of solute in each phase is determined by the following relationships (Jury etaL, 1990):. : F-3 CHEMRISK* - A DIVISION OF MCLAREN/HART R.-itJ.4066 Cf '- (£e0(GQ; Kd = " , ' , (5) where, - -. Kd = dissociation constant (cmVgj foe » fraction organic carbon (percent) Koc = octanol/water partition coefficient (mg/1) Kh » Henry=s Law Constant (cm3(liq)/cm3(gas)) When partitioning between the three phases is incorporated into the analysis, flux can be evaluated in terms of Cto. Simplifying Equation 2, given the relationships between Cto and Cg, CI and Cs, ' • ' . ' • ' • ' . yields (Jury etaL, 1990): ,' ' ' • F » -Dei $££] + VeCto (6) ^ dz J where, " '- " ; ' - ' • ' ; - • .- •-.;'.' De = effective solute diffusion coefficient (cmVs) Ve = effective solute convection velocity (crn/s) N - ' • • Specifically, De is the diffusion of the chemical through soil pore spaces (air and water) driven by the concentration gradient Ve describes the convective movement (Le., movement in rainwater) of solute through the soil Convection refers to the transport of a dissolved chemical by virtue of bulk movement of the host water phass e (Jury and Fluhler, 1992). ' '- • • . BAM predicts flux rates (F) based on Equation 6. The benefit of using this equation is that, in cases where only a one-phase flow is considered, total concentrations and losses can still be estimated (Jury et aL, 1983). De and Ve are further defined by the following equations (Jury et aL, 1983): — • "' —.-.... ^ —— - — . ———— ____ ' F-4 CHEMRISK* -A DIVISION OF MCLAREN/HART uji+067 Ve = .ti : -.. m JW W where, Rg = partition coefficient for the gaseous phase (cm3 (gas)/cm3 (gross)) RI = partition coefficient for the liquid phase (cm3 (liquid)/cm3 (gross)) . \ • i •' The partition coefficients (RI and Rg) identify the ratio of Cto to the concentration in each phase. For example, Rg is the ratio of the total concentration to the concentration in the vapor phase. Rs (partition coefficient for the solid phase), RI and Rg are calculated based on p, 6w, 6a, and chemical- specific Kh and Kd. , 7 At the ground surface, the diffusion of gas from the soil surface is controlled by the diffusion of air in the stagnant boundary layer. He, the effective transport coefficient of gas across the stagnant air boundary layer, is related to the upper boundary condition of the stagnant air layer and the gaseous diffusion from the site, and is defined by the following equation (Jury et aL. 1983): He * "**' (9) where, d = stagnant air boundary layer thickness (cm) F^S • CHEMRjSK* - A DIVISION OF MCLAREN/HART >—S . • • \ • '-'.•' '.. _ \ • . . ' " ' • ' ' •'••••' AR:iUt«068 By assumption, the VOC concentration at the top of the boundary or stagnant air layer, a height -HeCto m -Dd ZjZ.\ + VeCto (w) t The stagnant air boundary layer thickness, (H) In addition to the above transport mechanisms, BAM can incorporate a microbial or chemical degradation rate based on a selected chemical half-life in soil (tw). For this risk assessment, degradation or the effective solute decay rate (p) was conservatively set equal to zero. » ' ... BAM was programmed in Fortran code to solve for the time-averaged solute mass flow per area per time, or flux rate (F). Values for all model parameters, including chemical-specific and soil-specific variables, were determined from field samples and the scientific literature. The parameter values selected to describe site characteristics and physical and chemical behavior of each COPC are presented in Tables F-l and F-2, respectively. The derivation of diffusion coefficients in air and water were based on methods reported by Lyman et aL, 1990 or obtained from EPA (1993). The output sheets of BAM for the COPCs in .subsurface soil of the Middle Buildings Sector are provided in Tables F-3 through F-8 of this appendix. Because BAM determines time-averaged flux values using a series of small time steps, it is possible that the model could calculate a cumulative mass lost through volatilization greater than the initial mass. To ensure that, this does not occur, the model ' ' . F-6 CHEMRISK* - A DIVISION OF MCLAREN/HART calculates a mass-balance, the results of which are summarized for each run on Tables F-3 through U, / . "'•'••. . , F-8. The largest mass-balance error was 0.0698 percent. While BAM was used to predict soil vapor emission rates, on-site concentrations of vapors were developed using a mass balance equation that incorporates a theoretically enclosed space or box over the area of interest, known as a box model This model assumes that the chemical concentration within the box is a function of both input (emission rate from soil) and output (air exchange or dispersion by wind). . It further assumes that the soil-gas flux is instantly and uniformly mixed with " • . • • t - •' • • ' . . . ' . . . . air flowing across a specified .area. This is mathematically expressed as the mass rate entering the box divided by the volumetric rate of air that flows through the box. For indoor exposures, vapor concentrations were calculated Using the following box model equation: . (12) ' . • , • . ' ' • ' ' ' - J • . - ... - • where," '•;.'..'•'.•. • " '• ' , , , ' '.''•• Cv = Indoor vapor concentration (mg/m3) • •;'•.-. ,. , - . • • - f = Fraction of basement floor area through which vapors can enter ' / . - T = , Air exchange rate (s) F =, , Flux rate of COPC computed by BAM (mg/m2-s) h .• ' « Box height (m) v " '--.'' . J For outdoor exposures, vapor concentrations were calculated using the following box model equation: ' < Cv *(Fx Aemit)/( Vwind x Awind) (13) . , ' ' •.•••' i •.-.'• where, ' ' Cv = Outdoor vapor concentration'(mg/m3) F * Hux rate of COPC computed by B AM (mg/m2-s) F~7 CHEMRISK* - A DIVISION OF MCLAREN/HART Aemit = Emitting area (unpaved area) • " Vwind = Windspeed (m/s) N..X Awind • Area of wind (box height x wind width) (m2) The indoor scenario evaluated for the Middle Buildings Sector included the Construction Worker. For this scenario, the fraction of basement floor through which vapors enter was set equal to 0.01 (Le., 1%). for the indoor construction worker, it is unlikely that an area greater than 1 percent of the floor will be disturbed. An air exchange rate of 8500 seconds per exchange was applied the model, based on 0.42 air exchanges per hour, as recommended by the American Society for Heating, Refiidgerating, and Air-Conditioning Engineers (ASHRAE) (1990). For the Construction Worker scenario, the approximate height of the building, 60 feet (18.3 m), was used as the height of the box. For the Outdoor Construction Worker scenario, the emitting area, Aemit, was estimated to be 17,400 m2 from site drawings provided by Cummings/Riter. A typical value of 2 m/s was selected for Vwind, while Awind was calculated assuming a box height of 2 m and a site cross-sectional area (wind width) of 241m, again based on sitedrawings. Tables F- 9 and F-10 display the results of the BAM computations and the application of the box models. F'8 CHEMRISK* -A DIVISION OF MCLAREN/HART • • ' ' - . - lillli 1 ,.; s O O w C u . w L/. ;•. 2 2 2 2 3J als , aM M M M M 00 BQ So W M •| -| J S J -f ' . . ' . •' i r • 1 . .'* • , - asslsg • • • , ' ' ' ' H '1 'R f. '!3 f ' - f < . , '. ' ' '''""', 111 111 1 aM .MS) . SM 5W JM .MSf a 1 I I .3 In 1 • "'•••- " • '"'•' f*« f 6* fr fr B* 6* ft * ** »j to S~ ... 0 « ra SSS S f $ "S 5 1' CO CO CO tfl CO CO SO •> U (I tl i i i a • u u ' Q u u 1 ^ 5 £ 1 1 a -9 a a a a CO CO CO CO CO CO ^ , • ,•.."---. '• I kDMS Defaul t valu e fo r § >ase d o n Middl e S i 90 . Defaul t valu e o*90 . Defaul t valu e 9*90 . Defaul t valu e •83 . Mos t likel y e •M .-' * ' ' | • f*3 a 13 2 s « W 73 - ' , • 1 3 H 3 a a « C C - 13 K g K 8 K f K « o: ... Q. K Calculate d fi i 1 ^ 1 Jur y etaL * 1 9 i Assumptio n 1 . > \ 00 a VI '. .,[ , 1 * 3 : *! ». ^ S- o S > ''"' w ° ° "" ^ o' o d ™* (\*^,. SJ • ' ' - , - . • • |i ' ' :' ' *• 1, ' m ' *%« j M %-* P E -B R "a •a I • •< jS s» no G "g «^ 6 *£ ! a ' « , 9 *«9 • M> c g1 *^c ' c - ' - •'• • . 1' «r 1 *• cfi 1 I en5 \ ' '. # B? - OT : ' ' • " " BSb ' ** •" '•. -:-- ' ' •! i™. Jpill ' , ' 1 ;[.^-I.53 1 '. . i i|il< - ' • - -i 4ti? P-l ' ' - ' - i 1 ' ," " '• .- .;u- S ! 1 1 . - j| ; i c§ >, 1 i S • c t , i , _«e 1 ^ , : i '&'• c • • ' - 2- Et 1 J i 4 i • .* I 1 1 ' " • ' . Ii B S 1 ' x .5 1 J £ •'5 J 1 1 {/ 3-•a j a £ i ' ' ' 1 i .< Ol»0.72 <5 ?3 ffi . -- - _- ^ss w i i * TS 2 , r* £• i« ci ri Sj •jg-jgi "n 3 S * cR "* ss S 2 J ' c4 r>i ri ri cl CM 81 $ Si 31 s; s s; s; 3t s; fi •s> -a -a 1 .3 S -a -a" .5 .9 .9 .3 0c& -8» <3» gpo- i o& o o**• . \a- \a *a fl^ 0s O\ § 8 g 8 S 8 8 8 8 S 8 S -•^ a a a a * .111 -- ^a III. II ii u CJ UCJC o o u u g a g g g g SSSSSS OS -N ? O 00 — — ^ •» m trj «ri wS ^ I J« P4 ^ O 53sl £ri 3«N jjgaa ^ ^ •< «™ ^ >. <••. M *• e*"* ** "" 5* 55 S -S 55 •**III• u u ^u ii 3 II! 3 « < < < S » I- • - - a "I Table F-3. 1 year averaging time • Phenanthrene Final Solution Type =2 . - . Ve =-0.191000E-08 [cm/sec] De = 0.396000E-07 [cm**2/sec] He * 0.186000E-06 [cm/sec] Mu » O.OOOOOOE-fOO [I/sec] zl = O.OOOOOOE-fOO [cm] z2 m 0.335000E+Q3 (cm] Cto -m 0.386000E-02 [mg/cm**3] z • tm O.OOOOOOE400 [cm] Tpl = O.OOOOOOE400 [sec] Tp2 = 0,315400E-f08 [sec] Time averaged Ct and F values are: Ct(z) = 0.723914E-03 [mg/cm**3] F =-OJ34648E-09[mg/(sec*cm**2)3 Parameter At Time Tpl AttimeTp2 Time [sec] O.OOOOOE+00 0.31540E+08 Mass in soil column [mg/cm**2] 0.12931E+01 0.12889E+01 Integrated surface flux [mg/cm**2] ; -0.42468E-02 Integrated bottom flux [mg/cm* *2] O.OOOOOE+00 Integrated flux at zl [mg/cm**2] -0.42468E-02 Integrated flux at z2 [mg/cm**2] 0.23152E-02 A mass balance over this time period shows an error of 0.0000 % CHEMRISK* - A DIVISION OF MCLAREN/HART rtR30l»07U- Table F-4. 1 year averaging time * Acenaphthylene Final Solution - . - • Type-'* 2- -.."•••'•• " - Ve=-0.113000E-07 [cm/sec] De = 0.248000E-06 [cm**2/sec] He = 0.350000E-05 [cm/sec] Mu = O.OOOOOOE-fOO[ I/sec] zl m O.OOOOOOE+00 [cm] z2 = 0.335000E+03 [cm] Cto = 0.218000E-03[mg/cm**3] z = O.OOOOOOE-fOO [cm] ; Tpl = O.OOOOOOE-fOO [sec] Tp2 » 0.315400E-KJ8 [sec] - Time averaged Ct and F values are: Ct(z) = 0.645430E-05 [mg/cm**3] , F -=.0.225901E-10[mg/(sec*cm**2)} Parameter ; At Time Tpl AtTimeTp2 Tune [sec] Q.OOOOOE-fOO 0.31540E+08 Mass in soil column [mg/cm**2] 0.73030E-01 0.72318E-01 Integrated surface flux [mg/cm**2] -0.71249E-03 Integrated bottom flux [mg/cm**2] O.OOOOOE-KX) Integrated flux at zl [mgfcm**2] -0.71249E-03 Integrated flux at z2 [mg/cm+*2] 0.30595E-03 A mass balance over this time period shows an error of 0.0000% ttaJENT3\wEJtt«™iw7>roaJus^^ GI EM RISK* . A DIVISION OF MCLAREN/HART ' a.R30l»075 Table F-5. 1 year averaging time • Benzo(g,h4)perylene Final Solution Type « 2 Ve =^0.277000E-10 [cm/sec] De = 0.556000E-09 [cm**2/sec] He - 0.814000E-11 [cm/sec] Mu = O.OOOQOOE+OO [ I/sec] zl = O.OOOOOOE+00 [cm] z2 = 0.335000E+03 [cm] •Cto = 0.420000E-03 [mg/cm**3] z m O.OOOOOOE-fOO [cm] Tpl m O.OOOOOOE-KX) [sec] Tp2 • 0.315400E408 [sec] Time averaged Ct and F values are: Ct(z) = 0.421473E-03 [mg/cm**3] \ F =-0.343079E-14[mg/(sec*cm**2)] Parameter - At Time Tpl At Time Tp2 Time [sec] O.OOOOOE+00 0.31540E-f08 Mass in soil column [mg/cm**2] 0.14070E+00 0.14070E-KX) Integrated surface flux [mg/cm**2] -0.1082JE-06 Integrated bottom flux [mg/cm**2] O.OOOOOE-KX) Integrated flux at zl [mg/cih**2] -0.10821E-06 , Integrated flux at z2 [mg/cm**2] , 0.31143E-04 A mass balance over this time period shows an error of 0.0000 % CHEMRISK* - A DIVISION OF MCLAREN/HART Table F-6. 1 year averaging time - Aroclor 1242 Final Solution Type = 2 ' Ve =-0.277000E-08 [cm/sec] De = 0.150000E-06[cm**2/sec] He = 0.301000E-05 [cm/sec] Mu' m O.OOOOOOE400Cl/secI zl m O.OOOOOOE-fOO [cm] z2 m 0.335000E403 [cm] Cto = 0.227000E-02 [mg/cm**3] z * O.OOOOOOE+00 [cm] Tpl « O.OOOOOOE400[sec] Tp2 a 0.315400E408[sec] Time averaged Ct and F values are: Ct(z) = 0.585603E-04[mg/cm**3] F =-0.176266E-09[mg/(sec*cm**2)] .. ! Parameter At Time Tpl AtTimeTp2 Tune tsec] O.OOOOOE+00 0.31540E+08 / Mass in soil column [mg/cm* *2] Q.76045E+00 0.75489E400 Integrated surface flux [mg/cm**2] -0.55504E-02 Integrated bottom flux [mg/cm**2] O.OOOOOE+00 Integrated flux at zl [mg/cm**2] . -0.55594E-02 Integrated flux a^ z2 [mg/cm**2] / 0.26829E-02 A mass balance over this time period shows an error of 0.0000 % C HEM RISK* - A DIVISION OF MCLAREN/HART flR30l|077 Table F-7. 1 year averaging time • Aroclor 1254 Final Solution Type =2 ; ; Ve =-0.527000E-09 [cm/sec] De = 0.270000E-07 [cm**2/sec] He * 0.524000E-06 [cm/sec] Mu '- O.OOOOOOE400 [I/sec] zl » O.OOOOOOE+00[cm] , z2 = 0.335000E+03 [cm] Cto * 0.12800QE-01 [mg/cm**3] z = O.OOOOOOE+00 [cm] Tpl . '* O.OOOOOOE400[sec] Tp2 , = 0.315400E+08 [sec] Time averaged Ct and F values are: Ct(z) = 0.774250E-03 [mg/cm**3] F m -0.405707E-09 [mg/(sec*cm**2)] Parameter At Time Tpl AtTimeTp2 Time . [sec] O.OOOOOE+00 0.31540E+08 Mass in soil column [mg/cm**2] 0.42880E-»O1 0.42752&fOl Integrated surface flux [mg/cm**2J -0.127$f6E-6l Integrated bottom flux [mg/cm**2] O.OOOOOE-fOO Integrated flux at zl [mg/cm**2] -O.J2796E-01 Integrated flux at z2 [mg/cm**2] 0.65470E-02 A mass balance over this time period shows an error of 0.0000 % CHEMRISK* -A DIVISION OF MCLAREN/HART R 3 01*078 Table F-8.. 1 year averaging time - Aroclor 1260 Final Solution Type » 2 . . " '• • ". - Ve =-0.982000E-10 [cm/sec] De = 0.393000E-08 [cm*+2/sec] He = 0.625000E-07 [cm/sec] Mu -at O.OOOOOOE-KX) [I/sec] zl m Q.OOOOOOE"fOO [cm] z2 = 0.335000E+03 [cm] Cto = 0.185000E-01 [mg/cm**3] z = O.OOOOOOE+00 [cm] Tpl = O.OOOOOOE-fOO [sec] Tp2 = 0.315400E-f08[sec] Time averaged Ct and F values are: Ct(z) m 0.321093E-02 [mg/cm**3] F =-0.200683E-09[mg/(sec*cm**2)] ^ Parameter " AtTimeTpl AtTimeTp2 Time [sec] O.OOOOOE-KX) 0.31540E-f08 Mass in soil column [mg/cm**2] 0.61975E+01 0.61912E-f01 Integrated surface flux [mg/cm**2] ' -0.63295E-02 Integrated bottom flux [mg/cm* *2] O.OOOOOE+00 Integrated flux at zl [mg/cm**2] -0.63295E-02 Integrated flux at z2 [mg/cm**2] * 0.36399E-02 A mass balance over this time period shows ah error of 0.0000 % CHEMRISK* - A DIVISION OF MCLAREN/HART Table F-9. Estimated Indoor Air Exposure Concentrations via Flux From Subsurface Soil t , . . . ' Sector/Scenario: Middle Buildings/Indoor Construction Cv-(fxTxF)/h , . s' where, . > , Cv - Concentration of vapor-phase chemical in indoor air (mg/m3) f - Fraction of basement floor area through which vapors enter (0.01) T-Air exchang rate (8500$) ;' ~ F - Flux rate of chemical of interest,, computed by BAM (mg/m2-sec), from Tables F-3 through F-8. h - Box height (60 ft or 18.3 m) Soil Chemical Concentration t Js Cv ; (mg/kg wet soil) (mg/sec-cm2/mg/kg)) (mg/mj) StmivotatUt Organic Cktmlcats Acenaphthylene . ' . 0.13 2.26E-11 1.05E-06 Benzo 7JR30U080 Table F-10. Estimated Outdoor Air Exposure Concentrations via Flux From Subsurface Soil « Sector/Scenario: Middle Buildings/Outdoor Construction Cv - (F x Aemit)/(Vwind x Awind) where, Cv - Ambient concentration of vapor-phase chemical in air (mg/m3) , F - Flux rate of chemical of interest, computed by BAM (mg/m'-sec), from Tables F-3 through F-8. Aemit "Emitting area (unpaved area) (17,400m2) , . / Vwind - Windspeed (Zm/sec) • A wind-Area of wind (box height x wind width) (482m2) Soil Chemical Concentration F (mg/kg wet soil) (mg/sec-cm2/mg/kg)) (mg/m3) SemtotatSt Organic Chtmlcab Acenaphthylenc . 0.13 2.26E-11 5.30E-07 Behzo(g,tM}perylene 0.25 3.43E-15 1.S5B-IO Phenanthrene 2.30 1.35E-10 . 5.59E-05 Aroclor-1242 2.41 1.76E-10 7.67E-05 ArocloF-1254 8.31 4.06E-10 6.09E-04 ArocloM260 11 2.01E-IO 3.98E-04 I .' Appendix G i' Toxicological Profiles iiR3UI»082 Toxicity Profile . , 1,1-Dichloroethylene ^ Chemical Formula (y^Clj Merck, 1983 Molecular Weight 96.94 g/mol . Merck, 1983 Vapor Pressure . 591 ramHg @ 25°C Verschuerenj 1983 Boiling Point 304.8°K ATSDR, 1988 Melting Point _ -122.5°C Merck, 1983 Henry's Law Constant 0.19 atm-mVmol PankowandRosen, 1988 Solubility Practically insoluble Merck, 1983 Partition Coefficients tog Octanol-water 2.13 Mabey et aL, 1982 tog Octanol carbon-water 1.81 Mabey et aL, 1982 The major use of 1,1-dichloroethylene (1,1-DCE) is as an intermediate for captive organic chemical synthesis (ATSDR, 1988). It is also employed in the production of polyvinylidene chloride copolymers, which are important as flexible packaging materials, pipe coatings, adhesive applications, and as flame retardant coatings for fiber and carpet backing (USEPA, 1977). ' Because of its "high volatility, the majority of 1,1-DCE released to the environment partitions to the atmosphere (ATSDR, 1988). Once in the atmosphere, it is unlikely to adsorb to atmospheric particulates or partition to water (Cupitt, 1980). 1,1-DCE in the atmosphere reacts rapidly with hydroxyi radicals and photolyses readily in the presence of nitrogen oxides (Gay etaL, 1976; ATSDR, 1988). In addition, the atmospheric lifetime of 1,1-DCE has been reported to range from 16.1 hours to 2 days (Cupitt, 1980; USEPA, 1983). 