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TOWN OF SOUTHAMPTON SUFFOLK COUNTY, NEW YORK
NORTH SEA LANDFILL
Remedial Investigation
PUBLIC HEALTH EVALUATION
JULY 1989
'MGROU D
HOLZMACHER, McLENDON & MURRELL, P.C. CONSULTING ENGINEERS • ARCHITECTS • PLANNERS • SCIENTISTS • SURVEYORS MEL v iae. N.Y.
IN ASSOCIATION WITH
RIVERHEAO. N.Y. FAIRFIELD. N.J.
Clement Associates Incorporated
H2MGROUP HOLZMACHER, McLENDON & MURRELL, P.C. CONSULTING ENGINEERS • ARCHITECTS • PLANNERS • SCIENTISTS • SURVEYORS MELVILLE. N.Y. RIVERHEAO. N.Y. FAIRFIELD. N.J.
m^UTGRO D v_/
Holzmacher, McLendon and Murrell, P.C. • Holzmacher, McLendon and Murrell, Inc. • H2M Labs, Inc. Engineers, Architects, Planners, Scientists
575 Broad Hollow Road, Melville, N.Y. 11747-5076 (516) 756-8000 • (201) 575-5400 FAX: 516-6 .4^4^^2 ^ 2 , ^ g g g
Ms. Caroline Kwan United States Environmental Protection Agency, Region II 26 Federal Plaza New York, NY 10278
Re: North Sea Landfill Phase I RI SHMP 89-01
Dear Ms. Kwan:
Enclosed please find twenty-five (25) copies of the Public Health Evaluation for the above-referenced project. Please distribute these copies as required to the various agencies for review.
This docuTaent has been revised as per USEPA's coiainent letter dated June 12, 1989. As you recall, the superseded draft Public Health Evaluation (March 1989) employed the use of filtered as well as total metals groundwater data for the exposure estimates and risk characterization steps. We strongly support the inclusion of filtered metals data for the evaluation and, therefore, an addendum will follow shortly. The addendum will be a risk comparison of filtered and total metals data in groundwater. The Phase II Remedial Investigation Public Health Evaluation will be performed in the same manner.
Should you require additional copies or have any questions, please contact Christine Vilardi at (516) 756-8000, ext. 414.
Very truly yours,
HOLZMACHER, McLENDON & MURRELL, P.C.
P.E. Grosser,
CLV/kc End. cc: Pamela Hillis, Versar, Inc. (w/2 copies)
Supervisor Mardythe D. DiPirro Town Board, Town of Southampton John Bennett, Esq.
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MelviHe, N.Y, • Riverhead, N.Y. • Fairfield, N.J.
TOWN OF SOUTHAMPTON SUFFOLK COUNTY, NEW YORK
NORTH SEA LANDFILL
Remedial Investigation
PUBLIC HEALTH EVALUATION
JULY 1989
H2HGROUP r
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HOLZMACHER, McLENDON & MURRELL, P.C. \ CONSULTING ENGINEERS • ARCHITECTS • PLANNERS • SCIENTISTS • SURVEYORS \ ^ MELVILLe, N.Y. RIVERHEAD. N.Y. FAIRFIELD. N.J. , ^
. J
IN ASSOCIATION WITH \
Clement Associates Incorporated
H2MGROUP
NORTH SEA LANDFILL
PUBLIC HEALTH EVALUATION
TABLE OF CONTENTS
PAGE NO.
EXECUTIVE SUMMARY E.l
1.0 - INTRODUCTION 1.1
2.0 - SELECTION OF INDICATOR CHEMICALS 2.1
3.0 - EXPOSURE ASSESSMENT 3.1
3.1 - IDENTIFICATION OF EXPOSURE PATHWAYS 3.1 3.1.1 Surface Soils 3.2 3.1.2 Subsurface Soils 3.2 3.1.3 Surface Water . 3 . 3 3.1.4 Sediment 3.3 3.1.5 Air 3.4 3.1.6 Groundwater 3.5
3.2 - ESTIMATION OF EXPOSURE POINT CONCENTRATIONS 3.8 IN GROUNDWATER
4.0- COMPARISON OF APPLICABLE OR RELEVANT AND 4.1 APPROPRIATE REOUIREMENTS fARARs)
4.1
4.2
4.3
4.4
- GROUNDWATER
- SURFACE WATER
- SEDIMENT
- SOIL
5.0 - TOXICITY ASSESSMENT
5.1 - HEALTH EFFECTS CLASSIFICATION AND CRITERIA DEVELOPMENT
5.1.1 - Health Effects Criteria for Non-carcinogens
5.1.2 - Health Effects Criteria for Potential Carcinogens
4.2
4.9
4.12
4.12
5.1
5.1
5.2
5.2
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TABLE OF CONTENTS (CONT'D.)
6.0 - RISK CHARACTERIZATION
6.1 - POTENTIAL EXPOSURE TO GROUNDWATER
6.2
6.3
- DIRECT CONTACT WITH SURFACE SOILS BY LANDFILL WORKERS
- CONSUMPTION OF SHELLFISH FROM FISH COVE
REFERENCES
PAGE
6
6
6.
NO.
1
3
8
6.13
7.0 - CONCLUSIONS/RECOMMENDATIONS 7.1
7.1- SUMMARY OF COMPARISON TO ARARs 7.1
7.2 - SUMMARY OF THE QUALITATIVE RISK 7.3 CHARACTERIZATIONS
7.3 - RECOMMENDATIONS 7.6
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TABLE OF CONTENTS (CONT'D.)
LIST OF TABLES
TABLE NO. PAGE NO.
2-1 NORTH SEA LANDFILL INDICATOR CHEMICALS
3-1 NORTH SEA LANDFILL EXPOSURE PATHWAYS
3-2 GROUNDWATER EXPOSURE CONCENTRATION ESTIMATE
2.3
3.6
3.9
4-1 LIST OF POTENTIAL FEDERAL AND STATE ARARs
4-2 POTENTIAL GROUNDWATER ARARs FOR NORTH SEA LANDFILL
4.3
4.5
4-3 COMPARISON OF ARARs TO GROUNDWATER EXPOSURE ESTIMATES
4.7
4-4 POTENTIAL SURFACE WATER ARARs FOR NORTH SEA LANDFILL
4.10
4-5 POTENTIAL SEDIMENT ARARs FOR NORTH SEA LANDFILL
4.13
4-6 POTENTIAL SOIL ARARs FOR NORTH SEA LANDFILL 4.14
4-7 POTENTIAL SOIL ARARs VS. DETECTED VALUES 4.17 IN SOIL MEDIA FOR NORTH SEA LANDFILL
5-1 SUMMARY OF HEALTH EFFECTS CRITERIA FOR INDICATOR CHEMICALS
5.5
6-lA SUMMARY OF POTENTIAL EXPOSURES AND RISKS ASSOCIATED WITH INGESTION OF GROUNDWATER BASED ON SITE CONDITIONS
6.4
6-lB SUMMARY OF POTENTIAL EXPOSURES AND RISKS ASSOCIATED WITH INGESTION OF GROUNDWATER BASED ON GROUNDWATER CONDITIONS
6.5
6-2A SUMMARY OF POTENTIAL EXPOSURES AND RISKS ASSOCIATED WITH DIRECT CONTACT WITH SURFACE SOIL BY WORKERS
6.12
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TABLE OF CONTENTS (CONT'D.)
LIST OF TABLES
TABLE NO. PAGE NO.
6-2B SUMMARY OF POTENTIAL EXPOSURES AND RISKS 6.14 ASSOCIATED WITH DIRECT CONTACT WITH SURFACE SOIL BY WORKS - BASED ON BACKGROUND LEVELS OF INORGANICS
6-3 PHYSICOCHEMICAL PARAMTERS USED IN ESTI- 6.16 MATING UPTAKE OF CONTAMINANTS BY SHELLFISH - FISH COVE
6-4A SUMMARY OF POTENTIAL EXPOSURES AND RISKS 6.18 ASSOCIATED WITH INGESTION OF SHELLFISH FROM FISH COVE
6-4B SUMMARY OF POTENTIAL EXPOSURES AND RISKS 6.21 ASSOCIATED WITH INGESTION OF SHELLFISH FROM FISH COVE - BASED ON BACKGROUND LEVELS OF INORGANICS
LIST OF APPENDICES
APPENDIX A - CONCENTRATIONS OF CHEMICALS IN ENVIRONMENTAL MEDIA
APPENDIX B
APPENDIX C
GROUNDWATER EXPOSURE ESTIMATION METHOD
TOXICITY PROFILES
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Reference
Applicable or Relevant and Appropriate Requirements
Bioconcentration Factor
Carcinogen Assessment Group
Clean Air Act
Chronic Daily Intake
Cancer Potency Factor
Clean Water Act
Comprehensive Environmental Response, Compensation & Liability Act
Contract Laboratory Protocol
Food & Drug Administration
Health Effect Assessment
Integrated Risk Information System
Maximum Contaminant Levels
National Ambient Air Quality Standards
National Contingency Plan
New York State Department of Environmental Conservation
New York State Department of Health
Non-carcinogens
Occupational Safety & Health Act
Polynuclear Aromatic Hydrocarbons
Potential Carcinogens ;•
Public Health Evaluation!
Publicly-Owned Treatment Works Standards
ARARs
BCF
CAG
CAA
CDI
CPF
CWA
CERCLA
CLP
FDA
HEA
IRIS
MCLs
NAAQs
NCP
NYSDEC
NYSDOH
NCs
OSHA
PAHS
PCs
PHE
POTWs
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Reference
Remedial Investigation
Resource Conservation Recovery Act
Risk Reference Dose
Safe Drinking Water Act
Superfund Public Health Evaluation Manual
United States Department of Agriculture
United States Environmental Protection Agency
United States Geologic Survey
Water Quality Criteria
RI
RCRA
RfD
SDWA
SPHEM
US DA
USEPA
USGS
WQC
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EXECUTIVE SUMMARY
The Public Health Evaluation addresses the potential impacts
to human health associated with the Remedial Investigation at the
North Sea Landfill in the absence of remedial corrective actions,
This assessment therefore constitutes an evaluation of the no
action alternative required under Section 300.68 (f)(v) of the
National Contingency Plan.
It should be noted that the Public Health Evaluation has
been conducted using conseirvative assumptions according to the
general guidelines outlined by the United States Environmental
Protection Agency (USEPA). The purpose of using conservative
assumptions is to explore the potential for adverse health
effects using conditions that tend to overestimate risk. Con
sequently, the final estimates will usually be near or higher
than the upper end of the range of actual exposures and risks.
As a result, this risk assessment should not be construed as
presenting an absolute estimate of risk to human populations.
Rather, it is a conservative analysis intended to indicate the
potential for adverse impact to occur.
This assessment follows USEPA, Guidance for Risk Assessment
in General and for Superfund Sites in Particular (USEPA 1986a, b,
c, d). The Public Health Evaluation, thus, follows these steps: | , CO 1 w
1. Selection of indicator chemicals; ' >
2. Exposure assessment; §
3. Comparison with Applicable or Relevant and Appro
priate Requirements (ARARs);
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4. Toxicity assessment; and
5. Risk assessment.
Thirty (30) indicator chemicals were initially selected for
evaluation. The selection of chemicals is based on chemical
analytical data generated during the Remedial Investigation
conducted in the Fall of 1987 and Winter of 1988. These chemi
cals were detected in various environmental media including:
groundwater; Fish Cove surface water; landfill surface soil; Fish
Cove sediment; subsurface saturated soil at well installation
points; and subsurface landfill lagoon soil.
The chemicals detected in these environmental media which
were above defined background levels became the selected
"indicator" chemicals. The indicator chemicals were used for the
risk assessment, i.e., steps 2 through 5 as described above.
The major conclusions and recommendations, as presented
below, are based on the findings of the risk assessment. These
are grouped by potential exposure pathway. The selected po
tential exposure pathways by which populations may be exposed to
contaminants from the site are as follows:
» Exposure Pathway A - Ingestion of shellfish from
Fish Cove;
» Exposure Pathway B - Direct contact with surface
soil by landfill workers; and en
0 Exposure Pathway C - Ingestion of groundwater from ,
private wells by residents downgradient of the j o : if
landfill. The risk assessment was not really
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necessary for this exposure pathway because resi
dents downgradient from the landfill are already
hooked up to a public water system (Suffolk County
Water Authority). Nevertheless, a model was used
to estimate the potential migration of contami
nants from the landfill.
CONCLUSIONS
Conclusions for this Public Health Evaluation are based on
the risk characterizations for each exposure pathway and the
comparison of exposure estimates to available ARARs. ARARs are
not available for chemicals in the shellfish and soil media, and
thus, quantitative risk estimates are also developed by combining
the estimated intakes of potentially exposed populations with
health effects criteria. For groundwater, ARARs are available
and were compared with long-term concentration estimates.
Overall, remedial actions in each of the three exposure
pathways does not appear warranted. However, additional data is
needed to confirm that there is no risk to consumers of shellfish
from Fish Cove.
Potential Exposure Pathway A - Incfestion of shellfish from
Fish Cove. Exposure may occur as a result of the uptake of
contaminants from surface water into shellfish in Fish Cove sedi- ,
ments. This may be the exposure pathway with the most risk for , g
i the Remedial Investigation unless some data gaps are filled. I g
The risk characterization indicates that there does not I *>• i I I
appear to be any immediate risk to the consumers of shellfish^ ° i I °° 1
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from Fish Cove. Nevertheless, based on the conservative nature
of the assessment and the uncertainty in the lifetime cancer risk
assessment, resampling of sediments for DEHP is recommended.
In regards to ARARs, the Federal Water Supply Quality
Criteria (WQC) for selenium in the human health protection
category is the only available ARAR for comparison. This cri
teria is exceeded. Aquatic life protection criteria may also
apply.
Potential Exposure Pathway B - Direct contact with surface
soil. Exposure to surface soil may occur through incidental
ingestion of soil adhering to the hands of individuals working at
the landfill who eat, smoke, or drink following soil contact, and
by direct absorption of contaminants through the skin.
The remediation of surface soils at the landfill does not
appear warranted based on the assumptions and scenarios used in
the risk characterization. Furthermore, soil ARARs do not exist
at this time, but target cleanup levels can be used in place of
this. Based on this premise, further justification for no
remediation is given.
Potential Exposure Pathwav C - Ingestion of groundwater.
Exposure to groundwater may occur through the ingestion of
groundwater by residents downgradient of the landfill with I r CO
private supply wells that tap the Upper Glacial aquifer. How- } > I
ever, residents are not currently exposed to contaminants in , g
groundwater since all homes have been connected to Suffolk County \ ; o
Water Authority water supply. co 1 *»
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Despite this, the recently enforced drinking water standards
are exceeded in certain isolated cases. The Phase I Remedial
Investigation was performed before these more stringent standards
took effect. Because of this, and that the risk characterization
indicates concern, the wells should be resampled using lower
detection levels.
RECOMMENDATIONS
The conclusions for each exposure pathway indicate that
three major recommendations should be followed. These are:
1. Perform a study at Fish Cove.
This study will complete our understanding of human exposure
and potential risks to shellfish ingestion. A proposal is forth
coming which details a program that includes sediment sampling,
water quality measurements and shellfish analysis. The data
generated will also enable us to determine whether remediation is
necessary at Fish Cove.
The sediment sampling program would include experiments on
cores to determine the flux of leachate ions at the sediment-
surface water interface. This data, along with data generated
from the water sampling program would aid in determining the
amount of leachate being discharged into Fish Cove. In addition,
the sediments would be analyzed for phthalates to verify their
presence in Fish Cove sediments. DEHP is one phthalate ; M >
i identified in the risk characterization which is a potential
carcinogen.
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Finally, shellfish should be considered, since they exist in
the sediments and are filter feeders. Bioassays would be
performed on hard clam larvae to determine the toxicity
characteristics of leachate components. Adult hard clam tissue
should also be analyzed for bioaccumulated metals and leachate
components.
2. Further work in Exposure Pathway B is not warranted.
In regard to Exposure Pathway B (surface soil), there is no
apparent risk to human health. Therefore, sampling/analyses
and/or remediation is not warranted. However, obtaining a back
ground surface soil sample is recommended for comparative
purposes.
3. Resampling of groundwater monitoring wells
is warranted.
Resampling of groundwater monitoring wells will help deter
mine if there have been any changes in human health risk.
Groundwater remediation is not warranted in either case because
the human population is not exposed to groundwater; all residents
are hooked up to alternate public drinking water supplies.
It is recommended that the Remedial Investigation monitoring
wells be resampled and that samples be analyzed at lower
detection levels. The detection levels should be lower than the
more stringent New York State public drinking water standards.
The risk assessment will be performed using filtered as well as I co
total metals data for comparison. >
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1.0 - INTRODUCTION
This Public Health Evaluation (PHE) addresses the potential
impacts to human health associated with the North Sea Landfill in
the absence of remedial (corrective actions). This assessment,
therefore, constitutes an evaluation of the no action alternative
required under Section 300.68 (f)(v) of the National Contingency
Plan (NCP). Such an assessment will enable a determination to be
made of whether remedial actions beyond those already implemented,
(i.e., the installation of an alternate water supply for
residents near the landfill) are required for any areas of the
site.
It should be noted that this PHE has been conducted using
conservative assumptions according to the general guidelines
outlined by the United State Environmental Protection Agency
(USEPA). The purpose of using conservative assumptions is to
explore the potential for adverse health effects using conditions
that tend to overestimate risk. Consequently, the final
estimates will usually be near or higher than the upper end of
the range of actual exposures and risks. As a result, this risk
assessment should not be construed as presenting an absolute
estimate of risk to human populations. Rather, it is a
conservative analysis intended to indicate the potential for
adverse impact to occur. i
This assessment follows USEPA guidance for risk assessment ' > \
in general and for Superfund sites in particular (USEPA 1986a, b, ' %
c, d) and is based on data generated during the Remedial
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Investigation (RI) conducted in the Fall of 1987. The assessment
is organized as follows:
Section 2.0 - Selection of Indicator Chemicals.
Chemicals detected in environmental media samples
during the RI (groundwater, surface water, soil
and sediments) are identified. Those chemicals
present at levels above background are identified
for evaluation in the risk assessment.
Section 3.0 - Exposure Assessment. Potential
pathways by which populations may be exposed to
contaminants from the site are identified. Con
centrations of chemicals in environmental media at
potential exposure points are estimated. In the
case of groundwater, a model is developed to
estimate the potential migration of contaminants
from landfill cells.
Section 4.0 - Comparison to ARARs. Concentrations
of chemicals estimated from the groundwater model
are compared to Applicable or Relevant and Appro
priate Requirements (ARARs) such as Maximum
Contaminant Levels (MCLs) and New York State
Drinking Water Standards.
Section 5.0 - Toxicity Assessment. In this
section, the toxic characteristics of the
indicator chemicals are discussed and toxicity
criteria are identified. The methodology for the
quantitative risk assessment is.also reviewed.
1.2.
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Section 6.0 - Risk Characterization. Since ARARs
are not available for all chemicals in all media,
quantitative risk estimates are also developed by
combining the estimated intakes of potentially
exposed populations with health effects criteria.
Section 7.0 - Summary and Recommendations. In
this section the main features and conclusions of
the PHE are summarized and recommendations for
future actions are presented.
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2.0 - SELECTION OF INDICATOR CHEMICALS
USEPA Guidance on the Performance of Public Health
Evaluations (USEPA 1986a) states that in order to simplify the
assessment, if greater than 10 to 15 chemicals are present at a
site, those site-related chemicals most likely to contribute to
risk (referred to as indicator chemicals) may be selected for
evaluation in the assessment. As a conservative approach in this
PHE, all chemicals that were detected are selected as indicator
chemicals. Organic chemicals as well as inorganics may be
attributable to constituents placed in or released from the land
fill. However, the inorganics are also naturally occurring and
may be present in soil, water or sediment as a result of natural
background conditions. In this assessment all organics have been
retained for evaluation. However, where it has been determined
that a chemical is present at or near background levels, an
assessment of the risk associated with the background concen
tration is also presented. The chemicals are then dismissed as
contributing to potential risk, if the background risk is equal
to or greater than the risk at on-site or downgradient points.
Indicator chemicals were selected from the contaminants
detected in environmental media on-site and off-site. The
indicator chemicals were selected from the following environ
mental media sampled in the remedial investigation: on-site and
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off-site groundwater. Fish Cove surface water, landfill surface ; w
soil. Fish Cove sediment, lancJfill lagoon soils and on-site and
off-site subsurface saturated soil.
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Validated Contract Laboratory Protocol (CLP) analytical data
for the above media were reviewed in selecting indicator
chemicals. In some cases, organic chemicals were positively
detected below contract required detection levels. These values
are flagged with a "J"; however, they are considered valid
results and are to be used in the assessment. Some reported
values were rejected during the validation procedure but were
substituted with positively identified split samples. Values
flagged with a "B" indicate laboratory contamination. If these
•>B" values were not also rejected and were detected above
detection levels, they were also considered a detected value.
Selected reported data are summarized by environmental media
in Appendix A, Concentrations of Chemicals in Environmental
Media. For each chemical, the range of concentration values, the
representative concentration, the frequency of occurrence of
values detected above the detection level and the total number of
samples obtained are given. These values were determined for
sampling points in the study area and for background points.
The representative concentration is the mean of all values,
including those below detection levels per chemical. For those
reported below detection levels, one-half of the detection value
is used in calculating the mean. Additional specific details on
the determination of mean values is described in Appendix A.
Table 2-1, North Sea Landfill Indicator Chemicals, lists the ; [ CO
Pd chemicals and the environmental media in which they were >
detected. Several inorganics are noted in various media as being
at levels less than twice the background level. The potential
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TABLE 2-1
NORTH SEA LANDFILL
INDICATOR CHEMICALS
CHEMICAL
Benzene Chloroform 1,1-DCA
1,2-DCA
1.1-DCE
1,2-DCE Methylene chloride
Tetrachloroethylene Toulene
Trichloroethylene Phenol
DEHP
DNBP
DEP BBP Endosulfan
Carcinogenic PAHs (a)
Noncarcinogenic PAHs (b)
Ammonia arsenic
cadmium chromium
copper
iron
lead
manganese
mercury
nitrate/nitrite
nickel
selenium silver
thallium
zinc
• SURFACE WATER
--
----— — — — — ----— ----— — --
X --X (c) --— X — X --X — X — --—
GROUND
WATER
X X X X X X X X X X X X X X X X — —
X X X X X X X X X X X — X --X
(c)
(c) (c) (c)
(c)
(c)
(c)
(c)
SURFACE SOIL
— — --—
, --
— — — — — X X X X --X X
— X X X X — X — X — X — X --X
(c) (c) (c) (c)
(c)
(c)
(c)
SATURATED
SOIL
--. —
— ----~ — — — — X X X --— — —
— •
X X X X — X — — — X X X X X
(c) (c) (c) (c)
(c)
(c) (c) (c)
(c)
LAGOON
SOIL
X — ------X — — — --X --X — — — --
— X X X X — X — X — X — X — X
(c) (c.)
(c)
(c)
(c)
(c)
(c)
SEDIMENT
. .-
— — ----— — — — — X X --X
— •
— X
— — X (c) X (c) — — X (c)
— X (c) — — — •
— --X (c)
(a) benzo(a)anthracene, ben2o(a)pyrene, ben2o(b)flouranthene, benzo(k)flouranthene, chrysene, indeno(l,2,3-cd)pyrenp.
(b) benzo(g,h,i)perylene, fluoranthene, pryrene, phenanthrene. /
(c) Chemical was detected at less than 'twice the background level. Therefore, the PHE includes an
evaluation of the on-site concentration and the background concentration.
= Indicates that the chemical was not detected in this medium.
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exposures and risks from these chemicals were assessed relative
to the background concentrations.
Take the water media as an example. There are 29 chemicals
detected in groundwater. Based on the criteria noted above, 20
chemicals (16 organic and 4 inorganic) were identified as
occurring at greater than twice background and are retained for
assessment of both on-site and background levels. It is noted
here that total metals data in groundwater were used for this
revised groundwater assessment. It is our opinion that filtered
metals data should be included in the risk assessment along with
total metals data. An addendum will follow this revised
evaluation to support this premise.
In surface water there are six chemicals considered, and
five of these were identified occurring above iaackground. The
sampled soil media are summarized here in a similar manner.
There are 15 chemicals detected in landfill surface soils, and
eight were identified as occurring above background. As will be
explained in Section 5.0, polynuclear aromatic hydrocarbons
(PAHs) are divided into two groups according to whether they
exhibit carcinogenic or non-carcinogenic effects. Carcinogenic
and non-carcinogenic PAHs are each considered as one chemical for
risk assessment purposes in this PHE.
There are nine chemicals detected in Fish Cove sediments.
Four were selected as above background. None of the five
inorganics were present at greater than twice the background.
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There are 13 chemicals detected in landfill lagoon soils. Six of i ** o
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these were selected as above background. There are 13 chemicals
detected in subsurface landfill and off-site saturated soils.
Four of these were selected as above background.
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3.0 - EXPOSURE ASSESSMENT
3.1- IDENTIFICATION OF EXPOSURE PATHWAYS
Exposure pathways describe the mechanisms by which humans
may come in contact with (be exposed to) contaminants. An expo
sure pathway will depend on the physical and chemical properties
of the contaminants, use of the site and surrounding area, and
site characteristics such as geology, hydrology, soil properties
and climate. USEPA guidance on Superfund risk assessments
(1986c) defines an exposure pathway as consisting of the follow
ing elements:
1. a source and mechanism of chemical release to the
environment;
2. an environmental transport medium for the released
chemical (e.g., air, groundwater);
3. a point of potential human contact with the
contaminated medium (referred to as an exposure
point); and
4. a route of exposure at the exposure point (e.g.,
ingestion, dermal contact).
If all of the elements of the exposure pathway are present,
then that pathway is said to be "completed". Completed exposure
pathways are subject to evaluation in the PHE. For the purposes / ^
of this assessment, the sources of contamination at the North Sea/ *** / o
Landfill are the landfill Cell 1 and associated groundwater o
contamination. The following sections address release an(
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transport mechanisms, potentially exposed populations, and
exposure routes relative to each of the potential exposure media:
soil, surface water, sediment, air, groundwater.
In this assessment, both current and potential future expo
sure pathways are considered. Since the site is an active land
fill, future exposure pathways are developed assuming continued
use of the site as a landfill. Future development for resi
dential or industrial use is not anticipated in the foreseeable
future and is, therefore, not considered in this assessment.
3.1.1 - Surface Soils
Exposure to surface soils may occur as a result of direct
contact by trespassers or landfill workers. Soil may adhere to
the hands or other areas of exposed skin. Incidental ingestion
of soil may occur if individuals eat, drink. or smoke following
contact with soils. Organic contaminants may also be absorbed
directly through the skin. Exposure to trespassers is not
considered a completed pathway since site security prevents
access by trespassers. Security includes fencing to limit access
and a manned weigh scale to monitor all vehicles as they enter
and leave. Landfill workers, however, would be subject to expo
sure to surface soils. This exposure pathway is, therefore,
evaluated in this assessment.
3.1.2 - Subsurface Soils
Exposure to subsurface soils may occur as a result of CO
. . . . ' . w excavation or construction activities. Workers engaged in these ; > activities may be exposed through incidental ingestion, dermal o
o
o
en 3.2
H2MGROUP
absorption or inhalation of construction generated dust. This is
not considered a completed exposure pathway since the former
lagoon areas and landfill cells are closed and excavation in
these areas are not expected.
3.1.3 - Surface Water
The nearest surface water body to the North Sea Landfill is
Fish Cove. Contaminants may enter the cove via soil erosion,
surface runoff or groundwater discharge. Soil erosion and
surface runoff are not considered completed exposure pathways at
the North Sea Landfill because the site has a storm water
retention basin that prevents runoff from leaving the site. How
ever, shallow groundwater is believed to discharge into Fish
Cove. This provides a potential release and transport mechanism.
Populations potentially affected would include nearby residents
who swim or wade in the cove or who consume shellfish from the
cove. Swimming, wading or other recreational activities are not
known to take place in Fish Cove; consequently, these routes of
exposure do not represent completed exposure pathways: Consump
tion of shellfish is known to occur and will be assessed as a
completed exposure pathway.
3.1.4 - Sediment
Potential exposure pathways associated with sediments are
essentially the same as those for surface water. Contaminants
may reach the sediments in Fish Cove via soil erosion, surface CO w >
runoff or groundwater discharge. The storm water retention basin i o I o I **
on site prevents soil erosion and surface runoff from exiting the j o
1
3.3
H2MGROUP
site; however, groundwater discharge and subsequent sorption of
contaminants onto sediments represents a potentially completed
exposure pathway. As with surface water, contact with sediments
through swimming or wading are not expected to occur in Fish
Cove. However, contaminants in sediments may be transferred to
sediment pore water and thus be available for uptake by shell
fish. Shellfish consumption will therefore be evaluated as a
completed exposure pathway.
3.1.5 - Air.
Release and transport mechanisms associated with air
exposure include .wind erosion of contaminated surface soils,
volatilization or organics from surface soils and release of
chemicals through landfill gas emissions. At the North Sea Land
fill, most of the site is vegetated so that wind erosion is not
expected. The area of the future cell is not vegetated and dust
generation occurs in this area. However, soil sampling did not
reveal any contaminants in this area; therefore, this is not
considered a completed exposure pathway. The organic contami
nants detected in a few of the surface soils consisted of poly
nuclear aromatic hydrocarbons (PAHs) and phthalates. Both have
relatively low volatility and would not be expected to produce
significant air emissions. Therefore, volatilization from soils
is not considered a completed exposure pathway. Soil gas moni
toring with field instruments revealed the presence of chemicals
(primarily methane) in soil gas. These chemicals may diffuse ' en
I >
into the air and reach nearby residents, thus representing a 1 ° >i>
o 00
3.4
H2MGROUP
completed exposure pathway. Ambient air monitoring at the site,
however, did not reveal any detectable level of contamination.
Consequently, any potential risk from this completed exposure
pathway cannot be quantified.
3.1.6 - Groundwater
Contaminants may be released to groundwater by leaching from
contaminated soils or by generation of leachate within the land
fill cells. E.P. Toxicity tests of soils from the site suggest
little potential for leaching, therefore, this potential exposure
pathway is not considered. Leachate generation has resulted in
the migration of contaminants off-site. However, all residents
in the area have been placed on the Suffolk County Water
Authority public water system. . There is currently no use of
groundwater, as a drinking water supply in the impacted area; and
consequently, nc? completed groundwater exposure pathway. A
hypothetical exposure pathway exists if it is assumed that a
drinking water well could be established off-site at some time in
the future. In keeping with the conservative nature of this risk
assessment, the potential migration of leachate from the landfill
cells and its potential impact on off-site groundwater will be
evaluated in this assessment.
Table 3-1, North Sea Landfill Exposure Pathways^ summarizes
the discussion of exposure pathways presented above. The follow- .
ing potential exposure pathways will be evaluated in the follow- co . 1 M
ing sections: >
1 o
direct contact with surface soils by on-site land- \ °
fill workers; o [ *-
3.5
TABLE 3-1 NORTH SEA LANDFILL EXPOSURE PATHWAYS
I o d
Exposure medium Release/transport mechanism Potentially Exposed Population Completed exposure pathway ?
SURFACE SOIL
SUBSURFACE SOIL
Direct contact
Direct contact during excavation or construction.
Tresspassers
Workers on-site
Workers on-site
No - Site security would prevent tresspassing
Yes - Dermal absorption of organics and incidental soil ingestion while working on site.
No - Lagoon and cell areas are closed. No activities planned to disturb soil in these areas.
SURFACE WATER
CO
05
Discharge of leachate into Fish Cove
Runoff of contaminated surface water; erossion of contaminated surface soils.
Nearby residents who swim or wade in Fish Cove or who consume shellfish from Fish Cove.
Nearby residents who swim or wade in Fish Cove or who consume shellfish from Fish Cove.
Yes - shellfish consumption only. Fish Cove not subject to other recreational uses.
No - Drainage system prevents off-site migration of surface water or sediment.
SEDIMENT Discharge of leachate into Fish Cove; accumulation in sediments.
Nearby residents who swim or wade in Fish Cove or who consume shellfish from Fish Cove.
Yes - shellfish consumption only. Fish Cove not subject to other recreational uses.
Runoff of contaminated surface water; erossion of contaminated surface soils.
Nearby residents who swim or wade in Fish Cove or who consume shellfish from Fish Cove.
No - Drainage system prevents off-site migration of surface water or sediment.
ooso ^00 'tfas
TABLE 3-1 NORTH SEA LANDFILL EXPOSURE PATHWAYS
I o ~G
Exposure medium Release/transport mechanism Potentially Exposed Population Completed exposure pathway ?
AIR
GROUNDWATER
CO
<1
Release of chemicals through landfill gas emissions.
Volatilization from surface soils.
Wind erossion
Leachate migration
Leaching from contaminated soil.
Nearby residents.
Nearby residents.
Nearby residents.
Nearby residents using groundwater
Nearby residents using groundwater
Yes - however; no contaminants detected in air samples - risk cannot be quantified.
