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CDM FEDERAL PROGRAMS CORPORATION 7^. CO o
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FINAL RISK ASSESSMENT PART I - HUMAN HEALTH ASSESSMENT PART II - ENVIRONMENTAL ASSESSMENT
KIN BUG LANDFILL OPERABLE UNIT II EDISON, NEW JERSEY
Prepared for
U.S. ENVIRONMENTAL PROTECTION AGENCY Office of Waste Programs Enforcement
Washington, D.C. 20460
EPA Work. Assignment No. EPA Region Site No. Contract No. CDM Federal Programs Corporation Document No. Prepared By Work Assignment Project Manager Telephone Number EPA Work Assignment Manager Telephone Number Date Prepared
C02004 II 2P0A 68-W9-0002
TESy-C02004-FR-CJZL CDM FPC Jeanne Litvin (212) 393-9634 Alison Barry (212) 264-8678 February 27, 1992
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EXECUTIVE SUMMARY
The risk assessment (RA) for the Kin-Buc Landfill site - Operable Unit 2 is composed of two parts. Part I, Human Health Assessment, focuses on the human health effects of contaminants released from the site through ground water, surface water, and sediment. Part II, Environmental Assessment, addresses the risks to flora and fauna in the vicinity of the site, due to exposure to site-related contaminants in surface water and sediment. Biota data are used to evaluate risks to selected species. Contaminant fate and transport information presented in the Human Health Assessment applies to Environmental Assessment also. The two parts of the report will be presented as two stand alone sections, each with a distinctive and directed approach, to allow better access to the information contained therein.
To allow periodic review of the approach used in this RA, while it was still in progress, the EPA was informed about Data Handling, Indicator Chemical Selection, Exposure Pathways and Assumptions, and Risk Assessment in a series of milestones.
The following sections present details on the Human Health Assessment and the Environmental Assessment.
Human Health Assessment
The contaminants identified in samples from the Kin-Buc Landfill site were screened to identify the most hazardous compounds. The contaminant screening process identified 19 chemicals of potential concern: nine metals and ten organic compounds. These compounds or elements were selected because of their toxicological properties, potentially critical exposure routes, frequency of occurrence, and higher concentrations present in comparison to other contaminants.
Contaminant migration mechanisms were evaluated for each of the indicator chemicals based on the site's physical setting and thejjhysical and chemical properties of each contaminant. Exposed populations include local residents who fish and swim in the area streams, and potential future residential users of ground water.
Toxicology assessments, which include pharmacokinetics, human health effects, and dose response assessment, for each of the indicator chemicals were developed based on curtent EPA accepted health effects documents, and established toxicological sources.
Risk characterization included an assessment of risk associated with carcinogenic and noncarcinogenic effects. Noncarcinogenic health effects were addressed using a hazard quotient computed by comparing the daily intake levels to a reference dose, above which no human health effects are anticipated, and summed to obtain a hazard index. The index should not exceed one, ^ according to the NCP Superfund site remediation goals (EPA, 1989). ^
Many of the hazard indices computed indicated that the intake levels were below the § reference doses (i.e., hazard indices were below one). However, five of the exposure scenarios ^' had hazard indices (HI) above reference doses: ^
• ground-water ingestion by adults and children, and ^ fish ingestion by adults and children
m Potential carcinogenic risks were comouted by multiplying trie chronic daily intakes oy tiie criemicai-SDeciiic carcinogenic slope factor. Tine resulting carcinogenic risks were then compared to the Sucerfund Site remeaiation goal of 10'" to 10"° {E?A. 1GS9).
The following risks calculated for the potential exposure scenarios exceeded the upper limit of the guideline range:
ingestion of ground water by adults and children, ingestion of fish by adults and children
Overall, the greatest noncarcinogenic hazard indices and carcinogenic risks result from oral ingestion of the following constituents: arsenic, antimony, banum. bis(2-ethylhexyl)phthalate. chloroebenzene, 4,4'-DDT, manganese, PCBs. and vinyl chlonde.
Environmental Assessment
The potential impacts to fish, wildlife, and plants were evaluated in the environmental assessment. Because the environmental assessment estimates risks to discrete populations, the site was first divided into subsets representing separate areas for contaminant exposure. Media-specific chemicals of potential concern were identified for each area of the site. Spatial patterns in contaminant concentrations were evaluated to determine whether chemicals In specific media are likely to occur from site-related activities. Ecological receptors and potential exposure pathways were identified.
Aquatic life and marsh plants may be exposed to chemicals in surface water and sediments. Estimates were made of the exposure of predatory bird species through the food chain and surface water ingestion. After toxicity data were obtained, risks to aquatic life were assessed by comparing surface water and sediment concentrations with toxicity guidance values. Risks to birds were evaluated by comparing estimated dosages with toxicity reference values (TRVs) derived from the literature, which are measured or estimated "no observed effect" dosages. Risks to fish, fiddler crabs, and mammals were assessed by comparing tissue levels in Kin-Buc animals with levels reported to be associated with toxic effects.
Organic chemical concentrations in surface water do not pose risks to aquatic life. Although several metals were found in surface waters at concentrations above ambient water quality chteria. the spatial pattern of concentrations does not implicate site-related activities. The major site-related risks to aquatic life are posed by the presence of PCBs in sediments at Pool C and the Connecting Channel and tidal Edmonds Creek. These concentrations greatly exceeded guidance levels and, therefore, assumed to be toxic to bottom-dwelling organisms. In tidal Edmonds Creek sediments, concentrations of arsenic, copper, lead, mercury, nickel, and zinc appear to be elevated above background concentrations and exceed guidance values for sediment toxicity. The contribution of site activities to these concentrations is unknown. Sediments can be a source of PCBs to fish and fiddler crabs; PCB tissue levels in mummichogs collected at tidal Edmonds Creek exceed levels associated with toxic effects. Predatory birds do ^ not appear to be at risk from exposure to PCBs and metals through the pathways evaluated. ^ However, there are uncertainties associated with both the estimates of exposure and risk. Tissue concentrations in mammals are less than levels associated with toxic effects. Marsh plants may o be at risk from exposure to arsenic, copper, and lead, but there are considerable uncertainties S in the plant toxicity guidance values.
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FINAL RISK ASSESSMENT PART I - HUMAN HEALTH ASSESSMENT
KIN BUC LANDFILL OPERABLE UNIT II EDISON, NEW JERSEY
Prepared for
U.S. ENVIRONMENTAL PROTECTION AGENCY Office of Waste Programs Enforcement
Washington, D.C. 20460
EPA Work Assignment No. EPA Region Site No. Contract No. CDM Federal Programs Corporation Document No. Prepared By Work Assignment Project Manager Telephone Number EPA Work Assignment Manager Telephone Number Date Prepared
C02004 II 2P04 68-W9-0002
TESV-C02004-FR-CJZL CDM FPC Jeanne Li twin (212) 393-9634 Alison Barry (212) 264-8678 February 27, 1992
7
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TABLE OF CONTENTS
Page
1.0 INTRODUCTION , 1 1.1 Site Description and History 1 1.2 Remedial Investigation Summary 6 1.3 Contaminants Found at the Site , 7 1.4 Selection of Contaminants of Concern 8
1.4.1 Ground Water (13 Contaminants of Concern) 12 1.4.2 Surface Water (13 Contaminants of Concern) 15 1.4.3 Sediment (2 Contaminants of Concern) 15 1.4.4 Air (4 Contaminants of Concern) 15
2.0 ENVIRONMENTAL FATE AND TRANSPORT 21 2.1 Factors Affecting Migration : . 21
2.1.1 Geology and Soils 21 2.1.2 Topography and Drainage 25 2.1.3 Hydrogeology 26 2.1.4 Climatology 27
2.2 Contaminant Fate and Transport 28 2.2.1 Inorganics 28
2.2.1.1 Antimony 28 2.2.1.2 Arsenic 28 2.2.1.3 Barium 30 2.2.1.4 Beryllium 31 2.2.1.5 Cadmium 32 2.2.1.6 Chromium 33 2.2.1.7 Copper 34 2.2.1.8 Lead 35 2.2.1.9 Manganese 36 2.2.1.10 Nickel 37 2.2.1.11 Vanadium 38
2.2.2 Organics -38 2.2.2.1 Benzene 38 2.2.2.2 Bis(2-ethylhexyl)phthalate (BEHP) 39 2.2.2.3 Carbon Disulfide . 40 2.2.2.4 Chlorobenzene 40 2.2.2.5 Trans-1,2-Dichloroethene 40 2.2.2.6 DDT 41 2.2.2.7 Naphthalene 41 2.2.2.8 PCBs 42 2.2.2.9 Trichloroethene 42 w 2.2.2.10 Vinyl Chloride 43 • 2.2.2.11 Xylenes 44 ^
o 3.0 HUMAN EXPOSURE CALCULATION 45
3.1 Present and Potential Future Exposure Routes 45 >--3.2 Present and Future Exposed Populations 47 !^
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TABLE OF CONTENTS (Continued)
Paae
3.3 Human Intake Calculations 47 3.3.1 Ingestion of Ground Water 48 3.3.2 Inhalation of Chemicals Volatilizing during Showering 52 3.3.3 Dermal Exposure To Shower Water 55 3.3.4 Dermal Contact with Surface Water Bodies during Recreation 58 3.3.5 Ingestion of Surface Water during Recreation 61 3.3.6 Dermal Contact with Sediments during Recreation 64 3.3.7 Ingestion of Sediment during Recreation 67 3.3.8 Ingestion of Contaminated Fish from the Raritan River
or Edmonds Creek 72
4.0 CHEMICAL-SPECIFIC TOXICITY EVALUATION 75 4.1 Inorganics 76
4.1.1 Antimony 76 4.1.2 Arsenic 79 4.1.3 Barium 82 . 4.1.4 Beryllium 83 4.1.5 Cadmium 84 4.1.6 Copper 86 4.1.7 Lead 88 4.1.8 Manganese 90 4.1.9 Nickel 91 4.1.10 Vanadium 92
4.2 Organics 94 4.2.1 Benzene 94 4.2.2 bis(2-Ethylhexyl)phthalate (BEHP) 96 4.2.3 Carbon Disulfide 97 4.2.4 Chlorobenzene 99 4.2.5 4,4'-DDT 100 .4.2.6 Naphthalene 101 4.2.7 Trans-1,2-Dichloroethene 102 4.2.8 Polychlorinated Biphenyls (PCBs) 103 4.2.9 Trichloroethene 104 4.2.10 Vinyl Chloride 107 4.2.11 Xylenes 109
4.3 Applicable or Relevant and Appropriate Requirements (ARARS) 112
5.0 HUMAN HEALTH RISK CHARACTERIZATION 116 5
6.0 AREAS OF UNCERTAINTY AND DATA GAPS 134
7.0 CONCLUSIONS . 135
REFERENCES 138
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TABLE OF CONTENTS (Continued)
Pace
LIST OF FIGURES
1-1. Location of the Kin-Buc Landfill Site 2
1-2. Layout of Operable Units at Kin-Buc Landfill 4
2-1. Diagramatic hydrogeologic section of the New Jersey Coastal Plain 22
2-2. Geologic and hydrogeologic units in the New Jersey Coastal Plain After Zapecza. 1989 23
4-1. Generalized Dose-Response Curve 77
LIST OF TABLES
1 -1 . Ground-water Data Statistical Summary 9
1 -2. Surface Water Data Statistical Summary 10
1-3. Sediment Data Statistical Summary .' 11
1-4. Contaminants of Concern Selection for Ground Water 13
1-5. Contaminants of Concern Selection for Surface Water 16
1-6. Contaminants of Concern Selection for Sediment 18
1-7. Contaminants of Concern Chosen for Each Media at the Kin-Buc Superfund Site 20
2-1. Summary of Chemical, Physical, and Biological Properties for
Contaminants of Concern at Kin-Buc Landfill 29
3-1. Evaluation of Exposure Pathways 46
3-2. Variables used for Human Intake Calculations : . . . . 49 rs o
3-3a. Ground-water Ingestion Exposure Calculations, Adults 50 o o 3-3b. Ground-water Ingestion Exposure Calculations, Children 51
TABLE OF CONTENTS (Continued)
Page
3-4. tstimated Ambient Concentration for Contaminants Released During Showering 54
3-5a. Ground-water Inhalation of Volatlles While Showering, Adults 56
3-5b. Ground-water Inhalation of Volatiles While Showering, Children 57
3-6a. Ground-water Dermal Absorption Exposure While Showering, Adults 58
3-6b. Ground-water Dermal Absorption Exposure While Showering, Children 59
3-7a. Surface Water Dermal Absorption Exposure While Swimming, Adults 62
3-7b. Surface Water Dermal Absorption Exposure While Swimming, Children 63
3-8a. Surface Water Incidental Ingestion Exposure While Swimming, Adults 65
3-8b. Surface Water Incidental Ingestion Exposure While Swimming, Children 66
3-9a. Dermal Contact Exposure with Sediment, Adults 68
3-9b. Dermal Contact Exposure with Sediment, Children 69
3-1 Oa. Incidental Ingestion Exposure of Sediments, Adults 70
3-10b. Incidental Ingestion Exposure of Sediments, Children 71
3-11 a. Exposures from Fish Ingestion, Adults 73
3-1 lb. Exposures from Fish Ingestion, Children 74
4-1. Critical Toxicity Values for Oral and Inhalation Routes 78
4-2. Ground-Water ARARs/TBCs for Kin-Buc Landfill 114
4-3. Surface Water ARARs/TBCs for Kin-Buc Landfill 115
5-1 a. Ground-water Hazard Indices, Adults 118
5-1 b. Ground-water Hazard Indices, Children . 119
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5-2a. Surface Water Hazard Indices, Adults 120 o •
5-2b. Surface Water Hazard Indices, Children 121 ^
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TABLE OF CONTENTS (Continued)
p aos
5-3a. Sediment Hazard Indices, Adults 122
5-3b. Sediment Hazard Indices, Children 123
5-4a. Carcinogenic Risk Estimates for Ground Water, Adults 125
5-4b. Carcinogenic Risk Estimates for Ground Water, Children 126
5-5a. Carcinogenic Risk Estitnates for Surface Water, Adults 127
5-5b. Carcinogenic Risk Estimates for Surface Water, Children 128
5-6a. Carcinogenic Risk Estimates for Sediment, Adults 129
5-6b. Carcinogenic Risk Eslsnates for Sediment, Children . . i 130
5-7. Summary of Risks by Exposure Pathway 132
5-8. Summary of Risks Across Exposure Pathways 133
7^ OS n
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1.0 INTRODUCTION
The Kin-Buc Landfill site is an inactive municipar solid waste and industrial waste management facility located along the banks of the Raritan River in Edison Township, Middlesex County. New Jersey. The site is currently included on the National Priorities List (NPL) for remedial action under the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) and the Superfund Amendment and Reauthorization Act (SARA).
The Kin-Buc landfill site was used for liquid and solid waste disposal as early as 1947. Kin-Buc, Inc. operated the site from 1968 to closing in 1976. Kin-Buc operated as a state-approved landfill between 1971 and 1976 accepting industrial and municipal solid wastes. The state of New Jersey revoked Kin-Buc's operating license in 1976 due to numerous environmental violations.
Federal and state agencies, as well as various environmental consulting firms have collected samples at the site over the last 16 years. Samples collected from the landfill and Its environs detected contaminants in ground water, surface water and sediments. The source of these contaminants is believed to be the hazardous waste buried at the Kin-Buc property.
Under the Technical Enforcement Support (TES) V contract, CDM Federal Programs Corporation (FPC) was contracted by the U.S. Environmental Protection Agency (EPA) Region II to perform a risk assessment for Operable Unit 2 (including Mound B, Mill Brook/Martins Creek, Edmonds Creek and the connecting channel from Pool C, Edmonds Marsh and the Raritan River). This report was prepared by Versar, Inc. for FPC under EPA Contract No. 68-W9-0002, Work Assignment No. C02004.
This risk assessment (RA) is a Level 3 (quantitative) RA. The format and level of detail in this report are taken from the EPA Risk Assessment Guide for Superfund (EPA, 1989a), and the Superfund Exposure Assessment Manual (EPA, 1988).
1.1 Site Description and History
The entire Kin-Buc property covers an area of approximately 220 acres, which includes Kin-Buc I (30 acres) and Kin-Buc II (12 acres). The site is located at the end of Meadow Road g
in Edison Township, Middlesex County, New Jersey. The site is bordered by an industrial "
complex to the north and the Edison Township Municipal Landfill to the south. Marshlands and o
a former channel area are to the east. The Raritan River and additional industrial buildings are f
to the west of the property. Figure 1-1 shows the general location of the site. _,
en
- 1 5302.001-KIN-BUC_RA_FINAL_PT1
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I
t 2085QOO
[ 2082000
C 208 1000
C 2Q80000
E 2079000
E 2078000
•-- i^J? ft 0 c.
SCALE IN rccT I
'5S31: e o o :3a>J
The Site has been separated into two operable units. Operable Unit 1 (OP-1) addressed
the following areas of the Kin-Buc property:
Kin-Buc I mound Kin-Buc II mound Pool C Low-lying area between Kin-Buc I and the Edison Township Munipal Landfill
Operable Unit 2 (OP-2) as addressed in this RA comprises the following components:
Mound B Mill BrookyMartins Creek Edmonds Creek, including the connecting channel from Pool C Adjacent wetlands (often referred to as Edmonds Marsh) The Raritan River at mouths of Edmonds Creek and Martins Creek Ground-water contamination emanating from the site
Figure 1 -2 shows the general layout of the operable unit components.
Mound B covers approximately 9 acres along the shoreline of the Raritan River with a cap elevation of approximately 15 to 20 feet.
Mill Brook is located northwest of the site, and flows into Martins Creek. Martins Creek is tidally influenced and flows into the Raritan River, just north of Mound B.
Leachate is collected in Lagoons A, B, and C. Adjacent to these lagoons is a tidalpool
referred to as Pool C. Pool C discharges to Edmonds Creek via a small channel. Edmonds
Creek drains approximately 80 acres of tidal wetlands and subsequently discharges to the Raritan
River. These tidal wetlands are often referred to as Edmonds Marsh.
Little is known about site operation between 1947 and 1968. In 1968, the site was leased by the owner, Inmar Associates, to Kin-Buc, Inc., a division of Scientific, Inc. Kin-Buc, Inc. operated the site from 1968 to 1976. The site was a state-approved landfill for solid and liquid industrial and municipal waste between 1971 and 1976 and was registered with the New Jersey Department of Environmental Protection and Energy (NJDEPE) Solid Waste Administration.
The EPA estimates that at least 70 million gallons of liquid waste and one million tons of g
solid waste were disposed of at the Kin-Buc landfill between 1973 and 1976. The largest '- volumes consisted of industrial wastes, waste liquids and sludges. These wastes were handled o in three different ways: ^
-3 5302.001-KIN-BUC RA FINAL_PT1
cn
8921 200 Oa^
Buried on-site and then compacted. Discharged into a pit at the top of Kin-Buc I. or Discharged into temporary storage ponds along the side of Kin-Buc i and subsequently pumped into a pit located at the top of Kin-Buc I.
Investigation of the site began in 1976, which led to revocation of. Kin-Buos operating permit. Among the alleged violations were leachate seepage into the Raritan River, failure to provide records of hazardous wastes received, failure to maintain adequate cover over the landfill surface, and unauthorized excavations. In February 1979, a civil lawsuit was filed, directing the owners/operators to take corrective action under federal law. In 1980, Kin-Buc, Inc. installed a synthetic membrane and clay cap on Kin-Buc I and a clay cap on Kin-Buc II.
The EPA initiated remedial activities in February 1980, including drum reduction, and collection and disposal of Pool C leachate. In October 1981. the site was placed on the CERCLA Superfund NPL In 1982. Kin-Buc, Inc. assumed the responsibility of leachate removal operations at Pool C. The EPA then issued a unilateral CERCLA order mandating an RI/FS and remedial action for the site. A Record of Decision (ROD) for Operable Unit I was signed in September 1988.
The ROD evaluated four main remedial alternatives for Operable Unit I. Of the four alternatives, two have subalternatives associated with them. The first alternative (A) entailed no further action with monitoring. Alternatives C3 and C4, each include 4 subalternatives (C3a-d, C4a-d) deal with containment, capping, collection, treatment and discharge. The final alternative, D. was for complete excavation with off site incineration.
Alternative C4d was the selected remedy. It consists of the following components:
circumferential slurry wall installation to bedrock on all sides of the site;
maintenance, and upgrading if necessary, of the Kin-Buc 1 cap, and installation of a cap (in accordance with RCRA Subtitle C and State requirements on Kin-Buc II, portions of the low-lying area between Kin-Buc I and the Edison Landfill and Pool C);
collection of oily phase and offsite incineration;
collection and onsite treatment of aqueous phase leachate and contaminated ^ ground with direct surface water discharge;
o periodic monitoring; and, K
operation and maintenance.
- 5-5302.001-KIN-BUC RA_F1NAL_PT1
1.2 Remedial Investigation Summary
Between 1983 and 1988, Kin-Buc. Inc., and SCA Services, Inc. conducted a Remedial Investigation/Feasibility Study (Rl/FS) which resulted in a ROD from EPA presenting tiie recommended remedial action for Operable Unit 1. This inckided construction of a slurry wall enclosing Kin-Buc I. Kin-Buc II, Pool C, and a portion of the low-lying area between tfnem. Tiie ROD also concluded that another RI/FS was needed to determine the nature and extent of contamination from other portions of the site. Operable Unit 2.
A draft Rl report prepared by Wehran Engineering Corporation (WEC) on behalf of Kin-Buc, Inc. and SCA Services present the findings of the investigations conducted on Operable Unit 2. The Rl included a hydrogeological investigation; ground-water, surface water, sediment and biota sampling and analysis in adjacent streams and wetla nds; and ecological surveys. Field investigations were conducted between August 1989 and July 1990.
The findings of the Rl are summarized below:
Ground water at the site is present In four distin ct hydrostratigraphic units. These include the refuse in the Low-Lying Area and Mound 8, the buried marsh sediments underiying the refuse, a thin wedge) of sand and gravel beneath the meadow mat, and bedrock.
Ground water in the refuse occurs in unconfinetd water table conditions. This unit is separated from the sand and gravel unit by the low permeability meadow mat. The refuse unit is not tidally influenced by the Fiaritan River. Ground water in the refuse unit flows toward Pool C and the Raritan River.
Ground water in the sand and gravel unit is in hydraulic contact with the Raritan River and responds to tidal fluctuations. Groiund-water flow reverses direction diurnally near the river, with a net discharge to iihe river.
Ground water in the bedrock unit is mainly withiin the secondary fracture and joint system under semi-confined conditions. Ground water in this unit is 'tidally influenced by the Raritan River. Net discharge^ is to the Raritan River.
Substantial vertical flow exists between each of the hydrostratigraphic units. A substantial and consistant downward vertical flow component was detected between the refuse unit and the sand and graveil unit. Both upward and downward gradients were recorded between the sand and ci'ravel unit and bedrock unit. Tidal fluctuations appear to control the vertical direction of flow in the IViound B and Low-Lying areas and direction reversals were common. Vertical gradients were highest during low tide.
Ground water in the refuse unit contains variouu; concentrations of VOCs, BNAs, ^' metals, pesticides and PCBs. The predominant constituents associated with ^ industrial waste disposal at the site are aroimatic VOCs and BNAs. These o constituents appear to have originated from within the landfill mounds within Operable Unit 1 and have migrated towards Mound B and the Raritan River.
- 6 -5302.001-KIN-BUC _RA.FINAL_PT1
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The sand and gravel unit contains compounds similar (VOCs and BNAs) to those found in the refuse unit, but at much lower concentrations.
VOCs were also detected in the bedrock unit at lower levels than in the sand and gravel unit.
Surface water discharge from the Pool C connecting channel to Edmonds Creek contain trace levels of VOCs.
Sediments in the Edmonds Creek and surrounding marsh contain PCBs and PAHs. These constituents are distributed throughout the creek and marsh, extending to the Raritan River.
Sediments in Mill Brook/Martins Creek do not exhibit evidence of contamination attributable to the site. There is evidence of PAH deposition at the mouth of the creek.
PCBs were detected in resident aquatic and terrestrial biota collected in Edmonds Creek/Marsh, Mill Brook, and Martins Creek.
Edmonds Creek/Marsh specimens exhibited some of the highest PCB concentrations primarily in macroinvertebrates (fiddler crabs). However, additional sources of PCBs in the regional water and diet are suggested by the occurrence of PCBs in biota collected from the Reference Area.
No association has been seen between the area of capture and tissue burden within the Edmonds system. This suggests that PCB tissue concentrations are not exclusively a function of sediment concentrations.
Four target metals (cadmium, chromium, lead and mercury) were detected in biological tissue.
A feasibility study (FS), which outlines possible remedial actions and cleanup levels for
Operable Unit 2 will be submitted by the potential responsible party (PRP) following the
completion of the Risk Assessment.
1.3 Contaminants Found at the Site
The EPA transmitted the Draft Rl, dated October 1990, to Versar, Inc. for use in the risk
assessment. Data collected during the Rl were used in the RA. g o
Samples were collected from ground water, surface water, and sediment. The following o
types of contaminants were detected in all three media: Volatile organic compounds (VOCs), ro
base-neutral/acid extractable compounds (BNAs), polycyclic aromatic hydrocarbons (PAHs),
phthalates, polychlorinated biphenyls (PCBs), and metals. In addition, pesticides were detected
-7 -5302.001-KIN-BUC_RA FINAL PT1
• in ground water and surface water. Maximums, arithmetic means. 95 percent Upper Confidence
Limits (95% UCL) around the arithmetic mean, and frequencies of detections were calculated for
each compound. The following formula was used to calculate the 95 percent UCL values:
95% UCL = MEAN +/t,o5 * STD DEV
Tables 1-1. 1-2, and 1-3 contain statistical summaries for contaminants found in each media. Contaminants detected at a frequency of less than 5 percent are not listed on these tables.
1.4 Selection of Contaminants of Concern
This risk assessment focuses on those chemicals which pose the most significant threat to human health. These contaminants of concern were chosen based on intrinsic toxicity and concentrations present. The methods for evaluating contaminants of concern presented in the EPA's Risk Assessment Guidance for Superfund (EPA 1989a) Volume I: Human Health Evaluation Manual (HHEM) were used in the selection process.
The data reported in this document were derived from the Rl Report for the second operable unit, not from the Rl for the first operable unit, unless othenwise noted. First, to prepare the data for the evaluation process, all contaminants that were analyzed for but not detected at all or that were detected at a frequency of less than five percent in a given media were not evaluated. Second, all non-detects for compounds detected at a frequency of greater than 5 percent were given values of one-half the detection limit. PAH and Aroclor detections were summed with non-detects given values of one-half the detection limits. Aroclors are evaluated as Aroclor 1260 because only Aroclor 1260 has a toxicity value. Naphthalene, the only PAH selected as a contaminant of potential concern, has its own toxicity value. This was done to allow for the inclusion and evaluation of compounds that may be present at or below detection limits. For the showering inhalation scenario, values from ground water were used in an exposure model (see Section 3.0 for details on the model used) to estimate inhalation concentrations.
The evaluation process involves determining a risk factor for each contaminant. The risk factor is calculated by multiplying the upper 95th percentile confidence limit on the arithmetic mean of the contaminant concentrations (C) found at the site by the chemical-specific toxicity (T). For carcinogens, the toxicity value used is the slope factor (SF). For noncarcinogens, the toxicity g value used is the Inverse of the reference dose (RfD) or reference concentration (RfC). Slope ^
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TABLE 1-1 GROUND-WATER DATA STATISTICAL SUMMARY
15-Jan-92
VOCs (mg/L) Vinyl, Chloride Chloroethane Acetone Carbon Disulfide 1,1-Oichloroethane 1.2-Oichloroetnene (total) Trichloroethene Benzene 4-MethyI-2-pentanone Tetrachloroethene Toluene Chlorobenzene Ethyl benzene Total Xylenes
BNAs (rag/L) Phenol 2-ChloroDhenol 1,3-Dichlorobenzene 1.4-Oichlorobenzene 1,2-Oichlorobenzene 2-Methylphenol "i-Methyl phenol 2,4-Oimethylphenol Benzoic Acid 4-Chloro-3-Methylphenol N-Nitrosooiphenylamine (1)
PAHs (mg/L) Naphthalene 2-Hethylnaphthalene Acenaphthene Fluorene Phenanthrene Flouranthene Pyrene
Phthalates (mg/L) Diethylphthalate Oi-n-butylphthalate Butyl benzylphthalate bis(2-Ethylfiexyl)Phthalate pi-n-Octylphthalate
Total Metals (mg/L) Aluminum Antimony Arsenic Barium Beryl 1ium Cadmium Calcium Chromium Cobalt Copper Iron Lead Magnesium Manganese Nickel Potassium Selenium Sodium Vanadium Zinc
MAXIMUM ;
4.50E-02 2.70E-02 2.30E-0I 2.30E-02 1.80E-02 1.50E-01 5.50E-O2 2.80E-01 1.40E-01 8.50E-02 5.70E-01 1.30E• 00 8.20E-02 2.90E-01
3.10E+00 5.00E-O3 9.00E-03
' l.lOE-02 5.00E-03 1.10E• 00 1.30E• 00 3.60E-Q2 i.50E-t-01 7.50E-02 3.00E-03
1.3QE-01 I.40E-02 l.OOE-02 5.00E-03 9.00E-04 3.00E-04 l.OOE-03
4.00E-03 5.00E-03 5.00E-04 2.00E-01 5.00E-03
6.02Ef01 5.37E-02 4.05E-02 1.52E+00 4.40E-03 2.60E-03 2.80E-^02 8.85E-02 5.07E-02 2.50E-01 2.33E+02 5.27E-02 4.84E-^02 1.04E+01 1.09E-01 1.23E- 02 2.50E-03 4.00E-^03 1.76E-01 4.38E-01
ARITHMETIC MEAN C
7.37E-03 5.95E-03 2.67E-02 5.26E-03 3.S7E-03 1.32E-02 6.24E-03 3.80E-02 1.07E-02 S.93E-03 4.05E-02 8.22E-02 1.43E-02 2.71E-02
1.98E-01 4.81E-03 5.20E-03 5.30E-03 4.49E-03 7.58E-02 8.63E-02 7.94E-03 9.59E-01 1.31E-02 4.55E-03
1.13E-02 5.45E-03 5.25E-03 5.00E-O3 4.80E-03 4.50E-03 4.09E-03
4.61E-03 3.53E-03 3.67E-03 1.79E-02 4.38E-03
9.80E-t-00 2.95E-02 1.26E-02 5.55E-01 l.llE-03 1.19E-03 1.28E-^02 I.58E-02 1.15E-02 4.94E-02 5.07E+01 1.06E-02 2.30E+02 2.98E+00 3.14E-02 6.alE•^01 7,a3E-04 1.89£f03 3.89E-02 7.80E-02
S5% UPPER ONFIOENCE LIMIT
1.20E-02 7,90E-03 5.15E-02 3.47E-03 5.19E-03 2.89E-02 1.12E-02 7.12E-02 2.26E-02 1.44E-02 9.22E-02 1.98E-01 2.53E-02 5.47E-02
1.99E-01 4.81E-03 5.20E-03 5.30E-03 4,49£-03 7.59E-02 8.S4E-02 7.94E-Q3 9.50E-01 1.31E-02
. 4.55E-03
1.13E-02 5.45E-03 5.25E-03 5.00E-03 4.80E-03 4.50E-03 4.09E-03
4.51E-03 3.53E-d3 3.57E-03 I.79E-02 4.38E-03
1.70Ef01 3.54E-02 1.70E-02 7.14E-01 1.59E-03 1.40E-03 I.57E+02 2.56E-02 1.S7E-02 3.29E-02 7.27E+01 1.64E-02 2.86E+02 4.12E+00 4.59E-02 8.12E-H01 1.04E-03 2.29E+03 5.05E-02 1.29E-01
FREQUENCY
2/23 2/23 4/23 5/23 2/23 4/23 4/23 15/23 3/23 2/23 15/23 10/23 7/23 12/23
1/16 1/16 1/20 1/20 3/20 2/16 • 2/15 3/15 3/16 3/16. 2/20
4/19 1/20 1/20 1/20 1/20 2/19 4/20
3/21 11/21 6/20 4/20 3/21
18/18 19/22 21/22 23/23 8/23 3/23 22/22 8/23 11/23 14/19 23/23 17/23 23/23 23/23 15/23 23/23 2/23 23/23 18/23 14/20
ro o
o o
ro ->
TABLE 1-2 SURFACE WATER DATA STATISTICAL SUMMARY
21-Jan-92 1 Compound
VOCs (mg/L) •J.sthylene Chloride 1,2-Olchlroethene (total) 2-3utanone Benzene Tetrachloroethene Toluene Chlorooenzene Ethyl benzene Styrene Xylene (total)
BNAs (mg/L) Phenol N-Ni trosodi phenyl ami ne
PAHs (mg/L) Naphthalene 2-Methylnaphthalene
Phthalates (mg/L) Di-n-butylphthalate
Pesticides/PCBs (mg/L) Aidrin 4.4'-0DT Aroclor 1254
Metals (mg/L) Alumi num Antimony Arsenic Barium Beryl 1ium Calcium Chromi um Cobalt Copper Iron Lead Magnesium Manganese Mercury Nickel Potassium Sodium Vanadium Zinc Cyanide
MAXIMUM
2.00E-03 2.00E-03 1.20E-02 5.70E-02 2.00E-03 l.OOE-03 3.10E-01 5.30E-02 6.00E-04 5.00E-01
8,00E-03 4.00E-03
I.30E-02 l.OOE-03
l.OOE-03
4.90E-05 1.50E-04 3.30E-04
^.47E-^01 4.82E-02 7.00E-03 3.46E-01 1.90E-03 1.54E+02 1.20E-01 2.20E-01 1.33E-01 5.41E-f01 4.72E-02 4.55E•^02 7,90E-01 l.lOE-04 4.07E-01 1.43E• 02 4.19E+03 1.52E-01 3.97E-01 2.22E-02
ARITHMETIC 957. UPPER MEAN CONFIDENCE LIMIT
2.45E-03 2.45E-03 5.58E-03 6.51E-03 2.45E-03 2.13E-03 2.52E-02 5.27E-03 2.35E-03 4.84E-02
5.30E-03 4.90E-03
5.80E-03 4.50E-03
4.50E-03
2.68E-05 5.85E-05 4.87E-04
3.03E-t-00 l,99E-02 2.18E-03 9.71E-02 8.00E-04 7.05E• 01 1.19E-02 4.97E-02 5.25E-02 8.08E-K00 6.61E-03 1.47E- 02 2.94E-01 5.23E-05 9.10E-02 5.77E*01 1.25E- 03 1.49E-02 3.80E-02 6.82E-03
2.54E-03 2.54E-03 5.80E-03 1.53E-02 2.54E-03 2.54E-03 7.57E-02 1.44E-02 2.66E-03 1.45E-01
5.92E-03 5.11E-03
7.45E-03 5.43E-03
5.43E-03
3.07E-05 7.52E-05 5.14E-04
5.88E+00 2.98E-02 3.17E-03 1.59E-01 1.09E-03 9.50E+01 3.08E-02 9.06E-02 8.48E-02 1.74E+01 1.40E-02 2.40E•^02 4.48E-01 7.50E-05 1.56E-01 8.45E-f01 2.12E+03 3.88E-02 1.51E-01 9.70E-03
.-REOUENCY
1/13 1/13 1/12 3/13 1/13 3/13 1/13 2/13 1/13 3/13
1/10 1/10
1/10 1/10
1/10
1/13 1/13 1/13
13/13 6/13 7/13 13/13 4/13 13/13 5/13 5/13 11/11 13/13 10/13 13/13 13/13 1/13 12/13 13/13 13/13 5/13 5/13 2/13
7
O O
10-
i;-Jan-92 .<IN- BUC OPERABLE UNIT 2
Comoouna
VOCs (mg/kg) Acetone Carbon Disulfide 2-3utanone Benzene Toluene Chlorobenzene Ethyl benzene Xylene (total)
BNAs (mg/kg) 1,4-Oichlorobenzene Benzoic acid Dibenzofuran N-Ni trosoai phenyl ami ne 2-Chlorophenol
PAHs (mg/kg) Naohthalene 2-Methylnaphthalene Acenapnthylene Acenaphthene -1uorene Phenanthrene Anthracene Fluoranthene Pyrene Benzo(a)anthracene Chrysene Senzo(b)f1uoranthene Benzo(k)fluoranthene Benzo(a)pyrene Indeno(l,2,3-cd)pyrene Benzo(g,h,i)perylene
TOTAL PAHS:
Phthalates (mg/kg) Diethylphthalate Butyl benzylphthalate bis(2-Ethylhexyl)phthalate Di-n-octylphthalate
Pesticides/PCBs (mg/kg) Aroclor-1242 Aroclor-1248 Aroclor-1254 Aroclor-1260
TOTAL PCB:
Metals (mg/kg) Aluminum Antimony Arsenic Barium Beryl 1 ium Cadmi um Calcium Chromium Cobalt Copper Iron Lead Magnesium Manganese Mercury Nickel Potassium Selenium Silver Sodium Vanadium Zinc
TABLE 1-3 SEDIMENT DATA STATISTICAL
MAXIMUM
9.20E-01 1.50E-02 1.30E+00 1.20E-01 4.G0E-02 3.10E-01 1.60E+01 1.60E-1-01
1.90E-01 8.80E-H00 1.50E-01 1.20E+01. 1.40E-02
l.SOE-t-OO 3.90E-^00 I.35E+00 2.6QE-1-00 l.SOE-t-OO 1.40E•^01 1.20E-t-00 2.90E-^01 2.50E+01 . 1.20E-<-00 1.3QE+00 l.SOE-t-OO 9.00E-01 1.50E+Q0 1.50E-I-00 l.SOEfOO
5.40E-I-01
1.50E-01 4.20E+01 3.50E•^03 8.70E-1-00
6.00E-t-02 2.90E-^02 1.30E-^02 3.50E•^00
7.30E+02
2.98E-I-04 2.53E+01 2.57E+02 2.76E-I-02 2.20E-fOO 2.94E-t-01 1.71E+04 1.17E-^02 5.78E+01 4.41E+02 5.95Et-04 3.72Et-02 8.93£-t-03 7.04E+02 3.40E-t-00 1.76E+02 7.99E-t-03 1.38E+01 7.50E+00 1.S9E+04 9.76E+01 6.62E+02
ARITHMETIC MEAN CC
4.70E-02 3.09E-03 5.86E-02 7.52E-03 3.73E-03 1.75E-02 3.07E-01 3.33E-01
1.38E-02 6.40E-01 1.23E-02 2.52E-01 1.53E-01
3.22E-01 3.67E-01 1.87E-01 3.77E-01 3.14E-01 5.75E-01 1.75E-01 9.72E-01 9.29E-01 2.71E-01 3.04E-01 • 3.77E-01 1.92E-01
, 2.77E-01 2.26E-01 2.53E-01
3.38E-I-00
1.30E-01 1.22E-1-00 5.55E-^01 3.46E-01
l.I6E-t-01 5.37E-^00 1.78E-^00 1.93E-01
1.66E-f01
1.59E+04 6.26E+00 5.30Et-01 .7.33Ef01 1.19E-I-00 1.49E-t-00 2.41E+03 5.98E+01 1.76E+01 1.26Et02 2.82E+04 1.08E-t-02 5.42Et-03 1.83E+02 7.95E-01 4.36Ef01 3.04E-I-03 1.45E+00 1.41E+00 3.37E+03 4.78E-t-01 2.18E+02
SUMMARY
~S% UPPER NFIDENCE LIMIT
3.55E-02 3,75E-03 i.36E-01 1.30E-02 5.30E-03 3.20E-02 9.08E-01 9,34E-01
2.35E-02 1.14E-t-00 1.98E-02 7.UE-01 1.55E-01
3.87E-01 4.55E-01 2.35E-01 4,54E-01 3.75E-01 3.85E-01 2.20E-01 1.63E-t-00 1.47E•^00 3.19E-01 3.55E-01 4.41E-01 2.31E-01 3.25E-01 2.73E-01 3.07E-01
4.80E+00
1.46E-01 2.89E1-00 1.31E+02 5.94E-01
2.49E-t-01 1.02E+01 3.55EfOO 2.58E-01
3.02E-f01
1.79Ef04 7.15E+00
. 5.37E+01 8.56Ef01 1.33EfOO 2.10E-t-00' 3.12E-I-03 5.55E+01 2.06E+01 1.45E-t-02 3.17E+04 1.28E+02 5.06E+03 2.17Ef02 9.54E-01 4.95E-^01 3.43E-t-03 2.05E+00 1.72E+00 4.41E+03 5.29E+01 2.46E+02
-REQUENCY
3/53 5/53 15/52 7/53 4/53 7/53 3/53 13/53
6/52 29/49 5/52 7/52 4/52
13/96 24/95 14/97 25/96 10/96 13/97 32/97 25/97 47/96 46/97 14/97 16/96 28/97 18/97 22/97 15/96
93/97
15/52 10/52 35/94 24/50
13/129 56/129 81/145 10/130
111/147
51/51 8/93
37/78 50/51 47/51 5/93
48/48 51/93 49/51 51/93 51/51 51/80 49/49 51/51 30/93 51/93 51/51 21/51 23/76 48/48 50/51 35/77
-11 -
a- ^
factors, reference doses, and reference concentrations are cenved by EPA and were taken from the Integrated Risk Information System (IRIS) and the EPA's Health Effects Assessment Summary Tables, Fourth Quarter. FY-1990. EPA has not derived slope factors and reference doses for all contaminants; therefore, all of the contaminants found at the Kin-Buc site were not used in choosing contaminants of concern. Generally, the contaminants that were chosen represent the greatest amount of risk, and are representative of overall site risk. Once the risk factors have been determined, all contaminants that contribute greater than one percent of the total risk were selected for use in the RA.
