(Ri) and Risk Assessment Report, Volume 4 of 5

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FINAL REMEDIAL INVESTIGATION & RISK ASSESSMENT REPORT CENTRAL LANDFILL OPERABLE UNIT 2 JOHNSTON, RHODE ISLAND VOLUME IV OF V

PREPARED FOR: Rhode Island Resource Recovery Corporation Johnston, Rhode Island

PREPARED BY: GZA GeoEnvironmental, Inc. Providence, Rhode Island

August 2001 File No. 31866.2

REFERENCES REFERENCES

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Burmaster, David E., and J.H. Lehr, 1991. It's Time to Make Risk Assessment a Science, Groundwater Monitoring Review, 11:3.

Canton, S.P., and W.D. Van Derveer, 1997. Selenium Toxicity to Aquatic life: An Argument for Sediment-Based Water Quality Criteria. Env. Tox. Chem., Vol. 16, No. 6, pp 1255-1259.

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Clement Associates, 1988. Toxicity Profile for Polyaromatic Hydrocarbons. Written for U.S. EPA.

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Driver, J.H., J.J. Konz, and O.K. Whitmyre, 1989. Soil Adherence to Human Skin. Bulletin of Environmental Contaminant Toxicology. 43:814-820.

Eisler, R. 1991. Cyanide Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review. U.S. Fish and Wildlife Service. Biological Report 85 (1.23). pp. 55.

EPA, 1980. Ambient Water Quality Criteria (AWQC) for Silver - 1980. EPA Criteria and Standards Division. (EPA-440/5-80-071).

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A-l EPA, 1985a. AWQC for Cyanide -1984. (EPA 440/5-84-028).

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EPA, 1988a. Laboratory Data Validation Functional Guidelines for Evaluating Organic Analyses. November 1988.

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EPA, 1989b. Interim Procedures for Estimating Risks Associated with Exposures to Mixtures of Chlorinated Dibenzo-p-Dioxins and Dibenzofurans (CDDs and CDFs) and 1989 Update. (EPA/625/3-89/016).

EPA, 1989c. Laboratory Data Validation Functional Guidelines for Evaluating Inorganic Analyses. February 1989.

EPA, 1989d. Rapid Bioassessment Protocols for Use in Streams and Rivers: Benthic Macroinvertebrates and Fish. (EPA/440/4-89/001).

EPA, 1989e. Risk Assessment Guidance for Superfund, Volume I: Human Health Evaluation Manual (Part A), Interim Final. (EPA 540/01/89, December 1989)

A-2 EPA, 1989f. Risk Assessment Guidance for Superfund, Volume n - Environmental Evaluation Manual. Interim Final. Office of Emergency and Remedial Response. March 1989.

EPA, 1989g. Soil Sampling Quality Assurance User's Guide, Second Edition. Office of Research and Development. (EPA/600/8-89/046, March 1989).

EPA, 1990. National Primary and Secondary Drinking Water Regulations: Synthetic Organic Chemicals and Inorganic Chemicals. Proposed Rule. (EPA 55FR30370, July 25, 1990).

EPA, 1991. Human Health Evaluation Manual, Supplemental Guidance: Standard Default Exposure Factors. OSWER Directive 9285.6-03.

EPA, 1992a. An SAB Report: Reveiw of Sediment Criteria Development Methodology for Non-Ionic Organic Contaminants. Prepared by the Sediment Quality Subcommittee of the Ecological Processes and Effects Committee. (EPA/SAB/EPEC/93/002).

EPA, 1992b. Dermal Exposure Assessment: Principles and Applications. Office of Health and Environmental Assessment. (EPA/600/6-88/005CC).

EPA, 1992d. Human Health Evaluation Manual, Supplemental Guidance: Standard Default Exposure Factors, OSWER Directive 9285.6-03.

EPA, 1992e. Supplemental Guidance to RAGS: "Calculating the Concentration Term." May 1992.

EPA, 1992f. Framework for Ecological Risk Assessment

EPA, 1993a. Great Lakes Water Quality Initiative Criteria Documents for the Protection of Aquatic Life in Ambient Water. (EPA PB93-154656, February 1993).

EPA, 1993b. Provisional Guidance for Quantitative Risk Assessment of Poly- Aromatic Hydrocarbons. (EPA/600/R-93/089, July 1993, pp. 72).

EPA, 1994. Region I Waste Management Division, Risk Updates (No. 2, August 1994).

EPA, 1995a. An SAB Report: Review of the Agency's Approach for Developing Sediment Criteria for Five Metals. EPA Science Advisory Board. (EPA/SAB/EPEC/95/020, September 1995).

EPA, 1995b. EPA Region HI, Revised Region ffl BTAG Screening Levels, Memo from Robert S. Davis, Biologist Technical Support Section, August 1995.

A-3 EPA, 1995c. EPA Region 4 Ecological Screening Values. Supplemental Guidance to RAGS: Region 4 Bulletins, Ecological Risk Assessment. November 1995.

EPA, 1995d. GZA personal communication with Margaret McDonough from Region I on May 14, 1995.

EPA, 1995e. Integrated Risk Information System (IRIS). National Library of Medicine TOXNET System. (Files updated monthly.)

EPA, 1995f. OU1 RD/RA Statement of Work.

EPA, 1995g. Water Quality Standards; Establishment of Numeric Criteria for Priority Toxic Pollutants; States'Compliance - Revision of Metals Criteria. EPA Office of Water. Federal Register Vol. 60, No. 86. May 4, 1995.

EPA, 1996a. EPA Ecotox Thresholds, ECO Update, Intermittent Bulletin Vol. 3, No. 2. EPA Office of Emergency and Remedial Response, Publication 9345.0-12FSI. (EPA 540/F-95/038, January 1996).

EPA, 1997a. Ecological Risk Assessment Guidance for Superfund.

EPA, 1997b. Health Effects Assessment Summary Tables FY-1997 Update, EPA 540/R 97/036, July 1997.

EPA, 1997c. Exposure Factors Handbook, EPA/600/P-95/002Fa, August 1997.

EPA, 1999. Region 1 Risk Updates, Number 5, September 1999.

ESS, 1988. Trace Metals in Panfish from Rhode Island Fresh Waters. Environmental Science Services. Prepared for: Rhode Island Solid Waste Management Corp., 1988.

ESS, 1993. Central Landfill Fish Sampling and Tissue Analysis. Environmental Science Services. Prepared for: Rhode Island Solid Waste Management Corp.

GRI, 1988. Management of Manufactured Gas Plant Sites. Vol. IE Risk Assessment. GRI-87/0260.3.

Guthrie, R. and J. Stolgitis, 1997. Fisheries Investigations and Management in Rhode Island Lakes and Ponds. RIDEM Fisheries Report No. 3.

GZA, 1993a. Central Landfill Remedial Investigation Report, Operable Unit 1. March 1993.

A-4 GZA, 1993b. Draft Operable Unit 2 Remedial Investigation Work Plan, Central Landfill, Johnston, Rhode Island. May 1993.

GZA, 1993c. Final Feasibility Study, Operable Unit 1, Central Landfill. December 1993.

GZA, 1993d. Upper Simmons Reservoir Sediment Study Phase I Report/Phase II Work Plan. February 1993.

GZA, 1993e, Upper Simmons Reservoir Sediment Study Phase II Report. February 1993.

GZA, 1994a. Ecological Characterization Report. June 1994.

GZA, 1994b. HotSpotPumpTest-OU2-Task3. July 1994.

GZA, 1995a. Monitoring Well Installations - OU2/Task 4 Data Report. October 1995.

GZA, 1995b. Operable Unit 2/Task 5 Residential Well Survey Draft Data Report and Field Sampling Plan. July 1995.

GZA, 1995c. Quality Assurance Project Plan (QAPP). November 1995.

GZA, 1995d. Sampling and Analysis Plan (SAP). November 1995.

GZA, 1995e. Upper Simmons Reservoir Screening Level Risk Assessment for Sediments, Operable Unit 2 Remedial Investigation - Task 1. June 1995.

GZA, 1995f. Draft Work Plan for Baseline Risk Assessment of Operable Unit 2, Central Landfill, Johnston, Rhode Island, June 1995.

GZA, 1996a. Delineation of Groundwater Contamination Emanating From the OUl-Area Technical Memorandum. January 1996.

GZA, 1996b. Draft Multi-media Sampling and Analytical Program Report. June 1996.

GZA, 1996c. Draft Risk Screening and Recommendation Report. July 1996.

GZA, 1996d. Pentennial Water Quality Report. February 1996.

GZA, 1996e. OU2-Task 7-Hot Spot Test Pits. March 1996.

GZA, 1996f. Recommendation for Drilling Location of MW96-ML10 Technical Memorandum. November 1996.

GZA, 1997a. Revised Environmental Monitoring Plan - Central Landfill. May 1997.

A-5 GZA, 1997b. Residential Well Identification Survey Report - OU2/Task 5. July 1997.

GZA, 1997c. Surface Water Flow Monitoring Program - Central Landfill. June 1997.

GZA, 1997d. Task 4A - Deep Well Installations. September 1997.

GZA, 1998. Ecological Risk Assessment Technical Memorandum, January 1998.

Herman, S.G. and J.B. Bulger. 1979. Effects of a Forest Application of DOT on Nontarget Organisms. Wildlife Monographs. No. 69. pp. 5-62.

Hull, R.N. and G.W. Suter n, 1994. Toxicological Benchmarks for Screening Contaminants of Potential Concern for Effects on Sediment-Associated Biota: 1994 Revision. Prepared by Oak Ridge National Laboratory for U.S. Dept. of Energy, Office of Environmental Restoration and Waste Management. ES/ER/TM 95/R1.

Kondakis, X.G., N. Makris, M. Leotsinidis, M. Prinou, and M. Papapetropoulos, 1989. Possible health effects of high manganese concentration in drinking water. Archives of Environmental Health. 44: 175-188.

Long, E.R., Morgan, L.G., 1990. The Potential for Biological Effects of Sediment-Sorbed Contaminants Tested in the National Status and Trends Program. National Oceanic and Atmospheric Administration Technical Memorandum NOS OMA 52. pp. 175.

MA DEP, 1992. Documentation for the Risk Assessment Shortform Residential Scenario. (#WSC/OSC-142-92, October 1992).

Murdock, Alena, and S.D. Mac Knight, 1991. Handbook of Techniques for Aquatic Sediments Sampling. CRC Press, Boston, Massachusetts.

Persaud, D., Jaagumagi, and A. Hayton, 1992. Guidelines for the Protection and Management of Aquatic Sediment Quality in Ontario. Ontario Ministry of the Environment, Queen's Printer for Ontario.

Quebec, 1988. Contaminated Sites Rehabilitation Policy, Direction des Substances Dangereuses, Gouvernment du Quebec, Canada. Depot legal - 2e trimestre 1988. Envirodoq 880100. ISBN 2-550-18630-3.

Richmond, RI Planning Board, 1995. GZA telephone communication with Joe Lombardo. May 30, 1995.

RIDEM, 1992. Rhode Island Department of Water Quality. Community Water System Requirements.

A-6 RIDOH, 1992. Rhode Island Department of Health, Rules and Regulations for Lead Poisoning Prevention. (R 23-24.6PB, February 1992e).

Rojko, A.M., 1990. Heavy Metals in the Sediments of Massachusetts Lakes and Ponds. Master Thesis, Dept. of Civil Engineering, Northeastern University, Boston, Massachusetts.

Suter, G.W. n and J.B. Mabrey, 1994. Toxicological Benchmarks for Screening Potential Contaminants of Concern for Effects on Aquatic Biota: 1994 Revision. Prepared by Oak Ridge National Laboratory for U.S. Dept. of Energy, Office of Environmental Restoration and Waste Management. ES/ER/TM-96/R1.

Suter, G.W. n and C.L. Tsao, 1996. Toxicological Benchmarks for Screening Potential Contaminants of Concern for Effects on Aqatic Biota: 1996 Revision. Prepared by Oak Ridge National Laboratory for U.S. Dept. of Energy, Office of Environmental Restoration and Waste Management. ES/ER/TM-96/R2.

Todd, David Keith, 1980. Groundwater Hydrology. Second Edition. John Wiley & Sons, New York.

USDI, 1981. Groundwater Manual: A Guide for the Investigation, Development, and Management of Groundwater Resources. U.S. Department of the Interior.

Van Derveer, W.D., and S.P. Canton, 1997. Selenium Sediment Toxicity Thresholds and Derivation of Water Quality Criteria for Freshwater Biota of Western Streams. Env. Tox. Chem., Vol. 16, No. 6, pp. 1260-1269.

Verschueren, Karel, 1983. Handbook of Environmental Data on Organic Chemicals, Second Edition, Van Norstrand Reinhold, New York.

Wester, 1990. Wester, RC; HI Majbach; DAW Bucks, L. Sedik, J. Melendres, C.L. Laio, S. DeZio 1990. Percutaneous absorption of [14C]DDT and [14Cbenzo(a)pyrene from soil. Fundam. Appl. Toxicol. 15:510-516.

Wester, 1992. Wester, RC; ; HI Majbach; L. Sedik; J. Melendres; S. DeZio; M. Wade 1992a. In vitro percutaneous absorption of cadmium from water and soil into human skin. Fundam, Appl. Toxicol. 19:1-5.

Wester, 1993. Wester, RC; HI Majbach; L. Sedik; J. Melendres; M. Wade 1993a. In vivo and in vitro percutaneous absorption and skin decontamination of arsenic from water and soil. Fundam. Appl. Toxicol. 20:336-40.

Wetzel, R.G., 1983. Limnology. Second Edition. Saunders College Publishing. New York.

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A-7 APPENDIX B

OU1 RI REPORT SECTION 10 - CONCLUSIONS 10.00 CONCLUSIONS

The Remedial Investigation (RI) at the Central Landfill was separated into two parts. On- site source control issues were addressed in Operable Unit One (OU1) studies, and are described in this report. Issues associated with off-site impacts and ecological concerns are being addressed in Operable Unit Two (OU2) studies. This approach expedited the remedial process by allowing Feasibility Studies (FS), required to address clearly identified remedial needs to proceed, as other RI tasks were being performed

In reviewing our conclusions it is important to note that while the RI/FS process has proceeded, RISWMC has undertaken a number of actions to reduce the potential risks to human health and the environmental posed by site conditions. Most notable are: 1) making public water available to residents in proximity to the site; 2) the installation of a landfill gas (LFG) collection and electrical power generating facility which burns the LFG; 3) the taking of land within 1,000 feet of the licensed landfill to expand the buffer zone; and, 4) the capping of landfill areas as they reach design elevations. Capping was particularly significant in the northeast portion of the landfill where groundwater flow is towards the Almy Reservoir, See Section 10.30.

Our conclusions are based on factual information, scientific principals, and judgement. In order to understand how we reached these and other conclusions, the report must be read in it's entirety. Note that all our conclusions are subject to the Limitations presented in Section 11.00 of this report.

Four overall purposes of the OU1 RI were to: 1) evaluate the sources nature, and extent of environmental contamination; 2) characterize potential routes for off-site contaminant migrations; 3) identify potential receptors of contamination which originates at the site; and, 4) identify unresolved issues and make recommendations to help formulate the scope of the OU2 RI. The following subsections describe our major conclusions regarding each of these study objectives.

10.10 SOURCES OF CONTAMINATION

We identified four potential sources of environmental contamination at the Central Landfill site. These were, municipal wastes found both above and below the water table and industrial/hazardous wastes also found above and below the water table. More specifically:

• Disposal of municipal wastes began at the site in 1955. Based on February 1988 site topography, and assuming that the area had been excavated to bedrock, there are more than 17,000,000 cubic yards of refuse at the site. Using the same assumption regarding the depth of fill, and extrapolated groundwater contours, it appears that approximately 2,000,000 cubic yards of refuse lie below the water table.

Central Landfill - Operable Unit One RI Report - March 1993

10- 1 The refuse is a significant source of metals contamination in groundwater. Total metal concentrations in groundwater samples are typically higher than dissolved concentrations in the same samples. This suggests that the migration of metals is being attenuated by absorption onto other metals or organic matter.

• Prior to 1980 treated and untreated septage wastes were disposed of at the site. The portion of the site which received that material was subsequently covered with refuse. This area reportedly covered five to ten acres, and held septage up to fifteen feet in thickness.

At some time in the mid to late 1970's the site received an estimated 1.5 to 2.5 million gallons of industrial hazardous waste. A significant portion of that waste was reportedly disposed of in trenches cut to or into bedrock. Within the context of CERCLA guidance documents, that area is a "Hot Spot." Closure activities in 1981 did not address the area of those trenches. The trenches were located during the RI. In this report the area of the trenches is identified as Hazardous Waste Disposal Area Two (HWDA2). Only one Hot Spot was identified. The designation HWDA2 was used to distinguish it from the area closed in 1981 and does not mean two hazardous waste disposal areas were identified.

Dense non-aqueous phase liquids (DNAPLs) and sludges in HWDA2 are a major source of volatile organic compound (VOC) contamination in groundwater. DNAPLs are a more significant source of VOCs in groundwater than are either the chemical or septage sludges, and chemical sludges are a more significant source of VOCs than are septage sludges.

• HWDA2 was identified as the most significant source of groundwater VOC contamination. The general areal distribution of VOCs, however, also indicates that the landfill as a whole is a source of generally lower concentrations of VOCs.

A review of files at the RIDEM indicates there are a number of other sources of groundwater contamination in the area of the CLF. Consequently, all groundwater contamination identified in the area cannot be attributed to activities at the CLF. Also, over the course of the study sampling and analytical procedures have changed. Consequently, not all reported variations in contaminant concentrations should be attributed to site conditions.

10.20 POTENTIAL CONTAMINANT PATHWAYS

We evaluated three pathways by which contaminants at the site could migrate into the surrounding environment. These were groundwater, surface water, and air. We found groundwater migration in bedrock to be the most significant contaminant pathway. More Specifically:

Central Landfill - Operable Unit One RI Report - March 1993

10-2 We have located lineaments (or fracture traces) which may be associated with bedrock fracture zones which cross the site (a lineament is line, possibly representing a structural bedrock fracture, which is observed on aerial imagery). A statistical analyses of data obtained by drilling at the site indicates that the frequency of bedrock fracturing in the area of lineaments is not significantly different from other locations at the site.

The frequency of bedrock fracturing at depths of less than 150 feet is on the order of inches to feet. Statistical analyses of data on bedrock fracturing versus depth indicates that the frequency of fracturing decreases with depth. Furthermore, these analyses suggest that at depths on the order of two to four hundred feet the frequency of fracturing should be much less (on the order of tens of feet) than observed in the upper thirty feet. No test drilling was performed to confirm that trend.

On a site wide basis the orientations of fractures were found to lie in directions which are generally in agreement with the orientations identified by the fracture trace analyses. However, analyses of data on a borehole specific basis did not, in all cases, indicate a preferential orientation of fractures consistent with nearby lineaments. Consequently, we believe that the bedrock structure does not support a preferred direction of flow in a horizontal direction.

Bedrock was identified as the major pathway for off-site migration of groundwater; and for the purposes of this report the bedrock aquifer can be analyzed as a porous media. Hydraulic testing and piezometer measurements indicate that the lineaments have hydraulic properties similar to other portions of the bedrock mass. Therefore, these geologic features are not acting as a pathway for interbasin groundwater flow.

The hydraulic conductivity of the rock in the horizontal direction is believed to average approximately 0.5 feet/day. The average transmissivity of the rock was estimated in a very preliminary way (without the benefit of pumping test data) to be on the order of 150 to 300 feet2/day. This is in keeping with fracture frequency data indicating the depth of the flow field is on the order of 200 to 400 feet.

The decreases in VOC concentrations observed with increasing distances from HWDA2 cannot be explained by dispersion alone. The groundwater beneath the site is anoxic and it appears anaerobic biodegradation is responsible for some of the observed decreases. Volatilization may also be responsible for some of the observed decreases in VOC concentrations. It also appears, however, that the contaminant plume from HWDA2 is narrow and has not been intercepted by a monitoring well at the toe of the landfill.

Central Landfill - Operable Unit One RI Report - March 1993

10-3 Because they receive contaminated groundwater, the Quarry Stream and Cedar Swamp Brook are pathways for off-site contaminant migration. There are no surface releases of contaminants to these surface waters.

Based on the results of air monitoring and air dispersion modeling, we believe that the CLF, with the electrical power generating facility operating, does not have a significant adverse effect on local ambient air quality. That facility has a Rhode Island Air Permit. We found no data, however, indicating that stack testing for VOCs has been performed.

10.30 RECEPTORS

Based on identified contaminant pathways, we estimated contaminant loading at the two major receptors, the Upper Simmons and the Almy Reservoirs. In reviewing this and related sections note that we designed and executed studies to assess the potential of the Scituate Reservoir being a receptor. These studies have established that the Scituate Reservoir is not a receptor of groundwater contamination which originates at the CLF. The Army Corp of Engineers, the United States Geological Survey, and CH2M Hill (consultants for the Providence Water Supply Board owners of the Scituate Reservoir), agree with that finding.

• Based on the site's history of waste disposal and computed contaminant transport velocities, it appears that the VOCs which are contaminants of concern are, on average, in dynamic equilibrium with the groundwater flow system. That is, steady state conditions have been achieved and no significant increases in VOC loading to the Upper Simmons Reservoir should occur. Statistical analyses of time- contaminant concentration relationships did not confirm this opinion. We attributed this lack of statistical evidence to complex contaminant release mechanism and changes due to sampling/analytical procedures.

• The groundwater transport rate for the semi-volatile organic compounds (SVOCs) of concern was computed to be slow. That is, for these contaminants steady state conditions may not have been established in 1990. Consequently, the loading rate of these contaminants to the Upper Simmons Reservoir could increase with time. • Based on the limited area of the site which supports groundwater migration towards the Almy Reservoir, the capping of that portion of the landfill, and the observed concentrations of contaminants in groundwater samples collected from wells located between the site and the Almy Reservoir, we believe site conditions pose no unacceptable incremental risk to that surface water body. That opinion needs to be substantiated by OU2 studies.

There are no public wells in the area where groundwater was or will be degraded by activities at the CLF. The closest public well is more than a mile from the site, and the soil and bedrock in the vicinity of the site are not generally conducive to the development of wells with a yield of more than a few gallons per minute.

Central Landfill - Operable Unit One RI Report - March 1993

10-4 Public water has been made available to residents in the areas which could be affected by activities at the CLF. No door to door studies have been performed to be sure all residents have connected to the public system and have abandoned their private water supply wells.

10.40 RECOMMENDED STUDIES

During the course of completing the OU1 Remedial Investigation, we identified a number of issues which were not fully resolved by the data provided in this report. The studies required to address these issues will be performed either during the OU2 Remedial Investigation, or during the Remedial Design/Remedial Action (RD/RA) Phase of work. The following provides an overview of these needs. The specifics of suggested studies will be described in specific work plans.

-1 The depth to which groundwater contamination extends has not been confirmed. One additional well extending to a depth of at least elevation zero MSL is recommended. We believe that well should be located near the toe of the landfill between wells WE87-ML4 and MW90-29, downgradient of HWDA2.

-2 Additional information on contaminant concentrations in groundwater, as the groundwater migrates towards the Almy and Upper Simmons Reservoir, is needed. We believe two to three wells both south and north east of the landfill (4 to 6 wells total), extended 30 feet into bedrock, will address those needs.

-3 Studies undertaken to date have not provided direct measurements of the transmissivity of the bedrock. We believe two or three pumping tests, 24 to 72 hours in duration, should provide adequate information to allow for design of required withdrawal systems.

-4 Estimates of flows to the Upper Simmons Reservoir have been based on empirical relations. Data needs to be collected on actual stream flows to substantiate those estimates.

-5 Studies need to be undertaken to address that affects of the CLF has had on the ecological systems of the Almy and Upper Simmons Reservoirs. We believe these efforts should begin with additional sediment and surface water sampling programs, and be expanded (if necessary) based on the potential risks demonstrated by those findings.

-6 The effects, if any, activities at the CLF have had on nearby wetlands, and the ecology of adjacent woodlands need to be established. We believe that a wetland delineation and ecological characterization of the areas surrounding CLF to

Central Landfill - Operable Unit One RI Report - March 1993

10-5 identify potential off-site receptors is needed. This may be followed by sampling and analysis of media representing potential pathways of off-site contaminant migration to ecological receptors.

-7- There is a possibility that residents in the vicinity of the site not have taken advantage of public water. We believe a lot by lot canvassing of all properties within two thousand feet of the site, to document water use and assess what institutional controls are most applicable, is an appropriate OU2 task.

Central Landfill - Operable Unit One Rl Report - March 1993

10-6 APPENDIX C

BORING LOGS & HYDRAULIC CALCULATIONS C-l

BORING LOGS MMENTAL. INC. PROJECT RE PORT OF BORING NO.MW95-47 140 BROADWAY, PROVIDENCE RHODE ISLAND ————— SHE ET 1— OF— 2~ ' . CENTRAL LANDFILL-OU2 - TASK 4 FIL S No. 3TT79.2 GEOTECHNICAL/GtOHYDROLOGICAL CONSUL 1 AN IS ' JOHNS! UN. KHUUb ISLAND CHKI) . BY bAS BORING Co. D.L. MAHER DRILLING COMPANY BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN JOHN BUWbN GROUND SURFACE tLbVA T ION jiu.ro UAIUM NUVU GZA ENGINEER HAKK UALPb DAlb SIAKI 1-31-9b UAit tNU £-«:-yo GROUNDWATER READINGS SAMPLER: UNLESS OTHERWISE NOTED, SAMPLER CONSIST S OF A 2" SPLIT ——————— i——— —• ————— • —— - —— •——————————————— — I SPOON DRIVEN USING A 140 Ib. HAMMER FALLING 35 In. DATE TIME WATER CASING STABILIZATION TIME CASING: UNLESS OTHERWISE NOTED, CASING DRIVE N USING A 300 Ib. 2-6-95 11.4 33' 4 DAYS HAMMER FALLING 24 In. 3-9-95 13.5 33' 1 MONTH CASING SIZE: 6" ID OTHER: 97 '8" AIR HAMMER AND ———————— 6" AIR HAMMER D C B R E A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD E P S 0 INSTALLED M N W PEN./ DEPTH DESCRIPTION Locking Guard SCREENING K H G S No. REC. (Ft.) BLOWS/6" Burmister CLASSIFICATION i IK>. S S-1 24/16 0-2 6-22 Dense tan, coarse to fine SAND, ND 1 some* Gravel, trace* Silt, trace* GRAVELLY 19-7 Organics witfi REFUSE (FILt) SAND AND REFUSE FILL R S R 5' 5 S-2 24/7 5-7 2-5 Medium dense, black, coarse to SILTY SAND 7.0 fine SAND AN6 SILT, trace fine AND REFUSE 5-10 Gravel, changing at 6'± to tan/ FILL B brown, coarse to fine SAND, trace* E Gravel with REFUSE (FILL) N S 9' A WOOD FILL L 10 10' A Q BOULDER U A G S-3 24/6 13-15 10-22 Very dense, gray, coarse to fine 13' R 0.2 SAND AND GRAVEL, trace Silt (TILL) 0 30-20 BOULDERY U 15 TILL

17' BOULDERS

20 ND S-4 24/11 21-23 7-19 Dense, gray, coarse to fine SAND, 21' trace Gravel, trace Silt (TILL) 11-27 BOULDERY TILL

25 25' BOULDERS AND Stratigraphic descriptions are COBBLES based on the examination of drill cuttings and air hammer response.

30 S-5 GRAB 31' MIN/FT Tan/White GRANITE 0.2 2 1.5 31' 6" casing to 33 Feet BEDROCK 1.5 1.3 1.3 35 S-6 GRAB 35' 1.0 Highly weathered GRANITE 36' ND 3 (Feldspars are kaolinized) 0.3 HIGHLY WEATHERED 1.0 ZONE BEJijl S||| 1.0 37' 1.0 40 REMARKS: 1. Field screening performed with HNU, Photoionization Detector (PID) with a 11.7 eV lamp. Readings in parts per million (ppm); ND indicates less than 0.1 ppm. 2. Using a 9 7/8" air hammer, a 10" steel casing was spun to a depth of 33' where a 6" steel casing was set and grouted 2 ft into bedrock. The TO" casing was pulled and the grout seal was allowed to set up for a minimum of 12 hrs, before the boring was advanced to 55' using a 6" air hammer. 3. Pink kaolinized rock from 36-37': "silty sand-like wash".

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE G ?ADUAL . 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED, FLUCTUATIONS OF GR(XJNDWATE R MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS | BORING NQ.MW95-47 *PROVIDENCE?"RHODE ISLAND PROJECT RE PORT OFEBORING No .MW9S-47 ft Kmr CENTRAL LANDFILL - OU2-TASK 4 FILE No. 3T foff -* GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS tJUHN^IUN. KMUUt ISLAND CHKD. BY IE D C B A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD S C ? N h DEPTH DESCRIPTION INSTALLED SCREENING I H G S No. T&{ (Ft.) MIN/FT Bur-mister CLASSIFICATION 1.0 F — 4V 1.0 42' L P T V 0.5 HIGHLY C— Central er 4 WEATHERED 1.0 ZONE R S 1.0 43' R 45 A S-7 GRAB 45' 1.0 Weathered Granite WEATHERED N NO GRANITE D " 1.0 0.8 — 0.8 1.0 50' 50 S-8 GRAB 50' 1.0 Gray/Brown, silty, fine SAND, ND little* Granite rock (angular 1.0 fragments) VERY HIGHLY WEATHERED AND 1 1.0 FRACTURED ZONE 1.0 ROCK FRAGMENTS ray/Brown, silty, fine SAND, NO 7 S-9 GRAB 55' 1.0 it tie* Gran ite rock (angular) 55 f End of Exploration at 55't [ 1 (Borehole collapsed to 53't)

REMARKS: 4. Seam from 42-43'i. 5. Seam at 50-55' pumping 25. gpm; fractured zones with silty sand seam; borehole collapsed back to 50' i wash color was grayjsn. 6. Borjng was advanced (roller-bit) froa 50' to 55' (after collapse). Upon roller-bit withdrawl, the boring collapsed back to 53'. 7. A mm ma 1 amount of water was lost to the borehole during drilling. On 2/6/95. prior to in situ testing, the borehole was developed using a submersible pump. Approximately 400 gallons or 6 standing well volumes of water were developed with a final turbidity of 100 NTU, 8. On 2/6/95, the borehole was packer tested from 53 to 33 using 10 and 20 foot test intervals. Upon completion of packer testing, the contractor purged a volume of water equal to that lost to the formation during testing. 9. On 3/9/95, one shallow bedrock monjtoring well constructed of 2' ID Sch. 40 PVg well pipe was installed with a 10' screened section beginning at a depth of 5V and topped with 43.8' of solid PVC riser (extending approximately 2.8' above ground surface). The well is protected by a $" Sch. L 40 steel locking guara pipe which extends approximately 3.0' above ground surface. See equipment diagram for further construction details. NOTES: 1} STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES, TRANSITIONS MAY BE GRADUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF GROUNDWATER „„, HAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE iZA BORING NO.MW95-47 GZA GEOENVIRONMENTAL. INC. PROJECT REPORT OF BOftING NO.MW95-47S 140 BROADWAY, PROVIDENCE, RHODE ISLAND SHEET CENTRAL LANDFILL - OU2 - TASK 4 FILE No —31479:3 GEOTECHN I CAL/GEOH YDROLOG I CAL CONSULTANTS JUHNSIUN. KHUUt ISLAND CHKD. BY EAS BORING Co. D.L. MAKER DRILLING COMPANY BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN JUHN bUWLN GROUND SURFACE ELEVATION" 31U.O8 UAIL n NUVU GZA ENGINEER HAKK UALKt DATE START 2/8/95 DA Ik tNU il B/95 GROUNDWATER READINGS SAMPLER: UNLESS OTHERWISE NOTED. SAMPLER CONSISTS OF A 2«1 SPLIT SPOON DRIVEN USING A UO Ib. HAMMER FALLING 30 In. DATE TIME WATER CASING STABILIZATION TIME CASING: UNLESS OTHERWISE NOTED, CASING DRIVEN USING A 30() Ib. 2-9-95 0850 10' 10' 2 MIN HAMMER FALLING 24 In.' CASING SIZE: 6" ID OTHER: 6" AIR HAMMER

D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD S 0 INSTALLED F ? N W PEN./ DEPTH DESCRIPTION Locking Guard SCREENING K H G S No. REC. (Ft.) BLOWS/6" Burmister CLASSIFICATION OVM S Cem. 1 Seal FILL

3' BEN SEAL A 5 Q U A 6' REFUSE: PLASTIC, G GLASS, PAPER R £TC. 0 U T 9' 10 P S-1 24/16 10-12 4-6 Medium dense , brown TOPSOIL: 10' TILL V 3.0 medium to fin e SAND, some+ glass/ C 10-16 roots, littl e- Silt, changing at 10.5'+ to gr ay/tan, coarse to fine+ R SAND, some- Gravel, little- Silt S R 15 S-2 24/5 15-17 10-28 Very dense, gray/tan GRAVEL 15' (COBBLES) ND (angular; ap Darent cobble zone), 33-20 little- jpedi urn to fine+ SAND, ^ri;;;;;; trace- Silt SfiNTil &i*ili 18'

20 20' NO 2 P F V r L s E R R E- S 25 TILL E A S-3 24/14 25-27 13-40 Very dense, tan, coarse to fine N- N ND SAND AND GRA YEL, little- Silt D 40-42

30 30' 3

32' GRANITE

End of Exploration at 34' + 35

40 REMARKS: 1. Soil TVOC headspace screening was performed employing a TEI 580B OVM Photoionization Detector equipped with an 11.8 eV lamp. 2. Mild leachate odor during drilling operations. 3. 10' of .01" slotted, 2.0" diam., sch 40, PVC wellscreen was placed from 30'+ up to 20'+ and topped with 22.5' (above G.S.) of solid PVC riser tube. Filter sand was placed. See equipment diagram for further details. NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE 3RADUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF G WXINDWATER „„, "A* OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENtS WERE MADE GZA BORING NO.MW95-47S GZA GEOENVIRONMENTAL. INC. PROJECT REPORT OF BDRING NO.MW95-48 140 BROADWAY, PROVIDENCE, RHODE ISLAND SHEE1r 1— OF— z~ CENTRAL LANDFIL-OU2-TASK-4 FILE No. 3TC79.2 GEOTECHNI CAL/GEOHYDROLOG I CAL CONSULTANTS JOHNS (UN. KHUUb ISLANU CHKD BY EAS BORING Co. D.L. MAKER DRILLING COMPANY BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN JOHN HUWbN liKOUNU SUKI-AU: tLtVAl IUN J5U/-.5O UAIUM NUVU GZA ENGINEER SlbHHbN KLlNb UAlb SIART 1/2/793 DA It tNL) 1/30/95 ————— GROUNDWATER READINGS SAMPLER: UNLESS OTHERWISE NOTED. SAMPLER CON SISTS OF A 2" SPLIT ———————— I———— —•————— — •— — -— — •————————————————— — ' SPOON DRIVEN USING A 140 Ib. HAMMER FALLING 30 In. DATE TIME WATER CASINC STABILIZATION TIME CASING: UNLESS OTHERWISE NOTED, CASING DRIVE N USING A 300 Ib. 1-31-95 0850 11.3' +21' 2.5 Days HAMMER FALLING 24 In.' 2-2-95 1126 6.65' 38.5' 4 Days CASING SIZE: 6" ID OTHER: 9 7/R " A ID MAHMPD •AIR HAMMER D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD E P S 0 INSTALLED * N W PEN./ DEPTH DESCRIPTION LOCKING GUARD TESTING K H G S No. REC. (Ft.) BLOWS/6" Bumiister CLASSIFICATION , DTRC S-1 24/14 0-2 3-20 Very dense, brown SILT AND SAND, TOP SOIL ND 1 little Organics changing after 4" 31-50 to brown, fine to medium Sand, little Silt (trace Gravel at depth) (FROZEN) with REFUSE SAND AND V REFUSE FILL 0

C L 5 A Y 6' S-2 24/19 7-9 10-12 Medium dense, dark brown, fine SILTY SAND 6 SAND AND SILt, little wood chips, AND WOOD G 8-6 trace coarse Sand (Stump Dump?) FILL R P 0 V U 10 T R 11' I

OUTWASH R SAND

15 S-3 24/24 16-18 8-8 Medium dense, tan, fine SAND, trace 8 coarse Sand, changing after 12" to 10-12 gray fine SAND (saturated)

Stratigraphic descriptions are based on the examination of 20 drilling cuttings and air hammer response. 20' ND 2 S-4 GRAB 21 Gray, fine to coarse SAND, little* ND 3 Gravel, Silt S-5 24/7 21.5-23.5 2-3 Loose, gray, fine to medium SAND, some Silt, trace Gravel (angular 7-1 fragments) GRAY 25 BOULDERY TILL S-6 GRAB 26' Gray, fine to coarse SAND AND ND GRAVEL, little- Silt

S-7 GRAB 33' Gray, fine to coarse SAND AND ND GRAVEL, little- Silt A 34' + 35 BEDROCK (Fe STAINED QTZ) MIN/FT GRANITE |6" Casing to 38.5' 1.0 1.0 40 REMARKS: 1. Field screening performed with a TEI 580B OVM, Photoionization Detector (PID) with a 11.8 eV lamp. Readings are in parts per million (ppm); ND indicates less than 0.1 ppm. 2. Spun casing to 2V drilled open-hole to 24', need more 10" casing; have to shut down without grouting 6" casing in place (1/27/95). 3. S-5 is suspected to be "wash". 4. Spun 10" of casing to 34' bored open hole to 38.5', set 6" ID Sch. 40 steel well casing to a depth at 38.5' and grouted into place. NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITION S MAY BE GRAkDUA L . 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED, FLUCTUAT IONS OF GROLJNDWATE R MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MA DE BORING NO.MW95-48 GZA GEOENVIRONMENTAL. INC. PROJECT REPORT OF B MtlNG No .MW95-48 140 BROADWAY, PROVIDENCE, RHODE ISLAND SHEE1 U CENTRAL LANDFILL - OU2 - TASK 4 FILE Mo. 3T ffO.... f -£_ GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS JUHNS1UN. KHUUt ISLAND CHKD. BY EAS> C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD M PEN./ DEPTH DESCRIPTION INSTALLED TESTING K H §8G S No. REC. (Ft.) MIN/FT Burmjster CLASSIFICATION 1.0 41' R 1.0 Fractured Zot* V G 1.0 42' 0 R R S-8 GRAB 43' 1.0 Gray GRANITE (rock cuttings) 8 NO 5 1.0 A 45 Y 1.0 SCITUATE 1.0 GRANITE 1.0 48' 1.0 BENT, 1.0 ||| 50 1.0 50' 1.0 F 52' S-9 GRAB 52' 1.0 Gray GRANITE (rock cuttings) P- NO T V— 1.0 R 1.2 S— 55 c 1.2 A R N E 1.2 D Central zer 1.2 1.2 1.2 60' 60 1.2 WEATHERED ZONE 6 1.2 62' 62' 1.2 S-10 GRAB 63' 1.2 Gray GRANITE (rock cuttings) NO 1.2 65 SCITUATE 1.2 GRANITE Illfll 1.2 1.2 7 1.0 End of Exploration at 68.5't 70

REMARKS: 5. Large fracture at 42't. 6. Color change in rock cuttings from gray to tan/brown (Fe staining?) from 60-62'±. 7. Borehole was "flushed" with compressed air for 10 minutest. 8. A minimum of water was lost to the borehole during drilling.. On 2/2/95, prior to in situ testing the borehole was developed using a submersible pump. Approximately 225 gallons of 2.5 standing well volumes of water were developed with a final turbidity of 15 NTU. .... 9. On 2/2/95 and 2/3/95. the borehole was packer tested from 68.5 to 37.7 using a 5 ft test Interval. Upon completion of packer testing the contractor purged a volume of water equal to that lost to 10. On^lS^S/one^hatlow^bedrock Monitoring well constructed of 2" ID Sch. 40 Pyc well pipe was installed with a 10' screened section beginning at a depth of 62' and topped with 54.87 of solid PVC riser (extending approximately 2.8' above ground surface). The well is protected by a 6" Sch, 40 steel locking guard pipe which extends approximately 3.0' above ground surface. See equipment diagram for further construction details. NOTES: 1} STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE GRADUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED, FLUCTUATIONS OF GROUNDWATER MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE GZA BORING NO.MW95-48 GZA GEOENVIRONKENTAL. INC. PROJECT REPORT OF BORING NO.MU95-48S 140 BROADWAY, PROVIDENCE, RHODE ISLAND SHEET 1— OF— —P CENTRAL LANDFILL - OU2 - TASK 4 FILE No. — 31479:3" GEOTECHN I CAL/GEOHYDROLOG I CAL CONSULTANTS JUHNilUN, KHUUt ISLAND CHKu. BY fcAS BORING CO. D.L. MAHER DRILLING COMPANY BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN JOHN BUWhN GROUND iUKhALt bLtVAIlUN 3U • o JA1 (. H NUVU GZA ENGINEER HAKK UALPt DATE START 2-7-95 UAlb tHO d-l-Y3 GROUNDWATER READINGS SAMPLER: UNLESS OTHERWISE NOTED. SAMPLER CONSISTS OF A 2*1 SPLIT SPOON DRIVEN USING A 140 Ib. HAMMER FALLING 30 In. DATE TIME WATER CASING STABILIZATION TIME CASING: UNLESS OTHERWISE NOTED, CASING DRIVEN USING A 30() Ib. 2-7-95 1100 7.5 15 5 HIN HAMMER FALLING 24 In. CASING SIZE: 6" ID OTHER: 6" AIR STRAIGHT HAMMER

D C B R E A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD E P S 0 INSTALLED M N W PEN./ DEPTH DESCRIPTION LOCKING GUARD SCREENING K H G S No. REC. (Ft.) BLOWS/6" gut-mister CLASSIFICATION PIPE ————• HNU(11.7) S Cem. 1 SAND AND Seal GRAVEL FILL

3' 3' BEN COBBLES P SEAL 5 V A Q U R A I 7' S G WOOD R (NON-LUMBER) R 0 U T 10 S-1 14/3 10-11.2 4-45 Very dense, brown, coarse to fine 10' 0.2 SAND AND GRAVEL, little+ Wood, 100 61/2" trace Rope, trace Silt SAND AND GRAVEL FILL

15 15' +

TILL

ill SEAL:::: 19' 20 21' BOULDERS F V~ I C- L s 25 R R S E- A N D S-2 17/4 28-29.4 15-60 SANVerDy ANdenseD GRAVEL/COBBLE, gray, coars,e iit\ot finee+ * ND 100 61/5" silt 2 30 3 31'

End of Exploration at 33'

40 REMARKS: 1. Soil headspace TVOC readings were collected employing a HNU Systems Model PI-101 Photoionization Detector, equipped with a 11.7 eV lamp. 2. 10' of .01" slotted, 20" diam. , Sch 40. PVC wellscreen was placed from 31'+ up to 21'+ and topped with 23.5' of solid PVC riser tube (extended above GS). See equipment diagram for further details. 3. During drilling a mild leachate odor was noted from ground surface to 33'.

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES, TRANSITIONS MAY BE (GRADUA L . 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF G(HXJNDWATE R MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENtS WERE MADE BORING NO.MU95-48S GZA GEOENVIRONMENTAL. INC. REPORT OF BORING No,MW95-49 140 BROADWAY, PROVIDENCE, RHODE ISLAND CENTRAL LANDFILL - OU2 - TASK 4 FILE No. ~~31479:2~ GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS JUHNiilUN. KHUUh ISLANP~ CHKD. BY ES————————S BORING Co. PL. MAHER DRILLING COMPANY BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN JUHN bUWbN GROUND SURFACE I'LtVAIlUN ^3V.U<| UAIUH NUVU GZA ENGINEER SlbPHfcN H. RLlNb — DATE START 1/i!3/95 UAIfc bNU ' T/25/95 GROUNDWATER READINGS SAMPLER: UNLESS OTHERWISE NOTED. SAMPLER CONSISTS OF A 2" SPLIT SPOON DRIVEN USING A UO Ib. HAMMER FALLING 30 In. DATE TIME WATER CASING STABILIZATION TIME CASING: UNLESS OTHERWISE NOTED, CASING DRIVEN USING A 300 Ib. 1/26/95 12.0 18 1 DAY HAMMER FALLING 24 In. 2/1/95 11.92 18 8 DAYS CASING SIZE: 6" ID OTHER: 9 7/8" AIR HAMMER AND 6" AIR HAMMER C B A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD S 0 INSTALLED SCREENING N W PEN./ DEPTH DESCRIPTION Locking Guard G S No. REC. (Ft.) BLOWS/6" Burmister CLASSIFICATION Pipe S-1 13/8 0-1.1 8-30 Very dense, orange/brown, fine to LOOMY NO medium SAND, some Silt, trace TOPSOIL 100/1" Gravel BOULDER B E BROWN TILL N 4' S BOULDER A 6' L Stratigraphic descriptions are BROWN A based on the examination of GRAVELLY 0 drilling cuttings and air hammer TILL U response. A 9.5' G S-2 Grab 9.5 Gray GRANITE Fragments (some R 10 red iron staining) WEATHERED 0 BEDROCK U T 11' SEVERLY WEATHERED ZONE ND S-3 Grab 15 Rock Fragments very brown/red 15 and severly weathered. 16' S-4 Grab 17 Gray/Tan GRANITE HARDER 17' ROCK NO 16" Casing to 18' BENT;;;; SEAL;; 19' S-5 Grab 20 Fine Gray with red and black WEATHERED 19' 20 Flecks: Brown Silts ZONE

22'

GRAY GRANITE

25 25.5' Centra izer Weathered Zone at 25.5 to 26.5' Brown Si Its WEATHERED ZONE 26.5'

GRAY S-6 Grab 30 Gray/Tan GRANITE GRANITE 30 30' ND

32' ;;;;;;B'eritbhii;te:;i

34' 35 Benseal Pink/Tan Silt returns (Pink +37' Aqua-Grout Granite or Fracture ?) PINK GRANITE 3RAY GRANITE S-7 Grab 40 Pink GRANITE (pink Silt returns) +40' ND 40. REMARKS: Field screening performed with a TEI 580B OVM. Photoionization Detector (PID) with a 11.8eV lamp. Readings are in parts per million (ppm). ND indicates less than 0.1 ppm. Encountered severly weathered lineament between 11 and 13':borehole not staying open. Usin••---g- a 9 7/8" air hammer, a 10" steel casing was spun to a depth off 1818'' wher...... e. a 6" stee_._.._.... l casing_ was set and grouted 8.5' into bedrock. The 10" casing was pulled and the grout seal was allowed to set up for a minimum of 1212 Ihrs. before the boring was advanced to 48' using a 6n air hammer. 4. Returned on V to finish Borehole but grout had receeded to 13' below ground surface. NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE GRADUAL. 25 WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED, FLUCTUATIONS OF GROUNDWATER MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE GZA BORING NO.MW95-49 GZA GEOENVIRONMENTAL. INC. PROJECT REI>OR T OF BORING NO.MW95-49 TO BROADWAY. PROVINCE. RHODE ISLAND ^^ ^"^T^ . , SHEET TAS< FILE No. 3T579.2 —— GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS ' ' JOHNSJ1UN. RHOTJh ISLAND CHKD. BY tAS D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD P S 0 M N W PEN./ DEPTH DESCRIPTION INSTALLED SCREENING K H G S No. REC. (Ft.) MIN/FT Burmister CLASSIFICATION S Pink GRANITE PINK GRANITE

BENSEAL AQUA -GROUT

45 +46' GRAY (DARK ND 5 GRAY) S-8 Grab 48 Dark Gray GRANITE 6 End of Exploration at +48.4'

REMARKS: 4. (con'd) Placed 2 bags of finish bentonite chips into annulus around 6" casing brought level to 9' below ground surface. Finished grouting in casing and then advanced boring to 48.4 ft using a 6" air hammer. 5. A minimal amount of water was lost to the borehole during drilling. On 1/31/95, prior to in situ testing, the borehole was developed using surge blocks and a submersible pump. Approxmately 105 gallons or 1.9 standing well volumes of water were developed with a final turbidity of 3 NTU. 6. On 2/1/95 and 2/2/95, the borehole was packer tested from 48. 4' to 18' using a 5 foot test interval. Upon completion of packer testing, the contractor purged a volume of water equal to that lost to the formation during testing. 7. On 2/14/95, one shallow bedrock monitoring well constructed of 2" ID Sch. 40 PVC well pipe was installed with a 10' screened section beginning at a depth of 30.0' and topped with 22.8' of solid PVC riser (extending approximately 2.8' above ground surface). The well is protected by a 6" Sch. 40 steel locking guard pipe which extends approximately 3.0' above ground surface. See equipment diagram for further construction details. NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES, TRANSITIONS HAY BE GRADUAL. 2) WATER LEVEL READINGS HAVE BEEN HADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATION S OF GROUNDWATER MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE BORING NO.MW95-49 GZA GEOENVIRONMENTAL. INC. PROJECT REPORT OF BORING No ^HW95-SQ ft BROADWAY, PROVIDENCE, RHODE ISLAND ^^ ^^^ ^ . ^ , ^^ I47V.y 2 GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS JOHNS 1 UN. KHUUt IbLANU CHKD. Bl tAS BORING CO. MAHER DRILLING COMPANY BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN JUHN BUWbNS UKlAJND SUKFACb bLbVAIlUN 4U/.JO m NliVU GZA ENGINEER SlbPHbN RuiNt unit biAKi 1/i6/vi> unit tnu I/m 16 GROUNDWATER READINGS SAMPLER: UNLESS OTHERWISE NOTED. SAMPLER CON SISTS OF A 2" SPLIT ——————— f SPOON DRIVEN USING A UO Ib. HAHHE R FALLING 30 In. DATE TIME WATER CASING STABILIZATION TIME CASING: UNLESS OTHERWISE NOTED, CASING DRIVE N USING A 300 Ib. 1/26/95 42.1' 14 2 DAYS HAMMER FALLING 24 In. 1/30/95 37.5' 14 6 DAYS CASING SIZE: 6" CASING OTHER: 9 7 /o n CTDA 1 I*HT MAMMFD AIR HAMMER 2/7/95 32.0' 14 5 DAYS D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD P S 0 INSTALLED SCREENING C N W PEN./ DEPTH DESCRIPTION Locking Guard K H G S No. REC. (Ft.) BLOWS/6" Burmister CLASSIFICATION ' 'f" S S-1 24/6 0-2 6-12 Dense, dark brown SILT AND SAND SEEDED COVER ND 1 changing after 3" to gray/tan GRAY 18-17 medium to coarse SAND, little GRAVELLY Gravel SAND 3' B E BOULDER N S 2 5 A S-2 1/0 5-5.1 100/1" No Recovery S-3 GRAB 6 Gray Granite Boulder NO Stratigraphic descriptions are 8' based on the examination of drilling cuttings and air harmer LIGHT BROWN response. GRAVELLY S-4 GRAB 9.5 Gray, coarse to fine Gravel, SAND (TILL) ND 10 Uttle(-) red SILT (weathered rock) 9.5' WEATHERED BEDROCK Dry fracture at 11.5' 11.5' FRACTURE ZONE A S-5 GRAB 13.5 Highly weathered rock; brown with 0 powderly, fine SAND AND SILT con- 13.75' U sistency. Harder gray and brown GRAY A R ND 3 15 Granite at 13.75' (6" casing to ROCK I 14 feet) S G R R 0 Dry fracture at 17' 17' U GRAY ROCK T

S-6 GRAB 25 Gray GRANITE (with red and black ND 25 flecks)

Dry Fracture at 26' +26'

+32' 33' SOFT ROCK 8ENT;;;;; &*M\ +34' 35 34.8' S-7 GRAB 35 Fracture zone at 35': Red/Brown +35' ND SILTS (iron staining ?)

+37' SOFTER ROCK S A H 39.6' 39' D 4tt REMARKS: 1. Field screening performed with a TEI 5808 OVM, Photoionization Dectector (PID) with a 11.8 eV lamp. Readings are in parts per million (pom). 2- Broke 97,8" roller pit trying to core through boulder; switched to 9 7/8 straight hammer at 5 ft. 3. Using a 9 7/8" air hammer, a 10" steel casing was spun to a depth of 9.5 ft. Then the boring was advanced H additional feet, where a 6" steel casing was set and grouted 4.5' into bedrock. The 10" casing was pulled and grout seal was allowed to set up for a min. of 12 hrs, before the boring was advanced to 44' using a 6" air hammer. NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE 3RADUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF G ROUNDWATER MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE BORING NO.MW95-51 GZA GEOENVIRONMENTAL. INC. PROJECT REPORT OF BORING No .MW95-50 HO BROADWAY, PROVIDENCE. RHODE ISLAND ————— SHEET 2 w e. . . CENTRAL LANDFILL - OU2 - TASK 4 FILE No. 3rV70.~ 2 GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS JUHNyiUN. RHODb ISLAND CHKD. BY hi, 5 D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD E P S 0 N U PEN./ DEPTH DESCRIPTION INSTALLED SCREENING t H G S No. REC. (Ft.) BLOWS/6" Burmister CLASSIFICATION 41' F P I V WEATHERED ZONE at 41 to 43: WEATHERED L C- ND Red rock fragments and brown Silts ZONE E S- 43' Rr S-9 GRAB 44 Gray/White GRANITE R- 4 E— Centra Li :er c 45 s — A D

49.6' 50 S-10 GRAB 50 Gray/White GRANITE ND

53'

6 55 I!!!™!!!