1,1-DCB in surface soils is generally partitioned to the atmosphere. In subsurface sous, 1,1-DCE tends to partition between soil and water with small quantities migrating freely through soil to groundwater. Because of its high water solubility and tow soil organic carbon partition coefficient, 1,1-DCE is likely to migrate through soils without significant retardation by adsorption to organic carbon (ATSDR, 1988). &assmvEmimi99*ewu^^ G- 1 CHEMRi$K*-A DIVISION OF MCLAREN/HXRT . Because of its rapid volatilization to the atmosphere from water, l.KDCE is generally not persistent in surface waters (ATSDR, 1988). The primary transfonnation process for 1,1-DCE in water systems is btotTpUisfonnation, although k does not appear to be a significant process under aerobic conditions (Pearson and McConnel, 1975; Bouwer et aL, 1981; Tabak et aL, 1981; McCarty et aL, 1986). Likewise, photolysis, hydrolysis, and oxidation do not appear to be significant transformation processes (Mffl and Mabey, 1980; Mabey et aL, 1982). In addition, 1,1-DCE does not partition significantly to aquatic organisms, although, slight bioaccumulation is likely to occur based on its K^ value (Veith etaL, 1985). , The USEPA has classified 1,1-DCE as a Group C carcinogen; possible human carcinogen, based on inadequate human carcinogenicity data and limited animal carcinogenicity data. The available epidemiotogic studies are compromised by design faults. Studies by Ott et at (1976) and Thiess et al (1979) are not useful for assessing the carcinogenic potential of 1,1-DCE to humans due to limited cohort sizes, short observation periods, a lack of causal relationships, and the occurrence of other carcinogens (ATSDR, 1988). By contrast, a laboratory study has been conducted in which male Swiss mice exposed to 1,1-DCE via inhalation for 4-5 days a week for 1 year at a range of 10 to 25 pjpm exhibited a statistically significant increase in kidney adenocarcinoma (Maltoni et aL, 1985). Based on the results of this study, the USEPA has estimated an oral cancer slope factor of 0.6 (mg/kg-day)'1 (IRIS, 1996). In addition, supporting data for this value is based on mutagenicity studies which report that 1,1-DCE has been shown to bemutagenic and a metabolite is known to alkyiate and to bind covalently to DNA (Rcitz et aL, 1980; Bronzetti et aL, 1981). The USEPA has also determined an inhalation unit risk of 0.00005 ^g/ra3 based on the studies by Maltoni et aL (1977; 1985) which produced a response as a complete carcinogen (IRIS, 1996). The USEPA has published an inhalation cancer slope factor of 1.2 x 10"' (mg/kg-dayX1 for 1,1-DCE based on a 12-month inhalation exposure to mice which resulted in kidney adenocarcinpmas (IRIS, 1996). In a chronic animal study, Quast et al (1983) administered 50, 100,, and 200 ppm 1,1-DCE in drinking water to Sprague-Dawley rats for a 2-year period. Results indicated that female rats in all treatment groups and male rats at the highest dose had hepatic lesions characterized by minimal mid- zonal hepatoceHular fatty change and hepatoceHular swelling (Quast et al, 1983). The results of this study suggest that the liver may be the most «ensitive organ and that rats may be the most sensitive species (IRIS, 1996). Based on the results of this study, the USEPA has established an oral RfD of 0.009 mg/kg-day based on the LOAEL of 9.0 mg/kg-day for hepatic lesions in female rats (IRIS, WHWWD G-2 CHEMWSK'-Ar^VISIONOFMCUREN/HART ARilOUOBU 1996). Additionally, 1,1-DCE has been shown to be fetotoxic, but not tcratogenic to rodents after exposure in drinking water or by inhalation (Short et aL, 1977; Murray et aL, 1979). The USEPA has not established an inhalation RID for 1,1-DCE. For the purposes of this evaluation, the oral RfD value is used for the inhalation RfD. . i . .'-.•__ . References ATSDR. 1988. Toxicological Profile for Dichlorocthylene: Draft. Agency for Toxic Substances and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public Health Service. December. Bouwer, EJ., B.E. Rittman, and P.L. McCarthy. 1981. Anaerobic degradation of halogenated 1- and 2-carbon organic compounds. Environ. Set Technof. 15:596-599. (Cited in ATSDR, 1988) Bronzetti, G., C Bauer, C Corsi, C Leporini, R. Nieri, andR.DelCairatore. 1981. Genetic activity of vinylidene chloride in yeast Mutat Res. 89:179-185. (Cited in IRIS, Cupitt, L.T. 1980. Fate of Toxic and Hazardous Materials in the Air Environment U.S. Environmental Protection Agency, EnvironmemalS<^ncw Research Laboratory, Office of Research and Development, Research Triangle Park, NC. (Cited in ATSDR, 1988) Gay, B.WJ., P.L. Hanst, J.J. Bufalini et aL 1976. Atmospheric oxidation of chlorinated ethylenes. Environ. Set Technol 10:58-66. (Cited in ATSDR, 1988) HSDB. 1996. 1,1 -Dichlorocthylene. Hazardous Substances Data Bank, National Library of Medicine, National Institutes of Health, Bethesda, MD. ~\ ' ' ••' • .'.. IRIS. 1996. 1,1'Dichloroethylene. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH. Mabey, W.R..J.H. Smith, R.T.Podofl etaL 1982. Aquatic Fate Process Data for Organic Priority Pollutants. Report to U.S. Environmental Protection Agency, Office of Water Regulations and Standard^ Washington, D.C by SRI International, Mento Park, CA. EPA 440/4-81-014. (Cited in ATSDR, 1991) ; G-3 CHEMRlSK*-A DIVISION OF MCLAREN/HART URJOI»0'85 Maltoni, C, G. Ufcmine, P. Chieco, G. Cotti, and V. PateHa. 1985. Experimental Research on VmyKdene Chloride Carcinogenesis. In: Archives of Research on Industrial Carcinogenesis. Voi 3. Maltoni, C and M.A. McKenna (eds). Princeton, NJ: Princeton Scientific Publishers. (Cited in IRIS,'1996) Maltoni, C., G. Cotti, L. Morisi, and P. Chieco. 1977. Carcinogenicity bioassays of vinylidene chloride. Research plan and early results. Med. Lav. 68(4):241-262. (Cited in IRIS, 1996) McCarty, Pi., H. Siegrist, T.M. Vogel et aL 1986. Biotransformation of Groundwater Contaminants; final Report. Stanforf Universky, Oepartment of Civil Engineering, Stanford, CA. (Cited in ATSDR, 1988) Merck. 1983. The Merck Index. 10th Edition. Windholz, M. (ed.). New Jersey: Merck & Co. Inc. (Cited in ATSDR, 1988) MOLT, and W.R. Mabey. 1980. Test Protocols for Evaluating the Fate of Organic Chemicals in Air and Water. U.S. .Environmental Protection Agency, Office of Research and Development, Athens. GA. (Cited in ATSDR, 1988) Murray, FJ., K.D. Nitschke, L.W. Rampy, and B. Schwetz. 1979. Embryotoxicity and fetotoxicity of iiihaled or ingested vinylidene chbridem rats and r^ ToxicoL Appi Pharmacol 49:189-202. (Cited in IRIS, 1996) NTP. 1982. NTP Technical Report on the Carcinogenesis Bioassay of Vinylidene Chloride (CAS No. 75-35-4) in F344/NRats and B6CFlJMice {Gavage Study). NTP Report No. 80-82. Nffl Publication No. 82-1784. National Toxicology Program, National Cancer Institute. National Institute of Health, Public Health Services, U.S. Department of Health and Human Health Services, Bethesda, MD and NTP Research Triangle Park, NC. (Cited in IRIS, 1996) Ott,M.G.,W.AF.slTbacMCTownsher^ 1976. A health study of employees exposed to vmyUdene chloride. 7. Occup.Med. 18(li):735-738. (Cited in IRIS, 1996) Pankow, J.F. and M.E. Rosen. 1988. Determination of volatile compounds in water by purging directly to a capiflary'colum with whole colurnncryotrapping. Environ. Set TechnoL 22(4):398-405. (Cited in ATSDR, 1988) G-4 CHEMRjsK*-A DIVISION OF MCLAREN/HART Pearson, C.R. and G. McConneL 1975. Chlorinated CI and C2 hydrocarbons in the marine environment Proceedings R Soc Lond B (Great Britain) 189:305-332. (Cited in ATSDR, 1988) , ") *-' ' • ^.^ Quast, J.F., CG. Hamilton, C.E. Wade et aL 1983. A chronic toxicity and oncogenicity study in rats and subchronic toxicity study in dogs on ingested vinylidene chloride. Fund. Appl Toxicot 3:55-62. (Cited in IRIS, 1996) Reitz, R.H., P.O. Watanabe, M.J. McKenna, J.F. Quast, and P.J. Gehring. 1980. Effects of vinylidene chloride on DNA synthesis and DNA repair in the rat and mouse: A comparative study with dimethylnitrosamine. Toxicol AppL Pharmacol 52:357-370, (Cited in IRIS, 1996) Short, R.D.. J.M. Winston, JJL Minor, J. Seifter, and C.C. Lee. 1977. Effect of various treatments on toxicity of inhaled vinylidene chloride. Environ. Health Perspect. 21:125-129. (Cited in IRIS, 1996) Thiess, A.M., R. Frentzel-Beyme, and E. Penning 1979. Mortality study of vinylidene chloride exposed persons. In: Proceedings ofthe 5th Medichem Congress. Hien, C. and D J. Kilian (ed.). University of California at San Francisco, San Francisco, CA. 270-278. ' • i • USEPA. 1917, Market Input/Output Studies Task 2. Vinylidene Chloride. U.S. Environmental Protection, Office of Toxic Substances, Washington, D.C: PB-273-205. (Cited in ATSDR, 1988) USEPA. 1983. Administered Permit Programs: The National Pollutant Discharge Elimination System: Genral Permits. U.S. Environmental Protection Agency, 40 Code of Federal Regulations 122.28., 48 Federal Register 14153-14178. April 1. (Cited in ATSDR, 1988) Veith, G.D., D. DeFoe, and M. Knuth. 1985. Structure-activity relationships for screening organic chemicals for potential ecotoxicity effects. Drug Metabolism Reviews 15:1295-1303. (Cited in ATSDR, 1988) Verschueren, K. 1983. Handbook of Environmental Data on Organic Chemicals. New York, NY: Van NostrandReinhokL p. 1131-1135. G-5 CHEMRISK*-A DIVISION OP MCLAREN/HART Toxicological Profile • < • . 1,2-Dichlorobenzene j ' . ' " Chemical Formula C6H4C12 • HSDB, 1995 Molecular Weight 147.01 g/mol Weast, 1988 Vapor Pressure 1.47mmHg @ 25°C MackayandShiu, 1981 BoflingPoint 180.5°C ' Weast, 1988; Melting Point -17.0°C Weast, 1985 Henry's Law Constant 2.4xlfr3 atm-mVmol @ 25°C Hine and Mookerjee, 1975 Solubility 137 mg/L @ 25°C Bangerjee, 1984 Partition Coefficient 3-38 HSDB, 1995 280-1,480 HSDB, 1995 1,2-Dichtorobenzene is typically employed in solvent applications for a wide variety of manufacturing processes (HSDB, 1995). Released to the atmosphere, 1,2-dichlorobenzene exists primarily as a vapor. A half-fife of 24 days has been estimated for the vapor ph-ise rt^tton of W-dkhtorobenzene with photochemically-produced hydroxyl radicals. Removal of the compound via wet deposition is also likely to occur (HSDB, 1995). « I' ' . . , ' • ' • . In soils, 1,2-dichtorobenzene may adsorb to particulates or leach to groundwater. To a lesser extent, volatilization an biodegradation may also occur. Other soil transformation processes, such as hydrolysis, oxidation, or direct photolysis, are Hot expected to be significant for this compound (HSDB, 1995). • ..>*.' • -j In aquatic systems, its relatively tow vapor pressure and tow aqueous solubility permit 1,2- dichlorobenzene to undergo sorption, bioaccumulation, and volatilization. These competing processes regulate the fate of 1,2-dichtorobenzene in water. Adsorption to sediments is likely to be a predominant fate process for this compound, and it may persist in sediments for several decades. Bioaccumulation of 1^-dichlorobenzene among aquatic organisms may also be an important process, Other removal mechanisms, however, such as hydrolysis, oxidation, or direct photolysis, are not expected to be significant In addition, the half-life of 1^-^litoroteriKne in the water column has , ttci.BTOkw-siiN<.wiWnnNuus.^^ G-6 CHEMRISK*-A DIVISION OF MCLAREN/HART been estimated to range from 0.3 to 3 days, 3 to 30 days, and 30 to 300 days in rivers, lakes, and groundwaters, respectively (HSDB, 1995). f J '.-''' ' • " • ' m ^"r Toxicity studies with l,2-dichlorobenzene are sparse. The results of a 103-week gavage study in which F344/N rats and B6C3F1 mice were treated at doses of 0,60, or 120 mg/kg-day at 5 days per week suggested decreased survival among high dose rats and an increase of renal tubular regeneration in high dose mice. The study revealed no other evidence of treatment related effects (NTP, 1985). A similar 13-week btoassay at doses of 0, 30, 60, 125, 250, or 500 mg/kg-day resulted in liver necrosis in mice and rats administered 250 mg/kg-day. Effects of the highest dose level included death, liver necrosis and degeneration, slight decreases in hemoglobin, hemacrit, and red blood cell - count (NTP, 1985). Similarly, Hollingsworth et aL (1958) administered doses of 18.8, 188, 376 mg/kg/day 1,2-dichtorobenzene to rats via gavage for 192 days. Results indicated that treated rats at 188 mg/kg/day experienced increased liver and kidney weights, while increased spleen weights were observed at 276 mg/kg/day. Inhalation exposures of 1,2-dichlorobenzene to rats, guinea pigs, mice, and monkeys suggest a reduction in spleen weight in guinea pigs and body weight gain in rats at 93 ppm (Hollingsworth et aL, 1958). Likewise, Hayes et aL (1985) reported a reduction in body weight gain in .rats and rabbits exposed to 400 ppm 1,2-dichtorobenzene via inhalation. Also, rats exposed to the same dose experienced increased liver weights (Hayes et aL, 1985). In humans, exposures to 1,2-dichtorobenzene result primarily in injuries to the liver and kidneys. At high concentrations, central nervous system depression may occur, as well as jaundice and abdominal tenderness (HSDB, 1995). ~ The USEPA has classified 1,2-dichtorobenzene as a Group D carcinogen, not classifiable as to human carcinogenicity, based on the absence of human data and lack of evidence of both negative and positive trends for carcinogenic resportsea in mice and rats (IRIS, 1996). Consequently, the Agency has not established an oral or inhalation cancer slope factor for 1,2-dichlorobenzene. The USEPA has derived an oral RfD value of 0.09 mg/kg-day for 1,2-dkhtorobenzene based on the evidence of dose-related effects in treated rats resulting from a 2-year gavage study (NTP, 1985; IRIS. 1996). In addition, USEPA Region III (1996) has derived an inhalation RfD value of 0.04 mg/kg-day. This value is derived from the chronic RfC value of 0,2 mg/m3 which is based on the G-7 CHEMRISJC*.A DIVISION OF MCLAREN/HA?T results of a 7-month inhalation study which reported decreased weight gain among treated rats , (USEPA, 1995). ' References , Bangerjee,S. 1984. Environ. Sci. Technol. 18:587-591. (Cited in HSDB, 1995) Hayes, W.C.TJt Hanky, T.S. Gushow, K.A Johnson, and J.A. John. 1985. Teratogenic potential of inhaled dichlorobenzene in rats and tabbits. Fund. AppLToxicoL 5:190-202. (Cited in IRIS, ' '' ' ' ' ' '"' ' ' Hine, J. and P.K. Mookerjee. 1975. J. Org. Chem. 40:292. (Cited in HSDB, 1995) .HoDingsworth, ILL., V.K. Rowe, F. Oyen, t.R. Torkelson, and E.M. Adams. 1958. Toxicity of o- dichlorobenzene. Studies on animals and industrial experience, A.MA. Arch. Indust. Health. 17:180-187. (Cited in IRIS, 1996) HSDB. 1995. Chemical Search for 1,2-Dichlorobenzene. Hazardous Substances DataBank, National Librar••'"•'••y of Medicine, Bethesda• •", MD-. ^.-' ••;.•>::•• :.'- • : .:-..'• .-:-- IRIS. 1996. 1,2-Dichlorobenzene. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH. ' ' - ' . ' ' ' ' Mackay, D. and W.Y. Shiu. 1981. J. Phys. Ref. Data. 10:1193. (Cited in HSDB, 1995) NTP. 1985. Toxicpfagy and Carcinogenesis Stttdies of L2-Dichforoben&M (Cos No. 95-50-1) in F344/N Rats and B6C3F1 Mice (Gavage Studies). NTP-TR-255, Nffl .Publication No. 86-2511. National Toxicology Program (NTP), U.S. Department of Health and Human Services, National Institutes of Health. (Cited in IRIS, 1996) --.. • , ' . . • . '. > " -• . USEPA. 1995. Health Effects Assessment Summary Tables, FY- 1995 Annual. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, D.C. EPA/540/R- 95/036. May. G-8 CHEMRlSK*-A DIVISION OF McLAREN/HART USEPA. 1996. Risk-Based Concentration Table. January-June 1996. Dr. Roy L. Smith, U.S. Environmental Protection Agency, Region ta, Office of RCRA, Techiiical and Program Support Branch, PmTadelphia, PA. April 30. Weast. 1988. Handbook of Chemical and Physical Properties, 68th Edition. (Cited in HSDB, 1995) G-9' CHEMRISK*-A DIVISION OF MCLAR£N/HART 1R30U09 Toxiaty Profile 1,2-DichIoroethane •. i . ' Criemical Formula CAPi Merck, 1983 Molecular Weight 98.96 Merck, 1983 Vapor Pressure 61 ramHg @ 20°C Mabey et aL, 1982 Boiling Point 847flC. Merck, 1983 Melting Point -35.3°C Merck, 1983 Henry's Law Constant 4.5xlO"2 atm-mVmol Shen, 1982 Sohibility = 0.869 rag/L @20°C Merck, 1983 Liquid Diffusion Coefficient 8.75xlCT* craVsec Lyman et aL, 1D90 Gaseous Diffusion Coefficient 9.77xlO"2 cmVsec Lyman et aL, 1990 Partition Coefficients 1-48 Hansch and Leo, 1979 1.14 Mabey etaL; 1982 The primary use of 1,2-dichtoro^triane (1,2-DC^ is to 1978; Kirk-Othmer, 1979). 1 ,2-DCA is also used in the synthesis of other chemicals such as vinylidene chloride, 1,1,1-trichtoroethane, trichloroethylene, tetrachtoroethylene, aziridines, and ethylene diamines (USEPA, 1985). In addition, 1,2-DCA is employed in penetrating agents, fumigants, varnish removers, soaps and scouring compounds, and solvents (Kirk-Othmer, 1979; Merck, 1983; * USEPA.1985). The majority of 1,2-DCA released to the environment partition to the atmosphere via volatilization. It is likely to be transport long distances prior to removal from wet deposition (ATSDR, 1988). In the atmosphere, the primary fate process of 1,2-DCA is photooxidation with hydroxyl radicals, with an estimated lifetime of 1 to 4 months (USEPA, 1975; Howard and Evenson, 1976; Cupitt, 1980; Class and BalTschmiter, 1986). '"_.'• • . ' l • . ' ] 1,2-DCA released to soils systems win rapidly volatilize to the atmosphere. Any remaining compound on soil surfaces will leach to groundwater. 1,2-DCA is unlikely to sorb to soil participates, particularly if the organic content of the soil is tow (Wilson etaL, 1981; ATSDR, 1988). Hydrolysis and biodegradation are not expected to be significant fate processes (ATSDR, 1988). ^^•H^*^^^^Ha>'IHB^^^^^^^^^^^^^^^^^^^^^^^^^^^^H^BnM**'l''av^^^^^^K^^^^^Hll^^H^^.^B^^HHIII^^WM>.BB^H^BBBB*.