PCBs were not detected in the sand and gravel layer during the Operable Unit 2 Rl; however, because of the toxicity of PCBs and due to the fact that they were detected in the refuse layer in the Operable Unit 2 Rl, they will be evaluated. Additionally, although trichloroethene, copper, and lead do not have toxicity factors, they will be retained for qualitative assessment because of their prevalence at the site and their potential toxicities.
Versar selected nineteen contaminants of concern for the Kin-Buc site. The contaminants of concern include six VOCs, one PAH, one phthalate, one pesticide, nine metals, and PCBs. Not all of the contaminants of concern are present in each of the sampled media, however, all will be used in the evaluation of risk for every media. For Instance, compounds in ground water may volatize white showering; although these compounds may not have been detected in the air samples collected, they will be evaluated for inhalation exposures. Tables 1-4 through 1-7 present the contaminants of concern selection process for ground water, surface water, sediment, and air matrices. Table 1-8 presents the contaminants of concern by matrix.
1.4.1 Ground Water (13 Contaminants of Concern)
The thirteen contaminants of concern chosen (COC) for ground water (Table 1-4) contribute the majority to noncarcinogenic health effects and carcinogenic risk of the contaminants used in the selection process for ground water. These thirteen contaminants Include:
Antimony Chlorobenzene Arsenic 1,2-Dichloroethene Barium Manganese Benzene Naphthalene Beryllium Vanadium ro Cadmium Vinyl Chloride
PCBs
1 ;
O O
(7!
- 12 5302.001 -KIN-BUC_RA_FINAL_PT1
TABLE 1-4 ^CONTAMINANTS OF CONCERN SELECTION FOR GROUND WATER
GROUND WATER (mg/1) | 95% UCL Frequency!
Oral Noncarcinogenic CT Rank
VCCs: Acetone isnzene 2-Butanone Cdrbon Disulfide Chlorooenzene Chloroethane 1,1-Dichloroethane 1,2-Dichloroethene : total)
Ethyl benzene Methylene Chloride •i-Methyi -2-pentanone Styrene Te:racnioroethene Toluene Tr-chioroethene Vinyl Chloride Xylene (total)
POLYCYCLIC AROMATIC HYDROCARBONS:
Acenaphthene Acenaphthylene Anthracene Benzo(a)anthracen8 Benzo(a)pyrene Benzo(b)f 1 uoranthene Benzo(g,h,i)perylene 3enzo(k)f1uoranthene Chrysene Fluoranthene F" uorene :.'ideno( 1.2,3-cd)pyrene 2-Methylnaphthalene Nacnthalene Phenanthrene Pyrene
BNAS; cenzoic acid 2-ChlorGonenol 4-Chloro-3-Methylphenol Dibenzofuran 1.2-Dichlorobenzene 1.3-OichIorobenzene 1,4-Dichlorobenzene 2.4-01methylphenol 2-Methylphenol 4-Methylphenol N-Ni trosodiphenyl amine Phenol
5.15E-02 7.12E-02 NA
8.47E-03 1.98E-01 7.90E-03 S.19E-03 2.39E-02 NA
2.53E-02 NA
2.26E-02 NA
1.44E-Q2 3.22E-02 1.12E-02 I.20E-02 5.47E-02
5.25E-03 NA NA NA NA NA NA NA NA
4.50E-03 5.00E-03 NA
5.45E-03 1.13E-02 4.80E-03 4.09E-03
9.50E-01 4.81E-03 1.31E-02 NA
4.49E-03 5.20E-03 5.30E-03 7.94E-03 7.59E-02 8.64E-02 4.55E-03 1.99E-01
4/23 15/23 NA 5/23 10/23 2/23 2/23 4/23 NA
7/23 NA
3/23 NA
2/23 15/23 4/23 2/23 12/23
1/20 NA NA NA NA NA NA NA NA 2/19 1/20 NA . 1/20 4/19 1/20 4/20
3/15 1/16 3/15 NA 3/20 1/20 1/20 3/16 2/15 2/16 2/20 1/16
5.15E-01 NA NA
8.47E-02 9.39E-t-00
NA 5.19E-02 3.22E-t-00
NA 2.53E-Q1
NA NA NA
1.44E-01 3.07E-Q1
NA NA
2.74E-02
8.75E-02 NA NA NA NA NA NA NA NA
1.13E-01 1.25E-01 NA NA
2.a4E+00 NA
1.35E-01
2.40E-01 9.53E-01
NA NA
4.99E-02 NA NA
3.97E-01 NA NA NA
3.31E-01
14
27 5
28 7
19
22
30
25
25 24
23
20 11
29
15
16
Oral Carcinogenic
CT Rank
cntaminant " of
Concern
NA 2.07E-03
NA NA NA NA NA NA NA NA NA NA NA NA NA NA
2.75E-02 NA NA NA NA NA NA NA NA NA NA NA NA NA NA . NA NA NA NA NA NA NA NA NA NA NA NA NA NA
1.27E-04 NA NA NA
2.23E-05 NA
YES
YES
YES
YES
YES
03
O o ro
13-
TABLE 1-4 CONTAMINANTS OF CONCERN SELECTION FOR GROUND WATER
Compound
PHTHALATES: bis(2-Ethylhexyi)
phthalate Butylbenzylphthalate Diethylphthalate Oi-n-butylphthalate Di-n-octylphthalate
PESTICIDES: 4,4'-0DT
METALS: Alumi num Antimony Arsenic Barium Beryl 1ium Cadmium Calcium Chromium (III) Cobalt Copper Iron Lead Magnesium Manganese Mercury (Inorganic) Nickel Potassium Selenium Silver Sodium Vanadium Zinc Cyanide
GROUND WATER 95% UCL
1.79E-02
3.67E-03 4.61E-03 3.53E-03 4.38E-03
NA
1.70Ef01 3.54E-02 1.70E-02 7.14E-01 1.59E-03 1.40E-03 1.57Ef02 2.56E-02 1.67E-02 8.29E-02 7.27E-t-01 1.54E-02 2.86Ef02 4.12E-f00 NA
4.59E-02 8.12E•^01 1.04E-03 NA
2.29Ef03 6.05E-02 1.29E-01 NA
(mg/1) 'requency
4/20
5/20 3/21 11/21 3/21
NA
18/18 19/22 21/22 23/23 8/23 3/23 22/22 3/23 11/23 14/19 23/23 17/23 23/23 23/23 NA 15/23 23/23 2/23 NA 23/23 18/23 14/20 NA
Ora Noncarci CT
3.93E-01
NA 5.77E-03 3.53E-03 2.19E-01
NA
NA 3.85E• 01 1.70E-t-01 1.02Ef01 3.19E-01 2.79E-eOO NA
2.55E-02 NA NA NA NA NA
.4,12E-t-01 NA
2.30E-t-00 NA NA NA NA
3.54E•^00 6.45E-01 NA
1 nogenic
Rank
12
32 33 21
1 3 4 17 9
31
2
10
5 13
Oral Carcinogenic
CT Rank
NA 2.50E-04 NA NA NA NA NA NA NA NA NA NA NA NA NA NA
5.85E-03 NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA
4
2
Contaminant of
Concern
YES YES YES YES YES
YES
YES
Risk Factor Total: 1.92E+02 3.70E-02
% of Total from Cotaminants of Concern: 95.9 9 9 . 1 %
7^ CO
O O
14
Although PCBs were not detected in the sand and bedrock wells during the Rl, they were detected in the refuse layer monitoring wells. Because PCBs present a major health concern, PCBs will be retained as a COC using data obtained from the refuse layer monitoring wells during the Rl at OP-2.
1.4.2 Surface Water (12 Contaminants of Concern)
The twelve contaminants of concern chosen for surface water (Table 1-5) contribute the majority to noncarcinogenic health effects and carcinogenic risk of the contaminants used in the selection process for surface water. These twelve contaminants include:
Antimony 4,4'-Dichlorodiphenyltrichloroethane (DDT) Arsenic Manganese Barium Naphthalene Benzene Nickel Beryllium PCBs Chlorobenzene Vanadium
1.4.3 Sediment (8 Contaminants of Concern)
The eight contaminants of concern chosen for sediment (Table 1-6) contribute the majority to noncarcinogenic health effects and carcinogenic risk of the contaminants used in the selection process for sediment. These eight contaminants include bis(2-ethylhexyl)phthalate, PCBs, antimony, arsenic, cadmium, manganese, nickel, and vanadium.
1.4.4 Summary
Table 1-7 summarizes the contaminants of concern for each media. Indicator chemicals selected for each media ^yill be evaluated in all media in which they were detected. This ensures that greater than 95 percent of the potential health risks will be quantified.
- 1 5 -
7C CO
o
ro
TABLE 1-5 CONTAMINANTS OF CONCERN SELECTION FOR SURFACE WATER
VOCS: Acetone Benzene 2-Butanone Carbon Disulfide Chlorobenzene Chloroethane 1.1-Dichloroethane 1,2-Dichloroethene Ethylbenzene Methylene Chloride 4-Methyl-2-pentanone Styrene Tetrachloroethene Toluene Trichloroethene Vinyl Chloride Xylene (total )
POLYCYCLIC AROMATIC HYDROCARBONS: Acenaphthene Acenaphthylene Anthracene Benzo(a)anthracene Benzoia pyrene 3enzo(b)fluoranthene Benzo(g,h,1)perylene Benzo(k)f1uoranthene Chrysene Fluoranthene Fl uorene Indeno(1,2,3-cd)pyrene 2-Methylnaphtha! ene Naphthalene Phenanthrene Pyrene
BNAS; Benzoic acid 2-Chlorophenol 4-Chloro-3-Methylphenol Dibenzofuran 1,2-Dlchlorobenzene 1,3-Dichlorobenzene i ,4-Dichlorobenzene 2.4-Oimethylphenol 2-Methylphenol 4-Methylphenol N-NItrosodi phenyl ami ne Phenol
PHTHALATES: bis(2-Ethylhexyl)phthaIate Butylbenzylphthalate Diethylphthalate Di-n-butylphthalate Di-n-octylphthalate
PESTICIDES/PCSs: 4,4'-DOT PCBs "
SURFACE WATER 95% UCL .-r
NA 1.53E-02 5.80E-03 NA •
7.57E-02 NA NA
2.54E-03 1.44E-02 2.54E-03 NA
2.66E-03 2.54E-03 2.54E-03 NA NA
1.45E-01
NA NA NA NA NA NA NA NA NA NA NA NA
5.43E-03 7.45E-03 NA NA
NA NA NA NA NA NA NA NA NA NA
5.11E-03 5.92E-03
NA NA NA
5.43E-03 NA
7.52E-05 5.14E-04
(mg/1) equency
NA 3/13 1/12 NA 1/13 NA NA 1/13 2/13 1/13 NA 1/13 1/13 3/13 NA NA 4/13
NA NA NA NA NA NA NA NA NA NA NA NA 1/10 1/10 NA NA
NA NA NA NA NA NA NA NA NA NA 1/10 1/10
NA NA NA 1/10 NA
1/13 1/13
Noncarcinogenic CT
NA NA NA NA
3.78E+00 NA NA
2.82E-01 1.44E-01 4.24E-02 NA NA
2.54E-02 8.46E-03 NA NA
7.23E-02
NA NA NA NA NA NA NA NA NA NA NA NA NA
1.86E-f00 NA NA
NA NA NA NA NA NA NA NA NA NA NA
9.87E-03
NA NA NA
5.43E-03 NA
1.52E-01 NA
Sank
5
11 15 17
19 21
16
8
20
22
14
Carcinooenic CT Sank
NA 4.44E-Q4 NA NA NA NA NA NA NA
1.91E-05 NA
7.98E-05 NA NA
. NA NA NA
NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA
NA NA NA NA NA NA NA NA NA NA
2.50E-05 NA
NA NA NA NA NA
2.59E-05 3.96E-03
3'
7
4
5
5 2
Contaminant of
Concern
YES
YES
YES
YES YES
7^
O
o o
- A6
TABLE 1-5 CONTAMINANTS OF CONCERN SELECT !N FOR SURFACE WATER
Compound
ETALS: Aluminum Antimony Arsenic Barium Beryl 1i um Cadmium ' Calcium Chromium Cobalt Copper Iron Lead Magnesium Manganese Mercury Nickel Potassium Selenium SiIver Sodium Vanadium Zinc Cyanide
SURFACE WATER 95% UCL F
5.88E-^00 2.98E-02 3.17E-03 1.59E-01 1.09E-03 NA
9.60E+01 3.08E-02 9.05E-02 8.48E-02 1.74Ef01 1.40E-02 2.40E-t-02 4.48E-01 7.50E-05 1.66E-01 8.45E-t-01 NA NA
2.12E•^03 3.88E-02 1.61E-01 9.70E-03
(mg/l) •equency
13/13 5/13 7/13
13/13 4/13 NA 13/13 5/13 5/13 11/11 13/13 10/13 13/13 13/13 1/13
12/13 13/13 NA NA 13/13 5/13 6/13 2/13
Noncarcinogenic CT Sank
NA 7.46E-^01 1 3.17E+00 8 2.27E+00 7 2.18E-01 13 NA NA
3.08E-02 18 NA NA' NA NA NA
4.48E+00 4 2.53E-01 12 8.29E-I-00 2
NA -NA NA NA
5.55E-t-00 3 8.07E-Q1 9 4.85E-01 10
Carcinogenic CT Rank
NA . NA NA NA
4.58E-03 NA NA NA NA NA NA NA NA
• NA NA NA NA NA NA NA NA NA NA
1
Total Risk Factor: 1.05E-1-02
of Risk from Contaminants of Concern: 98.0
Contaminant of
Concern
YES YES YES YES
YES
YES
YES
9.24E-03
99.9%
* Value for cadmium RfD is for food. '* Value for PCBs is for Aroclor 1250.
CO o
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17- o
TABLE 1-5 CONTAMINANTS OF CONCERN SELECTION FOR SEDIMENT
1 1
CcmoQund j
VOCS: Acetone Benzene 2-3utanone Carbon Disulfide Chlorobenzene Chloroethane 1,1-Oichlorcethane 1.2-Oichloroethene Ethylbenzene Methylene Chloride 4-Methyl-2-pentanone Styrene Tetrachloroethene Toluene Trichloroeinene Vinyl Chloride Xylene (total)
BNAS: Benzoic acid 2-Chloropnenoi •i-Chloro-3-Methyl phenol Dibenzofuran 1,2-Oichlcrocenzene i.3-Oicnloronenzene 1.4-Oichlorooenzene 2,4-Oimethyiphenol 2-Methylphenol 4-Methylphenol N-Ni trosodi phenyl amine Phenol
POLYCYCLIC AROMATIC HYDROCARBONS: Acenaphthene Acenaphthylene Anthracene Benzt3(a)anthracene Benzo a pyrene Benzo b fluoranthene 3enzo(g,h,i)perylene Benzo(k)f1uoranthene Chrysene Fluoranthene Fl uorene Indeno(1.2.3-cd)pyrene 2-Methylnapntnalene Naphthalene Phenanthrene Pyrene
PHTHALATES: bis(2-Ethyihexyl phthalate Butyl benzylphtha ate Diethylphthalate Di-n-butylpnthalate Oi-n-octylphthalate
PESTICIDES/PCBs: 4.4'-0DT PCBs
SEDIMENT (x 95% UCL
a.55E-02 1.30E-02 1.35E-01 3.75E-03 3.20E-02 NA NA NA
• 9.08E-01 NA NA NA NA
5.30E-03 NA NA
9.34E-01
l.UE-t-OO 1.55E-01 NA
l,98E-02 NA NA
2.35E-02 NA NA NA
7,11E-01 NA
4.54E-01 2.35E-01 2.20E-01 3.19E-01
. 3.25E-01 4.41E-01 3.07E-01 2.31E-01 3,55E-01 1.53Ef00 3.75E-01 2.73E-01 4.56E-01 3.87E-01 8.85E-01 1.47EfOO
1.31E-t-02 2.89EfO0 i.46E-0I NA
5.94E-01
NA 3.02E-I-01
g/kg) rreauency
3/53 7/53 15/52 5/53 7/53 NA NA NA 8/53 NA NA NA NA 4/53 NA NA 13/53
29/49 4/52 NA 6/52 NA NA 5/52 NA NA NA 7/52 NA
25/96 14/97 32/97 46/97 18/97 15/96 15/96 28/97 14/97 25/97 10/95 22/97 24/96 13/96 13/97 47/96
35/94 10/52 15/52 NA 24/50
NA 111/147
Noncarcinoaenic i CT
3,55E-01 NA NA
3.75E-02 NA NA NA NA
9.08E-t-00 NA NA NA NA
1.77E-02 NA NA
4,67E-01
2.34E-01 3.29E-f01 NA NA NA NA NA NA NA NA NA NA
7.57Et-00 NA
7.33E-01 NA NA NA NA NA NA
4.08E-I-01 9.38E-t-00 NA NA
9.68E-I-01 NA
4.90E-t-01
5.55Et-03 NA
1;33E-0I NA
3.47E+01
NA NA
Rank |
22
27
20
23
24
'5
la
21
23
15 19
13
15
4
25
17
Carcinoaenic CT • Sank
NA 3.78E-04 6 NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA
NA NA NA NA NA NA
5.65E-04 5 NA NA NA
3.48E-03 4 NA
NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA
1.83E+00 3 NA NA NA NA
NA 3.78E-t-02 1
Contaminant Of
Concern
YES
YES g
O
O O r-j
\)
18-
TABLE 1-5 CONTAMINANTS OF CONCERN SELECTION FOR SEDIMENT
Compound
METALS: Aluminum Antimony Arsenic Barium Beryl 1ium Cadmium ' Calcium Chromium Cobalt Copper Iron Lead Magnesium Manganese Mercury Nickel Potassium Selenium Si Tver Sodium Vanadium Zinc Cyanide
SEDIMENT (ma, 95% UCL r
1.7.9E-t-04 7.16E+00 5.37Ef01 8.55E-t-01 •1.33E-t-00 2.10E-t-00 3.12E+03 6.55E-t-01 2.06E-f01 1.45Ef02 3.17Ef04 1.28E-t-02 5.06E-t-03 2.17E-f02 9.54E-01 4.95Ef01 3.43E+03 2.Q5E+00 1.72E+00 4.41E-.-03 5.29E-t-01 2.46E•^02 NA
kg) -equency
51/51 8/93 37/78 50/51 47/51 5/93
48/48 51/93 49/51 51/93 51/51 51/80 49/49 51/51 30/93 51/51 51/51 21/51 23/76 48/48 50/51 35/70 NA
Noncarcinoaenic CT
NA 1.79E-t-04 5.37E-t-04 1.22E-t-03 2.56E-I-02 2.10Et-03 NA
5.55E+01 NA NA NA NA NA
2.17Ef03 3.18E-I-03 2.48Ef03 NA NA
5.73E-t-02 NA
7.55E-I-03 1.23E-t-03 NA
Sank
2 1 9 12 8
14
7 5 5
11
3 10
Card nogenic CT Sank
Risk Factor Total : 1.09E-t-05
of Total from Contaminants of Concern: 95.5
Values for RfD is for food.
NA NA NA NA
5.72E1-00 NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA .• NA NA
3.86E-I-02
98.5
Contaminant Of
Concern
YES YES
YES
YES
YES
YES
CD O
O O fO
- 19-^1
21-Feb-92
TABLE 1-7 CHEMICALS OF CONCERN CHOSEN FOR EACH MEDIA
AT THE KIN-BUC SUPERFUND SITE OPERABLE UNIT 2
COMPOUND SEDIMENTS SURFACE WATER GROUNDWATER
VOCS: BENZENE X X CARBON DISULFIDE CHLOROBENZENE X X 1,2-DICHLOROETHENE X VINYL CHLORIDE X XYLENE
PAHS: NAPHTHALENE
PHTHALATES: BIS{2-ETHYLHEXYL)PKTHALATE X
PESTICIDES/PCBs: 4.4'-DDT X PCBs X X (1)
METALS: ANTIMONY X X X ARSENIC X X X BARIUM X X BERYLLIUM X X CADMIUM X X MANGANESE X X X NICKEL X X VANADIUM ^ X X X
NOTE: This table presents the contaminants of concern for tJie fiuman fiealth evaluation of the Kin-Buc RA.
Note that all of the contannlnants selected above will be evaluated for all of the pathways In which they were detected. For example: cadmium was selected for ground water and for sediments although it will also be evaluated for surface water. Because the air pathway involves volatilization, cadmium will not be evaluated for air. (1) - AlttTough PCBs were not detected in sand and gravel wells during the Rl, they were detected in the refuse layer monitoring wells. Due to their potential for adverse health effects, they were retained for analysis during the Rl at OP-2.
W o
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- 2 0 -
#
2.0 ENVIRONMENTAL FATE AND TRANSPORT
This section describes the characteristics of the site and the contaminants found onsite that may affect the fate and transport of site contamination. Section 2.2 details the regional and local geology and soils, topography and drainage, hydrogeology, and climate. Section 2.2 provides information on the chemical and physical charactenstics of site contaminants and describes the fate and transport processes that are expected to occur related to these compounds.
2.1 Factors Affecting Migration
The Kin-Buc Landfill Superfund site is located in Edison Township, Middlesex County, New Jersey (Figure 2-1). Operable Unit 2, which is the focus of this nsk assessment, consists of the following areas: Mound B. Mill Brook/Martins Creek. Edmonds Creek (including the connecting channel from Pool C), adjacent wetlands (often referred to as Edmonds Marsh), the Raritan River at the mouths of Edmonds Creek and Martins Creek, and ground-water contamination emanating from the site. To assess the migration potential of contaminants detected in the soils, sediments, surface water and ground water at the site, specific site characteristics affecting contaminant migration must be addressed.
Site characteristics influencing environmental fate and transport of contaminants at the Kin-Buc Landfill site are detailed below and include the following physical features' and characteristics: geology and soils: topography and drainage; hydrogeology; and climatology.
2.1.1 Geology and Soils
The Kin-Buc landfill site is located on the northwestern edge of the Atlantic coastal plairt, where Triassic and older sedimentary and crystalline bedrock is overlain by thin Cretaceous and younger sedimentary deposits (Figure 2-1). The following sections detail the geology of the underlying rocks in the vicinity of the site and the overlying soils derived from these rocks.
Bedrock
Pre-Cambrian and Lower Paleozoic crystalline rocks, including metamorphic schist and gneiss are the oldest rocks underlying the Cretaceous coastal plain deposits in the county. Pre- o
Cretaceous bedrock is represented by the Triassic Newark Group in the vicinity of the site (Figure 2-2). These deposits vary from soft red shale to dark, hard argillite and gray sandstone. The oldest formation within the Newark Group is the Stockton Formation, which unconformably
CD O
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-21 5302.001-KIN-BUC_RA_FiNAL_PT1
ro ro
H o l l y D o n c I )
W a l o r - b o a r l n g z o n e
A*
DELAWARE RIVER
A I I A N T I C O i l A N
N o t l o s c a l e
Fi i . i re 2 1 . DI B|r8i8llc hydto|eoto|lc section ol Itie Hey Jersey Coastal Plain.
S^2I 200 ,ja>
ri?urfl 2-2. GAOIO^IC ana hydrogeologic units in tne Mev Jersey Coasui Plain. After ZaMcsa. 1289.
I LTilT HT^RCLccic c:-{juucTi7.:sr:c:
d r s e t t c s S«ria. 1 1 1 : . ADS BiccK m a .
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Cjri»n«r» 5 ana co«rs« i r tLBca. gcooiy: local e i a r D«aa.
L'ndlf f « r t n -
I w.or'
S u r i i c i a i m a w r i A i , c i zen \
r.ycrauiiciiiv canneccea to I
-noprlYinq doui^ers. Lcoi iy !
sane \jMt.s r ay act as continina |
:^eas. 'Rioter unos are camsie f
c£ yieidinq Urqe quancicies oc j
' — wacer.
j i r i a t t i a n
i ror^acian i pr.... 4uar tx . ' . l ine eo lo rca .
i
lanov. 1
' aqu t i a r
A a«ior aauLi t r i T i t r a . Ctotina*w*tar oeeurt g«n*ral lT \a\a*r v a c i r - c a a l a e a n e t c i o n s . l3 CaD« r*.av Councv c.-.t C£»•»••• Sana i i under a r t c i t a n cona i c i ena .
1 Sana, a u a r t r . r ra* ana tart. y«rf t i n t to k:irtvooa j , , ,iijBi r r a i n t a . a i cac toua . ana ««r«"
''o'-^"^^" ] eoiorta dLacas«caoua ci«T.
Tarsal ion U n a . «u«rcs an* i i a u c s f i i c « . f ins to
Caccna | ^ J * ' * * ^ ' ' * ' | ^ J V ' 2 i i t y • " * ' s a r w / , q l j u o c m t i c - q rcen . (*f;afici_^__ , ^ ^ ^ ^ ^ O r a m , f i n e - q r a i n r d q i u r u u n a .
P a l e « c r n «
-iorr^vricown I Sand* c : j y T r ' q U u c o n i c i c * a i r e q reen , Cine
canMnin t B«a i .^.H.-.—— — j iorc coasi ana lot a S^CTI
Aio Gfan^ *r-c2T distance inljna. A tnin water-
I " " T ~ ' " " aearina una is oeeaenc^m ir.e
ACiAntlC CiiV I
300-(ooc u n a !
ftn«9 Poifti T i c i a i aod«rat« 4u«iii icLat ot
• • u i f « r wacvr l o c a i l v .
foo r IT p«ra«aol« t c a i s a n c a .
I ikina. c u a r i x . qray i r a qrecn, t i n e to coarse
vincentown i r j i f c o . q i a u c o n i t i c . ^no Drown ciayfY, very
rgnatla.-^ :=£sili£crous. Qiau^mitt *ro q u t r t :
1 c a i a r e n i t e .
FooTlT p t ra«a»l« »««k*aai».
.-^tsn Sana fana. «uarcx. ana i l a u c t t n i c i . brovw ana r r t T . [ ? ^ ^ ~ ""
l t d latui Sanat i^^t (o <«srs« ^TAiata. cLavvy, «icae»o«».
. .«»»i i ra I 3 i r a , c ; j y w . i i i t y , s j iducani t ic* a reen anc ro r sae ion | ; i a c » . r -o i i j a t o aoac:>e u t a v n e c .
Podriv r v r ^ a a e i * ivaLawaci .
5ar>.a
I ;ana. duarcx. a r m m ana arsv. ti.-.i ta
Ieoaria triinaa. ilicnclv ilauconittc.
ir i.-.i.. :;wr.
^no. very tine co cine arainea, gray anc
--•a-n, siitv, s m t l v glauconitic.
:-jy, siity, aam qre«nian qray,
I :'.Aint L^urti A ffu^or a q u i f e r .
; .".ar inai i csvn-
I -anonan A ItasT cont ' .ninc a t e .
- . • j f r i.:zi:itxx.svr» I land, duarez . :an ano t r a v . u n a to. aaavua
: recae*oui ' ' z r z A i : : - ; ; r » t r*g : local eiaT s«a«. •du i f r r
z a i e r a d u i i e r . .vo tasa -^r.;,:s
in r^oraoucn ana Cecan t ^^ jn^ i t i .
: rttaeac<4i , - . l lav. c rav ane : ; a c x . . - . i caaous s w t .
. . ' . j v . a l a u o c n i : : : , r . ' . ^ c c o u s . c r i y ar.2 " ' '="•*=*• ' • -••*! ; .*£<; : c c i i y v - r v J i n e - q r a i n s c q u a r t s
"sTTation i : - - - ; , a u c s r . i t ; z i a n o .
_ ! A a a i e r coni- . r inc a t e . - j s a t i T
; "^erenantvi; i«-1 c.-.t .TrfcnaatTi:'.« ."=. za^
i '.'aodBur^ eaneain a tT.'.n vac t r •?*a7*.:2
. e sn t in inx ? ta \ land-
•*.Ot"v *er=«ti07
I :ar.a. duarcf . . . ! . - . : | r a v . f.r.t CO eoars*
i .-;i-.n«a: locai :«ds ot d a r f c r i ' r t ^ i r . i i t :
K aa lo r adu i i e r aiona cn« c o a i c . I
lAViowa"* CL^v Hea»#r or rQw.yAitr.'. i
^ i vtneantwn I Tlrldi taati co Moaarata
* j lauilvr i duancicica ol wacvr in ana
o| ntsr ici ouceroo arra.
;j ^ j ^ jj^^ ,ri«laa naaii auancttics ot vattr
•• »ana •" •"* "*•'' *•'* <»«ceroo area. j
e k. t
•*ri:an
•^rsacicn
.•-3. suartz. . . i t i ' . era-/. (irt :o eoarta
z T f . r . w a . 8»03i-'. arKOsie. red. vnkit. ar.c
.artaaacta cii/
• : SCI
' u > * r I ', " t re tacecusi
: xl :»r!*-acint c;a-/ sand, and i r a v a i .
3 0
d «
acu i - r f -;:tr.ern C->itai ? l i ; - , cr.? -rp«f .
ic-i :?c IS «u iva ; tn t zz tr.e
CI- 2cica; a j - i i e : —"o -~.c " i s i i i i
•.tola I asui i t r 15 errjivai«n: i r "--.• 1
s--i:er' f2rr*.r.~3P. jouiccr. • * "-".r - c l J . 1
— • " — ?.ivef '•'a::e'/ c-.rs? ac--i:sr; j r j !
- ' • ^ " ' :*cocri:ea. ; - v^e at-apt =u=- I
l ^ « r I s-r ; jce, -r.its t e l * 3"f (
Pr>-Cr«ucccus
.-:7c;rir;i."; i.-= .j^er i^aicc;:;; ;:yst-i*.i.-.?
::<z\i, rie*_r:c:3^:c cr".;:t 1.*.: —.cisr: i a ^ i . v ^edroca
cam i.-.-.-z ^i>ai
c .-eUS c=t3;r. wats r : :5r .
•-.0 w.*i:-5» wactr-o^-irir-r : s
.-.c=::icc : : a - ZiJ .cs i . :33-;-
- 2 3 - KBC 002 1276
overlies crystalline basement rocks. The Stockton Formation is dominantly composed of
intercalated conglomerate, sandstone, and red shale, "he Lockatong Formation, which
conformably overlies the Stockton Formation, is characterized by well lithified shale and argillite.
The Brunswick Formation is the youngest unit of the Newark Group. Interbedded sandstone,
siltstone. and red shale comprise this deposit (Barksdale, 1943. as cited in Wehran, 1990).
Jurassic diabase dikes are locally present in cross-cutting relationships. In addition, all of these older rocks are locally intruded by Triassic basalt. These more resistant igneous dikes and sills tend to underlie areas of higher elevation in the vicinity of the site. Alteration from contact metamorphism and metasomatism has resulted in hardening and darkening of the original sedimentary deposits.
Block faulting, as a result of extensional stress, disrupted the pre-Cretaceous bedrock, forming a senes of highs and lows that affected sediment dispersal and accumulation patterns. The Kin-Buc Landfill site is located at the northern end of one of these basement structural lows, referred to as the Raritan Embayment. Although these basement lows tend to accumulate thicker deposits, the site is at the western edge, where the sediments thin significantly.
Coastal Plain Deposits
The Kin-Buc Landfill site is located at the northwest margin of the coastal plain and, as such, is in an area underlain by extremely thin sedimentar/ deposits. The depth to bedrock is less than fifty feet throughout the site (Wehran, 1990). Coastal plain deposits thicken to 6,500 feet in the southern portion of New Jersey and pinch out against the pre-Cretaceous bedrock at the fall line. The coastal plain deposits in Middlesex County consist mostly of alternating layers of dark glauconite. clay, fine sand, and coarse glauconitic sand. The site is at the extreme western edge of the coastal plain, and as such the only deposits likely to be present under the site are the oldest layers of the sedimentary coastal plain package. These deposits belong to the Lower Cretaceous Potomac Group. The Upper Cretaceous Raritan and Magothy Formations are located just southeast of the site (Zapecza, 1989). These three formations comprise the Potomac-Raritan Magothy Aquifer system, which is a significant water source for the northern coastal plain.
The Potomac Group lies unconformably upon Triassic bedrock. This unit consists of g alternating clay, silt, sand, and gravel deposited domininently in a non-marine environment. "'
These sediments were deposited by fluvial systems carrying piedmont-derived material which was o o
then deposited in a deltaic environment. The Farrington Sand Member of the Raritan Formation w
may also be present beneath the site. This unit includes fine to coarse grained, light gray, pebbly ^
Ni XI
- 24 -5302.0O1-KIN-BUC.RA_FINAL_PT1
quartz sand and arkosic sand. Red. white, and variegated clays are also present within this deposit. The Old Bridge Sand Member of the Magothy Formation is present at the surface east of the site, and is composed of tight gray, fine to coarse grained quartz sand. Beds of dark gray organic clay are locally present (Zapecza. et al, 1987).
Younger Deposits
Unconformably overlying the coastal plain sediments in Middlesex County are Quaternary deposits of glacial, glacio-fluvial, eolian, and fluvial ohgin. The early Quaternary Pensauken Formation consists of light colored, clayey and pebbly heterogeneous quartz sand, deposited in a fluvial environment overtop of and eroding the unconsolidated coastal plain deposits. This unit is present on the higher terraces along the Raritan River and in much of the southern portion of the county (Powley, 1987). The Cape May Formation, which overlies the Pensauken Formation in the vicinity of the site, is formed from outwash deposits flowing ahead of the glaciers. This unit is composed of stratified sand and gravel, with minor clay (Powley, 1987). The youngest deposits in the vicinity of the site are Recent alluvial and fluvial deposits. These unconsolidated deposits are present adjacent to the river systems in the county.
Soils
According to the Soil Conservation Service Soil Survey of Middlesex County (Powley, 1987), the soils at the site are classified as Psammants. Waste Substratum. This soil unit consists of excessively drained to well drained soils used to cover landfills. The characteristics ot this unit are variable. The material is generally 2-4 feet thick and covers layers of soil and household and industrial trash. The soils present in the vicinity of the site are the Sulfaquents-Sulfihemists-Psamments group. These soils are characterized as nearly level, deep, excessively drained to very poorly drained, mineral and organic soils. These soils are found on tidal flats and exhibit a grayish or black subsoil (Powley, 1987).
2.1.2 Topography and Drainage
The Kin-Buc Landfill is located in the Atlantic Coastal Plain physiographic province, just southeast of the fall line that divides the piedmont from the coastal plain. The site is contained
on two United States Geologic Survey topographic maps, the New Brunswick and South Amboy g
quadrangles (USGS, 1954). According to the topographic maps, the elevation of the site varies '^ from less than 10 feet above mean sea level (msl) to approximately 50 feet above msl. Accurate o
elevations of the abandoned landfill areas were acquired as part of the Rl, and suggest the ^^
elevation of the landfill ranges from approximately 15 feet above msl to 93 feet above msl ^
CO
-25 5302.001 -KIN-BUC _RA_FINAL_PT1
(Wehran. 1990). Most of the surrounding area is gently roiling, with elevations varying from 10
to 80 feet above msl. A northwesl'southeast trending topographic ridge 2-3 miles nortneast of
the site reaches elevations of 100 to 140 feet above msl. This ridge is a terminal moraine, which
marks the southern extent of glacial activity in Middlesex County. At the fall line, which is located
8 miles to the northwest, the elevation reaches 540 feet above msl.
The Kin-Buc site and surrounding environs are poorly drained with large areas of swampland and a multitude of small streams. The tidally influenced Raritan River is wide and slow moving in the vicinity of the site. The flood plain of the river is dominated by flat-lying tidal marshes. The Raritan River discharges into Rahtan Bay approximately 5 miles downstream of the site.
Several small streams and creeks are located on or adjacent to the site. Mill Brook is located northwest and west of the site, and originates approximately 2 miles north of the site. The stream drains a dominantly industhal area containing petroleum storage facilities, chemical manufacturers, and salvage yards (Wheran, 1990). Martins Creek originates on the site from an area between Kin-Buc I and II (USGS, 1954). This small stream is joined by Mill Brook approximately 1000 feet before discharging into the Raritan River. A stream draining the eastern portion of the site is unnamed on the topographic maps but is referred to as Edmonds Creek in site-related documents (Wehran, 1990; PRC, 1987). Edmonds Creek apparently originates as urban and industrial drainage before being channeled through a former sand and gravel borrow area north of the site (Wehran, 1990). Edmonds Creek flows through an area dissected by mosquito ditches before flowing south into the Raritan River. The stream also drains the Low-Lying Area and Pool C via shallow ditches. An additional small stream is located south of the site, within a meander bend of the Raritan River. This stream is designated Rum Creek on some of the site-related documents (Wehran, 1990) but is unnamed on USGS maps. According to the USGS (1954) Rum Creek is located northeast of the site, and flows from south of Mirror Lake'to the vicinity of the mosquito ditches east of the site (USGS, 1954). Additional surface runoff flows west and south from the site to enter the Raritan River.
2.1.3 Hydrogeology
The principle aquifers in New Jersey are classified as coastal plain aquifers south of the
fall line and non-coastal plain aquifers north of the fall line. The only non-coastal plain aquifer g
in the vicinity of the site is the Newark Group. The Newark Group, which underlies the coastal "
plain deposits at the site, consists of shale and sandstone. Water is generally present in o
weathered joint and fracture systems in the upper 200 or 300 feet (Barksdale, et al, 1958, as cited '--
in USGS, 1984). Below approximately 300 feet, the fractures are fewer and smaller, and water ^ hj
o - 26 -
5302.001-KIN-BUC .RA_FINAL_PT1
availibility is reduced. The aquifer is unconfined to semi-confined up to approximately 200 feet depth, and semi-confined at greater depths. In several counties in New Jersey, the shale and sandstone of the Newark Group are the most productive aquifers and yield as much as 1.500 gal/min (USGS, 1984). Yields from wells in the Newark Group, which are from 30 to 1.500 feet deep, range from 10 to 500 gallons per minute (GPM). The water from this aquifer is generally hard, and may have high concentrations of iron and sulfate. Saltwater has intruded areas of large ground-water withdrawal near coastal bays and estuaries (USGS. 1984).