57'

60 A S-11 GRAB 60 Gray/White GRANITE Q ND U B A N G S R E 0 A U L T 65

S-12 GRAB 68 Gray/White GRANITE ND 8

70 End of Exploration at +69.5' 9

R EMARKS: 4. Borehole makes very little water; Was blown dry in 3 minutes by air hammer development. Did not recover in 3 hrs. 5. Overdrjlled borehole on 2/2/95. Advanced 6" borehole to 69.5 feet. 6. Very little fracturing noted during drilling borehole, making very little water. 7. A minimal amount of water was lost to the borehole during drilling. On 2/7/95, prior to in situ testing, the borehole was developed using surge blocks and a submersible pump. Approximately 46 gallons (or 0.82 standing well volumes of water) were developed with a final turbidity of 40 NTU. Pumping was terminated due to slow well recovery. 8. On 2/7/95 and 2/8/95, the borehole was packer tested from 69.8' to 25.0' using a 5 foot test interval. Upon completion of packer testing, the contractor purged a volume of water equal to that lost to the formation during testing. 9. On 2/14/95, one shallow bedrock monitoring well constructed of 2" ID Sch. 40 PVC well pipe was in stalled with a 10' screened section beginning at a depth of 49.6' and topped with 42.V of solid PVC riser (extending approximately 2.8' above ground surface). The well is protected by a 6" Sch. 40 steel locking guard pipe which extends approximately 3.0' above ground surface. See equipment diagram for further construction details. NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES, TRANSITIONS CAY BE GRADUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED, FLUCTUATION S OF GROUNDWATER MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE BORING NO.MU95-50 GZA GEOENVIRONMENTAL. INC. PROJECT REPORT OF BORING NO.HW95-51 140 BROADWAY. PROVIDENCE, RHODE ISLAND ————— SHEET 1— OT— 2~ CENTRAL LANDFILL - OU2 - TASK/4 FILE No. 31579.2' ~ GEOTECHNI CAL/GEOHYDROLOG I CAL CONSULTANTS " JUHNSIUN, KHUUb ISLAND CHKI). BY bAS BORING CO. MAKER DRILLING COMPANY BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN JUHN bUUtNb GROUND SUKFAUb bLbVAHUN 5W.J1 UAIUN GZA ENGINEER STEPHEN KLINE DAIt S1ARI 1/ UAIt bNO 1/^/Vb GROUNDWATER READINGS SAMPLER : UNLESS OTHERWISE NOTED. SAMPLER CONSIST S OF A 2" SPLIT ——————— i- SPOON DRIVEN USING A U5 Ib. HAMMER FALLING 30 In. DATE TIME WATER CASING STABILIZATION TIME CASING: UNLESS OTHERWISE NOTED, CASING DRIVE N USING A 300 Ib. 2/9/95 20.0 15 13 DAYS HAMMER FALLING 24 In. 2/13/95 18.5 15 3 DAYS CASING SIZE: 6" CASING OTHER: 9 7W STRAIGHT HAMMER AIR HAMMER D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD E P S 0 INSTALLED SCREENING h N W PEN./ DEPTH DESCRIPTION LOCKING GUARD K H G S No. REC. (Ft.) BLOWS/6" Burmjster CLASSIFICATION OTDC s S-1 24/16 0-2 11-17 Medium dense, dark brown, fine LOOMY FILL NO 1 SAND, some organics changing after 2 4-28 6 inches to tan, fine to coarse TAN SANDY SAND, Iittle(-) Gravel FILL 3 (VERY SOFT)

(COBBLES) B R E I 5 FILL N S S-2 18/12 5-6.5 17-50 Very dense, tan, fine to coarse S ND SAND, some Gravel, trace Silt 6.5' E R 100/6" (rock chips in soil catch) A VOID 4 Straigraphic descriptions are based on the examination of 7.5' drilling cuttings and air hammer response. COBBLES 10 9.5' S-3 GRAB 10-10.5 Highly weathered bedrock (Brown ND Silts and fine Sand cuttings) HIGHLY WEATHERED BEDROCK A Still highly weathered bedrock and Q ND 5 S-4 GRAB 14 slightly harder rock (cuttings with U 15 A 1— 6" casing to 15' G R 0 U

S-5 GRAB 20 Red weathered bedrock (very silty) 20 21' HARDER ROCK ND WEATHERED ZONE from 22' to 23' (Red/Brown Silts) WEATHERED ROCK 23' 25 Fracture at 26'

26'

29' S-6 GRAB 30 Tan/Gray GRANITE (with red/black SOFTER ROCK SENT SEWl:;;!;;;!; ND 30 and blue flecks)

31' F I 33' 3 T V E 35 R 3 — S A l- N 38' D i- Centrali er Fracture Zone 38' (Pink/Brown PINK/BROUN Silts) 40. REMARKS: 1. Field screening performed with a TEI 5808 OVM. Photoionization Detector (PID) with a 11.8 eV lamp. Readings are in parts per million (ppm). Nd indicates less than 0.1 ppm. 2. 2-4" of frgst for first sample, may have created higher blow counts. 3. Easy drilling (VOID?); covered 1 foot in less than "5 seconds. 4. Dropped-Uke a VOID from 6.5 to 7.5'. 5. Using a 9 7/8" air hammer, a 10" steel casing was spun to a depth of 13.7'. Then the boring was advanced to NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE G RADUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED, FLUCTUATIONS OF GR DUNDWATER „«•» MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENfS WERE MADE aZA BORING NO.MW95-51 *!»^-RHOOE ISLAND t*^ «BW M"" "'.MW95-5 1 m raw —————: ———————— CENTRAL LANDFILL OU2/TASK 4 FILE No. JfaF>-L GEOTECHNICAL/'GtOHYOROLOUlCA L CONSULT AN IS ' JDHHSIUN. RHODt ISLAND " CHKD. BY ~bAS ———— 0 SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD ! P S 2 0 N U PEN./ DEPTH DESCRIPTION INSTALLED SCREENING i H G S No. REC. (Ft.) BLOWS/6" Burmister CLASSIFICATION < S-7 GRAB 40 — NO I — i Fracture at 42': (Brown Silts) 42' — 43' SAND 45 End of Exploration at +45.5' 45.5'

REMARKS: 5. (cont.'d) 15' where a 6" s{eel casing was set and grouted 5.5' into the bedrock. Could not pull the 10" casing; was grouted in place and the gcout seal was allowed to set up for a minimum of 12 hrs, before the boring was advanced to 45.5' using 6' air hammer. 6. A minimal amount of water was lost to fhe borehole during drilling. On 2/8/95, prior {o in situ testing, the borehole was developed using surge blocks and a submersible pump.. Approximately 42 gallons or T.T standing well volumes of water were developed with a final turbidity of 35 NTU. Pumping was terminated due to slow well recovery. 7. On 2/9/95 and 2/10/95, the borehole was packer tested from 45.5' to 15' using a 5 foot test inter val. Upon completion of packer testing, the contractor purged a volume of water equal to that lost to the formation during testing. 8. Qn 2/15/95, one shallow bedrock monitoring well constructed of 2" ID Sch. 40 PVC well pipe was installed with a 10' screened section beginning at a depth of 43.0'. and topped with 35. 7* of solid PVC riser (extending approx. 2.7' above ground surface). The well is protected by a 6" §ch. 40 steel locking guard pipe which extends approximately 3.0' above ground surface. See equipment diagram for further construction details. NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS HIAY BE GRADUAL. 25 WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATION S OF GROUNDWATER „ _ MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE GZA BORING NO.MW95-51 GZA GEOENV1RC 140 BROADWAY ' - CENTRAL LANDFILL - OU2 - TASK 4 F?LEENo. — 31479 rr- GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS JOHNS 1 UN. KHUUb 1SLANU CHKD. BY hAS> BORING Co. D.L. MAKER DRILLING COMPANY BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN JOHN BUWtN GROUND SURFACE bit VAI 1UN j&£. . UV DA UM NtiVU GZA ENGINEER STbPHbN KLINt UAlb SIARI 1/19/9 UAlb fcNU 1/23 'Vb GROUNDWATER READINGS SAMPLER: UNLESS OTHERWISE NOTED. SAMPLER CONSIST S OF A 2" SPLIT ______| —————• —————— • —— • ———• —————————————————— ' SPOON DRIVEN USING A HO ib. HAMMER FALLING 30 In. DATE TIME WATER CASING STABILIZATION TIME CASING: UNLESS OTHERWISE NOTED, CASING DRIVE N USING A 300 Ib. 1/23/95 10:30 12.2 18 1 HOUR HAMMER FALLING 24 In. 3/8/95 11.9 18 1.5 MONTHS CASING SIZE: 6" ID OTHER: 9 7'8 " AIR HAMMER AND ——————— AIR HAMMER 3/29/95 11.2 18 2 MONTHS D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD P S 0 INSTALLED V N U PEN./ DEPTH DESCRIPTION Locking Guard SCREENING K H G S No. REC. (Ft.) BLOWS/6" Burmister CLASSIFICATION S-1 15/12 0.5-1.25 9-18 Very dense, brown, fine to coarse ND 1 SAND, little(+) Silt, changing TAN GRAVELLY 100/3" after 6" to brown coarse SAND AND SAND B 2 FINE GRAVEL, trace Silt FILL N S BROKEN CONCRE CONSTRUCTION A DEBRIS 5 S-2 24/10 6-8 5-11 Medium dense, brown, fine to BROWN FILL A ND medium SAND, little Silt, trace CONSTRUCTION Q 18-20 Gravel, trace Wood DEBRIS U A G R 0 U 10 T VOID Stratigraphic description are based on the examination of drilling cuttings and air hammer BOULDERY response. TILL

15 15.5' S-3 GRAB 16 Grey/Red, highly weathered GRANITE (Has consistency of coarse SAND ND and fine GRAVEL, some Silt) 17' 3 1 6" casing to 18 feet HIGHLY WEATHERED BEDROCK BENT; •1 MIN/FT 20' 19' 20 0.8 Highly weathered/f ratured ROCK FRACTURE (High iron staining) ZONE F 21' 0.5 I p— L V 1.0 22' C E 1.0 R S S-4 GRAB 24 0.5 Fracture at 24': Brown Silts 24' S R- 3 25 A E 1.0 N E- D u 1.0 1.0 1.0 1.0 30 1.0 31' 0.8 Fracture zone at 31 to 32' FRACT ZONE 0.8 32' 0.8 1.0 35 1.0 S-5 GRAB 36 1.0 Gray GRANITE (some weathering) 1.0 37' 0.5 Fracture at 38' (Red/Brown Silts) 1.0 38' 38' AQUA GROUT 1.0 40 REMARKS: 1. Split -spoon refusE I (rock chips in the soil catch), 2. Field screening performed vjith HNU, Photoionization Detector (PID) with a 11.7 eV lamp. Reading in parts per million (pom), tID indicates les? than 0.1 ppm. 3. Using a 9 7/8" air hammer, a 10" steel casing was spun to a depth of 15.5'; then drilled openhole to 18' where a 6" steel casing was, set and grouted 2.5' into bedrock. An unacceptable amount of grout was being lost to the formation, ther efore bentonite chips were placed around v" casing from 12' to 10' \o bridge the void. The 10" casing was pulled tind the grout was allowed set up for a minimum of 12 hrs, before boring was advanced to 47.9 using a 6" air hamn ier NOTES 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES, TRANSITIONS MAY BE GRADUA L. ~r,~ ZJ WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS GZA OF GW MAY OCCUR DUE TO 0 THER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE BORING NO.MW95-52 GZA GEOENVIRONNENTAL. INC. PROJECT REPORT OF BORING NoLMW95-5 2 140 BROADWAY, PROVIDENCE, RHODE ISLAND ————— SHEET ——————————————— CENTRAL LANDFILL - OU2 - TASK 4 FILE No. 3T1J79. 2 —— GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS JOHNS 1 UN. KHUUb ISLAND CHUD. BY bAb! D C B R SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD E PEN./ DEPTH DESCRIPTION INSTALLED SCREENING 1 H iG s S No. REC. (Ft.) MIN/FT Burmister CLASSIFICATION 1.0 41' 4 0.5 Fracture Zone at 41' and 43' FRACTURE 1.0 (Brown Si Us) ZONE S-6 GRAB 43 1.0 43' 1.0 AQUA GROUT 1.0 45 1.0 1.0 47' Fracture at 47': (Brown Silts) 1.0 c: S-7 GRAB 47 0.8 6 End of Exploration at 47.9' 7

85 REMARKS: 4. Dirty fractures water highly silty. 5. Tools have rock debris on them (fractures may be silting in the borehole). 6. On 2/13/95, obstructions in the well were discovered at 22' and 38' below ground surface which hampered borehole development. On 2/21/95, the borehole was reamed out by drill rig. A least 1 foot of sediments were removed from bottom of well. Rig developed well for 15 minutes with air to clean out sediments. Well making approximately 2 gpm. 7. By 3/8/95, the borehole caved-jn a second time. On 3/19/95 using an auger rig, GZA spun 4-inch casing, and installed a well with a 16 foot screen starting at 37. See equipment diagram for further details.

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES, TRANSITIONS HAY BE GRADUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATION S OF GROUNDWATER MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE BORING NO.MW95-52 GZA GEOENVIRONMENTAL. INC. PROJECT REPORT OF BOfiING NO.MW95-53 140 BROADWAY, PROVIDENCE, RHODE ISLAND SHEET 1 OF— r CENTRAL LAN DFILL - OU2 - TASK 4 FILE No — 31479.~3~ GEOTECHNI CAL/GEOHYDROLOG I CAL CONSULTANTS JUHNSIUN, KMUUt ISLAND CHKD. BY tAS BORING Co. D.L. MAKER DRILLING COMPANY BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN JUHN bUWtN GROUND SURf-ACh bLbVAUUN 3Ui .VH BAILin NGVU GZA ENGINEER MAKK. DALHt DATE START 2/9/95 DA It bNU if 9/95 GROUNDWATER READINGS SAMPLER: UNLESS OTHERWISE NOTED. SAMPLER CONSISTS OF A 2 1 SPLIT SPOON DRIVEN USING A UO Ib. HAMMER FALLING 30 In. DATE TIME WATER CASING STABILIZATION TIME CASING: UNLESS OTHERWISE NOTED, CASING DRIVEN USING A 30(3 Ib. 2-9-95 0850 10' 10' 2 MIN HAMMER FALLING 24 In. CASING SIZE: 6" ID OTHER: 6" AIR HAMMER

D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD P S 0 INSTALLED K N W PEN./ DEPTH DESCRIPTION Locking Guard SCREENING K H G S No. REC. (Ft.) BLOWS/6" Burmister CLASSIFICATION HNU(11.7) S S-1 9/5 0-0.8 35-100/3" Very dense (Frost), gray, fine Cem. ND 1 SAND, some+ Silt Seal P FILL V C 2' A R Q 3' U A 5 REFUSE R G S-2 24/4 5-7 3-7 Medium dense , gray/black REFUSE: R 6.8 Paper, littl e+ glass, trace 0 17-4 coarse to fin e SAND U

111 10 ill S-3 24/16 10-12 7-17 Dense, gray, coarse to fine SAND 10' 10' 1.6 AND UEATHERED ROCK/GRAVEL 25-14 SAND AND GRAVEL 12' P V C F 14' S- I 15 MEDIUM TO r L S-4 24/22 15-17 8-26 Dense, tan/g ray, medium to fine+ FINE+ SAND R- 1.2 SAND, trace Silt, changing at F 15-16 16'+ to gray , coarse to fine SAND E- R AND GRAVEL, little- Silt 16' + S SAND AND A GRAVEL N D 20 S-5 24/2 21-23 2-3 Loose, gray, fine SAND, trace Silt 20' NO 2 4-7 FINE SAND 22' 24' 24' GRANITE H;iiii*E»TOH:tniEiii;;iii 25 End of Exploration at 25'+ (BEDROCK) 25'

40 REMARKS: 1. Soil TVOC headspace screening was performed employing a HNU Systems Model PI-101 Photoionization Detector equipped with an 11.7 eV Tamp. 2. Strong leachate odor noted at 20-25'+, 3. 10' of .01" slotted, 2.0" diam., Sch 4Q, PVC wellscreen was placed from 22'+ up to 12'+ and topped with 14.5' (above G.S.) of solid PVC riser tube. See equipment digram for further details.

S-1 GRAB 3-5 Brown/Black, coarse to fine SAND, , tittle-Debris, B trace* Silt (44) 5 N E A

A Q U S-2 GRAB 9 Brown/Gray, coarse to fine SAND, A 10 little* Silt (3.4) R R R I G S S R 2 0 R R R U T

TILL

S-3 GRAB 19-20 Tan/Gray, co arse to fine SAND AND 20 GRAVEL, I ittle - Silt (0.4)

S-4 GRAB 29-31 Tan/Gray, co arse to fine SAND AND 30 GRAVEL, I ittle - Silt (ND) MIN/FT 2 31' + BEDROCK 2 1.5 GRANITE 3 1.5 35 1.2 2.3 Fracture Zone: 37 to 38': Brown/ 37' Red Silts 1.0 FRACTURE ZONE 1.0 38' HARDER (ND) ROCK S-5 GRAB 39 1.2 Tan (iron-st

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES, TRANSITIONS MAY BE GR/IDUAL . 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF GROLJNDWATE R „„_ MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MAD GZA BORING NO.MW95-ML9 GZA GEOENVIRONMENTAL. INC. PROJECT REI>OR T OF BORIk G NO.MW ?S-ML9 W BROADWAY. PROVIDENCE, RHODE ISLAND ^"^T^. ^ , SHEET Jh 8 CEMTRAL FILE No. 3T575 .2 GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS JUHNS.IUN. KHUUb ISLAND CHKD. BY tAS D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT P S 0 t N U PEN./ DEPTH DESCRIPTION INSTALLED H G S No. REC. (Ft.) MIN/FT Burmister CLASSIFICATION A B C < NR NR NR NR B NR N 45 S 2.0 A 2.0 47' 2.0 WEATHERED ZONE at 47' to 48: WEATHERED A Brown Silts ZONE Q 2.0 U 48' A 2.0 50 G S-6 GRAB 49 2.0 Tan/Gray GRANITE cuttings, very 50' R 4 highly WEATHERED AND FRACtURED 0 1.0 ZONE at 50 to 55' (1.3) U FRACTURE 1.5 ZONE R R R I I 1.5 S s S 1.5 R R R 55 1.0 Tan/Gray GRANITE Cuttings 55' 5 1.0 110" casing to 57' 1.0 1.5 2.0 60 S-7 GRAB 59 1.0 Tan/Gray GRANITE Cuttings (0.5) 1.0 1.5 1.5 1.5 65 1.0 66' Fracture Zone at 66' to 67' Red 0.3 Silts and rock fragments FRACTURE ZONE 1.5 67' S-8 GRAB 67 1.5 Highly weathered, gray GRANITE GRAY rock fragments (0.3) GRANITE 1.0 70 6 1.0 Fracture Zone at 70' to 73: Red/ 70' Brown SILTS 1.0 FRACTURE ZONE 1.0 1.0 Brown/Gray/Tan GRANITE (smaller 73' sieces) 1.5 75 1.5 1.5 1.5 1.5 2.0 80 7 S-9 GRAB 80 2.0 Harder rock (small pieces) still 80' BENT. a, lot of weathering evident (ND) jSEAL :; 8 2.0 6" casing to 82.5' 1.0 82' s: 1.0 1.0 85 REMARKS: 4. Drill water effluent is slightly "FOAMY" (making approx. 30 gpm and borehole collapses at the Fracture Zone. 5. Began open-hole drilling with 9 7/8 straight hammer. Advanced to 8V. 6. Large fracture between 7Q' and 73' making less water. 7. 6" ID steel casing spun into rock to a depth of 82.5'; on 2/20/95 began drilling open borehole with 6" straight hammer. 8. On 2/21/95. the decision was made to leave the 10" steel casing in the ground. In order to protect nearby borings MW95-4.7 and MW94-47S, the 6" casing was sealed with a layer of bentonit? chip? from 82.5' to 54'; above which the annular space between the 10" and 6" casings were filled with "High Early" grout to ground surface.

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE GRA DUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF CROC NDWATER ___ MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENtS WERE MADE SZA BORING NO.MW95-ML9 GZA GEOENVIRONMENTAL, INC. PROJECT REPORT OF BORING NO.HW95 -HL9 140 BROADWAY, PROVIDENCE, RHODE ISLAND SHEET FILE No. 2 GEOTECHN I CAL/GEOH YDROLOGI CAL CONSULTANTS JUHNblUN, KHUUt ISLAND CHKD. BY fcAS D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT P S 0 N W PEN./ DEPTH DESCRIPTION INSTALLED K H G S NO. REC. (Ft.) MIN/FT Burmister CLASSIFICATION A B C < 1.0 F Fracture at 86': Brown Silts I 1.0 L S 1.0 C E GRAY R R 1.0 GRANITE S-10 GRAB 90 1.0 Gray GRANITE Bedrock (High Quartz) N S 90 (NO) A 0.7 N D 0.8 0.5 0.5 93 0.5 95 R R 0.5 96' Fracture 96' : Brown Silts S ; S 0.5 E R R SEAL]; 0.5 0.5 0.5 100' 100 Fracture at 100': Pink Silts 1.0 S-11 GRAB 102 1.0 Gray GRANITE (ND) 1.0 GRAY 1.0 B 1.0 E 105 N 1.0 1.0 A 0.5 108' Fracture at 108': Tan Silts A 1.0 0 U S-12 GRAB 110 2.0 Gray GRANITE (ND) GRAY A 110 1.0 111' G Fracture at 111': Tan/Brown Silts R 1.0 0 U 1.0 0.8 GRAY 0.8 115 0.8 0.5 0.5 118' Fracture at 118': Tan/Brown Silts 0.5 S-13 GRAB 120 0.5 Weathered GR UNITE (Tan/Brown LIGHT BROUN 120 Silts) (ND) ROCK 0.5 SOFTER 9 0.4 ROCK 0.4 0.4 0.4 125 S-14 GRAB 126 0.4 Gray/Cream GUNITE (ND) CHANGES FROM LIGHT BROWN 0.5 TO CREAM AT 126' 0.8 128.5' 0.8 FRACTURE? 129' Flint Olive/Tan GR/VNIT E (possible shot. 0.8 fracture at 129') Seal. 130 REMARKS: 9. Large weathered seam from 118' to 129' (borehole remains open).

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE (IRADUA L . 2) WATER LEVEL READINGS HAVE BEEN HADE AT TIMES AND UNDER CONDITIONS STATED, FLUCTUATIONS OF GFtOUNDWATE R MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE BORING NO.MU95-ML9 GZA GEOENVIRC* MENTAL. INC. PROJECT RE PORT OF [JOKING NO.HW95-HL9 140 BROADWAY, PROVIDENCE, RHODE ISLAND SHEE T 4— Uh 8 CENTRAL LANDFILL - OU2 - TASK 4 FILE No. 3T579.2 —— GEOTECHNICAL/C EOHYDROLOGICAL CONSULTANTS JUMNilUN, KMUUb ISLAND CHKD . BY hAS D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT E P S 0 N W PEN./ DEPTH DESCRIPTION INSTALLED II H G S No. REC. (Ft.) MIN/FT Burmister CLASSIFICATION B < 1.0 . • . . - • F 130.5' 1.0 GRAY L 1.0 1.0 133.4' R S-15 GRAB 135 0.5 Brown/Orange SILTS (0.1) FRACTURE 135' 135 S A 0.5 C- N WEATHERED D 0.5 ZONE E E- Cen 0.5 N- tralize ORANGE 10 0.5 SOFT 0.5 HO LARGE 0.5 CHUCKS OF R 0.5 ROCK 0.5 R 0.5 143.4' S-15 GRAB 145 0.5 Brown/Orange Silts (ND) 145 0.5 146' 146.1' 0.5 LIGHT BROUN PINK 0.5 GRANITE B 0.5 E N 0.5 S 150 0.5 A L 0.5 152' A 0.8 CREAM/GRAY Q U 1.0 A HARDER S-16 GRAB 155 1.0 Dark gray with black and red rock G 155 Chios GRANITE (Brown/Gray Silts) R 1.0 0 U 1.0 0.5 0.5 0.5 160 0.3 S-17 GRAB 162 0.3 Brown/Red SILTS (0.1) 162' 0.5 BROUN 11 0.3 SOFT ROCK 165' 0.3 Brighter red 165 0.3 RED/BROUN 0.8 166' 1.0 Gray SILTS GRAY ROCK 1.0 169' 1.0 Brown/Heavier SILT content BROWN/RED 170 1.0 1.0 1.0 1.0 lark Gray/Brown chips GRANITE, S-18 GRAB 175 1.0 brown Silts (NO) REMARKS: 10. Large, highly weathered seam at 135 to 146'; larger chunks of rock in cuttings (borehole remained 11. Large, highly weathered seam at 162 to 166': very bright red silts; suspect PID reading - probably NO •

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES, TRANSITIONS MAY BE GRADUAL . 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF GROUNOWATE R MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE BORING NO.MW95-ML9 GZA GEOENVIRONNENTAL. INC. PROJECT REPORT OF BORING NO.MW9S-ML9 140 BROADWAY. PROVIDENCE, RHODE ISLAND ————— SHEET CENTRAL LANDFILL - OU2 - TASK 4 FILE No. 31479. 2 —— GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS ' 'JUHNS10N, KHUDK ISLAND CHKD. BY tAS D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT S 0 M ? N U PEN./ DEPTH DESCRIPTION INSTALLED K H G S No. REC. (Ft.) MIN/FT Burmisjer CLASSIFICATION C S 1.0 176' 1.0 PINK/CREAM 1.0 SILT B 1.0 N S 1.0 E 180 R A 1.0 1.0 A R Q 0.8 183' U A 0.8 LIGHT BROUN SILT G 0.8 R 185 0 0.8 U S-19 GRAB 187 0.8 Dark Gray with Red & Black Chips (Brown Silts) (ND) 0.5 0.5 0.5 190 0.5 0.5 0.5 0.3 194' 0.3 195 BROUN/ORANGE S-20 GRAB 196 0.3 Blue/Cream/Black/Red Rock Chips (with brown/orange Silt) (ND) 0.3 12 0.3 0.5 199' 0.5 200 LIGHT BROUN 4.8 0.8 1.0 1.0 0.5 Blue/Cream/Black/Red Rock Chips 205' 205 (with brown/orange Silt: some 0.5 white flecks and Red Silts) 1.0 BROUN/RED SILTS S-21 GRAB 208 1.0 Blue/Cream/Black/Red Rock Chips (with brown/orange Silt: some 1.0 white flecks and Red Silts) (ND) 209' 1.0 GRAY/CREAM 210 SILTS 1.0 211' S-22 GRAB 212 0.5 White/Red/Dark Gray Chips BRIGHT RED (Bright Red Silts) (NO) 0.5 213'S1US 0.5 GRADING INTO PINK WITH 0.8 MORE LIGHT 215 GRAY 0.8 0.8 0.8 0.8 0.8 220 REMARKS: 12. Borehole remains open despite very weathered, soft rock with high silt content.

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITION S HAY BE GRAC)UAL . 2) WATER LEVEL READINGS HAVE BEEN HADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUAT IONS OF GROW1DWATE R __, MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE HA DE aZA BORING NO.MU95-ML9 GZA GEOENVIRONNENTAL. INC. PROJECT REPORT OF BORING NQ.MW95-ML9 1*8 BROADWAY. PROVIDENCE. RHODE ISLAND ^^ ^^ _^ _^ ^ SHEET 6— Ut- 8 FILE No. 3T579.2 GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS JUHNSIUN, KHUUb ISLAND CHKD. BY bAS D C B R A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT P S 0 M N U PEN./ DEPTH DESCRIPTION INSTALLED K H G S No. REC. (Ft.) MIN/FT Bunnjster CLASSIFICATION C S 1.0 221' S-23 GRAB 222 1.0 White/Light Gray (white/cream WHITE LIGHT GRAY 1.0 1.0 B 0.5 N 225 S 0.5 226' Fractured Zone at 226' to 228: A 13 0.5 Bright Red Silts BRIGHT RED L SILTS 0.5 228' A 0 0.8 Soft Zone 22? to 234: Green rock TAN/GRAY U chips (Tan Silts) A 0.8 230 R 0.8 G R 0.8 E 0 R U 1.0 1.5 234' S-24 GRAB 235 1.5 White/Light Green/Dark Gray chips OLIVE/TAN 235 (Olive/Tan Silts) (NO) HARDER ROCK 1.5 GRADING TO LIGHT GRAY 1.5 1.5 1.5 1.0 240 1.0 1.0 1.5 1.5 S-25 grab 245 1.5 Gray/White with Black Flecks 245 (Gray Silts) (NO) LIGHT GRAY 1.5 1.5 1.5 1.5 GRAY SILT 1.5 GRAY/WHITE 250 BLACK ROCK 1.5 1.5 1.5 1.5 « 1.5 255 1.5 S-26 GRAB 258 1.0 Green/Gray/Black Rock Fragments 257' (Tan/Olive Silts) - Possible 1.0 Fractured Zone (ND) TAN/OLIVE SILTS 1.0 1.0 260' 260 1.0 BLUE/GRAY 1.0 1.0 263.3' 1.0 ...... 1.0 265 REHARKS: 13. Deepest observed fracture zone 226' to 228'; more bright red Silts.

NOTES: 1} STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES, TRANSITIONS KAY BE GRADUAL. 2) WATER LEVEL READINGS HAVE BEEN HADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATION S OF GROUNDWATER MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE BORING NO.MW95-ML9 GZA GEOENVIRONMENTAL. INC. PROJECT REI>OR T OF BORING NO.MW95-HL9 W BROADWAY. PROVIDENCE. RHOOE ISLAND ^^ _^ _ ^ ^ SHEET 7 ui-_6 CEHTRAL FILE No. 3T.7V.2 GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS JOHNS 1 UN. KHUUfc INLAND CHKD. BY tfti D C B R E A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT P S 0 M N W PEN./ DEPTH DESCRIPTION INSTALLED K H G S No. REC. (Ft.) MIN/FT Burmister CLASSIFICATION 1.0 Flint. . Shot .. . 1.0 ".". .' Seal . . 1.5 R 1.5 S S-27 GRAB 270 1.5 Dark Gray/White/Light Gray GRANITE R 270 (Light Silts) (ND) HARDER ROCK 2.0 270' 2.0 2.0 2.0 273.3' 2.0 275 14 2.0 S 2.0 Central izer -R 2.0 -E~ 2.0 -N- F 2.0 Dark Gray/White/Light Gray GRANITE L 280 (Light Silts); did not grab sample 2.0 E R 2.0 2.0 A N 2.0 D 2.0 285 Centra 1 2.0 izer 2.0 S-28 GRAB 288 2.0 Dark Gray/White/Light Gray GRANITE GRAY (Light Silts); slightly sillier GRANITE 2.0 (ND) BEDROCK 2.0 290 2.5 2.5 2.5 2.5 293.3 294 2.5 Filter Sand & Grout 295 2.5 2.5 2.5 2.5 S-29 GRAB 300 2.5 Dark Gray/White/Light Gray GRANITE 300 (Light Silts); slightly bluer (ND) 2.0 Benseal Aqua Grout 2.0 2.0 303' 1.5 SLIGHTLY SOFTER 1.5 DRILLING 305 1.5 1.5 1.5 II 1.5 Dark Gray/White/Light Gray GRANITE 18 1.5 (Light ?i Its); slightly bluer 310 End of Exploration at 310.5'+ 2§ REMARKS: 4. Borehole still making water; rock much harder; > 2 gpqi rate. 5. Drilled to depth of 310' below ground surface at 14:14 hrs on 2/20/95. 16. After developing the well for 15 minutes with air; well making +5 gpm (measured with calibrated bucket). 17. Hager GeoScience, Inc. working with Colog, Inc. performed borehole geophysical logging. 3-arra borehole caliper and fluid tenperature testing was performed on 3/3/95. Acoustic borehole tele viewer logging was performed on 3/6/95. 18. A minimal amount of water was lost to the borehole during drilling. On 3/10/95, prior to packer NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES, TRANSITIONS MAY BE GRADUAL. 2) WATER LEVEL READINGS HAVE BEEN HADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATION S OF GROUNDWATER MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE BORING NO.MW95-ML9 GZA GEOENVIRONMENTAL, INC. REPORT OF BORING NO.HW95-ML9 140 BROADWAY, PROVIDENCE, RHODE ISLAND SHEET 8~~UF—fr~ CENTRAL LANDFILL OU2 - TASK 4 FILE No. 5TC79.2—— GEOTECHNICAL/GEOHYDROLOGICAL CONSULTANTS 'JUHNSIUN. KHUUb ISLAND CHKD. BY bAii —— C B A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT S 0 N U PEN./ DEPTH DESCRIPTION INSTALLED G S No. REC. (Ft.) MIN/FT Burmister CLASSIFICATION

REMARKS: 18. cont.'d. testing, the borehole was developed using surge blocks and a centrifigal pump. Approximateltelyy 870 aliens or 1.9 standing well volumes of water were developed with a final turbidity of 20 NTU. 19. rom 3/14/14/99 5 to 3/21/95, the borehole was packer tested from 82.5' to 310.5' using a 10 foot ttest ?interval. UpoL, n completion of packer testing, the contractor purged a volume of water equal to that tost to:o th...e. formatio. _.n. during testing. 20. Based on the resglts of' th'e ' renole geophysics, packer testing and discrete zone analytical sampling, 2 2.0-inch ID Sch. wells were installed to depths of 293,3 feet and 143.4.feet with a 20 foot and a 10 foot 0.01-inch slotted screen.__... , In addition, 1 1.0-inch ID Sch 40 well was installed to a depth of 93.1 feet with 1" fee' t' of screen. See equipment diagram for further de tails.

BORING CO DL. MAHER ENVIRONMENTAL BORING LOCATION SEE EXPLORATION LOCATION PLAN 1 FOREMAN DENNIS DUCHNOWKSI GROUND SURFACE ELEV 294 ee DATUM NGVD

GZA ENGINEER STEPHEN KLINE DATE START 1/21/97 DATE END 1/22/97

SAMPLER UNLESS OTHERWISE NOTED. SAMPLER CONSISTS OF GROUNDWATER READINGS A 2" SPLIT SPOON DRIVEN USING A 140 Ib HAMMER FALLING 30 IN DATE TIME WATER CASING STABILIZATION TIME

CASING UNLESS OTHERWISE NOTED. CASING DRIVEN USING 1/22/97 0700 72' 505 OPEN BOREHOLE A 300 LB HAMMER FALLING 24 IN IcASING SIZE: 6" OTHER 5 7/8" PNEUMATIC AIR HAMMER

'DPTH CASING SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD R (FT) BLOWS NO PEN/REC DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K

Stratum descriptions based on air r TOPSOIL 1 r Jj hammer cuttings and drill rig response • 25' l SAND AND B R GRAVEL FILL E I

5* N S 7' BOULDER T e I O R

9' N 6.0 2

G-1 8-10 Brown/gray, fine to coarse SAND, little NATURAL I Gravel, trace Silt SAND T GRADING TO E l GRAVEL 15 G-2 15* Brown, fine Gravel and medium to coarse R 1 5 Sand, trace Silt, trace Organics (roots and 0 I twigs) U FINE SAND & SILT T

I, SAND AND 1.1 3 G-3 20* Olive/gray, fine to coarse SAND, little fine GRAVEL Gravel, little* Silt (organic odor) I (COBBLES)

ND I* G-4 25* Olive (silt color). medium to coars e SAND and fine Gravel, little- Silt 28'

30 Bent.

31' Brown/tan, fine to coarse SAND, trace 3V (COBBLES) 31' Seal Gravel STRATI RED SAND AND 32' GRAVEL

ND 4 35 1I S-1 18/3 35-365 Pushed Tan, fine to coarse SAND, little Gravel, trace Silt REMARKS 11 Field screening performed with a Thermo Environmental Instruments Model 580 Organic Vapor Monitor (OVM) Photoionization Detector (PID) equipped with an 11 SeVlamp Readings are in parts per million (ppm). ND indicates less than 0 1 ppm in soil sample headspace 2 Estimated bottom of earthen dam. 3. Making more water at 17'* 14 Pushed 3" split spoon. Consolidated material. Very dense 1.000 Ibs pressure could only move 18" into material NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE GRADUAL 1 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF GROUNDWATER TABLE MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE ,GZA BORING NO MW97-54B GZA GEOENVIRONMENTAL INC. PROJECT REPORT OF BORING NO MW97-54 "1140 BROADWAY. PROVIDENCE. RHODE ISLAND CENTRAL LANDFILL OU2/T ASK 4A SHEET 2 OF 2 JOHNSTON. RHODE ISLAND RLE NO 31842 GEOTECH/GEOHYDROLOGICAL CONSULTANTS OHKDBY EAS

-TDPTI- CASING SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD R BLOWS NO PEN/REG DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K (More Gravelly)

45 G-5 44-45 Creamrtan, medium to coarse SAND and fine (More Silty) NO Gravel, little Silt

G-6 48 Tan. fine to coarse SAND, little Gravel, little 48' 47.5' ND 5 Silt ROTTEN ROCK I 6 S-2 6/4 51-51 5 Pushed Tan, fine to coarse SAND and sections • NO 7 of Granite cemented with Silts 1 I END OF EXPLORATION AT 51 5' * a T 1 60

T -j [REMARKS: 5 Air hammer on-soil holds more air after 48' ; 6 Push T split spoon with 1.000 Ibs pressure only able to work 6"» into strata 7 A groundwater monitoring well constructed of 2" ID Sch 40 PVC was installed with a 15' (10 slot) screen section to a depth of 47' and topped with 34 0' of solid riser pipe (2.0' above ground surface) on 1/22/97 The borehole annulus was backfilled with 4' of bentonite chips (515' to 47.5). 165' of filter sand around screen section (47 5' to 3V). a 3 bentonite seal (31' to 28'), and 28' of cement/bentonite ground (28' to 0> The well is protected by a 4" ID x 5' locking, steel guard pipe set 2 5' below ground surface in a concrete seal NOTE S: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE GRADUAL 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF GROUNDWATER TABLE MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE GZu(V | BORING NO MW97-54B GZA GEOENVIRONMENTAL INC PROJECT REPORT OF BORING NO MW97-54A 140 BROADWAY. PROVIDENCE. RHODE ISLAND CENTRAL LANDFILL OU2/TASK 4A SHEET 10F2 JOHNSTON. RHODE ISLAND FILE NO 31842 GEOTECH/GEOHYDROLOGICAL CONSULTANTS CHKD BY EAS

BORING CO D.L MAHER ENVIRONMENTAL BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN DENNIS DUCHNOWKSI GROUND SURFACE ELEV 2935' DATUM NGVD

GZA ENGINEER STEPHEN KLINE DATE START 1/20/97 DATE END 1/21/97

SAMPLER UNLESS OTHERWISE NOTED. SAMPLER CONSISTS OF GROUNDWATER READINGS A 2" SPLIT SPOON DRIVEN USING A 140 Ib HAMMER FALLING 30 IN DATE TIME WATER CASING STABILIZATION TIME

CASING UNLESS OTHERWISE NOTED. CASING DRIVEN USING 1/20/97 1630 776 34 05 HOURS A 300 LB HAMMER FALLING 24 IN 1/21/97 772 34 17 HOURS CASING SIZE 6" OTHER 5 7/8" PNEUMATIC AIR HAMMER

DPTH CASING SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD R (FT) BLOWS NO PEN/REC DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K

Stratum descriptions determined from V TOPSOIL 1

air hammer cuttings and drill ng response

SAND AND

5 Yellowrbrown, fine to coarse SAND, some GRAVEL FILL G

fine to coarse Gravel, trace Silt R

(COBBLES) U

9' T 2

10 NATURAL

Olive/brown, fine to coarse SAND, some GRAVELLY SAND

Silt, little fine Gravel (COBBLES)

15 15'

Gray, fine to medium GRAVEL, little medium

to coarse Sand, little Silt GRAY GRAVEL

AND SILTY SAND

Gray, fine Silty SAND, trace coarse Sand

Tan. fine to coarse SAND and fine Gravel SAND WITH

ORGANIC ODOR

Olive/green, fine to medium SAND, little

25 SiH 25'

2ff BOULDER

SAND WITH

Olive/brown, fine to coarse SAND, some ORGANIC ODOR 3 Silt, little fine Gravel 30

G-1 Tan/orange, medium to fine SAND and fine 3Z 4. GRAVEL, little Silt STRATIFIED SAND AND GRAVEL

35 G-2 Gray/brown, fine to coarse Gravel and medium to fine SAND (Gravel is blue/gray), little- Silt

3rown. fine to coarse SAND and fine to 40 G-3 medium Gravel, little Silt REMARKS 1 No field screening was performed 2 Estimated bottom of earthen dam 3 Very easy drilling 4 Making significant volumes of water, easy drilling drop 3 feet in 30 sec+ GZA BORING NO MW97-54A GZA GEOENV1RONMENTAL INC PROJECT REPORT OF BORING NO. MW97-54A 140 BROADWAY, PROVIDENCE. RHODE ISLAND CENTRAL LANDFILL OU2/TASK 4A SHEET 20F2 JOHNSTON. RHODE ISLAND RLE NO 31842 GEOTECH/GEOHYDROLOGICAL CONSULTANTS CHKDBY EAS

DPTH CASING SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT RELD R BLOWS NO PEN/REC DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K

Brown, fine to coarse SAND, little Silt, little STRATIRED SAND 5

fine Gravel AND GRAVEL G

Material grades to coarse Sand and Gravel 0

45 U

END OF EXPLORATION AT 47'* 7

REMARKS 5 Zone is producing a significant volume of water 6 Neither rotten rock nor bedrock interface encountered by 47'+ 7 Casing separated 13"+ from bottom of borehole - could not retrieve - borehole was abandoned and sealed using tremied in place bentonite/cement grout on 1/21/97

NOTES: 1) STRATIRCATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES; TRANSITIONS MAY BE GRADUAL 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF GROUNDWATER TABLE MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE GZA [SORING NO MW97-54A GZA GEOENVIRONMENTAL INC PROJECT REPORT OF BORING NO MW97-ML10 140 BROADWAY. PROVIDENCE. RHODE ISLAND CENTRAL LANDFILL OU2/TASK 4A SHEET 1 OF 8 JOHNSTON. RHODE ISLAND FILE NO 31842 GEOTECH/G6OHYDROLOGICAL CONSULTANTS CHKDBY EAS

BORING CO D.L. MAHER ENVIRONMENTAL BORING LOCATION SEE EXPLORATION LOCATION PLAN FOREMAN DENNIS DUCHNOWSKI GROUND SURFACE ELEV 29435' DATUM NGVD

GZA ENGINEER STEPHEN KLINE DATE START 1/8/97 DATE END 1/15/97

SAMPLER UNLESS OTHERWISE NOTED. SAMPLER CONSISTS OF GROUNDWATER READINGS A 3" SPLIT SPOON DRIVEN USING A 140 fc HAMMER FALLING 30 IN DATE TIME WATER CASING STABILIZATION TIME

CASING: UNLESS OTHERWISE NOTED, CASING DRIVEN USING 1/8/97 1300 SO 100 OS HOURS

A 3OO LB HAMMER FALLING 24 IN 1/16/97 0800 59 700 1 DAY CASING SIZE 10"/6" OTHER 9 7/8 & 5 7/8" PNEUMATIC AIR HAMMER

DPTH CASING SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD R (FT) BLOWS NO PEN/REC DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K

S-1 24/16 0-2 8-9 Medium dense, dark brown, fine to medium 10" TOPSOIL A B 55 1

12-7 SAND, some Silt (roots and other organics) SAND AND 2

changing after 10" to tan, fine lo coarse GRAVEL

SAND, some fine to coarse Gravel FILL B

5 (Cobbles) E R R 3

S-2 24/2 5-7 32-26 Very dense, olive/brown, fine to medium N I I 16

G-1 6 28-36 SAND and fine to medium Gravel. little* Silt S S S

(saturated) 8' E E E

A R R

10 L 4

S-3 24/8 10-12 3-6 Medium dense, olive/brown, fine to coarse STRATIFIED 1.5

4-10 SAND, some fine to coarse Grave trace SANDS A

Sill Q

15 (COBBLES) A

S-4 24/20 15-17 21-23 Dense, olive/green, fine SAND, little- Silt NO

18-19 intertjedded with layers of coarse Sand. G

some fine to medium Gravel R

20 U 5

S-5 20/2 20-21 7 9-3 Dense, gray, fine SAND, trace Silt 2V T 1 5

40-50/2"

GRAVEL

24.5'

BOULDER

S-6 24/7 27.5-295 2 Very loose, fine SAND, changing after 4" 275' NO 7

2-2 to gray, fine to coarse SAND, little blue and SANDY GRAVEL

30 3 orange, fine Gravel 30'

BOULDER

COBBLES

35 STRATIFIED SAND 16 8 S-7 510 35-355 SO+/5" Very dense, gray, fine lo coarse GRAVEL, AND GRAVEL G-2 35 trace fine to coarse Sand, trace Silt 1 Field screening performed with a Thermo Environmental Instruments organic vapor monitor (OVM) Photoionization Detector (PID) equipped with an 1 1 .8 eV lamp Readings are in parts per million (ppm) NO indicates less than 0.1 ppm in soil sample headspace Based on subsequent analytical testing it appears that the elevated headspace readings were potentially caused by water vapor and extreme cold. 2 Frosl lo 8 inches 3 Sample is saturated. Poor recovery - took grab sample (G-1 ) from hammer may have been pushing a cobble. Sample has organic odor (like black licorish) 4 Approximately 15" rounded gravel in soil catch of sampler resulted in low sample recovery. 5. Spirt spoon refusal - very poor recovery - drill cuttings indicate fine to coarse gravel (quartz, mica granite) rounded edges, trace fine sand, trace silt 6 Encountered granite boulder from 24 5'+ to 27 5'+ - Cyclone relumed angular granite chips Borehole making much more water 7 Began with split spoon sample on 1/9/97 only S of water in casing (i.e.. DTW=19 5') at 27 5ft - hydros atic surface at 5'+ 8. Split spoon refusal at S-7 took grab sample G-2 at 35'+ from cyclone BORING NO MW97-ML10 G2A GEOENVIRONMENTAL INC PROJECT REPORT OF BORING NO MW97-ML10 140 BROADWAY, PROVIDENCE. RHODE ISLAND CENTRAL LANDFILL OU2/TASK 4A SHEET 2 OF 8 JOHNSTON. RHODE ISLAND FILE NO 31842 GEOTECH/GEOHYDROLOGICAL CONSULTANTS CHKDBY EAS

OPTH MIN/FT SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD R NO PEN/REC DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K

A B

STRATIFIED SAND

AND GRAVEL B

R R

40 N I I 7.0 8

G-5 40+ Light brown, fine GRAVEL and medium to S S S

coarse Sand, trace Sift E

1 A R R

1- G-6 45+ Yellowish brown fine to coarse SAND and A ND Gravel, little (-) Silt Q - U 1 491 A 50 1 HIGHLY

1 G-7 51 + White and black GRANITE Fragments WEATHERED ND 1 2 Yellowish brown Sifts ROTTEN R 2 ROCK 0

2 U 1. 2 551 9 3 G-8 55+ White, GRANITE Fragments, cream colored GRANITE ND 10

2 Silts (more sand consistency) BEDROCK 1 2 G-9 58+ NO 2

60 2 1 0" ID steel casing installed to 60' 11 1 2 G-10 60+ ND 2 63'

2 Fracture zone: (Red Silt 63'+ to 64'- borehole FRACTURE ZONE 1 2 remains open) 64' 65 2

2 G-11 65+ -ight gray GRANITE (consistency of coarse 1 2 Sand with cream/white Silts) 67 ND 2 jj 2 6~ ID steel casing installed to 69.4' % n 70 2 G-12 70+ Light gray GRANITE (slightly more Silts) 69 ND

2 7CT 12

2 S 13 1 2 S A 3 c N 75 3 R D 3 G-13 75+ Light gray GRANITE (cream/white Silts) t 3 IT R ND 1 ; 3 racture zone (brown silts - easier drilling) FRACTURE ZONE N 1 78' 80'

REMARKS: 8. Air hammer returns are very silty. Borehole making approximately 10+ gpm. 9- Rock increases in hardness at 55'. - 10. On 1/9/97, spun casing to 58V Advanced bit in front of casing 2"-borehole is not self supporting. 11. On 1/10/97, spun casing to 60" borehole making less water - silts are cream colored - competent rock drilled open borehole 10" and rock remains open-grouted in 6-inch casing 12. During the grouting of the 6" casing, the 10" casing became stuck - could not be removed. 13. Grout allowed to set up over weekend before advancing 6-inch ID open borehole drilling on 1/13/97. ~|GZA IBORING MW97-ML10 'GZA GEOENVIRONMENTAL INC. PROJECT REPORT OF BORING NO. MW97-ML10 140 BROADWAY. PROVIDENCE. RHODE ISLAND CENTRAL LANDFILL OU2/TASK 4A SHEET 3 OF 8 JOHNSTON. RHODE ISLAND FILE NO 31842 IGEOTECH/GEOHYDROLOGICAL CONSULTANTS CHKDBY EAS

DPTH MIN/FT SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD R NO PEN/REC DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K 1 G-14 80+ Light gray GRANITE (cream/white Sins) ND t- I B 4

2 Fracture, brown Silts larger red granite 83' 83' I l 2 fragments (83'+) m 85 2 GRAY ™ I 1 GRANITE 85'

I 1 S

1 881 E

4 FRACTURE ZONE B R

90 4 G-15 90+ Fracture: brown Silts larger red granite 90' ND

4 fragments (erratic hammer movement) GRAY GRANITE N I 4 92' FRACTURE S 1

1 A I 2 Granite: gray Silts (quartz sand fragments) 2

2 A I 1 Fracture: (98'+) brown silts 98' Q 14 1 U

1100 1 SOFT GRAY A

1 GRANITE I 1 3

1 R

I 1 GRADUALLY O 105 1 G-16 105+ Gray GRANITE (fine to coarse Sand HARDER U ND

2 fragment - gray Silts) GRAY GRANITE I 2

2 I 2 110 2

2 I 2 2

2 u 1 G-17 115+ Fracture zone: red/orange GRANITE 15' 2 ragments with brown Silts FRACTURES ND

2 I 2 GRAY 2 GRANITE 120 1 1REMARKS: 14. Drill rig bucking-softer rock

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES; TRANSITIONS MAY BE GRADUAL 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNOE R CONDITIONS STATED; FLUCTUATIONS OF GROUNDWATER TABLE GZA MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE. BORING NO. MW97-ML10 GZA GEOENVIRONMENTAL INC. PROJECT REPORT OF BORING NO MW97-ML10 140 BROADWAY. PROVIDENCE, RHODE ISLAND CENTRAL LANDFILL OU2/TASK 4A SHEET 4 OF 8 JOHNSTON. RHODE ISLAND FILE NO 31842 GEOTECH/GEOHYDROLOGICAL CONSULTANTS CHKDBY EAS

DPTH MIN/FT SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD R NO PEN/REC DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K 121 1 Fracture: Brown Silt red/orange granite 12ff FRACTURES B

2 fragments

1.5 122'

1.5 FRACTURE R

125 1.5 G-18 125+ Large granite fragments (more orange i ND

1.5 pink/gray Silts) SOFTER STONE s

1 B

1 GRAY R

1 N

130 1 Sillier discharge. GRANITE is blue/black/dark 5

1 gray

0.5 132' A

0.5 Fracture zone: Tan/yellowftlack GRANITE FRACTURES

1 Fragments, tan Silts (132- to 133') 133'

135 1 A

1 Q

1.5 138' U

20 G-18 138+ Black and white GRANITE with gray Silts GRADUALLY A NO

8.0

140 5.0 HARDER GRAY 3 15

5.0 R

12.0 GRANITE O

3.0 U

3.0

145 3.0 Black and white GRANITE with green tint to

3.0 quartz - gray Silts

3.0

150 30 G-20 150+ Black and white GRANITE - gray Silts ND

3.0

0.5 Fracture: Large pieces in return with gray 52' 16

5.0 Silts (152>)

155 50

5.0

50 160 5.0

REMARKS 15 Granite became very hard hammer not progressing Pulled pneumatic hammer from 142. Replaced bit - continued drilling. 16. Drill head dropped 6"+ in approximately 30 seconds and then slowed again.

NOTES. 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE GRADUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED; FLUCTUATIONS OF GROUNDWATER TABLE GZA MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE. IBORING NO. MVWT-MLIO GZA GEOENV1RONMENTAL INC PROJECT REPORT OF BORING NO MW97-ML10 ,140 BROADWAY. PROVIDENCE. RHODE ISLAND CENTRAL LANDFILL OU2/TASK 4A SHEET 5OF8 JOHNSTON, RHODE ISLAND FILE NO 31842 GEOTECH/GEOHYDROLOGICAL CONSULTANTS CHKDBY EAS

DPTH MIN/FT. SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT RELD R NO PEN/REC DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K 1-161 5 G-21 160* Black and white GRANITE - gray Silts B ND

3 16? I 3 Small fractures? - drill rig jumped 163' FRACTURES 3 GRAY

165 3 GRANITE R

4 I

3 s

3 Fracture: (168'+) 168' E NO 17 I 3 R 170 3

3 G-22 170+ Black and white GRANITE fragments (fine 18 I 4 to coarse SAND sized particles- slight green B 5 tint to white fragments).

5 N u 5 S 5

5 A I 5 5

|1BO 5 A

5 G-23 180+ White and gray GRANITE (still tint of green) Q 11 19

5 white/gray Silts trace black/yellow and orange U

4 fragments A

185 3 Not making any more water, slightly sillier SOFTER ROCK G

3 R

3 O

4 U

4 T

190 5

5 G-24 190+ White and gray GRANITE (still tint of green) HARDER AGAIN 1.1

5 white/gray Silts trace black/yellow and orange

5 fragments

195 5

5 200 5

REMARKS 17 Drill rig jumped at 168' * larger rock fragments Borehole appears to be making more water. 18 Driller has increased pressure on downward head (he says won't drag along the inside of borehole when questioned) 19 P1D reading may be affected by moisture on the lamp, however. PID calibration check was acceptable NOTES 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES; TRANSITIONS MAY BE GRADUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED; FLUCTUATIONS OF GROUNDWATER TABLE GZA MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE (BORING NO MW97-ML10 GZA GEOENVIRONMENTAL INC. PROJECT REPORT OF BORING NO MW97-ML10 140 BROADWAY, PROVIDENCE, RHODE ISLAND CENTRAL LANDFILL OU2/TASK 4A SHEET 6 OF 8 JOHNSTON, RHODE ISLAND FILE NO 31842 GEOTECH/GEOHYDROLOGICAL CONSULTANTS CHKD BY EAS

DPTH MIN/FT. SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD R NO PEN/REC DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K 201 5 G-25 200+ White and gray GRANITE (still tint of green) HARD B ND

5 white/gray Silts trace black/yellow and orange GRAY

5 fragments (more silt and coarser fragments) GRANITE

4 R

205 4 I

4 s B

4 E E

4 R N

4 S

210 4

4 G-26 210+ Mostly white GRANITE fragments, little A ND

5 black (water is even sillier, fragments are

5 smaller)

7 A 20

215 3 More black flecks, return of green tint to SOFTER ROCK Q

3 white U

4 A

220 3 G-27 220+ Larger/coarser granite fragments R ND

3 black and while GRANITE O

3 U

225 3

230 3 G-28 230+ Larger/coarser granite fragments

3 with return to green tinrt ND

235 3 Dropped from 234.5'+ to 235'+ very quickly 34.5'+

3 no change in silt color) FRACTURES

4 35'+

3 240 3

REMARKS: 20. On 1/14/97, air hammer ringing more loudly at 213'+ - bit is not cutting the bedrock - borehole making 2+gpm Pulled tools to investigate Bit is broken, replaced bit and returned to drilling

NOTES: 1 ) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES; TRANSITIONS MAY BE GRADUAL . 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED; FLUCTUATIONS OF GROUNDV WATER TABLE GZA MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE [BORING NO MW97-ML10 'GZA GEOENV1RONMENTAL INC. PROJECT REPORT OF BORING NO MW97-ML10 1*0 BROADWAY. PROVIDENCE. RHODE ISLAND CENTRAL LANDFILL OU2/TASK 4A SHEET 7 OF 8 JOHNSTON. RHODE ISLAND FILE NO 31842 GEOTECH/GEOHYDROLOGICAL CONSULTANTS CHKD BY EAS

DPTH MIN/FT. SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT FIELD R NO PEN/REC DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K tr 3 G-29 240+ Black and white grained GRANITE (slight B ND 2 gray/green linit, fine to coarse Sand-sized SOFTER COARSER

2 grains). GRAINED l 2 GRANITE R 245 2 I

2 S

I 2 E B

3 R

3 N L 3 S 4 G-30 250+ Black and white grained GRANITE ND I 3 More gray Silt, larger granite fragments A 2 (no green) 253'

2 SOFT I 5 255' ZONE A 5 Q

3 U

3 A

3 HARDER

1260 3 ROCK 5

3 G-31 260+ Black and white GRANITE R ND

3 More medium to coarse fragments, trace 0

3 Gravel-more gray silt U

1 3

265 3

4 Large fragment, more white silt, drill rig 268'

5 bucks and grinds, purple and green crystals

270 2

2 G-32 270+ Green to gray GRANITE with little black and ND

2 race purple large flat fragments) 272'

1 273' FRACTURES

275 2 275' 275'

1 Fracture: (275'+) Flint

2 Shot

2 SOFTER Seal

1 1280 2 279'

REMARKS:

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES; TRANSITIONS MAY BE GRADUAL. 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED; FLUCTUATIONS OF GROUNDWATER TABLE | GZA MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE MADE. BORING NO. MW97-ML10 GZA GEOENV1RONMENTAL INC. PROJECT REPORT OF BORING NO. MW97-ML10 140 BROADWAY. PROVIDENCE. RHODE ISLAND CENTRAL LANDFILL OU2/TASK 4A SHEET 8 OF 8 JOHNSTON, RHODE ISLAND RLE NO. 31842 GEOTECH/GEOHYDROLOGICAL CONSULTANTS OHKDBY EAS

DPTH MIN/ SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT RELD R FT NO PEN-REG DEPTH (FT) BLOWS/6" BURMISTER CLASSIFICATION DESCRIPTION INSTALLED TESTING K 281 2 G-33 280+ Green/gray/white GRANITE fragments, gray GRAY GRANITE B

2 Silts F

3 1 S

3 L C

285 3 T R

3 E E

2 FRACTURE (287'+) 287' R E 21

2 FRACTURE ZONE N

2 S —— 290 2 290 A

2 G-34 290+ Green black/gray GRANITE fragments, gray N —— 3 Silts (fragments as large as fine GRAVEL) GRADUALLY D

3 HARDER GRANITE

295 7 White/gray trace black GRANITE

3 Green/gray /black GRANITE, fragments 22 —— 300 3 G-35 300+ gray Silts 23

END OF EXPLORATION AT 300'+ 24

REMARKS: 21. Air hammer returns medium to coarse GRAVEL fragments of broken rock. 22 Reached bottom 30ff at 11:10 hours on 1/15/97 -developed borehole for 4 hours pumping and surging with 6-inch surge blocks Borehole makes +1 5gpm. water is clear with rust tint 23. On 1/16/97 Colog. Inc. performed geophysical logging including 3-arm borehole caliper. fluid temperature and resistivity, acoutic borehole televiewer, and heat-pulse flow meter logging 24 Between 1/29 and 2/5/97. the borehole was packer tested using 16 10-foot long test intervals, selected based on geophysical logging, from 70 to 300 feet 25 On 2/24/97 a short duration specific capacity test was performed while purging a volume of water equal to that lost to the formation during packer testing 26 Based on the results of borehole geophysics, packer testing and discrete zone analytical sampling, two 2-inch ID Sch 80 monitoring wells were installed to depths of 3001 and 80* with 20" and 10* of 0 01" slot screen, respectively See equipment diagram for further installation details. 27 On 3/1 1/97, GZA installed QED "V\fell Wzard" dedicated bladder pump sampling systems in each monitoring well NOTES 1) STRATIRCATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS MAY BE GRADUAL 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF GROUNDWATER TABLE GZA MAY OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WEFtE MADE BORING NO MW97-ML10 GUILD DRILLING CO., INQ SHEET^ 1 ,.OF! TOO WATER STREET EAST PROVIDENCE, R 1 *"' DATT WELL ^ p flpnr^, P.T. HOLE NO BH-J TO C E Maguire, Inc. ,/innoccc rovi PR OJECT NA ME Hazardous Waste Closing |t rvAT,nN Johnston, R.I. LINEftSTA. ————————. RE PORT SEN T TO above / R.I. SW1C _1_ non, wn 3869 OFFSET .. , SA MPLES SI-KIT ™ " r*,OJnpNn 82-54 SURF Fl FV Timt GROUND WATER OBSERVATlONS CASING SAMPLER CORE BAR «/oq/«i 0 m START 8/25/81 ————— p.m. s Type HW S/S NXD3 COMPLETE 8/26/81 a.m. 4" Size: D 1 3/8" TOTAL HRS. 300^ BORING FOREMAN t , Ricci rs Hcnmer Wt Spun tSU INSPFCTOfl Kr/.. Hammer Fall 24" u*-a" SOILS ENGR. tor/mow nr RDRIWT,

Cosing Sample Type Blows per 6" Moisture SOIL IDENTIFICATION i Strata »- on Sampler SAMPLE o. Blows Depths of Density Remarks include color,groda1ion, Type of per From To or Change soil elc Rock -color, type, condition, hard- g From- To Somple foot 0-6 1 6-12 12-18 Consist, Elev ness , Drilling time , seams and etc No Pen Rec r 0'-1'6" D 9 9 12 Dry Loam - Brown fine Sand 1 18' 12" medium & Gravel (Road Fill) dense

5'-6'6" D 18 22 37 Wet Brown fine to coarse SAND 2 181 7" very & fine to medium Gravel, dense some silt

10' -11 ' 6" D 20 22 25 Wet " color change to Gray 3 181 7" dense Brown 13'6" Top of Rock 13' 6" -\8' 6' C Gray GRANITE, very hard Cl 60' 60h

18'6"-22'6' C C2 48' 45"

22'6" Bottom of Boring 22 "6"

GROUND SURFACE TO 13' 6" USED HW "CASING: THEN Cored Somple Ty je Proportions Used !40lbWt.*3 0"follon2"OD. Sompler SUMMARY: 0=Dry C = Core d W = Washed troce OtolO% Coneskmless Der Sity Cohesive Consistency Fry th Boring •*••* " UP^Undislur bed Piston se 0-4 Soft 30-t-Hord Rock Coring _5_ —— IO ens« 4-6 M/Stiff Samples . .„ 3 TP=TeM Pit A^Augcr V= Vane Test som™°e ?n20lo35fJ%° 30.5£S>M^0 ^D " .»-* *VV, f'Hnir un BH-J GOLDBERG-ZOINO & ASSOCIATES. INC. PROJECT REPORT OF BORING No_WE87^_ 140 BROADWAY, PROVIDENCE, RHODE ISLAND CENTRAL LANDFILL/R1/FS FILE No. -1^3002778 GEOTECHN I CAL/GEOHYDROLOGI CAL CONSULTANTS ——— Johnston, Rl— — CHKD. BY bAS BORING Co. Guild Dri I ing Co. BORING LOCATION Refer to Exploration Location Plan FOREMAN faul bresc 3 " (JKOUNO SURFACh bLbVAl ION 187.0 W fl NVUU GZA ENGINEER Hike Sherr 11 DA It SIAKI B-V-o/ UAlb bNU a-i \- tf GROUNDWATER READINGS SAMPLER: UNLESS OTHERWISE NOTED. SAMPLER CON SISTS OF A 2" SPLIT ————————| —————• ——————• —— - —— • —————————————————— ' SPOON DRIVEN USING A UO Ib. HAMME * FALLING 30 In. 8-19 23' 16' 17 Hours CASING: UNLESS OTHERWISE NOTED, CASING DRIVE X USING A 300 Ib. 8-19 27.7' 16' End of Core Drill HAMMER FALLING 24 In. 8-20 23.4' 16' 16 Hours CASING SIZE: PW 5", HW 4" OTHER: Cor<• » R -in rn 1 HV Dri lied Casing Do uble Tube 3.8" O.D. 8-21 23.1' 16' 16 Hours 3 C B 5 A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT P S 0 INSTALLED N U PEN./ DEPTH DESCRIPTION (. H G S No. REC. (Ft.) BLOWS/6" Burmister CLASSIFICATION S-1 18/13 0.0-1.5 17-25-42 Very dense, rust brown, coarse GRANULAR \. to tine SAND, little(-) fine FILL R-1 37" 1.9-5 Roller Bit Gravel, trace Silt; Fill. 2.0' Guardpipe 2. 4.

