NCD003188844_19901008_Carolina Transformer_FRBCERCLA RISK_Draft Baseline Risk Assessment Report-OCR

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DRAFT
Baseline Risk Assessment Report
Carolina Transformer Superfund Site
Fayetteville, North Carolina
October B, 1990
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DRAFT
Baseline Risk Assessment Report
for the
CAROLINA TRANSFORMER SUPERFUND SITE
FAYETTEVILLE, NORTH CAROLINA
EPA WORK ASSIGNMENT 06-4LN3
Prepared for
U.S. Environmental Protection Agency
Region IV
Atlanta, Georgia
Prepared by
B&V WASTE SCIENCE AND TECHNOLOGY CORP
October 8, 1990
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DRAFT BASELINE RISK ASSESSMENT
CAROLINA TRANSFORMER
Fayetteville, North Caro/Ina
1.0 Introduction
1.1 Overview
1. 1. 1 General Problem
Carolina Transformer is located in Cumberland County, North Carolina, approxi-
mately one mile northeast of Fayetteville. Carolina Transformer recycled electrical
transformers and capacitors from 1967 through 1982. Although the facility has been
inactive since 1986, several abandoned electrical transformers, empty tanks and
drums, and debris remain on site. Operations conducted during the active life of the
facility have resulted in contamination of the soil, groundwater, surface water, and
sediment with polychlorinated biphenyls (PCBs), chlorobenzene compounds, and
other organic and inorganic pollutants. The site is currently under investigation by
the U.S. Environmental Protection Agency (EPA), Region IV, Environmental
Services Division, Hazardous Waste Section (ESD-HWS) through the consulting
services of B&V Waste Science and Technology Corp (BVWST). The EPA
conducted a three-phase Remedial Investigation (RI) at the Carolina Transformer
site to characterize the types and extent of contamination on and around the site.
1. 1.2 Objectives of the Risk Assessment
The proposed revision of the National Oil and Hazardous Substances Pollution
Contingency Plan (NCP) states that the purpose of the remedial process is to
implement remedies that reduce, control, or eliminate risk to human health and the
environment. The main objective of the human health evaluation process is to
provide the information necessary to assist in the decision-making process at remedial
sites. The specific objectives of the human health evaluation process are to:
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• Provide analysis of baseline risks ( defined as risks that might exist if no
remediation or institutional controls were applied at the site) and help
determine what action is needed at the site;
• Provide a basis for determining the levels of chemicals that can remain onsite
and still not adversely impact public health;
• Provide a basis for comparing potential health impacts of various remedial
alternatives; and
o Provide a consistent process for evaluating and documenting the threat to
public health at sites (U.S. EPA 1989a).
The proposed revision of the NCP also calls for the selection of remedial actions that
are protective of environmental organisms and ecosystems. In addition, numerous
federal and state laws and regulations concerning environmental protection are
potentially "Applicable or Relevant and Appropriate Requirement" (ARARs).
This baseline risk assessment provides a human health evaluation of potential risk to
human health and the environment from exposure to the contaminants at the
Carolina Transformer site. An ecological assessment for the site is also provided in
this baseline risk assessment. The baseline risk assessment results will be used to
document the magnitude of risk at the site and the associated cause of that risk. The
results will also help determine what additional response actions may be necessary
and aid in establishing and modifying the preliminary remediation goals. A flowchart
of the risk assessment process is presented on Figure 1-1.
1.2 Site Background
The Carolina Transformer site is located in Cumberland County, North Carolina,
approximately one mile northeast of Fayetteville and north of the intersection of U.S.
Highway 301 and River Road (Figure 1-2). The approximate map coordinates are
latitude 35°03'08" N and longitudinal 78°50'07" W.
The site consists of approximately 4.8 acres of relatively flat terrain and is bounded
on the north by a wooded/swamp-like area which is adjacent to an agricultural field
and numerous homes; on the west by a dirt road which provides access to two homes;
to the south by Middle Road, Larry's Sausage Company, and Fayetteville Livestock
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Market (operated by Lundy Packing Company); and to the east by an abandoned
home site and an agricultural field.
A foundation and a variety of buildings of varying sizes are located on the site.
These are situated predominantly toward the front and northeast portions of the
property (Figure 1-3). The western portion of the site is relatively open. Much of
the area around the foundation and buildings has been paved with concrete.
The site is located in an area which is generally low-lying and swampy. After any
substantial rainfall, water tends to stand in pools on the site.
Major surface waters, the Cape Fear River and associated wetlands, are within one
mile of the site. Presently, surface water drains from the site into an 18-inch culvert
which runs along the southwest edge of the site. The culvert carries the surface water
to a natural stream channel which measures roughly 24 inches in width. The stream
channel flows through a nearby swampy area into an unnamed tributary, which is
approximately four feet wide. The water flow from the tributary proceeds to the
Cape Fear River. Other drainage ditches flow along Middle Road, west to the Cape
Fear River and east to Locks Creek (Figure 1-4).
The site may be underlain by as many as three aquifers. The alluvial deposits where
sand and gravel are present could provide large yields to wells. The available
information indicates that the alluvial aquifers are not presently used for water supply
in the area. The sands and clays of the Cape Fear and Middendorf Formations serve
as aquifers in the Fayetteville area. The bedrock possesses fracture permeability and
is utilized for industrial supplies.
During three initial site investigations conducted between 1978 and 1979, the EPA
collected and analyzed numerous well water samples from homes near the site. The
results of the analyses showed no evidence of PCBs, but did uncover evidence of
chlorobenzene and other chemical compounds in several of the wells located within
1,000 feet of the site. In addition, numerous soil/sediment and surface water samples
were collected from suspected contaminated areas on site. These samples showed
the presence of PCBs.
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CAROLINA TRANSFORMER
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FIGURE 1-3
SITE MAP
CAROLINA TRANSFORMER FAYETTEVILLE, NORTH CAROLINA
-------------------
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APPROXIMATE SCALE
0 3500 7000
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SITE DRAINAGE PATTERN
CAROLINA TRANSFORMER
FAYETTEVILLE, NORTH CAROLINA
FIGURE J-4
LOCKS CREEK
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After the company made no attempts to remove or control the contaminants
identified during the various sampling investigations, EPA began an immediate
removal action on August 13, 1984. Clean-up consisted of dewatering the contami-
nated swampy area of the site where PCB-contaminated surface water pooled and
soaked into the soil. The excavated areas were backfilled with uncontaminated soil.
Approximately 975 tons of PCB-contaminated material were removed from the site
and transported to the Chemical Waste Management Disposal Facility in Emelle,
Alabama. The site has been vacant since 1986.
EPA conducted a three-phased Remedial Investigation between August 1989 and
January 1990. Samples were collected from soil, groundwater, surface water, and
sediment. Samples were analyzed for the presence of the following general
categories of contaminants:
• PCBs
• Dioxins/furans and pesticides
o Extractable organic compounds
• Purgeable organic compounds
• Inorganics ·
Elevated concentrations of each of the contaminant categories have been detected
in one or more media at the site.
1.3 Scope of the Baseline Risk Assessment
The scope of this risk assessment is limited to the potential risks to human health and
the environment present due to exposure to contaminants in groundwater, soil,
sediment, surface water, and air associated with the Carolina Transformer Site. The
potential risks developed in this risk assessment are those directly related to
contaminants in the media at this site. No attempt has been made to differentiate
between the risk contributions from other sites and those being contn'buted from the
Carolina Transformer Site. This human health and environmental risk assessment
has been derived from data collected during Phase I, Phase II, and Phase III of the
Remedial Investigation performed by ESD-HWS.
The procedures used in the performance of this risk assessment and its scope are
consistent with and based on U.S. EPA guidance procedures and policies for the
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performance of risk assessments at hazardous waste sites. The primary guidance
relied upon was the Risk Assessment Guidance for Superfund (RAGs), Volume I
(Human Health Evaluation Manual), Volume II (Environmental Evaluation Manual),
and related documents (1,5].
1.4 Organization of the Baseline Risk Assessment
The Baseline risk assessment of the Carolina Transformer Site consists of:
• Identification of Chemicals of Potential Concern
• Exposure Assessment
• Toxicity Assessment
• Risk Characterization
• Environmental Evaluation
• Summary
1.4. 1 Identification of Chemicals of Potential Concern
This step in the risk assessment process involves gathering and analyzing the site data
relevant to the human health evaluation and identifying the contaminants present at
the site that will be included in the risk assessment process. This is shown on Figure
1.1 as the Data Collection and Evaluation section. The identification of target
chemicals per medium is performed in Chapter 2 of this report
1.4.2 ExposureAssessment
An exposure assessment is conducted to estimate the magnitude of actual ( current)
and potential (future) human exposures to site media, the frequency and duration of
these exposures, and the pathways that result in human exposures. In the exposure
assessment, conservative estimates of exposure are developed for both current and
future land-use assumptions. Current exposure estimates are used to determine if a
threat exists based on existing exposure conditions at the site. Future exposure
estimates are to provide decision-makers with an understanding of potential future
exposures and threats. Conducting an exposure assessment involves analyzing
contaminant releases, identifying exposed populations, identifying all the potential
pathways of exposure, estimating exposure point concentrations for specific pathways,
and estimating contaminant intakes for specific pathways. The results of the exposure
assessment are pathway-specific intakes for current and future exposures to
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contaminants at the site. The exposure assessment is presented in Chapter 3 of this
report.
1.4.3 Toxicity Assessment
The toxicity assessment involves determining the types of adverse health effects
associated with chemical exposures, the relationship between magnitude of exposure
and adverse effects, and the related uncertainties involved. Risk assessments rely
heavily on existing toxicity information developed for specific chemicals. The two
primary sources for this information is the Integrated Risk Information System
database (IRIS), and the Health Effects Assessment Summary Tables (HEAST). The
toxicity components in a risk assessment fall into two categories, those related to
noncarcinogenic risk, and those related to carcinogenic risk. To evaluate
noncarcinogenic risk, the intake of a contaminant is compared to the corresponding
reference dose (RID) of that compound. The RID used in the Risk Assessment is
a best estimate of the level at which there will be no observed adverse effect to the
exposed population. To evaluate carcinogenic risk the intake of a contaminant is
factored with the slope factor (SF) for that contaminant. The slope factor used in
the Risk Assessment is a best estimate of the carcinogenic potency of a contaminant,
or its ability to cause cancers in an exposed population. For humans both the Rills
and Sfs are derived from human epidemiology studies and animal dose-response
relationships. The toxicity assessment results are presented in Chapter 4 of this
report.
1.4.4 Risk Characterization
The risk characterization section of the risk assessment summarizes and combines the
exposure and toxicity assessments to characterize baseline risks, both quantitatively
and qualitatively. During risk characterization, chemical-specific toxicity information
is compared against the estimated exposure levels to determine whether contaminants
at the site pose current and future risks that are of a magnitude to be of concern.
This is presented in Chapter 5 of this report.
1.4.5 Environmental Evaluation
An environmental evaluation (EA) is a qualitative and/or quantitative appraisal of the
actual or potential effects of a hazardous waste site on plants and animals other than
people and domesticated species. It is important to emphasize, however, that the
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11
health of people and domesticated species is inextricably linked to the quality of the
environment shared with other species.
The goal of an environmental evaluation is to provide information on threats to the
natural environment associated with contaminants or with actions designed to
remediate the site. The environmental evaluation is also intended to reduce the
inevitable uncertainty associated with understanding the environmental effects of a
site and its remediation, and to give specific boundaries to that uncertainty.
However, it is important to recognize that environmental evaluations are not research
projects: they are not intended to provide absolute proof of damage, nor are they
designed to answer long-term research needs.
Information provided by the environmental evaluations may be used to:
• Decide if remedial action is necessary based on ecological considerations.
• Evaluate the potential ecological effects of the remedial action itself.
• Provide information necessary for mitigation of the threat.
• Design monitoring strategies for assessing the progress and effectiveness of
remediation.
The environmental evaluation is presented in Chapter 6 of this report.
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2.0 Identification of Chemicals of Potential Concern
2.1 Summary of Remedial Investigations
2. 1. 1 Geologic and Hydrogeologic Investigation
The Carolina Transformer Site may be underlain by as many as three aquifers. The
sand and gravel alluvial deposits are present could provide large yields to wells. The
available information indicates that the alluvial aquifers are not presently used for
water supply in the area. The sands and clays of the Cape Fear and Middendorf
Formations serve as aquifers in the Fayetteville area. Wells completed within these
formations can be screened over a large interval which could cover sands and
intervening clays. The sands provide much higher yield and are the most productive
aquifers in the region. The bedrock possesses fracture permeability and is utilized
for industrial supplies. A deep bedrock well was used by Larry's Sausage Company
which is located adjacent to the site. This well is 303 feet deep and is completed into
the bedrock from 212 feet to the total depth.
During Phase I of the RI, ESD-HWS installed and sampled eleven temporary sand
point wells on and around the site (Figure 2-1). The wells were installed where soil
samples with the same sample number were collected by advancing the borehole to
a depth of approximately two to three feet below the water table surface. After the
groundwater samples had been collected, piezometers were constructed. Five potable
water wells located to the north and east of the site were also sampled (Figure 2-2).
Table 2-1 presents the potable water well inventory and the current status informa-
tion for wells located in the immediate vicinity of the site.
During the installation of the groundwater monitoring wells and the piezometers, soil
samples were obtained from various horizons within the deposits. A lithologic profile
for each borehole is presented in Table 2-2.
In general, the site is located in the Coastal Plain physiographic province of North
Carolina. The main stratigraphic unit at and in the vicinity of the site is the
Tuscaloosa Formation of alluvial origin and Upper Cretaceous in age. The materials
comprising the Tuscaloosa Formation were derived from crystalline rocks such as
granites, gneisses, and schists which compose the adjacent Piedmont physiographic
A:.\CART\SECT2.0AA 2-1
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NOTE:
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PROPERTY
ALL ELEVATIONS ARE FEET ABOVE GEOGRAPHIC DATUM
TDC= TOP OF CASING
12
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FIGURE 2-1 TEMPORARY WELL LOCATIONS
CAROLINA TRANSFORMER FAYETTEVILLE, NORTH CAROLINA
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160 0 80 - -- - -C IN FEETl
EDGE PROPERTY
DRAINAGE DITCH
LARRY'S SAUSAGE ---ll
160
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1 INCH= 160 FT.
202 8
CAROLINA TRANSFORMER
0
.209
207,.
.., FIGURE 2-2
WATER WELL SAMPLE LOCATIONS
CAROLINA TRANSFORMER
FAYETTEVILLE, NORTH CAROLINA
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I Table 2-1
Water Well Inventory
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I Well Owner Depth
Number (as of 12/83) .illl Present Status
I J. K. Ellis 12 pulled and plugged
I 202 M. T. Ellis 12 no longer used
R. Ellis 12 pulled and plugged
I B. Edge 12 pulled and plugged
I Larry's Sausage 300 plugged
I J. Royster 165 still in use
207 A. McDaniel 260 still in use
I R. Williams still in use
I 209 T. R. Weeks 363 still in use
I Ms. Edge pulled and plugged
I C. Vansant pulled and plugged
Carolina Transformer not in use
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Source: Remedial Investigation Report, Carolina Transformer Site,
I Fayettville, North Carolina, U.S. EPA, June 1990.
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We 11 Location
1
6
12
16
19
21
25
. 31
36
44
47
TABLE 2-2
LITHOLOGIC PROFILE FROM TEMPORARY WELL LOCATIONS
CAROLINA TRANSFORMER
FAYETTEVILLE, NORTH CAROLINA
Depth (ft) Description
0 -0.5 Brown Soil
0.5 - 1
Sandy brown soil mixed with clay
1 - 2
Brown sandy soil
2 - 7
Orange brown sand
0 -2.5 Brown gray clay
2.5 - 4
Gray sandy clay
4 -4.5 Gray sand
0 -0.5 Light brown soil
0.5 -1.5 Light brown & orange soil mixed with rocks
1.5 -5 Orange clay
0 -1.5 Dark brown sandy soil
1.5 -3.5 Tan sand
0 - 1 Orange brown soil
1 - 6
Orange clay
6 - 7
Light tan-beige soil
0 - 1 Light brown soil
1 -2.5 Light brown soil gradually turning into clay
2.5 - 4
Light tan to peach clay
4 -4.3 Coarse white sand
0 -0.5 Light tan soil
0.5 - 3
Orange clay
3 -4.5 Dry orange clay with sand
4.5 - 6
Wet oranqe clay with sand
0 - 1
Orange brown sand
1 - 4 Orange clay
4 - 5
Orange clay mixed with some light gray sand
5 - 7
Liqht oranae sandy soil
0 -0.5 Brown sandy soil
0.5 -4.5 Sandy orange soil
4.5 - 5
Light tan sand
0 - 1 Orange brown sand
1 - 2
Bright gray sand
2 - 3
Soft dark gray clay
3 -. 4 Soft dark arav clay mixed with some aravel
0 -1.5 Light gray sand
1.5 -3 Saturated lfoht gray sand
--- -- -
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FIGURE 2-3 PERMANENT MONITORING WELL LOCATIONS
CAROLIN/\ TRANSFORMER
FAYETTEVILLE, NORTH CAROLINA
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province. The soils formed from these crystalline materials consist of brown to tan,
fine to coarse grained sands, tan, silty sands, clayey sands, sandy clays, and grey to
blue-grey sandy clays, and clays.
The surfical soils at the site consist of the Wickham Series and the Roanoke Series.
Wickham Series soils cover most of the former facility area. These are well-drained
soils that formed in loamy fluvial sediments on terraces of the Cape Fear River and
its major tributaries. The loamy horizon is typically 40 to 60 inches thick and is
underlain by sandy alluvial sediments. These underlying sediments are poorly drained
soils that formed in stratified clayey sediments on terraces of the Cape Fear River
and its major tributaries. The loamy and clayey horizons are generally 40 to 60
inches thick and overlie the stratified sediments deposited by the river.
The shallow aquifer under the site is located at a depth of five to eight feet below
ground surface elevation, and is flowing through a fine to coarse sand layer which
varies in thickness from six to 13 feet. The grey to blue-grey clay located under the
upper sand layer is very tough and dry (observed from samples) indicating that the
clay is a very good confining layer separating the shallow aquifer from the deeper
aquifers. The potentiometric surface of the surfical aquifer was developed by
obtaining groundwater elevations from the piezometers. The general direction of
groundwater flow in the surficial aquifer in this area is to the northeast toward Locks
Creek.
During Phase III of the RI, five permanent monitor wells were installed around the
site (Figure 2-3). The wells were installed to the clay confining layer which forms the
bottom of the surfical aquifer. The wells were installed to detect any present and/or
future contamination which may result from the site. Groundwater elevations in
these wells were also surveyed in order to develop the potentiometric surface map.
Analytical data derived from groundwater samples from the onsite and downgradient
wells were compared to data from wells located hydraulically upgradient of the site.
The upgradient wells which were sampled are MW-1, MW-2, 16-GW, 19-GW, and
21-GW.
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Analytical data derived from groundwater samples from the temporary wells indicated
that PCB-1260 (Aroclor 1260) was present in two onsite wells: sample 44-GW
contained 52 micrograms per liter (ug/l) and sample 47-GW contained 25 ug/l. Two
onsite samples contained bis (2-ethylhexyl) phthalate (24 ug/l and 920J ug/1). Various
purgeable organic compounds, such as benzene, toluene, and chlorobenzene, were
also detected in onsite wells. In comparison with upgradient samples, elevated
concentrations of metals were detected in both onsite and offsite groundwater.
The five potable well samples, 202-GW, 206-GW, 207-GW, 208-GW, and 209-GW,
contained no detectable concentrations of PCBs, pesticides, or extractable organic
compounds. Sample 202-GW contained the purgeable organic compound methyl
ethyl ketone at a concentration of lOJ ug/l.' This well is no longer used for drinking
water.
PCBs were not detected in any of the samples from the permanent monitor wells.
Of the extractable organic compounds, 1,2,4-trichlorobenzene was detected in two
wells at concentrations of 1.5J ug/l and 5.0J ug/1. A variety of purgeable organic
compounds were detected; however, each one was only detected once. Several
metals, including barium, chromium, copper, and manganese, were detected at
elevated concentrations when compared with the upgradient samples.
2. 1.2 Surface Water Investigation
Thirteen surface water samples were collected from on and around the site (Figure
2-4) during Phase I. Eight of the samples were collected from the drainage ditch
which runs through the site and into a wooded area southwest of the site. Two
samples were collected from Locks Creek which flows into the Cape Fear River. The
first sample was collected upgradient of the site and the other downgradient. Two
samples were collected from the swamp west of the site and one from north of the
site.
0 The Alpha suffix to analytical data is a result of the ESD-HIIS data
validation. The suffixes have the following meaning:
J -Estimated value
N -PresulTJ)tive evidence of the material
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160
I - ----9 s,o
C IN FEET!
EDGE
PROPERTY
LARRY'S SAUSAGE --u
160
I
l INCH= 160 FT.
1J CAROLINA TRANSFORMER
FIGURE 2-4 SURFACE WATER SAMPLING LOCATIONS CAROLINA TRANSFORMER FAYETTEVILLE, NORTH CAROLINA
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Samples 71-SW and 72-SW collected from Locks Creek, up-and downgradient,
respectively, contained no detectable concentrations of PCBs, pesticides, extractable
organic compounds, or volatile organic compounds. Both samples contained similar
metals at equivalent concentrations.
Samples 73-SW through 80-SW were collected from the drainage ditch which runs
through the site and into a wooded area southwest of the site. All of the samples
except 75-SW contained PCB 1260 at concentrations ranging from 2.8 ug/1 in sample
76-SW to 8.2 ug/1 in sample 80-SW. No pesticides were detected in these samples.
Sample 80-SW contained a single extractable organic compound, bis (2-ethylhexyl)
phthalate, at a concentration of 45 ug/1. The concentration of copper was also
elevated in all the samples when compared to the upgradient sample.
Samples 82-SW, 83-SW and 84-SW were collected from the low-lying marsh areas
west and north of the site. Sample 83-SW contained 12 ug/1 of PCB 1260. No
pesticides were detected in the samples. Sample 83-SW contained a single
extractable organic compound, bis (2-ethylhexyl) phthalate, at a concentration of 1001
ug/1. Samples 83-SW and 84-SW contained the purgeable organic compound carbon
disulfide at concentrations of 8.61 ug/1 and 381 ug/1, respectively. Sample 83-SW also
contained 0.621 ug/1 of toluene.
2. 1.3 Sediment Investigation
During Phase I of the RI, 16 sediment samples were collected from on and around
the site (Figure 2-5). Neither PCBs nor organic compounds were detected in the
upgradient sample, 71-SD.
Three types of PCBs were detected in the 11 samples collected from the drainage
ditches. Each sample contained at least one type of PCB. Total PCB concentrations
ranged from 41,900 micrograms per kilogram (ug/kg) to 4,400,000 ug/kg. Purgeable
organic compounds were detected in five of the samples collected from the drainage
ditches. These compounds include toluene (121 ug/kg to 1,200J ug/kg),
chlorobenzene ( 48J ug/kg to 641 ug/kg), and 1,2-dichlorobenzene (291 ug/kg to 50J
ug/kg). Concentrations of several metals were elevated in comparison with the
upgradient sample.
A:\CART\SECT2.0AA 2-4
-------------------
160 0 80
CIN FEETl
EDGE PROPERTY
160
1 INCH = l 60 FT.
CAROLINA
TRANSFORMER
FIGURE 2-5
SEDIMENT SAMPLING LOCATIONS
CAROLINA TRANSFORMER FAYETTEVILLE, NORTH CAROLINA
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Two sediment samples were collected from the low-lying area west of the site. This
area is usually underwater. Another sample was collected from a marsh area north
of the site. PCB concentrations in these three samples ranged from 93 ug/kg to 3,120
ug/kg. Two pesticides, 4,4'-DDD and heptachlor, were also detected in these
samples. Toluene and ethylbenzene were the only purgeable organic compounds that
were detected. Mercury was detected in one sample at a concentration of 60 ug/kg.
2. 1.4 Onsite Soil Investigation
Four vadose zone soil samples were collected during Phase I. PCB was detected in
one sample at a concentration of 45 ug/kg. A single pesticide, toxaphene, was
detected in one sample at a concentration of 1,400 ug/kg.
During Phase II, 123 onsite soil samples from 62 locations were collected (Figure 2-
6). The site consists of two main areas: the administration area (grids 1-13) and the
storage and operations area (grids 15-72). Three different PCBs were detected in the
samples: PCB-1242, PCB-1254, and PCB-1260. The concentrations of PCB-1260 in
the administrative area ranged from "not detected" to 7,500 ug/kg. The concentra-
tions of PCB-1260 in the storage and operations area ranged from "not detected" to
2,100,000 ug/kg. Several volatile organic compounds were also detected. Examples
of these compounds include toluene, trichlorothene, benzene, and tetrachloroethene.
A variety of metals, including barium, chromium, and copper, were detected at
elevated concentrations when compared to offsite background samples.
2. 1.5 Ottsite Soil Investigation
During Phase I, 57 off site soil samples from 27 locations were collected (Figure 2-7).
PCB-1260 was the only PCB detected in the offsite soil samples. PCB concentrations
ranged from 9.2J ug/kg to 110,000 ug/kg. Pesticides were detected in four samples
collected from three grids. Chlordane was detected at concentrations of 0.71 ug/kg
and 0.92 ug/kg. Dieldrin was detected in one sample location. Several organic
compounds were also detected. For example, toluene was detected in concentrations
ranging from 6.2J ug/kg to 891 ug/kg; 1, 2-dichlorobenzene was detected in concentra-
tions of 181 ug/kg and 22J ug/kg; and 1, 4-dichlorobenzene was detected at concentra-
tions of 32J ug/kg and 44 ug/kg. Various metals were detected in all of the samples.
A:.\CAAT\SECT2.0AA 2-5
-------------------
160 0 80
C IN FEETl
EDGE PROPERTY
DRAINAGE DITCH
160
1 INCH = 160 FT.
r
FIGURE 2-6
ON-SITE SAMPLING LOCATIONS CAROLINA TRANSFORMER FAYETTEVILLE, NORTH CAROLINA
-------------------
18 •
•20
21 •
--- - -
9 sp
C IN FEETl
EDGE PROPERTY
•l 4 el 3
DRAINAGE DITCH
•12 •ll
U7L-.-..L.I _____,
Lf\RRY'S Sf\USI\GE --U
160 I
24
23
2
1 INCH= 160 FT.
•10 9•
8 •
-~ 7• ~
1J
.s
It ::,,;
e4 " .Q:-
25
•3
Cf\ROLINA
TRANSFORMER
o2
FIGURE 2-7
OFF-SITE SOIL SAMPLING LOCATIONS
CAROLINA TRANSFORMER FAYETTEVILLE, NORTH CAROLIN/\
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Six samples were analyzed for dioxins and furans. All of the samples except one
contained dioxins and/or furans.
2.1.6 Waste/Tanklnvestigatton
During Phase I, a total of four tanks and six transformers were located onsite. Also,
a pit was discovered in the main building. Of these, three tanks, five transformers
and the pit were sampled. One tank and one transformer were empty. PCBs were
detected in only one sample. A sample collected from a half-buried tank next to the
maintenance building contained 15 milligram per kilogram (mg/kg) of PCB-1242 and
57 mg/kg of PCB-1260. No pesticides were detected in any of the samples.
Extractable organic compounds were identified in a sample collected from a half-
buried tank near the maintenance building. The sample contained 2,100 mg/kg of 2-
methylnapthalene, 5601 mg/kg of fluorene, and 1,200 mg/kg of phenanthrene. No
purgeable organic compounds were detected in the samples. Several metals were
identified in most of the samples including copper, zinc, aluminum, and iron.
Two of the samples were analyzed for dioxins and furans. A sample collected from
a transformer did not contain either dioxins or furans; however, the sample collected
from the half-buried tank contained several dioxins and furans.
2. 1. 7 Wipe and Building Sampling
Three buildings which were used as storage and work areas are located on site. The
main building on site which served as the office, warehouse, and work area has a
concrete floor. During Phase I, three samples were scraped from the soil and debris
remaining on the floor.
The maintenance building along the northern boundary of the site was divided into
three bays which appeared to be areas for working on vehicles and equipment. This
building also has a concrete floor. One composite soil/debris sample was scraped
from the floors in the three bays.
One soil/debris sample was collected from the small brick building used to burn
insulation from wire and other electrical components in order to recover the metals.
A:\CART\SECT2.DAA 2-6
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The wipe samples were collected by wiping a 10 centimeter (cm) by 10 cm area with
a cotton swab saturated with hexane. Each area was wiped three times. Three wipe
samples were collected from selected walls inside the main building. One wipe
sample was collected from the small brick burn building.
The composite soil samples scraped from the floors of the main, maintenance, and
burn buildings all contained PCB-1260. The three samples from the main building
contained 92,000 ug/kg, 80,000 ug/kg, and 91,000 ug/kg of PCB-1260. The composite
sample from the maintenance building contained 2,200,000 ug/kg of PCB-1260. The
sample collected from the burn building contained 42,000 ug/kg PCB-1260.
The pesticide, heptachlor epoxide, was detected in two of the main building samples.
No extractable organic compounds were detected in the soil samples. Purgeable
organic compounds were detected in two of the main building samples. One sample
contained 9801 ug/kg of acetone and the other sample contained 230 ug/kg of
toluene.
High concentrations of several metals were detected in all the building samples.
Mercury ranged from lJ mg/kg to 2.2 mg/kg. Arsenic ranged from 2.JJ mg/kg to 76J
mg/kg. Copper ranged from 2,6991 mg/kg to 130,000 mg/kg. Lead ranged from 120
mg/kg to 700 mg/kg. Manganese ranged from 440 mg/kg to 2,600 mg/kg.
The sample collected from the burn building was analyzed for dioxins and furans.
The sample contained high concentrations of several dioxins and furans. One
composite sample from the main building and one from the maintenance building
also contained dioxins and furans.
PCB-1260 was identified in two wipe samples from the main building. One sample
contained 5.6 ug/100 cm2 and the other sample contained 3.1 ug/100 cm2•
The sample collected from the bum building contained 5.3 ug/100 cm2 of PCB-1260.
No pesticides, extractable organic compounds, or purgeable organic compounds were
detected in the wipe samples.
The wipe samples were not analyzed for metals or dioxins and furans.
A:.\CART\SECT2.DAA 2-7
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2.2 Evaluation and Selection of Chemlcalsof Potential Concern
The process of determining the chemicals of potential concern for the Carolina
Transformer Site included a detailed evaluation of the analytical data, a careful
analysis of the sources of contamination and areas that the sources impact, and a
review of site characteristics. This evaluation is consistent with EPA guidance (1 ).
This process includes the following steps:
• Gather all available data from site investigations and sort the data by
medium.
o Evaluate the analytical methods used.
• Evaluate the quality of data with respect to sample quantitation limits.
• Evaluate the quality of data with respect to qualifiers and codes.
o Evaluate the quality of data with respect to blanks.
• Compare potential site-related contamination with background concentra-
tions.
• Develop a set of data for use in the risk assessment.
• If appropriate, further limit the number of chemicals to be carried through
the risk assessment.
The objectives of this evaluation process are to identify a set of chemicals that are
likely to be site-related and to assure that reported concentrations are of acceptable
quality for use in the quantitative risk assessment. In the evaluation, the data
validation processes for each phase of the RI were reviewed, and the appropriateness
of the data for the risk assessment was determined.
The scope of the risk assessment was limited to the data generated during Phase I,
Phase II, and Phase III of the RI. The RI data was believed to most accurately
represent the current state of the site and was, therefore, the primary source of
contaminant information.
A:\CART\SECT2.0AA 2-8
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During the initial evaluation, the data collected for the site was categorized as to
whether the sample locations were source-related or impacted by the source. There
are three basic categories for the sample locations, including one onsite category
(within the site boundaries), and two offsite categories (upgradient of the site and
impacted by past disposal activities). Sample locations influenced by the site have
been identified for the potential ability of contaminants to migrate from the site to
sample points through natural fate and transport mechanisms, including leaching,
precipitation runoff, groundwater migration, and erosion.
This qualitative identification has also been done for impacts of human activities such
as dumping, earthmoving operations, and tracking. Based on these evaluations, the
sample locations presented on Table 2-3 are evaluated to identify chemicals of
potential concern for the Carolina Transformer Site.
Two onsite temporary wells ( 44-GW and 47-GW) were considered to be the most
representative of site-related activities. PCBs were only detected in these two wells.
In addition, organic compounds and elevated concentrations of various metals were
also detected in these wells. For these reasons, samples 44-GW and 47-GW were
used to identify site-related chemicals of concern in groundwater. General
comparisons were also made between the constituents detected in these two samples
and those detected in the other media.
Tables 2-4 through 2-13 present the information used in determining the chemicals
of potential concern for the Carolina Transformer Site and the results. Table 2-14
presents the chemicals that have been selected as the chemicals of potential concern
in the associated media for the site.
The following steps eliminated potential chemicals of concern from further
consideration for the baseline risk assessment:
• Data qualifiers resulting in presumptive evidence of presence of material
resulted in compounds being eliminated from further consideration.
• If a chemical was detected only once in all samples analyzed for that
chemical in that media, the exposure potential for that chemical was
considered to be low. As a result, compounds were eliminated from further
consideration.
A:\CART\SECT2.DAA 2-9
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TABLE 2-3
SOURCE RELATED SAMPLE LOCATIONS AND NUMBERS
GROUNDWATER SURFACE WATER
Temporary Wells Permanent Wells Potable Wells
(1) IGW (III) MWI-GWI (UP) (I) 2(12.GW (OFF) (I) 7!SW (UP)
(1) 6GW (OFF) (III) MW2-GWI (UP) (I) 206GW (OFF) (1) 72SW (OFF)
(I) 12GW (OFF) (III) MW3-GWI (OFF) (I) 207GW (OFF) (I) 73SW
(I) i6GW (UP) (Ill) MW4-GWI (OFF) (I) 208GW (OFF) (I) 74SW
(I) !9GW(UP) (Ill) MW5-GWI (I) 209GW (OFF) (I) 75SW
(I) 2!GW (UP) (I) 76SW
(I) 25GW (OFF) (!) 77SW
(I) 3!GW (I) 78SW
(I) 36GW (!) 79SW
(I) 44GW (I) 80SW (OFF)
(I) 47GW (I) 82SW (OFF)
(I) 83SW (OFF)
(I) 84SW (OFF)
NOTES:
(1) Phase I Data
(Ill) Phase m Data
(UP) Upgradient sample IOOIJ:ion
(OFF) Off site and possibly impoctod by site.
SEDIMENT
(I) 71SD (UP)
(I) 72SD (OFF)
(I) 73SD
(I) 74SD
(I) 75SD
(I) 76SD
(I) 77SD
(I) 78SD
(I) 79SD
(I) 80SD (OFF)
(I) 8!SD (OFF)
(I) 82SD (OFF)
(I) 83SD (OFF)
(I) 84SD (OFF)
(I) 85SD
(I) 86SD
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TABLE 2-3 (Cont.)
SOURCE RELATED SAMPLE LOCATIONS AND NUMBERS
OFF-SITE SOIL
(I) ISLA (I) I0SLA (I) 19SLA
(I) ISLB (I) IOSLB (I) 19SLB
(I) !SLY (I) I ISLA (I) 19SLV
(I) 2SLA (I) IISLB (I) 20SLA (UP)
(I) 2SLB (I) 12SLA (I) 20SLB (UP)
(I) 3SLA (I) 12SLB (I) 21SLV (UP)
(I) 3SLB (I) 12SLV (I) 22SLA
(I) 4SLA (I) I 3SLA (I) 22SLB
(I) 4SLB (I) 13SLB (I) 23SLA
(I) 5SLA (I) 14SLA (I) 23SLB
(I) 5SLB (I) 14SLB (I) 24SLA
(I) 6SLA (I) 15SLA (I) 24SLB
(I) 6SLB (I) 15SLB (I) 25SLV
(I) 6SLV (I) 16SLA (I) 33SLA
(I) 7SLA (I) 16SLB (I) 33SLB
(I) 7SLB (I) 16SLV (I) 34-SLA
(I) 8SLA {I) I 7SLA (I) 34SLB
(I) 8SLB (I) 17SLB
(I) 9SLA (I) 18SLA
(I) 9SLB (I) 18SLB
NOTES:
(I) Phase I Data
A 0-6" below land surface (BLS)
B 6-12" below land surface (BLS)
V Vadose Zone (Only sample., tekcn at 0-6" BLS and 6-12" BLS will be used in this baseline risk assessment).
(UP) Upgradient or background sample location, all other samples possibly impacted by site.
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TABLE 2-3 (Cont.)
SOURCE RELATED SAMPLE LOCATIONS AND NUMBERS
I ON-SITE SOIL
I (II) ISLA (II) 2ISLA (II) 40SLA (II) 57SLB
I (II) ISLB (II) 2ISLB (II) 40SLB (II) 58SLA
(II) 2SLA (II) 22SLA (II) 4ISLA (II) 58SLB
(II) 2SLB (II) 22SLB (II) 4 ISLB (II) 59SLA
I (11) 3SLA (II) 23SLA (II) 42SLA (II) 59SLB
(II) 3SLB (II) 23SLB (II) 42SLB (II) 60SLA
(II) SSLA (II) 24SLA (II) 43SLA (II) 60SLB
I (II) SSLB (II) 24SLB (II) 43SLB (II) 6ISLA
(II) 6SLA (II) 2SSLA (II) 44SLA (II) 6ISLB
(II) 6SLB (II) 2SSLB (II) 44SLB (II) 62SLA
I (II) ?SLA (II) 26SLA (II) 45SLA (II) 62SLB
(II) ?SLB (11) 26SLB (II) 45SLB (II) 64SLA
(II) 8SLA (II) 27SLA (II) 46SLA (II) 64SLB
I (II) 8SLB (II) 27SLB (II) 46SLB (II) 65SLA
(II) I0SLA (II) 28SLA (II) 47SLA (II) 65SLB
(II) !OSLB (II) 30SLA (II) 47SLB (II) 66SLA
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(II) I ISLA (II) 30SLB (II) 48SLA (II) 66SLB
(II) I ISLB (II) 3 ISLA (]I) 48SLB (II) 67SLA
(II) 12SLA (II) 3ISLB (II) 49SLA (II) 67SLB
I
(II) I2SLB (II) 32SLA (II) 49SLB (II) 68SLA
(II) I 3SLA (II) 32SLB (II) 50SLA (II) 68SLB
(II) !3SLB (II) 33SLA (II) S0SLB (II) 69SLA
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(II) ISSLA (II) 33SLB (II) SISLA (II) 69SLB
(II) I5SLB (II) 34SLA (II) 52SLB (II) ?ISLA
(II) I6SLA (II) 34SLB (II) 54SLA (II) ?ISLB
I
(II) I6SLB (II) 36SLA (]I) 54SLB (II) 72SLA
(II) I8SLA (II) 36SLB (]I) 55SLA (II) 72SLB
(II) !8SLB (II) 37SLA (]I) 55SLB
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(II) I9SLA (II) 37SLB (]I) 56SLA
(II) I9SLB (II) 39SLA (II) 56SLB
(II) 20SLA (II) 39SLB (II) 57SLA
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(II) 20SLB
I NOTES:
(I) Phase I Data
(II) Phase II Data
I A 0-2" below land surfaee (BLS)
B 8-10" below land surface (BLS)
I
--- - - -
~•myto Chermcal or Parameter
1norganac Bement, Barium
1 Kerytl1um
Cobalt
1l,hrom1um
vopper
Nickel
Lead
Strontium
Titanium
Vanadium
Yttrium
Zinc
Aluminum
Manganese
Calcium
Magnesium
Iron
Sodium
Potassium
Mercury
Pfllldde/PCB Compound• PCB-1260 (Aroclor 1260)
Dieldrin
E:Ktractabl• Organic Compound• Naphthalene
01~2-t::lhyinex •••
Phenol
1,2.4-Trichlorobenzene
Purgeable Organic Compound• Carbon Dlaulfide
Methyl Ethyl Ketone
Benzene
Toluene
Chlorobenzene
Chloromethane
1, 1-Dlchloroethene
Acetone
1.1--0ichloroethane
Ci s-1,2--0ichloroethene
Chloroform
1, 1, 1-Trichloroethane
Bromodichloromethane
Trichloroethene
Tetrachloroethene
Ethyl Benzene
(M-and/or P-)Xylene
0-Xylene
1,3--0ichlorobenzene
1,4--0ichlorobenzeoe
J • Eatlmated value.
Blank • NOi Analyzed.
-- - - -- - -- - -
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN GROUNDWATER (UG/L)
CAROLINA TRANSFORMER
1GW 8GW 12GW 16GW 19GW 21GW
~requency ol Detection" 0 -L3/89 08J2;jilS\:I QK1:,,4/g9 08/23/89 ,=,~89
17/20 4,400 1,200 560 1,000 1,600 6,000
3120 - -- --
10/20 530 32 51 24 180 110
16120 1,300 150 170 130 640 590
17/20 780 90 140 58 340 270
13/20 620 61 76 46 -160
5120 ---- --
17/17 1,300 260 100 88 500 610
15/20 6,700 620 1,400 460 2,900 500
16/20 3,600 220 390 120 1,200 780
15/20 890 89 120 85 640 390
16/20 2,500 230 340 180 900 94()
17/20 1,900,000 130,000 260,000 180,000 740,000 610,000
17/20 25,000 370 610 470 2,300 2,700
19/20 84,000 9,600 4,200 8,200 27,000 38,000
18/20 110,000 8,400 11 .000 7.200 52,000 40,000
16/20 1,900,000 51,000 180,000 46,000 450,000 23,000
16/20 -20,000 8,100 - -
14,000
12120 - --4,900 --
4/20 - -- - - -
2120 --- - --
1/20 - - - ---
1/20 -- - - -
2120
1/20 --3.7J - -
2/20 --- - -
3120 - --- -
2/20 - - -
3120 -- - ---
1/20 - - -
-- -
2/20 -- - ---
1/20 -- -- -
1/20 - -- - --
1/20 - - - -- -
1/20 - - - ---
1/20 - - - - --
1/20 -- -- -
1/20
1/20 -
1/20
1/20
1/20 - - -- --
1/20 - - - - - -
1/20
1/20 -- - - - -
1/20 - - - - - -
Material was analyzed for but not detected.
25GW 31GW
08/23/89
2,300 600 -
250 91
840 260
370 130
520 n
--
740 180
5,100 1,600
2,000 830
490 190
1,200 260
1.000,000 260,000
11,000 2,000
40,000 13,000
48,000 14,000
1,100,000 260,000
-5,700 -14,000
----- --
- ------- -- -- ---
---- -
Frequency of Detection• Number of Samplea With Positive Detection Over TotaJ Number of Samples
:JJ;GW 44GW 47GW
08123/89 O=;,,;,,J89 •=mK9
420 19,000 5,800
--
38 670 -
94 2,900 860
57 3,000 1.000
59 1,200 ----
310 1,400 510
1,100 -1,000
150 4,900 950
40 1,500 -
150 3,500 1,200
100,000 3,100,000 1,400,000
520 8,900 2,400
22,000 79.000 62,000
11,000 140,000 59,000
63,000 1,000,000 210,000
24,000 73,000 26,000
4,900 --
- ---52 25
24 02~
6.7J 11J
8.2J
0.65J 2.8J -- -5.5
6.3 20 -
- - -- - -- -
--- - ----------- - --
Analyte Chemical or Parameter
Inorganic Bement• Barium
Beryllium
Cobalt
Chromium
Capper
Nickel
Lead
Strontium
Titanium
Vanadium
Yttrium
Zinc
Aluminum
Manganese
Calcium
Magnesium
Iron
Sodium
Potassium
Mercury
Pesdclde/PCB Ccmpounda PCB-1260 (Aroclor 1260)
Dleldrin
Extractable Organic Canpounda Naphthalene
Bis(2-Eth)1hex)1) Phthalate
Phenol
1,2,4-Trichlorobenzene
Purgeable Organic Compounds Carbon Di&Ulfide
Methyl Ethyl Ketone
Benzene
Toluene
Chlorobenzene
Chloromethane
1, 1--0lchloroethene
Acetone
1, 1--0ichloroethane
Cl &-1,2-0lchloroothene
Chloroform
1, 1, 1-Trichloroethane
Bromodlchloromethane
Trichloroethene
Tetrachloroethene
Ethyl Benzene
(M-and/or P-))()1ene
0-Xylene
1,3-0lchlorobenzene
1,4-0lchlorobenzene
J • Estimated vaJue.
Blank • NOi Analyzed,
TABLE 2--4 (Cont).
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN GROUNDWATER (UG/l.)
CAROLINA TRANSFORMER
202GW 206GW 207GW 208GW 209GW MW1
Frequency of Detection• 08/30/89 07/18/89 08/29/89 08/29/89 08/30/89 03/13/90
17/20 190 -250
3/20 -
10/20 -
16/20 32
17/20 12 ---25
13/20 -
6/20 18
17/17 270 190
15/20 320
16/20 so
15/20 20
16/20 13 --190 35
17/20 110 - --19,000
17/20 76 -270
18/20 26,000 7,100 13,000 -8,300
18/20 12,000 5,000 4,400 -5,400
16/20 22,000
16/20 11,000 140,000 3,400 170,000 rn.ooo
12120 5,900 13,000 17,000 8,200 2,100
4/20 -
2120 -- -- -
1/20 --- -
1/20 -- -- --
2120 -- -- --
1/20 -- -- -
2120 --1.SJ
3/20 -- -- --
2120 10.0J --- --
3/20 -- -- -
1/20 -- - --
2120 - -- -
1/20 --
1/20 -
1/20
1/20
1/20 --- -- -
1/20 --- -- -
1/20 - ---- -
1/20 - -- --
1120 ----
1/20
1/20 -- -- --
1/20 --- --
1/20 -- --
1/20 ---
1/20 --
Matenal was analyzed for but not detected.
MW2 MW3
03/13/90 03/13/90
1,500 1.600
26 -
37 110
260 240
130 180
94 160
110 140
350 180
1,300 3,100
460 580
190 88
240 490
210,000 390,000
860 2,900
16,000 13,000
16,000 18,000
120.000 340,000
46,000 9,400
7,300 9,400
0.22 0.40 ----
--
---
5.0J
5.9J -- --
-------
---
9.3J
37
Frequency of Detection • Number of Sample■ With Positive Detection Over Total Number or Sample■
MW4 MWS
03/13/90 03/13/90
1,200 910
20 21
220 110
300 290
210 280
180 200
150 190
460 230
5,000 3,000
890 820
180 200
480 410
410.000 280,000
13,000 2.200
30,000 18,000
30,000 17,000
560,000 400,000
19,000 5,100
13,000 14,000
0.37 0.37
- --0.029J
7.4J ----
- -- -
80
2.4J
27
66
31
42 --9.9
66
1.3.l
10.0J
16J
54
23
13J
-
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
ANALYTE
Inorganic Elements
Pesticide/PCB
Extractable Organics
Purgeable Organics
TABLE 2-5
RATIONALE FOR IDENTIFICATION OF
CHEMICALS OF POTENTIAL CONCERN
IN GROUNDWATER
CHEMICAL OR PARAMEfER RATIONALE
Barium Yes -Found at more than 2X upgradlent concentration.
Beryllium No -Not significantly (2X} greater than upgradlent.
Cobalt Yes -Found at more than 2X upgradlent concentration.
Chromium Yes -Found at more than 2X upgradlent concenlratlon.
Copper Yes -Found at more than 2X upgradlent concentration.
Nickel Yes -Found only downgradient.
Lead No -Not significantly (2X) greater than upgradient.
Strontium Yes -Found at more than 2X upgradlent concentration.
Titanium Yes -Found al more than 2X upgradlent concentration.
Vanadium Yes -Found at more than 2X upgradlent concentration.
Yttrium Yes -Found at more than 2X upgradient concentration.
Zinc Yes -Found al more than 2X upgradient concentration.
Aluminum Yes -Found al more than 2X upgradlent concentration.
Manganese Yes -Found at more than 2X upgradlent concentration.
Calcium No -Low toxicily and low concentrations.
Magnesium No -Low toxlclly and low concentrations.
Iron No -Low toxiclly and low concentrations.
Sodium No -Not significantly (2X) greater than upgradient.
Potassium No -Not significantly (2X) greater than upgradlent.
Mercury Yes -Found at more than 2X upgradlent concentration.
PCB-1260 (Aroclor 1260) Yes -Found only downgradient.
Dleldrin No -Found in only one sample at a low concentration.
Bls(2-Elhylhexyl) Phthalale Yes -Found only downgradlent.
Phenol No -Found In only one sample at a low concentration.
1,2,4-Trichlorobenzene Yes -Found only downgradient.
Naphthalene No -Found In only one sample at a low concenlratlon.
Carbon Disulfide Yes -Found only downgradlent.
Methyl Ethyl Ketone Yes -Found only downgradlent.
Benzene Yes -Found only downgradlent.
Toluene Yes -Found only downgradlent.
Chlorobenzene Yes -Found only downgradlent.
Chloromethane No -Found In only one sample.
1, 1-Dichloroethene No -Found In only one sample.
Acetone No -Found In only one sample.
1, 1-Dlchloroethane No -Found In only one sample.
Cls-1,2-Dlchloroethene No -Found in only one sample.
Chloroform No -Found in only one sample.
1, 1, 1-Trichloroethane No -Found In only one sample.
Bromodichloromethane No -Found In only one sample.
Trichloroethane No -Found In only one sample.
Tetrachloroethene No -Found In only one sample.
Ethyl Benzene No -Found In only one sample.
(M-and/or P-)Xylene No -Found In only one sample.
0-Xylene No -Found In only one sample.
1 ,3-Dichlorobenzene Yes -Found only downgradlent.
1,4-Dlchlorobenzene Yes -Found only downgradlent.
- --

-
--
1.~nem1rJ111 or Parameter 1 rrequency 01 uetectioo •
Inorganic Bement&
tianum 20,20
Cadmium 4/8
~~~t a,8
IChrormum 19/20
v<>pper 12118
Lead 20/21
Vanadium 20/20
Zinc 14/20
Aluminum 20/20
ManganeN 20/20
Calcium 18/20
Magnesium 8/16
Iron 20/20
Soolum 1/4
Antimony 1/4
PeatlcldelPCB Compcunde
PCB-1264 (Aroclor 1264) 6/115
PCB-1260 (Aroclor 1260) 107/115
PCB-1242 (Aroclor 1242) 1/115
Extractable Organic Compound a
1,2,4-Trlchlorobenzene 1/4
Purgeable Organic Compound•
Tetrachloroethene 4/12
Toluene 11/20
Trtchloroethene 3/10
Benzene 1/4
Chlorobenzene 1/4
Chloroform 1/2
Blank• Not Analyzed. .
J • Estimated value.
N • Presumptive evidence of presence of material.
Material wae analyzed for but not detected.
----

-
--TABLE 2--6
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA TRANSFORMER
1SLA 1SLB 2SLA 2SLB 3SLA 3SLB 5SLA
111 l"M"OII 11,,-89 11/14/89 11/14/89 11/14189 11/14/89 11/14189
MU<~U MG.-u MG/KG Mm~u MGIKG MG,~u MGmu
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
-

-
-

-
-

-

-
2,500 160.J 3,600 230.JN 3,800 220 2,100
-----

-

-
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG UGIKG UG/KG
Frequency of Detection• Number of Samples With Positive Detection Over Total Number of Samples
-

-
-

-
--
5SLB 6SLA 6SLB 7SLA 7SLB
1111 .... 09 11/14/89 11/14/89 11/14/89 11/14/89
Mu.-u MG,~u Mu,~G MG/KG Mm~G
21 28
2.4
4.2 4.2
23 8.1
6.2 7.2
19J -
2.100J 2,SOOJ
250 210
280.J 300.J
2,200J 2,400J
UG/KG UG/KG UG/KG UG/KG
-

-
-

-

-
160.J 350 -400 -
--

-
--
UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG -2J -4J
--- -- -
Chemical or Parameter Frequency of Detection•
Inorganic 89fnents
Barium 20/20
Cadmium 4/8
Cobalt 3/8
Chromium 19/20
Copper 12118
Lead 20/21
Vanadium 20/20
Zinc 14/20
Aluminum 20/20
Manganese 20/20
Calcium 16/20
Magnesium 6/16
Iron 20/20
Sodium 1/4
Antimony 1/4
Pesticide/PCB Compounds
PCB-1254 (Aroclor 1254) 6/115
PCS-1260 (Aroclor 1260) 107/116
PCB-1242 (Aroclor 1242) 1/115
Extractable Organic Compounde
1,2,4-Trichlorobenzene 1/4
Purgeable Organic Ccmpounda
Tetrachloroethene 4/12
Toluene 11/20
Trichloroethane 3/10
Benzene 1/4
Chlorobenzene 1/4
Chloroform 1/2
Blank• Not Analyzed.
J • Estimated value.
N .. Presumptive evidence of preeence of materiaJ.
Material wae analyzed tor but not detected.
--- ----TABLE 2-<l (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA TRANSFORMER
23SLA 23SLB 24SLA 24SLB 25SLA 25SLB 26SLA
11/15189 11/15/89 11/14189 11/14189 11/14/89 11/14/89 11/14/89
MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
-------
20,000J 740 14,000 22,000 28,000 57,000 140,000
-------
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
Frequency of Detection~ Number of Samplee With Positive Detection Over Total Number of Samples
-- -- - -
26SLB 27SLA 27SLB 28SLA
11/14/89 11/14/89 11/14/89 11/15189
MG/KG MG/KG MG/KG MG/KG
29 28
2.2 -
8.9 5.4
2.800.J 1,300J
140 38
5.5 7.7
100.J 59J
3,300J 2,200J
31 45
1,300J 490J
240 220
2,600J 2,800J
UG/KG UG/KG UG/KG UG/KG
----
72,000 39,000 51,000 100,000 ----
UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG
3J 3J
---- --
Chemical or Parameter Frequency of Detection•
Inorganic Bement,
Barium 20/20
Cadmium 4/8
Cobalt 3/8
Chromium 19/20
Copper 12/18
Lead 20/21
Vanadium 20/20
Zinc 14/20
Aluminum 20/20
Manganeee 20/20
Calcium 16/20
Magnesium 6/16
Iron 20/20
Sodium 1/4
Antimony 1/4
Pesticide/PCB Ccmpounda
PCB-1254 (Aroolor 1254) 6/115
PCB-1260 (Aroolor 1260) 107/115
PC_B-1242 (Aroolor 1242) 1/115
Extractable Organic Compounds
1,2,4-Trichlorobenzene 1/4
Purgoable Organic Compoondo
Tetrachloroethene 4/12
Toluene 11/20
Trichloroethene 3/10
Benzene 1/4
Chlorobenzene 1/4
Chloroform 1/2
Blank a Not Analyzed.
J • Eetlmated value.
N • Presumptive evidence of presence of material.
Material was analyzed for but not detected.
--- - ---TABLE 2--6 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA TRANSFORMER
30SLA 30SLB 31SLA 31SLB 32SLA 32SLB 33SLA
11/15/89 11/15/89 11/15189 11/15/89 11/16189 11/16189 11/16189
MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG
27
1.8
8.4
610J
2
170
5.8
69J
1,BOOJ
29
690
230
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
-------
140,000 12,000 44,000 2,400 260,000J 66,000 78,000
-------
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG -
2J
Frequency of Detection• Number of Samples With Positive Detection Over Total Number of Samplea
-- -- - -
33SLB 34SLA 34SLB 36SLA 36SLB
11/16/89 11/16189 11/16189 11/16189 11/16/89
MG/KG MG/KG MG/KG MG/KG MG/KG
12 -
5.4 --
8.8 .
10
33J
2,100.J
27
UG/KG UG/KG UG/KG UG/KG UG/KG
8,900 120,000 16,000 23,000 18.000 --- --
UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG
1J
4J
--- - - -
Chemical or Parameter Frequency of Detection•
Inorganic Bementa
Barium 20/20
Cadmium 418
Cobalt 3/8
Chromium 16120
Copper 12/18
Lead 20/21
Vanadium 20/20
Zlnc 14120
Aluminum 20/20
Manganeae 20/20
Calcium 16/20
Magneelum 16/20
Iron 20/20
Sodium 1/4
Antimony 1/4
Pesticide/PCB Compound&
PCB-1254 (Aroclor 1254) 6/115
PCB-1260 (Aroclor 1260) 107/115
PCB-1242 (Aroclor 1242) 1/115
Extractable Organic Compounds
1,2,4-Trichlorobenzene 1/4
Purgeable Organic Ccmpounda
Tetrachloroethene 4112
T~uene 1/20
Trichloroethene 3/10
Benzene 1/4
Chlorobenzene 1/4
Chloroform 1/2
Blank• Not Analyzed.
J .,. Estimated value.
N • Preaimptlve evidence of presence of material.
Material wae analyzed for but nOI detected.
---- ---TABLE 2--6 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA TFIANSFORMER
37SLA 37SLB 39SLA 39SLB 40SLA 40SLB 41SLA
11/15189 11/15/89 11/15189 11/15/89 11/15/89 11/15/89 11/15189
MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG
9.8
1.9 -
4.2
70J
38
5
31J
1,500.J
14
190J -
1,500J
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG --- ----
7,400 40,000J 58,000J 1,300 83,000 2,200 27,000
-- --- --
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
Frequency of Detection • Number of Samples With Positive Detection Over Total Number of Samples
--- - --
41SLB 42SLA 42SLB 43SLA 43SLB
11/15/89 11/15/89 11/15/89 11/15189 11/15/89
MG/KG MG/KG MG/KG MG/KG MG/KG
29 10 11
9.4 --
2.6 --
4.1 4.9 4.8
140J 88J 1,200.J
71 27 32
12 8.4 ,_,
52J 19J 38J
2,600.J 3,000J 1,400.J
56 19 33
410J 26-0J 16-0J
260 --
2.900 3,300.J 3.500.J
UG/KG UG/KG UG/KG UG/KG UG/KG
-- - --
7,600 37,000J 7,100 31.000 15,000J
--- --
UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG
2J
6 2J 2J
1J
--- ---
Chemical or Parameter Frequency of Detection•
Inorganic 88fnenta
Barium 20/20
Cadmium 4/8
Cobalt 3/8
Chromium 19/20
Copper 12/18
Load 20/21
Vanadium 20/20
Zinc 14/20
Aluminum 20/20
Manganese 20/20
Calcium 16/20
Ma.gne■um 6/16
Iron 20/20
Sodium 1/4
Antimony 1/4
Pesticide/PCB Cc:m.pound•
PCB-1254 (Aroolor 1254) 6/116
PCB-1260 (Aroclor 1260) 107/115
PCB-1242 (Aroclor 1242) 1/115
Extractable Organic Ccmpoundo
1,2,4-Trlchlorobenzene 1/4
Purgaable Organic Compounds
Tetrachloroethene 4/12
Toluene 11/20
Trlchloroethene 3/10
Benzene 1/4
Chlorobenzene 1/4
Chloroform 1/2
Blank • Not Analyzed.
J • Eldmated value.
N • Preaumptiw evidence of preeence of material.
Material waa analyzed for but not detected.
--- - ---TABLE 2-6 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA TRANSFORMER
44SLA 44SLB 45SLA 45SLB 46SLA 46SLB 47SLA
11/15/89 11/15189 11/16189 11/16189 11/16/89 11/16/89 11/16189
MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG
18 15 13
3.7 -4.8
500J -270J
32 7.3 43
3.3 4.7 5.3
35 -43J
1,400J 950J 1,SOOJ
9.5 14 15
250J -730J ---
2,200.J 970J 1.700J
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
-------
19,000 5,300 42,000 3,SOOJ 31,000 2,700 89,000
-------
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
---
Frequency of Detection• Number of Sa.mplee With Positive Detection Over TotaJ Number of Samples
-- ----
47SLB 48SLA 48SLB
11/16189 11/16189 11/16/89
MG/KG MG/KG MG/KG
12
4.7
-
16
7.2
22J
2,100J
23
7.900J
270
1,000J
UG/KG UG/KG UG/KG -140,000 -
9,300 -7,400
---
UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG
2J
---- - -
Chemical or Parameter Frequency of Detection•
Inorganic Bemente
Barium 20/20
Cadmium 4/8
Cobalt 3/8
Chromium 19/20
Copper 12/18
Lead 20/21
Vanadium 20/20
Zinc 14/20
Aluminum 20/20
Manganeee 20120
Calcium 16/20
Magnesium 6/16
Iron 20/20
Sodium 1/4
Antimony 1/4
Pesticide/PCB Ccmpounde
PCB-1254 (Arcclor 1254) 6/115
PCB-1280 (Arcclor 1280) 107/115
PCB-1242 (Arcclor 1242) 1/115
Extractable Organic Compound•
1,2,4-Trfchlorobenzene 1/4
Purgeable Organic Compound•
Tetraohloroethene 4/12
Toluene 11/20
Trfchloroethene 3/10
Benzene 1/4
Chlorobenzene 1/4
Chlorofonn 1/2
Blank• Not Analyzed.
J • Eetimated value.
N • Prewmptlve evidence of pretence of material.
Material wa, analyzed for but not detected.
--- - -- -
TABLE 2-6 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA TRANSFORMER
49SLA 49SLB SOSLA SOSLB 51SLA 51SLB 52SLA
11/18189 11/16/89 11/18189 11/18189 11/16189 11/16189 11/15/89
MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG
6.3 16
-1.6
4.1 5.9
150J 47J
21 1.8
5.1 12
42J -
1,500.J 2,100J
8.3 23
350J 280.J -220
1,600.J 2,500J
- -
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
- --- - --
35,000 25,000 5,500 25,000J 5,400J 23,000J 2,000 - -- -- --
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG --
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG -1J
-, ,
-3J -16 -93
Frequency of Detection • Number of Samples With Pofitlve Detection Over Total Number of Samples
- -----
52SLB 54SLA 54SLB SSSLA SSSLB
11/15189 11/15189 11/15/89 11/15189 11/15/89
MG/KG MG/KG MG/KG MG/KG MG/KG
6 9.1
--
5.5 3
- -
0.83 -
5.9 8.3 --
2,300.J 1 .800J
6.4 16 - ---
2,000J 2,500.J
-6.8
UG/KG UG/KG UG/KG UG/KG UG/KG - --- -
11,000 2,100,000 1.000.000 150,000 11,000 --- - -
UG/KG UG/KG UG/KG UG/KG UG/KG -4500J
UG/KG UG/KG UG/KG UG/KG UG/KG
------
--- ---
Chemical or Parameter Frequency of Detection•
Inorganic Bement&
Barium 20/20
Cadmium 4/8
Cobalt 3/8
Chromium 19/20
Copper 12/18
Lead 20/21
Vanadium 20/20
Zinc 14/20
Aluminum 20/20
Manganese 20/20
Calcium 16120
Magnesium 6/16
Iron 20/20
Sodium 1/4
Antimony 1/4
Pesticide/PCB Compounds
PCB-1254 (Aroclor 1254) 6/115
PCB-1260 (Aroclor 1260) 107/115
PCB-1242 (Aroclor 1242} 1/115
Extractable Organic Compound a
1,2,4-Trichlorobenzene 1/4
Purgeable Organic Compound a
Tetrachloroethene 4/12
Toluene 11/20
Trichloroethene 3/10
Benzene 1/4
ChlOt'obenzene 1/4
Chloroform 1/2
BJank • Not Analyzed.
J • Estimated value.
N • Presumptive evidence of presence of material.
Material was analyzed for but not detected.
-- - -- - -
TABLE 2-6 (Coot.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA TRANSFORMER
62SLA 62SLB 64SLA 64SLB 6SSLA 6SSLB 66SLA
11/16/89 11/16/89 11/16189 11/16/89 11/16189 11/16189 11/15/89
MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG
16 19
5.5 3.7
55J -
1.2J 0.86
8.9 7.8
23.J -
3,SOOJ 2,600J
13 17
4"0J 470J
3,000J 2,000J
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
------20,000J
52,000 38000J 110,000J 32,000 54,000 160,000J -
---- ---
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
8
2J
2J -
Frequency of Detection• Number or Samplee With Positive Detection Over Total Number of Samples
-- --- -
66SLB 67SLA 67SLB 68SLA 68SLB
11/15189 11/15/89 11/15/89 11/15189 11/15189
MG/KG MG/KG MG/KG MG/KG MG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG
- ----
32,000J 48,000J 12,000 32,000 42,000
UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG
--- - - --- -- -
TABLE 2-6 (Cont.)
EVALUATION OFCHEMICALSOF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA TRANSFORMER
31SLV 36SLV
Chenuca1 or Parameter i:'requency 01 Detection• U0129/89 08/23/89
Inorganic Elements MG/KG MG/KG
Banum 20/20 8.6 5.6
Cadmium 4/8
vobalt 3/8 2.4 -
Chromium 19/20 5.6 2.6
Copper 12/18 2.8 -
Lead 20/21 4.8 4.5
Vanadium . 20/20 163 3.5
Zinc 14/20 5.6 -
Aluminum 20/20 3.600 1,300
Manganese 20/20 73 15
Calcium 16120 140 110
Magnesium 6116 220 n
Iron 20/20 9.200 750
Sodium 1/4 - -
Antimony 1/4
Pesticide/PCB Compound• UG/KG UG/KG
PCB-1254 (Aroclor 1254) 6/116
PCB-1260 (Aroclor 1260) 107/115
PCB-1242 {Aroclor 1242) 1/116
Blank• Not Analyzed.
J • Estimated value.
N ~ Presumptive evidence of preaence of material.
Material was analyzed for but not detected.
--
44SLV 47SLV
08/22/89 08/22/89
MG/KG MGl)(G
79 16
2.2
15 3.0
9.2 2.5
13 -
26 4.1
10 3.3
15,000 2,700
38 20
430 190
640 170
3,600 710
210
UG/KG UG/KG
45
Frequency of Detection a Number of Sam plea With Positive Detection Over Total Number of Samples
-- -- - -
---- - -
Chemical or Parameter Frequency of Detection•
Pesticide/PCB Compounds
PCB-1254 (Aroclor 1254) 61115
PCB-1260 (Aroclor 1260) rn1111s
PCB-124.2 (Arocl0< 1242) 1/115
Blank a Not Analyzed.
J • Estimated value.
N • Preeumptlve evidence or presence of material.
Material wa, analyzed tor but not detected.