The only coastal plain aquifer exposed in the vicinity of the site is the Potomac-Raritan-Magothy Aquifer system, which is composed of alternating beds of sand, gravel, silt and clay. This semi-confined aquifer system is highly productive and one of the.most used aquifers in the northern coastal plain. The aquifer thins to a feather edge at the fall line and reaches a maximum thickness of 4,100 feet in southern New Jersey. The Farrington Sand Member of the Raritan Formation and the Old Bridge Sand Member of the Magothy Formation are the main waterbearing units in the northern coastal plain. The water quality from the aquifer system is excellent although high concentrations of iron are locally present. Saline water is present at depth and increases downdip, towards the southeast (USGS, 1984). Yields from wells in the Potomac-Raritan-Magothy aquifer system commonly range from 500 to 1,000 GPM, with maxima in excess of 2,000 GPM. Withdrawal wells in the unit vary from 50 to 1,800 feet in depth (USGS, 1984).
2.1.4 Climatology
The climate in the vicinity of the Kin-Buc Landfill site is classified as continental, charactenzed by cold winters, hot summers, and annually well distributed precipitation. The average temperature is 33° in winter and 73° in summer. A record low temperature of -6° was recorded in 1961 and a record high of 102° was recorded in 1957 (Powley, 1987). January is the coldest month, with average daily lows of 22.2°F and highs of 38.4 °F. The hottest month of the summer is July, with average daily lows of 64.TF and highs of 85.2 °F (NOAA, 1982).
Of the total annual precipitation, 24 inches, or 54 percent, usually falls in April through September. The heaviest 24-hour rainfall was 7.66 inches in 1971. Thunderstorms occur on about 25 days each year, and most occur in summer. The average seasonal snowfall is 17 inches, and the record from a single snowfall is 19 inches (Powley, 1987). The month with the 7:
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greatest average precipitation is August, with 4.90 inches. February gets the least precipitation o with 2.96 inches (NOAA, 1982). The relative humidity averages 54 percent in midafternoon anc ^ 73 percent at dawn when it is highest. The prevailing wind is from the southwest, with the highes g average speed, 12 miles per hour, in March (Powley, 1987). The mean wind speed for New York
o
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New York is 12.31 miles per hour, and the maximum recorded is 50.34 miles per hour (GRI.
1988).
2.2 Contaminant Fate and Transport
The environmental fate and transport analyses examine the possibility of offsite migration of contaminants based on the operational history of the Kin-Buc Operable Unit 2.
Possible release mechanisms at Kin-Buc include migration of contaminants into and through the soil, and then to ground water, surface water, and stream sediments. The sections that follow provide fate and transport information for the nineteen contaminants of concern. Table 2-1 presents chemical, physical, and biological properties of these contaminants.
2.2.1 Inorganics
2.2.1.1 Antimony
In most natural waters, antimony (Sb) is found as soluble oxide or antimonite (+3). Volatile stibine (SbHj) may be formed in reducing environments. At room temperature, stibine is a gas and soluble in water. In aerobic waters or air, stibine becomes unstable and oxidizes to produce Sb203. In bed sediments, the formation of stibine produces a reducing environment and may remobilize antimony that was taken from solution. Another process that may cause remobilization of antimony is biomethylation, a process which results in the formation of volatile stibine derivatives (Clement, 1985).
The most important process that reduces aqueous transport of antimony is sorption to clays and minerals. In addition, insoluble compounds can be formed by the reaction of heavy metals with antimonite or antimonate (-f5). It is likely that most species of antimony in natural waters are soluble and very mobile and are eventually transported to the ocean. Bioaccumulation, however, is only a minor fate process for antimony (Clement, 1985).
2.2.1.2 Arsenic
Though a rare element, arsenic (As) is ubiquitous in the earth's crust and occurs in 7
hundreds of minerals, often with sulfur. With four possible oxidation states (3-, 0, 3+, and 5-f-), o arsenic's speciation is both complex and important in determining its fate. Interconversions of the ^ 3+ and 5+ states and organic complexation have the greatest impact of any transformations g (Clement, 1985). Arsenic is generally mobile in all environments in comparison to other metals.
- 28 -5302.001 -KIN-BUC_RA_FINAL_PT1
TABLE 2 - 1 SOMMAHV OK ClltMtCAl., PHySICAL, AND B lOI.CX; 1 CA I, I'HOPKHT I K.S
FOR CONTKMIHANTS OF CONCERN AT KIH-BOC LANDFILI.
ro to
Indicator Chemical
Antimony Arsenic Barium Benzene Beryllium Bis(2-Ethylhexyl)Phtha Cadmium Carbon Dlsul(Ide Chlorobenzene Copper 1, 2-DlchloroetlienB * . * • -DDT Manganese Naphthalene Nickel PCBs Vanadium Vlnyi Chloride Xylene
CAS no.
7440-36.0 7440-38-2 7440-39-2
71-43-2 7440-41-7
ilate 117-81-7 7440-43-9
75-15-0 108-90-7
7440-50-9 540-59-0 50-29-3
7439-96-5 91-20-3
7440-02-0 1336-36-3 7440-62-2
75-01-4 1330-20-7
Molecular Height (g/mole) Bef. (11
122 74.92
137.36 78.11 9
391 112.41 76 113 63.54 97
355 54.94
128.16 58.71
328 51 63
106
Water Solubility
tmg/1)
H a l . (1)
- — 1,7 80
---2,940
466
6.3Et3 5.00E-03
34.4
3.lOE-02
2.67E«03 1.98Et02
Vapor Pressure (mm hg)
B8f. (11
1 0
76 0
0 360 117 0
3.Z4E»2 5.5QE-06
0.087 0
7.70E-05
2.66E*03 lEtl
ll*jiu y ' 3 Law
Con^jLaiit
atm-mV mol-'K But, (2)
IIR NA NA
b 59K -03 NA
NA 1:23E-02 3.73E-03 NA
6 5fct:-n3
5.13E-04 NA NA NA
1.07K-03 NA
8.19E-02 7.04E-03
K« Irol/g)
Baf. (2»
83
54 3 30
54 243,000
530,000
___ 57
240
l.otj K_
Bef. (2)
_ _
. 2.12
2 2.(14
0.48 6.19
3.37
6.04
1.38 3.26
UCf rish (1/Kgl
Rot. (2)
1 44
5.2 19
ni 0 10
.'00 1 6
S4, 001)
•17 100,000
1 .17
(1) Clement, 1985 (2) Superfund Public Health Evaluation Manual (F.FA, 1986)
z&zi zoo 3a>i
I he chemical form of arsenic and the properties of the surrounding medium determine the degree of mobility of the metal.
When atmosphehc deposition, runoff from soils, and industhal discharge send arsenic into aqueous environments, it tends to cycle through the water column, sediments, and biota. Arsenate (As'") is generally the dominant species in aquatic systems, but biological activities may produce arsenite (As'*), methylated arsenicals (As '), and the highly volatile arsenic hydrides (AsHj) (EPA, 1984a). Most salts and compounds of arsenic are soluble in water (U.S. DHHS, 1985). Ambient pH and Eh (reduction-oxidation potential) conditions determine the prevailing form of the metal and thus influence its fate (EPA, 1979). Adsorption and desorption to sediments dominates the aquatic cycling process. Iron concentration affects aqueous arsenic sorption, and coprecipitation with hydrous oxides of iron is a prevalent process (EPA, 1979). Transport in solution to ocean sediments is the major sink for arsenic in water. Volatilization of arsenic or methylarsenics through biotransformations and highly reducing conditions is also an-important mobilization process (Clement, 1985). Due to arsenic's toxicity, bioaccumulation is not an important fate in aqueous media and is significant only in lower trophic levels (EPA, 1979).
On land and in the atmosphere, arsenic is also quite mobile. In the air, arsenic trioxide (AS2O3) is the dominant species. Arsenic particles remain in the atmosphere for only a short period before continuing to cycle through the environment. Wet or dry deposition removes arsenic from the air. The properties of the soil determine the fate of arsenic on land. Soils containing clays and organic matter sorb arsenic well and retard its leachability. Arsenic will mobilize into the ground water from soils with low sorptive capacity (EPA, 1984a). As with aquatic biota, bioaccumulation of toxic arsenic by terrestrial organisms contributes little to its transport and fate.
2.2.1.3 Barium
Barium (Ba) is a naturally occurring metal found in many types of rock. Limestones, sandstones, and soils in the eastern United States may contain 300-500 ppm barium (Federal Register, 1985). Barium is extremely reactive, decomposes in water, and readily forms insoluble carbonate and sulfate salts. Barium is present in solution in surface or ground water only in trace amounts. Large amounts will not dissolve because natural waters usually contain sulfate, and 7 the solubility of barium sulfate is generally low. Barium is not soluble at more than a few parts o per million in water that contains sulfate at more than a few parts per million. The presence of Q chloride or other anions may increase barium sulfate solubility (Clement, 1985), Principal areas t j where high levels of barium have been found in drinking water include parts of Iowa, Illinois,
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Kentucky, and Georgia (Federal Register. 1985). Monitoring programs show that it is rare to find
barium in drinking water at concentrations greater than 1 mg/1 (Clement, 1985).
Anthropogenic sources of barium include oil and gas drilling muds, coal fired power plants,
fillers for automotive paints and specialty compounds used in bricks, tiles, and jet fuels (Federal
Register, 1985).
Atmospheric particulate barium is removed by wet and dry deposition and it has a residence time of several days. In aquatic media, barium is likely to be present primarily as suspended particulate matter or sediments. In soils, barium is not expected to be very mobile because of its formation of water-insoluble salts and its inability to form soluble complexes with humic and fulvic materials. Under acidic conditions, however, some of the water insoluble barium compounds may be solubilized and move back into ground water (EPA, 1984g).
2.2.1.4 Beryllium
Beryllium (Be) is a naturally occuring element found in the earth's crust at an average concentration of 2.5 ppm. Beryllium is a metal with a complicated coordination chemistry and it can form complexes, oxycarboxylates, and chelates with a variety of materials. Beryllium is found chiefly as the minerals beryl, bromellite, chrysoberyl, and beryllonite.
In industry, beryllium is extensively incorporated into alloys with a variety of uses, such as electrical connectors, springs, precision instruments, aircraft engine parts, wheels, and pinions. Beryllium oxide is used in high-technology ceramics, electronic heat sinks, electrical insulators, and microwave oven components. Beryllium metal is used in aircraft brakes, precision instruments, and mirrors.
Most common beryllium compounds are readily soluble in water. However,, in water,
soluble beryllium salts are hydrolized to form beryllium hydroxide. The solubility of beryllium
hydroxide is quite low (2 mg/liter) in the pH range of most natural waters. Formation of hydrated
complexes may increase the solubility of beryllium somewhat, especially at higher pH where
polynuclear hydroxide complexes may form. It is probable, however, that in most natural aquatic
environments beryllium is present in particulate 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 not evidence
CD O
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-31 5302.001 •KIN-BUC_RA FINAL PT1
of food chain magnification. Airborne transport of beryllium, generally in the form of particulates. may also occur.
2.2.1.5 Cadmium
Cadmium (Cd) is found in very low concentrations (usually <1 ppm) in most rocks, as well as in coal and petroleum and often in combination with zinc. Geologic deposits of cadmium can serve as sources to ground-water and surface water, especially when in contact with soft, acidic waters, it is introduced into the environment from mining and smelting operations, and industrial operations including electroplating, reprocessing cadmium scrap, and incinerating cadmium containing plastics. The remaining cadmium emissions are from fossil fuel use, fertilizer application, and sewage sludge disposal. Landfill leachates are also an important source of cadmium in the environment (Federal Register, 1985).
Cadrhium appears in nature in the zero valence state (in metals and alloys) and most
often in the complexes.
divalent state (in compounds). Cadmium may form both organic and inorganic
Relative to other heavy metals, cadmium is very mobile in aquatic environments, although certain forms are insoluble in water and therefore less mobile (EPA, 1979). Hydrated cations and organic or inorganic complexes account for the cadmium that remains in solution. The principal fate of any cadmium migrating offsite in aquatic media, however, is sedimentation via sorption by clays or organic matter following organic complexion, especially with humic acids (Clement, 1985). Cadmium concentrations in sediments are generally at least an order of magnitude greater than those in thelambient water (EPA, 1979). The speciation of the cadmium ion and the degree to which the water is polluted, control the fate of the metal. The divalent metal cation predominates in acidic and approximately neutral waters. Higher pH yields complexes with carbonate and hydroxide ions. Hydrated divalent cation is common in unpolluted water, and organically
1
Gomplexed cadmium is found in polluted water (EPA, 1979).
Though investigations have been limited, cadmium transport in soil appears to be a slow
process. Cadmium sorption in soil is strong and correlates well with the organic content of the
ground (EPA, 1979). After adsorption, however, cadmium may desorb from the soil and
remobilize, bften as a result of a decrease in pH below seven or an increase in salinity (EPA, CD
1984b). i I ' • o
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I I I
I - 32 -
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5302.001-KIN-BUC RA FINAU_PT1
Dust and fumes containing cadmium reside in the atmosphere. Chemical interaction usually results in speciation rather than decomposition. The removal mechanism of these particles occurs through wet and dry deposition (EPA, 1984b).
Organisms at all levels of the food chain accumulate cadmium often by the replacement . of zinc in metabolic functions. Bioaccumulation or bioconcentration factors (the ratio of the concentration in the organism to the concentration in the surrounding water, abbreviated BCF) in aquatic biota generally range from 1,000 to 3,000 but may reach several hundred thousand (EPA, 1979).
Terrestrial plants do not significantly deplete cadmium concentrations in soils by absorption through their roots. However, concentrations of cadmium in plants may be elevated sufficiently to cause potential exposure to humans and animals through ingestion (Clement, 1985).
2.2.1.6 Chromium I
i
Chro'mium (Or) geiieiatly appears in nature in either a trivalent (Cr *) or hexavalent (Cr *) oxidation state. Other valences are relatively unstable and therefore do not contribute significantly to total concentration of clirpmium in the environment. The speciation dominates the fate of the metal. Hexavalent chromium is very water soluble and remains very mobile. On the other hand, for trivalent chromium, precipitation and adsorption are important processes.
Hexavalent chromium, a strong oxidizing agent, forms stable complex anions, such as chromate (CrO/') and dichromate (Cr^O/')- The high solubility of these anions is responsible for their great mobility in aquatic environments (Clement, 1985). When reduced to the trivalent state, chromium is usually hydrolized and precipitated as chromium hydroxide (Cr(0H)3) (EPA, 1979). Trivalent chromium may also adsorb on sediments or be consumed by aquatic and marine biota. Ambient conditions, such aspH, and the types of other compounds present influence the oxidation state formed in aquatic environments (Clement, 1985). Thus, conditions favorable to the trivalent state will lead to precipitation, adsorption, and bioaccumulation, while soluble forms of chromium will accumulate in aquatic settings favorable to Cr * formation.
Trivalent chromium accounts for nearly ail the chromium present in soils and sediments. Trivalent chromium is strongly adsorbed onto clays and organic soils. Soil components, with the
I A
exception of activated carbon, ;do not readily adsorb hexavalent chromium, which remains soluble ^
and mobile in ground water and surface water (EPA, 1979). Little hexavalent chromium is
leached from soil; instead it quic
organic content (Clement, 1985).
- 33 -
o
leached from soil; instead it quickly reduces to the trivalent state, especially in soils of high o
(- CX>
o 5302.001 -KIN-BUC_RA_F1NAL_PT1
Chromium occurs in the atmosphere as particulate matter. This dust may spread miles from its source, depending on particle size and density, before returning to the ground via fallout or precipitation (Clement. 1985).
Chromium may pass through the food chain especially by accumulation in aquatic and marine biota, whose chromium levels are usually much, higher than in the surrounding water, though lower than chromium levels in sediments. This indicates that the food chain is a greater source of chromium for aquatic life than is direct uptake from seawater (EPA, 1979). On land, plants tend to retain chromium in their roots and rarely translocate it to their leaves. This: in turn, limits the availability of chromium to terrestrial animals.
2.2.1.7 Copper
Copper (Cu) is a metal belonging to the First Transitional Series of the periodic table. Copper occurs in nature as the elemental metal (zero valence), and in the -i-l and +2 valence states. In addition to a variety of inorganic compounds, copper forms a number of compounds with organic ligands. Both organic and inorganic copper compounds have a variety of uses. Most Cu*' compounds are not stable in the environment, particularly in the presence of water or moisture and air, and tend to change to the stable Cu*^ state (Kust, 1979, as cited in EPA, 1985).
The aquatic fate of copper has been studied more extensively than its atmospheric fate. The two processes that are likely to dominate the fate of copper in aquatic media are chemical speciation and sorption (Callahan et al., 1979, as cited in EPA, 1985). The nature of chemical speciation of copper in aquatic media is determined by the Eh of the particular copper compound and the pHof the aquatic media. In aquatic media of pH <7, copper may exist in Cu*^ form, whereas at pH >7, copper may exist as the carbonate complex. In polluted water bodies, copper may form complexes with organic material in the water. Various sorption processes reduce the level of ionic state carbonate complex or organic complex of copper in aquatic media. Sorption onto clay materials, hydrous iron, manganese oxides, and organic material are the primary controlling factors (Callahan et al., 1979, as cited in EPA, 1985). In organically rich sediments, the sorbed and precipitated copper may become redissolved through complexation and may persist in the water for a long time. No estimate of the aquatic half-life of copper is available in the literature (EPA, 1985).
The fate of copper in soil has been studied inadequately; however, the fate may depend upon the pH of the soil, its moisture content, and its clay and organic matter content (NAS, 1977, as cited in EPA, 1985). In acidic soils, the solubility of copper may be more soluble, which would g enhance its mobility; the reverse may be true in basic soils. Soils rich in organic matter may
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enhance the mobility of copper through complexation. Both clay and organic matter may facilitate
the sorotion of copper in soil, however, and may retard its leachability. Soils with suitable
moisture content may enhance the microorganism activity and the partial removal of copper
through uptake by microorganisms. No estimate of the half-life of copper in soils is available;
however, copper is expected to be leached more readily from acidic and sandy soils than from
basic soils containing a higher percentage of clay and/or organic matter (EPA, 1985).
2.2.1.8 Lead
Lead' (Pb), is a naturally occurring heavy metal and can pass through soils, aquatic environments, the atmosphere, and the food chain. The species (oxidation states) of lead formed and their associated solubilities are important in determining lead's environmental mobility.
Metallic lead is stable in dry air: however, in moist air. it quickly forms lead carbonate. In general, the chemical properties of inorganic lead compounds are similar to those of the alkaline earth metals. The nitrate, chlorate, and acetate salts are water soluble; the chloride is slightly soluble; and the sulfate, carbonate, chromate, phosphate, and sulfide are insoluble. The aromate, carbonate, nitrate, sulfide, and phosphate are soluble in acid, and the chloride is slightly soluble in acid. Lead forms stable tetraalkyl compounds with organic ligands, for example tetramethyl, tetraethyl, tetraprophyl, and tetrabutyl compounds. They are soluble in many organic solvents but are insoluble in water. The tetraorganolead compounds decompose to lead metal and free organic radicals at elevated temperatures or in the presence of light. In the presence of oxygen, the thermal decomposition of tetraethyl lead produces lead oxide rather than the free metal. Lead also forms stable metal complexes with polydetate chelating agents, for example penicillamine or ethylene diaminetetra acetic acid (EDTA) (ATSDR, 1988b).
The jorimary mechanisms controlling the distribution of lead in the environment appears to be sorption. Soils readily adsorb lead at a pH above 5, but soils tend to desorb lead as pH becomes more acidic. Consequently, lead exhibits greater mobility in acidic waters and tends to accumulate,in sediments under neutral or alkaline conditions. The observed sorption method varies with soil conditions (Clement, 1985). Because studies show that only 0.6 percent to 1.6 percent of the total lead in soils should be leachable, runoff of suspended particles, rather than the leaching of soluble lead, should be the dominant migration pathway for contaminants in soils
at a site (Penwak et al., 1980). ^ ro o
In the atmosphere, lead exists primarily in the particulate form. Upon release to the
atmospere (mostly from fuel combustion), lead particles are dispersed, transformed by physical o
and/or chemical processes, and ultimately removed from the atmposhere by wet or dry deposition.
- 3 5 -5302.001-KIN-BUC_RA_FINAL,PT1
The average residence time of lead panicles in the atmosphere is expected to range between 7 and 30 days (ATSDR. 1988b).
In the; aquatic environment, speciation of the lead influences its fate. The divalent form (Pb ") is the stable ionic species of lead; hydroxide, carbonate, sulfide, and more rarely, sulfate may act as solubility controls in its precipitation. Tetraalkyl leads may also form by a combination of chemical/biological alkylation of inorganic lead compounds under appropriate conditions. The amount of lead that remains in solution depends upon the pH of the water and the dissolved salt content (ATSDR, 1988b).
The accumulation of lead in most soils is primarily a function of the rate of deposition from the atmosphere. Most lead is retained strongly in soli, and very little is transported into surface water or ground water. The fate of lead in soil is affected by processes which are dependent on such factors as soil pH, organic content of soil, the presence of inorganic colloids and iron oxides,
i
ion exchange characteristics, and the amount of lead in the soil (ATSDR, 1988b).
Bioaccumulation of lead occurs in a variety of organisms, though lead concentrations tend to.decrease with increasing trophic level or distance from the primary source in the food chain (EPA, 1979).! Except for some shellfish (e,g,, mussells), lead does not appear to bioaccumulate significantly in most fish (ASTDR, 1988b).
2.2.1.9 Manganese
Although manganese (Mn) can exist in all valence states from -3 to •f7 the inorganic chemistry of manganese is dominated by compounds in the +2. +4, and +7 oxidation states. The principal sources of manganese in the atmosphere are natural processes including continental dust, volcanic gas and dust, and forest fires, while the main anthropogenic sources are industrial emissions and combustion of fossil fuels. Atmospheric fate of manganese is determined by tropospheric chemical reactions and physical removal processes, while aquatic fate may be controlled by its ability to undergo chemical and microbial reactions - as in the case for manganese in soil (EPA, 1985a).
In air, manganese may undergo photochemical and thermal reactions which result in ^ speciation, but these reactions may not be directly responsible for its removal from the ;? atmosphere. Manganese may be removed from air through dry fallout or wet precipitation. It has been estimated that the atmospheric residence time for manganese, due to such physical removal p process, is approximately 7 days (EPA, 1985a).
^ • .
- 3 6 -5302.001-KIN-BUC .RA_FINAL_PT1
The fate of manganese in aquatic systems may be determined by its ability to undergo chemical and microbiological reactions. In most natural aquatic systems, manganese is expected to be present predominantly in the suspended particulates and sediments as MnOj or MnjO^. A small amount of manganese ion may remain as soluble Mn''. The maximum concentration of soluble Mn'"; may be limited by the solubility product of MnCOo and. under certain reducing conditions, by the MnS solubility product. The concentration of soluble chelated manganese in aquatic systems is likely to be less than soluble free manganese ions. Thus, although manganese may undergo speciation through chemical and microbiological reactions in systems, it may persist in aquatic systems for a long period. By analogy with aquatic iron, the residence time of aquatic manganese may be a few hundred years (EPA, 1985a). The BCF for manganese in a species of edible fish (striped bass) has been reported to be less than 10. Also, significant bioaccumulation of manganese may not occur with organisms of high trophic level (EPA, 1985a).
Both chemical and microbiological interactions may cause speciation of manganese in soils; soil pH and oxidation-reduction potential of soil may influence the speciation process. It has been suggested that in acid water-logged soils, manganese passes freely into solution and may leach into ground water. Also, manganese can be leached readily from waste burial sites and from other natural soils into ground water (EPA, 1985a).
2.2.1.10 Nickel
A relatively mobile heavy metal, nickel (Ni) commonly occurs in the elemental and divalent
states. Sorption processes and plant uptake may limit its mobility somewhat. Photolysis,
volatilization, and biotransformation do not play important roles in the environmental transport and
fate of nickel (Clement, 1985).
The overall passage of atmospheric nickel may be characterized as a short-lived transport process. Various chemical forms of nickel appear in the atmosphere as dust and fumes, but any chemical interactions of nickel usually result in conversion to nickel oxide (EPA, 1985b), The. length of stay in the atmosphere of nickel particulates before removal by wet or dry deposition depends on particle size and density. The average half-life in air is much longer for smaller particles, allowing greater transport distances. The average residence time for nickel in air is 7 days.
Nickel usually occurs in the divalent oxidation state in aqueous media and has a great affinity for organic liquids, hydrous iron, and manganese oxides. Most of the common aquatic g
organic liquids of nickel are soluble in water and support the metal's high mobility. However, ^^ sorption and coprecipitation involving hydrous iron and manganese oxides moderately limit nickel ^
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5302.001-KIN-BUC
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mobility, especially at high pH (EPA. 1979). Another factor that regulates the mobility of nickel
in aqueous media is the degree of pollution. Nonpolluted water favors sorption and precipitation,
while polluted waters provide organic groups needed for the formation of soluble nickel
compounds. Bioaccumulation of nickel by aqueous organisms is limited; bioconcentration factors
are usually on the order of 100 to 1,000 (Clement, 1985). In general, most nickel introduced to
rivers and streams eventually settles in ocean basins (EPA, 1979).
Analogous to aqueous media, the composition of the soil exerts a dominating effect on the fate of nickel in terrestrial settings. Soil high in iron and manganese oxides sorbs nickel significantly and impedes its movement. The metal remains mobile in ground water with a high organic content (EPA. 1985b). Plants may take up some nickel, while other plants identified as nickel-accumulating plants extract great amounts of nickel from soil. Nickel is reasonably mobile
in low pH and cation exchange capacity mineral soils, but less mobile in basic mineral soils and soils with high organic content. Nickel present in dump sites will have higher mobility under acid rain conditions and will be more likely to contaminate underiying aquifers (ATSDR, 1987).
i I
2.2.1.11 V a n a d i u m
I Vanadium can exist in the 0, +2, +3, +4, and -i-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
organometall ic compounds.
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 niateriais. Some vanadium compounds are volati le, and atmospheric transport of
fumes, as well as part iculates, can occur. Some bioaccumulat ion of vanadium occurs. However,
in mammals , it appears that excess vanadium can be rapidly excreted in urine. In humans, it is
excreted as sodium metavanadate or ammonium vanadyl tartiate.
2.2.2 O r g a n i c s
2.2,2.1 Benzene
Benzene is a clear, colorless, highly f lammable liquid and is slightly soluble in water co
(Windholz et al. , 1983). Volati l ization is the primary transport process at the site. Based on
cloud-chamber data, photooxidat ive destruction in the troposphere is thought to be rapid and §
complete (Clement, 1985). The half-life of benzene in the atmosphere has been reported to /v>
- 3 8 -5302.001-KIN-BUC _RA_FINAL.PT1
h j
range from 2.4 to 50 hours, depending on relative reactivities. Due to the relatively rapid attack
of hydroxyl radicals, and because benzene does not absorb at wavelengths of light longer than
260 nm. ciffiiision to the stratosphere and subsequent photolysis are not expected (Callahan et
al., 1979).' : • i -
Volatilization appears to be the major transport process of benzene from landfill to the ambient air, and atmospheric transport of benzene occurs readily. Inasmuch as volatilization is likely to be the main transport process, the atmospheric destruction of benzene is probably the most likely fate process.
2.2.2i2 Bis(2-ethylhexyi^hthalate (BEHP) i • •
r Bis(2|-ethylhexyl)phthalate is used as a plasticizer for polyvinyl chloride (PVC) and othe polymers in large quantities and s likely to be released to air and water during production and disposal of these plastic products.
Phthalate esters are bioaccumulated by a variety of organisms. There is little evidence to suggest that any long-term bioaccumulation or biomagnification, such as that demonstrated for some of the persistent organoctdorine compounds (PCBs and DDT), will occur for phthalate esters. Phthalate esters, however, are concentrated by higher animals and man in specific tissues and organs. Phthalates sirongly partition into the lipids (fats) of both plants and animals. BEHP released to water systems will biodegrade fairly rapidly (half-life of 2 to 3 weeks). There is evidence ,that they are degraded by microbiota and metabolized by fish and animals. The degree to which biotransformation and biodegradation occur is important in determining the significance of bioaccumulation as an aquatic fate process; however, it is not clear to what extent their effect is exerted. As a resiit, phthalates are not likely to biomagnify (EPA, 1979).
i ' •
Mixed microbial systems can degrade phthalate esters under aerobic conditions. Degradation' is generally slower under anaerobic conditions and ceases to be effective for bis(2-ethylhexyl)phthalate. A variety of multicellular organisms have demonstrated the ability to biotransform and eliminate phthalate esters. Hydrolysis will occur in the water column, but it may be too slow to be environmentally significant. Bioaccumulation, biotransformation, and biodegradation are probably the most important processes in determining the aquatic fate of phthalate esters (EPA, 1979). Atmospheric BEHP will be carried long distances and be removed by rain. VVashout by rain appears to be a significant removal process (Atlas, 1984). It is ^
unknown whether direct photolysis and photooxidation are important atmospheric processes. o
o o
i -39 5302.001 -KIN-BUCLRA_FINAL_PT1
\0
The phthalates are sparingly soluble in water and have very high organic carbon partition coefficients (Koc). As a result, they tend to adsorb strongly to soils, sediments, and organic material, and be highly immobile in the environment with the possible exception of surface water. transport of sediments.
2.2.2.3 Carbon Disulfide
The fate of carbon disulfide in soil and water is volatilization. The volatilization halflife has been estimated at 2.6 hours for a model river (Howard, 1990). The vapor pressure of carbon disulfide, 297 mm Hg, combined with its volatization half-life indicates that it would volatilize rapidly from soil (Howard, 1990). In solution, carbon disulfide would not absorb significantly to soil (Howard,, 1990) and, therefore, be available for transport. In air, carbon disulfide reacts with atomic oxygen and photochemically produces hydroxyl radicals with a half-life of around 9 days
(Howard. 1990). i
2.2.2;.4 Chlorobenzene
Chlorobenzene is a derivative of benzene and is a coloriess liquid that has low solubility in water (Windholz et al., 1983). Unlike many priority pollutants, it is not possible to predict a predominant transport and fate process for chlorobenzene. It is thought to evaporate to the atmosphere, where it undergoes photooxidation at a relatively rapid rate, but this has not been quantified in, the available literature. There is some evidence that photooxidation occurs in the presence of nitric acid, but this is not conclusive (Callahan et al., 1979). No evidence of the direct photolysis of chlorobenzene was found.
It should be noted that chlorobenzene is persistent in the environment and has a high affinity for lipophilic materials (Callahan et al., 1979). Due to its relatively high log octanol/water partition coefficient of 2.84 (EPA, 1986a), chlorobenzene is expected to move slowly through soil, and consequently, adsorb to any organic materials present. Biodegradation probably occurs eventually, but not at a substantial rate. Bioaccumulation of chlorobenzene may help to regulate its fate (Clement, 1985). If the rate of volatilization is more rapid than the rates of sorption and bioaccumulation, then atmospheric fate processes will dominate. Aquatic processes will dominate if the converse is true.
2.2.2.5 Trans-1,2-dlchloroethene T CD
Trans-1,2-dichloroethene is a highly volatile liquid which has low solubility in water and o causes narcotic effects when encountered in high concentrations (Windholz et al., 1983). ro
ro - 40 - 'p..
5302.001-KIN-BUC_RA_FINAL_PT1 ^ j J
Volatization is believed to be the predominant transport process for trans-1,2-
dichloroethe.ne. In air. hydroxyl radicals attack the double bound to form formic acid, hydrochloric
acid, carbon monoxide, and formaldehyde; thus photooxidation is the primary fate process
(Clement, 1985). The lifetime of trans-1,2-dichloroethene has been extrapolated to be less than
1 day (Callahan et al,, 1979). Diffusion to the stratospehre, where direct photolysis occurs, is not
expected.
Although there is not much support evidence, properties of similar compounds suggest that direct photolysis, hydrolysis, oxidation, adsorption, bioaccumulation, and biodegradation occur, but are insignificant in the aquatic environment (Clement, 1985). The octanol/water coefficient for trans-1,2-dichloroethene is low (1.48), which further suggests that bioaccumulation does not occur at a significant rate. Biodegradation occurs, but the rate is expected to be slow (Callahan et al.. 1979).
2.2.2.6 DDT
DDTiis an organochlorine pesticide which, together with its metabolites, is very persistent in the environment. Volatilization is most likely the most important transport process for p,p'-DDT and o,p'-DDT from soil and water. In addition, for the DDT isomers, sorption and bioaccumulation are the most important transport processes. Ultimately, p,p'-DDT, o,p'-DDT, and DDD are biotransformed to form bis(2-chlorophenyl)methanone (DDCD). Indirect photolysis may also be important for p.p'-DDT and o,p'-DDT in aquatic environmental (Clement, 1985).
2.2.2.7 Naphthalene
Specific information on the fate and transport of naphthalene is not available but can be inferred from information for polycyclic aromatic hydrocarbons (PAHs) in general. Adsorption'is the most important aquatic transport process for naphthalene. The log octanol/water partition coefficient indicates that naphthalene can be strongly adsorbed onto suspended and sedimentary particulate matter, especially particulates high in organic content. In addition, depending on the mixing rates in both the water column and air column, volatilization may play a role in transport (Clement, 1985).
Naphthalene is rapidly metabolized and excreted by animals and, therefore, : ro
bioaccumulation is not an important fate process. Biodegradation by microorganisms, which o
seems to be more efficient in soil than in aquatic systems, is most likely the ultimate fate process ^ for naphthalene (Clement, 1985), ^
{ • : •
-&. -41 -
5302.001-KIN-BUC RA_FINAL_PT1
2.2.2.8 PCBs
Polychlorinated biphenys (PCBs) are a family of compounds which vary widely in physical, chem.ical. and biological properties. For those compounds with four or fewer chlorine atoms per molecule, biodegradation by soil microorganisms appear to be the dominant fate process and results in significant destruction and transformation. PCBs with five or more chlorine atoms per molecule can be photolyzed with UV light. This process is extremely slow, but it may be the most important degradation process for these very persistent compounds.
Non-destructive processes which affect the distribution and transport of PCBs are absorption, 'volatilization and bioaccumulation. In natural water systems, the greatest concentration of these compounds is sorbed to suspended and bed sediments due to their very low solubility in water. The tendency of PCBs for absorbtion increases with the degree of chlorination and with the organic content of the sorbent. Once bound, the PCBs may persist for years with slow desorbtion providing continuous, low level exposure to the surrounding locality. The biota are another environmental compartment into which these compounds are strongly partitioned. When bioaccumulation occurs most of the compound is stored in the adipose tissue of the body.'
PCBs are relatively inert and therefore persistent with low vapor pressures and high log octanol/water partition coefficients. Despite their low vapor pressures, they have a high activity coefficient in water, which causes a higher rate of volatilization than might be expected. Volatilization and transport as an aerosol followed by a fallout with dust or rain is the probable cause of the ubiquitous distribution of PCBs. The more highly chlorinated species are less volatile than the lighter species. The presence of suspended solids tends to reduce volatilization, presumably because the solids absorb the PCBs and reduce the concentration in solution.
Individual PCBs vary widely in their physical properties according to the degree and
position of chlorination. Since all of these compounds have very low water soiuability, low vapor
pressure and a high dielectric constant, they were widely used for industrial processes.
Additionally, they have excellent thermal stability and are strongly resistant to oxidation and both
acidic or basic hydrolysis.
2.2.2.9 Trichloroethene w o
Trichloroethene (TCE) is a nonflammable, highly toxic, mobile liquid. Although TCE is not _
very soluble in water, it is soluble at levels that are harmful to health. g
- 4 2 -5302.001 -KIN-BUC _RA_F1NAL_PT1
h>
The most important transport process for trichloroethene in surface water and in the upper layer of soil is volatilization. Trichloroethene enters the troposphere by evaporation: then hydroxyl radicals attack the double bond to form hydrochloric acid, carbon dioxide, carbon monoxide, and carboxylic acid (Clement.' 1985). Based on the reaction with hydroxyl radicals, the reported lifetime in the troposphere is approximately 4 days. Oxidation is the primary fate of trichloroethene in the troposphere, and reportedly, photooxidation is so radid that it never enters the stratosphere. Therefore, direct photolysis does not contribute to the fate, because photolysis occurs above the ozone layer (Callahan et al., 1979).
In the aquatic environment, direct photolysis, hydrolysis, and oxidation do not contribute significantly to the fate of trichloroethene due to the rapid volatilization and the subsequent attack of the hydroxyl radicals. Additionally, the process of adsorption occurs but is not thought to be important. Based on available information, it is unclear whether trichloroethene can be biodegraded'by microorganisms, or if it must be destroyed through desorption. At least two species of microorganisms have been isolated that metabolize tnchloroethene (Newsweek, 1988) and there is some evidence that it can be metabolized by highear organisms. Finally, bioaccumulation in marine organisms may occur, but no biomagnification in the food chain has been observed (Clement, 1985). Studies have shown that bioaccumulation is directly related to a compound's octanol/water partition coefficient, which for trichloroethene is 2.47. This indicates that bioaccumulation is possible but is probably not as Important as volatilization (Callahan et al.,
1979). i i
Volatilization from the landfill is considered to be the primary transport mechanism. i I
2.2.2|.10 Vinyl Chloride
Vinyl! chloride is an extremely toxic and hazardous material by all avenues of exposure and is a recognized human carcinogen. It is slightly soluble in water and has an extremely high vapor pressure.
Limited data are available on the persistence of vinyl chloride in the environment,
particularly in surface waters, soil, and ground water. Although a half-life for vinyl chloride in
surface water has been estimated, significant uncertainty exists. The half-lives in surface water
range from |l to 5 days. Due to lack of data, it was not possible to estimate a half-life for vinyl g
chloride in soil or ground water.
i 9
(—
- 4 3 -5302.001-KIN-BUC RA FINAL_PT1
#
The fate of vinyl chlonde in soil is not known with certainty. Evaporation is expected to
be the predominant loss mechanism from the soil surface. The half-life from soil evaporation
should be longer than its evaporation half-life from water.
Due tp the high vapor pressure, volatilization from aquatic and terrestrial systems is the most important transport process for the distribution of vinyl chloride throughout the environment (Clement. 1985). Under most natural conditions, vinyl chloride should not remain upon release to an aquatic ecosystem. Half-lives in aquatic systems range from several minutes to a few hours. Photdoxidation in the troposphere is the dominant environmental fate of vinyl chloride.
Vinyl chloride reacts rapidly with hydroxyl radicals in the air. forming hydrogen chloride or formyl chloride. Formyl chloride, with a half-life of about 20 minutes, is reported to decompose at ambient temperatures, to carbon monoxide and hydrogen chloride. As a result, vinyl chloride in the troposphere should be decomposed within a day or two of release (Callahan et al., 1979). The hydrogen chloride formed is removed from the troposphere during precipitation (Clement. 1985).
Based on the information found, it does not appear that oxidation, hydrolysis, and biodegradation are important fate processes for vinyl chloride in aquatic environments. There is little information pertaining specifically to the rate of adsorption of vinyl chloride to particulate matter. Based on a low log octanol/water partition coefficient (1.38), vinyl chloride typically travels rapidly through subsurface strata and is often found as a contaminant in ground-water supplies.
2.2.2.11 Xylenes
Volatilization and subsequent photooxidation by reaction with hydroxyl radicals in the atmosphere are probably important transport and fate processes for xylene in the upper layer.of soil and in aquatic environments. Products of the hydroxylation reaction include carbon dioxide, peroxy acetyl nitrate (PAN), and cresol. Xylene binds to sediment in water and to organics in soils and undergoes microbial degradation. Biodegradation is probably the most important fate process in both soils and the aquatic environment. Xylenes have been shown to persist for up to 6 months in soil. Because of their low water solubility and rapid biodegration, xylenes are unlikely to leach into ground water in high concentrations (Clement, 1985).
7 ro o
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- 4 4 - - 5302.001-KIN-BUC_RA_FINAL_PT1
3.0 HUMAN EXPOSURE CALCULATION
For an exposure to occur at the Kin-Buc Landfill site, the following must be present; source, release mechanism, migration pathway (transport medium/media), exposure route, and receptor population. The following sections detail the presence or absence of these criteria, and provide estimates where appropriate. In addition, the intake levels for exposed populations, which are used to estimate hazard indices and carcinogenic risk, are presented in the last section.