4.0' BOULDER 5 and S-2 6/5 5-5.5 82/Refusal Very dense, brown, medium to GRAVELLY fine SAND, littlef*) coarse to SAND R-2 42" 5.5-9 Roller Bit fine Gravel, little Silt. (TILL) 2.0" ID PVC Riser Pipe

S-3 24/15 9-11 23-41 Very dense, brown, medium to 10 fine SAND, little coarse to fine Native 51-63 Gravel, little Silt. Backtfll R-3 24" 12-14 Roller Bit

14' + ROTTEN 15 Very dense, brown, coarse(+) to ROCK 15' S-4 11/4 15-15.9 27-30/5" fine SAND, little fine angular 16.0' Gravel, trace Si It; wet. Bentonite C-1 54/54 16.5-21 4.5 Min C-1: Moderately weathered BEDROCK Seal SCITUATE GRANITE GNEISS, Slightly ROD 57X 4.5 open 60* to 70* angled joints at 1679', 17.5' to 18T2', 19.5' to 18' 5 20'. Broken quartz seam at 17.5' to 18. 4.5 20 20' 3/6" C-2 60/60 21-26 5 C-2: Severely stained and — weathered across open fractures ROD 58% 4.5 at 2l',™1.8' 23.T7 to 24.1' — and 25^2' to 25.6'. 4.1 3. 5.9 Moderately 2.0" 25 Weathered Slotted 5 To Fresh, - PVC Light Screen C-3 60/60 26-31 4.5 C-3: Same to 28 ft: Quartz zone .Gray, - with from 28' to 29.3'; From 28 ft, Hedi urn- Filter ROD 64X 4.3 rock is fresh with weathering Grained, Sand limited to staining of joint SCITUATE Pack 6.2 surfaces: Tight vertica joint GRANITE 27' to 28'; low angle, s ightly GNEISS 5 open joints at 28.1!', 28. 7? and 30 5 C-4 60/59 31-36 5.5 C-4: Fresh rock, withcture staines at d ROD 93X 4.3 $!?!)•: s§#°2nd 3l" 3.7 3.7 35 7 36' C-5 20/20 36-37.7 6 C-5 and C-6: Same: Tight low 37' ROD 100X 8 angle fracture at 37.7' and tight, vertical fracture from Bentonite C-6 39/39 37.7-41 6.5 38:5 ''to 41.6'. Seal ROD 52X 5.0 39.5' 40 REMARKS: 1. Drilled HW casing behind roller bit through bouldery soils to 16 feet; Roller bit advanced to 16.5 ft; Rock coring started at 16.5 feet.

NOTES: 1) STRATIFICATION LINES REPRESENT APPROXIMATE BOUNDARY BETWEEN SOIL TYPES. TRANSITIONS HAY BE GRA 2) WATER LEVEL READINGS HAVE BEEN MADE AT TIMES AND UNDER CONDITIONS STATED. FLUCTUATIONS OF GROUBOkt a in-. *** OCCUR DUE TO OTHER FACTORS THAN THOSE PRESENT AT THE TIME MEASUREMENTS WERE HADE 6ZA BORING HO.WE87-4 GOLDBERG-ZOINO & ASSOCIATES. INC. PROJECT REPORT OF BORING No. WE87-4 40 BROADWAY, PROVIDENCE, RHODE ISLAND SHEET i Up i CENTRAL LANOFILL/R1FS FILE No. "CTSOOZTTB" GEOTECHN I CAL/GEOHYDROLOG I CAL CONSULTANTS jonnston, KI CHKD. BY L-Ab C B A L SAMPLE SAMPLE DESCRIPTION STRATUM EQUIPMENT > S 0 INSTALLED N W PEN./ DEPTH DESCRIPTION 1 G S No. REC. (Ft.) BLOWS/6" Burmister CLASSIFICATION i 4.3 Filter C-7 60/59 41-46 5.5 C-7: Same; tight, low angle SCITUATE Sand stained fractures at 41.4' and GRANITE ROD 94% 6.5 45'. GNEISS 5.5 6.5 45 7.5 End of Exploration at 46'+

85 REMARKS: 2. Cored bedrock from 16.5 feet to 46 feet. Lost drilling water at 23.7 foot depth, with no subsequent return. 3. Bedrock zone between 21.9 feet and 43.5 feet was Packer pressure tested to evaluate bedrock hydraulic conductivity; Injected, a total pf 232 gallons; Bailed approximately 280 gallons. 4. installed one observation we.ll which consists Qf 16' of 2.0" I.D.TVC screen (0.01 inch slot) installed f rom ?0' to 36' with 2.0" I.D. PVC riser pipe to ground surface. On? (' by 4" locking guard pipe was then installed to 3' above ground surface and cemented in place. Refer to figure for additional details.

DEVELOP BUFFER ZONE FOR OU2 AREA GZA GE06NMRONMENTAL. WC. JOB. Engineers and Scientists O7\ SHEET NO. -OF. 140 BROADWAY PROVIDENCE. RHODE BLAND O29O3 (4O1)421-414O CALCULATED BY. -DATE. CHECKED BY __ .DATE.

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- C3 APPENDIX C-3

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-L_4 APPENDIX D

RESIDENTIAL WELL SUMMARY APPENDIX D COMPOUNDS IDENTIFIED IN OU2 AREA RESIDENTIAL WELLS Central Landfill - Johnston, Rhode Island

REPORTED # OF REPORTED/ MCL ABOVE I LOCATIONS) OU1 COMPOUND SAMPLED LOCATIONS (ug/L) MCL j ABOVE MCL COC

RIDOH ANALYTICAL SUMMARY 1,1,1 -Trichloroethane 3/46 200 Yes 43/036 Yes 1 , 1 ,2-Trichloroethane 1/46 5 No — No 1 , 1 -Dichloroethane 3/46 — — — Yes 1 ,1 -Dichloroethylene 2/46 7 Yes 43/036 No 1 ,2-Dichloroethane 3/46 5 Yes 43/174 No 1 ,2 -Dichloroethylene 2/46 70 No — No Bromodichlormethane 1/46 100P No — No Bromoform 2/46 100 P No — No Chlorobenzene 1/46 100 No — Yes Chloroform 14/46 SOP No — No Dibromodichloromethane 2/46 100 P No — No Ethylbenzene 1/46 700 No ... No Methylene Chloride 7/46 5 Yes 32/020 Yes 43/174 43/165 Tetrachloroethylene 4/46 5 UNK* 43/036 No Trichloroethylene 5/46 5 Yes 31/006 Yes

EPA ANALYTICAL SUMMARY Bis(2-ethylhexyl)phthalate 2/7 6 No — Yes Beryllium 2/7 4 Yes 43/174 Yes Calcium 7/7 — ... — No Copper 2/7 1,300 No — No Iron 3/7 — — — No Lead 5/7 15 Yes 43/153 Yes Magnesium 7/7 — — — No Manganese 4/7 — — — Yes Potassium 7/7 — — — No Sodium 7/7 — — — No Tin 1/7 — — — No Zinc 3/7 — — — No

GZA ANALYTICAL SUMMARY Acetone 1/10 — — — No Benzene 1/10 5 L Yes 43/036 Yes Carbon Tertrachloride 1/10 5 Yes 31/017 No Carbon Bisulfide 1/10 — ... — No Chloroethane 1/10 — ... — No Chloroform 1/10 SOP No — No Toluene 1/10 1,000 No — Yes VTICs 1/10 — — ... No Anthracene 1/10 — — — No Bis(2-ethylhexyl)phthalate 1/10 6 Yes 43/036 Yes Dibenzofuran 1/10 — — — No Phenanthracene 1/10 _ — — — No STICs 2/10 — — — No

G:\JOBS\CLF\31866-2.EASVOU2 REV3\APPENDDC-D.XLS Page 1 of 2 02/28/2001 APPENDIX D COMPOUNDS IDENTIFIED IN OU2 AREA RESIDENTIAL WELLS Central Landfill - Johnston, Rhode Island

REPORTED # OF REPORTED/ MCL ABOVE LOCATIONS) OU1 COMPOUND SAMPLED LOCATIONS (ug/L) MCL ABOVE MCL COC

INORGANICS Aluminum 3/10 ... — — No Arsenic 4/10 — — — Yes Barium 9/10 2,000 No — No Beryllium 9/10 5 Yes 31/002 Yes 31/004 43/007 43/167 43/275 Cadmium 4/10 5 Yes 31/002 Yes Calcium 10/10 ... — — No Chromium 1/10 100 No ... Yes Cobalt 2/10 — — ... No Copper 6/10 1,300 No — No Iron 7/10 — — — No Lead 1/10 15 Yes 31/002 Yes Magnesium 10/10 — — — No Manganese 8/10 — — — Yes Nitrates (N) 7/10 10,000 Yes 31/002 Yes Nitrites (N) 2/10 1,000 No ... No Potassium 10/10 — — — No Selenium 2/10 50 No ... No Sodium 9/10 ...... — No Sulfates (SO4) 4/10 500,000 No No Thallium 3/10 2 Yes 31/002 No 43/007 43/036 Vanadium 4/10 — — — Yes Zinc 3/10 ... — ... No ^slili! i|jii|ilj|p Illiil ^indicates Maximum Conta L Drinking Water Regulations

G:\JOBS\CLF\31866-2.EAS\OU2 REV3\APPENDK-D.XLS Page 2 of 2 02/28/2001 -STUDY." AREA ,\\' • 'A«&\ ."-... - *V:.- 15

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HUMAN HEALTH RISK DATA APPENDIX E-l

RISK CHARACTERIZATION FOR RESIDENTIAL WELLS 31/004, 43/167, 43/244T AND 43/070 APPENDIX E-l

RISK CHARACTERIZATION FOR RESIDENTIAL WELLS 31/004,43/167, 43/244T, AND 43/070

Four residential wells which were sampled as part of the RI/FS process have been determined to be outside the zone of influence of the groundwater plume associated with the landfill. Hydraulic modeling (refer to Section 5.00 of the Main Report) has indicated that these wells were outside the zone of influence of the landfill groundwater plume under pumping and non-pumping conditions. Because contaminants in these wells have source(s) other than the landfill, these wells have been evaluated separately and the risks are presented in this appendix.

The four residential wells are at lots 31/004, 43/167, 43/070 and 43/244t. The last well is only used for irrigation purposes; the house has been connected to the public water supply. However, this well was evaluated as if it were currently a drinking water source.

The risk characterization methodology followed for these wells is the same as that presented in Section 8.00 of the main report. Thus, exposure to groundwater is calculated separately for each well and cumulative risks including all applicable pathways calculated. The following discussion briefly presents the tables containing the information necessary for this risk characterization. Many of these tables are the same as those presented in Section 8.00; they are included here so that this appendix could serve as a "stand alone" document. Tables El-1 and El-2 contain information on the EPCs. Exposure assumptions are presented in Tables El-3 and El-4. All relevant chemical-specific information is shown in Tables El-5 through El-8.

The cumulative hazard indices and risk estimates are presented in Table El-9 and the relative contribution of various pathways to the cumulative risk is presented in Table El-10.

The high end exposure results are summarized as follows. The risks associated with ingestion of groundwater at residential well RW31/004, located near the Upper Simmons Reservoir, were summed to yield a total HI of 2.4. The total ILCR estimate for this receptor is 6 x 10". The cumulative, non-cancer and cancer risks for this receptor exceeded risk management criteria, primarily due to the detected concentrations of arsenic and beryllium. The risks associated with ingestion of groundwater at residential well RW43/167, located northwest of the landfill, were summed to yield a total HI of 1.4 and with an ILCR estimate of 4 x 10"4. The cumulative non-cancer and cancer risks for this receptor slightly exceed risk limits, primarily due to detected concentrations of arsenic, copper and beryllium. The risks associated with ingestion of groundwater at residential well RW43/244T located northwest of the landfill were summed to yield a total HI of 2.0 and a total ILCR estimate of 3x10"*. Both the estimated non-cancer and cancer risks for this receptor slightly exceed EPA risk limits/ranges, due to the detected levels of arsenic. However, as previously described, this residence is owned by RIRRC and has been connected to the municipal water supply. Neither the non-cancer or cancer risks estimated for residential well 43/070 located northwest of the landfill exceed EPA limits.

The following is a summary of groundwater ingestion risks for the central tendency exposure. Risks associated with central tendency exposure were approximately one-half of the risks associated with high end exposure. The risks at residential well RW31/004 were summed to yield a total HI of 1.3 and the total ILCR estimate is 2 x 10^. The estimated risks are associated with the presence of arsenic in groundwater. Central tendency risks for residential well RW 43/167 were 0.79 (HI) and 1 x \QA (ILCR). The non-cancer risk was slightly below the limit of 1, while the cancer risk is equivalent to the upper end of EPA's risk range of 1 x KT4- 1 x 10-6. RW43/244Thad a total HI (1.1) which slightly exceeded EPA's non- cancer risk limit, and an ILCR of 8 x 10"5 which is within EPA's target risk range. As with the upper end exposure, none of the estimated risks for 43/070 exceed target risk criteria.

Table E1 -17 presents a comparison of measured concentrations at these four wells to drinking water standards. Only one metal, beryllium, was detected in excess of enforceable standards. However, this metal was detected at concentrations consistent with background. Three other metals, aluminum, iron and manganese were detected at levels above secondary maximum contaminant levels (SMCLs). These SMCLs are based on aesthetics, not health effects; however, and are not enforceable.

G:\3I866.ZYN\31866-20.LJC\REPORTS\APP E2n.DOC File No. 31866.20 TABLE El-1 PlfC I 0( I 11/17/1999

EXPOSURE POINT CONCENTRATIONS Central Landfill - OU2 Johnston, Rhode Island

Resident Croundwater Groundwater Groundwater Groundwater Contaminants Concentration Concentration Concentration Concentration »t Well at Well at Well at Well RW31004 RW43I67 RW43244T RW43070 (mg/1) (mg/1) (mg/l) (mg/1)

Volatile Organic Compounds

,1,1-Trichloroethane ND ND ND ND , 1 ,2-Trichlof oethane ND ND ND ND . 1 -Dichloroethane ND ND ND ND ,1-Dichloroethene ND ND ND ND cis-1 ,2-Dichloroethene ND ND ND ND ,2-Dichlorobenzene ND ND ND ND ,3-Dichlorobenzcne ND ND ND ND ,4-Dichlorobenzene ND ND ND ND 4-Methyl-2-Penlanonc ND ND ND ND Acetone ND ND NA ND Benzene ND ND ND ND Carbon Tetrachloride ND ND ND ND Chlorobenzene ND ND ND ND Chloroform ND ND ND ND Elhylbenzene ND ND ND ND Methyl ethyl Ketone ND ND NA NA Tetrachloroethene ND ND ND ND Toluene ND ND ND ND Trichloroethcne ND ND ND ND Vinyl Chloride ND ND ND ND Xylenes ND ND ND ND

Sfntivolalilf Organic Compounds

2,4-Dichlorophenol ND ND ND ND 2-Chlorophenol ND ND ND ND 4-Methylphenol ND ND ND ND Benzo(a)an(hracene ND ND ND ND Benzo(a)pyrene ND ND ND ND Benzo(b)nuorantnene ND ND ND ND Benzo(g.h,i)perylene ND ND ND ND bis(2-Ethylhexyl)phthalate ND ND ND ND Chrysene ND ND ND ND Naphthalene ND ND ND ND Phenanthrene ND ND ND ND

Pesliddes/PCBs

Aldrin ND ND ND ND delta-BHC ND ND ND ND Dieldrin ND ND ND ND

Metals

Aluminum, total 4.1E-01 4.9E-OI ND ND \. Arsenic, total 8.4E-03 2.6E-O3 7.0E-03 ND Barium, total 2.2EXJ1 3.4E-02 X4E-02 2.3E-03 '<' !." Beryllium, total 6.3E-03 5.SE-03 2.0E-03 ND Cadmium, total ND ND 8.9E-04 ND Copper, total :;7.8E-02 Z6E-OI 5.3E-02 I.OtOl Iron, total 6.4E-01 5.3E-01 4.3E+00 ND Lead, total ND ND NA ND Manganese, total I.1E-OI 7.4E-02 I.8E-OI ND Mercury, total ND ND ND ND Nickel, total ND ND ND ND Thallium, total ND ND ND ND Vanadium, total 4.5E-03 ND 5.2E-04 ND Zinc, total 2.2E-01 l.OE+OO ND ND

Notes: 1. 95% UCL EPCs were calculated based on normal, lognormal or non-normal distribution. Refer to exposure point concentration section of the risk assessment text for more information. 2. Shade indicates consistent with background. 3. NA •= Not Analyzed; NCC = Not a Contaminant of Concern in this medium; ND = Not Detected.

C:\3l««2YN\3l(i66-K).UC\RW_E-2\Zyorwer«:iils\EPC File No. 31866.20 Page 1 of I 11/17/1999

TABLE El-2

SAMPLE LOCATIONS USED TO CALCULATE EXPOSURE POINT CONCENTRATIONS Central Landfill - OU2 Johnston, Rhode Island

Medium Exposure Point Sample Location and Identification

Residential Groundwater RW31004

RW43167

RW43244T

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TABLE El-5

CONTAMINANT-SPECIFIC PERMEABILITY COEFFICIENTS Central Landfill - OU2 Johnston, Rhode Island

Permeability Coefficient Contaminant Kp (cm/hour) Notes

Volatile Organic Compounds 1,1,1 -Trichloroethane 1.7E-02 b 1,1,2-Trichloroethane 8.4E-03 b 1 , 1 -Dichloroethane 8.9E-03 b 1, 1-Dichloroelhene 1.6E-02 b cis- 1 ,2-Dichloroethene l.OE-02 b 1 ,2-Dichlorobenzene 6. IE-02 b 1 ,3-Dichlorobenzene 8.7E-02 b 1 ,4-Dichlorobenzene 6.2E-02 b 4-Methyl-2-Pentanone 3.3E-03 b Acetone 5.7E-04 c Benzene 1. IE-01 a Carbon Tetrachloride 2.2E-02 b Chlorobenzene 4. IE-02 b Chloroform 1.3E-01 a Ethylbenzene l.OE+00 a Methyl ethyl Ketone 5.0E-03 a Tetrachloroethene 3.7E-01 a Toluene l.OE+00 a Trichloroethene 2.3E-01 a Vinyl Chloride 7.3E-03 b Xylenes 8.0E-02 b Semivolatile Organic Compounds

2,4-Dichlorophenol 6.0E-02 a 2-Chlorophenol 3.3E-02 a 4-Methylphenol 8.2E-03 e Benzo(a)anthracene • 8. IE-01 b Benzo(a)pyrene 1.2E+00 b Benzo(b)fluoranthene 1.2E+00 b Benzo(g,h,i)perylene 1.7E+00 c bis(2-Ethylhexyl)phthalate 3.3E-02 b Chrysene 8. IE-01 b Di-n-butylphthalate 3.3E-02 b Naphthalene 6.9E-02 b Phenanthrene 2.7E-01 b Pesticides/PCBs

Aldrin 1.6E-03 b delta-BHC Dieldrin 1.6E-02 b

G A31866.ZYN\31866-20.LJC\RW_E-2\Zynnvchm.xlsPC QA: CDS Date: 8/5/97 File No. 31866.20 Page 2 of 2 11/17/1999

TABLE El-5

CONTAMINANT-SPECIFIC PERMEABILITY COEFFICIENTS Central Landfill - OU2 Johnston, Rhode Island Permeability Coefficient Contaminant Kp (cm/hour) Notes

Metals Aluminum, total 1 .OE-03 d Arsenic, total l.OE-03 d Barium, total 1. OE-03 d Beryllium, total l.OE-03 d Cadmium, total l.OE-03 d Copper, total l.OE-03 d Iron, total l.OE-03 d Lead, total l.OE-03 d Manganese, total l.OE-03 d Mercury, total l.OE-03 d Nickel, total l.OE-03 d Thallium, total l.OE-03 d Vanadium, total l.OE-03 d Zinc, total l.OE-03 d

Priority of Sources: a. Experimentally measured Kp values obtained from US EPA, Dermal Exposure Assessment: Principals and Applications, Interim Report, Office of Research and Development, EPA/600/8-91/01 IB, Tables 5-3 and 5-8. b. Estimated Kp values obtained from US EPA, Dermal Exposure Assessment: Principals and Applications, Interim Report, Office of Research and Development, EPA/600/8-91/01 IB, Tables 5-7 and 5-8. c. Kp values calculated by GZA using Equation 5.8 from U.S. EPA, Dermal Exposure Assessment: Principles and Applications, Interim Report, Office of Research and Development, EPA/600/8-91/01 IB, January 1992. d. A default value of 0.001 cm/hr was used to represent the Kp for inorganic compounds not tested as recommended in U.S. EPA, Dermal Exposure Assessment: Principles and Applications, Interim Report, Office of Research and Development, EPA/600/8-91/01 IB. Notes: e. Experimentally measured value for phenol was used. Sufficient data are not available to calculate a value for this compound.

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t— 1— -. -."• .)•;•.: •-» '•"• V u s 1 s u u l tV rt n 1 *'" " ^vH I s 1 I S I a; XJ : c 1 1 c V-: 1 1 1 t 1 £ 2 O O 1 1 O O O O r «*- ---- s O o i o i 1O o - ' ^'ff e ?v-- - o •s "o "f > ja3ij ;ii |H § S | • . -.;;/i2£ "" r >• .•:' I !.! 1 M i (/> u 1 u u ! t> oo 00 oo 00 00 : 00 00 00 ^ c c C : C c

t- o 0 < .:'• £ £Tf r— i i i| 0 itn : 5<^1 t*} ••* m i "J •^~ S •q- s 5 ^ ? ? ^ ^ ? ? ^ "^ I01 K OL c< jet: of &. „ J, K a ?iS i3 o1. -i y. s" • t*1 *- Vt " — "D ^ u , • v>l.x U v.^tv.: : ;J^i u c - ' .S ^ '""' • *' j^~- .•2 (S : •. if~*r*- " '•=•---/" -7 "- ' 1 § ~~( 11/1 CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESnONOFGROUNDWATER(RW3l004) HIGH END EXPOSURE~~

~~RECEPTOR: Resident - Current CHRONIC NONCARCINOGENIC EFFECTS~~

Receptor- Chronic Oral Exposure Oral Specific Average Chronic Hazard Contaminants Point x Absorption x Exposure = Daily / Reference = Index Concentration Adjustment Factor Dose Dose (mg/1) Factor (l/kg-day) (mp/kg-day) (mg/kg-day)

Votarilt Organic Compound*

1,1,1 -Trichloroe thane ND 1.00 5.6E-02 NC 9.0E-02 NC 1 , 1 ,2-Trichloroethane ND 1.00 56E-02 NC 40E-03 NC 1 , 1 -Dichloroelhane ND 1.00 56E-02 NC I.OE-01 NC 1,1-Dichloroethene ND 1.00 56E-02 NC 9.0E-03 NC cis- 1 ,2-Dichloroethene ND 1.00 56E-02 NC I.OE-02 NC 1 ,2-Dichloro benzene ND 1.00 5.6E-02 NC 9.0E-02 NC 1 ,3-Dichlorobenzene ND 1.00 5.6E-02 NC NA NC 1 ,4-Dichlorobenzene ND 1.00 5.6E-02 NC NA NC 4-Mcthyl-2-Pen

~~Stmivotatile Organic Compounds~~

2,4-Dichlorophenol ND 1.00 5.6E-02 NC 3.0E-03 NC 2-ChIorophenol ND 1.00 5.6E-02 NC 5.0E-03 NC 4-Methylphenol ND 1.00 5.6E-02 NC 5.0E-03 NC Benzo(a)anthracene ND 1.00 5.6E-02 NC 3.0E-02 NC Benzo(a)pyrene ND 1.00 56E-02 NC 3.0E-02 NC Benzo(b)fluoranthcne ND 1.00 5.6E-02 NC 3.0E-02 NC Benzo<£,h,i)perylene ND 1.00 5.6E-02 NC 3.0E-02 NC bis(2-Ethylhexyl)phthalate ND 1.00 56E-02 NC 2.0E-02 NC Chrysene ND 1.00 5.6E-02 NC 3.0E-02 NC Di-n-butylphthalate ND 1.00 5.6E-02 NC l.OE-01 NC Naphthalene ND 1.00 5.6E-02 NC 2.0E-02 NC Phenanthrene ND 1.00 5.6E-02 NC 3.0E-02 NC

~~Feiticides/PCBs~~

~~SUBTOTAL: 2.4E+00~~

~~QA:MBGD«e:7/IW« File No 3IB6620 TABLE El-11 (CONTD) Piee2of2 \\mi\9V) CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTON OF GROUNDWATER (RW31004) HIGH END EXPOSURE~~

~~RECEPTOR: Resident - Current CARCINOGENIC EFFECTS~~

Receptor Lifetime Incremental Exposure Oral Specific Average Cancer Lifetime Contaminants Point x Absorption x Exposure = Daily x Slope = Cancer Concentration Adjustment Factor Dose Factor Risk (mg/l) Factor (l-hr/cm-kg-day) (mg/kg-day) (mg/kg-day)-' Estimate

~~Volatile Organic Compounds~~

1,1,1 -Trichloroethane ND 1.00 I.6E-02 NC NA NA 1,1.2-Trichloroethane ND 1.00 I.6E-02 NC 5.7E-02 NA I.l-Dichloroethane ND 1.00 I.6E-02 NC NA NA 1,1-Dichloroethene ND 1.00 1 .6E-02 NC 60E-01 NA cis- 1 ,2-Dichloroethene ND 1.00 1.6E-02 NC NA NA 1,2-Dichlorobenzene ND 1.00 1.6E-02 NC NA NA 1 ,3-Dichlorobenzene ND 1.00 I.6E-02 NC NA NA 1 ,4-Dichlorobenzene ND 1.00 I.6E-02 NC 2.4E-02 NA 4-Methyl-2-Pentanone ND 1.00 I.6E-02 NC NA NA Acetone ND 1.00 I.6E-02 NC NA NA Benzene ND 1.00 1.6E-02 NC 2.9E-02 NA Carbon Tetrachloride ND 1.00 1.6E-02 NC I.3E-01 NA Chlorobenzene ND 1.00 I.6E-02 NC NA NA Chloroform ND 1.00 1 .6E-02 NC 6. IE-03 NA Ethylbenzene ND 1.00 1.6E-02 NC NA NA Methyl ethyl Ketone ND 1.00 1 6E-02 NC NA NA Tetrachloroethene ND 100 I.6E-02 NC 5.2E-02 NA Toluene ND 1.00 1.6E-02 NC NA NA Trichloroethene ND 1.00 1 6E-02 NC 1. IE-02 NA Vinyl Chloride ND 1.00 I.6E-02 NC 1.9E+00 NA Xylenes ND 1.00 1.6E-02 NC NA NA

~~Sernivolatilf Organic Compounds~~

2,4-Dichlorophenol ND 1.00 I.6E-02 NC NA NA 2-Chlorophenol ND 1.00 I.6E-02 NC NA NA 4-Methylphenol ND 1.00 I.6E-02 NC NA NA Benzo(a)anthracene ND 1.00 I.6E-02 NC 7.3E-01 NA Benzo(a)pyrene ND 1.00 1.6E-02 NC 7.3E+00 NA Benzo(b)fluoranlhene ND 1.00 1.6E-02 NC 7.3E-01 NA Benzo(g,h,i)perylene ND 1.00 1.6E-02 NC NA NA bis(2-Elhylhexyl)phlhalate ND 1.00 1.6E-02 NC I.4E-02 NA Chrysene ND 1.00 I.6E-02 NC 7.3E-02 NA Di-n-butylphthalate ND 1.00 I.6E-02 NC NA NA Naphthalene ND 1.00 1.6E-02 NC NA NA Phenanthrene ND 1.00 1.6E-02 NC NA NA

~~Pesticides/PCBs~~

~~Aldrin ND 1.00 1.6E-02 NC I.7E+OI NA delta-BHC ND LOO 1.6E-02 NC NA NA Dieldrin ND 1.00 I.6E-02 NC 1.6E+01 NA Metals~~

Aluminum, total ; : ':; - i: 4.iE4i i;:-v ._.;; :;LOO '•; : I.6E-02 6JE-03 :; NA . NA Arsenic, total 8.4E-03 :; 1.00 1.6E-02 1.3E-04 1.5E+00 2.0E-04 Barium, total : i ; 2-jE-oi ::; ::: i.00 1.6E-C2 3.SE-03 NA NA Beryllium, total : V6.3frd3:..::U 1.00 L6E-02 l.OE-04 43E-IOO 4.4E-04 Cadmium, total ND : ! 1.00 I.6E-02 NC NA NA Copper, total ; ; :;7.8&o2: ' :^ :i.oo 1.6E-02 1-3E-03 NA '- NA Iron, total 6.4E-OI 1.00 1.6E-02 l.OE-02 NA NA Lead, total ND 1.00 1.6E-02 NC NA NA Manganese, total 1. IE-01 LOO 1.6E-02 I.7E-03 NA NA Mercury, total ND 1.00 I.6E-02 NC NA NA Nickel, total ND 1.00 1.6E-02 NC NA NA Thallium, total ND 1.00 1.6E-02 NC NA NA Vanadium, total 4.5E-03 1.00 1.6E-02 7.2E-05 NA NA Zinc, total 2.2E-01 LOO 1.6E-02 3.5E-03 NA NA

~~SUBTOTAL: 6.4E-04~~

~~Notes:~~

~~1. N A « Not Analyzed/Not Applicable: NC = Not Calculated; NSCC = Not a Study Chemical of Concern. 2. For constituents without an AAF value, a default value of LOO was used.~~

~~0:\3l866iYN\3l866.J01JORW_E-2\Z»iir«Tgw.«l«\llGWLR_3l4C QA:MBG Dace: 7(15W file No. 11866.20 TABLE El-12 Page I o<2 M/I7/I999~~

~~CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGEST1ON OF GROUNDWATER (RW43167) HIGH END EXPOSURE~~

~~RECEPTOR: Resident - Cunent CHRONIC NONCARCINOGEN1C EFFECTS~~

Receptor Chronic Oral Exposure Oral Specific Average Chronic Hazard Contaminants Point x Absorption x Exposure = Daily / Reference = Index Concentration Adjustment Factor Dose Dose (mp/1) Factor (1/kg-day) (mg/kg-day) (mg/kg-day)

~~Volatile Organic Compounds~~

Stmivotalilf Organic Compounds 2,4-Dichlorophenol ND 1.00 5.6E-02 NC 3.0E-03 NC 2-Chlorophenol ND 1.00 5.6E-02 NC 5.0E-03 NC 4-Methylphenol ND 1.00 5.6E-02 NC 5.0E-03 NC Benzo(a)anthracene ND 1.00 5.6E-02 NC 3.0E-02 NC Benzo(a)pyrene ND 1.00 5.6E-02 NC 3.0E-02 NC Benzo(b)fluoranthene ND 1.00 S.6E-02 NC 3.0E-02 NC Benzo(g,h,i)oerylene ND 1.00 5.6E-02 NC 3. OE-02 NC bis(2-Eihylhexyl)phthalate ND 1.00 5.6E-02 NC 2.0E-02 NC Chrysene ND 1.00 5.6E-02 NC 3.0E-02 NC Di-n-burylphthalate ND 1.00 5.6E-02 NC l.OE-OI NC Naphthalene ND 1.00 5.6E-02 NC 2.0E-02 NC Phenanthrene ND 1.00 5.6E-02 NC 3. OE-02 NC

~~PesriciJts/PCBs~~

~~Aldrin ND 1.00 5.6E-02 NC 3.0E-05 NC delta-BHC ND 1.00 5.6E-02 NC NA NC Dieldrin ND 1.00 5.6E-02 NC 5.0E-05 NC~~

Metals Aluminum, tool 4.9E-OI: •:;;;; : •-; I.o6.. ': /:• . : S.6E-02 2.7E-02 NA NC Arsenic, total 2.6E-03 1.00 5.6E-02 I.5E-04 3.0E-04 4.9E-01 ; Barium, total J.4E-02 : ; •• . : 1.00 : -3-6E-02 1.9E-03 7.0E-02 2.7E-02 Beryllium, total 5.5E-03 : •••• LOO \ !:L:5,6E-02 •',. 3.1E-04 2.0E-03 1.5E-OI Cadmium, total ND 1.00 5.6E-02 NC 5.0E-04 NC : : : : Copper, total :;:2.6E-01::;;r;;: • :; : too v:" ;: :;S.6E-02: : '• I.SE-02 3.7E-02 3.9E-01 Iron, total 5.3E-01 1.00 5.6E-02 3.0E-02 NA NC Lead, total ND 1.00 5.6E-02 NC NA NC Manganese, total 7.4E-02 1.00 5.6E-02 4.2E-03 2.4E-02 I.7E-01 Mercury, total ND 1.00 5.6E-02 NC 3.0E-04 NC Nickel, total ND 1.00 5.6E-02 NC 2.0E-02 NC Thallium, total ND 1.00 5.6E-02 NC 2.0E-OI NC Vanadium, total ND 1.00 5.6E-02 NC 7. OE-03 NC Zinc, total I.OE+00 1.00 5.6E-02 5.7E-02 3.0E-01 I.9E-01

~~SUBTOTAL: | 1.4E+00~~

C:\3l866ZYN\3IH66-20.1JORW.E-2\ZyiMWfjw.iUjMIGWLR_4JI6K QA: MUG Due: 7(15/99 Fik No. 31866.20 TABLE El-12 (CONTD) PiCe2o(2 11/17/1999 CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OF GROUNDWATER (RW43167) HIGH END EXPOSURE

~~RECEPTOR: Resident - Current CARCINOGENIC EFFECTS~~

~~Receptor Lifetime Incremental Exposure Oral Specific Average Cancer Lifetime Contaminants Point x Absorption x Exposure = Daily x Slope * Cancer Concentration Adjustment Factor Dose Factor Risk~~

~~Volatile Organic Compounds~~

~~Setnivotalile Organic Compounds~~

2,4-Dichlorophenol ND 1.00 1.6E-02 NC NA NA 2-Chlorophenol ND 1.00 1.6E-02 NC NA NA 4-Methylphenol ND 1.00 1.6E-02 NC NA NA Benzo(a)anthracene ND 1.00 1.6E-02 NC 7.3E-01 NA Benzo(a)pyrene ND 1.00 1.6E-02 NC 7.3E+00 NA Benzo(b)nuoranthene ND 1.00 1.6E-02 NC 7.3E-01 NA Benzo(g.h.i)perylene ND 1.00 1 .6E-02 NC NA NA bis(2-Etriylhexyl)phthaIate ND 1.00 1.6E-02 NC I.4E-02 NA Chrysene ND 1. 00 1.6E-02 NC 7.3E-02 NA Di-n-bulylphthalate ND 1.00 I.6E-02 NC NA NA Naphthalene ND 1.00 1.6E-02 NC NA NA Phenanthrene ND 1.00 I.6E-02 NC NA NA

~~PesliciJes/PCBs~~

~~Aldrin ND 1.00 1.6E-02 NC 1.7E+01 NA delta-BHC ND 1.00 I.6E-02 NC NA NA DieMrin ND 1.00 I.6E-02 NC 1.6E+01 NA~~

~~Mctah~~

Aluminum, tool 4-9E4JI i 1.00 1.6E-02 7.SE-03 NA ' :; : : NA ; Arsenic, total 2.6E-03 1.00 I.6E-02 4.2E-05 1.5E400 6.3E-05 ; Barium, total 3.4E-02,v; v i 1.00 I.6E-02 ':•• 5.4E-04 NA NA Beryllium, total • • 5.5E-03 '•••^•: 1.00 I.6E-02 8.8E-03 4JE+OO 3.8E-04 Cadmium, total ND 1.00 1.6E-02 NC NA NA : Copper, total ' • 2.6E-pl:Un : LOO 1.6E-02 4.1E-03 NA NA Iron, total 5.3E-OI 1.00 1.6E-02 8.5E-03 NA NA Lead, lota] ND 1.00 I.6E-02 NC NA NA Manganese, total 7.4E-02 1.00 I.6E-02 1.2E-03 NA NA Mercury, total ND 1.00 1.6E-02 NC NA NA Nickel, total ND 1.00 1 .6E-02 NC NA NA Thallium, total ND 1.00 1 .6E-02 NC NA NA Vanadium, total ND 1.00 I.6E-02 NC NA NA Zinc, total 1.0E400 1.00 I.6E-02 1.6E-02 NA NA

~~SUBTOTAL: 4.4E-04~~

~~Notes: 1. NA = Not Analyzed/Not Applicable; NC = Not Calculated: NSCC = Not a Study Chemical of Concern. 2. For constituents without an AAF value, a default value of 1.00 was used.~~

CA31866ZYNV3l«66-20JJCMlW_E-2\ZrIir«itw.«liyiCWLR.«l67C QA:MBGDae 7/IS/V9 File No. 31866.20 TABLE El-13 P.tclof2 II/I7M999 CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OF GROUNDWATER (RW43244T) HIGH END EXPOSURE

~~RECEPTOR: Resident - Current CHRONIC NONCARCINOGENIC EFFECTS~~

~~Volatile Organic Compounds~~

2,4-Dichlorophenol ND 1.00 5.6E-02 NC 3 OE-03 NC 2-Chlorophenol ND 1.00 5.6E-02 NC 5.0E-03 NC 4-Methylphenol ND 1.00 5.6E-02 NC 5 OE-03 NC Benzo(a)anthracene ND 1.00 5.6E-02 NC 3. OE-02 NC Benzo(a)pyrene ND 1.00 5.6E-02 NC 3.0E-02 NC Benzo(b)nuoranthene ND 1.00 5.6E-02 NC 3.0E-02 NC Benzo(g,h,i )perylene ND 1.00 5.6E-02 NC 3.0E-02 NC bis(2-Ethylhexyl)phthalate ND 1.00 5.6E-02 NC 2.0E-02 NC Chrysene ND 1.00 5.6E-02 NC 3. OE-02 NC Di-n-butylphthalate ND 1.00 5.6E-02 NC l.OE-01 NC Naphthalene ND 1.00 5.6E-02 NC 2.0E-02 NC Phenanthrene ND 1.00 5.6E-02 NC 3.0E-02 NC Pesticidrs/PCBs

~~Aldrin ND 1.00 5.6E-02 NC 3.0E-05 NC delta-BHC ND 1.00 5.6E-02 NC NA NC Dieldrin ND 1.00 5.6E-02 NC 5.0E-05 NC~~

Metals : :: :•: Aluminum, total '•• . ' •.- NP::: ...;; 1.00 5.6E-02 .NC NA NC Arsenic, total 7.0E-03 1.00 5.6E-02 3.9E-04 3.0E-04 I.3E+00 Barium, total 2.4E-02: i:oo 5.6E-02 1.3E-03 7.0E-02 I.9E-02 Beryllium, total lOE-03 ": ••• ;;:IXX> 5.6E-02 LIE-04 2.0E-03 S.6E-02 Cadmium, total 8.9E-04 1. 00 5.6E-02 5.0E-05 5.0E-04 l.OE-01 Copper, total 53E-02 1.00 5.6E-02 3.0E-03 3.7E-02 8.IE-02 Iron, total 4.3E400 1.00 5.6E-02 2.4E-01 NA NC Lead, total NA 1.00 5.6E-02 NC NA NC Manganese, total I.8E-OI 1.00 5.6E-02 l.OE-02 2.4E-02 42E-OI Mercury, total ND 1.0 0 5.6E-02 NC 3.0E-04 NC Nickel, total ND 1.00 5.6E-02 NC 2.0E-02 NC Thallium, total ND 1.00 5.6E-02 NC 2.0E-01 NC Vanadium, total 5.2E-04 1.00 5.6E-02 2.9E-05 7.0E-03 4.2E-03 Zinc, total ND 1. 00 5.6E-02 NC 3.0E-OI NC

~~SUBTOTAL: 2.0E+OO~~

C\S I B66.Z YNJ l«66-20.LJORW_E-2\Z>no«f w.xh\IIGWLR_<3244TC QA:MBGD«c:7/l5/W fik No 31866.20 TABLE El-lJ (CONTD) Fa«e2o<2 11/17/1999 CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OF GROUNDWATER (RW43244T) HIGH END EXPOSURE

~~RECEPTOR: Resident - Current CARCINOGENIC EFFECTS~~

Receptor- Lifetime Incremental Exposure Oral Specific Average Cancer Lifetime Contaminants Point x Absorption x Exposure = Daily x Slope = Cancer Concentration Adjustment Factor Dose Factor Risk (mg/1) Factor (I-hr/cm-kg-day) (mg/kg-day) (mg/kg-day)-1 Estimate

~~Volatile Organic Compounds~~

1,1,1 -Trichloroe thane ND 1.00 1.6E-02 NC NA NA 1 . 1 ,2-Trichloroe thane ND 1.00 1 .6E-02 NC 5.7E-02 NA I.l-Dichloroethane ND 1.00 16E-02 NC NA NA 1 , 1 -Dichloroethene ND 1.00 I.6E-02 NC 6.0E-01 NA cis- 1 ,2-Dichloroethene ND 1.00 1 .6E-02 NC NA NA 1 ,2-Dichlorobenzene ND 1.00 1.6E-02 NC NA NA 1 ,3-Dichlorobenzene ND 1.00 1.6E-02 NC NA NA 1 ,4-Dichlorobenzene ND 1.00 1.6E-02 NC 2.4E-02 NA 4-Methyl-2-Pentanone ND 1.00 1.6E-02 NC NA NA Acetone NA 1.00 1 .6E-02 NC NA NA Benzene ND 1.00 1 .6E-02 NC 2.9E-02 NA Carbon Tetrachloride ND 1.00 I.6E-02 NC I.3E-01 NA Chlorobenzene ND 1.00 1.6E-02 NC NA NA Chloroform ND 1.00 1 6E-02 NC 6. IE-03 NA Ethylbenzene ND 1.00 1.6E-02 NC NA NA Methyl ethyl Ketone NA 1 00 1 6E-02 NC NA NA Tetrachloroethene ND 1.00 1 .6E-02 NC 5.2E-02 NA Toluene ND 1.00 1 .6E-02 NC NA NA Trichloroethene ND 1.00 1.6E-02 NC 1. IE-02 NA Vinyl Chloride ND 1.00 1 .6E-02 NC I.9E+OO NA Xylenes ND 1.00 1.6E-02 NC NA NA

~~Semivolalile Organic Compounds~~

2,4-Dichlorophenol ND 1.00 I.6E-02 NC NA NA 2-Chlorophenol ND 1.00 I.6E-02 NC NA NA 4-Methylphenol ND 1.00 1.6E-02 NC NA NA Benzo(a)anthracene ND 1.00 I.6E-02 NC 7.3E-OI NA Benzo(a)pyrene ND 1.00 1.6E-02 NC 7.3E+OO NA BenzoO>)fluoranthene ND 1.00 1.6E-02 NC 7.3E-OI NA Benzo(g,h,i)perylene ND 1.00 I.6E-02 NC NA NA bis<2-Ethylhexy])phthalaie ND 1.00 I.6E-02 NC 1.4E-02 NA Chrysene ND 1.00 1.6E-02 NC 7.3E-02 NA Di-n-butylphthalate ND 1.00 1.6E-02 NC NA NA Naphthalene ND 1.00 1.6E-02 NC NA NA Phenanthrene ND 1.00 1.6E-02 NC NA NA

~~Ptslicidts/PCBs~~

~~Aldrin ND 1.00 1.6E-02 NC 1.7E+01 NA delta-BHC ND 1.00 1.6E-02 NC NA NA Dieldrin ND 1.00 1.6E-02 NC 1.6E+01 NA~~

~~Metals~~

! Aluminum, total ' .'ND ;L •} : -0;-i'i:JX» ' • L6E-02 NC NA . : :i: NA 1.6E-02 1. IE-04 1.5E+00 1.7E-04 Arsenic, total 7.0E-03 i 1.00 Barium, total •• 14E-02 .:; • ;::;- :Jni.6: 6 1.6E-02 3.8E-04 NA , NA Beryllium, lota] : -iOE-03. ":•:;;;!: - l-ioo ' •1.6E-02 ;.. 3.2E-05 4.3E+00 !• I.4E-04 Cadmium, total 8.9E-04 1.00 1.6E-02 I.4E-05 NA NA : Copper, total .;.5.3E-oi.;. ;!; ••'; jm-lM L6E-02 8.3E-04 : NA NA Iron, total 4.3E-KX) 1.00 1.6E-02 6.9E-02 NA NA Lead, total NA 1.00 1.6E-02 NC NA NA Manganese, total I.8E-01 1.00 I.6E-02 2.9E-03 NA NA Mercury, total ND 1.00 1.6E-02 NC NA NA Nickel, total ND 1.00 1 6E-02 NC NA NA Thallium, total ND 1.00 1 .6E-02 NC NA NA Vanadium, total 5.2E-04 1.00 I.6E-02 84E-06 NA NA Zinc, total ND 1.00 1.6E-02 NC NA NA

~~SUBTOTAL: 3.1E-04~~

~~Notes: 1. N A = Not Analyzed/Not Applicable: NC •= Not Calculated: NSCC = Not a Study Chemical of Concern. 2. For constituents without »n AAF value, a default value of 1.00 was used.~~

~~C:\31«« ZYNVl 1866-20.UORW_E-2\Zrnrwnw.«l««lOWlJl_43244TC QA: MBG Doe ^HVf^ Fik No. 31SM.20 TABLE El-14 rigcl~~

~~RECEPTOR: Resident - Current CHRONIC NONCARCINOGENIC EFFECTS~~

Sfmivolatitc Organic Compounds 2,4-Dichlorophenol ND 1.00 3.IE-02 NC 3.0E-03 NC 2-Chlorophenol ND 1.00 3. IE-02 NC 5.0E-03 NC 4-Methylphenol ND 1.00 3.IE-02 NC 5.0E-03 NC Benzo(a)anthracene ND 1.00 3. IE-02 NC 3. OE-02 NC Benzo(a)pyrene ND 1.00 3. IE-02 NC 3. OE-02 NC Benzo(b)fluoranthene ND 1.00 3.1E-02 NC 3.0E-02 NC Benzo(£,h,i)perylene ND 1.00 3.1E-02 NC 3.0E-02 NC bis(2-Eihylhexyl)phthalate ND 1.00 3. IE-02 NC 2.0E-02 NC Chrysene ND 1.00 3. IE-02 NC 3.0E-02 NC Di-n-butylphthalate ND 1.00 3. IE-02 NC l.OE-01 NC Naphthalene ND 1.00 3. IE-02 NC 2.0E-02 NC Phenanthrene ND 1.00 3.1E-02 NC 3. OE-02 NC

~~Peslicides/PCBs~~

Aldrin ND 1.00 3. IE-02 NC 3.0E-05 NC delta-BHC ND 1.00 3.1E-02 NC NA NC Dieldrin ND 1.00 3.1E-02 NC 5.0E-05 NC Meials Aluminum, total =; > 4.1E-OI :;; ;: i.oo 3.1E-02 IJE-02 NA NC Arsenic, total 8.4E-03 1.00 3.1E-02 2.6E-04 3.0E-04 8.7E-01 L Barium, total : :i 2.2E-OI ; : 1.00 3.1E-02 6.9E-03 7.0E-02 9.8E-02 Beryllium, total : 6.3E-03 ::::;: ; 1,00 3.1E-02 2.0E-04 10E-03 9.8E-02 Cadmium, lota] ND 1.00 3. IE-02 NC 5.0E-04 NC Copper, total ' 7.8E-02 :! ; ::;:.:. 10 0 • ••• • 3.1E-02 2.4E-03 3.7E-02 6.6E-02 Iron, total 6.4E-OI 1.00 3. IE-02 2.0E-02 NA NC Lead, total ND 1.00 3. IE-02 NC NA NC Manganese, total 1. IE-01 1.00 3. IE-02 3.3E-03 2.4E-02 1.4E-01 Mercury, total ND 1.00 3. IE-02 NC 3.0E-04 NC Nickel, total ND 1.00 3 IE-02 NC 2.0E-02 NC Thallium, total ND 1.00 3. IE-02 NC 2.0E-01 NC Vanadium, total 4.5E-03 1.00 3. IE-02 1.4E-04 7.0E-03 2.0E-02 Zinc, total 2.2E-01 1.00 3. IE-02 6.8E-03 3.0E-01 2.3E-02

~~SUBTOTAL: IJE+00~~

~~QA MBGDatt:7/IS/V9 Fik No 31866 20 TABLE El-14 (CONTD) rice2~~

~~RECEPTOR: Resident - Current CARCINOGENIC EFFECTS~~

~~Volatile Organic Compounds~~

1,1,1 -Trichloroethane ND 1.00 4.0E-03 NC NA NA 1 , 1 ,2-Trichlorocthane ND 1.00 4.0E-03 NC 5.7E-02 NA 1, 1 -Dichloroethane ND 1.00 4.0E-03 NC NA NA 1 , 1 -Dichloroethenc ND LOO 40E-03 NC 6.0E-OI NA cis- 1 ,2-Dichloroethene ND LOO 40E-03 NC NA NA 1 ,2-Dichlorobenzene ND 1.00 4.0E-03 NC NA NA 1 ,3-Dichlorobenzene ND LOO 4.0E-03 NC NA NA 1 ,4-Dichlorobenzene ND LOO 4.0E-03 NC 2.4E-02 NA 4-Methyl-2-Pentanone ND LOO 4.0E-03 NC NA NA Acetone ND 1.00 4.0E-03 NC NA NA Benzene ND LOO 4.0E-03 NC 29E-02 NA Carbon Tetrachlorkie ND LOO 4.0E-03 NC 1.3E-OI NA Chlorobenzene ND LOO 4.0E-03 NC NA NA Chloroform ND LOO 4.0E-03 NC 6 IE-03 NA Ethylbenzene ND LOO 4.0E-03 NC NA NA Methyl ethyl Ketone ND 1.00 4.0E-03 NC NA NA Tetrachloroethene ND 1.00 4.0E-03 NC 5.2E-02 NA Toluene ND 1.00 4.0E-03 NC NA NA Trichloroethene ND LOO 4.0E-03 NC 1. IE-02 NA Vinyl Chloride ND 1.00 4.0E-03 NC 1.9E+00 NA Xylenes ND 1.00 4.0E-03 NC NA NA

~~SftnivolatUt Organic Compounds~~

2,4-Dichlorophenol ND 1.00 4.0E-03 NC NA NA 2-Chlorophenol ND LOO 4.0E-03 NC NA NA 4-M«hylphenol ND LOO 4.0E-03 NC NA NA Benzo(a)anthracene ND 1.00 4.0E-03 NC 7.3E-01 NA Benzo(a)pyrene ND LOO 4.0E-03 NC 7.3E+00 NA Benzo(b)fluoranthene ND LOO 4.0E-03 NC 7.3E-01 NA Benzo(g,h,i Jperylene ND LOO 4.0E-03 NC NA NA bis(2-E(hylheKyl)phrhalate ND 1.00 4.0E-03 NC 1.4E-02 NA Chrysene ND 1.00 4.0E-03 NC 7.3E-02 NA Di-n-butylphthalate ND LOO 4.0E-03 NC NA NA Naphthalene ND LOO 4.0E-03 NC NA NA Phenanrhrene ND LOO 4.0E-03 NC NA NA rxA PesticiJes/PCBs

Aldrin ND LOO 4.0E-03 NC 1.7E+01 NA delta-BHC ND 1.00 4.0E-03 NC NA NA Dieldrin ND 1.00 4.0E-03 NC I.6E+01 NA Metals Aluminum, tool L 4.1E-OI ••;!% ; ; LOO 4.0E-03 1.6E-03 NA .; N\ ':.;• Arsenic, total 8.4E-03 LOO 4.0E-03 3.4E-05 1.5E400 5.1E-05 ; ! : Barium. UXal ;23EOI :: •;:;:. ;::^t.oo 4.0E-03 8.8E-04 NA .••'-/• : : 'V'NA'.:, v :i : : ; Beryllium, total . 6.3E-03 '••• k '::: : i-.:'j.OO 4.0E-03 Z5E-OS 4JE+00 ; LI&04 Cadmium, total ND 1.00 4.0E-03 NC NA NA :: Copper, total ; . 1.8E-02 'm.:' .- il.oo 4.0E-03 3.1E-04 NA V; "NA :-.:;•: Iron, total 6.4E-01 LOO 4.0E-03 2.6E-03 NA NA Lead, total ND LOO 4.0E-03 NC NA NA Manganese, total 1. IE-01 LOO 4.0E-03 4.3E-04 NA NA Mercury, total ND LOO 4.0E-03 NC NA NA Nickel, total ND 1.00 4.0E-03 NC NA NA Thallium, total ND 1.00 40E-03 NC NA NA Vanadium, total 4.5E-03 LOO 4.0E-03 I.8E-05 NA NA Zinc, total 2.2E-01 LOO 4.0E-03 8.7E-O4 NA NA

~~SUBTOTAL: I.6E-04~~

~~Notes:~~

~~1. NA c Not Analyzed/Not Applicable: NC •= Not Calculated. NSCC = Not a Study Chemical of Concern. 2. For constituents without an AAF value, a default value of LOO was used~~

GAJ I866.ZYNV! l«66-20.LIC\RW_E.2\Z>nfwtfw.xl»MIGWUOHC_ce« QA MBGD«K:7/I5»9 FikNo MS66M PIT: I 0(2 TABLE EMS 11/17/1999 CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OF GROUNDWATER (RW43070) HIGH END EXPOSURE

~~RECEPTOR: Resident - Current CHRONIC NONCARCINOGENIC EFFECTS~~

~~Volatile Organic Comttouncia~~

~~Stmivolatitf Organic Compounds~~

2.4-Dicnlorophenol ND 1.00 5.6E-02 NC 3.0E-03 NC 2-Chlorophenol ND 1.00 5.6E-02 NC S.OE-03 NC 4-Methylphenol ND 1.00 5.6E-02 NC 5.0E-O3 NC Benzophtha]ate ND 1.00 5.6E-02 NC 2.0E-02 NC Quyscne ND 1.00 5.6E-02 NC 3.0E-02 NC Di-n-butylphthalate ND 1.00 5.6E-02 NC l.OE-01 NC Naphthalene ND 1.00 5.6E-02 NC 2.0E-02 NC Phenanthrene ND 1.00 5.6E-02 NC 3.0E-02 NC

~~Peiticides/PCRs~~

~~Aldrin ND 1. 00 5.6E-02 NC 3.0E-05 NC delta-BHC ND 1.00 5.6E-02 NC NA NC Dieldrin ND 1.00 5.6E-02 NC 5.0E-05 NC~~

~~Mtlah~~

~~SUBTOTAL: 1.6E-OI SITE RELATED RISK: NC BACKGROUND RISK. 1.6E-01 Flic No 31166 20 Pip 2 01 2 TABLE El-15 (CONTD) 11/17/1999~~

~~CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OFGROUNDWATER (RW43070) HIGH END EXPOSURE~~

~~RECEPTOR: Resident - Current CARCINOGENIC EFFECTS~~

~~Receptor Lifetime Incremental Exposure Oral Specific Average Cancer Lifetime Contaminants Point x Absorption x Exposure = Daily x Slope = Cancer Concentration Adjustment Factor Dose Factor Risk~~

Volatile Organic Compound*

1.1,1 -Trichloroethane ND 1.00 1 6E-02 NC NA NA 1,1,2-Trichloroelhane ND 1.00 1 .6E-02 NC 5.7E-02 NA I.l-Dkhloroethane ND 1.00 1.6E-02 NC NA NA l.l-Dichloroethene ND 1.00 I.6E-02 NC 6.0E-OI NA cis-1.2-Dichloroethene ND 1.00 1 .6E-02 NC NA NA 1 ,2-Dichlorobenzene ND 1.00 1.6E-02 NC NA NA 1 ,3-Dichloroocnzcnc ND 1.00 1 .6E-02 NC NA NA 1 ,4-Dkhlorobenzene ND 1.00 1 .6E-02 NC 2.4E-02 NA 4-Mcthyl-2-Pcntanone ND 1.00 1.6E-02 NC NA NA Acetone ND 1.00 1.6E-02 NC NA NA Benzene ND 1.00 1 6E-02 NC 2.9E-02 NA Carbon Tetrachloride ND 1.00 1.6E-02 NC I.3E-OI NA Chlorobenzene ND 1.00 1 6E-02 NC NA NA Chloroform ND 1.00 I.6E-02 NC 6 IE-03 NA Ethylbenzene ND 1.00 1 6E-02 NC NA NA Methyl ethyl Ketone NA 1.00 1.6E-02 NC NA NA Tetrachloroethene ND 1.00 I.6E-02 NC 5.2E-02 NA Toluene ND 1.00 1 .6E-02 NC NA NA Trichloroelhcne ND 1.00 1 .6E-02 NC 1 IE-02 NA Vinyl Chloride ND 1.00 I.6E-02 NC 1.9E+00 NA Xylenes ND 1.00 1 .6E-02 NC NA NA

~~Sftnivolafite Organic Compounds~~

2.4-Dichlorophenol ND 1.00 1.6E-02 NC NA NA 2-Chlorophcnol ND 1.00 I.6E-02 NC NA NA 4-Methylphenol ND 1.00 1 .6E-02 NC NA NA Benzo(a)anthracene ND 1.00 I.6E-02 NC 7.3E-01 NA Benzo{a)pvrenc ND 1.00 I.6E-02 NC 7.3E+00 NA Benzo(b)fluoranthene ND 1.00 1.6E-02 NC 7.3E-OI NA Benzo(g,h,i)perylene ND 1.00 1.6E-02 NC NA NA bis(2-Elhylhexyl)phlha]ate ND 1.00 1.6E-02 NC 1.4E-02 NA Chrysene ND 1.00 I.6E-02 NC 7.3E-02 NA Di-n-butylphthalate ND 1.00 I.6E-02 NC NA NA Naphthalene ND 1.00 I.6E-02 NC NA NA Phenanthrene ND 1.00 1.6E-02 NC NA NA

~~Peslic'ults/PCBs~~

~~Aldrin ND 1.00 I.6E-02 NC 1 .7E+OI NA delta-BHC ND 1.00 I.6E-02 NC NA NA Dieldrin ND 1.00 I.6E-02 NC 1.6E+01 NA~~

~~Mnals~~

Aluminum, total ND 1.00 1.6E-02 NC NA NA Arsenic, total ND 1.00 I.6E-02 NC I.5E+00 NA Barium, total 2.3E-03 1.00 I.6E-02 3.7E-05 NA NA Beryllium, local ND 1.00 1.6E-02 NC 4.3E-KX) NA Cadmium, local ND 1.00 1.6E-02 NC NA NA Copper, total l.OE-01 1.00 1.6E-02 1.7E-03 NA NA Iron, total ND 1.00 I.6E-02 NC NA NA Lead, total ND 1.00 I.6E-02 NC NA NA Manganese, total ND 1.00 1 .6E-02 NC NA NA Mercury, total ND 1.00 1.6E-02 NC NA NA Nickel, total ND 1.00 1.6E-02 NC NA NA Thallium, total ND 1.00 I.6E-02 NC NA NA Vanadium, total ND 1.00 1.6E-02 NC NA NA Zinc, total ND 1.00 1 6E-02 NC NA NA

~~SUBTOTAL: NC SITE RELATED RISK: NC BACKGROUND RISK: NC~~

~~Notes:~~

~~1. NA = Not Analyzed/Not Applicable; NC = Not Calculated; NSCC = Not a Study Chemical of Concern. 2. For constituents without an AAF value, a default value of 1.00 was used.~~