-- - ----TABLE 2-6 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA TRANSFORMER
56SLA 56SLB 57SLA 57SLB 58SLA 58SLB 59SLA
11/15/89 11/15/89 11/15/89 11/15189 11/15189 11/15189 11/16189
UGIKG UGIKG UGIKG UGIKG UGIKG UGIKG UGIKG --29,000 -27,000 --
14,000 32,000 -6,000 -29,000 34,000
--60.000J ----
Frequency of Detection• Number of Samples With Positive Detection Over TotaJ Number of Samples
-- -- --
59SLB 60SLA 60SLB 61SLA 61SLB
11/16189 11/16189 11/16189 11/16189 11/16189
UGIKG UGIKG UGIKG UGIKG UGIKG -9,000 ---
4,000 -1,SOOJ 15,000 8.700
-----
- ---- -
Chemical or Parameter Frequency or Detection•
PeadcidelPCB Compound•
PCB-1254{Aroclor 1254) 6/119
PCB-1260 (Aroclor 1260) 108/119
PCB-1242 (Aroclor 1242) 1/119
Chemical or Parameter Frequency of Detection•
Pesllclde/PCB Canpoundo
PCB-1254(Aroclor 1254) 6/119
PCB-1260 (Aroclor 1260) 108/119
PCB-1242(Aroclor 1242) 1/119
Chemical or Parameter Frequency of Detection•
Pesticide/PCB Compound•
PCB-1254 (Aroclor 1254) 8/119
PCB-1260 (Aroclor 1260) 108/119
PCB-1242 (Aroclor 1242) 1/119
Blank • Not Analyzed.
J • Estimated value.
N • Prewmptlve evidence or prell8rlce of material.
Material waa analyzed for but not detected.
----- --TABLE 2-6 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA lRANSFORMEA
SSLA 8SLB 10SLA 10SLB 11SLA 11SLB 12SLA
11/14189 11/14/89 11/14/89 11/14189 11/14/89 11/14/89 11/14/89
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG -- - --- -
3,900 180 5,500 350 650 210 1,400J - --- -- -
16SLA 16SLB 18SLA 18SLB 19SLA 19SLB 20SLA
11/14/89 11/14/89 11/15.189 11/15189 11/15/89 11/15189 11/16189
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG --- -- --
9,800 560 10.000 120J 7,000 150J 1,400J -- -----
69SLA 69SLB 71SLA 71SLB 72SLA 72SLB
11/16189 11/16189 11/16189 11/16189 11/15189 11/15189
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG - -----
12,000 4,800 18,000 7,400 8,500 250 ------
Frequency of Oetecdon • Number of Samplee With Positive Detection Over Total Number of Sample&
----- -
12SLB 13SLA 13SLB 15SLA 15SLB
11/14189 11/14189 11/14/89 11/15189 11/15/89
UG/KG UG/KG UG/KG UG/KG UG/KG
- - -- -
290 7.600 450 6,800 850 - --- -
20SLB 21S1..A 21SLB 22SLA 22SLB
11/16189 11/16189 11/16189 , 1/16.189 11/16189
UG/KG UG/KG UG/KG UG/KG UG/KG
---60,000 -
1,900 21,000 120J -18,000 -----
- ---- ---------- --
Chemical or Parameter Frequency of Detection•
Dlaxine/Furana
Hexachlorodlbenzodioxin (Total) 1/10
Heptaohlorodibenzodloxin (Total) 7/10
Octachlorodlbenzodioxin 9/10
2,3,7.8 TCDF (Oibenzofuran) 9/10
Tetrachlorodlbenzoturan (TotsJ) 10/10
Pentachlorodlbenzofuran (Total) 10/10
Hexachlorodlbenzofuran (Total) 10/10
Heptachlorodlbenzoturan (Total) 10/10
Octachlorodlbenzofuran (Total) 4/10
TEO (TO>dclty Equivalent Value)
Blank• Not Analyzed,
J • Eetimated value.
N "" Prea.imptive evidence of preeence of material.
Material wa, analyzed for but not detected.
TABLE 2-6 (Cont.)
EVALUATION OF CHEMtCALS OF POTENTIAL CONCERN IN ONSITE SOIL
CAROLINA TRANSFORMER
27SLA 27SLB 33SLA 33SLB 47SLA 47SLB 49SLA
11/14/89 11/14/89 11/14/89 11/14/89 11/14189 11/14/89 11/14/89
NG/KG NG/KG NG/KG NG/KG NG/KG NG/KG NG/KG
- - - - - --
630J 300J - -460J 79J 420J
2,000J 8,000J 990J 2.300J 3.300J 2,900J BOOJ
650J 42J 940J 18J 1,100J 18J 290J
1,200J 260J 2,400J 30J 1,100J 41J 420J
3,400J 410J 6,200J 190J 3,000J 260J 4,200J
2,200J 4,900J 3,100J 130J 2,000J 160J 1,900J
600J 1,400J SOOJ 78J 630J 55J 280J
130J 110J 96J -69J --
420J 96J 750J 22J 520J 29J 470J
Frequency of Detection • Number of Samples With P081Uve Detection Over Total Number of Samples
49SLB 60SLA 60SLB
11/14/89 11/14/89 11/14/89
NG/KG NG/KG NG/KG
- -9.0J
130J -340J
4,200J -1,100J
45J 28J -
210J 200J 15J
1, 100J 480J 150J
570J 230J 94J
180J 1,400J 42J
---
120J 55J 17J
- -
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ANALYTE
Inorganic Elements
Pesticide/PCB
Extractable Organics
Purgeable Organics
Dioxins/Furans
TABLE 2-7
RATIONALE FOR IDENTIFICATION OF
CHEMICALS OF POTENTIAL CONCERN
IN ONSITE SOIL
CHEMICAL OR PARAMETER RATIONALE
Barium Yes -Found only downgradlent.
Cadmium Yes -Found only downgradlent.
Cobalt Yes -Found only downgradlent.
Chromium Yes -Found only downgradlent.
Copper Yes -Found only downgradlent.
Lead Yes -Found at more than 2X background concentration.
Vanadium No -Not significantly (2X) greater than background.
Zinc Yes -Found at more than 2X background concentration.
Aluminum No -Not significantly (2X) greater than background.
Manganese Yes -Found at more than 2X background concentration.
Calcium No -Low toxicity and low concentrations.
Magnesium No -Not significantly (2X) greater than background.
Iron No -Not significantly (2X) greater than background.
Sodium No -Found in only one sample.
Antimony No -Found in only one sample.
PCB-1254 Yes
PCB-1260 Yes
PCB-1242 No -Found In only one sample.
1,2,4-Trichlorobenzene Yes
Tetrachloroethene Yes
Toluene Yes
Trichloroethene Yes
Benzene Yes
Chlorobenzene Yes
Chloroform No -Found in only one sample at a low concentration.
Hexachlorodibenzodioxln Yes
Heptachlorodibenzodioxin Yes
Octachlorodibenzodiozin Yes
2,3,7,8 TCDF Yes
Tetrachlorodibenzofuran Yes
Pentachlorodibenzofuran Yes
Hexachlorodibenzofuran Yes
Heptachlorodlbenzofuran Yes
Octachlorodibenzofuran Yes
--- - ----- - ---- - ---
1SLA
unemlcaJ ot Parameter requency or Detection--=•9
Inorganic Bemente mumu
Arsenic a,22
Barium 27157 26
v~~t 7/46 2.9
... hrom1um 17/57 6.2
..,opper 19/57 3.4
Nickel 17/57 2.4
lead 52157 15
Strontium 17/17 4.2
Titanlum 17/17 300
Vanadium 57/57 12
Yttrium 17/17 4.0
Zinc 21/57 12
Aluminum 57/57 4,600
Manganese 57/57 230
Calcium 14/20 350
Magnesium 25/44 370
Iron 54/54 4,400
Potassium 41/43
Mercury 3/22
Pe611clde/PCB Compounds UG/KG
PCB-1260 (Aroclor 1260) 17/57 -
Gamma-Chlordane 2/18 0.71
IDiemnn 2/11
Extractable Organic Compound• UG/KG
Benzolo Acid 1111
Purgeable Organic Compounds UG/KG
Meth)'t Ethyl Ketone 2/11
Carbon Tetrachlortde 1/11
Trtchloroethene 2/11
Toluene 5/34
Ethyl Benzene 2/11
1,4-0lchlorobenzene 2/11
1.2~Ichlorobenzene 2/11
Blank• Not Analyzed.
J • Estimated value.
N .. Presumptive evidence of presence of material.
Material waa analyzed for but not detected.
TABLE2-8
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN
OFFSITE SOIL
CAROLINA lRANSFORMER
1SLB 1SLV 2SLA 2SLB 3SLA
08/22/89 08/22/89 08/29/89 08/29/89 08/29/89
mu,~u Mumu MGmu MumG MG,~u
32 7.9 -59 -
3.5
7.0 3.5
3.2 1.9
2.5 -3.2 3.3 -
4.6 -10 4.4 7
4.5 2.5
250 92
14 8.1 12 22 11
4.6 1.7
9.6 5.1 ---
6,600 3,300 4,300J 7,800J 3,000J
240 39 170 140 110
360 140
500 180 620 620 420
5.200 3,900 4,800 9,100 4,000
220 200 180
UG/KG UG/KG UG/KG UG/KG UG/KG
--------
UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG
Frequency of Detection• Number ol Samplaa With Positive Detection Over Total Number of Samplae
3SLB 4SLA 4SLB 5SlA SSLB
08/29/89 08/29/89 08129, ... 08/29/89 08/29/89
Mu,~u Mu,~G Mu,~u mumu mumu
58 ---50
3.6 -3.2 -3.1
4.5 7 5.1 6.3 5.5
33 8.6 34 7.7 24
-----
11,000J 2,600J 9.400J 2,600J 9,400J
99 79 50 73 28
760 -750 --
13,000 3,500 14.000 2,300 4,700
290 84 190 83 130
UG/KG UG/KG UG/KG UG/KG UG/KG
----------
UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG
-
--------- - - --- - - - -
6SLA
Chemical or Parameter Frequency of Oetecticn • 08/23/89
Inorganic Bements MG/KG
Arsenic 3/22
Barium 27/57 130
Cobalt 7/46 4.2
Chromium 17/57 11
Copper 19/57 5.3
Nickel 17/Sl -
Lead 521S7 17
Strontium 17/17 14
T1tanium 17/17 140
Vanadium 57/Sl 28
Yttrium 17/17 7.4
Zinc 21/57 15
Aluminum 57157 11,000
Manganeee S7/S7 170
Calcium 14/20 660
Magnesium 25/44 620
Iron 54/54 8,200
Sodium 1/3 -
Potassium 41/43 -
Mercury 3/22 0.10
Pesticide/PCB Compounds UGIKG
PCB-1260 (Arcx:lor 1260} 17/57 1,200
Gamma-Chlordane /2 2118
Dleldrin 2111
0ctractab1e Organic Compounde UGIKG
Benzolc Acid 1/11
Purgeable Organic Canpounds UG/KG
Methyl Ethyl Ketone 2111
Carbon Tetrachloride i/11
Trlchloroethene 2111
Toluene 5134
Ethyl Benzene 2111
1,4-0lchlorobenzene 2111
1,24'Ichlord>enzene 2111
Blank• Not Analyzed.
J • Estimated value.
N • Preaumptlve e'Jtdence of presence of material.
Material waa analyzed for but not detected.
TABLE 2-8 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN
OFFSITE SOIL
CAROLINA mANSFORMER
6SLB 6SLV 7SLA 7SLB SSLA
08/23/89 08/23/89 08/29189 08129/89 08/29/89
MG/KG MG/KG MG/KG MG/KG MG/KG
110 78 52 62 -
2.5 2.3 - - -
12 13 - - -
3.8 7.6 - - --5.3 -5.6 -
12 7.5 12J 6.4J 4.2J
15 14
130 280
28 22 12 13 9.1
6.0 7.6
9.8 13 -- -
12,000 9,800 4,BOOJ 5,600J 3,600J
48 31 80 100 55
640 500
550 580 - - -
5,400 2,300 3,400 3,100 2,400
-120
-250 200 200 160
0.08 - - - -
UGIKG UGIKG UG/KG UGIKG UG/KG
66 9.2J 31,000 9,700 500
0.92 - --
UGIKG UGIKG UGIKG UGIKG UGIKG
UGIKG UG/KG UGIKG UGIKG UGIKG
Frequency of Detection• Number of Samples With Positive Detection Over Total Number of Sample&
8SLB BSLA BSLB 10SLA 10SLB
08/29/89 08/29/89 08/29/89 08/29189 08/29189
MG/KG MG/KG MG/KG MG/KG MG/KG
-S7 83 ----- --- ----- - - - -- -2.9 - -
4.8.J 14J 7.1J 7.9J 4
15 17 29 11 16
- - - - -
3,000J 4,500.J B.700J 3,400.J 4,900.J
34 96 20 27 16
- -430 - -
2,000 5,900 10,000 3,400 5,500
170 100 140 110 100 -- -- -
UGIKG UGIKG UGIKG UG/KG UGIKG -350 -- -- -- --
UG/KG UG/KG UGIKG UGIKG UG/KG
UGIKG UGIKG UGIKG UG/KG UGIKG
-
-- - - --- - ------ - - --
11SLA
Chemical or Parameter Frequency of Detection• 08/29/89
Inorganic Bements MG/KG
Ar&enlc 3/22 -
Barium 27/57 -
Cobalt 7/46
Chromium 17/57 -
Copper 19/57 -
Nickel 17/57 -
Lead 52157 7.SJ
Strontium 17/17
Titanium 17/17
Vanadium 57/57 15
Yttrium 17/17
Zinc 21/57 52J
Aluminum 67/67 6,600J
Manganese 57/57 28
CaJcium 14/20
Magnesium 25/44
Iron 54154 22,000
Potassium 41/43 88
Mercury 3/22
Pesticide/PCB Compound• UG/KG
PCB-1260 (Aroclor 1260) 17/57
Gamma-Chlordane /2 2118
Oieldrln 2111
Extractable Organic Compound• UG/KG
Benzolc Acid 1/11
Purgeable Organic Compound• UG/KG
Methyl Eth~ Ketone 2111
Carboo Tetrachloride 1/11
Tr1chloroethene 2111 -
Toluene 5/34
Ethyl Benzene 2111
1,4-0ichlorobenzene 2111
1,2~ichlorobenzene 2111
Blank• NOi Analyzed.
J • Estimated value.
N • Pre-..mptive evidence of preeence of material.
Material waa analyzed kif but not detected.
TABLE 2-8 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN
OFFSITE SOIL
CAROLINA TRANSFORMER
11SLB 12SLA 12SLB 12SLV 13SLA
08/29/89 08/23189 08/23189 08/23/89 08/29/89
MG/KG MG/KG MG/KG MG/KG MG/KG
- - - -2.2J
-22 26 12 -
-10 9.7 4.7 --4.9 5.7 2.3 -- - -- -
1.6J 9.4 7.2 -21
2.2 3.8 2.6
180 160 140
9.1 23 28 11 18
2.6 4.6 3.5 -12 12 4.8 -
3,300J 11.000 12,000 5,300 5,500J
14 26 27 20 14
-180 120
510 610 240
8,400 1,200 15,000 4,600 9,200
58 130
UG/KG UG/KG UG/KG UG/KG UG/KG
24 -
UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG
----- --6.9J --- -5.2J
Frequency of Detection • Number of Samplee With Positive Detection Over Total Number of Samplee
13SLB 14SLA 14SLB 15SLA 15SL8
08/29189 08/30/89 08/30/89 08/30/89 08/30/89
MG/KG MG/KG MG/KG MG/KG MG/KG
3.4J -- - --- - --
---- ---- --
2.7 - - --
8.2J 12J 7.1J 5J 2J
31 6.4 2.5 7.4 7.3
--- --
7,900J 4,000J 1,BOOJ 3, 100.J 2,500J
19 14 5.3 84 48
19,000 1,900 1,000 3,100 3,300
200 120 40 110 87
UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG --400J
UG/KG UG/KG UG/KG UG/KG UG/KG -80J 370J --------18J --
17J 89J
-19J 43J
-
---- --- - -- - -- - - - - --
16SLA
Chemical or Parameter Frequency of Detection* 08/24189
Inorganic Elements MG/KG
Arsenic 3/22
Barium 27/57 15
Cobalt 7/48 -
Chromium 17/57 3.5
Copper 19/57 1.6
Nicke:I 17/57 -
Lead 52157 8.8
Strontium 17/17 2.0
Tltanlum 17/17 110
Vanadium 57/57 5.9
Yttrium 17/17 1.2
Zlnc 21/57 7.7
Aluminum 57/57 2,400
Manganese 57/57 58
Calcium 14/20 300
Magnesium 25/44 170
Iron 54/54 2.200
Potassium 41/43
Mercury 3/22 -
Peetfclde/PCB Compounds UG/KG
PCB-1280 (Aroclor 1280) 17/57 83
Gamma-Chlordane /2 2118
Dleldrin 2111
Extractable Organic Compound• UG/KG
Benzolc Acid 1/11
Purgeable Organic Compound• UG/KG
Methyi Ethyt Ketone 2111
Carbon Tetrachloride 1/11
Trichloroethene 2111
Toluene 5/34 -
Ethyl Benzene 2111
1 ,4-0lohlorobenzene 2111 -
1,2-0lchlorobenzene 2111 -
Blank• Not Analyzed.
J • Estimated value.
N • Preaumptlve evidence of presence ol material.
Material WH analyzed tor but not detected.
TABLE 2-8 (Cont.)
EVALUATION OFCHEMICALSOF POTENTIAL CONCERN IN
OFFSITE SOIL
CAROLINA TRANSFORMER
16SLB 16SLV 17SLA 17SLB 18SLA
08/24/89 08/24189 08/30/89 08/30/89 08/30/89
MG/KG MG/KG MG/KG MG/KG MG/KG
20 10 - -48
- - - - -
4.7 2.1 - - -
3.0 1.2 - - -- - - --
8.7 -3.4 10J 11
2.9 1.1
170 120
8.2 2.2 12 9.8 13
1.9 1.1
8.1 1.7 - --
3,700 1,700 4,700J 4,400J 5,600J
51 10 7.7 13 66
290 63 --1.200
230 72 --440
2.900 550 1,600 1,600 4,900
100 110 250
- - - - -
UG/KG UG/KG UG/KG UG/KG UG/KG
48 -22,000 110,000 75,000
UG/KG UG/KG UG/KG UGIKG UG/KG
UGIKG UG/KG UG/KG UGIKG UG/KG
-- -
14.J -
--44 32J -- -22J 18J -
Frequency of Detection• Number or Sample, With Positive Detection Over Total Number of Samplee
18SLB 19SLA 19SLB 19SLV 20SLA 20SLB
08/30/89 08/23/89 08/23/89 08/30/89 08/30189 08/30189
MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG
-26 31 10 - --2.1 2.1 -- --13 17 5.8 ---7.8 9.2 2.2 - ---4.8 2.5 -2.8
3.1J 10 8.2 4.2 22 8.6
3.4 3.8 3.6
250 280 410
9.5 31 44 11 12 28
2.3 3.4 6.6
-22 21 5.4 89J -
3,BOOJ 10,000 14,000 3,900 4,100J 8,400J
18 52 46 29 93 58
-- ---740
1,400 4.900 11,000
240 320 380
-0.08 - - - -
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
23,000 --- - -
UG/KG UG/KG UG/KG UG/KG UG/KG UGIKG
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
6.2J - --
-- ------- ---
---- -- - - -- - --- - - ---
21SLV
Chemical or Parameter Frequency of Detection* 08/24/89
lnorganic Bements MG/KG
Arsenic 3/22 -
Barium 27/ST 16
Cobalt 7/46 -
Chromium 17/57 2.2
Copper 19/57 1.0
Nickel 17/57 -
Load 52157 -
Strontium 17/17 2.4
Titanium 17/17 240
Vanadium 57/57 2.7
Yttrium 17/17 1.3
Zinc 21157 3.6
Aluminum 57157 1,500
Manganese 57/57 20
Calcium 14/20 150
Magnesium 25/44 150
Iron 54/54 660
Pota88ium 41/43
Mercury 3/22
Pesticide/PCB Compound• UG/KG
PCB-1260 (Aroclor 1260) 17/57 -
Gamma-Chlofdane /2 2118
Oleldrtn 2111 -
Extractable Organic Compound• UG/KG
Bon:rolc Acid ,,, 1
Purgeable Organic Compounds UG/KG
Methyl Ethyl Ketone 2111
Carbon Tetrachloride ,,, ,
Trtchloroethene 2111
Tduene 5134
Ethyl Benzene 2111
1,4-0ichlorobenzene 2111
1.2~Ichlorobenzene 2111
Blank• Not Analyzed.
J • Estimated value.
N • Prea,mptlve evidence of presence of material.
Material w■-analyzed for but not detected.
TABLE 2-8 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN
OFFSITE SOIL
CAROLINA TRANSFORMER
22SLA 22SLB 23SLA 23SLB 24SLA
08/30/89 08/30/89 08/30/89 08/30/89 08130/89
MG/KG MG/KG MG/KG MG/KG MG/KG
----2."-l
-----------------75J -50J ----3.9
13 6.6 56 9.5 27
13 13 9.8 19 24
--78J -55J
4.500.J 3,600J 2,200J 6,100J 5,BOOJ
92 73 14 29 41
---460 -
5,400 4,700 2,500 8,000 11,000
140 130 59 160 130
UG/KG UG/KG UG/KG UG/KG UG/KG
--3,300 250 530
160 44 ---
UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG
Frequency of Detection • Number of SamplH With Positive Detection Over Total Number ot Samples
24SLB 25SLV 33SLA 33SLB 34SLA 34SLB
08/30189 08/23189 08/29/89 08/29189 08/29/89 08/29189
MG/KG MG/KG MG/KG MG/KG MG/KG MG/KG
-------4.7 -53 -48
-------4.2 -----1.4 ----
3 --5.5 --
7.1 -7 3.3 11 6.1J
1.7
110
45 5.7 8 17 9.3 11
1.7
-4.0 ----
14,000J 2,300 3,700.J 7,000J 3,700J 4,800J
36 27 450 510 160 310
90
680 110 -580
19,000 6,300 3,200 6,800 3,900 4,600
240 140 210 180 210
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG ------
------
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
-- - ----
7SLA
Chemical or Parameter Frequency of Detection• 08/29/89
Oia,cine/Fu:rana NG/KG
Hexachlorodibenzodloxin 4/12 26J
Heptachlorodlbenzodlaxin 8/12 200J
Octachlorodibenzodioxin 10/12 2,200
2,3,7,8 TCOF 3/12 20
Tetrachlorodlbenzofuran 3/12 220J
Pentachlorodlbenzofuran 4/12 600J
Hexachlorodlbenzofuran 3/12 500J
Heptachlorodlbenzofuran 3/12 190J
Octachlorodlbenzofuran 2/12 140J
TEO (Toxicity Equivalent Value) 69J
Blank• Not Analyzed,
J • Elltimated value.
N • Pre8Umptive evidence of presence of material.
MatertaJ was analyzed for but not detected.
- --- --TABLE 2-<I (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN
OFFSITE SOIL
CAROLINA TRANSFCRMER
7SLB 10SLA 10SLB 12SLA 12SLB
08/29/89 08/29/89 08/29189 08/30/89 08/30/89
NG/KG NG/KG NG/KG NG/KG NG/KG
13.J -- --
160J - -16J 29J
2,100 470J 670 2,100 1,300
5.8 - - - -
49J - - - -
120J - - - -
120J - - --
67J -- - -
67 -- --
15J - -0.016J 0.29J
16SLA
08/30/89
NG/KG ---------
-
Frequency or Detection • Number of Samples With Positive Detection Over Total Number or Samples
- -- - --
16SLB 19SLA 19SLB 23SLA 23SLA
08/23/89 08/23/89 08/30/89 08/30/89 08/30/89
NG/KG NG/KG NG/KG NG/KG NG/KG
-- -
45J 9.6J
-140J 200J 320J 160J
-8,400 27,000J 3,100 12,000J
- - -10 ----93.J -- --240J 28J
- - -160J -- --70J --- - --
-0.14J 0.2J 29J 3.3.J
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ANALYTE
Inorganic Elements
Pesticide/PCB
Extractable Organics
Purgeable Organics
Dioxlns/Furans
TABLE 2-9
RATIONALE FOR IDENTIFICATION OF
CHEMICALS OF POTENTIAL CONCERN
IN OFFSITE SOIL
CHEMICAL OR PARAMETER RATIONALE
Arsenic Yes -Found only downgradlent.
Barium Yes -Found only downgradlent.
Cobalt Yes -Found only downgradlent.
Chromium Yes -Found only downgradlent.
Copper Yes -Found only downgradlent.
Nickel No -Not significantly (2X) greater than background.
Lead Yes -Found at more than 2X background concentration.
Strontium Yes -Found at more than 2X background concentration.
ntanium Yes -Found at more than 2X background concentration.
Vanadium No -Not significantly (2)() greater than background.
Yttrium Yes -Found at more than 2X background concenlralion.
Zinc Yes -Found at more than 2X background concentralion.
Aluminum No -Not significantly (2X) greater than background.
Manganese Yes -Found at more than 2X background concentration.
Calcium No -Low toxicity and low concentrations.
Magnesium No -Not significantly (2X) greater than background.
Iron No -Not significantly (2X) greater than background.
Sodium No -Found in only one sample.
Potassium No -Not significantly (2X) greater than background.
Mercury Yes -Found only downgradlent.
PCB-1260 (Aroclor 1260) Yes
Gamma-Chlordane No -Found in only two samples at low concentrations.
Dleldrln No -Found In only one sample location.
Benzoic Acid No -Found in only one sample.
Methyl Ethyl Ketone No -Found in only one sample localion.
Carbon Tetrachloride No -Found in only one sample.
Trichloroethene Yes
Toluene Yes
Ethyl Benzene No -Found in only one sample location.
1,4-Dlchlorobenzene Yes
1,2-Dlchlorobenzene Yes
Hexachlorodlbenzodioxln Yes
Heptachlorodlbenzodloxln Yes
Octachlorodlbenzodloxln Yes
2,3,7,8 TCDF Yes
Tetrachlorodlbenzofuran Yes
Pentachforodlbenzofuran Yes
Hexachlorodlbenzofuran Yes
Heptachlorodibenzofuran Yes
Octachlorodlbenzofuran Yes
--- - ----- - - ---- --TABLE2-10
EVALUATK>N OF CHEMICALS OF POTENTIAL CONCERN IN SEDIMENT
CAROLINA TRANSFORMER
71SO 72SO 73$0 7460 75SO 76SO
1.~n em•(!Jlll or Pa,ameter I Frequency of Detection" 08124'89 0lVLW89 Oru, 4/89 o~,~= 08124'89 08124,89
Inorganic Bemente MG/KG MGmu MG/KG Mu••" MG/KG MG, .... G
OJ:jnum 16116 4.4 72 22 30 30 29
I !:YirvlliUm 1/10 0.51
vadm1um 7/18 0.81 1.2 1.2 1.1
iGobaJI 11/16 -3.8 1.2 1.4 1.3 1.2
ctirormum 16/16 1.3 4.6 8.1 11 10 11
vopper 1t>116 150 230 120 100 130
Molybdenum 1/6
Nickel 5116 --2.5 --2.3
Lead 15/1B -7.9 31 54 55 43
Strontium 15/16 1.1 4.5 4.1 4.4 4.0 4.2
Tltanlum 16/16 120 200 96 100 90 89
Vanadium 16/16 2.2 11 15 26 21 16
Yttrium 13/16 -3.9 2.2 3.4 3.4 2.4
Zinc 16/16 2.0 8.3 53 65 52 61
Mercury 116
Aluminum 18/18 640 2,200 6,300 8.100 7,200 7,000
Manganeee 16/16 13 110 29 34 32 27
CaJcium 16/16 78 360 1,100 660 560 560
Magnellium 16/16 42 180 240 410 350 320
Iron 16/18 no 3,300 5,000 8,700 6,200 6,200
Peatlclde/PCB Compounds UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
4,4-0DD 1/6
PCB-1254 (Arcclor 1264) 3110 ----23,000J 72,000
PCB-1248 (Aroclor 1248) 4/16 --5,200 12,000 2,900 -
PCB-1260 (Arcclor 1260) 14/16 --68,000 100,000 39.000 140,000
Meptacmor 1/6
Extractable Organic Ccwnpounda UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
Benzolc Acid 1/6
Purgeablo Orgonlc Compound• UG/KG UG/KG UG/KG UG/KG UG/KG UG/KG
Benzene 1/10 ------
Toluene 4/16 -2,400 12J ---
Chlorobenzene 2/10 ---48J --
1,3-0lchlorobenzene 2/10 ---170J 16J -
1,4-0lchlorobenzene 3110 ---590 130 -
1.2-0lchlorobenzene 2/10 ---29J --
Ethyl Benzene 1/8
Blank• Not Analyzed.
J • Estimated value.
N • Pre1t.1mpUve evidence or preeence of material.
Material waa analyzed tor but not detected.
Frequency ofOetecUon • Number or Samples With PoelUve Detection Over Total Number or Samples
nso 78SO 79SO SOSO
Q8/2<uD9 o~,=•9 08J2<ua9 08/24/89
MGflliG MG/KG MG/KG MGIKG
35 48 12 140
1.8 4.7 ---5.1
7.9 7.4 4.2 29
1,100 3.200 12 590
---9.3
48 57 5.6 150
5.0 -2.4 16
140 100 200 160
15 11 8.1 47
--1.9 8.6
66 67 13 260
7.600 8,000 3,200 27,000
32 100 24 95
660 930 220 1,700
350 380 210 1,200
4,400 5,900 2,000 11.000
UG/KG UG/KG UG/KG UG/KG
100,000 -------
87,000 140,000 48,000 4.4E6
UG/KG UG/KG UG/KG UG/KG
UG/KG UG/KG UG/KG UG/KG --28J ----1,200J
--64J -------49.J ---50J -
- -
--- -- - -- - - - - --TABLE 2-10 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN SEDIMENT
CAROLINA TRANSFORMER
81SD 82S0 83SD 84SO 85SD
Chemical or Parameter Frequency of Detection• 08/24/89 08/24/89 08/24/89 08/24/89 08/24/89
Inorganic Elements MG/KG MG/KG MG/KG MG/KG MG/KG
Barium 16/16 25 38 89 11 56
Beryllium 1/10
Cadmium 7/16 ----0.61
Cobalt 11/16 1.3 1.3 4.3 -4.1
Chromium 16/16 5.5 6.2 20 4.8 11
Copper 15/18 15 7.9 14 6.3 120
Molybdenum 1/6 ----1.0
Nickel 5/16 -2.0 - -6.0
Lead 15/16 18 34 28 9.7 55
Strontium 15116 3.1 4.9 8.9 3.4 12
Titanium 16/16 100 140 120 97 200
Vanadium 16/16 10 12 51 8.5 23
Yttrium 13/16 1.9 2.0 7.0 1.4 7.2
Zinc 16116 18 18 78 4.0 66
Mercury 1/8 --0.06 --
Aluminum 16116 5,900 7,400 25,000 4,100 8,200
Manganese 16/16 19 23 77 18 150
Calcium 16/16 210 230 390 1,400 1,100
Magnesium 16116 250 380 1,300 200 650
Iron 16116 2,400 4,300 15,000 3,200 8,700
Pestlclde/PCBCompounda UG/KG UG/KG UG/KG UG/KG UG/KG
4,4-000 1/8 -18 -- -
PCB-1248 (Arcclor 1248) 4/16 ---220J -
PCB-1260 (Aroclor 1260) 14/16 260.000 180 93 2,900 15,000
Heptachlor 1/6 --1.8 -
Extractable Organic Compound• UG/KG UG/KG UG/KG UG/KG UG/KG
Benzolc Acid 1/6 -960J ---
Purgeabla Organic Ccmpounde UG/KG UG/KG UG/KG UG/KG UG/KG
Benzene 1/10
Tolene 4/16 -61J ---
Chlorobenzene 2/10
1,3-0lchlorobenzene 2/10
1,4-0lchlorobenzene 3/10
1,2-0lchlorobenzena 2/10
Eth)4 Benzene 1/8 15J -
Blank• Nol Analyzed.
J • Eetlmated value.
N • Preaimpdve evidence of preeence of material.
MatertaJ wa, analyzed for but not detected.
Frequen<:yof Detection• Number of Samplee With POtitive Detection Over Total Number of Sam plea
86SD 371SO
08/24/89 08/24/89
MG/KG MG/KG
47 40
--
3.8 1.0
15 1.4
100 ---- -
98 -
6.3 1.5
200 140
32 2.8
4.0 -
73 2.1 --
11,000 710
180 18
730 120
740 43
12,000 920
UG/KG UG/KG
--- -
11,000
UG/KG UG/KG
- -
UG/KG UG/KG
- -
- -- - -
----- --- - --TABLE 2-10 (Cont.)
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN SEDIMENT
CAROLINA TRANSFORMER
nso 81S0
Chemical or Parameter Frequency of Detection• 08/23/89 08/23189
Oloxina/Furane NG/KG NG/KG
2.3.7.8 TCOO (Dioxin) - -
Tetrachlorodibenzodioxln (Total) - -
Pentachlorodibenzodioxin {Total) - -
Hexachlorodibenzodioxln {Total) 1/4 48J -
Heptachlorodibenzodioxln (Total) 3/4 200J 180J
Octachlorodibenzodioxin 3/4 1,100 no
2,3,7,8 TCDF (Dibenzofuran) 2/4 70 76
Tetrachlorodlbenzofuran (Total) 2/4 630J 390J
Pentachlorodibenzofuran (Total) 3/4 1,500J 1,100J
Hexachlorodibenzofuran {Total) 3/4 760J 660J
Hepachlorodibenzofuran {Total) 2/4 190J 550J
Octachlorodibenzofuran (Total} 2/4 55 610
TEO (Toxicity Equivalent VeJue) 220J 160J
Blank • Not Analyzed.
J .,. Estimated value.
N • Presumptive evidence of preeence of material.
Material wae analyzed tor but not detected.
--
8350 8450
08/23/89 08/23/89
NG/KG NG/KG
- -- -- -- -
79J -
990 -- -- --32J
-9.6J - -- -
0,079J 3.3J
Fr4tquency of Detection • Number of Samplee With Positive Detection Over Total Number of Samplee
---- --
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ANALYTE
Inorganic Elements
Pesticide/PCB
Extractable Organics
Purgeable Organics
Dioxlns/Furans
TABLE 2-11
RATIONALE FOR IDENTIFICATION OF
CHEMICALS OF POTENTIAL CONCERN
IN SEDIMENT
CHEMICAL OR PARAMETER RATIONALE
Barium Yes -Found at more than 2X upgradlent concentration.
Beryllium No -Found In only one sample at a low concentration.
Cadmium Yes -Found only downgradlent.
Cobalt Yes -Found only downgradlent.
Chromium Yes -Found at more than 2X upgradlent concentration.
Copper Yes -Found only downgradlent.
Molybdenum No -Found In only one sample.
Nickel Yes -Found only downgradlent.
Lead Yes -Found only downgradlent.
Strontium Yes -Found at more than 2X upgradient concentration.
Titanium No -Not significantly (2X) greater than upgradient.
Vanadium Yes -Found at more than 2X upgradient concentration.
Yttrium Yes -Found only downgradienl.
Zinc Yes -Found at more than 2X upgradlent concentration.
Mercury No -Found In only one sample at a low concentration.
Aluminum Yes -Found at more than 2X upgradient concentration.
Manganese Yes -Found at more than 2X upgradlent concentration.
Calcium No -Low toxicity and low concentrations.
Magnesium No -Low toxicity and low concentrations.
Iron No -Low toxicity and low concentrations.
4,4-DDD No -Found in only one sample.
PCB-1254 (Aroclor 1254) Yes -Found only downgradlenl.
PCB-1248 (Aroclor 1248) Yes -Found only downgradient.
PCB-1260 (Aroclor 1260) Yes -Found only downgradlenl.
Heptachlor No -Found In only one sample.
Benzolc Acid No -Found In only one sample.
Benzene Yes -Found only downgradlenl.
Toluene Yes -Found only downgradlent.
Chlorobenzene Yes -Found only downgradlent.
1,3-Dlchlorobenzene Yes -Found only downgradlent.
1,4-Dlchlorobenzene Yes -Found only downgradlent.
1,2-Dlchlorobenzene Yes -Found only downgradlent.
Ethyl Benzene No -Found In only one sample at a low concentration.
2,3,7,8 TCDD (Dioxin} Yes
Tetrachlorodlbenzodloxln (Total} Yes
Penlachlorodibenzodioxin (Total} Yes
Hexachlorodlbenzodloxln (Total) Yes
Heptachlorodibenzodioxln (TotaQ Yes
Octachlorodlbenzodloxln Yes
2,3,7,8 TCDF (Dlbenzofuran} Yes
Tetrachlorodlbenzofuran (TotaQ Yes
Pentachlorodlbenzofuran (TotaQ Yes
Hexachlorodlbenzofuran (TotaQ Yes
Hepachlorodlbenzofuran (TotaQ Yes
Octachlorodibenzofuran (TotaQ Yes
--- - - -
Ch8ffl1r..A1 or Parameter t Frequency of Detection·
Inorganic Elements
•=•Um 13/13
1vopper 9/13
Strontium 13/13
Titanlum 2/13
Zinc 12/13
Alumlnum 10/13
Manganeee 13/13
Calcium 13/13
Magneeium 13/13
Iron 13/13
Sodium 13/13
Potasalum 8/13
PesdcidelPCB Canpounda
PCB-1280 (Aroclor 1280) 8/13
&:tractable Organlc Compound a
B18(2 Ethythoxyl) Phthalate 2/13
PurgeableOrganic Ccmpounde
Carbon Dlallftde 4/13
Toluene 1/13
Blank• Not Analyzed.
J • Eldmated value.
N • Preaumptlw evidence of presence of material.
Matertal waa analyzed for but not detected.
-- - - - ---TABLE 2-12
EVALUATION OF CHEMICALS OF POTENTIAL CONCERN IN SURFACE WATER
CAROLINA TRANSFORMER
71SW 72SW 73SW 74SW 7SSW 76SW 77SW 78SW 79SW
•-2~-un12-u~9 08/2~•9 08/24189 08/24189 0~24/89 08/24189 08/24/89 08/24/89
rn,/L UG/L UG/L UG/L UG/L UG/L UG/L UG/L UG/L
68 67 20 22 30 25 16 12 18
130 63 44 58 61 90 42
43 42 46 32 33 36 27 23 25
- - --- - - --
11 -27 31 38 54 57 24 78
660 570 -140 -100 110 130 140
62 48 74 170 440 340 71 78 200
MG/!. MG/!. MG/!. MG/!. MG/!. MG/!. MG/!. MG/!. MG/!.
4.4 4.3 17 11 10 9.7 7.2 6.1 6.7
2.0 2.0 1.3 0.94 0.85 0.78 0.60 0.54 0.60
0.87 0.86 0.31 1.2 1.2 0.61 0,33 0.26 2.8
4.9 4.9 2.3 1.8 1.5 1.6 1.4 1.2 1.7 --8.4 4.7 4.4 3.0 -2.6 -
UG/L UG/L UG/L UG/L UG/L UG/L UG/L UG/L UG/L --5.2 4.5 -2.8 3.9 3.7 4.0
UG/L UG/L UG/L UG/L UG/L UG/L UG/L UG/L UG/L
- -- - -
-- - -
UG/L UG/L UG/L UG/L UG/L UG/L UG/L UG/L UG/L
- -- -16J -8.1J - -- -- ---- - -
Frequency of Oetecdon • Number of Samples With Poaitive Detection Over Total Number of Samples
- -- - -
80SW 82SW 83SW 84SW
0&24.IR9 ' lll!/?4/89 08/24189 08/24189
UG/L u .... UG/L 7JGIL
26 45 47 17
130 13
25 36 30 35 -12 11 -
140 37 160 23
330 570 970 -
480 270 220 190
MG/!. MG/!. MG/!. MG/!.
7.0 4.0 3.0 12
0.74 1.2 0.91 1.4
4.0 8.3 6.1 1.8
1.8 3.2 3.1 1.1
- - -
9.6
UG/L UG/L UG/L UG/L
8.2 -12 -
UG/L UG/L UG/L UG/L
45 -100J -
UG/L UG/L UG/L UG/L
- -8.8.J 38J
- -0.82J -
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ANALYTE
Inorganic Elements
Pesticide/PCB
Extractable Organics
Purgeable Organics
TABLE 2-13
RATIONALE FOR IDENTIFICATION OF
CHEMICALS OF POTENTIAL CONCERN
IN SURFACE WATER
CHEMICAL OR PARAMETER RATIONALE
Barium No -Not significantly (2X) greater than upgradient.
Copper Yes -Found only downgradlent.
Strontium No -Not significantly (2X) greater than upgradient.
ntanium Yes -Found only downgradlenl.
Zinc Yes -Found only downgradlent.
Aluminum No -Not significantly (2X) greater than upgradlent.
Manganese Yes -Found al more than 2X upgradlenl concentration.
Calcium No -Low toxicity and low concentrations.
Magnesium No -Nol significantly (2X) greater than upgradlent.
Iron No -Low toxicity and low concentrations.
Sodium No -Not significantly (2X) greater than upgradient.
Potassium No -Low toxicity and low concentrations.
PCB-1260 (Aroclor 1260) Yes -Found only downgradlent.
Bis(2 Elhylhexyl) Phlhalate Yes -Found only downgradlent.
Carbon Disulfide Yes -Found only downgradlent.
Toluene No -Found In only one sample.
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MEDIA
Groundwater
On-Site Soils
TABLE 2-14
CHEMICALS OF POTENTIAL CONCERN
CAROLINA TRANSFORMER
ANALYTE CHEMICAL OR PARAMETER
Inorganic Elemenls Barium
Cobalt
Chromium
Copper
Nickel
Slronllum
Titanlum
Vanadium
Y!lrium
Zinc
Aluminum
Manganese
Mercury
Pesticide/PCB PCB-1260 (Aroclor 1260)
Extractable Organics Bis(2-Ethylhexyl) Phthalate
1,2,4-Trlchlorobenzene
Purgeable Organics Methyl Ethyl Ketone
Toluene
Carbon Disulfide
Benzene
Chlorobenzene
1,3-Dichlorobenzene
1,4-Dichlorobenzene
Inorganic Elements Barium
Cadmium
Cobalt
Chromium
Copper
Lead
Zinc
Manganese
Pesticide/PCB PCB-1254 (Aroclor 1254)
PCB-1260 (Aroclor 1260)
Extractable Organics 1,2,4-Trlchlorobenzene
Purgeable Organics Tetrachloroethene
Toluene
Trichloroethane
Benzene
Chlorobenzene
Dioxlns/Furans TEO
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MEDIA
Off-Site Soils
Sediments
Surface Water
TABLE 2-14 (cont.)
CHEMICALS OF POTENTIAL CONCERN
CAROLINA TRANSFORMER
ANALYTE CHEMICAL OR PARAMETER
Inorganic Elements Arsenic
Barium
Coball
Chromium
Copper
Lead
Sirontlum
ntanium
Yttrium
Zinc
Manganese
Mercury
Pesticide/PCB PCB-1260 (Aroclor 1260)
Purgeable Organics Trichloroethene
Toluene
1,4-Dichlorobenzene
1,2-Dichlorobenzene
Dioxlns/Furans TEQ
Inorganic Elements Barium
Cadmium
Coball
Chromium
Copper
Nickel
Lead
Slrontium
Zinc
Aluminum
Yttrium
Manganese
Vanadium
Pesticide/PCB PCB-1254 (Aroclor 1254)
PCB-1248 (Aroclor 1248)
PCB-1260 (Aroclor 1260)
Purgeable Organics Benzene
Toluene
Chlorobenzene
1,3-Dichlorobenzene
1,4-Dlchlorobenzene
1,2-Dichlorobenzene
Dioxins/Fu rans TEQ
Inorganic Elements Copper
ntanlum
Zinc
Manganese
Pesticide/PCB PCB-1260 (Aroclor 1260)
Extractable Organics Bis(2-Ethylhexyl) Phthalate
Purgeable Organics Carbon Disulfide
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• Metals were excluded that were detected at less than two times representa-
tive background.
• If a chemical was detected infrequently (two or three times) and at low
concentrations, it was eliminated from further consideration.
• If a chemical was naturally occuring, had very low toxicity, and was detected
at low concentrations, it was eliminated from further consideration.
2.3 Characteristics of Chemicals of Potential Concern
A discussion of the characteristics of the chemicals of potential concern is presented
in Appendix A.
2.4 Environmental Fate Characteristics of Chemicals of Potential
Concern
The environmental fate characteristics of the chemicals of potential concern are
presented in Appendix A.
k\CART\SECT2.0AA 2-10
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3.0 Exposure Assessment
3.1 Overview of Exposure Assessment
The objective of the exposure assessment is to estimate the type and magnitude of
exposures to the chemicals of potential concern that are present at or migrating from
a site. The results of the exposure assessment are combined with chemical-specific
toxicity information to characterize potential risk [1 ]. The assessment of exposures
presented in this section is based upon and consistent with current EPA guidance [1 ].
The exposure assessment process involves four main steps:
• Characterization of the exposure setting.
• Identification of the exposure pathways.
o Quantification of the exposure.
o Identification of uncertainties in the exposure assessment.
3.2 Characterization of the Exposure Setting
3.2. 1 Physical Setting
3.2.1.1 Demography. The Carolina Transformer Site is located in Cumberland
County, North Carolina, east of East Fayetteville. The site is bounded on the
northwest by an approximately 50 to 100 foot strip of wooded area. North of this
wooded area is an agricultural field and numerous homes. On the west, the site is
bounded by a dirt road which provides access to two homes. To the southeast, the
site is bounded by Middle Road, Larry's Sausage Company, and Fayetteville
Livestock Market (operated by Lundy Packing Company). To the northeast the site
is adjacent to an abandoned home site and an agricultural field. Small wetlands exist
in the north and far west portions of the site.
Cumberland County encompasses 661 square miles and, according to a 1980 census,
had a population of 247,160 people. Projections by the North Carolina Office of
State Budget and Management indicated that the population would rise to 261,839
/c\CART.SECT3.DRA 3-1
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people by 1990 and increase to 275,972 people by the year 2000. The City of
Fayetteville had a population of 59,507 in the 1980 census.
3.2. 1.2 Natural Resources.
Soils. The site is located in the Coastal Plain physiographic province of North
Carolina. Soils in this area are formed from crystalline materials, such as granites,
gneisses, and schists. The soils consist of brown to tan, fine to coarse grained sands,
tan, silty sands, clayey sands, sandy clays, and clays.
The surfical soils at the site consist of the Wickham Series and the Roanoke Series.
Wickham Series soils cover most of the former facility area. These are well-drained
soils that formed in loamy fluvial sediments on terraces of the Cape Fear River and
its major tributaries. Wickham soil is well suited to growing cultivated crops and
trees. The loamy horizon of this series is typically 40 to 60 inches thick and is
underlain by sandy alluvial sediments. These are poorly drained soils that formed in
stratified clayey sediments on terraces of the Cape Fear River and its major
tributaries. The loamy and clayey horizons overlie the stratified sediments deposited
by the river.
The Roanoke soils are somewhat poorly drained and typically have a surface layer
of grayish brown loam which is eight inches thick. The subsoil is 47 inches thick.
The seasonal high water table is at or near the surface during winter and early spring.
Surface runoff is slow, which results in ponding in some areas during wet periods.
Roanoke soils are suited to cultivated crops.
Surface Waters. The Carolina Transformer Site is situated in the path of, or very
near the headwaters of, an unnamed tributary which flows less than two miles from
the site to the Cape Fear River. The Cape Fear River is located approximately 3/4
of a mile west of the site. The site lies within the 100 year flood plain for the Cape
Fear River. Locks Creek is located less than one mile east of the site.
A:.\CART.SECT3.DRA. 3-2
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Surface runoff from the site flows into the unnamed tributary which flows from the
southwest corner of the site to the Cape Fear River, and to other drainage ditches
along Middle Road, west to the Cape Fear River and east to Locks Creek.
Geology and Hydrogeology.The Carolina Transformer Site may be underlain by
as many as three aquifers. These are, in ascending order, the Cape Fear Formation,
Middendorf Formation, and recent alluvial deposits. The sands and clays of the Cape
Fear and Middendorf Formations serve as aquifers in the Fayetteville area. Wells
completed within these formations can be screened over a large interval which could
cover sands and intervening clays. The sands in these aquifers provide much higher
yield and are the most productive strata in the region. The bedrock possesses
fracture permeability and is utilized for industrial water supply wells. A deep bedrock
well was used by Larry's Sausage Company, located adjacent to the site. This well
was 303 feet deep and is completed into the bedrock from 212 feet to the total depth.
Groundwater flow at the site is controlled by local surface water bodies. The Cape
Fear River is a major discharge point for all of the aquifers.
Mr. J. D. Parker, President of the Carolina Sand and Gravel Company, Incorporated,
indicated during a conversation on June 22, 1989 that exploration borings near the
site showed a thick clay lens starting at 90 feet below land surface (BLS) and
extending down to at least 120 feet BLS.
The shallow alluvial aquifer under the site is located at a depth of five to eight feet
below ground surface elevation, and includes a fine to coarse sand layer which varies
in thickness from six to thirteen feet. The shallow groundwater appears to flow in
a northeasterly direction toward Locks Creek. The grey to blue-grey clay located
under the upper sand layer is very tough and dry ( observed from samples) indicating
that the clay is potentially a very good confining layer separating the shallow aquifer
from the deeper aquifers. All of the temporary and permanent monitoring wells
were installed in the shallow aquifer. The alluvial deposits of the shallow aquifer
could provide large yields to wells; however, the available information indicates that
this aquifer is not presently used for water supply in the area.
A.:.\CART.SECT3.DRA 3-3
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3.2.1.3 Climatology
Climatology Summary. The Cumberland County area is hot and generally humid
in summer because of the moist, maritime air. Winter is moderately cold, but short
because the mountains to the west protect the area from many cold waves.
Precipitation is quite evenly distributed throughout the year and is adequate for all
crops.
The average temperature at Fayetteville in the winter is 44 degrees F. The average
daily minimum temperature is 31 F. The lowest temperature on record, which
occurred at Pinehurst in December 1962, is 3 F. In summer, the average tempera-
ture is 78 degrees at Fayetteville. The average daily maximum temperature is 89
degrees. The highest recorded temperature in Cumberland County, which occurred
at Fayetteville in June 1952, and at Pinehurst in July 1952, is 105 F. The average
daily temperature throughout the year is 61 F.
The total annual precipitation is 43 inches at Fayetteville. Of this, 60 percent usually
falls in April through September, which includes the growing season for most crops.
The heaviest 1-day rainfall for Fayetteville during the period of record was 5.12
inches on September 12, 1960. Thunderstorms occur on about 45 days each year,
and most are in summer.
The average seasonal snowfall is 3 inches at Fayetteville. In Fayetteville, the greatest
snow depth at any one time during the period of record was 4 inches. At least 1
inch of snow is on the ground an average of one day per year. The number of such
days varies greatly from year to year.
In winter, every few years, heavy snow covers the ground for a few days to a week.
Every few years, in late summer or autumn, a tropical storm moving inland from the
Atlantic Ocean causes extremely heavy rain for one to three days.
The average relative humidity in mid-afternoon is about 60 percent. Humidity is
higher at night and the average at dawn is about 85 percent. The sun shines 70
percent of the time possible in summer and 60 percent in winter. A summary of
weather information is provided in Table 3-1.
A:\CART.SECT3.0AA 3-4
-------------------TABLE 3-1 --TEMPERATURE AND PRECIPITATION
(Recorded in the period 1951-73 at Fayetteville, North Carolina, in Cumberland County)
Temperature Precipitation
2 years in 2 years in 10
10 will have-will have-Average
Month Average Average Average Maximum Minimum number of days Average
daily daily daily temperature temperature Average Less than-More than-with 0.10 snowfall
maximum minimum higher than-lower than-inch or more
Degree F Degree F Degree F Degree F Degree F ill ill lD. ill
January 54.0 30.0 42.0 78 12 3.51 2.22 4.67 8 0.7
February 57.0 32.9 44.9 80 15 4.10 2.42 5.59 8 0.5
March 63.9 38.5 51.2 84 23 4.10 2.59 5.45 8 0.1
April 73.5 47.4 60.2 91 30 3.21 1.87 4.40 5 0.0
May 80.7 56.3 68.5 96 37 3.54 2.20 4.74 6 0.0
June 87.5 64.7 76.1 100 49 4.56 2.50 6.37 7 0.0
July 90.1 68.9 79.6 101 57 4.94 3.02 6.66 9 0.0
August 89.1 67.9 78.5 99 55 5.67 3.81 7.36 8 0.0
September 84.5 61.8 73.2 96 45 3.53 1.41 5.36 5 0.0
October 75.4 50.1 62.7 90 28 3.15 0.78 5.03 5 0.0
November 66.0 38.4 52.2 84 19 2.40 0.94 3.61 4 0.0
December 56.0 30.8 43.4 79 12 2.85 1.27 4.19 6 1.9
Yearly:
Average 73.1 49.0 61.1 --------------
Extreme ----101 12 ----------
Total --------45.56 37.72 48.6 79 3.2
Source: National Climatic Center, Ashville, N.C.
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Dispersion Climatology. The dispersion capacity of the atmosphere is of primary
interest when estimating the potential for the atmospheric migration of site emissions.
As onsite meteorological monitoring was not within the scope of the remedial
investigation, the minimal atmospheric stability, wind speed, and wind direction can
be estimated based on data available from a first order national Weather Service
station at Fort Bragg, North Carolina.
The Cities of Fayetteville and East Fayetteville, and the residential areas northeast
of the site are the nearest population centers to the site. Winds from the northeast
and southwest would provide the most critical wind conditions. Winds in the range
of 3 to 5 miles per hour are the most critical with respect to volatilized chemicals as
they result in a steady movement of emissions with minimal dispersive mixing. In
order for wind erosion to occur from non-homogeneous surfaces, higher wind speeds
of about 22 mph would be required [11].
3.2.2 Potentially Exposed Populations/ Relative Locations of Populations with
Respect to Site
The Demography of the area surrounding the Carolina Transformer site was
described in Section 3.2.1.1.
3.2.2. 1. Current Residential Populations. Residential populations that may be
exposed to site-related contaminants include residents that live near the site and are
involved in recreational activities near the site, and potential site trespassers.
Residents living adjacent to the site or in the vicinity are most likely to trespass on
the property.
3.2.2.2 Current Worker Populations. Since the site is inactive and vacant,
worker populations that may be exposed to contaminants from the Carolina
Transformer site are limited to workers at neighboring businesses.
3.2.2.3 Future Residential Populations. The potential exists that future land-use
activities would alter current exposure scenarios. Based on current land use in the
area, the site and the surrounding area could be developed for residential use.
A:.\CART.SECT3.DRA 3-5
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3.2.2.4 Future Worker Populations. The site could be used for commercial
development in the future, thereby increasing the worker population that could
potentially be exposed to contaminants from the site.
3.3 Identification of Exposure Pathways
3.3. 1 Sources and Mechanisms of Chemical Release to the Environment
The sources of contaminant release for the Carolina Transformer Site are described
in the Work Plan and the RI Report [2,3]. In the course of its transformer rebuilding
business, Carolina Transformer handled and stored large numbers of electrical
transformers at the site which contained oil laden with PCBs. Several abandoned
transformers and unlabeled, full, sealed drums are located onsite.
3.3.2 Fate and Transport of Chemicals of Potential Concern
The chemicals of potential concern for the Carolina Transformer Site include PCBs,
volatile and semi-volatile organic compounds, pesticides, and metals. There are seven
transport mechanism that are the most likely to occur:
• Leaching from contaminated soil.
• Volatilization from contaminated soil.
• Wind and mechanical erosion of contaminated soil.
• Excavation of contaminated soil (future land use).
• surface water runoff.
• Groundwater flow (present and future).
• Groundwater seepage to surface water.
The fate and transport characteristics for the chemicals of potential concern are
covered in Appendix A This information was used in evaluating the potential for site
contaminants to migrate the source of contamination to some point of exposure.
3.3.3 Exposure Pathways and Routes
Exposure pathways describe the movement of contaminants from sources to exposure
points where exposed populations (receptors) come in contact with the contaminant.
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This movement usually involves the release of contaminants from the source to an
intermediate environmental transport medium between the source and the receptor
point. Exposure routes are the modes of contact with and intake of contaminated
media and contaminants at the exposure points. The following sections focus on an
evaluation of exposure points and exposure routes, in order to determine what
pathways of exposure exist.
3.3.3. 1 Current Land Use Conditions. The potential exposure pathways under
current land use conditions are summarized in Table 3-2. This table presents
potential routes of exposure, potential receptors, an evaluation of pathway
completeness, and an assessment of exposure potential. Based on this information,
the following current populations were further evaluated for potential exposures to
chemicals of potential concern in various media in the area of the site:
• Residents recreating near the site.
• Site trespassers.
• Offsite workers.
Although the surface waters at and around the site are defined as "Best Usage
Waters" (which includes fishing), neither sport nor commercial fish species were
observed in the shallow surface water bodies where samples were collected during
field investigations. Therefore, it is expected that exposure via ingestion of potentially
contaminated fish from the sampled areas would be minimal to nonexistent.
Water samples were not collected from the Cape Fear River, so it is not known
whether site-related contaminants can be detected in the river. There are no
commercial fisheries between the site and the Cape Fear River. The average PCB
concentration in offsite surface water was 10 ug/1. The sampled surface water bodies
empty into the Cape Fear River; however, copious dilution occurs and it is assumed
that potential exposure via ingestion of contaminated fish from the Cape Fear River
is negligible.
Due to the low concentrations of organic compounds detected in each medium (less
than 1 ppm), the air pathway will not be quantitatively evaluated as an exposure
A:\CART\SECT3.0RA 3 - 7
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I TABLE 3-2
SUMMARY OF EXPOSURE PATHWAYS -CURRENT LAND USE
I
POTENTIALLY PATHWAY
I EXPOSED EXPOSURE ROUTE QUANTITATIVELY REASON FOR SELECTION
POPULATION AND POINT MEDIUM EVALUATED OR EXCLUSION
Residenls Ingestion of and Deep No No chemicals of polentlal
I (Offsite) direct conlact wilh Aquifer concern detected In deep
conlaminanls from aquifer.
downgradlent wells.
I Resldenls Ingestion of garden Deep No No chemicals or polentlal
(Off site) produce irrlgaled from Aquifer concern detected In deep
I
downgradlent wells. aquifer.
Residents Ingestion of, direcl Shallow No Shallow aquifer wells in the
(Off site) contacl with, and Aquifer vicinity of site are not being
I inhalation of contamin-used for potable water.
ants from downgradient
wells.
I Residents Ingestion of garden Soil Yes Potential exists for exposure
(Off site) produce grown in to contaminated produce.
contaminated soil.
I Residents Incidental Ingestion of, Soll Yes Potential exists for exposure
(Off site) and direct contact with to contaminated soil.
I contaminants.
Residents Direct contact with Surface Yes Potential exists for exposure
(Offsite) contaminants. Water to contaminated surface water.
I Residents Direct contact with Sediment Yes Potential exists for exposure
(Offsite) contaminants. lo contaminated sediment In
I the creeks and river.
Workers Ingestion of, direct Shallow No No shallow Industrial wells.
I
(Off site) conlact with, and lnhal-Aquifer
atlon of contaminants
form downgradlent
Industrial wells.
I Workers Direct contact with Soll, No Exposure would be the same as
(Olfsite) contaminants. Sediment, for offsile residents bul with
I Surface Waler shorter durations.
Trespassers Incidental ingestion of Soll Yes Potential exists for exposure
(Onsite) and direct contact with contaminated solf.
I contaminants.
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TABLE 3-2 (CONTINUED)
SUMMARY OF EXPOSURE PATHWAYS -CURRENT LAND USE
POTENTIALLY PATHWAY
EXPOSED EXPOSURE ROUTE QUANTITATIVELY REASON FOR SELECTION
POPULATION AND POINT MEDIUM EVALUATED OR EXCLUSION
Trespassers Direct contact with Sediment Yes Potential exists for exposure
(Onslte) contaminants. to contaminated sediment.
Tresspassers Direct contact with Surface Yes Potential exists for exposure
(Onslte) contaminants. Water to contaminated surface water.
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pathway for volatilized chemicals. The air pathway was qualitatively evaluated as an
exposure pathway for particulate emissions from surface soils. In order for wind
erosion to occur, the surface must be dry and exposed to the wind. Particulate
emission rates from nonhomogeneous surfaces impregnated with non-erodible
elements (such as the surfaces present at the site) tend to decay rapidly during an
erosion event. AB indicated in Section 3.2.1.3, wind speeds of about 22 mph would
be required to cause wind erosion from such surfaces [11]. Since average wind
speeds in Fayetteville are in the range of 4.7 miles per hour (mph) to 8;3 mph
(Figure 3-1), the air pathway will not be quantitatively evaluated as an exposure
pathway for particulate emissions.
Residential Populations Under Current Land Use Conditions. Residential
populations that may be exposed to site-related contaminants include residents that
live near the site and potential site trespassers.
While involved in recreational activities near the site, residents could come in contact
with contaminated offsite soil, sediment, and surface water. Exposure to contami-
nants in surface water and sediment could occur during wading activities. Swimming
in onsite and surrounding surface water is unlikely due to the shallow depth of the
water. For this population, dermal contact with contaminants in surface water and
sediment were quantitatively evaluated. In addition, incidental ingestion of and
dermal contact with contaminants in soil were also evaluated.
Nearby residents could also cultivate garden produce in contaminated offsite soil.
This potential exposure route was quantitatively evaluated.
With respect to trespasser populations, exposure could occur if they contacted
contaminated soil, sediment, or surface water onsite. Each of these potential
exposure routes was quantitatively evaluated.
Worker Populations Under Current Land Use Conditions. The site is currently
inactive; therefore, the only potential worker exposure would occur to populations
working in the surrounding area. Industrial supplies of water in the area are
reportedly from the deeper aquifers (no chemicals of potential concern were detected
in the deeper aquifers). Soil, sediment, and surface water exposures may occur if
A.:\CART\SECT3.0AA 3 - 8
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N
5.3
5.6
6
I--_,_ _ ____, E
5.5
s
WINDS ARE FROM INDICATED DIRECTIONS
0-3 -6 -10 -16 -21 •21
KNOT
ANNUAL WINOROSE FOR FORT BRAGG/FAYETTEVILLE, N.C.
PERIOD OF RECORD: 1977 -1986
AVERAGE WIND SPEEDS !KNOTSl ARE SHOWN AT
THE ENO OF EACH DIRECTION
ONE KNOT= 1.1 MILES PER HOUR
FIGURE 3-1
NNJAL MINOROSE FOR FAYETTEVILLE, N.C.
PERIOD OF RECORD: 77-fJS
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workers enter offsite or onsite areas that are contaminated. These exposures would
be similar to those experienced by nearby residents or trespassers.
3.3.3.2 Future Land Use Conditions. The potential exposure pathways for
future land use conditions are summarized in Table 3-3. This table presents potential
routes of exposure, potential receptors, an evaluation of pathway completeness and
an assessment of exposure potential. Therefore, in addition to the populations
identified under current land use conditions, the future populations living onsite may
be exposed to chemicals of potential concern in the various media.
Onsite Residential Populations Under Future Land Use Conditions.For onsite
residential populations, exposure to contaminants onsite could occur if they contacted
contaminated soil (surface or subsurface), groundwater, surface water, or sediment.
Since surrounding land use is a mixture of residential, it is possible that the site may
be used as a residential agricultural, or commercial area in the future. Therefore,
future residential land use is a possibility.
For this population, ingestion and dermal contact with contaminants in drinking water
will be evaluated. To obtain a reasonable maximum exposure projection of future
residential exposure to groundwater, sample data obtained from Well #44 (an on-site
well) were used to evaluate exposure via ingestion and dermal contact. Most
residents in the area are currently using City water; therefore, there is low likelihood
of this scenario being realized in the future.
Residential exposure to surface water and sediment is not expected to be greatly
increased under future land use conditions ( e.g., off site PCB concentrations in surface
water and sediment are higher than onsite concentrations). Therefore, residential
exposure is considered the same as current offsite residential exposure and is
evaluated as such.
Residential exposure to onsite surface and subsurface soils could occur if the site was
developed residentially. For this population, incidental ingestion of and direct contact
k\CAAT\SECT3.0AA 3 -9
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I TABLE 3-3
SUMMARY OF EXPOSURE PATHWAYS-FUTURE LAND USE
I
POTENTlALL Y PATHWAY
I EXPOSED EXPOSURE ROUTE QUANTlTATlVEL Y REASON FOR SELECTION
POPULATION AND POINT MEDIUM EVALUATED OR EXCLUSION
Residents Ingestion of, direct Deep No The deep aquifer has not been
I (Onsite) contact with, and In-Aquifer Impacted by the site.
halatlon of contaminants.
I Residents Ingestion of, direct Shallow Yes Polenllal exists for the site
(Onsite) contact with, and in-Aquifer to be developed for residential
I
halation of contaminants. use.
Residents Ingestion of garden Soil Yes Potential exists for the site
I (Onsite) produce grown In to be developed for residential
contaminated soil. use.
I Residents Incidental Ingestion of Soil Yes Potential exists for the site
(Onsite) and direct contact with to be developed for residential
contaminants. use.
I Residents Direct contact with Surface Yes Same as under current land use.
(Onslte) contaminants. Water
I Residents Direct ~ontact with Sediments No Same as under current land use.
(Onsite) contaminants.
Residents Ingestion ol, direct Shallow No Exposure would be the same as
I (OHsite) contact with, and in-Aquifer onsite residents but with
halation of contaminants. lower contaminant levels.
I Residents Incidental ingestion ol, All No Same as under current land use.
(Offsite) or direct contact with
contaminants.
I Workers Incidental Ingestion of, All No Exposure would be the same as
(Onsite) direct contact with, for onslte residents but with
and inhalation ol contam-shorter exposure durations.
I inants.
Workers Incidental lngeslion ol, All No Exposure would be the same as
I (Offsite) direct contact with, current land use.
and inhalation of contam-
lnants.
I Trespassers Incidental Ingestion of, All No Exposure would be the same as
(Onslle) direct contact with, the current land use.
and Inhalation of contam-
I lnants.
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with contaminants was evaluated. Ingestion of contaminated, homegrown produce
was also evaluated.