No - Only low volatility organics (PAHs, phthalates) detected in soil.
No - most of site is vegetated and protected from wind erossion. Only dusty area Is the porposed future cell where no contaminants were detected in surface soil.
No - all residents on city water system. However this pathway will be evaluated in terms of a hypothetical well off-site.
No - EP tox results show little potential for leaching of inorganics. Only organics detected are phthalates which have high soil-water partition coefficients - would not be expected to leach.
XOSO ^00 >?3S
H2MGROUP
consumption of shellfish from Fish Cove; and
ingestions of groundwater from a hypothetical
downgradient well.
3.2 - ESTIMATION OF EXPOSURE POINT CONCENTRATIONS
IN GROUNDWATER
Exposure point concentrations were estimated in groundwater
using mean and maximum concentration values reported for each
groundwater indicator chemical. These values were used to
predict the concentration change as the chemicals migrate from
the landfill with groundwater flow. The mean and maximum values
are, thus, considered initial concentrations. The initial and
predicted exposure point concentrations are in Table 3-2, Ground
water Exposure Concentration Estimates, a. Site and b. Back
ground .
The source of contamination is assumed to be the inactive
landfill Cell 1. The release medium for this exposure pathway is
via groundwater. Leachate is generated at the source via perco
lating rainwater. The human receptor area is downgradient from
Cell 1 in a hypothetical future well near the local discharge
area (Fish Cove). The potential human exposure route is in
gestion.
The most conservative approach, aside to using the actual i \ Ui 1 w
detected concentrations, was used to estimate groundwater ; >
exposure concentrations. The groundwater exposure estimation
method is based on a soil contaminant evaluation methodology
o o
o 1 o IO
3.8
iTIMGRCUP
TABLE 3-2
GROUNDWATER EXPOSURE CONCENTRATION ESTIMATES
a. SITE * (mg/1)
Indicator Chemical
Benzene
Chloroform
1,1-DCA
1,2-DCA
1-,1-DCE
1,2-DCE
Methylene" Chloride
PCE Toluene
TOE Phenol
DEHP
DNBP
DEP
BBP Endosulfan I
Endosulfan 11
Anmonia
Arsenic
Cadmium
Chromium
Copper
Iron
Lead
Manganese
Mercury
Nickel
Nitrate/Nitrite
Si Iver
Zinc ;•
Initial Grot ndwater
Concentration
Mean
l.OOE-03 NR.
NA
2.70E-03-
' NA •
NA
2.7'0E-03
2.00E-03 NR
3.50E-03
2.50E-03
3.30E-03
2.00E-03 NR
3.50E-02
NA
NA
NA NA
NA
1.17E+01
7.60E-03
9.60E-03
2.90E-02
1.20E-01
3.09E+01
3.00E-02
1.41E-01
1.80E-04
4.30E-02
5.60E-02
NA
1.21E-01
Maximum
l.OOE-03
NA 3.00E-03
NA NA
4.bOE-03
2.00E-03
7.00E-03
3.00E-03
7.0OE-03
2.00E-03
1.40E-01
NA
NA,
NA NA
NA
4.45E+01
1.40E-02
2.00E-02
7.80E-02
2.70E-01
4.58E+01
6.30E-01'
3.04E-01
4.00E-04
I.OOE7OI
l.OOE+00
NA
3.00E-01
JB
J
J
JB
NE
Predicted
Concentrat
Best Case
9.7SE-04
NA
2.59E-03
NA NA
2.59E-03
1.95E-03
3.41E-03
2.44E-03
3.22E-03
1.95E-03
3.41E-02
NA
NA
NA
NA
NA
1.14E+01
7.40E-03
9.40E-03
2.83E-02
1.17E-01
3.01E+01
2.93E-02
1.38E-01
1.70E-04
4.20E-02 -
6.40E-02
NA
1.18E-01
ion
Worst Case
9.75E-04
NA 2.93E-03
NA
NA 3.90E-03
1.95E-03
6.83E-03
2.93E-03
6.83E-03
1.95E-03
1.36E-01
NA
NA
NA
NA
NA
4.34E+01
1.36E-02
1.95E-02
7.60E-02
2.63E-01
4.47E+01
6.14E-01
2.96E-01
3.90E-04
9.75E-02
9.75E-01
NA
2.93E-01
CO M >
o o
o en o 00
3.9
UZHGROUP
TABLE 3-2 (Continued)
GROUNDWATER EXPOSURE CONCENTRATION ESTIMATES
b. BACKGROUND + (mg/1)
Indicator
Benzene
Chloroform
1,1-DCA'
1,2-DCA
1,1-DCE-
l',2-DCE •.
Methylene
PCE
Toluene
TCE
Phenol
DEHP
DNBP
DEP
BBP
Endosulfan
Endosulfan
Ammonia
Arsenic
Cadmium
Chromium
Copper
Iron
Lead
Manganese
Mercury
Nickel
Nitrate/Ni
Silver
Zinc.
Chemical
Chloride
I
II
trite
Initial Grou ndwater
Concentration
Mean
l.OOE-03 NR
l.OOE-03 NR
NA
NA
NA
NA
1.40E-02
NA
2.00E-03 NR
NA
9.00E-04
l.OOE-02 •
NA
NA
.3.80E-03
NA
NA
5.00E-02 "
NA
1;80E-02
2.50E-02
1.30E-01
1.34E+01
1.02E-01
5.30E-01
2.00E-04 •
4.00E-02
2.00E-01
6.00E-03
1.97E-01 •
Maximum
l.OOE-03
l.OOE-03
NA
NA
NA
NA
1.50E-02
NA
;2.00E-03
NA
3.00E-03
1.90E-02
NA
NA
•l.lOE-02
NA
NA
1.70E-01
NA .•
5.00E-02
6.20E-02
1.80E-01
2.10E+0O
1.55E-01
8.40E-01
5.00E-04.
1.20E-01
4.00E-01
l.OOE-02
2.76E-01
JB
J
B
J
B
E
Predicted
Concent
Best Case
8.67E-04
8.67E-04
NA
NA
NA
NA
1.20E-03
NA
2.08E-03
NA
7.80E-04
8.67E-03
NA
NA
.3.29E-03
NA
NA
4.34E-02
NA
1.56E-02
2.17E-02
1.13E-01
1.16E+01
8.86E-Q2
4.59E-01
1.73E-04
1.73E-01
3.47E-02
5.20E-03
1.70E-01
ration
Worst Case
8.67E-04
8.67E-04
NA
NA
NA
NA-
1.30E-02
NA
1.70E-03
NA
2.60E-03
1.65E-02
NA
NA
9.50E-03
NA
NA
1.47E-01
NA
4.34E-02
5.40E-02
1.56E-01
1.82E+00
1.34E-01
7.28E-01
4.34E-04
1.04E-01
3.47E-01
8.70E-03
2.39E-01
*Mean and maximum values from well couplet MW-3, rounds 1 and 2.
+Mean and maximum values from well couplet MW-1, rounds .1 and 2.
NA = Not Applicable. Chemical was not detected in the wells used for the
initial concentration estimates.-
NR = Mean value was not reported; mean is greater than maximum due to
values below the detection limit. The maximum is used for both va.lues In
these cases.
J = Estimated value below the detection limit.
B = Chemical detected in blanks.
3.10
CO
>
o o
o Ln o
H2MGPOUP
(CH2M Hill Southeast, 1985). This simple model, with assumptions
is fully described in Appendix B, Groundwater Exposure Estimation
Method. The model contains several simplifying assumptions. It
does not account for loss/decay, chemical reaction, retardation,
longitudinal dispersion, or recharge dilution. Therefore, the
estimates will be conservative. As can be seen in Table 3-2, the
resulting exposure concentrations are only slightly less than the
initial concentrations under site conditions and are, therefore,
very conservative estimates. These estimates will be used in
comparison with ARARs and for the risk characterization.
CO
>
o o
o en o
3.11
H2MGROUP
4.0--- COMPARISON OF APPLICABLE OR RELEVANT AND
APPROPRIATE REOUIREMENTS
Federal and State potentially Applicable or Relevant and
Appropriate Requirements (ARARs) were compared to detected indi
cator chemical concentrations in groundwater, surface water,
sediment and surface soils.
The ARAR comparison helps to determine the extent to which
Federal, State and other environmental and public health require
ments are applicable or relevant and appropriate to the study
site. Such criteria, advisories or guidance and standards are to
be used in developing appropriate remedial action for the site.
"Applicable" requirements are defined as Federal require
ments for hazardous substances that would be legally applicable
or enforceable by either a Federal or an authorized State program
if this response were not undertaken pursuant to the Compre
hensive Environmental Response, Compensation and Liability Act
(CERCLA), Section 104 or 106. Certain Federal requirements, such
as those under the Resource Conservation Recovery Act (RCRA), are
"applicable" although other Federal requirements may not be
"applicable".
"Relevant and appropriate" requirements are defined as those
Federal requirements designed to apply to problems similar to 3
. • • . / ^ those encountered at the CERCLA site and their application is i
— ™ - - - " •'•"'" • — " ' i ^ the requirements discussed below with respect to the North Sea / o
o ,' <n ,
4.1
•H2MGROUP
Landfill are in the "relevant and appropriate" category. These
include the Safe Drinking Water Act (SDWA) Primary Drinking Water
Standards (MCLs), Federal Water Quality Criteria, Clean Water Act
(CWA), Federal and State Occupational Safety and Health Act
(OSHA) requirements, and State Drinking Water Standards.
Table 4-1, List of Federal and State ARARs. lists the proba
ble applicability of all available Federal and State ARARs for
this site. The applicable ARARs, except for RCRA, Clean Air Act
(CAA) and New York State Department of Environmental Conservation
(NYSDEC) Part 360, are discussed below in relation to Phase I RI
results.
4.1 - GROUNDWATER
Table 4-2, Potential Groundwater ARARs. provides the actual
concentration values of Federal and State ARARs for groundwater.
The most stringent ARARs listed in Table 4-2 were compared with
the estimated groundwater exposure point concentrations. The
comparison can be seen in Table 4-3, Comparison of ARARs to
Groundwater Exposure Estimates. For each indicator chemical the
following are listed: the most stringent ARAR, projected long-
term and short-term exposure concentrations and concentration to
standard ratios. | CO
The concentration to standard ratio is a comparison of the n
projected exposure concentration to the ARAR. If this value ^
exceeds one, then the ARARs are exceeded. Predicted concentra-
o
tions of PCE, TCE and BEHP exceed ARARs for the worst case only. | g o o
4.2
H2MGROUP
TABLE 4-1
LIST OF POTENTIAL FEDERAL AND STATE ARARs
Safe Drinking Water Act (SDWA)
Maximum Contaminant Levels (MCLs) MCL Goals (MCLGs) Secondary MCLs (SMCLs)
National Interim Primary Drinking Water Regulation (NIPDWR)
Clean Water Act
Ambient Water Quality Criteria (WQC) Publicly-Owned Treatment Works (POTW)
Standards Effluent Limitations and Guidelines Requirements for Dredge and File
Activities
Toxic Substances Control Act (TSCA)
Polychlorinated bipenals (PCB) Standards
Clean Air Act (CAA)
National Ambient Air Quality Standards (NAAQs)
Potentially Applicable Potentially Applicable Potentially Applicable
Potentially Applicable
Potentially Applicable
Not Applicable Not Applicable Not Applicable
Not Applicable
Potentially Applicable
Resource Conservation and Recovery Act (RCRA)
Subtitle C (Hazardous Waste Requirements)"
Subtitle D (Solid Waste Requirements)
Potential Soils ARARs
Potential Sediment ARARs
Food and Drug Administration (FDA) Guidelines
Not Applicable
Applicable
Applicable
Applicable
Applicable CO
cq >
o o
o en o 00
4.3 v_..
|-|2yHGROUP
TABLE 4-1 (CONT'D.)
NYSDEC. Groundwater Standards and Guidance Values Class 6A, 6 NYCRR Part 703
NYSDEC, Surface Water Standards, Class B, 6 NYCRR Part 703
NYSDOH. Public Drinking Water Standards, Sanitary Code Support S-1
Clean Air Act (CAA), Site Implementation Plan (SIP)
NYSDEC. Div. of Solid Waste, Solid Waste Management Facilities, 6 NYCRR Part 3 60
Applicable
Applicable
Applicable
Not Applicable
Applicable
CO
>
o o
o Ul o
4.4
TABLE 4-2 POTENTIAL GROUNDWATER ARARS
tft.
CJl
CHEMICAL (A)
Volatile organic compounds
Acetone Benzene Carbon dioxide Chlorobenzene (L) Chloroform 1,l-Dichloroethane 1,2-Dichloroethane 1, l-Dichloroethene 1,2-Dichloroethene
Dichloromethane (Methylene chloride) Hexane Tetrachloroethene Toluene
1,1,l-Trichloroethane Trichloroethane Vinyl Chloride
Semivolatile organic compounds
6-Amino-hexanoic acid b i s(2-ethy1hexy1)phthalate Butylbenzylphthalate Oi-N-octylphthalate Dodecanoic acid Molecular sulfur (H)
Pesticides
Endosulfan I Endosulfan II
Target analyte list
Aluminum Arsenic Barium Beryllium Cadmium Calcium Chromium Cobalt
NYSDEC GROUNDWATER. STANDARDS (CLASS GA) UG/L) (B)
NA ND NA
20 (6) 100
50 (G) 0.8 (G)
0.07 (Gl 50 (G) (G) NA
,0.7 (G) 50 (G 50 (G) 10 5
NA 4200 50 (G) 50 (G) NA " NA.
NA NA
NA . 2 5
1000 3 (G) 10 NA 50 NA
NYSDOH PUBLIC DRINKING WATER STANDARDS (UG/L) (C)
50 5 50 5 • 50 5 5 5 5 5 50 5 5 5 5
50
50 50 50 50 50 A
50 50
NA 50 1000 NA 10 NA 50 NA
NIPDWR (UG/L) (0)
NA NA NA NA 100 NA NA NA NA NA NA NA NA NA NA NA
NA NA NA NA NA NA
NA NA
NA 50 1000 NA 10 NA 50 NA
SOWA MCLG (UG/L) (E)
NA 0 NA NA NA NA 0 7 NA NA NA 0
2000 200 0 0
NA NA NA NA NA NA
NA NA
NA 0
5000 NA 5 NA 100 NA
SDWA MCL (UG/L) (F)
NA 5 NA NA NA NA 5 7 NA NA NA 5
2000 200 5 2
NA NA NA NA NA NA
NA NA
NA 30 5000 NA 5 NA 100 NA
SDWA SMCL (UG/L) (H)
NA • NA NA NA NA NA NA NA NA NA NA NA 40 NA NA NA
NA NA NA NA NA NA
NA NA
50 NA NA NA NA NA NA NA
RCRA MCLS (UG/L) (I)
NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA
NA NA NA NA NA NA
NA NA
NA 50 1000 NA 10 NA 50 NA
I o -D
Copper 1000 1000 NA NA NA 100 NA
0150 ^00 ^zas
TABLE 4-2 (Continued) POTENTIAL GROUNDWATER ARARs FOR NORTH SEA LANDFILL- I
o d "TO
•CHEMICAL (A)
NYSDEC GROUNDWATER STANDARDS CLASS GA) UG/L) (B)
NYSOOH PUBLIC DRINKING WATER STANDARDS (UG/L) (C)
NIPDWR (UG/L) (D)
SDWA MCLG (UG/L) (E) •
SDWA MCL (UG/L) (F)
SDWA SMCL (UG/L) (H)
RCRA MCLS (UG/L) (I)
Target analyte list (Continued)
Manganese Mercury Nickel Potassium SiIver Sod i urn • Thallium Vanadium Zinc
Miscellaneous-
.Anmonia Chlorides
• N i t r a t e - N i t r i t e Phenols Total dissolved solids Total organic carbon
300 2 NA NA 50 NA
4 (G) NA
5000
NA 250,000 10,000
1 1,000,000
NA
300 (J) 2 NA NA 50 NA NA NA 5000
NA 250,000
10,000 (K) NA NA NA
NA 2 NA NA 50 NA NA NA NA
NA -NA NA NA NA NA
NA-2 NA NA NA NA ' NA •. . NA NA
NA NA
10,000 NA NA NA
NA 2 NA NA NA NA NA NA NA
NA NA
. 10,000 NA NA NA
50 NA NA NA 50 NA NA NA
5000
NA 250.000 NA NA
500,000 NA
NA 2 NA NA 50 NA NA NA NA
NA NA NA NA NA NA
(A) (B) (C)
(D)
(E)
(n (G) (H) (1) (J) (K) (L) (M)
- Values provided by USEPA - New York State Department of Environmental Conservation. Groundwater Quality Regulation 6 NYCRR Part 703. - State of New York, Official Compilation of Codes, Vol. 10 Subpart 5-1. Revision of NYSOOH. Subpart 5-1 State Sanitary Code
effective 1/9/89. 5 ppb for principal organic compounds (POCs) and 50 ppb for unspecified organic compounds (UOCs) - National Interim Primary Drinking Water Regulation (NIPDWR). Interim enforceable drinking water regulations first established under the Safe Drinking Water Act (SDWA) that are protective of public health to the extent feasible. - SDWA MCL Goals (MCLGs) are nonenforceable health goals for public water systems (40 CFR 141.52 and 50 FR 46936). - SDWA Maximum Contaminant Level (MCLs) are adopted as enforceable standards for public drinking water systems (40 CFR 141.11-141 1.6). - Guidance value. - SDWA secondary MCLs based on taste and odor detection limits. - RCRA MCLs have been adopted as part of RCRA groundwater protection standards (40 CFR 264.94) - If iron and manganese are present, the total concentration of both should not exceed 0.3 mg/1. - Nitrate (as N ) . - Health based criteria for systemic toxicants is O.OOlug/1. Table 8-7 of Development of•an RFI Work Plan and General Considerations
for RCRA Facility Investigations. - Laboratory reported molecular sulfur under tentatively identified semi-volatiles.
TTso POO vas
li^AiGROUP
TABLE 4-3
COMPARISON OF ARARS TO GROUNDWATER EXPOSURE ESTIMATES
ARARs
Drinking Water Standards
Projected Exposure
Concentration (riig/l)
Concentration:Standard Ratio
(Projected Exposure
ConcentratIon:ARAR)
Chemical Standard Source Best Case Worst Case Best Case Worst Case
SITE *
Benzene
Chloroform
1,1-DCA
1,2-DCA
1,1-DCE
1,2-OCE
Methylene Chloride
PCE Toluene
TCE
Phenol
DEHP
DNBP
DEP BBP Endosulfan I
Endosulfan II
Armion i a
Arsenic
Cadmium
Chromium
Copper
Iron
Lead
Manganese
Mercury
Nickel
Nitrate/Nitrite
Silver
Zinc
5.00E-03
5.00E-02
5.00E-03
5.00E-03
5.00E-03
5.00E-03
5.00E-03
5.00E-03
5.00E-03
5.00E-03
l.OOE-03
5.00E-02
----
5.00E-02
5.00E-02
5.00E-02
__
2.50E-02
5.00E-03
5.00E-02
l.OOE-01
3.00E-01
5.00E-03
5.00E-02
2.00E-03
--
l.OOE+01
5.00E-02
5.00E+00
9.75E-04
NA
2.59E-03
NA
NA
2.59E-03
1.95E-03
3.41E-03
2.44E-03
3.22E-03
1.95E-03
3.41E-02
NA
NA
NA
NA
• NA
1.14E+01
7.40E-03
9.40E-03
2.83E-02
1.17E-01
3.01E+01
2.93E-02
1.38E-01
1.70E-04
4.20E-02
6.40E-02
NA
1.18E-01
9.75E-04
NA
2.93E-03
NA
NA
3.90E-03
1.95E-03
6.83E-03
2.93E-03
6.83E-03
1.95E-03
1.36E-01
NA
NA
NA
NA
NA
4.34E+01
1.36E-02
1.95E-02
7.60E-02
2.63E-01
4.47E•^01
6.14E-01
2.96E-01
3.90E-04
9.75E-02
9.75E-01
NA
2.93E-01
1.95E-01
NA
5.18E-01
NA
NA
5.18E-01
3.90E-01
6,82£-01
4.88E-01
6.44E-01
1.95E+00
6.82E-01
NA
NA
NA
NA
NA
2.96E-01
i;88E+00
5.66E-01
1.17E+00
l.OOE+02
5.86E+00
2.75E-f00
8.50E-02
6.40E-03
NA
2.36E-02
1.95E-01
NA
5.86E-01
NA
NA
7.80E-01
3.90E-01
1.37E-t-00
5.86E-01
1.37E-f00
1.95E+00
2.72E+00
NA
NA
NA
NA
NA
5.44E-01
3.90E+00
1.52E-^00
2.63E-^00
1.49E+02
1.23E+02
5.93E+00
1.95E-01
9.75E-02
NA
5.85E-02
i CO I ^ I > I o o
I. *>.
o en
lo
4.7
li2MGROUP
TABLE 4-3 (ConMnued)
COMPARISON OF ARARS TO GROUNDWATER EXPOSURE ESTIMATES
ARARs . Projected Exposure
Drinking Water Standards Concentration (mg/1)
Concentration:Standard Ratio
(Projected Exposure
Concentrat i on:ARAR)
Chemical Standard Source Best Case Worst Case Best Case Worst Case
b. BACKGROUND
Benzene
Chloroform
1,1-DCA
1,2-DCA
1,1-DCE
1,2-DCE
Methylene Chloride
PCE
Toluene
TCE'
Phenol
DEHP •
DNBP
DEP
BBP
Endosulfan I
Endosulfan II
Ammonia
Arsenic
Cadmium
Chromium
Copper
Iron
Lead
Manganese
Mercury
Nickel
Nitrate/Nitrite
Silver
Zinc
5.00E-03
5.00E-02
5.00E-03
5.00E-03
5.-00E-03
5.00E-03
5.00E-03
5.00E-03
5.00E-03
5.00E-03
l.OOE-03
5.00E-02
—
--
5.00E-02
5.00E-02
5.00E-O2
--
2.50E-02
5.00E-03
5.00E-02
l.OOE-01
3.00E-01
5.00E-03
5.00E-02
2.00E-03
-.-
l.OOE+01
5.00E-02
5.00E-I-00
a
a
a
a
a
a
a
a
a
a
b
a
a
a
a
b
c
a
d
a
. e
d
a
a
a
a
8.67E-04
8.67E-04
NA.
NA ,
NA
NA
1.20E-03 .
NA
1.70E-03
NA
7.80E-04
8.67E-03
NA
NA
3.29E-03
NA
NA
4.34E-02
NA
1.56Er02
2.17E-02
1.13E-01
1.16E+01
8.86E-02
4.59E-01
1.73E-04
1.73E-01 ,
3.47Er02
5.20E-03
1.70E-01
8.67E-04
8.67E-04
NA
NA
NA
NA
1.30E-02
NA
. 1.70E-03
NA
2.60E-03
1.65E-02
NA
NA
9.50E-03
NA
NA
1.47E-01
NA
4.34E-02
5.40E-02 ,
1.56E-01
1.82E+00
1.34E-01
7.28E-01
4.34E-04
1.04E-01
3.47E-01
8.70E-03
2.39E-01
1.73E-01
1.73E-02
• NA
NA
NA
NA
2.40E-01
NA
3.40E-01
NA
7.80E-01
1.73E-01
NA
NA
6.58E-02
NA
NA
—
NA
3.12E+Q0
4.34E-01
1.13E-I-00
3.87E+01
1.77E-t-01
9.18E+00
8.65E-02
--
3.47E-03
1.04E-01
3.40E-02
1.73E-01
1.73E-02
NA
NA
NA
NA
2.60E+00
NA
3.46E-01
NA
2.60E+00
3.30E-01
NA
NA.
1.90E-01
NA
NA
-- .
NA
8.68E+00
1.08E+00
1.58E+dO
6.07E+00
2.68E+01
1.45E+01
2.17E-01
—
3.47E-02
1.74E-01
4.78E-02
*Mean and maximum values from well couplet MW-3, rounds 1 and 2.
+Mean and maximum values from well couplet MW-1, rounds 1 and 2.
a - NYSDOH Public Drinking Water Standards
b - NYDEC Groundwater Standards (Class GA)
c - SDWA MCL (Proposed)
d - SDWA Secondary MCL (Based on organoleptic criteria)
CO IS
>
o o
o en
U)
4.8
H2MGROUP
Predicted concentrations for the best case do not exceed ARARs
for these compounds. The worst case is based on the maximum
detected value and the best case is based on the mean value of
the compound. Predicted concentrations of cadmium, chromium
(worst case only) copper, iron, lead and manganese also exceed
potential ARARs for both the predicted values based on site
conditions and those based on background conditions. This
suggests that naturally occurring levels of some inorganics may
exceed some health-based or secondary criteria. Concentrations
of phenol also exceed ARARs for both the on-site and background
cases. The background methylene chloride concentrations exceed
ARARs for the worst case only.
4.2 - SURFACE WATER
There are five selected indicator chemicals detected in Fish
Cove surface water. The applicable ARARs for New York State
ambient Class B waters and Federal ambient Water Quality Criteria
(WQC) can be seen in Table 4-4, Potential Surface Water ARARs.
The indicator chemicals exceeding ARARs are cadmium, iron,
manganese and selenium. Detected site and background concentra
tions are compared against potential surface water ARARs in Table
4-4.
Maximum and mean site and maximum background concentrations
of cadmium in Fish Cove surface waters exceeded Federal ambient
WQC for the protection of aquatic life in freshwater (both acute
and chronic criteria). The maximum site and background concen-
co
>
o o
trations were equivalent to the Federal ambient WQC for the ; o Ul
4.9
TABLE 4-4 POTENTIAL SURFACE WATER AREAS FOR NORTH SEA LANDFILL
5^
o d
CHEMICAL
N.Y.S. SURFACE WATER STANDARDS (CLASS B) (UG/L)
FEDERAL AMBIENT WATER QUALITY CRITERIA FOR THE PROTECTION OF AQUATIC LIFE (UG/L)
FEDERAL AMBIENT WATER QUALITY CRITERIA FOR THE PROTECTION OF HUMAN HEALTH (UG/L)
FRESH ACUTE CRITERIA
FRESH CHRONIC CRITERIA
MARINE ACUTE CRITERIA
MARINE CHRONIC CRITERIA
WATER AND FISH INGESTION
FISH ONLY
WATER ONLY
Total metals
4^
o
Aluminum Cadmium (*) Calcium Chromium (+) Chromium III Chromium IV Copper (*) • Iron Magnesium Manganese Potassium Selanium Sodium-Zinc
Miscellaneous
Ammonia (#) Chlorides Dissolved solids (salinity) Nitrates Nitrate-nitrite Total organic carbon
100 21.5 NA
4449 290 11 290 300 NA NA NA 1.0 30 58
2580 NA NA NA NA NA
NA 3.9 NA NA
18 (a) 16
18 (a) NA NA NA NA 260 NA 320
NA NA NA NA NA NA
NA 1.1 NA NA
210 (a) 11
. 12 (a) 1000 NA NA NA 35 NA 47
NA NA , NA NA NA NA
NA 43 NA NA
10300 (a) 1100 2.9 NA NA NA NA 410 NA-170
NA NA NA NA NA NA
NA 9.3 NA NA NA 50 2.9 NA NA NA NA 54 NA 58
NA NA NA NA NA NA
NA 10 NA NA
170,000 50
1000 - - . 300
NA 50 NA 10 NA 5
NA NA
250,000 10,000 NA NA
NA . • NA NA NA
3,433,000 NA NA •• NA NA 100 NA NA NA NA
NA NA NA NA NA NA
NA 10 NA NA
179,000 50
1000 NA NA NA NA 10 NA 5
NA NA NA NA NA NA
(a) - Insufficient data to develop criteria. Value presented is the the lowest observed effect level (LOEL).
{+) - Human criteria for carcinogens reported for 10-5 risk level. (*) - Average value of 238 ppm of calcium and 884 of magnesium was used to
to calculate hardness as follows: Hardness, mg equivalent CaC03/L - 2.497(ca, mg/L) -4.118(Mg, mg/L) - 4235
(#) - Average values of 15 C temperature and 7.5 pH were used.
SOURCES: Guidance on Remedial Actions for Contaminated Groundwater at Superfund Sites. Final Review Draft, August 1988. Superfund Public Health Evaluation Manual, EPA/540/1-86/060, October 1986. RFI Guidance Vol I of IV, Development of an RFI Work Plan and General
Considerations for RFIs. EPA 530/SW-87-001, July 1987. " Clean Water Act (CWA)
BDL = Below Detection Level
NA = Potential ARAR Not Available NR = Not Reported. No analysis for this chemical.
STSO ^00 vas
H2MGROUP
protection of human health for water and fish ingestion and for
water ingestion alone.
Maximum concentrations of iron for the site and background
and mean site concentrations exceeded the New York State surface
water standard for Class B waters and Federal ambient WQC for
protection of human health for the water and fish ingestion
category.
Site and background maximum and mean detected concentrations
of manganese exceeded Federal ambient WQC for human health
protection in the water and fish ingestion and fish only
ingestion categories.
It is noted that many ambient WQC for the protection of
human health are based on obsolete toxicological data. There
fore, they are generally not recommended for use as ARARs. In
addition, the human health ambient WQC are based .on use of
surface water as a drinking water supply. Fish Cove is not used
for drinking, therefore, the comparison to the ambient WQC is not
completely relevant for this exposure point. See Section 6.0 for
a discussion of potential quantitative human health risks associ
ated with Fish Cove.
Site maximum and mean concentrations of selenium exceeded
the New York State surface water standards for Class B waters.
Site maximum concentrations exceeded all available Federal ambi- j • C O
ent WQC for the protection of acjuatic life and for the protection | >
of human health. The mean value of selenium exceeded Federal WQC g
for the freshwater chronic categories listed under the protection ' o
' Ul of aquatic life and human health protection. i M
4.11
H2MGROUP
Directly related to the question of surface water quality is
the cjuality of edible shellfish tissue. The USEPA does not have
any ARAR listing per se. However, the Federal Food and Drug
Administration (FDA) has produced compliance policy guidelines
(7108.07 In-house) for mercury in fish or shellfish (1 ppb). No
other contaminated levels for heavy metals, such as selenium, are
available. If the FDA finds a concentration of heavy metal in
fish or shellfish it is usually due to a spill, at which time
they formulate a tolerance policy (Personal Communication, 1987).
4.3 - SEDIMENT
Potential sediment ARARs have been proposed by USEPA Region
II (refer to March 1989, final comments and conditional approval
letter). These ARARs are presented in Table 4-5, Potential Sedi
ment ARARs for North Sea Landfill. Table 4-5 also contains the
concentrations detected in Fish Cove sediments at three lo
cations. In comparison with the potential sediment ARARs, there
are no apparent exceedances.
4.4 - SOIL
Soil standards at the State level do not exist. In several
States (e.g.. New Jersey, California) there are "action levels"
or "target cleanup concentrations" for soil remediation. New
York State does not have definitive "action levels" at this time. ^
o Potential soil ARARs have been proposed by USEPA Region II o
(refer to March 1989, final comments and conditional approval
letter). These ARARs are presented in Table 4-6, Potential Soil
4.12
o Cn
H2MGROUP
TABLE 4-5 POTENTIAL SEDIMENT ARARs FOR NORTH SEA LANDFILL (A)
CHEMICAL
Semivolatile organic compounds
Di-N-butylphtha bis{2-ethylhaxy
ate )phthalate
Molecular sulfur (T) 1,13-Tetradecad BBP Fluoranthene Pyrene Phenanthrene Cadmium Chromium Copper Iron Lead Magnes ium Manganese Mercury Sodium Zinc
ene
SEDIMENT (B) (mg/kg)
. 2000 NA NA NA 220 NA 198 56 31 25 136 NA 132 NA NA 0.8 NA 760
SEDIMENT (C) (mg/g)
NA NA NA NA NA 0.9 4.95 1.4 NA NA NA NA NA NA NA NA NA NA
SEDIMENT (D) (mg/kg)
NA NA NA NA NA
4.25 20
4.71 NA NA NA NA NA NA NA NA NA NA
SITE CONCENTRATION MAXIMUM (mg/kg)
0.26J 19
TIC TIC
,0.36 0.06 J 0.051J 0.068J 1.7 2.8
BDL BDL
5.15 BDL SOL
0.1 BDL
27
MEAN
0.19 8.15 TIC TIC 0.22 NR NR NR 1.3 1.5
BDL BDL 4.1
BOL BDL 0.07 BDL 16.3
BACKGROUND RANGE (E)
(mg/kg)
NA NA NA NA NA NA NA NA
«:1 - 4.5 30 - 50 15 - 20
1500 -100000 <10 - 20
2000 - 16000 500 - 7000 0.082 - 5.1 3000 - 100000
45 - 74
A - National Perspective on Sediment Quality (May 10, 1985) Prepared By: Bolton, H.S., et al. Prepared For: EPA Criteria and Standards Divison
B - Pavlou and Weston, Acute permissible Sediment Contaminant Concentrations (1984)
C - U.S. EPA Elaboration of Sediment Normalization Theory for Nonpolar Hydrophobic Organic Chemicals (January, 1986) Prepared For: U.S. EPA Criteria and Standards Division ACUTE Permissible Sediment Contaminant Concentrations
D - Shacklette and Boerngen (1984) and Connor and Shacklette (1975) BDL = Below Detection Level TIC = Tentatively identified compound. NA = Not Available NR = Not Reported; mean is greater than maximum due to values below the detection limit.