OV3H06ZYNV)l»66-JOJJCVCAljCS«ltSIC.TA8\Zri«vn»wJil<«IOWLR.4370C QA: MBG Dalf: 7/1W9 FikNo. 3I8M.20 TABLE El-16 Pap: I of 2 II/17M999 CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OF GROUNDWATER (RW43167) CENTRAL TENDENCY EXPOSURE

~~RECEPTOR: Resident - Current CHRONIC NONCARCINOGENIC EFFECTS~~

~~Receptor Chronic Oral Exposure Oral Specific Average Chronic Hazard Contaminants Point x Absorption x Exposure = Daily / Reference = Index Concentration Adjustment Factor Dose Dose~~

~~Volatile Organic Compounds~~

~~Pesiicides/fCBs Aldrin ND 1.00 3.1E-02 NC 3.0E-05 NC delta-BHC ND 1.00 3. IE-02 NC NA NC Dieldrin ND 1.00 3. IE-02 NC 5.0E-05 NC~~

~~Metals~~

Aluminum, total 4:9E-01i; M; 1.00 3.1E-02 1-5E-02 NA NC Arsenic, total 2.6E-03 1.00 3. IE-02 8.IE-05 3.0E-04 2.7E-OI ; ;: Barium, total : :j.4E-02':: :' p:. 1.00 3. IE-02 l.OE-03 7.0E-02 1JE-02 Beryllium, total 5.5E-03.: ;;;-;::: . "r- v:; 1.00. 3.1E-02 I.7E-04 2.0E-03 8.6E-02 Cadmium, total ND 1.00 3.1E-02 NC 5.0E-04 NC ; ; ; : : : Copper, total :io«:i ;'; r ; l :i.0o ;. : 3.1E-02 8.0E-03 3.7E-02 Z2E-01 Iron, total 5.3E-OI 1.00 3. IE-02 1.6E-02 NA NC Lead, total ND 1.00 3. IE-02 NC NA NC Manganese, total 7.4E-02 1.00 3. IE-02 2.3E-03 2.4E-02 9.6E-02 Mercury, total ND 1.00 3. IE-02 NC 3.0E-04 NC Nickel, total ND 1.00 3. IE-02 NC 2.0E-02 NC Thallium, total ND 1.00 3. IE-02 NC 2.0E-01 NC Vanadium, total ND 1.00 3. IE-02 NC 7.0E-03 NC Zinc, total I.OE+00 1.00 3. IE-02 3. IE-02 3.0E-01 1. OE-01

~~SUBTOTAL: 7.9E-OI~~

~~QA: MBG Dale: 7/1VW RfcNn. 3186620 TABLE El-14 (CONTD) Pite2of2 11/17/1999 CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OF GROUNDWATER (RW43167) CENTRAL TENDENCY EXPOSURE~~

~~RECEPTOR: Resident - Current CARCINOGENIC EFFECTS~~

~~Volatile Ortanic Compounds~~

~~StmivolutHe Organic Compounds~~

2,4-Dichlorophenol ND 1.00 4.0E-03 NC NA NA 2-Chlorophenol ND 1.00 4.0E-03 NC NA NA 4-Methylphenol ND 1.00 4.0E-03 NC NA NA Benzo(a)anthracene ND 1.00 4.0E-03 NC 7.3E-OI NA Benzo(a)pyrene ND 1.00 4.0E-03 NC 7.3E+00 NA Benzo(b)fluoranthene ND 1.00 4.0E-03 NC 7.3E-01 NA Benzo(g,h,i)pcrylene ND 1.00 4.0E-03 NC NA NA bis(2-Eihylhexyl)phihalaie ND 1.00 4.0E-03 NC 1.4E-02 NA Chrysene ND 1.00 40E-03 NC 7.3E-02 NA Di-n-butylphthalate ND 1.00 4.0E-03 NC NA NA Naphthalene ND 1.00 4.0E-03 NC NA NA Phenanthrene ND 1.00 4.0E-03 NC NA NA Peaicides/PCBs

~~Aldrin ND 1.00 4.0E-03 NC 1.7E+OI NA delta-BHC ND 1.00 4.0E-03 NC NA NA Dteldrin ND 1.00 4.0E-03 NC I.6E+01 NA~~

~~Metals~~

Aluminum, total 4.9E-OI 1.00 4.0E-03 2.0E-03 •- NA '-,••-., ' NA Arsenic, total 2.6E-03 1.00 4.0E-03 l.OE-05 LSE-tOO 1.6E-05 Barium, total 3.4E-02 1.00 4.0E-03 1.3E-04 NA :.v. NA ; Beryllium, total 5JE-03 1.00 4.0E-03 2-2E-OS i 4JE+00 :.': 9.5E-OJ Cadmium, total ND 1.00 4.0E-03 NC NA NA Copper, total 2.6E-01 1-00 4.0E-03 l.OE-03 NA NA Iron, total SJE-01 1.00 4.0E-03 2.IE-03 NA NA Lead, total ND 1.00 4.0E-03 NC NA NA Manganese, total 7.4E-02 1.00 40E-03 3.0E-04 NA NA Mercury, total ND 1.00 40E-03 NC NA NA Nickel, total ND 1.00 4.0E-03 NC NA NA Thallium, total ND 1.00 40E-03 NC NA NA Vanadium, total ND 1.00 4.0E-03 NC NA NA Zinc, total l.OE+00 1.00 4.0E-03 4.0E-03 NA NA

~~SUBTOTAL: 1.1 E-W~~

~~Notes: 1. NA •= Not Analyzed/Not Applicable; NC « Not Calculated: NSCC = Not a Study Chemical of Concern. 2. For constituents without an AAF value, a default value of 1.00 was used.~~

G:\3IS66 ZYNU 1866^20 LJORW_E-2\Zy»r*«Jw.«liMIGWLR_43 l«C_coi QA:MBCD«c. file No 31866.20 TABLE El-17 Facelo<2 11/17(1999 CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OF GROUNDWATER (RW43244T) CENTRAL TENDENCY EXPOSURE

~~RECEPTOR: Resident - Cunent CHRONIC NONCARCINOGENIC EFFECTS~~

~~Volatile Organic Compounds~~

~~Sfmivolutilt Organic Compounds~~

~~SUBTOTAL: 1.1E+OO~~

C:\3IS66 ZYN\3l»66-20.1JORW.E2\Zynrwt(w«U«IGWLR_<32«TC_cell QA MBGD»r 7/I5W File No. 318*6.20 TABLE El-17 (CONTD) P»je2of2 11/17/1999 CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OF GROUNDWATER (RW43244T) CENTRAL TENDENCY EXPOSURE

~~RECEPTOR: Resident - Current CARCINOGENIC EFFECTS~~

~~Receptor Lifetime Incremental Exposure Oral Specific Average Cancer Lifetime Contaminants Point x Absorption x Exposure = Daily x Slope = Cancer Concentration Adjustment Factor Dose Factor Risk~~

~~Volatile Organic Compounds~~

~~Srmivolatilt Organic Compounds~~

: : Aluminum, total ; :ND V-;;. ; 1.00 4.0E-03 NC NA NA Arsenic, total 7.0E-03 1.00 4.0E-03 2.8E-05 I.5E4OO 4.2E-OS ; : Barium, total Z4E-02 : : ; ; LOO 4.0E-03 i 9JE-05 NA NA Beryllium, total 2.0E-03 LOO 4.0E-03 gjOE-06 4JE+00 3.4E-05 Cadmium, total 8.9E-04 1.00 4.0E-03 3.6E-06 NA NA - Copper, total ;;J3E-02'::'^;: LOO 4.0E-03 2.IE-04 : NA NA Iron, total 4.3E-KX) 1.00 4.0E-03 1.7E-02 NA NA Lead, total NA 1.00 4.0E-03 NC NA NA Manganese, total I.8E-OI 1.00 4.0E-03 7.3E-04 NA NA Mercury, total ND 1.00 4.0E-03 NC NA NA Nickel, total ND 1.00 4.0E-03 NC NA NA Thallium, total ND 1.00 4.0E-03 NC NA NA Vanadium, total 5.2E-04 1.00 4.0E-03 2. IE-06 NA NA Zinc, total ND 1.00 4.0E-03 NC NA NA

~~SUBTOTAL: 7.7E-05~~

~~Notes: 1. NA = Not Analyzed/Not Applicable; NC « No( Calculated: NSCC «= Not a Study Cnemical of Concern. 2. For constituents without an AAF value, a default value of 1.00 was used.~~

~~G:\5l866iYNV)l8(S6.20.LIC\RW_E-2AZx«r«rj».«tiUIGWLR_43244TC_cen QA: MBG Dale: 7/1 file No. }1M6 20 PlfcloC TABLE EMS 11/17/1999~~

~~CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OF GROUNDWATER (RW43070) CENTRAL TENDENCY EXPOSURE~~

~~RECEPTOR: Resident - Current CHRONIC NONCARCINOGENIC EFFECTS~~

~~Volatile Organic Compounds~~

~~Stntivolatilf Organic Compounds~~

~~Prslicides/PCBs~~

~~Aldrin ND 1.00 3. IE-02 NC 3.0E-05 NC delta-BHC ND 1.00 3. IE-02 NC NA NC Dieldrin ND 1.00 3. IE-02 NC 5.0E-05 NC~~

~~Metals~~

~~SUBTOTAL: &8E-02 SITE RELATED RISK: ( NC BACKGROUND RISK: | 8.8E-02~~

~~QA: MBG Dale: 7/1 Fife No 311166.20 Fife 2 0(2 TABLE El-18 (CONTD) 11/17/1999~~

~~CALCULATION OF AVERAGE DAILY DOSES AND RISK ESTIMATES FOR INGESTION OF GROUNDWATER (RW43070) CENTRAL TENDENCY EXPOSURE~~

~~RECEPTOR: Resident - Cuirenl CARCINOGENIC EFFECTS~~

~~Receptor Lifetime Incremental Exposure Oral Specific Average Cancer Lifetime Contaminants Point x Absorption x Exposure Daily x Slope = Cancer Concentration Adjustment Factor Dose Factor Risk~~

~~Volatile Organic Compound's~~

I.I.I -Trichloroethane ND 1.00 4.0E-03 NC NA NA 1 . 1 .2-Trichloroelhane ND 1.00 4.0E-03 NC 5.7E-02 NA 1 . 1 -Dichloroethane ND 1.00 4.0E-03 NC NA NA l.l-Dichloroethene ND 1.00 4.0E-03 NC 60E-01 NA cis 1 .2-Dichloroethene ND 1.00 4.0E-03 NC NA NA 1 ,2-Dichlorobenzcne ND 1.00 40E-03 NC NA NA 1 ,3-Dichlorobenzcne ND 1.00 4.0E-03 NC NA NA 1 ,4-Dichlorobenzene ND 1.00 4.0E-03 NC 2.4E-02 NA 4-Methyl-2-Penlanone ND 1.00 4.0E-03 NC NA NA Acetone ND 1.00 4.0E-03 NC NA NA Benzene ND 1.00 4.0E-03 NC 2.9E-02 NA Carbon Tetrachloride ND 1.00 4.0E-03 NC I.3E-01 NA Chlorobenzenc ND 1.00 4.0E-03 NC NA NA Chloroform ND 1.00 40E-03 NC 6 IE-03 NA Ethylbenzene ND 1.00 4.0E-03 NC NA NA Methyl ethyl Ketone NA 1.00 4.0E-03 NC NA NA Tetrachlofoclhene ND 100 4.0E-03 NC 5.2E-02 NA Toluene ND 1.00 4.0E-03 NC NA NA Trichloroethenc ND 1.00 4.0E-03 NC 1. IE-02 NA Vinyl Chloride ND 1.00 4.0E-03 NC I.9E+00 NA Xylenes ND 1.00 4.0E-03 NC NA NA

~~Semivolatile Organic Compounds~~

~~Petlicides/PCBs~~

~~Aklrin ND 1.00 4.0E-03 NC 1.7E+01 NA delta-BHC ND 1.00 4.0E-03 NC NA NA Dieldrin ND 1.00 4.0E-03 NC 1.6E-tOl NA~~

~~Metals~~

~~SUBTOTAL: NC SITE RELATED RISK: NC BACKGROUND RISK: NC~~

~~Notes:~~

1. NA = Not Analyzed/Not Applicable: NC = Not Calculated; NSCC = Not a Study Chemical of Concern. 2. For constituents without an AAF value, a default value of 1.00 was used. G:\3I W6-ZYW31166- 2O.LJOCALCS\RJSK_TAB\ZyiH>wfw.xfaUtGWLR_4370C_ix« File No. 31866.20 Page 1 of 1 11/17/1999

~~TABLE El-19~~

~~COMPARISON OF RESIDENTIAL WELL CONCENTRATIONS TO DRINKING WATER STANDARDS Central Landfill - OU2 Johnston, Rhode Island~~

Concentration Concentration Concentration Concentration RI EPA at Sampling at Sampling at Sampling at Sampling Gtoundwater Maximum Contaminate Location Location Location Location Quality Contaminant RW31004 RW43167 RW43244T RW43070 Standards Levels (mg/1) (mg/1) (mg/1) (mg/1) (mg/1) (mg/1)

~~Metals~~

Aluminum, total 4. IE-01 * ; ;-4;9E-01;* : ; ; ND ND NA 0.13 Arsenic, total 8.4E-03 2.6E-03 7.00E-03 ND NA 0.05 Barium, total . 2:2E-01 :-:• . '*t^%E&L*J:^: , 2.36E-02 •;-.' 2.3E-03 .-,-;•. 2 2 ; : ; : Beryllium, total :• ;-6.3E-03 H : ••-••• :.;«;s;5:5Ef03-H ;>*;:. '2.00E-03 -•:- ' :.'-" ND ^ • 0.004 0.004 Cadmium, total ND ND 8.90E-04 ND 0.005 0.005 : ; ; Copper, total : . 7.8E-02 -• : ^;^ .;2.6E-Qimy.;: :;; ; : :: 5.32E-02 . ; l.OE-01 NA 1.3 Iron, total 6.4E-01 * 5.3E-OI * 4.30E-I-00 * ND NA 0.3 Lead, total ND ND NA ND 0.015 0.015 Manganese, total 1. IE-01 * 7.4E-02 * 1.81E-01 * ND NA 0.05 Mercury, total ND ND ND ND 0.002 0.002 Nickel, total ND ND ND ND 0.1 0.14 Thallium, total ND ND ND ND 0.002 0.002 Vanadium, total 4.5E-03 ND 5.20E-04 ND NA NA Zinc, total 2.2E-01 l.OE+00 ND ND NA 5

~~Notes:~~

1. NA = Not Analyzed or Not Available; ND = Not Detected. 2. * = In exceedance of EPA maximum contaminant levels. n = In exceedance of EPA maximum contaminant levels and RI groundwater quality standards. ¥ = In exceedance of RI groundwater quality standards. 3. Values in italics are secondary MCLs. 4. Grey = Consistent with Background.

~~G:\31866ZYNV31866-20.LJC\RW_&2\Zynrv>riwq.xlsVCW_COM QA: MBG Date 7/15/99 APPENDIX E-2~~

~~METHODOLOGY OF THE KRUSKAL-WALLIS TEST APPENDIX E.2~~

~~METHODOLOGY OF THE KRUSKAL-WALLIS TEST~~

The Kruskal-Wallis test is a nonparametric analysis of variance (ANOVA) by ranks test. It is a generalization of the two-sample Mann-Whitney Test, and is similar to the parametric F test, with ranks replacing the original observations (Andrews, 1954).

The Kruskal-Wallis test is generally used to test for differences among more than two groups. When used to test for differences between two groups, the results are identical to those from the nonparametric two-group Mann-Whitney test. The test involves the calculation of a test statistic, and comparison of this statistic with a critical value for a specified significance level. If the test statistic exceeds the critical value, it can be concluded that the two groups are significantly different.

~~The test statistic, //, is calculated as:~~

where rc, is the number of observations in group i, N is the total number of observations in all groups, and R, is the sum of the ranks of the n, observations in group i. If there are any ties (observations of equal value, and therefore equal rank), a corrected H is calculated by dividing the original H by the following correction factor (C):

~~c- L~ (N'-N where f, is the number of ties in the ith group of ties and m is the number of groups of tied ranks.~~

The H distribution is similar to the Chi-Square distribution; the critical value is equal to the Chi- Square critical value, obtained from tables or calculated. For all of the comparisons, a significance level of 0.05 was used; the critical value for two groups (i.e., one degree of freedom) at this significance level is 3.841.

~~E-2-1 POWER~~

The power (efficiency) of a statistical test is its ability to detect differences between groups. Nonparametric tests may need larger sample sizes than parametric tests because: (1) these tests make fewer assumptions concerning the distribution of the data, and, (2) procedures based on ranks have a discrete distribution rather than the continuous distribution of the parametric tests (EPA 1992).

The Kruskal-Wallis test is generally considered to be among the most powerful of the nonparametric tests for inter-group differences. It is at least 86 percent as efficient as the analogous parametric ANOVA. When used with normally distributed data, it is 3/p = 95 percent as efficient as a parametric ANOVA test. When the data are not normally distributed, and/or when the population variances of the groups are not homogeneous, the test is much more powerful than the parametric test (Zar, 1984). In these cases, additional samples are not needed to match the power of a parametric test; power similar to that of a parametric test can be obtained with fewer samples. Statistical methods are not available to calculate the exact power of a nonparametric test.

The Kruskal-Wallis tests were performed with the combined Phase I and II data sets using The Monitor System software. The accuracy of the Monitor System's H and Chi-Square calculations provided on the ANOVA reports was checked and found to be correct. The results generally matched those performed with the t-tests. Although no exact power calculations can be provided, it is reasonable to assume that the actual power values for the nonparametric tests performed with the current data are higher than those calculated with the t-tests for the Phase I data because:

1. The departures from normality which may have reduced the power of some of the Phase I t-tests do not affect the nonparametric tests because these tests do make any assumptions about underlying distributions;

2. The large variances observed in many of the parameter groups which reduced the power of the t-test to identify differences with the given number of samples do not affect the nonparametric tests which are based on ranks, not measurement values; and,

~~3. Additional samples were collected for both background and SWMU data sets, increasing the power of all performed tests.~~

~~E-2-2 REFERENCES~~

~~Andrews, Fred C, 1954. "Asymptotic behavior of some rank test for analysis of variance." Ann. Math. Statist. 25:724-735.~~

Environmental Protection Agency (EPA), 1992. Statistical Analysis of Ground-water Monitoring Data at RCRA Facilities. Addendum to Interim Final Guidance. Office of Solid Waste, Permits and State Programs Division. Washington, D.C. July 1992.

~~Zar, Jerrold H., 1984. Biostatistical Analysis, 2nd. Edition. Prentice-Hall, Inc. Englewood Cliffs.~~

~~G:\31866.ZYNX31866-20.LJOREPORTS\appe2.doc~~

~~E-2-3 09/09/1997 Page: 1~~

~~DATA DISTRIBUTION FOR ALL DATES~~

~~COMPANY: ^'^:r^Brrt^Sl^nd^|^~~

~~iMtiW®fc^^^iM&-%tf&~~

~~LOCATION SAMPLE X SHAPIRO-WILK CALCULATED TABULAR COEFFICIENT ID SIZE N-Ds DISTRIBUTION W W SKEWNESS KURTOSIS OF VARIATION~~

~~Import~~

~~SED 40 0 Normal 0.9591 0.9400 0.08 1.84 0.47~~

~~SEO 34 24 Non-Normal 0.8998 0.9330 0.86 2.64 0.98~~

~~SED 34 0 Lognormal 0.9332 0.9330 0.84 2.31 1.02~~

~~SED 34 32 Non-Normal 0.8548 0.9330 1.16 3.43 1.17~~

~~SED 40 3 Non-Normal 0.9263 0.9400 1.09 3.17 0.94~~

~~(continues) 09/09/1997 Central Landfill Page: 2~~

~~DATA DISTRIBUTION FOR ALL DATES~~

~~LOCATION SAMPLE X SHAPIRO-WILK CALCULATED TABULAR COEFFICIEKT 10 SIZE N-Ds DISTRIBUTION W H SKEMNESS KURTOSIS OF VARIATION PARAMETERS M^irtgcirtfese,^ UNIT: mg/kg~~

~~SED 40 0 Lognormal 0.9596 0.9400 3.15 11.99 2.21~~

~~SEO 40 0 Non-Normal 0.9197 0.9400 0.93 3.47 0.67~~

~~DATA DISTRIBUTION FOR ALL DATES~~

~~LOCATION SAMPLE X SHAPIRO-WILK CALCULATED TABULAR COEFFICIENT ID SIZE N-Os DISTRIBUTION W W SKEWNESS KURTOSIS OF VARIATION~~

~~Import~~

~~SED BK Normal 0.9248 0.8030 -0.03 1.19 0.54~~

~~SED BK 29 Lognormal 0.8516 0.8030 0.22 0.87 0.91~~

~~SEO BK 7 0 Normal 0.8988 0.8030 0.02 1.06 0.57~~

~~SEO BK 7 14 Normal 0.8803 0.8030 0.48 1.57 1.01~~

~~SEO BK 7 14 Normal 0.8967 0.8030 0.19 1.16 0.81~~

~~(continues) 09/09/1997 Central Landfill Page: 2~~

~~DATA DISTRIBUTION FOR ALL DATES~~

~~LOCATION SAMPLE X SHAPIRQ-WILK CALCULATED TABULAR COEFFICIENT ID SIZE N-Ds DISTRIBUTION W W SKEWNESS KURTOSIS OF VARIATION~~

~~SED K 7 0 Normal 0.8392 0.8030 0.86 2.17 1.10~~

~~• ' ' : •• ••'-•'••' •-'• '-•• ' '-:-•"•. •~~

~~SEDBK Normal 0.8927 0.8030 0.48 1.350.84~~

~~ANOVA (KRUSKAL-WALLIS/NONPARAMETRIC) FOR ALL DATES~~

~~COMPANY-~~

~~Import~~

~~: ; :; : ; : :;: ::; PARAHETER; tArlsirilp ijptlil >|;•:;.- ;; : • ^;;'^:$&i ; " • • - • •• • ' --' ;.•';•:;' :-; ;': :; •:"• • •: -'. UN IT: mg/kg~~

~~Number of Ties > 0 Total Degrees Of Freedom: 1 Calculated H' Value: 0.043 Tabular H: 3.841~~

~~Since the calculated Kruskal-Wallis H' value Is less than the tabular value of H. it can be concluded that a statistically significant difference does not exist among the selected locations.~~

~~Number of Ties > 0 Total Degrees Of Freedom: 1 Calculated H' Value: 0.203 Tabular H: 3.841~~

~~Since the calculated Kruskal-Wallis H' value Is less than the tabular value of H. it can be concluded that a statistically significant difference does not exist among the selected locations.~~

~~Number of Ties > 0 Total Degrees Of Freedom: 1 Calculated H1 Value: 0.188 Tabular H: 3.841~~

~~Since the calculated Kruskal-WalUs H' value Is less than the tabular value of H. it can be concluded that a statistically significant difference does not exist among the selected locations.~~

~~Number of Ties > 0 Total Degrees Of Freedom: 1 Calculated H' Value: 1.032 Tabular H: 3.841~~

~~Since the calculated Kruskal-Wallis H' value is less than the tabular value of H. it can be concluded that a statistically significant difference does not exist among the selected locations.~~

~~(continues) 09/09/1997 Central Landfill Page: 2~~

~~ANOVA (KRUSKAL-WALLIS/NONPARAMETRIC) FOR ALL DATES~~

~~Al| N6ti-00tects Limit/2 Si gril i earice ( 1 - a] pha ) :~~

~~PARAMETER: Manganese; total i mg/kg~~

~~Number of Ties - 0 Total Degrees Of Freedom: 1 Calculated H Value: 5.294 Tabular H: 3.841~~

~~Since the calculated Kruskal-Wallis H value exceeds the tabular value of H. it can be concluded that a statistically significant difference may exist among the selected locations.~~

Additionally, based on the Bonferroni t-test. the location comparisons below with asterisks are considered statistically significant since the calculated critical values are less than or equal to the difference of the average ranks for each location comparison.

~~BACKGROUND LOCATION CRITICAL DIFFERENCE AVERAGE COMPLIANCE LOCATION VALUE OF RANKS RANK~~

~~SED N/A N/A 25.925 SED BK 9.240 -12.925 13.000~~

~~Number of Ties > 0 Total Degrees Of Freedom: 1 Calculated H1 Value: 1.157 Tabular H: 3.841~~

Since the calculated Kruskal-Wallis H' value is less than the tabular value of H. it can be concluded that a statistically significant difference does not exist among the selected locations. ——. ——.——— End of Report —— ——————— The Monitor System. TM Copyright (C) 1992-94. Entech Systems Incorporated 09/05/1997 Page: 1

~~T-TEST (CABF) FOR ALL DATES~~

~~:N!iSIlilffi!~~

~~Mdni tor iacat1 on SED Background Locat1on 5ED BK~~

~~BACK MON BACK MON SAMPLE SAMPLE T T SIGNIFICANT PARAhETtR UNIT SIZE SIZE VALUE VALUE tc DIFFERENCE~~

~~Import~~

~~DATA DISTRIBUTION FOR ALL DATES~~

~~LOCATION SAMPLE X SHAPIRO-WILK CALCULATED TABULAR COEFFICIEKT 10 SIZE N-Ds DISTRIBUTION W W SKEWNESS KURTOSIS OF VARIATION~~

~~Import ^^^^^l^^Mii^^^&^S^I^^B^M^i^M^^yM^l SW 36 100 Non-Normal 0.2507 0.9350 3.72 15.18 0.00~~

~~SW 38 55 Non-Normal 0.8245 0.9380 1.24 3.72 0.00~~

~~SW 38 11 Lognormal 0.9779 0.9380 1.77 6.22 0.00~~

~~SW 38 3 Non-Normal 0.9085 0.9380 3.33 13.44 2.18~~

~~SW 38 61 Non-Normal 0.8064 0.9380 1.98 6.49 0.00~~

~~DATA DISTRIBUTION FOR ALL DATES~~

~~LOCATION SAMPLE X SHAPIRO-WILK CALCULATED TABULAR COEFFICIENT ID SIZE N-Ds DISTRIBUTION W W SKEWNESS KURTOSIS OF VARIATION~~

~~Import~~

~~SW BK 100 Non-Normal 0.6008 0.8030 0.75 1.40 0.00~~

~~SW BK 8 50 Normal 0.8224 0.8180 0.29 1.17 0.00~~

~~SW BK Normal 0.9194 0.8180 0.46 1.69 0.00~~

~~SW BK 8 13 Normal 0.8266 0.8180 0.78 1.80 0.92~~

~~ANOVA (KRUSKAL-WALLIS/NONPARAMETRIC) FOR ALL DATES~~

~~llliilflif ii ••~~

~~Import UNIT: tng/1~~

~~Number of Ties > 0 Total Degrees Of Freedom: 1 Calculated H1 Value: 0.322 Tabular H: 3.841~~

~~Since the calculated Kruskal-Wallis H' value Is less than the tabular value of H. it can be concluded that a statistically significant difference does not exist among the selected locations.~~

~~Number of Ties > 0 Total Degrees Of Freedom: 1 Calculated H1 Value: 11.108 Tabular H: 3.841~~

~~Since the calculated Kruskal-Wallis H' value exceeds the tabular value of H. it can be concluded that a statistically significant difference may exist among the selected locations.~~

Additionally, based on the Bonferronl t-test. the location comparisons below with asterisks are considered statistically significant since the calculated critical values are less than or equal to the difference of the average ranks for each location comparison.

~~BACKGROUND LOCATION CRITICAL DIFFERENCE AVERAGE COMPLIANCE LOCATION VALUE OF RANKS RANK~~

~~DATA DISTRIBUTION FOR ALL DATES~~

~~COMPA:~~

~~LOCATION SAMPLE I SHAPIRO-WILK CALCULATED TABULAR COEFFICIENT ID SIZE N-Ds DISTRIBUTION W W SKEWNESS KURTOSIS OF VARIATION~~

~~Import (MIT;~~

~~GW 26 27 Lognormal 0.9648 0.9200 2.35 7.62 2.12~~

~~GW 26 42 Non-Normal 0.8338 0.9200 2.73 9.95 0.90~~

~~26 Lognormal 0.9406 0.9200 1.99 7.15 1.15~~

~~26 15 Lognonnal 0.9687 0.9200 2.52 9.25 0.00~~

~~26 65 Non-Normal 0.8164 0.9200 4.50 22.07 0.00~~

~~(continues) 09/09/1997 Central Landfill Page: 2~~

~~DATA DISTRIBUTION FOR ALL DATES~~

~~LOCATION SAMPLE t SHAPIRO-WILK CALCULATED TABULAR COEFFICIEKT ID SIZE N-Ds DISTRIBUTION W W SKEWNESS KURTOSIS OF VARIATION~~

~~PARAMETER: Cc$per ,: total ^§^i^'.f^:\ ! : : ::' :; • • - •:• . '. .~~

~~GW 26 42 Lognormal 0.9516 0.9200 3.09 13.00 1.81 IMSife- ••:^':|?f:^:^||;:;i^~~

~~GW 26 8 Lognormal 0.9484 0.9200 3.59 16.29 2.15 ; : PARAMETER: Lead•,;•' total•i/^gjjl^^j^ if |lf -; f ; - ^---- . •'^^~~

~~GW 26 65 Non-Normal 0.9029 0.9200 2.32 7.39 1.44 PARAMETER: Manganese ; ; ^Ottl '; i|;I W, ^mi--;- •. ". " v: ' UNIT: mg/1~~

~~GW 26 8 Lognormal 0.9751 0.9200 2.74 10.69 1.83~~

~~•^^^^^^:^^iS^'0K^-^: GW 26 50 Lognormal 0.9431 0.9200 2.62 10.29 0.00~~

~~DATA DISTRIBUTION FOR ALL DATES~~

~~COMPANY: -.<$ht&a1 Landfill~~

~~PRORAM:~~

~~LOCATION SAMPLE t SHAPIRO-WILK CALCULATED TABULAR COEFFICIENT 10 SIZE N-Ds DISTRIBUTION W W SKEWNESS KURTOSIS OF VARIATION~~

~~Import : rng/1~~

~~GW BK 4 0 Normal 0.8271 0.7480 0.62 1.22 0.68~~

~~GW BK 4 50 Normal 0.7913 0.7480 0.62 1.21 0.00~~

~~GW BK 4 0 Normal 0.7947 0.7480 0.67 1.26 1.01~~

~~GW BK 4 0 Normal 0.8087 0.7480 0.02 0.59 0.00~~

~~GW BK 4 0 Normal 0.9210 0.7480 0.43 1.07 0.00~~

~~(continues) 09/09/1997 Central Landfill Page: 2~~

~~DATA DISTRIBUTION FOR ALL DATES~~

~~LOCATION SAMPLE X SHAPIRO-WILK CALCULATED TABULAR COEFFICIEKT ID SIZE N-Ds DISTRIBUTION W W SKEWNESS KURTOSIS OF VARIATION PARAMETER: Copper.~~

~~GW BK 4 50 Normal 0.7545 0.7480 0.71 1.28 0.00~~

GW BK 4 50 Lognormal 0.9497 0.7480 0.73 1.30 1.54 : ; : V: : : : : PARAMETERS Lead, total ;.;fIf:;l^l lt:: W-•;: "- .-.'" ':; ; •• -i&: -;^'•'. UNIT: mg/1 GW BK 4 25 Normal 0.8874 0.7480 -0.03 0.65 0.45 PARAMETER:

~~GW BK 4 0 Normal 0.9661 0.7480 0.17 1.12 0.51 lîffl^^^l^fflî^^^^^^^BSft^'iii^fl^^f^^^^^B^MÎi GW BK 4 50 Normal 0.9861 0.7480 0.14 0.93 0.00~~

~~ANOVA (KRUSKAL-WALLIS/NONPARAMETRIC) FOR ALL DATES~~

~~COMPANY- Central Landfill SITE: Central Landf111 PROGRAM: Grbundwater PROGRAM TYPE- DATAGROOi i Groundwater KruskaI~~

~~Import PARAMETER: v tbtal UNIT: mg/1 Number of Ties - 0 Total Degrees Of Freedom: 1 Calculated H Value: 1.344 Tabular H: 3.841~~

~~Since the calculated Kruskal-Wallis H value 1s less than the tabular value of H. it can be concluded that a statistically significant difference does not exist among the selected locations.~~

~~Number of Ties - 0 Total Degrees Of Freedom: 1 Calculated H Value: 3.130 Tabular H: 3.841~~

~~Since the calculated Kruskal-Wallis H value 1s less than the tabular value of H. it can be concluded that a statistically significant difference does not exist among the selected locations.~~

~~Number of Ties > 0 Total Degrees Of Freedom: 1 Calculated H' Value: 0.411 Tabular H: 3.841~~

~~Since the calculated Kruskal-Wallis H' value 1s less than the tabular value of H. it can be concluded that a statistically significant difference does not exist among the selected locations.~~

Number of Ties > 0 Total Degrees Of Freedom: 1 Calculated H1 Value: 0.023 Tabular H: 3.841 Since the calculated Kruskal-Wallis H1 value is less than the tabular value of H. it can be concluded that a statistically significant difference does not exist among the selected locations.

~~(continues) 09/09/1997 Central Landfill Page: 2~~

~~ANOVA (KRUSKAL-WALLIS/NONPARAMETRIC) FOR ALL DATES~~

~~All Duplicates l|sed Non-Detects = Detection Limit/2 Sigrii fi cance Level (1 - al pha):~~

~~PARAMETER: UNIT: mg/T Number of Ties - 0 Total Degrees Of Freedom: 1 Calculated H Value: 6.257 Tabular H: 3.841~~

~~Since the calculated Kruskal-Wallis H value exceeds the tabular value of H. it can be concluded that a statistically significant difference may exist among the selected locations.~~

~~BACKGROUND LOCATION CRITICAL DIFFERENCE AVERAGE COMPLIANCE LOCATION VALUE OF RANKS RANK~~

~~TOXICITY PROFILES 1,1,1-TRICHLOROETHANE~~

~~GENERAL BACKGROUND INFORMATION~~

1,1,1-Trichloroethane (also known as 1,1,1-TCA) is a colorless man-made chemical. It can be found in a liquid state, vapor, or dissolved in water or other chemicals. When found as a liquid, it evaporates rapidly and becomes a vapor in the air. 1,1,1-TCA has a sweet, sharp odor (ATSDR, 1990). 1,1,1-Trichloroethane is often used as a solvent to dissolve other substances such as glue or paint Industrially, it is used to remove oil or grease from manufactured metal parts. Residentiary, it is used for spot removal cleaners, aerosol sprays and glues. 1,1,1-Trichloroethane can be found in hazardous waste sites in the soil, water and in the air (ATSDR, 1990). It can be found in rivers, lakes, soil, drinking water, and drinking water from underground wells.

~~PHARMACOKINETICS~~

1,1,1-Trichloroethane is rapidly and completely absorbed by ingestion and inhalation (U.S. EPA, 1984). It distributes throughout the body and crosses the blood-brain barrier (U.S. EPA, 1984). If spilled topically, absorption via the skin would occur in small amounts because of quick evaporation .into the air (U.S. EPA, 1984; ATSDR, 1990). Regardless of how 1,1,1-trichloroethane enters the body, most will quickly leave as exhalation occurs (ATSDR, 1990). What does not exit from expiration (metabolites) will be excreted through the urine and breath in a few days.

~~HUMAN TOXICOLOGICAL PROFILE~~

The toxic effects of 1,1,1-TCA are generally seen at concentrations well above those likely in an ambient environment. The most notable toxic effects of 1,1,1-TCA in humans are central nervous system depression, including anesthesia at very high concentrations, and impairment of coordination, equilibrium, and judgement at lower concentrations. Exposure to high concentrations may also result in cardiovascular effects, including premature ventricular contractions, decreased blood pressure and sensitization of the heart to epinephrine-induced arrhythmias, leading possibly to cardiac arrest (U.S. EPA, 1985; ATSDR, 1990). Acute exposure to niinjmal concentrations of 1,1,1-trichloroethane did not produce respiratory or lung volume effects (Dornette, 1960; Torkelson et al, 1958).

~~MA DEP, ORS & BWSC Documntation for the RUk /n«g«rm~~

~~Summary 1,1,2-Trichloroethane induced liver tumors and pheochromo cytomas in mice. It caused liver and kidney damage in dogs.~~

~~CAS Number: 79-00-5~~

~~Chemical Formula: CH2C1CHC12 IUPAC Name: 1,1,2-Trichloroethane Important Synonyms and Trade Names: Vinyl trichloride, ethane trichloride~~

Chemical and Physical Properties Molecular Weight: 133.41 Boiling Point: 133.8«C Melting Point: -36.5*C Specific Gravity: 1.4397 at 20«C Solubility in Water: 4,500 mg/liter at 20*C Solubility in Organics: Soluble in alcohol, ether, and chloroform Log Octanol/Water Partition Coefficient: 2.17 Vapor Pressure: 19 mat Hg at 20*C Vapor Density: 4.63

Transport and Fate Volatilization and subsequent photooxidation in the tropos phere are probably the primary transport and fate processes for 1,1,2-trichloroethane. Some sorption, bioaccumulation, and biodegradation may occur, but these processes are probably not very important processes for trichloroethane transport or fate.

~~1,1,2-Tr ichloroethane Page 1 October 1985 [Cl«m«nc Risk Concentration I0~l 6.0 Mg/liter 10"; 0.6 Mg/liter 10"' 0.06 Mg/liter CAG Unit Risk (USEPA): 5.7xlO"2 (mg/kg/day)"1~~

REFERENCES INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1979. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans. Vol. 20: Some Halogenated Hydro carbons. World Health Organization, Lyon, France, pp. 533-543 NATIONAL CANCER INSTITUTE (NCI). 1977. Bioassay of 1,1,2 Trichloroethane for Possible Carcinogenicity. CAS No. 79 00-5. NCI Carcinogenesis Technical Report Series No. 74, Washington, D.C. DHEW Publication No. (NIH) 78-1324 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1983. Registry of Toxic Effects of Chemical Substances. Data Base. Washington, D.C. October 1983 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1979. Water- Related Environmental Fate of 129 Priority Pollutants. Washington, D.C. December 1979. EPA 440/4-79-029 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1980. Ambient Water Quality Criteria for Chlorinated Ethanes. Office of Water Regulations and Standards, Criteria and Standards Division, Washington, D.C. October 1980. EPA 440/5-80-029 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984. Health Effects Assessment for 1,1,2-Trichloroethane. Environmental Criteria and Assessment Office, Cincinnati, Ohio. September 1984. ECAO-CIN-HO45 (Final Draft) U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985. Health Assessment Document for Dichloromethane (Methylene Chloride). Office of Health and Environmental Assessment. Washington, D.C. February 1985. EPA 600/8-82/004F VERSCHUEREN, K. 1977. Handbook of Environmental Data on Organic Chemicals. Van Nostrand Reinhold Co., New York. 656 pages WEAST, R.E., ed. 1981. Handbook of Chemistry and Physics. 62nd ed. CRC Press, Cleveland, Ohio. 2,332 pages

~~1,1,2-Trichloroethane Page 3 October 1985 1,1-DICHLOROETHANE~~

~~GENERAL BACKGROUND INFORMATION~~

1,1-Dichloroethane (1,1-DCA) is a colorless, oily, lipophilic liquid which evaporates quickly at room temperature and has an ether-like odor. Its liquid and vapor forms ignite easily and may pose a fire hazard when handled improperly. It does not dissolve easily in water. 1,1 DCA is used primarily as an industrial solvent and as a dissolving agent for paint, varnish, finish removers and grease (ATSDR, 1990).

~~PHARMACOKINETICS~~

Little information exists quantitating the absorption of 1,1-DCA. However, based on its chemical and physical properties, it would be predicted to be readily absorbed via any route of exposure (ATSDR, 1990). Once absorbed, it should be readily distributed to bodily tissues, with highest concentrations achieved in tissues of greatest lipid content (Sato and Nakajima, 1987). A large percentage of an administered dose is exhaled unchanged (Mitoma et al., 1985). The remainded undergoes biotranformation mediated by the microsomal mixed function oxidase enzyme system to yield reactive acylchloride metabolite(s) which covalently bind to cellular macro molecules

~~HUMAN TOXICOLOGICAL PROFILE~~

Relatively little information is available on the health effects of 1,1-dichloroethane in humans. It induces central nervous system depression and anesthesia upon inhalation. In fact, it was used as an inhalation anesthetic in the past. The use of 1,1-DCA as an inhalation anesthetic was discontinued when it was discovered that this compound induced cardiac arrhythmias in humans at anesthetic doses ((Reinhardt et aL, 1971). No studies were located concerning threshold effects of exposure on any other organ system.

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

Limited data indicate that 1,1-dichloroethane is less toxic than its isomer, 1,2-dichloroethane and most other chlorinated aliphatic solvents (Parker et al., 1979). Exposure of animals to 1,1-DCA results in central nervous system depression which may be fatal if exposure levels are high (Plaa and Larson, 1965). Nephrotoxicity has been observed in cats and mice

~~MA DEP. ORS £ BWSC DocumntAtion for th« RUk Ai««mm«nt ShortFonn R««kUntial Scenario rmion* 1.6 * It b - 10/92 B-55 1,1 -DICHLOROETHYLENE~~

~~GENERAL BACKGROUND INFORMATION~~

1,1-Dichloroethylene (1,1-DCE or vinylidene chloride) is a synthetic chemical used to make certain plastic products and flame retardant fabrics. It is released into the environment primarily as a result of air and water emissions coming from factories where 1,1-DCE is manufactured, hazardous waste sites where 1,1-DCE has been improperly disposed of, or as a result of accidental spills. 1,1-DCE is also found as a breakdown product of other chemicals present in the environment Although high percentages of 1,1-DCE in soil and water quickly escape to the air, gmall concentrations remain and undergo biodegradation into other compounds. Once in the air, the compound rapidly decomposes through a variety of processes. It is estimated that 1,1-DCE released into the atmosphere persists for only about two days (ATSDR, 1988).

~~PHARMACOKINETICS~~

1,1-DCE is rapidly absorbed by the oral and inhalation routes. In animal studies, it was found to accumulate preferentially in the kidney, liver, and lung. 1,1-DCE undergoes complex biotransfonnation processes and numerous metabolites have been identified1. The initial metabolic step is possibly the formation of an unstable reactive epoxide intermediate. Metabolites are ultimately conjugated with glutathione and excreted in urine (ATSDR, 1988).

~~HUMAN TOXICOLOGICAL PROFILE~~

Humans exposed to high concentrations of 1,1-DCE (approximately 4,000 ppm) show central nervous system depression which sometimes progresses to convulsions, spasm, and unconsciousness (Tieniey et aL, 1979). Repeated exposure to 1,1-DCE causes hepatotoxicity. Preliminary clinical findings on workers exposed to 1,1-DCE for up to 6 years in a polymerization plant in New Jersey revealed a high incidence of hepatotoxicity (U.S. EPA, 1985).

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

Signs of central nervous system toxitity are the predominant effects observed in animals acutely exposed to high concentrations of 1,1-DCE via the inhalation route. The toxic signs consist primarily of central nervous system depression, lacrimation, dyspnea, tremor, convulsions, and narcosis, finally resulting in death (KUmisch and Freisberg, 1979a,b; Zeller et aL, 1979). Rodents acutely exposed to high levels of 1,1-DCE (500 - 15,000 ppm) via inhalation show irritation of the mucous membranes and pulmonary edema, congestion and

MA DEP, ORS & BWSC DocumnUtkm for tb* Rick Aneitment SbortFonn Re*kU&ti*l Scenario wrion* 1.6 * Jc b - 10/92 B-63 active as a tumor-initiating agent (Van Duuren et al., 1979). U.S. EPA has classified 1,1-DCE as a Group C agent (possible human carcinogen) for which there is limited evidence of cardnogemcity in animals.

~~REFERENCES~~

~~Afency for Toxic Suhctance* and Dueaaa Registry (ATSDR) (1988) Toxicoloiritfl Pr?fil« tor 1.1-dichloroethene. US. Public Health Service.~~

~~Andereon, D.M, Hodge, CX. and Purchaae, LF.H. (1977) Dominant lethal studies with the halogenated olefins vinyl chloride and vinylidene chloride in male CD-1 mice. Environ. Health Penp. 21:712-78.~~

~~Gage, J.C. (1970) The subacute inhalation tcaddty of 109 industrial chemicals. Br. J. Ind. Mod. 27:1-18.~~

~~Jackaon, N.M. and Connoty, R-B. (1985) Acute nephrotoxidty of 1,1-dichloroethylene in the rat after inhalation exposure. ToxiooL Lett. 29:191.199.~~

~~Jaeger, RJ. (1977) Effect of 1,1-dichloroethylene exposure on hepatic mitochondria. Rea. Commun. Chem. PathoL PharmaooL 18 83-94.~~

~~Jonea, BJL and Hathway, DX. (1978) Tissue-mediated mutagenidty of vinylidene chloride in Salmonella typhimurium TA 1636. Cancer Lett. 6:1-6.~~

Rlhniarh, JJ. and Friaiberg, K.O. (1979*) Report on the determination of acute tcaddty (LCSO) by inhalation of vinylidene chloride in Chinese striped hamsters (fed) during a 4-hour exposure period. BASF AktlengeaeQaonan, Ludwigechafen:!!.

Klimiarh, JJ. and Frieaberg. K.O. (1979b) Report on the determination of acute toxicity (LCSO) by inhalation of vinylidene chloride in Chinese striped hamsters (fasting) during a 4-hour exposure period. BASF Aktiegnecellsohaft, Ludwigachafen: 11.

Makoni, C, T"•*•»"iM. G. and Chieoo, P. (19&6) Experimental research on vinylidene chloride cardnogenesis. In: Archive* of Reeearch on Industrial Carcinoggnetii. VoL 3, C. Mf H""' and M. M*itriMf^ eda. Princeton Scientific PubUahera, Princeton, NJ.

Prendergmit, J-A-, Jonea, R.A. and Jenkina, LJ. (1967) Effects on experimental animals of long-term inhalation of trichloroethylene, carbon tetrachloride, 1,1,1-trichloroethane, dichlorodifluoromelhane, and 1,1-dichloroethylene. ToxiooL AppL PharmaooL 10:270-289.

~~J, Humicton, C.G. and Wad*, CX. (1983) A chronic toxicity and oncogenidty study in rats and subchronic toxicity study in dog* on ingested vinylidene chloride. Fund. AppL ToxiooL 3:55-62.~~

Reitz, RJL, Watanaba, P.G. and M-K""". sLJ. (1980) Effects ofvinylidene chloride on DNA synthesis and DNA repair in the rat and mouse; a comparative study with dimethylniirosamine. ToxiooL AppL PharmaooL 62:357-370.

~~Reynold*, ILS, Moakn. M.T. and Boor, P J. (1980) 1.1-Dichloroethylene hepato toxicity. Am. J. PathoL 101:331-342.~~

Short, R-D^ Minor, Jl* *"^ Winiton, JJi. (1977) ToricitT «tudr of «el*ct*d ch«mical«. Talk II: Tht development of vinylideo* chlorid* 'i holed by rati and mice during gestation. U^. Environmental Protection Agency, Watnington, D.C. EPA 660/6-77-022.

~~Tierney, Di, Mackwood, TH. and Piana, MJL (1979) Statui a««c««m*nt of toxic chemical*: vinvlideng chloride. Cincinnati. Ohio: U 3. Environmental Protection Agency. EPA 600/2-79-2100.~~

~~MA DEP, ORS & BWSC Documntation for the Riak Aueaiment ShortForm Reaidential Scenario ««niona 1.6 a It b - 10/92 B-65 1,2-DICHLOROETHYLENE~~

~~GENERAL BACKGROUND INFORMATION~~

There are two isomere of 1,2-dichloroethene (1,2-DCE), cis and trans. Neither of these isomers has developed wide industrial usage in the United States partly due to their flammability. The trans isomer is more widely used in industry than either the cis isomer or the 60:40 cis/trans mixture. It is used as either a low-temperature extraction solvent or as a direct solvent in materials such as dyes, perfume oils, waxes, resins and thermoplastics. It is also used as a chemical intermediate in the synthesis of polymers. 1,2-DCE is highly volatile, weakly adsorbed by soil and has no significant potential for bioaccumulation. It may volatilize from soil surfaces, but that portion not subject to volatilization is likely to be mobile in groundwater (IRP, 1985).

~~PHARMACOKINETICS~~

1,2-DCE is absorbed by all routes of exposure (see section on Relative Absorption Factors) (ATSDR, 1989). Distribution is expected to be rapid. Due to the lipophilic nature of 1,2 DCE, tissues of high lipid content would be expected to attain the highest levels. 1,2-DCE is metabolised via the mixed function oxidase enzyme system to chloroethylene epoxides which undergo rearrangement to dichloroacetaldehyde or chloroacetic acids (Henschler, 1977; Liebman and Ortiz, 1977). Excretion of 1,2-DCE and its metabolites has been largely uncharacterized (ATSDR, 1989).

~~HUMAN TOXICOLOGICAL PROFILE~~

1,2-DCE was once used as a general inhalation anesthetic in humans (Proctor and Hughes, 1978). Exposure to the trans isomer at a level of 2000 ppm causes burning of the eyes, vertigo and nausea (Proctor and Hughes, 1978). Within the limited industrial usage, only one toxic effect in humans was reported • a fatality due to very high vapor inhalation in a gnmll enclosure (Rosenthal-Deussen, 1931). 1,2-DCE causes eye and skin irritation upon contact (Grant, 1974). There are no reports of long-term human exposure to 1,2-DCE isomers.

~~MA DEP. ORS & BWSC Documntatkm for th« Rick Ammment ShortFonn P*"^*"^*1 Scenario 1.6 • & b - 10/92 B-67 REFERENCES~~

Agency for Toxic Subetanoei and Di*e&M Regictry (ATSDR) (1989) Ttmoological profil* for 1.2-dichlororthene. VS. Public Health Service. Ameriren Conference of Inductrial HygianUtJ (ACGIH) (1980) Documentation of the Thrc«hold I JmH Vahier 4th ed. Cincinnati, Ohio.

Bronzetti, G., Bauar, C., D«l Carratore, R, Cord, C., Leporine, C., Nieri, R. «nd Galli, S. (1982) Genetic e/7eck o/' chlorinated eihylena: in vUro and in viuo ttudie* using D7 ttrain of S. eerivisioe. Effects on enzymes involved in xenobiotic meiabolitm. MuUt RM. 97:460.

~~Frwundt, KJ, LUl«ldt, GP. and Li«b«rwirth, E. (1977) Toxicology ttudies on trans-lj-dichlorocthylene. Tandoology. 7:141-163.~~

~~Grant, WJi. (1974) ToxicologT of The Era. 2nd «d- Springfold, DlinoU: CharlM C. Thotna* Pnbliahcr.~~

~~H*a«chlar. D. (1977) MetoooZum and mutagenidty of halogcnated ole/lnx A comparison of ttrvcturc and activity. EnTiroo. Health Panpeoi. 21:61-64.~~

InftfJIf fop R«toration Program Toiicology Guide (TRP). Vohinv* 1. (1985) Arthur D. Little, Iiv , Cambridgv, MA. Uebman, K.C. aad Ortix, E. (1977) Metabolism of halogcnated eihylena. Environ. Health P«rapeot. 21:91-97.

~~MatluM, V. (1970) Med. Klin. 63:463.~~

~~Proctor, NJI. atv4 Hugh**, JJ*. (1978) ^IrrmiT*! Hatard* of the Workplace. Philadelphia; Lippincott Company.~~

~~Roatathal-DwaMn, E. (1931) Arch. G«werb«paUioL G«w«rbehyg. 2: 92. Smyth, HJ. (1966) Improved communication • Hygienic standards for daily inhalation. Am. Ind. Hyg. A**oo. Q. 17:164.~~

~~MA DEP, ORS I BWSC Documntation for the RUk AiiMtment ShortForm Re«idential Scenario vmknw 1.6 a Jc b • 10/92 B-69 DICHLOROBENZENE~~

Summary Dlchlorobenzenc (DCB) is probably persistent in the natural environment. In rats, chronic oral exposure to dichlorobenzene caused liver and kidney damage and changes in the hematopoietic system. In humans/ DCB is a skin and eye irritant; inhalation exposure causes nausea and irritates the membranes.

CAS Number: 1,2-Dichlorobenzene (1,2-DCB) 95-50-1 1/3-Dichlorobenzene (1,3-DCB) 541-73-1 1,4-Dichlorobenzene (1,4-DCB) 106-46-7 Chemical Formula: CgH.Cl- IUPAC Name: Dichlorobenzene Important Synonyms and Trade Names: Dichlorobenzene, DCB

Chemical and Physical Properties Molecular Weight: 147.01 Boiling Point: 1,2-DCB: 180.5"C 1,3-DCB and 1,4-DCB: 173 "C Melting Point: 1,2-DCB:-17.0*C 1.3-DCB:-24*C 1.4-DCB:-53«C Specific Gravity: 1.3 at 2Q*C Solubility in Water: 1,2-DCB: 145 rag/liter at 25«C 1.3-DCB: 123 ing/liter at 25-C 1.4-DCB: 80 nig/liter at 25'C Solubility in Organics: Soluble in alcohol, ether, acetone, benzene, carbon tetrachloride, and ligroin Log Octanol/Water Partition Coefficient: 3.38 Vapor Pr««aur.e: 1 ma Hgv at 20"C Vapor Density: 5.OS

~~Dichlorobenzene Page 1 October 1985~~

~~Cl«m«nt~~

~~111 ACETONE~~

Summary* Aowtone is a commonly used solvent, which probably is not very persistent in the environment. It is considered to have rather low toxicity, and no chronic health hazards ha.ve been associated with exposure to it. Acetone is not very toxic to aquatic organisms.

~~GAS Number: 67-64-1 Chemical Formula: CH.-CO-CH, IUPAC Name: Propanone Important Synonyms and Trade Names: Dimethyl ketone, 2-propanone~~

Chemical and Physical Properties Molecular Weight: 58.08 Boiling Point: 56.2«C Melting Pointi -9S»C Specific Gravity: 0.7899 at 20«C Solubility in Water: miscible Solubility in Organic*: Soluble in alcohol, ether, benzene, and chloroform Log Octanol/Water Partition Coefficient: -0.24 Vapor Pressure! 190 mm Hg at 20«C Vapor Density: 2.00 Flash MtAt* -1«*C (closed cup)

Transodyt and Fate Very limited information on the transport and fate of acetone was found in the literature reviewed. However, ketones in general art probably not very persistent. Acetone has a high vapor pressure and therefore would be expected to volatilize readily, but because of its high water solubility, volatilization is probably limited. Once in the atmosphere, it is apparently Acetone Page 1 October 1985

33 REFERENCES AMERICAN INDUSTRIAL HYGIENE ASSOCIATION (AIHA). 1980. Hygienic Guide Series: Acetone McKEE, J.I., and WOLF, H.W. 1963. Water Quality Criteria. 2nd ed. California State Water Resources Control Board Publication 3A NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1978. Criteria for a Recommended Standard—Occupational Exposure to Ketones. Washington, D.C. DHEW Publication No. (NIOSH) 78-173 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1983. Registry of Toxic Effects of Cheaical Substances. Data Base. Washington, D.C. January 1984 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).- 1984. Health Effects Assessment for Acetone. Environmental Criteria and Assessment Office, Cincinnati, Ohio. Septeaber 1984. ECAO-CIN-H016 (Final Draft) VERSCHUEREN, K. 1977. Handbook of Environmental Data on Organic Chemicals. Van Nostrand Reinhold Co., New York. 659 pages? WEAST, R.E., ed. 1981. Handbook of Chemistry and Physics. 62nd ed. CRC Press, Cleveland, Ohio. 2,332 pages

~~Acetone Page 3 October 1985 BENZENE~~

~~GENERAL BACKGROUND INFORMATION~~

Benzene is a dear, volatile, highly flammable, aromatic hydrocarbon which exists naturally and is produced by volcanoes and forest fires. Benzene is also a very common industrial solvent, produced from petroleum. It is used as a solvent for fats, inks, paints, plastics, rubber, in the extraction of oils from seeds and nuts, in photogravure printing, as a chemical intermediate and in the manufacture of detergents, explosives, pharmaceuticals and dyestufls. It is also a component of gasoline and other petroleum-based fuels. Exposure to benzene can occur via inhalation, ingestion, especially of contaminated drinking water, and dermal contact (as in contact with liquid benzene found in gasoline.) (Sittig, 1981; ATSDR, 1989)

~~PHARMACOKINETICS~~

Benzene is readily absorbed through ingestion, moderately absorbed through inhalation and poorly absorbed through intact skin (see section on Relative Absorption Factors). Once in the bloodstream, benzene is distributed throughout the body, with the concentration in any one compartment dependent on the degree of perfusion of tissues by blood. Since benzene is lipid-soluble, it accumulates in fat, but the rate of accumulation is slow since fat is poorly perfused. The metabolites of benzene are responsible for its toxic effects. These include phenol (which is either formed via an unstable benzene oxide precursor or directly from benzene), catechol, hydroquinone and conjugated phenolic compounds. The primary site of benzene metabolism is the liver via the cytochrome P450 mixed function oxidase system. Some benzene metabolism may also occurs in the bone marrow via the same enzyme system. Benzene is excreted either unchanged from the lungs or as metabolites in the urine (ATSDR, 1989).

~~HUMAN TOXICOLOGICAL PROFILE~~

Benzene targets its effects on the hemopoietic, immune and nervous systems (ATSDR, 1989). Exposure to benzene has produced irritation of the skin, eyes and upper respiratory tract. Acute exposure has produced central nervous system depression, headache, dizziness, nausea, convulsions, coma and death at extremely high concentrations (Sittig, 1981). Health effects in humans have been reported starting as low as 50 ppm via inhalation. Twenty-five ppm for 6 hrs had no obvious effects though benzene was detected in blood (Sandmeyer, 1981). Early autopsy reports found benzene-induced hemorrhages of the brain, pericardium, urinary tract, mucous membranes and akin (Sittig, 1981). Chronic exposure to benzene produces blood changes involving an initial increase in levels of erythrocytes, leukocytes and

~~MA DEP, ORS & BW8C DocumntAtion for UM RUk Ajuntmant ShortForm Radde&twl Scenario venioiw 1.6 * tt b - 10/92 B- 13 CARBON TETRACHLORIDE~~

~~GENERAL BACKGROUND INFORMATION~~

Carbon Tetrachloride is a dear, heavy aromatic liquid with a sweet odor. Although this compound does not occur naturally, it is distributed extensively in the earth's atmosphere due to its extensive anthropogenic production and use. Carbon tetrachloride is currently widely used as a refrigerant and a propellant. Carbon tetrachloride is also used a solvent for oil, fats, lacquers, varnishes, rubber, waxes and resins. Until the mid-1960s, carbon tetrachloride was used as an industrial degreaser, as a household spot remover, and as a fire- extinguishing agent. Until 1986, carbon tetrachloride was used to fumigate grain. Carbon tetrachloride is very stable in the atmosphere, with a half-life in air of about 30-100 years. Thus, it persists in the environment for many years (Sittig, 1981; ATSDR, 1989).