^^H«^^^^BHMail..B G-10 CHEMRISK*-A DIVISION OF MCLAREN/HART . i . • . • . .' ' . . • ... In surface waters, most 1,2-DCA win partition rapidly to the atmosphere as suggested by its high vapor pressure. Volatilization of this compound from aqueous media is likely to occur prior to any .ugriificarit dieraical or biological degradation (ATDSR, 1988). An estimated volatilization half-life has been reported to range from 30 minutes to 10 days in surface waters depending on local wind speed and mixing conditions of the aquatic system (DiUing et aL, 1975; Diffing, 1977; ATSDR, 1988). The Kfetime of 1 ,2-DCA in groundwater systems has been reported to range from several months to a few years (USEPA, 1985). Additionally, direct oxidation or photolysis are not expected to be significant processes (ATDSR, 1988). "~ i % • • .' • . • ' * There are no available studies which provide sufficient evidence associating inhalation, ingestion, or dermal exposure to 1,2-DCA with the incidence of cancer in humans (ATSDR, 1988). No existing studies which suggest a correlation between 1,2-DCA exposure and human carcinogenicity focus exclusively on 1,2-DCA exposure (Austin and Schnatter, 1983a,b; Reeve et aL, 1983; Waxweiler et aL, 1983; Isacson et aL, 1985). . . ' - ....' i In a rodent bioassay, male and female Osborne-Mendel rats and B6C3F1 mice were administered 1,2- DCA via gavage for 78 weeks. Dosages were 47 and 95 mg/kg-day for rats, 97 and 195 mg/kg-day for male mice, and 149 and 299 mg/kg-day for female mice. Results indicated a dose-related incidence of effects in treated animals. A significantly increased incidence of forestomach squamous- i j cell carcinomas and circulatory system hemangiosarcomas was observed for male rats. Also, significant increases of mammary adenocarcinomas were reported for female rats and mice. Additionally, both male and female mice developed alveolar/bronchiolar adenomas, female mice exhibited endometrial stromal polyps and sarcomas, and male mice developed hepatocellular carcinomas (NCI, 1978). . . - ."''"', Additionally, results of dermal application of 1,2-DCA to mice in a lifetime study resulted in a statistically significant increase in the incidence of nonmalignant pulmonary tumors (Van Duren et : -' , ' ' , ' . - al, 1979). Theiss et aL (1977) reported dose-related increases of nonmalignant pulmonary tumors in mice exposed to 1,2-DCA via intraperitoneal injection age 3 times a week for 8 weeks. - . ' ' Inhalation exposures of 400 to 500 ppm 1,2-DCA to rats, guinea pigs, rabbits, and monkeys resulted in a variety of effects, including pulmonary congestion, diffused myocarditis, and increased plasma prothrombin time. Slight to moderate degeneration of USe Hv^, kiiney, adrenal gland, and heart were also observed (Heppel etaL, 1946; Spencer etaL, 1951; Hoffinan etaL, 1971). r wTTOi*.^^ ; G-ll CHEMRISK*-A DIVISION OF MCLAREN/HART s ' . , • i . ' ' ' • ' ' •' ' rtR30l«093 The USEPA has classified 1,2-DCA as a Group B2 carcinogen, probable human carcinogen* based on adequate animal carcinogenicity data (IRIS, 1996). The USEPA has established an oral cancer \ stopefcrtor of 0.091 (mg/kg-day^ >*..«/ treated via gavage and lung papillomas in mice following topical application (IRIS, 1996). The USEPA has also published an inhalation cancer slope factor of 0.091 (mg/kg-day)-1 for 1,2-DCA based 6n the same study (USEPA, 1995). The Agency, however, has also derived an inhalatton unit risk value of 0.000026 Mg/m* for 1,2-DCA Finally, an oral or inhalation RfD value has not been established for 1,2-DCA(IRIS, 1996). In lieu of verified values, a provisional inhalation RfD value of 0.00286 mg/kg-day was applied in this assessment This value was obtained from the USEPA Region HI (1996) guidance document for RCRA sites and is regarded as a provisional value. Furthermore, a value of 0.03 is also used as the oral RfD value. References .' ' " . , ATSDR. 1988. Toxicotogical Profile for 1,2'Dichtoroethane: Draft. Agency for Toxic Substances and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public .'••'•-Health Service. •. , Washington\.. ,• D.C• . December. : ' ' • x '' •' •-. '• ' ; Austin, S.G. and AR. Schnatter. 1983a. A case-control study of chemical exposures and brain tumors in petrochemical workers. /. Occup, Med. 25:313-320. (Cited in ATSDR, 1988) Austin, S.G. and AR. Schnatter. 1983b. A cohort mortality study of petrochemical workers. / Occup. Med. 25:304-312. (Cited in ATSDR, 1988) - i - Class, T.H. and K. BaHschmiter. 1986. Chemistry of organic traces in air VI: Distribution of chtorinated C1-C4 hydro<^irrx)n3 in ai Chemosphere 15:413-427. (Cited in ATSDR, 1988) ^ Cupitt, L.T. 1980. Fate of Toxic and Hazardous Materials in the Air Environment. US. Environmental Protection Agency, Office of Research and Development, Research Triangle Park, NC. EPA 60G/3-80-084. (Cited in ATSDR, 1988) G-12 CHEMRlSK*-A DIVISION OF MCLAREN/HART / , .,.' . •' • • • • - Dilling, W.L 1977. Interphase transfer processes. G. Evaporation rates of chloro methanes, ethanes, ethylenes, propanes, and propylenes from dilute aqueous solutions. Comparisons with theoretical predictions. Environ. Set Technol. 11:405-409. (Cited in ATSDR, 1988) Dilling, W.L., N.B. Tefertiller, and G.J. Kaltos. 1975. Evaporation rates and reactivities of methylene chloride, chloroform, 1,1,1-tricWoroethane, trichlofoethylene, tetrachtoroethylene, and other chtorinated comrwiinds m dib in ATSDR,1988) ' Hansch, C. and A. Leo. 1979. Substitueht Constants for Correlation Analysis in Chemistry and Biology. New York* NY: JohnWiley& Sons. (Cited in ATSDR, 1988) Heppel, L.A., P.A. Neal, T.L. Perrin, K.M. Endicott, and V.T. Porterfield. 1946. The toxicology of I,2-dicmoroeth.u.e(ethyki.edichloride). J.lndHyg.Tox. 28:113-120. (Cited in IRIS, 1996) Hoffman, H., H. Bimsteil, and P. Jobst. 1971. Zur ir-halationtoxicitat von 1,1- and 1,2- dichloroathan. Arch. Toxicol 27:27:248-265. (Cited in IRIS, 1996) Howard, C. J. and K.M. Evenson. 1976. Rate constants for the reactions of OH with ethane and somehalogen substituted ethanes at 296K. / Chem. Phys. 64:4303-4306. (Cited in ATSDR, 1988) HSDB. 1995. Chemical Search for 1,2-Dichloroethane. Hazardous Substances DataBank. National Library of Medicine, National Iiistitutes of Health, Bethe«ia, MD.\ IRIS- 1996; 1,2-Dichtoroethane. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH. Isacson, P.. J.A. Bean, R. Splinter et aL 1985. Drinking water and cancer incidence in Iowa. m. Associatton of c-ir-cervvim indices of contarnm 1988> ".••'•-,;-. - • ; ' • •"' . '-'-'' ••'-• .. • ' '....-• ' ' v ' . .'-'., "• '..' ' J ' . / . . , Kirk-Othmer. 1979. Kirk-Othmer Encyclopedia of Chemical Technology. New Yoric, NY: John Wiley&Sons. (Cited in ATSDR, 1988) . G-13 CHEMRISK*.A DIVISION OF MCLAREN/HAR' T Lyman,WJ,,W.F.ReehlandD.H.RosenbIatt. 1990. Handbookof Chemical Property Estimation Methods: Environmental Behavior of Organic Compounds. Washington, DC: American Chemical Society. ^ . ' . - ' . ' ' . . Mabey, \y.R., J.H. Smith, R.T, Podofl et aL 1982. Aquatic Fate Process Data for Organic Priority Pollutants. Prepared for U.S. Environmental Protection Agency, Office of Water Regulations and Standards, Washington, D.C. by SRI International, EPA 440/4-81-014. (Cited in ATSDR, 1988) Merck. 1983. The Merck Index: 10th Edition. Rahway, NJ: Merck & Co., Inc. (Cited in ATSDR, 1988) 1 '''•-' • NCI. 1978. Bioassay of 1,2-Dich faroethane for Possible Carcinogenicity. N Technical Report Series No. 55. DHEW Publication No. (Nffl) 78-1361. National Cancer Institute, Washington, D.C. (Cited in IRIS, 1996). NIOSH. 1978. Revised Recommended Standard: Occupational Exposure to Ethylene Dichloride, (1,2-Dichhrethane). U.S. Department of Health, Education, and Welfare, National Institute for Occupational Safety and Health, Division of Criteria Document and Standards Development, Cincinnati, OR PB80-1760092. (Cited in ATSDR. 1988) ' •'' '• •" ' '-' ' '• - - V -'• ' " - Reeve, G.R., G.G. Bond, J.W. Uyod et aL 1983. An investigation of brain tumors among chemical plant employees using a sample-based cohort method. / Occup. Med 25:387-393. (Cited in ATSDR, 1988) % Shen,T.T. 1982. Estimation olforganfccompoimdemisswnsfiro^ Control Assoc. 32:79-82. (Cited in ATSDR, 1988) Spencer, RC.,VXRowe,E.M. Adams, D.D. McCollister, and D.D. Irish. 1951. Vapor toxicity of ethylene dichtoride determined by experiments on laboratory animals. Ind. Hygt Occup. Med. 4:482-493. (Cited in MS, 1996) Theiss, 1C., G.D. Stoner, M.B. Shimkin et aL 1977. Test for carcinogenicity of organic contaminants of United States drinking waters by pulrrwnarytiurior response in strain a mice. Cancer Res. 37:2717-2720. (Cited in ATSDR, 1988) \ G-14 CHEMRISK*-A DIVISION OF MCLAREN/HART , j ;iR:iO'l»096- USEPA. 1975. Report on the Problem of Habgcnated Air Pollutots and St^ U.S. Environmental Protection Agency, Washington, D.C. EPA 600/9-75-008. (Cited in ATSDR, i J 1988) ^^--^* .'.'.,' ' \ ' \ USEPA 1985. Health Assessment Document for 1,2-Dichloroethane. U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Washington, D.C. EPA 600/8- 84-006F. (Cited in ATSDR, 1988) . ' USEPA 1995. Health Effects Assessment Summary Tables, FY- 1995 Annual. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, D.C. May. EPA/54(VR-95/036. • ' ' '. '•<•''.,'- ' '. V - > • • ' ' .• : , . /" v' : USEPA. 1996. Risk-Based Concentration Table, January -June 1996, Dr. Roy L. Smith, U.S. Environmental Protection Agency, Region m. Office of RCIbV, Techriical and Program Support Branch, Philadelphia, PA April 30. Van Duren, B.L., B.M. Goldschmidt, G. Loewengart et al 1979. Carcinogenicity of hatogenated ofefinic and aliphatic hydrocarbons in mice. JNCl 63: 1433- 1439. (Cited in ATSDR, 1988) i j Waxweiler, RJ., V. Alexander, S.S. Leffingwell et aL 1983. Mortality from brain tumor and other causes in a cohort of petrochemical workers. .JNCl 70:75-81. (Cited in ATSDR, 1988) Wilson, J.T., CG. Enfield, W.J. Dunlap et aL 1981. Transport and fate of selected organic pollutants in a sandy soil J. Environ. Qual 10:501-506. (Cited in ATSDR, 1988) G-15 CHEMRISK*- A DIVISION OF MCLAREN/HART AR30U097 Toxicological Profile i '' '..''•' • 1,2-DichloroethyIene . .' Chemical Formula CflzQ HSDB, 1995 Molecular Weight 9i6.94 g/mol HSDB, 1995 Vapor Pressure 395 ramHg d 30°C HSDB, 1995 Boiling Point 333°K HSDB, 1995 Melting Point -50°C HSDB, 1995 Henry's Law Constant 6,72xlCr3 atm-mVmol HSDB, 1995 Solubility 6.3g/L@25°C , HSDB, 1995 Partition Coefficient 36 HSDB, 1995 This lexicological profile addresses the chemical and physical properties, environmental fate and transport, and lexicological aspects of the trans isomer of 1,2-dichtoroethylene (1,2-DCE). Trans- 1,2-DCE is recognized by USEPA as a priority pollutant while cw-l,2-DCE is not Further, the standard USEPA methods of analysis dp not permit the isomers to be differentiated (HSDB, 1995). Trans- 1,2-DCE is used primarily as a solvent and extractant It is also used in the synthesis of organic chemicals and in the manufacture of perfumes, lacquers, and thermoplastics (HSDB, 1995). In the atmosphere, trans- 1,2-DCE is generally lost by reaction with photochemically produced hydroxyl radicals (CaHahan et al, 1979). Photooxidation is not expected to be a significant fate process. The primary removal process for trans- 1,2-DCE in the atmosphere is via wet deposition with an estimated half-life of 3.6 days (HSDB, 1995). rro/u-l,2-lXE in terrestrial environments typically evaporates and leaches to groundwater where it may biodegrade (HSDB, 1995). Vo.atili7at.nn is the most important transport process for iron.?-1,2-DCE in aquatic systems. Other processes, however, such as photodissociation, oxidation, hydrolysis, biodegradation or adsorption to sediments are not expected to be significant. Additionally, an estimated half-life of 3 hours has been estimated for *row-l,2-DCE in river systems (HSDB, 1995). G-16 . CHEMRlSK*-A DIVISION OF MCLAREN/HART iR:Hll»098 Inhalation of trans- 1,2-DCE in animals may cause nausea, vomiting, weakness, tremor, epigastric crainps, and cenfcri nervous depressfon. Contact with liquid/row-1,2-DCE may cause irritation of the eyes and skin (HSDB, 1995). •• - • . • i • •••".•'' ' • - Pregnant rats were exposed to i*cwj-l,2-DCE vk irihalation for 6 hours toy during days 7 to 16 of gestation at exposure levels of 0,2000,6000, or 12000 ppm. Maternal toxicity was expressed as reduction in weight gain at 12,000 ppm and at feed consumption at 6,000 and 12,000 ppm. Additionally, fetal weights were significantly reduced in the litters exposed to the highest dose, concentration (HSDB, 1995). , The USEPA has not determined the carcinogenic classification of either the trans- or the citr-isomer of 1,2-DCE. Likewise, the Agency has not established an oral or inhalation cancer slope factor. The USEPA has published tul oral RfD of 0.0093 mg/kg-day based for mixed 1,2-DCE based on values derived ifrom toxicity studies with 1,1-dichtoroethylene (1,1-DCE) (USEPA, 1995). Study results indicated the presence of liver lesions in rats administered 1,1-DCE via drinking water for two years. The USEPA has not established an inhalation RfD for 1,2-DCE. Reference.-• -.s : .-•'• / ,-'•• •:•••': •- " '• -;'•••/•••:' • "• ATSDR. 1995. ToxicohgicalProfiUforPofychlorinatedBiphenyls. Agency for Toxic Substances and Disease Registry, Atlanta, G A and U.S. Department of Health and Human Services, Public Health Service. August. . CaIlahan,M.A.,M.W. Sliraak,N.W. Gabcletal 1979. Water-Related Environmental Fate of 129 Priority Pollutants, Volume I. U.S. Environmental Protection Agency, Washington, D.C. EPA 440/4-79-029a. (Cited in ATSDR, 1995) HSDB. 1995. Chemical Search for 1,2-Dichloroethylene: Hazardous Substances Data Bank, National Library of Medicine, National Institutes of Health, Bethesda, MD. IRIS. 1996. 1,2-Dichloroethylenc. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH. , tmi^^ G-17 CHEMRISK*-A DIVISION OF MCLAREN/HART USEPA. 1995. Health Effects Assessment Summary Tables, FY-1995 Annual. U.S. Environmental Protection Agency, Office of Research and Development, Office of Emergency and Remedial Response, Washington, D.C. EPA/540/R-95/036. May. G-18 CHEMRlSK*-A DTVISION OF MCLAREN/HART , Toxidty Profile > 1,2,4-Trichlorobenzene Chemical Formula QHjClj Howard, 1989 Molecular Weight 181.46 Howard, 1989 Vapor Pressure i 0.29 mmHg @ 25°C , USEPA, 1980 1.0 mmHg @ 38.4°C USEPA, 1980 BoaingPoint 213°C Verschueren, 1983 MeltingPoint 17°C Verschueren, 1983 Henry's Law Constant 1.42xlOr3 atm-mVmol Lyman et aL* 1982 Solubility 48.8 mg/L @ 20°C Chiou et aL, 1983 19.0rag/L@22°C Verschueren, 1983 Liquid Diffusion Coefficient 6.68xl(X*cmVsec Lyman etaL, 1990 Gaseous Diffusion Coefficient 6.95x10^ cmVsec Lyman et aL, 1990 Partition Coefficients / 4.02 ; Hansch and Leo, 1985 3.87 JuryetaL,1983 1,2,4-TricMorotenzerie (TCB) has been rrian^ These include: dye carrier, intermediate in manufacture of herbicides and higher chlorinated benzenes, v dielectric fluid, solvent, degreasing agent; septic tank/drain cleaner, wood preservative, and in abrasives (HSDB, 1995). Releases to the environment have occurred as a result of these uses. In the atmosphere, TCB is estimated to have a vapor phase half-life of 18.5 days based on reaction with hydroxyl radicals (HSDB, 1995). In soils, TCB is expected to adsorb to organic matter and leaching to groundwater is not expected to be significant (HSDB, 1995). Some btodegradation may occur slowly in soils (HSDB, 1995). In aquatic systems, TCB is expected to adsorb to sediments. Dissolved TCB may evaporate relatively rapidly from waterbodies (HSDB, 1995). • v • • - r i ' In humans, TCB has been reported to cause dernial inimion ami skin burris .^ter dermal exposure; dermal exposure in animals has resulted in thickening and keratinizatipn of the epidermis (HSDB, 1995). G-19 CHEMRISK*-A DIVISION OF MCLAREN/HART fVR30M 01 In animals, the primary target organs after oral TCB exposure appear to be the liver and adrenal glands, with adrenal enlargement and increased liver and kidney weights observed in some species (Cicmanec, 1991; Smith and Carbon, 1980). Robinson et aL (1981) conducted a multigeneration reproduction study of 1,2,4-trichto re benzene in rats. The study results were used to determine a NOAEL of 100 ppm and a LOAEL of 400 ppm based on a significance increase in adrenal gland weights among male and female rats in the 400 ppm dose group (IRIS, 1996). The increase in adrenal gland weight may be associated with vacuolization of the zona fasciulata (Cicmanec, 1991; Dilley, 1977). Adrenal glands exhibit the highest initial concentration. After dosing, however, significant concentration increases may be observed in abdominal fat, kidney, and liver (Smith and Carison, 1980). TCB may also induce some liver enzymes (HSDB, 1995). Other investigators have reported different results from exposures of TCB to laboratory animals. An oral dose of 90 mg/kg 1,2,4-trichlorobenzene administered to rhesus monkeys caused hepatic induction. Death occurred within 30 days to rhesus monkeys receiving an oral dose of 173.6 mg/kg. Subjects at this dose experienced tremors and severe weight toss (Smith et aL, 1978). Carison and Tardiff (1976) determined a NOAEL of 20 mg/kg/day and a LOAEL of 40 mg/kg/day for male rats administered oral doses resulting in an increase in Uver-to-body weight ratios. Watanabe etaL (1977; 1978) estimated a LOAEL of 10 ppm and a NOAEL of 3 ppm for rats based upon evidence of a sporadic increase in urinary porphyrins in rats exposed for 90 days via inhalation. '• v ' • .'•'. •-. • '"••• •' 'v "; '' .. •••' . ••"'. Yamamoto et aL (1982) conducted dermal exposure studies with mice administered up to 60% 1,2,4- trichlorobenzene at 0.03 mLVapplication twice weekly for two years. Results at this dose group indicated increases of nonneoplastic lesions for lung, liver, kidney, adrenal spleen and lymph nodes. * In addition, mean survival days within the dose group were significantly reduced, Kitchin and Ebron (1980) reported significant retardation among the offspring of rats administered 360 mg/kg/day during gestation. Results, however/did not indicate increased resorptions, embryolethaUty, or teratogenicity. The USEPA has classified 1,2,4-trichtorobenzene as a Group D carcinogen, not classifiable as a human carcinogen, based on the absence of human carcinogenicity data and inadequate animal data (IRIS, 1996). In addition, the Agency has not established an oral or inhalation cancer stope factor for this compound (IRIS, 1996). The USEPA has derived an oral RfD value of 0.01 mg/kg-day for 1,2,4-trichtorobenzene based on the results of a rat reproductive study which indicate an increase in adrenal weights and the _^^^^»^» -•" G-20 CHEMRISK*-A DIVISION OF MCLAREN/HART . TheUSEPAhas not deten-.ined.minh.totionRfD value for 1,2,4-trichtorobenzene (IRIS, 1996). In fieu of verified values, a provisional inhalation RfD value of 0.0571 mg/kg-day was applied in this assessment. This value was obtained from the USEPA Region HI ( 1996) guidance document for RCRA sites and is regarded as a provisional value. •References • • ' ", '. - - - ••' •_.. . ; ..'