CO M >
o o
o (Jl
00
4.13
li^AiGROUP
TABLE 4-6
POTENTIAL SOIL ARARs FOR NORTH SEA LANDFILL (A)
CHEMICAL
HEALTH BASED CRITERIA
CARCINOGENS
(B) (mg/kg)
SYSTEMATIC
TOXICANTS
(C) (mg/kg)
COMMON
AVERAGE
CONCENTRATIONS
(D) (mg/kg)
TYPICAL
CONCENTRATION
RANGES
(E) (mg/kg)
Volatile organic compounds
Benzene
2-Benzene
1,l-Dichloroethane
1,1-Dlchloroethene
Dichloromethane (Methylene Chloride)
Hexane
4-Methyl-3-Pantanoic acid
Tetrachloroethene
Toluene
Trichloromethane (Chloroform)
1,1,2-Trlchlorotrlf luoroethane
Xylenes
Semivolatile organic compounds
Benzo(a)pyrene
Benzo{b)fluoranthane
Benzo(g,h,f)perylene
Benzo(k)fluoranthene
Benz(a)anthracene
, 4-Bromophenyl phenyl ether,'
Buthylbenzylphthalate
Di-N-Butylphthalate
Chryzene
Diethyl phthalate
4,6-Dintro-2-methylphenol
D1-n-butylphthalate
bis(2-Ethylhexyl)phthalate
Fluoranthene
1-Hexadecane
Hexadecanoic acid
Hexanedioic acid, dioctyl ester
4-Hydroxy-4-Methyl-2-pentanone
Indeno(l,2,3-cd)pyrene
Pentachlorophenol
Pyrene
1,1,2,2-Tetrachloroethane
0.04
NA NA
0.02
NA
NA
NA
0.2
NA
0.01
NA
NA
NA NA NA
10
70
NA NA
20
400
10
NA NA
NA
NA NA
NA NA
NA
NA
NA
NA NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
0.0001
NA
NA •
NA
0.0004
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA NA
NA
NA
NA
NA
NA 0.06
NA NA
NA
NA
NA
NA
NA
NA
NA
20,000'
NA
100
NA
NA NA
NA
NA
NA
NA
NA
NA NA
NA NA
NA
NA
NA
NA
• NA
NA
NA
NA
NA
NA
NA NA
NA
NA
NA
NA
NA
NA
NA NA
NA NA
NA
NA
NA
NA
NA ,
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA NA
NA
NA NA
f 1 !• cn
1 > 1 o o
' o ! (Jl
yo
4.14
li^AiGROUP
TABLE 4-6 (Continued)
POTENTIAL SOIL ARARs FOR NORTH SEA LANDFILL (A)
HEALTH BASED CRITERIA
CHEMICAL CARCINOGENS
(B) (mg/kg)
SYSTEMATIC
TOXICANTS
(C) (mg/kg)
COMMON
AVERAGE
CONCENTRATIONS
(D) (mg/kg)
TYPICAL
CONCENTRATION
RANGES
(E) (mg/kg)
Target analyte list
Antimony
Arsenic
Barium
Cadmium
Chromium III
Chromium VI
Chromium (Total)
Cobalt
Copper
Iron
Lead
Magnesium
Manganese
Mercury
Nickel
Potassium
Si Tver
Sodium
Vanadium
Zinc
NA 0.00008
NA
NA
NA
NA
NA NA
NA
NA NA NA NA
NA
NA
NA
NA
NA
NA
NA
0.5 NA
60
NA
1000
8 NA
NA NA NA
NA NA
NA
600 NA
NA 4
NA
NA
NA
2-10
5 430
0.06
NA
NA
100
8 30 NA
10 5000
600
0.03
40 NA
0.05
NA
100 50
1.3 - 10
4.1 - 10
300 - 500
<1 - 4.5
NA
NA 30 - 50
7 - 70
15 - 20
1500 - 100000
<10 - 20
2000 - 7000
500 - 7000
0.082 - 5.1
15
2200 - 16000
<0.5 - 3
3000 - 100000
30 - 500
45 -74
A - Potential ARARs and Common Average Concentrations provided by USEPA.
B - Health-Based Criteria for Carcinogens, Oral Exposure Route RSQ
Table 8-5 of Development of an RFI Work plan and General
Considerations for RCRA Facility Investigations.
EPA 530/SW-87-001, July 1987.
C - Health-Based Criteria for Systemic Toxicants
Table 8-7 of Development of an RFI Work Plan and General
Considerations for RCRA Facility Investigations.
EPA 530/SW87-001, July 1987.
D - SU 846 Hazardous Waste Land Treatment (Lindsay 1979)
E - Shacklette and Boerngen (1984) and Connor and Shacklette (1975).
NA Not Available.
cn w
o o
o (Jl to o
4.15
H2MGROUP
ARARs for the North Sea Landfill. These are: typical concentra
tion ranges and average concentrations for metals in soil (these
are not available for organic compounds because they do not
naturally occur in soil) and human health based criteria for a
few organic compounds and metals.
Table 4-7, Potential Soil ARARs vs. Detected Values in Soil
Media, compares the values detected in landfill surface soils,
lagoon soils and saturated subsurface soils with potential soil
ARARs. As can be seen, background soil samples were not
collected during the Phase I RI for comparison. Nevertheless,
the typical concentration ranges for metals are based on two
United States Geological Survey (USGS) reports. These are: (1)
Shacklette, H.T. and Boerngen, J.G., 1984, Elemental Concentra
tions in Soils and Other Surficial Materials of the Conterminous
United States. USGS Professional Paper 1270; and (2) Connor, J.J.
and Shacklette, H.T., 1975, Background Geochemistry of Some
Rocks^ Soils. Plants and Vegetables in the Conterminous United
States. USGS Professional Paper 574-F.
Reference (1) discusses samples collected at sites in
Connecticut and Northern New Jersey and is applicable to all
priority pollutant metals except thallium. Reference (2) dis
cusses samples collected from glaciated soil in Missouri and
applies to cadmium and silver. Comparison of the typical
background ranges for metals vs. the common average concentra
tions, reveals that the common average concentrations fall within °
the background concentration range. Apparently maximum values o
for arsenic, copper and silver in lagoon soil do not fall within
4.16
o
(Jl ' to
li^MGROUP
TABLE 4-7 POTENTIAL SOIL ARARs VS DETECTED VALUES IN SOIL MEDIA FOR NORTH SEA LANDFILL
HEALTH BASED CRITERIA
CHEMICAL CARCINOGENS , (A) (mg/kg)
SYSTEMATIC TOXICANTS
(B) (mg/kg)
COMMON TYPICAL AVERAGE BACKGROUND CONCENTRATIONS RANGE
(C) (D) (mg/kg)
MAXIMUM (mg/kg)
MEAN (mg/kg)
Surface Soil:
Benzo(a)pyrene Benzofbjfluoranthane Benzo(g,h,f)perylene Benzo(k)fluoranthene Benz(a)anthracene
D1-N-Butylphthalate Chryzene Butyl Benzyl Phthalate Diethyl phthalate
2-Ethylhexyl)phthalate Fluoranthene Indeno(1,2,3-cd)pyrene Pyrene
bis
Arsenic Ca(Jmium Chromium Copper Lead Mercury Nickel SiIver Zinc
'Total)
Laggon Soils:
Dichloromethane (Methylene Chloride) Trichloromethane (Chloroform) Diethyl phthalate
bis(2-Ethylhexyl)phthalate Arsenic Cadmium Chromium Copper Lead Mercury Nickel Silver Zinc
•Total)
Saturated Soils
Di-N-Butylphthalate Diethyl phthalate
bis(2-Ethylhexyl)phthalate Arsenic CacJmium Chromium (Total) Copper Lead Nickel Selenium SiIver Thallium Zinc
0.0001 NA NA NA
0.0004 NA NA NA NA NA NA NA NA
0.00008 NA NA NA NA NA NA NA NA
NA 0.01 NA NA
0.00008 NA NA NA NA. NA NA NA NA
. NA NA NA •
0.00008 NA NA NA NA NA -NA NA • •NA NA
NA NA NA NA NA NA NA NA
20,000 NA NA NA NA NA NA NA NA NA 600 NA
. 4 NA
70 10
20.000 NA NA NA NA
. NA NA 600 NA .4 NA
NA 20,000 NA NA NA NA NA
- NA NA NA
- 4 NA NA
NA NA NA NA NA NA NA NA NA NA NA NA NA 5
0.06 100 30 10
0.03 40-
0.05 50
NA NA NA NA 5
0.06 100 30 10.
0.03 40
0.05 50
NA NA NA 5
0.06 100 30 10 40 NA
0.05 NA 50
NA NA NA NA NA NA NA NA NA NA NA
, NA NA
.4.1 -<1 -30 -15 -
<10 -0.082 -
15 <0.5 -45 -
NA NA NA NA
4.1 -<1 -30 -15 -
<10 -0.082 -
15 <0.5 -
45 -
NA NA NA
4.1 -<1 -30 -15 -
<10 -15 0.5
'<0.5 -NA
45 -
10 4.5 50 20 20 5.1
3 74
10 4.5 50 20 20 5.1
3 74
10 4.5 50 20 20
3
74
O.llJ 0.25J 0.057J O.llJ 0.095J 0.35J 0.15J 0.175 0.063J 9.9 0.14J 0.071J 0.14J 8.1 2.2 7.2 9.8 17.1 1.9 21 0.6 11.2
0.14 O.OIJ 0.27J 6.6 31 2.3 16 35 13 0.1 6.5 110 50
0.11 0.49 8.7 4.5 1.2 6 9.8 16 3.4 0.6 19 1.2 12
A - Health-Based Criteria for Carcinogens, Oral Exposure Route RSQ Table 8-5 of Development of an RFI Work plan and General Considerations for RCRA Facility Investigations. EPA 530/SW-87-001, July 1987.
B - Health-Based Criteria for Systemic Toxicants Table 8-7 of Development of an RFI Work Plan and General Considerations for RCRA Facility Investigations., EPA 530/SW87-001, July 1987. SW 846 Hazardous Waste Land Treatment (Lindsay 1979) Shacklette and Boerngen (1984) and Connor and Shacklette (1975)
NR 0.235
NR NR NR
0.19 NR NR NR
2.4 NR NR NR
2.9 0.73 2.8 6.2 5.7
0.17 7.2 0.6 11.2
0.12 0.007
NR 4.1 12.9 0.8 9.9 9.7 5.3
0.05 3.5 9.7 17.6
NR-0.21 2.0 o:9-0.6 3.5 4.3 7.1 2.4 0.3 2.2 0.6 5.6
cn
o o
O Ul
, IO \ to
C -D -BDL = Below Detection Level
DL = Detection Level NA = Not Available NR = Not Reported; mean is greater than maximum due to values below the detection limit.
4.17
H2MGROUP
the typical background range. Silver falls above the typical
range in a saturated soil sample.
Potential human health based criteria are available for
benzo(a)pyrene, benzo(a)anthracene, diethyl phthalate, methylene
chloride, chloroform, diethyl phthalate, arsenic, mercury and
silver. For surface soils, human health criteria are potentially
exceeded for benzo(a)pyrene, benzo(a)anthracene and arsenic. For
lagoon soils, human health criteria are potentially exceeded for
arsenic and silver. For saturated soils, human health criteria
are potentially exceeded for arsenic and silver.
The values listed in Table 4-7 are described as health based
values; however, the basis for this designation was not provided
by USEPA. The listed value for arsenic is five orders of magni
tude below the background level and several orders of magnitude
below normal detection limits. Consequently, the value is not
recommended as a realistic cleanup standard for the North Sea
Landfill. Similarly, the value for PAHs is also several orders
of magnitude below the detection limit and, as such, does not
represent a realistic cleanup standard. The reader is referred
to Section 6.0 where a quantitative assessment of potential
exposures and risks from surface soils based on actual site
conditions is given.
CO
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4.18
ii2MGROUP
5.0 - TOXICITY ASSESSMENT
5.1 - HEALTH EFFECTS CLASSIFICATION AND CRITERIA
DEVELOPMENT
For risk assessment purposes, individual pollutants are
separated into two categories of chemical toxicity, depending on
whether they exhibit non-carcinogenic or carcinogenic effects.
This distinction relates to the currently held scientific opinion
that the mechanism of action for each category is different.
USEPA has adopted, for the purpose of assessing risks associated
with potential carcinogens, the scientific position that a small
number of molecular events can cause changes in a single cell or
a small number of cells that can lead to tumor formation. This
is described as a "no threshold" mechanism, since there is
essentially no level of exposure (i.e., a threshold) to a
carcinogen which will not result in some finite possibility of
causing the disease. In the case of chemicals exhibiting
non-carcinogenic effects, however, it is believed that organisms
have protective mechanisms that must be overcome before the toxic
endpoint is manifested. For example, if a large number of cells
perform the same or similar functions, it would be necessary for
significant damage or depletion of these cells to occur before an
effect could be seen. This threshold view holds that a range of r
exposures from just above zero to some finite value can be , !• cn
tolerated by the organism without appreciable risk of causing the i w
disease (USEPA, 1986c) o o
S ! 5.1
to
H2MGROUP
5.1.1 - Health Effects Criteria for Non-Carcinogens
Health criteria for chemicals exhibiting non-carcinogenic
effects are generally developed using risk reference doses (RfDs)
developed by the USEPA RfD Work Group as listed in USEPA's
Integrated Risk Information System (IRIS) database, or RfDs
obtained from Health Effect Assessments (HEAs). The RfD,
expressed in units of mg/kg/day, is an estimate of the daily
exposure to the human population (including sensitive subpopula-
tions) that is likely to be without an appreciable risk of
deleterious effects during a lifetime. These RfDs are usually
derived either from human studies involving workplace exposures
or from animal studies and are adjusted using uncertainty
factors. The RfD provides a benchmark to which chemical intakes
by other routes (e.g., via exposure to contaminated environmental
media) may be compared.
5.1.2 - Health Effects Criteria for Potential Carcinogens
Cancer potency factors (CPFs), developed by USEPA's Carcino
gen Assessment Group (CAG) for potentially carcinogenic chemicals
and expressed in units of (mg/kg/day)~, are derived from the
results of human epidemiological studies or chronic animal bio
assays. The animal studies must usually be conducted using rela
tively high doses in order to detect possible adverse effects.
Since humans are expected to be exposed at lower doses than those
used in the animal studies, the data are adjusted by using ''- cn
mathematical models. The data from animal studies are typically >
fitted to the linearized multistage model to obtain a ° o
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5.2
iH2MGROUP
dose-response curve. The 95th percentile upper confidence limit
slope of the dose-response curve is subjected to various
adjustments and an interspecies scaling factor is applied to
derive the CPF for humans. Thus, the actual risks associated
with exposure to a potential carcinogen (quantitatively evaluated
based on animal data are not likely to exceed the risks estimated
using these CPFs, but they may be much lower. Dose-response data
derived from human epidemiological studies are fitted to dose-
time-response curves on an ad hoc basis. These models provide
rough, but plausible estimates of the upper limits on lifetime
risk. CPFs based on human epidemiological data are also derived
using very conservative assumptions and, as such, they too are
unlikely to underestimate risks. Therefore, while the actual
risks associated with exposures to potential carcinogens are
unlikely to be higher than the risks calculated using a CPF, they
could be considerably lower.
USEPA assigns weight-of-evidence classifications to
potential carcinogens. Under this system, chemicals are classi
fied as either Group A, Group Bl, Group B2, Group C, Group D, or
Group E. Group A chemicals (human carcinogens) are agents for
which there is sufficient evidence to support the casual associ
ation between exposure to the agents in human and cancer. Groups
Bl and B2 chemicals (probable human carcinogens) are agents for i
I' CO which there is limited (Bl) or inadequate (B2) evidence of i a
carcinogenicity from animal studies. Group C chemicals (possible
human carcinogens) are agents for which there is limited evidence
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5.3
(H2AiGROUP
of carcinogenicity in animals, and Group D chemicals (not classi
fied as to human carcinogenicity) are agents with inadequate
human and animal evidence of carcinogenicity or for which no data
are available. Group E chemicals (evidence of non-carcino-
genicity in humans) are agents for which there is no evidence of
carcinogenicity in adequate human or animal studies.
Table 5-1, Summary of Health Effects Criteria for Indicator
Chemicals. summarizes the toxicity criteria used in this
assessment along with their associated safety factors (for non-
carcinogens) and weight-of-evidence classifications (for carcino
gens) . The. table also lists the source of the criteria.
Table 5-1.lists the criteria for oral exposure only, since,
as noted in Section 3.0, no exposures via inhalation are
considered in this assessment. The table lists subchronic as
well as chronic criteria for non-carcinogens. USEPA has not
established subchronic RfDs; however, many of the HEA documents
list subchronic criteria. These criteria apply to short-term
exposures of 90 days or less.
A summary of the toxic effects of each of the chemicals and
the basis for the derivation of the CPF and RfD is given in
Appendix D.
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':|i2MGROUP TABLE 5-1 SUMMARY OF HEALTH EFFECTS CRITERIA FOR INDICATOR CHEMICALS
NORTH SEA LANDFILL
CHEMICAL
Benzene Chloroform 1,1-DCA 1,2-OCA 1,1-OCE 1.2-DCE Methylene chloride Tetrachloroethylene Toluene Trichloroethylene Phenol DEHP DNBP DEP BBP Endosulfan Carcinogenic PAHs (a) Noncarcinogenic PAHs (b)
Ammon i a
arsenic cadmium
chromium copper iron lead manganese mercury nitrate nitrite nickel selenium. silver thai 1ium zinc
Reference Dose (RfD)
(mg/kg/d)
* lE-02 lE-Ol
-9.3E-03 2E-02 6E-02 lE-02
. 3E-01 7.35E-03
6E-01 2E-02 lE-01 8E-01 2E-01 5E-05 -
4.1E-01 *
34 mg/1iter drinking wat
lE-03 lE-03 (e) 5E-04 (e)
5E-03 1.3 mg/1 (f)
-
2E-01 2E-03 1
lE-01 2E-02 3E-03 3E-03 7E-05 2E-01
Chronic
Safety Factor (a
. 1000 1000 -
1000 1000 100
1000 100
1000 100
1000 1000 1000 1000 3000 -100
er (d) 1
500 --
100 1000 1 10 300 15 2
3000 100
NON-CARCINOGENIC EFFECTS
Source (b) )
IRIS IRIS HEA -
IRIS IRIS IRIS IRIS IRIS HA HEA IRIS IRIS IRIS HEA IRIS -
HEA
HEA
HEA
IRIS HEA -
HEA HEA IRIS IRIS IRIS HEA IRIS HEA HEA
Reference Dose (RfD)
(mg/kg/d)
. lE-02 lE+00 -
9.3E-03 -
6E-02 lE-01 4E-01 -
6E-01 2E-02 lE+00 8E+00 2E+00 2E-04 -
4.1E-01 *
34 mg/1iter drinking wa
lE-03
2E-02 1.3 mg/1 (e)
-
5E-01 3E-04 --
2E-02 4E-03 -7E-04
Subchronic
Safety Factor (a)
. 1000 100 -1000 -100 100 100 . -100
1000 100 100 100
1000 -100
ter (d) 1
100 --
100 10 --300 100 -300 •
Source (b)
.
HEA HEA -HEA -HEA HEA HEA -HEA HEA HEA HEA HEA HEA -
HEA
HEA
HEA
HEA HEA -
HEA HEA --HEA HEA -HEA
CARCINOGENIC
EPA/CAG Cancer Potency
EFFECTS
Weight of
Factor Evidence (c) (mg/kg/d)-l
2.9E-03 6.1E-03 9.1E-02 9.1E-02 6.1E-1
-7.5E-03
5.1E-02 * -
l.lE-02 -
1.4E-02 ----
11.5 * -
-
, 1.75
--.-
--------
A B2 C 82
-B2 --82 -B2 ----B2 -
-
A
---
--------
(a) Safety factors used to develop reference doses consist of multiples of 10; each factor representing a specific area of uncertainty inherent in the data available, data available. The standard uncertainty factors Include:
0 A ten-fold factor to account for. the variation in sensitivity among the members of the human population;
0 A ten-fold factor to account for the uncetalnty In extrapolating animal data to the case of humans;
0 A ten-fold factor to account for the uncertainty In extrapolating from less than chronic No Observed Adverse Effects Levels (NOAELs) to chronic (NOAELs)
0 A ten-fold factor.to account for the uncertainty in extrapolating from Lowest Observed Adverse Effect Levels (LOAELs) to NOAELs.
(b) Sources of Reference Doses: IRIS = chemical files of the Integrated Risk Information System. HEA = Health Effects Assessment; HA = Health Advisory.
(c) Weight of evidence classification scheme for carcinogens: A -- Human Carcinogen, sufficient evidence from human epidemiological studies; 81 -- Probable Human Carcinogen, limited evidence from epidemiological studies
and adequate evidence from animal studies; 82 -- Probable Human Carcinogen, inadequate evidence from epidemiological studies
and adequate evidence from animal studies; C -- Possible Human Carcinogen, limited evidence in animals in the absence of human studies; D -- Not Classified as to human carcinogenicity; and E -- Evidence of Noncarcinogenlcity.
(d) Organoleptic basis; inadequate data to report a safe concentration, which may be higher.
(e) The value of 5E-04 is used for drinking water exposure, and the value of lE-03 is used for non-drinking water exposures such as food or soil Ingestion
(f) Current drinking water standard; inadequate toxicity data exists to calculate RfD according to Drinking Water Criteria Document.
* Review pending. - No criteria have been established by EPA for for these endpolnts of exposure.
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5.5
H2MGROUP
6.0 - RISK CHARACTERIZATION
To quantitatively assess the potential risks to human health
associated with the exposure scenarios considered in this assess
ment, the exposure point concentrations developed in the previous
sections are converted to chronic daily intakes (CDIs). CDIs are
expressed as the amount of a substance taken into the body per
unit bo<iy weight per unit time or mg/kg/day. A CDI is averaged
over a lifetime for carcinogens (USEPA, 1986b) and over the expo
sure period for non-carcinogens (USEPA, 1986c). For potential
carcinogens, excess lifetime cancer risks are obtained by
multiplying the daily intake of the contaminant under
consideration by its cancer potency factor. USEPA has imple
mented actions under Superfund associated with total cancer risks
ranging from" lO"'* to 10~' (i.e., the probability of one excess
cancer is one in 10,000 to 10,000,000, respectively, under the
conditions of exposure). A risk level of 10" , representing a
probability of one in 1,000,000 that an individual could contract
cancer due to exposure to the potential carcinogen, is often used
as a benchmark by regulatory agencies.
Potential risks for non-carcinogens are presented as the
ratio of the chronic daily intake exposure to the reference dose
(CDI:RfD). The sum of the ratios of chemicals under consider
ation is called the hazard index. The hazard index is useful as j
a reference point for gauging the potential effects of environ- ' >
mental exposures to complex mixtures. In general, hazard indices' ' o
6.1
*. I
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•i^MGROUP
which are less than one are not likely to be associated with any
health risk and are therefore less likely to be of concern than
hazard indices greater than one. A conclusion should not be
categorically drawn, however, that all hazard indices less than
one are "acceptable" or that hazard indices of greater than one
are "unacceptable". This is a consequence of the perhaps order
of magnitude or greater uncertainty inherent in estimates of the
RfD and CDI in addition to the fact that the uncertainties asso
ciated with the individual terms in the hazard index calculation
are additive.
In accordance with USEPA's guidelines for evaluating the
potential toxicity of complex mixtures (USEPA, 1986c), it was
assumed that the toxic effects of the site-related chemicals
would be additive. Thus, lifetime excess cancer risks and the
CDI:RfD ratios were summed to indicate the potential risks asso
ciated with mixtures of potential carcinogens and non-carcino
gens, respectively. In the absence of specific information on
the toxicity of the mixture to be assessed or on similar mixture,
USEPA guidelines generally recommend assuming that the effects of
different components of the mixture are additive when affecting a
particular organ or system. Synergistic or antagonistic inter
actions may be taken into account if there is specific inform
ation on particular combinations of chemicals. In this risk
assessment, it was assumed that the potential effects of site-
related chemicals would be additive.
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6.2
H2AiGROUP
Risk characterizations were done for three potential human
exposure routes: groundwater ingestion, surface soil intake and
shellfish ingestion.
6.1 - POTENTIAL EXPOSURE TO GROUNDWATER
Exposure to groundwater may occur through ingestion of
groundwater from private supply wells. The chronic daily inta:ke
(CDI) estimate of groundwater ingestion is based on the following
expression:
CDI = (Cp) : (I) . (6-1)
where, CDI = chronic daily intake (mg/kg/d)
Cp = predicted long-term concentration in
groundwater (mg/1)
I = groundwater ingestion rate (L/kg/day)
The predicated long-term concentrations, in groundwater were
estimated using initial mean and maximum detected concentrations
(refer to Section 3.2, Estimation of Exposure Point Concentra
tions in Groundwater). The groundwater ingestion rate (or human
intake factor) is ecjual to 0.029 L/kg/day. This is based on the
standard drinking water intake per day (roughly 2 L/day) divided
by the standard adult body weight (70 kg).
Tables 6-lA and 6-lB, Summary of Potential Exposures and
Risks Associated with Ingestion of Groundwater. Based on Site - — ^
• • I 1
Conditions aind Based on Background Conditions, lists the indi
cator chemicals predicted concentrations, and chronic daily
cn • j
o intake values. The indicator chemicals are grouped into two 1 °
6.3
1 (>> 1
li2MGROUP TABLE 6 - lA
SUMMARY OF POTENTIAL EXPOSURES AND RISKS ASSOCIATED WITH INGESTION OF GROUNDWATER Based on Site Conditions
Indicator Chemica1
Projected
Best Case
Concentrations (mg/1)
Worst Case
Chronic Dai ly Intake (CDI)
Best Case (mg/kg/d)
Worst Case (mg/kg/d)
Cancer Potency Factor ' (mg/kg/d)-.I
Excess L Cancer
Best Case
ifetime Risk
Worst Case
Arsenic Benzene DEHP Chloroform 1,1-DCA 1,2-OCA 1,1-DCE Methylene Chloride PCE TCE
7.40E-03 9.75E-04 3.41E-02
NA 2.59E-03
NA NA
1.95E-03 3.41E-03 3.22E-03
1.36E-02 9.75E-04 1.36E-01
NA 2.93E-03
NA . NA • •
• 1.95E-03 6.83E-03 6.83E-03
2.I5E-04 2.83E-05 9.89E-04
NA 7.51E-05
NA NA
5.65E-05 9.89E-05 9.34E-05
3.94E-04 2.83E-05 3.94E-03
NA 8.50E-05
NA NA
5.65E-05 1.98E-04 1.98E-04
1.75E+00 2.90E-02 1.40E-02 6.10E-03 9.10E-02 9.10E-02 6.10E-01 7.50E-03 (1) 5.10E-02 l.lOE-02
3.76E-04 8.20E-07 1.38E-05
NA 6.84E-06 .
NA NA
4.24E-07 5.04E-06 1.03E-06
6.90E-04 8.20E-07 5.52E-05 NA
7.73E-06. • NA NA
4.24E-07 l.OlE-05
. 2.18E-06
Ammonia Arsenic Benzene DEHP BBP Cadmium Chloroform Chromium Copper 1,1-OCA 1.2-OCA 1,1-OCE 1,2-OCE DEP Endosulfan I Endosulfan II Iron Lead Manganese Mercury Methylene Chloride Nickel
Nitrate/Nitrite Phenol PCE Silver Toluene TCE Zinc
1.14E+01 • 7.40E-03 9.75E-04 3.41E-02 2.-44E-03
• 9.40E-03 •NA
2.83E-02 1.17E-01 2.59E-03
NA NA.
2.59E-03 . NA NA NA
3.01E+01 2.93E-02 1.38E-01 1.70E-04 2.24E-03 4.20E-02
•6.40E-02 1.95E-03 3.41E-03 • NA • 2.44E-03 3.22E-03 1.18E-01
4.34E+01 1.36E-02 9.75E-04 1.36E-01 4.88E-03 1.95E-02
NA • 7.60E-02
2.63E-01 2.93E-03
NA NA
3.90E-03 NA NA NA
4.47E+01 6.14E-01 2.96E-01 3.90E-04 1.95E-03 9.75E-02
9.75E-01 1.95E-03 6.83E-03
NA 2.93E-03 6.83E-03 2.93E-01
TOTAL RISK: 4.04E-04 7.67E-04
-NONCARCINOGEN - — -r Reference CDI:RfO Ratio Dose - Chroni (mg/kg/d) . Best Case Worst Case
3.31E-01 1.26E+00 34 mg/1 ( z ) — .' . — 2.15E-04 •3.94E-O4 l.OOE-03 NA NA 2.83E-05 2.83E-05 -- -- — 9.89E-04 3.94E-03 2.00E-02 4.94E-02 r.97E-01 7.08E-05 1.42E-04 2.00E-02 3.54E-03 7..08E-03 2.73E-04 5.66E-04 5.00E-04 5.45E-01 1.13E+00 • NA NA l.OOE-02 NA. NA' 8.21E-04 2.20E-03- 5.00E-03 1.64E-01 4.41E-01 3.39E-03 7.63E-03 1.3 mg/1 (3) 7.51E-05 . 8.50E-05 l.OOE-01 7.51E-04 8.50E-04 . NA NA — — • — •
NA NA 9 .00E-03 ( 4 ) NA NA 7.51E-05 1.13E-04 2.00E-02 3.76E-03 5.65E-03
NA NA 8.00E-01 NA NA NA NA 5.00E-05 NA N A NA NA 5.00E-05 NA NA
8.73E-01 1.30E+00 8.50E-04 1.78E-02 6.00E-04 1.42E+00 2.97E+01 4.00E-03 8.58E-03 2.00E-01 2.00E-02 4.29E-02 4.93E-06 1.13E-05 .2.00E-03 2.47E-03 5.66E-03 6.50E-05 5.65E-05 6.00E-02 1.08E-03 9.42E-04 1.22E-03 2.83E-03 2.00E-02 6.09E-02 1.41E-01
1.86E-03 2.83E-02 l.OOE-01 (5) 1.86E-02 2.83E-01 5.65E-05 5.65E-05 6.00E-01 9.43E-05 9.43E-05 9.89E-05 1.98E-04 l.OOE-02 9.89E-03 1.98E-02
NA NA 3.00E-03 , NA NA 7.08E-05 8.50E-05 3.00E-01 2.36E-04 2.83E-04 9.34E-05 1.98E-04 7;35E-03 (6) 1.27E-02 •2.69E-02 3.42E-03 8.50E-03 2:00E-01 1.71E-02 4.25E-02
HAZARD INDEX: 2.33E+00 -- = No health criteria available for this chemical. NA = Not Applicable. Chemical was nor detected in the wells used for the initial concentration estimates. Human Intake Factor = 0.029 1/day/kg. CDI = 0.029 X predicted concentration • .
NOTES:
Carcinogens
1. PCE - Review pending.
Noncarcinogens
3.20E+01
2. NHS -.34 mg/1 in drinking water. Organoleptic basis, inadequate data to report a safe concentration, which may be higher.
3. Cu - Current drinking water standards, inadequate toxicity data exists to calculate an RfD according to
DWCD (Drinking Water Criteria Document)!
4. 1,2;DCE - Value .for trans-l,2-DCE. Value for cis-1,2-DCE Is l.OOE-02.