3.4 Summary of Exposure Pathways
Based on this evaluation process, the following pathways were selected for evaluation
in the assessment:
o Current exposure of offsite residents to contaminants in soil through
incidental ingestion and dermal contact, and in surface water and sediment
through dermal contact. Exposure through ingestion of garden produce
planted in contaminated soil was also evaluated.
• Current exposure of offsite residents to contaminants in fish through
ingestion of contaminated fish.
• Current exposure of onsite trespassers to contaminants in soil through
incidental ingestion and dermal contact, and in surface water and sediment
through dermal contact.
• Future exposure of onsite residents to contaminants in groundwater through
ingestion and direct contact and inhalation; and to contaminants in soil
through incidental ingestion and dermal contact.
• Future exposure to onsite residents to contaminants in garden produce
through ingestion of contaminated produce.
3.5 Quantification of Exposure
The basic equation used to calculate human intake of an environmental contaminant
was:
DI= C x HIF
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where:
DI = Daily Intake (mg of chemical per kg of body weight per day)
C = Concentration of the chemical in mg/kg/ (ppm)
HIF = Human Intake Factor (kg of medium per kg body weight per day)
Each intake variable in the above equation has a range of values. The intake
variable values for a given pathway were selected so that the combination of all
intake variables results in an estimate of the reasonable maximum exposure (RME)
for that pathway. The RME is defined as the maximum exposure that is reasonably
expected to occur at or near a site. This section describes the way in which the
exposure concentrations and the human intake factors are derived.
3.5.1 Exposure Concentration
The concentration term (C) in the intake equation generally utilizes the arithmetic
average of the concentration that is contacted over the exposure period. Due to the
uncertainty associated with any estimate of exposure concentrations, the upper 95
percent confidence limit on the arithmetic mean was used for this variable. Standard
statistical methods (t-test) were used to calculate the upper confidence limit on the
arithmetic mean. Where this value exceeded the highest observed concentration, the
highest observed concentration was used as the exposure point concentration.
Contaminant concentrations reported as "not detected" were assumed to be one-half
the detection limit for the calculation of exposure point concentrations. Exposure
point concentrations were estimated for the chemicals of potential concern that were
detected in the following media and area subsets:
Current Exposure:
• Offsite sediment
• Offsite soil
• Offsite surface water
• Onsite soil
• Onsite sediment
• Onsite surface water
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Future Exposure:
• Onsite soil
• Onsite groundwater (shallow aquifer)
o Offsite sediment
• Offsite surface water
Table 3-4 summarizes the exposure concentrations derived for each pathway in each
medium. The estimates of future soil, sediment, groundwater, and surface water
exposure concentrations presented here assume that concentrations will remain
constant over the duration of exposure (up to 30 years). This is a conservative
assumption since nearly all chemicals, especially volatiles, are subject to a variety of
fate processes. Based on the presence of distinct areas of PCB-contamination in on-
site soils, the site was divided into two areas: the administration area and the
operations/storage area. This method of evaluating PCB contamination was chosen
to more clearly define the contaminated areas and to aid in selecting appropriate
remedial alternatives for the site.
3.5.2 Human Intake Factors
Human Intake Factors (H!Fs) are site-specific terms that quantify the degree of
contact between humans and environmental media at the exposure points. The
USEPA has developed several guidance documents that provide information for
deriving HIFs. The RAGS manual [1] summarizes much of the information for these
other sources, and was used as the primary source for information used for deriving
the HIFs. The sections that follow detail the derivation of these HIFs values.
3.5.2.1 Intake From Incidental Ingestion of Soll or _Sediment. Incidental
ingestion of contaminated soil or sediment was calculated using the following
equation [1]:
Intake = CS x IR x CF x FI x EF x ED
(mg/kg-day BW x AT x 365 days/yr
where:
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CS = Chemical Concentration in Soil or Sediment (mg/kg)
IR = Ingestion Rate (mg soil/day)
CF = Conversion Factor (10 .;; kg/mg)
FI = Fraction Ingested from Contaminated Source (unitless)
EF = Exposure Frequency (days/year)
ED = Exposure Duration (years)
BW = Body Weight (kg)
AT = Averaging Time (period over which exposure is averaged -years)
Current Adult Trespassers Onsite (Soil). For current adult site trespassers
exposed to soil onsite, the values of these parameters are as follows:
CS = Site specific value (Table 3-4)
IR = 100 mg/day (age groups greater than 6 years old, [1])
CF = 10"° kg/mg
FI = 0.083 (based on 2 hr/day exposure)
EF = 5 days/yr (1 day/week, 5 wks/yr)
ED = .5 years (subchronic); 10 years (chronic); 30 years (lifetime)
BW = 70 kg (adult average)
AT = 0.5 years (subchronic); 10 years (chronic); 70 years (lifetime)
Based on these values, average daily intakes of soil via incidental ingestion by adult
trespassers are:
DI (subcontract) = CS (mg/kg) x 1.6E -9 (kg/kg/day)
DI (chronic) = CS (mg/kg) 1.6E-9 (kg/kg/day)
DI (lifetime) = CS (mg/kg) 7.0E -10 (kg/kg/day)
Current Child Trespassers Onsite (Soll). For current child site trespassers
exposed to soil onsite, the values of these parameters are as follows:
CS = Site specific value (Table 3-4)
IR = 200 mg/day ( children 1 through 6 years old, [1])
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EXPOSED
POPULATION
Current OIi-Site
Residents
TABLE 3-4
SUMMARY OF EXPOSURE POINT CONCENTRATIONS
OF CHEMICALS OF POTENTIAL CONCERN
EXPOSURE EXPOSURE POINT CONCENTRA TIONS(a)
MEDIUM CHEMICAL (MG/KG SOIL, UG/L WATIER)
Groundwater Barium 4.3E+03
Cobalt 2.3E+02
Chromium 7.6E+02
Copper 4.7E+02
Nickel 3.6E+02
Strontium 7.0E+02
ntanlum 4.7E+03
Vanadium 1.6E+03
Yttrium 5.4E+02
Zinc 1.1E+03
Aluminum 8.8E+0S
Manganese 4.0E+03
Mercury 3.0E-01
PCB-1260 (Aroclor 1260) 6.SE+00
Bis(2-Ethylhexyl) Phthaiate 9.8E+01
1,2,4-Trichlorobenzene 1.SE+01
Methyl Ethyl Ketone 6.7E+00
Toluene 5.SE+00
Carbon Disulfide 4.4E+00
Benzene 4.6E+01
Chlorobenzene 3.1 E+00
1,3-Dichlorobenzene 9.3E+00
1,4-Dichlorobenzene 3.7E+01
Soils o-s• s•-12•
Arsenic 2.2E+OO 3.4E+00
Barium 7.4E+01 8.7E+01
Cobalt 2.SE+00 2.4E+OO
Chromium 9.4E+OO 1.1 E+01
Copper 4.0E+01 5.6E+OO
Lead 3.4E+01 1.1E+01
Strontium 1.4E+01 1.SE+01
lltanlum 3.0E+02 2.SE+02
Yttrium 7.4E+OO 6.0E+OO
Zinc 5.9E+01 1.3E+01
Manganese 2.8E+02 3.1E+02
Mercury 9.0E-02 6.0E-02
PCB-1260 (Aroclor 1260) 3.7E+01 4.9E+01
Trichloroethane 1.6E-02 2.SE-03
Toluene 1.4E-02 6.4E-02
1,4-Dichlorobenzene 4.4E-02 3.2E-02
1,2-Dlchlorobenzene 2.2E-02 1.SE-02
Dloxlns/Furans 6.9E-05 1.SE-05
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EXPOSED
POPULATION
Current Off-Site
Residents,
Future On-Site
Residents
TABLE 3-4 (Cont.)
SUMMARY OF EXPOSURE POINT CONCENTRATIONS
OF CHEMICALS OF POTENTIAL CONCERN
EXPOSURE EXPOSURE POINT CONCENTRA TIONS(a)
MEDIUM CHEMICAL (MG/KG SOIL, UG/L WATER)
Sediments Barium 1.4E+02
Cadmium 3.9E+00
Cobalt 5.9E+00
Chromium 2.9E+01
Copper 5.0E+02
Nickel 7.9E+00
Lead 1.2E+02
Strontium 1.5E+00
Zinc 2.2E+02
Aluminum 3.1E+04
Yttrium 8.6E+00
Manganese 1.2E+02
Vanadium 5.1 E+01
PCB-1254 (Aroclor 1254) 2.SE-03
PCB-1248 (Aroclor 1248) 1.8E-01
PCB-1260(Aroclor 1260) 2.2E+02
Benzene 2.SE-03
Toluene 2.2E+00
Chlorobenzene 2.SE-03
1,3-Dichlorobenzene 5.0E-03
1,4-Dichlorobenzene 5.0E-03
1,2-Dlchlorobenzene 5.0E-03
Dioxins/Furans 1.6E-04
Surface Water Copper 1.1E+02
Titanlum 1.2E+01
Zinc 1.6E+02
Manganese 5.0E+02
PCB-1260(Aroclor 1260) 1.0E+01
Bls(2-Ethylhexyl) Phthalate 7.7E+01
Carbon Disulfide 2.8E+01
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EXPOSED
POPULATION
Current On-Site
Trespassers
TABLE 3-4 (Cont.)
SUMMARY OF EXPOSURE POINT CONCENTRATIONS
OF CHEMICALS OF POTENTIAL CONCERN
EXPOSURE EXPOSURE POINT CONCENTRATIONS(a)
MEDIUM CHEMICAL (MG/KG SOIL, UG/L WATER)
Soll 0-2· 8'-10'
Barium 2.9E+01 2.9E+01
Cadmium 2.2E+00 9.4E+OO
Cobalt 5.0E-01 2.6E+OO
Chromium 8.9E+00 5.9E+OO
Copper 1.3E+03 8.0E+02
Lead 7.9E+01 4.3E+OO
Zinc 6.9E+01 4.5E+01
Manganese 7.6E+02 9.0E+02
1,2,4-Trichlorobenzene 2.SE-03 4.SE+OO
Tetrachloroelhene 5.0E-04 2.0E-03
Toluene 6.2E-03 9.4E-03
Trichloroethane 2.0E-03 3.0E-03
Benzene 2.5E-03 1.6E-03
Chlorobenzene 2.SE-03 9.3E-03
Dioxins/Fu rans 7.5E-04 1.2E-04
Administrative
0-2· a•-10·
PCB-1254 (Aroclor 1254) 2.5E-03 2.5E-03
PCB-1260 (Aroctor 1260) 7.1E+00 4.5E-01
Operations/Storage
0-2· s·-10•
PCB-1254 (Aroclor 1254) 4.8E+01 2.5E-03
PCB-1260 (Aroclor 1260) 6.5E+02 3.1 E+02
Sediment Barium 5.6E+01
Cadmium 1.9E+00
Cobalt 4.1 E+00
Chromium 1 .5E+01
Copper 2.5E+03
Nickel 4.3E+OO
Lead 9.5E+01
Strontium 1.1 E+01
Zinc 7.3E+01
Aluminum 1.1E+04
Yttrium 6.7E+OO
Manganese 1.8E+02
Vanadium 3.3E+01
PCB-1254 (Aroclor 1254) 9.2E+01
PCB-1248 (Aroctor 1248) 9.8E+OO
PCB-1260 (Aroclor 1260) 1.6E+02
Benzene 2.1E-02
Toluene 9.4E-03
Chlorobenzene 5.9E-02
1,3-Dlchlorobenzene 1.3E-01
1,4-Dichlorobenzene 4.4E-01
1,2-Dlchlorobenzene 4.2E-02
Dioxlns/Furans 2.2E-04
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EXPOSED
POPULATION
Current On-Site
Trespassers
Future On-Site
Residents
TABLE 3-4 (Cont.)
SUMMARY OF EXPOSURE POINT CONCENTRATIONS
OF CHEMICALS OF POTENTIAL CONCERN
EXPOSURE EXPOSURE POINT CONCENTRATIONS(a)
MEDIUM CHEMICAL (MG/KG SOIL, UG/L WATER)
Surface Water Copper 1 .2E+02
Titanium 5.0E+00
Zinc 8.0E+01
Manganese 4.6E+02
PCB-1260 (Aroclor 1260) 6.2E+00
Bis(2-Ethylhexyl) Phthalate 2.5E+00
Carbon Disulfide 1.4E+02
Groundwater Barium 1.7E+04
Cobalt 7.4E+02
Chromium 2.8E+03
Copper 2.9E+03
Nickel 1.2E+03
Strontium 1.6E+03
Titanium 6.SE+03
Vanadium 5.3E+03
Yttrium 1.5E+03
Zinc 3.8E+03
Aluminum 3.4E+06
Manganese 2.4E+04
Mercury 3.0E-01
PCB-1260 (Aroclor 1260) 5.1E+01
Bis(2-Ethylhexyl) Phthalate 8.2E+02
1,2,4-Trlchlorobenzene 1.5E+00
Methyl Ethyl Ketone 7.6E+00
Toluene 5.5E+00
Carbon Disulfide 1.1E+01
Benzene 3.7E+00
Chforobenzene 1.BE+01
1,3-Dichlorobenzene 9.3E+00
1,4-Dichlorobenzene 3.7E+01
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CF = 10 "° kg/mg
FI = 0.083 (based on 2 hr/day exposure)
EF = 5 days/yr (1 day/wk, 5 wks/yr)
ED = 0.5 years (subchronic); 5 years (lifetime)
BW = 16 kg ( children through 6 years old, 50th percentile)
AT = 0.5 years ( subchronic ); 70 years (lifetime)
Based on these values, average daily intakes of soil via incidental ingestion by child
trespassers are:
DI (subchronic) = CS (mg/kg) x 1.4E-8 (kg/kg/day)
DI (lifetime) = CS (mg/kg) x 1.0E-9 (kg/kg/day)
Current Adult Offsite (Soil). For current adult residents exposed to soil offsite,
the values of these parameters are as follows:
CS = Site specific value (Table 3-4)
IR = 100 mg/day (age groups greater than 6 year old; (1))
CF = 10"° kg/mg
FI = 0.33 (based on 8 hr/day Recreational Activity)
EF = 6 day/year (based on 0.94 hrs/week mean outdoor activity -men &
women and 8 hour/day exposure)
ED = .5 years (subchronic); 10 years (chronic); 30 years (lifetime)
BW = 70 kg (adult average)
AT= 0.5 years (subchronic); 10 years (chronic); 70 years (lifetime)
Based on these values, average daily intakes of soil via incidental ingestion by current
adult offsite residents are:
DI (subchronic) = CS (mg/kg) x 7.7 E-9 (kg/kg/day)
DI (chronic) = CS (mg/kg) x 7.7 E-9 (kg/kg/day)
DI (lifetime) = CS (mg/kg) x 3.3 E-9 (kg/kg/day)
Current Child Offsite (Soll). For current child residents exposed to soil offsite,
the values of these parameters are as follows:
k\CART\8"CT3.0RA 3 -14
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CS = Site specific value (Table 3-4)
IR = 200 mg/day (children 1 through 6 years old, [1])
CF = 10--0 kg/mg
FI = 0.33 (based on 8 hr/day recreational activity)
EF = 10 days/year (based on 1.59 mean hrs/week, boys & girls, outdoor
activity)
ED = 0.5 years (subchronic); 5 years (lifetime)
BW = 16 kg (children through 6 years old, 50th percentile)
AT = 0.5 years (subchronic); 70 years (lifetime)
Based on these values, average daily intakes of soil via incidental ingestion by current
child offsite residents are:
DI (subchronic) = CS (mg/kg) x 1.lE-7 (kg/kg/day)
DI (lifetime) = CS (mg/kg) x 8.lE-9 (kg/kg/day)
Future Adult Onsite (Soil). For future adult residents exposed to soil onsite, the
values of these parameters are as follows:
CS = Site specific value (Table 3-4)
IR = 100 mg/day (age groups greater than 6 years old, [1])
CF = 10--0 kg/mg
FI = 0. 72 (based on the summation of active & passive leisure, housework,
yardwork, and personal care)
EF = 365 days/year
ED = .5 years (subchronic); 10 years (chronic); 30 years (lifetime)
BW = 70 kg (adult average)
AT = 0.5 years (subchronic); 10 years (chronic); 70 years (lifetime)
Based on these values, average daily intakes of soil via incidental ingestion by future
adult residents are:
DI (subchronic) = CS (mg/kg) x 1.0E-6 (kg/kg/day)
DI (chronic) = CS (mg/kg) x l.OE-6 (kg/kg/day)
DI (lifetime) = CS (mg/kg) x 4.4E-7 (kg/kg/day)
A:\CART\SECT3.0RA 3 -15
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Future Child Onsite (Soil). For future child residents exposed to soil onsite, the
values of these parameters are as follows:
CS = Site Specific Value (Table 3-4)
IR = 200 mg/day (children 1 through 6 years old, [1])
CF= 10--0 kg/mg
FI = 0.75 (based on the summation of active & passive leisure, housework,
yardwork, and personal care)
EF = 365 days/year
ED = 0.5 years (subchronic); 5 years (lifetime)
BW = 16 kg ( children through 6 years old, 50th percentile)
AT = 0.5 years (subchronic); 70 years (lifetime)
Based on these values, average daily intakes of soil via incidental ingestion by future
onsite child residents are:
DI (subchronic) = CS (mg/kg) x 9.4E-6 (kg/kg/day)
DI (lifetime) = CS (mg/kg) x 6.7E-7 (kg/kg/day)
3.5.2.2 Intake from Dermal Contact with Soll or Sediment. Intake ( expressed
as absorbed dose) from dermal exposure to soil or sediment is given by the following
equation [1 ]:
where:
Absorbed dose = CS x CF x SA x AF x AB x EF x ED
(mg/kg-day) BW x AT x 365 days/yr
CS = Chemical Concentration in Soil or Sediment (mg/kg)
CF = Conversion Factor (10--0 kg/mg)
SA = Surface Area Exposed (cm2)
AF = Soil Adherence Factor (mg/cm2)
AB = Absorption Factor (unitless)
A:\CART\SECT3.0RA 3 -16
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EF = Exposure Frequency (days/yr)
ED = Exposure Duration (years)
BW = Body Weight (kg)
AT = Averaging Time (years)
Current Adult Trespassers Onsite (Soil or Sediment). For current adult
trespassers exposed to soil or sediment onsite, the values of these parameters are as
follows:
CS = Site specific value (Table 3-4)
CF = 10-6 kg/mg
'fj';}.9 SA = 8,620 cm2 (adult: hands, arms, legs) [1]
AF = 1.45 mg/cm2 (EPA, 1989b)
AB = Chemical specific dermal absorption and soil description factor
assumed to be 0.25 for volatiles 0.1 for semivolatiles, and 0.01 for metals
[8].
\'\0 EF = 5 days/yr (1 days/wk, 5 wks/yr)
,.,o t;0 ED = 0.5 years (subchronic); 10 years (chronic) 30 years (lifetime)
r_
_,,, BW = 70 kg (adult average)
,;p 1~o AT = 0.5 years ( subchronic ); 10 years (chronic); 70 years (lifetime)
S,
Based on these values, the daily absorbed doses from dermal contact with soil or
sediment for adult trespassers are:
DI (subchronic) = CS (mg/kg) (ABS) 2.4E-6 (kg/kg/day)
DI (chronic) = CS (mg/kg)(ABS) 2.4E-6
DI (lifetime) = CS (mg/kg)(ABS) 1.0E-6 (kg/kg/day)
Current Child Trespasser Onsite (Soil or Sediment). For current child
trespassers exposed to soil or sediment onsite, the values of these parameters are as
follows:
CS = Site specific value (Table 3-4)
CF = 10"° kg/mg
.A.:\CART\SECT3.0RA 3 -17
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SA = 3,160 cm2 (child: hands, arms, legs, [1])
AF = 1.45 mg/cm2
AB = Chemical specific dermal absorption and soil desorption factor
assumed to be 0.25 for volatiles, 0.1 for semivolatiles, and 0.01 for metals
[8].
EF = 5 days/yr (1 day/wk, 5 weeks/yr)
ED = 0.5 years (subchronic); 5 years ( child)
BW = 16 kg (children 1 through 6 years old, 50th percentile)
AT = 0.5 years (subchronic); 70 years (lifetime)
Based on these values, the daily absorbed doses from dermal contact with soil or
sediment for child trespassers are:
DI (subchronic) = CS (mg/kg) (ABS) 3.9E-6 (kg/mg/day)
DI (lifetime) = CS (mg/kg) (ABS) 2.8E-7 (kg/mg/day)
Current Adult Off site (Soil or Sediment). For curr.ent adult residents exposed
to soil or sediment offsite, the values of these parameters are as follows:
CS = Site Specific Value (Table 3-4)
CF = 10'° kg/mg
SA = 8,620 cm2 ( adult: hands, arms, legs)
AF = 1.45 mg/cm
AB = Chemical specific dermal absorption and soil desorption factor
assumed to be 0.25 for volatiles, 0.1 for semivolatiles and 0.01 for metals
[8].
EF = 6 days/year (based on 0.94 hours/wk mean outdoor activity -men and
women, and 8 hr/day exposure.
ED = .5 years (subchronic); 10 years (chronic); 30 years (lifetime)
BW = 70 kg (adult average)
AT = 0.5 years (subchronic); 10 years (chronic); 70 years (lifetime)
Based on these values, average daily intakes of soil or sediment from dermal contact
by current adult offsite residents are:
A:\CART\SECT3.0RA 3 -18
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DI (subchronic) = CS (mg/kg) (ABS) x 2.9E-6 (kg/kg/day)
DI (chronic) = CS (mg/kg (ABS) x 2.9E-6 (kg/kg/day)
DI (lifetime) = CS (mg/kg) (ABS) x l.3E-6 (kg/kg/day)
Current Child Offslte (Soil or Sediment). For current child residents exposed
to soil or sediment offsite, the values of these parameters are as follows:
CS = Site Specific Value (Table 3-4)
CF = 10'° kg/mg
SA = 3,160 cm2 (child, hands, arms, legs, [1])
AF = 1.45 mg/cm2
AB = Chemical specific dermal absorption and soil desorption factor
assumed to be 0.25 for volatiles, 0.1 for sernivolatilves, and 0.01 for
metals (8].
EF = 10 Days/year (based on 1.59 mean _hrs/wk boys & girls outdoor activity)
ED = 0.5 years (subchronic); 5 years (child)
BW = 16 kg ( children 1 through 6 years old, 50th percentile)
AT = 0.5 years (subchronic); 70 years (lifetime)
Based on these values, average daily intakes of soil or sediment from dermal contact
by current child offsite residents are:
DI (subchronic) = CS (mg/kg) (ABS) 7.SE-6 (kg/kg/day)
DI (lifetime) = CS (mg/kg) (ABS) 5.6E-7 (kg/kg/day)
Future Adult Onslte (Soil). For future adult residents exposed to soil onsite, the
values of these parameters are as follows:
CS = Site specific value (Table 3-4)
CF = 10'° kg/mg
SA = 8,620 cm2 (Adult: hands, arms, legs, [1])
AF = 1.45 mg/cm2
k\CAAT\SECT3.DAA 3 -19
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AB = Chemical specific dermal absorption and soil desorption factor
assumed to be 0.25 for volatiles, 0.1 for semivolatiles, and 0.01 for
metals [8].
EF = 365 days/yr
ED = 0.5 years (subchronic); 10 years (chronic); 30 years (lifetime)
BW = 70 kg (adult, average; [1]
AT = 0.5 years (subchronic); 10 years (chronic); 70 years (lifetime)
Based on these values, average daily intakes of soil by dermal absorption by future
onsite residents are:
DI (subchronic) = CS (mg/kg) (ABS) x 1.8E-4 (kg/kg/day)
DI (chronic) = CS (mg/kg (ABS) x l.8E-4 (kg/kg/day)
DI (lifetime) = CS (mg/kg) (ABS) x 7.7E-5 (kg/kg/day)
Future Child Onsite (Soil). For future child residents exposed to soil onsite, the
values of these parameters are as follows:
CS = Site specific value (Table 3-4)
CF = 10-,; kg/mg
SA = 3,160 cm2 (Adult: hands, arms, legs, [1])
AF = 1.45 mg/cm2
AB = Chemical specific dermal absorption and soil desorption factor
assumed to be 0.25 for volatiles, 0.1 for semivolatiles, and 0.01 for
metals [8].
EF = 365 days/yr
ED = 0.5 years (subchronic); 5 years (child)
BW = 16 kg (children 1 through 6 years old, 50th percentile)
AT= 0.5 years (subchronic); 70 years (lifetime)
Based on these values, average daily intakes of soil via dermal absorption for future
child onsite residents are:
DI (subchronic) = CS (mg/kg) (ABS) 2.9E-4 (kg/kg/day)
DI (lifetime) = CS (mg/kg) (ABS) 2.0E-5 (kg/kg/day)
A:.\CART\SECT3.0RA 3 -20
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3.5.2.3 Intake From Ingestion of Groundwater or Surface Water Intake from
ingestion of groundwater is given by the following equation (1 ]:
Intake (mg/kg/day) = CW x IR x EF x ED
BW x AT x 365 days/yr
Future Adult Residents Onsite (Groundwater). For future onsite adult residents
using groundwater for drinking purposes, the values of these parameters are as
follows:
CW = Site Specific Values (Table 3-4)
IR = 2.0 Uday (adult 90th percentile)
EF = 365 days/yr
ED = 0.5 years (subchronic), 10 years (chronic); 30 years (lifetime)
BW = 70 kg (adult average.)
AT = 0.5 years (subchronic); 10 years (chronic); 70 years (lifetime)
Based on these values, the only intakes of groundwater via ingestion by onsite
residents are:
DI (subchronic) = C (rng/L) x 2.9E-2 Ukg/day)
DI (chronic) = C (mg/L) x 2.9E-2 L/kg/day)
DI (lifetime) = C (mg/L) x 1.2E-2 L/kg/day)
Future Child Onsite (Groundwater). For future onsite child residents using
groundwater for drinking purposes, the values of these parameters are as follows:
CW = Site specific values (Table 3-4)
IR = 1.4 Uday ( child 90th percentile)
EF = 365 days/yr
ED = 0.5 years (subchronic), 5 years (chronic)
A:\CART\SECT3.0RA 3 -21
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BW = 16 kg (children 1-6 year old average)
AT = 0.5 years (subchronic); 70 years (lifetime)
Based on these values, the only intakes of groundwater via ingestion by onsite child
residents are:
DI (subchronic) = CW (mg/L) X 8.7E-2 L/kg/day)
DI (lifetime) = CW (mg/L) X 6.2E-3 L/Kg/day)
3.5.2.4 Intake From Dermal/Contact with Groundwater or Surface Water.
Intake from dermal contact with groundwater is given by the following equation [1]:
Absorbed Dose = CW x SA x PC x ET x EF x ED x CF
(mg/kg/day) BW x AT x 365 days/yr
where:
CW = Chemical Concentration in Water (mg/L)
SA = Skin surface area available for contact ( cm2)
PC = Chemical specific dermal permeability constant ( cm/hr)
ET = Exposure Time (hours/day)
EF = Exposure Frequency (days/yr)
ED = Exposure Duration (year)
CF = Volumetric Conversion factor for water (lUlO00 cm3)
BW = Body weight (kg)
AT = Averaging time (years)
Future Adults Residents{OnsiteGroundwater) For future onsite adult residents
using groundwater for showering purposes, the values of these parameters are as
follows:
CW = Site specific measure or modeled value (Table 3-4)
SA = 18,150 cm2 (average adult, (1])
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PC = Chemical specific permeability ( cm/hr) [Table 3-5]
ET = .20 hours/day (assumes one 12 minute shower 90th percentile shower)
EF = 365 days/year
ED = 0.5 years (subchronic), 10 years (chronic), 30 years (lifetime)
CF = lL/1000 cm 3
BW = 70 kg (adult, average)
AT = 0.5 years (subchronic), 10 years (chronic), 70 years (lifetime)
Based on these values, the daily absorbed doses from dermal contact with groundwa-
ter for adult residents are:
DI (subchronic) = CS (mg/L) x PC (cm/hr) x 5.E-2 (hrs) (L)
(kg) (day)(cm)
DI (chronic) = CS (mg/L) PC x (cm/hr) 5.2E-2 (hrs) (L)
(kg) ( day) ( cm)
DI (lifetime) = CS (mg/L) PC x (cm/hr) 2.2E-2 (hrs) (L)
(kg) (day) (cm)
Future Child Residents Onsite (GroundWater).For future onsite child residents
using groundwater for showering purposes, the values of these parameters are as
follows:
CW = Site specific measure or modeled value (Table 3-4)
SA = 13,000 cm2 (average child, [1])
PC = Chemical specific permeability (cm/hr) (Table 3-5]
ET = .20 hours/day (assumes one 12 minute shower-90th percentile shower)
EF = 365 days/year
ED = 0.5 years (subchronic), 5 years (chronic)
CF = lL/1000 cm3
BW = 16 kg (children 1-6 year old average)
AT= 0.5 years (subchronic) 70 years (lifetime)
A:\CART\SECT3.DAA. 3 -23
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Based on these values the daily absorbed doses from dermal contact with groundwa-
ter for child residents are:
DI (subchronic) = CS (mg/L) x PC (cm/hr) x l.6E-1 (hrs) (L)
(kg) (day)( cm)
DI (lifetime) = CS (mg/L) PC x (cm/hr) l.2E-2 (hrs) (L)
(kg) (day) (cm)
Current Adult Trespassers Onsite/Current Adult Residents Offsite. For
current onsite adult trespassers and offsite residents wading in surface water, the
values of these parameters are as follows:
CW = Site specific measured or modeled value [Table 3-4]
SA = 4,912 cm2 (average feet, lower legs, hands and forearms, adult)
PC = Chemical specific permeability ( cm/hr) [Table 3-5]
ET= 1 hr/day
ED = 0.5 years (subchronic); 10 years (chronic); 70 years (lifetime)
EF = 5 days/yr
CF = 1 Ul,000 cm3
BW = 70 Kg (adult average)
AT = 0.5 years (subchronic); 10 years (chronic); 70 years (lifetime)
Based on these values, the daily absorbed doses for current onsite adult trespassers
and current adult resident off site from dermal contact with surface water from wading
are as follows:
DI (chronic) = CW (mg/L) x PC (cm/hr) x 9.6E-4 (hrs) (L)
(kg) ( day)( cm)
DI (lifetime) = CW (mg/L) x PC (cm/hr) 4.2E-4 (hrs) (L)
(kg) (day) (cm)
A:\CAR1\SECT3.DRA 3 -24
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TABLE 3-5
SUMMARY OF DERMAL PERMEABILITY CONSTANTS
FOR CHEMICALS OF POTENTIAL CONCERN
Compound PC (cm/hr)
Aluminum 7.20E-6
Carbon disulfide 5.SE-2
Cadmium 8E-4(a)
Thallium 8E-4(a)
Vanadium 8E-4(a)
Titanium 8E-4(a)
Barium 8E-4(a)
Cobalt 8E-4(a)
Copper 8E-4(a)
Manganese 8E-4(a)
Zinc 8E-4(a)
Chromium 8E-4(a)
Nickel 8E-4(a)
Strontium 8E-4(a)
Mercury 8E-4(a)
Yttrium 8E-4(a)
PCB-1260 8E-4(a)
Bis (2-Ethylhexyl) Phthlate 8E-4(a)
Benzene 4.lOE-1
Toluene 9.00E-4
Methyl Ethyl Ketone 5.0E+0
Chlorobenzene 8E-4(a)
1,3-Dichlorobenzene 8E-4(a)
1,4-Dichlorobenzene 8E-4(a)
1,2,4-Trichlorobenzene 8E-4(a)
(a) PC for Water
Source: Superfund Exposure Assessment Manual [6]
"\CART\SECT3.0AA
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Current Child Trespassers Onsite/Current Child Resident Offsite. For
current onsite child trespassers and offsite child residents wading in surface water, the
values of these parameters are as follows:
CW = Site specific measured or modeled value [Table 3-4)
SA = 3,500 cm2 ( average feet, lower legs, hands and forearms, child)
PC = Chemical specific permeability ( cm/hr) [Table 3-5)
ET= 1 hr/day
ED= 8 years
EF = 5 days/yr
CF = 1 Ul,000 cm3
BW = 40 Kg (8-16 year old average)
AT = 8 years (chronic), 70 years (lifetime)
Based on these values, the daily absorbed doses for current onsite child trespassers
and current child resident offsite from dermal contact with surface water from wading
are as follows:
DI (chronic) = CW (mg/L) x PC (cm/hr) x 1.2E-3 (hrs) (L)
(kg) (day)(cm)
DI (lifetime) = CW (mg/L) x PC (cm/hr) 1.4E-4 (hrs) (L)
(kg) ( day) ( cm)
3.5.2.5 Intake From Inhalation of ContamlnantsVolatilized From Groundwa-
ter.
Intake from inhalation of contaminants volatilized from groundwater is given by the
following equation [1]:
where:
Intake =
(mg/kg/day)
A:.\CART\SECT3.0RA.
CA X IR X ET X EF X ED
BW x AT x 365 days/yr
3 -25
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CA = Contaminant Concentration in air (mg/m3)
IR = Inhalation Rate (m3,'hour)
ET = Exposure time (hours/day)
EF = Exposure Frequency (days/year)
ED = Exposure Duration (years)
BW = Body weight (kg)
AT = Averaging time (years)
The air concentration from volatilization is calculated as follows (assumes 100%
volatilization):
Water concentration (mg/L) x water used (L)
size of room ( m3)
where: Water concentration = compound specific
Water Use = 200 L (per shower)
Size of room = 12 m3 (bathroom)
Shower air concentrations for chemicals of potential concern from offsite groundwa-
ter:
PCB -1260 = 5.4E-2 mg/m3
Carbon Disulfide = 7.3E-2 mg!m3
Bis (2-Ethylhexyl) Phthalate = 8.2E-1 mg!m3
1,2,4-Trichlorobenzene = 1.3 E-1 mg/m3
Methyl Ethyl Ketone = 1.1 E-1 mg!m3
Chlorobenzene = 5.2E-2 mg!m3
1,3-Dichlorobenzene = l.6E-1 mg!m3
1,4-Dichlorobenzene = 6.2E-1 mg!m3
Toluene = 9.2E-2 mg/m3
Benzene = 7.7E-1 mg!m3
A:.\CAAT\SECT3.0AA 3 -26
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Shower air concentrations for chemicals of potential concern from onsite groundwa-
ter:
PCB -1260 = 4.3E-1 mg/m3
Carbon Disulfide = l.8E-1 mg/m3
Bis (2-Ethylhexyl) Phthalate = 6.8E+O mg/m3
1,2,4-Trichlorobenzene = l.3E-2 mg/m3
Methyl Ethyl Ketone = l.3E-2 mg/m3
Toluene = 9.2E-2 mg/m3
Benzene = 6.2E-1 mg/m3
Chlorobenzene = 3.0E-1 mg!m3
1,3-Dichlorobenzene = l.6E-1 mg/m3
1,4-Dichlorobenzene = 6.2E-1 mg/m3
Shower air concentrations for chemicals of potential concern from groundwater
collected from Well #44:
PCB-1260 = 4.3E-1 mg/m3
Carbon Disulfide = l. lE-1 mg/m3
Benzene = 4.7 E-2 mg!m3
Chlorobenzene = 3.3E-1 mg!m3
Future Adult Onsite Residents(GroundWater).For future adult onsite residents
using groundwater for showering purposes, the values of these parameters are as
follows:
CA = Site specific value
IR = 0.6 m3/hour (all age groups)
ET = 0.2 hours/day (one-12 minute shower)
EF = 365 days/year
ED = 0.5 years (subchronic), 10 years (chronic), 30 years (lifetime)
BW = 70 kg (adult, average)
AT = 0.5 years (subchronic), 10 years (chronic), 70 years (lifetime)
A.:\CART\SECT3.DRA 3 -27
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Based on these values, the daily intakes from inhalation of contaminants in the
shower for adult residents are:
DI (subchronic) = CA (mg/m3) x l.7E-3 (m3/kg/day)
DI (chronic) = CA (mg/m3) x l.7E-3 (m3/kg!day)
DI (lifetime) = CA (mg/m3 x 7.3E-4 (m3/kg!day)
Future Child Onsite Residents(Groundwater). For future onsite child residents
using ground water for showering purposes, the values of these parameters are as
follows:
CA = Site specific value
IR = 0.6 m3/hour (all age groups)
ET = 0.2 hours/day ( one 12 minute shower)
EF = 365 days/year
ED = 0.5 years ( subchronic ), 5 years (chronic),
BW = 16 kg (1-6 years average)
AT = 0.5 years (subchronic), 70 years (lifetime)
Based on these values, the daily intake from inhalation of contaminants in the shower
for child residents are:
DI (subchronic) = CA (mg/rn3) x 7.5E-3 (m3/kg/day)
DI (chronic) = CA (mg/m3) x 7.SE-3 (m3/kg/day)
DI (lifetime) = CA (mg/m3 x 5.4E-4 (m3/kg/day)
A:\CART\_SECT3.DAA 3 -28
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3.5.2.6 Intake From Ingestion of Contaminated Produce. Intake From
Ingestion of Contaminated Produce
Intake =
(mg/kg/day)
CF X IR X Fl X EF X ED
BWxAT
where:
CF = Contaminant Concentration in Food (mg/kg)
IR = Ingestion Rate (kg/day)
Fl = Fraction Ingested from Contaminated Source (unitless)
EF = Exposure Frequency (days/year)
ED = Exposure Duration (years)
BW = Body Weight (kg)
AT = Average Time (days)
The concentration of PCBs taken up in the plants can be calculated using a
correlation developed by Travis and Arms (Travis and Arms, 1988) between
bioconcentration factors and octanol-water partition coefficients:
Log BCF -1.588 -0.578 log Kow
where:
BCF = Concentration Factor of PCB-1260
Kow = the octanol-water partition coefficient = 8.2E+6
Based on the above equation, the bioconcentration factor for PCB-1260 for plants is
3.9E-3. The concentration in the produce can be calculated as follows:
CF= BCFx CS
Where:
A:\CAR1\SECT3.DRA 3 -29
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CS = Contaminant concentration in soil (mg/kg)
Current Adult Offsite Residents/FutureAdult Onsite Residents.For current
adult offsite and future adult onsite residents ingesting contaminated homegrown
produce,the valves of these parameters are as follows:
CF = Site-specific measured or modeled value
IR = 0.201 kg/day [7]
FI = 0.40 [7]
EF = 120 days/yr
ED = 0.5 year (subchronic), 30 years (lifetime)
BW = 70 kg (adult average)
AT = 70 years x 365 days/year
Based on these values, the daily intakes from ingestion of contaminated produce for
adult residents are:
DI (subchronic) = CS (mg/kg) x BCF x 2.7E-6 (kg/kg day)
DI (lifetime) = CS (mg/kg x BCF x l.6E-4 (kg/kg day)
Current Child Offsite Residents/Future Child Onsite Residents.For current
child offsite and future child onsite residents ingesting contaminated homegrown
produce, the values of these parameters are as follows:
CF = Site-specific measured or modeled value
IR = 0.201 kg/day [7]
FI = 0.40 [7]
EF = 120 days/yr
ED = 0.5 year (subchronic), 5 years ( child)
BW = 16 kg (1-6 years average)
AT = 70 years x 365 days/year
A:\CART\SECT3.DPA 3 -30
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Based on these values, the daily intakes from ingestion of contaminated produce for
child residents are:
DI (subchronic) = CS (mg/kg) x BCF x l.2E-5 (kg/kg day)
DI (child) = CS (mg/kg x BCF x l.2E-4 (kg/kg day)
3.5.3. Results
Based on the previous equations, average daily intakes were calculated using the
exposure point concentrations from Table 3-4. Average daily intake values will be
used to calculate noncarcinogenic and carcinogenic risk values. A summary of results
of these calculations are presented on Tables 3-6, 3-7 and 3-8.
3.5.4 Uncertainties in Exposure Assessment
The estimated average daily exposure levels to chemical contaminants at Carolina
Transformer were generated with a number of uncertainties. These uncertainties are
generally inherent in risk assessments associated with remedial investigations
particularly because of the type of and amount of data that can be collected in the
short durations of sampling episodes. The most important of these uncertainties are
summarized in this section as follows:
• Although current exposure levels are based on measured concentrations in
the media of concern, these values are uncertain due to limited sampling and
analytical variation. To account for this, the upper 95th percentile confi-
dence limit of the mean concentration values were used in dose calculations.
This is likely to result in an overestimation of the actual average dose.
• Although site-specific contaminants are expected to be confined to the
shallow aquifer, the samples and sample locations in the deep aquifer may
not adequately characterize water quality in that aquifer. Based on the
available data, the deep aquifer was deleted from this risk assessment.
However, additional characterization of the water quality in the deep aquifer
downgradient of the site is necessary to adequately assess whether the deep
aquifer has been impacted by the site.
A:\CART\SECT3.DRA 3 -31
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I TABLE 3-6
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
I CURRENT LAND USE
Average Daily Intake
(mg/kg/day)
I Population Exposure Pathwal Chemical Chronic Lifetime
Adult Onsite Ingestion ol Onsile Barium 4.6E-08 2.0E-08
Trespassers Soll Cadmium 3.SE-09 1.SE-09
Cobalt 8.0E-10 3.SE-10
I Chromium 1.4E-08 6.2E-09
Copper 2.1E-06 9.1E-07
Lead 1.3E-07 5.5E-08
I Zinc 1.1E-07 4.8E-08
Manganese 1.2E-06 5.3E-07
1,2,4-Trichlorobenzene 4.0E-12 1.BE-12
Tetrachloroethene 8.0E-13 3.5E-13
I Toluene 9.9E-12 4.3E-12
Trichloroelhene 3.2E-12 1.4E-12
Benzene 4.0E-12 1.8E-12
I Chlorobenzene 4.0E-12 1.BE-12
PCB-1254 (Aroclor 1254) 7.?E-08 3.4E-08
PCB-1260 (Aroclor 1260) 1.0E-06 4.6E-07
Dioxins Furans 1.2E-12 5.3E-13
I Dermal Contact with Barium 7.0E-07 2.9E-07
Onsite Soll Cadmium 5.3E-08 2.2E-08
I Cobalt 1.2E-08 5.0E-09
Chromium 2.1 E-07 8.9E-08
Copper 3.1 E-05 1.3E-05
I Lead 1.9E-06 7.9E-07
Zinc 1.?E-06 6.9E-07
Manganese 1.8E-05 7.6E-06
1,2,4-Trlchlorobenzene 6.0E-10 2.5E-10
I Tetrachloroethene 3.0E-10 1.3E-10
Toluene 3.?E-09 1.5E-09
Trichloroethane 1.2E-09 5.0E-10
I Benzene 1.5E-09 6.3E-10
Chlorobenzene 1.5E-09 6.3E-10
PCB-1254 (Aroclor 1254) 1.2E-05 4.SE-06
PCB-1260 (Aroclor 1260) 1.6E-04 6.5E-05
I Dioxins/Fu rans 1.SE-10 7.5E-11
Dermal Contact with Barium 1.3E-06 5.6E-07
I Onslte Sediment Cadmium 4.6E-08 1.9E-08
Cobalt 9.8E-08 4.1E-08
Chromium 3.SE-07 1.5E-07
Copper 6.0E-05 2.5E-05
I Nickel 1.0E-07 4.3E-08
Lead 2.3E-06 9.5E-07
Strontium 2.SE-07 1.1E-07
I Zinc 1.8E-06 7.3E-07
Aluminum 2.SE-04 1.1E-04
Yttrium 1.SE-07 6.?E-08
I Manganese 4.3E-06 1.8E-06
Vanadium 7.9E-07 3.3E-07
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I TABLE 3-6 (continued)
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
I CURRENT LAND USE
Average Daily Intake
(mg/kg/day)
Population Exposure Pathwa~ Chemical Chronic lifetime
I Dermal Contact with PCB-1254 (Aroclor 1254) 2.2E-05 9.2E-06
Onsite Sediment PCB-1248 (Aroclor 1248) 2.4E-06 9.8E-07
(continued) PCB-1260 (Aroclor 1260) 3.8E-05 1.SE-05
I Benzene 1.3E-08 5.3E-09
Toluene 5.SE-09 2.4E-09
Chlorobenzene 3.SE-08 1.SE-08
1,3-Dlchlorobenzene 3.1E-08 1.3E-08 I 1,4-Dlchlorobenzene 1.1E-07 4.4E-08
1,2-Dlchlorobenzene 1.0E-08 4.2E-09
Dloxin/furans 5.3E-11 2.2E-11
I Dermal Contact with Copper 9.2E-08 3.9E-08
Onsite Surface Water Titanium 3.8E-09 1.6E-09
I Zinc 6.1 E-08 2.SE-08
Manganese 3.SE-07 1.SE-07
PCB-1260 (Aroclor 1260) 4.8E-09 2.0E-09
Bis(2-Ethylhexyl) Phthalate 1.9E-09 8.2E-10
I Carbon Disulfide 7.3E-06 3. lE-06
Child Onsite Ingestion of Onsite Barium 4.1E-07 2.9E-08
I Trespassers Soll Cadmium 3.1E-08 2.2E-09
Cobalt 7.0E-09 5.0E-10
Chromium 1.2E-07 8.9E-09
Copper 1.8E-05 1.3E-06
I Lead 1.lE-06 7.9E-08
Zinc 9.7E-07 6.9E-08
Manganese 1.1E-05 7.6E-07
I 1,2,4-Trichlorobenzene 3.SE-11 2.SE-12
Tetrachloroethene 7.0E-12 5.0E-13
Toluene 8. 7E-11 6.2E-12
Trichloroethane 2.8E-11 2.0E-12 I Benzene 3.SE-11 2.SE-12
Chlorobenzene 3.SE-11 2.SE-12
PCB-1254 (Aroclor 1254) 6.7E-07 4.8E-08
I PCB-1260 (Aroclor 1260) 9.1E-06 6.SE-07
Dioxins Furans 1.1E-11 7.SE-13
I Dermal Contact with Barium 1.1E-06 8.1E-08
Onslte Soll Cadmium 8.SE-08 6.2E-09
Cobalt 2.0E-08 1.4E-09
Chromium 3.SE-07 2.SE-08
I Copper 5.1E-05 3.6E-06
Lead 3.1E-06 2.2E-07
Zinc 2.7E-06 1.9E-07
I Manganese 3.0E-05 2.1E-06
1,2,4-Trlchlorobenzene 9.8E-10 7.0E-11
Tetrachloroethene 4.9E-10 3.SE-11
Toluene 6.0E-09 4.3E-10
I Trichloroethane 2.0E-09 1.4E-10
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I TABLE 3-6 (continued)
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
I CURRENT LAND USE
Average Daily lnlake
(mg/kg/day)
I Population ExQosure Pathwal Chemical Chronic Lifetime
Dermal Contact with Benzene 2.4E-09 1.BE-10
Onsite Soil Chlorobenzene 2.4E-09 1.BE-10
(continued) PCB-1254 (Aroclor 1254) 1.9E-05 1.3E-06
I PCB-1260 (Aroclor 1260) 2.SE-04 1.BE-05
Dioxins/Fur ans 2.9E-10 2.1E-11
I Dermal Contact with Barium 2.2E-06 1.6E-07
Onsite Sediment Cadmium 7.4E-08 5.3E-09
Cobalt 1.6E-07 1.1E-08
Chromium 5.9E-07 4.2E-08
I Copper 9.SE-05 7.0E-06
Nickel 1.7E-07 1.2E-08
Lead 3.?E-06 2.?E-07
I Strontium 4.3E-07 3.1E-08
Zinc 2.SE-06 2.0E-07
Aluminum 4.3E-04 3.1 E-05
Yttrium 2.6E-07 1.9E-08
I Manganese 7.0E-06 5.0E-07
Vanadium 1.3E-06 9.2E-08
PCB-1254 (Aroclor 1254) 3.6E-05 2.6E-06
I PCB-1248 (Aroclor 1248) 3.SE-06 2.?E-07
PCB-1260 (Aroclor 1260) 6.2E-05 4.SE-06
Benzene 2.0E-08 1.SE-09
I Toluene 9.2E-09 6.6E-10
Chlorobenzene 5.SE-08 4.1E-09
1,3-Dichlorobenzene 5.1E-08 3.6E-09
1,4-Dichlorobenzene 1. ?E-07 1.2E-08
I 1,2-Dichlorobenzene 1.6E-08 1.2E-09
Dioxin/furans 8.6E-11 6.2E-12
I Dermal Contact with Copper 1.2E-07 8.3E-09
Onsite Surface Water Titanium 4.SE-09 3.4E-10
Zinc 7.7E-08 5.SE-09
Manganese 4.4E-07 3.2E-08
I PCB-1260 (Aroclor 1260) 6.0E-09 4.3E-10
Bis(2-Ethylhexyl) Phthalate 2.4E-09 1.7E-10
Carbon Disulfide 9.2E-06 6.6E-07
I Adult Offslte Ingestion of Soll Arsenic 1.7E-08 7.3E-09
Resident Barium 5.7E-07 2.4E-07
Coball 2.2E-08 9.2E-09
I Chromium 7.2E-08 3.1E-08
Copper 3.1E-07 1.3E-07
Lead 2.6E-07 1.1E-07
I Strontium 1.1E-07 4.6E-08
Titanium 2.3E-06 9.9E-07
Yttrium 5.7E-08 2.4E-08
I Zinc 4.SE-07 1.9E-07
Manganese 2.2E-06 9.2E-07
I
I
I TABLE 3-6 (continued)
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
I CURRENT LAND USE
Average Daily Intake
(mg/kg/day)
I Population Exposure Pathwa~ Chemical Chronic Lifetime
Ingestion of Soil Mercury 6.9E-10 3.0E-10
(continued) PCB-1260 (Aroclor 1260) 2.BE-07 1.2E-07
Trichloroethane 1.2E-10 5.3E-11
I Toluene 1.1E-10 4.6E-11
1,4-Dlchlorobenzene 3.4E-10 1.SE-10
1,2-Dlchlorobenzene 1.7E-10 7.3E-11
I Dioxin/furans 5.3E-13 2.3E-13
Dermal Contact with Arsenic 6.4E-08 2.9E-08
Off site Soll Barium 2.1 E-06 9.6E-07
I Cobalt 8.1 E-08 3.6E-08
Chromium 2.7E-07 1.2E-07
Copper 1.2E-06 5.2E-07
I Lead 9.9E-07 4.4E-07
Strontium 4.1 E-07 1.BE-07
Titanium 8.7E-06 3.9E-06
Yttrium 2.1 E-07 9.6E-08
I Zinc 1.7E-06 7.7E-07
Manganese 8.1E-06 3.6E-06
Mercury 2.6E-09 1.2E-09
I PCB-1260 (Aroclor 1260) 1.1E-05 4.BE-06
Trichloroethane 1.2E-08 5.2E-09
Toluene 1.0E-08 4.6E-09
1,4-Dichlorobenzene 1.3E-08 5.7E-09
I 1,2-Dichlorobenzene 6.4E-09 2.9E-09
Dloxin/furans 2.0E-11 9.0E-12
I Dermal Contact with Barium 4.1 E-06 1.BE-06
Off site Sediment Cadmium 1.1E-07 5.1 E-08
Cobalt 1.7E-07 7.7E-08
I Chromium 8.4E-07 3.BE-07
Copper 1.5E-05 6.5E-06
Nickel 2.3E-07 1.0E-07
Lead 3.5E-06 1.6E-06
I Strontium 4.4E-08 2.0E-08
Zinc 6.4E-06 2.9E-06
Aluminum 9.0E-04 4.0E-04
I Yttrium 2.5E-07 1.1 E-07
Manganese 3.SE-06 1.SE-06
Vanadium 1.SE-06 6.SE-07
PCB-1254 (Aroclor 1254) 7.3E-10 3.3E-10
I PCB-1248 (Aroclor 1248) 5.2E-08 2.3E-08
PCB-1260 (Aroclor 1260) 6.4E-05 2.9E-05
Benzene 1.BE-09 8.1E-10
I Toluene 1.SE-06 7.2E-07
Chlorobenzene 1.BE-09 8.1E-10
1,3-Dichlorobenzene 1.5E-09 6.SE-10
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I
I TABLE 3-6 (continued)
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
I CURRENT LAND USE
Average Daily lnlake
(mg/kg/day)
I Population Exposure Pathwal Chemical Chronic Lifetime
Dermal Contact with 1,4-Dichlorobenzene 1.SE-09 6.SE-10
Offsite Sediment 1,2-Dichlorobenzene 1.SE-09 6.SE-10
(continued) Dioxins/furans 4.6E-11 2.1E-11
I Dermal Contact with Copper 8.4E-08 3.6E-08
Off site Surface Water ntanium 9.2E-09 3.9E-09
I (Wading) Zinc 1.2E-07 5.2E-08
Manganese 3.8E-07 1.6E-07
PCB-1260 (Aroclor 1260) 7.7E-09 3.3E-09
I Bis(2-Ethylhexyl) Phthalate 5.9E-08 2.SE-08
Carbon Disulfide 1.SE-06 6.3E-07
Ingestion of Produce PCB-1260 (Aroclor 1260) 3.9E-07 2.3E-05
I 1,2-Dichlorobenzene 2.SE-08 1.SE-06
1,4-Dichlorobenzene 5.2E-08 3.1 E-06
I Child Offsite Ingestion of Soil Arsenic 2.4E-07 1.8E-08
Resident Barium 8.1E-06 6.0E-07
Cobalt 3.1E-07 2.3E-08
Chromium 1.0E-06 7.6E-08
I Copper 4.4E-06 3.2E-07
Lead 3.7E-06 2.8E-07
Strontium 1.SE-06 1.1E-07
I ntanium 3.3E-05 2.4E-06
Yttrium 8.1E-07 6.0E-08
Zinc 6.SE-06 4.SE-07
Manganese 3.1E-05 2.3E-06
I Mercury 9.9E-09 7.3E-10
PCB-1260 (Aroclor 1260) 4.1E-06 3.0E-07
Trichloroethane 1.8E-09 1.3E-10
I Toluene 1.SE-09 1.1E-10
1,4-Dichlorobenzene 4.SE-09 3.6E-10
1,2-Dichlorobenzene 2.4E-09 1.8E-10
Dioxin/furans 7.6E-12 5.6E-13
I Dermal Contact with Arsenic 1.7E-07 1.2E-08
Offslte Soll Barium 5.SE-06 4.1E-07
I Cobalt 2.2E-07 1.6E-08
Chromium 7.3E-07 5.3E-08
Copper 3.1E-06 2.2E-07
Lead 2.7E-06 1.9E-07
I Strontium 1.1E-06 7.BE-08
ntanium 2.3E-05 1.7E-06
Yttrium 5.BE-07 4.1E-08
I Zinc 4.6E-06 3.3E-07
Manganese 2.2E-05 1.6E-06
Mercury 7.0E-09 5.0E-10
I PCB-1260 (Aroclor 1260) 2.9E-05 2.1E-06
I
I
I TABLE 3-6 (continued)
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
I CURRENT LAND USE
Average Daily Intake
(mg/kg/day)
I Population Exposure Pathwal Chemical Chronic Lifetime
Dermal Contact with Trichloroethene 3. lE-08 2.2E-09
Off site Soll Toluene 2.7E-08 2.0E-09
(continued) 1,4-Dichlorobenzene 3.4E-08 2.5E-09
I 1,2-Dichlorobenzene 1.7E-08 1.2E-09
Dioxin/furans 5.4E-11 3.9E-12
I Dermal Contact with Barium 1.1E-05 7.8E-07
Off site Sediment Cadmium 3.0E-07 2.2E-08
Cobalt 4.6E-07 3.3E-08
Chromium 2.3E-06 1.6E-07
I Copper 3.9E-05 2.8E-06
Nickel 6.2E-07 4.4E-08
Lead 9.4E-06 6.?E-07
I Strontium 1.2E-07 8.4E-09
Zinc 1. 7E-05 1.2E-06
Aluminum 2.4E-03 1.?E-04
Yttrium · 6.?E-07 4.8E-08
I Manganese 9.4E-06 6.?E-07
Vanadium 4.0E-06 2.9E-07
PCB-1254 (Aroclor 1254) 2.0E-09 1.4E-10
I PCB-1248 (Aroclor 1248) 1.4E-07 1.0E-08
PCB-1260 (Aroclor 1260) 1.7E-04 1.2E-OS
Benzene 4.9E-09 3.SE-10
I Toluene 4.3E-06 3. lE-07
Chlorobenzene 4.9E-09 3.SE-10
1,3-Dichlorobenzene 3.9E-09 2.8E-10
1,4-Dichlorobenzene 3.9E-09 2.8E-10
I 1,2-Dichlorobenzene 3.9E-09 2.8E-10
Oioxins/furans 1.2E-10 9.0E-12
I Dermal Contact with Copper 1.lE-07 4.5E-08
Off site Surface Water Titanium 1.2E-08 4.9E-09
(Wading) Zinc 1.SE-07 6.SE-08
Manganese 4.8E-07 2.0E-07
I PCB-1260 (Aroclor 1260) 9.6E-09 4.1E-09
Bis(2-Ethylhexyl) Phthafate 7.4E-08 3.1E-08
Carbon Disulfide 1.8E-06 7.9E-07
I Ingestion of Produce PCB-1260 (Aroclor 1260) 1.7E-06 1.7E-OS
1,2-Dlchlorobenzene 1.1E-07 1.lE-06
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1,4-Dlchlorobenzene 23E-07 2.3E-06
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I
I TABLE 3-7
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
I FUTURE LAND USE
Average Dally Intake
(mg/kg/day)
Population Exposure Pathwa~ Chemical Chronic Liletime
I Adult Onsite Ingestion of Onsite Barium 2.9E-05 1.3E-05
Resident Soil Cadmium 2.2E-06 9.7E-07
Cobalt 5.0E-07 2.2E-07
I Chromium 8.9E-06 3.9E-06
Copper 1.3E-03 5.7E-04
Lead 7.9E-05 3.SE-05
I Zinc 6.9E-05 3.0E-05
Manganese 7.6E-04 3.3E-04
1,2,4-Trlchlorobenzene 2.5E-09 1.1E-09
Tetrachloroethene 5.0E-10 2.2E-10
I Toluene 6.2E-09 2.7E-09
Trichloroethene 2.0E-09 8.BE-10
Benzene 2.5E-09 1.1E-09
I Chlorobenzene 2.5E-09 1.1E-09
PCB-1254 (Aroclor 1254) 4.BE-05 2.1 E-05
PCB-1260 (Aroclor 1260) 6.5E-04 2.9E-04
Dioxin/furans 7.5E-10 3.3E-10
I Dermal Contact with Barium 5.2E-05 2.2E-05
Onsite Soil Cadmium 4.0E-06 1.7E-06
I Cobalt 9.0E-07 3.9E-07
Chromium 1.6E-05 6.9E-06
Copper 2.3E-03 1.0E-03
Lead 1.4E-04 6.1 E-05
I Zinc 1.2E-04 5.3E-05
Manganese 1.4E-03 5.9E-04
1,2,4-Trichlorobenzene 4.5E-09 1.9E-09
I Tetrachloroelhene 9.0E-10 3.9E-10
Toluene 1.lE-08 4.BE-09
Trichloroethane 3.6E-09 1.5E-09
I Benzene 4.5E-08 1.9E-08
Ch lorobenzene 1.1E-07 4.8E-08
PCB-1254 (Aroclor 1254) 2.2E-03 9.2E-04
PCB-1260 (Aroclor 1260) 1.2E-02 5.0E-03
I Dioxln/furans 1.4E-08 5.8E-09
Dermal Contact with Barium 4.1E-06 1.8E-06
I Offslte Sediment Cadmium 1.1E-07 5.1 E-08
Cobalt 1.7E-07 7.7E-08
Chromium 8.4E-07 3.8E-07
Copper 1.SE-05 6.5E-06
I Nickel 2.3E-07 1.0E-07
Lead 3.SE-06 1.6E-06
Strontium 4.4E-08 2.0E-08
I Zinc 6.4E-06 2.9E-06
Aluminum 9.0E-04 4.0E-04
Yttrium 2.SE-07 1.1E-07
Manganese 3.5E-06 1.6E-06
I Vanadium 1.SE-06 6.6E-07
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I TABLE 3-7 (continued)
EXPOSURE ASSESSMENT RESULTS-DAILY INTAKES
I FUTURE LAND USE
Average Daily Intake
(mg/kg/day)
I Population Exposure Pathwa~ Chemical Chronic Lifetime
Dermal Contact with PCB-1254 (Aroclor 1254) 7.3E-10 3.3E-10
Off site Sediment PCB-1248 (Aroclor 1248) 5.2E-08 2.3E-08
(continued) PCB-1260 (Aroclor 1260) 6.4E-05 2.9E-05
I Benzene 1.8E-09 8.1E-10
Toluene 1.6E-06 7.2E-07
Chlorobenzene 1.BE-09 8.1E-10
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1,3-Dlchlorobenzene 1.SE-09 6.SE-10
1,4-Dichlorobenzene 1.SE-09 6.SE-10
1,2-Dlchlorobenzene 1.SE-09 6.SE-10
Dloxlns/furans 4.6E-11 2.1E-11
I Ingestion of Onsite Barium 4.9E-01 2.0E-01
Groundwater Cobalt 2.1 E-02 8.9E-03
I Chromium 8.1 E-02 3.4E-02
Copper 8.4E-02 3.SE-02
Nickel 3.SE-02 1.4E-02
Strontium 4.6E-02 1.9E-02
I Titanium 1.9E-01 7.BE-02
Vanadium 1.SE-01 6.4E-02
Yttrium 4.4E-02 1.8E-02
I Zinc 1.1E-01 4.6E-02
Aluminum 9.9E+01 4.1 E+01
Manganese 7.0E-01 2.9E-01
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Mercury 8.7E-06 3.6E-06
PCB-1260 (Aroclor 1260) 1.SE-03 6.1E-04
Bis(2-Ethylhexyl) Phthalate 2.4E-02 9.BE-03
1,2,4-Trlchlorobenzene 4.4E-05 1.BE-05
I Methyl Ethyl Ketone 2.2E-04 9.1E-05
Toluene 1.6E-04 6.6E-05
Carbon Disulfide 3.2E-04 1.3E-04
I Benzene 1.1 E-04 4.4E-05
Chlorobenzene 5.2E-04 2.2E-04
1,3-Dlchlorobenzene 2.7E-04 1.1E-04
1,4-Dlchlorobenzene 1.1E-03 4.4E-04
I Dermal Contact with Barium 7.1E-04 3.0E-04
Onsile Groundwater Cobalt 3.1E-05 1.3E-05
I (Showers) Chromium 1.2E-04 4.9E-05
Copper 1.2E-04 5.1 E-05
Nickel 5.0E-05 2.1 E-05
Strontium 6.7E-05 2.8E-05
I Titanium 2.7E-04 1.1E-04
Vanadium 2.2E-04 9.3E-05
Yttrium 6.2E-05 2.6E-05
I Zinc 1.6E-04 6.7E-05
Aluminum 1.3E-03 5.4E-04
Manganese 1.0E-03 4.2E-04
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Mercury 1.2E-08 5.3E-09
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POQUlation
TABLE 3-7 (continued)
EXPOSURE ASSESSMENT RESULTS-OAILY INTAKES
FUTURE LAND USE
Average Daily Intake
(mg/kg/day)
B<Qosure Pathwar Chemical Chronic Lifetime
Dermal Contact with PCB-1260 (Aroclor 1260) 2.1 E-06 9.0E-07
Onsite Groundwater Bis(2-Ethylhexyl) Phthalate 3.4E-05 1.4E-05
(Showers)(continued) 1,2,4-Trlchlorobenzene 6.2E-08 2.6E-08
Methyl Ethyl Ketone 2.0E-03 8.4E-04
Toluene 2.6E-07 1.1E-07
Carbon Disulfide 3.1E-05 1.3E-05
Benzene 7.9E-05 3.3E-05
Chlorobenzene 7.SE-07 3.2E-07
1,3-Dichlorobenzene 3.9E-07 1.6E-07
1,4-Dlchlorobenzene 1.SE-06 6.SE-07
Dermal Contact with Copper 8.4E-08 3.6E-08
Off site Surface Water Titanium 9.2E-09 3.9E-09
(Wading) Zinc 1.2E-07 5.2E-08
Manganese 3.8E-07 1.6E-07
PCB-1260 (Aroclor 1260) 7. 7E-09 3.3E-09
Bis(2-Ethylhexyl) Phthalate 5.9E-08 2.SE-08
Carbon Disulfide 1.SE-06 6.3E-07
Inhalation of Onsite PCB-1260 (Aroclor 1260) 7.4E-04 3.1 E-04
Groundwater (Shower) Bis(2-Ethylhexyt) Phthalate 1.2E-02 4.9E-03
1,2,4-Trichlorobenzene 2.2E-05 9.0E-06
Methyl Ethyl Ketone 2.2E-04 9.1 E-05
Toluene 1.6E-04 6.6E-05
Carbon Disulfide 3.2E-04 1.3E-04
Benzene 1.1E-04 4.4E-05
Chlorobenzene 5.2E-04 2.2E-04
1,3-Dichlorobenzene 2.7E-04 1.1E-04
1,4-Dichlorobenzene 1.1E-03 4.4E-04
Ingestion of Produce PCB-1260 (Aroclor 1260) 6.8E-06 4.1E-04
I
I TABLE 3-7 (continued)
EXPOSURE ASSESSMENT RESULTS-DAILY INTAKES
I FUTURE LAND USE
Average Dally lnlake
(mg/kg/day)
Population Exposure Pathwa~ Chemical Chronic Liletime
I Child Onsite Ingestion ol Onsite Barium 2.?E-04 1.9E-05
Resident Soll Cadmium 2.1E-05 1.5E-06
Cobalt 4.7E-06 3.4E-07
I Chromium 8.4E-05 6.0E-06
Copper 1.2E-02 8.7E-04
Lead 7.4E-04 5.3E-05
Zinc 6.5E-04 4.6E-05
I Manganese 7.1E-03 5.1 E-04
1,2,4-Trlchlorobenzene 2.4E-08 1.?E-09
Tetrachloroethene 4.?E-09 3.4E-10
I Toluene 5.SE-08 4.2E-09
Trichloroethane 1.9E-08 1.3E-09
Benzene 2.4E-08 1. ?E-09
I
Chlorobenzene 2.4E-08 1. 7E-09
PCB-1254 (Aroclor 1254) 4.SE-04 3.2E-05
PCB-1260 (Aroclor 1260) 6.1E-03 4.4E-04
Dioxin/lurans 7.1E-09 5.0E-10
I Dermal Contact with Barium 8.4E-05 5.SE-06
Onsite Soil Cadmium 6.4E-06 4.4E-07
I Cobalt 1.SE-06 1.0E-07
Chromium 2.6E-05 1.SE-06
Copper 3.BE-03 2.6E-04
Lead 2.3E-04 1.6E-05
I Zinc 2.0E-04 1.4E-05
Manganese 2.2E-03 1.5E-04
1,2,4-Trichlorobenzene 7.3E-09 5.0E-10
I T etrachloroelhene 1.SE-09 1.0E-10
Toluene 1.BE-08 1.2E-09
Trichloroethane 5.SE-09 4.0E-10
Benzene 7.3E-08 5.0E-09
I Chlorobenzene 1.SE-07 1 .3E-08
PCB-1254 (Aroclor 1254) 3.SE-03 2.4E-04
PCB-1260 (Aroclor 1260) 1.9E-02 1.3E-03
I Dloxln/furans 2.2E-08 1.SE-09
Dermal Contact with Barium 4.4E-06 3.1E-07
Off site Sediment Cadmium 1.SE-07 1.1E-08
I Cobalt 3.2E-07 2.3E-08
Chromium 1.2E-06 8.4E-08
Copper 2.0E-04 1.4E-05
I Nickel 3.4E-07 2.4E-08
Lead 7.4E-06 5.3E-07
Strontium 8.6E-07 6.2E-08
Zinc 5.7E-06 4.1E-07
I Aluminum 8.6E-04 6.2E-05
Yttrium 5.2E-07 3.SE-08
Manganese 1.4E-05 1.0E-06
I Vanadium 2.6E-06 1.SE-07
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I TABLE 3-7 (conilnued)
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
I FUTURE LAND USE
Average Daily Intake
(mg/kg/day)
I Population Exposure Palhwal Chemical Chronic Lifetime
Dermal Contact wilh PCB-1254 (Aroclor 1254) 7.2E-0S S.2E-06
Offsite Sediment PCB-1248 (Aroclor 1248) 7.6E-06 S.SE-07
(continued) PCB-1260 (Aroclor 1260) 1.2E-04 9.0E-06
I Benzene 4.1 E-08 2.9E-09
Toluene 1.SE-08 1.3E-09
Chforobenzene 1.2E-07 8.3E-09
I 1,3-Dichlorobenzene 1.0E-07 7.3E-09
1,4-Dichlorobenzene 3.4E-07 2.SE-08
1,2-Dlchlorobenzene 3.3E-08 2.4E-09
Dloxlns/furans 1.7E-10 1.2E-11
I Ingestion of Onsite Barium 1.SE+0O 1.1E-01
Groundwater Cobalt 6.SE-02 4.7E-03
I Chromium 2.SE-01 1.SE-02
Copper 2.6E-01 1.SE-02
Nickel 1.1E-01 7.6E-03
Strontium 1.4E-01 1.0E-02
I Titanium S. 7E-01 4.1E-02
Vanadium 4. 7E-01 3.3E-02
Yttrium 1.3E-01 9.SE-03
I Zinc 3.3E-01 2.4E-02
Aluminum 3.0E+02 2.1 E+01
Manganese 2.1E+OO 1.SE-01
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Mercury 2.6E-0S 1.9E-06
PCB-1260 (Aroclor 1260) 4.SE-03 3.2E-04
Bis(2-Ethylhexyl) Phthalate 7.2E-02 5.2E-03
1,2.4-Trichlorobenzene 1.3E-04 9.SE-06
I Methyl Ethyl Ketone 6.7E-04 4.SE-05
Toluene 4.SE-04 3.SE-05
Carbon Disulfide 9.7E-04 6.9E-OS
I Benzene 3.3E-04 2.3E-05
Chlorobenzene 1.6E-03 1.1E-04
1,3-Dlchlorobenzene 8.2E-04 5.9E-OS
1 .4-Dichlorobenzene 3.3E-03 2.3E-04
I Dermal Contact with Barium 2.2E-03 1.6E-04
Onslte Groundwater Cobalt 9.SE-05 7.1E-06
I (Showers) Chromium 3.6E-04 2.7E-OS
Copper 3.7E-04 2.SE-05
Nickel 1.SE-04 1.2E-OS
Strontium 2.0E-04 1.SE-05
I Titanium 8.3E-04 6.2E-OS
Vanadium 6.SE-04 5.1 E-05
Yttrium 1.9E-04 1.4E-05
I Zinc 4.9E-04 3.6E-OS
Aluminum 3.9E-03 2.9E-04
Manganese 3.1E-03 2.3E-04
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Mercury 3.SE-08 2.9E-09
PCB-1260 (Aroclor 1260) 6.SE-06 4.9E-07
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PoQulation
TABLE 3-7 (continued}
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
FUTURE LAND USE
Average Daily Intake
(mg/kg/day}
Exeosure Pathwa~ Chemical Chronic Lifetime
Dermal Contact with Bls(2-Elhylhexyl} Phthalate 1.0E-04 7.9E-06
Onsite Groundwater 1,2,4-Trichlorobenzene 1.9E-07 1.4E-08
(ShowersXcontinued} Methyl Ethyl Ketone 6.lE-03 4.SE-04
Toluene 7.9E-07 5.9E-08
Carbon Disulfide 9.7E-05 7.3E-06
Benzene 2.4E-04 1.8E-05
Chlorobenzene 2.3E-06 1.7E-07
1,3-Dichlorobenzene 1.2E-06 8.9E-08
1,4-Dlchlorobenzene 4.7E-06 3.SE-07
Dermal Contact with Copper 1.1E-07 4.5E-08
Off site Surface Water ntanlum 1.2E-08 4.9E-09
(Wading} Zinc 1.5E-07 6.5E-08
Manganese 4.8E-07 2.0E-07
PCB-1260 (Aroclor 1260) 9.SE-09 4.1 E-09
Bis(2-Ethylhexyl} Phthalate 7.4E-08 3.1E-08
Carbon Disulfide 1.BE-06 7.9E-07
Inhalation of Onsite PCB-1260 (Aroclor 1260) 3.3E-03 2.3E-04
Groundwater (Shower} Bis(2-Ethylhexyl} Phlhalate 5.3E-02 3.6E-03
1,2,4-Trichlorobenzene 9.BE-05 6.7E-06
Methyl Ethyl Ketone 9.9E-04 6.BE-05
Toluene 7.2E-04 4.9E-05
Carbon Disulfide 1.4E-03 9.8E-05
Benzene 4.BE-04 3.3E-05
Chlorobenzene 2.3E-03 1.6E-04
1,3-Dichlorobenzene 1.2E-03 8.3E-05
1,4-Dlchlorobenzene 4.BE-03 3.3E-04
Ingestion of Produce PCB-1260 {Aroclor 1260) 3.0E-05 3.0E-04
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PoQulatlon
Adult Onslte
Resident
TABLE 3-8
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
FUTURE LAND USE -WELL NO. 44
Average Dally Intake
(mg/kg/day)
B<Qosure Pathwa~ Chemical Chronic Lifetime
Ingestion of Well Barium 5.5E-01 2.3E-01
No. 44 Groundwater Cobalt 1.9E-02 8.0E-03
Chromium 8.4E-02 3.SE-02
Copper 8.7E-02 3.6E-02
Nickel 3.5E-02 1.4E-02
Strontium 4. lE-02 1.7E-02
Vanadium 1.4E-01 S.9E-02
Yttrium 4.4E-02 1.SE-02
Zinc 1.0E-01 4.2E-02
Aluminum 9.0E+01 3.7E+01
Manganese 2.6E-01 1.lE-01
PCB-1260 (Aroclor 1260) 1.SE-03 6.2E-04
Carbon Disulfide 1.9E-04 8.0E-05
Benzene 8. lE-05 3.4E-05
Chlorobenzene 5.SE-04 2.4E-04
Dermal Contact With Barium 7.9E-04 3.3E-04
No. 44 Groundwater Cobalt 2.SE-05 1.2E-05
(ShOwers) Chromium 1.2E-04 5.1 E-05
Copper 1.2E-04 5.3E-05
Nickel 5.0E-05 2.1E-05
Strontium S.SE-05 2.SE-05
Vanadium 2.0E-04 8.6E-05
Yttrium 6.2E-05 2.6E-05
Zinc 1.SE-04 6.2E-05
Aluminum 1.2E-03 4.9E-04
Manganese 3.?E-04 1 .6E-04
PCB-1260 (Aroclor 1260) 2.2E-06 9.2E-07
Carbon Disulfide 1.9E-05 8.1E-06
Benzene 6.0E-05 2.5E-05
Chlorobenzene 8.3E-07 3.SE-07
Inhalation of PCB-1260 (Aroclor 1260) 7.SE-01 3.1E-01
No. 44 Groundwater Carbon Disulfide 1.9E-01 8.0E-02
(Showers) Benzene 8. lE-02 3.4E-02
Chlorobenzene 5.SE-01 2.4E-01
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Child Onslte
Resident
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TABLE 3-8 (continued)
EXPOSURE ASSESSMENT RESULTS -DAILY INTAKES
FUTURE LAND USE -WELL NO. 44
Exposure Pathway
Ingestion of Well
No. 44 Groundwater
Dermal Contact With
No. 44 Groundwater
(Showers)
Inhalation of
No. 44 Groundwater
(Showers)
Chemical
Barium
Cobalt
Chromium
Copper
Nickel
Strontium
Vanadium
Yttrium
Zinc
Aluminum
Manganese
PCB-1260 (Aroclor 1260)
Carbon Disulfide
Benzene
Chlorobenzene
Barium
Cobalt
Chromium
Copper
Nickel
Strontium
Vanadium
Yttrium
Zinc
Aluminum
Manganese
PCB-1260 (Aroclor 1260)
Carbon Disulfide
Benzene
Chlorobenzene
PCB-1260 (Aroclor 1260)
Carbon Disulfide
Benzene
Chlorobenzene
Average Dally Intake
(mg/kg/day)
Chronic
1.7E+OO
5.9E-02
2.6E-01
2.6E-01
1.lE-01
1.2E-01
4.3E-01
1.3E-01
3.1E-01
2.7E+02
7.SE-01
4.6E-03
5.9E-04
2.SE-04
1.SE-03
2.4E-03
8.6E-05
3.?E-04
3.SE-04
1.SE-04
1.SE-04
6.3E-04
1.9E-04
4.SE-04
3.6E-03
1.1E-03
6.?E-06
5.9E-05
1.SE-04
2.6E-06
3.4E+00
8. 7E-01
3.6E-01
2.6E+00
Lifetime
1.2E-01
4.2E-03
1.SE-02
1.9E-02
7.6E-03
8.SE-03
3. lE-02
9.SE-03
2.2E-02
2.0E+0l
5.6E-02
3.3E-04
4.2E-05
1.BE-05
1.3E-04
1.SE-04
6.4E-06
2.SE-05
2.9E-05
1.2E-05
1.3E-05
4.?E-05
1.4E-05
3.4E-05
2.?E-04
8.SE-05
5.0E-07
4.4E-06
1.4E-05
1.9E-07
2.3E-01
6.0E-02
2.SE-02
1.BE-01
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• Contaminant concentrations that could occur under the future land use
scenario are highly uncertain. Contaminant concentrations in the soil were
determined to a depth of one foot below ground surface; however, samples
were not obtained from the deeper soil. It was assumed that the highest soil
contaminant concentrations occur in the surficial soils. It is uncertain
whether this will result in an overestimation or underestimation of actual
dose during periods of excavation.