•'' • .''..' Carison, G.P. and R.G.Tardiff. 1976. Effect of chlorinated benzenes on the metabolism of foreign 'organic compounds. Toxicol AppL Pharmacol. 36:383-394. (Cited in IRIS, 1996) Chiou, P.E. et aL 1983. Environ. Sci. Tech. 17:227-231. (Cited in Howard, 1989) , ' ' ' • \ - - v 1 . "• N ' ' ' ' 1 Cicmanec, J. 1991. U.S. Environmental Protection Agency, Cincinnati, OH Memorandum to the RfD/RfC Work Group, U.S. Environmental Protection Agency. November 15. (Cited in IRIS, 1996) DiUey.J.V, 1977. Toxic Evaluation of Inhaled Chlorobcnzene(Monochlorobenzcne). Prepared by Stanford Research Institute for NIOSH, DHEW, Cii-cinnati, OH. NTIS PB-276-623. Cited in IRIS, ' " ; Hansch, C. and A.J. Leo. 1985. MedChem Project. Issue No. 26. ClaremonU CA: Pomona College. (Cited in Howard, 1989) Howard, P.H. (ed). 1989. 1,2,4-Trichlorobenzene. Handbook of Environmental Fate and Exposure Data for Organic Chemicals^ Volume /; Large Production and Priority Pollutants. Chelsea, MI: Lewis Publishers, Inc. 518-527. HSDB. 1995. 1,2,4-Trichlorobenzene. Hazardous Substance Data Base. National Library of Medicine, Bethesda, MD. IRIS. 1996. It2t4-Trichlorobenzene. Integrated Risk Inforrnation System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH. Jury, W A., W.F. Spencer, and W.J. Farmer. 1983. Behavior assessment model for trace organics in soil: I. Model description. J. Environ. QuaL 12(4):558-564. "- ;: •- " -'-' '• '-•'''•; G-2' 1 ; CHEMRISK*-•• •'';A •DIVISIO N OF -MCLAREN/HAR. -'r- •T ' Kitchin, K.T. and M.T. Ebron. 1983. Maternal hepatic and embryonic effects of-1,2,4- trichtorobenzene in the rat Environ. Res. 31:362-373., (Cited IRIS, 1996) • ' - ,' \ . - ' i; i. \---*^ Lym-ui,WJ.,WJ'.R.xhlandD.aRosenb^att 1990. Handbook of Chemical Property Estimation Methods: Environmental Behavior of Organic Compounds. Washington, D.C.: American Chemical Society. Lyman, WJ., W.F. Reehl and D.H. Rosenblatt. 1982. Handbook of Chemical Property Estimation Methods. New York, NY: McGraw-Hifl Book Co. (Cited in Howard, 1989) Robinson, K.S., R.J. Kavtock, N. Chernoff, and E. Gray. 1981. Multi-generation study of 1,2,4- trichtorobenzene in rats. / Toxicol Environ. Health. 8:489-500. (Cited in IRIS, 1996) Smith, B.N. and G.P. Carison. 1980. Various pharmacokinetic parameters in relation to enzyme- inducing abilities of 1 A4-trichtorobenzene and 1,2,4-tribromobenzene. J. Toxicol Environ. Health. 6(4):737-749. (Cited in IRIS. 1996) * . . i Smith, CC,S.T.Cragg, and GJ.Wolte. 1978. Subacute toxicity of 1,2,4-trichtorobenzene (TCB) in sub-human primates. Fed. Proc. Fed. Am, Soc. Exp. Biol 37(3):248. (Abstract). (Cited in IRIS, 1996) 7 ' ' ' • - { . '. ' ' ' • • ' . ' USEPA. 1980. Ambient Water Quality Criteria for Chlorinated Benzenes. U.S. Environmental Protection Agency, Office of Water Regulations and Standards, Washington, D.C. EPA-44Q/5-80- 028. (Cited in Howard, 1989) USEPA. 1996. Risk-Based Concentration Table, January - June 1996. Dr. Roy L. Smith, U.S. Environmental Protection Agency, Region HI, Office of RCRA, Technical and Program Support Brarch. Philadelphia, PA. April 30. . Verschueren, K. (ed). 1983. 1,2,4-Trkhtorobenzene. Handbook of Environmental Data on Organic Chemicals, 2nd Edition. New York, NY: Van Nostrand Reinhold. 1122-1123. ' " - ' - ' . .' • • : \ . Watanabe, P:G., RJ. Kociba, R.E. Hefher, H.O. Yakel and B.K.J. Leong. 1978. Subchronic toxicity studies of 1,2,4-trichtorobenzene in experimental animals. Toxicol Appl Pharmacol 45(l):332-33l (Abstract). (Cited in IRIS, 1996) G-22 CHEMRISK*-A DIVISION OF MCLAREN/HART Watanabe, P.O., H.O. Yankel and R.J. Kociba. 1977. Subchronic Toxicity Study of/nhaledJ,2,4- Trichlorobenzene in Rats. Internal Report. Dow Chemical Company, Toxicology Research Laboratory, Midland, MI. (Cited in IRIS, 1996) Yamamoto, H. Y. Ohno, K. Nakamori, T. Okuyama, S. Imai, and Y. Tsubura. 1982. Chronic toxicity and o.rcinogenicity test of 1^,4-trichtorobenzene on mice by dermal painting. /. .Vara. Med. Assoc. 33:132-145. (Cited in IRIS, 1996) > G«23 CHEMRlSI-*-A DIVISION OF MCLAREN/HART Toxicity Profile • • . . ' . " • ' ' 1,3-Dichtorobenzene Chemical Formula C^dj HSDB, 1995 Molecular Weight 147 , HSDB, 1995 Vapor Pressure 2.3mmHg@25°C Mackay and Shiu, 1981 Boiling Point 173,53°C HSDB, 1995 Melting Point -24.7°C HSDB, 1995 Henry's Law Constant 6.0018 atm-mVmol @ 20°C HSDB, 1995 Solubility . 123 mg/L @ 25°C USEPA, 1980 Liquid Diffusion Coefficient 7.16x10* cmVsec 1-yman et aL, 1990 Gaseous Diffusion Coefficient 7.62X10"1 cmVsec - Lyman et aL,1990 Partition Coefficients 3.55 Mackay etaL, 1992 3.23 Mackay etaL, 1992 13-Dichtorobenzene in the atmosphere exists primarily in the vapor phase and may be removed via reaction with photochemicaHy produced hydroxyl radicals. A half-life of 14 days has been estimated for this removal process. Wet deposition or direct photolysis are not expected to be significant removal mechanisms for atmospheric 1.3-dichlorobenzene (HSDB, 1995). '"...' In soil systems, 1,3-dichtorobenzene may be tightly adsorbed to soil particulates, although some leaching to groundwater can occur. Volatilization from soil surfaces may be an active transport mechanism if the compound is not attenuated by adsorption or leaching. Under aerobic conditions, 13-dichtoroberizer.ernaybestowlybto^ photolysis, oxidation, or hydrolysis are not likely to occur (HSDB, 1995). A significant fate process for 13-dichtorobenzene in aquatic systems is adsorption to sediment (Oliver and NicoL 1983). When not attenuated by adsorption to sediment, 1,3-dichtorobenzene may volatilize from water with an estimated half-life of 4.1 hours in river systems at a depth of 1 meter. Additionally, under aerobic conditions, 1,3-dichlorobenzene may biodegrade after rnicrobial adaptation (HSDB, 1995). Other aquatic fate processes such as direct photolysis, hydrolysis, and oxidation, are hot considered to be significant mechanisms (Oliver and Niimi, 1983). G-24 CHEMRISK*. A DIVISION OP MCLAREN/HART • / \ .' • " ' * • • "^""^^ In humans, several studies involving exposures to 1,3-dichtorobenzene have reported leukemias. These studies are compromised, however, by the presence of chemkiU mixtures which prohibit the identification of a single carcinogenic agent (HSDB, 1995). Human exposure to varying concentrations of 1,3-dichlorobenzene may irritate the eyes, nose, or throat. 13-Dichtorobenzene may cause nausea, vomiting, diarrhea, and liver or kidney damage if swallowed (HSDB, 1995). Similarly, few animal studies reported conclusive evidence of 1,3-dichtorobenzene toxicity. A study with rats administered oral doses of 250 mg/kg daily for 3 days resulted in enhanced activities of aminopyrine demcthylase and aniline hydroxylase. Study results also indicate that delta-ammo levuhnic acid synthetase activity was enhanced by 32 percent (Ariyoshi et aL, 1975). Mohtashamipur etaL (1987) reported the induction of clastogenic activities in 8-week oM mice administered 4 doses of 13-dichtorobenzene via injection. Clastogenic activity was observed in the femoral bones of the treated group and described as increased formation of microhucleated polychromatic erythrocytes. In addition, Prasad and Pramer (1968) reported an increase in the quantity of revertants of an auxotrophic strain ofAspergillu s nidulans foflowing spore treatment with 1,3-dichlorobenzene. The increase, however, was not statistically significant. I j The USEPA has classified 13-dicWDrorxn.Krie as a Group Dc^rcirwgen, not classifiable as to ; ^^"^^ • . 'carcinogenicity ' , base; ' d 'o 'nf the absenc: .e of humai n or anima' ' l carcinogenkity data and limited genetic data (IRIS, 1996). The Agency has not established an oral or inhalation cancer slope factor or RfD value for 13-dichtorobenzene (IRIS, 1996) . In lieu of verified values, a provisional oral RfD value of 0.089 mg/kg-day was applied in this assessment This value was obtained from the USEPA Region ....'' in (1996) guidance document for RCRA sites and is regarded as a provisional value. References ; v ;'- , ' '. ' ) ".. . ' •' ' ' • • ' '..''- i' ' '- " " . -.' ' .."•'' ' -' - Ariyoshi etaL 1975, Chem. Pharm. Bull 23(4):&24-*3Q. (CitrtmKSDX, 1995): HSDB. 1995. 1,3-Dichlorobenzene. Hazardous Substances DataBank. National Library of Medicine, National Institutes of Health, Bethesda, MD. / , . IRIS. 1996. 1,3'Dichlorobenzcne. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Environmental and Health Assessment, Cincinnati, OH. 1 '• ' ' ' G-25 CHEMRISK*- A DIVISION OF MCLAREN/HART <1R30t»l07 Lyman, WJ., WJi Redd, and D.R Rosenblatt 1990. Handbook of Chemical Property Estimation Methods: Environmental Behavior of Organic Compounds. Washington, DC: American Chemical " Society. • . • Mackay, D. and W.Y. Shiu. 1981. J. Phys, Ref. Data. 10:1193. (Cited in HSDB, 1995) i . . . . , '• . Mackay, D., W.Y. Shiu, and K.C. Ma. (eds). 1992. Illustrated Handbook of Physical-Chemical Properties and Environmental Fate for Organic Chemicals. Volume 1: Monoaromatic Hydrocarbons, Chhrobenzenes, and PCBs. Chelsea, MI: Lewis Publishers, Inc. MohtasJiaraipur, E. et al 1987- Mutagenesis. 2(2):111-114. (Cited in HSDB, 1995). Oliver, B.G. and K.D. NicoL 1983. Environ. Sci. Technol 16:532. (Cited in HSDB, 1995). Oliver, B.G. and AJ. NiiraL 1983. Environ. Sci. Technol 17:287. (Cited in HSDB, 1995). Prasad, I. and D. Pramer. 1968. Mutagenic activity of some chloroanilines and chtorobenzenes. Genetics. 60:212-213. (Cited in IRIS, 1996). . USEPA. 1980. Ambient Water Quality Criteria Document for It4-Dichlorobenzene. U.S. Environmental Protection Agency, Office of Water, Washington, D.C. EPA-44G/5-80-039. USEPA. 1996. Risk-Based Concentration Table, January' June 1996. Dr. Roy L. Smith, U.S. Environmental Protection Agency, Region m. Office of RCRA, Technical and Program Support Branch, Philadelphia. PA. April 30. G-26 .. CHEMRISK"-A DIVISION OF MCLAREN/HART IR3UI»I08 Toxicity Profile 1,4-Dichlorobenzene , Chemical Formula QHA Howard, 1990 Molecular Weight 147.01 Howard, 1990 Vapor Pressure . 1.76 raraHg @ 25°C Howard, 1990 Bofling Point V74°C Howard, 1990 MeltingPoint * 53.1°C Howard, 1990 Henry's Law Constant > 1.5x10-* Howard, 1990 Solubility 79mg/L@25°C Verscheuren, 1983 Liquid Diffusfon Coefficient 7.16xlO-*cmVsec Lyman et aL, 1990 Gaseous Diffusion Coefficient 7.62xlO-2 cmVsec Lyman et aL, 1990 Partition Coefficients , togK,. 3.52 Howard, 1990 2.4-3.26 Bahnick arid Doucette, 1988 1,4-Dichtorobenzene is a synthetic chemical used primarily as a space deodorant in toilets and refuse containers. It is also emptoyed as a fumigant for control of moths, molds, and raiMew^^ It may also be utilized as an intermediate in the production of other chemicals and in the control of certain seed molds and tree-boring insects (HSDB, 1995; ATSDR, 1991). In the atmosphere, 1,4-dichtorobenzene reacts with photochemically generated hydroxyl radicals with a predicted reaction rate of 3x10*" cmVmol-sec (Atkinson et aL, 1985; Singh et aL, 1981). In addition, Singh et aL (1981) calculated an atmospheric residence of about 39 days for 1,4- dichlorobenzene. ' 1,4-Dichtorobenzene is expected to sorb to soils and sediments (ATSDR, 1991). Sorption of 1,4- dichtorobenzene in soils is highly dependent upon the organic content. Sorption may be reversible, however, permitting 1,4-dichtorobenzene to migrate through the soil from surface water to groundwater (Newsom, 1985; Schwarzenbach and WestaU, 1981). The most prominent fate process for 1,4-dichtorobenzene in surface soils is volatilization, although biodegradation by soil organisms and leaching to groundwater may also occur (ATSDR, 1988; USEPA, 1985). ., ' . G-27 CHEMRISK*-A DWISION OF MCLAREN/HART 1,4-Dichtorobenzene has a relatively high potential for bioconcentration and bioaccumulatiori in aquatic organisms, BCFs for 1,4-dichtorobenzene hav$ been calculated for rainbow trout and guppies at 370-720 and 1,800, respectively (Chiou, 1985; Oliver and Niimi, 1983). Estimated volatilization half-lives for 1,4-dichtorobenzene in river and seawater systems have been estimated at 4.3 hours and 10-18 days, respectively (Howard, 1990; Wakeham et aL, 1983). Additionally, biodegradatkm may also be a significant transformation process for 1,4-dichtorobenzene in aerobic water systems, but not under anaerobic conditions (Bouwer and McCarty, 1982, 1983, 1984; Spain and Nishino, 1987; Tabak etaL, 1981). Exposure to 1,4-dichtorobenzene occurs primarily through ingestion of contaminated water and inhalation. There is no evidence that adverse health effects can be attributed to brief, low, or moderate level exposures to household products containing 1,4-dichtorobenzene. Inhalation of higher concentrations, such as those that might occur in industrial settings may cause headaches, diarrhea, numbness, or weight toss (ATSDR, 1991). Such exposures, however, are generally associated with intolerable odors which normally serve as a warning (USEPA, 1985). .''•"• Dose related increases of renal tubular ceU adenocarcinomas have been observed in male rats administered doses of 150 to 600 mg/kg-day via gavage in a two year bioassay. A similar study of mice receiving comparable doses (300 to 600 mg/kg-day) yielded results indicating increased hepatocellular carcinomas in male mice (NTP, 1987). Based on the results of these studies, 150 mg/kg-day is the cancer effect level for renal tubular cell adenomas in male rats and 600 mg/kg-day is the cancer effect level for hepatocellular carcinomas and hepatoblastomas in mice (NTP, 1987). The USEPA has classified 1,4-dichlorobenzene a class C human carcinogen. The Agency has published an oral cancer slope factor of 0.024 (mg/kg-day)'1 based on the presence of liver tumors in mice exposed to 1,4-dichtorobenzene in a 103-week gavage study (USEPA, 1995). The USEPA has not established an inhalation cancer slope factor or an oral or inhalation RfD value for 1,4-dichtorobenzene (MS, 1996). The USEPA, however, has derived an inhalation reference concentration (RfC) of 0.8 mg/rn3 based on increased liver weights in male Sprague-Dawley rats for 10 weeks (Chlorobenzene Producers Association, 1986). The results of this two-generation investigation indicated increased liver and kidney weights for both parental males and females. The NOAEL calculated from this study was 301 mg/m3 and the LOAEL was 902 mg/m3 based on the significant increase in liver weights of parental males (IRIS, 1996). , • _ ' ' • , ( ; ' G-28 CHEMRISK*-A DIVISION OF MCLAREN/HART / . 1 . . : • ^-»»^ • rtR30iil.ro In feu of verified values, a provisional inhalation RfD value of 0.229 mg/kg-day was appfiedJn this ; assessment. This value was obtained from the USEPA Region m (1996) guidance document for \^y RCRA sites and is regarded as a provisional value. v ATSDR. 1991; Toxicological Profile for 1,4-Dichtorobenzene: Draft.. Agency for Toxic Substances and Disease Registry, Atlanta. GA and U.S. Department of Health and Human Services, Public Health Service. October. / Bouwer, EJ. and P.L. McCarty. ' 1982. Removal of trace chlorinated organic cortipounds by activated carbon and fixed-film bacteria. Environ. Sci. Technol 16:336-343. (eked in ATSDR, Bouwer, E.J. and P.L. McCarty. 1983. Transformations of halogenated organic compounds under denitrification conditions. Appl Environ. Microbiol 45:1295-1299. (ATSDR, 1991) Bouwer, E.J. and P.L. McCarty. 1984. Modeling of trace organics biotransformation in, the subsurface. Ground Water 22:433-44$. (cited in ATSDR, 1991) O. ' - ' '." '"; - /:' ' -•' '. •.••.'-•••' " ' '• •' • :• * - Chiou, C.T. 1985. . Partition coefficient of organic compounds in Hpid-water systems and correlations with fish bioconcentration factors. Environ. 5ci/7>cfeu?^ 19:57-62. (cited in ATSDR, 1991) Chtorobenzene Producers Association. 1986. Parachlorobenzene: Two-Generation Reproduction Study in Sprague-Dawley Rats. Study 86-81-90605. MRTO No. 41 1088-1. (Cited in IRIS, 1996) Howard, P.H., ed. 199Q. Handbook of Environmental Fate and Exposure Data for Organic Chemicals. VolL Large Production and Priority Pollutants. Chelsea,MI: Lewis Publishers, Inc. p.250-262. (Cited in IRIS, 1996) HSDB. 1995. 1,4-Dichhrobenzene. Hazardous Substances DataBank, National Library of Medicine, Bethesda, MD. - IRIS. 1996. 1,4-Dichtorobenzene. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH. G-29 CHEMRJSK*- A DIVISION OF MCLAREN/HART ' Lyni.u.,WJ.,WJ.ReehCar.dD.R 1990; Handbook of Chemical Property Estimation Methods: Environmental Behavior of Organic Compo^ Society. \ : ~ NTP. 1987. Toxicology and Carcinogenesis Studies of l,4-dichlorobenzene(CAS no. 106-46-7) in F344/N Rats and B6C3F1 Mice (Gavage Studies); National Toxicology Program, Research Triangle Park, NC. NTP TR 319. NIH Publication No. 87-2575. (Cited in ATSDR, 1991) Oliver, B.G. and A. J. NiimL 1983. Bioconcentration of chlorobenzcnes from water by rainbow trout: Correlations with partition coefficients and environmental residues. Environ. Sci. Technol 17:287-291. (Cited in ATSDR, 1991) : Spain, J.C. and S.F. Nishino. 