3.1 Present and Potential Future Exposure Routes and Receptor Populations
The Kin-Buc Landfill, located in Edison Township, Middlesex County, New Jersey, is primarily an industrial and commercial area. The population of Edison Township in 1986 was 81.934 persons.
Two residential populations are within 1 mile of the Kin-Buc Landfill: a densely populated residential area located northwest of the site across the New Jersey Turnpike by Meadow Road; and an apartment complex located north-northeast near the Middlesex County College. There are three additional populationsto the north and east of the site. First, Middlesex County College is approximately % of a mile norfri-northeast, of Kin-Buc Landfill. Second, Heller Industrial Park is a light industrial park complex '72 mile northeast of the site. Third, the Mirror Lake Beach Club is approximately Vz mile northeast of the site. It is used by the employees and families of the Heller Industrial Park on a seasonal basis for swimming, boating, and tennis.
Based on a review of an available file information and discussions with representatives of the local health department, there are no private or potable wells presently drawing ground water from contaminated aquifers immediately downgradient of the Kin-Buc Landfill. Most of the public water supply in the area s from the Raritan River upstream of the site. Edison Township has six resen/e wells screened in the Brunswick" formation (bedrock) approximate 2y2 miles upgradient of Kin-Buc II. According to local health officials, these wells are currently not in use. In addition, Edison Township has 700 to 800 private and industrial wells upgradient of the site. None of these wells are located between the site and the Raritan River.
Eight exposure pathways were evaluated for the Kin-Buc Operable Unit 2 RA. The following is a discussion of the exposure pathways that were evaluated for each exposure media (soil, water, and air) and the reasons why other pathways were not evaluated. Table 3-1 presents a summary of all exposure pathtways evaluated and discounted.
•CD
O o
- 4 5 -5302.001 -KIN-BUC_RA_FINAL_PT1
TABLE 3-1 EVALUATION OF EXPOSURE PATHWAYS
SOIL
Onsite (Present) Ingestion - Not evaluated. No site excavation work is anticipated. No data. Dermal Absorption - Not evaluated. No site excavation work is anticipated. No data.
Offsite - Not evaluated. No data.
Sediments (Present) Ingestion - Evaluated for exposure during recreational activities. Dermal Absorption - Evaluated for exposure during recreational activities.
WATER ;
Ground Water (Future) Inhalation - Evaluated for exposure during showering. Ingestion - Evaluated for exposure from water consumption. Dermal Absorption - Evaluated for exposure during showering.
Surface Water (Present) Inhalation - Not evaluated. Other routes are adequate to assess surface water risks. Ingestion - Evaluated for exposure during recreational activities. Absorption - Evaluated for exposure during recreational activities. Fish Ingestion - Evaluated for exposure from fish consumption.
AIR
Onsite (Present and Future) Dust Inhalation - Not evaluated. Heavy machinery is not anticipated at this site. No
mechanism for dust release. VOC Inhalation - Not evaluated. Previous remediation eliminated exposure pathway.
Offsite (Present and Future) Dust Inhalation - Not evaluated. No mechanism for dust release. VOC Inhalation - Not evaluated. Early reports indicate landfill cap eliminated much of the
vapor migration.
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- 46 - ^ 5302.001-KIN-BUC_RA_F1NAL_PT1
Soil samples were not collected because the surficial soil on the landfill area is fill material and not natural soil; therefore, exposures from onsite soils were not evaluated in this risk assessment. The Kin-Buc Landfill site is fenced and access to the site controlled. Therefore, exposure of trespassers to contaminants in soils by inhalation, ingestion, or dermal absorption is not likely. In addition, no work is presently in progress onsite that would allow workers to come into contact with contaminated soils.
Ingestion or dermal absorption of contaminants in sediment will be evaluated for exposures during recreational activities in the surface waters surrounding the Kin-Buc Landfill. This exposure scenario will be evaluated for present use by adults and children living nearby.
Inhalation and dermal absorption exposures to ground water during showering were evaluated for potential future residents, both children and adults. Ingestion of ground water as a source of drinking water for potential future residents, adults and children, was also evaluated.
Ingestion and dermal absorption of surface water were evaluated for recreational exposures for present residents, both adults and children. Exposure to contaminants in surface water from the consumption of contaminated fish will also be evaluated. Inhalation effects of contaminants in surface water were considered negligable with respect to ingestion and dermal absorption exposures adequately address surface water exposures.
Exposure to contaminants in onsite air will not be evaluated. Previous studies indicated that some airborne vapors may have been a problem offsite but the capping of the landfill and the remediation of Pool C reduced or eliminated the vapors. Additionally, fugitive dust releases generated by wind and heavy machinery are not expected to occur.
3.2 Present and Future Exposed Populations
The Kin-Buc Landfill is located in Edison Township, Middlesex County, New Jersey, an
area that is primarily industrial and commercial. The population of Edison Township in 1986 was
• 81,934 persons.
Populations potentially exposed to contaminants that may migrate from the site include future residents who may use ground water for their basic water supply (e.g., drinking, showenng), residents who presently use the surrounding surface waters for recreation, and residents who presently consume fish caught in the surface waters surrounding the Kin-Buc site.
3.3 Human Intake Calculations c o
This section discusses the exposure equations used to estimate chemical intakes for >-'10
adults and children, for the contaminants of concern via exposure pathways discussed in g Section 3.2. Exposure equations for human exposure pathways were taken from the EPA's Risk
- 4 7 -5302.001-KIN-BUC _RA_FINAL^PT1
Assessment Guidance for Superfund. Volume I, Human Health Evaluation Manual (Part A) (EPA.
1990). Table 3-2 summarizes the variables used for intake calculations for each exposure
pathway,
3.3.1 Ingestion of Ground Water
Ingestion of contaminants will occur when an individual consumes tap water and beverages made from water withdrawn from a residential ground-water well. The ingestion rate used is based on the assumption that 100 percent of the fluid intake for the resident is from the contaminated ground-water source. PCBs were not detected in sand and gravel wells during the Operable Unit 2 Rl, but were detected during earlier investigations at the Kin-Buc site. In light of this, the PCB ground-water concentration used in this RA is from the 1987 RA for Operable Unit 1 (PRC, 1987).
Chronic exposure from ingestion ot contaminated ground water was calculated as follows
(EPA. 1989a): CDI = CWx IR X EFx ED
BW X AT Where:
CDI= Chronic Daily Intake (mg/kg-day) CW = Chemical Concentration in Water (mg/liter) IR = Ingestion Rate (liters/day) EF = Exposure Frequency (days/year) ED = Exposure Duration (years) BW = Body Weight (kg) AT = Averaging Time (days)
Variables: CW = Measured value IR = 2 liters/day (adult) (EPA, 19S9b)
0.8 liters/day (child) (EPA, 1989b) EF = 365 days/year ED = 30 years (adult)
9 years (child) BW = 70 kg (adult) (EPA, 1989b)
25 kg (child) (EPA, 1989b) AT = 70 years x 365 days/year (carcinogens)
30 years x 365 days/year (noncarcinogens for adults) T 9 years x 365 days/year (noncarcinogens for children) o
Table 3-3a presents exposures calculated for adults ingesting ground water and g
Table 3-3b presents the ground-water intakes for children. '^
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21-Feh-92
TABLE 3-2 VARIABLES USED FOR HUMAN INTAKE CALCULATIONS
4 ^
I
Contaminant
Source and Exposed
Population
Ground Water
Adults Children
Adults Children
Adults Children
Surface Water
Adults Children
Adults Children
Sediment
Adults Children
Adults Children
Fish
Adults Children
Exposure Route
Ingestion Ingestion
Inhalation Inhalation
Dermal Dermal
Dermal Dermal
Ingestion Ingestion
Dermal Dermal
Ingestion Ingestion
Ingestion Ingestion
CW
(nrxj/l)
RIDala RIData
-
RIData RIDala
RIData RIData
RIData RIData
-
-
CA (mq/mS)
-
(5) (5)
-
-
-
OS (mg/kg)
-
-
RIData RIData
RIData RIData
-
CF(1) (mg/kg)
-
-
(5) (5)
SA (cm2)
-
18150 9250
18150 9250
8620 4970
PC (cnVhr)
(6) (6)
(6) (6)
-
IR(2)
2 I/day 0.8 I/day
0.6 m3/hr 0.6m3/hr
-
lOOmg/day 200 mg/day
0.054 kg/day 0.054 kg/day
AF (mq/cm2)
-
.
1 45 1.45
-
-
ABS
(7) (7)
-
OR
-
0.05 0.05
Fl ET EF (hr/day) (day/yr)
0 2 0.2
0 2 0.2
1 2
1 2
-
1 1
1 1
365 365
365 365
365 365
7 21
7 21
7 21
7 21
365 365
ED (Yrs|_
30 9
30 9
30 9
30 9
30 9
30 9
30 9
30 9
OF (3)
1E-3 l/cm3 1 E-3 l/cm3
1 E-3 i/cm3 1 E-3 l/cm3
1E-6 kg/mg 1E-6kg/mg
1E-6kg/mg 1E-6kg/mg
BW
(kq)
70 25
70 25
70 25
70 25
70 25
70 25
70 25
70 25
AT (4) (years
70(30) 70(9)
70(30) 70(9)
70(30) 70(9)
70(30) 70(9)
70(30) 70(9)
70(30) 70(9)
70(30) 70(9)
70(30) 70(9) J
(1) Contaminant corKentratlon in fish (2) Ingestion or inhalation rate (3) Conversion Factor (4) 70 years (or carcinogens, 30 years lor noncarcinogens (or adults, 9 years lor noncarcinogens for children (multiplied by 365 days) (5) This value was modeled from Rl Data. (6) This value Is a chemical-specific permeability constant. (7) Sediment dermal contact absorption factors: 1%'=inorganics, 10%ssemi-volatiles organics and 25%':volatile organics other Abbreviations:
CW ' Contaminant corx:entralion in water CA - Contaminant concentration In air CS ~ Contaminant concentration in sediments SA •> Skin surface area available tor dermal contact AF > Soil-to-skin adherance factor CR - Contact Rate Ft •• Fraction ingested from contaminant source ET - Exposure Time
EF > Exposure Frequency
ED - Exposure Duration BW - Body Weight AT - Averaging Time
'oex '300
16-Jan-92
TABLE 3-3a GROUND-UATER INGESTION EXPOSURE CALCULATIONS
ADULTS
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs* (C)
4,4'-DDT (NC)
^ 4,A'-DDT (C)
O , Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Beryllium (C)
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadium (NC) (C) - Carcinogen (NO - Noncarcinogen
95% UCL Ground-water Concentration
(mg/l)
7.12E-02
8.47E-03
1.98E-01
2.89E-02
1 1.20E-02
5.47E-02
1.13E-02
1.79E-02
1.79E-02
2.00E-03
NA
NA
3.5AE-02
1.70E-02
1.70E-02
7.1AE-01
1.59E-03
1.59E-03
1.40E-03
A.12E+00
4.59E-02
6.05E-02
Ingestion Rate
(l/day)
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
2.00
Exposure Frequency (days/year)
365
365
365
365
365
365
365
365
365
365
365
365
365
. 365
365
365
365
365
365
365
Exposure Duration (years)
30
30
30
30
30
.30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
Body Weight (kg)
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
Averaging Time (days)
25550
10950
10950
10950
25550
10950
10950
10950
25550
25550
10950
10950
25550
10950
10950
25550
10950
10950
10950
10950
CDI (mg/kg-day)
8.72E-04
2.42E-0/.
5.66E-03
8.26E-0'i
LA/E-C
1.56E-03
3.23E-04
5.11E-04
2.19E-0A
2.45E-05
NA
NA
1.01E-03
A.86E-04
2.08E-04
2.0'iE-02
4.54E-05
1.95E-05
A.OOE-05
1.18E-01
1.31E-03
1.73E-03
NOTES: NA - Not Analyzed, Not Applicable, or Not Available * PCBs were detected in the refuse layer only.
eocT' ' 00 Da>j
16-Jan-92
TABLE 3-3b GROUND-WATER INGESTION EXPOSURE CALCULATIONS
CHILDREN
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Oichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs* (C)
( 4.4'-D0T (NC)
• 4.4'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Beryllium (C)
Cadmiun (NC)
Manganese (NC)
Nickel (NC)
Vanadium (NC) (C) - Carcinogen (NC) - Noncarcinogen
95X UCL Ground-water Concentration
(mg/l)
7.12E-02
8.47E-03
1.98E-01
2.89E-02
1.20E-02
5.47E-02
1.13E-02
1.79E-02
1.79E-02
2.00E-03
NA
NA
3.5AE-02
1.70E-02
1.70E-02
7.UE-01
1.59E-03
1.59E-03
1.A0E-03
A.12E+00
A.59E-02
6.05E-02
Ingestion Rate
(l/day)
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
0.80
Exposure F requency (days/year)
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
Expos Durat (yea
jre ion rs)
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
Body Weight (kg)
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
Averaging Time (days)
25550
3285
3285
3285
25550
3285
3285
3285
25550
25550
3285
3285
25550
3285
3285
25550
3285
3285
3285
3285
CDI (mg/kg-day)
2.93E-0A
2.71E-0A
6.3AE-03
9.25E-0A
A.9AE-05
1.75E-03
3.62E-0A
5.73E-0A
7.36E-05
8.23E-06
NA
NA
1.13E-03
5.AAE-0A
6.99E-05
2.28E-02
5.09E-05
6.5AE-06
A.A8E-05
1.32E-01
1.A7E-03
1.9AE-03
NOTES: NA - Not Analyzed, Hot Applicable, or Not Available * PCBs were detected in the refuse layer only.
t'oei 200 oaM
3.3.2 Inhalation of Cheinicals Volatilizing During Showering
Most of the exposures expectecj to occur at the Kin-Buc Landfill site involve direct ingestion of. or contact with, contaminated ground water, surface water, and sediment. Evaluation of these direct exposures does not involve the estimation of contaminant release or migration. However, to evaluate the exposures from inhalation of vapors during showering, an estimation model is required. Only VOCs are evaluated for this scenario, because of their superior vaporization capacity.
VOCs can be emitted when heated household water is sprayed out of a shower head. Because potential receptors may use ground water contaminated by site activities, they may be exposed to the VOCs identified in the ground water. To evaluate the risks associated with the emission of VOCs from shower water, equations are used which estimate the release efficiency of contaminants of concern by comparing them to the release efficiency of trichloroethene (TCE) which has been determined experimentally. Scaling to other chemicals is accomplished by assuming that the rate of volatilization between shower water and the air is proportional to the Henry's Law constant. The ratio of a contaminant's Henry's Law constant and TCE's Henry's Law constant can provide the efficiency of release for the contaminant in question. Henry's Law constants are based on standard temperature and pressure. Accordingly, as the temperature of water increases, the partial pressure of the gas is increased, as is the rate of volatilization. The method is derived from work by Andelman (1984, 1985a, and 1985b) and is outlined in the Gas Research Institute's (GRI) risk assessment manuals, (1988). This exposure scenaho will be evaluated for residents, both adult and children, who may potentially use ground water for showering.
In order to estimate the emission rate for VOCs from shower water, the release efficiency,
E, of the contaminant in question was first determined using the following relationship:
E = (E,CE) (H) / (H,CE)
Where:
E cE = efficiency of release of trichloroethene from water to air based on controlled experiments; 0.6 is a typical value (GRI, 1988) (unitless),
C3 O
H = Henry's Law constant for an organic compound m^-atm/mol, (Verschuren,1977), and p
52-O Cn
5302.001-KIN-BUC RA_FINAL_PT1
HTCE = Henry's Law constant for trichloroethene, 9.10E-03 m'-atm/mol (Verschuren. 1977).
As the contaminants are emitted into the shower area over a long period (approaching infinity), the concentration asymptotically approaches a maximum value. C„,. The time required to reach C: , is much longer than typical showering times of 5-15 minutes (GRI, 1988). O , is determined with the following relationship: .
C„=[(E)(FJ(C,)]/F3
Where:
C;n, = concentration of contaminant in air (mg/m )
E = release efficiency of the contaminant in question (unitless)
F, = flow rate of water in shower, typical value is 8 l/min (GRI, 1988)
C, = concentration of contaminant in shower water from onsite monitoring well
data (mg/l)
Fg = flow rate of air in the shower, typical value is 2.4 m /min
The rate constant, k, for the exponential function describing the contaminant air concentration over time is defined as the ratio between the air flow rate and the volume of the bathroom. A typical bathroom volume of 12 m was used.
With these parameters describing the concentration as it asymptotically approaches Ci„,
one can calculate the average concentration of a contaminant in the shower air over a duration
of ts minutes:
Ca = C„ [1 +(1/(kg)(exp(-kt3)-1)]
Ambient concentrations for contaminants released during showering are presented in ^
Table 3-4. ro
o o
- 5 3 -5302.001 -KIN-BUC_RA_FINAL_PT1
OJ
o
TABLE 3-A eSTlHAlEO AHBiam CONCENTRATION FOR CONTAMINANTS RELEASED DURING SHOWERING
COHPOUNO
Benzene Carbon Disulfide Chlorobenzene 1,2-Dichloroethene Vinyl Chloride Xylene (total)
WATER CONCENTRATION 95X UCL (mg/l)
Ct(mean) (a)
7.12E-02 8.A7E-03 1.98E-01 2.89E-02 1.20E-02 5.A7E-02
SHOWER TIME (min) ts (b)
12 12 12 12 12 12
FLOW RATES WATER (l/min)
Fw (c)
8 8 8 8 8 8
AIR (m3/min)
Fa (d)
2.A 2.A 2.A 2.A 2.A 2.A
BATHROOM VOLUME (m3) Vb (e)
12 12 12 12 12 12
HENRY'S LAW
(m3-atm/mol) H (f)
5.59E-03 1.23E-02 3.72E-03 7.00E-03 8.19E-02 7.0AE-03
ASYMPTOTIC AIR CONC (mg/ni3)
Cinf(mean) (9)
8.75E-02 2.29E-02 1.62E-01 A.A5E-02 A.01E-02 8.A7E-02
RATE CONST (1/min)
k (h)
0.2 0.2 0.2 0.2 0.2 0.2
RELEASE EFFICIENCY
COMPOUND E (i)
O.A 0.8 0.2 0.5 1.0 0.5
TCE E TCE (j)
0.6 0.6 0.6 0.6 0.6 0.6
HENRY'S LAW
(m3-atm/mol) H TCE (k)
9.10E-03 9.10E-03 9.10E-03 9.10E-03 9.10E-03 9.10E-03
AIR CONC
(mg/m3) Cs(mean) (I)
5.A3E-02 1.A2E-02 l.OOE-01 2.77E-02 2.A9E-02 5.26E-02
Ul
NOTES: a - Mean concentrations of contaminants found in ground water from onsite monitoring wells. b - Time that shower is used, average of 12 minutes used, c - Estimated flow rate of water in shower, typical value from GRI, 1988. d - Estimated flow rate of air in shower, typical value from GRI, 1988. e - Volune of bathroom, typical value from GRI, 1988. f - Henry's Law for conpound, from the Handbook: of Environmental Data (Verschuren, 1977) g - Asymptotic air concentration if shower ran for a long time (much longer than 5 minutes), calculated as,described in text. h - Rate constant for exponential function, calculated as described in text. i - Efficiency of release of compounds from water to air, calculated as described in text. j - Efficiency of release for trichloroethene, as determined through research (GRI, 1988). k - Henry's Law for trichloroethene. I - Air concentration in shower, calculated as described in text.
zoex ::oo oax
This scenario involves exposure of potential future residents, both adults and children, to contaminants in ground water through inhalation of volatiles during showenng.
Daily Intake (mg/kg-day) = CA x IR x ET x EF x ED BW X AT
Where: CA = Contaminant Concentration in Air (mg/m-) IR = inhalation Rate (m^/hour) ET = Exposure Time (hours/day) EF = Exposure Frequency (days/year) ED = Exposure Duration (years) BW = Body Weight (kg) AT = Averaging Time (days)
Variables: CA = Modeled from ground-water data IR = 0.6 m /hour (EPA, 1989b) ET = 0.2 hours/day (GRI, 1988) EF = 1 Bath (shower) per day, 365 days/yr ED = 30 years (adult)
9 years (child) BW = 70 kg (adult) (EPA, 1989b)
25 kg (child) (EPA, 1989b) AT = 70 years x 365 days/year (carcinogens)
30 years x 365 days/year (noncarcinogens for adults) 9 years x 365 days/year (noncarcinogens for children)
Tables 3-5a and 3-5b present exposures for vapors inhaled during showering for adults
and children.
3.3.3 Dermal Exposure To Shower Water
This scenario involves the exposure of potential future residents, both adults and children, to contaminants in ground water through dermal contact. All values were obtained from the Exposure Factors Handbook (EPA 1989b) unless othenwise noted.
Daily Intake (mg/kg-day) = CW x SA x PC x ET x EF x ED x CF BW x AT
Where:
o CW = Chemical Concentration in Water (mg/liter) 8 SA = Skin Surface Area Available for Contact (cm ) PC = Chemical-specific Permeability Constant (cm/hour)
o ET = Exposure Time (hours/day) o EF = Exposure Frequency (days/year) ED = Exposure Duration (years)
- 5 5 -
o <3D
530^001-KIN-BUC RA_F1NAL_PT1
16-Jan-92
TABLE 3-5a GROUND-WATER INHALATION OF VOLATILES WHILE SHOWERING
ADULTS
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dtchloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs* (C)
A,A'-DOT (NC)
A.A'-OOT (C)
OJ Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NO
Beryllium (NC)
Beryllium (C)
Cadmiun (NO
Manganese (NC)
Nickel (NO
Vanadium (NC) (C) - Carcinogen (NC) - Noncarcinogen
Modeled Air Concentration
(mg/m3)
5.A3E-02
1.A2E-02
1.00E-01
2.77E-02
2.A9E-02
5.26E-02
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
Inhalation Rate
(m3/hr)
0.60
0.60
0.60
0.60
0.60
0.60
Exposure Time
(hours/day)
0.2
0.2
0.2
0.2
0.2
0.2
Exposure frequency (days/year)
365
365
365
365
365
365
Exposure Duration (years)
30
30
30
30
30
30
Body Weight (kg)
70
70
70
70
70
70
Averaging Time (days)
25550
10950
10950
10950
25550
10950
CDI (mg/kg-day)
3.99E-05
2.A3E-05
1.71E-0A
A.75E-05
1.83E-05
9.02E-05
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NOTES: NA - Not Analyzed, Not Applicable, or Not Available
6081 300 oa>j
16-Jan-92
TABLE 3-5b GROUND-WATER INHALATION OF VOLATILES WHILE SHOWERING
CHILDREN
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Oichloroethene (NC)
Vinyl Chloride (C)
Xylene (NO
Naphthalene (NO
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyt)phthalate (C)
PCBs* (O
i^ A.A'-DDT (NO
A.A'-DOT (O
Antimony (NO
Arsenic (NO
Arsenic (O
Barium (NO
Beryllium (NO
Beryllium (C)
Cadmium (NO
Manganese (NC)
Nickel (NO
Vanadiun (NO
Modeled Air Concentration
(mg/m3)
5
1
1
2
2
5
.A3E
.A2E
OOE
77E
A9E
26E
-02
-02
-01
-02
-02
-02
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
Inhalation Rate
(m3/hr)
0.60
0.60
0.60
0.60
0.60
0.60
Exposure Time
(hours/day)
0.2
0.2
0.2
0.2
0.2
0.2
Exposure Frequency (days/year)
365
365
365
365
365
365
Exposure Duration (years)
9
9
9
9
9
9
Body Weight (kg)
25
25
25
25
25
25
Averaging Time (days)
25550
3285
3285
3285
25550
3285
CDI (mg/kg-day)
3.35E-05
6.82E-05
A.80E-0A
1.33E-0A
1.5AE-05
2.52E-0A
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA (C) - Carcinogen (NC) - Noncarcinogen
NOTES: NA - Not Analyzed, Not Applicable, or Not Available
o ie i zoo ,3ax
CF = Volumethc Conversion Factor for Water (1 liter/1000 cm') BW = Body Weight (kg) AT = Averaging Time (days)
Variables: CW = Measured value SA = l8,150cmMadult)
9,250cm' (child) PC = Chemical specific, from Table A-4 of the EPA, 1988 (EPA, 1988).
The PC for water is used if no PC is available ET = 0.2 hours/day EF = 1 bath (shower) per day, 365 days/year ED = 30 years (adult)
9 years (child) CF = 1 liter/1000 cm^ BW = 70 kg (adult)
25 kg (child) AT = 70 years x 365 days/year (carcinogens)
30 years x 365 days/year (noncarcinogens for adults) 9 years x 365 days/year (noncarcinogens for children)
Estimated exposures from dermal contact with contaminated ground water during
showering are presented in Tables 3-6a and 3-6b.
3.3.4 Derinal Contact With Surface Water Bodies During Recreation
This scenario involves the exposure of nearby residents, both adults and children, to
contaminants in surface water duhng recreational activities in the waters surrounding the Kin-Buc
site. All values were obtained from the Exposure Factors Handbook (EPA, 1989b) unless
otherwise noted.
Daily Intake (mg/kg-day) = CW x SA x PC x ET x EF x ED x CF BWx AT
Where: CW = Chemical Concentration in Water (mg/liter) SA = Skin Surface Area Available for Contact (cm ) PC = Chemical-specific Dermal Permeability Constant (cm/hr) ET = Exposure Time (hours/day) EF = Exposure Frequency (days/year) ^ ED = Exposure Duration (years) ra CF = Volumetric Conversion Factor for Water (1 liter/IOOO cm ) BW = Body Weight (kg) o AT = Averaging Time (days) °
00
- 5 8 -5302.001-KIN-BUC_RA FiNAL_PT1
16-Jan-92
TABLE 3-6a GROUND-WATER DERMAL ABSORPTION EXPOSURE WHILE SHOWERING
ADULTS
CHEMICAL
bis
bis
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dichloroethene (NC)
Vinyl Chloride ( O
Xylene (NO
Naphthalene (NC)
(2-Ethylhexyl)phthalate (NC)
{2-Ethylhexyl)phthalate (C)
PCBs* ( O
A.A'-DDT (NO
A,A'-ODT ( O
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Berylliun ( O
Cadmiun (NC)
Manganese (NC)
Nickel (NO
Vanadium (NC) (C) - Carcinogen (NC) - Noncarcinogen
95% UCL Ground-water Concentration
(mg/L)
7.12E-02
8.A7E-03
1.98E-01
2.89E-02
1.20E-02
5.A7E-02
1.13E-02
1.79E-02
1.79E-02
2.00E-03
NA
NA
3.5AE-02
1.70E-02
1.70E-02
7.1AE-01
1.59E-03
1.59E-03
1.A0E-O3
A.12E+00
A.59E-02
6.05E-02
Skin Surface Area (cm2)
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
Permeabi I ity Constant (cm/hr)
A.10E-01
5.50E-02
8.A0E-O;
8.A0E-0A
8.A0E-OA
8.A0E-0A
8.A0E-0A
8.A0E-OA
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
Exposure Time
(hours/day)
0.2
0.2
) 0.2
) 0.2
) 0.2
) 0.2
) 0.2
) 0.2
> 0.2
) 0.2
0.2
0.2
0.2
0.2
0.2
0.2
0.2
0.2
0.2
0.2
Exposure Frequency (days/year)
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
Exposure Duration (years)
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
Conversion Factor (L/cm3)
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
'0.001
0.001
0.001
0.001
0.001
Body Weight (kg)
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
Averaging Time (days)
25550
10950
10950
10950
25550
10950
10950
10950
25550
25550
10950
10950
25550
10950
10950
25550
10950
10950
10950
10950
GDI (dig/kg-day)
6.A9E-0A
2.A2E-05
8.62E-06
1.26E-06
2.2AE-07
2.38E-06
A.92E-07
7.80E-07
3.3AE-07
3.73E-08
NA
NA
1.5'.t-06
7.A1E-07
3.17E-07
3.11E-05
6.93E-08
2.97E-0a
6.10E-08
1.79E-0A
2.00E-06
2.6AE-06
NOTES: NA - Not Analyzed, Not Applicable, or Not Available (1) - Permeability Constant of water used in lieu of compourxl-specific values. * PCBs were detected in the refuse layer only.
STCT 200 oa><
21-Jan-92
TABLE 3-6b GROUND-WATER DERMAL ABSORPTION EXPOSURE WHILE SHOWERING
CHILDREN
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dichloroethene (NC)
Vinyl Chloride (C)
Xylene ( N O
Naphthalene (NO
bis(2-Ethythexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs* (C)
A,A'-DDT (NC)
g A.A'-DDT ( O
Antimony (NC)
Arsenic ( N O
Arsenic (C)
Barium ( N O
Berylliun ( N O
Beryllium (C)
Cadmium ( N O
Manganese ( N O
Nickel (NC)
Vanadium ( N O ( O - Carcinogen ( N O - Noncarcinogen
95X UCL Ground-water Concentration
(mg/L)
7.12E-02
8.A7E-03
1.98E-01
2.89E-02
1.20E-02
5.A7E-02
i.13E-02
1.79E-02
1.79E-02
2.00E-03
NA
NA
3.5AE-02
1.70E-02
1.70E-02
7.1AE-01
1.59E-03
1.59E-03
1.A0E-03
A.12E+00
A.59E-02
6.05E-02
Skin Surface Area (cm2)
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
Permeabi I i ty Constant (cm/hr)
A.lOE-01
5.50E-02
8.A0E-04
8.A0E-04
8.A0E-0A
8.AaE-0A
8.A0E-0A
8.A0E-0A
8.40E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
8.A0E-0A
Exposure Time
(hours/day)
0.2
0.2
) 0.2
) 0.2
) 0.2
) 0.2
) 0.2
) 0.2
) 0.2
) 0.2
0.2
0.2
0.2
0.2
0.2
0.2
0.2
0.2
0.2
0.2
Exposure Frequency (days/year)
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
Exposure Duration (years)
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
Conversion Factor (L/cm3)
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
Body Weight (kg)
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
Averaging Time (days)
25550
3285
3285
3285
25550
3285
3285
3285
25550
25550
3285
3285
25550
3285
3285
25550
25550
3285
3285
25550
CDI (rmj/kg-day)
2. 7aE-OA
3.A5E-05
1.23E-05
1.80E-06
9.59C-08
3.A0E-06
7.02E-07
1.11E-06
1.43E-07
1.60E-08
NA
NA
2.20E-06
1.06E-06
1.36E-07
A.AAE-05
9.88E-08
1.27E-08
1.12E-08
2.56E-0A
2.85E-06
A.8AE-07
NOTES: NA - Hot Analyzed. Not Applicable, or Not Available * PCBs were detected in the refuse layer only.
CTCT 300 OaM
Variables: CW = Measured value SA = 18.150cm' (adult)
9,250cm^ (child) PC = Chemical Specific value from Table A-4, EPA. 1988 (EPA, 1988).
PC for water is used if no PC is available ET = 1 hour (adult)
2 hours (child) EF = 7 days/year (adult)
21 days/year (child) ED = 30 years (adult)
9 years (child) CF = 1 liter/1000 cm^ BW = 70 kg (adult)
25 kg (child) AT = 70 years x 365 days/year (carcinogens)
30 years x 365 days/year (noncarcinogens for adults) 9 years x 365 days/year (noncarcinogens for children)
Exposure estimates for surface water contact are presented in Tables 3-7a and 3-7b.
3.3.5 Ingestion of Surface Water During Recreation
This scenario involves the exposure of nearby residents, both adults and children, to contaminants in surface water during recreational activities in the waters surrounding the Kin-Buc site. Values used were obtained from Exposure Factors Handbook (EPA, 1989b) unless otherwise noted.
Daily Intake (mg/kg-day) = CW x CR x ET x EF x ED BW X AT
Where: CW = Chemical Concentration in Water (mg/liter) CR = Contact Rate (liters/hour) ET = Exposure Time (hours/day) EF = Exposure Frequency (days/year) ED = Exposure Duration (years) BW = Body Weight (kg) AT = Averaging Time (days)
Variables: - CW = Measured value ro CR = 0.05 liters/hour ^ ET = 1 hour/day (adult) o
2 hours/day (child) g
- 6 1 - S 5302.001-KIN-BUC_RA_FINAL_PT1 *
t 16-Jan-92
TABLE 3-7a SURFACE WATER DERMAL ABSORPTION EXPOSURE WHILE SWIMMING
ADULTS
CHEMICAL
Benzene ( O
Carbon Disulfide (NC)
Chlorobenzene (NC)
1.2-Dichloroethene (NC)
Vinyl Chloride (C)
Xylene (NO
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs* ( O
A.A'-DDT (NC)
A.A'-DDT ( O
Antimony (NC)
^ Arsenic (NC)
Arsenic (C)
Barium (NC)
BerylliiOT (NC)
Beryllium (C)
Cadmium ( N O
Manganese (NC)
Nickel ( N O
Vanadium ( N O ( O - Carcinogen (NC) - Noncarcinogen
Surface Water Concentration
(mg/L)
1.53E-02
NA
7.57E-02
2.5AE-03
NA
1.A5E-01
7.A5E-03
NA
NA
5.1AE-0A
7.62E-05
7.62E-05
2.98E-02
3.17E-03
3.17E-03
1.59E-01
1.09E-03
1.09E-03
NA
A.A8E-01
1.66E-01
3.88E-02
Skin Surface Area (cm2)
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
18150
PermeabiIity Constant (cm/hr)
A.10E-01
8.A0E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
a.AOE-04 (1)
8.A0E-04 (1)
8.40E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
Exposure Time
(hours/day)
Exposure Frequency (days/year)
Exposure Duration (years)
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
Conversion Factor (L/cm3)
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
Body Weight (kg)
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
Averaging Time (days)
25550
10950
10950
10950
10950
25550
10950
25550
10950
10950
25550
10950
10950
25550
10950
10950
10950
CDI (mg/kg-day)
1.3AE-05
NA
3.16E-07
1.06E-08
NA
6.06E-07
3.11E-08
NA
NA
9.20E-10
3.18E-10
1.36E-10
1.2AE-07
1.32E-08
5.67E-09
6.64E-07
A.55E-09
1.95E-09
NA
1.87E-06
6.93E-07
1.62E-07
NOTES: NA
(1) -' Not Analyzed, Not Applicable, or Not Available Permeability Constant of water used in lieu of compound-specific values.
T£'T 200 3a>j
16-Jan-92
TABLE 3-7b SURFACE WATER DERMAL ABSORPTION EXPOSURE WHILE SWIMMING
CHILDREN
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1.2-Dichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NO
bis(2-Ethylhexyl)phthalate (C)
PCBs* ( O
A.A'-DDT (NO
a> A.A'-DDT ( O
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Beryllium (C)
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadium (NC) ( O - Carcinogen (NO - Noncarcinogen
Surface Water Sk Concentration
(mg/L)
1.53E-02
NA
7.57E-02
2.5AE-03
NA
1.A5E-01
7.A5E-03
NA
NA
5.14E-OA
7.62E-05
7.62E-05
2.98E-02
3.17E-03
3.17E-03
1.59E-01
1.09E-03
1.09E-03
NA
A.A8E-01
1.66E-01
3.88E-02
in Surface Area (cm2)
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
9250
^ermeabiIi ty Constant (cm/hr)
A.10E-01
8.A0E-0A (1)
8'.A0E-0A (1)
8.A0E-04 (1)
8.A0E-0A (1)
8.A0E-04 (1)
8.A0E-0A (1)
8.A0E-0A (1)
8.40E-0A (1)
8.40E-04 (1)
8.40E-0A (1)
8.40E-0A (1)
8.A0E-0A (1)
8.AOE-0A (1)
8.40E-0A (1)
8.A0E-0A (1)
8.A0E-0A (1)
Exposure Time
(hours/day)
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
Exposure frequency (days/year)
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
Exposure Durat i on (years)
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
Conversion Factor (L/cm3)
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
Body Weight (kg)
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
Averaging Time (days)
25550
3285
3285
3285
3285
25550
3285
25550
3285
3285
25550
3285
3285
25550
3285
3285
3285
COl (mg/kg-day)
3.A3E-05
NA
2.71E-06
9.08E-08
NA
5.19E-06
2.66E-07
NA
NA
2.36E-09
2.73E-09
3.50E-10
1.07E-06
1.13E-07
1.46E-08
5.69E-06
3.90E-08
5.01E-09
NA
1.60E-05
5.94E-06
1.39E-06
NOTES: NA Not Analyzed, Not Applicable, or Not Available
9I£I eoo oax
EF = 7 days/year (adult) 21 days/year (child)
ED = 30 years (adult) 9 years (child)
BW = 70 kg (adult) 25 kg (child)
AT = 70 years x 365 days/year (carcinogens) . 30 years x 365 days/year (noncarcinogens for adults) 9 years x 365 days/year (noncarcinogens for children)
Tables 3-8a and 3-8b present the levels for adults and children for ingestion of surface
water during swimming.
3.3.6 Dermal Contact With Sediments During Recreation
This scenario involves the exposure of nearby residents to contaminants found in sediments during recreational activities in the waters surrounding the Kin-Buc site. Values were obtained from the Exposure Factors Handbook (EPA. 1989b) unless othenA/ise noted.
Daily Intake (mg/kg-day) = CS x CF x SA x AF x ABS x EF x ED BW X AT
Where: CS = Chemical Concentration in Sediment (mg/kg) CF = Conversion Factor (10'® kg/mg) SA = Skin Surface Area Available for Contact (cm /event) AF = Soil to Skin Adherence Factor (mg/cm^) ABS = Absorption Factor (unitless) EF = Exposure Frequency (events/year) ED = Exposure Duration (years) BW = Body Weight (kg) AT = Averaging Time (days)
Variables: CS = Measured value CF = 10' kg/mg SA = 8,620 cm^/event (arms, hands, and legs) (adult)
4,970 cm^/event (arms, hands, and legs) (child) AF = 1.45 mg/cm^ (commercial potting soil) ABS = 0.01 for inorganics, 0.10 for semivolatiles, and 0.25 for volatiles, as ^
defined by New Jersey Department of ,S; Environmental Protection and Energy (NJDEPE)
EF = 7 events/year (adult) o 21 events/year (child) r-o
ED = 30 years (adult) 9 years (child) ^
- 6 4 -5302.001 -KIN-BUC _RA_FINAL_PT1
16-Jan-92
TABLE 3-8a SURFACE WATER INCIDENTAL INGESTION EXPOSURE WHILE SWIMMING
ADULTS
CHEMICAL
Benzene ( O
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dichloroethene (NO
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs* ( O
A,A'-DDT (NC)
, A,A'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Bariun (NC)
Beryllium (NO
Berylliun (C)
Cadmiun (NC)
Manganese (NC)
Nickel (NO
Vanadiun (NO (C) - Carcinogen (NC) - Noncarcinogen
Surface Water Concentration
(mg/l)
1.53E-02
NA
7.57E-02
2.5AE-03
NA
1.A5E-01
7.A5E-03
NA
NA
5.1AE-04
7.62E-05
7.62E-05
2.98E-02
3.17E-03
3.17E-03
1.59E-01
1.09E-03
1.09E-03
NA
A.A8E-01
1.66E-01
3.88E-02
Contact Rate (L/hr)
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
Exposure Time
(hr/event)
Exposure Frequency
(events/year)
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
Exposure Duration (years)
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
Body Weight (kg)
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
Averaging Time (days)
25550
10950
10950
10950
10950
25550
10950
25550
10950
10950
25550
10950
10950
25550
10950
10950
10950
CDI (mg/kg-day)
8.98E-08
NA
1.04E-06
3.A8E-08
NA
1.99E-06
1.02E-O7
NA
NA
3.02E-09
1.04E-09
A.47E-10
A.08E-07
4.34E-0a
1.86E-08
2.18E-06
1.49E-08
6.A0E-09
NA
6.14E-06
2.27E-06
5.32E-07
NOTES: NA - Not Analyzed, Not Applicable, or Not Available
8I£I '00 ;3a>
16-Jan-92
TABLE 3-8b SURFACE WATER INCIDENTAL INGESTION EXPOSURE WHILE SWIMMING
CHILDREN
CHEMICAL
Benzene (O
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Oichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs* (O
0» A,A'-DDT (NO Oi • A.A'-DDT (O
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Berylliun (NC)
Berylliun (C)
Cadnium (NC)
Manganese (NO
Nickel (NO
Vanadiun (NO (C) - Carcinogen (NC) - Noncarcinogen
Surface Water Concentration
(mg/l)
1.53E-02
NA
7.57E-02
2.5AE-03
NA
1.A5E-01
7.A5E-03
NA
NA
5.1AE-0A
7.62E-05
7.62E-05
2.98E-02
3.17E-03
3.17E-03
1.59E-01
1.09E-03
1.09E-03
NA
A.A8E-01
1.66E-01
3.88E-02
Contact Rate (L/hr)
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
0.05
Exposure Time
(hr/event)
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
Exposure Frequency
(events/year)
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
Exposure Duration (years)
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
Body Weight (kg)
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
Averaging Time (days)
25550
3285
3285
3285
3285
25550
3285
25550
3285
3285
25550
3285
3285
25550
3285
3285
3285
CDI (mg/kg-day)
A.53E-07
NA
1.7AE-05
5.85E-07
NA
3.3AE-05
1.71E-06
NA
NA
1.52E-08
1.75E-08
2.25E-09
6.B6E-06
7.30E-07
9.38E-08
3.66E-05
2.51E-07
3.23E-08
NA
.1.03E-0A
3.82E-05
8.93E-06
NOTES: NA - Not Analyzed, Not Applicable, or Not Available
'TCI 200 oa.^j
BW = 70 kg (adult) . 25 kg (child)
AT = 70 years x 365 days (carcinogens) 30 years x 365 days (noncarcinogens for adults) 9 years x 365 days (noncarcinogens for children)
Tables 3-9a and 3-9b present intake levels with sediment duhng recreation.