~~PHARMACOKINETICS~~

Carbon tetrachloride is readily absorbed through ingestion and inhalation and poorly absorbed through the skin (see section on Relative Absorption Factors). The metabolism of carbon tetrachloride occurs primarily in the liver, where a specific form of hepatic cytochrome P-450 initiates a reductive dehalogenation yielding a trichloromethyl free radical and a chloride ion. The trichloromethyl radical is then further reacted upon either anaerobically or aerobically. Anaerobically, either CHCL,, CL,CCCL, or CO*/HCOO' can be produced depending on which of several anaerobic reactions take place. Aerobically, the precursor, CL^CO, could be produced, leading to formation of phosgene (COClj). Hydrolytic cleavage of COC1, leads to formation of HCL Although it is known that metabolism of carbon terachloride plays an important role in its toxitity, the specific mechanism relating the metabolites to toxitity has not yet been determined. Excretion of carbon tetrachloride from the body has been found to occur largely in the form of the parent compound. Exposure studies in animals have shown that about 30-40% of an inhaled dose of carbon tetrachloride is recovered in expired air and about 50-60% is recovered in feces. Via oral exposure, one rat study indicated that about 70-90% of an administered oral dose was recovered in expired air and lower amounts were recovered as COa or CHCL, or as nonvolatile metabolites in feces or urine. Via dermal exposure, carbon tetrachloride excretion has also been found to occur rapidly through expired air, but this was not quantified (ATSDR, 1989).

~~HUMAN TOXICOLOGICAL PROFILE~~

Most of the human health data for carbon tetrachloride come from acute exposure case studies in individuals who have been exposed to large doses for short periods of tune. Health effects of carbon tetrachloride include defatting of skin leading to a dry, fissured dermatitis

MA DEP, ORS & BWSC Documntatkm for the Ri«k Awirmnnt ShortForm Residential Scenario v*nioo< 1.6 a tc b - 10/92 B-33 International Agency for Research on Cancer (IARC) that sufficient evidence exists to designate this compound carcinogenic in experimental nnimnls (ATSDR, 1989).

~~REFERENCES~~

~~Agency for Toxic Subctancw and DUeaM Regutry (ATSDR) (1989) Torieological profile for carbon tetrachloride. U.S. Public Haakh Strric*.~~

~~Callm, DJ, Vfolt, C.R. and Philpot, R-M. (1980) Cytochmme P-450 mediated genetic activity and cytatoxidty of seven haiogenated aliphatic hydrocarbon* in Saocharomyce* ocrevuiae. Mutat. Re*. 77:55-63.~~

~~Could, VJL and Smuckier, EA. (1971) Alveolar injury in acute carbon tetrachloride intoxication. Arab. Intern. Med. 128:109-117.~~

~~Stttig. M. (1981) Handbook of Toxic and Haxardom Chemical*. Nojre* Publications.~~

~~WiUoa, J.G. (1954) Influence ofofftpring of altered phyfiologic ttatet during pregnancy in the rat. Ann NY Aoad ScL 67:617^26.~~

~~MA DEP. ORS & BW3C Documntation for the Riak rt««fnrmont ShortForm Residential Sotnario 1.6 a tt b - 10/92 B-35 CHLOROBENZENE~~

~~GENERAL BACKGROUND INFORMATION~~

Chlorobenzene is a dear liquid with an almond-like odor. Although chlorobenzene does not occur naturally in the environment, it is used in industry as a solvent, in the manufacture of aniline, phenol and chloronitrobenzene, and as an intermediate in the manufacture of dyestuffs and pesticides (ATSDR, 1990; Sittig, 1981).

~~PHARMACOKENETICS~~

Chlorobenzene is assumed to be readily absorbed via ingestion, moderately absorbed through inhalation and poorly absorbed through the skin, based on its structural similarity to benzene (see section on Relative Absorption Factors). The major metabolites of chlorobenzene are p-chlorophenylmercapturic acid and 4-chlorocatechol. Excretion of chlorobenzene occurs via urine in the form of its two metabolites, with the excretion of p-chlorophenylmercapturic acid reported to be much lower than of 4-chlorocatechol. A portion of an absorbed dose is excreted as unchanged chlorobenzene through the lungs (ATSDR, 1990).

~~HUMAN TOXICOLOGICAL PROFILE~~

Acute exposure to chlorobenzene has produced the following health effects in workers exposed to high levels: irritation of the eyes and nose, skin irritation, central nervous system depression with symptoms such as drowsiness, incoherence, numbness, nausea and vomiting. However, these workers were simultaneously exposed to other solvents so it is not clear whether chlorobenzene is responsible for these effects (ATSDR, 1990; Sittig, 1989).

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

Acute lethality via both inhalation and ingestion is relatively low in animals. One study produced 100% mortality in mice after 2 hrs of exposure to 4,300 ppm. In rats exposed to a single dose of 4000 mg/kg and mice exposed to a single dose of 1000 mg/kg via corn oil by gavage, death occurred in 2-3 days (ATSDR, 1990). Animal studies indicate that exposure to chlorobenzene via either inhalation or ingestion can produce severe kidney and liver damage. Typical signs of liver damage reported include increased serum enzymes, changes in liver weights, degeneration, necrosis and interference with porphyrin metabolism. Signs of kidney damage include degeneration or focal necrosis of proximal tubules and increased kidney weights. Animal evidence also exists that chlorobenzene is immunotoxic via ingestion with the potential of producing thymic necrosis and lymphoid or myeloid depletion of bone marrow, spleen or thymus. Neurological effects, manifested by miscellaneous spasms and

~~MA DEP, ORS & BWSC Documntation for the Ruk AoaoMmcnt ShortFonn P»«i/<«t.»i«l Scenario vmrion* 1.6 • A b - 10/92 B-37 CHLOROFORM~~

~~GENERAL BACKGROUND INFORMATION~~

Chloroform is a dear, colorless, liquid with a characteristic odor, which exists both naturally and as a man-made compound. Chloroform was one of the earliest general anaesthetics but was later banned because of toxic effects. Chloroform is largely used in the production of fluorocarbon 22 (used as a coolant hi air conditioners and to make fluoropolymers) (ATSDR, 1989). In addition, chloroform is used as a solvent, in the extraction and purification of pharmaceuticals, in the manufacture of pesticides and dyes and in various products including fire extinguishers, dry cleaning agents, artificial silk, plastics and floor polishes. Chloroform is also widely found in drinking water supplies as a byproduct of chlorination (ATSDR, 1989; Sittig, 1981).

~~PHARMACOKINETICS~~

Chloroform is readily absorbed via inhalation and ingestion and poorly absorbed through the skin, unless the dose is occluded, in which case it is very well absorbed (see section on Relative Absorption Factors). Chloroform is lipid-soluble and passes through cell membranes easily. Thus it will reach the central nervous system and cross the placenta! barrier. It has been found in fresh cow's milk and is thus expected to reach human millc too. Chloroform is metabolized via cytochrome P450 by oxidative dechlorination to form phosgene. The phosgene either reacts with glutathione to form diglutathionyl dithiocarbonate or causes cytotoxicity directly by reacting with other cellular constituents. Inorganic chloride ion and carbon monoxide are minor metabolites of chloroform metabolism. Although there are species differences as to relative amounts metabolized, chloroform is largely excreted unchanged through the lungs. Carbon dioxide is also a major endproduct of chloroform metabolism, most of which is excreted via the lungs but some of which is also incorporated into endogenous metabolites and excreted as bicarbonate, urea, methionine and other amino acids. Carbon monoxide is a minor metabolite also excreted through the lungs. In addition, inorganic chloride ions are excreted via the urine (ATSDR, 1989).

~~HUMAN TOXICOLOGICAL PROFILE~~

Skin contact with chloroform can produce burns. Chloroform is a central nervous system depressant and was used in the past as an anaesthetic until it was determined that it caused liver and kidney toxicity. Specific central nervous system symptoms resulting from acute exposure include fatigue, dizziness, headache, digestive disturbance and mental dullness, as well as

~~MA DEP. ORS & BWSC Documnution for the Risk AiMument ShortForm Residential Scenario venion* 1.6 a It b - 10/92 B-39 REFERENCES~~

~~Agtnc7 far Toxic SubitanoM and DUMBM lUgutty (AT3DR) (1989) Tcncicological profile for chloroform. UJ. Public Haalth S«Tvic*.~~

Chu, I, Vfflracuv*, D.C, Secoun, V.E. and B«ckin, G.C. (1982) Toxidty of trihalomethanes. I. The acute and tubocute taadty of chloroform, bromodichloromcthane, chlorodibromomethanc and bromoform in rat*. J. Environ. SoL Health. 817:205-224. Dmrinfftr. MJC. Dunn, T.B. and HMton, WJJ. ( 19S3) Rettdtt of exposure ofttrain C3B mice to chloroform. Proo. 800. Erp. BioL Mod. 83.474-479.

~~TjL, M«i«rh«irjr. EJ. and Riuhbrook, CJ. (1985) Caranogenicify of chloroform in drinking water to male Otbornc-Mendcl rat* and female B6C3F1 mice. Fund. AppL ToxiooL 6:760-769.~~

~~Kunurm, E.T., Ebert, DAJ. and Dodg«, B.W. (1971) Acute teaddty and limits of tolvent residue for sixteen organic •olvents. Toidoot AppL PharmaooL 19:699-704.~~

1-, P-M«H M., Kroocvi, T., Udonu, V. and Lundberg, S. (1986) Relative hepatotoxieity of tome industrial tolvenis after intraperitoneal injection or inhalation exposure to rats. Environ. RM. 40:411-420.

~~NCI (1976) Report on carcinogcnxU bioaa«ay of chloroform. NTIS PB-264018.~~

~~Roa, FJ.C, Palmn-, A-iUC, Worden, AJJ. and Van Abb*, NJ. (1979) Safety evaluation of toothpaste containing chloroform. I. Long-term studies in mice. J. Environ. ToxiooL 2:799-819.~~

~~Sittig. M. (1981) Handbook of Tone and Hatardom Chemical*. NOT** Publication*.~~

~~MA DEP. ORS & BWSC Documntation for the Ruk AjMum«nt ShortForm R«*id«ntial Scenario 1.6 a It b - 10/92 B-41 ETHYLBENZENE~~

~~GENERAL BACKGROUND INFORMATION~~

Ethylbenzene is a colorless liquid that smells like gasoline. It is volatile and flammable. Ethylbenzene occurs naturally in coal tar and petroleum, and is also manufactured for commercial uses in paints, inkq, and insecticides (ATSDR, 1990). The two major uses of ethylbenzene are in the plastic and rubber industry, where it is used in the synthesis of styrene (U.S. EPA, 1980). Gasoline contains about 2% (by weight) ethylbenzene (ATSDR, 1990). Ethylbenzene has a wide environmental distribution due to its widespread use.

~~PHARMACOKINETICS~~

Ethylbenzene has been shown to be readily absorbed via inhalation, ingestion, and dermal exposure in humans as well as in laboratory animals (see section on Relative Absorption Factors). Following exposure, ethylbenzene is distributed throughout the body, with the highest levels detected in the kidney, lung, adipose tissue, digestive tract, and liver (Chin et aL, 1980). There appears to be quantitative differences in metabolism of the chemical in humans and laboratory animals However, in all species, ethylbenzene undergoes a variety of microsomally-mediated side-chain hydroxylations to yield the major metabolites, mandelic acid and phenylglyoxylic acid (Engstrom et aL, 1984). The oxidation products are conjugated followed by urinary excretion which appears to be complete within 2 days of exposure (ATSDR, 1990).

~~HUMAN TOXICOLOGICAL PROFILE~~

Humans exposed to low levels of ethylbenzene in air for short periods of time experience eye and throat irritation. Exposure to higher levels may cause more severe effects such as central nervous system depression, decreased movement and dizziness, and more severe mucous membrane irritation. No studies have reported death in humans following exposure to ethylbenzene. No information was located to indicate that ethylbenzene produces toxicity in other organ systems upon short-term or prolonged exposure (ATSDR, 1990).

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

Animal studies indicate that the primary symptoms resulting from acute exposure to ethylbenzene are manifested as neurological and respiratory depression. Other studies suggest that the liver, kidney and hematopoietic system may also be targets of ethylbenzene toxicity (ATSDR, 1990). Studies indicate that ethylbenzene exposure of pregnant rats can produce fetotoxic effects at doses that also induce maternal toxicity (Andrew et aL, 1981).

~~MA DEP. ORS & BWSC Documntation for the Rink Anoomant ShortForm RandBntud Scenario vmwoa* 1.6 • & b - 10/92 B-71 MFTHYL ETHYL KETONE~~

~~GENERAL BACKGROUND INFORMATION~~

Methyl ethyl ketone (also known as MEK or 2-butanone) is a colorless liquid with an acetone-like odor, moderate water solubility and high volatility. The major uses of MEK are as a solvent for coatings, adhesives and printing inlcs, as a deaning/degreasing agent and as a chemical intermediate in the production of synthetic leathers, transparent paper and aluminum foiL MEK is a highly flammable substance and may pose a fire hazard if handled improperly (ATSDR, 1990).

~~PHARMACOKINETICS~~

MEK is readily absorbed by all routes of exposure (see section on Relative Absorption Factors). It is readily soluble in blood and appears to distribute uniformly to all organs (Perbellini et al, 1984). MEK is metabolized by both oxidative and reductive pathways (DiVincenzo et aL, 1976). It undergoes reduction to 2-butanol and oxidation to 3-hydroxy-2 butanone, which is further reduced to 2,3-butanediol. Small amounts of unmetabolized MEK can be excreted in urine or exhaled air. All metabolites are excreted in the urine as glucuronides or sulfate conjugates.

~~HUMAN TOXICOLOGICAL PROFILE~~

MEK can produce irritation to the eyes, respiratory tract and skin following high level exposure. Central nervous system effects have been reported, including headache, dizziness, nausea and fatigue (ATSDR, 1990). No studies were located regarding the possible consequences of exposure on the liver, kidney, reproductive organs or developing fetus. This ketone has been demonstrated to be very hazardous in combination with other solvents by potentiating the neurotoxicity of n-hexane, methyl-n-butyl ketone and ethyl-n-butyl ketone (Altenkirch et aL, 1979).

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

High level inhalation exposure to MEK results in upper respiratory tract and ocular irritation. Exposure to high level MEK by the inhalation or oral route resulted in liver congestion, increase liver weight and renal tubular necrosis (Patty, 1935; Cavender et al., 1983). Narcosis and incoordination, indicators of central nervous system effects, were also observed, with no signs of periphereal neuropathy. Inhalation exposure during gestation resulted in fetotoxic effects such as reduced fetal weight, skeletal variations and delayed

~~MA DEP, ORS & BWSC Documntation for UM Rick Ac*«*«tn«nt ShortFonn RMidential Scenario v«rnon* 1.6 • tt b - 10/92 B -91 TETRACHLOROETHYLENE~~

~~GENERAL BACKGROUND INFORMATION~~

The major use for tetrachloroethylene (perchloroethylene, PCE) is in the dry-cleaning industry. Its popularity in this area is due to its nonflammability, ease of recovery for reuse and its compatibility with various fabrics. It is also used in cold cleaning and vapor degreasing of metals. Its remaining uses are as a chemical intermediate in the synthesis of fluorocarbons, various manufacturing and industrial processes as well as medicinal uses (IRP, 1985).

~~PHARMACOKINETICS~~

PCE is readily absorbed by humans through the lungs into the blood. Pulmonary uptake is proportional to ventilation rate, duration of exposure and (at lower concentrations of PCE) to the concentration of PCE in the inspired air (Hake and Stewart, 1977). PCE is also rapidly aborbed following oral administration, but is poorly absorbed following dermal exposure (see section on Relative Absorption Factors). Distribution occurs rapidly with the highest concentrations of PCE achieved in tissues of high fat content (ATSDR, 1990). Metabolism of PCE is believed to be mediated by the microsomal mixed function oxidase enzyme system involving the formation of an epoxide intermediate. Major metabolites of PCE are trichloroacetic acid and trichloroethanoL Unmetabolized PCE is excreted largely by exhalation with urinary excretion of metabolites representing a small percentage (ATSDR, 1990).

~~HUMAN TOXICOLOGICAL PROFILE~~

Stewart et al. (1977) found that exposure of 11 subjects to a mean PCE concentration of 101 ppm for 7 hours produced symptoms of headache, dizziness, difficulty in speaking, and sleepiness. Long-term exposed subjects are also reported to experience effects such as short- term memory defects, ataxia, irritability, disorientation, and sleep disturbances (USEPA, 1985). PCE causes hepatotoxicity in humans. A number of reports of liver damage after inhalation of PCE in acute or chronic exposure situations have been documented (Hake and Stewart, 1977). PCE ingestion in humans results in symptoms indicative of liver damage, including elevated SCOT and SGPT levels, hepatomegaly, and fatty degeneration of the liver cells (Koppel et al., 1985).

MA DEP. ORS & BWSC Documntaticm for the RUk Aji««im«nt ShortForm Residential Scenario vmion* 1.6 • & b - 10/92 B- 115 carrinogenicity in humans, the U.S. EPA places PCE in Group B2, mining that is considered a probable human carcinogen.

~~REFERENCES~~

~~Agency tar Toxic 8ub*tancae and Dieaea* Reguftry (ATSDR) (1990) Toxicological orofila for tetrachlorotthylgne. U.S. Public Health Service.~~

~~Blair, A, Deoouflt, P. and Grauman, D. (1979) Cor/art of death among laundry and dry cleaning workers. Am. J. Pub. Health 69:608-611.~~

~~Broncetti. G.C., et aL (1983) Genetic and biochemical studies on pcrchloroethylene in vitro and in vivo. MutaL Roe. 116:323-331.~~

~~Haka, C.L. and Stewart, RJ). (1977) Human exposure to tetrachloroethylene: inhalation and tkin contact. Environ. Health Perap, 21:231-238.~~

~~Hayea, JJL, Condia, L.W. and BorzelUca, JJ. (1986) TTwr »u6cft/wuc toxidty of tetrachloroethylene (perchloroethylene) adminitiered in the drinking water of rats. Fund. AppL ToxiooL 7:119-125.~~

~~Tttt Imf^Uf **>n lUrtoration Program Torieologv Guid« ORP). Vol 1. (1985) Arthur D. LfttU, Inc. Cambridg., MA.~~

~~Kaplan. 8J). (1980) Drr-C\e»r]jj}f worken etpo««i to p«rchlorocthyl*ne. A retrorpactivc cohort mortality «tudr. Cincinnati, OH.~~

~~Koppal, Cn Arndt, I, Arandt, U. and Koepp*, P. (1985) Acute tetraehloroethylene poisoning: Blood elimination kinetic* during hyperventUation therapy. J. ToxiooL Clin. ToxiooL 23:103-116.~~

~~Eylin, B., Raichard, H^ Sunwgi, I. and YUnar, S. (1963) Hepatotoriiity of inhaled trichloroethylene, tetrachloroethylene, and chloroform -tingle exposure. Aota. Pharmaool. ToxiooL 20: 16-26.~~

~~National Cancer Inatituta (NCI) ( 1977) Bioa«««Tof tetrachlorocthylgno for poxibU carcinogenicity. OHEW Publication No. (NIH) 77-813.~~

~~National Toxicology Program (NTP) ( 1986) Toxicology and carcinoggnoi* of tgtrachloroethyl~~

~~Price, ?J~, Haaectt, CJf. and Manafiald, JI. (1978) Transforming activities of trichloroethylene and proposed industrial alternative*. In Vitro U(3).290-293.~~

~~Roaangren, LXM Ejelktrand, P. and Haglid, E.G.(1986) Tetrachloroethylene: levels ofDNA and S-100 in the gerbil CNS after chronic exposure. Neurobehav. ToxiooL TermtoL 8:201-206.~~

~~Row*. V^, McCollifUr, DJ)., Spancer. H.C, Adana, EM. and Iriah, DJ). (1952) Vapor toadty of tetrachloroethylene for laboratory animals and human subjects. AMA Arch. Ind. Hyg. Oooup. Med. 5:566-579.~~

BJL, Laong. BJLJ. and Gehriag, PJ. (1975) The effect of maternally inhaled trichloroethylene, perchloroethylene, meihylchlorofbrm, and methylene chloride on embryonal and fetal development in mice and rats. ToxiooL AppL PharmaooL 32:84-96.

~~Stawart, R.D.. Haka, Ci. and Wu, A. ( 1977) EffeeU of p«rchloroethylene/drug interaction on behavior and neurological function. Final Report.~~

~~U.S. Environmental Protection Agency (U.3. EPA) (1985) Health a««c««ment document for tetrachloroethvlene (ixrcnloroethyl~~

~~MA DEP, ORS & BWSC Documntation for the Ruk Aaaeaament ShortForm P^VUt^^l Scenario v«nion« 1.6 a & b - 10/92 B- 117 TOLUENE~~

~~GENERAL BACKGROUND INFORMATION~~

Toluene is a clear, colorless organic liquid with a sweet smell and a high degree of lipid solubility. It is used as an industrial solvent/degreaser, as an intermediate in the manufacture of chemicals and pharmaceuticals, and is present as a component of gasoline and other fuels, paints, lacquers, adhesives, rubber and printing ink. Toluene is a volatile molecule with relatively low water solubility. It is flammable and may pose a fire hazard if handled improperly (ATSDR, 1989).

~~PHARMACOKINETICS~~

Toluene is readily absorbed by all routes of exposure (see section on Relative Absorption Factors). Once absorbed, it is rapidly distributed to all organ systems, including fetal tissue, with highest concentrations occuring in organs with high lipid content such as adipose tissue, brain and bone marrow. Toluene undergoes primarily oxidative metabolism to benzyl alcohol mediated by the mixed function oxidase enzyme system. Benzyl alcohol is further oxidized by alcohol and aldehyde dehydrogenase to produce benzole acid which is primarily conjugated with glycine or glucuronic acid and excreted in urine as hippuric acids or benzoyl glucuronide. Toluene may also be excreted unchanged in exhaled air. Metabolism and excretion occurs rapidly, with the major portion occurring within 12 hours of exposure (Fishbein, 1985).

~~HUMAN TOXICOLOGICAL PROFILE~~

In humans, the most profound effects of toluene are on the central nervous system. Acute exposure results in reversible depression of the central nervous system, neurological dysfunction, impaired performance and narcosis. Chronic exposure has been reported to result in permanent central nervous system effects such as ataxia, tremors and impaired speech, hearing and vision (ATSDR, 1989). Toluene vapors cause irritation of the upper respiratory tract, mucous membranes and eyes, and may produce cardiac arrhythmias upon chronic exposure (Anderson et aL, 1982). Reports of effects on the hematological system, liver, kidney, immune system, reproductive organs and the developing fetus are confounded by exposure to multiple solvents (ATSDR, 1989).

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

~~Toluene has been demonstrated to produce similar effects in humans and animals. The major target organ following acute or chronic exposure is the central nervous system. Signs~~

MA DEP. ORS & BWSC Documntation for the RUk AMeamtnt ShortForm Rackkntial Scenario wnion* 1.6 • & b - 10/92 B- 123 FUhbcin, L. (1985) An overview of environmental and Umoological aspects of aromatic hydrocarbon*, n. Toluene. SoL ToUl Environ. 42:267-288.

~~H^ghuvi. U, Lundbtrg. I. and Zech. L, (1980) Chromotome aberration* and titter chromatid exchanges in Swedith paint induttry worker*. Bonn. J. Environ. Health 6:291-298.~~

Hobara, T., Kobavathi, H. and Higuhihara, E. (1984) Acute effects of 1.1,1-trichloroethane, trichloroethylene and toluene on the hanatological parameter* in dog*. Arch. Environ. Contain. ToxtooL 13:589-593.

~~t£aki-Paakkan«n, J., Hu«gafv«l-Pur*iain«n, K. and K«Hi/Mn«iri PL. (1980) Toluene-expoted workers and chromosome aberration*. J, ToxtooL Environ. Health 6:775-781.~~

~~NTP. (1989) NTP tee^uy^l report on th« toxicology and carcinogen««U «tudie« of toluene (CA3 No. 108-88-3) in F344/K nttf and B6C3F, mic*. NIH Publication No. 89-2826.~~

~~ftr*K«»i/l E^ Baucoi&gw, M. and Haul, R- (1985) Chromotome changes with time in lymphocyte* after occupational exposure to toluene. Mutat. lUa. 142:37-39.~~

~~Ungvmiy, GM Tatrai. E. «"^ SMbtrtnyi, S. (1982) Effect of toluene exposure on the liver under different experimental condition*. Exp. MoL PathoL 36:347-360.~~

Ungvary, G. (1985) The possible contribution of industrial chemicals (organic tolvents) to the incidence of congenital defect* caused by (erotogenic drug* and consumer goods: An experimental study. In: Maroii, M_ «cL Prevention of phyrical and menta] congenital defecU. Part B: Epidemiology, early detecton and therapy, and environmental facton. New York: Alan R. UM, Inc. pp. 295-300.

~~MA DEP, ORS & BWSC Documntatkm for the Rick AMeM&wnt ShortForm Rendential Scenario version* 1.6 a It b - 10/92 B- 125 TRICHLOROETHYLENE~~

~~GENERAL BACKGROUND INFORMATION~~

Trichloroethylene (TCE) is widely used as an industrial solvent, particularly in metal degreasing, which consumes about 90% of TCE produced annually in the U.S. TCE is also used for dry-cleaning, as a low-temperature heat exchange fluid, as a fumigant, as a diluent in paints and adhesives, in aerospace operations, and in textile processing. Previously, TCE was used as an extractant in food-processing. These uses were discontinued in 1975 due to evidence of possible carcinogenic activity. Its earlier use in anesthetics was also discontinued (IRP, 1985).

~~PHARMACOKINETICS~~

Absorption of TCE from the gastrointestinal and respiratory tracts is extensive. TCE is extensively metabolized in humans to trichloroethanol, trichloroethanol glucuronide, and trichloroacetic acid. Although the liver is the primary site of TCE metabolism, there is evidence for extrahepatic metabolism, in the lungs and kidneys (ATSDR, 1988).

~~HUMAN TOXICOLOGICAL PROFILE~~

TCE is assumed to be responsible for the deaths of four men employed at degreasing operations using TCE as the solvent (Kleinfeld and Tabershaw, 1954). Toxicologies! analysis revealed TCE in varying concentrations in various tissues. Kleinfeld and Tabershaw (1954) reported that, despite treatment, a y»«n died 11 days after he accidentally drank an unknown quantity of TCE. TCE has been shown to affect the central nervous system. Short-term exposure to high concentrations of TCE caused dizziness, headache, nausea, confusion, facial numbness, blurred vision, and, at very high levels, unconsciousness. Longer exposures cause ataxia, decreased appetite, sleep disturbances, and trigeminal neuropathy (U.S. EPA, 1985). Information regarding hepatotoxirity in humans is limited and derived from acute overexposures. U.S. EPA (1985) has concluded that it is unlikely that chronic exposure to trichloroethylene at concentrations found or expected in ambient air would result in liver damage.

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

In laboratory animals, the acute toxicity of trichloroethylene is low. Oral LD^ values of 4920 mg/kg in the rat, 3200 mg/kg in the mouse and 2800 mg/kg in the dog have been reported. In a study by Baker (1958), several dogs died within 20 minutes of being exposed to TCE at 30,000 ppm. Rats exposed to 20,000 ppm for 5 hours died (Adams, 1951). A 2-year study

MA DEP. ORS & BWSC Documntatkm for the RUk AMaommt ShortForm Reddential Scenario vtnknu 1.6 • & b - 10/92 B- 129 F.lcotnh*. CJt, ROM, M.S. mad Pratt, I.S. (1985) Biochemical, hittological and ultrastructural changes in rat and mouse liver following the administration of trichloroethylene: Pottible relevance to tpede* difference* in hepatocardnogenicity ToxiooL AppL PharmaooL 79:365-376.

~~Gu, Z.W., 8«k, B. and Jattwrt, P. (1981) Induction d'echange* entre let chromatide* toeurt (SCE) par le trichloroethylene et te* metabolite*. ToxiooL Eur. Rt*. 3:63-67.~~

~~The Installation Restoration Program Toxicology Guide (IRP). 1985. VoL 1. Arthur D. LittU, Inc., Cambridge, MA.~~

Kjellstrand, P., Holmquist, B, Aim, P., Kaaje, M, Romare, SM JonMon. I., Uamuoo, L. end Bjerkamo, M. (1983) Trichloroethylene: Further ttudiet of the effect* on body and organ weight* and plasma butyryl cholinesterate activity in mice. Act* PharmMoL ToxiooL 53:375-384.

~~Klmn&ld, M. «nd T«b«nh«w, IJL (1954) Trichloroethene toxidty. Report of five fatal cotes. AMA: Arab. Ind. Hyf. Oooup. Mod. 10:134-141.~~

National Toxicologjr Program (NTP) (1986a) Toxicology and carcinoggne«u «tudi« of trichlorogthylcne in F344/N rati and B6C3F1 mic». NTP TR 243. National Torinolngy Program (NTP). (1986b) TrichloroethTkne: Reproduction and fertility a«<««m«nt in F344 rat« whm >^m'"'«t«r»d in the feed. Final Report. NTP-86-085.

~~Ptroooo, P. and Prodi, G. (1981) DNA damage by haloalkanes in human lymphocytes cultured in vitro. Canoer Latt. 13:213-218.~~

~~SUrmnan, AJ. and Wflliama, H. (1975) Behaviour of rat* expoted to trichloroethylene vapor*. Br. J. Ind. Mad. 32:308 315.~~

~~UJS. Enrironm«ntal Protection Agency (U.S. EPA) (1985) Health a«*emngnt document for trichloroethyl«ne. Final Report. Washington, DC. NTIS PB85-249696.~~

~~\J3. EnTironmantal Protection Agency (VS. EPA) (1987) Addendum to the health a«c««ment document for •: Update carcinogenicity aiMnnxnt for trichloroethTknc. EPA/600/8-82/006FA.~~

~~MA DEP, ORS & BWSC Documntation for the Risk Aaceatment ShortForm RMiHonfrial Scenario wtiona 1.6 a ft b - 10/92 B- 131 VINYL CHLORIDE~~

~~GENERAL BACKGROUND INFORMATION~~

About 90% of the vinyl chloride produced in the U.S. is used to manufacture polyvinyl chloride (PVC) and other vinyl polymers. The remainder is used to synthesize 1,1,1-trichloroethane. The major uses of PVC are in the building and construction industries, in consumer goods, packaging and electrical ~~wire insulation. PVC is also used in packaging, such as plasticized film, bottles and bottle-cap liners and gaskets (IRP, 1985).~~

~~PHARMACOKINETICS~~

Respiratory and gastrointestinal absorption of vinyl chloride is rapid and nearly complete. Distribution may be widespread with the highest concentration of the parent compound located in the fat Metabolism and excretion occur rapidly. The highest levels of excretory products are located in the liver and kidney (ATSDR, 1989).

~~HUMAN TOXICOLOGICAL PROFILE~~

Several epidemiologic studies have associated occupational exposure with impaired liver function and biochemical or histologies! evidence of liver damage (U.S. EPA, 1985a,b). Symptoms and signs of liver disease associated with occupational exposure to vinyl chloride include pain or discomfort, hepatomegaly, portal hypertension, thrombocytopenia, esophageal varices (Lee et al, 1977). Acute toxicity at high levels has resulted in lethality among occupationally exposed workers. Death appeared to be due to narcosis (U.S. EPA, 1985a). Acute inhalation exposure to high levels of vinyl chloride leads to CNS effects. Exposures to 8,000 to 20,000 ppm have been associated with dizziness, giddiness, euphoria, ataxia, headache, and narcosis (Nicholson et al, 1975; Lester et al., 1963). Dinceva et al (1985) reported electroencephalogram changes that they thought were indicative of early evidence of neurotoxicity in workers exposed to vinyl chloride along with other organic solvents. Vinyl chloride disease is the name given to the total Hiniral syndrome associated with occupational exposure. It includes a syndrome known as acroosteolysis or dissolution of the ends of the distal phalanges of the hands, circulatory disturbance in the extremities, Raynaud syndrome, scleroderma, hematologic effects, and lung and liver effects (ATSDR, 1989).

~~MA DEP, ORS it EWSC Documntation for tb* RUk Anxnnent ShortForm RMkUntial Scenario vvrnom 1.6 a & b - 10/92 B- 133 REFERENCES~~

~~Agency tor Toxic Subetanca* and Di*ea*e Regutry (ATSDR) (1989) Toxicological profile for vinvl chloride. US. Publk Health Service.~~

Anderaon, D., Richardson, C JL, Weight, T .M . and Adam*. W.G.( 1980) Chromosomal analyse* in vinyl chloride r*i***td worker*. Results from analysis 18 and 42 month* after an initial sampling. Mutat. Re*. 40:273-276.

~~Anderaon, D. and Richardaon, C JL ( 1981)Issues relevant to the assessment of chemically induced chromosome damage in vivo and their relationship to chemical mutagenesu. Mutat. Res. 90:261-272.~~

~~Bi, W., Wang, Y., Huang, M. and Meng, D. (1985) Effect of vinyl chloride on tesOs in rats. Eootox. Environ. Safety 10:281-289.~~

~~Dinceva, E, Kolev, P. and Dalbokova, D. (1985) EEO changes in workers exposed to long-term combined effect of a mixture of organic solvents and vinyl chloride. Khlg. Zdraveopaz. 29:8-15.~~

~~Dow Chemical Company ( 1984) Sununarr of report on LUe«pan oral carcinogenicitv rtudy of vinyl chloride in rat*.~~

~~Installation Restoration Program Toxicology Guide (TRP). 1985. Vol 1. Arthur D. Little, Tt»r. Cambridge, MA.~~

~~Lee, FX, Harry, D.S., Adam*, W.G. and Litchfiald, M. (1977) Screening for liver disease in vinyl chloride workers. Br. J. Ind. Med. 34:142-147.~~

~~Lecter, D., Gr*«nb«rg, LA. and Adanu, WJt (1963) Effects of single and repeated exposures of humans and rats to vinyl chloride. Am. Ind. Hyg. AMOO, J. 24:265-275.~~

Laib, RJ., Doag«r, G. and Boh, KM. ( 1985)Detection of If 2, N-3-cthenoguanine in liver-DNA hydrolysates of young rats and after exposure of the animals to (^C) vinyl chloride. J. Cano»r Rea, Clin. One. 109iA7.

Mahoni. C^ T^f«it.»>. G, Cfliberti, A-, Cotti, G. and Carretti. D. (1981) Cardnogenidty bioassays of vinyl chloride monomer: A model of risk assessment on an experimental basis. Environ. Health Penpeot. 41:3-29.

~~NichoUon, W J., Hammond, E.C., Saidman, H. and S^Weott, LJ. (1975) Mortality experience of a cohort of vinyl chloride- polyvinyl chloride workers. Ann. N.Y. Aoad. ScL 246:225-230.~~

~~Patty, F A, Yapt, WP. and WaiU, C J>. ( 1930) Acute response of guinea pigs to vapors of some new commercial organic compound*. V. Vinyl chloride. Pub. Health Report* 45:1963-1971.~~

~~Stytea, J.A. (1977) A method for detecting carcinogenic organic chemicals using mammalian cells in culture. Br. J. Canoer 36:658-663.~~

~~Tamburro, C.H. (1984) Relationship of vinyl monomer* and liver cancers: Angiosarcoma and hepatoccllular carcinoma. Sem. Livw Oia. 4:168-169.~~

U^. EnTironmantal Protection Agency (U.S.EPA) (1980) Ambient water quality criteria for vinyl chloride. EPA Report No. 440/5-80-078. Waahington, DC: Criteria and Standard* Divinon, Office of Water Regulation* and Standard*. PB81 117889.

~~U.S. Knirip'?f't*i*n^f 1 Protection Agfftvcr (TJ^. CPA) (19S5ft) PripJP-T1g-_y!fttgr crjtgrifl docurocnt for vinyl cfaloridg. Washington. DC: Offica of Drinking Water. NTIS PB86-1 18320.~~

~~U^. Earironmental Protection Agency (VJS. EPA) (1986b) Health and tnvironmental effect* profile for chlorrthene. Cincinnati, OH: Environmental Criteria and AMeeament Office. ECAO-CIN. P155.~~

~~Verburgt, F.G. and Vogal, E. (1977) Vinyl chloride mutagenesis in D. melanogaster. MutaL Re*. 48:327-336.~~

~~MA DEP, ORS & BWSC Documntatkm for the Riak i"miMiiiiiini ShortFonn Po»«H«titi«| Scenario reroon* 1.6 a tt b - 10/92 B- 135 XYLENES~~

~~GENERAL BACKGROUND INFORMATION~~

Xylenes are colorless liquid organic molecules with a sweet odor and a high degree of lipid solubility. There are three isomers of xylene: meta- ortho- and para-xylene (m-, o- and p-xylene, respectively). The term "total xylenes" is used to designate a mixture of the three possible isomers, in any proportions. They are commonly used as industrial solvents, as components of paints, varnishes, cleaners, degreasers and gasoline and as chemical intermediates in the manufacture of other chemicals, plastics and synthetic fibers. Xylenes are volatile molecules and therefore, evaporate quickly. They are also flammable and may pose a fire hazard if handled improperly (ATSDR, 1990).

~~PHARMACOBINETICS~~

Xylenes are readily absorbed by all routes of exposure (see section on Relative Absorption Factors). Xylenes are very soluble in blood and therefore are absorbed easily into the systemic circulation during exposure (Astrand, 1982). Following absorption, distribution occurs rapidly to all organs, including fetal tissue, with greatest distribution occuring to organs having a high lipid content, such as adipose tissue, bone marrow and brain (Astrand, 1982; Engstron and Bjurstrom, 1978; RiihiTrmki et al., 1979). In humans, xylenes are primarily metabolized by the mixed function oxidase enzyme system to methylbenzyl alcohols which are further oxidized by alcohol and aldehyde dehydrogenase to yield methyl benzole acids. The acids are readily conjugated and excreted in urine (Fishbein, 1985). In addition, a small percentage (3-6%) is exhaled unchanged due to the volatile nature of these compounds.

~~HUMAN TOXICOLOGICAL PROFILE~~

Human data suggests that the three xylene isomers all produce qualitatively similar effects, although the individual isomers are not necessarily equal in potency with regard to a given effect (ATSDR, 1990). Exposure, by any route, results in primarily central nervous system effects that may include headaches, nausea, mental confusion, narcosis, impaired learning and memory, dizziness, tremors, unconscienceness and coma, depending on dose and length of exposure. High doses may result hi death. The respiratory system may also be a target of xylene toxicity in humans, producing respiratory tract irritation, pulmonary edema and inflammation after inhalation. Ocular irritation may result following exposure to xylene vapors. Skin irritation, dryness and scaling may result following dermal exposure. Limited data are available concerning effects of exposure on the hepatic, renal, cardiovascular,

~~MA DEP. ORS It BWSC Documntatioa for th« Rick AiMtament ShortFonn Raddmtid Scenario r»r«on» 1.6 « it b - 10/92 B - 137 REFERENCES~~

~~Agency for Tack Substance* and Dice*** Regirtry (ATSDR) (1990) Toiicological profile for total irl«n«. U.S. Publk Health Service.~~

~~Actrand, I. (1982) Work load and uptake of solvents in tissues of man. In: Mehlman, MA., ed. Advance* in modern environmental toxicology. VoL 2, Priac«ton Junction, N J.: Senate Prew, pp. 141-152.~~

~~Goodie, L.W., Hill, J3L and Borzelleca, J J. (1988) Ora/toxicology studies with xylene isomen and mixed xylenes. Drug Chem. TmdooL 11:329-364.~~

~~Elovaara, E. (1982) .Date-related effects of m-xylene inhalation on the xenobiotic metabolism of the rat. XenobloUoa 12:345-352.~~

~~Eloraara, E., ColUn, Y. and PfafOi, P. (1980) The combined tenacity of technical grade xylene and ethanol in the rat. Xanobiotioa 10.436-445.~~

~~Engstrom, J. and Bjuntrom, R- (1978) Exposure to xylene and ethylbenzene. n. Concentration in subcutaneous adipose tissue. Soand. J. Work EnTiroo. Health 4:195-203.~~

~~FUhbcin, L. (1985) An overview of the environmental and toxicological aspects of aromatic hydrocarbons: m. Xylene. SoL Total EnYiron. 43:166-183.~~

~~Marka, TA^ I^admiz, TA. and Moor*. JA. (1982) Teratogenicity of a commercial xylene mixture in the mouse. J. ToxiooL Environ. Health 9:97-105.~~

~~Morrai, V, Hudak, A. and Ungvary, G. (1976) ECO changes in benxene, toluene and xylene poisoned rats. Aota. M«d. Aoad. Set Hunf. 33:275-286.~~

~~Morvai, V^ Ungvmry, G. and Hemnann, HJ. ( 1987) Effects of quantitative undernourishment, ethanol and xylene on coronary microvessels of rats. Aota MorphoL Hung. 35:199-206.~~

^ pfaffli, P. and Savolain«n. K. (1979) Kinrt"* of m-xylene in man: General features of absorption, distribution, biotransformation and excretion in repetitive inhalation exposure. Soand. J. Work Environ. Health 5:217 231.

~~Toftgard, R. and N3a«n, O.G. (1982) Effects of xylene and xylene isomers on cytochrome P-460 and in vitro enzymatic activities in rat liver, kidney and lung. Tmdoolofy 23:197-212.~~

~~Ungvaiy, G^ Tatrai, E^ Hudak, A. ( 1980) Studies on the embryotoxic effects ofortho-, meta- and para-xylene. Toxicology 18:61-74.~~

~~MA DEP. ORS & BWSC Documntation for the Rick AMeaonent ShortForm Residential Scenario venion* 1.6 a & b - 10/92 B- 139 2,4-DICHLOROPHENOL~~

Summary 2,4-Dichlorophenol (2,4-DCP) is not very persistent in the environment. There is equivocal evidence suggesting that it may act as a tumor promoter. Subcutaneous administration of 2,4-di cnlorophenol to pregnant mice induced minor teratogenic effects. Chronic exposure caused nonspecific liver changes in mice.

~~CAS Number: 120-83-2 Chemical Formula: CgH^CljOH IUPAC Name: 2,4-Dichlorophenol Important Synonyms and Trade Names: 2,4-DCP~~

Chemical and Physical Properties Molecular Weight: 163.0 Boiling.Point: 210«C Melting Point: 45«C Specific Gravity: 1.383 at 25«C Solubility in Water: 4,500 mg/liter Solubility in Organicst Soluble in benzene, alcohol, ether, and chloroform Log Octanol/Water Partition Coefficient: 2.75 Vapor Pressure: 0.12 mm Hg at 20*C (calculated) Vapor Density: 5.62 pKa: 7.48 v Flash Point: 114«C

2,4-Oichlorophenol Page 1 October 1985 O Toxicity to Wildlife and Domestic Animals Special mean acute values reported for the freshwater species Daphnia magna, fathead minnow, and bluegill are 2,605, 8,230, and 2,020 yg/liter, respectively. A chronic value of 365 ng/liter and an acute-chronic ratio of 23 are reported for the fathead minnow. The only Information available con cerning saltwater species indicates that the mountain bass Kuhlia sandvicensis exhibits a moderate reaction in response to 20 rag/liter 2,4-DCP. Complete destruction of chlorophyll and 56.4% reduction of photosynthetic oxygen production are observed after exposure of the freshwater alga Chlorella py renoidosa to 100 and 50 mg/liter, respectively. The weighted average bioconcentration factor for 2,4-DCP and the edible portion of all freshwater and estuarine organisms consumed by Americans is calculated to be 40.7. 2,4-DCP residues have been detected in the liver and kidneys of cattle and chickens, and in chicken eggs. Concentrations of 2,4-DCP in aninaal tissues are reported to diminish rapidly after withdrawal of the 2,4-DCP precursor, 2,4-dichlorophenoxy acetic acid (2,4-D). No information concerning toxicity of 2,4-DCP to domestic animals is available.

Regulations and Standards Ambient Water Quality Criteria (USEPA): Aquatic Life The available data are not adequate for establishing criteria. Human Health Health criterion: 3.09 mg/liter Organoleptic criterion: 0.3

REFERENCES NATIONAL INSTITUTE POR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1984. Registry of Toxic Effects of Chemical Substances. Data Base. Washington, D.C. January 1984 SAX, N.I. 1975. Dangerous Properties of Industrial Materials. 4th ed. Van Nostrand Reinhold Co., New York. 1,258 pages U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1979. Water- Related Environmental Fate of 129 Priority Pollutants. Washington, D.C. December 1979. EPA 440/4-79-029

~~2,4-Dichlorophenol Page 3 October 1985 4-METHYLPHENOL~~

I. CHEMICAL AND PHYSICAL INFORMATION A. Synonyms: p-cresol; l-hydroxy-4-methylbenzene; 4-hydroxytoluene B. GAS No. : 106-44-5 C. Molecular Formula: C7HsO D. Molecular Weight: 108.13 E. Chemical and physical properties: 1. Physical State; Crystalline solid 2. Odor/Odor Threshold; Phenolic; sweet and tarry; 0.0005 ppm 3. Melting point: 34.8'C 4. Boiling point: 201.9'C at 760 mmHg 5. Vapor pressure: 0.13 mmHg at 25°C 6. Specific gravity; 7. Vapor density; 3.72 8. Refractive index: 9. Solubility in water: 22.6 g/1 at 40°C 10. Solubility in organic solvents: 11. Log octanol/water partition coefficient: 1.94 12. Henry's Law Constant;9.6 x 10~7 atm-m3/mol. F. Uses:

II. TRANSPORT AND FATE When released to the atmosphere, 4-methylphenol will react with photochemically produced hydroxyl radicals during the day (half life of 10 hours) and react with nitrate radicals at night (half life of 4 minutes). It will also be scavenged by rain and oxidized by metal cations in rain water and fogwater. Biodegradation is expected to be the dominant loss mechanism when 4-methylphenol is released into water. Volatilization, bioconcentration in fish, and adsorption to sediment will be unimportant and photolysis is only expected to be significant in surface waters of oligiotrophic lakes. III. TOXICITY A. Human: Toxic properties from short-term exposure of 4-methylphonal are similar to those of phenol. 4-methylphenol may be absorbed through the skin and this is a major route of exposure. Contact with skin may cause inflammation, blistering and scarring. Respiratory hazard is low because of its low volatility. However, exposure to high vapor concentrations may cause irritation to the respiratory tract. Ingestion has caused pneumonia, irritation, kidney and nervous system damage. BENZO[a]ANTHRACENE

~~GENERAL BACKGROUND INFORMATION~~

Benzo[a]anthracene (BaA) is a member of the polycyclic aromatic hydrocarbons (PAH). PAHs are a class of non-polar compounds that contain two or more aromatic rings. They are ubiquitous in nature and are both naturally occurring and man-made. The overall database for benzo[a]anthracene is limited. Human exposures to BaA can come from the oral, inhalation or dermal routes. BaA is produced when gasoline or other organic material is burned. It is also found in cigarette smoke and cooked food. People most at risk from exposure to BaA are those in the coal tar and asphalt production industries, cooking plants, coal gasification plants, smoke houses and industrial plants that burn wood, trash, coal or oil.

~~PHARMACOKINETICS~~

BaA is absorbed by the dermal and oral routes. There is no information on absorption by inhalation. Biotransformation to reactive intermediates is necessary for toxitity (ATSDR, 1990). BaA accumulates in adipose tissue. The metabolism of BaA is similar to the metabolism of benzo[a]pyrene (Cooper et aL, 1983). In brief, the aromatic ring is oxidized by arene oxides to form reactive intermediates. The reactive intermediates are subsequently hydrolyzed to diols (Suns and Grover, 1974). The diols are conjugated with glutathione and excreted.

~~HUMAN TOXICOLOGICAL PROFILE~~

~~There are no reports directly correlating human exposure to BaA with the development of excess tumors.~~

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

The only toxitity endpoint that has been adequately studied for BaA is dermal carcinogenicity. There is some evidence that benz[a]anthracene is carcinogenic in laboratory by the oral route (Klein, 1963; Bock and King, 1959) and also by subcutaneous injection (IARC, 1973). BaA has been shown to cause skin tumors after dermal application (Bingham and Falk, 1969). Tumorigenicity of the diol epoxide metabolite has been shown (Levin et aL, 1978) as well as the mutagenirity of the diol epoxide (Wood et aL, 1977).

~~MA DEP. ORS & BWSC Documntation for UM Rick Aiiimmiint ShortForm Residential Scenario v*nion« 1.6 • & b - 10/92 B- 15 BENZO[a]PYRENE~~

~~GENERAL BACKGROUND INFORMATION~~

Benzo[a]pyrene (BaP) is a member of the class of compounds generally referred to as polyaromatic hydrocarbons (PAH). PAHs contain two or more aromatic rings. They are ubiquitous in nature and are both naturally occurring and man-made. BaP is a component of fossil fuels and is produced from the incomplete combustion of organic compounds. BaP and other PAHs are found in coal tar, creosote oils and pitches formed from the distillation of coal tars (ATSDR, 1990).

~~PHARMACOKINETICS~~

BaP is readily absorbed by dermal, inhalation and oral routes (see section on Relative Absorption Factors). Distribution of BaP is rapid among several tissues. Following inhalation exposure to *H labeled BaP, ma-rimnm levels of radioactivity were found in the liver, esophagus, small intestine and blood after 30 minutes. After 12 hours, TTMTJTTIIITTI levels were found in the cecum, stomach and large intestine (Sun et aL, 1982). This and other studies provide evidence for the enterohepatic circulation of BaP metabolites.

Mammalian metabolism of BaP follows the mechanism established for smaller aromatic compounds (Williams, 1959). There is an initial oxidation of a double bond on one of the rings to an arene oxide. The oxide is then hydrolyzed to the dioL Oxidations may occur at multiple sites on the BaP molecule. Phase n metabolism is considered the detoxication pathway and involves the conjugation of the activated Phase I metabolites with easily eliminated substrates such as glutathione, glucuronide or sulfate (Cooper et aL, 1983). In addition to being conjugated, the diol intermediate can undergo (1) further oxidation to several uncharacterized metabolites via the P-450 monooxygenase system, (2) spontaneous rearrangement to the phenol or (3) hydration to the trans-diols through a reaction catalyzed by epoxide hydrolase (Cooper et aL, 1983). BaP 7,8-diol-9,10-epoxide has been established as an ultimate carcinogen (ATSDR, 1990). The primary route of excretion of BaP is through the feces. BaP undergoes first-pass metabolism and is reabsorbed via enterohepatic circulation (Chipman et aL, 1982). Rats exposed by gavage to "C labeled BaP in peanut oil excreted up to 85% in the feces. Excretion in the urine was 1 to 3% of the administered dose (Hecht et aL, 1979).

~~MA DEP. ORS & BWSC Documnution for the Ri«k AcMMsnant SbortForm Rtddrotud Scenario wrrion* 1.6 a ti b - 10/92 B- 17 REFERENCES~~

~~Agencj tor Toxic Subetancea and Diaeaaa Registry (ATSDR) ( 1990) Toxicological profile for benzoCahnrrene. U. S. Public Health Service.~~

Chspman, J5L, Hirom, P.C, Front, G£. tad Milbura, 8. ( 1982) Bento(a)pyrene metabolism and enterohepatic circulation in the rat. In: Snyder, R. et al ed*. Biological Reactive Intermediate* P. Chemical Mechanism* and Biological Effect*. Pan A. Plenum Preac. New York, ppe. 761-768. Chu, E.W. and Malmgren, RA. (1965) An inhibitory effect of vitamin A on the induction of tumor* in the forettomach and cervix in the Syrian hamtter by carcinogenic polyeydic hydrocarbons. Canoer Re*. 25: 884-895.

Cooper, C.S., Grow, Pi. and Sim*. P. (1983) The metabolism and activation of benzo(a)pyrene. In: Bridge*, J.W., Chaae, LJ. tat, Progreee in drug metabolinn. VoL 7. John Wiley and Sona, N»w York. ppa. 295-395.

~~Davidaon, GX. and Daw*on, G.W J>. ( 1976) Chemically induced presumed somatic mutation* in the mouse. Mutat. Ra*. 38:151-154.~~

~~Dairidaon, G£. and Dawaon, G.WJ. (19TT) Induction of somatic mutations in mouse embryo* by benzo(a)pyrene. Aroh. T~~

~~Hacht, 8^^ Grabowmki. W. and Groth, K. (1979) Analysis of faeces for BaP after consumption of charcoal-broiled beef by rat* and human*. Food CoameC ToxtaoL 17223-227.~~

~~Huggina, C. and Yang, N.C. (1962) Induction and extinction of mammary cancer. Soi«noe 137:257-262.~~

~~International Agvncy for B-rrtr-h on Canoar (IARC) (1983) IARC monograph on the evaluation of carcinogenic riik of cKg**'"**^ to tnan. Vol 32 IARC, L^on, Franca.~~

~~Me Cormick, D. at aL (1981) Inhibition of bento(a)pyrene induced mammary cardnogenesis by retinyl acetate. J. NatL Cancer Inat. 66:559-564.~~

~~Naal, J. and Rigdon, RH. ( 1967) Oastic tumor* in mice fed bento(a)pyrene: A quantitative study. T«x. Rep. BloL Med. 25:553-657.~~

~~Sandara, CX, Skinner. C. and Gvlman, RJL (1986) Percutaneous absorption of 7.10 ^C-benzo(a)pyrene and 7,12 ^C dimethylbenz(a)oj\ihracene in mice. JEPTO 2^25-34.~~

~~Sparnina, VJ^, Mott, A.W^ Baraney, G. and Wattanberg. G. (1986) Effects ofaUyl methyl tritulfide on glutathione-* trantferatf activity. Nutr. Canoar 8:211-215.~~

Sun, JD-, Wolff, R.K^ and EanapiUy, Gil., (1982) Deposition, retention and biological fate of inhaled pure bento(a)pyrene adsorbed onto ultraflne particles; and a* a pure aerosol. TojdooU AppL PbarmaooL 65:231-244.

Wattanberg, L.W. and Bueding, E. (19&6) Inhibitory effects of6-(2-pyrazonyl>-4-methyl-13-dUhiol-3-thione (Oltiprat) on cardnogenetis induced by bento(a)pyrme, diethylnitrosomine, and uracil mustard. Carcinogen«aia 7:1379-1381.

~~WatUnberg, L.W. and Laong, J J* (1970) Inhibition of the carcinogenic action ofbento(a)pyrene by flavones. Canoer Rea. 30:1922-1925.~~

~~WQliana, R.T. (1959) Detaacication MechanUnu. 2nd ed. Chapman and Hall, London.~~

~~MA DEP, ORS & BWSC Documntation for tha Riak Aaaeaanent ShortFonn Rtnifirntiil Scenario 1.6 a tc b - 10/92 B- 19 BENZO[b]FLUORANTHENE~~

~~GENERAL BACKGROUND INFORMATION~~

Benzo[b]fluoranthene (BbF) is a member of the class of compounds referred to as polycydic aromatic hydrocarbons (PAHs). PAHs contain two or more aromatic rings. PAHs are ubiquitous in nature and are both naturally occurring and man-made. Exposure to BbF can come from air, water, or soil. As a PAH, BbF is present in the emissions from industrial plants that produce coal tar, cooking plants, asphalt production plants, and home heating with wood and coal. BbF is also present in charcoal-broiled foods and cigarette smoke (ATSDR, 1990).

~~PHARMACOKINETICS~~

No data on the absorption, distribution or excretion of BbF were identified. BbF is metabolized under in vitro incubation conditions to phenol and dihydrodiol metabolites (Amin et al, 1982). The general metabolic pathways elucidated for benzo(a)pyrene are also active on BbF (Cooper et aL, 1983; Levin et al., 1982; Grover et al., 1986). The reactive metabolites associated with the tumorigenic effects of BbF may not be the diol epoxides (Amin et aL, 1982; Amin et aL, 1985). As for the other PAHs, the material excreted is expected to consist primarily of dihydrodiol and phenol conjugates (Grover et al., 1986).

~~HUMAN TOXICOLOGICAL PROFILE~~

The database for human toxicity is very limited. There are no studies correlating exposure to BbF and cancer or systemic toxicity. The only data implicating BbF as a carcinogen come from carcinogenicity studies using a mixture of PAHs.

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

The database on the toxicity of BbF is limited. Intratracheal administration of BbF to rats resulted in an increase in respiratory tract tumors (Deutsch-Wenzel et al, 1983). BbF has caused skin tumors in mice following dermal application (Wynder and Hoffman, 1959). The skin tumor initiating ability of BbF has been demonstrated in mice using a standard initiation/promotion protocol with either croton oil or phorbol myristate acetate as a tumor promoter (Amin et al., 1985; LaVoie et al., 1979, 1982).

~~MA DEP. ORS Jc BWSC Documntation for th« Ri*k AiMMnMnt ShortForm P^Htn*'*1 Scenario 1.6 • ft b - 10/92 B-21 BENZO[g,h,i]PERYLENE~~

~~GENERAL BACKGROUND INFORMATION~~

Benzo[g,hti]perylene is a member of the polyaromatic hydrocarbons (PAH). PAHs constitute a class of non-polar compounds that contain two or more aromatic rings. They are ubiquitous in nature and are both naturally occurring and man-made. The data regarding benzo[g,h,i]perylene are limited. As a PAH, it is found in food (charcoal broiled meats), vegetables, tobacco smoke and soot (U.S. EPA, 1980). Exposure occurs by inhalation, ingestion and by dermal contact

~~PHARMACOKINETICS~~

~~No data were found regarding the pharmacokinetics of benzo[g,h,i]perylene.~~

~~HUMAN TOXICOLOGICAL PROFILE~~

~~No data were found regarding the human toxicology of benzo[g,h,i]perylene.~~

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

~~No data were found regarding the mnmtnalifln toxicity of benzo[g,h,i]perylene.~~

~~GENOTOXICrrY~~

~~No data were found regarding the genotoxicity of benzo[g,h,i]perylene.~~

~~REFERENCES~~

~~U.S. Environment*] Protection Agency (U.S. EPA). (1980) An exposure riik a««e««inent of polycyclic aromatic hydrocarbon* fb*nio~~

~~MA DEP. ORS & BWSC Documntatkra for to* Ri*k AiMannent ShortFonu Evidential Scenario vwnon* 1.6 a & b . 10/92 B-23 BIS(2-ETHYLHEXYL)PHTHAIATE~~

~~GENERAL BACKGROUND INFORMATION~~

Bis(2-ethylhexyl)phthalate, often referred to as Di(2-ethylhexyl)phthalate (DEHP), exists as a colorless, oily liquid at room temperature. It is used industrially as a plasticizer for resins, to make plastic materials more flexible. DEHP is contained in many plastic products such as imitation leather, rainwear, footwear and toys. It is used in the manufacture of tubing and containers used for blood transfusions and kidney dialysis. DEHP is also used in the manufacture of organic pump fluids in electrical capacitors. DEHP may migrate into the environment under improper use/disposal conditions. As a result, exposure could occur via air, water and food. Patients receiving blood transfusions or kidney dialysis can also be exposed to DEHP (ATSDR, 1989; Sittig, 1981).