• Contaminant concentrations in groundwater for future use was assumed to
be the same as currently onsite, with no adjustment due to dilution,
biodegradation, or volatilization. This will result in an overestimation of
dose.
• For chronic and lifetime exposures, the simplifying assumption has been
made that all concentration values will remain constant. This is likely to
results in an overestimation of chronic or lifetime exposure for the volatile
organic compounds since these are expected to be biologically broken down
or volatizile relatively quickly. It is also likely to lead to an overestimation
of semivolatile exposure, even though semivolatiles undergo slower biological
breakdown in soil and are less volatile in nature. For metals, these factors
are not expected to have much of an effect on the exposure calculations, as
they are typically persistent in soils.
• Dermal uptake of chemicals from soil is especially difficult to estimate, since
this is dependent on both the characteristics of the specific chemical and the
soil. The values of absorbance employed to estimate dermal uptake are
highly uncertain, and are almost certainly conservative, leading to an
overestimation of dose.
• The permeability constants employed in the derivation of dermal uptake in
water are not available for all chemicals identified as chemicals of concern.
The assumption that all metals and unavailable organic compounds have the
same PC as water is a simplifying assumption, and it is not known whether
it overestimates or underestimates dose.
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• When deriving concentrations of chemicals, all chemicals that are not
detected are assumed to be at one-half the detection limit. Whether this
assumption results in an overestimation or an underestimation of actual dose
is uncertain.
o When evaluating exposure via ingestion of contaminated fish, it was assumed
that contaminant concentrations (PCB) in the Cape Fear River were
negligible. However, water samples and/or tissue cultures from fish should
be collected from the Cape Fear River to adequately assess potential
exposure via ingestion of contaminated fish.
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4.0 TOXICITY ASSESSMENT
The purpose of the toxicity assessment is to evaluate available information regarding
the potential for particular chemical contaminants to cause adverse effects in exposed
populations, and to provide an estimate of the relationship between the extent of
exposure to a contaminant and the increased likelihood or severity of adverse effects.
Appendix A provides a summary of important information on the chemicals of
potential concern at the Carolina Transformer Site. The toxicity assessment is
intended to provide an overview of key observations and issues on the toxicity of each
of the chemicals of potential concern.
4.1 Summary of Critical Toxicity Values
Health risks for chemicals exhibiting noncarcinogenic effects are evaluated using
reference doses (RfDs) developed by the EPA's RID work group, or obtained from
Health Effects Assessments (HEAs). The RID is an estimate of the daily exposure
to the human population that is likely to be without an appreciable risk of deleterious
effects during a lifetime. RfDs are expressed in units of mg/kg/day and include
exposure to sensitive subpopulations within their derivation. The Rills are usually
derived from human studies involving workplace exposures or from animal studies.
They are adjusted using uncertainty factors to account for unknown interpolations
from the available studies and data. The RID is a reference point for comparison
of chemical intakes.
Health risks for chemicals exhibiting carcinogenic effects are evaluated using slope
factors (SFs) developed by the Carcinogen Assessment Group of EPA, which
estimate the upper bound excess lifetime cancer risk associated with lifetime exposure
to potential human carcinogens. Excess cancer risk is calculated based on the
average daily intake over a lifetime and the cancer slope factor. The SF is an
estimate of a chemical's slope of the chronic dose-response curve at low doses. Since
it is generally not possible to measure this slope directly, it is calculated from the
chronic dose-response data at high dose levels. These calculations assume linearity
of the dose-response curve at low doses, and that it has no threshold, passing through
the origin. Although it is recognized that there are some grounds for debating these
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assumptions, this approach is currently the most appropriate means recommended
by the USEPA for estimating cancer risks in exposed humans.
The USEPA has developed a weight-of-evidence classification system for potential
carcinogens. Using this system, chemicals are classified as either Group A, Bl, B2,
C, D or E. Group A chemicals are classified as human carcinogens with sufficient
evidence from epidemiologic studies to support a causal association between human
exposure and cancer. Group Bl and B2 chemicals are classified as probable human
carcinogens. Group Bl applies to chemicals with limited evidence of carcinogenicity
in humans from epidemiologic studies, and Group B2 applies to chemicals with
inadequate evidence of carcinogenicity in humans but sufficient evidence of
carcinogenicity in animals. Group C applies to chemicals with limited evidence of
carcinogenicity in animals. Group D is not classified due to inadequate evidence of
carcinogenicity in animals, and Group E applies to chemicals which show no evidence
of carcinogenicity in humans where there is at least two adequate animal tests or both
epidemiologic and animal studies.
Table 4-1 presents oral and inhalation Rills and SFs for chemicals designated as
chemicals of potential concern for the Carolina Transformer site.
The dermal exposures at this site require dermal Rills and SFs. Since the USEPA
has not developed dermal Rills or SFs, these critical toxicity values must be derived
based on available oral RFDs and SFs. This derivation is to convert the RFDs and
SFs to absorbed dose rather than the administered dose since dermal intakes are
calculated as absorbed doses. Approximate values for dermal Rills and SFs were
derived by simple extrapolation from oral Rills and SFs. For Rills, this is done by
multiplying the oral RID value by the oral absorption fraction. For SFs, this is done
by dividing the oral SF by the oral absorption fraction. This approach has a high
level of associated uncertainty, as does any route to route extrapolation. The results
of these extrapolations are presented in Table 4-2.
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CHEMICALS
Carbon Ol&Ulflde
2-8utanooe
Trichloroethane
Benzene
Tol!achloroothene
Toluene ·
Chlorobenzene
1,3-0lchlorobonzone
1,4-0ichlorobenzene
1,2-0lchlorobonzene
1,2,4-Trlchlorobenzeno
bls(2-Ethylhexyl)Phlhalale
Aluminum
Arsenic
Barium
Cadmium
Chromium
Cobalt
Copper
Lead
Manganese
Mercury
Nickel
Strontium
Titanium
Vanadium
Yttrium
Zinc
Oleldrln
Arochlor-1016
Arochlor-1221
Arochlor-1232
Arochtor-1242
AIOchlor-1248
Arochlor-1254
Arochlor-1260
2,3,7,8-Tetra-COO
1,2,3,7 ,8-Ponta-CDO
1,2,3,4,7,8-Hexa-COO
1,2,3,4,6, 7,8-Hepta-COO
Octa-COD
2,3,7,8-Tetra.-COO
1,2,3,7,8-Ponta-CDO
1,2,3,4,7,8-Hoxa-COO
1,2,3,4,6, 7 ,8-Hepta.-COF
Ocla-CDF
NOTES:
TABLE 4-1
TOXICITY VALUES
OF\AL
SLOPE RID REFERENCE
FACTOR
1.0E--01 IRIS
5.0E--02 IRIS
1.1 E-02 7.3E-03 HEALTH ADV.
2.9E--02 IRIS
5.1 E--02 1.0E--02 HEASTnRIS
2.0E--01 IRIS
2.0E--02 IRIS
2.4E--02 HEAST
9.0E--02 IRIS
2.0E--02 HEAST
1.4E--02 2.0E--02 IRIS
2.0E+-00 1.0E--03 HEAST
7.0E--02 IRIS
5.0E--04 HEAST
5.0E--03 IRIS
1.0E--01 IRIS
3,0E-04 HEAST
2.0E--02 HEAST
7.0E--03 HEAST
2.0E-01 HEAST
1.eE+-01 5.0E--05 IRIS
7.7E+O0 IRIS
7.7E+-OO IRIS
7.7E+-OO IRIS
7.7E+-OO IRIS
7.7E+-OO IRIS
7.7E+-OO IRIS
7.7E+-OO IRIS
1.6E+-05 HEAST
6.2E+-03 IRIS
6.2E+-03 IRIS
IRIS-INTEGRATED RESEARCH INFORMATION SYSTEM. (9/00)
INHALATION
SLOPE RIO
FACTOR
9.0E--02
1.3E--02
2.BE--02
3.3E--03
5.0E--03
4.0E--02
3.0E--03
5.0E+-01
1.0E-04
6.1 E+-00
4.1 E+01
3.0E--04
1.6E+-01
1.SE+-05
6.2E+-03
6.2E+-03
HEAST-HEALTH EFFECTS ASSESSMENT SUMMARY TABLES (3RD QUARTER, FY 1990)
RIO -REFERENCE DOSE
CT/SECT4
9/20/90
REFERENCE
HEAST
IRIS
IRIS
HEAST
HEAST
HEAST
HEAST
HEAST
HEAST
HEAST
IRIS
HEAST
IRIS
HEAST
IRIS
IRIS
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I TABLE4-2
I DERIVATION OF DERMAL CRITICAL TOXICITY VALVES
ORAL DERMAL
I Absorption
Chemical RID SF Faclo[{al fl!Q(Ql SF{cl
Aluminum 0.2
I Arsenic 1E-3 2E♦0 1.0 1E-3 ---(d)
Barium 7E-2 0.2 1E-2
Cadmium 5E-4 0.2 1E-4
I Chromium VI 5E-3 0.2 1E-3
Cobalt 0.2
Copper 0.2
I Lead 0.2
Manganese 1E-1 0.2 2E-2
Mercury 3E-4 0.2 6E-5
I Nickel 2E-2 0.2 4E-3
Slronllum 0.2
Tilanlum 0.2
I Vanadium 7E-3 0.2 1E-3
Yttrium 0.2
Zinc 2E-1 0.2 4E-2
I Benzene 2.9E-2 0.8 3.6E-2
2-Bulanone (MEK) 5E-2 0.8 4E-2
Carbon Disulfide 1E-1 0.8 8E-2
I Chlorobenzene 2E-2 0.8 2E-2
1,2-Dlchlorobenzene 9E-2 0.8 7E-2
1,3-Dichlorobenzene 0.8
I 1,4-Dichlorobenzene 2.4E-2 0.8 3.0E-2
Tetrachloroelhene 1E-2 5.1E-2 0.8 8E-3 6.4E-2
Toluene 2E-1 0.8 2E-1
I 1,2,4-Trlchlorobenzene 2E-2 0.8 2E-2
Trlchloroelhene 7E-3 1.1 E-2 0.8 6E-3 1.4E-2
Bls(2-elhylhexyl)phlhalale 2E-2 1.4E-2 0.5 1E-2 2.8E-2
I PCBs 7.7E+0 0.5 1.5E+1
Dleldrin 5E-5 1.6E+1 0.5 2E-5 3.2E+1
Dloxlns/Furans (TEO) 1.5E+5 0.5 3.0E+5
I (a) Based on USEPA HEAs and ATSDR documents
(b) Dermal Rid• Oral RID X Absorption Factor
I (c) Dermal SF -Oral SF/Absorption Factor
(d) Dermal extrapolation of Arsenic Inappropriate due lo localized effects
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9/20/90
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4.2 Uncertainties in Toxicology Prediction of Health Effects
The prediction of human health consequences likely to occur following exposure to
a given dose of a chemical is imprecise due to many uncertainties in the toxicological
information available on dose-response relationships. For example, the slope factor
for evaluation of Dioxins is based on 2,3,7,8-TCDD, and the rest of the dioxins and
furans are assigned an equivalency factor to adjust them to 2,3,7,8-TCDD. The
quantity of toxicity information for the chemicals evaluated is typically limited, with
correspondingly varying degrees of uncertainty associated with the calculated toxicity
values.
Sources of uncertainty associated with the toxicity values may include (1 ]:
• Using dose-response information from effects observed at high doses to
predict the adverse health effects that may occur following exposure to the
low levels expected from human contact with the agent in the environment;
• Using dose-response information from short-term exposure studies to predict
the effects of Jong-term exposures, and vice-versa;
• Using dose-response information from animal studies to predict effects in
humans; and
• Using dose-response information from homogeneous animal populations to
predict the effects likely to be observed in the general population consisting
of individuals with a wide range of sensitivities.
Site specific uncertainties include:
• Not assessing risks for chemicals without critical toxicity values;
• Using the toxic equivalency approach for Dioxins/Furans;
• Assuming all PCBs are the same toxicologically;
A:\CART\SECT <I.ORA 4-3
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5.0 RISK CHARACTERIZATION
A detailed risk characterization is presented in this section.
5.1 Evaluation of Noncarcinogenic Risks
The risk of adverse noncarcinogenic effects from chemical exposure is expressed in
terms of the Hazard Quotient (HQ). The HQ is the ratio of the estimated dose (DI)
which a human receives to the Rill, the estimated dose below which it is unlikely for
even sensitive populations to experience adverse health effects. TI1e HQ is calculated
as follows [1 ]:
HQ= DI/Rill
Where:
HQ = Hazard Quotient (unitless)
DI = Daily Intake (mg/kg/day)
Rill = Reference Dose (mg/kg/day)
All the HQ values for chemicals within each exposure pathway are summed to yield
the hazard index (HI). If the value of HI is less than 1.0, it is interpreted to mean
that the risk of noncarcinogenic injury is low. If the HI is greater than 1.0, it is
indicative of some degree of noncarcinogenic risk, or effect. Using the HQ equation,
the DI values from Tables 3-6 and 3-7, and the Rill values in Tables 4-1 and 4-2, a
Hazard Index for each of the exposure scenarios considered in this risk assessment
were calculated for each chemical of potential concern associated with that pathway
and exposure point. Only chronic are derived, as the subchronic risks will always be
equal to or less than the chronic risks. This will slightly overestimate risks associated
with exposures to children. The results of these calculations are summarized in Table
5-1 and Table 5-2, and have been rounded to one significant figure.
An evaluation of the results of the risk calculations presented in Tables 5-1 and 5-2
indicates that. hazard indices for all current scenarios are below 1.0, the level of
concern for noncarcinogens. For future scenarios onsite resident hazard indices are
all above 1.0. Adult and child onsite residents have of 6E+0l and 2E+02,
respectively, primarily due to ingestion of metals in groundwater. Exposure to
A:\CART\SECTli.ClRA 5 · 1
I TABLE 5-1
I SUMMARY OF CHRONIC HAZARD INDEX ESTIMATES
CURRENT LAND USE
I CDI RID Hazard
Population Exposure Pathwa~ Chemical (mQ/KgLda~l (mQ/KQ/da)1 Quotient
Adult Onsite Ingestion ol Onslte Barium 4.6E-08 7E-02 ?E-07
I Trespassers Soll Cadmium 3.SE-09 SE-04 7E-06
Chromium 1.4E-08 SE-03 3E-06
Zinc 1.1E-07 2E-01 6E-07
I Manganese 1.2E-06 1E-01 1E-05
1,2,4-Trlchlorobenzene 4.0E-12 2E-02 2E-10
Tetrachloroethene 8.0E-13 1E-02 8E-11
I Toluene 9.9E-12 2E-01 SE-11
Trichloroethane 3.2E-12 7E-03 SE-10
Chlorobenzene 4.0E-12 2E-02 2E-10
I Pathway Hazard Index = 2E-05
Dermal Contact with Barium 7.0E-07 1E-02 7E-05
I Onsite Soil Cadmium 5.3E-08 1E-04 SE-04
Chromium 2.1E-07 1E-03 2E-04
Zinc 1. 7E-06 4E-02 4E-05
I Manganese 1.SE-05 2E-02 9E-04
1,2,4-Trichlorobenzene 6.0E-10 2E-02 3E-08
Tetrachloroethene 3.0E-10 SE-03 4E-08
I Toluene 3.7E-09 2E-01 2E-08
Trichloroethane 1.2E-09 6E-03 2E-07
Chlorobenzene 1.SE-09 2E-02 8E-08
I Pathway Hazard Index = 2E-03
Dermal Contact with Barium 1.3E-06 1E-02 1E-04
I Onsite Sediment Cadmium 4.6E-08 1E-04 SE-04
Chromium 3.6E-07 1E-03 4E-04
Nickel 1.0E-07 4E-03 3E-05
I Zinc 1.SE-06 4E-02 4E-05
Manganese 4.3E-06 2E-02 2E-04
Vanadium 7.SE-07 1E-03 8E-04
I Toluene 5.6E-09 2E-01 3E-08
Chlorobenzene 3.SE-08 2E-02 2E-06
1,2-Dichlorobenzene 1.0E-08 7E-02 1E-07
I Pathway Hazard Index = 2E-03
Dermal Contact With Zinc 6.1 E-08 4E-02 2E-06
I Onslte Surface Water Manganese 3.SE-07 2E-02 2E-05
Bis(2-Ethylhexyl) Phthalate 1.9E-09 1E-02 2E-07
Carbon Disulfide 7.3E-06 8E-02 9E-05
I Pathway Hazard Index= 1E-04
Total Exposure Index= 4E-03
I CT/SECTS
10/3/90
I
I TABLE 5-1
I SUMMARY OF CHRONIC HAZARD INDEX ESTIMATES
CURRENT LAND USE
(CONTINUED)
I CDI RID Hazard
Population Ex~osura Pathwal Chemical (mg/Kg/dal'.} (mg/Kg/dal'.} Quotient
Child Onsite Ingestion of Onslte Barium 4.1 E-07 7E-02 6E-06
I Trespassers Solt Cadmium 3.1E-08 SE-04 6E-05
Chromium 1.2E-07 SE-03 2E-05
Zinc 9.7E-07 2E-01 SE-06
I Manganese 1.1E-05 1E-01 1E-04
1,2,4-Trichlorobenzene 3.SE-11 2E-02 2E-09
Tetrachloroethene 7.0E-12 lE-02 7E-10
I Toluene 8.7E-11 2E-01 4E-10
Trichloroethane 2.BE-11 7E-03 4E-09
Chlorobenzene 3.SE-11 2E-02 2E-09
I Pathway Hazard Index = 2E-04
Dermal Contact with Barium 1.1 E-06 1E-02 1E-04
I Onsite Soil Cadmium 8.6E-08 1E-04 9E-04
Chromium 3.SE-07 lE-03 3E-04
Zinc 2.7E-06 4E-02 7E-05
I Manganese 3.0E-05 2E-02 lE-03
1 ,2,4-Trichlorobenzene 9.BE-10 2E-02 SE-08
Tetrachloroethene 4.9E-10 BE-03 6E-08
I Toluene 6.0E-09 2E-01 3E-08
Trichloroethane 2.0E-09 6E-03 3E-07
Chlorobenzene 2.4E-09 2E-02 1E-07
I Pathway Hazard Index = 3E-03
Dermal Contact with Barium 2.2E-06 1E-02 2E-04
I Onslte Sediment Cadmium 7.4E-08 1E-04 7E-04
Chromium 5.9E-07 1E-03 6E-04
Nickel 1.7E-07 4E-03 4E-05
I Zinc 2.BE-06 4E-02 7E-05
Manganese 7.0E-06 2E-02 4E-04
Vanadium 1.3E-06 lE-03 lE-03
I Toluene 9.2E-09 2E-01 SE-08
Chlorobenzene 5.BE-08 2E-02 3E-06
1 ,2-Dichlorobenzene 1.6E-08 7E-02 2E-07
I Pathway Hazard Index = 3E-03
Dermal Contact with Zinc 7.7E-08 4E-02 2E-06
I Onsite Surface Water Manganese 4.4E-07 2E-02 2E-05
B1s(2-Ethylhexyl) Phthalate 2.4E-09 1E-02 2E-07
Carbon Dlsulflde 9.2E-06 8E-02 1E-04
I Pathway Hazard Index = 1E-04
Total Exposure Index= 7E-03
I CT/SECTS
10/3/90
I
I TABLE 5-1
I SUMMARY OF CHRONIC HAZARD INDEX ESTIMATES
CURRENT LAND USE
(CONTINUED)
I CDI RIO Hazard
Population Exposure Pathwa~ Chemical (mg(Kg/da,'.l (mg(Kg(da,1 Quotient
Adult Oflsite Ingestion ol Soll Arsenic 1. 7E-08 4E-04 4E-05
I Resident Barium 5.7E-07 7E-02 SE-06
Chromium 7.2E-08 SE-03 1E-05
Zinc 4.SE-07 2E-01 2E-06
I Manganese 2.2E-06 1E-01 2E-05
Mercury 6.9E-10 3E-04 2E-06
Trichloroethane 1.2E-10 7E-03 2E-08
I Toluene 1.1E-10 2E-01 SE-10
1,2-Dichlorobenzene 1.7E-10 9E-02 2E-09
Pathway Hazard Index = 9E-05
I Dermal Contact with Arsenic 6.4E-08 1E-03 6E-05
Off site Soll Barium 2.1 E-06 1E-02 2E-04
I Chromium 2.7E-07 1E-03 3E-04
Zinc 1.?E-06 4E-02 4E-05
Manganese 8.1 E-06 2E-02 4E-04
I Mercury 2.6E-09 6E-05 4E-05
Trichloroethane 1.2E-08 6E-03 2E-06
Toluene 1.0E-08 2E-01 SE-08
I 1,2-Dichlorobenzene 6.4E-09 7E-02 9E-08
Pathway Hazard Index = 1E-03
I Dermal Contact with Barium 4.1 E-06 1E-02 4E-04
Oflsite Sediment Cadmium 1.1E-07 1E-04 1E-03
Chromium 8.4E-07 1E-03 SE-04
I Nickel 2.3E-07 4E-03 6E-05
Zinc 6.4E-06 4E-02 2E-04
Manganese 3.SE-06 2E-02 2E-04
I Vanadium 1.SE-06 1E-03 1E-03
Toluene 1.SE-06 2E-01 SE-06
Chlorobenzene 1.SE-09 2E-02 9E-08
I 1,2-Dlchlorobenzene 1.SE-09 7E-02 2E-08
Pathway Hazard Index= 4E-03
I Dermal Contact with Zinc 1.2E-07 4E-02 3E-06
Off site Surface Water Manganese 3.SE-07 2E-02 2E-05
(Wading) 8Is(2-Ethylhexyl) Phthalate 6.0E-08 1E-02 6E-06
I Carbon Disulfide 1.SE-06 SE-02 2E-05
Pathway Hazard Index= SE-05
I Total Exposure Index= SE-3
I CT/SECTS
10/3/90
I
I TABLE 5-1
I SUMMARY OF CHRONIC HAZARD INDEX ESTIMATES
CURRENT LAND USE
(CONTINUED)
I COi RID Hazard
Population ExQosure Pathwa~ Chemical {mQ/KQ/da~J {m9LK9Lda~J Quotient
Child Offsite Ingestion of Soll Arsenic 2.4E-07 lE-03 2E-04
I Resident Barium 8.1 E-06 7E-02 lE-04
Chromium 1.0E-06 SE-03 2E-04
Zinc 6.SE-06 2E-01 3E-05
I Manganese 3.1 E-05 1E-01 3E-04
Mercury 9.9E-09 3E-04 3E-05
Trichloroethane 1.8E-09 7E-03 3E-07
I Toluene 1.SE-09 2E-01 8E-09
1,2-Dichlorobenzene 2.4E-09 9E-02 3E-08
Pathway Hazard Index= 9E-04
I Dermal Contact with Arsenic 1.7E-07 1E-03 2E-04
Offsile Soil Barium 5.8E-06 1 E-02 6E-04
I Chromium 7.3E-07 1E-03 7E-04
Zinc 4.6E-06 4E-02 1E-04
Manganese 2.2E-05 2E-02 1E-03
I Mercury 7.0E-09 6E-05 1E-04
Trichloroethane 3.1 E-08 6E-03 SE-06
Toluene 2.7E-08 2E-01 lE-07
I 1,2-Dichlorobenzene 1.7E-08 7E-02 2E-07
Pathway Hazard Index = 3E-03
I Dermal Contact with Barium 1.1E-05 1E-02 1E-03
Offslte Sediment Cadmium 3.0E-07 1E-04 3E-03
Chromium 2.3E-06 1E-03 2E-03
I Nickel 6.2E-07 4E-03 2E-04
Zinc 1.7E-05 4E-02 4E-04
Manganese 9.4E-06 2E-02 SE-04
I Vanadium 4.0E-06 1E-03 4E-03
Toluene 4.3E-06 2E-01 2E-05
Chlorobenzene 4.9E-09 2E-02 2E-07
I 1,2-Dichlorobenzene 3.9E-09 7E-02 6E-08
Pathway Hazard Index = 1E-02
I Dermal Contact with Zinc 1.SE-07 4E-02 4E-06
Offslte Surface Water Manganese 4.8E-07 2E-02 2E-05
(Wading) Bis(2-Ethylhexyl) Phthalate 7.SE-08 1E-02 8E-06
I Carbon Disulfide 1.8E-06 8E-02 2E-05
Pathway Hazard Index= 6E-05
I Total Exposure Index= 2E-02
I CT/SECTS
10/3/90
I
I TABLE 5-2
I SUMMARY OF CHRONIC HAZARD INDEX ESTIMATES
FUTURE LAND USE
I CDI RID Hazard
Population Exposure Pathway Chemical {ma/Ko/day} {mgfil9!da)1 Quotient
Adult Onslte Ingestion of Onslte Barium 2.9E-05 7E-02 4E-04
I Resident Soil Cadmium 2.2E-06 SE-04 4E-03
Chromium 8.9E-06 SE-03 2E-03
Zinc 6.9E-05 2E-01 3E-04
I Manganese 7.SE-04 lE-01 BE-03
1,2,4-Trichlorobenzene 2.SE-09 2E-02 lE-07
Tetrachloroelhene 5.0E-10 lE-02 SE-08
I Toluene 6.2E-09 2E-01 3E-08
Trichloroethane 2.0E-09 7E-03 3E-07
Chlorobenzene 2.SE-09 2E-02 lE-07
I Pathway Hazard Index = 1E-02
Dermal Conlact with Barium 5.2E-05 lE-02 SE-03
I Onsite Soil Cadmium 4.0E-06 lE-04 4E-02
Chromium 1.SE-05 lE-03 2E-02
Zinc 1.2E-04 4E-02 3E-03
I Manganese 1.4E-03 2E-02 7E-02
1,2,4-Trichlorobenzene 4.SE-09 2E-02 2E-07
Tetrachloroethene 9.0E-10 8E-03 lE-07
I Toluene 1.lE-08 2E-01 SE-08
Trichloroethane 3.SE-09 SE-03 SE-07
Chlorobenzene 1.lE-07 2E-02 SE-06
I Pathway Hazard Index = 1E-01
Dermal Contact with Barium 4. lE-06 lE-02 4E-04
I Off site Sediment Cadmium 1.1 E-07 1E-04 lE-03
Chromium 8.4E-07 lE-03 SE-04
Nickel 2.3E-07 4E-03 SE-05
I Zinc 6.4E-06 4E-02 2E-04
Manganese 3.SE-06 2E-02 2E-04
Vanadium 1.SE-06 lE-03 2E-03
I Toluene 1.SE-06 2E-01 BE-06
Chlorobenzene 1.SE-09 2E-02 9E-08
1,2-Dichlorobenzene 1.SE-09 7E-02 2E-08
I Pathway Hazard Index = 4E-03
lngesllon of Onslte Barium 4.9E-01 7E-02 7E+OO
I Groundwater Chromium 8. lE-02 SE-03 2E+01
Nickel 3.SE-02 2E-02 2E+OO
Vanadium 1.SE-01 7E-03 2E+01
I Zinc 1.lE-01 2E-01 6E-01
Manganese 7.0E-01 lE-01 7E+OO
I CT/SECTS
10/3/90
I
I TABLE 5-2
I SUMMARY OF CHRONIC HAZARD INDEX ESTIMATES
FUTURE LAND USE
(CONTINUED)
I CDI RID Hazard
Population Exposure Pathway Chemical (mg/Kg/dal'] (mg/Kg/day) Quotient
Adult Onsite Ingestion ol Onsite Mercury 8.?E-06 3E-04 3E-02
I Resident Groundwaler Bis(2-Ethylhexyl) Phlhalate 2.4E-02 2E-02 1E+00
(Continued) (Continued) 1,2,4-Trichlorobenzene 4.4E-05 2E-02 2E-03
Methyl Ethyl Ketone 2.2E-04 5E-02 4E-03
I Toluene 1.6E-04 2E-01 BE-04
Carbon Disulfide 3.2E-04 1E-01 3E-03
Chlorobenzene 5.2E-04 2E-02 3E-02
I Pathway Hazard Index = 6E+01
Dermal Contact with Barium 7.1E-04 1E-02 7E-02
I Onsite Groundwater Chromium 1.2E-04 1E-03 1E-01
(Showers) Nickel 5.0E-05 4E-03 1E-02
Vanadium 2.2E-04 1E-03 2E-01
I Zinc 1.6E-04 4E-02 4E-03
Manganese 1.0E-03 2E-02 SE-02
Mercury 1.2E-08 6E-05 2E-04
I Bis(2-Ethylhexyl) Phthalate 3.5E-05 1E-02 3E-03
1,2,4-Trichlorobenzene 6.2E-08 2E-02 3E-06
Methyl Ethyl Ketone , 2.0E-03 4E-02 5E-02
I Toluene 2.6E-07 2E-01 1E-06
Carbon Disulfide 3.1E-05 SE-02 4E-04
Chlorobenzene 7.SE-07 2E-02 4E-05
I Pathway Hazard Index = 5E-01
Dermal Contact with Zinc 1.2E-07 4E-02 3E-06
I Onslte Surface Water Manganese 3.BE-07 2E-02 2E-05
(Wading) Bis(2-Ethylhexyl) Phlhalate 6.0E-08 1E-02 SE-06
Carbon Disulfide 1.5E-06 BE-02 2E-05
I Pathway Hazard Index = 5E-05
Inhalation of Onslte 1,2,4-Trichlorobenzene 4.4E-05 3E-03 1E-02
I Groundwater (Shower) Methyl Ethyl Ketone 2.2E-04 9E-02 2E-03
Chlorobenzene 5.2E-04 SE-03 1E-01
Pathway Hazard Index = 1 E-01
I Total Exposure Index = 6E+01
I
I
I CT/SECTS
I 10/3/90
I TABLE 5-2
I SUMMARY OF CHRONIC HAZARD INDEX ESTIMATES
FUTURE LAND USE
(CONTINUED)
I CDI RID Hazard
Population B<gosure Pathwa~ Chemical (ma/Kaid al') (ma/Ka/day} Quotient
Child Onslte Ingestion of Onslte Barium 2.7E-04 7E-02 4E-03
I Resident Soll Cadmium 2.1 E-05 SE-04 4E-02
Chromium 8.4E-05 SE-03 2E-02
Zinc 6.SE-04 2E-01 3E-03
I Manganese 7.1 E-03 1E-01 7E-02
1 ,2,4-Trichlorobenzene 2.4E-08 2E-02 1E-06
Tetrachloroethene 4.7E-09 1E-02 SE-07
I Toluene 5.8E-08 2E-01 3E-07
Trichloroethene 1.9E-08 7E-03 3E-06
Chlorobenzene 2.4E-08 2E-02 1E-06
I Pathway Hazard Index = 1 E-01
Dermal Contact with Barium 8.4E-05 1E-02 8E-03
I Onslte Soll Cadmium 6.4E-06 1E-04 6E-02
Chromium 2.6E-05 1E-03 3E-02
Zinc 2.0E-04 4E-02 SE-03
I Manganese 2.2E-03 2E-02 1E-01
1 ,2,4-Trichlorobenzene 7.3E-09 2E-02 4E-07
Tetrachloroethene 1.SE-09 8E-03 2E-07
I Toluene 1 .8E-08 2E-01 9E-08
Trichloroethene 5.8E-09 6E-03 lE-06
Chlorobenzene 1 .BE-07 2E-02 9E-06
I Pathway Hazard Index = 2E-01
Dermal Contact with Barium 1.1E-05 1E-02 1E-03
I Offsite Sediment Cadmium 3.0E-07 1E-04 3E-03
Chromium 2.3E-06 1E-03 2E-03
Nickel 6.2E-07 4E-03 2E-04
I Zinc 1.?E-05 4E-02 4E-04
Manganese 9.4E-06 2E-02 SE-04
Vanadium 4.0E-06 1E-03 4E-03
I Toluene 4.3E-06 2E-01 2E-05
Chlorobenzene 4.9E-09 2E-02 2E-07
1,2-Dichlorobenzene 3.9E-09 7E-02 6E-08
I Pathway Hazard Index = 1E-02
Ingestion of Onsite Barium 1.SE+OO 7E-02 2E+01
I Groundwater Chromium 2.SE-01 SE-03 5E+01
Nickel 1.1E-01 2E-02 SE+OO
Vanadium 4.7E-01 7E-03 7E+01
I Zinc 3.3E-01 2E-01 2E+OO
Manganese 2.1E+OO 1E-01 2E+01
I CT/SECTS
10/3/90
I
I TABLE 5-2
I SUMMARY OF CHRONIC HAZARD INDEX ESTIMATES
FUTURE LAND USE
I
(CONTINUED)
CDI RID Hazard
Population Exposure Pathwai Chemical {ma/Kg/da~l {mg/Kg/da,1 Quotient
I Child Onsite Ingestion of Onsite Mercury 2.6E-05 3E-04 9E-02
Resident Groundwater Bis(2-Ethylhexyl) Phthalate 7.2E-02 2E-02 4E+OO
(Continued) (Continued) 1,2,4-Trichlorobenzene 1.3E-04 2E-02 7E-03
Methyl Ethyl Ketone 6.7E-04 5E-02 1E-02
I Toluene 4.8E-04 2E-01 2E-03
Carbon Disulfide 9.7E-04 1E-01 1E-02
Chlorobenzene 1.6E-03 2E-02 8E-02
I Pathway Hazard Index = 2E+02
Dermal Contact with Barium 2.2E-03 1E-02 2E-01
I Onsite Groundwater Chromium 3.6E-04 1E-03 4E-01
(Showers) Nickel 1.5E-04 4E-03 4E-02
Vanadium 6.8E-04 1E-03 7E-01
I Zinc 4.9E-04 4E-02 1E-02
Manganese 3.1E-03 2E-02 2E-01
I
Mercury 3.8E-08 6E-05 6E-04
Bis(2-Ethylhexyl) Phthalate 1.1E-04 1 E-02 1E-02
1,2,4-Trichlorobenzene ).9E-07 2E-02 lE-05
Methyl Ethyl Ketone 6. lE-03 4E-02 2E-01
I Toluene 7.9E-07 2E-01 4E-06
Carbon Disulfide 9.7E-05 8E-02 lE-03
Chlorobenzene 2.3E-06 2E-02 1E-04
I Pathway Hazard Index = 2E+OO
Dermal Contact with Zinc 1.1E-07 4E-02 3E-06
I Onslte Surface Water Manganese 4.BE-07 2E-02 2E-05
(Wading) Bis(2-Ethylhexyl) Phthalate 7.5E-08 1E-02 8E-06
Carbon Disulfide 1.8E-06 8E-02 2E-05
I Pathway Hazard Index= 6E-05
I
Inhalation of Onslte 1,2,4-Trichlorobenzene 2.0E-04 3E-03 7E-02
Groundwater (Shower) Methyl Ethyl Ketone 9.9E-04 9E-02 1E-02
Chlorobenzene 2.3E-03 5E-03 SE-01
I Pathway Hazard Index = SE-01
Total Exposure Index= 2E+02
I
I
I CT/SECTS
I 10/3190
I TABLE 5-2
I SUMMARY OF CHRONIC HAZARD INDEX ESTIMATES
FUTURE LAND USE
(CONTINUED)
I CDI RID Hazard
Population Exposure Pathwa~ Chemical (mg,'Kg/da~l (mg/Kg/da:i} Quotient
Adult Onslte Ingestion of Well Barium 5.SE-01 7E-02 8E+OO
I Resident No. 44 Groundwater Chromium 8.4E-02 SE-03 2E+01
Nickel 3.SE-02 2E-02 2E+OO
Vanadium 1.4E-01 7E-03 2E+01
I Zinc 1.0E-01 2E-01 SE-01
Manganese 2.6E-01 1E-01 3E+00
Carbon Disulfide 1.9E-04 1E-01 2E-03
I Chlorobenzene 5.8E-04 2E-02 3E-02
Pathway Hazard Index = 5E+01
I Dermal Contact With Barium 7.9E-04 1E-02 8E-02
No. 44 Groundwater Chromium 1.2E-04 1E-03 1E-01
(Showers) Nickel 5.0E-05 4E-03 1E-02
I Vanadium 2.0E-04 1 E-03 2E-01
Zinc 1.SE-04 4E-02 4E-03
Manganese 3.7E-04 2E-02 2E-02
I Carbon Disulfide 1 .9E-05 8E-02 2E-04
Chlorobenzene 8.3E-07 2E-02 4E-05
Pathway Hazard Index = 4E-01
I Inhalation of Chlorobenzene 5.8E-01 SE-03 1E+02
No. 44 Groundwater Pathway Hazard Index = 1E+02
I (Showers)
Total Exposure Index= 2E+02
I Child Onslte Ingestion of Well Barium 1. 7E+OO 7E-02 2E+01
I Resident No. 44 Groundwater Chromium 2.6E-01 SE-03 5E+01
Nickel 1.1E-01 2E-02 6E+OO
Vanadium 4.3E-01 7E-03 6E+01
Zinc 3.1E-01 2E-01 2E+OO
I Manganese 7.8E-01 1E-01 8E+OO
Carbon Disulfide 5.9E-04 1E-01 6E-03
Chlorobenzene 1 .8E-03 2E-02 9E-02
I Pathway Hazard Index = 2E+02
I
I
I CT/SECTS
I 10/3/90
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PoQulation
Child Onsita
Resident
(Conlinued)
CT/SECTS
10/3/90
TABLE 5-2
SUMMARY OF CHRONIC HAZARD INDEX ESTIMATES
FUTURE LAND USE
(CONTINUED)
CDI RID
El<QOSure Pathwa~ Chemical (mg,'Kg,'da~l (mg,'Kg,'dal'}
Dermal Contact With Barium 2.4E-03 1E-02
No. 44 Groundwater Chromium 3.7E-04 1E-03
(Showers) Nickel 1.SE-04 4E-03
Vanadium 6.3E-04 1E-03
Zinc 4.SE-04 4E-02
Manganese 1.1 E-03 2E-02
Carbon Disulfide 5.9E-05 8E-02
Chlorobenzene 2.6E-06 2E-02
Hazard
Quotient
2E-01
4E-01
4E-02
SE-01
1E-02
6E-02
7E-04
1E-04
Pathway Hazard Index = 1 E+00
Inhalation of Chlorobenzene 2.6E+00 SE-03 SE+02
No. 44 Groundwater Pathway Hazard Index = 5E+02
(Showers)
Total Exposure Index= 7E+02
5-14
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groundwater well No. 44 results in noncarcinogenic risk of 2E+02 for adults, and
7E+02 for children, again due to metals in groundwater and a significant contribution
to risk from chlorobenzene being inhaled in the showering scenario.
5.2 Evaluation of Carcinogenic Risks
The risk of cancer from exposure to a chemical is described in terms of the
probability that an individual exposed will develop cancer during his or her lifetime
from that exposure. This value is calculated from the average daily intake over a
lifetime (CDI) and the slope factor (SF) for the chemical as follows [1]):
Risk = CDI x SF
When the product of CDI x SF is greater than 0.01, this expression may be estimated
as:
Risk = 1 -EXP(-CDI x SF)
Using the simplified equation where appropriate and employing the CDI values
calculated for lifetime exposure (Tables 3-6 and 3-7) along with the SF values (Tables
4-1 and 4-2), cancer risks were calculated for lifetime exposures which may occur at
this site. A summary of the results is presented in Tables 5-3 and 5-4. It is important
to note that the carcinogenic risk estimates presented in Tables 5-3 and 5-4
represent the summation of the individual risks associated with each of the chemicals
of potential concern for which cancer information is adequately available.
All populations show carcinogenic risk in excess of the accepted EPA benchmark of
1 x 10--0. For current adult onsite trespassers, the lifetime excess cancer risk is lE-3,
primarily from PCBs. For current child trespassers, the lifetime excess cancer risk
is 4E-4, again primarily from PCBs. For current adult offsite residents, the lifetime
excess cancer risk is 7E-4, while current offsite child residents have a risk of 3E-04,
primarily from dermal contact with PCBs in sediment and ingestion of PCBs in
produce.
For future (hypothetical) adult onsite residents, the lifetime excess cancer risk is lE-1,
primarily from dermal contact with PCBs in soil. For future child onsite residents, the
A:.\CART\SECT5.DRA 5-2
I TABLE 5-3
I SUMMARY OF CANCER RISK ESTIMATES
CURRENT LAND USE
I COi SF
Population Ex~osure Pathwa~ Chemical (mgL!5g(day) 1/(mg(Kg(day) Risk
Adult Onsite Ingestion of Onsite Tetrachloroethene 3.5E-13 5.1 E-02 2E-14
I Trespassers Solt Trichloroethane 1.4E-12 1.1E-02 2E-14
Benzene 1.8E-12 2.SE-02 5E-14
PCB-1254 (Aroclor 1254) 3.4E-08 7.7E+OO 3E-07
I PCB-1260 (Aroclor 1260) 4.SE-07 7.7E+OO 4E-06
Dioxlns/Furans 5.3E-13 1.5E+05 8E-08
Pathway Risk = 4E-06
I Dermal Contact with Tetrachloroethene 1.3E-10 6.4E-02 8E-12
Onsite Soil Trichloroethene 5.0E-10 1.4E-02 7E-12
I Benzene 6.3E-10 3.6E-02 2E-11
PCB-1254 (Aroclor 1254) 4.8E-06 1.5E+01 7E-05
PCB-1260 (Aroclor 1260) 6.5E-05 1.5E+01 1E-03
I Dioxins/Furans 7.5E-11 3.0E+OS 2E-05
Pathway Risk = 1E-03
I Dermal Contact with PCB-1254 (Aroclor 1254) 9.2E-06 1.5E+01 1E-04
Onsite Sediment PCB-1248 (Aroclor 1248) 9.8E-07 1.5E+01 1E-05
PCB-1260 (Aroclor 1260) 1.6E-05 1.5E+01 2E-04
I Benzene 5.3E-09 3.6E-02 2E-10
1,4-0ichlorobenzene 4.4E-08 3.0E-02 1E-09
Oioxin/furans 2.2E-11 3.0E+OS 7E-06
I Pathway Risk = 4E-04
Dermal Contact with PCB-1260 (Aroclor 1260) 2.0E-09 1.5E+01 3E-08
I Onsite Surface Water Bis(2-Ethylhexyl) Phthalate 8.3E-10 2.8E-02 2E-11
Pathway Risk = 3E-08
I Total Exposure Risk = 1E-03
I Child Onsite Ingestion of Onslte Tetrachloroethene 5.0E-13 5.1 E-02 3E-14
Trespassers Soll Trichloroethane 2.0E-12 1.1E-02 2E-14
Benzene 2.5E-12 2.9E-02 7E-14
I PCB-1254 (Aroclor 1254) 4.BE-08 7.7E+OO 4E-07
PCB-1260 (Aroclor 1260) 6.5E-07 7.7E+OO 5E-06
Dioxins Furans 7.SE-13 1.SE+OS 1E-07
I Pathway Risk = 5E-06
I
I CT/SECTS
10/3/90
I
I TABLE 5-3
I SUMMARY OF CANCER RISK ESTIMATES
CURRENT LAND USE
(CONTINUED)
I COi SF
Populalion Exposure Pathwa~ Chemical {mg/Kg/dal'} 1/{mg/Kg/da~l Risk
Child Onsile Dermal Contact with Tetrachloroethene 3.SE-11 6.4E-02 2E-12
I Trespassers Onsile Soll Trichloroethane 1.4E-10 1.4E-02 2E-12
(Continued) Benzene 1.SE-10 3.6E-02 6E-12
PCB-1254 (Aroclor 1254) 1.3E-06 1.5E+01 2E-05
I PCB-1260(Aroclor 1260) 1.SE-05 1.5E+01 3E-04
Dioxins/Furans 2.1E-11 3.0E+OS 6E-06
Pathway Risk = 3E-04
I Dermal Contact with PCB-1254 (Aroclor 1254) 2.6E-06 1.5E+01 4E-05
Onsite Sediment PCB-1248 (Aroclor 1248) 2.7E-07 1.SE+01 4E-06
I PCB-1260 (Aroclor 1260) 4.SE-06 1.5E+01 7E-05
Benzene 1.SE-09 3.6E-02 SE-11
1,4-Dichlorobenzene 1.2E-08 3.0E-02 4E-10
I Dioxin/furans 6.2E-12 3.0E+OS 2E-06
Pathway Risk = 1E-04
I Dermal Contact with PCB-1260 (Aroclor 1260) 4.3E-10 1.5E+01 6E-09
Onsite Surface Water Bis(2-Ethylhexyl) Phthalate 1.7E-10 2.SE-02 SE-12
Pathway Risk = 6E-09
I Total Exposure Risk = 4E-04
I Adult Offsite Ingestion of Soil Arsenic 1.7E-08 2.0E+OO 3E-08
Resident PCB-1260 (Aroclor 1260) 1.2E-07 7.7E+OO 9E-07
I Trichloroethene 5.3E-11 1.1E-02 6E-13
1,4-Dichlorobenzene 1.SE-10 2.4E-02 3E-12
Dioxin/furans 2.3E-13 1.SE+OS 3E-08
I Pathway Risk = 1 E-06
Dermal Contact wi\h PCB-1260(Aroclor 1260) 4.SE-06 1.SE+01 ?E-05
I Off site Soll Trlchloroethene 5.2E-09 1.4E-02 7E-11
1,4-Dichlorobenzene 5.7E-09 3.0E-02 2E-10
Dloxln/furans 9.0E-12 3.0E+OS 3E-06
·1 Pathway Risk = 7E-05
Dermal Contact with PCB-1254 (Aroclor 1254) 3.3E-10 1.SE+01 SE-09
I Offslte Sediment PCB-1248 (Aroclor 1248) 2.3E-08 1.SE+0l 4E-07
PCB-1260 (Aroclor 1260) 2.9E-05 1.5E+01 4E-04
Benzene 8.1E-10 3.6E-02 3E-11
I 1,4-Dlchlorobenzene 6.SE-10 3.0E-02 2E-11
Dloxlns/furans 2.1E-11 3.0E+OS 6E-06
Pathway Risk = 4E-04
I CT/SECTS
10/3/90
I
I TABLE 5-3
I SUMMARY OF CANCER RISK ESTIMATES
CURRENT LAND USE
(CONTINUED)
I CDI SF
Population Exposure Pathwa~ Chemical (m9L!S9ldal') 1/(m9L!S9ldal') Risk
Adull Ollsite Dermal Contact with PCB-1260 (Aroclor 1260) 3.3E-09 1.5E+01 SE-08
I Resident Offslle Surface Waler Bis(2-Ethylhexyl) Phthalate 2.6E-08 2.SE-02 7E-10
(Continued) (Wading) Pathway Risk = SE-08
I Ingestion of Produce PCB-1260 (Aroclor 1260) 2.3E-05 7.7E+OO 2E-04
Pathway Risk = 2E-04
I Total Exposure Risk= 7E-04
I Ingestion of Soil Arsenic 1.SE-08 2.0E+OO 4E-08
PCB-1260 (Aroclor 1260) 3.0E-07 7.7E+OO 2E-06
Trichloroethane 1.3E-10 1.1E-02 1E-12
I 1.4-Dichlorobenzene 3.6E-10 2.4E-02 9E-12
Dioxin/furans 5.6E-13 1.SE+OS BE-08
Pathway Risk = 2E-06
I Dermal Contact with PCB-1260 (Aroclor 1260) 2.1 E-06 1.5E+01 3E-05
Ollsite Soll Trichloroethane 2.2E-09 1.4E-02 3E-11
I 1,4-Dlchlorobenzene 2.SE-09 3.0E-02 7E-11
Dioxin/furans 3.9E-12 3.0E+OS 1E-06
Pathway Risk = 3E-05
I Child Offsite Dermal Contact with PCB-1254 (Aroclor 1254) 1.4E-10 1.5E+01 2E-09
Resident Offsite Sediment PCB-1248 (Aroclor 1248) 1.0E-08 1.5E+01 2E-07
PCB-1260 (Aroclor 1260) 1.2E-05 1.5E+01 2E-04
I Benzene 3.SE-10 3.SE-02 1 E-11
1,4-Dichlorobenzene 2.SE-10 3.0E-02 BE-12
Dioxins/furans 9.0E-12 3.0E+OS 3E-06
I Pathway Risk = 2E-04
Dermal Contact with PCB-1260 (Aroclor 1260) 4.1E-09 1.5E+01 GE-08
I Off site Surface Water Bis(2-Ethylhexyl) Phthalate 3.1E-08 2.BE-02 9E-10
(Wading) Pathway Risk = 6E-08
I Ingestion of Produce PCB-1260 (Aroclor 1260) 1. 7E-05 7.7E+OO 1E-04
Pathway Risk = 1E-04
I Total Exposure Risk = 3E-04
I
I CT/SECTS
10/3/90
I
I TABLE 5-4
I SUMMARY OF CANCER RISK ESTIMATES
FUTURE LAND USE
I CDI SF
Population Exposure Pathwal Chemical (mQ/KQ/da)1 1/(mg/Kg/da)1 Risk
Adult Onsile Ingestion of Onsite Telrachloroelhene 2.2E-10 5. lE-02 1 E-11
I Resident Soll Trichloroethane 8.BE-10 1.lE-02 1 E-11
Benzene 1.lE-09 2.9E-02 3E-11
PCB-1254 (Aroclor 1254) 2.1 E-05 7.7E+00 2E-04
I PCB-1260 (Aroclor 1260) 2.9E-04 7.7E+00 2E-03
Oioxln/furans 3.3E-10 1.5E+05 SE-05
Pathway Risk = 2E-03
I Dermal Contact with Tetrachloroethene 3.9E-10 6.4E-02 2E-11
Onsite Soll Trichloroethane 1.SE-09 1.4E-02 2E-11
I Benzene 1.9E-08 3.6E-02 7E-10
PCB-1254 (Aroclor 1254) 9.2E-04 1.SE+01 lE-02
PCB-1260 (Aroclor 1260) 5.0E-03 1.SE+01 BE-02
I Dioxin/furans 5.BE-09 3.0E+0S 2E-03
Pathway Risk = 9E-02
I Dermal Contact with PCB-1254 (Aroclor 1254) 3.3E-10 1.SE+01 SE-09
Olfsite Sediment PCB-1248 (Aroclor 1248) 2.3E-08 1.5E+01 3E-07
PCB-1260 (Aroclor 1260) 2.9E-05 1.5E+01 4E-04
I Benzene 8.lE-10 3.6E-02 3E-11
1,4-Dichlorobenzene 6.SE-10 3.0E-02 2E-11
Dloxlns/furans 2.lE-11 3.0E+0S 6E-06
I Pathway Risk = 4E-04
Ingestion of Onslte PCB-1260 (Aroclor 1260) 6. lE-04 7.7E+00 SE-03
I Groundwater Bis(2-Ethylhexyl) Phthalate 9.BE-03 1.4E-02 lE-04
Benzene 4.4E-05 2.9E-02 lE-06
1,4-Dichlorobenzene 4.4E-04 2.4E-02 lE-05
I Pathway Risk = 5E-03
Dermal Contact with PCB-1260 (Aroclor 1260) 9.0E-07 1.5E+01 lE-05
I Onsite Groundwater Bis(2-Ethylhexyl) Phthalate 1.SE-05 2.BE-02 4E-07
(Showers) Benzene 3.3E-05 3.6E-02 lE-06
1,4-Dlchlorobenzene 6.SE-07 3.0E-02 2E-08
I Pathway Risk = 2E-05
Dermal Contact with PCB-1260 (Aroclor 1260) 3.3E-09 1.5E+01 SE-08
I Onsite Surface Water Bis(2-Ethylhexyl) Phthalate 2.6E-08 2.8E-02 7E-10
(Wading) Pathway Risk = 5E-08
I Inhalation of Onslte Benzene 4.4E-05 2.9E-02 lE-06
Groundwater (Shower) Pathway Risk = 1E-06
I CT/SECTS
10/3190
I
I TABLE 5-4
I SUMMARY OF CANCER RISK ESTIMATES
FUTURE LAND USE
(CONTINUED)
I CDI SF
Population Exposure Pathwa1 Chemical (mg!Kg!da~l 1/(mg!Kg!da~l Risk
Adult Onsite Ingestion of Produce PCB-1260 (Aroclor 1260) 4.1E-04 7.7E+OO 3E-03
I Resident Pathway Risk = 3E-03
(Continued)
Total Exposure Risk= 1 E-01
I
Child Onsite Ingestion of Onsite Tetrachloroethene 3.4E-10 5.1 E-02 2E-11
I Resident Soil Trichloroethene 1.3E-09 1.lE-02 1 E-11
Benzene 1 .7E-09 2.9E-02 5E-11
PCB-1254 (Aroclor 1254) 3.2E-05 7.7E+OO 2E-04
I PCB-1260 (Aroclor 1260) 4.4E-04 7.7E+00 3E-03
Dioxin/furans 5.0E-10 1.5E+05 BE-05
Pathway Risk = 4E-03
I Dermal Contact with Tetrachloroethene 1.0E-10 6.4E-02 6E-12
Onsite Soil Trichloroethene 4.0E-10 1.4E-02 6E-12
I Benzene 5.0E-09 3.6E-02 2E-10
PCB-1254 (Aroclor 1254) 2.4E-04 1.5E+01 4E-03
PCB-1260 (Aroclor 1260) 1.3E-03 1 .5E+01 2E-02
I Oioxin/furans 1 .5E-09 3.0E+05 5E-04
Pathway Risk = 2E-02
I Dermal Contact with PCB-1254 (Aroclor 1254) 1.4E-10 1 .5E+01 2E-09
Off site Sediment PCB-1248 (Aroclor 1248) 1.0E-08 1.5E+01 2E-07
PCB-1260 (Aroclor 1260) 1.2E-05 1.5E+01 2E-04
I Benzene 3.5E-10 3.6E-02 1 E-11
1,4-Dlchlorobenzene 2.BE-10 3.0E-02 BE-12
Dioxins/furans 9.0E-12 3.0E+05 3E-06
I Pathway Risk = 2E-04
Ingestion of Onslte PCB-1260 (Aroclor 1260) 3.2E-04 7.7E+OO 2E-03
I Groundwater Bis(2-Ethylhexyl) Phthalate 5.2E-03 1.4E-02 7E-05
Benzene 2.3E-05 2.SE-02 7E-07
1,4-Dichlorobenzene 2.3E-04 2.4E-02 6E-06
I Pathway Risk = 3E-03
Dermal Contact with PCB-1260 (Aroclor 1260) 4.9E-07 1 .5E+01 7E-06
I Onsite Groundwater Bis(2-Ethylhexyl} Phthalate 8.0E-06 2.BE-02 2E-07
(Showers) Benzene 1.SE-05 3.6E-02 7E-07
1 ,4-Dlchlorobenzene 4.?E-06 3.0E-02 1E-07
I Pathway Risk = BE-06
I CT/SECTS
10/3190
I
I TABLE 5-4
I SUMMARY OF CANCER RISK ESTIMATES
FUTURE LAND USE
(CONTINUED)
I CDI SF
Population ExQosure Pathwa~ Chemical {mQ/Kg/dal'.} 1/(mQ/Kg/dal'.} Blfil!.