1987. Degradation of 1,4-dichtorobenzene by a Pseudomonas sp. Appl Environ. Microbiol 53:1010-1019. (Cited in ATSDR, 1991) ^ ' Tabak,H.H.,S.A Quave, and C.L Mashni etaL 1981, BtodegradabOity studies with organic priority poUutant compounds. /. Water Pollut. Contr. Fed. 53:1503-1518. (Cited in ATSDR, 1991) USEPA. 1985. Health Assessment Document for Chlorinated Benzenes. U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Washington, D.C. EPA/600/8- 84AM5F. USEPA 1995. Health Effects Assessment Summary Tables, FY-1995 Annual U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, D.C. May. EPA/540/R-95/036. USEPA. 1996. Risk-Based Concentration Tablet January - June 1996. Dr. Roy L. Smith, U.S. Environmental Protection Agency, Region m, Office of RCRA, Technical and Program Support Branch, Philadelphia, PA. April 30. Verscheuren, K. 1983. Handbook of Environmental Data on Organic Chemicals. 2nd edition. NewYori_;NY; Van Nostrand Reinhold Company, p. 477-478. (Cited in ATSDR, 1991) Walceham, S.G., A.C. Davis, J.L. Karas et aL 1983. Mescocosm experiments to determine the fate and persistence of volatile organic compounds in coastal seawater. Environ. Sci Technol 17:611* 617. (Cited in ATSDR. 1991) G-30 CHEMRlSK*-A DIVISION OF MCLAREN/HART '''' 4R.WI 12 Toxidty Profile - • . . . • ' '.'•'. i ' ' .... i 2,4-Dichlorophenol . . Chemical Formula C^ClzO HSDB, 1995 Molecular Weight 163 Weast, 1972 Vapor Pressure 0.067 mmHg @ 25°C Bidleman and Renberg, 1985 'Boiling Point 210°C '•.'. , Hawley, 1981 Melting Point 45°C Hawley, 1981 Henry's Law Constant 3-16x10* atm-mVmol , Thomas, 1982 Solubility 4,500 mg/L <§• 25°C Verschueren, 1983 Partition Coefficients 2-92 V Hansch and Leo, 1985 '2.10 , Boyd.1982 2,4-Dichtorophenol is used primarily as an intermediate in the production of other organic compounds such as herbicides, fungicides, antiseptics, and mothproofing compounds (ATSDR, 19?9) Very little '••••-;'•'2,4-dichlorophenol is •allowe •—'-"d for direc•t usag' e (Scow, 1982).' ' --••••...';"•••'-•'•••' Released to the atmosphere, 2,4-dichlorophenors reactivity will fimit its potential for transport. Based on its chemical properties, 2,4-dichtorophenol may not partition from the Vapor to the paniculate phase (Eisenreich et aL, 1981). An atmospheric half-life ranging from 0.8 hours to 5.3 days has been estimated for 2,4-dichlorophenol (Atkinson, 1987; ATSDR, 1989). The primary atmospheric removal process for 2,4-dichtorophenol occurs via direct photolysis or reaction with photochcmically-produced hydroxyl radicals. It may also be removed via wet deposition (ATSDR, 1989). ..-."„ fasoflsysterris,the..dsorpttonof2,4-dk Fortuny and Fuller, 1982; Isaacson and Frink, 1984; Schellenberg et aL, 1984; Seip et aL, 1986). Adsorption may also be influenced by the soil content of iron oxide, clay, or silt (Artiola-Fortuny and Fuller, 1982). Biodegradation acts as the primary removal process for 2,4-dichlorophenol in soils (ATSDR. 1989). A half-life of 2,4-dichtorophenol in sandy loam soil under aerobic conditions has been estimated at 1.5 days (Namkoong etaL, 1989). • G*31 CHEMRjSK*-A DIVISION OF MCLAREN/HART In water, direct photolysis half-lives have been estimated to range from 0.8 to 62 hours depending on theaquatjcpH and other conditions (Hwang et aL, 1986; Scully and Hoigne, 1987). On the other hand, estimated voMzation half-lives of 2,4-dichlorophenol in aquatic systems have been reported to range from 14.8 to 223 days (Thomas, 1982). In addition, photolysis and biodegradatton may also act as removal processes for 2,4-dichtorophenol in both water and sediments (Aly and Faust, 1964; Baker et aL, 1980; Banerjee et aL, 1984; ATSDR, 1989). The pH of the water system wiH likely determine the partitioning of 2,4-dichlorophenol between water and sediments. Adsorption to sediments and particulate matter may also be a significant removal process for 2,4-dichtorophcnoi in some waters (ATSDR, 1989). ' , . . " i ' " .,','* ' Some existing studies suggest that exposure of 2,4-dichtorophenol to humans via inhalation may result in carcinogenic effects (Eriksson et aL, 1981; Hardell etaL, 1981; Woods etaL, 1987). these data are confounded, however, due to the presence of other volatile compounds. There is no evidence associating oral or dermal exposure to 2,4-dichlorophenol and carcinogenic effects in humans (ATSDR. 1989). Exon and Roller (1985) exposed female rats to 3, 30, or 300 ppm 2,4-dichtorophenol in drinking water from weaning age through breeding at 90 days, parturition, and weaning of pups. The results suggest decreased delayed-type hyperserisitivityrespoiTseta Dams exposed to 300 ppm resulted in a significant decrease in litter sizes (Exon and KoHer, 1985). Dennal administration of 2,4-dichlorophenol with tumor initiators has been reported to result in tumor promotion in mice. Boutwelland Bosch (1959) applied about 0.005 mg 2,4-dichtorophenol to the mid-dorsal region of mice twice weekly for 15 weeks. Results indicated a significant increase in ihe incidence of papillomas and carcinomas. The USEPA has not classified 2,4-dichtorophenol as to human carcinogenic potentiaL Likewise, the Agency has not established an oral or inhalation cancer slope factor for 2,4-dichlorophenol (IRIS, 1996). i • ' • , "i ' • The USEPA has derived an oral RfD value of 0.003 mg/kg-day for 2,4-dichtorophenol based on the results of chronic animal studies which suggest a decreased delayed hypersensitivity response in rats (IRIS, 1996). The Agency has not established an inhalation RfD value for 2,4-dichlorophenol (IRIS, 1996). , G~32 CHEMRISK*- A DIVISION OP MCLAREN/HART IR.'WI ll* . • Reference~ s ' '"'' • i ' . . •: , • • *• . ' • ' -" ' • ! . • •• Aly, O.M. and SD. Faust 1964. Studies on the fete of 2,4-D and ester derivatives in natural surface waters. J.Agric. FdChem. 12:541-546. (Cited in ATSDR, 1989) Artiola-Fortuny, J. and W.H. FuUer. 1982. Adsorption of some monohydroxybenzene derivatives by soils. Soil Science 133:18-26. (Cited in ATSDR, 1989) . i , '. ' . ATSDR. 1989. Toxicofogical Profiltfor 2,4-Dicforophenol Draft. ^ and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public ,,\ Health Service, Washington, D.C. October. . Baker, M.D., C.L Mayfield, and W.E Inniss. 1980. Degradation of chlorophenols in soil, sediment 'and water at tow temperature. Wat. Res. 14:1765-1771. (Cited in ATSDR, 1989) Banerjee, S., P.H. Howard, A.M. Rosenberg et al 1984. Development of a general kinetic model for biodegradation and its application to chlorophenols and related compounds. Environ. Sci. Technol. 18:416-422. (Cited in ATSDR, 1989) L / Bidleman, T.F. and L. Renberg. 1985. Determination of vapor pressures for chtoroguaiacols, chtoroveratroles, and nonylphenol by gas chromatography. Chemosphere 14:1475-1481. (Cited in ATSDR, 1989) ; ' BoutweH, R.K. and D.K. Bosch. 1959, The tumor-promoting action of phenol and related compounds for mouse skin. Cancer Res. 19:413-424. (Cited in ATSDR, 1989) --1 . • ' . ' : . '- . . . . ,/ Boyd,S.A 1982. Adsorption of substituted phenols by soil SoilScience 134:337-343. (Cited in ATSDR, 1989) / . ' ••'.'"-•.• 1 •-.•'. ' - .. ', . • \ ' , •.•'., Eisenreich, SJ., BJJ. Looney, and ID. Thomton. 1981. Airborne organic contaminants in the Great Lakes ecosystem. Environ. Sci. Technol 15:30-38. (Cited in ATSDR, 1989) ' •. •' i . - . '' . -^ . . Eriksson, M.. L. HardeU, N. Berg et aL 1981. Soft-tissue sarcoma and exposure to chemical substances: A case-reference study. Brit. /. Ind. Med. 38:27^33. (Cited in ATSDR, 1989) G-33 CHEMRISK*- A DIVISION OF MCLAREN/HART VR30t»l IS Exon, J.H. and L.D. KoHer. 1985. Toxicity of 2-Chlorophenol, 2,4-Dfchlorophenol, and-2,4,6- TrichtorophenoL In; Water Chlorination: Chemistry, Environmental Impact and Health Effects. Volume5. JoDeyetaL (eds). (Cited in IRIS, 1996) Har-sch, C and AJ. Leo. 1985. Medchem project: Issue #26. Claremont, CA: Pomona College. (Cited in ATSDR, 1989) \ • • • HardeQ, L., M. Eriksson, P. Lenner et aL 1981. Malignant lymphoma and colon cancer to phenoxy acids, chlorophenols and other agents. Scand. J. Work Environ. Health 7:119-130. (Cited in ATSDR, 1989) / • , , f ' ' • . • '.• . • '• ' ... - Hawley, G.G. 1981. The Condensed Chemical Dictionary, 10th edition. New York, NY: Van NostrandReinholdCo. (Cited in ATSDR, 1989) HSDB. 1995. 2,4-Dichlorophenol Hazardous Substances DataBank, National Lirfary of Medicine, National Institutes of Health, Bethesda, MD. Hwang, H.M., R.E. Hodson, and R.F. Lee. 1986. Degradation of phenol and chlorophenols by sunfight and microbes in estuarine water. Environ. Sci. TechnoL2Q:lQQ2-\(Xn, (Cited in ATSDR, 1989) IRIS. 1996. 2,4-Dichlorophenol. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OIL Isaacson, P.J. and C.R. Frinlc 1984. Nonreversible sorption of phenolic compounds by sediment fractions: The role of sediment organic matter. Environ. Sci Technol 18:43-48. (Cited in ATSDR, 1989) Namkoong, W., R.C Loehr, and IF. Malina. 1989. Effects of mixture and acclimation on removal of phenolic compounds in soiL /. Wat Pollut Contrl Fed. 61:242-250. (Cited in ATSDR, 1989) ScheQenberg. 1C, C. Leuenberger. and R.P. Schwarzehbach. 1984. Sorption of chlorinated phenols by natural sediments and aquifer materials. Environ. Sci. Technol 18:652-657. (Cited in ATSDR, 1989) G-34' •• CHEMRlSK*-:- '. A DIVISIO.. N OF MCLAREN/HAR: • T . '\J /'"" Scow, K., M. Goyer, J. Perwak et aL 1982. An Exposure end Risk Assessment for Chlorinated Phenols (2-Chlorophenol, 2,4-Dichlorophenol, 2,4,6-Trichlorophenol). Arthur D. Little Inc., '\ *——^J - Cambridge- , MA. i EPA 440/4-85-007- -... PB85-211951. . -(Cite d i^ n ATSDR, 1989^). ^ . \ • • ! , • . ' • *• . . ^ . • Scully, F.E. and J. Hoigne. 1987. Rate constants for reactions of single oxygen with phenols and Other compounds in water. Chemosphere16:681-694. (Cited in ATSDR, 1989) i • • -',•'' Seip, H.M., J. Alstad, G.E. Carlberg et aL 1986. Measurement of mobility of organic compounds in soils. Sci Tot Environ. 50:87-101. (Cited in ATSDR, 1989) » ' . ., ' . Thomas, R.G. 1982. Environmental behavior of organic compounds. In: Handbook of Chemical Property Estimation Methods. New York, NY: McGraw-Hffl Book Co. (Cited in ATSDR, 1989) • ' >> • . ' . . i Verschueren, K. 1983. Handbook of Environmental Data on Organic Chemicals. 2ntf Edition. New York, NY: Van Nostrand ReinhbW Company. (Cited in ATSDR, 1989) Weast, R.C. 1972. CRC Handbook for Chemistry and Physics. 53rdEdition. Boca Raton, FL: CRCPress. (Cited in ATSDR, 1989) Woods, J.S., L. Polissar, R.K. Severson et aL 1987. Soft tissue sarcoma and non-Hodgkin's ' ' ' - lymphoma in relation to phenoxyherbicide and chlorinated phenol exposure in western Washington. Cancer Inst. 78:899-910. (Cited in ATSDR, 1989) , G-35 CHEMRISK*-A DIVISION OF MCLAREN/HART Toxicity Profile • • - - " • "^ Aluminum : . X..X Chemical Fbrmula ^ HSDB, 1995 Molecular Weight 26.98 Windholz, 1983 Vapor Pressure 1 mmHg @ 1284°C Sax and Lewis, 1989 Boiling Point 2327°C Windholz, 1983 Melting Point 660°C Windholz, 1983 - Henry's Law Constant NA ATSDR, 1990 Solubility Insoluble ' Weast, 1989 Partition Coefficients togK^ NA ATSDR, 1990 togK,. NA ATSDR,1990 Aluminum metals are used in a wide variety of capacities. The primary use of aluminum is as a structural material for the construction, automotive, and aircraft industries. It is also used in the production of metal alloys, electrical materials, cooking utensils, highway signs, and fencing. To a lesser extent, aluminum metals are also employed in the production of cans, food packaging, foils, corrosion resistant chemical equipment, and dental materials (ATSDR, 1990). Aluminum is not found as a free metal in the natural environment (Bodek et aL, 1988). Transport and partitioning of aluminum, then, is likely to be dictated by the chemical properties of the element, as wen as those of the immediate environmental matrix. Because it is an element, aluminum does not degrade in the environment and only one trivalent oxidation state is possible (ATSDR, 1990). Aluminum in the atmosphere may be transported via particulate matter. Atmospheric transformations, however, are unlikely to occur during transport (ATSDR, 1990). In soils, aluminum is present in marry priniary minerals. It may partition between solid and liquid phases by reacting with water molecules and anions such as fluoride, chloride, sulfate, nitrate, phosphate, clay, and humic materials (ATSDR, 1990). In general, mobility of aluminum increases with decreasing pH (Goenaga and WiHiams, 1988). G-36 CHEMRISK*.A DIVISION OF MCLAREN/HART il.R30-jM8 Aluminum in aquatic systems establishes an equilibrium with a solid phase which controls the -extent of dissolution. It may also be removed from solution by compiexing with phosphate at a pH within u the range of 5 to 6. Aluminum is also removed from aquatic systems via hydrolysis as the result of a stepwise replacement of molecules by hydroxyl ions (ATSDR, 1990). ' In healthy human adults, the bodyburden of aluminum is 30 to 50 mg. Half of the total body burden of aluminum occurs in the bones while one quarter occurs in the lungs. Normal human exposure to aluminum through utensils, foils, antacids, or antiperspirants is not considered harmful Some individuals, however, have experienced minor dermal irritation from exposure to aluminum in antiperspirants (ATSDR, 1990). Certain subpopulations, including patients undergoing renal dialysis and Alzheimer patients, may be more sensitive to aluminum's harmful effects. Individuals undergoing renal dialysis who have been exposed to large amounts of aluminum orally or intravenously may develop encephalopathy or a bone disease known as osteomalacia (ATSDR, 1990). Additionally, Alzheimer's patients often have elevated levels of aluminum in their brains, hippocampiis, and cerebral cortex. Defiiute cause-and- effect relationships between the presence of alurruniim and these degereradve problems have not been established (ATSDR, 1990). , Generally, aluminum causes toxic effects to animals when exposed to very large doses. In one \~~s experiment, mice died after a one-day acute exposure of 4,053 ppm aluminum in drinking water (ATSDR, 1990). Subchronic studies with pregnant rats exposed to 3, 100 ppm aluminum in food had fewer live newborns; and rats exposed for 100 days to 3,857 ppm in drinking water exhibited decreased weight gain (ATSDR, 1990). Genotoxicity tests indicate that aluminum may adversely affect DNA bases and phosphate, increase histone-DNA binding, t-Iter sister chromatic exchange, and decrease cell division (ATSDR, 1990). Results from an experiment involving in vivo intraperitoneal exposure of! aluminum chloride to mice indicate that this compound may be clastogenic. Other available data suggest that aluminum does not directly interact with DNA in mutagenicity tests (ATSDR, 1990). The USEPA has not classified aluminum as to potent Also, the Agency has not established an oral or inhalation cancer stope factor for aluminum. Likewise, the USEPA has not determined an oral or inhalation RfD value for aluminum (IRIS, 1996). In lieu of verified values, a provisional oral RfD value of 1 mg/kg-day was applied in this assessment. This value was obtained G-37 CHEMRjSK*-A DtVEION OF MCLAREN/HART 19 from the USEPA Region m (1996) guidance document for RCRA sites and is based on developmental effect• s in ••-"the• centra l nervou. -.. s system'•••"',.'. • - - '•'-. •"• ••-. • ;. References .'.,.'' - V ATSDR. 1990. Toxicological Profile for Aluminum: Draft. Agency forToxic Substances and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public Health Service, Washington, D.C. October. . , > Bodek, I., W. J. Lyman, W.F. Reehl et aL 1988. Environmental Inorganic Chemistry-Properties Processes, and Estimation Methods. New York, NY: Pergammon Press. (Cited in ATSDR, 1990) / . - ' . . '•.'-- Goenaga, X. and D.J.A. Williams. 1988. Aluminum speciation in surface waters from a Welsh upland area. Environ. Poltoi. 52:131-149. (Cited in ATSDR, 1990) HSDB. 1995. Chemical Search far Aluminum.. Hazardous Substances DataBank. National Library. of Medicine, Nationa' l Institutes of Health, Bethesda• , MD. . ^ IRIS. 1996. Aluminum. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH. . \ J Sax, N.L and RJ. Lewis. 1989. Dangerous Properties of Industrial Materials. Volume 2, 7th Edition. New York, NY: Van Nostrand ReinhoM. (Cited in ATSDR, 1990) USEPA. 