3.3.7 Ingestion of Sediment During Recreation
This scenano involves the exposure of nearby residents to contaminants fround in sediments during recreational activities in the water surrounding the Kin-Buc site. All values were obtained from the Exposure Factors Handbook (EPA, 1989b) unless othenwise noted.
• Daily Intake (mg/kg-day) = CS x IR x CF x Fl x EF x ED BW X AT
Where: CS = Chemical Concentration in Soil (mg/kg) IR = Ingestion Rate (mg soil/day) CF = Conversion Factor (10'® kg/mg) Fl = Fraction Ingested from Contaminated Source (unitless) EF = Exposure Frequency (days/year) ED = Exposure Duration (years) BW = Body Weight (kg) AT = Averaging Time (days)
\/ariables: CS = 1R =
CF = Fl = EF =
ED =
BW
AT =
: Measured value 100 mg/day (adult) (EPA, 1989a) 200 mg/day (child) (EPA, 1989a)
: 10' kg/mg 1
: 7 days/year (adult) 21 days/year (child)
= 30 years (adult) 9 years (child)
= 70 kg (adult) 25 kg (child)
= 70 years x 365 days/year (carcinogens) 30 years x 365 days/year (noncarcinogens for adults) 9 years x 365 days/year (noncarcinogens for children)
7\ CD
Tables 3-1 Oa and 3-1 Ob present exposure levels with sediment during recreation. o
o o
- 67 - '- 5302.001-KIN-BUC_RA_FINAL_PT1 O
21-Jan-92
TABLE 3-9a DERMAL CONTACT EXPOSURE WITH SEDIMENT
ADULTS
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dichloroethene (NO
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs (O
A.A'-DDT (NC)
*J° A.A'-DDT (O
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Berylliun (O
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadiun (NC) (O - Carcinogen (NC) - Noncarcinogen
Sediment 95% UCL Sk Concentration
(mg/kg)
1.30E-02
3.76E-03
3.20E-02
NA
NA
9.34E-01
3.87E-01
1.31Et02
1.31E+02
3.02E+01
NA
NA
7.16E+00
6.37E+01
6.37E+01
8.56E+01
1.33E+00
1.33E+00
2.10E+00
2.17E+02
A.95E+01
5.29E+01
n Surface Area (cm2)
8620
8620
8620
8620
8620
8620
8620
8620
8620
8620
8620
8620
8620
8620
8620
8620
8620
8620
Adherance Factor (nig/crn2)
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
1.45
Absorption Factor
(unitless)
0.25
0.25
0.25
0.25
0.1
0.1
0.1
0.1
,
0.01
0.01
0.01
0.01
0.01
0.01
0.01
0.01
0.01
0.01
Exposure Frequency (days/year)
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
Exposure Duration (years)
30
30
30
30
30
30,
30
30
30
30
30
30
30
30
30
30
30
30
Conversion Factor (kg/mg)
1E-06
1E-06
lE-06
lE-06
1E-06
1E-06
1E-06
lE-06
1E-06
1E-06
1E-06
lE-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
Body Weight (kg)
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
Averaging Time (days)
25550
10950
10950
10950
10950
10950
25550
25550
10950
10950
25550
10950
10950
25550
10950
10950
10950
10950
CDI (mg/kg-day)
A.77E-09
3.22E-09
2.74E-08
NA
NA
8.00E-07
1.33E-07
4.49E-05
1.92E-05
4.43E-06
NA
NA
2.A5E-07
2.18E-06
9.35E-07
2.93E-06
A.55E-08
1.95E-08
7.19E-08
7.43E-06
1.70E-06
1.81E-06
NOTES: NA - Not Analyzed, Not Applicable, or Not Available
I Z t l 200 Da>i
21-Jan-92
CHEMICAL
Benzene (O
Carbon Disulfide (NO
Chlorobenzene (HO
1,2-Oichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs* (O
^ A.A'-DDT (NC)
A.A'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic ( O
Bariun (NC)
Berylliun (NC)
Berylliun ( O
Cadmium ( N O
Manganese (NC)
Nickel (NO
Vanadiun (NC) (C) - Carcinogen (NC) - Noncarcinogen
DERMAL CONTACT
95% UCL Sediment Concentration
(mg/kg)
1.30E-02
3.76E-03
3.20E-02
NA
NA
9.3AE-01
3.87E-01
1.31E+02
1.31E+02
3.02E+01
NA
NA
7.16E+00
6.37E*01
6.37E-^01
8.56E+01
1.33E+00
1.33E+00
2.10E+00
2.17E+02
A.95E+01
5.29E+01
Skin Surface Area (cm2)
A970
A970
A970
A970
A970
A970
A970
A970
A970
4970
A970
A970
A970
A970
A970
A970
A970
A970
TABLE 3-9b EXPOSURE WITH SEDIMENT CHILDREN
Adherance factor
(m9/ciii2)
1.A5
1.A5
1.A5
1.45
1.A5
1.A5
1.45
1.A5
1.A5
1.A5
1.45
1.A5
1.A5
1.A5
1.A5
1.A5
1.A5
1.A5
Absorption Factor
(uni tless)
0.25
0.25
0.25
0.25
0.1
0.1
0.1
0.1
0.01
0.01
0.01
0.01
0.01
0.01
0.01
0.01
0.01
0.01
Exposure Frequency
(days/year)
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
Exposure Duration (years)
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
Conversion factor (kg/mg)
1E-06
lE-06
1E-06
lE-06
1E-06
1E-06
1E-06
lE-06
1E-06
1E-06
lE-06
IE-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
Body Weight (kg)
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
Averaging Time (days)
25550
3285
3285
3285
3285
3285
25550
25550
3285
3285
25550
3285
3285
25550
3285
3285
3285
3285
CDI (mg/kg-day)
6.93E-09
1.56E-08
1.33E-07
NA
NA
3.87E-06
6.A2E-07
2.17E-04
2.79E-05
6.44E-06
NA
NA
1.19E-06
1.06E-05
1.36E-06
1.42E-05
2.21E-07
2.84E-08
3.A8E-07
3.60E-05
8.21E-06
8.77E-06
NOTES: NA - Not Analyzed. Not Applicable, or Not Available
^^€.^ 200 •J8 . ;W
21-Jan-92
#
TABLE 3-10a INCIDENTAL INGESTION EXPOSURE OF SEDIMENTS
ADULTS
CHEMICAL
bis
bis
o
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1.2-Dfchloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
(2-Ethylhexyl)phthalate (NC)
{2-Ethylhexyl)phthalate (C)
PCBs ( O
A.A'-DDT (NC)
A.A'-DDT ( O
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Bariun (NC)
Berylliun (NC)
Beryllium (C)
Cadmiun (NC)
Manganese (NC)
Nickel (NO
Vanadiun (NC) ( O - Carcirwgen (NC) - Noncarcinogen
Sediment 95% UCL Concentration
(mg/ky)
1.30E-02
3.76E-03
3.20E-02
NA
NA
9.3AE-01
3.87E-01
1.31E+02
1.31E+02
3.02E+01
NA
NA
7.16E+00
6.37E+01
6.37E+01
8.56E+01
1.33E-»00
1.33E+00
2.10E+00
2.17E+02
A.95E+01
5.29E+01
Ingestion Rate
(mg/event)
100
100
100
100
100
100
6o
100
100
100
100
100
100
100
100
100
100
100
Exposure Frequency
(events/year)
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
7
Exposure Duration (years)
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
Conversion Factor (kg/mg)
1E-06
1E-06
1E-06
1E-06
lE-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
Body Weight (kg)
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
70
Averaging Time (days)
25550
10950
10950
10950
10950
10950
25550
25550
10950
10950
25550
10950
10950
25550
10950
10950
10950
10950
CDI (iiig/kg-diiy)
1.53E-10
1.03E-10
8.77E-10
NA
NA
2.56E-08
1.06E-08
3.59E-06
1.54E-06
3.55E-07
NA
NA
1.96E-07
1.75E-06
7.48E-07
2.35E-06
3.64E-08
1.56E-08
5.75E-08
5.95E-06
1.36E-06
1.A5E-()6
NOTES: NA Not Analyzed, Not Applicable, or Not Available
escT 200 a>
21-Jan-92
TABLE 3-10b INCIDENTAL INGESTION EXPOSURE OF SEDIMENT
CHILDREN
CHEMICAL
Benzene ( O
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dichloroethene (NC)
Vinyl Chloride (C)
Xylene (NO
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs* ( O
A.A'-DOT (NC) -4 -^ A.A'-DDT ( O
Antimony (NC)
Arsenic (NC)
Arsenic ( O
Bariun (NC)
Beryllium (NO
Beryllium (C)
Cadmium (NO
Manganese (NC)
Nickel (NO
Vanadiun (NO ( O - Carcinogen (NC) - Noncarcinogen
95% UCL ScdimcnLlngcst ion Concentration Rate
(mg/kg) (mg/event)
1.30E-02
3.76E-03
3.20E-02
NA
NA
9.3AE-01
3.87E-01
1.31E+02
1.31E+02
3.02E+01
NA
NA
7.16E+00
6.37E+01
6.37E+01
8.56E+01
1.33E+00
1.33E+00
2.10E+00
2.17E+02
A.95E+01
5.29E+01
NOTES: NA - Not Analyzed,
200
200
200
200
200
200
200
200
200
200
200
200
200
200
200
200
200
200
Not
Exposure Frequency (everus/year
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
21
Exposure Duration (years)
Applicable, or Not
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
ConversionBody Factor Weight (kg/mg) (kg)
1E-06
lE-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
1E-06
lE-06
1E-06
1E-06
1E-06
lE-06
Available
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
Averaging T i me (days)
25550
3285
3285
3285
3285
. 3285
25550
25550
3285
3285
25550
3285
3285
25550
3285
3285
3285
3285
COl (mg/kg-djy)
7.69E-10
1.73E-09
1.A7E-08
NA
NA
4.30E-07
1.78E-07
6.03E-05
7.75E-06
1.79E-06
NA
NA
3.30E-06
2.93E-05
3.77E-06
3.94E-05
6.12E-07
7.87E-08
9.67E-07
9.99E-05
2.28E-05
2.A3E-05
^Z£X Zoo 08)-/
3.3.8 Ingestion of Contaminated Fish From The Raritan River or Edmonds Creek
This scenario involves the exposure of nearby residents, both adults and children, to contaminants found in surface water as a result of consuming contaminated fish. All values are from the Exposure Factors Handbook (EPA, 1989b) unless otherwise noted.
Daily Intake (mg/kg-day) = CF x IR x Fl x EF x ED BWx AT
Where: CF = Contaminant Concentration in Fish (mg/kg) IR = Ingestion Rate (kg/meal) Fl = Fraction Ingested from Contaminated Source (unitless) EF = Exposure Frequency (meals/year) ED = Exposure Duration (years) BW = Body Weight (kg) AT = Averaging Time (days)
Variables: CF = Modeled Value by multiplying surface water concentration by the
bioconcentration factor (mg/l x 1/kg = mg/kg) IR = 0.054 kg/day (EPA, 1991) Fl = 1 EF = 365 days/year ED = 30 years (adult)
9 years (child) BW = 70 kg (adult)
25 (child) AT = 70 years x 365 days/year (carcinogens)
30 years x 365 days/year (noncarcinogens for adults) 9 years x 365 days/year (noncarcinogens for children)
The bioconcentration factors (BCF) for many of the compounds were acquired from the Ambient Water Quality Criteria documents for each chemical (EPA, 1980). The BCF for PCBs was obtained from the Handbook of Chemical Property Estimation Methods (Lyman, 1982). Additional BCFs were determined from the chemical's logarithmic octanol/water partition coefficient (log k^) using the following approximation (Veith, et al., 1979).
Log BCF = 0.85 Log K^ -0.70
A BCF of one was used for compounds that had no BCF or Log K^ Tables 3-1 la and 3-1 lb ^ present exposure levels from fish ingestion. •'
o o !\)
)-^ i o
- 72 - . iM
20Feb-92
TABLE 3-1 la EXPOSURES FROM FISH INGESTION
ADULTS
I
I
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Oichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Elhylhexyl)phlhalale (NC)
bls(2-Elhylhexyl)phlhalate (C)
PCBs* (C)
4.4'-DDT (NC)
4,4'-DDT (C)
Antimony (NC)
/Krsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Beryllium (C)
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadium (NC)
Surface W/aler Concentration
(mg/l)
1.53E-02
NA
7.57E-02
2.54E-03
NA
1.45E-01
7.45E-03
NA
NA
5.14E-04
7.62E-05
7.62E^5
2.98E-02
3.17E-03
3.17E-03
1.59E-01
1.09E-03
1.09E-03
NA
4.48E-01
1.66E-01
3.88E-02
BCF (I/kg)
5.2
0.0
100
1.6
1.2
117.8 (1)
229.1 (1)
741.3 (1)
741.3 (1)
100000.0
54000.0
54000.0
1.0
44.0
44.0
1.0 (2)
19.0
19.0
81.0
1.0 (2)
47.0
1.0 (2)
Amount Ingested (kg/day)
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
Exposure Frequency (days/year)
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
Exposure Duration (years)
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
30
Body
(kg)
70
70
70
70
70
70
70
70
70
70.
70
70
70
70
70
70
70
Averaging Time (days)
25550
10950
10950
10950
10950
25550
10950
25550
10950
10950
25550
10950
10950
25550
10950
10950
10950
CDI (mg/kg-day)
2.63E05
NA
5.84E-04
3.14E-06
NA
1.32E-02
1.32E-03
NA
NA
1.70E-02
3.17E-03
1.36E-03
2.30E-05
1.08E-04
4.61 E-05
1.23E-04
1.60E-O5
6.85E-06
NA
3.46E04
6.02E03
2.99E-05
(C) - (^rcinogen (NC) - Noncarcinogen
(1) - It no BCF was available in the literature, BCF was cak:ulated from the log Kow using Uie Veith equatk>n, (Veilh, el al, (2) - A BCF of one was used for compounds with no BCF or Log Kow. NA - Not Analyzed, Not Applicable, or 1^1 Available
1979).
9cCT 200 3a>)
20-Feb-92
TABLE 3-1 l b EXPOSURES FROM FISH INGESTION
CHILDREN
1
1
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1.2-0k:hloroelhene (NC)
Vinyl Chk>ride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Elhylhexyl)phthalate (NC)
bis{2-Ethylhexyl)phthalate (C)
PCBs- (C)
4,4-DDT (NC)
4,4'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Beryllium (C)
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadium (NC)
(C) - Carcinogen (NC) - Noncarcinogen
Surface Water (^rKenlration
(mg/l)
1.53E-02
NA
7.57E-02
2.54E-03
NA
1.45E-01
7.45E-03
NA
NA
5.14E-04
7.62E05
762E-05
2.98E-02
3.17E-03
3.17E-03
1.59E-01
1.09E-03
1.09E-03
NA
4.48E-01
1.66E-01
3.88E-02
BCF (1/kg)
5.2
0.0
10.0
1.6
12
117.8 (1)
229.1 (1)
741.3 (1)
741.3 (1)
100000.0
54000.0
54000.0
1.0
44.0
44.0
1.0 (2)
19.0
19.0
81.0
1.0 (2)
47.0
1.0 (2)
Amount Ingested (kg/day)
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
0.054
Exposure Frequency (days/year)
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
365
Exposure Duration (years)
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
Body Weight
(kg)
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
25
Averaging Time (days)
25550
3285
3285
3285
3285
25550
3285
25550
3285
3285
25550
3285
3285
25550
3285
3285
3285
CDI (mg/kq-day)
2.21 E-05
NA
1.64E-03
8.78E-06
NA
3.69E-02
3.69E-03
NA
NA
1.43E 02
8.89E-03
1.14E-03
6.44E-05
3.01 E-04
3.e7E-05
3.43E-04
4.47E-05
5.75E-06
NA
9.68E-04
1.69E-02
8.38E-05
(1) - If no BCF was available In the literature. BCF was cak:ulated from the Ljog Kow using the Veith equatk>n, (Veith, el al, (2) - A BCF of one was used for compounds with no BCF or Log Kow. NA - Not Analyzed, Not Applicable, or Not Available
1979).
L7.Z \ ZOO Da>i
4.0 CHEMICAL-SPECIFIC TOXICITY EVALUATION
The objective of this toxicity assessment is to descnbe, through the exposure routes identified in Section 3.0 of this report, the nature and extent of potential health and environmental hazards that may be associated with the contaminants of concern at the Kin-Buc Landfill site. This section contains information on pharmacokinetics, human health effects, and dose-response assessments for the contaminants of concern.
in the pharmacokinetic sections, the absorption, distribution, metabolism, and excretion of particular chemicals are discussed. Under human health effects, the various human side effects from exposure to a chemical will be listed. These effects may include toxicity, carcinogenicity, mutagenicity, and teratogenicity. The dose-response sections will discuss the correlation between a particular dose of a chemical and the response in the exposed individual. These sections will also include several human health criteria, such as carcinogenic slope factors, and the chemical concentrations associated with specific cancer risk levels.
EPA has developed water quality criteria to help protect human health and aquatic life. Human health criteria include toxicity and carcinogenicity protection factors. For carcinogens, EPA established concentrations corresponding to several incremental lifetime cancer risk levels (i.e., 1E-05, 1E-06, and 1E-07). A risk of 1E-05, for example, indicates a probability of one additional case of cancer for every 100,000 people exposed (Federal Register, 1980).
Maximum Contaminant Levels are standards established under the Safe Drinking Water Act and represent the allowable concentrations in public water systems. In general, MCLs are based on lifetime exposure (70 years) to the contaminant of concern for a 70-kilogram adult who consumes 2 liters of water per day. In addition to health factors, EPA's development of MCLs also considered the technological and economic feasibility of removing the contaminant from the water supply (EPA, 1989a).
EPA is also developing maximum contaminant level goals (MCLGs). Unlike MCLs, the
MCLGs are entirely health-based. They are, therefore, always less than or equal to MCLs.
Carcinogenic slope factors (SFs) are frequently used to help compare the carcinogenic
effects among various chemicals. These values are also used to determine risks to individuals. -
The slope values (or unit risks) are upper 95-percent confidence limits on the slope of the o
dose-response curve. Assuming low-dose linearity, the slope value represents the excess lifetime ^
risk due to a continuous lifetime exposure of one unit of carcinogen concentration. A generalized g
-75 5302.001 -KIN-BUC_RA_F1NAL_PT1
ro
dose-response curve is shown in Figure 4-1. For inhalation and ingestion, typical exposure units are milligrams per kilogram of body weight per day.
Table 4-1 lists the carcinogenic slope factors and other toxicity values for the selected chemicals at the Kin-Buc Landfill site.
EPA has also developed acceptable intake toxicity values for noncarcinogens. The acceptable toxicity values are chronic and subchronic Reference Doses (RfD and RfD ) for oral exposure and Reference Concentrations (RfC) for inhalation exposures. The RfD is the toxicity value most used in evaluating noncarcinogenic effects resulting from exposure at Superfund sites, and has replaced the acceptable daily intake (ADI) as the EPA's preferred value. These values are expressed in units of milligrams per kilogram of body weight per day. Subchronic RfDs are estimates of a daily exposure level for the human population, including sensitive subpopulations, that are not expected to present an appreciable risk of deleterious effects if the exposure were to occur for a pehod of less than 7 years. Chronic RfD is an estimate of a lifetime daily exposure level that is not expected to present an appreciable risk. Because there are no subchronic exposure scenarios likely to occur at the Kin-Buc site, subchronic reference doses (RfDj) will not be used in this report. Table 4-1 contains chronic RfD and RfC values for both oral and inhalation routes of exposure. Oral RfDs and slope factors are used for dermal exposures.
4.1 Inorqanics
4.1.1 Antimony
Antimony is a metal which is a byproduct of base metal and silver ores. It is primarily used in industry for flame proofing textiles and vulcanizing rubber. It is also used in the manufacture of paint, electronic semiconductors, and thermoelectric devices. In addition, . antimony has been used in the treatment of leishmaniasis. Antimony has two valence states: +3 and +5. It is estimated that the human daily intake of antimony from all sources is about 100 ug/day, or 1.4 ug/kg-day for a 70 kg adult (Schroeder, 1970).
Pharmacokinetics
Antimony is metal which is a byproduct of base metal and silver ores. It is primarily used 7\
in the manufacture of paints, electronic semiconductors, and thermoelectric devices. In addition, (~>
antomony has been used in the treatment of leishmaniasis. Antimony has two valence states: Q o
CO h>
-76 5302.001 -KIN-BUC_RA_FINAL.PT1
FIGURE 4-1 GENERALIZED DOSE-RESPONSE CURVE
tu
z o a. Ui Ui
c
z at u c LU
I I I i t ; i i 1 I ' 'i 11 1 I I I I 111 i
5 10 20 50 100 200 400 800 2,000 DOSS (mg/kg-day)
7\ CD O
O
o
- 7 7 -
co o
21-Jan-92
TABLE A-1 CRITICAL TOXICITY VALUES FOR ORAL AND INHALATION ROUTES
00
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs (C)
4,4'-0DT (NC)
4,4'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Beryllium (C)
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadiun (NC) (C) - Carcinogen (NC) - Noncarcinogen
Oral RfD *
(mg/kg-day)
NA
l.OOE-01 (1)
2.OOE-02 (1)
9.00E-03 (1)
NA
2.00E+00 (1)
4.00E-03
2.00E-02 (1)
NA
NA
5.00E-04 (1)
NA
4.0OE-0A (1)
l.OOE-03
NA
7.00E-02 (1)
5.00E-03 (1)
NA
5.00E-0A (1)
1.00E-01 (1)
2.00E-02 (1)
7.OOE-03
SF •• 1/(mg/kg-day)
2.90E-02 (1)
NA
NA
NA
2.30E+00 (1)
NA
NA
NA
1.40E-02 (1)
7.70E+00 (1)
NA
3.40E-01 (1)
NA
NA
NA
NA
NA
4.30E+00 (1)
NA
NA
NA
NA
Inhalation RfC •
(mg/kg-day)
3
6
9
NA
OOE-03
OOE-03 (1)
NA
NA
OOE-02
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
SF ** 1/(mg/kg-day)
2.90E-02
NA
NA
NA
2.94E-01
NA
NA
NA
NA
NA
NA
3.40E-01
NA
NA
5.00E+01
NA
NA
8.40E+00
NA
NA
NA
NA
NA - Not Analyzed, Not Applicable, or Not Available • Reference Dose/Reference Concentration
** Carcinogenic Slope Factor (1) Values obtained from IRIS (1990). A l l other values obtained from HEAST FY90.
TCCI 2 0 0 oa>j
-r3 and -H5. It is estimated that the human daily intake of antimony from all sources is about 100 ug/day, or 1.4 ug/kg/day for a 70 kg adult (Schroeder, 1970).
Human Health Effects
Little is known concerning the health effects of antimony, its toxicity appears to be similar to arsenic, although there is no evidence of carcinogenicity for antimony. In humans, antimony is acutely irritating to the gastrointestinal tract following ingestion. Antimony can also affect the heart, skin, respiratory tract, and liver. The primary cardiac effects are altered electrocardiograms bradycardia, and lowered blood pressure (NIOSH, 1978; Brieger et al., 1954). Little information is available concerning the dose response relationship in humans.
In animals, the toxicity of antimony is dependent on the form of antimony. For instance, water soluble antimony (e.g., antimony potassium tartrate) is more acutely toxic than a water insoluble form (e.g., antimony trioxide). Overall, the toxic effects are similar in animals and humans. Rats administered 130 mg/kg antimony trichloride developed myocardial degeneration. Lower doses (12 or 20 mg/kg-day) of antimony trichloride in guinea pigs resulted in altered blood values (decreased hemoglobin, increased reticulocyte count) (Arzamastsev, 1964).
Schroeder et al. (1970) exposed rats to 5 ppm antimony tartrate in the water for a lifetime. The authors estimate that the actual dose of antimony was 0.35 mg/kg-day. No significant pathology was observed, however, exposed rats had significantly shorter life spans. Similar results were obtained in studies in mice (Kanisawa and Schroeder, 1969). There is evidence that the toxicity results from inhibition of glucose metabolism.
There was no evidence found to suggest carcinogenicity due to antimony ingestion.
Dose-Response Assessment
EPA has derived an oral RfD of 0.4. ug/kg-day from the Schroeder et al. (1970) study
(IRIS, 1989).
4.1.2 Arsenic
Pharmacokinetics
In mice, approximately 90 percent of orally administered trivalent arsenic (As^*) or
pentavalent arsenic (As^*) was absorbed through the gastrointestinal (Gl) tract (Casarett and
-79 5302.OO1-KIN-BUC_RA_FINAL_PT1
7^ CD O
O o rv'
CO CO
ro
Doull. 1986). In humans, up to 95 percent of administered inorganic arsenic is absorbed (EPA, 1984a). Following absorption into the blood, arsenic was rapidly and widely distributed to all body tissues. The highest percentage of arsenic was found in the liver and kidneys (Clayton and Clayton, 1981).
Arsenic is excreted primarily in urine. The biological half-life of ingested inorganic arsenic is about 10 hours, and the half-life of methylated arsenic in humans is about 30 hours. Arsenic is also excreted through desquamation of skin and in sweat (Casarett and Doull, 1986).
Results of studies indicate that placental transfer of arsenic is possible (Casarett and
Doull, 1986).
Human Health Effects
Arsenic poisoning produces a variety of effects in humans. Acute poisoning of humans who have ingested as little as 130 mg of arsenic has been reported. Acute poisoning is characterized by nausea, vomiting, diarrhea, abdominal pain, and severe gastrointestinal damage.
Chronic arsenic poisoning is associated with digestive and nervous system problems, liver damage, and kidney problems. Dermal effects of chronic toxicity include hyperkeratosis and arsenical melanosis. Mucous membrane effects of chronic toxicity include irritation of the nose and pharynx. Arsenic is a recognized carcinogen of the skin, lungs, and liver. It is a cumulative poison in mammals, although a small percentage is considered essential for normal life (Clayton and Clayton, 1981). The NIOSH permissible exposure limit for arsenic is 10 ag/m^ (USDHHS, 1985). The time weighted average (TWA) for arsenic is 0.2 mg/m^ The MCL for arsenic is currently set at 0.05 mg/L.
Dose-response Assessment
Studies discussed in the Arsenic Health Effects Assessment document (EPA, 1984a)
present useful human dose-response information. One study involved 74 individuals who had
ingested arsenic-containing antiasthmatic herbal preparations for periods ranging from less than
6 months (intermittent ingestion) to 15 years. Doses were estimated to be 2.5 mg arsenic/day
as arsenic oxide (trivalent arsenic) or 10.3 mg arsenic/day as arsenic sulfides. The following ^
systems of the individuals were affected: cutaneous (91.9 percent), neurological (51.3 percent),
gastrointestinal (23 percent), hematological (23 percent), and renal and other (19 percent); 5.4 o
percent of the patients had internal malignancies.
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7^
In this study, the major effects in more than 10 percent of the subjects were generalized hyperpigmentation (arsenical melanosis), hyperkeratosis of palms and soles, "raindrop" dipigmentations, palmar and plantar hyperhidrosis, multiple arsenical keratoses, sensorimotor polyneuropathy, fine finger tremors, persistent chronic headache, lethargy, weakness and insomnia, psychosis, gastritis or gastroenteritis, mild iron deficiency anemia as a result of toxic marrow suppression, and transient albuminuria without azotemia. The-internal malignancies consisted of two squamous-cell carcinomas of the lungs, one squamous-cell carcinoma of the gall bladder, and one hemangiosarcoma of the liver. Similar neurological effects were obsen/ed in people who consumed approximately 3 mg arsenic/day in contaminated soy sauce for 2 to 3 weeks.
Other studies have indicated that airborne .arsenic compounds are associated with skin lesions, cardiovascular and respiratory effects, and peripheral neuropathy, but no adequate exposure information is available for any of the studies (EPA. 1984a).
Chronic inhalation exposure to arsenic compounds results in symptoms similar to those obsen/ed following oral exposure (EPA, 1984a). For example, a direct relationship has been reported between the length and intensity of exposure of smelter workers to airborne arsenic, predominantly as arsenic trioxide, and alterations in peripheral nerve function. No studies were available in which exposure levels are characterized sufficiently for the determination of dose-response relationships (EPA, 1984a).
Numerous arsenic compounds, particularly trivalent inorganics, have been associated with lung and skin carcinomas in humans. In two studies, (EPA. 1984a), investigators surveyed 40.421 residents of Taiwan who had consumed artesian well water containing 0.01-1.8 mg/l arsenic for 45 to 60 years. A dose-response relationship was established between the prevalence of skin cancer and arsenic consumption, which was based on arsenic concentrations in different wells and length of exposure (age). The overall incidence of skin cancer was 10.6/1,000; the maximum incidence was 209.6/1,000 in males over 70 years of age (EPA, 1984a). The EPA Risk Assessment Council has recently recommended that the risk associated with ingestion exposure of inorganic arsenic be scaled down by a factor of 10 based on the Council's judgment that exposures by this route are less likely to induce lethal cancers (Moore, 1987, as cited in EPA, 1984a). The reference dose for arsenic is presently set at 1E-03 mg/kg-day (EPA, 1990). The Q
Federal Water Quality Criteria (WQC) for arsenic in freshwater are 360 and 190 [xg/L for
subcronic and chronic exposures respectively. WQC for saltwater are 69 and 36 jig/L for g subchronic and chronic exposures respectively.
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4.1.3 Barium
Pharmacokinetics
Barium is at least partially absorbed by the human body following ingestion. McCauley and Washington (1983, as cited in EPA. 1984b) studied the absorption of various barium salts and reported the relative absorption rate to be: barium chloride > barium sulfate > barium carbonate.
Human Health Effects
Acute exposure to barium results in a variety of cardiac, gastrointestinal, and neuromuscular effects (Federal Register, 1985). There are no reports of carcinogenicity, mutagenicity, or teratogenicity associated with barium or its compounds (Clement. 1985).
Insoluble forms of barium, particulariy barium sulfate, are not toxic by ingestion or inhalation because only minimal amounts are absorbed. However, soluble barium compounds are highly toxic in humans after exposure by either route. The most important effect of acute barium poisoning is a prolonged stimulant action on muscle (Clement, 1985). Welch, et al., (1983, as cited in EPA, 1984b) reported that the antinociceptive and lethal effects of barium chloride could be reversed by naloxone or atropine.
Effects on the hematopoietic system and cerebral cortex have also been reported in humans. Accidental ingestion of soluble barium salts has resulted in gastroenteritis, muscular paralysis, and ventricular fibrillation and extra systoles. Potassium deficiency can occur in cases of acute poisoning. Baritosis, a benign pneumoconiosis, is an occupational disease arising from the inhalation of barium sulfate dust, barium oxide dust, and barium carbonate. The radiologic changes produced in the lungs are reversible with cessation of exposure (Clement, 1985). The TWA limit for barium is 0.5 mg/m^.
Dose-response Assessment
Doses of barium carbonate and barium chloride of 57 mg/kg and 11.4 mg/kg respectively, T
have been reported to be fatal in humans (Clement, 1985). Based on a no-obsen/ed effect level * '
(NOEL) in animal studies, the RfDs/AIS has been set at 0.0098 mg/kg-day. For chronic Q exposure, the RfD for oral exposure to barium has been set at 0.07 mg/kg-day and the RCC for S inhalation exposure set at 0.0001 mg/kg-day (IRIS, 1990). An MCL of 1.0 mg/L has been set for
barium. There is a proposed MCL (PMCL) for 2 mg/L. The MCLG is also set at 2 mg/L. , Y\
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4.1.4 Beryllium
Pharmacokinetics
Beryllium is pooriy absorbed from the gastrointestinal tract and is expected to have low toxicity by the oral route of administration.
Human Health Effects
The major toxicologic effects of beryllium are on the lungs and skin. 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 inflamation of the conjunctiva from splash burns or in association with contact dermatitis. The most common clinical symptoms caused by chronic beryilium exposure are granulomatous lung inflamation. with, accompanying couch, chest pain, and general weakness. Systemic effects include right heart enlargement with accompanying cardiac failure, liver and spleen enlargement, cyanosis, digital clubbing, and kidney stone development.
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 know to be carcinogenic in several animal species. Inhalation exposure to beryilium 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 polymerization, there is not other evidence of mutagenic or ciastogenic 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.
Dose Response Assessment
Estimates of human carcinogenic risks associated with lifetime exposure to various concentrations of beryllium in water are:
Risk Concentration
10-' 0.37 ng/liter
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10"' 37 ng/liter o 10"' 3.7 ng/liter 3
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I he GAG Unit Risk Value is 2.6 (mg/kg-day)"'. OSHA publishes the following criteria for beryllium air concentrations:
2 ^ig/m- TWA
5 ,Lig/m^ Ceiling Level
25 ug/m /30 min Peak Concentration
The ACGIH Threshold Limit Value is 2 ug/m^ and it is listed as a suspected human carcinogen. NIOSH has established an airborn criteria of 0.5 .ug/m . The reference dose for oral ingestion of beryllium is 5.OOE-03 mg/kg-day (IRIS, 1990). The PMCL for beryllium is 2 ag/L, and the MCLG has been set at 0 mg/L.
4.1.5 Cadmium
Pharmacokinetics
In humans, both the respiratory and gastrointestinal tracts absorb cadmium. The rate of gastrointestinal absorption is about 5 percent to 8 percent. This rate is affected by dietary factors. Diets that are low in calcium. Vitamin D, protein, zinc, iron, and copper significantly increase cadmium absorption in the gastrointestinal tract: A deficiency in ascorbic acid has been shown to increase cadmium toxicity (EPA, 1984b).
In blood, cadmium binds to red blood cells and high-molecular-weight proteins in plasma.
The blood cadmium level in adults without excessive exposure is usually less than 1 ag/dl
(Casarett, 1986).
The liver and kidneys contain approximately 5 percent to 75 percent of the body burden
of cadmium. The half-life of cadmium in the body is at least several years and may be as long
as 30 years. With continued retention, cadmium progressively accumulates in soft tissues
(especially the kidney) until about age 50 when levels begin to slowly decline (Casarett, 1986).
The placenta may be a partial barrier to maternal cadmium, but the fetus may become exposed with increased maternal exposure (Casarett, 1986). 5
populations, much more cadmium is excreted in urine than in feces (Clayton and Clayton, 1981).
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Human Health Effects
An ingestion dose of 15-30 mg (1/1.000 oz.) of metal or soluble compounds may cause increased salivation, choking, vomiting, abdominal pain, anemia, kidney malfunction, diarrhea, and persistent desire to micturate. Symptoms may occur within 15-30 minutes after ingestion (NYSDOH, 1984).
Studies indicate that there is an increased incidence of prostatic cancer and possible kidney and respiratory cancer in workers who are exposed to airborne cadmium. Cadmium causes birth defects in rats, mice, and hamsters; whether or not it does so in humans is not known (NYSDOH, 1984).
Cadmium toxicity also affects calcium metabolism. Persons with severe cadmium nephropathy may develop kidney stones and excrete excess calcium. Corresponding skeletal changes include bone pain, osteomalacia, and osteoporosis (Casarett, 1986).
The International Agency for Research on Cancer has placed cadmium and certain cadmium compounds in Group 2B. This group consists of substances for which there is limited evidence of carcinogenicity in humans, sufficient evidence of carcinogenicity in animals, and inadequate evidence of activity in short-term tests. This classification is based on exposure to cadmium by inhalation. Inhalation of cadmium dust primarily affects the respiratory tract. Brief exposures to high cadmium concentrations may be fatal. No evidence has been found linking ingestion of cadmium with carcinogenicity in animals or humans (Federal Register, 1985).
Cadmium is an animal teratogen and reproductive toxin but this has not been adequately supported in a human model. Evidence concerning the mutagenicity of cadmium in animals is
, equivocal (EPA, 1984b).
Dose-Response Assessment
EPA has calculated a temporary adjusted acceptable daily intake (AADI) for cadmium of 0.018 mg/l. These calculations used the value of 200 ig/g for the critical (threshold) concentration of cadmium in the renal cortex resulting in renal dysfunction, and a lowest observed adverse effects level (LOAEL) value of 0.352 mg Cd/day. The LOAEL value was derived by _
assuming that 4.5 percent of the daily oral dose was absorbed and 0.01 percent per day of the ^ total body burden was excreted. The AADI was developed using an uncertainty factor of 10 and assuming 2 l/day of water were consumed. o
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The current MCL for cadmium is 0.01 mg/l. This level was based on the critical concentration of cadmium in the renal cortex (200 ag/g), 5 percent gastrointestinal absorption, rapid excretion of 10 percent of the absorbed dose, and 0.05-percent daily excretion of the total body burden.
The National Academy of Sciences and the World Health Organization (WHO) have determined a guideline of 0.005 mg/l cadmium. EPA is proposing that 0.005 mg Cd/I be the recommended maximum contaminant level (RMCL), or maximum contaminant level goal (MCLG). The reference dose for cadmium (oral) is 5.00E-04 mg/kg-day (IRIS. 1990). The present MCL is 0.005 mg/L; however. New Jersey's MCL for cadmium is 0.010 mg/L. Freshwater WQC for cadmium are 3.9 and 1.1 jig/L for chronic and subchronic exposures respectively. Saltwater WQCs for cadmium are 43 and 9.3 ug/L for chronic and subchronic exposures respectively.
4.1.6 Copper
Pharmacokinetics
According to Schroeder et al. (1986), humans ingest an average of 2.5 to 5 mg of copper per day from dietary sources. These authors estimated that gastrointestinal absorption of -3.2 and 0.2 mg of copper occurs from food and fluid intake, respectively. The actual quantities of copper absorbed depend on geography, climate, soil chemistry, diet, water softness and pH.
Weber et al. (1969) administered ""Cu as copper acetate to seven fasted human subjects without liver damage. Because of the short half-life of °*Cu (12.8 hours), labeled ( ^Zr) zirconium oxylate was given as a non-absorbable stool marker to enable location of the copper acetate bolus. The radionuclides were counted daily for 4 days in a whole body scintillation counter, and gastrointestinal movement of the administered bolus was monitored with a scintillation camera. Radioactive copper in blood was determined houriy for 6 hours and in urine and stools daily.