Child Onslte Dermal Contact with PCB-1260 (Aroclor 1260) 4.1 E-09 1.5E+01 6E-08
I Resident Onslte Surface Water Bis(2-Ethylhexyl) Phthalate 3.2E-08 2.BE-02 9E-10
(Continued) (Wading) Pathway Risk = 6E-08
I Inhalation of Onsite Benzene 3.3E-05 2.9E-02 1E-06
Groundwater (Shower) Pathway Risk = 1E-06
I Ingestion of Produce PCB-1260 (Aroclor 1260) 3.0E-04 7.7E+00 2E-03
Pathway Risk = 2E-03
I Total Exposure Risk = 3E-02
I Adult Onsite Ingestion of Well PCB-1260 (Aroclor 1260) 6.2E-04 7.7E+00 5E-03
Residents No. 44 Groundwater Benzene 3.4E-05 2.9E-02 1E-06
Pathway Risk = 5E-03
I Dermal Contact With PCB-1260 (Aroclor 1260) 9.2E-07 1.SE+01 1E-05
No. 44 Groundwater Benzene 2.SE-05 3.6E-02 9E-07
I (Showers) Pathway Risk = 1E-05
I Inhalation of Benzene 3.4E-02 2.9E-02 1E-03
No. 44 Groundwater Pathway Risk= 1 E-03
(Showers)
I Total Exposure Risk = 6E-03
I Child Onsite Ingestion of Well PCB-1260 (Aroclor 1260) 3.3E-04 7.7E+00 3E-03
Residents No. 44 Groundwater Benzene 1.BE-05 2.9E-02 SE-07
Pathway Risk = 3E-03
I Dermal Contact With PCB-1260 (Aroclor 1260) 5.0E-07 1.5E+01 BE-06
No. 44 Groundwater Benzene 1.4E-05 3.6E-02 SE-07
I (Showers) Pathway Risk = SE-06
I Inhalation of Benzene 2.SE-02 2.9E-02 7E-04
No. 44 Groundwater Pathway Risk = 7E-04
(Showers)
I Total Exposure Risk= 3E-03
I CT/SECTS
10/3/90
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excess cancer risk is 3E-2, again primarily dermal contact with PCBs in soil.
Exposure to groundwater in Well No. 44 results in risks of 6E-3 for future adult
onsite residents, and 4E-3 for future child onsite residents.
According to EPA policy, the target total individual risk resulting from exposures at
a Superfund site may range anywhere between 10-4 to 10.{j. Thus, remedial
alternatives being considered should be capable of reducing total potential
carcinogenic risks to individuals to levels within this range. EPA further suggests that
the 10.{j risk level should be used as a starting point.
5.3 Uncertainties in the Risk Characterization
The factors that contribute uncertainty to the estimates of exposure concentrations,
daily intakes, and toxicity information also contribute uncertainty to the estimates of
risk. These factors include:
• Chemicals not included
• Exposure pathways not considered
• Derivation of exposure point concentrations
• Intake uncertainty
• Toxicological dose-response and toxicity values.
There are uncertainties associated with summing cancer risks or hazard indices for
different chemicals. This assumption of dose additivity ignores possible synergism or
antagonism among chemicals and differences in mechanisms of action and
metabolism. It is not known what effects this has on the total risk numbers.
Another important uncertainty surrounds the fact that risk calculations for dermal
exposure to all compounds except arsenic assume a relationship between the oral
toxicity values and the extrapolated dermal value. These uncertainties and the
uncertainties discussed in previous sections need to be considered when evaluating
the results of the risk assessment and when making risk management decisions for
the site.
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6.0 ENVIRONMENTAL EVALUATION
6.1 INTRODUCTION
This section provides an assessment of potential impacts to biotic receptors due to
potential exposures to the chemicals of concern released from the Carolina Trans•
former Site. In this analysis, chemicals of potential concern identified for the
human health risk assessment were not necessarily the same as those used for the
environmental evaluation. Further discussions of chemicals of concern are present
in Section 6.3. The assessment is comprised of five major sections: 1) introduc-
tion; 2) site and study area description; 3) contaminants of concern; 4) exposure
characterization; and 5) risk characterization. The assessments of risk are limited
primarily to the population (species) level because data on community and ecosys-
tem level responses to environmental pollutants generally are lacking. However,
where possible, the implications of population level impacts on the community or
ecosystem are discussed.
6. 1. 1 Objectives
The objective of the environmental evaluation is to determine the extent of envi-
ronmental injury caused by contaminant releases at the Carolina Transformer Site.
The objective is attained by documenting injury to environmental receptors (i.e.,
natural resources including air, surface water, ground water, soil, geological units,
agricultural operations, and naturally occurring communities), assessing the impact
to receptors of continued release and exposure, and assessing potential for envi-
ronmental recovery.
6. 1.2 Scope of the Investigation
This environmental evaluation incorporates data collected during the RI ( conduct-
ed by Region IV EPA) along with information from other literature resources to
provide an assessment of potential impacts to biota due to releases of contami-
nants from the Carolina Transformer Site. Detailed field surveys and toxicity
testing were not completed as part of the scope of this assessment.
A:\CART\SECTe.ORA 6-1
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6.2 SITE AND STUDY AREA DESCRIPTION
6.2.1 Zoning/Site Description
The site is currently not being used for commercial or industrial purposes. The
4.8 acre site is bounded on the north by a wooded/wetland areas which are adja-
cent to agricultural areas and residential properties. The site is bordered to the
west by a dirt road which provides access to two homes; to the south by Middle
Road, Larry's Sausage Company and Lundy Packing Company; and to the east by
an abandoned home site and an agricultural field.
Although various habitats exist onsite ( descriptions in Section 6.2.2) at Carolina
Transformer, it should be noted that all of the areas are relatively small and prob-
ably do not support large populations of any animal or plant species.
The first habitat, consisting of a wooded area north and west of the site, is bound-
ed by an agricultural region and River Road. This habitat resembles loblolly-
shortleaf pine forests. This type of forest is more than fifty percent pine species
and red and white oaks, gum, hickory, and yellow-poplar. Soil properties and
features that affect the growth of trees and shrubs are depth of the root zone, the
available water capacity, and wetness. The wildlife attracted to these areas in-
clude bobwhite quail, mourning doves, red fox, cottontail rabbit, and many species
of songbirds.
The following tree species are commonly found in this region (not necessarily at
the site): white, scarlet, water, pin, schumard, post, willow, blackjack, and other
southern species of oak (Quercus austrina, Q.,_ coccinea, Q.,_ nigra, Q. palustris, Q.,_
shumardi, Q.,_ stellata, Q. phellos, Q,. marilandica, and Q.,_ falcata). Local species of
hickory include nutmeg, pecan, bitternut, water, pale, mockernut and sweet pignut
(Carya myristicaeformis, C. illinoensis, C. cordiformis, C. aguatica, C. pallida, C.
tomentosa, and C. ovalis ). Flowering and other species of dogwoods are populous
in this region (Cornus florida, C. alternifolia, C. amomum, C. racemosa. C. stricta,
and C. asperifolia). Other types of trees include: yellow poplar (tulip
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tree)(Liriodendron tulipifera); sweetgum (Liguidambar styraciflua); redbay (Persea
borbonia); titi (Cyrilla racemiflora); blueberry (Vacciunium corymbosum. V.
atrococcum. and V. cassifolium); blackberry (Rubus cuneifolius. R. canadensis. R.
allegheniensis. R. betulifolius. R. argutus. and R. laciniatus); red maple (Acer
rubrum); loblolly. longleaf and shortleaf pine (Pious taeda. P. palustris. and P.
echinata); american beech (Fagus grandifolia); bayberry (Myrica pennsylvanica);
wintergreen (Gaultheria procumbens); sycamore (Platarius occidentalis); cotton-
wood (Populus deltoides); black tupelo(Nyssa sylvanica); and american elm
(Ulm as americana ).
Foliage found in the woody understory of forested areas of this region include:
wax myrtle (Myrica cerifera), sassafras (Sassafras albidum), hackberry (Celtis
accidentalis), winged elm (Ulmas alata). carolina and american holly (Ilex ambigua
and 1 opaca). sourwood (Oxydendrum aboreum), american hornbeam (Carpinus
caroliniena), eastern hophornbeam (Ostrya virgniana), paw paw (Asimiria triloba),
serviceberry (Amelancher arborea). poison ivy (Rhus radicans), and poison oak
(Rhus toxicodendron).
Wild herbaceous plants are native or naturally established grasses and forbs, in-
cluding weeds. Examples of common wild herbaceous plants found in wooded
areas include: goldenrod (So!idago stricta. S. altissima and S. caesia), beggarweed
(Desmodium tortuosum), partridgegrass (Mitchelle), pokeweed (Phytolacca ameri-
cana). wild ginger (Asarum canadense). spring beauty (Claytonia virginica), chick-
weed (Stellaria pubera and S. media), mayapple (Podophyllum peltatum), twinleaf
(Jeffersonia diphylla). bloodroot (Sanguinaria canadensis), toothwort (Dentaria
multifida and D. diphylla), early saxifrage (Saxifraga virginiensis), foamflower
(Tiarella cordifolia), partridge pea (Cassia fasciculata), violet (violaceae family).
spotted wintergreen (Chimaphia maculata), trailing-arbutus (Epigaea repens),
pennywort (Obolaria virginica), trout lily (Eiythronium americanum). and showy
orchid (Orchis spectabilis).
On the central part of the site bound by the wooded area to the north and the
barren area to the south lies a small wetlands area. Another wetland area is
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located at the far west end of the site. Wetland plants are generally annual, and
wild herbaceous plants that grow on moist or wet areas. Soil properties and fea-
tures affecting wetland plants are texture of the surface layer, wetness, reaction,
and slope. Some of the wildlife commonly attracted to such areas are ducks,
muskrat, raccoon, and red-wing blackbirds.
Examples of wetlands vegetation commonly found in this area include giant reeds
(Arundo donax), millet (Pennisetum glaucum), cutgrass (Leersia hexandra, L.
virginica and L. oryzoids), cat-tail (Typha latifolia, T. glauca, T. augustifolia, and
T. domingensis), and sedges (Cyperaceae family).
The grassy areas of the Carolina Transformer Site are bordered by roads and
buildings found on site. In these areas, grasses, legumes, and wild herbaceous
plants are prevalent. Soil properties and features that affect the growth of grass-
es, legumes, and wild herbs are depth of the root zone, texture of the surface
layer, available water capacity, wetness, surface stoniness, flood hazard, and slope.
Soil temperature and moisture are also considerations. The wildlife attracted to
these areas include bobwhite quail, mourning doves, red fox, cottontail rabbit, and
many species of songbirds.
The grasses generally found m the Carolina Transformer area include fescue
(Festuca myuros, F. octaflora, F. sciurea, F. elatior, F. paradoxa, F. obtusa, and F.
capillata), lovegrass (Eragrostis cilianensis, E. curvula, E. hisuta, E. pilosa, E.
spectabilis, E. refracta, E. cilaris, and E. amabilis), switchgrass, clover (Trifolium
genus), bahiagrass (Paspalum notatum), trefoil, and crownvetch (Coronilla varia).
The most common legumes found in this region is soybean (Glycine max).
Wildflowers and herbs located in the grassland region area include those previous
listed for wooded regions.
Even though four distinct communities have been outlined at the site, it is expect-
ed that species of birds and mammals typical of these areas will be found in more
than one habitat. For a description of typical species in these habitats ( environ-
mental receptors) found at the Carolina Transformer Site, see Section 6.4.1.
A:\CART\SECT6.DRA 6-4
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6.2.2 Observations from Site Visits.
A site visit was conducted on September 18 and 19, 1990. Areas on site and adja-
cent off site were visually surveyed for species composition and evidence of envi-
ronmental stress or damage.
Numerous plant species were noted on and offsite. Four main types of habitat
were evident. First, in most areas on site and in some offsite areas, adjacent her-
baceous vegetation and grasses were growing in unpaved areas. However, there
were some areas where no plant growth was noted in sandy soils.
The second habitat type was a wooded area to the north and west of the site.
Vegetation in this area was not obviously stressed. Only one dead or dying pine
tree was noted and this may or may not have been due to contaminant releases
since surrounding trees were apparently healthy.
The third habitat type was embodied in two small wetland areas, one to the north
of site and one to the west of the site. No standing water was evident in either of
these areas at the time of the site visit. There was no evidence of stressed vegeta-
tion in either wetland area.
The fourth habitat type was an agricultural area to the northeast of the site. Soy-
beans were the crop at the time of the site visit. There was no evidence of impact
from site contaminants on the agricultural area.
Soils in many areas on site and in the drainage ditch along the north boundary of
the site were stained or coated with dark colored residue material. These soils
generally either lacked vegetation or had lesser growth than adjacent areas.
Animal species noted during the site visit included gray squirrel, mourning dove,
white-breasted nuthatch, and common crow. Deer tracks were also observed on
site.
A:.\ CART\ SECT6. OAA. 6-5
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6.2.3 Water Classification
According to the North Carolina Environment Management Commission on Wa-
ter Quality Standards, the Cape Fear River is classified as WS-II waters. Class
WS-11 are waters which are to be suitable as a source of water supply for drinking,
culinary, or food processing purposes, for users desiring maximum protection for
their water supplies. The unnamed tributary which drains the Carolina Trans-
former Site is classified as a Class C stream. Class C waters are waters which are
suitable for fishing, secondary contact recreation, agriculture, and any other uses
except for primary processing purposes.
6.2.4 Management or Preserve Areas and Parks
The Carolina Transformer Site is located in the general area of Pope Park and
Clark Park. However, both of these parks are located at a distance far enough
away that they would not be impacted by the site.
6.2.5 Critical or Sensitive Habitats and Species
Endangered or threatened species that may be found in the region of the site
include red-cockaded woodpecker and red wolf. The presence of these species at
the site has not been documented. Large populations of the red-cockaded wood-
pecker are located on nearby Fort Bragg, approximately 5 miles from the site.
The red wolf has been extirpated from the area since colonial times. Although
recent attempts have been made to reintroduce this animal to the region, contin-
ued human pressures and hybridization with expanding coyote populations have
likely resulted in extinction of genetically pure red wolves in the wild.
6.2.6 Mortality
During site visits, there was no evidence of tree dead zones or animal mortality.
Stressed vegetation was sighted in areas of spills of unknown substances in the
grassy areas near the southwest and northeast corners of the site. Other areas of
no vegetation were sighted in the region north of the main building of Carolina
Transformer.
A.:\CART\SECT6.DRA 6-6
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6.3 CONTAMINANTS OF CONCERN
6.3.1 Chemicals and Concentrations
The chemicals that were evaluated in this environmental evaluation were for the
most part the same chemicals evaluated for the human health risk assessment.
Special consideration was made for environmental exposure media that have the
greatest potential for injury to environmental receptors (i.e. surface water, sedi-
ment and soil). Therefore, due to the threat of adverse environmental impact on
surface water and sediment biota, several additional chemicals were included in
the environmental evaluation. The chemicals of concern were selected on the
basis of: 1) the presence of the chemical at the site at concentrations above
upgradient or background levels, 2) high frequency of detection, or 3) toxicity. A
list of the chemicals of concern for the environmental evaluation are provided in
Table 6-1. The ranges of the contaminant concentrations in soil and sediment at
the site are provided in Table 6-2.
6.3.2 Toxicity and Chemical Characteristics.
This section includes a brief description of the toxicity of the chemicals of concern
to environmental receptors.
6.3.2.1 Inorganic Elements. The inorganic element of concern are aluminum,
arsenic, barium, cadmium, cobalt, chromium, copper, lead, manganese, mercury,
nickel, strontium, titanium, vanadium, yttrium, and zinc. Due to the lace of perti-
nent toxicity data for strontium and yttrium, descriptions of the toxicity of these
two elements are not included in this discussion.
Aluminum. Aluminum is one of the most abundant metals in the earth's crust.
Because of its frequent use and common occurrence, aluminum enters the envi-
ronment from point and non-point sources. Aluminum has moderate acute toxici-
ty to aquatic life and high acute toxicity to birds. Insufficient data are available to
evaluate or predict the short-term effects of aluminum to plants or land animals.
Aluminum has high chronic toxicity to aquatic life. Insufficient data are available
A:\CART\SECT6.0RA 6-7
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TABLE 6-1
CHEMICALS OF CONCERN FOR ENVIRONMENTAL EVALUATION
SOIL SURFACE WATER SEDIMENT
TOLUENE TOLUENE TOLUENE
TETFlACHLOROETHENE BIS(2-ETHYLHEXYL)PHTHALATE BENZENE
TRICHLOROETHENE CARBON DISULFIDE ETHYLBENZENE
1,2-DICHLOROBENZENE CHLOROBENZENE
1,4-DICHLOROBENZENE 1,2-DICHLOROBENZENE
CHLOROBENZENE 1,3-DICHLOROBENZENE
BENZENE 1.4-DICHLOROBENZENE
CARBON TETRACHLORIDE
ETHYL BENZENE
PCB-1260 PCB-1260 PCB-1260
PCB-1254 PCB-1254
PCB-1242 PCB-1248
DIELDRIN 4.4-DDD
CHLORDANE HEPTACHLOR
ARSENIC COPPER BARIUM
BARIUM TITANIUM CADMIUM
COBALT ZINC COBALT
CHROMIUM MANGANESE CHROMIUM
COPPER COPPER
LEAD MERCURY
STRONTIUM NICKEL
TITANIUM LEAD
YTTRIUM STRONTIUM
ZINC ZINC
MANGANESE ALUMINUM
MERCURY YTTRIUM
MANGANESE
VANADIUM
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TABLE 6-2
RANGE OF CONCENTRATIONS IN SEDIMENT AND SOIL
SEDIMENT SOIL
CHEMICAL RANGE OF CHEMICAL RANGE OF
CONCENTRATION (mg/kg) CONCENTRATION (mg/kg)
TOLUENE BDL-2.4 TOLUENE BDL--0.088
ETHYLBENZENE BDL--0.015 TRICHLORDETHENE BDL--0.018
CHLOROBENZENE BDL-0.064 1,2-DICHLOROBENZENE BDL--0.022
1,2-DICHLOROBENZENE BDL--0.05 1,4-DICHLORDBENZENE BDL--0.044
1,4-0ICHLOROBENZENE BDL--0.58 BENZENE BDL--0.20
1,3-0ICHLOROBENZENE BDL--0.17 CARBON TETRACHLORIDE BDL--0.0068
BENZENE BDL--0.028 ETHYL BENZENE BDL--0.043
PCB-1260 BDL--4400 PCB-1260 BDL-110
PCB-1254 BDL-100 DIELDRIN BDL--0.160
PCB-1248 BDL-12 CHLORDANE BDL--0.0008
4,4-000 BOL--0.016 ARSENIC BDL-3.4
HEPTACHLOR BDL-0.0018 BARIUM BDL-130
BARIUM 4.4-140 COBALT BDL-53
CADMIUM BDL-4.7 CHROMIUM BDL-17
COBALT BDL-5.1 COPPER BDL-75
CHROMIUM 1.3-29 LEAD BDL-56
COPPER BDL-3200 STRONTIUM 0.0011-15
MERCURY BDL-0.08 TITANIUM 0.110-490
NICKEL BDL-8.3 YTTRIUM BDL-7.6
LEAD BDL-150 ZINC BDL-78
STRONTIUM BDL-16 MANGANESE 0.0053-510
ZINC 2.0-260 MERCURY BDL--0.1
ALUMINUM 640-27000
YTTRIUM BDL-6.6
MANGANESE 13-180
VANADIUM 2.2-61
NOTES:
BDL -BELOW DETECTION LIMIT
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to evaluate or predict the long-term effects of aluminum to plants, birds, or land
animals.
Aluminum solubility in water is dependent upon pH -as pH increases of decreas-
es from near neutrality, solubility increases. Aluminum is highly persistent in
water, with a half-life greater than 200 days. Aluminum will not accumulate in
fish tissues [13].
Arsenic. Arsenic is a naturally occurring element which is used to make glass,
cloth, and electrical semiconductors. It is also commonly used in fungicides, wood
preservatives, growth stimulants for plants and animals, and in veterinary uses.
Arsenic metabolism and effects are significantly influenced by the animal/plant
tested, the route of administration, the physical and chemical form of the arsenic,
and the dose. Inorganic arsenic compounds are more toxic than organic arsenic
compounds. Arsenic has high acute toxicity to aquatic life, birds and land animals.
Except where soil arsenic content is high ( around smelters and where arsenic-
based pesticides have been used heavily), arsenic does not accumulate in plants to
toxic levels. Where soil arsenic content is high, growth and crop yields can be
decreased. Arsenic has high chronic toxicity to aquatic life, and moderate chronic
toxicity to birds and land animals.
Arsenic and its salts have low solubility in water ( < 1 mg/I). It is highly persistent
in water, with a half-life of more than 200 days. It is also expected to be found at
higher levels in fish tissue, than in the surrounding waters.
Barium. Barium is a yellowish-white solid which exists in a variety of salt forms.
Barium may enter the environment from industrial and municipal waste treatment
plant discharges, or spills. Barium and its salts have moderate acute toxicity to
aquatic life. Insufficient data are available to evaluate or predict the short-term
effects of barium or its salts to plants, birds, or land animals. Barium and its salts
have moderate chronic toxicity to aquatic life. Insufficient data are available to
evaluate or predict the short-term effects of barium or its salts to plants, birds, or
land animals.
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Most of the barium salts are either highly or moderately soluble in water. Con-
centrations of 1 to 1,000 mg.IL and greater possible. Barium is highly persistent in
water, with a half-life greater than 200 days. The concentration of barium found
in fish tissues is expected to be about the same as the average concentration of in
the water from which the fish was taken [13].
Cadmium. Cadmium is a naturally occurring element used in metal alloys, electro-
plating, process engraving, photoelectric cells and in nickel-cadmium electrical
storage batteries. Cadmium enters the environment primarily through industrial
effluents and landfill leaching. In fresh waters, cadmium toxicity is influenced by
water hardness -the harder the water, the lower the toxicity. Cadmium has high
acute toxicity to aquatic life. No data are available on the short-term effects of
cadmium on plants, birds, or land animals. Cadmium has high chronic toxicity to
aquatic life. No data are available on the long-term effects of cadmium to plants,
birds, or land animals.
Cadmium is slightly soluble in water. The solubility in water is less than 1 mg/1. It
is highly persistent in water, with a half-life of greater than 200 days. It is also
expected to be found at higher levels in fish tissue, than in the surrounding waters.
Cobalt. Cobalt is a natural element present in certain ores of the earth's crust,
and is essential to life in trace amounts. Cobalt and its salts have high acute and
chronic toxicity to aquatic life. Insufficient data are available to evaluate or pre-
dict the short-term and long-term effects of cobalt and its salts to plants, birds, or
land animals.
The water solubility of cobalt and its salts range from highly soluble to practically
insoluble. Cobalt and its salts are highly persistent in water, with a half-life of
greater than 200 days. It is also expected to be found at higher levels in fish tis-
sue, than in the surrounding waters.
Chromium. Chromium is a metallic element which exists mainly in the 3 + (III) or
6+ (VI) oxidation states in natural bodies of water, and each form can be convert-
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ed to the other form under appropriate environmental conditions. Chromium is
more toxic in soft water than in hard water. Chromium (VI) has high acute toxici-
ty to aquatic life, and chromium (III) has moderate acute toxicity to aquatic life.
Chromium (III) and chromium (VI) both have high chronic toxicity to aquatic life.
No data are available on the short-term or long-term effects of chromium to
plants, birds, or land animals.
Water solubility of chromium and its salts ranges from low to high. It is highly
persistent in water, with a half-life of greater than 200 days. It is also expected to
be found at higher levels in fish tissue, than in the surrounding waters.
Copper. The toxicity of copper and its compounds to aquatic life varies with the
physical and chemical conditions of the water. Factors such as water hardness,
alkalinity and pH influence copper toxicity. At low concentrations it is an essen-
tial element for both plants and animals. At slightly higher concentrations it is
toxic to aquatic life. Copper and its compounds have high acute and chronic
toxicity to aquatic life. No data are available on the short and long-term effects of
copper to plants, birds, or land animals.
Copper and its salts are highly soluble in water (up to 1,000 mg/I). It is also highly
persistent with a half-life of greater than 200 days. It is also expected to be found
at higher levels in fish tissue, than in the surrounding waters.
Lead. Toxicity of lead to aquatic life is affected by water hardness-the softer the
water, the greater the toxicity. Insufficient data are available to evaluate or pre-
dict the short-term effects of lead and its compounds to plants, birds, or land
animals. Lead and its compounds have high chronic toxicity to aquatic life. Lead
causes nerve and behavioral effects in humans and could cause similar long-term
effects in birds and land animals exposed to lead and its compounds.
Lead and its compounds range in their respective water solubilities from highly
soluble to practically insoluble. It is also highly persistent with a half-life of great-
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er than 200 days. It is also expected to be found at higher levels in fish tissue,
than in the surrounding waters.
Manganese. Manganese occurs in many minerals that are widely distributed in the
earth's crust and, in trace amounts, is an essential element for both plants and
animals. The many different possible manganese compounds may enter the
aquatic environment from natural and industrial sources. Manganese and its com-
pounds have moderate acute and chronic toxicity to aquatic life. Insufficient data
are available to evaluate or predict the short-term and long-term effects to plants,
birds, or land animals.
Manganese and its compounds range m their respective water solubilities from
very soluble to insoluble. It is also highly persistent with a half-life of greater than
200 days. Manganese is expected to be found at about the same levels in fish
tissue, as in the surrounding waters.
Mercury. Elemental mercury is a heavy and relatively inert liquid which is oxi-
dized to inorganic mercury (II) under natural conditions. Bacteria may combine
mercury (II) with an organic fraction to form methylmercury. Mercury (II) and
methylmercury have high acute toxicity to aquatic life. Insufficient data are avail-
able to evaluate or predict the short term effects of mercury (II) or methylmercury
to plants, birds, or land animals. Mercury (II) and methylmercury have high
chronic toxicity to aquatic life. Birds or land animals are subject to secondary
poisoning from consumption of fish contaminated with mercury.
Mercury is highly persistent in water, with a half-life greater than 200 days.
Bioaccumulation is expected in aquatic life (13).
Nickel. Nickel is one of the most common metals occurring in surface waters. It
occurs naturally in surface waters from the weathering of rocks. Other sources of
nickel and compounds to the environment include the burning of coal and other
fossil fuels and discharges from such industries as electroplating and smelting.
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Water hardness affects nickel toxicity to aquatic organisms -the softer the water,
the higher the toxicity. Nickel and its compounds have higher acute toxicity to
aquatic life. Insufficient data are available to evaluate or predict the short-term
effects of nickel and its compounds to plants, birds, or land animals. Nickel and
its compounds have high chronic toxicity to aquatic life. Insufficient data are
available to evaluate or predict the long-term effects of nickel and its compounds
to plants, birds, or land animals.
Nickel and its compounds have water solubilities ranging from low to high.
Nickel and its compounds are highly persistent in water, with half-lives greater
than 200 days. The concentration of nickel and its compounds found in fish tis-
sues is expected to be somewhat higher than the average concentration of nickel
and its compounds in the water from which the fish was taken [13].
Titanium. Titanium dioxide occurs in nature in several mineral (rutile, anatase or
octahedrite, brookite, ilemite and perovskite ). Titanium dioxide occurs naturally
in the environment and also enters the environment from industrial and municipal
waste treatment plant discharges. Titanium dioxide is highly toxic to birds. Insuf-
ficient data are available to evaluate or predict the short-term effects of titanium
dioxide to plants, aquatic life; or land animals. Insufficient data are available to
evaluate or predict the long-term effects of titanium dioxide to aquatic life, plants,
birds, or land animals.
Titanium dioxide is slightly soluble in water (1 mg/Lor less). Titanium dioxide is
highly persistent in water, with a half-life greater than 200 days. The concentra-
tion of titanium dioxide found in fish tissues is expected to be about the same as
the average concentration of titanium dioxide in the water from which the fish was
taken [13].
Vanadium. Vanadium (fume or dust) is an element which is widely dispersed in
the earth's crust at low concentrations. The acute toxicity of elemental vanadium
(fume or dust) to aquatic life is unknown, but the compound ammonium vanadate
is moderately toxic to aquatic life. Insufficient data are available to evaluate or
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predict the short-term effects of elemental vanadium (fume or dust) to plants,
birds, or land animals. The chronic toxicity of elemental vanadium (fume or dust)
to aquatic life is unknown, but ammonium vanadate has high chronic toxicity to
aquatic life. Insufficient data are available to evaluate or predict the long-term
effects of vanadium (fume or dust) to plants, birds, or land animals.
Elemental vanadium is not likely to dissolve in surface water. It will probably be
highly persistent in aquatic ecosystems, but will not accumulate in edible tissues or
aquatic species [13].
Zinc. The toxicity of zinc to aquatic life is related to water hardness, with in-
creased toxicity occurring in softer waters. Zinc and its salts have high acute and
chronic toxicity to aquatic life. Insufficient data are available to evaluate or pre-
dict the short-term or long-term effects of zinc and its compounds to plants, birds,
or land animals.
Zinc exists as a variety of salts, many of which are highly soluble in water. It is
also highly persistent with a half-life of greater than 200 days. Zinc is expected to
be found at about the same levels in fish tissue, as in the surrounding waters.
6.3.2.2 PCBs/Pesticldes. The pesticide contaminants of interest include
chlorodane, dieldrin, heptachlor, and 4,4,4-DDD. Due to a lack of toxicity data
for dieldrin, heptachlor, and 4,4,4-DDD, this contaminant are not included in the
following discussion.
PCBs (Archlor 1242, 1248, 1254. and 1260). Acute toxic effects of PCBs may in-
clude the death of animals, birds, or fish, and death or low growth rate in plants.
Acute effects are seen two to four days after animals or plants come in contact
with the substance. PCBs have high acute toxicity to aquatic life. Insufficient data
are available to evaluate or predict the short-term effects of PCBs to plants or
animals. Chronic toxic effects may include shortened lifespan, reproductive prob-
lems, lower fertility, and changes in appearance or behavior. Chronic effects can
be seen long after first exposure(s) to PCBs. PCBs have high chronic toxicity to
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aquatic life. Insufficient data are available to evaluate or predict the long-term
effects of PCBs to plants, birds or land animals.
PCBs are slightly soluble in water (1 mg/L or less). The relative distribution of
the various PCBs depends on the level of chlorination. Some PCBs will probably
be highly persistent in water, with half-lives greater than 200 days. Potential PCB
distribution in the various environmental compartments can have the following
ranges: air, 0-34 percent; terrestrial soils, 33-52 percent; water, 0-1.8 percent;
suspended solids, 0.05-0.08 percent; aquatic biota, 0.02-0.03 percent; aquatic sedi-
ments, 30-50 percent. Bioaccumulation of PCBs is expected in fish, birds, or land
animals.
Chlordane. Chlordane is an insecticide of the polycyclic chlorinated hydrocarbon
class of pesticides. Chlordane has high acute and chronic toxicity to aquatic life.
Insufficient data are available to evaluate or predict the short-term or long-term
effects of chlordane to birds or land animals.
Chlordane is slightly soluble in water ( < 1 mg/I). It is highly persistent in water,
with a half-life of greater than 200 days. About 50.7 percent of chlordane will
eventually end up in terrestrial soil; about 47.3 percent will end up in aquatic
sediments; the rest will end up in the water. Bioaccumulation is expected to be
considerably high [13].
6.3.2.3 Organics. Organic contaminants of concern include bis (ethyl-
hexyl)phthalate; 1,2,4-trichlorobenzene; benzene; carbon tetrachloride;
chlorobenzene; 1,2-dichlorobenzene; 1,3-dichlorobenzene; ethylbenzene; tetrachlo-
roethylene; toluene; and trichloromethane. Pertinent toxicity data are not avail-
able for 1,3-dichlorobenzene and 1,4-dichlorobenzene, therefore, toxicity descrip-
tions are not included for those chemicals.
Bis (2-ethylhexyl) phthalate. No ambient water quality criteria is available for this
chemical. EPA reported acute and chronic LOELs for phthalate esters for aquat-
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ic organisms of 940 and 3 ug/1, respectively [20]. Daphnia magna exposed to bis
(2-ethylhexyl) phthalate had an LC50 of 11,000 ug/L. Chronic toxicity was ob-
served at 8.4 ug/L in rainbow trout. Daphnia magna had significant adverse re-
productive effects at 3 ug/L [14].
Information on the toxicity of bis (2-ethylhexyl) phthalate to wildlife is unavailable.
The LD50 for mice is 30,000 mg/kg [15]. Bis (2-ethyl-hexyl) phthalate has caused
cancer in laboratory animals. Other toxic effects in laboratory animals include
decreased growth, increased liver and kidney weights, reduced fetal weight, and
increased number of fetal resorptions [16]. The lowest chronic effect level in lab
animals is 19 mg/kg based on increased liver weights in guinea pigs [17].
J,2,4-Trichlorobenzene. 1,2,4-Trichlorobenzene has been used as a carrier to
apply dyes to polyester materials, a termite pesticide, an aquatic herbicide, an
herbicide intermediate, a heat transfer medium, a dielectric fluid in transformers,
a degreaser, and a lubricant. 1,2,4-trichloro-benzene may enter the environment
from industrial discharges, municipal waste treatment discharges, spills, or in run-
off following insect control applications. 1,2,4-Trichlorobenzene has high acute
toxicity to aquatic life. Its use as an herbicide indicates it can be expected to have
high acute toxicity to plants. Insufficient data are available to evaluate or predict
the short-term effects of 1,2,4-trichlorobenzene to birds of land animals. 1,2,4-
Trichlorobenzene has high chronic toxicity to aquatic life. Insufficient data are
available to evaluate or predict the long-term effects of 1,2,4-trichlorobenzene to
plants, birds, or land animals.
1,2,4-Trichlorobenzene is moderately soluble in water ( < 1000 mg/I). 1,2,4-
Trichlorobenzene is slightly persistent in water, with a half-life of between 2 to 20
days. About 93 percent of 1,2,4-trichlorobenzene will eventually end up in air;
about 2.6 percent and 2.4 percent, respectively, will end up in terrestrial soil and
aquatic sediments; the remainder will end up in the water. The concentration of
1,2,4-trichlorobenzene found in fish tissues is expected to be much higher than the
average concentration of 1,2,4-trichlorobenzene in the water from which the fish
was taken [13].
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Benzene. Benzene has high acute toxicity to aquatic life. It can cause death in
plants and roots and membrane damage in leaves of various agricultural crops.
No data are available on the short-term effects of benzene on birds of land ani-
mals. Benzene has high chronic toxicity to aquatic life. No data are available on
the long-term effects of benzene on plants, birds, or land animals.
Benzene is moderately soluble in water ( < 1000 mg/I). Benzene is slightly persis-
tent in water, with a half-life of between 2 to 20 days. About 99.5 percent of
benzene will eventually end up in air; the rest will end up in the water. The
concentration of benzene found in fish tissues is expected to be somewhat higher
than the average concentration of benzene in the water from which the fish was
taken [13].
Carbon Tetrachloride. Carbon tetrachloride is a clear, colorless, non-flammable
liquid which is heavier than water. Carbon tetrachloride has high acute toxicity to
aquatic life. No data are available on the short-term effects of carbon tetrachlo-
ride on plants, birds, or land animals. Carbon tetrachloride has high chronic toxic-
ity to aquatic life. No data are available on the long-term effects of carbon tetra-
chloride on plants, birds, or land animals.
Carbon tetrachloride is moderately soluble in water ( < 1000 mg/I). Carbon tetra-
chloride is nonpersistent in water, with a half-life of less than two days. About
99.9 percent of carbon tetrachloride will eventually end up in air. The concentra-
tion of carbon tetrachloride found in fish tissues is expected to be somewhat high-
er than the average concentration of carbon tetrachloride in the water from which
the fish was taken [13].
Chlorobenzene. Chlorobenzene has moderate acute toxicity to aquatic life. The
acute toxicity of chlorobenzene in small mammals was found to be low. An esti-
mated acute inhalation LC50 of 20 mg/I (4,300 ppm) was reported in mice exposed
for 2 hours. In acute (single exposure) studies in cats , all animals died 2 hours
after removal from exposure following inhalation of 8,000 ppm and after 7 hours
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at 3,700 ppm [18]. Insufficient data are available to evaluate or predict the short-
term effects of chlorobenzene to plants, birds, or land animals.
Chlorobenzene has moderate chronic toxicity to aquatic life. Insufficient data are
available to evaluate or predict the long-term effects of chloro-benzene to plants,
birds, or land animals.
Chlorobenzene is moderately soluble in water ( < 1000 mg/I). Chlorobenzene is
slightly persistent in water, with a half-life of between 2 to 20 days. About 99.25
percent of chlorobenzene will eventually end up in air; the remainder will end up
in the water.
1,2-Dichlorobenzene. 1,2-Dichlorobenzene has moderate acute toxicity to aquatic
life and has caused injury, stunting and harvest yield decrease in various agricultur-
al crops. Insufficient data are available to evaluate or predict the short-term ef-
fects of 1,2-dichlorobenzene to birds or land animals. 1,2-Dichlorobenzene has
moderate chronic toxicity to aquatic life. Insufficient date are available to evalu-
ate or predict the long-term effects of 1,2-dichlorobenzene to plants, birds, or land
animals.
1,2-Dichlorobenzene is slightly soluble in water ( < 1 mg/I). It is slightly persistent
in water, with a half-life of between 2 to 20 days. About 97.5 percent of 1,2 di-
chlorobenzene will end up in water; about 0.5 percent will end up in terrestrial
soil; and the remainder will end up in aquatic sediments. Some bioaccumulation
is expected in fish [13).
Ethylbenzene. No information on the toxicity of ethylbenzene to terrestrial wild-
life was available (14). Laboratory studies have found an oral LD50 of 3,000mg/kg
in the rat. Test animals subjected to both acute and chronic exposures developed
liver and kidney pathologies and nervous system disorders. No toxic effects were
seen .during a 6-month oral exposure of 13.6 and 136 mg ethylbenzene/kg of body
weight/day to rats (14). No information is available for birds.
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Tetrachloroethylene. Tetrachloroethylene is heavier than water; it may enter the
environment from industrial discharges, municipal waste treatment plant discharg-
es, or spills. Tetrachloroethylene has moderate acute and chronic toxicity to
aquatic life. Insufficient data are available to evaluate or predict the short-term or
long-term effects of tetrachloro-ethylene to plants, birds, or land animals.
Tetrachloroethylene is moderately soluble in water ( < 1000 mg/I). Tetra-
chloroethylene is non-persistent in water, with a half-life of less than two days.
About 99.8 percent of tetrachloroethylene will eventually end up in air; the re-
mainder will end up in the water. The concentration of tetrachloroethylene found
in fish tissues is expected to be somewhat higher than the average concentration
of tetrachloroethylene in the water from which the fish was taken (13].
Toluene. Toluene is obtained mainly from tar oil. It is a commonly used solvent
for extraction processes and may enter the environment mainly from industrial
discharges. Toluene has moderate acute and chronic toxicity to aquatic life. Tolu-
ene has caused leaf membrane damage in plants. Insufficient data are available to
evaluate or predict the short-term or long-term effects of toluene to birds or land
animals.
Little information is available on the toxicity of toluene to terrestrial species.
Rabbits given a single oral dose of 275 mg/kg body weight, excreted 74 percent of
the total dose within 24 hours, indicating a short biologic half-life (19]. Oral LD50
for rats range from 4,300 to 7,500 mg/kg (USEPA 1981). A NOEL of 30
mg/kg/day has been reported for a study with rats. Information on avian toxicity is
not available.
Toluene is slightly soluble and non-persistent in water. It has a half-life in water
of less than 2 days. About 99.5 percent of toluene will eventually end up in air;
the rest will end up in water. The concentration of toluene found in fish tissues is
expected to be somewhat higher than the average concentration of toluene in the
water from which the fish was taken.
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Trichloromethane. Trichloromethane is a clear, colorless nonflammable liquid
and is heavier than water. Trichloromethane may enter the environment from
industrial discharges, municipal waste treatment plant discharges, or spills. Tri-
chloromethane has moderate acute and chronic toxicity to aquatic life. Insufficient
data are available to evaluate or predict the short-term or long-term effects of
trichloromethane to plants, birds, or land animals.
Trichloromethane is moderately soluble in water ( < 1000 mg/I). Trichloro-ethylene
is nonpersistent in water, with a half-life of less than 2 days. About 99.6 percent
of trichloromethane will eventually end up in air; the remainder will end up in
the water. The concentration of trichloromethane found in fish tissues is expected
to be somewhat higher than the average concentration of trichloromethane in the
water from which the fish was taken (13].
6.4 EXPOSURE CHARACTERIZATION
6.4.1 Potential Receptors.
In this section the plant, animal and aquatic species which are either documented
to occur or expected to occur at the Carolina Transformer Site are identified.
6.4. 1. 1 Terrestrial Receptors. For continuity and clarity, the plants, mammals
and birds will be identified according to their predominant habitat. As mentioned
in section 6.2.1 some species overlap between habitats is expected to occur.
Plants. The principal vegetation of the wooded environment is loblolly, longleaf
and shortleaf pine (Pinus taeda, P. palustris, and P. echinata), and sycamore
(Platnus occidentalis). A variety of wild herbs and plants in the woody understory
are. found in the forested area. Although there are no predominant species found
onsite, species that may be present are listed in Section 6.2.1. Vegetation found in
the wetland area of the site include cat-tail (Typha) and sedges (Cyperaceae fami-
ly). The foliage of the grassland area is diverse with a variety of grasses.
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Mammals. Species of mammals that occur in the forested areas of North Carolina
included eastern cottontail rabbit (Sylvilagus floridanus), eastern chipmunk
(Tamias striatus), gray squirrel (Sclurus carolinensis), red squirrel (Tamia sciurus
hucisonicus), white footed mouse (Peromyscus leucopus), cotton mouse
(Peromyscus gossypinus), golden mouse (Ochrotomys nuttalli), woodland vole
(Microtus pirietorum), long tailed weasel (Mustela frenata), striped skunk
(Mephitis memphitis), racoon (Procyonlotor), white-tailed deer (Odocoileus
virginianus ), silver-haired bat (Lasionycteris noctivagons ), eastern pipistrelle
(Pipistrellus subflavus), and red bat (Lasiurus borealis).
The following are potential mammal species of the grassland area; eastern cotton-
tail rabbit (Sylvilagus floridanus), eastern mole (Scalopus aguaticus), white footed
mouse (Perornyscus leucopus ), meadow vole (Microtus pennsylvanicus ), house
mouse (Mus musculus), meadow jumping mouse (Microtus pennsylvanicus), east-
ern harvest mouse (Reithrodontomys humulis), norway rat (Rattlus norvegicus),
hispid cotton rat (Sigrnodon hispidus), black rat (Rattus rattus), long-tailed weasel
(Mustela frenata) and red fox (Vulpes vulpes).
Common species of the wetlands habitat is 'the muskrat (Ondatra zibethicus),
raccoon (Procyon lotor), marsh rabbit (Sylviagus palustris), virgin opossum
(Dideophis virginian), southeastern shrew (Sorex longirostris), southern short-
tailed shrew (Blarina carolinensis), least shrew (Cryptotis parva), marsh rice rat
(Oryzomys palustris) and mink (Mustela vison).
Birds. Birds of the wooded regions in the area of the site include broad-winged
hawk (Buteco platypterus), screech owl (Otus asis), great horned owl (Bubo
virginianus), barn owl (Iy!.Q alba), barred owl (Strica varia), long-eared owl (Asia
otus), common flicker (Colaptes auratus),yellow-shafted flicker (Colaptes auratus),
hairy woodpecker (Dendrocopus villosus), downy woodpecker (Dendrocopus
pubescens), pileated woodpecker (Dryocupus pileatus), red-bellied woodpecker
(Melanerpes carolinus), red-headed woodpecker (Melanerpes erythrocephalus),
yellow-bellied sapsucker (Sphyrapicu varius), red-cockaded woodpecker (Picoides
pubescens), blue jay (C_yanocitla cristata), red-eyed vireos, (Vireo olivaceus), soli-
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tary vireo (Vireo solitrius), warbling vireo (Vireo gilvus), prothonotary warbler
(Protonotaria citrea), pine warbler (Dendroica pinus),black and white warbler
(Mniotilta varia), ovenbird (Seirus aurocapillus), cardinal (Cardinalis cardinalis),
evening grosbeak (Hesiperiphona vespertina), robin (Turdus migratorius), tufted
titmouse (Dendroica discolor), wood thrush (Hylocichla mustelina), eastern wood
peewee (Coritopus virens), eastern bluebird (Sialia sialis), carolina chickadee
(Parus carolinensis), brown-headed nuthatch (Sitla pusilla), Bachman's sparrow
(Aimophila aestivalis),and english sparrow (Passer domesticus).
The following birds may potentially be found in grassland areas of the Carolina
Transformer region: prairie warbler (Dendroica discolor), grey catbird (Dumetella
carolinerisis), yellow warbler (Pendroica petechia), yellow throat (Geothlypis
trichas), song sparrow (Melospiza melodia), white-throated sparrow (Zonotrichia
albicollis), field sparrow (Spizella pusilla),white crowned sparrow (Zonotrichia
Jeucoprys), savannah sparrow (Ipswich sparrow), grasshopper sparrow
(Ammodramus savannarum), rufous-sided towhee (Pipilo erythrophthalmus), bob-
white quail (Colinus virginianus), mourning doves (Zenaida macroura), and spar-
row hawk (Falso sparverius ).
Bird species that are probable to occur at the wetland area of the site include,
green heron (Bu tori des virescens ), spotted sandpiper (Actitus Macularia ),
woodduck (Aix sponsa), pintails (Anas acuta), blue-wing teal (Anas discors), mal-
lard (Anas platyrhynchos), black duck (Anas rubripes), and swamp sparrow
(Melospiza georgiana ).
Amphibians. The types of amphibians found in the forested area include: grey
treefrogs (Hyla chrysoscelis, H. versicolor), green treefrog (Hyla cinerea), spring
peeper (Hyla crucifer), pine woods treefrog (Hyla gratiosa), squirrel treefrog
(Hyla squirella), little grass frog (Limnaoedus ocularis), Brimley's chorus frog
(Pseudacris brimleyi), southern chorus frog (Pseudacris nigrita), ornate chorus frog
(Pseudacris ornata), pickerel frog (Rana palustris), carpenter frog (Rana
virgatipes), oak toad (Bufo quercicus), and american toad (Bufo americanus).
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The wetland areas of the coastal plains region of North Carolina are home to
many amphibians including: eastern spadefoot toad (Scaphiopus holbrooki), south-
ern toad (Bufo terrestris), Fowler's toad (Bufo woodhousei), american toad (Bufo
americanus), southern cricket frog (Acrid gryllis), pine barrens treefrog (Hyla
andersoni), bullfrog (Rana catesbeiana), southern leopard frog (Rana
sphenocephala), and eastern narrowmouth toad (Gastrophryne carolinensis).
Reptiles. A variety of reptiles are present in the wooded areas of this region.
Species of turtle found in this area include: yellowbelly slider (Chrysemys scripta),
chicken turtle (Deirochelys reticularia ), and eastern box turtle (Terrapene caroli-
na ). Lizards found in this region include: carolina anole (Anolis carolinensis ),
eastern fence lizard (Sceloporus undulatus), five-lined skink (Eumeres fasciatus),
and ground skink (Scincella lateralis).
Snakes, both non-poisonous and poisonous, are common to the wooded coastal
plains area of North Carolina. Non-poisonous species of snakes include: worm
snake (Carphophis amoenus), scarlet snake (Cemophora coccinea), ringneck snake
(Diadophus punctatus), rat snake (Elapha obsoleta), southern hognose snake
(Heterodon Simus), mole king snake (Lampropeltis calligaster), eastern milk
snake or scarlet king snake (Lampropeltis triangulum), rough green snake
(Opheodrys aestivus), pine woods snake (Rhadinaea flavilata), brown snake
(Storeria dekayi), redbelly snake (Storeria occipitomaculata), southeastern
crowned snake (Tantilla coronata), rough earth snake (Virginia stratula), and
smooth earth snake (Virginia va!eriae ). Poisonous species of snakes found in this
region include: eastern coral snake (Micrurus fulvius), copperhead (Alkistrodon
contortrix), timber rattlesnake (Crotalus horridus), and pygmy rattlesnake
(Sistrurus miliarius ).
Reptiles common to the marshy areas of this region include: snapping turtle
(Chelydra serpentina), eastern musk turtle (Sternotherus odaratus), eastern mud
turtle (Kinosternon subrubrum), spotted turtle (Clemmys guttata), mud snake
(Farancia abacura), rainbow snake (Farancia erytrogramma), eastern ribbon snake
(Thamnophis sauritus), and cottonmouth (poisonous)(Agkistrodon piscuvorus).
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In the grassland areas of this region, reptiles commonly found include: slender
grass lizard (Ophisaurus attenuatus), eastern grass lizard (Ophisaurus ventralis),
black racer (Coluber constrictor), corn snake (Elapha guttata), eastern hognose
snake (Geterodon platyrhinos), eastern king snake (Lampropeltis getulus), and
eastern garter snake (Thamnophis sirtalis ).
6.4. 1.2 Aquatic Receptors. On the Carolina Transformer Site, surface water is
not permanent enough to support fish populations. Only amphibians and reptiles,
previously listed, are potential aquatic receptors.
The nearby Cape Fear River does support a variety of fishes, amphibians and
reptiles. Seventy-one species of fishes are found in the Cape Fear River. The
families of fishes indigenous to the Cape Fear River include: lampreys
(Pctromyuzontide ), sturgeons (Acipenseridae ), gars (Lepisosteidae ), bowfin
(Amiidae), eels (Anguillidae), herrings (Clupeidae), mudminnows (Umbridae),
pikes (Esocidae), native minnows (Cyprinidae), suckers (catastomidae), catfishes
(lctaluridae ), cavefishes (Amblyopsidae), pirate perch (Aphredoderidae), kill fishes
(Cyprinodontidae ), live bearers (Poecilidae ), basses (Percichthyidae ), sunfishes
(Centrarchidae), and perches (Percidae).
Amphibians and reptiles found in the Cape Fear habitat include: green frog (Rana
clamintans), river frog (Rana hecksheri), river coater (Chrysemys concinna), flori-
da coater (Chrysemys floridana), rainbow snake (Farancia erythrogaster), banded
water snake (Nerodia fasciata), and brown water snake (Nerodia taxispilota).
6.4.2 Exposure Pathways.
This section identifies exposure pathways for animals, and plants at or potentially
entering the site. There are a number of direct and indirect pathways by which
wildlife can be exposed to the chemicals of concern at the Carolina Transformer
Site. Direct pathways would be direct contact or ingestion of contaminated media
such as soil, sediment, or water. Indirect pathways, for the purpose of this assess-
ment, are those in which an animal consumes other previously contaminated or-
ganisms.
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Exposure media and routes may differ between various organisms due to their
physiological and behavioral differences. For example, fish may be exposed to
contaminants directly via absorption of contaminated water and indirectly via
ingestion of other previously contaminated organisms. Likewise, duck species rely
on both aquatic animals (i.e., insects, crustaceans, and snails) and plants for some
portion of their dietary intake. However, the percentage of animal food versus
plant food in the diet differs from species to species ( e.g. blue winged teal con-
sumes approximately 30 percent animal food, while mallards consume approxi-
mately 20 percent animal food, and wood ducks approximately 10 percent animal
food). Variables such as these must be considered in assessing exposure to eco-
logical receptors.
Some contaminants of concern at the site, especially cadmium, mercury, and PCBs
are known to bioaccumulate in various organisms and therefore increase the
chance for exposure via the food chain. Consequently, predators using the habitat
around the Carolina Transformer Site exclusively may potentially be at greater risk
because they may be exposed both to contaminated biota and to contaminated
drinking water.
6.4.2. 1 Exposure of Aquatic Species. Fish and other aquatic wildlife found in
the Cape Fear River habitat are not likely to be impacted by the contaminants
found at Carolina Transformer. Although no sampling was performed at the
Cape Fear River, the site is small enough and too far away to contaminate the
river.
The Cape Fear River is potential habitat for both invertebrate and vertebrate
species. A comparison between available surface water concentrations and ambi-
ent water quality criteria (A WQC) is presented in Table 6-3.
6.4.2.2. Exposure of Birds. Birds may be exposed either directly or indirectly to
contaminants at the Carolina Transformer Site. Direct pathways for birds include
ingestion of contaminants in sediments or water, and direct contact with contami-
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TABLE 6-3
AMBIENT WATER QUALITY CRITERIA FOR CHEMICALS OF CONCERN
CHEMICAL MAX. CONG. FRESHWATER
IN SW (ug/1) CHRONIC AWQC ACUTEAWQC
COPPER 130 12 (b) 18 (b)
TITANIUM 12
ZINC 180 110 (b) 120 (b)
MANGANESE 480
TOLUENE 0.62 17500 (a)
CARBON DISULFIDE 38
BIS(2-ETHYLHEXYL)PHTHALATE 100 3 (a) 940 (a)
PCB-1260 12 0.014 2.0
NOTES:
(a) EQUALS LOWEST OBSERVED EFFECT LEVEL
(b) EQUALS HARDNESS DEPENDENT ON 100 mg/I OF CaCO3
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nated soil or sediments. Some birds, such as belted kingfishers, build their nests
by burrowing into the soil along river banks, road cuts, and other exposed bank
area. Activities such as dust bathing also increase exposure to contaminated soil.
Unfortunately, estimates of exposure via these pathways are not easily quantified
using available data.
Birds may be exposed to chemicals indirectly by ingesting contaminated food.
Exposure via this pathway is the greatest in those species which consume food
items which tend to bioaccumulate or bioconcentrate contaminants. For example,
many aquatic invertebrates and fish are known to bioaccumulate some heavy
metals and organic chemicals. Therefore this pathway may be significant for
ducks which rely on aquatic invertebrates for a portion of their dietary intake.
A large portion of the diet of smaller birds consists of insects such as grasshoppers
and crickets. Hawks also may be exposed to contaminants via food, as primary
food sources for most hawks are rodents ( e.g. field mice). Available data are not
sufficient to estimate uptake and accumulation of contaminants in insects or ro-
dents.
6.4.2.3 Exposure of Mammals. Mammals may be exposed to contaminants at
the Carolina Transformer Site via the ingestion of food, water, or soil or via direct
contact with contaminated media. For example, the raccoon and skunk are known
to prey on small rabbits and rodents and they may be exposed to chemicals that
have accumulated in these animals. Omnivorous or herbivorous mammals such as
rabbits and muskrats could be exposed to chemicals of concern by ingesting con-
taminated vegetation such as grasses and other small land plants. These mammals
may also inadvertently ingest contaminated soil while feeding. Direct contact of
contaminated soil could frequently occur among burrowing animals. Skunks dig
and root in the soil while searching for insects and grubs. Rabbits and raccoons
groom frequently and are likely to ingest contaminated soil while grooming. Rac-
coons and muskrats prey on fish and crustaceans. Terrestrial organisms using the
surface water at the site as a source of drinking water might also be exposed to
chemicals of potential concern.
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6.4.2.4 Exposure of Amphibians and Reptiles. Amphibians and reptiles may
be exposed to contaminants in soil, sediment, and water via ingestion and direct
contact with contaminated medias and air. Amphibians and reptiles may also be
exposed to contaminants at the site via inhalation of particulates due to their close
association with soil and sediment. Turtles could be exposed to chemicals of con-
cern by ingesting contaminated vegetation such as grasses and other small land
plants. These reptiles may also inadvertently ingest contaminated soil while feed-
ing. Direct contact of contaminated soil could frequently occur among burrowing
snakes and turtles. Some turtles and snakes bury their eggs by burrowing into the
soil or sediments. This activity may also potentially expose the eggs to contami-
nants in soils and sediments.
Amphibians and reptiles using the surface water at the site as a source of drinking
water might also be exposed to chemicals of concern.
6.4.2.5 Exposure of Plants. Plants may be exposed to contaminants in soil, and
water. Surface water runoff from contaminated areas may percolate into plant
root zones, and plants may then be exposed to these contaminants as they are
taken up through the roots. Phytotoxicity data are limited and plant uptake values
vary greatly from species to species.
6.5 RISK CHARACTERIZATION
The environmental receptors discussed in Section 6.4.1 may be exposed to chemicals
present in the area via surface water, sediment, and soil. This section consists of a
qualitative assessment of the potential hazards to environmental receptors that may
exist at the Carolina Transformer Site. This assessment is structured around the po-
tential toxicity of the chemicals of concern, identified in section 6.4.1.3.
6.5.1 Risks to Aquatic Organisms.
Table 6-3 presents the comparison between maximum surface water concentrations
detected at the site and the chronic ambient water quality criteria (A WQC). Of the
eight chemicals of concern detected in surface water at levels above background, five
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chemicals had water quality criteria. Of these, copper, zinc, plthalate and PCB con-
centrations exceed toluene, bis (2-ethylhexy) the chronic A WQC or toxicity value.
However, these chemicals were detected in surface water samples from locations
80SW, 82SW which do not retain water throughout the year. Surface water organisms
or receptors may not be present at these locations. Therefore, the exposure to sur-
face water onsite by fish and other aquatic organisms would be unlikely.
6.5.2 Risks To Terrestrial Animals.
Estimates of risks to terrestrial animals at Carolina Transformer are difficult to make
because toxicity data are limited and animal toxicity may vary greatly from species to
species. Some chemicals of concern in soil, sediment, and surface water at the site
demonstrate the potential for toxic effects and bioaccumulation which may cause ad-
verse effects to some species via the food chain. Chemicals detected in soil and sedi-
ment which are known to cause adverse effects in animals include lead, PCB-1260,
benzene, and chlorobenzenes. The magnitude of any potential adverse effects cannot
be estimated based on current available data. However, especially the PCB soil and
sediment concentrations are at levels of potential concern.
6.5.3 Risks To Birds.
The possible exposure pathways for birds have been discussed in Section 6.4.2.2. Due
to exposure pathways of waterfowl, they may be exposed to risks from chemicals of
concern due to direct sediment exposures. In addition, predatory avian species may
be at risk due to food chain exposures. Data to accurately assess the potential risk
associated with exposure of birds to chemicals of concern are not available. However,
as with terrestrial animals, exposure to PCB's in soil, sediment, and surface water may
have adverse effects on avian species.
6.5.4 Risks To Plants.
As mentioned earlier, stressed or the absence of vegetation was observed in areas
onsite. The contaminants detected in soil may be responsible for these areas. Ac-
cording to toxicity information provided in Section 6.3.2. 1,2,4-trichlorobenzene, ben-
zene, 1,2 -dichlorobenzene, toluene and PCBs have potential for causing damage to
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plants. Assessment of adverse effects to plants at the site are difficult to make be-
cause toxicity data are limited and plant toxicity varies greatly from species to species.
6.5.5 Risks to Amphibians and Reptiles.
The possible exposure pathways for amphibians and reptiles have been discussed in
Section 6.4.2.4. Due to exposure pathways for turtles and snakes, they may be ex-
posed to risks from chemicals of concern due to direct surface water sediment, and
soil exposures. In addition, herbivorous reptilian species may be at risk due to food
chain exposure
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6.6 BIBLIOGRAPHY
Although not specifically cited, the following were referenced during the preparation
of this section.
Conant, R. (1975). "A Field Guide to Reptiles and Amphibians of Eastern and Cen-
tral North America." Houghton Mifflin Company, Boston.
Duncan, W. and Foote, L. (1975). Wildflowers of the Southeastern United State.
University of Georgia Press, Athens.
North Carolina Department of Parks and Recreation. Personal Interview (Sep 13,
1990)
Potter, E., Parnell, J. and Telings, R.P. (1980). Birds of the Carolinas. University of
North Carolina Press, Chapel Hill.
Radford, A., Ahles, H., and Bell, C. (1968). Manual of the Vascular Flora of the
Carolinas. University of North Carolina Press, Chapel Hill.
U.S. Department of Agriculture, Soil Conservation Service (1984). Soil Survey of
Cumberland and Hoke Counties. North Carolina. USDA
U.S. Environmental Protection Agency. (1980). Ambient Water Quality teria for
Phthalate Esters. Office of Water Regulations and Standards. Criteria and Standards
Division. October, 1980. EPA 40/5-8-067.
Wangersky, P.J. (1977). "The Role of Particulate Matter in the Productivity of Sur-
face Waters." Helga!. Wiss. Meeresunters 30, 546-564.
Webster, W.D., Parnell, J. and Biggs, W. (1985). Mammals of the Carolinas. Virginia,
and Maryland. University of North Carolina Press, Chapel Hill.
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7.0 Summary
7 .1 Data Collection and Evaluation
The data collected and used in the risk assessment for the Carolina Transformer Site
included data from Phases I, II, and III of the Remedial Investigation. The evalua-
tion of the data from the three investigations was the basis for determining the chemi-
cals of potential concern.
Chemicals identified as chemicals of potential concern which were us_ed in the actual
calculation of risk are listed in Table 2-14.
The following steps eliminated chemicals of potential concern from further consider-
ation in the baseline risk assessment:
• Data qualifiers resulting in presumptive evidence of presence of material
resulted in compounds being eliminated from further consideration.
• If a chemical was detected only once in all samples analyzed for that chemi-
cal in that media, the exposure potential for that chemical was considered to
be low. A5 a result, compounds were eliminated from further consideration.
• Metals were excluded that were detected at less than two times representa-
tive background.
• If a chemical was detected infrequently (two to three times) and at low
concentrations, it was eliminated from further consideration.
• If a chemical had very low toxicity and was detected at low concentrations, it
was eliminated from further consideration.
7.2 Exposure Assessment
Based on a detailed evaluation of exposure pathways and receptors, the following
exposure scenarios were selected for quantitative evaluation in this assessment:
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• Current exposure of offsite residents to contaminants in soil through inci-
dental ingestion and dermal contact, and in surface water and sediment
through dermal contact. Exposure through ingestion of garden produce
planted in contaminated soil was also evaluated.
• Current exposure of onsite trespassers to contaminants in soil through inci-
dental ingestion and dermal contact, and in surface water and sediment
through dermal contact.
• Future exposure of onsite residents to contaminants in groundwater through
ingestion, direct contact, and inhalation; and to contaminants in soil through
incidental ingestion and dermal contact.
• Future exposure to onsite residents to contaminants in garden produce
through ingestion of contaminated produce.
The following media were not evaluated in exposure scenarios:
• Groundwater ( deep aquifer), because of the inability to assess contamina-
tion due to lack of data.
• Air, because of low concentrations of volatile and semi-volatile organic
compounds in the remaining media and low average wind speeds in the
area.
• Fish, because of the inability to assess contamination due to lack of data
from the Cape Fear River.
Average daily intakes were calculated for each chemical of potential concern for each
exposure scenario. These calculations were based on validated data from the three
phases of the RI, and employed EPA recommended equations for calculating doses.
7.3 Toxicity Assessment
A toxicity assessment was performed for each of the chemicals of potential concern.
This assessment included information on the critical toxicity values employed in the
risk characterization. The toxicity assessment presents important information on the
toxicologic properties of each of the chemicals of potential concern.
7.4 Risk Characterization
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7.4. 1 Non-Carcinogenic Risk
An evaluation of the results of the risk calculations indicates that hazard indices
for all current scenarios are below 1.0, the level of concern for noncarcinogens.
For future scenarios, however, onsite resident hazard indices are all above 1.0.
Adult and child onsite residents have His of 6E + 01 and 2E + 02, respectively,
primarily due to ingestion of metals in groundwater. Exposure to groundwater
Well No. 44 results in noncarcinogenic risk of 2E + 02 for adults, and 7E + 02
for children, again due to metals in groundwater and a significant contribution to
risk from chlorobenzene being inhaled in the showering scenario.
7.4.2 Carcinogenic Risk
All populations show carcinogenic risk in excess of the accepted EPA benchmark
of 1 x 10-6. For current adult onsite trespassers, the lifetime excess cancer risk is
lE-3, primarily from PCBs. For current child trespassers, the lifetime excess can-
cer risk is 4E-4, again primarily from PCBs. For current adult offsite residents,
the lifetime excess cancer risk is ?E-4 while current offsite child residents have a
risk of 3E-04 primarily from dermal contact with PCBs in sediment and ingestion
of PCBs in produce.
For future (hypothetical) adult onsite residents, the lifetime excess cancer risk is
lE-1 primarily from dermal contact with PCBs in soil. For future child onsite
residents, the excess cancer risk is 3E-2, again primarily dermal contact with PCBs
in soil. Exposure to groundwater in Well No. 44 results in risks of 6E-3 for future
adult onsite residents, and 4E-3 for future child onsite residents.
According to EPA policy, the target total individual risk resulting from exposures
at a Superfund site may range anywhere between 104 to 10-6. Thus, remedial
alternatives being considered should be capable of reducing total potential carci-
nogenic risks to individuals to levels within this range. EPA further suggests that
the 10-6 risk level should be used as a starting point.
7.4.3 Uncertainties In the Risk Characterization
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There are uncertainties associated with summing cancer risks or hazard indices for
different chemicals. This assumption of dose additivity ignores possible synergism
or antagonism among chemicals and differences in mechanisms of action and
metabolism. It is not known what effects this has on the total risk numbers.
Another important uncertainty surrounds the fact that risk calculations for dermal
exposure to all compounds except arsenic assume a relationship between the oral
toxicity values and the extrapolated dermal value. These uncertainties and the
uncertainties discussed in previous sections need to be considered when evaluating
the results of the risk assessment and when making risk management decisions for
the site.
7.5 Ecological Assessment
An ecological assessment of the Carolina Transformer site was completed to de-
termine the extent of environmental injury. The ecological assessment was based
on data collected during the RI, site visits, and literature sources.
The site habitat consists of four types: wooded area, wetlands, agricultural, and
grassy area. No special management, preserve areas or parks are located at the
site and threatened or endangered species have not been documented at the site.
Many areas onsite and in the drainage ditch along the north boundary of the site
either lack vegetation or had lesser growth than adjacent areas.
Terrestrial and aquatic populations at the site were not surveyed in detail as part
of this study. Thus, quantitative assessments of potential risks were not derived.
A total of 36 chemicals of concern were identified and qualitatively evaluated for
potential ecological risks.
Surface water concentrations of several chemicals of concern ( copper, zinc, tolu-
ene, PCB) were above ambient water quality criteria for those chemicals with
available criteria. However, these chemicals were detected in surface water sam-
ples from locations which did not retain water throughout the year. Surface water
organisms or receptors may not be present at these locations. Therefore, the
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exposure to surface water onsite by fish and other aquatic organisms would be
unlikely.
Sediment and surface soil exposures could not be fully evaluated due to lack of
site specific ecological data and toxicity information for the chemicals of concern.