5. N03/N02 - Value for nitrite. Value for nitrate is l.OOE+00.
6. TCE - Review pending. . . .- .
6.4
the
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TABLE 6-18
m \ j t ^ 7 A < ( 7 u r SUMMARY OF POTENTIAL EXPOSURES AND RISKS ASSOCIATED WITH INGESTION OF GROUNDWATER Based on Background Conditions
Indicator Chemical
Projected
Best Case
Concentrations (mg/1)
Worst Case
Chronic
Best Case (mg/kg/d)
Dai ly Intake (CDI)
Worst Case (mg/kg/d)
Cancer Potency Factor
(mg/kg/d)-1
Excess L Cancer
Best Case
fetime Risk
Worst Case
Arsenic Benzene DEHP Chloroform 1,1-DCA 1,2-DCA 1,1-DCE Methylene Chloride PCE TCE
NA 8.67E-04 8.67E-03 8.67E-04
NA NA NA
1.20E-03 NA NA
NA 8.67E-04 I.65E-02 8.67E-04
NA NA NA
1.30E-02 NA NA
NA 2.51E-05 2.51E-04 2.51E-05
NA NA NA
3.48E-05 NA NA
NA 2.5IE-05 4.79E-04 2.51E-05
NA NA NA
3.77E-04 NA NA
1.75E+00 2.90E-02 1.40E-02 6.10E-03 9.10E-02 9.10E-02 6.10E-01 7.50E-03 5.10E-02 l.lOE-02
(1)
NA 7.29E-07 3.52E-06 1.53E-07
NA NA NA
2.61E-07 NA NA
NA 7.29E-07 6.70E-06 1.53E-07
NA NA NA
2.83E-06 NA NA
Ammonia Arsenic Benzene DEHP BBP Cadmium Chloroform Chromium Copper 1,1-DCA 1,2-DCA 1,1-DCE 1,2-OCE DEP Endosulfan I Endosulfan II Iron Lead Manganese Mercury Methylene Chloride Nickel Nitrate/Nitrite Phenol PCE Silver
Toluene TCE Zinc
5.00E-02 NA
8.67E-04 8.67E-03 3.29E-03 1.56E-02 8.67E-04 2.17E-02 1.13E-01
NA NA NA NA NA NA NA
1.16E+00 8.86E-02 4.59E-01 1.73E-04 1.20E-03 1.73E-01 3.47E-02 7.80E-04
NA 5:20E-03
2.08E-03 NA
1.70E-01
1.70E-01 NA
8.67E-04 1.65E-02 9.50E-03 4.34E-02 8.57E-04 5.40E-02 1.56E-02
NA NA NA NA NA NA NA
1.82E+00 1.34E-01 7.28E-01 4.34E-04 1.30E-02 1.04E-01 3.47E-01 2.60E-03
NA 8.70E-03
1.70E-03 NA
2.39E-01
TOTAL RISK: 4.66E-06 1.04E-05
-NONCARCINOGENS -Reference CDhRfD Ratio Dose - Chronic (mg/kg/d) Best Case Worst Case
1.45E-03 4.93E-03 34 mg/1 (2) NA NA l.OOE-03 NA NA
6.35E-05 2.83E-05 6.35E-05 2.83E-05 2.00E-02 3.18E-03 1.41E-03 6.35E-05 2.83E-05 2.00E-02 3.18E-03 1.41E-03 6.35E-05 2.83E-05 5.00E-04 1.27E-01 5.65E-02 6.35E-05 2.83E-05 l.OOE-02 6.35E-03 2.83E-03 6.35E-05 2.83E-05 5.00E-03 1.27E-02 5.65E-03 6.35E-05 2.83E-05 1.3 mg/1 (3)
NA NA l.OOE-01 NA NA NA NA NA NA 9.00E-03 (4) NA NA NA NA 2.00E-02 NA NA NA NA 8.00E-01 NA NA NA NA 5.00E-05 NA NA NA NA 5.00E-05 NA NA
3.36E-02 5.28E-02 2.57E-03 3.89E-03 6.00E-04 4.28E+00 6.48E+00 1.33E-02 2.11E-02 2.00E-01 6.66E-02 1.06E-01 5.02E-06 1.26E-05 2.00E-03 2.51E-03 6.29E-03 3.48E-05 3.77E-04 6.00E-02 5.80E-04 6.28E-03 5.02E-03 3.02E-03 2.00E-02 2.51E-01 1.51E-01 l.OlE-03 l.OlE-02 l.OOE-01 (5) l.OlE-02 l.OlE-01 2.26E-05 7.54E-05 6.00E-01 3.77E-05 1.26E-04
NA NA l.OOE-02 NA NA 1.51E-04 2.52E-04 3.00E-03 5.03E-02 8.41E-02
6.03E-05 4.93E-05 3.00E-01 2.01E-04 1.64E-04 NA NA 7.35E-03 (6) NA NA
4.93E-03 6.93E-03 2.00E-01 2.47E-02 3.47E-02
HAZARD INDEX: 4.84E+00
-- = No health criteria available for this chemical. NA = Not Applicable. , Chemical was nor detected in the wells used for the initial concentration estimates. Human Intake Factor = 0.029 1/day/kg. CDI = 0.029 X predicted concentration
NOTES:
Carcinogens
1. PCE - Review pending.
Noncarcinogens
7.03E+00
2. NH3 - 34 mg/1 In drinking water. Organoleptic basis, inadequate data to report a safe concentration, which may be higher.
cn
3. Cu - Current drinking water standards, inadequate toxicity data exists to calculate an RfD according to the i O DWCD (Drinking Water Criteria Document). , 1 O
4. 1,2-DCE - Value for trans-l,2-0CE. Value for cis-1,2-DCE is l.OOE-02.
5. N03/N02 - Value for nitrite. Value for nitrate Is l.OOE+OO.
6. TCE - Review pending.
6.5
o Ul (jj
y/i
H2MGROUP
categories: the potential carcinogens (PCs) and the non-
carcinogens (NCs). The PC chemicals are benzene, DEHP, chloro
form, 1,1-DCA, 1,2-DCA, 1,1-DCE, methylene chloride, PCE and TCE.
The NC chemicals are ammonia, DEHP, BBP, chloroform, chromium
(Cr), copper (Cu), 1,1-DCE, 1,2-DCE, endosulfan, iron (Fe),
manganese (Mn), methylene chloride, nickel (Ni), nitrate/nitrite,
phenol, PCE, toluene and TCE.
For the PCs, the cancer potency factor (CPF) is mg/kg/d-1.
The lifetime cancer risk is determined by multiplying the CPF by
the mean or maximum CDI value. For the NCs, the reference dose
(or RfD expressed in units of mg/kg/d) is given. The hazard
index is determined by the summation of the ratios of the CDI to
RfD values. Tables 6-lA and 6-lB list the CPF and RfD values for
each indicator PC or NC value, respectively, and presents a total
summation of the CPF and RfD values as well.
Table 6-lA presents the potential exposures and risks based
on the site conditions, i.e., based on concentration estimates
using downgradient monitoring wells as input. Table 6-lB gives
the estimates based on predicted concentrations using data
obtained from background wells. The total excess lifetime cancer
risk based on site conditions is 4 x 10" for the best case
(average conditions) and 8 x 10"'* for the worst case. The major
contributor to this risk is arsenic which is a naturally occur
ring compound. Table 6-lB indicates that the excess lifetime
cancer risks associated with background conditions is 5 x 10"°
for the best case and 1 x 10" for the worst case, with the risk \ *»
cn
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6.6
H2MGROUP
mainly attributable to DEHP and methylene chloride. Remedial
actions at Superfund sites are generally designed to achieve risk
levels in the range of 1 x 10"'* to 1 x 10"^ with 1 x 10"^ as a
commonly used benchmark. It is emphasized that there are no
current users of groundwater in the vicinity of the North Sea
Landfill, and that a public water supply system is available in
the area. Therefore, the analysis presented above does not
represent an actual or potential exposure pathway. As noted
above, arsenic is the major contributor to the risk. Since
arsenic is naturally occurring, some portion of the risk is
attributable to background levels. It is emphasized that the
predicted arsenic concentrations do not exceed any drinking water
ARARs. Further, from among the carcinogens ARARs are only
exceeded for PCE, TCE and DEHP under worst case conditions.
Given these limiting factors, the risk level presented under this
analysis does not strongly suggest that remediation of ground
water is recjuired.
For the non-carcinogens, hazard indices exceed one for both
best and worst cases for. both the on-site conditions and the
background conditions. The individual CDI:RfD ratios exceed one
for only cadmium and lead. Ratios for lead exceed one for both
site arid background conditions, suggesting that any potential
risks from this chemical are largely due to background levels.
The CDI:RfD ratio for cadmium exceeds one only under the worst
case. CDI:RfD ratios are less than one for all other chemicals. j
I
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6.7
' o ( : Ul I r (jj i
i ^ .
H2AiGROUP
6.2 - DIRECT CONTACT WITH SURFACE SOILS BY LANDFILL WORKERS
Exposure to surface soils may occur through incidental
ingestion of soil adhering to the hands by individuals who eat,
smoke, or drink following soil contact, and by direct absorption
of contaminants through the skin. In estimating exposure to
landfill workers, it is assumed that outdoor work involving soil
contact will occur twice per week during 38 weeks of the year for
the average exposure case and five times per week during 38 weeks
per year for the maximum case. The 38 week exposure is based on
the period when weather conditions are amenable to outdoor
activity. Average temperatures are near or below freezing for
approximately three months (12 weeks) of the year. Subtracting
12 weeks from a typical 50 week work year etjuals 38 weeks. The
rate of incidental soil ingestion is taken as 100/mg/day based on
USEPA guidance (1989).
The PAHs and phthalates are likely to be strongly sorbed to
the soil and consecjuently may be less bioavailable in the
gastrointestinal tract than they would be if they were present in
drinking water or food, which are the typical media in animal
studies used to derive toxicity criteria. Values of 15 percent
and 50 percent are used in the average and maximum cases to
reflect this diminished bioavailability based in physicochemical
properties and analogy to studies by Poiger and Schlatter (1980)
with 2,3,7,8-TCDD. Poiger and Schlatter found 2,3,7,8-TCDP
bioavailability to range from 3 percent from fly ash to 80 cn
percent from soil, with 15 to 50 percent as typical values. The) o o
6.8
o Ul (jj
l71MGRO[P
organic carbon content of the soils at the North Sea Landfill may
be less than those of the soils used by Poiger and Schlatter.
Therefore, chemicals might be less tightly bound to soils at the
North Sea Landfill and more bioavailable. However, TCDD is
likely to be more strongly bound to soil than PAHs or phthalates.
Consecjuently, the values from Poiger and Schlatter represent
reasonable estimates for the exposure at the North Sea Landfill.
A value of 100 percent bioavailability is used for the
inorganics.
Using these assumptions, chronic daily intake (CDI) esti
mates of incidental soil ingestion are calculated as follows:
CDI =. fC^)(I)VAI^(E) fYr^(X) (6-2) (BW)(DY)(YL)
where, CDI = chronic daily intake (mg/kg/d)
Cs = concentration in soil (mg/kg)
I = soil ingestion rate (mg/d)
Al = differential absorption factor (dimensionless)
E = number of exposure events per year
(events/year)
Yr = years exposed (yr)
X = conversion factor (1 kg/10"^mg)
Bw = average body weight (70 kg) 1 i cn
DY = days per year (365) ! w
YL = lifetime (70 years) for carcinogens, or length:
of exposure (5 years or 40 years) for non-\ o ' o 1 *> I
• • °
carcinogens '• u \
6.9
H2MGROUP
Following USEPA guidelines, risks from carcinogens are
averaged over a 70-year lifetime and risks from non-carcinogens
are averaged over the period of exposure.
Concentrations of indicator chemicals in soil are taken as
the mean value for the average case and the. maximum detected
value for the maximum case.
Significant exposure via dermal absorption of inorganics is
not expected, because of the low permeability of skin to metal
ions (Schaefer et al., 1983). However, the organic chemicals of
concern are more likely to be absorbed through skin. The data
from Feldman and Maibach (1970, 1974), Yang.et al. (1986), Poiger
and Schlatter (1980), and Wester et al. (1987) can be used to
approximate dermal absorption factors for the organic indicator
chemicals. For the PAHs, rates of 5.8 percent and 10 percent are
used for the average and maximum cases, respectively. For the
phthalates, rates of 5 percent are used for both average and
maximum cases.
Values of 400 and 900 g/day are used as the ayerage and
maximum estimates of soil contact rates for dermal exposure.
These values are based on a consideration of contact rates in mg
soil/cm^ skin (0.5-1.5 mg/cm^) from Schaiim (1984) and surface
area of parts of the body that are likely to come in contact
with soil (EPA 1985). The CDI for dermal cibsorption is cal-• • • • . " . • • ' - . " ;• c n
culated as follows: i w • 1 >
CDI = fCs)fCD)(E)(Yr)(Z) fABSV (6-3) (BW)(DY)(YL)
• o
i ° I o I (Jl
I 00
6.10
H2MGROUP
where, CD = contact rate for soil (g/event)
Z = conversion factor (1 kg/1000 g)
ABS = dermal absorption factor
and Cs, E, Yr, BW, DY, Yl are defined as above. The total CDI
associated with direct contact with soils is the sum of the CDIs
from incidental ingestion and dermal absorption.
Table 6-2a, Summary of Potential Exposures and Risks Associ
ated with Direct Contact with Surface Soil bv Workers, summarizes
the CDIs and risks associated with potential exposure to surface
soils by landfill workers.. Under the average exposure case, the
excess lifetime cancer risk is 9 x 10 , and under the maximum
exposure, the risk is 1 x 10"^. Hazard indices for both the
average and maximum cases are less than one. The average case is
based on the mean concentration of contaminants in soil and aver
age exposure parameters and the maximum case is based on the
maximum detected value and upper-bound exposure parameters,
since the maximum concentration occurs at only one location, the
maximum case amounts to exposure scenario where the worker
returns to the same location every day for 40 years, and the
concentration remains the same at that spot for that period. As
such, the maximum case should not be construed as an actual
exposure, but rather as an extreme upper bound on potential
exposure. Approximately half of the risk (5 x 10"°) is
contributed by arsenic, which is present at background concentra
tion target risk levels normally cited for remedial action. The
cn cq >
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average case exposure is an order of magnitude below | •'
6.11
TABLE 6-2a SUMMARY OF POTENTIAL EiXPOSURES AND RISKS ASSOCIATED WITH DIRECT
CONTACT WITH SURFACE SOIL BY WORKERS NORTH SEA LANDFILL o
CHEMICAL SURFACE SOIL CONCENTRATION
MEAN MAXIMUM (mg/kg) (mg/kg)
CDI - Ingestion CDI-Dermal contact Ave. Max. Ave. Max.
(mg/kg/d) (mg/kg/d) (mg/kg/d) (mg/kg/d)
CDI Total Ave. Max.
(mg/kg/d) (mg/kg/d)
CANCER POTENCY FACTOR
(mg/kg/d)-l
EXCESS LIFETIME CANCER RISK Ave. Max.
CARCINOGENIC PAHs 7.76E-01 7.87E-01 BIS(2-ETHYLHEXYL)PHTHALATE 2.40E+00 9.90E+00 ARSENIC 2.90E+00 8.10E+00
CARCINOGENS -2.47E-09 1.67E-07 3.83E-09 3.O1E-07 6.30E-09 4.68E-07 1.15E+01 7.24E-08 5.38E-06 7.65E-09 2.10E-06 1.02E-08 1.89E-06 1.27E-08 4.00E-06 1.40E-02 1.77E-10 5.60E-08 4.93E-08 2.75E-06 NA NA 7.65E-09 2.75E-06 1.75E+00 1.34E-08 4.82E-06
TOTAL RISK: 8.60E-08 1.03E-05
^^——NONCARCINOGENS —
05
to
NONCARCINOGENIC PAHs B1S(2-ETHYLHEXYL)PHTHALATE DI-n-BUTLYL PHTHALATE DIETHYL PHTHALATE BUTYL BENZYL PHTHALATE ARSENIC CADMIUM CHROMIUM COPPER LEAD MERCURY NICKEL SILVER
3.37E-01 2.40E+00 1.90E-01 6.30E-02 1.70E-01 2.90E+00 7.30E-01 2.80E+00 6.20E+00 5.70E+00 1.70E-01 7.20E+00 6.00E-01
3.37E-01 9.90E+00 3.50E-01 6.30E-02 1.70E-01 8.10E+00 2.20E+00 7.20E+00 9.80E+00 1.71E+01 1.90E+00 2.10E+01 2.20E+00
1.50E-08 1.07E-07 8.48E-09 2.81E-09 7.59E-09 8.63E-07 2.17E-07 8.33E-07 1.84E-06 1.70E-06 5.06E-08 2.14E-06 1.78E-07
1.25E-07 3.68E-06 1.30E-07 2.34E-08 6.32E-08 6.02E-06 1.64E-06 5.35E-06 7.29E-06 1.27E-05 1.41E-06 1.56E-05 1.64E-06
2.33E 1.43E 1.13E 3.75E I.OIE-NA NA NA NA NA NA NA NA
-08 -07 -08 -09 -08
2 3 1 2 5
.26E
.31E
.17E-
.llE-
.69E-NA NA NA NA NA NA NA NA
-07 -06 -07 -08 -08
3.83E-08 2.50E-07 1.98E-08 6.56E-09 1.77E-08 8.63E-07 2.17E-07 8.33E-07 1.84E-06 1.70E-06 5.06E-08 2.14E-06 1.78E-07
_
3.51E-07 6.99E-06 2.47E-07 4.45E-08 1.20E-07 6.02E-06 1.64E-06 5.35E-06 7.29E-06 1.27E-05 1.41E-06 1.56E-05 1.64E-06
REFERENCE DOSE
(mg/kg/d)
4.00E-01 2.00E-02 l.OOE-01 8.00E-01 2.00E-0I l.OOE-03 l.OOE-03 5.00E-03 3.70E-02 6.00E-04 2.00E-03 2.00E-02 3.00E-03
CDI:RfD RATIO Ave.
9.57E-08 1.25E-05 1.98E-07 8.20E-09 8.85E-08 8.63E-04 2.17E-04 1.67E-04 4.98E-05 2.83E-03 2.53E-05 1.07E-04 5.95E-05
Max.
8.77E-07 3.50E-04 2.47E-06 5.56E-08 6.00E-07 6.02E-03 1.64E-03 1.07E-03 1.97E-04 2.12E-02 7.06E-04 7.81E-04 5.45E-04
* ZINC 1.12E-I-01 1.12E-1-01 3.33E-06 8.33E-06 NA NA 3.33E-06 8.33E-06 2.00E-0I
HAZARD INDEX:
1.67E-05 4.16E-05
4.34E-03 3.25E-02
* These chemicals are present at less than twice the background concentrations. See Table 8b for an assessment of exposures and risks due to background levels. NA = Deramal exposure to inorganics is not applicable. Average exposure and risk is based on mean soil concentration and average exposure conditions. Maximum exposure and risk is based on maximum soil concentration and upper-bound exposure conditions.
Of'SO t'OO vas
li2MGROUP
the 10" level. Consecjuently, remediation of surface soils does
not appear warranted.
Table 6-2b, Summary of Potential Exposures and Risks Associ
ated with Direct Contact with Surface Soils by Workers - Based on
Background Levels of Inorganics, presents the CDIs and risks
associated with background levels of inorganics. The soil
concentration for the average case is taken as the lowest value
from.the range given by Shacklette and Boerngen (1984), or Conner
and Shacklette (1975) in the case of cadmium and silver, as shown
in Table A-4. The concentration for the plausible maximum case
is the highest value from the references cited above. All other
exposure parameters are as given previously. The table shows
that, under the average case, the excess lifetime cancer risk for
arsenic based on the background concentration is greater than
that based on the on-site concentration - lE-07 versus lE-08.
For the plausible maximum case the risks are virtually the same -
6E-06 based on background levels and 5E-06 based on the on-site
levels. This suggests that arsenic is not contributing to the
risk above background levels.
6.3 - CONSUMPTION OF SHELLFISH FROM FISH COVE
Exposure may occur as a result of the uptake of contaminants
from; surface water into shellfish in Fish Cove and subsequent
consumption of the shellfish by nearby residents. The chronic
r cn >
daily intake for this potential exposure may be calculated as o • • -i o
follows: ; . ' •' ' • .• I o
•. I ( J l • ." ife.
6.13
TABLE 6-2b SUMMARY OF POTENTIAL EXPOSURES AND RISKS ASSOCIATED WITH DIRECT
CONTACT WITH SURFACE SOIL BY WORKERS -BASED ON BACKGROUND LEVELS OF INORGANICS NORTH SEA LANDFILL
CHEMICAL SURFACE SOIL
CONCENTRATION (a) MEAN MAXIMUM
(mg/kg) (mg/kg)
CDI - Ingestion Ave. Max.
(mg/kg/d) (mg/kg/d)
CDI-Dermal contact Ave. Max.
(mg/kg/d) (mg/kg/d)
CDI Total Ave. Max.
(mg/kg/d) (mg/kg/d)
CANCER POTENCY FACTOR
(mg/kg/d)-l
EXCESS LIFETIME CANCER RISK Ave. Max
ARSENIC - CARCINOGENS
4.10E-^00 l.OOE-i-01 6.97E-08 3.40E-06 NA NA 6.97E-08 3.40E-06 1.75E-i 00 1.22E-07 5.95E-06
TOTAL RISK: 1.22E-07 5.95E-06
NONCARCINOGENS r
05
ARSENIC CADMIUM CHROMIUM COPPER LEAD MERCURY NICKEL SILVER ZINC
4.10E•^00 5.00E-01 3.00E-1-01 1.50E-^01 5.00E-^00 8.20E-02 1.50E•^01 2.50E-01 4.50E-t-01
l.OOE-fOl 4.50E-t-00 5.00E-f01 2.00E-e01 2.00E+01 5.10E+00 1.50E•^01 3.00E•^00 7.40E-e01
1.22E-06 1.49E-07 8.92E-06 4.46E-06 1.49E-06 2.44E-08 4.46E-06 7.44E-08 1.34E-05
7.44E-06 3.35E-06 3.72E-05 1.49E-05 1.49E-05 3.79E-06 1.12E-05 2.23E-06 5.50E-05
NA NA NA NA NA NA NA NA NA
NA NA NA NA NA NA NA NA NA
1.22E-06 1.49E-07 8.92E-06 4.46E-06 1.49E-06 2.44E-08 4.46E-06 7.44E-08 1.34E-05
7.44E-06 3.35E-06 3.72E-05 1.49E-05 1.49E-05 3.79E-06 1.12E-05 2.23E-06 5.50E-05
REFERENCE DOSE
(mg/kg/d)
l.OOE-03 l.OOE-03 5.00E-03 3.70E-02 6.00E-04 2.00E-03 2.00E-02 3.00E-03 2.00E-01
HAZARD INDEX:
CDhRfD RATIO Ave.
1.22E-03 1.49E-04 1.78E-03 1.21E-04 2.48E-03 1.22E-05 2.23E-04 2.48E-05 6.69E-05
6.08E-03
Max.
7.44E-03 3.35E-03 7.44E-03 4.02E-04 2.48E-02 1.90E-03 5.58E-04 7.44E-04 2.75E-04
4.69E-02
(a) Concentrations are taken from ranges given by Conner and Shacklette 1975 and Shacklette and Boerngen 1984, see Table A-4. NA = Deramal exposure to inorganics is not applicable. Average exposure and risk is based on lowest reported soil concentration and average exposure conditions. Maximum exposure and risk Is based on highest reported soil concentration and upper-bound exposure conditions.
3^90 t'OO vas
H2MGROUP
CDI = ( C w ) ( B C F ) ( I R ) ( X ) / ( B W ) ( 6 - 4 )
where, CDI = chronic daily intake (mg/kg/d)
Cw = surface water concentration (mg/1)
IR = shellfish ingestion rate (g/day)
X = conversion factor (1 kg/1000 g)
BW .= average body weight (70 kg)
Surface water cioncentrations (Cw) for selenium and manganese
are taken directly from the. surface water monitoring data.
Concentrations for the organic chemicals were estimated based on
equilibrium partitioning with sediments as follows:
Cw = Cs/(Koc)(foe) (6-5)
I
where, Cw = surface water concentration (mg/1)
Cs = sediment cioncentration (mg/kg)
Koc = organic carbon partition coefficient (1/kg)
foe = fraction of organic carbon in the sediment
(dimensionless)
Organic carbon analyses for sediments from Fish Cove are not
available; therefore, a default value of 1.7 percent was used
based on sediment samples collected by USEPA (1980). Koc values
used in the analysis are listed in Table 6-3, Physicochemical
Parameters Used in Estimating Uptake of Contaminants by Shell
fish.
The bioconcentration factor (BCF) relates the concentration
of the contaminant in surface water to the concentration in the cn
>
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to 1
6.15
H2yHGROUP
TABLE -6-3
PHYSICOCHEMICAL PARAMETERS USED IN ESTIMATING
UPTAKE OF CONTAMINANTS BY SHELLFISH
FISH COVE, NORTH SEA, NY
CHEMICAL
CADMIUM
MANGANESE SELENIUM
BIS(2-ETHYLHEXYL)PHTHALATE
OI-n-BUTYL PHTHALATE
BUTYL BENZYL PHTHALATE
FLUORANTHENE
PHENANTHRENE
PYRENE
log Koc
Organic carbon Partition coefficient
NA NA NA
4.94 3.14
. 4.23
5.11
4.25
5.11
BCF Bioconcentration factor
(1/kg)
200 1
16 4470
420 1580 1150
2630 6460
NA = Not applicable
cn
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6.16
H2MGROUP
aquatic organism. For selenium, fluoranthene, and phenanthrene
bioconcentration factors were taken from the Superfund Public
Health Evaluation Manual (SPHEM). For the remaining organic
chemicals values were derived from log Koc values using the
method of Lyman et al. (1982). The BCF for manganese was assumed
to be one. Ammonia, nitrate and nitrite were also selected as
indicator chemicals in surface waters. However, it is assumed
that these chemicals will metabolize in acjuatic organisms and
will not bioaccumulate. Iron was also selected as an indicator
chemical; however, there is no established reference dose for
iron; therefore, it cannot be included in the assessment. Bio
concentration factors used in . the assessment are listed in
Table 6-3.
The shellfish ingestion rate is taken as 6.5 g/day. This is
the value established by United States Department of Agriculture
(USDA, 1982), which includes the consumption of fish and shell
fish from all sources (i.e., recreational and store bought).
Therefore, it represents an upper bound on the possible consump
tion of shellfish from Fish Cove.
Although recreational fishing is not believed to take place
in Fish Cove, the bioconcentration factors and shellfish
ingestion rates are also applicable to the consumption of fish.
Therefore, the exposures and risks estimated for shellfish
consumption can also be used to represent fish consumption.
Table 6-4a, Summary of Potential Exposures and Risks o o
Associated with Ingestion of Shellfish from Fish Cove^ j *»
•' o
Ul ;• > ^
• Ul
6.17 ^^
cn >
TABLE 6-4a
SUMMARY OF POTENTIAL EXPOSURES AND RISKS ASSOCIATED WITH
INGESTION OF SHELLFISH FROM FISH COVE
NORTH SEA, NY
o
CHEMICAL
SEDIMENT CONCENTRATION
MEAN MAX
(rag/kg) (mg/kg)
SURFACE WATER
CONCENTRATION
MEAN MAX
(mg/1) (mg/1)
CANCER
CHRONIC DAILY INTAKE POTENCY
AVE. MAX FACTOR
(mg/kg/d) (mg/kg/d) (mg/kg/d)-l
EXCESS LIFETIME
CANCER RISK
AVE. MAX
(3)
(-•
00
BIS(2-ETHYLHEXYL)PHTHALATE 8.50E-fOO 1.90E-I-01
CARCINOGENS---
5.74E-03 1.28E-02 2.38E-03 5.33E-03 I.40E-02 3.34E-05 7.46E-05
NONCARCINOGENS
REFERENCE CDI:RfD RATIO
DOSE
(mg/kg/d) AVE. MAX
CADMIUM — — 6.00E-03 l.OOE-02 l.llE-04 1.86E-04
MANGANESE - - 7.20E-01 8.50E-01 6.69E-05 7.89E-05
SELENIUM - — 8.00E-02 5.00E-01 1.19E-04 7.43E-04
BIS(2-ETHYLHEXYL)PHTHALATE 8.50E-f00 1.90E+01 5.74E-03 1.28E-02 2.38E-03 5.33E-03
DI-n-BUTYL PHTHALATE ' 1.90E-01 2.60E-01 7.92E-03 1.08E-02 3.09E-04 4.23E-04
BUTYLBENZYL PHTHALATE 2.20E-01 3,60E-01 7.59E-04 1.24E-03 l.llE-04 1.82E-04
FLUORANTHENE 6.00E-02 6.00E-02 2.71E-05 2.71E-05 2.90E-06 2.90E-06
PHENANTHRENE 5.00E-02 5.00E-02 1.67E-04 1.67E-04 4.07E-05 4.07E-05
PYRENE 6.80E-02 6.80E-02 3.08E-05 3.08E-05 1.85E-05 1.85E-05
l.OOE-03
2.00E-0I
3.00E-03
2.00E-02
l.OOE-01
2.00E-01
4.00E-01
4.00E-01
4.00E-01
HAZARD INDEX:
l.llE-01
3.34E-04
3.96E-02
1,19E-01
3.09E-03
5.57E-04
7.25E-06
1.02E-04
4.61E-05
I.86E-0I
3.95E-04
2.48E-01
2.66E-01
4.22E-03
9.I1E-04
7.25E-06
1.02E-04
4.61E-05
2.74E-01 7.05E-01
9fS0 f'OO
* This chemical is present at less than twice the background concentration. See Table 9b for an assessment of
exposures and risks due to background levels.
NOTES: (1) Surface water concentrations for organics based on equilibrium partitioning with sediments.
(2) Average case based on mean concentrations. Maximum case based on maximum concentrations.
W l r n r based on ingestion of 6.5 g/day of shellfish.
vas 1 )
H2MGROUP
summarizes the potential exposures and risks associated with
consumption of shellfish from Fish Cove. The hazard' indices for
non-carcinogens are less than one under both the average and
maximum cases. Thus adverse health effects would not be expected
from non-carcinogens under this potential exposure scenario. The
excess lifetime cancer risk associated with shellfish consumption
is 3 X 10"^ under the average case and 7 x 10"^ under the maximum
case. These are within USEPAs typical target risk range of 10"^
to 10~'; however, they are above the 10" target risk level.
Several factors suggest that the actual risk should be lower than
was estimated above. As noted,. the shellfish ingestion rate
probably overestimates consumption. In addition, the estimate
assumes a lifetime (70) year consumption period, which probably
over-estimates the length of time that residents will spend near
Fish Cove. The concentrations are based on only three sediment
samples. Bis(2-ethylhexyl)phthalate (DEHP), the chemical
contributing to the potential carcinogenic risk was also detected
in field blanks; therefore, there is uncertainty as to the actual
level present. Given this uncertainty, and the conservative
nature of the assessment, there does not appear to be any immedi
ate risk to consumers of shellfish from fish Cove. Resampling of
sediments may be necessary . to verify if DEHP is present and, if
so, at what levels.
Although recreational fishing is not believed to take place . a >
in Fish Cove, the bioconcentration factors and shellfish ' ! o
ingestion rates are also applicable to the consumption of fish. : ** . ' • , ' I ••jo
. ' (Jl
6.19
H2MGROUP
Therefore, the exposures and risks estimated for shellfish
consumption can also be used to represent fish consumption.
Hazard indices for both the average and plausible maximum
cases are less than one, suggesting no adverse health effects
from exposure to non-carcinogens under the assumed exposure
conditions. Table 6-4b, Summary of Potential Exposures and Risks
Associated with Ingestion of Shellfish from Fish Cove - Based on
Background Levels of Inorganics, shows similar CDI:RfD ratios as
for the off-site concentrations. This suggests that the risks
from cadmium and manganese are attributable primarily to
naturally occurring background levels.
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6.20
TABLE 6-4b SUMMARY OF POTENTIAL EXPOSURES AND RISKS ASSOCIATED WITH
INGESTION OF SHELLFISH FROM FISH COVE -BASED ON BACKGROUND LEVELS OF INORGANICS . NORTH SEA, NY .
o
05
to
CHEMICAL
CADMIUM
MANGANESE
SELENIUM
SURFACE WATER
CONCENTRATION
MEAN
(mg/l)
l.OOE-02
1.90E-01
ND
MAX • (mg/1)
l.OOE-02
3.80E-01
ND
CHRONIC DAILY INTAKE.
AVE.
(mg/kg/(J)
1.86E-04
1.76E-05
ND
MAX (mg/kg/d)
1.86E-04
3.53E-05
ND
CANCER
POTENCY
• FACTOR
(mg/kg/d)-l
- l.OOE-03
2.00E-01
3.00E-03
HAZARD INDEX
EXCESS LIFETIME
CANCER
AVE.
1.86E-01
8.82E-05
ND
1.86E-01
RISK
MAX
1.86E-01
1.76E-04
ND
1.86E-01
NOTES: (1) Average case based on mean concentrations. Maximum case based on maximum concentrations. (2) CDI based on ingestion of 6.5 g/day of shellfish. NO = Chemical not detected In background samples.
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7.0 - CONCLUSIONS AND RECOMMENDATIONS
Conclusions and recommendations are discussed in this
section. Conclusions related to the ARAR comparisons and the
qualitative risk characterizations are given. These are grouped
by the following exposure pathways in decreasing order of
importance:
(1) Exposure Pathway A - ingestion of shellfish from
Fish Cove;
(2) Exposure Pathwav B - direct contact with surface
soil by landfill workers; and
(3) Exposure Pathwav C - ingestion of groundwater from
private wells by residents downgradient of the
landfill.
Recommendations for additional remedial investigation work
are proposed thereafter, primarily in the area of sampling.
7.1 - SUMMARY OF COMPARISON TO ARARs
Surface Water (Exposure Pathway A) -
THE FEDERAL WATER QUALITY CRITERIA (WQC) FOR
SELENIUM IN THE HUMAN HEALTH PROTECTION CATEGORY
IS THE ONLY AVAILABLE ARAR FOR COMPARISON. THIS ,' !• cn
CRITERIA IS EXCEEDED. AQUATIC LIFE PROTECTION . "
CRITERIA MAY ALSO APPLY.