1996. Risk-Based Concentration Table, January *June 1996. Dr. Roy L. Smith, U.S. Environmental Protection Agency, Region m. Office of RCRA, Technical and Program Support Branch, Philadelphia, PA. April 30. Weast, R.C. 1989. CRC Handbook of Chemistry and Physics, 70th Edition. Boca Ratpn, FL:. CRC Press, Inc. (Cited in ATSDR, 1990) Wind-iob; E. ed 1983. The Merck Index* 10th Edition. Rahway. NJ: Merck & Co., 'Inc. 48:50-53. (Cited in ATSDR, 1990) G-38 CHEMRISK*- A DIVISION OP MCLAREN/HART ilR30.».l20 Toxicological Profile \ ' ' -' ' Arsenic Chemical Formula As . ATSDR, 1993 Molecular Weight 74.92 g/mol ; Weast^ 1985 Vapor Pressure 1 mmHg @ 372°C HSDB, 1995 Boiling Point 613°C Sublimes Weast, 1985 Melting Point 817°C@28atm Weast, 1985 Henry's Law Constant No data ATSDR, 1993 Solubility Insoluble Weast, 1985 Partition Coefficient ; Nodata ATSDR, 1993 Arsenic is an element that exists in various chemical states, including elemental inorganic arsenic, arsenic trioxide, arid arsenic pentoxide, with each form having different toxicological potential (ATSDR, 1993). The major sources of environmental arsenic are natural forces such as volcanic activity and weathering of arsenic-containing rocks, and human activity associated with metal smelting, glass inanufacturing, pesticide production and use, and fossil fuel burning. Arsenic is also present in small amounts in mainstream cigarette smoke (ATSDR, 1993). In air, arsenic is adsorbed to paniculate matter, with a residence time of about 9 days, depending on particle size. In surface waters, arsenic is predominantly adsorbed to clays, iron oxides, manganese compounds, and organic material Therefore, sediment serves as a reservoir for arsenic, where it exists mainly in insoluble complexes (ATSDR, 1993). Arsenic also occurs in soil primarily in an insoluble, adsorbed form. Binding of arsenic via organic material, or chemical interaction with iron or calcium, represents an important fixation phenomenon for arsenic in soil (ATSDR, 1993). ' ' -' " . * . • j Arsenic has been known as a human poison since ancient times because large ingested doses cause death (ATSDR, 1993). Sublethal doses cause stomach and intestinal irritation, decreased production of red and white blood cells, abnormal heart rhythm, blood-vessel damage, and impaired nerve function (ATSDR, 1993). Long-term oral exposure causes darkening of the skin and the appearance of small corns Or warts on palms, soles, and torso, which potentially develop into skin cancer. OAO-P^WETWCHUWW^ G-39 CHEMR-SK'-A DIVISION OF MCLAREN/HART Arsenic has also been reported to increase the risk of liver, bladder, kidney, and lung cancer (ATSDR, 1993). • "":• : . •' •-.' -: "•"- - " • • '.'• ' - • -.'•' • Arsenic is classified by USEPA as a Group A carcinogen, a human carcinogen, based on sufficient evidence from human data (IRIS, 1996). This classification is based on evidence of lung cancer in human populations exposed via inhalation, and increased incidence of skin cancer in populations exposed to arsenic in drinking water (HUS, ,1996). In addition, USEPA has stated that the carcinogenicity assessment for arsenic may be revised, pending a review of data regarding internal cancers associated with oral exposure to arsenic (IRIS, 1996). The USEPA has established an oral slope factor of 1.5 (mg/kg-day)'1 for arsenic, based on skin cancer in a Taiwanese population exposed to arsenic in drinking water (Tseng, 1977). However, due to uncertainties associated with the unit risk, USEPi A has state•d tha' t ris\ k estimate. s for oral exposur' e to' arsenic may be overstated by as much as an order of magnitude (IRIS. 1996). The USEPA has also established an inhalation unit risk of 0.0043 Mg/m3 for arsenic based on increased lung cancer mortality observed in multiple populations exposed primarily through inhalation (IRIS, 1996). For the purposes of this assessment, the inhalation unit risk value is converted to an inhalation slope factor of 15 (mg/kg-day)-1 (USEPA, 1995). - " . , . In addition, the oral RfD for arsenic of 0.0003 mg/kg-day is based on a study of chronic human exposur*' e to arseni" c in drinking wate' ' r (IRIS..— , 1996). Hyperpigmentation, keratosis' , and possible vascular complications were identified as critical effects. The oral RfD was calculated from a NOAEL of 0.009 mg arsenic/L water (0.008 mg/kg-day) and the application of an uncertainty factor of 3 (IRIS, 1996). This value is currently under reevaluation by USEPA (IRIS, 1996). The Agency has not determined an inhalation RfD value for arsenic. References ATSDR. 1993. Toxicologicaf Profile for Arsenic. Ageiicy for Toxic Substances and Disease Registry, U.S. Public Health Service, Atlanta, Georgia. April HSDB. 1995. Arsenic. Hazardous Substances DataBank, National Library of Medicine, Bethesda, MD. G-40 CHEMRlSK*-A DIVISION OF MCLAREN/HART IRIS. 1996. Arsenic. Integrated Risk Information System, U.S. Environmental Protection Agency, 'Offic ' e of Healt• ' h• an•'-,d Environmenta' ' ..- 'l Assessment. . ,,' Cincinnati;• ,''. OH. . . • ' Tseng, W.P. 1977. Effects and dose-response rehtionships of skin cancer and blackfoot disease with arsenic. Environ. Health Perspect. 19:1*09-119. (As cited in IRIS, 1996). USEPA 1995. Health Effects Assessment Summary Tables, FY-1995 Annual. U.S. Environmental Protection Agency, Office of Solid Waste and Emt^gency RtMpor.se, Washington, D.C EPA/54(yR- 95/036. May. : Weast, R.C(ed). 1985. CRC Handbook of Chemistry and Physics. 66th Edition. Boca Raton, FL: CRC Press, Inc. (Cited in ATSDR, 1993) G-41 OlEMRlSK*-A DIVISION OF MCLAREN/HART Toxicological Profile . Barium -...•' '" - - . - • Chemical Formula Ba * ATSDR. 1990 Molecular Weight ' 137.3 g/mol Weast, 1989 Vapor Pressure 10 mmHg @ 1049°C USEPA, 1984 Boiling Point 1640°C Weast, 1989 MeltingPoint ,725°C ; Weast, 1989 Henry's Law Constant No data ATSDR, 1990 Solubility Decomposes Weast, 1989 Partition Coefficient No data ; Barium and its compounds are used industrially for several purposes. Barium salts are used for drilling mud, pigment, and as x-ray contrast medium. Barium is also used in automotive paints, plastics stabilizers, bricks, tiles, jet fuels, and pesticides. The largest use of mined barite is oil and gas we. n driffin- g (ATSDR- - , 1990).:' '- " - .• •: ;•" • , • Industrial releases of barium are generally in forms which are not likely to be widely dispersed (Ng and Patterson, 1982). Barium in the atmosphere is typically in the paniculate form and removed via wet and dry deposition (USEPA, 1984). It is readily oxidized in moist air, arid maintains an approximate residence time of several days depending on environmental factors and its precise particulate form (Kunesh, 1978; USEPA, 1984) In soil systems barium may be absorbed by vegetation or precipitated through soil matrices (Bates, 1988). The rate of transport is influenced by cation exchange capacity and calcium carbonate content The mobility of barium in soils with high cation exchange capacity will be limited (Kabatas- Pendias and Pendias, 1984; Bates, 1988). Soils with high calcium carbonate content also limit barium's mobility by precipitation of barium as barium carbonate (Lagas et aL, 1984). Additionally, barium mobility in soils may be reduced by the precipitation of barium sulfate (USEPA. 1984). Barium in aquatic systems may adsorb to suspended particulate matter or may precipitate from solution as an insoluble salt such as barium sulfate or barium carbonate (Lagas et aL, 1984; USEPA, G-42 CHEMRJSJC*- A DIVISION OF MCLAREN/HART V flR-30l»l2ij 1984; Bodek et aL, 1988), In sediments, barium is usually present as barium sulfate (Mecefield, 1987). The uptake of barium by aquatic organisms may also be an important removal mechanism. Bioconcentration factors of barium have been estimated for marine animals, plankton, and brown algae at 100,120, and 260, respectively (Bowen, 1966; Schroeder, 1970)i In humans, the insoluble forms of barium are slightly toxic as only minimal amounts can be absorbed. Soluble barium, however, may be highly toxic via ingestion or inhalation. Acute oral exposures to soluble barium compounds may result in cardiovascular effects such as hypertension and ventricular fibrillation (Das and Singh, 1970). Other adverse effects in humans may include gastroenteritis, muscular paralysis, and central nervous system damage. Several researchers have identified acute barium toxicity associated with hypokalemia and electrocardiographs alterations (Diengott et aL, 1964; Gould et aL, 1973; Talwar and Sherma, 1979). .The results of epidemiologicaj studies conducted by Wones et aL (1990) and Brenniman and Levy (1984) indicate conflicting effects after drinking water exposures. Wones et aL (1990) found no significant impacts in subjects administered 5 to 10 mg/L barium chloride for up to 10 weeks. Brenniman and Levy (1984), however, reported significant increases in blood pressure, prevalence of hypertension, stroke, and heart and renal diseases within a community exposed to barium in drinking water at a relative dose of 0.2 mg/kg-day. ( f There are iwava3.u)fei^rts of muttg^ Some reproductive effects have been noted in laboratory -.nimals after inhalation of barium comrwunds.^ For example, a decrease in sperm count, motile sperm percentage, and osmotic resistance of sperm were observed in male rats exposed to 15.8 mg/mj barium carbonate dust via inhalation for one spermatogenesis cycle (Tarasenko et aL, 1977). fateniiediate and chroiiic oral exposure of rats to nominal concentrations of barium in drinking water was not associated with any gross or histopathological lesions of the uterus, ovaries, or testes (McCauley etaL, 1985). USEPA has not classified barium as to potential human carcinogenicity. Likewise, the Agency has not established an oral or inhalation cancer slope factor for barium. ' The USEPA has determined a lifetime RfD of 0.07 mg/kg-day for barium based on a weight-of- evidence approach utilizing various epidemiologic and rodent assays which indicate a potential increase in Wood pressure (Schroeder and Mitchener, 1975a,b; Tardiff et aL, 1980; Perry et aL, 1983; Brenniman and Levy, 1984; McCauley el aL,.1985; Wones et aL, 1990). G-43 CHEMRisK*-A DIVISION OF MCLAREN/HART ' HR30M25 The USEPA has determined an inhalation reference concentration (RfC) of 0.0005 mg/m3 for barium based on fetotoxic eftects in rats exposed to barium via inhalation for 4 months (USEPA, 1995). For the purposes of this assessment, the inh.uation RfC value is converted to an irir^ 0.000143 mg/kg-day as reported in USEPA Region in (1996). / ' ' ' - '. ' . - . " '\ • References , I ~ ' ! . ' ' ATSDIt 1990. Toxicological Profile for Barium: Draft. Agency for Toxic Substances and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public Health Service, Washington, D.C. October. Bates, M.H. 1988. Land farming of reserve pit fluids and sludges: Fates of selected contaminants. Wat Res. 22:793-797. (Cited in ATSDR, 1990). • . : . ' • - ' • , - • ' - ' i • Bodelc, L, W.J. Lyman, W.F. Reehl, et aL (eds). 1988. Environmental Inorganic Chemistry: Properties, Processes, and Estimation Methods. New York, NY: Peramagon Press. (Cited in ATSDR, 1990). Bowen, H.J.M. 1966. Trace Elements in Biochemistry. New York, NY: Academic Press, Inc. '(Cited in ATSDR, 1990). L J Brenniman, G.R. and P.S. Levy. 1984. Epidemiological study of barium in Illinois drinking water supplies. In: Advances in Modern Environmental Toxicology IX, Calabrese, E.J., R.W. Tuthill, and L. Condic (eds). Princeton, NJ: Princeton Scientific Publications, p. 231-240. (Cited in IRIS, 1996) Das, N.C and V. Singh. 1970. Unusual type of cardiac arrest: Case Report. Armed Forces Med. J.India 26:344-352. (Cited in ATSDR, 1990). Diengott, D., O. Rozsa, N. Levy, et aL 1964. Hypokalemia in barium poisoning. Lancet 2:343-344. ' (Cited in ATSDR, 1990). Gould, D.B., M.R. SorreU, and A.D. Lupariello. 1973. Barium sulfide poisoning: Some factors contributing to survivaL Arch. Intern. Med. 132:891-894. (Cited in ATSDR, 1990). G-44 CHEMRisjc*-A DIVISION OF MCLAREN/HART - ' "•'-•. "-' . '' -:' IRIS. 1996. Barium. Integrated ^Information System, U.S. Envirorahental Protection Agency, ' Offic•'e• of•'•'•..:.v.; Health and Environmenta: l•••:-,-. Assessment, Cincinnati- ; ;••, OH'. ..:.. ••-.-... ••..'•• Kabatas-Pendias, A. and H. Pendias. 1984. Trace Elements in Soils and Plants. Boca Raton, FL: CRC Press, Inc. (Cited in ATSDR, 1990). \ Kunesh,C.J. 1978. Bariurn. In: Kirk-Othmer Encyclopedia of Chemical Technology of Chemical Technology. Volume 3, Third Editwn. GraysoivM. and D. Eckroth (^ Wiley and Sons. p. 457-463. (Cited in ATSDR, 1990). Lagas, P., J.P.G. Loch, C.M. Bom., et aL 1984. The behavior of barium in a landfill and the underlying soiL Water, Air, Soil Poll 22:121-129. (Cited in ATSDR, 1990). McCauley, P.T., B.H. Douglas, R.D, Laurie, and R.J. BulL 1985. Investigations into the effect of drinkin1996) g"• watel- r bariu' m/ •o n ^rats .' . Environ.; .•• Healt. •-''h Perspec; . t Vo•'L• - 'DC . ; p. 197-210,-v . (Cited in IRIS, Merefield, J.R. 1987. Ten years of barium build-up in the Teign. Mor. Poll Bull 18:220-222. (Cited in ATSDR,1990). Ng-- , A.'• an' d' C.C' .' • Patterso""^ a 1982^ "•":••. Change•s of•- lea d 'an 'd' bariu'• ' m wit' h timei' • •n Californi' ;". a offshor'••••" '"'e basi"n sediments. Geochim. Cosmochim. Acta 46:2307-2321. (Cited in ATSDR, 1990). Perry, H.M., S.J. Kopp, M.W. Erlanger, and E.F. Perry. 1983. Cardiovascular Effects of Chronic Barium Ingestion. In: Trace Substances in Environmental Health, XVII. Hemphffl, D.D. (ed). Columbia, MO: University of Missouri Press. (Cited in IRIS, 1996) Schroeder, H.A. 1970. Barium: Air Quality Monograph. American Petroleum institute. Washington, D.C. Air Quality Monograph No. 70-12. (Cited in ATSDR, 1990). Schroeder, H.A. and M. Mkchcner. 1975a. Life-term effects of mercury, methyl mercury, and nine other trace metals on mice. / Nutr. 105:452-4.58. (Cited in IRIS, 1996) Schroeder, H.A. and M. Mitchener. 1975b. Life-term studies in rats: Effects of aluminum, barium, beryllium, and tungsten. J.Nutr. 105:421-427. (Cited in IRIS, 1996) r '-*>''•' ' ' ' ,....Vff...... *...V...^...... HHH.flH^^....I.^.^B"B"«V.|.B.H G-45 CHEMRISK*.A DlVTSION OF MCLAREN/HART Tahvar, K.K. and B.K. Sherma. 1979. Myocardial damage due to barium chloride poisoning. Indian . Hear• t J.' 31:244-245.'•--. (Cite, d .-'in ATSDR. , 1990).-' .:- . '••'•--. .'• •-_• ••• (J Tardiff, R.a, M. Robinson, and N.S. Ulmer. 1980. Subchronic oral toxicity of BaClj in rats. /. Environ. Pathol Toxicol 4:267-275. (Cited in IRIS, 1996) Tarasenko, N.Y., O.A. Pronin, and A. A Sflaev. 1977. Barium compounds as industrial poisons (an experimental study). J.Hyg.EpidemolMicrobioilmmunoL 21:361-373. (Cited in ATSDR, 1990). USEPA. 1984. Health Effects Assessment for Barium. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, Cincinnati, OH. EPA/540/1-86/021. USEPA. 1995. Health Effects Assessment Summary Tables, FY-1995 Annual. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, D.C. EPA/540/R- 95/036. May. USEPA. 1996. Risk-Based Concentration Tables, January - June 1996. Dr. Roy L, Smith, U.S. Environmental Protection Agency, Region Hi, Office of RCRA, Technical and Program Support Branch, Philadelphia, PA. ApriI30. Weast, R.C. (ed). 1989. CRC Handbook of Chemistry and Physics. 70th Edition. BocaRaton, .7"^ FL: CRC Press, Wones, R.G., B.L. Stadler, and L.A. Frohman. 1990. Lack of effect of drinking water barium on cardiovascular risk factor. Environ. Health, ferspect 85:1-13. (Cited in IRIS, 1996) G-46' CHEMRlSK*-A DIVISION OF MCLAREN/HART Toxidty Profile Ui , . . ' . • . Benzene , , . , • - . ' •,..;/ . ' : Chemical Formula C^ HSDB, 1995 Molecular Weight 78.11 , ' HSDB, 1995 VaporPressure 95.2 mmHg @ 25°C OHM/TADS, 1990 Boiling Point 80.1°C HSDB, 1995 Melting Point 5.5°C HSDB, 1995 Henry's Law Constant 5.5xlQ"3 atm-mVmol Mackay and Leinonen, 1975 Solubility 1,780 mg/L @ 25°C Mackay and Leinonen, 1975 Liquid Diffusion Coefficient 8.65x10"* cm'/sec Lyman et aL, 1990 Gaseous Diffusion Coefficient 9.84xlO~2 cmVsec Lyman et aL, 1990 Partition Coefficients ; logK,,. 2.15 Gossett etaL, 1983 1.9 HSDB, 1995 Benzene is used primarily as an intermediate in the manufacture of other chemicals such as f j ethylbenzene, cumene, cyclohexane, and nitrobenzene (ATSDR, 1995). It is also employed as a solvent, reactant, and component of gasoline (Brief et aL, 1980; Holmberg and Lundberg, 1985; OSHA, 1987). In addition, benzene may be used in such products as paints, rubber cements, adhesives, paint removers, leathers, printing, pesticides, and fumigants OSHA, 1977; ATSDR, 1995). In the environment, benzene vplatifizes readily from water and soils to the atmosphere where it exists primarily in the vapo, r phase (Eisenreic'\ 'h et aL,' 198 1). Th.e primar' ' y degradation proces• s for benzen> . e in the atmosphere is reaction with hydroxyl radicals (ATSDR, 1995). Residence time for benzene has been estimated within a range of 2.1 hours to 8 days based on a vapor phase reaction with photochemically produced hydroxyl radicals (Gaflhey and Levihe, 1979; Lyman et aL, 1982). It may also be removed from the atmosphere via wet deposition, although benzene removed due to this process is likely to revolatilize to the atmosphere (ATSDR, 1995). Additionally, direct photolysis of benzene in the atmosphere is not likely (Bryce-Smith and Gilbert, 1976). Released to soil systems, benzene may volatilize to the atmosphere, partition to surface water through runoff, and leach to groundwater. Tucker et aL (1986) estimated that 67 percent of benzene released 'G-47 CHEMRJSK*. A DIVISION OF MCLAREN/HART to soil would volatilize while 29 percent would leach to groundwater. Additionally, benzene may also biodegrade in aerobic soils. Study models indicate that 1 percent benzene released to soils would biodegrade over a 17-month period (Tucker et aL, 1986; ATSDR, 1995). Benzene in aquatic systems is readily released to the atmosphere via volatilization. A volatilization ' half-life of 4.81 hours has been estimated for benzene at 1-meter deep and 25°C (Mackay and Leinonen, 1975). Additionally, a half-life of 16.9 days was reported for the photolysis of benzene dissolved in oxygen-saturated deionized water (ATSDR. 1995). Another half-life of 0.71 years has been estimated for a benzene reaction with hydroxyl radicals (Anbar and Neta, 1967). Benzene in surface and groundwater may undergo biodegradation via microorganisms. Reported half-lives for aquatic btodegradatton of benzene range from 8 to 28 days (Delfino and Miles, 1985; Vaishnav and Babeu, 1987; Chiang et aL, 1989; ATSDR, 1995). Btoconcentration and biomagnification of benzene within aquatic organisms and foodchains is expected to be minimal (Gossett et aL, 1983; Geyer et aL, 19«4; Ogataet aL, 1984; Miller et aL, 1985; ATSDR, 1995; HSDB, 1995). 