However, some chemicals of concern (lead, benzene, chlorobenzene, PCBs) in
soil, sediment and surface water at the site demonstrate the potential for toxic
effects and bioaccumluation which may cause adverse effects to some species via
the food chain. Especially the PCB concentrations are at levels of potential con-
cern.
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8.0 References
[l) U.S. Environmental Protection Agency, 1989. Risk Assessment Guidance for
Superfund. Volume I: Human Health Evaluation Manual. Interim Final. Wash-
ington, DC: U.S. Environmental Protection Agency. July 1989.
(2) U.S. Environmental Protection Agency, 1990. Carolina Transformer
Superfund Site, Remedial Investigation, prepared by EPA Region IV.
(3) U.S. Environmental Protection Agency, 1989. Work Plan for Carolina Trans-
former Site, Remedial Investigation/Feasibility Study, Fayetteville, North Carolina,
prepared by EPA Region IV.
(4) B&V Waste Science and Technology Corp., 1990. Risk Assessment/Feasibility
Study Work Plan for the Carolina Transformer Superfund Site, Fayetteville, North
Carolina, Volume I, prepared for U.S. Environmental Protection Agency, Region
IV, Atlanta, Georgia.
[5) U.S. Environmental Protection Agency, 1989. Risk Assessment Guidance for
Superfund. Volume II: Environmental Evaluation Manual. Interim Final. Wash-
ington, DC: U.S. Environmental Protection Agency. March 1989.
[6) EPA, 1988; EPA, Superfund Exposure Assessment Manual, EPN540/l-88/001,
April 1988.
[7) U.S. Environmental Protection Agency, 1989. Exposure Factors Handbook.
EPN600/8-89/043, July 1989.
[8) Ryan EA, Hawkins ET, Magee B, Santos SL. 1987. Assessing Risk from Der-
mal Exposure at Hazardous Waste Sites. Superfund, 1987. Proceedings of the
8th National Conference (November 16-18, 1987, Washington, DC). Sponsored by
the Hazardous Material Control Research Institute. Pages 166-168.
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[9) U.S. Environmental Protection Agency, 1989. Draft Guidance on Selecting
Remedies for Superfund Sites with PCB Contamination, September 22, 1989.
[10) U.S. Department of Agricultural, Soil Conservation Service, 1984. Soil Sur-
vey of Cumberland Hoke Counties North Carolina, October 1984.
[11) U.S. Environmental Protection Agency, 1985. Rapid Assessment of Expo-
sure to particulate Emissions from Surface Contamination Sites, Office of Health
and Environmental Assessment, February 1985. EP N600/8-85/002.
[12) U.S. Environmental Protection Agency, 1988. Estimating Toxicity of Indus-
trial Chemicals to Aquatic Organisms Using Structure Activity Relationships, Vol-
ume I, Office of Toxic Substances, July 1988. EPA 560/6-88/001.
[13) U.S. Environmental Protection Agency, Chemline Database, September 1990.
[14) U.S. Environmental Protection Agency, Office of Waste Programs Enforce-
ment, 1985. Chemical, Physical, and Biological Properties of Compounds Present
at Hazardous Waste Sites. Prepared by Clement Associates, Inc. For GCA Cor-
poration. October, 1985.
[15) Sax, N. Irving, 1984. Dangerous Properties of Industrial Materials, Sixth
Edition. Van Nostrand-Reinhold Co., New York, 3124 pp.
(16) U.S. Environmental Protection Agency, 1980. Ambient Water Quality Crite-
ria for Phthalate Esters. Office of Water Regulations and Standards, Criteria and
Standards Division. October, 1980. EPA 40/5-8-067.
(17] Carpenter, C.P. , Weil, C.S. and Smyth, H.F. 1953. Chronic Oral Toxicity of
Di(2-ethylhexyl) phthalate for Rats, Guinea Pigs and Dogs. Arch. Indus!. Hyg.
Occup. Med. 8:219-226.
(18) Agency for Toxic Substances and Disease Registry, 1989. Toxicological Pro-
file for Chlorobenzene. U.S. Public Health Service. Draft. October 1989.
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[l 9) U.S. Environmental Protection Agency, Office of Drinking Water, 1981.
Toluene Health Advisory. Washington, D.C.
[20) U.S. Environmental Protection Agency, 1986. Office of Regulations and
Standards, Quality Criteria for Water for 1986. May 1, 1986. EPA 440/5-86-001.
Washington, D.C.
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APPENDIX A
INFORMATION ON CHEMICALS OF CONCERN
A1 Aromatic Hydrocarbons
A 1.1 Characteristics
Aromatic hydrocarbons, which include BETXs, (benzene, ethyl benzene, toluene, and
xylenes) are found in crude light oils. Aromatic hydro-carbons are recovered after
distillation and used as fuels or blended with other petroleum stocks. Compared to
polynuclear aromatic hydrocarbons that are discussed later, aromatic hydrocarbons
have lower molecular weights, are less dense (lighter than water), have higher water
solubilities, have higher vapor pressures, have a lower affinity for soil, and generally
have shorter half-lives. Table A-1 shows chemical and physical properties for
aromatic hydrocarbons.
A1 .2 Environmental Fate
Aromatic hydrocarbons are primarily found as components of complex mixtures,
particularly petroleum sources. Because benzene is one of the more toxic aromatic
hydrocarbons, it has been studied more than the other compounds in this group. The
discussion of environmental occurrence of aromatic hydrocarbons will focus on
benzene because there is a relatively large amount of data available and because
benzene's characteristics are representative of other aromatic hydrocarbons.
Environmental sources of benzene include gasoline filling stations, industrial facilities
using benzene or producing it as a byproduct, vehicle exhaust emissions, cigarette
smoke, leaking underground storage tanks, contaminated leachate from landfills,
chemical spills, and foods that contain benzene as a natural constituent. Aromatic
hydrocarbons are found in consumer products such as plastics, glues, and adhesives,
household cleaning products, paint strippers, and art supplies (ATSDR 1987).
A1.2.1 Benzene
Benzene in surface water or ground water tends to be mobile because of its relatively
high solubility in water and relatively low affinity for soils and sediment. Because
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TABLE A-1
PHYSIOCHEMICAL PROPERTIES OF BETX COMPOUNDS
VAP HENRY'S
COMPOUND CASRN FORMULA MW MP BP DENSITY WATER SOL PRESS LAW
(•C) (•C) (gfcm3) (mgfl) (mm Hg) (atm-m3Jmol)
Benzene n-43-2 C6H6 78.1 6.6 80 0.879 1760 95.2 5.4E-3
Totuone 108-88-3 C7H8 92.1 -95 110.6 0,886 534.8 28.7 5.9E-3
Sources: CAC 1970, MERCK 1976, USEPA IRIS, USEPA HEA, USHPS ATSDA
PARTITION
COEF.
(log Kow)
2.13
2.73
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benzene has a relatively high volatility, it tends to evaporate into the air from soil and
water, with a half-life of four to five hours for evaporation (A TSDR 1987).
Benzene is degraded in air by reacting with hydroxyl radicals. The half-life in air
ranges from several hours to several days, depending upon atmospheric conditions.
Microbial degradation of benzene occurs in water and soil, with the rate and extent
of degradation depending upon specific conditions such as microbes present,pH, and
oxygen level (ATSDR 1987).
Although large amounts of benzene are released to the environment by both natural
and manmade sources, environmental levels are relatively low due to efficient
removal processes. Benzene concentrations in the air are normally higher in urban
areas than in rural areas, primarily because of vehicle and industrial emissions.
Benzene concentrations in air have been reported to range from 0.8 to 60 ppb in
urban and industrial areas and from 0.02 to 1.4 ppb in rural areas (ATSDR 1987).
Benzene has been detected in rainwater, surface water, sea water, drinking water, and
ground water samples collected throughout the United States, Canada, and the
United Kingdom. Benzene levels detected range from 0.005 ppb in the Gulf of
Mexico to 330 ppb in contaminated ground water in New York, New Jersey, and
Connecticut. Very high concentrations of benzene; up to 24,000 ppb, have been
recorded in subsurface water samples collected near extensive gas and oil reserves
(ATSDR 1987).
Limited data are available for benzene concentrations in soils. However, one study
found benzene levels ranging from less than 2 ppb to 191 ppb in samples collected
near several industrial facilities that either used or produced benzene (A TSDR 1987).
A 1 _2,2 Toluene
Most toluene that is released into the environment evaporates into the air because
of its moderate volatility. Toluene is also moderately soluble in water, so it can be
transported by surface or ground water. Toluene is not usually persistent in the
environment. In air, toluene has a half-life of about thirteen hours. In water and
soil, it is rapidly degraded by microbial processes with usual half-lives of one to seven
days (ATSDR 1988).
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A 1.3 Health Effects
A1.3.1 Benzene
Noncarcinogenic Effects of Benzene. Acute inhalation exposure to benzene at
concentrations from 50 to 3000 ppm results in a range of effects on the nervous
system, depending on level and duration. Common signs include dizziness, nausea,
headache, sleepiness, and loss of coordination. These effect are generally fully
reversible, although exposure to a very high level (20,000 ppm) can induce coma and
even cause death (A TSDR 1987).
Long-term exposure to lower levels of benzene can injure the hematopoietic (blood-
forming) system. Pancytopenia, aplastic anemia, and other abnormalities of blood
cells have been reported to occur more frequently in groups of workers exposed to
benzene in the workplace at level perhaps as low as 20 to 30 ppm (Goldwater, 1941;
Aksoy, 1971; Goldstein, 1977). Similar blood dyscrasias have been reported in many
animal studies of inhalation exposure to levels of around one hundred ppm or higher
or oral doses of 50 to 500 mg/kg/day (Wolfe, 1956; NTP, 1986a). Abnormalities in
the immune system have also been detected in humans and animals exposed to
benzene (ATSDR 1987).
Because benzene is a potent carcinogen (see following section), the EPA has not yet
derived inhalation or oral RID values (lRIS, 1990). Based on studies in mice and
rats, a minimal risk level (MRL) of 0.01 ppm for short-term inhalation exposure and
0.0001 mg/kg/day for chronic oral exposure was estimated and assigned to benzene
(ATSDR 1987).
Carcinogenic Effects of Benzene. There is convincing data from both human and
animal studies that chronic exposure to benzene leads to increased of leukemia (NAS
1977; ATSDR 1987), and EPA has ranked benzene as a Group A carcinogen for
both inhalation and oral exposure (IRIS 1990).
Several studies provide useful data for estimating the carcinogenic potency of
benzene in humans. Based on the epidemiological data of Rinskey et al. (1981), Ott
et al. (1978), and Wong (1983), the EPA calculated a geometric mean inhalation
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slope factor of 2.9 x 10·2 mg/kg/day. This value assumes 100 percent absorption of
inhaled benzene, so it is the same value taken as the oral slope factor (IRIS 1990).
A 1.3.2 Toluene
Noncarcinogenic Effects of Toluene. The principal effect associated with exposure
to toluene is depression of the central nervous system. In humans, inhalation of
toluene in air at concentrations of 100 ppm can cause sleepiness and decreased
dexterity. Exposure to levels of 200 to 800 ppm can lead to narcosis, characterized
by impaired mental and motor functions. These effects appear to be fully reversible,
although very high exposures can lead to permanent central nervous system damage
and may produce such profound central nervous system depression that death ensues
(EPA 1985).
Inhalation exposure to toluene does not usually lead to significant effects on tissues
other than the central nervous system (Bruckner, 1981), although lung irritation,
decreased immunological function, and developmental effects have been noted in
some studies of animals or humans exposed to levels of 200 ppm or higher (Courtney,
1942). Based on a two-year inhalation study in rats, the EPA identified a dose of 300
ppm (1,130 mg/m3) as a no observable adverse effect level (NOAEL), and calculated
an inhalation RID of 5 mg/m3 (1.3 ppm) (HEAST 1989). The EPA is currently
reviewing this value (IRIS 1988).
Humans are rarely exposed to toluene orally at doses high enough to cause
measurable effects. Limited studies of animals indicate that doses of 590 mg/kg/day
for six months do not significantly effect rats (Wolf, 1956). Based on a chronic (2-
year) inhalation study of rats, the EPA has calculated a chronic oral RID of 0.3
mg/kg/day (IRIS 1988). This was based on absence of effects on the central nervous
system, liver, or kidneys. Dermal or ocular contact with toluene can result in
irritation and skin damage, but neurological or systemic effects have not been noted
(ATSDR 1988).
Carcinogenic Effects of Toluene. There are no studies of humans that indicate that
toluene is carcinogenic, and cancer studies of animals exposed by inhalation (CIIT
1980) or dermal contact (Weiss 1986) have been negative. However, due to
limitations in these studies, the EPA does not consider the weight of evidence
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adequate to rank toluene as a noncarcin-ogen. Consequently, toluene has been
placed in Group D-not classified (IRIS 1988).
A 1.4 Bibliography
Benzene
ATSDR 1987 ATSDR, Draft Toxicological Profile for Benzene, Oak Ridge
National Laboratory, Oak Ridge, October 1987.
HOWARD Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH/OSHA NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Benzene, Supplement II, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No 89-104,
1988.
EPA
IRIS 1990
Toluene
EPA, Health Effects Assessment for Benzene, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Integrated Risk Information System (IRIS), Slope Factor for
Carcinogenicity Assessment for Benzene, on-line, Office of Health
and Environmental Assessment, Cincinnati, OH, verification date.
ATSDR 1988 ATSDR, Draft Toxicological Profile for Toluene, Oak Ridge
National Laboratory, Oak Ridge, 1988.
HOWARD
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Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
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EPA 1985 EPA, Chemical, Physical, and Biological Properties of Compounds
Present at Hazardous Waste Sites, U.S. Environmental Protection
Agency, Office of Waste Program Enforcement, Washington, DC,
1985.
EPA EPA, Health Effects Assessment for Toluene, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
HEAST 1989 EPA, Health Effects Assessment Summary Table, Forth Quarter,
FY 1989, 1989.
IRIS 1988 EPA, Integrated Risk Information System (IRIS), Reference Dose
(Rill) for Toluene, on-line, Office of Health and Environmental
Assessment, Cincinnati, OH, verification date March 1, 1988.
EPA EPA, Integrated Risk Information System (IRIS), Slope Factor for
Carcinogenicity Assessment for Toluene, on-line, Office of Health
and Environmental Assessment, Cincinnati, OH, verification date
February 1, 1989.
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A2 2-Butanone
A2.1 Characteristics
2-Butanone, Chemical Abstract Service Registry No. 78-93-3, is an aliphatic ketone
also known as MEI<, Methyl Ethyl Ketone, and ethyl methyl ketone. 2-Butanone is
a clear and colorless liquid with an odor like acetone (NIOSH 1988). 2-Butanone is
soluble in about four parts water; with solubility decreasing at higher temperatures,
miscible with alcohol, ether, and benzene. (MERCK 1976). Table A-2 shows
chemical and physical properties for 2-Butanone.
A2.2 Environmental Fate
2-Butanone has been used as a solvent in the surface coating industry and the
manufacturing of colorless synthetic resins (MERCK 1976). 2-Butanone's natural
sources include volcanos, forest fires, products of biological degradation, and natural
component of food. (HOW ARD 1990)
Large quantities of 2-Butanone are used as a solvent especially in the coatings
industry. 2-Butanone will be discharged into the atmosphere from this and other
industrial uses. It will also be discharged into wastewater. In addition, high
atmospheric 2-Butanone levels are associated with photochemical smog episodes
although it is generally absent from ambient air. If 2-Butanone is released to soil, it
will partially evaporate into the atmosphere from near-surface soil and may leach into
the ground water. Biodegradability studies in anaerobic systems suggest that 2-
Butanone present in the ground water may degrade slowly after a long acclimation
period. If released into water, 2-Butanone will be lost by evaporation (half-life 3-12
days) or be slowly biodegraded. It will not significantly indirectly photooxidize in
surface waters, absorb to sediment or bioconcentrate in aquatic organisms. If
released into the atmosphere, it will exist primarily in the gas phase. It will
photodegrade at a moderate rate (half-life 2-3 days or less) and it may be subject to
direct photolysis (HOWARD 1990).
A2.3 Health Effects
Noncarcinogenic Effects of 2-Butanone. Adequate chronic toxicity testing has not
been performed with 2-Butanone. The NOAEL of the Labelle and Brieger (1955)
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TABLE A-2
PHYSIOCHEMICAL PROPERTIES OF VOLATILE COMPOUNDS
HENRY'S
COMPOUND CASRN FORMULA MW MP BP DENSITY WATER SOL VAP PRESS LAW
('C) ('C) (gfcm3) (rno/L) (mm Hg) (atm-m3/mol)
2-Bulanone 78-93-3 C4H8O 72.1 -88,4 79.8 0.805 268000 TT.5@ 20'C 1.05E-5
Carbon Olaulfide 75-15--0 CS2 76.13 -110.8 48.6 1.28 2940 3eO 1.4E-3
Chlorobenzene 108-90-7 C6H5CI 112.8 --45.8 132.0 1.11 500 8.8 3.BE-3
Sourcos: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA. USPHS ATSDR
PARTITION
COEF.
(log Kow)
0.28
1.7-4.2
2.8
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study provides the lowest and most protective dose for deriving an RfD. In this
study, 25 rats were exposed to 235 ppm of 2-Butanone for 7 hour/day, 5 day/week for
12 weeks. No effects were observed, but only a few parameters were measured. 2-
Butanone has also been tested for teratogenicity by Schwetz et al. in 1974 and
Deacon et al in 1981, and the observed LOAELs for fetotoxicity were higher than the
NOAEL of LaBelle and Brieger (1955) (IRIS 1987).
Carcinogenic Effects of 2-Butanone. There is no data available to assess the
carcinogenic potential of 2 Butanone by the oral or inhalation routes. In a skin
carcinogenicity study, two groups of ten mice received dermal applications of 50 mg
of a solution containing 25 to 29 percent 2-Butanone twice a week for one year.
After 27 weeks, only one mouse of ten receiving 29 percent 2-Butanone developed
a skin tumor (IRIS 1987).
A2.4 Bibliography
HOW ARD 1990 Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH 1988
EPA
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NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; 2-Butanone, Supplement II, U.S.Department
of Health and Human Services, DHHS NIOSH Publication No
89-104, 1988.
EPA, Health Effects Assessment for Methyl Ethyl Ketone,
prepared by the Office of Health and Environmental
Assessment, Cincinnati, September 1984.
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989
EPA, Integrated Risk Information System (IRIS), Methyl Ethyl
Ketone, on-line, Office of Health and Environmental
Assessment, Cincinnati, OH, January 31, 1987.
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IRIS 1988
IRIS 1989
WEAST
MERCK 1976
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EPA, Integrated Risk Information System (IRIS), Reference
Dose (RfD) for Methyl Ethyl Ketone, on-line, Office of Health
and Environmental Assessment, Cincinnati, OH, verification
date March 1, 1988.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Methyl Ethyl Ketone,
on-line, Office of Health and Environmental Assessment,
Cincinnati, OH, verification date December 1, 1989.
Weast, Robert C., et al., Handbook of Chemistry and Physics,
51st Edition, The Chemical Rubber Co., Cleveland, 1970.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
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A3 Carbon Disulfide
A3.1 Characteristics
Carbon sulfide, Chemical Abstract Registry Service No. 75-15-0, is also known as
carbon disulphide, carbon disulphide, and carbon sulphide. Pure carbon disulfide is
an odorless, clear, colorless, flammable liquid (NIOSH 1977). The usual commercial
and reagent grades are foul smelling. Carbon Disulfide's solubility in water at 20°C
is 2.9 grams in 1 liter of water (MERCK 1976). Table A-2 shows chemical and
physical properties for carbon disulfide.
A3.2 Environmental Fate
Carbon disulfide is used in the manufacturing of rayon and cellophane, carbon
tetrachloride, and rubber accelerators. It is also used as a grain fumigant, laboratory
reagent, and solvent for phosphorus, sulphur, selenium, bromine, iodine, fats, resins,
and rubbers.
Carbon disulfide is a natural product of anaerobic biodegradation and is released to
the atmosphere from oceans and land masses. Geothermal sources also contribute
to carbon disulfide emissions. It also may be released as emissions and in wastewater
during its production and use, in the production of viscose rayon, cellophane, and
carbon tetrachloride, and as a solvent and fumigant. If released on land, carbon
disulfide will be primarily lost by volatilization. It may also readily leach into the
ground where it may biodegrade. If released into water, carbon disulfide will be
primarily lost due to volatilization (half-life 2.6 hr in a model river). Adsorption to
sediment and bioconcentration in fish should not be significant. In the atmosphere,
carbon disulfide degrades by reacting with atomic oxygen and photochemically
produced hydroxyl radicals (half-life 9 days). The soil may be a natural sink for the
chemical by adsorbing and subsequently biodegrading on it. Exposure to carbon
disulfide is mostly occupational and primarily by inhalation. Only workers in the
viscose rayon industry are exposed to high concentration. The general population
may be exposed to carbon disulfide from ambient air as well as food items containing
grain that has been fumigated with the chemical. (HOWARD 1990)
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A3.2 Health Effects
Noncarcinogenic Effects of Carbon Disulfide. Hardin et al. (1981) observed no
effects on fetal development in rats or rabbits following inhalation exposure to 62.3
or 124.6 mg/m3, which corresponds to estimated equivalent oral dosages of 5 and 10
mg/kg for rats, and 11 and 22 mg/kg for rabbits. The highest no observable effect
level (NOEL) from this study, 22 mg/kg for the rabbit, should not be used for a Rill
estimate because adverse effects were seen in rabbit fetuses following oral exposure
of pregnant does to 25 mg/kg (Price et al., 1984). Therefore, the highest no
observable adverse effect level (NOAEL) that is below an effect level is the
estimated low dose from the Hardin et al. (1981) inhalation study using rabbits. This
dose level, 11 mg/kg, is the most appropriate basis for Rill derivation. (IRIS 1989).
Price et al. (1984) observed 25 mg/kg/day in rabbits results in fetal reabsorption.
Fetal toxicity and fetal malformation were not observed in rats at the lowest level
(100 mg/kg/day) of carbon disulfide exposure. The data from this study also suggest
that the rabbit fetus is more sensitive than the rat fetus to carbon disulfide induced
toxicity. (IRIS 1989).
Carcinogenic Effects of Carbon Disulfide. This chemical has not been evaluated by
the EPA for evidence of human carcinogenic potential (IRIS 1987). No reports on
carcinogenesis resulting from exposure to carbon disulfide have been found in the
literature (NIOSH 1977).
A3.4 Bibliography
HOW ARD 1990 Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH 1977
EPA
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NIOSH, Criteria For a Recommended Standard, Occupational
Exposure to Carbon Disulfide, U.S. Department of Health,
Education and Welfare, DHEW(NIOSH) Publication No.
77-156, May 1977.
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989.
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IRIS 1987
IRIS 1989
MERCK 1976
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EPA, Integrated Risk Information System (IRIS), Carbon
Disulfide, on-line, Office of Health and Environmental
Assessment, Cincinnati, OH, September 30, 1987.
EPA, Integrated Risk Information System (IRIS), Reference
Dose (RID) for Carbon Disulfide, on-line, Office of Health and
Environmental Assessment, Cincinnati, OH, verification date
February 1, 1989.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
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A4 Chlorobenzene
A4.1 Characteristics
Chlorobenzene, Chemical Abstract Service Registry No. 108-90-7, is a colorless liquid
with an almond-like odor. The compound does not occur widely in nature, but is
manufactured for use as a solvent and is used in the production of other chemicals.
500 mg of chlorobenzene is soluble in 1 liter of water .. The vapor pressure of
chlorobenzene is 8.8 mm Hg (ATSDR 1989).
Table A-2 shows some of the chemical and physical properties of chloro-benzene.
A4.2 Environmental Fate
Chlorobenzene will enter the atmosphere from fugitive emissions connected with its
use as a solvent in pesticide formulations and as an industrial solvent. Once released
it will decrease in concentration due to dilution and photooxidation. Releases into
water and onto land will decrease in concentration due to vaporization into the
atmosphere and slow biodegradation in the soil and water. Chlorobenzene has
potential to percolate into the ground water, particularly if soil is sandy and poor in
organic matter. This will result in leaching into groundwater. Little bioconcentration
is expected into fish and food products. Primary human exposure is expected to be
from ambient air, especially near point and sources (Howard 1989).
Chlorobenzene is loss from water primarily by evaporation. Biodegrada-tion, another
loss process, will occur during the warmer seasons and will proceed more rapidly in
fresh water than in estuarine and marine systems. One reported half-life for an
estuarine river with near natural conditions is 75 days. A moderate amount of
adsorption will occur onto organic sediments (Howard 1989).
If released to the atmosphere, chlorobenzene is expected to exist almost entirely in
the vapor phase based upon the vapor pressure. Reaction with hydroxyl radicals is
the dominant removal mechanism with an estimated half-life of 17 days with the
formation of chlorophenols. Reaction in polluted air is faster, resulting in the
A-13
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formation of chloronitrobenzene and chloronitrophenols. Photolysis would proceed
at a much slower rate, with monochlorobiphenyl being produced (Howard 1989).
A4.3 Health Effects
Noncarcinogenic Effects of Chlorobenzene. A subacute oral toxicity test using male
and female beagles derived a no observable adverse effect level (NOAEL) of 27.3
mg/kg/day. The chlorobenzene was administered orally by capsules at does of 27.3,
54.5 and 272.5 mg/kg/day, 5 day/week for 13 weeks. At the 54.5 mg/kg/day dose,
adverse effects were detected. The histopathologic changes noted in the liver
included slight bile proliferation, cytologic alternations, and leukocytic infiltration of
the stroma.
Based on the above test, and other supportive studies, an RID value of 2 x 10·2
mg/kg/day is assigned to chlorobenzene (IRIS 1989).
Carcinogenic Effects of Chlorobenzcne. The evaluation for this chemical is presently
under review by the EPA and therefore a slope factor has not been assigned (IRIS
1989a).
A4.3 Bibliography
ATSDR 1989 ATSDR, Draft Toxicological Profile for Chlorobenzene,
prepared by Life Systems, Inc., Oak Ridge National Laboratory,
Oak Ridge, October 1989.
HOWARD 1989
IRIS 1989
IRIS 1989a
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Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume I, Lewis
Publishers, Chelsea, Michigan, 1990.
EPA, Integrated Risk Information System (IRIS), Reference
Dose (RID) for Chlorobenzene, on-line, Office of Health and
Environmental Assessment, Cincinnatti, OH, August 1, 1989.
EPA Integrated Risk Information System. (IRIS),
Carcinogenicity Assessment for Chlorobenzene, on-line, Office
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AS 1,3 Dichlorobenzene
AS.1 Characteristics
1,3-Dichlorobenzene, Chemical Abstract Service Registry No. 541-73-1, is also known
as 1,3-dichloro-m-DCB and 1,3-DCB. It is a liquid which boils at 173° C. The
solubility in water is 111 mg/I at 20° C. Its Log Octanol/Water Partition coefficient
is 3.60 (Howard 1990). The physical and chemical properties of 1,3-dichlorobenzene
are presented in Table A-3.
AS.2 Environmental Fate
Chemical waste dump leachates and direct manufacturing effluents are reported to
be the major source of pollution of the chlorobenzenes (including the
· dichlorobenzenes) to Lake Ontario. Use of 1,3 dichlorobenzene (1,3-DCB) as a
fumigant will release it directly to the atmosphere. If released to soil, 1,3-DCB can
be moderately to tightly adsorbed. Leaching from hazardous waste disposal areas has
occurred and the detection of 1,3-DCB in various ground waters indicates that
leaching can occur. Volatilization from soil surfaces may be an important transport
mechanism. It is possible that 1,3-DCB will be slowly biodegraded in soil under
aerobic conditions. Chemical transformation by hydrolysis, oxidation, or direct
photolysis are not expected to occur in soil. If released to water, adsorption to
sediment will be a major environmental fate process based upon extensive monitoring
data in the Great Lakes area and Koc values. Analysis of Lake Ontario sediment
cores has indicated the presence and persistence of 1,3-DCB since before 1940. 1,3-
DCB is volatile from the water column, with an estimated half-life of 4.1 hours from
a river one meter deep flowing 1 m/sec with a wind velocity of 3 m/sec at 20 °C;
adsorption to sediment will attenuate volatilization. Aerobic biodegradation in water
may be possible; however, anaerobic biodegradation is not expected to occur.
Experimental BCF values of 89-740 have been reported and 1,3-DCB has been
detected in trout from Lake Ontario. Hydrolysis, oxidation, and direct photolysis in
aquatic environment are not expected to be important. If released to air, 1,3-DCB
will exist predominantly in the vapor phase and will react with photochemically
produced hydroxyl radicals at an estimated half-life rate of 14 days in a typical
atmosphere. Direct photolysis in the troposphere is not expected to be important.
The detection of 1,3-DCB in rainwater suggests that atmospheric removal via wash-
CT/Af'PA
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TABLE A-3
PHYSIOCHEMICAL PROPERTIES OF SEMIVOLATILE COMPOUNDS
WATER VAP HENRY'S PART
COMPOUND CASRN FORMULA MW MP BP DENSITY SOL PRESS LAW COEF
{°C) (•C) (lj/om3) (mg/L) (mm Hg) (atm-ms.'mol) (log Kow)
1,3-Dichlorobenzene 106-48-7 C6H4Cl2 147.01 -25 173 1.29 1.23E-t-02 2.28-t-OO 3.59-03 3.6
1,4-Dichlorobonzene 106-46--7 C6H4Cl2 147.01 53.1 174 1.25 80 1.8E-t-O 2.9E-3 3.6
Bis (2-othylhexyl) Phthalate 117-81-7 C24H38O4 390.54 -50 385 0.9861 0.285 3.4E-7 1.0E-4 4.88
2,3,7,8-TCDD 174~1-6 C12H4Cl4O2 322.0 305.0 412.2 1.827 3.17E-04 1.40E-09 2.10E--06 6.5
Aroclor-1016 12674-11-2 C12H7Cl3 257.9 325.0 1.33 4.2E-01 4.0E-04 2.9E--04 5.6
Aroclor-1221 11104-28-2 C12H9CI 200.7 275.0 1.16 5.9E--01 6.7E-03 3.5E--03 4.7
Aroclor-1232 11141-16-5 C12H9CI 232.2 290.0 1.24 4.1 E--03 6.1
Aroclor-1242 53469-21-9 C12H7Cl3 266.5 325.0 1.35 1.0E--01 4.1 E--04 5.2E--04 5.6
Aroclor-1248 12672-29--6 C12HBCl4 299.5 340.0 1.41 6.0E--02 4.9E--04 2.8E--03 6.2
Aroclor-1254 11097-e9-1 C12H5C15 328.4 365.0 1.5 5.7E-02 7.7E--05 2.0E--03 6.5
Aroclor-1260 11096-82-5 C12H3Cl7 375.7 385.0 1.58 2.7E--03 4.1 E--05 4.6E--03 6.8
Source: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA. USHPS ATSDA
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out is possible. General population exposure to 1,3-DCB may occur through oral
consumption of contaminated drinking water and food (particularly fish) and through
inhalation of contaminated air since 1,3-DCB has been widely detected in ambient
air (Howard 1990).
A5.3 Health Effects
Noncarcinogenic Effects of 1,3-Dichlorobenzene
The dichlorobenzenes are of relatively low acute toxicity in experimental animals.
Oral LD50s of about 500 mg/kg have been reported in rats and rabbits, while much
higher figures of 2950 mg/kg and 2800 mg/kg have been reported in mice and guinea-
pigs, respectively.
In Sprague-Dawley rats, intraperitoneal injection of either 1.33 mmol/kg (196 mg/kg)
of ortho-dichlorobenzene or 1.31 mmol/kg (193 mg/kg) of meta-dichlorobenzene
induced only limited hepatic necrosis. Pretreatment with phenobarbital markedly
enhanced the hepatotoxic potential of these two compounds. Intraperitoneal
injection of 3.4 mmol/kg (500 mg/kg) of para-dichlorobenzene had little effect on the
liver. Pretreatment with phenobarbital was not found to enhance the hepatotoxicity
of this isomer. Hepatic porphyria was reported in rats given oral doses of 900-1000
mg/kg/day of meta-dichlorobenzene for 5 days. A single oral dose of 800 mg/kg para-
dichlorobenzene in day-old White Leghorn chicks has also been reported to increase
hepatic and biliary porphyrin content. Unlike ortho-and para-dichlorobenzene, the
meta isomer has been shown to enhance liver aminopyrine demethylase and aniline
hydroxylase activities in rats given oral doses of 250 mg/kg day for 3 days. Hepatic
cytochrome P-450 content was not altered significantly by treatment with any of the
isomers, but hepatic delta-ALA synthetase activity was enhanced by 63, 32 and 42%
by ortho-, meta-and para-dichlorobenzene, respectively (Fawell and Hunt 1988).
USEP A has not currently evaluated 1,3-dichlorobenzene under the IRIS system.
Carcinogenic Effects of 1,3-Dichlorobenzene
No reports on carcinogenesis resulting from exposure to 1,3-dichlorobenzene have
been found in the literature. This chemical has not been evaluated by the USEP A
for evidence of human carcinogenic potential (IRIS 1990).
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A5.4 Bibliography
ALDRICH
ATSDR 1987
CLAYTON
CRC
FAWELL
HOWARD
NIOSH/OSHA
SIELER
USEPA
IRIS 1990
Cf/APPA
9/2Dl90
Aldrich Catalog Handbook of Fine Chemicals, Aldrich
Chemical Company, Inc. 1988.
ATSDR, Draft Toxicological Profile for Benzene, Oak Ridge
National Laboratory, Oak Ridge, October 1987.
Clayton, G.D. and Clayton, F.E., Patty's Industrial Hygiene and
Toxicology, John Wiley and sons, NY, 1981.
Weast, R. (editor), CRC Handbook of Chemistry and Physics,
58th ed., CRC Press, Inc., West Palm Beach, FL, 1977.
Fawell, J. and Hunt, S., Environmental Toxicology, Ellis
Horwood Ltd., England, 1988.
Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Benzene, Supplement II, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No
89-104, 1988.
Seiler, H.G., Sigel, G. and Sigel, A., Handbook on Toxicity of
Inorganic Compounds, Marcel Dekker, Inc., 1988.
EPA, Health Effects Assessment for Benzene, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Benzene, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date.
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A6 1,4-DICHLOROBENZENE
A6.1 Characteristics
1,4-Dichlorobenzene, Chemical Abstract Service Registry No. 106-46-7, is monoclyclic
halogenated aromatic hydrocarbon also known as p-DCB or paradichlorobenzene.
1,4-Dichlorobenzene is a colorless solid with a mothball-like odor (NIOSH 1981).
1,4-Dichlorobenzene is practically insoluble in water; soluble in alcohol, ether,
benzene, chloroform, and carbon disulphide, and sublimes at ordinary temperatures
(MERCK 1976). Table A-3 shows chemical and physical properties for 1,4-
Dichlorobenzene.
A6.2 ENVIRONMENTAL FATE
The major uses of 1,4-dichlorobenzene are as space deodorizers, moth repellant and
an intermediate in the production of polyphenylene sulfide resins. These uses
account for over 90 percent of the 1,4-dichlorobenzene used in the United States in
recent years. About 95 percent of the environmental releases of 1,4-dichlorobenzene
occur during its use rather than during manufacturing or processing (ATSDR 1987).
1,4-dichloroben-zenes are not known to occur as such in nature (HOWARD 1989).
1,4-Dichlorobenzene can be moderately to tightly absorbed if released to soil. It is
possible 1,4-dichlorobenzene can be biodegraded in soil under aerobic conditions.
The detection of 1,4-dichlorobenzene in various ground waters indicates leaching can
occur (HOWARD 1989).
When released to water, volatilization may be the dominant removal process. The
volatilization half-life is estimated to be 4.3 hours. If released to air, 1,4-
dichlorobenzene will exist predominantly in the vapor phase and will react with
photochemically produced hydroxyl radicals at an estimated half-life rate of 31 days.
Because of its ability to sublime at ambient temperatures, it is expected to volatilize
from dry surfaces (HOW ARD 1989).
A6.3 HEAL TH EFFECTS
Noncarcinogenic Effects of 1,4-Dichlorobenzene. There is no evidence that brief low-
level or moderate-level exposures to household · products contain-ing 1,4-
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dichlorobenzene cause human health problems. Higher 1,4-dichloro-benzene levels
in air, such as the levels that are sometimes associated with industrial exposure, can
cause headaches and dizziness. Levels that would result in death would be associated
with a odor so intense that it would be very unpleasant, if not intolerable, and would
serve as a danger warning (ATSDR 1987).
Carcinogenic Effects of 1,4-Dichlorobcnzene. In laboratory animals, breathing or
ingestion of 1,4-dichlorobenzene can cause toxic effects in the liver and kidney.
Although there is no evidence that 1,4-dichloroben-zene can cause cancer in humans,
laboratory animals administered with 1,4-dichlorobenzene by gavage in lifetime
studies had increased rates of cancer of the liver and kidneys when compared with
animals not treated to 1,4-dichlorobenzene. Based on the results of these animals
studies, a potential exists that 1,4-dichlorobenzene may cause cancer in humans.
Based on two animal studies, there is some evidence that 1,4-dichloroben-zene
exposure can result in birth defects (ATSDR 1987).
A6.4 BIBLIOGRAPHY
ATSDR 1987 ATSDR, Draft Toxicological Profile for 1,4-Dichlorobenzene,
prepared by Life Science, Inc., Oak Ridge National Laboratory,
Oak Ridge, December 1987.
HOW ARD 1989 Howard, Philip H., et al., Handbook of Environmental Fate
and Exposure Data for Organic Chemicals, Volume I, Lewis
Publishers, Chelsea, Michigan, 1989.
NIOSH 1981 NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; p-Dichlorobenzene, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No
81-123, January 1981.
EPA EPA, Health Effects Assessment for Dichlorobenzene, prepared
by the Office of Health and Environmental Assessment,
Cincinnati, September 1984.
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EPA
EPA
EPA
MERCK 1976
r:f/M'PA
9/2fJl90
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989
EPA, Integrated Risk Information System (IRIS),
Dichlorobenzene, on-line, Office of Health and Environmental
Assessment, Cincinnati, OH, August 1, 1989.
EPA, Integrated Risk Information System (IRIS), Reference
Dose (RID) for Dichlorobenzene, on-line, Office of Health and
Environmental Assessment, Cincinnati, OH, verification date
August 1, 1989.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
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A7 BIS (2-ETHYLHEXYL) PHTHALATE
A7.1 CHARACTERISTICS
Bis (2-ethylhexyl) phthalate, Chemistry Abstract Service Registry No. 117-81-7, is a
phthalate ester also known as BEHP, dioctyl phthalate, di-n-butylphthalate and
Octoil. Bis (2-ethylhexyl) phthalate is a nonvolatile, colorless liquid, only slightly
soluble in water. It is widely used as a plasticizer. Bis (2-ethylhexyl) phthalate has
been suggested as a possible natural product in animal and plants (HOWARD 1989).
Table A-3 shows chemical and physical properties for bis (2-ethylhexyl) phthalate.
A7.2 ENVIRONMENTAL FATE
Plastics may contain up to 40 percent Bis (2-ethylhexyl) phthalate by weight and are
widely used in consumer products such as imitation leather, rainwear, footwear,
upholstery, flooring, food packaging materials, and children's toys. They are also used
for tubing and containers for blood transfusions and blood products. Bis (2-
ethylhexyl) phthalate is also used as a hydraulic fluid and as a dielectric fluid for use
in electrical capacitors (ATSDR 1987).
Bis (2-ethylhexyl) phthalate is used as a plasticizer for polyvinyl chloride and other
polymers in large quantities and is likely to be released to air and water during
production and waste disposal of these plastic products. Bis (2-ethylhexyl) phthalate
will be carried Jong distances and be removed by rain. Human exposure will occur
in occupational settings and from air, consumption of drinking water, food ( especially
fish, etc., where bioaccumulation can occur), and food wrapped in PVC, as well as
during blood transfusions from PVC blood bags. (HOWARD 1989)
A7.3 HEALTH EFFECTS
Noncarcinogenic Effects of Bis (2-ethylhexyl) Phthalate. Carpenter et al. (1953)
conducted chronic oral toxicity studies on rats, guinea gigs and dogs. The guinea pigs
were fed diets containing bis (2-ethylhexyl) phthalate for a period of one year at
levels corresponding to 19 and 64 mg/kg/day. Significant increases were observed in
relative liver weights in both treated groups.
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Groups of rats were maintained for 2 years on diets containing bis (2-ethylhexyl)
phthalate. The results of this study demonstrated that guinea pigs offer the more
sensitive animal model for bis (2-ethylhexyl) phthalate toxicity. A lowest observable
adverse effect level (LOAEL) in the guinea pigs is determined to be 19 mg/kg/day.
EPA has established an oral reference dose of 2 x 10·2 mg/kg/day based on the above
studies. (IRIS 1989)
Carcinogenic Effects of Bis (2-ethylhexyl) Phthalate. There is inadequate human
carcinogenicity data for bis (2-ethylhexyl) phthalate. A mortality study conducted by
Thiess et al. (1978) was limited by a short follow-up period and unquantified bis (2-
ethylhexyl) phthalate worker exposure.
In an NTP (1982) study, rats and mice were fed diets containing bis (2-ethylhexyl)
phthalate for 103 weeks. A statistically significant increase in the incidence of
hepatocellular carcinomas and combined incidence of carcinomas and adenomas were
observed in female rats and both sexes of the mice. (IRIS 1989)
Based on a significant oral dose related increase in liver tumor responses in rats and
mice EPA classed bis (2-ethylhexyl) phthalate as B2; probable human carcinogen.
The oral slope factor assigned for bis (2-ethylhexyl) phthalate is 1.4 x 10·2 mg/kg/day.
An inhalation slope factor is not available (IRIS 1989).
A7.4 BIBLIOGRAPHY
ATSDR 1987 A TSDR, Draft Toxicological Profile for Di-(2-ethylhexyl)
phthalate, prepared by Life Systems, Inc., Oak Ridge National
Laboratory, Oak Ridge, December 1987.
HOW ARD 1989 Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume I, Lewis
Publishers, Chelsea, Michigan, 1989.
NIOSH/OSHA NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Di (2-ethylhexyl) Phthalate, Supplement I,
U.S.Department of Health and Human Services, DHHS NIOSH
Publication No 88-118, 1988.
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EPA
IRIS 1989
IRIS 1989
CT/N'f'A
9/2IJ/90
EPA, Integrated Risk Information System (IRIS), Bis
(2-ethylhexyl) Phthalate, on-line, Office of Health and
Environmental Assessment, Cincinnati, OH, January 31, 1987.
EPA, Integrated Risk Information System (IRIS), Reference
Dose (RID) for Bis (2-ethylhexyl) Phthalate, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date August 1, 1989.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Bis (2-ethyl-hexyl) Phthalate,
on-line, Office of Health and Environ-mental Assessment,
Cincinnati, OH, verification date February 1, 1989.
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AS DIOXINS/FURANS
A8.1 CHARACTERISTICS
Dioxin and Furans are otheIWise known as chlorinated dibenzo-p-dioxins (CDDs) and
chlorinated dibenzofurans (CDFs) respectively. Chlorinated dibenzo-p-dioxins and
dibenzofurans (CDDs/CDFs) constitute a family of 210 structurally related chemical
compounds. Because of the large number of similar compounds and the lack of
specific toxicity data for the compounds, EPA has adopted a Toxicity Equivalency
Factor (TEF) that relates the toxicity of all 210 CDDs and CDFs to 2,3,7,8-
Tetrachloro dibenzo-p-dioxin (2,3,7,8-TCDD) (EPA 1989). For the purpose of this
risk assessment, 2,3,7,8-TCDD will be used as an equivalent to the other 209 CDDs
and CDFs compounds.
2,3,7,8-TCDD, Chemicals Abstract Service Registry No. 1746-01-6, is a colorless solid
with no distinguishable odor. 2,3,7,8-TCDD is stable towards heat, acids, and alkalies,
but begins to decompose at 500°C. The decomposition is virtually complete within
21 seconds at 800°C. 2,3,7,8-TCDD is susceptible to photodegradation in the
presence of ultraviolet light, especially in the presence of a hydrogen-donating solvent
(A TSDR 1987). The physicochemical properties for 2,3,7,8-TCDD are listed in Table
A-3.
A8.2 ENVIRONMENTAL FATE
The major sources of 2,3,7,8-TCDD in the environment are production and use of
certain herbicides and chlorophenols, incineration of municipal and industrial wastes,
and improper disposal of chemical wastes produced during the manufacture of 2,4,5-
trichlorophenol, 2,4,5-T, and related herbicides, hexachlorophene, and chlorinated
benzenes (ATSDR 1987).
The fate of 2,3,7,8-TCDD in the air may undergo photolysis and may be removed by
wet and dry deposition. The half-life of atmospheric 2,3,7,8-TCDD is such that it can
be transported long distances in the air. The ultimate sink of airborne 2,3, 7,8-TCDD
is sediments of surface waters. The two processes that are likely to remove 2,3,7,8-
TCDD from water and soils are vaporization and photolysis. The estimated half-life
of 2,3,7,8-TCDD in surface water is greater than one year, and the ultimate sink of
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aquatic 2,3,7,8-TCDD is sediments. The bioconcentration factor of 2,3,7,8-TCDD in
the fathead minnow (Pimephales promelas) is 7900 to 9300 (ATSDR 1987).
2,3,7,8-TCDD is immobile in most soils, but horizontal movement of soil-bound
2,3,7,8-TCDD may occur in runoff water during flooding. As observed in Seveso,
Italy; a site of a major dioxin release, minimal vertical movement may occur in soils
containing low organic matter. The estimated half-life of 2,3, 7,8-TCDD is one to
three years in soil surfaces and 10 to 12 years in the interior of soils (ATSDR 1987).
2,3, 7,8-TCDD present on leaves of plants as a result of spraying herbicides will
photolyze with a half-life of a few hours. The chemical is absorbed by higher plants
and is probably translocated, but it is not accumulated. The absorption by
underground parts may be at the same level as soil, but the aerial parts contain
approximately 50 percent lower concentrations (ATSDR 1987).
A8.3 HEAL TH EFFECTS
CDDs and CDFs constitute a family of 210 structurally related chemical compounds.
Confronted with the need to determine the risks associated with exposure to
materials such as soot, incinerator ash, industrial wastes, and soils which contain
complex mixtures of CDDs and CDFs, EPA adopted a toxicity equivalency factor
(TEF) procedure. This interim procedure is used to assess the risks associated with
exposures to complex mixtures of CDDs and CDFs. By relating the toxicity of the
209 CDDs and CDFs to the highly studied 2,3,7,8-tetrachlorodibenzo-p-dioxin
(2,3,7,8-TCDD), the approach simplifies the assessment of risks involving exposures
to mixtures of CDDs and CDFs. Based on the interim TEF method, the toxicity of
2,3,7,8-TCDD will be discussed in this section and be representative of the 209 other
CDDs and CDFs compounds (EPA 1989).
Noncarcinogenic Effects of 2,3,7,8-TCDD. Although humans have been exposed to
2,3,7,8-TCDD as a contaminant of herbicides and industrial chemicals, there have
been no reported deaths from acute exposure. Lethal oral doses of 2,3,7,8-TCDD
vary from 0.6 to 5000 micrograms/kg for guinea pigs and hamsters, respectively.
Subchronic LD5o values for cumulative (total) exposure during a 90-day oral study
with guinea pigs were essentially the same as those observed after acute exposure.
A 9-month feeding study of a small number of monkeys indicated that a dose of 2 to
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3 micrograms/kg resulted in death. Inhalation experiments have not been conducted
to test the toxicity of 2,3,7,8-TCDD.
The only effect clearly demonstrated to be produced in humans following 2,3,7,8-
TCDD exposure is chloracne. This lesion is a systematic toxic effect and not solely
a dermal effect. In animals, the major toxic effect of 2,3,7,8-TCDD exposure is the
wasting syndrome, in which the animal progressively lose body weight prior to death,
with no clear signs of altered organ function. Although this syndrome is observed in
all species tested, it occurs predominantly only at doses that are lethal or near lethal.
The wasting syndrome has not been observed in humans. There is evidence; some
suggestive, that the liver and nervous systems are affected in humans and animals.
In addition, animals studies demonstrate effects on the digestive system and the
kidney (ATSDR 1987).
Human and animal data indicate that 2,3,7,8-TCDD can be absorbed following
ingestion, and although bioavailability is affected by binding to soils, the extent of
absorption is only decreased by approximately 50 percent. In addition, animal data
indicate 2,3,7,8-TCDD is absorbed well through the skin. Following absorption,
2,3,7,8-TCDD is distributed to tissues in proportion to the lipid content. 2,3,7,8-
TCDD can cross the placenta with subsequent exposure to the fetus. Unmetabolized
2,3,7,8-TCDD is excreted through lactation and direct intestinal elimination (ATSDR
1987).
Data from studies in laboratory mice and rats clearly demonstrate that 2,3,7,8-TCDD
is a developmental toxicant and fetotoxic in several species. These studies have
demonstrated a variety of developmental abnormalities and have resulted in
spontaneous abortions in several species. In contrast, evidence from studies of
human populations exposed to herbicides and other industrial chemicals known to be
contaminated with 2,3,7,8-TCDD is inadequate to demonstrate that 2,3,7,8-TCDD is
a human developmental toxicant or adversely affects reproductive health (A TSDR
1987).
EPA has not assigned 2,3,7,8-TCDD a oral or inhalation reference dose (HEAST
1990).
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Carcinogenic Effects of2,3,7,8-TCDD. The human evidence that 2,3,7,8-TCDD is a
carcinogen is conflicting, with both positive and negative findings reported in cohorts
exposed to herbicides and other chlorinated chemicals known to be contaminated
with 2,3,7,8-TCDD. As a result, the human data only provide suggestive evidence
that 2,3,7,8-TCDD is a human carcinogen. The animal data, however, provide clear
evidence that 2,3,7,8-TCDD is carcinogenic in animals (ATSDR 1987).
Oral administration of 2,3,7,8-TCDD results in the induction of hepato-cellular
carcinoma in both sexes of mice and in female rats, squamous cell carcinomas of the
hard palate in both sexes of rats, and follicular-cell adenomas of the thyroid in male
rats and female mice (HEA 1984).
Kociba et al. (1978) fed rats diets of 0.0, 0.001, 0.01, or 0.1 microgram of 2,3,7,8-
TCDD/kg bw/day to groups of 50 male and 50 female rats for 2 years. The control
group consisted of 86 male and 86 female rats. Tumor incidences were increased in
both sexes in the high-dose group. The tumors that were observed were located in
the hard palate, tongue and adrenal cortex of male and in the liver, tongue and lungs
of female. The most common finding was hepatocellular carcinoma in the females
(HEA 1984).
NTP (1980) tested 2,3,7,8-TCDD for carcinogenicity in mice and rats. Groups of 50
male and 50 female animals received 2,3,7,8-TCDD by gavage in corn oil: acetone,
2 days/week for 104 weeks. Male mice and male and female rats received 0.0, 0.01,
0.05, or 0.5 micrograms of 2,3,7,8-TCDD/kg bw/week. In mice, significant increases
in hepatocellular carcinomas and neoplastic nodules were noted in the high-dose-
males, and increased incidences of hepatocellular carcinomas and adenomas,
fibrosarcoma, histiocytic lymphoma, thyroid Follicular-cell adenoma and cortical
adenoma or carcinoma were observed in high-dose females. A statistically significant
increase in the incidence of follicular-cell adenomas occurred in all treated groups of
male rats. In female rats, significant tumor incidences were noted in subcutaneous
tissue fibromas, adrenal cortical adenomas, and hepatocellular carcinomas and
neoplastic nodules (HEA 1984).
EPA has classified 2,3, 7,8-TCD D as group B2 -sufficient evidence of carcinogenicity
in animals with inadequate evidence in humans. Mixtures consisting of phenoxy
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herbicides and/or chlorophenols with 2,3,7,8-TCDD as a contaminant are classified
as Bl carcinogens -limited evidence of carcinogenicity in humans. An oral and
inhalation slope factor of 1.5 x 105 (mg/kg/day)"1 has been assigned to 2,3,7,8 TCDD
(HEAST 1990).
A8.4 BIBLIOGRAPHY
ATSDR 1987
HEA 1984
HEAST 1990
EPA 1989
CT/APPA
9/20/90
ATSDR, Draft Toxicological Profile for 2,3,7,8-Tetrachloro-
dibenzo-p-dioxin prepared by Syracuse Research Corporation,
Oak Ridge National Laboratory, Oak Ridge, November 1987.
EPA, Health Effects Assessment for 2,3,7,8-Tetrachlorodibenzo-
p-dioxin, Office of Health and Environmental Assessment,
Cincinnati, September 1984.
EPA, Health Effects Assessment Summary Tables, Third
Quarter, FY-1990, Office of Health and Environmental
Assessment, Washington DC, July 1990.
EPA, Interim Procedures for Estimating Risks Associated with
Exposures to Mixtures of Chlorinated Dibenzo-p-Dioxins and
Dibenzo Furans (CDDs and CDFs) and 1989 update, Risk
Assessment Forum, Washington DC, March 1989.
A-29
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A9 POLYCHLORINATED BIPHENOLS (PCB)
A9.1 CHARACTERISTICS
Polychlorinated Biphenyls (PCBs) are a family of man-made chemicals that contain
209 individual compounds. Structurally PCBs consist of a mixture of chlorinated
biphenyls that contain a variable number of substituted cWorine atoms on the
aromatic ring. The commercial PCBs manufactured in the United States are known
as Aroclors. Aroclor products are identified by a four-digit numbering code in which
the first two digits indicate that the parent molecule is a biphenyl and the last two
digits indicate the chlorine content by weight. An exception to this is Aroclor 1016
which retained its developmental designation. Aroclor 1016 is very similar to Aroclor
1242 (ATSDR 1987).
PCBs vary widely in chemical, physical, and biological properties. All PCBs have a
very low water solubility, low vapor pressure, and a high dielectric constant. The
more highly chlorinated species are less volatile than the lighter species (EPA 1979).
Table A-3 lists the physicochemical properties for the Aloclor mixtures.
A9.2 ENVIRONMENTAL FATE
At present, the major source of PCB exposure in the general environment appears
to be environmental cycling of PCBs previously introduced into the environment.
This cycling process involves volatilization from ground surfaces into the atmosphere
with subsequent removal from the atmosphere via wet/dry deposition and then
revolatilization. The environmental persistence of PCBs generally increases with an
increase in the degree of chlorination of the congener. The Aloclors with a high
degree of chlorin-ation (1248, 1254,1260) are resistant to biodegradation and appear
to be degraded very slowly in the environment. The chemical composition of the
original commercial Aloclor mixtures which were released to the environ-men! has
changed over time since the individual congeners degrade and partition at different
rates (ATSDR 1987).
In water, absorption to sediments or other organic matter is a major environmental
fate process for the PCBs. Studies have shown that PCB concentrations are higher
in sediment and suspended matter than in the associated water column. Based on
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their water solubilities and octanol-water partition coefficients, the lower chlorinated
components of Aloclor will sorb less strongly than the higher chlorinated isomers.
Although absorption can immobilize PCBs in the aquatic environment, resolution into
the water column has been shown to occur on the environmental level. The
substantial quantities of PCBs contained in the aquatic sediments can therefore act
as an environmental sink for environmental redistribution of PCBs. Volatilization is
also an important environmental fate process for the PCBs that exist in water in the
dissolved state. The values of the estimated Henry's gas constants for Aloclors are
indicative of significant volatilization from environmental waters (A TSRD 1987).
The low water solubility , high octanol-water partition coefficients of the PCBs and
demonstrated strong absorption of PCBs to soils and sediment indicate that
significant leaching should not occur in soil under most conditions. The tendency of
the lower chlorinated PCBs to leach will be greater than the highly chlorinated PCBs.
In the presence of organic solvents, however, PCBs can leach significantly in soil
(ATSDR 1987).
The vapor pressures of the Aloclors indicate that they should exist primarily in the
vapor phase in the atmosphere. Monitoring data has shown that between 87 and 100
percent of the PCBs in air are operationally in the vapor phase. The tendency of
PCBs to absorb to particulates will increase as the degree of chlorination increases
(ATSDR 1987).
PCBs in the atmosphere are physically removed by wet and dry deposition. Dry
deposition occurs only for PCBs associated in the particulate phase. The PCB
concentration of rain water anywhere in the world may typically range between 1 and
250 nanogram/L, which is an indication of the importance of wet deposition.
The ability of PCBs to be degraded or transformed in the environment is dependent
upon the degree of chlorination of the bi phenyl molecule. In general, the persistence
of PCB congeners increases as the degree of chlorination increases. A summary of
experimentally determined biocon-centration factors of various Aroclors in aquatic
species (fish, shrimp, oyster) has found Aloclor bioconcentration factors ranging from
26,00 to 660,00 (ATSDR 1987).
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A9.3 HEAL TH EFFECTS
Evaluation of the toxicity of PCBs is complicated by the fact that PCBs are mixtures
of a variety of different congeners and impurities, each with its own characteristics.
Impurities include the highly toxic polychlorin-ated dibenzofurans (PCDFs). Many
toxicity studies used mixtures of PCBs other than Aroclor, particularly Keneclors.
Keneclors are similar to Aroclors but are produced in Japan rather than the United
States and differ in the method of production, chlorine content, and PCDF contamin-
ation. The reported range of PCDFs in Keneclors and Aroclors is 5 to 20 ppm and
O to 2ppm, respectively. Reference to Keneclors is made occasion-ally to support
statements about Aroclors because the effects produced by Aroclors and Keneclors
are similar (ATSDR 1987).
Noncarcinogenic Effects of PCBs. Aroclors appear to have a low order of acute
lethality. Data indicate that mice and guinea pigs are more sensitive than rats.
Aroclors are lethal at much lower total doses when administered subchronically or
chronically than acutely, indicating PCBs bioaccumulate to concentrations that are
toxic.
Animal studies have shown that the liver and cutaneous tissues are the major target
organs for Aroclor. Aroclors have also been shown to produce stomach.and thyroid
alterations, imm unosuppressive effects, and porphyria in animals. Gross toxic effect
other than reversible skin lesion have not been associated with Aro cl or exposure in
humans. Biochemical effects, however, such as increased liver enzyme levels, have
been associated with Aroclor exposure in workers and in the general population.
Aroclors appear to be fetotoxic but not teratogenic in various of animals, including
rats, mice, rabbits, and monkeys, but the possibility that contaminants (e.g. PCDFs)
may be responsible for the effects should be recognized. Effects such as decreased
birth weight, shortened gestation age, and neonatal behavioral alterations have been
associated with PCB exposure in humans. Oral exposure to Aroclors produced
deleterious effects on reproduction in monkeys, mink, and at higher doses, rodents
(ATSDR 1987).
Carcinogenic Effects of PCBs. Although there are many studies involving humans,
the data are inadequate due to confounding exposures or lack of exposure
quantification. The first documentation of carcinogenicity associated with PCBs
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exposure was reported at a New Jersey petrochemical plant involving 31 research and
development employees and 41 refinery workers. Although a statistically significant
increase in malignant melanomas was reported, the two studies failed to report a
quantified exposure level and to account for the presence of other potential or known
carcinogens (IRIS 1990).
Two occurrences of ingestion of PCBs-contaminated rice oil have been reported: the
Yusho incident of 1968 in Japan and the Yu-Cheng incident of 1979 in Taiwan.
Amano et al. (1984) completed a 16-year retrospective cohort mortality study of 581
male and 505 female victims of the Yusho incident. A consistently high risk of liver
cancer in females over the entire 16 years was observed; liver cancer in males was
also significantly increased. Several serious limitations are evident in this study.
There was a lack of information regarding job histories or the influence of alcoholism
or smoking. The information concerning the diagnosis of liver cancer was obtained
from the victims' families, and it is not clear whether this information was
independently verified by health profession-als. For some of the cancers described,
the latency period is shorter than would be expected. Furthermore, the contaminated
oils contained polychlorinated dibenzofurans and polychlorinated quinones as well
as PCBs, and the study lacks data regarding exposure to the first two classes of
compounds. There is strong evidence indicating that the health effects seen in
Yusho victims were due to ingestion of polychlorinated dibenzofurans, rather than to
PCBs themselves. The results of the Amano et al. study can, therefore, be
considered as no more than suggestive of carcinogenicity of PCBs (IRIS 1990).
Sufficient evidence is available in animal studies to support the carcinogenicity of
PCBs. PCB mixtures assayed in the following studies were commercial preparations
and may not be the same as mixtures of isomers found in the environment. Although
animal feeding studies demon-strate the carcinogenicity of commercial PCB
preparations, it is not known which of the PCB congeners in such preparations are
responsible for these effects, or if decomposition products, contaminants or
metabolites are involved in the toxic response. Early bioassays with rats were
inadequate to assess carcinogenicity due to the small number of animals and short
duration of exposure to PCBs. A Jong-term bioassay of Aroclor 1260 reported by
Kimbrough et al. (1975) produced hepatocellular carcinomas in female rats when 100
ppm was administered for 630 days to 200 animals. Hepatocellular carcinomas and
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neoplastic nodules were observed in 14 and 78 percent, respectively, of the dosed
animals, compared with 0.58 and O percent, respectively,of the controls (IRIS 1990).
Orally administered PCBs resulted in increased incidences of hepatocell-ular
carcinomas in two mouse strains. Ito et al. (1973) treated male mice with Keneclors
500, 400 and 300 each at dietary levels of 100, 250 or 500 ppm for 32 weeks. The
group fed 500 ppm of Kanechlor 500 had a 41. 7 percent incidence of hepatocellular
carcinomas and a 58.3 percent incidence of nodular hyperplasia. Hepatocellular
carcinomas and nodular hyperplasia were not observed in mice fed 100 or 250 ppm
of Kanechlor 500, nor among those fed Kanechlors 400 or 300 at any concentrations
(IRIS 1990).
Schaeffer et al. (1984) fed male rats diets containing 100 ppm of the PCBs mixtures
Clophen A 30 (30 percent chlorine by weight) or Clophen A 60 (60 percent chlorine
by weight) for 800 days. The PCBs mixtures were reported to be free of furans.
Clophen A 30 was administered to 152 rats, Clophen A 60 to 141 rats, and 139 rats
received a standard diet. Mortality and histologic lesions were reported for animals
necropsied during each 100-day interval for all three groups. Of the animals that
survived the 800-day treatment period, 1/53 rats (2 percent) in the control group,
3/87 (3 percent) in the Clophen A 30 group and 52/85 (61 percent) in the Clophen
A 60 group had developed hepatocellular carcinoma. The incidence in the Clophen
A 60 group was significantly elevated in comparison to the control group. The
incidence of nodules was significantly increased in both treatment groups in
comparison to the control group. Neoplastic liver nodules and hepatocellular
carcinomas appeared earlier and at higher incidence in the Clophen A 60 group
relative to the Clophen A 30 group. The authors interpreted the results as indicative
of a carcinogenic effect related to the degree of chlorination of the PCBs mixture.
The authors also suggested that these findings support those of others, including Ito
et al. (1973) and Kimbrough et al. (1975), in which hepatocellular carcinomas were
produced by more highly chlorinated mixtures (IRIS 1990).
Chlorinated dibenzofurans (CDFs), known contaminants of PCBs, and chlorin-ated
dibenzodioxins (CDDs) are structurally related to and produce certain biologic effects
similar to those of PCBs congeners. While the CDDs are known to be carcinogenic,
the carcinogencity of CDFs is still under evalu-ation (IRIS 1990).
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A9.4 BIBLIOGRAPHY
ATSDR
HEA 1984
IRIS 1990
EPA 1979
CT/1\Pf'A
9/2!J/90
A TSDR, Draft Toxicological Profile for Selected PCBs prepared
by Syracuse Research Corporation, Oak Ridge National
Laboratory, Oak Ridge, November 1987.
EPA Health Effects Assessment for Poluchlorinated Biphenyls
(PCBs), Office of Health and Environmental Assessment,
Cincinnati, September 1984.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogencity Assessment for Polychlorinated biphenyls
(PCBs), on-line, Office of Health and Environ-mental
Assessment, Cincinnati, OH, January 1, 1990.
EPA, Water Related Environmental Fate of 129 Priority
Pollutants Volume I: Polychlorinated Biphenyls, Versar, Inc.,
Washington DC, December 1979.
A-35
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A 10 1,2,4 Trichlorobenzene
A 10.1 Characteristics
1,2,4-Trichlorobenzene, Chemical Abstract Service Registry No. 120-82-1, is a low
melting solid or liquid with a pleasant aroma. It melts at 17° C and boils at 213.5°
C. 1,2,4-Trichlorobenzene has a solubility in water of <30 mg/I at 20°C. It has a
threshold odor concentration of 0.005-0.05 mg/I in water (Fawell & Hunt 1988).
Table A-4 shows chemical and physical properties of 1,2,4-Trichlorobenzene.
A 10.2 Environmental Fate
1,2,4-Trichlorobenzene's (1,2,4-TCB) release to the environment will occur through
its manufacture and use as a dye carrier (major use), intermediate in the manufacture
of herbicides and higher chlorinated benzenes, dielectric fluid solvent, heat-transfer
medium, and its use in degreasing agents, septic tank and drain cleaners, wood
preservatives, and abrasive formulations. If it is released to soil, it will probably
adsorb to soil and therefore will not leach appreciably to ground water. However,
1,2,4-TCB has been detected in some ground water samples, which indicates that it
can be transported there by some process. 1,2,4-TCB will not hydrolyze or
biodegrade in ground water, but it may biodegrade slowly in the soil based upon the
data from one experiment. If 1,2,4-TCB is released to water it will adsorb to the
sediments and may bioconcentrate in aquatic organisms. It will not hydrolyze in
surface waters but it may be subject to significant biodegradation. It is expected to
significantly evaporate from water with half-lives of 11-22 days for evaporation from
a study of a mixed, 5.4 m deep seawater microcosm, and a half-life of 4.2 hr
predicted for evaporation from a model river. Adsorption to sediments or absorption
by microorganisms may retard the rate of evaporation. It will not appreciably directly
photolyze in surface waters based on a reported half-life for sunlight photolysis in
surface water at 40 deg latitude in summer of 450 years. If 1,2,4-TCB is released to
the atmosphere it will react with photochemically produced hydroxyl radicals with a
resulting estimated vapor phase half-life in the atmosphere of 18.5 days. Exposure
to 1,2,4-TCB will result mainly from occupational exposure during its manufacture
and use, while general population exposure will result from the ingestion of
contaminated drinking water and food, especially contaminated fish (Howard 1990).