This applies directly to Exposure Pathway A - the ingestion o
o of shellfish from Fish Cove. There are five selected indicator i
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7.1
H2MGROUP
chemicals detected in Fish Cove surface water. ARARs for New
York State ambient Class SB waters and Federal ambient WQC are
available for only selenium. For human health protection, the
toxicity protection level, when ingesting both water and
organisms, is 0.01 mg/1. The mean (0.8 mg/1) concentrations
detected in surface water samples exceed this value. Federal
ambient WQC for aquatic life protection for selenium are also
exceeded.
USEPA does not have any ARARs for the quality of edible
shellfish tissue. However, the FDA has produced guidelines for
mercury in shellfish (1.0 ppb). Recommended levels for other
metals, in shellfish, are not available.
Soil (Exposure Pathway B) -
SOIL ARARs DO NOT EXIST AT THIS TIME, BUT TARGET
CLEANUP LEVELS CAN BE USED IN PLACE OF THIS
DEFICIENCY. BASED ON THIS PREMISE, SOIL REMEDI
ATION IS NOT WARRANTED AT THIS SITE.
This applies directly to Exposure Pathwav B) - the direct
contact (i.e., potential ingestion and dermal absorption) with
surface soil by landfill workers. ARARs for surface soil in the
Federal and State sector do not exist at this time. Remediation
of soils is not warranted based on a comparison of the risk
characterization total risk value for potential carcinogens and -fi ' w
the Federal target level of 10 °. ^ > I 1 o o
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7.2
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Groundwater (Exposure Pathway C) -
PREDICTED LONG-TERM GROUNDWATER EXPOSURE CONCEN
TRATIONS EXCEEDED THE MOST STRINGENT ARARs FOR
CERTAIN INDICATOR CHEMICALS, BUT ONLY BY A SMALL
MARGIN.
This applies to Exposure Pathway C - the ingestion of
groundwater from private wells by residents downgradient of the
landfill. Refer to Section 4.0 - Comparison of ARARs for a full
discussion.
NOTE: The New York State Department of Health ARAR for
volatile organics in drinking water is low, 5.0 ppb (effective
1/89). At the time these groundwater samples were run (Fall
1987), the detection level was 5.0 ppb. This alone warrants
resampling.
7.2 - SUMMARY OF THE OUALITATIVE RISK CHARACTERISTICS
Exposure Pathway A - Ingestion of Shellfish from
Fish Cove -
THERE DOES NOT APPEAR TO BE ANY IMMEDIATE RISK TO
CONSUMERS OF SHELLFISH AT FISH COVE. NEVERTHE
LESS, BASED ON THE CONSERVATIVE NATURE OF THE
ASSESSMENT AND THE UNCERTAINTY IN THE LIFETIME
CANCER RISK ASSESSMENT, RESAMPLING OF SEDIMENTS
cn FOR DEHP IS RECOMMENDED. , Cd
\ > The lifetime cancer risk associated with shellfish consump- o
o tion is 3 X 10 ^ under the average case and 7 x 10 ^ under the ; *"
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7.3
H2yViGROUP
maximum case. The risk estimates exceed the USEPA target risk
level of 1 X 10"°, but are within the risk range of 1 x lO"' to
1 X 10"^. The PC considered is DEHP.
The actual risk may be lower than the above based on these
factors: (1) the consumption rate may be an overestimate; (2)
the lifetime (70 years) consumption period may be an overesti
mate; (3) the concentrations are based only on three sediment
samples; and (4) DEHP was detected in field blanks.
Adverse health effects from NCs are not expected as based on
the hazard indices for average (2 x lO"-'-) and maximum (5 x 10"- )
conditions. The NC indicator chemicals are: Mn, Se, DEHP, DNBP,
BBP, fluoranthene, phenanthrene and pyrene.
Exposure Pathway B - Direct Contact (Dermal Ab
sorption and Ingestion) with Surface Soil by Land
fill Workers -
REMEDIATION OF SURFACE SOILS DOES NOT APPEAR
WARRANTED BASED ON THE ASSUMPTIONS AND SCENARIOS
USED.
Adverse health effects from NCs are not expected based on
the calculated hazard indices for average (10 x 10"^) and maximum
(2 X 10"- ) conditions. The NC indicator chemicals are: PAHs,
DEHP, DNBP, DEP, BBP, Hg and Ag.
Lifetime cancer risk for the average condition (4 x 10"^) is
below the USEPA target risk of 1 x 10"^. However, the risk for cn
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maximum (5 x 10~°) is only slightly above the target risk level, j o
The maximum should not be construed as an actual exposure, but i o
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7.4
H2MGROUP
rather as an extreme condition of potential exposure. The PC
indicator chemicals are PAHs and DEHP.
Exposure Pathway C - Ingestion of Groundwater by
Residents, Downgradient from the Landfill -
RESIDENTS ARE NOT CURRENTLY EXPOSED TO CONTAMI
NANTS IN GROUNDWATER, SINCE ALL HOMES HAVE BEEN
CONNECTED TO PUBLIC WATER SUPPLY. BASED ON THE
RISK CHARACTERIZATION, HOWEVER, ADDITIONAL GROUND
WATER MONITORING IS RECOMMENDED.
Under Superfund guidance the lifetime cancer risk should be
within the 10" to 10~ range. The average is 4 x 10"'^ and the
maximum is 8 x io"^; although arsenic, a naturally occurring
compound is the major contributor to this risk. The PC indicator
chemicals are: arsenic, benzene, bis(2-ethylhexyl) phthalate
(DEHP), chloroform, 1,1-dichloroethane (1,1-DCA), 1,1-dichloro-
ethane (1,2-DCA), 1,1-dichloroethene (1,1-DCE), methylene
chloride, tetrachloroethene (PCE) and trichloroethene (TCE).
Adverse health effects from most NCs are not expected based
on the hazard indices for average (2.3) and maximum (32) condi
tions. The NC indicator chemicals are: ammonia, bis(2-ethyl-
hexyl) phthalate (DEHP), butylbenzyl phthalate (BBP), calcium
(Ca), chloroform, chromium (Cr), copper (Cu), 1,1-dichloroethene
(1,1-DCE), 1,2-dichloroethene (1,2-DCE), endosulfan, iron (Fe),
lead (Pb), manganese (Mn), methylene chloride. Nickel (Ni),I ^
nitrate/nitrite, phenol, silver (Ag), tetrachloroethene (PCE),/ o
toluene, trichloroethene (TCE) and zinc (Zn). CDI:RfD ratios for
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7.5 ---
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ii2MGROUP
lead exceed one for both site and background conditions. The
CDI:RfD ratio for cadmium exceeds one only for the worst case.
All other CDI:RfD ratios are less than one.
7.3 - RECOMMENDATIONS
Recommendations for additional sampling as based on the
comparison with ARARs and the qualitative risk characterization
are as follows by exposure pathway:
Exposure Pathway A - Shellfish Ingestion -
A small scale study of Fish Cove should be pursued to
complete our understanding of the human exposure to shellfish
ingestion. The study would also examine the magnitude of
leachate release into Fish Cove and evaluate.the impacts on hard
clam populations. Three media should be sampled: (1) sediments;
(2) surface water; and (3) shellfish.
Experiments should be performed on sediment cores from Fish
Cove. These experiments would measure the flux of leachate indi
cator solutes across the sediment-surface water interface. Also,
the sediments should be analyzed for phthalates (i.e., DEHP).
DEHP was identified as a potential carcinogen in the risk
characterization, and the presence and concentration of DEHP in
sediments needs to be verified. _ • - r
A water sampling program in Fish Cove would include ' cn
measurement of leachate concentrations at the sediment sampling I >
locations between high and low tide. This data, combined with
the sediment-surface water flux experiments data and a
7.6
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bathymetric survey of fish, will help determine the amount of
leachate discharging into Fish Cove, if any.
Shellfish exist in the sediments and are filter feeders.
Therefore, clam tissue analyses is necessary to determine
leachate bioaccumulation. Clams would be collected at select
stations at Fish Cove and analyzed for metals and leachate indi
cators. Also, bioassays using hard clam larvae would be
performed to determine the impact, i.e., toxicity, in terms of
LD50 of leachate components. Clam larvae is the most sensitive
stage of moiluscan development.
Exposure Pathwav B - Surface Soil Intake -
The major conclusions for Exposure Pathwav B (Surface Soil
Intake) do not warrant additional sampling. This is so primarily
because the risk characterization does not indicate a risk to
human health.
Exposure Pathway C - Groundwater Intake -
The results warrant additional sampling.
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7.7
H2MGROUP
REFERENCES
CH2M HILL SOUTHEAST, INC., 1985. Soil Contamination Evaluation Methodology, Preliminary Draft Memorandum Report, Subtask 2.3, Contract No. 68-01-2090 W61501.A0, Reston, Virginia.
CONNOR, J.J. AND SHACKLETTE, H.T., 1975. Background Geochemistry of Some Rocks, Soils, Plants and Vegetables in the Conterminous U.S., USGS Professional Paper: 574-F.
DOMENICO, P.A. AND V.V. PALCIAUSKAS, 1982. Alternative Boundaries in Solid Waste Management Groundwater 20(3):303-311.
ENVIRONMENTAL PROTECTION AGENCY (EPA), 1989. Letter from Carole Petersen (Chief, EPA NY/Caribbean Compliance Branch) to Mardythe DiPirro, Town Supervisor of the Town of Southampton on Remedial Investigation Response Document, North Sea Municipal Landfill, Town of Southampton, Suffolk County, New York, March 27, 1989.
ENVIRONMENTAL PROTECTION AGENCY (EPA), 1989. Memorandum from J. Winston Porter to Regional Administrators on Interim Final Guidance for Soil Ingestion Rates. OSWER Directive 9850.4, January 27, 1989.
ENVIRONMENTAL PROTECTION AGENCY (EPA), 1986a. Superfund Public Health Evaluation Manual. Prepared by ICF, Inc. for Office of Emergency and Remedial Response, Washington, D.C. October, 1986. EPA"400/168-060
ENVIRONMENTAL PROTECTION AGENCY (EPA), 1986b. Guidelines for Carcinogen Risk Assessment. Fed. Reg. 51:33992-34002 (September 25, 1986)
ENVIRONMENTAL PROTECTION AGENCY (EPA), 1986c. Guidelines for the Health Risk Assessment of Chemical Mixtures. Fed. Reg. 51:34014-34023 (September 24, 1986)
ENVIRONMENTAL PROTECTION AGENCY (EPA), 1986. Superfund Public Health Evaluation Manual, OSWER Directive 9285.4-1, EPA 540/1-86/060.
ENVIRONMENTAL PROTECTION AGENCY (EPA), 1985. Protection of Public Ground Water Supplies from Ground Water Contamination. Seminars Publication EPA/625/H-85/D16.
ENVIRONMENTAL PROTECTION AGENCY (EPA), 1985. Development of w Statistical Distributions or Ranges of Standard Factors Used in Exposure Assessments. Office of Health and Environmental
>
o Assessment, Washington, D.C. March 1985. OHEA-E-161. ] o
o Ul cn
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ENVIRONMENTAL PROTECTION AGENCY (EPA), 1980. Sorption Properties of Sediments and Energy Related Pollutants. EPA 600/3-80-041. Environmental Research Laboratory, Athens, GA.
FELDMANN, R.J., and MAIBACH, H.I., 1970. Absorption of Some Organic Compounds Through the Skin in Man. J. Invest. Dermatol. 54: 399-404.
FELDMANN, R.J., and MAIBACH, H.I., 1974. Percutaneous Penetration of Some Pesticides and Herbicides in Man. Toxicol. Appl. Pharmacol. 28:126-132.
HOLZMACHER, McLENDON & MURRELL, 1986. South Fork Supplemental Water Resources Study, Phase III. Groundwater Modeling and Recommendations for SCDHS in Cooperation with SCWA and Town of East Hampton.
LYMAN, W.J., REEHL, W.F., and ROSENBLATT, D.H., 1982. Handbook of Chemical Property Estimation Methods; Environmental Behavior of Organic Compounds. McGraw-Hill.
POIGER, H., and SCHLATTER C , 1980. Influence of Solvents and Absorbents on Dermal and Intestinal Absorption of 2,3,7,8-TCDD. Food Cosmet. Toxicol. 18: 477-481.
SHACKLETTE, H.T. AND BOERNGEN J.G., 1984. Elemental Concentrations in Soils and Other Surficial Materials of the Conterminous U.S., USGS Professional Paper: 1270.
SCHAEFER, H. , ZESCH, A., and STUTTGEN. G. , 1983. Skin Permeability. Springer-Verlag, New York.
SCHAUM, J.L., 1984. Risk Analysis of TCDD Contaminated Soil. U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Washington, D.C. November 1984. EPA 600/8-84-031.
USDA, 1982. Foods Commonly Eaten by Individuals: Amounts Per Day and Per Eating Occasion. Home Economics Research Report No. 44.
WEBSTER, R.C., MOBAYEN, M., and MAIBACH, H.I., 1987. In Vivo and In vitro Absorption and Binding to Powered Stratum Corneium as Method to Evaluate Skin Absorption of Environmental Chemical Contaminants from Ground and Surface Waters. J. Toxicol. Environ. Health 20: 367-374.
WILSON,: J.L. and P.J. MILLER, 1978. Two Dimensional Plume in Uniform Groundwater Flow. Journal Hydraulic Div. Assn. Soc, Civil Engineering Paper No. 13665, HY4: 503-514.
cn
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YANG, J.J., ROY, T.A. and MICKERER, CR. , 1986a. Percutaneous Absorption of Benzo(a)pyrene in the Rat. Toxicol, and Indust. Health 2:409-415.
YANG, J.J., ROY, T.A. and MICKERER, CR. , 1986b. Percutaneous Absorption of Anthracene in the Rat. Toxicol, and Indust. Health 2:409-415.
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APPENDIX A
CONCENTRATIONS OF CHEMICALS IN ENVIRONMENTAL MEDIA
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APPENDIX A
NOTES FOR TABLES LISTING CONCENTRATIONS OF CHEMICALS IN ENVIRONMENTAL MEDIA
1. General:
The tables list each detected chemical in the media of concern. For each chemical the range of concentration values, the representative concentration, the frequency of occurrence of values detected above the detection level (DL) and the total number of samples are given for the study area and for background conditions. The representative concentration is a mean of all detected values. Those values reported below the detection level are also included in the mean and count as one-half the detection level.
2. Groundwater (Table A-1):
Thirty samples were analyzed for inorganics. This includes all wells samples in Round 1 (19 wells) and 11 stainless steel wells in Round 2. The samples were analyzed for priority pollutant metals (total and filtered) and leachate indicator inorganics. Samples from residential and supply wells in Round 1 were not filtered.
A total of 22 samples were analyzed for organics analysis. Eleven stainless steel wells were sampled for organics in Round 1 and Round 2. Samples were analyzed for purgeable organics and semivolatiles (acid extractables, base neutrals and pesticides and PCBs). Even though split samples were used to substitute for rejected DEHP reported values, a total of 16 reported values (out of 22) were used to determine the representative concentration of DEHP.
Background values are based on the average of two round of values in upgradient well cluster MW-1.
3. Surface Water (Table A-2):
Twelve samples were analyzed from 6 locations at high and low tide. Samples were analyzed for priority pollutant metals cn
! cq and selected leachate indicators. One exception are the 6 values ' > rejected for copper analysis.
• o 1 C2
Background values are averaged from the values from sample i *» locations 5 and 6. This is a total of 4 samples representing j high and low tide. Out of these 12 samples, 8 are representative I ° of the site. ' <y>
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4. Soil (Tables A-3. A-4. A-5 and A-6);
A total of 46 samples were obtained in various soil media on and off the site. These are: landfill surface soils, subsurface saturated soils obtained at the stainless steel well locations, surface and subsurface soils at the filled scavenger lagoon site and sediments from Fish Cove.
All soil samples were analyzed for priority pollutant metals. However, 33 samples were used for the average of copper because 13 values were rejected in the surface soil package. All soil samples were also analyzed for semivolatiles (acid extractables and base neutrals). Lagoon soil samples were analyzed for purgeable organics and pesticides and PCBs in addition to the above.
Background samples were not obtained for the soil media. Background values for metals are based on two USGS reports. These are: (1) Shacklette, H.T. and Boerngen, J.G., 1984. Elemental Concentrations in Soils and Other Surficial Materials of the Conterminous U.S.. USGS Professional Paper 1270.; and (2) Connor, J.J. and Shacklette, H.T., 1975, Background Geochemistry of Some Rocks. Soils. Plants, and Vegetables in the conterminous U.S.. USGS Professional Paper 574-F. Reference (1) discusses samples collected at sites in Connecticut and northern New Jersey and is applicable to all priority pollutant metals except thallium. Reference (2) discusses samples collected from glaciated soil in Missouri and applies to cadmium and silver. Background values for thallium and organics are not available.
5. Air: \
Air samples were analyzed for purgeable organics. All reported values of air samples analyzed were below detection levels and thus not included in this evaluation.
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TABLE A-1
CONCENTRATIONS OF CHEMICALS IN ENVIRONMENTAL MEDIA - GROUNDWATER
Chemical
Ammonia Arsenic Arsenic * Cadmium Cadmium * Chromium Chromium * Copper Copper * Iron Iron * Lead Lead * Manganese *. Manganese Mercury Mercury * Nickel Nickel * Nitrate/Nitrite SiIver SiIver * Zinc Zinc * Benzene Chloroform 1,1-DCA 1,2-DCA 1,1-DCE 1.2-DCE Methylene.Chloride TCE Toluene PCE Phenol DEHP BBP Endosulfan I Endosulfan II
BOL = Below Detection OL = Detection Level
NA = Not Available
Range of Concentrat
(mg/1)
B0L(0.02) BDL(0.01 -BDL(O.Ol) -BOL(0.005 -BDL(0.005 -BDL(O.Ol) -BDL(O.Ol) -BDL(0.025 -BDL(0.025 -
0.15 -0.04 -
BOL(0.005) -BDL(0.005) -BDL{0.02) -BDL 0.02) -BDL(0.0002) -BDL(0.0002) -BDL(0.04) BDL(0.04) -BDL(O.IO) BDL(O.Ol) -BDL{0.01 BDL 0.02 -BDL(0.02) BDL(0.005) -BDL(0.005) -BDL(0.005) -BDL(0.005) -BDL(0.005) -BDL(0.005) -BDL 0.005) -BDL(0.005) -B0L{0.005) -BOL 0.005 -BDL(O.OOl) -BDL(O.Ol) -BDL 0.01) -BDL 0.0001) -BDL(O.OOOl) -
Level
ion
44.5 0.014 0.013 0.05 0.02 0.55 0.53 0.28 0.88 61.4 30 0.185 0.165 9.1 9.6 0.0007 0.0005 0.15 0.20 11.8 0.07 0.03 0.30 0.36 O.OOIJ 0.003J 0.003J 0.002J 0.016B 0.004J 0.024B 0.007J 0.003J 0.007J 0.003 0.14
0.00027 0.00019
NR = Not Reported; mean is greater than maximum * = FiItered metals (1) 8/24 rejected (round 2). (2) 8/24 rejected (round 2; 2/24 rejec
Site *
Mean Concentration
(mg/l)
4.6 0.006 0.005 0.013 0.005 0.053 0.03 0.091 0.08 18.4 5.6
0.024 0.01 1.3 1.52
0.0002 0.0001 0.04 0.02 1.2
0.008 0.006 0.13 0.07
0.0024. 0.0025 0.0025
NR 0.003 0.0026 0.0045
- 0.0029 0.0019 0.0027 0.0011 0.0285 0.005
0.00005 0.00007
due to values below
ted (round 1).
Frequency of Occurence Values
16 / 2 / 1 / 14 / 5 / 12 / 13 / 12 / 18 / 24 / 24 / 10 / 8 / 21 / 23 / 19 / 2 / 9 / 7 / 12 / 2 / 2 / 15 / 22 / 1 / 4 / 3 / 2 / 2 / 2 / 8 / 2 / 5 /
• 3 /
2 / 11 / 3 / 2 / 1 /
> DL
24 24 24 24 24 16 24 16 23 24 24 14 22 24 24 24 24 24 24 24 24 24 16 24 16 16 16 16 16 16 16 16 13 16 16 13 16 16 16
the detection
(1)
(1)
(2)
(1)
limit
Range of Concentrat
(mg/1)
8DL(0.02) -BDL(O.Ol) BDL(O.Ol)
0.01 -BOL(O.Ol) -B0L(0.002) -BDL(O.Ol) -
BDL(0.007) -BDL(0.025) -
6.5 -0.03 -
B0L(0.O02) -0.006 -
BDL(0.02) -0.22 -
B0L(0.O002) -B0L(0.0002) -BDL(0.04) -BDL(0.04) BDL(0.1 -BDL(O.Ol) -BDL(O.OI)
0.10 -BDL(0.02) -BDL(0.005 -BOL 0.005) -BDL(0.005) BOL 0.005) B0L(0.005) BDL(0.005) BDL(0.005) -BDL(0.005) BDL 0.005) -BDL(0.005) BDL(O.OOl) -
0.01 -BDL(O.Ol) -BDL 0,95 BDL(O.IO)
\
ion
.17
0.05 0.01-0.062 0.02 0.18 0.08 21 0.32 0.155S 0.05 0.39 0.84 0.0005 0.0002 0.12
0.40 0.01
0.276E 0.10 O.OOIJB O.OOIJ
0.015B
0.002J
0.003 0.019B 0.011
Background +
Mean Concentration
(mg/1)
0.05 0.005 0.005 0.018 0.006 0.025 0.0075 0.13
, 0.04 13.4 0.14
0.1022 0.02 0.14 0.53
0.0002 0.0001 0.04 --0.2
0.006 _-
0.1965 0.05 NR NR --------
0.0074 --NR --
0.0009 0.01
0.0038 — --
Frequency of Occurence Values
2 / 0 / 0 / 6 / 3 / 5 / 1 / 5 / 4 / 6 / 6 / 5 / 6 / 3 / 6 / 3 / 1 / 2 / 0 / 4 / 1 / 0 / 4 / 4 / 1 / 2 / 0/ 0 / 0 / 0 •/
3 / 0 / 1 / 0 / 1 / 3 / 3 / 0 / 0 /
> DL
6 6 6 6 6 5 6 5 (3) 6 6 6 5 (3) 6 6 6 6 5 . 5 6 6 6 6 4 5 5 5 6 6, 6 6 6 6 6 5 6 6 3 6 6
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APPENDIX B
GROUNDWATER EXPOSURE ESTIMATION METHOD
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GROUNDWATER EXPOSURE ESTIMATION METHOD APPENDIX B
The most conservative approach, aside to using the actual detected concentrations, was used to estimate groundwater exposure concentrations. The groundwater exposure estimation method is based on a soil contaminant evaluation methodology (CH2M Hill Southeast, 1985) and is referred to as "SOCEM".
Some of the major assumptions are summarized below:
This is a simple model. The simpler the model, the more conservative the estimates will be. One can move up to more complex models as needed later on.
The initial source concentration at Well #3 is diluted by vertical and lateral dispersion during transport. No other attenuation mechanisms are assumed to occur (i.e., loss/decay, chemical reactions, retardation, longitudinal dispersivity or recharge dilution).
•> Leachate contaminants present in the source soil (Cell 1) are leached to groundwater downgradient. The worst case is assumed, i.e., no liner and no cap on top or sides.
The contaminants exist downgradient of the source through a vertical plane with dimensions equal to the source width and depth of detected contamination.
The steady state condition is assumed, i.e., the source is constant and therefore contaminant flux to groundwater does not increase or decrease over time.
The groundwater transport equation is:
Cx = Co * erf (Z/(2(d*x)l/2) ) * erf (y/(4 (d*x) 1/2)) 1 ]
where, Cx = Contaminant concentration in groundwater at the receptor well (ug/1).
The receptor well is couplet MW-4 along Fish Cove Road (refer to Figure B-1).
*****
t ^ If the groundwater flow zone is limited in vertical extent by a relatively impermeable layer (i.e., acjuifer thickness less than two times 2), then the equation is:
Cx = Co * Z/H * erf (y/(4(4*x)1/2))
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However, this geologic limitation does not apply to this ^ o site, and therefore, was not used in the calculations. ' *£;
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FIGURE B-1
SCALE IN FEET
DIRECTION OF GROUNDWATER FLOW
SEA LANDFILL
LEGEND
= STAINLESS STEEL MONITORING WELL
( = EXISTING PVC WELL
+ = RESIDENVAL WELL
' X » = DISTANCE FROM SOURCE TO RECEPTOR WELL
' X B = DISTANCE FROM BACKGROUND TO RECEPTOR WELL
Y = WIDTH OF CONTAINMENT ZONE
H2MGRQUP ENGINEERS u a M L U . N.T.
ARCHITECTS • PLANNERS RVCnCAD, N.Y.
SCIENTISTS fMXPOO. N.JL
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Co = Initial contaminant concentration in groundwater at the waste boundary and for background (ug/1).
The waste boundary is represented by detected concentrations of indicator chemicals in well couplet MW-3. The background conditions are represented by detected concentrations in upgradient well couplet MW-1 (refer to Figure B-1) .
For waste boundary and background conditions, two scenarios are run:
The best case scenario represents short-term conditions and uses an average of detected values from Rounds 1 and 2 of the Phase I RI. Where detected values were rejected for certain indicator chemicals, these values were substituted with split sample values. This applies mainly to Round 2 results for certain metals (chromium, copper, lead and zinc) and several organic indicator chemicals (methylene chloride, toluene, butyl benzyl phthalate and DEHP).
The worst case scenario represents long-term conditions. The maximum value is selected from two rounds of groundwater sample results for this scenario.
If an indicator chemical was detected below detection levels for all cases, the detection level was used for the worst case scenario. An average of one-half the detection level was used for the best case scenario.
It is important to note that the detection level for volatile organics for the Phase I RI sample is 5 ppb. This is now the NYSDOH ARAR for public drinking water.
erf = error function (the exponential integral function).
= Transverse dispersivity (feet).
The assumed value is 0.66 feet and is presented in the South Fork Study (H2M, 1986). The transverse dispersivity in this study is assumed to be one-fifth of the longitudinal dispersivity (3.281 feet).
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X = Distance to the receptor well in the direction of groundwater flow (feet).
The approximate distance from well couplet MW-3 (waste boundary) to receptor well couplet MW-4 is 1,500 feet. The approximate distance from well couplet MW-1 (background) to receptor well couplet MW-1 is 3,350 feet (refer to Figure B-1).
y = Width of the contaminated zone at the waste boundary measured perpendicular to the direction of groundwater flow (feet).
For both waste boundary and background conditions, the approximate inferred width of the source (Cell 1) was used as the most conservative value (700 feet) (refer to Figure B-1).
z = Thickness of the contaminated zone at the waste boundary measured downward from the water table surface.
The total saturated thickness of the Upper Glacial aquifer at the waste boundary is about 150 to 160 feet. The inferred extent of the leachate plume was drawn in cross section and is about 90 to 100 feet (refer to Figure B-2). The more conservative value (100 feet) is assumed for the model.
The "SOCEM" computer program is written in GWBASIC (refer to Figure B-3).
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SILTY OR CLAYEY SANDS SAND - SILT MIXTURE SAND - CLAY MIXTURE
HaMGROUP ENGINEERS MELVLLE, N.Y.
ARCHITECTS PLANNERS RIVERHEAO, N.Y.
SaENTISTS SURVEYORS FAIRFIELD. N.J.
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FIGURE B-3
SOCEM PROGRAM
10 INPUT "ENTER INITIAL CONCENTRATION, CO (US/L)"; CO: PRINT 11 D=.66 12 X=1500 1.3 Y=700 14 Z=100 20 Bl=Z/(2!*( <D*X)'--,5) ) 21 GOSUB 150 30 B2=Y/(4!*( (D*X.)'-.5) ) 31 GOSUB 250 32 REM 40 CX=C0*ERFB1*ERFB2 41 DF=CO/CX 50 PRINT "CONCENTRATION AT RECEPTOR CX"; CX; "UG/L": 60 PRINT "DILUTION FACTOR (CO/CX) ="; DF: 120 END 130 REM COMPUTE ERFBl 150 T1=1!/(1!+(.3275911»B1)) 160 Al=.254a29592tt 170 A2=-.234496736# 180 A3=1.421413741# 190 A4=-l.453152027tt 200 A5=1.061405429tt .
210 ERFB1 = 1 !-( ( (Al*Tl) + (A2*Tl--2) + (A3*Tl-'^3) + (A4*Tl'--4) + (A5*Tl'"-5) ) *EXP (-Bl'-2' ) ) : RE TURN 240 REM COMPUTE ERFB2 250 T2=l!/(I!+(.3275911*B2)) 260 Cl=.254a29592# " .. 270 C2=-.284496736t+ ' 280 C3=1.421413741# 290 C4=-1.453152027# 300 C5=1.061405429#
310 ERFB2=1 !-( ( (C1*T2) + (C2*T2-'-2) + (C3*T2'^3) + (C4*T2"-4) + (C5*T2-"-5) ) *EXP (-B2-'-2 ! ) ) : RE TURN
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H2MGROUP
APPENDIX C
TOXICITY PROFILES
APPENDIX C
H2MGROUP TOXICITY PROFILES
AMMONIA
Ammonia is absorbed by inhalation and ingestion; absorption by dermal or
ocular exposure is likely at concentrations high enough to cause tissue injury
(Wands 1982). Acute dermal exposure may result in second degree skin burns
(Levy et al. 1964). Acute exposure to ammonia vapors results in a burning
sensation of the nose and throat, laryngitis, pharyngitis and rhinitis in
humans (NIOSH 1974). Long-term symptoms such as pulmonary edema,
bronchopneumonia, and pneumonitis have been reported in individuals
accidentally exposed to ammonia gas (NIOSH 1974). Accidental poisoning or
intentional ingestion of ammonia solutions by humans, frequently results in
severe burning pain in the mouth, throat, and stomach (NIOSH 1974). In
experimental animals, acute inhalation exposure has been found to produce eye
and respiratory tract irritation (Propkopieva et al. 1973) and to reduce
ciliary activity in rat tracheas (Dalhamn 1956). Subchronic inhalation
exposures in animals produce congestion of the spleen, liver, and kidney,
degenerative changes in the adrenal gland, and nonspecific lung inflammation
(Weatherby 1952, Coon et al. 1970).
EPA (1989) has reported a value of 34 mg/liter as a chronic and subchronic
oral reference dose. This value is equivalent to 0.97 mg/kg/day assuming a 70
kilogram individual consumes 2 liters of water per day. A safe concentration
may be higher, but the data are inadequate to assess. The oral RfD was based
upon the taste threshold (EPA 1981, WHO 1986). EPA (1989) has also derived
an inhalation RfD of 0.36 mg/m^ based upon the odor threshold (Carson et al.
1981, Campbell et al. 1958). No safety factors were used to develop the RfDs.
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CAMPBELL, C.L., DAWES, R.K., DEOLALKA, S., and MERRITT, M.C. 1958. Effect of certain chemicals in water on the flavor of brewed coffee. Food Res. 23:575-579. (Cited in U.S. EPA, 1981)
CARSON, B.L., BEALL, CM., ELLIS, H.V.III, and BAKER. L.H. 1981. Ammonia Health Effects. Prepared by Midwest Research Institute for Office of Mobile Source Air Pollution Control, Emission Control Technology Division, U.S. EPA, Ann Arbor, MI. EPA 460/3-81-027
COON, R.A., JONES, R.A.. JENKINS, L.L., Jr., and SIEGEL, J. 1970. Animal inhalation studies on ammonia, ethylene glycol, formaldehyde, dimethylamine, and ethanol. Toxicol. Appl. Pharmacol. 16:646-655
DAHLMANN, T. 1956. Mucus flow and ciliary activity in the trachea of healthy rats and rats exposed to respiratory irritant gases. Acta Physiol. Scand. 36 (Suppl. 123):93-97 (As cited in NIOSH 1974)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1981. Ambient Water Quality Criterion for the Protection of Human Health: Ammonia. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria Assessment Office, Cincinnati, Ohio, for the Office of Water Regulations and Standards, Washington, DC
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
LEVY, D.M., DIVERTIE, M.B., LITZOW, T.J., and HENDERSON, J.W.. 1964. Ammonia burns of the face and respirktory tract. JAMA 190:873-876
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1974. Criteria for a Recommended Standard. . . Occupational Exposure to Ammonia. U.S. DHEW (NIOSH) Publication No. 74-136
PROPKOPIEVA, A.S., YUSHOV., G.G., and UBASHEEV, I.O. 1973. [Materials for a . toxicological characteristics of the one-term effect of ammonia on the organism of animals after brief exposure] Gig. Tr. Prof. Zabol. 6:56-57 (as cited in WHO 1976)
WANDS, R.C. 1982. Alkaline Materials. In Clayton, G.D.. and Clayton, F.E. (eds.). Pattys Industrial Hygiene and Toxicology. 3rd edition. John Wiley and Sons, New York
WEATHERBY-, J.H. 1952. Chronic toxicity of ammonia fumes by inhalation - -(1985). Proc. Soc. Exp. Biol. Med. 81:300-301 j
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WORLD HEALTH ORGANIZATION (WHO). 1986. Environmental Health Criteria. 54. , M Ammonia. WHO, Geneva, Switzerland
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ARSENIC
Both inorganic and organic forms of arsenic are readily absorbed via the oral
and inhalation routes. Soluble forms are more readily absorbed than the
insoluble forms (EPA 1984). Approximately 95% of soluble inorganic arsenic
administered to rats is absorbed from the gastrointestinal tract (Coulson et
al. 1935, Ray-Bettley and O'Shea 1975). Approximately 70%-80% of arsenic
deposited in the respiratory tract of humans has been shown to be absorbed
(Holland et al. 1959). Dermal absorption is not significant (EPA 1984).