1 '• . • . ' A number of studies indicate carcinogenic effects among humans exposed to benzene. A study of Turkish shoe workers indicated an increased incidence of leukemia for individuals employed for 1 to 15 >ears and subjected to peak exposures of 210 to 650 ppm (Aksoy et aL, 1974). A retrospective cohort mortality study of males exposed to benzene in the manufacturing of rubber products also suggests a significant increase of leukemias (Infante etaL, 1977a,b). Likewise, Rinsky etaL (1981) t j observed a statistically significant increase of leukemia in a subsequent retrospective cohort mortality study with the same study group. Ott et aL (1978) and Wong et aL (1983) have also reported mortality due to leukemia among chemical workers exposed to benzene. In animals, the development of neoplasia has been reported as a result of benzene exposure via inhalation and gavage. Maltoni and Scamato (1979) and Maltoni et aL (1983) reported dose-related increased incidences of mammary tumors, Zymbal gland carcinomas, oral cavity carcinomas, and leukemias in Sprague-Dawtey rats administered benzene via gavage at concentrations of 0,50,250, or 500 mg/kg-bw for life. Another gavage study with rats and mice treated at concentrations of 0, 25. 50, 100, or 200 mg/kg-bw for 103 weeks resulted in a significantly increased incidences of Zymbal gland carcinomas in rats and mice of both sexes. Additionally, oral cavity tumors were observed in rats of both sexes, while males also showed increased incidences of skin tumors. Lympnomas and lung tumors were reported for both male and female mice. In general, the effects were considered dose-related (NTP, 1986). . oflojriwwBinNcwi9ntfTMJusiwMAi.pwihwmj.wpD G-48 < CHEMRISK*-A DIVISION OF MCLAREN/HART «R30'lil30 The USEPA has classified benzene as a Group A carcinogen, human carcinogen, based on adequate evidence in humans and animals (IRIS, 1996). The Agency has established an oral cancer slope factor of 0.029 (mgfcg-day)*1 for benzene based on the results of several studies which suggest an increased incidence of nonlyraphocytic leukemia from occupational exposure (Aksoy et aL, 1974; Infante, i97,7a,b; Ott et aL, 1978; Aksoy, 1980; Rinsky et aL, 1981; Wong etaL, 1983), and an increased incidence of neoplasia in rats and mice exposed via inhalation and gavage (Maltoni and Scarnato, 1979; Maltoni et aL, 1983; NTP, 1986). The Agency has not established an inhalation cancer slope factor for benzene. However, the USEPA has derived an inhalation unit risk value of 0.0000083 (IRIS, 1996). ' • Finally, the USEPA has not developed an oral or inhalation RfD value for benzene (IRIS, 1996). In lieu of verified values, a provisional inhalation RfD value of 0.00171 mg/kg-day and a provisional oral RfD value of 0.003 mg/kg-day was applied in this assessment. These values were obtained from the USEPA Region in guidance documents for RCRA sites and is regarded as a provisional value. References Aksoy, M., S. Erdem, and G. DincoL 1974. Leukemia in shoeworkers exposed chronically to benzene. S/ww/. 44(j6):837-841. (Cited in IRIS, 1996) ~ ' Aksoy, M. 1980. Different types of malignancies due to occupational exposure to benzene: A review of recent observations in Turkey. Environ. Res. 23:181. (Cited in IRIS, 1996) i ... > ' • - ' • ' • '' Anbar, M. and P. Neta. 1967. A compilation of specific bimolecular rate constants for the reaction of hydrated electrons, hydrogen atoms and hydroxyl radicals with inorganic and organic compounds in aqueous solutions. Internal. J. ApplRad. Isotopes 18:493-523. (Cited in ATSDR, 1995) ) " ' • ' , .- ' . • x '" ATSDR. 1995. Toxicological Profile for Benzene: Draft. Agency for Toxic Substances and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public Health Sente, Washington, D.C. August. Brief, R.S..J. Lynch, T. Bernath et aL 1980. Benzene in the workplace. Am. Ind. Hyg.Assoc. J. 41:616-623. (Cited in ATSDR, 1995) ! G-49 CHEMRJSK*-A DIVISION OF MCLAREN/HART Bryce-Smith, D. and A. Gilbert 1976. Inorganic photochemistry of benzene: I. Tetrahedron. 32:1309-1326. (Cited in ATSDR, 1995) Chiang,C.Y.,J.P.Slanitro,EY.ChaietaL 1989. Aerobic biodegradation of benzene, toluene, and xyfene in a sandy-aquifer-data anarysis and computer modeling. Ground Water 27:823-834. (Cited in ATSDR, 1995) Delfino, J.J. and CJ. Mites. 1985. Aerobic and anaerobic degradation of organic contaminants in Florida groundwater. Soil and Crop Science Society of Florida 44:9-14. (Cited in ATSDR, 1995) •, ' ' N ' ' * X . Eisenreich, S.J., B.B. Looney, and J.D. Thomton. 1981. Airborne organic contaminants in the Great Lakes ecosystem. Environ. Sci Technol 15:30-38. (Cited in ATSDR, 1995) Gafihey, J.S. and S.Z. Levine. 1979. Predicting gas phase organic molecular reaction rates using linear free-energy correlations: I. O(3P) and OH addition and subtraction reactions. Int J. Chem. •JBnietXI:1197-1209. (Cited in ATSDR, 1995) "--.•• \ * - ' • - ' 1 . ' . Geyer, H., G. Politzki, and D. Freitag. 1984. Prediction of ecotoxicological behavior of chemicals: Relationship between n-octanol/water coefficient and bioaccumulation of organic chemicals by alga Cruorella. Chemosphere 13(2):269-284. (Cited in ATSDR, 1995) Gossett, R.W., D.A. Brown, and D.R. Young. 1983. Predicting the bioaccumulation of organic compounds in marine organisms using octanol/water partition coefficients. Mar. Pottut Bull 14(10)387-392. (Cited in ATSDR. 1995) Holmberg, B. and P. Lundberg. 1985. Benzene: Standards, occurrence, and exposure. Am. J. Ind. Med. 7:375-383. (Cited in ATSDR, 1995) HSDB. 1995. Benzene. Hazardous Substances DataBank, National Library of Medicine, Nattonal Institutes of Health, Bethesda, MD. . "/ Infante, P.F., R.A./ Rinsky, J.K. Wagoner, and R.J. Young. 1977a. Benzene and leukemia. The Lancet. 2(8043):867-869. (Cited in IRIS. 1996) G-50 CHEMRISK*- A DIVISION OF MCLAREN/HART -1ROM3-2 Infinite, PJF., R.A. Rinsky, J.K. Wagoner, and R.J. Young. 1977b. Leukemia in benzene workers. Th• e Lancet•• .'.•'•.- 19:76-78.• (Cite-:d- i•...,-.-••n IRIS, 1996) • -. i;.' '• - ."- •-'•• y •.• •-"•' IRIS. 19?6. Benzene. Integrated Risk mfonnation Systen\ IJ.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati. OH. '. ' ' i . ' • , . - , Lyman, WJ. 1982. Atmospheric Residence Time. In: Handbook of Chemical Property Estimation Methods: Environmental Behavior of Organic Compounds. W.J, Lyman, W.F. Reehl, and D.H Rosenblatt (eds.). New York, NY: McGraw-HilL (Cited in ATSDR, 1995) Lyman, WJ., W.H. Reehl, and D.H. RosenblatL 1990. Handbook of Chemical Property Estimation Methods: Environmental Behavior of Organic Compounds. Washington, DC: American Chemical • ' •• . • Society. • " . ; ; . .: • '._'•', v • , ! Mackay, D. and PJ. Leinonen. 1975. Rate of evaporation of low-solubility contaminants from water bodies to atmosphere. Environ. Sci. Technol 9:1178-1180. (Cited in ATSDR, 1995) 1 ,'"''' ' •, Maltoni, C, B. Conti, and G. Cotti. 1983. Benzene: A multipotential carcinogen. Results of long - term bioassays performed at the Bologna Institute of Oncology. Am. J. Ind. Med. 4:589-630. (Cited I inlRIS, 1996) ' , i -.-.•' ' ' Maltoni, C. and C Scamato. 1979. First experimental demonstration of the carcinogenic effects of benzene. Long-term bioassays on Sprague-Dawley rats by oral administration. Aftfdl £^v. 70:352- 357. (Cited in IRIS, 1996) Mflkr, M.M., S.P. Wasik, G.L. Huang et aL 1985. Relationships between octanol-water partition coefficients and aqueous solubility. Environ. Sci. Technol 19:522-529. (Cited in ATSDR, 1995) NTP. 1986. Tmdcohgya^ Carcinogenesis Studies of Benzene (C^ and B6C3F1 Mice (Gavage Studies). NTP Techru\;al Report Series No. 289. Nattor^ Toxkotogy Program, National Institutes of Health. Ogata, M., K. Fujisawa, Y. Ogino et aL 1984. Partition coefficients as a measure of bioconcentration potential of crude oil compounds in fish and shellfish. Bull Environ. Contam. Toxicol 33:561-567. (Cited in ATSDR, 1995) iM*M^ G'51 CHEMRlSK*.ADrVISION OFMCLAREN/HART AR30I»'I33 OHMS/TADS. 1990. Oil and Hazardous Materials/Technical Assistance Data System. Chemical Information Systems, Inc., Baltimore, MD. (Cited in ATSDR, 1995) - . • -:' '• • . ."• '• - ' - •: ''. '• ' •-': "••' -V OSHA. 1977. Final Environmental Impact Statement: Benzene. U.S. Department of Labor, Occupational Safety and Health Administration, Washington, D.C. Federal Register 42:22516- 22529. (Cited in ATSDR, 1995) OSHA. 1987. Time-Weighted Average Limit. Occupational Safety and Health Standards. Benzene. U.S. Occupational Safety and Health Administration. Code of Federal Regulations 40 CFR 1910.1028(c)(l). (Cited in ATSDR, 1995) - Ott, M.G., J.C. Townsend, W.A. Fishbeck, and R.A Langner. 1978. Mortality among individuals occupationally exposed to benzene. Arch. Environ. Health. 33:3-10. (Cited in IRIS, 1996) Rinsky, R.A., A.B. Smith, R. Hornung et aL 1987. Benzene and leukemia. New England J. Med. 316(17):1044-1050. (Cited: in IRIS, 1996) Rinsky, R.A., RJ. Young, and AB. Smith. 1981. Leukemia in benzene workers. Am, J. Ind. Med. 2:217-245. (Cited in IRIS. 1996) .- ' '. •-•:• = , •' ••-..-' -.' ' -: •'••" .' -• '- Tucker, W.A., C. Huang. J.M. Bral et aL 1986. Validation of transport model In: Benzene in Florida Groundwater: An Assessment of the Significance to Human Health. Florida Petroleum Council, American Petroleum Institute, Tallahassee, FL. (Cited in ATSDR, 1995) USEPA. 1996. Risk-Based Concentration Table, January - June 1996. Dr. Roy L. Smith, U.S. Environmental Protection Agency, Region m, Office of RCRA, Technical and Program Support Branch, Philadelphia. PA. April 30. Vaishnav, D.D. and L. Babeu. 1987. Comparison of occurrence and rates of chemical biodegradation in natural waters. Bull Environ. Contam. Toxicol 39:237-244. (Cited in ATSDR, 1995) Wong,O.,R. W.Morgan, and MJXWhorton. 1983. Comments ontheNIOSHStudy ofLeukemia in Benzene Workers. Technical Report submitted to Gulf Canada, Ltd. by Environmental Health Associates. (Cited in IRIS, 1996) " G-52 CHEMR^K*-A DIVISION OF MCLAREN/HART Toxidty Profile 1 • ' > ' ; . ' - " ' •' ' - Beryllium ' . Chemical Formula Be ATSDR, 1991. Molecular Weight 9.012 Weast, 1985 Vapor Pressure 1 mrnHg @ 1,520°C Weast. 1985* BoilingPoint 2,970°C Ballance et aL, 1978 Melting Point 1,287-1,292°C Ballance et aL, 1978 Henry's Law Constant No data ATSDR, 1991 Solubility Insoluble USEPA, 1987 Partition Coefficients , -No data ATSDR, 1991 . Nodata . ATSDR, 1991 Beryllium can be mobilized in the environment from natural or anthropogenic sources The largest emission of beryllium is the combustion of coal and fuel oil ( ATSDR, 1991). Ore processing, metal fabrication, beryllium oxide production and use, and municipal waste combustion represent much more minor sources of beryllium mobilization. Beryllium can be transported to surface waters ' through weathering of soils and rocks, effluents from beryllium industries, and runoff from beryllium ^ — * containing waste sites (ATSDR, 1991). Beryllium may exist naturally in soils or be deposited in sous as a result of disposal of wastes containing beryllium or atmospheric deposition of airborne beryllium (ATSDR, 1991). In the atmosphere, beryllium particulates will be removed by wet and dry deposition. In water and . soil, beryllium will likely be relatively immobile, existing in insoluble form in sediments and soils. Beryllium in water is not expected to bioconcentrate significantly in aquatic organisms; however, bottom-feeding organisms may bioconcentrate beryllium from sediments to some degree (ATSDR, 1991). '..'.' • '. . . \ The respiratory system is a major target for beryllium toxicity in both humans and animals (ATSDR, 1991). Inhalation of high concentrations of soluble beryllium compounds is associated with chemical pneumonitis; inhalation of less soluble forms may lead to chronic beryllium disease with reductions in lung function. Information on effects after oral exposure to beryllium indicates lower toxicity by G-53 CHEMRISK*-A DIVISION OF MCLAREN/HART * ' - this route; studies in animals suggest few systemic effects after oral exposure. Rats exposed to beryllium intheir diets developed rickets (ATSDR, 1991). . The USEPA has classified beryllium as a Group B2 carcinogen, probable human carcinogen, based on inadequate data in humans and sufficient data in animals. Beryllium has been shown to induce various types of tumors in primates and rats via, inhalation and intratracheal instillation exposures, and in rabbits via intravenous or intramedullary injection (IRIS, 1996). The USEPA has established an oral cancer slope factor of 4,3 (mg/kg-day)'1 for beryllium based upon ' the numbers of observed tumors in the exposed group of a study in which male Long-Evans rats were given drinking water containing 5 ppm beryllium sulfate for a lifetime (Schroeder and Mitchener, 1975; IRIS, 1996). The Agency has also published an inhalation cancer slope factor of 8.4 (mg/kg- day)*1 based on the presence of lung tumors in humans due to occupational exposures to beryllium (USEPA, 1995). In addition, the USEPA has determined an inhalation unit risk value of 0.0024 Mg/m3 (IRIS, 1996). The chronic oral RfD value for beryllium is based upon the same study as the oral cancer slope factor. Upon natural death, the animals were examined for gross and microscopic changes in the heart, kidney, liver, and spleen as well as some serum chemistry parameters. No adverse effects were observed in the group dosed at 5 ppm beryllium sulfate in drinking water. The water concentration I J of 5 ppm was assumed to represent a NOAEL and was converted to 0.54 mg/kg-day. An uncertainty factor of 100 to account for interspecies and interindividual variability was applied to the NOAEL to derive the oral RfD value of 0.005 mg/kg-day (IRIS, 1996). Additionally, the USEPA has not proposed an inhalation RfD value for beryllium. References ATSDR. 1991. Toxicological Profile for Beryllium; Draft for Public Comment Agency for Toxic Substances and Disease Registry, Atlanta. GA and U.S. Department of Health and Human Services, Public Health Service. October. , / Ballance, J., AJ. Sonehouse, R. Sweeney et aL 1978. Beryllium and Beryllium Alloys, IK Kirk- r Othmer Encyclopedia of Chemical Technology, 3rd Edition, Volume 3. Grayson, M. and D. . Eckroth. (eds). New York, NY: John Wiley & Sons, Inc. 803-823. (Cited in ATSDR, 1991) G-54 CHEMRis K*. A DIVISION OF MCLAREN/HART ;iR30U'!36 HSDB. 1995. Beryllium. Hazardous Substances DataBank, National Library of Medicine, National u •'Institute • s o.f Health- ••, Bethesda• •• ,••••;•. MD. • - ••'•"•• •-'•• -" '.'.•••' IRIS. 1996. Beryllium. Integrated Risk Information System, U.S. Environmental Protection Agency,Office of Health and Environmental Assessment, Cincinnati, OH. ' • • ' ! . ' " •' ' ' , - . •"'',-•• ' ,' ' " ' '' Schroeder, HA and M. Mitchener. 1975. Life-term studies in rats: Effects of aluminum, barium, beryllium, and tungsten. J.Nutr. 105:421-427. (Cited in IRIS,; 1996) USEPA. 1987. Health Assessment Document for Beryllium. U.S. Environmental Protection , .- Agency, Environmental Criteria and Assessment Office, Office of Health and Environmental Assessment, Research Triangle Park, NC. EPA/600/8-84/026F. (Cited in ATSDR, 1991) USEPA 1995. Heal^ Effects Assessment Summary Tables, FY-1995 Annual. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, D.C. May. EPA/54(VR-95/036. -, Weast, R.C. (ed). 1985. CRC Handbook of Chemistry and Physics, 66^ Edition, ^oca^ion,^ CRC Press, Inc. (Cited in ATSDR, 1991) G-55 CHEMRJSK*- A DIVISION OF MCLAREN/HART ;»R3'O.I»-I37 Toxicity Profile ..... -. ; (.''-1 * , '., ,. •' • ' Cadmium Chemical Formula ,< Cd , ATSDR, 1991 Molecular Weight 112.4g/mol , Sax and Lewis, 1987 VaporPressure lmmHg@394°C Sax and Lewis, 1989 Boiling Point 767°C ^ / Sax and Lewis, 1987 MeltingPoint 320.9°C Sax and Lewis, 1987 Henry's Law Constant No data . ATSDR, 1991 Solubility Insoluble Sax and Lewis, 1987 Partition Coefficient No data ATSDR, 1991 Cadmium is a naturaUy-occurring silver-white metal which is used for a number of industrial purposes. These include electroplating, color pigmenting of plastics and paints, as an electrode component in batteries, and in the production of copper-cadmium alloys (Friberg et aL, 1986; ATSDR, 1991) • ": :'-. ."