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TABLEA-4
PHYSIOCHEMICAL PROPERTIES OF VOLATILE COMPOUNDS
WATER VAP HENRY'S PART
COMPOUND CASRN FORMULA MW MP BP DENSITY SOL PRESS LAW COEF
('C) ('C) (g/cm3) (mg/L} (mm Hg) (alm-m31mol) (log Kow)
1.2,4-Trichlorobenzene 120-82-1 C6H3Cl3 181.46 17 213.5 1.45 3,00E+-01 2.00E--01 2.31E--03 4.3
Totrach!orelheno 127-18-4 CC12CC12 165.83 -19 121 1.62 1.SOE+-02 1.78E+-01 2.59E--02 2.6
Trlchtorethene 79--01--6 CHC1CC12 131.39 -73 87 1.46 1.10E+03 5,79E+-01 9.10E--03 2.4
Source: EPA 1990, CAC 10n
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A 10.3 Health Effects
Non-Carcinogenic Effects of 1,2,4-Trichlorobcnzene
Trichlorobenzenes are of relatively low acute toxicity in experimental animals. Oral
LD50s in rodents range from 300 to 800 mg/kg.
Lethargy and retarded weight gain were reported in rats exposed by inhalation to 200
ppm of 1,2,4-trichlorobenzene, 6 hours/day for 15 days. Similar effects were found
in rats exposed to 70 ppm, though no sighs of toxicity were evident at 20 ppm. No
histopathological changes were found at any concentration. Female rats given 250
or 500 mg/kg/day of 1,2,4-trichlorobenzene by intraperitoneal injection for 3 days
exhibited elevated liver weight and adrenal weight. Lowered body weight ant uterus
weight were also reported, but there was no evidence that 1,2,4-trichlorobenzene had
oestrogenic activity. In rhesus monkeys, daily oral doses of 173.6 mg/kg were lethal
within 20-30 days. Doses of up to 25 mg/kg were without effect.
A single oral dose of 200 mg/kg of 1,2,4-trichlorobenzene was found markedly to
enhance hepatic porphyrins in both adult male Japanese quail and day-old White
Leghorn chicks. In a further study, Japanese quail given oral doses of 50 or 200
mg/kg/day for 8 days also exhibited induction of a number of liver constituents and
enzymes involved in haem biochemistry and drug metabolism. Several other studies
have shown that 1,2,4-trichlorobenzene readily induces hepatic mixed function oxidase
activity. The 1,2,3-and 1,3,5-isomers do not appear to be as potent as the 1,2,4-
isomer in this respect.
lntraperitoneal injection of 5 mmol/kg (905 mg/kg) of 1,2,4-trichlorobenzene in rats
was found to increase bile-duct pancreatic fluid flow but had no effect on plasma
alanine aminotransferase activity. However, in rats given the same dose of 1,3,5-
trichlorobenzene, plasma alanine aminotransferase activity was elevated, while there
was little effect on bile-duct pancreatic fluid flow.
In a comprehensive multigeneration study, Charles River rats were exposed to 1,2,4-
trichlorobenzene in their drinking water from birth of the F(O) generation to weaning
of the F(2) generation at concentrations of 0, 25, 100 or 400 mg/1. No effects were
found on fertility, growth, viability, locomotor activity or blood parameters of either
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the F(0), F(l) or F(2) generations. Slightly elevated adrenal weights, however, were
reported in the F(0) and F(l) generations at 95 days of age at the high dose.
Hepatic cytochrome P-450 and cytochrome c reductase were induced by 1,2,4-
trichlorobenzene in a 90-day study in which rats were given daily oral doses of 10-40
mg/kg. A slight increase in liver weight/body weight ratio was found at 40 mg/kg but
no changes in haemoglobin, haematocrit or liver histopathology were evident at any
dose level. Daily oral doses of 1-25 mg/kg of 1,2,4-trichlorobenzene for 120 days did
not produce any evidence of toxicity in rhesus monkeys. At 125 mg/kg, temporary
body-weight loss and some induction of cytochrome P-450 were found.
Histopathological changes were found in the liver and kidney or rats exposed by
inhalation to 25, 50 and 100 ppm of 1,2,4-trichlorobenzene, 7 hours/day, 5 days/week,
for 4 or 13 weeks. No treatment-related effects were observed in either rats, rabbits
or monkeys exposed to 25, 50 or 100 ppm for 26 weeks. Rats, rabbits and dogs
exposed by inhalation to 30 or 100 ppm of 1,2,4-trichlorobenzene, 7 hours/day, 5
days/week for 30 exposures in 44 days did not exhibit changes in body weight,
haematology, clinical chemistry or histopathology. At the high dose, however, there
was elevated liver weight in rats and dogs and elevated kidney weight in rats.
Increased urinary excretion of uroporphyrin and coproporphyrin was found in rats at
both 30 and 100 ppm. Urinary excretion of porphyrins was also elevated in rats
exposed to 10 ppm of 1,2,4-trichlorobenzene for 90 days but not at 3 ppm. A 90-day
inhalation study of 1,3,5-trichlorobenzene in CD rats failed to show significant
changes in haematology, clinical chemistry or histopathology at 1.3, 13 or 130 ppm.
In a Polish study, body weight loss and lowered white blood cell counts were found
in Swiss mice exposed by inhalation to 0.02 mg/I of trichlorobenzene, 7 hours/day for
3 months (Fawell and Hunt 1988).
The USEP A has withdrawn the Oral FRD for 1,2,4-trichlorobenzene pending further
review by the RFD work group. ACGIH has set the ceiling occupational limit at 5
ppm (ACGIH 1989).
Carcinogenic Effects of 1,2,4-Trichlorobenzene
Histopathology showed some organ sites had increased nonneoplastic lesions. All 75
animals in the treated groups and all 50 in the control groups appear to have been
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examined. Increases in nonneoplastic lesions (i.e., amyloid) were reported in lung,
liver, kidney, adrenal, spleen and lymph node of the male high-dose group and in all
these organs except lymph node of the female high-dose group.
No single tumor type was increased significantly over the control incidence; there
was no significant difference in total tumor incidence between treated and control
groups. Among males, nine different tumors were found in the high-dose group as
compared with two in the low-dose and two in the control group. In females there
were 11 different tumors in the high-dose group as compared with 3 in the low-dose
and 8 in the control group. However, no adjustment was made for reduced survival,
and there was no indication of the time for first tumor appearance. The authors do
not state whether these tumors were all found in different individual animals or
whether these were multiple tumors in the same animal. This study has several
limitations. Although male mice were housed individually, female mice were group-
housed. The animals were only treated twice a week, and no pharmacokinetic studies
were performed. There was a low survival rate: 80% of the control mice and 90%
of the treated mice died before the end of the study.
Yamamoto et al. applied 1,2,4-trichlorobenzene in acetone to the dorsal skin of mice
twice weekly for 2 years. The solution of 1,2,4-trichlorobenzene was 60% for the high
dose and 30% for the low dose and the volume applied was 0.03 mUapplication.
Each treated group contained 75 animals of each sex. There were 50 vehicle control
animals for each sex. Growth rates in treated and control mice were comparable
through 83 weeks. Mean survival days were significantly reduced in the 60% 1,2,4-
trichlorobenzene groups of males and females and also in the 30% treatment group
of females. All males and treated females showed as poor as 60% survival by week
40.
Results of two reports on mutagenicity tests with Salmonella typhimurium test strains
were negative. Grover and Sims reported trichlorobenzene to be a metabolite of
gamma-hexachlorocyclohexane (Lindane) which is a possible or probable human
carcinogen. The authors isolated 2,4,5-and 2,3,5-trichlorophenol, which are
metabolites of trichlorobenzene, from urine of Lindane treated rats. This suggested
that dehydrochlorination via trichlorobenzene is one metabolic pathway of gamma-
hexachlorocyclohexane (IRIS 1990).
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1,2,4-trichlorobenzene is classified as a D carcinogen. No slope factor exists because
of the uncertainty of human carcinogenicity (IRIS 1990).
A 10.4 Bibliography
ALDRICH
ATSDR 1987
CLAYTON
CRC
FAWELL
HOWARD
NIOSH/OSHA
SIELER
USEPA
Aldrich Catalog Handbook of Fine Chemicals, Aldrich Chemical
Company, Inc. 1988.
ATSDR, Draft Toxicological Profile for Benzene, Oak Ridge
National Laboratory, Oak Ridge, October 1987.
Clayton, G.D. and Clayton, F.E., Patty's Industrial Hygiene and
Toxicology, John Wiley and sons, NY, 1981.
Weast, R. (editor), CRC Handbook of Chemistry and Physics,
58th ed., CRC Press, Inc., West Palm Beach, FL, 1977.
Fawell, J. and Hunt, S., Environmental Toxicology, Ellis
Horwood Ltd., England, 1988.
Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Benzene, Supplement II, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No
89-104, 1988.
Seiler, H.G., Sigel, G. and Sigel, A., Handbook on Toxicity of
Inorganic Compounds, Marcel Dekker, Inc., 1988.
EPA, Health Effects Assessment for Benzene, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
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IRIS 1990
Cf/APPA
9/2!J/OO
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Benzene, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date.
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A 11 Tetrachloroethene
A 11.1 Characteristics
Tetrachloroethene Chemical Abstract Service Registry No. 127-18-4 is known as
perchloroethylene, tetrachloroethylene, ethylene tetrachloride, PER, PCE, and PERC.
It is a clear, water-white liquid at ordinary temperatures with an odor like ether or
chloroform. It is completely miscible with most organic liquids. Tetrachloroethene
has a solubility in water of 150 mg/I at 25°C (Howard 1990). Table A-4 shows
chemical and physical properties of tetrachloroethene.
A 11.2 Environmental Fate
Tetrachloroethylene (PCE) is likely to enter the environment by fugitive air emissions
from dry cleaning and metal degreasing industries and by spills or accidental releases
to air, soil, or water. If PCE is released to soil, it will be subject to evaporation into
the atmosphere and to leaching to the ground water. Biodegradation may be an
important process in anaerobic soils based on laboratory tests with methanogenic
columns. Slow biodegradation may occur in ground water where acclimated
populations of microorganisms exist. If PCE is released to water, it will be subject
to rapid volatilization with estimated half-lives ranging from < 1 day to several weeks.
It sill not be expected to significantly biodegrade, bioconcentrate in aquatic
organisms, or adsorb to sediment. PCE will not be expected to significantly hydrolyze
in soil or water under normal environmental conditions. If PCE is released to the
atmosphere, it will exist mainly in the gas-phase and it will be subject to
photooxidation with estimates of degradation time scales ranging from an
approximate half-life of 2 months to complete degradation in an hour. some of the
PCE in the atmosphere may be subject to washout in rain based on the solubility of
PCE in water; PCE has been detected in rain. Major human exposure is from
inhalation of contaminated urban air, especially near point sources such as dry
cleaners, drinking contaminated water from contaminated aquifers and drinking water
distributed in pipelines with vinyl liners, and inhalation of contaminated occupational
atmospheres in metal degreasing and dry cleaning industries (Howard 1990).
World-wide production of PCE in 1973 was estimated to be just over one million
tons, and it is likely that over 80% of this was lost to the atmosphere by evaporation
Cif/APPA
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during subsequent use. There have been a number of reports of the detection of
PCE in air. In New York City, levels ranged between 0.1 and 8.7 ug!m3, whereas
concentrations in rural areas were much loser. This solvent was detected at
concentrations as high as 20-300 mg/m3 near dry-cleaning firms.
PCE was detected in 11 out of 14 drinking water samples examined in a WRC survey.
Concentrations varied from less than 1 ug/1 to about 10 ug/1 in some groundwaters.
There are many reports of contamination of water supplies by PCE, in both Europe
and the United States.
PCE has been found in rainwater at 0.15 ug/1, groundwaters and rivers, and in
tapwater at 45 ug/1. Drinking water supplies in Milan contained levels between 4 and
20 ug/1. Chlorination at sewage treatment plants can result in small quantities of PCE
being present in water.
Although ingestion is the main route of exposure for most waterborne chemicals,
inhalation may also be important for compounds such as PCE which are particularly
volatile. Andelman has measured air concentrations of TCE in showers using TCE-
contaminated groundwater, and has shown that this can be a substantial source of
exposure.
Leaching of PCE from vinyl-toluene-lined asbestos-cement pipes was reported in two
American studies. Concentrations ranged from a few micrograms per litre to 3.5 mg/I
PCE in the dead-end pipes of water distribution systems lined with vinyl-toluene.
PCE is used to extract oil and fat from meat so contamination of food may result
from this process. Levels of 1 ug/kg have been detected in beef, up to 2 ug/kg in
fruit and vegetables, 3 ug/kg in tea and coffee, and ranging from 7 ug/kg in olive oil
to 13 ug/kg in butter (Fawell and Hunt 1988).
A 11.3 Health Effects
Noncarcinogenic Effects of Tetrachloroethene
Buben and O'Flaherty exposed Swiss-Cox mice to PCE in corn oil by gavage at doses
of 0, 20, 100, 200, 500, 1500, and 2000 mg/kg, 5 days/week for 6 weeks. Liver toxicity
was evaluated by several parameters including liver weight/body weight ratio, hepatic
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triglyceride concentration, DNA content, histopathological evaluation, and serum
enzyme levels. Increased liver triglycerides were first observed in mice treated with
100 mg/kg. Liver weight/body weight ratios were significantly higher than controls for
animals treated with 100 mg/kg. At higher doses, hepatotoxic effects included
decreased DNA content, increased SGPT, decreased levels of G6P and hepatocellular
necrosis, degeneration and polypolody.
A NOEL of 14 mg/kg/day was established in a second study, as well. Groups of 20
Sprague-Dawley rats of both sexes were administered doses of 14,400, or 1400
mg/kg/day in drinking water. Males in the high-dose group and females in the two
highest groups exhibited depressed body weights. Equivocal evidence of
hepatotoxicity (increased liver and kidney weight/body weight ratios) were also
observed at the higher doses (IRIS 1990). Based on these studies, an oral RFD of
lE-2 mg/kg/day was derived under the IRIS system.
Most of the infonnation on the chronic effects of PCE in humans is from occupations
data on dry-cleaners. The common symptoms of toxicity are dizziness, sleepiness, and
irritation to the eyes, nose and throat. Russian authors have reported other
neurophysiological effects following occupational exposure, such as a reduced ability
to perceive color.
Neurological, physiological and behavioral tests were carried out on ten male and
nine female volunteers exposed for 1, 3 or 7.5 hours/day, 5 days/week (for an
unspecified period of time) to 20, 100 or 150 ppm PCE. No effects were observed
at exposure levels of 20 ppm. Males showed a decrease in coordination skills at 100
and 150 ppm.
Behavioral, renal, hepatic and pulmonary tests were carried out on two groups of
subjects: those occupationally exposed to PCE and a control group. The exposed
group consisted of 26 subjects (24 female and 2 male) working in dry-cleaning
establishments and occupationally exposed to 21 ppm PCE (time-weighted average
exposure) over a period of 6 years; the control group was composed of 33 subjects
(31 female and 2 male) working in a chocolate factory and who had never been
occupationally exposed to organic solvents. No differences were found between the
two groups.
A-44
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Chronically exposed individuals may develop a tolerance to the solvent. Single and
repeated experimental exposures to 100 ppm PCE vapor were carried out in subjects
for either a single 7-hour period, or 7 hours/day for 5 days. Subjects repeatedly
exposed had fewer subjective and objective complaints (headaches, speech difficulty,
dizziness, nose and throat irritation) than those who were exposed for only a single,
7-hour period (Howard and Hunt 1988).
Both OSHA and ACGIH have set an occupational exposure limit of 50 ppm 8 hr
TWA for tetrachloroethene (OSHA 1989, ACGIH 1989).
Carcinogenic Effects of Tetrachloroethene
In the National Cancer Institute study groups of 48 B6C3Fl mice and Osborne-
Mendel rats of both sexes were given doses of 500 or 1000 mg/kg body weight of
PCE in corn oil by gavage, 5 days/ week for 78 weeks. A significant increase in
hepatocellular carcinomas was found in treated male and female B6C3Fl mice at
both low and high dose levels. No other organs or tissues appeared to be affected.
In contrast there was no evidence of an increase in liver tumors in Osborne-Mendel
rats treated with the same dose levels of PCE administered in corn oil. However, the
survival rate was poor.
In an inhalation study by Rampy et al, there was no significantly increased incidence
of any type of tumor in either male or female Sprague-Dawley rats exposed to 315
ppm or 602 ppm PCE for 6 hours/day, 5 days/week for 12 months. Observations
were carried out over the animals' lifetime. However, inhalation of PCE for two
years at 200 or 400 ppm in rats and 100 or 200 ppm in mice resulted in an increased
incidence of leukaemia in rats and liver tumors in mice.
Evidence that PCE causes cancer in humans is unclear. Blair et al investigated a
group of 330 dry-cleaning and laundry workers who had been exposed to PCE for
periods of up to 20 years. The frequency of specific causes of deaths for this group
was compared with that for the general population, and the frequency of deaths from
cancer was higher than the predicted frequency for the normal population (87
recorded; 68 expected), although the difference was only small. Lung, cervical and
skin cancer were mainly responsible for the increased mortality rate, but there was
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also a slightly elevated occurrence of leukaemia and liver cancer. Although PCE was
the main constituent of the cleaning fluid, other solvents such as carbon tetrachloride
and TCE were also present, so any effects cannot be attributed to PCE alone. Also,
a high incidence of Jung cancer is associated with low socio-economic class. Since
laundry workers tend to belong to this social group, this could have been an
important contributing factor to the elevated mortality rate from cancer, rather than
the single effect of exposure to PCE.
Another study reported an unspecified excess of bladder and kidney cancers among
1690 cry-cleaning workers exposed to PCE. However, since exposure cannot be
attributed to this solvent alone, due to the presence of other solvent compounds, the
significance of the results is unclear (Fawell and Hunt 1988).
The USEP A is currently evaluating tetrachloroethene under the IRIS system.
The World Health Organization wet a tentative guideline value of 10 ug/1 for PCE
in drinking water. This was based on data from the mouse carcinogenicity study,
using corn oil as the solvent. However, it is possible that the use of corn oil as a
vehicle may overestimate the toxicity that might be expected following exposure
through water (Fawell and Hunt 1988).
A 11.4 Bibliography
ALDRICH
ATSDR 1987
CLAYTON
CRC
CT/N"PA
9/2!J/90
Aldrich Catalog Handbook of Fine Chemicals, Aldrich Chemical
Company, Inc. 1988.
ATSDR, Draft Toxicological Profile for Benzene, Oak Ridge
National Laboratory, Oak Ridge, October 1987.
Clayton, G.D. and Clayton, F.E., Patty's Industrial Hygiene and
Toxicology, John Wiley and sons, NY, 1981.
Weast, R. (editor), CRC Handbook of Chemistry and Physics,
58th ed., CRC Press, Inc., West Palm Beach, FL, 1977.
A-46
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FAWELL
HOWARD
NIOSH/OSHA
SIELER
USEPA
IRIS 1990
CT/APPA
9/2Dl90
Fawell, J. and Hunt, S., Environmental Toxicology, Ellis
Horwood Ltd., England, 1988.
Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Benzene, Supplement II, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No
89-104, 1988.
Seiler, H.G., Sigel, G. and Sigel, A, Handbook on Toxicity of
Inorganic Compounds, Marcel Dekker, Inc., 1988.
EPA, Health Effects Assessment for Benzene, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Benzene, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date.
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A 12 Trlchloroethene
A 12.1 Characteristics
Trichloroethene, Chemical Abstract Service Registry No. 75-00-3, is also known as
TCE, acetylene trichloride, ethylene trichloride, tri, trilene, and TCE (Fawell and
Hunt 1988). It is a colorless liquid with a sweet odor like chloroform (NIOSW 1985).
One gram of trichloroethene can be dissolved in one liter of water at 20°C.
Trichloroethene has an odor threshold of 10 mg/I in water (Fawell and Hunt 1988).
Table A-4 shows chemical and physical properties of trichloroethene.
A 12 Environmental Fate
Over 155 million pounds of TCE are used for vapor degreasing of metals which
should result in releases to the environment through evaporation, spills, and leaks in
storage tanks. TCE released to the atmosphere will exist primarily in the vapor
phase based on its relatively high vapor pressure. It will react fairly rapidly, especially
under smog conditions. Atmospheric residence time of 5 days has been reported with
formation of phosgene, dichloroacetyl chloride, and formyl chloride. It is not subject
to direct photolysis (Howard 1990).
TCE is a common contaminant of air, and has been detected at levels normally in the
range 1-20 ug/m3• Analyses of concentrations of TCE in air in Western Europe
during the period 1972-1976 indicated that levels were between 0.5 and 10 ug/m3•
However, concentrations up to 90 ug/m3 have been reported in an urban area
containing many dry-cleaning establishments. Atmospheric contamination with TCE
has been implicated as a possible factor in the depletion of the ozone layer (Fawell
and Hunt 1988).
If TCE is released to water, the primary removal process will be evaporation with a
half-life of minutes to hours, depending upon turbulence. Biodegradation, hydrolysis,
and photooxidation are extremely slow by comparison. Adsorption to sediment and
bioconcentration in aquatic organisms are not important processes. Releases to soil
will be partially evaporated and partially leached into ground water, where it may
remain for a long time. However, there is some monitoring data that suggests
degradation to other chlorinated alkenes. High levels of exposure are expected for
CT/AI'f'A
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workers in degreasing plants due to inhalation of vapors or adsorption through the
skin. Lower exposure by inhalation is expected in persons living near degreasing
plants or at spill sites. Broad population exposure to low levels is expected from
inhalation of contaminated ambient air and ingestion of contaminated drinking water
(Howard 1990).
TCE was identified in 13 out of 14 drinking water samples examined in a WRc
survey. Concentrations between 0.02 and 5.4ug/l have been detected in domestic
drinking water supplies in the United States. In rainwater, TCE was detected at
levels of up to 0.07 ug/1. This compound was found as a common contaminant in
groundwater in Britain, the Netherlands, France, Italy and the United States of
America. In general, levels are below 2 ug/1 and 40 000 ug/1 have been reported.
Since TCE is virtually insoluble in water, and has a specific gravity heavier than
water, any pollution of groundwater is likely to persist. There is no indication that
TCE is produced from chlorination of natural waters (Fawell and Hunt 1988).
Although ingestion is the main route of exposure for most waterborne chemicals,
inhalation may also be important for compounds such as TCE which are particularly
volatile. Andelman measured air concentrations of TCE in showers, using TCE-
contaminated groundwater, and has shown that this can be a substantial source of
exposure (Fawell and Hunt 1988).
TCE is used as a solvent in food processing, and this may account for its occurrence
in food. It has been detected at levels of 10 ug/kg in butter, 16 ug/kg in steak and
60 ug/kg in tea. Wallace et al found 920 ug/kg TCE in margarine, but concentrations
in other foodstuffs were negligible. There have been proposals by the U.S. Food and
Drug Administration to discontinue the use of TCE in food processing. At present,
the level of TCE in coffee is limited to 10 mg/kg dry weight in decaffeinated instant
coffee and 25 mg/kg in decaffeinated ground coffee. Some manufacturers now use
methylene chloride as an alternative for decaffeinating coffee (Fawell and Hunt
1988).
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A 12.3 Health Effects
Noncarcinogenic Effects of Trichloroethene
TCE is of moderate to low acute toxicity via the oral route. The oral LD50 in female
mice was 2443 mg/kg body weight, and in male mice it was 2402 mg/kg, when this
compound was administered by gavage, in a 10% solution of Emulphor. The oral
LD50 in the rat was 4920 mg/kg (Fawell and Hunt 1988).
Male Swiss-Cox mice exposed to doses of 100-3200 mg/kg/day TCE in corn oil, by
gavage, for 6 weeks, showed an increase in relative liver weight in all dose groups,
with an increase of 75% compared to controls in the highest dose group. Hepatic
glucose-6-phosphatase activity was depressed at dose levels of 800 mg/kg/day and
above, but the levels of liver triglycerides or serum glutamate-pyruvate transaminase
were unaffected, even at the highest dose (Fawell and Hunt 1988).
Workers chronically exposed to TCE may suffer central nervous effects such as
headaches, dizziness and impaired sensitivity to touch and pain. The trigeminal nerve
appears to be particularly affected from long-term exposure. Disturbance in heart
muscle conduction was reported in dry-cleaning workers (Fawell and Hunt 1988).
Where work involves frequent skin contact with TCE, this solvent causes defatting of
tissues, so hands and skin become rough and chapped. Dermatitis and secondary
infections may develop as a consequence (Fawell and Hunt 1988).
Both OSHA and ACGIH have set an occupational exposure limit of 50 ppm 8 hr
TWA for trichloroethene (OSHA 1989 ACGIH 1989).
Carcinogenic Effects of Trichloroethene
In the National Cancer Institute study (1976) groups of 50 male B6C3Fl mice were
given doses of 1200 or 2400 mg/kg body weight and females were given 900 or 1800
mg/kg body weight of TCE (99% purity, 0.19% epoxybutane stabiliser) in corn oil,
by gavage, 5 days/week for 78 weeks. Twenty animals of each sex and species were
given the vehicle alone, as controls. A significant increase in hepatocelluar
carcinomas was found in treated mice of both sexes compared with control animals.
There was also a slightly increased incidence of lung tumors in both sexes. No
evidence of liver tumors was observed in groups of 50 Osborne-Mendel rats of both
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sexes given doses of 500 or 1000 mg/kg body weight of TCE (99% purity, 0.19%
epoxybutane) in corn oil, by gavage, 5 days/week for 78 weeks.
Recent evidence from long-term gavage studies suggests that concentrations of 250
mg/kg body weight TCE produce a low incidence of renal adenocarcinomas in male
rats. This type of tumor occurs very rarely in untreated control animals (Fawell and
Hunt 1988).
The carcinogenicity of TCE, with or without two epoxide stabilisers, epichlorohydrin
(0.8% w/w) and epoxybutane (0.8% w/w) was investigated in Swiss mice, a strain with
a low frequency of spontaneous liver tumors. Males were dosed with 2.4 g/kg and
females were dosed with 1.8 g/kg TCE in corn oil, or TCE with epichlorohydrin
and/or epoxybutane, by gavage, 5 days/week, for 18 months. Gross and microscopic
examination of liver, stomach, spleen, kidney, adrenal, lung and heart tissue indicated
a statistically significant increase in the incidence of forestomach tumors in mice
treated with TCE plus epichlorohydrin, and mice treated with TCE plus
epichlorohydrin and epoxybutane. No effect was observed in mice treated with pure,
epoxybutane-stabilized and amine-stabilized TCE.
At present, epidemiological studies are inadequate to evaluate the risk of cancer in
man from exposure to TCE. Limitations include uncertain estimation of the degree
and duration of exposure to the chemical, simultaneous exposure to other potentially
carcinogenic chemicals, small cohort size, and a follow-up period which may be
shorter than the latency period for a cancer to develop. The risk of death from
cancer due to exposure to dry-cleaning fluids, including TCE, was investigated from
the mortality figures of 330 dry-cleaning and laundry workers recorded between 1957
and 1977. The frequency of deaths from cancer was compared with the predicted
frequently of deaths from cancer in the normal population. There was an increased
occurrence of lung cancer, cervical cancer and leukaemia in the exposed group,
although the difference was not significant. Lung cancer is often associated with low
socio-economic status, and it is likely that this was a major contributing factor to the
increased frequency observed. The results were also unclear because PCE, carbon
tetrachloride and petroleum solvents were also present in the dry-cleaning fluids. In
Finland, no significant difference was observed in either total mortality or cancer
mortality between a cohort of 1148 men and 969 women, occupationally exposed to
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TCE between 1963 and 1976, and the national average mortality figures. However,
the period of exposure to TCE was not specified. In a retrospective study, comparing
two information sources, the Cancer Registry of liver cancer and a list of past
employees at Imperial Chemical Industries, Runcorn, there was only one probable
match, and one possible match between the occurrence of liver cancer and
occupational exposure. However, on further investigation these two possibilities
proved to be negative since the subjects diagnosed with liver cancer had never
worked on the Runcorn site (Fawell and Hunt 1988).
The USEP A has withdrawn the carcinogen assessment summary for trichloroethene
under the IRIS program pending further review.
Based on data from the mouse carcinogenicity study (National Cancer Institute 1976)
the World Health Organization derived a tentative guideline level of 30 ug/1 for TCE
in drinking water. However, the guideline value was calculated using a low-dose
extrapolation model based on a genotoxic mechanism of action, but there is evidence
that this is not the case with TCE (Fawell and Hunt 1988).
A 12.4 Bibliography
ALDRICH
ATSDR 1987
CLAYTON
CRC
FAWELL
CT/APPA
9/',JJ/90
Aldrich Catalog Handbook of Fine Chemicals, Aldrich Chemical
Company, Inc. 1988.
ATSDR, Draft Toxicological Profile for Benzene, Oak Ridge
National Laboratory, Oak Ridge, October 1987.
Clayton, G.D. and Clayton, F.E., Patty's Industrial Hygiene and
Toxicology, John Wiley and sons, NY, 1981.
Weast, R. (editor), CRC Handbook of Chemistry and Physics,
58th ed., CRC Press, Inc., West Palm Beach, FL, 1977.
Fawell, J. and Hunt, S., Environmental Toxicology, Ellis
Horwood Ltd., England, 1988.
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HOWARD
NIOSH/OSHA
SIELER
USEPA
IRIS 1990
CT/Pi'PA
9/20/90
Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Benzene, Supplement II, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No
89-104, 1988.
Seiler, H.G., Sigel, G. and Sigel, A., Handbook on Toxicity of
Inorganic Compounds, Marcel Dekker, Inc., 1988.
EPA, Health Effects Assessment for Benzene, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Benzene, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date.
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A13 DIELDRIN
A13.1 CHARACTERISTICS
Dieldrin, Chemical Abstract Service Registry No. 60-57-1, is an organo-chlorine
insecticide also known as HEOD, Octalox, and Panorain D-31. Dieldrin is a buff to
light tan solid with a mild odor. Dieldrin's solubility in water is reported to be 0.19
mg/L (ATSDR 1988). Table A-5 shows chemical and physical properties for dieldrin.
A13.2 ENVIRONMENTAL FATE
Dieldrin was widely used by farmers to kill insects in seed and agricul-tural crops,
notably corn, citrus, and cotton between the 1950s to the early 1970s. Dieldrin was
also used for soil treatment as well as by exterminators to kill termites through the
treatment of soil under slab houses. Most uses of dieldrin were banned in 1975
(ATSDR 1988).
Dieldrin sorbs tightly to soil and volatilizes more slowly than its structural counterpart
aldrin. However, the relatively rapid loss of dieldrin from soil during the first few
months after application is plausibly attributed to loss by volatilization. It is probable
that atmospheric degradation prevent accumulation of dieldrin in the air (ATSDR
1988).
Dieldrin is resistant to biodegradation, resulting in microbial degrada-tion being a
minor route of environmental loss. Movement of dieldrin in waterborne sediment is
a major pathway of loss from treated soil. The potential for soil runoff is supported
by reports of small amounts of dieldrin in surface waters (ATSDR 1988).
The resistance of dieldrin to soil leaching generally precludes their appearance in
groundwater, as in evident from the absence of dieldrin from groundwater samples.
Volatilization of dieldrin from water is slow, with an estimated half-life from a 1
meter column of water of 539 days (ATSDR 1988).
A13.3 HEALTH EFFECTS
Non-carcinogenic Effects of Dieldrin. Waler et al. (1969) administered dieldrin to
rats for two years at dietary levels of 0, 0.005, 0.05, and 0.5 mg/kg/day. At the end
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TABLE A-5
PHYSIOCHEMICAL PROPERTIES OF PESTICIDE COMPOUNDS
WATER VAP HENRY'S
COMPOUND CASRN FORMULA MW MP BP DENSITY SOL PRESS LAW
(•C) ('C) (g/cm3) (mg/l) (mm Hg) (atm-m3/mol)
Dleldrln 60-57-1 C12HBCl6O 380.93 176 1.75 1.9E+2 3.1E-6 2.0E-7
Sources: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA, USHPS ATSDR
PART
COEF
(log Kow)
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of two years, rats treated with 0.05 and 0.5 mg/kg/day had increased liver weights and
liver-to-body weight ratios. Histopathological examinations revealed liver lesions that
are considered to be characteristic of exposure to an organochlorine insecticide (IRIS
1988).
Based on the study by Walker et al. (1969), an oral reference dose of 5 x 10·5
mg/kg/day has been established for dieldrin (IRIS 1988).
There is no inhalation reference dose for dieldrin available at this time (IRIS 1988).
Carcinogenic Effects of Dieldrin. Human carcinogenicity data is inadequate for
evidence of dieldrin being a human carcinogen. Animal studies, however, are
sufficient to classify dieldrin as a probable human carcinogen or Group B2. Dieldrin
has been shown to be carcinogenic in various strains of mice of both sexes. At
different dose levels the effects range from benign liver tumors, to heptocarcinomas
with trans-plantation confirmation to pulmonary metastases. Dieldrin is structurally
related to compounds ( aldrin, chlordane, heptachlor, heptachlor epoxide, and
chlorendic acid) which produce tumors in rodents (IRIS 1988).
The oral and inhalation slope factor of dieldrin is 1.6 x 101 mg/kg/day. This value is
the geometric mean of 13 oral slope factors calculated from liver carcinoma data in
both sexes of several strains of mice (IRIS 1988).
A 13.4 BIBLIOGRAPHY
EPA
EPA
Cf/M'PA
9/2Dl90
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989.
EPA, Integrated Risk Information System (IRIS), Dieldrin,
on-line, Office of Health and Environmental Assessment,
Cincinnati, OH, January 1, 1989.
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ATSDR 1988
NIOSH/OSHA
IRIS 1988
IRIS 1988
Cf/APPA
9/'20/90
ATSDR, Draft Toxicological Profile for Aldrin/Dieldrin,
prepared by Dynamac Corporation, Oak Ridge National
Laboratory, Oak Ridge, 1988.
NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Dieldrin, Supplement I, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No
88-118, 1988.
EPA, Integrated Risk Information System (IRIS), Reference
Dose (RID) for Dieldrin, on-line, Office of Health and
Environmental Assessment, Cincinnati, OH, verification date
September 7, 1988.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Dieldrin, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date September 7, 1988.
A-56
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A14 ALUMINUM
A14.1 CHARACTERISTICS
Aluminum, Chemical Abstract Service Registry No. 7429-90-5, is a tin-white,
malleable, ductile metal with somewhat bluish tint; capable of taking on a brilliant
shine which is retained in dry air. In moist air, an oxide film forms which protects
the metal from corrosion (MERCK 1976). Aluminum is the third most abundant of
all elements on earth (ACGIH 1986). Table A-6 shows chemical and physical
properties for aluminum.
A14.2 ENVIRONMENTAL FATE
Although no information on the environmental fate of aluminum could be located in
the literature, aluminum containing materials would be expected to participate in all
of the environmental fate processes. Aluminum metal and insoluble compounds
would act as particulates, alkyl aluminum compounds would act as
volatile/semivolatile compounds, and soluble aluminum compounds would be
influenced by water.
A14.3 HEALTH EFFECTS
Concarcinogenic Effects of Aluminum. No information on the environmental
toxicology of aluminum could be located in the literature. There does exist data on
the industrial exposure to aluminum via the inhalation route. From industrial
toxicologic information, there would appear to be a need for different allowable
exposure levels based on the form of aluminum in the air. Metal dusts have been
assigned an allowable exposure limit of 10 mg Al/M3 for an 8-hour workday. Pyro
powders and welding fumes containing aluminum have been assigned an allowable
exposure limit of 5 mg Al/M3• Soluble salts and aluminum alkyl compounds have
been assigned an allowable exposure limit of 2 mg Al/M3•
EPA has not assigned an oral or inhalation reference dose (RID) for aluminum or
aluminum compounds with the exception of aluminum phosphide. The critical
toxicity value for aluminum phosphide is based on the acute toxicity associated with
the decomposition product; phosphine gas. Therefore, the critical toxicity values for
aluminum phosphide are not applicable for aluminum (IRIS 1988).
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COMPOUND
Aluminum (metal)
Aluminum chlorate
Aluminum chloride
Aluminum fluoride
Aluminum hydroxide
Aluminum oxide
Aluminum phosphate
TABLEA-6
PHYSIOCHEMICAL PROPERTIES OF ALUMINUM
AND SELECTED COMPOUNDS
CASAN FORMULA MW MP BP DENSITY
(•C) ('C) (g/om3)
7429-90-6 Al 26.98 660 2327 2.7
15477-33-5 AICl3O9 277.35
7448-70--0 AICl3 133.34
7784-18-1 AIF3 83.98 1272 (sublimes)
21645-51-2 AIH3O3 77.99
1344-28-1 Al2O3 101.94 2000 4
7784-30-7 AIO4P 121.95 1460 2.58
Sou,ces: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA, USPHS ATSDR
WATER SOLUBLE
(mgfl)
Insoluble
soluble
soluble
5590
insoluble
insoluble
Insoluble
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Carcinogenic Effects of Aluminum. Aluminum has not been evaluated by the EPA
for evidence of human carcinogenic potential. Aluminum is not recognized as an
industrial carcinogen by either the National Toxicology Program (NTP), International
Agency for Research on Cancer (IARC), National Institute of Occupational Safety
and Health (NIOSH), or the Occupational Safety and Health Administration
(OSHA).
A14.4 BIBLIOGRAPHY
MERCK 1976
ACGIH 1986
IRIS 1988
CT/APPA
9f;JJ/OO
Windholz, Martha, ed., the Merck Index, An Encyclopedia of
Chemical and Drugs, Ninth Edition, Merck & Co., Inc. Rahway,
New Jersey, 1976.
ACGIH, Documentation of Threshold Limit Values and
Biological Exposure Indices, Aluminum, Fifth Edition,
Cincinnati, 1986.
EPA, Integrated Risk Information System (IRIS), Reference
dose (RID) for Aluminum Phosphide, on-line, Office of Health
and Environmental Assessment, Cincinnati, OH, March 1, 1988.
A-58
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A15 ARSENIC
A15.1 CHARACTERISTICS
Arsenic, Chemical Abstract Service Registry No. 7440-38-2, is also known as gray
arsenic or arsen. Arsenic is a naturally occurring metalloid element. Pure arsenic is
not commonly found in the environment. It is usually found combined with one or
more other elements, such as oxygen, chlorine, or sulphur. Arsenic combined with
these elements is referred to as inorganic arsenic, while arsenic combined with carbon
and hydrogen is referred to as organic arsenic. The organic arsenic forms are usually
less toxic than the inorganic forms (ATSDR 1987). Table A-7 lists pertinent physical
and chemical properties of arsenic and several arsenic salts, oxides, and organic
derivatives. These arsenic compounds were selected because their toxicity or
presence in the environment identified them as compounds of concern. The
inorganic compounds of arsenic are solids at normal temperatures and are not likely
to volatilize. The solubility of these compounds in water ranges from quite soluble
( sodium arsenite and arsenic acid) to practically insoluble ( arsenic trisulfide ). Some
organic arsenic compounds are gases or low-boiling liquids at normal temperatures.
Except the organic acid compounds, they are not readily soluble in water (ATSDR
1987).
A15.2 ENVIRONMENTAL FATE
Arsenic released to the atmosphere as a gas, vapor, or adsorbed to partic-ulate
matter may be transported to other media by wet or dry deposition, making the
atmosphere an important route of arsenic transfer to other media. Trivalent arsenic
may undergo oxidation in the air, and arsenic in the atmosphere is usually a mixture
of the trivalent and pentavalent forms. Most arsenic in air is adsorbed to particulate
matter, especially small-diameter particles. The residence time of particulate-bound
arsenic in the air depends on particle size, but a typical value is about nine days,
although it may persist longer under conditions of limited atmospheric mixing or low
precipitation. Photolysis is not considered an important fate process for arsenic
compounds (ATSDR 1987).
Arsenic in surface water can undergo a complex pattern of transformation, including
oxidation-reduction reactions, ligand exchange, biotransform-ation, precipitation, and
,:;rJN'PA
9/20/00 A-59
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COMPOUND
Arsenic
Arsenic Pentoxlde
Arsenic Trioxide
Arsenic Trisulfide
Calcium Arsenate
Sodium Arsenate
Sodium Arsenite
TABLEA-7
PHYSIOCHEMICAL PROPERTIES OF ARSENIC
AND SELECTED COMPOUNDS
CASRN FORMULA MW MP BP DENSITY WATER SOLUBLE
(•C) ('C) (glom3) (moll)
7440-38-2 As 74.92 818@ 36 atm 5.727
1303-28-2 As2O5 229.84 315 (decomp) 4.32 freely soluble
1327-53-3 As2O3 197.82 312.3 465 3.74 2100
1303-33-9 As2S3 246 300-325 707 3.46 prac. soluble
7778-44-1 Ca3(AsO4)2 77.93 -117 -62.5 2.695 130
7778-43-0 Na2HAsO4 398.08 1455 3.62 very soluble
7784-46-5 NaAsO2 185.91 57 ND 1.87 freely soluble
Sources: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA, USPHS ATSDR
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adsorption. This complexity results in extremely mobile behavior in aquatic systems,
with much of the arsenic entering rivers and eventually traveling to oceans. Sorption
onto clays, iron oxides, manganese compounds, and organic material is an important
fate of arsenic in surface water, and sediment serves as a reservoir for much of the
arsenic. Sediment-bound arsenic (arsenate/arsenite) that has been methylated by
aerobic and anaerobic microorganisms may be released back to the water column
(ATSDR 1987).
Soluble forms of arsenic interact with soil and travel with the ground water mass with
which they are associated. Shifts in oxidation state may occur in either direction,
depending upon the particular physical and chemical characteristics of the soil and
ground water. Volatilization of methylated forms from ground water is possible.
Nonporous soil and heavy vegetation cover are expected to impede volatilization, and
oxidation may transform volatile forms into nonvolatile species or species that will
adsorb to clay, organic matter, and iron and aluminum complexes (ATSDR 1987).
Arsenic occurs in soil predominately in an insoluble, adsorbed form. Arsenic leaching
is usually important only in the top 30 cm of soil. Leaching carries arsenic deeper
in sandy soils than in clay or loam soils, although the EPA reported that no leached
arsenic could be detected below 90 cm in any study. While arsenate dominates in
aerobic soils, arsenite is the predominate form in slightly reduced soils (temporary
flooded soil), and arsine, methylated arsenic, and elemental arsenic predominate in
very reduced conditions (swamps and bogs) (ATSDR 1987).
As noted previously arsenic in water and soil may be reduced and methylated by
fungi, yeasts, algae, and bacteria, and these forms may volatilize and escape into the
air with the volatilization rate varying considerably, depending upon soil conditions,
the pH value of the soil, and microbes present. Bioconcentration of arsenic occurs
in aquatic organisms, primarily in algae and lower invertebrates. Biomagnification
in aquatic food chains does not appear to be significant, although some fish and
invertebrates contain high levels of arsenic compounds that are relatively inert
tox:icologically. Plants may accumulate arsenic by root uptake from soil solution, and
certain species may accumulate substantial levels. In addition to species differences,
the amount of arsenic taken up depends upon soil arsenic concentration, soil
characteristics, and other factors (A TSDR 1987).
Cf/N'f'A
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A15.3 HEALTH EFFECTS
Investigation and analysis of the toxicity of arsenic is complicated by the finding that
different chemical forms of arsenic are not equally toxic. Inorganic arsenic tends to
be more toxic, and exposure for human studies must be expressed in terms of total
inorganic arsenic. An additional difficulty is that most studies indicate that animals
are less sensitive to the toxic effects of arsenic than humans are. Although there is
good evidence that arsenic is carcinogenic in humans by both the oral and inhalation
routes, evidence of arsenic-induced carcinogenicity in animals is mostly negative. For
these reasons, dose-response data from animals are not judged to be reliable for
determining levels of signifi-cant human exposure and will not be considered except
in the absence of any human data.
Noncarcinogenic Effects of Arsenic. The results of human studies indicate that doses
as low as 20 to 60 ug/kg/day may produce the characteristic signs of arsenic toxicity,
including gastrointestinal irritation, anemia, neuropathy, skin lesions, vascular lesions,
and lepatic or renal injury. There does not appear to be a strong trend toward
cumulative toxicity because doses of about fifty ug/kg/day produce similar effects after
both short and long-term exposure. In most cases of subchronic or chronic exposure,
many or all of the signs of arsenic toxicity are detected together, indicating systemic
end points are similar. Doses of around ten ug/kg/day do not generally cause
measurable signs of arsenic intoxication (ATSDR 1987).
Studies in animals have revealed that very high oral doses of sodium arsenate (more
than one hundred mg/kg) may be teratogenic and fetotoxic, but doses of 60 to 100
mg/kg/day have no significant effect. Sodium arsenite appears to be somewhat more
toxic, causing increased malformations and prenatal mortality in mice and hamsters
dosed at levels of 25 to 40 mg/kg/day. These dose levels that may cause maternal
lethality in exposed animals are considerably higher than levels which may cause
lethality in humans (0.6 mg/kg/day). The effects of arsenic exposure on reproductive
parameters have not been well studied. Limited data in mice suggest that ingestion
of water containing 5 mg/L of arsenite for three generations does not significantly
impair reproductive success. Arsenic appears to be either inactive or extremely weak
to the induction of specific gene mutations in vivo (ATSDR 1987).
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Many reports indicate that dermal exposure to inorganic arsenic compounds leads to
dermatitis. However, none of these reports provides quantitative information on
dose-duration relationships. No reports indicating that dermal exposure is associated
with increased risk of cancer have been located (A TSDR 1987).
The oral reference dose (RID) for arsenic, both chronic and subchronic exposure, is
1 ug/kg/day (HEAST 1989). No inhalation RID has been developed. The current
MCL (maximum contaminant level) for arsenic in drinking water 0.05 mg/I, which is
an interim measure the EPA is using that was previously derived by the Public Health
Service (IRIS 1989).
Carcinogenic Effects of Arsenic. Studies have indicated that skin cancer prevalence
are proportional to arsenic exposure level. Other studies show the same results,
which increased frequency of skin cancer or internal cancer in individuals exposed to
water containing 0.3 mg/I or more. Failure to detect significant increases at lower
doses may be due to lack of statistical power in the studies, or it could suggest that
arsenic-induced cancers have a threshold dose. Although toxicokinetic data regarding
arsenic methylation provide some support for this concept, at present it is judged
inadequate to conclude that arsenic-induced cancer has a nonzero threshold (ATSDR
1987).
It was originally calculated that a dose of 1 ug/kg/day corresponded to a skin cancer
risk of 1.58 x 10·2• The EPA has more recently refined these calculations, having
estimated that a dose of 1 ug/kg/day corresponds to a risk of 1 x 10·3• As with any
cancer risk calculation, there is a considerable amount of uncertainty in this value,
especially when extrapo-lated to very low exposure levels. None of the available
studies provide adequate dose-response data to calculate the risk of internal cancers
following exposure to arsenic (ATSDR 1987).
Many studies report above-average lung cancer rates in groups of people with above-
average exposure to airborne arsenic. It has been concluded that arsenic is a more
potent lung carcinogen than previously believed, with a dose-response relationship
concaved downward at exposure levels below 10,000 ug/m3/year. The relationship
between lung cancer and urinary arsenic levels was linear, suggesting that
Cf/APf'A
9/2fJl90 A-62
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bioavailability and Jung absorption of arsenic tend to be proportionately greater at
low exposure levels than at high exposure levels (ATSDR 1987).
An inhalation slope factor of 50 mg/kg/day has been derived for arsenic. An oral
slope factor of 1.75 has been developed for arsenic (IRIS 1990).
A15.4 BIBLIOGRAPHY
ATSDR 1987
MERCK
EPA
IRIS 1989
CT/N'PA
9/'2JJIOO
ATSDR, Draft Toxicological Profile for Arsenic, prepared by
Life Science, Inc., Oak Ridge National Laboratory, Oak Ridge,
November 1987.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
EPA, Integrated Risk Information System (IRIS), Arsenic,
on-line, Office of Health and Environmental Assessment,
Cincinnati, OH February 10, 1988.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Arsenic, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date September 1, 1989.
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A16 Barium
A 16.1 Characteristics
Barium, CASRN 7440-39-3, is a silvery white metallic element which oxidizes very
easily. It is one of the less expensive metals that have the distinctive properties of
absorbing gases. It belongs to the alkaline earth group, resembling calcium
chemically. The most important compounds are the peroxide, chloride, sulfate,
carbonate, nitrate, and chlorate. Naturally occurring barium is a mixture of seven
stable isotopes (CRC 1973). Table A-8 lists some chemical and physical properties
of barium and barium compounds.
A 16.2 Environmental Fate
Traces of barium are very widely distributed. No data exist concerning its presence
or its amount in dust; the content of barium wiJl probably be proportionally related
total calcium content (Seiler, et al 1983).
A 16.3 Health Effects
Noncarcinogenic Effects of Barium
Compounds of barium are highly toxic, unlike others in its chemical group. The fatal
dose of BaCl2 for man is reported to be between 0.8 and 0.9 g (0.55 to 0.6 g as Ba).
A benign pneumoconiosis, baritosis, in workers exposed to finely ground BaS04, first
described in Italy, was later confirmed by Arrigoni. Baritosis was later reported in
the United States in bariet miners by Pendergrass and Leopold, in Germany, and in
Czechoslovakia. Baritosis also occurred among workers handling lithopone. Baritosis
causes no specific symptoms and no changes in pulmonary function (Gayton and
Clayton 1981).
Brenniman, et. al. concluded that there was no statistically significant difference in
blood pressure between human ingesting drinking water containing barium at 7.3
mg/L compared with 0.1 mg/L. A concentration of 7.3 mg/L corresponds to a dose
of 0.20 mg/kg/day (assuming that a 70-kg adult drinks 2 Uday).
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TABLE A-8
PHYSIOCHEMICAL PROPERTIES OF BARIUM AND SOME OF ITS COMPOUNDS
CASRN FORM OF BA
7440-39-3 Barium (Ba)
7727-43-7 Barium sulfale
(BaS04)
12230-71-6 Barium hydroxide
[Ba(OH)2 8H2O}
513-77-6 Barium carbonale
(BaCO2)
10361-37-2 Barium chloride
(BaCl2)
10022-31-8 Barium nllrate
1Ba(NO3)2!
7787-32-8 Barium lluoride
(BaF2)
(a) Tr. -transition
(b) -90 atm.
AT.OR
MOL. Wf. SP. GR. M.P.(°C)
137.36 3.5 (20°C) 752
233.43 4.5 (15°C) 1580
171.38 2.18(16°C) 78
197.37 4.43 1740(b)
208.25 3.86 (24°C) Tr. to cub.
261.35 3.24 (23°C) 592
175.34 4.89 1355
B.P.(°C)
1640
Tr.(a) 1149
monocl.
SOLUBILITY
Dec. with evoln. ol H2; sol. alcohol;
lnsol. C6H6
2.46 mg/liter (25°C), 4.13 mg/liter
(100°C), sl. sol. HCI, H2S04
-8H2O,780 16.7 g/liter (0°C); 947 g/liter
(100°C)
Dec. 20 mg/liter (20°C); 60 mg/liter
(100°C); sol. acid, NH4CI; lnsol.
alcohol
1560
Dec.
2137
375 g/llter (26°C), 590 g/llter
(100°C); sl. sol. HCI, HNO8;
v. sl. sol. alcohol
87 g/liter (20°C), 342 g/llter
(100°C); insol. alcohol; sl
sol. acid
1.2 g/liter (25°C); sl. lnsol. hot water;
sol. acid, NH4CI
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Perry, et. al. exposed weaning rats to barium at 1, 10, or 100 ppm in drinking water
for up to 16 months (average daily barium doses of 0.051, 0.51, and 5.1 mg/kg,
respectively). There were no signs of toxicity at any barium dose level. Systolic blood
pressure measurements revealed no increase in pressure in animals exposed to 1 ppm
barium for 16 months, an increase of 4 mm Hg (p<0.01) in animals exposed to 10
ppm barium for 16 months, and an increase of 16 mm HG (p<0.001) in animals
exposed to 100 ppm barium for 16 months. The animals in this study were
maintained in a special contaminant-free environment and fed a diet designed to
reduce exposure to trace metals. It is possible that the restricted intake of certain
beneficial metals (e.g., calcium and potassium) may have predisposed the test animals
to the hypertensive effects of barium.
The LOAEL identified in the Perry, et. al. study (5.1 mg/kg/day) has been used in the
derivation of the oral RID without an additional 10-fold uncertainty factor for the
lack of a NOAEL. The oral reference dose is Sx10·2 mg/kg/day with an uncertainty
factor of 100 (IRIS 1990).
Carcinogenic Effects of Barium
No evidence of the carcinogenicity of barium could be located in the literature.
A 16.4 Bibliography
ALDRICH
ATSDR 1987
CLAYTON
CRC
FAWELL
Cf/APPA
9/2!Jl'iXl
Aldrich Catalog Handbook of Fine Chemicals, Aldrich Chemical
Company, Inc. 1988.
ATSDR, Draft Toxicological Profile for Benzene, Oak Ridge
National Laboratory, Oak Ridge, October 1987.
Clayton, G.D. and Clayton, F.E., Patty's Industrial Hygiene and
Toxicology, John Wiley and sons, NY, 1981.
Weast, R. (editor), CRC Handbook of Chemistry and Physics,
58th ed., CRC Press, Inc., West Palm Beach, FL, 1977.
Fawell, J. and Hunt, S., Environmental Toxicology, Ellis
Horwood Ltd., England, 1988.
A-65
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HOW~D
NIOSHJOSHA
SIELER
USEPA
IRIS 1990
CT/N'f'A
9f2D/90
Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Benzene, Supplement II, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No
89-104, 1988.
Seiler, H.G., Sigel, G. and Sigel, A, Handbook on Toxicity of
Inorganic Compounds, Marcel Dekker, Inc., 1988.
EPA, Health Effects Assessment for Benzene, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Benzene, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH.
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A17 CADMIUM
A17.1 CHARACTERISTICS
Cadmium, Chemical Abstract Service Registry No. 7440-43-9, is a silver-blue-white
metal. Pure metallic cadmium is not common in the environment. It is most often
encountered in combination with other elements such as oxygen, chlorine, or sulfur.
Metallic cadmium has a low melting point for metals (321°C) and is insoluble in
water. (ATSDR 1987) Table A-9 Iists the chemical and physical properties of some
cadmium compounds.
A17.2 ENVIRONMENTAL FATE
Cadmium enter the environment to a limited extent from the natural weathering of
minerals, but to a much greater degree from pollutant sources such as discarded
metal-containing products, phosphate fertilizers, and fuel combustion (A TSDR 1987).
Although overall natural sources of cadmium are relatively low, the metal is widely
distributed in the Earth's crust and is commonly found at detectable levels in soil,
surface water, and groundwater (ATSDR 1987).
Atmospheric cadmium is in the form of very small particulate matter, produced by
combustion of fuel containing cadmium. This material is subject to dry deposition
and rainwash, so that cadmium levels in the atmosphere are generally less than 3
ng!m3 near specific cadmium emitting industries. Cadmium in surface water is usually
present at less than 1 ng/L; industrial contaminations can result in concentrations up
to 10 ng/L. There is some concern that soil cadmium levels are increasing largely
from the use of cadmium-contaminated phosphate fertilizer and land disposal of
some sewage sludges containing particularly high levels of cadmium. Consumption
of food represents the greatest sources of human exposure, since plants take up
cadmium from the soil (ATSDR 1987).
Combustion of coal and petroleum products tend to produce cadmium that is
adsorbed to small (1 to 2 micron) particles that are persistent in the atmosphere and
are easily respirable. In this form, cadmium can be trans-ported to some distance
CT/APf'A
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TABLEA-9
PHYSIOCHEMICAL PROPERTIES OF CADMIUM
AND SELECTED COMPOUNDS
COMPOUND CASRN FORMULA MW MP BP DENSITY
(•C) ('C) (g/""3)
Cadmium 7440-43-9 Cd 112.4 321 765 B.65
Cadmium Chloride 10108-64-2 CdCl2 183,32 568 960 4.047
Cadmium Oxide 1306-19-(l CdO 128.4 1426 8.15
Cadmium Sulfide 1306-23--8 Cd$ 144.48 1750@ 100 atm 2.455
Cadmium Nitrate 10325-94-7 Cd(NO3)2 238.43 350
Sources: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA, USPHS ATSDR
WATER SOLUBLE
(mg/1.)
Insoluble
1.4E+5
insofuble
1.3E-3
1090@ 0°C
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and transferred to other environmental compartments via wet or dry deposition
(ATSDR 1987).
Compared to most other heavy metals, cadmium is relatively mobile in the aqueous
environment. In natural waters, cadmium may exist as the hydrated ion; as metal-
inorganic complexes with co3·2, OH-, er-or SO/; or as metal-organic complexes
with humic acids. Cadmium does not form volatile compounds in the aquatic
environment, nor does biological methylation occur (ATSDR 1987).
Concentrations of cadmium in groundwater are kept low by sorption by mineral
matter and clay, binding by humic substances, precipitation as cadmium sulfide in the
presence of sulfide, and precipitation as the carbonate at relatively high alkalinities
(ATSDR 1987).
Cadmium may be present in soil as free cadmium compounds or in solution dissolved
in soil water. It may also be held to soil mineral or organic constituents by cation
exchange. High soil acidity favors release of cadmium and its uptake by plants
(ATSDR 1987). Cadmium is mobile in soil, as evidenced by the detection of this
element in 100 percent of the groundwater samples collected from New Jersey (HEA
1984).
A17.3 HEALTH EFFECTS
Non carcinogenic Effects of Cadmium. EPA (1985) conducted a toxico-kinetic model
to determine the highest level of exposure associated with the lack of significant
proteinuria of the human renal cortex (i.e., the critical effect). An oral reference
dose of 5 x 104 mg/kg/day has been established based on this model. At the present
time, a risk assessment for cadmium is under review by an EPA work group (IRIS
1987).
Carcinogenic Effects of Cadmium. Human epidemiological studies of cadmium
smelter workers supply limited evidence of human lung carcinogenicity. The study
by Thun et al. (1985) was reported by the EPA Carcinogen Assessment Group as not
adequately accounting for the possible confounding factors due to the presence of
arsenic or to smoking.
r;r/M'PA
9l20l90 A-68
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Three other studies observed an excess lung cancer risk but they were compromised
by the presence of other carcinogens, such as arsenic and smoking. Four other
studies showed a positive association between cadmium and prostate cancer, but the
total number of cases was small in each study. Studies of human ingestion of
cadmium are inadequate to assess carcinogenicity.
There is sufficient animal evidence to support an association of inhalation of
cadmium to carcinogenicity. Several studies of oral exposure to cadmium have shown
no evidence of a carcinogenic response. EPA has classified cadmium as Group Bl;
probable human carcinogen by inhalation (IRIS 1988). A slope factor of 6.1 x 10°
mg/kg/day for inhala-tion to cadmium has been assigned. No slope factor for oral
exposure has been assigned due to insufficient data to classify cadmium as
carcinogenic to humans by the oral route (IRIS 1988).
A17.4 BIBLIOGRAPHY
NIOSH
HEA 1984
EPA
MERCK
ATSDR 1987
NIOSH, Criteria For a Recommended Standard, Occupational
Exposure to Cadmium, U.S. Department of Health, Education
and Welfare, DHEW (NIOSH) Publication No. 76-192, August
1976.
EPA, Health Effects Assessment for Cadmium, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
A TSDR, Draft Toxicological Profile for Cadmium, prepared by
Life Systems Inc., Oak Ridge National Laboratory, Oak Ridge,
November 1987.
A-69
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IRIS 1987
EPA
IRIS 1988
r;T/APPA
9l2IJ/90
EPA, Integrated Risk Information System (IRIS), Cadmium,
on-line, Office of Health and Environmental Assessment,
Cincinnati, OH, March 31, 1987.
EPA, Integrated Risk Information System (IRIS), Reference
Dose (RID) for Cadmium, on-line, Office of Health and
Environmental Assessment, Cincinnati, OH, verification date
October 1, 1989.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Cadmium, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date March 1, 1988.
A-70
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A18 CHROMIUM
A18.1 CHARACTERISTICS
The ammonium and alkali metal salts of hexavalent chromium are generally water-
soluble, but the alkaline metal salts ( calcium, strontium) are sparingly soluble or
insoluble in water. Hexavalent chromium rarely occurs in nature apart from man-
made sources because it is readily reduced in the presence of oxidizable organic
matter; however, hexavalent chromium compounds that occur most commonly in the
form of chromate and dichromate are stable in many natural waters because of the
low concentration of reducing matter. Except acetate and nitrate salts, the trivalent
chromium compounds are generally insoluble in water. In most biological systems,
chromium is present in the trivalent form. The physical or chemical forms and the
mode by which chromium (III) compounds are incorporated into bio-logical systems
are poorly characterized (A TSDR 1987). Table A-10 lists some chemical and
physical properties of chromium and chromium compounds.
A18.2 ENVIRONMENTAL FATE
Chromium occurs naturally in the earth's crust. Continental dust is the primary
source of natural chromium present in the environment; however, chromium is
released to the environment because of human activities in much larger amounts.
Chromium is primarily removed from the atmosphere by fallout and precipitation.
Atmospheric chromium removed by physical processes predominantly enters surface
water or soil; however, before their removal, chromium particles of aerodynamic
diameter less than 20 um may remain airborne for long periods and may be
transported long distances (ATSDR 1987).
Because there are no known chromium compounds that can volatilize from water,
transport of chromium from water to the atmosphere is not likely other than by
transport in windblown sea sprays. Most of the chromium (III) is eventually expected
to precipitate in sediments. Small amounts of chromium (III) may remain in solution
as soluble complexes. Chromium (YI) will be present predominantly in soluble form.
These soluble forms of chromium may be stable enough to undergo intramedia
transport; however, organic matters present in water will eventually reduce chromium
CT/M'PA
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TABLE A-10
PHYSIOCHEMICAL PROPERTIES OF CHROMIUM
AND SELECTED COMPOUNDS
COMPOUND CASRN FORMULA MW MP BP DENSITY
(•C) (•C) (g/cm3)
Chromium 7440-47-3 Cr 51.996 1000 2642 7.14
Chromic Nitrate 13548-38-4 Cr(NO3)3 9H2O 400.16 60 100 (decomp)
Chromic Oxide 1308-38-9 Cr203 151,99 2266 4000 5.21
Calclum Chromate 13765-19-0 CaCr04 156.07
Lead Chromate 7758-97-6 PbCr04 323.18 844 decomposes 8.12 (15°C)
Potassium Chromate 7789-00~ K2Cr04 194.2 968.3 2.73 (18•C)
Potassium Dichromate m8-so-e K2Cr2O7 294.18 398 500 (docomp) 2.as (2s•c)
Sources: CRC 1970, MERCK 1978, USEPA IRIS, USEPA HEA, USPHS ATSDR
WATER SOLUBLE
(mg/I.)
Insoluble
soluble
Insoluble
22300
Insoluble
soluble
soluble
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(VI) to chromium (III). It has been estimated that the residence time of chromium
in lake water is from 4.6 to 18 years (ATSDR 1987).
Chromium probably occurs as insoluble Cr20 3_H20 in soil because the organic matter
in soil is expected to convert soluble chromate to insoluble Cr 203• Chromium in soil
may be transported to the atmosphere in the aerosol form, and runoff and leaching
may transport chromium from soil to surface waters and ground water. Runoff could
remove both soluble and bulk precipitate with final deposition on either a different
land area or a water body. Flooding of soils and the subsequent anaerobic
decomposition of plant matter may increase mobilization of chromium in soils
because of the form-ation of soluble complexes. The half-life of chromium in soils
may be several years (ATSDR 1987).
A18.3 HEALTH EFFECTS
Noncarcinogenic Effects of Chromium. The estimated safe and adequate daily
dietary recommendations of chromium, considered to be an essential nutrient, is 50-
200 ug/day for adults. Effects observed after chromium (VI), hexavalent chromium,
and chromium (III), trivalent chromium, oral exposure have not been well defined.
Chronic oral studies of chromium compounds have not identified any adverse effects
on toxicological end points including body and organ weights, clinical chemistry
values, and histologic appearance of tissue (ATSDR 1987).
Studies indicate that oral chromium (VI) may result in reproductive toxicity (ATSDR
1987). Inhalation exposure has several key effects including respiratory tract effects,
irritation of the nasal mucosa; transient decreases in lung function; and induction of
cancer. Many cases of nasal mucosa! ulceration and perforation have been reported
in workers exposed to chromium (VI). Slight effects on lung function have also been
observed in exposed workers (ATSDR 1987).
Studies of chromosome effects in lymphocytes of workers exposed to chromium (VI)
have given mixed results. In vitro assays for gene mutations, chromosome effects,
and cell transformation have consistently given positive results for chromium (VI) and
negative results for chromium (III). The positive dominant lethal study considered
Cf/APPA
9/2D/90 A-72
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with positive results in human somatic cells raises concern that chromium (VI) may
be a potentially human germ-cell mutagen (ATSDR 1987).
An oral RID for chromium (III) (insoluble salts) was calculated to be 1 mg/kg/day.
The value includes an uncertainty factor of 100 for inter-species and intraspecies
variability and 10 as a modifying factor to reflect uncertainty around the (NOAEL),
which was the basis of the calculation. An oral RID of .005 mg/kg/day has been
calculated for chromium (YI), with a modifying factor of 100 for interspecies and
intraspecies extrapolation and a modifying factor of 5 for less-than-lifetime exposure
duration (ATSDR 1987).
Carcinogenic Effects of Chromium. The limited chronic oral studies of chromium
(YI) and chromium (III) compounds have not resulted in signif-icant tumor incidence
(ATSDR 1987).
Case studies and epidemiological studies for the inhalation route of exposure indicate
that occupational exposure to chromium compounds is associated with respiratory
cancer. Although these studies do not clearly implicate specific compounds or the
valence state of chromium involved, the results of animal testing implicate chromium
(YI). The key epidemio-logical study used for quantitative risk assessment found a
dose-related increase in lung cancer death rates in chromate production workers
exposed to chromium at 1-8 mg/m3/year. Chronic inhalation studies of chromium
(YI) in animals provide sufficient evidence that certain chromium (VI) compounds
are carcinogens (ATSDR 1987).
The dose of chromium (YI) associated with an increased lifetime cancer risk level of
10-{j is 8 x 10·5 ug/m3 ( A TSD R 1987).