Acute exposure of humans to metallic arsenic has been associated with
gastrointestinal effects, hemolysis, and neuropathy (EPA 1984). Chronic
exposure of humans to this metal can produce toxic effects on both the
peripheral and central nervous systems, keratosis, hyperpigmentation,
precancerous dermal lesions, and cardiovascular damage (EPA 1984). Arsenic is
embryotoxic, fetotoxic, and teratogenic in several animals species (EPA 1984).
Arsenic is a known human carcinogen. Epidemiological studies of workers in
smelters and in plants manufacturing arsenical pesticides have shown that
inhalation of arsenic is strongly associated with lung cancer and perhaps with
hepatic angiosarcoma (EPA 1984). Ingestion of arsenic has been linked to a
form of skin cancer and more recently to bladder, liver, and lung cancer
(Tseng 1977, Tseng et al. 1968, Chen et al. 1986).
EPA has classified arsenic in Group A—Human Carcinogen—and has developed
inhalation (EPA 1989) and oral cancer potency factors (EPA 1988) of
50 mg/kg/day)"^ and 2.0 (mg/kg/day)'^, respectively. The inhalation potency
factor is the geometric mean value of potency factors derived from four
occupational exposure studies on two different exposure populations (EPA
1984). The oral cancer potency factor was based on an epidemiological study
in Taiwan which indicated an increased incidence of skin cancer in individuals
exposed to arsenic in drinking water (Tseng 1977). A risk assessment for
noncarcinogenic effects of arsenic is currently under review by EPA (1989). 03
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CHEN, C , CHUANG,.Y., YOU, S., LIN, T. , and WU, H. 1986. A retrospective study on malignant neoplasms of bladder, lung, and liver an blackfoot disease endemic area in Taiwan. Br. J. Cancer 53:399-4051
I
COULSON, E.J., REMINGTON, R.E., and LYNCH, K.M. 1935. Metabolism in the rat of the naturally occurring arsenic of shrimp as compared with arsenic trioxide. J. Nutr. 10:255-270 ,
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Assessment Document for Inorganic Arsenic. Office of Health and Environmental Assessment, Washington D.C. EPA 600/8-83-021F i
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1988. Special Report oh Ingested Inorganic Arsenic Skin Cancer: Nutritional Essentiality.: Risk Assessment Forum. U.S. Environmental Protection Agency, Washington, D.C. EPA/625/3-87/013F. July 1988 .
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated Risk Information System (IRIS). Health Criteria and Assessment Office, Cincinnati, Ohio. Revised June 1, 1989
HOLLAND, R.H., McCALL, M.S., and LANZ, H.C. 1959. A study of inhaled arsenic-74 in man. Cancer Res. 19:1154-1156
RAY-BETTLEY, F., and O'SHEA, J.A. 1975. The absorption of arsenic and its relation to carcinoma. Br. J. Dermatol. 92:563-568
TSENG, W.P., CHU, H.M., HOW, S.W., FONG, J.M., LIN, C.S., andYEH, S. 1968. Prevalence of skin cancer in an endemic area of chronic arsenic ism in Taiwan. J. Natl. Cancer Inst. 40:453-463
TSENG, W.P. 1977. Effects and dose-response relationships of skin cancer and blackfoot disease with arsenic. Environ. Health Perspect. 19:109-119
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BENZENE
Benzene is readily absorbed following oral and inhalation exposure (EPA 1985).
The.toxic effects of benzene in humans and other animals following exposure by
inhalation include central nervous system effects, hematological effects, and
immune system depression. In humans, acute exposures to high concentrations
of benzene vapors has been associated with dizziness, nausea, vomiting,
headache, drowsiness, narcosis, coma, and death (NAS 1976). Chronic exposure
to benzene vapors can produce reduced leukocyte, platelet, and red blood cell
counts (EPA 1985). Benzene induced both solid tumors and leukemias in rats
exposed by gavage (Maltoni et al. 1985). Many studies have also described a
causal relationship between exposure to benzene by.inhalation (either alone or
in combination with other chemicals) and leukemia in humans (lARC 1982).
Applying EPA's criteria for evaluating the overall evidence of carcinogenicity
to humans, benzene is classified in Group A (Human Carcinogen) based on
adequate evidence of carcinogenicity from epidemiological studies. EPA (1989)
derived both an oral and an inhalation cancer potency factor for benzene of
2.9x10"^ (mg/kg/day)"^. This value was based on several studies in which
increased incidences of nonlymphbcytic leukemia were observed in humans
occupationally exposed to benzene principally by inhalation (Rinsky 1981, Ott
1978, Wong 1983). EPA (1989) is currently reviewing an oral RfD for benzene
and its status is pending.
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Drinking Water Criteria document for Benzene (Final Draft). Office of Drinking Water, Washington, D.C. April 1985
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised May 1, 1989
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (lARC). 1982. lARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Volume 27: Some Aromatic Amines, Anthraquinones and Nitroso Compounds, and Inorganic Fluorides Used in Drinking-Water and Dental Preparations. World Health Organization, Lyon, France
MALTONI, C , CONTI, B., COTTI, C , and BELPOGGI, F. 1985. Experimental studies on benzene carcinogenicity at the Bologna Institute of Oncology: Current results and ongoing research. Am. J. Ind. Med. 7:415-446
NATIONAL ACADEMY OF SCIENCE (NAS). 1976. Health Effects of Benzene: A Review Committee on Toxicology, Assembly of Life Sciences. National Research Council, Washington, D.C.
OTT, M.G., TOWNSEND, J.C, FISHBECK, W.A.. and LANGNER, R.A. 1978. 'Mortality among individuals occupationally exposed to benzene. Arch. Environ. Health 33:3-10
RINSKY, R.A., YOUNG, R.J., and SMITH, A.B. 1981. Leukemia in benzene workers. Am. J. Ind. Med. 3:217-245
WONG, 0., MORGAN, R.W., AND WHORTON, M.D. 1983. Comments on the NIOSH Study of Leukemia in Benzene Workers. Technical report submitted to Gulf Canada, Ltd. by Environmental Health Associates
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BIS(2 -ETHYLHEXYL)PHTHALATE
Bis(2-ethylhexyl)phthalate, also known as di-ethylhexyl phthalate (DEHP), is
readily absorbed following oral or inhalation exposure (EPA 1980). Chronic
exposure to relatively high concentrations of DEHP in the diet can cause
retardation of growth and increased liver and kidney weights in laboratory
animals (NTP 1982, EPA 1980, Carpenter et al. 1953). Reduced fetal weight and
increased number of resorptions have been observed in rats exposed orally to
DEHP (EPA 1980). DEHP is reported to be carcinogenic in rats and mice,
causing increased incidences of hepatocellular carcinomas or neoplastic
nodules following oral administration (NTP 1982) .
DEHP has been classified in Group B2--Probable Human Carcinogen (EPA 1986,
1989a). EPA (1989a) calculated an oral cancer potency factor for DEHP of -2 -1
1.4x10 (mg/kg/day) based on data from the NTP (1982) study. EPA has
recommended both chronic and subchrnoic oral reference doses (RfD) for DEHP of
0.02 mg/kg/day based on a study by Carpenter et al. (1953) in which increased
liver weight was observed in female guinea pigs exposed to 19 mg/kg bw/day in
Che diet for 1 year (EPA 1989a,b); an uncertainty factor of 1,000 was used to
develop the RfD.
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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. Indust. Hyg. Occup. Med. 8:219-226
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Phthalate Esters. Office of Water Regulations and Standards, Criteria and Standards Division, Washington, D.C. October 1980. EPA 40/5-80-067
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Superfund Public Health Evaluation Manual. Office of Emergency and Remedial Response, Washington, D.C. EPA 540/1-86-060
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised May 1, 1989
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
NATIONAL TOXICOLOGY PROGRAM (NTP). 1982. Carcinogenesis Bioassay of Di(2-ethylhexyl)phthalate in F344 Rats and B6C3Fi Mice. Feed Study. NTP Technical Report Series No. 217, U.S. Department of Health and Human Services. NIH Publication No. 82-1773. NTP-80-37
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H2MGROUP
BUTYL BENZYL PHTHALATE
Butyl benzyl phthalate is absorbed following oral exposure. Butyl benzyl
phthalate is not especially toxic. Acute oral doses of 50,000 or
100,000 mg/kg administered to male rats resulted in testicular degeneration.
Thymic atrophy was reported in both male and female rats given 100,000 mg/kg
for 14 days (NTP 1982). Depressed body weight gain, testicular degeneration,
and liver and' kidney effects have been observed in animals subchronically
administered benzyl butyl phthalate in the diet (NTP 1982, NTP 1985). Butyl
benzyl phthalate has been tested for carcinogenicity in chronic feeding
studies using mice and female rats, and via intraperitoneal injection in male
mice (NTP 1982). In female rats, an increased incidence of myelomonocytic
leukemia was observed in the high exposure group. No increased tumor
incidence was noted for mice (NTP 1982).
EPA has classified butyl benzyl phthalate in Group C--Possible Human
Carcinogen. EPA (1989) derived an oral RfD of 2x10"^ mg/kg/day for butyl
benzyl phthalate based on a subchronic study in rats in which effects on body
weight gain, testes, liver, and kidney were observed (NTP 1985). An
uncertainty factor of 1,000 was used to derive the oral RfD. EPA (1989) also
developed a subchronic RfD of 2.0 mg/kg/day based on the same, NTP (1985)
study; a safety factor of 100 was used to calculate the subchronic RfD. No
inhalation criteria have been developed for butyl benzyl phthalate.
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health Effects Assessment Summary Tables. Prepared by the Office of Health and Environmental Assessment, Environmental Assessment and Criteria Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
NATIONAL TOXICOLOGY PROGRAM (NTP). 1982. Bioassay of Butyl Benzyl Phthalate for Possible Carcinogenicity. U.S. Department of Health and Human Services, Washington, D.C. DHHS (NIH) Publication No. 82-1769. NTP Technical Report Series No. 213
NATIONAL TOXICOLOGY PROGRAM (NTP). 1985. Project #12307-02,-3. Hazelton Laboratories of America, Inc. Unpublished study (As cited in EPA 1989)
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CADMIUM
Gastrointestinal absorption of cadmium in humans ranges from 5-6% (EPA 1985a).
Pulmonary absorption of cadmium in humans is reported to range from 10% to 50%
(CDHS 1986). Cadmium bioaccumulates in humans, particularly in the kidney and
liver (EPA 1985a,b). Chronic oral or inhalation exposure of humans to cadmium
has been associated with renal dysfunction, itai-itai disease (bone damage),
hypertension, anemia, endocrine alterations, and immunosuppression. Renal
toxicity occurs in hiimans at a renal cortex concentration of cadmium of
200 Mg/g (EPA 1985b). Epidemiological studies have demonstrated a strong
association between inhalation exposure to cadmium and cancers of the lungs,
kidney, and prostate (EPA 1985b, Thun et al. 1985). In experimental animals,
cadmium induces injection-site sarcomas and testicular tumors. When
administered by inhalation, cadmium chloride is a potent pulmonary carcinogen
in rats. Cadmium is a well-documented animal teratogen (EPA 1985b).
EPA (1989a,b) classified cadmium as a Group Bl agent (Probable Human
Carcinogen) by inhalation. This classification applies to agents for which
there is limited evidence of carcinogenicity in humans from epidemiologic
studies. EPA (1989a,b) derived an inhalation cancer potency factor of 6.1
(mg/kg/day)"^ for cadmium based on epidemiologic studies in which respiratory
tract tumors were observed (Thun et al. 1985, EPA 1985b). Using renal
toxicity as an endpoint, and a safety factor of 10, EPA (1980, 1987, 1989b)
has derived two separate oral reference doses (RfD). The RfD associated with
oral exposure to drinking water is 5x10"* mg/kg/day, and is based upon the
lowest-observed-adverse-effect level (LOAEL) of 0.005 mg/kg in homians (Friberg
et al. 1974). The RfD associated with exposure to cadmium in food or other
nonaqueous oral exposures is 1x10"^ mg/kg/day.
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CALIFORNIA DEPARTMENT OF HEALTH SERVICES (CDHS). 1986. Report to the Scientific Review Panel on Cadmium. Part B. Health Effects of Cadmium. Revised. Prepared by the Epidemiological Studies and Surveillance Section, Berkeley, California. September 19, 1986
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria Document for Cadmium. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio for the Office of Water Regulations and Standards, Washington, D.C. EPA 440/5-80-025
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985a. Drinking Water Criteria Document for Cadmium. Final Draft. Office of Drinking Water, Washington, D.C. April 1985. PB86-117934
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. ' Updated Mutagenicity and Carcinogenicity Assessment of Cadmium. Addendum to the Health Assessment Document for Cadmium (May 1981; EPA/600/8-81/023). Office of Health and Environmental Assessment, Washington, D.C. June 1985. EPA 600/8-83-025F
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisory for Cadmium. Office of Drinking Water, Washington, D.C. March 31, 1987
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised June 1, 1989
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Environmental Assessment and Criteria Office, Cincinnati, Ohio for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. March 1989
FRIBERG, L., PISCATOR, M., NORDBERG, G.F.. and KJELLSTROM, T. 1974. Cadmium in the Environment. 2nd ed. CRC Press, Inc., Boca Raton, Florida
THUN, M.J., SCHNORR, T.M., SMITH, A.B., HALPERIN, W.E., and LEMEN, B.A. 1985. Mortality among a cohort of U.S. cadmium production workers—an update. JNCI 74:325-333
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CHLOROFORM
Chloroform, a trihalomethane, is rapidly absorbed through the respiratory and
gastrointestinal tracts in humans and experimental animals; dermal absorption
from contact of the skin with liquid chloroform can also occur (EPA 1985). In
humans, acute exposures to chloroform may result in depression of the central
nervous system, hepatic and renal damage and death caused by ventricular
fibrillation following an acute ingested dose of 10 ml (EPA 1984). Acute
exposure to chloroform may also cause irritation to the skin, eyes, and
gastrointestinal tract (EPA 1984, 1985). In experimental animals, chronic
exposure may lead to fatty cyst formation in the liver (Heywood et al. 1979),
renal, and cardiac effects and central nervous system depression (EPA 1985).
Chloroform has been reported to induce renal epithelial tumors in rats
(Jorgenson et al. 1985) and hepatocellular carcinomas in mice (NCI 1976).
Suggestive evidence from human epidemiological studies indicates that long-
term exposure to chloroform and other trihalomethanes in contaminated water
supplies may be associated with an increased incidence of bladder tumors (EPA
1985).
Chloroform has been classified by EPA as a Group B2 Carcinogen (Probable Human
Carcinogen) (EPA 1989a). EPA (1989a) developed an oral cancer potency factor
for chloroform of 6.1x10''' (mg/kg/day)"^ based on a study in which kidney
tumors were observed in rats exposed to chloroform in drinking water
(Jorgenson et al. 1985). An inhalation cancer potency factor of 8.1x10"
(mg/kg/day)"^ has been developed by EPA (1989a) based on an NCI (1976)
bioassay in which liver tumors were observed in mice. EPA (1989b) also
derived both a chronic and subchronic oral reference dose (RfD) of 0.01
mg/kg/day for chloroform based on a chronic bioassay in dogs in which liver
effects were observed at 12.9 mg/kg/day (Heywood et al. 1979); an uncertainty
factor of 1,000 was used to derive both RfDs.
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Effects Assessment for Chloroform. Environmental Criteria and Assessment Office, Cincinnati, Ohio. September 1984. EPA 540/1-86-010
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Health Assessment Document for Chloroform. Environmental Criteria and Assessment Office, Research Triangle Park, North Carolina. September 1985. EPA 600/8-84-004F
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised May 1, 1989
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health.and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
HEYWOOD, R., SORTWELL, R.J. NOEL, P.R.B., et al. 1979. Safety evaluation of toothpaste containing chloroform. III. Long-term study in beagle dogs. J. Environ. Pathol. Toxicol. 2:835-85L
JORGENSON, T.A., MEIERHENRY, E.F., RUSHBROOK, C.J., et al. 1985. Carcinogenicity of chloroform in drinking water to male Osborne-Mendel rats and female B6C3F1 mice. Fund. Appl. Toxicol. 5:760-769
NATIONAL CANCER INSTITUTE (NCI). 1976. Carcinogenesis Bioassay of Chloroform. CAS No. 67-66-3. NCI Carcinogenesis Technical Report Series No. 0. Bethesda, M.D. DHEW (NIH) Publication No. 76
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CHROMIUM
Chromium exists in two states, as chromium(III) and as chromium(VI) .
Following oral exposure, absorption of chromium(III) is low while absorption
of chromium(VI)-is high (EPA 1987)'. Chromium is an essential micronutrient
and. is not toxic in trace quantities (EPA 1980). High levels of soluble
chromium(VI) and chromium(III) can produce kidney and liver damage following
acute oral exposure; target organs affected by chronic oral exposure remain
unidentified (EPA 1984). Chronic inhalation exposure may cause respiratory
system damage .(EPA 1984). Further, epidemiological studies of worker
populations have clearly established that inhaled chromium(VI) is a human
carcinogen; the respiratory passages and the lungs are the target organs
(Mancuso 1975, EPA 1984). Inhalation of chromium(III) or ingestion of
chromium(VI) or (III) has not been associated with carcinogenicity in humans
or experimental animals (EPA 1984) . Certain chromium salts have been shown to
be teratogenic and embryotoxic in mice and hamsters following intravenous or
intraperitoneal injection (EPA 1984).
EPA has classified inhaled chromium(VI) in Group A--Probable Hvmian Carcinogen
by the inhalation route (EPA 1989a). Inhaled chromium(III) and ingested
chromium(III) and (VI) have not been classified with respect to
carcinogenicity (EPA 1989a). EPA (1989a) developed an inhalation cancer
potency factor of 41 (mg/kg/day)"^ for chromium(VI) based on an increased
incidence of lung cancer in workers exposed to chromium over a 6 year period,
and followed for approximately 40 years (Mancuso 1975). EPA (1989a) derived a
chronic oral reference dose (RfD) of 5.OxlO''^-mg/kg/day for chromium(VI) based
on a study by MacKenzie et al. (1958) in which no observable adverse effects
were observed in rats.exposed to .2.4 mg chromium(VI)/kg/day in drinking water
for 1 year. A-safety factor of 500 was used to derive the RfD. EPA (1989b)
calculated a subchronic oral reference dose of 2.0x10'^ mg/kg/day for
chromium(Vl) based on the same study; a safety factor of 100 was applied to
the NOAEL to derive the RfD. EPA (1989a) developed an oral RfD of 1 mg/kg/day
for chromiLmi(III) based on a study in which rats were exposed to chromic oxide CO w >
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H2MGROUP
baked in bread; no effects due to chromic oxide treatment were observed at any
dose level (Ivankovic and Preussman 1975) . A safety factor of 1,000 was used
to calculate the oral RfD. EPA (1989b) also developed a subchronic RfD of
10 mg/kg/day for chromium(III) using the Ivankovic and Preussman (1975) study
and a safety factor of 100.
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Chromium. Office of Water Regulations and Standards. Washington, D.C. EPA.440/5-80-035
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Assessment Document for Chromium. Environmental Criteria and Assessment Office, Research Triangle Park, N.C. EPA 600/8-83-014F
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Draft Health Advisory for Chromium. Office of Drinking Water, Washington, D.C. March 31, 1987
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised June 1, 1989
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
IVANKOVIC, S.., and PREUSSMAN, R. 1975. Absence of toxic and. carcinogenic effects after administration of high doses of chromic oxide pigment in subacute and long-term feeding experiments in rats. Fd. Cosmet. Toxicol. 13:347-351
MANCUSO, T.F. .1975. International Conference on Heavy Metals in the Environment. . Toronto, Canada
MACKENZIE, R.D.., BYERRUM, R.V. , DECKER, C.F., HOPPERT, C.A., AND LONGHAM, F,L. 1958. Chronic toxicity studies II. Hexavalent and trivalent chromium administered in drinking water to rats. Arch. Ind. Health 18:232-234
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COPPER
Copper is an essential element. A daily copper intake of 2 mg is considered
to be adequate for normal health and nutrition; the minimum daily requirement
is 10 n g / ' k g (EPA 1985). In humans, absorption of copper following oral
exposure is approximately 60% and is influenced by competition with other
metals and the level of dietary protein and ascorbic acid in both humans and
animals (EPA 1984). Copper is absorbed following inhalation exposures,
although quantitative data on the extent of absorption are unavailable (EPA
1984) . Adverse effects in humans resulting from acute exposure to copper at
concentrations that exceed these recommended levels by ingestion include
salivation, gastrointestinal irritation, nausea, vomiting, hemorrhagic
gastritis, and diarrhea (ACGIH 1986). Dermal or ocular exposure of humans to
copper salts can produce irritation (ACGIH 1986). Acute inhalation of dusts
or mists of copper salts by humans may produce irritation of the mucous
membranes and pharynx, ulceration of the nasal septum, and metal fume fever.
The latter condition is characterized by chills, fever, headache, and muscle
pain. Limited data are available on the chronic toxicity of copper; however,
chronic over-exposure to copper by humans has been associated with anemia
(ACGIH 1986) and local gastrointestinal irritation (EPA 1987). Results of
several animal bioassays suggest that copper compounds are not carcinogenic by
oral administration; however, some copper compounds can induce injection-site
tumors in mice (EPA 1985).
EPA (1989) has reported the drinking water standard of 1.3 mg/liter as an oral
chronic and subchronic reference dose (RfD) based on local gastrointestinal
irritation (EPA 1987). Assuming a 70-kg adult ingests 2 liters of water per
day, this concentration is equivalent to a dose of 3.7x10'^ mg/kg/day.
However, EPA (1987) concluded toxicity data were inadequate for the
calculation of a reference dose (RfD) for copper.
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AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1986. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, Ohio
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Effects Assessment for Copper. Environmental Criteria and Assessment Office, Cincinnati, Ohio. EPA/540-1-86-025
ENVIRONMENTAL PROTECTION AGENCY (EPA).. 1985. National primary drinking water regulations; synthetic organic chemicals, inorganic chemicals and microorganisms. Fed. Reg. 50:46937-47025 (November 13, 1985)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Drinking Water Criteria Document for Copper. Prepared by the Office of Health and Environmental Assessment. Environmental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Drinking Water, Washington, D.C.
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment. Environmental Assessment and Criteria Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
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Dl-n-BUTYL PHTHALATE • .
Di-n-butyl phthalate is readily absorbed following oral and inhalation
exposure (EPA 1980). Acute exposures of di-n-butyl phthalate aerosol in mice
have produced irritation of the eyes and upper, respiratory tract mucous
membranes. Extreme exposures result in labored breathing, ataxia, paresis,
convulsions and death from paralysis of the respiratory system (ACGIH 1986).
Workers chronically.exposed to di-n-butyl phthalate in combination with other
phthalate plasticizers have exhibited pain, numbness and spasms in the upper
and .lower extremities. Further evaluation revealed vestibular dysfunction and
polyneuritis (ACGIH 1986). Reduced fetal weight, increased numbers of
resorptions, and dose-related musculoskeletal abnormalities have been observed
among.fetuses from rats and mice exposed to very high doses of di-n-butyl
phthalate during gestation (Shiota and Nishimura 1982).
EPA (1989a) calculated a. chronic oral reference dose (RfD) for di-n-butyl
phthalate based on a study by Smith (1953) in which male Sprague-Dawley rats
were fed a diet containing dibutyl phthalate for a period of 1 year. One-half
of all rats receiving the highest dibutyl phthalate concentration (1.25% of
diet, or 600 mg/kg/day) died during the first week of exposure. The remaining
animals survived the study with no apparent adverse effects. Using a NOAEL of
125 mg/kg/day (0.25% dibutyl phthalate.in diet) and an uncertainty factor of
1,000, an oral reference dose (RfD) of 0.1 mg/kg/day was derived; a LOAEL of
600 mg/kg/day (1.25% dibutyl phthalate in.diet) was observed in this study.
.Using this same study and a safety factor of 100, EPA (1989b) derived a
subchronic RfD of 1.0 rag/kg/day. .
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AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1986. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH.
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Phthalate Esters. Office of Water Regulations and Standards, Washington, D.C. October 1980. EPA 440/5-80-067
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised May 1, 1989
ENVIRONMENTAL PROTECTION AGENCY. (EPA). 1989b. Health Effects Assessment Summary Tables;. Prepared by Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
SHIOTA, K., and NISHIMURA, H. 1982. Teratogenicity of di(2-ethylhexyl) phthalate (DEHP) and di-n-butyl phthalate (DBP) in mice. Environ. Health Perspect. 45:65-70
SMITH, CC. 1953. Toxicity of butyl stearate, dibutyl sebacate, dibutyl phthalate, and methoxyethyl oleate. . Arch. Ind. Hyg. 7:310
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H2MGROUP
1,1-DICHLOROETHANE
1,1-DCA is probably less coxic than the 1,2-isoraer (EPA 1980). At one time,
the compound was used as an anesthetic, but it induced cardiac arrhythmias and
its use was discontinued. It is probable that human exposure to sufficiently
high levels of 1,1-DCA would cause central nervous system depression and
respiratory tract and skin irritation, since many of the chlorinated
aliphatics cause these effects (Parker at al. 1979). However, no
dose-response data concerning these effects are available. Renal damage was
observed in cats exposed by inhalation in a subchronic study (Hpfmann et al.
1971). Inhalation exposure of pregnant rats to high doses of 1,1-DCA
(6,000 ppm) retarded fetal development (Schwetz et al. 1974). A
carcinogenicity bioassay of 1,1-DCA was limited by poor survival of both
treatment and control groups, and the physical conditions of the treated
animals was markedly stressed. Dose-related marginal increases in mammary
gland adenocarcinomas and in hemangiosarcomas were seen in female rats, and a
statistically significant increase in endometrial stromal polyps was seen in
female mice; however, these data were not interpreted as providing conclusive
evidence for the carcinogenicity of 1,1-DCA because of the previously
mentioned limitations of the bioassay (NCI 1978).
EPA (1989) has classified 1,1-DCA as a Group B2 agent (Probable Human
Carcinogen) and reported an oral cancer potency factor of 9.1x10"
(mg/kg/day)'^. This potency factor is based on structure-activity
relationship to the isomer-1,2-dichloroethane, a Group B2 carcinogen and on
the increased incidence of hemangiosarcomas observed in rats administered
1,1-DCA via gavage (NCI 1978). EPA (1989) developed a chronic oral and
inhalation reference dose of 0.1 mg/kg/day based on adverse renal effects seen
in cats following subchronic inhalation exposure (Hofmann et al. 1971). A
safety factor of 1000 was used to develop the RfD. EPA (1989) also derived a'
subchronic RfD of 1.0 mg/kg/day for both oral and inhalation exposures based j ^
on this same study and end point and applying a safety factor of 100. '< >
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for 1,l-Dichloroethane. Office of Water Regulations and Standards, Washington, D.C EPA 440/5-80-029
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Effects Assessment for 1,l-Dichloroethane. Environmental Criteria and Assessment Office, Cincinnati, Ohio.. EPA 540/1-86-027
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989;. Health Effects Assessment Summary Tables Prepared by Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati Ohio for the Office"of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. March 1989
HOFMANN, H.T., BIRNSTIEL, H., and JOBST, P. 1971. The inhalation toxicity of 1,1- and 1,2-dichloroethane. Arch. Toxikol. 27:248-265
NATIONAL CANCER INSTITUTE (NCI). 1978. Bioassay of 1,l-Dichloroethane for Possible Carcinogenicity. CAS No. 75-34-3. NCI Carcinogenesis Technical Report Series No. 66, Washington, D.C. DHEW Publication No. (NIH) 78-1316
PARKER, J.C, CASEY, G.E., and BAHLNON, L.J. 1979.' NIOSH current intelligence bulletin No. 27. Chloroethanes:: Review of toxicity. Am. Ind. Hyg. Assoc. J. 40:A46-A60
SCHWETZ, B.A., LEONG, B.K.J., andCEHRING, P.J. 1974. Embryo and fetotoxicity of inhaled carbon tetrachloride, 1,1-dichloroethane, and methyl ethyl ketone. Toxicol. Appl. Pharmacol. 28:452-464
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1,2-DICHLOROETHANE
Data on the toxicokinetics of 1.2-dichloroethane (1,2-DCA) in humans are
limited, but data from animal studies suggest that the chemical is rapidly
absorbed following oral and inhalation exposure and after dermal contact with
the liquid form of the compound (EPA 1985). Effects of acute inhalation
exposure in humans include irritation of mucous membranes in the respiratory
tract and central nervous system depression (EPA 1985) . Death may occur as a
result of respiratory and circulatory failure. Pathological examinations
typically show congestion, degeneration, necrosis, and hemorrhagic lesions of
the respiratory and gastrointestinal tracts, liver, kidney, spleen, and lungs
(EPA 1985). Adverse effects caused by less extreme exposures are generally
associated with the gastrointestinal and nervous systems. Occupational
exposures to 1,2-DCA vapors result in anorexia, nausea, vomiting, fatigue,
nervousness, epigastric pain, irritation of the eyes and respiratory tract,
and gastrointestinal, liver, and gallbladder disease (EPA 1984, 1985).
Chronic studies in animals also have revealed toxic effects following
inhalation exposure including degeneration of the liver (EPA 1985). Available
data suggest that 1,2-DCA does not adversely affect reproductive or
developmental processes in experimental animals except at maternally toxic
levels (EPA 1985). In long-term oral bioassays sponsored by the National
Cancer Institute (NCI 1978), increased incidences of squamous-cell carcinomas
of the forestomach, mammary gland adenocarcinomas, and hemangiosarcomas have
been observed in rats exposed to 1,2-DCA; pulmonary adenomas, mammary
adenocarcinomas, and uterine endometrial tumors have been observed in mice
exposed to this chemical.
EPA (1989) has classified 1,2-DCA in Group B2 (Probable Human Carcinogen)
based on inadequate evidence of carcinogenicity from human studies and
sufficient evidence of carcinogenicity from animal studies. EPA (1989)
derived an oral and an inhalation cancer potency factor (qi*) of 9.1x10
(mg/kg/day)'^ for 1,2-DCA based on the incidences of hemangiosarcomas in / ^ ; ;' S" /
Osborne-Mendel male rats observed in the NCI (1978) gavage study. ; ,
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Effects Assessment for 1,2-Dichloroethane. Environmental Criteria and Assessment Office, Cincinnati, Ohio. September 1984. EPA 540/1-86-002
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Health Assessment Document for 1,2-Dichloroethane. Office of Health and Environmental Assessment, Washington, D.C. September 1985. EPA 600/8-84-006F
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised May 1, 1989
NATIONAL CANCER INSTITUTE (NCI). 1978. Bioassay of 1,2-Dichloroethane for Possible Carcinogenicity. NCI Carcinogenesis Technical Report Series No. 55. Washington, D.C. DHEW (NIH) Publication No. 78-1361
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1,1-DICHLOROETHENE
r, l-Dichloroethene (1,1-DCE) is rapidly absorbed after oral and inhalation
exposures (EPA 1984, 1987). Humans acutely exposed to 1,1-DCE vapors exhibit
central nervous system depression. In animals, the liver is the principal
target of 1,1-DCE toxicity. Acute exposures result in liver damage which
ranges from fatty infiltration to necrosis (EPA 1987). Workers chronically
exposed to 1,1-DCE in combination with other vinyl compounds exhibit liver
dysfunction', headaches, vision problems, weakness, fatigue and neurological
sensory disturbances (EPA 1987). Chronic oral administration of 1,1-DCE to
experimental animals results in both hepatic and renal toxicity (EPA 1984,.
Quast et al. 1983). Inhalation or oral exposure of rats and rabbits has
produced fetotoxicity and minor skeletal abnormalities, but only at maternally
toxic doses. 1,1-DCE vapors produced kidney tumors and leukemia in a single
study of mice exposed by inhalation, but the results of other studies were
equivocal or negative (EPA 1987, Maltoni et al. 1985).