Absorption of '"Cu appeared to be diphasic. Maximum absorption from the stomach and duodenum occurred within 1 hour of administration. A second and slower absorption phase was
. obsen/ed >3.5 hours post-administration. At 2 hours post-administration the '"Cu acetate bolus had left the stomach of the subjects and was located in the small intestine; 3 hours later it was located in the terminal ileocecal region and proximal large intestine. Average net absorption of '"Cu was -60 percent, with a range of 15 to 97 percent (Weber et al., 1969). Evans (1973) stated 5
<•> that, in mammals, alimentary absorption of copper occurs only from the upper gastrointestinal tract and that the extent of absorption may be influenced by competition of other metals for ^
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metallathione in binding sites (necessary for active transport of copper), levels of dietary protein.
kinds and amounts of anions present and the level of dietan/ asorbic acid.
• Quantitative data regarding absorption of copper from inhalation exposure could not be located in the available literature; however, presumptive evidence has been located. Villar (1974) observed copper-containing granulomas in the lung, liver, and kidney upon necropsy of an individual occupationally exposed to Bordeaux mixture (an aqueous solution of lime and 1 to 2 percent copper sulfate) used in spraying vineyards. Pimental and Menezes (1975) noted copper-containing liver granulomas in three patients who used Bordeaux mixture while spraying vineyards to prevent mildrew. Gleason (1968) reported symptoms of "metal fume fever" (general discomfort, fever, chills, stuffiness of the head) in three workers exposed to fine copper dust at concentrations of 0.03 to 0.12 mg/m^ Installation of an exhaust fan that reduced air levels to <0.008 mg/m^ promptly alleviated these symptoms.
Batsura (1969) exposed rats (strain, sex and number not specified) for 15, 30, 45, 60, or 180 minutes to 50 to 80 mg copper oxide/m^ Electron microscopy showed that copper absorption had occurred in rats exposed for 180 minutes. Copper oxide particles had penetrated the epithelial cells of the pulmonary alveoli and were found in plasma 6 hours after exposure began. Particles were also found in the proximal convoluted tubules of the kidney.
Human Health Effects
Copper appears to increase the mutagenic activity of those reductone and ascorbic acid in bactenal test systems. However, copper itself does not appear to have mutagenic, teratogenic, or carcinogenic effects in animals or humans. Dietary levels of trace elements such as molybdenum, sulfur, zinc, and iron can affect the level of copper that produces certain deficiency or toxicity symptoms. In general, more attention is given to the problems associated with copper deficiency than to problems of excess copper in the environment. However, high levels of copper can be toxic to humans (Clement, 1985).
Exposure to metallic copper dust can cause a short-term illness similar to metal fume fever that is characterized by chills, fever, aching muscles, dryness of mouth and throat, and headache. Exposure to copper fumes can produce upper respiratory tract irritation, a metallic or sweet taste, - nausea, metal fume fever, and sometimes discoloration, of skin and hair. Individuals exposed to o dusts and mists of copper salts may exhibit congestion of nasal mucous membranes, sometimes of the pharynx, and occasionally ulceration with perforation of the nasal septum (Clement, 1985). o
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If sufficient concentrations of copper salts reach the gastrointestinal 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 bleeding,
oliguria, azotemia, hemoglobinuria, hematuria, proteinuria, hypertension, tachycardia, convulsions,
and death. Chronic exposure may result in anemia (Clement, 1985).
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 (Clement, 1985).
Dose-Response Assessment
The ACGIH (1983) has set the TWA-TLV for copper fumes at 0.2 mg Cu/m^ and the TLV for copper dusts and mists at 1 mg Cu/m^ of air. Although Gleason (1986. as cited in EPA 1984h) reported symptoms of metal fume fever in workers exposed to 0.1 mg copper dust/m^ air, the ACGIH felt that extensive industrial experiences with copper welding and refining experience in Great Britain supported the view that no ill effects result from exposure to fumes at concentrations up to 0.4 mg Cu/m^ (EPA, 1984h).
The National Academy of Sciences (NAS, 1977a) has given 15 ppm copper in pig feed a GRAS (generally regarded as safe) categorization. Levels up to 200 ppm are often used in market hogs as a growth promoter (EPA, 1984h).
Copper has a secondary MCL (SMCL) of 1,000 ug/L and a PMCL of 1,300 ug/L. The MCLG is set at 1,300 (ig/L. WQC for freshwater are 18 and 12 ug/L for chronic and subchronic exposures respectively. WQC for saltwater are 2.9 |a.g/L for both chronic and subchronic exposure. The EPA (1980b), based on the organoleptic threshold of copper, has set the ambient water quality criterion for human effects at 1.0 mg/L. EPA recommended this same level as the criterion for drinking water based on organoleptic criteria (EPA, 1984h).
4.1.7 Lead
Pharmacokinetics
world. It is estimated that Americans take in between 0.1 and 2 mg lead per day [Kehoe, 1961; National Academy of Sciences (NAS), 1972]. All people have lead in their bloodstream from
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sources such as food or water [Worid Health Organization (WHO), 1977], with average blood
concentrations between 10 and 25 ug/dl (Tsuchiyaetal.. 1975: McLaughlin etal.. 1973), although
concentrations as high as 35 ug/dl are reported in occupationally unexposed populations in Italy
and France (Zurio et al.. 1970; Boudene et al., 1975). It is estimated that adults absorb between
5 and 10 percent of ingested lead (Kehoe. 1961; Rabinowitz.et al.. 1974) although children and
infants may absorb a greater percentage, possibly as high as 50 percent (Alexander et al., 1973;
Ziegler et al., 1978).
Human Health Effects
The primary concern of lead toxicity is neurotoxicity. Lead is particularly of concern for its effects on the central nen/ous system (CNS) in children. Children appear especially sensitive • to the CNS effects of lead which may result in encephalopathy. Symptoms include ataxia, coma, and convulsions. Physiologically, the encephalopathy is characterized by severe cerebral edema, increased cerebral spinal fluid pressure, glial cell proliferation, and neuronal degeneration and necrosis. Its toxicity has been extensively investigated in both animals and humans and is correlated with blood lead levels. The NAS (1972) has summarized the dose response relationship between blood level and CNS toxicity in children, based on data from Chisolm (1962, 1965) and Chisolm and Harrison (1956). Adverse effects on the CNS of children have been detected at blood lead concentrations as low as 60 ug/dl blood, while CNS effects in adults occur at concentrations greater tha 100 ug/dl.
In addition to causing CNS toxicity, lead can also cause peripheral nervous system (PNS) toxicity characterized by neuropathy. The toxic lesion is characterized by a axonal degeneration causing muscle weakness and symptoms such as "wrist drop". It is difficult to characterize the doses needed to cause these effects since the effects are observed primarily in older sutides and no reports of blood lead levels were available for these cases. However, muscle nen/e conduction rates were decreased at blood lead levels as low as 50 ug/dl (Seppalainen et al., 1975).
Lead can also affect body function, although only at concentrations which affect the nen/ous system (WHO, 1977). Two general effects have been described. The first is Fanconi Syndrome, which is characterized by renal tubular damage and generalized animoaciduria, hypophosphatemia and glycosuria (Chisolm, 1962). These 'effects have been obsen/ed in children exposed with lead toxicity and blood lead levels of 50 to 120 ug/dl, but the blood lead •
levels for the children with nephropathy were not cited (Pueschel et al., 1972). These effects *"
have also been observed in adults, but associated blood lead levels were not given. Lead c
exposure is also associated with another renal syndrome characterized by diffuse interstitial and fo
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peritubular fibrosis. This syndrome is called chronic lead nephropathy and results from chronic blood lead levels greater than 70 ug/dl.
Lead exposure is also associated with anema. This is caused by-inhibition of heme synthesis and decreased red blood cell life span, but these effects occur only at concentrations greater than 80 ug/dl, and are not common today (Goyer, 1986).
The effects of lead on intelligence in children has been extensively investigated. (EPA, 1986). There are many problems with these studies, since they rely on IQ measurements which are subject to great variations. In addition, there are numerous potentially confounding variables which make interpretation difficult. Nevertheless, there is a trend that associates lead with decrements of 10 at low blood lead concentrations.
Dose-Response Assessment
There is some evidence that lead is carcinogenic in animals; however, there is not enough information available in humans (EPA, 1986). EPA classifies lead as a B2 carcinogen, but does not provide estimate slope factors. In addition, the EPA has not derived any oral RfD or inhalation RfC for lead.
4.1.8 Manganese
Pharmacokinetics
Daily manganese intake ranges from 2 to 9 mg. Gastrointestinal absorption is less than 5 percent. It is transported in plasma bound to a (3,-globulin, thought to be transferrin, and is widely distributed in the body. Manganese concentrates in mitochondria so that tissues rich in these organelles have the highest concentrations of manganese including pancreas, liver, kidney, and intestines. Biologic half-life in the body is 37 days. It readily crosses the blood-brain barrier and the half-life in the brain is longer than in the whole body (Casarett, 1986).
Manganese is eliminated in the bile and is reabsorbed in the intestine, but the principal
route of excretion is with feces. This system apparently involves the liver, auxiliary
gastrointestinal mechanisms for excreting excess manganese, and perhaps the adrenal cortex. a: o
This regulating mechanism, plus the tendency for extremely large doses of manganese salts to cause gastrointestinal irritation, accounts for the lack of systemic toxicity following oral g administration or dermal application (Casarett, 1986). ' '
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Human Health Effects
In humans, manganese dusts and compounds have relatively low oral and dermal toxicity, but they can cause a variety of toxic effects after inhalation exposure. Acute exposure to very high concentrations can cause manganese pneumonitis, increased susceptibility to respiratory disease, and pathologic changes including epithelial necrosis and mononuclear proliferation. Chronic manganese poisoning is more common, but generally occurs only among persons occupationally exposed to manganese compounds. Degenerative changes in the central nervous system are the major toxic effects. Eariy symptoms include emotional changes, followed by a masklike face, retropulsion or propulsion, and a Parkinson's-like syndrome. Liver changes are also frequently seen. Individuals with an iron deficiency may be more susceptible to chronic poisoning (Clement. 1985).
Dose-Response Assessment
The acceptable daily intake of manganese from subchronic exposure (RfDs) for oral exposure routes is 0.53 mg/kg-day. The corresponding acceptable daily intake for chronic exposure (RfD) is 0.1 mg/kg-day (EPA, 1986a). The EPA has set the freshwater criterion at 0.05 mg/l based on the organoleptic threshold for manganese, and the marine water criterion at 0.1 mg/l to protect consumers of seafood (EPA, 1985a).
4.1.9 Nickel
Pharmacokinetics
Human and animal studies indicate that 1 to 10 percent of dietary nickel is absorbed (ATSDR, 1987). Nickel solutions penetrate human skin, and depending on type of nickel compound in solution and application conditions, up to 77 percent of the nickel can be absorbed. Distribution of nickel occurs in humans in the nasal mucosa and lungs following inhalation and in the blood following oral exposure. In animals, nickel was found in the lungs and kidneys following inhalation; in the kidneys, lungs, liver, heart, testes, and central nervous system following oral exposure; and in various tissues following dermal exposure (ATSDR, 1987).
Once absorbed, nickel binds to a number of serum bimolecular components. A number
of disease states and physiological stresses (i.e., myocardial infarction) have been reported to a alter the metabolism of nickel in man and animals (ATSDR, 1987).
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Nickel is removed from the body in urine, feces, hair, and perspiration. The 1/2-life of nickel in nasal mucosa has'been estimated at 3.5 years, and at 100 hours in blood serum. EPA concluded that age-dependent accumulation of nickel in soft tissue appears to occur only in the lungs (ATSDR, 1987).
Human Health Effects
The lung is the primary target of inhalation exposure to nickel and its compounds in humans and animals. Dermal exposure to nickel is associated with contact dermatitis and effects only those sensitive to nickel (<15 percent of the human population). Oral and inhalation exposure to nickel has effects on the immune system, the kidney, and hematological and hematopoietic systems (ATSDR, 1987).
Some nickel compounds associated with nickel refinery dust are classified as known human carcinogens via the inhalation exposure route. Other data suggest that nickel compounds may be mutagenic and elastogenic, processes that are thought to be related to carcinogenesis. Warner (1979, as cited in 1987) reported that there were no clinical data on developmental effects from women working at a nickel refinery in Wales. No human studies on reproductive toxicity are available.
Dose-Response Assessment
For drinking water, EPA advises that the following concentrations are probably associated with minimal risk: 1 mg l/NI for 10 days for children, 3.5 mg/l for 10 days for adults, and 0.35 mg/l/NI for lifetime exposure for adults. The oral RfD for nickel is 2.00E-02 mg/kg-day (IRIS, 1990). The PMCL and MCLG for nickel are set at 0.1 mg/L. WQC for freshwater life are 1,400 and 160 jig/L for subchronic and chronic exposures respectively. Marine WQC are set at 75 and 8.3 ug/L for subchronic and chronic exposures respectively.
4.1.10 Vanadium
Pharmacokinetics
The rate of pulmonary absorption of vanadium compounds has not been experimentally
determined, but it has been estimated that approximately 25 percent of soluble vanadium
compounds may be absorbed. Vanadium salts are poorly absorbed from the human
gastrointestinal tract. Only 0.1-1.0 percent of the very soluble oxytartarovanadate has been
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reported as being absorbed through the gut (IPCS 1988). ingested vanadium is partially
eliminatea in the feces, while absorbed vanadium is principally eliminated througn the kidneys.
There is no convincing evidence that vanadium is an essential element. Vanadium interferes with a multitude of biochemical processes. Vanadium can penetrate the blood-brain barrier and is found in breast milk.
Human Health Effects
There are no data available to suggest that vanadium has carcinogenic, mutagenic, teratogenic, or reproductive effects in humans or experimental animals. Occupational exposure to airborne vanadium compounds can produce eye and skin irritation. Oral exposure, may produce gastrointestinal disturbances and discoloration of the oral mucosa and tongue. There is no evidence of chronic oral toxicity. The most important toxic effects of vanadium are associated with inhalation exposure. Symptoms include acute upper and lower respiratory irritation with mucous discharge and bronchitis, cough, bronchospasm, and chest pain. Acute effects are reported to occur at concentrations as low as 0.1 mg/m^ Effects on various enzyme systems may also occur, especially after chronic exposure.
Vanadium is toxic to experimental animals by all routes of administration. Its toxicity generally increases with valence number. The pentavalent chemical forms, such as vanadium pentoxide and the vanadates are the most toxic compounds. In albino mice, an oral LDjg of 130 mg/kg vanadium trioxide is reported; a value of mg/kg is reported for vanadium pentoxide and vanadium trichloride.
Dose Response Assessment
The ACGIH TLV is 0.05 mg/m^ (vanadium pentoxide. repirable dust and fume). The NIOSH recommended standards are 1 mg/m^ (TWA) and 0.05 mg/m^ (ceiling level). The oral RfD for vanadium is 7.00E-03 mg/kg-day (EPA, 1990).
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4.2 Organics
4.2.1 Benzene
Pharmacokinetics
According to the Health Effects Assessment document for benzene (EPA, 1984d), quantitative data on the rate and extent of benzene absorption are not available. Absorption can, however, be inferred from various studies. A significant portion of any dose of benzene is exhaled unchanged or is stored in fat in both animals and humans (Casarett and Doull, 1986).
Evidence suggests that benzene toxicity is caused by one or more metabolites of benzene • rather than by benzene itself (Synder [1981] cited in Casarett and Doull [1986]). Some of the metabolites resulting from benzene's biotransformation in animals include the following: phenol, catechol, hydroquinone, and 1,2,4-trihydroxybenzene (Parke [1953] cited in Casarett and Doull [1986]).
The metabolites of benzene also covalently bond to cellular macromolecules. Many researchers believe this bonding is related to the mechanism of benzene's toxicity or carcinogenicity or to both (Casarett and Doull, 1986). In mice, benzene metabolites reportedly bind to proteins in the liver, bone marrow, kidney, spleen, blood, and muscle [Longacre (1981) cited in Casarett and Doull (1986)]. Other studies have shown covalent bonding to protein in bone marrow preparations [Irons (1980) cited in Casarett and Doull (1986)].
Human Health Effects
Benzene is a volatile aromatic hydrocarbon present in fossil fuels, including gasoline and other petroleum-based products. Humans are most frequently exposed to benzene through inhalation, and therefore, much of the human health information is based on exposure by this route. Acute exposure to high concentrations of benzene depresses the central nen/ous system and may cause unconsciousness and death. Acute exposures can also cause fetal cardiac arrhythmias [Synder (1975) cited in Casarett and Doull (1986)]. Milder exposures to benzene can produce vertigo, drowsiness, headache, nausea, menstrual irregularities, and unconsciousness. ^ Benzene can also be dermaily absorbed, causing blistering, erythema, and dermatitis (Clement ^ Associates, Inc., 1985).
In humans, the primary adverse effect of benzene is hematopoietic toxicity, that is, interterence with the formation of blood or blood cells (Casarett and Doull, 1986). Chronic
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exposure to low levels of benzene is associated with blood disorders including aplastic anemia and leukemia [Synder (1975) cited in Casarett and Doull (1986)]. The bone marrow toxicity of benzene is characterized by a progressive decrease in the number of circulating blood cells (i.e., erythrocytes, thrombocytes, and leukocytes). Blood cell depletion correlates to the degree of benzene exposure (Casarett and Doull, 1986). If the depression of the number of blood cells is severe, the condition is called pancytopenia and is characterized by necrosis (death of living tissue) and fatty replacement of bone marrow (Casarett and Doull, 1986).
Many epidemiology studies have associated occupational exposure to benzene (via inhalation) with an increased incidence of leukemia (EPA, 1984d). The most common leukemia associated with these exposures is acute myelogenous (bone marrow) leukemia. EPA has classified benzene as a Group A carcinogen (i.e., there is sufficient evidence from epidemiologic studies to support a causal association between exposure and cancer).
Benzene has been thoroughly tested for genotoxic properties; however, it has not been shown to be mutagenic in several bacterial and yeast systems (EPA, 1984d).
Many people have studied the effect of benzene on the chromosomes of bone marrow cells and peripheral lymphocytes. The results of most of these studies indicate significant increases in chromosomal aberrations in both symptomatic and asymptomatic groups who were exposed at some time to benzene (EPA, 1984d).
Dose-response Assessment
Because benzene is a carcinogen, no level of exposure is recognized as safe (nonthreshold concept). The EPA calculated a range of concentrations for benzene corresponding to cancer risk levels of 1 E-05,1E-06, and 1E-07. In calculating these values, EPA assumed an intake of 2 liters per day of drinking water, 6.5 grams per day of fish, and a human body weight of 70 kilograms. The corresponding criteria for these levels for various conditions are listed below:
Consumption of Consumption of Consumption of Water and Fish Fish Only .Water Only
Risk Level ( 1) ( 1) ( il) CD
1 E-05 1E-06 1E-07
6.60 0.66 0.066
400.0 40.0 4.0
6.70 0.67 0.067
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The carcinogenic slope factor for benzene via inhalation is 2.9E-02 (mg/kg-day)' (IRIS, 1990). This calculation assumes complete absorption and an inhalation rate of 20 cubic meters (m ) per day for a 70-kg man.
The lower limit of benzene exposure via inhalation that will elicit hematologic effects is thought to be less than 100 parts per million (ppm). Occupational exposure to benzene at 300 to 700 ppm has been linked to blood abnormalities (EPA, 1984d).
The TLV-TWA for benzene is 10 ppm or 30 mg/m^ (ACGIH, 1988). EPA has established
an MCL of 0.005 mg/l for benzene (Federal Register, 1985). Although the federal MCL is set at
5 ug/L, the New Jersey MCL is set substantially lower at 1 ug/L. The MCLG for benzene is set
atO.
4.2.2 bis(2-Elhylhexy<)phthalate(BEHP)
Pharmacokinetics
Phthalate esters such as BEHP are well absorbed from the gastrointestinal tract following oral administration. Hydrolysis to the corresponding monoester metabolite (MEHP), with release of an alcoholic constituent, 2-ethylhexanol, largely occurs prior to intestinal absorption. Once absorbed, BEHP and MEHP are widely distributed in the body, the liver being the major initial respiratory organ. Clearance- from the body is rapid, and there is only a slight cumulative potential. BEHP is converted principally to polar deriatives of the monoesters by oxidative metabolism prior to excretion, primarily through the urinan/ tract (USDHHS. 1987). When administered by the oral, extraperitoned, intravenous and inhalation routes. BEHP has a low order of acute toxicity.
Human Health Effects
BEHP is carcinogenic in rats and mice, causing hepatocellular carcinomas. Teratogenic
and reproductive effects have been obsen/ed in experimental animals. Chronic exposure to
BEHP retarded growth and increased liver and kidney weights in animals. BEHP status as a
human carcinogen is considered indeterminate by the International Agency for Research on
Cancer (lARC). BEHP appears to have a relatively low toxicity in experimental animals. BEHP ro
is pooriy absorbed through the skin and no irritant response or sensitizing potential from dermal
application has been noted in experimental animals or humans (Clement Associates, Inc., 1985). §
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Studies in rats and mice suggest that BEHP is developmentally toxic. In the rat, a variety
of congenital abnormalities have been obsen/ed in the offspring of BEHP-treated rats. In the
mouse, the developing nervous appears to be the major target site, producing cyencephaly and
spina bifida. BEHP is a reproductive toxicant in male and female mice, resulting in reduced
fertility and both production of fewer litters by breeding pairs and decreased litter size (USDHHS,
1987).
For the protection of human health from the toxic properties of BEHP ingested through contaminated aquatic organisms alone, the ambient water quality criterion is determined to be 50 mg/l for BEHP and 34 mg/l for diethyl butyl phthalate.
Dose-response Assessment
The OSHA threshold limit value TWA is 5 mg/m^. TheOSHASTELfor BEHP is 10 mg/m^ (ACGIH, 1988). The reference dose for BEHP is 2E-02 (IRIS. 1989). The PMCL for BEHP is 4 mg/L and the MCLG is currently 0.
4.2.3 Carbon Disulfide
Pharmacokinettics
Experimental animal studies have shown that embryonic animals repeatedly exposed to high concentrations of CSj had a high incidence of malformations. These effects were probably secondary to illness caused to the dam. On the other hand. Eastern European studies (Tabacova et al.. 1978: Tabacova et al., 1983) have suggested that exposure to very low levels of CSj (10 ppb and 3,300 ppb) can produce subtle behavioral modifications in newborns who had been in utero to doses below those that caused maternal toxicity. The adequacy of these studies is difficult to evaluate, due to the lack of details of the methods and results. However, there appear to be inconsistencies in the results, since prenatal exposure to 17,000 ppb CS2 increased open field activity. In cause-effect relationships, a dose-response relationship is expected to exist (that is, as the dose level is decreased, a proportional decrease in the measure of toxic response should occur, and not a reversal of polarity). Consequently, for the present, these behavioral teratology effects of CS2 reported at concentraions below 20,000 ppb must be regarded as unproven.
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Human Health Effects
The toxic effects of overexposure in humans to OS, have been well documented as complex (see Worid Health Organization, 1979 and Seppaiainen and Haltia. 1980 for reviews). The discussion of the toxic properties of CS, has been organized into chronic toxicity and acute toxicity, because of the differences in toxic manifestations and potency and type of exposure pattern for each form of injury.
Three forms of chronic toxicity of carbon disulfide have been identified: neurotoxicity,
cardiovascular effects, and reproductive effects. Each of these effects will be discussed in turn.
The neurotoxicity of CSj is well characterized. Repeated exposure has resulted in disturbances of the central (CNS) and peripheral (PNS) nervous systems. The CNS effects may take the form of altered mental status, impaired psychomotor function (i.e.. dexterity), and neurasthenic symptoms (mood swings, headaches, irritability). The PNS effects include a neuropathy characterized by weakness in the legs and slowed nerve condition. In general, the severe CNS effects (e.g., psychic disturbances) are the result of exposure to high concentrations of CS2. Because most of these cases date from a time prior to the development of good industrial hygiene practices, it is not possible to precisely estimate these concentrations, but Viglianni (1950) estimated that these effects were seen primarily with daily exposure to levels in excess of 100,000 ppb (300,000 jig/m^). Milder symptoms of neurotoxicity may be observed between 20,000 and 100,000 ppb. These effects are not expected to occur when CS, levels are maintained below 20,000 ppb.
CS, has been shown to injure the cardiovascular system. Studies of workers have found an assoication between CS, exposure and vascular changes similar to atherosclerosis (Tiller et al., 1968). These lesions were obsen/ed (a) primarily in the CNS and kidneys, (b) largely in older studies (relating effects derived from very high exposures), and (c) as being reversible upon cessation of exposure. Recent evidence suggests that with the reduction in CSj levels since the 1960s, the risk-and correspondingly, the incidence~of cardiovascular disease has decreased (MacMahon and Monson, 1988). This has led MacMahon (1988) to conclude that the CSj concentrations to which workers are at increased risk of cardiovascular disease are far in excess of 20,000 ppm.
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CSj has been shown to alter the male reproductive system of humans. The obsen/ed < effects included impotence and loss of libido, which were seen primarily in early reports of CSj Q poisoning. Recent evidence suggests that no effect on male reproductive performance is to be M expected at levels below 20,000 ppm (Albright et al., 1984).
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Other toxic effects of CS, exposure have been noted on other organ systems, most
notably the eye. These effects have generally been secondary to alterations of the nervous and
cardiovascular systems. Thus, dose levels of CSj which do not cause damage to the nen/ous
and cardiovascular systems would not likely injure these other organs.
Acute CS2 toxicity in humans results from short exposure to very high concentrations of (1,000,000 to 1,670.000 ppb). Symptoms of acute toxicity are predominantly psychiatric including extreme irritability, rapid mood changes, paranoia, and suicidal tendencies. Other symptoms include insomnia, anorexia, nightmares, and fatigue (Worid Health Organization, 1979).
The EPA has calculated an oral RfD of 0.1 mg/kg-day based on reproductive effects in rabbits. The RfC for CSj is E-2 mg/kg-day (IRIS. 1989).
Evidence was not found to suggest that CS, causes cancer.
4.2.4 Chlorobenzene
Pharmacokinetics
Chlorobenzene can enter the body through ingestion, inhalation, and skin absorption. According to several animal studies, chlorobenzene is rapidly absorbed into the blood stream from the lungs and gastrointestinal tract (EPA, 1984e). It has also been reported that the ingestion of fats and oils facilitates the Gl absorption of chlorobenzene (EPA, 1984e).
Human Health Effects
Chlorobenzene is irritating to the skin, eyes, and mucous membranes of the upper respiratory tract, and can cause central nervous system depression. Animals chronically exposed to chlorobenzene have shown histological changes in the liver, kidneys, and lungs (AIHA, 1985).
A 70-year-old woman exposed for 6 years to a glue containing 70-percent chlorobenzene
experienced headaches and irritation of the respiratory mucosa, and eventually exhibited reduced
marrow development. Workers exposed to chlorobenzene for 1 to 2 years complained of
headaches, somnolence, indigestion, and numbness and stiffness in the extremities (EPA,
1984e). §
cause abnormal blood conditions, increased plasma lipids, and cardiac dysfunction (Clement
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Associates, Inc., 1985). There is currently no evidence indicating that chlorobenzene is a human carcinogen. Animal studies have failed to confirm or deny the carcinogenicity of chlorobenzene in rats or mice (EPA. 1984e).
Dose-response Assessment
The RfC for this compound is 2E-02 mg/kg-day and the RfD is 0.02 mg/kg-day (IRIS. 1990).
Currently there is no MCL for chlorobenzene. The PMCL is 4 ug/L and the MCLG is 5 ug/L. The Water Quality Criteria Document for chlorinated benzenes recommends a maximum concentration for chlorobenzene of 488 ul to protect the public health (Federal Register, 1980).
A chlorobenzene concentration of 75 ppm in the air causes discomfort in humans; at 200 ppm, symptoms of illness begin; and at 400 ppm, severe toxic effects are exhibited (Verschueren, 1983). The TLV-TWA for chlorobenzene is 75 ppm or 350 mg/m^ (ACGIH, 1988).
4.2.5 4,4'-DDT
Pharmacokinetics
DDT, DDD, and DDE are bioconcentrated and stored in the adipose tissues of most animals.
Human Health Effects
DDT, DDE, and DDD have been shown to be carcinogenic to mice, primarily causing liver tumors, but also causing lung tumors and lymphonas (Clement, 1985). DDT does not appear to be mutagenic, but it has caused chromosomal damage. There is no evidence that DDT is a teratogen; but it is a reproductive toxin, causing reduced fertility, reduced growth of offspring, and fetal mortality (Clement, 1985).
Chronic exposure to DDT causes a number of adverse effects, especially to the liver and
central nen/ous system (CNS). DDT induces various microsomal enzymes and therefore probably g
affects the metabolism of steroid hormones and exogenous chemicals. Other effects on the liver "
include hypertrophy of the parenchymal cells and increased fat deposition (Clement, 1985). In ©
the CNS, exposure to DDT causes behavioral effects such as decreased aggression and rj
decreased conditional reflexes (Clement,1985). Acute exposure to large doses or chronic
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exposure to lower doses causes seizures. The oral LD;^ is between 113 and 450 mg/kg for the rate and is generally higher for other animals (Clement. 1985).
Dose-Response Assessment
Estimates of the carcinogenic risks associated with lifetime exposure to various concentrations of DDT in water are:
Risk Concentration
10" 0.24 ng/liter 10"' 0.024 ng/liter 10"' 0.0024 ng/liter
The carcinogenic slope factor for DDT is 0.34 (mg/kg-day)"'. The OSHA TWA Standard in air is 1 mg/m^ and the ACGIH TLV-TWA is 1 mg/m^. The chronic oral RfD is 5E-04 mg/kg/day (IRIS. 1990). The freshwater WQC for DDT are 1.1 and 0.001 ug/L for subchronic and chronic exposures, respectively. Marine WQC are 0.13 and 0.001 ug/L for subchronic and chronic exposures respectively.
4.2.6 Naphthalene
Pharmacokinetics
Naphthalene is rapidly absorbed by inhalation but absorption through the skin or gastrointestinal tract is slower. It is methabolized to 1-naphthol. 2-naphthol, 1-naphthoquinone, and 2-naphthoquinone (Gerarde, 1960; Brown, 1957), probably through naphthalene-1,2-oxide (Juchau and Namkung, 1974). This last compound is thought to be the most toxic of the metabolites (Sandmeyer, 1981). The detoxification of naphthalene-1,2-oxide may be slowed in individuals with glucose-6-phosphate dehydrogenase or gluthathione deficiencies and newborns (Sandmeyer, 1981). The naphthols are excreted as the glucuronide conjugates (Sandmeyer, 1981).
Human Health Effects
Ingestion of large concentrations of naphthalene can cause moderate to severe anemia ^
and hemoglobinuria. There may also be gastro-intestinal distress and renal dysfunction (Moeschlin, 1965; Sandmeyer, 1981). Naphthalene is also acutely irritating to the eyes and skin § (Key etal., 1977).
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Chronic exposure to naphthalene is associated with the development of corneal ulcerations and, cataracts, which resemble the effects of aging (Adams. 1930). Similar effects are noted in experimental animals following repeated administration of 1 g/kg naphthalene orally (Van Heyningen and Pine, 1967) and in rabbits administered 1.5 g/kg-day (Shimotori. 1972).
No information is available on the potential carcinogenicity of naphthalene.
Dose Response Assessment
The ACGIH TLV-TWA and TLV-STEL are 50 mg/m" and 75 mg/m^ respectively. The OSHA TWA is 50 mg/m^ (Clement Associates, Inc., 1985). The oral chronic RfD for naphthalene is set by the EPA at 4E-03 mg/kg-day (IRIS, 1990).
4.2.7 Trans-1,2-Dichloroethene
Pharmacokinetics
EPA estimates that almost 100 percent of ingested dichloroethene and 35 to 50 percent of inhaled dichloroethene may be absorbed systemically (EPA, 1984d).
The metabolism of trans-1,2-dichloroethene yields dichloroacetylaldehyde, presumably via the formation of an epoxide compound. The exact intermediary metabolism, however, has not been determined (Casarett, 1986).
Human Health Effects
Little information is available concerning human exposure to trans-1,2-dichloroethene. Exposure to high vapor concentrations has been found to cause nausea, vomiting, weakness, tumors, and cramps (Clement, 1985).
There are no reports of carcinogenic or teratogenic results from exposure to trans-1,2-
dichloroethene (Clement Associates, Inc., 1985). In rats, repeated exposure via inhalation of 900
mg/m^ for 16 weeks produced fatty degeneration of the liver (Clement Associates. Inc., 1985). ^
This compound was also found to inhibit in-vitro aminopyrine demethylation in rat liver
microsomes. This indicates that trans-1,2-dichloroethene may interact with certain aspects of g
drug-metabolizing system of the liver (Clement Associates, Inc., 1985). r j
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Dose Response Assessment
Because inadequate data, EPA has not been able to derive acceptable intakes for trans-
1,2-dichloroethene. Based on data from animal studies, EPA calculated a human MED (minimum
effective dose) of 189 mg/day (EPA, 1984d).
One animal study showed that no adverse effects occurred following inhalation exposure to a 1,000-ppm mixture of 1,2-dichloroethene isomers for 6 months (EPA, 1984d). In contrast, other researchers obsen/ed fatty changes in the liver and minor changes in the lungs following exposure to 200 ppm trans-1,2-dichloroethene for 16 weeks (EPA, 1984d).
The TLV-TWA for 1,2-dichloroethene is 200 ppm (ACGIH, 1987). The oral RfD for 1.2-dichloroethene is 9E-03 mg/kg-day (IRIS, 1989). The federal MCL and MCLG are 100 ug/L The New Jersey MCL is set at 10 ug/L.
4.2.8 Polychlorinated Biphenyls (PCBs)
Pharmacokinetics
Not enough data is available at this time.
Human Health Effects
In humans exposed to PCBs (in the work place or via accidental contamination of food), reported adverse effects include chloracne (a long-lasting, disfiguring skin disease), impairment of liver function, a variety of neurobehavioral and affective symptoms, menstrual disorders, minor birth abnormalities, and probably increased incidence of cancer. Animals experimentally exposed to PCBs have shown most of the same symptoms, as well as impaired reproduction; pathological changes in the liver, stomach, skin, and other organs; and suppression of immunological functions. PCBs are carcinogenic in rats and mice and, in appropriate circumstances, enhance the effects of other carcinogens. Reproductive and neurobiological effects of PCBs have been reported in rhesus monkeys at the lowest dose level tested, 11 |a.g/kg body weight/day over a period of several months. There is indadequate, yet suggestive evidence of excess liver cancer in humans exposed through by ingestion, inhalation or dermal contact.
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PCBs are bioaccumulated and can be biomagnified. Therefore, their toxicity increases f ' with length of exposure and position of the exposed species on the food chain. The toxicity of ^ the various PCB mixtures is also dependent on their composition. There is some evidence that 'm
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the mixtures containing more highly chlorinated biphenyls are more potent inducers of
hepatocellular carcinoma in rats than mixtures containing less chlorine by weight (IRIS, 1990).
Dose-Response Assessment
EPA has assigned a drinking water unit risk value of 2.2E-4 ug/1 and a value for human exposure to PCB of 4.3396 (mg/kg-day)"'. The slope factor for PCBs is 7.7 (mg/kg-day)' (IRIS, 1990). WQC for PCBs are 0.14 and 0.03 ug/L for freshwater and marine life respectively.
4.2.9 Trichloroethene
Chemical Characteristics
Trichloroethene (TCE) is a colorless volatile liquid. It has a vapor pressure of 77 mm Hg at 25'C. TCE is soluble in polar and non-polar solvents. It is primarily used as a degreaser of fabricated metal parts. It is also used as a solvent in the textile industry and as a low temperature heat transfer fluid.
Pharmacokinetics
Following absorption, TCE is distributed throughout the body. Because of its high lipid solubility, TCE can concentrate in the fatty tissue, from which it is slowly removed [half-life between 3.5 and 5 hours (EPA, 1985)]. In contract, TCE has a shorter half-life in blood due to removal of TCE by exhalation, metabolism, and urinary excretion. By combining the information of the various body compartments together, the half-life for TCE in the human body has been determined to be approximately 10 hours, ranging from 7 to 14 hours (EPA, 1985).
The metabolism of TCE has been studied in humans. These studies (e.g., Monster et al., 1979) suggest that absorbed TCE is extensively metabolized with 60 to 90 percent of the absorbed dose metabolized, and the remainder excreted unchanged through the lungs (EPA, 1985). The principal site of TCE metabolism is the liver, although extrahepatic metabolism may play an important role in the toxic effects of TCE observed in other organs, such as the kidney. The importance of exhalation as a route of excretion increases as the metabolic pathways for ^ TCE conversion become saturated. However, saturation of metabolism in humans is not expected to occur except at extremely high (anesthetic) doses of TCE (Feingold and Holaday, g 1977). ^
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TCE is metabolized by cytochrome P-450 to trichloroethylene oxide and chloral hydrate, although the pathways for this conversion are not completely understood. Bonse and Henschler (1976) suggested that TCE is metabolized to TCE-oxide. which then forms chloral hydrate. However. Miller and Guengerich (1983) suggest that TCE forms a complex with cytochrome P-450 which then decomposes to TCE-oxide or chloral hydrate. EPA (1985) has speculated that the conversion of TCE to chloral hydrate involves a chloronium ion transition state which they suggest is a reactive intermediate able to bind to cellular components, possibly calusing the obsen/ed toxicity. Chloral hydrate has a short half-life (only a few minutes) and is metabolized and/or is decomposed to trichloroethanol or trichloroacetic acid. Trichloroethanol can be conjugated with glucuronic acid. Thus, the primar/ metabolites obsen/ed in the urine are trichloroacetic acid, 1,1,1-trichloroethanol, and trichloroethanol-glucuronide. Various minor metabolites (accounting for less than 10 percent of the absorbed TCE) have been identified in various rodent species (EPA, 1985), but of these, only monochloroacetic acid and N-(hydroxyacetyl)-aminoethanol have been identified in humans following exposure to TCE. Most of the metabolites are excreted TCE.
Experiments have been conducted to correlate metabolism of TCE with a toxic endpoint. In particular, attempts have been made to identify a metabolite of TCE which binds to DNA. This would be expected if TCE were a genotoxic carcinogen. Highly sensitive studies of DNA adducts following administration of '"C-labelled TCE found that TCE interacts weakly with DNA, as compared to known carcinogens such as dimethylnitrosamine (Parchmand and Magee, 1982). In addition, no specific DNA adduct was identified, possibly due to the inability of TCE to bind to DNA. As a result, there is a preponderance of evidence that TCE is an epigenetic carcinogen.
Non-Cancer Toxicitv
The toxic effects produced in humans exposed repeatedly to TCE include alterations of the central nen/ous system and the immune system.
In laboratory animals chronically exposed to TCE, toxic effects were manifested in the
liver, kidneys, and central nen/ous system. The lowest dose of TCE which has been reported to
affect kidney and liver function adversely is 393 mg/kg-day administered in the drinking water to
male mice, while doses which had no adverse effect on liver and kidney function were 216 and -y-
437 mg/kg-day in male and female mice respectively (Tucker et al., 1982). CD
In another study cited by EPA (1985) and ATSDR (1988), the lowest dose of TCE which g has been reported to cause slight adverse effects is 17.9 mg/kg body weight per day for six ' ^
months which had an adverse effect on the immune system exhibited as bone marrow stem cell ^ 01
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colonization (Sanders et al., 1982). These effects were obsen/ed inconsistently in this study (e.g.,
female mice exposed for four months were more affected than mice exposed for six months).
Because of these inconsistencies in this study, and because of the unknown relevance of these
findings to humans, the significance of this work for human health is uncertain.
Relatively high doses of inhaled TCE (300 ppm for 7 hours/days, days 6-15 of gestation) have been shown to be fetotoxic in laboratory animals, but only at levels which cause toxicity to the dams (Schwetz et al., 1975), It is possible, therefore, that the damage to the unborn fetuses observed were only secondary to the adverse effects on the pregnant animals.
EPA has not derived an oral RfD or inhalation RfC for TCE as of this writing.