~~PHARMACOKINETICS~~

DEHP is readily absorbed through ingestion and inhalation and poorly absorbed through the skin (see section on Relative Absorption Factors). DEHP is largely metabolized prior to intestinal absorption, via hydrolysis, to its corresponding monoester metabolite (MEHP), with the release of 2-ethylhexanol. Once absorbed, DEHP and its metabolites are distributed throughout the body, with most of the compounds initially going to the liver. In general, DEHP and its metabolites are converted to more polar derivatives and are then excreted. DEHP is rapidly cleared from the body, with little potential for accumulation. There are differences in the way DEHP is metabolized among species. Although phase I reactions are essentially the same across species except for quantitative differences, phase n reactions differ among species as to the ability to glucuronidate DEHP and its metabolites. The relationship between pharmacokinetics and toxicity is not known due to gaps in knowledge regarding mechanisms of toxic action (ATSDR, 1989).

~~HUMAN TOXICOLOGICAL PROFILE~~

Acute toxicity from DEHP is relatively low by both inhalation and ingestion. A 1-hr exposure to 23,670 mg/ms DEHP did not result in any deaths. The oral LD50 for DEHP ranges from 26,000 to 49,000 mg/kg (ATSDR, 1989). Exposure to DEHP has produced irritation of the eyes, and mucous membranes, nausea and diarrhea (Sittig, 1981). Liver biopsies from dialysis patients showed liver abnormalities (peroxisome proliferation) (ATSDR, 1989). Most of the toxicity data for DEHP originate from animal studies.

~~MA DEP. ORS & BWSC Documnution for the RUk AM*«m*nt ShortForm RMidantud Scenario vwnioo* 1.6 • It b - 10/92 B-27 CHRYSENE~~

~~GENERAL BACKGROUND INFORMATION~~

Chrysene is one of the polycydic aromatic hydrocarbon (PAH) compounds which are formed during the combustion of organic material. Chrysene often exists in particulate form, adsorbing to existing particulate material in air. Human exposure can occur in the workplace (coal and asphalt production plants, cooking plants, smoke houses) or in the environment due to chrysene contamination of air, food, soil and water (ATSDR, 1990).

~~PHARMACOKINETICS~~

Chrysene can be absorbed by all routes of exposure (see section on Relative Absorption Factors). Its absorption is believed to be qualitatively similar to benzo[a]pyrene (ATSDR, 1990). Following absorption, chrysene distributes to all organs, reaching the highest concentration in tissues with large fat content (adipose tissue, mammary tissue, brain) (Modica et aL, 1983). Chrysene undergoes metabolic biotransformation mediated by the mixed function oxidase enzyme system to form reactive intermediates hypothesized to be responsible for its toxicity. The major metabolites include trans-dihydrodiols, phenols, diol epoxides and triol epoxides (Thakker et aL, 1985). The reactive metabolites are conjugated and excreted primarily in feces (Schlede et aL, 1970).

~~HUMAN TOXICOLOGICAL PROFILE~~

There is no information available on threshold toxic effects of chrysene in humans. Since it is structurally similar to benzo[a]pyrene, it would be expected to produce effects similar to B[a]P following acute or chronic exposure (see Toxicity Profile on Benzo[a]pyrene).

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

There is no information available on threshold toxic effects of chrysene in animals. Since it is structurally «imilflr to benzo[a]pyrene, it would be expected to produce effects similar to B[a]P following acute or chronic exposure (see Toxicity Profile for Benzo[a]pyrene).

~~MA DEP, ORS & BWSC Documntmtion for the Rick Aueument ShortForm RaricUntial Scenario veraion* 1.6 • It b - 10/92 B-47 DI-N-BUTYL PHTHALATE~~

SUMMARY Dibutyl phthalate is used extensively as a plasticizer, as a solvent in the lacquer industry and as an insect repellent on clothing. Industrially, the material has proven relatively innocuous except for cases of accidental human ingestion where symptoms have been reported. CAS Number: 84-74-2 Chemical Formula: C6-H22~°4 Important Synonyms and Trade Names: DBF; Phthalic Acid, Dibutyl Ester; O-Benzene dicarboxylic Acid.

CHEMICAL AND PHYSICAL PROPERTIES Molecular Weight: 278.4 Boiling Point: 644'F (340'C) Melting Point: -31°F (-35°C) Specific Gravity: 1.0 Solubility in Water: 13 mg/1 Solubility in Solvents: Alcohol, Ether, Benzene Log Octanol/Water Partition Coefficient: 5.60 Vapor Pressure: l.OOE-05 mm Hg at 20* to 30*C Flash Point: 315°F (157*C)

TRANSPORT AND FATE --- •-- Very little specific information on the fate and transport of di n-butyl phthalate is available. The fate of this compound is to a large extent inferred from data for phthalate esters as a group (see bis(2-ethylhexyl) phthalate).

HEALTH EFFECTS Delayed symptoms resulting from ingestion include nausea, vomiting, and dizziness, followed later by headache, pain, and irritation in the eyes, lacrimation, photophobia, and conjunctivitis. Slight, temporary renal effects may also occur. Animal experiments have shown that the material has generally low acute and chronic toxicity.

~~TOXICITY TO WILDLIFE AND DOMESTIC ANIMALS See bis(2-ethylhexyl) phthalate NAPHTHALENE~~

~~GENERAL BACKGROUND INFORMATION~~

Naphthalene is a white solid substance at room temperature. It has a distinct odor of mothballs or tar. Humidity and sunshine cause evaporation into the air within a few hours. When placed in water or soil, bacteria will destroy naphthalene, or will render it airborne within a few hours (ATSDR, 1990). Tobacco smoke is known to release 3 ug of naphthalene per cigarette (U.S. EPA, 1982). The compound is used in the production of dyes, solvents, lubricants, motor fuels (U.S. EPA, 1980) and is a major component of many moth ball preparations.

~~PHARMACOKINETICS~~

Humans can absorb naphthalene by dermal, inhalation and oral routes (see section on Relative Absorption Factors). Metabolism occurs via the P450 mixed function oxidase enzyme system to yield multiple intermediates which are then conjugated. Key metabolites are responsible for each toxicity endpoint following intraperitoneal administration: 2 naphthoquinones —> hemolysis; 1,2-naphthoquinones —> cataracts; 3-GSH adducts —> pulmonary toxicity (Buckpitt et al., 1984). Excretion of metabolites occurs via urine and feces (ATSDR, 1990).

~~HUMAN TOXICOLOGICAL PROFELE~~

Adults and children exposed to airborne naphthalene experience vomiting, abdominal pain and anemia (ATSDR, 1990). Most of the data is for inhalation of naphthalene from mothballs. The primary site of toxicity is the erythrocyte resulting in hemolytic crisis (hemolytic anemia). Jaundice is seen upon dermal, inhalation, and oral exposures, as are kidney effects (ATSDR, 1990). Near-blindness resulted in male and female subjects with 5 gram ingestion (ATSDR, 1990).

~~MAMMALIAN TOXICOLOGY PROFILE~~

~~Oral doses in rats have hepatic effects. Dogs (1800 mg/kg) for 5 days of exposure showed signs of lethargy and ataxia, and decreased hemoglobin levels (ATSDR, 1990)~~

~~GENOTOXICITY~~

~~No studies of genotoxic effects in Humans or laboratory animals were located. No human epidemiological evidence for cancer.~~

~~MA DEP. ORS & BWSC Documntation for the Rkk Aite*tmant ShortFonn Residential Scenario wrrioni 1.6 • & b - 10/92 B -97 PHENANTHRENE~~

~~GENERAL BACKGROUND INFORMATION~~

Phenanthrene is a member of the polyaromatic hydrocarbons (PAH). PAHs constitute a class of non-polar compounds that contain two or more aromatic rings. They are ubiquitous in nature and are both naturally occurring and man-made. The database on the potential health effects of phenanthrene is limited.

~~PHARMACOKINETICS~~

Little data are available regarding the pharmacokinetics of phenanthrene. The intestinal absorption of phenanthrene is less dependent on the presence of bile in the stomach than is the absorption of the larger PAHs (such as benzo(a)pyrene) (Rahman et al, 1986).

~~HUMAN TOXICOLOGICAL PROFILE~~

~~Phenanthrene has been shown to be a «kin photosensitizer in humans (Sax, 1934).~~

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

~~Phenanthrene has a reported LD 50 of 700 mg/kg in mice (Simmon et al., 1979). Rats injected intraperitoneally evidenced liver effects (Yoshikawa et al, 1987).~~

There is equivocal evidence for cancer from dermal application of phenanthrene in rats (IARC, 1983). Phenanthrene is not a complete skin carcinogen (ATSDR, 1990). It is neither an initiator (LaVoie et al, 1981; Roe, 1962) nor a promoter (Roe and Grant, 1964). Higgins and Yang (1962) reported no tumor production within two months after the ingestion of 200 mg of phenanthrene by rats.

~~GENOTOXICnT~~

~~There are limited data that suggest that phenanthrene is mutagenic (Wood et al., 1979). However, the majority of tests are negative (ATSDR, 1990).~~

~~MA DEP. ORS & BWSC DociuxmtJition for tH* Risk AMiutmfint ShorlFonn R^ vwr»ion« 1.6 • & b - 10/92 B- 101 POLYCHLORINATED BIPHENYLS (PCBs)~~

~~GENERAL BACKGROUND INFORMATION~~

The thermal stability, nonflammobility, and dielectric capability of PCBs resulted in their use in electrical capacitors and transformers (NIOSH, 1986). The manufacturing, processing, distribution in commerce, and use of PCBs after January 1, 1978 was prohibited under Section 6(e) of the Toxic Substances Control Act PCBs can be released to the environment during fires involving electrical equipment containing these compounds. PCBs are strongly adsorbed on solid surfaces, including glass and metal surfaces in laboratory apparatus, and onto soils, sediments, and particulates in the environment.

~~PHARMACOKINETICS~~

Gastrointestinal absorption of most PCB isomers is large. PCBs can also be absorbed by the inhalation and dermal routes but limited data are available (see section on Relative Absorption Factors). Distribution of PCBs follows a biphasic pattern. Initially, PCBs distribute to liver and muscle tissue. They are then redistributed to the fat, skin, and other fat-containing organs (ATSDR, 1989). PCBs are poorly metabolized in humans with major metabolites being 3- or 4-hydroxy compounds. Metabolism may proceed through formation of arene oxide intermediates (UJS. EPA, 1988). The slow metabolism of PCB congeners to more polar compounds is responsible for long biological half-lives of PCBs. Excretion occurs primarily through the feces (Goto et at, 1974).

~~HUMAN TOXICOLOGICAL PROFILE~~

Dermatologic signs are the most persistent indicator of PCB toxitity. Skin manifestations have been observed also in newborn infants of mothers exposed to high levels of PCBs and related compounds. Cases of severe chloracne were reported in a work environment in which PCB air levels were found to be between 6.2 and 6.8 rng/m*. The workers developing chloracne had been exposed for 2 to 4 years. Other analyses revealed worker complaints of dry sore throat, akin rash, gastrointestinal disturbances, eye irritation, and headache at work area concentrations of 0.013 to 0.16 mg PCB/m3. Higher blood PCB levels are associated with higher serum triglyceride and/or cholesterol levels, as well as high blood pressure. Air PCB concentrations as low as 0.1 mg/m3 can produce toxic effects, and exposure to levels producing no overt toxicity can affect liver function. Recovery after termination of exposure occurs but is slow and depends upon the amount of PCBs stored in adipose tissue (Clayton and Clayton, 1981). Human exposures to PCBs resulting in toxic effects have almost all resulted from the ingestion of rice oil contaminated with "Kanechlor 400" in Japan (resulting in Yusho or rice oil disease) or from industrial exposure. Clinical symptoms of poisoning

MA DEP, ORS & BWSC Don limitation for the Rick AueMment ShortForm RMidential Scenario rei-non* 1.6 a & b - 10/92 B- 105 Immunological effects (decreased IgM, IgG induction) were noted in monkeys following a 27 month exposure at a dose of 0.005 mg/kg/day (Tryphonos et al., 1989).

~~GENOTOXICITY~~

Most genotoxicity assays of PCBs have been negative. The majority of microbial assays of PCB mixtures and various congeners show no evidence of mutagenic effects (U.S. EPA, 1980). The carcinogenic effects of PCBs have been studied in rats and mice. In a study conducted by Kimbrough et al. (1975) rats were exposed via the diet to 100 ppm Aroclor 1260 for 21 months. Hepatocellular carcinomas were observed in 26 of the 184 treated rats but only in one of the 173 controls. Neoplastic nodules were not found in controls but occurred in 144/184 of treated rats. The National Cancer Institute (NCI, 1978) reported a high incidence of hepatocellular proliferative lesions in male and female Fischer 344 rats fed three dose levels of Aroclor 1254 for 104-105 weeks, but, in part due to the small number of flnimnla tested, carcrnogenicity was not statistically demonstrable. Norback and Weltman (1985) fed a diet containing relatively high concentrations Aroclor 1260 (100 ppm for 16 months followed by 50 ppm for an additional 8 months) to Sprague-Dawley rats. In the PCB-exposed group, neoplastic nodules were observed at 12 months followed by trabecular carcinoma at 15 months and adenocarcinoma at 24 months (52/93). In the control rats, the incidence of hepatocellular neoplasms was low (1/81). Metastases to distant organs was not observed and mortality in the PCB exposed unimfllH was not increased. The incidence of these slow-growing hepatocellular neoplasms was strikingly higher in female rats than in male rats.

PCBs (Clophen C) have also been shown to be cocartinogenic. When PCBs were mixed with diethylnitrosamine (DENA), twice as many tumors were observed as were observed in treated with DENA alone (Brunn, 1987).

Based on the positive evidence for carcinogenicity of Aroclor 1254, Aroclor 1260, Kaneclor 500, and Clophen A-30 and A-60 in ^nitnalg, along with adequate evidence in humans, the U.S. EPA has placed these PCBs in categroy B2 - probable human carcinogen (U.S. EPA, 1988).

MA DEP, ORS t. BWSC DocumntAtion for the RUk AjfTttmtnt ShortForm R-r*Hintinl Scenario v«rnona 1.6 • i b- 10/92 B- 107 Ovmnann. SSL, Kottaj, J., Wibon, LJL, Shain, W. end Biuh, B. (1987) Neuroochavioral and somatic effects of perinatal PCB exposure in rats. Environ. Roc. 44:66-70.

Tr/phono*. U, CharbonoMU, S., Tryphonaj, H., Zawidzka, Z., MM, J., Wong, M. and Arnold, D.L. (1986a) Comparative aspects of Arocior 1254 laxtdty in adult cynomoigus and Rhesus monkeys: A pilot study. Arch. Environ. Contain. ToriooL 15:169-169.

~~Tryphono*. L, Arnold, DXu, Zawidrka, Z., MM, J^ Charbonnaau, S. and Wong, J. (1986b) Apilot study on adult Rhesus monkey* (M. mulatto) treated with Ancior 1254 for two yean. ToxiooL PathoL 14:1-10.~~

~~TiTphono*, L., at al (1989) Immunotaxidty Studies of PCB (Arochlor 1264) in the Adult Rhesus (Macca mulatto) Monkey - Preliminary Report. Int. J. ImmunopnarnukooL 11:199-206.~~

~~UJS. Environmantal Protection Agency (UJ. EPA) (1980) Ambient water quality criteria for polvchlorinatcd biphenyli. EPA-440/6-80-068. OOie* of Wat«r Regulation* and Standarda, Waahington, DC.~~

~~U.S. EnvironmAntal Protection Agency (U.S. EPA) (1988) Drinking water criteria document for polychlorinat«d biohenTU (PCB«). EACO-CIK-414.~~

~~MA DEP. ORS & BWSC DocumaUtion for the Rick rtiaoiitiuint ShortFonn R«*v<«"ti''l Scenario vernon* 1.6 a ti b - 10/92 B- 109 ALDRIN/DIELDRIN~~

Sumaary Aldrtw degrades to dieldrin, which is very persistent in the €nrironp«nt. Both pesticides are carcinogenic in rats and mice and arc teratogenic and reproductive toxicants. Aldrin and dieldrin cause liver toxicity and central nervous system abnormalities fallowing chronic exposure. Both are also acutely toxic*- with oral LD-0 values of about 50 mg/kg. Both pesticides are very toxic to aquatic organisms and have been associated with large-scale kills of terrestrial wildlife in treated areas.

Background Information Dieldrin is the 6,7-epoxide of aldrin and is readily ob tained from aldrin under normal environmental conditions and by metabolism in animals. CAS Numberi Aldrint 309-00-2 Dieldrint 60-57-1 Chemical Formula* Aldrint < Dieldrint ** p a IUPAC Naaet Aldrint 1,2,3,4,10,10-hexachloro-l,4,4a,5,8,8a hexahydro-1,413,8-exo-dimethanonaphthalene Dieldrint l,2,3,4,10,10-hexachloro-6,7-epoxy l,4,4a,5,6,7,8,8»-octahydro-endo,exo-l,4»5,8-di metnajionaphthalene

~~Chemical asrf TfaCTJcal properties Molecular tm^hts Aldrint 365 Dieldrint 381 Melting Pointt Aldrint 104MC Dieldrint 176«C~~

Aldrin/Dieldrln Page 1 October 1985 webbed foot, and skeletal anomalies. Chronic effects attributed to aldrin and dieldcin include liver toxicity and central nervous system abnormalities. Both chemicals are acutely toxic; the oral LDcft is around SO mg/kg, and the dermal LD,rt ij about 100 mg/*gV 50

Toxicity to Wildlife and Domestic Animals Aldrin and dieldrin are both acutely toxic to freshwater species at low concentrations. Tests in fish showed that the two chemicals had similar toxicities, with LCen values ranging from 1 to 46 pg/liter for different species. Final acute values for freshwater species were determined to be 2.5 wg/liter for dieldrin and 3.0 pg/liter foe aldrin. Saltwater species were also quite sensitive to aldrin and dieldrin. The range of LC«-n values was similar to that for freshwater species: 2 to 100 pg/ liter for aldrin and 1 to 34 ug/liter for dieldrin. The salt water Final Acute Values were 1.3 tig/liter for- aldrin and 0.71 pg liter for dieldrin. Chronic studies have been conducted on the effects of dieldrin on freshwater and saltwater species. For freshwater organisms, chronic values as low as 0.2 iig/liter were obtained. . The Final Acute Chronic Ratio was determined to be 3.5, and the : calculated Freshwater Final Chronic Value was 0.29 ug/liter. Only one chronic study was done on saltwater species. Therefore, the saltwater Final Chronic Value-of 0.084 ug/liter was deter mined by dividing the Final Acute Value by the acute-chronic ratio. Mo chronic studies were performed on alJrin* but because its acute toxicity is comparable to that of dieldrin and because it is readily converted to dieldrin in animals and in the environ ment, it probably has similar chronic toxicity.. Both pesticides, and especially dieldrin, have been associ ated with large-scale bird and mammal kills in treated areas. Experimental feeding studies have shown that the chemicals are quite toxic to terrestrial wildlife and domestic animals at low levels.

~~Regulation* and Standards Ambient 4|HF Qu4U£y Criteria (USEPA)t Agualfe Lif e Freshwater Acute toxicity! Aldrint 3.0 jig/liter Oieldrins 2.5 pg/liter~~

Aldrin/Dieldrin Page 3 October 1985 U.S. ENVIRONMENTAL PROTECTION AGENCY (OSEPA). 1980. Anbient Water Quality Criteria for Aldrin/Dieldrin. Office of Water Regulations and Standards, Criteria and Standards Division, Washington, D.C. October 1980. EPA 440/5-80-019 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985. Health Assessment Document for Dichloronethane (Methylene Chloride). Office of Health and Environmental Assessment. Washington, D.C. February 1985. EPA 600/8-82/004F VERSCHUEREN, K. 1977. Handbook of Environmental Data on Organic Chemicals. Van Nostrand Reinhold Co., New York. 659 pages WEAST, R.E., ed. 1981. Handbook of Chemistry and Physics. 62nd ed. CRC Press, Cleveland, Ohio. 2332 pages

~~Aldrin/Dieldrin Page 5 October 1985~~

~~a Q ARSENIC~~

~~GENERAL BACKGROUND INFORMATION~~

The toxicity of arsenic depends upon its chemical form along with the route, dose, and duration of exposure. In general, arsenites (As**) are potentially more toxic than arsenates, soluble arsenic compounds are potentially more toxic than insoluble compounds, and inorganic arsenic compounds are potentially more toxic than organic derivatives (U.S. EPA, 1985).

~~PHARMACOKINETICS~~

Absorption from the gastrointestinal tract is dependent upon the solubility of the specific arsenic compound and the dose. Absorption from the respiratory tract is also dependent upon the specific arsenic compound, along with particle size (see section on Relative Absorption Factors).

~~HUMAN TOXICOLOGICAL PROFILE~~

Depending upon dose and exposure route, arsenic is an irritant of the gfcin, mucous membranes, and the gastrointestinal tract Acute toxicity from the ingestion of higher doses of arsenic may result in vomiting, diarrhea, convulsions,a severe drop in blood pressure, and cardiovascular effects. The lethal dose for humans is reported to be 1.0 to 2.6 mg/kg-bw (Vallee et al, 1960). Acute toxicity from inhalation exposure to arsenic adsorbed to particulate matter may result in conjunctivitis and pharyngitis. Subchronic effects included hyperpigmentation (melanosis), multiple arsenical keratoses, sensory-motor polyneuropathy, persistent chronic headache, lethargy, gastroenteritis, and mild iron deficiency anemia. Inhaled arsenic compounds have been reported to be associated with skin lesions, cardiovascular and respiratory effects, and peripheral neuropathy (Stokinger, 1981; IARC, 1980). Chronic oral exposure of humans to inorganic arsenic compounds has been reported to cause skin lesions, peripheral vascular disease, and peripheral neuropathy (Silver and Wainman, 1952). The incidence of blackfoot disease, a peripheral circulatory disease characterized by gangrene of the extremities, has reportedly been related to the presence of arsenic in the drinking water of residents of the southwest of Taiwan (Tseng, 1977). The symptoms of chronic inhalation exposure to arsenic compounds are similar to those associated with chronic oral toxicity.

~~MA DEP. ORS IL BWSC Documntation for the Ri«k /Imminent ShortForm Randcntial Scenario vnviotui 1.6 * It b - 10/92 B-9 BARIUM~~

Summary In its pure form, barium is an extremely reactive metal that decomposes in water. In natural waters it forms insoluble carbonate or sulfate salts and is usually present at concentra tions of less than 1 mg/liter. Insoluble forms of barium are not very toxic; but soluble barium salts are highly toxic after acute exposure, and they have a prolonged stimulant effect on muscles. A benign pneumoconiosis, baritosis, can result from inhaling barium dusts. The EPA Interim Primary Drinking Water Standard is 1 mg/liter.

~~CAS Number: 7440-39-3 Chemical Formula: Ba IUPAC Name: Barium~~

Chemical and Physical Properties Atomic Weight: 137.3 Boiling Point: 1,640«C Melting Point: 725"C Specific Gravity: 3.5 Solubility in Water: Decomposes; combines with sulfate present in natural waters to form Basp., which has a solubility of 1.6 ig/liter at 2Q*C Solubility in Organics: Soluble in alcohol; insoluble in benzene

Transport and Fate Barium is extremely reactive, decomposes in water, and readily forms insoluble carbonate and sulfate salts. -Barium is generally present in solution in surface or groundwater only in trace amounts. Large amounts will not dissolve because natural waters usually contain sulfate, and the solubility of barium sulfate is generally low. Barium is not soluble at more than a few parts per million in water that contains sulfate at more than a few parts per million. However, barium sulfate may become considerably more soluble in the presence

Barium Page 1 October 1985 Regulations and Standards Interim Primary Drinking Water Standard: 1 mg/liter OSHA Standard: 0.5 mg/m (soluble compounds, as Ba) ACGIH Threshold Limit Value: 0.5 mg/ra3 (soluble compounds, as Ba)

REFERENCES AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1980. Documentation of the Threshold Limit Values. 4th ed. Cincinnati, Ohio. 488 pages DOULL, J., KLAASSEN, C.D., and AMDOR, M.O., eds. 1980. Casarett and Doull's Toxicology: The Basic Science of Poisons. 2nd ed. Macmillan Publishing Co., New York. 778 pages NATIONAL ACADEMY OF SCIENCES (NAS). 1977. Drinking Water and Health. Safe Drinking Water Committee, Washington, D.C. 939 pages NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH) . 1984. Registry of Toxic Effects of Chemical Substances. Data Base. Washington, D.C. July 1984 SAX, N.I. 1975. Dangerous Properties of Industrial Materials. 4th ed. van Nostrand Reinhold Co., New York. 1,258 pages U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984. Health Effects Assessment for Barium. Environmental Criteria and Assessment Office, Cincinnati, Ohio. September 1984. ECAO-CIN-H021 (Final Draft) WEAST, R.E., ed. 1981. Handbook of Chemistry and Physics. 62nd ed. CRC Press, Cleveland, Ohio. 2332 pages

Barium Page 3 October 1985 Although little Information concerning adsorption of beryl lium is available, based on its geochemical similarity to alu minum it is expected to be adsorbed onto clay mineral surfaces at low pH and to be complexed into some insoluble compounds at high pfl. In most natural environments, beryllium is likely to be present in sorbed or precipitated, rather than dissolved, form. Beryllium may be accumulated to a slight extent by aquatic organisms. Although it has a low solubility in water, it is possible that benthos could accumulate beryllium from sediment and thereby transfer the metal to higher organisms via the food chain. However, there is no evidence for food chain mag nification. Airborne transport of beryllium, generally in the form of particulates, may also occur.

Health Effects The results of some epidemiological studies of workers occupationally exposed to beryllium indicate that beryllium may cause lung cancer in humans. Although this evidence is equivocal, beryllium and many of its compounds are known to be carcinogenic in several animal' species. Inhalation exposure to beryllium has resulted in the development of lung or bone cancer in animals, and exposure by injection has produced bone cancer. Although beryllium compounds may impair DNA polymeri zation, there is no other evidence of mutagenic or clastogenic activity. However, the number of compounds tested and the types of tests conducted have been limited. There is little information concerning the possible teratogenic effects of beryllium. It is reported to inhibit embryonic development of the snail and regeneration of the limbs of the salamander. Acute respiratory effects due to beryllium exposure include rhinitis, pharyngitis, tracheobronchitis, and acute pneumonitis. Dermal exposure to soluble beryllium compounds can cause contact dermatitis. Ocular effects include inflammation of the conjunc tiva from splash burns or in association with contact dermatitis. The most common clinical symptoms caused by chronic beryllium exposure are granulomatous lung inflammation, with accompanying cough, chest pain, and general weakness. Systemic effects include right heart enlargement with accompanying cardiac fail ure, liver and spleen enlargement, cyanosis, digital clubbing, and kidney stone development.

Toxicity to Wildlife and Domestic Animals Data for several freshwater fish species indicate that the acute toxicity of beryllium decreases by about two orders of magnitude with an increase in hardness from about 20 to

~~Beryllium Page 2 October 1985 Risk Concentration~~

~~10~5 37 ng/liter 10 , 3.7 ng/liter 10"7 0.37 ng/liter~~

~~GAG Unit Risk (USEPA)» 2.6 (ag/kg/day)"1 OS HA Standards (air): 2 pg/a TWA 5 Mg/a^Ceiling Level 25 ng/m /30 ain Peak Concentration ACGIH Threshold Limit Value: Suspected huaan carcinogen 2 ug/m3~~

REFERENCES AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH) 1980. Documentation of the Threshold Liait Values. 4th ed. Cincinnati/ Ohio. 488 P*ges NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AHD HEALTH (NIOSH). 1983. Registry of Toxic Effects of Cheaical Substances. Data Base. Washington, D.C. October 1983 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1979. Water- Related Environaental Fate of 129 Priority Pollutants. Washington, D.C. December 1979. SPA 440/4-79-029 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1980. Ambient Water Quality Criteria for Berylliua. Office of Water Regulations and Standards, Criteria and Standards Division, Washington, D.C. 'October 1980. EPA 440/5-80-024 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985. Health Assessment Docuaent for Dichlorome thane (Kethylene Chloride) Office of Health and Environaental Assessment. Washington, D.C. February 1995. EPA 600/8-82/004F WEAST, R.S., ed. 1981. Handbook of Chemistry and Physics. 62nd ed. CRC Press, Cleveland, Ohio. 2332 pages

~~Berylliua Page 4 October 1985 CADMIUM~~

~~GENERAL BACKGROUND INFORMATION~~

Cadmium typically exists in the environment as a salt of the +2 valence state or as a metal. It forms no stable organic compounds. Cadmium releases are generally associated with mining, smelting, manufacturing operations, and from the disposal of alkaline batteries containing cadmium (Doull, 1980; U.S. EPA, 1981).

~~PHARMACOKINETICS~~

Cadmium is absorbed by all routes of exposure (see section on Relative Absorption Factors). Absorption through the gastrointestinal tract is low, respiratory absorption more efficient and dermal absorption relatively insignificant (ATSDR, 1989). Absorbed cadmium is widely distributed throughout the body, with the major portion of the body burden located in liver and kidney (Sumino et aL, 1975). The distribution of cadmium is linked to the distribution of metallothionein, a low-moleculer-weight protein, rich in cadmium-binding sites. Cadmium is not known to undergo any direct metabolic conversions in vivo. The principle excretory route for absorbed cadmium is urinary. Excretion is slow, accounting for the long half-life of cadmium in the body (17-38 years) (ATSDR, 1989).

~~HUMAN TOXICOLOGICAL PROFILE~~

Cadmium is a local respiratory tract irritant Systemic symptoms occur in a few hours after an acute exposure to cadmium dust or fumes. Upper respiratory tract irritation is followed by coughing, chest pain, sweating, and chills. These symptoms resemble nonspecific upper respiratory infection (Sittig, 1985). Within 24 hours severe pulmonary irritation may develop, with progressively increasing pain in the chest, dyspnea, pulmonary edema, cough, and generalized weakness. Chronic exposure to cadmium fumes may result in emphysema- like lung damage (Sittig, 1984). Renal dysfunction may ensue (Friberg, 1950). Bernard and Lauwerys (1984) observed that the gastrointestinal tract is adversely affected by acute oral exposure with such symptoms as nausea, vomiting, salivation, abdominal pain, cramps, and diarrhea. The principal effects of chronic cadmium exposure are osteomalaria and osteoporosis (Itai Itai disease) secondary to glomerular and tubular necrosis in the kidney. The Itai Itai Couch-ouch") disease is endemic areas in Japan, which have been contaminated with mining wastes containing cadmium. Victims display the osteomalacia and osteoporosis as primary symptoms, as well as protein, sugar and amino acids not normally found in the urine. Other chronic effects include immunosuppression and decreases in measures of respiratory fitness (ventilation capacity, vital capacity, forced expiratory volume, etc.) (U.S. EPA, 1981).

~~MA DEP. ORS & BWSC DocumnUtion for the Ruk A**e««ment ShortFonn Residential Scenario verrion* 1.6 « & b • 10/92 B-29 REFERENCES~~

~~Agency for Tone Subetancee and DUeaM RagUtry (ATSDR) (1989) Toxicological profile for cadmium. U.S. Public Health Service.~~

~~Bernard, A. «nd Lauwery*, R. (1984) Cadmium in the human population. Experiment! 40:143-152.~~

~~Doall. J, ffliteen. CD. and Amdur, MJ>. (1980) Caaarttt and Doull'i Toiicologr. 2nd ed., M«rMilUn Publishing Co Inc. New York.~~

~~Fitxhugh, O.G. and Meiller, FJi. (1941) The chronic toaddty of cadmium. J, Pharm. Erp, Ther. 72:15.~~

~~Friberg, L. (1950) Health hazards in the manufacture of alkaline accumulator* with special reference to chronic cadmium poitoning. Aota. Mod. Soand. 138(SuppL 240): 1-124.~~

~~Friberg, L, Piacatcr, M^ Nordberg, GJ. and KjelUtrom, T. (1974) Cadmium in the Environment. 2nd «d., CRC Preu, Boca Raton. FL.~~

~~Eaniaawa, M. and Schroadtr, H-A. (1969) Life term ttudin on the effect of trace elements on spontaneous tumors in mice and rat*. Canoer Rea. 29:892-895.~~

~~Kqikawa, K., Nakaniahi, I. and Kuroda, E. (1981) Morphological changes of the kidney and bone of rats in chronic cadmium poitoning. Exp. Molao. PathoL 34:9-24.~~

~~KolUr, LD., Exon, J.H. and Roan, J.G. (1975) Antibody suppression by cadmium. Arch. Environ. Health 30:698.~~

~~Schroadar, H.A., B«U««a. JJ. and Vinton, WJI. (1964) Chromium, lead, cadmium, nickel, and titanium in mice: Effects on mortality, tumor* and tissue level*. J. Nutr. 83:239-250.~~

~~Sittig, M. (1985) Handbook of Toxic and Hatardou* Chemical* and Carrinogcnj. Noy»« Publication; Park Ridgv, NJ.~~

~~Sumino, K^ Hajnakawa, K-, Shibata, T. and Kitamura, 8. (1975) Heavy metals in normal Japanese tissue*. Arch, Environ. Health 30:487-494.~~

~~Thun, MJ., Schnorr, TAI^ Smith, A.. Halpuia, W£. and L»w«n. R-A. (1985) Mortality among a cohort of US. cadmium production worker* . anupdate. J. Natl. Canoer Iiut. 74:325-333.~~

U^. Environmental Protection Agmcy (EPA) (1981) Health a«««««ment document for cadmium. Environmental Criteria and Aaeeeament Office. EPA-600/8-81/023. \}JB. Environmental Protection Agtncy (EPA) (1985) Cadmium contamination of the environment: an a»»e««mant of nationwide rUk. Office of Health and Environmental AMeacment. EPA-440/4-85-023.

~~Yuhaa, E.M., Mqra, T^. and Schnell, R.C. (1979) Do*t-relattd alteration* in growth and mineral deposition by chronic oral cadmium administration in the male rat. Toxicology 12:19-29.~~

~~MA DEP, ORS IL BWSC Documntation for the RUk A*eee~~

Summary Copper is among th« mort nob lit metals in the environment. It is toxic to humans at high levels; it causes irritation following acute exposure and anemia following chronic exposure Sheep are very susceptible to copper toxicosis, as are many aquatic organisms. Background Information Copper exists in a valence state of +1 or +2. It is a lustrous, reddish metal. The physical properties of copper include ductility and conductivity of heat and electricity. Copper is found in nature as sulfide, oxide, or carbonate ore. CAS Humbert 7440-50-8 Chemical Formula: Cu IUPAC Name: Copper

Chemical and Physical Properties Atomic Weight: 63.546 Boiling Pointt 2,567*C Melting Point: 1,083«C Specific Gravity: 8.92 Solubility in Water: Most copper salts are insoluble, with the exception of CuSO4, Cu(N03)2, and CuCL, (the more comon copper silts). The fatal is insoluble in water. j Vapor Pressure: 1 •• Bg at 1,628*C

Transport and Fate Copper has two oxidation states, +1 (cuprous) and +2 (cupric Cuprous copper is unstable in aerated water over the pH range of most natural waters (6 to 8) and oxidises to the cupric state. Several processes determine the fate of copper in the aquatic environments formation of complexes, «specially witn humic substances) sorption to hydrous aetal oxides, clays, and organic materials* and bioaccumulation. In waters pollutea

Coppe r Page 1 October 1985 jlj respiratory tract irritation, a metallic or sweet taste, nausea, metal fume fever, and sometimes discoloration of skin and hair. Individuals exposed to dusts and aists of copper salts nay exhibit congestion of nasal mucous membranes, sometimes of the pharynx, and occasionally ulceration with perforation of the nasal septum. If sufficient concentrations of copper salts reach the gastro intestinal tract, they act as irritants and can produce salivation, nausea, vomiting, gastritis, and diarrhea. Elimination of ingested ionic copper by vomiting and diarrhea generally protects the patient from more serious systemic toxic effects, which can include hemolysis, hepatic necrosis, gastrointestinal bleed ing, oliguria, azotemia, hemoglobinuria, hematuria, proteinuria, hypotension, tachycardia, convulsions, and death. Chronic exposure may result in anemia* Copper salts act as skin irritants producing an itching eczema. Conjunctivitis or even ulceration and turbidity of the cornea may result from direct contact of ionic copper with the eye.

Toxicity to Wildlife and Domestic Animals Mean acute toxicity values for a large number of freshwater animals range from 7.2 |ig/liter for Daphnia pulicaria to 10,200 pg/liter for the bluegill. Toxicity tends to decrease as hard ness, alkalinity, and total organic carbon increase. Chronic values for a variety of freshwater species range from 3.9 }ig/liter for brook trout to 60.4 ng/liter for northern pike. Hardness does not appear to affect chronic toxicity. The acute-chronic ratios for different species range from 3 to 156. The more sensitive species tend to have lower ratios than the less sensi tive species. In addition, the ratio seems to increase with hardness. Acute toxicity values for saltwater organisms range from 17 jig/liter for a calanoid copepod to 600 ug/liter for the shore crab. A chronic value of 54 tig/liter* and an acute- chronic ratio of 3.4 is reported for the mysid shrimp. Long term exposure to 5 ng/llter is fatal to the bay scallop. Bioconcentratlon factors in freshwater species range from zero for the bluegill to 2,000 for the alga Chlorella rcgularts. Among saltwater species, the highest bioaccumulation factors are those for the bivalve molluscs. Oysters can bioaccumulate copper up to 28,200 times without any significant mortality. Sheep are very susceptible to copper toxicosis, and pois oning may be acute or chronic. Acute poisoning is caused by direct action of copper salts on the gastrointestinal -tract, resulting in gastroenteritis, shock, and death. The toxic dose is about 200 mg/kg and is usually obtained through an

~~Copper Page 3 October 1985 IRON~~

Summary There it some evidence that high concentrations of certain soluble icon salts may be teratogenic. The ingestion of excess amounts of iron can irritate the gastrointestinal tract. Inhaling some iron-containing dusts and fumes can cause siderosis, a type of benign pneumoconiosis.

Background Information Iron is the fourth most abundant element in the earth's crust. The pure metal is very reactive chemically, it corrodes readily in the presence of oxygen and moisture, forming iron (III) hydroxide [Fe(OH}.3]. GAS Number: 7439-89-6 .Chemical Formula: Fe

Chemical and Physical properties Atomic Weight: 55.847 Boiling Point: 2,750«C Melting Point: 1,535*C Specific Gravity: 7.86 Solubility in Water: Insoluble Solubility in Organics: Soluble in alcohol and ether

Transport and Fate Elemental iron and many iron compounds, including Fe(OH). and the iron oxides, are insoluble in water. Iron also tends to chelate with organic and inorganic natter. Consequently, much of the iron present in aquatic systems tends to partition into the bottom sediments. Iron has relatively low mobility in soil. Atmospheric transport of iron can occur.

~~Iron Page 1 October 1985~~

339 REFERENCES AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1980. Documentation of the Threshold Limit Values. 4th ed. Cincinnati, Ohio. 488 pages DOULL, J., KLAASSEN, C.D., and AMDUR, M.O. 1980. Casarett and Doull's Toxicology: The Basic Science of Poisons. 2nd ed. Macmillan Publishing Company, New York. 778 pages NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1984. Registry of Toxic Effects of Chemical Substances. Data Base. Washington, D.C. NATIONAL RESEARCH COUNCIL. 1982. Diet, Nutrition, and Cancer. National Academy Press, Washington, D.C. U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984. Health Effects Assessment for Iron. Environmental Criteria and Assessment Office, Cincinnati, Ohio. September 1984. ECAO-CIN-H054 (Final Draft) WEAST, R.E., ed. 1981. Handbook of Chemistry and Physics. 62nd ed. CRC Press, Cleveland, Ohio. 2332 pages

~~Iron Page 3 October 1985 0Cl«m«nt LEAD~~

~~GENERAL BACKGROUND INFORMATION~~

Lead is used extensively in the manufacture of storage batteries and was used in gasoline and paint. Lead is also a natural constituent of many soils, for which concentrations normally range from 10 to 30 mg lead per kilogram of soil (U.S. EPA, 1980).

~~PHARMACOKINETICS~~

Lead can be absorbed by the oral, inhalation or dermal exposure routes (see section on Relative Absorption Factors). Gastrointestinal absorption of lead varies considerably depending upon chemical form, dietary intake, and age (Forbes and Reina, 1974; Barltrop and Meek, 1975). The deposition and absorption of inhaled lead depends upon particle size, chemical form and the rate and depth of breathing (Randall et al., 1975; Nozaki, 1966; Chamberlain et al., 1975). Once absorbed, lead is distributed to the various organs of the body, with most distribution occurring into mineralized tissues (ATSDR, 1990). Placenta! transfer to the developing fetus is possible (Bellinger et al., 1987). Inorganic lead is not known to be biotransformed within the body. Absorbed lead is excreted via the urinary or fecal routes (ATSDR, 1990)

~~HUMAN TOXICOLOGICAL PROFILE~~

Cases of acute lead poisoning in humans are not common and have not been studied in experimental ^nimal^ as thoroughly as chronic lead poisoning. Symptoms of acute lead poisoning from deliberate ingestion by humans may include vomiting, abdominal pain, hemolysis, liver damage, and reversible tubular necrosis (U.S. EPA, 1984). Subacute exposures in humans reportedly may produce a variety of neurological effects including dullness, restlessness, irritability, poor attention span, headaches, muscular tremor, hallucinations, and loss of memory. Nortier et al., (1980) report encephalopathy and renal damage to be the most serious complications of chronic toxicity in man and the hematopoietic system to be the most sensitive. For this reason, most data on the effects of lead exposure in humans are based upon blood lead levels. The effects of lead on the formation of hemoglobin and other hemoproteins, causing decreased levels, are reportedly detectable at lower levels of lead exposure than in any other organ system (Betts et al., 1973). Peripheral nerve dysfunction is observed in adults at levels of 30 to 50 /ig/dL-blood. Children's nervous systems are reported to be affected at levels of 15 /zg/dL-blood and higher (Benignus et al., 1981). In high doses, lead compounds may potentially cause abortions, premature delivery, and early membrane rupture (Rom, 1976).

MA DEP, ORS & BWSC Docomntatioo for tb* Ri«k AtMMioent ShortForm Evidential Scenario 1.6 a & b - 10/92 B - 81 Agmey tor Toxic SMhatanoaa And DIMM* Ragirtry (ATSDR) (1990) Toricological profile for load. UJJ. Public Health Service.

~~Barfcrop, D. and Meek. F. (1976) Absorption of different lead compound*. Poetgrad. Med. J. 61:806-809.~~

Bellinger, D.C, Leviton, A.. Wataroaux, C., Needleman, H. and Rabinowitz, M. ( 1987)Longitudinal analyse* of prenatal and postnatal lead exposure and early cognitive development. N. EngL J. Med. 316: 1037-1043.

Benignue, V.A, Otto. D.A, MulUr, ICE. and Saipla, KJ. (1981) f/Tecto of <»e «u/ tody lead burden on CffS function in young children. U: EEQ ipectra. Eleotroeooephalograph. Clin. NeurophyaioL 62:240-248.

~~Betta, PJL, Aatley. R. and Rain*. RJi. (1973) Lead intoxication in children in Birmingham. Br. Mod. J. 1:402-406.~~

~~Boyland, E., Duke*. C.E, Grow, Pi. and Mitchley, B.C.V. (1962) 77i« induction of renal tumor* by feeding lead acetate to ratt. Br. J. Caaoer 16:283-288.~~

~~Chambatiain. D. «t aL (1976) Uptake of lead by inhalation of motor exhautt. Proo. Roy. Soc. London B. 192:77-110.~~

~~Forbac, G £. and Raina, J.C. (1974) Effect of age on gattrointestinal absorption (Fe, Sr, Pb) in the rat. J. Nutr. 102:647 652.~~

~~Fowlar. BA. «t aL (1980) Chronic low level lead tenacity in the rot: HI. An integrated at*e**ment of long-term tcaddty with ipedal reference to the kidney. ToxiooL AppL PbarmaooL 56:59-77.~~

~~Grant, LJ}. «t aL (1980) Chronic lout-level lead tcaddty in the rat: H. Effect* on postnatal physical and behavioral development. ToxiooL AppL PharmaooL 66:42-68.~~

~~HOdartorand, D.C. at ai (1973) Effect of lead acetate on reproduction. Am. J. ObatoC GynoooL 115:1058-1065.~~

~~Ito, N. (1973) Experimental thidirt on tumor* on the urinary system of rat* induced by chemical carcinogen*. Aota. PatboL (Jap.) 23:87.109.~~

~~Kang, HJD. at aL (1980) Occupational lead exposure and cancer. Letter to the Editor. Sofonoe 207:935.~~

~~Kopp, L. at aL (1980a) Altered metabolism and function of rat heart following chronic low level cadmium/lead feeding. J. MoL CelL CardioL 12:1407-1425.~~

~~Kopp, L. at aL (1980b) Cardiac physiological-metabolic change* after chronic low-level heavy metal feeding. Am. J. PhytrioL 239:H22-H30.~~

~~Nortiar, J.W., Sangitar, B. and Van Kaatam, R.G. (1980) Acute lead poisoning with hemolysi* and liver tcaddty after ingettion of red lead. Vet Hum. ToxiooL 22:145-147.~~

~~Nocaki, K. (1966) Method for studies on inhaled particle* in human respiratory system and retention of lead fume. Ind. Health (Jap.) 4:118-128.~~

~~RandaU, K. at aL (1975) The effect of particle toe on absorption of inhaled lead. J. Am. Ind. Hyg. Asaoo. 36:207-213.~~

~~Rom, WJf. (1976) Effects of lead on female reproduction: A review. ML Sinai J. Med. 43:542-552.~~

~~Scbroadar, P. at aL (1970) Zirconium, niobium, tin, vanadium, and lead in rats: Lifcierm studies. J. Nutr. 100:59-68.~~

~~MA DEP. ORS & BWSC Documntation for UM Riak AMaaamant ShortForm Raaidantial Scenario 1.6 a It b - 10/92 B-83 MANGANESE~~

Summary Manganese chloride produced lymphomas and manganese sulfate, tumor* afttr injestion into vice. In humans, chronic exposure to manganese causes degenerative changes in the central nervous system in the form of a Parfcinson-like disease; liver changes also occur. Acute exposure causes manganese pneumonitis.

~~CAS Number: 7439-96-5 Chemical Formula: Mn IUPAC Name: Manganese~~

~~Chemical and Physical Properties Atomic Weight: 54.938 Boiling Point: 1962«C Melting Point: 1244«C Specific Gravity: 7.20 Solubility in Hater: Decomposes; some compounds are soluble~~

Transport and Fate Manganese occurs most commonly in the +2 and +4 oxidation states in aquatic systems. Its solubility depends to a great extent on pH, dissolved oxygen, and presence of complexing agents. In saltwater, it is estimated that 85% or more of the manganese present exists in a soluble form. In freshwater, manganese can occur as the soluble ion, in complex organic ions, or in colloidal suspensions. Manganese often occurs at higher concentrations near the bottom of stratified lakes because it can be released from sediments, as the manganous ion, under reducing conditions. In the toil, the concentration and chemical form in which manganese occur can b« affected by pH, cation exchange capacity, drainage, organic matter content, and other factors. The solu bility of manganese is increased at low pH and under reducing conditions. The presence of high concentrations of chlorides, nitrates, or sulfates may also increase solubility. Under these conditions, manganese is more easily taken up by plants

Manganese Page 1 October 198S A «a-nouc LV-CQ vaj-ue of 16 »g/licec oc etanganese is reported for embryos of the oyster Crassostrea virginica. For the softshell clam Mya arenaria a 168-hour LCC^ vaiu» of 300 mg/liter is reported. 50

~~Regulations and Standards OSHA Standard: 5 «g/ra3 Ceiling Level ACGIH Threshold Limit Values: 1 rag/ra^ TWA (fume) 3 mg/ra^ STEL (fume) 5 mg/ra Ceiling Level (dust and compounds)~~

~~REFERENCES~~

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1980. Documentation of the Threshold Limit Values. 4th ed. Cincinnati, Ohio. 488 pages DOULL, J., KLAASSEN, C.D., and AMDUR, M.O., eds. 1980. Casarett and Doull's Toxicology: The Basic Science of Poisons. 2nd ed. Macmillan Publishing Co., New York. 778 pages EISLER, R. 1977. Acute toxicities of selected heavy metals to the softshell clam, Mya arenaria. Bull. Environ. Contam. Toxicol. 17:137-145 NATIONAL ACADEMY OF SCIENCE (HAS). 1973. Medical and Biolo gical Effects of Environmental Pollutants: Manganese. Washington, D.C. 191 pages NATIONAL ACADEMY OF SCIENCES (NAS). 1977. Drinking Water and Health. Safe Drinking Water Committee, Washington, D.C. 939 pages NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1983. Registry of Toxic Effects of Chemical Substances. Data Base. Washington, D.C. October 1983 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984. Health Effects Assessment for Manganese. Environmental Criteria and Assessment Office, Cincinnati, Ohio. September 1984. ECAO-CIN-HO57 (Final Draft) WEAST, R.E., ed. 1981. 'Handbook of Chemistry and Physics. 62nd ed. CRC Press, Cleveland, Ohio. 2332 pages

~~Manganese Page 3 October 1985~~

~~[O««rrc Associates MERCURY~~

~~GENERAL BACKGROUND INFORMATION~~

Mercury has been used in the past for medicinal purposes (Gosselin et al., 1984). There are a number of occupations associated with mercury exposure, particularly through inhalation. These include mining, smelting, chloralkali production, and the manufacture of mercury- containing products such as batteries, measuring devices (thermometers) and paints. Mercury has also been used agriculturally as a seed and cereal protectant and as a fungicide.

~~PHARMACOKINETICS~~

The pharmacokinetics and pharmacodynamics of mercury depend largely on its chemical form, organic, inorganic or elemental Absorption efficiencies vary depending on route of exposure and chemical form (see section on Relative Absorption Factors). Distribution, metabolism and excretion depend largely on the lipid solubility, ionization state and molecular size of the specific chemical form (ATSDR, 1989).

~~HUMAN TOXICOLOGICAL PROFILE~~

Exposure to most forms of mercury is associated with a high degree of toxicity. Elemental (metallic) mercury causes behavioral effects and other nervous system damage. Inorganic mercury salts do not generally reach the brain, but will produce kidney damage. Divalent (mercuric) mercury is substantially more toxic in this regard than the monovalent (mercurous) form. Organic mercury compounds are also toxic. Symptoms of chronic mercury poisoning can be both neurological and psychological in nature as the central nervous system is the primary target organ. Hand and finger tremors, slurred or scanning speech patterns, and drunken, stupor-like (ataxic) gait are some motor-control impairments that have been observed in chronic mercurial toxicity. Visual disturbances may also occur, and the peripheral nervous system may be affected. A psychological syndrome known as erethism is know to occur. It is characterized by changes in behavior and personality including depression, fearfulness, restlessness, irritability, irascibility, timidity, indecision, and early embarrassment Advanced cases may also experience memory loss, hallucination, and mental deterioration.

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

In a study by Mitsumori et al. (1981), male and female mice were fed methyl mercury chloride in their diet for up to 78 weeks. Most of the high dose group died from neurotoxicity before the 26th week. Renal tumors developed in 13 of 16 males in the

~~MA DEP, ORS & BWSC DocumnUtion for UM Rkk A«Mttm«nt ShortForm P*"^*™! Scenario wnion* 1.6 • & b - 10/92 B-85 NICKEL~~

~~GENERAL BACKGROUND INFORMATION~~

Nickel in the ambient atmosphere typically exists as a constituent of suspended particulate matter (U.S. EPA, 1985). The greatest volume of nickel emitted into the atmosphere is the result of fossil fuel combustion. Other sources of nickel emissions are primary production, incinerators, metallurgy, chemical manufacturing, cement manufacturing, coke ovens, nickel recovery, asbestos mining/milling and cooling towers.

~~PHARMACOKINETICS~~

Studies of nickel absorption have shown that it is absorbed by all routes of exposure to varying degrees, primarily dependent on the chemical form (see section on Relative Absorption Factors). Absorbed nickel is bound to serum components and distributed to body organs, reaching highest concentrations in kidney and lung tissue (Whanger, 1973). Nickel is not known to be biotransformed. Excretion of absorbed nickel is primarily through urine, with minor excretory routes through hair and sweat (ATSDR, 1988).

~~HUMAN TOXICOLOGICAL PROFILE~~

Nickel carbonyl Ni(CO)4 is a particularly toxic form of nickel upon inhalation and causes chest pain, dry coughing, hyperpnea, cyanosis, occasional gastrointestinal symptoms, sweating, visual disturbances and severe weakness. This is often followed by pulmonary hemorrhage, edema and cellular derangement Survivors may be left with pulmonary flbrosis. In the workplace, nickel dermatitis may result at high nickel concentrations. At lower concentrations some susceptible individuals develop eczema-like lesions. The threshold for these health effects is much greater than exposures which occur in the ambient environment. The major adverse effects of nickel in nym are dermatitis, chemical pneumonitis, and lung and "qgfl cancers.

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

Deaths occurred in rats and mice at concentrations greater than 3.3 and 1.7 mg/m3 nickel, respectively, upon extended inhalation exposure to NiS04 (Dunnick et al, 1987). Mice exposed to NijSj died due to necrotizing pneumonia at 7.3 mg/m3 nickel (Benson et al, 1987). Prolonged exposure of hamsters to nickel oxide at 41.7 mg/m3 resulted in decreased survival due to emphysema (Wehner et al., 1975). Oral LO^s in rats vary depending upon the nickel-containing compound to which the rats were exposed. These range from 355 mg compound/kg (118 mg Ni/kg) for nickel acetate (Haro, 1968) to greater than 5000 mg

~~MA OEP. ORS & BWSC Documntation for the Ruk AMemnant ShortForm R»«i~~

~~GENERAL BACKGROUND INFORMATION~~

Pure thallium is a soft bluish-white metal that is widely distributed in trace amount in the earth's crust. It is used in the manufacture of electronic devices, switches, and closures. It is also used to a limited extent in the manufacture of special glasses and for medical procedures that evaluate heart disease. Up until 1972, thallium was also used as a rat poison (ATSDR, 1991).

~~PHARMACOKINETICS~~

Thallium appears to be nearly completely absorbed from the gastrointestinal tract No information was located on absorption following inhalation or dermal exposure. However, animal studies following intratracheal administration suggested that uptake through respiratory epithelium was rapid and complete. There is little information on the distribution of thallium in humans. Analysis of human tissues indicates that thallium is distributed throughout the body. The highest levels were found in the scalp hair, kidney, heart, bone, and spleen. In animala, the highest levels are found in the kidneys and liver. Excretion of thallium occurs by both the urinary and fecal routes (ATSDR, 1991).

~~HUMAN TOXICOLOGICAL PROFILE~~

Thallium is acutely lethal to humans following oral exposure at doses of 54-110 mg thallium/kg of body weight as thallium sulfate (Davis et aL, 1981). The estimated lethal dose is approximately 14-15 mg/kg (Gosselin et aL, 1984). Thallium compounds can affect the respiratory, cardiovascular, and gastrointestinal systems, the liver, kidneys and the male reproductive system. Alopecia (hair loss) and changes in the nervous system are characteristic of thallium exposure. A retrospective study was conducted which compared the incidence of congenital abnormalities in children born to mothers who had been exposed to thallium during pregnancy (Dolgner et aL, 1983). The number of anomalies in the exposed group did not exceed the number of expected birth defects in the general population.

~~MAMMALIAN TOXICOLOGICAL PROFILE~~

In animals, the lowest doses showing lethality for a brief exposure period ranged from 5 to 30 mg/kg body weight for several species (Downs et aL, 1960). Exposure to low doses (1.4 mg thallium as thallium sulfate/kg body weight/day) for longer durations (40-240 days) also cause death (Manzo et aL, 1983). Electromyographic abnormalities without changes in

~~MA DEP. ORS & BWSC Documntation for the Ri*k Ai»e««n«nt ShortForm ReMdeatikl Scenario 1.6 « ti b - 10/92 B- 119 REFERENCES~~

~~Agraey for Toxic Substance* and DIMM* Registry (ATSDR) ( 199 1) Toxicologieal profile for thallium. U.S. Public Health Service.~~

M, Herfctn, R. and Neubert, D. (1981) Stadia on embryotaxic effects of thallium using the whole embryo culture technique. In: Neubert D., Merker HJ., eds. Culture Technique*: Applicability for Studio on Prenatal Differentiation and Torintr: 6th Symposium on Prenatal Development. Berlin, W. Germany, pp. 67-66.

~~Catto, B.C., Merer*, J. and DiPaolo, J.A. (1979) Enhancement of viral transformation for evaluation of the carcinogenic or mutagenic potential of inorganic metal salt*. Cancer Re*. 39: 193-198.~~

~~DavU, L.E., Standeftr, J.C., and Kornfeld, M. (1981) Acute thallium poisoning: Toxicological and morphological studies of the nervous system. Ann. NeuroL 10:38-44.~~

Dolgner E., Brockhaus, A. and Ewers, U. (1983) Repeated surveillance of exposure to thallium in a population living in the inanity of a cement plant emitting dust containing thallium. Int. Arab. Oooup. Environ. Health 62:79-94.

~~Downs, Wj,,, Scott, JJC and Steadman, L.T. (1960) Acute and tub-acute taadty studies of thallium compounds. Am. lad. Hyg. AMOO. J. 21:399-406.~~

~~GQwon, J-E. and Becker, B-A- (1970) Placenta! transfer, embryoUaddty and teratogenicity of thallium sulfate in normal and potassium-deficient rats. ToxiooL AppL PbarmaooL 16:120-132.~~

~~GocMlin, ILE, Smith, RJ». and Hodge, H.C. (1984) ^lini"*1 Taxicolosrr of Commercial Product*. 5th ed. Baltimore, MD; William, and WOkitw, H-139, IH-379-383.~~

Grunfeld, O^ RattiUnM, G. and Aldana, L. ( 1963) Electrocardiographic changes in experimental thallium poisoning. Am. J. Vet. Ret. 24:1291-1296. Kanematau, N, Harm, M. and Dada, T. (1980) Rec assay and mutagenicity studies on metal compounds. Mutat. Re*. 77:109-116. Manzo, L^ SoaUi, R. and Mogiia, A. (1983) Long-term toxtdty of thallium in the rat. In: Chemical Toxicology and Clinical Chemistry of Metal*. London, tttifli*^ fa*A*m\/- Preu, pp. 401-406.

~~)., Vacilywa, IM and Sdirkova, NX (1983) Mutagenic effect of thallium and mercury salts on rodent cells with different repair activities. Mutat. Re*. 124:163-173.~~

~~MA DEP. ORS & BWSC Documntation for the Ri*k Af*e**ment ShortFonn Residential Scenario versions 1.6 a & b - 10/92 B- 121 VANADIUM~~

Summary Occupational exposure to airborne vanadium has been shown to irritate the skin, eyes, and respiratory tract and to cause bronchitis, bronchospasms, and chest pain. Oral exposure has been associated with gastrointestinal disturbances and discolor ation of the oral mucosa. Chronic exposure to vanadium may have an adverse effect on various enzyme systems.