A18.4 BIBLIOGRAPHY
ATSDR 1987
NIOSH
(;f/APPA
9/20/90
A TSDR, Draft Toxicological Profile for Chromium, prepared by
Syracuse Research Corporation, Oak Ridge National
Laboratory, Oak Ridge, October 1987.
NIOSH, Criteria For a Recommended Standard, Occupational
Exposure to Chromium (VI), U.S. Department of Health,
A-73
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EPA
EPA
EPA
EPA
EPA
EPA
MERCK
CT/N'PA
9/2Dl90
Education and Welfare, DHEW (NIOSH) Publication No.
76-129, 1975.
EPA, Health Effects Assessment for Chromium, prepared by
the Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Health Effects Assessment for Trivalent Chromium,
prepared by the Office of Health and Environmental Assess-
ment, Cincinnati, September 1984.
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989.
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989.
EPA, Integrated Risk Information System (IRIS), Chromium,
on-line, Office of Health and Environmental Assessment,
Cincinnati, OH, January 1, 1987.
EPA, Integrated Risk Information System (IRIS), Reference
Dose (RfD) for Chromium, on-line, Office of Health and
Environmental Assessment, Cincinnati, OH, verification date
March 1, 1988.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
A-74
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A19 COBALT
A19.1 CHARACTERISTICS
Cobalt, Chemical Abstract Service Registry No. 7440-48-4, is a relatively rare
element, composing but 0.001 percent of the earth's crust. The metallic form is silver
gray to bluish white and is magnetic. There are three oxides of cobalt: colbaltous
oxide, cobaltic oxide, and cobaltous colbaltic oxide. Ionic cobalt can exist in either
a divalent or a tri-valent form. The cobaltous form can form numerous inorganic and
organic salts, and cobalt can form complexes with amines, nitrites, and cyanides
(NIOSH 1981). Table A-11 lists some chemical and physical properties of cobalt and
cobalt compounds.
A19.2 ENVIRONMENTAL FATE
No information in the fate of cobalt in the environment could be located m the
literature.
Cobalt is present in low concentrations in ambient air. Several studies have
measured cobalt in urban and rural areas at levels of 2.6 and 0.95 ng/m3 respectively
(NIOSH 1981).
A19.3 HEALTH EFFECTS
Noncarcinogcnic Effects of Cobalt. Pulmonary involvement consisting of chronic
interstitial pneumonitis has now been reported with sufficient frequency in workers
associated with the cemented tungsten-carbide industry to give credence to the belief
of Miller et al. and others that cobalt is the probable etiologic agent, although the
carbides of tungsten, thallium and titanium are commonly present in the exposure
atmosphere.
Lung changes frequently were not progressive and often improved consider-ably upon
removal from exposure. Hypersensitivity appears to be involved, because the
pulmonary responses occurred at low incidence, varied in intensity and time of onset.
Animal studies tended to confirm the hyper-sensitivity theory, but were not
productive of the characteristic lung lesion seen in workers; increases in serum A-
CT/APPA
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TABLE A-11
PHYSIOCHEMICAL PROPERTIES OF COBALT
AND SELECTED COMPOUNDS
COMPOUND CASRN FORMULA MW MP BP DENSITY
("C) ("C) (gfcm3)
Cobalt 7440-48-4 Co 58.9 1483 3100 8.9
Cobaltous Oxide 1307-98-6 CoO 74.93 1935 6.45
Cobaltlc Oxide 1308-04-9 Co2O3 165.86 895 (decomp) 4.81-5.6
Cobaltous Colbatlc Oxide 1308-06-1 Co304 240.8 925 (CoO) 6.07
Cobaltous Chloride 7646-79-9 CoCl2 129.84 735 3.356
Cobaltous Nitrate 10141--05-6 Co(NO3)2 182.96 100 (decomp) 2.49
Cobaltous Cyanide Dihydrate 14965-99-2 Co(CN)2.2H2O 147 300 (decomp) 1.87
Sources: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA, USPHS ATSDR
WATER SOLUBLE
(mgfl)
insoluble
4.SE+S @7°C
41.8
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globulin and neuraminic acid were found in dogs and rabbits exposed by inhalation
to Co metal, metal fume, carbide blend, or by injection of CoC12 (ACGIH 1986).
A dermatitis of the allergic type has been described by Schwartz from contact with
cobalt and its compounds; a carboloy-itch has also been described (ACGIH 1986).
Investigation by Kerfoot, Fredrich and Domeier on miniswine exposed by inhalation
to Co metal dust resulted in early appearance (3 months) of pulmonary disease at the
TLV of 0.1 mg!m3 as evidenced by a marked decrease in lung compliance and an
increase in the amount of collagen in the central areas of the pulmonary alveolar
septa. Exposures at both 1.0 and 0.1 mg/m3 were performed for 3 months daily, 6
hours per day, 5 days per week. Wheezing was taken as evidence of hypersensitivity
that occurred during the fourth week of exposure following a one-week sensitizing
dose (ACGIH 1986).
Carcinogenic Effects of Cobalt. No evidence of the carcinogenicity of cobalt could
be located in the literature.
A 19.4 BIBLIOGRAPHY
ACGIH 1986
NIOSH 1981
WEAST
MERCK
Cf/APPA
9/2fJ/90
ACGIH, Documentation of Threshold Limit Values and
Biological Exposure Indices, Cobalt, Fifth Edition, Cincinnati,
1986.
NIOSH, Criteria For a Recommended Standard, Occupational
Exposure to Cobalt, U.S. Department of Health, Education and
Welfare, DHEW (NIOSH) Publication No. 82-107, 1981.
Weast, Robert C., et al., Handbook of Chemistry and Physics,
51st Edition, The Chemical Rubber Co., Cleveland, 1970.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
A-76
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A20 COPPER
A20.1 CHARACTERISTICS
Copper, Chemical Abstract Service Registry No. 7440-50-8, is a reddish metal that
occurs naturally in rock, soil, water, sediment, and air. Its average concentration in
the earth's crust is about 50 parts per million. Copper has the ability to alloy with
many metals, such as zinc, tin, and beryllium. Next to copper metal, copper sulfate
is the most commercially important use of copper. Copper sulfate is also produced
as a by product of copper production by ore-leaching with sulfuric acid (ATSDR
1989). Table A-12 shows some chemical and physical properties of copper and
copper compounds.
A20.2 ENVIRONMENTAL FATE
Copper occurs in nature as the elemental metal (zero valence), and in the + 1 and
+ 2 valence states. In addition to a variety of inorganic compounds, copper forms a
number of compounds with organic ligands. Most cu+1 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+2 state.
In the atmosphere, copper is present as dusts and fumes from copper smelting
industries, iron and steel industries, coal burning power plants and other
miscellaneous fabricating operations involving copper. The atmospheric fate of
copper has not been studied comprehensively. Any chemical interaction of copper
compounds in the atmosphere is likely to result in the formation of a more stable
species, such as CuO, not in its direct removal throughout decomposition as
frequently occurs with organic chemicals. The principal removal mechanism for
atmospheric copper are probably wet and dry deposition. No estimate for the
atmosphere half-life of copper is available (HEA 1984).
The aquatic fate of copper has been studied more extensively that its atmospheric
fate. The two processes that are likely to dominate the fate of copper in aquatic
media are chemical speciation and sorption. The nature of chemical speciation is
determined by the oxidation-reduction potential of the copper compound and the pH
of the aquatic media. In polluted water bodies, copper may form complexes with
Cf/APPA
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TABLE A-12
PHYSIOCHEMICAL PROPERTIES OF COPPER
AND SELECTED COMPOUNDS
COMPOUND CASRN FORMULA MW MP BP DENSITY
('C) ('C) (g/cm3)
Copper 7440-50-8 Cu 63.55 1083 2595 8.94
Copper Sulfate TTSB-98-7 CuSO4 159.6 sl d >200 650 (decamp) 3.803
Copper Oxide 1317-39-1 CuO 79.54 1026 (docomp) 6.4
Sources: CRC 1970, MERCK 1978 USEPA IRIS, USEPA HEA, USPHS ATSDR
WATER SOLUBLE
(mg/L)
143
insoluble
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organic material in the water. Various sorption processes reduce the level of copper
compounds from aquatic media. Sorption into clay materials, hydrous iron,
manganese oxides and organic material in the primary controlling factor. 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 (HEA 1984).
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. In acidic soils, copper may be more soluble, which would enhance its
mobility; the reverse may be true in basic soils. Soils rich in organic material may
enhance the mobility of copper. Both clay and organic matter may facilitate the
sorption 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 soil is available (HEA 1984 ).
A20.3 HEALTH EFFECTS
Noncarcinogenic Effects of Copper. There are a number of human cases where they
were exposed to acute levels of copper. For example, cases where the single copper
dose was estimated to be between 0.1 mg/kg and 0.14 mg/kg, symptoms of diarrhea,
vomiting, and nausea were common.
Little information exists concerning subchronic toxicity of copper in the usual
laboratory species. The one study in the literature that used rats (Howell, 1959),
noted an accumulation of copper in the liver and kidney but no accumulation was
found in the cornea or brain. No criteria of toxicity were mentioned. Several studies
on pigs revealed accelerated weight gain at doses between 1.8 -3.2 mg/kg/day. At
5.5 mg/kg/day, reduced growth and hemoglobin levels were noted, as well as
increased liver copper concentrations (HEA 1984).
Carcinogenic Effects of Copper. There is no human carcinogenicity data available
for exposure to copper. Animal data is inadequate in that copper fed to mice did not
elicit tumor growth where as subcutaneous injections of an organic copper compound
to mice and intramuscular injections of inorganic copper to rats resulted in a very low
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incidence in tumors among the treated groups. EPA has assigned Group D, not
classified, to copper based on no human data and inadequate animal data. A slope
factor for copper has not been assigned (IRIS 1988).
A20.4 BIBLIOGRAPHY
HEA 1984
EPA
EPA
IRIS 1988
MERCK
ATSDR 1989
c:T/N'PA
9/2!)/90
EPA, Health Effects Assessment for Copper, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989.
EPA, Integrated Risk Information System (IRIS), Copper,
on-line, Office of Health and Environmental Assessment,
Cincinnati, OH, September 7, 1988.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Copper, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date September 7, 1988.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
ATSDR, Draft Toxicological Profile for Copper, prepared by
Syracuse Research Corporation, Oak Ridge National
Laboratory, Oak Ridge, October 1989.
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A21 LEAD
A21.1 CHARACTERISTICS
Metallic lead is stable in dry air; however, in moist air, it quickly forms lead
monoxide, which in turn produces lead carbonate with carbon dioxide in air. Table
A-13 lists pertinent physical and chemical proper-ties of lead and some of its
compounds. In general, the chemical proper-ties of inorganic lead compounds are
similar to those of the alkaline earth metals. The nitrate, chlorate, and acetate salts
are water soluble; chloride is slightly soluble; and sulfate, carbonate, chromate,
phosphate, and sulfide are insoluble. Aromate, carbonate, nitrate, sulfide, and
phosphate are soluble in acid, and chloride is slightly soluble in acid. Lead forms
stable tetraalkyl compounds with organic ligands, such as tetramethyl, tetraethyl,
tetrapropyl, and tetrabutyl compounds. They are soluble in many organic solvents
but are insoluble in water. The tetra-organolead compounds decompose to lead
metal and free organic radicals at elevated temperatures or in 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 polydentate
chelating agents, such as penicillamine or EDTA (ATSDR 1988).
A21.2 ENVIRONMENTAL FATE
In the atmosphere, lead exists primarily in the particulate form .. Upon release to the
atmosphere, lead particles are dispersed, transformed by physical or chemical
processes, and ultimately removed by wet or dry deposition. An important factor in
determining the atmospheric transport of lead is particle size distribution. Large ·
particles, particularly those with aerodynamic diameters greater than 2 um, settle out
of the atmosphere fairly rapidly and are deposited relatively close to emission
sources, but small particles may be transported thousands of kilometers. Wet
deposition is expected to remove larger amounts of lead in areas with acid rain
(northeastern United States), because aid rain has a tendency to make lead soluble.
The average residence time of lead particles in the atmosphere is expected to be
between 7 and 30 days (ATSDR 1988).
The chemistry of lead in aqueous solution is highly complex because this element can
be found in many forms. Lead has a tendency to form compounds of low solubility
CT/N'f'A
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COMPOUND
lead
Lead Chloride
Lead Nilrate
lead Oxide
Tetraethyl Lead
Tetramethyl Lead
TABLE A-13
PHYSIOCHEMICAL PROPERTIES OF LEAD
AND SELECTED COMPOUNDS
CASRN FORMULA MW MP BP
(•C) (•C)
7439-92-1 Pb 207.2 327.4 1740
TT58-95-4 PbCl2 278.11 501 950
10099-74-8 Pb(NO3)2 331.21 470 (decomp)
1317-38-8 PbO 223.2 886 1472 (decomp)
78-00-2 (C2H5)4Pb 323.45 -136 198-202 (decamp)
(CH3)4Pb 267.35 -27.5 110 (decamp)
Sources: CAC 1970, MERCK 1976, USEPA IRIS, USEPA HEA, USPHS ATSDR
DENSITY WATER SOLUBLE
(g/cm3) (mg/l)
11.34 Insoluble
5.85 9.9E+3
4.53 4.7E+5
8 1.7E+1
1.65 8.0E-1
1.995 9.0E+-0
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with the major anions of natural water. In the natural environment, the divalent form
(Pb2+) is the stable ionic species of lead. Hydroxide, carbonate, sulfide, and, more
rarely, sulfate may act as solubility controls in precipitating lead from water.
Tetraalkyl leads may also form by a combination of chemical/biological alkylation of
inorganic lead compounds under appropriate conditions. A significant fraction of
lead carried by river water is expected to be in an undissolved form, which can consist
of colloidal particles or larger undissolved particles of lead carbonate, lead oxide, lead
hydroxide, or other lead compounds incorporated in other components of surface
partic-ulate matters from runoff. Lead may occur either as absorbed ions or surface
coatings on sediment mineral particles, or it may be carried as a part of suspended
living or nonliving organic matter in water (ATSDR 1988).
Except in some shellfish, such as mussels, lead does not appear to bioaccumulate
significantly in most fish (ATSDR 1988).
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 soil, and very little
is transported into surface water or ground water. The fate of lead in soil is affected
by the specific or exchange adsorp-tion at mineral interfaces, the precipitation of
sparingly soluble solid phases, and the formation of relatively stable organic-metal
complexes or chelates with soil organic matter. These processes are dependent upon
factors such as soil pH, organic content of soil, the presence of inorganic colloids and
iron oxides, ion-exchange characteristics, and the amount of lead in soil. There is
evidence that atmospheric lead enters the soil as lead sulfate or it is converted rapidly
to lead sulfate at the soil surface. Lead sulfate is relatively soluble and could leach
through soil if it were not transformed. In soils with pH of 5 or greater and with at
least 5 percent organic content, atmospheric lead is retained in the upper 2 to 5 cm
of undisturbed soil. Because many plants commonly take up lead from soil, lead may
eventually return to soil when these plants decay, unless they are harvested or
removed (ATSDR 1988).
A21.3 HEALTH EFFECTS
Lead is a naturally occurring element which is dispersed throughout the environment
primarily as the result of anthropogenic activities. Environ-mental fate processes may
transform one lead compound to another, but lead itself is not degraded and is still
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available for human exposure. The general population is exposed to lead in ambient
air, in many foods, in drinking water, and in dust. The average baseline intake of
lead in 1982-1983 by 2-year old children, adult females, and adult males was 46.6
ug/day, 37.5 ug/day, and 50.7 ug/day, respectively. These reflect minimum levels of
exposure during normal daily living. The highest and most prolonged lead exposures
are found among workers in the lead smelting, refining, and manufacturing industries
(ATSDR, 1988).
The database for lead is unusual in that it contains a great deal of data concerning
dose-effect relationships in humans. However, the dose data for humans are
generally expressed in terms of internal exposure, usually measured as levels of lead
in the blood. Human body burdens of lead result from a combination of inhalation
and oral exposure primarily to inorganic lead. Dose-effect data in terms of external
exposure levels by a single route of exposure are not generally available for humans,
therefore, experimental studies of lead toxicity in animals provide support for
observations in human studies, with some consistency in types of effects and blood-
lead-effects relationships (A TSDR 1988).
Noncarcinogenic Effects of Lead. For oral exposure, the end points of greatest
concern for human health are heme synthesis and erythropoiesis, neurobehavioral
toxicity, cardiovascular toxicity, and vitamin D metabolism and growth (ATSDR
1988).
In humans, studies have shown ingestion of lead produces a decrease in erythrocyte
aminolerulinic acid dehydrase (ALA-D) and an increase in erythrocyte
protoporphyrin. Lead ingestion has also shown delays in reflex development in rats;
poorer performance on a spatial discrimination task was reported in rats fed 1.25
ug/kg/day. Monkeys given 0.05 mg/kg/day from birth performed significantly poorer
in learning discrim-ination-reversal and delayed alternation. Studies have also shown
that rats given drinking water with lead at 7 mg/kg/day lead showed markedly
increased blood pressures, but rats given water with 3.5 mg/kg/day lead showed no
effect on blood pressure. A review of 65 pertinent animal studies concluded that low-
level exposure to lead during prenatal or early postnatal life results in retarded
growth in the absence of overt signs of toxicity. Studies have shown reproductive
toxicity at levels as low as 0.014 mg/kg/day (ATSDR 1988).
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The only pertinent dose-effect data found in the available literature on lead
inhalation were from a study of hematological effects in humans and a study of the
developmental toxicity to animals. In the human study, exposure to particulate lead
at 3.2 or 10.9 ug/m3 in air for three months showed a decrease of 85 percent and 56
percent decrease after four months in erythrocyte levels of ALA-D. Maternal and
fetal ALA-D were inhibited in rats exposed to 1, 3, and 10 mg/m3 lead throughout
gestation (ATSDR 1988).
The EPA has not derived a reference dose for oral or inhalation exposure to lead.
Carcinogenic Effects of Lead. In the most adequate study available, rats exposed to
lead acetate at 25 mg/kg/day in the diet for two years showed statistically increased
incidence of kidney tumors. No kidney tumors were seen at the next lower dietary
level, 5 mg/kg/day (ATSDR 1988).
No slope factor has been developed for lead.
A21.4 BIBLIOGRAPHY
HSDB
EPA
MERCK
ATSDR 1988
Cf/APPA
9/2fJ/90
HSDB, Hazardous Substance Data Base On-Line Data Base.
Profiles for Arsenic, Arsenic Trioxide, Arsenic Trisulfide,
Calcium Arsenate, Sodium Arsenate, Sodium Arsenite, and
Lead, 1987.
EPA, Health Effects Assessment for Lead, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
ATSDR, Draft Toxicological Profile for Lead, prepared by
Syracuse Research Corporation, Oak Ridge National
Laboratory, Oak Ridge, February 1988.
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EPA
EPA
Cf/Af'f'A
9/2JJ/OO
EPA, Integrated Risk Information System (IRIS), Lead, on-line,
Office of Health and Environmental Assessment, Cincinnati,
OH, February 1, 1989.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Lead, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date December 1, 1989.
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A22 MANGANESE
A22.1 CHARACTERISTICS
Manganese, Chemical Abstract Service Registry No. 7439-96-5, is a steel gray,
lustrous, hard, brittle metal. Manganese occurs in a great variety of minerals widely
scattered over the earth (Merck 1976). Manganese, a highly reactive metal, exists in
all seven valence oxidation states from -3 to + 7. The bivalent form is the most stable
and its common salts, with the exceptions of carbonate, phosphate and sulfide, are
water soluble (PATTY 1963). Table A-14 shows chemical and physical properties
for manganese and selected compounds.
A22.2 ENVIRONMENTAL FATE
The principal sources of manganese in the atmosphere are natural processes
including continental dust, volcanic gas and dust, and forest fires. The atmospheric
flux of manganese due to burning of forests and wood fuel may exceed the combined
flux due to other natural and anthropogenic sources. The main anthropogenic
sources of manganese are industrial emissions and combustion of fossil fuels. In the
atmosphere, manganese is expected to be present in particulate form. The two main
mechanisms that may deter-mine the fate of atmospheric manganese are tropospheric
chemical reactions and physical removal processes. Atmospheric manganese may
undergo photo-chemical and thermal reaction. Thus, manganese dioxide may react
with SO2 or NO2 in the atmosphere, forming MnSO3 and Mn(NO3)z, respectively.
Although such reactions may change the chemical nature of manganese, these
reactions may not be directly responsible for the removal of manganese from the
atmosphere. Manganese aerosol may be removed from the air through dry fallout
or wet precipitation. It has been estimated that the atmospheric residence time for
manganese due to such physical removal processes is approximately 7 days (HEA
1984).
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 MnO2 and Mn3O4 or both. A small amount of manganese may remain in the
soluble form, the concentration of which is limited by the solubility product of
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COMPOUND
Manganese (dust)
Manganoso Oxide
Manganese Nitrate
Manganese Dioxide
Manganese Carbonate
TABLE A-14
PHYSIOCHEMICAL PROPERTIES OF MANGANESE
AND SELECTED COMPOUNDS
CASRN FORMULA MW MP BP DENSITY
('C) ("C) (g/crn3)
7439-96-5 Mn 54.93 1260 1900 7.47
1317-35-7 Mn304 228.79 4.7
10377--66-9 Mn(NO3)2 178.85 37.1 2.129
1313-13-9 Mn02 86.94 5.028
598--82-9 MnCO3 114.94 decomposes 3.1
Sources: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HES, USPHS ATSDR
WATER SOLUBLE
(mg/L)
very soluble
Insoluble
insoluble
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MnC03 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 speci-
ation 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 (HEA 1984).
A bioconcentration factor for manganese in a species of edible fish (striped bass) has
been reported to be less than 10. Bioaccumulation of manganese may not occur
significantly with organisms of higher tropic level (HEA 1984).
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 groundwater. Also, manganese can be
leached directly from waste burial sites and from other natural soils into groundwater
(HEA 1984).
A bioconcentration factor for manganese in a species of edible fish (striped bass) has
been reported to be less than 10. Bioaccumulation of manganese may not occur
significantly with organisms of higher tropic level (HEA 1984).
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 groundwater. Also, manganese can be
leached directly from waste burial sites and from other natural soils into groundwater
(HEA 1984).
A22.3 HEAL TH EFFECTS
Noncarcinogcnic Effects of Manganese. A no observable affect exposure level
(NOAEL) of 10 mg/day (0.14 mg/kg day for 70 kg adult) for chronic human
consumption of manganese is based on a composite of data from the following
studies. The World Health Organization reported no adverse effects in humans
consuming supplements of 8-9 mg/day (0.11-0.13 mg/kg/day). Schroeder et al. (1966)
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reported a chronic human NOAEL of 11.5 mg/day (0.16 mg/kg/day). The National
Research Council determined "safe and adequate" levels to be 2-5 mg/day for adults
(0.03 -0.07 mg/kg/day). It is important to recognize that manganese is an essential
element in human nutrition and that the oral reference dose (RfD) is based on a
total dietary intake, and this amount of manganese alone is not necessarily acceptable
if the intake were from drinking water alone. This difference is due to the fact that
manganese in drinking water is more bioavailable than manganese in food.
Based on the above studies, EPA assigned manganese an oral reference dose (RfD)
of 1 x 10-1 mg/kg/day (IRIS 1990).
Carcinogenic Effects of Manganese. Existing studies are inadequate to assess the
carcinogenicity of manganese. According to EP A's carcinogenic classification scheme,
manganese can be assigned an EPA classification of D-not classifiable as to human
carcinogenicity (IRIS 1990).
A22.4 BIBLIOGRAPHY
MERCK 1976
PATTY 1963
HEA 1984
IRIS 1990
IRIS 1990
c;r/APPA
9/'2!J/90
Windholz, Martha, ed., the Merck Index, An Encyclopedia of
Chemical and Drugs, Ninth Edition, Merck & Co., Inc., Rahway,
New Jersey, 1976.
Patty, F.A. Industrial Hygiene and Toxicology, Volume II, 2nd
Ed. Interscience, New York, 1963.
EPA. Health Effects Assessment for Manganese, prepared by
the Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA. Integrated Risk Information System (IRIS), Reference
Dose (RfD) for Manganese, on-line, Office of Health and
Environmental Assessment, Cincinnati, OH, August 1, 1990.
EPA. Integrated Risk Information System (IRIS),
Carcinogenicity Assessment for Manganese On-line, Office of
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CT/APPA
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Health and Environmental Assessment, Cincinnati, OH, August
1, 1990.
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A23 MERCURY
A23.1 CHARACTERISTICS
Mercury, Chemical Abstract Service No. 7439-97-6, is a silver-white, liquid metal also
known as liquid silver, quicksilver, and hydrargyrum. Mercury's melting point in -
38.8°C. At 25°C, Mercury has a vapor pressure of 2x10·3 mm Hg and a water
solubility of 81.3xl0·3 mg/Lat 30°C (ATSDR 1988). Table A-15 lists some chemical
and physical properties of mercury and mercury compounds.
A23.2 ENVIRONMENTAL FATE
In the environment, mercury exists in three oxidation states: 0 ( elemental), + 1
(mercurous compounds), and +2 (mercuric compounds). Elemental mercury is
insoluble when compared to mercury compounds, with mercuric compounds being the
most solubles.
Besides a variety of inorganic compounds, mercury forms a number of compounds
with organic ligands. These compounds are toxicologically and environmentally
significant. Methylmercury, ethylmercury, phenylmercury, and alkoxyphenylmercury
are some of the prominent compounds belonging to the organomercuric compounds
(HEA 1984).
It is difficult to estimate the abundance of mercury in the earth's crust. Fleisher
(1970) reported that concentrations vary between 5 and 1000 ppb in common natural
materials.
Mercury that is released into the environment will remain there indefin-itely. The
form of mercury exists in ( organic or inorganic) may change with time. For example,
some or all of released organic mercury will slowly decompose to become inorganic
mercury. On the other hand, some portion of released inorganic mercury will be
slowly transformed into organic mercury by bacteria in soil or water (ATSDR 1988).
Mercury's major removal mechanism from a natural water system is adsorp-tion onto
the surfaces of particulate phases and subsequently settling to the bed sediment. A
majority of any dissolved mercury is removed in this manner within a relatively short
time, generally in the immediate vicinity of the source. A much smaller portion of
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COMPOUND
Mercury
Mercuric Acolate
Mercuric Chloride
Mercurous Chloride
Methymercuric Chloride
Phenylmercury Ac~late
TABLE A-15
PHYSIOCHEMICAL PROPERTIES OF MERCURY
AND SELECTED COMPOUNDS
CASRN FORMULA MW MP BP DENSITY
l'C) ('C) (g/c:m3)
7439-97-ll Hg 200.59 -38.9 356.72 13.53
1600-27-7 HgC4H604 318.7 179 3.28
7487-94-7 HgCl2 271.52 277 302 5.4
10112-91-1 Hg2Cl2 472.09 sublimes 7.15
115---09-3 CH3HgCI 251.08 170 4.063
62-38--4 C8H8HgO2 336.75 149
Sources: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA, USPHS ATSDR
WATER SOLUBLE
(mg/L)
8.1E-2
4.0E+S
7.4E+4
2.0E.O
4.4E+3
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the dissolved mercury is ingested by aquatic biota or transported by current
movement and dilution (Callahan 1979).
A23.3 HEAL TH EFFECTS
Noncarcinogenic Effects of Mercury. A risk assessment for mercury is under review
by a EPA work group at this time (IRIS 1988).
Inhalation of metallic mercury vapors has been associated with systemic toxicity in
both humans and animals. At low levels of exposure, the major target organs of
mercury-induced toxicity are the kidney and central nervous system (ATSDR 1988).
Ashe et al. (1953) studied the effect inhalation of mercury has on rats. A NOAEL
of 0.01 mg/m3 mercury was determined based on two studies that exposed rats for 72
and 83 weeks respectively (ATSDR 1988).
Schuckmann (1979) demonstrated a NOAEL of 0.075 mg/m3 for mercury to prevent
adverse effects to the neurological system in humans (ATSDR 1988).
Carcinogenic Effects of Mercury. No human data exists to associate mercury with
carcinogenicity (IRIS 1988).
Inadequate animal studies exist to support mercury as being a carcinogen. Based on
this, EPA has classed mercury in group D, not classifiable as to human
carcinogenicity (IRIS 1988).
A23.4 BIBLIOGRAPHY
ATSDR 1988 ATSDR, Draft Toxicological Profile for Mercury, prepared by
Clement Associates, Oak Ridge National Laboratory, Oak
Ridge, December 1988.
CALLAHAN 1979 Callahan, Michael A. et al., Water-Related Environmental Fate
of 129 Priority Pollutants, Volume I, prepared by Versar,
Incorporated for EPA, Washington D.C., 1979.
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NIOSH
HEA 1984
EPA
IRIS 1988
MERCK
IRIS 1988
CT/Af'PA
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NIOSH, Criteria For a Recommended Standard, Occupational
Exposure to Mercury, U.S. Department of Health, Education
and Welfare, I-ISM Publication No. 73-11024, 1973.
EPA, Health Effects Assessment for Mercury, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989.
EPA, Integrated Risk Information System (IRIS), Mercury,
on-line, Office of Health and Environmental Assessment,
Cincinnati, OH, December 1, 1988.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Mercury, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH,
verification date September 7, 1988.
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A24 NICKEL
A24.1 CHARACTERISTICS
Nickel, Chemistry Abstract Service Registry No. 7440-02-0, is a naturally occurring
silvery metal that is found in small quantities in the earth's crust of 0.018 percent
(MERCK 1976). In the environment, nickel almost always occurs in the O and + 2
valence states. Besides a varie_ty of inorganic compounds, nickel forms a number of
complexes with organic ligands (HEA 1984). Table A-16 lists some chemical and
physical properties of nickel and nickel compounds.
A24.2 ENVIRONMENTAL FATE
Nickel is a naturally occurring element which cannot be degraded in the environment.
Environmental fate processes may transform one nickel compound into another, but
the nickel is still available for human exposure (A TSDR 1987).
The primary source of nickel in the atmosphere is from the burning of fuel oil.
Nickel levels in soils may be elevated by application of nickel-containing sewage
sludge, use of certain fertilizers, and deposition of aerosol particles. Industrial
pollution and waste disposal practices are responsible for higher levels of nickel found
in surface water or ground-water. Nickel is continuously transferred between air,
water and soil by natural chemical and physical processes, such as weathering,
erosion, runoff, precipitation, stream/river flow, and leaching. Nickel aerosols are
removed from the atmosphere primarily by wet and dry deposition. The average
residence time for nickel in the atmosphere is 7 days. Over this period of time, long-
distance transport is expected to take place. Nickel is extremely persistent in both
water and soil. Oceans act as the ulti-mate sink for nickel in the environment. The
residence time for nickel in deep oceans and near shore coastal waters have been
estimated to be 23,000 and 19 years, respectively. Nickel may be removed from
oceans in sea spray aerosols (ATSDR 1987).
A24.3 HEALTH EFFECTS
Noncarcinogenic Effects of Nickel. Ambrose et al. (1976) conducted a two-year
feeding study using rats. Nickel sulfate hexahycrate was adminis-tered in
concentrations of 0, 5, 50, or 125 mg/kg/day as nickel. No significant effects were
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COMPOUND
Nickel
Nickel Oxide. green
Nickel Oxide, black
Nickol Chloride
Nickel Sulfate
TABLE A-16
PHYSIOCHEMICAL PROPERTIES OF NICKEL
AND SELECTED COMPOUNDS
CASRN FORMULA MW MP BP DENSITY
(•C) (•C) (g/cm3)
7440-02-0 NI 58.7 1555 2837 8.9
12054-48-7 Ni(OH)2 74.7 1984 unknown 6.67
1314--06-3 Ni03 185.4 600 (decomp) NA unknown
n1s-54-9 NiCl2 129.6 1001 973 (subllmes) 3.55
7786-81-4 Ni04S 154.77
Sources: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA. USPHS ATSDR
WATER SOLUBLE
(mgll)
insoluble
insoluble
insoluble
6.4E+5
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noted at the 5 mg/kg/ day level. At 50 mg/kg/day, adverse effects noted were
decreased body and organ weights (IRIS 1990).
EPA (1986) reported that a 90 day subchronic study conducted for them by American
Biogenics Corp. also found 5 mg/kg/day to be a NOAEL, thus supporting Ambrose
et al. (1976) chronic study.
Based on the above two studies and other supporting data, EPA has assigned nickel
an oral reference dose of 2 x 10·2 mg/kg/day. A risk assessment for the inhalation of
nickel is under review by an EPA work group. An inhalation reference dose has not
been assigned by EPA (IRIS 1990).
Carcinogenic Effects of Nickel. The EPA has not evaluated soluble salts of nickel,
as a class of compounds, for potential human carcino-genicity. However, nickel
refinery dust and specific nickel compounds -nickel carbonyl and nickel subsulfide -
have been evaluated. Summaries of these evaluations are available on IRIS (IRIS
1987).
A24.4 BIBLIOGRAPHY
ATSDR 1987
NIOSH
HEA 1984
HEAST 1989
Cf/APPA
9l2D/OO
ATSDR, Draft Toxicological Profile for Nickel, prepared by
Syracuse Research Corporation, Oak Ridge National
Laboratory, Oak Ridge, October 1987.
NIOSH, Criteria For a Recommended Standard, Occupational
Exposure to Inorganic Nickel, U.S. Department of Health,
Education and Welfare, DHEW (NIOSH) Publication No.
77-164, May 1977.
EPA, Health Effects Assessment for Nickel, prepared by the
Office of Health and Environmental Assessment, Cincinnati,_
September 1984.
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989.
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IRIS 1987
IRIS 1990
MERCK 1976
CT/M'PA
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EPA, Integrated Risk Information System (IRIS), Nickel,
on-line, Office of Health and Environmental Assessment,
Cincinnati, OH, September 30, 1987.
EPA, Integrated Risk Information System (IRIS), Reference
Dose (RID) for Nickel, soluble salts, on-line, Office of Health
and Environmental Assessment, Cincinnati, OH, verification
date April, 1990.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
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A25 Strontium
A25.1 Characteristics
Strontium, CASRN 7440-24-6, has a silvery appearance, but rapidly turns a yellowish
color with the formation of the oxide. The finely divided metal ignites spontaneously
in air. Volatile strontium salts impart and beautiful crimson color to flames, and
these salts are used in pyrotechnics. Natural strontium is a mixture of four stable
isotopes (CRC 1978). Table A-17 shows chemical and physical properties for
strontium.
A25.2 Environmental Fate
Strontium is found as strontianite (SrCO3) and celestite (SrSO4). Worldwide
sampling of soils revealed Sr contents around 300 mg/kg. Total input into oceans
results mainly (80%) from weathering of sedimentary carbonates and sulfates.
Seawater contains about 7 mg/L and is unsaturated relative to celestite deposition.
The ratio of Sr content to salinity is about 221 ug/g. The average Sr/Ca ratio in
world rivers is 5x10·3 and a (minimum) estimate of their Sr input into oceans gives
2.2 mio tons/year based on the average river Sr content of 68.5 ug/L. Celestite forms
the skeletal material of the planktonic species Acantharia (21.8% Sr in ash). There
is evidence for a higher content of Sr in animal than in human skeletons (Seiler et
al 1988).
A25.3 Health Effects
Noncarcinogenic Effects of Strontium
Compounds of stable isotopic Sr have a low to moderate toxicity as indicated by
range-finding and acute toxicity tests and subchronic feeding studies in rats. On the
other hand, since the advent of nuclear fission, which results in several species of Sr
radioisotopes, 90Sr has been found to be highly radiotox:ic, because of its characteristic
deposition in growing bone.
The ingestion of mice of 16,000 ppm Sr lactate in the drinking water for 402 days
produced an immediate stunting of growth, which later was recovered, according to
Alexander et al. At this level, Sr actively inhibited calcification of growing bone.
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TABLE A-17
PHYSIOCHEMICAL PROPERTIES OF STRONTIUM AND SOME OF ITS COMPOUNDS
AT.OR DENSITY OR
CASRN FORM OF SR MOL WT. SP.GR. M.P.(°C) B.P.(°C) SOLUBILITY
7440-24-6 Strontium (Sr) 87.62 2.6 (20°C) 769 1384 Dec. hot or cold H2/O;
sol. acid, alcohol, liq. NH3
Strontium oxide 103.62 4.7 2430 3000 6.9 g/liter (20°C), 228.5 g/liter
(SrO) (100°C); sl. sol. alcohol;
insol. ether, acetone
Strontium hydroxide 121.63 3.63 375 710 4.1 g/liter (0°C), 218.3 g/liter
iSr(OH)2] (in H2, -H2O) (100°C); sol. acid, NH4CI
1633-05-2 Strontium carbonate 147.63 3.70 1497 -CO2, 1340 11 mg/liter (18°C), 650 mg/liter
(native, strontlalile) (69 aim) (100°C); sol. acid, NH4 salts
(SrCO2)
7789-06-2 Strontium chromate 203.61 3.895 (15°C) 1.2 glliter (15°C), 30 g/liter
(SrCrO4) (100°C); sol. HCI, HNO3; acetic
acid, NH4 salts
Strontium molybdate 247.56 4.54 Dec. 0.104 g/liter (17°C); sol. acid
(SrMoO4)
10042-76-9 Strontium nitrate 211.63 2.986 570 401 g/liter (0°C); 1 kg
[Sr(NO3)2] liter (90°C); v. sol.
NH3; sl. sol. HAc
Strontium sulfate 183.68 3.96 1605 Dec. 113 mg/liter (0°C); 114 mg/liter
(native, celestlte) (30°C); 140 g/llter H2S04
(SrSO4) (70°C); sl. sol. acid, lnsol.
alcohol, dil. H2S04
Sources: Patty's 1981, Aldrich 1989
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Repeated intraperitoneal injections of SrCli, to the extent of Sr deposition as 7
percent of inorganic content of bone, did not produce rickets in rats.
Ingestion of doses of Sr(NO3 of 50 mg/kg (1030 ppm) are well tolerated for 8 weeks
by either weanling or adult rats, as evidenced by normal amount of food intake,
normal weight gains, total bone ash, or Ca and P composition of the skeleton.
In contrast to the well-tolerated 50 mg/kg doses of Sr(NO3)2 by the oral route,
inhalation exposures of slightly less than 50 mg/m3 were not well tolerated by the
same species. At the end of 1 month of 4-hr daily exposures at 44.6 + 1.4 mg/m3,
particle size 83 percent <5 um, male rats showed functional changes in the kidney
and liver, and histological changes in the cardiovascular, hematopoietic, and nervous
systems and respiratory organs. Tests of renal function showed a lower excretion of
chloride in the urine and higher level of residual nitrogen in the blood, with a daily
diuresis after caffeine loading greater than controls. In the liver, increased
biosynthesis of hippuric acid was considered a compensatory mechanism in response
to the toxicity of Sr(NO3)2• A disorder in mineral metabolism was interpreted from
an increase in elimination of Ca in the urine and an increase in serum alkaline
phosphatase.
Although no animal died as a result of the exposure, histological changes of moderate
degree were seen in the lungs, heart, liver, kidneys, and spleen. In the lungs,
interstitial pneumonia was accompanied by hyperemia and hemorrhage. In the heart,
changes were limited to hyperemia, principally of the alveoli, and dystrophic changes
in muscular fibers. Similar changes were seen in the liver and kidney with granular
dystrophy of the epithelia of the convoluted tubules.
Sr(NO3)2 proved to be highly irritating to the skin of both rats and guinea pigs but
only slightly irritating to the mucosa (Clayton and Clayton 1981).
No oral or inhalation RFD or occupational exposure limits have been set by the
USEP A at this time (IRIS 1990).
Carcinogenic Effects of Strontium
No evidence of the carcinogenicity of strontium could be located in the literature.
CT/N'PA
9/20/90 A-96
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A25.4 Bibliography
ALDRICH
ATSDR 1987
CLAYTON
CRC
FAWELL
HOWARD
NIOSH/OSHA
SIELER
USEPA
IRIS 1990
CT/N'PA
9/2D/90
Aldrich Catalog Handbood of Fine Chemicals, Aldrich Chemical
Company, Inc. 1988.
ATSDR, Draft Toxicological Profile for Benzene, Oak Ridge
National Laboratory, Oak Ridge, October 1987.
Clayton, G.D. and Clayton, F.E., Patty's Industrial Hygiene and
Toxicology, John Wiley and sons, NY, 1981.
Weast, R. (editor), CRC Handbood of Chemistry and Physics,
58th ed., CRC Press, Inc., West Palm Beach, FL, 1977.
Fawell, J. and Hunt, S., Environmental Toxicology, Ellis
Horwood Ltd., England, 1988.
Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Benzene, Supplement II, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No
89-104, 1988.
Seiler, H.G., Sigel, G. and Sigel, A., Handbook on Toxicity of
Inorganic Compounds, Marcel Dekker, Inc., 1988.
EPA, Health Effects Assessment for Benzene, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Benzene, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH.
A-97
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A26 Titanium
A26.1 Characteristics
Titanium, CASRN 7440-32-6, when pure, is a lustrous white metal. It has a low
density, good strength, is easily fabricated, and has excellent corrosion resistance.
The metal burns in air and is the only element that burns in nitrogen.
Natural titanium consists of five isotopes with atomic masses from 46 to 50. The
metal is dimorphic. It is important as an alloying agent with aluminum, molybdenum,
manganese, iron, and other metals. The element is the ninth most abundant in the
crust of the earth. It is almost always present in igneous rock and in the sediments
derived from them. It occurs in the minerals, rutile, ilmenite, and sphere, and is
present in titanates and in many iron ores (CRC 1978). Table A-18 shows the
chemical and physical properties of titanium and some if its compounds.
A26.2 Environmental Fate
Due to the stability of its tetravalent state and its affinity to oxygen, titanium is not
found in elementary form in nature. Being the ninth most abundant element in the
earth's crust, it is thus found and industrially used in the minerals ilmenite (FeTiO3)
and to a lesser extent in rutile (TiO2).
The two other TiO2 modifications, anatase and brookite, as well as other minerals
containing titanium (CaTiO3, CaTiSiO5, MnTiO3) do not constitute large areas of
potential industrial interest. Rocks brought back by Apollo 17 lunar missions
revealed 12.1 % TiOz, whose spectral bands have also been detected in M-type stars.
Effects of Ti2+ and Ti3+ compounds on algae, plants, and invertebrates have been
summarized but the instability of these cations together with their small-scale use as
compared to TiO2 makes it questionable if these results can raise environmental
concern. Effects of industrial titanium dioxide effluents have been investigated on
fish (perch, bleak, flounder) with main effects of a deposition on the gills being
found. Road traffic near Frankfurt airport left titanium ( and other metal)
concentrations below the limits for raw and drinking water. This situation is changed
in the vicinity of steel mills where drinking water contained titanium. Sediment
analysis showed low levels of biological available titanium even near TiO2 effluents,
the poor solubility of TiO2 being established by different digestion procedures. In
A-98
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TABLE A-18
PHYSIOCHEMICAL PROPERTIES OF TITANIUM AND SOME OF ITS COMPOUNDS
AT.OR DENSITY OR
CASRN FORM OFTI MOL. WT. SP. GR. M.P.(°C) B.P.(°C) SOLUBILITY
7440-32-6 Titanium (Tl) 47.90 4.5 (20°C) 1660=10 3287 lnsol. cold H2O; dee. hot
H2O sol. dll. acids
13463-67-7 Titanium dioxide 79.90 4.26 1830-1850 2500-3000 lnsol. hot or cold H2O; sol.
(rutile) H2SO4, alkalies; lnsol. acids
(TiO2)
Titanium diboride 69.52 4.50 2900
(TiB2)
12070-08-5 Titanium carbide 59.91 4.93 3140=90 4820 lnsol. hot or cold H2O;
(TiC) sol. aqua regia, HNO3
7705-07-9 litanium trichloride 154.26 2.64 d440 660 lnsol. hot or cold H2O; v. sol.
(TiCl3) (69 atm) (108) alcohol; sol. HCI; lnsol. ether
7750-45-0 nIanium tetrachlorid 189.71 Liq. 1. 726 -25 136.4 Sol. cold H2O; dee. hot H2O;
(TiCl4) sol. dil. HCI, alcohol
7704-98-5 Titanium hydride 49.92 3.9 (12°ci d400
(TiH2)
Titanium disulfide 112.03 322 (20°C) Hyd. sl. cold H2O; dee. In steam,
(TiS2) HCI; sol. dil. HNO3, H2S04
Titanium sulfate 383.98 lnsol. hot or cold H20;
[fl2(S04)3] sol. dil. acids; lnsol. alcohol,
ether, cone. H2SO$
Sources: Patty's 1981, Aldrich 1989
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other cases titanium content of sediments was related to geological factors. Titanium
content of urban aerosols and street dust was found to be soil-derived and a Japanese
study showed that titanium falls in the same category as Si, Fe, or Al with no
correlation to anthropogenic sources. This general situation is changed in the vicinity
of coal-fired power plants and more specifically in metal alloy and metal carbide
plants. In most cases titanium occurs as a ballast element whose sparingly soluble
oxide and silicates may also be the reason that it is not essential in human or animal
nutrition. The finding of Pais that a complex of Ti4+ with ascorbic acid has beneficial
effects on plant growing is noteworthy. Other authors reported decreased growth and
some chlorosis of beans exposed to titanium compounds (Seiler et al 1988).
A26.3 Health Effects
The toxicologic history of Ti is one of dichotomy as a result on the one hand of
overwhelming evidence of the physiological inertness of Ti metal and its oxide and
carbide, and on the other hand, of the highly injurious action of the tetrachloride in
particular and the dicyclopentadienyl derivatives secondarily.
Noncarcinogenic Effects of Titanium
Of the more than a dozen and a half commercially available Ti substances, only eight
have been tested for their acute toxic action. some, such as Ti oxide, diboride, and
carbide, have been recognized to be so inert as to require no such tests. Among
those of more toxic nature, the tetrachloride had a lowest lethal concentration (LCL0 )
of 10 mg/m3 for the mouse, one of the more resistant species, in a 2-hr inhalation
exposure, and Ti dicyclopentadienyl dichloride had an intramuscular LDLO of 83
mg/kg for the hamster and an intraperitoneal LD50 of 30 mg/kg for the rat.
Considerably less acutely toxic was potassium hexafluorotitanate, T~F.,, which had
an oral LDLo of 200 mg/kg for the guinea pig, and a subcutaneous LDLO of 450
mg/kg. Titanium acetylacetonate, TiO[OC(CH3):CHCOCH3Ji., had 650 mg/kg as an
intraperitoneal LD50 for the rat.
The acute oral and intraperitoneal toxicity of a group of four metal titanates, Ba, Bi,
Ca, and Pb, found in World War I to have wide, but low volume uses as dielectrics,
was determined by Brown and Mastromatteo. All four were found to have extremely
low toxicity for the rat; the acute oral LD50 exceeded 12,000 mg/kg for all; the
intraperitoneal LD50 for the most toxic, Pb titanate, was 2000 mg/kg (1,5000 to
CT/M'PA
9/2!J/90 A-99
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2,7000); Bi titanate, 2200 mg/kg (1700 to 2900), Ba titanate, 3000 mg/kg (1800 to
5100); and Ca titanate, 5300 mg/kg (3100 to 8900).
No acute toxicity data were found on Ti dioxide, borides, hydrides, sulfate, or halides
other than that on the tetrachloride.
Following in the steps of Fredrick and Bradley, who found Ti02 administered to rats
to be essentially inert, Christie et al. exposed rats to an air-dried mist of Ti02 slurry
at 2-hr intervals, four times daily, 5 days a week for a maximum of 13 months
followed by 7 months' observation period without exposure. As expected under such
conditions, dust counts varied from 42 to 328 mppcf during the first hour to 10 to 46
at the end of the second hour, with large variations from day to day. At all times,
dust counts were far above any permissible industrial limit. Despite this massive and
although the inorganic content of the lungs showed dust accumulation, no increase
in the wet weight of the lungs occurred, nor was there any sigh of activity or specific
lesion produced by Ti02• In conformity with metabolic findings noted below, no
appreciable elimination of accumulated Ti02 in the lungs occurred in the 7 months
without exposure. The Ti02 reaching the alveoli and ducts was phagocytosed and
carried to the sump areas in the subpleura to remain there.
Other evidences for the physiological inertness of Ti and its ;highly insoluble,
nonhydrolyzable compounds follow: (1) TiOz, used as a protective film on exposed
parts of the body as a prevention of flash burns during World War II, was without
consequence, indicating no capacity of Ti02 to produce contact dermatitis, allergic
sensitization, or appreciable dermal absorption. (2) Disks of Ti metal implanted in
muscle of dogs and left in situ for 7 months were inert; the wound healed and the
metal was encapsulated with fibrous tissue.
In a study to determine the long-term effects from inhaling TiC14, four dogs were
exposed 6 hr/day, 5 days a week for 9 weeks, after a 6-week observation period when
measurements of blood pressure, body temperature, pulse and respiration rates, and
blood and urine samples were taken to determine base-line values. Atmospheric
concentrations of Ti averaged 8.4 ppm (1.6 to 17.1); volatile chloride averaged 6.8
ppm (1.2 to 16) (Oayton and Oayton 1981).
CrJN'PA
9/2fJ/90 A-100
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Both OSHA and ACGIH have set occupational exposure limits for titanium dioxide
at 15 and 10 mg/m3 8 hr TWA respectively (OSHA 1989, ACGIH 1989).
Carcinogenic Effects of Titanium
Titanium dioxide of the anatase variety, approved by the FDA for use in foods, fed
to Fischer 344 rats and B6C3F1 mice at levels of 25,000 and 50,000 ppm for 103
weeks showed no evidence of toxicity and not rumors in excess of those occurring
spontaneously in the control rats and mice. No evidence of carcinogenicity was found
also when another inorganic compound, TiK oxalate, was administered to Swiss
albino mice at 5 ppm in the drinking water for their life-span.
When, however, an organo Ti compound, titanocene, a dicyclopentadiene dichloride,
was injected intramuscularly into C57 Blk mice, a strain resistant to tumors, a variety
of tumors, hepatomas, fibrosarcoma, lymphoblastoma, and others, developed at the
injection site and in organs some distance away (Clayton and Clayton 1981).
The USEPA has not evaluated titanium or titanium compounds under the IRIS
system (IRIS 1990).
A26.4 Bibliography
ALDRICH
ATSDR 1987
CLAYTON
CRC
FAWELL
CT/M'PA
9/2fJ/90
Aldrich Catalog Handbood of Fine Chemicals, Aldrich Chemical
Company, Inc. 1988.
ATSDR, Draft Toxicological Profile for Benzene, Oak Ridge
National Laboratory, Oak Ridge, October 1987.
Clayton, G.D. and Clayton, F.E., Patty's Industrial Hygiene and
Toxicology, John Wiley and sons, NY, 1981.
Weast, R. (editor), CRC Handbood of Chemistry and Physics,
58th ed., CRC Press, Inc., West Palm Beach, FL, 1977.
Fawell, J. and Hunt, S., Environmental Toxicology, Ellis
Horwood Ltd., England, 1988.
A-101
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HOWARD
NIOSH/OSHA
SIELER
USEPA
IRIS 1990
c;[/APPA
9/2D/90
Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Benzene, Supplement II, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No
89-104, 1988.
Seiler, H.G., Sigel, G. and Sigel, A., Handbook on Toxicity of
Inorganic Compounds, Marcel Dekker, Inc., 1988.
EPA, Health Effects Assessment for Benzene, prepared by the
Office of Health and Environmental Assessment, Cincinnati,
September 1984.
EPA, Integrated Risk Information System (IRIS), Slope Factor
for Carcinogenicity Assessment for Benzene, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH.
A-102
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A27 VANADIUM
A27.1 CHARACTERISTICS
Vanadium, Chemical Abstract Service Registry No. 1314-62-1, is a light gray metal.
Vanadium occurs in ores at about 0.02 percent of the earth's crust. It may occur in
oxidation states of 0, II, III, IV, and V. Penta-valent compounds are industrially
important compounds (NIOSH 1977).
Vanadium pentoxide is a yellow to rust-brown, noncombustible crystalline compound
(ACGIH 1986). Table A-19 list some chemical and physical properties of vanadium
and vanadium compounds.
A27.2 ENVIRONMENTAL FATE
No information on the fate of Vanadium in the environment could be located in the
literature.
A27.3 HEALTH EFFECTS
Noncarcinogenic Effects of Vanadium. Vanadium is poisonous to all animals in any
but very small doses, no matter how it is administered. The penta-valent compounds,
such as vanadium pentoxide and vanadates, are more toxic than other forms (ACGIH
1986).
EPA has assigned an oral reference dose for vanadium pentoxide. Based on a
chronic study (Stokinger et al., 1953) where rats were fed 0.89 or 8.9 mg/kg/day of
vanadium pentoxide for 2.5 years, an oral reference dose of 9 x 10·3 mg/kg/day was
assigned. This is based on finding no adverse effect from the 0.89 mg/kg/day
exposure. The lowest adverse effect noted was a decrease in the amount of cystine
in the hair of animals ingesting vanadium (IRIS 1988).
No inhalation reference dose is available through EPA at this time for vanadium or
vanadium pentoxide (IRIS 1988).
Carcinogenic Effects of Vanadium. There are no data in the available literature that
show whether vanadium and its compounds are carcinogenic except for a negative
CT/N'PA
9/2D/90 A-103
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TABLE A-19
PHYSIOCHEMICAL PROPERTIES OF VANADIUM
AND SELECTED COMPOUNDS
COMPOUND CASRN FORMULA MW MP BP DENSITY
('C) ('C) (g/cm3)
Vanadium 7440--62-2 V 50.94 1917 8.11
Vanadium Pentoxide 1314--62-1 V2O5 149.88 1970 4.87
Vanadium Oxide 1314-34-7 V2O4 149.9 1940 4.87
Vanadium Oxytrichloride 7727-18--6 VOCl3 173.3 -77 126.7 1.829
Sources: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA. USPHS ATSDA
WATER SOLUBLE
(rng/l)
Insoluble
slightly
Insoluble
decomp
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finding where mice were administered vanadyl sulfate at 19.8 mg of vanadium/100
gram of body weight/year for a lifetime (NIOSH 1977).
A27.4 BIBLIOGRAPHY
ACGIH 1986
NIOSH 1977
EPA
EPA
IRIS 1988
MERCK
ACGIH, Documentation of Threshold Limit Values and
Biological Exposure Indices, Vanadium, Fifth Edition,
Cincinnati, 1986.
NIOSH, Criteria For a Recommended Standard, Occupational
Exposure to Vanadium, U.S. Department of Health, Education
and Welfare, DHEW (NIOSH) Publication No. 77-222, August
1977.
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989.
EPA, Integrated Risk Information System (IRIS), Reference
Dose (RID) for Vanadium Pentoxide, Office of Health and
Environmental Assessment, Cincinnati, OH, verification date
June 30, 1988.
EPA, Integrated Risk Information System (IRIS), Vanadium
Pentoxide, on-line, Office of Health and Environmental
Assessment, Cincinnati, OH, June 30, 1988.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.
A-104
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A28 Yttrium
A28.1 Characteristics
Yttrium, CASRN 7440-65-5, has a silvery-metallic luster and is relatively stable in air.
Turnings of the metal, however, ignite in air if their temperature exceeds 400°C and
finely divided yttrium is very unstable in air. Yttrium oxide is one of the most
important compounds of yttrium and accounts for the largest use. Yttrium occurs in
nearly all of the rare-earth minerals. Natural yttrium contains but one isotope, Y89•
A28.2 Environmental Fate
An examination of the literature reveals no evidence of environmental harm from
yttrium. In the following account of the levels of yttrium in soils and its movements
to plants, it is evident that increased industrial usage of yttrium is unlikely to lead to
its accumulation in a plant-based food chain back to man.
The levels of the rare earth elements (REEs) in soils area certainly not low; Connor
and Shacklette cited levels of 27 and 33 ppm for yttrium and lanthanum, respectively,
in uncultivated soils. In comparison, barium, cobalt, copper, nickel, strontium, and
zinc are present at levels of 300, 10, 15, 17, 67, and 36 ppm, respectively. The
insolubility of their phosphates and fluorides limits movement of the REE through
the environment. From the reports on the uptake of REEs into plants, it is apparent
that the reducing conditions which might generate europium (II) are not present in
soils. Reports of uptake of REEs into plants comes from many groups although it
is recognized that the leaves of mockernut hickory can accumulate 2300 ppm of
REEs in contrast to leaves of other species which take up only 60 ppm. A lowered
abundance of cerium in the mockernut leaves points to the production of cerium (IV)
in the subsoils. Cowgill reported the uptake and accumulation of lanthanum, cerium,
praseodymium, samarium, dysprosium, erbium, and ytterbium by aquatic plants such
as the water lily. It might be concluded that the partial enrichment of some of these
REEs in the water lily indicates some essential element status. Ure and Bacon,
however, were unable to find any evidence of accumulation in water lilies gathered
in Scotland (Seiler et al 1988).
CT/N'PA
9/2fJIOO A-105
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A28.3 Health Effects
Noncarcinogenic Effects of Yttrium
Although Y behaves chemically sufficiently similar to La to be included with the
lanthanides, toxicologically it has been found to differ sufficiently to single it out from
the lanthanides. The Y citrate-chloride complex was found by Graca et al., for
example, to be the most acutely toxic both to guinea pigs and mice by the
intraperitoneal route of all the lanthanides (with LD50 values of 42 and 78 mg/kg,
respectively, compared with a close member in the series, Ce, with respective LD50
values of 82 and 150 mg/kg). Further, in a comparative investigation of the oxides
of Y, Ce, and Nd in rats, intratracheally administered at a dose of 50 mg (0.222,
0.152, and 0.148 mM, respectively Y20 3 showed the most pronounced changes in the
Jung of the three oxides tested. At 8 months, in the lung tissue in which Y 20 3 was
present characteristic granulomatous nodules developed, consisting of crystalline
deposits of the oxide and cellular elements. Nodules in the peribronchial tissue
compressed and deformed several bronchi, and the surrounding lung areas were
emphysematous, the interalveolar walls were thin and sclerotic, and the alveolar
cavities dilated. By contrast, Ce20 3 did not elicit serious changes, and produced
neither diffuse nor nodular fibrotic processes. Although Nd20 3 granulomas
resembled those induced by Y 20 3, their further development differed; their
characteristic was very poor formation of connective tissue fibers, which around the
granulomas were extremely weak; and sclerosis of the interalveo!ar walls was only
moderate. It was concluded that, regardless of the similarity of their chemical and
physical properties, Y 20 3 exhibited specific toxicologic actions which were the most
severe of the three oxides studied. A still further toxicologic difference is the lesser
degree of skeletal deposition. YC13, administered to rats intraperitoneally alternate
days, for as many as 83 injections totaling 936 mg, did not accumulate large amounts
of Y in femoral bone. Yttrium never exceeded 330 ppm of bone ash, and after Y
had been deposited to the extent of 150 to 200 ppm ( corresponding to about 50 mg
injected YC½), further accumulation proceeded at a very slow rate; with age, the
ratio of Y in spongy to compact bone approached 1. By comparison, skeletal
deposition amounts to 20 percent for La, ranging to 70 percent for Lu (Clayton and
Clayton 1981).
Both OSHA and ACGilI have set occupational exposure limit of 1 mg/m3 for yttrium
and yttrium compounds (OSHA 1989, ACGilI 1989).
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Carcinogenic Effects of Yttrium
No reports on the carcinogenicity of yttrium and its compounds could be found in the
literature.
A28.4 Bibliography
ALDRICH
ATSDR 1987
CLAYTON
CRC
FAWELL
HOWARD
NIOSH/OSHA
SIELER
USEPA
c;r/APPA
9/2!)/90
Aldrich Catalog Handbook of Fine Chemicals, Aldrich Chemical
Company, Inc. 1988.
ATSDR, Draft Toxicological Profile for Benzene, Oak Ridge
National Laboratory, Oak Ridge, October 1987.
Clayton, G.D. and Clayton, F.E., Patty's Industrial Hygiene and
Toxicology, John Wiley and sons, NY, 1981.
Weast, R. (editor), CRC Handbook of Chemistry and Physics,
58th ed., CRC Press, Inc., West Palm Beach, FL, 1977.
Fawell, J. and Hunt, S., Environmental Toxicology, Ellis
Horwood Ltd., England, 1988.
Howard, Philip H., et al., Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Volume II, Lewis
Publishers, Chelsea, Michigan, 1990.
NIOSH, NIOSH/OSHA Occupational Health Guidelines for
Chemical Hazards; Benzene, Supplement II, U.S.Department of
Health and Human Services, DHHS NIOSH Publication No
89-104, 1988.
Seiler, H.G., Sigel, G. and Sigel, A., Handbook on Toxicity of
Inorganic Compounds, Marcel Dekker, Inc., 1988.
EPA, Health Effects Assessment for Benzene, prepared by the
Office of Health and Environmental Assessment, Cincinnat~
September 1984.
A-107
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I for Carcinogenicity Assessment for Benzene, on-line, Office of
Health and Environmental Assessment, Cincinnati, OH.
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A29 ZINC
A29.1 CHARACTERISTICS
Zinc, Chemical Abstract Service Registry No. 7440-66-6, is a bluish white, lustrous
metal that occurs in nature in the zero valence (metal and alloys) and +2 valence
(compounds) states. Besides a variety of inorganic compounds, zinc forms a number
of compounds with organic ligands (HEA 1984). Zinc's abundance in the earth's
crust in 0.02 percent by weight (MERCK 1976). Table A-20 list some chemical and
physical properties of zinc and zinc compounds.
A29.2 ENVIRONMENTAL FATE
In the atmosphere, zinc is expected to be present as dust and fumes from zinc
production facilities, lead smelts, brass works automobile emissions, fuel combustion,
incineration and soil erosion. The atmospheric fate of zinc has not been
comprehensively studied. Any chemical interaction of zinc compounds in the
atmosphere may result in conversion of zinc into a stable species such as zinc oxide,
and not its removal through decomposi-tion as frequently occurs with organic
compounds. Zinc oxide emitted from high-temperature processes may emit particle
sizes in the 0.01-0.4 micron range, resulting in a long residence time in the
atmosphere, although no estimate for the atmospheric lifetime for zinc is available
at this time (HEA 1984).
Information regarding the fate of zinc in soil is inadequate. However, zinc is likely
to be strongly sorbed onto soil. Soil conditions not amenable for the sorption of zinc
may lead to the leaching of zinc. The tendency of zinc to be sorbed is affected by
the pH and salinity of soils. Decrease of pH ( < 7) and increase of soil salinity favors
desorption. In a study of groundwater from New Jersey, zinc was detected in 100
percent of the samples. This indicates that leaching of zinc from soil may be
prevalent (HEA 1984).
Zinc introduced into the aquatic environment is partitioned into sediments through
sorption onto hydrous iron and manganese oxides, clay minerals and organic material;
a small part may be partitioned into the aquatic phase through speciation into soluble
zinc compounds. Precipitation of the sulfide is an important control on the mobility
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COMPOUND
Zinc
Zinc Oxide
Zinc Chloride
Zinc Sulfide
Zinc Chromate H
TABLE A-20
PHYSIOCHEMICAL PROPERTIES OF ZINC
AND SELECTED COMPOUNDS
CASRN FORMULA MW MP BP DENSITY
('C) ('C) (g/cm3}
7440-66---6 Zn 65.37 419.6 911 7.14
1314-13-2 ZnO 81.37 >1800 sublimes 5.6
7646-85-7 ZnCl2 136.3 283 732 2.91
1314-98-3 SZn 97.45
1308-13-0 ZnCr04(0H)2 280.74
Source,: CRC 1970, MERCK 1976, USEPA IRIS, USEPA HEA. USPHS ATSDR
WATER SOLUBLE
(mg/L)
Insoluble
Insoluble
8.1E+5
insoluble
slightly soluble
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of zinc in reducing environments, and precipitation of hydroxides, carbonate or basic
sulfate may occur at high zinc concentration. Formation of complexes with organic
and inorganic ligands may increase the mobility of zinc in aquatic media, but these
complexes also have a tendency to be absorbed more strongly onto the sediments.
Sorption of zinc is probably the dominant fate of zinc in the aquatic environment
(HEA 1984).
A29.3 HEALTH EFFECTS
Noncarcinogenic Effect of Zinc. There is a considerable body of informa-tion
concerning the toxicology of orally administered zinc in both humans and
experimental animals. A synthesis of the available human data supported by the
experimental animal data resulted in an oral acceptable intake chronic and
subchronic (AIC and AIS respectively) of 14.9 mg/day as defined by EPA in their
Health Effect Assessment for Zinc (HEA 1984). There is no EPA reference dose
for ingestion of zinc.
The data base for inhalation of exposure is much more limited. No adequate animal
data were located pertinent to either subchronic or chronic inhalation exposures.
Based on the occupational Threshold Limit Value (TLV) established for zinc oxide
by the American Conference of Governmental Industrial Hygienist, EPA established
an inhalation acceptable intake chronic and subchronic (AIC and AIS respectively)
of 7.1 mg/day and 0.7 mg/day respectively. Zinc chloride was used to establish the
AIC and AIS because it is the zinc compound with the lowest TLV, except for zinc
chromate, which is a suspected human carcinogen (HEA 1984).
Carcinogenic Effects of Zinc. Pertinent data associating cancer in humans from zinc
or bioassays of zinc and its compounds for carcinogenicity could not be located in the
available literature. One group of compounds, the zinc chromates, are suspected
carcinogens (HEA 1984). Since the suspected carcinogenicity of these compounds
is associated with the chromate moiety rather than the element zinc, no further
discussion of zinc chromate will be made here. Discussion of the carcinogenic effects
of chromium compounds is found under the section addressing chromium.
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29.4 BIBLIOGRAPHY
LANGE
HEA 1984
EPA
MERCK 1976
(;r/Af'PA
WO/OO
Dean, John A., Lange's Handbook of Chemistry, McGraw-Hill
Book Company, Thirteenth Edition, New York, 1985.
EPA, Health Effects Assessment for Zinc (and Compounds),
prepared by the Office of Health and Environmental
Assessment, Cincinnati, September 1984.
EPA, Health Effects Assessment Summary Table, Forth
Quarter, FY 1989, 1989.
Windholz, Martha, ed., The Merck Index, An Encyclopedia of
Chemical and Drugs,, Ninth Edition, Merck & Co., Inc.,
Rahway, New Jersey, 1976.d.
A-111