Carcinoqencity
TCE is a member of a group of chemicals known as chlorinated hydrocarbons. Some of these compounds including TCE have been reported to cause liver tumors in mice; however, the significance of these tumors for human health is uncercain. This strain of mice has a high spontaneous rate of liver cancer, so that responses in these animals may likely overestimate the risk of cancer to man. In addition, chemicals which cause liver tumors in other species (such as rats) or in other organs. There is little evidence that TCE causes tumors in other species or other organs in the mouse. In addition, there is no consistency in the carcinogenic response in mice. There have been three studies which found no excess of tumors in mice treated with TCE (Herren-Freund et al., 1987; Van Duuren et al., 1983; Henschler et al., 1984). Because of these weak and inconsistent findings, the International Agency for Research on Cancer has rated TCE as having only limited evidence of carcinogencity in animals; and while EPA classified TCE as an animal carcinogen (EPA, 1985), the evidence for this conclusion h as been questioned recently by its Science Advisory Board. Despite repeated attempts in epidemiological studies, TCE has not been associated with human cancer. There are no credible studies establishing a link between birth defects and TCE exposure in humans.
One characteristic of a large class of carcinogens is that the individual compounds consistently cause mutations (alterations of DNA) in whole animals and in various non-mammalian systems. Many studies have examined the ability of TCE to cause mutations. In most of these g tests, TCE failed to produce mutations. There was a lack of consistent results, even within very similar tests. This has led some experts to conclude that TCE is, at best, only weekly genotoxic. o Likewise, TCE did not act as an initiator in a mouse skin painting study (Van Duuren, 1983). ^
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causing effects of TCE are related to its ability to act through a mechanism (epigenetic) for which there may more likely be a threshold.
4.2.10 Vinyl Chloride
Pharmacokinetics
The pharmacokinetics of vinyl chloride in humans exposed by inhalation is well understood, but little information is known of oral and dermal pharmacokinetics. The pharmacokinetics of oral vinyl chJoride in relevant animal models is well understood, and dermal exposure is not likely to be significant. Metabolism to an epoxide and an aldehyde provides reactive intermediates thought to be responsible for the carcinogenicity and probably the hepatotoxicity of the compound in animals and humans.
Metabolism proceeds via oxidation and subsequent conjugation with suifhydryi groups. An important oxidative pathvay involves mixed-function oxidase and results in reactive electrcphilic intermediates, 2-chioroethylene oxide and 2-chloroacetaldehyde, which bind to live macromolecules and may be responsible for the toxicity and oncogenicity associated with vinyl chloride. Excretion of polar metabolites is predominantely through the urine. When metabolic pathways are saturated, substantial amounts of unmetabolized vinyl chloride are exhaled.
Respiratory and gastrointestinal absorption of vinyl chloride appears to be rapid. Humans retain 42 percent of vinyl chlortle inhaled at concentrations of 3 to 24 ppm. Animals studies suggest that gastrointestinal absorption is nearly complete. Dermal absorption of vinyl chloride vapors is not likely to result in toxicity. Distribution of absorbed vinyl chloride may be widespread, with highest levels of parent ccmipound located in fat, but metabolism and excretion occur so rapidly that highest levels of excretory products are located in the liver and kidney, the primary organs of metabolism and excretion.
Human Health Effects
The most likely route of exposure for vinyl chloride is through inhalation. Short-term exposures to very high levels in contaminated air can cause dizziness, giddiness, stumbling and . y\ uncoordination, headache, unconsciousness, and death. Long-term exposure to lower o concentrations, for example, in factories where vinyl chloride was made or processed, has caused "vinyl chloride disease," which is characterized by severe damage to the liver, effects on the lungs, poor circulation in the fingers, changes in the bones at the end of the fingers, thickening
of the skin, and changes in the blood, as well as increased risk of cancer of the liver, brain, lungs, ^ o
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and possibly other organs. An increased risk of miscarriage has been associated with breathing air in factories containing vinyl chloride.
Vinyl chloride can be detected in urine and body tissues, but the tests are not a reliable indicator of exposure.
Hepatotoxicity, liver disease, is probably the most common adverse effect associated with exposure to vinyl chloride.
Humans can be exposed to vinyl chloride from environmental and occupational sources. The low levels of vinyl chloride found in the environment are usually more than a thousand times lower than levels found in occupational locations. Highest background levels have been measured in air near vinyl chloride factories or over chemical waste storage areas.
Background levels in drinking water may come from sources such as factories that release wastes into rivers and lakes, from seepage into water in areas where chemical wastes are stored, or from contact with polyvinyl chloride pipes.
Dose-response Assessment
From available data in animal studies, the EPA has estimated that breathing air containing 1 ppm vinyl chloride every day, all day, for 70 years, increases, at the most, the risk of 1,100 persons in a population of 10,000 developing cancer (1E-01). These risk values are upper-limit estimates. Actual risk levels are unlikely to be higher and may be lower.
Oral lethality data are limited to an LDj in rats of 500 mg/kg (Sax, 1984), an effect level
of 1.3 (mg/kg-day), and a NOEL of 0.13 mg/kg-day in a lifetime dietary study in rats.
EPA calculated estimated levels of vinyl chloride in water from the following:
Fish ar Risk Level
1E-04 1E-05 1E-06 1E-07
Id Shellfish Oil (ul)
5246.0 525.0 52.5
Ambient Water Onlv (an
20.0 2.0 0.2
Daily Drinking Water Consumotion (ul)
1.5 0.15 0.015
The carcinogenic slope value for vinyl chloride is 2.3 (mg/kg-day)' via ingestion (IRIS, 1990). EPA has classified vinyl chloride as a Group A carcinogen in the same group as benzene.
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The TLV-TWA for vinyl chloride is 5 ppm and 10 mg/m' (ACGIH, 1988). The MCL for vinyl
chloride is 2 ug/L and the MCLG is set at 0.
4.2.11 Xylenes
Xylene can exist in three isomeric forms: o-xylene, m-xylene, and p-xylene. Commercial xylene is a mixture of the three isomers and is generally in the following percentage ranges: o-xylene. 10-25 percent; m-xylene, 45-70 percent; and p-xylene 6-15 percent.
Pharmacokinetics
Gastrointestinal absorption of xylenes can be inferred from oral studies where up to 90 percent of the administered dose could be accounted for in the urine (EPA 1984m). Studies have evaluated the inhalation absorption rate of xylenes in humans exposed to 100 to 1300 mg/m^ These studies indicate approximately 60 percent of the xylene present in inhaled air is absorbed (Astrand et al 1978, Gamberale 1978, Sedivec and FIek 1976, EPA 1985).
Human Health Effects
The current occupational exposure standard for xylene is based primarily upon its effect on the central nervous system. Reports on occupational exposure to xylene have been published; However, due to the lack of quantitative evidence regarding the relationship between exposure and the resulting adverse effects, as well as the impurity of the materials to which the workers were exposed, limited conclusions can be made regarding neurotoxic effects. Several acute inhalation studies have been conducted where human volunteers were exposed to xylene. Although the focus of this toxicological summary is chronic effects, these studies will be discussed because of their direct relevance to human health effects. Although the exposure duration is not relevant, the effects observed are relevant when compared to effects from chronic exposure.
No data were found concerning the dermal toxicity of xylenes.
No data concerning the carcinogenicity of xylenes in humans were found in the available y CD
l i terature. The EPA (1990) classi f ies xy lenes as Group D carc inogens~not classif iable as to o
human carcinogenici ty. In an NTP (1986) study, 50 male and 50 female rats were adminis tered
a xylene mixture in corn oil at doses of 0, 250, or 500 mg/kg-day, 5 days per week, for 103 g
. weeks . Although an apparent dose-re la ted increase in mortality w a s repor ted for male rats,
iterstitial cell tumors of the testes in male rats could not be attr ibuted to xy lene exposure. NTP co o (1986) concluded that there were no signif icant changes in the inc idence of neoplast ic or . -''
-109-5302.001-KIN-BUC_RA FINAL_PT1
nonneoplastic lesions that could be related to xylene exposure. Maltoni et al. (1985) reported
higher incidences of malignant tumors in male and female sprague-dawley rats treated by oral
(gavage) administration with xylene in olive oil at 500 mg/kg-day, 4 or 5 days per week, for 104
weeks. However, the study did not specify tumor types or sun/ival rates. The EPA (1990)
concluded that the results could not be appropriately interpreted.
Mutagenicity studies indicate that xylene isomers are not DNA-reactive. Further, the frequency of chromosomal aberrations and sister chromatid exchanges were nearly identical between a group of 17 paint industry workers exposed to xylene and their matched controls (Haglund et al. 1980). Rats exposed to xylene via inhalation did not show chromosomal aberrations in their bone marrow cells (Donner et al. 1980).
Dose Response Assessment
Nelson et al. (1943) exposed groups of human volunteers to concentrations of a mixture of xylene isomers (65.0 percent m-xylene, 7.8 percent p-xylene, and 7.6 percent o-xylene), 19.3 percent ethylbenzene and traces of other compounds. Volunteers detected the odor of xylene at 14 ppm; none detected xylene at 0.14 ppm; 1.4 ppm was detected 67 percent of the time. The authors concluded that the odor threshold is approximately 1.0 ppm (0.0045 mg/liter). In a separate experiment volunteers inhaled concentration of the xylene mixture of 110,230,460, and 690 ppm for 15 minutes duration. At the highest concentration, 4 of the 6 volunteers experienced eye irritation and dizziness, two reported throat irritation, and three detected a taste sensation. During exposure to 110 ppm (0.46 mg/liter), mild throat irritation was the only symptom reported by one volunteer. The authors concluded that 100 ppm or less would not be objectionable to most persons exposed.
Gamberale et al. (1978) examined the effects of inhalation exposure to a mixture of xylenes (79 percent) and ethylbenzene (21 percent) and 15 human subjects. In one experiment, the 15 subjects were exposed for 70 minutes to approximately 100 or 300 ppm xylene vapor. In a second experiment, subjects were exposed for 70 minutes to 300 ppm xylene. This experiment involved a 30 minute work period at the beginning of the exposure. No adverse effects were seen in the first experiment at either the 100 or 300 ppm exposures with regard to numerical ability, reaction time, short-term memory, or critical flicker fusion. The estimated average dose of xylene in this experiment was 180 mg at the 100 ppm exposure level and 540 mg at the 300 ^, ppm exposure level. In the second experiment, the physical exercise resulted in an increased
uptake of the xylene. The average dose at the 300 ppm exposure level was estimated to be o ro
1200 mg. Significant performance decrements were observed in this experiment. )-» CO (> CO
- 110-5302.001-KIN-BUC RA FINAL .PTl
7^
•
Savolainen et al. (1979) conducted human volunteer experiments with six male subjects. These subjects were exposed via inhalation to m-xylene for 6 hours per day. 3 days per week, for 2 weeks. Concentrations of m-xylene in one experiment were constantly 100 to 200 ppm and in a second experiment the concentration was either 100 or 200 as a time-weighted average. Slight impairment of equilibrium and significant increases in reaction time were reported at 100 ppm during the first week. These effects were not persistent, suggesting the development of tolerance by the exposed subjects. There was no obsen/ation of significant alterations in manual dexterity, flicker fusion, or extraocular muscle balance. Salvolainen et al. (1978. 1982), in other studies, using similar exposure schedules and concentrations of xylene, obsen/ed acute effects at 90 ppm after 10 minutes of exercise. These acute effects were changes in reaction time and equilibrium and did not persist until the end of the first week of exposure; however, they were again observed during the second week of exposure.
Marks et al. (1982) conducted an oral study to assess the reproductive effects of xylene exposure to pregnant CD-I mice on days 6-15 gestation. Oral exposures of 3.10 g/kg body weight/day produced a mortality incidence of 12/38. Doses of 2.06 and 2.58 mg/kg body weight/ day resulted in increased resorptions, fetal malformations, and decreased fetal body weights. Doses of 1.03 and 0.52 g/kg body weight/day had no apparent effects on fetal or maternal toxicity. Ungvary et al. (1980) exposed pregnant CF4 rats to 150 mg/m^ (34.6 ppm), 15,000 mg/m^ (346.1), or 3,000 mg/m^ (692.2) of each of the isomers of xylene continuously on days 7-14 of gestation. Exposure to 1,500 mg/m^ (346.1 ppm) of m-xylene produced no adverse effects on litters. Exposure of 150 mg/m^ (34.6 ppm) of o-xylene produced no adverse effects on litters. However, exposure of 150 mg/m^ (34.6 ppm) of p-xylene resulted in fetotoxicity obsen/ed as delays in skeletal ossification.
The EPA (1989) has calculated an oral Reference Dose (RfD) for xylene based on a study
. conducted by the National Toxicology Program (NTP, 1986). This oral RfD is based on the assumption that thresholds exist for non-carcinogenic effects. The NTP (1986) study involved exposure of male and female Fischer 344 and B6C3F1 mice to gavage doses of 0, 250, or 500
mg/kg body weight/day of a mixture of xylenes (60.2 percent m-xylene, 13.6 percent p-xylene,
9.1 percent o-xylene, and 17.0 percent ethylbenzene). The animals were exposed for 5 days/week for 103 weeks. Mice in the high dose (500 mg/kg) group exhibited hyperactivity, and
there was a dose-related increased mortality in the male rats in the high dose group (500 mg/kg). A statistically non-significant increase in mortality was obsen/ed at 250 mg/kg in male rats. The ^
250 mg/kg body weight/day dose level was determined to be a no-obsen/ed-adverse-effect-level (NOAEL) for hyperactivity, decreased body weight, and male animal mortality. This was 8
r j converted to a human oral RfD of 2 mg/kg body weight/day using a conversion factor for the gavage schedule (5 days/week) and an uncertainty factor of 100 (10 for animal to human ^
( IN
- I l l -5302.001 •KIN-BUC_RA_FINAL.PT1
extrapolation and 10 to protect sensitive individuals). The level of confidence in the oral RfD for xylene is medium based upon the lack of monitoring of clinical chemistry, hemotology (e.g., enzymatic levels), and urine, as well as the lack of a lowest-obsen/ed-effects-level (LOEL) for chronic oral exposure (IRIS. 1990).
The ACGIH (1989) recommends a TWA-TLV of 100 ppm (435 mg/m ) for occupational inhalation exposures to xylenes (ACGIH, 1986). NIOSH also recommends a workplace standard of 100 ppm. with a 10 minute ceiling concentration of 200 ppm (ACGIH, 1986). The federal MCL and MCLG are both 10 mg/L; New Jersey has set the state MCL substantially lower. 0.044 mg/L.
4.3 Applicable or Relevant and Appropriate Requirements (ARARs)
The 1986 Superfund Amendments and Re-authorization Act (SARA) mandates that site remediation under CERCLA comply with all applicable or relevant and appropriate Federal. State, environmenal, and public health laws. These are known as ARARs for the site. Applicable requirements are specific to the conditions present on the site for which all jurisdictional prerequisites of the law or requirements are satisfied. Relevant and appropriate requirements are those that do not have jurisdictional authority over particular circumstances on the site, but that are meant to address similar situations and are, therefore, suitable for use at the site. The determination of applicability or relevance and appropriateness is made by the EPA and the responsible state authority, on a case-by-case basis. Comparisons of the mean and the 95 percent UCL concentrations to the applicable ARARs for ground-water and surface water samples at Kin-Buc are listed in Table 4-2 and Table 4-3 respectively.
The mean and 95 percent UCL concentrations for benzene, chlorobenzene. 1,2-dichloroethene, vinyl chloride, and nickel exceeded the maximum contaminant levels (MCL) of both the New York and the New Jersey Safe Drinking Water Standards. The maximum and 95 percent UCL concentrations for benzene, 1,2-dichloroethene, and vinyl chloride exceeded the MCLs established under the Federal Safe Drinking Water Standards. The 95 percent UCL concentrations for xylene and PCBs exceeded the New Jersey, New York, and the federal standards.
A comparison of the surface water data to the ARARs shows that the mean and the 95 percent UCL concentrations for PCBs, 4,4'-DDT, antimony, arsenic, beryllium, and nickel w exceed the Federal Water Quality Critera for Human Health. Of this list, PCBs and 4,4'-DDT also
exceed the New Jersey Surface Water Quality Criteria. g hj
CO
cn
- 112 5302.001 -KIN-BUC _RA_FINAL_PT1
All total carcinogenic risks for both adults and children are greater than 10 . For adults and children, the greatest carcinogenic risk results from combining fish ingestion and total residential resulting in risks of 1.32E-01 and l.llE-01 respectively.
7\ CD r- ,
O O ro
113-. 'i
Table 4-2 Groundwater ARARs/TBCs f o r i<in-Buc L a n d f i l l
CHEMICAL
Benzene Carbon D i s u l f i d e
Chlorobenzene 1 .2 -D ich lo re thene V iny l Ch lo r i de
Xylene Naohthalene
b i s { 2 - E t h y l h e x y l ) p h t h a l a t e PCBs
4,4'-DOT Antimony
Arsen ic Barium
Beryl 1Ium Cadmium Copper
Manganese Nickel
Vanadium
Mean Cone. (ppm)
3.80E-02 5.25E-03 8.22E-02 1.32E-02 7.37E-03 2.71E-02 1.13E-02 1.79E-02
-NA
2.95E-02 1.25E-02 5.55E-01 l . l l E - 0 3 1.19E-03 4.94E-02 2.98E---00 3.14E-02 3.89E-Q2
95% UCL Cone. (ppm)
7.12E-02 8.47E-03 1.98E-01 2.98E-02 1.20E-02 5.47E-02 1.13E-02 1.79E-02 2.OOE-03
NA 3.54E-02 1.70E-02 7.14E-01 1.59E-03 1.40E-03 a.29E-02 4.12E+00 4.59E-02 5.Q5E-Q2
NJSDUA MCU's (ppm)
l.OE-03
4.0E-03 2.0E-03 2.0E-03 4.4E-02
5.0E-04
5.0E-02 1 . 0E•^00
l.OE-02
1.3E-02
NJAC Groundwater Stds. (ppm)
l.OE-06 l.OE-06
5.0E-02 l.OE-^00
l .OE-02'
New York MCL's . ;?pm)
5.0E-O3
5.0E-03 5.0E-03 2.0E-03
•5.0E-03
S.OE-02 i.OE•^00
l.OE-02
Federal D r i nk i ng Water Standards (ppm)
MCL
5.0E-03
7.0E-03 2.QE-03 l,0E-^01
5.0E-04
S.OE-02 1 . 0E• O0
5.0E-03
PMCL
- •
. 01 / .005 (1)
2.0E•^00 l .OE-03
1.3E•^00
l .OE-01
MCLG
O.OE-t-00
7.0E-03 O.OE-^00 l.OE+01
O.OE+00
3.0E-03
2.0E-K00 O.OE-hOO 5.0E-03 1.3E+00
l .OE-Ol
Notes:
(1) = EPA is considering two alternative MCLs basea uDon a Practical Quanitative Level (PQL) of five times the Method Detection Limit (MDL) or ten times the MOL.
7\ CO
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LO
114
Table 4-3 Surface Water ARARs/TBCs for Kin-Buc
CHEMICAL
Benzene Carbon Disulfide Chlorobenzene
1,2-OJchlorethene Vinyl Chloride
Xylene Naphthalene
bis(2-Ethylhexyl)phtha(ate PCBs
4,4'-D0T Antimony Arsenic Barium
Berylliun Cadmium Copper
Manganese Nickel
Vanadium
Mean Concentration
(ppm)
i.5lE-03 NA 2.62E-02 2.46E-03 HA
4.84E-02 5.80E-03 HA
4.87E-04 5.85E-05 1.99E-02 2.18E-03 9.71E-02 8.00E-04 HA
5.25E-02 2.94E-01 9.10E-02 1.49E-02
95X UCL Concentration
(ppm)
1.53E-02 NA 7.57E-02 2.54E-03 NA 1.45E-01 7.45E-03 NA
5.UE-04 7.62E-05 2.98E-02 3.17E-03 1.59E-01 1.09E-03 HA
8.48E-02 4.48E-01 1.66E-01 3.88E-02
HJAC 7:9-4 Surface Water Criteria (ppm)
1.4E-05 1E-06
5E-02 1E+00
1E-02
federal Water Oual Freshwater
Maximum Concentration
1.1E-03
3.6E-01
3.9E-03 1.8E-02
1.4E+00
ity Criteria
Continuous Concentration
1.4E-05 l.OE-06
1.9E-01
1.1E-03 1.2E-02
1.6E-01
(ppm) Saltwater
Maximum Concentration
1.3E-04
6.9E-02
4.3E-02
7.5E-02
Continuous Human
Water and Concentration Organisms
3E-05 l.OE-06
3.6E-02
9.3E-03
8.3E-03
1.2E-05
4.9E-01 7.0E-01 2.0E-03
1.8E-03 4.4E-08 5.9E-07 1.4E-02 l.eE-05
7.6E-06 l.OE-02 1.3E+00
1.4E-04
Health Organisms
Only
7.1E-02"
1.4E*02 5.3E-01
5.9E-03 4.5E-08 5.9E-07 4.3E+00 1.4E-04
1.3E-04 1.7E-01
3.8E+00
cn
89e '00 oa,v
5.0 HUMAN HEALTH RISK CHARACTERIZATION
The objective of this risl< characterization is to integrate information from the human exposure evaluation (Section 3.0) and the toxicity evaluation (Section 4.0) in order to evaluate present and future human health impacts associated with the Kin-Buc Landfill site - Operable Unit 2. Carcinogenic risl< is estimated as the incremental probability of an individual developing cancer over a lifetime as a result of exposure to a potential carcinogen. Carcinogenic risk is generally expressed in scientific notation. An individual lifetime risl< of one in 10,000 is represented as 1 x 10^ or lE-04.
Impacts of noncarcinogenic chemicals on human health are evaluated by comparing projected or estimated intakes with reference levels for the chemicals of concern. A reference level represents an estimated exposure level at which there is not expected to be an appreciable risk of deleterious effects. Noncarcinogenic reference levels used in risk assessment are referred to as reference doses (RfD) or reference concentration (RfC). The impact of carcinogenic chemicals is assessed by comparing predicted risks with target risks for known or suspected carcinogens. Target risks for carcinogens are referred to as slope factors.
Noncarcinogenic Effects
Versar evaluated the potential noncarcinogenic effects due to exposures to the contaminants of concern for all applicable exposure routes. Any potential health effects are identified by computing hazard indices derived from chronic daily intake levels. The hazard index is computed as follows:
CDI. + CDI^ + CDL Hazard Index = RJD^ Rfo^" Rfp^
for oral exposure routes, and,
CDI. + CDI^ , CDi, Hazard index = pfc, Rfc^" RfC„
for inhalation exposures.
accurate. Actual effects may be multiplicative or may not be related at all. However, it is generally agreed that if the hazard index is less than one, deleterious health effects are unlikely. If the hazard index is greater than one, then the individual effects of each chemical should be considered to determine the likelihood of ill effects.
- 116-53O2.0O1-K1N-BUC_RA_FINAL_PT1
7\ CD
The assumption that the combined effects of the chemicals will be additive may not be § hJ
cr-
Hazard indices for ground-water exposure scenarios for adults and children are presented in Table 5-la and 5-lb. Exposures during showering/bathing, such as vapor inhalation and dermal absorption, have hazard indices less than 1. Hazard indices for ground-water ingestion for both adults and children exceed 1, with values of 5.37 and 6.01, respectively. The compounds or chemicals that contribute the greatest to the hazard indices are antimony, at 2.53 for adults and 2.83 for children, and manganese, at 1.18 for adults and 1.32 for children. These two metals contribute approximately 70 percent of the hazard indices for ground-water ingestion for both adults and children. Exposures to arsenic, barium, vanadium, and chlorobenzene contribute an additional 24 percent to the hazard indices for adults and children.
Surface water hazard indices for adults and children are presented in Tables 5-2a and 5-2b. For adults, the highest hazard index occurs from ingestion of contaminated fish caught in surface water on or adjacent to the site. The hazard index of 7.19 is due mostly to the hazard quotient for 4,4'-DDT (6.34) which is responsible for approximately 88 percent of the hazard index. The remaining hazard indices for adult exposures to surface water are less than one. For children, the highest hazard index also occurs for fish ingestion (20.1). 4,4'-DDT, which has a hazard quotient of 17.8 is responsible for approximately 88 percent of the hazard index.
Sediment exposure hazard indices, which are shown in Table 5-3a and 5-3b, are all less then one. Approximately 89 percent of the hazard indices is from arsenic, bis(2-ethylhexyl)phthalate, and antimony.
Carcinogenic Effects
For potential carcinogens, risks are estimated by the probability of increased cancer incidence. A carcinogenic slope factor (SF) represents the upper 95-percent confidence limit of the probability of response per unit intake of the contaminant over a lifetime, and converts estimated intakes directly to incremental risk (EPA, 1989a).
The carcinogenic risks via exposure pathways for the Kin-Buc Landfill - Operable Unit 2 were calculated as:
Risk = CDI X SF
Where:
CDI = chronic daily intake (mg/kg-day) CO
SF = carcinogenic slope factor l/(mg/kg-day) 6
o o
CO
o
- 117
21-Jan-92
00
CHEMICAL
Benzene (C)
Carbon Disulfide (NO
Chlorobenzene (NC)
1,2-Dichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC
bis{2-Ethylhexyl)phthalate (C)
PCBs (C)
4.4'-D0T (NC)
4,4'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Bariun (NC)
Beryllium (NC)
Beryllium (C)
Cadmiun (NC)
Manganese (NC)
Nickel (NC)
Vanadiun (NC) (C) - Carcinogen (NC) - Noncarcinogen
GU Ingestion CDI
(mg/kg-day)
8.72E-04
2.42E-04
5.66E-03
8.26E-04
1.47E-04
1.56E-03
3.23E-04
5.11E-04
2.19E-04
2.45E-05
NA
NA
1.01E-03
4.86E-04
2.08E-04
2.04E-02
4.54E-05
1.95E-05
4.00E-05
1.18E-01
1.31E-03
Oral RfD
(mg/kg-day)
NA
l.OOE-01
2.00E-02
9.OOE-03
NA
2.00E+00
4.00E-03
2.00E-02
NA
NA
5.00E-04
NA
4.00E-04
l.OOE-03
NA
7.00E-02 ,
5.OOE-03
HA
5.00E-04
l.OOE-01
2.00E-02
1.73E-03 7.OOE-03
Total Hazard Index =
GROUND
Hazard Index
(Intake/RfO)
NA
2.42E-03
2.83E-01
9.17E-02
HA
7.81E-04
8.07E-02
2.56E-02
HA
NA
NA
NA
2.53E+00
4.86E-01
NA
2.91E-01
9.09E-03
NA
8.00E-02
1.18E+00
6.56E-02
2.47E-01
5.37E+00 •
TABLE 5-la -WATER HAZARD INDICES
ADULTS
GW Inhalation CDI
(mg/kg-day)
3.99E-05
2.43E-05
1.71E-04
4.75E-05
1.83E-05
9.02E-05
HA
HA
HA
NA
NA
NA
HA
NA
HA
HA
NA
HA
NA
HA
HA
Inhalation RfC
(mg/kg-day)
NA
3.OOE-03
6.OOE-03
NA
HA
9.00E-02
NA
NA
NA
HA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
HA NA
Total Hazard Index =
Hazard Index
(Intake/RfC)
NA
8.11E-03
2.86E-02
NA
HA
1.00E-03
NA
NA
NA
NA
HA
HA
HA
NA
NA
HA
HA
HA
HA
HA
HA
HA
3.77E-02
GW Dermal Abs. CDI
(mg/kg-day)
6.49E-04
2.42E-05
8.62E-06
1.26E-06
2.24E-07
2.38E-06
4.92E-07
7.80E-07
3.34E-07
3.73E-08
HA
NA
1.54E-06
7.41E-07
3.17E-07
3.11E-05
6.93E-0a
2.97E-08
6.10E-08
1.79E-04
2.00E-06
Oral RfD
(mg/kg-day)
NA
l.OOE-01
2.00E-02
9.OOE-03
NA
2.00E+00
4.OOE-03
2.00E-02
NA
HA
5.00E-04
NA
4.00E-04
l.OOE-03
NA
7.00E-02
5.OOE-03
NA
5.00E-04
l.OOE-01
2.00E-02
2.64E-06 7.00E-03
Total Hazard Index =
Hazard Index
(Intake/RfD)
NA
2.42E-04
4.31E-04
1.40E-04
HA
1.19E-06
1.23E-04
3.90E-05
HA
HA
HA
NA
3.86E-03
7.41E-04
HA
4.44E-04
1.39E-05
HA
1.22E-04
1.79E-03
1.00E-04
3.76E-04
8.42E-03
NA - Not Analyzed, Not Applicable, or Not Available Hazard index exceeds 1 for the exposure route.
IZCX 200 :)a>i
21-Jan-92
TABLE 5-1b GROUND WATER HAZARD INDICES
CHILDREN
CHEMICAL
bis
bis
:; (O
Benzene (C)
Carbon Disulfide (NO
Chlorobenzene (NC)
1,2-Dichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
(2-Ethylhexyl)phthalate (NO
(2-Ethylhexyl)phthalate ( O
PCBs* (C)
4,4'-0DT (NO
4,4'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Berylliun (NC)
Beryllium (C)
Cactniun (NC)
Manganese (NC)
Nickel (NC)
Vanadiun (NC) (C) - Carcinogen (NC) - Noncarcinogen
GW Ingestion CDI
(mg/kg-day)
2.93E-04
2.71E-04
6.34E-03
9.25E-04
4.94E-05
1.75E-03
3.62E-04
5.73E-04
7.36E-05
8.23E-06
NA
NA
1.13E-03
5.44E-04
6.99E-05
2.28E-02
5.09E-05
6.54E-06
4.48E-05
1.32E-01
1.47E-03
Oral RfD
(mg/kg-day)
NA
l.OOE-01
2.00E-02
9.OOE-03
NA
2.00E^00
4.OOE-03
2.00E-02
NA
NA.
5.00E-04
NA
4.00E-04
l.OOE-03
NA
7.00E-02
5.OOE-03
NA
5.OOE-04
l.OOE-01
2.00E-02
1.94E-03 7.00E-03
Total Hazard Index =
NA - Not Analyzed. Not A D
Hazard Index
(Intake/RfD)
NA
2.71E-03
3.17E-01
i.03E-01
NA
8.75E-04
9.04E-02
2.86E-02
NA
NA
NA
HA
2.83E+00
5.44E-01
HA
3.26E-01
1.02E-02
NA
8.96E-02
1.32E-t 00
7.34E-02
2.77E-01
6.01E+00 *
olicable. or Not
GW Inhalation CDI
,(mg/kg-day)
3.35E-05
6.82E-05
4.80E-04
1.33E-04
1.54E-05
2.52E-04
NA
NA
NA
NA
NA
NA
HA
HA
NA
NA
NA
NA
NA
NA
HA
Inhalation RfC
(mg/kg-day)
HA
3.OOE-03
6.OOE-03
HA
NA
9.00E-02
HA
NA
HA
HA
HA
NA
NA
NA
NA
NA
HA
NA
NA
HA
HA
NA HA
Total Hazard Index =
vailable
Hazard Index
(Intake/RfC)
NA
2.27E-02
8.00E-02
NA
HA
2.81E-03
HA
HA
HA
NA
NA
HA
HA
NA
HA
HA
HA
HA
HA
HA
HA
HA
1.06E-01
GW Dermal Abs. CDI
(mg/kg-day)
2.78E-04
3.45E-05
1.23E-05.
1.80E-06
9.59E-08
3.40E-06
7.02E-07
1.11E-06
1.43E-07
1.60E-08
NA
NA
2.20E-06
1.06E-06
1.36E-07
4.44E-05
9.88E-0a
1.27E-08
1.12E-08
2.56E-04
2.85E-06
Oral RfD
(mg/kg-day)
NA
l.OOE-01
2.00E-02
9.OOE-03
HA
2.00E*00
4.OOE-03
2.00E-02
HA
HA
5.00E-04
HA
4.00E-04
l.OOE-03
HA
. 7.00E-02
5.OOE-03
HA
5.00E-04
l.OOE-01
2.00E-02
4.84E-07 7.OOE-03
Total Hazard Index =
Hazard Index
(Intake/RfD)
NA
3.45E-04
6.15E-04
2.00E-04
NA
1.70E-06
1.76E-04
5.56E-05
NA
NA
NA
HA
5.50E-03
1.06E-03
NA
6.34E-04
1.98E-05
NA
2.24E-05 -
2.56E-03
1.43E-04
6.91E-05
1.14E-02
Hazard index exceeds 1 for the exposure route.
3zex 200 oa>i
20-Fe^92
TABLE 5-2a SURFACE WATER HAZARD INDICES
ADULTS
O I
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chtorobenzene (NC)
t.2-Dichloroelhene (NC)
Vinyl Chtorlde (C)
Xylene (NC)
Naphthalene (NC)
bi8(2-Ethylhexyl)phthalale (NC)
bis(2-Ethylhexyl)phlhalale (C)
PCBs* (C)
4.4'-DDT (NC)
4,4'-DDT (C)
Antinwny (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beiyllium (NC)
Beryllium (C)
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadium (NC)
(C) - Carcinogen
(NC) - Noncarcinogen
Fish Ingestion CDI
(mq/kg-day)
2.63E-05
NA
5.84E-04
3.14E-06
NA
1.32E-02
132E-03
NA
NA
1.70E-02
3 17E-03
1.36E-03
2.30E-05
1.06E-04
4.61E-05
1.23E-04
1.60E-05
6.85E-06
NA
3.46E-04
6.02E-03
2.99E-05
Oral RfD
(mg/kg-day)
NA
l.OOE-01
2.00E-02
9.00E-03
NA
2.00E^OO
4.00E-03
2.00E-02
NA
NA
5.00E-04
NA
4.00E-04
1.00E-03
NA
7.00E-02
5.00E-03
NA
5.00E-04
1.00E-01
2.00E-02
7.00E-03
Hazard Index-
Hazard Index
(Inlake/RID)
NA
NA
2.92E-02
3.49E-04
NA
6.60E03
3.30E-01
NA
NA
NA
6.34E+00
NA
5.75E-02
1.08E-01
NA
1.76E-03
320E-03
NA
NA
3.46E-03
3.01E-01
4.27E-03
7.19E+00-
Incidental Ingestion CDI
(mg/kg-day)
8 98E-08
NA
1.04E-06
3.48E-08
NA
1.99E-06
1.02E-07
NA
NA
3.02E-09
1.04E-09
4.47E-10
4 08E-07
4.34E-08
1.86E-08
2.18E-06
1.49E-08
6.40E-09
NA
6.14E-06
2.27E-06
5.32E-07
Oral RfD
(mg/kg-day)
NA
1.00E-01
2.00E-02
9.00E-O3
NA
2.00E+00
4.00E-O3
2.00E-02
NA
NA
5.00E-04
NA
4.00E-04
1.00E-03
NA
7.00E-02
5.00E-03
NA
5.00E-04
1.00E-01
2.00E-02
7.00E-03
Hazard Index -
Hazard Index
(Intake/RID)
NA
NA
5.20E-05
3.87E-06
NA
9.95E-07
2.55E-05
NA
NA
NA
2.08E-06
NA
1 02E-03
4.34E-05
NA
3.11 E-05
2.98E-06
NA
NA
6 14E-05
1.14E-04
7.60E-05
1.43E-03
Dermal Absorption CDI
(mg*q-day)
1.34E-05
NA
3.16E-07
1.06E-08
NA
6.06E-07
3.11E-08
NA
NA
9.20E-10
3.18E-10
1.36E-10
1.24 E-07
1.32E-08
5.67E-09
6.64E-07
4.55E-09
1.95E-09
NA
1 87E-06
6.93E-07
1.62E-07
Oral RID
(mg/kg-day)
NA
l.OOE-01
2.00E-02
9.OOE-03
NA
2.00E+00
4.OOE-03
2.00E-02
NA
NA
5.00E-04
NA
4.00E-04
1.00E-03
NA
7.00E-02
5.00E-03
NA
5.00E-04
1 OOE 01
2.00E-02
7.00E-03
Hazard Index -
Hazard Index
(Intake/RID)
NA
NA
1 58E-05
1.18E-06
NA
3.03E-07
7.78E-06
NA
NA
NA
6.36E-07
NA
3.10E-04
1.32E05
NA
9.49E-06
9.10E-07
NA
NA
1.87E-05
3 47E-05
2.31 E-05
4.36E-04
NA - Not Analyzed, Not Applicable, or Not Available *- Hazard index exceeds 1 for the exposure route.
czex soo 3a>i
20-Feb-92
1
tV)
1
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chtorobenzene (NC)
1,2-Dichk]roethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs* (C)
4,4'-DDT (NC)
4,4'-DDT (C)
Antiriwny (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Beryllium (C)
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadium (NC)
(C) - Carcinogen
(NC) - Noncarcinogen
Fish Ingestion COl
(mg*g-day)
2 21 E-05
NA
1.64E-03
8.78E-06
NA
369E-02
369E-03
NA
NA
1.43E-02
8.89E-03
1.14E-03
6.44E-05
3.01 E-04
3.87E-05
3.43E-04
4.47E-05
5.75E-06
NA
9.68E-04
1.69E-02
8.38E05
Oral RfD
(mg/kg-day)
NA
1 OOE-OI
2.00E-02
9.00E-03
NA
2.00E+00
4.00E-03
2.00E-02
NA
NA
5.00E-04
NA
4.00E-04
l.OOE-03
NA
7.00E-02
5.00E-03
NA
5.00E-04
1 OOE-OI
2.00E-02
7.00E-03
Hazard Index-
Hazard Index
(Intake/RID)
NA
NA
8.20E-02
9.76E-04
NA
1.85E-02
9.23E-01
NA
NA
NA
1.78E+01
NA
1 61E-01
3.01 E-01
NA
4.90E-03
8.94E-03
NA
NA
9.68E-03
8.45E-01
120E-02
2.01 E + o r
TABLE 5-2b SURFACE WATER HAZARD INDICES
CHILDREN
Incidental lngeslk)n CDI
(mg/kg-day)
4.53E-07
NA
1.74E-05
585E-07
NA
3.34E-05
1.71 E-06
NA
NA
152E-08
1.75E-08
2.25E-09
686E-06
7.30E-07
9.38E-08
3.66E-05
2.51 E-07
3.23E-08
NA
1.03E-04
3.82E-05
e.93E-06
Oral RfD
(mg/kg-day)
NA
1.OOE-OI
2.00E-02
9.00E-03
NA
2.00E+00
4.00E-03
2.00E-02
NA
NA
5.00E-04
NA
4.00E-04
l.OOE-03
NA
7.00E-02
5.00E-03
NA
5.00E-04
1.00E-01
2.00E-02
7.00E-03
Hazard Index -
Hazard Index
(Intake/RfD)
NA
NA
870E-04
650E-05
NA
1.67E-05
4.28E-04
NA
NA
NA
3.50E-05
NA
1.72E-02
7.30E04
NA
5.23E-04
5.02E-05
NA
NA
1 03E-03
1.91E03
1.28E-03
2.41E-02
Dermal Absorption CDI
(mg/kg-day)
3.43E-05
NA
2.71 E-06
9.08 E-08
NA
5.19E-06
2.66E-07
NA
NA
2.36E-09
2.73E-09
3.50E-10
1.07E-06
1.13E07
1.46E-08
5.69E-06
3.90E-0e
5.01 E-09
NA
1.60E-05
5.94E-06
1.39E:06
Oral RfD
(mg/kg-day)
NA
1.OOE 01
2 0 0 E 0 2
900E-03
NA
2.00E+00
4.OOE-03
2.00E-02
NA
NA
, 5.00E-04
NA
4.00E-04
1.OOE 03
NA
7.00E-02
5.00E-03
NA
5.00E-04
l.OOE-01
2.00E-02
7.00E-03
Hazard Index -
Hazard Index
(Inlake/RID)
NA
NA
1.36E-04
1.01 E-05
NA
2.60E-06
6.65E-05
NA
NA
NA
5.46E-06
NA
2.68E-03
1 13E04
NA
8.13E-05
7.80E-06
NA
NA
1 60E-04
2.97E-04
1.99E-04
3.75E-03
NA - Not Aruilyzed, Nol Applicable, or Not Available ' Hazard index exceeds 1 for the exposure route.
t^ZCT 200 3a>l
22-Jan-92
TABLE 5-3a SEDIMENT HAZARD INDEX
AOOLrS
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Oichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyt)phthalate (C)
PCBs (C)
4,4'-DDT (NC)
M 4,4'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NO
Beryllium (NO
Berylliun (C)
Cadmiun (NO
Manganese (NC)
Nickel (NC)
Vanadium (NC) <C> - Carcinogen (NO - Noncarcinogen
Dermal Contact CDI
(mg/kg-day)
4.77E-09
3.22E-09
2.74E-08
NA
NA
8.00E-07
U33E-07
4.49E-05
1.92E-05
4.43E-06
NA
NA
2.45E-07
2.18E-06
9.35E-07
2.93E-06
4.55E-08
1.95E-08
7.19E-08
7.43E-06
1.70E-06
1.81E-06
Hazard
Oral RfD
(mg/kg-day)
NA
l.OOE-01
2.00E-02
9.00E-03
NA
2.00E+00
4.OOE-03
2.00E-02
NA
NA
5.00E-04
NA
4.00E-04
l.OOE-03
HA
7.00E-02
5.OOE-03
HA
5.00E-04
l.OOE-01
2.00E-02
7.OOE-03
Index =
Hazard Index
(Intake/RfD)
HA
3.22E-08
1.37E-06
NA
HA
4.00E-07
3.31E-05
2.24E-03
HA
HA
HA
NA
6.13E-04
2.18E-03
NA
4.19E-05
9.11E-06
HA
1.44E-04
7.43E-05
8.48E-05
2.59E-04
5.68E-03
Incidental Ingestion CDI
(mg/kg-day)
1.53E-10
1.03E-10
8.77E-10
NA
HA
2.56E-08
1.06E-08
3.59E-06
1.54E-06
3.55E-07
NA
NA
1.96E-07
1.75E-06
7.48E-07
2.35E-06
3.64E-08
1.56E-08
5.75E-08
5.95E-06
1.36E-06
Oral RfO
(mg/kg-day)
HA
l.OOE-01
2.00E-02
9.OOE-03
HA
2.00E+00
.4.OOE-03
2.00E-02
NA
HA
5.00E-04
HA
4.00E-04
l.OOE-03
HA
7.00E-02
5.OOE-03
NA
5.00E-04
l.OOE-01
2.00E-02
1.45E-06 7.OOE-03
Hazard Index =
Hazard Index
(Intake/RfD)
NA
1.03E-09
4.38E-08
NA
NA
1.28E-08
2.65E-06
1.79E-04
NA
HA
HA
HA
4.90E-04
1.75E-03
NA
3.35E-05
7.29E-06
NA
1.15E-04
5.95E-05
6.78E-05
2.07E-04
2.91E-03
NA - Not Analyzed, Not Applicable, or Not Available
SZCI 300 oax
22-Jan-92
TABLE 5-3b SEDIMENT HAZARD INDEX
CHILDREN
Dermal Contact CDI
(mg/kg-day)
Oral Hazard RfD Index
(mg/kg-day) (Intake/RfD)
Incidental Ingestion Oral Hazard CDI RfD Index
(mg/kg-day) (mg/kg-day) (Intake/RfD) CHEMICAL
JS
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Oichloroethene (NC)
Vinyl Chloride (O
Xylene (NO
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NO
bis(2-Ethylhexyl)phthalate (O
PCBs (O
4,4'-DDT (NO
4,4'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NO
Beryllium (NC)
Berylliun (O
Cadmium (NO
Manganese (NC)
Nickel (NO
vanadiun (NC) (C) - Carcinogen (NC) - Noncarcinogen
6.93E-09
1.56E-08
1.33E-07
NA
NA
3.87E-06
6.42E-07
2.17E-04
2.79E-05
6.44E-06
NA
NA
1.19E-06
1.06E-05
1.36E-06
1.42E-05
2.21E-07
2.84E-08
3.48E-07
3.60E-05
8.21E-06
8.77E-06
Hazard
NA
l.OOE-01
2.00E-02
9.OOE-03
NA
2.00E+00
4.OOE-03
2.00E-02
NA
NA
5.00E-04
NA
4.00E-04
l.OOE-03
HA
7.00E-02
5.OOE-03
NA
5.00E-04
l.OOE-01
2.00E-02
7.00E-03
Index =
NA
1.56E-07
6.63E-06
NA
NA
1.94E-06
1.60E-04
1.09E-02
NA
NA
HA
NA
2.97E-03
1.06E-02
NA
2.03E-04
4.41E-05
NA
6.97E-04
3.6aE-04
4.10E-04
1.25E-03
2.75E-02
7.69E-10
1.73E-09
1.47E-08
HA
HA
4.30E-07
1.78E-07
6.03E-05
7.75E-06
1.79E-06
NA
HA
3.30E-06
2.93E-05
3.77E-06
3.94E-05
6.12E-07
7.87E-08
9.67E-07
9.99E-05
2.28E-05
2.43E-05
Hazard
NA
l.OOE-01
2.00E-02
9.OOE-03
NA
2.00E+00
4.OOE-03
2.00E-02
HA
HA
5.00E-04
NA
4.00E-04
l.OOE-03
HA
7.00E-02
5.OOE-03
NA
5.00E-04
l.OOE-01
2.00E-02
7.OOE-03
Index =
NA
1.73E-08
7.36E-07
NA
NA
2.15E-07
4.45E-05
3.01E-03
HA
NA
HA
NA
8.24E-03
2.93E-02
MA
5.63E-04
1.22E-04
NA
1.93E-03
9.99E-04
1.14E-03
3.48E-03
4.89E-02
NA - Not Analyzed, Not Applicable, or Not Available
9<^er •^oo oa>/
Evaluation of carcinogenic risks are used to determine if the site contaminants pose sufficient risk to human health to exceed 10^ to 10^ (EPA, 1989).