Background Information Vanadium can exist in the 0, +2, +3, +4, and +5 oxidation states. Elemental vanadium is insoluble in water. Vanadium usually occurs in some oxidized form, and soluble and insoluble vanadium compounds can occur. Vanadium can bind covalently to organic molecules to yield organometallic compounds. CAS Humbert 7440-62-2 Chemical Formula: V IUPAC Name: Vanadium

~~Chemical and Physical Properties Atomic Weight: 50.9 Boiling Point: 3,380*C Melting Point: 1,890«C Specific Gravity: 5.96 Solubility in Water: Insoluble~~

Transport and Fate The extent to which vanadium is transported in aqueous media is largely .determined by the chemical species present and by environmental factors determining its solubility and binding to organic materials. Some vanadium compounds are volatile, and atmospheric transport of fumes as well as partic ulates can occur. Some bioaccumulation of vanadium occurs. However, in mammals, it appears that excess vanadium can be rapidly excreted in the urine. In humans, it is excreted as sodium metavanadate or ammonium vanadyl tartiate.

Vanadium Page 1 October 1985 REFERENCES AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH) 1980. Documentation of the Threshold Limit Values. 4th ed. Cincinnati, Ohio. 488 pages DOULL, J.» KLAASSEN, C.D., and AMDUR, M.O., «ds. 1980. Casarett and Doull's Toxicology: The Basic Science of Poisons. 2nd ed. Macmillan Publishing Co., New York. 778 pages EA ENGINEERING, SCIENCE, AND TECHNOLOGY, INC. (EA). 1985. Vanadium: Environmental and Community Health Impact. Prepared for American Petroleum Institute, Washington D.C., January 1985. EA Report API 37 D NATIONAL ACADEMY OF SCIENCE (NAS). 1977. Drinking Water and Health. Safe Drinking Water Committee, Washington, D.C. 939 pages NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1977. Criteria for a Recommended Standard—Occupational Exposure to Vanadium. Washington, D.C. DHEW Publication No. (NIOSH) 77-222

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1984. Registry of Toxic Effects of Chemical Substances. Data Base. Washington, D.C. July 1984 WEAST, R.E., ed. 1981. Handbook of Chemistry and Physics. 62nd ed. CRC Press, Cleveland, Ohio. 2,332 pages

~~Vanadium Page 3 October 1985 Co«m«nc A»«ooat«« ZINC~~

~~GENERAL BACKGROUND INFORMATION~~

Zinc is used most commonly as a protective coating for other metals and in alloys such as bronze and brass. Zinc is emitted to the atmosphere during mining and refining, manufacturing processes, and combustion of zinc-containing materials. Zinc is an essential trace element in nutrition and is found in many foods (ATSDR, 1989).

~~PHARMACOKINETICS~~

It has been reported that about 20 to 30 percent of ingested zinc is absorbed and the mechanism may be homeostatically controlled and carrier-mediated. When zinc levels in the body are sufficient to sustain normal physiological functions, zinc absorption decreases. Absorption occurs by the inhalation and dermal routes as well. Once absorbed, zinc is distributed throughout the body where it is used as an essential cofactor in many enzyme systems. Excretion occurs primarily through the feces (ATSDR, 1989).

~~HUMAN TOXICOLOGICAL PROFILE~~

Zinc compounds are of relatively low toxicity by ingestion. In humans, exposure to 2 g or more of zinc produces symptoms of fever, nausea, vomiting, stomach cramps, and diarrhea 3-12 hours after ingestion. Zinc chloride is a primary component of smoke bombs, and pathologic changes in humans due to acute inhalation exposure to ZnCl include laryngeal, trachea!, and bronchial mucosal edema and ulceration, interstitial edema, interstitial fibrosis, alveolar obliteration and bronchiolitis obliterans. Severe acute injury is associated with a high mortality (Matarese and Matthews, 1986). Metal fume fever results from occupational inhalation of freshly formed fumes of zinc oxides. It is characterized by transient chills and fever, profuse sweating, and weakness some hours after exposure. The fumes usually consist of extremely fine particles containing other metals in addition to zinc. The very small size (submicronic) of the fume particles with their potential for alveolar deposition is thought to be an important aspect of this phenomenon. It has generally been estimated that fume fever does not occur at zinc oxide levels less than 15 mg/m9 although some occurrence of fume fever has been reported at levels as low as 5 mg/m9. This occupational hazard is not considered to be a general public health problem (U.S. EPA, 1987a; U.S. EPA, 1987b). Poorly ionized zinc compounds have low dermal toxicity and have been used therapeutically and cosmetically for many years as mild astringents, antiseptics and perspirants (Oilman et aL, 1985).

~~MA DEP, ORS £ BWSC Documntation for the Rick AMewment ShortForm Retktontial Scenario vcniotu 1.6 * tt b • 10/92 B- 141 REFERENCES~~

~~Agency for Toxic Subatancee and DUea*e Regiatry (ATSDR) (1989) Tmcicological profile for rine. U.S. Public Health Service.~~

~~Amdur, M.O., McCarthy, JS. and Gill, M.W. (1982) Respiratory response of guinea pigs to zinc oxide fume. Am. Ind. Hyg. AMOO. J. 43:887489.~~

~~Bauchinger, M., Schmid, £., Einbrodt, HJ. and Drwp, J. (1976) Chromosome aberrations in lymphocytes after occupational exposure to lead and chromium. Mutat. Ree. 40:67-62.~~

~~Clayton, FJ). and Clayton, F.E. (1981) Patty'1 Industrial Hveigne and Toxicology. Third RevUed Edition, Volume 2A, Toxicology. John Wiliy and Sou, New York, NY. pp. 2033-2049.~~

~~Chang, CM.. Mann, DJ£. and Gautieri, RJ. (1977) Teratogenicity of tine chloride, 1,10-phenanthroUne, and a zinc-1.10 phenanthnUne complex in mice. J. Pharm. Sot 66:1755-1758.~~

~~Oilman, A.G., Goodman, L.S., Rail, T.W. and Murad, F. (1985) The Pharmacological BajU of Therapeutic*. 7th EM. \tm*-'Uin** Puhliahing Company. NY, NY.~~

Lam, HJ., Pench, R. and Amdur, M.O. (1982) Changes in lung volume and diffusing capacity in guinea pigs exposed to a combination of sulfur dioxide and submicron zinc oxide mixed in a humidified furnace. ToxiooL AppL Pharmaool. 66:427-433.

Lam, HJ., Conner, J.W., Rodgen, AX., Fitzgerald, S. and Amdur, M.O. (1985) Functional and morphological changes in the lungs of guinea pigs exposed to freshly-generated ultrofine tine oxide. ToxiooL AppL PharmaooL 78:29-38.

~~Leonard, A. (1985) Chromosomal damage in individuals exposed to heavy metals. In: H. Sigel (ed)., Metal lorn in Biological Syttenu.~~

~~Mataraee Si. and Matthew*. JJ. (1986) Zinc chloride (smoke bomb) inhalation lung injury. Che*t. 89:308-9.~~

~~Miyaki, M^ Murata, 1^ Oaabe, M. and Ohno, T. (1977) Effect of metal cations on mis-incorporation by E. Coli DNA polymerases. Bioohem. Biophys. Ree. Commun. 77:854-860.~~

Sirovw, MJV. and Loeb, L-A. (1976a) Metal-induced infidelity during DNA synthesis. Proc. NaU. Acad. Sci. 73:2331 2335. Sirorer, M-A. and Loeb, L.A. (1976b) Infidelity of DNA synthesis in vitro: Screening for potential metal mutagens or carcinogen*. Soionoe 194:1434-1436.

VS. Environmental Protection Agency (UJ. EPA) (1987a) Summary review of the health effects associated with zinc and zinc oxide. Health lame Aaieetmeat. EPA/600/8-87/022F. Office of Heahh and Environmental Aueument. Washington, D.C. UJ. Environmental Protection Agency (U.S. EPA) (1987b) Assessment of zinc and zinc oxide as potentially toxic u> pollutants. Federal Register

~~MA DEP. ORS & BWSC Documntation for the RUk Aiengimrnt ShortForm Retidential Scenario venion* 1.6 a tt b - 10/92 B- 143 APPENDIX E-4~~

~~FUGITIVE DUST MODEL APPENDIX E-4~~

~~FUGITIVE DUST MODEL~~

~~ESTIMATION OF FUGITIVE DUST EXPOSURE POINT CONCENTRATIONS FROM ON-SITE DIRT BIKER ACTIVITY~~

~~1.00 INTRODUCTION~~

Exposure point concentrations (EPCs) for potential on-site dirt bike riders on Central Landfill property were calculated using Environmental Protection Agency (EPA) AP-42 emission factors and the Near Field Box dispersion model. The AP-42 emission factor for unpaved roads (Section 13.2.2) was used to determine emission rates from dirt bikers dust generation. These emission rates were used in a transport and dispersion model (Near Field Box) to estimate concentrations of individual compounds in ambient air on-site (EPCs).

~~2.00 EMISSION FACTOR~~

The derived emission rates from fugitive dust activities from dirt bikers was based on the highest concentrations of individual compounds detected in surficial soil (0-3 feet) based on previous Central Landfill soil sample collection. The USEPA AP-42 emission factors for unpaved roads was selected to quantify emission rates of fugitive dusts generated from dirt bikers. The emission rate is based on the following equations. Details regarding the modeling assumptions are provided in Table E.4-1 through E.4-3.

~~Emission Rate:~~

~~Q(10) = (a)(Et)(VMT)~~

~~where:~~

Q10 = emission rate of individual compound (mg/hr) (a) = mass fraction of individual compounds in soil (mg/hr) (Et) = emission rate of particles 10 microns and smaller due to dirt bike travel over unpaved surfaces (Ibs/VMT) (VMT) = vehicle miles traveled per hour (miles)

~~where:~~

~~(Et) = k(5.9) [s/12] [S/30] [W/3]07 [w/4]05 [365-p/365] where:~~

k = particle size multiplier (dimensionless) s = silt content of road surface (%) S = mean vehicle speed (miles per hour) W = mean vehicle weight (tons) w = mean number of wheels P = number of days of at least .254 mm of precipitation per year

~~The predicted emission rate is presented Table E.4-4~~

The emission factor derived is based on mean vehicle weights and number of wheels greater than dirt bikes (i.e., trucks). However, based on discussions with personnel from Research Triangle Park (RTF) the developers of the unpaved road emission factor, the application of the unpaved road emission factor for dirt bikes is adequate and is a conservative estimate in the absence of a specific emission factor for dirt bikes at the time of this report.

~~3.00 DISPERSION MODEL~~

The Near Field Box model was used to estimate ambient air concentrations of compounds detected in soils on-site, based on compound-specific emission rates estimated by emission factors for dirt bike generating fugitive dusts, dimensions of the area, and average wind speed at the Site. The dimensions of the contaminant area (box) and the average annual wind speed at the Site, were used to set the downward height of the box and the average wind speed through the box, respectively.

~~G:\31866.ZYNX31866-20.LJC\REPORTS\appende4.doc File No. 31864.00 Page I of 2 TABLE E.4-1 "/I7/1999~~

~~MODELING OF FUGITIVE DUST EMISSION RATES FROM VEHICLE TRAFFIC AND AIR CONCENTRATIONS~~

~~Vehicle Traffic Fugitive Dust Emission Rate Calculations For Unpaved Roads~~

Emission rates of individual compounds in soil and debris were calculated by multiplying the mass fraction of the individual compounds in soil by the total fugitive dust emission rate. The total fugitive dust emission rate from motorcycle traffic was estimated to be equivalent to the fugitive dust generated by vehicle traffic on unpaved roads based on the AP-42 emission factors.

~~Q(10) = (a) (Et)(VMT)~~

~~Q (10) = emission rate of individual compound (mg/hr)~~

~~a — mass fraction of individual compounds in soil, debris (mg/kg)~~

~~Et = total fugitive dust emission rate (kg/hr)~~

~~VMT = vehicle miles traveled per hour (miles)~~

~~G:\31864.Z23V31864-OO.LJC\CALCS\RISK_TAB\Z2300fds.xls\M_BLDZR File No. 31864.00 Page 2 of 2 11/17/1999~~

~~TABLE E.4-2~~

~~MODELING OF FUGITIVE DUST EMISSION RATES FROM VEHICLE TRAFFIC AND AIR CONCENTRATIONS~~

~~E10 - Fugitive Dust Generated by Motor Vehicle Activity~~

~~AP-42 EMISSION FACTOR - UNPAVED ROADS (U.S. EPA AP-42 1/95, Sec. 13.2.2)~~

This formula is used to estimate the emission rate of fugitive dusts into the air from motor vehicle traffic on unpaved roads based on the number of vehicle miles traveled at the site and the silt content of the soils, speed and weight of the vehicle, number of wheels, and precipitation. This equation provides conservative estimates of fugitive dust concentrations from unpaved roads. Actual dust emissions at the site are likely to be less than calculated by this model.

~~E t = k(5.9) x {(s/12)(S/30)((W/3)A0.7)} x {w/4}A0.5 x {365-p/365}~~

~~Et = emission rate of particles 10 microns and smaller due to motor vehicle travel over unpaved surfaces (Ibs/VMT)~~

k = particle size multiplier (dimensionless) k = 0.4 s = silt content of road surface (%) s= 6.4 % S = mean vehicle speed, miles per hour S= 20 W = mean vehicle weight, tons W= 0.3 w = mean number of wheels w = 2 p = number of days of at least .254 mm of precip. per year p= 120

~~conversion factor: 1 Ibs. = 0.454 kg~~

~~Et = 2.9E-02 k|~~

~~VMT= 20 miles traveled~~

~~G:\31864.Z23V31864-OO.UC\CALCS\RISK_TAB\Z2300fds.xls\M_BLDZR File No. 31864.00 Page I of I TABLE E.4-3 11/17/1999~~

~~MODELING OF FUGITIVE DUST EMISSION RATES FOR UNPAVED ROADS AND AIR CONCENTRATIONS~~

~~Air Concentration Calculations~~

~~NEAR FIELD BOX MODEL (Pasquill, 1975; Horst, 1979)~~

This model is used to estimate air concentrations of compounds based on emission rates, dimensions of the site (box) and average wind speeds at the site. The model is accurate at short downwind distances (i.e., less than 100 meters) and is appropriate for estimation of on-site exposures.

~~Ca = Q10/((Hb)(Wb)(Um))~~

~~Ca = concentration of compounds in ambient air on site (mg/m3)~~

~~Q10 = emission rate of compounds (mg/s) where: Q10 = concentration (mg/hr) x hr/3600 s~~

~~Hb = downwind height of box (m) Hb= 6.2 m (determined from length of box 100m (x) and model constraints) Wb = width of box (m) Wb = 1950 m (determined based on site area)~~

~~Um = average wind speed through the box (m/s) Urn = 0.22 (ulO)ln(2.5Hb)~~

~~ulO = wind speed at 10 m (m/s) ulO= 5 m/s (annual wind speed for Providence, RI; National Climatic Data Center, observations Um = 2.77 m/s from 1961 through 1990)~~

~~Ca (mg/m3) = Q10 (mg/s)/Dispersion Factor(ms/s), where~~

~~Dispersion Factor = (Hb) (Wb) (Um) m3/s (HbHWbHUm) = 3.35E+04 mVs~~

~~G:\31864.Z23V31864-OO.UC\CALCS\RISK_TAB\Z2300f~~

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~~S oo 5 APPENDIX E-5~~

~~ABSORPTION ADJUSTMENT FACTORS Table 4. Recommended Dermal Absorption Factor from Soil~~

Compound Dermal Reference Absorption Factor Arsenic 0.03 Wester, et al (1993a) Cadmium 0.001 Wester, et al (1992a) USEPA(1992) Chlordane 0.04 Wester, et al (1992b) 2,4-Dichlorophenoxyacetic 0.05 Wester, et al ( 1996) acid DOT 0.03 Wester, et al ( 1990) Dioxins TCDD < 10% organic soil 0.03 USEPA (1992) >10% organic soil 0.001 PAHs Benzo(a)pyrene 0.13 Wester, et al ( 1990) PCBs Aroclor 1254 and 1242 0.14 Wester etal(1993b)

~~3,3'4,4'-Tetrachlorobiphenyl 0.02 USEPA (1992) Pentachlorophenol 0.25 Wester etal(1993c) Generic Defaults Semivolatile organic 0.1 - compounds Inorganics 0.01 ARSENIC GAS #: 7440382~~

~~TOXICnY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.0003 mg/kg/day (2) Chronic Oral Reference Dose: 0.0003 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: 1.8 (mg/kg/day)"' (If) Inhalation Cancer Unit Risk: Not Volatile~~

Human studies support the assumption that the soluble salts of inorganic arsenic are almost completely absorbed by the oral route. Literature sources cite an absorption efficiency of 98% for arsenic in humans and laboratory animals (Vahter, 1983; EPA, 1984, 1985; Goyer, 1986).

~~Vahter, M. (1983) Meiabolum of Arsenic. In: Fowler, B.A., ed. Biological and Environmental Effect of Arxnic. New York: ElMvur, pp. 171-198.~~

~~U.S. Environmental Protection Agency (U.S. EPA) (1985) Health AdvUorie* for 52 Chemical* Which Have Been ig water.~~

~~U.S. Environmental Protection Agency (U.S. EPA) (1984) Health A«M««ment Document for Inorganic Artenic. Final report. Ruiarch Triangle Park, NC: Environmental Protection Agency. EPA 600/8-83-02 IF.~~

~~Coyer, R-A. (1986) Caearett and Doull'i Toxicology. (CJ). Klaaceen, M.O. Amdur and J. Doull, Eds.) 3rd «d-, pp. 682-635, M^-Miii.^ New York.~~

No quantitative studies were located to evaluate the dermal absorption of arsenic compounds. However, clinical symptoms of arsenic poisoning have been reported in humans after accidents where the only route of exposure was through the skin, suggesting that dermal absorption does occur. An absorption efficiency of 3% may be considered a conservative upper-bound based on EP toxicity studies where the extraction of arsenic from soil (Ph. 5, 24 hours) averaged 3%.

~~MA DEP. ORS & BWSC Documentation for the RUk AtMoment ShortForm Rmiriential Scenario 1.6 a & b - 10/92 C- 11 ARSENIC~~

The oral RfD for arsenic of 3E-04 mg/kg-day and the proposed oral unit risk factor of 5E-5(ug/L)'1 (backcalculated CSF of (1.8mg/kg-day)'1) are based on epidemiological studies that characterized health effects in a large population of Taiwanese who consumed drinking water containing arsenic. The exact form of arsenic is unknown. For the purposes of development of the AAFs, it has been assumed that the arsenic was a soluble inorganic arsenic salt. The solubility of the various arsenic forms is reported to be a critical factor in their bioavailability (U.S. EPA, 1984).

Several investigators have estimated the extent of arsenic absorption following ingestion. Pomroy et al. (1980) administered radiolabeled arsenic acid in gelatin capsules followed by a glass of water. In one subject, approximately 11% was excreted in the feces with most of that (8%) excreted in 3 days. It is not possible to determine what fraction of this fecally excreted arsenic was unabsorbed and what fraction was absorbed and subsequently excreted in the feces. Thus, 89% represents a minimum estimate of absorption. These data are supported by the data from the other five subjects in the study. The average minimum absorption (assumes fecally excreted arsenic was unabsorbed) across all six subjects was 94%. This absorption estimate is supported by a study by Bettley and O'Shea (1975) whose data indicate a minimum absorption of 96%. These studies indicate that virtually all of an orally administered dose of arsenic can be absorbed from the gastrointestinal tract.

If site-specific data indicate that an insoluble form of arsenic is present, than the conservative AAFs calculated below may need to be modified. GZA utilized AAFs derived by the MADEP (1992) for all pathways, when available. However, MADEP did not derive an AAF for dermal contact with chemicals in water, thus GZA derived one.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral RfD and unit risk for arsenic are based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the RfD and unit risk to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals 1/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose-response criteria (multiplying the RfD or dividing the CSF by the absorption). For arsenic, the AAF (dermal-water) is 1/(100%) = 1.

~~REFERENCES~~

Bettley and O'Shea. 1975. The absorption of arsenic and its relation to carcinoma. British Journal of Dermatology, 92:563-568. Page 1 of 2 Pomroy, C, S.M. Charbonneau, R.S. McCollough and G.K.H. Tarn. 1980. Human retention studies with 74As. Toxicology and Applied Pharmacology, 53:550-556.

~~U.S. EPA. 1984. Health Effects Assessment for Arsenic. Office of Research and Development, Office of Emergency and Remedial Response. EPA/540/1-86-020.~~

~~M:\RSK_STND\HH\AAF_TEXT\AAFS\ARSENIC.DOC~~

~~Page 2 of 2 ARSENIC (INORGANIC)~~

Several studies in humans indicate that the soluble arsenates and arsenites (salts of the oxyacid forms of arsenic) are well absorbed across the gastrointestinal tract. ATSDR (1997) reports that in one study by Bettley and O'Shea, (1975) less than 5% of an oral dose given to humans was excreted in the feces indicating that absorption was at least 95% (the specific study conditions were not presented by ATSDR). ATSDR states that other studies in humans reported that urinary excretion (the primary route of elimination) accounted for 55-80% of daily oral intakes of arsenate or arsenite (Buchet et al 1981; Crecelius, 1977; Mappes, 1977; Tam et al., 1979). The MADEP (1992) utilizes an absorption efficiency of 98% for the soluble salts of inorganic arsenic, based on both U.S. EPA and other published literature sources. The solubility of the various arsenic forms is reported to be a critical factor in their bioavailability (U.S. EPA, 1984). Gastrointestinal absorption may be much lower if highly insoluble forms of arsenic are ingested such as arsenic triselinide, arsenic trisulfide, and lead arsenate (ATSDR, 1997).

Arsenic exhibits varying physiochemical properties depending on its valence state. In the environment, the transport and partitioning of arsenic in water is dependent upon the chemical form (oxidation state and counter ion) of the arsenic and on interactions with other materials present. Soluble forms move with the water in the environment. These forms are also more bioavailable when human exposure occurs. However, arsenic may be adsorbed from water onto sediments or soils, especially clays, iron oxides, aluminum hydroxides, manganese compounds and organic materials (ATSDR, 1997). Once adsorbed, arsenic is less soluble and less bioavailable.

~~Oral-Soil AAF~~

The relative Absorption Adjustment Factor (AAF) is used to account for differences in absorption of arsenic when exposure occurs via a route different than that used in the dose- response study (drinking water) and/or when the arsenic is present in a different environmental medium. The Texas Risk Reduction Program (1996) presented data from four studies on the oral bioavailability of arsenic from soil. The mean bioavailability reported in its Draft Document ranged from 8 to 24 percent in dogs, monkeys, swine and rabbits. Based upon these data, the Texas Natural Resource Conservation Commission (TNRCC) chose 20% because its the upper- end of the mean bioavailability determined in three models (monkey, dog and swine) reportedly having similar gastrointestinal systems relative to humans and because 20% is consistent with the mean bioavailabilty for soil arsenic obtained using the rabbit. (The TNRCC apparently assumed that the absorption of arsenic from the drinking water in the Taiwanese population was 100%, since they used the oral-soil value directly as the relative bioavailability factor.) The ATSDR, however, reports that the rabbit has a similar ratio of metabolites as humans, and suggests that this may be the best model for the toxicokinetics in humans.

7/24/97, revised 10/5/99 GZA reviewed the two published studies cited by TNRCC (the dog study by Groen et al., 1994, and the rabbit study by Freeman et al., 1993; the other two were unpublished) and determined that the rabbit study was the most appropriate study from which to derive the AAF. The shortcomings of the dog study were that a total of only six animals were used, the arsenic-soil matrix consisted of arsenic in bog ore-containing soil from the Netherlands which is not representative of the type of soil found near the site, and the fact that the dog was not the recommended animal model. The bioavailability of the arsenic from the soil in the dog study (relative to intravenous administration of arsenic pentoxide (As2Os)) was 8%, the lowest value reported by TNRCC. It is likely that this low bioavailability value is reflective of the high adsorption potential of the soil matrix used.

In the rabbit study, the bioavailability of arsenic-containing soil obtained from an area near a smelter in Anaconda, Montana was determined relative to both intravenous (28%, reported by TNRCC as 24% based on normalized i.v. data) and oral gavage (48%) administration of sodium arsenate. The percent bioavailability value presented in this paper for the oral soil arsenic relative to the oral gavage can be used directly as the oral-soil AAF. This allows the relative bioavailability estimate to be based on a single species, thereby eliminating the uncertainties introduced by calculating a relative absorption factor using data obtained from different exposure matrices and animal species, as well as from different study protocols. Thus, although it is possible that the absolute bioavailability in the rabbit may differ somewhat from that in the human, the use of relative bioavailability data from within a single species allows one to evaluate the affect of the soil matrix itself. One would assume that this relative affect (decreased bioavailability due to adsorption to soil matrix) would be the same across species.

Freeman et al. (1993) exposed fasted prepubescent male and female SPF New Zealand White Rabbits (5/sex/treatment group) to a single oral administration of arsenic-containing soil (3900 ppm As) at three different dose levels (0.2,0.5 and 1.0 g soil/kg body weight, corresponding to 0.78, 1.95 and 3.9 mg As/kg, respectively). The arsenic-containing soil was administered in a gelatin capsule. The test soil contained primarily enargite [Cu3AsS4] (48%), and goldfieldite [Cu7(Te,As,Sb)S4] (14%), with the remainder being present as As(V) oxides and solid solutions of arsenic with copper and iron. Some of the arsenic-bearing solid phases were encapsulated by insoluble silicate minerals, effectively preventing the release of arsenic into the gastrointestinal tract. Thus, the majority of the arsenic in the soil was present in forms that are less soluble than the forms typically found dissolved in water, which, as discussed above, is generally the case in environmental exposures. The particle size of the soil is reported to be similar to the size of ingested particles commonly found to adhere to children's hands.

Other exposure groups included untreated controls, an intravenous sodium arsenate group (1.95 mg As/kg) and a gavage aqueous sodium arsenate group (1.95 mg As/kg). Urine, cage rinse and feces were collected at 24-hour intervals for 5 days and analyzed for total arsenic. Using the

7/24/97, revised 10/5/99 urinary excretion data, the average oral bioavailability of arsenic in soil relative to that of an aqueous solution of sodium arsenate administered by gavage was 48% indicating that the soluble form of arsenic used in the gavage exposures was about twice as bioavailable as the forms of arsenic present in the test soil. Thus, the AAF (oral-soil) is 0.48.

This relative bioavailability value can be used as the oral-soil AAF since it is based on the bioavailability of arsenic in soil relative to that following oral exposure to sodium arsenate in water (the dose response values for inorganic arsenic are based on drinking water exposures). Although some arsenic is excreted in the feces (an average of 8% following intravenous administration), the primary route of elimination is via the urine, and the amount excreted in the urine should be directly proportional to the bioavailability. The use of a relative bioavailability factor calculated from urinary excretion data should provide a reasonable estimate of the relative absorption, assuming that there are no significant differences in elimination of absorbed arsenic following intravenous and oral exposures.

~~Oral-Water AAF~~

The dose-response values were based on an epidemiological study involving drinking water exposures. Therefore no adjustment for relative absorption differences is necessary as the absorption following oral water exposures is assumed to be the same as in the dose-response study. The AAF (oral-water), therefore, is 1.

~~Oral-Diet AAF~~

Due to a lack of data on the bioavailability of inorganic arsenic present in food (data do indicate that methylated forms of arsenic present in fish are well absorbed), GZA assumed that the absorption would be the same as when it is present in drinking water. Thus, the AAF (oral-diet) equals 98%/98% = 1. This assumption is consistent with MADEP, 1992.

~~Dermal-Soil AAF~~

Due to a lack of quantitative data on the dermal absorption of arsenic from soil, the default assumption for inorganics of 1%, recommended by the Michigan Department of Environmental Quality's Environmental Response Division Staff (1995), was used in calculating the AAF. Based upon the assumed absorption utilized by the MADEP (1992), which is supported by information presented by ATSDR (1997), it was assumed that the gastrointestinal absorption of arsenic in the Taiwanese population was virtually complete (98%). Thus, the AAF (oral-soil) for the soluble forms of inorganic arsenic is l%/98% = 0.01.

~~7/24/97, revised 10/5/99 Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this process is an absorbed dose. The oral RfD is based on administered dose. An absorption adjustment factor is necessary to convert the RfD to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment was made to the RfD in the risk calculation. The Dose-Response Absorption Correction Factor (DRACF) for dermal-water equals the absorption in the dose-response study. The RfD was multiplied by the DRACF whereas the CSF (which is in inverse units of dose) was divided by the DRACF to obtain absorbed dose based values. Using an assumed gastrointestinal absorption of 98% in the dose-response study (based on MADEP, 1992 and ATSDR, 1997), GZA calculated the DRACF, for use with both the oral RfD and CSF, as 0.98.

~~REFERENCES~~

~~ATSDR (Agency for Toxic Substances and Disease Registry). 1997. Toxicological Profile for Arsenic. CRC Press, Inc.~~

~~Bettley and O'Shea. 1975. The absorption of arsenic and its relation to carcinoma. British Journal of Dermatology, 92:563-568.~~

Buchet, J.P., Lauwerys, R. and Roels, H. 1981. Comparison of the urinary excretion of arsenic metabolites after a single oral dose of sodium arsenite, monomethyl arsonate or dimethyl arsinate in man. Int. Archives of Occupational Environmental Health. 48:71-79

~~Crecelius, E.A. 1977. Changes in the chemical speciation of arsenic following ingestion by man. Environmental Health Perspectives. 19:147-150.~~

Freeman, G.B., J.D. Johnson, J.M. Killinger, S.C. Liao, A.O. Davis, M.V. Ruby, R.L. Chaney, S.C. Lovre, and P.D. Bergstrom. 1993. Bioavailability of arsenic in soil impacted by smelter activities following oral administration in rabbits. Fundamental and Applied Toxicology, 21:83 88.

Groen, K., H. Vaessen, J. Kliest, J. De Boer, T. Van Ooik, A. Timmerman and R. Vlug. 1994. Bioavailability of inorganic arsenic from bog ore-containing soil in the dog. Environmental Health Perspectives, 102(2): 182-184.

~~7/24/97, revised 10/5/99 Mappes, R. 1977. [Experiments on excretion of arsenic in urine.] Int. Archives of Occupational Environmental Health. 40:267-272. (German)~~

Massachusetts Department of Environmental Protection (MADEP). 1992.Documentation of the Risk Assessment Shortform, Residential Scenario, Office of Research and Standards and the Bureau of Waste Site Cleanup, Policy #WSC/ORS-142-92, October 1992.

Michigan Department of Environmental Quality (MDEQ), Environmental Response Division (ERD) Staff. 1995. ERD Operational Memorandum #14 - Revision 2. Generic Remedial Action Plans Using Generic Industrial or Generic Commercial Cleanup Criteria and Other Requirements, June 6, 1995.

Tarn, G.K., Charbonneau, S.M. and Lacroix, G. 1979. Confirmation of inorganic arsenic and dimethylarsenic acid in urine and plasma of dog by ion-exchange and TLC. Bull. Environ. Contam. Toxicol. 21:371-374.

~~Texas Risk Reduction Program. May 14, 1996. Draft Appendix I Contaminant-Specific Approaches, p. 185-194. TNRCC.~~

~~Tseng W.P., H.M. Chu, S.W. How, J.M. Fong, C.S. LinandS. Yeh. 1968. Prevalence of skin cancer in an endemic area of chronic arsenicism in Taiwan. Journal of the National Cancer Institute, 40:453-46.~~

~~Tseng, W.P. 1977. Effects and dose-response relationships of skin cancer and blackfoot disease with arsenic. Environmental Health Perspectives, 19:109-119.~~

~~U.S. EPA. 1984. Health Effects Assessment for Arsenic. Office of Research and Development, Office of Emergency and Remedial Response. EPA/540/1-86-020.~~

~~M :\RSK_STND\HH\TOXICITY\AAF\AAF_TEX'r\ARSEN 1 .DOC~~

~~7/24/97, revised 10/5/99 BENZENE CAS#: 71432~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.05 mg/kg/day (4) Chronic Oral Reference Dose: 0.005 mg/kg/day (4)~~

~~Subchronic Inhalation Reference Concentration: 32 ng/m* (4) Chronic Inhalation Reference Concentration: 9 jug/m* (3)~~

~~Oral Cancer Potency Factor: 0.029 (mg/kg/day)*1 (1) Inhalation Cancer Unit Risk: 0.0000083 (Mg/m3)'1 (D~~

The oral absorption efficiency of pure benzene is estimated to be essentially 100% based on rabbit data in which 100% of an oral dose was either metabolized or exhaled unchanged (Sabourin et aL, 1986). The oral bioavailability of benzene was slightly but not significantly increased by adsorption to clay soil (Turkall, et ai, 1988). Human (Parke and Williams, 1953) and animal studies suggest that virtually all (100%) of an oral dose of benzene is absorbed.

~~Parka, D.V. and William*, R.T. (1963) Studio in Detoxuation. 49. The Metabolism of Benzene Containing f^CJ Bentene. Biooham. J. 64:231-238.~~

~~Sabourin, P., Chan. B, Headanon, R. Luciar, G. and Birnbaum, L. (1986) Effect of Dose on Absorption and Excretion of -^C-Benxene Administered Orally or by Inhalation. The ToxioolofUt. 6:163.~~

Turkall, R.M.. Skowronaki. G, G«rg»«, S., Van H*fn. S. and Abdal-Rahmen, ILS. (1988) Soil Adsorption Alters Kinetic* and Bioavailability of Bentene in Orally Exposed Male Rats. Arch. Environ. Contain. ToxiooL 17:159 164.

For dermal absorption, the controlling factor is contact time with the skin. One study (Susten et aL, 1990) estimated the non-occluded dermal absorption of benzene in hairless mice to be approximately 1% of the applied dose in 4 hour (or 6% in 24 hours), with volatilization occurring rapidly. In a second study (Susten et aL, 1985), the dermal absorption efficiency (non-occluded) of benzene was 1% of the applied dose in 2.5 hours (or 10% in 24 hours). In an occluded study (Lam and Bisgaard, 1989), the dermal absorption efficiency of 1,3-diaminobenzene was 100% of the applied dose in 24 hours for aqueous solutions and hydrogen peroxide-based solutions of this benzene analog. This suggests that the dermal absorption of benzene is highly dependent on whether an occluded or non-occluded study design is utilized. An average non-occluded dermal absorption efficiency (24 hour) of 10% was selected as a protective estimate from these studies while an occluded 24-hr dose would be absorbed 100%. The dermal bioavailability of benzene was slightly reduced by its adsorption to soil (Skowronski, et al., 1988). The

MA DEP, ORS & BWSC Documentation for the Riak AiMaonent ShortFonn t?««i4tff«i«1 Scenario venioni 1.6 a &. b - 10/92 C- 13 The oral and dermal subchronic reference dose for benzene was derived from an animal inhalation study. An absorption efficiency of 50% was used to calculate an absorbed dose. The RAFs for all scenarios are the absorption efficiencies of benzene by the route in question.

BENZENE RAF* Evaluation of Subohroolo Exposure*

~~SOIL SOIL WATER VEGETABLE moEsnoN DERMAL DIGESTION INGESTION~~

~~1 0.08 1 1~~

~~MA DEP. ORS & BWSC Documentation for the Rick Anotment ShortForm Recidential Scenario wwion* 1.6 a & b • 10/92 C- 15 BENZENE~~

The MADEP (1992) derived AAFs for evaluation of both the noncancer and cancer effects of benzene. However, MADEP did not derive dermal-water AAFs for this chemical. Thus, GZA has derived dermal-water AAFs for benzene, as described below.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral CSF for benzene is based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the CSF to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose- response criteria (multiplying the RfD, or dividing the CSF, by the percent absorption).

The oral CSF for benzene is based on an occupational study wherein human exposure was via inhalation. The U.S. EPA (1992) assumed that the fraction of the administered dose absorbed systemically via inhalation was the same as that via drinking water. Thus, no absorption adjustment was made to convert the inhalation dose to an ingestion dose. (This is in contrast to what MADEP indicated in the ShortForm. MADEP stated that EPA's CSF was based on an absorbed dose.) MADEP (1992) assumed that the oral absorption of benzene was complete (100%). Thus, GZA assumed that the absorption from the occupational study was 100%. Therefore, the AAF (dermal water) for use with the CSF equals 1/100% = 1.

The oral RfD for benzene was derived by MADEP (1992), assuming 50% gastrointestinal absorption. Therefore, no further adjustment is necessary. Since this RfD based on absorbed dose, it can be used directly with the absorbed dose calculated for the dermal-water exposure scenario. For consistency, an AAF (oral-water) of 1 was included in the spreadsheets. However, this resulted in no adjustment of the dose.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~U.S. EPA. 1992. Integrated Risk Information System (IRIS).~~

~~M:\RSK STND\HH\AAF TEXT\AAFS\BENZENE.DOC~~

~~Page 1 of 1 BENZO[a]ANTHRACENE GAS #i 56553~~

~~TOXICnY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.04 mg/kg/day (2b) Chronic Oral Reference Dose: 0.04 mg/kg/day (2f)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: 7.3 (mg/kg/day)"1 (Ig) Inhalation Cancer Unit Risk: Not Volatile~~

~~No specific quantitative information found on oral or dermal route. Assume same as B[a]P.~~

~~The oral and dermal cancer potency value for benzo[a]anthracene is based on a dietary study in which B[a]P was administered to mice. In this study, an applied dose was used.~~

~~BENZOfalANTHRACENE RAF* Evaluation of Caroinofenloity~~

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION 0.91 0.18 0.91 0.91 —————— . 1 ————— -0.2 0.91 0.91 0.91 0.91~~

~~The oral and dermal chronic reference dose for benzo[a]anthracene is based on a naphthalene oral gavage study conducted in rats, hi this study, an applied dose was used.~~

BENZOl.lANTHRACENE RAF* Evaluation of Chronic Exposure*

~~SOIL SOIL WATER VEGETABLE DIGESTION DERMAL DIGESTION INGESTION 0.91 0.18 0.91 0.91 —————— 0.91 ————— 0.18 .. ..._.. — 031 ————— 0.91 1 1 1 1~~

~~MA DEP, ORS & BWSC Documentation for th* Ruk ShortFonn T?MiH~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.04 mg/kg/day (2b) Chronic Oral Reference Dose: 0.04 mg/kg/day (2f)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: 7.3 (mg/kg/day)' (1) Inhalation Cancer Unit Risk: Not Volatile~~

The oral absorption of "C-labeled BfaJP, dissolved in peanut oil and administered by gavage, was studied in rats (Hecht et al, 1979). Absorption was determined by recovery of label in urine and feces. Unchanged B[a]P recovered in feces was estimated at 9% of the total dose, with all other fecal radioactivity (85% of applied dose) recovered as metabolites. This suggests an oral absorption efficiency of 91%.

~~Haeht, BJS., Grabomki, W. and Groth, K. (1979) Analysis of Feces for BfaJP After Consumption of Charcoal-Broiled Beef by Rait and Human*. Food Co*m«t. ToxiooL 17:223-227.~~

The percutaneous absorption of "C-B[a]P was studied in vivo in Swiss Webster mice (Sanders et al., 1986) and in Sprague-Dawley rats (Yang et al., 1986). Absorption was determined by analyzing radioactivity in urine, feces and tissues, and by analysis of residual label at the site of application. Dermal absorption efficiency was measured as 40% (in mice) and 6% (in rats) in 24 hrs. The higher value of 40% is selected as a protective estimate for human dermal exposure to pure compound. In vitro estimates are lower, ranging from 0.1%-15% in humans and animals (Kao et al., 1985; Kao et al., 1988) and are not considered applicable to human exposure. The in vivo percutaneous absorption of soil-adsorbed B[a]P was determined in rats by Yang et al. (1989). The range of absorbed doses was 1.3% - 9.2% depending on the amount of soil applied. More efficient absorption occurred at lower soil application rates. Wester et al. (1990) confirms a low absorption for soil-associated B[a]P in the rhesus monkey with a range of 9% - 18%. The upper limit of 18% is selected as a protective estimate for human exposure to B[a]P contaminated soil

~~Kao, J-. P*H. J. and Hainan, G. (1988) In Vitro Pereuianou* Absorption in Mouse Skin: Influence of Skin Appendage*. ToxiooL AppL PharmaooL 94: 93-103.~~

Kao, J JL. Pattanon. F.K, and Hall, J. (1985) Skin Penetration and Metabolism of Topically Applied Chemicals in Six Mammalian Species, Including Man: An In Vitro Study With Benzo(a)pyrene and Testosterone. ToxiooL AppL PhamaooL 81:602-518.

MA DEP. ORS & BWSC Documentation for tha RUk Aiaaamant ShortForm Raiiriantiil Scenario vcnion* 1.6 a & b - 10/92 C - 19 The oral and dermal chronic reference dose for benzo[a]pyrene is based on a naphthalene oral gavage study conducted in rats. In this study, an applied dose was used. The chronic inhalation reference concentration for benzo[a]pyrene is based on a naphthalene inhalation study in humans. In this study, an applied dose was used.

BENZO(a]PYRENERAF . Evaluation at Chiruni c Exposure*

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION 0.91 0.18 0.91 0.91 —————— 0.91 ... . . _ n in ————— 0.91 1 1 1 1~~

The oral and dermal subchronic reference dose for benzo[a]pyrene is based on a naphthalene oral gavage study conducted in rats. In this study, an applied dose was used. The subchronic inhalation reference concentration for benzo[a]pyrene is based on a naphthalene inhalation study in humans. In this study, an applied dose was used.

~~BENZOU1PYRENE RAF* EvftltiAtion of flubchranio Expoffum~~

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION 0.91 0.18 0.91 0.91 —————— 0.91 ————— 0.18 ———— 0.91 ,. _...,. ™ ft 01 1 1 1 1~~

~~MA DEP, ORS * BWSC Documentation for tin Rick Aiaeaament ShortForm Residential Scenario v»roona 1.6 a &. b - 10/92 C-21 BENZO[b]FLUORANTHENE CAS #i 205992~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.04 ing/kg/day (2b) Chronic Oral Reference Dose: 0.04 mg/kg/day (2f)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: 7.3 (mg/kg/day)"1 (Ig) Inhalation Cancer Unit Risk: Not Volatile~~

~~No specific quantitative information found on any route of exposure. Assume same as B[a]P.~~

~~The oral and dermal cancer potency value for benzo[b]fluoranthene is based on a dietary study in which B[a]P was administered to mice. In this study, an applied dose was used.~~

~~BENZO[b]FLUORANTHENE RAF« Evaluation of Cardnoffeniolty~~

~~SOIL SOIL WATER VEGETABLE DIGESTION DERMAL DIGESTION DIGESTION 0.91 0.18 0.91 0.91 —————— 1 .__ _ nt ———— 1 ———— 1 0.91 O.fll 0.91 0.91~~

~~The oral and dermal chronic reference dose for benzo[b]fluoranthene is based on a naphthalene oral gavage study conducted in rats. In this study, an applied dose was used.~~

BENZO(b]FLUOR.ANTHENERAF * Evaluation of Chironi o Exposure*

~~SOIL SOIL WATER VEGETABLE DIGESTION DERMAL DIGESTION DIGESTION 0.91 0.18 0.91 0.91 —————— 0.91 ———— 0.91 ———— 0.91 1 1 1 1~~

~~MA DEP, ORS XL BWSC Documentation for the Ri«k Ataeament ShortForm Residential Scenario venion* 1.6 a it b - 10/92 C-23 BENZO[g,h,i]PERYlENE CAS #: 191242~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.04 mg/kg/day (2b) Chronic Oral Reference Dose: 0.04 mg/kg/day (20~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: Not Volatile~~

~~No specific quantitative information found on any route of exposure. Assume same as BtalP.~~

~~The oral and dermal chronic reference dose for benzo[g,h,i]perylene is based on a naphthalene oral gavage study conducted in rats. In this study, an applied dose was used.~~

BENZOUMUIPERYLENE RAF* Evaluation of Chronlo Exposure*

~~son, son. WATER VEGETABLE DIGESTION DERMAL INGESTION INGESTION 0.91 0.18 0.91 0.91 —————— 0.91 __._. ... _ AID ———— 0.91 ————— 0.91 1 1 1 1~~

~~The oral and dermal subchronic reference dose for benzo[g,h,i]perylene is based on a naphthalene oral gavage study conducted in rats. In this study, an applied dose was used.~~

BENZOljvhJlPERYLENE RAF. Evaluation of Subohronio Exposure*

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION 0.91 0.18 0.91 0.91 —————— 0.91 ————— 0.18 ———— 0.91 ————— 0.91 1 1 1 1~~

~~MA DEP, ORS & BWSC Documentation for the Ri*k A*MMnvent ShortForm Brridtn+itl Scenario vanioni 1.6 a & b - 10/92 C-25 BIS(2-ETHYLHEXYL)PHTHAIATE CAS #: 117817~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.02 mg/kg/day (2) Chronic Oral Reference Dose: 0.02 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: 0.014 (mg/kg/day)"1 (1) Inhalation Cancer Unit Risk: Not Volatile~~

"C-DEHP appears to be efficiently absorbed from the gastrointestinal tract of the rat (Williams and Blanchfield, 1974). More than 90% of the radiolabel was excreted in urine. Fecal excretion was not quantified, suggesting oral absorption is probably dose to 100%. A second study (Chadwick et aL, 1982) demonstrated virtually complete absorption of "C DEHP administered in the diet to F344 rats.

Chadwick. M., Branfinan. AJC. and Sihrnr*. DM. (1982) Do»e-Dgndenc« of and Effect of Prior Erpo«ure on the Metabolism of DEHP Administered in the Diet to Rat*. Report to Chemical Manufacturer* A**ociation. Arthur D. Little. Inc.

~~William*, D.T. and Blanchfi*U, BJ. (1974) Retention, Excretion and Metabolism of DEHP Administered Orally to the Rat. BuIL Environ. Contain. ToxiooL 11:371-387.~~

DEHP appears to be poorly absorbed through skin (Elsisi et al., 1985). Only 7% of an occluded applied dose of MC-DEHP was absorbed through shaved rat skin, as evidenced by the appearance of radiolabel hi urine, feces and tissues. In a semi-occluded study (Elsisi et al., 1989), the shaved «lrin of F344 rats was exposed to 14C-phthalates in ethanol and covered with a perforated plastic cap. Radioactivity was monitored in urine and feces as an index of excretion. Bis(2-ethylhexyl)phthalate was poorly absorbed with less than 2% of the applied dose recovered in biological material (98% recovered at the site of application). The value of 2% is selected as the most appropriate since the experimental protocol most closely represents the human exposure scenario.

~~Eltiri. A. E., Carter, D. E. and Sip**, I. G. (1975). Dermal Absorption and Tissue Distribution ofPhlhalate Esters. Tonoolofist. 5:246.~~

~~aMj. E., Carter, D.E. and Sip**, I.G. (1989) Dermal Absorption of Phthalate Diesters in Rats. Fund. AppL ToxiooL 12:70-77.~~

~~MA OEP. ORS & BWSC Documentation for the RUk Ai*e*cment ShortForm Residential Scenario venion* 1.6 a & b - 10/92 C- 29 CADMIUM GAS #: 7440439~~

~~TOXICnY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.001 mg/kg/day (2e) Chronic Oral Reference Dose: 0.001 mg/kg/day (2d)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile ,^-- '"' Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: Not Volatile~~

Human studies have measured the oral absorption efficiency of cadmium compounds with a reported range of 1% - 7% (McLellan et aL, 1978; Shaikh and Smith, 1980). The range of reported oral absorption efficiencies in experimental animals is lower than in humans, from 0.5% - 3% (Engstrom and Nordberg, 1979; Moore et aL, 1973; Friberg et al., 1974). Higher doses tend to be absorbed less efficiently as do doses administered in food or milk, when compared to aqueous doses. Iron deficiency has been observed to increase the oral absorption of cadmium in humans and ?nimal« (ATSDR, 1989). Therefore, the upper- bounds of 7% (humans) and 3% (animals) are selected as protective estimates.

Agmey for Toxic SubrtaacM and Diaaaaa Regutry (ATSDR) (1989) Toxicological Profile for Cadmium. Agency for Tone Suhftancaa and Diaeaae Regutry. U.S. Public Health Service, pp. 46-49. EngBtrem. B. and Nordberg, GS. (1979) Dote-Dependencc of Gastrointestinal Absorption and Biological Half-Time of Cadmium in Mice. Toxicology 13:215-222.

~~Friberg, L* Piaeator, M., Nordberg, GJ". «"^ BJallatmn, T. (1974) C°^m"im in the Environment. 9n/l ad. Boca Baton. FL: CRC Preae.~~

~~McUUan. JJS^ Flanagan, P^. Chamberlain, if J. and VaBMrg, LJS. (1978) Measurement of Dietary Cadmium Absorption in Human*. J. ToxiooL Eaviroo. H«alth 4: 131-138.~~

~~Moor*. W., Stara, JJ, Crockar, W.C^ M«u~.fc,«> M. and Dti*. B, (1973) Comparison of^Cd Retention in Rats Following Different Route* of Administration. Environ. Raa, 6:473-478.~~

Shaikh. ZX and Smith. J.C. (1980) Metabolism of Orally Ingested Cadmium in Humans. In: HolmsUdt, B. «t aL. •da. M^chanimy of ToxicitT and "rlfttrd Evalhtf ticn. ^mat^r^*"1 * FlIiavMtr/MfTrth-HT^""^. pp< 669*574.

~~Cadmium is poorly absorbed by the dermal route (ATSDR, 1989). An upper-bound estimate of 1% is probably appropriate and protective for human exposure (see chromium).~~

~~for Tone SobctanoM and Diaaao Bagirtry (ATSDR) ( 1989) Toricoloacal Profile for Cadmium. Agency for Toxic Stibttanow and Diaaaa* Ragiftry, U.S. PubUc Haakh Service, pp. 46-49.~~

~~MA DEF. ORS & BWSC Documentation for the Riak Aaaeaament ShortForm R»«H»P»i«| Scenario weraion* 1.6 a tt b - 10/92 C-31 CADMIUM~~

The oral RfDs for cadmium of IE-3 and 5E-4 mg/kg-day for food and water exposures, respectively, are based on a toxicokinetic model that evaluated a large quantity of both human and animal data. The RfDs are based on the highest level of cadmium in the human renal cortex not associated with significant proteinuria (i.e., the critical effect). To derive the RfD, it was assumed that 5% of cadmium was absorbed from water, while only 2.5% was absorbed from the diet. Although these RfDs account for matrix-specific differences in absorption, they are applicable to administered media-specific doses (U.S. EPA, 1992).

GZA evaluated the AAFs derived by the MADEP (1992) for noncancer effects and determined that they were not derived correctly. The MADEP only considered the RfD derived for dietary exposure and, thus, failed to consider that the U.S. EPA-derived RfDs already accounted for media-specific absorption differences. MADEP calculated an AAF for drinking water exposure, for use with the cadmium RfD intended for dietary exposure, assuming that absorption from the diet is the same as that from drinking water. This assumption is inconsistent with EPA's derivation of two RfDs. GZA derived AAFs for all pathways. However, the AAFs for oral exposure to soil, food, and water are numerically the same as those presented by MADEP. The difference is in their derivation, and in their intended use (e.g., oral-water AAF is used with RfD for water).

~~Derivation of Oral-Diet AAF~~

As discussed above, the oral RfD (food) for cadmium of 0.001 mg/kg-day is based on a toxicokinetic model with an assumed dietary absorption rate of 2.5%. Thus, no further adjustment is necessary when it is used for dietary exposures. Therefore, the AAF (oral-diet) is 1.0 (assumes equal absorption for basis of RfD, and for exposure). This AAF is only applicable when the AAF for food is used.

~~Derivation of Oral-Water AAF~~

As discussed above, the oral RfD (water) for cadmium of 0.0003 mg/kg-day is based on a toxicokinetic model with an assumed absorption rate of cadmium from water, of 5%. Thus, no further adjustment is necessary for drinking water exposures. Therefore, the AAF (oral-water) is 1.0 (assumes equal absorption for basis of RfD, and for exposure). This AAF is only applicable when the RfD for water is used.

~~Derivation of Oral-Soil AAF~~

~~GZA conservatively assumed that the absorption of cadmium from soil is equal to that from the diet. Thus the AAF (oral-soil) = 1.0. This AAF is for use with the RfD developed for dietary exposure.~~

~~Page 1 of 2 Derivation of Dermal-Soil AAF~~

Dermal absorption of inorganics, especially from soil, is reported to be poor. Dermal absorption of cadmium is also expected to be poor, although no specific estimates were located. The MADEQE (1989) recommended a default dermal absorption (absolute) value of from 0.1% to 1% for inorganics. Thus, GZA calculated a dermal-soil relative absorption adjustment factor (AAF) of 0.1%/2.5% = 0.04 for the low end of the range and an AAF of l%/2.5% = 0.4 for the high end of the recommended absorption range. To be conservative, GZA used the AAF (dermal-soil) of 0.4 in this risk assessment. This AAF is intended for use with the oral RfD for cadmium derived for food (lE-3mg/kg-day).

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral RfD for cadmium is applicable to an administered dose, as discussed above. Therefore, an adjustment is necessary to convert the RfD to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose- response criteria (multiplying the RfD by the absorption). For cadmium, the AAF (dermal-water) is 11(2.5%) = 40. This AAF is for use with the RfD derived for the diet. If the oral RfD derived for water is used, then the AAF (dermal-water) is l/(5%) = 20. Care must be taken to ensure that the appropriate AAF is used with the corresponding RfD.

~~REFERENCES~~

MADEQE (Massachusetts Department of Environmental Quality Engineering). 1989. Guidance for Disposal Site Risk Characterization and Related Phase H Activities - In Support of the Massachusetts Contingency Plan. MADEQE Office of Research and Standards.

~~U.S. EPA. 1992. Integrated Risk Information System (IRIS).~~

~~M:\RSK_STND\HH\AAF_TEXT\AAFS\CADM1UM.DOC~~

~~Page 2 of 2 CARBON TETRACHLORIDE CAS#: 56235~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.007 mg/kg/day (2) Chronic Oral Reference Dose: 0.0007 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: 430 M£/m* (3a) Chronic Inhalation Reference Concentration: 430 Mg/m9 (3)~~

~~Oral Cancer Potency Factor: 0.13 (mg/kg/day)'1 (1) Inhalation Cancer Unit Risk: 0.000015 (pg/mY (1)~~

The oral absorption efficiency in nnimnl« is extensive. Studies have reported that 80-85% of an administered dose is recovered in expired air (Marchand et al, 1970; Paul and Rubinstein, 1963). This indicates that GI absorption is probably close to 100% since CC1< is metabolized with metabolites appearing in urine and feces.

~~C., McLaan, S. and Plaa, G.L. (1970) The Effect of SKF626A on the Distribution of Carbon Tetraehloride in Rats. J. Ph«rm»nol. Exp. Therap. 714:232-238.~~

~~Paul. B-B. and Rubnutain, D. (1963) MctabolUm of Carbon Tetraehloride and Chloroform by the Rat. J. PharmaooL Exp. Tberap. 141:141-148.~~

No studies were located containing quantitative information on the dermal absorption efficiency of carbon tetrachloride. Assume that the dermal absorption is similar to that of other volatile organics such as benzene whose dermal absorption efficiency has been estimated to be 10% of a non-occluded applied dose in 24 hours.

~~The oral and dermal cancer potency value for carbon tetrachloride is based on a gavage study in rodents. This toxirity value is based on applied dose.~~

~~CARBON TETRAiCHLORID E RAF* Evaluation of <3aittiaog«niclt y~~

~~SOIL son, WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION 1 0.1 1 1 —————— 1 ————— -0.1 ———— 1 — 1 1 1 1 1~~

~~MA DEP, ORS & BWSC Documentation for th« Rick Ajimrment ShortForm RMtdcntial Scenario reniou 1.6 a it b - 10/92 C-33 CHLOROBENZENE CAS#: 108907~~

~~TOXTCITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.2 mg/kg/day (2) Chronic Oral Reference Dose: 0.02 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: 200 Mg/ni3 (2) Chronic Inhalation Reference Concentration: 20 Mg/ms (2)~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: NC~~

The oral absorption efficiency of chlorobenzene has been reported to range from at least 18% in rats to at least 31% in humans (Lindsay-Smith et al., 1972; Ogata and Shimada, 1983). These estimates are probably low since the studies failed to quantitate exhaled compounds. A more conservative estimate may be 100%, based on its structural similarity to benzene.

~~Lindcay-Snuta, JSL, Shaw, B-AJ. and FoulkM, D.M. (1972) Mechanisms of Mammalian Hydraxylation: Some Novel Metabolites of Chlorobenxene. Xenoblotioc 2:215-226.~~

~~Ogata, M. and Shimada, Y. (1983) Differences in Urinary Monachlorobenzene Metabolites Between Rats and Humans. Int. Arch. Oooup. Environ. Health 63:61-57.~~

~~No studies were located regarding the dermal absorption of chlorobenzene. Assume it to be similar to benzene (10% non-occluded, 24 hours).~~

~~The oral and dermal chronic reference dose for chlorobenzene is based on an oral (capsule) study in dogs. In this study, an applied dose was used.~~

CHLOR013ENZEN E Evaluation of Ctironi c Exposure*

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL DIGESTION INGESTION 1 0.1 1 1 —————— . i ————— -0.1 ———— I ———— 1 1 1 1 1~~

~~MA DEP, ORS & BWSC Documentation for the Ruk AMeument ShortForm R*ti4«rti*l Scenario version* 1.6 a & b - 10/92 C-35 CHLOROBENZENE~~

The MADEP (1992) assumed 100% gastrointestinal absorption of VOCs when developing AAFs. No consideration was given to possible matrix attenuation affects when the VOC was administered in the diet versus drinking water. GZA, therefore, assumed 100% gastrointestinal absorption of chlorobenzene in the dose-response study wherein it was administered to dogs in capsule form.

~~Derivation of Oral-Soil. Oral-Water, and Oral-Diet AAFs~~

The MADEP (1992) typically assumed 100% gastrointestinal absorption for the VOCs, when specific data were not available. The oral RfD for chlorobenzene is based on an oral study, thus, GZA assumed 100% absorption in this study. It was further assumed that the absorption was 100%, when administered in soil, water and the diet. Therefore, the AAF (oral-soil), the AAF (oral-water), and the AAF (oral-diet) are all equal to 100%/100% = 1.

~~Derivation of Dermal-Soil AAFs~~

The MADEQE (1989) recommended a default range of absorption estimates for VOCs in soil of 10% to 25%. GZA has conservatively assumed that the dermal absorption of chlorobenzene from soil is 25%. Thus, the AAF (dermal-soil) for this chemical equals (the absorption from soil)/(absorption in the dose-response study) which equals 25%/100% = 0.25.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral RfD for chlorobenzene is based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the RfD to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose-response criteria (multiplying the RfD by the percent absorption). For chlorobenzene the AAF (dermal-water) is 1/(100%) = 1.0.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

MADEQE (Massachusetts Department of Environmental Quality Engineering). 1989. Guidance for Disposal Site Risk Characterization and Related Phase II Activities - In Support of the Massachusetts Contingency Plan. MADEQE Office of Research and Standards.