•'. -• •' ' •• .;/:, • •- : •'• Cadmium emitted to the atmosphere is usually present as small particles (below 10 fan) in the respirable range (ATSDR, 1991). These particles may be subject to long range transport from 100 km to a few thousand km and maintain a typical residence time of 1 to 10 days (Keitz, 1980). Atmospheric levels of cadmium may be removed via wet and dry deposition (USEPA, 1984). Smaller particles (<3 ^m) of cadmium may remain longer in the atmosphere prior to removaL The common cadmium compounds in the atmosphere are stable and not subject to photochemical reactions (ATSDR, 1991). Cadmium concentrations in U.S. ambient air generally range from 0.001 to 0.02 ^g/m3 (USEPA, 1981). Concentrations as high as 0.5 g/m3, however, may be found in industrialized urban areas (Friberg et aL, 1974). In soil systems, cadmium may leach into water under acklic conditions (Callahan et aL, 1979; Elinder, 1985). Transformation processes for cadmium in soils includes precipitation, dissolution, comptexation, and ion exchange. Factors affecting cadmium transformation in soils include cation exchange capacity. pH, and the content of clay minerals, carbonate minerals, oxides, organic matter, and oxygen (McComish and Ong, 1988). G-56 CHEMRJSK*.A DIVISION OF MCLAREN/HART IR3UM38 In natural waters, cadmium exists primarily in the +2 oxidation state and is not influenced by the oxidizing or reducing potential of the water. In aquatic systems, cadmium concentration is inversely related to pH and organic material concentration (Callahan et aL, 1979). The primary removal processes are precipitation and sorption to organic materials and mineral surfaces. (ATSDR, 1991). Callahan et aL (1*979) reported that cadmium concentrations in sediments may reach more than one order of magnitude higher than in the water column. In addition, cadmium may bioaccumulate within aquatic food chains hundreds to thousands of times greater than in the water. Bioconcentration factors for invertebrates and fish have been reported ranging from 113 to 18000 and from 3 to 2213, respectively (USEPA, 1985; van Hattum et al, 1989). , Cadmium is poorly absorbed after exposure via ingestion. Inhaled cadmium, particularly as soluble compounds, is more extensively absorbe^. Once absorbed, cadmium has a strong affinity for the liver and kidney and tends to accumulate in the body. The main route of excretion is through urine. No '"'•''homeostati.c i mechanis ' . m is known for' cadmium and the removal' of absorbe'd cadmiu• m from the body is a slow process (USEPA, 1984). •.., • ' . ' • . ^ The major adverse health effect associated with long-term cadmium exposure is kidney dysfunction, which can lead to disturbances in mineral metabolism and ultimately to the formation of kidney stones. Proteinuria, excretion of unmetabolized proteins in the urine, is one of the most sensitive • L j indicators of renal damage. Hypertension has also been associated with cadmium exposure. The potential role of cadmium in hypertension or the levels at which this effect might occur, however, are currently unknown (ATSDR, 1991). Thun etaL (1985) reported a two-fold excess risk of lung cancer in cadmium smelter workers. This study, however, is considered to supply limitei d evidence of' huma' J n carcinogenicit• y due to low/ ' observed standard mortality ratios and a lack of evidence of a causal relationship of cadmium exposure (IRIS, 1996). Similar investigations have also reported excess lung cancer risk due to cadmium exposure, but these studies may have been Compromised by a small study population or by the presence of other carcinogens such as arsenic or smoking (Armstrong and Kazantzis, 1983; Sorahan and Waterhouse, 1983; Varner, 1983). The most typical effect of chronic, low-level exposure to cadmium by experimental animals is renal dysfunction. Significant immune suppression has also been noted with oral exposures in mice and rabbits to cadmium chloride (USEPA, 1981). Additionally, a significant increase in lung tumors was G-57 CHEMRlSK*-A DIVISION OF MCLAREN/HART ' ,1RJOI»I39 observed by Takenaka et aL (1983) in Wistar rats exposed to concentrations ranging from 12.5 to 50 Mg/m3 for 18 months. x \ Available data suggest that cadmium a mutagenic in mammalian rrif culture assay 3y:teni3, Cadmium has been demonstrated to be mutagenic in both the mouse lymphoma assay and in the Chinese hamster cell assay (ATSDR, 1991). 1 . '" /' • v , ' ' Cadmium has not been found to cause reproductive or developmental effects in humans. Decreased ~ birth weight as well as teratogenic effects, however, have been reported following cadmium exposure in experimental animals; Perineal doses of cadmium have caused severe injury to the gonads of - experimental animals resulting in reduced fertility or complete sterility. Oral exposure of cadmium to both male and female animals have not significantly affected reproductive function (ATSDR, 1991). Cadmium is classified by the USEPA as a Group B1 carcinogen, probable human carcinogen, by inhalation (IRIS, 1996). An association between lung cancer and inhalation exposure to cadmium has been suggested by epidemiologic studies of occupational exposures. No epideraiologic studies of cancer induction in humans due to exposure to the oral route have been conducted (ATSDR, 1991). While studies with experimental animals have also shown cadmium to be carcinogenic by inhalation, oral studies in animals have found no significant carcinogenic effects. The USEPA has not established an oral cancer slope factor for cadmium. The Agency has published an inhalation unit risk of 0.0018 Mg/m3 based on a study by Thun et aL (1985) and an inhalation slope factor of 6.3 (mg/kg-day)"1. In this study, lung, trachea, and bronchus tumors were elevated relative to controls (IRIS, 1996). Oral RfDs were calculated separately by USEPA for ingestion of cadmium in food and in water. Both values are based on a level of cadmium in humans in the renal cortex of 200 Mg/g, identified as a no^bserved-adverse-eSect-level (NOAEL) for proteinuria. A toxicokinetic model was applied to determine the level of chronic cadmium exposure which would result in 200 Mg/g in the renal cortex. It was assumed that absorption of cadmium from water and food are 5% and 2.5%, respectively. In calculating the RfDs, a modifying factor of 10 was applied to account for sensitive individuals within the human population. The resultant RfDs for cadmium are 0.0005 mg/kg-day in water, and 0.001 mg/kg-day in food (IRIS, 1996). Finally, the Agency has hot published an inhalation RfD value for cadmium. , G*58 CHEMRisic'-A DIVISION OF MCLAREN/HART '•• References . •/ • __ /"•,•., '". • . • - ;; ;-., ' ,.,!".'.'•'.'. V_y Armstrong, B.G. and G.Kazantzis. 1983. The mortality of cadmium workers. Lancet 1425-1427. (Cited m IRIS, 1996) : *• ' . .'•'.• , - • ' ' i .•''.. ' , - '; ' • 1 ' ' ATSDR. 1991. Toxicological Profile for Cadmium: Draft. Agency for Toxic Substances and Disease Registry, Atlanta, GA and U.S. Department of Health and Human Services, Public Health Service, Washington, D.C. October. ' Callahan, M.A., KtW. Slimak, N.W. Gable, et aL 1979.. Water-Related Fate of 129 Priority Pollutants. U.S. Environmental Protection Agency, Office of Water Planning and Standards, Washington, D.C. EPA-440/4-79-029a. Blinder, C.G. 1985. Cadmium: Uses, occurrence and intake. In: Cadmium and Health: A Toxicological and Epidemiological Appraisal. Volume I. Exposure, Dose, and Metabolism. Friberg, U. C.G. EKnder, T. Kjellstrom, G.F. Nordberg (eds.). Boca Raton, FL: CRC Press, p. 23- 64. (Cited in ATSDR, 1991) Friberg, L., M. Piscator, G.F. Nordberg, et aL 1974. Cadmium in the Environment 2nd Edition. Boca Raton, FL: CRC Press. (Cited in ATSDR, 1991) : < . . ^ - . , . , ' • , ••,'-. . ^ Friberg, L., C.G. Blinder, T. Kjellstrom, et aL 1986. Cadmium and Health: A Toxicological and Epidemiological Appraisal Volume 2. Effects and Response. Boca Raton, FL: CRC Press. (Cited mATSDR,1991) IRIS. 1996. Cadmium. Integrated Risk Information System, U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Cincinnati, OH. Keitz, E.L. 1980. Atmospheric Cycles of Cadmium and Lead1 Emissions, Transport, Transformation and Removal The Mitre Corporation, McLean, VA. (Cited in ATSDR, 1991) McComish, M.F. and J.H. Ong. 1988. Trace metals. In: Environmental Inorganic Chemistry: Properties, Processes, and Estimation Methods. New York, NY: Pergamon Press. (Cited in ATSDR, 1991) ; ' : G-59 , CHEMRlSK*-A DIVISION OF MCLAREN/HART Thun,MJ.,T.M.Schnorr,AB. Smith, and W.E. Halperin. 1985. Mortality among a cohort of U.S. cadmium production workers: An update. 'J. Natl Cancer Inst 74(2):325-333. (Cited b IRIS, / 1996) ' " '. - . i /" .. - • Sax, N.L. and RJ. Lewis. 1987. Hawley's Condensed Chemical Dictionary, llth Edition. New York, NY: Van Nostrand Reinhold Company. p. 196*198. Sax, N.I. and RJ. Lewis. 1989. Dangerous Properties of Industrial Materials: Volume II. 7th Edition. New York* NY: ,Van Nostrand Reinhold Company, p. 664-672. Sorahan* T. and J.A.R Waterhouse. 1983. Mortality study of nickel-cadmium battery workers by the method of regression models in life tables. Br. / //^ A/«£ 40:293-300. (Cited in IRIS, 1996) Takenaka, S., R Oldiges, R Konig, D. Hochrainer, and G. Oberdoerster. 1983. Carcinogenicity of cadmium aerosols in Wistar rats. /. Natl Cancer Inst 70:367-373. (Cited in IRIS, 1996) i / ^ • • * "• ' . , USEPA. 1981. : Health Assessment Document for Cadmium. U.S. Environmental Protection Agency, Office of Research arid Development, Research Triangle Park, NC. EPA-600/8-81-023. USEPA. 1984. Health Effects Assessment for Cadmium, U.S. ErivirQi^n^ Environmental Criteria and Assessment Office, Cincinnati, OR EPA/540/1-86/038. * - r' ' • •''•'- i , ''..-- . USEPA.1 1985. Cadmium Contamination of the Environment: An Assessment of Nationwide Risk. U.S. Environmental Protection Agency, Office of Water Regulations and Standards, Washington, D.C EPA-440/4-85-023. Van Hattum,B., P. Van den, L. Bosch, etaL 1989. Bioaccumulation of cadmium by the freshwater w^Asellusaquaticus(L) from aqueous and dietary sources. Environ. Poll 62:129-152. (Cited in ATSDR, 1991) \ ' , , ' . - , ~ ' Vamer,M.O. 1983. Updated Epidemiologic Study of Cadmium Smelter Workers. Presented at the Fourth International Cadmium Conference. Unpublished. (Cited in IRIS, 1996) o«*in»WEfnj«(Mi«fT«NLRisiHtaiAppw»rtAmj.wpo G-60 CHEMRlSK*-A DIVISION OF MCLAREN/HART ' Toxidty Profile ; ," • '•'... ". " • , i - . • ". ' ' . ' , . " ! ('i.1' • Chlorobenzene / . Chemical Formula QHjCl HSDB, 1995 r-1 Molecular Weight ", . ' 112.56 Merck; 1989 Vapor Pressure 11.8 mmHg © 25°C HSDB, 1995 Boiling Point 132°C / HSDB, 1995 Melting Point -45.6°C HSDB, 1995 Henry's Law Constant , 3.56x10^ atra-mVmol HSDB, 1995 Solubility ' 448ppm Kenaga, 1980 Liquid Diffusion Coefficient 7.79x10^ cmVsec Lyman et aL, 1990 Gaseous Diffusion Coefficient S.SOxlO"2 cm2/sec Lyman et aL, 1990 Partition Coefficients . i ,.,...• logK,/ , 2.84 Mackay etaL, 1992 2.52 MackayetaL,1992 Chlorobenzene is used extensively as a solvent in pesticide formulation. It is also used in degreasing and other industrial applications (HSDB, 1995). Most Chlorobenzene released to the environment wfll be rapidly volatilized to the atmosphere (HSDB, 1995). The dominant removal mechanism occurs via reaction with hydroxyl radicals with an estimated atmospheric half-life of 9 days with the formation of chbronitrophenols (Singh etaL, 1981). Reaction with nitric oxide in polluted air occurs more rapidly and produces chloronitrophenols and chloronitrobenzene (Kanno and Nojima, 1979). Chlorobenzene in the atmosphere is also influenced by photolysis, but this process occurs slowly and produces monochlorobiphenyl (Uyetta etaL, 1976). Chlorobenzene released to soil systems is likely to volatih^ to the atmosphere (Mackay and Yeun, 1983). The remaining Chlorobenzene not volatilized to the atmosphere is relatively mobile in sandy soils and aquifer material and may leach to groundwater. Moderate adsorption to organic soils is also possibfe. If retained in soil long enough, chlorobenzerte may niineralize or slowly biodegrade (Haider et aL, 1974; Rittmann et aL, 1980; Roberts et aL, 1980; Schwarzenbach and WestaH 1981; Tornson etaL, 1981; Wilson etaL, 1981,1983). :''•'', ' » oKUNTninn«cnt>n\in»JiBii>n>Aii1ndburpaw'n ' G-61 CHEMRBK*-A DIVISION OF MCLAREN/HART ...... f •'•'•. ' " . • . In aquatic systems, Chlorobenzene will be lost primarily due to evaporation. The half-life fpr this process has been estimated at apr^ximate 1983). Biodegradation may also occur during warmer months, occurring more rapidly in freshwater systems than in estuarine or marine waters (Pfaender and Bartholomew, 1982; Bartholomew and Pfaender, 1985). A half-life of 75 days has been reported for Chlorobenzene in an estuarine river system (Lee and Ryan, 1979). Additionally, some adsorption to organic sediments may also occur (Voice etaL, 1983). Carcinogenicity data for human exposure to Chlorobenzene does not exist (HSDB, 1995; IRIS, 1996). The toxic effects of human exposures to Chlorobenzene seem to be primarily liver and kidney injury. Slight skin irritation may occur as a result of dernial application, with repeated contact resulting in moderate erythema and slight superficial necrosis (HSDB, 1995). In one animal study, beagle dogs were administered chtorobenzene orally via capsule at doses of 27.25,54.5, or 272^ mg/kg-day for 13 weeks. Treated animals at the highest dosage were observed to develop histopathologic liver effects such as bile duct hyperplasia, cytotogic alterations, teukocytic infiltration, and centrotobular degeneration. Other reported effects at this concentration included body weight toss and changes in kidney, gastrointestinal mucosa, and hematopoietic tissue (Monsanto Company, 1967). Similar results of fiver effects have also been reported motrier studies with rats and mice exposed to Chlorobenzene via gavage (Irish, 1963; Knapp et aL; 1971; NTP, 1985) ' • '"'"•• ' * " ' '. The USEPA has classified Chlorobenzene as a Group D carcinogen, not classifiable as to human carcinogenicity, based on the absence of human carcinogenicity data, inadequate animal carcinogenic evidence,and predominantly negative genetic toxicity dau in bacterH yeast, arrf mouse lymphoma cells (Monsanto Company, 1976a,b; Lawlor et aL, 1979; Simmon et aL, 1979; IRIS, 1996). In addition, the Agency has not established an oral or inhalation cancer slope factor for chtorobenzene (IRIS, 1996). The USEPA has determined an oral RfD value of 0.02 mg/kg-day based on the results of dog studies in which oral exposure to chtorobenzene produced histopathologic changes in the liver (Monsanto Company, 1967; Knapp et aL, 1971). The Agency has not derived an inhalation RfD value for chtorobenzene (IRIS, 1996). In lieu of a verified value, a provisional inhalation RfD value of 0.00571 mg/kg-day was applied in this assessment This value was obtained from the USEPA Region III (1996) guidance document for RCRA sites and is regarded as a provisional value. G-62 CHEMRISK*-A DIVISION OF MCLAREN/HART ' References Bartholomew, G.W. and F.K. Pfaender. 1983. Appl Environ. Microbiol 45:103-109. (Cited in HSDB.1995) Haider, K. et aL 1974. Arch. Microbiol 96:183-200. (Cited in HSDB, 1995) HSDB. 1995. Chlorobenzene. Hazardous Substances DataBank, National Library of Medicine, National Institutes of Health, Bethesda, MD. IRIS. 1996. Chlorobenzene. Integrated Risk Infonnation System, U.S. Environmental Protec^^ Agency, Office of Environmental and Health Assessment, Cmcinnati, OH. Irish, D.D. 1963. Halogenated Hydrocarbons. D. Cyclic. In: Patty's Industrial Hygiene and Toxicology, Volume II. Fassett, D.W. and D.D. Irish (eds). New York, NY: Interscience Publishers. (Cited in IRIS, 1996) Kanno, S. and K. Nojima. 1979. Chemosphere. 8:225-232. (Cited in HSDB, 1995) Kenaga,E.E. 1980. Ecotox. Environ. Safety. 4:26-38. (Cited in HSDB, 1995) Kjiapp,W.K.,W.MBusey,arriW.Kundzjns. 1971. SubacutcoraltoxKityofmonochtorobenzene on dogs and rats. Toxicol Appl Pharmacol 19:393.-(Cited in IRIS, 1996) Lawtor, T., S.R. Haworth, and P. Voytek. 1979. Evaluation of the genetic activity of nine chlorinated phenols, seven chlorinated benzenes, and three chlorinated hexanes. \Environ. Mutagen. 1:143. (Cited in IRIS. 1996) Lee, R.F. and C.C. Ryan. 1979. Microbial Degradation of Pollutants in Marine Environments. U.S. Environmental Protection Agency, Washington, D.C. EPA-600/9-79-012. (Cited in HSDB, 1995) • " r . ' ' Lyman, WJ..W.R Reehl, and D.R Rosenblatt 1990. Handbook of Chemical Property Estimation Methc&: Environmental Behavfar of Organic Compound Society. G-63 CHEMRlSK*-A DIVISION OF MCLAREN/HART '' 1FUOMI+5 Mackay, D. and A.T.K. Yeun. 19*3. Environ. Sci Technol 17:211-217. (Cited in HSDB..1995) ; .'.-.' '- ;". . -' ' /. ' Mackay, D., W.Y. Shiu, and K.C. Ma. (eds). 1992. Illustrated Handbook of Physical-Chemical Properties and Environmental Fate for Organic Chemicals.. Volume I: Monoaromatic Hydrocarbons, Chlorobenzenes, and PCBs. Chelsea, MI: Lewis Publishers, Inc. Merck. 1989. The Merck Index, llth Edition. Rahway, NJ: Merck & Co., Inc. Monsanto Company. 1976a. Mutageniciiy Evaluation of B10-76*86-CP-5535 (WGK). Final Report. LBI Project No. 2457. Litton Bionetics, Kensington, MD. (Cited in IRIS, 1996) ,. ' --> ' i Monsanto Company. 1976b. Mutagenicity Evaluation ofB10-76-86-CP-5535(LOX). FinalReport LBI Project No. 2457. Uttpn Bionetics, Kensington, MD. (Cited in IRIS, 1996) Monsanto Company. 1967. 13-Week Oral Administration - Dogs. Afonochlorobenzene. Final Report Prepared by Hazleton Laboratories, Project No. 241-105. February24. (Cited in IRIS, 1996) NTP. 1985. Toxicology and Carcinogenesis Studies of Chlorobenzene (CAS M>. 108-90-7) in F344/N Rats and B6C3F1 Mice (Gavage Studies). National Toxicotogy Program, U.S. bepartmcnt of Health and Human Services,^Public Health Service, Natiorol Institutes of Health. NTP No. 261. Nffl Publication No. 83-2517. (Cited in IRIS, 1996) ,.••'•(. Pfaender, F.K. and G.W. Barthotomew. 1982. Appl Environ. Microbiol 44:159-164. (Cited in HSDB.1995) Rittmann, B.E. et aL 1980. Ground Water. 18:236-243. (Cited in HSDB, 1995) Roberts, P.V. etaL 1980. J. Water Pollut Control Fed. 52:161-171. (Cited in HSDB, 1995) Schwarzenbach.R.P.andJ.WestalL 1981. Environ. Sci Technol 15:1360-1367. (Cited in HSDB, G-64 CHEMRISK*-A DIVISION OF MCLAREN/HART Simmon, V.F., EC Ricco, and M.V. Pierce. 1979. In Vitro Microbiological Genotoxicity Ttsts of Chlorobenzene, m-Dichlorobenzene, o-Dichlorobenzene, and p-Dichhrobenzene. Final Report. SRI International, Mento Park, CA ,Unpublished. (Cited in IRIS, 1996) Singh, RB. et aL 1981. Atmos. Environ. 15:601-612. (Cited in HSDB, 1995) • , • . . •'.••' ' - - _ • • • ^ ••• Tomson, M.B. et aL 1981. WaterRes. 15:1109-1116. (Cited in HSDB, 1995) USEPA. 1996. Risk-Based Concentration Table, January-June 7996. Dr. Roy L. Smith, U.g. Environmental Protection Agency, Region m. Office of RCRA, Technical and Program Support Branch,Philadelphia,PA April30. Uyetta> M. et aL 1976. Nature. 264:583-584. (Cited in HSDB, 1995) Voice, T.C. et aL 1983. Environ. Sci. Technol 17:513-518. (Cited in HSDB, 1995) Wilson, J.T. et aL 1983. Devel Indust Microbiol 24. (Cited m HSDB, 1995) .Wilson, J.T. etaL 1981. J. Environ. Qual 10:501-506. (Cited in HSDB. 1995) G-65 CHEMRJSK*-A DIVISION OF MCLAREN/HART