EPA has classified 1,1-DCE as a Group C agent (Possible Human Carcinogen) and
has developed inhalation and oral cancer potency factors of 1.2 (mg/kg/day)'^
and 0.6 (mg/kg/day)'^, respectively (EPA 1985, 1989a). The inhalation
potency factor was based on the increased incidence of renal adenocarcinomas
in male mice exposed to 1,1-DCE via inhalation for 52 weeks and observed for a
total of 121 weeks (Maltoni et al. 1985). The oral potency factor was derived
by estimating an upper-limit value from negative bioassay data and assuming
that a carcinogenic response occurs via ingestion, although there is no direct
evidence that this is true. EPA (1989b) developed both a chronic and
subchronic oral reference dose (RfD) of 9x10"'' mg/kg/day based on the
occurrence of hepatic lesions in rats chronically exposed to 1,1-DCE in
drinking water (Quast et al. 1983). A safety factor of 1,000 was applied to
the lowest-observed-adverse-effect level (LOAEL) of 9 mg/kg/day to derive the
oral RfD. CO M >
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ENVIRONMENTAL PROTECTION AGENCY (EPA). ' 1984. Health.Effects Assessment for 1,1-Dichloroethylene. Environmental Criteria and Assessment Office, Cincinnati,. Ohio. September 1984. EPA 540/1-86-051
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Health Assessment Document for Vinylidene .Chloride. Final Report. Environmental Criteria and Assessment Office, Research Triangle Park, North Carolina-. August 1985
. EPA 600/8-83/031F
ENVIRONMENTAL PROTECTION AGENCY (EPA). . 1987. Health Advisory for 1,l-Dichloroethene . Office of Drinking Water, Washington, D.C. March 31, 1987.
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office. Cincinnati, Ohio. Revised May 1, 1989 '
ENVIRONMENTAL PROTECTION AGENCY (EPA).. 1989b. Health Effects Assessment • Summary Tables. Prepared by Office of Health and Environmental . Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington,, D.C April 1989
MALTONI, C , LEFEMINE, C , COTTI, G., CHIECO, P., and PATELLA, V. 1985. Experimental Research on Vinylidine Chloride Carcinogenesis. In Archives of Research on Industrial Carcinogenesis. Princeton Scientific Publishers, Princeton, New Jersey. 3 vols.
QUAST, J.F., HUMISTON, C C , WADE, C.E., BALLARD, J., BEYER, J.E., SCHWETZ, R.W., and NORRIS, J.M. 1983. A chronic toxicity and oncogenicity study in rats and subchronic toxicity study in dogs on ingested vinylidene chloride. Fund. Appl. Toxicol. 3:55-62
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crans-1,2 -DICHLOROETHYLENE
trans-1,2-Dichloroethylene is expected to be absorbed by any route of
exposure. Information on the health effects of crans-1,2-dichloroethylene is
limited. In humans, trans-1,2-dichloroethylene is a central nervous system
depressant, and exposure to high concentrations can result in anesthetic
effects (Irish 1963). Inhalation exposure of rats to 200 ppm has been
associated with pneumonic infiltration of the lungs and progressive fatty
degeneration of the liver (Freundt et al. 1977). Acute exposure to higher
dose levels can cause narcosis and death in rats (Torkelson and Rowe 1981).
EPA (1985) proposed a maximum contaminant level goal (MCLG) of 70 |ig/liter for
both c i s - and trans-1,2-dichloroethylene based on the adjusted acceptable
daily intake (AADI) of 350 f i g / l i t e r , assuming 20% of the exposure is via
drinking water. EPA (1989) has derived an oral reference dose (RfD) of 2x10"^
mg/kg/day for trans-1,2-dichloroethylene based on a 90-day drinking water
study conducted in mice (Barnes et al. 1985). A no-observed-adverse-effect
level (NOAEL) of 17 mg/kg/day for increased serum alkaline phosphatase and an
uncertainty factor of 1,000 were used to derive the RfD.
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BARNES, D.W.,• SANDERS, V.M., WHITE, K.L., Jr., et al. 1985. Toxicology of crans-1,2-dichloroethylene in the mouse. Drug Chem. Toxicol. 8:373-392
ENVIRONMENTAL.PROTECTION AGENCY (EPA). 1985. National primary drinking water regulations; synthetic organic chemicals, inorganic chemicals and microorganisms. Fed. Reg. 50:46937-47025 (November 13, 1985)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. May 1,. 1989
FREUNDT, K.J., LIEBALDT, G.P., and LIEBERWIRTH, E. 1977. Toxicity studies on trans-1,2-dichloroethylene.. Toxicology 7:141-153
IRISH, D.D. 1963. Vinylidene chloride. In Patty, F.A., ed. Industrial Hygiene and Toxicology. 2nd ed. John Wiley and Sons, New York. Vol. II., pp. 1305-1309
TORKELSON, T.R., and ROWE, V.K. 1981. Halogenated aliphatic hydrocarbons. In Clayton, CD., and Clayton, P.B., eds. Patty's Industrial Hygiene and Toxicology. • 3rd ed. John Wiley and Sons, New York.- Vol. 2B, pp. 3550-3555
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DIETHYLPHTHALATE
Diethylphthalate (DEP) is absorbed following ingestion and inhalation
exposures. Its acute toxicity for laboratory animals by most routes of
administration is very low (NIOSH 1986). Exposure of humans to the heated
vapor may cause respiratory irritation (ACGIH 1986). No specific lesions were
observed in subchronic or chronic feeding studies of DEP to rats and dogs.
However, decreased consumption of food and increased relative organ weights
were observed in some of the animals (EPA 1980. EPA 1986, Brown et al. 1978).
Workers chronically exposed to DEP experienced pain, numbness and spasms in
the upper and lower extremities (ACGIH 1985). Reduced fetal weight,
resorptions and dose-related musculoskeletal abnormalities were observed among
fetuses from rats exposed to DEP intraperitoneally during gestation (EPA
1980). DEP is also reported to be mutagenic in bacterial test systems (EPA
1986, Seed 1982). Currently, there are no reports that DEP is carcinogenic in
humans or animals.
EPA (1989a) calculated an oral reference dose (RfD) of 8x10"^ mg/kg/day based
on a subchronic rat study in which decreased growth rate, food conscmiption and
altered organ weights were the observed effects (Brown et al. 1978). The oral
RfD was derived using a no-observed-adverse effect level (NOAEL) of
750 mg/kg/day and an uncertainty factor of 1,000. EPA (1989b) also developed
a subchronic RfD of 8.0 mg/kg/day from this same study in which a safety
factor of 100 was used.
HaMGROUP
AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRli\L HYGIENISTS (ACGIH). 1986. ' Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. AGCIH, Inc., Cincinnati, Ohio
BROWN, D., BUTTERWORTH, K.R., GAUNT, I.F., GRASSO, P., and GANGOLLI, S. 1978. Short-term toxicity study of diethyl phthalate in the rat. Food Cosmet. Toxicol. 16:415-422
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Phthalate Esters. Office of Water Regulations and Standards, Criteria and Standards Division, Washington, D.C. October 1980. EPA 440/5-80-057
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Verified Reference Doses (RfDs) of the USEPA. The ADI Work Group of the Risk Assessment Forum. Cincinnati, Ohio. January 1986. ECAO-CIN-475
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised June 1, 1989
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Enviror^mental Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1986. Registry of Toxic Effects of Chemical Substances. Data Base. Washington, D.C.
SEED, J.L. 1982. Mutagenic activity of phthalate esters in bacterial liquid suspension assays. Environ. Health Perspect. 45:111-114
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ENDOSULFAN-
Technical grade endosulfan is composed of two isomers, endosulfan I (a) and
endosulfan II (fi) in approximately a 7:3 ratio, respectively (Hayes 1982).
Absorption'of the j3-isomer exceeds that of the a-isomer and occurs in mammals
following both oral and dermal exposure (EPA 1980).. Absorption.is enhanced by
alcohols, oils, and emulsifiers (Maier-Bode 1968). Substantial absorption
following inhalation exposure to endosulfan is not expected to occur, due to
the substance's low vapor pressure (EPA 1980). Endosulfan is distributed
initially "to the liver and then subsequently to the brain, heart, kidney,
lungs, spleen, testes, thymus gland and other tissues and organs following
ingestion (EPA 1980). Acute endosulfan poisoning in humans produces symptoms
which include gagging, vomiting, diarrhea, agitation, tonic-clonic
convulsions, dyspnea, apnea, cyanosis, loss of consciousness, and death in
some cases (Hayes 1982). Acute exposure in animals causes signs of CNS
toxicity including hyperactivity, tremors, and convulsions followed by death
(WHO 1984). Subchronic oral exposure to rats has resulted in adverse renal
effects -(Hoeschst Aktiengesellschaft 1984). Chronic exposure results in
reduced survival, enlarged kidneys and signs of renal tubular damage with
interstitial nephritis and hepatocellular changes in rats (WHO 1984). Diets
deficient in protein are reported to increase the toxicity of technical grade
endosulfan in rats (EPA 1980, Hayes 1982). Adverse reproductive effects
including testicular degeneration and atrophy have been reported in mice and
rats following chronic exposure (EPA 1980).
EPA. (1989a) has derived an oral risk reference dose (RfD) for endosulfan of
5x10"^ mg/kg/day based on an unpublished reproduction study (Hoeschst
Aktiengesellschaft 1984). In this study, rats were administered endosulfan at
dietary concentrations of 0, .3, 15, or.75 ppm for two generations.'. Renal
toxicity was observed at an endosulfan concentration of 3 ppm
(0-15 mg/kg/day)-; an uncertainty factor of'3,000 was used to derive the RfD.
EPA (1989b) developed a subchronic RfD of.2.OxlO'* mg/kg/day also based on- ' CO
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mild kidney lesions in rats administered 0.15 mg/kg/day. A safety factor of
1,000 was used to calculate the subchronic RfD.
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Endosulfan. Office of Water Regulations and Standards. Washington, D.C October 1980. EPA 440/5-80-046
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). Health Criteria and Assessment Office, Cincinnati, Ohio. Revised June 1, 1989
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
GUPTA, P, CHANDRA, S., and SAXENA, D. 1978. Teratogenic and embryonic effects of endosulfan in rats. Acta Pharmacol. Toxicol 42:150-152
HAYES, W., Jr. 1982. Pesticides Studied in Man. Williams and Wilkins. Baltimore, Maryland
HOESCHST AKTIENGESELLSCHAFT. 1984. Unpublished two-generation reproduction study in rats. Ace. Nos. 256127, 257727 (As cited in EPA 1987)
NATIONAL CANCER INSTITUTE (NCI). 1978. Bioassay of endosulfan for possible carcinogenicity. Natl. Cancer Inst. Div. Cancer Cause and Prevention. Bethesda, Maryland. DHEW Pub. No. (NIH) 78-1312
WORLD HEALTH ORGANIZATION (WHO). 1984. Endosulfan. Environmental Health Criteria 40. World Health Organization. Geneva
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IRON
Gastrointestinal absorption of iron in humans ranges from 1% to 25% (EPA
1984). Absorption'of iron following inhalation exposure has not been
thoroughly studied. Iron is an essential element and is therefore nontoxic at
doses necessary for maintaining normal health and nutrition (EPA 1984).
However, overexposure to iron can cause adverse health effects.
Gastrointestinal irritation is the primary effect observed in humans following
acute oral overexposure to iron. Chronic oral overexposure of hLunans to iron
has been associated with gastrointestinal bleeding, metabolic acidosis,
hepatic toxicity, hemosiderosis, and hemochromatosis (EPA 1984). Human
fatalities have occurred following ingestion of iron at doses of 100 mg/kg/day
(Venugopal and Luckey 1978). Chronic inhalation overexposure of humans to•
iron-containing dusts and fumes produces respiratory irritation and various
pulmonary lesions (EPA 1984). There is limited evidence from studies with
experimental animals that certain soluble iron salts are teratogenic. Certain
iron compounds are also reported to be genotoxic. Iron oxide enhances the
carcinogenic action of various organic carcinogens (benzo[a]pyrene for
example) and may act as a tumor promoter.. Local sarcomas have been induced by
subcutaneous injection of iron-dextran (EPA 1984). • .
The National Research Council of the National Academy of Sciences (NRG 1980)
has suggested the recommended dietary allowances (RDAs) for iron of between 10
and 60 mg. Therefore, the maximum recommended daily intake of iron can be
used as a conservative allowable intake for chronic exposure. No .health based
criteria have been deri-ved by EPA.
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Effects Assessment for Iron. Environmental Criteria and Assessment Office, Cincinnati, Ohio. September 1984. ECA0-CIN-H054 (Final Draft)
NATIONAL RESEARCH COUNCIL (NRC) . 1980. Drinking Water a.nd Health. Safe Drinking Water Committee. National Academy Press, Washington, D.C. Vol. 3, 415 pp.
VENUGOPAL, B. and LUCKEY, T.D. 1978. Metal Toxicity in Mammals. In Chemical Toxicity of Metals and Metalloids. Plenum Press, New York.
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MANGANESE
Manganese is absorbed at low levels following oral or inhalation exposure (EPA
1984a). The effects following acute exposure to manganese are unknown.
Chronic oral and inhalation exposure of humans to high levels of manganese
causes pneumonitis in exposed workers and has been associated with a condition
known as manganism, a progressive neurological disease characterized by speech
disturbances, tremors, and difficulties in walking (Kawamura et al. 1941).
Altered hematologic parameters (hemoglobin concentrations, erythrocyte counts)
have also been observed in persons exposed chronically. Chronic oral exposure
of rats to manganese chloride results in central nervous system dysfunction
(Leung et al. 1981, Lai et al. 1982). Manganese has not been reported to be
teratogenic; however, this metal has been observed to cause depressed
reproductive performance and reduced fertility in humans and experimental
animals (EPA 1984a). Certain manganese compounds have been shown to be
mutagenic in a variety of bacterial tests. Manganese chloride and potassium
permanganate caused chromosomal aberrations in mouse mammary carcinomal cells.
Manganese was moderately effective in enhancing viral transformation of Syrian
hamster embryo cells (EPA 1984a,b).
EPA (1989) established a chronic oral reference dose (RfD) of 2.0x10"^
mg/kg/day for manganese based on no observed adverse effects (NOAEL) in rats
exposed chronically to manganese in drinking water (Leung et al. 1981, Lai et
al. 1982). An uncertainty factor of 100 was used to derive the reference
dose. A subchronic oral RfD of 0.5 mg/kg/day was derived by EPA (1989) based
on a study by Laskey et al. (1982) in wich rats exposed to 52.5 mg/kg/day
manganese from day 1 of gestation through 224 days of age exhibited
reproductive effects. A safety factor of 100 was used to calculate the
subchronic RfD. EPA (1989) calculated an inhalation reference dose based upon
an occupational study conducted by Saric et al. (1977). Using a NOAEL of i
2,1 mg/day and an uncertainty factor of 100, an inhalation RfD of i co
3.0x10''' mg/kg/day was derived. Both the inhalation and oral intake values j ^
are based upon central nervous system effects (EPA 1989). o
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984a. Health Assessment Document for Manganese. Final Report. Environmental Criteria and Assessment Office, Environmental Protection Agency, Cincinnati. Ohio. August 1984. EPA 600/8-83-013F
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984b. Health Effects Assessment for Manganese (and compounds). Environmental Criteria and Assessment Office, Washington, D.C. EPA 540/1-86-057
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Guidelines for carcinogen risk assessment. Fed. Reg. 51:33992-34003 (September 24, 1986)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Environmental Assessment and Criteria Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washignton, D.C. April 1989
KAWAMURA, R., IKUTA, H., FUKUZUMI, S., et al. 1941. Intoxication by manganese in well water. Kitasato Arch. Exp. Med. 18:145-149
LAI, J.O.K., LEUNG, T.K.C, and LIM, L. 1982 Activities of the mitochondrial NAD-linked isocitric dehydrogenase in different regions of the rat brain. Changes in aging and the effect of chronic manganese chloride administration. Gerontology 28:81-85
LASKEY, J.W., REHNBERG, G.L., HEIN, J.F., CARTER, S.D. 1982. Effects of chronic manganese (Mn30 ) exposure on selected reproductive parameters in rats. J. Toxicol. Environ. Health 9;677-687
LEUNG, T.K.C, LAI, J.O.K., and LIM, L. 1981. The regional distribution of monoamine oxidase activities towards different substrates: Effects' in rat brain of chronic administration of manganese chloride and of aging. J. Neurochem. 36:2037-2043
SARIC, M., MARKICEVIC, S., and HRUSTIC, 0. 1977. manganese. Br. J. Ind. Med. 34:114-118
Occupational exposure to
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MERCURY
In humans, inorganic mercury is absorbed following inhalation and oral
exposure, however only 7% to 15% of administered inorganic mercury is absorbed
following oral exposure (EPA 1984, Rahola et al. 1971, Task Group on Metal
Accumulation 1973). Organic mercury is almost•completely absorbed from the
gastrointestinal tract and is assumed to be well absorbed via inhalation in
humans (EPA 1984). A primary target organ for inorganic compounds is the
kidney. • Acute and chronic exposures.of-humans to inorganic mercury compounds
have been associated with anuria, polyuria, proteinuria, and renal lesions
(Hammond and Bellies 1980). Chronic occupational exposure of workers to
elemental mercury vapors (0.1 to 0.2 mg/m'') has been associated with mental
disturbances, tremors, and gingivitis (EPA 1984). Animals exposed to
inorganic mercury for 12 weeks have exhibited proteinuria, nephrotic syndrome
and renal disease (Druet et al. - 1978). Rats chrpnically administered
inorganic mercury (as mercuric acetate) in their diet have exhibited decreased
body weights and significantly increased kidney weights (Fitzhugh et al.
1950). The central nervous system is a major target for organic mercury
compounds. Adverse effects in humans, resulting from subchronic and chronic
oral exposures to organic mercury compounds have included destruction of
cortical cerebral neurons, damage to Purkinje cells, and lesions of the
cerebellum.- Clinical symptoms following exposure to organic mercury compounds
have included paresthesia, loss- of sensation in extremities, ataxia, and
hearing and visual impairment (WHO 1976). Embryotoxic and teratogenic
effects, including malformations of the skeletal and genitourinary systems,
have been observed in animals exposed orally to organic mercury (EPA..1984).
Both organic and inorganic compounds are reported to be genotoxic in
eukaryotic systems (Leonard et al. 1984!).
EPA (1989). has reported both a chronic and subchronic oral RfD for alkyl and
inorganic mercury of 3x10'* mg/kg/day based on studies investigating central
nervous system effects in humans exposed, to mercury (EPA 1980); an uncertainty , W
factor-of 10 was used to develop the RfD. EPA (1989) has also reported a
chronic-and subchronic oral reference dose of 3x10'* mg/kg/day for inorganic o o
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mercury based on a chronic rat study in which kidney effects were observed
(Fitzhugh et al. 1950). An uncertainty factor of 1,000 was used to derive the
RfD.
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DRUET, P., DRUET", E., POTDEVIN,. F., and SAPIN ,• C 1978. Immune type glomerulonephritis induced by HgCl2 in the brown Norway rat. Ann. Immunol. 1290:777-792
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria Document for Mercury. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio for the Office of Water Regulation and Standards, Washington, D.C. EPA 440/5-80-058. NTIS PB 81-117699
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. -Health Effects Assessment for Mercury. Environmental Criteria and Assessment Office, Cincinnati, Ohio-. ' EPA 540/1-85-042 • •
ENVIRONMENTAL PROTECTION AGENCY (EPA). • 1989. Health Effects Assessment Summary Tables. Prepared .by Office of Health and Environmental Assessment. Environmental Assessment and Criteria Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Resposne, Office of Emergency and Remedial Response, Washington, D.C. April 1989
FITZHUGH, O.C, NELSON, A.A., LAUG, E.P., and KUNZE, F.M. 1950. Chronic oral toxicities of mercury-phenyl and mercuric salts. Arch. Ind. Hyg. Occup. Med 2:433-441
HAMMOND, P.B., and.BELILES, R.P. 1980. Metals. InDoull, J., Klaassen, CD., and;Ajndur, M.O., eds. Casarett and Doull's Toxicology: The Basic Science of Poisons. 2nd ed. Macmillan Publishing Co., New York. Pp. 421-428'
LEONARD,- A., GERBER, G.B., JACQUET, P., and LAUWERYS, R.R-. 1984. Mutagenicity, .carcinogenicity, and teratogenicity of industrially used metals. In Kirsch-Volders, M., ed. Mutagenicity, Carcinogenicity and Teratogenicity of Industrial Pollutants. Plenum Press, New York. Pp. 59-126
RAHOLA, T., HATTULA, T.,-KORLAINEN, A., AND MIETTINEN, J.K. 1971. The biological half time of inorganic mercury (Hg "*") in man. Scand. J. Clin. Invest. 27(suppl. 116):77 (Abstract)'
TASK GROUP ON METAL ACCUMULATION. 1973. Accumulation of toxic metals with special reference to their absorption, excretion and biological halftimes. Environ. Phys.- Biochem. 3:65-67
WORLD HEALTH ORGANIZATION (WHO).' 1976. Environmental Health Criteria, Mercury. Geneva ' ' f
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METHYLENE CHLORIDE (Dichloromethane)
Methylene chloride is absorbed following oral and inhalation exposure. The
amount of airborne methylene chloride absorbed following inhalation exposure
increases in direct proportion to its concentration in inspired air, the dura
tion of exposure, and physical activity. Dermal absorption has not been
accurately measured (EPA 1985a). Acute human exposure to methylene chloride
may result in irritation of eyes, skin, and respiratory tract; central nervous
system depression; elevated carboxyhemoglobin levels; and circulatory
disorders that may be fatal (EPA 1980). Chronic exposure of animals can
produce renal and hepatic toxicity (NCA 1982). Methylene chloride is
mutagenic for Salmonella cyphimurium and produces mitotic recombination in
yeast (EPA 1989A). Several inhalation studies conducted in animals provide
clear evidence of methylene chloride's carcinogenicity. There is only
suggestive evidence in experimental animals that hepatocellular carcinomas and
neoplastic nodules arise from oral exposure (EPA 1985a,b).
EPA (1989a) classified methylene chloride in Group B2--Probable Human Carcino
gen. It has been concluded by EPA (1985b) that the induction of distant site
tumors from inhalation exposure and the borderline significance for induction
of tumors in a drinking water study are an adequate basis for concluding that
methylene chloride be considered a probable human carcinogen via ingestion as
well as inhalation. EPA (1989a) derived an inhalation cancer potency factor
of 1.4x10'^ (mg/kg/day)'^ based on the results of a National Toxicology Program
(NTP) inhalation bioassay conducted in rats and mice (NTP 1986). Mammary tu
mors were noted in rats, while lung and liver tumors were observed in mice.
EPA (1989a) determined an oral cancer potency factor of 7.5x10''' (mg/kg/day)"^
based on the results of the NTP (1986) inhalation bioassay and on an ingestion
bioassay conducted by the National Coffee Association . (NCA 1983). In the NCA.
study, hepatocellular adenomas .and/or carcinomas were observed in male mice. _
Both a chronic and subchronic oral reference dose (RfD) of 0.06 mg/kg/day has CO
been developed by EPA (1989b) based on a 2-year rat drinking water bioassay | tq (NCA 1982) that identified no-observed-effect levels (NOELs) of 5.85 and 6.47
I o "•g/ g/day for male and female rats, respectively. Liver toxicity was observed j o
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at doses of 52.58 and 58.32 mg/kg/day for males and females, respectively. An
uncertainty factor of 100 was used to derive the RfD. EPA (1989b) has
established an inhalation RfD of 3 mg/m'' based on a study by Nitschke et
al. (1988) in which rats were exposed to 200 ppm (694.8 mg/rn^) for 2 years. A
safety factor of 100 was used to derive the RfD. This RfD is currently
undergoing verification by EPA (1989a).
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Halomethanes. Office of Water Regulations and Standards, Criteria and Standards Division, Washington, D.C. October 1980, EPA 440.5-80-051
ENVIRONMENTAL PROTECTION AGENCY-(EPA). 1985a. Health Assessment Document for Dichloromethane. Office of Health and Environmental Assessment,
• Washington, D.C. February 1985. EPA/600/8-82004F
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. Addendum to the Health Assessment Document for Dichloromethane. Office of Health and Environmental Assessment, Washington, D.C. September 1985. EPA/600/8-82-004F
ENVIRONMENTAL PROTECTION AGENCY (EPA). ' 1989a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised May 1, 1989
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989h. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment. Environmental Assessment and Criteria Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. March 1989
NATIONAL COFFEE ASSOCIATION (NCA). 1982. Twenty-four Month Chronic Toxicity and Oncogenicity Study of Methylene Chloride in Rats. Final Report. Prepared, by Hazelton Laboratories America, Inc., Vienna, Virginia. August 11, 1982
NATIONAL COFFEE ASSOCIATION (NCA). 1983. Twenty-fourth-Month Oncogenicity Study of Methylene Chloride in Mice. Unpublished report prepared by Hazelton Laboratories, Inc., Vienna, Virginia
NATIONAL TOXICOLOGY PROGRAM (NTP). 1986. NTP Technical Report on the Toxicology and Carcinogenesis Studies of Dichloromethane in F344/N Rats and B6C3F1 Mice (Inhalation Studies).. NTP TR306
NITSCHKE, K.D., BURED, J.D., BELL, T.J., et al. 1988. Methylene Chloride: A 2 year inhalation toxicity and oncogenicity study in rats. Fund. Appl. Toxicology (in press) (as cited by EPA 1989b)
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NICKEL
Nickel compounds can be absorbed following inhalation, ingestion, or dermal
exposure. The amount absorbed depends on the dose administered and the
chemical and physical form of the particular nickel compound (EPA 1986).
Dermal exposure of humans to nickel produces allergic contact dermatitis (EPA
1986). Adverse effects associated with acute exposure in animals have
included depressed weight gain, altered hematological parameters, and
increased iron deposition in blood, heart, liver, and testes (EPA 1987).
Chronic or subchronic exposure of experimental animals to nickel has been
associated with reduced weight gain, degenerative lesions.of the male
reproductive tract, asthma, nasal septal perforations, rhinitis, sinusitis,
hyperglycemia, decreased prolactin levels, decreased iodine uptake, and
vasoconstriction of the coronary vessels (EPA 1986). Teratogenic and
fetotoxic.effects have been observed in the offspring of exposed animals (EPA
1986). Inhalation exposure of experimental animals to nickel carbonyl or
nickel subsulfide induces pulmonary tumors (EPA 1986). Several nickel salts
cause localized tcunors when administered by subcutaneous injection or
implantation. Epidemiological evidence indicates that inhalation of nickel
refinery dust and nickel subsulfide is associated with cancers of the nasal
cavity, lung, larynx, kidney, and prostate (EPA 1986).
Nickel refinery dust and nickel subsulfide are both categorized in Group
A--Human Carcinogens. These classifications are based on an increase
incidence of lung and nasal tumors observed in workers occupationally exposed
to nickel refinery dust. These materials have inhalation cancer potency
factors of 0.84 (mg/kg/day)'^ and 1.7 (mg/kg/day)'\ respectively (EPA 1989a).
Nickel carbonyl is categorized in Group B2--Probable Human Carcinogen;
however, a potency factor has not been derived for nickel carbonyl (EPA
1989a). EPA (1989a) derived a chronic oral reference dose (RfD) for nickel of
2x10'^ mg/kg/day based on a study by Ambrose et al. (1976) in which rats , —
administered 5 mg/kg/day (NOAEL) nickel in the diet for 2 years did not . CO
experience decreased weight gain observed in animals administered 50 mg/kg/day; w
(LOAEL). A safety factor of 300 was used to calculate the RfD. A subchronic , I o
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oral RfD was also calculated from this same study using a safety factor of 300
(EPA 1989b) .
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AMBROSE. A.M., LARSON, P.S., BORZELLECA, J.R., and HENNIGAR, CR. 1976. Long-term toxicologic assessment of nickel in dogs and rats. J. Food Sci. Techriol. 13:181-187
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Health Assessment Document for 'Nickel and Nickel compounds. Office of Health and Environmental Assessment, Research Triangle Park, North Carolina. EPA 600/8-83-012FF
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisory for Nickel. Office for Drinking Water, Washington, D.C. March 31, 1987
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information •System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio... Revised May 1, 1989
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
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NITRATE/NITRITE
Both nitrate and nitrite are readily absorbed from the gastrointestinal tract
after oral exposure (EPA 1987). Following intratracheal instillation or i.v.
injection, nitrate is reduced to nitrite by bacteria in the stomach (Parks et
al. 1981). Nitrite reacts with hemoglobin in blood producing methemoglobin,
thereby reducing the oxygen-carrying ability of red blood cells: Oral
exposure to nitrite has been reported to result in acute toxic effects such as
nausea, palpitations, numbness, and cyanosis due to methemoglobinemia in
humans (EPA 1985, Walton 1951). Similar cardiovascular effects were observed
in animals following acute oral exposure to high levels of nitrate (EPA 1987) .
Ingestion of large doses of sodium nitrate and sodium nitrite resulted in
amyloidosis and hemosiderosis in ICR mice (EPA 1987). Chronic exposure to
both nitrate and nitrite may lead to central nervous system toxicity in
animals (EPA 1985). Nitrate and nitrite have not been associated with
teratogenic effects in humans or laboratory animals and studies completed on
livestock have not shown any relationship between nitrate and reproductive
effects. However, developmental effects such as growth retardation and
histological abnormalities of the liver, lungs and spleens were obseirved in a
three-generation study in rats following oral ingestion of nitrite (EPA 1985) .
An oral reference dose (RfD) of 1 mg/kg/day and 0.1 mg/kg/day for nitrate and
nitrite respectively have been derived by EPA (1989). These values were based
on an epidemiologic study by Walton (1951) in which the occurrence of
methemoglobinemia was evaluated in infants that consumed formula that was
prepared with water containing various levels of nitrate. A no-observed-'
effect-level (NOAEL) of 1.0 mg/kg/day was derived for both nitrite and nitrate
and a safety factor of 1 and 10 were used in the calculation of the RfD's for
nitrate and nitrite respectively (EPA 1989).
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Final Draft for the Drinking Water Criteria Document on Nitrate/Nitrite. Prepared for the Criteria and Standard Division, Office of Drinking Water, Washington, D.C. PB86-117959
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisory: Nitrate/Nitrite. Office of Drinking WAter. Washington, D.C. (March 31 1987)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised June 1, 1989
PARKS, N., KROHN, K., MATHIS, C , CHASKO, J., GEIGER, K., GREGOR, M., and PEEK, N. 1981. Nitrogen 13-labeled nitrite and nitrate: Distribution and metabolism after intratracheal administration. Science 212:58-61 (As cited in EPA 1987)
WALTON, C 1951. Survey of literature relating to infant methemoglobinemia due to nitrate-contaminated water. Am. J. Public Health. 41:986-996
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PHENOL
Phenol is readily absorbed through the gut, by inhalation, and percutaneously
(EPA 1980). Signs of acute phenol toxicity in humans and experimental animals
are central nervous system depression, collapse, coma, cardiac arrest, and
death. Acutely toxic doses can also cause extensive necrosis at the site of
exposure (eyes, skin, oropharynx) (EPA 1980). In experimental animals
subchronic oral and inhalation studies suggest that kidney, pulmonary,
myocardial,' and liver damage are associated with exposure, although many of
these studies were poorly designed (EPA 1980, 1984). Oral administration of
phenol.to pregnant rats during gestational days 6 to 15 resulted in a
significant reduction in fetal body weight (NTP 1983). Phenol exhibited
tumor-promoting activity in the mouse skin painting system following
initiation with 9,10-dimethyl-l,2-ben2anthracene (DMBA) or benzo[a]pyrene
(B[a]P), and it exhibited cutaneous carcinogenic activity in a sensitive mouse
strain when applied at concentrations that produced repeated skin damage (EPA
1980).
EPA (1989a) has established an oral reference dose (RfD) of 0.6 mg/kg/day for
phenol based on reduced fetal body weight in rats (NTP 1983). A no-observed-
adverse-effect level (NOAEL) of 60 mg/kg/day and a safety factor of 100 were
used to derive RfD. EPA (1989b).reported a subchronic RfD of 0.6 mg/kg/day
also based on the same NTP (1983) study; a safety factor of 100 was used to
derive the RfD. EPA has not yet established an inhalation RfD (EPA 1989).
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Phenol. Office of Water Regulations and Standards, Criteria and Standards Division, Washington, D.C. October 1980. EPA 440/5-80-066
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Effects Assessment for '. Phenol. Environmental Criteria and Assessment Office, Cincinnati, Ohio. September 1984. EPA 540/1-86-007
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio (Revised June 1, 1989)
ENVIRONMENTAL PROTECTION AGENCY (EPA).' I989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Envirorimental Criteria and Assessment Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
NATIONAL TOXICOLOGY PROGRAM (NTP). 1983. Teratologic evaluation of phenol in CD rats and mice. Report prepared by Research Triangle Institute, Research Triangle Park, NC. NTIS PB83-247726. Gov. Rep. Announce. Index 83(25):5247 •
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SELENIUM
Results of studies with humans and experimental animals indicate that certain
selenium compounds are readily absorbed from the gastrointestinal tract
following oral exposure (EPA 1984). The pulmonary absorption of selenium
following inhalation exposure has not been well studied, although there are
reports suggesting that selenium is absorbed to some extent by this route (EPA
1984). Selenium is an essential element and therefore is nontoxic at doses
necessary for normal health and nutrition. NAS (1980) reported that an
adequate and safe selenium intake for an adult human ranges from 0.05 mg/day
to 0.2 mg/day. However, exposure to selenium at levels that exceed these
standards has been associated with adverse health effects. Such effects
observed in experimental animals following subchronic or chronic oral exposure
to various selenium compounds have included anemia, reduced growth, increased
mortality, and lesions of the liver, heart, kidney, and spleen (EPA 1984). In
humans, chronic oral exposure to selenium has been associated with alopecia,
dermatitis, discoloration of the skin, loss of fingernails, muscular
dysfunction, convulsions, paralysis, and increased incidences of dental caries
(EPA 1984). Headaches and respiratory irritation have been noted in humans
following acute inhalation exposure (EPA 1984). Studies with a variety of
animals have suggested that selenium may be teratogenic; however, these
studies are limited in that exposure levels are not well characterized (EPA
1984).