~~U.S. EPA. 1992. Integrated Risk Information System (IRIS). M:\RSK_STND\HH\AAF_TEXT\AAFS\CHLORBEN.DOC Page 1 of 1 CHLOROFORM CAS#: 67663~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.01 mg/kg/day (2) Chronic Oral Reference Dose: 0.01 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: 660 fig/m* (3a) Chronic Inhalation Reference Concentration: 660 Mg/m* (3)~~

~~Oral Cancer Potency Factor: 0.0061 (mg/kg/day)'' (1) Inhalation Cancer Unit Risk: 0.000023 (jxg/mV (D~~

~~Oral absorption efficiency of chloroform in humans and animals is essentially 100% (Fry et aL, 1972; Brown et at, 1974; Taylor et aL, 1974).~~

~~Brown, D3L, Langlqr, P-F-. Smith, D. and Taylor. D.C. (1974) Metabolism of Chloroform. I. The Metabolism of^C- Chloroform by Different Species. Xanobiotioa. 4:151-163.~~

~~Fry, B J., Taylor, T. and Hathaway, D.E. (1972) Pulmonary Elimination of Chloroform and its Metabolites in Man. Arofa. IaC Pharmaoodyn, 196:98-11.~~

~~Taylor, D.C., Brown, D.M., Ruble, R. and Langiey, PJ. (1974) Metabolism of Chloroform. H. A Sex Difference in the Metabolism of ^C^hloroform in Mice. XanobioUoa. 4:165-174.~~

Dermal absorption of chloroform is rapid and quite large (329 umol/min/cm2) across mouse skin (Tsurata, 1975). This suggests that an occluded dose would be 100% absorbed with a non-occluded dose being absorbed less efficiently (perhaps 10% as with benzene) due to rapid volatilization.

~~Tcurata, H. (1975) Percutaneous Absorption of Organic Solvents. I. Comparative Study of the in Vivo Percutaneous Absorption of Chlorinated Solvents in Mice. Ind. Health. 13:227-236.~~

~~MA DEP, ORS it BW8C Documentation for th* Riak Aiaairnmnt ShortForm Reaidantial Scenario wniocs 1.6 a & b - 10/92 C-37 CHLOROFORM~~

The MADEP (1992) assumed 100% gastrointestinal absorption of chloroform when developing AAFs. The MADEP, has not, however, derived dermal-water AAFs for this compound. Thus, GZA has derived a dermal-water AAF for chloroform, assuming 100% gastrointestinal absorption of chloroform in the oral drinking water study upon which the oral/dermal dose-response value is based.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral CSF for chloroform is based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the CSF to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose- response criteria (dividing the CSF by the percent absorption). For chloroform, the AAF (dermal water) is 17(100%) = 1.0.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~M:\RSK_STNEAHHV^AF_TEXT\AAFS\CHLORFRM.DOC~~

~~Page 1 of 1 CHRYSENE GAS #i 218019~~

~~TOXICnY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.04 mg/kg/day (2b) Chronic Oral Reference Dose: 0.04 mg/kg/day (2f)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: 7.3 (mg/kg/day)"1 (Ig) Inhalation Cancer Unit Risk: Not Volatile~~

~~No specific quantitative information found on the absorption via the oral or dermal route. Assume same as B[a]P.~~

~~The oral and dermal cancer potency value for chrysene is based on a dietary study in which B[a]P was administered to mice. In this study, an applied dose was used.~~

~~CHRYSENE RAFi Evaluation of Caroinogenioity~~

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION 0.91 0.18 0.91 0.91 —————— . 1 ————— 1 ———— 1 0.91 0.91 0.91 0.91~~

~~The oral and dermal chronic reference dose for chrysene is based on a naphthalene oral gavage study conducted in rats. In this study, an applied dose was used.~~

~~CHRYSETTCRAF i Evaluation of Chironi o ExpocuTM~~

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION~~

~~0.91 0.18 0.91 0.91 —————— 0.91 _ /\ 10 ————— 0.91 ———— 0.91 1 i 1 1~~

~~MA DEP. ORS & BWSC Documentation for UM Risk i"iiimiiiniil ShortForm R»«i/u«»;al Scenario venion* 1.6 a & b - 10/92 C-41 1,1-DICHLOROETHANE GAS #: 75343~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 1 mg/kg/day (2) Chronic Oral Reference Dose: 0.1 mg/kg/day (2)~~

~~Subchronic Inhalation Reference Concentration: 5000 Mg/ma (2) Chronic Inhalation Reference Concentration: 500 HS/m3 (2)~~

~~Oral Cancer Potency Factor: Not Quantified Inhalation Cancer Unit Risk: Not Quantified~~

No specific studies were located quantifying the respiratory absorption efficiency of 1,1 dichloroethane. The blood/air partitioning coefficient of 1,1-dichloroethane is approximately 4 times less than that of 1,2-dichloroethane suggesting less efficient pulmonary absorption of 1,1-dichloroethane than 1,2-dichloroethane. However, assume the 75% inhalation efficiency of 1,2-dichloroethylene is applicable.

~~No specific studies were located quantifying the oral absorption efficiency of 1,1 dichloroethane. Assume it to be the same as 1,2-dichloroethane (100%).~~

No specific studies were located quantifying the dermal absorption efficiency of 1,1 dichloroethane. Assume it to be similar to that of other volatile compounds (benzene) whose dermal absorption efficiency may reach 10% of a non-occluded applied dose in 24 hours.

~~The oral and dermal chronic reference dose for 1,1-dichloroethane is based on an inhalation study conducted in rats. In this study, an applied dose was used.~~

U-DCA RAF* Evaluation of Chronic Exposure*

~~SOIL son. WATER VEGETABLE DIGESTION DERMAL mcEsnoN mCESTION 1 0.1 1 1 —————— . u - 1.3 m 1 ? 0.75 0.76 0.76 0.76~~

~~MA DEP, ORS & BWSC Documentation for the Riik Atummant ShortFonn Scenario vercton* 1.6 a & b - 10/92 C-47 1,1-DICHLOROETHANE~~

The MADEP (1992) derived AAFs for ingestion of soil, water and food, and for dermal exposure to soil. The MADEP, has not however, derived dermal-water AAFs for this compound. Thus, GZA has derived a dermal-water AAF for this chemical. MADEP assumed 75% absorption in the inhalation dose-response study used to derive the chronic oral RfD of l.OE-01 mg/kg-day. GZA assumed the same absorption when deriving the dermal-water AAF.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral CSF for 1,1-dichloroethane is based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the CSF to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose- response criteria (dividing the CSF by the percent absorption). For 1,1-dichloroethane, the AAF (dermal-water) is l/(75%) = 1.33.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~M:\RSK_STND\HH\AAF_TEXT\AAFS\11DCA.DOC~~

~~Page 1 of 1 1,1-DICHLOROETHYLENE CAS #: 75354~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subcfaronic Oral Reference Dose: 0.009 nig/kg/day (2) Chronic Oral Reference Dose: 0.009 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: 5 /x&/ni3 (3a) Chronic Inhalation Reference Concentration: 5 n%/ra (3)~~

~~Oral Cancer Potency Facton 0.6 (mg/kg/day)'' (1) Inhalation Cancer Unit Risk: 0.00005 (jig/mV (1)~~

Since 1,1-dichloroethylene is a small organic molecule with chemical and physical properties similar to the lipid soluble anaesthetics, it is expected to penetrate the pulmonary epithelium rapidly and efficiently. An inhalation absorption efficiency of 98% is derived from metabolic excretion data of inhaled radiolabeled 1,1-dichloroethylene data in the rat (McKenna et ai, 1977).

~~J^ Watanab*, P.G. and Gthring, P J. (1977) Pharmacoiunetics of Vinylidene Chloride in the Rat. Environ. Health Pcnpw*. 21:99-105.~~

The oral absorption of 1,1-dichloroethylene in animals has been demonstrated to be rapid and essentially complete (100%). (Reichert et al, 1979; Jones and Hathaway, 1978; McKenna et aL, 1978; Putcha et aL, 1986).

MrKenna, M-T. Zampte. JJL, Madrid, E.O., Braun, WJL and Gehring, P J. (1978) Metabolism and PharmacokinetK Profile of Vinylidene Chloride in Rats Following Oral Administration. ToxiooL AppL PhannaooL 45:821-835.

~~Rafehart, D., WWIMT, HE. «ad M«Ukr, M. (1979) Molecular Mechanism of 1,1-Dichloroethylene Toxidty: Excreted Metabolite* Rental Different Pathway* of Rtactwe Intermediate*. Aroh. TmdooL 42: 159-169.~~

~~JOBM, PJL and Hathawmy, DJ1 (1978) Difference* in Metabolism of Vinylidene Chloride Between Mice and Rats. Br. J. Caimr. 37:411-417.~~

~~Puteha. I_ Bruchnw, J.V. and D'Sojn, R. (1986) ToxicoJiinetic* and BioatxiilabilUy of Oral and Intravenous 1,1 Dichloroethylene. Fund. Appi ToxiooL 6:240-250.~~

No studies were located regarding the dermal absorption of 1,1-dichloroethylene. Due to its chemical and physical properties, dermal absorption is expected to be 100% of an occluded applied dose or 10% of a non-occluded applied dose (same as benzene).

~~MA DEP. ORS & BWSC Documentation for th« RUk AMcument ShortForm Residential Scenario vemon» 1.6 a A b - 10/92 C -61 1,1-DICHLOROETHYLENE~~

The MADEP (1992) derived AAFs for ingestion exposure to soil, water and food and for dermal exposure to soil, assuming 100% gastrointestinal absorption of 1,1-dichloroethylene in the oral drinking water study upon which the chronic oral RfD of 9.0E-03 mg/kg-day was based, and 98% absorption in the mouse inhalation study upon which the oral CSF of 6.0E-1 (mg/kg-day)"1 was based. MADEP has not derived dermal-water AAFs for this compound. GZA, therefore, derived dermal-water AAFs for use with the oral RfD and CSF, using the same absorption assumptions as those used by the MADEP.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral RfD and CSF for 1,1 -dichloroethene are based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the RfD and CSF to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose-response criteria (multiplying the RfD or dividing the CSF by the percent absorption). For 1,1-dichloroethene, the AAF (dermal-water) is 1/(100%) = 1.0 for use with the RfD, and 1/98% = 1.02 for use with the CSF.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~U.S. EPA. 1992. Integrated Risk Information System (IRIS).~~

~~M:\RSK STND\HH\AAF_TEXT^AAFS\11DCE.DOC~~

~~Page 1 of 1 1,2-DICHLOROETHYLENE CAS #: 156605~~

~~TOXTCITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

Subchronic Oral Reference Dose: 0.2 mg/kg/day (2) Chronic Oral Reference Dose: 0.02 mg/kg/day (1) ». Subchronic Inhalation Reference Concentration: 1100 ng/m (3a) Chronic Inhalation Reference Concentration: 1100 /xg/m3 (3)

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: NC~~

No studies were located addressing the oral or dermal absorption efficiency of 1,2 dichloroethylene. Assume behavior nimibtr to 1,1-dichloroethylene and benzene (100% oral and 10% non-occluded dermal absorption efficiencies).

~~The oral and dermal chronic reference dose for 1,2-dichloroeth.ylene is based on an oral drinking water study conducted in mice. In this study, an applied dose was used.~~

U3-DC1ZRAF * Evaluation of Clironi c Exposure*

~~son, SOIL WATER VEGETABLE mcEsnoN DERMAL INGESTION INGESTION i 0.1 1 1 ———— - i ———— - 1 ————— - 1 i 1 1 1~~

~~The oral and dermal subchronic reference dose for 1,2-dichloroethylene is based on an oral drinking water study conducted in mice. In this study, an applied dose was used.~~

U-DCE RAF* Evaluation of Subchronio Exposure*

~~son, son, WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION 1 0.1 1 1 —————— 1 ————— 0.1 ———— 1 — \ 1 1 1 1~~

~~MA DEP, ORS & BWSC Documentation for to* Riik AcMtoncnt ShortForm R*«iH»t«tiai Scenario venion* 1.6 a & b - 10/92 C-53 ETHYLBENZENE CAS #: 100414~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Sub chronic Oral Reference Dose: 1 mg/kg/day (2) Chronic Oral Reference Dose: 0.1 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: 1000/ig/m9 (2) Chronic Inhalation Reference Concentration: 1000Mg/m9 (1)~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: NC~~

Animal studies indicate that ethylbenzene is quickly and efficiently absorbed by the oral route. Estimates range from 72%-92% in one study (El Masry et aL, 1956) to 84% in a second study (Climie et aL, 1983). A value of 100% is selected since these studies underestimated oral absorption by not controlling for respiratory volatilization following oral absorption.

~~ClimM. U.G., HuUon. DM. and Stoydin, G. (1983) The Metabolism of Ethylbentene Hydroperoxide in the Rot. X0nobioUoa 13:611-618.~~

~~El Maary, AJM., Smith, J.N. and William*. R.T. (195«) The Metabolism of Alkyloenxenes: n-Propylbenzene and n- Butylbenxene with Further Observation* on Ethylbenxtne. Bioohem. J. 64:50-56.~~

Absorption of pure liquid ethylbenzene and aqueous solutions containing ethylbenzene through human flkin is rapid and substantial (20-30 mg/cmVhr) (Gromiec and Piotrowski, 1984). Occluded doses could potentially be 100% absorbed. The non-occluded dermal absorption of ethylbenzene has been measured to be 3.4% of an applied dose in 4 hours (Susten et aL, 1990). This calculates to a 24 hour dermal absorption efficiency of 20%.

~~SucUn. AJ3., NiemaUr, R.W. and Simon, 3D. (1990) In Vivo Percutaneous Absorption Studies of Volatile Organic Solvents in Hairless Mice U. Toluene, Ethylbentene and Aniline. J. AppL ToxiooL 10:217-225.~~

~~GromiK, JJ>. and PiotrowaJd, J.K. (1984). Urinary Mandelic Acid as an Exposure Test for Ethylbenzene. Int. Arch. Oooup, Environ. Health 55:61-72.~~

~~MA DEF, ORS &. BWSC Documentation for the Ruk Aiieetment ShortForm Retidential Scenario venioni 1.6 a & b - 10/92 C-55 ETHYLBENZENE~~

The MADEP (1992) assumed 100% gastrointestinal absorption of ethylbenzene when developing AAFs. GZA, therefore, assumed 100% gastrointestinal absorption of ethylbenzene in the dose- response study. The MADEP derived AAFs for ethylbenzene for the oral route, but not for the dermal-water AAFs exposure route. Thus, GZA has derived dermal-water AAFs for ethylbenzene.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral RfD for ethylbenzene is based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the RfD to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose-response criteria (multiplying the RfD by the percent absorption). For ethylbenzene, the AAF (dermal-water) is 1/(100%)= 1.0.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~U.S. EPA. 1992. Integrated Risk Information System (IRIS).~~

~~M:\RSK STND\HH\AAF TEXT\AAFS\ETHYLJBEN.DOC~~

~~Page 1 of 1 LEAD GAS #: 7439921~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.00075 mg/kg/day (4) Chronic Oral Reference Dose: 0.00075 mg/kg/day (4)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: Not Quantified Inhalation Cancer Unit Risk: Not Volatile~~

The oral absorption efficiency of lead compounds in adult experimental animnlg and adult humans ranges from 1% - 15% (EPA, 1986; Hammond, 1982; Chamberlain et al, 1978). Young humans and experimental animals absorb lead with higher efficiency, estimates ranging up to 60% (Hammond, 1982; Kostial et al., 1971, 1978; Forbes and Reina, 1972). The estimate of 50% is considered as being a conservative upper-bound for humans and experimental animnlg,

~~Chamberlain. A.. Hard. C. and Little, MJ. (1978) Invartigationj into Lead from Motor Vehicle*. Harwell. U.K.: United Kingdom Atomic Energy Authority. R«p. No. AERE-9198.~~

U£. Environmental Protection Agency (EPA) (1986) Air Quality Criteria for Lead. June 1986 and Addendum. September. 1986. Reeearch Triangle Park. NC: Office of Reeearch and Development, Office of Health and Environmental Aeaeeament, Environmental Criteria and Aueeonent Office, EPA. EPA 600/8-83-018F.

~~Forbee, GJJ. and Reina, J.C. (1972) Effect of Age on Gastrointestinal Absorption (Ft, Sr, Pb) in the Rat. J. Nutr. 102:647452.~~

Hammnnd, PS. (1982) Metabolism of Lead. In: Chuolm. JJ. and OUara. D .M.. ed*. Lead Abeorotion in Children: Management. diflK*! and Environmental Atpecte. Baltimore, MD: Urban and Schwarzenberg, pp. 11-20.

~~Knetiel, 1C, Simonovie, J. and Pieonic, M. (1971) Lead Absorption from the Intestine in Newborn Rats. Nature 233:664-667.~~

The dermal absorption efficiency for lead as lead acetate has been reported to be 0.3% (12 hours) of an applied dose in humans, or 0.6% in 24 hours (Moore et al., 1980). Organic lead compounds are absorbed more rapidly and extensively than inorganic lead compounds.

Moore. Mi, Meredith. P.A., Wateon. W.S., Stunner, DJ., Taylor, MJL and Goldberg, A. (1980) The Percutaneous Absorption of Lead-203 in Humans from Cosmetic Preparations Containing Lead Acetate, As Assessed by Whole-Body Counting and Other Techniques. Food. CoameC ToxiooL 18:399-405.

~~MA DEP, ORS & BWSC Documentation for the Riik Asceument ShortForm Residential Scenario venion* 1.6 a & b - 10/92 C -65 LEAD~~

The oral dose-response value for lead of 7.5E-4 mg/kg-day was calculated from a Treatment Technology Action Level (TTAL) of 15 ppb set for drinking water at the tap. The gastrointestinal absorption of lead ranges from 8% (Hammond, 1992) to 15% (Chamberlain, et al., 1978) for adults. For children, absorption of lead from the diet has been reported to be higher, with estimates ranging from 40 to 50% (ATSDR, 1989). When calculating the dose-response value, the MADEP assumed a 50% absorption of lead from drinking water. Thus, this value is based on an absorbed dose.

~~Derivation of Dermal-Water AAF~~

~~REFERENCES~~

~~ATSDR (Agency for Toxic Substances and Disease Registry). 1989. Toxicological Profile for Lead. ATSDR, Centers for Disease Control, Atlanta, GA.~~

Chamberlain, A.C., MJ. Heard, P. Little, D. Newton, A.C. Wells and R.D. Wiffen. 1978. Investigations into lead from motor vehicles. United Kingdom Atomic Energy Authority, Harwell, United Kingdom. Report No. AERE-R9198. As cited in ATSDR, 1989.

Hammond, B. 1982. Metabolism of Lead. In: J.J. Chisolm and D.M. O'Hara (eds). Lead Absorption in Children: Management. Clinical and Environmental Aspects. Urban and Schwarzenberg. Baltimore, MD. As cited in ATSDR, 1989.

~~M:\RSK_STND\HH\AAF_TEXTAAFS\LEAD.DOC~~

~~Page 1 of 1 MERCURY CAS #: 7439976~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.0003 mg/kg/day (2) Chronic Oral Reference Dose: 0.0003 mg/kg/day (2)~~

~~Subchronic Inhalation Reference Concentration: 0.3 Hg/m* (2) Chronic Inhalation Reference Concentration: 0.3 MB/m3 (2)~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: NC~~

~~MERCURY (elemental)~~

Oral absorption of metallic mercury has been estimated to be, at most, 0.10% (Friberg and Nordberg, 1973). The oral absorption efficiency of 0.01% in humans and laboratory animals is most frequently cited in the literature (Owen, 1990). The value of 0.1% is suggested as a conservative upper limit for human exposure.

Fribcrg. L-, Nordberg, F. (1973) Inorganic Mercury • A Taxicolngical and Epidemiological Appraisal. In: Miller, M.W., Clarkaon, T.W., «d. M«fcurv. Mercurial* and Mercaptapj. Springfield, Dlinou: Charla* C. Thomaj, pp. 5-22.

~~Own. B.A. (1990) Literature-Derived Abtorption Coefficient* for 39 Chemicals Via Oral and Inhalation Route* of Exposure. lUfuL TmdooL Ph«rm«ooL 11:237-262.~~

Hursh et at (1989) report maximum systemic mercury as a fraction of initial amounts of. mercury on the «Hn The average percentage absorbed (from data obtained from 5 human volunteers) can be calculated as 40% of the free mercury deposited on the skin. Assuming that 10% of the mercury in soil could be extracted and available for dermal absorption (Landa, 1978), a dermal absorption factor of 0.04 is obtained.

Hur«h. J£., Clarkaon, T.W., Mil**, EJ., «t «L (1989) Percutaneous Absorption of Mercury Vapor by Man. Arch. Environ. Health 44:120-127. Landa, EJt (1978) The Retention of Metallic Mercury Vapor by Soils. G*ooh«m. Coimochlm. Act*. 42:1407-1411.

~~MA DEP, ORS & BWSC Documentation for the Risk AMcument ShortForm Evidential Scenario vantoni 1.6 a It b - 10/92 C-67 MERCURY~~

The oral RfD for inorganic mercury of 3E-4 mg/kg-day is based on three subchronic rat studies in which rats were dosed with mercuric chloride by either gavage or by subcutaneous injection. The U.S. EPA converted the subcutaneously injected dose to an oral dose by assuming 7% gastrointestinal absorption of mercuric chloride. The assumption of a 7% gastrointestinal absorption was based on a paper by Rahola et al. (1973). A later publication (Miettinen, 1973) by one of the authors of the study indicates that the gastrointestinal absorption in this study was 15%, not 7%. The MADEP (1992) also recommends a conservative estimate of gastrointestinal absorption of inorganic mercury of 15%. Thus, this value was assumed for the dose-response studies. The RfD is based on an administered dose of mercuric chloride in aqueous solution via gavage.

This RfD and accompanying AAFs are intended for use with water, soils and sediments containing unspeciated mercury, or in situations where speciation indicates the presence of inorganic mercury. This RfD and accompanying AAFs should not be used for risk assessments in which exposure to mercury taken up by fish is a concern. In such a case, the RfD for methyl mercury should be used and AAFs specific for methyl mercury should be derived.

~~Derivation of Oral-Water and Oral-Diet AAFs~~

The RfD for inorganic mercury is based on ingestion of aqueous solutions of mercuric chloride. GZA assumed that the gastrointestinal absorption of mercury from water and the diet is the same. Thus, the oral-water and oral-diet AAFs are both 1.

~~Derivation of Oral-Soil AAF~~

~~The MADEP (1992) estimated that ingestion of mercury in soil is absorbed at about one half the extent of mercury in water. Thus, GZA calculated an AAF (oral-soil) of 0.5.~~

~~Derivation of Dermal-Soil AAF~~

Absorption data specific to inorganic mercury are presented in the text, however. These data were used below to derive AAFs for inorganic mercury. The MADEP estimated that 6.5% of a dermal dose of inorganic mercury adsorbed to soil would be absorbed. MADEP also estimated that up to 15% of an oral dose of inorganic mercury could be absorbed from the gastrointestinal tract. From this estimate, GZA derived an AAF (dermal-soil) of 6.5%/15% = 0.43.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this process is an absorbed dose. The oral RfD is based on administered dose. In order to use Page 1 of 2 consistent dose-response criteria across all exposure pathways, the adjustment was made to the absorbed dermal dose in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to multiplying the RfD by the percent absorption in the applicable dose-response study. Using an assumed gastrointestinal absorption of 15% in the dose-response study, GZA calculated an AAF (dermal water) of 1/15% = 6.7 for use with the oral RfD.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation of the Risk Assessment ShortForm-Residential Scenario.~~

Meittinen, J.K. 1973. Absorption and Elimination of Dietary Mercury (Hg2+) and Methylmercury in Man. In: Miller, M.W. and T.W. Clarkson (eds). Mercury, Mercurials and Mercaptens. C.C. Thomas, Springfield.

~~Rahola, T., T. Hattula, T. Korolainen and J.K. Meittinen. 1973. Elimination of free and protein- bound ionic mercury 203 Hg2+ in man. Annals of Clinical Research, 5:214-219.~~

~~U.S. EPA. 1992. Integrated Risk Information System (IRIS).~~

~~M:\RSK_STND\HHWAF_TEXTW\AFS\MERCURY.DOC~~

~~Page 2 of 2 MERCURY (organic)~~

The oral absorption efficiency of methylmercury is reported as 95% (Aberg et al., 1969; Owen, 1990). Other forms of organic mercury may be orally absorbed less efficiently, with estimates ranging down to 80% (Fitzhugh et al., 1950).

~~Owra, B. A. (1990) Literature-Derived Absorption Coefficient* for 39 Chemical* Via Oral and Inhalation Route* of Exposure. R*fuL TmdooL PharmaooL 11:237-252.~~

~~Abarg, B., FIITTMB It, Falk, U., «t «L (1969) Metabolism of Methylmercury (Hg ) Compounds in Man: Excretion and Distribution. Arab. Environ. Health 19:478-484.~~

~~Fitzhugh, O.G, N«Uon, A-A., Laug, EJ5., et aL (1950) Chronic Oral Toricitirt of Mercuri-phenyl and Mercuric Salt*. Aron, Ind. Hyg. Oooup. Med. 2:433-442~~

Methyl mercury (in water) applied to the skin of guinea pigs at two dose levels resulted in 3.4% and 4.5% of the applied dose being absorbed (Skog and Wahlberg, 1964). Given the lipophilicity of organomercurials, an absorption value of 4.5% was chosen.

Skog, £. and WahUxirg, J.E. (1964) A Comparative Investigation of the PercutaneoujA.bsorotion of Metal Compounds in the Guinea Pig by Means of the Radioactive Isotopes; *%>, &Co. -Zn, •U2!vV, •U52Cd, — Hg. J. Invent. DermatoL 43:187-192.

~~MA DEP, OES &. BWSC Dooimentation for the Rick Aaieument Short-Form Residential Scenario version* 1.6 a &. b - 10/92 C-69 METHYL ETHYL KETONE GAS #: 78933~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Sub chronic Oral Reference Dose: 0.5 mg/kg/day (2) Chronic Oral Reference Dose: 0.05 mg/kg/day (2)~~

~~Subchronic Inhalation Reference Concentration: 3000 Mg/m9 (2) Chronic Inhalation Reference Concentration: 1000 ng/tn3 (1)~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: NC~~

No information was located to quantitatively determine the oral or dermal absorption efficiency of methyl ethyl ketone. Assume a 100% absorption efficiency by the oral route and a 10% dermal absorption efficiency (non-occluded, 24 hour).

The oral and dermal chronic reference dose for methyl ethyl ketone is based on an inhalation study conducted in rats. An absorption efficiency of 50% was used to calculate an absorbed dose. The RAFs to be used for all exposure pathways are the absorption efficiencies of methyl ethyl ketone by the route in question.

~~METHYL ETHYL KETONE RAF* Evaluation of Chronic Expocura~~

~~SOIL SOIL WATER VEGETABLE INGE3TION DERMAL mcEsnoN DIGESTION~~

~~1 0.1 1 1~~

~~MA DEP, ORS & BWSC Documentation for th* Ri«k AcMumant ShortFonn Raiidantial Scenario wnion< 1.6 • & b • 10/92 C - 73 2-BUTANONE (A.K.A. METHYL ETHYL KETONE)~~

The MADEP (1992) has derived AAFs for 2-butanone (MEK) for the oral route and for dermal exposure to soil, but has not derived dermal-water AAFs for this compound. Thus, GZA has derived dermal-water AAFs for MEK. The MADEP (1992) assumed 100% gastrointestinal absorption of MEK when developing other AAFs. GZA, therefore, assumed 100% gastrointestinal absorption of MEK in the dose-response study upon which the chronic RfD of 5.0E-2 mg/kg-day was based.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral RfD for MEK is based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the RfD to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose-response criteria (multiplying the RfD by the percent absorption). For MEK, the AAF (dermal-water) is 1/(100%) = 1.0.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~U.S. EPA. 1992. Integrated Risk Information System (IRIS).~~

~~M:\RSK_STND\HH\AAF TEXT\AAFS\MEK.DOC~~

~~Page 1 of 1 NAPHTHALENE and CAS #: 91203 2-METHYLNAPHTHALENE GAS #: 91576 TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.04 mg/kg/day (2) Chronic Oral Reference Dose: 0.04 mg/kg/day (2)~~

~~Subchronic Inhalation Reference Concentration: 71 ng/m* (3a) Chronic Inhalation Reference Concentration: 71 jig/m3 (3b)~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: NC~~

~~Oral absorption, based on fecal recovery of metabolites, has been demonstrated to be essentially 100% in tbe rat (Cbang, 1943).~~

~~Chang, L H. (1943) The Fecal Excretion ofPolyeyclic Hydrocarbons Following Their Administration to the Rat. J. BioL Cbem. 151:93-102.~~

No information exists quantifying the dermal absorption efficiency of naphthalene. However, toxicity has been documented following exposure by this suggesting absorption has occurred. Assume 10% to represent the dermal absorption efficiency (same as non ocdude, 24 hour benzene value).

~~The oral and dermal chronic reference dose for naphthalene and 2-methylnaphthalene is based on an oral gavage study conducted in rats. In this study, an applied dose was used.~~

NAPHTHALENE It 2-METHYLNAPHTHALENE RAF. Evaluation of Chronic Exposure*

~~SOIL son. WATER VEGETABLE DIGESTION DERMAL " mcEsnoN INGESTION 1 0.1 i i —————— . 1 ——— - i 1 1 i i~~

~~MA DEP. ORS & BWSC Documentation for the Risk Aue**ment ShortForm Residential Scenario veniotu 1.6 a & b - 10/92 C-77 NICKEL GAS #: 7440020~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.02 mg/kg/day (2) Chronic Oral Reference Dose: 0.02 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: Not Volatile~~

Human and animal studies indicate that the oral absorption efficiency of nickel from food or water ranges from 1%- 10% (Christensen and Lagesson, 1981; Schroeder et al., 1974; Tedeschi and Sunderman, 1956; Ambrose et al., 1976; Nielsen et al., 1986; Ho and Furst, 1973). The upper-bound of 10% is selected as a protective estimate of the oral absorption efficiency of nickel.

~~ChrwUawn. OJJ. tad LageMon, V. (1981) Nickel Concentrations of Blood and Urine After Oral Administration. Ann. CUa, Lab. SoL 11:119-125.~~

~~Schroeder, H-A-. Mitchener. M. and Nacon. AJ». (1974) Life-Term Effects of Nickel in Rats: Survival, Tumors, Interaction* with Trace Elements and Tissue Levels. J. Nutr. 104:239-243.~~

~~TedMchi, R-E. and Sunderaan, F.W. (1957) Nickel Poisoning V. The Metabolism of Nickel Under Normal Conditions and After Exposure to Nickel CarbonyL Ann. Ind. Health 16:486-488.~~

~~AmbroM, AJ4., Lanon, P.3., Borzelleca, JJL and Hraaigar, GJt (1976) Long Term Toacologic Assessment of Nickel in Rats and Dogs. J. Food. SoL TeohnoL 13:181-187.~~

Nialatn, GJ}M Anderecn, O, Jen*e&, M. and Grandjean, P. (1986) Gastrointestinal Nickel Absorption. A New Experimental Model Using the Qamma-EmiUing Isotope &Ni. In; The Sixth UOEH Int. Symp.. 3rd COMTOX on Bio- and Toricoidnetia of MetaU. Kitakyuihu City, Japan, Int. Conf. Clin. Chant., Chain. Toxicol., July 27-31.

~~Ho., W. and Funt, A. (1973) Nickel Excretion by Rats Following a Single Treatment. Proo. We*C PharmaooL Soc. 16:245-248.~~

Aqueous solutions of various forms of nickel can penetrate occluded human skin with absorption efficiencies ranging from 55% - 77%, most absorption occurring in the first 24 hours (Norgaard, 1955). It is unclear whether the nickel was absorbed into the deep layers of the skin or into the bloodstream. Studies in guinea pigs (Lloyd, 1980) demonstrated that much of the nickel absorbed remained in the skin, primarily in the jighly keratinized areas, while approximately 0.005 - 0.51 % of the applied nickel chloride was recovered from the blood and urine. A more recent study on excised human skin (Fullerton et al., 1986) indicated that 3.5% of an applied dose of nickel chloride

~~MA DEP, ORS it BWSC Documentation for the RUk As*e*«ment ShortForm Residential Scenario version* 1.6 a £ b - 10/92 C-79 NICKEL~~

The oral RfD value for nickel of 2E-2 mg/kg-day is based on a dietary study of nickel sulfate in rats. The RfD is based on administered dose. Human and animal studies indicate that the oral absorption of nickel from the diet or water ranges from 1% to 10% (Christiansen and Lagesson, 1981; Schroeder et al., 1974; Tedeschi and Sunderman, 1956; Ambrose et al., 1976; Ho and Furst, 1973; MADEP, 1992). MADEP chose the upperbound estimate of 10% as a protective estimate of the oral absorption efficiency of nickel. This is a conservative estimate of absorption of nickel from the diet, which is likely to be less than that from drinking water. However, in order to be consistent with MADEP, GZA assumed that the absorption of nickel from the diet in the dose-response study was 10%.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral RfD for nickel is based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the RfD to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals 1/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose-response criteria (multiplying the RfD by the percent absorption). For nickel, the AAF (dermal-water) is 1/(10%) = 10.

~~REFERENCES~~

~~Ambrose, A.M., P.S. Larson, J.R. Borzelleca and G.R. Hennigar. 1976. Long term lexicological assessment of nickel in rats and dogs. Journal of Food Science and Technology, 13:181-187.~~

~~Christiansen, O.B. and V. Lagesson. 1981. Nickel concentrations of blood and urine after oral administration. Annals of Clinical Laboratory Science, 11:119-125.~~

~~Ho, W. and A. Furst. 1973. Nickel excretion by rats following a single treatment. Proc. West Pharmacol. Soc. 16:245-248.~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

Nielson, G.D., O. Anderson, M. Jensen and P. Grandjean. 1986. Gastrointestinal nickel absorption. A new experimental model using the gamma-emitting isotope 7Ni. In: The Sixth UOEH Int. Symp., 3rd COMTOX on Bio- and Toxicokinetics of Metals. Kitakyushu City, Japan, Page 1 of 2 Int. Conf. Clin. Chem., Chem. Toxicol., July 27-31.

~~Schroeder, H.A., M. Mitchener, and A.P. Nason. 1974. Life-term effects of nickel in rats: Survival, tumors, interactions with trace elements and tissue levels. Journal of Nutrition, 104:239 243.~~

~~Tedeschi, R.E. and F.W. Sunderman. 1957. Nickel poisoning V. The metabolism of nickel under normal conditions and after exposure to nickel carbonyl. Archives of Industrial Health, 16:486 488.~~

~~M ARS K_STND\HH\AAF_TEX1\AAFS\NICKEL.DOC~~

~~Page 2 of 2 PHENANTHRENE CAS#: 85018~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.04 mg/kg/day (2b) Chronic Oral Reference Dose: 0.04 mg/kg/day (2f)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: NC~~

~~No specific quantitative information found on the absorption via the oral or dermal route. Assume same as B[a]P.~~

~~The oral and dermal chronic reference dose for phenanthrene is based on a naphthalene oral gavage study in rats, hi this study, an applied dose was used.~~

PHENANTHRENE RAF* Evaluation of Chronic Exposure*

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION~~

~~0.91 0.18 0.91 0.91 —————— 0.91 • AIR - 0.91 1 i 1 1~~

~~The oral and dermal subchronic reference dose for phenanthrene is based on a naphthalene oral gavage study conducted in rats, hi this study, an applied dose was used.~~

PHENANTHRENE RAFi Evaluation of Subohrooio Exposure*

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION 0.91 0.18 0.91 0.91 —————— 0.91 ———— 0.91 ———— 0.91 1 1 1 1~~

~~MA DEP, ORS & BWSC Documentation for the Ri»k Ai*e**ment ShortFonn Residential Scenario venioni 1.6 « & b - 10/92 C-81 TETRACHLOROETHYLENE GAS #: 127184~~

~~TOXTCITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.1 mg/kg/day (2) Chronic Oral Reference Dose: 0.01 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: 4600 Hg/ia* (3a) Chronic Inhalation Reference Concentration: 4600 p.g/m3 (3)~~

~~Oral Cancer Potency Factor: 0.052 (mg/kg/day)' (2h) Inhalation Cancer Unit Risk: 0.0.0000058 (jig/mY (2h)~~

Results from several animal studies (Pegg et aL, 1979; Schumann et al., 1980; Frantz and Wantanabe, 1983) indicate that tetrachloroethylene is rapidly and virtually completely absorbed following oral administration.

~~Frantz, S.W. and Wantanabe, P.G. (1983) Tetraehloroethylene: Balance and Tissue Distribution in Male Sprague- Dawley Rats by Drinking Water Administration. ToxiooL AppL PharmaooL 69:66-72.~~

~~P«gg, D.G., Zeznple, J.A., Braun, W.H. and Watanaba, P.G. (1979) Disposition of (^OTetrachloroethylene Following Oral and Inhalation Exposure in Rats. ToxiooL AppL PharmaooL 51:465-474.~~

Schumann, A.M., Quart, J.F., and Watanabe, P.G. (1980) The Pharmaookinetics and Macromoleular Interactions of Perchloroethylene in Mice and Rats as Related to Oneogeniaty. ToxiooL AppL PharmacoL 55:207-219.

Dermal absorption of tetrachloroethylene appears to be poor (0.24 mg/cm2/hr) (Tsuruta, 1975). Therefore, the absorption efficiency by the dermal route in a non-occluded exposure probably does not exceed 10% (see benzene).

~~Tcuruta, H. (1975) Percutaneous absorption of organic solvents. I. Comparative study of + 6 percutaneous absorption of chlorinated solvents in mice. Ind. Health 13:227-236.~~

~~The oral and dermal cancer potency value for tetrachloroethylene is based on a gavage study in mice. This toxicity value is not based on absorbed dose.~~

~~TETRACHLOROETHYLENE RAF* Evaluation of Carcinogeniolty~~

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION 1 0.1 1 1 —————— = 1 ———— 0.1 ———— 1 •• 1 1 1 1 1~~

~~MA DEP, ORS & BWSC Documentation for the Risk Aueument ShortForm Evidential Scenario venions 1.6 a & b • 10/92 C-93 THALLIUM CAS#: 7440280~~

~~TOXTCITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.0007 mg/kg/day (2) Chronic Oral Reference Dose: 0.00007 mg/kg/day (2)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: Not Volatile~~

Limited human data suggest that most of an oral dose of thallium (applied as thallium nitrate) is absorbed from the gastrointestinal tract (Barclay et al., 1953). Animal studies suggest that thallium is completely absorbed when ingested. A single trace dose of thallium204 (as thallium nitrate) was administered orally to rats (Lie et al., 1960). The body burden of thallium204, as percent dose, decreased with a single exponential function which extrapolated to 100% at zero time. It was concluded that thallium is completely absorbed from the gastrointestinal tract. A 100% oral absorption efficiency is therefore assumed for thallium compounds.

~~Barclay, RJC. Pencock, W.C.. Kanofty, D-A- (1953) Distribution and Excretion of Radioactive Thallium in the Chick Embryo. Rat and Man. J. PtvarmaooL Exp. Ther. 107:178-187.~~

~~Lie, R., Thoma*, R. and Scott. J. (1960) The Distribution and Excretion of Thallium— in the Rat, with Suggested MFC's and a Bio-Assay Procedure. Health Phys. 2:334-340.~~

No quantitative studies were located regarding the dermal absorption of thallium in humans or animals. Assume a dermal absorption efficiency of 1% as a conservative upper- bound estimate (see chromium).

~~MA DEP, ORS &. BWSC Documentation for the RUk Aiuesjment ShortForm Residential Scenario vemons 1.6 a & b - 10/92 C-95 THALLIUM~~

~~The oral RfD for thallium of 7E-5 mg/kg-day is based on a rat study in which thallium sulfate was administered by gavage. The MADEP (1992) assumed that thallium was completely absorbed in this study.~~

~~Derivation of Dermal-Water AAF~~

The methodology for estimating risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this process is an absorbed dose. The oral RfD is based on administered dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment was made to the absorbed dermal dose in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to multiplying the RfD by the percent absorption in the applicable dose-response study. The AAF (dermal-water) for use with the RfD is 1/100% = 1.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation of the Risk Assessment ShortForm-Residential Scenario.~~

~~M:\RSK_STND\HHUAF_TEX-nAAFS\THALLIUM.DOC~~

~~Page 1 of 1 TOLUENE CAS #: 108883 TOXZCITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 2 mg/kg/day (2) Chronic Oral Reference Dose: 0.2 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: 2000 Hg/m3 (2) Chronic Inhalation Reference Concentration: 400 jxg/m3 (1)~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: NC~~

Rabbit studies indicate that essentially 100% of an oral dose of toluene is either excreted as metabolites or exhaled unchanged, implying 100% absorption efficiency by the oral route (Smith et al., 1954; El Masry et al., 1956). Oral absorption efficiency of soil- adsorbed toluene was not changed from that of the pure compound even though absorption was delayed in time by the presence of sandy soil (Turkall et al., in press).

El Many. A.M., Smith, J.N. and Williams, R.T. (1956) Studies in Detoxication 69. The Metabolism of Alkylbentenes: n-Propylbentene and n-Butylbenzene with Further Observations on Ethylbenzene. Biochem. J. 64:60-56.

~~Smith, J.N., Smithies, RJi. and William*, R.T. (1954) Studies in Detoxication 65. The Metabolism of Alkylbentenes. Bioohem. J. 56:317-325.~~

~~Turkall, RJ4., Skowronski, G-A. and Abdel-Rahmen, M.S. (in press) Differences in Kinetics of Pun and Soil- Adsorbed Toluene in Orally Exposed Male Rats. Arch, Environ. Contain. TojtiooL~~

The dermal absorption of toluene has been measured to be approximately 2% of the applied dose in 4 hours, or 12% in 24 hours (Susten et al., 1990). This study allowed for volatilization of toluene, rapidly decreasing the actual applied dose. In a second study (Skowronski, et al., 1989), volatilization loss was minimised to less than 10% of the applied dose by occlusion. The dermal absorption efficiency was estimated to be approximately 90% with volatilization loss accounting for the remainder of the dose (essentially 100% dermal absorption). The estimate was based on recovery of radioactivity in urine, feces and expired air. The dermal absorption of toluene was unaffected by its adsorption to clay or sandy soils. The 24 hour non-occluded value (12%) is assumed to be the most appropriate and protective for human exposure.

Susten. A.S., Niem«i«r, R.W. and Simon, S.D. (1990) In Vivo Percutaneous Absorption Studies of Volatile Organic Solvents in Hairless Mice II. Toluene, Ethylbenzene and Aniline. J. AppL Toxicol. 10:217-225.

~~Skowronski, G.A.. Turkall. R.M. and Abdel-Rahman, M.S. (1989) Effects of Soil on Percutaneous Absorption of Toluene in Male Rats. J. ToxiooL Environ. Health 26:373-384.~~

~~MA DEP. ORS & BWSC Documentation for the Risk Assessment Short Form Residential Scenario versions 1.6 a & b • 10/92 C - 97 TOLUENE~~

The MADEP (1992) assumed 100% gastrointestinal absorption of toluene when developing AAFs. GZA, therefore, assumed 100% gastrointestinal absorption of toluene in the dose-response study. The MADEP has derived AAFs for toluene for the oral route, but not for the dermal-water exposure route. Thus, GZA has derived dermal-water AAFs for toluene.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral RfD for toluene is based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the RfD to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose-response criteria (multiplying the RfD by the percent absorption). For toluene, the AAF (dermal-water) is 1/(100%) = 1.0.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~U.S. EPA. 1992. Integrated Risk Information System (IRIS).~~

~~M:\RSK STND\HH\AAF TEXT\AAFS\TOUJENE.DOC~~

~~Page 1 of 1 1,1,1-TRICHLOROETHANE GAS #: 71556~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.9 mg/kg/day (2) Chronic Oral Reference Dose: 0.09 mg/kg/day (2)~~

~~Subchronic Inhalation Reference Concentration: 10,000 /zg/m3 (2) Chronic Inhalation Reference Concentration: 1000 Mg/m3 (2)~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: NC~~

No studies were located containing information to quantitate the oral absorption efficiency of 1,1,1-trichloroethane. However, it can be assumed to be rapidly and completely absorbed in a manner similar to other chlorinated volatiles.

No studies were located containing information to quantitate the dermal absorption efficiency of 1,1,1-trichloroethane. Assume a 10% absorption efficiency (non-occluded, 24 hour), comparable to other volatile compounds.

The oral and dermal chronic reference dose for 1,1,1-trichloroethane is based on an inhalation study conducted in guinea pigs. An absorption efficiency of 30% was used to calculate an absorbed dose. The RAFs to be used for all exposure pathways are the absorption efficiencies of 1,1,1-trichloroethane by the route in question.

l.l.l-TRICHLOROETHANE RAF. Evaluation of Chronic Exposure*

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION~~

~~1 0.1 1 1~~

~~MA DEP. ORS &. BWSC Documentation for the RUk As*e«*ment ShortForm Residential Scenario venions 1.6 a & b - 10/92 C-99 1,1,1-TRICHLOROETHANE~~

The MADEP (1992) derived AAFs for ingestion exposure to soil, water and food and for dermal exposure to soil. MADEP has not derived dermal-water AAFs for any of the VOCs. The chronic oral RfD of 9.0E-02 mg/kg-day is based on an absorbed dose in an inhalation study, wherein U.S. EPA assumed 30% absorption. GZA derived a dermal-water AAF for this chemical as described below.

~~Derivation of Dermal-Water AAF~~

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~U.S. EPA. 1992. Integrated Risk Information System (IRIS).~~

~~M:\RSK_STND\HH\AAF_TEXT\AAFS\L 1 ITCA.DOC~~

~~Page 1 of 1 TRICHLOROETHYLENE CAS#: 79016~~

~~TOXTCITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.02 mg/kg/day (4) Chronic Oral Reference Dose: 0.002 mg/kg/day (4)~~

~~Subchronic Inhalation Reference Concentration: 180 ng/m3 (3a) Chronic Inhalation Reference Concentration: 180 Mg/m3 (3)~~

~~Oral Cancer Potency Factor: 0.011 (mg/kg/day)"1 (2h) Inhalation Cancer Unit Risk: 0.0000017 (jig/mY (2h)~~

Oral absorption studies in experimental animals indicate that trichloroethylene is extensively absorbed by the oral route. Absorption efficiency was measured as 91% - 98% of an applied oral dose (Prout et al., 1985; Dekant et al., 1984) determined as radioactivity in expired air and urine. Radioactivity in the carcass was not determined. Absorption, therefore, is assumed to be complete.

~~Dekant, W., Metzler, M. and Heojchler. D. ( 1984) Hovel Metabolites of Trichloroethylene Through Dechlorination Reactions in Rats, Mice and Humans. Bioohem. Pharmaool. 33:2021-2027.~~

~~Prout, M.S., Provan, W.M. and Gr*«n, T. (1985) Specie* Differences in Response to Trichloroethylene. ToxiooL AppL PharmaooL 79:389-400.~~

No studies were located regarding the dermal absorption efficiency of trichloroethylene. Assume 10% dermal absorption (non-occluded, 24 hour) based on physical and chemical properties similar to the other volatile compounds.

~~The oral and dermal cancer potency value for trichloroethylene is based on a gavage study in mice. This toxicity value is not based on absorbed dose.~~

~~TRICHLOROETHYLENE RAF* Evaluation of Caroinog«nioity~~

~~SOIL SOIL WATER VEGETABLE INGESTION DERMAL INGESTION INGESTION 1 0.1 1 1 —————— = 1 ———— •= 0.1 m j 1 1 1 1~~

~~MA DEP. ORS & BWSC Documentation for the Risk Assessment Short Form Residential Scenario versions 1.6 a & b - 10/92 C - 101 TRICHLOROETHYLENE~~

The MADEP (1992) assumed 100% gastrointestinal absorption of trichloroethylene when developing AAFs. The MADEP, has not, however, derived dermal-water AAFs for any of the VOCs. Thus, GZA has derived a dermal-water AAF for trichloroethylene, assuming 100% gastrointestinal absorption of trichloroethylene in the gavage study upon which the oral/dermal dose-response value is based.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral CSF for trichloroethylene is based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the CSF to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose- response criteria (dividing the CSF by the percent absorption). For trichloroethylene, the AAF (dermal-water) is 17(100%) = 1.0.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~M:\RSK_STND\HH\AAF_TEXT\AAFS\TCE.DOC~~

~~Page 1 of 1 VINYL CHLORIDE GAS #: 75014~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.001 mg/kg/day (4) Chronic Oral Reference Dose: 0.001 mg/kg/day (4)~~

~~Subchronic Inhalation Reference Concentration: 17 Mg/m3 (3a) Chronic Inhalation Reference Concentration: 17 HS/m* (3)~~

~~Oral Cancer Potency Factor: 1.9 (mg/kg/day)"1 (2) Inhalation Cancer Unit Risk: 0.000084 (/xg/m3)"' (2)~~

In young human volunteers administered vinyl chloride monomer for 6 hours, an average retention of 42% was estimated. It was not reported whether steady state had been achieved. Maximum retention was achieved at 15 minutes and retention declined after 30 minutes after which it increased to a relatively constant value. The percentage retained seemed to be independent of the concentration inhaled. A range of reported inhalation absorption efficiencies is 40% - 98%, 64% being suggested as representative and protective (Owen, 1990)

~~Owen. B.A- ( 1990) Literature-Derived Absorption Coefficients for 39 Chemicals Via Oral and Inhalation Routes of Exposure. ReguL ToxiooL PharmaooL 11:237-252.~~

~~Krajewiki. J., Oobecki, M. and Gromiec, J. (1980) Retention of Vinyl Chloride in the Human Lung. Br. J. Ind. Med. 37:373-374.~~

Rats were administered single gavage doses of uC-vinyl chloride hi corn oil and radioactivity levels excreted in expired air, urine and feces, as well as the amount remaining in the carcass, were measured at 72 hours. 0.47-2.39% of the administered dose was recovered in the feces indicating that absorption was nearly complete. Total recovery ranged from 82.3-91.3% suggesting a substantial loss of radioactivity. An oral absorption efficiency of 98% is assumed to be protective for human exposure.

~~Watanabe, P.O.. McGowan, CJL and Gearing. PJ. (1976) Fate of l^C] Vinyl Chloride After Single Oral Administration. ToxiooL AppL PhamaooL. 36:339-352.~~

Two rhesus monkeys exposed from the neck down to 14C-vinyl chloride vapor were found to have dermal absorptions of 0.031% and 0.023%, respectively. The dermal absorption of neat vinyl chloride or soil contaminated with vinyl chloride would be expected to be greater due to increased time of dermal contact. Therefore, the dermal absorption efficiency is assumed to be similar to the 10% estimate derived for other volatile compounds (non-occluded, 24 hour).

~~MA DEP. ORS & BWSC Documentation for the Risk Assessment ShortForm Residential Scenario versions 1.6 a & b - 10/92 C- 103 VINYL CHLORIDE~~

The MADEP (1992) derived AAFs for vinyl chloride assuming that the oral CSF was based on an inhalation study. This is incorrect. The oral CSF of 1.9 (mg/kg-day)"1 is based on a dietary study in rats (U.S. EPA, 1992). After a review of the literature, MADEP (1992) assumed that the oral absorption efficiency of vinyl chloride is 98%. GZA derived revised AAFs for use with the oral CSF, assuming that the CSF was based upon an oral study and that the absorption in this study was 98%. This is the absorption MADEP assumed in the noncancer dose-response study. However, it is not clear why this value was used, since this is the upper end of the range (40-98%) reported for inhalation studies. For oral studies, MADEP (1992) reported an absorption range of 82.3-91.3%. To be conservative, and to be consistent with MADEP's assumed absorption in the noncancer dose- response study, GZA assumed 98% absorption in the oral cancer dose-response study.

~~Derivation of Oral-Soil, Oral-Water and Oral-Diet AAFs~~

GZA assumed that the oral absorption of vinyl chloride in the oral cancer dose-response study was 98%. GZA also assumed that the oral absorption by humans of vinyl chloride in soil, water or the diet is also 98%. Thus, the AAFs (oral-soil, oral-water, and oral-diet) are all equal to 98%/98% = 1.00.

~~Derivation of Dermal-Soil AAF~~

~~The MADEP (1992) assumed that the dermal absorption of vinyl chloride in soil was about 10% of the applied dose. The AAF (dermal-soil), therefore, equals 10%/98% = 0.1.~~

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral RfDs and CSFs for vinyl chloride are based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the RfDs and CSFs to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose-response criteria (multiplying the RfD, or dividing the CSF, by the percent absorption).

The oral CSF and oral RfD for vinyl chloride are based on an oral dietary study in rats. The MADEP (1992) and GZA assumed that the oral absorption from these studies was 98%. Therefore, for vinyl chloride, the AAF (dermal-water) is equal to 1/98% = 1.02.

~~Page 1 of 2 REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~U.S. EPA, 1992. Health Effects Assessment Summary Tables (HEAST).~~

~~M:\RSK STND\HH\AAF TEXT\AAFS\VINYLCHUDOC~~

~~Page 2 of 2 XYLENES CAS #: 1330207~~

~~TOXICITY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 4 mg/kg/day (2) Chronic Oral Reference Dose: 2 mg/kg/day (1)~~

~~Subchronic Inhalation Reference Concentration: 300 ^g/m3 (2) Chronic Inhalation Reference Concentration: 300 ng/m3 (2)~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: NC~~

The oral absorption efficiency of 100% is estimated from limited excretion data specifying that more than 98% of an oral dose of p-xylene was absorbed and excreted as metabolites in urine and expired air of the rabbit.

~~Bray, H.C.. Humphric, B.C. and Thorpe, W.V. (1949) Metabolism of Derivatives of Toluene 3. o-,m- and p-Xylene*. Bioohem. J. 45:241-244.~~

The dermal absorption efficiency of m-xylene, adsorbed to either sand or clay, has been demonstrated to be essentially 100% of an occluded dose when applied to the shaved skin of male rats (Skowronski et al., 1990). Absorption was rapid with 50% of the dose absorbed in less than 1 hour. Soil adsorption slightly delayed the dermal absorption of m-xylene relative to pure parent compound. The dermal absorption of soil adsorbed mixed xylene isomers is assumed to behave as m-xylene. No information exists on non- occluded dermal uptake, however, it would be assumed to be similar to that of its structural analog, toluene (12% in 24 hours).

~~Skowronjki, Gj\_. Turkail. R.M.. Kadry, A.R.M. and Abdal-Rahmen, M.S. (1990) Effects of soil on the dermal buxwailability of m-xylene in male rats.~~

~~MA DEP. ORS & BWSC Documentation for the Risk Aaseument Shonform Residential Scenario versions 1.6 a & b - 10/92 C - 105 XYLENE~~

The MADEP (1992) assumed 100% gastrointestinal absorption of xylene when developing AAFs. GZA, therefore, assumed 100% gastrointestinal absorption of xylene in the dose-response study. The MADEP has derived AAFs for xylene for the oral route, but has not derived dermal-water AAFs for any of the VOCs. Thus, GZA has derived dermal-water AAFs for xylene.

~~Derivation of Dermal-Water AAF~~

The methodology for estimating the risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this procedure is an absorbed dose. The oral RfD for xylene is based on an administered (exposure) dose. Therefore, an adjustment is necessary to convert the RfD to be based on an absorbed dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment is made to the absorbed dermal dose in the exposure assessment, rather than to the dose-response criteria. This approach also enables all absorption adjustments (all pathways) to be performed in the exposure assessment section. The AAF for dermal-water equals 1/(absorption in the dose-response study), which is mathematically equivalent to adjusting the dose-response criteria (multiplying the RfD by the percent absorption). For xylene, the AAF (dermal-water) is 1/(100%) = 1.0.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation for the Residential Short Form.~~

~~U.S. EPA. 1992. Integrated Risk Information System (IRIS).~~

~~M :\RSK_STND\HH\AAF_TEXT\AAFS\XYUENE.DOC~~

~~Page 1 of 1 ZINC CAS #: 7440666~~

~~TOXICrTY INFORMATION FROM THE RESIDENTIAL SHORTFORM:~~

~~Subchronic Oral Reference Dose: 0.2 mg/kg/day (2) Chronic Oral Reference Dose: 0.2 mg/kg/day (2)~~

~~Subchronic Inhalation Reference Concentration: Not Volatile Chronic Inhalation Reference Concentration: Not Volatile~~

~~Oral Cancer Potency Factor: NC Inhalation Cancer Unit Risk: Not Volatile~~

The absorption of zinc in humans from the diet has been determined to range from 22% 46% (Sandstrom et al., 1987) with the upper limit of the range suggested as an appropriate estimate. Zinc is more efficiently absorbed from drinking water with absorption estimates ranging up to 58% (Dinsmore et al., 1985; Farah et al., 1984; Valberg et al., 1985).

~~Dimmer*, W., Calendar, M.E., McMasMr, D.. Todd, S J. and Love, A-H.G. (1985) Zinc Absorption in Alcoholics Using Zinc-65. Digest. 32:238-242.~~

~~Farah. DA., Hall, M J.. Mills, PJR. and Russell, RJ. (1984) Effect of Wheat Bran on Zinc Absorption. Human Nutr. Clin.Nutr. 380:433-441.~~

Sandstrora, B., Davuon. L., Kivisto, B., Hasselbland, C. and Cedarbland, A. (1987) The Effect of Vegetables and Beet Fibre on the Absorption of Zinc in Humans from Composite Meals. Brit. J. Nutr. 58:49-57.

~~Valberg, L.S., Flanagan, PS.., Ghent, C.N. and Chemberlai, MJ. (1985) Zinc Absorption and Leukocyte Zinc in Alcoholic and Nonalcoholic Cirrhosis. Digest. Dim. SoL 30:329-333.~~

~~No studies were located quantitatively describing the dermal absorption of zinc compounds. Assume a dermal absorption efficiency of 1% as a conservative upper-bound estimate (see chromium).~~

~~MA DEP, ORS & BWSC Documentation for the Risk Assessment ShortForm Residential Scenario version* 1.6 a & b - 10/92 C - 107 ZINC~~

The oral RfD for zinc of 2E-1 mg/kg-day is based on a human study with zinc sulfate in the diet. The MADEP (1992) assumed that the gastrointestinal absorption of zinc from the diet in the human subjects was 46%, the upper end of the range (22-46%) reported by Sandstrom et al. (1987).

~~Derivation of Dermal-Water AAF~~

The methodology for estimating risks posed by dermal exposure to chemicals of concern in water utilizes a chemical-specific permeability constant that estimates the rate at which the chemical passes into and through the skin from an aqueous solution. By definition, the dose estimated by this process is an absorbed dose. The oral RfD is based on administered dose. In order to use consistent dose-response criteria across all exposure pathways, the adjustment was made to the absorbed dermal dose in the exposure assessment section. The AAF for dermal-water equals l/(absorption in the dose-response study), which is mathematically equivalent to multiplying the RfD by the percent absorption in the applicable dose-response study. The AAF (dermal-water) for use with the RfD is 1/46% = 2.2.

~~REFERENCES~~

~~MADEP (Massachusetts Department of Environmental Protection). 1992. Documentation of the Risk Assessment ShortForm-Residential Scenario.~~

Sandstrom, B., L. Davidson, B. Kivisto, C. Hasselbland and A. Cederbland. 1987. The effect of vegetables and beet fibre on the absorption of zinc in humans from composite meals. British Journal of Nutrition, 58:49-57.

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~~Page 1 of 1~~