Carcinogenic risks for ground-water exposures are presented in Table 5-4a and 5-4b. For adults, the risk from ground-water ingestion dominates ground-water exposure, with a total risk value of 6.39E-04. Approximately 82 percent of the risk is due to the ingestion of vinyl chloride and PCBs, whose chemical-specific risks are 3.38E-04 and 1.89E-04 respectively. For children, the risk from ground-water ingestion also dominates ground-water exposure. Approximately, 96 percent of the total value of 2.15E-04 is a result of exposure to vinyl chloride, PCBs, and beryllium at 1.14E-04, 6.34E-05, and 2.81E-05, respectively. The risk values for ground-water ingestion exposures exceed the EPA-specified target range of 10^ to 10"*. Risks due to dermal absorption and inhalation ground-water exposures do not exceed 10" and fall within the target range.
Risk values for surface water exposures (Tables 5-5a and 5-5b) were greatest for fish ingestion, which yielded 1.31E-01 for adults and l.llE-01 for children. The major contaminant yielding risk was PCBs, with risks of 1.31E-01 and l.lOE-01 for adults and children, respectively. These high risk values are due to the conservative assumptions used (i.e., an exposure frequency of 365 days per year for 9 and 30 years for children and adults, respectively, averaged over a lifetime for carcinogens) as per EPA 1989a and EPA 1991.
Sediment-related risk values, presented in Table 5-6a and 5-6b, were also within the target level of 10"* and 10"*. Dermal contact resulted in a risk of 3.45E-05 for adults and 5.01E-05 for children. The dominant risk driving compound was again PCBs. Sediment ingestion exposure risks for adults were also within the target range at 2.82E-06 and 1.42E-05 for adults and children respectively.
Summary
In summary, four exposure scenarios have hazard indices above 1: ground-water ingestion by adults (5.37), ground water ingestion by children (6.01), fish ingestion by adults (7.19) and fish ingestion by children (20.1).
Exposure pathways resulting in an excess cancer risk include: ingestion of ground water by adults (6.39E-04) and children (2.15E-04), and, fish, ingestion by adults (1.31E-01) and children (1.1 lE-01).
Risk associated with multiple exposure pathways were also evaluated. Risks were grouped by population, i.e., residential, recreational, and fishers. Residential risks include 5
124
^ >
O O
( A )
22-Jan-92
TABLE 5-4a CARCINOGENIC RISK ESTIMATES FOR GROUND-WATER
ADULTS
CHEMICAL
Benzene (C)
Carbon Disulfide (HC)
Chlorobenzene (NC)
1,2-Dichloroethene (HC)
Vinyl Chloride ( O
Xylene ( N O
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NO
bi8(2-Ethylhexyl)phthalate ( O
PCBs ( O
{fl 4,4'-DDT (NC)
4,4'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Bariun (NC)
Beryllium (NC)
Berylliun (C)
Cadmium (NC)
Manganese ( N O
Nickel ( N O
Vanadiun ( N O ( O - Carcinogen (NO - Noncarcinogen
GU Ingestion CDI
(mg/kg-day)
8.72E-04
2.42E-04
5.66E-03
8.26E-04
1.47E-04
1.56E-03
3.23E-04
5.11E-04
2.19E-04
2.45E-05
NA
NA
1.01E-03
4.86E-04
2.08E-04
2.04E-02
4.54E-05
1.95E-05
4.00E-05
1.18E-0I
1.31E-03
SF 1/(mg/kg-day)
2.90E-02
HA
NA
NA
2.30E+00
NA
NA
NA
1.40E-02
7.70E+00
HA
3.40E-01
HA
NA
HA
NA
HA
4.30E+00
HA
NA
HA
1.73E-03 HA
Total Carcinogenic Risk =
Chemical-specific Risk
(lntake*SF)
2.53E-05
HA
HA
HA
3.38E-04
HA
HA .
HA
3.07E-06
1.89E-04
NA
NA
HA
NA
NA
NA
HA
8.37E-05
HA
NA
NA
HA
6.39E-04 •
GU (nhatatron CDI
(mg/kg-day)
3.99E-05
2.43E-05
1.71E-04
HA
1.83E-05
9.02E-05
NA
NA
NA
NA
NA
HA
HA
HA
NA
NA
HA
HA
NA
NA
NA
Sf 1/(mg/kg-day)
2.90E-02
NA
NA
NA
2.94E-01
HA
HA
NA
NA
NA
NA
HA
HA
NA
NA
NA
HA
HA
HA
NA
HA
NA NA
Total Carcinogenic Risk =
Chemical-specific Risk
(lntake*SF)
1.16E-06
NA
NA
HA
5.38E-06
HA
HA
HA
HA
HA
HA
HA
HA
HA
NA
HA
HA
HA
HA
NA
HA
HA
6.54E-06
GW Dermal Abs. CDI
(mg/kg-day)
6.49E-Q4
2.42E-05
8.62E-06
1.26E-06
2.24E-07
2.38E-06
4.92E-07
7.80E-07
3.34E-07
3.73E-08
NA
NA
1.54E-06
7.41E-07
3.17E-07
3.11E-05
6.93E-08
2.97E-08
6.10E-08
I.79E-04
2.00E-06
SF 1/(mg/kg-day)
2.90E-02
NA
NA
NA
2.30E100
NA
NA
HA
1.40E-02
7.70E+00
NA
3.40E-01
NA
NA
NA
NA
NA
4.30Et00
HA
NA
NA
2.64E-06 NA
Total Carcinogenic Risk =
Cheat i ca l - spec i f i c Risk
(lntake*SF)
1.B8E-05
NA
NA
NA
5.15E-07
NA
HA
HA
4.68E-09
2.87E-07
NA
HA
NA
NA
NA
NA
NA
1.2aE-07
HA
NA
NA
NA
1.98E-05
NA - Not Analyzed, Not Applicable, or Not Available * Total carcinogenic risk exceeds the target range of 1E-04 to 1E-06.
8./e.T .300 3a><
22-Jan-92
TABLE 5-4b CARCINOGENIC RISK ESTIMATES FOR GROUND-WATER
CHILDREN
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dichloroethene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (C)
PCBs ( O
4,4'-DDT (NC)
M 4,4'-DDT ( O
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NO
Beryllium (NC)
Beryllium ( O
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadiun (NC) ( O - Carcinogen (NC) - Noncarcinogen
IGU Ingestion CDI
(mg/kg-day)
2.93E-04
2.71E-04
6.34E-03
9.25E-04
4.94E-05
1.75E-03
3.62E-04
5.73E-04
7.36E-05
8.23E-06
NA
NA
1.13E-03
5.44E-04
6.99E-05
2.28E-02
5.09E-05
6.54E-06
4.48E-05
1.32E-01
1.47E-03
SF 1/(mg/kg-day)
2.90E-02
NA
NA
NA
2.30E+00
NA
NA
HA
1.40E-02
7.70E+00
HA
3.40E-01
HA
NA
HA
NA
HA
4.30E+00
NA
HA
HA
1.94E-03 NA
Total Carcinogenic Risk =
Chemical-specific Risk
(lntake*SF)
8.50E-06
NA
NA
HA
1.14E-04
HA
NA
NA
1.03E-06
6.34E-05
HA
HA
HA
NA
NA
NA
HA
2.81E-05
HA
HA
HA
NA
2.15E-04 *
GU Inhalation CDI
(mg/kg-day)
3.35E-05
6.82E-05
4.80E-04
1.33E-04
1.54E-05
2.52E-04
HA
NA
HA
HA
HA
NA
HA
NA
HA
HA
NA
HA
NA
HA
NA
SF 1/(mg/kg-day)
2.90E-02
NA
HA
NA
2.94E-01
HA
NA
NA
HA
HA
HA
HA
. HA
NA
HA
NA
NA
NA
NA
HA
NA
NA NA
Total Carcinogenic Risk =
Chemical-specific Risk
(lntake*SF)
9.72E-07
HA
HA
HA
4.52E-06
HA
HA
HA
HA
NA
NA
HA
HA
NA
HA
NA
NA
HA
NA
NA
HA
NA
5.49E-06
GU Dermal Abs. CDI
(mg/kg-day)
2.78E-04
3.45E-05
1.23E-05
1.80E-06
9.59E-08
3.40E-06
7.02E-07
1.11E-06
1.43E-07
1.60E-08
NA
NA
2.20E-06
1.06E-06
1.36E-07
4.44E-05
9.88E-08
1.27E-08
1.12E-08
2.56E-04
2.85E-06
SF 1/{iii9/kg-day)
2.90E-02
. NA
NA
NA
2.30E+00
NA
. NA
NA
1.40E-02
7.70E+0a
NA
3.40E-01
NA
NA
NA
NA
NA
4.30E*00
NA
NA
NA
4.84E-07 NA
Total Carcinogenic Risk =
Chemical-speci fie Risk
(lntake*SF)
8.06E-06
NA
NA
NA
2.21E-07
NA
NA
NA
2.00E-09
1.23E-07
NA
NA
NA
NA
NA
NA
NA
5.46E-08
NA
HA
HA
HA
8.46E-06
HA - Hot Analyzed, Not Applicable, or Not Avai table * Total carcinogenic risk exceeds the target range of lE-04 to 1E-06.
" ST eoo oax
20-Feb92
TABLE S^Sa
CARCINOGENIC RISK ESTIMATES FOR SURFACE WATER
ADULTS
CHEMICAL
Benzene (C)
Carbon Disulfkie (NC)
Chlorobenzene (NC)
1,2-Dichloroelhene (NC)
Vinyl Chloride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Elhylhexyt)phthalale (C)
PCBs- (C)
4,4'-DDT (NC)
4,4'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Beryllium (C)
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadium (NC)
(C) - Carcinogen
(NC) - Noncarcirwgen
Fish Ingestion COl
(mg/kg-day)
2.63E-05
NA
5.84E-04
3.14E-06
NA
1.32E-02
1.32E-03
NA
NA
1.70E-02
3.17E-03
1.36E-03
2.30E-05
1.08E-04
4.61 E-05
1.23E-04
1.60E-05
6.85E-06
NA
3.46E-04
602E-03
2.99E-05
SF 1/(mg/kg-day)
2.90E-02
NA
NA
NA
2.30E+00
NA
NA
NA
1.40E-02
7.70E+00
NA
3.40E-01
NA
NA
NA
NA
NA
4.30E+00
NA
NA
NA
NA
Total Carcinogenic Risk -
Chemk^al - specific Risk
(Inlake-SF)
7.63E-07
NA
NA
NA
NA
NA
NA
NA
NA
1.31E-01
NA
4.62E-04
NA
NA
NA
NA
NA
2.95E-05
NA
NA
NA
NA
1.31 E-01 •
SW Ingestnn CDI
(mg/kg-day)
8.98E-08
NA
1.04E-06
3.48E-08
NA
1.99E-06
1.02E-07
NA
NA
302E09
1.04E-09
4.47E-10
4.08E-07
4.34E-08
1.86E-08
2.18E-06
1.49E-08
6.40E-09
NA
6.14E-06
2.27E-06
5.32E-07
SF 1/(mg/kg-day)
2.90E-02
NA
NA
NA
2.30E+00
NA
NA
NA
1.40E-02
7.70E+00
NA
3.40E-01
NA
NA
NA
NA
NA
4.30E-f00
NA
NA
NA
NA
Total Cafcinogenic Risk -
Chemical - specific Risk
(Inlake'SF)
2.60E-09
NA
NA
NA
NA
NA
NA
NA
NA
2.33E-0e
NA
152E-10
NA
NA
NA
NA
NA
2.75E-08
NA
NA
NA
NA
535E-08
Denrul Absorption CDI
(rrxj/kg-day)
134E-05
NA
3.16E-07
1.06E-08
NA
6.06E07
3.11 E-08
NA
NA
9.20E-10
3.18E-10
1.36E-10
1.24E-07
1.32E-08
5.67E-09
6.64E-07
4.55E-09
1.95E-09
NA
1.87E-06
6.93E-07
1.62E07
SF 1/(mg/kg-day)
2.90E-02
NA
NA
NA
2.30E+00
NA
NA
NA
1.40E02
7.70E+00
NA
3.40E-01
NA
NA
NA
NA
NA
4.30E+00
NA
NA
NA
NA
Total Carcinogenic Risk -
Chemical - spedtic Risk
(Inlake-SF)
3.89E-07
NA
NA
NA
NA
NA
NA
NA
NA
7.08E-09
NA
4.62E11
NA
NA
NA
NA
NA
8.39E-09
NA
NA
NA
NA
4.04E-07
oeer eoo
NA - Not Analyzed, Not Applk»ble, or Not Available *- Total carcinogenic risk exceeds the target range of 1 E-04 to 1 E-06.
20-Feb-92
TABLE 5-5b CARCINOGENIC RISK ESTIMATES FOR SURFACE W/ATER
CHILDREN
o o
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dk:hloroethene (NC)
Vinyl Chtoride (C)
Xylene (NC)
Naphthalene (NC)
bis(2-Elhylhexyl)phthalale (NC)
bis(2-Ethythexyl)phthalate (C)
PCBs* (C)
4.4'-DDT (NC)
4,4'-DDT (C)
Antiiix>ny (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Beryllium (NC)
Beryllium (C)
Cadmium (NC)
Manganese (NC)
Nk^el (NC)
Vanadium (NC)
(C) - Carcinogen
(NC) - Noncarcinogen
Fish Ingestion CDI
(mgAg-day)
2.21 E-05
NA
1.64E-03
878E-06
NA
369E-02
3.69E-03
NA
NA
1.43E^)2
8.89E-03
1.14E-03
6.44 E-OS
3.01 E-04
3.87E-05
3.43E-04
4.47E-05
5.75E-06
NA
9.68E-04
1.69E-02
8.38E-05
SF 1/(mg/kg-day)
2.90E-02
NA
NA
NA
2.30E+00
NA
NA
NA
1.40E-02
7.70E+00
NA
3.40E-01
NA
NA
NA
NA
NA
4.30E+00
NA
NA
NA
NA
Total Carcinogenic Rtsk-
Chemical-specific Risk
(Inlake'SF)
6.41 E-07
NA
NA
NA
NA
NA
NA
NA
NA
1.10E-01
NA
3.88E-04
NA
NA
NA
NA
NA
2.47E-05
NA
NA
NA
NA
i . i i E - o r
SW Ingestion CDI
(mg/kg-day)
4.53E-07
NA
1.74E-05
5.85E-07
NA
3.34E-05
1.71E-06
NA
NA
1.S2E-08
1.75E-08
2.25E-09
6.86E-06
7.30E-07
9.38E-08
3.66E-05
2.51 E-07
3.23E-08
NA
1.03E-04
3.82E-05
8.93E-06
Total (^ ic irwgenic
SF 1/(mg/kg-day)
2.90E-02
NA
NA
NA
2.30E+00
NA
NA
NA
1.40E-02
7.70E-^00
NA
3.40E-01
NA
NA
NA
NA
NA
4.30E+OO
NA
NA
NA
NA
Risk-
Che mk:al-specillc Risk
(Inlake'SF)
131 E-08
NA
NA
NA
NA
NA
NA
NA
NA
1.17E-07
NA
7.65E-10
NA
NA
NA
NA
NA
1.39E-07
NA
NA
NA
NA
2.70E-07
1 Dermal Absorption CDI
(mg/kg-day)
3.43E-05
NA
2.71 E-06
9.08E-08
NA
5.19E-06
266E-07
NA
NA
2.36E-09
2.73E-09
3.50E-10
1.07E-06
1.13E-07
1.46E-08
5.69E-06
3.90E-08
5.01 E-09
NA
1.60E-05
5.94E-06
1.39E-06
SF 1/(mg/kg-day)
2.90E-02
NA
NA
NA
2.30E+00
NA
. NA
NA
1.40E-02
7.70E+00
NA
3.40E-01
NA
NA
NA
NA
NA
4.30E-t-00
NA
NA
NA
NA
Total Carcinogenic Risk-
Chemk:al specific Risk
(Inlake'SF)
9 95E07
NA
NA
NA
NA
NA
NA
NA
NA
1.82E-08
NA
1.19E-10
NA
NA
NA
NA
NA
215E-08
NA
NA
NA
NA
1.03E-06
NA - Not Analyzed, Not Appik:able, or Not Available *- Total carcinogenic risk exceeds the target range of 1E-04 lo 1E-06.
i^ect 200 oax
22-Jan-92
TABLE 5-6a CARCINOGENIC RISK ESTIMATES FOR SEDIMENTS
ADULTS
CHEMICAL
Benzene (C)
Carbon Disulfide (NC)
Chlorobenzene (NC)
,2-Dichloroethene (NO
Vinyl Chloride ( O
Xylene (NC)
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate
bis(2-Ethylhexyl)phthalate
ro «o
(C) -(NC)
PCBs (C)
4,4'-DDT (NC)
4,4'-DDT (C)
Antimony (NC)
Arsenic (NC)
Arsenic (C)
Barium (NC)
Berylliun (NC)
Beryllium (C)
Cadmium (NC)
Manganese (NC)
Nickel (NC)
Vanadiun ( N O Carcinogen - Noncarcinogen
(HO
(C)
Dermal Contact CDI
(mg/kg-day) 1/(
4.77E-09
3.22E-09
2.74E-08
NA
NA
8.00E-07
1.33E-07
4.49E-05
1.92E-05
4.43E-06
NA
NA
2.45E-07
2.18E-06
9.35E-07
2.93E-06
4.55E-08
1.95E-08
7.19E-08
7.43E-06
1.70E-06
1.81E-06
Total Carcinogenic
SF mg/kg-day)
2.90E-02
HA
NA
NA
2.30E+00
NA
HA
HA
1.40E-02
7.70E+00
HA
3.40E-01
NA
HA
NA
NA
NA
4.30E+00
NA
NA
NA
NA
Risk =
Chemical-specific Risk
(lntake*SF)
1.38E-10
NA
NA
NA
NA
NA
NA
HA
2.69E-07
3.41E-05
NA
HA
NA
NA
NA
NA
NA
8.39E-08
NA
NA
NA
NA
3.45E-05
Sediment Ingest CDI
(mg/kg-day)
1.53E-10
1.03E-10
8.77E-10
NA
NA
2.56E-08
1.06E-08
3.59E-06
1.54E-06
3.55E-07
NA
NA
1.96E-07
1.75E-06
7.48E-07
2.35E-06
3.64E-08
1.56E-08
5.75E-08
5.95E-06
1.36E-06
ion
1/(
1.45E-06
Total Carcinogenic
SF nig/icg-day)
2
2
1
7
3
4
Rl
.90E
.30E
.40E
.70E
.40E
30E
sk =
-02
NA
NA
NA
+ 00
NA
NA
NA
-02
+ 00
NA
-01
NA
NA
NA
NA
NA
00
NA
HA
HA
HA
Chemical-s Risk
(Intake
4
2
2
6
2.
pecific
»Sf)
.43E-12
HA
HA
HA
NA
NA
NA
NA
.15E-08
73E-06
HA
HA
HA
HA
HA
HA
NA
72E-08
NA
NA
NA
HA
82E-06
NA Not Analyzed, Not Applicable, or Hot Available
^sei 200 oa ^
22-Jan -92
TABLE 5-6b CARCINOGENIC RISK ESTIMATES FOR SEDIMENTS
CHILDREN
CHEMICAL
Benzene (O
Carbon Disulfide (NC)
Chlorobenzene (NC)
1,2-Dichloroethene (HC)
Vinyl Chloride (C)
Xylene (NO
Naphthalene (NC)
bis(2-Ethylhexyl)phthalate (NC)
bis(2-Ethylhexyl)phthalate (O
O
(C) -(NO
PCBs (C)
4,4'-DDT (NC)
4,4'-DDT (O
Antimony (NC)
Arsenic (NC)
Arsenic ( O
Bariun (NO
Beryllium (NC)
Beryllium (O
Cadmiun (NO
Manganese (NC)
Nickel (NO
Vanadiun (NC) Carcinogen - Noncarcinogen
Dermal Contact CDI
(mg/kg-day)
6.93E-09
1.56E-08
. 1.33E-07
NA
NA
3.87E-06
6.42E-07
2.17E-04
2.79E-05
6.44E-06
NA
NA
1.19E-06
1.06E-05
1.36E-06
1.42E-05
2.21E-07
2.84E-08
3.48E-07
3.60E-05
8.21E-06
8.77E-06
Total Carci
SF 1/(mg/kg-day)
2
2
1
7
3.
4.
nogenic
90E
30E
40E
70E
40E
30E
Ri
-02
HA
NA
NA
+00
HA
NA
NA
-02
+00
NA
-01
NA
NA
HA
NA
NA
+00
NA
NA
HA
NA
sk =
Chemical-speci fie Risk
(Intake'SF)
2.01E-10
NA
NA
NA
HA
HA
HA
HA
3.91E-07
4.96E-05
HA
NA
HA
HA
NA
NA
NA
1.22E-07
NA
HA
NA
NA
5.01E-O5
Sediment Ingestion CDI SF
(mg/kg-day) 1/(m9/kg-day)
7.69E-10 2.90E-02
1.73E-09 NA
1.47E-08 NA
NA NA
NA 2.30E+00
4.30E-07 NA
1.78E-07 NA
6.03E-05 NA
7.75E-06 1.40E-02
1.79E-06 7.70E+00
NA NA
HA 3.40E-01
3.30E-06 HA
2.93E-05 HA
3.77E-06 HA
3.94E-05 HA
6.12E-07 NA
7.87E-08 4.30E+00
9.67E-07 NA
9.99E-05 NA
2.28E-05 NA
2.43E-05 NA
Total Carcinogenic Risk =
Chemical-s Risk
(Intake
2
1
1
3
1.
pecific
»SF)
.23E-11
NA
NA
NA
NA
NA
NA
NA
.09E-07
.38E-05
HA
NA
NA
NA
NA
NA
NA
38E-07
NA
NA
NA
NA
42E-05
NA Not Analyzed, Not Applicable, or Not Available
£88T ?.00 Oa>l
inhalation, ingestion, and absorption of ground water for both children and adults. Recreational risks included ingestion and absorption of sediments, and ingestion and absorption of surface water for both children and adults. The total noncarcinogenic health effects of each group was determined by summing the hazard indices for each pathway. Total carcinogenic risk for each group was determined by summing the carcinogenic risks for each pathway. The evaluation is shown in Table 5-7.
The highest noncarcinogenic hazard indices for both adults and children is from fish ingestion exposure with hazard indices of 7.19 and 20.1 respectively. Residential exposure to ground water for adults (5.42) and children (6.13) also exceeded one. All other population hazard indices for both adults and children were less than one.
Adult carcinogenic risks were 6.65E-04 for residents, 3.78E-05 for recreational users of the site, and 1.31E-01 for recreational fishers. The highest carcinogenic risk to children was l.llE-01 from the ingestion of contaminated fish tissue. The carcinogenic risk for child recreational users of the site was 6.56E-05, and for residential children 2.29E-04.
Risks were also evaluated across all reasonable exposure pathway combinations for both noncarcinogens and carcinogens. Table 5-8 shows a summary of all possible combinations of exposure pathways for adults and children. All pathway combinations for noncarcinogenic exposure to adults are greater than one. The highest noncarcinogenic hazard index to adults occurs by combining the total residential and total fish ingestion pathways yielding a hazard index of 12.6. The risk to adults from the combination of total recreational and total residential exposure is 5.43. The risk to adults from combining fish ingestion and recreational exposures is 7.21. All combinations of carcinogenic risks were above the target range of lE-04 to lE-06. The highest carcinogenic risk (1.32E-01) resulted from combining the fish ingestion and residential scenarios, accounting for the case where site residents utilize site streams for recreational fishing. The combined carcinogenic risks for adults ranged from 7.03E-04 to 1.32E-01.
For children, the highest noncarcinogenic hazard index is associated with combining fish ingestion and residential exposures yielding a hazard index of 26.2. The total recreational and residential and total fish ingestion and recreational hazard indices for children are also greater than one, with hazard indices of 6.23 and 20.2, respectively. For children, all combinations of carcinogenic risks were above the target range. A carcinogenic risk of l.llE-01 resulted from combining the fish ingestion and residential scenarios and also the fish ingestion and recreational scenarios. The total recreational and residential scenario combination resulted in a carcinogenic risk of 2.95E-04. ^
O O ,v.
- 131 -
CO
20-Feb-92
TABLE 5-7 SUMMARY OF RISKS BY EXPOSURE PATHWAY
Route of
Exposure RESIDENTIAL ADULT
Ground water Inhalaton Ingestion
Absorption
TOTAL
CHILD Ground water
Inhalation Ingestion
Absorption
TOTAL
RECREATIONAL ADULT
Sediments Ingestion
Absorption
TOTAL
Surface Water Ingestion
Absorption
TOTAL TOTAL RECREATIONAL:
CHILD Sediments
Ingestion Absorption
TOTAL
Surface Water Ingestion
Absorption
TOTAL TOTAL RECREATIONAL:
FISH INGESTION ADULT
i CHILD
Noncarcinogenic Hazard Index
3.77E-02 5.37E+00 8.42E-03
5.42E+00
1.06E-01 6.01 E+00 1.14E-02
6.13E-(O0
2.91 E-03 5.68E-03
8.59E-03
1.43E-03 4.37E-04
1.87E-03 1.05E-02
4.89E-02 2.75E-02
7.64E-02
2.41 E-02 3.74E-03
2.78E-02 1.04E-01
7.19E+00
2.01 E+01
Carcinogenic Risk
6.54E-06 6.39E-04 1.98E-05
6.65E-04
5.49E-06 2.15E-04 8.46E-06
2.29E-04
2.82E-06 3.45E-05
3.73E-05
5.35E-08 4.03E-07
4.57E-07 3.78E-05
1.42E-05 5.01 E-05
6.43E-05
2.70E-O7 1.04E-06
1.31 E-06 6.56E-05
1.31 E-01
1.11 E-01 7^ CC
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20-Feb-92
TABLE 5-8 SUMMARY OF RISKS ACROSS EXPOSURE PATHWAYS
1 Route of
Exposure
ADULT Total Recreational:
Total Resklential:
TOTAL
CHILD Total Recreational:
Total Reskiential:
TOTAL
ADULT Fish Ingestion:
Total Residential:
TOTAL
CHILD Fish Ingestion:
Total Resklential:
TOTAL
ADULT Fish Ingestion:
Total Recreatksnal:
TOTAL
CHILD Fish Ingestion:
Total Recreational:
TOTAL
Noncarcinogenic | Hazard i index
1.05E-02 5.42E+00
5.43E+00
1.04E-01 6.13E+00
6.23E+00
7.19E+00
5.42E+00
1.26E+01
2.01 E+01 6.13E+00
2.62E+01
7.19E+00
1.50E-02
'7.21 E+00
2.01 E+01
1.04E-01
2.02E+01
Carcinogenic
Risk
3.78E-05
6.65E-04
7.03E-04 1
6.56E-05 2.29E-04
2.95E-04
1.31 E-01
6.65E-04
1.32E-01
1.11E-01 2.29E-04
1.11E-01
1.31 E-01
3.78E-05
1.31 E-01
1.11E-01 6.56E-05
1.11E-01
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6.0 AREAS OF UNCERTAINTY AND DATA GAPS
Because all inputs into the exposure assessments are conservatively based, the resulting risks identified for the Kin-Buc Landfill site represent upper-bound risk estimates, and may overestimate the actual risk from exposure to the chemicals of concern studied. Additional data would be required to derive a statistically valid estimate of error in the exposure and risk calculations.
Although the methods used to calculate carcinogenic risk comply with EPA and industry standards, there are uncertainties associated with the carcinogenic risk estimates discussed above. These uncertainties are introduced because of (1) the need to extrapolate below the dose range of experimental tests, (2) the variability of the receptor population (e.g., smoker vs. nonsmoker, genetic predisposition), (3) assumed dose-response relationship between animals and humans, (4) differences in exposure routes expected onsite, (5) overly conservative assumptions, and (6) ignoring background risks. The recognized uncertainties in these issues listed are raised to point out the limitations of this type of study. The assumptions used to estimate exposure were consistently conservative in nature and biased towards protecting human health and may have overestimated the risks asscx:iated with exposure. Parameters such as the absorption factor (AF) and diet fraction may also have been over estimated.
In addition to contaminant concentration, route, and duration of exposure, there are many other factors that may influence the likelihcxxi of developing cancer. These include differences in individual nutrition, health status, age, sex, and inherited characteristics which may affect susceptibility (U.S. DHHS, 1985). Risk addition across scenarios for a given population also assumes that intake levels will be small without synergistic or antagonistic chemical effects, and that individuals will be exposed to each of the indicator chemicals that elicit a carcinogenic response.
Additionally, there are chemicals that do not have toxicity values and therefore could not contribute a quantifiable risk. These chemicals of concern are primarily copper, lead and trichloroethane. Toxicity profiles including pharmacokinetics, non-cancer toxicity, and carcinogenicity, for these chemicals are provided in Section 4. The arithmetic mean, maximum and 95 percent UCL concentrations for copper are below the PMCL and SMCL of 1.3 and 1.0 ppm respectively. Only the arithmetic mean concentration for lead (1.06E-02) is below the interim MCL value of 1.50E-02 ppm. The maximum and 95 percent UCL lead concentrations exceed this value. The trichloroethene mean concentration of 6.24E-03 ppm and the 95 percent UCL of 1.12E-02 ppm are both greater than the MCL of 5E-03 ppm and may cause some health effects to humans.
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7.0 CONCLUSIONS
Contaminant screening was performed on analytical results from Wehran's sediment, surface water, and ground water samples from the Kin-Buc Landfill Operable Unit II Superfund site. The contaminant screening process identified 19 chemicals of concern: nine metals and ten organic compounds. The indicator chemicals chosen for this risk assessment were antimony, arsenic, barium, benzene, beryllium, bis(2-ethylhexyl)phthalate, cadmium, carbon disulfide, chlorobenzene, copper, 1,2-dichloroethene, 4,4'-DDT, manganese, napthalene, nickel, polychlorinated biphenyls (PCBs), vanadium, vinyl chloride, and xylene. These compounds or elements were selected because of their toxicological properties, potentially critical exposure routes, and higher concentrations present in comparison to other contaminants.
^ Applicable or relevant and appropriate requirements (ARARs) are presented in Tables 4-2 and 4-3 for the chosen contaminants of concern. These ARARs include National Primary Drinking Water Regulations (NPDWR) Maximum Contaminant Levels (MCLs), which are enforceable drinking water regulations first established under the Safe Drinking Water Act (SDWA) that are protective of public health to the extent feasible: MCL goals (MCLGs), which are nonenforceable health goals for public water systems; proposed MCLs (PMCLs) and proposed MCLGs (PMCLGs); and Occupational Safety and Health Act (OSHA) Permissible Exposure Limits (PELs), both Time Weighted Average (TWA) and Short Term Exposure Limit-(STEL).
Environmental fate and transport mechanisms were evaluated for each of the indicator chemicals based on an, assessment of the site's physical setting and the physical and chemical properties of each contaminant. Predominant transport mechanisms for originally landfilied contaminants include leachate percolation into soils, leachate migration through soils to groundwater supply wells, and vapor releases from contaminated ground water. Exposed populations include local residents and potential future residential users of ground water.
Eight possible exposure scenarios were evaluated: (1) residential ingestion of contaminated ground water from on-site sand & gravel wells, (2) dermal absorption of contaminated ground water during showering, (3) inhalation of vapors released from contaminated ground water during showering, (4) ingestion of contaminated fish from on-site and adjacent streams, (5) accidental ingestion of surface water while recreating in on-site and adjacent streams, (6) dermal absorption of contaminated surface water while recreating in local streams,
(7) dermal absorption of contaminated sediments within the on-site and adjacent streams, and (8) accidental ingestion of sediments from within the on-site and adjacent streams.
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Total body burden rates were computed based on all potential exposure routes using an average adult body weight of 70 kg, and a childrens body weight of 25 kg. It was assumed that ingestion and showering in ground water from on site would occur for 30 years for adults and 9 years for children. The noncarcinogenic exposures were averaged over a 9-year period for children. For adults, the noncarcinogenic exposures were averaged over a 30-year period. An exposure period of 70 years was used for carcinogenic compounds.
Time-weighted average doses for chemicals of concern varied considerably. The lowest chronic daily intake (CDI) was 1.03E-10 milligrams per kilogram per day (mg/kg-day) for incidental ingestion of carbon disulfide (noncarcinogenic effects) in sediments by adults during recreation activities. The highest CDI was 1.32E-01 mg/kg-day for ingestion of manganese in ground water by children.
Toxicity profiles for each of the contaminants of concern were developed based on current EPA accepted health effects documents, and established toxicological sources. Toxicity evaluation included pharmacokinetics, human health effects, and dose-response assessment. Toxicity information is dependent to a large extent on animal models upon which any potential adverse human health effects must be extrapolated.
Risk characterization included an assessment of risk associated with carcinogenic and non-carcinogenic effects caused by the contaminants of concern. Non-carcinogenic effects were addressed using a hazard index computed by multiplying the daily intake level by the inverse of
. the reference dose. The number should not exceed one, according to the NCP Superfund site remediation goals (EPA, 1989).
Many of the hazard indices computed indicated that the intake levels were below the reference doses (i.e., hazard indices were below one). However, four of the exposure scenarios liave hazard indices (HI) above one: ground-water ingestion by adults (HI = 5.37), groundwater ingestion by children (HI = 6.01), fish ingestion by adults (HI = 7.19), and fish ingestion by children (20.1).
Potential carcinogenic risks were computed by multiplying the chronic daily intakes by the chemical-specific carcinogenic slope factor. The resulting carcinogenic risks were then compared to the target of 10^ to 10"*.
CD' Several of the risks calculated for the potential exposure scenarios exceeded the target o range. The following risk values were in excess of the upper limit of the target range.
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ingestion of ground water by adults (6.39E-04) ingestion of ground water by children (2.15E-04) fish ingestion by adults (1.31E-01) fish ingestion by children (1.1 lE-01)
Overall, the greatest non-carcinogenic hazard indices and carcinogenic risks result from oral ingestion and dermal absorption of the following compounds and metals: arsenic, antimony, beryllium, bis(2-ethylhexyl)phthalate, chlorobenzene, 4,4'-DDT, manganese, PCBs, and vinyl chloride. Any corrective action implemented at the site to eliminate risks posed by site contaminants should reduce concentrations of these indicator chemicals and other contaminants with similar physical and chemical characteristics.
Upon evaluation of all available information on the site and the most recent analytical data collected from the site, potential threat to human health exists. This conclusion is based on an evaluation of the site history and operations, the overall physical setting, and on chemical analysis of affected media.
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