Chronic oral and inhalation reference doses (RfD) of S.OxlO''' mg/kg/day and
l.OxlO''' mg/kg/day, respectively, have been derived by EPA (1984, 1989). The
oral RfD value was based on a study by Yang et al. (1983) in which humans
exposed to selenium in the diet at doses of 3.2 mg/day developed loss of hair,
loss of fingernails, dermatitis, and muscular dysfunction. By applying an
uncertainty factor of 15 and a LOAEL of 3.2 mg/day,-EPA (1989) determined the
oral RfD value of 3x10'^ mg/kg/day. The oral RfD is currently under review by
the oral RfD Work Group at EPA (1989). A subchronic oral RfD was calculated
by EPA (1989) based on increased mortality in rats administered 0.4 mg/kg/day
for 6 weeks (Halverson et al. 1966). A safety factor of 100 was used to
CO Cd >
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derive the RfD. The inhalation RfD value was based on an occupational study
by Glover (1967) in which workers exposed to airborne concentrations of
selenium developed dermatitis and gastrointestinal disturbances. An
uncertainty factor of 10 was used to determine the inhalation RfD (EPA 1989).
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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Effects Assessment for Selenium (and Compounds). Office of Emergency and Remedial Response, Washington, D.C. EPA 540/1-86-058. September 1984
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Environmental Assessment and Criteria Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
GLOVER, J.R. 1967. Selenium in human urine: A tentative maximum allowable concentration for industrial and rural populations. Ann. Occup. Hyg. 10:3-10
NATIONAL ACADEMY OF SCIENCES (NAS). 1980. Drinking Water and Health. National Academy Press, Washington, D.C. Vol. 3
YANG, C , WANG, S., ZHOU, R. , and SUN, S. 1983. Endemic selenium intoxication of humans in China. Am. J. Clin. Nutr. 37:872-881
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SILVER
Silver in various forms is absorbed to a limited extent following oral and
inhalation exposures (EPA 1985). The acute toxic effects in humans following
oral exposure to silver include corrosive damage to the GI tract leading to
shock, convulsions, and death. In animals, acute exposure has been shown to
affect the central nervous system and to cause respiratory paralysis (Hill and
Pillsbury 1939). The primary effect of silver in hLunans following chronic
exposures, 'is argyria, a permanent bluish-metallic discoloration of the skin
and mucous membranes, which can be either localized or generalized. Silver
also accumulates in the blood vessels and connective tissue (EPA 1985).
EPA (1989) derived an oral reference dose (RfD) of 3.0x10"^ mg/kg/day for
silver based on the human case reports of Gaul and Staud (1935), Blumberg and
Carey (1934), and East et al. (1980). In these studies, argyria was observed
at an average dose of silver of 0.0052 mg/kg/day, to which an uncertainty
factor of 2 was applied.
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BLUMBERG, H. and CAREY, t.N. 1934. Argyremia: Detection of unsuspected and obscure argyria by the spectrographic demonstration of high blood silver. J'. Am. Med. Assoc. 103:1521-1524
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Drinking Water Criteria Document for Silver. Environmental Criteria and Assessment Office, Cincinnati, Ohio. PB 86-118288
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised June 1, 1989
EAST, B.W., BODDY,'K., WILLIAMS, E.D., MACINTYRE, D. and McLAY, A.L.C 1980. Silver retention, total body silver and tissue silver concentrations in argyria associated with exposure to an anti-smoking remedy containing silver acetate. Clin. Exp. Dermatol. 5:305-311
GAUL, L.E. and STAUD, A.H. 1935. Clinical spectroscopy. Seventy cases of generalized argyrosis following organic and colloidal silver medication. J. Am. Med. Assoc. 104:1387-1390
HILL, W.R. and PILLSBURY-, D.M. 1939. Argyria, the Pharmacology of Silver. Williams and Wilkins Co.-, Baltimore, Maryland.
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TETRACHLOROETHYLENE
Tetrachloroethylene is absorbed following inhalation (lARC 1979) and oral (EPA
1985a,b). exposure. Tetrachloroethylene vapors and liquid also can be absorbed
through the skin (EPA 1985a,b). The principal toxic effects of tetrachloro
ethylene in humans and animals following acute and longer-term exposures in
clude central nervous system (CNS) depression and fatty infiltration of the
liver and kidney with concomitant changes in serum enzyme activity levels in
dicative of tissue damage (EPA 1985a,b). Humans exposed to doses of between
136 and 1,018 mg/m- for 5 weeks develop central ner-vous system effects, such
as lassitude and signs of inebriation (Stewart et al. 1974). The offspring of
female rats and mice exposed to high concentrations of tetrachloroethylene for
7 hours daily on days- 6-15 of gestation developed toxic effects, including a
decrease in fetal body weight in mice and a small but significant increase in
fetal resorption in rats (Schwetz et al. 1975). Mice also exhibited develop
mental effects, including subcutaneous edema and delayed ossification of skull
bones and sternebrae (Schwetz et al. 1975). In a National Cancer Institute
bioassay (NCI 1977), increased incidences of hepatocellular carcinoma was
observed in both sexes of B6C3F1 mice administered tetrachloroethylene in corn
oil by gavage for 78 weeks. Increased incidences of mononuclear cell leukemia
and. renal adenomas and carcinomas (combined) have also been observed in long
term bioassays in which rats were exposed to tetrachloroethylene by inhalation
(NTP. 1986):.
EPA (1989b) classifies tetrachloroethylene as a Group B2 carcinogen (Probable
Human Carcinogen). EPA (1989a, 1985b) has derived an oral cancer potency - 2 - 1
factor (q,*) of 5.1x10 (mg/kg/day) based on liver tumors observed in the
NCI (1977) gavage bioassay for mice. The inhalation cancer potency factor for
tetrachloroethylene of 3.3x10'^ (mg/kg/day)'^ is based on an NTP (1986) bio
assay in rats and mice in which leukemia and liver tumors were observed (EPA
1989b). Both cancer potency factors are currently under review by EPA
(1989a). EPA (1989a,b) also has derived a chronic oral reference dose (RfD)
of 1x10'^ mg/kg/day for tetrachloroethylene based on a gavage study by Bubert
and O'Flaherty (1985). In this study, liver weight/body weight ratios were
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significantly increased in mice and rats treated with 71 mg/kg/day
tetrachloroethylene but not in animals treated with 14 mg/kg/day. Using a
NOAEL of 14 mg/kg/day and applying an uncertainty factor of 1,000, the RfD was
derived. EPA (1989b) has also derived a subchronic RfD of 0.1 mg/kg/day based
on the same Buben and O'Flaherty (1985) study; a safety factor of 100 was used
to calculate the RfD.
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BUBEN, J.A., and O'FLAHERTY, E.J. 1985. Delineation of the role of metabolism in the hepatotoxicity of trichloroethylene and perchloroethylene: A dose-effect study. Toxicol. Appl. Pharmacol. 78:105-122 . -
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985a. Health Assessment '-Document for Tetrachloroethylene (Perchloroethylene). Office of Health and Environmental Assessment, Washington, D.C. July 1985. EPA 600/8-82-O05F'
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. Drinking Water Criteria Document for Tetrachloroethylene. Office of Drinking Water, Criteria and Standards Division, Washington, D.C. April 1985
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). . Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised May 1, 1989 \
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office, of Health and Environmental Assessment, Environmental Assessment and Criteria Office, Cincinnati, Ohio, for the Office of Solid Waste and- Emergency Response, Office of Remedial Response, Washington, D.C. March 1989
INTERNATIONAL AGENCY FOR RESAERCH ON CANCER (lARC). 1979. lARC Monographs on the evaluation of the carcinogenic risks of chemicals to humans. Vol. 20: Some Halogenated Hydrocarbons. World Health Organization, Lyon France
NATIONAL CANCER INSTITUTE (NCI). 1977. Bioassay of Tetrachloroethylene for Possible Carcinogenicity. CAS No. 127-18-4. NCt Carcinogenesis Technical Report Series No. 13, Washington, D.C. DHEW (NIH) Publication No. 77-813
NATIONAL TOXICOLOGY PROGRAM (NTP). 1986. Toxicology and Carcinogenesis Studies of Tetrachloroethylene (Perchloroethylene) (CAS No. 127-18-4) in F344/N Rats and B6C3F1 Mice (Inhalation Studies). NTP Technical Report Series No. 311, Research Triangle Park, North Carolina. DHEW (NIH) Publication No. 86-2567
SCHWETZ, B.A., LEONG, B.K.J., and GEHRING, P.J. 1975. The effect of maternally inhaled trichloroethylene, perchloroethylene, methyl chloroform, and methylene chloride on embryonal and fetal development in mice and rats. Toxicol. Appl. Pharmacol. 55:207-219
STEWART, R.D., HAKE, C.L., FORSTER, H.V., LEBRUN, A.J., PETERSON, J..F., and WU, A. 1974. Tetrachloroethylene: Development of a biologic standard, for the industrial worker by breath analysis.• Medical College of ; Wisconsin, Milwaukee, Wisconsin. NIOSH-MCOW-ENUM-PCE-74-6 '' ^
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THALLIUM
Thallium and its salts are readily and rapidly absorbed through the skin,
lungs, and mucous membranes of the mouth and gastrointestinal tract.
Percutaneous absorption has also been reported to occur through rubber gloves
(Rumack 1986). Thallium is acutely toxic to humans regardless of the chemical
form of the compound or route of administration. Hundreds of cases of
thallotoxicosis due to ingestion of thallium-based pesticides have been
reported (ACGIH 1985) . Children poisoned by thallium ingestion have exhibited
neurological abnormalities including mental retardation and psychoses (ACGIH
1986). The effects of thallium toxicity are similar in humans and animals.
The most commonly noted response to thallium exposure is alopecia, but
neurological and gastrointestinal findings are frequently found. Such effects
include ataxia, lethargy, painful extremities, peripheral neuropathies,
convulsions, endocrine disorders, psychoses, nausea, vomiting, and abdominal
pains (Bank 1980). It has been noted that the degree and duration of exposure
to thallium and its salts can influence the clinical picture of thallium
intoxication. Subchronic feeding studies conducted with weanling rats observed
marked growth depression and a nearly complete loss of hair (Clayton and
Clayton 1981) . Exposure to thallium salts during critical developmental stages
in chicks and rats has been reported to be associated with the induction of
adverse developmental outcomes (Karnofsky et al. 1950). Pre- and postnatally
exposed rat pups have exhibited hydronephrosis, fetal weight reduction and
growth retardation (Clayton and Clayton 1981, Gibson and Becker 1970).
Thallium has also been shown to cross the placenta and, presumably, enter the
fetal blood system (Clayton and Clayton 1981) . Thallium has not been
demonstrated to be carcinogenic in humans or experimental animals and may have
some antitumor activity (Clayton and Clayton 1981) .
EPA (1989b) developed a chronic oral reference dose (RfD) of 7x10" mg/kg/day
for thallium in soluble salts based on a subchronic feeding study in which rats
received 0.20 mg/thallium/kg/day administered as thallium sulfate (.HRI 1986,
EPA 1986). Increased blood chemistry parameters (SCOT and serum LDH) and CO Cd >
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alopecia were observed. An uncertainty factor of 3,000 was used to calculate
the RfD. A subchronic oral RfD of 7.0x10''' for thallium in soluble salts was
also derived by EPA (1989b) based on the same studies and parameters. A safety
factor of 300 was used in calculating the subchronic RfD. EPA (1989a) also
derived oral RfDs for certain thallium salts (i.e., thallium acetate, thallium
carbonate, thallium chloride, thallium nitrate, thallium seleinte and thallium
(I) sulfate) of between 8-9x10' mg/kg/day based on the same EPA (1986) 90 day
subchronic rat study. The same endpoints of toxicity were observed and an
uncertainty factor of 3,000 was used to derive the RfDs.
CO Cd >
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AMERICAN CONFE.RENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1986.. "Documentation of the Threshold-Limit Values and Biological Exposure Indices. ACGIH, Cincinnati, Ohio
BANK, W.J. 1980. Thallium. In Spencer, P.S., and Schaumberg, H.H., eds. Experimental and Clinical Neurotoxicology. Williams and Wilkins, Baltimore. P. 571
CLAYTON, C D . , and CLAYTON, F.E., eds. 1981. Patty's Industrial Hygiene and Toxicology. 3rd ed. John Wiley and Sons, New York. P. 1915
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Subchronic (90-day) toxicity of thallium (I) sulfate in Sprague-Dawley rats. Final Report. Prepared for the Office of Solid Waste, U.S. EPA, Washington, D.C. Project No. 8702-1(18) . • ,
ENVIRONMENTAL PROTECTION AGENCY (EPA): 1989a. Integrated'Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised June 1, 1989 .' • '
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Criteria Office, Cincinnati,-Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response. Washington, D.C. April 1989
GIBSON, J.E., and BECKER, B.A. 1970. Placental transfer, embryo toxicity, and teratogenicity of thallium sulfate in normal and potassium-deficient rats. Toxicol. Appl. Pharmacol. 16:120-132
KARNOFSKY, D.A., RIDGWAY, L.P., and PATTERSON, P.A. 1950. Production of • achondroplasia in the chick embryo with thallium. Proc. Soc. Exp. Biol. • Med. 73:255-259
MIDWEST RESEARCH INSTITUTE (MRI).' 1986. Subchronic (90-day) toxicity study of thallium sulfate in Sprague-Dawley rats. Off ice ' of Solid Wastre . U. S . EPA Washington, D.C : •
RUMACK, B.H., ed. 1986. Poisindex. Microfiche ed. Micromedix, Inc., Denver, Colorado, in association with the National Center for Poison Information, with updates, 1975-present
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TOLUENE
Toluene is absorbed in humans following both inhalation and dermal exposure
(EPA 1985). In humans, the primary acute effects of toluene vapor are central
nervous system (CNS) depression and narcosis. These effects occur at
concentrations of 200 ppm (754 mg/m'') (von Oettingen et al. 1942a,b) . In
experimental animals, acute oral and inhalation exposures to toluene can
result in central nervous system (CNS) depression and lesions of the lungs,
liver, and kidneys (EPA 1987). The earliest observable sign of acute oral
toxicity in animals is depression of the CNS, which becomes evident at
approximately 2,000 mg/kg (Kimura et al. 1971). In humans, chronic exposure
to toluene vapors at concentrations of approximately 200 and 800 ppm has been
associated with CNS and peripheral nervous system effects, hepatomegaly, and
hepatic and renal function changes (EPA 1987) . Toxic effects following
prolonged exposure of experimental animals to toluene are similar to those
seen following acute exposure (Hanninen et al. 1976, von Oettingen et al.
1942a). A dose-related reduction in hematocrit values was observed in rats
chronically exposed to toluene (CUT 1980) . There is some evidence in mice
that oral exposure to greater than 0.3 ml/kg toluene during gestation results
in embryotoxicity (Nawrot and Staples 1979). Inhalation exposure of up to
1,000 mg/m'' by pregnant rats during gestation has been associated with
significant increases in skeletal retardation (Hudak and Ungvary 1978).
EPA (1989a) has derived an oral risk reference dose (RfD) of 0.3 mg/kg/day for
toluene based on a 24-month inhalation study in which rats were exposed to
concentrations as high as 300 ppm (29 mg/kg/day) and hematological parameters
were examined (CUT 1980). No adverse effects were observed in any of the
treated animals. Using a no-observed-adverse-effect level (NOAEL) of
29 mg/kg/day and an uncertainty factor of 100, the oral RfD was derived. EPA
(1989b) reported a subchronic RfD of 0.4 mg/kg/day based on a rat study
conducted by Wolf et al. (1956) in which central nervous system effects were .—
observed. A safety factor of 100 was used to derive the RfD. EPA (1989b)
also reported an inhalation RfD for toluene of 1.0 mg/kg/day based on this i W
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CUT (1980) study in which CNS effects were noted and an uncertainty factor of
LOO was used.
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CHEMICAL INDUSTRY INSTITUTE OF TOXICOLOGY (CUT). 1980. A Twenty-Four Month Inhalation Toxicology Study in Fischer 344 Rats Exposed to Atmospheric Toluene. Executive Summary and Data Tables. October 15, 1980
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Drinking Water Criteria Document for Toluene. Final Draft. Office of Drinking Water, Washington, D.C. March 1985
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisory for Toluene. Office of Drinking Water, Washington, D.C. March 1987
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk Information System' (IRIS). Environmental Criteria and Assessment Office,.Cincinnati, Ohio. Revised May 1, 1989
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Environmental Assessment and Criteria Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
HANNINEN, H., ESKELININ, L., HUSMAN, K., and'NUEIMINEEN, M. 1975. Behavioral effects of long-term exposure to a mixture of organic solvents. Scand. J. Work Environ. Health 2:240-255 (As cited in EPA 1987)
HUDAK, A., and UNGVARY, C 1978. Embryotoxic effects of benzene and its methyl derivatives: Toluene, xylene. Toxicology 11:55-63
KIMURA, E.T., EBERT, D.M., and DODGE, P.W. 1971. Acute toxicity and limits of solvent residue for sixteen organic solvents. Toxicol. Appl. Pharmacol. 19:699-704
NAWROT, P.S., and STAPLES, R.E. 1979. Embryo-fetal toxicity and teratogenicity of benzene and toluene in the mouse. Teratology 19:41A
VON OETTINGEN, W.F., NEAL, P.A.,. DONAHUE, D.D., et al. 1942a. The Toxicity and Potential Dangers of Toluene, with Special Reference to its Maximal Permissible Concentration. PHS Publication No. 279. P. 50 (As cited in EPA 1987)
VON OETTINGEN, W.F., NEAL, P.A., DONAHUE, D.D., et al. 1942b. The toxicity and potential dangers of toluene—preliminary report. J. Am. Med. Assoc. 118:579-584 (As cited in EPA 1987)
WOLF, M.A., ROWE, V.K., McCOLLISTER, D.D., et al. 1956. Toxicological ,-"—"', studies of certain alkylated benzenes and benzene. Arch. Ind. Health . i 14:387 (As cited in EPA 1985) '; CO
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TOLUENE
Toluene is absorbed in humans following both inhalation and dermal exposure,
(EPA 1985). In humans, the primary acute effects of toluene vapor are central
nervous system (CNS) depression and narcosis. These effects occur at
concentrations of 200 ppm (754 mg/m- ) (von Oettingen et al. 1942a,b). In
experimental animals, acute oral and inhalation exposures to toluene can
result in central nervous system (CNS) depression and lesions of the lungs,
liver, and kidneys (EPA 1987). The earliest observable sign of acute oral
toxicity in animals is depression of the CNS, which becomes evident at
approximately 2,000 mg/kg (Kimura et al. 1971). In humans, chronic exposure
to toluene vapors at concentrations of approximately 200 and 800 ppm has been
associated with CNS and peripheral nervous system effects, hepatomegaly, and
hepatic and renal function changes (EPA 1987) . Toxic effects following
prolonged exposure of experimental animals to toluene are similar to those
seen following acute exposure (Hanninen et al. 1976, von Oettingen et al.
1942a). A dose-related reduction in hematocrit values was observed in rats
chronically exposed to toluene (CUT 1980) . There is some evidence in mice
that oral exposure to greater than 0.3 ml/kg toluene during gestation results
in embryotoxicity (Nawrot and Staples 1979). Inhalation exposure of up to
1,000 mg/m'' by pregnant rats during gestation has been associated with
significant increases in skeletal retardation (Hudak and Ungvary 1978).
EPA (1989a) has derived an oral risk reference dose (RfD) of 0.3 mg/kg/day for
toluene based on a 24-month inhalation study in which rats were exposed to
concentrations as high as 300 ppm (29 mg/kg/day) and hematological parameters
were examined (CUT 1980). No adverse effects were observed in any of the
treated animals. Using a no-observed-adverse-effect level (NOAEL) of
29 mg/kg/day and an uncertainty factor of 100, the oral RfD was derived. EPA
(1989b) reported a subchronic RfD of 0.4 mg/kg/day based on a rat study .
conducted by Wolf et al. (1955) in which central nervous system effects were
observed. A safety factor of 100 was used to derive the RfD. EPA (1989b) (
also reported an inhalation RfD for toluene of 1.0 mg/kg/day based on this | co '• ^
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CUT (1980) study in which CNS effects were noted and an uncertainty factor of
100 was used.
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CHEMICAL INDUSTRY INSTITUTE OF TOXICOLOGY (CUT). 1980. A Twenty-Four Month Inhalation Toxicology Study in Fischer 344 Rats Exposed to Atmospheric Toluene. Executive Summary and Data Tables. October 15, 1980
ENVIRONMENTAL PROTECTION AGENCY (EPA).' 1985. Drinking Water Criteria Document for Toluene. Final Draft. Office of Drinking Water, Washington, D.C. March 1985
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisory for Toluene. Office of Drinking Water, Washington, D.C. March 1987
ENVIRONMENTAL PROTECTION .AGENCY (EPA). 1989a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised May 1, 1989
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects Assessment Summary Tables. Prepared by Office of Health and Environmental Assessment, Environmental Assessment and Criteria Office, Cincinnati, Ohio, for the Office of Solid Waste and Emergency Response, Office of Emergency and Remedial Response, Washington, D.C. April 1989
HANNINEN, H., ESKELININ, L., HUSMAN, K., and NURMINEEN, M. 1976. Behavioral effects of long-term exposure to a mixture of organic solvents. Scand. J. Work Environ. Health 2:240-255 (As cited in EPA 1987)
HUDAK, A., and UNGVARY, C 1978. Embryotoxic effects of benzene and its methyl derivatives: Toluene, xylene. Toxicology 11:55-63
KIMURA, E.T., EBERT, D.M., and DODGE, P.W. 1971.. Acute toxicity and limits of solvent residue for sixteen organic solvents. Toxicol. Appl. Pharmacol. 19:699-704
NAWROT, P.S., and STAPLES, R.E. 1979. Embryo-fetal toxicity and teratogenicity of benzene and toluene in the mouse. Teratology 19:41A
VON OETTINGEN, W.F., NEAL, P.A., DONAHUE, D.D., et al. l?42a. The Toxicity and Potential Dangers of Toluene, with Special Reference to its Maximal Permissible Concentration. PHS Publication No. 279. P. 50 (As cited in EPA 1987)
VON OETTINGEN, W.F., NEAL, P.A., DONAHUE, D.D., et al. 1942b. and potential dangers of toluene—preliminary report. J. 118:579-584 (As cited in EPA 1987)
The toxicity Am. Med. Assoc
WOLF, M.A., ROWE, V.K., McCOLLISTER, D.D., et al. 1956. Toxicological studies of certain alkylated benzenes and benzene. Arch. Ind. Health 14:387 (As cited in EPA 1985) CO
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TRICHLOROETHYLENE
Absorption of trichloroethylene (TCE) from the gastrointestinal tract is
virtually complete. Absorption following inhalation exposure is proportional
to concentration and duration of exposure (EPA 1985). TCE is a central
nervous system depressant following acute and chronic exposures. In humans,
single oral doses of 15 to 25 ml (21 to 35 grams) of TCE have resulted in
vomiting and abdominal pain, followed by transient unconsciousness (Stephens
1945). High-level exposure can result in death due to respiratory and cardiac
failure (EPA 1985). Hepatotoxicity has been reported in human and animal
studies following acute exposure to TCE (EPA 1985). Nephrotoxicity has been
observed in animals following acute exposure to TCE vapors (ACGIH 1986,
Torkelson and Rowe 1981). Subacute inhalation exposures of mice have resulted
in transient trichloroethylene-induced increased liver weights (Kjellstrand et
al. 1983). Industrial use of TCE is often associated with adverse
dermatological effects including reddening and skin burns on contact with the
liquid form, and dermatitis resulting from vapors. These effects are usually
the result of contact with concentrated solvent, however, and no effects have
been reported after exposure to TCE in dilute, aqueous solutions (EPA 1985).
Trichloroethylene has caused significant increases in the incidence of
hepatocellular carcinomas in mice (NCI 1976) and renal tubular-cell neoplasms
in rats exposed by gavage (NTP 1983), and pulmonary adenocarcinomas in mice
following inhalation exposure (Fukuda et al. 1983). Trichloroethylene was
mutagenic in S a l m o n e l l a C y p h i m u r i u m and in E. c o l i (strain K-12), utilizing
liver microsomes for activation (Greim et al. 1977).
EPA (1989) classified trichloroethylene in Group B2--Probable Human Carcinogen
based on inadequate evidence in humans and sufficient evidence of
carcinogenicity from animals studies. An oral cancer potency factor of .3
1.1x10'^ (mg/kg/day)'^ and an inhalation cancer potency factor of 4.6x10 -1 ' ' ~
(mg/kg/day) (EPA 1984) have been derived for trichloroethylene based on the mouse liver tumor data in the NCI (1976) and NTP (1983) gavage studies. EPA ^
-3 ' > (1987) developed an oral reference dose (RfD) of 7.35x10 mg/kg/day based on .
a subchronic inhalation study in rats in which elevated liver weights were | o 1 Ji
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observed following exposure to 55 ppm^ 5 days/week for 14 weeks (Kimmerle and
Eben 1973). A safety factor of 1,000 was used to calculate the RfD.' However,
this RfD is currently under review by EPA.
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AMERICAN CONFERENCE OF GOVERNME.N'TAL INDUSTRIAL HYGIENISTS (ACGIH). 1986. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. ACGIH, Cincinnati, Ohio
ENVIRONMENTAL PROTECTION AGENCY (EPA'). 1984. Health Effects Assessment for Trichloroethylene. Environmental Criteria and Assessment Office, Cincinnati, Ohio. EPA 540/1-86-045
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Health Assessment Document for Trichloroethylene. Environmental Criteria and Assessment Office. Research Triangle Park, North Carolina. EPA/600/8-82/006F
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisory for Trichloroethylene. Office of Drinking Water, Washington, D.C. March 31, 1987
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised May 1, 1989
FUKUDA, K., TAKEMOTO, K., andTSURUTA, H. 1983. Inhalation carcinogenicity of trichloroethylene in mice and rats. Ind. Health 21:243-254
GREIM, H., BIMBOES, D., EGERT, C , GIGGELMANN, W., and KRAMER, M. 1977. Mutagenicity and chromosomal aberrations as an analytical tool for in vitro detection of mammalian enzjmie-mediated formation of reactive metabolites. Arch. Toxicol. 39:159
KIMMERLEE, C , and EBEN, A. 1973. Metabolism, excretion and toxicology of trichloroethylene after inhalation. 1. Experimental exposure on rat. Arch. Toxicol. 30:115
KJELLSTRAND,P., HOLQUIST,B., ALM,P., KANJE, M., ROMARE, S., JONSSON, I., MANNSON, L., and BJERKEMO, M. 1983. Trichloroethylene: Further studies of the effects on body and organ weights and plasma butyl cholinesterase activity in mice. Acta. Pharmacol. Toxicol. 53:375-384 (As cited in EPA 1985)
NATIONAL CANCER INSTITUTE (NCI). 1976. Carcinogenesis Bioassay of Trichloroethylene. CAS No. 79-01-6. Carcinogenesis Technical Report Series No. 2. PB-264 122
NATIONAL TOXICOLOGY PROGRAM (NTP). 1983. Carcinogenesis Studies of Trichloroethylene (Without Epichlorohydrin), CAS No. 79-01-6, in F344/N rats and B6C3F mice (Gavage Studies). Draft. August 1983. NTP 81-84, NTP TR 243.
/' STEPHENS, C 1945. Poisoning by accidental drinking of trichloroethylene. ;
Br. Med. J. 2:218 V cn PI
1. t> TORKELSON, T.R., and ROWE, V.K. 1981. Halogenated aliphatic hydrocarbons. \
In Clayton, CD., and Clayton, P.B., eds. Patty's Industrial Hygiene am. o
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Toxicology. 3rd ed. John Wiley and Sons, New York. Vol. 2B, Pp. 3553-3559
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POLYCYCLIC AROMATIC HYDROCARBONS (Carcinogenic)
PAHs occur in the environment as complex mixtures containing numerous PAHs of
varying carcinogenic potencies. Only a few components of these mixtures have
been adequately characterized, and only limited information is available on
the relative potencies of different compounds.
PAH absorption following oral exposure is inferred from the demonstrated
toxicity of PAHs following ingestion (EPA 1984a). PAH absorption following
inhalation exposure is inferred from the demonstrated toxicity of PAHs
following inhalation (EPA 1984a). PAHs are also absorbed following dermal
exposure (Kao et al. 1985). It has been suggested that simultaneous exposure
to carcinogenic PAHs such as benzo[a]pyrene and particulate matter can
increase the effective dose of the compound (ATSDR 1987). Acute effects from
direct contact with PAHs and related materials are limited primarily to
phototoxicity; the primary effect is dermatitis (NIOSH 1977). PAHs have also
been shown to cause cytotoxicity in rapidly proliferating cells throughout the
body; the hematopoietic system, lymphoid system, and testes are frequent
targets (Santodonato et al. 1981). Destruction of the sebaceous glands.,
hyperkeratosis, hyperplasia, and ulceration have been observed in mouse skin
following dermal application of the carcinogenic PAHs (Santodonato et
al. 1981). The carcinogenic PAHs have also been shown to have an
immunosuppressive effect in animals (ATSDR 1987). Nonneoplastic lesions have
been observed in animals exposed to the more potent carcinogenic PAHs but only
after exposure to levels well above those required to elicit a carcinogenic
response. Carcinogenic PAHs are believed to induce tumors both at the site of
application and systemically. Neal and Rigdon (1967) reported that oral
administration of 250 ppm benzo[a]pyrene for approximately 110 days led to
forestomach tumors in mice. Thyssen et al. (1981) observed respiratory tract
tumors in hamsters exposed to up to 9.5 mg/m'' benzo [a] pyrene for up to 96
u • 7 " ' weeks.
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Benzo[a]pyrene is representative of the carcinogenic PAHs and is classified bv
EPA in Group B2--Probable Human Carcinogen--based on sufficient evidence of i o
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carcinogenicity from animal studies and inadequate evidence from
epidemiological studies (EPA 1984|c) . EPA (1984a) calculated an oral cancer
potency factor of 11.5 (mg/kg/day) for carcinogenic PAHs (specifically
benzo[a]pyrene) based on the study by Neal and Rigdon (1967). EPA (1984a)
calculated an inhalation cancer potency factor of 6.1 (mg/kg/day) for
benzo[a]pyrene based on the study by Thyssen et al. (1981). These potency
factors are currently undergoing a reevaluation based on recalculation of the
data (EPA 1989).
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AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY (ATSDR). 1987. Draft Toxicological Profile for Benzo[ajpyrene. October 1987
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984a. Health Effects Assessment for Polycyclic Aromatic Hydrocarbons (PAHs). Environmental Criteria and Assessment Office, Cincinnati, Ohio. September 1984. EPA 540/1-85-013
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984c. Health Effects Assessment for Benzo[a]pyrene. Environmental Criteria and Assessment Office, Cincinnati, Ohio. September 1984. EPA 540/1-86-022
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Health and Environmental Effects Profile for Naphthalene. Environmental Criteria and Assessment Office, Cincinnati, Ohio
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio. Revised May 1, 1989
KAO, J.K., PATTERSON, F.K., and HALL, J. 1985. Skin penetration and metabolism of topically applied chemicals in six mammalian species including man: An i n vitro study with benzo[a]pyrene and testosterone. Toxicol. Appl. Pharmacol. 81:502-515 (As cited in ATSDR 1987)
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1977. Criteria for a Recommended Standard--Occupational Exposure to Coal Tar Products. DHEW (NIOSH) 78-107
NEAL, J., and RIGDON, R.H. 1967. Gastric tumors in mice fed benzo(a)pyrene: A quantitative study. Tex. Rep. Biol. Med. 25:553-557
SANTODONATO, J., HOWARD, P., and BASU, D. 1981. Health and ecological assessment of polynuclear aromatic hydrocarbons. J. Environ. Pathol. Toxicol. 5:1-364
THYSSEN, J., ALTHOFF, J., KIMMERLE, G., and MOHR, U. .1981. Inhalation . studies with benzo(a)pyrene in Syrian golden hamsters. J. Natl. Cancer Int. 66:575-577
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H2MGROUP HOLZMACHER, McLENDON & MURRELL, P.C. CONSULTING ENGINEERS • ARCHITECTS • PLANNERS • SCIENTISTS • SURVEYORS MELVILLE. N.Y. RIVERHEAD. N.Y. FAIRFIELD. N.J.
